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yesno | Is there high nucleotide diversity in the Drosophila suzukii species? | ['yes'] | [
"yes"
]
| ['Native to Asia, the soft-skinned fruit pest Drosophila suzukii has recently invaded the United States and Europe. The eastern United States represents the most recent expansion of their range, and presents an opportunity to test alternative models of colonization history. There are high levels of nucleotide diversity in this species and research suggests that the recent invasions of Europe and the continental United States are independent demographic events.', 'Yes, there is high nucleotide diversity in the Drosophila suzukii species. There is a lot of genetic diversity in this species, and it is thought that the recent expansion of the species into Europe and the continental United States are independent demographic events. This means that there is a high level of diversity within the species.', 'Yes, there is high nucleotide diversity in the Drosophila suzukii species. There is a lot of genetic diversity in this species, and it is thought that the recent expansion of the species into Europe and the Americas are independent demographic events.', 'Yes. There is high nucleotide diversity within the Drosophila suzukii species.', 'Yes. There is high nucleotide diversity within and between populations of Drosophila suzukii, as shown by the presence of 12.1% single-nucleotide variants and 43.6% double-stranded DNA.', 'Yes. There is high nucleotide diversity within and between populations of Drosophila suzukii, across all developmental stages examined from only one genome.', 'Yes. There is high nucleotide diversity within and between populations of Drosophila suzukii, manifesting both in gene expression patterns and genomic locations.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/25158796"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25158796",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 852,
"text": "Native to Asia, the soft-skinned fruit pest Drosophila suzukii has recently invaded the United States and Europe. The eastern United States represents the most recent expansion of their range, and presents an opportunity to test alternative models of colonization history. Here, we investigate the genetic population structure of this invasive fruit fly, with a focus on the eastern United States. We sequenced six X-linked gene fragments from 246 individuals collected from a total of 12 populations. We examine patterns of genetic diversity within and between populations and explore alternative colonization scenarios using approximate Bayesian computation. Our results indicate high levels of nucleotide diversity in this species and suggest that the recent invasions of Europe and the continental United States are independent demographic events. "
}
]
| 11 | BioASQ-training11b | null | null | 60290c2b1cb411341a00010a | 107 |
yesno | Has "RNA interference" been awarded Nobel prize? | ['yes'] | [
"yes"
]
| ['Since the first unequivocal description of RNA interference (RNAi) in 1998, it has remained one of the hottest topics under investigation, culminating in the award of a Nobel Prize to its discoverers in 2006.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/20717561",
"http://www.ncbi.nlm.nih.gov/pubmed/24235106",
"http://www.ncbi.nlm.nih.gov/pubmed/26648823",
"http://www.ncbi.nlm.nih.gov/pubmed/25048083"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20717561",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "Since the first unequivocal description of RNA interference (RNAi) in 1998, it has remained one of the hottest topics under investigation, culminating in the award of a Nobel Prize to its discoverers in 2006."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24235106",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 341,
"text": "RNA interference (RNAi) is considered one of the most powerful genomic tools which allows the study of drug discovery and understanding of the complex cellular processes by high-content screens. This field of study, which was the subject of 2006 Nobel Prize of medicine, has drastically changed the conventional methods of analysis of genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26648823",
"endSection": "abstract",
"offsetInBeginSection": 187,
"offsetInEndSection": 373,
"text": " Almost 10 years after Fire and Mello received the Nobel Prize for the discovery of this mechanism in flat worms, RNA interference is on the edge of becoming a new class of therapeutics."
}
]
| 6 | BioASQ-training6b | null | null | 58bbb68b22d3005309000015 | 108 |
yesno | Is abdominal pain a common symptom in autism? | ['yes'] | [
"yes"
]
| ['Yes, although there are no precise data. There is data that Lactase deficiency, not associated with intestinal inflammation or injury, is common in autistic children and may contribute to abdominal discomfort, pain and observed aberrant behavior.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23371507",
"http://www.ncbi.nlm.nih.gov/pubmed/22997101",
"http://www.ncbi.nlm.nih.gov/pubmed/22850932",
"http://www.ncbi.nlm.nih.gov/pubmed/21415091",
"http://www.ncbi.nlm.nih.gov/pubmed/21114016",
"http://www.ncbi.nlm.nih.gov/pubmed/19329445",
"http://www.ncbi.nlm.nih.gov/pubmed/14523189",
"http://www.ncbi.nlm.nih.gov/pubmed/12846385"
]
| [
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23371507",
"endSection": "sections.0",
"offsetInBeginSection": 222,
"offsetInEndSection": 381,
"text": "Participants included 132 children with ASD and 81 with special educational needs (SEN) but no ASD, aged 10-14 years plus 82 typically developing (TD) children"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23371507",
"endSection": "sections.0",
"offsetInBeginSection": 807,
"offsetInEndSection": 946,
"text": "The ASD group had significantly increased past vomiting and diarrhoea compared with the TD group and more abdominal pain than the SEN group"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22997101",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "Many children with autism spectrum disorders (ASDs) suffer from gastrointestinal problems such as diarrhoea, constipation and abdominal pain"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22850932",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "Children with autism spectrum disorders (ASD) experience high rates of anxiety, sensory processing problems, and gastrointestinal (GI) problems"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22850932",
"endSection": "sections.0",
"offsetInBeginSection": 963,
"offsetInEndSection": 1142,
"text": "The results indicate that anxiety, sensory over-responsivity and GI problems are possibly interrelated phenomenon for children with ASD, and may have common underlying mechanisms."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21415091",
"endSection": "sections.0",
"offsetInBeginSection": 699,
"offsetInEndSection": 883,
"text": "Lactase deficiency not associated with intestinal inflammation or injury is common in autistic children and may contribute to abdominal discomfort, pain and observed aberrant behavior."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21114016",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 160,
"text": "Autistic behavior is often accompanied by numerous disturbing symptoms on the part of gastrointestinal system, such as abdominal pain, constipation or diarrhea."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19329445",
"endSection": "sections.0",
"offsetInBeginSection": 152,
"offsetInEndSection": 386,
"text": "Information on children's stool patterns and gut symptoms collected by questionnaire at 4 weeks and at 6, 18, 30 and 42 months of age were available for 12,984 children from the Avon Longitudinal Study of Parents and Children (ALSPAC)"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19329445",
"endSection": "sections.0",
"offsetInBeginSection": 583,
"offsetInEndSection": 794,
"text": "Comparison of the ASD and control group during the first 3.5 years of life showed no major differences in stool colour or consistency, or in frequency of diarrhoea, constipation, bloody stools or abdominal pain."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14523189",
"endSection": "sections.0",
"offsetInBeginSection": 1654,
"offsetInEndSection": 2032,
"text": "Constipation is a frequent finding in children with gastrointestinal symptoms and autism, particularly in the rectosigmoid colon, often with acquired megarectum. The absence of any correlation between the clinical history and the degree of fecal impaction in autistic children confirms the importance of an abdominal radiograph in the assessment of their degree of constipation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12846385",
"endSection": "sections.0",
"offsetInBeginSection": 311,
"offsetInEndSection": 590,
"text": "In a sample of 137 children, age 24-96 months, classified as having autism or ASD by the Autism Diagnostic Observation Schedule-Generic, 24 percent had a history of at least one chronic gastrointestinal symptom. The most common symptom was diarrhea, which occurred in 17 percent."
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D015746",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D001321"
]
| null | 515debe7298dcd4e51000026 | 109 |
yesno | Is RET the major gene involved in Hirschsprung disease? | ['yes'] | [
"yes"
]
| ['The RET proto-oncogene is the major gene associated to Hirschsprung disease (HSCR) with differential contributions of its rare and common, coding and noncoding mutations to the multifactorial nature of this pathology.', 'RET is the major gene associated to Hirschsprung disease (HSCR) with differential contributions of its rare and common, coding and noncoding mutations to the multifactorial nature of this pathology ', 'RET is the major gene associated to Hirschsprung disease (HSCR) with differential contributions of its rare and common, coding and noncoding mutations to the multifactorial nature of this pathology ', 'RET is the major gene associated to Hirschsprung disease (HSCR) with differential contributions of its rare and common, coding and noncoding mutations to the multifactorial nature of this pathology ', 'RET is the major gene associated to Hirschsprung disease (HSCR) with differential contributions of its rare and common, coding and noncoding mutations to the multifactorial nature of this pathology ', 'RET is the major gene associated to Hirschsprung disease (HSCR) with differential contributions of its rare and common, coding and noncoding mutations to the multifactorial nature of this pathology '] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23372769",
"http://www.ncbi.nlm.nih.gov/pubmed/22574178",
"http://www.ncbi.nlm.nih.gov/pubmed/22131258",
"http://www.ncbi.nlm.nih.gov/pubmed/21995290",
"http://www.ncbi.nlm.nih.gov/pubmed/17965226",
"http://www.ncbi.nlm.nih.gov/pubmed/17108762",
"http://www.ncbi.nlm.nih.gov/pubmed/22584707",
"http://www.ncbi.nlm.nih.gov/pubmed/17397038",
"http://www.ncbi.nlm.nih.gov/pubmed/16441254",
"http://www.ncbi.nlm.nih.gov/pubmed/10790203",
"http://www.ncbi.nlm.nih.gov/pubmed/20598273",
"http://www.ncbi.nlm.nih.gov/pubmed/16986122",
"http://www.ncbi.nlm.nih.gov/pubmed/22344793",
"http://www.ncbi.nlm.nih.gov/pubmed/23400839",
"http://www.ncbi.nlm.nih.gov/pubmed/16448984",
"http://www.ncbi.nlm.nih.gov/pubmed/12865274",
"http://www.ncbi.nlm.nih.gov/pubmed/9727738",
"http://www.ncbi.nlm.nih.gov/pubmed/7883791",
"http://www.ncbi.nlm.nih.gov/pubmed/16877807",
"http://www.ncbi.nlm.nih.gov/pubmed/16816022",
"http://www.ncbi.nlm.nih.gov/pubmed/18285831",
"http://www.ncbi.nlm.nih.gov/pubmed/10664228"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23372769",
"endSection": "abstract",
"offsetInBeginSection": 284,
"offsetInEndSection": 477,
"text": "The RET proto-oncogene is the major gene associated to HSCR with differential contributions of its rare and common, coding and noncoding mutations to the multifactorial nature of this pathology"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22574178",
"endSection": "abstract",
"offsetInBeginSection": 282,
"offsetInEndSection": 465,
"text": "The RET proto-oncogene is the major gene for HSCR with differential contributions of its rare and common, coding and noncoding mutations to the multifactorial nature of this pathology"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22131258",
"endSection": "abstract",
"offsetInBeginSection": 156,
"offsetInEndSection": 238,
"text": "The rearranged during transfection gene (RET) is considered the major gene in HSCR"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21995290",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 209,
"text": "RET is the major gene associated to Hirschsprung disease (HSCR) with differential contributions of its rare and common, coding and noncoding mutations to the multifactorial nature of this pathology"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17965226",
"endSection": "abstract",
"offsetInBeginSection": 640,
"offsetInEndSection": 988,
"text": "While all Mendelian modes of inheritance have been described in syndromic HSCR, isolated HSCR stands as a model for genetic disorders with complex patterns of inheritance. The tyrosine kinase receptor RET is the major gene with both rare coding sequence mutations and/or a frequent variant located in an enhancer element predisposing to the disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22584707",
"endSection": "abstract",
"offsetInBeginSection": 264,
"offsetInEndSection": 545,
"text": " The rearranged during transfection (RET) proto-oncogene is the major susceptibility gene for Hirschsprung disease, and germline mutations in RET have been reported in up to 50% of the inherited forms of Hirschsprung disease and in 15-20% of sporadic cases of Hirschsprung disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16441254",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 209,
"text": "The RET proto-oncogene is the major gene involved in the complex genetics of Hirschsprung disease (HSCR), or aganglionic megacolon, showing causative loss-of-function mutations in 15-30% of the sporadic cases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20598273",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 88,
"text": "The major gene for Hirschsprung disease (HSCR) encodes the receptor tyrosine kinase RET."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17108762",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "The RET proto-oncogene is considered to be the major susceptibility gene involved in Hirschsprung disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16986122",
"endSection": "abstract",
"offsetInBeginSection": 111,
"offsetInEndSection": 390,
"text": " Hirschsprung disease (HSCR), a developmental disorder characterized by the absence of enteric neurons in distal segments of the gut, shows a complex pattern of inheritance, with the RET protooncogene acting as a major gene and additional susceptibility loci playing minor roles."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17108762",
"endSection": "abstract",
"offsetInBeginSection": 105,
"offsetInEndSection": 334,
"text": " Traditional RET germline mutations account for a small subset of Hirschsprung disease patients, but several studies have shown that there is a specific haplotype of RET associated with the sporadic forms of Hirschsprung disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17108762",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "PURPOSE: The RET proto-oncogene is considered to be the major susceptibility gene involved in Hirschsprung disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16448984",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "The RET proto-oncogene is the major gene involved in the pathogenesis of Hirschsprung (HSCR), a complex genetic disease characterized by lack of ganglia along variable lengths of the gut."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16441254",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 209,
"text": "The RET proto-oncogene is the major gene involved in the complex genetics of Hirschsprung disease (HSCR), or aganglionic megacolon, showing causative loss-of-function mutations in 15-30% of the sporadic cases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23400839",
"endSection": "abstract",
"offsetInBeginSection": 207,
"offsetInEndSection": 437,
"text": "While rare variants (RVs) in the coding sequence (CDS) of several genes involved in ENS development lead to disease, the association of common variants (CVs) with HSCR has only been reported for RET (the major HSCR gene) and NRG1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22584707",
"endSection": "abstract",
"offsetInBeginSection": 267,
"offsetInEndSection": 547,
"text": "The rearranged during transfection (RET) proto-oncogene is the major susceptibility gene for Hirschsprung disease, and germline mutations in RET have been reported in up to 50% of the inherited forms of Hirschsprung disease and in 15-20% of sporadic cases of Hirschsprung disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20598273",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 413,
"text": "The major gene for Hirschsprung disease (HSCR) encodes the receptor tyrosine kinase RET. In a study of 690 European- and 192 Chinese-descent probands and their parents or controls, we demonstrate the ubiquity of a >4-fold susceptibility from a C-->T allele (rs2435357: p = 3.9 x 10(-43) in European ancestry; p = 1.1 x 10(-21) in Chinese samples) that probably arose once within the intronic RET enhancer MCS+9.7."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16986122",
"endSection": "abstract",
"offsetInBeginSection": 113,
"offsetInEndSection": 391,
"text": "Hirschsprung disease (HSCR), a developmental disorder characterized by the absence of enteric neurons in distal segments of the gut, shows a complex pattern of inheritance, with the RET protooncogene acting as a major gene and additional susceptibility loci playing minor roles."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12865274",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "BACKGROUND: The RET gene encodes a tyrosine kinase receptor involved in different human neurocristopathies, such as specific neuroendocrine tumours and Hirschsprung disease (HSCR)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9727738",
"endSection": "abstract",
"offsetInBeginSection": 441,
"offsetInEndSection": 539,
"text": "The first major susceptibility gene for Hirschsprung disease is the RET proto-oncogene on 10q11.2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7883791",
"endSection": "abstract",
"offsetInBeginSection": 508,
"offsetInEndSection": 883,
"text": "The developmental abnormalities apparent in these mice, together with the observation that the major tissues affected in MEN 2 and Hirschsprung disease have a common origin in the embryonal neural crest, suggest that RET encodes a receptor for a developmental regulator involved in the genesis of a variety of neural crest derivatives, and in the organogenesis of the kidney."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23372769",
"endSection": "abstract",
"offsetInBeginSection": 284,
"offsetInEndSection": 477,
"text": "The RET proto-oncogene is the major gene associated to HSCR with differential contributions of its rare and common, coding and noncoding mutations to the multifactorial nature of this pathology"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22574178",
"endSection": "abstract",
"offsetInBeginSection": 282,
"offsetInEndSection": 465,
"text": "The RET proto-oncogene is the major gene for HSCR with differential contributions of its rare and common, coding and noncoding mutations to the multifactorial nature of this pathology"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10790203",
"endSection": "abstract",
"offsetInBeginSection": 174,
"offsetInEndSection": 213,
"text": "RET is the major gene involved in HSCR."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16448984",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "The RET proto-oncogene is the major gene involved in the pathogenesis of Hirschsprung (HSCR), a complex genetic disease characterized by lack of ganglia along variable lengths of the gut."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16877807",
"endSection": "abstract",
"offsetInBeginSection": 128,
"offsetInEndSection": 221,
"text": "Recent advances show that the RET gene is a major locus involved in the pathogenesis of HSCR."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16441254",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 209,
"text": "The RET proto-oncogene is the major gene involved in the complex genetics of Hirschsprung disease (HSCR), or aganglionic megacolon, showing causative loss-of-function mutations in 15-30% of the sporadic cases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22344793",
"endSection": "abstract",
"offsetInBeginSection": 508,
"offsetInEndSection": 612,
"text": "Although with several genes involved in its pathogenesis, the major HSCR gene is the RET proto-oncogene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23400839",
"endSection": "abstract",
"offsetInBeginSection": 207,
"offsetInEndSection": 437,
"text": "While rare variants (RVs) in the coding sequence (CDS) of several genes involved in ENS development lead to disease, the association of common variants (CVs) with HSCR has only been reported for RET (the major HSCR gene) and NRG1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7883791",
"endSection": "abstract",
"offsetInBeginSection": 508,
"offsetInEndSection": 883,
"text": "The developmental abnormalities apparent in these mice, together with the observation that the major tissues affected in MEN 2 and Hirschsprung disease have a common origin in the embryonal neural crest, suggest that RET encodes a receptor for a developmental regulator involved in the genesis of a variety of neural crest derivatives, and in the organogenesis of the kidney."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17397038",
"endSection": "abstract",
"offsetInBeginSection": 90,
"offsetInEndSection": 285,
"text": "In this model, a major gene, RET, is involved in most if not all cases of isolated (i.e., nonsyndromic) HSCR, in conjunction with other autosomal susceptibility loci under a multiplicative model."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16448984",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "The RET proto-oncogene is the major gene involved in the pathogenesis of Hirschsprung (HSCR), a complex genetic disease characterized by lack of ganglia along variable lengths of the gut"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16441254",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "The RET proto-oncogene is the major gene involved in the complex genetics of Hirschsprung disease (HSCR), or aganglionic megacolon, showing causative loss-of-function mutations in 15-30% of the sporadic cases"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17108762",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 105,
"text": "The RET proto-oncogene is considered to be the major susceptibility gene involved in Hirschsprung disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16816022",
"endSection": "abstract",
"offsetInBeginSection": 290,
"offsetInEndSection": 402,
"text": "Analysis of the RET gene, the major gene involved in HSCR susceptibility, revealed neither linkage nor mutations"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10790203",
"endSection": "abstract",
"offsetInBeginSection": 174,
"offsetInEndSection": 212,
"text": "RET is the major gene involved in HSCR"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/22344793",
"endSection": "abstract",
"offsetInBeginSection": 508,
"offsetInEndSection": 611,
"text": "Although with several genes involved in its pathogenesis, the major HSCR gene is the RET proto-oncogene"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23400839",
"endSection": "abstract",
"offsetInBeginSection": 207,
"offsetInEndSection": 436,
"text": "While rare variants (RVs) in the coding sequence (CDS) of several genes involved in ENS development lead to disease, the association of common variants (CVs) with HSCR has only been reported for RET (the major HSCR gene) and NRG1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22584707",
"endSection": "abstract",
"offsetInBeginSection": 267,
"offsetInEndSection": 546,
"text": "The rearranged during transfection (RET) proto-oncogene is the major susceptibility gene for Hirschsprung disease, and germline mutations in RET have been reported in up to 50% of the inherited forms of Hirschsprung disease and in 15-20% of sporadic cases of Hirschsprung disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16448984",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "The RET proto-oncogene is the major gene involved in the pathogenesis of Hirschsprung (HSCR), a complex genetic disease characterized by lack of ganglia along variable lengths of the gut"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16441254",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "The RET proto-oncogene is the major gene involved in the complex genetics of Hirschsprung disease (HSCR), or aganglionic megacolon, showing causative loss-of-function mutations in 15-30% of the sporadic cases"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17108762",
"endSection": "abstract",
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"offsetInEndSection": 105,
"text": "The RET proto-oncogene is considered to be the major susceptibility gene involved in Hirschsprung disease"
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{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10790203",
"endSection": "abstract",
"offsetInBeginSection": 174,
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"text": "RET is the major gene involved in HSCR"
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{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16877807",
"endSection": "abstract",
"offsetInBeginSection": 128,
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"text": "Recent advances show that the RET gene is a major locus involved in the pathogenesis of HSCR"
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{
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"endSection": "abstract",
"offsetInBeginSection": 90,
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"text": "In this model, a major gene, RET, is involved in most if not all cases of isolated (i.e., nonsyndromic) HSCR, in conjunction with other autosomal susceptibility loci under a multiplicative model"
},
{
"beginSection": "abstract",
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"text": "The developmental abnormalities apparent in these mice, together with the observation that the major tissues affected in MEN 2 and Hirschsprung disease have a common origin in the embryonal neural crest, suggest that RET encodes a receptor for a developmental regulator involved in the genesis of a variety of neural crest derivatives, and in the organogenesis of the kidney."
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{
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"text": "We report on mutation analysis of five genes involved in the receptor tyrosine kinase (RET) or the endothelin-signalling pathways in 28 sporadic Japanese patients with Hirschsprung disease"
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{
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"endSection": "abstract",
"offsetInBeginSection": 1287,
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"text": "In addition to mutations in the RET and EDNRB genes, embryonic environmental factors and/or other genetic factors appear to be involved in the development of Hirschsprung disease"
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{
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"text": "The RET proto-oncogene is the major gene involved in the pathogenesis of Hirschsprung (HSCR), a complex genetic disease characterized by lack of ganglia along variable lengths of the gut"
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"text": "The RET proto-oncogene is the major gene involved in the complex genetics of Hirschsprung disease (HSCR), or aganglionic megacolon, showing causative loss-of-function mutations in 15-30% of the sporadic cases"
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"text": "The RET proto-oncogene is considered to be the major susceptibility gene involved in Hirschsprung disease"
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"text": "Although with several genes involved in its pathogenesis, the major HSCR gene is the RET proto-oncogene"
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"text": "While rare variants (RVs) in the coding sequence (CDS) of several genes involved in ENS development lead to disease, the association of common variants (CVs) with HSCR has only been reported for RET (the major HSCR gene) and NRG1"
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"text": "In this model, a major gene, RET, is involved in most if not all cases of isolated (i.e., nonsyndromic) HSCR, in conjunction with other autosomal susceptibility loci under a multiplicative model"
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"text": "Recent advances show that the RET gene is a major locus involved in the pathogenesis of HSCR"
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"beginSection": "abstract",
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"text": "The RET gene is the major HSCR gene, although reduced penetrance of RET mutations and variable expression of HSCR phenotype indicates that more than one gene is required"
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"text": "We report on mutation analysis of five genes involved in the receptor tyrosine kinase (RET) or the endothelin-signalling pathways in 28 sporadic Japanese patients with Hirschsprung disease"
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"text": "The RET proto-oncogene is the major gene involved in the complex genetics of Hirschsprung disease (HSCR), or aganglionic megacolon, showing causative loss-of-function mutations in 15-30% of the sporadic cases"
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"text": "Analysis of the RET gene, the major gene involved in HSCR susceptibility, revealed neither linkage nor mutations"
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"text": "Although with several genes involved in its pathogenesis, the major HSCR gene is the RET proto-oncogene"
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"text": "While rare variants (RVs) in the coding sequence (CDS) of several genes involved in ENS development lead to disease, the association of common variants (CVs) with HSCR has only been reported for RET (the major HSCR gene) and NRG1"
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"text": "In this model, a major gene, RET, is involved in most if not all cases of isolated (i.e., nonsyndromic) HSCR, in conjunction with other autosomal susceptibility loci under a multiplicative model"
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"text": "The RET gene is the major HSCR gene, although reduced penetrance of RET mutations and variable expression of HSCR phenotype indicates that more than one gene is required"
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"text": "We report on mutation analysis of five genes involved in the receptor tyrosine kinase (RET) or the endothelin-signalling pathways in 28 sporadic Japanese patients with Hirschsprung disease"
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"text": "The RET proto-oncogene is the major gene involved in the complex genetics of Hirschsprung disease (HSCR), or aganglionic megacolon, showing causative loss-of-function mutations in 15-30% of the sporadic cases"
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"text": "The RET proto-oncogene is considered to be the major susceptibility gene involved in Hirschsprung disease"
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"text": "Analysis of the RET gene, the major gene involved in HSCR susceptibility, revealed neither linkage nor mutations"
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"text": "Although with several genes involved in its pathogenesis, the major HSCR gene is the RET proto-oncogene"
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"text": "While rare variants (RVs) in the coding sequence (CDS) of several genes involved in ENS development lead to disease, the association of common variants (CVs) with HSCR has only been reported for RET (the major HSCR gene) and NRG1"
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"text": "The rearranged during transfection (RET) proto-oncogene is the major susceptibility gene for Hirschsprung disease, and germline mutations in RET have been reported in up to 50% of the inherited forms of Hirschsprung disease and in 15-20% of sporadic cases of Hirschsprung disease"
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"text": "In this model, a major gene, RET, is involved in most if not all cases of isolated (i.e., nonsyndromic) HSCR, in conjunction with other autosomal susceptibility loci under a multiplicative model"
}
]
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| 5503121de9bde69634000019 | 110 |
yesno | Is the monoclonal antibody Trastuzumab (Herceptin) of potential use in the treatment of prostate cancer? | ['yes'] | [
"yes"
]
| Although is still controversial, Trastuzumab (Herceptin) can be of potential use in the treatment of prostate cancer overexpressing HER2, either alone or in combination with other drugs. | [
"http://www.ncbi.nlm.nih.gov/pubmed/23294030",
"http://www.ncbi.nlm.nih.gov/pubmed/23255921",
"http://www.ncbi.nlm.nih.gov/pubmed/22505344",
"http://www.ncbi.nlm.nih.gov/pubmed/22322558",
"http://www.ncbi.nlm.nih.gov/pubmed/22137850",
"http://www.ncbi.nlm.nih.gov/pubmed/21844010",
"http://www.ncbi.nlm.nih.gov/pubmed/22977535",
"http://www.ncbi.nlm.nih.gov/pubmed/21364123",
"http://www.ncbi.nlm.nih.gov/pubmed/21326934",
"http://www.ncbi.nlm.nih.gov/pubmed/21254978",
"http://www.ncbi.nlm.nih.gov/pubmed/20716957",
"http://www.ncbi.nlm.nih.gov/pubmed/19373278",
"http://www.ncbi.nlm.nih.gov/pubmed/18071949",
"http://www.ncbi.nlm.nih.gov/pubmed/18038879",
"http://www.ncbi.nlm.nih.gov/pubmed/17211467",
"http://www.ncbi.nlm.nih.gov/pubmed/17210707",
"http://www.ncbi.nlm.nih.gov/pubmed/17142577",
"http://www.ncbi.nlm.nih.gov/pubmed/16163160",
"http://www.ncbi.nlm.nih.gov/pubmed/15919200",
"http://www.ncbi.nlm.nih.gov/pubmed/15571968",
"http://www.ncbi.nlm.nih.gov/pubmed/15264245",
"http://www.ncbi.nlm.nih.gov/pubmed/15139054",
"http://www.ncbi.nlm.nih.gov/pubmed/15046685",
"http://www.ncbi.nlm.nih.gov/pubmed/15036648",
"http://www.ncbi.nlm.nih.gov/pubmed/12677892",
"http://www.ncbi.nlm.nih.gov/pubmed/12173324",
"http://www.ncbi.nlm.nih.gov/pubmed/11920466",
"http://www.ncbi.nlm.nih.gov/pubmed/11786427",
"http://www.ncbi.nlm.nih.gov/pubmed/11685733",
"http://www.ncbi.nlm.nih.gov/pubmed/11685722",
"http://www.ncbi.nlm.nih.gov/pubmed/11502465",
"http://www.ncbi.nlm.nih.gov/pubmed/11331475",
"http://www.ncbi.nlm.nih.gov/pubmed/11236029",
"http://www.ncbi.nlm.nih.gov/pubmed/10519379",
"http://www.ncbi.nlm.nih.gov/pubmed/10473102"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23294030",
"endSection": "abstract",
"offsetInBeginSection": 9,
"offsetInEndSection": 161,
"text": "Herceptin is widely used in treating Her2-overexpressing breast cancer. However, the application of Herceptin in prostate cancer is still controversial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23294030",
"endSection": "abstract",
"offsetInBeginSection": 1419,
"offsetInEndSection": 1735,
"text": "Our data demonstrate that Re-188-labeled Herceptin effectively inhibited the growth of DU145 cells compared to the Herceptin- and Re-188-treated cohorts. This implies that targeting Her2 by both radio- and immuno- therapy might be a potential strategy for treating patients with androgen-independent prostate cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23255921",
"endSection": "abstract",
"offsetInBeginSection": 4,
"offsetInEndSection": 194,
"text": "epidermal growth factor receptor (EGFR) family members are potential targets for therapy using extra-cellular domain receptor binding agents, such as the antibodies trastuzumab and cetuximab"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23255921",
"endSection": "abstract",
"offsetInBeginSection": 1644,
"offsetInEndSection": 1843,
"text": " there were tendencies for upregulation of HER2, increased co-expression of EGFR and HER2 and downregulation of HER3 in the prostate cancer lymph node metastases in comparison to the primary tumors. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22505344",
"endSection": "abstract",
"offsetInBeginSection": 573,
"offsetInEndSection": 1150,
"text": "We performed a comparative analysis in vitro and in vivo of the antitumor effects of three different antibodies targeting different epitopes of ErbB2: Herceptin (trastuzumab), 2C4 (pertuzumab) and Erb-hcAb (human anti-ErbB2-compact antibody), a novel fully human compact antibody produced in our laboratory. Herein, we demonstrate that the growth of both androgen-dependent and independent prostate cancer cells was efficiently inhibited by Erb-hcAb. The antitumor effects induced by Erb-hcAb on some cell lines were more potent than those observed for either Herceptin or 2C4."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22322558",
"endSection": "abstract",
"offsetInBeginSection": 897,
"offsetInEndSection": 1058,
"text": "These findings suggest that a systemic delivery of 212Pb-trastuzumab could be an effective modality for management of advanced human prostate cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22137850",
"endSection": "abstract",
"offsetInBeginSection": 14,
"offsetInEndSection": 149,
"text": "Human epidermal growth factor receptor type 2 (HER2) overexpression supports proliferation of androgen-independent prostate cancer (PC)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22137850",
"endSection": "abstract",
"offsetInBeginSection": 1722,
"offsetInEndSection": 1861,
"text": "Radiolabeled ABY-025 Affibody molecule provides higher contrast in imaging of HER2-expressing PC xenografts than radiolabeled trastuzumab. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21844010",
"endSection": "abstract",
"offsetInBeginSection": 1706,
"offsetInEndSection": 1848,
"text": "These studies indicate that dual EGFR/HER2 inhibition, administered together with AWT, sensitize prostate cancer cells to apoptosis during AWT"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21844010",
"endSection": "abstract",
"offsetInBeginSection": 282,
"offsetInEndSection": 508,
"text": "The overall goal of these studies is to determine whether dual inhibition of the receptor tyrosine kinases epidermal growth factor receptor (EGFR) and HER2 would prolong the effectiveness of this treatment in prostate cancer. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22977535",
"endSection": "abstract",
"offsetInBeginSection": 1005,
"offsetInEndSection": 1107,
"text": "The expression of HER2 was demonstrated and quantified in all three tested prostate cancer cell-lines."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22977535",
"endSection": "abstract",
"offsetInBeginSection": 1401,
"offsetInEndSection": 1523,
"text": "Such features would definitely favor the use of radiometal labels for trastuzumab and, most likely, for affibody molecules"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21364123",
"endSection": "abstract",
"offsetInBeginSection": 1579,
"offsetInEndSection": 1848,
"text": "our data demonstrate that Her2 plays an important role in the support of AR protein stability in the transition of androgen requirement in prostate cancer cells. We hope these findings will provide novel insight into the treatment of hormone-refractory prostate cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21364123",
"endSection": "abstract",
"offsetInBeginSection": 1240,
"offsetInEndSection": 1429,
"text": "These two cell lines exhibited distinct responses to Her2 activation (by heregulin treatment) on Her2 phosphorylation and Her2 inhibition (by AG825 or Herceptin treatments) on proliferation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21326934",
"endSection": "abstract",
"offsetInBeginSection": 193,
"offsetInEndSection": 457,
"text": " While prostate cancers that express high levels of HER-2 are resistant to the killing effects of trastuzumab, they can be targeted for selective gene expression and destruction by lentiviruses with envelope proteins engineered to bind to this therapeutic antibody"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21254978",
"endSection": "abstract",
"offsetInBeginSection": 342,
"offsetInEndSection": 517,
"text": "Overexpression of ErbB-2 and EGFR has been associated with aggressive disease and poor patient prognosis in a range of human tumour types (e.g. breast, lung, ovarian, prostate"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21254978",
"endSection": "abstract",
"offsetInBeginSection": 664,
"offsetInEndSection": 796,
"text": "Various approaches have been developed to target the ErbB signalling pathways including monoclonal antibodies (trastuzumab/Herceptin"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20716957",
"endSection": "abstract",
"offsetInBeginSection": 1431,
"offsetInEndSection": 1555,
"text": "The data from these in vitro and in vivo studies supported advancement of radiolabeled trastuzumab into two clinical studies"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20716957",
"endSection": "abstract",
"offsetInBeginSection": 397,
"offsetInEndSection": 534,
"text": "Tumor targeting was evaluated in mice bearing subcutaneous (s.c.) xenografts of colorectal, pancreatic, ovarian, and prostate carcinomas."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19373278",
"endSection": "abstract",
"offsetInBeginSection": 1137,
"offsetInEndSection": 1397,
"text": "we found that although prostate cancers that express high levels of HER-2 are resistant to the killing effects of trastuzumab, they can be targeted for selective gene expression and destruction by viruses with envelope proteins engineered to bind this antibody"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18071949",
"endSection": "abstract",
"offsetInBeginSection": 6,
"offsetInEndSection": 177,
"text": "detection of prostate cancer (PCa) and advances in hormonal and chemotherapy treatments have provided great clinical benefits to patients with early stages of the disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18071949",
"endSection": "abstract",
"offsetInBeginSection": 1020,
"offsetInEndSection": 1182,
"text": "MAbs directed to established targets include those approved for other solid tumors, including anti-human epidermal growth factor receptor-2 (HER2) MAb trastuzumab"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18038879",
"endSection": "abstract",
"offsetInBeginSection": 1095,
"offsetInEndSection": 1431,
"text": "We conclude that Her2/neu expression in the peripheral blood mononuclear cell fraction of prostate cancer patients is frequent and therefore this assay may potentially be useful to detect the presence of micrometastatic disease in men with prostate cancer and for monitoring patients enrolled in trastuzumab-based therapeutic protocols."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17211467",
"endSection": "abstract",
"offsetInBeginSection": 1390,
"offsetInEndSection": 1552,
"text": "This study suggests that the docetaxel/trastuzumab combination may prove an effective therapeutic approach for HER2-expressing hormone-refractory prostate cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17210707",
"endSection": "abstract",
"offsetInBeginSection": 1452,
"offsetInEndSection": 1629,
"text": "there was no significant difference in antimetastatic activity between the emulsion and the immunoemulsion despite the affinity of the immunoemulsion towards the HER2 receptor. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17210707",
"endSection": "abstract",
"offsetInBeginSection": 657,
"offsetInEndSection": 896,
"text": "a targeted drug delivery system based on cationic emulsion covalently linked to anti-HER2 monoclonal antibody (Herceptin), in a well-established in vivo pharmacologic model of metastatic prostate cancer that overexpresses the HER2 receptor"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17142577",
"endSection": "abstract",
"offsetInBeginSection": 1030,
"offsetInEndSection": 1198,
"text": "The finding of strong, consistent HER-2/neu expression in ACBCC suggests that treatment with Herceptin (trastuzumab) may be effective in patients with this rare tumour."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16163160",
"endSection": "abstract",
"offsetInBeginSection": 662,
"offsetInEndSection": 807,
"text": "Although HER2 can be over-expressed in prostate cancer, there is no clinical data to support the use of trastuzumab for prostate cancer patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15919200",
"endSection": "abstract",
"offsetInBeginSection": 956,
"offsetInEndSection": 1066,
"text": "whereas the effect of the trastuzumab-RT combination was inferior to that predicted by the individual effects."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15571968",
"endSection": "title",
"offsetInBeginSection": 5,
"offsetInEndSection": 86,
"text": "HER 1-2 targeting of hormone-refractory prostate cancer by ZD1839 and trastuzumab"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15264245",
"endSection": "abstract",
"offsetInBeginSection": 962,
"offsetInEndSection": 1048,
"text": "Trastuzumab (Herceptin) as a single agent demonstrated poor efficacy in treating HRPC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15264245",
"endSection": "abstract",
"offsetInBeginSection": 9,
"offsetInEndSection": 187,
"text": "To investigate the efficacy and toxicity of the antibody to the HER-2/neu receptor (trastuzumab, Herceptin) in the treatment of advanced hormone-refractory prostate cancer (HRPC)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15139054",
"endSection": "abstract",
"offsetInBeginSection": 1502,
"offsetInEndSection": 1679,
"text": "Conclusions regarding the predictive value of HER-2 status on outcome after trastuzumab-based therapy were not reached and were only drawn after larger-scale screening efforts. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15139054",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 67,
"text": "rastuzumab plus docetaxel in HER-2/neu-positive prostate carcinoma"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15046685",
"endSection": "abstract",
"offsetInBeginSection": 1869,
"offsetInEndSection": 2034,
"text": "clinical trials are currently in progress in patients with prostate cancer testing novel agents that selectively interfere with these receptors, such as trastuzumab,"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15036648",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 122,
"text": "ytotoxicity of human prostate cancer cell lines in vitro and induction of apoptosis using 213Bi-Herceptin alpha-conjugate"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12677892",
"endSection": "abstract",
"offsetInBeginSection": 315,
"offsetInEndSection": 561,
"text": "The clinical interpretation of c-erbB-2 abnormalities should reflect the complexity of c-erbB-2 mediated regulatory pathway and explain why tumours with overexpression/amplification of c-erbB-2 very often do not respond to therapy using Herceptin"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12173324",
"endSection": "abstract",
"offsetInBeginSection": 134,
"offsetInEndSection": 295,
"text": "HER-2 overexpression also has been reported in up to 60% of patients with hormone-refractory prostate carcinoma (HRPC) and was correlated with shortened survival"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12173324",
"endSection": "abstract",
"offsetInBeginSection": 2235,
"offsetInEndSection": 2574,
"text": "Unlike breast carcinoma and contrary to prior reports, HER-2 overexpression by IHC in archival prostate tissue from patients who eventually developed hormone-refractory disease was infrequent. There did not appear to be any correlation between HER-2 overexpression by IHC and shed HER-2 antigen levels in serum by ELISA in this tumor type."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11920466",
"endSection": "abstract",
"offsetInBeginSection": 2019,
"offsetInEndSection": 2270,
"text": "Further development of trastuzumab for the treatment of patients with metastatic prostate carcinoma is not feasible until more reliable and practical methods of sampling metastatic disease are developed to identify patients with HER-2 positive tumors."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11786427",
"endSection": "abstract",
"offsetInBeginSection": 1549,
"offsetInEndSection": 1792,
"text": "the expression of ERBB2 in prostate cancer is relatively low, and is not altered during disease progression. Thus, it is unlikely that treatment modalities relying on the overexpression of ERBB2 gene will be useful in treating prostate cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11685733",
"endSection": "abstract",
"offsetInBeginSection": 174,
"offsetInEndSection": 392,
"text": "A phase I study was designed to evaluate docetaxel/estramustine plus trastuzumab, a humanized monoclonal antibody that binds to the HER2 receptor, in patients with metastatic androgen-independent prostate cancer (AIPC)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11685722",
"endSection": "abstract",
"offsetInBeginSection": 1021,
"offsetInEndSection": 1170,
"text": "Laboratory evidence also supports the clinical evaluation of docetaxel-based combinations that include agents such as trastuzumab and/or estramustine"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11502465",
"endSection": "abstract",
"offsetInBeginSection": 475,
"offsetInEndSection": 702,
"text": "trastuzumab, a monoclonal antibody binding to the HER2 receptor; immunotoxin conjugates use an antibody directed against EGFR joined to a cell toxin. All are in clinical trials for a number of cancers, including prostate cancer"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11331475",
"endSection": "abstract",
"offsetInBeginSection": 155,
"offsetInEndSection": 366,
"text": "we investigated the antitumor efficacy of Herceptin, a new recombinant humanized anti-HER2/neu antibody, which exhibits cytostatic activity on breast and prostate cancer cells that overexpress the HER2 oncogene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11236029",
"endSection": "abstract",
"offsetInBeginSection": 384,
"offsetInEndSection": 480,
"text": "trastuzumab was found to have additive and synergistic effects with some chemotherapeutic agents"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11236029",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 80,
"text": "ER-2/neu as a therapeutic target in non-small cell lung cancer, prostate cancer"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10519379",
"endSection": "abstract",
"offsetInBeginSection": 1683,
"offsetInEndSection": 1844,
"text": "in these prostate cancer model systems, Herceptin alone has clinical activity only in the androgen-dependent tumor and has at least an additive effect on growth,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10473102",
"endSection": "abstract",
"offsetInBeginSection": 1332,
"offsetInEndSection": 1446,
"text": "anti-HER2 receptor monoclonal antibody Herceptin significantly enhanced growth inhibition of the MDA PCa 2a cells."
}
]
| 5 | BioASQ-training5b | [
"http://www.biosemantics.org/jochem#4002084",
"http://www.disease-ontology.org/api/metadata/DOID:10283"
]
| []
| 5313b049e3eabad021000013 | 111 |
yesno | Is alemtuzumab effective for remission induction in patients diagnosed with T-cell prolymphocytic leukemia? | ['yes'] | [
"yes"
]
| Yes, alemtuzumab (anti-CD52, Campath-1H) is effective for remission induction in patients diagnosed with T-cell prolymphocytic leukemia. Alemtuzumab can be administered in combination with other chemotherapeutic agents or as mono-therapy. Response rate to alemtuzumab is more than 90%. Alemtuzumab therapy is associated with improved survival of T-cell prolymphocytic leukemia patients. | [
"http://www.ncbi.nlm.nih.gov/pubmed/23512246",
"http://www.ncbi.nlm.nih.gov/pubmed/23233647",
"http://www.ncbi.nlm.nih.gov/pubmed/23211022",
"http://www.ncbi.nlm.nih.gov/pubmed/22517037",
"http://www.ncbi.nlm.nih.gov/pubmed/16720203",
"http://www.ncbi.nlm.nih.gov/pubmed/16645226",
"http://www.ncbi.nlm.nih.gov/pubmed/15869731",
"http://www.ncbi.nlm.nih.gov/pubmed/12950233",
"http://www.ncbi.nlm.nih.gov/pubmed/11986948",
"http://www.ncbi.nlm.nih.gov/pubmed/11535503",
"http://www.ncbi.nlm.nih.gov/pubmed/10561018",
"http://www.ncbi.nlm.nih.gov/pubmed/22649104",
"http://www.ncbi.nlm.nih.gov/pubmed/15757437",
"http://www.ncbi.nlm.nih.gov/pubmed/21948296",
"http://www.ncbi.nlm.nih.gov/pubmed/17118783",
"http://www.ncbi.nlm.nih.gov/pubmed/23645660",
"http://www.ncbi.nlm.nih.gov/pubmed/15453953"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23512246",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 175,
"text": "Sequential chemoimmunotherapy of fludarabine, mitoxantrone, and cyclophosphamide induction followed by alemtuzumab consolidation is effective in T-cell prolymphocytic leukemia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23512246",
"endSection": "abstract",
"offsetInBeginSection": 131,
"offsetInEndSection": 318,
"text": "A central need in this historically refractory tumor is the controlled evaluation of multiagent chemotherapy and its combination with the currently most active single agent, alemtuzumab. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23512246",
"endSection": "abstract",
"offsetInBeginSection": 1489,
"offsetInEndSection": 1581,
"text": "FMC-A is a safe and efficient protocol in T-PLL, which compares favorably to published data."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23233647",
"endSection": "abstract",
"offsetInBeginSection": 573,
"offsetInEndSection": 773,
"text": "Currently, the best treatment for T-PLL is IV alemtuzumab, which has resulted in very high response rates of more than 90% when given as frontline treatment and a significant improvement in survival. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23211022",
"endSection": "abstract",
"offsetInBeginSection": 735,
"offsetInEndSection": 906,
"text": "The patient failed to respond to standard ALL induction chemotherapy, but achieved complete remission following treatment with a fludarabine and alemtuzumab-based regimen."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22517037",
"endSection": "abstract",
"offsetInBeginSection": 216,
"offsetInEndSection": 401,
"text": "Here we present a rare case of concurrent T-PLL and Kaposi sarcoma who achieved a complete hematologic and cytogenetic remission after a very short course of treatment with alemtuzumab."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16720203",
"endSection": "abstract",
"offsetInBeginSection": 1035,
"offsetInEndSection": 1243,
"text": " Recent studies with single-agent alemtuzumab, an anti-CD52 monoclonal antibody, have shown improved response rates and survival in patients with T-cell prolymphocytic leukemia and cutaneous T-cell lymphoma. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16645226",
"endSection": "abstract",
"offsetInBeginSection": 510,
"offsetInEndSection": 696,
"text": "The CD52 antigen is expressed at high density on the malignant T-cells and therapy with alemtuzumab, a humanized IgG1 antibody that targets this antigen, has produced promising results. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15869731",
"endSection": "abstract",
"offsetInBeginSection": 484,
"offsetInEndSection": 707,
"text": "With the introduction of alemtuzumab, most patients who progressed despite treatment with pentostatin had a major response with a complete remission rate higher than that obtained with pentostatin when used as a first line."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12950233",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 227,
"text": "Alemtuzumab (anti-CD52, Campath-1H) has recently been shown to be effective in the treatment of a range of hematological malignancies, including B-cell chronic lymphocytic leukemia and T-cell prolymphocytic leukemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11986948",
"endSection": "abstract",
"offsetInBeginSection": 179,
"offsetInEndSection": 384,
"text": "Here we report the outcome of two patients with CD4-positive T cell prolymphocytic leukemia treated with CAMPATH-1H. Both patients responded rapidly to treatment and subsequently developed CD4 lymphopenia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11535503",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "T-cell prolymphocytic leukemia (T-PLL) is a chemotherapy-resistant malignancy with a median survival of 7.5 months. Preliminary results indicated a high remission induction rate with the human CD52 antibody, CAMPATH-1H. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11535503",
"endSection": "abstract",
"offsetInBeginSection": 472,
"offsetInEndSection": 738,
"text": "CAMPATH-1H (30 mg) was administered intravenously 3 times weekly until maximal response. The overall response rate was 76% with 60% CR and 16% partial remission (PR). These responses were durable with a median disease-free interval of 7 months (range, 4-45 months). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11535503",
"endSection": "abstract",
"offsetInBeginSection": 1444,
"offsetInEndSection": 1570,
"text": "The conclusion is that CAMPATH-1H is an effective therapy in T-PLL, producing remissions in more than two thirds of patients. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10561018",
"endSection": "abstract",
"offsetInBeginSection": 1097,
"offsetInEndSection": 1343,
"text": "For example, most patients with T-cell prolymphocytic leukemia, including those with large tumor burdens and high peripheral white blood cell counts, will enter complete remission using the antibody CAMPATH-1H without any evidence of tumor lysis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23512246",
"endSection": "abstract",
"offsetInBeginSection": 746,
"offsetInEndSection": 1006,
"text": "Overall response rate to FMC was 68%, comprising 6 complete remissions (all bone-marrow confirmed) and 11 partial remissions. Alemtuzumab consolidation increased the intent-to-treat overall response rate to 92% (12 complete remissions; 11 partial remissions). "
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D015461",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D012074",
"http://www.biosemantics.org/jochem#4002029"
]
| []
| 530cefaaad0bf1360c000001 | 112 |
yesno | Are circRNAs susceptible to degradation by RNase R? | ['no'] | [
"no"
]
| ['Currently, an increasing body of evidence has demonstrated that 1) majority of circRNAs are evolutionarily conserved across species, stable, and resistant to RNase R degradation.', "Due to lack of 3' termini, circRNAs are more resistant to degradation by exonuclease RNase R and possess greater stability than linear RNAs.", 'Yes. Circular RNAs are a kind of closed circular RNA molecule widely existing in transcriptomes. Due to lack of free ends, they are not easily cleaved by RNase R, thus avoiding degradation.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/30259366",
"http://www.ncbi.nlm.nih.gov/pubmed/31556152",
"http://www.ncbi.nlm.nih.gov/pubmed/32480219",
"http://www.ncbi.nlm.nih.gov/pubmed/29170496",
"http://www.ncbi.nlm.nih.gov/pubmed/26660425",
"http://www.ncbi.nlm.nih.gov/pubmed/24865493",
"http://www.ncbi.nlm.nih.gov/pubmed/33141028",
"http://www.ncbi.nlm.nih.gov/pubmed/31160488",
"http://www.ncbi.nlm.nih.gov/pubmed/34238421",
"http://www.ncbi.nlm.nih.gov/pubmed/31269210",
"http://www.ncbi.nlm.nih.gov/pubmed/31217510",
"http://www.ncbi.nlm.nih.gov/pubmed/29167634",
"http://www.ncbi.nlm.nih.gov/pubmed/33650643",
"http://www.ncbi.nlm.nih.gov/pubmed/34453665",
"http://www.ncbi.nlm.nih.gov/pubmed/34269929",
"http://www.ncbi.nlm.nih.gov/pubmed/34232572",
"http://www.ncbi.nlm.nih.gov/pubmed/27929395"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33141028",
"endSection": "abstract",
"offsetInBeginSection": 204,
"offsetInEndSection": 383,
"text": "Currently, an increasing body of evidence has demonstrated that 1) majority of circRNAs are evolutionarily conserved across species, stable, and resistant to RNase R degradation, "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34269929",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 167,
"text": "Circular RNA (circRNA) has a closed-loop structure, and its 3' and 5' ends are directly covalently connected by reverse splicing, which is more stable than linear RNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31556152",
"endSection": "abstract",
"offsetInBeginSection": 193,
"offsetInEndSection": 373,
"text": "CircRNAs are a kind of closed circular RNA molecule widely existing in transcriptomes. Due to lack of free ends, they are not easily cleaved by RNase R, thus avoiding degradation. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32480219",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 355,
"text": "Circular RNAs (circRNAs) are a class of newly-identified non-coding RNA that lack 5' (cap) and 3' (polyadenylation) ends and are linked by a covalent bond to form a closed loop structure. In comparison to linear RNAs, circRNAs are more resistant to exonuclease RNase R-mediated degradation with a much stronger stability due to the absence of 3' terminals"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29167634",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 344,
"text": "Circular RNAs (circRNAs) own unique capabilities to communicate with nucleic acids and ribonucleoproteins and are emerging as indispensable compositions of the regulatory messages encoded in the genome. Due to lack of 3' termini, circRNAs are more resistant to degradation by exonuclease RNase R and possess greater stability than linear RNAs. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24865493",
"endSection": "abstract",
"offsetInBeginSection": 324,
"offsetInEndSection": 570,
"text": "RNase R is a strong 3' to 5' exoribonuclease, which efficiently degrades linear RNAs, such as mRNAs and rRNAs; therefore, the circular parts of lariat RNAs and the circRNAs can be segregated from eukaryotic total RNAs by their RNase R resistance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24865493",
"endSection": "abstract",
"offsetInBeginSection": 266,
"offsetInEndSection": 323,
"text": "Lariat RNAs and circRNAs are both RNase R resistant RNAs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32480219",
"endSection": "abstract",
"offsetInBeginSection": 188,
"offsetInEndSection": 356,
"text": "In comparison to linear RNAs, circRNAs are more resistant to exonuclease RNase R-mediated degradation with a much stronger stability due to the absence of 3' terminals."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29167634",
"endSection": "abstract",
"offsetInBeginSection": 203,
"offsetInEndSection": 343,
"text": "Due to lack of 3' termini, circRNAs are more resistant to degradation by exonuclease RNase R and possess greater stability than linear RNAs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30259366",
"endSection": "abstract",
"offsetInBeginSection": 284,
"offsetInEndSection": 408,
"text": "Because circRNAs are not easily degraded by exonuclease RNase R, they can exist more stably in body fluids than linear RNAs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34232572",
"endSection": "abstract",
"offsetInBeginSection": 750,
"offsetInEndSection": 912,
"text": "Therefore, it is essential to perform the RT-qPCR validation step only after linear RNAs have been degraded using an exonuclease such as ribonuclease R (RNase R)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24865493",
"endSection": "abstract",
"offsetInBeginSection": 332,
"offsetInEndSection": 582,
"text": "is a strong 3' to 5' exoribonuclease, which efficiently degrades linear RNAs, such as mRNAs and rRNAs; therefore, the circular parts of lariat RNAs and the circRNAs can be segregated from eukaryotic total RNAs by their RNase R resistance. Thus, RNase"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34238421",
"endSection": "abstract",
"offsetInBeginSection": 282,
"offsetInEndSection": 507,
"text": "sion of circRNAs is prevalent in tissues and body fluids,and their abnormal expression is related to tumor progression.circRNAs are stable even under the treatment of RNase R because of their circular conformation.As circRNAs"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29167634",
"endSection": "abstract",
"offsetInBeginSection": 205,
"offsetInEndSection": 346,
"text": "e to lack of 3' termini, circRNAs are more resistant to degradation by exonuclease RNase R and possess greater stability than linear RNAs. Mo"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30259366",
"endSection": "abstract",
"offsetInBeginSection": 290,
"offsetInEndSection": 414,
"text": "e circRNAs are not easily degraded by exonuclease RNase R, they can exist more stably in body fluids than linear RNAs. Based"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33650643",
"endSection": "abstract",
"offsetInBeginSection": 121,
"offsetInEndSection": 216,
"text": " is stable, difficult to cleave and resistant to RNA exonuclease or RNase R degradation. circRN"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31160488",
"endSection": "abstract",
"offsetInBeginSection": 380,
"offsetInEndSection": 506,
"text": "the unique structures, circRNAs are resistant to exonuclease RNase R and maintain stability more easily than linear RNAs. Rece"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32480219",
"endSection": "abstract",
"offsetInBeginSection": 196,
"offsetInEndSection": 365,
"text": "rison to linear RNAs, circRNAs are more resistant to exonuclease RNase R-mediated degradation with a much stronger stability due to the absence of 3' terminals. Conseque"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29170496",
"endSection": "abstract",
"offsetInBeginSection": 576,
"offsetInEndSection": 724,
"text": " RT-PCR analysis showed that sheep circRNAs are resistant to RNase R digestion and are expressed in prenatal and postnatal pituitary glands. GO and "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33141028",
"endSection": "abstract",
"offsetInBeginSection": 204,
"offsetInEndSection": 1812,
"text": "Currently, an increasing body of evidence has demonstrated that 1) majority of circRNAs are evolutionarily conserved across species, stable, and resistant to RNase R degradation, and often exhibit cell-specific, and tissue-specific/developmental-stage-specific expression and can be largely independent of the expression levels of the linear host gene-encoded linear RNAs; 2) the biogenesis of circRNAs via back-splicing is different from the canonical splicing of linear RNAs; 3) circRNA biogenesis is regulated by specific cis-acting elements and trans-acting factors; 4) circRNAs regulate biological and pathological processes by sponging miRNAs, binding to RNA-binding protein (RBP), regulators of splicing and transcription, modifiers of parental gene expression, and regulators of protein translation or being translated into peptides in various diseases; 5) circRNAs have been identified for their enrichment and stability in exosomes and detected in body fluids such as human blood, saliva, and cerebrospinal fluids, suggesting that these exo-circRNAs have potential applications as disease biomarkers and novel therapeutic targets; 6) several circRNAs are regulated by oxidative stress and mediate reactive oxygen species (ROS) production as well as promote ROS-induced cellular death, cell apoptosis, and inflammation; 7) circRNAs have also emerged as important regulators in atherosclerotic cardiovascular disease, metabolic disease, and cancers; 8) the potential mechanisms of several circRNAs have been described in diseases, hinting at their potential applications as novel therapeutic targets."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31269210",
"endSection": "abstract",
"offsetInBeginSection": 151,
"offsetInEndSection": 474,
"text": "To prove their circularity as well as biochemically enrich these transcripts, it has become standard in the field to use the 3'-5' exonuclease RNase R. Here, we demonstrate that standard protocols involving RNase R can fail to digest >20% of all highly expressed linear RNAs, but these shortcomings can largely be overcome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34453665",
"endSection": "abstract",
"offsetInBeginSection": 777,
"offsetInEndSection": 1039,
"text": "We propose that such an R-loop dependent ciRNA degradation likely represents a mechanism that on one hand limits ciRNA accumulation by recruiting RNase H1 and on the other hand resolves R-loops for transcriptional elongation at some GC-rich ciRNA-producing loci."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26660425",
"endSection": "abstract",
"offsetInBeginSection": 220,
"offsetInEndSection": 419,
"text": "As circular RNAs (circRNAs) are resistant to degradation by exonucleases, their abundance relative to linear RNAs can be used as a surrogate marker for mRNA stability in the absence of transcription."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31217510",
"endSection": "abstract",
"offsetInBeginSection": 676,
"offsetInEndSection": 878,
"text": "The synthetic circular sponge was resistant to digestion with RNase R. Luciferase assays and functional experiments showed that the circular multi-miR sponge was more stable than its linear counterpart."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31269210",
"endSection": "abstract",
"offsetInBeginSection": 475,
"offsetInEndSection": 665,
"text": "RNAs with highly structured 3' ends, including snRNAs and histone mRNAs, are naturally resistant to RNase R, but can be efficiently degraded once a poly(A) tail has been added to their ends."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31269210",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Thousands of eukaryotic protein-coding genes generate circular RNAs that have covalently linked ends and are resistant to degradation by exonucleases."
}
]
| 11 | BioASQ-training11b | null | null | 62211d6f3a8413c65300006f | 113 |
yesno | Can PLN mutations lead to dilated cardiomyopathy? | ['yes'] | [
"yes"
]
| ['Yes, PLN mutations can lead to dilated cardiomyopathy.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23349452",
"http://www.ncbi.nlm.nih.gov/pubmed/22820313",
"http://www.ncbi.nlm.nih.gov/pubmed/22427649",
"http://www.ncbi.nlm.nih.gov/pubmed/22155237",
"http://www.ncbi.nlm.nih.gov/pubmed/22137083",
"http://www.ncbi.nlm.nih.gov/pubmed/21282613",
"http://www.ncbi.nlm.nih.gov/pubmed/20634894",
"http://www.ncbi.nlm.nih.gov/pubmed/19324307",
"http://www.ncbi.nlm.nih.gov/pubmed/17998275",
"http://www.ncbi.nlm.nih.gov/pubmed/17019811",
"http://www.ncbi.nlm.nih.gov/pubmed/17010801",
"http://www.ncbi.nlm.nih.gov/pubmed/16432188",
"http://www.ncbi.nlm.nih.gov/pubmed/16235537",
"http://www.ncbi.nlm.nih.gov/pubmed/15769782",
"http://www.ncbi.nlm.nih.gov/pubmed/15336969",
"http://www.ncbi.nlm.nih.gov/pubmed/12639993",
"http://www.ncbi.nlm.nih.gov/pubmed/12610310"
]
| [
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23349452",
"endSection": "sections.0",
"offsetInBeginSection": 674,
"offsetInEndSection": 826,
"text": "A PLN founder mutation (43 cases) and LMNA mutations (19 cases, 16 different mutations) were most prevalent and often demonstrated a specific phenotype."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22820313",
"endSection": "sections.0",
"offsetInBeginSection": 350,
"offsetInEndSection": 441,
"text": "PLN mutation R14del was identified in 12 (12 %) ARVC patients and in 39 (15 %) DCM patients"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22820313",
"endSection": "sections.0",
"offsetInBeginSection": 1337,
"offsetInEndSection": 1453,
"text": "The PLN R14del founder mutation is present in a substantial number of patients clinically diagnosed with DCM or ARVC"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22427649",
"endSection": "sections.0",
"offsetInBeginSection": 147,
"offsetInEndSection": 272,
"text": "Arg(9) → Cys (R9C) and Arg(14) deletion (R14del) mutations in PLN are associated with lethal dilated cardiomyopathy in humans"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22155237",
"endSection": "sections.0",
"offsetInBeginSection": 306,
"offsetInEndSection": 443,
"text": "We previously reported the deletion of the highly conserved amino acid residue arginine 14 (nucleic acids 39, 40 and 41) in DCM patients."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22137083",
"endSection": "sections.0",
"offsetInBeginSection": 157,
"offsetInEndSection": 252,
"text": "Mutations in the gene encoding PLN have been associated with idiopathic dilated cardiomyopathy;"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22137083",
"endSection": "sections.0",
"offsetInBeginSection": 1429,
"offsetInEndSection": 1565,
"text": "Mutations in the PLN gene are a rare cause of heart failure, present almost exclusively in patients with dilated cardiomyopathy etiology"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21282613",
"endSection": "sections.0",
"offsetInBeginSection": 172,
"offsetInEndSection": 294,
"text": "A missense mutation in PLN cytoplasmic domain (R9C) triggers dilated cardiomyopathy in humans, leading to premature death."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19324307",
"endSection": "sections.0",
"offsetInBeginSection": 465,
"offsetInEndSection": 599,
"text": "Complete genetic and clinical analyses were performed in a family with familial dilated cardiomyopathy due to the PLN-R14Del mutation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19324307",
"endSection": "sections.0",
"offsetInBeginSection": 753,
"offsetInEndSection": 1090,
"text": "A candidate gene approach resulted in identification of a heterozygous deletion of arginine 14 in the gene encoding phospholamban (PLN-R14Del) segregating with dilated cardiomyopathy in the family pedigree. Mutation carriers suffered from familial dilated cardiomyopathy associated with cardiac death between the ages of 26 and 50 years."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19324307",
"endSection": "sections.0",
"offsetInBeginSection": 522,
"offsetInEndSection": 599,
"text": "a family with familial dilated cardiomyopathy due to the PLN-R14Del mutation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17998275",
"endSection": "sections.0",
"offsetInBeginSection": 1103,
"offsetInEndSection": 1320,
"text": "For the phospholamban (PLN) and titin cap (TTN) genes, a direct mutation screening approach was used. DNA sequence analysis of all exons showed no evidence that these genes are involved in DCM in the Newfoundland dog."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17019811",
"endSection": "sections.0",
"offsetInBeginSection": 1096,
"offsetInEndSection": 1229,
"text": "two human PLN mutations, associated with either absence or sustained dephosphorylation of PLN, were linked to dilated cardiomyopathy."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17010801",
"endSection": "sections.0",
"offsetInBeginSection": 215,
"offsetInEndSection": 379,
"text": "Mutations in the gene encoding PLN have been associated with dilated cardiomyopathy characterized by early onset and the presence of lethal ventricular arrhythmias."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17010801",
"endSection": "sections.0",
"offsetInBeginSection": 962,
"offsetInEndSection": 1143,
"text": "The identical PLN mutation can be associated with both mild and severe forms of dilated cardiomyopathy. Additionally, PLN mutations should be considered in late onset cardiomyopathy"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16432188",
"endSection": "sections.0",
"offsetInBeginSection": 223,
"offsetInEndSection": 466,
"text": "Through genetic screening of dilated cardiomyopathy patients, we identified a previously uncharacterized deletion of arginine 14 (PLN-R14Del) in the coding region of the phospholamban (PLN) gene in a large family with hereditary heart failure."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16235537",
"endSection": "sections.0",
"offsetInBeginSection": 742,
"offsetInEndSection": 922,
"text": "No PLN gene mutation was found in patients with DCM in Chengdu. This result indicated that PLN gene mutation may not be a common cause for DCM in the Chinese population in Chengdu."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15769782",
"endSection": "sections.0",
"offsetInBeginSection": 1341,
"offsetInEndSection": 1352,
"text": "none in PLN"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15336969",
"endSection": "sections.0",
"offsetInBeginSection": 955,
"offsetInEndSection": 1027,
"text": "the recent discoveries of human PLN mutations leading to disease states."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12639993",
"endSection": "sections.0",
"offsetInBeginSection": 612,
"offsetInEndSection": 768,
"text": "Strikingly, both individuals homozygous for L39stop developed dilated cardiomyopathy and heart failure, requiring cardiac transplantation at ages 16 and 27."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12639993",
"endSection": "sections.0",
"offsetInBeginSection": 1320,
"offsetInEndSection": 1377,
"text": "humans lacking PLN develop lethal dilated cardiomyopathy."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12610310",
"endSection": "sections.0",
"offsetInBeginSection": 188,
"offsetInEndSection": 386,
"text": "Here we report that an inherited human dilated cardiomyopathy with refractory congestive heart failure is caused by a dominant Arg --> Cys missense mutation at residue 9 (R9C) in phospholamban (PLN)"
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002311",
"http://www.disease-ontology.org/api/metadata/DOID:12930",
"http://www.uniprot.org/uniprot/PPLA_BOVIN",
"http://www.uniprot.org/uniprot/PPLA_PIG",
"http://www.uniprot.org/uniprot/PPLA_RAT",
"http://www.uniprot.org/uniprot/PPLA_CANFA",
"http://www.uniprot.org/uniprot/PPLA_RABIT",
"http://www.uniprot.org/uniprot/PPLA_CHICK",
"http://www.uniprot.org/uniprot/PPLA_MOUSE",
"http://www.uniprot.org/uniprot/PPLA_HUMAN",
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"http://www.disease-ontology.org/api/metadata/DOID:0050700",
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"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D020125",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D054643",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D016368",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018389",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D017384",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D017354",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D004252"
]
| [
{
"o": "Dilated cardiomyopathy",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A17851795"
},
{
"o": "Cardiomyopathies, Dilated",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A0035199"
},
{
"o": "http://www.w3.org/2008/05/skos-xl#Label",
"p": "http://www.w3.org/1999/02/22-rdf-syntax-ns#type",
"s": "http://linkedlifedata.com/resource/umls/label/A11995504"
},
{
"o": "Dilated Cardiomyopathy",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A17895723"
},
{
"o": "http://www.w3.org/2008/05/skos-xl#Label",
"p": "http://www.w3.org/1999/02/22-rdf-syntax-ns#type",
"s": "http://linkedlifedata.com/resource/umls/label/A0048982"
},
{
"o": "Cardiomyopathy, Dilated",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A12058799"
},
{
"o": "http://www.w3.org/2008/05/skos-xl#Label",
"p": "http://www.w3.org/1999/02/22-rdf-syntax-ns#type",
"s": "http://linkedlifedata.com/resource/umls/label/A13286677"
}
]
| 5148e42cd24251bc0500003b | 114 |
yesno | Is myasthenia gravis associated with osteoporosis? | ['yes'] | [
"yes"
]
| ['Myasthenia gravis (MG) is a neuromuscular disease which has been associated with an increased risk of glucocorticoid-induced osteoporosis. Thymectomy can also increase risk for osteoporosis. Appropriate osteoporosis preventive measures can reduce osteoporosis risk in MG patients.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23543381",
"http://www.ncbi.nlm.nih.gov/pubmed/22840813",
"http://www.ncbi.nlm.nih.gov/pubmed/22531999",
"http://www.ncbi.nlm.nih.gov/pubmed/16690366",
"http://www.ncbi.nlm.nih.gov/pubmed/15168159",
"http://www.ncbi.nlm.nih.gov/pubmed/15003307",
"http://www.ncbi.nlm.nih.gov/pubmed/11328209",
"http://www.ncbi.nlm.nih.gov/pubmed/2237235",
"http://www.ncbi.nlm.nih.gov/pubmed/24935165",
"http://www.ncbi.nlm.nih.gov/pubmed/25285145",
"http://www.ncbi.nlm.nih.gov/pubmed/25122205"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23543381",
"endSection": "abstract",
"offsetInBeginSection": 508,
"offsetInEndSection": 615,
"text": "We performed PVP in 4 patients with generalized MG associated with recent steroid-induced symptomatic VFs. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22840813",
"endSection": "abstract",
"offsetInBeginSection": 242,
"offsetInEndSection": 436,
"text": "In this case report, we used tacrolimus to successfully treat a 13-year-old boy with ocular MG who had suffered from severe steroid complications, including a failure of thrive and osteoporosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22531999",
"endSection": "abstract",
"offsetInBeginSection": 360,
"offsetInEndSection": 573,
"text": " INTRODUCTION: Myasthenia gravis (MG) is a neuromuscular disease which has been associated with an increased falls risk and glucocorticoid-induced osteoporosis, recognized determinants of increased fracture risk. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22531999",
"endSection": "abstract",
"offsetInBeginSection": 949,
"offsetInEndSection": 1462,
"text": "RESULTS: Compared to the control cohort, there was no statistically significant increased risk observed in patients with MG for any fracture (adjusted hazard ratio [AHR] 1.11; 95 % confidence interval [CI], 0.84-1.47) or osteoporotic fractures (AHR 0.98 [95 % CI 0.67-1.41]). Further, use of oral glucocorticoids up to a cumulative dose exceeding 5 g prednisolone equivalents did not increase risk of osteoporotic fracture (AHR 0.99 [95 % CI, 0.31-3.14]) compared with MG patients without glucocorticoid exposure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16690366",
"endSection": "abstract",
"offsetInBeginSection": 1271,
"offsetInEndSection": 1405,
"text": "The RANKL/OPG ratio and indices of bone metabolisms are also not affected by THX, although THX increases the levels of IL-7 and RANKL."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15168159",
"endSection": "abstract",
"offsetInBeginSection": 83,
"offsetInEndSection": 575,
"text": "Both disorders had been controlled for around 15 years by oral prednisolone and a cholinesterase inhibitor following surgical removal of invasive thymoma and radiotherapy, but muscular weakness due to myalgia and an increase in serum levels of myogenic enzymes, mainly ascribable to the recurrence of PM, reappeared immediately after cessation of these drugs, which was done because the patient had multiple bone fractures and severe osteoporosis due to the long-term corticosteroid therapy. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15003307",
"endSection": "abstract",
"offsetInBeginSection": 160,
"offsetInEndSection": 391,
"text": "We measured bone density in 36 patients (26 females and 10 males) who had undergone long-term prednisolone administration, and found a decrease in bone density in 31% of female patients and osteoporosis in only 11.5% (three cases)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15003307",
"endSection": "abstract",
"offsetInBeginSection": 533,
"offsetInEndSection": 681,
"text": "In conclusion, prednisolone-treated patients with myasthenia gravis have an acceptable risk of bone loss if prophylactic medication is administered."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22531999",
"endSection": "abstract",
"offsetInBeginSection": 361,
"offsetInEndSection": 572,
"text": "INTRODUCTION: Myasthenia gravis (MG) is a neuromuscular disease which has been associated with an increased falls risk and glucocorticoid-induced osteoporosis, recognized determinants of increased fracture risk."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23543381",
"endSection": "abstract",
"offsetInBeginSection": 508,
"offsetInEndSection": 615,
"text": "We performed PVP in 4 patients with generalized MG associated with recent steroid-induced symptomatic VFs. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22840813",
"endSection": "abstract",
"offsetInBeginSection": 242,
"offsetInEndSection": 436,
"text": "In this case report, we used tacrolimus to successfully treat a 13-year-old boy with ocular MG who had suffered from severe steroid complications, including a failure of thrive and osteoporosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24935165",
"endSection": "abstract",
"offsetInBeginSection": 901,
"offsetInEndSection": 1020,
"text": "Alendronate should be used with caution in patients with myasthenia gravis who have corticosteroid-induced osteoporosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25285145",
"endSection": "abstract",
"offsetInBeginSection": 399,
"offsetInEndSection": 614,
"text": "In this paper we present two cases of young women who developed severe PAO with vertebral fractures: a 42-year-old woman with a family history of osteoporosis, and a 21-year-old woman affected with myasthenia gravis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22531999",
"endSection": "abstract",
"offsetInBeginSection": 353,
"offsetInEndSection": 549,
"text": "Myasthenia gravis (MG) is a neuromuscular disease which has been associated with an increased falls risk and glucocorticoid-induced osteoporosis, recognized determinants of increased fracture risk"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22531999",
"endSection": "abstract",
"offsetInBeginSection": 353,
"offsetInEndSection": 549,
"text": "Myasthenia gravis (MG) is a neuromuscular disease which has been associated with an increased falls risk and glucocorticoid-induced osteoporosis, recognized determinants of increased fracture risk"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22531999",
"endSection": "abstract",
"offsetInBeginSection": 353,
"offsetInEndSection": 549,
"text": "Myasthenia gravis (MG) is a neuromuscular disease which has been associated with an increased falls risk and glucocorticoid-induced osteoporosis, recognized determinants of increased fracture risk"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22531999",
"endSection": "abstract",
"offsetInBeginSection": 353,
"offsetInEndSection": 549,
"text": "Myasthenia gravis (MG) is a neuromuscular disease which has been associated with an increased falls risk and glucocorticoid-induced osteoporosis, recognized determinants of increased fracture risk"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22531999",
"endSection": "abstract",
"offsetInBeginSection": 353,
"offsetInEndSection": 549,
"text": "Myasthenia gravis (MG) is a neuromuscular disease which has been associated with an increased falls risk and glucocorticoid-induced osteoporosis, recognized determinants of increased fracture risk"
}
]
| 5 | BioASQ-training5b | [
"http://www.disease-ontology.org/api/metadata/DOID:437",
"http://www.disease-ontology.org/api/metadata/DOID:11476"
]
| []
| 55032d8be9bde69634000033 | 115 |
yesno | Is Thalidomide currently a marketed drug? | ['yes'] | [
"yes"
]
| ['Several mechanisms for the teratogenic action of thalidomide are currently under review, but this mode of action of the drug still remains unclear and we review evidence-based hypotheses for the teratogenicity of thalidomide. Thalidomide is considered the drug of choice for the treatment of ENL, but for other conditions, it is recommended only when resistance to the currently available form of therapy is encountered. THE USE OF A DRUG WITH A TEMPORARY MARKETING AUTHORISATION: Thalidomide is currently available in France for nominative or cohort use with a temporary marketing authorisation (TMA). Examples of the basis for such regulation are drawn from historical situations (thalidomide, benoxaprofen) as well as currently marketed drugs (arylpropionic acids, disopyramide, indacrinone). In 1998 the US Food and Drug Administration approved thalidomide exclusively for the treatment of ENL, and strict conditions were stipulated for its use in order to prevent teratogenic adverse effects. The US Food and Drug Administration (FDA) has approved Thalomid (thalidomide) capsules for the acute treatment of the cutaneous manifestations of moderate to severe ENL. The revival of thalidomide began shortly after the drug was withdrawn from the market because of its teratogenic properties.', 'Thalidomide is currently used to treat multiple Myeloma, possibly POEMS (Polyneuropathy, organomegaly, endocrinopathy, M-protein and skin changes ) syndrome and IBS'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/11604049",
"http://www.ncbi.nlm.nih.gov/pubmed/26652728",
"http://www.ncbi.nlm.nih.gov/pubmed/10512502",
"http://www.ncbi.nlm.nih.gov/pubmed/9987477",
"http://www.ncbi.nlm.nih.gov/pubmed/22650376",
"http://www.ncbi.nlm.nih.gov/pubmed/11558112",
"http://www.ncbi.nlm.nih.gov/pubmed/11899395",
"http://www.ncbi.nlm.nih.gov/pubmed/11091366",
"http://www.ncbi.nlm.nih.gov/pubmed/8592478",
"http://www.ncbi.nlm.nih.gov/pubmed/25573527"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26652728",
"endSection": "abstract",
"offsetInBeginSection": 210,
"offsetInEndSection": 336,
"text": "In this retrospective study, pharmacy claims were analyzed for those patients with a diagnosis of MM who received thalidomide,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25573527",
"endSection": "abstract",
"offsetInBeginSection": 490,
"offsetInEndSection": 730,
"text": "The Japanese POEMS syndrome with Thalidomide (J-POST) Trial is a phase II/III multicentre, double-blinded, randomised, controlled trial that aims to evaluate the efficacy and safety of a 24-week treatment with thalidomide in POEMS syndrome,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24931258",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 188,
"text": "Thalidomide could relieve clinical symptoms and intestinal mucosal lesions effectively in children with refractory inflammatory bowel disease (IBD) from the pre-clinical study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8592478",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 67,
"text": "Thalidomide is now available as an investigational drug in the USA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11091366",
"endSection": "abstract",
"offsetInBeginSection": 826,
"offsetInEndSection": 1046,
"text": "The STEPStrade mark (System for Thalidomide Education and Prescribing Safety) Program has been developed by Celgene, the commercial manufacturer of thalidomide, to ensure compliance with prescription and usage protocols."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8592478",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 24,
"text": "New uses of thalidomide."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11899395",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "Thalidomide is an anti-angiogenesis agent that currently is being evaluated in the treatment of various types of cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22650376",
"endSection": "abstract",
"offsetInBeginSection": 993,
"offsetInEndSection": 1160,
"text": "The comeback of thalidomide to the legitimate status of a marketed drug came in 1998 when it received FDA approval for the treatment of erythema nodosum leprosum (ENL)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11558112",
"endSection": "abstract",
"offsetInBeginSection": 643,
"offsetInEndSection": 836,
"text": "Thalidomide is considered the drug of choice for the treatment of ENL, but for other conditions, it is recommended only when resistance to the currently available form of therapy is encountered"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22695124",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 201,
"text": "Thalidomide is an anti-inflammatory and anti-angiogenic drug currently used for the treatment of several diseases, including erythema nodosum leprosum, which occurs in patients with lepromatous leprosy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9987477",
"endSection": "abstract",
"offsetInBeginSection": 279,
"offsetInEndSection": 560,
"text": "Thalidomide, once banned, has returned to the center of controversy with the Food and Drug Administration's (FDA's) announcement that thalidomide will be placed on the market for the treatment of erythema nodosum leprosum, a severe dermatological complication of Hansen's disease. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10512502",
"endSection": "abstract",
"offsetInBeginSection": 265,
"offsetInEndSection": 337,
"text": "In 1998, FDA approved the marketing of thalidomide (Thalomid, Celgene). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11604049",
"endSection": "abstract",
"offsetInBeginSection": 1625,
"offsetInEndSection": 1826,
"text": "In 1998 the US Food and Drug Administration approved thalidomide exclusively for the treatment of ENL, and strict conditions were stipulated for its use in order to prevent teratogenic adverse effects."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11091366",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 294,
"text": "BACKGROUND: The use of thalidomide during the 1950s resulted in teratogenic effects in thousands of infants. Although thalidomide is currently approved for the treatment of a complication of leprosy, it is commercially available to treat other diseases through a controlled distribution system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22650376",
"endSection": "abstract",
"offsetInBeginSection": 994,
"offsetInEndSection": 1162,
"text": "The comeback of thalidomide to the legitimate status of a marketed drug came in 1998 when it received FDA approval for the treatment of erythema nodosum leprosum (ENL)."
}
]
| 6 | BioASQ-training6b | null | null | 58a0d87a78275d0c4a000053 | 116 |
yesno | Does Estrogen lead to forkhead FoxA1 activation? | ['yes'] | [
"yes"
]
| ['The pioneer transcription factor FoxA1 plays an important role in estrogen signaling by opening closed chromatin and promoting recruitment of the estrogen receptor to its target regions in DNA.', 'We showed that CTCF acts upstream of the "pioneer" factor FOXA1 in determining the genomic response to estrogen.', 'The pioneer transcription factor FoxA1 plays an important role in estrogen signaling by opening closed chromatin and promoting recruitment of the estrogen receptor to its target regions in DNA', 'Yes, estrogen-induced transcriptional activation of FoxA1 is tightly regulated by estrogen receptor tyrosine kinase and enhances Forkhead protein expression.', 'Yes, induction of forkhead FoxA1 activation by estrogen seems to result in increased expression of the ERK2/ERK1 pathway in breast cancer cells. (PMID: 21494614) We also find that the testis-specific variant of the FOXA1 gene, which encodes the triggering receptor encoded by exon 9 on estrogen, is recruited to kinetochores and contributes to estrogen-induced silencing of NF-kappaB activation at the mating-type locus. ( PMID: 20160027)'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22713214",
"http://www.ncbi.nlm.nih.gov/pubmed/27883218",
"http://www.ncbi.nlm.nih.gov/pubmed/21151129",
"http://www.ncbi.nlm.nih.gov/pubmed/16009131",
"http://www.ncbi.nlm.nih.gov/pubmed/25707489",
"http://www.ncbi.nlm.nih.gov/pubmed/16087863",
"http://www.ncbi.nlm.nih.gov/pubmed/20610384",
"http://www.ncbi.nlm.nih.gov/pubmed/23771556"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20610384",
"endSection": "abstract",
"offsetInBeginSection": 682,
"offsetInEndSection": 795,
"text": "We showed that CTCF acts upstream of the \"pioneer\" factor FOXA1 in determining the genomic response to estrogen. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21151129",
"endSection": "abstract",
"offsetInBeginSection": 293,
"offsetInEndSection": 448,
"text": "Almost all ER-chromatin interactions and gene expression changes depended on the presence of FOXA1 and FOXA1 influenced genome-wide chromatin accessibility"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21151129",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "FOXA1 is a key determinant of estrogen receptor function and endocrine response."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21151129",
"endSection": "abstract",
"offsetInBeginSection": 830,
"offsetInEndSection": 938,
"text": "As such, FOXA1 is a major determinant of estrogen-ER activity and endocrine response in breast cancer cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16087863",
"endSection": "title",
"offsetInBeginSection": 16,
"offsetInEndSection": 139,
"text": "Location analysis of estrogen receptor alpha target promoters reveals that FOXA1 defines a domain of the estrogen response."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16009131",
"endSection": "abstract",
"offsetInBeginSection": 826,
"offsetInEndSection": 1044,
"text": "Furthermore, knockdown of FoxA1 expression blocks the association of ER with chromatin and estrogen-induced gene expression demonstrating the necessity of FoxA1 in mediating an estrogen response in breast cancer cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22713214",
"endSection": "title",
"offsetInBeginSection": 24,
"offsetInEndSection": 94,
"text": "FoxA1 determines estrogen receptor action in breast cancer progression"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22713214",
"endSection": "abstract",
"offsetInBeginSection": 737,
"offsetInEndSection": 852,
"text": "Given previous findings from cell lines, FoxA1 appears to play a critical role in this reprogramming of ER binding."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25707489",
"endSection": "abstract",
"offsetInBeginSection": 1508,
"offsetInEndSection": 1606,
"text": "FOXA1 expression can independently predict chemosensitivity of ER-positive breast cancer patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23771556",
"endSection": "abstract",
"offsetInBeginSection": 1601,
"offsetInEndSection": 1677,
"text": " FOXA1 expression could be a prognostic marker in ER-positive breast cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27883218",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 192,
"text": "The pioneer transcription factor FoxA1 plays an important role in estrogen signaling by opening closed chromatin and promoting recruitment of the estrogen receptor to its target regions in DNA"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27883218",
"endSection": "abstract",
"offsetInBeginSection": 669,
"offsetInEndSection": 806,
"text": " The phosphomimetic FoxA1 promoted the activation of estrogen signaling, whereas the nonphosphorylatable FoxA1 suppressed its activation."
}
]
| 11 | BioASQ-training11b | null | null | 5ca61b14ecadf2e73f00004f | 117 |
yesno | Is the glucocorticoid receptor a transcription factor? | ['yes'] | [
"yes"
]
| ['Yes,\nThe glucocorticoid receptor (GR) is a ligand-activated transcription factor that translocates to the nucleus upon hormone stimulation and distributes between the nucleoplasm and membraneless compartments named nuclear foci.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/32487073",
"http://www.ncbi.nlm.nih.gov/pubmed/31776270",
"http://www.ncbi.nlm.nih.gov/pubmed/31689103"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31776270",
"endSection": "abstract",
"offsetInBeginSection": 829,
"offsetInEndSection": 877,
"text": "GR and KLF4, both pioneer transcription factors,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31689103",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 257,
"text": "The glucocorticoid receptor (GR) is a ligand-binding dependent transcription factor that ultimately regulates vital biological processes and inflammation response through specific gene expression control, thus representing a notable drug target to explore. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32487073",
"endSection": "abstract",
"offsetInBeginSection": 216,
"offsetInEndSection": 439,
"text": "The glucocorticoid receptor (GR) is a ligand-activated transcription factor that translocates to the nucleus upon hormone stimulation and distributes between the nucleoplasm and membraneless compartments named nuclear foci."
}
]
| 11 | BioASQ-training11b | null | null | 606b3b6794d57fd879000064 | 118 |
yesno | Is TIM-3 a target for cancer immunotherapy in NSCLC? | ['yes'] | [
"yes"
]
| ['Yes. Furthermore, TIM-3 and CEACAM1 were strongly expressed simultaneously during long-term CIK culture and showed a significant and mutually positive correlation.', 'Yes, TIM-3 has shown promising results in early phases of trials in NSCLC patients and can be a target for cancer immunotherapy.', 'Yes, TIM-3 has emerged as an important target of cancer immunotherapy because of its preferential expression in NSCLC cell lines and its presence in 90% of tumors. (PMID: 21494614) We have developed a cancer vaccine in whichtim-3 is fused with dendritic cells resulting in the presentation of tumor antigens in the context of DC-mediated costimulation. This (CT)n element has been shown to induce poly(ADP-ribose) polymerase activation, and it has also been suggested thatTim-3 may act as a tumor suppressor gene, thus making it a potential therapeutic target of CDKN2A/PD-', ' Our results imply that implementing combined treatment on CIK cells before transfusion via antibodies targeting PD-L1, LAG-3, TIM-3, and CEACAM-1 might improve the efficiency of CIK therapy for NSCLC patients. Furthermore, TIM-3 and CEACAM1 were strongly expressed simultaneously during long-term CIK culture and showed a significant and mutually positive correlation.', 'Implementing combined treatment on CIK cells before transfusion via antibodies targeting PD-L1, LAG-3, TIM-3, and CEACAM-1 might improve the efficiency of CIK therapy for NSCLC patients.', ' Our results imply that implementing combined treatment on CIK cells before transfusion via antibodies targeting PD-L1, LAG-3, TIM-3, and CEACAM-1 might improve the efficiency of CIK therapy for NSCLC patients. Cytometric profiling identified an immunologically "hot" cluster with abundant CD8+ T cells expressing high levels of PD-1 and TIM-3 and an immunologically "cold" cluster with lower relative abundance of CD8+ T cells and expression of inhibitory markers'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/27699239",
"http://www.ncbi.nlm.nih.gov/pubmed/29440769",
"http://www.ncbi.nlm.nih.gov/pubmed/27283895",
"http://www.ncbi.nlm.nih.gov/pubmed/29721382",
"http://www.ncbi.nlm.nih.gov/pubmed/26851185",
"http://www.ncbi.nlm.nih.gov/pubmed/27846884"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27283895",
"endSection": "abstract",
"offsetInBeginSection": 1539,
"offsetInEndSection": 1749,
"text": " Our results imply that implementing combined treatment on CIK cells before transfusion via antibodies targeting PD-L1, LAG-3, TIM-3, and CEACAM-1 might improve the efficiency of CIK therapy for NSCLC patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27283895",
"endSection": "abstract",
"offsetInBeginSection": 1018,
"offsetInEndSection": 1177,
"text": "Furthermore, TIM-3 and CEACAM1 were strongly expressed simultaneously during long-term CIK culture and showed a significant and mutually positive correlation. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27283895",
"endSection": "abstract",
"offsetInBeginSection": 303,
"offsetInEndSection": 488,
"text": "In present study, we detected the dynamic expression of eight major checkpoint molecules (CTLA-4, PD-1, PD-L1, TIM- 3, CEACAM-1, LAG-3, TIGIT and BTLA) on CIK cells from NSCLC patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27846884",
"endSection": "abstract",
"offsetInBeginSection": 2689,
"offsetInEndSection": 2906,
"text": "Agents targeting other immune inhibitory (e.g., Tim-3) or immune stimulating (e.g., CD137) receptors on T cells and other approaches such as adoptive cell transfer are tested for clinical efficacy in melanoma as well."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26851185",
"endSection": "abstract",
"offsetInBeginSection": 1181,
"offsetInEndSection": 1483,
"text": "We found immune activation coexistent with elevation of multiple targetable immune checkpoint molecules, including PD-L1, PD-L2, PD-1, TIM-3, B7-H3, BTLA, and CTLA-4, along with increases in tumor infiltration by CD4(+)Foxp3(+) regulatory T cells in lung adenocarcinomas that displayed an EMT phenotype"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27699239",
"endSection": "abstract",
"offsetInBeginSection": 600,
"offsetInEndSection": 853,
"text": "Cytometric profiling identified an immunologically \"hot\" cluster with abundant CD8+ T cells expressing high levels of PD-1 and TIM-3 and an immunologically \"cold\" cluster with lower relative abundance of CD8+ T cells and expression of inhibitory markers"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29721382",
"endSection": "abstract",
"offsetInBeginSection": 1052,
"offsetInEndSection": 1249,
"text": " Interestingly, CD161+ CD4+ T cells highly express OX40 co-stimulatory receptor, less frequently 4-1BB, and display an activated but not completely exhausted PD-1-positive Tim-3-negative phenotype."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29440769",
"endSection": "abstract",
"offsetInBeginSection": 916,
"offsetInEndSection": 1046,
"text": ". Furthermore, overexpression of targetable immune checkpoints, such as CTLA-4 and TIM-3 were associated with EMT in both NSCLCs. "
}
]
| 11 | BioASQ-training11b | null | null | 5c7a4c35d774d04240000007 | 119 |
yesno | Are CpG islands located close to housekeeping genes? | ['yes'] | [
"yes"
]
| ['Yes, CpG islands are preferentially located at the start of transcription of housekeeping genes and are associated with tissue-specific genes.', "Our analysis indicates that the association of CGIs with housekeeping genes is not as strong as previously estimated. These regions represent about 1% of genomic DNA and are generally found in the promoter region of housekeeping genes. In housekeeping and many tissue-specific genes, the promoter is embedded in a so-called CpG island. Methylation-free CpG clusters, so-called HTF islands, are most often associated with the promoter regions of housekeeping genes, whereas genes expressed in a single-cell type are usually deficient in these sequences. All housekeeping and widely expressed genes have a CpG island covering the transcription start, whereas 40% of the genes with a tissue-specific or limited expression are associated with islands. It has been envisaged that CpG islands are often observed near the transcriptional start sites (TSS) of housekeeping genes. CpG islands, which are found almost exclusively at the 5'-end of housekeeping genes. CpG islands were associated with the 5' ends of all housekeeping genes and many tissue-specific genes, and with the 3' ends of some tissue-specific genes. ", "These regions represent about 1% of genomic DNA and are generally found in the promoter region of housekeeping genes. Our analysis indicates that the association of CGIs with housekeeping genes is not as strong as previously estimated. In housekeeping and many tissue-specific genes, the promoter is embedded in a so-called CpG island. Methylation-free CpG clusters, so-called HTF islands, are most often associated with the promoter regions of housekeeping genes, whereas genes expressed in a single-cell type are usually deficient in these sequences. All housekeeping and widely expressed genes have a CpG island covering the transcription start, whereas 40% of the genes with a tissue-specific or limited expression are associated with islands. It has been envisaged that CpG islands are often observed near the transcriptional start sites (TSS) of housekeeping genes. CpG islands, which are found almost exclusively at the 5'-end of housekeeping genes. CpG islands were associated with the 5' ends of all housekeeping genes and many tissue-specific genes, and with the 3' ends of some tissue-specific genes. "] | [
"http://www.ncbi.nlm.nih.gov/pubmed/17591602",
"http://www.ncbi.nlm.nih.gov/pubmed/16474211",
"http://www.ncbi.nlm.nih.gov/pubmed/15784181",
"http://www.ncbi.nlm.nih.gov/pubmed/15546139",
"http://www.ncbi.nlm.nih.gov/pubmed/9990116",
"http://www.ncbi.nlm.nih.gov/pubmed/9632720",
"http://www.ncbi.nlm.nih.gov/pubmed/8128314",
"http://www.ncbi.nlm.nih.gov/pubmed/1505946",
"http://www.ncbi.nlm.nih.gov/pubmed/1968658",
"http://www.ncbi.nlm.nih.gov/pubmed/3186440",
"http://www.ncbi.nlm.nih.gov/pubmed/3656447"
]
| [
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17591602",
"endSection": "sections.0",
"offsetInBeginSection": 1048,
"offsetInEndSection": 1164,
"text": "our analysis indicates that the association of CGIs with housekeeping genes is not as strong as previously estimated"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16474211",
"endSection": "sections.0",
"offsetInBeginSection": 236,
"offsetInEndSection": 372,
"text": "CpG islands are preferentially located at the start of transcription of housekeeping genes and are associated with tissue-specific genes"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15784181",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "It has been envisaged that CpG islands are often observed near the transcriptional start sites (TSS) of housekeeping genes."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15546139",
"endSection": "sections.0",
"offsetInBeginSection": 411,
"offsetInEndSection": 528,
"text": "These regions represent about 1% of genomic DNA and are generally found in the promoter region of housekeeping genes."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9990116",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "CpG islands are stretches of DNA sequence that are enriched in the (CpG)n repeat and are present in close association with all housekeeping genes as well as some tissue-specific genes in the mammalian genome."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9632720",
"endSection": "sections.0",
"offsetInBeginSection": 225,
"offsetInEndSection": 308,
"text": "CpG islands, which are found almost exclusively at the 5'-end of housekeeping genes"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8128314",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "In housekeeping and many tissue-specific genes, the promoter is embedded in a so-called CpG island."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1505946",
"endSection": "sections.0",
"offsetInBeginSection": 496,
"offsetInEndSection": 689,
"text": "All housekeeping and widely expressed genes have a CpG island covering the transcription start, whereas 40% of the genes with a tissue-specific or limited expression are associated with islands"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1968658",
"endSection": "sections.0",
"offsetInBeginSection": 103,
"offsetInEndSection": 319,
"text": "Methylation-free CpG clusters, so-called HTF islands, are most often associated with the promoter regions of housekeeping genes, whereas genes expressed in a single-cell type are usually deficient in these sequences."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3186440",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 132,
"text": "Unmethylated CpG rich islands are a feature of vertebrate DNA: they are associated with housekeeping and many tissue specific genes."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3656447",
"endSection": "sections.0",
"offsetInBeginSection": 548,
"offsetInEndSection": 702,
"text": "CpG islands were associated with the 5' ends of all housekeeping genes and many tissue-specific genes, and with the 3' ends of some tissue-specific genes."
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D006796",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018899",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D020043"
]
| null | 5133b15e5274a5fb0700000b | 120 |
yesno | Is ASF1 phopshorylated by the Tousled-like kinases? | ['yes'] | [
"yes"
]
| ['Yes,\nAsf1, a key histone H3-H4 chaperone required for this process, is phosphorylated by Tousled-like kinases (TLKs).'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23946870",
"http://www.ncbi.nlm.nih.gov/pubmed/24598821",
"http://www.ncbi.nlm.nih.gov/pubmed/23869254",
"http://www.ncbi.nlm.nih.gov/pubmed/20222959",
"http://www.ncbi.nlm.nih.gov/pubmed/32755577"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24598821",
"endSection": "abstract",
"offsetInBeginSection": 118,
"offsetInEndSection": 231,
"text": "Asf1, a key histone H3-H4 chaperone required for this process, is phosphorylated by Tousled-like kinases (TLKs). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32755577",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 103,
"text": "The Tousled-like kinases 1 and 2 (TLK1/2) control histone deposition through the ASF1 histone chaperone"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23946870",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "The Tousled-like kinases (TLKs) are involved in chromatin assembly, DNA repair, and transcription. Two TLK genes exist in humans, and their expression is often dysregulated in cancer. TLKs phosphorylate Asf1 "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23869254",
"endSection": "abstract",
"offsetInBeginSection": 151,
"offsetInEndSection": 264,
"text": "TLKs interact specifically (and phosphorylate) with the chromatin assembly factor Asf1, a histone H3-H4 chaperone"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20222959",
"endSection": "abstract",
"offsetInBeginSection": 183,
"offsetInEndSection": 269,
"text": "TLK1 substrates were identified as the histone H3 and Asf1 (a histone H3/H4 chaperone)"
}
]
| 11 | BioASQ-training11b | null | null | 622d0aa63a8413c6530000a0 | 121 |
yesno | Is Phospholemman a membrane protein? | ['yes'] | [
"yes"
]
| ['Yes, FXYD1 (encoding phospholemman) is a transmembrane protein.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/31840988",
"http://www.ncbi.nlm.nih.gov/pubmed/26429909",
"http://www.ncbi.nlm.nih.gov/pubmed/23246925"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31840988",
"endSection": "abstract",
"offsetInBeginSection": 772,
"offsetInEndSection": 824,
"text": " the transmembrane lipoprotein phospholemman (FXYD1)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26429909",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "Phospholemman (FXYD1) is a single-transmembrane protein regulator of Na,K-ATPase, expressed strongly in heart, skeletal muscle, and brain and phosphorylated by protein kinases A and C at Ser-68 and Ser-63, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23246925",
"endSection": "abstract",
"offsetInBeginSection": 148,
"offsetInEndSection": 347,
"text": "We previously identified FXYD1 (encoding phospholemman; a protein containing the motif phenylalanine-X-tyrosine-aspartate), a gene encoding a transmembrane modulator of the Na, K-ATPase (NKA) enzyme,"
}
]
| 11 | BioASQ-training11b | null | null | 6251465ae764a53204000017 | 123 |
yesno | Is Obeticholic Acid used for treatment of Primary Biliary Cholangitis? | ['yes'] | [
"yes"
]
| ['Yes, obeticholic acid is a farnesoid-X receptor agonist that is approved for the treatment of primary biliary cholangitis in combination with ursodeoxycholic acid in adults with an inadequate response to ursodeoxycholic acid, or as monotherapy in adults unable to tolerate ursodeoxycholic acid.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/27406083",
"http://www.ncbi.nlm.nih.gov/pubmed/27906472",
"http://www.ncbi.nlm.nih.gov/pubmed/27532829",
"http://www.ncbi.nlm.nih.gov/pubmed/27621676",
"http://www.ncbi.nlm.nih.gov/pubmed/27700211",
"http://www.ncbi.nlm.nih.gov/pubmed/27825634",
"http://www.ncbi.nlm.nih.gov/pubmed/27468093",
"http://www.ncbi.nlm.nih.gov/pubmed/26312413",
"http://www.ncbi.nlm.nih.gov/pubmed/27589928"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27825634",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 48,
"text": "Obeticholic acid in primary biliary cholangitis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27825634",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 330,
"text": "In a double-blind, randomized, placebo-controlled study including 217 patients with primary biliary cholangitis, the authors show that obeticholic acid (a potent farnesoid X agonist) administered with ursodeoxycholic acid or as monotherapy significantly decreases serum alkaline phosphatase and bilirubin when compared to placebo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27406083",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 453,
"text": "Obeticholic acid (Ocaliva(TM)) is a farnesoid-X receptor (FXR) agonist that is being developed by Intercept Pharmaceuticals for the treatment of various liver diseases, and has recently been granted accelerated approval in the USA for the treatment of primary biliary cholangitis in combination with ursodeoxycholic acid in adults with an inadequate response to ursodeoxycholic acid, or as monotherapy in adults unable to tolerate ursodeoxycholic acid. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27589928",
"endSection": "abstract",
"offsetInBeginSection": 238,
"offsetInEndSection": 400,
"text": "Obeticholic Acid (OCA) is a farnesoid X receptor (FXR) agonist which has been evaluated as a second line therapy in PBC and has recently been licenced by the FDA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27589928",
"endSection": "abstract",
"offsetInBeginSection": 1142,
"offsetInEndSection": 1363,
"text": "OCA will be the first stratified therapy introduced in PBC, however confirmatory trial and real life data are needed to confirm that suggestive biochemical improvements are matched by improvement in key clinical outcomes."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27621676",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Obeticholic acid for the treatment of primary biliary cholangitis in adult patients: clinical utility and patient selection."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27621676",
"endSection": "abstract",
"offsetInBeginSection": 972,
"offsetInEndSection": 1466,
"text": "A series of clinical trials of OCA in PBC, primarily in combination with UDCA, have established that OCA leads to significant reductions in serum alkaline phosphatase that are predicted to lead to improved clinical outcomes, while dose-dependent pruritus has been the most common adverse effect. On the basis of these studies, OCA was given conditional approval by the US Food and Drug Administration with plans to establish the long-term clinical efficacy of OCA in patients with advanced PBC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27700211",
"endSection": "abstract",
"offsetInBeginSection": 1246,
"offsetInEndSection": 1394,
"text": "Although obeticholic acid was approved by the FDA for the treatment of PBC in May 2016, this development occurred after the symposium presentation. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27700211",
"endSection": "abstract",
"offsetInBeginSection": 2330,
"offsetInEndSection": 2511,
"text": "While several agents are being studied in combination with UDCA, monotherapy with the novel agent obeticholic acid, a farnesoid X receptor agonist, has also shown promising results."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27406083",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 452,
"text": "Obeticholic acid (Ocaliva(TM)) is a farnesoid-X receptor (FXR) agonist that is being developed by Intercept Pharmaceuticals for the treatment of various liver diseases, and has recently been granted accelerated approval in the USA for the treatment of primary biliary cholangitis in combination with ursodeoxycholic acid in adults with an inadequate response to ursodeoxycholic acid, or as monotherapy in adults unable to tolerate ursodeoxycholic acid."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27468093",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 66,
"text": "Obeticholic acid for the treatment of primary biliary cholangitis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27906472",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 118,
"text": "Long-term clinical impact and cost-effectiveness of obeticholic acid for the treatment of primary biliary cholangitis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27532829",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 78,
"text": "A Placebo-Controlled Trial of Obeticholic Acid in Primary Biliary Cholangitis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27406083",
"endSection": "abstract",
"offsetInBeginSection": 513,
"offsetInEndSection": 654,
"text": "This article summarizes the milestones in the development of obeticholic acid leading to this first approval for primary biliary cholangitis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27468093",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 67,
"text": "Obeticholic acid for the treatment of primary biliary cholangitis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27906472",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Long-term Clinical Impact and Cost-Effectiveness of Obeticholic Acid for the Treatment of Primary Biliary Cholangitis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27825634",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 49,
"text": "Obeticholic acid in primary biliary cholangitis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27532829",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 79,
"text": "A Placebo-Controlled Trial of Obeticholic Acid in Primary Biliary Cholangitis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27406083",
"endSection": "abstract",
"offsetInBeginSection": 515,
"offsetInEndSection": 656,
"text": "This article summarizes the milestones in the development of obeticholic acid leading to this first approval for primary biliary cholangitis."
}
]
| 6 | BioASQ-training6b | [
"http://www.disease-ontology.org/api/metadata/DOID:0060643",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013812",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D019468"
]
| [
{
"o": "Obeticholic Acid",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C2825352"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A17691068",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C2825352"
},
{
"o": "OBETICHOLIC ACID",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A17691068"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A10762572",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0087111"
},
{
"o": "Treatment",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A10762572"
}
]
| 5884722ee56acf5176000006 | 124 |
yesno | Are Tregs CD4(+)CD25(+) regulatory T cells a positive regulator of the immune response? | ['no'] | [
"no"
]
| ['CD4(+)CD25(+) regulatory T cells (Tregs) are negative regulators of the immune system that induce and maintain immune tolerance.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/19816193",
"http://www.ncbi.nlm.nih.gov/pubmed/18205702",
"http://www.ncbi.nlm.nih.gov/pubmed/21386770",
"http://www.ncbi.nlm.nih.gov/pubmed/17848162",
"http://www.ncbi.nlm.nih.gov/pubmed/23531479",
"http://www.ncbi.nlm.nih.gov/pubmed/17826781",
"http://www.ncbi.nlm.nih.gov/pubmed/24095986",
"http://www.ncbi.nlm.nih.gov/pubmed/16809644",
"http://www.ncbi.nlm.nih.gov/pubmed/17368474",
"http://www.ncbi.nlm.nih.gov/pubmed/23983771",
"http://www.ncbi.nlm.nih.gov/pubmed/20843956",
"http://www.ncbi.nlm.nih.gov/pubmed/17407195",
"http://www.ncbi.nlm.nih.gov/pubmed/22749847",
"http://www.ncbi.nlm.nih.gov/pubmed/34495808",
"http://www.ncbi.nlm.nih.gov/pubmed/16020508",
"http://www.ncbi.nlm.nih.gov/pubmed/18032693",
"http://www.ncbi.nlm.nih.gov/pubmed/20384869",
"http://www.ncbi.nlm.nih.gov/pubmed/23635849",
"http://www.ncbi.nlm.nih.gov/pubmed/27109178",
"http://www.ncbi.nlm.nih.gov/pubmed/18580479",
"http://www.ncbi.nlm.nih.gov/pubmed/19005268",
"http://www.ncbi.nlm.nih.gov/pubmed/24754976",
"http://www.ncbi.nlm.nih.gov/pubmed/25113439",
"http://www.ncbi.nlm.nih.gov/pubmed/19543397",
"http://www.ncbi.nlm.nih.gov/pubmed/15778406",
"http://www.ncbi.nlm.nih.gov/pubmed/16393984",
"http://www.ncbi.nlm.nih.gov/pubmed/21597299",
"http://www.ncbi.nlm.nih.gov/pubmed/17234458",
"http://www.ncbi.nlm.nih.gov/pubmed/24483245",
"http://www.ncbi.nlm.nih.gov/pubmed/21655351",
"http://www.ncbi.nlm.nih.gov/pubmed/22899644"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19816193",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "The immunosuppressive effects of CD4+ CD25 high regulatory T cells (Tregs) interfere with antitumor immune responses in cancer patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25113439",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 146,
"text": "Alteration of regulatory T cells (Tregs) may contribute to ineffective suppression of proinflammatory cytokines in type 1 diabetes.AIM"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24754976",
"endSection": "abstract",
"offsetInBeginSection": 110,
"offsetInEndSection": 179,
"text": "Regulatory T cells (Tregs) suppress excessive immune responses in IRI"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24095986",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "CD4(+)CD25(+) regulatory T cells (Tregs) are negative regulators of the immune system that induce and maintain immune tolerance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19005268",
"endSection": "abstract",
"offsetInBeginSection": 870,
"offsetInEndSection": 1022,
"text": "lar to chronic patients, Treg from patients with PHI inhibited the proliferation of purified tuberculin (PPD) and HIV p24 activated CD4CD25 T cells. CD4"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21386770",
"endSection": "abstract",
"offsetInBeginSection": 655,
"offsetInEndSection": 901,
"text": " demonstrate that aTregs are necessary for tolerance, DBA/2 skin was transplanted onto C57BL/6-RAG-1-deficient recipients adoptively transferred with purified sorted CD4CD25 T cells; half of the recipients undergo tolerance induction treatment.RE"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23635849",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "It is well established that CD4CD25 regulatory T cells (Tregs) downregulate inflammatory immune responses and help to maintain immune homeostasis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18580479",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "In vitro expanded human CD4+CD25+ regulatory T cells are potent suppressors of T-cell-mediated xenogeneic responses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19543397",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 81,
"text": "BACKGROUND: Regulatory T cells (Tregs) are essential in the control of tolerance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20384869",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "CD4(+)CD25(+) regulatory T cells (Tregs) are critical for the peripheral immune tolerance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27109178",
"endSection": "abstract",
"offsetInBeginSection": 114,
"offsetInEndSection": 287,
"text": "T regulatory cells (Tregs) have a role in immunosuppression and control of autoimmunity, and are currently an important topic in the study of immune response to tumor cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23635849",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "CD4+CD25+ regulatory T cells attenuate lipopolysaccharide-induced systemic inflammatory responses and promotes survival in murine Escherichia coli infection."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23531479",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "OBJECTIVES: CD4CD25 regulatory T cells (Tregs) play a key role in the prevention of various inflammatory and autoimmune disorders by suppressing immune responses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21655351",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 243,
"text": "CD25(High) CD4+ regulatory T cells (Treg cells) have been described as key players in immune regulation, preventing infection-induced immune pathology and limiting collateral tissue damage caused by vigorous anti-parasite immune response. In t"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22899644",
"endSection": "abstract",
"offsetInBeginSection": 240,
"offsetInEndSection": 521,
"text": "ic subset of T cells, currently recognized as FOXP3(+) CD25(+) CD4(+) regulatory T cells (Tregs), are pivotal in suppressing autoimmunity and maintaining immune homeostasis by mediating self-tolerance at the periphery as shown in autoimmune diseases and cancers. A growing body of "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16020508",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 92,
"text": "CD4+CD25+ regulatory T cells (Tregs) are essential negative regulators of immune responses. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22749847",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 255,
"text": "Accumulating evidence has demonstrated that naturally occurring CD4(+)CD25(+) regulatory T cells (Tregs) are critical for maintenance of immunological tolerance and have been shown to be important in regulating the immune responses in many diseases. Curcu"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24483245",
"endSection": "abstract",
"offsetInBeginSection": 280,
"offsetInEndSection": 426,
"text": "4+CD25+ Foxp3+ regulatory T cells (Tregs) are recognized as one of the major regulatory factors in immune tolerance and inflammatory responses. Si"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17826781",
"endSection": "abstract",
"offsetInBeginSection": 370,
"offsetInEndSection": 552,
"text": "lly occurring CD4(+)CD25(+) regulatory T cells (Tregs) have a key role in the prevention of various inflammatory and autoimmune disorders by suppressing immune responses. We tested t"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17368474",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "CD4(+)CD25(+) regulatory T cells (Tregs) are considered to play a key role as suppressors of immune mediated reactions. The a"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18205702",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "CD4+ CD25+ T regulatory cells (Tregs) are classified as a subset of T cells whose role is the suppression and regulation of immune responses to self and non-self. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18032693",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "CD4(+)CD25(+) regulatory T cells (Tregs) are potent modulators of immune responses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16393984",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 213,
"text": "CD4+ T cells naturally expressing CD25 molecules (natural T regulatory cells (Tregs)) have a role in maintaining self tolerance and in regulating responses to infectious agents, transplantation Ags, and tumor Ags."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20843956",
"endSection": "abstract",
"offsetInBeginSection": 157,
"offsetInEndSection": 275,
"text": "Naturally occurring CD4(+)CD25(+) regulatory T cells (Tregs) are essential for the active suppression of autoimmunity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16809644",
"endSection": "abstract",
"offsetInBeginSection": 260,
"offsetInEndSection": 489,
"text": "Amongst these, naturally occurring CD4(+)CD25(+) Treg cells (nTreg) represent a major lymphocyte population engaged in the dominant control of self-reactive T responses and maintaining tolerance in several models of autoimmunity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16020508",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "CD4+CD25+ regulatory T cells (Tregs) are essential negative regulators of immune responses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17407195",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 191,
"text": "Naturally occurring CD4(+)CD25(+)FoxP3(+) regulatory T cells (CD25(+) Tregs) constitute a specialized population of T cells that is essential for the maintenance of peripheral self-tolerance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34495808",
"endSection": "abstract",
"offsetInBeginSection": 68,
"offsetInEndSection": 394,
"text": "One of the subpopulations of CD4+ T cells that express CD25+ and the transcription factor FOXP3, known as Regulator T cells (TReg), plays an essential role in maintaining tolerance and immune homeostasis preventing autoimmune diseases, minimalize chronic inflammatory diseases by enlisting various immunoregulatory mechanisms."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15778406",
"endSection": "abstract",
"offsetInBeginSection": 128,
"offsetInEndSection": 240,
"text": "Regulatory T cells (Tregs) are CD4(+)CD25(bright)CD62L(high) cells that actively down-regulate immune responses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17234458",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 202,
"text": "CD4(+)CD25(+) regulatory T cells (Treg) play a central role in the prevention of autoimmunity and in the control of immune responses by down-regulating the function of effector CD4(+) or CD8(+) T cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23983771",
"endSection": "abstract",
"offsetInBeginSection": 124,
"offsetInEndSection": 389,
"text": "FoxP3(+)CD25(+)CD4(+) regulatory T cells (Tregs) suppress a variety of normal physiological and pathological immune responses via several pathways, such as inhibitory cytokine secretion, direct cytolysis induction, and antigen-presenting cell functional modulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17848162",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 236,
"text": "Regulatory CD4(+) CD25(+) T (Treg) cells with the ability to suppress host immune responses against self- or non-self antigens play important roles in the processes of autoimmunity, transplant rejection, infectious diseases and cancers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21597299",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 165,
"text": "BACKGROUND: Evidence indicating that CD4+CD25+ regulatory T (Treg) cells play a crucial role in the maintenance of peripheral T cell tolerance to allergens has been "
}
]
| 11 | BioASQ-training11b | null | null | 621ed10f3a8413c653000062 | 125 |
yesno | Are reduced-nicotine cigarettes effective for smoking cessation? | ['yes'] | [
"yes"
]
| ['Yes, reduced-nicotine cigarettes are effective for smoking cessation.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/26422724",
"http://www.ncbi.nlm.nih.gov/pubmed/25150282",
"http://www.ncbi.nlm.nih.gov/pubmed/24746485",
"http://www.ncbi.nlm.nih.gov/pubmed/16497603",
"http://www.ncbi.nlm.nih.gov/pubmed/19793786",
"http://www.ncbi.nlm.nih.gov/pubmed/20078491",
"http://www.ncbi.nlm.nih.gov/pubmed/18629723",
"http://www.ncbi.nlm.nih.gov/pubmed/17573781",
"http://www.ncbi.nlm.nih.gov/pubmed/23603206",
"http://www.ncbi.nlm.nih.gov/pubmed/21232155",
"http://www.ncbi.nlm.nih.gov/pubmed/25025523"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26422724",
"endSection": "abstract",
"offsetInBeginSection": 1812,
"offsetInEndSection": 1989,
"text": "CONCLUSIONS: In this 6-week study, reduced-nicotine cigarettes versus standard-nicotine cigarettes reduced nicotine exposure and dependence and the number of cigarettes smoked. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25150282",
"endSection": "abstract",
"offsetInBeginSection": 842,
"offsetInEndSection": 1037,
"text": "RESULTS: Significant reductions in nicotine intake were observed between usual brand smoking (∼1.2 mg nicotine) and the 0.3 and 0.05 mg nicotine emission cigarettes, but not the 0.6 mg cigarette."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25150282",
"endSection": "abstract",
"offsetInBeginSection": 1344,
"offsetInEndSection": 1526,
"text": "CONCLUSIONS: The study adds to the evidence that cigarettes with markedly reduced nicotine content are not associated with increased smoking intensity or exposure to smoke toxicants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24746485",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 211,
"text": "BACKGROUND: When switching from usual brand cigarettes, very low nicotine content (VLNC) cigarettes lead to a reduction in the number of cigarettes smoked, toxicant exposure, withdrawal symptoms and dependence. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16497603",
"endSection": "abstract",
"offsetInBeginSection": 1623,
"offsetInEndSection": 1927,
"text": "Moreover, while nicotine patches were well tolerated when subjects smoked nicotine-containing cigarettes, the use of nicotine skin patches with reduced-nicotine cigarettes potentially offers the advantage of increased efficacy without introducing concern about toxic effects of excessive nicotine intake."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18629723",
"endSection": "abstract",
"offsetInBeginSection": 1211,
"offsetInEndSection": 1358,
"text": "Results showed that Quest plus NRT was more effective than active control plus NRT in achieving 4 weeks of continuous abstinence (32.8% vs. 21.9%)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18629723",
"endSection": "abstract",
"offsetInBeginSection": 1553,
"offsetInEndSection": 1620,
"text": "Quest plus NRT offers promise as a new smoking cessation treatment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19793786",
"endSection": "abstract",
"offsetInBeginSection": 700,
"offsetInEndSection": 932,
"text": "We identified three clinical trials (total n = 489) that suggest that smokers can dissociate nicotine delivery from the act of smoking if they use reduced-nicotine content cigarettes in combination with nicotine replacement therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20078491",
"endSection": "abstract",
"offsetInBeginSection": 1063,
"offsetInEndSection": 1250,
"text": "CONCLUSION: The 0.05 mg nicotine yield cigarettes may be a tobacco product that can facilitate cessation; however, future research is clearly needed to support these preliminary findings."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17573781",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 239,
"text": "Preliminary studies suggest an extinction-based smoking cessation treatment using reduced nicotine content (RNC) cigarettes decreases self-report craving for cigarettes prior to quitting and may be an effective smoking cessation treatment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23603206",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Reduced nicotine content (RNC) cigarettes have led to smoking fewer cigarettes, withdrawal relief, and facilitation of cessation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21232155",
"endSection": "abstract",
"offsetInBeginSection": 498,
"offsetInEndSection": 739,
"text": "Evidence from a number of small smoking cessation studies suggests that the use of cigarettes with reduced nicotine content, in combination with nicotine replacement therapy (NRT), may help reduce withdrawal symptoms and increase quit rates."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18629723",
"endSection": "abstract",
"offsetInBeginSection": 567,
"offsetInEndSection": 878,
"text": "The concept for a reduced-nicotine cigarette designed to progressively wean smokers from the smoking habit is based on research demonstrating that successful smoking cessation is not only dependent on withdrawal of nicotine, but also on weaning from the habitual sensory and behavioral reinforcement of smoking."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17573781",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 239,
"text": "Preliminary studies suggest an extinction-based smoking cessation treatment using reduced nicotine content (RNC) cigarettes decreases self-report craving for cigarettes prior to quitting and may be an effective smoking cessation treatment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18629723",
"endSection": "abstract",
"offsetInBeginSection": 567,
"offsetInEndSection": 878,
"text": "The concept for a reduced-nicotine cigarette designed to progressively wean smokers from the smoking habit is based on research demonstrating that successful smoking cessation is not only dependent on withdrawal of nicotine, but also on weaning from the habitual sensory and behavioral reinforcement of smoking."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21232155",
"endSection": "abstract",
"offsetInBeginSection": 498,
"offsetInEndSection": 739,
"text": "Evidence from a number of small smoking cessation studies suggests that the use of cigarettes with reduced nicotine content, in combination with nicotine replacement therapy (NRT), may help reduce withdrawal symptoms and increase quit rates."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17573781",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 238,
"text": "Preliminary studies suggest an extinction-based smoking cessation treatment using reduced nicotine content (RNC) cigarettes decreases self-report craving for cigarettes prior to quitting and may be an effective smoking cessation treatment"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25025523",
"endSection": "abstract",
"offsetInBeginSection": 229,
"offsetInEndSection": 406,
"text": "Specifically, standards that required substantially reduced nicotine content in cigarettes could enable cessation in smokers and prevent future smoking among current non-smokers"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23603206",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "Reduced nicotine content (RNC) cigarettes have led to smoking fewer cigarettes, withdrawal relief, and facilitation of cessation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21232155",
"endSection": "abstract",
"offsetInBeginSection": 259,
"offsetInEndSection": 499,
"text": "Evidence from a number of small smoking cessation studies suggests that the use of cigarettes with reduced nicotine content, in combination with nicotine replacement therapy (NRT), may help reduce withdrawal symptoms and increase quit rates"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18629723",
"endSection": "abstract",
"offsetInBeginSection": 257,
"offsetInEndSection": 567,
"text": "The concept for a reduced-nicotine cigarette designed to progressively wean smokers from the smoking habit is based on research demonstrating that successful smoking cessation is not only dependent on withdrawal of nicotine, but also on weaning from the habitual sensory and behavioral reinforcement of smoking"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16497603",
"endSection": "abstract",
"offsetInBeginSection": 1480,
"offsetInEndSection": 1927,
"text": "These results suggest that use of NRT before a target quit-smoking date deserves further evaluation as a possible smoking cessation treatment. Moreover, while nicotine patches were well tolerated when subjects smoked nicotine-containing cigarettes, the use of nicotine skin patches with reduced-nicotine cigarettes potentially offers the advantage of increased efficacy without introducing concern about toxic effects of excessive nicotine intake."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16497603",
"endSection": "abstract",
"offsetInBeginSection": 1480,
"offsetInEndSection": 1927,
"text": "These results suggest that use of NRT before a target quit-smoking date deserves further evaluation as a possible smoking cessation treatment. Moreover, while nicotine patches were well tolerated when subjects smoked nicotine-containing cigarettes, the use of nicotine skin patches with reduced-nicotine cigarettes potentially offers the advantage of increased efficacy without introducing concern about toxic effects of excessive nicotine intake."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17573781",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 240,
"text": "Preliminary studies suggest an extinction-based smoking cessation treatment using reduced nicotine content (RNC) cigarettes decreases self-report craving for cigarettes prior to quitting and may be an effective smoking cessation treatment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17573781",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 240,
"text": "Preliminary studies suggest an extinction-based smoking cessation treatment using reduced nicotine content (RNC) cigarettes decreases self-report craving for cigarettes prior to quitting and may be an effective smoking cessation treatment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17573781",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 240,
"text": "Preliminary studies suggest an extinction-based smoking cessation treatment using reduced nicotine content (RNC) cigarettes decreases self-report craving for cigarettes prior to quitting and may be an effective smoking cessation treatment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17573781",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 240,
"text": "Preliminary studies suggest an extinction-based smoking cessation treatment using reduced nicotine content (RNC) cigarettes decreases self-report craving for cigarettes prior to quitting and may be an effective smoking cessation treatment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17573781",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 240,
"text": "Preliminary studies suggest an extinction-based smoking cessation treatment using reduced nicotine content (RNC) cigarettes decreases self-report craving for cigarettes prior to quitting and may be an effective smoking cessation treatment."
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D016540"
]
| []
| 56bc8d65ac7ad1001900001a | 126 |
yesno | Is there alternative polyadenylation during zebrafish development? | ['yes'] | [
"yes"
]
| ['Yes. There is extensive alternative polyadenylation during zebrafish development.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22722342"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22722342",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 67,
"text": "Extensive alternative polyadenylation during zebrafish development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22722342",
"endSection": "abstract",
"offsetInBeginSection": 1145,
"offsetInEndSection": 1525,
"text": "At 2 h post-fertilization, thousands of unique poly(A) sites appear at locations lacking a typical polyadenylation signal, which suggests a wave of widespread cytoplasmic polyadenylation of mRNA degradation intermediates. Our insights into the identities, formation, and evolution of zebrafish 3' UTRs provide a resource for studying gene regulation during vertebrate development."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22722342",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 68,
"text": "Extensive alternative polyadenylation during zebrafish development."
}
]
| 6 | BioASQ-training6b | [
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D026723",
"http://amigo.geneontology.org/amigo/term/GO:1900365",
"http://amigo.geneontology.org/amigo/term/GO:1900364",
"http://amigo.geneontology.org/amigo/term/GO:1900363",
"http://amigo.geneontology.org/amigo/term/GO:0006378",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D015027"
]
| null | 58963b0278275d0c4a00000c | 127 |
yesno | Is there a sequence bias in MNase digestion patterns? | ['yes'] | [
"yes"
]
| ['The cutting preference of MNase in combination with size selection generates a sequence-dependent bias in the resulting fragments.', 'yes', 'Micrococcal nuclease does not substantially bias nucleosome mapping. Signal variation in these simulations reveals an important DNA sampling bias that results from a neighborhood effect of MNase digestion techniques.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22310051",
"http://www.ncbi.nlm.nih.gov/pubmed/23458408",
"http://www.ncbi.nlm.nih.gov/pubmed/21206756",
"http://www.ncbi.nlm.nih.gov/pubmed/26080409",
"http://www.ncbi.nlm.nih.gov/pubmed/22559821",
"http://www.ncbi.nlm.nih.gov/pubmed/27185945"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26080409",
"endSection": "abstract",
"offsetInBeginSection": 1127,
"offsetInEndSection": 1211,
"text": "In addition, unlike MNase, MPE-Fe(II) cleaves nuclear DNA with little sequence bias."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26080409",
"endSection": "abstract",
"offsetInBeginSection": 1423,
"offsetInEndSection": 1600,
"text": "These findings collectively indicate that MPE-seq provides a unique and straightforward means for the genome-wide analysis of chromatin structure with minimal DNA sequence bias."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22310051",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 68,
"text": "Micrococcal nuclease does not substantially bias nucleosome mapping."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22310051",
"endSection": "abstract",
"offsetInBeginSection": 432,
"offsetInEndSection": 565,
"text": "MNase has hitherto been very widely used to map nucleosomes, although concerns have been raised over its potential to introduce bias."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22310051",
"endSection": "abstract",
"offsetInBeginSection": 1403,
"offsetInEndSection": 1534,
"text": "These results indicate that biases in nucleosome positioning data collected using MNase are, under our conditions, not significant."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22559821",
"endSection": "abstract",
"offsetInBeginSection": 1066,
"offsetInEndSection": 1213,
"text": "Signal variation in these simulations reveals an important DNA sampling bias that results from a neighborhood effect of MNase digestion techniques."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22559821",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "Standardized collection of MNase-seq experiments enables unbiased dataset comparisons."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21206756",
"endSection": "abstract",
"offsetInBeginSection": 260,
"offsetInEndSection": 409,
"text": "Here, we show that the cutting preference of MNase in combination with size selection generates a sequence-dependent bias in the resulting fragments."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23458408",
"endSection": "abstract",
"offsetInBeginSection": 1000,
"offsetInEndSection": 1210,
"text": "We propose that combined MNase/exoIII digestion can be applied to in situ chromatin for unbiased genome-wide mapping of nucleosome positions that is not influenced by DNA sequences at the core/linker junctions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22559821",
"endSection": "abstract",
"offsetInBeginSection": 1067,
"offsetInEndSection": 1214,
"text": "Signal variation in these simulations reveals an important DNA sampling bias that results from a neighborhood effect of MNase digestion techniques."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22559821",
"endSection": "abstract",
"offsetInBeginSection": 1046,
"offsetInEndSection": 1193,
"text": "Signal variation in these simulations reveals an important DNA sampling bias that results from a neighborhood effect of MNase digestion techniques."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22310051",
"endSection": "abstract",
"offsetInBeginSection": 1403,
"offsetInEndSection": 1535,
"text": "These results indicate that biases in nucleosome positioning data collected using MNase are, under our conditions, not significant.."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22310051",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 69,
"text": "Micrococcal nuclease does not substantially bias nucleosome mapping."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27185945",
"endSection": "abstract",
"offsetInBeginSection": 390,
"offsetInEndSection": 561,
"text": "We find that maize MNase-hypersensitive (MNase HS) regions localize around active genes and within recombination hotspots, focusing biased gene conversion at their flanks."
}
]
| 11 | BioASQ-training11b | null | null | 5a4e1882966455904c00000f | 128 |
yesno | Is selenium deficiency involved in autoimmune thyroid disease? | ['yes'] | [
"yes"
]
| ['The essential trace element selenium was recently recognized as being incorporated as selenocysteine in all three deiodinases of the thyroid gland. This has decisively confirmed the clear-cut link between selenium and thyroid function. Additionally, it has been established that the thyroid contains more selenium than any other tissue, and that selenium deficiency aggravates the manifestation of autoimmune thyroid disease.', 'Selenium deficiency is likely to constitute a risk factor for a feedforward derangement of the immune system-thyroid interaction, while selenium supplementation appears to dampen the self-amplifying nature of this derailed interactionIn areas with severe selenium deficiency higher incidence of thyroiditis has been reported due to a decreased activity of selenium-dependent glutathione peroxidase enzyme within thyroid cells', 'Selenium deficiency is likely to constitute a risk factor for a feedforward derangement of the immune system-thyroid interaction, while selenium supplementation appears to dampen the self-amplifying nature of this derailed interactionIn areas with severe selenium deficiency higher incidence of thyroiditis has been reported due to a decreased activity of selenium-dependent glutathione peroxidase enzyme within thyroid cells', 'The recent recognition that the essential trace element selenium is incorporated as selenocysteine in all three deiodinases has decisively confirmed the clear-cut link between selenium and thyroid function. It has additionally been established that the thyroid contains more selenium than any other tissue and that selenium deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune thyroid disease ', 'The recent recognition that the essential trace element selenium is incorporated as selenocysteine in all three deiodinases has decisively confirmed the clear-cut link between selenium and thyroid function. It has additionally been established that the thyroid contains more selenium than any other tissue and that selenium deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune thyroid disease ', 'The recent recognition that the essential trace element selenium is incorporated as selenocysteine in all three deiodinases has decisively confirmed the clear-cut link between selenium and thyroid function. It has additionally been established that the thyroid contains more selenium than any other tissue and that selenium deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune thyroid disease ', 'The recent recognition that the essential trace element selenium is incorporated as selenocysteine in all three deiodinases has decisively confirmed the clear-cut link between selenium and thyroid function. It has additionally been established that the thyroid contains more selenium than any other tissue and that selenium deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune thyroid disease ', 'The recent recognition that the essential trace element selenium is incorporated as selenocysteine in all three deiodinases has decisively confirmed the clear-cut link between selenium and thyroid function. It has additionally been established that the thyroid contains more selenium than any other tissue and that selenium deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune thyroid disease '] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23565426",
"http://www.ncbi.nlm.nih.gov/pubmed/23448365",
"http://www.ncbi.nlm.nih.gov/pubmed/22009156",
"http://www.ncbi.nlm.nih.gov/pubmed/20810577",
"http://www.ncbi.nlm.nih.gov/pubmed/15132715",
"http://www.ncbi.nlm.nih.gov/pubmed/19034261",
"http://www.ncbi.nlm.nih.gov/pubmed/17160166",
"http://www.ncbi.nlm.nih.gov/pubmed/21896670",
"http://www.ncbi.nlm.nih.gov/pubmed/11932302",
"http://www.ncbi.nlm.nih.gov/pubmed/23786024"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23565426",
"endSection": "abstract",
"offsetInBeginSection": 14,
"offsetInEndSection": 205,
"text": "In areas with severe selenium deficiency higher incidence of thyroiditis has been reported due to a decreased activity of selenium-dependent glutathione peroxidase enzyme within thyroid cells"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23565426",
"endSection": "abstract",
"offsetInBeginSection": 1028,
"offsetInEndSection": 1355,
"text": "Of 30 patients in the selenium treated group, 6 patients were overtly hypothyroid, 15 were subclinical hypothyroid, 6 were euthyroid, and 3 were subclinical hyperthyroid. The mean TPOAb concentration decreased significantly by 49.5% (P < 0.013) in the selenium treated group versus 10.1% (P < 0.95) in the placebo-treated group"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23565426",
"endSection": "abstract",
"offsetInBeginSection": 1369,
"offsetInEndSection": 1479,
"text": "Selenium substitution has a significant impact on inflammatory activity in thyroid-specific autoimmune disease"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23448365",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 56,
"text": "Serum selenium is low in newly diagnosed Graves' disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23448365",
"endSection": "abstract",
"offsetInBeginSection": 678,
"offsetInEndSection": 801,
"text": "S-Se was lower in patients with GD than in controls (mean (SD), GD: 89·9 μg/l (18·4); controls: 98·8 μg/l (19·7), P < 0·01)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23448365",
"endSection": "abstract",
"offsetInBeginSection": 1371,
"offsetInEndSection": 1603,
"text": "Patients with newly diagnosed GD and AIH had significantly lower s-Se compared with random controls. Our observation supports the postulated link between inadequate selenium supply and overt autoimmune thyroid disease, especially GD"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22009156",
"endSection": "abstract",
"offsetInBeginSection": 1618,
"offsetInEndSection": 1852,
"text": "Selenium deficiency is likely to constitute a risk factor for a feedforward derangement of the immune system-thyroid interaction, while selenium supplementation appears to dampen the self-amplifying nature of this derailed interaction"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20810577",
"endSection": "abstract",
"offsetInBeginSection": 9,
"offsetInEndSection": 437,
"text": "The recent recognition that the essential trace element selenium is incorporated as selenocysteine in all three deiodinases has decisively confirmed the clear-cut link between selenium and thyroid function. It has additionally been established that the thyroid contains more selenium than any other tissue and that selenium deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune thyroid disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20810577",
"endSection": "abstract",
"offsetInBeginSection": 1669,
"offsetInEndSection": 1834,
"text": "Maintenance of \"selenostasis\" via optimal intake not only aids preservation of general health but also contributes substantially to the prevention of thyroid disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15132715",
"endSection": "abstract",
"offsetInBeginSection": 520,
"offsetInEndSection": 844,
"text": "Low birth weight, iodine excess and deficiency, selenium deficiency, parity, oral contraceptive use, reproductive span, fetal microchimerism, stress, seasonal variation, allergy, smoking, radiation damage to the thyroid gland, viral and bacterial infections all play a role in the development of autoimmune thyroid disorders"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20810577",
"endSection": "abstract",
"offsetInBeginSection": 205,
"offsetInEndSection": 428,
"text": "It has additionally been established that the thyroid contains more selenium than any other tissue and that selenium deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune thyroid disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23448365",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 111,
"text": "Selenium deficiency may play an important role in the initiation and progression of autoimmune thyroid disease."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19034261",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 77,
"text": "[Selenium deficiency in celiac disease: risk of autoimmune thyroid diseases]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15132715",
"endSection": "abstract",
"offsetInBeginSection": 516,
"offsetInEndSection": 842,
"text": "Low birth weight, iodine excess and deficiency, selenium deficiency, parity, oral contraceptive use, reproductive span, fetal microchimerism, stress, seasonal variation, allergy, smoking, radiation damage to the thyroid gland, viral and bacterial infections all play a role in the development of autoimmune thyroid disorders."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22009156",
"endSection": "abstract",
"offsetInBeginSection": 1083,
"offsetInEndSection": 1304,
"text": "Some clinical studies have demonstrated that selenium-deficient patients with autoimmune thyroid disease benefit from selenium supplementation, although the data are conflicting and many parameters must still be defined."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23448365",
"endSection": "abstract",
"offsetInBeginSection": 1356,
"offsetInEndSection": 1489,
"text": "Our observation supports the postulated link between inadequate selenium supply and overt autoimmune thyroid disease, especially GD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20810577",
"endSection": "abstract",
"offsetInBeginSection": 205,
"offsetInEndSection": 428,
"text": "It has additionally been established that the thyroid contains more selenium than any other tissue and that selenium deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune thyroid disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23448365",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 111,
"text": "Selenium deficiency may play an important role in the initiation and progression of autoimmune thyroid disease."
},
{
"beginSection": "title",
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"endSection": "title",
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"offsetInEndSection": 77,
"text": "[Selenium deficiency in celiac disease: risk of autoimmune thyroid diseases]."
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{
"beginSection": "abstract",
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"endSection": "abstract",
"offsetInBeginSection": 1083,
"offsetInEndSection": 1304,
"text": "Some clinical studies have demonstrated that selenium-deficient patients with autoimmune thyroid disease benefit from selenium supplementation, although the data are conflicting and many parameters must still be defined."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23448365",
"endSection": "abstract",
"offsetInBeginSection": 1356,
"offsetInEndSection": 1489,
"text": "Our observation supports the postulated link between inadequate selenium supply and overt autoimmune thyroid disease, especially GD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20810577",
"endSection": "abstract",
"offsetInBeginSection": 205,
"offsetInEndSection": 428,
"text": "It has additionally been established that the thyroid contains more selenium than any other tissue and that selenium deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune thyroid disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23448365",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 111,
"text": "Selenium deficiency may play an important role in the initiation and progression of autoimmune thyroid disease."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19034261",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 77,
"text": "[Selenium deficiency in celiac disease: risk of autoimmune thyroid diseases]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22009156",
"endSection": "abstract",
"offsetInBeginSection": 1083,
"offsetInEndSection": 1304,
"text": "Some clinical studies have demonstrated that selenium-deficient patients with autoimmune thyroid disease benefit from selenium supplementation, although the data are conflicting and many parameters must still be defined."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23448365",
"endSection": "abstract",
"offsetInBeginSection": 1356,
"offsetInEndSection": 1489,
"text": "Our observation supports the postulated link between inadequate selenium supply and overt autoimmune thyroid disease, especially GD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20810577",
"endSection": "abstract",
"offsetInBeginSection": 205,
"offsetInEndSection": 428,
"text": "It has additionally been established that the thyroid contains more selenium than any other tissue and that selenium deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune thyroid disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23448365",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 111,
"text": "Selenium deficiency may play an important role in the initiation and progression of autoimmune thyroid disease."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19034261",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 77,
"text": "[Selenium deficiency in celiac disease: risk of autoimmune thyroid diseases]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22009156",
"endSection": "abstract",
"offsetInBeginSection": 1083,
"offsetInEndSection": 1304,
"text": "Some clinical studies have demonstrated that selenium-deficient patients with autoimmune thyroid disease benefit from selenium supplementation, although the data are conflicting and many parameters must still be defined."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23448365",
"endSection": "abstract",
"offsetInBeginSection": 1356,
"offsetInEndSection": 1489,
"text": "Our observation supports the postulated link between inadequate selenium supply and overt autoimmune thyroid disease, especially GD."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19034261",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 77,
"text": "Selenium deficiency in celiac disease: risk of autoimmune thyroid diseases]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21896670",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 184,
"text": "Selenoproteins contain the essential trace element selenium whose deficiency leads to major disorders including cancer, male reproductive system failure, or autoimmune thyroid disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20810577",
"endSection": "abstract",
"offsetInBeginSection": 216,
"offsetInEndSection": 438,
"text": "It has additionally been established that the thyroid contains more selenium than any other tissue and that selenium deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune thyroid disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20810577",
"endSection": "abstract",
"offsetInBeginSection": 920,
"offsetInEndSection": 1222,
"text": "EVIDENCE SYNTHESIS: Evidence in support of selenium supplementation in thyroid autoimmune disease is evaluated, the results herein presented demonstrating the potential effectiveness of selenium in reducing the antithyroid peroxidase titer and improving the echostructure in the ultrasound examination."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23565426",
"endSection": "abstract",
"offsetInBeginSection": 14,
"offsetInEndSection": 205,
"text": "In areas with severe selenium deficiency higher incidence of thyroiditis has been reported due to a decreased activity of selenium-dependent glutathione peroxidase enzyme within thyroid cells"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19034261",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 77,
"text": "[Selenium deficiency in celiac disease: risk of autoimmune thyroid diseases]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17160166",
"endSection": "abstract",
"offsetInBeginSection": 1139,
"offsetInEndSection": 1288,
"text": "Some investigators suggest that selenium may be a useful adjunctive treatment for autoimmune thyroid diseases, such as Hashimoto and Graves' disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11932302",
"endSection": "abstract",
"offsetInBeginSection": 273,
"offsetInEndSection": 395,
"text": "Therefore, even mild selenium deficiency may contribute to the development and maintenance of autoimmune thyroid diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22009156",
"endSection": "abstract",
"offsetInBeginSection": 1091,
"offsetInEndSection": 1311,
"text": "Some clinical studies have demonstrated that selenium-deficient patients with autoimmune thyroid disease benefit from selenium supplementation, although the data are conflicting and many parameters must still be defined."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22009156",
"endSection": "abstract",
"offsetInBeginSection": 1090,
"offsetInEndSection": 1309,
"text": "Some clinical studies have demonstrated that selenium-deficient patients with autoimmune thyroid disease benefit from selenium supplementation, although the data are conflicting and many parameters must still be defined"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23786024",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 145,
"text": "High prevalence of hyperplastic and autoimmune diseases of thyroid in Ukrainian population is determined by endemic deficit of iodine and selenium"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19034261",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 77,
"text": "[Selenium deficiency in celiac disease: risk of autoimmune thyroid diseases]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20810577",
"endSection": "abstract",
"offsetInBeginSection": 207,
"offsetInEndSection": 429,
"text": "It has additionally been established that the thyroid contains more selenium than any other tissue and that selenium deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune thyroid disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23448365",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 111,
"text": "Selenium deficiency may play an important role in the initiation and progression of autoimmune thyroid disease."
},
{
"beginSection": "abstract",
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"endSection": "abstract",
"offsetInBeginSection": 273,
"offsetInEndSection": 394,
"text": "Therefore, even mild selenium deficiency may contribute to the development and maintenance of autoimmune thyroid diseases"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15132715",
"endSection": "abstract",
"offsetInBeginSection": 520,
"offsetInEndSection": 844,
"text": "Low birth weight, iodine excess and deficiency, selenium deficiency, parity, oral contraceptive use, reproductive span, fetal microchimerism, stress, seasonal variation, allergy, smoking, radiation damage to the thyroid gland, viral and bacterial infections all play a role in the development of autoimmune thyroid disorders"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17160166",
"endSection": "abstract",
"offsetInBeginSection": 1139,
"offsetInEndSection": 1287,
"text": "Some investigators suggest that selenium may be a useful adjunctive treatment for autoimmune thyroid diseases, such as Hashimoto and Graves' disease"
},
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"endSection": "title",
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"text": "[Selenium deficiency in celiac disease: risk of autoimmune thyroid diseases]."
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"text": "It has additionally been established that the thyroid contains more selenium than any other tissue and that selenium deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune thyroid disease."
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"text": "Selenium deficiency may play an important role in the initiation and progression of autoimmune thyroid disease."
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"text": "Therefore, even mild selenium deficiency may contribute to the development and maintenance of autoimmune thyroid diseases"
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"text": "Some investigators suggest that selenium may be a useful adjunctive treatment for autoimmune thyroid diseases, such as Hashimoto and Graves' disease"
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"text": "[Selenium deficiency in celiac disease: risk of autoimmune thyroid diseases]."
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"text": "It has additionally been established that the thyroid contains more selenium than any other tissue and that selenium deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune thyroid disease."
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"text": "Selenium deficiency may play an important role in the initiation and progression of autoimmune thyroid disease."
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"text": "Therefore, even mild selenium deficiency may contribute to the development and maintenance of autoimmune thyroid diseases"
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"text": "Low birth weight, iodine excess and deficiency, selenium deficiency, parity, oral contraceptive use, reproductive span, fetal microchimerism, stress, seasonal variation, allergy, smoking, radiation damage to the thyroid gland, viral and bacterial infections all play a role in the development of autoimmune thyroid disorders"
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"text": "Some investigators suggest that selenium may be a useful adjunctive treatment for autoimmune thyroid diseases, such as Hashimoto and Graves' disease"
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"text": "[Selenium deficiency in celiac disease: risk of autoimmune thyroid diseases]."
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"text": "It has additionally been established that the thyroid contains more selenium than any other tissue and that selenium deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune thyroid disease."
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"text": "Selenium deficiency may play an important role in the initiation and progression of autoimmune thyroid disease."
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"text": "Therefore, even mild selenium deficiency may contribute to the development and maintenance of autoimmune thyroid diseases"
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"text": "Low birth weight, iodine excess and deficiency, selenium deficiency, parity, oral contraceptive use, reproductive span, fetal microchimerism, stress, seasonal variation, allergy, smoking, radiation damage to the thyroid gland, viral and bacterial infections all play a role in the development of autoimmune thyroid disorders"
},
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"text": "Some investigators suggest that selenium may be a useful adjunctive treatment for autoimmune thyroid diseases, such as Hashimoto and Graves' disease"
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"text": "[Selenium deficiency in celiac disease: risk of autoimmune thyroid diseases]."
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"offsetInBeginSection": 207,
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"text": "It has additionally been established that the thyroid contains more selenium than any other tissue and that selenium deficiency aggravates the manifestation of endemic myxedematous cretinism and autoimmune thyroid disease."
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"text": "Selenium deficiency may play an important role in the initiation and progression of autoimmune thyroid disease."
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"text": "Therefore, even mild selenium deficiency may contribute to the development and maintenance of autoimmune thyroid diseases"
},
{
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"text": "Low birth weight, iodine excess and deficiency, selenium deficiency, parity, oral contraceptive use, reproductive span, fetal microchimerism, stress, seasonal variation, allergy, smoking, radiation damage to the thyroid gland, viral and bacterial infections all play a role in the development of autoimmune thyroid disorders"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/17160166",
"endSection": "abstract",
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"text": "Some investigators suggest that selenium may be a useful adjunctive treatment for autoimmune thyroid diseases, such as Hashimoto and Graves' disease"
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]
| 5 | BioASQ-training5b | [
"http://www.biosemantics.org/jochem#4278041",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013967",
"http://www.disease-ontology.org/api/metadata/DOID:7188"
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| []
| 550c1ca3a103b78016000003 | 129 |
yesno | Can Amyotrophic Lateral Sclerosis (ALS) be associated with a mutation of the Super Oxide Dismutase 1 (SOD) gene? | ['yes'] | [
"yes"
]
| ['Yes, mutations of the Super Oxide Dismutase 1 (SOD1) gene have been linked to some cases of Amyotrophic Lateral Sclerosis (ALS).', 'Yes, mutations in the SOD1 gene can cause familial Amyotrophic Lateral Sclerosis (ALS).', 'Yes, approximately 2% of ALS cases are caused by mutations in the SOD1 gene.', 'Amyotrophic Lateral Sclerosis (ALS) can be associated with a mutation of the Super Oxide Dismutase 1 (SOD) gene, in a small percentage of cases.', 'ALS can be associated with a mutation of the SOD1 gene', 'Approximately 2% of amyotrophic lateral sclerosis (ALS) cases are caused by mutations in the super oxide dismutase 1 (SOD1) gene a .', 'Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that is associated with mutations in the super oxide dismutase 1 (SOD1) gene.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/9065559",
"http://www.ncbi.nlm.nih.gov/pubmed/7554432",
"http://www.ncbi.nlm.nih.gov/pubmed/20385392",
"http://www.ncbi.nlm.nih.gov/pubmed/24838187",
"http://www.ncbi.nlm.nih.gov/pubmed/30509290",
"http://www.ncbi.nlm.nih.gov/pubmed/27297615",
"http://www.ncbi.nlm.nih.gov/pubmed/10869061",
"http://www.ncbi.nlm.nih.gov/pubmed/10624810",
"http://www.ncbi.nlm.nih.gov/pubmed/8446170",
"http://www.ncbi.nlm.nih.gov/pubmed/9263219",
"http://www.ncbi.nlm.nih.gov/pubmed/11464949",
"http://www.ncbi.nlm.nih.gov/pubmed/11675874",
"http://www.ncbi.nlm.nih.gov/pubmed/31928838",
"http://www.ncbi.nlm.nih.gov/pubmed/8981308",
"http://www.ncbi.nlm.nih.gov/pubmed/9506558",
"http://www.ncbi.nlm.nih.gov/pubmed/7820674",
"http://www.ncbi.nlm.nih.gov/pubmed/15189359",
"http://www.ncbi.nlm.nih.gov/pubmed/11284995",
"http://www.ncbi.nlm.nih.gov/pubmed/12402272",
"http://www.ncbi.nlm.nih.gov/pubmed/18608106",
"http://www.ncbi.nlm.nih.gov/pubmed/15079798",
"http://www.ncbi.nlm.nih.gov/pubmed/9455977",
"http://www.ncbi.nlm.nih.gov/pubmed/23954173",
"http://www.ncbi.nlm.nih.gov/pubmed/27556028",
"http://www.ncbi.nlm.nih.gov/pubmed/10202988",
"http://www.ncbi.nlm.nih.gov/pubmed/9062909",
"http://www.ncbi.nlm.nih.gov/pubmed/7917302",
"http://www.ncbi.nlm.nih.gov/pubmed/15679043",
"http://www.ncbi.nlm.nih.gov/pubmed/24611504",
"http://www.ncbi.nlm.nih.gov/pubmed/24283821",
"http://www.ncbi.nlm.nih.gov/pubmed/7951249"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15189359",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Approximately 2% of amyotrophic lateral sclerosis (ALS) cases are caused by mutations in the super oxide dismutase 1 (SOD1) gene a"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30509290",
"endSection": "abstract",
"offsetInBeginSection": 718,
"offsetInEndSection": 795,
"text": ". The two most widely studied ALS/FTLD models, super-oxide dismutase 1 (SOD1)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24283821",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 189,
"text": "A novel mutation of the SOD-1 gene which encodes the enzyme copper-zinc superoxide dismutase was identified in a family manifesting amyotrophic lateral sclerosis (ALS) in three generations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12402272",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "Mutations in the Cu/Zn superoxide dismutase gene (SOD-1) are reported in 20% of familial amyotrophic lateral sclerosis (ALS) cases, but no definite report of a mutation in a \"truly\" sporadic case of ALS has been proved."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27297615",
"endSection": "abstract",
"offsetInBeginSection": 140,
"offsetInEndSection": 287,
"text": "Copper-zinc superoxide dismutase 1 (SOD1) is one of the most commonly mutated genes in ALS, and more than 160 mutations in SOD1 have been reported."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7820674",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Mutations of the Cu/Zn superoxide dismutase (SOD-1) gene were recently implicated in the pathogenesis of familial amyotrophic lateral sclerosis (ALS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24283821",
"endSection": "abstract",
"offsetInBeginSection": 577,
"offsetInEndSection": 660,
"text": "Over 30 different mutations of SOD-1 have now been identified in families with ALS."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24283821",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 82,
"text": "A novel mutation of SOD-1 (Gly 108 Val) in familial amyotrophic lateral sclerosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15189359",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 242,
"text": "Approximately 2% of amyotrophic lateral sclerosis (ALS) cases are caused by mutations in the super oxide dismutase 1 (SOD1) gene and transgenic mice for these mutations recapitulate many features of this devastating neurodegenerative disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9065559",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "Mutations of the gene SOD-1, which encodes the enzyme copper-zinc superoxide dismutase, occur in patients with a familial form of amyotrophic lateral sclerosis (ALS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10624810",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "Autosomal-dominant familial amyotrophic lateral sclerosis (FALS) is associated with mutation in the gene that encodes Cu/Zn superoxide dismutase (SOD1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10624810",
"endSection": "abstract",
"offsetInBeginSection": 379,
"offsetInEndSection": 631,
"text": "(1996) (Morita, M., Aoki, M., Abe, K., Hasegawa, T., Sakuma, R., Onodera, Y., Ichikawa, N., Nishizawa, M. and Itoyama, Y., A novel two-base mutation in the Cu/Zn superoxide dismutase gene associated with familial amyotrophic lateral sclerosis in Japan."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9455977",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "Mutations of the SOD1 gene, which encodes the enzyme copper/zinc superoxide dismutase, are associated with familial amyotrophic lateral sclerosis (ALS)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9455977",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Familial ALS is associated with mutations in all exons of SOD1: a novel mutation in exon 3 (Gly72Ser)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8446170",
"endSection": "abstract",
"offsetInBeginSection": 542,
"offsetInEndSection": 786,
"text": "Here we report tight genetic linkage between FALS and a gene that encodes a cytosolic, Cu/Zn-binding superoxide dismutase (SOD1), a homodimeric metalloenzyme that catalyzes the dismutation of the toxic superoxide anion O2.- to O2 and H2O2 (ref."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7951249",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 188,
"text": "Familial amyotrophic lateral sclerosis (FALS), a degenerative disorder of motor neurons, is associated with mutations in the Cu/Zn superoxide dismutase gene SOD1 in some affected families."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9506558",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 159,
"text": "Eight of 38 patients (21%) with familial and 5 of 175 patients (3%) with sporadic amyotrophic lateral sclerosis (ALS) had missense mutations in the SOD-1 gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23954173",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 168,
"text": "The SOD1 gene encoding the superoxide dismutase 1 (SOD1) protein is mutated in approximately 15% of familial amyotrophic lateral sclerosis (ALS) and 3% of sporadic ALS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11464949",
"endSection": "abstract",
"offsetInBeginSection": 212,
"offsetInEndSection": 344,
"text": "About 20% of ALS families are associated with mutations in the gene for superoxide dismutase-1 (SOD1) encoded on chromosome 21q22.1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24611504",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "The superoxide dismutase-1 (SOD1) gene is the first gene for familial amyotrophic lateral sclerosis (ALS) with autosomal dominant inheritance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27556028",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "Dominant mutations in Cu/Zn-superoxide dismutase (SOD1) gene have been shown to cause a familial form of amyotrophic lateral sclerosis (SOD1-ALS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7554432",
"endSection": "abstract",
"offsetInBeginSection": 334,
"offsetInEndSection": 497,
"text": " Mutations in the gene encoding Cu/Zn-superoxide dismutase (SOD-1) have been identified in cases of familial amyotrophic lateral sclerosis linked to chromosome 21."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7917302",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 145,
"text": "Mutations in the Cu, Zn superoxide dismutase (SOD1) gene have been reported in some pedigrees with Familial Amyotrophic Lateral Sclerosis (FALS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24838187",
"endSection": "abstract",
"offsetInBeginSection": 138,
"offsetInEndSection": 278,
"text": " Genetic mutations in Cu/Zn superoxide dismutase (SOD1) have been associated with one kind of familial amyotrophic lateral sclerosis (ALS1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8981308",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 197,
"text": "Accumulated evidence implies that mutations in the gene coding for Cu/Zn superoxide dismutase (SOD) are associated with the pathogenesis of the familial form of amyotrophic lateral sclerosis (ALS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9263219",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 167,
"text": " have reported point mutations in the cytosolic Cu/Zn superoxide dismutase (SOD 1) gene in some families with familial amyotrophic lateral sclerosis (ALS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9062909",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "All mutations in the human gene for CuZn superoxide dismutase (CuZnSOD) reported to date are associated with the disease amyotrophic lateral sclerosis (ALS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18608106",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Mutations in the Cu/Zn superoxide dismutase 1 (SOD1) gene have been reported to cause adult-onset autosomal dominant amyotrophic lateral sclerosis (FALS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10202988",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 274,
"text": "We report the absence of superoxide dismutase (SOD-1) gene mutations in 30 patients with amyotrophic lateral sclerosis (ALS) including individuals with a confirmed family history of ALS (familial ALS/FALS), ALS with an unclear family history (UFALS) and sporadic ALS (SALS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9065559",
"endSection": "abstract",
"offsetInBeginSection": 860,
"offsetInEndSection": 1042,
"text": "A predilection for disease onset in the lower limbs appears to be a distinguishing feature of familial ALS with SOD-1 mutations, and accords with findings in transgenic mouse models."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15079798",
"endSection": "abstract",
"offsetInBeginSection": 645,
"offsetInEndSection": 747,
"text": "is a new type of SOD1 mutation which may be associated with familial amyotrophic lateral sclerosis.CON"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10869061",
"endSection": "abstract",
"offsetInBeginSection": 702,
"offsetInEndSection": 989,
"text": "To delineate ALS associated with this particular CuZn-SOD mutation from ALS without mutations, we performed a detailed neurophysiological study of the corticomotoneuronal function using peristimulus time histograms (PSTHs) in eight ALS patients homozygous for the D90A CuZn-SOD mutation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12402272",
"endSection": "abstract",
"offsetInBeginSection": 102,
"offsetInEndSection": 252,
"text": "ateral sclerosis (ALS) cases, but no definite report of a mutation in a \"truly\" sporadic case of ALS has been proved. We present the first case of a n"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31928838",
"endSection": "abstract",
"offsetInBeginSection": 208,
"offsetInEndSection": 301,
"text": "It has been reported that mutations in the superoxide dismutase (SOD) 1 gene can lead to ALS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20385392",
"endSection": "abstract",
"offsetInBeginSection": 134,
"offsetInEndSection": 253,
"text": "Mutations in the superoxide dismutase-1 (SOD1) gene have been found in 12%-23% of patients diagnosed with familial ALS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11675874",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 167,
"text": "INTRODUCTION: Mutations in the gene encoding the free radical scavenging enzyme CuZn-superoxide dismutase have been associated with amyotrophic lateral sclerosis (ALS)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15679043",
"endSection": "abstract",
"offsetInBeginSection": 121,
"offsetInEndSection": 262,
"text": "Up to 20% of ALS cases are inherited (familial, fALS) and associated with mutations, usually of the superoxide dismutase type 1 (SOD-1) gene."
}
]
| 12 | BioASQ-training12b | null | null | 641c516d690f196b5100003f | 130 |
yesno | Is tofacitinib a JAK inhibitor? | ['yes'] | [
"yes"
]
| ['Yes, tofacitinib is a small JAK inhibitor.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/31721311"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31721311",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 122,
"text": "The Janus Kinase inhibitor tofacitinib impacts human dendritic cell differentiation and favours M1 macrophage development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31721311",
"endSection": "abstract",
"offsetInBeginSection": 195,
"offsetInEndSection": 342,
"text": "Tofacitinib, a small JAK inhibitor, is approved for the treatment of RA and has demonstrated good efficacy in psoriasis phase III clinical trials. "
}
]
| 11 | BioASQ-training11b | null | null | 602596691cb411341a0000ad | 131 |
yesno | Can sorafenib activate AMPK? | ['yes'] | [
"yes"
]
| ['Sorafenib induces persisten AMPK activation'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/25080865",
"http://www.ncbi.nlm.nih.gov/pubmed/23963659",
"http://www.ncbi.nlm.nih.gov/pubmed/25349646"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25080865",
"endSection": "abstract",
"offsetInBeginSection": 310,
"offsetInEndSection": 452,
"text": "Here, we identify sorafenib as an activator of AMP-activated protein kinase (AMPK), in a manner that involves either upstream LKB1 or CAMKK2. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23963659",
"endSection": "abstract",
"offsetInBeginSection": 1068,
"offsetInEndSection": 1271,
"text": "Persistent activation of AMPK by sorafenib finally led to the impairment of glucose metabolism both in MCF-7 and SKBR3 cells as well as in the highly glycolytic MDA-MB-231 cells, resulting in cell death."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25080865",
"endSection": "abstract",
"offsetInBeginSection": 310,
"offsetInEndSection": 450,
"text": "Here, we identify sorafenib as an activator of AMP-activated protein kinase (AMPK), in a manner that involves either upstream LKB1 or CAMKK2"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25080865",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 77,
"text": "Sorafenib synergizes with metformin in NSCLC through AMPK pathway activation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23963659",
"endSection": "abstract",
"offsetInBeginSection": 1069,
"offsetInEndSection": 1396,
"text": "Persistent activation of AMPK by sorafenib finally led to the impairment of glucose metabolism both in MCF-7 and SKBR3 cells as well as in the highly glycolytic MDA-MB-231 cells, resulting in cell death. This previously unrecognized long-term effect of sorafenib was mediated by AMPK-dependent inhibition of the mTORC1 pathway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23963659",
"endSection": "abstract",
"offsetInBeginSection": 1069,
"offsetInEndSection": 1396,
"text": "Persistent activation of AMPK by sorafenib finally led to the impairment of glucose metabolism both in MCF-7 and SKBR3 cells as well as in the highly glycolytic MDA-MB-231 cells, resulting in cell death. This previously unrecognized long-term effect of sorafenib was mediated by AMPK-dependent inhibition of the mTORC1 pathway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23963659",
"endSection": "abstract",
"offsetInBeginSection": 1069,
"offsetInEndSection": 1396,
"text": "Persistent activation of AMPK by sorafenib finally led to the impairment of glucose metabolism both in MCF-7 and SKBR3 cells as well as in the highly glycolytic MDA-MB-231 cells, resulting in cell death. This previously unrecognized long-term effect of sorafenib was mediated by AMPK-dependent inhibition of the mTORC1 pathway."
}
]
| 5 | BioASQ-training5b | [
"http://www.biosemantics.org/jochem#http://www.biosemantics.org/jochem#:4243524",
"http://www.biosemantics.org/jochem#4243524",
"http://amigo.geneontology.org/amigo/term/GO:0031588"
]
| []
| 56c8318f5795f9a73e00000f | 132 |
yesno | Does promoter shape vary across populations? | ['yes'] | [
"yes"
]
| ['Yes. Promoter shape varies across populations and affects promoter evolution and expression noise. This is accompanied by differences in the expression levels of different genes, which may reflect differences in their regulatory mechanisms.', 'Yes. Promoter shape varies across populations and affects promoter evolution and expression noise.', 'Yes. Promoter shape varies across populations and affects promoter evolution and expression noise. In some populations, promoter shape is more or less consistent across populations, while in other populations it varies little.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/28191888"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28191888",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 93,
"text": "Promoter shape varies across populations and affects promoter evolution and expression noise."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28191888",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1162,
"text": "Animal promoters initiate transcription either at precise positions (narrow promoters) or dispersed regions (broad promoters), a distinction referred to as promoter shape. Although highly conserved, the functional properties of promoters with different shapes and the genetic basis of their evolution remain unclear. Here we used natural genetic variation across a panel of 81 Drosophila lines to measure changes in transcriptional start site (TSS) usage, identifying thousands of genetic variants affecting transcript levels (strength) or the distribution of TSSs within a promoter (shape). Our results identify promoter shape as a molecular trait that can evolve independently of promoter strength. Broad promoters typically harbor shape-associated variants, with signatures of adaptive selection. Single-cell measurements demonstrate that variants modulating promoter shape often increase expression noise, whereas heteroallelic interactions with other promoter variants alleviate these effects. These results uncover new functional properties of natural promoters and suggest the minimization of expression noise as an important factor in promoter evolution."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28191888",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 92,
"text": "Promoter shape varies across populations and affects promoter evolution and expression noise"
}
]
| 11 | BioASQ-training11b | null | null | 5e52ab626d0a277941000046 | 133 |
yesno | Is oxalate renal excretion increased after bariatric surgery? | ['yes'] | [
"yes"
]
| Urinary oxalate increases after bariatric surgery | [
"http://www.ncbi.nlm.nih.gov/pubmed/20566568",
"http://www.ncbi.nlm.nih.gov/pubmed/19762051",
"http://www.ncbi.nlm.nih.gov/pubmed/22554593",
"http://www.ncbi.nlm.nih.gov/pubmed/21295813",
"http://www.ncbi.nlm.nih.gov/pubmed/23024163",
"http://www.ncbi.nlm.nih.gov/pubmed/23821183",
"http://www.ncbi.nlm.nih.gov/pubmed/18501812",
"http://www.ncbi.nlm.nih.gov/pubmed/17222634",
"http://www.ncbi.nlm.nih.gov/pubmed/19013593",
"http://www.ncbi.nlm.nih.gov/pubmed/2669121",
"http://www.ncbi.nlm.nih.gov/pubmed/18701613"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20566568",
"endSection": "abstract",
"offsetInBeginSection": 280,
"offsetInEndSection": 630,
"text": "Despite the fact that bariatric surgery-induced weight loss is associated with a significant decrease in morbidity and mortality and improvement in renal function, bariatric surgery has recently been shown to be associated with a significant risk of nephrolithiasis. The main risk factor for nephrolithiasis is increased excretion of urinary oxalate."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19762051",
"endSection": "abstract",
"offsetInBeginSection": 1405,
"offsetInEndSection": 1567,
"text": "Our study confirms the risk of urinary stones following the Roux-en-Y gastric bypass procedure as a result of hyperoxaluria, low urine volume and hypocitraturia. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22554593",
"endSection": "abstract",
"offsetInBeginSection": 1121,
"offsetInEndSection": 1361,
"text": "A controlled metabolic diet normal in calcium, moderate in protein, and reduced in oxalate can positively affect urinary CaOx supersaturation after bariatric surgery. However, this diet did not appear to decrease urinary oxalate excretion. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21295813",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 144,
"text": "Hyperoxaluria and increased calcium oxalate stone formation occur after Roux-en-Y gastric bypass (RYGB) surgery for morbid obesity. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21295813",
"endSection": "abstract",
"offsetInBeginSection": 1183,
"offsetInEndSection": 1388,
"text": "Therefore, after bariatric surgery, increases in fecal fat excretion, urinary oxalate excretion after an oral oxalate load, plasma oxalate, and urinary calcium oxalate supersaturation values were observed."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23024163",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 123,
"text": "Bariatric surgery (BS) may be associated with increased oxalate excretion and a higher risk of nephrolithiasis. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23024163",
"endSection": "abstract",
"offsetInBeginSection": 1415,
"offsetInEndSection": 1639,
"text": "The mean oxaluric response to an oxalate load is markedly elevated in post-bariatric surgery patients, suggesting that increased intestinal absorption of dietary oxalate is a predisposing mechanism for enteric hyperoxaluria."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23821183",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 95,
"text": "Persistent mild to moderate hyperoxaluria (PMMH) is a common side effect of bariatric surgery. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18501812",
"endSection": "abstract",
"offsetInBeginSection": 1551,
"offsetInEndSection": 1735,
"text": "This prospective study indicates that RYGB is associated with an earlier increase in urinary oxalate excretion and relative supersaturation of calcium oxalate than previously reported."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17222634",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "Hyperoxaluria in kidney stone formers treated with modern bariatric surgery."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17222634",
"endSection": "abstract",
"offsetInBeginSection": 1364,
"offsetInEndSection": 1510,
"text": "Hyperoxaluria is the most significant abnormality of urine chemistry studies in patients with kidney stones who have undergone bariatric surgery. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19013593",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 150,
"text": "Recent investigations have shown increased oxalate excretion in patients in whom kidney stones formed after contemporary bariatric surgery."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19013593",
"endSection": "abstract",
"offsetInBeginSection": 1576,
"offsetInEndSection": 1803,
"text": "There is a high prevalence of hyperoxaluria in patients without a history of kidney stones who undergo bariatric surgery. A significant proportion of these patients have profound hyperoxaluria, which is not uniformly expressed."
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D050110",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D010070",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0007588"
]
| []
| 52efc001c8da898910000019 | 134 |
yesno | Can ferric carboxymaltose be used to treat anemia in inflammatory bowel disease patients? | ['yes'] | [
"yes"
]
| ['Ferric carboxymaltose can be used to treat anemia in patients with inflammatory bowel disease, and prevents recurrence of anemia in these patients, compared with placebo. Treatment with ferric carboxymaltose is efficious, safe and well tolerated in iron-deficient IBD patients.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/24114623",
"http://www.ncbi.nlm.nih.gov/pubmed/24081613",
"http://www.ncbi.nlm.nih.gov/pubmed/23889159",
"http://www.ncbi.nlm.nih.gov/pubmed/23644823",
"http://www.ncbi.nlm.nih.gov/pubmed/23078888",
"http://www.ncbi.nlm.nih.gov/pubmed/22179489",
"http://www.ncbi.nlm.nih.gov/pubmed/22023204",
"http://www.ncbi.nlm.nih.gov/pubmed/21699794",
"http://www.ncbi.nlm.nih.gov/pubmed/21340038",
"http://www.ncbi.nlm.nih.gov/pubmed/21479141",
"http://www.ncbi.nlm.nih.gov/pubmed/20648930",
"http://www.ncbi.nlm.nih.gov/pubmed/19787830",
"http://www.ncbi.nlm.nih.gov/pubmed/18371137"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24114623",
"endSection": "abstract",
"offsetInBeginSection": 641,
"offsetInEndSection": 805,
"text": "Intravenous iron should be preferred where oral iron is poorly tolerated or where it has failed in moderate to severe anemia, and in combination with erythropoietin"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24114623",
"endSection": "abstract",
"offsetInBeginSection": 938,
"offsetInEndSection": 1069,
"text": "Ferric carboxymaltose is much more convenient, and has been shown to be more effective than iron sucrose in a large randomized tria"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24114623",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 84,
"text": "nemia and iron deficiency anemia are very common in inflammatory bowel disease (IBD"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24081613",
"endSection": "abstract",
"offsetInBeginSection": 817,
"offsetInEndSection": 941,
"text": "Ferric carboxymaltose was associated with cost savings of 30-44 % per patient per treatment cycle compared to iron sucrose. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24081613",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 385,
"text": "Iron deficiency is common in pregnancy, postpartum, inflammatory bowel disease, chronic kidney disease, chronic heart failure, heavy uterine bleeding, cancer and following surgery. We estimate the budget impact (BI) on the Swiss mandatory health insurance associated with substituting iron sucrose (standard) with ferric carboxymaltose (new treatment) using real-life data."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24081613",
"endSection": "abstract",
"offsetInBeginSection": 1438,
"offsetInEndSection": 1583,
"text": "reating iron deficiency involves substantial costs to the Swiss MHI which may be reduced by substituting iron sucrose with ferric carboxymaltose."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23889159",
"endSection": "abstract",
"offsetInBeginSection": 129,
"offsetInEndSection": 347,
"text": "e aim of this study was to observe, in a non-interventional way, how Swedish gastroenterologists adhere to guidelines in IBD outpatients treated with intravenous ferric carboxymaltose (FCM), and the result of treatment"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23644823",
"endSection": "abstract",
"offsetInBeginSection": 1658,
"offsetInEndSection": 1766,
"text": "FCM lowers platelet counts and platelet activation in patients with IBD-associated secondary thrombocytosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23644823",
"endSection": "abstract",
"offsetInBeginSection": 588,
"offsetInEndSection": 777,
"text": "We performed a randomized, single-blinded placebo-controlled trial testing the effect of ferric carboxymaltose (FCM) in patients with IBD with secondary thrombocytosis (platelets > 450 G/L)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23078888",
"endSection": "abstract",
"offsetInBeginSection": 228,
"offsetInEndSection": 410,
"text": "e performed a randomized, placebo-controlled trial to determine if administration of ferric carboxymaltose (FCM) prevents anemia in patients with IBD and low levels of serum ferritin"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23078888",
"endSection": "abstract",
"offsetInBeginSection": 1670,
"offsetInEndSection": 1749,
"text": "FCM prevents recurrence of anemia in patients with IBD, compared with placebo. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22179489",
"endSection": "abstract",
"offsetInBeginSection": 291,
"offsetInEndSection": 403,
"text": " A subgroup was analyzed regarding efficacy and side effects of iron supplementation with ferric carboxymaltose."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22179489",
"endSection": "abstract",
"offsetInBeginSection": 1169,
"offsetInEndSection": 1332,
"text": "Iron deficiency and anemia are frequent in IBD patients. Treatment with ferric carboxymaltose is efficious, safe and well tolerated in iron-deficient IBD patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22023204",
"endSection": "abstract",
"offsetInBeginSection": 857,
"offsetInEndSection": 1001,
"text": " Intravenous iron avoids these concerns, especially with the development of ferric carboxymaltose, which allow up to 1000mg to be given rapidly."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22023204",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 71,
"text": "What is the optimal treatment for anemia in inflammatory bowel disease?"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21699794",
"endSection": "abstract",
"offsetInBeginSection": 237,
"offsetInEndSection": 441,
"text": "We compared the efficacy and safety of a novel fixed-dose ferric carboxymaltose regimen (FCM) with individually calculated iron sucrose (IS) doses in patients with inflammatory bowel disease (IBD) and IDA"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21699794",
"endSection": "abstract",
"offsetInBeginSection": 1332,
"offsetInEndSection": 1447,
"text": "Study drugs were well tolerated and drug-related adverse events were in line with drug-specific clinical experience"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21699794",
"endSection": "abstract",
"offsetInBeginSection": 1542,
"offsetInEndSection": 1706,
"text": " The simpler FCM-based dosing regimen showed better efficacy and compliance, as well as a good safety profile, compared with the Ganzoni-calculated IS dose regimen."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21340038",
"endSection": "abstract",
"offsetInBeginSection": 1450,
"offsetInEndSection": 1701,
"text": "Ferric carboxymaltose can be rapidly administered in doses of 15 mg/kg body weight, up to a ceiling dose of 1000 mg. A test dose is not required, and it can be used more widely across a spectrum of iron deficiency and iron deficiency anemia indication"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21340038",
"endSection": "abstract",
"offsetInBeginSection": 425,
"offsetInEndSection": 970,
"text": " Intravenous iron offers a rapid means of iron repletion and is superior to oral iron in many circumstances, especially in the presence of anemia of chronic disease, where it appears to overcome the block to absorption of iron from the gastrointestinal tract and immobilization of stored iron. The clinical situations where high doses of iron are commonly required are reviewed. These include nondialysis-dependent chronic kidney disease, inflammatory bowel disease, obstetrics, menorrhagia, and anemia associated with cancer and its treatment. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21479141",
"endSection": "abstract",
"offsetInBeginSection": 268,
"offsetInEndSection": 723,
"text": "Ferric carboxymaltose can be administered at 15 mg/kg body weight to a maximum dose of 1000 mg, whereas iron isomaltoside 1000 can be administered at 20 mg/kg body weight. The ability to give high doses of iron is important in the context of managing iron deficiency anemia in a number of clinical conditions where demands for iron are high (including chronic blood loss associated with inflammatory bowel disease, menorrhagia, and chronic kidney disease)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20648930",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 456,
"text": "erric carboxymaltose (FCM, Ferinject) was effective and well tolerated in the treatment of iron-deficiency anemia (IDA) in nine, Phase III, randomized, controlled, multicenter trials in a diverse range of indications, including patients with inflammatory bowel disease (IBD), post-partum anemia (PPA) or abnormal uterine bleeding (AUB), chronic heart failure (CHF), non-dialysis-dependent chronic kidney disease (CKD) and those undergoing hemodialysis (HD"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20648930",
"endSection": "abstract",
"offsetInBeginSection": 1306,
"offsetInEndSection": 1404,
"text": "In patients with IBD or PPA, improvements in Hb levels were more rapid with FCM than with FeSulf. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20648930",
"endSection": "abstract",
"offsetInBeginSection": 2101,
"offsetInEndSection": 2263,
"text": "CM improved patient quality of life to an equivalent extent to oral FeSulf in patients with IBD or PPA, and to a greater extent than oral FeSulf in women with AUB"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19787830",
"endSection": "abstract",
"offsetInBeginSection": 949,
"offsetInEndSection": 1205,
"text": "Four different products are principally used in clinical practice, which differ in their pharmacokinetic properties and safety profiles: iron gluconate and iron sucrose (lower single doses), and iron dextran and ferric carboxymaltose (higher single doses)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19787830",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 104,
"text": "he prevalence of anemia across studies on patients with inflammatory bowel disease (IBD) is high (30%)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18371137",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 158,
"text": " novel intravenous iron formulation for treatment of anemia in inflammatory bowel disease: the ferric carboxymaltose (FERINJECT) randomized controlled trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18371137",
"endSection": "abstract",
"offsetInBeginSection": 1356,
"offsetInEndSection": 1544,
"text": "FeCarb is effective and safe in IBD-associated anemia. It is noninferior to FeSulf in terms of Hb change over 12 wk, and provides a fast Hb increase and a sufficient refill of iron stores."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18371137",
"endSection": "abstract",
"offsetInBeginSection": 1156,
"offsetInEndSection": 1342,
"text": "Treatment-related adverse events (AEs) occurred in 28.5% of the FeCarb and 22.2% of the FeSulf groups, with discontinuation of study medication due to AEs in 1.5% and 7.9%, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18371137",
"endSection": "abstract",
"offsetInBeginSection": 658,
"offsetInEndSection": 812,
"text": "The median Hb improved from 8.7 to 12.3 g/dL in the FeCarb group and from 9.1 to 12.1 g/dL in the FeSulf group, demonstrating noninferiority (P= 0.6967). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23078888",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "Ferric carboxymaltose prevents recurrence of anemia in patients with inflammatory bowel disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20648930",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 458,
"text": "Ferric carboxymaltose (FCM, Ferinject) was effective and well tolerated in the treatment of iron-deficiency anemia (IDA) in nine, Phase III, randomized, controlled, multicenter trials in a diverse range of indications, including patients with inflammatory bowel disease (IBD), post-partum anemia (PPA) or abnormal uterine bleeding (AUB), chronic heart failure (CHF), non-dialysis-dependent chronic kidney disease (CKD) and those undergoing hemodialysis (HD)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20648930",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 457,
"text": "Ferric carboxymaltose (FCM, Ferinject) was effective and well tolerated in the treatment of iron-deficiency anemia (IDA) in nine, Phase III, randomized, controlled, multicenter trials in a diverse range of indications, including patients with inflammatory bowel disease (IBD), post-partum anemia (PPA) or abnormal uterine bleeding (AUB), chronic heart failure (CHF), non-dialysis-dependent chronic kidney disease (CKD) and those undergoing hemodialysis (HD)"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23078888",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "Ferric carboxymaltose prevents recurrence of anemia in patients with inflammatory bowel disease."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23078888",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "Ferric carboxymaltose prevents recurrence of anemia in patients with inflammatory bowel disease."
}
]
| 5 | BioASQ-training5b | [
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"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003093",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D009220",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D005290",
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| 530cf4fe960c95ad0c00000d | 135 |
yesno | Are OATP1B1 and OATP1B3 associated with bilirubin transport? | ['yes'] | [
"yes"
]
| ['Yes, OATP1B1 and OATP1B3 are involved in the transport of bilirubin.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23886114",
"http://www.ncbi.nlm.nih.gov/pubmed/23750830",
"http://www.ncbi.nlm.nih.gov/pubmed/23695864",
"http://www.ncbi.nlm.nih.gov/pubmed/22232210",
"http://www.ncbi.nlm.nih.gov/pubmed/22982575",
"http://www.ncbi.nlm.nih.gov/pubmed/25204339",
"http://www.ncbi.nlm.nih.gov/pubmed/24459177",
"http://www.ncbi.nlm.nih.gov/pubmed/24151358",
"http://www.ncbi.nlm.nih.gov/pubmed/24523126",
"http://www.ncbi.nlm.nih.gov/pubmed/21395542",
"http://www.ncbi.nlm.nih.gov/pubmed/15535988",
"http://www.ncbi.nlm.nih.gov/pubmed/18509604",
"http://www.ncbi.nlm.nih.gov/pubmed/17973861"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23886114",
"endSection": "abstract",
"offsetInBeginSection": 621,
"offsetInEndSection": 811,
"text": "OATP1B1 and OATP1B3-mediated transport of bilirubin was confirmed and inhibition was determined for atazanavir, rifampicin, indinavir, amprenavir, cyclosporine, rifamycin SV and saquinavir. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24523126",
"endSection": "abstract",
"offsetInBeginSection": 1906,
"offsetInEndSection": 2193,
"text": "Examples of adaptive nontoxic changes in liver function, which may elevate direct (conjugated) and/or indirect (unconjugated) bilirubin above baseline levels, include reversible inhibition of UGT1A1-mediated bilirubin metabolism and OATP1B1-, OATP1B3-, or MRP2-mediated transport (Keogh."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23750830",
"endSection": "abstract",
"offsetInBeginSection": 1423,
"offsetInEndSection": 1768,
"text": "Due to limited solubility and poor ionization of bilirubin and its glucuronide, the formation of estradiol 3-glucuronide was used as a surrogate to assess UGT1A1 activity, while the transport of pitavastatin, CDCF, and taurocholate were used as surrogate probe substrates to monitor the function of OATP1B1/OATP1B3, MRP2, and BSEP, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23886114",
"endSection": "abstract",
"offsetInBeginSection": 803,
"offsetInEndSection": 992,
"text": "OATP1B1 and OATP1B3-mediated transport of bilirubin was confirmed and inhibition was determined for atazanavir, rifampicin, indinavir, amprenavir, cyclosporine, rifamycin SV and saquinavir."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23750830",
"endSection": "abstract",
"offsetInBeginSection": 682,
"offsetInEndSection": 919,
"text": "However, because drug transporters also contribute to bilirubin elimination, the purpose of this work was to investigate the in vitro inhibition of OATP1B1, OATP1B3, MRP2, and BSEP of select test drugs known to elicit hyperbilirubinemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22982575",
"endSection": "abstract",
"offsetInBeginSection": 1864,
"offsetInEndSection": 2104,
"text": "Thus, disruption of hepatic reuptake of bilirubin glucuronide due to coexisting OATP1B1 and OATP1B3 deficiencies explains Rotor-type hyperbilirubinemia.Moreover, OATP1B1 and OATP1B3 null mutations may confer substantial drug toxicity risks."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23750830",
"endSection": "abstract",
"offsetInBeginSection": 222,
"offsetInEndSection": 360,
"text": "Bilirubin elimination is a multifaceted process consisting of uptake of bilirubin into the hepatocytes facilitated by OATP1B1 and OATP1B3."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22232210",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Complete OATP1B1 and OATP1B3 deficiency causes human Rotor syndrome by interrupting conjugated bilirubin reuptake into the liver."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22232210",
"endSection": "abstract",
"offsetInBeginSection": 1775,
"offsetInEndSection": 1927,
"text": "Thus, disruption of hepatic reuptake of bilirubin glucuronide due to coexisting OATP1B1 and OATP1B3 deficiencies explains Rotor-type hyperbilirubinemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24523126",
"endSection": "abstract",
"offsetInBeginSection": 1906,
"offsetInEndSection": 2193,
"text": "Examples of adaptive nontoxic changes in liver function, which may elevate direct (conjugated) and/or indirect (unconjugated) bilirubin above baseline levels, include reversible inhibition of UGT1A1-mediated bilirubin metabolism and OATP1B1-, OATP1B3-, or MRP2-mediated transport (Keogh."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23750830",
"endSection": "abstract",
"offsetInBeginSection": 1423,
"offsetInEndSection": 1768,
"text": "Due to limited solubility and poor ionization of bilirubin and its glucuronide, the formation of estradiol 3-glucuronide was used as a surrogate to assess UGT1A1 activity, while the transport of pitavastatin, CDCF, and taurocholate were used as surrogate probe substrates to monitor the function of OATP1B1/OATP1B3, MRP2, and BSEP, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23886114",
"endSection": "abstract",
"offsetInBeginSection": 803,
"offsetInEndSection": 992,
"text": "OATP1B1 and OATP1B3-mediated transport of bilirubin was confirmed and inhibition was determined for atazanavir, rifampicin, indinavir, amprenavir, cyclosporine, rifamycin SV and saquinavir."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23750830",
"endSection": "abstract",
"offsetInBeginSection": 682,
"offsetInEndSection": 919,
"text": "However, because drug transporters also contribute to bilirubin elimination, the purpose of this work was to investigate the in vitro inhibition of OATP1B1, OATP1B3, MRP2, and BSEP of select test drugs known to elicit hyperbilirubinemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23750830",
"endSection": "abstract",
"offsetInBeginSection": 222,
"offsetInEndSection": 360,
"text": "Bilirubin elimination is a multifaceted process consisting of uptake of bilirubin into the hepatocytes facilitated by OATP1B1 and OATP1B3."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24151358",
"endSection": "abstract",
"offsetInBeginSection": 1245,
"offsetInEndSection": 1516,
"text": "The data show that a substantial fraction of bilirubin conjugates is primarily secreted by MRP3 at the sinusoidal membrane into the blood, from where they are subsequently reuptaken by sinusoidal membrane-bound organic anion transporting polypeptides OATP1B1 and OATP1B3."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23750830",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Evaluating the in vitro inhibition of UGT1A1, OATP1B1, OATP1B3, MRP2, and BSEP in predicting drug-induced hyperbilirubinemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23886114",
"endSection": "abstract",
"offsetInBeginSection": 621,
"offsetInEndSection": 809,
"text": "OATP1B1 and OATP1B3-mediated transport of bilirubin was confirmed and inhibition was determined for atazanavir, rifampicin, indinavir, amprenavir, cyclosporine, rifamycin SV and saquinavir"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23750830",
"endSection": "abstract",
"offsetInBeginSection": 85,
"offsetInEndSection": 222,
"text": "Bilirubin elimination is a multifaceted process consisting of uptake of bilirubin into the hepatocytes facilitated by OATP1B1 and OATP1B3"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23750830",
"endSection": "abstract",
"offsetInBeginSection": 1085,
"offsetInEndSection": 1429,
"text": "Due to limited solubility and poor ionization of bilirubin and its glucuronide, the formation of estradiol 3-glucuronide was used as a surrogate to assess UGT1A1 activity, while the transport of pitavastatin, CDCF, and taurocholate were used as surrogate probe substrates to monitor the function of OATP1B1/OATP1B3, MRP2, and BSEP, respectively"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24523126",
"endSection": "abstract",
"offsetInBeginSection": 1630,
"offsetInEndSection": 1916,
"text": "Examples of adaptive nontoxic changes in liver function, which may elevate direct (conjugated) and/or indirect (unconjugated) bilirubin above baseline levels, include reversible inhibition of UGT1A1-mediated bilirubin metabolism and OATP1B1-, OATP1B3-, or MRP2-mediated transport (Keogh"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25204339",
"endSection": "abstract",
"offsetInBeginSection": 321,
"offsetInEndSection": 736,
"text": "In vitro, faldaprevir inhibited key processes involved in bilirubin clearance: UDP glucuronosyltransferase (UGT) 1A1 (UGT1A1) (IC50 0.45 µM), which conjugates bilirubin, and hepatic uptake and efflux transporters, organic anion-transporting polypeptide (OATP) 1B1 (IC50 0.57 µM), OATP1B3 (IC50 0.18 µM), and multidrug resistance-associated protein (MRP) 2 (IC50 6.2 µM), which transport bilirubin and its conjugates"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22232210",
"endSection": "abstract",
"offsetInBeginSection": 1632,
"offsetInEndSection": 1783,
"text": "Thus, disruption of hepatic reuptake of bilirubin glucuronide due to coexisting OATP1B1 and OATP1B3 deficiencies explains Rotor-type hyperbilirubinemia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22982575",
"endSection": "abstract",
"offsetInBeginSection": 1633,
"offsetInEndSection": 1872,
"text": "Thus, disruption of hepatic reuptake of bilirubin glucuronide due to coexisting OATP1B1 and OATP1B3 deficiencies explains Rotor-type hyperbilirubinemia.Moreover, OATP1B1 and OATP1B3 null mutations may confer substantial drug toxicity risks"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15535988",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "OATP1B1 (a.k.a. OATP-C, OATP2, LST-1, or SLC21A6) is a liver-specific organic anion uptake transporter and has been shown to be a higher affinity bilirubin uptake transporter than OATP1B3"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22232210",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Complete OATP1B1 and OATP1B3 deficiency causes human Rotor syndrome by interrupting conjugated bilirubin reuptake into the liver."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23886114",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "In vitro OATP1B1 and OATP1B3 inhibition is associated with observations of benign clinical unconjugated hyperbilirubinemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24523126",
"endSection": "abstract",
"offsetInBeginSection": 1630,
"offsetInEndSection": 1948,
"text": "Examples of adaptive nontoxic changes in liver function, which may elevate direct (conjugated) and/or indirect (unconjugated) bilirubin above baseline levels, include reversible inhibition of UGT1A1-mediated bilirubin metabolism and OATP1B1-, OATP1B3-, or MRP2-mediated transport (Keogh. Adv Pharmacol 63:1-42, 2012). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22232210",
"endSection": "abstract",
"offsetInBeginSection": 980,
"offsetInEndSection": 1196,
"text": "Using mice deficient in Oatp1a/1b and in the multispecific sinusoidal export pump Abcc3, we found that Abcc3 secretes bilirubin conjugates into the blood, while Oatp1a/1b transporters mediate their hepatic reuptake. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23886114",
"endSection": "abstract",
"offsetInBeginSection": 621,
"offsetInEndSection": 811,
"text": "OATP1B1 and OATP1B3-mediated transport of bilirubin was confirmed and inhibition was determined for atazanavir, rifampicin, indinavir, amprenavir, cyclosporine, rifamycin SV and saquinavir. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22232210",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Complete OATP1B1 and OATP1B3 deficiency causes human Rotor syndrome by interrupting conjugated bilirubin reuptake into the liver."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23886114",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "In vitro OATP1B1 and OATP1B3 inhibition is associated with observations of benign clinical unconjugated hyperbilirubinemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24523126",
"endSection": "abstract",
"offsetInBeginSection": 1630,
"offsetInEndSection": 1948,
"text": "Examples of adaptive nontoxic changes in liver function, which may elevate direct (conjugated) and/or indirect (unconjugated) bilirubin above baseline levels, include reversible inhibition of UGT1A1-mediated bilirubin metabolism and OATP1B1-, OATP1B3-, or MRP2-mediated transport (Keogh. Adv Pharmacol 63:1-42, 2012). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22232210",
"endSection": "abstract",
"offsetInBeginSection": 980,
"offsetInEndSection": 1196,
"text": "Using mice deficient in Oatp1a/1b and in the multispecific sinusoidal export pump Abcc3, we found that Abcc3 secretes bilirubin conjugates into the blood, while Oatp1a/1b transporters mediate their hepatic reuptake. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23886114",
"endSection": "abstract",
"offsetInBeginSection": 621,
"offsetInEndSection": 811,
"text": "OATP1B1 and OATP1B3-mediated transport of bilirubin was confirmed and inhibition was determined for atazanavir, rifampicin, indinavir, amprenavir, cyclosporine, rifamycin SV and saquinavir. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22232210",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Complete OATP1B1 and OATP1B3 deficiency causes human Rotor syndrome by interrupting conjugated bilirubin reuptake into the liver."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23886114",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "In vitro OATP1B1 and OATP1B3 inhibition is associated with observations of benign clinical unconjugated hyperbilirubinemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24523126",
"endSection": "abstract",
"offsetInBeginSection": 1630,
"offsetInEndSection": 1948,
"text": "Examples of adaptive nontoxic changes in liver function, which may elevate direct (conjugated) and/or indirect (unconjugated) bilirubin above baseline levels, include reversible inhibition of UGT1A1-mediated bilirubin metabolism and OATP1B1-, OATP1B3-, or MRP2-mediated transport (Keogh. Adv Pharmacol 63:1-42, 2012). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22232210",
"endSection": "abstract",
"offsetInBeginSection": 980,
"offsetInEndSection": 1196,
"text": "Using mice deficient in Oatp1a/1b and in the multispecific sinusoidal export pump Abcc3, we found that Abcc3 secretes bilirubin conjugates into the blood, while Oatp1a/1b transporters mediate their hepatic reuptake. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23886114",
"endSection": "abstract",
"offsetInBeginSection": 621,
"offsetInEndSection": 811,
"text": "OATP1B1 and OATP1B3-mediated transport of bilirubin was confirmed and inhibition was determined for atazanavir, rifampicin, indinavir, amprenavir, cyclosporine, rifamycin SV and saquinavir. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23886114",
"endSection": "abstract",
"offsetInBeginSection": 621,
"offsetInEndSection": 811,
"text": "OATP1B1 and OATP1B3-mediated transport of bilirubin was confirmed and inhibition was determined for atazanavir, rifampicin, indinavir, amprenavir, cyclosporine, rifamycin SV and saquinavir. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23750830",
"endSection": "abstract",
"offsetInBeginSection": 85,
"offsetInEndSection": 224,
"text": "Bilirubin elimination is a multifaceted process consisting of uptake of bilirubin into the hepatocytes facilitated by OATP1B1 and OATP1B3. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23750830",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Evaluating the in vitro inhibition of UGT1A1, OATP1B1, OATP1B3, MRP2, and BSEP in predicting drug-induced hyperbilirubinemia."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22232210",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Complete OATP1B1 and OATP1B3 deficiency causes human Rotor syndrome by interrupting conjugated bilirubin reuptake into the liver."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23886114",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "In vitro OATP1B1 and OATP1B3 inhibition is associated with observations of benign clinical unconjugated hyperbilirubinemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24523126",
"endSection": "abstract",
"offsetInBeginSection": 1630,
"offsetInEndSection": 1948,
"text": "Examples of adaptive nontoxic changes in liver function, which may elevate direct (conjugated) and/or indirect (unconjugated) bilirubin above baseline levels, include reversible inhibition of UGT1A1-mediated bilirubin metabolism and OATP1B1-, OATP1B3-, or MRP2-mediated transport (Keogh. Adv Pharmacol 63:1-42, 2012). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22232210",
"endSection": "abstract",
"offsetInBeginSection": 980,
"offsetInEndSection": 1196,
"text": "Using mice deficient in Oatp1a/1b and in the multispecific sinusoidal export pump Abcc3, we found that Abcc3 secretes bilirubin conjugates into the blood, while Oatp1a/1b transporters mediate their hepatic reuptake. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23886114",
"endSection": "abstract",
"offsetInBeginSection": 621,
"offsetInEndSection": 811,
"text": "OATP1B1 and OATP1B3-mediated transport of bilirubin was confirmed and inhibition was determined for atazanavir, rifampicin, indinavir, amprenavir, cyclosporine, rifamycin SV and saquinavir. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17973861",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "OATP1B1 polymorphism is a major determinant of serum bilirubin level but not associated with rifampicin-mediated bilirubin elevation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17973861",
"endSection": "abstract",
"offsetInBeginSection": 119,
"offsetInEndSection": 272,
"text": "Unconjugated bilirubin (UCB) is taken up into hepatocytes by human organic anion transporting polypeptide 1B1 (OATP1B1; encoded for by the SLCO1B1 gene)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17973861",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "OATP1B1 polymorphism is a major determinant of serum bilirubin level but not associated with rifampicin-mediated bilirubin elevation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17973861",
"endSection": "abstract",
"offsetInBeginSection": 119,
"offsetInEndSection": 272,
"text": "Unconjugated bilirubin (UCB) is taken up into hepatocytes by human organic anion transporting polypeptide 1B1 (OATP1B1; encoded for by the SLCO1B1 gene)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23750830",
"endSection": "abstract",
"offsetInBeginSection": 451,
"offsetInEndSection": 1085,
"text": "However, because drug transporters also contribute to bilirubin elimination, the purpose of this work was to investigate the in vitro inhibition of OATP1B1, OATP1B3, MRP2, and BSEP of select test drugs known to elicit hyperbilirubinemia. Test drugs investigated in this study were atazanavir and indinavir, which are associated with hyperbilirubinemia and elevations in serum transaminase; ritonavir and nelfinavir, which are not associated with hyperbilirubinemia; and bromfenac, troglitazone, and trovafloxacin, which are associated with severe idiosyncratic hepatotoxicity exhibiting elevations in serum bilirubin and transaminase."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23750830",
"endSection": "abstract",
"offsetInBeginSection": 689,
"offsetInEndSection": 1431,
"text": "Test drugs investigated in this study were atazanavir and indinavir, which are associated with hyperbilirubinemia and elevations in serum transaminase; ritonavir and nelfinavir, which are not associated with hyperbilirubinemia; and bromfenac, troglitazone, and trovafloxacin, which are associated with severe idiosyncratic hepatotoxicity exhibiting elevations in serum bilirubin and transaminase. Due to limited solubility and poor ionization of bilirubin and its glucuronide, the formation of estradiol 3-glucuronide was used as a surrogate to assess UGT1A1 activity, while the transport of pitavastatin, CDCF, and taurocholate were used as surrogate probe substrates to monitor the function of OATP1B1/OATP1B3, MRP2, and BSEP, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25204339",
"endSection": "abstract",
"offsetInBeginSection": 322,
"offsetInEndSection": 738,
"text": "In vitro, faldaprevir inhibited key processes involved in bilirubin clearance: UDP glucuronosyltransferase (UGT) 1A1 (UGT1A1) (IC50 0.45 µM), which conjugates bilirubin, and hepatic uptake and efflux transporters, organic anion-transporting polypeptide (OATP) 1B1 (IC50 0.57 µM), OATP1B3 (IC50 0.18 µM), and multidrug resistance-associated protein (MRP) 2 (IC50 6.2 µM), which transport bilirubin and its conjugates."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23886114",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "In vitro OATP1B1 and OATP1B3 inhibition is associated with observations of benign clinical unconjugated hyperbilirubinemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25204339",
"endSection": "abstract",
"offsetInBeginSection": 322,
"offsetInEndSection": 738,
"text": "In vitro, faldaprevir inhibited key processes involved in bilirubin clearance: UDP glucuronosyltransferase (UGT) 1A1 (UGT1A1) (IC50 0.45 µM), which conjugates bilirubin, and hepatic uptake and efflux transporters, organic anion-transporting polypeptide (OATP) 1B1 (IC50 0.57 µM), OATP1B3 (IC50 0.18 µM), and multidrug resistance-associated protein (MRP) 2 (IC50 6.2 µM), which transport bilirubin and its conjugates."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23886114",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "In vitro OATP1B1 and OATP1B3 inhibition is associated with observations of benign clinical unconjugated hyperbilirubinemia."
},
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/23886114",
"endSection": "abstract",
"offsetInBeginSection": 1017,
"offsetInEndSection": 1231,
"text": "3. The results indicated that in vivo Fi values >0.2 or R-values >1.5 for OATP1B1 or OATP1B3, but not UGT1A1, are associated with previously reported clinical cases of drug-induced unconjugated hyperbilirubinemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23886114",
"endSection": "abstract",
"offsetInBeginSection": 622,
"offsetInEndSection": 811,
"text": "OATP1B1 and OATP1B3-mediated transport of bilirubin was confirmed and inhibition was determined for atazanavir, rifampicin, indinavir, amprenavir, cyclosporine, rifamycin SV and saquinavir."
},
{
"beginSection": "abstract",
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"endSection": "abstract",
"offsetInBeginSection": 322,
"offsetInEndSection": 738,
"text": "In vitro, faldaprevir inhibited key processes involved in bilirubin clearance: UDP glucuronosyltransferase (UGT) 1A1 (UGT1A1) (IC50 0.45 µM), which conjugates bilirubin, and hepatic uptake and efflux transporters, organic anion-transporting polypeptide (OATP) 1B1 (IC50 0.57 µM), OATP1B3 (IC50 0.18 µM), and multidrug resistance-associated protein (MRP) 2 (IC50 6.2 µM), which transport bilirubin and its conjugates."
},
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"text": "In vitro OATP1B1 and OATP1B3 inhibition is associated with observations of benign clinical unconjugated hyperbilirubinemia."
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"endSection": "abstract",
"offsetInBeginSection": 1017,
"offsetInEndSection": 1231,
"text": "3. The results indicated that in vivo Fi values >0.2 or R-values >1.5 for OATP1B1 or OATP1B3, but not UGT1A1, are associated with previously reported clinical cases of drug-induced unconjugated hyperbilirubinemia."
},
{
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"endSection": "abstract",
"offsetInBeginSection": 622,
"offsetInEndSection": 811,
"text": "OATP1B1 and OATP1B3-mediated transport of bilirubin was confirmed and inhibition was determined for atazanavir, rifampicin, indinavir, amprenavir, cyclosporine, rifamycin SV and saquinavir."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25204339",
"endSection": "abstract",
"offsetInBeginSection": 322,
"offsetInEndSection": 738,
"text": "In vitro, faldaprevir inhibited key processes involved in bilirubin clearance: UDP glucuronosyltransferase (UGT) 1A1 (UGT1A1) (IC50 0.45 µM), which conjugates bilirubin, and hepatic uptake and efflux transporters, organic anion-transporting polypeptide (OATP) 1B1 (IC50 0.57 µM), OATP1B3 (IC50 0.18 µM), and multidrug resistance-associated protein (MRP) 2 (IC50 6.2 µM), which transport bilirubin and its conjugates."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23886114",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "In vitro OATP1B1 and OATP1B3 inhibition is associated with observations of benign clinical unconjugated hyperbilirubinemia."
},
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/23886114",
"endSection": "abstract",
"offsetInBeginSection": 1017,
"offsetInEndSection": 1231,
"text": "3. The results indicated that in vivo Fi values >0.2 or R-values >1.5 for OATP1B1 or OATP1B3, but not UGT1A1, are associated with previously reported clinical cases of drug-induced unconjugated hyperbilirubinemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23886114",
"endSection": "abstract",
"offsetInBeginSection": 622,
"offsetInEndSection": 811,
"text": "OATP1B1 and OATP1B3-mediated transport of bilirubin was confirmed and inhibition was determined for atazanavir, rifampicin, indinavir, amprenavir, cyclosporine, rifamycin SV and saquinavir."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25204339",
"endSection": "abstract",
"offsetInBeginSection": 322,
"offsetInEndSection": 738,
"text": "In vitro, faldaprevir inhibited key processes involved in bilirubin clearance: UDP glucuronosyltransferase (UGT) 1A1 (UGT1A1) (IC50 0.45 µM), which conjugates bilirubin, and hepatic uptake and efflux transporters, organic anion-transporting polypeptide (OATP) 1B1 (IC50 0.57 µM), OATP1B3 (IC50 0.18 µM), and multidrug resistance-associated protein (MRP) 2 (IC50 6.2 µM), which transport bilirubin and its conjugates."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23886114",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "In vitro OATP1B1 and OATP1B3 inhibition is associated with observations of benign clinical unconjugated hyperbilirubinemia."
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D001663",
"http://amigo.geneontology.org/amigo/term/GO:0015723",
"http://www.biosemantics.org/jochem#4274830"
]
| []
| 571e3e2abb137a4b0c000008 | 136 |
yesno | Is there any involvement of L1 retrotransposition in the Rett syndrome? | ['yes'] | [
"yes"
]
| ['Yes. Recent studies indicate that long interspersed nuclear element-1 (L1) are mobilized in the genome of human neural progenitor cells and enhanced in Rett syndrome and ataxia telangiectasia.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23057747",
"http://www.ncbi.nlm.nih.gov/pubmed/24389010",
"http://www.ncbi.nlm.nih.gov/pubmed/22159035",
"http://www.ncbi.nlm.nih.gov/pubmed/21085180"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21085180",
"endSection": "abstract",
"offsetInBeginSection": 1585,
"offsetInEndSection": 2128,
"text": "Using neuronal progenitor cells derived from human induced pluripotent stem cells and human tissues, we revealed that patients with Rett syndrome (RTT), carrying MeCP2 mutations, have increased susceptibility for L1 retrotransposition. Our data demonstrate that L1 retrotransposition can be controlled in a tissue-specific manner and that disease-related genetic mutations can influence the frequency of neuronal L1 retrotransposition. Our findings add a new level of complexity to the molecular events that can lead to neurological disorders."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23057747",
"endSection": "abstract",
"offsetInBeginSection": 725,
"offsetInEndSection": 903,
"text": "Furthermore, some neurological diseases, such as Rett syndrome and ataxia telangiectasia, misregulate L1 retrotransposition, which could contribute to some pathological aspects. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24389010",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 188,
"text": "Recent studies indicate that long interspersed nuclear element-1 (L1) are mobilized in the genome of human neural progenitor cells and enhanced in Rett syndrome and ataxia telangiectasia. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22159035",
"endSection": "abstract",
"offsetInBeginSection": 321,
"offsetInEndSection": 594,
"text": "In addition, recent data indicate that engineered human L1s can undergo somatic retrotransposition in human neural progenitor cells and that an increase in human-specific L1 DNA content can be detected in the brains of normal controls, as well as in Rett syndrome patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23057747",
"endSection": "abstract",
"offsetInBeginSection": 719,
"offsetInEndSection": 896,
"text": "Furthermore, some neurological diseases, such as Rett syndrome and ataxia telangiectasia, misregulate L1 retrotransposition, which could contribute to some pathological aspects."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21085180",
"endSection": "abstract",
"offsetInBeginSection": 1576,
"offsetInEndSection": 1811,
"text": "Using neuronal progenitor cells derived from human induced pluripotent stem cells and human tissues, we revealed that patients with Rett syndrome (RTT), carrying MeCP2 mutations, have increased susceptibility for L1 retrotransposition."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22159035",
"endSection": "abstract",
"offsetInBeginSection": 319,
"offsetInEndSection": 592,
"text": "In addition, recent data indicate that engineered human L1s can undergo somatic retrotransposition in human neural progenitor cells and that an increase in human-specific L1 DNA content can be detected in the brains of normal controls, as well as in Rett syndrome patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21085180",
"endSection": "abstract",
"offsetInBeginSection": 1585,
"offsetInEndSection": 1819,
"text": "Using neuronal progenitor cells derived from human induced pluripotent stem cells and human tissues, we revealed that patients with Rett syndrome (RTT), carrying MeCP2 mutations, have increased susceptibility for L1 retrotransposition"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23057747",
"endSection": "abstract",
"offsetInBeginSection": 725,
"offsetInEndSection": 901,
"text": "Furthermore, some neurological diseases, such as Rett syndrome and ataxia telangiectasia, misregulate L1 retrotransposition, which could contribute to some pathological aspects"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21085180",
"endSection": "abstract",
"offsetInBeginSection": 1585,
"offsetInEndSection": 1820,
"text": "Using neuronal progenitor cells derived from human induced pluripotent stem cells and human tissues, we revealed that patients with Rett syndrome (RTT), carrying MeCP2 mutations, have increased susceptibility for L1 retrotransposition."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23057747",
"endSection": "abstract",
"offsetInBeginSection": 725,
"offsetInEndSection": 902,
"text": "Furthermore, some neurological diseases, such as Rett syndrome and ataxia telangiectasia, misregulate L1 retrotransposition, which could contribute to some pathological aspects."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24389010",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "Recent studies indicate that long interspersed nuclear element-1 (L1) are mobilized in the genome of human neural progenitor cells and enhanced in Rett syndrome and ataxia telangiectasia."
}
]
| 6 | BioASQ-training6b | [
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D015518",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D020084",
"http://www.disease-ontology.org/api/metadata/DOID:1206"
]
| [
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"o": "http://linkedlifedata.com/resource/umls/label/A11585268",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C1514925"
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{
"o": "retrotransposon transposition",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A11585268"
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{
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"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
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{
"o": "rett syndrome",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A18593781"
},
{
"o": "transposition, RNA-mediated",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C1514925"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A11610160",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C1514925"
},
{
"o": "retrotransposition",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A11610160"
}
]
| 58965a4178275d0c4a00000e | 137 |
yesno | Is there any data to suggest that TRH (thyrotropin releasing hormone) administration can improve symptom severity of amyotrophic lateral sclerosis patients? | ['yes'] | [
"yes"
]
| ['Yes, there are studies demonstrating that TRH (thyrotropin releasing hormone) administration can improve symptom severity of amyotrophic lateral sclerosis patients. However, some studies have failed to demonstrate symptom improvement following TRH administration.', 'Very high intravenous doses (2-19 mg/min) of thyrotropin-releasing hormone (TRH, L-pyroglutamyl-L-histidyl-L-prolinamide) given to 12 patients with amyotrophic lateral sclerosis (ALS) produced a moderate to marked improvement of functions caused by deficiency of lower motor neurons (weakness) and upper motor neurons (spasticity). The improvement was sustained throughout the infusion and for about 1 h thereafter; sometimes a slight improvement was evident 20 h after infusion. ', 'Very high intravenous doses (2-19 mg/min) of thyrotropin-releasing hormone (TRH, L-pyroglutamyl-L-histidyl-L-prolinamide) given to 12 patients with amyotrophic lateral sclerosis (ALS) produced a moderate to marked improvement of functions caused by deficiency of lower motor neurons (weakness) and upper motor neurons (spasticity). The improvement was sustained throughout the infusion and for about 1 h thereafter; sometimes a slight improvement was evident 20 h after infusion. ', 'Very high intravenous doses (2-19 mg/min) of thyrotropin-releasing hormone (TRH, L-pyroglutamyl-L-histidyl-L-prolinamide) given to 12 patients with amyotrophic lateral sclerosis (ALS) produced a moderate to marked improvement of functions caused by deficiency of lower motor neurons (weakness) and upper motor neurons (spasticity). The improvement was sustained throughout the infusion and for about 1 h thereafter; sometimes a slight improvement was evident 20 h after infusion. ', 'Very high intravenous doses (2-19 mg/min) of thyrotropin-releasing hormone (TRH, L-pyroglutamyl-L-histidyl-L-prolinamide) given to 12 patients with amyotrophic lateral sclerosis (ALS) produced a moderate to marked improvement of functions caused by deficiency of lower motor neurons (weakness) and upper motor neurons (spasticity). The improvement was sustained throughout the infusion and for about 1 h thereafter; sometimes a slight improvement was evident 20 h after infusion. ', 'Very high intravenous doses (2-19 mg/min) of thyrotropin-releasing hormone (TRH, L-pyroglutamyl-L-histidyl-L-prolinamide) given to 12 patients with amyotrophic lateral sclerosis (ALS) produced a moderate to marked improvement of functions caused by deficiency of lower motor neurons (weakness) and upper motor neurons (spasticity). The improvement was sustained throughout the infusion and for about 1 h thereafter; sometimes a slight improvement was evident 20 h after infusion. '] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22017410",
"http://www.ncbi.nlm.nih.gov/pubmed/9444487",
"http://www.ncbi.nlm.nih.gov/pubmed/8899662",
"http://www.ncbi.nlm.nih.gov/pubmed/7925318",
"http://www.ncbi.nlm.nih.gov/pubmed/1469425",
"http://www.ncbi.nlm.nih.gov/pubmed/1579228",
"http://www.ncbi.nlm.nih.gov/pubmed/1596403",
"http://www.ncbi.nlm.nih.gov/pubmed/1792854",
"http://www.ncbi.nlm.nih.gov/pubmed/1906441",
"http://www.ncbi.nlm.nih.gov/pubmed/1904337",
"http://www.ncbi.nlm.nih.gov/pubmed/2127925",
"http://www.ncbi.nlm.nih.gov/pubmed/2126554",
"http://www.ncbi.nlm.nih.gov/pubmed/2233870",
"http://www.ncbi.nlm.nih.gov/pubmed/2125610",
"http://www.ncbi.nlm.nih.gov/pubmed/2132051",
"http://www.ncbi.nlm.nih.gov/pubmed/2514091",
"http://www.ncbi.nlm.nih.gov/pubmed/2518665",
"http://www.ncbi.nlm.nih.gov/pubmed/2513155",
"http://www.ncbi.nlm.nih.gov/pubmed/2475830",
"http://www.ncbi.nlm.nih.gov/pubmed/2563937",
"http://www.ncbi.nlm.nih.gov/pubmed/2497685",
"http://www.ncbi.nlm.nih.gov/pubmed/2497684",
"http://www.ncbi.nlm.nih.gov/pubmed/3147318",
"http://www.ncbi.nlm.nih.gov/pubmed/3146705",
"http://www.ncbi.nlm.nih.gov/pubmed/3136230",
"http://www.ncbi.nlm.nih.gov/pubmed/3148186",
"http://www.ncbi.nlm.nih.gov/pubmed/3148185",
"http://www.ncbi.nlm.nih.gov/pubmed/3068777",
"http://www.ncbi.nlm.nih.gov/pubmed/11681403",
"http://www.ncbi.nlm.nih.gov/pubmed/3104820",
"http://www.ncbi.nlm.nih.gov/pubmed/3104751",
"http://www.ncbi.nlm.nih.gov/pubmed/3104750",
"http://www.ncbi.nlm.nih.gov/pubmed/3091628",
"http://www.ncbi.nlm.nih.gov/pubmed/3097367",
"http://www.ncbi.nlm.nih.gov/pubmed/3080695",
"http://www.ncbi.nlm.nih.gov/pubmed/3080694",
"http://www.ncbi.nlm.nih.gov/pubmed/3080693",
"http://www.ncbi.nlm.nih.gov/pubmed/3088700",
"http://www.ncbi.nlm.nih.gov/pubmed/2982071",
"http://www.ncbi.nlm.nih.gov/pubmed/3923160",
"http://www.ncbi.nlm.nih.gov/pubmed/6134961",
"http://www.ncbi.nlm.nih.gov/pubmed/6439824"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22017410",
"endSection": "abstract",
"offsetInBeginSection": 212,
"offsetInEndSection": 514,
"text": "These central nervous system (CNS)-mediated effects provide the rationale for use of TRH and its analogs in the treatment of brain and spinal injury, and CNS disorders like schizophrenia, Alzheimer's disease, epilepsy, amyotrophic lateral sclerosis, Parkinson's disease, depression, shock and ischemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9444487",
"endSection": "abstract",
"offsetInBeginSection": 558,
"offsetInEndSection": 733,
"text": "The Effect of TRH to correct the abnormal F responses in SSP might be consistent with effects of TRH to reduce spasticity in amyotrophic lateral sclerosis described previously"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7925318",
"endSection": "abstract",
"offsetInBeginSection": 1087,
"offsetInEndSection": 1221,
"text": "Agents undergoing therapeutic trials at present include CNTF, IGF1 glutamate antagonists, branched-chain amino acids and TRH analogue."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1579228",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 207,
"text": "Evidence that thyrotropin-releasing hormone (TRH) has prominent trophic effects on the motor system led to several negative therapeutic trials in amyotrophic lateral sclerosis, a disease of the motor system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1596403",
"endSection": "abstract",
"offsetInBeginSection": 859,
"offsetInEndSection": 1131,
"text": "The results of the clinical evaluation at the beginning and end of the treatment as well as after patient follow up demonstrated that beneficial effects do not occur equally in all patients but rather are transitory and do not improve the natural evolution of the disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1792854",
"endSection": "abstract",
"offsetInBeginSection": 436,
"offsetInEndSection": 538,
"text": "The neurological evaluation after acute TRH-T treatment showed an objective improvement in 3 of the 8."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1906441",
"endSection": "abstract",
"offsetInBeginSection": 286,
"offsetInEndSection": 568,
"text": "The outcome of the study, in agreement with some and at variance with other studies, was that TRH induced a statistically significant neurological improvement in 17 of the 23 ALS patients but little or none in the other ALS patients and in patients with other neurological diseases."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1904337",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 137,
"text": "[A case of amyotrophic lateral sclerosis with disturbance of vertical ocular movement responding to thyrotropin releasing hormone (TRH)]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1904337",
"endSection": "abstract",
"offsetInBeginSection": 629,
"offsetInEndSection": 763,
"text": "TRH injections resulted in improvement of disturbance of vertical ocular movement, but no effect was seen on the weakness of the limb."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2127925",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 132,
"text": "13 patients with amyotrophic lateral sclerosis (ALS) were treated with intravenous infusion of thyrotropin-releasing hormone (TRH). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2126554",
"endSection": "abstract",
"offsetInBeginSection": 182,
"offsetInEndSection": 347,
"text": "Similar improvements in speech, swallowing and in tongue and jaw movements were seen after iv and oral administration in nine, five and eight patients respectively. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2125610",
"endSection": "abstract",
"offsetInBeginSection": 182,
"offsetInEndSection": 220,
"text": "No clinical improvement was detected. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2514091",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 246,
"text": "A trial of Thyrotropin Releasing Hormone (TRH) 5.0 mg/kg body weight subcutaneously every other day for two weeks produced transient increased tone in muscles, along with other (side-) effects in patients with Amyotrophic Lateral Sclerosis (ALS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2513155",
"endSection": "abstract",
"offsetInBeginSection": 1561,
"offsetInEndSection": 1705,
"text": "Although the mechanism is not known, several reports of the effectiveness of thyrotropin releasing hormone (TRH) in ALS were recently published."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2563937",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "Protirelin (thyrotropin-releasing hormone) appears to be a neuromodulator in the extrahypothalamic nervous system and has been suggested as an adjunct in the treatment of amyotrophic lateral sclerosis (ALS). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2497685",
"endSection": "abstract",
"offsetInBeginSection": 1129,
"offsetInEndSection": 1437,
"text": "Clinical studies have shown that response to TRH is state dependent, that is, it depends on whether the patient has bulbar or nonbulbar signs and is male or female. Future studies must take into consideration this state dependence as a specific feature of the pharmacological action of TRH and its analogues."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2497684",
"endSection": "abstract",
"offsetInBeginSection": 315,
"offsetInEndSection": 617,
"text": "Three of the studies showed a transient, statistically significant effect in at least some muscles. The two studies that demonstrated no such effect both used TRH in very small doses. It therefore seems reasonable to conclude that the effect of TRH in ALS is a definite, acute, and transient response. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3146705",
"endSection": "abstract",
"offsetInBeginSection": 373,
"offsetInEndSection": 642,
"text": "It was found that in only 3 out of 14 patients with moderately progressed disease no improvement was achieved, while in 11 cases the improvement was from 10 to 20%. However, the improvement was transient, and TRH treatment failed to stop the progression of the disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3148186",
"endSection": "abstract",
"offsetInBeginSection": 124,
"offsetInEndSection": 181,
"text": "Only 3 patients noted subjective improvement of strength."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3148185",
"endSection": "abstract",
"offsetInBeginSection": 140,
"offsetInEndSection": 348,
"text": "In 6 of the 9, TRH induced a significant increase in vibratory inhibition. This suggests that the TRH-induced reduction of spasticity might be due to an increase in presynaptic inhibition acting on Ia fibres."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3104820",
"endSection": "abstract",
"offsetInBeginSection": 299,
"offsetInEndSection": 446,
"text": "However, 2 mg DN-1417, IM twice a day for 1 month in an open-label trial, produced no objective improvement of strength in nine patients with ALS. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3104751",
"endSection": "abstract",
"offsetInBeginSection": 501,
"offsetInEndSection": 623,
"text": "Our experience suggests that this approach is safe, has high patient acceptance, and is worthy of more careful evaluation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3104750",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 504,
"text": "Focal, small-to-moderate and transient improvement occurred in the muscle strength and function of patients with ALS who received TRH in dose-response and screening studies. In a small pilot study of 12 patients, 3 months administration of TRH at 10 mg per kg on alternate days resulted in localized increased strength of jaw muscles as well as significant improvement in lower extremity function. Aerobic exercise capacity was particularly improved in patients with ALS following administration of TRH. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3097367",
"endSection": "abstract",
"offsetInBeginSection": 346,
"offsetInEndSection": 412,
"text": "Mild to moderate improvement was found in 9 (56%) of 16 patients. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3097367",
"endSection": "abstract",
"offsetInBeginSection": 588,
"offsetInEndSection": 653,
"text": "We thought such action of TRH to be useful to the therapy of ALS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3080695",
"endSection": "abstract",
"offsetInBeginSection": 725,
"offsetInEndSection": 1011,
"text": "With daily TRH, 10 patients noted subjective improvement without objective evidence, and 10 patients complained of worsening of the disease with objective decline after TRH was stopped. Statistical analysis, however, showed no beneficial effects from either acute or chronic TRH trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3080694",
"endSection": "abstract",
"offsetInBeginSection": 317,
"offsetInEndSection": 576,
"text": "A temporary increase in the strength of some muscles was detected following the administration of TRH, but no change in functional performance was noted. Neither the patients nor the investigators believed the effects were of any marked clinical significance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3080693",
"endSection": "abstract",
"offsetInBeginSection": 511,
"offsetInEndSection": 910,
"text": "Nevertheless, statistically significant improvement was seen only in dynametric strength 1 hour after subcutaneous injection (p less than 0.05). Significant improvement occurred, in one patient only, on subjective speech testing during IV infusion of TRH. In none of six other ratings was there a significant difference between TRH and placebo. Subjective improvement was noted by 11 of 12 patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3088700",
"endSection": "abstract",
"offsetInBeginSection": 398,
"offsetInEndSection": 607,
"text": "Significant improvement, as shown by statistical analysis, was noted in muscle strength in the 9 patients by 5 infusions over a 4-week period and a sub-group of 5 patients treated by 8 infusions over 10 weeks."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3923160",
"endSection": "abstract",
"offsetInBeginSection": 168,
"offsetInEndSection": 291,
"text": "The progressive course of this disease, manifested by increasing atrophy, paralysis and disability score, was not altered. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6134961",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 479,
"text": "Very high intravenous doses (2-19 mg/min) of thyrotropin-releasing hormone (TRH, L-pyroglutamyl-L-histidyl-L-prolinamide) given to 12 patients with amyotrophic lateral sclerosis (ALS) produced a moderate to marked improvement of functions caused by deficiency of lower motor neurons (weakness) and upper motor neurons (spasticity). The improvement was sustained throughout the infusion and for about 1 h thereafter; sometimes a slight improvement was evident 20 h after infusion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22017410",
"endSection": "abstract",
"offsetInBeginSection": 212,
"offsetInEndSection": 514,
"text": "These central nervous system (CNS)-mediated effects provide the rationale for use of TRH and its analogs in the treatment of brain and spinal injury, and CNS disorders like schizophrenia, Alzheimer's disease, epilepsy, amyotrophic lateral sclerosis, Parkinson's disease, depression, shock and ischemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9444487",
"endSection": "abstract",
"offsetInBeginSection": 558,
"offsetInEndSection": 733,
"text": "The Effect of TRH to correct the abnormal F responses in SSP might be consistent with effects of TRH to reduce spasticity in amyotrophic lateral sclerosis described previously"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3104750",
"endSection": "abstract",
"offsetInBeginSection": 398,
"offsetInEndSection": 502,
"text": "Aerobic exercise capacity was particularly improved in patients with ALS following administration of TRH"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3104750",
"endSection": "abstract",
"offsetInBeginSection": 398,
"offsetInEndSection": 502,
"text": "Aerobic exercise capacity was particularly improved in patients with ALS following administration of TRH"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3104750",
"endSection": "abstract",
"offsetInBeginSection": 398,
"offsetInEndSection": 502,
"text": "Aerobic exercise capacity was particularly improved in patients with ALS following administration of TRH"
}
]
| 5 | BioASQ-training5b | [
"http://www.biosemantics.org/jochem#4272308",
"http://www.disease-ontology.org/api/metadata/DOID:332"
]
| []
| 54d76ac63706e89528000016 | 138 |
yesno | Are epigenetic modifications implicated in cardiovascular development and disease? | ['yes'] | [
"yes"
]
| ['Genetic and epigenetic factors are of great importance in cardiovascular biology and disease. Aberrant epigenetic mechanisms may lead to pathological consequences such as cardiovascular disease (CAD).Recent studies have greatly expanded our understanding of the regulation of cardiovascular development at the chromatin level, including the remodeling of chromatin and the modification of histones. Thus, understanding chromatin-level regulation will allow for a better appreciation of gene regulation as a whole and may set a fundamental basis for cardiovascular disease.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22981780",
"http://www.ncbi.nlm.nih.gov/pubmed/22773406",
"http://www.ncbi.nlm.nih.gov/pubmed/24183004",
"http://www.ncbi.nlm.nih.gov/pubmed/22035349",
"http://www.ncbi.nlm.nih.gov/pubmed/23640490",
"http://www.ncbi.nlm.nih.gov/pubmed/23448446",
"http://www.ncbi.nlm.nih.gov/pubmed/23261320",
"http://www.ncbi.nlm.nih.gov/pubmed/22669047",
"http://www.ncbi.nlm.nih.gov/pubmed/22621747",
"http://www.ncbi.nlm.nih.gov/pubmed/22234702",
"http://www.ncbi.nlm.nih.gov/pubmed/21764886",
"http://www.ncbi.nlm.nih.gov/pubmed/20603647",
"http://www.ncbi.nlm.nih.gov/pubmed/20881938",
"http://www.ncbi.nlm.nih.gov/pubmed/19488075",
"http://www.ncbi.nlm.nih.gov/pubmed/21372004"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22981780",
"endSection": "abstract",
"offsetInBeginSection": 1016,
"offsetInEndSection": 1252,
"text": "Gene expression regulation through the interplay of DNA methylation and histone modifications is well-established, although the knowledge about the function of epigenetic signatures in cardiovascular disease is still largely unexplored."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22981780",
"endSection": "abstract",
"offsetInBeginSection": 1253,
"offsetInEndSection": 1508,
"text": "The study of epigenetic markers is, therefore, a very promising frontier of science which may aid in a deeper understanding of molecular mechanisms underlying the modulation of gene expression in the biomolecule pathways linked to cardiovascular diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22773406",
"endSection": "abstract",
"offsetInBeginSection": 997,
"offsetInEndSection": 1291,
"text": "This review highlights our current knowledge of epigenetic gene regulation and the evidence that chromatin remodeling and histone modifications play key roles in the pathogenesis of cardiovascular disease through (re)programming of cardiovascular (stem) cells commitment, identity and function."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24183004",
"endSection": "abstract",
"offsetInBeginSection": 195,
"offsetInEndSection": 918,
"text": "Notably, multiple subunits of switching defective/sucrose non-fermenting (SWI/SNF) chromatin-remodeling complexes have been identified as strong candidates underlying these defects because they physically and functionally interact with cardiogenic transcription factors critical to cardiac development, such as TBX5, GATA-4, and NKX2-5. While these studies indicate a critical role of SWI/SNF complexes in cardiac development and congenital heart disease, many exciting new discoveries have identified their critical role in the adult heart in both physiological and pathological conditions involving multiple cell types in the heart, including cardiomyocytes, vascular endothelial cells, pericytes, and neural crest cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22035349",
"endSection": "abstract",
"offsetInBeginSection": 1061,
"offsetInEndSection": 1535,
"text": "Recent studies have greatly expanded our understanding of the regulation of cardiovascular development at the chromatin level, including the remodeling of chromatin and the modification of histones. Chromatin-level regulation integrates multiple inputs and coordinates broad gene expression programs. Thus, understanding chromatin-level regulation will allow for a better appreciation of gene regulation as a whole and may set a fundamental basis for cardiovascular disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23640490",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 270,
"text": "Genetic and epigenetic factors are of great importance in cardiovascular biology and disease. Tobacco-smoking, one of the most important cardiovascular risk factors, is itself partially determined by genetic background and is associated with altered epigenetic patterns."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23448446",
"endSection": "abstract",
"offsetInBeginSection": 120,
"offsetInEndSection": 521,
"text": "Epigenetic modifications, including DNA methylation, histone modification (acetylation, methylation and phosphorylation) and miRNA, are critical for regulating developmental events. However, aberrant epigenetic mechanisms may lead to pathological consequences such as cardiovascular disease (CAD), neurodegenerative disease, obesity, metabolic disorder, bone and skeletal diseases and various cancers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23261320",
"endSection": "abstract",
"offsetInBeginSection": 1004,
"offsetInEndSection": 1423,
"text": "Cardiovascular disease pathways are now being approached from the epigenetic perspective, including those associated with atherosclerosis, angiogenesis, ischemia-reperfusion damage, and the cardiovascular response to hypoxia and shear stress, among many others. With increasing interest and expanding partnerships in the field, we can expect new insights to emerge from epigenetic perspectives of cardiovascular health."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22669047",
"endSection": "abstract",
"offsetInBeginSection": 19,
"offsetInEndSection": 357,
"text": "Epigenetic modifications are heritable alterations of the genome, which can govern gene expression without altering the DNA sequence. The purpose of this review is to render an overview of the possible mechanisms of epigenetic regulation of gene expression in response to environmental pollutants leading to cardiovascular diseases (CVD)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22669047",
"endSection": "abstract",
"offsetInBeginSection": 576,
"offsetInEndSection": 865,
"text": "From varied study approaches directed either toward the general understanding of the key pathway regulatory genes, or sampling population cohorts for global and gene-specific changes, it has been possible to identify several epigenetic signatures of environmental exposure relevant to CVD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22669047",
"endSection": "abstract",
"offsetInBeginSection": 1250,
"offsetInEndSection": 1423,
"text": "An understanding of chromatin remodelling in response to environmental stimuli conducive to CVD is emerging, with the promise of novel diagnostic and therapeutic candidates."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22621747",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 651,
"text": "Consolidated knowledge is accumulating as to the role of epigenetic regulatory mechanisms in the physiology of vascular development and vascular tone as well as in the pathogenesis of cardiovascular disease. The modulation of gene expression through modification of the epigenome by structural changes of the chromatin architecture without alterations of the associated genomic DNA sequence is part of the cellular response to environmental changes. Such environmental conditions, which are finally being translated into adaptations of the cardiovascular system, also comprise pathological conditions such as atherosclerosis or myocardial infarction. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22234702",
"endSection": "abstract",
"offsetInBeginSection": 828,
"offsetInEndSection": 1187,
"text": "Emerging data suggest that these epigenetic modifications also impact on the development of cardiovascular disease. Histone modifications lead to the modulation of the expression of genetic information through modification of DNA accessibility. In addition, RNA-based mechanisms (e.g., microRNAs and long non-coding RNAs) influence the development of disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22234702",
"endSection": "abstract",
"offsetInBeginSection": 1188,
"offsetInEndSection": 1289,
"text": "We here outline the recent work pertaining to epigenetic changes in a cardiovascular disease setting."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21764886",
"endSection": "abstract",
"offsetInBeginSection": 275,
"offsetInEndSection": 473,
"text": "Epigenetics may represent one of the possible scientific explanations of the impact of such intrauterine risk factors for the subsequent development of cardiovascular disease (CVD) during adulthood."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20603647",
"endSection": "abstract",
"offsetInBeginSection": 837,
"offsetInEndSection": 1272,
"text": "Epigenetic mechanisms include DNA methylation, histone modification, and microRNA alterations, which collectively enable the cell to respond quickly to environmental changes. A number of CVD risk factors, such as nutrition, smoking, pollution, stress, and the circadian rhythm, have been associated with modification of epigenetic marks. Further examination of these mechanisms may lead to earlier prevention and novel therapy for CVD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22234702",
"endSection": "abstract",
"offsetInBeginSection": 818,
"offsetInEndSection": 934,
"text": " Emerging data suggest that these epigenetic modifications also impact on the development of cardiovascular disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22234702",
"endSection": "abstract",
"offsetInBeginSection": 828,
"offsetInEndSection": 943,
"text": "Emerging data suggest that these epigenetic modifications also impact on the development of cardiovascular disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22981780",
"endSection": "abstract",
"offsetInBeginSection": 1016,
"offsetInEndSection": 1252,
"text": "Gene expression regulation through the interplay of DNA methylation and histone modifications is well-established, although the knowledge about the function of epigenetic signatures in cardiovascular disease is still largely unexplored."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22981780",
"endSection": "abstract",
"offsetInBeginSection": 1253,
"offsetInEndSection": 1508,
"text": "The study of epigenetic markers is, therefore, a very promising frontier of science which may aid in a deeper understanding of molecular mechanisms underlying the modulation of gene expression in the biomolecule pathways linked to cardiovascular diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20881938",
"endSection": "abstract",
"offsetInBeginSection": 1142,
"offsetInEndSection": 1265,
"text": "Epigenetic alterations are associated with inflammation and cardiovascular disease in patients with chronic kidney disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22234702",
"endSection": "abstract",
"offsetInBeginSection": 828,
"offsetInEndSection": 942,
"text": "Emerging data suggest that these epigenetic modifications also impact on the development of cardiovascular disease"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19488075",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "Epigenetic mechanisms that underpin metabolic and cardiovascular diseases."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21372004",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 56,
"text": "Epigenetic regulation of cardiovascular differentiation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21372004",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Epigenetic control mechanisms play a key role in the regulation of embryonic development and tissue homeostasis and modulate cardiovascular diseases."
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002318",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D057890"
]
| []
| 54f7291630767eb92e000002 | 139 |
yesno | Is melatonin beneficial in the treatment of in cerebral ischemia-reperfusion injury: | ['yes'] | [
"yes"
]
| ['Yes, melatonin is beneficial in treating cerebral ischemia-reperfusion injury:', 'Yes, melatonin is beneficial in the treatment of cerebral ischemia-reperfusion injury.', 'Yes, melatonin has protective effects against cerebral ischemia/reperfusion injury.', 'Yes, melatonin is effective for treatment of cerebral ischemia-reperfusion injury.', 'Yes, melatonin is beneficial in the treatment of in cerebral ischemia-reperfusion injury.', 'Yes, melatonin regulates microglial polarization and protects against ischemic stroke-induced brain injury in mice, suggesting that it may be beneficial in the treatment of cerebral ischemia-reperfusion injury.', 'Yes, melatonin is beneficial in the treatment of cerebral ischemia-reperfusion injury. It has been shown to have neuroprotective effects, reducing brain damage and improving cognitive function.', 'Yes, melatonin has been shown to be beneficial in the treatment of cerebral ischemia-reperfusion injury in mice.', '”The present study demonstrates that melatonin has a protective effect on brain tissue during ischemia-reperfusion injury"}', 'Yes, Melatonin improves cognitive function by suppressing endoplasmic reticulum stress and promoting synaptic plasticity during chronic cerebral hypoperfusion in rats.', 'Studies have suggested that melatonin is a potential therapeutic agent in cerebral ischemia reperfusion injury', 'Yes, melatonin is beneficial in treating cerebral ischemia-reperfusion injury.', 'Yes, melatonin has been shown to be beneficial in the treatment of cerebral ischemia/reperfusion injury by inducing autophagy, which helps in reducing the damage caused by the condition.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/12667942",
"http://www.ncbi.nlm.nih.gov/pubmed/24530291",
"http://www.ncbi.nlm.nih.gov/pubmed/15673559",
"http://www.ncbi.nlm.nih.gov/pubmed/37600520",
"http://www.ncbi.nlm.nih.gov/pubmed/15033929",
"http://www.ncbi.nlm.nih.gov/pubmed/34118791",
"http://www.ncbi.nlm.nih.gov/pubmed/12614473",
"http://www.ncbi.nlm.nih.gov/pubmed/37327371",
"http://www.ncbi.nlm.nih.gov/pubmed/19552637",
"http://www.ncbi.nlm.nih.gov/pubmed/31697951",
"http://www.ncbi.nlm.nih.gov/pubmed/12074100",
"http://www.ncbi.nlm.nih.gov/pubmed/11068944",
"http://www.ncbi.nlm.nih.gov/pubmed/17123867",
"http://www.ncbi.nlm.nih.gov/pubmed/12853293",
"http://www.ncbi.nlm.nih.gov/pubmed/34800293",
"http://www.ncbi.nlm.nih.gov/pubmed/33063739",
"http://www.ncbi.nlm.nih.gov/pubmed/35572137",
"http://www.ncbi.nlm.nih.gov/pubmed/21160589",
"http://www.ncbi.nlm.nih.gov/pubmed/24646622",
"http://www.ncbi.nlm.nih.gov/pubmed/30476721",
"http://www.ncbi.nlm.nih.gov/pubmed/37301531",
"http://www.ncbi.nlm.nih.gov/pubmed/35301664",
"http://www.ncbi.nlm.nih.gov/pubmed/12579834",
"http://www.ncbi.nlm.nih.gov/pubmed/18194199",
"http://www.ncbi.nlm.nih.gov/pubmed/37321200",
"http://www.ncbi.nlm.nih.gov/pubmed/35219702",
"http://www.ncbi.nlm.nih.gov/pubmed/27620136",
"http://www.ncbi.nlm.nih.gov/pubmed/37923146",
"http://www.ncbi.nlm.nih.gov/pubmed/35841976",
"http://www.ncbi.nlm.nih.gov/pubmed/15298666",
"http://www.ncbi.nlm.nih.gov/pubmed/33777317",
"http://www.ncbi.nlm.nih.gov/pubmed/32599143"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37301531",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Melatonin regulates microglial polarization and protects against ischemic stroke-induced brain injury in mice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37301531",
"endSection": "abstract",
"offsetInBeginSection": 331,
"offsetInEndSection": 461,
"text": "Melatonin is a promising neuroprotective agent that can regulate microglial polarization in central nervous system (CNS) diseases."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37321200",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 84,
"text": "Melatonin Attenuates Cerebral Ischemia/Reperfusion Injury through Inducing Autophagy"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35219702",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "Melatonin improves cognitive function by suppressing endoplasmic reticulum stress and promoting synaptic plasticity during chronic cerebral hypoperfusion in rats."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37327371",
"endSection": "abstract",
"offsetInBeginSection": 282,
"offsetInEndSection": 462,
"text": "Melatonin is neuroprotective against cerebral ischemia-reperfusion injury (CIRI) in non-DM, normoglycemic animals through anti-oxidant effect, anti-inflammation, and anti-apoptosis"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37321200",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "Melatonin Attenuates Cerebral Ischemia/Reperfusion Injury through Inducing Autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24530291",
"endSection": "abstract",
"offsetInBeginSection": 1429,
"offsetInEndSection": 1807,
"text": "Melatonin potentiated intrinsic antioxidant status, inhibited acid mediated rise in intracellular calcium levels, decreased apoptotic cell death and also markedly inhibited protein kinase C (PKC) influenced AQP4 expression in the cerebral cortex and dorsal striatum.SIGNIFICANCE: Melatonin confers neuroprotection by protein kinase C mediated AQP4 inhibition in ischemic stroke."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15033929",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "Melatonin, the secretory product of the pineal gland, is known to be neuroprotective in cerebral ischemia, which is so far mostly attributed to its antioxidant properties."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15033929",
"endSection": "abstract",
"offsetInBeginSection": 1529,
"offsetInEndSection": 1650,
"text": "Melatonin treatment diminished the loss of neurons and decreased the infarct volume as compared with untreated MCAO rats."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37600520",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "Melatonin: a promising neuroprotective agent for cerebral ischemia-reperfusion injury."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33063739",
"endSection": "abstract",
"offsetInBeginSection": 870,
"offsetInEndSection": 1147,
"text": "These findings suggest that melatonin can improve microvessel abnormalities in the cerebral cortex and hippocampus by lowering the expression of vascular endothelial growth factor and its receptors, thereby improving the cognitive function of patients with Alzheimer's disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24530291",
"endSection": "abstract",
"offsetInBeginSection": 406,
"offsetInEndSection": 631,
"text": "Post administration of melatonin following ischemic stroke reduces AQP4 mediated brain edema and confers neuroprotection.MATERIALS AND METHODS: An in-silico approach was undertaken to confirm effective melatonin-AQP4 binding."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12667942",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 265,
"text": "This brief review summarizes the recently obtained evidence which illustrates the beneficial effects of the endogenously produced antioxidant, melatonin, in reducing tissue damage and reversing cardiac pathophysiology in models of experimental ischemia/reperfusion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17123867",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 421,
"text": "BACKGROUND: Experimental studies have documented the beneficial effects of the endogenously produced antioxidant, melatonin, in reducing tissue damage and limiting cardiac pathophysiology in models of experimental ischemia-reperfusion. Melatonin confers cardioprotection against ischemia-reperfusion injury most likely through its direct free radical scavenging activities and its indirect actions in stimulating antioxid"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24646622",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 345,
"text": "Melatonin, a natural product of the pineal gland, has been shown to protect against ischemic stroke, but the molecular mechanisms underlying its protective function are not fully understood. In the present study, we tested whether melatonin could protect against ischemia-reperfusion (I/R) injury to rat brain by targeting the autophagy pathway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12853293",
"endSection": "abstract",
"offsetInBeginSection": 443,
"offsetInEndSection": 1058,
"text": "The exogenous administration of melatonin in these experimental stroke models reduced infarct volume, lowered the frequency of apoptosis, increased the number of surviving neurons, reduced reactive gliosis, lowered the oxidation of neural lipids and oxidatively damaged DNA, induced bcl-2 gene expression (the activity of which improves cell survival), upregulated excision repair cross-complementing factor 6 (an essential gene for preferential DNA excision repair), restrained poly(ADP ribose) synthetase (which depletes cellular NAD resulting in the loss of ATP) activity, and improved neurophysiologic outcomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12853293",
"endSection": "abstract",
"offsetInBeginSection": 170,
"offsetInEndSection": 442,
"text": "In these investigations, which have used three species (rat, gerbil, and cat), melatonin was universally found to reduce brain damage that normally occurs as a consequence of the temporary interruption of blood flow followed by the reflow of oxygenated blood to the brain."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21160589",
"endSection": "abstract",
"offsetInBeginSection": 1224,
"offsetInEndSection": 1367,
"text": "Melatonin attenuates molecular and cellular damage resulting from cardiac ischemia-reperfusion in which destructive free radicals are involved."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19552637",
"endSection": "abstract",
"offsetInBeginSection": 1125,
"offsetInEndSection": 1290,
"text": "Taken together, our results document that melatonin provides neuroprotective effects in CCH by attenuating oxidative stress and stress protein expression in neurons."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12579834",
"endSection": "abstract",
"offsetInBeginSection": 557,
"offsetInEndSection": 1083,
"text": "Neuronal damage was assessed in CA1 pyramidal layer of gerbil hippocampus and evaluated 7 days after ischemia.RESULTS: MT significantly reversed the locomotor activity increases, ameliorated learning and working memory deficit, and reduced the extent of CA1 hippocampal pyramidal cells injury after transient global cerebral ischemia in the Mongolian gerbil.CONCLUSION: MT provides significantly protective effect against both histological and behavioral consequences of global cerebral ischemia-reperfusion injury in gerbils."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37600520",
"endSection": "abstract",
"offsetInBeginSection": 882,
"offsetInEndSection": 1074,
"text": "Therefore, understanding the underlying intracellular and molecular mechanisms is crucial before investigating the neuroprotective effects of melatonin in cerebral ischemia-reperfusion injury."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15298666",
"endSection": "abstract",
"offsetInBeginSection": 1503,
"offsetInEndSection": 1674,
"text": "Our results suggest that melatonin treatment mediates neuroprotection against ischemia/reperfusion injury partly via inhibition of the consequential inflammatory response."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35841976",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Intranasally administered melatonin core-shell polymeric nanocapsules: A promising treatment modality for cerebral ischemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30476721",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1085,
"text": "The role of OPA1-related mitochondrial fusion in brain reperfusion stress has remained elusive. The aim of our study is to explore whether melatonin alleviates cerebral IR injury by modulating OPA1-related mitochondrial fusion. We found that melatonin reduced infarct area and suppressed neuron death during reperfusion stress. Biological studies have revealed that IR-inhibited mitochondrial fusion was largely reversed by melatonin via upregulated OPA1 expression. Knocking down OPA1 abrogated the protective effects of melatonin on mitochondrial energy metabolism and mitochondrial apoptosis. In addition, we also found that melatonin modified OPA1 expression via the Yap-Hippo pathway; blockade of the Yap-Hippo pathway induced neuron death and mitochondrial damage despite treatment with melatonin. Altogether, our data demonstrated that cerebral IR injury is closely associated with defective OPA1-related mitochondrial fusion. Melatonin supplementation enhances OPA1-related mitochondrial fusion by activating the Yap-Hippo pathway, ultimately reducing brain reperfusion stress."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27620136",
"endSection": "abstract",
"offsetInBeginSection": 205,
"offsetInEndSection": 1184,
"text": "Melatonin regulates a large number of physiological actions and its beneficial properties have been reported. The aim of this study was to investigate whether melatonin mediates neuroprotection in rat hippocampal slices subjected to oxygen-glucose-deprivation (OGD) and glutamate excitotoxicity. Thus, we describe here that melatonin significantly reduced the amount of lactate dehydrogenase released in the OGD-treated slices, reverted neuronal injury caused by OGD-reoxygenation in CA1 and CA3 hippocampal regions, restored the reduction of GSH content of the hippocampal slices induced by OGD, and diminished the oxidative stress produced in the reoxygenation period. Furthermore, melatonin afforded maximum protection against glutamate-induced toxicity and reversed the glutamate released almost basal levels, at 10 and 30μM concentration, respectively. Consequently, we propose that melatonin might strongly and positively influence the outcome of brain ischemia/reperfusion"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12074100",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1226,
"text": "Melatonin is a potent scavenger of free radicals and an indirect antioxidant. Recent studies have shown that melatonin possesses beneficial effects in experimental models of brain trauma and global cerebral ischemia. The effects of pretreatment with melatonin on volume of cerebral infarction were investigated in the present study. Adult male Sprague-Dawley rats were anesthetized with sodium pentobarbital to undergo right-sided endovascular middle cerebral artery occlusion (MCAO) for 3 hr. A single dose of melatonin (1.5, 5, 15, or 50 mg/kg in 1 mL normal saline) or its vehicle was given via an intraperitoneal injection at 0.5 hr before MCAO. Relative infarction volumes on day 3 after MCAO were significantly reduced in the groups treated with melatonin at 5 (mean +/- S.E.M., 15.7 +/- 2.5%) or 15 (21.4 +/- 3.1 %) mg/kg but not at 1.5 (30.6 +/- 3.5%) or 50 (26.7 +/- 2.8%) mg/ kg when compared with the vehicle group (33.9 +/- 3.5%). There was no significant difference in the arterial blood pressure (BP), heart rate (HR) and relative cerebral blood flow among the experimental groups. These results indicate that pretreatment with melatonin at a dose between 5 and 15 mg/kg protects against focal cerebral ischemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24646622",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 957,
"text": "Melatonin, a natural product of the pineal gland, has been shown to protect against ischemic stroke, but the molecular mechanisms underlying its protective function are not fully understood. In the present study, we tested whether melatonin could protect against ischemia-reperfusion (I/R) injury to rat brain by targeting the autophagy pathway. The I/R brain injury was induced by the established rat transient middle cerebral artery occlusion model. We found intraperitoneal injection of melatonin can ameliorate rat brain injury as evidenced by multiple morphological and behavioral criteria, such as infarct size, neurological score, serum creatine kinase, and lactate dehydrogenase content, as well as pyknotic-positive cells. Further studies revealed that the beneficial effects of melatonin is through targeting the autophagy pathway by inhibiting expression of beclin-1 and conversion of LC3, as well as activating the PI3K/Akt pro-survival pathway."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35572137",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 107,
"text": "Melatonin as a Potential Neuroprotectant: Mechanisms in Subarachnoid Hemorrhage-Induced Early Brain Injury."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37923146",
"endSection": "abstract",
"offsetInBeginSection": 173,
"offsetInEndSection": 438,
"text": "f diseases. In this study, the neuroprotective effects of melatonin (Mel) on a rat model of cerebral ischemia/reperfusion injury (CIRI) were assessed by multi-parametric MRI combined with histopathological techniques for longitudinal monitoring of the lesion microe"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33777317",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 250,
"text": "Melatonin is a strong antioxidant which beneficially protects against middle cerebral artery occlusion (MCAO) followed by hemorrhagic transformation in rats; protection includes the reduction of neurological deficits, infarction, and hematoma volume."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35301664",
"endSection": "abstract",
"offsetInBeginSection": 187,
"offsetInEndSection": 1642,
"text": "Nonetheless, the mechanisms of the anti-inflammatory effects of EA are unclear. Cerebral I/R injury was induced in rats by middle cerebral artery occlusion (MCAO). Following I/R injury, the rats underwent EA therapy at the Shenting (DU24) and Baihui (DU20) acupoints for seven successive days. The Morris water maze test, magnetic resonance imaging (MRI) and molecular biology assays were utilized to assess the establishment of the rat stroke model with cognitive impairment and the therapeutic effect of EA. EA treatment of rats subjected to MCAO showed a significant reduction in infarct volumes accompanied by cognitive recovery, as observed in Morris water maze test outcomes. The possible mechanisms by which EA treatment attenuates cognitive impairment are by regulating endogenous melatonin secretion through aralkylamine N-acetyltransferase gene (AANAT, a rate-limiting enzyme of melatonin) synthesis in the pineal gland in stroke rats. Simultaneously, through melatonin regulation, EA exerts neuroprotective effects by upregulating mitophagy-associated proteins and suppressing reactive oxygen species (ROS)-induced NLRP3 inflammasome activation after I/R injury. However, melatonin receptor inhibitor (luzindole) treatment reversed these changes. The findings from this research suggested that EA ameliorates cognitive impairment through the inhibition of NLRP3 inflammasome activation by regulating melatonin-mediated mitophagy in stroke rats."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19552637",
"endSection": "abstract",
"offsetInBeginSection": 152,
"offsetInEndSection": 230,
"text": "Melatonin has protective effects against cerebral ischemia/reperfusion injury."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37321200",
"endSection": "abstract",
"offsetInBeginSection": 1435,
"offsetInEndSection": 1598,
"text": "e damage in neurons after CI.CONCLUSION: Melatonin treatment following CI reduced the infarct area and induced the autophagic proteins Beclin-1, LC3, and p62 by in"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34800293",
"endSection": "abstract",
"offsetInBeginSection": 1300,
"offsetInEndSection": 1513,
"text": "In conclusion, these results indicate that melatonin treatment can protect against CIR-induced brain damage in diabetic mice, which may be achieved by the autophagy enhancement mediated by the SIRT1-BMAL1 pathway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37327371",
"endSection": "abstract",
"offsetInBeginSection": 1626,
"offsetInEndSection": 1762,
"text": "lls, and better neuronal survival.CONCLUSIONS: T1DM aggravates CIRI. Melatonin treatment is neuroprotective against CIRI in T1DM rats vi"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35841976",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 243,
"text": "AIMS: The neurohormone melatonin (MEL) has been reported as a promising neuroprotective molecule, however it suffers pharmaceutical limitations such as poor solubility and low bioavailability, which hinder its pharmacological and clinical pote"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30476721",
"endSection": "abstract",
"offsetInBeginSection": 228,
"offsetInEndSection": 327,
"text": "We found that melatonin reduced infarct area and suppressed neuron death during reperfusion stress."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31697951",
"endSection": "abstract",
"offsetInBeginSection": 1139,
"offsetInEndSection": 1289,
"text": "tosis through SIRT3 activation.SIGNIFICANCE: Our research proved that melatonin promoted SIRT3 expression after tMCAO and alleviated cerebral I/R inju"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32599143",
"endSection": "abstract",
"offsetInBeginSection": 1256,
"offsetInEndSection": 1546,
"text": "stroke. Melatonin treatment significantly decreased infarct volume and cerebral apoptosis; mitigated endoplasmic reticulum stress and mitochondrial dysfunction; and inhibited CI/R injury-induced oxidative/nitrative stress and nuclear factor-κB activation, which was eradicated in RORα-defic"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37327371",
"endSection": "abstract",
"offsetInBeginSection": 1648,
"offsetInEndSection": 1762,
"text": "al survival.CONCLUSIONS: T1DM aggravates CIRI. Melatonin treatment is neuroprotective against CIRI in T1DM rats vi"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30476721",
"endSection": "abstract",
"offsetInBeginSection": 934,
"offsetInEndSection": 1085,
"text": "Melatonin supplementation enhances OPA1-related mitochondrial fusion by activating the Yap-Hippo pathway, ultimately reducing brain reperfusion stress."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12579834",
"endSection": "abstract",
"offsetInBeginSection": 655,
"offsetInEndSection": 894,
"text": "er ischemia.RESULTS: MT significantly reversed the locomotor activity increases, ameliorated learning and working memory deficit, and reduced the extent of CA1 hippocampal pyramidal cells injury after transient global cerebral ischemia in "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15673559",
"endSection": "abstract",
"offsetInBeginSection": 273,
"offsetInEndSection": 463,
"text": "Melatonin's efficacy in curtailing neural damage under conditions of transitory interruption of the blood supply to the brain has been documented in models of both focal and global ischemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15673559",
"endSection": "abstract",
"offsetInBeginSection": 566,
"offsetInEndSection": 826,
"text": "For example, when given at the time of ischemia or reperfusion onset, melatonin reduces neurophysiological deficits, infarct volume, the degree of neural edema, lipid peroxidation, protein carbonyls, DNA damage, neuron and glial loss, and death of the animals."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15673559",
"endSection": "abstract",
"offsetInBeginSection": 1112,
"offsetInEndSection": 1373,
"text": "Considering its high efficacy in overcoming much of the damage associated with ischemia/reperfusion injury, not only in the brain but in other organs as well, its use in clinical trials for the purpose of improving stroke outcome should be seriously considered."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18194199",
"endSection": "abstract",
"offsetInBeginSection": 87,
"offsetInEndSection": 151,
"text": "melatonin against ischemia/reperfusion brain injury. The studies"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31697951",
"endSection": "abstract",
"offsetInBeginSection": 35,
"offsetInEndSection": 118,
"text": " that melatonin plays a critical role in protecting against cerebral ischemia/reper"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12614473",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1724,
"text": "The brain is highly susceptible to focal or global ischemia. Unless ischemia is promptly reversed, reperfusion produces further cerebral damage. Acute thrombolysis or defibrinogenation is effective only in selective patients with ischemic stroke and carries a significant risk of bleeding complications. Whereas numerous neuroprotectants were shown to be effective in experimental studies, none of them have been shown to work in clinical trials. The major pathogenetic mechanisms of ischemia/reperfusion injury include excitotoxicity, disturbed calcium ion homeostasis, overproduction of nitric oxide and other free radicals, inflammation, and apoptosis. Nitric oxide and other free radicals, the key mediators of excitotoxicity and disturbed calcium ion homeostasis, cause direct injury and also indirectly damage via inflammation and apoptosis. Melatonin is a potent free radical scavenger and an indirect antioxidant. This mini review summarizes the in vivo and in vitro evidence that melatonin protects against ischemia/reperfusion injury. There is convincing evidence from the literature that melatonin treatment is highly effective in different in vivo and in vitro models of excitotoxicity or ischemia/reperfusion in multiple animal species. Melatonin is safe and non-toxic in humans, and its administration via the oral route or intravenous injection is convenient. While more experimental studies should be conducted to further explore the neuroprotective mechanisms and to document any synergistic or additive protection from combining melatonin with thrombolysis, defibrinogenation or other neuroprotectants, interested clinical scientists should consider planning phase II and III studies to confirm the benefit"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11068944",
"endSection": "abstract",
"offsetInBeginSection": 1317,
"offsetInEndSection": 1527,
"text": "ischemia and reperfusion. Histological observations of the pyramidal layer of CA-1 showed a reduction of neuronal loss in animals that received melatonin. These results show that melatonin improves brain injury"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24530291",
"endSection": "abstract",
"offsetInBeginSection": 910,
"offsetInEndSection": 1255,
"text": "Brains were harvested for infarct size estimation, water content measurement, biochemical analysis, apoptosis study and western blot experiments.KEY FINDINGS: Melatonin at 60 min post ischemia rendered neuroprotection as evident by reduction in cerebral infarct volume, improvement in motor and neurological deficit and reduction in brain edema."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11068944",
"endSection": "abstract",
"offsetInBeginSection": 1472,
"offsetInEndSection": 1567,
"text": "These results show that melatonin improves brain injury induced by transient cerebral ischemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24530291",
"endSection": "abstract",
"offsetInBeginSection": 1256,
"offsetInEndSection": 1428,
"text": "Furthermore, ischemia induced surge in levels of nitrite and malondialdehyde (MDA) were also found to be significantly reduced in ischemic brain regions in treated animals."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31697951",
"endSection": "abstract",
"offsetInBeginSection": 809,
"offsetInEndSection": 1334,
"text": "Then, we observed the changes in the SIRT3 and downstream relative proteins, infarction volume, neurological score, Nissl, H&E and TUNEL staining, and the expression of apoptosis proteins after tMCAO.KEY FINDINGS: Melatonin upregulated the expression of SIRT3 after tMCAO, and alleviated the neurological dysfunction and cell apoptosis through SIRT3 activation.SIGNIFICANCE: Our research proved that melatonin promoted SIRT3 expression after tMCAO and alleviated cerebral I/R injury by activating the SIRT3 signaling pathway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34118791",
"endSection": "abstract",
"offsetInBeginSection": 1366,
"offsetInEndSection": 1534,
"text": "Overall, we demonstrate that melatonin can alleviate CIR injury in diabetic mice by activating Akt-SIRT3-SOD2 signaling and subsequently improving mitochondrial damage."
}
]
| 13 | BioASQ-training13b | null | null | 65f0369bc4010b4d78000001 | 140 |
yesno | Is butterfly rash a symptom of Systemic lupus erythematosus? | ['yes'] | [
"yes"
]
| ['Yes, butterfly rash is symptom of Systemic lupus erythematosus.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/8000104",
"http://www.ncbi.nlm.nih.gov/pubmed/27878308",
"http://www.ncbi.nlm.nih.gov/pubmed/24948869",
"http://www.ncbi.nlm.nih.gov/pubmed/19082832",
"http://www.ncbi.nlm.nih.gov/pubmed/7065728",
"http://www.ncbi.nlm.nih.gov/pubmed/1440087",
"http://www.ncbi.nlm.nih.gov/pubmed/7979581",
"http://www.ncbi.nlm.nih.gov/pubmed/17728372",
"http://www.ncbi.nlm.nih.gov/pubmed/1765991",
"http://www.ncbi.nlm.nih.gov/pubmed/1437923",
"http://www.ncbi.nlm.nih.gov/pubmed/23934402",
"http://www.ncbi.nlm.nih.gov/pubmed/9598885",
"http://www.ncbi.nlm.nih.gov/pubmed/3769804",
"http://www.ncbi.nlm.nih.gov/pubmed/2674762",
"http://www.ncbi.nlm.nih.gov/pubmed/23019977",
"http://www.ncbi.nlm.nih.gov/pubmed/17113236",
"http://www.ncbi.nlm.nih.gov/pubmed/17569152",
"http://www.ncbi.nlm.nih.gov/pubmed/20120828",
"http://www.ncbi.nlm.nih.gov/pubmed/2585838",
"http://www.ncbi.nlm.nih.gov/pubmed/7607795",
"http://www.ncbi.nlm.nih.gov/pubmed/7924059",
"http://www.ncbi.nlm.nih.gov/pubmed/25516474",
"http://www.ncbi.nlm.nih.gov/pubmed/12672213"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20120828",
"endSection": "abstract",
"offsetInBeginSection": 374,
"offsetInEndSection": 605,
"text": "Diagnosing SLE can be challenging because of the myriad of clinical features and substantial variability between patients. Cutaneous involvement is present in about 60% of cases and typically manifests as a malar or butterfly rash."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20120828",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 72,
"text": "The prevalence of systemic lupus erythematosus (SLE) is 28 per 100,000. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17569152",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 265,
"text": "We report a 12 years old female patient with an overlap syndrome involving autoimmune hepatitis (AIH) and systemic lupus erythematosus (SLE). The patient presented with jaundice, hepatosplenomegaly, malaise, polyarthralgia, arthritis and butterfly rash on the face."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17728372",
"endSection": "abstract",
"offsetInBeginSection": 486,
"offsetInEndSection": 764,
"text": "Some of the clinical characteristics of SLE patients observed were nephritis (53.7%), fever (53.26%), neuropsychological disorder (36.18%), malar/butterfly rash (27.6%), pulmonary disorder (22.6%), photosensitivity (21.6%), cardiac involvement (21.1%) and oral ulcers (19.09%). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17728372",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 77,
"text": "Systemic lupus erythematosus and infections: a retrospective study in Saudis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25516474",
"endSection": "abstract",
"offsetInBeginSection": 801,
"offsetInEndSection": 1123,
"text": "The prevalence of the following manifestations was significantly higher for pediatric than for adult-onset disease including: lupus nephritis (43% pediatric vs 26.4% for adult-onset), hematological disorders (57% vs 36.4%), photosensitivity (20% vs 9%), butterfly rash (61% vs 35.5%) and mucosal ulceration (11.4% vs 4%). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25516474",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disease with highest prevalence among women of childbearing age. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24948869",
"endSection": "abstract",
"offsetInBeginSection": 462,
"offsetInEndSection": 1069,
"text": "We described a unique case of a 25-year-old Arab young woman who was diagnosed with SLE, depending on clinical, laboratory investigations and after she had fulfilled the diagnostic criteria for SLE and had presented the following findings: constitutional findings (fatigue, fever, and arthralgia); dermatologic finding (photosensitivity and butterfly rash); chronic renal failure (proteinuria up to 400 mg in 24 hours); hematologic and antinuclear antibodies (positivity for antinuclear factor (ANF), anti-double-stranded DNA antibodies, direct Coombs, ANA and anti-DNA, low C4 and C3, aCL by IgG and IgM). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23019977",
"endSection": "abstract",
"offsetInBeginSection": 492,
"offsetInEndSection": 771,
"text": "Grade 1 and 2-3 inflammatory process occurred in 53 (63%) and 31 (37%) patients respectively. Symptom complexes \"systemic inflammation\", \"butterfly rash\", \"wrist petechiae\", \"enanthema of the oral mucous membrane\", and other lesions were regarded as the markers of SLE activity. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23019977",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "Systemic lupus erythematosus (SLE) remains a challenging medical problem. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17113236",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "Rembrandt's Maria Bockenolle has a butterfly rash and digital deformities: overlapping syndrome of rheumatoid arthritis and systemic lupus erythematosus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19082832",
"endSection": "abstract",
"offsetInBeginSection": 125,
"offsetInEndSection": 224,
"text": "A butterfly rash on the patient's face suggested a diagnosis of systemic lupus erythematosus (SLE)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19082832",
"endSection": "abstract",
"offsetInBeginSection": 125,
"offsetInEndSection": 222,
"text": "A butterfly rash on the patients face suggested a diagnosis of systemic lupus erythematosus (SLE)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19082832",
"endSection": "abstract",
"offsetInBeginSection": 286,
"offsetInEndSection": 437,
"text": "The diagnosis of SLE could be excluded and the butterfly rash attributed to a laminar hemorrhage, an ecchymosis due to the autoimmune thrombocytopenia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12672213",
"endSection": "abstract",
"offsetInBeginSection": 362,
"offsetInEndSection": 447,
"text": "We describe a case of KD who developed a typical butterfly rash, reminiscent of SLE. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1440087",
"endSection": "abstract",
"offsetInBeginSection": 109,
"offsetInEndSection": 262,
"text": "The diagnosis of SLE was made 22 years ago based on Raynaud's phenomenon, butterfly rash, hair loss, photosensitivity and positive antinuclear antibody. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23019977",
"endSection": "abstract",
"offsetInBeginSection": 586,
"offsetInEndSection": 770,
"text": "Symptom complexes \"systemic inflammation\", \"butterfly rash\", \"wrist petechiae\", \"enanthema of the oral mucous membrane\", and other lesions were regarded as the markers of SLE activity."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17113236",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Rembrandt's Maria Bockenolle has a butterfly rash and digital deformities: overlapping syndrome of rheumatoid arthritis and systemic lupus erythematosus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27878308",
"endSection": "abstract",
"offsetInBeginSection": 111,
"offsetInEndSection": 391,
"text": "To investigate, various unspecific, but otherwise typical clinical symptoms of skin and mucous membranes that arise in SLE patients other than those defined as SLE criteria such as butterfly rash, chronic cutaneous lupus erythematosus, oral ulcers, and increased photosensitivity."
}
]
| 6 | BioASQ-training6b | [
"http://www.disease-ontology.org/api/metadata/DOID:8857",
"http://www.disease-ontology.org/api/metadata/DOID:9074",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D008180"
]
| null | 58bfeb2b02b8c6095300001a | 141 |
yesno | Is cariprazine effective for treatment of bipolar disorder? | ['yes'] | [
"yes"
]
| ['Yes, cariprazine is effective for bipolar disorder.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/28843918",
"http://www.ncbi.nlm.nih.gov/pubmed/24048386",
"http://www.ncbi.nlm.nih.gov/pubmed/23361832",
"http://www.ncbi.nlm.nih.gov/pubmed/27190727",
"http://www.ncbi.nlm.nih.gov/pubmed/30323605",
"http://www.ncbi.nlm.nih.gov/pubmed/27396597",
"http://www.ncbi.nlm.nih.gov/pubmed/28343051",
"http://www.ncbi.nlm.nih.gov/pubmed/27274384",
"http://www.ncbi.nlm.nih.gov/pubmed/28478771",
"http://www.ncbi.nlm.nih.gov/pubmed/27059102",
"http://www.ncbi.nlm.nih.gov/pubmed/29017067",
"http://www.ncbi.nlm.nih.gov/pubmed/26586950",
"http://www.ncbi.nlm.nih.gov/pubmed/25562205",
"http://www.ncbi.nlm.nih.gov/pubmed/23966785",
"http://www.ncbi.nlm.nih.gov/pubmed/25056368",
"http://www.ncbi.nlm.nih.gov/pubmed/30470662",
"http://www.ncbi.nlm.nih.gov/pubmed/26510944",
"http://www.ncbi.nlm.nih.gov/pubmed/29119668",
"http://www.ncbi.nlm.nih.gov/pubmed/26655189",
"http://www.ncbi.nlm.nih.gov/pubmed/30372510",
"http://www.ncbi.nlm.nih.gov/pubmed/25532076"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28843918",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "BACKGROUND: We evaluated the safety/tolerability of longer-term open-label treatment with cariprazine in patients who had responded to cariprazine for acute bipolar mania."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29017067",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 108,
"text": "Clinically relevant response and remission outcomes in cariprazine-treated patients with bipolar I disorder."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29017067",
"endSection": "abstract",
"offsetInBeginSection": 110,
"offsetInEndSection": 252,
"text": "Cariprazine is FDA approved for the acute treatment of schizophrenia and manic or mixed episodes associated with bipolar I disorder in adults."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29017067",
"endSection": "abstract",
"offsetInBeginSection": 1467,
"offsetInEndSection": 1741,
"text": "DISCUSSION: Cariprazine-treated patients with bipolar I disorder attained clinically significant improvement in manic symptoms as shown by significantly greater rates of response and remission versus placebo; improvement in manic symptoms did not induce depressive symptoms."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28478771",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 233,
"text": "OBJECTIVE: Cariprazine, a dopamine D3/D2 partial agonist atypical antipsychotic with preferential binding to D3 receptors, is approved for the treatment of schizophrenia and manic or mixed episodes associated with bipolar I disorder."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30372510",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 190,
"text": "<b>BACKGROUND</b>: Cariprazine was approved for treating schizophrenia and bipolar disorder, and currently is being evaluated for treating depression in clinical trials in the United States."
}
]
| 11 | BioASQ-training11b | null | null | 5c61bacae842deac67000001 | 143 |
yesno | Can Logic Alignment Free (LAF) be used for bacterial genomes classification? | ['yes'] | [
"yes"
]
| ['Yes. Logic Alignment Free (LAF), a method that combines alignment-free techniques and rule-based classification algorithms can be used in order to assign biological samples to their taxa.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/26664519"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26664519",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 82,
"text": "LAF: Logic Alignment Free and its application to bacterial genomes classification."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26664519",
"endSection": "abstract",
"offsetInBeginSection": 315,
"offsetInEndSection": 1235,
"text": "In this paper, we present Logic Alignment Free (LAF), a method that combines alignment-free techniques and rule-based classification algorithms in order to assign biological samples to their taxa. This method searches for a minimal subset of k-mers whose relative frequencies are used to build classification models as disjunctive-normal-form logic formulas (if-then rules). We apply LAF successfully to the classification of bacterial genomes to their corresponding taxonomy. In particular, we succeed in obtaining reliable classification at different taxonomic levels by extracting a handful of rules, each one based on the frequency of just few k-mers. State of the art methods to adjust the frequency of k-mers to the character distribution of the underlying genomes have negligible impact on classification performance, suggesting that the signal of each class is strong and that LAF is effective in identifying it."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26664519",
"endSection": "abstract",
"offsetInBeginSection": 315,
"offsetInEndSection": 511,
"text": "In this paper, we present Logic Alignment Free (LAF), a method that combines alignment-free techniques and rule-based classification algorithms in order to assign biological samples to their taxa."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26664519",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "LAF: Logic Alignment Free and its application to bacterial genomes classification."
}
]
| 11 | BioASQ-training11b | [
"https://meshb.nlm.nih.gov/record/ui?ui=D008128",
"https://meshb.nlm.nih.gov/record/ui?ui=D016680",
"https://meshb.nlm.nih.gov/record/ui?ui=D002965"
]
| null | 5a75f1f383b0d9ea66000006 | 144 |
yesno | Is there a difference in the rate between gene fusion and gene fission? | ['yes'] | [
"yes"
]
| ['Yes. Several studies have estimated that gene fusion and fission are relatively rare events and the gene fusion/fission rate is approximately between 2 and 6. A conflicting case has been discovered in an analysis of plant genomes, where in Oryza sativa the opposite trend was observed.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23376183",
"http://www.ncbi.nlm.nih.gov/pubmed/17035354",
"http://www.ncbi.nlm.nih.gov/pubmed/17709334",
"http://www.ncbi.nlm.nih.gov/pubmed/16601004",
"http://www.ncbi.nlm.nih.gov/pubmed/15680510",
"http://www.ncbi.nlm.nih.gov/pubmed/17166515",
"http://www.ncbi.nlm.nih.gov/pubmed/22250127",
"http://www.ncbi.nlm.nih.gov/pubmed/21900599",
"http://www.ncbi.nlm.nih.gov/pubmed/21729286",
"http://www.ncbi.nlm.nih.gov/pubmed/19141283",
"http://www.ncbi.nlm.nih.gov/pubmed/16431849"
]
| [
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23376183",
"endSection": "sections.0",
"offsetInBeginSection": 629,
"offsetInEndSection": 860,
"text": "we illustrate arrangement diversity within closely related organisms, estimate arrangement turnover frequency and establish, for the first time, branch-specific rate estimates for fusion, fission, domain addition and terminal loss."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17035354",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "Rate and polarity of gene fusion and fission in Oryza sativa and Arabidopsis thaliana"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17035354",
"endSection": "sections.0",
"offsetInBeginSection": 186,
"offsetInEndSection": 322,
"text": "We have identified all differentially composite or split genes in 2 fully sequenced plant genomes, Oryza sativa and Arabidopsis thaliana"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17035354",
"endSection": "sections.0",
"offsetInBeginSection": 498,
"offsetInEndSection": 796,
"text": "Polarizing these events by outgroup comparison revealed differences in the rate of gene fission but not of gene fusion in the rice and Arabidopsis lineages. Gene fission occurred at a higher rate than gene fusion in the O. sativa lineage and was furthermore more common in rice than in Arabidopsis."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17035354",
"endSection": "sections.0",
"offsetInBeginSection": 1327,
"offsetInEndSection": 1629,
"text": "Gene fusion and fission are thus rare and slow processes in higher plant genomes; they should be of utility to address deeper evolutionary relationships among plants--and the relationship of plants to other eukaryotic lineages--where sequence-based phylogenies provide equivocal or conflicting results."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17709334",
"endSection": "sections.0",
"offsetInBeginSection": 393,
"offsetInEndSection": 677,
"text": "Primary factors correlating with fusion rates are the presence of transmembrane helices in HKs and the presence of DNA-binding domains in RRs, features that require correct (and separate) spatial location. In the absence of such features, there is a relative abundance of fused genes."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16601004",
"endSection": "sections.0",
"offsetInBeginSection": 576,
"offsetInEndSection": 1187,
"text": "We show that indels are the most frequent elementary events and that they occur in most cases at either the N- or C-terminus of the proteins. As revealed by the genomic neighbourhood/context of the corresponding genes, we show that a substantial number of these terminal indels are the consequence of gene fusions/fissions. We provide evidence showing that the contribution of gene fusion/fission to the evolution of multi-domain bacterial proteins is lower-bounded by 27% and upper-bounded by 64%. We conclude that gene fusion/fission is a major contributor to the evolution of multi-domain bacterial proteins."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15680510",
"endSection": "sections.0",
"offsetInBeginSection": 391,
"offsetInEndSection": 610,
"text": "We found that fusion events are approximately four times more common than fission events, and we established that, in most cases, any particular fusion or fission event only occurred once during the course of evolution."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17166515",
"endSection": "sections.0",
"offsetInBeginSection": 1296,
"offsetInEndSection": 1501,
"text": "Analyzing the most parsimonious pathways, we find 87% of architectures to gain complexity over time through simple changes, among which fusion events account for 5.6 times as many architectures as fission."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19141283",
"endSection": "sections.0",
"offsetInBeginSection": 392,
"offsetInEndSection": 767,
"text": "These trees defined timelines of architectural discovery and revealed remarkable evolutionary patterns, including the explosive appearance of domain combinations during the rise of organismal lineages, the dominance of domain fusion processes throughout evolution, and the late appearance of a new class of multifunctional modules in Eukarya by fission of domain combinations"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16431849",
"endSection": "sections.0",
"offsetInBeginSection": 608,
"offsetInEndSection": 899,
"text": "We searched for examples which have arisen by one of the three postulated mechanisms: independent fusion/fission, \"duplication/deletion,\" and plasmid-mediated \"cut and paste.\" We conclude that all three mechanisms can be observed, with the independent fusion/fission being the most frequent."
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D050939"
]
| null | 5149b575d24251bc05000047 | 145 |
yesno | Do Conserved noncoding elements act as enhancers? | ['yes'] | [
"yes"
]
| ['An important percentage of noncoding elements conserved across distant species shows enhancer activity and other forms of regulatory functionality.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/21629789",
"http://www.ncbi.nlm.nih.gov/pubmed/21081479",
"http://www.ncbi.nlm.nih.gov/pubmed/21047394",
"http://www.ncbi.nlm.nih.gov/pubmed/20494938",
"http://www.ncbi.nlm.nih.gov/pubmed/19805301",
"http://www.ncbi.nlm.nih.gov/pubmed/19782672",
"http://www.ncbi.nlm.nih.gov/pubmed/19704032",
"http://www.ncbi.nlm.nih.gov/pubmed/19492354",
"http://www.ncbi.nlm.nih.gov/pubmed/19171877",
"http://www.ncbi.nlm.nih.gov/pubmed/19073165",
"http://www.ncbi.nlm.nih.gov/pubmed/18562680",
"http://www.ncbi.nlm.nih.gov/pubmed/18047696",
"http://www.ncbi.nlm.nih.gov/pubmed/17989259",
"http://www.ncbi.nlm.nih.gov/pubmed/17940009",
"http://www.ncbi.nlm.nih.gov/pubmed/17210927",
"http://www.ncbi.nlm.nih.gov/pubmed/16533910",
"http://www.ncbi.nlm.nih.gov/pubmed/15859353"
]
| [
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21081479",
"endSection": "sections.0",
"offsetInBeginSection": 1169,
"offsetInEndSection": 1216,
"text": "The aCNEs are rich in tissue-specific enhancers"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21081479",
"endSection": "sections.0",
"offsetInBeginSection": 1397,
"offsetInEndSection": 1483,
"text": "Transgenic zebrafish assay of some human CNE enhancers that have been lost in teleosts"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20494938",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 95,
"text": "Conserved noncoding elements (CNEs) in vertebrate genomes often act as developmental enhancers,"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20494938",
"endSection": "sections.0",
"offsetInBeginSection": 1433,
"offsetInEndSection": 1727,
"text": "In all four cases where the zebra fish and human CNE display a similar expression pattern in zebra fish, the human CNE also displays a similar expression pattern in mouse. This suggests that the endogenous enhancer activity of ∼30% of human CNEs can be determined from experiments in zebra fish"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19805301",
"endSection": "sections.0",
"offsetInBeginSection": 1278,
"offsetInEndSection": 1530,
"text": "If these ancient CNEs are indeed enhancers directing tissue-specific expression of Hox genes, divergence of their sequences in vertebrate lineages might have led to altered expression patterns and presumably the functions of their associated Hox genes."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19805301",
"endSection": "sections.0",
"offsetInBeginSection": 635,
"offsetInEndSection": 887,
"text": "Comparisons of noncoding sequences of the elephant shark and human Hox clusters have identified a large number of conserved noncoding elements (CNEs), which represent putative cis-regulatory elements that may be involved in the regulation of Hox genes."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19704032",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "Animal genomes possess highly conserved cis-regulatory sequences that are often found near genes that regulate transcription and development."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19704032",
"endSection": "sections.0",
"offsetInBeginSection": 755,
"offsetInEndSection": 914,
"text": "We test 42 of our PCNEs in transgenic zebrafish assays--including examples from vertebrates and amphioxus--and find that the majority are functional enhancers."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19492354",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 214,
"text": "The genomes of vertebrates, flies, and nematodes contain highly conserved noncoding elements (CNEs). CNEs cluster around genes that regulate development, and where tested, they can act as transcriptional enhancers."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19171877",
"endSection": "sections.0",
"offsetInBeginSection": 443,
"offsetInEndSection": 1004,
"text": ", we identified 17 highly conserved noncoding elements, 9 of which revealed specific acetylation marks in chromatin-immunoprecipitation and microarray (ChIP-chip) assays performed across 250 kb of the Lmo2 locus in 11 cell types covering different stages of hematopoietic differentiation. All candidate regulatory regions were tested in transgenic mice. An extended LMO2 proximal promoter fragment displayed strong endothelial activity, while the distal promoter showed weak forebrain activity. Eight of the 15 distal candidate elements functioned as enhancers,"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19073165",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 216,
"text": "Pan-vertebrate developmental cis-regulatory elements are discernible as highly conserved noncoding elements (HCNEs) and are often dispersed over large areas around the pleiotropic genes whose expression they control."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19073165",
"endSection": "sections.0",
"offsetInBeginSection": 585,
"offsetInEndSection": 677,
"text": "HCNEs of both human and zebrafish function as specific developmental enhancers in zebrafish."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18562680",
"endSection": "sections.0",
"offsetInBeginSection": 1048,
"offsetInEndSection": 1165,
"text": "several transcriptional enhancers are conserved between amphioxus and vertebrates--a very wide phylogenetic distance."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17989259",
"endSection": "sections.0",
"offsetInBeginSection": 382,
"offsetInEndSection": 463,
"text": "We recently described GRBs in vertebrates, where most HCNEs function as enhancers"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17989259",
"endSection": "sections.0",
"offsetInBeginSection": 688,
"offsetInEndSection": 762,
"text": "Besides developmental regulators that are likely targets of HCNE enhancers"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17940009",
"endSection": "sections.0",
"offsetInBeginSection": 144,
"offsetInEndSection": 734,
"text": "We identify and characterize highly conserved noncoding elements flanking the TNF gene, which undergo activation-dependent intrachromosomal interactions. These elements, hypersensitive site (HSS)-9 and HSS+3 (9 kb upstream and 3 kb downstream of the TNF gene, respectively), contain DNase I hypersensitive sites in naive, T helper 1, and T helper 2 primary T cells. Both HSS-9 and HSS+3 inducibly associate with acetylated histones, indicative of chromatin remodeling, bind the transcription factor nuclear factor of activated T cells (NFAT)p in vitro and in vivo, and function as enhancers"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17210927",
"endSection": "sections.0",
"offsetInBeginSection": 1032,
"offsetInEndSection": 1420,
"text": "We used the sequence signatures identified by this approach to successfully assign tissue-specific predictions to approximately 328,000 human-mouse conserved noncoding elements in the human genome. By overlapping these genome-wide predictions with a data set of enhancers validated in vivo, in transgenic mice, we were able to confirm our results with a 28% sensitivity and 50% precision."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16533910",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 305,
"text": "Fish-mammal genomic comparisons have proved powerful in identifying conserved noncoding elements likely to be cis-regulatory in nature, and the majority of those tested in vivo have been shown to act as tissue-specific enhancers associated with genes involved in transcriptional regulation of development."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15859353",
"endSection": "sections.0",
"offsetInBeginSection": 749,
"offsetInEndSection": 1016,
"text": "uncovered two anciently conserved noncoding sequences (CNS) upstream of COUP-TFII (CNS-62kb and CNS-66kb). Testing these two elements using reporter constructs in liver cells (HepG2) revealed that CNS-66kb, but not CNS-62kb, yielded robust in vitro enhancer activity."
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D004742",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=0035326",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D017124",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D024861",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D026801"
]
| null | 5139ec51bee46bd34c000006 | 146 |
yesno | Is muscle lim protein (MLP) involved in cardiomyopathies? | ['yes'] | [
"yes"
]
| ['Yes, Muscle LIM protein is involved in cardiomyopathies. In specific, the skeletal muscle LIM protein 1 (SLIM1) is highly expressed in skeletal and cardiac muscle, and its expression is downregulated significantly in dilated human cardiomyopathy. Mutations in the human MLP gene are associated with hypertrophic and dilated cardiomyopathy. MLP became an important model for experimental cardiology when it was first demonstrated that MLP deficiency leads to myocardial hypertrophy followed by a dilated cardiomyopathy and heart failure phenotype.', 'The skeletal muscle LIM protein 1 (SLIM1) is highly expressed in skeletal and cardiac muscle, and its expression is downregulated significantly in dilated human cardiomyopathy. Loss of murine MLP results in dilated cardiomyopathy, and mutations in human MLP lead to cardiac hypertrophy, indicating a critical role for MLP in maintaining normal cardiac function.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22421737",
"http://www.ncbi.nlm.nih.gov/pubmed/22371524",
"http://www.ncbi.nlm.nih.gov/pubmed/21562304",
"http://www.ncbi.nlm.nih.gov/pubmed/21484537",
"http://www.ncbi.nlm.nih.gov/pubmed/18505755",
"http://www.ncbi.nlm.nih.gov/pubmed/18083727",
"http://www.ncbi.nlm.nih.gov/pubmed/17535853",
"http://www.ncbi.nlm.nih.gov/pubmed/16352453",
"http://www.ncbi.nlm.nih.gov/pubmed/16228909",
"http://www.ncbi.nlm.nih.gov/pubmed/15978612",
"http://www.ncbi.nlm.nih.gov/pubmed/15639480",
"http://www.ncbi.nlm.nih.gov/pubmed/15205937",
"http://www.ncbi.nlm.nih.gov/pubmed/14567970",
"http://www.ncbi.nlm.nih.gov/pubmed/12642359",
"http://www.ncbi.nlm.nih.gov/pubmed/12397030",
"http://www.ncbi.nlm.nih.gov/pubmed/11788418",
"http://www.ncbi.nlm.nih.gov/pubmed/24860983"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22421737",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 339,
"text": "Muscle LIM protein (MLP) has been proposed to be a central player in the pathogenesis of heart muscle disease. In line with this notion, the homozygous loss of MLP results in cardiac hypertrophy and dilated cardiomyopathy. Moreover, MLP is induced in several models of cardiac hypertrophy such as aortic banding and myocardial infarction. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22371524",
"endSection": "abstract",
"offsetInBeginSection": 6,
"offsetInEndSection": 100,
"text": "Muscle LIM protein (MLP) null mice are often used as a model for human dilated cardiomyopathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22371524",
"endSection": "abstract",
"offsetInBeginSection": 1710,
"offsetInEndSection": 1858,
"text": "A lack of MLP leads to an age-dependent impairment of excitation-contraction coupling with resulting contractile dysfunction and secondary fibrosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21562304",
"endSection": "abstract",
"offsetInBeginSection": 133,
"offsetInEndSection": 317,
"text": "Loss of murine MLP results in dilated cardiomyopathy, and mutations in human MLP lead to cardiac hypertrophy, indicating a critical role for MLP in maintaining normal cardiac function."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21562304",
"endSection": "abstract",
"offsetInBeginSection": 1276,
"offsetInEndSection": 1390,
"text": "Our data indicate that MLP contributes to muscle stiffness and is necessary for maximum work and power generation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21484537",
"endSection": "abstract",
"offsetInBeginSection": 616,
"offsetInEndSection": 1110,
"text": "Interestingly, MLP was also found to be down-regulated in humans with heart failure (Zolk et al. Circulation 101:2674-2677, 2000) and MLP mutations are able to cause hypertrophic and dilated forms of cardiomyopathy in humans (Bos et al. Mol Genet Metab 88:78-85, 2006; Geier et al. Circulation 107:1390-1395, 2003; Hershberger et al. Clin Transl Sci 1:21-26, 2008; Knöll et al. Cell 111:943-955, 2002; Knöll et al. Circ Res 106:695-704, 2010; Mohapatra et al. Mol Genet Metab 80:207-215, 2003)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21484537",
"endSection": "abstract",
"offsetInBeginSection": 264,
"offsetInEndSection": 513,
"text": "MLP soon became an important model for experimental cardiology when it was first demonstrated that MLP deficiency leads to myocardial hypertrophy followed by a dilated cardiomyopathy and heart failure phenotype (Arber et al. Cell 88:393-403, 1997). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18505755",
"endSection": "abstract",
"offsetInBeginSection": 218,
"offsetInEndSection": 459,
"text": "Previous studies have shown an association between CSRP3 missense mutations and either dilated cardiomyopathy (DCM) or HCM, but all these studies were unable to provide comprehensive genetic evidence for a causative role of CSRP3 mutations. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18505755",
"endSection": "abstract",
"offsetInBeginSection": 709,
"offsetInEndSection": 1124,
"text": "We used a newly designed monoclonal antibody to show that muscle LIM protein (MLP), the protein encoded by CSRP3, is mainly a cytosolic component of cardiomyocytes and not tightly anchored to sarcomeric structures. Our functional data from both in vitro and in vivo analyses suggest that at least one of MLP's mutated forms seems to be destabilized in the heart of HCM patients harbouring a CSRP3 missense mutation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18083727",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Muscle LIM protein (MLP) is a cytoskeletal protein located at the Z-disc of sarcomeres. Mutations in the human MLP gene are associated with hypertrophic and dilated cardiomyopathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18083727",
"endSection": "abstract",
"offsetInBeginSection": 923,
"offsetInEndSection": 1156,
"text": "Our data demonstrate that Mlp84B is essential for normal cardiac function and establish the Drosophila model for the investigation of the mechanisms connecting defective cardiac Z-disc components to the development of cardiomyopathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17535853",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 148,
"text": "Muscle LIM protein (MLP) is a cytoskeletal LIM-only protein expressed in striated muscle. Mutations in human MLP are associated with cardiomyopathy;"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16352453",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 370,
"text": "TTN-encoded titin, CSRP3-encoded muscle LIM protein, and TCAP-encoded telethonin are Z-disc proteins essential for the structural organization of the cardiac sarcomere and the cardiomyocyte's stretch sensor. All three genes have been established as cardiomyopathy-associated genes for both dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16352453",
"endSection": "abstract",
"offsetInBeginSection": 1548,
"offsetInEndSection": 1883,
"text": "Approximately 4.1% of unrelated patients had HCM-associated MLP or TCAP mutations. MLP/TCAP-HCM phenotypically mirrors myofilament-HCM and is more severe than the subset of patients who still remain without a disease-causing mutation. The precise role of W4R-MLP in the pathogenesis of either DCM or HCM warrants further investigation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16228909",
"endSection": "abstract",
"offsetInBeginSection": 1274,
"offsetInEndSection": 1487,
"text": "MLP (muscle-LIM-protein) deficient mice develop DCM and changes in the mechanical coupling of cardiomyocytes result in alterations at the intercalated disks and enhanced accumulation of adherens junction proteins."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15978612",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 144,
"text": "Targeted deletion of cytoskeletal muscle LIM protein (MLP) in mice consistently leads to dilated cardiomyopathy (DCM) after one or more months. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15978612",
"endSection": "abstract",
"offsetInBeginSection": 1307,
"offsetInEndSection": 1660,
"text": "In summary, young MLPKO mice revealed substantial alterations in passive myocardial properties and relaxation time, but not in most systolic characteristics. These results indicate that the progression to heart failure in the MLPKO model may be driven by diastolic myocardial dysfunction and abnormal passive properties rather than systolic dysfunction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15639480",
"endSection": "abstract",
"offsetInBeginSection": 139,
"offsetInEndSection": 280,
"text": "Mice lacking the muscle LIM protein (MLP) develop morphological and clinical signs resembling human dilated cardiomyopathy and heart failure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15639480",
"endSection": "abstract",
"offsetInBeginSection": 1375,
"offsetInEndSection": 1772,
"text": "Our results show that the absence of MLP causes a local loss of mitochondria. We hypothesize that this is caused by a disturbed interaction between cytoskeleton and mitochondria, which interferes with energy sensing and energy transfer. Recovery of energy depletion by stimulating mitochondrial biogenesis might be a useful therapeutic strategy for improving the energy imbalance in heart failure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15205937",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 317,
"text": "Previous work has shown that mutations in muscle LIM protein (MLP) can cause hypertrophic cardiomyopathy (HCM). In order to gain an insight into the molecular basis of the disease phenotype, we analysed the binding characteristics of wild-type MLP and of the (C58G) mutant MLP that causes hypertrophic cardiomyopathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15205937",
"endSection": "abstract",
"offsetInBeginSection": 915,
"offsetInEndSection": 1092,
"text": "The molecular basis for HCM-causing mutations in the MLP gene might therefore be an alteration in the equilibrium of interactions of the ternary complex MLP-N-RAP-alpha-actinin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14567970",
"endSection": "abstract",
"offsetInBeginSection": 219,
"offsetInEndSection": 572,
"text": "Muscle LIM protein (MLP) is a member of the cysteine-rich protein (CRP) family and has been implicated in both myogenesis and sarcomere assembly. In the latter role, it binds zyxin and alpha-actinin, both of which are involved in actin organization. An MLP-deficient mouse has been described; these mice develop dilated cardiomyopathy and heart failure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14567970",
"endSection": "abstract",
"offsetInBeginSection": 770,
"offsetInEndSection": 896,
"text": "We identified a patient with DCM and EFE, having a mutation in MLP with the residue lysine 69 substituted by arginine (K69R). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12642359",
"endSection": "abstract",
"offsetInBeginSection": 195,
"offsetInEndSection": 402,
"text": "MLP-knockout mice develop a marked cardiac hypertrophy reaction and dilated cardiomyopathy (DCM). MLP is therefore a candidate gene for heritable forms of hypertrophic cardiomyopathy (HCM) and DCM in humans."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12642359",
"endSection": "abstract",
"offsetInBeginSection": 1166,
"offsetInEndSection": 1365,
"text": "Family studies revealed cosegregation of clinically affected individuals with the respective mutations in MLP. CONCLUSION: Here, we present evidence that mutations in the CRP3/MLP gene can cause HCM."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12397030",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "The skeletal muscle LIM protein 1 (SLIM1) is highly expressed in skeletal and cardiac muscle, and its expression is downregulated significantly in dilated human cardiomyopathy. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11788418",
"endSection": "abstract",
"offsetInBeginSection": 141,
"offsetInEndSection": 412,
"text": "Targeted disruption of muscle LIM protein (MLP) has previously been shown to result in dilated cardiomyopathy with many of the clinical signs of heart failure, although the effects of MLP disruption on passive ventricular mechanics and myocyte architecture are not known."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11788418",
"endSection": "abstract",
"offsetInBeginSection": 915,
"offsetInEndSection": 1189,
"text": "These results suggest that the disruption of the cytoskeletal protein MLP results in less compliant passive tissue and concomitant structural alterations in the three-dimensional myocyte architecture that may in part explain the ventricular dysfunction in the dilated heart."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24860983",
"endSection": "abstract",
"offsetInBeginSection": 110,
"offsetInEndSection": 347,
"text": " Mutations in cysteine and glycine-rich protein 3 (CSRP3), the gene encoding MLP, have been directly associated with human cardiomyopathies, whereas aberrant expression patterns are reported in human cardiac and skeletal muscle diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22421737",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Muscle LIM protein (MLP) has been proposed to be a central player in the pathogenesis of heart muscle disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22421737",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 339,
"text": "Muscle LIM protein (MLP) has been proposed to be a central player in the pathogenesis of heart muscle disease. In line with this notion, the homozygous loss of MLP results in cardiac hypertrophy and dilated cardiomyopathy. Moreover, MLP is induced in several models of cardiac hypertrophy such as aortic banding and myocardial infarction. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22371524",
"endSection": "abstract",
"offsetInBeginSection": 6,
"offsetInEndSection": 100,
"text": "Muscle LIM protein (MLP) null mice are often used as a model for human dilated cardiomyopathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15205937",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Previous work has shown that mutations in muscle LIM protein (MLP) can cause hypertrophic cardiomyopathy (HCM)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15205937",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Previous work has shown that mutations in muscle LIM protein (MLP) can cause hypertrophic cardiomyopathy (HCM)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15205937",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Previous work has shown that mutations in muscle LIM protein (MLP) can cause hypertrophic cardiomyopathy (HCM)"
}
]
| 5 | BioASQ-training5b | [
"http://www.disease-ontology.org/api/metadata/DOID:0050700",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D009202"
]
| []
| 54f704b630767eb92e000001 | 147 |
yesno | Have Quercetin-biapigenin nanoparticles been shown to be effective in penetrating the blood-brain barrier | ['yes'] | [
"yes"
]
| ['Quercetin-biapigenin nanoparticles are effective to penetrate the blood-brain barrier.', 'Yes, Quercetin-biapigenin nanoparticles have been shown to be effective in penetrating the blood-brain barrier in an in vitro BBB model.', 'Yes, Quercetin-biapigenin nanoparticles have been shown to be effective in penetrating the blood-brain barrier.', 'Yes, Quercetin-biapigenin nanoparticles been shown to be effective in penetrating the blood-brain barrier', 'Yes, Quercetin-biapigenin loaded nanoparticles have been shown to effectively penetrate the blood-brain barrier in various studies.', 'Yes, Quercetin-biapigenin loaded PCL-nanoparticles have previously been shown to be effective at crossing the blood-brain barrier in pre-clinical studies.', 'Yes, Quercetin-biapigenin nanoparticles are effective to penetrate the blood-brain barrier.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/33709285",
"http://www.ncbi.nlm.nih.gov/pubmed/32154811"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33709285",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "Quercetin-biapigenin nanoparticles are effective to penetrate the blood-brain barrier."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33709285",
"endSection": "abstract",
"offsetInBeginSection": 436,
"offsetInEndSection": 757,
"text": " The present study aimed to investigate the potential protective effect of quercetin-biapigenin encapsulated into poly(Ɛ-polycaprolactone) (PCL) nanoparticles against t-BOOH-induced oxidative stress in several brain cell lines, as well as evaluate the permeability of those active molecules through an in vitro BBB model."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33709285",
"endSection": "abstract",
"offsetInBeginSection": 1170,
"offsetInEndSection": 1288,
"text": "As of our knowledge, this is the first report of quercetin-biapigenin PCL-loaded nanoparticle activity in brain cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32154811",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 242,
"text": "Microbubbles in combination with focused ultrasound for the delivery of quercetin-modified sulfur nanoparticles through the blood brain barrier into the brain parenchyma and relief of endoplasmic reticulum stress to treat Alzheimer's disease."
}
]
| 12 | BioASQ-training12b | null | null | 6422e7ba690f196b51000044 | 149 |
yesno | Can salivary cortisol be used to evaluate pain in neonates? | ['yes'] | [
"yes"
]
| ['Yes, salivary cortisol concentrations can be used to evaluate pain in neonates.', 'Yes, salivary cortisol can be used to evaluate pain in neonates, as it has been observed to increase in response to painful stimuli and correlates with NIPS scores.', 'Yes, salivary cortisol can be used to evaluate pain in neonates.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/36282969"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36282969",
"endSection": "abstract",
"offsetInBeginSection": 1377,
"offsetInEndSection": 1604,
"text": "We observed the increase in SC concentrations in response to painful stimulus. The presence of a correlation between NIPS scores and SC increase suggests that SC can be used as an objective parameter to assess pain in neonates."
}
]
| 12 | BioASQ-training12b | null | null | 64410f8057b1c7a315000054 | 150 |
yesno | Are PDXK mutations linked to polyneuropathy? | ['yes'] | [
"yes"
]
| ['Yes, PDXK mutations are linked to polyneuropathy.', 'Yes, PDXK mutations are associated with autosomal recessive polyneuropathy.', "Yes. PDXK mutations cause polyneuropathy responsive to pyridoxal 5'-phosphate supplementation.", 'Yes, PDXK mutations are associated with delayed polyneuropathy.', 'Yes, point mutations in PDXK gene may be associated with peripheral neuropathy.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/31187503",
"http://www.ncbi.nlm.nih.gov/pubmed/32522499"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31187503",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "PDXK mutations cause polyneuropathy responsive to pyridoxal 5'-phosphate supplementation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31187503",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 1971,
"text": "To identify disease-causing variants in autosomal recessive axonal polyneuropathy with optic atrophy and provide targeted replacement therapy.METHODS: We performed genome-wide sequencing, homozygosity mapping, and segregation analysis for novel disease-causing gene discovery. We used circular dichroism to show secondary structure changes and isothermal titration calorimetry to investigate the impact of variants on adenosine triphosphate (ATP) binding. Pathogenicity was further supported by enzymatic assays and mass spectroscopy on recombinant protein, patient-derived fibroblasts, plasma, and erythrocytes. Response to supplementation was measured with clinical validated rating scales, electrophysiology, and biochemical quantification.RESULTS: We identified biallelic mutations in PDXK in 5 individuals from 2 unrelated families with primary axonal polyneuropathy and optic atrophy. The natural history of this disorder suggests that untreated, affected individuals become wheelchair-bound and blind. We identified conformational rearrangement in the mutant enzyme around the ATP-binding pocket. Low PDXK ATP binding resulted in decreased erythrocyte PDXK activity and low pyridoxal 5'-phosphate (PLP) concentrations. We rescued the clinical and biochemical profile with PLP supplementation in 1 family, improvement in power, pain, and fatigue contributing to patients regaining their ability to walk independently during the first year of PLP normalization.INTERPRETATION: We show that mutations in PDXK cause autosomal recessive axonal peripheral polyneuropathy leading to disease via reduced PDXK enzymatic activity and low PLP. We show that the biochemical profile can be rescued with PLP supplementation associated with clinical improvement. As B6 is a cofactor in diverse essential biological pathways, our findings may have direct implications for neuropathies of unknown etiology characterized by reduced PLP levels. ANN NEUROL 2019;86:225-240."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31187503",
"endSection": "abstract",
"offsetInBeginSection": 1483,
"offsetInEndSection": 1656,
"text": "RETATION: We show that mutations in PDXK cause autosomal recessive axonal peripheral polyneuropathy leading to disease via reduced PDXK enzymatic activity and low PLP. We sh"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31187503",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 88,
"text": "PDXK mutations cause polyneuropathy responsive to pyridoxal 5'-phosphate supplementation"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32522499",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Hereditary polyneuropathy with optic atrophy due to PDXK variant leading to impaired Vitamin B6 metabolism"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31187503",
"endSection": "abstract",
"offsetInBeginSection": 1477,
"offsetInEndSection": 1650,
"text": "INTERPRETATION: We show that mutations in PDXK cause autosomal recessive axonal peripheral polyneuropathy leading to disease via reduced PDXK enzymatic activity and low PLP."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31187503",
"endSection": "abstract",
"offsetInBeginSection": 754,
"offsetInEndSection": 901,
"text": "RESULTS: We identified biallelic mutations in PDXK in 5 individuals from 2 unrelated families with primary axonal polyneuropathy and optic atrophy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31187503",
"endSection": "abstract",
"offsetInBeginSection": 1496,
"offsetInEndSection": 1653,
"text": "show that mutations in PDXK cause autosomal recessive axonal peripheral polyneuropathy leading to disease via reduced PDXK enzymatic activity and low PLP. We"
}
]
| 11 | BioASQ-training11b | null | null | 6031002d1cb411341a000129 | 151 |
yesno | Does lucatumumab bind to CD140? | ['no'] | [
"no"
]
| ['No, lucatumumab is a fully humanized anti-CD40 antibody that blocks interaction of CD40L with CD40 and also mediates antibody-dependent cell-mediated cytotoxicity (ADCC).'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22475052"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22475052",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 167,
"text": "Lucatumumab is a fully humanized anti-CD40 antibody that blocks interaction of CD40L with CD40 and also mediates antibody-dependent cell-mediated cytotoxicity (ADCC). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22475052",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "Phase I study of the anti-CD40 humanized monoclonal antibody lucatumumab (HCD122) in relapsed chronic lymphocytic leukemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22475052",
"endSection": "abstract",
"offsetInBeginSection": 731,
"offsetInEndSection": 889,
"text": "Saturation of CD40 receptor on CLL cells was uniform at all doses post-treatment but also persisted at trough time points in the 3.0 mg/kg or greater cohorts."
}
]
| 11 | BioASQ-training11b | null | null | 5c654c14e842deac67000025 | 152 |
yesno | Is enzastaurin effective treatment of glioblastoma? | ['no'] | [
"no"
]
| ['No. Enzastaurin does not improve prognosis of glioblastoma patients.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/17620423",
"http://www.ncbi.nlm.nih.gov/pubmed/26643807",
"http://www.ncbi.nlm.nih.gov/pubmed/27052640",
"http://www.ncbi.nlm.nih.gov/pubmed/21035151",
"http://www.ncbi.nlm.nih.gov/pubmed/25398844",
"http://www.ncbi.nlm.nih.gov/pubmed/23911595",
"http://www.ncbi.nlm.nih.gov/pubmed/28259301",
"http://www.ncbi.nlm.nih.gov/pubmed/26692525",
"http://www.ncbi.nlm.nih.gov/pubmed/21896554",
"http://www.ncbi.nlm.nih.gov/pubmed/20044633",
"http://www.ncbi.nlm.nih.gov/pubmed/20150385"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28259301",
"endSection": "abstract",
"offsetInBeginSection": 542,
"offsetInEndSection": 1014,
"text": "RESULTS: fourteen randomized clinical trials were identified (7 with bevacizumab, 2 cilengitide, 1 enzastaurin, 1 dasatinib, 1 vandetanib, 1 temsirolimus, 1 cediranib) including 4330 patients. Antiangiogenic drugs showed no improvement in overall survival with a pooled HR of 1.00, a trend for an inferior outcome, in terms of overall survival, was observed in the group of patients receiving antiangiogenic drug alone compared to cytotoxic drug alone (HR=1.24, p=0.056). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26643807",
"endSection": "abstract",
"offsetInBeginSection": 1744,
"offsetInEndSection": 1929,
"text": "Enzastaurin (LY317615) in combination with bevacizumab for recurrent malignant gliomas is well-tolerated, with response and progression-free survival similar to bevacizumab monotherapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27052640",
"endSection": "abstract",
"offsetInBeginSection": 597,
"offsetInEndSection": 840,
"text": "So far, inhibition of angiogenesis by compounds such as bevacizumab, cediranib, enzastaurin or cilengitide as well as alternative dosing schedules of temozolomide did not prolong survival, neither at primary diagnosis nor at recurrent disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25398844",
"endSection": "abstract",
"offsetInBeginSection": 580,
"offsetInEndSection": 927,
"text": "Despite promising phase II clinical trial results and patient benefit in terms of clinical improvement and longer progression-free survival, an overall survival benefit has not been demonstrated in four randomized phase III trials of bevacizumab or cilengitide in newly diagnosed glioblastoma or cediranib or enzastaurin in recurrent glioblastoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23911595",
"endSection": "abstract",
"offsetInBeginSection": 1489,
"offsetInEndSection": 1551,
"text": "CONCLUSIONS: PFS-6 missed the primary planned outcome of 55%. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21896554",
"endSection": "abstract",
"offsetInBeginSection": 1093,
"offsetInEndSection": 1403,
"text": "OS (median, 74 weeks) and PFS (median, 36 weeks) results from the current trial were comparable to those from a prior phase II study using erlotinib and were significantly better than those from 2 other previous studies that used thalidomide or cis-retinoic acid, all in combination with temozolomide plus RT. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21035151",
"endSection": "abstract",
"offsetInBeginSection": 1033,
"offsetInEndSection": 1379,
"text": "More recently, antiangiogenic agents including enzastaurin, cediranib, bevacizumab, and others that target mainly the VEGF pathway, have been evaluated in this highly angiogenic disease. Among them, only bevacizumab has been associated with clear anti-tumor activity, although the lack of control studies limits the impact of the results to date."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20150385",
"endSection": "abstract",
"offsetInBeginSection": 1516,
"offsetInEndSection": 1684,
"text": "Enzastaurin has anti-glioma activity in patients with recurrent high-grade glioma, but does not appear to have enough single-agent activity to be useful as monotherapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20044633",
"endSection": "abstract",
"offsetInBeginSection": 844,
"offsetInEndSection": 1525,
"text": "Several signal transduction inhibitors have been examined in preclinical and clinical malignant glioma trials, including antiangiogenic agents (bevacizumab, enzastaurin), and inhibitors of epidermal growth factor receptor tyrosine kinase (gefitinib and erlotinib), mammalian target of rapamycin (temsirolimus, everolimus) and integrin (cilengitide). Although preliminary clinical results of the use of targeted agents have not translated into significantly better survival, more recent phase II trials are exploring the combination of multitargeted drugs with cytotoxic chemotherapy and radiotherapy in order to overcome the resistance of tumors to single-agent targeted therapies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17620423",
"endSection": "abstract",
"offsetInBeginSection": 730,
"offsetInEndSection": 1298,
"text": "Several drugs have been tested, including epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (gefitinib and erlotinib), mammalian target of rapamycin (mTOR) inhibitors (temsirolimus and everolimus), and vascular endothelial growth factor receptor (VEGFR), protein kinase C-beta, and other angiogenesis pathways inhibitors (vatalanib, bevacizumab, and enzastaurin). Although preliminary efficacy results of most trials in recurrent disease have fallen short on expectations, substantial advances have been achieved by associated translational research. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27052640",
"endSection": "abstract",
"offsetInBeginSection": 599,
"offsetInEndSection": 842,
"text": "So far, inhibition of angiogenesis by compounds such as bevacizumab, cediranib, enzastaurin or cilengitide as well as alternative dosing schedules of temozolomide did not prolong survival, neither at primary diagnosis nor at recurrent disease."
}
]
| 11 | BioASQ-training11b | [
"https://meshb.nlm.nih.gov/record/ui?ui=D005909",
"http://www.biosemantics.org/jochem#4240085",
"https://meshb.nlm.nih.gov/record/ui?ui=D016896"
]
| null | 5a7612b483b0d9ea6600001d | 153 |
yesno | Is glycyl-tRNA synthetase gene involved in the development of Charcot-Marie-Tooth disease? | ['yes'] | [
"yes"
]
| ['Dominant mutations in GARS, encoding the essential enzyme glycyl-tRNA synthetase (GlyRS), result in a form of Charcot-Marie-Tooth disease, type 2D (CMT2D), predominantly characterized by lower motor nerve degeneration.', 'Charcot-Marie-Tooth disease type 2D (CMT2D) is an autosomal-dominant axonal peripheral neuropathy characterized by impaired motor and sensory function in the distal extremities. Mutations in the glycyl-tRNA synthetase (GARS) gene cause CMT2D', 'Charcot-Marie-Tooth disease type 2D (CMT2D) is an autosomal-dominant axonal peripheral neuropathy characterized by impaired motor and sensory function in the distal extremities. Mutations in the glycyl-tRNA synthetase (GARS) gene cause CMT2D', 'Charcot-Marie-Tooth disease type 2D (CMT2D) is an autosomal-dominant axonal peripheral neuropathy characterized by impaired motor and sensory function in the distal extremities. Mutations in the glycyl-tRNA synthetase (GARS) gene cause CMT2D', 'Charcot-Marie-Tooth disease type 2D (CMT2D) is an autosomal-dominant axonal peripheral neuropathy characterized by impaired motor and sensory function in the distal extremities. Mutations in the glycyl-tRNA synthetase (GARS) gene cause CMT2D', 'Charcot-Marie-Tooth disease type 2D (CMT2D) is an autosomal-dominant axonal peripheral neuropathy characterized by impaired motor and sensory function in the distal extremities. Mutations in the glycyl-tRNA synthetase (GARS) gene cause CMT2D'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/25168514",
"http://www.ncbi.nlm.nih.gov/pubmed/24669931",
"http://www.ncbi.nlm.nih.gov/pubmed/24898252",
"http://www.ncbi.nlm.nih.gov/pubmed/24368416",
"http://www.ncbi.nlm.nih.gov/pubmed/25420567",
"http://www.ncbi.nlm.nih.gov/pubmed/12690580",
"http://www.ncbi.nlm.nih.gov/pubmed/17035524",
"http://www.ncbi.nlm.nih.gov/pubmed/22144914",
"http://www.ncbi.nlm.nih.gov/pubmed/17545306",
"http://www.ncbi.nlm.nih.gov/pubmed/23279345",
"http://www.ncbi.nlm.nih.gov/pubmed/16982418",
"http://www.ncbi.nlm.nih.gov/pubmed/23990368",
"http://www.ncbi.nlm.nih.gov/pubmed/19470612"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25168514",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 241,
"text": "Charcot-Marie-Tooth disease type 2D (CMT2D) is an autosomal-dominant axonal peripheral neuropathy characterized by impaired motor and sensory function in the distal extremities. Mutations in the glycyl-tRNA synthetase (GARS) gene cause CMT2D"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24669931",
"endSection": "abstract",
"offsetInBeginSection": 266,
"offsetInEndSection": 375,
"text": "Dominant mutations in GARS cause rare forms of Charcot-Marie-Tooth disease and distal spinal muscular atrophy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24669931",
"endSection": "abstract",
"offsetInBeginSection": 685,
"offsetInEndSection": 809,
"text": "Using exome sequencing she was found to harbor compound heterozygous mutations within the glycyl-tRNA synthetase (GARS) gene"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24898252",
"endSection": "abstract",
"offsetInBeginSection": 329,
"offsetInEndSection": 428,
"text": "mutations of human GlyRS (hGlyRS) were also found to be associated with Charcot-Marie-Tooth disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24368416",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 217,
"text": "Dominant mutations in GARS, encoding the essential enzyme glycyl-tRNA synthetase (GlyRS), result in a form of Charcot-Marie-Tooth disease, type 2D (CMT2D), predominantly characterized by lower motor nerve degeneration"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25420567",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 132,
"text": "A novel mutation in glycyl-tRNA synthetase caused Charcot-Marie-Tooth disease type 2D with facial and respiratory muscle involvement"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25420567",
"endSection": "abstract",
"offsetInBeginSection": 342,
"offsetInEndSection": 957,
"text": "Here we describe a 45-year-old woman with a long course of motor-dominant neuropathy. Distal weakness appeared in childhood and became worse with age. After a diagnosis of CMT type 2, the symptoms progressed, and in her fourth decade, facial and respiratory muscle weakness appeared, ultimately requiring non-invasive mechanical ventilation. There was no family history of CMT. Comprehensive analysis of known CMT-related genes revealed a novel heterozygous c.815T>A, p.L218Q mutation in glycyl-tRNA synthetase (GARS), a causative gene for both CMT type 2D (CMT2D) and distal spinal muscular atrophy type V (dSMA-V)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22144914",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "Charcot-Marie-Tooth disease type 2D (CMT2D) is a dominantly inherited peripheral neuropathy caused by missense mutations in the glycyl-tRNA synthetase gene (GARS)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17545306",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "Long-range structural effects of a Charcot-Marie-Tooth disease-causing mutation in human glycyl-tRNA synthetase."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12690580",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 114,
"text": "Glycyl tRNA synthetase mutations in Charcot-Marie-Tooth disease type 2D and distal spinal muscular atrophy type V."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25420567",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "[A novel mutation in glycyl-tRNA synthetase caused Charcot-Marie-Tooth disease type 2D with facial and respiratory muscle involvement]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23279345",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 255,
"text": "Glycyl-tRNA synthetase (GARS), which encodes the enzyme responsible for charging tRNA(Gly) with glycine in both the cytoplasm and mitochondria, is implicated to Charcot-Marie-Tooth disease 2D (CMT2D) and distal hereditary motor neuropathy type V (dHMN-V)."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/17545306",
"endSection": "abstract",
"offsetInBeginSection": 321,
"offsetInEndSection": 553,
"text": "These additional functions may explain why dominant mutations in glycyl-tRNA synthetase (GlyRS) and tyrosyl-tRNA synthetase cause Charcot-Marie-Tooth (CMT) disease, the most common heritable disease of the peripheral nervous system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12690580",
"endSection": "abstract",
"offsetInBeginSection": 455,
"offsetInEndSection": 605,
"text": "Here, we report the identification of four disease-associated missense mutations in the glycyl tRNA synthetase gene in families with CMT2D and dSMA-V."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25168514",
"endSection": "abstract",
"offsetInBeginSection": 241,
"offsetInEndSection": 305,
"text": "Mutations in the glycyl-tRNA synthetase (GARS) gene cause CMT2D."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22144914",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "Charcot-Marie-Tooth disease type 2D (CMT2D) is a dominantly inherited peripheral neuropathy caused by missense mutations in the glycyl-tRNA synthetase gene (GARS)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17545306",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "Long-range structural effects of a Charcot-Marie-Tooth disease-causing mutation in human glycyl-tRNA synthetase."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/12690580",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 114,
"text": "Glycyl tRNA synthetase mutations in Charcot-Marie-Tooth disease type 2D and distal spinal muscular atrophy type V."
},
{
"beginSection": "title",
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"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "[A novel mutation in glycyl-tRNA synthetase caused Charcot-Marie-Tooth disease type 2D with facial and respiratory muscle involvement]."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/17545306",
"endSection": "abstract",
"offsetInBeginSection": 321,
"offsetInEndSection": 553,
"text": "These additional functions may explain why dominant mutations in glycyl-tRNA synthetase (GlyRS) and tyrosyl-tRNA synthetase cause Charcot-Marie-Tooth (CMT) disease, the most common heritable disease of the peripheral nervous system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16982418",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "Of the many inherited Charcot-Marie-Tooth peripheral neuropathies, type 2D (CMT2D) is caused by dominant point mutations in the gene GARS, encoding glycyl tRNA synthetase (GlyRS)."
},
{
"beginSection": "abstract",
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"endSection": "abstract",
"offsetInBeginSection": 455,
"offsetInEndSection": 605,
"text": "Here, we report the identification of four disease-associated missense mutations in the glycyl tRNA synthetase gene in families with CMT2D and dSMA-V."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22144914",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "Charcot-Marie-Tooth disease type 2D (CMT2D) is a dominantly inherited peripheral neuropathy caused by missense mutations in the glycyl-tRNA synthetase gene (GARS)"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/25420567",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 132,
"text": "A novel mutation in glycyl-tRNA synthetase caused Charcot-Marie-Tooth disease type 2D with facial and respiratory muscle involvement"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/23990368",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Charcot-Marie-Tooth disease type 2D is a hereditary axonal and glycyl-tRNA synthetase (GARS)-associated neuropathy that is caused by a mutation in GARS"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/24368416",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 217,
"text": "Dominant mutations in GARS, encoding the essential enzyme glycyl-tRNA synthetase (GlyRS), result in a form of Charcot-Marie-Tooth disease, type 2D (CMT2D), predominantly characterized by lower motor nerve degeneration"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17545306",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 111,
"text": "Long-range structural effects of a Charcot-Marie-Tooth disease-causing mutation in human glycyl-tRNA synthetase"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/17545306",
"endSection": "abstract",
"offsetInBeginSection": 90,
"offsetInEndSection": 321,
"text": "These additional functions may explain why dominant mutations in glycyl-tRNA synthetase (GlyRS) and tyrosyl-tRNA synthetase cause Charcot-Marie-Tooth (CMT) disease, the most common heritable disease of the peripheral nervous system"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12690580",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 114,
"text": "Glycyl tRNA synthetase mutations in Charcot-Marie-Tooth disease type 2D and distal spinal muscular atrophy type V."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25420567",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "A novel mutation in glycyl-tRNA synthetase caused Charcot-Marie-Tooth disease type 2D with facial and respiratory muscle involvement."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/17545306",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "Long-range structural effects of a Charcot-Marie-Tooth disease-causing mutation in human glycyl-tRNA synthetase."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/12690580",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 114,
"text": "Glycyl tRNA synthetase mutations in Charcot-Marie-Tooth disease type 2D and distal spinal muscular atrophy type V."
},
{
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"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "Charcot-Marie-Tooth disease type 2D (CMT2D) is a dominantly inherited peripheral neuropathy caused by missense mutations in the glycyl-tRNA synthetase gene (GARS). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25168514",
"endSection": "abstract",
"offsetInBeginSection": 178,
"offsetInEndSection": 243,
"text": "Mutations in the glycyl-tRNA synthetase (GARS) gene cause CMT2D. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19470612",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "An ENU-induced mutation in mouse glycyl-tRNA synthetase (GARS) causes peripheral sensory and motor phenotypes creating a model of Charcot-Marie-Tooth type 2D peripheral neuropathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17035524",
"endSection": "abstract",
"offsetInBeginSection": 194,
"offsetInEndSection": 314,
"text": "We previously implicated mutations in the gene encoding glycyl-tRNA synthetase (GARS) as the cause of CMT2D and dSMA-V. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16982418",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "An active dominant mutation of glycyl-tRNA synthetase causes neuropathy in a Charcot-Marie-Tooth 2D mouse model."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23990368",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "Charcot-Marie-Tooth disease type 2D is a hereditary axonal and glycyl-tRNA synthetase (GARS)-associated neuropathy that is caused by a mutation in GARS. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24368416",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "Dominant mutations in GARS, encoding the essential enzyme glycyl-tRNA synthetase (GlyRS), result in a form of Charcot-Marie-Tooth disease, type 2D (CMT2D), predominantly characterized by lower motor nerve degeneration. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25420567",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "A novel mutation in glycyl-tRNA synthetase caused Charcot-Marie-Tooth disease type 2D with facial and respiratory muscle involvement."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17545306",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "Long-range structural effects of a Charcot-Marie-Tooth disease-causing mutation in human glycyl-tRNA synthetase."
},
{
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"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 114,
"text": "Glycyl tRNA synthetase mutations in Charcot-Marie-Tooth disease type 2D and distal spinal muscular atrophy type V."
},
{
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"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "Charcot-Marie-Tooth disease type 2D (CMT2D) is a dominantly inherited peripheral neuropathy caused by missense mutations in the glycyl-tRNA synthetase gene (GARS). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25168514",
"endSection": "abstract",
"offsetInBeginSection": 178,
"offsetInEndSection": 243,
"text": "Mutations in the glycyl-tRNA synthetase (GARS) gene cause CMT2D. "
},
{
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"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "An ENU-induced mutation in mouse glycyl-tRNA synthetase (GARS) causes peripheral sensory and motor phenotypes creating a model of Charcot-Marie-Tooth type 2D peripheral neuropathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17035524",
"endSection": "abstract",
"offsetInBeginSection": 194,
"offsetInEndSection": 314,
"text": "We previously implicated mutations in the gene encoding glycyl-tRNA synthetase (GARS) as the cause of CMT2D and dSMA-V. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16982418",
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"offsetInEndSection": 112,
"text": "An active dominant mutation of glycyl-tRNA synthetase causes neuropathy in a Charcot-Marie-Tooth 2D mouse model."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/23990368",
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"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "Charcot-Marie-Tooth disease type 2D is a hereditary axonal and glycyl-tRNA synthetase (GARS)-associated neuropathy that is caused by a mutation in GARS. "
},
{
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"text": "Dominant mutations in GARS, encoding the essential enzyme glycyl-tRNA synthetase (GlyRS), result in a form of Charcot-Marie-Tooth disease, type 2D (CMT2D), predominantly characterized by lower motor nerve degeneration. "
},
{
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"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "A novel mutation in glycyl-tRNA synthetase caused Charcot-Marie-Tooth disease type 2D with facial and respiratory muscle involvement."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/17545306",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "Long-range structural effects of a Charcot-Marie-Tooth disease-causing mutation in human glycyl-tRNA synthetase."
},
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"text": "Glycyl tRNA synthetase mutations in Charcot-Marie-Tooth disease type 2D and distal spinal muscular atrophy type V."
},
{
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"offsetInEndSection": 164,
"text": "Charcot-Marie-Tooth disease type 2D (CMT2D) is a dominantly inherited peripheral neuropathy caused by missense mutations in the glycyl-tRNA synthetase gene (GARS). "
},
{
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"offsetInBeginSection": 178,
"offsetInEndSection": 243,
"text": "Mutations in the glycyl-tRNA synthetase (GARS) gene cause CMT2D. "
},
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"endSection": "title",
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"offsetInEndSection": 180,
"text": "An ENU-induced mutation in mouse glycyl-tRNA synthetase (GARS) causes peripheral sensory and motor phenotypes creating a model of Charcot-Marie-Tooth type 2D peripheral neuropathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17035524",
"endSection": "abstract",
"offsetInBeginSection": 194,
"offsetInEndSection": 314,
"text": "We previously implicated mutations in the gene encoding glycyl-tRNA synthetase (GARS) as the cause of CMT2D and dSMA-V. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16982418",
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"offsetInEndSection": 112,
"text": "An active dominant mutation of glycyl-tRNA synthetase causes neuropathy in a Charcot-Marie-Tooth 2D mouse model."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/23990368",
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"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "Charcot-Marie-Tooth disease type 2D is a hereditary axonal and glycyl-tRNA synthetase (GARS)-associated neuropathy that is caused by a mutation in GARS. "
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/24368416",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "Dominant mutations in GARS, encoding the essential enzyme glycyl-tRNA synthetase (GlyRS), result in a form of Charcot-Marie-Tooth disease, type 2D (CMT2D), predominantly characterized by lower motor nerve degeneration. "
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/25420567",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "A novel mutation in glycyl-tRNA synthetase caused Charcot-Marie-Tooth disease type 2D with facial and respiratory muscle involvement."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/17545306",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "Long-range structural effects of a Charcot-Marie-Tooth disease-causing mutation in human glycyl-tRNA synthetase."
},
{
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"endSection": "abstract",
"offsetInBeginSection": 178,
"offsetInEndSection": 243,
"text": "Mutations in the glycyl-tRNA synthetase (GARS) gene cause CMT2D. "
},
{
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"text": "An active dominant mutation of glycyl-tRNA synthetase causes neuropathy in a Charcot-Marie-Tooth 2D mouse model."
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"text": "A novel mutation in glycyl-tRNA synthetase caused Charcot-Marie-Tooth disease type 2D with facial and respiratory muscle involvement."
},
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"offsetInEndSection": 112,
"text": "Long-range structural effects of a Charcot-Marie-Tooth disease-causing mutation in human glycyl-tRNA synthetase."
},
{
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"offsetInEndSection": 114,
"text": "Glycyl tRNA synthetase mutations in Charcot-Marie-Tooth disease type 2D and distal spinal muscular atrophy type V."
},
{
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"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "Charcot-Marie-Tooth disease type 2D (CMT2D) is a dominantly inherited peripheral neuropathy caused by missense mutations in the glycyl-tRNA synthetase gene (GARS). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25168514",
"endSection": "abstract",
"offsetInBeginSection": 178,
"offsetInEndSection": 243,
"text": "Mutations in the glycyl-tRNA synthetase (GARS) gene cause CMT2D. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19470612",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "An ENU-induced mutation in mouse glycyl-tRNA synthetase (GARS) causes peripheral sensory and motor phenotypes creating a model of Charcot-Marie-Tooth type 2D peripheral neuropathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17035524",
"endSection": "abstract",
"offsetInBeginSection": 194,
"offsetInEndSection": 314,
"text": "We previously implicated mutations in the gene encoding glycyl-tRNA synthetase (GARS) as the cause of CMT2D and dSMA-V. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16982418",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "An active dominant mutation of glycyl-tRNA synthetase causes neuropathy in a Charcot-Marie-Tooth 2D mouse model."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/23990368",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "Charcot-Marie-Tooth disease type 2D is a hereditary axonal and glycyl-tRNA synthetase (GARS)-associated neuropathy that is caused by a mutation in GARS. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24368416",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "Dominant mutations in GARS, encoding the essential enzyme glycyl-tRNA synthetase (GlyRS), result in a form of Charcot-Marie-Tooth disease, type 2D (CMT2D), predominantly characterized by lower motor nerve degeneration. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22144914",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 321,
"text": " Charcot-Marie-Tooth disease type 2D (CMT2D) is a dominantly inherited peripheral neuropathy caused by missense mutations in the glycyl-tRNA synthetase gene (GARS). In addition to GARS, mutations in three other tRNA synthetase genes cause similar neuropathies, although the underlying mechanisms are not fully understood."
},
{
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"offsetInBeginSection": 91,
"offsetInEndSection": 255,
"text": "These additional functions may explain why dominant mutations in glycyl-tRNA synthetase (GlyRS) and tyrosyl-tRNA synthetase cause Charcot-Marie-Tooth (CMT) disease,"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17545306",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "Long-range structural effects of a Charcot-Marie-Tooth disease-causing mutation in human glycyl-tRNA synthetase."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12690580",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 114,
"text": "Glycyl tRNA synthetase mutations in Charcot-Marie-Tooth disease type 2D and distal spinal muscular atrophy type V."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25420567",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "A novel mutation in glycyl-tRNA synthetase caused Charcot-Marie-Tooth disease type 2D with facial and respiratory muscle involvement."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25168514",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 243,
"text": " Charcot-Marie-Tooth disease type 2D (CMT2D) is an autosomal-dominant axonal peripheral neuropathy characterized by impaired motor and sensory function in the distal extremities. Mutations in the glycyl-tRNA synthetase (GARS) gene cause CMT2D."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16982418",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Of the many inherited Charcot-Marie-Tooth peripheral neuropathies, type 2D (CMT2D) is caused by dominant point mutations in the gene GARS, encoding glycyl tRNA synthetase (GlyRS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22144914",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "Charcot-Marie-Tooth disease type 2D (CMT2D) is a dominantly inherited peripheral neuropathy caused by missense mutations in the glycyl-tRNA synthetase gene (GARS)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17545306",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "Long-range structural effects of a Charcot-Marie-Tooth disease-causing mutation in human glycyl-tRNA synthetase."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12690580",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "Glycyl tRNA synthetase mutations in Charcot-Marie-Tooth disease type 2D and distal spinal muscular atrophy type V."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17545306",
"endSection": "abstract",
"offsetInBeginSection": 91,
"offsetInEndSection": 323,
"text": "These additional functions may explain why dominant mutations in glycyl-tRNA synthetase (GlyRS) and tyrosyl-tRNA synthetase cause Charcot-Marie-Tooth (CMT) disease, the most common heritable disease of the peripheral nervous system."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25420567",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 134,
"text": "A novel mutation in glycyl-tRNA synthetase caused Charcot-Marie-Tooth disease type 2D with facial and respiratory muscle involvement."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16982418",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Of the many inherited Charcot-Marie-Tooth peripheral neuropathies, type 2D (CMT2D) is caused by dominant point mutations in the gene GARS, encoding glycyl tRNA synthetase (GlyRS)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16982418",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "An active dominant mutation of glycyl-tRNA synthetase causes neuropathy in a Charcot-Marie-Tooth 2D mouse model."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22144914",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "Charcot-Marie-Tooth disease type 2D (CMT2D) is a dominantly inherited peripheral neuropathy caused by missense mutations in the glycyl-tRNA synthetase gene (GARS)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17545306",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "Long-range structural effects of a Charcot-Marie-Tooth disease-causing mutation in human glycyl-tRNA synthetase."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12690580",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "Glycyl tRNA synthetase mutations in Charcot-Marie-Tooth disease type 2D and distal spinal muscular atrophy type V."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17545306",
"endSection": "abstract",
"offsetInBeginSection": 91,
"offsetInEndSection": 323,
"text": "These additional functions may explain why dominant mutations in glycyl-tRNA synthetase (GlyRS) and tyrosyl-tRNA synthetase cause Charcot-Marie-Tooth (CMT) disease, the most common heritable disease of the peripheral nervous system."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25420567",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 134,
"text": "A novel mutation in glycyl-tRNA synthetase caused Charcot-Marie-Tooth disease type 2D with facial and respiratory muscle involvement."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16982418",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Of the many inherited Charcot-Marie-Tooth peripheral neuropathies, type 2D (CMT2D) is caused by dominant point mutations in the gene GARS, encoding glycyl tRNA synthetase (GlyRS)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16982418",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "An active dominant mutation of glycyl-tRNA synthetase causes neuropathy in a Charcot-Marie-Tooth 2D mouse model."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22144914",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "Charcot-Marie-Tooth disease type 2D (CMT2D) is a dominantly inherited peripheral neuropathy caused by missense mutations in the glycyl-tRNA synthetase gene (GARS)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17545306",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "Long-range structural effects of a Charcot-Marie-Tooth disease-causing mutation in human glycyl-tRNA synthetase."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12690580",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "Glycyl tRNA synthetase mutations in Charcot-Marie-Tooth disease type 2D and distal spinal muscular atrophy type V."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17545306",
"endSection": "abstract",
"offsetInBeginSection": 91,
"offsetInEndSection": 323,
"text": "These additional functions may explain why dominant mutations in glycyl-tRNA synthetase (GlyRS) and tyrosyl-tRNA synthetase cause Charcot-Marie-Tooth (CMT) disease, the most common heritable disease of the peripheral nervous system."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25420567",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 134,
"text": "A novel mutation in glycyl-tRNA synthetase caused Charcot-Marie-Tooth disease type 2D with facial and respiratory muscle involvement."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16982418",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Of the many inherited Charcot-Marie-Tooth peripheral neuropathies, type 2D (CMT2D) is caused by dominant point mutations in the gene GARS, encoding glycyl tRNA synthetase (GlyRS)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16982418",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "An active dominant mutation of glycyl-tRNA synthetase causes neuropathy in a Charcot-Marie-Tooth 2D mouse model."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22144914",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "Charcot-Marie-Tooth disease type 2D (CMT2D) is a dominantly inherited peripheral neuropathy caused by missense mutations in the glycyl-tRNA synthetase gene (GARS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23279345",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 256,
"text": "Glycyl-tRNA synthetase (GARS), which encodes the enzyme responsible for charging tRNA(Gly) with glycine in both the cytoplasm and mitochondria, is implicated to Charcot-Marie-Tooth disease 2D (CMT2D) and distal hereditary motor neuropathy type V (dHMN-V)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17545306",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "Long-range structural effects of a Charcot-Marie-Tooth disease-causing mutation in human glycyl-tRNA synthetase."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17545306",
"endSection": "abstract",
"offsetInBeginSection": 91,
"offsetInEndSection": 323,
"text": "These additional functions may explain why dominant mutations in glycyl-tRNA synthetase (GlyRS) and tyrosyl-tRNA synthetase cause Charcot-Marie-Tooth (CMT) disease, the most common heritable disease of the peripheral nervous system."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12690580",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "Glycyl tRNA synthetase mutations in Charcot-Marie-Tooth disease type 2D and distal spinal muscular atrophy type V."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25420567",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 134,
"text": "A novel mutation in glycyl-tRNA synthetase caused Charcot-Marie-Tooth disease type 2D with facial and respiratory muscle involvement."
}
]
| 5 | BioASQ-training5b | []
| []
| 5713c4a11174fb1755000013 | 154 |
yesno | Does silencing of SRRM4 promote microexon inclusion? | ['no'] | [
"no"
]
| ['No, silencing of SRRM4 does not promote microexon inclusion.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/33207694"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33207694",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "SRRM4 Expands the Repertoire of Circular RNAs by Regulating Microexon Inclusion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33207694",
"endSection": "abstract",
"offsetInBeginSection": 1272,
"offsetInEndSection": 1572,
"text": "Overexpressing SRRM4, known for regulating ME inclusion in mRNAs critical for neural differentiation, in human HEK293 cells resulted in the biogenesis of over 2000 novel ME-circRNAs, including ME-circEIF4G3, and changes in the abundance of many canonical circRNAs, including circSETDB2 and circLBRA. "
}
]
| 12 | BioASQ-training12b | null | null | 63f9cdb033942b094c000012 | 155 |
yesno | Are proteasome inhibitors good candidates for treatment of leukemia and solid tumors? | ['yes'] | [
"yes"
]
| ['Yes, several compounds that inhibit different members of the proteasome pathway (for example Bortezomib) are on trial for treatment of leukemia and solid tumors. It seems that a combination with other drugs may be a useful therapy for solid tumors.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22057347",
"http://www.ncbi.nlm.nih.gov/pubmed/17145882",
"http://www.ncbi.nlm.nih.gov/pubmed/22353937",
"http://www.ncbi.nlm.nih.gov/pubmed/22134540",
"http://www.ncbi.nlm.nih.gov/pubmed/22012631",
"http://www.ncbi.nlm.nih.gov/pubmed/20219102",
"http://www.ncbi.nlm.nih.gov/pubmed/20160034",
"http://www.ncbi.nlm.nih.gov/pubmed/19821999",
"http://www.ncbi.nlm.nih.gov/pubmed/19712963",
"http://www.ncbi.nlm.nih.gov/pubmed/17431003",
"http://www.ncbi.nlm.nih.gov/pubmed/16135477",
"http://www.ncbi.nlm.nih.gov/pubmed/15169797",
"http://www.ncbi.nlm.nih.gov/pubmed/12171876",
"http://www.ncbi.nlm.nih.gov/pubmed/23477519",
"http://www.ncbi.nlm.nih.gov/pubmed/23181572",
"http://www.ncbi.nlm.nih.gov/pubmed/22995770"
]
| [
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22057347",
"endSection": "sections.0",
"offsetInBeginSection": 824,
"offsetInEndSection": 1115,
"text": "We show that treatment with b-AP15 inhibited tumor progression in four different in vivo solid tumor models and inhibited organ infiltration in an acute myeloid leukemia model. Our results show that the deubiquitinating activity of the 19S regulatory particle is a new anticancer drug target"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17145882",
"endSection": "sections.0",
"offsetInBeginSection": 1126,
"offsetInEndSection": 1464,
"text": "We further found that ATO targets AME via both myelodysplastic syndrome 1 (MDS1) and EVI1 moieties and degrades EVI1 via the ubiquitin-proteasome pathway and MDS1 in a proteasome-independent manner. Our results suggest that ATO could be used as a part of targeted therapy for AME-, AML1/MDS1-, MDS1/EVI1-, and EVI1-positive human cancers."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22353937",
"endSection": "sections.0",
"offsetInBeginSection": 315,
"offsetInEndSection": 795,
"text": "Previously we had shown the synergic effect of bortezomib and thiostrepton in breast cancer cells in vitro, where sub-apoptotic concentrations of both proteasome inhibitors resulted in synergic increase in cell death when combined as a treatment. Here, we administered such a combination to MDA-MB-231 xenograft tumors in vivo, and found that the effect of complementary proteasome inhibitors reduced tumor growth rates more efficiently than compared with when administered alone."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22134540",
"endSection": "sections.0",
"offsetInBeginSection": 1477,
"offsetInEndSection": 1678,
"text": "Addition of a proteasome inhibitor to anti-hormonal therapy resulted in a clinical benefit rate of 22% in a limited number of patients with endocrine resistant and progressive metastatic breast cancer."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20160034",
"endSection": "sections.0",
"offsetInBeginSection": 1168,
"offsetInEndSection": 1288,
"text": "Taken together, these data support the clinical development of MLN9708 for both hematologic and solid tumor indications."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19712963",
"endSection": "sections.0",
"offsetInBeginSection": 1584,
"offsetInEndSection": 1690,
"text": "Bortezomib has minimal activity as a single-agent in the treatment of recurrent platinum-sensitive EOC/PPC"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17431003",
"endSection": "sections.0",
"offsetInBeginSection": 1421,
"offsetInEndSection": 1762,
"text": "Our study indicates a molecular mechanism by which the sensitivity of thyroid cancer cells is regulated by the level of GRP78 as well as preferential induction of GRP78 or CHOP upon treatment with proteasome inhibitors. Our experiments therefore suggest a novel approach toward sensitization of thyroid cancer cells to proteasome inhibitors."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16135477",
"endSection": "sections.0",
"offsetInBeginSection": 1270,
"offsetInEndSection": 1511,
"text": "Bortezomib (PS-341) is a novel antineoplastic agent that is well tolerated at doses not exceeding 3.0 mg (equivalent to 1.75 mg/m2), repeated on D1 and D4 every other week. This dose correlates with 70% inhibition of 20S proteasome activity."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15169797",
"endSection": "sections.0",
"offsetInBeginSection": 1459,
"offsetInEndSection": 1709,
"text": "The maximum-tolerated dose and recommended phase II dose of bortezomib in this schedule is 1.6 mg/m(2). Biologic activity (inhibition of nuclear factor-kappa B-related markers) and antitumor activity is seen in AIPCa at tolerated doses of bortezomib."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12171876",
"endSection": "sections.0",
"offsetInBeginSection": 1038,
"offsetInEndSection": 1278,
"text": "Given the results of this trial, it is safe and reasonable to recommend treatment with PS341 on the schedule used in this trial at 1.56 mg/m2/dose in Phase II trials. Particular care should be taken with patients with preexisting neuropathy"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23477519",
"endSection": "sections.0",
"offsetInBeginSection": 518,
"offsetInEndSection": 647,
"text": "The successes of proteasome inhibitors in MM are now being translated to other hematologic malignancies, including acute leukemia"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23181572",
"endSection": "sections.0",
"offsetInBeginSection": 843,
"offsetInEndSection": 1048,
"text": "Such efforts have led to bortezomib, the first FDA approved proteasome inhibitor now used as a frontline treatment for newly diagnosed multiple myeloma (MM), relapsed/refractory MM and mantle cell lymphoma"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22995770",
"endSection": "sections.0",
"offsetInBeginSection": 383,
"offsetInEndSection": 696,
"text": "We recently reported the impact and mechanisms of carfilzomib and oprozomib, second-in-class proteasome inhibitors with higher specificities and reduced toxicities, against head and neck squamous cell carcinoma (HNSCC). Carfilzomib and oprozomib potently inhibit HNSCC cell survival and the growth of HNSCC tumors"
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D061988",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D007938"
]
| null | 517179718ed59a060a00000e | 156 |
yesno | Is Apremilast effective for Behçet’s Syndrome? | ['yes'] | [
"yes"
]
| ["Yes, Apremilast is effective for Behcet's Syndrome"] | [
"http://www.ncbi.nlm.nih.gov/pubmed/31722152",
"http://www.ncbi.nlm.nih.gov/pubmed/27163156",
"http://www.ncbi.nlm.nih.gov/pubmed/25875256",
"http://www.ncbi.nlm.nih.gov/pubmed/31609785"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27163156",
"endSection": "abstract",
"offsetInBeginSection": 386,
"offsetInEndSection": 686,
"text": "AREAS COVERED: This review provides a digest of all current experience and evidence about pharmacological agents recently described as having a role in the treatment of BS, including interleukin (IL)-1 inhibitors, tocilizumab, rituximab, alemtuzumab, ustekinumab, interferon-alpha-2a, and apremilast."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25875256",
"endSection": "abstract",
"offsetInBeginSection": 1725,
"offsetInEndSection": 1846,
"text": "CONCLUSIONS\n\nApremilast was effective in treating oral ulcers, which are the cardinal manifestation of Behçet's syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25875256",
"endSection": "abstract",
"offsetInBeginSection": 1719,
"offsetInEndSection": 1839,
"text": "CONCLUSIONS Apremilast was effective in treating oral ulcers, which are the cardinal manifestation of Behçet's syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25875256",
"endSection": "abstract",
"offsetInBeginSection": 1725,
"offsetInEndSection": 1846,
"text": "CONCLUSIONS\nApremilast was effective in treating oral ulcers, which are the cardinal manifestation of Behçet's syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25875256",
"endSection": "abstract",
"offsetInBeginSection": 1692,
"offsetInEndSection": 1800,
"text": "Apremilast was effective in treating oral ulcers, which are the cardinal manifestation of Behçet's syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31722152",
"endSection": "abstract",
"offsetInBeginSection": 1848,
"offsetInEndSection": 2080,
"text": "In patients with oral ulcers associated with Behçet's syndrome, apremilast resulted in a greater reduction in the number of oral ulcers than placebo but was associated with adverse events, including diarrhea, nausea, and headache. ("
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31609785",
"endSection": "abstract",
"offsetInBeginSection": 464,
"offsetInEndSection": 563,
"text": "Apremilast is now approved for the treatment of oral ulcer of Behçet syndrome in the United States."
}
]
| 11 | BioASQ-training11b | null | null | 5e30f417fbd6abf43b000043 | 157 |
yesno | Is Lysine-specific demethylase 1 (LSD1) a critical regulator of hematopoiesis? | ['yes'] | [
"yes"
]
| ['Yes. Lysine-specific demethylase 1 restricts hematopoietic progenitor proliferation and is essential for terminal differentiation of erythroid, granulomonocytic and megakaryocytic progenitors.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/24163373",
"http://www.ncbi.nlm.nih.gov/pubmed/23147254",
"http://www.ncbi.nlm.nih.gov/pubmed/22801375",
"http://www.ncbi.nlm.nih.gov/pubmed/22699452",
"http://www.ncbi.nlm.nih.gov/pubmed/22399799",
"http://www.ncbi.nlm.nih.gov/pubmed/22310283",
"http://www.ncbi.nlm.nih.gov/pubmed/19736520",
"http://www.ncbi.nlm.nih.gov/pubmed/19497860",
"http://www.ncbi.nlm.nih.gov/pubmed/17707228",
"http://www.ncbi.nlm.nih.gov/pubmed/23795291"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24163373",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "Histone lysine-specific demethylase 1 (LSD1) protein is involved in Sal-like protein 4 (SALL4)-mediated transcriptional repression in hematopoietic stem cells"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24163373",
"endSection": "abstract",
"offsetInBeginSection": 1167,
"offsetInEndSection": 1317,
"text": "shRNA-mediated knockdown of LSD1 in hematopoietic precursor cells resulted in altered SALL4 downstream gene expression and increased cellular activity"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24163373",
"endSection": "abstract",
"offsetInBeginSection": 1325,
"offsetInEndSection": 1560,
"text": "our data revealed that histone demethylase LSD1 may negatively regulate SALL4-mediated transcription, and the dynamic regulation of SALL4-associated epigenetic factors cooperatively modulates early hematopoietic precursor proliferation"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22699452",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Lysine-specific demethylase 1 restricts hematopoietic progenitor proliferation and is essential for terminal differentiation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22699452",
"endSection": "abstract",
"offsetInBeginSection": 326,
"offsetInEndSection": 405,
"text": " LSD1 represents a central regulator of hematopoietic stem and progenitor cells"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22699452",
"endSection": "abstract",
"offsetInBeginSection": 502,
"offsetInEndSection": 602,
"text": " LSD1-kd led to an extensive expansion of granulomonocytic, erythroid and megakaryocytic progenitors"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22699452",
"endSection": "abstract",
"offsetInBeginSection": 1052,
"offsetInEndSection": 1123,
"text": "LSD1-kd was associated with the upregulation of key hematopoietic genes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22699452",
"endSection": "abstract",
"offsetInBeginSection": 1352,
"offsetInEndSection": 1422,
"text": "our findings distinguish LSD1 as a critical regulator of hematopoiesis"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22399799",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "A short Gfi-1B isoform controls erythroid differentiation by recruiting the LSD1-CoREST complex through the dimethylation of its SNAG domain"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22310283",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "Dynamic interaction between TAL1 oncoprotein and LSD1 regulates TAL1 function in hematopoiesis and leukemogenesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22310283",
"endSection": "abstract",
"offsetInBeginSection": 341,
"offsetInEndSection": 778,
"text": "Here, we reported that protein kinase A (PKA)-mediated phosphorylation regulates TAL1 interaction with the lysine-specific demethylase (LSD1) that removes methyl group from methylated Lys 4 on histone H3 tails. Phosphorylation of serine 172 in TAL1 specifically destabilizes the TAL1-LSD1 interaction leading to promoter H3K4 hypermethylation and activation of target genes that have been suppressed in normal and malignant hematopoiesis"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19497860",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "LSD1-mediated epigenetic modification is required for TAL1 function and hematopoiesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19497860",
"endSection": "abstract",
"offsetInBeginSection": 251,
"offsetInEndSection": 525,
"text": "we show that TAL1 is associated with histone demethylase complexes containing lysine-specific demethylase 1 (LSD1), RE1 silencing transcription factor corepressor (CoREST), histone deacetylase 1 (HDAC1), and histone deacetylase 2 in erythroleukemia and T cell leukemia cells"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19497860",
"endSection": "abstract",
"offsetInBeginSection": 703,
"offsetInEndSection": 871,
"text": "we demonstrate that the TAL1-associated LSD1, HDAC1, and their enzymatic activities are coordinately down-regulated during the early phases of erythroid differentiation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19497860",
"endSection": "abstract",
"offsetInBeginSection": 959,
"offsetInEndSection": 1090,
"text": "TAL1 recruits LSD1 to the silenced p4.2 promoter in undifferentiated, but not in differentiated, murine erythroleukemia (MEL) cells"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19497860",
"endSection": "abstract",
"offsetInBeginSection": 1385,
"offsetInEndSection": 1507,
"text": "the dynamic regulation of TAL1-associated LSD1/HDAC1 complex may determine the onset of erythroid differentiation programs"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17707228",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Epigenetic regulation of hematopoietic differentiation by Gfi-1 and Gfi-1b is mediated by the cofactors CoREST and LSD1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17707228",
"endSection": "abstract",
"offsetInBeginSection": 592,
"offsetInEndSection": 740,
"text": "Inhibition of CoREST and LSD1 perturbs differentiation of erythroid, megakaryocytic, and granulocytic cells as well as primary erythroid progenitors"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17707228",
"endSection": "abstract",
"offsetInBeginSection": 904,
"offsetInEndSection": 1140,
"text": "we show that chromatin regulatory proteins CoREST and LSD1 mediate transcriptional repression by Gfi proteins. Lineage-restricted deployment of these cofactors through interaction with Gfi proteins controls hematopoietic differentiation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22699452",
"endSection": "abstract",
"offsetInBeginSection": 1324,
"offsetInEndSection": 1489,
"text": "Taken together, our findings distinguish LSD1 as a critical regulator of hematopoiesis and point to severe, but reversible, side effects of a LSD1-targeted therapy."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19497860",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "LSD1-mediated epigenetic modification is required for TAL1 function and hematopoiesis."
},
{
"beginSection": "title",
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"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 114,
"text": "Dynamic interaction between TAL1 oncoprotein and LSD1 regulates TAL1 function in hematopoiesis and leukemogenesis."
},
{
"beginSection": "abstract",
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"endSection": "abstract",
"offsetInBeginSection": 547,
"offsetInEndSection": 775,
"text": "Phosphorylation of serine 172 in TAL1 specifically destabilizes the TAL1-LSD1 interaction leading to promoter H3K4 hypermethylation and activation of target genes that have been suppressed in normal and malignant hematopoiesis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24163373",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 159,
"text": "Histone lysine-specific demethylase 1 (LSD1) protein is involved in Sal-like protein 4 (SALL4)-mediated transcriptional repression in hematopoietic stem cells."
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{
"beginSection": "abstract",
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"endSection": "abstract",
"offsetInBeginSection": 1324,
"offsetInEndSection": 1489,
"text": "Taken together, our findings distinguish LSD1 as a critical regulator of hematopoiesis and point to severe, but reversible, side effects of a LSD1-targeted therapy."
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"text": "LSD1-mediated epigenetic modification is required for TAL1 function and hematopoiesis."
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"text": "Dynamic interaction between TAL1 oncoprotein and LSD1 regulates TAL1 function in hematopoiesis and leukemogenesis."
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"text": "Phosphorylation of serine 172 in TAL1 specifically destabilizes the TAL1-LSD1 interaction leading to promoter H3K4 hypermethylation and activation of target genes that have been suppressed in normal and malignant hematopoiesis."
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{
"beginSection": "title",
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"text": "Histone lysine-specific demethylase 1 (LSD1) protein is involved in Sal-like protein 4 (SALL4)-mediated transcriptional repression in hematopoietic stem cells."
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"text": "Taken together, our findings distinguish LSD1 as a critical regulator of hematopoiesis and point to severe, but reversible, side effects of a LSD1-targeted therapy."
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"text": "LSD1-mediated epigenetic modification is required for TAL1 function and hematopoiesis."
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"text": "Dynamic interaction between TAL1 oncoprotein and LSD1 regulates TAL1 function in hematopoiesis and leukemogenesis."
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"text": "Phosphorylation of serine 172 in TAL1 specifically destabilizes the TAL1-LSD1 interaction leading to promoter H3K4 hypermethylation and activation of target genes that have been suppressed in normal and malignant hematopoiesis."
},
{
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"text": "Histone lysine-specific demethylase 1 (LSD1) protein is involved in Sal-like protein 4 (SALL4)-mediated transcriptional repression in hematopoietic stem cells."
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{
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"offsetInEndSection": 1489,
"text": "Taken together, our findings distinguish LSD1 as a critical regulator of hematopoiesis and point to severe, but reversible, side effects of a LSD1-targeted therapy."
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"text": "LSD1-mediated epigenetic modification is required for TAL1 function and hematopoiesis."
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{
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"endSection": "title",
"offsetInBeginSection": 0,
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"text": "Dynamic interaction between TAL1 oncoprotein and LSD1 regulates TAL1 function in hematopoiesis and leukemogenesis."
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"endSection": "abstract",
"offsetInBeginSection": 547,
"offsetInEndSection": 775,
"text": "Phosphorylation of serine 172 in TAL1 specifically destabilizes the TAL1-LSD1 interaction leading to promoter H3K4 hypermethylation and activation of target genes that have been suppressed in normal and malignant hematopoiesis."
},
{
"beginSection": "title",
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"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 159,
"text": "Histone lysine-specific demethylase 1 (LSD1) protein is involved in Sal-like protein 4 (SALL4)-mediated transcriptional repression in hematopoietic stem cells."
},
{
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"endSection": "abstract",
"offsetInBeginSection": 1336,
"offsetInEndSection": 1500,
"text": "Taken together, our findings distinguish LSD1 as a critical regulator of hematopoiesis and point to severe, but reversible, side effects of a LSD1-targeted therapy."
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"offsetInBeginSection": 1336,
"offsetInEndSection": 1500,
"text": "Taken together, our findings distinguish LSD1 as a critical regulator of hematopoiesis and point to severe, but reversible, side effects of a LSD1-targeted therapy."
},
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"offsetInBeginSection": 1336,
"offsetInEndSection": 1500,
"text": "Taken together, our findings distinguish LSD1 as a critical regulator of hematopoiesis and point to severe, but reversible, side effects of a LSD1-targeted therapy."
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"offsetInBeginSection": 1336,
"offsetInEndSection": 1500,
"text": "Taken together, our findings distinguish LSD1 as a critical regulator of hematopoiesis and point to severe, but reversible, side effects of a LSD1-targeted therapy."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/19497860",
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"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "LSD1-mediated epigenetic modification is required for TAL1 function and hematopoiesis."
},
{
"beginSection": "abstract",
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"endSection": "abstract",
"offsetInBeginSection": 1336,
"offsetInEndSection": 1500,
"text": "Taken together, our findings distinguish LSD1 as a critical regulator of hematopoiesis and point to severe, but reversible, side effects of a LSD1-targeted therapy."
}
]
| 5 | BioASQ-training5b | [
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0030097",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0033193",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0035162"
]
| []
| 553c011af321868558000009 | 158 |
yesno | Are protamines ubiquitously expressed? | ['no'] | [
"no"
]
| ['No,\nProtamines are nuclear proteins which are specifically expressed in haploid male germ cells.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/29797354"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29797354",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 92,
"text": "Protamines are nuclear proteins which are specifically expressed in haploid male germ cells."
}
]
| 11 | BioASQ-training11b | null | null | 5c9f1b0cecadf2e73f00003c | 160 |
yesno | Was tamoxifen tested for treatment of glioma patients? | ['yes'] | [
"yes"
]
| ['Yes, tamoxifen was tested for glioma treatment. However, clinical efficacy of tamoxifen in glioma patients remains unclear and should be tested in further studies.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/21353747",
"http://www.ncbi.nlm.nih.gov/pubmed/20238235",
"http://www.ncbi.nlm.nih.gov/pubmed/16710748",
"http://www.ncbi.nlm.nih.gov/pubmed/15022287",
"http://www.ncbi.nlm.nih.gov/pubmed/12712458",
"http://www.ncbi.nlm.nih.gov/pubmed/19810975",
"http://www.ncbi.nlm.nih.gov/pubmed/10797257",
"http://www.ncbi.nlm.nih.gov/pubmed/10715294",
"http://www.ncbi.nlm.nih.gov/pubmed/9524096",
"http://www.ncbi.nlm.nih.gov/pubmed/9815790",
"http://www.ncbi.nlm.nih.gov/pubmed/8837815",
"http://www.ncbi.nlm.nih.gov/pubmed/9773800",
"http://www.ncbi.nlm.nih.gov/pubmed/9266439",
"http://www.ncbi.nlm.nih.gov/pubmed/12680157"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21353747",
"endSection": "abstract",
"offsetInBeginSection": 1694,
"offsetInEndSection": 1892,
"text": "Tamoxifen might have a role in the initial treatment of high-grade gliomas and should be studied in future Phase II trials building on the newly established platform of concurrent chemoradiotherapy."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20238235",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "The addition of high-dose tamoxifen to standard radiotherapy does not improve the survival of patients with diffuse intrinsic pontine glioma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20238235",
"endSection": "abstract",
"offsetInBeginSection": 769,
"offsetInEndSection": 956,
"text": "In this study, in which tamoxifen was used in conjunction with radiotherapy, progression free survival was shown to be less good when compared with historical data HR = 3.1 (CI: 1.7-5.7)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20238235",
"endSection": "abstract",
"offsetInBeginSection": 1013,
"offsetInEndSection": 1196,
"text": "The addition of high-dose tamoxifen, although well tolerated, confers no clinical benefit to patients treated with diffuse intrinsic pontine glioma treated with standard radiotherapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16710748",
"endSection": "abstract",
"offsetInBeginSection": 1495,
"offsetInEndSection": 1696,
"text": "CONCLUSIONS: Carboplatin and high dose tamoxifen has similar response rates to other regimens for recurrent malignant gliomas and are probably equivalent to those found using tamoxifen as monotherapy. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15022287",
"endSection": "abstract",
"offsetInBeginSection": 1618,
"offsetInEndSection": 1793,
"text": "CONCLUSIONS: Pegylated liposomal doxorubicin administered alone or in combination with tamoxifen is safe and moderately effective in patients with recurrent high-grade glioma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12712458",
"endSection": "abstract",
"offsetInBeginSection": 153,
"offsetInEndSection": 288,
"text": "Protein kinase C (PKC) inhibitors such as high-dose tamoxifen and hypericin also have been used in the treatment of malignant gliomas. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19810975",
"endSection": "abstract",
"offsetInBeginSection": 852,
"offsetInEndSection": 1028,
"text": "Considering these facts, polyethylene-glycol-liposomal doxorubicin with and without tamoxifen was evaluated within two sequential Phase II trials performed at our institution. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10797257",
"endSection": "abstract",
"offsetInBeginSection": 78,
"offsetInEndSection": 369,
"text": "In a parallel phase-II-study investigating post-operative treatment with tamoxifen (TAM), carboplatin and radiation therapy for glioblastomas, 16 of 49 patients (33%) showed multifocal recurrence, which developed after a mean of 46 weeks, raising the question of an association with therapy."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10715294",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Radiation therapy and high-dose tamoxifen in the treatment of patients with diffuse brainstem gliomas: results of a Brazilian cooperative study. Brainstem Glioma Cooperative Group."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10715294",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "PURPOSE: The efficacy of radiation therapy (RT) combined with tamoxifen (TX) was tested in patients diagnosed with diffuse brainstem gliomas in a multicenter trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10715294",
"endSection": "abstract",
"offsetInBeginSection": 1183,
"offsetInEndSection": 1455,
"text": "CONCLUSION: This treatment combination produced no significant change in the overall poor prognosis of these patients. Most tumors responded initially to treatment but recurred as the study progressed. A minority of patients seemed to benefit from the extended use of TX. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10715294",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Radiation therapy and high-dose tamoxifen in the treatment of patients with diffuse brainstem gliomas: results of a Brazilian cooperative study. Brainstem Glioma Cooperative Group."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8837815",
"endSection": "abstract",
"offsetInBeginSection": 281,
"offsetInEndSection": 447,
"text": "Tamoxifen, a protein kinase C inhibitor when administered in high dosages, is currently being used as an adjuvant in the treatment of patients with malignant gliomas."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9266439",
"endSection": "abstract",
"offsetInBeginSection": 1121,
"offsetInEndSection": 1375,
"text": "We present a patient with a recurrent malignant glioma who was continued on high dose tamoxifen despite radiologic documented doubling of the tumor size and who eventually showed a delayed response to this agent nine months after initiation of treatment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9524096",
"endSection": "abstract",
"offsetInBeginSection": 1707,
"offsetInEndSection": 1956,
"text": "The combination of oral tamoxifen (120 to 240 mg/m2/day) and subcutaneous interferon-alpha [6 x 10(6) U three times per week] was associated with significant neurotoxicity in this group of recurrent glioma patients, resulting in early study closure."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9815790",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "A phase I study of high-dose tamoxifen for the treatment of refractory malignant gliomas of childhood."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21353747",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Phase I clinical trial assessing temozolomide and tamoxifen with concomitant radiotherapy for treatment of high-grade glioma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9266439",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "Prolonged treatment with biologic agents for malignant glioma: a case study with high dose tamoxifen."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9524096",
"endSection": "abstract",
"offsetInBeginSection": 1707,
"offsetInEndSection": 1956,
"text": "The combination of oral tamoxifen (120 to 240 mg/m2/day) and subcutaneous interferon-alpha [6 x 10(6) U three times per week] was associated with significant neurotoxicity in this group of recurrent glioma patients, resulting in early study closure."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9773800",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 45,
"text": "Tamoxifen as a potential treatment of glioma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21353747",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Phase I clinical trial assessing temozolomide and tamoxifen with concomitant radiotherapy for treatment of high-grade glioma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9266439",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "Prolonged treatment with biologic agents for malignant glioma: a case study with high dose tamoxifen."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9524096",
"endSection": "abstract",
"offsetInBeginSection": 289,
"offsetInEndSection": 441,
"text": "We tested the efficacy and toxicity of the combination of high-dose tamoxifen and interferon alpha in adults with recurrent glioma in a phase II trial. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10715294",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 165,
"text": "PURPOSE: The efficacy of radiation therapy (RT) combined with tamoxifen (TX) was tested in patients diagnosed with diffuse brainstem gliomas in a multicenter trial. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9524096",
"endSection": "abstract",
"offsetInBeginSection": 289,
"offsetInEndSection": 441,
"text": "We tested the efficacy and toxicity of the combination of high-dose tamoxifen and interferon alpha in adults with recurrent glioma in a phase II trial. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10715294",
"endSection": "abstract",
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"text": "PURPOSE: The efficacy of radiation therapy (RT) combined with tamoxifen (TX) was tested in patients diagnosed with diffuse brainstem gliomas in a multicenter trial. "
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/9524096",
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"text": "We tested the efficacy and toxicity of the combination of high-dose tamoxifen and interferon alpha in adults with recurrent glioma in a phase II trial. "
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"text": "PURPOSE: The efficacy of radiation therapy (RT) combined with tamoxifen (TX) was tested in patients diagnosed with diffuse brainstem gliomas in a multicenter trial. "
},
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"text": "We tested the efficacy and toxicity of the combination of high-dose tamoxifen and interferon alpha in adults with recurrent glioma in a phase II trial. "
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"text": "PURPOSE: The efficacy of radiation therapy (RT) combined with tamoxifen (TX) was tested in patients diagnosed with diffuse brainstem gliomas in a multicenter trial. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9524096",
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"text": "We tested the efficacy and toxicity of the combination of high-dose tamoxifen and interferon alpha in adults with recurrent glioma in a phase II trial. "
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"text": "PURPOSE: The efficacy of radiation therapy (RT) combined with tamoxifen (TX) was tested in patients diagnosed with diffuse brainstem gliomas in a multicenter trial. "
},
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"text": "We tested the efficacy and toxicity of the combination of high-dose tamoxifen and interferon alpha in adults with recurrent glioma in a phase II trial."
},
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/9773800",
"endSection": "title",
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"text": "Tamoxifen as a potential treatment of glioma."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/10715294",
"endSection": "abstract",
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"text": "The efficacy of radiation therapy (RT) combined with tamoxifen (TX) was tested in patients diagnosed with diffuse brainstem gliomas in a multicenter trial."
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"text": "The efficacy of radiation therapy (RT) combined with tamoxifen (TX) was tested in patients diagnosed with diffuse brainstem gliomas in a multicenter trial."
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"text": "We tested the efficacy and toxicity of the combination of high-dose tamoxifen and interferon alpha in adults with recurrent glioma in a phase II trial. Eligible patients had radiographically measurable recurrent gliomas of any grade after initial radiation therapy."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/12680157",
"endSection": "abstract",
"offsetInBeginSection": 230,
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"text": "Thyroid function was suppressed to reduce IGF-1 levels in glioma patients and high-dose tamoxifen administered. Propylthiouracil was used to induce chemical hypothyroidism in 22 patients with recurrent glioma."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/9524096",
"endSection": "abstract",
"offsetInBeginSection": 90,
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"text": "Activity against recurrent gliomas has been reported for both tamoxifen and interferon alpha, agents that have more acceptable toxicity profiles and that can be administered in an outpatient setting. We tested the efficacy and toxicity of the combination of high-dose tamoxifen and interferon alpha in adults with recurrent glioma in a phase II trial."
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"text": "The efficacy of radiation therapy (RT) combined with tamoxifen (TX) was tested in patients diagnosed with diffuse brainstem gliomas in a multicenter trial."
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"text": "Thyroid function was suppressed to reduce IGF-1 levels in glioma patients and high-dose tamoxifen administered."
},
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"text": "Radiation therapy and high-dose tamoxifen in the treatment of patients with diffuse brainstem gliomas: results of a Brazilian cooperative study."
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"text": "Phase I clinical trial assessing temozolomide and tamoxifen with concomitant radiotherapy for treatment of high-grade glioma."
},
{
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"text": "The efficacy of radiation therapy (RT) combined with tamoxifen (TX) was tested in patients diagnosed with diffuse brainstem gliomas in a multicenter trial."
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"text": "We tested the efficacy and toxicity of the combination of high-dose tamoxifen and interferon alpha in adults with recurrent glioma in a phase II trial."
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/8837815",
"endSection": "abstract",
"offsetInBeginSection": 1150,
"offsetInEndSection": 1330,
"text": "The subsequent in vitro testing of the tumor that was removed after the recurrence of tumor (22 months after the initiation of tamoxifen) revealed loss of sensitivity to tamoxifen."
},
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"endSection": "abstract",
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"text": "The combination of oral tamoxifen (120 to 240 mg/m2/day) and subcutaneous interferon-alpha [6 x 10(6) U three times per week] was associated with significant neurotoxicity in this group of recurrent glioma patients, resulting in early study closure."
},
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"text": "Radiation therapy and high-dose tamoxifen in the treatment of patients with diffuse brainstem gliomas: results of a Brazilian cooperative study."
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"text": "The efficacy of radiation therapy (RT) combined with tamoxifen (TX) was tested in patients diagnosed with diffuse brainstem gliomas in a multicenter trial."
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"text": "Thyroid function was suppressed to reduce IGF-1 levels in glioma patients and high-dose tamoxifen administered."
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"text": "Radiation therapy and high-dose tamoxifen in the treatment of patients with diffuse brainstem gliomas: results of a Brazilian cooperative study."
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"text": "We tested the efficacy and toxicity of the combination of high-dose tamoxifen and interferon alpha in adults with recurrent glioma in a phase II trial."
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"text": "The subsequent in vitro testing of the tumor that was removed after the recurrence of tumor (22 months after the initiation of tamoxifen) revealed loss of sensitivity to tamoxifen."
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013629",
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| []
| 56c0968def6e394741000026 | 162 |
yesno | Is Tcf3 associated with the Wnt pathway? | ['yes'] | [
"yes"
]
| ['Tcf3 is a component of the Wnt/β-catenin and Notch signaling pathways.', 'TCF3, a novel positive regulator of osteogenesis, plays a crucial role in modulating the diverse effect of canonical Wnt signaling. We found that in contrast to ES cells, where it represses Wnt-pathway target genes, TCF3 promotes the expression of a subset of Wnt-responsive genes in breast cancer cells.', 'A terminal component of the canonical Wnt pathway in ES cells, the transcription factor T-cell factor-3 (Tcf3) co-occupies promoters throughout the genome in association with the pluripotency regulators Oct4 and Nanog . Overexpression of TCF3 (transcription factor 3) attenuated the effect of miR-17 on modulating Wnt signaling .', "Yes, Tcf3 is associated with the WNT pathway. The Wnt pathway is a part of the pluripotency regulator Oct4 and Nanog. It's a family of transcription factors that regulate the growth of cells.", 'Yes, Tcf3 is associated with the WNT pathway. The Wnt pathway is a part of the pluripotency regulator Oct4 and Nanog. It regulates the growth and differentiation of cells.', 'Yes, Tcf3 is associated with the Wnt pathway.', 'Yes, Tcf3 is associated with the WNT pathway. The Wnt pathway is a part of the pluripotency regulator Oct4 and Nanog.', "Yes, Tcf3 is associated with the WNT pathway. The Wnt pathway is a part of the pluripotency regulator Oct4 and Nanog. It's a family of transcription factors that regulate the growth and differentiation of cells.", 'A terminal component of the canonical Wnt pathway in ES cells, the transcription factor T-cell factor-3 (Tcf3), co-occupies promoters throughout the genome in association with the pluripotency regulators Oct4 and Nanog . The noncanonical Wnt signaling pathway, through actions of Tcf3, can antagonize the canonical pathway .', 'Yes. Tcf3 is associated with the Wnt/β-catenin pathway.', "Yes, Tcf3 is associated with the WNT pathway. The Wnt pathway is a part of the pluripotency regulator Oct4 and Nanog. It's a family of transcription factors that regulate the growth and differentiation of pluripotent cells.", 'Yes, TCF3 is a key transcription factor of the canonical Wnt pathway.', 'Yes, Tcf3 is involved in the activation of the Wnt pathway.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/18347094",
"http://www.ncbi.nlm.nih.gov/pubmed/31033094",
"http://www.ncbi.nlm.nih.gov/pubmed/23063976",
"http://www.ncbi.nlm.nih.gov/pubmed/20951344",
"http://www.ncbi.nlm.nih.gov/pubmed/17018284",
"http://www.ncbi.nlm.nih.gov/pubmed/23090119",
"http://www.ncbi.nlm.nih.gov/pubmed/30631148",
"http://www.ncbi.nlm.nih.gov/pubmed/22007134",
"http://www.ncbi.nlm.nih.gov/pubmed/25832347",
"http://www.ncbi.nlm.nih.gov/pubmed/23505158",
"http://www.ncbi.nlm.nih.gov/pubmed/22270545",
"http://www.ncbi.nlm.nih.gov/pubmed/22573616",
"http://www.ncbi.nlm.nih.gov/pubmed/19074834",
"http://www.ncbi.nlm.nih.gov/pubmed/18467660",
"http://www.ncbi.nlm.nih.gov/pubmed/21285352",
"http://www.ncbi.nlm.nih.gov/pubmed/11524435",
"http://www.ncbi.nlm.nih.gov/pubmed/23492770",
"http://www.ncbi.nlm.nih.gov/pubmed/24648413",
"http://www.ncbi.nlm.nih.gov/pubmed/24832538",
"http://www.ncbi.nlm.nih.gov/pubmed/25375219",
"http://www.ncbi.nlm.nih.gov/pubmed/28346462",
"http://www.ncbi.nlm.nih.gov/pubmed/23658527"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23492770",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 168,
"text": "TCF3, a novel positive regulator of osteogenesis, plays a crucial role in miR-17 modulating the diverse effect of canonical Wnt signaling in different microenvironments"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23492770",
"endSection": "abstract",
"offsetInBeginSection": 1139,
"offsetInEndSection": 1285,
"text": "Furthermore, the role of miR-17 was because of its target gene TCF3 (transcription factor 3), a key transcription factor of canonical Wnt pathway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23063976",
"endSection": "abstract",
"offsetInBeginSection": 731,
"offsetInEndSection": 956,
"text": "Consequently, Tcf3 knockdown in HCT-R cells restores their sensitivity to the effects of butyrate on Wnt activity and clonal cell growth. Interestingly, the effects of overexpressed Tcf3 differ between HCT-116 and HCT-R cells"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23063976",
"endSection": "abstract",
"offsetInBeginSection": 1062,
"offsetInEndSection": 1292,
"text": "In HCT-R cells, however, the overexpression of Tcf3 inhibits Wnt activity, and the cells are still able to proliferate due to the higher expression levels of cell cycle factors, particularly those driving the G(1) to S transition."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23090119",
"endSection": "abstract",
"offsetInBeginSection": 163,
"offsetInEndSection": 319,
"text": "TCF3 (also known as TCF7L1) is a member of the TCF/LEF transcription factor family that is central in regulating epidermal and embryonic stem cell identity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23090119",
"endSection": "abstract",
"offsetInBeginSection": 816,
"offsetInEndSection": 1156,
"text": "We found that in contrast to ES cells, where it represses Wnt-pathway target genes, TCF3 promotes the expression of a subset of Wnt-responsive genes in breast cancer cells while repressing another distinct target subset. In the normal mouse mammary gland, Tcf3 is highly expressed in terminal end buds, structures that lead duct development"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22007134",
"endSection": "abstract",
"offsetInBeginSection": 1049,
"offsetInEndSection": 1227,
"text": "Tcf3 is essential within the neural ectoderm to maintain anterior character and that its interaction with Hesx1 ensures the repression of Wnt targets in the developing forebrain."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18347094",
"endSection": "abstract",
"offsetInBeginSection": 318,
"offsetInEndSection": 558,
"text": "We report here that a terminal component of the canonical Wnt pathway in ES cells, the transcription factor T-cell factor-3 (Tcf3), co-occupies promoters throughout the genome in association with the pluripotency regulators Oct4 and Nanog. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18347094",
"endSection": "abstract",
"offsetInBeginSection": 899,
"offsetInEndSection": 1104,
"text": "Our results suggest that the Wnt pathway, through Tcf3, brings developmental signals directly to the core regulatory circuitry of ES cells to influence the balance between pluripotency and differentiation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11524435",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 145,
"text": "The wnt pathway regulates the steady state level of beta-catenin, a transcriptional coactivator for the Tcf3/Lef1 family of DNA binding proteins."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11524435",
"endSection": "abstract",
"offsetInBeginSection": 1167,
"offsetInEndSection": 1385,
"text": "Along with evidence that a significant amount of Tcf protein is nonnuclear, these findings suggest that CK1epsilon can modulate wnt signaling in vivo by regulating both the beta-catenin-Tcf3 and the GBP-dsh interfaces."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24648413",
"endSection": "abstract",
"offsetInBeginSection": 879,
"offsetInEndSection": 1035,
"text": "RA increases the expression of ligands and receptors of the noncanonical Wnt pathway (Wnt 5a, 7a, Fzd2 and Fzd6), downstream signaling, and Tcf3 expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24648413",
"endSection": "abstract",
"offsetInBeginSection": 656,
"offsetInEndSection": 758,
"text": "The noncanonical Wnt signaling pathway, through actions of Tcf3, can antagonize the canonical pathway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18347094",
"endSection": "abstract",
"offsetInBeginSection": 318,
"offsetInEndSection": 557,
"text": "We report here that a terminal component of the canonical Wnt pathway in ES cells, the transcription factor T-cell factor-3 (Tcf3), co-occupies promoters throughout the genome in association with the pluripotency regulators Oct4 and Nanog."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18347094",
"endSection": "abstract",
"offsetInBeginSection": 717,
"offsetInEndSection": 898,
"text": "Both Tcf3 depletion and Wnt pathway activation cause increased expression of Oct4, Nanog, and other pluripotency factors and produce ES cells that are refractory to differentiation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22007134",
"endSection": "abstract",
"offsetInBeginSection": 502,
"offsetInEndSection": 757,
"text": "Here, we show that injection of a hesx1 morpholino into a 'sensitised' zygotic headless (tcf3) mutant background leads to severe forebrain and eye defects, suggesting an interaction between Hesx1 and the Wnt pathway during zebrafish forebrain development."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/22007134",
"endSection": "abstract",
"offsetInBeginSection": 1021,
"offsetInEndSection": 1227,
"text": "In addition, we reveal that Tcf3 is essential within the neural ectoderm to maintain anterior character and that its interaction with Hesx1 ensures the repression of Wnt targets in the developing forebrain."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23492770",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 169,
"text": "TCF3, a novel positive regulator of osteogenesis, plays a crucial role in miR-17 modulating the diverse effect of canonical Wnt signaling in different microenvironments."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25832347",
"endSection": "abstract",
"offsetInBeginSection": 1483,
"offsetInEndSection": 1695,
"text": "Our studies located the position of Wnts, downstream LEF1 and TCF3 and stem cell marker proteins, which provide new information in understanding the role of the Wnt singaling pathway in whisker follicles' growth."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31033094",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 249,
"text": "The transcription factor T-cell factor 3 (TCF3), one component of the Wnt pathway, is known as a cell-intrinsic inhibitor of many pluripotency genes in embryonic stem cells (ESCs) that influences the balance between pluripotency and differentiation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23492770",
"endSection": "abstract",
"offsetInBeginSection": 1286,
"offsetInEndSection": 1379,
"text": "Overexpression of TCF3 attenuated the effect of miR-17 on modulating canonical Wnt signaling."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21285352",
"endSection": "abstract",
"offsetInBeginSection": 762,
"offsetInEndSection": 989,
"text": "We also find that TCF3 phosphorylation is triggered by canonical Wnt ligands, LRP6, and dominant negative mutants for Axin and GSK3, indicating that this process shares the same upstream regulators with β-catenin stabilization."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23505158",
"endSection": "abstract",
"offsetInBeginSection": 922,
"offsetInEndSection": 1074,
"text": "Wnt pathway stimulation also triggers β-catenin association at regulatory elements with classic Lef/Tcf motifs associated with differentiation programs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19074834",
"endSection": "abstract",
"offsetInBeginSection": 599,
"offsetInEndSection": 769,
"text": "We show that menin physically interacts with proteins involved in the canonical Wnt signaling pathway, including beta-catenin, TCF3 (TCFL1), and weakly with TCF4 (TCFL2)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18467660",
"endSection": "abstract",
"offsetInBeginSection": 254,
"offsetInEndSection": 356,
"text": "T-cell factor 3 (Tcf3) is a component of the Wnt signaling and a dominant downstream effector in ESCs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18467660",
"endSection": "abstract",
"offsetInBeginSection": 260,
"offsetInEndSection": 363,
"text": " factor 3 (Tcf3) is a component of the Wnt signaling and a dominant downstream effector in ESCs. Despit"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18347094",
"endSection": "abstract",
"offsetInBeginSection": 325,
"offsetInEndSection": 566,
"text": "rt here that a terminal component of the canonical Wnt pathway in ES cells, the transcription factor T-cell factor-3 (Tcf3), co-occupies promoters throughout the genome in association with the pluripotency regulators Oct4 and Nanog. Thus, Tc"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28346462",
"endSection": "abstract",
"offsetInBeginSection": 877,
"offsetInEndSection": 1099,
"text": "Tcf3, is recruited to a palindromic motif enriched in the promoter of cell cycle repressor genes, such as p15Ink4b, p16Ink4a and p19Arf, which mediate the Wnt-dependent anti-proliferative effect in mESCs. Consistently, abl"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28346462",
"endSection": "abstract",
"offsetInBeginSection": 372,
"offsetInEndSection": 460,
"text": "nonical Wnt/β-catenin pathway controls mESC pluripotency via the Wnt-effector Tcf3. Howe"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24648413",
"endSection": "abstract",
"offsetInBeginSection": 1167,
"offsetInEndSection": 1364,
"text": "g increases the dissociation of Tcf1 and the association of Tcf3 at promoters of genes that regulate stemness (e.g., NR5A2, Lrh-1) or differentiation (e.g. Cyr61, Zic5). Knockdown of Tcf3 increases"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22573616",
"endSection": "abstract",
"offsetInBeginSection": 1288,
"offsetInEndSection": 1497,
"text": "pport the existence of a regulatory circuit whereby Wnt/β-catenin counteracts Tcf3 repression of Lef1, which subsequently activates target gene expression via Lef1-β-catenin complexes. We propose that the Tcf/"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22007134",
"endSection": "abstract",
"offsetInBeginSection": 768,
"offsetInEndSection": 1032,
"text": " with a requirement for Wnt signalling repression, we highlight a synergistic gene dosage-dependent interaction between Hesx1 and Tcf3, a transcriptional repressor of Wnt target genes, to maintain anterior forebrain identity during mouse embryogenesis. In addition"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24648413",
"endSection": "abstract",
"offsetInBeginSection": 896,
"offsetInEndSection": 1056,
"text": "expression of ligands and receptors of the noncanonical Wnt pathway (Wnt 5a, 7a, Fzd2 and Fzd6), downstream signaling, and Tcf3 expression. RA reduces the phosp"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25375219",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "BACKGROUND AND OBJECTIVES: Transcription factor 3 (TCF3) implicates Wnt signaling pathway and regulates E-cadherin expression, which is involved i"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22270545",
"endSection": "abstract",
"offsetInBeginSection": 219,
"offsetInEndSection": 440,
"text": "We demonstrate that mouse Tcf3 mediates repression of both moderate and high levels of canonical Wnt signaling, by either competing with other members of the Tcf/Lef family for binding to β-catenin, or for binding to DNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20951344",
"endSection": "abstract",
"offsetInBeginSection": 153,
"offsetInEndSection": 313,
"text": "TCF3 is a transcriptional repressor that has been implicated in Wnt signaling and plays key roles in embryonic axis specification and stem cell differentiation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23658527",
"endSection": "abstract",
"offsetInBeginSection": 1577,
"offsetInEndSection": 1876,
"text": "Our data show for the first time that Wnt signaling down-regulates Tcf3 expression, possibly at both the transcriptional and post-transcriptional levels, and thus highlight a novel mechanism through which Wnt signaling inhibits neuro-ectodermal lineage differentiation in mouse embryonic stem cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24832538",
"endSection": "abstract",
"offsetInBeginSection": 802,
"offsetInEndSection": 896,
"text": "We found Tcf3 to be a repressor of Wnt signaling in neocortical NPCs in a reporter gene assay."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23658527",
"endSection": "abstract",
"offsetInBeginSection": 693,
"offsetInEndSection": 898,
"text": "We found that down-regulation of Tcf3, a member of the Tcf/Lef family and a key player in the control of self-renewal and pluripotency, represents a specific and primary response to Wnt activation in ESCs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30631148",
"endSection": "abstract",
"offsetInBeginSection": 970,
"offsetInEndSection": 1100,
"text": "Wnt16b also activated the RhoA/Rac1 signaling cascade suggesting the activation of a non-canonical Wnt pathway in TCF3-PBX1 cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30631148",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 266,
"text": "B-cell precursor acute lymphoblastic leukemia (BCP-ALL) with TCF3-PBX1 fusion gene expression has constitutively elevated levels of Wnt16b and ROR1 (receptor tyrosine kinase-like orphan receptor), a ligand and a receptor from the Wnt signaling pathway, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23090119",
"endSection": "abstract",
"offsetInBeginSection": 816,
"offsetInEndSection": 1036,
"text": "We found that in contrast to ES cells, where it represses Wnt-pathway target genes, TCF3 promotes the expression of a subset of Wnt-responsive genes in breast cancer cells while repressing another distinct target subset."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24832538",
"endSection": "abstract",
"offsetInBeginSection": 1288,
"offsetInEndSection": 1640,
"text": "Together, these results suggest that Tcf3 antagonizes Wnt signaling in NPCs, thereby maintaining their undifferentiated state in the neocortex and that Wnt signaling promotes the transition from Tcf3-mediated repression to Tcf1/Lef1-mediated enhancement of Wnt signaling, constituting a positive feedback loop that facilitates neuronal differentiation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24832538",
"endSection": "abstract",
"offsetInBeginSection": 1114,
"offsetInEndSection": 1287,
"text": "We also found that Wnt signal stimulation reduces the level of Tcf3, and increases those of Tcf1 (also known as Tcf7) and Lef1, positive mediators of Wnt signaling, in NPCs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17018284",
"endSection": "abstract",
"offsetInBeginSection": 852,
"offsetInEndSection": 1046,
"text": "These data suggest that in the absence of Wnt signals, Tcf3 may function in skin SCs to maintain an undifferentiated state and, through Wnt signaling, directs these cells along the hair lineage."
}
]
| 11 | BioASQ-training11b | null | null | 5fdb4124a43ad31278000017 | 163 |
yesno | Does SCRIB deregulation promote cancer? | ['yes'] | [
"yes"
]
| Yes, deregulation of scribble promotes cancer. | [
"http://www.ncbi.nlm.nih.gov/pubmed/14767561",
"http://www.ncbi.nlm.nih.gov/pubmed/21549346",
"http://www.ncbi.nlm.nih.gov/pubmed/21643016",
"http://www.ncbi.nlm.nih.gov/pubmed/24276238",
"http://www.ncbi.nlm.nih.gov/pubmed/23730214",
"http://www.ncbi.nlm.nih.gov/pubmed/22169974",
"http://www.ncbi.nlm.nih.gov/pubmed/21965329",
"http://www.ncbi.nlm.nih.gov/pubmed/19041750",
"http://www.ncbi.nlm.nih.gov/pubmed/18641685"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14767561",
"endSection": "abstract",
"offsetInBeginSection": 134,
"offsetInEndSection": 211,
"text": "human homologs of Drosophila dlg, scrib, and lgl are cancer-associated genes."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21549346",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 77,
"text": "Aberrant overexpression of the cell polarity module scribble in human cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21549346",
"endSection": "abstract",
"offsetInBeginSection": 140,
"offsetInEndSection": 318,
"text": "we show that Scrib is nearly universally overexpressed in cultured tumor cell lines and genetically disparate cancer patient series compared with matched normal tissues in vivo. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21549346",
"endSection": "abstract",
"offsetInBeginSection": 762,
"offsetInEndSection": 939,
"text": "These data uncover a previously unrecognized exploitation of Scrib for aberrant tumor cell motility and invasion, thus potentially contributing to disease progression in humans."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21643016",
"endSection": "abstract",
"offsetInBeginSection": 578,
"offsetInEndSection": 737,
"text": "oss of miR-296 causes aberrantly increased and mislocalized Scrib in human tumors, resulting in exaggerated random cell migration and tumor cell invasiveness. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21643016",
"endSection": "abstract",
"offsetInBeginSection": 832,
"offsetInEndSection": 904,
"text": "Scrib levels predict tumor relapse in hepatocellular carcinoma patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24276238",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 47,
"text": "Scrib heterozygosity predisposes to lung cancer"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24276238",
"endSection": "abstract",
"offsetInBeginSection": 754,
"offsetInEndSection": 859,
"text": "loss of Scrib and activated oncogenic KRas cooperate in vivo, resulting in more aggressive lung tumors, l"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23730214",
"endSection": "abstract",
"offsetInBeginSection": 406,
"offsetInEndSection": 463,
"text": "Scribble, a product of a well-known tumor suppressor gene"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23730214",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 105,
"text": "CD74-dependent deregulation of the tumor suppressor scribble in human epithelial and breast cancer cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22169974",
"endSection": "abstract",
"offsetInBeginSection": 247,
"offsetInEndSection": 358,
"text": " scribble (SCRIB) complexes) is intricately related to advanced stages of tumour progression and invasiveness. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21965329",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 57,
"text": "SCRIB expression is deregulated in human prostate cancer,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21965329",
"endSection": "abstract",
"offsetInBeginSection": 531,
"offsetInEndSection": 582,
"text": "Scrib heterozygosity initiated prostate hyperplasia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21965329",
"endSection": "abstract",
"offsetInBeginSection": 984,
"offsetInEndSection": 1153,
"text": "The clinical significance of the work in mice was highlighted by our observation that SCRIB deregulation strongly correlated with poor survival in human prostate cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19041750",
"endSection": "abstract",
"offsetInBeginSection": 839,
"offsetInEndSection": 1051,
"text": "we demonstrate that scribble inhibits breast cancer formation and that deregulation of polarity pathways promotes dysplastic and neoplastic growth in mammals by disrupting morphogenesis and inhibiting cell death."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19041750",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Deregulation of scribble promotes mammary tumorigenesis and reveals a role for cell polarity in carcinoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18641685",
"endSection": "abstract",
"offsetInBeginSection": 637,
"offsetInEndSection": 743,
"text": "loss of Scribble promotes invasion of cells through extracellular matrix in an organotypic culture system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18641685",
"endSection": "abstract",
"offsetInBeginSection": 1131,
"offsetInEndSection": 1195,
"text": "Scribble expression is decreased in many invasive human cancers."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18641685",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Loss of human Scribble cooperates with H-Ras to promote cell invasion through deregulation of MAPK signalling."
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D009369",
"http://www.disease-ontology.org/api/metadata/DOID:162",
"http://www.uniprot.org/uniprot/SCRIB_DANRE",
"http://www.uniprot.org/uniprot/LAP4_DROME"
]
| [
{
"o": "C36345",
"p": "http://www.w3.org/2004/02/skos/core#notation",
"s": "http://linkedlifedata.com/resource/umls/label/A7659777"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A7659777",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C1514542"
},
{
"o": "Protein Deregulation",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A7659777"
}
]
| 53314c98d6d3ac6a3400003b | 164 |
yesno | Is AND-1/Ctf4 essential for proliferation? | ['yes'] | [
"yes"
]
| ['Yes. AND-1 fork protection function prevents fork resection and is essential for proliferation.', 'Yes. AND-1/Ctf4 bridges the CMG helicase and DNA polymerase alpha, facilitating replication. AND-1 depletion is incompatible with proliferation, owing to cells accumulating in G2 with activated DNA damage checkpoint. Replication without AND-1 causes fork speed slow-down and accumulation of long single-stranded DNA (ssDNA) gaps at the replication fork junction, with these regions being converted to DNA double strand breaks (DSBs) in G2.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/30082684"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30082684",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "AND-1 fork protection function prevents fork resection and is essential for proliferation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30082684",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1036,
"text": "AND-1/Ctf4 bridges the CMG helicase and DNA polymerase alpha, facilitating replication. Using an inducible degron system in avian cells, we find that AND-1 depletion is incompatible with proliferation, owing to cells accumulating in G2 with activated DNA damage checkpoint. Replication without AND-1 causes fork speed slow-down and accumulation of long single-stranded DNA (ssDNA) gaps at the replication fork junction, with these regions being converted to DNA double strand breaks (DSBs) in G2. Strikingly, resected forks and DNA damage accumulation in G2, but not fork slow-down, are reverted by treatment with mirin, an MRE11 nuclease inhibitor. Domain analysis of AND-1 further revealed that the HMG box is important for fast replication but not for proliferation, whereas conversely, the WD40 domain prevents fork resection and subsequent DSB-associated lethality. Thus, our findings uncover a fork protection function of AND-1/Ctf4 manifested via the WD40 domain that is essential for proliferation and averts genome instability."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30082684",
"endSection": "abstract",
"offsetInBeginSection": 890,
"offsetInEndSection": 1055,
"text": "Thus , our findings uncover a fork protection function of AND-1/Ctf4 manifested via the WD40 domain that is essential for proliferation and averts genome instability"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30082684",
"endSection": "abstract",
"offsetInBeginSection": 871,
"offsetInEndSection": 1037,
"text": "Thus, our findings uncover a fork protection function of AND-1/Ctf4 manifested via the WD40 domain that is essential for proliferation and averts genome instability."
}
]
| 11 | BioASQ-training11b | null | null | 5e36d924b5b409ea5300000b | 165 |
yesno | Should PDYD polymorphism determination be routinely performed in patients with colorectal cancer patients? | ['yes'] | [
"yes"
]
| ['Yes, determining DPYD polymorphism should be routinely performed in colorectal cancer patients to improve patient safety by allowing for dose adjustments of fluoropyrimidine treatment based on genetic predisposition to toxicity.', 'Yes, prospective DPYD genotyping should be routinely performed in colorectal cancer patients treated with fluoropyrimidines (FP). DPYD genetic variants are associated with extremely severe, early-onset FP toxicity. Prospective DPYD genotyping is feasible in routine clinical practice, and DPYD genotype-based FP dose reductions improve patient safety.', 'Yes, DPYD polymorphism determination should be routinely performed in patients with colorectal cancer patients.', 'Yes, DPYD polymorphism determination should be considered for routine performance in patients with colorectal cancer who are candidates for fluoropyrimidine treatment such as 5-fluorouracil or capecitabine. This is because genetic variants in the dihydropyrimidine dehydrogenase (DPYD) gene have been associated with an increased risk of severe and potentially life-threatening toxicity, particularly when patients carry certain DPYD alleles that result in reduced enzyme activity. By identifying these polymorphisms before initiating treatment, clinicians can adjust the fluoropyrimidine dose to reduce the likelihood of severe toxic effects, thereby improving patient safety and outcomes.', "There is currently no consensus on the routine determination of PDYD polymorphism in colorectal cancer patients. The clinical utility of this test is still under investigation and its use should be based on individual patient's needs and the availability of resources. It is recommended to consult with a healthcare provider to determine the most appropriate course of action.", 'The question of whether PDYD polymorphism determination should be routinely performed in patients with colorectal cancer is a complex one. The literature suggests that DPD deficiency, which is caused by genetic variations in the DPYD gene, is a significant risk factor for severe toxicities associated with 5-fluorouracil (5-FU) therapy. However, the current methods for determining DPD status are not yet suitable for routine clinical practice. While complete genotyping of the DPYD gene would be ideal, it is not currently feasible for routine use. Prospective genotyping for specific polymorphisms, such as the exon 14-skipping and 2846A>T-polymorphisms, may reduce the risk of serious toxic events by about 25%. However, the cost-effectiveness of such screening methods would need to be evaluated before they could be widely implemented in', 'Yes, DPYD genotyping is feasible in routine clinical practice, and DPYD genotype-based dose reductions improved patient safety of fluoropyrimidine treatment.', 'Yes, DPYD polymorphism determination should be routinely performed in patients with colorectal cancer. Host genetic variants in the DPYD gene have been found to be associated with severe toxicity in patients treated with fluoropyrimidine drugs. Prospective DPYD genotyping has been shown to be feasible in routine clinical practice and has led to improved patient safety by allowing for genotype-based dose reductions. Therefore, routine DPYD polymorphism determination can help identify patients who are at higher risk of toxicity and guide personalized treatment strategies.', 'The determination of the PDYD polymorphism should not be routinely performed in patients with colorectal cancer. Although polymorphisms in certain genes, such as p53 and hMLH1, have been shown to play a role in the pathogenesis of colorectal cancer, there is currently insufficient evidence to support the routine use of PDYD polymorphism determination in clinical practice. Further research is needed to establish the clinical significance and prognostic value of PDYD polymorphism in colorectal cancer patients.', 'Yes, prospective DPYD genotyping was feasible in routine clinical practice, and DPYD genotype-based dose reductions improved patient safety of fluoropyrimidine treatment.', 'PDYD polymorphism determination should not be routinely performed in patients with colorectal cancer.The PDYD gene encodes a protein involved in the biosynthesis of the amino acid proline. The PDYD polymorphism is associated with altered proline metabolism, which may have implications for cancer development and progression. However, the clinical utility of PDYD polymorphism determination in colorectal cancer patients is not well established.The clinical utility of PDYD polymorphism determination in colorectal cancer patients is not well established.The PDYD polymorphism is associated with altered proline metabolism, which may have implications for cancer development and progression. However, the clinical utility of PDYD polymorphism determination in colorectal cancer patients is not well established.', 'Based on the current evidence, there is no strong recommendation for routine PDYD polymorphism determination in patients with colorectal cancer. The available studies have focused on other gene polymorphisms such as p53 and IRS-2, and there is limited data on the association between PDYD polymorphism and colorectal cancer. Further research is needed to determine the clinical significance and utility of PDYD polymorphism determination in colorectal cancer patients.', 'PDYD polymorphism determination should not be routinely performed in patients with colorectal cancer.The PDYD gene encodes a protein involved in the regulation of the immune response and is associated with the risk of colorectal cancer. However, the clinical utility of PDYD genotyping in colorectal cancer patients is still unclear.The clinical utility of PDYD genotyping in colorectal cancer patients is still unclear.The PDYD gene encodes a protein involved in the regulation of the immune response and is associated with the risk of colorectal cancer. However, the clinical utility of PDYD genotyping in colorectal cancer patients is still unclear.The PDYD gene encodes a protein involved in the regulation of the immune response and is associated with the risk of colorectal cancer. However, the clinical utility of PDYD genotyping in colorectal cancer patients is still unclear.The PDYD gene encodes a protein involved in the regulation of the immune response and is associated with the risk of colorectal cancer. However, the clinical utility of PDYD genotyping in colorectal cancer patients is still unclear.The PDYD gene encodes a protein involved in the regulation of the immune response and is associated with the risk of colorectal cancer. However, the clinical utility of PDYD genotyping in colorectal cancer patients is still unclear.The PDYD gene encodes a protein involved in the regulation of the immune response and is associated with the risk of colorectal cancer. However, the clinical utility of PDYD genotyping in colorectal cancer patients is still unclear.The PDYD gene encodes a protein involved in the regulation of the immune response and is associated with the risk of colorectal cancer. However, the clinical utility of PDYD genotyping in colorectal cancer patients is still unclear.The PDYD gene encodes a protein involved in the regulation of the immune response and is', 'Yes, PDYD polymorphism determination should be routinely performed in patients with colorectal cancer before they start receiving Fluorouracil (FP) treatment.', 'Prospective DPYD genotyping was feasible in routine clinical practice, and DPYD genotype-based dose reductions improved patient safety of fluoropyrimidine treatment.', "Currently, there is no consensus on routine PDYD polymorphism determination in colorectal cancer patients. The decision to perform such testing should be made on a case-by-case basis, taking into account factors such as the patient's medical history, treatment goals, and availability of alternative treatment options. However, it is important for healthcare providers to be aware of the potential for fluoropyrimidine-induced cardiotoxicity and to consider alternative regimens, such as s-MOX, in patients who have experienced this toxicity or who have abnormalities in the DYPD gene.", 'yes, PDYD polymorphism determination should be routinely performed in patients with colorectal cancer. This is because genetic variants in the DPYD gene can lead to severe toxicity in patients treated with fluoropyrimidine. Prospective DPYD genotyping has been shown to be feasible in routine clinical practice, and using the genotype to guide dose adjustments can significantly improve patient safety.', 'The question of whether PDYD polymorphism determination should be routinely performed in patients with colorectal cancer is a topic of ongoing debate. Some argue that genetic testing for DPYD variants can help identify patients who are at risk of developing severe side effects from fluoropyrimidine chemotherapy, such as 5-FU and capecitabine. This could potentially spare patients from experiencing life-threatening adverse reactions and reduce the need for costly and time-consuming medical interventions. However, others argue that the frequency of DPYD variants is relatively low, and the cost and time required for genetic testing may not be justified for all patients with colorectal cancer. Moreover, there are still concerns about the accuracy and reproducibility of current genotyping methods, and the clinical utility of genetic testing in this setting remains uncertain. Therefore, it is crucial to weigh the potential benefits and', 'The routine determination of PDYD polymorphism in patients with colorectal cancer is not currently a standard practice. However, further research and clinical studies may provide insights into the potential relevance and impact of PDYD polymorphism in the management and treatment of colorectal cancer patients. It is advisable to consult with a healthcare provider or genetic counselor for personalized recommendations regarding genetic testing and its implications in colorectal cancer care.', 'Yes, in summary, polypeptide diversity analysis (PDYD) is a valuable technique for characterizing coloreactal cancer and should be considered for routine use in clinical oncology. It allows for the assessment of genetic, epigenetic, and biological diversity within a tumor population, providing valuable insights into cancer progression and response to treatment. ', 'Yes, PDYD polymorphism determination should be routinely performed in patients with colorectal cancer, particularly those with high-risk stage II resected colorectal cancer enrolled in the TOSCA trial. The presence of the PDYD polymorphism has been associated with improved response to capecitabine and oxaliplatin in these patients.', 'Yes, PDYD polymorphism determination should be routinely performed in patients with colorectal cancer. The XPD Lys751Gln and XRCC1 Arg399Gln polymorphisms have been associated with increased sensitivity to oxaliplatin-based chemotherapy in colorectal cancer patients.', 'Yes, PDYD polymorphism determination should be routinely performed in patients with colorectal cancer. PDYD genetic variants are associated with severe toxicity in patients treated with fluoropyrimidines, which are commonly used in colorectal cancer treatment. Prospective genotyping for PDYD polymorphisms allows for dose individualization and reduces the risk of severe fluoropyrimidine-related toxicity. Implementing PDYD genotype-guided dosing as a standard of care can improve patient safety and treatment outcomes.', 'Yes, DPYD polymorphism determination should be routinely performed in patients with colorectal cancer who are planned to receive fluoropyrimidine treatment. The presence of certain genetic variants in the DPYD gene can result in extremely severe and early onset toxicity in these patients. Prospective DPYD genotyping has been shown to be feasible in routine clinical practice, and DPYD genotype-based dose reductions have been shown to improve patient safety of fluoropyrimidine treatment. By identifying patients who are at risk for severe toxicity, healthcare providers can take steps to minimize the risk of adverse events and optimize treatment outcomes.', 'Yes, PDYD (dihydropyrimidine dehydrogenase) polymorphism determination should be routinely performed in colorectal cancer patients treated with fluoropyrimidines. The abstract describes a prospective study that demonstrated reduced severe toxicity in patients who received genotype-guided dosing of fluoropyrimidines based on PDYD variants. Specifically, DPYD*2A and c.1679T>G carriers benefited from a 50% initial dose reduction, while c.1236G>A and c.2846A>T carriers may require a larger dose reduction of 50%. Given that fluoropyrimidines are commonly used anticancer agents, the implementation of PDYD genotype-guided individualized dosing should be considered a new standard of care to improve patient safety and treatment outcomes.', 'Yes, determining DPYD polymorphism should be routinely performed in patients with colorectal cancer before starting fluoropyrimidine-based chemotherapy. This is because certain genetic variants in the DPYD gene can lead to severe toxicity in patients treated with fluoropyrimidines. Identifying these variants through genotyping can help tailor the treatment dose to improve safety and efficacy for the patient', 'Yes, DPYD polymorphism determination should be routinely performed in patients with colorectal cancer to improve patient safety during fluoropyrimidine treatment.', 'This question is too specific and does not reflect the scope of the study. PDYD polymorphisms are not associated with colorectal cancer in general. The study focuses on a specific subset of colorectal cancer patients, and even for that subset, PDYD polymorphism determination is not routinely recommended, but rather it is suggested as an optional tool to improve clinical management of patients with stage II/III disease.', 'Yes, PDYD polymorphism determination should be routinely performed in patients with colorectal cancer patients to identify those who may be at risk for severe toxicity from fluoropyrimidine-based chemotherapy.', 'Yes, DPYD polymorphism determination should be routinely performed in patients with colorectal cancer to improve patient safety of fluoropyrimidine treatment.', "yes, PDYD polymorphism determination should be routinely performed in patients with colorectal cancer to improve patient safety by allowing for dose adjustments of fluoropyrimidine treatment based on the patient's genetic profile.", 'Yes, PDYD polymorphism determination should be routinely performed in patients with colorectal cancer. This is because genetic variants in the DPYD gene can lead to severe toxicity in patients treated with fluoropyrimidine. As mentioned, "Prospective DPYD genotyping was feasible in routine clinical practice, and DPYD genotype-based dose reductions improved patient safety of fluoropyrimidine treatment." This indicates that knowing a patient\'s DPYD genotype can help tailor their treatment plan to reduce the risk of severe side effects and enhance treatment safety.', 'Yes, determining dihydropyrimidine dehydrogenase (DPYD) polymorphisms should be considered routine practice for patients with colorectal cancer who are candidates for fluoropyrimidine-based chemotherapy. This is because DPYD plays a crucial role in the metabolism of these drugs and genetic variations can significantly impact both drug efficacy and toxicity. By identifying individuals with variants that may lead to reduced or absent enzyme activity, clinicians can adjust treatment plans accordingly, potentially avoiding severe adverse reactions while optimizing therapeutic outcomes.', 'Yes, complete genotyping of the encoding DPYD gene is desirable, in the interest of drug safety, before treatment is started.', 'No, according to current guidelines from major cancer organizations such as the National Comprehensive Cancer Network (NCCN) and the American Society of Clinical Oncology (ASCO), routine PDYD polymorphism determination is not recommended in patients with colorectal cancer. However, some experts suggest that PDYD genotyping may be considered in certain situations, such as in patients with a history of severe fluoropyrimidine toxicity or in those receiving high-dose fluoropyrimidine therapy. Therefore, the decision to perform PDYD polymorphism determination should be made on a case-by-case basis in consultation with a healthcare provider.', 'Yes, determining DPYD polymorphisms should be routinely performed in patients with colorectal cancer as it can help predict the risk of severe toxicity from fluoropyrimidine treatment and guide personalized dose adjustments to improve patient safety and treatment outcomes.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/36524458",
"http://www.ncbi.nlm.nih.gov/pubmed/18597209",
"http://www.ncbi.nlm.nih.gov/pubmed/35582139",
"http://www.ncbi.nlm.nih.gov/pubmed/29372689",
"http://www.ncbi.nlm.nih.gov/pubmed/34780066",
"http://www.ncbi.nlm.nih.gov/pubmed/36297556",
"http://www.ncbi.nlm.nih.gov/pubmed/11051215",
"http://www.ncbi.nlm.nih.gov/pubmed/36980706",
"http://www.ncbi.nlm.nih.gov/pubmed/31653159",
"http://www.ncbi.nlm.nih.gov/pubmed/25906475",
"http://www.ncbi.nlm.nih.gov/pubmed/25253112",
"http://www.ncbi.nlm.nih.gov/pubmed/21461655",
"http://www.ncbi.nlm.nih.gov/pubmed/12749725",
"http://www.ncbi.nlm.nih.gov/pubmed/23781135",
"http://www.ncbi.nlm.nih.gov/pubmed/20637356",
"http://www.ncbi.nlm.nih.gov/pubmed/23335937",
"http://www.ncbi.nlm.nih.gov/pubmed/35880438",
"http://www.ncbi.nlm.nih.gov/pubmed/23942539",
"http://www.ncbi.nlm.nih.gov/pubmed/25137161",
"http://www.ncbi.nlm.nih.gov/pubmed/33274825",
"http://www.ncbi.nlm.nih.gov/pubmed/19239324",
"http://www.ncbi.nlm.nih.gov/pubmed/16537192",
"http://www.ncbi.nlm.nih.gov/pubmed/20920994",
"http://www.ncbi.nlm.nih.gov/pubmed/15213713",
"http://www.ncbi.nlm.nih.gov/pubmed/30348537",
"http://www.ncbi.nlm.nih.gov/pubmed/36890284",
"http://www.ncbi.nlm.nih.gov/pubmed/32546132",
"http://www.ncbi.nlm.nih.gov/pubmed/24817302",
"http://www.ncbi.nlm.nih.gov/pubmed/33280607",
"http://www.ncbi.nlm.nih.gov/pubmed/30551678"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35582139",
"endSection": "abstract",
"offsetInBeginSection": 569,
"offsetInEndSection": 759,
"text": "Host genetic variants in the rate limiting enzyme dihydropyrimidine dehydrogenase (DPYD) gene are related to the occurrence of extremely severe, early onset toxicity in FP treated patients. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30348537",
"endSection": "abstract",
"offsetInBeginSection": 3168,
"offsetInEndSection": 3333,
"text": "Prospective DPYD genotyping was feasible in routine clinical practice, and DPYD genotype-based dose reductions improved patient safety of fluoropyrimidine treatment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20637356",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1014,
"text": "Colorectal cancer (CCR), which is one of the most common causes of cancer, has benefited from the major advances in the understanding of the intracellular signaling pathways implicated in the initiation, growing and local and metastasis dissemination of tumor, which have occurred during the 20 past years. The pharmacogenomics approach, especially the determination of the genetic polymorphisms, tries to find prognosis and predictive biomarkers permitting to identify patients who could benefit from a particular treatment or those exhibiting higher risks of toxicity. Among the numerous biomarkers, which have been studied, few are currently in use in clinical practice. The phenotyping of DPD and UGT1A1 activities, and to a lesser extent, its genotyping, appears as the most useful tool in terms of prediction of toxicities induced by two major drugs: 5-FU and irinotecan. For oxaliplatin, the determination of the polymorphisms of reparases and detoxification systems such as GSTpi seems interesting, but its"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18597209",
"endSection": "abstract",
"offsetInBeginSection": 22,
"offsetInEndSection": 1708,
"text": "forms the basis for the chemotherapy of advanced colorectal cancer and of other solid tumours. About 9% of patients suffer from serious, sometimes even life-threatening adverse effects of a 5-FU therapy, such as haemotoxicity, which cannot be reliably predicted by conventional clinical and pharmacokinetic criteria. The systemic exposure to 5-FU is fundamentally determined by the genetically polymorphic enzyme dihydropyrimidine dehydrogenase (DPD). This deficiency is closely related to 5-FU-induced toxicity and a variety of non-synonymous variants has been detected in affected patients. The exon14-skipping mutation is the gene defect most frequently associated with serious 5-FU-related adverse effects and it has been reported ten times more often in affected individuals than in the general population. The 2846A>T polymorphism, which leads to an amino acid substitution, appears to be of comparable importance. While the causative role of premature stop codons - presumably resulting from spontaneous mutations - is very likely, the pathophysiological relevance of various other amino acid changes is still unclear. Patients who harbour a high-risk genotype should not be treated with 5-FU if therapeutic alternatives are available. The present data indicate that complete genotyping of the encoding DPYD gene is desirable, in the interest of drug safety, before treatment is started, although only a small number of patients would actually benefit. A method for the quantification of the DPD activity in vivo would have the advantage of reflecting all genetic and non-genetic influences.' However, no such method is currently available for routine use. Prospective genotyping"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34780066",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "AIMS: Cancer patients with reduced dihydropyrimidine dehydrogenase (DPD) activity are at increased risk of severe fluoropyrimidine (FP)-related adverse events (AE)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34780066",
"endSection": "abstract",
"offsetInBeginSection": 768,
"offsetInEndSection": 1270,
"text": "For each of the tested polymorphisms, variant allele carriers were matched to respective wild type controls (optimal full matching combined with exact matching, in respect to: age, sex, type of cancer, type of FP, DPYD activity score, use of irinotecan/UGT1A1, adjuvant therapy, radiotherapy, biological therapy and genotype on the remaining two tested polymorphisms).RESULTS: Of the 503 included patients (82.3% colorectal cancer), 283 (56.3%) developed grade ≥3 AEs, mostly diarrhoea and neutropenia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34780066",
"endSection": "abstract",
"offsetInBeginSection": 320,
"offsetInEndSection": 767,
"text": "We evaluated the relationship between three further DPYD polymorphisms: c.496A>G (rs2297595), *6 c.2194G>A (rs1801160) and *9A c.85T>C (rs1801265) and the risk of severe AEs.METHODS: Consecutive FP-treated adult patients were genotyped for \"standard\" and tested DPYD variants, and for UGT1A1*28 if irinotecan was included, and were monitored for the occurrence of grade ≥3 (National Cancer Institute Common Terminology Criteria) vs. grade 0-2 AEs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18597209",
"endSection": "abstract",
"offsetInBeginSection": 1265,
"offsetInEndSection": 1481,
"text": "The present data indicate that complete genotyping of the encoding DPYD gene is desirable, in the interest of drug safety, before treatment is started, although only a small number of patients would actually benefit."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25906475",
"endSection": "abstract",
"offsetInBeginSection": 1227,
"offsetInEndSection": 1487,
"text": "The studies we reviewed indicate that pharmacogenetic testing is promising to direct personalised dosing of fluoropyrimidines, although further investigations are needed to establish the role of DPD in severe toxicity in patients treated for colorectal cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34780066",
"endSection": "abstract",
"offsetInBeginSection": 165,
"offsetInEndSection": 319,
"text": "Guidelines recommend FP dosing adjusted to genotype-predicted DPD activity based on four DPYD variants (rs3918290, rs55886062, rs67376798 and rs56038477)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25137161",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 847,
"text": "OBJECTIVE: To validate the associations previously found in three cohorts of patients from the General University Hospital Gregorio Marañón, between the polymorphisms rs1128503, rs2032582 and rs1045642 of the ABCB1 gene and the hand-foot syndrome and diarrhea in colorectal cancer patients treated with chemotherapy regimes containing Capecitabine and 5-Fluorouracil, respectively, and between the polymorphisms rs2297595 of the DPYD gene and nausea/vomiting, rs11615 of ERCC1 and neutropenia, and rs28399433 CYP2A6 and neutropenia, in colorectal cancer patients treated with FOLFOX or XELOX as adjuvant therapy.METHOD: Colorectal cancer patients treated with chemotherapy regimes, containing Capecitabine (n = 157), 5-Fluorouracil (n = 99) were included in the study, as well as patients treated with XELOX or FOLFOX (n = 83) as adjuvant therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18597209",
"endSection": "abstract",
"offsetInBeginSection": 1686,
"offsetInEndSection": 1842,
"text": "Prospective genotyping for the exon 14-skipping and the 2846A>T-polymorphisms may result in a reduction of serious, 5-FU-induced, toxic events of about 25%."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32546132",
"endSection": "abstract",
"offsetInBeginSection": 1343,
"offsetInEndSection": 1589,
"text": "There was no association between IVS14 + 1 G > A polymorphism and the occurrence of adverse reactions.CONCLUSION: FOLFOX and FOLFIRI were the most common regimens in CRC patients and their toxicity profile was different in some adverse reactions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18597209",
"endSection": "abstract",
"offsetInBeginSection": 117,
"offsetInEndSection": 338,
"text": "About 9% of patients suffer from serious, sometimes even life-threatening adverse effects of a 5-FU therapy, such as haemotoxicity, which cannot be reliably predicted by conventional clinical and pharmacokinetic criteria."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36980706",
"endSection": "abstract",
"offsetInBeginSection": 1113,
"offsetInEndSection": 1273,
"text": "These findings suggest the identification of future predictive biomarkers of effectiveness and toxicity in colorectal cancer patients treated with capecitabine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36980706",
"endSection": "abstract",
"offsetInBeginSection": 947,
"offsetInEndSection": 1112,
"text": "This systematic review reveals that several SNPs other than the four DPYD variants that are screened in clinical practice could have an impact on treatment outcomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33274825",
"endSection": "abstract",
"offsetInBeginSection": 1275,
"offsetInEndSection": 1587,
"text": "DPYD*2A test results were available in an average of 6 days, causing no significant delays in treatment initiation.CONCLUSION: Upfront genotyping before fluoropyrimidine-based treatment is feasible in clinical practice and can prevent severe toxicities and hospitalizations without delaying treatment initiation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36890284",
"endSection": "abstract",
"offsetInBeginSection": 1156,
"offsetInEndSection": 1592,
"text": "Our patient may also have benefitted from compound heterozygosis, as shown by no evidence of disease (NED) at 6-month follow-up.CONCLUSION: Pharmacogenetic-guided dosing of DPYD intermediate metabolizer compound heterozygous HapB3 and c.2194G>A variant carries should be managed by a multidisciplinary team with a dose reduction ranging from 25 to 50% to maintain effectiveness and close clinical monitoring for early detection of ADRs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19239324",
"endSection": "abstract",
"offsetInBeginSection": 437,
"offsetInEndSection": 933,
"text": " The frequency of the polymorphism was examined in 156 patients with colorectal cancer and in 293 healthy controls. The polymorphism analysis was performed by amplifying exon 4 of p53 and digesting the products with restriction enzyme. The frequencies of genotypes: Arg/Arg, Arg/Pro and Pro/Pro were 34.6% (54/156), 43.0% (67/156) and 22.4% (35/156), respectively, in the cases with colorectal cancer, and 28.9% (114/293), 47.8% (140/293) and 13.3% (39/293), respectively, in the healthy controls"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24817302",
"endSection": "abstract",
"offsetInBeginSection": 67,
"offsetInEndSection": 184,
"text": "+1 G > A genotype of the dihydropyrimidine dehydrogenase (DPD) gene with plasma concentration of 5-fluorouracil (5-FU"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20637356",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1686,
"text": "Colorectal cancer (CCR), which is one of the most common causes of cancer, has benefited from the major advances in the understanding of the intracellular signaling pathways implicated in the initiation, growing and local and metastasis dissemination of tumor, which have occurred during the 20 past years. The pharmacogenomics approach, especially the determination of the genetic polymorphisms, tries to find prognosis and predictive biomarkers permitting to identify patients who could benefit from a particular treatment or those exhibiting higher risks of toxicity. Among the numerous biomarkers, which have been studied, few are currently in use in clinical practice. The phenotyping of DPD and UGT1A1 activities, and to a lesser extent, its genotyping, appears as the most useful tool in terms of prediction of toxicities induced by two major drugs: 5-FU and irinotecan. For oxaliplatin, the determination of the polymorphisms of reparases and detoxification systems such as GSTpi seems interesting, but its exact place should be more defined. It is in the field of targeted therapies that the pharmacogenomics approach seems to be the more relevant. KRAS mutation is a dramatic example of single nucleotide polymorphism, which is able to identify a priori patients that could receive or not an anti-EGFR monoclonal antibody such as cetuximab or panitumumab. It is obvious that pre-clinical identification of molecular biomarkers predictive of the sensitivity of the drug targets, which subsequently implicate the selection of patients and the rational evaluation of responses, will be the cornerstone of any clinical trials concerning targeted therapies. Besides the determinati"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12749725",
"endSection": "abstract",
"offsetInBeginSection": 1538,
"offsetInEndSection": 2091,
"text": "Alterations in gene expression, protein expression and polymorphic variants in genes encoding thymidylate synthase, dihydropyrimidine dehydrogenase, dUTP nucleotidehydrolase and thymidine phosphorylase (for fluoropyrimidine-based chemotherapy), uridine diphosphate glucosyltransferase (UGT) 1A1 and carboxylesterase (for irinotecan therapy), and excision repair cross-complementing genes (ERCC1 and ERCC2) and glutathione-S-transferase P1 (for oxalilplatin-based regimens) may be useful as markers for clinical drug response, survival and host toxicity."
}
]
| 13 | BioASQ-training13b | null | null | 65f77596c4010b4d7800002c | 166 |
yesno | Does steroid 5A-Reductase deficiency lead to hermaphroditism? | ['yes'] | [
"yes"
]
| ['Yes, steroid 5A-reductase deficiency can lead to hermaphroditism.', '5α steroid reductase deficiency (5αSRD) is an autosomal recessive enzymatic deficiency and mutations in the 5α steroid reductase type 2 gene (SRD5A2) result in male pseudohermaphrodism caused by decreased dihydrotestosterone (DHT) synthesis. The diagnosis of steroid-5-alpha-reductase deficiency is rarely considered by the paediatrician.', 'Yes, steroid 5A-reductase deficiency is a rare autosomal recessive disorder.', 'Yes, steroid 5A-Reductase deficiency is associated with hermaphroditism.', '5α steroid reductase deficiency (5αSRD) is an autosomal recessive enzymatic deficiency and mutations in the 5α steroid reductase type 2 gene (SRD5A2) result in male pseudohermaphrodism caused by decreased dihydrotestosterone (DHT) synthesis.', 'Male pseudo hermaphroditism caused by steroid 5 alpha reductase deficiency is a rare autosomal recessive disorder. This enzyme catalyses the conversion of testosterone to dihydrotestosterone (DHT) in genital tissue.', 'Yes, steroid 5A-reductase deficiency is associated with hermaphroditism.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/11515490",
"http://www.ncbi.nlm.nih.gov/pubmed/23633205",
"http://www.ncbi.nlm.nih.gov/pubmed/10458450",
"http://www.ncbi.nlm.nih.gov/pubmed/20850730",
"http://www.ncbi.nlm.nih.gov/pubmed/27693263",
"http://www.ncbi.nlm.nih.gov/pubmed/8110760",
"http://www.ncbi.nlm.nih.gov/pubmed/10564874",
"http://www.ncbi.nlm.nih.gov/pubmed/21147889",
"http://www.ncbi.nlm.nih.gov/pubmed/24383016",
"http://www.ncbi.nlm.nih.gov/pubmed/3489839",
"http://www.ncbi.nlm.nih.gov/pubmed/8001864",
"http://www.ncbi.nlm.nih.gov/pubmed/1944596",
"http://www.ncbi.nlm.nih.gov/pubmed/17663907",
"http://www.ncbi.nlm.nih.gov/pubmed/20511729",
"http://www.ncbi.nlm.nih.gov/pubmed/8302780",
"http://www.ncbi.nlm.nih.gov/pubmed/20132346",
"http://www.ncbi.nlm.nih.gov/pubmed/8768837"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20511729",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 253,
"text": "5α steroid reductase deficiency (5αSRD) is an autosomal recessive enzymatic deficiency and mutations in the 5α steroid reductase type 2 gene (SRD5A2) result in male pseudohermaphrodism caused by decreased dihydrotestosterone (DHT) synthesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20132346",
"endSection": "abstract",
"offsetInBeginSection": 413,
"offsetInEndSection": 510,
"text": "The diagnosis of steroid-5-alpha-reductase deficiency is rarely considered by the paediatrician. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21147889",
"endSection": "abstract",
"offsetInBeginSection": 10,
"offsetInEndSection": 213,
"text": "n 46,XY disorders of sex development, 5α-reductase deficiency is rare and is not usually the first-intention diagnosis in newborn ambiguous genitalia, contrary to partial androgen insensitivity syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21147889",
"endSection": "abstract",
"offsetInBeginSection": 214,
"offsetInEndSection": 345,
"text": "Yet the cause of ambiguous genitalia may guide sex assignment, and rapid, precise diagnosis of 5α-reductase deficiency is essential"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20850730",
"endSection": "abstract",
"offsetInBeginSection": 1102,
"offsetInEndSection": 1384,
"text": "Our data clearly demonstrate that 5α-reductase deficiency should be considered in XY adolescents with primary amenorrhea and no breast development associated with virilization at puberty and high plasma T. Positive parental consanguinity should reinforce the diagnostic orientation."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23633205",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "Molecular diagnosis of 5α-reductase deficiency in 4 elite young female athletes through hormonal screening for hyperandrogenism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23633205",
"endSection": "abstract",
"offsetInBeginSection": 1289,
"offsetInEndSection": 1550,
"text": "The hormonal analysis evidenced plasma T within the male range, the karyotype was 46, XY, and molecular analysis of the 5α-reductase type 2 (srd5A2) gene identified a homozygotic mutation in 2 cases, a heterozygotic compound in 1 case, and a deletion in 1 case."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23633205",
"endSection": "abstract",
"offsetInBeginSection": 1562,
"offsetInEndSection": 1754,
"text": "5α-Reductase deficiency should be investigated in elite young female athletes with primary amenorrhea and high male T levels detected during antidoping programs to identify undiagnosed XY DSD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27693263",
"endSection": "abstract",
"offsetInBeginSection": 14,
"offsetInEndSection": 389,
"text": "Few studies exist on the psychosexual outcome of homogeneous groups of individuals with 5α-reductase deficiency type 2 (5α-RD-2) and the relation between gender changes and parental hostile and benevolent sexism, which are two components of ambivalent sexism that assume a stereotypical approach toward women in an overtly negative way or a chivalrous, seemingly positive way"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27693263",
"endSection": "abstract",
"offsetInBeginSection": 1849,
"offsetInEndSection": 2039,
"text": "The high prevalence of gender change and gender dysphoria reported in the literature was confirmed in this relatively large and homogeneous sample of Iranians with 5-α-RD-2 raised as female."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11515490",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 114,
"text": "Male pseudo hermaphroditism caused by steroid 5 alpha reductase deficiency is a rare autosomal recessive disorder."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11515490",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "[Male pseudo-hermaphroditism due to partial 5 alpha-reductase deficiency, a case report]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17663907",
"endSection": "abstract",
"offsetInBeginSection": 249,
"offsetInEndSection": 357,
"text": "We report two cases of male pseudohermaphroditism, a true hermaphroditism and a 5-alfa-reductase deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8302780",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 205,
"text": "Contrary to what is observed in true hermaphroditism and in male pseudo-hermaphroditism, there is no erroneous transmission of the genetic gonadal differentiation programme in female pseudohermaphroditism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10458450",
"endSection": "abstract",
"offsetInBeginSection": 822,
"offsetInEndSection": 1039,
"text": "To our knowledge neither the A49T nor the L113V mutation has been previously reported in association with 5alpha-reductase type 2 deficiency and to date they have only been identified in cases of isolated hypospadias."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8001864",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "The deficiency of steroid 5 alpha-reductase leads to the disturbances in sex differentiation that cause symptoms of male pseudohermaphroditism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10564874",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 108,
"text": "Male pseudohermaphroditism caused by steroid 5alpha-reductase deficiency is an autosomal recessive disorder."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3489839",
"endSection": "abstract",
"offsetInBeginSection": 1705,
"offsetInEndSection": 1930,
"text": "This study reveals that 5 alpha-reductase deficiency occurs with a frequency of 13 per cent as a cause of male pseudohermaphroditism in the Dominican Republic with approximately the same frequency as XO/XY gonadal dysgenesis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1944596",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 75,
"text": "Deletion of steroid 5 alpha-reductase 2 gene in male pseudohermaphroditism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3489839",
"endSection": "abstract",
"offsetInBeginSection": 812,
"offsetInEndSection": 1080,
"text": "In 5 of 33 male pseudohermaphrodites with a normal testosterone response to human chorionic gonadotropin 5 alpha-reductase deficiency was suspected by elevated plasma testosterone/dihydrotestosterone ratios before and/or after human chorionic gonadotropin stimulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1944596",
"endSection": "abstract",
"offsetInBeginSection": 981,
"offsetInEndSection": 1114,
"text": "A deletion in this gene is present in two related individuals with male pseudohermaphroditism caused by 5 alpha-reductase deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24383016",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 189,
"text": "Steroid 5-alpha-reductase 2 deficiency is a rare disorder leading to male pseudohermaphroditism, a condition characterized by incomplete differentiation of male genitalia in 46,XY patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8768837",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 200,
"text": "The present report describes a cluster of eight patients with male pseudohermaphroditism from a large pedigree with steroid 5 alpha-reductase 2 deficiency (5 alpha RD), who reside in Southern Lebanon."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8110760",
"endSection": "abstract",
"offsetInBeginSection": 485,
"offsetInEndSection": 640,
"text": "Inherited deficiencies of 5 alpha-reductase type 2 result in a form of male pseudohermaphroditism in which the external genitalia fail to develop normally."
}
]
| 11 | BioASQ-training11b | null | null | 5fd78702a43ad31278000005 | 167 |
yesno | Has amantadine ER been approved by the FDA? | ['yes'] | [
"yes"
]
| ['Yes, amantadine ER is an US FDA-approved treatment.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/29532440"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29532440",
"endSection": "abstract",
"offsetInBeginSection": 270,
"offsetInEndSection": 404,
"text": "ADS-5102 (amantadine) extended-release (ER) capsules (GOCOVRITM) is a recent US FDA-approved treatment for dyskinesia in PD patients. "
}
]
| 11 | BioASQ-training11b | null | null | 5e2db15cfbd6abf43b000014 | 168 |
yesno | Are there mammalian promoters with distal enhancer functions? | ['yes'] | [
"yes"
]
| ['Yes. Several studies have suggested that some promoters might have enhancer functions. By exploiting a high-throughput enhancer reporter assay, scientists have unraveled a set of mammalian promoters displaying enhancer activity. These promoters have distinct genomic and epigenomic features and frequently interact with other gene promoters. Extensive CRISPR-Cas9 genomic manipulation demonstrated the involvement of these promoters in the cis regulation of expression of distal genes in their natural loci.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/28581502"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28581502",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "Genome-wide characterization of mammalian promoters with distal enhancer functions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28581502",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 902,
"text": "Gene expression in mammals is precisely regulated by the combination of promoters and gene-distal regulatory regions, known as enhancers. Several studies have suggested that some promoters might have enhancer functions. However, the extent of this type of promoters and whether they actually function to regulate the expression of distal genes have remained elusive. Here, by exploiting a high-throughput enhancer reporter assay, we unravel a set of mammalian promoters displaying enhancer activity. These promoters have distinct genomic and epigenomic features and frequently interact with other gene promoters. Extensive CRISPR-Cas9 genomic manipulation demonstrated the involvement of these promoters in the cis regulation of expression of distal genes in their natural loci. Our results have important implications for the understanding of complex gene regulation in normal development and disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28581502",
"endSection": "abstract",
"offsetInBeginSection": 367,
"offsetInEndSection": 499,
"text": "Here, by exploiting a high-throughput enhancer reporter assay, we unravel a set of mammalian promoters displaying enhancer activity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28581502",
"endSection": "abstract",
"offsetInBeginSection": 138,
"offsetInEndSection": 219,
"text": "Several studies have suggested that some promoters might have enhancer functions."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28581502",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "genome wide characterization of mammalian promoters with distal enhancer functions"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28581502",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 892,
"text": "gene expression in mammals is precisely regulated by the combination of promoters and gene distal regulatory regions known as enhancers several studies have suggested that some promoters might have enhancer functions however the extent of this type of promoters and whether they actually function to regulate the expression of distal genes have remained elusive here by exploiting a high throughput enhancer reporter assay we unravel a set of mammalian promoters displaying enhancer activity these promoters have distinct genomic and epigenomic features and frequently interact with other gene promoters extensive crispr cas9 genomic manipulation demonstrated the involvement of these promoters in the cis regulation of expression of distal genes in their natural loci our results have important implications for the understanding of complex gene regulation in normal development and disease."
}
]
| 11 | BioASQ-training11b | [
"http://amigo.geneontology.org/amigo/term/GO:0001206",
"http://amigo.geneontology.org/amigo/term/GO:0001205",
"http://amigo.geneontology.org/amigo/term/GO:0035326",
"https://meshb.nlm.nih.gov/record/ui?ui=D011401",
"http://amigo.geneontology.org/amigo/term/GO:0003705",
"http://amigo.geneontology.org/amigo/term/GO:0071733",
"https://meshb.nlm.nih.gov/record/ui?ui=D004742"
]
| null | 5a6fabfeb750ff4455000062 | 169 |
yesno | Is Sotatercept effective for Pulmonary Arterial Hypertension? | ['yes'] | [
"yes"
]
| ['Sotatercept was shown to be effective for Pulmonary Arterial Hypertension.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/33789009",
"http://www.ncbi.nlm.nih.gov/pubmed/33733610"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33789009",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 65,
"text": "Sotatercept for the Treatment of Pulmonary Arterial Hypertension."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33789009",
"endSection": "abstract",
"offsetInBeginSection": 1920,
"offsetInEndSection": 2094,
"text": "CONCLUSIONS: Treatment with sotatercept resulted in a reduction in pulmonary vascular resistance in patients receiving background therapy for pulmonary arterial hypertension."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33789009",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 64,
"text": "Sotatercept for the Treatment of Pulmonary Arterial Hypertension"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33789009",
"endSection": "abstract",
"offsetInBeginSection": 1920,
"offsetInEndSection": 2092,
"text": "CONCLUSIONS: Treatment with sotatercept resulted in a reduction in pulmonary vascular resistance in patients receiving background therapy for pulmonary arterial hypertensio"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33789009",
"endSection": "abstract",
"offsetInBeginSection": 1821,
"offsetInEndSection": 2051,
"text": "n hematologic adverse events. One patient in the sotatercept 0.7-mg group died from cardiac arrest.CONCLUSIONS: Treatment with sotatercept resulted in a reduction in pulmonary vascular resistance in patients receiving background t"
}
]
| 11 | BioASQ-training11b | null | null | 61f7cca7882a024a1000002b | 170 |
yesno | Is there an association between TERT promoter mutation and survival of glioblastoma patients? | ['yes'] | [
"yes"
]
| ['Telomerase reverse transcriptase (TERT) promoter are associated with shorter survival of glioblastoma patients. Prognostic value of TERT mutations for poor survival is largely due to their inverse correlation with IDH1 mutations.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23955565",
"http://www.ncbi.nlm.nih.gov/pubmed/23393205",
"http://www.ncbi.nlm.nih.gov/pubmed/24937153"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23955565",
"endSection": "abstract",
"offsetInBeginSection": 993,
"offsetInEndSection": 1734,
"text": "Glioblastoma patients with TERT mutations showed a shorter survival than those without TERT mutations in univariate analysis (median, 9.3 vs. 10.5 months; P = 0.015) and multivariate analysis after adjusting for age and gender (HR 1.38, 95 % CI 1.01-1.88, P = 0.041). However, TERT mutations had no significant impact on patients' survival in multivariate analysis after further adjusting for other genetic alterations, or when primary and secondary glioblastomas were separately analysed. These results suggest that the prognostic value of TERT mutations for poor survival is largely due to their inverse correlation with IDH1 mutations, which are a significant prognostic marker of better survival in patients with secondary glioblastomas."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23393205",
"endSection": "abstract",
"offsetInBeginSection": 1593,
"offsetInEndSection": 1825,
"text": "Patients with tumors lacking hTERT expression/TA showed a significant survival benefit (Kaplan-Meier test, both P < .01), which, however, was based exclusively on the younger patient subgroup (≤60 y, both P < .005; >60 y, both ns). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23955565",
"endSection": "abstract",
"offsetInBeginSection": 993,
"offsetInEndSection": 1734,
"text": "Glioblastoma patients with TERT mutations showed a shorter survival than those without TERT mutations in univariate analysis (median, 9.3 vs. 10.5 months; P = 0.015) and multivariate analysis after adjusting for age and gender (HR 1.38, 95 % CI 1.01-1.88, P = 0.041). However, TERT mutations had no significant impact on patients' survival in multivariate analysis after further adjusting for other genetic alterations, or when primary and secondary glioblastomas were separately analysed. These results suggest that the prognostic value of TERT mutations for poor survival is largely due to their inverse correlation with IDH1 mutations, which are a significant prognostic marker of better survival in patients with secondary glioblastomas."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23393205",
"endSection": "abstract",
"offsetInBeginSection": 1593,
"offsetInEndSection": 1825,
"text": "Patients with tumors lacking hTERT expression/TA showed a significant survival benefit (Kaplan-Meier test, both P < .01), which, however, was based exclusively on the younger patient subgroup (≤60 y, both P < .005; >60 y, both ns). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23955565",
"endSection": "abstract",
"offsetInBeginSection": 993,
"offsetInEndSection": 1133,
"text": "Glioblastoma patients with TERT mutations showed a shorter survival than those without TERT mutations in univariate analysis (median, 9.3 vs"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23955565",
"endSection": "abstract",
"offsetInBeginSection": 993,
"offsetInEndSection": 1133,
"text": "Glioblastoma patients with TERT mutations showed a shorter survival than those without TERT mutations in univariate analysis (median, 9.3 vs"
}
]
| 5 | BioASQ-training5b | [
"http://www.disease-ontology.org/api/metadata/DOID:3073"
]
| []
| 55032bbfe9bde69634000032 | 171 |
yesno | Is Hunter's disease is associated with the X Chromosome? | ['yes'] | [
"yes"
]
| ["Yes, Hunter's disease is associated with the X Chromosome.", 'Yes, the X Chromosome is associated with the X chromosome.', "Hunter's disease is associated with the X chromosome."] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22246721",
"http://www.ncbi.nlm.nih.gov/pubmed/31046699",
"http://www.ncbi.nlm.nih.gov/pubmed/21062272",
"http://www.ncbi.nlm.nih.gov/pubmed/25044788",
"http://www.ncbi.nlm.nih.gov/pubmed/3100113",
"http://www.ncbi.nlm.nih.gov/pubmed/9604546",
"http://www.ncbi.nlm.nih.gov/pubmed/1294876",
"http://www.ncbi.nlm.nih.gov/pubmed/9611068",
"http://www.ncbi.nlm.nih.gov/pubmed/6418082",
"http://www.ncbi.nlm.nih.gov/pubmed/9375851",
"http://www.ncbi.nlm.nih.gov/pubmed/20052546",
"http://www.ncbi.nlm.nih.gov/pubmed/23634718",
"http://www.ncbi.nlm.nih.gov/pubmed/1481858",
"http://www.ncbi.nlm.nih.gov/pubmed/17345554",
"http://www.ncbi.nlm.nih.gov/pubmed/21834048",
"http://www.ncbi.nlm.nih.gov/pubmed/2499679",
"http://www.ncbi.nlm.nih.gov/pubmed/1908009",
"http://www.ncbi.nlm.nih.gov/pubmed/8807335",
"http://www.ncbi.nlm.nih.gov/pubmed/1642233",
"http://www.ncbi.nlm.nih.gov/pubmed/1678247"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1908009",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 198,
"text": "Segregation analysis on five samples of families with Hunter's syndrome (158 cases overall) shows that the mutant allele segregates in agreement with Mendelian expectations for an X linked recessive"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9604546",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 281,
"text": "The utility of polymerase chain reaction (PCR) amplification of amelogenin gene as a reliable and rapid means of determination of sex chromosomes was tested in 20 patients of X-linked disorders (Duchenne muscular dystrophy, haemophilia and Wiscott-Aldrich and Hunter's syndromes), "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6418082",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 118,
"text": "We describe a 3 year old girl with the typical clinical features of the X linked recessive condition, Hunter's disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6418082",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "We describe a 3 year old girl with the typical clinical features of the X linked recessive condition, Hunter's disease."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6418082",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Hunter's disease in a girl: association with X:5 chromosomal translocation disrupting the Hunter gene."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2499679",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 109,
"text": "Further evidence localising the gene for Hunter's syndrome to the distal region of the X chromosome long arm."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3100113",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "Full expression of Hunter's disease in a female with an X-chromosome deletion leading to non-random inactivation."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9375851",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Hunter disease in a girl caused by R468Q mutation in the iduronate-2-sulfatase gene and skewed inactivation of the X chromosome carrying the normal allele."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9375851",
"endSection": "abstract",
"offsetInBeginSection": 1060,
"offsetInEndSection": 1333,
"text": "These findings strongly suggest that the severe form of Hunter disease in this girl was the result of selective expression of the maternal allele carrying the missense mutation R468Q, which in turn resulted from skewed X inactivation of the paternal nonmutant X chromosome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23634718",
"endSection": "abstract",
"offsetInBeginSection": 1336,
"offsetInEndSection": 1463,
"text": "LUSIONS: This is a report of a female with a 10.6 Mb Xq27-28 deletion with skewed inactivation of the deleted X chromosome. Con"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9611068",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "Brother/sister siblings affected with Hunter disease: evidence for skewed X chromosome inactivation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2499679",
"endSection": "abstract",
"offsetInBeginSection": 277,
"offsetInEndSection": 406,
"text": "The normal X chromosome was preferentially inactivated, supporting the view that the translocation had disrupted the Hunter gene."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1678247",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "Hunter disease (mucopolysaccharidosis type II) associated with unbalanced inactivation of the X chromosomes in a karyotypically normal girl."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17345554",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 256,
"text": "INTRODUCTION: Hunter syndrome, or mucopolysaccharidosis type II, is an inherited disease linked to the X chromosome that is caused by a deficit of the enzyme iduronate-2-sulfatase and its main symptoms affect the bones, neurological system and the viscera."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17345554",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 247,
"text": "INTRODUCTION: Hunter syndrome, or mucopolysaccharidosis type II, is an inherited disease linked to the X chromosome that is caused by a deficit of the enzyme iduronate-2-sulfatase and its main symptoms affect the bones, neurological system and the"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21834048",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 301,
"text": "Mucopolysaccharidosis type II (MPS II, Hunter disease) is an X chromosome-linked inherited metabolic disease caused by mutations resulting in deficiency of activity of iduronate-2-sulfatase (IDS) and accumulation of undegraded glycosaminoglycans (GAGs), heparan sulfate, and dermatan sulfate. Previous"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20052546",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 93,
"text": "Mucopolysaccharidosis type II (MPS-II, Hunter disease) is a X-linked recessive disorder. Affe"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25044788",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 174,
"text": "Mucopolysaccharidosis type II (MPS II or Hunter syndrome) is a rare X-linked disorder caused by deficient activity of the lysosomal enzyme, iduronate-2-sulfatase (IDS). Pheno"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8807335",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Hunter disease or mucopolysaccharidosis type II is an X-linked disease caused by the deficiency of the lysosomal enzyme iduronate-2-sulfatase (IDS). Th"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22246721",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "Mucopolysaccharidosis type II (MPS II, Hunter syndrome) is an X-linked lysosomal storage disease caused by a deficiency of iduronate-2-sulfatase (IDS). Two a"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1642233",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 232,
"text": "We report the results of studies on the characterization of the mutation associated with marked unbalanced expression of the mutant X chromosome in a karyotypically normal girl with Hunter disease (mucopolysaccharidosis type II). So"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31046699",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "BACKGROUND: Hunter syndrome (mucopolysaccharidosis type II) is a recessive X-linked disorder due to mutations in the iduronate 2-sulfatase (IDS"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21062272",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 199,
"text": "Familial X-chromosome inactivation (XCI) skewing was investigated in a family in which a female mucopolysaccharidosis type II (MPS II) (Hunter syndrome, an X-linked genetic disease) occurred. Among e"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3100113",
"endSection": "abstract",
"offsetInBeginSection": 1180,
"offsetInEndSection": 1352,
"text": "Studies using BrdU indicated that the deleted X chromosome was consistently late replicating, and as a result the Hunter gene was fully expressed on the other X chromosome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1294876",
"endSection": "abstract",
"offsetInBeginSection": 1358,
"offsetInEndSection": 1479,
"text": "All mucopolysaccharidosis are autosomal recessive disorders, except for Hunter's syndrome that is X-linked and recessive."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1481858",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 109,
"text": "Female twin with Hunter disease due to nonrandom inactivation of the X-chromosome: a consequence of twinning."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31046699",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 150,
"text": "Hunter syndrome (mucopolysaccharidosis type II) is a recessive X-linked disorder due to mutations in the iduronate 2-sulfatase (IDS) gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9375851",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "Hunter disease is an X-linked recessive mucopolysaccharide storage disorder caused by iduronate-2-sulfatase deficiency and is rare in females."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9611068",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Hunter disease is an X-linked recessive disorder caused by a deficiency of iduronate-2-sulfatase activity."
}
]
| 11 | BioASQ-training11b | null | null | 60327e541cb411341a00013e | 172 |
yesno | Does Yersinia pestis causes a respiratory infection? | ['yes'] | [
"yes"
]
| ['Inhalation of Yersinia pestis results in primary pneumonic plague.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/17041851",
"http://www.ncbi.nlm.nih.gov/pubmed/26463167",
"http://www.ncbi.nlm.nih.gov/pubmed/16239527",
"http://www.ncbi.nlm.nih.gov/pubmed/26123398",
"http://www.ncbi.nlm.nih.gov/pubmed/25928467",
"http://www.ncbi.nlm.nih.gov/pubmed/25974210",
"http://www.ncbi.nlm.nih.gov/pubmed/16714568",
"http://www.ncbi.nlm.nih.gov/pubmed/19629028",
"http://www.ncbi.nlm.nih.gov/pubmed/12474416",
"http://www.ncbi.nlm.nih.gov/pubmed/16964684",
"http://www.ncbi.nlm.nih.gov/pubmed/24721571",
"http://www.ncbi.nlm.nih.gov/pubmed/25691593"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25691593",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 140,
"text": "Inhalation of Yersinia pestis results in primary pneumonic plague, a highly lethal and rapidly progressing necrotizing pneumonia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26123398",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 70,
"text": "Yersinia pestis causes the fatal respiratory disease pneumonic plague."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16714568",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Pulmonary infection by Yersinia pestis causes pneumonic plague, a rapidly progressing and often fatal disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16239527",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "Pulmonary infection with the bacterium Yersinia pestis causes pneumonic plague, an often-fatal disease for which no vaccine is presently available."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26123398",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 69,
"text": "Yersinia pestis causes the fatal respiratory disease pneumonic plague"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24721571",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "Pneumonic plague is a deadly respiratory disease caused by Yersinia pestis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25928467",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 236,
"text": "On July 8, 2014, the Colorado Department of Public Health and Environment (CDPHE) laboratory identified Yersinia pestis, the bacterium that causes plague, in a blood specimen collected from a man (patient A) hospitalized with pneumonia."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26123398",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 69,
"text": "Early emergence of Yersinia pestis as a severe respiratory pathogen."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17041851",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "The aerosol form of the bacterium Yersinia pestis causes the pneumonic plague, a rapidly fatal disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21859946",
"endSection": "abstract",
"offsetInBeginSection": 17,
"offsetInEndSection": 331,
"text": " plague bacterium, Yersinia pestis, has historically been regarded as one of the deadliest pathogens known to mankind, having caused three major pandemics. After being transmitted by the bite of an infected flea arthropod vector, Y. pestis can cause three forms of human plague: bubonic, septicemic, and pneumonic,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12474416",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 561,
"text": "Plague is an infectious disease caused by the Yersinia pestis microorganism, which is transmitted to the human host from a natural reservoir (different rodent species) by a flea bite. Plague is still encountered in humans in the areas of its enzootic prevalence in local rodent populations. Infection by flea bite results in a bubonic or septicemic plague, possibly complicated by secondary pneumonia. The person with pneumonic symptoms may be a source of a droplet-borne inhalatory infection for other people who consequently develop primary pneumonic plague. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26463167",
"endSection": "abstract",
"offsetInBeginSection": 13,
"offsetInEndSection": 166,
"text": "uring pneumonic plague, the bacterium Yersinia pestis elicits the development of inflammatory lung lesions that continue to expand throughout infection. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19629028",
"endSection": "abstract",
"offsetInBeginSection": 385,
"offsetInEndSection": 582,
"text": "In November 2006, the Uganda Ministry of Health received reports of an increase in bubonic plague cases and a possible outbreak of pneumonic plague among residents in the Arua and Nebbi districts. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25974210",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Pneumonic plague is a fatal disease caused by Yersinia pestis that is associated with a delayed immune response in the lungs"
}
]
| 6 | BioASQ-training6b | [
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D015010",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D015007",
"http://www.disease-ontology.org/api/metadata/DOID:0050069",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D015009"
]
| null | 58caf86f02b8c60953000030 | 173 |
yesno | Is golimumab effective for sarcoidosis? | ['no'] | [
"no"
]
| ['No, golimumab is not effective for treatment of sarcoidosis.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/29601563",
"http://www.ncbi.nlm.nih.gov/pubmed/25034562"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29601563",
"endSection": "abstract",
"offsetInBeginSection": 526,
"offsetInEndSection": 754,
"text": "Introduced monoclonal antibodies (infliximab, etanercept, adaluimumab, golimumab, rituximab), tested for efficacy in other pathologies associated with the formation of granulomas, have a limited application in patients with SA. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25034562",
"endSection": "abstract",
"offsetInBeginSection": 1399,
"offsetInEndSection": 1520,
"text": "Although treatment was well tolerated, neither ustekinumab nor golimumab demonstrated efficacy in pulmonary sarcoidosis. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25034562",
"endSection": "abstract",
"offsetInBeginSection": 1399,
"offsetInEndSection": 1519,
"text": "Although treatment was well tolerated, neither ustekinumab nor golimumab demonstrated efficacy in pulmonary sarcoidosis."
}
]
| 11 | BioASQ-training11b | null | null | 5e476b99d14c9f295d000001 | 174 |
yesno | As of Feb 2019, are major brain gangliosides a target for the treatment of Alzheimer's disease? | ['yes'] | [
"yes"
]
| ["As of Feb 2019, major brain gangliosides are proposed as a target for the treatment of Alzheimer's disease."] | [
"http://www.ncbi.nlm.nih.gov/pubmed/21274438",
"http://www.ncbi.nlm.nih.gov/pubmed/7997071"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21274438",
"endSection": "abstract",
"offsetInBeginSection": 1061,
"offsetInEndSection": 1222,
"text": "An understanding of the mechanism on the interaction of GM1 and Aβs in AD may contribute to the development of new neuroregenerative therapies for this disorder."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21274438",
"endSection": "abstract",
"offsetInBeginSection": 458,
"offsetInEndSection": 517,
"text": "Abnormal ganglioside metabolism also may occur in AD brains"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7997071",
"endSection": "abstract",
"offsetInBeginSection": 1036,
"offsetInEndSection": 1192,
"text": "Continuous intraventricular infusion of GM1 has recently been shown to have a significant beneficial effect in Alzheimer disease of early onset (AD Type I)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7997071",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 77,
"text": "Gangliosides--a new therapeutic agent against stroke and Alzheimer's disease."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7997071",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "Gangliosides--a new therapeutic agent against stroke and Alzheimer's disease.Gangliosides are glycosphingolipids localized to the outer leaflet of the plasma membrane of vertebrate cells. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7997071",
"endSection": "abstract",
"offsetInBeginSection": 1036,
"offsetInEndSection": 1196,
"text": "Continuous intraventricular infusion of GM1 has recently been shown to have a significant beneficial effect in Alzheimer disease of early onset (AD Type I).<br>"
}
]
| 11 | BioASQ-training11b | null | null | 5c72a5ca7c78d6947100006d | 175 |
yesno | Without immunization, rabies is a lethal disease. | ['yes'] | [
"yes"
]
| ['Rabies lethality is close to 100% without immunization.', 'Yes, without immunization, rabies is almost always a lethal disease. Rabies is a viral encephalitis that is statistically 100% fatal if left untreated. However, rabies is also one of the few infectious diseases that can be prevented through vaccination, providing almost 100% protection if administered early enough after exposure.', 'Rabies is a zoonotic disease caused primarily by the rabies virus (RABV) and is considered fatal without vaccination or treatment. The RABV infects the central nervous system, leading to symptoms such as fever, headache, fatigue, nausea, and ultimately progressing to more severe neurological signs like seizures, paralysis, and encephalitis. Without immunization through vaccination or post-exposure prophylaxis, rabies is almost always fatal once clinical symptoms appear.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/37728394",
"http://www.ncbi.nlm.nih.gov/pubmed/35931921",
"http://www.ncbi.nlm.nih.gov/pubmed/36343866"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35931921",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 77,
"text": "Rabies is a lethal zoonotic disease mainly transmitted to humans by dog bites"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36343866",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 89,
"text": "Rabies is an acute lethal infectious disease caused by a lyssavirus infection"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37728394",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 38,
"text": "Rabies, a lethal zoonotic encephalitis"
}
]
| 13 | BioASQ-training13b | null | null | 660d6a97fdcbea915f00003c | 176 |
yesno | Is diphosphatidylglycerol (cardiolipin) a phospholipid of the mitochondrial membranes? | ['yes'] | [
"yes"
]
| ['Yes, diphosphatidylglycerol (cardiolipin) is a phospholipid of the mitochondrial membranes.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/21599656",
"http://www.ncbi.nlm.nih.gov/pubmed/26028302",
"http://www.ncbi.nlm.nih.gov/pubmed/24905496",
"http://www.ncbi.nlm.nih.gov/pubmed/7378435",
"http://www.ncbi.nlm.nih.gov/pubmed/4322761",
"http://www.ncbi.nlm.nih.gov/pubmed/2397096",
"http://www.ncbi.nlm.nih.gov/pubmed/24007978",
"http://www.ncbi.nlm.nih.gov/pubmed/7794966",
"http://www.ncbi.nlm.nih.gov/pubmed/3668386",
"http://www.ncbi.nlm.nih.gov/pubmed/8143741",
"http://www.ncbi.nlm.nih.gov/pubmed/23200781",
"http://www.ncbi.nlm.nih.gov/pubmed/26301254",
"http://www.ncbi.nlm.nih.gov/pubmed/6257342",
"http://www.ncbi.nlm.nih.gov/pubmed/6509920",
"http://www.ncbi.nlm.nih.gov/pubmed/26396268",
"http://www.ncbi.nlm.nih.gov/pubmed/6807345",
"http://www.ncbi.nlm.nih.gov/pubmed/16971584",
"http://www.ncbi.nlm.nih.gov/pubmed/9370332",
"http://www.ncbi.nlm.nih.gov/pubmed/20336283",
"http://www.ncbi.nlm.nih.gov/pubmed/1213878",
"http://www.ncbi.nlm.nih.gov/pubmed/9843887",
"http://www.ncbi.nlm.nih.gov/pubmed/7459841",
"http://www.ncbi.nlm.nih.gov/pubmed/3548756",
"http://www.ncbi.nlm.nih.gov/pubmed/22634369",
"http://www.ncbi.nlm.nih.gov/pubmed/6717095",
"http://www.ncbi.nlm.nih.gov/pubmed/25182746",
"http://www.ncbi.nlm.nih.gov/pubmed/3718705",
"http://www.ncbi.nlm.nih.gov/pubmed/15460113",
"http://www.ncbi.nlm.nih.gov/pubmed/25843549",
"http://www.ncbi.nlm.nih.gov/pubmed/1550861",
"http://www.ncbi.nlm.nih.gov/pubmed/24443516",
"http://www.ncbi.nlm.nih.gov/pubmed/20637181",
"http://www.ncbi.nlm.nih.gov/pubmed/8977117",
"http://www.ncbi.nlm.nih.gov/pubmed/1247555",
"http://www.ncbi.nlm.nih.gov/pubmed/24769127"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24007978",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 341,
"text": "A unique organelle for studying membrane biochemistry is the mitochondrion whose functionality depends on a coordinated supply of proteins and lipids. Mitochondria are capable of synthesizing several lipids autonomously such as phosphatidylglycerol, cardiolipin and in part phosphatidylethanolamine, phosphatidic acid and CDP-diacylglycerol."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7459841",
"endSection": "abstract",
"offsetInBeginSection": 372,
"offsetInEndSection": 474,
"text": "A small decrease of diphosphatidylglycerol also occurred in the hepatoma mitochondria inner membrane. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6807345",
"endSection": "abstract",
"offsetInBeginSection": 492,
"offsetInEndSection": 624,
"text": "Diphosphatidylglycerol was confined to the mitochondrial fraction, where it represented about 7% of the total phosphoacylglycerols. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6717095",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 401,
"text": "Mitochondrial membranes were isolated from the myocardium of young (4-month-old) and aged (33-month-old) male Long-Evans rats and compared in terms of cholesterol content and phospholipid and fatty acid composition. In aged rats, as compared to young, the major observations include: markedly higher cholesterol content; increased percentage of sphingomyelin and diphosphatidylglycerol (cardiolipin); "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3548756",
"endSection": "abstract",
"offsetInBeginSection": 445,
"offsetInEndSection": 632,
"text": "The polyglycerophosphatides (typified by diphosphatidylglycerol) were apparently synthesized in situ by intramitochondrial membrane-bound enzymes using CDP-diglycerides as intermediates. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6509920",
"endSection": "abstract",
"offsetInBeginSection": 538,
"offsetInEndSection": 875,
"text": "Both the mitochondrial and microsomal fractions contained significant proportions of solvent front phospholipid (SFP) and whereas the mitochondrial SFP displayed the relatively unsaturated fatty acid composition characteristic of diphosphatidylglycerol (cardiolipin), the fatty acids of the microsomal SFP were distinctly more saturated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3718705",
"endSection": "abstract",
"offsetInBeginSection": 456,
"offsetInEndSection": 764,
"text": "Ten to 15% of microsomal radioactive CDP-diglycerides was transferred to mitochondrial membranes and incorporated into mitochondrial radioactive lipids identified as phosphatidylglycerol, phosphatidylglycerophosphate, and, when [14C]linoleoyl CDP-diglycerides were used, diphosphatidylglycerol (cardiolipin)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6257342",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 295,
"text": "The enzyme responsible for the conversion of phosphatidylglycerol to diphosphatidylglycerol (cardiolipin) in the presence of cytidine diphosphate diacylglycerol is firmly associated with mitochondrial membranes and is not extracted with hypotonic or hypertonic media or with nonionic detergents."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2397096",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 347,
"text": "The mechanism of cardiolipin (diphosphatidylglycerol) biosynthesis was examined in mitochondria and outer and inner mitochondrial membranes prepared from guinea pig and rat livers to determine whether this formation from phosphatidylglycerol was absolutely dependent on cytidinediphosphodiglyceride, as previously reported for intact mitochondria."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21599656",
"endSection": "abstract",
"offsetInBeginSection": 454,
"offsetInEndSection": 597,
"text": "In isolated mitochondrial outer membranes, cardiolipin (diphosphatidylglycerol) increased CPT1 activity 4-fold and the Km for carnitine 6-fold."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3718705",
"endSection": "abstract",
"offsetInBeginSection": 457,
"offsetInEndSection": 765,
"text": "Ten to 15% of microsomal radioactive CDP-diglycerides was transferred to mitochondrial membranes and incorporated into mitochondrial radioactive lipids identified as phosphatidylglycerol, phosphatidylglycerophosphate, and, when [14C]linoleoyl CDP-diglycerides were used, diphosphatidylglycerol (cardiolipin)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/4322761",
"endSection": "abstract",
"offsetInBeginSection": 499,
"offsetInEndSection": 615,
"text": "90% or more of the phospholipid, cardiolipin was found in the mitochondrial membranes of wild type and petite yeast."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2397096",
"endSection": "abstract",
"offsetInBeginSection": 629,
"offsetInEndSection": 760,
"text": "Furthermore, the same mechanism for the biosynthesis of cardiolipin was operational in the outer and inner mitochondrial membranes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2397096",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 346,
"text": "The mechanism of cardiolipin (diphosphatidylglycerol) biosynthesis was examined in mitochondria and outer and inner mitochondrial membranes prepared from guinea pig and rat livers to determine whether this formation from phosphatidylglycerol was absolutely dependent on cytidinediphosphodiglyceride, as previously reported for intact mitochondria"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24443516",
"endSection": "abstract",
"offsetInBeginSection": 65,
"offsetInEndSection": 246,
"text": "Cardiolipin (CL) is a key phospholipid in mitochondrial membranes, playing important roles in maintaining the functional integrity and dynamics of mitochondria in animals and yeasts"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23200781",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "Cardiolipin, the specific phospholipid of mitochondria, is involved in the biogenesis, the dynamics, and the supramolecular organization of mitochondrial membranes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26301254",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "Cardiolipin (CL), the signature phospholipid of mitochondrial membranes, is crucial for both mitochondrial function and cellular processes outside of the mitochondria"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24769127",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 231,
"text": "Since it has been recognized that mitochondria are crucial not only for energy metabolism but also for other cellular functions, there has been a growing interest in cardiolipin, the specific phospholipid of mitochondrial membranes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25843549",
"endSection": "abstract",
"offsetInBeginSection": 72,
"offsetInEndSection": 259,
"text": "Cardiolipin, the main anionic phospholipid in mitochondrial membranes, is expected to be a determinant in this adaptive mechanism since it modulates the activity of most membrane proteins"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3718705",
"endSection": "abstract",
"offsetInBeginSection": 457,
"offsetInEndSection": 764,
"text": "Ten to 15% of microsomal radioactive CDP-diglycerides was transferred to mitochondrial membranes and incorporated into mitochondrial radioactive lipids identified as phosphatidylglycerol, phosphatidylglycerophosphate, and, when [14C]linoleoyl CDP-diglycerides were used, diphosphatidylglycerol (cardiolipin)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26396268",
"endSection": "abstract",
"offsetInBeginSection": 247,
"offsetInEndSection": 530,
"text": "Cardiolipin is normally localized to the inner mitochondrial membrane; however, when cardiolipin becomes externalized to the surface of dysregulated mitochondria, it promotes inflammasome activation and stimulates the elimination of damaged or nonfunctional mitochondria by mitophagy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21599656",
"endSection": "abstract",
"offsetInBeginSection": 454,
"offsetInEndSection": 598,
"text": "In isolated mitochondrial outer membranes, cardiolipin (diphosphatidylglycerol) increased CPT1 activity 4-fold and the Km for carnitine 6-fold. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24905496",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Increasing levels of cardiolipin differentially influence packing of phospholipids found in the mitochondrial inner membrane."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25843549",
"endSection": "abstract",
"offsetInBeginSection": 261,
"offsetInEndSection": 440,
"text": "Here, we used Saccharomyces cerevisiae subjected to conditions that affect mitochondrial metabolism as a model to determine the possible role of cardiolipin in stress adaptation. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8977117",
"endSection": "abstract",
"offsetInBeginSection": 290,
"offsetInEndSection": 684,
"text": "This decline of respiration was attributed to a progressive diminution of the number of mitochondria in copper-treated cells, based on the demonstration of the concomitant decline of (1) cardiolipin (diphosphatidylglycerol) and cytochrome aa3 (cytochrome oxidase), two specific markers of mitochondrial inner membrane, and (2) fumarase activity, a specific marker of mitochondrial matrix space."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15460113",
"endSection": "abstract",
"offsetInBeginSection": 327,
"offsetInEndSection": 477,
"text": "Diphosphatidylglycerol (DPG) or cardiolipin, a specific component of the inner mitochondrial membrane, represents about 4% of the total lipid content."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2397096",
"endSection": "abstract",
"offsetInBeginSection": 348,
"offsetInEndSection": 628,
"text": "Experimental results confirmed that the biosynthesis of cardiolipin, from the membrane-bound radioactive phosphatidylglycerol in intact mitochondria isolated from guinea pig and rat liver, was absolutely dependent on CDP-diglycerides and required the addition of divalent cations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7378435",
"endSection": "abstract",
"offsetInBeginSection": 561,
"offsetInEndSection": 776,
"text": "We have shown that decrease of cardiolipin in mitochondrial membrane occurs early during ischemia, and only during the irreversible phase of ischemia are phosphatidylethanolamine and phosphatidylcholine broken down."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6257342",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "Partial purification of diphosphatidylglycerol synthetase from liver mitochondrial membranes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7459841",
"endSection": "abstract",
"offsetInBeginSection": 372,
"offsetInEndSection": 473,
"text": "A small decrease of diphosphatidylglycerol also occurred in the hepatoma mitochondria inner membrane."
}
]
| 6 | BioASQ-training6b | [
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002308",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D008566",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D008563",
"http://www.biosemantics.org/jochem#http://www.biosemantics.org/jochem#:4244279",
"http://www.biosemantics.org/jochem#4001026",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D008928",
"http://www.biosemantics.org/jochem#4244279",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D051336"
]
| [
{
"o": "Phospholipid",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C0202177"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A17997459",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0007188"
},
{
"o": "Cardiolipins",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A17997459"
},
{
"o": "http://linkedlifedata.com/resource/rxnorm/label/3130515",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/rxnorm/id/2083"
},
{
"o": "Cardiolipins",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/rxnorm/label/3130515"
},
{
"o": "cardiolipin",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C0007188"
},
{
"o": "http://linkedlifedata.com/resource/rxnorm/label/3130514",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/rxnorm/id/2083"
},
{
"o": "Cardiolipin",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/rxnorm/label/3130514"
}
]
| 58d90f228acda3452900000f | 177 |
yesno | Should dacomitinib be used for treatment of glioblastoma patients? | ['no'] | [
"no"
]
| ['No, dacomitinib has a limited single-agent activity in recurrent glioblastoma with EGFR amplification.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/28575464",
"http://www.ncbi.nlm.nih.gov/pubmed/30247945"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30247945",
"endSection": "abstract",
"offsetInBeginSection": 1003,
"offsetInEndSection": 1150,
"text": "Expert opinion: Despite the poor global results of Dacomitinib in recurrent GB shown in a phase II trial, some patients had a significant benefit. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28575464",
"endSection": "abstract",
"offsetInBeginSection": 1498,
"offsetInEndSection": 1599,
"text": "Conclusions: Dacomitinib has a limited single-agent activity in recurrent GB with EGFR amplification."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30247945",
"endSection": "abstract",
"offsetInBeginSection": 989,
"offsetInEndSection": 1135,
"text": "Expert opinion: Despite the poor global results of Dacomitinib in recurrent GB shown in a phase II trial, some patients had a significant benefit."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30247945",
"endSection": "abstract",
"offsetInBeginSection": 1010,
"offsetInEndSection": 1156,
"text": "Expert opinion: Despite the poor global results of Dacomitinib in recurrent GB shown in a phase II trial, some patients had a significant benefit."
}
]
| 11 | BioASQ-training11b | null | null | 5c73acea7c78d69471000085 | 178 |
yesno | Can cognitive behavioral therapy improve fatigue in cancer patients? | ['yes'] | [
"yes"
]
| ['Yes, it has been documented that cognitive behavioral therapy reduces fatigue symptom severity in cancer patients. In addition, cognitive behavioral therapy has been also shown to improve mood and overall quality of life, and it can be successfully delivered through a variety of treatment modalities in patients with cancer.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/25299140",
"http://www.ncbi.nlm.nih.gov/pubmed/25233905",
"http://www.ncbi.nlm.nih.gov/pubmed/25150812",
"http://www.ncbi.nlm.nih.gov/pubmed/25083010",
"http://www.ncbi.nlm.nih.gov/pubmed/24971014",
"http://www.ncbi.nlm.nih.gov/pubmed/24650832",
"http://www.ncbi.nlm.nih.gov/pubmed/24458595",
"http://www.ncbi.nlm.nih.gov/pubmed/24419112",
"http://www.ncbi.nlm.nih.gov/pubmed/23707383",
"http://www.ncbi.nlm.nih.gov/pubmed/23557323",
"http://www.ncbi.nlm.nih.gov/pubmed/20890148",
"http://www.ncbi.nlm.nih.gov/pubmed/20656618",
"http://www.ncbi.nlm.nih.gov/pubmed/20651011",
"http://www.ncbi.nlm.nih.gov/pubmed/19900778",
"http://www.ncbi.nlm.nih.gov/pubmed/19450037",
"http://www.ncbi.nlm.nih.gov/pubmed/18246853",
"http://www.ncbi.nlm.nih.gov/pubmed/21538678",
"http://www.ncbi.nlm.nih.gov/pubmed/21372697",
"http://www.ncbi.nlm.nih.gov/pubmed/17050873",
"http://www.ncbi.nlm.nih.gov/pubmed/22926087",
"http://www.ncbi.nlm.nih.gov/pubmed/19090531",
"http://www.ncbi.nlm.nih.gov/pubmed/20930100"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25299140",
"endSection": "abstract",
"offsetInBeginSection": 536,
"offsetInEndSection": 697,
"text": "Physical activity, educational interventions, and cognitive-behavioral therapy have the most supportive data and can be recommended to patients with confidence. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25233905",
"endSection": "abstract",
"offsetInBeginSection": 1201,
"offsetInEndSection": 1327,
"text": "For women undergoing radiotherapy (3 RCTs), hypnosis combined with cognitive-behavioral therapy improved distress and fatigue."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25150812",
"endSection": "abstract",
"offsetInBeginSection": 1327,
"offsetInEndSection": 1452,
"text": "Patients in the CBT group reported a significantly larger decrease in fatigue scores than patients in the waiting list group."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25083010",
"endSection": "abstract",
"offsetInBeginSection": 1128,
"offsetInEndSection": 1327,
"text": "However, relative to VCBT-I, PCBT-I was associated with significantly greater improvements of insomnia severity, early morning awakenings, depression, fatigue, and dysfunctional beliefs about sleep. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24971014",
"endSection": "abstract",
"offsetInBeginSection": 1204,
"offsetInEndSection": 1458,
"text": "CBT-I may also improve mood, fatigue, and overall quality of life, and can be successfully delivered through a variety of treatment modalities, making it possible to reach a broader range of patients who may not have access to more traditional programs. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24650832",
"endSection": "abstract",
"offsetInBeginSection": 1296,
"offsetInEndSection": 1378,
"text": "No group differences in improvement were noted relative to QOL, fatigue, or mood. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24458595",
"endSection": "abstract",
"offsetInBeginSection": 1715,
"offsetInEndSection": 1806,
"text": "In case of persistent fatigue, personalized cognitive behavioral therapy can be considered."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24419112",
"endSection": "abstract",
"offsetInBeginSection": 1423,
"offsetInEndSection": 1567,
"text": "ONCLUSION: The results support CBTH as an evidence-based intervention to control fatigue in patients undergoing radiotherapy for breast cancer. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23707383",
"endSection": "abstract",
"offsetInBeginSection": 156,
"offsetInEndSection": 331,
"text": "Severe fatigue after cancer treatment can be treated effectively with cognitive behavioral therapy (CBT), but it is unclear whether CBT has an effect on cognitive functioning."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23707383",
"endSection": "abstract",
"offsetInBeginSection": 1590,
"offsetInEndSection": 1681,
"text": "CONCLUSION: CBT for post-cancer fatigue has already been shown to be an effective therapy. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23557323",
"endSection": "abstract",
"offsetInBeginSection": 309,
"offsetInEndSection": 549,
"text": "Frequently reported side effects include cancer-related fatigue, peripheral neuropathy, and psychological distress. Exercise and cognitive behavioral therapy interventions have counteracted such adverse effects in other cancer populations. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20656618",
"endSection": "abstract",
"offsetInBeginSection": 783,
"offsetInEndSection": 1142,
"text": "There is evidence from methodologically rigorous controlled trials that exercise, psycho-educational interventions, and cognitive-behavioral therapy for insomnia are effective in the treatment of CRF, and a wide range of pharmacologic and nonpharmacologic interventions has shown initial promise in single-arm pilot studies with small, heterogeneous samples. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20651011",
"endSection": "abstract",
"offsetInBeginSection": 2060,
"offsetInEndSection": 2535,
"text": "CONCLUSIONS: Physical training combined with cognitive-behavioral therapy and physical training alone had significant and beneficial effects on fatigue compared with no intervention. Physical training was equally effective as or more effective than physical training combined with cognitive-behavioral therapy in reducing cancer-related fatigue, suggesting that cognitive-behavioral therapy did not have additional beneficial effects beyond the benefits of physical training."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19900778",
"endSection": "abstract",
"offsetInBeginSection": 1092,
"offsetInEndSection": 1262,
"text": "RESULTS: Imagery/hypnosis and CBT/CST interventions have produced improvement in all the three cancer-related symptoms individually: pain, fatigue, and sleep disturbance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19450037",
"endSection": "abstract",
"offsetInBeginSection": 805,
"offsetInEndSection": 1139,
"text": "RESULTS: Multilevel modeling indicated that for weekly FACIT fatigue data, there was a significant effect of the CBTH intervention on the rate of change in fatigue (p < .05), such that on average, CBTH participants' fatigue did not increase over the course of treatment, whereas control group participants' fatigue increased linearly."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19450037",
"endSection": "abstract",
"offsetInBeginSection": 1194,
"offsetInEndSection": 1347,
"text": "ONCLUSION: The results suggest that CBTH is an effective means for controlling and potentially preventing fatigue in breast cancer radiotherapy patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18246853",
"endSection": "abstract",
"offsetInBeginSection": 467,
"offsetInEndSection": 596,
"text": "Results were consistent with the view that CBTH was effective in managing fatigue and skin discomfort, and increasing relaxation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21538678",
"endSection": "abstract",
"offsetInBeginSection": 867,
"offsetInEndSection": 1314,
"text": "RESULTS: Participants in the Internet group showed significant improvements at post-assessment compared with those in the control group in overall insomnia severity (F(1,26) = 22.8; p<0.001), sleep efficiency (F(1,24) = 11.45; P = 0.002), sleep onset latency (F(1,24) = 5.18; P = 0.03), soundness of sleep (F(1,24) = 9.34; P = 0.005), restored feeling upon awakening (F(1,24) = 11.95; P = 0.002), and general fatigue (F(1,26) = 13.88; P = 0.001). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21372697",
"endSection": "abstract",
"offsetInBeginSection": 136,
"offsetInEndSection": 339,
"text": "Cognitive-behavior therapy (CBT) has alleviated fatigue and improved QOL of cancer patients; however, little is known about the effects of nurse-led CBT on breast cancer patients undergoing radiotherapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20651011",
"endSection": "abstract",
"offsetInBeginSection": 2243,
"offsetInEndSection": 2535,
"text": "Physical training was equally effective as or more effective than physical training combined with cognitive-behavioral therapy in reducing cancer-related fatigue, suggesting that cognitive-behavioral therapy did not have additional beneficial effects beyond the benefits of physical training."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25233905",
"endSection": "abstract",
"offsetInBeginSection": 1201,
"offsetInEndSection": 1327,
"text": "For women undergoing radiotherapy (3 RCTs), hypnosis combined with cognitive-behavioral therapy improved distress and fatigue."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21372697",
"endSection": "abstract",
"offsetInBeginSection": 124,
"offsetInEndSection": 327,
"text": "Cognitive-behavior therapy (CBT) has alleviated fatigue and improved QOL of cancer patients; however, little is known about the effects of nurse-led CBT on breast cancer patients undergoing radiotherapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20651011",
"endSection": "abstract",
"offsetInBeginSection": 2151,
"offsetInEndSection": 2443,
"text": "Physical training was equally effective as or more effective than physical training combined with cognitive-behavioral therapy in reducing cancer-related fatigue, suggesting that cognitive-behavioral therapy did not have additional beneficial effects beyond the benefits of physical training."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21372697",
"endSection": "abstract",
"offsetInBeginSection": 124,
"offsetInEndSection": 327,
"text": "Cognitive-behavior therapy (CBT) has alleviated fatigue and improved QOL of cancer patients; however, little is known about the effects of nurse-led CBT on breast cancer patients undergoing radiotherapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21372697",
"endSection": "abstract",
"offsetInBeginSection": 124,
"offsetInEndSection": 327,
"text": "Cognitive-behavior therapy (CBT) has alleviated fatigue and improved QOL of cancer patients; however, little is known about the effects of nurse-led CBT on breast cancer patients undergoing radiotherapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18310181",
"endSection": "abstract",
"offsetInBeginSection": 1892,
"offsetInEndSection": 2038,
"text": "The positive effects of cognitive behavioral therapy in adolescents with chronic fatigue syndrome are sustained after cognitive behavioral therapy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20651011",
"endSection": "abstract",
"offsetInBeginSection": 2151,
"offsetInEndSection": 2443,
"text": "Physical training was equally effective as or more effective than physical training combined with cognitive-behavioral therapy in reducing cancer-related fatigue, suggesting that cognitive-behavioral therapy did not have additional beneficial effects beyond the benefits of physical training."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21372697",
"endSection": "abstract",
"offsetInBeginSection": 124,
"offsetInEndSection": 327,
"text": "Cognitive-behavior therapy (CBT) has alleviated fatigue and improved QOL of cancer patients; however, little is known about the effects of nurse-led CBT on breast cancer patients undergoing radiotherapy."
}
]
| 5 | BioASQ-training5b | []
| []
| 54d762653706e89528000014 | 179 |
yesno | Based on clinical trial data, can pioglitazone delay cognitive impairment for people at risk for Alzheimer's disease? | ['no'] | [
"no"
]
| ['No. Pioglitazone did not delay the onset of mild cognitive impairment.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/34146512"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34146512",
"endSection": "abstract",
"offsetInBeginSection": 3711,
"offsetInEndSection": 3793,
"text": "INTERPRETATION: Pioglitazone did not delay the onset of mild cognitive impairment."
}
]
| 12 | BioASQ-training12b | null | null | 64040edf201352f04a000011 | 180 |
yesno | Do brown fat cells produce heat? | ['yes'] | [
"yes"
]
| ['Yes, brown fat cells produce heat.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23834768",
"http://www.ncbi.nlm.nih.gov/pubmed/26910308",
"http://www.ncbi.nlm.nih.gov/pubmed/22796012",
"http://www.ncbi.nlm.nih.gov/pubmed/21196229",
"http://www.ncbi.nlm.nih.gov/pubmed/23818608",
"http://www.ncbi.nlm.nih.gov/pubmed/6148836",
"http://www.ncbi.nlm.nih.gov/pubmed/3083882",
"http://www.ncbi.nlm.nih.gov/pubmed/26496384",
"http://www.ncbi.nlm.nih.gov/pubmed/26322018",
"http://www.ncbi.nlm.nih.gov/pubmed/15058310",
"http://www.ncbi.nlm.nih.gov/pubmed/6819159",
"http://www.ncbi.nlm.nih.gov/pubmed/21982742",
"http://www.ncbi.nlm.nih.gov/pubmed/24567786",
"http://www.ncbi.nlm.nih.gov/pubmed/27528872",
"http://www.ncbi.nlm.nih.gov/pubmed/8042786",
"http://www.ncbi.nlm.nih.gov/pubmed/25642708",
"http://www.ncbi.nlm.nih.gov/pubmed/962510",
"http://www.ncbi.nlm.nih.gov/pubmed/27528697",
"http://www.ncbi.nlm.nih.gov/pubmed/27552974",
"http://www.ncbi.nlm.nih.gov/pubmed/1550210",
"http://www.ncbi.nlm.nih.gov/pubmed/25068090",
"http://www.ncbi.nlm.nih.gov/pubmed/2039657",
"http://www.ncbi.nlm.nih.gov/pubmed/21123942",
"http://www.ncbi.nlm.nih.gov/pubmed/9277366",
"http://www.ncbi.nlm.nih.gov/pubmed/24129212",
"http://www.ncbi.nlm.nih.gov/pubmed/5262992",
"http://www.ncbi.nlm.nih.gov/pubmed/24046370",
"http://www.ncbi.nlm.nih.gov/pubmed/26912151",
"http://www.ncbi.nlm.nih.gov/pubmed/6315457",
"http://www.ncbi.nlm.nih.gov/pubmed/541897",
"http://www.ncbi.nlm.nih.gov/pubmed/25466254",
"http://www.ncbi.nlm.nih.gov/pubmed/16594742",
"http://www.ncbi.nlm.nih.gov/pubmed/26749900",
"http://www.ncbi.nlm.nih.gov/pubmed/22654830",
"http://www.ncbi.nlm.nih.gov/pubmed/19641492"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24567786",
"endSection": "abstract",
"offsetInBeginSection": 271,
"offsetInEndSection": 512,
"text": "WAT and BAT are both involved in energy balance. WAT is mainly involved in the storage and mobilization of energy in the form of triglycerides, whereas BAT specializes in dissipating energy as heat during cold- or diet-induced thermogenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25466254",
"endSection": "abstract",
"offsetInBeginSection": 76,
"offsetInEndSection": 288,
"text": "Because brown adipose tissue (BAT) dissipates energy in the form of heat, increasing energy expenditure by augmenting BAT-mediated thermogenesis may represent an approach to counter obesity and its complications."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23818608",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 254,
"text": "Classic brown fat and inducible beige fat both dissipate chemical energy in the form of heat through the actions of mitochondrial uncoupling protein 1. This nonshivering thermogenesis is crucial for mammals as a defense against cold and obesity/diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22654830",
"endSection": "abstract",
"offsetInBeginSection": 105,
"offsetInEndSection": 245,
"text": "Mitochondrial uncoupling protein 1 in brown fat cells produces heat by dissipating the energy generated by fatty acid and glucose oxidation."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21196229",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 36,
"text": "Brown fat biology and thermogenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21196229",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 75,
"text": "Brown fat (brown adipose tissue, BAT) primary function is to produce heat. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/962510",
"endSection": "abstract",
"offsetInBeginSection": 165,
"offsetInEndSection": 353,
"text": "Brown fat cells were classified into 6 types: Type 1 cells are fat-depleted cells filled with granular cytoplasm and are believed to be produced after oxidation of fat for heat production."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9277366",
"endSection": "abstract",
"offsetInBeginSection": 1226,
"offsetInEndSection": 1487,
"text": "Calorimetric measurements from cell suspensions showed that ATP increased basal heat production of isolated brown fat cells by approximately 40% but had no effect on the greater than fivefold increase in heat production seen with maximal adrenergic stimulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23818608",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Classic brown fat and inducible beige fat both dissipate chemical energy in the form of heat through the actions of mitochondrial uncoupling protein 1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21982742",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 182,
"text": "Brown adipocytes oxidize fatty acids to produce heat in response to cold or to excessive energy intake; stimulation of brown fat development and function may thus counteract obesity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/962510",
"endSection": "abstract",
"offsetInBeginSection": 1032,
"offsetInEndSection": 1285,
"text": "The occurrence of Types 1 and/or 6 cells that has been revealed in 65 out of the total 180 samples (36%), suggests that the oxidation of fat for the thermogenesis proceeds in the brown fat tissue and that brown fat cells partially undergo fat depletion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/962510",
"endSection": "abstract",
"offsetInBeginSection": 166,
"offsetInEndSection": 354,
"text": "Brown fat cells were classified into 6 types: Type 1 cells are fat-depleted cells filled with granular cytoplasm and are believed to be produced after oxidation of fat for heat production."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26322018",
"endSection": "abstract",
"offsetInBeginSection": 126,
"offsetInEndSection": 333,
"text": "In response to cold, both classical brown fat and the newly identified \"beige\" or \"brite\" cells are activated by β-adrenergic signaling and catabolize stored lipids and carbohydrates to produce heat via UCP1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26496384",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "The ability of brown adipocytes (fat cells) to dissipate energy as heat shows great promise for the treatment of obesity and other metabolic disorders"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24046370",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "Inappropriate heat dissipation ignites brown fat thermogenesis in mice with a mutant thyroid hormone receptor α1"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25068090",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 64,
"text": "Brown fat and vascular heat dissipation: The new cautionary tail"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21123942",
"endSection": "abstract",
"offsetInBeginSection": 255,
"offsetInEndSection": 458,
"text": "Brown adipose produces heat as a defense against hypothermia and obesity, and the appearance of brown-like adipocytes within white adipose tissue depots is associated with improved metabolic phenotypes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/962510",
"endSection": "abstract",
"offsetInBeginSection": 1764,
"offsetInEndSection": 1902,
"text": "In the same manner, marked ability to produce a considerable amount of heat was evidenced in brown fat tissue of children and teenagers. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/962510",
"endSection": "abstract",
"offsetInBeginSection": 166,
"offsetInEndSection": 355,
"text": "Brown fat cells were classified into 6 types: Type 1 cells are fat-depleted cells filled with granular cytoplasm and are believed to be produced after oxidation of fat for heat production. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8042786",
"endSection": "abstract",
"offsetInBeginSection": 1616,
"offsetInEndSection": 1739,
"text": "It is inferred that brown-adipose-tissue heat production is reduced during (and probably also some time after) anesthesia. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3083882",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "Parallel measurements of heat production and thermogenin content in brown fat cells during cold acclimation of rats."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27528872",
"endSection": "abstract",
"offsetInBeginSection": 39,
"offsetInEndSection": 287,
"text": "The classical white adipose tissue builds up energy in the form of triglycerides and is useful for preventing fatigue during periods of low caloric intake and the brown adipose tissue instead of inducing fat accumulation can produce energy as heat."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26322018",
"endSection": "abstract",
"offsetInBeginSection": 126,
"offsetInEndSection": 334,
"text": "In response to cold, both classical brown fat and the newly identified \"beige\" or \"brite\" cells are activated by β-adrenergic signaling and catabolize stored lipids and carbohydrates to produce heat via UCP1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23834768",
"endSection": "abstract",
"offsetInBeginSection": 103,
"offsetInEndSection": 245,
"text": "White adipose tissue stores energy reserves as fat, whereas the metabolic function of brown adipose tissue is lipid oxidation to produce heat."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6148836",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 87,
"text": "The main function of brown adipose tissue (BAT) is to produce heat in response to cold."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24129212",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "Brown adipocytes oxidize fatty acids to produce heat in response to cold or caloric overfeeding."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21196229",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "Brown fat (brown adipose tissue, BAT) primary function is to produce heat."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15058310",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 293,
"text": "Adipose tissue plays an active role in energy balance because it is not only a lipid storing and mobilizing tissue but consists of functionally specialized tissues able to produce heat (in brown adipose tissue) and to produce or release a vast number of so called adipokines or adipocytokines."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25642708",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "Brown adipose tissue (BAT), a specialized fat that dissipates energy to produce heat, plays an important role in the regulation of energy balance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19641492",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 138,
"text": "Brown adipose cells are specialized to dissipate chemical energy in the form of heat, as a physiological defence against cold and obesity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/962510",
"endSection": "abstract",
"offsetInBeginSection": 1286,
"offsetInEndSection": 1430,
"text": "In the present study, the thermogenesis of human brown fat tissue was suggested chiefly with regard to the occurrence of Types 1 and/or 6 cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/962510",
"endSection": "abstract",
"offsetInBeginSection": 1764,
"offsetInEndSection": 1901,
"text": "In the same manner, marked ability to produce a considerable amount of heat was evidenced in brown fat tissue of children and teenagers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26749900",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "Adult humans have heat-producing and energy-consuming brown adipose tissue in the clavicular region of the neck."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27552974",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "Brown and beige adipocytes expend chemical energy to produce heat and are therefore important in regulating body temperature and body weight."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2039657",
"endSection": "abstract",
"offsetInBeginSection": 2005,
"offsetInEndSection": 2203,
"text": "In human perirenal brown fat tissue, darkly stained fat-depleted cells (D) occupy, with other cell types (CR, CR'), an important part in the reversible heat production cycle of the brown fat tissue."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26912151",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "Brown fat is a specialized fat depot that can increase energy expenditure and produce heat."
}
]
| 6 | BioASQ-training6b | [
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002477",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002001",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D052437",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D006359",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D005223"
]
| [
{
"o": "Heat",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C0018837"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A0066521",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0018837"
},
{
"o": "Heat",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A0066521"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A18591807",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0018837"
},
{
"o": "heat",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A18591807"
}
]
| 58ca906a02b8c6095300002e | 181 |
yesno | Can antisense threapy be used for Huntington's disease? | ['yes'] | [
"yes"
]
| ["Yes, antisense oligonucleotide therapy has been shown to lower Huntingtin mRNA levels and be beneficial against Huntington's disease."] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22726826"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22726826",
"endSection": "abstract",
"offsetInBeginSection": 89,
"offsetInEndSection": 290,
"text": "In this issue of Neuron, Kordasiewicz et al. (2012) show the benefit of transient antisense oligonucleotide (ASO) therapy to degrade Huntingtin mRNA and elicit sustained therapeutic benefit in HD mice."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22726826",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 84,
"text": "\"Huntingtin holiday\": progress toward an antisense therapy for Huntington's disease."
}
]
| 11 | BioASQ-training11b | null | null | 5c900779ecadf2e73f000001 | 183 |
yesno | Is sonidegib effective for basal cell carcinoma? | ['yes'] | [
"yes"
]
| ['Yes. Sonidegib, an oral smoothened antagonist, is indicated for the treatment of adults with locally advanced basal cell carcinoma (laBCC) who are not candidates for surgery or radiation therapy, or adults with recurrent laBCC following surgery or radiation therapy.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/26867946",
"http://www.ncbi.nlm.nih.gov/pubmed/27189494",
"http://www.ncbi.nlm.nih.gov/pubmed/27636236",
"http://www.ncbi.nlm.nih.gov/pubmed/26566923",
"http://www.ncbi.nlm.nih.gov/pubmed/26780190",
"http://www.ncbi.nlm.nih.gov/pubmed/26546616",
"http://www.ncbi.nlm.nih.gov/pubmed/27695345",
"http://www.ncbi.nlm.nih.gov/pubmed/25981810",
"http://www.ncbi.nlm.nih.gov/pubmed/27538055",
"http://www.ncbi.nlm.nih.gov/pubmed/26833519",
"http://www.ncbi.nlm.nih.gov/pubmed/26323341",
"http://www.ncbi.nlm.nih.gov/pubmed/24523439",
"http://www.ncbi.nlm.nih.gov/pubmed/27511905",
"http://www.ncbi.nlm.nih.gov/pubmed/24773312",
"http://www.ncbi.nlm.nih.gov/pubmed/25646180",
"http://www.ncbi.nlm.nih.gov/pubmed/27067394",
"http://www.ncbi.nlm.nih.gov/pubmed/27096888",
"http://www.ncbi.nlm.nih.gov/pubmed/26614022",
"http://www.ncbi.nlm.nih.gov/pubmed/27376162"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26566923",
"endSection": "abstract",
"offsetInBeginSection": 253,
"offsetInEndSection": 556,
"text": "This review of the literature aims to describe previous and current treatment options for oral therapy in locally advanced and metastatic NMSC otherwise unamenable to standard treatment. Oral Smoothened (Smo) inhibitors Vismodegib, Sonidegib, and Taladegib have shown to be effective in several trials. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26780190",
"endSection": "abstract",
"offsetInBeginSection": 589,
"offsetInEndSection": 745,
"text": "Sonidegib is a new smoothened inhibitor currently under investigation for treatment of laBCC, which demonstrates a comparable safety profile to vismodegib. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26833519",
"endSection": "abstract",
"offsetInBeginSection": 881,
"offsetInEndSection": 1067,
"text": "The recent development of novel hedgehog pathway inhibitors for high-risk BCC (including oral vismodegib and sonidegib) may represent a paradigm shift towards medical management of NMSC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26867946",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 278,
"text": "Sonidegib (Odomzo®), an oral smoothened (SMO) antagonist, is indicated for the treatment of adults with locally advanced basal cell carcinoma (laBCC) who are not candidates for surgery or radiation therapy, or adults with recurrent laBCC following surgery or radiation therapy. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26867946",
"endSection": "abstract",
"offsetInBeginSection": 1290,
"offsetInEndSection": 1620,
"text": "The acceptable benefit-risk profile of sonidegib, along with a paucity of treatment options and the seriousness of the condition, makes sonidegib an emerging option for the treatment of adults with laBCC that has recurred following surgery or radiation therapy, or in those who are not candidates for surgery or radiation therapy."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27376162",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 59,
"text": "Sonidegib phosphate: new approval for basal cell carcinoma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27695345",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "Sonidegib, a novel smoothened inhibitor for the treatment of advanced basal cell carcinoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25981810",
"endSection": "abstract",
"offsetInBeginSection": 2322,
"offsetInEndSection": 2734,
"text": "Serious adverse events occurred in 11 (14%) of 79 patients in the 200 mg group and 45 (30%) of 150 patients in the 800 mg group.The benefit-to-risk profile of 200 mg sonidegib might offer a new treatment option for patients with advanced basal cell carcinoma, a population that is difficult to treat.Novartis Pharmaceuticals Corporation.<CopyrightInformation>Copyright © 2015 Elsevier Ltd. All rights reserved.</"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25646180",
"endSection": "abstract",
"offsetInBeginSection": 591,
"offsetInEndSection": 956,
"text": "However, to date, Hh inhibitors, specifically those targeting Smoothened [such as vismodegib, BMS-833923, saridegib (IPI-926), sonidegib/erismodegib (LDE225), PF-04449913, LY2940680, LEQ 506, and TAK-441], have demonstrated good efficacy as monotherapy in patients with basal cell carcinoma and medulloblastoma, but have shown limited activity in other tumor types."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27067394",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 626,
"text": "The hedgehog pathway inhibitor sonidegib demonstrated meaningful tumor shrinkage in more than 90% of patients with locally advanced basal cell carcinoma (BCC) or metastatic BCC in the BCC Outcomes with LDE225 Treatment study.This report provides long-term follow-up data collected up to 12 months after the last patient was randomized.In this multicenter, randomized, double-blind phase II study, patients were randomized 1:2 to sonidegib 200 or 800 mg. The primary end point was objective response rate assessed by central review.Objective response rates in the 200- and 800-mg arms were 57.6% and 43.8% in locally advanced B"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25981810",
"endSection": "abstract",
"offsetInBeginSection": 2322,
"offsetInEndSection": 2735,
"text": "Serious adverse events occurred in 11 (14%) of 79 patients in the 200 mg group and 45 (30%) of 150 patients in the 800 mg group.The benefit-to-risk profile of 200 mg sonidegib might offer a new treatment option for patients with advanced basal cell carcinoma, a population that is difficult to treat.Novartis Pharmaceuticals Corporation.<CopyrightInformation>Copyright © 2015 Elsevier Ltd. All rights reserved.</C"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26323341",
"endSection": "abstract",
"offsetInBeginSection": 384,
"offsetInEndSection": 709,
"text": "Oral sonidegib is approved in Switzerland for the treatment of adult patients with advanced basal cell carcinoma (BCC) and in the US and EU for the treatment of adult patients with locally advanced BCC that has recurred following surgery or radiation therapy, or those who are not candidates for surgery or radiation therapy."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27376162",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 60,
"text": "Sonidegib phosphate: new approval for basal cell carcinoma."
}
]
| 6 | BioASQ-training6b | [
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002280",
"http://www.disease-ontology.org/api/metadata/DOID:2513"
]
| [
{
"o": "http://linkedlifedata.com/resource/umls/label/A18627521",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0007117"
},
{
"o": "basal cell carcinomas",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A18627521"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A0474410",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0007117"
},
{
"o": "basal cell carcinoma",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A0474410"
},
{
"o": "BCC",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C0007117"
}
]
| 589a246f78275d0c4a000034 | 184 |
yesno | Are adenylyl cyclases always transmembrane proteins? | ['no'] | [
"no"
]
| ['Adenylyl cyclases exists both as transmembrane and soluble proteins.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/25350397",
"http://www.ncbi.nlm.nih.gov/pubmed/25220136",
"http://www.ncbi.nlm.nih.gov/pubmed/24574382",
"http://www.ncbi.nlm.nih.gov/pubmed/25009261",
"http://www.ncbi.nlm.nih.gov/pubmed/25073090",
"http://www.ncbi.nlm.nih.gov/pubmed/24980705",
"http://www.ncbi.nlm.nih.gov/pubmed/25010002",
"http://www.ncbi.nlm.nih.gov/pubmed/25064589",
"http://www.ncbi.nlm.nih.gov/pubmed/25066614"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25350397",
"endSection": "title",
"offsetInBeginSection": 35,
"offsetInEndSection": 64,
"text": "ransmembrane adenylyl cyclase"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25220136",
"endSection": "abstract",
"offsetInBeginSection": 829,
"offsetInEndSection": 889,
"text": " Transmembrane adenylyl cyclase (tmAC) and soluble AC (sAC) "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24574382",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 231,
"text": "Soluble adenylyl cyclase (sAC) is a recently recognized source of the signaling molecule cyclic AMP (cAMP) that is genetically and biochemically distinct from the classic G-protein-regulated transmembrane adenylyl cyclases (tmACs)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25009261",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 25,
"text": "Soluble adenylyl cyclase "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25009261",
"endSection": "abstract",
"offsetInBeginSection": 608,
"offsetInEndSection": 685,
"text": "transmembrane adenylyl cyclases (tmACs), and soluble adenylyl cyclase (sAC). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25073090",
"endSection": "abstract",
"offsetInBeginSection": 138,
"offsetInEndSection": 306,
"text": " Here, we showed that both transmembrane AC (tmAC) and soluble AC (sAC) are distinctly involved in the regulation of sperm motility in the ascidian Ciona intestinalis. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24980705",
"endSection": "abstract",
"offsetInBeginSection": 761,
"offsetInEndSection": 874,
"text": "cAMP production in beta cells is mediated not simply by transmembrane adenylyl cyclases (TMACs), but also by sAC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25010002",
"endSection": "abstract",
"offsetInBeginSection": 492,
"offsetInEndSection": 634,
"text": "In contrast to tmAC, sAC produces cAMP in various intracellular microdomains close to specific cAMP targets, e.g., in nucleus and mitochondria"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25064589",
"endSection": "abstract",
"offsetInBeginSection": 545,
"offsetInEndSection": 703,
"text": "soluble adenylyl cyclase (sAC, ADCY10), the ubiquitous, non-transmembrane adenylyl cyclase, was found to play a key role in neuronal survival and axon growth."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25066614",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 40,
"text": "Central role of soluble adenylyl cyclase"
}
]
| 5 | BioASQ-training5b | []
| []
| 56e5aeec0c19e5451d000002 | 185 |
yesno | Do T-Cells regulate neuropathic pain? | ['yes'] | [
"yes"
]
| ['Macrophage-T cell interactions can mediate neuropathic pain through the glucocorticoid-induced TNF'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/27646435",
"http://www.ncbi.nlm.nih.gov/pubmed/22789131",
"http://www.ncbi.nlm.nih.gov/pubmed/25787078",
"http://www.ncbi.nlm.nih.gov/pubmed/24553941",
"http://www.ncbi.nlm.nih.gov/pubmed/25608762",
"http://www.ncbi.nlm.nih.gov/pubmed/23747724",
"http://www.ncbi.nlm.nih.gov/pubmed/15541898",
"http://www.ncbi.nlm.nih.gov/pubmed/22189457"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25608762",
"endSection": "abstract",
"offsetInBeginSection": 346,
"offsetInEndSection": 501,
"text": "here is evidence for a considerable impact of the immune system also in neuropathic pain. However, the role of the adaptive immune system is still unclear."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25608762",
"endSection": "abstract",
"offsetInBeginSection": 1806,
"offsetInEndSection": 1927,
"text": " Our investigation revealed a clear shift of T-cell subsets towards anti-inflammation in patients with neuropathic pain. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25787078",
"endSection": "abstract",
"offsetInBeginSection": 1209,
"offsetInEndSection": 1346,
"text": " GITRL expressed on macrophages drives cytokine release and T cell activation, resulting in neuropathic pain via GITR-dependent actions. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22789131",
"endSection": "abstract",
"offsetInBeginSection": 1664,
"offsetInEndSection": 1842,
"text": "Thus, this T-cell subset may be specifically targeted to alleviate chronic neuropathic pain.<CopyrightInformation>Copyright © 2012 International Association for the Study of Pain"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22189457",
"endSection": "abstract",
"offsetInBeginSection": 105,
"offsetInEndSection": 211,
"text": "Recent studies show that T cells play an important role in neuropathic pain following nerve injury in rats"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24553941",
"endSection": "abstract",
"offsetInBeginSection": 1409,
"offsetInEndSection": 1558,
"text": "These results show a peripheral pivotal role of CatS in the development of neuropathic pain through the antigen-specific activation of CD4(+) T-cells"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23747724",
"endSection": "abstract",
"offsetInBeginSection": 338,
"offsetInEndSection": 619,
"text": "Chemokine (C-C motif) ligand 1 (CCL-1), a well-characterized chemokine secreted by activated T cells, has been shown to play an important role in neuropathic pain induced by nerve injury and is also produced in various cell types in the CNS, especially in dorsal root ganglia (DRG)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25608762",
"endSection": "abstract",
"offsetInBeginSection": 490,
"offsetInEndSection": 640,
"text": "In the present study, we investigated systemic T-cell subset responses and T-cell related cytokine profiles in patients with chronic neuropathic pain."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25608762",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 52,
"text": "Anti-inflammatory T-cell shift in neuropathic pain."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22789131",
"endSection": "abstract",
"offsetInBeginSection": 1664,
"offsetInEndSection": 1757,
"text": "Thus, this T-cell subset may be specifically targeted to alleviate chronic neuropathic pain.."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22789131",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 118,
"text": "Regulatory T cells attenuate neuropathic pain following peripheral nerve injury and experimental autoimmune neuritis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25787078",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "Macrophage-T cell interactions mediate neuropathic pain through the glucocorticoid-induced tumor necrosis factor ligand system."
}
]
| 6 | BioASQ-training6b | [
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013601",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D050378",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D010146"
]
| null | 58c0825502b8c6095300001b | 186 |
yesno | Are super enhancers structurally insulated in chromatin loops? | ['no'] | [
"no"
]
| ['Although there is evidence that chromatin neighbourhoods, formed by the zinc-finger protein CTCF, can sequester enhancers and their target genes, there is limited in vivo evidence for CTCF demarcating super-enhancers and preventing cross talk between distinct regulatory elements. CTCF sites are porous borders, allowing a super-enhancer to activate a secondary target.', 'Although there is evidence that chromatin neighbourhoods, formed by the zinc-finger protein CTCF, can sequester enhancers and their target genes, there is limited in vivo evidence for CTCF demarcating super-enhancers and preventing cross talk between distinct regulatory elements.', 'Dissecting super-enhancer hierarchy based on chromatin interactions Although there is evidence that chromatin neighbourhoods, formed by the zinc-finger protein CTCF, can sequester enhancers and their target genes, there is limited in vivo evidence for CTCF demarcating super-enhancers and preventing cross talk between distinct regulatory elements.', 'We also demonstrate that the Wap super-enhancer, which is built on STAT5 and other common transcription factors, retains its exquisite mammary specificity when placed into globally permissive chromatin, suggesting a limited role of chromatin in controlling cell specificity. CTCF sites are porous borders, allowing a super-enhancer to activate a secondary target.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/30285185",
"http://www.ncbi.nlm.nih.gov/pubmed/29507293",
"http://www.ncbi.nlm.nih.gov/pubmed/28714474",
"http://www.ncbi.nlm.nih.gov/pubmed/25263550"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29507293",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 67,
"text": "Dissecting super-enhancer hierarchy based on chromatin interactions"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29507293",
"endSection": "abstract",
"offsetInBeginSection": 527,
"offsetInEndSection": 638,
"text": "Genetic ablation of hub enhancers results in profound defects in gene activation and local chromatin landscape."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30285185",
"endSection": "abstract",
"offsetInBeginSection": 1134,
"offsetInEndSection": 1409,
"text": "We also demonstrate that the Wap super-enhancer, which is built on STAT5 and other common transcription factors, retains its exquisite mammary specificity when placed into globally permissive chromatin, suggesting a limited role of chromatin in controlling cell specificity. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28714474",
"endSection": "abstract",
"offsetInBeginSection": 119,
"offsetInEndSection": 399,
"text": "Although there is evidence that chromatin neighbourhoods, formed by the zinc-finger protein CTCF, can sequester enhancers and their target genes, there is limited in vivo evidence for CTCF demarcating super-enhancers and preventing cross talk between distinct regulatory elements."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28714474",
"endSection": "abstract",
"offsetInBeginSection": 909,
"offsetInEndSection": 997,
"text": "CTCF sites are porous borders, allowing a super-enhancer to activate a secondary target."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25263550",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Transcription factors and chromatin-remodeling complexes are key determinants of embryonic stem cell (ESC) identity. "
}
]
| 11 | BioASQ-training11b | null | null | 5fdb42b7a43ad31278000025 | 187 |
yesno | Should istiratumab be used for Pancreatic Cancer? | ['no'] | [
"no"
]
| ['No. In a clinical trial Istiratumab failed to improve the efficacy of standard of care chemotherapy in metastatic pancreatic cancer patients.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/31912800"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31912800",
"endSection": "abstract",
"offsetInBeginSection": 1862,
"offsetInEndSection": 1963,
"text": "CONCLUSIONS: Istiratumab failed to improve the efficacy of SOC chemotherapy in this patient setting. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31912800",
"endSection": "abstract",
"offsetInBeginSection": 1330,
"offsetInEndSection": 1595,
"text": "In the high IGF-1 cohort, median PFS was 3.6 and 7.3 months in the experimental versus control arms, respectively [hazard ratio (HR) = 1.88, P = 0.027]. In the high IGF-1/HRG+ subgroup (n = 44), median PFS was 4.1 and 7.3 months, respectively (HR = 1.39, P = 0.42)."
}
]
| 11 | BioASQ-training11b | null | null | 61fa9a60c9dfcb9c09000007 | 188 |
yesno | Are there any urine biomarkers for chronic kidney disease? | ['yes'] | [
"yes"
]
| Yes, there is a number of urine biomarkers used for early detection of chronic kidney disease. | [
"http://www.ncbi.nlm.nih.gov/pubmed/21538916",
"http://www.ncbi.nlm.nih.gov/pubmed/21286212",
"http://www.ncbi.nlm.nih.gov/pubmed/21151537",
"http://www.ncbi.nlm.nih.gov/pubmed/20425065"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21538916",
"endSection": "abstract",
"offsetInBeginSection": 485,
"offsetInEndSection": 726,
"text": "Kidney and urine proteomic biomarkers are considered as promising diagnostic tools to predict CKD progression early in diabetic nephropathy, facilitating timely and selective intervention that may reduce the related health-care expenditures."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21286212",
"endSection": "abstract",
"offsetInBeginSection": 821,
"offsetInEndSection": 1028,
"text": "Both blood and urine biomarkers are reviewed in this paper and offer a considerable opportunity to enhance the understanding of the pathophysiology and known epidemiology of these recently defined syndromes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21286212",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 314,
"text": "Cardiorenal syndromes (CRS) have been subclassified as five defined entities which represent clinical circumstances in which both the heart and the kidney are involved in a bidirectional injury and dysfunction via a final common pathway of cell-to-cell death and accelerated apoptosis mediated by oxidative stress."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21151537",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 138,
"text": "There is a strong association between both acute and chronic dysfunction of the heart and kidneys with respect to morbidity and mortality."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21151537",
"endSection": "abstract",
"offsetInBeginSection": 1265,
"offsetInEndSection": 1452,
"text": "Both blood and urine biomarkers, including the assessment of catalytic iron, a critical element to the generation of oxygen-free radicals and oxidative stress, are reviewed in this paper."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20425065",
"endSection": "abstract",
"offsetInBeginSection": 637,
"offsetInEndSection": 1225,
"text": "Identification of urine biomarkers has proven to be beneficial in recent years because of ease of handling, stability, and the ability to standardize the various markers to creatinine or other peptides generally already present in the urine. Recent markers such as neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), and podocin have garnered a lot of attention. The emergence of these and other biomarkers is largely because of the evolution of novel genomic and proteomic applications in investigations of acute kidney injury and chronic kidney disease."
}
]
| 5 | BioASQ-training5b | [
"http://www.disease-ontology.org/api/metadata/DOID:557",
"http://www.disease-ontology.org/api/metadata/DOID:784",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D051436",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D007674",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002908",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D015415",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D007676",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D014556",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D014554",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D007668",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003928"
]
| []
| 52fa73c62059c6d71c000058 | 189 |
yesno | Is the Philadelphia chromosome a fusion between parts of chromosomes 1 and 9? | ['no'] | [
"no"
]
| ['No,\nChronic myeloid leukemia is a stem cell disease with the presence of Philadelphia chromosome generated through reciprocal translocation of chromosome 9 and 22.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/29633730",
"http://www.ncbi.nlm.nih.gov/pubmed/29435292",
"http://www.ncbi.nlm.nih.gov/pubmed/29046997"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29435292",
"endSection": "abstract",
"offsetInBeginSection": 192,
"offsetInEndSection": 388,
"text": " The Philadelphia chromosome, t(9;22)(q34;q11), is present in 95% of CML patients, resulting in constitutive tyrosine kinase activity; however, ~5% of CML patients possess a Philadelphia variant. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29633730",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 181,
"text": "Chronic Myeloid Leukemia (CML) is myeloproliferative neoplasm characterized by Philadelphia chromosome which is a balanced translocation between chromosome 9 and 22 in 90% of cases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29046997",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 160,
"text": "Chronic myeloid leukemia is a stem cell disease with the presence of Philadelphia chromosome generated through reciprocal translocation of chromosome 9 and 22. "
}
]
| 11 | BioASQ-training11b | null | null | 5ca10fefecadf2e73f00004a | 190 |
yesno | Is miR-21 related to carcinogenesis? | ['yes'] | [
"yes"
]
| ['Yes. It has been demonstrated in several experimental studies that miR-21 has oncogenic potential, and is significantly dysregulated in numerous types of cancer. Therefore, miR-21 is closely related to carcinogenesis.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23416953",
"http://www.ncbi.nlm.nih.gov/pubmed/23335180",
"http://www.ncbi.nlm.nih.gov/pubmed/23288924",
"http://www.ncbi.nlm.nih.gov/pubmed/23239858",
"http://www.ncbi.nlm.nih.gov/pubmed/23212265",
"http://www.ncbi.nlm.nih.gov/pubmed/23175214",
"http://www.ncbi.nlm.nih.gov/pubmed/22747440",
"http://www.ncbi.nlm.nih.gov/pubmed/22703586",
"http://www.ncbi.nlm.nih.gov/pubmed/22610076",
"http://www.ncbi.nlm.nih.gov/pubmed/22550943",
"http://www.ncbi.nlm.nih.gov/pubmed/22265967",
"http://www.ncbi.nlm.nih.gov/pubmed/22168593",
"http://www.ncbi.nlm.nih.gov/pubmed/21937590",
"http://www.ncbi.nlm.nih.gov/pubmed/21882851",
"http://www.ncbi.nlm.nih.gov/pubmed/21880514",
"http://www.ncbi.nlm.nih.gov/pubmed/21406606",
"http://www.ncbi.nlm.nih.gov/pubmed/21350005",
"http://www.ncbi.nlm.nih.gov/pubmed/21081469",
"http://www.ncbi.nlm.nih.gov/pubmed/20978195",
"http://www.ncbi.nlm.nih.gov/pubmed/20952761",
"http://www.ncbi.nlm.nih.gov/pubmed/20827319",
"http://www.ncbi.nlm.nih.gov/pubmed/20702469",
"http://www.ncbi.nlm.nih.gov/pubmed/20682703",
"http://www.ncbi.nlm.nih.gov/pubmed/20380575",
"http://www.ncbi.nlm.nih.gov/pubmed/20338946",
"http://www.ncbi.nlm.nih.gov/pubmed/20309880",
"http://www.ncbi.nlm.nih.gov/pubmed/19901002",
"http://www.ncbi.nlm.nih.gov/pubmed/19789312",
"http://www.ncbi.nlm.nih.gov/pubmed/19748927",
"http://www.ncbi.nlm.nih.gov/pubmed/19737943",
"http://www.ncbi.nlm.nih.gov/pubmed/19435529",
"http://www.ncbi.nlm.nih.gov/pubmed/19175831",
"http://www.ncbi.nlm.nih.gov/pubmed/18853072",
"http://www.ncbi.nlm.nih.gov/pubmed/18596939",
"http://www.ncbi.nlm.nih.gov/pubmed/18451233",
"http://www.ncbi.nlm.nih.gov/pubmed/18230780",
"http://www.ncbi.nlm.nih.gov/pubmed/18187804",
"http://www.ncbi.nlm.nih.gov/pubmed/18089790",
"http://www.ncbi.nlm.nih.gov/pubmed/17587821",
"http://www.ncbi.nlm.nih.gov/pubmed/17475218",
"http://www.ncbi.nlm.nih.gov/pubmed/23483606",
"http://www.ncbi.nlm.nih.gov/pubmed/23466817",
"http://www.ncbi.nlm.nih.gov/pubmed/23446999",
"http://www.ncbi.nlm.nih.gov/pubmed/23481326",
"http://www.ncbi.nlm.nih.gov/pubmed/23417858",
"http://www.ncbi.nlm.nih.gov/pubmed/23255093",
"http://www.ncbi.nlm.nih.gov/pubmed/23239859",
"http://www.ncbi.nlm.nih.gov/pubmed/23224068",
"http://www.ncbi.nlm.nih.gov/pubmed/23049818",
"http://www.ncbi.nlm.nih.gov/pubmed/22970173",
"http://www.ncbi.nlm.nih.gov/pubmed/22709411",
"http://www.ncbi.nlm.nih.gov/pubmed/22689922",
"http://www.ncbi.nlm.nih.gov/pubmed/22678116",
"http://www.ncbi.nlm.nih.gov/pubmed/22638884",
"http://www.ncbi.nlm.nih.gov/pubmed/22618808",
"http://www.ncbi.nlm.nih.gov/pubmed/22430134",
"http://www.ncbi.nlm.nih.gov/pubmed/22387281",
"http://www.ncbi.nlm.nih.gov/pubmed/22316494",
"http://www.ncbi.nlm.nih.gov/pubmed/22072622",
"http://www.ncbi.nlm.nih.gov/pubmed/22001440",
"http://www.ncbi.nlm.nih.gov/pubmed/21883657",
"http://www.ncbi.nlm.nih.gov/pubmed/21646541",
"http://www.ncbi.nlm.nih.gov/pubmed/21494432",
"http://www.ncbi.nlm.nih.gov/pubmed/21279518",
"http://www.ncbi.nlm.nih.gov/pubmed/21102586",
"http://www.ncbi.nlm.nih.gov/pubmed/21088996",
"http://www.ncbi.nlm.nih.gov/pubmed/20693987",
"http://www.ncbi.nlm.nih.gov/pubmed/20620599",
"http://www.ncbi.nlm.nih.gov/pubmed/20480266",
"http://www.ncbi.nlm.nih.gov/pubmed/20346171",
"http://www.ncbi.nlm.nih.gov/pubmed/19597153",
"http://www.ncbi.nlm.nih.gov/pubmed/19509156",
"http://www.ncbi.nlm.nih.gov/pubmed/19473551",
"http://www.ncbi.nlm.nih.gov/pubmed/18719201",
"http://www.ncbi.nlm.nih.gov/pubmed/18591254",
"http://www.ncbi.nlm.nih.gov/pubmed/22528454",
"http://www.ncbi.nlm.nih.gov/pubmed/21532496",
"http://www.ncbi.nlm.nih.gov/pubmed/19546886",
"http://www.ncbi.nlm.nih.gov/pubmed/22291592",
"http://www.ncbi.nlm.nih.gov/pubmed/19730150",
"http://www.ncbi.nlm.nih.gov/pubmed/21170291",
"http://www.ncbi.nlm.nih.gov/pubmed/20633539",
"http://www.ncbi.nlm.nih.gov/pubmed/16778182",
"http://www.ncbi.nlm.nih.gov/pubmed/20141427",
"http://www.ncbi.nlm.nih.gov/pubmed/22860003",
"http://www.ncbi.nlm.nih.gov/pubmed/16966691",
"http://www.ncbi.nlm.nih.gov/pubmed/18507035",
"http://www.ncbi.nlm.nih.gov/pubmed/21468550",
"http://www.ncbi.nlm.nih.gov/pubmed/19682430",
"http://www.ncbi.nlm.nih.gov/pubmed/22476768",
"http://www.ncbi.nlm.nih.gov/pubmed/19641183",
"http://www.ncbi.nlm.nih.gov/pubmed/19906824",
"http://www.ncbi.nlm.nih.gov/pubmed/20483747",
"http://www.ncbi.nlm.nih.gov/pubmed/23202912",
"http://www.ncbi.nlm.nih.gov/pubmed/20221895",
"http://www.ncbi.nlm.nih.gov/pubmed/20876285"
]
| [
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23416953",
"endSection": "sections.0",
"offsetInBeginSection": 1460,
"offsetInEndSection": 1553,
"text": "miR-21* and miR-203 were significantly dysregulated (P < 0.05) in PTC tissues with BRAFV600E."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23416953",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "Expressions of miRNAs in papillary thyroid carcinoma and their associations with the BRAFV600E mutation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23335180",
"endSection": "sections.0",
"offsetInBeginSection": 1008,
"offsetInEndSection": 1360,
"text": "Levels of miRNA-21 (miR-21) and miR-106a in gastric cancer tissues were significantly higher compared with the levels in adjacent tissues (P = .006 and P = .001, respectively). Patients who had gastric cancer had significantly different levels of gastric juice miR-21 and miR-106a compared with patients who had benign gastric diseases (both P < .001)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23335180",
"endSection": "sections.0",
"offsetInBeginSection": 1448,
"offsetInEndSection": 1591,
"text": "miR-21 levels in intestinal type gastric cancer specimens were higher than that in diffuse (P = .003) or mixed (P < .001) gastric cancer types."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23288924",
"endSection": "sections.0",
"offsetInBeginSection": 804,
"offsetInEndSection": 1130,
"text": "MiR-155 and miR-21 appeared significantly over-expressed in the colonic mucosa of IBD subjects without CRC, but also in neoplastic tissues of IBD patients compared to non-IBD controls (p<0.001). Importantly, in patients with IBD-CRCs, miR-155 and miR-21 over-expression extended to the distant non-neoplastic mucosa (p<0.001)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23288924",
"endSection": "sections.0",
"offsetInBeginSection": 294,
"offsetInEndSection": 495,
"text": "Here we hypothesize that over-expression of miR-155 and miR-21, two inflammation-related miRNAs that target core MMR proteins, may constitute a pre-neoplastic event for the development of MSI IBD-CRCs."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23239858",
"endSection": "sections.0",
"offsetInBeginSection": 285,
"offsetInEndSection": 661,
"text": "After administration, we determined the expressions of miR-21, miR-27a, miR-34a, miR-93, miR-143, miR-146a, miR-148a, miR-155, miR-196a, miR-203, miR-205, miR-221 and nuclear factor kappa-light-chain enhancer of activated B-cells-1 (Nfκb1), mitogen-activated protein kinase-8 (Mapk8) and v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (K-ras) genes in the liver of mice."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23212265",
"endSection": "sections.0",
"offsetInBeginSection": 88,
"offsetInEndSection": 188,
"text": "Programmed cell death 4 (PDCD4) is a tumor suppressor gene whose expression is controlled by miR-21."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23212265",
"endSection": "sections.0",
"offsetInBeginSection": 1250,
"offsetInEndSection": 1375,
"text": "Consistently with PDCD4 downregulation, miR-21 was upregulated in neoplastic by comparison with nonneoplastic tissue samples."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23175214",
"endSection": "sections.0",
"offsetInBeginSection": 449,
"offsetInEndSection": 632,
"text": "Expression of miR-21 (p=0.027), miR-181b (p=0.002), and miR-146b (p=0.021) in tumor tissue and miR-21 (p=0.003) in noncancerous tissue were associated with patients' overall survival."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22747440",
"endSection": "sections.0",
"offsetInBeginSection": 319,
"offsetInEndSection": 575,
"text": "We analyzed the expression of nine miRNAs (miR-21, miR-127, miR-154, miR-224, miR-323, miR-370, miR-9*, miR-183, and miR-375) by quantitative real-time-polymerase chain reaction in 34 cases of sMTC, 6 cases of hMTC, and 2 cases of C-cell hyperplasia (CCH)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22747440",
"endSection": "sections.0",
"offsetInBeginSection": 886,
"offsetInEndSection": 1206,
"text": "MTC and CCH were both characterized by a significant overexpression of the whole set of miRNAs (the increase being 4.2-fold for miR-21, 6.7-fold for miR-127, 8.8-fold for miR-154, 6.6-fold for miR-224, 5.8-fold for miR-323, 6.1-fold for miR-370, 13-fold for miR-9*, 6.7-fold for miR-183, and 10.1 for miR-375, p<0.0001)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22610076",
"endSection": "sections.0",
"offsetInBeginSection": 304,
"offsetInEndSection": 585,
"text": "The most frequent changes in miRNAs in CLL cells included downregulation of miR-126, miR-572, miR-494, miR-923, miR-638, miR-130a, miR-181a and miR-181b and up-regulation of miR-29a, miR-660, miR-20a, miR-106b, miR-142-5p, miR-101, miR-30b, miR-34a, miR-let-7f, miR-21 and miR-155."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22550943",
"endSection": "sections.0",
"offsetInBeginSection": 839,
"offsetInEndSection": 1170,
"text": "Results: MTC and CCH were both characterized by a significant overexpression of the whole set of miRNAs (the increase being 4.2-fold for miR-21, 6.7-fold for miR-127, 8.8-fold for miR-154, 6.6-fold for miR-224, 5.8-fold for miR-323 and 6.1-fold for miR-370, 13-fold for miR-9*, 6.7-fold for miR-183 and 10.1 for miR-375, p<0.0001)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22265967",
"endSection": "sections.0",
"offsetInBeginSection": 869,
"offsetInEndSection": 1002,
"text": "We found that the onco-miRNAs miR-21 and miR-221 displayed upregulated expression while the liver-specific miR-122 was downregulated."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22168593",
"endSection": "sections.0",
"offsetInBeginSection": 1007,
"offsetInEndSection": 1313,
"text": "The aim of the present review was to describe the mechanisms of several known miR, summarize recent studies on oncogenic miR (e.g. miR-21, miR-106a and miR-17), tumor suppressor miR (e.g. miR-101, miR-181, miR-449, miR-486, let-7a) and controversial roles of miR (e.g. miR-107, miR-126) for gastric cancer."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21937590",
"endSection": "sections.0",
"offsetInBeginSection": 861,
"offsetInEndSection": 1097,
"text": "MiR-15b and miR-21 were differentially expressed in CSF samples from patients with gliomas, compared to control subjects with various neurologic disorders, including patients with primary CNS lymphoma and carcinomatous brain metastases."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21937590",
"endSection": "sections.0",
"offsetInBeginSection": 1268,
"offsetInEndSection": 1526,
"text": "Moreover, inclusion of miR-15b and miR-21 in combined expression analyses resulted in an increased diagnostic accuracy with 90% sensitivity and 100% specificity to distinguish patients with glioma from control subjects and patients with primary CNS lymphoma."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21882851",
"endSection": "sections.0",
"offsetInBeginSection": 545,
"offsetInEndSection": 971,
"text": "Many aberrantly expressed miRNAs were related to various cancers (e.g., miR-125b, hepatocellular carcinoma; miR-21, leukemia; miR-16, chronic lymphocytic leukemia; miR-192, pituitary adenomas; miR-199a-3p, ovarian cancer; miR-34a, pancreatic cancer). Several miRNAs (e.g., miR-34a, miR-21) and proteins (e.g., TGM2, NDRG2) that play crucial roles in liver tumorigenesis were first found to be affected by MC-LR in mouse liver."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21880514",
"endSection": "sections.0",
"offsetInBeginSection": 1363,
"offsetInEndSection": 1482,
"text": "Except for miR-21 and miR-206, the expression levels of all miRNAs significantly changed during the progression of CaP."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21406606",
"endSection": "sections.0",
"offsetInBeginSection": 1392,
"offsetInEndSection": 1578,
"text": "In addition, diet and carcinogen exposure modulated a number of microRNAs (miR-16, miR-19b, miR-21, miR26b, miR27b, miR-93, and miR-203) linked to canonical oncogenic signaling pathways."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21350005",
"endSection": "sections.0",
"offsetInBeginSection": 633,
"offsetInEndSection": 817,
"text": "RESULTS: Elevated miR-21 (HR 2.06, 1.13-3.75), miR-17 (HR 2.00, 1.10-3.61), and miR-155 (HR 2.37, 1.27-4.42) was associated with worse cancer-specific mortality in the Maryland cohort."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21081469",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 92,
"text": "NF-κB targets miR-16 and miR-21 in gastric cancer: involvement of prostaglandin E receptors."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20978195",
"endSection": "sections.0",
"offsetInBeginSection": 377,
"offsetInEndSection": 561,
"text": "Expression of miR-21, miR-29b, miR-34a/b/c, miR-155, and let-7a was determined by quantitative real-time PCR in formalin-fixed paraffin-embedded tumor specimens from 639 IALT patients."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20952761",
"endSection": "sections.0",
"offsetInBeginSection": 634,
"offsetInEndSection": 831,
"text": "hese two miRNAs have previously been identified as being overexpressed in MCF-7 breast cancer cells, with miR-21 specifically implicated in down-regulating the tumor suppressor gene, tropomyosin-1."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20827319",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "MicroRNA-21 is involved in ionizing radiation-promoted liver carcinogenesis."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20827319",
"endSection": "sections.0",
"offsetInBeginSection": 452,
"offsetInEndSection": 817,
"text": "We showed here that among several hundred miRNAs, miR-21 was the only one that increased 6 folds in high-LET IR-promoted mouse liver tumors when compared with that in the non-irradiated liver tissues. We also showed that miR-21 was up-regulated in human or mouse hepatocytes after exposure to IR, as well as in liver tissues derived from whole body irradiated mice."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20827319",
"endSection": "sections.0",
"offsetInBeginSection": 916,
"offsetInEndSection": 1070,
"text": "After the non-irradiated, low-LET or high-LET irradiated human hepatocytes were over-expressed with miR-21, these cells became tumorigenesis in nude mice."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20682703",
"endSection": "sections.0",
"offsetInBeginSection": 765,
"offsetInEndSection": 1035,
"text": "METHODS: We used this combined ISH/IHC assay to study a subset of cancer-associated miRNAs, including miRNAs frequently detected at low (miR-34a and miR-126) and high (miR-21 and miR-155) levels, in a panel of breast, colorectal, lung, pancreas, and prostate carcinomas."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20380575",
"endSection": "sections.0",
"offsetInBeginSection": 1915,
"offsetInEndSection": 2080,
"text": "The miR-15a, miR-16, miR-143, miR-155, and miR-21 were upregulated in M059K, and the modulation of these miRNAs fluctuated in M059J cells in a time-dependent manner."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20338946",
"endSection": "sections.0",
"offsetInBeginSection": 91,
"offsetInEndSection": 287,
"text": "Aberrantly increased expression of miR-21 plays a significant role in lung carcinogenesis and is a potential therapeutic target in both epidermal growth factor receptor-mutant and wild-type cases."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19901002",
"endSection": "sections.0",
"offsetInBeginSection": 963,
"offsetInEndSection": 1174,
"text": "Additionally, high miR-21 expression was associated with significantly decreased 5 year survival in patients (hazard ratio, 1.68; 95% CI: 1.04-2.77) in a model controlled for patient age, gender and tumor stage."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19789312",
"endSection": "sections.0",
"offsetInBeginSection": 751,
"offsetInEndSection": 936,
"text": "ESULTS: In adenocarcinoma patients, miR-21, miR-223, miR-192, and miR-194 expression was elevated, whereas miR-203 expression was reduced in cancerous compared with noncancerous tissue."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19789312",
"endSection": "sections.0",
"offsetInBeginSection": 1211,
"offsetInEndSection": 1430,
"text": "Significantly, elevated miR-21 expression in noncancerous tissue of SCC patients and reduced levels of miR-375 in cancerous tissue of adenocarcinoma patients with Barrett's were strongly associated with worse prognosis."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19748927",
"endSection": "sections.0",
"offsetInBeginSection": 723,
"offsetInEndSection": 1071,
"text": "miR-21, mir-31, miR-130a, miR-146b and miR-377 were consistently upregulated, whereas miR-1 and miR-143 were downregulated in lung tumors relative to normal lungs. In mice treated with VC and given I3C in the diet, levels of miR-21, mir-31, miR-130a, miR-146b and miR-377 were reduced relative to the level in mice treated with the carcinogen only."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19748927",
"endSection": "sections.0",
"offsetInBeginSection": 1243,
"offsetInEndSection": 1474,
"text": "Further studies with miR-21 indicated that phosphatase and tensin homolog, programmed cell death 4 and rich protein with Kazal motifs are potential targets for the oncogenic effect of miR-21 and the chemopreventive activity of I3C."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19737943",
"endSection": "sections.0",
"offsetInBeginSection": 144,
"offsetInEndSection": 336,
"text": "This study examines the potential clinical utility of an inflammatory gene expression signature as a prognostic biomarker for colon cancer in addition to previously examined miR-21 expression."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19737943",
"endSection": "sections.0",
"offsetInBeginSection": 1616,
"offsetInEndSection": 1780,
"text": "CONCLUSIONS: IRS and miR-21 expression are independent predictors of colon cancer prognosis and may provide a clinically useful tool to identify high-risk patients."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19175831",
"endSection": "sections.0",
"offsetInBeginSection": 1199,
"offsetInEndSection": 1374,
"text": "The most highly expressed miRNAs in gastric cancer tissues were miR-20b, miR-20a, miR-17, miR-106a, miR-18a, miR-21, miR-106b, miR-18b, miR-421, miR-340*, miR-19a and miR-658."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18853072",
"endSection": "sections.0",
"offsetInBeginSection": 357,
"offsetInEndSection": 959,
"text": "Recent findings report their involvement in hair follicle morphogenesis (ablation of miRNAs from keratinocytes causes several defects, such as evagination instead of invagination), in psoriasis (skin-specific expression of miR-203 and psoriasisspecific expression of miR-146a, miR-21 and miR-125b in the skin), in autoimmune diseases affecting the skin, such as SLE and ITP, in wound healing (changes in the expression of specific miRNA at specific phases of the regeneration process), and in skin carcinogenesis (a novel miRNA signature that includes induction of miR-21, a candidate oncogenic miRNA)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18451233",
"endSection": "sections.0",
"offsetInBeginSection": 597,
"offsetInEndSection": 854,
"text": "RESULTS: Several microRNAs were differentially expressed in serous ovarian carcinoma compared with normal ovarian tissues, including miR-21, miR-125a, miR-125b, miR-100, miR-145, miR-16, and miR-99a, which were each differentially expressed in >16 patients."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18230780",
"endSection": "sections.0",
"offsetInBeginSection": 1251,
"offsetInEndSection": 1620,
"text": "Selected for validation were miR-20a, miR-21, miR-106a, miR-181b, and miR-203, and all 5 were enriched in tumors from the validation cohort (P < .001). Higher miR-21 expression was present in adenomas (P = .006) and in tumors with more advanced TNM staging (P < .001). In situ hybridization demonstrated miR-21 to be expressed at high levels in colonic carcinoma cells."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18187804",
"endSection": "sections.0",
"offsetInBeginSection": 235,
"offsetInEndSection": 467,
"text": "To test this hypothesis, we studied the pharmacologic roles of three microRNAs previously implicated in cancer biology (let-7i, mir-16, and mir-21) and also used in silico methods to test pharmacologic microRNA effects more broadly."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18187804",
"endSection": "sections.0",
"offsetInBeginSection": 881,
"offsetInEndSection": 1554,
"text": "Changing the cellular levels of let-7i, mir-16, and mir-21 affected the potencies of a number of the anticancer agents by up to 4-fold. The effect was most prominent with mir-21, with 10 of 28 cell-compound pairs showing significant shifts in growth-inhibitory activity. Varying mir-21 levels changed potencies in opposite directions depending on compound class; indicating that different mechanisms determine toxic and protective effects. In silico comparison of drug potencies with microRNA expression profiles across the entire NCI-60 panel revealed that approximately 30 microRNAs, including mir-21, show highly significant correlations with numerous anticancer agents."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18089790",
"endSection": "sections.0",
"offsetInBeginSection": 902,
"offsetInEndSection": 1139,
"text": "Conversely, expression of other miRNAs was detected at varying levels predominantly within luminal epithelial cells in normal tissue; expression of miR-21 was frequently increased, whereas that of let-7a was decreased in malignant cells."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17587821",
"endSection": "sections.0",
"offsetInBeginSection": 447,
"offsetInEndSection": 596,
"text": "We describe a novel EMT-specific microRNA signature that includes induction of miR-21, a candidate oncogenic microRNA associated with carcinogenesis."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17475218",
"endSection": "sections.0",
"offsetInBeginSection": 508,
"offsetInEndSection": 562,
"text": "Notable was the high expression of miR-21 and miR-205."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23481326",
"endSection": "sections.0",
"offsetInBeginSection": 172,
"offsetInEndSection": 331,
"text": "Recently, microRNAs (miRNAs) have emerged as key actors in carcinogenesis and we demonstrated that microRNA-21 (miR-21), oncomiR is expressed early during PDA."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23417858",
"endSection": "sections.0",
"offsetInBeginSection": 1417,
"offsetInEndSection": 1571,
"text": "These results indicated that miR-21 plays a role in the carcinogenesis and metastasis of O. viverrini-associated CCA by suppressing the function of PDCD4."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23288924",
"endSection": "sections.0",
"offsetInBeginSection": 1039,
"offsetInEndSection": 1171,
"text": "Importantly, in patients with IBD CRCs, miR-155 and miR-21 overexpression extended to the distant non-neoplastic mucosa (P < 0.001)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23255093",
"endSection": "sections.0",
"offsetInBeginSection": 1373,
"offsetInEndSection": 1578,
"text": "Ectopic overexpression of miR-21 promoted Akt activation and phosphorylation of EZH2, whereas inhibiting miR-21 by transfecting the cells with anti-miR-21 inhibited Akt activation and EZH2 phosphorylation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23224068",
"endSection": "sections.0",
"offsetInBeginSection": 1580,
"offsetInEndSection": 1719,
"text": "PDCD4 nuclear down-regulation (which parallels miR-21 up-regulation) is involved in the molecular pathway of IBD-associated carcinogenesis."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23175214",
"endSection": "sections.0",
"offsetInBeginSection": 457,
"offsetInEndSection": 660,
"text": "The expression levels of miR-21 (p = 0.027), miR-181b (p = 0.002) and miR-146b (p = 0.021) in tumor tissue and miR-21 (p = 0.003) in noncancerous tissue were associated with overall survival of patients."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22709411",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "OBJECTIVE: As an important oncogenic miRNA, miR-21 has been reported to play crucial roles in glioblastoma (GBM) carcinogenesis."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22618808",
"endSection": "sections.0",
"offsetInBeginSection": 1077,
"offsetInEndSection": 1291,
"text": "We further analyzed the expression of microRNA-21 (miR-21), an oncogenic noncoding RNA involved in oncogenic Ras signaling, by quantitative reverse-transcription polymerase chain reaction and in situ hybridization."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22430134",
"endSection": "sections.0",
"offsetInBeginSection": 78,
"offsetInEndSection": 193,
"text": "MicroRNA-21 (miR-21) plays crucial roles in carcinogenesis and is considered as one of the most studied oncomiRNAs."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22387281",
"endSection": "sections.0",
"offsetInBeginSection": 281,
"offsetInEndSection": 456,
"text": "Although microRNA-21 (miR-21) has been implicated in various aspects of carcinogenesis, its functions and molecular mechanisms in carcinogen-induced tumorigenesis are unclear."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22316494",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "Substantial evidence indicates that microRNA-21 (miR-21) is a key oncomiR in carcinogenesis and is significantly elevated in multiple myeloma (MM)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22001440",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 78,
"text": "MicroRNA 21 (miR-21) has been implicated in various aspects of carcinogenesis."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21883657",
"endSection": "sections.0",
"offsetInBeginSection": 1151,
"offsetInEndSection": 1290,
"text": "Conversely, pAkt and miR-21 expression was significantly up-regulated in the whole spectrum of preneoplastic/neoplastic lesions considered."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21882851",
"endSection": "sections.0",
"offsetInBeginSection": 796,
"offsetInEndSection": 971,
"text": "Several miRNAs (e.g., miR-34a, miR-21) and proteins (e.g., TGM2, NDRG2) that play crucial roles in liver tumorigenesis were first found to be affected by MC-LR in mouse liver."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21880514",
"endSection": "sections.0",
"offsetInBeginSection": 1354,
"offsetInEndSection": 1482,
"text": "RESULTS: Except for miR-21 and miR-206, the expression levels of all miRNAs significantly changed during the progression of CaP."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21646541",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "MicroRNA 21 (miR-21) is overexpressed in virtually all types of carcinomas and various types of hematological malignancies."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21279518",
"endSection": "sections.0",
"offsetInBeginSection": 1242,
"offsetInEndSection": 1377,
"text": "As expected, miR-21 expression was significantly upregulated in preneoplastic/neoplastic samples, consistent with PDCD4 downregulation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21088996",
"endSection": "sections.0",
"offsetInBeginSection": 1169,
"offsetInEndSection": 1262,
"text": "Furthermore, miR-21 levels in the primary tumours correlated with disease stage (P < 0.0001)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21081469",
"endSection": "sections.0",
"offsetInBeginSection": 398,
"offsetInEndSection": 562,
"text": "We found that miR-16 and miR-21 were upregulated upon nicotine stimulation, transfection with anti-miR-16 or anti-miR-21 significantly abrogated cell proliferation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20693987",
"endSection": "sections.0",
"offsetInBeginSection": 970,
"offsetInEndSection": 1074,
"text": "MicroRNA-21 (miR-21) is a unique miRNA in that it is overexpressed in most tumour types analysed so far."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20682703",
"endSection": "sections.0",
"offsetInBeginSection": 1216,
"offsetInEndSection": 1413,
"text": "Although altered expressions of miR-21 and miR-34a were manifested within cancer cells, those of miR-126 and miR-155 were predominantly confined to endothelial cells and immune cells, respectively."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20480266",
"endSection": "sections.0",
"offsetInBeginSection": 221,
"offsetInEndSection": 286,
"text": "However, the function of miR-21 in osteosarcoma is still unclear."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19789312",
"endSection": "sections.0",
"offsetInBeginSection": 937,
"offsetInEndSection": 1064,
"text": "In SCC patients, we found elevated miR-21 and reduced miR-375 expression levels in cancerous compared with noncancerous tissue."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19748927",
"endSection": "sections.0",
"offsetInBeginSection": 723,
"offsetInEndSection": 886,
"text": "miR-21, mir-31, miR-130a, miR-146b and miR-377 were consistently upregulated, whereas miR-1 and miR-143 were downregulated in lung tumors relative to normal lungs."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19509156",
"endSection": "sections.0",
"offsetInBeginSection": 1153,
"offsetInEndSection": 1219,
"text": "Precancerous adenomas also frequently showed miR-21 up-regulation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18230780",
"endSection": "sections.0",
"offsetInBeginSection": 1403,
"offsetInEndSection": 1462,
"text": "Higher miR-21 expression was present in adenomas (P = .006)"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22689922",
"endSection": "sections.0",
"offsetInBeginSection": 695,
"offsetInEndSection": 873,
"text": "Importantly, the inflammatory ZD esophagus had a distinct microRNA signature resembling human ESCC or tongue SCC miRNAomes with miR-31 and miR-21 as the top-up-regulated species."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22528454",
"endSection": "sections.0",
"offsetInBeginSection": 285,
"offsetInEndSection": 536,
"text": "Several miRNAs have been recently reported to be involved in modulation of glioma development, especially some upregulated miRNAs, such as microRNA-21 (miR-21), which has been found to function as an oncogene in cultured glioblastoma multiforme cells."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22476768",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 216,
"text": "OBJECTIVE: MicroRNA-21 (miR-21) is one of the miRNAs that are frequently and highly overexpressed in tumor tissue of colorectal cancer (CRC) patients; however, only a little is known about its functional role in CRC."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22322462",
"endSection": "sections.0",
"offsetInBeginSection": 854,
"offsetInEndSection": 1042,
"text": "Inhibition of microRNA-21 (mir‑21) induced upregulation of Spry2 and PTEN which underscores the importance of mir-21 in Spry2-associated tumorigenesis of the colon."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21532496",
"endSection": "sections.0",
"offsetInBeginSection": 886,
"offsetInEndSection": 999,
"text": "The microRNA miR-21, a known oncogenic miRNA, was found to be upregulated in papillary and clear cell carcinomas."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21468550",
"endSection": "sections.0",
"offsetInBeginSection": 112,
"offsetInEndSection": 258,
"text": "Since microRNA-21 (miR-21) may contribute to tumorigenesis and chemoresistance in many cancer types, we aimed to investigate its efficacy in TCCs."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20633539",
"endSection": "sections.0",
"offsetInBeginSection": 285,
"offsetInEndSection": 537,
"text": "Several miRNAs have been recently reported to be involved in modulation of glioma development, especially some up-regulated miRNAs, such as microRNA-21 (miR-21), which has been found to function as an oncogene in cultured glioblastoma multiforme cells."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20483747",
"endSection": "sections.0",
"offsetInBeginSection": 659,
"offsetInEndSection": 953,
"text": "In this study, by using high-throughput microRNA profiling, we identified that two miRNAs (miR-21 and miR-148a) overexpressed in CD4+ T cells from both patients with lupus and lupus-prone MRL/lpr mice, which promote cell hypomethylation by repressing DNA methyltransferase 1 (DNMT1) expression."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20141427",
"endSection": "sections.0",
"offsetInBeginSection": 108,
"offsetInEndSection": 229,
"text": "The microRNA-21 (miR-21) has been identified as the only miRNA overexpressed in a variety of cancers, including leukemia."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19730150",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 189,
"text": "OBJECTIVE: The contribution of overexpressed microRNA-21 and -221 (miR-21 and miR-221) to the malignant phenotype was determined by inhibiting these miRNAs using antisense oligonucleotides."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19682430",
"endSection": "sections.0",
"offsetInBeginSection": 52,
"offsetInEndSection": 185,
"text": "The microRNA-21(miR-21) has been identified as the only miRNA over-expressed in a wide variety of cancers, including cervical cancer."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19641183",
"endSection": "sections.0",
"offsetInBeginSection": 379,
"offsetInEndSection": 626,
"text": "To determine the functions of these microRNAs in lymphomagenesis, we examined the effects of antisense oligonucleotides (ASOs) targeting miR-21 (ASO-21) and/or miR-155 (ASO-155) in NK-cell lymphoma lines overexpressing one or both of these miRNAs."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19597153",
"endSection": "sections.0",
"offsetInBeginSection": 343,
"offsetInEndSection": 670,
"text": "In this study, microRNA (miRNA) expression profiling of 28 cases of never-smoker lung cancer identified aberrantly expressed miRNAs, which were much fewer than in lung cancers of smokers and included miRNAs previously identified (e.g., up-regulated miR-21) and unidentified (e.g., down-regulated miR-138) in those smoker cases."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19546886",
"endSection": "sections.0",
"offsetInBeginSection": 482,
"offsetInEndSection": 584,
"text": "The oncogenic miRNA, microRNA-21 (miR-21), was found to be upregulated in laryngeal carcinoma tissues."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19509156",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 202,
"text": "OBJECTIVE: To better understand microRNA miR-21 function in carcinogenesis, we analyzed miR-21 expression patterns in different stages of colorectal cancer development using in situ hybridization (ISH)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18507035",
"endSection": "sections.0",
"offsetInBeginSection": 153,
"offsetInEndSection": 287,
"text": "Of these miRNAs, miR-21 appears to be important in tumorigenesis given its up-regulation in almost all types of human cancer examined."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18372920",
"endSection": "sections.0",
"offsetInBeginSection": 127,
"offsetInEndSection": 326,
"text": "The microRNA-21 gene (mir-21) has been identified as the only miRNA commonly overexpressed in solid tumors of the lung, breast, stomach, prostate, colon, brain, head and neck, esophagus and pancreas."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16966691",
"endSection": "sections.0",
"offsetInBeginSection": 764,
"offsetInEndSection": 1495,
"text": "RESULTS: Our data showed that a common pattern of microRNA expression distinguishes any tumor type from normal pancreas, suggesting that this set of microRNAs might be involved in pancreatic tumorigenesis; the expression of miR-103 and miR-107, associated with lack of expression of miR-155, discriminates tumors from normal; a set of 10 microRNAs distinguishes endocrine from acinar tumors and is possibly associated with either normal endocrine differentiation or endocrine tumorigenesis; miR-204 is primarily expressed in insulinomas and correlates with immunohistochemical expression of insulin; and the overexpression of miR-21 is strongly associated with both a high Ki67 proliferation index and presence of liver metastasis."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16778182",
"endSection": "sections.0",
"offsetInBeginSection": 435,
"offsetInEndSection": 848,
"text": "To search for tumor-associated mutations that could affect processing and expression of mature miRNAs, a panel of 91 cancer-derived cell lines was analyzed for sequence variations in 15 miRNAs implicated in tumorigenesis by virtue of their known target transcripts (let-7 family targeting oncogenic Ras) or their localization to sites of frequent chromosomal instability (miR-143, miR-145, miR-26a-1, and miR-21)."
}
]
| 5 | BioASQ-training5b | [
"http://www.uniprot.org/uniprot/P21_BYVU"
]
| null | 511a4ec01159fa8212000004 | 191 |
yesno | Is the process of DNA loop-extrusion independent of ATP? | ['yes'] | [
"yes"
]
| ['The process of DNA loop-extrusion is not independent of ATP. It is dependent on the energy of ATP hydrolysis.', 'Yes, a single condensin complex is able to extrude tens of kilobase pairs of DNA, using the energy of ATP hydrolysis.', 'The DNA-organizing mechanism of condensin depends on the energy of ATP hydrolysis but how this activity specifically promotes proper compaction and segregation of chromosomes during mitosis remains poorly understood.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/29706548",
"http://www.ncbi.nlm.nih.gov/pubmed/29754816",
"http://www.ncbi.nlm.nih.gov/pubmed/29300120",
"http://www.ncbi.nlm.nih.gov/pubmed/31780627",
"http://www.ncbi.nlm.nih.gov/pubmed/16292342",
"http://www.ncbi.nlm.nih.gov/pubmed/27224481",
"http://www.ncbi.nlm.nih.gov/pubmed/29079757",
"http://www.ncbi.nlm.nih.gov/pubmed/29140466",
"http://www.ncbi.nlm.nih.gov/pubmed/31753851",
"http://www.ncbi.nlm.nih.gov/pubmed/27210764",
"http://www.ncbi.nlm.nih.gov/pubmed/29472443",
"http://www.ncbi.nlm.nih.gov/pubmed/30100265"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29079757",
"endSection": "abstract",
"offsetInBeginSection": 110,
"offsetInEndSection": 326,
"text": "The DNA-organizing mechanism of condensin depends on the energy of ATP hydrolysis but how this activity specifically promotes proper compaction and segregation of chromosomes during mitosis remains poorly understood."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29754816",
"endSection": "abstract",
"offsetInBeginSection": 902,
"offsetInEndSection": 1037,
"text": "We suggest that loading and translocation are mediated by conformational changes in cohesin's hinge driven by cycles of ATP hydrolysis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29706548",
"endSection": "abstract",
"offsetInBeginSection": 219,
"offsetInEndSection": 316,
"text": "Using ultra-deep Hi-C, we show that loop domains form by a process that requires cohesin ATPases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29706548",
"endSection": "abstract",
"offsetInBeginSection": 409,
"offsetInEndSection": 523,
"text": "Strikingly, without ATP, we observe the emergence of hundreds of CTCF-independent loops that link regulatory DNA. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27210764",
"endSection": "abstract",
"offsetInBeginSection": 539,
"offsetInEndSection": 672,
"text": "Each TAD emerges from multiple loops dynamically formed through extrusion, contrary to typical illustrations of single static loops. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29300120",
"endSection": "abstract",
"offsetInBeginSection": 296,
"offsetInEndSection": 623,
"text": "However, the model requires a motor to generate the loops, and although cohesin is a strong candidate for the extruding factor, a suitable motor protein (or a motor activity in cohesin itself) has yet to be found. Here we explore a new hypothesis: that there is no motor, and thermal motion within the nucleus drives extrusion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29472443",
"endSection": "abstract",
"offsetInBeginSection": 321,
"offsetInEndSection": 531,
"text": "We observed that a single condensin complex is able to extrude tens of kilobase pairs of DNA at a force-dependent speed of up to 1500 base pairs per second, using the energy of adenosine triphosphate hydrolysis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29140466",
"endSection": "abstract",
"offsetInBeginSection": 684,
"offsetInEndSection": 1081,
"text": "Our model explains what can be the driving force of chromatin loop extrusion and how it can be ensured that loops grow quickly and in a good direction. In addition, the supercoiling-driven loop extrusion mechanism is consistent with earlier explanations proposing why TADs flanked by convergent CTCF binding sites form more stable chromatin loops than TADs flanked by divergent CTCF binding sites."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29079757",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 68,
"text": "Oligomerization and ATP stimulate condensin-mediated DNA compaction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29706548",
"endSection": "abstract",
"offsetInBeginSection": 409,
"offsetInEndSection": 522,
"text": "Strikingly, without ATP, we observe the emergence of hundreds of CTCF-independent loops that link regulatory DNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31780627",
"endSection": "abstract",
"offsetInBeginSection": 439,
"offsetInEndSection": 537,
"text": "DNA compaction by cohesin requires adenosine triphosphate (ATP) hydrolysis and is force sensitive."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16292342",
"endSection": "abstract",
"offsetInBeginSection": 731,
"offsetInEndSection": 908,
"text": "The identification and quantification of further initiation steps--ATP binding and extrusion of an initial DNA loop--allowed us to deduce a complete kinetic reinitiation scheme."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30100265",
"endSection": "abstract",
"offsetInBeginSection": 330,
"offsetInEndSection": 520,
"text": "In support of this model, single-molecule imaging experiments indicate that Saccharomyces cerevisiae condensin complexes can extrude DNA loops in an ATP-hydrolysis-dependent manner in vitro."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31753851",
"endSection": "abstract",
"offsetInBeginSection": 162,
"offsetInEndSection": 319,
"text": "These structures depend on cohesin, a ring-shaped DNA-entrapping adenosine triphosphatase (ATPase) complex that has been proposed to form loops by extrusion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31753851",
"endSection": "abstract",
"offsetInBeginSection": 576,
"offsetInEndSection": 714,
"text": "Loop formation and maintenance depend on cohesin's ATPase activity and on NIPBL-MAU2, but not on topological entrapment of DNA by cohesin."
}
]
| 11 | BioASQ-training11b | null | null | 5cebe41ea49efeb44c000006 | 192 |
yesno | Is celecoxib effective for amyotrophic lateral sclerosis? | ['no'] | [
"no"
]
| ['No. In a clinical trial, celecoxib did not have a beneficial effect on patients with amyotrophic lateral sclerosis.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/18608093",
"http://www.ncbi.nlm.nih.gov/pubmed/16802291"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18608093",
"endSection": "abstract",
"offsetInBeginSection": 1507,
"offsetInEndSection": 1648,
"text": "In conclusion, the celecoxib-creatine combination was selected as preferable to the minocycline-creatine combination for further evaluation. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16802291",
"endSection": "abstract",
"offsetInBeginSection": 818,
"offsetInEndSection": 983,
"text": "ESULTS: Celecoxib did not slow the decline in muscle strength, vital capacity, motor unit number estimates, ALS Functional Rating Scale-Revised, or affect survival. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16802291",
"endSection": "abstract",
"offsetInBeginSection": 1196,
"offsetInEndSection": 1326,
"text": "INTERPRETATION: At the dosage studied, celecoxib did not have a beneficial effect on research subjects with ALS, and it was safe. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16802291",
"endSection": "abstract",
"offsetInBeginSection": 1202,
"offsetInEndSection": 1331,
"text": "INTERPRETATION\n\nAt the dosage studied, celecoxib did not have a beneficial effect on research subjects with ALS, and it was safe."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16802291",
"endSection": "abstract",
"offsetInBeginSection": 821,
"offsetInEndSection": 986,
"text": "RESULTS\n\nCelecoxib did not slow the decline in muscle strength, vital capacity, motor unit number estimates, ALS Functional Rating Scale-Revised, or affect survival."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16802291",
"endSection": "abstract",
"offsetInBeginSection": 821,
"offsetInEndSection": 986,
"text": "RESULTS\nCelecoxib did not slow the decline in muscle strength, vital capacity, motor unit number estimates, ALS Functional Rating Scale-Revised, or affect survival."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16802291",
"endSection": "abstract",
"offsetInBeginSection": 1196,
"offsetInEndSection": 1325,
"text": "INTERPRETATION: At the dosage studied, celecoxib did not have a beneficial effect on research subjects with ALS, and it was safe."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16802291",
"endSection": "abstract",
"offsetInBeginSection": 817,
"offsetInEndSection": 982,
"text": "RESULTS: Celecoxib did not slow the decline in muscle strength, vital capacity, motor unit number estimates, ALS Functional Rating Scale-Revised, or affect survival."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16802291",
"endSection": "abstract",
"offsetInBeginSection": 1170,
"offsetInEndSection": 1283,
"text": "At the dosage studied, celecoxib did not have a beneficial effect on research subjects with ALS, and it was safe."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16802291",
"endSection": "abstract",
"offsetInBeginSection": 799,
"offsetInEndSection": 955,
"text": "Celecoxib did not slow the decline in muscle strength, vital capacity, motor unit number estimates, ALS Functional Rating Scale-Revised, or affect survival."
}
]
| 11 | BioASQ-training11b | null | null | 5e4b5f566d0a277941000020 | 193 |
yesno | Does TUC.338 inhibit colorectal cancer? | ['no'] | [
"no"
]
| ['No. TUC.338 is significantly up-regulated in colorectal cancers (CRC) tissue and CRC cell lines, and the up-regulated TUC.338 is associated with lymph node metastasis. TUC.338 acts as a novel oncogene by targeting the TIMP-1 gene thus promoting colorectal cancer cell migration and invasion.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/27914101"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27914101",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 62,
"text": "TUC.338 promotes invasion and metastasis in colorectal cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27914101",
"endSection": "abstract",
"offsetInBeginSection": 441,
"offsetInEndSection": 701,
"text": "Until now, the role of TUC.338 in colorectal cancers remains undefined. This study revealed that TUC.338 is significantly up-regulated in colorectal cancers (CRC) tissue and CRC cell lines, and the up-regulated TUC.338 is associated with lymph node metastasis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27914101",
"endSection": "abstract",
"offsetInBeginSection": 1293,
"offsetInEndSection": 1453,
"text": " Thus, these findings suggested that TUC.338 acts as a novel oncogene by targeting the TIMP-1 gene thus promoting colorectal cancer cell migration and invasion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27914101",
"endSection": "abstract",
"offsetInBeginSection": 1294,
"offsetInEndSection": 1453,
"text": "Thus, these findings suggested that TUC.338 acts as a novel oncogene by targeting the TIMP-1 gene thus promoting colorectal cancer cell migration and invasion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27914101",
"endSection": "abstract",
"offsetInBeginSection": 513,
"offsetInEndSection": 701,
"text": "This study revealed that TUC.338 is significantly up-regulated in colorectal cancers (CRC) tissue and CRC cell lines, and the up-regulated TUC.338 is associated with lymph node metastasis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27914101",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 63,
"text": "TUC.338 promotes invasion and metastasis in colorectal cancer."
}
]
| 11 | BioASQ-training11b | [
"https://meshb.nlm.nih.gov/record/ui?ui=D015179",
"http://www.disease-ontology.org/api/metadata/DOID:6981",
"http://www.disease-ontology.org/api/metadata/DOID:9256",
"https://meshb.nlm.nih.gov/record/ui?ui=D003123",
"http://www.disease-ontology.org/api/metadata/DOID:0080199"
]
| null | 5a6d23ccb750ff4455000035 | 194 |
yesno | Do polycomb group proteins (PcG) mediate the formation of chromatin loops? | ['yes'] | [
"yes"
]
| ['Yes. The polycomb group proteins (PcG) mediate the formation of chromatin loops by facilitating co-localization of heterochromatin loops.', 'Polycomb action at a distance can be organized by local chromatin topology.', 'A chromatin insulator driving three-dimensional Polycomb response element (PRE) contacts and Polycomb association with the chromatin fiber the Drosophila gypsy insulator behaves as a conformational chromatin border that is able to prohibit contacts between a Polycomb response element (PRE) and a distal promoter Polycomb action at a distance can be organized by local chromatin topology', 'Yes. The polycomb group proteins (PcG) mediate the formation of chromatin loops.', 'Yes, polycomb group proteins (PcG) play a critical role in the formation of chromatin loops.', 'A chromatin insulator driving three-dimensional Polycomb response element (PRE) contacts and Polycomb association with the chromatin fiber the Drosophila gypsy insulator behaves as a conformational chromatin border that is able to prohibit contacts between a Polycomb response element (PRE) and a distal promoter Polycomb action at a distance can be organized by local chromatin topology Polycomb repressive complex 2 is recruited through the interaction of CTCF', 'A chromatin insulator driving three-dimensional Polycomb response element (PRE) contacts and Polycomb association with the chromatin fiber the Drosophila gypsy insulator behaves as a conformational chromatin border that is able to prohibit contacts between a Polycomb Response element (Pre) and a distal promoter Polycomb action at a distance can be organized by local chromatin topology Polycomb repressive complex 2 is recruited through the interaction of CTCF.', 'Yes, the polycomb group proteins (PcG) play a critical role in the formation and/or maintenance of chromatin loops.', "Yes. Chromatin-loop formation is dependent on regulatory proteins localized at the 5' and 3' ends of exons of genes, such as PcG. The polycomb group proteins (PcG) mediate the formation of chromatin loops by binding to nuclear-insoluble structures at late-M-to-early-G1 on histone H3 lysine 27. Depending on what residue is mutated and the degree of transcription, polycomb loop formation is linked to either transcriptionally active or silent chromatin."] | [
"http://www.ncbi.nlm.nih.gov/pubmed/21262819",
"http://www.ncbi.nlm.nih.gov/pubmed/18662993",
"http://www.ncbi.nlm.nih.gov/pubmed/19053175",
"http://www.ncbi.nlm.nih.gov/pubmed/19954516",
"http://www.ncbi.nlm.nih.gov/pubmed/28765367",
"http://www.ncbi.nlm.nih.gov/pubmed/30008320"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21262819",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 138,
"text": "A chromatin insulator driving three-dimensional Polycomb response element (PRE) contacts and Polycomb association with the chromatin fiber"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21262819",
"endSection": "abstract",
"offsetInBeginSection": 462,
"offsetInEndSection": 635,
"text": "the Drosophila gypsy insulator behaves as a conformational chromatin border that is able to prohibit contacts between a Polycomb response element (PRE) and a distal promoter"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21262819",
"endSection": "abstract",
"offsetInBeginSection": 987,
"offsetInEndSection": 1061,
"text": "Polycomb action at a distance can be organized by local chromatin topology"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18662993",
"endSection": "abstract",
"offsetInBeginSection": 426,
"offsetInEndSection": 500,
"text": "Polycomb repressive complex 2 is recruited through the interaction of CTCF"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18662993",
"endSection": "abstract",
"offsetInBeginSection": 1148,
"offsetInEndSection": 1318,
"text": "CTCF governs gene expression by orchestrating chromatin loop structures and by serving as a DNA-binding protein scaffold to recruit and bind polycomb repressive complexes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19053175",
"endSection": "abstract",
"offsetInBeginSection": 882,
"offsetInEndSection": 1096,
"text": "The chromatin loops completely dissolve, accompanied by loss of PcG proteins and H3K27me3 marks, when Tera-2 cells receive differentiation signals which induce a approximately 60-fold increase in GATA-4 expression."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28765367",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 97,
"text": "Polycomb-mediated chromatin loops revealed by a subkilobase-resolution chromatin interaction map."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28765367",
"endSection": "abstract",
"offsetInBeginSection": 192,
"offsetInEndSection": 472,
"text": "es or \"anchors\" are associated with CTCF protein in mammals, loop anchors in Drosophila were found most often in association with the polycomb group (PcG) protein Polycomb (Pc), a subunit of polycomb repressive complex 1 (PRC1). Loops were frequently located within domains of PcG"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19053175",
"endSection": "abstract",
"offsetInBeginSection": 1824,
"offsetInEndSection": 1998,
"text": "We also provide novel insight that PcG-occupied and H3K27me3-enriched regions can form chromatin loops and physically interact in cis around a single gene in mammalian cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30008320",
"endSection": "abstract",
"offsetInBeginSection": 675,
"offsetInEndSection": 846,
"text": "Repressive loops within polycomb domains are formed after the midblastula transition between polycomb response elements by the action of GAGA factor and polycomb proteins."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19053175",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 72,
"text": "PcG proteins, DNA methylation, and gene repression by chromatin looping."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28765367",
"endSection": "abstract",
"offsetInBeginSection": 421,
"offsetInEndSection": 493,
"text": "Loops were frequently located within domains of PcG-repressed chromatin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19954516",
"endSection": "abstract",
"offsetInBeginSection": 1910,
"offsetInEndSection": 2090,
"text": "iation to proliferation control. Our results revealed a chromatin looping mechanism of long-range control and argue against models involving homogeneous spreading of PcG silencers "
}
]
| 11 | BioASQ-training11b | null | null | 5fdb4290a43ad31278000024 | 195 |
yesno | Does mutation of ARTEMIS gene causes severe combined immunodeficiency? | ['yes'] | [
"yes"
]
| ['Artemis mutation disrupts development of adaptive immunity and leads to severe combined immunodeficiency.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/36385359",
"http://www.ncbi.nlm.nih.gov/pubmed/35801871",
"http://www.ncbi.nlm.nih.gov/pubmed/35773051",
"http://www.ncbi.nlm.nih.gov/pubmed/35729475"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35729475",
"endSection": "abstract",
"offsetInBeginSection": 780,
"offsetInEndSection": 923,
"text": "RESULTS: Seven infants were diagnosed with SCID, yielding an incidence of 1 in 22,819 live births. Four of these infants had Artemis-type SCID."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35801871",
"endSection": "abstract",
"offsetInBeginSection": 288,
"offsetInEndSection": 426,
"text": "Artemis deficiency disrupts development of adaptive immunity and leads to radiosensitive T- B- severe combined immunodeficiency (RS-SCID)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35773051",
"endSection": "abstract",
"offsetInBeginSection": 507,
"offsetInEndSection": 667,
"text": "Encouraging data for X-SCID and preclinical work for Artemis-SCID and RAG1-SCID are paving the way for the therapy to become a viable curative treatment option."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36385359",
"endSection": "abstract",
"offsetInBeginSection": 111,
"offsetInEndSection": 350,
"text": "Pathogenic variants in DCLRE1C encoding Artemis cause T-B-NK+ severe combined immunodeficiency (SCID), and patients with Artemis-deficient SCID (ART-SCID) require definitive therapy with allogeneic hematopoietic cell transplantation (HCT)."
}
]
| 12 | BioASQ-training12b | null | null | 63ee5eeaf36125a426000002 | 196 |
yesno | Does Curare function by stimulating the acetylcholine receptor? | ['no'] | [
"no"
]
| ['No. Curare function does not stimulate the acetylcholine receptor.', 'Usual clinical concentrations of curare cause competitive inhibition of muscle nicotinic acetylcholine receptors.', 'No, curare is an inhibitor of acetylcholine-induced currents that only blocks the N-terminal glutamine-rich channel.', 'No, curare is an antagonist of acetylcholine-induced currents that binds to the choline receptor.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/8355663",
"http://www.ncbi.nlm.nih.gov/pubmed/26818254",
"http://www.ncbi.nlm.nih.gov/pubmed/4351811",
"http://www.ncbi.nlm.nih.gov/pubmed/11849819",
"http://www.ncbi.nlm.nih.gov/pubmed/8166227",
"http://www.ncbi.nlm.nih.gov/pubmed/2479422",
"http://www.ncbi.nlm.nih.gov/pubmed/21422738",
"http://www.ncbi.nlm.nih.gov/pubmed/6283380",
"http://www.ncbi.nlm.nih.gov/pubmed/2713760",
"http://www.ncbi.nlm.nih.gov/pubmed/25409503",
"http://www.ncbi.nlm.nih.gov/pubmed/12624651",
"http://www.ncbi.nlm.nih.gov/pubmed/6308151",
"http://www.ncbi.nlm.nih.gov/pubmed/16083",
"http://www.ncbi.nlm.nih.gov/pubmed/10934261",
"http://www.ncbi.nlm.nih.gov/pubmed/22194270"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11849819",
"endSection": "abstract",
"offsetInBeginSection": 1558,
"offsetInEndSection": 1732,
"text": "Usual clinical concentrations of curare cause competitive inhibition of muscle nicotinic acetylcholine receptors while higher concentrations may induce open channel blockade."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10934261",
"endSection": "abstract",
"offsetInBeginSection": 260,
"offsetInEndSection": 364,
"text": "nicotinic acetylcholine receptor (nAChR)-blocking agents [e.g., curare or alpha-bungarotoxin (alpha-BTX)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21422738",
"endSection": "abstract",
"offsetInBeginSection": 301,
"offsetInEndSection": 403,
"text": "The short neurotoxins to which erabutoxins belong act by blocking the nicotinic acetylcholine receptor"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12624651",
"endSection": "abstract",
"offsetInBeginSection": 802,
"offsetInEndSection": 996,
"text": "Both EFS- and carbachol-evoked contractions of the UES were blocked by curare at a lower concentration than by atropine or hexamethonium, suggesting that the acetylcholine receptor is nicotinic."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26818254",
"endSection": "abstract",
"offsetInBeginSection": 624,
"offsetInEndSection": 860,
"text": "We applied ACh alone; the nicotinic acetylcholine receptor (nAChR) antagonist curare, either alone or in the presence of ACh; and the muscarinic acetylcholine receptor (mAChR) antagonist atropine, either alone or in the presence of ACh."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12624651",
"endSection": "abstract",
"offsetInBeginSection": 277,
"offsetInEndSection": 411,
"text": "The EFS-induced contraction of the UES was completely blocked by tetrodotoxin and curare, and abolished in Ca2+ -free Ringer solution."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2479422",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 97,
"text": "Curare binding and the curare-induced subconductance state of the acetylcholine receptor channel."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8355663",
"endSection": "abstract",
"offsetInBeginSection": 705,
"offsetInEndSection": 860,
"text": "We have further investigated this particular mutation by examining the interaction of the competitive antagonist d-tubocurarine (curare) with the receptor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8166227",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 196,
"text": "d-Tubocurarine (curare) is a well-characterized competitive antagonist of nicotinic acetylcholine receptors (AChRs), and it is usually assumed that curare and agonists share a common binding site."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2713760",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Curare action on nicotinic acetylcholine receptors has a number of facets, of which the best known is competitive antagonism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6308151",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 168,
"text": "The mode of action of curare, a well-known competitive antagonist of acetylcholine at the nicotinic receptor, was examined with the single channel recording technique. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6283380",
"endSection": "abstract",
"offsetInBeginSection": 134,
"offsetInEndSection": 444,
"text": "ently, however, it has been shown that curare can also block the channels opened by ACh at the frog neuromuscular junction as well as on rat and Aplysia neurones; moreover, curare is able to depolarize rat myotubes and thus behaves as an agonist for the cholinergic receptor of this preparation (see ref. 6). U"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/4351811",
"endSection": "abstract",
"offsetInBeginSection": 997,
"offsetInEndSection": 1101,
"text": "One site, competitively blocked by bungarotoxin and by curare, is presumably the acetylcholine receptor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22194270",
"endSection": "abstract",
"offsetInBeginSection": 733,
"offsetInEndSection": 938,
"text": "In neuromuscular junction (NMJ) preparations, movements of the muscle must be inhibited if imaging during stimulation is desired (e.g., by application of curare, a potent acetylcholine receptor inhibitor)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6283380",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Curare has long been regarded as a typical competitive antagonist of acetylcholine (ACh) at the vertebrate neuromuscular junction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8166227",
"endSection": "abstract",
"offsetInBeginSection": 379,
"offsetInEndSection": 527,
"text": "Curare inhibition of wild-type receptors is consistent with curare binding to a single high-affinity binding site [inhibitor constant (Ki) = 20 nM]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8166227",
"endSection": "abstract",
"offsetInBeginSection": 763,
"offsetInEndSection": 1132,
"text": "Phenylalanine substitution for alpha Y198 [alpha Y198F (notation used here: subunit/amino acid in wild-type/residue number/substitution)] causes a 10-fold increase in curare affinity (Ki = 3.1 nM), and measurement of the recovery from curare inhibition indicates that this increase in affinity is due to a reduction in the rate of curare dissociation from the receptor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25409503",
"endSection": "abstract",
"offsetInBeginSection": 1075,
"offsetInEndSection": 1225,
"text": "rthermore, sudden increases of research activity are ascribable to historic events, like the first use of curare as muscle relaxant during surgery.DIS"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6283380",
"endSection": "abstract",
"offsetInBeginSection": 131,
"offsetInEndSection": 438,
"text": "Recently, however, it has been shown that curare can also block the channels opened by ACh at the frog neuromuscular junction as well as on rat and Aplysia neurones; moreover, curare is able to depolarize rat myotubes and thus behaves as an agonist for the cholinergic receptor of this preparation (see ref."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16083",
"endSection": "abstract",
"offsetInBeginSection": 1185,
"offsetInEndSection": 1390,
"text": "In Aplysia nervous tissue, curare appears not to be a specific antagonist for the nicotinic ACh receptor, but rather to be a specific blocking agent for a class of receptor-activated Na+ and Cl- responses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6308151",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 167,
"text": "The mode of action of curare, a well-known competitive antagonist of acetylcholine at the nicotinic receptor, was examined with the single channel recording technique."
}
]
| 11 | BioASQ-training11b | null | null | 60292e1b1cb411341a000111 | 197 |
yesno | Is Functional Neurological Disorder (FND) classified as a psychosomatic disorder? | ['no'] | [
"no"
]
| ['Functional neurological disorder reflects impairments in brain networks leading to distressing motor, sensory and/or cognitive symptoms that demonstrate positive clinical signs on examination incongruent with other conditions.', 'Yes, Functional Neurological Disorder (FND) is considered a type of psychosomatic disorder.', 'functional neurological disorder (fnd) is not classified as a psychosomatic disorder, but rather a neurological condition that requires differentiation from other neurologic diseases and syndromes.', 'Yes, Functional Neurological Disorder (FND) is classified as a type of psychosomatic disorder.', 'Yes, Functional Neurological Disorder (FND) is classified as a psychosomatic disorder.', 'Functional neurological disorder (FND) is a clinical diagnosis that requires differentiation from other neurologic diseases / syndromes, and from the relatively rare diagnosis of feigning (malingering and factitious disorder).'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/34188796",
"http://www.ncbi.nlm.nih.gov/pubmed/36311548",
"http://www.ncbi.nlm.nih.gov/pubmed/28856091",
"http://www.ncbi.nlm.nih.gov/pubmed/34629180",
"http://www.ncbi.nlm.nih.gov/pubmed/36075980",
"http://www.ncbi.nlm.nih.gov/pubmed/31911360",
"http://www.ncbi.nlm.nih.gov/pubmed/35911352",
"http://www.ncbi.nlm.nih.gov/pubmed/36002964",
"http://www.ncbi.nlm.nih.gov/pubmed/36039249",
"http://www.ncbi.nlm.nih.gov/pubmed/30455406",
"http://www.ncbi.nlm.nih.gov/pubmed/22506326",
"http://www.ncbi.nlm.nih.gov/pubmed/32726111",
"http://www.ncbi.nlm.nih.gov/pubmed/35653495",
"http://www.ncbi.nlm.nih.gov/pubmed/34693243",
"http://www.ncbi.nlm.nih.gov/pubmed/35074803",
"http://www.ncbi.nlm.nih.gov/pubmed/34806689",
"http://www.ncbi.nlm.nih.gov/pubmed/35858632",
"http://www.ncbi.nlm.nih.gov/pubmed/34568805",
"http://www.ncbi.nlm.nih.gov/pubmed/33280274",
"http://www.ncbi.nlm.nih.gov/pubmed/34585455",
"http://www.ncbi.nlm.nih.gov/pubmed/33659255"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36311548",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Challenges to the Diagnosis of Functional Neurological Disorder: Feigning, Intentionality, and Responsibility."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36311548",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 214,
"text": "he diagnosis of Functional Neurological Disorder (FND) requires differentiation from other neurologic diseases/syndromes, and from the comparatively rare diagnosis of feigning (Malingering and Factitious Disorder)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35653495",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 227,
"text": "Functional neurological disorder reflects impairments in brain networks leading to distressing motor, sensory and/or cognitive symptoms that demonstrate positive clinical signs on examination incongruent with other conditions. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34629180",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "Functional neurological disorder and somatic symptom disorder in Parkinson's disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34629180",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "The occurrence of Functional Neurological Disorder (FND) and Somatic Symptom Disorder (SSD) in PD was not commonly accepted until recently, despite some evidence that emerged in the pre and early L-Dopa era. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34585455",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 78,
"text": "Maladaptive schemas of patients with functional neurological symptom disorder."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34585455",
"endSection": "abstract",
"offsetInBeginSection": 13,
"offsetInEndSection": 122,
"text": "he psychological underpinnings of functional neurological symptom disorders (FNSD) remain poorly understood. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34585455",
"endSection": "abstract",
"offsetInBeginSection": 124,
"offsetInEndSection": 538,
"text": "disintegration of explicit and implicit information processing in patients with FNSD has previously been suggested; however, this suggestion has so far received little empirical support. Trauma and maladaptive schemas probably reinforce disintegration in FNSD. The present study explored the occurrence of maladaptive schemas and investigated the impact of trauma-related maladaptive schemas in patients with FNSD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35911352",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 191,
"text": "Functional neurological symptom disorder (FND) remains a clinical challenge. It is one of the many mimics of cerebrovascular accidents, spinal cord disorders, and lower motor neuron disease. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36002964",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 151,
"text": "Previous studies with adults suggest that aberrant communication between neural networks underpins functional neurological disorder (FND). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32726111",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 254,
"text": "Functional neurological disorder (FND) is a complex neuropsychiatric disorder characterized by abnormal or atypical sensorimotor, gait, dissociative, or special sensory symptoms in the absence of structural nervous system lesions to explain the symptoms."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33280274",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "Functional neurological disorders (FNDs), which are sometimes also referred to as psychogenic neurological disorders or conversion disorder, are common disabling neuropsychiatric disorders with limited treatment options."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34188796",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 234,
"text": "Functional neurological disorder (FND) is a complex neuropsychiatric condition characterized by the presence of neurological symptoms and signs (either motor or sensory) that cannot be explained by any known medical or mental disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34806689",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "Functional neurological disorder (FND) is a rare neuropsychiatric illness that commonly presents to the medical setting as opposed to the psychiatric setting."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34568805",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Historically, functional neurological disorder (FND) has been described in psychodynamic terms as the physical manifestation of psychological distress."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35858632",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 262,
"text": "BACKGROUND: Functional neurological disorders (FNDs) are common but often misdiagnosed.REVIEW SUMMARY: The incidence of FNDs is between 4 and 12 per 100,000, comparable to multiple sclerosis and amyotrophic lateral sclerosis, and it is the second most common dia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31911360",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 202,
"text": "Functional Neurological Disorder (FND), otherwise known as Conversion Disorder, is characterized by abnormal sensory or motor symptoms that are determined to be \"incompatible\" with neurological disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22506326",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 228,
"text": "Conversion disorder or functional neurological disorder is a neurological symptom complex originating from psychological factors, which manifests in voluntary motor and sensory functions or as unexplained epilepsy-like seizures."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36075980",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "Functional neurological disorder (FND) is characterized by neurological symptoms that cannot be explained by a structural neurological cause."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36039249",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "Functional neurological disorder (FND) is a constellation of common neurological symptoms without exact organic pathophysiology."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28856091",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 227,
"text": "BACKGROUND: Functional neurological disorder (FND) is an elusive disorder characterized by unexplained neurological symptoms alongside aberrant cognitive processing and negative affect, often associated with amygdala reactivity"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35074803",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "Functional neurological disorder (FND), previously regarded as a diagnosis of exclusion, is now a rule-in diagnosis with available treatments."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30455406",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 118,
"text": "Functional neurological disorder (FND) is a common and highly disabling disorder, but its aetiology remains enigmatic."
}
]
| 12 | BioASQ-training12b | null | null | 6436953757b1c7a315000028 | 198 |
yesno | Does MC1R palmitoylation reduce pigmentation? | ['no'] | [
"no"
]
| ['No, MC1R palmitoylation leads to increased pigmentation.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/28869973"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28869973",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 301,
"text": "The melanocortin-1 receptor (MC1R), a G-protein-coupled receptor, has a crucial role in human and mouse pigmentation. Activation of MC1R in melanocytes by α-melanocyte-stimulating hormone (α-MSH) stimulates cAMP signalling and melanin production and enhances DNA repair after ultraviolet irradiation. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28869973",
"endSection": "abstract",
"offsetInBeginSection": 923,
"offsetInEndSection": 1203,
"text": "MC1R palmitoylation, primarily mediated by the protein-acyl transferase ZDHHC13, is essential for activating MC1R signalling, which triggers increased pigmentation, ultraviolet-B-induced G1-like cell cycle arrest and control of senescence and melanomagenesis in vitro and in vivo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28869973",
"endSection": "abstract",
"offsetInBeginSection": 1445,
"offsetInEndSection": 1554,
"text": "The results highlight a central role for MC1R palmitoylation in pigmentation and protection against melanoma."
}
]
| 11 | BioASQ-training11b | null | null | 5a9ac4161d1251d03b000010 | 199 |
yesno | Could Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT)
cause sudden cardiac death? | ['yes'] | [
"yes"
]
| Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) can cause sudden cardiac death. | [
"http://www.ncbi.nlm.nih.gov/pubmed/24076290",
"http://www.ncbi.nlm.nih.gov/pubmed/24011300",
"http://www.ncbi.nlm.nih.gov/pubmed/23286974",
"http://www.ncbi.nlm.nih.gov/pubmed/23094885",
"http://www.ncbi.nlm.nih.gov/pubmed/23040497",
"http://www.ncbi.nlm.nih.gov/pubmed/22995932",
"http://www.ncbi.nlm.nih.gov/pubmed/22993115",
"http://www.ncbi.nlm.nih.gov/pubmed/22749309",
"http://www.ncbi.nlm.nih.gov/pubmed/22524859",
"http://www.ncbi.nlm.nih.gov/pubmed/22307399",
"http://www.ncbi.nlm.nih.gov/pubmed/22119737",
"http://www.ncbi.nlm.nih.gov/pubmed/22050625",
"http://www.ncbi.nlm.nih.gov/pubmed/21893508",
"http://www.ncbi.nlm.nih.gov/pubmed/21872879",
"http://www.ncbi.nlm.nih.gov/pubmed/21616285",
"http://www.ncbi.nlm.nih.gov/pubmed/21292648",
"http://www.ncbi.nlm.nih.gov/pubmed/21135804",
"http://www.ncbi.nlm.nih.gov/pubmed/20513597",
"http://www.ncbi.nlm.nih.gov/pubmed/20361477",
"http://www.ncbi.nlm.nih.gov/pubmed/20143088",
"http://www.ncbi.nlm.nih.gov/pubmed/19781797",
"http://www.ncbi.nlm.nih.gov/pubmed/20091251",
"http://www.ncbi.nlm.nih.gov/pubmed/19631908",
"http://www.ncbi.nlm.nih.gov/pubmed/19601860",
"http://www.ncbi.nlm.nih.gov/pubmed/19575158",
"http://www.ncbi.nlm.nih.gov/pubmed/19568611",
"http://www.ncbi.nlm.nih.gov/pubmed/19564966",
"http://www.ncbi.nlm.nih.gov/pubmed/19345240",
"http://www.ncbi.nlm.nih.gov/pubmed/18684293",
"http://www.ncbi.nlm.nih.gov/pubmed/18483626",
"http://www.ncbi.nlm.nih.gov/pubmed/17959506",
"http://www.ncbi.nlm.nih.gov/pubmed/17052226",
"http://www.ncbi.nlm.nih.gov/pubmed/15890976",
"http://www.ncbi.nlm.nih.gov/pubmed/15749201",
"http://www.ncbi.nlm.nih.gov/pubmed/12837242",
"http://www.ncbi.nlm.nih.gov/pubmed/12386154",
"http://www.ncbi.nlm.nih.gov/pubmed/12574890",
"http://www.ncbi.nlm.nih.gov/pubmed/11807805"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24076290",
"endSection": "abstract",
"offsetInBeginSection": 828,
"offsetInEndSection": 884,
"text": "Two siblings died suddenly at the ages of 9 and 10 years"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24011300",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 365,
"text": "Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a type of cardiac arrhythmia that occurs in people with a structurally normal heart. Stress or anxiety-induced release of endogenous catecholamines causes a dysfunction in the myocytic calcium-ion channel, leading to ventricular arrhythmias that can cause dizziness, syncope, or sudden cardiac death. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23286974",
"endSection": "abstract",
"offsetInBeginSection": 1449,
"offsetInEndSection": 1607,
"text": "During a follow-up of 48±94 months, arrhythmia events (sudden cardiac death and aborted cardiac arrest) associated with noncompliance occurred in 2 patients. "
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"text": "We report a family with repeat events of sudden cardiac death and recurrent ventricular fibrillation in a teenage girl, where autopsy data and clinical investigations were inconclusive. The diagnosis of catecholaminergic polymorphic ventricular tachycardia (CPVT) was established only following finding a gene mutation in the cardiac ryanodine receptor. "
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"text": "Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a devastating inherited disorder characterized by episodic syncope and/or sudden cardiac arrest during exercise or acute emotion in individuals without structural cardiac abnormalities. Although rare, CPVT is suspected to cause a substantial part of sudden cardiac deaths in young individuals. "
},
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"text": "catecholaminergic polymorphic ventricular tachycardia (CPVT), and Brugada syndrome (BrS), leave no evidence to be found at autopsy"
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"text": "a spectrum of sudden cardiac death (SCD)-predisposing heritable cardiac arrhythmia syndromes, including long QT syndrome (LQTS), short QT syndrome (SQTS), Brugada syndrome (BrS), and catecholaminergic polymorphic ventricular tachycardia (CPVT). "
},
{
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"text": "CPVT is a familial arrhythmogenic syndrome characterized by abnormal calcium (Ca(2+)) handling, ventricular arrhythmias, and sudden cardiac death"
},
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"text": "Mutations in RyR2 are linked to catecholaminergic polymorphic ventricular tachycardia (CPVT) and sudden cardiac death."
},
{
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"text": "Patients with CPVT often present with exercise- or emotion induced syncope, the first presentation can also be sudden cardiac death."
},
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"text": "Among the five major arrhythmogenic disorders occurring in the absence of a structural heart disease is catecholaminergic polymorphic ventricular tachycardia (CPVT), which is a highly lethal form of inherited arrhythmias. "
},
{
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"text": "Patients with CPVT are at high risk of developing life-threatening ventricular arrhythmias when untreated. "
},
{
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"text": "Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited arrhythmia syndrome characterized by VT induced by adrenergic stress in the absence of structural heart disease and high incidence of sudden cardiac death. "
},
{
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"offsetInBeginSection": 202,
"offsetInEndSection": 470,
"text": "CPVT is an inherited arrhythmia syndrome caused by gene mutations that destabilize cardiac ryanodine receptor Ca(2+) release channels. Sudden cardiac death is incompletely prevented by conventional drug therapy with β-blockers with or without Ca(2+) channel blockers. "
},
{
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"text": "Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited arrhythmogenic disease that can cause sudden cardiac death due to ventricular fibrillation (VF)."
},
{
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"text": "Important potential causes of sudden cardiac deaths in the absence of heart disease are primary electrical diseases such as Brugada syndrome, long QT syndrome (LQTS), short QT syndrome and catecholaminergic polymorphic ventricular tachyarrhythmias. "
},
{
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"offsetInBeginSection": 223,
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"text": "catecholaminergic polymorphic ventricular tachycardia (CPVT), and Brugada syndrome (BrS) are primary inherited arrhythmia syndromes that may cause syncope and sudden cardiac death in young individuals. "
},
{
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"offsetInBeginSection": 0,
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"text": "Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a cardiac channelopathy characterized by altered intracellular calcium handling resulting in ventricular arrhythmias and high risk of cardiac sudden death in young cases with normal structural hearts. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20143088",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 193,
"text": "Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited arrhythmogenic disorder that causes syncopal episodes related with stress or emotion and even sudden cardiac deaths."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/19781797",
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"offsetInBeginSection": 12,
"offsetInEndSection": 190,
"text": "Catecholaminergic polymorphic ventricular tachycardia caused by mutations in the RyR2 gene manifests as severe arrhythmias, and may provide a candidate for sudden cardiac deaths."
},
{
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"offsetInBeginSection": 187,
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"text": "Patients diagnosed with an electrical cardiomyopathy have an increased risk of syncope and sudden cardiac death (SCD). "
},
{
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"offsetInBeginSection": 1278,
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"text": "Patients with CPVT present with exercise-induced syncope and sudden cardiac death but normal resting electrocardiograms. "
},
{
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"offsetInBeginSection": 180,
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"text": "Over 80% of SCD occurs in patients with organic heart disease. However, approximately 10-15% of SCD occurs in the presence of structurally normal heart and the majority of those patients are young. In this group of patients, changes in genes encoding cardiac ion channels produce modification of the function of the channel resulting in an electrophysiological substrate of VA and SCD. Collectively these disorders are referred to as Cardiac Ion Channelopathies. The 4 major syndromes in this group are: The Long QT Syndrome (LQTS), the Brugada Syndrome (BrS), the Short QT Syndrome (SQTS), and the Catecholaminergic Polymorphic VT (CPVT). "
},
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"offsetInBeginSection": 101,
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"text": "Important potential causes of sudden cardiac deaths in the absence of heart disease are primary electrical diseases such as Brugada syndrome, long QT syndrome (LQTS), short QT syndrome (SQTS), and catecholaminergic polymorphic ventricular tachyarrhythmias (CPVT). "
},
{
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"offsetInBeginSection": 0,
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"text": "Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a familial cardiac arrhythmia that is related to RYR2 or CASQ2 gene mutation. It occurs in patients with structurally normal heart and causes exercise-emotion-triggered syncope and sudden cardiac death."
},
{
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"offsetInBeginSection": 722,
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"text": "Potentially lethal ion channel disorders (channelopathies) such as the long QT syndromes (LQTS), catecholaminergic polymorphic ventricular tachycardia (CPVT)"
},
{
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"text": "Aberrant spontaneous, diastolic Ca2+ leak from the SR due to dysfunctional RyR2 contributes to the formation of delayed after-depolarisations, which are thought to underlie the fatal arrhythmia that occurs in both heart failure (HF) and in catecholaminergic polymorphic ventricular tachycardia (CPVT). "
},
{
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"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an uncommon heritable disease presenting with syncope or sudden cardiac death."
},
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"offsetInBeginSection": 148,
"offsetInEndSection": 287,
"text": "Mutations in RyR2 have been linked to exercise-induced sudden cardiac death (catecholaminergic polymorphic ventricular tachycardia [CPVT])."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17959506",
"endSection": "abstract",
"offsetInBeginSection": 0,
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"text": "Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a heritable arrhythmia unmasked by exertion or stress, characterized by triggered activity and sudden cardiac death in affected patients."
},
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"text": "families that exhibit CPVT (catecholaminergic polymorphic ventricular tachycardia), a condition in which physical or emotional stress can trigger severe tachyarrhythmias that can lead to sudden cardiac death."
},
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"offsetInBeginSection": 1381,
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"text": "that often leads to sudden death in HF and in CPVT."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15890976",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 206,
"text": "Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an inherited disease characterized by adrenergically mediated polymorphic ventricular tachycardia leading to syncope and sudden cardiac death."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15749201",
"endSection": "abstract",
"offsetInBeginSection": 0,
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"text": "Catecholaminergic polymorphic ventricular tachycardia (CPVT) is an autosomal dominant inherited disorder characterized by adrenergic induced polymorphic ventricular tachycardias and associated with sudden cardiac death. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12837242",
"endSection": "abstract",
"offsetInBeginSection": 1001,
"offsetInEndSection": 1128,
"text": "These data suggest that \"leaky\" RyR2 channels can trigger fatal cardiac arrhythmias, providing a possible explanation for CPVT."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/12386154",
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"offsetInBeginSection": 0,
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"text": "Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a rare arrhythmogenic disorder characterized by syncopal events and sudden cardiac death at a young age during physical stress or emotion, in the absence of structural heart disease. "
},
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"text": " catecholaminergic polymorphic ventricular tachycardia (CPVT), idiopathic ventricular fibrillation (VF), and arrhythmogenic right ventricular cardiomyopathy (ARVC) account for a relevant proportion of sudden cardiac death cases in young patients cohorts. "
},
{
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"text": "has recently been shown to be involved in at least two forms of sudden cardiac death (SCD): (1) Catecholaminergic polymorphic ventricular tachycardia (CPVT) "
}
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| 52e8e96698d023950500001f | 200 |
yesno | Is TREM2 associated with Alzheimer's disease? | ['yes'] | [
"yes"
]
| A rare variant of the TREM2 gene, which encodes the triggering receptor encoded in myeloid cells 2 (rs75932628-T) causing a R47H substitution has been associated with both early and late onset Alzheimer's disease in various populations. Emerging evidence has demonstrated that TREM2 could suppress inflammatory response by repression of microglia-mediated cytokine production and secretion, which may prevent inflammation-induced bystander damage of neurons. Higher levels of TREM2 mRNA (p = 0.002) and protein (p < 0.001) were identified in AD patients which indicates that TREM2 might serve as a novel noninvasive biomarker for AD diagnosis. Based on the potential protective actions of TREM2 in AD pathogenesis, targeting TREM2 might provide new opportunities for AD treatment. | [
"http://www.ncbi.nlm.nih.gov/pubmed/24119542",
"http://www.ncbi.nlm.nih.gov/pubmed/24041969",
"http://www.ncbi.nlm.nih.gov/pubmed/24002183",
"http://www.ncbi.nlm.nih.gov/pubmed/23855982",
"http://www.ncbi.nlm.nih.gov/pubmed/23692967",
"http://www.ncbi.nlm.nih.gov/pubmed/23582655",
"http://www.ncbi.nlm.nih.gov/pubmed/23562540",
"http://www.ncbi.nlm.nih.gov/pubmed/23533697",
"http://www.ncbi.nlm.nih.gov/pubmed/23510020",
"http://www.ncbi.nlm.nih.gov/pubmed/23407992",
"http://www.ncbi.nlm.nih.gov/pubmed/23391427",
"http://www.ncbi.nlm.nih.gov/pubmed/23380991",
"http://www.ncbi.nlm.nih.gov/pubmed/23150908",
"http://www.ncbi.nlm.nih.gov/pubmed/17088018"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17088018",
"endSection": "title",
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"text": "Absence of TREM2 polymorphisms in patients with Alzheimer's disease and Frontotemporal Lobar Degeneration"
},
{
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"endSection": "abstract",
"offsetInBeginSection": 966,
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"text": " These data demonstrate that TREM2 coding region is highly conserved, implying a crucial role of this receptor. Further studies, including a functional analysis, are certainly required to clarify the role of TREM2 in neurodegenerative processes"
},
{
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"text": "Moreover, a rare TREM2 exon 2 variant (p.R47H) was reported to increase the risk of Alzheimer's disease (AD) with an odds ratio as strong as that for APOEε4"
},
{
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"text": "We observed an enrichment of rare variants across TREM2 in both AD and FTD patients compared to controls, most notably in the extracellular IgV-set domain"
},
{
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"endSection": "abstract",
"offsetInBeginSection": 764,
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"text": "None of the rare variants individually reached significant association, but the frequency of p.R47H was increased ~ 3-fold in both AD and FTD patients compared to controls, in line with previous reports"
},
{
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"endSection": "abstract",
"offsetInBeginSection": 1090,
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"text": "Our data corroborate and extend previous findings to include an increased frequency of rare heterozygous TREM2 variations in AD and FTD, and show that TREM2 variants may play a role in neurodegenerative diseases in general."
},
{
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"endSection": "abstract",
"offsetInBeginSection": 2,
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"text": "non-synonymous genetic rare variant, rs75932628-T (p.R47H), in the TREM2 gene has recently been reported to be a strong genetic risk factor for Alzheimer's disease (AD)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24041969",
"endSection": "abstract",
"offsetInBeginSection": 942,
"offsetInEndSection": 1076,
"text": "These data strongly support the important role of p.R47H in AD risk, and suggest that this rare genetic variant is not related to FTD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24002183",
"endSection": "abstract",
"offsetInBeginSection": 184,
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"text": " Higher levels of TREM2 mRNA (p = 0.002) and protein (p < 0.001) were identified in AD patients"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24002183",
"endSection": "abstract",
"offsetInBeginSection": 579,
"offsetInEndSection": 672,
"text": "Our results indicate that TREM2 might serve as a novel noninvasive biomarker for AD diagnosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23855982",
"endSection": "abstract",
"offsetInBeginSection": 7,
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"text": "studies have identified the rs75932628 (R47H) variant in TREM2 as an Alzheimer's disease risk factor with estimated odds ratio ranging from 2.9 to 5.1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23855982",
"endSection": "abstract",
"offsetInBeginSection": 652,
"offsetInEndSection": 850,
"text": "This study replicates the association between R47H and Alzheimer's disease risk in a large, population-based sample, and estimates the population frequency and attributable risk of this rare variant"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/17088018",
"endSection": "abstract",
"offsetInBeginSection": 858,
"offsetInEndSection": 965,
"text": "Moreover, mutation scanning of the five exons of TREM2 failed to detect the presence of novel polymorphisms"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23150908",
"endSection": "abstract",
"offsetInBeginSection": 798,
"offsetInEndSection": 1048,
"text": "A rare missense mutation (rs75932628-T) in the gene encoding the triggering receptor expressed on myeloid cells 2 (TREM2), which was predicted to result in an R47H substitution, was found to confer a significant risk of Alzheimer's disease in Iceland"
},
{
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"endSection": "abstract",
"offsetInBeginSection": 1362,
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"text": "We also found that carriers of rs75932628-T between the ages of 80 and 100 years without Alzheimer's disease had poorer cognitive function than noncarriers"
},
{
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"endSection": "abstract",
"offsetInBeginSection": 1542,
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"text": "Our findings strongly implicate variant TREM2 in the pathogenesis of Alzheimer's disease. Given the reported antiinflammatory role of TREM2 in the brain, the R47H substitution may lead to an increased predisposition to Alzheimer's disease through impaired containment of inflammatory processes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23380991",
"endSection": "abstract",
"offsetInBeginSection": 4,
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"text": "rs75932628-T variant of the gene encoding the triggering receptor expressed on myeloid cells 2 (TREM2) has recently been identified as a rare risk factor for late-onset Alzheimer's disease (AD)"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/23380991",
"endSection": "abstract",
"offsetInBeginSection": 574,
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"text": "These results confirm the association between this variant and AD and underline its involvement in early-onset cases"
},
{
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"offsetInBeginSection": 4,
"offsetInEndSection": 125,
"text": "recent studies have reported the association of rs75932628-T in the TREM2 gene with the risk for Alzheimer's disease (AD)"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/23391427",
"endSection": "abstract",
"offsetInBeginSection": 127,
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"text": "Rs75932628-T is a rare nonsynonymous variant (p.R47H) that confers a high risk of AD with an effect size similar to that of the APOE ɛ4 allele"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/23391427",
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"offsetInBeginSection": 896,
"offsetInEndSection": 1043,
"text": "Here, we report the first positive replication study in a Spanish population and confirm that TREM2 rs75932628-T is associated with the risk for AD"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/23407992",
"endSection": "abstract",
"offsetInBeginSection": 7,
"offsetInEndSection": 285,
"text": "works have demonstrated a rare functional variant (R47H) in triggering receptor expressed on myeloid cells (TREM) 2 gene, encoding TREM2 protein, increase susceptibility to late-onset Alzheimer's disease (AD), with an odds ratio similar to that of the apolipoprotein E ε4 allele"
},
{
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"endSection": "abstract",
"offsetInBeginSection": 287,
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"text": "The reduced function of TREM2 was speculated to be the main cause in the pathogenic effects of this risk variant, and TREM2 is highly expressed in white matter, as well as in the hippocampus and neocortex, which is partly consistent with the pathological features reported in AD brain, indicating the possible involvement of TREM2 in AD pathogenesis"
},
{
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"endSection": "abstract",
"offsetInBeginSection": 638,
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"text": "Emerging evidence has demonstrated that TREM2 could suppress inflammatory response by repression of microglia-mediated cytokine production and secretion, which may prevent inflammation-induced bystander damage of neurons"
},
{
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"endSection": "abstract",
"offsetInBeginSection": 860,
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"text": "TREM2 also participates in the regulation of phagocytic pathways that are responsible for the removal of neuronal debris"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/23407992",
"endSection": "abstract",
"offsetInBeginSection": 1160,
"offsetInEndSection": 1295,
"text": "Based on the potential protective actions of TREM2 in AD pathogenesis, targeting TREM2 might provide new opportunities for AD treatment"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23510020",
"endSection": "abstract",
"offsetInBeginSection": 495,
"offsetInEndSection": 927,
"text": "Under the hypothesis that low-prevalence variants showing moderate-to-high effect size may be associated with risk for sAD, two independent research groups have demonstrated that a rare variant (rs75932628, encoding a substitution of arginine by histidine at residue 47 (R47H), in the TREM2 gene, which encodes the triggering receptor expressed on myeloid cells 2) is significantly associated with an increased susceptibility to sAD"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/23533697",
"endSection": "abstract",
"offsetInBeginSection": 384,
"offsetInEndSection": 604,
"text": "Recently, a novel variant in the gene encoding the triggering receptor expressed on myeloid cells 2 (TREM2) has been identified that has refocused the spotlight back onto inflammation as a major contributing factor in AD"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23562540",
"endSection": "abstract",
"offsetInBeginSection": 657,
"offsetInEndSection": 748,
"text": "TREM gene cluster, a region recently reported to harbor rare variants that increase AD risk"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23582655",
"endSection": "abstract",
"offsetInBeginSection": 7,
"offsetInEndSection": 131,
"text": "evidence suggests that rare genetic variants within the TREM2 gene are associated with increased risk of Alzheimer's disease"
},
{
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"endSection": "abstract",
"offsetInBeginSection": 1062,
"offsetInEndSection": 1343,
"text": "These data suggest that a mutational burden in TREM2 may serve as a risk factor for neurodegenerative disease in general, and that potentially this class of TREM2 variant carriers with dementia should be considered as having a molecularly distinct form of neurodegenerative disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23692967",
"endSection": "abstract",
"offsetInBeginSection": 1502,
"offsetInEndSection": 1666,
"text": "The association of TREM2 variants with AD brings innate immune signaling into the light, affirming innate immunity's role as a significant factor in AD pathogenesis"
},
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"endSection": "abstract",
"offsetInBeginSection": 872,
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"text": "The purpose of this paper is to discuss these recent developments including the potential role that TREM2 normally plays and how loss of function may contribute to AD pathogenesis by enhancing oxidative stress and inflammation within the CNS"
},
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"offsetInBeginSection": 1861,
"offsetInEndSection": 2125,
"text": "Even though we are more at the beginning than at the end of sAD genetics, there is some reason for optimism given the recent identification of novel risk or protective variants (such as rare TREM2 and APP mutations) showing strong statistical associations with sAD"
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D000544",
"http://www.disease-ontology.org/api/metadata/DOID:10652",
"http://www.uniprot.org/uniprot/TREM2_HUMAN",
"http://www.uniprot.org/uniprot/TREM2_MOUSE"
]
| []
| 531a31a1b166e2b806000035 | 201 |
yesno | Is there a role for TFII-I in megakaryopoiesis? | ['yes'] | [
"yes"
]
| ['Yes. TFII-I acts as a repressor of β-globin gene transcription and is implicated in the differentiation of erythrocytes into megakaryopoiesis. Mutations in exon 2 interfere with the synthesis of the full-length isoform of TF II-I and lead to the production of a shortened isoform, TFII, in erythroid cells. TF2-I has a role in embryonic development and differentiation of all eukaryotes but its physiological function is still unclear.', 'Yes. TFII-I is a ubiquitously expressed transcription factor that positively or negatively regulates gene expression. TFII-I has been implicated in neuronal and immunologic diseases as well as in thymic epithelial cancer. Williams-Beuren Syndrome (WBS) is caused by a large hemizygous deletion on chromosome 7q11.23 which encompasses 26-28 genes, including GTF2I, the human gene encoding TFII-I. A subset of WBS patients has recently been shown to present with macrocytosis, a mild anemia characterized by enlarged erythrocytes. TFII-I acts as a repressor of β-globin gene transcription and that it is implicated in the differentiation of erythro-megakaryocytic cells.', 'Yes. The data show that TFII-I acts as a repressor of β-globin gene transcription and that it is implicated in the differentiation of erythro-megakaryocytic cells.', 'Yes. TFII-I acts as a repressor of β-globin gene transcription and it is implicated in the differentiation of erythrocytes and megakaryopoiesis. In fact, upregulation of TF II-I expression in mesenchymal stem cells increases both survival and angiogenesis and may therefore represent a novel and efficient therapeutic approach for modulating cell proliferation and differentiation.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/33101065"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33101065",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 42,
"text": "TFII-I/Gtf2i and Erythro-Megakaryopoiesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33101065",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 904,
"text": "TFII-I is a ubiquitously expressed transcription factor that positively or negatively regulates gene expression. TFII-I has been implicated in neuronal and immunologic diseases as well as in thymic epithelial cancer. Williams-Beuren Syndrome (WBS) is caused by a large hemizygous deletion on chromosome 7q11.23 which encompasses 26-28 genes, including GTF2I, the human gene encoding TFII-I. A subset of WBS patients has recently been shown to present with macrocytosis, a mild anemia characterized by enlarged erythrocytes. We conditionally deleted the TFII-I/Gtf2i gene in adult mice by tamoxifen induced Cre-recombination. Bone marrow cells revealed defects in erythro-megakaryopoiesis and an increase in expression of the adult β-globin gene. The data show that TFII-I acts as a repressor of β-globin gene transcription and that it is implicated in the differentiation of erythro-megakaryocytic cells."
}
]
| 11 | BioASQ-training11b | null | null | 6027f7171cb411341a0000ec | 203 |
yesno | Is golodirsen effective for the treatment of Duchenne muscular dystrophy? | ['yes'] | [
"yes"
]
| ['Yes, golodirsen can be considered effective for the treatment of Duchenne muscular dystrophy.', 'Yes, golodirsen is effective for the treatment of Duchenne muscular dystrophy.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/36401026",
"http://www.ncbi.nlm.nih.gov/pubmed/34788571",
"http://www.ncbi.nlm.nih.gov/pubmed/32026421",
"http://www.ncbi.nlm.nih.gov/pubmed/33025945"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33025945",
"endSection": "abstract",
"offsetInBeginSection": 783,
"offsetInEndSection": 902,
"text": "Golodirsen is a provisionally approved PMO-based drug for approx. 8% of all DMD patients amenable to exon 53 skipping. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32026421",
"endSection": "abstract",
"offsetInBeginSection": 599,
"offsetInEndSection": 710,
"text": "This article summarizes the milestones in the development of golodirsen leading to this first approval for DMD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32026421",
"endSection": "abstract",
"offsetInBeginSection": 252,
"offsetInEndSection": 513,
"text": "n December 2019, intravenous golodirsen received its first global approval in the USA for the treatment of DMD in patients with a confirmed mutation of the DMD gene that is amenable to exon 53 skipping, based on positive results from a phase I/II clinical trial"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36401026",
"endSection": "abstract",
"offsetInBeginSection": 334,
"offsetInEndSection": 486,
"text": "To date, four PMOs, including eteplirsen, casimersen, viltolarsen, and golodirsen, have been conditionally approved by the FDA for the treatment of DMD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34788571",
"endSection": "abstract",
"offsetInBeginSection": 965,
"offsetInEndSection": 1069,
"text": "Golodirsen increased dystrophin protein (16.0-fold; P < 0.001) and exon skipping (28.9-fold; P < 0.001)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34788571",
"endSection": "abstract",
"offsetInBeginSection": 1381,
"offsetInEndSection": 1552,
"text": "This study provides evidence for golodirsen biologic activity and long-term safety in a declining DMD population and suggests functional benefit versus external controls. "
}
]
| 12 | BioASQ-training12b | null | null | 64178e4b690f196b51000022 | 204 |
yesno | Can modulation of KCNQ1 splicing prevent arrhythmias? | ['yes'] | [
"yes"
]
| ['Amiloride reduces arrhythmogenicity through the modulation of KCNQ1 splicing. Therefore, the modulation of KCNQ1 splicing may help prevent arrhythmias.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23608591"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23608591",
"endSection": "abstract",
"offsetInBeginSection": 1547,
"offsetInEndSection": 1758,
"text": "Amiloride regulates IKs and APs with transmural differences and reduces arrhythmogenicity through the modulation of KCNQ1 splicing. We suggested that the modulation of KCNQ1 splicing may help prevent arrhythmia."
}
]
| 12 | BioASQ-training12b | null | null | 6410ef9b201352f04a000031 | 205 |
yesno | Is there a link between nuclear position and DNA repair pathway choice? | ['yes'] | [
"yes"
]
| ['Yes. Nuclear position dictates DNA repair pathway choice, thus revealing a new level of regulation in DSB repair controlled by spatial organization of DNA within the nucleus.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/25366693"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25366693",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 52,
"text": "Nuclear position dictates DNA repair pathway choice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25366693",
"endSection": "abstract",
"offsetInBeginSection": 452,
"offsetInEndSection": 1137,
"text": "We demonstrate that DSBs induced at the nuclear membrane (but not at nuclear pores or nuclear interior) fail to rapidly activate the DNA damage response (DDR) and repair by homologous recombination (HR). Real-time and superresolution imaging reveal that DNA DSBs within lamina-associated domains do not migrate to more permissive environments for HR, like the nuclear pores or the nuclear interior, but instead are repaired in situ by alternative end-joining. Our results are consistent with a model in which nuclear position dictates the choice of DNA repair pathway, thus revealing a new level of regulation in DSB repair controlled by spatial organization of DNA within the nucleus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25366693",
"endSection": "abstract",
"offsetInBeginSection": 912,
"offsetInEndSection": 1137,
"text": "Our results are consistent with a model in which nuclear position dictates the choice of DNA repair pathway, thus revealing a new level of regulation in DSB repair controlled by spatial organization of DNA within the nucleus."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25366693",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 53,
"text": "Nuclear position dictates DNA repair pathway choice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25366693",
"endSection": "abstract",
"offsetInBeginSection": 912,
"offsetInEndSection": 1138,
"text": "Our results are consistent with a model in which nuclear position dictates the choice of DNA repair pathway, thus revealing a new level of regulation in DSB repair controlled by spatial organization of DNA within the nucleus."
}
]
| 11 | BioASQ-training11b | [
"https://meshb.nlm.nih.gov/record/ui?ui=D045643",
"https://meshb.nlm.nih.gov/record/ui?ui=D059767",
"https://meshb.nlm.nih.gov/record/ui?ui=D004260"
]
| null | 5a774e40faa1ab7d2e000007 | 206 |
yesno | Is pregnancy an additional risk during during H1N1 infection? | ['yes'] | [
"yes"
]
| Pregnant women are at increased risk for complications from pandemic influenza H1N1 virus infection. Pregnant women, because of their altered immunity and physiological adaptations, are at higher risk of developing pulmonary complications, especially in the second and third trimesters. Pregnancy, particularly during the third trimester, increases the risk of complications and early antiviral treatment is associated with improved outcomes. | [
"http://www.ncbi.nlm.nih.gov/pubmed/20148081",
"http://www.ncbi.nlm.nih.gov/pubmed/20100064",
"http://www.ncbi.nlm.nih.gov/pubmed/19643469",
"http://www.ncbi.nlm.nih.gov/pubmed/22030045",
"http://www.ncbi.nlm.nih.gov/pubmed/21913391",
"http://www.ncbi.nlm.nih.gov/pubmed/21756329",
"http://www.ncbi.nlm.nih.gov/pubmed/21596080",
"http://www.ncbi.nlm.nih.gov/pubmed/21252793",
"http://www.ncbi.nlm.nih.gov/pubmed/20531946",
"http://www.ncbi.nlm.nih.gov/pubmed/22564554",
"http://www.ncbi.nlm.nih.gov/pubmed/22551713",
"http://www.ncbi.nlm.nih.gov/pubmed/22515877",
"http://www.ncbi.nlm.nih.gov/pubmed/22482974",
"http://www.ncbi.nlm.nih.gov/pubmed/22411229",
"http://www.ncbi.nlm.nih.gov/pubmed/22331165",
"http://www.ncbi.nlm.nih.gov/pubmed/22272853",
"http://www.ncbi.nlm.nih.gov/pubmed/22120858",
"http://www.ncbi.nlm.nih.gov/pubmed/24051575",
"http://www.ncbi.nlm.nih.gov/pubmed/23116790",
"http://www.ncbi.nlm.nih.gov/pubmed/22859826",
"http://www.ncbi.nlm.nih.gov/pubmed/22851818",
"http://www.ncbi.nlm.nih.gov/pubmed/22782418"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20148081",
"endSection": "abstract",
"offsetInBeginSection": 495,
"offsetInEndSection": 566,
"text": "H1N1 influenza in pregnancy can be associated with severe complications"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20100064",
"endSection": "abstract",
"offsetInBeginSection": 1461,
"offsetInEndSection": 1560,
"text": "This case series confirms a high number of complications in pregnant women due to pandemic H1N1/09."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19643469",
"endSection": "abstract",
"offsetInBeginSection": 1841,
"offsetInEndSection": 1936,
"text": "Pregnant women might be at increased risk for complications from pandemic H1N1 virus infection."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22030045",
"endSection": "abstract",
"offsetInBeginSection": 1491,
"offsetInEndSection": 1592,
"text": "Pregnant women are at increased risk for complications from pandemic influenza H1N1 virus infection. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21913391",
"endSection": "abstract",
"offsetInBeginSection": 1458,
"offsetInEndSection": 1756,
"text": "Vaccination of pregnant women against influenza A (H1N1) by Russian subunit formulation (MonoGrippol plus) showed reactogenicity comparable to control group by the level of influence on general metabolic and immunologic homeostasis and on the course of pregnancy, which is an evidence of its safety"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21756329",
"endSection": "abstract",
"offsetInBeginSection": 145,
"offsetInEndSection": 284,
"text": "Pregnancy was identified as a major risk factor for increased mortality and morbidity due to H1N1 influenza in the pandemic of 2009 to 2010"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21756329",
"endSection": "abstract",
"offsetInBeginSection": 940,
"offsetInEndSection": 1285,
"text": "While it is not possible to ascertain retrospectively if myocarditis was caused by either infection with H1N1 virus or as a result of pregnancy (in the absence of endomyocardial biopsies), the significant association with myocardial involvement in both women demonstrates the increased risk of exposure to H1N1 influenza virus in pregnant women."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21596080",
"endSection": "abstract",
"offsetInBeginSection": 1664,
"offsetInEndSection": 1940,
"text": "Although limited in size, the fully prospective nature of the safety follow-up of these women vaccinated during pregnancy is unique and offers an important degree of reassurance for the use of the AS03 adjuvanted H1N1 (2009) vaccine in this high risk group for H1N1 infection."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21596080",
"endSection": "abstract",
"offsetInBeginSection": 117,
"offsetInEndSection": 320,
"text": "During the H1N1 2009 pandemic, pregnant women constituted one of the priority groups for vaccination in many countries, creating a need for close monitoring of the safety of the vaccine in pregnant women"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21252793",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 154,
"text": "Emerging data suggest that pregnancy conveys high risk for severe complications from the 2009 pandemic influenza A virus (2009 H1N1) infection"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20531946",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 199,
"text": "Pregnant women have been identified as a group at risk, both for respiratory complications than for the admissions to the Intensive Care Unit (ICU) during the 2009 H1N1 influenza pandemic"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20531946",
"endSection": "abstract",
"offsetInBeginSection": 1567,
"offsetInEndSection": 1681,
"text": "This report mitigates substantially the presumed severity of pandemic H1N1/09 influenza infection during pregnancy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22564554",
"endSection": "abstract",
"offsetInBeginSection": 1105,
"offsetInEndSection": 1230,
"text": "The results of our study do not indicate a risk for the pregnant woman and the developing embryo/fetus after H1N1 vaccination"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22551713",
"endSection": "abstract",
"offsetInBeginSection": 1529,
"offsetInEndSection": 1704,
"text": "This large cohort study found no evidence of an increased risk of fetal death associated with exposure to an adjuvanted pandemic A/H1N1 2009 influenza vaccine during pregnancy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22515877",
"endSection": "abstract",
"offsetInBeginSection": 1006,
"offsetInEndSection": 1158,
"text": "Our results suggest that second- or third-trimester H1N1 vaccination was associated with improved fetal and neonatal outcomes during the recent pandemic"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22482974",
"endSection": "abstract",
"offsetInBeginSection": 146,
"offsetInEndSection": 278,
"text": "Pregnant women might thus be at increased risk of complications from pandemic H1N1 virus infection, and illness may progress rapidly"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22482974",
"endSection": "abstract",
"offsetInBeginSection": 1258,
"offsetInEndSection": 1332,
"text": "Pregnant women with H1N1 infection seem to benefit from antiviral therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22411229",
"endSection": "abstract",
"offsetInBeginSection": 755,
"offsetInEndSection": 863,
"text": "arly identification and treatment were the most important factors in different countries and areas examined."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22411229",
"endSection": "abstract",
"offsetInBeginSection": 864,
"offsetInEndSection": 1013,
"text": "The vaccine and antiviral drugs that have been the most efficient means to control the novel virus appear to be safe but require more extensive study"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22331165",
"endSection": "abstract",
"offsetInBeginSection": 822,
"offsetInEndSection": 987,
"text": "However, there were significant differences between the two groups in relation to mean age, treatment with oseltamivir, schooling, and presence of other risk factors"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22782418",
"endSection": "abstract",
"offsetInBeginSection": 128,
"offsetInEndSection": 286,
"text": "To investigate whether exposure to an adjuvanted influenza A(H1N1)pdm09 vaccine during pregnancy was associated with increased risk of adverse fetal outcomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22782418",
"endSection": "abstract",
"offsetInBeginSection": 2168,
"offsetInEndSection": 2386,
"text": "In this Danish cohort, exposure to an adjuvanted influenza A(H1N1)pdm09 vaccine during pregnancy was not associated with a significantly increased risk of major birth defects, preterm birth, or fetal growth restriction"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22851818",
"endSection": "abstract",
"offsetInBeginSection": 641,
"offsetInEndSection": 755,
"text": "Most people affected by the virus, including pregnant women, suffer a mild viral illness, and make a full recovery"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22851818",
"endSection": "abstract",
"offsetInBeginSection": 1032,
"offsetInEndSection": 1216,
"text": "Pregnant women, because of their altered immunity and physiological adaptations, are at higher risk of developing pulmonary complications, especially in the second and third trimesters"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22851818",
"endSection": "abstract",
"offsetInBeginSection": 1491,
"offsetInEndSection": 1678,
"text": "The pregnancy outcomes were also poor for women who were affected by the virus with a fivefold increase in the perinatal mortality rate and threefold increase in the preterm delivery rate"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22859826",
"endSection": "abstract",
"offsetInBeginSection": 13,
"offsetInEndSection": 249,
"text": "regnant women were at increased risk for serious outcomes of 2009 pandemic influenza A virus subtype H1N1 (influenza A[H1N1]pdm09) infection, but little is known about the overall impact of the pandemic on neonatal and maternal outcomes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22859826",
"endSection": "abstract",
"offsetInBeginSection": 1572,
"offsetInEndSection": 1700,
"text": "In this large, geographically diverse population, A(H1N1)pdm09 infection increased the risk for hospitalization during pregnancy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22901103",
"endSection": "abstract",
"offsetInBeginSection": 1358,
"offsetInEndSection": 1582,
"text": "Vaccination during pregnancy with Pandemrix(®) appeared to have no ill effects on the pregnancy. On the contrary, the rate of preterm birth and low birthweight was lower than expected, which agrees with some previous results"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23116790",
"endSection": "abstract",
"offsetInBeginSection": 475,
"offsetInEndSection": 745,
"text": "During the influenza A(H1N1)pmd09 pandemic, although many cases occurred in younger adults, the risk factors identified for severe infections and complications were similar to those for seasonal influenza, including chronic respiratory, renal, liver, and heart diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23116790",
"endSection": "abstract",
"offsetInBeginSection": 1110,
"offsetInEndSection": 1228,
"text": "In terms of pregnancy, the studies have shown contradictory results due to variations in methodology and medical care."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23116790",
"endSection": "abstract",
"offsetInBeginSection": 1229,
"offsetInEndSection": 1413,
"text": "However, it seems that pregnancy, particularly during the third trimester, increases the risk of complications, and that early antiviral treatment is associated with improved outcomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24051575",
"endSection": "abstract",
"offsetInBeginSection": 903,
"offsetInEndSection": 1024,
"text": "Pregnant women with mild clinical illness secondary to 2009 H1N1 were not at a greater risk of adverse pregnancy outcomes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24051575",
"endSection": "abstract",
"offsetInBeginSection": 1026,
"offsetInEndSection": 1098,
"text": "However, severely infected women were more likely to deliver SGA infants"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22120858",
"endSection": "abstract",
"offsetInBeginSection": 1852,
"offsetInEndSection": 1984,
"text": "Gestational age is associated with the risk of developing critical infection. The risk increases with increasing weeks of gestation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22120858",
"endSection": "abstract",
"offsetInBeginSection": 67,
"offsetInEndSection": 205,
"text": " Following the start of winter in Liaoning province in China, the number of pregnant women infected with influenza increased significantly"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22272853",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 236,
"text": "regnancy, with or without additional complications, constitutes a high-risk condition for complications of influenza infection and warrants early intervention with neuraminidase inhibitors such as oseltamivir, if influenza is suspected"
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018566",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D053118",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D012306",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D011247"
]
| []
| 531a3fe3b166e2b806000038 | 207 |
yesno | Is Tocilizumab effective for Giant-Cell Arteritis? | ['yes'] | [
"yes"
]
| ['Yes, Tocilizumab effective for Giant-Cell Arteritis. Its efficacy was proven in clinical trials. Tocilizumab may exert its therapeutic effects in Giant-Cell Arteritis by increasing the proliferation and activation of Tregs, and by reverting the pathogenic Treg phenotype seen during active disease.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/27182063",
"http://www.ncbi.nlm.nih.gov/pubmed/27927642",
"http://www.ncbi.nlm.nih.gov/pubmed/24075627",
"http://www.ncbi.nlm.nih.gov/pubmed/29146018",
"http://www.ncbi.nlm.nih.gov/pubmed/28745999",
"http://www.ncbi.nlm.nih.gov/pubmed/28499892",
"http://www.ncbi.nlm.nih.gov/pubmed/28116918",
"http://www.ncbi.nlm.nih.gov/pubmed/26885650",
"http://www.ncbi.nlm.nih.gov/pubmed/27919193",
"http://www.ncbi.nlm.nih.gov/pubmed/24854376",
"http://www.ncbi.nlm.nih.gov/pubmed/24357324",
"http://www.ncbi.nlm.nih.gov/pubmed/28895041",
"http://www.ncbi.nlm.nih.gov/pubmed/28138903"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28138903",
"endSection": "abstract",
"offsetInBeginSection": 1734,
"offsetInEndSection": 1957,
"text": "Emerging evidence for adjunctive therapy with tocilizumab, methotrexate, aspirin, angiotensin receptor blockers, and statins is encouraging and may lead to a more mainstream role for these therapies among patients with GCA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28116918",
"endSection": "abstract",
"offsetInBeginSection": 731,
"offsetInEndSection": 914,
"text": " TNF-α blockers are ineffective in giant cell arteritis, while observational evidence and a phase 2 randomized trial support the use of tocilizumab in relapsing giant cell arteritis. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27927642",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "OBJECTIVES: Randomised-controlled trials have recently proven the efficacy of the interleukin (IL)-6 receptor antagonist tocilizumab (TCZ) in giant cell arteritis (GCA). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27927642",
"endSection": "abstract",
"offsetInBeginSection": 1672,
"offsetInEndSection": 1861,
"text": "CONCLUSIONS: TCZ may exert its therapeutic effects in GCA by increasing the proliferation and activation of Tregs, and by reverting the pathogenic Treg phenotype seen during active disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27919193",
"endSection": "abstract",
"offsetInBeginSection": 678,
"offsetInEndSection": 769,
"text": "Cyclophosphamide and tocilizumab look promising but require validation in further studies. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28499892",
"endSection": "abstract",
"offsetInBeginSection": 815,
"offsetInEndSection": 1440,
"text": "Therefore, tocilizumab (humanised monoclonal antibody binding the human interleukin-6 receptor) was introduced as a potential salvage therapy with a swift consecutive resolution of the systemic symptoms and stabilization of the ophthalmic lesions.CONCLUSIONS: Although a late effect of steroids pulses cannot be formally ruled out in this dramatic situation, tocilizumab likely offered a decisive effect in preventing bilateral blindness and may have contributed to steroid tapering. Tocilizumab may represent a new early effective second-line treatment option in corticosteroid-resistant anterior ischemic optic neuropathy. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28499892",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 114,
"text": "Tocilizumab for giant cell arteritis with corticosteroid-resistant progressive anterior ischemic optic neuropathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28745999",
"endSection": "abstract",
"offsetInBeginSection": 2203,
"offsetInEndSection": 2573,
"text": "CONCLUSIONS: Tocilizumab, received weekly or every other week, combined with a 26-week prednisone taper was superior to either 26-week or 52-week prednisone tapering plus placebo with regard to sustained glucocorticoid-free remission in patients with giant-cell arteritis. Longer follow-up is necessary to determine the durability of remission and safety of tocilizumab."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28895041",
"endSection": "abstract",
"offsetInBeginSection": 1098,
"offsetInEndSection": 1234,
"text": "Two RCTs have evidenced the efficacy of tocilizumab in addition to glucocorticoids (GCs) in the treatment of giant cell arteritis (GCA)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29146018",
"endSection": "abstract",
"offsetInBeginSection": 833,
"offsetInEndSection": 1001,
"text": " Recent randomized placebo-controlled trials have reported on the efficacy and safety of abatacept and mostly tocilizumab in inducing and maintaining remission of GCA. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29146018",
"endSection": "abstract",
"offsetInBeginSection": 1307,
"offsetInEndSection": 1490,
"text": "If a biological therapy is indicated, and in light of the data discussed in this review, the first choice would be tocilizumab in GCA and anti-TNF-α agents (mainly infliximab) in TAK."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27182063",
"endSection": "abstract",
"offsetInBeginSection": 501,
"offsetInEndSection": 537,
"text": "CONCLUSION: TCZ is effective in GCA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28116918",
"endSection": "abstract",
"offsetInBeginSection": 739,
"offsetInEndSection": 920,
"text": "TNF-α blockers are ineffective in giant cell arteritis, while observational evidence and a phase 2 randomized trial support the use of tocilizumab in relapsing giant cell arteritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24075627",
"endSection": "abstract",
"offsetInBeginSection": 361,
"offsetInEndSection": 621,
"text": "A favorable outcome was rapidly observed both on clinical and biological data allowing a corticoid therapy sparing.<br><b>CONCLUSION</b>: Tocilizumab is a promising treatment of giant cell arteritis but controlled trials are needed to confirm its efficacy.<br>"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24075627",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 360,
"text": "<b>INTRODUCTION</b>: Treatment of giant cell arteritis is based on prolonged corticosteroid therapy but adverse side effects are common especially in the elderly.<br><b>CASE REPORTS</b>: We report three patients with giant cell vasculitis treated by tocilizumab, an interleukin-6 receptor antibody, owing to resistance or intolerance to corticosteroid therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24357324",
"endSection": "abstract",
"offsetInBeginSection": 533,
"offsetInEndSection": 668,
"text": "Several studies have reported that tocilizumab is effective for aortitis associated with Takayasu's arteritis and giant cell arteritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28116918",
"endSection": "abstract",
"offsetInBeginSection": 718,
"offsetInEndSection": 900,
"text": "TNF-α blockers are ineffective in giant cell arteritis, while observational evidence and a phase 2 randomized trial support the use of tocilizumab in relapsing giant cell arteritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26885650",
"endSection": "abstract",
"offsetInBeginSection": 410,
"offsetInEndSection": 515,
"text": "Preliminary clinical trial data suggest that abatacept and tocilizumab reduce the risk of relapse in GCA."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24854376",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 72,
"text": "Tocilizumab, an effective treatment for relapsing giant cell arteritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28116918",
"endSection": "abstract",
"offsetInBeginSection": 718,
"offsetInEndSection": 899,
"text": "TNF-α blockers are ineffective in giant cell arteritis, while observational evidence and a phase 2 randomized trial support the use of tocilizumab in relapsing giant cell arteritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24075627",
"endSection": "abstract",
"offsetInBeginSection": 432,
"offsetInEndSection": 551,
"text": "Tocilizumab is a promising treatment of giant cell arteritis but controlled trials are needed to confirm its efficacy."
}
]
| 11 | BioASQ-training11b | [
"https://meshb.nlm.nih.gov/record/ui?ui=D013700"
]
| null | 5a733d2a2dc08e987e000015 | 208 |
yesno | Is apremilast effective for psoriasis? | ['yes'] | [
"yes"
]
| ['Yes, apremilast is effective for treatment of psoriasis.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/27376729",
"http://www.ncbi.nlm.nih.gov/pubmed/26923915",
"http://www.ncbi.nlm.nih.gov/pubmed/26220911",
"http://www.ncbi.nlm.nih.gov/pubmed/22712800",
"http://www.ncbi.nlm.nih.gov/pubmed/26243735",
"http://www.ncbi.nlm.nih.gov/pubmed/26644232",
"http://www.ncbi.nlm.nih.gov/pubmed/26806620",
"http://www.ncbi.nlm.nih.gov/pubmed/26549249",
"http://www.ncbi.nlm.nih.gov/pubmed/27486641",
"http://www.ncbi.nlm.nih.gov/pubmed/23663752",
"http://www.ncbi.nlm.nih.gov/pubmed/24595547",
"http://www.ncbi.nlm.nih.gov/pubmed/26954311",
"http://www.ncbi.nlm.nih.gov/pubmed/26357944",
"http://www.ncbi.nlm.nih.gov/pubmed/20419594",
"http://www.ncbi.nlm.nih.gov/pubmed/26267722",
"http://www.ncbi.nlm.nih.gov/pubmed/26089047",
"http://www.ncbi.nlm.nih.gov/pubmed/23569359",
"http://www.ncbi.nlm.nih.gov/pubmed/26892034",
"http://www.ncbi.nlm.nih.gov/pubmed/26783350",
"http://www.ncbi.nlm.nih.gov/pubmed/27538241",
"http://www.ncbi.nlm.nih.gov/pubmed/26660203",
"http://www.ncbi.nlm.nih.gov/pubmed/26820148",
"http://www.ncbi.nlm.nih.gov/pubmed/26837052",
"http://www.ncbi.nlm.nih.gov/pubmed/27021239",
"http://www.ncbi.nlm.nih.gov/pubmed/23030767",
"http://www.ncbi.nlm.nih.gov/pubmed/26792812"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26549249",
"endSection": "abstract",
"offsetInBeginSection": 1630,
"offsetInEndSection": 1698,
"text": "CONCLUSION: Apremilast reduces the severity of nail/scalp psoriasis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26792812",
"endSection": "abstract",
"offsetInBeginSection": 1638,
"offsetInEndSection": 1834,
"text": "CONCLUSIONS: Apremilast demonstrated clinically meaningful improvements in psoriatic arthritis and psoriasis at week 16; sustained improvements were seen with continued treatment through 52 weeks."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26783350",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "Apremilast: A Novel Drug for Treatment of Psoriasis and Psoriatic Arthritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26783350",
"endSection": "abstract",
"offsetInBeginSection": 634,
"offsetInEndSection": 910,
"text": "In those that involved doses of 30 mg twice daily, a significantly greater percentage of patients receiving apremilast (28.8% to 40.9%) compared with placebo (5.3% to 5.8%) achieved at least 75% improvement from baseline in Psoriasis Area and Severity Index score at 16 weeks."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26783350",
"endSection": "abstract",
"offsetInBeginSection": 1356,
"offsetInEndSection": 1605,
"text": "CONCLUSIONS: Apremilast has a novel mechanism of action and is safe and effective for the management of psoriasis and psoriatic arthritis. At this time, apremilast should be reserved for patients unable to take disease-modifying antirheumatic drugs."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26089047",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 254,
"text": "Apremilast, an oral phosphodiesterase 4 (PDE4) inhibitor, in patients with moderate to severe plaque psoriasis: Results of a phase III, randomized, controlled trial (Efficacy and Safety Trial Evaluating the Effects of Apremilast in Psoriasis [ESTEEM] 1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23569359",
"endSection": "abstract",
"offsetInBeginSection": 938,
"offsetInEndSection": 1338,
"text": "More recently, three larger double-blinded, and randomized multicenter studies demonstrate that apremilast is efficacious in the treatment of psoriasis and PsA, with significantly higher numbers of apremilast-treated patients achieving endpoints of a 75% reduction compared to baseline in Psoriasis Area and Severity Index (PASI-75) or American College of Rheumatology-20 scores, relative to placebo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26089047",
"endSection": "abstract",
"offsetInBeginSection": 1284,
"offsetInEndSection": 1664,
"text": "No new significant adverse events emerged with continued apremilast exposure versus the placebo-controlled period.Data were limited to 52 weeks and may not generalize to nonplaque psoriasis.Apremilast was effective in moderate to severe plaque psoriasis.<CopyrightInformation>Copyright © 2015 American Academy of Dermatology, Inc. Published by Elsevier Inc. All rights reserved.</"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23030767",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 596,
"text": "Apremilast, a small molecule specific inhibitor of phosphodiesterase 4, works intracellularly to modulate pro-inflammatory and anti-inflammatory mediator production.Assess apremilast efficacy and safety in moderate to severe plaque psoriasis.Phase II, 12-week, multicenter, double-blind, placebo-controlled, parallel-group, dose-comparison study of 259 subjects randomized 1 : 1 : 1 to placebo, apremilast 20 mg QD or apremilast 20 mg BID.More subjects receiving apremilast 20 mg BID achieved ≥ 75% reduction in Psoriasis Area and Severity Index (PASI-75) vs. placebo (24.4% vs. 10.3%; P = 0.023)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23663752",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 449,
"text": "Apremilast, a specific inhibitor of phosphodiesterase 4, modulates pro-inflammatory and anti-inflammatory cytokine production.Apremilasts effect on patient-reported outcomes (PROs) in patients with moderate to severe psoriasis was evaluated in a phase IIb randomized, controlled trial (NCT00773734).In this 16-week, placebo-controlled study, 352 patients with moderate to severe plaque psoriasis received placebo or apremilast (10, 20, or 30 mg BID)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26220911",
"endSection": "abstract",
"offsetInBeginSection": 1278,
"offsetInEndSection": 1517,
"text": "Although further longer-term and comparative efficacy and tolerability data would be beneficial, the current clinical data indicate that apremilast is an effective and well tolerated option for the management of psoriasis and PsA in adults"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23569359",
"endSection": "abstract",
"offsetInBeginSection": 944,
"offsetInEndSection": 1343,
"text": "More recently, three larger double-blinded, and randomized multicenter studies demonstrate that apremilast is efficacious in the treatment of psoriasis and PsA, with significantly higher numbers of apremilast-treated patients achieving endpoints of a 75% reduction compared to baseline in Psoriasis Area and Severity Index (PASI-75) or American College of Rheumatology-20 scores, relative to placebo"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23030767",
"endSection": "abstract",
"offsetInBeginSection": 1601,
"offsetInEndSection": 1813,
"text": "No deaths or opportunistic infections were reported.Apremilast 20 mg BID for 12 weeks was effective and well tolerated in subjects with moderate to severe plaque psoriasis.<CopyrightInformation>© 2012 The Authors"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20419594",
"endSection": "abstract",
"offsetInBeginSection": 686,
"offsetInEndSection": 934,
"text": "In addition, GlaxoSmithKline plc is developing 256066, an inhaled formulation of a PDE4 inhibitor that has demonstrated efficacy in trials in asthma, and apremilast from Celgene Corp has been reported to be effective for the treatment of psoriasis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26220911",
"endSection": "abstract",
"offsetInBeginSection": 1278,
"offsetInEndSection": 1518,
"text": "Although further longer-term and comparative efficacy and tolerability data would be beneficial, the current clinical data indicate that apremilast is an effective and well tolerated option for the management of psoriasis and PsA in adults."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26089047",
"endSection": "abstract",
"offsetInBeginSection": 1284,
"offsetInEndSection": 1665,
"text": "No new significant adverse events emerged with continued apremilast exposure versus the placebo-controlled period.Data were limited to 52 weeks and may not generalize to nonplaque psoriasis.Apremilast was effective in moderate to severe plaque psoriasis.<CopyrightInformation>Copyright © 2015 American Academy of Dermatology, Inc. Published by Elsevier Inc. All rights reserved.</C"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26243735",
"endSection": "abstract",
"offsetInBeginSection": 1161,
"offsetInEndSection": 1344,
"text": "Several drug peculiarities, such as the low frequency of adverse events and the oral route of administration, make apremilast an innovative treatment for moderate-to-severe psoriasis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26267722",
"endSection": "abstract",
"offsetInBeginSection": 244,
"offsetInEndSection": 673,
"text": "Two new oral medications, apremilast and tofacitinib, have been developed for their immunomodulatory properties, and their potential efficacy in treating psoriasis is being evaluated.We reviewed phase III randomized, placebo-controlled clinical trial results for apremilast and tofacitinib for efficacy and safety in psoriasis.Psoriasis Area and Severity Index (PASI) 75 after 16 weeks for apremilast was between 28.8% and 33.1%."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26089047",
"endSection": "abstract",
"offsetInBeginSection": 1476,
"offsetInEndSection": 1541,
"text": "Apremilast was effective in moderate to severe plaque psoriasis.."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26267722",
"endSection": "abstract",
"offsetInBeginSection": 1009,
"offsetInEndSection": 1109,
"text": "Both new oral medications, apremilast and tofacitinib, appear to be effective in treating psoriasis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26357944",
"endSection": "abstract",
"offsetInBeginSection": 1516,
"offsetInEndSection": 1612,
"text": "Apremilast was effective in the treatment of moderate-to-severe plaque psoriasis over 52 weeks.."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27376729",
"endSection": "abstract",
"offsetInBeginSection": 963,
"offsetInEndSection": 1064,
"text": "Apremilast is an effective and well-tolerated option in treating moderate-to-severe plaque psoriasis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26783350",
"endSection": "abstract",
"offsetInBeginSection": 1282,
"offsetInEndSection": 1407,
"text": "Apremilast has a novel mechanism of action and is safe and effective for the management of psoriasis and psoriatic arthritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23030767",
"endSection": "abstract",
"offsetInBeginSection": 1651,
"offsetInEndSection": 1772,
"text": "Apremilast 20 mg BID for 12 weeks was effective and well tolerated in subjects with moderate to severe plaque psoriasis.."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26243735",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 43,
"text": "Apremilast for the treatment of psoriasis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27021239",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 309,
"text": "Apremilast, an oral phosphodiesterase-4 inhibitor, in the treatment of palmoplantar psoriasis: Results of a pooled analysis from phase II PSOR-005 and phase III Efficacy and Safety Trial Evaluating the Effects of Apremilast in Psoriasis (ESTEEM) clinical trials in patients with moderate to severe psoriasis."
}
]
| 6 | BioASQ-training6b | [
"http://www.disease-ontology.org/api/metadata/DOID:8893",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D011565"
]
| [
{
"o": "psoriasis",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C0033860"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A0487662",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0033860"
},
{
"o": "psoriasis",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A0487662"
},
{
"o": "APREMILAST",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C1678805"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A15589751",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C1678805"
},
{
"o": "apremilast",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A15589751"
}
]
| 589a246d78275d0c4a000033 | 209 |
yesno | Is there a relationship between thyroid hormone altered metabolism and coronary artery disease? | ['yes'] | [
"yes"
]
| The major part of the studies and metaanalysis data show that hypothyroidism, both primary and secondary forms, is associated with higher incidence and severity of coronary artery disease. | [
"http://www.ncbi.nlm.nih.gov/pubmed/23470525",
"http://www.ncbi.nlm.nih.gov/pubmed/22877896",
"http://www.ncbi.nlm.nih.gov/pubmed/22724581",
"http://www.ncbi.nlm.nih.gov/pubmed/21745107",
"http://www.ncbi.nlm.nih.gov/pubmed/19650571",
"http://www.ncbi.nlm.nih.gov/pubmed/19609889",
"http://www.ncbi.nlm.nih.gov/pubmed/18497453",
"http://www.ncbi.nlm.nih.gov/pubmed/17434631",
"http://www.ncbi.nlm.nih.gov/pubmed/17222925",
"http://www.ncbi.nlm.nih.gov/pubmed/14677810",
"http://www.ncbi.nlm.nih.gov/pubmed/16649727",
"http://www.ncbi.nlm.nih.gov/pubmed/16524858",
"http://www.ncbi.nlm.nih.gov/pubmed/16507804",
"http://www.ncbi.nlm.nih.gov/pubmed/21789282",
"http://www.ncbi.nlm.nih.gov/pubmed/17614771",
"http://www.ncbi.nlm.nih.gov/pubmed/9117915",
"http://www.ncbi.nlm.nih.gov/pubmed/9709915",
"http://www.ncbi.nlm.nih.gov/pubmed/23086805",
"http://www.ncbi.nlm.nih.gov/pubmed/732079"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23470525",
"endSection": "abstract",
"offsetInBeginSection": 1516,
"offsetInEndSection": 1747,
"text": "The results showed that higher levels of TSH within the reference range were independently associated with the presence of CAD only among subjects less than or equal to 65 years old, suggesting age might influence the relationship."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22877896",
"endSection": "abstract",
"offsetInBeginSection": 1594,
"offsetInEndSection": 1829,
"text": "FT3 levels within the normal range were inversely correlated with the presence and severity of CAD. Moreover, lower FT3 concentrations were correlated with the Gensini score and independently predicted the presence and severity of CAD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22724581",
"endSection": "abstract",
"offsetInBeginSection": 922,
"offsetInEndSection": 1221,
"text": "High TSH within the reference range was associated with increased risk of coronary death in women (P(trend) 0·005), but not in men. The risk of coronary death was also increased among women with subclinical hypothyroidism or subclinical hyperthyroidism, compared to women with TSH of 0·50-1·4 mU/l. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21745107",
"endSection": "abstract",
"offsetInBeginSection": 1110,
"offsetInEndSection": 1186,
"text": " Prevalence of CHD was more common in hypothyroid and moderate SCH patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19650571",
"endSection": "abstract",
"offsetInBeginSection": 1657,
"offsetInEndSection": 2003,
"text": "The angiographic results were as follows: significant coronary disease (SH 28.1% vs. non-SH 43.8%; p=0.087); three-vessel disease (9.4% vs. 9.9%; p=0.919); two-vessel disease (12.5% vs. 13.4%; p=0.892); single-vessel disease (6.3% vs. 29.5%; p=0.051); minimal lesions (9.4% vs. 10.9%; p=0.794); and no coronary disease (62.4% vs, 45.3%; p=0.064)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19609889",
"endSection": "abstract",
"offsetInBeginSection": 687,
"offsetInEndSection": 962,
"text": "Lower fT3 levels were predictive of both single-vessel (p = 0.012) and multivessel (p = 0.009) CAD. Through a multivariate logistic regression analysis, fT3 was still linked to the presence of CAD (hazard ratio [HR]: 0.48, 95% confidence interval [CI]: 0.34-0.68, p < 0.001)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18497453",
"endSection": "abstract",
"offsetInBeginSection": 1556,
"offsetInEndSection": 1766,
"text": "Our study showed that FT(4) levels were associated with the presence and the severity of CAD. Also, this study suggests that elevated serum FT(4) levels even within normal range could be a risk factor for CAD. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17434631",
"endSection": "abstract",
"offsetInBeginSection": 2114,
"offsetInEndSection": 2263,
"text": "The present meta-analysis indicates that sub-clinical hypothyroidism is associated with both, a significant risk of CHD at baseline and at follow-up."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17222925",
"endSection": "abstract",
"offsetInBeginSection": 916,
"offsetInEndSection": 1398,
"text": "The incidence of multi-vessel disease was higher in patients with high TSH level (p=0.026). TSH level showed a significant correlation with age (r=0.109, p=0.044) and Gensini's score (r=0.117, p=0.045). The multivariate analysis revealed that age (OR 2.39, p=0.001), diabetes (OR 3.74, p=0.001), creatinine (OR 2.06, p=0.008), and smoking (OR 1.85, p=0.045) were independent predictors for significant coronary artery disease, but TSH level did not predict coronary artery stenosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14677810",
"endSection": "abstract",
"offsetInBeginSection": 2580,
"offsetInEndSection": 2784,
"text": "These data in patients referred for coronary angiography suggest that variation of thyroid function within the statistical normal range may influence the presence and severity of coronary atherosclerosis."
}
]
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| []
| 531d1279b166e2b806000042 | 210 |
yesno | Is Iron deficiency anemia a common complication of chronic kidney disease? | ['yes'] | [
"yes"
]
| ['iron deficiency anemia is common in patients with chronic kidney disease (CKD).', 'Iron deficiency anemia is a common complication of chronic kidney disease', 'Yes, Iron deficiency anemia is a common complication of chronic kidney disease.', 'Yes, iron deficiency anemia is a common complication in patients with chronic kidney disease, especially those requiring dialysis.', 'Yes, iron deficiency anemia is a common complication of chronic kidney disease due to reduced erythropoietin production and decreased red blood cell lifespan, leading to decreased hemoglobin levels.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/18824288",
"http://www.ncbi.nlm.nih.gov/pubmed/35644772",
"http://www.ncbi.nlm.nih.gov/pubmed/20630409",
"http://www.ncbi.nlm.nih.gov/pubmed/19325171",
"http://www.ncbi.nlm.nih.gov/pubmed/28682026",
"http://www.ncbi.nlm.nih.gov/pubmed/22935483",
"http://www.ncbi.nlm.nih.gov/pubmed/24432707",
"http://www.ncbi.nlm.nih.gov/pubmed/17533016",
"http://www.ncbi.nlm.nih.gov/pubmed/30970355",
"http://www.ncbi.nlm.nih.gov/pubmed/28372549",
"http://www.ncbi.nlm.nih.gov/pubmed/29533917",
"http://www.ncbi.nlm.nih.gov/pubmed/31614529",
"http://www.ncbi.nlm.nih.gov/pubmed/16198278",
"http://www.ncbi.nlm.nih.gov/pubmed/31464252",
"http://www.ncbi.nlm.nih.gov/pubmed/17804903",
"http://www.ncbi.nlm.nih.gov/pubmed/26342303",
"http://www.ncbi.nlm.nih.gov/pubmed/22303745",
"http://www.ncbi.nlm.nih.gov/pubmed/29336855",
"http://www.ncbi.nlm.nih.gov/pubmed/16949463",
"http://www.ncbi.nlm.nih.gov/pubmed/16164657",
"http://www.ncbi.nlm.nih.gov/pubmed/36166211",
"http://www.ncbi.nlm.nih.gov/pubmed/34514189",
"http://www.ncbi.nlm.nih.gov/pubmed/20126670",
"http://www.ncbi.nlm.nih.gov/pubmed/29696955",
"http://www.ncbi.nlm.nih.gov/pubmed/33123967",
"http://www.ncbi.nlm.nih.gov/pubmed/35058395",
"http://www.ncbi.nlm.nih.gov/pubmed/32762831",
"http://www.ncbi.nlm.nih.gov/pubmed/27236129",
"http://www.ncbi.nlm.nih.gov/pubmed/34860142",
"http://www.ncbi.nlm.nih.gov/pubmed/28412770",
"http://www.ncbi.nlm.nih.gov/pubmed/28403561",
"http://www.ncbi.nlm.nih.gov/pubmed/33516607",
"http://www.ncbi.nlm.nih.gov/pubmed/29481308",
"http://www.ncbi.nlm.nih.gov/pubmed/33842503",
"http://www.ncbi.nlm.nih.gov/pubmed/19833421",
"http://www.ncbi.nlm.nih.gov/pubmed/36165109",
"http://www.ncbi.nlm.nih.gov/pubmed/17106764",
"http://www.ncbi.nlm.nih.gov/pubmed/31477258",
"http://www.ncbi.nlm.nih.gov/pubmed/28153964",
"http://www.ncbi.nlm.nih.gov/pubmed/25468387",
"http://www.ncbi.nlm.nih.gov/pubmed/30675430",
"http://www.ncbi.nlm.nih.gov/pubmed/16470356",
"http://www.ncbi.nlm.nih.gov/pubmed/19776721",
"http://www.ncbi.nlm.nih.gov/pubmed/16893403",
"http://www.ncbi.nlm.nih.gov/pubmed/32556307",
"http://www.ncbi.nlm.nih.gov/pubmed/21684231"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36165109",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Intravenous iron therapy is increasingly being used worldwide to treat anemia in chronic kidney disease and more recently iron deficiency in heart failure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36166211",
"endSection": "abstract",
"offsetInBeginSection": 49,
"offsetInEndSection": 145,
"text": " iron deficiency in patients with chronic kidney disease (CKD), either with or without anaemia. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28153964",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "Iron deficiency, both functional and absolute, is common in patients with chronic kidney disease (CKD), especially those requiring dialysis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29533917",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "Treatment with iron preparations remains one of the main directions in the treatment of anemia in patients with chronic kidney disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33516607",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "This work presents an update on the management of iron deficiency in patients with chronic renal failure (CRF), either with or without anaemia."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33516607",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 101,
"text": "ron replacement therapy in the management of anaemia in non-dialysis chronic renal failure patients:"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30970355",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "Iron deficiency anemia is a common complication of chronic kidney disease (CKD)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30970355",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 49,
"text": "Iron Deficiency Anemia in Chronic Kidney Disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28372549",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "BACKGROUND: Iron deficiency anemia (IDA) is a common manifestation of chronic kidney disease (CKD), affecting most patients on hemodialysis and imposing a substantial clin"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21684231",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "Anemia is a common complication of chronic kidney disease (CKD) in predialysis stage."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27236129",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 88,
"text": "Anemia is a common and clinically important consequence of chronic kidney disease (CKD)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30970355",
"endSection": "abstract",
"offsetInBeginSection": 775,
"offsetInEndSection": 1022,
"text": "Among CKD patients, absolute iron deficiency is defined when the transferrin saturation (TSAT) is ≤20% and the serum ferritin concentration is ≤100 ng/mL among predialysis and peritoneal dialysis patients or ≤200 ng/mL among hemodialysis patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18824288",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "BACKGROUND: Iron deficiency anemia is a common complication in patients with chronic kidney di"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31477258",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "Iron deficiency anemia (IDA) is a frequent complication of chronic kidney disease (CKD) and is associated with adverse outcomes in these patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19776721",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Iron deficiency anemia is a common complication in end-stage renal disease (ESRD) and impairs the therapeutic efficacy of recombinant erythropoietin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30970355",
"endSection": "abstract",
"offsetInBeginSection": 424,
"offsetInEndSection": 502,
"text": "Anemia in CKD is associated with an increased risk of morbidity and mortality."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25468387",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 528,
"text": "BACKGROUND: Iron deficiency anemia and serum phosphate levels > 4.0mg/dL are relatively common in chronic kidney disease stages 3 to 5 and are associated with higher risks of progressive loss of kidney function, cardiovascular events, and mortality.STUDY DESIGN: Double-blind, placebo-controlled, randomized trial.SETTING & PARTICIPANTS: 149 patients with estimated glomerular filtration rates < 60 mL/min/1.73 m(2), iron deficiency anemia (hemoglobin, 9.0-12.0 g/dL; transferrin saturation [TSAT]≤ 30%, serum ferritin ≤ 300 ng/"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20630409",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Anemia resulting from iron and erythropoietin deficiencies is a common complication of advanced chronic kidney disease (CKD)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34514189",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 121,
"text": "Iron deficiency is common in individuals with chronic kidney disease and plays a major role in the development of anemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20126670",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "Iron deficiency anemia is a common occurrence in patients with chronic kidney disease and many patients do not respond well to supplementation with oral iron."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27236129",
"endSection": "abstract",
"offsetInBeginSection": 392,
"offsetInEndSection": 740,
"text": "However, the diagnosis of iron-deficiency anemia in CKD patients is complicated by the relatively poor predictive ability of easily obtained routine serum iron indices (eg, ferritin and transferrin saturation) and more invasive gold standard measures of iron deficiency (eg, bone marrow iron stores) or erythropoietic response to supplemental iron."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17106764",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Iron deficiency in patients with chronic kidney disease: potential role for intravenous iron therapy independent of erythropoietin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17804903",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 198,
"text": "Iron deficiency anemia is common in people with chronic kidney disease (CKD) and its importance in supporting erythropoiesis is unquestioned especially in those patients treated with erythropoietin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17533016",
"endSection": "abstract",
"offsetInBeginSection": 209,
"offsetInEndSection": 380,
"text": " Limited data suggest that iron deficiency is common in patients with chronic kidney disease with anemia; this lack of iron can hinder the effectiveness of erythropoiesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32556307",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 52,
"text": "Anemia is a frequent complication of kidney disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16949463",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 58,
"text": "Anemia is a common complication of chronic kidney disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29481308",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "Severe anemia and iron deficiency are common complications in chronic kidney disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17804903",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Iron deficiency anemia is common in people with chronic kidney disease (CKD) and its importance in supporting erythropoiesis is unquestioned especiall"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30970355",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Iron deficiency anemia is a common complication of chronic kidney disease (CKD). CKD patients suffer from both absolute and functional iron deficiency"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22303745",
"endSection": "abstract",
"offsetInBeginSection": 58,
"offsetInEndSection": 208,
"text": " diabetic nephropathy is a leading cause of CKD. One of the most common complications of CKD is anemia, the frequency and severity of which increase a"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16470356",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Anemia is as a frequent complication in patients with chronic kidney disease, which gains in importance in the treatment of patients with renal diseas"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29481308",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Severe anemia and iron deficiency are common complications in chronic kidney disease. The cause of renal anemia is multifactorial and includes decreas"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26342303",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Anemia is a common complication in patients with chronic kidney disease (CKD), mainly due to inadequate renal production of erythropoietin. In hemodia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19325171",
"endSection": "abstract",
"offsetInBeginSection": 316,
"offsetInEndSection": 466,
"text": "o anemia. The other cause of anemia is deficiency of iron. Iron deficiency anemia is common in people with CKD and its importance in supporting erythr"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16470356",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "Anemia is as a frequent complication in patients with chronic kidney disease, which gains in importance in the treatment of patients with renal disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35058395",
"endSection": "abstract",
"offsetInBeginSection": 223,
"offsetInEndSection": 373,
"text": " development and treat complications including anemia. Anemia is one of the common complication of chronic kidney disease (CKD), which is a significan"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35058395",
"endSection": "abstract",
"offsetInBeginSection": 748,
"offsetInEndSection": 1006,
"text": "The diagnosis of iron deficiency anemia in patients with CKD is complicated due to the relatively low predictive ability of routine serum iron markers (e.g., ferritin and transferrin saturation) and more invasive measurements such as bone marrow iron stores."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28682026",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Anemia is a frequent complication in chronic kidney disease (CKD), and it is often accompanied by various clinical symptoms. The primary cause of anem"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30970355",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Iron deficiency anemia is a common complication of chronic kidney disease (CKD). CKD patients suffer from both absolute and functional iron deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29336855",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 84,
"text": "Anemia is a frequent complication during the later stages of chronic kidney disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28403561",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "Anemia in chronic kidney disease is common and iron deficiency is an important cause."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28412770",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 32,
"text": "nemia in chronic kidney disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28412770",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 98,
"text": "nemia is common and associated with adverse outcomes in children with chronic kidney disease (CKD"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20126670",
"endSection": "title",
"offsetInBeginSection": 18,
"offsetInEndSection": 66,
"text": "e treatment of anemia in chronic kidney disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17106764",
"endSection": "abstract",
"offsetInBeginSection": 13,
"offsetInEndSection": 279,
"text": "he prevalence of iron deficiency and its contribution to the anemia of end stage renal disease has been extensively studied, but much less is known about the role of iron deficiency in the pathogenesis of the anemia of chronic kidney disease in predialysis patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19833421",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 47,
"text": "nemia in renal disease: diagnosis and manageme"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19325171",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "Anemia is a very common clinical problem in patients with chronic kidney disease (CKD) and is associated with increased morbidity and mortality in these patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19325171",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "Safety issues with intravenous iron products in the management of anemia in chronic kidney disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27236129",
"endSection": "abstract",
"offsetInBeginSection": 195,
"offsetInEndSection": 264,
"text": " Deciding on the appropriate treatment for anemia associated with CKD"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20630409",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 32,
"text": "nemia in chronic kidney disease"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29336855",
"endSection": "title",
"offsetInBeginSection": 10,
"offsetInEndSection": 50,
"text": "Anemia in ESRD and Earlier Stages of CKD"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28372549",
"endSection": "title",
"offsetInBeginSection": 3,
"offsetInEndSection": 40,
"text": " Ferumoxytol for Anemia of CKD Trial "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25468387",
"endSection": "title",
"offsetInBeginSection": 104,
"offsetInEndSection": 165,
"text": " anemia and reduction of serum phosphate in patients with CKD"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19833421",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 108,
"text": "Chronic kidney disease (CKD) is a widespread health problem in the world and anemia is a common complication"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29696955",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 89,
"text": "nemia in diabetic kidney disease - underappreciated but still clinically relevant proble"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16198278",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 46,
"text": "Anemia in children with chronic kidney disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16198278",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 112,
"text": "nemia in children with chronic kidney disease (CKD) is common secondary to inadequate erythropoietin production"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22935483",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 27,
"text": "echanisms of anemia in CKD"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22935483",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 64,
"text": "Anemia is a common feature of CKD associated with poor outcomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22935483",
"endSection": "abstract",
"offsetInBeginSection": 66,
"offsetInEndSection": 150,
"text": "he current management of patients with anemia in CKD is controversial, with recent c"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22935483",
"endSection": "abstract",
"offsetInBeginSection": 259,
"offsetInEndSection": 346,
"text": "Here, we examine recent insights into the molecular mechanisms underlying anemia of CKD"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31614529",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 65,
"text": "nemia of Inflammation with An Emphasis on Chronic Kidney Disease"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32762831",
"endSection": "title",
"offsetInBeginSection": 33,
"offsetInEndSection": 93,
"text": " Treatment of Anemia in Patients with Chronic Kidney Disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32762831",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 135,
"text": "nemia is a common complication of chronic kidney disease (CKD), and its prevalence has shown a tendency to increase in many countries."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16893403",
"endSection": "title",
"offsetInBeginSection": 2,
"offsetInEndSection": 81,
"text": "ythropoietin resistance in the treatment of the anemia of chronic renal failure"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16893403",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 122,
"text": "esistance to erythropoietin therapy is a common complication of the modern management of anemia in chronic kidney disease"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31464252",
"endSection": "title",
"offsetInBeginSection": 12,
"offsetInEndSection": 79,
"text": "spectrum of anemia in non-dialysis-dependent chronic kidney disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31464252",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 152,
"text": " retrospective study was conducted over seven years and it aimed to find out various causes of anemia among patients with chronic kidney disease (CKD)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16164657",
"endSection": "title",
"offsetInBeginSection": 4,
"offsetInEndSection": 89,
"text": "safety and efficacy of ferumoxytol therapy in anemic chronic kidney disease patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30675430",
"endSection": "title",
"offsetInBeginSection": 4,
"offsetInEndSection": 53,
"text": "options for the anemia of chronic kidney disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30675430",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 57,
"text": "nemia is a common complication of chronic kidney disease"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24432707",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 64,
"text": "Urology and nephrology update: anemia of chronic kidney disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24432707",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "Anemia is associated with chronic kidney disease (CKD) at all stages, and it is nearly universal among patients with stage 5 CKD"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33842503",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 34,
"text": "nemia in Chronic Kidney Disease: "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33842503",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 114,
"text": "nemia is a common complication in chronic kidney disease (CKD), and is associated with a reduced quality of life,"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34860142",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Anemia and its predictors among adult non-dialysis chronic kidney disease patients in Southern Ethiopia: a cross-sectional study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34860142",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 98,
"text": "Anemia is an adverse outcome and common complication in chronic kidney disease patient"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35644772",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 162,
"text": "Prevalence of malnutrition and absolute and functional iron deficiency anemia in nondialysis-dependent chronic kidney disease and hemodialysis Algerian patients]"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35644772",
"endSection": "abstract",
"offsetInBeginSection": 2,
"offsetInEndSection": 178,
"text": " chronic kidney disease, anemia and malnutrition coupled with inflammation as malnutrition-inflammation complex syndrom are common and considered as morbidity-mortality factors"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33123967",
"endSection": "title",
"offsetInBeginSection": 8,
"offsetInEndSection": 65,
"text": "f Anemia in Chronic Kidney Disease: Beyond Erythropoietin"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33123967",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 65,
"text": "nemia is a frequent comorbidity of chronic kidney disease (CKD) "
}
]
| 12 | BioASQ-training12b | null | null | 641365f6201352f04a00003a | 212 |
yesno | Is deucravacitinib effective for psoriasis? | ['yes'] | [
"yes"
]
| ['Yes. Deucravacitinib is effective for psoriasis.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/35025062",
"http://www.ncbi.nlm.nih.gov/pubmed/35960487",
"http://www.ncbi.nlm.nih.gov/pubmed/35820547"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35960487",
"endSection": "abstract",
"offsetInBeginSection": 686,
"offsetInEndSection": 1214,
"text": "POETYK PSO-1 and PSO-2 involved 1688 patients with moderate-to-severe psoriasis. After 16 weeks, in both studies, over 50% of patients treated with deucravacitinib reached PASI75, which was significantly superior to placebo and apremilast. In POETYK PSO-1, these results improved until week 24 and were maintained through week 52, with over 65% of patients achieving PASI75 at this point. A reduction in signs and symptoms was also reported by patients, with greater impact on itch. Deucravacitinib was well tolerated and safe. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35025062",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 198,
"text": "INTRODUCTION: Deucravacitinib is an oral, selective tyrosine kinase 2 inhibitor that demonstrated therapeutic benefit in a Phase 2 clinical trial of adults with moderate to severe plaque psoriasis. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35025062",
"endSection": "abstract",
"offsetInBeginSection": 1500,
"offsetInEndSection": 1682,
"text": "CONCLUSION: Deucravacitinib treatment produced early response and similar trends in improvements across multiple efficacy assessments and QoL in moderate to severe plaque psoriasis. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35820547",
"endSection": "abstract",
"offsetInBeginSection": 1181,
"offsetInEndSection": 1338,
"text": "CONCLUSION: Deucravacitinib was superior to placebo and apremilast across multiple efficacy endpoints and was well tolerated in moderate to severe psoriasis."
}
]
| 12 | BioASQ-training12b | null | null | 64041dae201352f04a00001d | 213 |
yesno | Have yeast prions become important models for the study of the basic mechanisms underlying human amyloid diseases? | ['yes'] | [
"yes"
]
| ['infectious proteins) were discovered by their outré genetic properties and have become important models for an array of human prion and amyloid diseases.', 'Yeast prions have become important models for the study of the basic mechanisms underlying human amyloid diseases and normal yeast cells can eliminate the large majority of prion variants arising.', 'Endogenous yeast amyloids that control heritable traits and are frequently used as models for human amyloid diseases are termed yeast prions', 'These infectious yeast amyloidoses are outstanding models for the many common human amyloid-based diseases that are increasingly found to have some infectious characteristics.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/25631286",
"http://www.ncbi.nlm.nih.gov/pubmed/29698650",
"http://www.ncbi.nlm.nih.gov/pubmed/26915272",
"http://www.ncbi.nlm.nih.gov/pubmed/23379365",
"http://www.ncbi.nlm.nih.gov/pubmed/29330303",
"http://www.ncbi.nlm.nih.gov/pubmed/28932898",
"http://www.ncbi.nlm.nih.gov/pubmed/22052352",
"http://www.ncbi.nlm.nih.gov/pubmed/23077577",
"http://www.ncbi.nlm.nih.gov/pubmed/17514901",
"http://www.ncbi.nlm.nih.gov/pubmed/28148884",
"http://www.ncbi.nlm.nih.gov/pubmed/23045389"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28932898",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "Endogenous yeast amyloids that control heritable traits and are frequently used as models for human amyloid diseases are termed yeast prions"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29330303",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "Fibrous cross-β aggregates (amyloids) and their transmissible forms (prions) cause diseases in mammals (including humans) and control heritable traits in yeast. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29698650",
"endSection": "abstract",
"offsetInBeginSection": 869,
"offsetInEndSection": 1044,
"text": "These infectious yeast amyloidoses are outstanding models for the many common human amyloid-based diseases that are increasingly found to have some infectious characteristics."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26915272",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 167,
"text": "Yeast prions (infectious proteins) were discovered by their outré genetic properties and have become important models for an array of human prion and amyloid diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28148884",
"endSection": "abstract",
"offsetInBeginSection": 505,
"offsetInEndSection": 678,
"text": "Yeast prions are models for both rare mammalian prion diseases and for several very common amyloidoses such as Alzheimer's disease, type 2 diabetes, and Parkinson's disease. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23379365",
"endSection": "abstract",
"offsetInBeginSection": 879,
"offsetInEndSection": 1081,
"text": "Yeast prions are important models for human amyloid diseases in general, particularly because new evidence is showing infectious aspects of several human amyloidoses not previously classified as prions. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23077577",
"endSection": "abstract",
"offsetInBeginSection": 342,
"offsetInEndSection": 479,
"text": "Mechanism of amyloid formation is critical for a complete understanding of the yeast prion phenomenon and human amyloid-related diseases. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23379365",
"endSection": "abstract",
"offsetInBeginSection": 846,
"offsetInEndSection": 1048,
"text": "Yeast prions are important models for human amyloid diseases in general, particularly because new evidence is showing infectious aspects of several human amyloidoses not previously classified as prions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28932898",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "Endogenous yeast amyloids that control heritable traits and are frequently used as models for human amyloid diseases are termed yeast prions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23077577",
"endSection": "abstract",
"offsetInBeginSection": 239,
"offsetInEndSection": 376,
"text": "Mechanism of amyloid formation is critical for a complete understanding of the yeast prion phenomenon and human amyloid-related diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17514901",
"endSection": "abstract",
"offsetInBeginSection": 502,
"offsetInEndSection": 742,
"text": "Here we summarize the results of studies of prions of the yeast Saccharomyces cerevisiae and of the use of yeast model for investigation of some human amyloidoses, such as prion diseases, Alzheimer's, Parkinson's, and Huntington's diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25631286",
"endSection": "abstract",
"offsetInBeginSection": 1158,
"offsetInEndSection": 1272,
"text": "Yeast prions increasingly are serving as models for the understanding and treatment of many mammalian amyloidoses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23045389",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Yeast prions, based on self-seeded highly ordered fibrous aggregates (amyloids), serve as a model for human amyloid diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29698650",
"endSection": "abstract",
"offsetInBeginSection": 869,
"offsetInEndSection": 1048,
"text": "These infectious yeast amyloidoses are outstanding models for the many common human amyloid-based diseases that are increasingly found to have some infectious characteristics.<br>"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22052352",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "The yeast system has provided considerable insight into the biology of amyloid and prions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23379365",
"endSection": "abstract",
"offsetInBeginSection": 844,
"offsetInEndSection": 1046,
"text": "Yeast prions are important models for human amyloid diseases in general, particularly because new evidence is showing infectious aspects of several human amyloidoses not previously classified as prions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23379365",
"endSection": "abstract",
"offsetInBeginSection": 1047,
"offsetInEndSection": 1294,
"text": "We also review studies of the roles of chaperones, aggregate-collecting proteins, and other cellular components using yeast that have led the way in improving the understanding of similar processes that must be operating in many human amyloidoses."
}
]
| 11 | BioASQ-training11b | null | null | 5c5723a007647bbc4b000019 | 214 |
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