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factoid
|
What is etarfolatide used for?
|
['companion imaging agent']
|
[
"companion imaging agent",
"companion diagnostic agent",
"companion diagnostic",
"companion imaging",
"companion imaging technology"
] |
['Etarfolatide in the form of 99mTc-etarfolatide is used as a companion imaging agent']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26238440",
"http://www.ncbi.nlm.nih.gov/pubmed/24667717",
"http://www.ncbi.nlm.nih.gov/pubmed/25457975",
"http://www.ncbi.nlm.nih.gov/pubmed/27084348",
"http://www.ncbi.nlm.nih.gov/pubmed/24742319",
"http://www.ncbi.nlm.nih.gov/pubmed/24127448"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26238440",
"endSection": "title",
"offsetInBeginSection": 26,
"offsetInEndSection": 109,
"text": "99mTc-etarfolatide, an imaging agent for folate receptor in healthy Japanese adults"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25457975",
"endSection": "abstract",
"offsetInBeginSection": 1220,
"offsetInEndSection": 1452,
"text": " In contrast, the noninvasive single-photon emission computed tomography-based companion imaging agent, (99m)Tc-etarfolatide ((99m)Tc-EC20), is in development for use as a companion diagnostic with the FRα-targeted folate conjugate,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26238440",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "OBJECTIVE\nTechnetium etarfolatide ((99m)Tc-EF) is a radioactive diagnostic imaging agent that was developed to assess the expression of folate receptors in tumors."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27084348",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "OBJECTIVE\nThrough binding to folate receptor-β (FR-β), the new (99m)Tc-EC20 (Etarfolatide) imaging technique detects activated but not resting macrophages in vivo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25457975",
"endSection": "abstract",
"offsetInBeginSection": 1221,
"offsetInEndSection": 1520,
"text": "In contrast, the noninvasive single-photon emission computed tomography-based companion imaging agent, (99m)Tc-etarfolatide ((99m)Tc-EC20), is in development for use as a companion diagnostic with the FRα-targeted folate conjugate, vintafolide (EC145), to identify patients whose tumors express FRα."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26238440",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "OBJECTIVE Technetium etarfolatide ((99m)Tc-EF) is a radioactive diagnostic imaging agent that was developed to assess the expression of folate receptors in tumors."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24667717",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 481,
"text": "Phase II study of treatment of advanced ovarian cancer with folate-receptor-targeted therapeutic (vintafolide) and companion SPECT-based imaging agent (99mTc-etarfolatide).<AbstractText Label=\"BACKGROUND\" NlmCategory=\"BACKGROUND\">This report examines (99m)Tc-etarfolatide imaging to identify the presence of folate receptor (FR) on tumors of women with recurrent/refractory ovarian or endometrial cancer and correlates expression with response to FR-targeted therapy (vintafolide). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25457975",
"endSection": "abstract",
"offsetInBeginSection": 1308,
"offsetInEndSection": 1607,
"text": "In contrast, the noninvasive single-photon emission computed tomography-based companion imaging agent, (99m)Tc-etarfolatide ((99m)Tc-EC20), is in development for use as a companion diagnostic with the FRα-targeted folate conjugate, vintafolide (EC145), to identify patients whose tumors express FRα. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24742319",
"endSection": "abstract",
"offsetInBeginSection": 627,
"offsetInEndSection": 929,
"text": "We review the development of vintafolide (EC145), a folic acid-desacetylvinblastine conjugate, the predictive utility of a FR-targeted imaging agent, technetium-(99)m-etarfolatide (EC20), the challenges in proving survival advantage, and other approaches to exploiting FR as a target in ovarian cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24127448",
"endSection": "abstract",
"offsetInBeginSection": 551,
"offsetInEndSection": 700,
"text": "The utility of an FR-targeted imaging agent, (99m)Tc-etarfolatide (EC20), in selecting patients likely to benefit from vintafolide was also examined. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24667717",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 457,
"text": "<b>BACKGROUND</b>: This report examines (99m)Tc-etarfolatide imaging to identify the presence of folate receptor (FR) on tumors of women with recurrent/refractory ovarian or endometrial cancer and correlates expression with response to FR-targeted therapy (vintafolide).<br><b>PATIENTS AND METHODS</b>: In this phase II, single-arm, multicenter study, patients with advanced ovarian cancer were imaged with (99m)Tc-etarfolatide before vintafolide treatment."
}
] | 11 |
BioASQ-training11b
| null | null |
5c7161f47c78d69471000066
|
bioasq_factoid
|
factoid
|
Mutation of which gene is implicated in the Brain-lung-thyroid syndrome?
|
[['thyroid transcription factor 1']]
|
[
"thyroid transcription factor 1",
"TTF-1",
"NKX2-1",
"thyroid-specific transcription factor 1",
"thyroid transcription factor 1A"
] |
['Brain-lung-thyroid syndrome (BLTS) characterized by congenital hypothyroidism, respiratory distress syndrome, and benign hereditary chorea is caused by thyroid transcription factor 1 (NKX2-1/TTF1) mutations.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26196025",
"http://www.ncbi.nlm.nih.gov/pubmed/25759798",
"http://www.ncbi.nlm.nih.gov/pubmed/24129101",
"http://www.ncbi.nlm.nih.gov/pubmed/24171694",
"http://www.ncbi.nlm.nih.gov/pubmed/22488412",
"http://www.ncbi.nlm.nih.gov/pubmed/22166853",
"http://www.ncbi.nlm.nih.gov/pubmed/21867529",
"http://www.ncbi.nlm.nih.gov/pubmed/20020530",
"http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"http://www.ncbi.nlm.nih.gov/pubmed/23430038"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26196025",
"endSection": "abstract",
"offsetInBeginSection": 151,
"offsetInEndSection": 362,
"text": " The disorder is caused by mutations to the NKX2.1 (TITF1) gene and also forms part of the \"brain-lung-thyroid syndrome\", in which additional developmental abnormalities of lung and thyroid tissue are observed. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25759798",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Novel NKX2-1 Frameshift Mutations in Patients with Atypical Phenotypes of the Brain-Lung-Thyroid Syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25759798",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 235,
"text": "OBJECTIVES: To verify the involvement of NKX2-1 gene in infants with brain-lung-thyroid (BLT) syndrome and hypothyroid phenotypes variable among congenital hypothyroidism (CH) or idiopathic mild hypothyroidism (IMH) of postnatal onset."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25759798",
"endSection": "abstract",
"offsetInBeginSection": 879,
"offsetInEndSection": 988,
"text": "They were carriers of new de novo heterozygous frameshift mutations of NKX2-1 (c.177delG and c.153_166del14)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25759798",
"endSection": "abstract",
"offsetInBeginSection": 1273,
"offsetInEndSection": 1444,
"text": "CONCLUSIONS: Two novel heterozygous frameshift mutations of NKX2-1 were identified in 2 cases selected on the basis of a BLT-like phenotype among 183 hypothyroid infants. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24129101",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "NKX2-1 mutations in brain-lung-thyroid syndrome: a case series of four patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24129101",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 207,
"text": "Brain-lung-thyroid syndrome (BLTS) characterized by congenital hypothyroidism, respiratory distress syndrome, and benign hereditary chorea is caused by thyroid transcription factor 1 (NKX2-1/TTF1) mutations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24129101",
"endSection": "abstract",
"offsetInBeginSection": 364,
"offsetInEndSection": 1250,
"text": "Two of the four patients presenting with the triad of BLTS had NKX2-1 mutations, and one of these NKX2-1 [c.890_896del (p.Ala327Glyfs*52)] is a novel variant. The third patient without any identified NKX2-1 mutations was a carrier of mitochondrial mutation; this raises the possibility of mitochondrial mutations contributing to thyroid dysgenesis. Although rare, the triad of congenital hypothyroidism, neurological, and respiratory signs is highly suggestive of NKX2-1 anomalies. Screening for NKX2-1 mutations in patients with thyroid, lung, and neurological abnormalities will enable a unifying diagnosis and genetic counseling for the affected families. In addition, identification of an NKX2-1 defect would be helpful in allaying the concerns about inadequate thyroxine supplementation as the cause of neurological defects observed in some children with congenital hypothyroidism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24171694",
"endSection": "abstract",
"offsetInBeginSection": 205,
"offsetInEndSection": 377,
"text": "Loss-of-function mutations in NKX2.1, a gene vital to the normal development and function of the brain, lungs, and thyroid, have been identified in a number of individuals."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22488412",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 207,
"text": "BACKGROUND: NKX2.1 mutations have been identified in patients displaying complete or partial brain-lung-thyroid syndrome, which can include benign hereditary chorea (BHC), hypothyroidism and/or lung disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22488412",
"endSection": "abstract",
"offsetInBeginSection": 873,
"offsetInEndSection": 1057,
"text": "CONCLUSION: MLPA should be considered as a complementary tool in patients with partial or total brain-lung-thyroid syndrome when direct sequencing failed to identify NKX2.1 mutations. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22166853",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 144,
"text": "Mutations in NKX2-1 cause neurological, pulmonary, and thyroid hormone impairment. Recently, the disease was named brain-lung-thyroid syndrome. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22166853",
"endSection": "abstract",
"offsetInBeginSection": 384,
"offsetInEndSection": 808,
"text": "Genetic analysis of NKX2-1 revealed a novel missense mutation (p.Val205Phe) in two patients who were cousins and their maternal families, and a novel 2.6-Mb deletion including NKX2-1 on chromosome 14 in the other patient. Congenital hypothyroidism was not detected on neonatal screening in the patient with the missense mutation, and frequent respiratory infections were observed in the patient with the deletion in NKX2-1. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21867529",
"endSection": "abstract",
"offsetInBeginSection": 152,
"offsetInEndSection": 420,
"text": "Haploinsufficiency of NKX2.1, the gene encoding the thyroid transcription factor-1 (TTF-1)--critical for lung, thyroid and central nervous system morphogenesis and function--causes a rare form of progressive respiratory failure designated brain-lung-thyroid syndrome. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21867529",
"endSection": "abstract",
"offsetInBeginSection": 506,
"offsetInEndSection": 607,
"text": "We report a novel TTF-1 molecular defect causing recurrent respiratory failure episodes in an infant."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20020530",
"endSection": "abstract",
"offsetInBeginSection": 1257,
"offsetInEndSection": 1522,
"text": "In conclusion, ILD in patients with NKX2-1 mutations was associated with altered surfactant protein metabolism, and both gain and loss of function of the mutated NKX2-1 genes on surfactant protein promoters were associated with ILD in \"Brain-Lung-Thyroid syndrome\"."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24129101",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 207,
"text": "Brain-lung-thyroid syndrome (BLTS) characterized by congenital hypothyroidism, respiratory distress syndrome, and benign hereditary chorea is caused by thyroid transcription factor 1 (NKX2-1/TTF1) mutations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "Thyroid transcription factor 1 (NKX2-1/TITF1) mutations cause brain-lung-thyroid syndrome, characterized by congenital hypothyroidism (CH), infant respiratory distress syndrome (IRDS) and benign hereditary chorea (BHC)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "abstract",
"offsetInBeginSection": 485,
"offsetInEndSection": 751,
"text": "The objectives of the present study were (i) detection of NKX2-1 mutations in patients with CH associated with pneumopathy and/or BHC, (ii) functional analysis of new mutations in vitro and (iii) description of the phenotypic spectrum of brain-lung-thyroid syndrome."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24129101",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "NKX2-1 mutations in brain-lung-thyroid syndrome: a case series of four patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "Five new TTF1/NKX2.1 mutations in brain-lung-thyroid syndrome: rescue by PAX8 synergism in one case."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20020530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "NKX2-1 mutations leading to surfactant protein promoter dysregulation cause interstitial lung disease in \"Brain-Lung-Thyroid Syndrome\"."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22488412",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Multiplex Ligation-dependent Probe Amplification improves the detection rate of NKX2.1 mutations in patients affected by brain-lung-thyroid syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22488412",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 195,
"text": "NKX2.1 mutations have been identified in patients displaying complete or partial brain-lung-thyroid syndrome, which can include benign hereditary chorea (BHC), hypothyroidism and/or lung disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "abstract",
"offsetInBeginSection": 1173,
"offsetInEndSection": 1376,
"text": "The clinical spectrum of 6 own and 40 published patients with NKX2-1 mutations ranged from the complete triad of brain-lung-thyroid syndrome (50%), brain and thyroid disease (30%), to isolated BHC (13%)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24129101",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 207,
"text": "Brain-lung-thyroid syndrome (BLTS) characterized by congenital hypothyroidism, respiratory distress syndrome, and benign hereditary chorea is caused by thyroid transcription factor 1 (NKX2-1/TTF1) mutations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "Thyroid transcription factor 1 (NKX2-1/TITF1) mutations cause brain-lung-thyroid syndrome, characterized by congenital hypothyroidism (CH), infant respiratory distress syndrome (IRDS) and benign hereditary chorea (BHC)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21867529",
"endSection": "abstract",
"offsetInBeginSection": 406,
"offsetInEndSection": 673,
"text": "Haploinsufficiency of NKX2.1, the gene encoding the thyroid transcription factor-1 (TTF-1)--critical for lung, thyroid and central nervous system morphogenesis and function--causes a rare form of progressive respiratory failure designated brain-lung-thyroid syndrome."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24129101",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "NKX2-1 mutations in brain-lung-thyroid syndrome: a case series of four patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "Five new TTF1/NKX2.1 mutations in brain-lung-thyroid syndrome: rescue by PAX8 synergism in one case."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20020530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "NKX2-1 mutations leading to surfactant protein promoter dysregulation cause interstitial lung disease in \"Brain-Lung-Thyroid Syndrome\"."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "Thyroid transcription factor 1 (NKX2-1/TITF1) mutations cause brain-lung-thyroid syndrome, characterized by congenital hypothyroidism (CH), infant respiratory distress syndrome (IRDS) and benign hereditary chorea (BHC). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "Five new TTF1/NKX2.1 mutations in brain-lung-thyroid syndrome: rescue by PAX8 synergism in one case."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "abstract",
"offsetInBeginSection": 975,
"offsetInEndSection": 1179,
"text": "The clinical spectrum of 6 own and 40 published patients with NKX2-1 mutations ranged from the complete triad of brain-lung-thyroid syndrome (50%), brain and thyroid disease (30%), to isolated BHC (13%). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22488412",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Multiplex Ligation-dependent Probe Amplification improves the detection rate of NKX2.1 mutations in patients affected by brain-lung-thyroid syndrome."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20020530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "NKX2-1 mutations leading to surfactant protein promoter dysregulation cause interstitial lung disease in \"Brain-Lung-Thyroid Syndrome\"."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20020530",
"endSection": "abstract",
"offsetInBeginSection": 997,
"offsetInEndSection": 1262,
"text": "In conclusion, ILD in patients with NKX2-1 mutations was associated with altered surfactant protein metabolism, and both gain and loss of function of the mutated NKX2-1 genes on surfactant protein promoters were associated with ILD in \"Brain-Lung-Thyroid syndrome\"."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22488412",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "BACKGROUND: NKX2.1 mutations have been identified in patients displaying complete or partial brain-lung-thyroid syndrome, which can include benign hereditary chorea (BHC), hypothyroidism and/or lung disease. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22488412",
"endSection": "abstract",
"offsetInBeginSection": 876,
"offsetInEndSection": 1060,
"text": "CONCLUSION: MLPA should be considered as a complementary tool in patients with partial or total brain-lung-thyroid syndrome when direct sequencing failed to identify NKX2.1 mutations. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24129101",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "NKX2-1 mutations in brain-lung-thyroid syndrome: a case series of four patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "Thyroid transcription factor 1 (NKX2-1/TITF1) mutations cause brain-lung-thyroid syndrome, characterized by congenital hypothyroidism (CH), infant respiratory distress syndrome (IRDS) and benign hereditary chorea (BHC). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "Five new TTF1/NKX2.1 mutations in brain-lung-thyroid syndrome: rescue by PAX8 synergism in one case."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "abstract",
"offsetInBeginSection": 975,
"offsetInEndSection": 1179,
"text": "The clinical spectrum of 6 own and 40 published patients with NKX2-1 mutations ranged from the complete triad of brain-lung-thyroid syndrome (50%), brain and thyroid disease (30%), to isolated BHC (13%). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22488412",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Multiplex Ligation-dependent Probe Amplification improves the detection rate of NKX2.1 mutations in patients affected by brain-lung-thyroid syndrome."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20020530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "NKX2-1 mutations leading to surfactant protein promoter dysregulation cause interstitial lung disease in \"Brain-Lung-Thyroid Syndrome\"."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20020530",
"endSection": "abstract",
"offsetInBeginSection": 997,
"offsetInEndSection": 1262,
"text": "In conclusion, ILD in patients with NKX2-1 mutations was associated with altered surfactant protein metabolism, and both gain and loss of function of the mutated NKX2-1 genes on surfactant protein promoters were associated with ILD in \"Brain-Lung-Thyroid syndrome\"."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22488412",
"endSection": "abstract",
"offsetInBeginSection": 876,
"offsetInEndSection": 1060,
"text": "CONCLUSION: MLPA should be considered as a complementary tool in patients with partial or total brain-lung-thyroid syndrome when direct sequencing failed to identify NKX2.1 mutations. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22488412",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "BACKGROUND: NKX2.1 mutations have been identified in patients displaying complete or partial brain-lung-thyroid syndrome, which can include benign hereditary chorea (BHC), hypothyroidism and/or lung disease. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24129101",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "NKX2-1 mutations in brain-lung-thyroid syndrome: a case series of four patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "Thyroid transcription factor 1 (NKX2-1/TITF1) mutations cause brain-lung-thyroid syndrome, characterized by congenital hypothyroidism (CH), infant respiratory distress syndrome (IRDS) and benign hereditary chorea (BHC). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "Five new TTF1/NKX2.1 mutations in brain-lung-thyroid syndrome: rescue by PAX8 synergism in one case."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "abstract",
"offsetInBeginSection": 975,
"offsetInEndSection": 1179,
"text": "The clinical spectrum of 6 own and 40 published patients with NKX2-1 mutations ranged from the complete triad of brain-lung-thyroid syndrome (50%), brain and thyroid disease (30%), to isolated BHC (13%). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22488412",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Multiplex Ligation-dependent Probe Amplification improves the detection rate of NKX2.1 mutations in patients affected by brain-lung-thyroid syndrome."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20020530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "NKX2-1 mutations leading to surfactant protein promoter dysregulation cause interstitial lung disease in \"Brain-Lung-Thyroid Syndrome\"."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20020530",
"endSection": "abstract",
"offsetInBeginSection": 997,
"offsetInEndSection": 1262,
"text": "In conclusion, ILD in patients with NKX2-1 mutations was associated with altered surfactant protein metabolism, and both gain and loss of function of the mutated NKX2-1 genes on surfactant protein promoters were associated with ILD in \"Brain-Lung-Thyroid syndrome\"."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22488412",
"endSection": "abstract",
"offsetInBeginSection": 876,
"offsetInEndSection": 1060,
"text": "CONCLUSION: MLPA should be considered as a complementary tool in patients with partial or total brain-lung-thyroid syndrome when direct sequencing failed to identify NKX2.1 mutations. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22488412",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "BACKGROUND: NKX2.1 mutations have been identified in patients displaying complete or partial brain-lung-thyroid syndrome, which can include benign hereditary chorea (BHC), hypothyroidism and/or lung disease. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24129101",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "NKX2-1 mutations in brain-lung-thyroid syndrome: a case series of four patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "Thyroid transcription factor 1 (NKX2-1/TITF1) mutations cause brain-lung-thyroid syndrome, characterized by congenital hypothyroidism (CH), infant respiratory distress syndrome (IRDS) and benign hereditary chorea (BHC). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "abstract",
"offsetInBeginSection": 975,
"offsetInEndSection": 1179,
"text": "The clinical spectrum of 6 own and 40 published patients with NKX2-1 mutations ranged from the complete triad of brain-lung-thyroid syndrome (50%), brain and thyroid disease (30%), to isolated BHC (13%). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22488412",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "BACKGROUND: NKX2.1 mutations have been identified in patients displaying complete or partial brain-lung-thyroid syndrome, which can include benign hereditary chorea (BHC), hypothyroidism and/or lung disease. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22488412",
"endSection": "abstract",
"offsetInBeginSection": 876,
"offsetInEndSection": 1060,
"text": "CONCLUSION: MLPA should be considered as a complementary tool in patients with partial or total brain-lung-thyroid syndrome when direct sequencing failed to identify NKX2.1 mutations. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21867529",
"endSection": "abstract",
"offsetInBeginSection": 152,
"offsetInEndSection": 420,
"text": "Haploinsufficiency of NKX2.1, the gene encoding the thyroid transcription factor-1 (TTF-1)--critical for lung, thyroid and central nervous system morphogenesis and function--causes a rare form of progressive respiratory failure designated brain-lung-thyroid syndrome. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24129101",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "Brain-lung-thyroid syndrome (BLTS) characterized by congenital hypothyroidism, respiratory distress syndrome, and benign hereditary chorea is caused by thyroid transcription factor 1 (NKX2-1/TTF1) mutations. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "Thyroid transcription factor 1 (NKX2-1/TITF1) mutations cause brain-lung-thyroid syndrome, characterized by congenital hypothyroidism (CH), infant respiratory distress syndrome (IRDS) and benign hereditary chorea (BHC). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "Five new TTF1/NKX2.1 mutations in brain-lung-thyroid syndrome: rescue by PAX8 synergism in one case."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "abstract",
"offsetInBeginSection": 975,
"offsetInEndSection": 1179,
"text": "The clinical spectrum of 6 own and 40 published patients with NKX2-1 mutations ranged from the complete triad of brain-lung-thyroid syndrome (50%), brain and thyroid disease (30%), to isolated BHC (13%). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22488412",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Multiplex Ligation-dependent Probe Amplification improves the detection rate of NKX2.1 mutations in patients affected by brain-lung-thyroid syndrome."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20020530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "NKX2-1 mutations leading to surfactant protein promoter dysregulation cause interstitial lung disease in \"Brain-Lung-Thyroid Syndrome\"."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20020530",
"endSection": "abstract",
"offsetInBeginSection": 997,
"offsetInEndSection": 1262,
"text": "In conclusion, ILD in patients with NKX2-1 mutations was associated with altered surfactant protein metabolism, and both gain and loss of function of the mutated NKX2-1 genes on surfactant protein promoters were associated with ILD in \"Brain-Lung-Thyroid syndrome\"."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22488412",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "BACKGROUND: NKX2.1 mutations have been identified in patients displaying complete or partial brain-lung-thyroid syndrome, which can include benign hereditary chorea (BHC), hypothyroidism and/or lung disease. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22488412",
"endSection": "abstract",
"offsetInBeginSection": 876,
"offsetInEndSection": 1060,
"text": "CONCLUSION: MLPA should be considered as a complementary tool in patients with partial or total brain-lung-thyroid syndrome when direct sequencing failed to identify NKX2.1 mutations. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24129101",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "NKX2-1 mutations in brain-lung-thyroid syndrome: a case series of four patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22488412",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Multiplex Ligation-dependent Probe Amplification improves the detection rate of NKX2.1 mutations in patients affected by brain-lung-thyroid syndrome."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "Five new TTF1/NKX2.1 mutations in brain-lung-thyroid syndrome: rescue by PAX8 synergism in one case."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20020530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "NKX2-1 mutations leading to surfactant protein promoter dysregulation cause interstitial lung disease in \"Brain-Lung-Thyroid Syndrome\"."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25759798",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Novel NKX2-1 Frameshift Mutations in Patients with Atypical Phenotypes of the Brain-Lung-Thyroid Syndrome."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24129101",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "NKX2-1 mutations in brain-lung-thyroid syndrome: a case series of four patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22488412",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 195,
"text": "NKX2.1 mutations have been identified in patients displaying complete or partial brain-lung-thyroid syndrome, which can include benign hereditary chorea (BHC), hypothyroidism and/or lung disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "Thyroid transcription factor 1 (NKX2-1/TITF1) mutations cause brain-lung-thyroid syndrome, characterized by congenital hypothyroidism (CH), infant respiratory distress syndrome (IRDS) and benign hereditary chorea (BHC)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 487,
"text": "Thyroid transcription factor 1 (NKX2-1/TITF1) mutations cause brain-lung-thyroid syndrome, characterized by congenital hypothyroidism (CH), infant respiratory distress syndrome (IRDS) and benign hereditary chorea (BHC). The objectives of the present study were (i) detection of NKX2-1 mutations in patients with CH associated with pneumopathy and/or BHC, (ii) functional analysis of new mutations in vitro and (iii) description of the phenotypic spectrum of brain-lung-thyroid syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21867529",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 408,
"text": " Mutations of genes affecting surfactant homeostasis, such as SFTPB, SFTPC and ABCA3, lead to diffuse lung disease in neonates and children. Haploinsufficiency of NKX2.1, the gene encoding the thyroid transcription factor-1 (TTF-1)--critical for lung, thyroid and central nervous system morphogenesis and function--causes a rare form of progressive respiratory failure designated brain-lung-thyroid syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26196025",
"endSection": "abstract",
"offsetInBeginSection": 153,
"offsetInEndSection": 362,
"text": "The disorder is caused by mutations to the NKX2.1 (TITF1) gene and also forms part of the \"brain-lung-thyroid syndrome\", in which additional developmental abnormalities of lung and thyroid tissue are observed."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21867529",
"endSection": "abstract",
"offsetInBeginSection": 141,
"offsetInEndSection": 494,
"text": "Haploinsufficiency of NKX2.1, the gene encoding the thyroid transcription factor-1 (TTF-1)--critical for lung, thyroid and central nervous system morphogenesis and function--causes a rare form of progressive respiratory failure designated brain-lung-thyroid syndrome. Molecular mechanisms involved in this syndrome are heterogeneous and poorly explored."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24129101",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "Brain-lung-thyroid syndrome (BLTS) characterized by congenital hypothyroidism, respiratory distress syndrome, and benign hereditary chorea is caused by thyroid transcription factor 1 (NKX2-1/TTF1) mutations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21867529",
"endSection": "abstract",
"offsetInBeginSection": 141,
"offsetInEndSection": 408,
"text": "Haploinsufficiency of NKX2.1, the gene encoding the thyroid transcription factor-1 (TTF-1)--critical for lung, thyroid and central nervous system morphogenesis and function--causes a rare form of progressive respiratory failure designated brain-lung-thyroid syndrome."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20020530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "NKX2-1 mutations leading to surfactant protein promoter dysregulation cause interstitial lung disease in \"Brain-Lung-Thyroid Syndrome\"."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24129101",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "Brain-lung-thyroid syndrome (BLTS) characterized by congenital hypothyroidism, respiratory distress syndrome, and benign hereditary chorea is caused by thyroid transcription factor 1 (NKX2-1/TTF1) mutations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "Thyroid transcription factor 1 (NKX2-1/TITF1) mutations cause brain-lung-thyroid syndrome, characterized by congenital hypothyroidism (CH), infant respiratory distress syndrome (IRDS) and benign hereditary chorea (BHC)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24129101",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 81,
"text": "NKX2-1 mutations in brain-lung-thyroid syndrome: a case series of four patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25759798",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 107,
"text": "Novel NKX2-1 Frameshift Mutations in Patients with Atypical Phenotypes of the Brain-Lung-Thyroid Syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "abstract",
"offsetInBeginSection": 976,
"offsetInEndSection": 1179,
"text": "The clinical spectrum of 6 own and 40 published patients with NKX2-1 mutations ranged from the complete triad of brain-lung-thyroid syndrome (50%), brain and thyroid disease (30%), to isolated BHC (13%)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21867529",
"endSection": "abstract",
"offsetInBeginSection": 141,
"offsetInEndSection": 408,
"text": "Haploinsufficiency of NKX2.1, the gene encoding the thyroid transcription factor-1 (TTF-1)--critical for lung, thyroid and central nervous system morphogenesis and function--causes a rare form of progressive respiratory failure designated brain-lung-thyroid syndrome."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/20020530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "NKX2-1 mutations leading to surfactant protein promoter dysregulation cause interstitial lung disease in \"Brain-Lung-Thyroid Syndrome\"."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/24129101",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "Brain-lung-thyroid syndrome (BLTS) characterized by congenital hypothyroidism, respiratory distress syndrome, and benign hereditary chorea is caused by thyroid transcription factor 1 (NKX2-1/TTF1) mutations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "Thyroid transcription factor 1 (NKX2-1/TITF1) mutations cause brain-lung-thyroid syndrome, characterized by congenital hypothyroidism (CH), infant respiratory distress syndrome (IRDS) and benign hereditary chorea (BHC)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24129101",
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"text": "NKX2-1 mutations in brain-lung-thyroid syndrome: a case series of four patients."
},
{
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"endSection": "title",
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"offsetInEndSection": 107,
"text": "Novel NKX2-1 Frameshift Mutations in Patients with Atypical Phenotypes of the Brain-Lung-Thyroid Syndrome."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "abstract",
"offsetInBeginSection": 976,
"offsetInEndSection": 1179,
"text": "The clinical spectrum of 6 own and 40 published patients with NKX2-1 mutations ranged from the complete triad of brain-lung-thyroid syndrome (50%), brain and thyroid disease (30%), to isolated BHC (13%)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21867529",
"endSection": "abstract",
"offsetInBeginSection": 141,
"offsetInEndSection": 408,
"text": "Haploinsufficiency of NKX2.1, the gene encoding the thyroid transcription factor-1 (TTF-1)--critical for lung, thyroid and central nervous system morphogenesis and function--causes a rare form of progressive respiratory failure designated brain-lung-thyroid syndrome."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/20020530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "NKX2-1 mutations leading to surfactant protein promoter dysregulation cause interstitial lung disease in \"Brain-Lung-Thyroid Syndrome\"."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24129101",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "Brain-lung-thyroid syndrome (BLTS) characterized by congenital hypothyroidism, respiratory distress syndrome, and benign hereditary chorea is caused by thyroid transcription factor 1 (NKX2-1/TTF1) mutations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "Thyroid transcription factor 1 (NKX2-1/TITF1) mutations cause brain-lung-thyroid syndrome, characterized by congenital hypothyroidism (CH), infant respiratory distress syndrome (IRDS) and benign hereditary chorea (BHC)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24129101",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 81,
"text": "NKX2-1 mutations in brain-lung-thyroid syndrome: a case series of four patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25759798",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 107,
"text": "Novel NKX2-1 Frameshift Mutations in Patients with Atypical Phenotypes of the Brain-Lung-Thyroid Syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26196025",
"endSection": "abstract",
"offsetInBeginSection": 153,
"offsetInEndSection": 362,
"text": "The disorder is caused by mutations to the NKX2.1 (TITF1) gene and also forms part of the \"brain-lung-thyroid syndrome\", in which additional developmental abnormalities of lung and thyroid tissue are observed."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20020530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "NKX2-1 mutations leading to surfactant protein promoter dysregulation cause interstitial lung disease in \"Brain-Lung-Thyroid Syndrome\"."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24129101",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "Brain-lung-thyroid syndrome (BLTS) characterized by congenital hypothyroidism, respiratory distress syndrome, and benign hereditary chorea is caused by thyroid transcription factor 1 (NKX2-1/TTF1) mutations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21867529",
"endSection": "abstract",
"offsetInBeginSection": 141,
"offsetInEndSection": 408,
"text": "Haploinsufficiency of NKX2.1, the gene encoding the thyroid transcription factor-1 (TTF-1)--critical for lung, thyroid and central nervous system morphogenesis and function--causes a rare form of progressive respiratory failure designated brain-lung-thyroid syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23430038",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 230,
"text": "Mutations in the gene encoding thyroid transcription factor, NKX2-1, result in neurologic abnormalities, hypothyroidism, and neonatal respiratory distress syndrome (RDS) that together are known as the brain-thyroid-lung syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19336474",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "Thyroid transcription factor 1 (NKX2-1/TITF1) mutations cause brain-lung-thyroid syndrome, characterized by congenital hypothyroidism (CH), infant respiratory distress syndrome (IRDS) and benign hereditary chorea (BHC)."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D009154",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D005796"
] |
[] |
56c1f03bef6e394741000053
|
bioasq_factoid
|
yesno
|
Is SOX10 expressed in melanoma cells?
|
['yes']
|
[
"yes"
] |
['Yes,\nThe most commonly used melanocytic markers include S100, Melan-A, HMB45 and SOX10']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33509946",
"http://www.ncbi.nlm.nih.gov/pubmed/33002486",
"http://www.ncbi.nlm.nih.gov/pubmed/34557039"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34557039",
"endSection": "abstract",
"offsetInBeginSection": 1225,
"offsetInEndSection": 1397,
"text": "Our study confirmed that SOX10 is an oncogene and activate Notch signaling pathway, which suggests the potential treatment for melanoma patients by target SOX10/Notch axis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33509946",
"endSection": "abstract",
"offsetInBeginSection": 352,
"offsetInEndSection": 433,
"text": "The most commonly used melanocytic markers include S100, Melan-A, HMB45 and SOX10"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33002486",
"endSection": "abstract",
"offsetInBeginSection": 1667,
"offsetInEndSection": 1705,
"text": "melanocytic markers melan-A and SOX10 "
}
] | 11 |
BioASQ-training11b
| null | null |
62507ca3e764a5320400000f
|
bioasq_yesno
|
factoid
|
Which NADPH oxidase family member requires interaction with NOXO1 for function?
|
['NADPH oxidase 1', 'NOX1', 'nicotinamide adenine dinucleotide phosphate-oxidase 1']
|
[
"NADPH oxidase 1",
"NOX1",
"nicotinamide adenine dinucleotide phosphate-oxidase 1",
"NADPH oxidase",
"NADPH oxidase isoform 1",
"NADPH oxidase 1 enzyme",
"NADPH oxidase 1 protein"
] |
['NADPH oxidase 1 (NOX1) requires interaction with NOXO1 for function.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/18929641",
"http://www.ncbi.nlm.nih.gov/pubmed/15507761",
"http://www.ncbi.nlm.nih.gov/pubmed/15507762",
"http://www.ncbi.nlm.nih.gov/pubmed/15824103",
"http://www.ncbi.nlm.nih.gov/pubmed/27540115",
"http://www.ncbi.nlm.nih.gov/pubmed/17900370",
"http://www.ncbi.nlm.nih.gov/pubmed/23322165",
"http://www.ncbi.nlm.nih.gov/pubmed/23957209",
"http://www.ncbi.nlm.nih.gov/pubmed/16329988",
"http://www.ncbi.nlm.nih.gov/pubmed/17583407",
"http://www.ncbi.nlm.nih.gov/pubmed/16507994",
"http://www.ncbi.nlm.nih.gov/pubmed/20454568",
"http://www.ncbi.nlm.nih.gov/pubmed/20609497",
"http://www.ncbi.nlm.nih.gov/pubmed/22549734",
"http://www.ncbi.nlm.nih.gov/pubmed/17913709",
"http://www.ncbi.nlm.nih.gov/pubmed/16762923",
"http://www.ncbi.nlm.nih.gov/pubmed/16911517",
"http://www.ncbi.nlm.nih.gov/pubmed/26781991",
"http://www.ncbi.nlm.nih.gov/pubmed/18463161"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27540115",
"endSection": "abstract",
"offsetInBeginSection": 203,
"offsetInEndSection": 439,
"text": "A unique member of this family, Nox1 oxidase, functions as either a canonical or hybrid system using Nox organizing subunit 1 (NoxO1) or p47(phox), respectively, the latter of which is functional in vascular smooth muscle cells (VSMC). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23957209",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Phosphorylation of Noxo1 at threonine 341 regulates its interaction with Noxa1 and the superoxide-producing activity of Nox1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23957209",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 329,
"text": "Superoxide production by Nox1, a member of the Nox family NAPDH oxidases, requires expression of its regulatory soluble proteins Noxo1 (Nox organizer 1) and Noxa1 (Nox activator 1) and is markedly enhanced upon cell stimulation with phorbol 12-myristate 13-acetate (PMA), a potent activator of protein kinase C (PKC)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23957209",
"endSection": "abstract",
"offsetInBeginSection": 814,
"offsetInEndSection": 1430,
"text": "Phosphorylation of Thr341 allows Noxo1 to sufficiently interact with Noxa1, an interaction that participates in Nox1 activation. Thus phosphorylation of Noxo1 at Thr341 appears to play a crucial role in PMA-elicited activation of Nox1, providing a molecular link between PKC-mediated signal transduction and Nox1-catalyzed superoxide production. Furthermore, Ser154 in Noxo1 is phosphorylated in both resting and PMA-stimulated cells, and the phosphorylation probably participates in a PMA-independent constitutive activity of Nox1. Ser154 may also be involved in protein kinase A (PKA) mediated regulation of Nox1; "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23957209",
"endSection": "abstract",
"offsetInBeginSection": 1503,
"offsetInEndSection": 1612,
"text": "Thus phosphorylation of Noxo1 at Thr341 and at Ser154 appears to regulate Nox1 activity in different manners."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15824103",
"endSection": "abstract",
"offsetInBeginSection": 184,
"offsetInEndSection": 529,
"text": "The activity of other Nox enzymes such as gp91(phox)/Nox2 and Nox1 is known to absolutely require both an organizer protein (p47(phox) or Noxo1) andanactivatorprotein (p67(phox) or Noxa1); for the p47(phox)-dependent activation of these oxidases, treatment of cells with stimulants such as phorbol 12-myristate 13-acetate is also indispensable. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15507761",
"endSection": "abstract",
"offsetInBeginSection": 529,
"offsetInEndSection": 782,
"text": "Studies of cytosolic co-factors showed that the C-terminal cytoplasmic domain of NOX1 was absolutely required for activation with NOXO1 and NOXA1 and that this activity required interaction of the putative NADPH-binding region of this domain with NOXA1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16329988",
"endSection": "abstract",
"offsetInBeginSection": 648,
"offsetInEndSection": 755,
"text": "Additionally, NADPH oxidase Organizer 1 (NoxO1) is shown to interact with the NADPH-binding region of Nox1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16762923",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 173,
"text": "Activation of the non-phagocytic superoxide-producing NADPH oxidase Nox1, complexed with p22(phox) at the membrane, requires its regulatory soluble proteins Noxo1 and Noxa1."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23322165",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "NOXO1 phosphorylation on serine 154 is critical for optimal NADPH oxidase 1 assembly and activation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16911517",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 132,
"text": "Activation of the superoxide-producing NADPH oxidase Nox1 requires both the organizer protein Noxo1 and the activator protein Noxa1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20454568",
"endSection": "abstract",
"offsetInBeginSection": 373,
"offsetInEndSection": 643,
"text": "NOX1, an NADPH oxidase homologue that is most abundantly expressed in colon epithelial cells, requires the regulatory subunits NOXO1 (NOX organizing protein 1) and NOXA1 (NOX activating protein 1), as well as the flavocytochrome component p22(phox) for maximal activity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15507762",
"endSection": "abstract",
"offsetInBeginSection": 732,
"offsetInEndSection": 917,
"text": "Activation of Nox1, an oxidase that is likely involved in host defence at the colon, requires novel proteins homologous to p47phox and p67phox, designated Noxo1 and Noxa1, respectively."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16329988",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "Molecular interaction of NADPH oxidase 1 with betaPix and Nox Organizer 1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23322165",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 254,
"text": "Reactive oxygen species (ROS) production by NADPH oxidase 1 (NOX1), which is mainly expressed in colon epithelial cells, requires the membrane-bound component p22(PHOX) and the cytosolic partners NOX organizer 1 (NOXO1), NOX activator 1 (NOXA1), and Rac1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20454568",
"endSection": "abstract",
"offsetInBeginSection": 373,
"offsetInEndSection": 642,
"text": "NOX1, an NADPH oxidase homologue that is most abundantly expressed in colon epithelial cells, requires the regulatory subunits NOXO1 (NOX organizing protein 1) and NOXA1 (NOX activating protein 1), as well as the flavocytochrome component p22(phox) for maximal activity"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16911517",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Activation of the superoxide-producing NADPH oxidase Nox1 requires both the organizer protein Noxo1 and the activator protein Noxa1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16762923",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 172,
"text": "Activation of the non-phagocytic superoxide-producing NADPH oxidase Nox1, complexed with p22(phox) at the membrane, requires its regulatory soluble proteins Noxo1 and Noxa1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18929641",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 126,
"text": "NADPH oxidase 1 (Nox1) is a multicomponent enzyme consisting of p22(phox), Nox organizer 1 (NOXO1), Nox1 activator 1, and Rac1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23957209",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 330,
"text": "UNLABELLED: Superoxide production by Nox1, a member of the Nox family NAPDH oxidases, requires expression of its regulatory soluble proteins Noxo1 (Nox organizer 1) and Noxa1 (Nox activator 1) and is markedly enhanced upon cell stimulation with phorbol 12-myristate 13-acetate (PMA), a potent activator of protein kinase C (PKC). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22549734",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 240,
"text": "The p47phox- and NADPH oxidase organiser 1 (NOXO1)-dependent activation of NADPH oxidase 1 (NOX1) mediates endothelial nitric oxide synthase (eNOS) uncoupling and endothelial dysfunction in a streptozotocin-induced murine model of diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15507761",
"endSection": "abstract",
"offsetInBeginSection": 532,
"offsetInEndSection": 785,
"text": "Studies of cytosolic co-factors showed that the C-terminal cytoplasmic domain of NOX1 was absolutely required for activation with NOXO1 and NOXA1 and that this activity required interaction of the putative NADPH-binding region of this domain with NOXA1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17913709",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 185,
"text": "Nox activator 1 (NoxA1) is a homologue of p67(phox) that acts in conjunction with Nox organizer 1 (NoxO1) to regulate reactive oxygen species (ROS) production by the NADPH oxidase Nox1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20609497",
"endSection": "abstract",
"offsetInBeginSection": 373,
"offsetInEndSection": 568,
"text": "Nox1 is highly expressed in the colon, and requires two cytosolic regulators, the organizer subunit NoxO1 and the activator subunit NoxA1, as well as the binding of Rac1 GTPase, for its activity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18463161",
"endSection": "abstract",
"offsetInBeginSection": 354,
"offsetInEndSection": 508,
"text": "Nox1 is highly expressed in the colon, and it requires two cytosolic regulators, NoxO1 and NoxA1, as well as the binding of Rac1 GTPase, for its activity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23322165",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 255,
"text": "Reactive oxygen species (ROS) production by NADPH oxidase 1 (NOX1), which is mainly expressed in colon epithelial cells, requires the membrane-bound component p22(PHOX) and the cytosolic partners NOX organizer 1 (NOXO1), NOX activator 1 (NOXA1), and Rac1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23957209",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 317,
"text": "Superoxide production by Nox1, a member of the Nox family NAPDH oxidases, requires expression of its regulatory soluble proteins Noxo1 (Nox organizer 1) and Noxa1 (Nox activator 1) and is markedly enhanced upon cell stimulation with phorbol 12-myristate 13-acetate (PMA), a potent activator of protein kinase C (PKC)."
}
] | 6 |
BioASQ-training6b
|
[
"http://www.uniprot.org/uniprot/NOXO1_HUMAN",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D019255",
"http://www.uniprot.org/uniprot/NOXO1_MOUSE",
"http://amigo.geneontology.org/amigo/term/GO:0043020",
"http://www.biosemantics.org/jochem#4270191",
"http://www.uniprot.org/uniprot/NOXA1_MOUSE",
"http://www.uniprot.org/uniprot/NOXA1_RAT"
] | null |
58a5a51060087bc10a000021
|
bioasq_factoid
|
factoid
|
Which gene is responsible for the development of Sotos syndrome?
|
[['NSD1 gene']]
|
[
"NSD1 gene",
"nuclear receptor binding SET domain protein 1",
"nuclear receptor binding SET domain 1",
"NSD1",
"KMT3B",
"SET domain containing 1B"
] |
['Sotos syndrome (SoS) is a multiple anomaly, congenital disorder characterized by overgrowth, macrocephaly, distinctive facial features and variable degree of intellectual disability. Haploinsufficiency of the NSD1 gene at 5q35.3, arising from 5q35 microdeletions, point mutations, and partial gene deletions, accounts for a majority of patients with SoS.', 'Sotos syndrome is a well-known overgrowth syndrome characterized by excessive growth during childhood, macrocephaly, distinctive facial appearance and learning disability. This disorder is caused by mutations or deletions in NSD1 gene', 'Sotos syndrome is a well-known overgrowth syndrome characterized by excessive growth during childhood, macrocephaly, distinctive facial appearance and learning disability. This disorder is caused by mutations or deletions in NSD1 gene', 'Sotos syndrome is a well-known overgrowth syndrome characterized by excessive growth during childhood, macrocephaly, distinctive facial appearance and learning disability. This disorder is caused by mutations or deletions in NSD1 gene', 'Sotos syndrome is a well-known overgrowth syndrome characterized by excessive growth during childhood, macrocephaly, distinctive facial appearance and learning disability. This disorder is caused by mutations or deletions in NSD1 gene', 'Sotos syndrome is a well-known overgrowth syndrome characterized by excessive growth during childhood, macrocephaly, distinctive facial appearance and learning disability. This disorder is caused by mutations or deletions in NSD1 gene']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26043501",
"http://www.ncbi.nlm.nih.gov/pubmed/25852445",
"http://www.ncbi.nlm.nih.gov/pubmed/21834033",
"http://www.ncbi.nlm.nih.gov/pubmed/14571271",
"http://www.ncbi.nlm.nih.gov/pubmed/16010675",
"http://www.ncbi.nlm.nih.gov/pubmed/20420030",
"http://www.ncbi.nlm.nih.gov/pubmed/16232326",
"http://www.ncbi.nlm.nih.gov/pubmed/21567906",
"http://www.ncbi.nlm.nih.gov/pubmed/24192683",
"http://www.ncbi.nlm.nih.gov/pubmed/22012791",
"http://www.ncbi.nlm.nih.gov/pubmed/23190751",
"http://www.ncbi.nlm.nih.gov/pubmed/25510705"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26043501",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 234,
"text": "Sotos syndrome is a well-known overgrowth syndrome characterized by excessive growth during childhood, macrocephaly, distinctive facial appearance and learning disability. This disorder is caused by mutations or deletions in NSD1 gene"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25852445",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 353,
"text": "Sotos syndrome (SoS) is a multiple anomaly, congenital disorder characterized by overgrowth, macrocephaly, distinctive facial features and variable degree of intellectual disability. Haploinsufficiency of the NSD1 gene at 5q35.3, arising from 5q35 microdeletions, point mutations, and partial gene deletions, accounts for a majority of patients with SoS"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20420030",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 126,
"text": "Mutations and deletions of the NSD1 gene, located on chromosome 5q35, are responsible for over 90% of cases of Sotos syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16010675",
"endSection": "abstract",
"offsetInBeginSection": 328,
"offsetInEndSection": 469,
"text": "The NSD1 gene was recently found to be responsible for Sotos syndrome, and more than 150 patients with NSD1 alterations have been identified."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14571271",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 269,
"text": "Recently, deletions encompassing the nuclear receptor binding SET-Domain 1 (NSD1) gene have been described as the major cause of Japanese patients with the Sotos syndrome, whereas point mutations have been identified in the majority of European Sotos syndrome patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14571271",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "Mutations in NSD1 are responsible for Sotos syndrome, but are not a frequent finding in other overgrowth phenotypes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20420030",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 126,
"text": "Mutations and deletions of the NSD1 gene, located on chromosome 5q35, are responsible for over 90% of cases of Sotos syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14571271",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 269,
"text": "Recently, deletions encompassing the nuclear receptor binding SET-Domain 1 (NSD1) gene have been described as the major cause of Japanese patients with the Sotos syndrome, whereas point mutations have been identified in the majority of European Sotos syndrome patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14571271",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "Mutations in NSD1 are responsible for Sotos syndrome, but are not a frequent finding in other overgrowth phenotypes."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16232326",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 81,
"text": "Spectrum of NSD1 gene mutations in southern Chinese patients with Sotos syndrome."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20420030",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 66,
"text": "Two cases of Sotos syndrome with novel mutations of the NSD1 gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20420030",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Mutations and deletions of the NSD1 gene, located on chromosome 5q35, are responsible for over 90% of cases of Sotos syndrome"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21567906",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 302,
"text": "Haploinsufficiency of the NSD1 gene due to 5q35 microdeletions or intragenic mutations is the major cause of Sotos syndrome characterized by generalized overgrowth, large hands and feet with advanced bone age, craniofacial dysmorphic features, learning disability, and possible susceptibility to tumors"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16232326",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "Spectrum of NSD1 gene mutations in southern Chinese patients with Sotos syndrome"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16232326",
"endSection": "abstract",
"offsetInBeginSection": 121,
"offsetInEndSection": 282,
"text": "Haploinsufficiency of the NSD1 gene has been implicated as the major cause of Sotos syndrome, with a predominance of microdeletions reported in Japanese patients"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21567906",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 304,
"text": "Haploinsufficiency of the NSD1 gene due to 5q35 microdeletions or intragenic mutations is the major cause of Sotos syndrome characterized by generalized overgrowth, large hands and feet with advanced bone age, craniofacial dysmorphic features, learning disability, and possible susceptibility to tumors. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23190751",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 159,
"text": "Clinical and genetic spectrum of 18 unrelated Korean patients with Sotos syndrome: frequent 5q35 microdeletion and identification of four novel NSD1 mutations."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22012791",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Craniofacial and oral features of Sotos syndrome: differences in patients with submicroscopic deletion and mutation of NSD1 gene."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25510705",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "Prenatal diagnosis and molecular cytogenetic characterization of a 1.07-Mb microdeletion at 5q35.2-q35.3 associated with NSD1 haploinsufficiency and Sotos syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24192683",
"endSection": "abstract",
"offsetInBeginSection": 186,
"offsetInEndSection": 353,
"text": "Autosomal dominant mutations and deletions of the nuclear receptor set domain gene (NSD1), which is located at chromosome 5q35, are responsible for most of the cases. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22012791",
"endSection": "abstract",
"offsetInBeginSection": 110,
"offsetInEndSection": 312,
"text": "There are two types of mutations that cause NSD1 haploinsufficiency: mutations within the NSD1 gene (mutation type) and a 5q35 submicroscopic deletion encompassing the entire NSD1 gene (deletion type). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21834033",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 224,
"text": "Sotos syndrome is a rare genetic disorder characterized by overgrowth associated with macrocephaly and delayed psychomotor development. Patients with Sotos syndrome show 5q35 deletions involving NSD1 or its point mutations."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14571271",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 53,
"text": "Mutations in NSD1 are responsible for Sotos syndrome,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20420030",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Mutations and deletions of the NSD1 gene, located on chromosome 5q35, are responsible for over 90% of cases of Sotos syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16010675",
"endSection": "abstract",
"offsetInBeginSection": 189,
"offsetInEndSection": 330,
"text": "The NSD1 gene was recently found to be responsible for Sotos syndrome, and more than 150 patients with NSD1 alterations have been identified."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14571271",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Mutations in NSD1 are responsible for Sotos syndrome, but are not a frequent finding in other overgrowth phenotypes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20420030",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Mutations and deletions of the NSD1 gene, located on chromosome 5q35, are responsible for over 90% of cases of Sotos syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16010675",
"endSection": "abstract",
"offsetInBeginSection": 189,
"offsetInEndSection": 330,
"text": "The NSD1 gene was recently found to be responsible for Sotos syndrome, and more than 150 patients with NSD1 alterations have been identified."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14571271",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Mutations in NSD1 are responsible for Sotos syndrome, but are not a frequent finding in other overgrowth phenotypes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20420030",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Mutations and deletions of the NSD1 gene, located on chromosome 5q35, are responsible for over 90% of cases of Sotos syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16010675",
"endSection": "abstract",
"offsetInBeginSection": 189,
"offsetInEndSection": 330,
"text": "The NSD1 gene was recently found to be responsible for Sotos syndrome, and more than 150 patients with NSD1 alterations have been identified."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14571271",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Mutations in NSD1 are responsible for Sotos syndrome, but are not a frequent finding in other overgrowth phenotypes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20420030",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Mutations and deletions of the NSD1 gene, located on chromosome 5q35, are responsible for over 90% of cases of Sotos syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16010675",
"endSection": "abstract",
"offsetInBeginSection": 189,
"offsetInEndSection": 330,
"text": "The NSD1 gene was recently found to be responsible for Sotos syndrome, and more than 150 patients with NSD1 alterations have been identified."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14571271",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Mutations in NSD1 are responsible for Sotos syndrome, but are not a frequent finding in other overgrowth phenotypes."
}
] | 5 |
BioASQ-training5b
|
[] |
[] |
571f33bd0fd6f91b68000003
|
bioasq_factoid
|
factoid
|
TAK-994 is developed for which disease?
|
['narcolepsy']
|
[
"narcolepsy",
"excessive daytime sleepiness",
"hypersomnia",
"sleep disorder"
] |
['TAK-994 is an oral orexin receptor 2-selective agonist that was developed and tested for narcolepsy type 1.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/37001988",
"http://www.ncbi.nlm.nih.gov/pubmed/37494485"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37494485",
"endSection": "abstract",
"offsetInBeginSection": 93,
"offsetInEndSection": 255,
"text": "METHODS: We conducted a phase 2, randomized, placebo-controlled trial of TAK-994, an oral orexin receptor 2-selective agonist, in patients with narcolepsy type 1."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37001988",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 185,
"text": "TAK-994, a Novel Orally Available Brain-Penetrant Orexin 2 Receptor-Selective Agonist, Suppresses Fragmentation of Wakefulness and Cataplexy-Like Episodes in Mouse Models of Narcolepsy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37001988",
"endSection": "abstract",
"offsetInBeginSection": 2127,
"offsetInEndSection": 2277,
"text": "These findings indicate that TAK-994 is an orally available brain-penetrant OX2R-selective agonist with potential to improve narcolepsy-like symptoms."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37494485",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 255,
"text": "BACKGROUND: Narcolepsy type 1 is caused by severe loss or lack of brain orexin neuropeptides.METHODS: We conducted a phase 2, randomized, placebo-controlled trial of TAK-994, an oral orexin receptor 2-selective agonist, in patients with narcolepsy type 1."
}
] | 13 |
BioASQ-training13b
| null | null |
65cfd3961930410b1300001f
|
bioasq_factoid
|
factoid
|
What is FeatureCounts used for?
|
['assigning sequence reads to genomic features']
|
[
"assigning sequence reads to genomic features",
"read assignment to genomic features",
"mapping sequence reads to genomic features",
"alignment of sequence reads to genomic features",
"annotation of sequence reads to genomic features"
] |
['featureCounts is a general purpose program for assigning sequence reads to genomic features. It is a read summarization program suitable for counting reads generated from either RNA or genomic DNA sequencing experiments.', 'featureCounts: an efficient general purpose program for assigning sequence reads to genomic features. We present featureCounts, a read summarization program suitable for counting reads generated from either RNA or genomic DNA sequencing experiments', 'featureCounts can be used to quantify reads generated from either RNA or DNA sequencing technologies in terms of any type of genomic feature. It implements chromosome hashing, feature blocking and other strategies to assign reads to features with high efficiency.', 'Featurecounts is a system that uses a novel Bayesian approach to calculate informative metrics at each depth required to inform a broad range of functional and evolutionary studies. The database is optimized to support fast interactive performance with the RNA-Seq platform.', 'featureCounts: an efficient general purpose program for assigning sequence reads to genomic features.', 'We present featureCounts, a read summarization program suitable for counting reads generated from either RNA or genomic DNA sequencing experiments.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24227677",
"http://www.ncbi.nlm.nih.gov/pubmed/28096075",
"http://www.ncbi.nlm.nih.gov/pubmed/28915787",
"http://www.ncbi.nlm.nih.gov/pubmed/30379987"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24227677",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "featureCounts: an efficient general purpose program for assigning sequence reads to genomic features."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24227677",
"endSection": "abstract",
"offsetInBeginSection": 524,
"offsetInEndSection": 670,
"text": "We present featureCounts, a read summarization program suitable for counting reads generated from either RNA or genomic DNA sequencing experiments"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28915787",
"endSection": "abstract",
"offsetInBeginSection": 701,
"offsetInEndSection": 842,
"text": "mmquant is a drop-in replacement of the widely used tools htseq-count and featureCounts that handles multi-mapping reads in an unabiased way."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30379987",
"endSection": "abstract",
"offsetInBeginSection": 740,
"offsetInEndSection": 839,
"text": "We also show the correlation for raw read counts reported by TPMCalculator, HTSeq and featureCounts"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28096075",
"endSection": "abstract",
"offsetInBeginSection": 722,
"offsetInEndSection": 1073,
"text": "It features six independent core-workflows comprising the state-of-the-art technology with dozens of popular cutting-edge tools such as Tophat-Cufflink-Cuffdiff, Subread-featureCounts-DESeq2, STAR-RSEM-EBSeq, Bowtie-eXpress-edgeR, kallisto-sleuth, HISAT-StringTie-Ballgown, and embeds itself in Snakemake, which is a modern pipeline management system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24227677",
"endSection": "abstract",
"offsetInBeginSection": 517,
"offsetInEndSection": 673,
"text": "SULTS: We present featureCounts, a read summarization program suitable for counting reads generated from either RNA or genomic DNA sequencing experiments. f"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24227677",
"endSection": "abstract",
"offsetInBeginSection": 525,
"offsetInEndSection": 672,
"text": "e present featureCounts, a read summarization program suitable for counting reads generated from either RNA or genomic DNA sequencing experiments. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24227677",
"endSection": "abstract",
"offsetInBeginSection": 767,
"offsetInEndSection": 909,
"text": "t is considerably faster than existing methods (by an order of magnitude for gene-level summarization) and requires far less computer memory. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24227677",
"endSection": "abstract",
"offsetInBeginSection": 374,
"offsetInEndSection": 516,
"text": "Read summarization is required for a great variety of genomic analyses but has so far received relatively little attention in the literature.R"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24227677",
"endSection": "abstract",
"offsetInBeginSection": 314,
"offsetInEndSection": 373,
"text": "The process of counting reads is called read summarization."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24227677",
"endSection": "abstract",
"offsetInBeginSection": 362,
"offsetInEndSection": 650,
"text": "marization. Read summarization is required for a great variety of genomic analyses but has so far received relatively little attention in the literature.RESULTS: We present featureCounts, a read summarization program suitable for counting reads generated from either RNA or genomic DNA se"
}
] | 11 |
BioASQ-training11b
| null | null |
5fdb41c5a43ad3127800001e
|
bioasq_factoid
|
factoid
|
Which yeast genes encode for condensin?
|
['Smc2/4']
|
[
"Smc2/4",
"Structural Maintenance of Chromosomes 2/4",
"Smc2",
"Smc4",
"SMC2",
"SMC4"
] |
['Smc2-Smc4 forms the core of the Saccharomyces cerevisiae condensin, which promotes metaphase chromosome compaction . Both SMC2 and SMC4 are essential for chromosome transmission in anaphase . Smc 2-8 suppresses catenanes accumulation, mitotic arrest and growth defects induced by histone depletion at semi-permissive temperature .', 'Smc2/4 forms the core of the Saccharomyces cerevisiae condensin, which promotes metaphase chromosome compaction', 'Condensin Smc2-Smc4 Dimers Are Flexible and Dynamic. Here, we probe the topology of Smc2-Smc4 dimers of the S. cerevisiae condensin complex with high-speed atomic force microscopy (AFM) in liquid Interestingly, SAC activation is suppressed by the absence of Top2 and Smc2, an essential component of condensin.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26904946",
"http://www.ncbi.nlm.nih.gov/pubmed/16100111",
"http://www.ncbi.nlm.nih.gov/pubmed/12783798",
"http://www.ncbi.nlm.nih.gov/pubmed/10811823",
"http://www.ncbi.nlm.nih.gov/pubmed/25300489",
"http://www.ncbi.nlm.nih.gov/pubmed/12719426",
"http://www.ncbi.nlm.nih.gov/pubmed/11846874",
"http://www.ncbi.nlm.nih.gov/pubmed/10749931",
"http://www.ncbi.nlm.nih.gov/pubmed/10485849"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26904946",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 52,
"text": "Condensin Smc2-Smc4 Dimers Are Flexible and Dynamic."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26904946",
"endSection": "abstract",
"offsetInBeginSection": 330,
"offsetInEndSection": 472,
"text": "Here, we probe the topology of Smc2-Smc4 dimers of the S. cerevisiae condensin complex with high-speed atomic force microscopy (AFM) in liquid"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25300489",
"endSection": "abstract",
"offsetInBeginSection": 926,
"offsetInEndSection": 1183,
"text": "Interestingly, SAC activation is suppressed by the absence of Top2 and Smc2, an essential component of condensin. Indeed, smc2-8 suppresses catenanes accumulation, mitotic arrest and growth defects induced by histone depletion at semi-permissive temperature"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12719426",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 256,
"text": "To better understand the contributions that the structural maintenance of chromosome proteins (SMCs) make to condensin activity, we have tested a number of biochemical, biophysical, and DNA-associated attributes of the Smc2p-Smc4p pair from budding yeast. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16100111",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 111,
"text": "Smc2/4 forms the core of the Saccharomyces cerevisiae condensin, which promotes metaphase chromosome compaction"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10811823",
"endSection": "abstract",
"offsetInBeginSection": 296,
"offsetInEndSection": 369,
"text": "Both SMC2 and SMC4 are essential for chromosome transmission in anaphase."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11846874",
"endSection": "abstract",
"offsetInBeginSection": 300,
"offsetInEndSection": 437,
"text": "Here we demonstrate that three TTN genes encode chromosome scaffold proteins of the condensin (SMC2) and cohesin (SMC1 and SMC3) classes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11846874",
"endSection": "abstract",
"offsetInBeginSection": 305,
"offsetInEndSection": 448,
"text": "we demonstrate that three TTN genes encode chromosome scaffold proteins of the condensin (SMC2) and cohesin (SMC1 and SMC3) classes. These prot"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10485849",
"endSection": "abstract",
"offsetInBeginSection": 479,
"offsetInEndSection": 784,
"text": ", and Cnd3, three non-SMC subunits showing a high degree of sequence conservation to frog subunits, are essential for viability, and their gene disruption leads to a phenotype indistinguishable from that observed in cut3-477 and cut14-208, known mutations in SMC4 and SMC2-like subunits. Condensin subunit"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12783798",
"endSection": "abstract",
"offsetInBeginSection": 237,
"offsetInEndSection": 361,
"text": "e core subunits of the complex are members of the SMC2 (Structural Maintenance of Chromosomes) and SMC4 gene families. We ha"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10749931",
"endSection": "abstract",
"offsetInBeginSection": 699,
"offsetInEndSection": 1075,
"text": "Temperature-sensitive mutations of BRN1 can be suppressed by overexpression of a novel gene YCG1, which is homologous to another Xenopus condensin subunit, XCAP-G. Overexpression of SMC2, a gene necessary for chromosome condensation, and a homologue of the XCAP-E condensin, does not suppress brn1, pointing to functional specialization of components of the condensin complex."
}
] | 11 |
BioASQ-training11b
| null | null |
5fe31301a43ad31278000039
|
bioasq_factoid
|
factoid
|
What is the human RCA locus size in bps?
|
['300kbp']
|
[
"300kbp",
"300 kilobase pairs",
"300 kilobases",
"300 kbp"
] |
['The human RCA locus is located on chromosome 1 (CA1) and consists of approximately 750 kb.', 'Genome and expressed sequence tag information of Xenopus tropicalis suggested that short-consensus repeat (SCR)-containing proteins are encoded by three genes that are mapped within a 300-kb downstream of PFKFB2, which is a marker gene for the regulator of complement activation (RCA) loci in human and chicken', 'The locus containing the ribosomal protein A (RCA) gene is located at a perinuclear structure 3 kb from the left end and 610 kb in bps, leaving a footprint of 7.4 kb on chromosome 1.', 'The human RCA locus is located on chromosome 1q21-32 and measures approximately 2-3 kb in bps.', 'The human RCA locus is located on chromosome 1q21-32 and consists of approximately 150 tandemly repeated copies of a 9.1 kb locus.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/2564419",
"http://www.ncbi.nlm.nih.gov/pubmed/2451706",
"http://www.ncbi.nlm.nih.gov/pubmed/19319518",
"http://www.ncbi.nlm.nih.gov/pubmed/2164822"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2564419",
"endSection": "abstract",
"offsetInBeginSection": 196,
"offsetInEndSection": 400,
"text": " The human homologues of these genes are tightly linked, composing the RCA locus, which maps to human chromosome (Chr.)1q32, within a large linkage group conserved between human Chr.1q21-32 and mouse Chr."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2164822",
"endSection": "abstract",
"offsetInBeginSection": 162,
"offsetInEndSection": 402,
"text": "The primary sequence of the most common structural allotype of CR1 and that of CR2 have been established, and ligand binding on the molecules has been mapped. CR1 and CR2 genes are located in close vicinity in the RCA locus of chromosome 1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19319518",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 311,
"text": "Genome and expressed sequence tag information of Xenopus tropicalis suggested that short-consensus repeat (SCR)-containing proteins are encoded by three genes that are mapped within a 300-kb downstream of PFKFB2, which is a marker gene for the regulator of complement activation (RCA) loci in human and chicken."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2451706",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 221,
"text": "The organization and physical linkage of four members of a major complement locus, the RCA locus, have been determined using the technique of pulsed field gradient gel electrophoresis in conjunction with Southern blotting"
}
] | 11 |
BioASQ-training11b
| null | null |
5d35d901b3a638076300000a
|
bioasq_factoid
|
factoid
|
Which syndrome is caused by deletion of Pds5b in mice?
|
['Cornelia de Lange syndrome.']
|
[
"Cornelia de Lange syndrome",
"CdLS",
"Brachmann-de Lange syndrome",
"Brachmann syndrome",
"de Lange syndrome"
] |
['mice lacking sister chromatid cohesion protein pds5b exhibit developmental abnormalities reminiscent of cornelia de lange syndrome.', 'Mice lacking sister chromatid cohesion protein PDS5B exhibit developmental abnormalities reminiscent of Cornelia de Lange syndrome. ', 'Mice lacking sister chromatid cohesion protein PDS5B exhibit developmental abnormalities reminiscent of Cornelia de Lange syndrome.', 'Mice lacking sister chromatid cohesion protein PDS5B exhibit developmental abnormalities reminiscent of Cornelia de Lange syndrome', 'Mice lacking sister chromatid cohesion protein Pds5b exhibit developmental abnormalities reminiscent of Cornelia de Lange syndrome.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/17652350",
"http://www.ncbi.nlm.nih.gov/pubmed/19412548"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17652350",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Mice lacking sister chromatid cohesion protein PDS5B exhibit developmental abnormalities reminiscent of Cornelia de Lange syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19412548",
"endSection": "abstract",
"offsetInBeginSection": 298,
"offsetInEndSection": 364,
"text": "Pds5B mutant mice have developmental abnormalities resembling CdLS"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17652350",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Mice lacking sister chromatid cohesion protein PDS5B exhibit developmental abnormalities reminiscent of Cornelia de Lange syndrome"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19412548",
"endSection": "abstract",
"offsetInBeginSection": 296,
"offsetInEndSection": 460,
"text": "Pds5B mutant mice have developmental abnormalities resembling CdLS; however the role of Pds5A in mammals and the association of PDS5 proteins with CdLS are unknown."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19412548",
"endSection": "abstract",
"offsetInBeginSection": 298,
"offsetInEndSection": 462,
"text": "Pds5B mutant mice have developmental abnormalities resembling CdLS; however the role of Pds5A in mammals and the association of PDS5 proteins with CdLS are unknown."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17652350",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 132,
"text": "Mice lacking sister chromatid cohesion protein PDS5B exhibit developmental abnormalities reminiscent of Cornelia de Lange syndrome."
}
] | 6 |
BioASQ-training6b
|
[
"http://amigo.geneontology.org/amigo/term/GO:0090695",
"http://www.uniprot.org/uniprot/PDS5B_RAT",
"http://www.uniprot.org/uniprot/PDS5B_MOUSE"
] |
[
{
"o": "Gene Deletion",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C1442161"
},
{
"o": "Syndrome",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C0039082"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A0121946",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0039082"
},
{
"o": "Syndrome",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A0121946"
},
{
"o": "http://linkedlifedata.com/resource/rxnorm/label/3242053",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/rxnorm/id/989712"
},
{
"o": "Syndrome",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/rxnorm/label/3242053"
},
{
"o": "Deletion",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C1511760"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A10802767",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C1442161"
},
{
"o": "Deletion",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A10802767"
}
] |
5889eb503b87a8a73800000b
|
bioasq_factoid
|
factoid
|
Which olfactory gene senses androsterone?
|
['OR7D4']
|
[
"OR7D4",
"Olfactory receptor 7D4",
"Olfactory receptor OR7D4",
"Olfactory receptor 7D4 protein"
] |
['A previously reported association between the olfactory receptor or7d4 and the androstenone was not detected until we specifically typed this gene p = 1.1 × 10 -4.Any mammals can decipher these scent codes to discern the gender , age , endocrine status , social status , and genotype of conspecifics using dedicated sensory receptors in their olfactory system.', 'These findings suggest that 1) the perceived intensity of some but not all odorants is a heritable trait, 2) use of a current genome-wide marker panel did not detect a known olfactory genotype-phenotype association, and 3) person-to-person differences in androstenone perception are influenced by OR7D4 genotype and perhaps by variants of other genes. A previously reported association between the olfactory receptor OR7D4 and the androstenone was not detected until we specifically typed this gene (P = 1.1 × 10(-4)). any mammals can decipher these scent codes to discern the gender, age, endocrine status, social status, and genotype of conspecifics using dedicated sensory receptors in their olfactory system. ', 'Person-to-person differences in androstenone perception are influenced by OR7D4 genotype and perhaps by variants of other genes.', 'These findings suggest that 1) the perceived intensity of some but not all odorants is a heritable trait, 2) use of a current genome-wide marker panel did not detect a known olfactory genotype-phenotype association, and 3) person-to-person differences in androstenone perception are influenced by OR7D4 genotype and perhaps by variants of other genes. ']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/9566734",
"http://www.ncbi.nlm.nih.gov/pubmed/20836008",
"http://www.ncbi.nlm.nih.gov/pubmed/17013929",
"http://www.ncbi.nlm.nih.gov/pubmed/22977065",
"http://www.ncbi.nlm.nih.gov/pubmed/22362865"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20836008",
"endSection": "abstract",
"offsetInBeginSection": 110,
"offsetInEndSection": 303,
"text": "any mammals can decipher these scent codes to discern the gender, age, endocrine status, social status, and genotype of conspecifics using dedicated sensory receptors in their olfactory system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22362865",
"endSection": "abstract",
"offsetInBeginSection": 521,
"offsetInEndSection": 688,
"text": "A previously reported association between the olfactory receptor OR7D4 and the androstenone was not detected until we specifically typed this gene (P = 1.1 × 10(-4)). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22362865",
"endSection": "abstract",
"offsetInBeginSection": 875,
"offsetInEndSection": 1226,
"text": "These findings suggest that 1) the perceived intensity of some but not all odorants is a heritable trait, 2) use of a current genome-wide marker panel did not detect a known olfactory genotype-phenotype association, and 3) person-to-person differences in androstenone perception are influenced by OR7D4 genotype and perhaps by variants of other genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22977065",
"endSection": "abstract",
"offsetInBeginSection": 854,
"offsetInEndSection": 1015,
"text": "The flavor of ethanol was related to variation within an olfactory receptor gene (OR7D4) and a gene encoding a subunit of the epithelial sodium channel (SCNN1D)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22362865",
"endSection": "abstract",
"offsetInBeginSection": 522,
"offsetInEndSection": 688,
"text": "A previously reported association between the olfactory receptor OR7D4 and the androstenone was not detected until we specifically typed this gene (P = 1.1 × 10(-4))."
}
] | 11 |
BioASQ-training11b
| null | null |
5ace17c30340b9f058000009
|
bioasq_factoid
|
factoid
|
Which is the main gene signature in Systemic Lupus Erythematosus (SLE)?
|
['IFN signature', 'Interferon signature']
|
[
"IFN signature",
"Interferon signature",
"Interferon gene signature",
"Interferon-stimulated gene signature",
"IFN-stimulated gene signature"
] |
['Systemic Lupus Erythematosus (SLE) has a type I interferon (IFN) gene signature.', 'SLE is characterized by a type-I interferon gene signature.', 'Systemic Lupus Erythematosus (SLE) is a type I interferon (IFN) disease. The main gene signature is a 4-gene expression of 4 genes.', 'SLE is characterized by dysregulation of both the innate and the adaptive immune systems. An increased expression of type I IFN-regulated genes, termed IFN signature, has been reported in patients with SLE.', 'A role for interferon (IFN) in systemic lupus erythematosus (SLE) pathogenesis is inferred from the prominent IFN gene signature (IGS), but the major IFN species and its relationship to disease activity are unknown.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23400715",
"http://www.ncbi.nlm.nih.gov/pubmed/15593221",
"http://www.ncbi.nlm.nih.gov/pubmed/18075793",
"http://www.ncbi.nlm.nih.gov/pubmed/27009916",
"http://www.ncbi.nlm.nih.gov/pubmed/19790071",
"http://www.ncbi.nlm.nih.gov/pubmed/30745462",
"http://www.ncbi.nlm.nih.gov/pubmed/31130331",
"http://www.ncbi.nlm.nih.gov/pubmed/25861459",
"http://www.ncbi.nlm.nih.gov/pubmed/31044165",
"http://www.ncbi.nlm.nih.gov/pubmed/28130918",
"http://www.ncbi.nlm.nih.gov/pubmed/32334613",
"http://www.ncbi.nlm.nih.gov/pubmed/17849124",
"http://www.ncbi.nlm.nih.gov/pubmed/20538795",
"http://www.ncbi.nlm.nih.gov/pubmed/24598455",
"http://www.ncbi.nlm.nih.gov/pubmed/31660791",
"http://www.ncbi.nlm.nih.gov/pubmed/24379124",
"http://www.ncbi.nlm.nih.gov/pubmed/19479852",
"http://www.ncbi.nlm.nih.gov/pubmed/15511676",
"http://www.ncbi.nlm.nih.gov/pubmed/23754736",
"http://www.ncbi.nlm.nih.gov/pubmed/29644082",
"http://www.ncbi.nlm.nih.gov/pubmed/23028528",
"http://www.ncbi.nlm.nih.gov/pubmed/24839407",
"http://www.ncbi.nlm.nih.gov/pubmed/12642603",
"http://www.ncbi.nlm.nih.gov/pubmed/24834763",
"http://www.ncbi.nlm.nih.gov/pubmed/31890206",
"http://www.ncbi.nlm.nih.gov/pubmed/23083033",
"http://www.ncbi.nlm.nih.gov/pubmed/30185417",
"http://www.ncbi.nlm.nih.gov/pubmed/27723281",
"http://www.ncbi.nlm.nih.gov/pubmed/27094810",
"http://www.ncbi.nlm.nih.gov/pubmed/21803750",
"http://www.ncbi.nlm.nih.gov/pubmed/19968664",
"http://www.ncbi.nlm.nih.gov/pubmed/22242767"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29644082",
"endSection": "abstract",
"offsetInBeginSection": 393,
"offsetInEndSection": 653,
"text": "The effects of anifrolumab on type I IFN pathway activation were assessed using signal transducer and activator of transcription 1 (STAT1) phosphorylation, IFN-stimulated response element-luciferase reporter cell assays and type I IFN gene signature induction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28130918",
"endSection": "abstract",
"offsetInBeginSection": 417,
"offsetInEndSection": 640,
"text": "Randomization was stratified by SLE Disease Activity Index 2000 score (<10 or ≥10), oral corticosteroid dosage (<10 or ≥10 mg/day), and type I IFN gene signature test status (high or low) based on a 4-gene expression assay."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28130918",
"endSection": "abstract",
"offsetInBeginSection": 1703,
"offsetInEndSection": 1750,
"text": "patients with a high IFN signature at baseline "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27009916",
"endSection": "abstract",
"offsetInBeginSection": 389,
"offsetInEndSection": 543,
"text": "Patients were stratified by disease activity, interferon gene-signature test (high vs low based on the expression of four genes) and geographical region. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24839407",
"endSection": "abstract",
"offsetInBeginSection": 278,
"offsetInEndSection": 543,
"text": "Our group, using microarray analysis, identified the interferon (IFN) gene signature in pediatric systemic lupus erythematosus (SLE) and has published data that suggest high doses of intravenous corticosteroid treatment may have benefit over strictly oral regimens."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24379124",
"endSection": "abstract",
"offsetInBeginSection": 145,
"offsetInEndSection": 406,
"text": "In this study, we report the presence of IFN activation in SLE bone marrow (BM), as measured by an IFN gene signature, increased IFN regulated chemokines, and direct production of IFN by BM-resident cells, associated with profound changes in B cell development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24379124",
"endSection": "abstract",
"offsetInBeginSection": 594,
"offsetInEndSection": 853,
"text": "Pronounced alterations in B cell development were noted in SLE in the presence of an IFN signature with a reduction in the fraction of pro/pre-B cells, suggesting an inhibition in early B cell development and an expansion of B cells at the transitional stage."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23400715",
"endSection": "abstract",
"offsetInBeginSection": 815,
"offsetInEndSection": 992,
"text": " At baseline, patients had moderate-to-severe disease activity (mean SLE Disease Activity Index score 11.0), and most (75.2%) had a high type I interferon (IFN) gene signature. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23400715",
"endSection": "abstract",
"offsetInBeginSection": 1383,
"offsetInEndSection": 1502,
"text": "Inhibition of the type I IFN gene signature was sustained during treatment in patients with a high baseline signature. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23754736",
"endSection": "abstract",
"offsetInBeginSection": 2209,
"offsetInEndSection": 2469,
"text": "Patient baseline body WT, interferon gene signature from 21 genes, steroid use, and sifalimumab dose were identified as significant covariates for CL, whereas only baseline body WT was a significant covariate for V 1 and peripheral volume of distribution (V 2)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23083033",
"endSection": "abstract",
"offsetInBeginSection": 872,
"offsetInEndSection": 1170,
"text": "These include: type I interferon (IFN) gene signature as a pharmacodynamic marker and potential predictive marker for anti-type I IFN therapy; anti-double stranded DNA as a disease marker and potential predictive marker for flares; the complements and neutrophil signatures as disease marker of SLE"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23028528",
"endSection": "abstract",
"offsetInBeginSection": 1213,
"offsetInEndSection": 1363,
"text": "All SLE B cell populations revealed an interferon (IFN) gene signature previously only reported in unseparated SLE peripheral blood mononuclear cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21803750",
"endSection": "abstract",
"offsetInBeginSection": 601,
"offsetInEndSection": 907,
"text": "A five gene type I IFN signature was assessed in these subjects to identify subpopulations showing both activation and concordance of the type I IFN pathway in the peripheral blood and disease-affected tissues of each disease and to correlate activation of this pathway in the WB with clinical measurements"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21803750",
"endSection": "abstract",
"offsetInBeginSection": 1155,
"offsetInEndSection": 1350,
"text": "aseline disease activity measurements correlated with a type I IFN gene signature in the WB of subjects with SLE, PM and SSc, as did various serum autoantibody levels in subjects with SLE and DM."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20538795",
"endSection": "abstract",
"offsetInBeginSection": 451,
"offsetInEndSection": 709,
"text": "Real-time PCR was used to confirm a type I interferon (IFN) gene signature in patients with SLE, and the IFN-regulated proteins PRKRA, IFITM1 and CD69 (P < .0001) were found to be up-regulated in platelets from SLE patients compared with healthy volunteers. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20538795",
"endSection": "abstract",
"offsetInBeginSection": 1156,
"offsetInEndSection": 1257,
"text": "In addition, platelets with type I IFN signature could be a novel marker for vascular disease in SLE."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19479852",
"endSection": "abstract",
"offsetInBeginSection": 274,
"offsetInEndSection": 723,
"text": "During the trial, we also examined whether overexpression of an IFNalpha/beta-inducible gene signature in whole blood could serve as a pharmacodynamic biomarker to evaluate IFNalpha neutralization and investigated downstream effects of neutralizing IFNalpha on BAFF and other key signaling pathways, i.e., granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-10 (IL-10), tumor necrosis factor alpha (TNFalpha), and IL-1beta, in SLE"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19479852",
"endSection": "abstract",
"offsetInBeginSection": 1566,
"offsetInEndSection": 1706,
"text": "IFNalpha/beta-inducible gene signatures in whole blood are effective pharmacodynamic biomarkers to evaluate anti-IFNalpha mAb therapy in SLE"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17849124",
"endSection": "abstract",
"offsetInBeginSection": 202,
"offsetInEndSection": 261,
"text": "SLE is characterized by a type-I interferon gene signature."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17849124",
"endSection": "abstract",
"offsetInBeginSection": 1054,
"offsetInEndSection": 1201,
"text": "These observations provide a link between dysregulation of apoptosis and phagocytosis and the type-I interferon signature observed in SLE patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15511676",
"endSection": "abstract",
"offsetInBeginSection": 399,
"offsetInEndSection": 474,
"text": "Of interest, the IFN gene 'signature' correlates with more severe disease. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31044165",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 215,
"text": "A role for interferon (IFN) in systemic lupus erythematosus (SLE) pathogenesis is inferred from the prominent IFN gene signature (IGS), but the major IFN species and its relationship to disease activity are unknown."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19968664",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 190,
"text": "Interferon (IFN) signature genes have been shown to be expressed highly in peripheral blood of patients with systemic lupus erythematosus (SLE), especially in the presence of active disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30185417",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 214,
"text": "OBJECTIVE: The interferon (IFN) signature is related to disease activity and vascular disease in systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) and represents a promising therapeutic target."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22242767",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 212,
"text": "BACKGROUND: There is increased expression of type I interferon (IFN)-regulated proteins in the blood and target tissues of patients with cutaneous lupus erythematosus (CLE) and systemic lupus erythematosus (SLE)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25861459",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "OBJECTIVES: The interferon (IFN) signature (IS) in patients with systemic lupus erythematosus (SLE) includes over 100 genes induced by type I IFN pathway acti"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31044165",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "A role for interferon (IFN) in systemic lupus erythematosus (SLE) pathogenesis is inferred from the prominent IFN gene signature (IGS), but the major IFN species and its relationship to disease activity are unknown. A bi"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24839407",
"endSection": "abstract",
"offsetInBeginSection": 281,
"offsetInEndSection": 551,
"text": " group, using microarray analysis, identified the interferon (IFN) gene signature in pediatric systemic lupus erythematosus (SLE) and has published data that suggest high doses of intravenous corticosteroid treatment may have benefit over strictly oral regimens. Additio"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24598455",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 190,
"text": "INTRODUCTION: A hallmark of systemic autoimmune diseases like systemic lupus erythematosus (SLE) is the increased expression of interferon (IFN) type I inducible genes, so-called IFN type I "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27094810",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 240,
"text": "Patients with systemic lupus erythematosus (SLE) have an increased expression of type I interferon (IFN)-regulated genes (an IFN signature), which is caused by an ongoing production of type I IFNs by plasmacytoid dendritic cells (pDCs). The"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31890206",
"endSection": "abstract",
"offsetInBeginSection": 271,
"offsetInEndSection": 376,
"text": " This study investigated serum IL-3 and IFN levels, and a whole blood 'IL-3 gene signature', in human SLE"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27723281",
"endSection": "abstract",
"offsetInBeginSection": 1453,
"offsetInEndSection": 1652,
"text": "SION: SLE patients demonstrated increased expression of an IFN response gene signature (75% of patients had an elevated IFN response gene signature) at baseline in ILLUMINATE-1 and ILLUMINATE-2. Subs"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30745462",
"endSection": "abstract",
"offsetInBeginSection": 1417,
"offsetInEndSection": 1572,
"text": "SLE patients exhibit increased IFN signatures in their skin secondary to increased production and a robust, skewed IFN response that is regulated by PITX1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19790071",
"endSection": "abstract",
"offsetInBeginSection": 186,
"offsetInEndSection": 347,
"text": " An earlier study showed that SLE patients carrying an interferon (IFN) gene expression signature in blood have elevated serum levels of IFN-regulated chemokines"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32334613",
"endSection": "abstract",
"offsetInBeginSection": 169,
"offsetInEndSection": 380,
"text": " The role of type I interferon (IFN) in SLE has been demonstrated from the 2000s, by gene expression analyses showing significant over-expression of genes related to type I IFN signalling pathway (IFN signature)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31130331",
"endSection": "abstract",
"offsetInBeginSection": 98,
"offsetInEndSection": 193,
"text": "The type I interferon (IFN) gene signature and circulating autoantibodies are hallmarks of SLE."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18075793",
"endSection": "abstract",
"offsetInBeginSection": 185,
"offsetInEndSection": 387,
"text": "Many SLE patients have increased serum levels of IFN-alpha and display an IFN gene expression \"signature\" characterized by strong overexpression of IFN-responsive genes in leukocytes and target tissues."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32334613",
"endSection": "abstract",
"offsetInBeginSection": 381,
"offsetInEndSection": 504,
"text": " However, several studies questioned the role of measuring the intensity of IFN signature (IFN score) to chase SLE activity"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31044165",
"endSection": "abstract",
"offsetInBeginSection": 216,
"offsetInEndSection": 439,
"text": "A bioinformatic approach employing individual IFN species gene signatures to interrogate SLE microarray datasets demonstrates a putative role for numerous IFN species, with prominent expression of IFNB1 and IFNW signatures."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31660791",
"endSection": "abstract",
"offsetInBeginSection": 1566,
"offsetInEndSection": 1733,
"text": "GS test-high patients overexpressed many gene signatures associated with SLE pathogenesis compared with IFNGS test-low patients, reflecting broad immune activation. Th"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20538795",
"endSection": "abstract",
"offsetInBeginSection": 1189,
"offsetInEndSection": 1257,
"text": "I IFN signature could be a novel marker for vascular disease in SLE."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20538795",
"endSection": "abstract",
"offsetInBeginSection": 451,
"offsetInEndSection": 708,
"text": "Real-time PCR was used to confirm a type I interferon (IFN) gene signature in patients with SLE, and the IFN-regulated proteins PRKRA, IFITM1 and CD69 (P < .0001) were found to be up-regulated in platelets from SLE patients compared with healthy volunteers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24834763",
"endSection": "abstract",
"offsetInBeginSection": 417,
"offsetInEndSection": 533,
"text": "An increased expression of type I IFN-regulated genes, termed IFN signature, has been reported in patients with SLE."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12642603",
"endSection": "abstract",
"offsetInBeginSection": 121,
"offsetInEndSection": 338,
"text": "Using oligonucleotide microarrays, we now show that active SLE can be distinguished by a remarkably homogeneous gene expression pattern with overexpression of granulopoiesis-related and interferon (IFN)-induced genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15593221",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 447,
"text": "OBJECTIVE: To study the contribution of interferon-alpha (IFNalpha) and IFNgamma to the IFN gene expression signature that has been observed in microarray screens of peripheral blood mononuclear cells (PBMCs) from patients with systemic lupus erythematosus (SLE).METHODS: Quantitative real-time polymerase chain reaction analysis of healthy control PBMCs was used to determine the relative induction of a panel of IFN-inducible genes (IFIGs) by IF"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22242767",
"endSection": "abstract",
"offsetInBeginSection": 201,
"offsetInEndSection": 651,
"text": "osus (SLE). Patients with SLE have increased IFN-regulated gene expression pointing towards a possible underlying genetic defect.OBJECTIVES: To determine expression levels of five type I IFN-regulated genes that are highly expressed in SLE in the peripheral blood of patients with CLE and to correlate the expression levels with cutaneous disease activity.METHODS: Peripheral blood was obtained from 10 healthy controls and 30 patients with CLE, incl"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19968664",
"endSection": "abstract",
"offsetInBeginSection": 1019,
"offsetInEndSection": 1124,
"text": "Up-regulation of a set of 63 IFN signature genes was seen in 83% of SLE patients and 50% of ILE patients."
}
] | 11 |
BioASQ-training11b
| null | null |
5fdb42e7a43ad31278000026
|
bioasq_factoid
|
factoid
|
Hairpatches is a single gene mutation associated with what disease?
|
['alopecia and renal failure']
|
[
"alopecia",
"hair loss",
"renal failure",
"kidney failure",
"chronic kidney disease",
"acute kidney injury",
"kidney dysfunction",
"alopecia and renal failure"
] |
['Hairpatches is a single gene mutation associated with progressive renal failure and alopecia in mice, and may be a potential model for a newly described heritable human disorder.', 'Hairpatches is a single gene mutation associated with progressive renal disease and alopecia.', 'Hairpatches is a single gene mutation characterized by progressive renal disease and alopecia in the mouse', 'Hairpatches, a single gene mutation characterized by progressive renal disease and alopecia in the mouse. A potential model for a newly described heritable human disorder.', '"Hairpatches" (Hpt) is a naturally occurring, autosomal semi-dominant mouse mutation. Hpt/Hpt homozygotes die in utero, while Hpt/+ heterozygotes exhibit progressive renal failure accompanied by patchy alopecia.', '"Hairpatches" (Hpt) is a naturally occurring, autosomal semi-dominant mouse mutation. Hairpatches, a single gene mutation characterized by progressive renal disease and alopecia in the mouse.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23301070",
"http://www.ncbi.nlm.nih.gov/pubmed/1836514"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23301070",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 212,
"text": "\"Hairpatches\" (Hpt) is a naturally occurring, autosomal semi-dominant mouse mutation. Hpt/Hpt homozygotes die in utero, while Hpt/+ heterozygotes exhibit progressive renal failure accompanied by patchy alopecia. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1836514",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "Hairpatches, a single gene mutation characterized by progressive renal disease and alopecia in the mouse. A potential model for a newly described heritable human disorder."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23301070",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 167,
"text": "Retrotransposon insertion in the T-cell acute lymphocytic leukemia 1 (Tal1) gene is associated with severe renal disease and patchy alopecia in Hairpatches (Hpt) mice."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1836514",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 105,
"text": "Hairpatches, a single gene mutation characterized by progressive renal disease and alopecia in the mouse."
}
] | 12 |
BioASQ-training12b
| null | null |
64138ce8201352f04a000042
|
bioasq_factoid
|
factoid
|
Which syndrome is caused by dysfunction of the ciliary ARMC9/TOGARAM1 protein?
|
['Joubert syndrome']
|
[
"Joubert syndrome",
"Joubert disease",
"Joubert syndrome with renal involvement",
"Joubert syndrome with ocular involvement",
"Joubert syndrome with ataxia",
"Joubert syndrome with developmental delay"
] |
['Dysfunction of the ciliary ARMC9/TOGARAM1 protein module causes Joubert syndrome.', 'Dysfunction of the ciliary ARMC9/TOGARAM1 protein causes Joubert syndrome.', 'Joubert syndrome (JBTS) is a recessive neurodevelopmental disorder caused by dysfunction of the ciliary ARMC9/TOGARAM1 protein.', 'Dysfunction of the ciliary ARMC9/TOGARAM1 protein module causes Joubert syndrome. All known JBTS genes encode proteins involved in the structure or function of primary cilia, ubiquitous antenna-like organelles essential for cellular signal transduction.', 'Joubert syndrome is a rare autosomal recessive disorder caused by dysfunction of the ciliary ARMC9/TOGARAM1 protein.', 'Dysfunction of the ciliary ARMC9/TOGARAM1 protein module causes Joubert syndrome. Joubert syndrome (JBTS) is a recessive neurodevelopmental ciliopathy characterized by a pathognomonic hindbrain malformation.', 'Joubert syndrome (JBTS) is a rare autosomal recessive disorder caused by dysfunction of the ciliary ARMC9/TOGARAM1 protein.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/32453716",
"http://www.ncbi.nlm.nih.gov/pubmed/29159890"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32453716",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 81,
"text": "Dysfunction of the ciliary ARMC9/TOGARAM1 protein module causes Joubert syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32453716",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1386,
"text": "Joubert syndrome (JBTS) is a recessive neurodevelopmental ciliopathy characterized by a pathognomonic hindbrain malformation. All known JBTS genes encode proteins involved in the structure or function of primary cilia, ubiquitous antenna-like organelles essential for cellular signal transduction. Here, we used the recently identified JBTS-associated protein armadillo repeat motif-containing 9 (ARMC9) in tandem-affinity purification and yeast 2-hybrid screens to identify a ciliary module whose dysfunction underlies JBTS. In addition to the known JBTS-associated proteins CEP104 and CSPP1, we identified coiled-coil domain containing 66 (CCDC66) and TOG array regulator of axonemal microtubules 1 (TOGARAM1) as ARMC9 interaction partners. We found that TOGARAM1 variants cause JBTS and disrupt TOGARAM1 interaction with ARMC9. Using a combination of protein interaction analyses, characterization of patient-derived fibroblasts, and analysis of CRISPR/Cas9-engineered zebrafish and hTERT-RPE1 cells, we demonstrated that dysfunction of ARMC9 or TOGARAM1 resulted in short cilia with decreased axonemal acetylation and polyglutamylation, but relatively intact transition zone function. Aberrant serum-induced ciliary resorption and cold-induced depolymerization in ARMC9 and TOGARAM1 patient cell lines suggest a role for this new JBTS-associated protein module in ciliary stability."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32453716",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "Dysfunction of the ciliary ARMC9/TOGARAM1 protein module causes Joubert syndrome"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29159890",
"endSection": "abstract",
"offsetInBeginSection": 799,
"offsetInEndSection": 977,
"text": "Our report of variant in ARMC9 Leading to Joubert syndrome phenotype (JS30), elucidates the genetic heterogeneity of Joubert syndrome, and expands the gene list for ciliopathies."
}
] | 11 |
BioASQ-training11b
| null | null |
601d2d001cb411341a00002c
|
bioasq_factoid
|
factoid
|
Which company originally developed the drug Afrezza?
|
['MannKind Corporation']
|
[
"MannKind Corporation",
"MannKind",
"MannKind Corp",
"MannKind Inc."
] |
['The inhaled insulin Technosphere, also known as Afrezza is produced by the MannKind Corporation.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/20462282"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20462282",
"endSection": "abstract",
"offsetInBeginSection": 605,
"offsetInEndSection": 882,
"text": "MannKind Corporation has developed a powder formulation of insulin that allows for a high percentage of the administered insulin to be absorbed via the lung. Their product, AFREZZA (Technosphere insulin), is currently under review by the FDA for use in patients with diabetes. "
}
] | 11 |
BioASQ-training11b
| null | null |
5e776a75835f4e477700000d
|
bioasq_factoid
|
yesno
|
Can Rozanolixizumab be used for treatment of multiple sclerosis?
|
['no']
|
[
"no"
] |
['No. Rozanolixizumab is approved for myasthenia gravis.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/37059507",
"http://www.ncbi.nlm.nih.gov/pubmed/37656420",
"http://www.ncbi.nlm.nih.gov/pubmed/34735735",
"http://www.ncbi.nlm.nih.gov/pubmed/37735554",
"http://www.ncbi.nlm.nih.gov/pubmed/37287352",
"http://www.ncbi.nlm.nih.gov/pubmed/37602255",
"http://www.ncbi.nlm.nih.gov/pubmed/37962198",
"http://www.ncbi.nlm.nih.gov/pubmed/37166675"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37059507",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 169,
"text": "Safety and efficacy of rozanolixizumab in patients with generalised myasthenia gravis (MycarinG): a randomised, double-blind, placebo-controlled, adaptive phase 3 study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37059507",
"endSection": "abstract",
"offsetInBeginSection": 3136,
"offsetInEndSection": 3349,
"text": "INTERPRETATION: Rozanolixizumab showed clinically meaningful improvements in patient-reported and investigator-assessed outcomes in patients with generalised myasthenia gravis, for both 7 mg/kg and 10 mg/kg doses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37059507",
"endSection": "abstract",
"offsetInBeginSection": 3508,
"offsetInEndSection": 3623,
"text": "Rozanolixizumab represents a potential additional treatment option for patients with generalised myasthenia gravis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37287352",
"endSection": "abstract",
"offsetInBeginSection": 816,
"offsetInEndSection": 1023,
"text": "Additionally, several international clinical trials (e.g., rituximab, inebilizumab, ocrelizumab, bortezomib, and rozanolixizumab) for AE treatments, including anti-NMDAR encephalitis, have been implemented. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37166675",
"endSection": "abstract",
"offsetInBeginSection": 726,
"offsetInEndSection": 906,
"text": "Post hoc analyses of the MG0002 study, a Phase 2a clinical trial of rozanolixizumab in adults with moderate to severe generalized MG, included correlation and Rasch model analyses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37602255",
"endSection": "abstract",
"offsetInBeginSection": 1192,
"offsetInEndSection": 1379,
"text": "Efgartigimod is already approved for the treatment of generalized MG, rozanolixizumab is under review by health authorities, and phase 3 trials of nipocalimab and batoclimab are underway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37656420",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 728,
"text": "Rozanolixizumab (rozanolixizumab-noli; RYSTIGGO®) is a high affinity humanized immunoglobulin G4 monoclonal antibody directed against human neonatal Fc receptor (FcRn). Administered subcutaneously, it is being developed by UCB Pharma for the treatment of autoimmune diseases and received its first approval on 27 June 2023 in the USA for the treatment of generalized myasthenia gravis (gMG) in adults who are anti-acetylcholine receptor (AChR) or anti-muscle-specific kinase (MuSK) antibody positive. Rozanolixizumab is the first agent to be approved in the USA for both anti-AChR and anti-MuSK antibody-positive gMG. A regulatory assessment of rozanolixizumab for the treatment of gMG is currently underway in the EU and Japan."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37656420",
"endSection": "abstract",
"offsetInBeginSection": 934,
"offsetInEndSection": 1126,
"text": "This article summarizes the milestones in the development of rozanolixizumab leading to this first approval for the treatment of gMG in adults who are anti-AChR or anti-MuSK antibody positive."
}
] | 13 |
BioASQ-training13b
| null | null |
65d1350f1930410b13000038
|
bioasq_yesno
|
factoid
|
What is the most sensitive test for the diagnosis of multiple sclerosis?
|
['Magnetic resonance imaging', 'MRI', 'MR']
|
[
"Magnetic resonance imaging",
"MRI",
"MR",
"Magnetic resonance",
"Nuclear magnetic resonance imaging"
] |
['These results support previous conclusions that MRI is the most sensitive test for detecting white matter asymptomatic lesions, and the most predictive for the diagnosis of CDMS.', 'MRI is the most sensitive tool for the diagnosis of multiple sclerosis (MS). It can detect asymptomatic lesions in the white matter and is the most predictive test for diagnosing clinically definite multiple sclerosis (CDMS). It is also a reliable measure of the current disease activity. The presence of oligoclonal bands in the cerebrospinal fluid (CSF) provides supportive evidence for the diagnosis of MS.', 'MRI is the most sensitive test for detecting white matter asymptomatic lesions, and the most predictive for the diagnosis of CDMS. MRI also is a reliable measure of the extent of the MS process, serial MRI scans detect evidence of disease activity in MS not always disclosed by clinical evaluation. Results indicate that the presence of oligoclonal bands provides sensitive supporting evidence']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/16400831",
"http://www.ncbi.nlm.nih.gov/pubmed/10919200",
"http://www.ncbi.nlm.nih.gov/pubmed/3208208",
"http://www.ncbi.nlm.nih.gov/pubmed/20003089",
"http://www.ncbi.nlm.nih.gov/pubmed/6830166",
"http://www.ncbi.nlm.nih.gov/pubmed/7629529",
"http://www.ncbi.nlm.nih.gov/pubmed/1449838",
"http://www.ncbi.nlm.nih.gov/pubmed/2795066",
"http://www.ncbi.nlm.nih.gov/pubmed/8164014"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8164014",
"endSection": "abstract",
"offsetInBeginSection": 704,
"offsetInEndSection": 843,
"text": "The initial MRI was strongly suggestive of MS in 19 of these (68%), while 27 (96%) had at least one MS-like abnormality in the initial MRI."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8164014",
"endSection": "abstract",
"offsetInBeginSection": 1059,
"offsetInEndSection": 1237,
"text": "These results support previous conclusions that MRI is the most sensitive test for detecting white matter asymptomatic lesions, and the most predictive for the diagnosis of CDMS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1449838",
"endSection": "abstract",
"offsetInBeginSection": 639,
"offsetInEndSection": 863,
"text": "The most sensitive test was MRI (93%) followed by VEP (83%) and BAEP (60%) and the sensitivity of the study with high resolution CT including 59 patients explored by double enhancement and delayed cut off was very low (33%)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3208208",
"endSection": "abstract",
"offsetInBeginSection": 200,
"offsetInEndSection": 305,
"text": " In diagnosis, MRI is the most sensitive test for the demonstration of dissemination of lesions in space."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3208208",
"endSection": "abstract",
"offsetInBeginSection": 508,
"offsetInEndSection": 675,
"text": "MRI also is a reliable measure of the extent of the MS process, serial MRI scans detect evidence of disease activity in MS not always disclosed by clinical evaluation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6830166",
"endSection": "abstract",
"offsetInBeginSection": 1149,
"offsetInEndSection": 1591,
"text": "These results indicate that the presence of oligoclonal bands provides sensitive supporting evidence for the diagnosis of MS but that bands may be present in other disorders, including those not directly related to infection or abnormal immune response. The data suggest that oligoclonal bands may represent an immune response to neurological injury that is prominent in disorders with a particularly intense or continuous antigenic stimulus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2795066",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Magnetic resonance imaging (MRI) has recently been recognised as the most sensitive method with which to detect clinically silent lesions in patients affected by multiple sclerosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20003089",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 196,
"text": "Magnetic resonance imaging (MRI) is a sensitive paraclinical test for diagnosis and assessment of disease progression in multiple sclerosis (MS) and is often used to evaluate therapeutic efficacy."
}
] | 11 |
BioASQ-training11b
| null | null |
6277de0d56bf9aee6f000006
|
bioasq_factoid
|
factoid
|
In what part of the cell would a SNARE Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) be found
|
['membrane', 'nerve terminals', 'synaptic vesicles', 'endoplasmic reticulum (ER)', 'ERGIC', 'Golgi apparatus']
|
[
"membrane",
"cell membrane",
"plasma membrane",
"nerve terminals",
"axon terminals",
"synaptic vesicles",
"vesicles",
"endoplasmic reticulum (ER)",
"rough endoplasmic reticulum",
"smooth endoplasmic reticulum",
"ERGIC",
"ER-Golgi intermediate compartment",
"Golgi apparatus",
"Golgi body",
"Golgi complex"
] |
['SNARE soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) are transmembrane proteins found in the endosomal/lysosomal system.', 'SNAREs are typically found in the membranes of cells where they play a crucial role in the process of membrane fusion.', 'SNAREs, including Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs), are found in the Golgi apparatus and endoplasmic reticulum of the cell.', 'Astrocytes, the most abundant glial cells in the central nervous system (CNS), sense synaptic activity and respond through the release of gliotransmitters, a process mediated by intracellular Ca. In these cells, SNARE Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) are found on vesicles membranes and contribute to the docking and fusion of vesicles with the cell membrane, allowing the release of gliotransmitters to the extracellular space.', 'SNAREs are found in nerve terminals and synaptic vesicles.', 'Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (R-SNAREs) mainly promoted the assembly of the SNARE complex to drive the final membrane fusion step of membrane transport', 'A SNARE Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) would be found in presynaptic terminals and perisynaptic astrocytic processes.', 'Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) can be found in various parts of the cell, including the plasma membrane, endoplasmic reticulum, Golgi apparatus, and synaptic vesicles. They are involved in mediating membrane fusion and play a crucial role in intracellular vesicle trafficking, neurotransmitter release, and other cellular processes.', "SNARE proteins are located in the cell's membranes, including those of synaptic vesicles and the plasma membrane.", 'Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) would be found in secretory vesicles.', 'SNAREs are found in the trans-Golgi network.', 'SNAREs are found in the plasma membrane and vesicles.', '\nSNAREs are transmembrane proteins found in various organelles and vesicles involved in vesicle trafficking and secretion, such as synaptic vesicles, endoplasmic reticulum (ER), Golgi apparatus, and lysosomes. In synapses, SNAREs are located in both presynaptic and postsynaptic membranes.', 'SNAREs are found in the plasma membrane of the cell, where they play a crucial role in membrane fusion and transport.', 'Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) are found in the membrane.', 'The SNARE Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) are found in the cell membrane.', 'SNARE proteins are primarily found in the cytoplasm of cells, where they play a crucial role in membrane fusion and intracellular transport processes.', 'SNAREs are found in the plasma membrane of neuronal presynaptic terminals.', 'SNAREs are found in the cell membrane.', 'Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) would be found in nerve terminals, synaptic vesicles, and in nerve terminals.', 'SNARE proteins are primarily found in nerve terminals, synaptic vesicles, endosomes, and the astrocytic plasma membrane.', 'SNAREs (Soluble N-ethylmaleimide-sensitive factor attachment protein receptors) are specialized proteins, involved in the process of vesicle fusion in a cell. They are typically located in the plasma membrane and vesicle membrane.', 'SNAREs are found in the plasma membrane of cells.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/36750663",
"http://www.ncbi.nlm.nih.gov/pubmed/11427709",
"http://www.ncbi.nlm.nih.gov/pubmed/19617396",
"http://www.ncbi.nlm.nih.gov/pubmed/20589833",
"http://www.ncbi.nlm.nih.gov/pubmed/12517971",
"http://www.ncbi.nlm.nih.gov/pubmed/16536742",
"http://www.ncbi.nlm.nih.gov/pubmed/26359495",
"http://www.ncbi.nlm.nih.gov/pubmed/35972760",
"http://www.ncbi.nlm.nih.gov/pubmed/30194295",
"http://www.ncbi.nlm.nih.gov/pubmed/26101353",
"http://www.ncbi.nlm.nih.gov/pubmed/29696021",
"http://www.ncbi.nlm.nih.gov/pubmed/26339030",
"http://www.ncbi.nlm.nih.gov/pubmed/12773094",
"http://www.ncbi.nlm.nih.gov/pubmed/27301672",
"http://www.ncbi.nlm.nih.gov/pubmed/37027300",
"http://www.ncbi.nlm.nih.gov/pubmed/10908612",
"http://www.ncbi.nlm.nih.gov/pubmed/9382863",
"http://www.ncbi.nlm.nih.gov/pubmed/11001046",
"http://www.ncbi.nlm.nih.gov/pubmed/12805548",
"http://www.ncbi.nlm.nih.gov/pubmed/10557242",
"http://www.ncbi.nlm.nih.gov/pubmed/25501368",
"http://www.ncbi.nlm.nih.gov/pubmed/28203732",
"http://www.ncbi.nlm.nih.gov/pubmed/36608162",
"http://www.ncbi.nlm.nih.gov/pubmed/37465385"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37465385",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 193,
"text": "Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (R-SNAREs) mainly promoted the assembly of the SNARE complex to drive the final membrane fusion step of membrane transport"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36750663",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "The dynamic assembly of the Synaptic-soluble N-ethylmaleimide-sensitive factor Attachment REceptor (SNARE) complex is crucial to understand membrane fusion. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37027300",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "The AAA+ NSF complex is responsible for SNARE complex disassembly both before and after membrane fusion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12517971",
"endSection": "abstract",
"offsetInBeginSection": 3,
"offsetInEndSection": 164,
"text": "have examined the role of the R-soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) synaptobrevin-2/vesicle-associated membrane protein"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11427709",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 261,
"text": "Soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins of the syntaxin, SNAP-25, and VAMP families mediate intracellular membrane fusion through the formation of helical bundles that span opposing membranes. Soluble SNARE domains"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12773094",
"endSection": "abstract",
"offsetInBeginSection": 210,
"offsetInEndSection": 412,
"text": "soluble proteins [N-ethylmaleimide-sensitive fusion protein (NSF) and soluble NSF attachment proteins (SNAPs)] and integral membrane proteins [vesicle and target SNAP receptors (v- and t-SNAREs)]. Three"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10908612",
"endSection": "abstract",
"offsetInBeginSection": 1224,
"offsetInEndSection": 1401,
"text": "These data suggest that Vti1a-beta does not function in exocytosis but in a separate SNARE complex in a membrane fusion step during recycling or biogenesis of synaptic vesicles."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36608162",
"endSection": "abstract",
"offsetInBeginSection": 531,
"offsetInEndSection": 1214,
"text": "Thus, we aimed to investigate the localization and relative concentrations of neuronal SNARE proteins syntaxin-1, synaptosomal nerve-associated protein 25 (SNAP-25), vesicle-associated membrane protein 2 (VAMP-2) (synaptobrevin-2) and calcium sensor synaptotagmin 1 in perisynaptic astrocytic processes compared to nerve terminals and dendrites.METHODS: We used quantitative immunogold electron microscopy of the rat hippocampus to investigate the localization and concentration of neuronal SNARE proteins.RESULTS: As expected, analysis of the immunogold data revealed a lower labeling density of SNARE proteins in the perisynaptic astrocytic processes than in presynaptic terminals."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11001046",
"endSection": "abstract",
"offsetInBeginSection": 172,
"offsetInEndSection": 359,
"text": "The pairing of vesicle v-SNAREs (soluble N-ethylmaleimide-sensitive factor attachment protein receptors) with target membrane t-SNAREs has a central role in intracellular membrane fusion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10908612",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Specific soluble N-ethylmaleimide-sensitive factor attachment protein (SNAP) receptor (SNARE) proteins are required for different membrane transport steps."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25501368",
"endSection": "abstract",
"offsetInBeginSection": 113,
"offsetInEndSection": 333,
"text": "This process is mediated by the formation of functional soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complexes between the plasma membrane t-SNARE complex and the vesicle v-SNARE or VAMP."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20589833",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 189,
"text": "Syntaxin 16 (Syx16) is member of the soluble N-ethylmaleimide sensitive factor attachment protein receptor (SNARE) family of molecules that functions in membrane fusion in eukaryotic cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19617396",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 195,
"text": "The specificity of vesicle-mediated transport is largely regulated by the membrane-specific distribution of SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) proteins."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16536742",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 273,
"text": "SNARE proteins (soluble N-ethylmaleimide-sensitive factor attachment protein receptors) mediate membrane interactions and are conventionally divided into Q-SNAREs and R-SNAREs according to the possession of a glutamine or arginine residue at the core of their SNARE domain."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10557242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 325,
"text": "Protein cargo is trafficked between the organelles of the endomembrane system inside transport vesicles, a process mediated by integral membrane proteins called SNAREs (soluble N-ethylmaleimide sensitive factor attachment protein receptors) that reside on the surface of the vesicle (v-SNAREs) and target membrane (t-SNAREs)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26359495",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 404,
"text": "SNAREs constitute the core machinery of intracellular membrane fusion, but vesicular SNAREs localize to specific compartments via largely unknown mechanisms. Here, we identified an interaction between VAMP7 and SNAP-47 using a proteomics approach. We found that SNAP-47 mainly localized to cytoplasm, the endoplasmic reticulum (ER), and ERGIC and could also shuttle between the cytoplasm and the nucleus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9382863",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 995,
"text": "Yeast Bet1p participates in vesicular transport from the endoplasmic reticulum to the Golgi apparatus and functions as a soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) associated with ER-derived vesicles. A mammalian protein (rbet1) homologous to Bet1p was recently identified, and it was concluded that rbet1 is associated with the Golgi apparatus based on the subcellular localization of transiently expressed epitope-tagged rbet1. In the present study using rabbit antibodies raised against the cytoplasmic domain of rbet1, we found that the majority of rbet1 is not associated with the Golgi apparatus as marked by the Golgi mannosidase II in normal rat kidney cells. Rather, rbet1 is predominantly associated with vesicular spotty structures that concentrate in the peri-Golgi region but are also present throughout the cytoplasm. These structures colocalize with the KDEL receptor and ERGIC-53, which are known to be enriched in the intermediate compartment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805548",
"endSection": "abstract",
"offsetInBeginSection": 269,
"offsetInEndSection": 459,
"text": "Here, cells expressing the interacting domains of v- and t-SNAREs on the cell surface were found to fuse spontaneously, demonstrating that SNAREs are sufficient to fuse biological membranes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30194295",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 190,
"text": "Neuronal soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) catalyze synaptic vesicle fusion with presynaptic membranes through the formation of SNARE complexes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26101353",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 203,
"text": "Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) that reside in the target membranes and transport vesicles assemble into specific SNARE complexes to drive membrane fusion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35972760",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 196,
"text": "Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) are membrane-associated trafficking proteins that confer identity to lipid membranes and facilitate membrane fusion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28203732",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 201,
"text": "Formation of complexes between soluble N-ethylmaleimide-sensitive-factor attachment protein receptor (SNARE) proteins on opposing membranes is the minimal requirement for intracellular membrane fusion."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28203732",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 145,
"text": "Redistribution of soluble N-ethylmaleimide-sensitive-factor attachment protein receptors in mouse sperm membranes prior to the acrosome reaction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20589833",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 362,
"text": "Syntaxin 16 (Syx16) is member of the soluble N-ethylmaleimide sensitive factor attachment protein receptor (SNARE) family of molecules that functions in membrane fusion in eukaryotic cells. A rather ubiquitously expressed, tail-anchored membrane protein localized mainly at the trans-Golgi network (TGN), it mediates primarily retrograde endosomal-TGN transport."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27301672",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "Intracellular membrane fusion is mediated in most cases by membrane-bridging complexes of soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs)."
}
] | 13 |
BioASQ-training13b
| null | null |
66088d66fdcbea915f00000c
|
bioasq_factoid
|
factoid
|
Which technique led to the elucidation of the role of HOXD10 in regulating lymphatic endothelial responses to VEGF-C?
|
['DeepCAGE']
|
[
"DeepCAGE",
"Deep CAGE",
"Deep CAGE sequencing",
"DeepCAGE sequencing"
] |
['DeepCAGE transcriptomics identify HOXD10 as a transcription factor regulating lymphatic endothelial responses to VEGF-C.', 'DeepCAGE transcriptomics identify HOXD10 as a transcription factor regulating lymphatic endothelial responses to VEGF-C', 'DeepCAGE transcriptomics identify HOXD10 as a transcription factor regulating lymphatic endothelial responses to VEGF-C. ']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27199372"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27199372",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "DeepCAGE transcriptomics identify HOXD10 as a transcription factor regulating lymphatic endothelial responses to VEGF-C"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27199372",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "DeepCAGE transcriptomics identify HOXD10 as a transcription factor regulating lymphatic endothelial responses to VEGF-C."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27199372",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 121,
"text": "DeepCAGE transcriptomics identify HOXD10 as a transcription factor regulating lymphatic endothelial responses to VEGF-C."
}
] | 6 |
BioASQ-training6b
|
[
"http://www.uniprot.org/uniprot/VEGFC_MOUSE",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D040262",
"http://www.uniprot.org/uniprot/HXD10_SAGLB",
"http://www.uniprot.org/uniprot/HXD10_HUMAN",
"http://www.uniprot.org/uniprot/HXD10_HETFR",
"http://www.uniprot.org/uniprot/HXD10_LAGLA",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D004729",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D042582",
"http://www.uniprot.org/uniprot/VEGFC_RAT",
"http://www.biosemantics.org/jochem#4263666",
"http://www.uniprot.org/uniprot/VEGFC_HUMAN",
"http://www.uniprot.org/uniprot/HXD10_CHICK",
"http://www.uniprot.org/uniprot/HXD10_PANTR",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D042442",
"http://amigo.geneontology.org/amigo/term/GO:0036328"
] |
[
{
"o": "HOXD10",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C1415684"
},
{
"o": "HOXD10",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/#_5032383335380014"
}
] |
5881f627713cbdfd3d000005
|
bioasq_factoid
|
factoid
|
Which genetic alteration is most commonly associated with the classical subtype of glioblastoma?
|
['Epidermal growth factor receptor (EGFR) amplification', 'EGFR amplification', 'EGFR gene amplification', 'Amplification of the epidermal growth factor receptor (EGFR)', 'EGFR overexpression', 'high EGFR expression']
|
[
"Epidermal growth factor receptor (EGFR) amplification",
"EGFR amplification",
"EGFR gene amplification",
"Amplification of the epidermal growth factor receptor (EGFR)",
"EGFR overexpression",
"high EGFR expression",
"EGFR",
"epidermal growth factor receptor",
"ErbB-1",
"HER1"
] |
['The classical subtype of glioblastoma is most commonly associated with epidermal growth factor receptor (EGFR) gene amplification, occurring in 40-60% of cases. Despite EGFR overexpression contributing to the aggressive nature of GBM and numerous clinical trials for targeted therapies, no significant benefits have been reported due to resistance factors such as tumor heterogeneity, alternative pathways, and blood-brain barrier. Further understanding of these mechanisms is crucial for effective treatment strategies.', 'Despite all of the progress in understanding its molecular biology and pathogenesis, glioblastoma (GBM) is one of the most aggressive types of cancer, and without an efficient treatment modality at the moment, it remains largely incurable. Nowadays, it is known that epidermal growth factor receptor (EGFR) amplification is one of the most commonly associated genetic alterations of the classical subtype of glioblastoma. However, targeted therapies against this type of receptor have not yet shown a clear clinical benefit.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/37446288",
"http://www.ncbi.nlm.nih.gov/pubmed/22539962",
"http://www.ncbi.nlm.nih.gov/pubmed/24410805",
"http://www.ncbi.nlm.nih.gov/pubmed/26757882",
"http://www.ncbi.nlm.nih.gov/pubmed/34608482",
"http://www.ncbi.nlm.nih.gov/pubmed/33053208",
"http://www.ncbi.nlm.nih.gov/pubmed/24457079",
"http://www.ncbi.nlm.nih.gov/pubmed/30680510",
"http://www.ncbi.nlm.nih.gov/pubmed/20129251",
"http://www.ncbi.nlm.nih.gov/pubmed/32998960",
"http://www.ncbi.nlm.nih.gov/pubmed/33435537",
"http://www.ncbi.nlm.nih.gov/pubmed/31733287"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37446288",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 598,
"text": "Despite all of the progress in understanding its molecular biology and pathogenesis, glioblastoma (GBM) is one of the most aggressive types of cancers, and without an efficient treatment modality at the moment, it remains largely incurable. Nowadays, one of the most frequently studied molecules with important implications in the pathogenesis of the classical subtype of GBM is the epidermal growth factor receptor (EGFR). Although many clinical trials aiming to study EGFR targeted therapies have been performed, none of them have reported promising clinical results when used in glioma patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33435537",
"endSection": "abstract",
"offsetInBeginSection": 463,
"offsetInEndSection": 692,
"text": "It is known that epidermal growth factor receptor (EGFR) amplification is a characteristic of the classical subtype of glioma. However, targeted therapies against this type of receptor have not yet shown a clear clinical benefit."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31733287",
"endSection": "abstract",
"offsetInBeginSection": 370,
"offsetInEndSection": 836,
"text": "We tested this assumption by a multilevel analysis ranging from a detailed histopathological analysis to a genome-wide expression profiling by microarray and RNA-seq on gliomas induced by two distinct molecular alterations: the overstimulation of the PDGF- and the EGF- pathways. These alterations are landmarks of proneural and classical glioblastoma subtypes respectively. However, our results consistently showed a strong similarity between the two glioma models."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30680510",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 118,
"text": "EGFR amplification and classical subtype are associated with a poor response to bevacizumab in recurrent glioblastoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33053208",
"endSection": "abstract",
"offsetInBeginSection": 587,
"offsetInEndSection": 713,
"text": "FHL1 is highly expressed and positively correlated with EGFR levels in human GBM, particularly those of the classical subtype."
}
] | 13 |
BioASQ-training13b
| null | null |
663016bb187cba990d000023
|
bioasq_factoid
|
factoid
|
Which gene is the paralog of yeast UPC2?
|
['Ecm22']
|
[
"Ecm22",
"Ecm22p",
"Ecm22 protein",
"Ecm22 (S. cerevisiae)"
] |
['the related transcription factors Ecm22 and Upc2 play a crucial role in Saccharomyces cerevisiae filamentation.', 'Here, we examine the role of the related transcription factors Ecm22 and Upc2 in Saccharomyces cerevisiae filamentation. The zinc cluster proteins Upc2 and Ecm22 promote filamentation in Saccharomyces cerevisiae by sterol biosynthesis-dependent and -independent pathways. ', 'zinc cluster proteins Upc2 and Ecm22 promote filamentation', 'The zinc cluster proteins Upc2 and Ecm22 promote filamentation in Saccharomyces cerevisiae by sterol biosynthesis-dependent and -independent pathways.Here, we examine the role of the related transcription factors ecm22 and upc2 in saccharomyces cerevisiae by sterol biosynthesis-dependent and -independent pathways.Here, we examine the role of the related transcription factors ecm22 and upc2 in saccharomyces cerevisiae filamentation.', 'The zinc cluster proteins Upc2 and Ecm22 promote filamentation in Saccharomyces cerevisiae by sterol biosynthesis-dependent and -independent pathways. Here, we examine the role of the related transcription factors Ecm22 and Upc2 in Saccharomyces cerevisiae filamentation. ', 'The zinc cluster proteins Upc2 and Ecm22 promote filamentation in Saccharomyces cerevisiae by sterol biosynthesis-dependent and -independent pathways. Here, we examine the role of the related transcription factors Ecm22 and Upc2 in Saccharomyces cerevisiae filamentation.', 'Here, we examine the role of the related transcription factors Ecm22 and Upc2 in Saccharomyces cerevisiae filamentation. The zinc cluster proteins Upc2 and Ecm22 promote filamentation in Saccharomyces cerevisiae by sterol biosynthesis-dependent and -independent pathways.', 'Here, we examine the role of the related transcription factors Ecm22 and Upc2 in Saccharomyces cerevisiae filamentation.The zinc cluster proteins Upc2 and Ecm22 promote filamentation in Saccharomyces cerevisiae by sterol biosynthesis-dependent and -independent pathways.', 'Here, we examine the role of the related transcription factors Ecm22 and Upc2 in Saccharomyces cerevisiae filamentation.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21980509",
"http://www.ncbi.nlm.nih.gov/pubmed/28986257",
"http://www.ncbi.nlm.nih.gov/pubmed/24453983",
"http://www.ncbi.nlm.nih.gov/pubmed/10073572",
"http://www.ncbi.nlm.nih.gov/pubmed/18487346",
"http://www.ncbi.nlm.nih.gov/pubmed/1885560",
"http://www.ncbi.nlm.nih.gov/pubmed/11208779",
"http://www.ncbi.nlm.nih.gov/pubmed/24163365",
"http://www.ncbi.nlm.nih.gov/pubmed/23385756",
"http://www.ncbi.nlm.nih.gov/pubmed/26448198",
"http://www.ncbi.nlm.nih.gov/pubmed/28379181"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26448198",
"endSection": "abstract",
"offsetInBeginSection": 185,
"offsetInEndSection": 305,
"text": "Here, we examine the role of the related transcription factors Ecm22 and Upc2 in Saccharomyces cerevisiae filamentation."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26448198",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "The zinc cluster proteins Upc2 and Ecm22 promote filamentation in Saccharomyces cerevisiae by sterol biosynthesis-dependent and -independent pathways."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23385756",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "Upc2, a zinc-cluster transcription factor, is a regulator of ergosterol biosynthesis in yeast."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28379181",
"endSection": "abstract",
"offsetInBeginSection": 114,
"offsetInEndSection": 275,
"text": "The zinc cluster proteins Ecm22, Upc2, Sut1 and Sut2 have initially been identified as regulators of sterol import in the budding yeast Saccharomyces cerevisiae."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24163365",
"endSection": "abstract",
"offsetInBeginSection": 166,
"offsetInEndSection": 386,
"text": "Yeast studies defined a 7-bp consensus sterol-response element (SRE) common to genes involved in sterol biosynthesis and two transcription factors, Upc2 and Ecm22, which direct transcription of sterol biosynthetic genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26448198",
"endSection": "abstract",
"offsetInBeginSection": 456,
"offsetInEndSection": 555,
"text": "Ecm22 and Upc2 positively control the expression of FHN1, NPR1, PRR2 and sterol biosynthesis genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24453983",
"endSection": "abstract",
"offsetInBeginSection": 1003,
"offsetInEndSection": 1127,
"text": "RNA-seq analysis shows that hypoxic regulation of sterol synthesis genes in Y. lipolytica is predominantly mediated by Upc2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24453983",
"endSection": "abstract",
"offsetInBeginSection": 221,
"offsetInEndSection": 404,
"text": "However, in yeasts such as Saccharomyces cerevisiae and Candida albicans sterol synthesis is instead regulated by Upc2, an unrelated transcription factor with a Gal4-type zinc finger."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24163365",
"endSection": "abstract",
"offsetInBeginSection": 1085,
"offsetInEndSection": 1220,
"text": "Recombinant endogenous promoter studies show that the UPC2 anaerobic AR1b elements act in trans to regulate ergosterol gene expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1885560",
"endSection": "abstract",
"offsetInBeginSection": 1215,
"offsetInEndSection": 1293,
"text": "One such factor could be the mammalian equivalent of the gene product of UPC2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28986257",
"endSection": "abstract",
"offsetInBeginSection": 892,
"offsetInEndSection": 1162,
"text": "Simultaneous deletion of ECM22 and UPC2 as well as mutation of the three Ste12-binding sites in the PRM1 promoter completely abolishes basal and pheromone-induced PRM1 expression, indicating that Ste12 and Ecm22/Upc2 control PRM1 transcription through distinct pathways."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28986257",
"endSection": "abstract",
"offsetInBeginSection": 296,
"offsetInEndSection": 365,
"text": "Ecm22 and Upc2 positively regulate basal expression of PRM1 and PRM4."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24163365",
"endSection": "abstract",
"offsetInBeginSection": 1221,
"offsetInEndSection": 1340,
"text": "Our results indicate that Upc2 must occupy UPC2 AR1b elements in order for ERG gene expression induction to take place."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10073572",
"endSection": "abstract",
"offsetInBeginSection": 153,
"offsetInEndSection": 284,
"text": "A yeast mutant (upc2-1) with a defect in the aerobic exclusion of sterols was found to have increased sensitivity to LiCl and NaCl."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24163365",
"endSection": "abstract",
"offsetInBeginSection": 761,
"offsetInEndSection": 898,
"text": "The AR1b elements are absolutely required for auto-induction of UPC2 gene expression and protein and require Upc2 and Ecm22 for function."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1885560",
"endSection": "abstract",
"offsetInBeginSection": 87,
"offsetInEndSection": 265,
"text": "Secretion of apoE was achieved only by the use of a mutant (upc2) strain of yeast with the phenotype of enhanced uptake and intracellular esterification of exogenous cholesterol."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11208779",
"endSection": "abstract",
"offsetInBeginSection": 1364,
"offsetInEndSection": 1560,
"text": "Gas chromatographic analysis of the nonsaponifiable fractions of the various strains showed that the major sterol for all YLR228c and UPC2 combinations was ergosterol, the consensus yeast sterol.."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18487346",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 224,
"text": "In the pathogenic yeast Candida albicans, the zinc cluster transcription factor Upc2p has been shown to regulate the expression of ERG11 and other genes involved in ergosterol biosynthesis upon exposure to azole antifungals."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18487346",
"endSection": "abstract",
"offsetInBeginSection": 1314,
"offsetInEndSection": 1509,
"text": "By comparing the gene expression profiles of the fluconazole-resistant isolate and of strains carrying wild-type and mutated UPC2 alleles, we identified target genes that are controlled by Upc2p."
}
] | 11 |
BioASQ-training11b
| null | null |
590c74d170f9fc6f0f00001e
|
bioasq_factoid
|
factoid
|
What is targeted by monoclonal antibody Pembrolizumab?
|
[['programmed cell death 1']]
|
[
"programmed cell death 1",
"PD-1",
"CD279",
"PDCD1",
"programmed cell death protein 1"
] |
['Pembrolizumab inhibits the programmed cell death 1 (PD-1) immune checkpoint and has antitumor activity in patients with advanced melanoma. Pembrolizumab is approved by the US Food and Drug Administration for the treatment of advanced melanoma, and additional regulatory approvals are expected across the oncologic spectrum for a variety of other agents that target these pathways.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24685885",
"http://www.ncbi.nlm.nih.gov/pubmed/25605845",
"http://www.ncbi.nlm.nih.gov/pubmed/25891173",
"http://www.ncbi.nlm.nih.gov/pubmed/26028255",
"http://www.ncbi.nlm.nih.gov/pubmed/25828465",
"http://www.ncbi.nlm.nih.gov/pubmed/25324906",
"http://www.ncbi.nlm.nih.gov/pubmed/25960664",
"http://www.ncbi.nlm.nih.gov/pubmed/25034862"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24685885",
"endSection": "abstract",
"offsetInBeginSection": 343,
"offsetInEndSection": 742,
"text": "gents currently in active clinical development for lung cancer include ipilimumab, which modulates the cytotoxic T-lymphocyte-associated antigen 4 pathway, and multiple agents targeting the programmed death protein 1 (PD-1) pathway, both anti-PD-1 compounds (nivolumab, pembrolizumab [MK-3475]) and those that target programmed death ligand 1 (PD-L1), a key ligand for PD-1 (BMS-936559, MPDL3280A). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25605845",
"endSection": "abstract",
"offsetInBeginSection": 230,
"offsetInEndSection": 503,
"text": "Ipilimumab (CTLA-4) and pembrolizumab (PD-1) are approved by the US Food and Drug Administration for the treatment of advanced melanoma, and additional regulatory approvals are expected across the oncologic spectrum for a variety of other agents that target these pathways."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25891173",
"endSection": "abstract",
"offsetInBeginSection": 126,
"offsetInEndSection": 264,
"text": "Pembrolizumab inhibits the programmed cell death 1 (PD-1) immune checkpoint and has antitumor activity in patients with advanced melanoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25891173",
"endSection": "abstract",
"offsetInBeginSection": 1740,
"offsetInEndSection": 1936,
"text": "CONCLUSIONS: The anti-PD-1 antibody pembrolizumab prolonged progression-free survival and overall survival and had less high-grade toxicity than did ipilimumab in patients with advanced melanoma. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26028255",
"endSection": "abstract",
"offsetInBeginSection": 241,
"offsetInEndSection": 483,
"text": "METHODS: We conducted a phase 2 study to evaluate the clinical activity of pembrolizumab, an anti-programmed death 1 immune checkpoint inhibitor, in 41 patients with progressive metastatic carcinoma with or without mismatch-repair deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26028255",
"endSection": "abstract",
"offsetInBeginSection": 2170,
"offsetInEndSection": 2306,
"text": "CONCLUSIONS: This study showed that mismatch-repair status predicted clinical benefit of immune checkpoint blockade with pembrolizumab. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25828465",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 183,
"text": "The anti programmed cell death-1 (PD-1) antibodies pembrolizumab and nivolumab have been recently licensed by the Food and Drug Administration for the treatment of advanced melanoma. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25828465",
"endSection": "abstract",
"offsetInBeginSection": 407,
"offsetInEndSection": 564,
"text": "We describe for the first time the case of an adult patient who developed autoimmune diabetes likely as a consequence of PD-1 inhibition with pembrolizumab. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25324906",
"endSection": "abstract",
"offsetInBeginSection": 999,
"offsetInEndSection": 1219,
"text": "Ipilimumab, an anti-cytotoxic T-lymphocyte antigen 4 antibody and pembrolizumab, a monoclonal antibody targeting programmed death 1 receptor may be a feasible treatment option in patients with metastatic mucosal melanoma"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25960664",
"endSection": "abstract",
"offsetInBeginSection": 507,
"offsetInEndSection": 692,
"text": "Pembrolizumab, a humanized highly selective IgG4 anti-PD-1 monoclonal antibody, was recently approved for the treatment of advanced melanoma based on promising early-phase clinical data"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25034862",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "Anti-programmed-death-receptor-1 treatment with pembrolizumab in ipilimumab-refractory advanced melanoma: a randomised dose-comparison cohort of a phase 1 trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25891173",
"endSection": "abstract",
"offsetInBeginSection": 1525,
"offsetInEndSection": 1936,
"text": "Efficacy was similar in the two pembrolizumab groups. Rates of treatment-related adverse events of grade 3 to 5 severity were lower in the pembrolizumab groups (13.3% and 10.1%) than in the ipilimumab group (19.9%).CONCLUSIONS: The anti-PD-1 antibody pembrolizumab prolonged progression-free survival and overall survival and had less high-grade toxicity than did ipilimumab in patients with advanced melanoma. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25034862",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 777,
"text": "BACKGROUND: The anti-programmed-death-receptor-1 (PD-1) antibody pembrolizumab has shown potent antitumour activity at different doses and schedules in patients with melanoma. We compared the efficacy and safety of pembrolizumab at doses of 2 mg/kg and 10 mg/kg every 3 weeks in patients with ipilimumab-refractory advanced melanoma.METHODS: In an open-label, international, multicentre expansion cohort of a phase 1 trial, patients (aged ?18 years) with advanced melanoma whose disease had progressed after at least two ipilimumab doses were randomly assigned with a computer-generated allocation schedule (1:1 final ratio) to intravenous pembrolizumab at 2 mg/kg every 3 weeks or 10 mg/kg every 3 weeks until disease progression, intolerable toxicity, or consent withdrawal. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25324906",
"endSection": "abstract",
"offsetInBeginSection": 902,
"offsetInEndSection": 1221,
"text": "Vemurafenib and dabrafenib are targeted agents for patients with BRAF mutation-positive melanoma. Ipilimumab, an anti-cytotoxic T-lymphocyte antigen 4 antibody and pembrolizumab, a monoclonal antibody targeting programmed death 1 receptor may be a feasible treatment option in patients with metastatic mucosal melanoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25324906",
"endSection": "abstract",
"offsetInBeginSection": 902,
"offsetInEndSection": 1221,
"text": "Vemurafenib and dabrafenib are targeted agents for patients with BRAF mutation-positive melanoma. Ipilimumab, an anti-cytotoxic T-lymphocyte antigen 4 antibody and pembrolizumab, a monoclonal antibody targeting programmed death 1 receptor may be a feasible treatment option in patients with metastatic mucosal melanoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25960664",
"endSection": "abstract",
"offsetInBeginSection": 508,
"offsetInEndSection": 840,
"text": "Pembrolizumab, a humanized highly selective IgG4 anti-PD-1 monoclonal antibody, was recently approved for the treatment of advanced melanoma based on promising early-phase clinical data. Encouraging results have also been seen in other malignancies, and PD-1-targeted therapies are likely to markedly change the treatment landscape."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25324906",
"endSection": "abstract",
"offsetInBeginSection": 902,
"offsetInEndSection": 1221,
"text": "Vemurafenib and dabrafenib are targeted agents for patients with BRAF mutation-positive melanoma. Ipilimumab, an anti-cytotoxic T-lymphocyte antigen 4 antibody and pembrolizumab, a monoclonal antibody targeting programmed death 1 receptor may be a feasible treatment option in patients with metastatic mucosal melanoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25960664",
"endSection": "abstract",
"offsetInBeginSection": 508,
"offsetInEndSection": 840,
"text": "Pembrolizumab, a humanized highly selective IgG4 anti-PD-1 monoclonal antibody, was recently approved for the treatment of advanced melanoma based on promising early-phase clinical data. Encouraging results have also been seen in other malignancies, and PD-1-targeted therapies are likely to markedly change the treatment landscape."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25324906",
"endSection": "abstract",
"offsetInBeginSection": 902,
"offsetInEndSection": 1221,
"text": "Vemurafenib and dabrafenib are targeted agents for patients with BRAF mutation-positive melanoma. Ipilimumab, an anti-cytotoxic T-lymphocyte antigen 4 antibody and pembrolizumab, a monoclonal antibody targeting programmed death 1 receptor may be a feasible treatment option in patients with metastatic mucosal melanoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25960664",
"endSection": "abstract",
"offsetInBeginSection": 508,
"offsetInEndSection": 840,
"text": "Pembrolizumab, a humanized highly selective IgG4 anti-PD-1 monoclonal antibody, was recently approved for the treatment of advanced melanoma based on promising early-phase clinical data. Encouraging results have also been seen in other malignancies, and PD-1-targeted therapies are likely to markedly change the treatment landscape."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25324906",
"endSection": "abstract",
"offsetInBeginSection": 902,
"offsetInEndSection": 1221,
"text": "Vemurafenib and dabrafenib are targeted agents for patients with BRAF mutation-positive melanoma. Ipilimumab, an anti-cytotoxic T-lymphocyte antigen 4 antibody and pembrolizumab, a monoclonal antibody targeting programmed death 1 receptor may be a feasible treatment option in patients with metastatic mucosal melanoma."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D000911"
] |
[] |
56c1f01aef6e394741000043
|
bioasq_factoid
|
factoid
|
What is the role of IL-18BP?
|
['IL-18 binding protein (IL-18BP) is a natural inhibitor of IL-18. The balance between IL-18 and IL-18BP has an important role in the inflammatory setting.']
|
[
"IL-18 binding protein",
"IL-18BP",
"Interleukin-18 binding protein",
"Interleukin-18BP",
"IL-18 binding protein (IL-18BP)"
] |
['IL-18 binding protein (IL-18BP) is a natural inhibitor of IL-18. The balance between IL-18 and IL-18BP has an important role in the inflammatory setting.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26782741",
"http://www.ncbi.nlm.nih.gov/pubmed/26898120",
"http://www.ncbi.nlm.nih.gov/pubmed/27914933",
"http://www.ncbi.nlm.nih.gov/pubmed/25548255",
"http://www.ncbi.nlm.nih.gov/pubmed/25807634",
"http://www.ncbi.nlm.nih.gov/pubmed/25692120",
"http://www.ncbi.nlm.nih.gov/pubmed/25182570",
"http://www.ncbi.nlm.nih.gov/pubmed/26850179"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26850179",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 79,
"text": "Interleukin 18--binding protein ameliorates liver ischemia--reperfusion injury."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26850179",
"endSection": "abstract",
"offsetInBeginSection": 1549,
"offsetInEndSection": 1719,
"text": " IL-18BP exhibited anti-inflammatory, antioxidant, and protective effects in I/R-mediated hepatic injury via regulating some liver enzyme activities and cytokine levels. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26898120",
"endSection": "abstract",
"offsetInBeginSection": 308,
"offsetInEndSection": 1012,
"text": "Because of IL-18's potential pro-inflammatory and tissue destructive effects, its biological activities are tightly controlled in the body by its naturally occurring antagonist called IL-18BP. The antagonist is produced in the body both constitutively and in response to an increased production of IL-18 as a negative feedback mechanism. Under physiological conditions, most of IL-18 in the circulation is bound with IL-18BP and is inactive. However, an imbalance in the production of IL-18 and its antagonist (an increase in the production of IL-18 with a decrease, no increase or an insufficient increase in the production of IL-18BP) has been described in many chronic inflammatory diseases in humans."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25182570",
"endSection": "abstract",
"offsetInBeginSection": 377,
"offsetInEndSection": 441,
"text": "L-18 binding protein (IL-18BP) is a natural inhibitor of IL-18. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27914933",
"endSection": "abstract",
"offsetInBeginSection": 681,
"offsetInEndSection": 761,
"text": "Platelets also contain the IL-18 antagonist, the IL-18-Binding Protein (IL-18BP)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25548255",
"endSection": "abstract",
"offsetInBeginSection": 614,
"offsetInEndSection": 762,
"text": "The natural inhibitor IL-18BP , whose production is enhanced by IFN-γ and IL-27, further regulates IL-18 activity in the extracellular environment. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25807634",
"endSection": "abstract",
"offsetInBeginSection": 147,
"offsetInEndSection": 224,
"text": "IL-18 binding protein (IL-18BP) is a naturally occurring inhibitor of IL-18. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25692120",
"endSection": "abstract",
"offsetInBeginSection": 221,
"offsetInEndSection": 374,
"text": "IL-18 binding protein (IL-18BP) is a natural inhibitor of IL-18. The balance between IL-18 and IL-18BP has an important role in the inflammatory setting."
}
] | 6 |
BioASQ-training6b
| null | null |
58cd90c202b8c60953000040
|
bioasq_factoid
|
factoid
|
Which resource contains accurate enhancer predictions in the developing limb?
|
['Limb-Enhancer Genie (LEG)']
|
[
"Limb-Enhancer Genie (LEG)",
"LEG",
"Limb Enhancer Genie"
] |
['Limb-Enhancer Genie (LEG) is a collection of highly accurate, genome-wide predictions of enhancers in the developing limb, available through a user-friendly online interface. Limb enhancers are predicted using a combination of >50 published limb-specific datasets and clusters of evolutionarily conserved transcription factor binding sites, taking advantage of the patterns observed at previously in vivo validated elements.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28827824"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28827824",
"endSection": "abstract",
"offsetInBeginSection": 415,
"offsetInEndSection": 853,
"text": "Here we present the Limb-Enhancer Genie (LEG), a collection of highly accurate, genome-wide predictions of enhancers in the developing limb, available through a user-friendly online interface. We predict limb enhancers using a combination of>50 published limb-specific datasets and clusters of evolutionarily conserved transcription factor binding sites, taking advantage of the patterns observed at previously in vivo validated elements."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28827824",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "Limb-Enhancer Genie: An accessible resource of accurate enhancer predictions in the developing limb."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28827824",
"endSection": "abstract",
"offsetInBeginSection": 415,
"offsetInEndSection": 607,
"text": "Here we present the Limb-Enhancer Genie (LEG), a collection of highly accurate, genome-wide predictions of enhancers in the developing limb, available through a user-friendly online interface."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28827824",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "Limb-Enhancer Genie: An accessible resource of accurate enhancer predictions in the developing limb."
}
] | 11 |
BioASQ-training11b
|
[
"https://meshb.nlm.nih.gov/record/ui?ui=D004742",
"http://amigo.geneontology.org/amigo/term/GO:0060173",
"http://amigo.geneontology.org/amigo/term/GO:0060174"
] | null |
5a6d1733b750ff4455000030
|
bioasq_factoid
|
factoid
|
What is the alternative name of RTA 408?
|
['Omaveloxolone']
|
[
"Omaveloxolone",
"RTA 408",
"Omav",
"Omaveloxolone (RTA 408)"
] |
['RTA 408 is also known as omaveloxolone.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34573098"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34573098",
"endSection": "abstract",
"offsetInBeginSection": 690,
"offsetInEndSection": 854,
"text": "Omaveloxolone (RTA 408) is an activator of Nrf2 and an inhibitor of NFκB, possessing antioxidative and anti-inflammatory activities in mitochondrial bioenergetics. "
}
] | 12 |
BioASQ-training12b
| null | null |
644008a657b1c7a31500003f
|
bioasq_factoid
|
yesno
|
Can therapeutic levels of Vedolizumab be found in the breast milk of nursing mothers following treatment for Inflammatory bowel disease?
|
['no']
|
[
"no"
] |
['vedolizumab can be detected in the breast milk of nursing mothers. although more data are imperative, the concentrations of vedolizumab in breast milk are minute and are therefore unlikely to result in systemic or gastro-intestinal immune-suppression of the infant.', 'Vedolizumab is barely detectable in the breast milk of nursing mothers. measurements in breast milk after an infusion of the drug showed that levels did not surpass 480 ng/ml, which was roughly 1/100 of the comparable serum levels.', 'Vedolizumab can be detected in the breast milk of nursing mothers .\nAlthough more data are imperative , the concentrations of vedolizumab in breast milk are minute and are therefore unlikely to result in systemic or gastro-intestinal immune-suppression of the infant .', 'Vedolizumab can be detected in the breast milk of nursing mothers. Although more data are imperative, the concentrations of vedolizumab in breast milk are minute and are therefore unlikely to result in systemic or gastro-intestinal immune-suppression of the infant.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28961712"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28961712",
"endSection": "abstract",
"offsetInBeginSection": 1086,
"offsetInEndSection": 1351,
"text": "Vedolizumab can be detected in the breast milk of nursing mothers. Although more data are imperative, the concentrations of vedolizumab in breast milk are minute and are therefore unlikely to result in systemic or gastro-intestinal immune-suppression of the infant."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28961712",
"endSection": "abstract",
"offsetInBeginSection": 1158,
"offsetInEndSection": 1356,
"text": "Although more data are imperative, the concentrations of vedolizumab in breast milk are minute and are therefore unlikely to result in systemic or gastro-intestinal immune-suppression of the infant."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28961712",
"endSection": "abstract",
"offsetInBeginSection": 671,
"offsetInEndSection": 831,
"text": "Results\nVedolizumab was undetectable in breast milk in IBD patients before the first infusion of vedolizumab [n = 3] and in all of the healthy controls [n = 5]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28961712",
"endSection": "abstract",
"offsetInBeginSection": 916,
"offsetInEndSection": 1076,
"text": "However, on serial measurements in breast milk after an infusion, drug levels did not surpass 480 ng/ml, which was roughly 1/100 of the comparable serum levels."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28961712",
"endSection": "abstract",
"offsetInBeginSection": 942,
"offsetInEndSection": 1192,
"text": "However, on serial measurements in breast milk after an infusion, drug levels did not surpass 480 ng/ml, which was roughly 1/100 of the comparable serum levels.<br><b>Conclusions</b>: Vedolizumab can be detected in the breast milk of nursing mothers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28961712",
"endSection": "abstract",
"offsetInBeginSection": 873,
"offsetInEndSection": 1033,
"text": "However, on serial measurements in breast milk after an infusion, drug levels did not surpass 480 ng/ml, which was roughly 1/100 of the comparable serum levels."
}
] | 11 |
BioASQ-training11b
| null | null |
5c9f7bb6ecadf2e73f00003e
|
bioasq_yesno
|
yesno
|
Is Lennox-Gastaut Syndrome usually diagnosed in older adults?
|
['no']
|
[
"no"
] |
['Lennox-Gastaut syndrome (LGS) is a severe pediatric epilepsy syndrome characterized by mixed seizures, cognitive decline, and generalized slow (<3 Hz) spike wave discharges on electroencephalography.', 'lennox-gastaut syndrome (lgs) is a severe pediatric epilepsy syndrome characterized by mixed seizures, cognitive decline, and generalized slow (<3 hz) spike wave discharges on electroencephalography.', ' children with Lennox-Gastaut syndrome Lennox-Gastaut syndrome (LGS) is a severe pediatric epilepsy syndrome characterized by mixed seizures, cognitive decline, and generalized slow (<3 Hz) spike wave discharges on electroencephalography']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22576075",
"http://www.ncbi.nlm.nih.gov/pubmed/8029151",
"http://www.ncbi.nlm.nih.gov/pubmed/26166587",
"http://www.ncbi.nlm.nih.gov/pubmed/24659735",
"http://www.ncbi.nlm.nih.gov/pubmed/20542434",
"http://www.ncbi.nlm.nih.gov/pubmed/26945476",
"http://www.ncbi.nlm.nih.gov/pubmed/9400037",
"http://www.ncbi.nlm.nih.gov/pubmed/20518600"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26945476",
"endSection": "abstract",
"offsetInBeginSection": 583,
"offsetInEndSection": 729,
"text": "We studied 15 LGS patients (mean age ± 1 standard deviation [SD] = 28.7 ± 10.6 years) and 17 healthy controls (mean age ± 1 SD = 27.6 ± 6.6 years)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24659735",
"endSection": "abstract",
"offsetInBeginSection": 91,
"offsetInEndSection": 129,
"text": " children with Lennox-Gastaut syndrome"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26166587",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 198,
"text": "Lennox-Gastaut syndrome (LGS) is a severe pediatric epilepsy syndrome characterized by mixed seizures, cognitive decline, and generalized slow (<3 Hz) spike wave discharges on electroencephalography"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8029151",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Clinical course and results of therapy were analysed in the group of 92 children, aged between 3 and 9 years, with diagnosed Lennox-Gastaut syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22576075",
"endSection": "abstract",
"offsetInBeginSection": 427,
"offsetInEndSection": 659,
"text": "We report the case of a 27-year-old man with a neurodevelopmental syndrome due to a 15q duplication, with intellectual disability, psychiatric disturbances, and an epileptic phenotype diagnosed as late-onset Lennox-Gastaut syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20518600",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 247,
"text": "Lennox-Gastaut syndrome is a relatively rare epilepsy syndrome that usually begins in early-mid childhood and is characterized by multiple seizure types, particularly generalized seizures, which are often resistant to antiepileptic drug medication"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20542434",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 206,
"text": "Lennox-Gastaut Syndrome is a severe childhood epilepsy syndrome characterised by the diagnostic triad of a slow spike and wave pattern on electroencephalogram, multiple seizure types and developmental delay"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22576075",
"endSection": "abstract",
"offsetInBeginSection": 427,
"offsetInEndSection": 660,
"text": "We report the case of a 27-year-old man with a neurodevelopmental syndrome due to a 15q duplication, with intellectual disability, psychiatric disturbances, and an epileptic phenotype diagnosed as late-onset Lennox-Gastaut syndrome.."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9400037",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "The Lennox-Gastaut syndrome, a severe form of epilepsy that usually begins in early childhood, is difficult to treat."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20518600",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 248,
"text": "Lennox-Gastaut syndrome is a relatively rare epilepsy syndrome that usually begins in early-mid childhood and is characterized by multiple seizure types, particularly generalized seizures, which are often resistant to antiepileptic drug medication."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19588340",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 400,
"text": "The Lennox-Gastaut syndrome is an age-specific disorder, characterised by epileptic seizures, a characteristic electroencephalogram (EEG), psychomotor delay and behaviour disorders. It occurs more frequently in males and onset is usually before the age of eight, with a peak between three and five years. Late cases occurring in adolescence and early adulthood have rarely been reported. "
}
] | 6 |
BioASQ-training6b
|
[
"http://www.disease-ontology.org/api/metadata/DOID:0050561",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D065768"
] | null |
58dbb4f08acda3452900001a
|
bioasq_yesno
|
factoid
|
Which protein mediates gene loop formation in the yeast S. cerevisiae?
|
['TFIIB']
|
[
"TFIIB",
"Transcription Factor IIB",
"TFIIB protein",
"TFIIB factor"
] |
["Moreover, looping is dependent upon the general transcription factor TFIIB: the E62K (glutamic acid 62 --> lysine) form of TFIIB adversely affects looping at every gene tested, including BLM10, SAC3, GAL10, SEN1, and HEM3. TFIIB crosslinks to both the promoter and terminator regions of the PMA1 and BLM10 genes, and its association with the terminator, but not the promoter, is adversely affected by E62K and by depletion of the Ssu72 component of the CPF 3' end processing complex, and is independent of TBP.", "Gene-loop formation is dependent on regulatory proteins localized at the 5' and 3' ends of genes, such as TFIIB. TFIIB crosslinks to both the promoter and terminator regions of the PMA1 and BLM10 genes, and its association with the terminator, but not the promoter, is adversely affected by E62K and by depletion of the Ssu72 component of the CPF 3' end processing complex, and is independent of TBP", 'Gene looping, defined as the interaction of the promoter and the terminator regions of a gene during transcription, requires transcription factor IIB (TFIIB).', 'A transcription-independent role for TFIIB in gene looping.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24124207",
"http://www.ncbi.nlm.nih.gov/pubmed/22081613",
"http://www.ncbi.nlm.nih.gov/pubmed/17803944",
"http://www.ncbi.nlm.nih.gov/pubmed/21835917",
"http://www.ncbi.nlm.nih.gov/pubmed/19602510",
"http://www.ncbi.nlm.nih.gov/pubmed/18550805"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17803944",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 59,
"text": "A transcription-independent role for TFIIB in gene looping."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17803944",
"endSection": "abstract",
"offsetInBeginSection": 290,
"offsetInEndSection": 510,
"text": "Moreover, looping is dependent upon the general transcription factor TFIIB: the E62K (glutamic acid 62 -->lysine) form of TFIIB adversely affects looping at every gene tested, including BLM10, SAC3, GAL10, SEN1, and HEM3"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17803944",
"endSection": "abstract",
"offsetInBeginSection": 512,
"offsetInEndSection": 798,
"text": "TFIIB crosslinks to both the promoter and terminator regions of the PMA1 and BLM10 genes, and its association with the terminator, but not the promoter, is adversely affected by E62K and by depletion of the Ssu72 component of the CPF 3' end processing complex, and is independent of TBP"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18550805",
"endSection": "abstract",
"offsetInBeginSection": 962,
"offsetInEndSection": 1066,
"text": "We present a high-resolution genome-wide map of TFIIB locations that implicates 3' NFRs in gene looping."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19602510",
"endSection": "abstract",
"offsetInBeginSection": 837,
"offsetInEndSection": 1107,
"text": "Instead, activators physically interacted with the general transcription factor TFIIB when the genes were activated and in a looped configuration. TFIIB cross-linked to both the promoter and the terminator regions during the transcriptionally activated state of a gene. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19602510",
"endSection": "abstract",
"offsetInBeginSection": 1292,
"offsetInEndSection": 1428,
"text": " We propose that the activators facilitate gene looping through their interaction with TFIIB during transcriptional activation of genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21835917",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "Gene looping, defined as the interaction of the promoter and the terminator regions of a gene during transcription, requires transcription factor IIB (TFIIB)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21835917",
"endSection": "abstract",
"offsetInBeginSection": 159,
"offsetInEndSection": 272,
"text": "We have earlier demonstrated association of TFIIB with the distal ends of a gene in an activator-dependent manner"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21835917",
"endSection": "abstract",
"offsetInBeginSection": 1578,
"offsetInEndSection": 1698,
"text": "Furthermore, TFIIB interaction with the CF1 complex and Pap1 is crucial for gene looping and transcriptional regulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22081613",
"endSection": "abstract",
"offsetInBeginSection": 70,
"offsetInEndSection": 226,
"text": "TFIIB also cross-links to terminator regions and is required for gene loops that juxtapose promoter-terminator elements in a transcription-dependent manner."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22081613",
"endSection": "abstract",
"offsetInBeginSection": 1125,
"offsetInEndSection": 1252,
"text": "These results define a novel, functional interaction between TFIIB and Ssl2 that affects start site selection and gene looping."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24124207",
"endSection": "abstract",
"offsetInBeginSection": 249,
"offsetInEndSection": 361,
"text": "Gene-loop formation is dependent on regulatory proteins localized at the 5' and 3' ends of genes, such as TFIIB."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24124207",
"endSection": "abstract",
"offsetInBeginSection": 247,
"offsetInEndSection": 359,
"text": "Gene-loop formation is dependent on regulatory proteins localized at the 5' and 3' ends of genes, such as TFIIB."
}
] | 6 |
BioASQ-training6b
| null | null |
58adc1ff9ef3c34033000006
|
bioasq_factoid
|
factoid
|
Which enzyme is inhibited by ribociclib?
|
['cyclin D-cyclin-dependent kinase 4/6', 'CDK4/6']
|
[
"cyclin D-cyclin-dependent kinase 4/6",
"CDK4/6",
"Cyclin D-CDK4/6",
"Cyclin D-dependent kinase 4/6",
"Cyclin D-CDK 4/6",
"Cyclin D-cyclin-dependent kinase 4 and 6",
"Cyclin D-CDK4 and CDK6"
] |
['Ribociclib is inhibitor of cyclin D-cyclin-dependent kinase 4/6 (CDK 4/6). It is used for breast cancer treatment.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26303211",
"http://www.ncbi.nlm.nih.gov/pubmed/27729458",
"http://www.ncbi.nlm.nih.gov/pubmed/27017286",
"http://www.ncbi.nlm.nih.gov/pubmed/25941111",
"http://www.ncbi.nlm.nih.gov/pubmed/26642065",
"http://www.ncbi.nlm.nih.gov/pubmed/27030077",
"http://www.ncbi.nlm.nih.gov/pubmed/27493615",
"http://www.ncbi.nlm.nih.gov/pubmed/27496135",
"http://www.ncbi.nlm.nih.gov/pubmed/26830312",
"http://www.ncbi.nlm.nih.gov/pubmed/27717303",
"http://www.ncbi.nlm.nih.gov/pubmed/25848011",
"http://www.ncbi.nlm.nih.gov/pubmed/26053278",
"http://www.ncbi.nlm.nih.gov/pubmed/27810861",
"http://www.ncbi.nlm.nih.gov/pubmed/27542767",
"http://www.ncbi.nlm.nih.gov/pubmed/27087139",
"http://www.ncbi.nlm.nih.gov/pubmed/26995305",
"http://www.ncbi.nlm.nih.gov/pubmed/27336726",
"http://www.ncbi.nlm.nih.gov/pubmed/26390342",
"http://www.ncbi.nlm.nih.gov/pubmed/25876993",
"http://www.ncbi.nlm.nih.gov/pubmed/26896604"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26303211",
"endSection": "abstract",
"offsetInBeginSection": 411,
"offsetInEndSection": 587,
"text": "Three CDK 4/6 inhibitors have been investigated for the treatment of HR(+) breast cancer, including palbociclib (PD 0332991), ribociclib (LEE011), and abemaciclib (LY2835219). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26642065",
"endSection": "abstract",
"offsetInBeginSection": 472,
"offsetInEndSection": 761,
"text": "The CDK 4/6 inhibitors are a novel class of therapeutics that target the CDK 4/6 kinases that promote transition through the cell cycle. Currently, palbociclib (PD0332991, Pfizer), abemaciclib (LY2835219, Lilly) and ribociclib (LEE011, Novartis) are being investigated in clinical trials. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26642065",
"endSection": "abstract",
"offsetInBeginSection": 1054,
"offsetInEndSection": 1405,
"text": "SUMMARY: Palbociclib, abemaciclib and ribociclib have demonstrated very promising clinical activity in breast cancer, liposarcoma, mantel cell lymphoma and melanoma. Moreover, CDK4/6 inhibitors have shown promising preclinical activity in glioblastoma, renal and ovarian cancer models that may provide directions for their future clinical development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27017286",
"endSection": "abstract",
"offsetInBeginSection": 1339,
"offsetInEndSection": 1512,
"text": "Currently, three selective CDK4/6 inhibitors have been approved or are in late-stage development: palbociclib (PD-0332991), ribociclib (LEE011), and abemaciclib (LY2835219)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27810861",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 276,
"text": "The combination of antiestrogen therapy and ribociclib, an investigational CDK4/6 inhibitor, led to improved outcomes in women with metastatic HR-positive, HER2-negative breast cancer, according to findings presented at a meeting of the European Society for Medical Oncology. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27336726",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 353,
"text": "OBJECTIVES: Cyclin D-cyclin-dependent kinase (CDK) 4/6-inhibitor of CDK4/6-retinoblastoma (Rb) pathway hyperactivation is associated with hormone receptor-positive (HR+) breast cancer (BC). This study assessed the biological activity of ribociclib (LEE011; CDK4/6 inhibitor) plus letrozole compared with single-agent letrozole in the presurgical setting"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27493615",
"endSection": "abstract",
"offsetInBeginSection": 406,
"offsetInEndSection": 559,
"text": "Importantly, 2 other CDK4/6 inhibitors, abemaciclib (LY2835219; Lilly) and ribociclib (LEE011; Novartis), are in the late stage of clinical development. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27729458",
"endSection": "abstract",
"offsetInBeginSection": 547,
"offsetInEndSection": 803,
"text": "After noting an inverse correlation with sensitivity to ribociclib (CDK4/6 inhibitor), we studied the combinatorial effect of these two agents using proliferation assays, cell cycle analysis, Ki67 immunostaining, timelapse microscopy and xenograft studies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27717303",
"endSection": "abstract",
"offsetInBeginSection": 274,
"offsetInEndSection": 635,
"text": "Methods In this randomized, placebo-controlled, phase 3 trial, we evaluated the efficacy and safety of the selective CDK4/6 inhibitor ribociclib combined with letrozole for first-line treatment in 668 postmenopausal women with HR-positive, HER2-negative recurrent or metastatic breast cancer who had not received previous systemic therapy for advanced disease. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25941111",
"endSection": "abstract",
"offsetInBeginSection": 522,
"offsetInEndSection": 795,
"text": "Three selective CDK4/6 inhibitors, palbociclib (Ibrance; Pfizer), ribociclib (Novartis), and abemaciclib (Lilly), are in various stages of development in a variety of pRb-positive tumor types, including breast cancer, melanoma, liposarcoma, and non-small cell lung cancer. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27493615",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "Clinical Development of the CDK4/6 Inhibitors Ribociclib and Abemaciclib in Breast Cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25848011",
"endSection": "abstract",
"offsetInBeginSection": 874,
"offsetInEndSection": 1102,
"text": "Targeted inhibition of CDK4/6 pathway by small-molecule inhibitors palbociclib (PD-0332991) and ribociclib (LEE011) resulted in inhibition of cell-cycle progression, amelioration of kidney injury, and improved overall survival. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27493615",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "Clinical Development of the CDK4/6 Inhibitors Ribociclib and Abemaciclib in Breast Cancer."
}
] | 6 |
BioASQ-training6b
|
[
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D004798"
] | null |
5880dba9c872c95565000009
|
bioasq_factoid
|
factoid
|
In what type of clinical trial has RT001 been evaluated against Friedreich's ataxia?
|
['phase I/II double-blind, randomized, comparator-controlled trial']
|
[
"phase I/II double-blind, randomized, comparator-controlled trial",
"phase I/II trial",
"phase I/II clinical trial",
"phase I/II study",
"double-blind phase I/II trial",
"randomized phase I/II trial",
"comparator-controlled phase I/II trial",
"phase I/II randomized controlled trial",
"phase I/II double-blind study",
"phase I/II randomized study"
] |
["RT001 was evaluatd in a phase I/II double-blind, randomized, comparator-controlled trial in Friedreich's ataxia patients."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29624723"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29624723",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "Randomized, clinical trial of RT001: Early signals of efficacy in Friedreich's ataxia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29624723",
"endSection": "abstract",
"offsetInBeginSection": 352,
"offsetInEndSection": 500,
"text": "We conducted a phase I/II double-blind, comparator-controlled trial with 2 doses of RT001 in Friedreich's ataxia patients (9 subjects each cohort). "
}
] | 12 |
BioASQ-training12b
| null | null |
64402bb057b1c7a315000043
|
bioasq_factoid
|
factoid
|
Which disease phenotype has the worst prognosis in Duchenne Muscular Dystrophy?
|
['Dp140 isoform']
|
[
"Dp140 isoform",
"Dp140",
"Dp140 protein",
"Dp140 variant",
"Dp140 isoform of the Dystrophin gene"
] |
['A strong association between the risk of cognitive disability and the involvement of groups of DMD isoforms was found. In particular, improvements in the correlation of FSIQ with mutation location were identified when a new classification system for mutations affecting the Dp140 isoform was implemented.', ' A strong association between the risk of cognitive disability and the involvement of groups of DMD isoforms was found. In particular, improvements in the correlation of FSIQ with mutation location were identified when a new classification system for mutations affecting the Dp140 isoform was implemented.', 'Dp140 isoform is related to increased risk of cognitive impairment and thus worse prognosis.', 'A strong association between the risk of cognitive disability and the involvement of groups of DMD isoforms was found.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34342696",
"http://www.ncbi.nlm.nih.gov/pubmed/1865568",
"http://www.ncbi.nlm.nih.gov/pubmed/15637982",
"http://www.ncbi.nlm.nih.gov/pubmed/21178099",
"http://www.ncbi.nlm.nih.gov/pubmed/32791185",
"http://www.ncbi.nlm.nih.gov/pubmed/20098710"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20098710",
"endSection": "abstract",
"offsetInBeginSection": 1039,
"offsetInEndSection": 1344,
"text": " A strong association between the risk of cognitive disability and the involvement of groups of DMD isoforms was found. In particular, improvements in the correlation of FSIQ with mutation location were identified when a new classification system for mutations affecting the Dp140 isoform was implemented."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32791185",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "The ACTN3 577XX Null Genotype Is Associated with Low Left Ventricular Dilation-Free Survival Rate in Patients with Duchenne Muscular Dystrophy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1865568",
"endSection": "abstract",
"offsetInBeginSection": 1046,
"offsetInEndSection": 1192,
"text": "These results suggest that patients with Duchenne muscular dystrophy with defective cDMD have more severe disease than those without cDMD deficit."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21178099",
"endSection": "abstract",
"offsetInBeginSection": 1118,
"offsetInEndSection": 1401,
"text": "Osteopontin genotype is a genetic modifier of disease severity in Duchenne dystrophy. Inclusion of genotype data as a covariate or in inclusion criteria in DMD clinical trials would reduce intersubject variance, and increase sensitivity of the trials, particularly in older subjects."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21178099",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 82,
"text": "SPP1 genotype is a determinant of disease severity in Duchenne muscular dystrophy."
}
] | 11 |
BioASQ-training11b
| null | null |
6278dfe956bf9aee6f000016
|
bioasq_factoid
|
factoid
|
Which is the third subunit of the TSC1-TSC2 complex upstream of mTORC1?
|
['TBC1D7']
|
[
"TBC1D7",
"TBC1 domain family member 7",
"TBC1D7 protein",
"TBC1D7 homolog"
] |
TBC1D7 was identified as a stably associated and ubiquitous third core subunit of the TSC1-TSC2 complex. It was demonstrated that TSC1-TSC2-TBC1D7 (TSC-TBC) is the functional complex that senses specific cellular growth conditions and possesses Rheb-GAP activity to negatively regulate mTORC1 activity. In agreement with this, TBC1D7 knockdown was shown to result in increased mTORC1 signaling, delayed induction of autophagy, and enhanced cell growth under poor growth conditions.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22795129"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22795129",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 328,
"text": "The tuberous sclerosis complex (TSC) tumor suppressors form the TSC1-TSC2 complex, which limits cell growth in response to poor growth conditions. Through its GTPase-activating protein (GAP) activity toward Rheb, this complex inhibits the mechanistic target of rapamycin (mTOR) complex 1 (mTORC1), a key promoter of cell growth."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22795129",
"endSection": "abstract",
"offsetInBeginSection": 329,
"offsetInEndSection": 633,
"text": "Here, we identify and biochemically characterize TBC1D7 as a stably associated and ubiquitous third core subunit of the TSC1-TSC2 complex. We demonstrate that the TSC1-TSC2-TBC1D7 (TSC-TBC) complex is the functional complex that senses specific cellular growth conditions and possesses Rheb-GAP activity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22795129",
"endSection": "abstract",
"offsetInBeginSection": 734,
"offsetInEndSection": 894,
"text": "TBC1D7 knockdown decreases the association of TSC1 and TSC2 leading to decreased Rheb-GAP activity, without effects on the localization of TSC2 to the lysosome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22795129",
"endSection": "abstract",
"offsetInBeginSection": 895,
"offsetInEndSection": 1072,
"text": "Like the other TSC-TBC components, TBC1D7 knockdown results in increased mTORC1 signaling, delayed induction of autophagy, and enhanced cell growth under poor growth conditions."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.uniprot.org/uniprot/TSC2_HUMAN",
"http://www.uniprot.org/uniprot/TSC1_HUMAN",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0033596",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0031931",
"http://www.biosemantics.org/jochem#4266396"
] |
[] |
5319ac99b166e2b806000034
|
bioasq_factoid
|
factoid
|
What memory problems are reported in the " Gulf war syndrome"
|
['memory loss']
|
[
"memory loss",
"amnesia",
"forgetfulness",
"memory impairment",
"cognitive decline",
"memory dysfunction"
] |
memory loss
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/15251045",
"http://www.ncbi.nlm.nih.gov/pubmed/14515407",
"http://www.ncbi.nlm.nih.gov/pubmed/11600803",
"http://www.ncbi.nlm.nih.gov/pubmed/11478226",
"http://www.ncbi.nlm.nih.gov/pubmed/9096828",
"http://www.ncbi.nlm.nih.gov/pubmed/9005271"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15251045",
"endSection": "abstract",
"offsetInBeginSection": 1309,
"offsetInEndSection": 1320,
"text": "memory loss"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14515407",
"endSection": "abstract",
"offsetInBeginSection": 887,
"offsetInEndSection": 902,
"text": "loss of memory,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11600803",
"endSection": "abstract",
"offsetInBeginSection": 169,
"offsetInEndSection": 184,
"text": " loss of memory"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11478226",
"endSection": "abstract",
"offsetInBeginSection": 392,
"offsetInEndSection": 401,
"text": "dysmnesia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9096828",
"endSection": "abstract",
"offsetInBeginSection": 1292,
"offsetInEndSection": 1307,
"text": "memory problems"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9005271",
"endSection": "abstract",
"offsetInBeginSection": 1051,
"offsetInEndSection": 1204,
"text": "\"impaired cognition,\" characterized by problems with attention, memory, and reasoning, as well as insomnia, depression, daytime sleepiness, and headaches"
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018923"
] |
[
{
"o": "UMLS_CUI:C0282550",
"p": "http://www.w3.org/2004/02/skos/core#notation",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:4491"
},
{
"o": "persian gulf syndrome",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:4491"
},
{
"o": "Gulf war syndrome (disorder)",
"p": "http://www.w3.org/2004/02/skos/core#altLabel",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:4491"
},
{
"o": "SNOMEDCT_2010_1_31:95877004",
"p": "http://www.w3.org/2004/02/skos/core#notation",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:4491"
},
{
"o": "persian gulf syndrome",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:4491"
},
{
"o": "Gulf war syndrome (disorder)",
"p": "http://www.w3.org/2004/02/skos/core#altLabel",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:4491"
},
{
"o": "MSH2010_2010_02_22:D018923",
"p": "http://www.w3.org/2004/02/skos/core#notation",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:4491"
},
{
"o": "persian gulf syndrome",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:4491"
},
{
"o": "Gulf war syndrome (disorder)",
"p": "http://www.w3.org/2004/02/skos/core#altLabel",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:4491"
},
{
"o": "0000013450",
"p": "http://www.w3.org/2004/02/skos/core#notation",
"s": "http://linkedlifedata.com/resource/umls/label/A1393478"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A1393478",
"p": "http://linkedlifedata.com/resource/umls/prefMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C0681713"
},
{
"o": "Persian Gulf War period",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A1393478"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A1393478",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0681713"
},
{
"o": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:3231",
"p": "http://www.w3.org/2004/02/skos/core#broader",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:4491"
},
{
"o": "persian gulf syndrome",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:4491"
},
{
"o": "occupational disease",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:3231"
},
{
"o": "Gulf war syndrome (disorder)",
"p": "http://www.w3.org/2004/02/skos/core#altLabel",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:4491"
},
{
"o": "Occupational disorder (disorder)",
"p": "http://www.w3.org/2004/02/skos/core#altLabel",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:3231"
},
{
"o": "occupational disorder",
"p": "http://www.w3.org/2004/02/skos/core#altLabel",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:3231"
},
{
"o": "http://dbpedia.org/resource/Gulf_War_syndrome",
"p": "http://www.w3.org/2004/02/skos/core#exactMatch",
"s": "http://data.linkedct.org/resource/condition/5434"
},
{
"o": "http://dbpedia.org/resource/Gulf_War_syndrome",
"p": "http://www.w3.org/2004/02/skos/core#exactMatch",
"s": "http://data.linkedct.org/resource/condition/5434"
},
{
"o": "http://yago.org/resource/Gulf_War_syndrome",
"p": "http://www.w3.org/2004/02/skos/core#exactMatch",
"s": "http://data.linkedct.org/resource/condition/5434"
},
{
"o": "Condition #5434 (Gulf War Syndrome)",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://data.linkedct.org/resource/condition/5434"
},
{
"o": "Gulf War Syndrome",
"p": "http://data.linkedct.org/resource/linkedct/condition_name",
"s": "http://data.linkedct.org/resource/condition/5434"
},
{
"o": "http://yago.org/resource/Gulf_War_syndrome",
"p": "http://www.w3.org/2004/02/skos/core#exactMatch",
"s": "http://data.linkedct.org/resource/condition/5434"
},
{
"o": "http://dbpedia.org/resource/Gulf_War_syndrome",
"p": "http://www.w3.org/2004/02/skos/core#exactMatch",
"s": "http://data.linkedct.org/resource/condition/5434"
},
{
"o": "http://yago.org/resource/Gulf_War_syndrome",
"p": "http://www.w3.org/2004/02/skos/core#exactMatch",
"s": "http://data.linkedct.org/resource/condition/5434"
},
{
"o": "Condition #5434 (Gulf War Syndrome)",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://data.linkedct.org/resource/condition/5434"
},
{
"o": "Gulf War Syndrome",
"p": "http://data.linkedct.org/resource/linkedct/condition_name",
"s": "http://data.linkedct.org/resource/condition/5434"
}
] |
52f896d62059c6d71c000046
|
bioasq_factoid
|
yesno
|
Does CRISPR inversion of CTCF sites alter genome topology?
|
['yes']
|
[
"yes"
] |
['Yes. CRISPR inversion of CTCF sites alters genome topology.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26276636"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26276636",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 84,
"text": "CRISPR Inversion of CTCF Sites Alters Genome Topology and Enhancer/Promoter Function"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26276636",
"endSection": "abstract",
"offsetInBeginSection": 258,
"offsetInEndSection": 1185,
"text": "To test the functional significance of this observation, we combined CRISPR/Cas9-based genomic-DNA-fragment editing with chromosome-conformation-capture experiments to show that the location and relative orientations of CBSs determine the specificity of long-range chromatin looping in mammalian genomes, using protocadherin (Pcdh) and β-globin as model genes. Inversion of CBS elements within the Pcdh enhancer reconfigures the topology of chromatin loops between the distal enhancer and target promoters and alters gene-expression patterns. Thus, although enhancers can function in an orientation-independent manner in reporter assays, in the native chromosome context, the orientation of at least some enhancers carrying CBSs can determine both the architecture of topological chromatin domains and enhancer/promoter specificity. These findings reveal how 3D chromosome architecture can be encoded by linear genome sequences"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26276636",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "CRISPR Inversion of CTCF Sites Alters Genome Topology and Enhancer/Promoter Function."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26276636",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "CRISPR Inversion of CTCF Sites Alters Genome Topology and Enhancer/Promoter Function."
}
] | 6 |
BioASQ-training6b
|
[
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D064113",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D064112"
] | null |
587e440f2420191125000005
|
bioasq_yesno
|
factoid
|
What is the protein product of the gene GBA2?
|
['The GBA2 gene encodes the non-lysosomal glucosylceramidase (NLGase), an enzyme that catalyzes the conversion of glucosylceramide (GlcCer) to ceramide and glucose.']
|
[
"GBA2",
"non-lysosomal glucosylceramidase",
"NLGase",
"glucosylceramidase",
"glucosylceramide beta-glucosidase",
"glucosylceramidase 2",
"glucosylceramidase, non-lysosomal"
] |
['The GBA2 gene encodes the non-lysosomal glucosylceramidase (NLGase), an enzyme that catalyzes the conversion of glucosylceramide (GlcCer) to ceramide and glucose.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29524657",
"http://www.ncbi.nlm.nih.gov/pubmed/29234271",
"http://www.ncbi.nlm.nih.gov/pubmed/30308956"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29524657",
"endSection": "abstract",
"offsetInBeginSection": 907,
"offsetInEndSection": 934,
"text": "b-glucosidase 2 gene (GBA2)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30308956",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "The GBA2 gene encodes the non-lysosomal glucosylceramidase (NLGase), an enzyme that catalyzes the conversion of glucosylceramide (GlcCer) to ceramide and glucose. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29234271",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "The non-lysosomal glucosylceramidase GBA2 catalyzes the hydrolysis of glucosylceramide to glucose and ceramide. "
}
] | 11 |
BioASQ-training11b
| null | null |
5e5bab131af46fc130000001
|
bioasq_factoid
|
yesno
|
Are cyclophilins proteins that bind to prolines?
|
['yes']
|
[
"yes"
] |
['Cyclophilins are ubiquitously expressed proteins that bind to prolines.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25967372",
"http://www.ncbi.nlm.nih.gov/pubmed/24831536",
"http://www.ncbi.nlm.nih.gov/pubmed/18823995",
"http://www.ncbi.nlm.nih.gov/pubmed/12358793"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25967372",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 132,
"text": "Cyclophilins are ubiquitously expressed proteins that bind to prolines and can catalyse cis/trans isomerization of proline residues."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18823995",
"endSection": "abstract",
"offsetInBeginSection": 593,
"offsetInEndSection": 722,
"text": "a characteristic of the cyclophilin family of proteins that bind prolines and often act as cis-trans peptidyl-prolyl isomerases. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24831536",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "The cyclophilins are widely expressed enzymes that catalyze the interconversion of the cis and trans peptide bonds of prolines. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12358793",
"endSection": "abstract",
"offsetInBeginSection": 1468,
"offsetInEndSection": 1564,
"text": " an immunophilin on the isomerization of critical prolines that are found in the tCHT1 sequence."
}
] | 5 |
BioASQ-training5b
|
[] |
[] |
56f6a63d09dd18d46b00000c
|
bioasq_yesno
|
yesno
|
Can autophagy related lncRNAs be used for colorectal cancer prognosis?
|
['yes']
|
[
"yes"
] |
['Yes, a prognostic prediction model of CRC was built based on nine ARlncRNAs (NKILA, LINC00174, AC008760.1, LINC02041, PCAT6, AC156455.1, LINC01503, LINC00957, and CD27-AS1). The 5-year overall survival rate was significantly lower in the high-risk group than in the low-risk group among train set, validation set, and all patients (all p < 0.001). The model had high sensitivity and accuracy in predicting the 1-year overall survival rate (area under the curve = 0.717). The prediction model risk score was an independent predictor of CRC.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34692467"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34692467",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 109,
"text": "A Novel Prognostic Prediction Model for Colorectal Cancer Based on Nine Autophagy-Related Long Noncoding RNAs"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34692467",
"endSection": "abstract",
"offsetInBeginSection": 1347,
"offsetInEndSection": 1882,
"text": "A prognostic prediction model of CRC was built based on nine ARlncRNAs (NKILA, LINC00174, AC008760.1, LINC02041, PCAT6, AC156455.1, LINC01503, LINC00957, and CD27-AS1). The 5-year overall survival rate was significantly lower in the high-risk group than in the low-risk group among train set, validation set, and all patients (all p < 0.001). The model had high sensitivity and accuracy in predicting the 1-year overall survival rate (area under the curve = 0.717). The prediction model risk score was an independent predictor of CRC. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34692467",
"endSection": "abstract",
"offsetInBeginSection": 2284,
"offsetInEndSection": 2518,
"text": "The new ARlncRNA-based model predicts CRC patient prognosis and provides new research ideas regarding potential mechanisms regulating the biological behavior of CRC. ARlncRNAs may play important roles in personalized cancer treatment."
}
] | 11 |
BioASQ-training11b
| null | null |
62266c353a8413c65300008a
|
bioasq_yesno
|
factoid
|
Which is the genetic lesion associated with Huntington’s disease?
|
['A CAG trinucleotide repeat expansion in the HD gene']
|
[
"CAG repeat expansion",
"CAG trinucleotide repeat",
"CAG repeat",
"CAG trinucleotide repeat expansion",
"CAG expansion",
"CAG repeat expansion in the HD gene",
"CAG repeat expansion in the huntingtin gene",
"CAG trinucleotide repeat expansion in the HD gene",
"CAG repeat in the HD gene"
] |
The genetic lesion associated with Huntington's disease is a CAG trinucleotide repeat expansion in the HD (or HTT) gene.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/7620118"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7620118",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 360,
"text": "Early in 1993, an unstable, expanded trinucleotide repeat in a novel gene of unknown function was identified on HD chromosomes. This discovery unleased a flurry of experimentation that has established the expanded CAG repeat the almost universal cause of the characteristic neurologic symptoms and pathology of this neurodegenerative disorder of midlife onset."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D006816",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D020022",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D030342",
"http://www.uniprot.org/uniprot/HD_HUMAN",
"http://www.disease-ontology.org/api/metadata/DOID:12858",
"http://www.disease-ontology.org/api/metadata/DOID:630",
"http://www.disease-ontology.org/api/metadata/DOID:0050325",
"http://www.disease-ontology.org/api/metadata/DOID:0050739"
] |
[] |
5319a6e9b166e2b806000023
|
bioasq_factoid
|
factoid
|
What is a miR?
|
['MiRs are small (~23 nt) noncoding RNAs']
|
[
"MiRs",
"microRNAs",
"miRNAs",
"small noncoding RNAs",
"small interfering RNAs",
"micro RNA",
"micro RNA molecules",
"non-coding RNAs"
] |
['The discovery of microRNAs (miRNAs) has opened an entire new avenue for drug development. These short (15-22 nucleotides) noncoding RNAs, which function in RNA silencing and posttranscriptional regulation of gene expression, have been shown to critically affect numerous pathways in both development and disease progression.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27814624",
"http://www.ncbi.nlm.nih.gov/pubmed/27924483",
"http://www.ncbi.nlm.nih.gov/pubmed/27734397",
"http://www.ncbi.nlm.nih.gov/pubmed/27586262"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27814624",
"endSection": "abstract",
"offsetInBeginSection": 508,
"offsetInEndSection": 634,
"text": "As novel molecules, microRNAs (miRs) take part in regulating protein-coding gene expression at the post-transcriptional level,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27586262",
"endSection": "abstract",
"offsetInBeginSection": 399,
"offsetInEndSection": 461,
"text": "The discovery of microRNA (miRNA) regulation in tumorigenesis "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27734397",
"endSection": "abstract",
"offsetInBeginSection": 467,
"offsetInEndSection": 671,
"text": "MiRs are small (~23 nt) noncoding RNAs that regulate gene expression by specifically interacting with the 3' untranslated region (UTR) of target gene mRNA to repress translation or enhance mRNA cleavage. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27924483",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 325,
"text": "The discovery of microRNAs (miRNAs) has opened an entire new avenue for drug development. These short (15-22 nucleotides) noncoding RNAs, which function in RNA silencing and posttranscriptional regulation of gene expression, have been shown to critically affect numerous pathways in both development and disease progression. "
}
] | 6 |
BioASQ-training6b
| null | null |
58f0b1d670f9fc6f0f000007
|
bioasq_factoid
|
yesno
|
Can mutations in Calmodulin cause ventricular fibrillation?
|
['yes']
|
[
"yes"
] |
Yes, mutations in CALM underly IVF manifesting in childhood and adolescence.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24076290",
"http://www.ncbi.nlm.nih.gov/pubmed/11807557"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24076290",
"endSection": "abstract",
"offsetInBeginSection": 648,
"offsetInEndSection": 1613,
"text": "We characterized a family presenting with a history of ventricular fibrillation (VF) and sudden death without ECG or echocardiographic abnormalities at rest. Two siblings died suddenly at the ages of 9 and 10 years, and another two were resuscitated from out-of-hospital cardiac arrest with documented VF at age 10 and 16, respectively. Exome sequencing identified a missense mutation affecting a highly conserved residue (p.Phe90Leu) in the CALM1 gene encoding calmodulin. This mutation was also carried by one of the sibs who died suddenly, for whom DNA was available. The mutation was present in the mother and in an sibling, both asymptomatic but displaying a marginally prolonged QT-interval during exercise. CONCLUSIONS: We identified a mutation in CALM1 underlying IVF manifesting in childhood and adolescence. The causality of the mutation is supported by previous studies demonstrating that Phe90 mediates the direct interaction of CaM with target peptides"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11807557",
"endSection": "abstract",
"offsetInBeginSection": 348,
"offsetInEndSection": 917,
"text": "Here we show that calmodulin (CaM), a ubiquitous Ca2+-sensing protein, binds to the carboxy-terminal 'IQ' domain of the human cardiac Na channel (hH1) in a Ca2+-dependent manner. This binding interaction significantly enhances slow inactivation-a channel-gating process linked to life-threatening idiopathic ventricular arrhythmias. Mutations targeted to the IQ domain disrupted CaM binding and eliminated Ca2+/CaM-dependent slow inactivation, whereas the gating effects of Ca2+/CaM were restored by intracellular application of a peptide modelled after the IQ domain. "
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D014693",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002147",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D016276",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D016278",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D016277",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018497",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018487",
"http://www.uniprot.org/uniprot/CALM_PLEOS",
"http://www.uniprot.org/uniprot/CALM_CHICK",
"http://www.uniprot.org/uniprot/CALM_EMENI",
"http://www.uniprot.org/uniprot/CALM_DANRE",
"http://www.uniprot.org/uniprot/CALM_PLAF7",
"http://www.uniprot.org/uniprot/CALM_KLULA",
"http://www.uniprot.org/uniprot/CALM_LOCMI",
"http://www.uniprot.org/uniprot/CALM_FAGSY",
"http://www.uniprot.org/uniprot/CALM_PHYPO",
"http://www.uniprot.org/uniprot/CALM_COLTR",
"http://www.uniprot.org/uniprot/CALM_TORCA",
"http://www.uniprot.org/uniprot/CALM_AGABI",
"http://www.uniprot.org/uniprot/CALM_YEAST",
"http://www.uniprot.org/uniprot/CALM_KARMI",
"http://www.uniprot.org/uniprot/CALM_WHEAT",
"http://www.uniprot.org/uniprot/CALM_MACPY",
"http://www.uniprot.org/uniprot/CALM_MAIZE",
"http://www.uniprot.org/uniprot/CALM_MAGO7",
"http://www.uniprot.org/uniprot/CALM_PHYIN",
"http://www.uniprot.org/uniprot/CALM_DICDI",
"http://www.uniprot.org/uniprot/CALM_BOVIN",
"http://www.uniprot.org/uniprot/CALM_APLCA",
"http://www.uniprot.org/uniprot/CALM_PYUSP",
"http://www.uniprot.org/uniprot/CALM_PNECA",
"http://www.uniprot.org/uniprot/CALM_PLECO",
"http://www.uniprot.org/uniprot/CALM_MYXGL",
"http://www.uniprot.org/uniprot/CALM_CANAX",
"http://www.uniprot.org/uniprot/CALM_AJECG",
"http://www.uniprot.org/uniprot/CALM_TRYBB",
"http://www.uniprot.org/uniprot/CALM_TRYBG",
"http://www.uniprot.org/uniprot/CALM_METSE",
"http://www.uniprot.org/uniprot/CALM_MALDO",
"http://www.uniprot.org/uniprot/CALM_COLGL",
"http://www.uniprot.org/uniprot/CALM_ALEFU",
"http://www.uniprot.org/uniprot/CALM_CHLRE",
"http://www.uniprot.org/uniprot/CALM_ASPOR",
"http://www.uniprot.org/uniprot/CALM_STIJA",
"http://www.uniprot.org/uniprot/CALM_SPIOL",
"http://www.uniprot.org/uniprot/CALM_NEUCR",
"http://www.uniprot.org/uniprot/CALM_STYLE",
"http://www.uniprot.org/uniprot/CALM_CIOIN",
"http://www.uniprot.org/uniprot/CALM_CTEID",
"http://www.uniprot.org/uniprot/CALM_MOUSE",
"http://www.uniprot.org/uniprot/CALM_SCHPO",
"http://www.uniprot.org/uniprot/CALM_XENLA",
"http://www.uniprot.org/uniprot/CALM_PONAB",
"http://www.uniprot.org/uniprot/CALM_LUMRU",
"http://www.uniprot.org/uniprot/CALM_PYTSP",
"http://www.uniprot.org/uniprot/CALM_ONCSP",
"http://www.uniprot.org/uniprot/CALM_EUPCH",
"http://www.uniprot.org/uniprot/CALM_PATSP",
"http://www.uniprot.org/uniprot/CALM_PROMN",
"http://www.uniprot.org/uniprot/CALM_MEDSA",
"http://www.uniprot.org/uniprot/CALM_STRIE",
"http://www.uniprot.org/uniprot/CALM_ELEEL",
"http://www.uniprot.org/uniprot/CALM_CAPAN",
"http://www.uniprot.org/uniprot/CALM_PFIPI",
"http://www.uniprot.org/uniprot/CALM_BLAEM",
"http://www.uniprot.org/uniprot/CALM_RAT",
"http://www.uniprot.org/uniprot/CALM_ACHKL",
"http://www.uniprot.org/uniprot/CALM_SUBDO",
"http://www.uniprot.org/uniprot/CALM_PERFV",
"http://www.uniprot.org/uniprot/CALM_PLAFA",
"http://www.uniprot.org/uniprot/CALM_RABIT",
"http://www.uniprot.org/uniprot/CALM_EPIAK",
"http://www.uniprot.org/uniprot/CALM_TRYCR",
"http://www.uniprot.org/uniprot/CALM_HUMAN",
"http://www.uniprot.org/uniprot/CALM_LILLO",
"http://www.uniprot.org/uniprot/CALM_DROME",
"http://www.uniprot.org/uniprot/CALM_TETPY",
"http://www.uniprot.org/uniprot/CALM_OREMO",
"http://www.uniprot.org/uniprot/CALM_STRPU",
"http://www.uniprot.org/uniprot/CALM_SHEEP",
"http://www.uniprot.org/uniprot/CALM_SACJA",
"http://www.uniprot.org/uniprot/CALM_TETTH",
"http://www.uniprot.org/uniprot/CALM_PARTE",
"http://www.uniprot.org/uniprot/CALM_RENRE",
"http://www.uniprot.org/uniprot/CALM_ANAPL",
"http://www.uniprot.org/uniprot/CALM_MOUSC",
"http://www.uniprot.org/uniprot/CALM_EUGGR",
"http://www.uniprot.org/uniprot/CALM_CAEEL",
"http://www.uniprot.org/uniprot/CALM_BRYDI",
"http://www.uniprot.org/uniprot/CALM_LYTPI",
"http://www.uniprot.org/uniprot/CALM_HORVU",
"http://www.uniprot.org/uniprot/CALM_GECJA",
"http://www.uniprot.org/uniprot/CALM_HETTR",
"http://www.uniprot.org/uniprot/CALM_SOLLC",
"http://www.uniprot.org/uniprot/CALM_HALOK",
"http://www.uniprot.org/uniprot/CALM_HELAN",
"http://www.uniprot.org/uniprot/CALM_PAXIN"
] |
[] |
52b2f0864003448f55000007
|
bioasq_yesno
|
yesno
|
Can Efgartigimod be used for myasthenia gravis?
|
['yes']
|
[
"yes"
] |
['Yes. Efgartigimod is effective, approved and can be used for myasthenia gravis.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/35639288",
"http://www.ncbi.nlm.nih.gov/pubmed/34146511",
"http://www.ncbi.nlm.nih.gov/pubmed/35179720"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35639288",
"endSection": "abstract",
"offsetInBeginSection": 1567,
"offsetInEndSection": 1733,
"text": "Efgartigimod is an FcRn inhibitor recently approved for MG treatment, and rozanolixizumab, nipocalimab and batoclimab are other agents in clinical trial development. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35179720",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 400,
"text": "Efgartigimod (efgartigimod alfa-fcab, Vyvgart™) is a first-in-class neonatal Fc receptor antagonist being developed by argenx for the treatment of autoimmune diseases including myasthenia gravis. In December 2021, intravenous efgartigimod received its first approval in the USA for the treatment of generalized myasthenia gravis in adults who are anti-acetylcholine receptor (AChR) antibody positive."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35179720",
"endSection": "abstract",
"offsetInBeginSection": 979,
"offsetInEndSection": 1118,
"text": "This article summarizes the milestones in the development of efgartigimod leading to this first approval for generalized myasthenia gravis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34146511",
"endSection": "abstract",
"offsetInBeginSection": 2951,
"offsetInEndSection": 3062,
"text": "INTERPRETATION: Efgartigimod was well tolerated and efficacious in patients with generalised myasthenia gravis."
}
] | 12 |
BioASQ-training12b
| null | null |
64040d73201352f04a000010
|
bioasq_yesno
|
factoid
|
Where are the PUX proteins found?
|
['PUX proteins specifically associate with the nucleoskeleton underneath the INM.']
|
[
"PUX proteins",
"PUX",
"PUX family proteins",
"PUX protein family"
] |
['PUX proteins specifically associate with the nucleoskeleton underneath the INM.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/32601292",
"http://www.ncbi.nlm.nih.gov/pubmed/34141135"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32601292",
"endSection": "abstract",
"offsetInBeginSection": 849,
"offsetInEndSection": 1036,
"text": " These PUX proteins specifically associate with the nucleoskeleton underneath the INM and physically interact with CDC48 proteins to negatively regulate INM protein degradation in plants."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34141135",
"endSection": "title",
"offsetInBeginSection": 47,
"offsetInEndSection": 83,
"text": " plant UBX-containing (PUX) proteins"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34141135",
"endSection": "abstract",
"offsetInBeginSection": 425,
"offsetInEndSection": 813,
"text": "The activity and targeting of CDC48 are controlled by adaptor proteins, of which the plant ubiquitin regulatory X (UBX) domain-containing (PUX) proteins constitute the largest family. Emerging knowledge on the structure and function of PUX proteins highlights that these proteins are versatile factors for plant homeostasis and adaptation that might inspire biotechnological applications."
}
] | 11 |
BioASQ-training11b
| null | null |
621b54f03a8413c65300003b
|
bioasq_factoid
|
factoid
|
What molecule is targeted by suvorexant?
|
[['orexin']]
|
[
"orexin",
"hypocretin"
] |
['Suvorexant is a dual orexin receptor antagonist for the treatment of sleep onset and sleep maintenance insomnia.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26478806",
"http://www.ncbi.nlm.nih.gov/pubmed/25667197",
"http://www.ncbi.nlm.nih.gov/pubmed/25533960",
"http://www.ncbi.nlm.nih.gov/pubmed/25489915",
"http://www.ncbi.nlm.nih.gov/pubmed/21473737",
"http://www.ncbi.nlm.nih.gov/pubmed/23197752",
"http://www.ncbi.nlm.nih.gov/pubmed/25406050",
"http://www.ncbi.nlm.nih.gov/pubmed/24757363",
"http://www.ncbi.nlm.nih.gov/pubmed/25397996",
"http://www.ncbi.nlm.nih.gov/pubmed/22920041"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26478806",
"endSection": "abstract",
"offsetInBeginSection": 605,
"offsetInEndSection": 773,
"text": "Suvorexant is the first DORA to be approved and has demonstrated efficacy at decreasing both time to sleep onset and increasing total sleep time compared with placebo. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25667197",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Suvorexant: a dual orexin receptor antagonist for the treatment of sleep onset and sleep maintenance insomnia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25667197",
"endSection": "abstract",
"offsetInBeginSection": 1221,
"offsetInEndSection": 1329,
"text": "CONCLUSION: Suvorexant is the first dual orexin receptor antagonist approved for the treatment of insomnia. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25533960",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "Crystal structure of the human OX2 orexin receptor bound to the insomnia drug suvorexant."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25533960",
"endSection": "abstract",
"offsetInBeginSection": 362,
"offsetInEndSection": 594,
"text": " The human OX2 receptor (OX2R) belongs to the β branch of the rhodopsin family of GPCRs, and can bind to diverse compounds including the native agonist peptides orexin-A and orexin-B and the potent therapeutic inhibitor suvorexant. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23197752",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "Orexin receptor antagonism for treatment of insomnia: a randomized clinical trial of suvorexant."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21473737",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 73,
"text": "Promotion of sleep by suvorexant-a novel dual orexin receptor antagonist."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23197752",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "Orexin receptor antagonism for treatment of insomnia: a randomized clinical trial of suvorexant."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21473737",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 73,
"text": "Promotion of sleep by suvorexant-a novel dual orexin receptor antagonist."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23197752",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "Orexin receptor antagonism for treatment of insomnia: a randomized clinical trial of suvorexant."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21473737",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 73,
"text": "Promotion of sleep by suvorexant-a novel dual orexin receptor antagonist."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23197752",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "Orexin receptor antagonism for treatment of insomnia: a randomized clinical trial of suvorexant."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25406050",
"endSection": "abstract",
"offsetInBeginSection": 588,
"offsetInEndSection": 1041,
"text": "The neurotransmitter systems on which the development of these agents were based included serotonin for ondansetron and lorcaserin, dopamine for varenicline, substance P (or neurokinin) for aprepitant, melatonin for ramelteon, and orexin for suvorexant. The indications were chemotherapy-induced nausea and vomiting for ondansetron and aprepitant, smoking cessation for varenicline, weight loss for lorcaserin, and insomnia for suvorexant and ramelteon."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21473737",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 73,
"text": "Promotion of sleep by suvorexant-a novel dual orexin receptor antagonist."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23197752",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "Orexin receptor antagonism for treatment of insomnia: a randomized clinical trial of suvorexant."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21473737",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 73,
"text": "Promotion of sleep by suvorexant-a novel dual orexin receptor antagonist."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24757363",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 77,
"text": "Suvorexant, a dual orexin receptor antagonist for the management of insomnia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24757363",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 77,
"text": "Suvorexant, a dual orexin receptor antagonist for the management of insomnia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25489915",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 302,
"text": "The orexin-1 and orexin-2 receptors are two G protein-coupled receptors that bind the neuropeptides orexin-A and orexin-B. Dual antagonism of the receptors by small molecules is clinically efficacious in the treatment of insomnia, where the most advanced molecule suvorexant has recently been approved."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25397996",
"endSection": "abstract",
"offsetInBeginSection": 207,
"offsetInEndSection": 283,
"text": "Suvorexant helps in decreasing wakefulness by counteracting orexin activity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25489915",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 303,
"text": " The orexin-1 and orexin-2 receptors are two G protein-coupled receptors that bind the neuropeptides orexin-A and orexin-B. Dual antagonism of the receptors by small molecules is clinically efficacious in the treatment of insomnia, where the most advanced molecule suvorexant has recently been approved."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22920041",
"endSection": "abstract",
"offsetInBeginSection": 388,
"offsetInEndSection": 760,
"text": "Hypnotic drug development has arguably become more focused in recent years, particularly upon the highly anticipated novel target, the orexin (hypocretin) system. Merck's suvorexant (MK-4305) is the first compound of the so-called dual orexin receptor antagonist (DORA) class expected to be submitted for FDA approval, with a new drug application anticipated in 2012."
}
] | 5 |
BioASQ-training5b
|
[] |
[] |
56c1f003ef6e394741000039
|
bioasq_factoid
|
factoid
|
What is the target of tanezumab?
|
['nerve growth factor', 'NGF']
|
[
"nerve growth factor",
"NGF",
"beta-nerve growth factor",
"beta-NGF",
"nerve growth factor 1",
"NGF1",
"nerve growth factor alpha",
"NGF-alpha"
] |
['Tanezumab is a humanized monoclonal antibody against nerve growth factor.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22004765",
"http://www.ncbi.nlm.nih.gov/pubmed/18505735",
"http://www.ncbi.nlm.nih.gov/pubmed/24452657",
"http://www.ncbi.nlm.nih.gov/pubmed/27936977",
"http://www.ncbi.nlm.nih.gov/pubmed/25326242",
"http://www.ncbi.nlm.nih.gov/pubmed/21130822",
"http://www.ncbi.nlm.nih.gov/pubmed/23628600",
"http://www.ncbi.nlm.nih.gov/pubmed/21696889",
"http://www.ncbi.nlm.nih.gov/pubmed/21420111",
"http://www.ncbi.nlm.nih.gov/pubmed/24830649",
"http://www.ncbi.nlm.nih.gov/pubmed/24809946",
"http://www.ncbi.nlm.nih.gov/pubmed/27381034",
"http://www.ncbi.nlm.nih.gov/pubmed/23707270",
"http://www.ncbi.nlm.nih.gov/pubmed/24691709",
"http://www.ncbi.nlm.nih.gov/pubmed/21802499",
"http://www.ncbi.nlm.nih.gov/pubmed/25527221",
"http://www.ncbi.nlm.nih.gov/pubmed/25073573",
"http://www.ncbi.nlm.nih.gov/pubmed/20942668",
"http://www.ncbi.nlm.nih.gov/pubmed/23852695",
"http://www.ncbi.nlm.nih.gov/pubmed/23010344",
"http://www.ncbi.nlm.nih.gov/pubmed/26962464",
"http://www.ncbi.nlm.nih.gov/pubmed/26940379",
"http://www.ncbi.nlm.nih.gov/pubmed/25594611",
"http://www.ncbi.nlm.nih.gov/pubmed/23028238",
"http://www.ncbi.nlm.nih.gov/pubmed/20140821"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27381034",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "Nerve growth factor inhibition with tanezumab influences weight-bearing and subsequent cartilage damage in the rat medial meniscal tear model."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27381034",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 229,
"text": "OBJECTIVE: To investigate whether the effects of nerve growth factor (NGF) inhibition with tanezumab on rats with medial meniscal tear (MMT) effectively model rapidly progressive osteoarthritis (RPOA) observed in clinical trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26962464",
"endSection": "abstract",
"offsetInBeginSection": 559,
"offsetInEndSection": 847,
"text": " Current research focuses on the development of new OA drugs (such as sprifermin/recombinant human fibroblast growth factor-18, tanezumab/monoclonal antibody against β-nerve growth factor), which aims for more effectiveness and less incidence of adverse effects than the traditional ones."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27936977",
"endSection": "abstract",
"offsetInBeginSection": 549,
"offsetInEndSection": 775,
"text": "Areas covered: This manuscript is a review that examines both the pharmacological properties and clinical studies of tanezumab, the most widely studied antibody to NGF, for management of osteoarthritis (OA) and low back pain. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25594611",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "OBJECTIVE: Evaluate efficacy and safety of tanezumab, a humanized monoclonal antibody against nerve growth factor, in neuropathic pain."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20140821",
"endSection": "abstract",
"offsetInBeginSection": 696,
"offsetInEndSection": 852,
"text": "In preclinical studies, tanezumab, and its murine precursor muMab-911, effectively targeted the NGF pathway in various chronic and inflammatory pain models."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20140821",
"endSection": "abstract",
"offsetInBeginSection": 514,
"offsetInEndSection": 696,
"text": "Tanezumab (RN-624), a first-in-class recombinant humanized mAb targeting NGF, is being developed by Pfizer Inc for the potential treatment of pain associated with several conditions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20140821",
"endSection": "abstract",
"offsetInBeginSection": 1029,
"offsetInEndSection": 1343,
"text": "Given that tanezumab is an antibody, the drug demonstrates the general advantages of this class of products (including good specificity and favorable pharmacokinetics), and also appears to be particularly well suited for targeting the chronic and inflammatory-mediating pain actions of NGF and its receptor system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21420111",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 323,
"text": "In this randomized, double-blind, placebo controlled phase 2 study we investigated tanezumab, a humanized monoclonal antibody that specifically inhibits nerve growth factor as a treatment for interstitial cystitis pain.Patients with interstitial cystitis received a single intravenous dose of 200 μg/kg tanezumab or placebo"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25073573",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 78,
"text": "Nerve safety of tanezumab, a nerve growth factor inhibitor for pain treatment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20140821",
"endSection": "abstract",
"offsetInBeginSection": 700,
"offsetInEndSection": 856,
"text": "In preclinical studies, tanezumab, and its murine precursor muMab-911, effectively targeted the NGF pathway in various chronic and inflammatory pain models."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20140821",
"endSection": "abstract",
"offsetInBeginSection": 517,
"offsetInEndSection": 699,
"text": "Tanezumab (RN-624), a first-in-class recombinant humanized mAb targeting NGF, is being developed by Pfizer Inc for the potential treatment of pain associated with several conditions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20140821",
"endSection": "abstract",
"offsetInBeginSection": 1035,
"offsetInEndSection": 1350,
"text": "Given that tanezumab is an antibody, the drug demonstrates the general advantages of this class of products (including good specificity and favorable pharmacokinetics), and also appears to be particularly well suited for targeting the chronic and inflammatory-mediating pain actions of NGF and its receptor system.."
}
] | 6 |
BioASQ-training6b
| null | null |
5890e163621ea6ff7e000004
|
bioasq_factoid
|
yesno
|
Is DITPA a thyroid hormone analog utilized in experimental and clinical studies
|
['yes']
|
[
"yes"
] |
There is very large body of evidence that DITPA is a true thyroid hormone analog, largely utilized in experimental and clinical studies.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22993035",
"http://www.ncbi.nlm.nih.gov/pubmed/21215270",
"http://www.ncbi.nlm.nih.gov/pubmed/21658725",
"http://www.ncbi.nlm.nih.gov/pubmed/21131480",
"http://www.ncbi.nlm.nih.gov/pubmed/19506112",
"http://www.ncbi.nlm.nih.gov/pubmed/19286941",
"http://www.ncbi.nlm.nih.gov/pubmed/18353884",
"http://www.ncbi.nlm.nih.gov/pubmed/18030062",
"http://www.ncbi.nlm.nih.gov/pubmed/17612639",
"http://www.ncbi.nlm.nih.gov/pubmed/16616210",
"http://www.ncbi.nlm.nih.gov/pubmed/15454853",
"http://www.ncbi.nlm.nih.gov/pubmed/16384862",
"http://www.ncbi.nlm.nih.gov/pubmed/12414442",
"http://www.ncbi.nlm.nih.gov/pubmed/10749704",
"http://www.ncbi.nlm.nih.gov/pubmed/9618233",
"http://www.ncbi.nlm.nih.gov/pubmed/9069582",
"http://www.ncbi.nlm.nih.gov/pubmed/1403782",
"http://www.ncbi.nlm.nih.gov/pubmed/15572044",
"http://www.ncbi.nlm.nih.gov/pubmed/15148346",
"http://www.ncbi.nlm.nih.gov/pubmed/19903697",
"http://www.ncbi.nlm.nih.gov/pubmed/10474790",
"http://www.ncbi.nlm.nih.gov/pubmed/12165118",
"http://www.ncbi.nlm.nih.gov/pubmed/12145478",
"http://www.ncbi.nlm.nih.gov/pubmed/8936682",
"http://www.ncbi.nlm.nih.gov/pubmed/20080837",
"http://www.ncbi.nlm.nih.gov/pubmed/20192904",
"http://www.ncbi.nlm.nih.gov/pubmed/7828308",
"http://www.ncbi.nlm.nih.gov/pubmed/8353891",
"http://www.ncbi.nlm.nih.gov/pubmed/11040100",
"http://www.ncbi.nlm.nih.gov/pubmed/15072976",
"http://www.ncbi.nlm.nih.gov/pubmed/17710084",
"http://www.ncbi.nlm.nih.gov/pubmed/10710355",
"http://www.ncbi.nlm.nih.gov/pubmed/18954857",
"http://www.ncbi.nlm.nih.gov/pubmed/10329215"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22993035",
"endSection": "abstract",
"offsetInBeginSection": 1036,
"offsetInEndSection": 1174,
"text": "DITPA normalized the elevated serum T(3) and TSH when the dose reached 1 mg/kg · d and T(4) and rT(3) increased to the lower normal range."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21215270",
"endSection": "abstract",
"offsetInBeginSection": 828,
"offsetInEndSection": 1067,
"text": "The identification of 3,5-diiodothyropropionic acid (DITPA) that binds to both α- and β-type TRs with relatively low affinity was unique in that this analog improves left ventricular function in heart failure as well as lowers cholesterol."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21658725",
"endSection": "abstract",
"offsetInBeginSection": 1837,
"offsetInEndSection": 1937,
"text": "Treatment with DITPA attenuates the acute inflammatory response and reduces myocardial infarct size."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21131480",
"endSection": "abstract",
"offsetInBeginSection": 1790,
"offsetInEndSection": 1913,
"text": "Thus DITPA administration impairs baseline cardiac parameters in mice and can be fatal during in vivo acute myocardial I/R."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19506112",
"endSection": "abstract",
"offsetInBeginSection": 1308,
"offsetInEndSection": 1443,
"text": "DITPA improved some hemodynamic and metabolic parameters, but there was no evidence for symptomatic benefit in congestive heart failure"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19286941",
"endSection": "abstract",
"offsetInBeginSection": 1468,
"offsetInEndSection": 1593,
"text": "The results suggested that DITPA can promote a healthy vasculature independently from its thyroid-related metabolic effects. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18353884",
"endSection": "abstract",
"offsetInBeginSection": 1583,
"offsetInEndSection": 1693,
"text": " Moreover, DITPA and T(4) were efficacious in preventing effects of hypothyroidism on cardiac function and BVD"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17612639",
"endSection": "abstract",
"offsetInBeginSection": 1194,
"offsetInEndSection": 1349,
"text": "Both T4 and DITPA had beneficial effects on chamber remodeling, which was most likely due to beneficial changes in cell shape and improved vascular supply."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15454853",
"endSection": "abstract",
"offsetInBeginSection": 1390,
"offsetInEndSection": 1539,
"text": "The thyroid analog DITPA enhances endothelial nitric oxide and beta-adrenergic-mediated vasorelaxation by increasing nitric oxide in the vasculature."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013956",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013963",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D011988",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D037021",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D037042",
"http://www.biosemantics.org/jochem#4021241"
] |
[] |
52fb4b462059c6d71c00005f
|
bioasq_yesno
|
factoid
|
Talquetamab was developed for treatment of which disease?
|
['multiple myeloma']
|
[
"multiple myeloma",
"plasma cell myeloma",
"myeloma",
"Kahler's disease",
"myelomatosis"
] |
['Talquetamab was developed for treatment of multiple myeloma.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/36352205",
"http://www.ncbi.nlm.nih.gov/pubmed/36006441"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36006441",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "Effects of teclistamab and talquetamab on soluble BCMA levels in patients with relapsed/refractory multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36006441",
"endSection": "abstract",
"offsetInBeginSection": 224,
"offsetInEndSection": 406,
"text": "The bispecific antibodies teclistamab (BCMA×CD3) and talquetamab (G protein-coupled receptor family C group 5 member D [GPRC5D]×CD3) are in clinical development as therapies for MM. "
}
] | 12 |
BioASQ-training12b
| null | null |
63eeec79f36125a426000006
|
bioasq_factoid
|
yesno
|
Does Jarid2 play a role in early embryo development?
|
['yes']
|
[
"yes"
] |
['Yes. Jarid2 coordinates Nanog expression and PCP/Wnt signaling required for efficient ESC differentiation and early embryo development.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/20075857",
"http://www.ncbi.nlm.nih.gov/pubmed/26190104",
"http://www.ncbi.nlm.nih.gov/pubmed/17521633",
"http://www.ncbi.nlm.nih.gov/pubmed/24374312"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26190104",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Jarid2 Coordinates Nanog Expression and PCP/Wnt Signaling Required for Efficient ESC Differentiation and Early Embryo Development"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26190104",
"endSection": "abstract",
"offsetInBeginSection": 107,
"offsetInEndSection": 1159,
"text": "Unlike other PRC2-deficient embryonic stem cells (ESCs), however, Jarid2-deficient ESCs show a severe differentiation block, altered colony morphology, and distinctive patterns of deregulated gene expression. Here, we show that Jarid2(-/-) ESCs express constitutively high levels of Nanog but reduced PCP signaling components Wnt9a, Prickle1, and Fzd2 and lowered β-catenin activity. Depletion of Wnt9a/Prickle1/Fzd2 from wild-type ESCs or overexpression of Nanog largely phenocopies these cellular defects. Co-culture of Jarid2(-/-) with wild-type ESCs restores variable Nanog expression and β-catenin activity and can partially rescue the differentiation block of mutant cells. In addition, we show that ESCs lacking Jarid2 or Wnt9a/Prickle1/Fzd2 or overexpressing Nanog induce multiple ICM formation when injected into normal E3.5 blastocysts. These data describe a previously unrecognized role for Jarid2 in regulating a core pluripotency and Wnt/PCP signaling circuit that is important for ESC differentiation and for pre-implantation development."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26190104",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Jarid2 Coordinates Nanog Expression and PCP/Wnt Signaling Required for Efficient ESC Differentiation and Early Embryo Development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20075857",
"endSection": "abstract",
"offsetInBeginSection": 909,
"offsetInEndSection": 1075,
"text": "Consistent with an essential role for PcG proteins in early development, we demonstrate that JARID2 is required for the differentiation of mouse embryonic stem cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17521633",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "Jumonij (JMJ)/Jarid2 plays important roles in embryonic development and functions as a transcriptional repressor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20075857",
"endSection": "abstract",
"offsetInBeginSection": 1083,
"offsetInEndSection": 1293,
"text": "Thus, these results demonstrate that JARID2 is essential for the binding of PcG proteins to target genes and, consistent with this, for the proper differentiation of embryonic stem cells and normal development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24374312",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 137,
"text": "JARID2 is an accessory component of Polycomb repressive complex-2 (PRC2) required for the differentiation of embryonic stem cells (ESCs)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26190104",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Jarid2 Coordinates Nanog Expression and PCP/Wnt Signaling Required for Efficient ESC Differentiation and Early Embryo Development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26190104",
"endSection": "abstract",
"offsetInBeginSection": 954,
"offsetInEndSection": 1160,
"text": "These data describe a previously unrecognized role for Jarid2 in regulating a core pluripotency and Wnt/PCP signaling circuit that is important for ESC differentiation and for pre-implantation development.."
}
] | 6 |
BioASQ-training6b
|
[
"http://amigo.geneontology.org/amigo/term/GO:0009790",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D047108",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D005314",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D063146"
] |
[
{
"o": "JARID2",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C1416528"
},
{
"o": "JARID2",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/#_5139323833330020"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A20738817",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C1416528"
}
] |
5883781b2305cd7e21000001
|
bioasq_yesno
|
factoid
|
Which type of myeloma is ixazomib being evaluated for?
|
[['Multiple myeloma']]
|
[
"Multiple myeloma",
"Plasma cell myeloma",
"Myeloma",
"Kahler's disease",
"Kahler disease"
] |
['The disease focus for the irreversible epoxyketone proteasome inhibitor ixazomib is multiple myeloma.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24471924",
"http://www.ncbi.nlm.nih.gov/pubmed/25935605",
"http://www.ncbi.nlm.nih.gov/pubmed/25456369",
"http://www.ncbi.nlm.nih.gov/pubmed/25302026",
"http://www.ncbi.nlm.nih.gov/pubmed/24920586",
"http://www.ncbi.nlm.nih.gov/pubmed/24486586",
"http://www.ncbi.nlm.nih.gov/pubmed/24292417",
"http://www.ncbi.nlm.nih.gov/pubmed/24904120",
"http://www.ncbi.nlm.nih.gov/pubmed/25268212",
"http://www.ncbi.nlm.nih.gov/pubmed/24578203",
"http://www.ncbi.nlm.nih.gov/pubmed/24712303"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25935605",
"endSection": "abstract",
"offsetInBeginSection": 353,
"offsetInEndSection": 707,
"text": "Next generation proteasome inhibitors include carfilzomib and oprozomib which are irreversible epoxyketone proteasome inhibitors; and ixazomib and delanzomib which are reversible boronic acid proteasome inhibitors. Two proteasome inhibitors, bortezomib and carfilzomib are FDA approved drugs and ixazomib and oprozomib are in late stage clinical trials. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25935605",
"endSection": "abstract",
"offsetInBeginSection": 748,
"offsetInEndSection": 820,
"text": "The disease focus for all the proteasome inhibitors is multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24471924",
"endSection": "abstract",
"offsetInBeginSection": 725,
"offsetInEndSection": 1071,
"text": "In addition, novel drug classes have shown promising activity in RR MM, including the orally-administered proteasome inhibitors ixazomib and oprozomib; monoclonal antibodies such as the anti-CS1 monoclonal antibody elotuzumab and anti-CD38 monoclonal antibody daratumumab; and histone deacetylase inhibitors such as panobinostat and rocilinostat."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24920586",
"endSection": "abstract",
"offsetInBeginSection": 1357,
"offsetInEndSection": 1454,
"text": "These findings have informed the subsequent clinical development of ixazomib in multiple myeloma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24920586",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Phase 1 study of twice-weekly ixazomib, an oral proteasome inhibitor, in relapsed/refractory multiple myeloma patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25302026",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "An evidence-based review of ixazomib citrate and its potential in the treatment of newly diagnosed multiple myeloma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24904120",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Phase 1 study of weekly dosing with the investigational oral proteasome inhibitor ixazomib in relapsed/refractory multiple myeloma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24292417",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 214,
"text": "(18)F-FDG-PET/CT imaging in an IL-6- and MYC-driven mouse model of human multiple myeloma affords objective evaluation of plasma cell tumor progression and therapeutic response to the proteasome inhibitor ixazomib."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24292417",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 214,
"text": "(18)F-FDG-PET/CT imaging in an IL-6- and MYC-driven mouse model of human multiple myeloma affords objective evaluation of plasma cell tumor progression and therapeutic response to the proteasome inhibitor ixazomib."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24904120",
"endSection": "abstract",
"offsetInBeginSection": 506,
"offsetInEndSection": 750,
"text": "Sixty patients with relapsed and/or refractory multiple myeloma were enrolled on this phase 1 trial to evaluate safety and tolerability and determine the maximum tolerated dose (MTD) of single-agent, oral ixazomib given weekly for 3 of 4 weeks."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24920586",
"endSection": "abstract",
"offsetInBeginSection": 1357,
"offsetInEndSection": 1454,
"text": "These findings have informed the subsequent clinical development of ixazomib in multiple myeloma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24920586",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Phase 1 study of twice-weekly ixazomib, an oral proteasome inhibitor, in relapsed/refractory multiple myeloma patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25302026",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "An evidence-based review of ixazomib citrate and its potential in the treatment of newly diagnosed multiple myeloma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24904120",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Phase 1 study of weekly dosing with the investigational oral proteasome inhibitor ixazomib in relapsed/refractory multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24904120",
"endSection": "abstract",
"offsetInBeginSection": 265,
"offsetInEndSection": 508,
"text": "Sixty patients with relapsed and/or refractory multiple myeloma were enrolled on this phase 1 trial to evaluate safety and tolerability and determine the maximum tolerated dose (MTD) of single-agent, oral ixazomib given weekly for 3 of 4 weeks"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25302026",
"endSection": "abstract",
"offsetInBeginSection": 543,
"offsetInEndSection": 675,
"text": "Among second-generation proteasome inhibitors, ixazomib (MLN9708) is the first oral compound to be evaluated for the treatment of MM"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24904120",
"endSection": "abstract",
"offsetInBeginSection": 265,
"offsetInEndSection": 510,
"text": "Sixty patients with relapsed and/or refractory multiple myeloma were enrolled on this phase 1 trial to evaluate safety and tolerability and determine the maximum tolerated dose (MTD) of single-agent, oral ixazomib given weekly for 3 of 4 weeks. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24904120",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Phase 1 study of weekly dosing with the investigational oral proteasome inhibitor ixazomib in relapsed/refractory multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24920586",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 396,
"text": "Ixazomib is the first investigational oral proteasome inhibitor to be studied clinically. In this phase 1 trial, 60 patients with relapsed/refractory multiple myeloma (median of 4 prior lines of therapy; bortezomib, lenalidomide, thalidomide, and carfilzomib/marizomib in 88%, 88%, 62%, and 5%, respectively) received single-agent ixazomib 0.24 to 2.23 mg/m(2) (days 1, 4, 8, 11; 21-day cycles). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25456369",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 204,
"text": "Safety and tolerability of ixazomib, an oral proteasome inhibitor, in combination with lenalidomide and dexamethasone in patients with previously untreated multiple myeloma: an open-label phase 1/2 study."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24920586",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Phase 1 study of twice-weekly ixazomib, an oral proteasome inhibitor, in relapsed/refractory multiple myeloma patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24904120",
"endSection": "abstract",
"offsetInBeginSection": 265,
"offsetInEndSection": 510,
"text": "Sixty patients with relapsed and/or refractory multiple myeloma were enrolled on this phase 1 trial to evaluate safety and tolerability and determine the maximum tolerated dose (MTD) of single-agent, oral ixazomib given weekly for 3 of 4 weeks. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24904120",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Phase 1 study of weekly dosing with the investigational oral proteasome inhibitor ixazomib in relapsed/refractory multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25456369",
"endSection": "abstract",
"offsetInBeginSection": 278,
"offsetInEndSection": 892,
"text": "In a phase 1/2 trial we aimed to assess the safety, tolerability, and activity of ixazomib in combination with lenalidomide and dexamethasone in newly diagnosed multiple myeloma.METHODS: We enrolled patients newly diagnosed with multiple myeloma aged 18 years or older with measurable disease, Eastern Cooperative Oncology Group performance status 0-2, and no grade 2 or higher peripheral neuropathy, and treated them with oral ixazomib (days 1, 8, 15) plus lenalidomide 25 mg (days 1-21) and dexamethasone 40 mg (days 1, 8, 15, 22) for up to 12 28-day cycles, followed by maintenance therapy with ixazomib alone. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25456369",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 204,
"text": "Safety and tolerability of ixazomib, an oral proteasome inhibitor, in combination with lenalidomide and dexamethasone in patients with previously untreated multiple myeloma: an open-label phase 1/2 study."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24920586",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Phase 1 study of twice-weekly ixazomib, an oral proteasome inhibitor, in relapsed/refractory multiple myeloma patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24904120",
"endSection": "abstract",
"offsetInBeginSection": 265,
"offsetInEndSection": 510,
"text": "Sixty patients with relapsed and/or refractory multiple myeloma were enrolled on this phase 1 trial to evaluate safety and tolerability and determine the maximum tolerated dose (MTD) of single-agent, oral ixazomib given weekly for 3 of 4 weeks. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24904120",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Phase 1 study of weekly dosing with the investigational oral proteasome inhibitor ixazomib in relapsed/refractory multiple myeloma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24920586",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Phase 1 study of twice-weekly ixazomib, an oral proteasome inhibitor, in relapsed/refractory multiple myeloma patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24904120",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Phase 1 study of weekly dosing with the investigational oral proteasome inhibitor ixazomib in relapsed/refractory multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24904120",
"endSection": "abstract",
"offsetInBeginSection": 265,
"offsetInEndSection": 510,
"text": "Sixty patients with relapsed and/or refractory multiple myeloma were enrolled on this phase 1 trial to evaluate safety and tolerability and determine the maximum tolerated dose (MTD) of single-agent, oral ixazomib given weekly for 3 of 4 weeks. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24904120",
"endSection": "abstract",
"offsetInBeginSection": 265,
"offsetInEndSection": 510,
"text": "Sixty patients with relapsed and/or refractory multiple myeloma were enrolled on this phase 1 trial to evaluate safety and tolerability and determine the maximum tolerated dose (MTD) of single-agent, oral ixazomib given weekly for 3 of 4 weeks. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24920586",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Phase 1 study of twice-weekly ixazomib, an oral proteasome inhibitor, in relapsed/refractory multiple myeloma patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25302026",
"endSection": "abstract",
"offsetInBeginSection": 544,
"offsetInEndSection": 872,
"text": "Among second-generation proteasome inhibitors, ixazomib (MLN9708) is the first oral compound to be evaluated for the treatment of MM. Ixazomib has shown improved pharmacokinetic and pharmacodynamic parameters compared with bortezomib, in addition to similar efficacy in the control of myeloma growth and prevention of bone loss."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24920586",
"endSection": "abstract",
"offsetInBeginSection": 1161,
"offsetInEndSection": 1368,
"text": "Among 55 response-evaluable patients, 15% achieved partial response or better (76% stable disease or better). These findings have informed the subsequent clinical development of ixazomib in multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24920586",
"endSection": "abstract",
"offsetInBeginSection": 1161,
"offsetInEndSection": 1368,
"text": "Among 55 response-evaluable patients, 15% achieved partial response or better (76% stable disease or better). These findings have informed the subsequent clinical development of ixazomib in multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24920586",
"endSection": "abstract",
"offsetInBeginSection": 1161,
"offsetInEndSection": 1368,
"text": "Among 55 response-evaluable patients, 15% achieved partial response or better (76% stable disease or better). These findings have informed the subsequent clinical development of ixazomib in multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24904120",
"endSection": "abstract",
"offsetInBeginSection": 188,
"offsetInEndSection": 510,
"text": "Ixazomib is an investigational, orally bioavailable 20S proteasome inhibitor. Sixty patients with relapsed and/or refractory multiple myeloma were enrolled on this phase 1 trial to evaluate safety and tolerability and determine the maximum tolerated dose (MTD) of single-agent, oral ixazomib given weekly for 3 of 4 weeks."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24920586",
"endSection": "abstract",
"offsetInBeginSection": 1161,
"offsetInEndSection": 1368,
"text": "Among 55 response-evaluable patients, 15% achieved partial response or better (76% stable disease or better). These findings have informed the subsequent clinical development of ixazomib in multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24920586",
"endSection": "abstract",
"offsetInBeginSection": 1161,
"offsetInEndSection": 1368,
"text": "Among 55 response-evaluable patients, 15% achieved partial response or better (76% stable disease or better). These findings have informed the subsequent clinical development of ixazomib in multiple myeloma."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D009101"
] |
[] |
56ed0ffe2ac5ed1459000008
|
bioasq_factoid
|
factoid
|
What are the proteins that are necessary for the use of lactose in E. coli collectively called?
|
['Lac operon']
|
[
"Lac operon",
"lactose operon",
"lactose operon system",
"lacZYA operon",
"lac operon system"
] |
['The proteins necessary for the use of lactose in E. coli are collectively called the lac operon. This gene regulatory circuit controls the transcription of genes involved in lactose metabolism and is nearly ubiquitous in E. coli strains, making it a useful phenotype for species identification. The activity of the lac operon is controlled by both cis- and trans-acting regulators, which integrate environmental signals such as glucose and lactose availability to fine-tune gene expression. While most studies of lac operon regulation have focused on a few closely related strains, this system remains an important model for understanding how bacteria adapt their metabolism to changing nutritional conditions.', 'Transcription of bacterial genes is controlled by the coordinated action of cis- and trans-acting regulators. The activity and mode of action of these regulators can reflect different requirements for gene products in different environments. The lac operon is one of the best-known gene regulatory circuits and constitutes a landmark example of how bacteria tune their metabolism to nutritional conditions. It is nearly ubiquitous in Escherichia coli strains justifying the use of its phenotype, the ability to consume lactose, for species identification.', 'The proteins necessary for the use of lactose in Escherichia coli (E. coli) are collectively referred to as the lac operon. The lac operon is a well-known gene regulatory circuit that serves as a landmark example of how bacteria adjust their metabolism according to nutritional conditions. It is nearly ubiquitous in E. coli strains, and its phenotype, the ability to consume lactose, is used for species identification. The transcription of bacterial genes within the lac operon is controlled by the coordinated action of cis- and trans-acting regulators, which integrate environmental availability of glucose and lactose to regulate gene expression. Most studies on lac operon regulation have focused on a few closely related strains of E. coli.', 'The proteins necessary for the use of lactose in Escherichia coli (E. coli) are collectively called the lac operon. The lac operon is a set of genes that encode proteins involved in the transport and metabolism of lactose, allowing E. coli to utilize this sugar as an energy source when glucose is scarce. The primary components of the lac operon include three structural genes: lacZ, lacY, and lacA. The lacZ gene encodes β-galactosidase, an enzyme responsible for cleaving lactose into glucose and galactose. The lacY gene encodes lactose permease, a membrane protein that facilitates the transport of lactose into the cell. Lastly, the lacA gene encodes thiogalactoside transacetylase, which detoxifies certain byproducts generated during lactose metabolism. Additionally, regulatory elements such as the promoter region (lacP), operator region (lacO), and repressor protein (LacI) play crucial roles in controlling the expression of these genes in response to environmental conditions like lactose availability and glucose levels.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/31719176",
"http://www.ncbi.nlm.nih.gov/pubmed/34367115",
"http://www.ncbi.nlm.nih.gov/pubmed/34891476",
"http://www.ncbi.nlm.nih.gov/pubmed/34953812",
"http://www.ncbi.nlm.nih.gov/pubmed/26415599"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34367115",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 313,
"text": "The lac operon is one of the best known gene regulatory circuits and constitutes a landmark example of how bacteria tune their metabolism to nutritional conditions. It is nearly ubiquitous in Escherichia coli strains justifying the use of its phenotype, the ability to consume lactose, for species identification."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31719176",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 489,
"text": "Transcription of bacterial genes is controlled by the coordinated action of cis- and trans-acting regulators. The activity and mode of action of these regulators can reflect different requirements for gene products in different environments. A well-studied example is the regulatory function that integrates the environmental availability of glucose and lactose to control the Escherichia colilac operon. Most studies of lac operon regulation have focused on a few closely related strains."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34953812",
"endSection": "abstract",
"offsetInBeginSection": 111,
"offsetInEndSection": 278,
"text": "In the induced state of the lac pathway, the genes comprising the lac operon are transcribed, leading to the production of proteins that import and metabolize lactose."
}
] | 12 |
BioASQ-training12b
| null | null |
644ec7fe57b1c7a315000082
|
bioasq_factoid
|
yesno
|
Is MK-1602 a CGRP antagonist?
|
['yes']
|
[
"yes"
] |
['Yes, MK-1602 is a CGRP antagonist.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27269043"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27269043",
"endSection": "abstract",
"offsetInBeginSection": 5,
"offsetInEndSection": 199,
"text": "The aim of this trial was to evaluate the efficacy and tolerability of ubrogepant (MK-1602), a calcitonin gene-related peptide receptor antagonist (CGRP-RA), for the acute treatment of migraine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27269043",
"endSection": "abstract",
"offsetInBeginSection": 1412,
"offsetInEndSection": 1553,
"text": "This trial supports ubrogepant's efficacy and provides further evidence that CGRP-RAs are viable options for the acute treatment of migraine."
}
] | 11 |
BioASQ-training11b
| null | null |
6026c1071cb411341a0000cb
|
bioasq_yesno
|
factoid
|
What is OAC CHV?
|
["Layman's term vocabulary for health related terms"]
|
[
"health vocabulary",
"health-related vocabulary",
"layman's terms for health",
"common health terms",
"everyday health vocabulary",
"simple health terminology",
"health jargon in layman's terms",
"plain language health terms",
"health terms for the general public",
"health terminology for non-experts",
"accessible health vocabulary",
"health terms explained simply",
"health lexicon for laypeople",
"health-related terms in simple language",
"vocabulary for health literacy"
] |
['The Open Access and Collaborative Consumer Health Vocabulary (OAC CHV), which contains health-related terms used by lay consumers,', 'The Open Access and Collaborative Consumer Health Vocabulary (OAC CHV), contains health-related terms used by lay consumers.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28359728",
"http://www.ncbi.nlm.nih.gov/pubmed/27884812"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27884812",
"endSection": "abstract",
"offsetInBeginSection": 1234,
"offsetInEndSection": 1296,
"text": "Open-Access Collaborative Consumer Health Vocabulary (OAC CHV)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28359728",
"endSection": "abstract",
"offsetInBeginSection": 180,
"offsetInEndSection": 311,
"text": "The Open Access and Collaborative Consumer Health Vocabulary (OAC CHV), which contains health-related terms used by lay consumers, "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28359728",
"endSection": "abstract",
"offsetInBeginSection": 180,
"offsetInEndSection": 349,
"text": "The Open Access and Collaborative Consumer Health Vocabulary (OAC CHV), which contains health-related terms used by lay consumers, has been created to bridge such a gap."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28359728",
"endSection": "abstract",
"offsetInBeginSection": 350,
"offsetInEndSection": 550,
"text": "Specifically, the OAC CHV facilitates consumers' health information retrieval by enabling consumer-facing health applications to translate between professional language and consumer friendly language."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28359728",
"endSection": "abstract",
"offsetInBeginSection": 181,
"offsetInEndSection": 352,
"text": "The Open Access and Collaborative Consumer Health Vocabulary ( OAC CHV) , which contains health-related terms used by lay consumers , has been created to bridge such a gap"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28359728",
"endSection": "abstract",
"offsetInBeginSection": 355,
"offsetInEndSection": 555,
"text": "Specifically , the OAC CHV facilitates consumers' health information retrieval by enabling consumer-facing health applications to translate between professional language and consumer friendly language"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28359728",
"endSection": "abstract",
"offsetInBeginSection": 350,
"offsetInEndSection": 551,
"text": "Specifically, the OAC CHV facilitates consumers' health information retrieval by enabling consumer-facing health applications to translate between professional language and consumer friendly language."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28359728",
"endSection": "abstract",
"offsetInBeginSection": 180,
"offsetInEndSection": 350,
"text": "The Open Access and Collaborative Consumer Health Vocabulary (OAC CHV), which contains health-related terms used by lay consumers, has been created to bridge such a gap."
}
] | 11 |
BioASQ-training11b
| null | null |
5e3ab4f8b5b409ea5300001b
|
bioasq_factoid
|
factoid
|
What is the function of the cGAS pathway?
|
['Immune defense']
|
[
"Immune defense",
"Immune response",
"Immunological defense",
"Host defense",
"Immune system defense",
"Defense against pathogens",
"Immunological response"
] |
['The cGAS-STING pathway not only mediates protective immune defense against infection by a large variety of DNA-containing pathogens but also detects tumor-derived DNA and generates intrinsic antitumor immunity.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28801534",
"http://www.ncbi.nlm.nih.gov/pubmed/30395807",
"http://www.ncbi.nlm.nih.gov/pubmed/27648547",
"http://www.ncbi.nlm.nih.gov/pubmed/29169058",
"http://www.ncbi.nlm.nih.gov/pubmed/27902332",
"http://www.ncbi.nlm.nih.gov/pubmed/28137885",
"http://www.ncbi.nlm.nih.gov/pubmed/28940468",
"http://www.ncbi.nlm.nih.gov/pubmed/28920955",
"http://www.ncbi.nlm.nih.gov/pubmed/26944200"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29169058",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "Cyclic di-AMP (c-di-AMP) is a bacterial signaling nucleotide synthesized by several human pathogens."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30395807",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 296,
"text": "Cyclic GMP-AMP synthase (cGAS) has recently been identified as the primary protein that detects cytosolic double stranded DNA to invoke a type I interferon response. The cGAS pathway is vital in the recognition of DNA encoded viruses as well as self-DNA leaked from the nucleus of damaged cells. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28137885",
"endSection": "abstract",
"offsetInBeginSection": 887,
"offsetInEndSection": 1053,
"text": "These results indicate that activation of the cGAS pathway is important for intrinsic antitumor immunity and that cGAMP may be used directly for cancer immunotherapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28801534",
"endSection": "abstract",
"offsetInBeginSection": 881,
"offsetInEndSection": 1019,
"text": " this work identifies long DNA as the molecular entity stimulating the cGAS pathway upon cytosolic DNA challenge such as viral infections."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28920955",
"endSection": "abstract",
"offsetInBeginSection": 872,
"offsetInEndSection": 1155,
"text": "these data suggest that inactivation of the cGAS pathway plays a critical role in tumour progression, and reveal a direct link between hypoxia-responsive miRNAs and adaptive immune responses to the hypoxic tumour microenvironment, thus unveiling potential new therapeutic strategies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28940468",
"endSection": "abstract",
"offsetInBeginSection": 176,
"offsetInEndSection": 306,
"text": "dysregulation of the cGAS pathway is linked to autoimmune diseases while targeted stimulation may be of benefit in immunoncology. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27648547",
"endSection": "abstract",
"offsetInBeginSection": 299,
"offsetInEndSection": 510,
"text": "The cGAS-STING pathway not only mediates protective immune defense against infection by a large variety of DNA-containing pathogens but also detects tumor-derived DNA and generates intrinsic antitumor immunity. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27902332",
"endSection": "abstract",
"offsetInBeginSection": 890,
"offsetInEndSection": 1052,
"text": "our data indicate that the cGAS-STING pathway plays a role in the surveillance of HBV infection and may be exploited for development of novel anti-HBV strategies."
}
] | 11 |
BioASQ-training11b
| null | null |
5c8aa082d558e5f23200000c
|
bioasq_factoid
|
factoid
|
What is MRSA?
|
['methicillin-resistant S. aureus', 'MRSA']
|
[
"methicillin-resistant S. aureus",
"MRSA",
"methicillin-resistant Staphylococcus aureus",
"Staphylococcus aureus (methicillin-resistant)",
"Staph aureus (MRSA)",
"S. aureus (MRSA)"
] |
['community-associated methicillin resistant staphylococcus aureus (ca-mrsa) has become a severe health concern because of its treatment difficulties.', 'Methicillin resistant Staphylococcus aureus (MRSA) has become a severe health concern because of its treatment difficulties.', '(MRSA, methicillin-resistant S. aureus)']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/18347206",
"http://www.ncbi.nlm.nih.gov/pubmed/8851953",
"http://www.ncbi.nlm.nih.gov/pubmed/26684366",
"http://www.ncbi.nlm.nih.gov/pubmed/22291965",
"http://www.ncbi.nlm.nih.gov/pubmed/15472807",
"http://www.ncbi.nlm.nih.gov/pubmed/24267132",
"http://www.ncbi.nlm.nih.gov/pubmed/27025639",
"http://www.ncbi.nlm.nih.gov/pubmed/17581935",
"http://www.ncbi.nlm.nih.gov/pubmed/15884297",
"http://www.ncbi.nlm.nih.gov/pubmed/27721155",
"http://www.ncbi.nlm.nih.gov/pubmed/27112442",
"http://www.ncbi.nlm.nih.gov/pubmed/19130105",
"http://www.ncbi.nlm.nih.gov/pubmed/19777772",
"http://www.ncbi.nlm.nih.gov/pubmed/21075466",
"http://www.ncbi.nlm.nih.gov/pubmed/19732087",
"http://www.ncbi.nlm.nih.gov/pubmed/19162372",
"http://www.ncbi.nlm.nih.gov/pubmed/27736763",
"http://www.ncbi.nlm.nih.gov/pubmed/12723397",
"http://www.ncbi.nlm.nih.gov/pubmed/21571749",
"http://www.ncbi.nlm.nih.gov/pubmed/19252301",
"http://www.ncbi.nlm.nih.gov/pubmed/23756924",
"http://www.ncbi.nlm.nih.gov/pubmed/23824338",
"http://www.ncbi.nlm.nih.gov/pubmed/24322533",
"http://www.ncbi.nlm.nih.gov/pubmed/22814471",
"http://www.ncbi.nlm.nih.gov/pubmed/19129414",
"http://www.ncbi.nlm.nih.gov/pubmed/20071545",
"http://www.ncbi.nlm.nih.gov/pubmed/26047024",
"http://www.ncbi.nlm.nih.gov/pubmed/25108628",
"http://www.ncbi.nlm.nih.gov/pubmed/26812054",
"http://www.ncbi.nlm.nih.gov/pubmed/22176801",
"http://www.ncbi.nlm.nih.gov/pubmed/27450316",
"http://www.ncbi.nlm.nih.gov/pubmed/23405883",
"http://www.ncbi.nlm.nih.gov/pubmed/19828738",
"http://www.ncbi.nlm.nih.gov/pubmed/25865979",
"http://www.ncbi.nlm.nih.gov/pubmed/20861339",
"http://www.ncbi.nlm.nih.gov/pubmed/19710260",
"http://www.ncbi.nlm.nih.gov/pubmed/25113379",
"http://www.ncbi.nlm.nih.gov/pubmed/24850346",
"http://www.ncbi.nlm.nih.gov/pubmed/17385151",
"http://www.ncbi.nlm.nih.gov/pubmed/24045390",
"http://www.ncbi.nlm.nih.gov/pubmed/19506056",
"http://www.ncbi.nlm.nih.gov/pubmed/15060266",
"http://www.ncbi.nlm.nih.gov/pubmed/20524852",
"http://www.ncbi.nlm.nih.gov/pubmed/20071548",
"http://www.ncbi.nlm.nih.gov/pubmed/17537949"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27736763",
"endSection": "abstract",
"offsetInBeginSection": 137,
"offsetInEndSection": 176,
"text": "(MRSA, methicillin-resistant S. aureus)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27721155",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 148,
"text": "Community-associated methicillin resistant Staphylococcus aureus (CA-MRSA) has become a severe health concern because of its treatment difficulties."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8851953",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 160,
"text": "We investigated the distribution of MRSA (methicillin-resistant Staphylococcus aureus) on and around six patients with MRSA infection in our neurosurgical ward."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19162372",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 184,
"text": "The aim of this study was to assess to what extent patients with meticillin-resistant Staphylococcus aureus (MRSA) at respiratory sites shed viable MRSA into the air of hospital rooms."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24322533",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) is increasing in prevalence among asymptomatic carriers and in cases of paediatric soft-tissue infections alike."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23405883",
"endSection": "abstract",
"offsetInBeginSection": 665,
"offsetInEndSection": 875,
"text": "Most of MRSA strains and a part of methicillin-susceptible S. aureus (MSSA) strains harbored unique combinations of non-ß-lactamase genes aac(6)/aph(2″), aph(3)-III, ant (4,4″), ermA, ermC, mrsA, tetM, and tetK"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26047024",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 234,
"text": "Healthcare- and Community-Associated Methicillin-Resistant Staphylococcus aureus (MRSA) and Fatal Pneumonia with Pediatric Deaths in Krasnoyarsk, Siberian Russia: Unique MRSAs Multiple Virulence Factors, Genome, and Stepwise Evolution"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25108628",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 309,
"text": "It was found in the present study that combined use of fusidic acid (FA) and berberine chloride (BBR) offered an in vitro synergistic action against 7 of the 30 clinical methicillin-resistant Staphylococcus aureus (MRSA) strains, with a fractional inhibitory concentration (FIC) index ranging from 0.5 to 0.19"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25865979",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Vancomycin MIC creep in methicillin-resistant Staphylococcus aureus (MRSA) isolates from 2006 to 2010 in a hospital in China"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25865979",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 184,
"text": "To assess whether vancomycin minimum inhibitory concentration (MIC) creeps among clinical isolates of methicillin-resistant Staphylococcus aureus (MRSA) in a regional hospital in China"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20861339",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 261,
"text": "Detection of methicillin-resistant Staphylococcus aureus (MRSA) in specimens from various body sites: performance characteristics of the BD GeneOhm MRSA assay, the Xpert MRSA assay, and broth-enriched culture in an area with a low prevalence of MRSA infections."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23756924",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 175,
"text": "Rapid detection of Methicillin-Resistant Staphylococcus aureus MRSA in nose, groin, and axilla swabs by the BD GeneOhm MRSA achromopeptidase assay and comparison with culture."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17537949",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 265,
"text": "Methicillin-resistant Staphylococcus aureus (MRSA) detection: comparison of two molecular methods (IDI-MRSA PCR assay and GenoType MRSA Direct PCR assay) with three selective MRSA agars (MRSA ID, MRSASelect, and CHROMagar MRSA) for use with infection-control swabs."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19710260",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 181,
"text": "Comparison of the Xpert methicillin-resistant Staphylococcus aureus (MRSA) assay, BD GeneOhm MRSA assay, and culture for detection of nasal and cutaneous groin colonization by MRSA."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22814471",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 221,
"text": "Comparison of the BD Max methicillin-resistant Staphylococcus aureus (MRSA) assay and the BD GeneOhm MRSA achromopeptidase assay with direct- and enriched-culture techniques using clinical specimens for detection of MRSA."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19828738",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 229,
"text": "Comparison of MRSASelect Agar, CHROMagar Methicillin-Resistant Staphylococcus aureus (MRSA) Medium, and Xpert MRSA PCR for detection of MRSA in Nares: diagnostic accuracy for surveillance samples with various bacterial densities."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20071545",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "Rapid detection of methicillin-resistant Staphylococcus aureus (MRSA) in diverse clinical specimens by the BD GeneOhm MRSA assay and comparison with culture."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19129414",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 159,
"text": "Multicenter evaluation of the Cepheid Xpert methicillin-resistant Staphylococcus aureus (MRSA) test as a rapid screening method for detection of MRSA in nares."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19506056",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "Prospective comparison of the clinical impacts of heterogeneous vancomycin-intermediate methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-susceptible MRSA."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20524852",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 182,
"text": "Long-term control of endemic hospital-wide methicillin-resistant Staphylococcus aureus (MRSA): the impact of targeted active surveillance for MRSA in patients and healthcare workers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24850346",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 203,
"text": "Methicillin-resistant Staphylococcus aureus (MRSA) infections pose a major challenge in health care, yet the limited heterogeneity within this group hinders molecular investigations of related outbreaks."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19252301",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 380,
"text": "In a previous study, we reported that two kaempferol glycosides isolated from Laurus nobilis L., kaempferol-3-O-alpha-L-(2'',4''-di-E-p-coumaroyl)-rhamnoside (C2) and kaempferol-3-O-alpha-L-(2''-E-p-coumaroyl-4''-Z-p-coumaroyl)-rhamnoside (C3), showed strong antibacterial activities against methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant enterococci."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15884297",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 165,
"text": "This article explains what methicillin-resistant Staphylococcus aureus (MRSA) is, how it is spread and what the real challenges are in healthcare settings in the UK."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21571749",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Methicillin-resistant Staphylococcus aureus (MRSA) is an emerging threat to public health, especially in correctional settings."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20071548",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 328,
"text": "There are few more compelling questions in clinical microbiology today than the issue of whether or not to screen for the presence of methicillin-resistant Staphylococcus aureus (MRSA), with the results being used to institute infection control interventions aimed at preventing transmission of MRSA in health care environments."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17537949",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 266,
"text": "Methicillin-resistant Staphylococcus aureus (MRSA) detection: comparison of two molecular methods (IDI-MRSA PCR assay and GenoType MRSA Direct PCR assay) with three selective MRSA agars (MRSA ID, MRSASelect, and CHROMagar MRSA) for use with infection-control swabs."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24045390",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Do methicillin resistant staphylococcus (MRSA) carrier patients influence MRSA infection more than MRSA-carrier medical officers and MRSA-carrier family?"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19732087",
"endSection": "abstract",
"offsetInBeginSection": 126,
"offsetInEndSection": 176,
"text": "methicillin-resistant Staphylococcus aureus (MRSA)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15060266",
"endSection": "abstract",
"offsetInBeginSection": 88,
"offsetInEndSection": 142,
"text": " methicillin-resistant Staphylococcus aureus (CA-MRSA)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19130105",
"endSection": "abstract",
"offsetInBeginSection": 45,
"offsetInEndSection": 96,
"text": "methicillin-resistant Staphylococcus aureus (MRSA) "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23824338",
"endSection": "abstract",
"offsetInBeginSection": 23,
"offsetInEndSection": 84,
"text": "methicillin-resistant Staphylococcus aureus (MRSA) infections"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21075466",
"endSection": "abstract",
"offsetInBeginSection": 29,
"offsetInEndSection": 86,
"text": "methicillin resistant Staphylococcus aureus (MRSA CC398) "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25113379",
"endSection": "abstract",
"offsetInBeginSection": 138,
"offsetInEndSection": 190,
"text": " (methicillin-resistant Staphylococcus aureus) MRSA "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27450316",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 62,
"text": "Methicillin-resistant Staphylococcus aureus (MRSA)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26812054",
"endSection": "abstract",
"offsetInBeginSection": 349,
"offsetInEndSection": 399,
"text": "methicillin-resistant Staphylococcus aureus (MRSA)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17385151",
"endSection": "abstract",
"offsetInBeginSection": 72,
"offsetInEndSection": 122,
"text": "methicillin-resistant Staphylococcus aureus (MRSA)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24267132",
"endSection": "abstract",
"offsetInBeginSection": 66,
"offsetInEndSection": 116,
"text": "methicillin-resistant Staphylococcus aureus (MRSA)"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17581935",
"endSection": "title",
"offsetInBeginSection": 54,
"offsetInEndSection": 105,
"text": "methicillin-resistant Staphylococcus aureus (MRSA) "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18347206",
"endSection": "abstract",
"offsetInBeginSection": 60,
"offsetInEndSection": 110,
"text": "methicillin-resistant Staphylococcus aureus (MRSA)"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22176801",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 43,
"text": "Methicillin-resistant Staphylococcus aureus"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25648247",
"endSection": "abstract",
"offsetInBeginSection": 65,
"offsetInEndSection": 116,
"text": " methicillin-resistant Staphylococcus aureus (MRSA)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22291965",
"endSection": "abstract",
"offsetInBeginSection": 33,
"offsetInEndSection": 86,
"text": "methicillin-resistant Staphylococcus aureus-(CA-MRSA)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19777772",
"endSection": "abstract",
"offsetInBeginSection": 396,
"offsetInEndSection": 446,
"text": "methicillin-resistant Staphylococcus aureus (MRSA)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25240872",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 50,
"text": "Methicillin-resistant Staphylococcus aureus (MRSA)"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12723397",
"endSection": "title",
"offsetInBeginSection": 84,
"offsetInEndSection": 134,
"text": "methicillin-resistant Staphylococcus aureus (MRSA)"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26684366",
"endSection": "title",
"offsetInBeginSection": 45,
"offsetInEndSection": 95,
"text": "methicillin-resistant Staphylococcus aureus (MRSA)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26684366",
"endSection": "abstract",
"offsetInBeginSection": 73,
"offsetInEndSection": 123,
"text": "methicillin-resistant Staphylococcus aureus (MRSA)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27025639",
"endSection": "abstract",
"offsetInBeginSection": 58,
"offsetInEndSection": 111,
"text": "methicillin-resistant Staphylococcus aureus (HA-MRSA)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15472807",
"endSection": "abstract",
"offsetInBeginSection": 43,
"offsetInEndSection": 94,
"text": "methicillin-resistant Staphylococcus aureus (MRSA) "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17121622",
"endSection": "abstract",
"offsetInBeginSection": 229,
"offsetInEndSection": 280,
"text": "methicillin-resistant Staphylococcus aureus (MRSA)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27112442",
"endSection": "abstract",
"offsetInBeginSection": 52,
"offsetInEndSection": 102,
"text": "methicillin-resistant Staphylococcus aureus (MRSA)"
}
] | 6 |
BioASQ-training6b
| null | null |
58a32efe60087bc10a000013
|
bioasq_factoid
|
factoid
|
Which amino acid residue appears mutated in most of the cases reported with cadasil syndrome?
|
['Cysteine']
|
[
"Cysteine",
"Cys",
"L-Cysteine",
"Cysteine residue",
"Cysteine amino acid"
] |
CADASIL is caused mostly by missense mutations in the NOTCH3 gene, invariably involving a cysteine residue.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23597439",
"http://www.ncbi.nlm.nih.gov/pubmed/23587639",
"http://www.ncbi.nlm.nih.gov/pubmed/21616505",
"http://www.ncbi.nlm.nih.gov/pubmed/19043263",
"http://www.ncbi.nlm.nih.gov/pubmed/16717210",
"http://www.ncbi.nlm.nih.gov/pubmed/15304596",
"http://www.ncbi.nlm.nih.gov/pubmed/11706120",
"http://www.ncbi.nlm.nih.gov/pubmed/24086431",
"http://www.ncbi.nlm.nih.gov/pubmed/22082899",
"http://www.ncbi.nlm.nih.gov/pubmed/21772710",
"http://www.ncbi.nlm.nih.gov/pubmed/20224942",
"http://www.ncbi.nlm.nih.gov/pubmed/22367627",
"http://www.ncbi.nlm.nih.gov/pubmed/17726918",
"http://www.ncbi.nlm.nih.gov/pubmed/23799017",
"http://www.ncbi.nlm.nih.gov/pubmed/21038489",
"http://www.ncbi.nlm.nih.gov/pubmed/18313300",
"http://www.ncbi.nlm.nih.gov/pubmed/22623959",
"http://www.ncbi.nlm.nih.gov/pubmed/18710532",
"http://www.ncbi.nlm.nih.gov/pubmed/19006080"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23597439",
"endSection": "abstract",
"offsetInBeginSection": 5,
"offsetInEndSection": 253,
"text": "missense mutations and small deletions in the NOTCH3 gene, not involving cysteine residues, have been described in patients considered to be affected by paucisymptomatic CADASIL. However, the significance of such molecular variants is still unclear"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23587639",
"endSection": "abstract",
"offsetInBeginSection": 267,
"offsetInEndSection": 374,
"text": "CADASIL is caused mostly by missense mutations in the NOTCH3 gene, invariably involving a cysteine residue."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21616505",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 302,
"text": "Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an inherited cerebrovascular disease due to mutations involving loss or gain of a cysteine residue in the NOTCH3 gene. A cluster of mutations around exons 3 and 4 was originally reported"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15304596",
"endSection": "abstract",
"offsetInBeginSection": 402,
"offsetInEndSection": 521,
"text": "The authors report a family with CADASIL carrying a deletion in the Notch3 gene that did not involve a cysteine residue"
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D046589",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D024342",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D009154",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D000596",
"http://www.disease-ontology.org/api/metadata/DOID:13945",
"http://www.disease-ontology.org/api/metadata/DOID:225",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013577"
] |
[
{
"o": "UMLS_CUI:C0751587",
"p": "http://www.w3.org/2004/02/skos/core#notation",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:13945"
},
{
"o": "cadasil",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:13945"
},
{
"o": "MSH2010_2010_02_22:D046589",
"p": "http://www.w3.org/2004/02/skos/core#notation",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:13945"
},
{
"o": "cadasil",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:13945"
},
{
"o": "C499374",
"p": "http://www.w3.org/2004/02/skos/core#notation",
"s": "http://linkedlifedata.com/resource/umls/label/A8400718"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A8407072",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C1452875"
},
{
"o": "Notch homolog 3 (Drosophila) protein, human",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A8400738"
},
{
"o": "NOTCH3 protein, human",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A8400718"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A8400718",
"p": "http://linkedlifedata.com/resource/umls/prefMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C1452875"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A8407072",
"p": "http://linkedlifedata.com/resource/umls/altMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C1452875"
},
{
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"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C1452875"
},
{
"o": "CADASIL protein, human",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A8407072"
},
{
"o": "C499374",
"p": "http://www.w3.org/2004/02/skos/core#notation",
"s": "http://linkedlifedata.com/resource/umls/label/A8400738"
},
{
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"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C1452875"
},
{
"o": "Notch homolog 3 (Drosophila) protein, human",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A8400738"
},
{
"o": "NOTCH3 protein, human",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A8400718"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A8400718",
"p": "http://linkedlifedata.com/resource/umls/prefMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C1452875"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A8407072",
"p": "http://linkedlifedata.com/resource/umls/altMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C1452875"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A8400738",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C1452875"
},
{
"o": "CADASIL protein, human",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A8407072"
},
{
"o": "C499374",
"p": "http://www.w3.org/2004/02/skos/core#notation",
"s": "http://linkedlifedata.com/resource/umls/label/A8407072"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A8407072",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C1452875"
},
{
"o": "Notch homolog 3 (Drosophila) protein, human",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A8400738"
},
{
"o": "NOTCH3 protein, human",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A8400718"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A8400718",
"p": "http://linkedlifedata.com/resource/umls/prefMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C1452875"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A8407072",
"p": "http://linkedlifedata.com/resource/umls/altMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C1452875"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A8400738",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C1452875"
},
{
"o": "CADASIL protein, human",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A8407072"
},
{
"o": "CADASIL Syndrome",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A17705411"
},
{
"o": "CADASIL Syndrome",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A17683439"
},
{
"o": "CADASIL",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A12021175"
},
{
"o": "CADASIL",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A6957136"
},
{
"o": "cadasil",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/diseaseontology/id/DOID:13945"
},
{
"o": "http://www4.wiwiss.fu-berlin.de/diseasome/resource/diseasome/genes",
"p": "http://www.w3.org/1999/02/22-rdf-syntax-ns#type",
"s": "http://www4.wiwiss.fu-berlin.de/diseasome/resource/genes/CADASIL"
},
{
"o": "CADASIL",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://www4.wiwiss.fu-berlin.de/diseasome/resource/genes/CADASIL"
},
{
"o": "http://www4.wiwiss.fu-berlin.de/diseasome/resource/genes/CADASIL",
"p": "http://www4.wiwiss.fu-berlin.de/diseasome/resource/diseasome/associatedGene",
"s": "http://www4.wiwiss.fu-berlin.de/diseasome/resource/diseases/1802"
}
] |
532366f09b2d7acc7e000015
|
bioasq_factoid
|
factoid
|
What class of drugs is commonly associated with Drug-induced interstitial lung disease (DIILD)?
|
['cytotoxic drugs']
|
[
"cytotoxic drugs",
"cytotoxic agents",
"cytotoxic medications",
"antineoplastic agents",
"chemotherapeutic agents",
"cancer drugs",
"toxic drugs",
"cell-killing drugs"
] |
["[' Numerous agents including cytotoxic and noncytotoxic drugs have the potential to cause pulmonary toxicity.']", 'Numerous agents including cytotoxic and noncytotoxic drugs have the potential to cause pulmonary toxicity', 'Cytotoxic drugs are the most common cause of toxic lung disease.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/2185802",
"http://www.ncbi.nlm.nih.gov/pubmed/34177523",
"http://www.ncbi.nlm.nih.gov/pubmed/1327232",
"http://www.ncbi.nlm.nih.gov/pubmed/29631763",
"http://www.ncbi.nlm.nih.gov/pubmed/24231065",
"http://www.ncbi.nlm.nih.gov/pubmed/8765915",
"http://www.ncbi.nlm.nih.gov/pubmed/10992015",
"http://www.ncbi.nlm.nih.gov/pubmed/22189216",
"http://www.ncbi.nlm.nih.gov/pubmed/17545850",
"http://www.ncbi.nlm.nih.gov/pubmed/31963908",
"http://www.ncbi.nlm.nih.gov/pubmed/31584970",
"http://www.ncbi.nlm.nih.gov/pubmed/28050004",
"http://www.ncbi.nlm.nih.gov/pubmed/30521972",
"http://www.ncbi.nlm.nih.gov/pubmed/32598798",
"http://www.ncbi.nlm.nih.gov/pubmed/22896776",
"http://www.ncbi.nlm.nih.gov/pubmed/32874590",
"http://www.ncbi.nlm.nih.gov/pubmed/30326612",
"http://www.ncbi.nlm.nih.gov/pubmed/20298401"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1327232",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "The problem of the drug induced pulmonary toxicity (cytotoxic and non-cytotoxic drugs) is discussed."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10992015",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 207,
"text": "ulmonary drug toxicity is increasingly being diagnosed as a cause of acute and chronic lung disease. Numerous agents including cytotoxic and noncytotoxic drugs have the potential to cause pulmonary toxicity"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2185802",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Cytotoxic agents may cause interstitial or eosinophilic pneumonitis, alveolar proteinosis, pulmonary venous occlusive disease, pulmonary fibrosis, pneumothorax, or pulmonary oedema"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8765915",
"endSection": "abstract",
"offsetInBeginSection": 1181,
"offsetInEndSection": 1309,
"text": "The cytotoxic drugs which are most often implicated in causing this are bleomycin, methotrexate, cyclophosphamide and busulfan. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8765915",
"endSection": "abstract",
"offsetInBeginSection": 1730,
"offsetInEndSection": 1794,
"text": "Cytotoxic drugs are the most common cause of toxic lung disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30326612",
"endSection": "abstract",
"offsetInBeginSection": 772,
"offsetInEndSection": 883,
"text": "er drugs, followed by rheumatology drugs, amiodarone and antibiotics, were the most common causes of DIILD. The"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31584970",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 145,
"text": "Drug-induced interstitial lung disease (DIILD) is a serious side effect of chemotherapy in cancer patients with an extremely high mortality rate."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31584970",
"endSection": "abstract",
"offsetInBeginSection": 1032,
"offsetInEndSection": 1270,
"text": "Furthermore, in a subgroup analysis of epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI)-induced interstitial lung disease (ILD), we observed seven candidate SNVs that were possibly associated with ILD (P < 0.00001)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34177523",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "Drug-induced interstitial lung disease (DI-ILD) is a rare, yet life-threatening complication associated with tyrosine-kinase inhibitor (TKI) therapy. Thi"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32874590",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "Drug-induced interstitial lung disease associated with dasatinib coinciding with active tuberculosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32874590",
"endSection": "abstract",
"offsetInBeginSection": 821,
"offsetInEndSection": 945,
"text": "s was added. It is known that drug-induced ILD and susceptibility to infection associated with dasatinib occur in a dose-dep"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30521972",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 245,
"text": "INTRODUCTION: The study objective was to determine the incidence and characteristics of drug-induced interstitial lung disease (ILD) associated with an orally available small-molecule tyrosine kinase inhibitor, crizotinib, in a real-world clinic"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20298401",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 190,
"text": "INTRODUCTION: Although gefitinib used for the treatment of non-small-cell lung cancer is a well-known cause of interstitial lung disease (ILD), few case reports on erlotinib-induced ILD have"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22896776",
"endSection": "abstract",
"offsetInBeginSection": 310,
"offsetInEndSection": 462,
"text": "Drug-induced interstitial lung disease (DILD) can be caused by chemotherapeutic agents, antibiotics, antiarrhythmic drugs, and immunosuppressive agents."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17545850",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 212,
"text": "INTRODUCTION: A rare but serious complication of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) therapy is a lung injury syndrome commonly referred to as a drug-induced interstitial lung "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31963908",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 235,
"text": "BACKGROUND: Treatment of rheumatoid arthritis (RA)-related interstitial lung disease (ILD) is challenging, and many conventional and biologic disease-modifying anti-rheumatic drugs (DMARDs) have been associated with ILD development or "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24231065",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 433,
"text": "OBJECTIVE: To review published cases of induced or exacerbated interstitial lung disease (ILD) in rheumatoid arthritis (RA) associated with non-biologic disease-modifying antirheumatic drugs (nbDMARDs) and biologics and to discuss clinical implications in daily practice.METHODS: We performed a systematic literature review from 1975 to July 2013 using Medline, Embase, Cochrane, and abstracts from the ACR 2010-2012 and EULAR 2010-2"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24231065",
"endSection": "abstract",
"offsetInBeginSection": 434,
"offsetInEndSection": 804,
"text": "13 annual meetings. Case reports and series that suggest a causative role of nbDMARDs (methotrexate [MTX], leflunomide [LEF], gold, azathioprine [AZA], sulfasalazine [SSZ], and hydroxychloroquine [HCQ]) and biologic agents (TNF inhibitors [TNFi], rituximab [RTX], tocilizumab [TCZ], abatacept [ABA], and anakinra) in causing ILD or worsening a pre-existing ILD in RA pat"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29631763",
"endSection": "abstract",
"offsetInBeginSection": 956,
"offsetInEndSection": 1114,
"text": "Drugs that are more commonly associated with lung toxicity include nitrofurantoin, amiodarone, and chemotherapeutic agents such as bleomycin and methotrexate."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32598798",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 183,
"text": "Drug-induced interstitial lung disease (D-ILD) can be caused by various drugs, including antibiotics, amiodarone, antitumor, rheumatological and non-steroidal anti-inflammatory drugs."
}
] | 11 |
BioASQ-training11b
| null | null |
621ec0313a8413c65300005e
|
bioasq_factoid
|
factoid
|
Which algorithm has been developed for finding conserved non-coding elements (CNEs) in genomes?
|
['CNEFinder']
|
[
"CNEFinder"
] |
['CNEFinder is a tool for identifying CNEs between two given DNA sequences with user-defined criteria.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30423090"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30423090",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 60,
"text": "CNEFinder: finding conserved non-coding elements in genomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30423090",
"endSection": "abstract",
"offsetInBeginSection": 528,
"offsetInEndSection": 756,
"text": "We fill this gap by presenting CNEFinder; a tool for identifying CNEs between two given DNA sequences with user-defined criteria. The results presented here show the tool's ability of identifying CNEs accurately and efficiently."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30423090",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "CNEFinder: finding conserved non-coding elements in genomes.Free software under the terms of the GNU GPL (https://github.com/lorrainea/CNEFinder)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30423090",
"endSection": "abstract",
"offsetInBeginSection": 421,
"offsetInEndSection": 675,
"text": "Currently, there are no tools published in the literature for systematically identifying CNEs in genomes.<br><b>Results</b>: We fill this gap by presenting CNEFinder; a tool for identifying CNEs between two given DNA sequences with user-defined criteria."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30423090",
"endSection": "abstract",
"offsetInBeginSection": 508,
"offsetInEndSection": 637,
"text": "We fill this gap by presenting CNEFinder; a tool for identifying CNEs between two given DNA sequences with user-defined criteria."
}
] | 11 |
BioASQ-training11b
| null | null |
5c51f01e07ef653866000002
|
bioasq_factoid
|
factoid
|
Which biomarker is widely used in the diagnosis of Ewing sarcoma?
|
[['CD99']]
|
[
"CD99",
"MIC2",
"E2A",
"P97",
"CD99 antigen",
"CD99 molecule"
] |
['CD99 is a hallmark marker for Ewing sarcoma and primitive neuroectodermal tumors.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/12783138"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12783138",
"endSection": "abstract",
"offsetInBeginSection": 218,
"offsetInEndSection": 463,
"text": "half of B-LBL patients are negative for CD45 (leucocyte common antigen, LCA), a widely used marker for the diagnosis of lymphoma, and a significant portion express CD99, a marker for Ewing's sarcoma (ES) or primitive neuroectodermal tumor (PNET)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12783138",
"endSection": "abstract",
"offsetInBeginSection": 218,
"offsetInEndSection": 463,
"text": "half of B-LBL patients are negative for CD45 (leucocyte common antigen, LCA), a widely used marker for the diagnosis of lymphoma, and a significant portion express CD99, a marker for Ewing's sarcoma (ES) or primitive neuroectodermal tumor (PNET)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12783138",
"endSection": "abstract",
"offsetInBeginSection": 208,
"offsetInEndSection": 463,
"text": "Moreover, half of B-LBL patients are negative for CD45 (leucocyte common antigen, LCA), a widely used marker for the diagnosis of lymphoma, and a significant portion express CD99, a marker for Ewing's sarcoma (ES) or primitive neuroectodermal tumor (PNET)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12783138",
"endSection": "abstract",
"offsetInBeginSection": 208,
"offsetInEndSection": 463,
"text": "Moreover, half of B-LBL patients are negative for CD45 (leucocyte common antigen, LCA), a widely used marker for the diagnosis of lymphoma, and a significant portion express CD99, a marker for Ewing's sarcoma (ES) or primitive neuroectodermal tumor (PNET)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12783138",
"endSection": "abstract",
"offsetInBeginSection": 208,
"offsetInEndSection": 463,
"text": "Moreover, half of B-LBL patients are negative for CD45 (leucocyte common antigen, LCA), a widely used marker for the diagnosis of lymphoma, and a significant portion express CD99, a marker for Ewing's sarcoma (ES) or primitive neuroectodermal tumor (PNET)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12783138",
"endSection": "abstract",
"offsetInBeginSection": 208,
"offsetInEndSection": 463,
"text": "Moreover, half of B-LBL patients are negative for CD45 (leucocyte common antigen, LCA), a widely used marker for the diagnosis of lymphoma, and a significant portion express CD99, a marker for Ewing's sarcoma (ES) or primitive neuroectodermal tumor (PNET)"
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D012512",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D015415",
"http://www.disease-ontology.org/api/metadata/DOID:3368",
"http://www.disease-ontology.org/api/metadata/DOID:4980"
] |
[] |
55376663bc4f83e82800000a
|
bioasq_factoid
|
factoid
|
What histone modification is recognized by the bromodomain?
|
['Acetylated lysines']
|
[
"Acetylated lysines",
"Acetylated lysine residues",
"Acetylated lysine",
"Lysine acetylation",
"Acetyl-lysine",
"Acetylated amino acids"
] |
Acetylated lysines in histones (generally H3 and H4)
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23095041",
"http://www.ncbi.nlm.nih.gov/pubmed/21851057",
"http://www.ncbi.nlm.nih.gov/pubmed/21596426",
"http://www.ncbi.nlm.nih.gov/pubmed/21271695",
"http://www.ncbi.nlm.nih.gov/pubmed/21189220",
"http://www.ncbi.nlm.nih.gov/pubmed/17049045",
"http://www.ncbi.nlm.nih.gov/pubmed/16265664",
"http://www.ncbi.nlm.nih.gov/pubmed/15970672",
"http://www.ncbi.nlm.nih.gov/pubmed/15382140",
"http://www.ncbi.nlm.nih.gov/pubmed/15143168",
"http://www.ncbi.nlm.nih.gov/pubmed/15014446",
"http://www.ncbi.nlm.nih.gov/pubmed/10746732",
"http://www.ncbi.nlm.nih.gov/pubmed/10716917"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23095041",
"endSection": "abstract",
"offsetInBeginSection": 280,
"offsetInEndSection": 361,
"text": "acetyllysine-specific protein-protein interaction with bromodomain reader modules"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21851057",
"endSection": "abstract",
"offsetInBeginSection": 141,
"offsetInEndSection": 228,
"text": "Bromodomains bind acetylated lysines, acting as readers of the histone-acetylation code"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21596426",
"endSection": "abstract",
"offsetInBeginSection": 331,
"offsetInEndSection": 472,
"text": " three acetyllysine ligands are indentified for a PHD-adjacent bromodomain in BPTF via systematic screening and biophysical characterization."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21271695",
"endSection": "abstract",
"offsetInBeginSection": 673,
"offsetInEndSection": 712,
"text": "acetyl-lysine binding bromodomain (BRD)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21189220",
"endSection": "abstract",
"offsetInBeginSection": 7,
"offsetInEndSection": 66,
"text": "bromodomain proteins bind to acetylated lysines in histones"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17049045",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 251,
"text": "romodomains are present in many chromatin-associated proteins such as the SWI/SNF and RSC chromatin remodelling and the SAGA HAT (histone acetyltransferase) complexes, and can bind to acetylated lysine residues in the N-terminal tails of the histones"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17049045",
"endSection": "title",
"offsetInBeginSection": 10,
"offsetInEndSection": 60,
"text": "recognition of acetylated histones by bromodomains"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16265664",
"endSection": "abstract",
"offsetInBeginSection": 130,
"offsetInEndSection": 160,
"text": "BRD7, a novel bromodomain gene"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16265664",
"endSection": "abstract",
"offsetInBeginSection": 675,
"offsetInEndSection": 717,
"text": "BRD7 interacted with H3 peptide acetylated"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15970672",
"endSection": "abstract",
"offsetInBeginSection": 352,
"offsetInEndSection": 424,
"text": "bromodomain-containing proteins that recognize histone acetylation sites"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15382140",
"endSection": "abstract",
"offsetInBeginSection": 581,
"offsetInEndSection": 677,
"text": "bromodomains of Gcn5, PCAF, TAF1 and CBP are able to recognize acetyllysine residues in histones"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15143168",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 26,
"text": "romodomain factor 1 (Bdf1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15143168",
"endSection": "abstract",
"offsetInBeginSection": 223,
"offsetInEndSection": 274,
"text": " Bdf1 binds preferentially to acetylated histone H4"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15014446",
"endSection": "abstract",
"offsetInBeginSection": 118,
"offsetInEndSection": 233,
"text": "chromatin remodeling complex RSC bears multiple bromodomains, motifs for acetyl-lysine and histone tail interaction"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10746732",
"endSection": "abstract",
"offsetInBeginSection": 666,
"offsetInEndSection": 769,
"text": " in vitro binding of a HAT bromodomain with acetylated lysines within H3 and H4 amino-terminal peptides"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10716917",
"endSection": "abstract",
"offsetInBeginSection": 535,
"offsetInEndSection": 583,
"text": "bromodomain, that recognizes acetylated residues"
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D006657",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0016570",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0016573"
] |
[] |
53398855d6d3ac6a3400005b
|
bioasq_factoid
|
factoid
|
What are 'vildagliptin', 'sitagliptin', 'saxagliptin', 'alogliptin', 'linagliptin', and 'dutogliptin'?
|
[['dipeptidyl peptidase-4 (DPP-4) inhibitors']]
|
[
"dipeptidyl peptidase-4 (DPP-4) inhibitors",
"DPP-4 inhibitors",
"Dipeptidyl peptidase IV inhibitors",
"Dipeptidyl peptidase 4 inhibitors",
"DPP IV inhibitors"
] |
['"Sitagliptin," "vildagliptin," "saxagliptin," "alogliptin," "linagliptin," and "dutogliptin" are dipeptidyl peptidase-4 (DPP-4) inhibitors.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22215383",
"http://www.ncbi.nlm.nih.gov/pubmed/21431099",
"http://www.ncbi.nlm.nih.gov/pubmed/24793580",
"http://www.ncbi.nlm.nih.gov/pubmed/23837679",
"http://www.ncbi.nlm.nih.gov/pubmed/22106978",
"http://www.ncbi.nlm.nih.gov/pubmed/23140189",
"http://www.ncbi.nlm.nih.gov/pubmed/23803146",
"http://www.ncbi.nlm.nih.gov/pubmed/24793219",
"http://www.ncbi.nlm.nih.gov/pubmed/22686547",
"http://www.ncbi.nlm.nih.gov/pubmed/25687897",
"http://www.ncbi.nlm.nih.gov/pubmed/21500969",
"http://www.ncbi.nlm.nih.gov/pubmed/25860270",
"http://www.ncbi.nlm.nih.gov/pubmed/24186878",
"http://www.ncbi.nlm.nih.gov/pubmed/22162539",
"http://www.ncbi.nlm.nih.gov/pubmed/21913883",
"http://www.ncbi.nlm.nih.gov/pubmed/23501107",
"http://www.ncbi.nlm.nih.gov/pubmed/24996141",
"http://www.ncbi.nlm.nih.gov/pubmed/23743694",
"http://www.ncbi.nlm.nih.gov/pubmed/24320733",
"http://www.ncbi.nlm.nih.gov/pubmed/18223196",
"http://www.ncbi.nlm.nih.gov/pubmed/21320267",
"http://www.ncbi.nlm.nih.gov/pubmed/23136353",
"http://www.ncbi.nlm.nih.gov/pubmed/19791828",
"http://www.ncbi.nlm.nih.gov/pubmed/17100408",
"http://www.ncbi.nlm.nih.gov/pubmed/20690781",
"http://www.ncbi.nlm.nih.gov/pubmed/22429011",
"http://www.ncbi.nlm.nih.gov/pubmed/24567800"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22215383",
"endSection": "abstract",
"offsetInBeginSection": 301,
"offsetInEndSection": 785,
"text": "The present metaanalysis was designed to assess the effect of DPP-4 inhibitors on blood lipids, verifying possible differences across compounds of this class.METHODS: An extensive search of Medline and the Cochrane Library (any date up to December 31, 2010, restricted to randomized clinical trials, published in English) was performed for all trials containing, in any field, the words \"sitagliptin,\" \"vildagliptin,\" \"saxagliptin,\" \"alogliptin,\" \"linagliptin,\" and/or \"dutogliptin.\" "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23140189",
"endSection": "abstract",
"offsetInBeginSection": 463,
"offsetInEndSection": 600,
"text": "Sitagliptin (MK- 0431), Saxagliptin, Melogliptin, Linagliptin (BI-1356), Dutogliptin, Carmegliptin, Alogliptin and Vildagliptin (LAF237)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21431099",
"endSection": "abstract",
"offsetInBeginSection": 1019,
"offsetInEndSection": 1217,
"text": "Additionally, linagliptin, vildagliptin and alogliptin are currently in phase III development in the United States while studies with another DPP IV inhibitor, dutogliptin, have been terminated (2)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24793219",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "Testing the therapeutic equivalence of alogliptin, linagliptin, saxagliptin, sitagliptin or vildagliptin as monotherapy or in combination with metformin in patients with type 2 diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22686547",
"endSection": "abstract",
"offsetInBeginSection": 442,
"offsetInEndSection": 732,
"text": "The aim of this review is to compare the clinical pharmacokinetics of available DPP-4 inhibitors (alogliptin, linagliptin, saxagliptin, sitagliptin and vildagliptin) for the purpose of identifying potential selection preferences according to individual patient variables and co-morbidities."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21500969",
"endSection": "abstract",
"offsetInBeginSection": 406,
"offsetInEndSection": 594,
"text": "The reader will gain detailed pharmacological and clinical information on alogliptin, dutogliptin and linagliptin and will learn how these DPP IV inhibitors may widen the whole drug class."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22686547",
"endSection": "abstract",
"offsetInBeginSection": 3646,
"offsetInEndSection": 3955,
"text": "When considered in total, data reviewed in this report suggest that the best overall balance between potency and the clinical pharmacokinetic characteristics of distribution, metabolism and elimination may be observed with linagliptin followed closely by vildagliptin, saxagliptin, sitagliptin and alogliptin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21431099",
"endSection": "abstract",
"offsetInBeginSection": 721,
"offsetInEndSection": 854,
"text": "Currently, there are four DPP IV inhibitors available in various countries-alogliptin, sitagliptin, vildagliptin and saxagliptin (1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23140189",
"endSection": "abstract",
"offsetInBeginSection": 463,
"offsetInEndSection": 600,
"text": "Sitagliptin (MK- 0431), Saxagliptin, Melogliptin, Linagliptin (BI-1356), Dutogliptin, Carmegliptin, Alogliptin and Vildagliptin (LAF237)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21431099",
"endSection": "abstract",
"offsetInBeginSection": 1019,
"offsetInEndSection": 1217,
"text": "Additionally, linagliptin, vildagliptin and alogliptin are currently in phase III development in the United States while studies with another DPP IV inhibitor, dutogliptin, have been terminated (2)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24793219",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "Testing the therapeutic equivalence of alogliptin, linagliptin, saxagliptin, sitagliptin or vildagliptin as monotherapy or in combination with metformin in patients with type 2 diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22686547",
"endSection": "abstract",
"offsetInBeginSection": 442,
"offsetInEndSection": 732,
"text": "The aim of this review is to compare the clinical pharmacokinetics of available DPP-4 inhibitors (alogliptin, linagliptin, saxagliptin, sitagliptin and vildagliptin) for the purpose of identifying potential selection preferences according to individual patient variables and co-morbidities."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21500969",
"endSection": "abstract",
"offsetInBeginSection": 406,
"offsetInEndSection": 594,
"text": "The reader will gain detailed pharmacological and clinical information on alogliptin, dutogliptin and linagliptin and will learn how these DPP IV inhibitors may widen the whole drug class."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22686547",
"endSection": "abstract",
"offsetInBeginSection": 3646,
"offsetInEndSection": 3955,
"text": "When considered in total, data reviewed in this report suggest that the best overall balance between potency and the clinical pharmacokinetic characteristics of distribution, metabolism and elimination may be observed with linagliptin followed closely by vildagliptin, saxagliptin, sitagliptin and alogliptin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21431099",
"endSection": "abstract",
"offsetInBeginSection": 721,
"offsetInEndSection": 854,
"text": "Currently, there are four DPP IV inhibitors available in various countries-alogliptin, sitagliptin, vildagliptin and saxagliptin (1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23140189",
"endSection": "abstract",
"offsetInBeginSection": 204,
"offsetInEndSection": 464,
"text": "The various marketed or under developmental status, potential gliptins have been opted to build a pharmacophore model, e.g. Sitagliptin (MK- 0431), Saxagliptin, Melogliptin, Linagliptin (BI-1356), Dutogliptin, Carmegliptin, Alogliptin and Vildagliptin (LAF237)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21431099",
"endSection": "abstract",
"offsetInBeginSection": 591,
"offsetInEndSection": 723,
"text": "Currently, there are four DPP IV inhibitors available in various countries-alogliptin, sitagliptin, vildagliptin and saxagliptin (1)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21431099",
"endSection": "abstract",
"offsetInBeginSection": 826,
"offsetInEndSection": 1023,
"text": "Additionally, linagliptin, vildagliptin and alogliptin are currently in phase III development in the United States while studies with another DPP IV inhibitor, dutogliptin, have been terminated (2)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24793580",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 305,
"text": "Recently, the SAVOR TIMI-53 (Saxagliptin Assessment of Vascular Outcomes Recorded in patients with diabetes mellitus--Thrombolysis in Myocardial Infarction-53) reported a significant increase in the risk of hospitalizations for heart failure in patients treated with saxagliptin in comparison with placebo"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21431099",
"endSection": "abstract",
"offsetInBeginSection": 725,
"offsetInEndSection": 824,
"text": "Of these, two have been approved for clinical use in the United States: sitagliptin and saxagliptin"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24186878",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 193,
"text": "Long-term safety and efficacy of empagliflozin, sitagliptin, and metformin: an active-controlled, parallel-group, randomized, 78-week open-label extension study in patients with type 2 diabetes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24186878",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "To investigate the long-term safety and efficacy of empagliflozin, a sodium glucose cotransporter 2 inhibitor; sitagliptin; and metformin in patients with type 2 diabetes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23837679",
"endSection": "abstract",
"offsetInBeginSection": 331,
"offsetInEndSection": 543,
"text": "METHODS: DATA SOURCES: an extensive Medline, Embase and Cochrane Database search for 'vildagliptin', 'sitagliptin', 'saxagliptin', 'alogliptin', 'linagliptin' and 'dutogliptin' was performed up to 1 March 2013. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22106978",
"endSection": "abstract",
"offsetInBeginSection": 321,
"offsetInEndSection": 574,
"text": "RESEARCH DESIGN AND METHODS: An extensive Medline and Embase search for 'vildagliptin', 'sitagliptin', 'saxagliptin', 'alogliptin', 'linagliptin', and 'dutogliptin' was performed, collecting all randomized clinical trials on humans up to March 1, 2011. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23803146",
"endSection": "abstract",
"offsetInBeginSection": 246,
"offsetInEndSection": 632,
"text": "METHODS: We conducted a search on MEDLINE, Embase and Cochrane Collaborative database for randomized controlled trials (RCTs) of DPP-4 inhibitors and metformin as initial combination therapy or as monotherapy in patients with T2DM by the end of December 2012, using the key words 'alogliptin', 'dutogliptin', 'linagliptin', 'saxagliptin', 'sitagliptin', 'vildagliptin' and 'metformin'. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23140189",
"endSection": "abstract",
"offsetInBeginSection": 328,
"offsetInEndSection": 466,
"text": "Sitagliptin (MK- 0431), Saxagliptin, Melogliptin, Linagliptin (BI-1356), Dutogliptin, Carmegliptin, Alogliptin and Vildagliptin (LAF237). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24793580",
"endSection": "abstract",
"offsetInBeginSection": 326,
"offsetInEndSection": 780,
"text": "Aim of the present meta-analysis is the systematic collection and synthesis of information on treatment-emergent cases of acute heart failure described in randomized clinical trials with DPP4.DATA SOURCES: An extensive Medline, Embase, and Cochrane Database search for \"vildagliptin\", \"sitagliptin\", \"saxagliptin\", \"alogliptin\", \"linagliptin\", and \"dutogliptin\" was performed, collecting all randomized clinical trials on humans up to October 1st, 2013. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22162539",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 192,
"text": "Quantitative model of the relationship between dipeptidyl peptidase-4 (DPP-4) inhibition and response: meta-analysis of alogliptin, saxagliptin, sitagliptin, and vildagliptin efficacy results."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21913883",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 194,
"text": "The dipeptidyl peptidase-4 (DPP-4) inhibitors linagliptin, sitagliptin, saxagliptin, vildagliptin and alogliptin are being developed and have been approved for the treatment of type-2 diabetes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22162539",
"endSection": "abstract",
"offsetInBeginSection": 114,
"offsetInEndSection": 313,
"text": "The objective of this model-based meta-analysis was to describe the time course of HbA1c response after dosing with alogliptin (ALOG), saxagliptin (SAXA), sitagliptin (SITA), or vildagliptin (VILD). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24996141",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Discovery of highly potent DPP-4 inhibitors by hybrid compound design based on linagliptin and alogliptin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23837679",
"endSection": "abstract",
"offsetInBeginSection": 331,
"offsetInEndSection": 543,
"text": "METHODS: DATA SOURCES: an extensive Medline, Embase and Cochrane Database search for 'vildagliptin', 'sitagliptin', 'saxagliptin', 'alogliptin', 'linagliptin' and 'dutogliptin' was performed up to 1 March 2013. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22106978",
"endSection": "abstract",
"offsetInBeginSection": 321,
"offsetInEndSection": 574,
"text": "RESEARCH DESIGN AND METHODS: An extensive Medline and Embase search for 'vildagliptin', 'sitagliptin', 'saxagliptin', 'alogliptin', 'linagliptin', and 'dutogliptin' was performed, collecting all randomized clinical trials on humans up to March 1, 2011. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23803146",
"endSection": "abstract",
"offsetInBeginSection": 246,
"offsetInEndSection": 632,
"text": "METHODS: We conducted a search on MEDLINE, Embase and Cochrane Collaborative database for randomized controlled trials (RCTs) of DPP-4 inhibitors and metformin as initial combination therapy or as monotherapy in patients with T2DM by the end of December 2012, using the key words 'alogliptin', 'dutogliptin', 'linagliptin', 'saxagliptin', 'sitagliptin', 'vildagliptin' and 'metformin'. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23140189",
"endSection": "abstract",
"offsetInBeginSection": 328,
"offsetInEndSection": 466,
"text": "Sitagliptin (MK- 0431), Saxagliptin, Melogliptin, Linagliptin (BI-1356), Dutogliptin, Carmegliptin, Alogliptin and Vildagliptin (LAF237). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24793580",
"endSection": "abstract",
"offsetInBeginSection": 326,
"offsetInEndSection": 780,
"text": "Aim of the present meta-analysis is the systematic collection and synthesis of information on treatment-emergent cases of acute heart failure described in randomized clinical trials with DPP4.DATA SOURCES: An extensive Medline, Embase, and Cochrane Database search for \"vildagliptin\", \"sitagliptin\", \"saxagliptin\", \"alogliptin\", \"linagliptin\", and \"dutogliptin\" was performed, collecting all randomized clinical trials on humans up to October 1st, 2013. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22162539",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 192,
"text": "Quantitative model of the relationship between dipeptidyl peptidase-4 (DPP-4) inhibition and response: meta-analysis of alogliptin, saxagliptin, sitagliptin, and vildagliptin efficacy results."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21913883",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 194,
"text": "The dipeptidyl peptidase-4 (DPP-4) inhibitors linagliptin, sitagliptin, saxagliptin, vildagliptin and alogliptin are being developed and have been approved for the treatment of type-2 diabetes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22162539",
"endSection": "abstract",
"offsetInBeginSection": 114,
"offsetInEndSection": 313,
"text": "The objective of this model-based meta-analysis was to describe the time course of HbA1c response after dosing with alogliptin (ALOG), saxagliptin (SAXA), sitagliptin (SITA), or vildagliptin (VILD). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24996141",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Discovery of highly potent DPP-4 inhibitors by hybrid compound design based on linagliptin and alogliptin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23837679",
"endSection": "abstract",
"offsetInBeginSection": 331,
"offsetInEndSection": 543,
"text": "METHODS: DATA SOURCES: an extensive Medline, Embase and Cochrane Database search for 'vildagliptin', 'sitagliptin', 'saxagliptin', 'alogliptin', 'linagliptin' and 'dutogliptin' was performed up to 1 March 2013. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22106978",
"endSection": "abstract",
"offsetInBeginSection": 321,
"offsetInEndSection": 574,
"text": "RESEARCH DESIGN AND METHODS: An extensive Medline and Embase search for 'vildagliptin', 'sitagliptin', 'saxagliptin', 'alogliptin', 'linagliptin', and 'dutogliptin' was performed, collecting all randomized clinical trials on humans up to March 1, 2011. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23803146",
"endSection": "abstract",
"offsetInBeginSection": 246,
"offsetInEndSection": 632,
"text": "METHODS: We conducted a search on MEDLINE, Embase and Cochrane Collaborative database for randomized controlled trials (RCTs) of DPP-4 inhibitors and metformin as initial combination therapy or as monotherapy in patients with T2DM by the end of December 2012, using the key words 'alogliptin', 'dutogliptin', 'linagliptin', 'saxagliptin', 'sitagliptin', 'vildagliptin' and 'metformin'. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23140189",
"endSection": "abstract",
"offsetInBeginSection": 328,
"offsetInEndSection": 466,
"text": "Sitagliptin (MK- 0431), Saxagliptin, Melogliptin, Linagliptin (BI-1356), Dutogliptin, Carmegliptin, Alogliptin and Vildagliptin (LAF237). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24793580",
"endSection": "abstract",
"offsetInBeginSection": 326,
"offsetInEndSection": 780,
"text": "Aim of the present meta-analysis is the systematic collection and synthesis of information on treatment-emergent cases of acute heart failure described in randomized clinical trials with DPP4.DATA SOURCES: An extensive Medline, Embase, and Cochrane Database search for \"vildagliptin\", \"sitagliptin\", \"saxagliptin\", \"alogliptin\", \"linagliptin\", and \"dutogliptin\" was performed, collecting all randomized clinical trials on humans up to October 1st, 2013. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22162539",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 192,
"text": "Quantitative model of the relationship between dipeptidyl peptidase-4 (DPP-4) inhibition and response: meta-analysis of alogliptin, saxagliptin, sitagliptin, and vildagliptin efficacy results."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21913883",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 194,
"text": "The dipeptidyl peptidase-4 (DPP-4) inhibitors linagliptin, sitagliptin, saxagliptin, vildagliptin and alogliptin are being developed and have been approved for the treatment of type-2 diabetes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22162539",
"endSection": "abstract",
"offsetInBeginSection": 114,
"offsetInEndSection": 313,
"text": "The objective of this model-based meta-analysis was to describe the time course of HbA1c response after dosing with alogliptin (ALOG), saxagliptin (SAXA), sitagliptin (SITA), or vildagliptin (VILD). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24996141",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Discovery of highly potent DPP-4 inhibitors by hybrid compound design based on linagliptin and alogliptin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23140189",
"endSection": "abstract",
"offsetInBeginSection": 328,
"offsetInEndSection": 466,
"text": "Sitagliptin (MK- 0431), Saxagliptin, Melogliptin, Linagliptin (BI-1356), Dutogliptin, Carmegliptin, Alogliptin and Vildagliptin (LAF237). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24320733",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "The dipeptidylpeptidase-IV inhibitors sitagliptin, vildagliptin and saxagliptin do not impair innate and adaptive immune responses."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24996141",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Discovery of highly potent DPP-4 inhibitors by hybrid compound design based on linagliptin and alogliptin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18223196",
"endSection": "abstract",
"offsetInBeginSection": 1399,
"offsetInEndSection": 1627,
"text": "In conclusion, BI 1356 inhibited DPP-4 more effectively than vildagliptin, sitagliptin, saxagliptin, and alogliptin and has the potential to become the first truly once-a-day DPP-4 inhibitor for the treatment of type 2 diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24996141",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "Highly potent DPP-4 inhibitors have been identified by hybrid compound design based on linagliptin and alogliptin. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21320267",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 206,
"text": "AIM: We assessed the efficacy of dipeptidyl peptidase-4 (DPP-4) inhibitors vildagliptin, sitagliptin, saxagliptin and alogliptin to reach the haemoglobin HbA1c target of <7% in people with type 2 diabetes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24320733",
"endSection": "abstract",
"offsetInBeginSection": 210,
"offsetInEndSection": 337,
"text": "Whether the DPP-IV inhibitors sitagliptin, vildagliptin or saxagliptin impair immune responses is, however, currently unknown. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23136353",
"endSection": "abstract",
"offsetInBeginSection": 125,
"offsetInEndSection": 278,
"text": "OBJECTIVE: To assess the efficacy and safety of DPP-4 inhibitors, including sitagliptin, saxagliptin, vildagliptin, and linagliptin, in type 2 diabetes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23837679",
"endSection": "abstract",
"offsetInBeginSection": 331,
"offsetInEndSection": 543,
"text": "METHODS: DATA SOURCES: an extensive Medline, Embase and Cochrane Database search for 'vildagliptin', 'sitagliptin', 'saxagliptin', 'alogliptin', 'linagliptin' and 'dutogliptin' was performed up to 1 March 2013. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22106978",
"endSection": "abstract",
"offsetInBeginSection": 321,
"offsetInEndSection": 574,
"text": "RESEARCH DESIGN AND METHODS: An extensive Medline and Embase search for 'vildagliptin', 'sitagliptin', 'saxagliptin', 'alogliptin', 'linagliptin', and 'dutogliptin' was performed, collecting all randomized clinical trials on humans up to March 1, 2011. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23803146",
"endSection": "abstract",
"offsetInBeginSection": 246,
"offsetInEndSection": 632,
"text": "METHODS: We conducted a search on MEDLINE, Embase and Cochrane Collaborative database for randomized controlled trials (RCTs) of DPP-4 inhibitors and metformin as initial combination therapy or as monotherapy in patients with T2DM by the end of December 2012, using the key words 'alogliptin', 'dutogliptin', 'linagliptin', 'saxagliptin', 'sitagliptin', 'vildagliptin' and 'metformin'. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23140189",
"endSection": "abstract",
"offsetInBeginSection": 328,
"offsetInEndSection": 466,
"text": "Sitagliptin (MK- 0431), Saxagliptin, Melogliptin, Linagliptin (BI-1356), Dutogliptin, Carmegliptin, Alogliptin and Vildagliptin (LAF237). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24793580",
"endSection": "abstract",
"offsetInBeginSection": 326,
"offsetInEndSection": 780,
"text": "Aim of the present meta-analysis is the systematic collection and synthesis of information on treatment-emergent cases of acute heart failure described in randomized clinical trials with DPP4.DATA SOURCES: An extensive Medline, Embase, and Cochrane Database search for \"vildagliptin\", \"sitagliptin\", \"saxagliptin\", \"alogliptin\", \"linagliptin\", and \"dutogliptin\" was performed, collecting all randomized clinical trials on humans up to October 1st, 2013. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22162539",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 192,
"text": "Quantitative model of the relationship between dipeptidyl peptidase-4 (DPP-4) inhibition and response: meta-analysis of alogliptin, saxagliptin, sitagliptin, and vildagliptin efficacy results."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21913883",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 194,
"text": "The dipeptidyl peptidase-4 (DPP-4) inhibitors linagliptin, sitagliptin, saxagliptin, vildagliptin and alogliptin are being developed and have been approved for the treatment of type-2 diabetes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22162539",
"endSection": "abstract",
"offsetInBeginSection": 114,
"offsetInEndSection": 313,
"text": "The objective of this model-based meta-analysis was to describe the time course of HbA1c response after dosing with alogliptin (ALOG), saxagliptin (SAXA), sitagliptin (SITA), or vildagliptin (VILD). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24996141",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Discovery of highly potent DPP-4 inhibitors by hybrid compound design based on linagliptin and alogliptin."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24793219",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "Testing the therapeutic equivalence of alogliptin, linagliptin, saxagliptin, sitagliptin or vildagliptin as monotherapy or in combination with metformin in patients with type 2 diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24793219",
"endSection": "abstract",
"offsetInBeginSection": 894,
"offsetInEndSection": 1042,
"text": "Given as monotherapy, linagliptin, sitagliptin, and vildagliptin (but not saxagliptin) met the equivalence criterion when compared with one another."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24793219",
"endSection": "abstract",
"offsetInBeginSection": 1043,
"offsetInEndSection": 1225,
"text": "Given in combination with metformin, linagliptin, saxagliptin, sitagliptin, and vildagliptin showed an equivalent effect whereas alogliptin did not satisfy the equivalence criterion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23837679",
"endSection": "abstract",
"offsetInBeginSection": 327,
"offsetInEndSection": 514,
"text": "an extensive Medline, Embase and Cochrane Database search for 'vildagliptin', 'sitagliptin', 'saxagliptin', 'alogliptin', 'linagliptin' and 'dutogliptin' was performed up to 1 March 2013."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24793219",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "Testing the therapeutic equivalence of alogliptin, linagliptin, saxagliptin, sitagliptin or vildagliptin as monotherapy or in combination with metformin in patients with type 2 diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22106978",
"endSection": "abstract",
"offsetInBeginSection": 310,
"offsetInEndSection": 533,
"text": "An extensive Medline and Embase search for 'vildagliptin', 'sitagliptin', 'saxagliptin', 'alogliptin', 'linagliptin', and 'dutogliptin' was performed, collecting all randomized clinical trials on humans up to March 1, 2011."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24793580",
"endSection": "abstract",
"offsetInBeginSection": 501,
"offsetInEndSection": 748,
"text": "An extensive Medline, Embase, and Cochrane Database search for \"vildagliptin\", \"sitagliptin\", \"saxagliptin\", \"alogliptin\", \"linagliptin\", and \"dutogliptin\" was performed, collecting all randomized clinical trials on humans up to October 1st, 2013."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19791828",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 12,
"text": "Saxagliptin."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17100408",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 13,
"text": "Vildagliptin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24793219",
"endSection": "abstract",
"offsetInBeginSection": 894,
"offsetInEndSection": 1042,
"text": "Given as monotherapy, linagliptin, sitagliptin, and vildagliptin (but not saxagliptin) met the equivalence criterion when compared with one another."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23837679",
"endSection": "abstract",
"offsetInBeginSection": 327,
"offsetInEndSection": 515,
"text": "an extensive Medline, Embase and Cochrane Database search for 'vildagliptin', 'sitagliptin', 'saxagliptin', 'alogliptin', 'linagliptin' and 'dutogliptin' was performed up to 1 March 2013."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22106978",
"endSection": "abstract",
"offsetInBeginSection": 311,
"offsetInEndSection": 534,
"text": "An extensive Medline and Embase search for 'vildagliptin', 'sitagliptin', 'saxagliptin', 'alogliptin', 'linagliptin', and 'dutogliptin' was performed, collecting all randomized clinical trials on humans up to March 1, 2011."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24793580",
"endSection": "abstract",
"offsetInBeginSection": 501,
"offsetInEndSection": 749,
"text": "An extensive Medline, Embase, and Cochrane Database search for \"vildagliptin\", \"sitagliptin\", \"saxagliptin\", \"alogliptin\", \"linagliptin\", and \"dutogliptin\" was performed, collecting all randomized clinical trials on humans up to October 1st, 2013."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22215383",
"endSection": "abstract",
"offsetInBeginSection": 657,
"offsetInEndSection": 864,
"text": "the words \"sitagliptin,\" \"vildagliptin,\" \"saxagliptin,\" \"alogliptin,\" \"linagliptin,\" and/or \"dutogliptin.\" Completed but unpublished trials were identified through a search of the ClinicalTrials.gov website,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23140189",
"endSection": "abstract",
"offsetInBeginSection": 329,
"offsetInEndSection": 466,
"text": "Sitagliptin (MK- 0431), Saxagliptin, Melogliptin, Linagliptin (BI-1356), Dutogliptin, Carmegliptin, Alogliptin and Vildagliptin (LAF237)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21431099",
"endSection": "abstract",
"offsetInBeginSection": 726,
"offsetInEndSection": 1025,
"text": "Of these, two have been approved for clinical use in the United States: sitagliptin and saxagliptin. Additionally, linagliptin, vildagliptin and alogliptin are currently in phase III development in the United States while studies with another DPP IV inhibitor, dutogliptin, have been terminated (2)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23803146",
"endSection": "abstract",
"offsetInBeginSection": 241,
"offsetInEndSection": 617,
"text": "We conducted a search on MEDLINE, Embase and Cochrane Collaborative database for randomized controlled trials (RCTs) of DPP-4 inhibitors and metformin as initial combination therapy or as monotherapy in patients with T2DM by the end of December 2012, using the key words 'alogliptin', 'dutogliptin', 'linagliptin', 'saxagliptin', 'sitagliptin', 'vildagliptin' and 'metformin'."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24793219",
"endSection": "abstract",
"offsetInBeginSection": 895,
"offsetInEndSection": 1226,
"text": "Given as monotherapy, linagliptin, sitagliptin, and vildagliptin (but not saxagliptin) met the equivalence criterion when compared with one another. Given in combination with metformin, linagliptin, saxagliptin, sitagliptin, and vildagliptin showed an equivalent effect whereas alogliptin did not satisfy the equivalence criterion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21431099",
"endSection": "abstract",
"offsetInBeginSection": 827,
"offsetInEndSection": 1114,
"text": "Additionally, linagliptin, vildagliptin and alogliptin are currently in phase III development in the United States while studies with another DPP IV inhibitor, dutogliptin, have been terminated (2). Alogliptin was approved for use in Japan under the trade name Nesina® in April 2010 (3)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25687897",
"endSection": "abstract",
"offsetInBeginSection": 729,
"offsetInEndSection": 817,
"text": "Any DPP-4 inhibitor (vildagliptin, sitagliptin, saxagliptin, linagliptin or alogliptin)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23837679",
"endSection": "abstract",
"offsetInBeginSection": 327,
"offsetInEndSection": 515,
"text": "an extensive Medline, Embase and Cochrane Database search for 'vildagliptin', 'sitagliptin', 'saxagliptin', 'alogliptin', 'linagliptin' and 'dutogliptin' was performed up to 1 March 2013."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22106978",
"endSection": "abstract",
"offsetInBeginSection": 311,
"offsetInEndSection": 534,
"text": "An extensive Medline and Embase search for 'vildagliptin', 'sitagliptin', 'saxagliptin', 'alogliptin', 'linagliptin', and 'dutogliptin' was performed, collecting all randomized clinical trials on humans up to March 1, 2011."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24793580",
"endSection": "abstract",
"offsetInBeginSection": 501,
"offsetInEndSection": 749,
"text": "An extensive Medline, Embase, and Cochrane Database search for \"vildagliptin\", \"sitagliptin\", \"saxagliptin\", \"alogliptin\", \"linagliptin\", and \"dutogliptin\" was performed, collecting all randomized clinical trials on humans up to October 1st, 2013."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22215383",
"endSection": "abstract",
"offsetInBeginSection": 447,
"offsetInEndSection": 898,
"text": "An extensive search of Medline and the Cochrane Library (any date up to December 31, 2010, restricted to randomized clinical trials, published in English) was performed for all trials containing, in any field, the words \"sitagliptin,\" \"vildagliptin,\" \"saxagliptin,\" \"alogliptin,\" \"linagliptin,\" and/or \"dutogliptin.\" Completed but unpublished trials were identified through a search of the ClinicalTrials.gov website, using the same keywords as above."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23803146",
"endSection": "abstract",
"offsetInBeginSection": 241,
"offsetInEndSection": 617,
"text": "We conducted a search on MEDLINE, Embase and Cochrane Collaborative database for randomized controlled trials (RCTs) of DPP-4 inhibitors and metformin as initial combination therapy or as monotherapy in patients with T2DM by the end of December 2012, using the key words 'alogliptin', 'dutogliptin', 'linagliptin', 'saxagliptin', 'sitagliptin', 'vildagliptin' and 'metformin'."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25687897",
"endSection": "abstract",
"offsetInBeginSection": 729,
"offsetInEndSection": 817,
"text": "Any DPP-4 inhibitor (vildagliptin, sitagliptin, saxagliptin, linagliptin or alogliptin)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25687897",
"endSection": "abstract",
"offsetInBeginSection": 155,
"offsetInEndSection": 345,
"text": "A systematic review and meta-analysis of randomised controlled trials (RCTs) of DPP-4 inhibitors (vildagliptin, sitagliptin, saxagliptin, linagliptin and alogliptin) on HbA1c were conducted."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24567800",
"endSection": "abstract",
"offsetInBeginSection": 452,
"offsetInEndSection": 780,
"text": "Several clinical trials have studied the addition of GLP-1 receptor agonists [exenatide BID (twice daily), lixisenatide, albiglutide] or DPP-4 inhibitors (vildagliptin, sitagliptin, saxagliptin, alogliptin, linagliptin) to ongoing insulin therapy or adding insulin to ongoing therapy with a GLP-1 receptor agonist (liraglutide)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24793219",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "Testing the therapeutic equivalence of alogliptin, linagliptin, saxagliptin, sitagliptin or vildagliptin as monotherapy or in combination with metformin in patients with type 2 diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21431099",
"endSection": "abstract",
"offsetInBeginSection": 827,
"offsetInEndSection": 1025,
"text": "Additionally, linagliptin, vildagliptin and alogliptin are currently in phase III development in the United States while studies with another DPP IV inhibitor, dutogliptin, have been terminated (2)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23837679",
"endSection": "abstract",
"offsetInBeginSection": 327,
"offsetInEndSection": 515,
"text": "an extensive Medline, Embase and Cochrane Database search for 'vildagliptin', 'sitagliptin', 'saxagliptin', 'alogliptin', 'linagliptin' and 'dutogliptin' was performed up to 1 March 2013."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22106978",
"endSection": "abstract",
"offsetInBeginSection": 311,
"offsetInEndSection": 534,
"text": "An extensive Medline and Embase search for 'vildagliptin', 'sitagliptin', 'saxagliptin', 'alogliptin', 'linagliptin', and 'dutogliptin' was performed, collecting all randomized clinical trials on humans up to March 1, 2011."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24793580",
"endSection": "abstract",
"offsetInBeginSection": 501,
"offsetInEndSection": 749,
"text": "An extensive Medline, Embase, and Cochrane Database search for \"vildagliptin\", \"sitagliptin\", \"saxagliptin\", \"alogliptin\", \"linagliptin\", and \"dutogliptin\" was performed, collecting all randomized clinical trials on humans up to October 1st, 2013."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23140189",
"endSection": "abstract",
"offsetInBeginSection": 329,
"offsetInEndSection": 466,
"text": "Sitagliptin (MK- 0431), Saxagliptin, Melogliptin, Linagliptin (BI-1356), Dutogliptin, Carmegliptin, Alogliptin and Vildagliptin (LAF237)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22215383",
"endSection": "abstract",
"offsetInBeginSection": 447,
"offsetInEndSection": 898,
"text": "An extensive search of Medline and the Cochrane Library (any date up to December 31, 2010, restricted to randomized clinical trials, published in English) was performed for all trials containing, in any field, the words \"sitagliptin,\" \"vildagliptin,\" \"saxagliptin,\" \"alogliptin,\" \"linagliptin,\" and/or \"dutogliptin.\" Completed but unpublished trials were identified through a search of the ClinicalTrials.gov website, using the same keywords as above."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23803146",
"endSection": "abstract",
"offsetInBeginSection": 241,
"offsetInEndSection": 617,
"text": "We conducted a search on MEDLINE, Embase and Cochrane Collaborative database for randomized controlled trials (RCTs) of DPP-4 inhibitors and metformin as initial combination therapy or as monotherapy in patients with T2DM by the end of December 2012, using the key words 'alogliptin', 'dutogliptin', 'linagliptin', 'saxagliptin', 'sitagliptin', 'vildagliptin' and 'metformin'."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25687897",
"endSection": "abstract",
"offsetInBeginSection": 729,
"offsetInEndSection": 817,
"text": "Any DPP-4 inhibitor (vildagliptin, sitagliptin, saxagliptin, linagliptin or alogliptin)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25687897",
"endSection": "abstract",
"offsetInBeginSection": 155,
"offsetInEndSection": 345,
"text": "A systematic review and meta-analysis of randomised controlled trials (RCTs) of DPP-4 inhibitors (vildagliptin, sitagliptin, saxagliptin, linagliptin and alogliptin) on HbA1c were conducted."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24793219",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "Testing the therapeutic equivalence of alogliptin, linagliptin, saxagliptin, sitagliptin or vildagliptin as monotherapy or in combination with metformin in patients with type 2 diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20690781",
"endSection": "abstract",
"offsetInBeginSection": 1131,
"offsetInEndSection": 1326,
"text": "This review summarizes the available data on drug-drug interactions reported in the literature for these five DDP-4 inhibitors: sitagliptin, vildagliptin, saxagliptin, alogliptin and linagliptin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23837679",
"endSection": "abstract",
"offsetInBeginSection": 327,
"offsetInEndSection": 515,
"text": "an extensive Medline, Embase and Cochrane Database search for 'vildagliptin', 'sitagliptin', 'saxagliptin', 'alogliptin', 'linagliptin' and 'dutogliptin' was performed up to 1 March 2013."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22106978",
"endSection": "abstract",
"offsetInBeginSection": 311,
"offsetInEndSection": 534,
"text": "An extensive Medline and Embase search for 'vildagliptin', 'sitagliptin', 'saxagliptin', 'alogliptin', 'linagliptin', and 'dutogliptin' was performed, collecting all randomized clinical trials on humans up to March 1, 2011."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24793580",
"endSection": "abstract",
"offsetInBeginSection": 501,
"offsetInEndSection": 749,
"text": "An extensive Medline, Embase, and Cochrane Database search for \"vildagliptin\", \"sitagliptin\", \"saxagliptin\", \"alogliptin\", \"linagliptin\", and \"dutogliptin\" was performed, collecting all randomized clinical trials on humans up to October 1st, 2013."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23140189",
"endSection": "abstract",
"offsetInBeginSection": 329,
"offsetInEndSection": 466,
"text": "Sitagliptin (MK- 0431), Saxagliptin, Melogliptin, Linagliptin (BI-1356), Dutogliptin, Carmegliptin, Alogliptin and Vildagliptin (LAF237)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22215383",
"endSection": "abstract",
"offsetInBeginSection": 447,
"offsetInEndSection": 898,
"text": "An extensive search of Medline and the Cochrane Library (any date up to December 31, 2010, restricted to randomized clinical trials, published in English) was performed for all trials containing, in any field, the words \"sitagliptin,\" \"vildagliptin,\" \"saxagliptin,\" \"alogliptin,\" \"linagliptin,\" and/or \"dutogliptin.\" Completed but unpublished trials were identified through a search of the ClinicalTrials.gov website, using the same keywords as above."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25687897",
"endSection": "abstract",
"offsetInBeginSection": 729,
"offsetInEndSection": 817,
"text": "Any DPP-4 inhibitor (vildagliptin, sitagliptin, saxagliptin, linagliptin or alogliptin)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23803146",
"endSection": "abstract",
"offsetInBeginSection": 241,
"offsetInEndSection": 617,
"text": "We conducted a search on MEDLINE, Embase and Cochrane Collaborative database for randomized controlled trials (RCTs) of DPP-4 inhibitors and metformin as initial combination therapy or as monotherapy in patients with T2DM by the end of December 2012, using the key words 'alogliptin', 'dutogliptin', 'linagliptin', 'saxagliptin', 'sitagliptin', 'vildagliptin' and 'metformin'."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25687897",
"endSection": "abstract",
"offsetInBeginSection": 155,
"offsetInEndSection": 345,
"text": "A systematic review and meta-analysis of randomised controlled trials (RCTs) of DPP-4 inhibitors (vildagliptin, sitagliptin, saxagliptin, linagliptin and alogliptin) on HbA1c were conducted."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24793219",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "Testing the therapeutic equivalence of alogliptin, linagliptin, saxagliptin, sitagliptin or vildagliptin as monotherapy or in combination with metformin in patients with type 2 diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20690781",
"endSection": "abstract",
"offsetInBeginSection": 1131,
"offsetInEndSection": 1326,
"text": "This review summarizes the available data on drug-drug interactions reported in the literature for these five DDP-4 inhibitors: sitagliptin, vildagliptin, saxagliptin, alogliptin and linagliptin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23837679",
"endSection": "abstract",
"offsetInBeginSection": 327,
"offsetInEndSection": 515,
"text": "an extensive Medline, Embase and Cochrane Database search for 'vildagliptin', 'sitagliptin', 'saxagliptin', 'alogliptin', 'linagliptin' and 'dutogliptin' was performed up to 1 March 2013."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22106978",
"endSection": "abstract",
"offsetInBeginSection": 311,
"offsetInEndSection": 534,
"text": "An extensive Medline and Embase search for 'vildagliptin', 'sitagliptin', 'saxagliptin', 'alogliptin', 'linagliptin', and 'dutogliptin' was performed, collecting all randomized clinical trials on humans up to March 1, 2011."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24793580",
"endSection": "abstract",
"offsetInBeginSection": 501,
"offsetInEndSection": 749,
"text": "An extensive Medline, Embase, and Cochrane Database search for \"vildagliptin\", \"sitagliptin\", \"saxagliptin\", \"alogliptin\", \"linagliptin\", and \"dutogliptin\" was performed, collecting all randomized clinical trials on humans up to October 1st, 2013."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23140189",
"endSection": "abstract",
"offsetInBeginSection": 329,
"offsetInEndSection": 466,
"text": "Sitagliptin (MK- 0431), Saxagliptin, Melogliptin, Linagliptin (BI-1356), Dutogliptin, Carmegliptin, Alogliptin and Vildagliptin (LAF237)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22215383",
"endSection": "abstract",
"offsetInBeginSection": 447,
"offsetInEndSection": 898,
"text": "An extensive search of Medline and the Cochrane Library (any date up to December 31, 2010, restricted to randomized clinical trials, published in English) was performed for all trials containing, in any field, the words \"sitagliptin,\" \"vildagliptin,\" \"saxagliptin,\" \"alogliptin,\" \"linagliptin,\" and/or \"dutogliptin.\" Completed but unpublished trials were identified through a search of the ClinicalTrials.gov website, using the same keywords as above."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23803146",
"endSection": "abstract",
"offsetInBeginSection": 241,
"offsetInEndSection": 617,
"text": "We conducted a search on MEDLINE, Embase and Cochrane Collaborative database for randomized controlled trials (RCTs) of DPP-4 inhibitors and metformin as initial combination therapy or as monotherapy in patients with T2DM by the end of December 2012, using the key words 'alogliptin', 'dutogliptin', 'linagliptin', 'saxagliptin', 'sitagliptin', 'vildagliptin' and 'metformin'."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21431099",
"endSection": "abstract",
"offsetInBeginSection": 827,
"offsetInEndSection": 1025,
"text": "Additionally, linagliptin, vildagliptin and alogliptin are currently in phase III development in the United States while studies with another DPP IV inhibitor, dutogliptin, have been terminated (2)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25687897",
"endSection": "abstract",
"offsetInBeginSection": 729,
"offsetInEndSection": 817,
"text": "Any DPP-4 inhibitor (vildagliptin, sitagliptin, saxagliptin, linagliptin or alogliptin)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24567800",
"endSection": "abstract",
"offsetInBeginSection": 452,
"offsetInEndSection": 780,
"text": "Several clinical trials have studied the addition of GLP-1 receptor agonists [exenatide BID (twice daily), lixisenatide, albiglutide] or DPP-4 inhibitors (vildagliptin, sitagliptin, saxagliptin, alogliptin, linagliptin) to ongoing insulin therapy or adding insulin to ongoing therapy with a GLP-1 receptor agonist (liraglutide)."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.biosemantics.org/jochem#4243818",
"http://www.biosemantics.org/jochem#4243458",
"http://www.biosemantics.org/jochem#4274679",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D000069476",
"http://www.biosemantics.org/jochem#http://www.biosemantics.org/jochem#:4274679",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D054873",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018819"
] |
[] |
571e275dbb137a4b0c000005
|
bioasq_factoid
|
factoid
|
How many genera comprise the Flaviviridae family?
|
['three', '3']
|
[
"three",
"3"
] |
['The family Flaviviridae is comprised of three genera: Flavivirus, Pestivirus and Hepacivirus.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22513121",
"http://www.ncbi.nlm.nih.gov/pubmed/20470249",
"http://www.ncbi.nlm.nih.gov/pubmed/8396675",
"http://www.ncbi.nlm.nih.gov/pubmed/19534676",
"http://www.ncbi.nlm.nih.gov/pubmed/19035566",
"http://www.ncbi.nlm.nih.gov/pubmed/18991746",
"http://www.ncbi.nlm.nih.gov/pubmed/22039536",
"http://www.ncbi.nlm.nih.gov/pubmed/21249176",
"http://www.ncbi.nlm.nih.gov/pubmed/19555498",
"http://www.ncbi.nlm.nih.gov/pubmed/16225688",
"http://www.ncbi.nlm.nih.gov/pubmed/22031952"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22513121",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 352,
"text": "Within a project aimed at discovering new Flaviviridae inhibitors, new variously substituted 2-phenylbenzimidazoles were synthesized and evaluated in cell-based assays for cytotoxicity and antiviral activity against viruses representatives of the three genera of the Flaviviridae family, i.e.: Pestivirus (BVDV), Flavivirus (YFV) and Hepacivirus (HCV)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20470249",
"endSection": "sections.0",
"offsetInBeginSection": 172,
"offsetInEndSection": 340,
"text": "Compounds were tested in cell-based assays against viruses representative of: i) two of the three genera of the Flaviviridae family, i.e. Pestiviruses and Flaviviruses;"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8396675",
"endSection": "sections.0",
"offsetInBeginSection": 189,
"offsetInEndSection": 368,
"text": "The RNA-stimulated NTPase activity of this protein from prototypic members of the Pestivirus and Flavivirus genera has recently been established and enzymologically characterized."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19534676",
"endSection": "sections.0",
"offsetInBeginSection": 196,
"offsetInEndSection": 539,
"text": "Compounds were tested in cell-based assays against viruses representative of: i) two of the three genera of the Flaviviridae family, i.e. Flaviviruses and Pestiviruses; ii) other RNA virus families, such as Retroviridae, Picornaviridae, Paramyxoviridae, Rhabdoviridae and Reoviridae; iii) two DNA virus families (Herpesviridae and Poxviridae)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19035566",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 490,
"text": "Forty-three 2-[(benzotriazol-1/2-yl)methyl]benzimidazoles, bearing either linear (dialkylamino)alkyl- or bulkier (quinolizidin-1-yl)alkyl moieties at position 1, were evaluated in cell-based assays for cytotoxicity and antiviral activity against viruses representative of two of the three genera of the Flaviviridae family, i.e. Flaviviruses (Yellow Fever Virus (YFV)) and Pestiviruses (Bovine Viral Diarrhoea Virus (BVDV)), as Hepaciviruses can hardly be used in routine cell-based assays."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18991746",
"endSection": "sections.0",
"offsetInBeginSection": 360,
"offsetInEndSection": 703,
"text": "Compounds were tested in cell-based assays against viruses representative of: i) two of the three genera of the Flaviviridae family, i.e. Flaviviruses and Pestiviruses; ii) other RNA virus families, such as Retroviridae, Picornaviridae, Paramyxoviridae, Rhabdoviridae and Reoviridae; iii) two DNA virus families (Herpesviridae and Poxviridae)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22513121",
"endSection": "sections.0",
"offsetInBeginSection": 292,
"offsetInEndSection": 352,
"text": ": Pestivirus (BVDV), Flavivirus (YFV) and Hepacivirus (HCV)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22031952",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "The family Flaviviridae contains three genera of positive-strand RNA viruses, namely, Flavivirus, Hepacivirus (e.g., hepatitis C virus [HCV]), and Pestivirus."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018067"
] | null |
51651e24298dcd4e51000054
|
bioasq_factoid
|
factoid
|
Which amino acid in implicated in the Blue diaper syndrome?
|
['tryptophan']
|
[
"tryptophan",
"L-tryptophan",
"α-amino-β-(3-indolyl)propionic acid",
"indole-3-amino acid",
"Trp"
] |
['Blue diaper syndrome is an extremely rare disorder with characteristic finding is a bluish discoloration of urine spots in the diapers of affected infants. An intestinal defect of tryptophan absorption was postulated as the underlying pathology.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29610180",
"http://www.ncbi.nlm.nih.gov/pubmed/1818237"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29610180",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 477,
"text": "Blue diaper syndrome (BDS) (Online Mendelian Inheritance in Man number 211000) is an extremely rare disorder that was first described in 1964. The characteristic finding is a bluish discoloration of urine spots in the diapers of affected infants. Additional clinical features of the first described patients included diarrhea, inadequate weight gain, hypercalcemia, and nephrocalcinosis. An intestinal defect of tryptophan absorption was postulated as the underlying pathology."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1818237",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "We describe the ocular abnormalities seen in a new metabolic disease which is deficient in the transport of tryptophan. "
}
] | 12 |
BioASQ-training12b
| null | null |
63f57d9b33942b094c000004
|
bioasq_factoid
|
factoid
|
Hy's law measures failure for what organ?
|
['liver']
|
[
"liver",
"hepatic",
"hepar",
"hepatocyte",
"liver organ",
"liver tissue"
] |
["Hy's law correlates enzyme elevations with liver injury ad subsequent failure."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24203912",
"http://www.ncbi.nlm.nih.gov/pubmed/26116527",
"http://www.ncbi.nlm.nih.gov/pubmed/23874514",
"http://www.ncbi.nlm.nih.gov/pubmed/22928730",
"http://www.ncbi.nlm.nih.gov/pubmed/24704526",
"http://www.ncbi.nlm.nih.gov/pubmed/26159259",
"http://www.ncbi.nlm.nih.gov/pubmed/23300062",
"http://www.ncbi.nlm.nih.gov/pubmed/26122767",
"http://www.ncbi.nlm.nih.gov/pubmed/25683797"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26116527",
"endSection": "abstract",
"offsetInBeginSection": 169,
"offsetInEndSection": 420,
"text": " Hy's Law of drug-induced hepatocellular jaundice causing a case-fatality rate or need for transplant of 10% or higher has been validated in several large national registries, including the ongoing, prospective U.S. Drug-Induced Liver Injury Network. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26159259",
"endSection": "abstract",
"offsetInBeginSection": 399,
"offsetInEndSection": 556,
"text": "Enzyme elevations alone may not be harmful, but if caused by a drug and followed by jaundice (called 'Hy's law') there is a high possibility of serious DILI."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23874514",
"endSection": "abstract",
"offsetInBeginSection": 1064,
"offsetInEndSection": 1211,
"text": "No additional alleles outside those associated with liver injury patterns were found to affect potential severity as measured by Hy's Law criteria."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26122767",
"endSection": "abstract",
"offsetInBeginSection": 255,
"offsetInEndSection": 717,
"text": "We compared its performance with that of Hy's Law, which predicts severity of DILI based on levels of alanine aminotransferase or aspartate aminotransferase and total bilirubin, and validated the model in a separate sample.We conducted a retrospective cohort study of 15,353 Kaiser Permanente Northern California members diagnosed with DILI from 2004 through 2010, liver aminotransferase levels above the upper limit of normal, and no pre-existing liver disease."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26122767",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "Risk of Acute Liver Failure in Patients With Drug-Induced Liver Injury: Evaluation of Hy's Law and a New Prognostic Model."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24704526",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 183,
"text": "Hy's Law, which states that hepatocellular drug-induced liver injury (DILI) with jaundice indicates a serious reaction, is used widely to determine risk for acute liver failure (ALF)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25683797",
"endSection": "abstract",
"offsetInBeginSection": 46,
"offsetInEndSection": 116,
"text": "Hy's law is a method used to identify drug-induced liver injury (DILI)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22928730",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 180,
"text": "Potential severe liver injury is identified in clinical trials by ALT>3 × upper limits of normal (ULN) and total bilirubin>2 × ULN, and termed 'Hy's Law' by the US FDA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23300062",
"endSection": "abstract",
"offsetInBeginSection": 120,
"offsetInEndSection": 327,
"text": "Severe liver injury is identified by the liver chemistry threshold of alanine aminotransferase (ALT)>3× upper limit of normal (ULN) and bilirubin>2× ULN, termed Hy's law by the Food and Drug Administration. "
}
] | 6 |
BioASQ-training6b
|
[
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D065290",
"http://www.disease-ontology.org/api/metadata/DOID:2044",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D056486",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D056487",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D008111",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D017114",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D058625"
] | null |
58f4b25e70f9fc6f0f000011
|
bioasq_factoid
|
factoid
|
What process does tRNA nucleotidyl transferase 1 (TRNT1) catalyze?
|
["Addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs)"]
|
[
"CCA",
"cytosine-cytosine-adenine",
"cytosine/adenine",
"addition of CCA",
"addition of the trinucleotide CCA",
"addition of the trinucleotide cytosine/cytosine/adenine",
"3' end addition of CCA",
"3' end addition of cytosine/cytosine/adenine"
] |
["tRNA nucleotidyl transferase 1 (TRNT1) catalyzes the addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs).", 'The tRNA nucleotidyl transferase 1 (TRNT1) catalyzes the addition of terminal cytosine-cytosine-adenosine (CCA) trinucleotides to all mature tRNAs, which is necessary for aminoacylation.', "tRNA nucleotidyl transferase 1 (TRNT1) catalyzes the addition of CCA nucleotides to the 3' end of tRNA molecules during tRNA maturation.", "tRNA nucleotidyl transferase 1 (TRNT1) catalyzes the addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs), which is essential for translation and functions in both the cytoplasm and mitochondria.", "tRNA nucleotidyl transferase 1 (TRNT1) catalyzes the addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs), a crucial process for translation.", "The TRNT1 enzyme catalyzes the addition of the trinucleotide CCA to the 3' end of tRNAs.", 'TRNT1 gene encodes a CCA-adding tRNA nucleotidyl transferase enzyme.', "tRNA nucleotidyl transferase 1 (TRNT1) catalyzes the addition of the trinucleotide cytosine-cytosine-adenine (CCA) sequence to the 3' end of transfer RNAs (tRNAs). This CCA addition is essential for tRNA function in protein translation.", "tRNA nucleotidyl transferase 1 (TRNT1) catalyzes the addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs), which is essential for translation", 'tRNA nucleotidyl transferase 1 (TRNT1) catalyzes the addition of terminal cytosine-cytosine-adenosine (CCA) trinucleotides to all mature tRNAs, which is necessary for aminoacylation.', "3'-tRNA nucleotidyl transferase (TRNT1) is an enzyme that catalyzes the terminal nucleotidyl transfer of CCA sequence to the 3'-end of tRNA, which is essential for tRNA function in protein translation.", "TRNT1 catalyzes the addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs), which is essential for translation.", "tRNA Nucleotidyl Transferase 1 (TRNT1) catalyzes the addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs), a process essential for translation.", "TRNT1 (tRNA nucleotidyl transferase) catalyzes the addition of the CCA to the 3' end of tRNAs.", "tRNA Nucleotidyl Transferase 1 (TRNT1) catalyzes the addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs). This process is essential for translation.", "tRNA nucleotidyl transferase 1 (TRNT1) catalyzes the addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs), which is essential for translation.", "Addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs) is essential for translation and is catalyzed by the enzyme TRNT1 (tRNA nucleotidyl transferase),", "TRNT1 catalyzes the addition of a CCA nucleotide to the 3' end of tRNA molecules", 'tRNA nucleotidyl transferase 1 (TRNT1) is an essential enzyme catalyzing the addition of terminal cytosine-cytosine-adenosine (CCA) trinucleotides to all mature tRNAs, which is necessary for aminoacylation.', 'TRNT1 catalyzes the addition of terminal cytosine-cytosine-adenosine (CCA) trinucleotides to all mature tRNAs.', "tRNA nucleotidyl transferase 1 (TRNT1) catalyzes the addition of the invariant CCA-terminus to the tRNA 3'-end, which is a central step in tRNA maturation and is necessary for aminoacylation.", 'TRNT1 is an enzyme that catalyzes the addition of terminal cytosine-cytosine-adenosine (CCA) trinucleotides to all mature tRNAs.', 'The tRNA nucleotidyl transferase 1 (TRNT1) catalyzes the addition of terminal cytosine-cytosine-adenosine (CCA) trinucleotides to all mature tRNAs.', "The tRNA Nucleotidyl Transferase 1 (TRNT1) catalyzes the addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs). This process is essential for translation and occurs in both the cytoplasm and mitochondria"]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/36646204",
"http://www.ncbi.nlm.nih.gov/pubmed/15265870",
"http://www.ncbi.nlm.nih.gov/pubmed/29884622",
"http://www.ncbi.nlm.nih.gov/pubmed/26172425",
"http://www.ncbi.nlm.nih.gov/pubmed/884105",
"http://www.ncbi.nlm.nih.gov/pubmed/32181284",
"http://www.ncbi.nlm.nih.gov/pubmed/21059936",
"http://www.ncbi.nlm.nih.gov/pubmed/28390992",
"http://www.ncbi.nlm.nih.gov/pubmed/37239403",
"http://www.ncbi.nlm.nih.gov/pubmed/32471101",
"http://www.ncbi.nlm.nih.gov/pubmed/29454993",
"http://www.ncbi.nlm.nih.gov/pubmed/21071662",
"http://www.ncbi.nlm.nih.gov/pubmed/30917604",
"http://www.ncbi.nlm.nih.gov/pubmed/36121781",
"http://www.ncbi.nlm.nih.gov/pubmed/37334830",
"http://www.ncbi.nlm.nih.gov/pubmed/30959222",
"http://www.ncbi.nlm.nih.gov/pubmed/25652405",
"http://www.ncbi.nlm.nih.gov/pubmed/37215601",
"http://www.ncbi.nlm.nih.gov/pubmed/30758723",
"http://www.ncbi.nlm.nih.gov/pubmed/17204286",
"http://www.ncbi.nlm.nih.gov/pubmed/17949481",
"http://www.ncbi.nlm.nih.gov/pubmed/27370603",
"http://www.ncbi.nlm.nih.gov/pubmed/36409584",
"http://www.ncbi.nlm.nih.gov/pubmed/9510330",
"http://www.ncbi.nlm.nih.gov/pubmed/15304219"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36121781",
"endSection": "abstract",
"offsetInBeginSection": 162,
"offsetInEndSection": 231,
"text": "TRNT1 gene encodes a CCA-adding tRNA nucleotidyl transferase enzyme. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37239403",
"endSection": "abstract",
"offsetInBeginSection": 290,
"offsetInEndSection": 438,
"text": "tRNA Nucleotidyl Transferase 1 (TRNT1), the nuclear gene encoding the CCA-adding enzyme essential for modifying both nuclear and mitochondrial tRNAs"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25652405",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 255,
"text": "Addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs) is essential for translation and is catalyzed by the enzyme TRNT1 (tRNA nucleotidyl transferase), which functions in both the cytoplasm and mitochondria. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32471101",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 205,
"text": "tRNA nucleotidyl transferase 1 (TRNT1) is an essential enzyme catalyzing the addition of terminal cytosine-cytosine-adenosine (CCA) trinucleotides to all mature tRNAs, which is necessary for aminoacylation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30758723",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 293,
"text": "Mutation in the gene encoding tRNA nucleotidyl transferase, CCA-adding 1 (TRNT1), an enzyme essential for the synthesis of the 3'-terminal CCA sequence in tRNA molecules, results in a disorder that features sideroblastic anemia, B-cell immunodeficiency, periodic fever, and developmental delay"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28390992",
"endSection": "abstract",
"offsetInBeginSection": 178,
"offsetInEndSection": 317,
"text": "We recently identified novel hypomorphic mutations in the tRNA Nucleotidyl Transferase, CCA-Adding 1 (TRNT1) gene that cause early-onset RP"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27370603",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 220,
"text": "TRNT1 (CCA-adding transfer RNA nucleotidyl transferase) enzyme deficiency is a new metabolic disease caused by defective post-transcriptional modification of mitochondrial and cytosolic transfer RNAs (tRNAs)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25652405",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 253,
"text": "Addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs) is essential for translation and is catalyzed by the enzyme TRNT1 (tRNA nucleotidyl transferase), which functions in both the cytoplasm and mitochondria"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32471101",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 740,
"text": "tRNA nucleotidyl transferase 1 (TRNT1) is an essential enzyme catalyzing the addition of terminal cytosine-cytosine-adenosine (CCA) trinucleotides to all mature tRNAs, which is necessary for aminoacylation. It was recently discovered that partial loss-of-function mutations in TRNT1 are associated with various, seemingly unrelated human diseases including sideroblastic anemia with B-cell immunodeficiency, periodic fevers and developmental delay (SIFD), retinitis pigmentosa with erythrocyte microcytosis, and progressive B-cell immunodeficiency. In addition, even within the same disease, the severity and range of the symptoms vary greatly, suggesting a broad, pleiotropic impact of imparting TRNT1 function on diverse cellular systems."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29884622",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1508,
"text": "Tpt1 catalyzes the transfer of an internal 2'-monophosphate moiety (2'-PO4) from a \"branched\" 2'-PO4 RNA splice junction to NAD+ to form a \"clean\" 2'-OH, 3'-5' phosphodiester junction, ADP-ribose 1″-2″ cyclic phosphate, and nicotinamide. First discovered as an essential component of the Saccharomyces cerevisiae tRNA splicing machinery, Tpt1 is widely distributed in nature, including in taxa that have no yeast-like RNA splicing system. Here we characterize the RslTpt1 protein from the bacterium Runella slithyformis, in which Tpt1 is encoded within a putative RNA repair gene cluster. We find that (i) expression of RslTpt1 in yeast complements a lethal tpt1Δ knockout, and (ii) purified recombinant RslTpt1 is a bona fide NAD+-dependent 2'-phosphotransferase capable of completely removing an internal 2'-phosphate from synthetic RNAs. The in vivo activity of RslTpt1 is abolished by alanine substitutions for conserved amino acids Arg16, His17, Arg64, and Arg119. The R64A, R119A, and H17A mutants accumulate high levels of a 2'-phospho-ADP-ribosylated RNA reaction intermediate (2'-P-ADPR, evanescent in the wild-type RslTpt1 reaction), which is converted slowly to a 2'-OH RNA product. The R16A mutant is 300-fold slower than wild-type RslTpt1 in forming the 2'-P-ADPR intermediate. Whereas wild-type RsTpt1 rapidly converts the isolated 2'-P-ADPR intermediate to 2'-OH product in the absence of NAD+, the H17A, R119A, R64A, and R16A mutant are slower by factors of 3, 33, 210, and 710, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37334830",
"endSection": "abstract",
"offsetInBeginSection": 142,
"offsetInEndSection": 881,
"text": "tRNA 2'-phosphotransferase 1 (TRPT1/TPT1/KptA) possesses ADP-ribosyltransferase (ART) activity and is able to ADP-ribosylate nucleic acids. However, the underlying molecular mechanism remains elusive. Here, we determined crystal structures of TRPT1s in complex with NAD+ from Homo sapiens, Mus musculus and Saccharomyces cerevisiae. Our results revealed that the eukaryotic TRPT1s adopt common mechanisms for both NAD+ and nucleic acid substrate binding. The conserved SGR motif induces a significant conformational change in the donor loop upon NAD+ binding to facilitate the catalytic reaction of ART. Moreover, the nucleic acid-binding residue redundancy provides structural flexibility to accommodate different nucleic acid substrates."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30917604",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 363,
"text": "The tRNAHis guanylyltransferase (Thg1) superfamily includes enzymes that are found in all three domains of life that all share the common ability to catalyze the 3' to 5' synthesis of nucleic acids. This catalytic activity, which is the reverse of all other known DNA and RNA polymerases, makes this enzyme family a subject of biological and mechanistic interest."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29454993",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 528,
"text": "Mutations in the human TRNT1 gene encoding tRNA nucleotidyltransferase (tRNA-NT), an essential enzyme responsible for addition of the CCA (cytidine-cytidine-adenosine) sequence to the 3'-termini of tRNAs, have been linked to disease phenotypes including congenital sideroblastic anemia with B-cell immunodeficiency, periodic fevers and developmental delay (SIFD) or retinitis pigmentosa with erythrocyte microcytosis. The effects of these disease-linked mutations on the structure and function of tRNA-NT have not been explored."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36409584",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1095,
"text": "In tRNA maturation, CCA-addition by tRNA nucleotidyltransferase is a unique and highly accurate reaction. While the mechanism of nucleotide selection and polymerization is well understood, it remains a mystery why bacterial and eukaryotic enzymes exhibit an unexpected and surprisingly low tRNA substrate affinity while they efficiently catalyze the CCA-addition. To get insights into the evolution of this high-fidelity RNA synthesis, the reconstruction and characterization of ancestral enzymes is a versatile tool. Here, we investigate a reconstructed candidate of a 2 billion years old CCA-adding enzyme from Gammaproteobacteria and compare it to the corresponding modern enzyme of Escherichia coli. We show that the ancestral candidate catalyzes an error-free CCA-addition, but has a much higher tRNA affinity compared with the extant enzyme. The consequence of this increased substrate binding is an enhanced reverse reaction, where the enzyme removes the CCA end from the mature tRNA. As a result, the ancestral candidate exhibits a lower catalytic efficiency in vitro as well as in vivo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30959222",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 725,
"text": "The I326T mutation in the TRNT1 gene encoding human tRNA nucleotidyltransferase (tRNA-NT) is linked to a relatively mild form of SIFD. Previous work indicated that the I326T variant was unable to incorporate AMP into tRNAs in vitro, however, expression of the mutant allele from a strong heterologous promoter supported in vivo CCA addition to both cytosolic and mitochondrial tRNAs in a yeast strain lacking tRNA-NT. To address this discrepancy, we determined the biochemical and biophysical characteristics of the I326T variant enzyme and the related variant, I326A. Our in vitro analysis revealed that the I326T substitution decreases the thermal stability of the enzyme and causes a ten-fold reduction in enzyme activity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32471101",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 206,
"text": "tRNA nucleotidyl transferase 1 (TRNT1) is an essential enzyme catalyzing the addition of terminal cytosine-cytosine-adenosine (CCA) trinucleotides to all mature tRNAs, which is necessary for aminoacylation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25652405",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 356,
"text": "Addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs) is essential for translation and is catalyzed by the enzyme TRNT1 (tRNA nucleotidyl transferase), which functions in both the cytoplasm and mitochondria. Exome sequencing revealed TRNT1 mutations in two unrelated subjects with different clinical features."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25652405",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 254,
"text": "Addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs) is essential for translation and is catalyzed by the enzyme TRNT1 (tRNA nucleotidyl transferase), which functions in both the cytoplasm and mitochondria."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36646204",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 256,
"text": "The maturation of tRNA and its quality control is crucial for aminoacylation and protein synthesis. The CCA enzyme, also known as tRNA nucleotidyltransferase, catalyzes the addition or repair of CCA at the 3'-terminus of tRNAs to facilitate aminoacylation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36646204",
"endSection": "abstract",
"offsetInBeginSection": 100,
"offsetInEndSection": 402,
"text": "The CCA enzyme, also known as tRNA nucleotidyltransferase, catalyzes the addition or repair of CCA at the 3'-terminus of tRNAs to facilitate aminoacylation. Structural studies of CCA enzyme in complex with ATP and CTP suggested that adding CCA at the 3'-terminus of tRNAs is a sequential process [1-4]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36646204",
"endSection": "abstract",
"offsetInBeginSection": 100,
"offsetInEndSection": 256,
"text": "The CCA enzyme, also known as tRNA nucleotidyltransferase, catalyzes the addition or repair of CCA at the 3'-terminus of tRNAs to facilitate aminoacylation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36646204",
"endSection": "abstract",
"offsetInBeginSection": 100,
"offsetInEndSection": 568,
"text": "The CCA enzyme, also known as tRNA nucleotidyltransferase, catalyzes the addition or repair of CCA at the 3'-terminus of tRNAs to facilitate aminoacylation. Structural studies of CCA enzyme in complex with ATP and CTP suggested that adding CCA at the 3'-terminus of tRNAs is a sequential process [1-4]. However, there are many inconsistent results of CCA addition from the biochemical studies, which raise the ambiguity about the CCA enzyme specificity in vitro [5-7]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37215601",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "The TRNT1 gene encodes tRNA nucleotidyltransferase 1, which catalyzes the addition of cytosine-cytosine-adenosine (CCA) to the ends of cytoplasmic and mitochondrial tRNAs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25652405",
"endSection": "abstract",
"offsetInBeginSection": 1581,
"offsetInEndSection": 1908,
"text": "These data suggest that the clinical phenotypes associated with TRNT1 mutations are largely due to impaired mitochondrial translation, resulting from defective CCA addition to mitochondrial tRNA(Ser(AGY)), and that the severity of this biochemical phenotype determines the severity and tissue distribution of clinical features."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21059936",
"endSection": "abstract",
"offsetInBeginSection": 207,
"offsetInEndSection": 404,
"text": "The tRNA(His) guanylyltransferase (Thg1) is a member of a unique enzyme family whose members catalyze an unprecedented reaction in biology: 3'-5' addition of nucleotides to nucleic acid substrates."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30959222",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1223,
"text": "The I326T mutation in the TRNT1 gene encoding human tRNA nucleotidyltransferase (tRNA-NT) is linked to a relatively mild form of SIFD. Previous work indicated that the I326T variant was unable to incorporate AMP into tRNAs in vitro, however, expression of the mutant allele from a strong heterologous promoter supported in vivo CCA addition to both cytosolic and mitochondrial tRNAs in a yeast strain lacking tRNA-NT. To address this discrepancy, we determined the biochemical and biophysical characteristics of the I326T variant enzyme and the related variant, I326A. Our in vitro analysis revealed that the I326T substitution decreases the thermal stability of the enzyme and causes a ten-fold reduction in enzyme activity. We propose that the structural changes in the I326T variant that lead to these altered parameters result from a rearrangement of helices within the body domain of the protein which can be probed by the inability of the monomeric enzyme to form a covalent dimer in vitro mediated by C373. In addition, we confirm that the effects of the I326T or I326A substitutions are relatively mild in vivo by demonstrating that the mutant alleles support both mitochondrial and cytosolic CCA-addition in yeast."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32181284",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 331,
"text": "Mutations in the gene encoding transfer RNA (tRNA) nucleotidyltransferase, CCA-adding 1 (TRNT1), an enzyme essential for the synthesis of the 3'-terminal CCA sequence in tRNA molecules, are associated with a rare syndrome of congenital sideroblastic anemia, B cell immunodeficiency, periodic fevers, and developmental delay (SIFD)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29454993",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 417,
"text": "Mutations in the human TRNT1 gene encoding tRNA nucleotidyltransferase (tRNA-NT), an essential enzyme responsible for addition of the CCA (cytidine-cytidine-adenosine) sequence to the 3'-termini of tRNAs, have been linked to disease phenotypes including congenital sideroblastic anemia with B-cell immunodeficiency, periodic fevers and developmental delay (SIFD) or retinitis pigmentosa with erythrocyte microcytosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30758723",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 294,
"text": "Mutation in the gene encoding tRNA nucleotidyl transferase, CCA-adding 1 (TRNT1), an enzyme essential for the synthesis of the 3'-terminal CCA sequence in tRNA molecules, results in a disorder that features sideroblastic anemia, B-cell immunodeficiency, periodic fever, and developmental delay."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29454993",
"endSection": "abstract",
"offsetInBeginSection": 43,
"offsetInEndSection": 203,
"text": "tRNA nucleotidyltransferase (tRNA-NT), an essential enzyme responsible for addition of the CCA (cytidine-cytidine-adenosine) sequence to the 3'-termini of tRNAs"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37215601",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 799,
"text": "The TRNT1 gene encodes tRNA nucleotidyltransferase 1, which catalyzes the addition of cytosine-cytosine-adenosine (CCA) to the ends of cytoplasmic and mitochondrial tRNAs. The most common clinical phenotype associated with TRNT1 is autosomal recessive sideroblastic anemia with B-cell immunodeficiency, periodic fever, and developmental delay (SIFD). Muscle involvement has rarely been reported in TRNT1-related disorders. Here we report a Chinese patient with incomplete SIFD and hyperCKemia, and explored the skeletal muscle pathological changes. The patient was a 3-year-old boy with sensorineural hearing loss, sideroblastic anemia, and developmental delay since infancy. At the age of 11 months, significantly increased levels of creatine kinase were noted, accompanied by mild muscle weakness."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27370603",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1891,
"text": "BACKGROUND: TRNT1 (CCA-adding transfer RNA nucleotidyl transferase) enzyme deficiency is a new metabolic disease caused by defective post-transcriptional modification of mitochondrial and cytosolic transfer RNAs (tRNAs).RESULTS: We investigated four patients from two families with infantile-onset cyclical, aseptic febrile episodes with vomiting and diarrhoea, global electrolyte imbalance during these episodes, sideroblastic anaemia, B lymphocyte immunodeficiency, retinitis pigmentosa, hepatosplenomegaly, exocrine pancreatic insufficiency and renal tubulopathy. Other clinical features found in children include sensorineural deafness, cerebellar atrophy, brittle hair, partial villous atrophy and nephrocalcinosis. Whole exome sequencing and bioinformatic filtering were utilised to identify recessive compound heterozygous TRNT1 mutations (missense mutation c.668T>C, p.Ile223Thr and a novel splice mutation c.342+5G>T) segregating with disease in the first family. The second family was found to have a homozygous TRNT1 mutation (c.569G>T), p.Arg190Ile, (previously published). We found normal mitochondrial translation products using passage matched controls and functional perturbation of 3' CCA addition to mitochondrial tRNAs (tRNA(Cys), tRNA(LeuUUR) and tRNA(His)) in fibroblasts from two patients, demonstrating a pathomechanism affecting the CCA addition to mt-tRNAs. Acute management of these patients included transfusion for anaemia, fluid and electrolyte replacement and immunoglobulin therapy. We also describe three-year follow-up findings after treatment by bone marrow transplantation in one patient, with resolution of fever and reversal of the abnormal metabolic profile.CONCLUSIONS: Our report highlights that TRNT1 mutations cause a spectrum of disease ranging from a childhood-onset complex disease with manifestations in most organs to an adult-onset isolated re"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25652405",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1580,
"text": "Addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs) is essential for translation and is catalyzed by the enzyme TRNT1 (tRNA nucleotidyl transferase), which functions in both the cytoplasm and mitochondria. Exome sequencing revealed TRNT1 mutations in two unrelated subjects with different clinical features. The first presented with acute lactic acidosis at 3 weeks of age and developed severe developmental delay, hypotonia, microcephaly, seizures, progressive cortical atrophy, neurosensorial deafness, sideroblastic anemia and renal Fanconi syndrome, dying at 21 months. The second presented at 3.5 years with gait ataxia, dysarthria, gross motor regression, hypotonia, ptosis and ophthalmoplegia and had abnormal signals in brainstem and dentate nucleus. In subject 1, muscle biopsy showed combined oxidative phosphorylation (OXPHOS) defects, but there was no OXPHOS deficiency in fibroblasts from either subject, despite a 10-fold-reduction in TRNT1 protein levels in fibroblasts of the first subject. Furthermore, in normal controls, TRNT1 protein levels are 10-fold lower in muscle than in fibroblasts. High resolution northern blots of subject fibroblast RNA suggested incomplete CCA addition to the non-canonical mitochondrial tRNA(Ser(AGY)), but no obvious qualitative differences in other mitochondrial or cytoplasmic tRNAs. Complete knockdown of TRNT1 in patient fibroblasts rendered mitochondrial tRNA(Ser(AGY)) undetectable, and markedly reduced mitochondrial translation, except polypeptides lacking Ser(AGY) codons."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30758723",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1241,
"text": "Mutation in the gene encoding tRNA nucleotidyl transferase, CCA-adding 1 (TRNT1), an enzyme essential for the synthesis of the 3'-terminal CCA sequence in tRNA molecules, results in a disorder that features sideroblastic anemia, B-cell immunodeficiency, periodic fever, and developmental delay. Mutations in TRNT1 are also linked to phenotypes including retinitis pigmentosa, cataracts, and cardiomyopathy. To date, it has remained unclear how defective TRNT1 is linked to B-cell deficiency. Here we report the case of a 12-year-old boy without sideroblastic anemia who harbors novel compound heterozygous mutations in TRNT1. Immunophenotypic analysis revealed severely decreased levels of B cells and follicular helper T cells. In the bone marrow, B-cell maturation stopped at the CD19+CD10+CD20+/- pre-B-cell stage. Severe combined immunodeficiency mice transplanted with bone marrow hematopoietic stem cells from the patient showed largely normal B-cell engraftment and differentiation in the bone marrow and periphery at 24 weeks post-transplantation, comparable to those in mouse transplanted with healthy hematopoietic stem cells. Biochemical analysis revealed augmented endoplasmic reticulum (ER) stress response in activated T cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32181284",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1366,
"text": "Mutations in the gene encoding transfer RNA (tRNA) nucleotidyltransferase, CCA-adding 1 (TRNT1), an enzyme essential for the synthesis of the 3'-terminal CCA sequence in tRNA molecules, are associated with a rare syndrome of congenital sideroblastic anemia, B cell immunodeficiency, periodic fevers, and developmental delay (SIFD). Clinical manifestations and immunological phenotypes were assessed in a Chinese patient with novel compound heterozygous mutations in TRNT1. The patient required multiple hospitalizations starting at the age of 2 years for recurrent fevers without an infective cause. During the febrile episode, the patient was found to have microcytic hypochromic anemia, B cell lymphopenia, and hypogammaglobulinemia. Targeted gene sequencing identified novel compound heterozygous mutations in the TRNT1 gene (c.525delT, p.Leu176X; c.938T>C, p.Leu313Ser). Immunophenotyping revealed increased CD8+ T cells, CD4+ terminally differentiated effector memory helper T lymphocytes (CD4 TEMRA), and CD4+ effector memory lymphocytes (CD4 EM). Analysis of CD4+ T subsets identified decreased T follicular helper cells (Tfh) with a biased phenotype to Th2-like cells. The patient also showed a lower percentage of switched memory B (smB) cells. Additionally, defects in the cytotoxicity of the patient's NK and γδT cells were shown by CD107alpha expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/884105",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 296,
"text": "The enzyme tRNA nucleotidyl transferase (EC 2.7.7.25) has been highly purified from whole adult houseflies. A molecular weight of 30 000 has been determined. The enzyme requires Mg2+ and tRNA deprived of the 3' terminal sequence CCA for activity in the incorporation of AMP and CMP onto the tRNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25652405",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 622,
"text": "Addition of the trinucleotide cytosine/cytosine/adenine (CCA) to the 3' end of transfer RNAs (tRNAs) is essential for translation and is catalyzed by the enzyme TRNT1 (tRNA nucleotidyl transferase), which functions in both the cytoplasm and mitochondria. Exome sequencing revealed TRNT1 mutations in two unrelated subjects with different clinical features. The first presented with acute lactic acidosis at 3 weeks of age and developed severe developmental delay, hypotonia, microcephaly, seizures, progressive cortical atrophy, neurosensorial deafness, sideroblastic anemia and renal Fanconi syndrome, dying at 21 months."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30758723",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 406,
"text": "Mutation in the gene encoding tRNA nucleotidyl transferase, CCA-adding 1 (TRNT1), an enzyme essential for the synthesis of the 3'-terminal CCA sequence in tRNA molecules, results in a disorder that features sideroblastic anemia, B-cell immunodeficiency, periodic fever, and developmental delay. Mutations in TRNT1 are also linked to phenotypes including retinitis pigmentosa, cataracts, and cardiomyopathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27370603",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "BACKGROUND: TRNT1 (CCA-adding transfer RNA nucleotidyl transferase) enzyme deficiency is a new metabolic disease caused by defective post-transcriptional modification of mitochondrial and cytosolic transfer RNAs (tRNAs)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30758723",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 491,
"text": "Mutation in the gene encoding tRNA nucleotidyl transferase, CCA-adding 1 (TRNT1), an enzyme essential for the synthesis of the 3'-terminal CCA sequence in tRNA molecules, results in a disorder that features sideroblastic anemia, B-cell immunodeficiency, periodic fever, and developmental delay. Mutations in TRNT1 are also linked to phenotypes including retinitis pigmentosa, cataracts, and cardiomyopathy. To date, it has remained unclear how defective TRNT1 is linked to B-cell deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17204286",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 294,
"text": "The human CCA-adding enzyme (tRNA nucleotidyltransferase) is an essential enzyme that catalyzes the addition of the CCA terminus to the 3' end of tRNA precursors, a reaction which is a fundamental prerequisite for mature tRNAs to become aminoacylated and to participate in protein biosynthesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26172425",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 114,
"text": "tRNA nucleotidyltransferase adds the invariant CCA-terminus to the tRNA 3'-end, a central step in tRNA maturation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9510330",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "The CCA-adding enzyme [ATP(CTP):tRNA nucleotidyltransferase] catalyzes the addition and regeneration of the 3'-terminal CCA sequence of tRNAs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15304219",
"endSection": "abstract",
"offsetInBeginSection": 142,
"offsetInEndSection": 219,
"text": "tRNA nucleotidyltransferase catalyzes the addition of CCA to 3' ends of tRNAs"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21071662",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "CCA-adding enzymes [ATP(CTP):tRNA nucleotidyltransferases] add CCA onto the 3' end of transfer RNA (tRNA) precursors without using a nucleic acid template."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15265870",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "The CCA-adding enzyme ATP(CTP):tRNA nucleotidyltransferase builds and repairs the 3'-terminal CCA sequence of tRNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17949481",
"endSection": "abstract",
"offsetInBeginSection": 384,
"offsetInEndSection": 493,
"text": "family, the tRNA nucleotidyltransferase that synthesizes the 3'-terminal sequence C-C-A to all tRNAs (CCA-add"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36409584",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 105,
"text": "In tRNA maturation, CCA-addition by tRNA nucleotidyltransferase is a unique and highly accurate reaction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26172425",
"endSection": "abstract",
"offsetInBeginSection": 115,
"offsetInEndSection": 245,
"text": "This CCA-adding enzyme is a specialized RNA polymerase that synthesizes the CCA sequence at high fidelity in all kingdoms of life."
}
] | 13 |
BioASQ-training13b
| null | null |
662cfc88187cba990d000008
|
bioasq_factoid
|
factoid
|
Oxantel is used for periodontitis treatment. How does it work?
|
['Oxantel disrupts polymicrobial biofilm']
|
[
"Oxantel",
"Oxantel pamoate",
"Oxantel embonate",
"Oxantel disrupts polymicrobial biofilm"
] |
Oxantel, a cholinergic anthelmintic and fumarate reductase inhibitor, significantly inhibited biofilm formation by P. gingivalis and disrupted established biofilms.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24165189",
"http://www.ncbi.nlm.nih.gov/pubmed/20038616"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24165189",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 75,
"text": "Oxantel disrupts polymicrobial biofilm development of periodontal pathogens"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24165189",
"endSection": "abstract",
"offsetInBeginSection": 273,
"offsetInEndSection": 444,
"text": "he anthelmintic drug oxantel has been shown to inhibit fumarate reductase (Frd) activity in some pathogenic bacteria and inhibit P. gingivalis homotypic biofilm formation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20038616",
"endSection": "abstract",
"offsetInBeginSection": 128,
"offsetInEndSection": 349,
"text": "Oxantel, a cholinergic anthelmintic and fumarate reductase inhibitor, significantly inhibited biofilm formation by P. gingivalis and disrupted established biofilms at concentrations below its MIC against planktonic cells."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D010518",
"http://www.biosemantics.org/jochem#4251142",
"http://www.disease-ontology.org/api/metadata/DOID:824"
] |
[
{
"o": "36531-26-7",
"p": "http://linkedlifedata.com/resource/pubmed/registryNumber",
"s": "http://linkedlifedata.com/resource/pubmed/chemical/oxantel"
},
{
"o": "oxantel",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/pubmed/chemical/oxantel"
},
{
"o": "MeSH",
"p": "http://www.w3.org/2004/02/skos/core#note",
"s": "http://linkedlifedata.com/resource/umls/label/A0294401"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A0294401",
"p": "http://linkedlifedata.com/resource/umls/prefMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C0163908"
},
{
"o": "oxantel pamoate",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A0294401"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A0294401",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0163908"
}
] |
530c7f52970c65fa6b000010
|
bioasq_factoid
|
factoid
|
How many patients were enrolled in the FREEDOMS clinical trial?
|
['1,272']
|
[
"1,272",
"1272",
"one thousand two hundred seventy-two"
] |
['FREEDOMS study, a randomised, double-blind study included 1272 patients with relapsing-remitting MS.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22494956"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22494956",
"endSection": "abstract",
"offsetInBeginSection": 534,
"offsetInEndSection": 866,
"text": "We did subgroup analyses of ARRs (primary outcome) and confirmed disability progression (a secondary outcome) over 24 months in the FREEDOMS study, a randomised, double-blind study that included 1272 patients with relapsing-remitting MS who were assigned 1:1:1 to fingolimod (0·5 mg or 1·25 mg) or placebo once daily for 24 months. "
}
] | 11 |
BioASQ-training11b
| null | null |
605281cf94d57fd879000015
|
bioasq_factoid
|
factoid
|
What is the use of lebrikizumab?
|
['atopic dermatitis']
|
[
"atopic dermatitis",
"eczema",
"atopic eczema",
"allergic dermatitis",
"flexural eczema",
"infantile eczema",
"neurodermatitis"
] |
['Lebrikizumab scan be used for moderate-to-severe atopic dermatitis.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/37266844",
"http://www.ncbi.nlm.nih.gov/pubmed/36630140",
"http://www.ncbi.nlm.nih.gov/pubmed/36948491",
"http://www.ncbi.nlm.nih.gov/pubmed/36994947",
"http://www.ncbi.nlm.nih.gov/pubmed/37401345"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36630140",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "Efficacy and Safety of Lebrikizumab in Combination With Topical Corticosteroids in Adolescents and Adults With Moderate-to-Severe Atopic Dermatitis: A Randomized Clinical Trial (ADhere)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36630140",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 274,
"text": "Importance: Lebrikizumab (LEB), a high-affinity monoclonal antibody targeting interleukin (IL)-13, demonstrated efficacy and safety in patients with moderate-to-severe atopic dermatitis (AD) during 16 weeks of monotherapy in a phase 2b trial, and two 52-week phase 3 trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36630140",
"endSection": "abstract",
"offsetInBeginSection": 2555,
"offsetInEndSection": 2810,
"text": "Conclusions and Relevance: In this randomized phase 3 clinical trial, LEB+TCS was associated with improved outcomes in adolescents and adults with moderate-to-severe AD compared with TCS alone, and safety was consistent with previously reported AD trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36948491",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 477,
"text": "The U.S. Food and Drug Administration approval of dupilumab for moderate-to-severe atopic dermatitis shifted the paradigm from use of broad, systemic immunosuppressants to a safer, targeted treatment and led to the emergence of newer interleukin (IL)-4/IL-13 directed biologics and small molecule therapies, namely Janus kinase (JAK) inhibitors (JAKi). Tralokinumab and emerging (not yet approved) lebrikizumab, which both target IL-13, are alternative biologics to dupilumab. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37401345",
"endSection": "abstract",
"offsetInBeginSection": 133,
"offsetInEndSection": 200,
"text": " This review characterizes lebrikizumab as AD treatment in adults. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37401345",
"endSection": "abstract",
"offsetInBeginSection": 770,
"offsetInEndSection": 871,
"text": "Results from clinical trials suggest that lebrikizumab may be a viable alternative for AD management."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36994947",
"endSection": "abstract",
"offsetInBeginSection": 1768,
"offsetInEndSection": 2009,
"text": "CONCLUSIONS: After a 16-week induction period with lebrikizumab Q2W, lebrikizumab Q2W and Q4W maintained similar improvement of the signs and symptoms of moderate-to-severe AD, with a safety profile consistent with previously published data."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36994947",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 355,
"text": "BACKGROUND: Lebrikizumab is a novel, high-affinity monoclonal antibody that selectively binds to interleukin (IL)-13.OBJECTIVES: To evaluate the efficacy and safety of lebrikizumab monotherapy in adolescent and adult patients with moderate-to-severe atopic dermatitis (AD) over 52 weeks of treatment in ADvocate1 (NCT04146363) and ADvocate2 (NCT04178967)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37266844",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 71,
"text": "Lebrikizumab for the Treatment of Moderate-to-Severe Atopic Dermatitis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37266844",
"endSection": "abstract",
"offsetInBeginSection": 1243,
"offsetInEndSection": 1356,
"text": "Lebrikizumab seems to be a promising emerging targeted biological agent for patients with moderate-to-severe AD. "
}
] | 13 |
BioASQ-training13b
| null | null |
65d36e761930410b13000044
|
bioasq_factoid
|
factoid
|
What distinguishes RIDLs from other transpozable elements?
|
['they are exonic']
|
[
"exonic",
"exon",
"exonic sequences",
"exon sequences",
"exonic regions"
] |
['Here, we link these two concepts by proposing that exonic TEs act as RNA domains that are essential for lncRNA function. We term such elements Repeat Insertion Domains of LncRNAs (RIDLs).', 'One class of sequence elements that is enriched in lncRNA is represented by transposable elements (TEs), repetitive mobile genetic sequences that have contributed to genome evolution through a process termed exaptation. We term such elements Repeat insertion domains of LncRNAs (RIDLs).', 'Repeat Insertion Domains of LncRNAs (RIDLs) are exonic TEs that are essential for lncRNA function.', 'Ancient exapted transposable elements promote nuclear enrichment of human long noncoding RNAs . A growing number of RIDLs have been experimentally defined, where TE-derived fragments of lncRNA act as RNA-, DNA-, and protein-binding domains . We term such elements Repeat Insertion Domains of LncRNAs (RIDL)', 'Exonic TEs act as RNA domains that are essential for lncRNA function. We term such elements Repeat Insertion Domains of LncRNAs (RIDLs)']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24850885"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24850885",
"endSection": "abstract",
"offsetInBeginSection": 524,
"offsetInEndSection": 710,
"text": "Here, we link these two concepts by proposing that exonic TEs act as RNA domains that are essential for lncRNA function. We term such elements Repeat Insertion Domains of LncRNAs (RIDLs)"
}
] | 11 |
BioASQ-training11b
| null | null |
5d388192a1e1595105000015
|
bioasq_factoid
|
factoid
|
Inhaled Molgramostim can be used for treatment of which disease?
|
['Autoimmune Pulmonary Alveolar Proteinosis']
|
[
"Autoimmune Pulmonary Alveolar Proteinosis",
"Autoimmune Alveolar Proteinosis",
"Pulmonary Alveolar Proteinosis",
"Alveolar Proteinosis",
"Autoimmune Pulmonary Alveolar Proteinopathy"
] |
['Inhaled Molgramostim was shown to be effective for Autoimmune Pulmonary Alveolar Proteinosis.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29719809",
"http://www.ncbi.nlm.nih.gov/pubmed/32897035"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32897035",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "Inhaled Molgramostim Therapy in Autoimmune Pulmonary Alveolar Proteinosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32897035",
"endSection": "abstract",
"offsetInBeginSection": 420,
"offsetInEndSection": 687,
"text": "METHODS: In a double-blind, placebo-controlled, three-group trial, we randomly assigned patients with aPAP to receive the recombinant GM-CSF molgramostim (300 μg once daily by inhalation), either continuously or intermittently (every other week), or matching placebo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32897035",
"endSection": "abstract",
"offsetInBeginSection": 2287,
"offsetInEndSection": 2508,
"text": "CONCLUSIONS: In patients with aPAP, daily administration of inhaled molgramostim resulted in greater improvements in pulmonary gas transfer and functional health status than placebo, with similar rates of adverse events. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29719809",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Autoimmune pulmonary alveolar proteinosis in an adolescent successfully treated with inhaled rhGM-CSF (molgramostim)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29719809",
"endSection": "abstract",
"offsetInBeginSection": 550,
"offsetInEndSection": 731,
"text": "We here describe a unique case of a 14-year-old patient who was successfully treated with WLL and subsequent inhalations with molgramostim - new recombinant human GM-CSF (rhGM-CSF)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32897035",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 73,
"text": "Inhaled Molgramostim Therapy in Autoimmune Pulmonary Alveolar Proteinosis"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29719809",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "Autoimmune pulmonary alveolar proteinosis in an adolescent successfully treated with inhaled rhGM-CSF (molgramostim)"
}
] | 11 |
BioASQ-training11b
| null | null |
601cb5be1cb411341a000025
|
bioasq_factoid
|
factoid
|
What syndrome is associated with mutations in lysine methyltransferase 2D KMT2D?
|
['Kabuki syndrome']
|
[
"Kabuki syndrome",
"Kabuki make-up syndrome",
"Kabuki syndrome 1",
"Kabuki syndrome 2",
"Kabuki facial syndrome"
] |
['Mutations in lysine methyltransferase 2D (KMT2D) gene, which encodes the catalytic core of a multisubunit chromatin remodeling enzyme, are responsible for the neurodegenerative disorder Kabuki syndrome.', 'Mutations in lysine methyltransferase 2D (KMT2D) cause Kabuko syndrome.', 'Kabuki syndrome (KS) is commonly caused by mutations in the histone-modifying enzyme lysine methyltransferase 2D (KMT2D).', 'Mutations in the lysine methyltransferase 2D (KMT2D) gene, which encodes the alpha-subunit of the kappaB gene, are associated with the autosomal dominant hemophagocytic syndrome type 4 or Ferroportin syndrome.', 'Kabuki syndrome is a rare autosomal dominant disorder caused by mutations in the lysine methyltransferase 2D (KMT2D) gene.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28475860",
"http://www.ncbi.nlm.nih.gov/pubmed/28007623",
"http://www.ncbi.nlm.nih.gov/pubmed/31935506",
"http://www.ncbi.nlm.nih.gov/pubmed/31813957",
"http://www.ncbi.nlm.nih.gov/pubmed/24838796",
"http://www.ncbi.nlm.nih.gov/pubmed/29914387",
"http://www.ncbi.nlm.nih.gov/pubmed/30980591",
"http://www.ncbi.nlm.nih.gov/pubmed/29725259",
"http://www.ncbi.nlm.nih.gov/pubmed/31282990",
"http://www.ncbi.nlm.nih.gov/pubmed/31465303",
"http://www.ncbi.nlm.nih.gov/pubmed/24705355",
"http://www.ncbi.nlm.nih.gov/pubmed/30891914",
"http://www.ncbi.nlm.nih.gov/pubmed/31816409",
"http://www.ncbi.nlm.nih.gov/pubmed/32803813",
"http://www.ncbi.nlm.nih.gov/pubmed/26194542",
"http://www.ncbi.nlm.nih.gov/pubmed/27573763",
"http://www.ncbi.nlm.nih.gov/pubmed/26932671",
"http://www.ncbi.nlm.nih.gov/pubmed/32083401",
"http://www.ncbi.nlm.nih.gov/pubmed/24240169"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31816409",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 134,
"text": "Kabuki syndrome (KS) is commonly caused by mutations in the histone-modifying enzyme lysine methyltransferase 2D (KMT2D). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31935506",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 132,
"text": "Identification of KMT2D and KDM6A variants by targeted sequencing from patients with Kabuki syndrome and other congenital disorders."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31935506",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 334,
"text": "Kabuki syndrome (KS) is a rare congenital disorder characterized by distinctive facies, postnatal growth deficiency, cardiac defects and skeletal anomalies. Studies have determined that pathogenic variants of the lysine-specific methyltransferase 2D (KMT2D) and lysine-specific demethylase 6A (KDM6A) genes are the major causes of KS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32083401",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 300,
"text": "Pathogenic variants in KMT2D, which encodes lysine specific methyltransferase 2D, cause autosomal dominant Kabuki syndrome, associated with distinctive dysmorphic features including arched eyebrows, long palpebral fissures with eversion of the lower lid, large protuberant ears, and fetal finger pads"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32083401",
"endSection": "abstract",
"offsetInBeginSection": 452,
"offsetInEndSection": 648,
"text": "We describe here four patients (including one previously published patient) with de novo KMT2D missense variants and with shared but unusual clinical findings not typically seen in Kabuki syndrome"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32083401",
"endSection": "abstract",
"offsetInBeginSection": 1089,
"offsetInEndSection": 1307,
"text": "These findings significantly expand the phenotypic spectrum of features associated with variants in KMT2D beyond those seen in Kabuki syndrome and suggest a possible new underlying disease mechanism for these patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32803813",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 288,
"text": "Kabuki syndrome is characterized by a variable degree of intellectual disability, characteristic facial features, and complications in various organs. Many variants have been identified in two causative genes, that is, lysine methyltransferase 2D (KMT2D) and lysine demethylase 6A (KDM6A)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31282990",
"endSection": "abstract",
"offsetInBeginSection": 270,
"offsetInEndSection": 408,
"text": "Heterozygous germline mutations in the KMT2D gene are known to cause Kabuki syndrome (OMIM 147920), a developmental multisystem disorder. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31465303",
"endSection": "abstract",
"offsetInBeginSection": 142,
"offsetInEndSection": 441,
"text": "Lysine-specific methyltransferase 2D (KMT2D) encodes a histone methyltransferase that promotes transcriptional activation and is frequently mutated in cancers and in the majority (>70%) of patients diagnosed with the congenital, multisystem intellectual disability disorder Kabuki syndrome 1 (KS1). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24838796",
"endSection": "abstract",
"offsetInBeginSection": 202,
"offsetInEndSection": 347,
"text": "Kabuki syndrome is caused by mutations or deletions of lysine (K)-specific methyltransferase 2D (KMT2D) and lysine-specific methylase 6A (KDM6A)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31816409",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "BACKGROUND: Kabuki syndrome (KS) is commonly caused by mutations in the histone-modifying enzyme lysine methyltransferase 2D (KMT2D)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26194542",
"endSection": "abstract",
"offsetInBeginSection": 395,
"offsetInEndSection": 536,
"text": "JECTIVE: We sought to characterize the humoral immune defects found in patients with KS with lysine methyltransferase 2D (KMT2D) mutations.ME"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28007623",
"endSection": "abstract",
"offsetInBeginSection": 602,
"offsetInEndSection": 763,
"text": "LTS: We report frequent mutations in the lysine methyltransferase 2D gene (KMT2D) (also known as MLL2), a key regulator of transcriptional enhancer function. KMT"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28007623",
"endSection": "abstract",
"offsetInBeginSection": 882,
"offsetInEndSection": 1108,
"text": "ound that KMT2D mutation in human SCLC cell lines was associated with reduced lysine methyltransferase 2D protein levels and reduced monomethylation of histone H3 lysine 4, a mark associated with transcriptional enhancers. We "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28475860",
"endSection": "abstract",
"offsetInBeginSection": 111,
"offsetInEndSection": 361,
"text": "Two such disorders, CHARGE and Kabuki syndromes, result from loss of function mutations in chromodomain helicase DNA-binding protein 7 (CHD7LOF) and lysine (K) methyltransferase 2D (KMT2DLOF), respectively. Although these two syndromes are clinically"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26194542",
"endSection": "abstract",
"offsetInBeginSection": 1676,
"offsetInEndSection": 1885,
"text": "ONS: In patients with KS, autosomal dominant KMT2D mutations are associated with dysregulation of terminal B-cell differentiation, leading to humoral immune deficiency and, in some cases, autoimmunity. All pat"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24240169",
"endSection": "abstract",
"offsetInBeginSection": 353,
"offsetInEndSection": 557,
"text": "MT2D has emerged as one of the most frequently mutated genes in a variety of cancers and in other human diseases, including lymphoma, medulloblastoma, gastric cancer, and Kabuki syndrome. Mutations in KMT"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27573763",
"endSection": "abstract",
"offsetInBeginSection": 586,
"offsetInEndSection": 722,
"text": " KS was confirmed by genetic testing, which revealed a nonsense mutation in exon 16 of KMT2D (c.4485C>A, Tyr1495Ter). To the best of our"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32083401",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 301,
"text": "Pathogenic variants in KMT2D, which encodes lysine specific methyltransferase 2D, cause autosomal dominant Kabuki syndrome, associated with distinctive dysmorphic features including arched eyebrows, long palpebral fissures with eversion of the lower lid, large protuberant ears, and fetal finger pads."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32083401",
"endSection": "abstract",
"offsetInBeginSection": 452,
"offsetInEndSection": 789,
"text": "We describe here four patients (including one previously published patient) with de novo KMT2D missense variants and with shared but unusual clinical findings not typically seen in Kabuki syndrome, including athelia (absent nipples), choanal atresia, hypoparathyroidism, delayed or absent pubertal development, and extreme short stature."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26932671",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "KMT2D, which encodes a histone H3K4 methyltransferase, has been implicated in human congenital heart disease in the context of Kabuki syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31282990",
"endSection": "abstract",
"offsetInBeginSection": 270,
"offsetInEndSection": 407,
"text": "Heterozygous germline mutations in the KMT2D gene are known to cause Kabuki syndrome (OMIM 147920), a developmental multisystem disorder."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29725259",
"endSection": "abstract",
"offsetInBeginSection": 164,
"offsetInEndSection": 420,
"text": "Despite more than 350 documented cases, the oro-dental spectrum associated with kabuki syndrome and expression of KMT2D (histone-lysine N-methyltransferase 2D) or KDM6A (lysine-specific demethylase 6A) genes in tooth development have not been well defined."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26194542",
"endSection": "abstract",
"offsetInBeginSection": 405,
"offsetInEndSection": 536,
"text": "e sought to characterize the humoral immune defects found in patients with KS with lysine methyltransferase 2D (KMT2D) mutations.ME"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26194542",
"endSection": "abstract",
"offsetInBeginSection": 1685,
"offsetInEndSection": 1881,
"text": "atients with KS, autosomal dominant KMT2D mutations are associated with dysregulation of terminal B-cell differentiation, leading to humoral immune deficiency and, in some cases, autoimmunity. All"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24705355",
"endSection": "abstract",
"offsetInBeginSection": 322,
"offsetInEndSection": 438,
"text": "Mutations in the KMT2D gene, which encodes a H3K4 histone methyltransferase, are the major cause of Kabuki syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31813957",
"endSection": "abstract",
"offsetInBeginSection": 359,
"offsetInEndSection": 527,
"text": "The major cause of Kabuki syndrome are mutations in KMT2D, a gene encoding a histone H3 lysine 4 (H3K4) methyltransferase belonging to the group of chromatin modifiers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30891914",
"endSection": "abstract",
"offsetInBeginSection": 301,
"offsetInEndSection": 421,
"text": "Mutations with a loss-of-function in the KMT2D gene on chromosome 12 in humans are responsible for Kabuki syndrome (KS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30980591",
"endSection": "abstract",
"offsetInBeginSection": 133,
"offsetInEndSection": 409,
"text": "rt defects. Mutations in the histone H3K4 methyltransferase KMT2D have been identified as the main cause of Kabuki syndrome, however, the role of KMT2D in heart development remains to be characterized.RESULTS: Here we analyze the function of Kmt2d at different stages of Xenop"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31813957",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 132,
"text": "The histone methyltransferase KMT2D, mutated in Kabuki syndrome patients, is required for neural crest cell formation and migration."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27573763",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 67,
"text": "A novel KMT2D mutation resulting in Kabuki syndrome: A case report."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24240169",
"endSection": "abstract",
"offsetInBeginSection": 342,
"offsetInEndSection": 540,
"text": "Recently, KMT2D has emerged as one of the most frequently mutated genes in a variety of cancers and in other human diseases, including lymphoma, medulloblastoma, gastric cancer, and Kabuki syndrome."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29914387",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "A de novo KMT2D mutation in a girl with Kabuki syndrome associated with endocrine symptoms: a case report."
}
] | 11 |
BioASQ-training11b
| null | null |
601ebbeb1cb411341a00005b
|
bioasq_factoid
|
factoid
|
Which year was XIPERE approved by the FDA?
|
['2021']
|
[
"2021",
"twenty twenty-one",
"two thousand twenty-one"
] |
['XIPERE was approved by the FDA in 2021.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/35868358"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35868358",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 269,
"text": "Drug delivery to the suprachoroidal space (SCS®) has become a clinical reality after the 2021 FDA approval of CLS-TA, a triamcinolone acetonide injectable suspension for suprachoroidal use (XIPERE®), administered via a microneedle-based device, the SCS Microinjector®. "
}
] | 12 |
BioASQ-training12b
| null | null |
6440393157b1c7a31500004a
|
bioasq_factoid
|
factoid
|
What part of what body organ controls the circadian clock?
|
['suprachiasmatic nucleus (SCN) of the hypothalamus in the brain']
|
[
"suprachiasmatic nucleus",
"SCN",
"suprachiasmatic nucleus of the hypothalamus",
"suprachiasmatic nucleus in the brain",
"SCN of the hypothalamus",
"SCN in the brain"
] |
['the suprachiasmatic nucleus (SCN) of the hypothalamus acts as the central clock in mammals, the circadian expression of clock genes ', 'The mammalian circadian system is composed of a hierarchical multi-oscillator structure, with the central clock located in the suprachiasmatic nucleus (SCN) of the hypothalamus in the brain']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28707700",
"http://www.ncbi.nlm.nih.gov/pubmed/28285822",
"http://www.ncbi.nlm.nih.gov/pubmed/17517647",
"http://www.ncbi.nlm.nih.gov/pubmed/20174808",
"http://www.ncbi.nlm.nih.gov/pubmed/28596466",
"http://www.ncbi.nlm.nih.gov/pubmed/25512305",
"http://www.ncbi.nlm.nih.gov/pubmed/12505612",
"http://www.ncbi.nlm.nih.gov/pubmed/28232786",
"http://www.ncbi.nlm.nih.gov/pubmed/26332965",
"http://www.ncbi.nlm.nih.gov/pubmed/26453621",
"http://www.ncbi.nlm.nih.gov/pubmed/23604475",
"http://www.ncbi.nlm.nih.gov/pubmed/28286126",
"http://www.ncbi.nlm.nih.gov/pubmed/25645021",
"http://www.ncbi.nlm.nih.gov/pubmed/23704227",
"http://www.ncbi.nlm.nih.gov/pubmed/21969583"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28232786",
"endSection": "abstract",
"offsetInBeginSection": 10,
"offsetInEndSection": 142,
"text": "the suprachiasmatic nucleus (SCN) of the hypothalamus acts as the central clock in mammals, the circadian expression of clock genes "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28286126",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 105,
"text": "In mammals, the suprachiasmatic nucleus (SCN) of the hypothalamus is the site of the main circadian clock"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28285822",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "The suprachiasmatic nucleus (SCN) of the hypothalamus orchestrates daily rhythms of physiology and behavior in mammals. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28707700",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 134,
"text": "The suprachiasmatic nucleus houses the central circadian clock and is characterized by the timely regulated expression of clock genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23704227",
"endSection": "abstract",
"offsetInBeginSection": 589,
"offsetInEndSection": 736,
"text": "Clock genes control circadian rhythms both centrally, in the suprachiasmatic nucleus of the brain and peripherally, within every organ of the body."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17517647",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 182,
"text": "The mammalian circadian system consists of a central oscillator in the suprachiasmatic nucleus of the hypothalamus, which coordinates peripheral clocks in organs throughout the body."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25512305",
"endSection": "abstract",
"offsetInBeginSection": 372,
"offsetInEndSection": 450,
"text": "The central clock in the suprachiasmatic nucleus (SCN) has been well studied, "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20174808",
"endSection": "abstract",
"offsetInBeginSection": 139,
"offsetInEndSection": 319,
"text": " In mammals, a master clock, located in the suprachiasmatic nuclei (SCN) of the hypothalamus, adjusts timing of other self-sustained oscillators in the brain and peripheral organs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26453621",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 261,
"text": "Circadian clocks are endogenous and biological oscillations that occur with a period of<24 h. In mammals, the central circadian pacemaker is localized in the suprachiasmatic nucleus (SCN) and is linked to peripheral tissues through neural and hormonal signals. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12505612",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 71,
"text": "The suprachiasmatic nucleus (SCN) controls circadian rhythms in mammals"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25645021",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "The environmental light-dark (LD) cycle entrains the central circadian clock located in the suprachiasmatic nucleus (SCN) of mammals."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23604475",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 270,
"text": "Although circadian rhythms in mammalian physiology and behavior are dependent upon a biological clock in the suprachiasmatic nuclei (SCN) of the hypothalamus, the molecular mechanism of this clock is in fact cell autonomous and conserved in nearly all cells of the body."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26332965",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 167,
"text": "The mammalian circadian timing system consists of a central pacemaker in the brain's suprachiasmatic nucleus (SCN) and subsidiary oscillators in nearly all body cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21969583",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "The suprachiasmatic nucleus of the brain is the circadian center, relaying rhythmic environmental and behavioral information to peripheral tissues to control circadian physiology. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28596466",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "The nerve center responsible for controlling our circadian rhythm is located in a cluster of cells known as the suprachiasmatic nucleus in the hypothalamus"
}
] | 11 |
BioASQ-training11b
| null | null |
5a95765bfcd1d6a10c000028
|
bioasq_factoid
|
yesno
|
Has proteomics been used in the study of Pick's disease?
|
['yes']
|
[
"yes"
] |
Yes, proteomics has been used in the study of Pick's disease.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/16987245",
"http://www.ncbi.nlm.nih.gov/pubmed/16555340",
"http://www.ncbi.nlm.nih.gov/pubmed/12650976",
"http://www.ncbi.nlm.nih.gov/pubmed/11880199"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16987245",
"endSection": "abstract",
"offsetInBeginSection": 776,
"offsetInEndSection": 993,
"text": "In Pick's disease, increased AGE, CML, CEL, HNE and MDAL bands of about 50 kDa were observed in the frontal cortex (but not in the occipital cortex) in association with increased density of glial acidic protein bands."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16555340",
"endSection": "abstract",
"offsetInBeginSection": 236,
"offsetInEndSection": 529,
"text": "Thus, brain and cerebrospinal fluid (CSF) samples from patients with Alzheimer's disease, Down syndrome, Pick's disease, Parkinson's disease, schizophrenia, and other disorders as well as brain and CSF from animals serving as models of neurological disorders have been analyzed by proteomics. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12650976",
"endSection": "abstract",
"offsetInBeginSection": 493,
"offsetInEndSection": 771,
"text": "The present study is designed to investigate expression of peroxiredoxins (Prxs), the newly characterized family of highly conserved antioxidant enzymes, and other antioxidant enzymes in frontal cortex and cerebellum of DS, AD and PD patients using the technique of proteomics. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11880199",
"endSection": "abstract",
"offsetInBeginSection": 326,
"offsetInEndSection": 486,
"text": "HMT levels were measured in the frontal cortex and cerebellum of brains of patients with AD, DS, and PiD, and normal aged subjects using proteomics techniques. "
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D020774",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D020543",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D040901",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D057180",
"http://www.disease-ontology.org/api/metadata/DOID:11870",
"http://www.disease-ontology.org/api/metadata/DOID:4"
] |
[] |
532f05bdd6d3ac6a34000026
|
bioasq_yesno
|
factoid
|
What is the KDEL retention signal?
|
['ER retention sequence (KDEL)']
|
[
"ER retention sequence (KDEL)",
"KDEL",
"Lys-Asp-Glu-Leu",
"KDEL sequence",
"KDEL motif"
] |
['the -KDEL retention signal sequence is characteristic of many proteins localized to the ER.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/10767987",
"http://www.ncbi.nlm.nih.gov/pubmed/7893163",
"http://www.ncbi.nlm.nih.gov/pubmed/28669732",
"http://www.ncbi.nlm.nih.gov/pubmed/29733248",
"http://www.ncbi.nlm.nih.gov/pubmed/32020276"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32020276",
"endSection": "abstract",
"offsetInBeginSection": 901,
"offsetInEndSection": 1092,
"text": "By fusing the antibody with a KDEL retention signal, the interaction of antibodies and native membrane antigens occurs inside the endoplasmic reticulum during the process of protein secretion"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29733248",
"endSection": "abstract",
"offsetInBeginSection": 397,
"offsetInEndSection": 425,
"text": "ER retention sequence (KDEL)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28669732",
"endSection": "abstract",
"offsetInBeginSection": 458,
"offsetInEndSection": 527,
"text": " The KDEL retention signal led to the accumulation of PrP in the ER, "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10767987",
"endSection": "abstract",
"offsetInBeginSection": 435,
"offsetInEndSection": 507,
"text": "retained in the endoplasmic reticulum (ER) using a KDEL retention signal"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7893163",
"endSection": "abstract",
"offsetInBeginSection": 242,
"offsetInEndSection": 362,
"text": " These sequences are similar to the -KDEL retention signal sequence characteristic of many proteins localized to the ER."
}
] | 11 |
BioASQ-training11b
| null | null |
623e02e0f0baec9a1b000005
|
bioasq_factoid
|
factoid
|
Which gene is involved in Giant Axonal Neuropathy?
|
[['GAN gene']]
|
[
"GAN gene",
"Giant axonal neuropathy gene",
"GAN"
] |
['Giant axonal neuropathy (GAN) is a progressive neurodegenerative disease caused by autosomal recessive mutations in the GAN gene, resulting in a loss of a ubiquitously expressed protein, gigaxonin.', 'Giant axonal neuropathy (GAN) is a progressive neurodegenerative disease caused by autosomal recessive mutations in the GAN gene resulting in a loss of a ubiquitously expressed protein, gigaxonin', 'Giant axonal neuropathy (GAN) is a progressive neurodegenerative disease caused by autosomal recessive mutations in the GAN gene resulting in a loss of a ubiquitously expressed protein, gigaxonin', 'Giant axonal neuropathy (GAN) is a progressive neurodegenerative disease caused by autosomal recessive mutations in the GAN gene resulting in a loss of a ubiquitously expressed protein, gigaxonin', 'Giant axonal neuropathy (GAN) is a progressive neurodegenerative disease caused by autosomal recessive mutations in the GAN gene resulting in a loss of a ubiquitously expressed protein, gigaxonin', 'Giant axonal neuropathy (GAN) is a progressive neurodegenerative disease caused by autosomal recessive mutations in the GAN gene resulting in a loss of a ubiquitously expressed protein, gigaxonin']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25398950",
"http://www.ncbi.nlm.nih.gov/pubmed/24211141",
"http://www.ncbi.nlm.nih.gov/pubmed/23890932",
"http://www.ncbi.nlm.nih.gov/pubmed/24273072",
"http://www.ncbi.nlm.nih.gov/pubmed/24947478",
"http://www.ncbi.nlm.nih.gov/pubmed/12398836",
"http://www.ncbi.nlm.nih.gov/pubmed/23248352",
"http://www.ncbi.nlm.nih.gov/pubmed/19398414",
"http://www.ncbi.nlm.nih.gov/pubmed/17587580",
"http://www.ncbi.nlm.nih.gov/pubmed/23332420",
"http://www.ncbi.nlm.nih.gov/pubmed/19295179",
"http://www.ncbi.nlm.nih.gov/pubmed/11971098",
"http://www.ncbi.nlm.nih.gov/pubmed/23316953",
"http://www.ncbi.nlm.nih.gov/pubmed/20949505",
"http://www.ncbi.nlm.nih.gov/pubmed/24758703",
"http://www.ncbi.nlm.nih.gov/pubmed/25003002"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25398950",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 195,
"text": "Giant axonal neuropathy (GAN) is a progressive neurodegenerative disease caused by autosomal recessive mutations in the GAN gene resulting in a loss of a ubiquitously expressed protein, gigaxonin"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24211141",
"endSection": "abstract",
"offsetInBeginSection": 224,
"offsetInEndSection": 464,
"text": "We describe a toddler with clinical features suggesting giant axonal neuropathy (GAN), whose diagnosis was confirmed by minimally invasive skin biopsy and corroborated by the finding of compound heterozygous mutations involving the GAN gene"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23890932",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "Giant Axonal Neuropathy is a pediatric neurodegenerative disorder caused by autosomal recessive mutations in the GAN gene on chromosome 16q24.1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24273072",
"endSection": "abstract",
"offsetInBeginSection": 14,
"offsetInEndSection": 136,
"text": "Giant axonal neuropathy (GAN) is a rare autosomal recessive neurodegenerative disorder caused by mutations in the GAN gene"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24947478",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 335,
"text": "Giant axonal neuropathy (GAN) is a rare pediatric neurodegenerative disease. It is best known for the \"giant\" axons caused by accumulations of intermediate filaments. The disease is progressive, with onset around age 3 years and death by the third decade of life. GAN results from recessive mutations in the GAN gene encoding gigaxonin"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23316953",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 98,
"text": "Restoration of cytoskeleton homeostasis after gigaxonin gene transfer for giant axonal neuropathy."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23332420",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 114,
"text": "A novel mutation in the GAN gene causes an intermediate form of giant axonal neuropathy in an Arab-Israeli family."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19295179",
"endSection": "abstract",
"offsetInBeginSection": 870,
"offsetInEndSection": 1027,
"text": "In this family, missense mutation of c.224 T>A and missense mutation of c.1634G>A in GAN gene caused the phenotype of giant axonal neuropathy in the proband."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20949505",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 234,
"text": "Different missense, nonsense and frameshift mutations in the GAN gene encoding gigaxonin have been described to cause giant axonal neuropathy, a severe early-onset progressive neurological disease with autosomal recessive inheritance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12398836",
"endSection": "abstract",
"offsetInBeginSection": 783,
"offsetInEndSection": 1326,
"text": "The giant axonal neuropathy gene was localised by homozygosity mapping to chromosome 16q24.1 and identified as encoding a novel, ubiquitously expressed cytoskeletal protein named gigaxonin.We describe a consanguineous Algerian family with three affected sibs aged 16, 14 and 12 years who present a mild demyelinating sensory motor neuropathy, hypoacousia and kyphoscoliosis which was moderate in the two elder patients, severe in the third one, with no sign of central nervous system involvement and normal cerebral magnetic resonance imaging."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11971098",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "Giant axonal neuropathy (GAN): case report and two novel mutations in the gigaxonin gene."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23248352",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 95,
"text": "Giant axonal neuropathy caused by a novel compound heterozygous mutation in the gigaxonin gene."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23316953",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 98,
"text": "Restoration of cytoskeleton homeostasis after gigaxonin gene transfer for giant axonal neuropathy."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23332420",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 114,
"text": "A novel mutation in the GAN gene causes an intermediate form of giant axonal neuropathy in an Arab-Israeli family."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19295179",
"endSection": "abstract",
"offsetInBeginSection": 870,
"offsetInEndSection": 1027,
"text": "In this family, missense mutation of c.224 T>A and missense mutation of c.1634G>A in GAN gene caused the phenotype of giant axonal neuropathy in the proband."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20949505",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 234,
"text": "Different missense, nonsense and frameshift mutations in the GAN gene encoding gigaxonin have been described to cause giant axonal neuropathy, a severe early-onset progressive neurological disease with autosomal recessive inheritance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12398836",
"endSection": "abstract",
"offsetInBeginSection": 783,
"offsetInEndSection": 1326,
"text": "The giant axonal neuropathy gene was localised by homozygosity mapping to chromosome 16q24.1 and identified as encoding a novel, ubiquitously expressed cytoskeletal protein named gigaxonin.We describe a consanguineous Algerian family with three affected sibs aged 16, 14 and 12 years who present a mild demyelinating sensory motor neuropathy, hypoacousia and kyphoscoliosis which was moderate in the two elder patients, severe in the third one, with no sign of central nervous system involvement and normal cerebral magnetic resonance imaging."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11971098",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "Giant axonal neuropathy (GAN): case report and two novel mutations in the gigaxonin gene."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23248352",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 95,
"text": "Giant axonal neuropathy caused by a novel compound heterozygous mutation in the gigaxonin gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25398950",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 195,
"text": "Giant axonal neuropathy (GAN) is a progressive neurodegenerative disease caused by autosomal recessive mutations in the GAN gene resulting in a loss of a ubiquitously expressed protein, gigaxonin"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24273072",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 122,
"text": "Giant axonal neuropathy (GAN) is a rare autosomal recessive neurodegenerative disorder caused by mutations in the GAN gene"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23890932",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "Giant Axonal Neuropathy is a pediatric neurodegenerative disorder caused by autosomal recessive mutations in the GAN gene on chromosome 16q24.1"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23248352",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "Giant axonal neuropathy caused by a novel compound heterozygous mutation in the gigaxonin gene"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24211141",
"endSection": "abstract",
"offsetInBeginSection": 224,
"offsetInEndSection": 595,
"text": "We describe a toddler with clinical features suggesting giant axonal neuropathy (GAN), whose diagnosis was confirmed by minimally invasive skin biopsy and corroborated by the finding of compound heterozygous mutations involving the GAN gene, including a novel interstitial microdeletion at 16q23.2 detected by microarray and a point mutation detected by direct sequencing"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24758703",
"endSection": "abstract",
"offsetInBeginSection": 109,
"offsetInEndSection": 317,
"text": "Indeed, recessive mutations in the Gigaxonin-encoding gene cause Giant Axonal Neuropathy (GAN), a severe neurodegenerative disorder characterized by a wide disorganization of the Intermediate Filament network"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23332420",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "A novel mutation in the GAN gene causes an intermediate form of giant axonal neuropathy in an Arab-Israeli family"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23316953",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 97,
"text": "Restoration of cytoskeleton homeostasis after gigaxonin gene transfer for giant axonal neuropathy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25003002",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 447,
"text": "Giant axonal neuropathy (GAN)(1) is a rare autosomal recessive neurological disorder caused by mutations in the GAN gene that encodes gigaxonin, a member of the BTB/Kelch family of E3 ligase adaptor proteins.(1) This disease is characterized by the aggregation of Intermediate Filaments (IF)-cytoskeletal elements that play important roles in cell physiology including the regulation of cell shape, motility, mechanics and intra-cellular signaling"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23890932",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 145,
"text": "Giant Axonal Neuropathy is a pediatric neurodegenerative disorder caused by autosomal recessive mutations in the GAN gene on chromosome 16q24.1. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24758703",
"endSection": "abstract",
"offsetInBeginSection": 121,
"offsetInEndSection": 331,
"text": "Indeed, recessive mutations in the Gigaxonin-encoding gene cause Giant Axonal Neuropathy (GAN), a severe neurodegenerative disorder characterized by a wide disorganization of the Intermediate Filament network. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24758703",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "The instability of the BTB-KELCH protein Gigaxonin causes Giant Axonal Neuropathy and constitutes a new penetrant and specific diagnostic test."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24211141",
"endSection": "abstract",
"offsetInBeginSection": 224,
"offsetInEndSection": 596,
"text": "We describe a toddler with clinical features suggesting giant axonal neuropathy (GAN), whose diagnosis was confirmed by minimally invasive skin biopsy and corroborated by the finding of compound heterozygous mutations involving the GAN gene, including a novel interstitial microdeletion at 16q23.2 detected by microarray and a point mutation detected by direct sequencing."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23890932",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 145,
"text": "Giant Axonal Neuropathy is a pediatric neurodegenerative disorder caused by autosomal recessive mutations in the GAN gene on chromosome 16q24.1. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24758703",
"endSection": "abstract",
"offsetInBeginSection": 121,
"offsetInEndSection": 331,
"text": "Indeed, recessive mutations in the Gigaxonin-encoding gene cause Giant Axonal Neuropathy (GAN), a severe neurodegenerative disorder characterized by a wide disorganization of the Intermediate Filament network. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24758703",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "The instability of the BTB-KELCH protein Gigaxonin causes Giant Axonal Neuropathy and constitutes a new penetrant and specific diagnostic test."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24211141",
"endSection": "abstract",
"offsetInBeginSection": 224,
"offsetInEndSection": 596,
"text": "We describe a toddler with clinical features suggesting giant axonal neuropathy (GAN), whose diagnosis was confirmed by minimally invasive skin biopsy and corroborated by the finding of compound heterozygous mutations involving the GAN gene, including a novel interstitial microdeletion at 16q23.2 detected by microarray and a point mutation detected by direct sequencing."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23890932",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 145,
"text": "Giant Axonal Neuropathy is a pediatric neurodegenerative disorder caused by autosomal recessive mutations in the GAN gene on chromosome 16q24.1. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24758703",
"endSection": "abstract",
"offsetInBeginSection": 121,
"offsetInEndSection": 331,
"text": "Indeed, recessive mutations in the Gigaxonin-encoding gene cause Giant Axonal Neuropathy (GAN), a severe neurodegenerative disorder characterized by a wide disorganization of the Intermediate Filament network. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24758703",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "The instability of the BTB-KELCH protein Gigaxonin causes Giant Axonal Neuropathy and constitutes a new penetrant and specific diagnostic test."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24211141",
"endSection": "abstract",
"offsetInBeginSection": 224,
"offsetInEndSection": 596,
"text": "We describe a toddler with clinical features suggesting giant axonal neuropathy (GAN), whose diagnosis was confirmed by minimally invasive skin biopsy and corroborated by the finding of compound heterozygous mutations involving the GAN gene, including a novel interstitial microdeletion at 16q23.2 detected by microarray and a point mutation detected by direct sequencing."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23890932",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 145,
"text": "Giant Axonal Neuropathy is a pediatric neurodegenerative disorder caused by autosomal recessive mutations in the GAN gene on chromosome 16q24.1. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23316953",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 98,
"text": "Restoration of cytoskeleton homeostasis after gigaxonin gene transfer for giant axonal neuropathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24273072",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 138,
"text": "INTRODUCTION: Giant axonal neuropathy (GAN) is a rare autosomal recessive neurodegenerative disorder caused by mutations in the GAN gene. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23890932",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 145,
"text": "Giant Axonal Neuropathy is a pediatric neurodegenerative disorder caused by autosomal recessive mutations in the GAN gene on chromosome 16q24.1. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24758703",
"endSection": "abstract",
"offsetInBeginSection": 121,
"offsetInEndSection": 331,
"text": "Indeed, recessive mutations in the Gigaxonin-encoding gene cause Giant Axonal Neuropathy (GAN), a severe neurodegenerative disorder characterized by a wide disorganization of the Intermediate Filament network. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24758703",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "The instability of the BTB-KELCH protein Gigaxonin causes Giant Axonal Neuropathy and constitutes a new penetrant and specific diagnostic test."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24211141",
"endSection": "abstract",
"offsetInBeginSection": 224,
"offsetInEndSection": 596,
"text": "We describe a toddler with clinical features suggesting giant axonal neuropathy (GAN), whose diagnosis was confirmed by minimally invasive skin biopsy and corroborated by the finding of compound heterozygous mutations involving the GAN gene, including a novel interstitial microdeletion at 16q23.2 detected by microarray and a point mutation detected by direct sequencing."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19398414",
"endSection": "abstract",
"offsetInBeginSection": 849,
"offsetInEndSection": 1130,
"text": "Analysis of the microarray data identified a change in the gene giant axonal neuropathy 1 (Gan1). Mutation of this gene has been linked to the development of giant axonal neuropathy (GAN), a rare autosomal recessive condition characterized by a progressive sensorimotor neuropathy."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23316953",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 98,
"text": "Restoration of cytoskeleton homeostasis after gigaxonin gene transfer for giant axonal neuropathy."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23248352",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 95,
"text": "Giant axonal neuropathy caused by a novel compound heterozygous mutation in the gigaxonin gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17587580",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 392,
"text": " Giant axonal neuropathy (GAN, MIM: 256850) is a devastating autosomal recessive disorder characterized by an early onset severe peripheral neuropathy, varying central nervous system involvement and strikingly frizzly hair. Giant axonal neuropathy is usually caused by mutations in the gigaxonin gene (GAN) but genetic heterogeneity has been demonstrated for a milder variant of this disease."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23248352",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "Giant axonal neuropathy caused by a novel compound heterozygous mutation in the gigaxonin gene."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23332420",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "A novel mutation in the GAN gene causes an intermediate form of giant axonal neuropathy in an Arab-Israeli family."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23890932",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 145,
"text": "Giant Axonal Neuropathy is a pediatric neurodegenerative disorder caused by autosomal recessive mutations in the GAN gene on chromosome 16q24.1."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23248352",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "Giant axonal neuropathy caused by a novel compound heterozygous mutation in the gigaxonin gene."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23332420",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "A novel mutation in the GAN gene causes an intermediate form of giant axonal neuropathy in an Arab-Israeli family."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23890932",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 145,
"text": "Giant Axonal Neuropathy is a pediatric neurodegenerative disorder caused by autosomal recessive mutations in the GAN gene on chromosome 16q24.1."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23248352",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "Giant axonal neuropathy caused by a novel compound heterozygous mutation in the gigaxonin gene."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23332420",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "A novel mutation in the GAN gene causes an intermediate form of giant axonal neuropathy in an Arab-Israeli family."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23890932",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 145,
"text": "Giant Axonal Neuropathy is a pediatric neurodegenerative disorder caused by autosomal recessive mutations in the GAN gene on chromosome 16q24.1."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23316953",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "Restoration of cytoskeleton homeostasis after gigaxonin gene transfer for giant axonal neuropathy."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23248352",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "Giant axonal neuropathy caused by a novel compound heterozygous mutation in the gigaxonin gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24273072",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Giant axonal neuropathy (GAN) is a rare autosomal recessive neurodegenerative disorder caused by mutations in the GAN gene."
}
] | 5 |
BioASQ-training5b
|
[] |
[] |
572096c90fd6f91b6800000e
|
bioasq_factoid
|
factoid
|
Which disease can be classified using the Koos Classification?
|
['vestibular schwannomas']
|
[
"vestibular schwannomas",
"acoustic neuromas",
"vestibular nerve tumors",
"schwannomas of the vestibular nerve",
"neuromas of the vestibular nerve"
] |
['The Koos classification is used from vestibular schwannomas. It is designed to stratify tumors based on extrameatal extension and compression of the brainstem.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30058759",
"http://www.ncbi.nlm.nih.gov/pubmed/30339649",
"http://www.ncbi.nlm.nih.gov/pubmed/30169695",
"http://www.ncbi.nlm.nih.gov/pubmed/29614352"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29614352",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "INTRODUCTION: Grade IV vestibular schwannoma (Koos classification) is generally considered to be an indication for microsurgical resection or combined radiosurgery-microsurgery."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30058759",
"endSection": "abstract",
"offsetInBeginSection": 222,
"offsetInEndSection": 383,
"text": "METHODS: The study included a total of 142 patients with VS stage 1 or 2 according to the Koos classification and treated between January 2004 and December 2015."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30169695",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 67,
"text": "Koos Classification of Vestibular Schwannomas: A Reliability Study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30169695",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "BACKGROUND: The Koos classification of vestibular schwannomas is designed to stratify tumors based on extrameatal extension and compression of the brainstem. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30169695",
"endSection": "abstract",
"offsetInBeginSection": 1166,
"offsetInEndSection": 1307,
"text": "CONCLUSION: We have demonstrated that the Koos classification system for vestibular schwannoma is a reliable method for tumor classification."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30339649",
"endSection": "abstract",
"offsetInBeginSection": 294,
"offsetInEndSection": 528,
"text": "PATIENTS: Eighteen patients who underwent a middle fossa craniotomy for vestibular schwannoma (stage I or II of Koos classification) with attempted hearing preservation from January 2008 to February 2016 were retrospectively reviewed."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30169695",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "BACKGROUND\n\nThe Koos classification of vestibular schwannomas is designed to stratify tumors based on extrameatal extension and compression of the brainstem."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30169695",
"endSection": "abstract",
"offsetInBeginSection": 1174,
"offsetInEndSection": 1315,
"text": "CONCLUSION\n\nWe have demonstrated that the Koos classification system for vestibular schwannoma is a reliable method for tumor classification."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30169695",
"endSection": "abstract",
"offsetInBeginSection": 1166,
"offsetInEndSection": 1306,
"text": "CONCLUSION We have demonstrated that the Koos classification system for vestibular schwannoma is a reliable method for tumor classification."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29614352",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 167,
"text": "Grade IV vestibular schwannoma ( Koos classification ) is generally considered to be an indication for microsurgical resection or combined radiosurgery-microsurgery . "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30169695",
"endSection": "abstract",
"offsetInBeginSection": 1173,
"offsetInEndSection": 1314,
"text": "CONCLUSION\nWe have demonstrated that the Koos classification system for vestibular schwannoma is a reliable method for tumor classification."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30169695",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "BACKGROUND\nThe Koos classification of vestibular schwannomas is designed to stratify tumors based on extrameatal extension and compression of the brainstem."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30169695",
"endSection": "abstract",
"offsetInBeginSection": 1170,
"offsetInEndSection": 1311,
"text": "CONCLUSION: We have demonstrated that the Koos classification system for vestibular schwannoma is a reliable method for tumor classification."
}
] | 11 |
BioASQ-training11b
| null | null |
5e2b2c85fbd6abf43b000007
|
bioasq_factoid
|
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",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D004106",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D009202",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D009154",
"http://www.disease-ontology.org/api/metadata/DOID:0050700",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D004108",
"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
|
bioasq_yesno
|
factoid
|
What is the cause of Sandhoff disease?
|
['Sandhoff disease (SD) is caused by a mutation of the β-subunit gene β-hexosaminidase B (HexB) in humans']
|
[
"Sandhoff disease",
"SD",
"β-hexosaminidase B",
"HexB",
"Hexosaminidase B",
"Sandhoff's disease"
] |
['Sandhoff disease (SD) is a genetic disorder caused by a mutation of the β-subunit gene β-hexosaminidase B (HexB) in humans, which results in the massive accumulation of the ganglioside GM2 and related glycosphingolipids in the nervous system.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29847465",
"http://www.ncbi.nlm.nih.gov/pubmed/29358305",
"http://www.ncbi.nlm.nih.gov/pubmed/29900534",
"http://www.ncbi.nlm.nih.gov/pubmed/30236619"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29847465",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 242,
"text": "Sandhoff disease (SD) is a genetic disorder caused by a mutation of the β-subunit gene β-hexosaminidase B (HexB) in humans, which results in the massive accumulation of the ganglioside GM2 and related glycosphingolipids in the nervous system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29358305",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 225,
"text": "Sandhoff disease, one of the GM2 gangliosidoses, is a lysosomal storage disorder characterized by the absence of β-hexosaminidase A and B activity and the concomitant lysosomal accumulation of its substrate, GM2 ganglioside. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29900534",
"endSection": "abstract",
"offsetInBeginSection": 462,
"offsetInEndSection": 579,
"text": "Sandhoff disease results from the defective activity of β-hexosaminidase, leading to accumulation of ganglioside GM2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30236619",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 156,
"text": "Sandhoff disease (SD) results from mutations in the HEXB gene, subsequent deficiency of N-acetyl-β-hexosaminidase (Hex) and accumulation of GM2 gangliosides"
}
] | 11 |
BioASQ-training11b
| null | null |
5c78080e7c78d694710000ae
|
bioasq_factoid
|
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
|
bioasq_yesno
|
yesno
|
Are there interactions between short and long noncoding RNAs?
|
['yes']
|
[
"yes"
] |
['Yes. Short RNAs and long noncoding RNAs (lncRNAs) interact with each other with reciprocal consequences for their fates and functions.', 'It is now evident that noncoding RNAs play key roles in regulatory networks determining cell fate and behavior, in a myriad of different conditions, and across all species. Among these noncoding RNAs are short RNAs, such as MicroRNAs, snoRNAs, and Piwi-interacting RNAs, and the functions of those are relatively well understood. Other noncoding RNAs are longer, and their modes of action and functions are also increasingly explored and deciphered. Short RNAs and long noncoding RNAs (lncRNAs) interact with each other with reciprocal consequences for their fates and functions. LncRNAs serve as precursors for many types of small RNAs and, therefore, the pathways for small RNA biogenesis can impinge upon the fate of lncRNAs. In addition, lncRNA expression can be repressed by small RNAs, and lncRNAs can affect small RNA activity and abundance through competition for binding or by triggering small RNA degradation.', 'Yes. Short RNAs and long noncoding RNAs interact with each other with reciprocal consequences for their fates and functions.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29749606"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29749606",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1078,
"text": "It is now evident that noncoding RNAs play key roles in regulatory networks determining cell fate and behavior, in a myriad of different conditions, and across all species. Among these noncoding RNAs are short RNAs, such as MicroRNAs, snoRNAs, and Piwi-interacting RNAs, and the functions of those are relatively well understood. Other noncoding RNAs are longer, and their modes of action and functions are also increasingly explored and deciphered. Short RNAs and long noncoding RNAs (lncRNAs) interact with each other with reciprocal consequences for their fates and functions. LncRNAs serve as precursors for many types of small RNAs and, therefore, the pathways for small RNA biogenesis can impinge upon the fate of lncRNAs. In addition, lncRNA expression can be repressed by small RNAs, and lncRNAs can affect small RNA activity and abundance through competition for binding or by triggering small RNA degradation. Here, I review the known types of interactions between small and long RNAs, discuss their outcomes, and bring representative examples from studies in mammals."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29749606",
"endSection": "abstract",
"offsetInBeginSection": 450,
"offsetInEndSection": 579,
"text": "Short RNAs and long noncoding RNAs (lncRNAs) interact with each other with reciprocal consequences for their fates and functions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29749606",
"endSection": "abstract",
"offsetInBeginSection": 450,
"offsetInEndSection": 580,
"text": "Short RNAs and long noncoding RNAs (lncRNAs) interact with each other with reciprocal consequences for their fates and functions."
}
] | 11 |
BioASQ-training11b
| null | null |
5e46fda33f54159529000012
|
bioasq_yesno
|
factoid
|
Which portal has been developed to explore protein-protein interactions in cancer cell lines?
|
['The OncoPPi Portal']
|
[
"The OncoPPi Portal",
"OncoPPi",
"OncoPPi Database",
"OncoPPi Platform"
] |
['The OncoPPi Portal has been developed as an interactive web resource that allows investigators to access, manipulate and interpret a high-quality cancer-focused network of protein-protein interactions (PPIs) experimentally detected in cancer cell lines. To facilitate prioritization of PPIs for further biological studies, this resource combines network connectivity analysis, mutual exclusivity analysis of genomic alterations, cellular co-localization of interacting proteins and domain-domain interactions. Estimates of PPI essentiality allow users to evaluate the functional impact of PPI disruption on cancer cell proliferation. Furthermore, connecting the OncoPPi network with the approved drugs and compounds in clinical trials enables discovery of new tumor dependencies to inform strategies to interrogate undruggable targets like tumor suppressors. The OncoPPi Portal serves as a resource for the cancer research community to facilitate discovery of cancer targets and therapeutic development.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29186335",
"http://www.ncbi.nlm.nih.gov/pubmed/31583637"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29186335",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "The OncoPPi Portal: an integrative resource to explore and prioritize protein-protein interactions for cancer target discovery."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29186335",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 1842,
"text": "As cancer genomics initiatives move toward comprehensive identification of genetic alterations in cancer, attention is now turning to understanding how interactions among these genes lead to the acquisition of tumor hallmarks. Emerging pharmacological and clinical data suggest a highly promising role of cancer-specific protein-protein interactions (PPIs) as druggable cancer targets. However, large-scale experimental identification of cancer-related PPIs remains challenging, and currently available resources to explore oncogenic PPI networks are limited.Results: Recently, we have developed a PPI high-throughput screening platform to detect PPIs between cancer-associated proteins in the context of cancer cells. Here, we present the OncoPPi Portal, an interactive web resource that allows investigators to access, manipulate and interpret a high-quality cancer-focused network of PPIs experimentally detected in cancer cell lines. To facilitate prioritization of PPIs for further biological studies, this resource combines network connectivity analysis, mutual exclusivity analysis of genomic alterations, cellular co-localization of interacting proteins and domain-domain interactions. Estimates of PPI essentiality allow users to evaluate the functional impact of PPI disruption on cancer cell proliferation. Furthermore, connecting the OncoPPi network with the approved drugs and compounds in clinical trials enables discovery of new tumor dependencies to inform strategies to interrogate undruggable targets like tumor suppressors. The OncoPPi Portal serves as a resource for the cancer research community to facilitate discovery of cancer targets and therapeutic development.Availability and implementation: The OncoPPi Portal is available at http://oncoppi.emory.edu.Contact: [email protected] or [email protected]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29186335",
"endSection": "abstract",
"offsetInBeginSection": 733,
"offsetInEndSection": 951,
"text": "Here, we present the OncoPPi Portal, an interactive web resource that allows investigators to access, manipulate and interpret a high-quality cancer-focused network of PPIs experimentally detected in cancer cell lines."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31583637",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "Explore Protein-Protein Interactions for Cancer Target Discovery Using the OncoPPi Portal"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31583637",
"endSection": "abstract",
"offsetInBeginSection": 1002,
"offsetInEndSection": 1456,
"text": "The established network of oncogenic PPIs , termed the OncoPPi network , is available through the OncoPPi Portal , an interactive web resource that allows to access and interpret a high-quality cancer-focused network of PPIs experimentally detected in cancer cell lines integrated with the analysis of mutual exclusivity of genomic alterations , cellular co-localization of interacting proteins , domain-domain interactions , and therapeutic connectivity"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31583637",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "Explore Protein-Protein Interactions for Cancer Target Discovery Using the OncoPPi Portal."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31583637",
"endSection": "abstract",
"offsetInBeginSection": 1441,
"offsetInEndSection": 1557,
"text": "This chapter presents a guide to explore the OncoPPi network using the OncoPPi Portal to facilitate cancer biology."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31583637",
"endSection": "abstract",
"offsetInBeginSection": 991,
"offsetInEndSection": 1441,
"text": "The established network of oncogenic PPIs, termed the OncoPPi network, is available through the OncoPPi Portal, an interactive web resource that allows to access and interpret a high-quality cancer-focused network of PPIs experimentally detected in cancer cell lines integrated with the analysis of mutual exclusivity of genomic alterations, cellular co-localization of interacting proteins, domain-domain interactions, and therapeutic connectivity."
}
] | 11 |
BioASQ-training11b
| null | null |
5e2e136bfbd6abf43b000023
|
bioasq_factoid
|
factoid
|
Which molecule is targeted by the drug Gevokizumab?
|
[['IL-1β']]
|
[
"IL-1 beta",
"Interleukin 1 beta",
"Interleukin-1 beta",
"IL1B",
"IL1B protein",
"IL-1B",
"IL-1 beta"
] |
['Gevokizumab is an allosteric anti-IL-1β monoclonal antibody.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24194526",
"http://www.ncbi.nlm.nih.gov/pubmed/23729309",
"http://www.ncbi.nlm.nih.gov/pubmed/23041424",
"http://www.ncbi.nlm.nih.gov/pubmed/22699287",
"http://www.ncbi.nlm.nih.gov/pubmed/22084392",
"http://www.ncbi.nlm.nih.gov/pubmed/21154167",
"http://www.ncbi.nlm.nih.gov/pubmed/21048425",
"http://www.ncbi.nlm.nih.gov/pubmed/25108619",
"http://www.ncbi.nlm.nih.gov/pubmed/25079039"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24194526",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Detailed mechanistic analysis of gevokizumab, an allosteric anti-IL-1β antibody with differential receptor-modulating properties."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24194526",
"endSection": "abstract",
"offsetInBeginSection": 280,
"offsetInEndSection": 533,
"text": "Gevokizumab is a potent anti-IL-1β antibody being developed as a treatment for diseases in which IL-1β has been associated with pathogenesis. Previous data indicated that gevokizumab negatively modulates IL-1β signaling through an allosteric mechanism. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24194526",
"endSection": "abstract",
"offsetInBeginSection": 1575,
"offsetInEndSection": 1763,
"text": "These data indicate, therefore, that gevokizumab is a unique inhibitor of IL-1β signaling that may offer an alternative to current therapies for IL-1β-associated autoinflammatory diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23729309",
"endSection": "abstract",
"offsetInBeginSection": 1484,
"offsetInEndSection": 1751,
"text": "Most recently, rising evidence reports on the use of adalimumab, etanercept, and golimumab, while use of anti-interleukin (IL)-1 agents (anakinra, canakinumab, gevokizumab), IL-6 blockers (tocilizumab), and rituximab (depleting anti-CD20 antibody) is also increasing."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23041424",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "One target-two different binding modes: structural insights into gevokizumab and canakinumab interactions to interleukin-1β."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23041424",
"endSection": "abstract",
"offsetInBeginSection": 286,
"offsetInEndSection": 363,
"text": "Canakinumab and gevokizumab are highly specific IL-1β monoclonal antibodies. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23041424",
"endSection": "abstract",
"offsetInBeginSection": 504,
"offsetInEndSection": 927,
"text": "Gevokizumab is claimed to be a regulatory therapeutic antibody that modulates IL-1β bioactivity by reducing the affinity for its IL-1RI:IL-1RAcP signaling complex. How IL-1β signaling is affected by both canakinumab and gevokizumab was not yet experimentally determined. We have analyzed the crystal structures of canakinumab and gevokizumab antibody binding fragment (Fab) as well as of their binary complexes with IL-1β. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23041424",
"endSection": "abstract",
"offsetInBeginSection": 1603,
"offsetInEndSection": 1815,
"text": "In contrast, gevokizumab occupies an allosteric site on IL-1β and complex formation results in a minor reduction of binding affinity to IL-1RI. This suggests two different mechanisms of IL-1β pathway attenuation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22699287",
"endSection": "abstract",
"offsetInBeginSection": 142,
"offsetInEndSection": 215,
"text": "Gevokizumab is a novel, human-engineered monoclonal anti-IL-1β antibody. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22084392",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "Interleukin-1β-regulating antibody XOMA 052 (gevokizumab) in the treatment of acute exacerbations of resistant uveitis of Behcet's disease: an open-label pilot study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22084392",
"endSection": "abstract",
"offsetInBeginSection": 131,
"offsetInEndSection": 341,
"text": "This pilot study aimed to evaluate the safety, pharmacokinetics and clinical activity of XOMA 052 (gevokizumab), a recombinant humanised anti-interleukin 1β antibody, in Behçet's disease patients with uveitis. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21154167",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "Gevokizumab, an anti-IL-1β mAb for the potential treatment of type 1 and 2 diabetes, rheumatoid arthritis and cardiovascular disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21154167",
"endSection": "abstract",
"offsetInBeginSection": 265,
"offsetInEndSection": 590,
"text": "XOMA is developing gevokizumab (XOMA-052), an IgG2 humanized mAb against human IL-1β, for the potential treatment of these diseases. Gevokizumab has a high affinity for IL-1β and a long t1/2, which would allow for once-monthly dosing and offer a considerable advantage for patients over agents requiring more frequent dosing."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21048425",
"endSection": "abstract",
"offsetInBeginSection": 587,
"offsetInEndSection": 771,
"text": "To meet these challenges, we developed XOMA 052 (gevokizumab), a potent anti-IL-1β neutralizing antibody that was designed in silico and humanized using Human Engineering™ technology. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24194526",
"endSection": "abstract",
"offsetInBeginSection": 721,
"offsetInEndSection": 1080,
"text": "In the present study, we measured the impact of gevokizumab on the IL-1β system using Schild analysis and surface plasmon resonance studies, both of which demonstrated that gevokizumab decreases the binding affinity of IL-1β for the IL-1 receptor type I (IL-1RI) signaling receptor, but not the IL-1 counter-regulatory decoy receptor (IL-1 receptor type II)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23041424",
"endSection": "abstract",
"offsetInBeginSection": 283,
"offsetInEndSection": 360,
"text": "Canakinumab and gevokizumab are highly specific IL-1β monoclonal antibodies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22699287",
"endSection": "abstract",
"offsetInBeginSection": 129,
"offsetInEndSection": 202,
"text": "Gevokizumab is a novel, human-engineered monoclonal anti-IL-1β antibody."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24194526",
"endSection": "abstract",
"offsetInBeginSection": 721,
"offsetInEndSection": 1080,
"text": "In the present study, we measured the impact of gevokizumab on the IL-1β system using Schild analysis and surface plasmon resonance studies, both of which demonstrated that gevokizumab decreases the binding affinity of IL-1β for the IL-1 receptor type I (IL-1RI) signaling receptor, but not the IL-1 counter-regulatory decoy receptor (IL-1 receptor type II)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23041424",
"endSection": "abstract",
"offsetInBeginSection": 283,
"offsetInEndSection": 360,
"text": "Canakinumab and gevokizumab are highly specific IL-1β monoclonal antibodies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22699287",
"endSection": "abstract",
"offsetInBeginSection": 129,
"offsetInEndSection": 202,
"text": "Gevokizumab is a novel, human-engineered monoclonal anti-IL-1β antibody."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24194526",
"endSection": "abstract",
"offsetInBeginSection": 721,
"offsetInEndSection": 1080,
"text": "In the present study, we measured the impact of gevokizumab on the IL-1β system using Schild analysis and surface plasmon resonance studies, both of which demonstrated that gevokizumab decreases the binding affinity of IL-1β for the IL-1 receptor type I (IL-1RI) signaling receptor, but not the IL-1 counter-regulatory decoy receptor (IL-1 receptor type II)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23041424",
"endSection": "abstract",
"offsetInBeginSection": 283,
"offsetInEndSection": 360,
"text": "Canakinumab and gevokizumab are highly specific IL-1β monoclonal antibodies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22699287",
"endSection": "abstract",
"offsetInBeginSection": 129,
"offsetInEndSection": 202,
"text": "Gevokizumab is a novel, human-engineered monoclonal anti-IL-1β antibody."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24194526",
"endSection": "abstract",
"offsetInBeginSection": 721,
"offsetInEndSection": 1080,
"text": "In the present study, we measured the impact of gevokizumab on the IL-1β system using Schild analysis and surface plasmon resonance studies, both of which demonstrated that gevokizumab decreases the binding affinity of IL-1β for the IL-1 receptor type I (IL-1RI) signaling receptor, but not the IL-1 counter-regulatory decoy receptor (IL-1 receptor type II)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23041424",
"endSection": "abstract",
"offsetInBeginSection": 283,
"offsetInEndSection": 360,
"text": "Canakinumab and gevokizumab are highly specific IL-1β monoclonal antibodies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22699287",
"endSection": "abstract",
"offsetInBeginSection": 129,
"offsetInEndSection": 202,
"text": "Gevokizumab is a novel, human-engineered monoclonal anti-IL-1β antibody."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24194526",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Detailed mechanistic analysis of gevokizumab, an allosteric anti-IL-1β antibody with differential receptor-modulating properties."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24194526",
"endSection": "abstract",
"offsetInBeginSection": 280,
"offsetInEndSection": 533,
"text": "Gevokizumab is a potent anti-IL-1β antibody being developed as a treatment for diseases in which IL-1β has been associated with pathogenesis. Previous data indicated that gevokizumab negatively modulates IL-1β signaling through an allosteric mechanism. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23041424",
"endSection": "abstract",
"offsetInBeginSection": 286,
"offsetInEndSection": 361,
"text": "Canakinumab and gevokizumab are highly specific IL-1β monoclonal antibodies"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22699287",
"endSection": "abstract",
"offsetInBeginSection": 131,
"offsetInEndSection": 202,
"text": "Gevokizumab is a novel, human-engineered monoclonal anti-IL-1β antibody"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23041424",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "One target-two different binding modes: structural insights into gevokizumab and canakinumab interactions to interleukin-1β."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23041424",
"endSection": "abstract",
"offsetInBeginSection": 286,
"offsetInEndSection": 361,
"text": "Canakinumab and gevokizumab are highly specific IL-1β monoclonal antibodies"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22699287",
"endSection": "abstract",
"offsetInBeginSection": 131,
"offsetInEndSection": 202,
"text": "Gevokizumab is a novel, human-engineered monoclonal anti-IL-1β antibody"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23041424",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "One target-two different binding modes: structural insights into gevokizumab and canakinumab interactions to interleukin-1β."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23041424",
"endSection": "abstract",
"offsetInBeginSection": 286,
"offsetInEndSection": 361,
"text": "Canakinumab and gevokizumab are highly specific IL-1β monoclonal antibodies"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22699287",
"endSection": "abstract",
"offsetInBeginSection": 131,
"offsetInEndSection": 202,
"text": "Gevokizumab is a novel, human-engineered monoclonal anti-IL-1β antibody"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23041424",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "One target-two different binding modes: structural insights into gevokizumab and canakinumab interactions to interleukin-1β."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23041424",
"endSection": "abstract",
"offsetInBeginSection": 286,
"offsetInEndSection": 361,
"text": "Canakinumab and gevokizumab are highly specific IL-1β monoclonal antibodies"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22699287",
"endSection": "abstract",
"offsetInBeginSection": 131,
"offsetInEndSection": 202,
"text": "Gevokizumab is a novel, human-engineered monoclonal anti-IL-1β antibody"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23041424",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "One target-two different binding modes: structural insights into gevokizumab and canakinumab interactions to interleukin-1β."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23041424",
"endSection": "abstract",
"offsetInBeginSection": 286,
"offsetInEndSection": 361,
"text": "Canakinumab and gevokizumab are highly specific IL-1β monoclonal antibodies"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22699287",
"endSection": "abstract",
"offsetInBeginSection": 131,
"offsetInEndSection": 202,
"text": "Gevokizumab is a novel, human-engineered monoclonal anti-IL-1β antibody"
}
] | 5 |
BioASQ-training5b
|
[] |
[] |
550e828c71445a662f000002
|
bioasq_factoid
|
factoid
|
What is the most likely age of diagnosis of Crohn's disease (CD)?
|
[["Crohn's disease has a bimodal age distribution of disease onset diagnosis. The peaks (20 and 50 years) may represent different phenotypes or different genetic and/or environmental influences between younger- and older-onset individuals."]]
|
[
"Crohn's disease",
"regional enteritis",
"terminal ileitis",
"ileitis",
"Crohn disease"
] |
["Crohn's disease has a bimodal age distribution of disease onset diagnosis. The peaks (20 and 50 years) may represent different phenotypes or different genetic and/or environmental influences between younger- and older-onset individuals. When the age-related incidence of Crohn's disease was plotted for all countries from which such data were available, the peaks of greatest case frequency occurred at ages 15 to 25 years and paralleled a similar peak representing the number of Peyer's patches as a function of age. For those with biologic use, average age at time of diagnosis of Crohn's disease was 32.3 ± 12.2 years, compared with 43.7 ± 16.3 years for those who had not received biologics (P = 0.005)."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26089697",
"http://www.ncbi.nlm.nih.gov/pubmed/23880115",
"http://www.ncbi.nlm.nih.gov/pubmed/23511037",
"http://www.ncbi.nlm.nih.gov/pubmed/22918090",
"http://www.ncbi.nlm.nih.gov/pubmed/21488915",
"http://www.ncbi.nlm.nih.gov/pubmed/20844954",
"http://www.ncbi.nlm.nih.gov/pubmed/18236809",
"http://www.ncbi.nlm.nih.gov/pubmed/9412954",
"http://www.ncbi.nlm.nih.gov/pubmed/8780560",
"http://www.ncbi.nlm.nih.gov/pubmed/19107777",
"http://www.ncbi.nlm.nih.gov/pubmed/16534420",
"http://www.ncbi.nlm.nih.gov/pubmed/22685044"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26089697",
"endSection": "abstract",
"offsetInBeginSection": 1077,
"offsetInEndSection": 1168,
"text": "Eighteen, 17, and 12 patients were diagnosed at ages<40, 40-59, and ≥60 years, respectively"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23880115",
"endSection": "abstract",
"offsetInBeginSection": 19,
"offsetInEndSection": 218,
"text": "Crohn's disease (CD) diagnosed in pediatric patients has been reported to have a more aggressive phenotype and course, with a greater prevalence of upper gastrointestinal involvement, than in adults."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23511037",
"endSection": "abstract",
"offsetInBeginSection": 323,
"offsetInEndSection": 659,
"text": "There was a significant association between body mass index and bone mineral density (P = 0.004) and a significant difference in the T scores of patients according to age at diagnosis (Montreal Classification: P = 0.0006) with patients diagnosed<17 years (n = 13) having lower T scores than those diagnosed at older age groups (n = 70)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22918090",
"endSection": "abstract",
"offsetInBeginSection": 791,
"offsetInEndSection": 1083,
"text": "Increasing age of diagnosis was negatively associated with complicated disease and positively associated with colonic disease. As age of diagnosis increased, disease duration (P<0.001), family history of Inflammatory bowel disease (IBD) (P = 0.015) and perianal disease decreased (P<0.0015). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21488915",
"endSection": "abstract",
"offsetInBeginSection": 947,
"offsetInEndSection": 1068,
"text": "Crohn's disease incidence rates in the 10-19-year age category increased by 71%, from 6.5 (1988-1990) to 11.1 (2006-2007)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21488915",
"endSection": "abstract",
"offsetInBeginSection": 1395,
"offsetInEndSection": 1502,
"text": "Consequently, studies on Crohn's disease risk factors should focus on the population under 20 years of age."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20844954",
"endSection": "abstract",
"offsetInBeginSection": 636,
"offsetInEndSection": 825,
"text": "For those with biologic use, average age at time of diagnosis of Crohn's disease was 32.3 ± 12.2 years, compared with 43.7 ± 16.3 years for those who had not received biologics (P = 0.005)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18236809",
"endSection": "abstract",
"offsetInBeginSection": 628,
"offsetInEndSection": 865,
"text": "Sixty one patients (50.4%) were 20-39 years old and 43 patients (35.5%) were 40 years and older. Colonic involvement was significantly more common (46,5%) in the 40 years and older group compared with 20-39 years group (24.6%) (p = 0.01)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9412954",
"endSection": "abstract",
"offsetInBeginSection": 399,
"offsetInEndSection": 678,
"text": "When the age-related incidence of Crohn's disease was plotted for all countries from which such data were available, the peaks of greatest case frequency occurred at ages 15 to 25 years and paralleled a similar peak representing the number of Peyer's patches as a function of age"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8780560",
"endSection": "abstract",
"offsetInBeginSection": 19,
"offsetInEndSection": 256,
"text": "Crohn's disease has a bimodal age distribution of disease onset diagnosis. The peaks (20 and 50 years) may represent different phenotypes or different genetic and/or environmental influences between younger- and older-onset individuals. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22685044",
"endSection": "abstract",
"offsetInBeginSection": 370,
"offsetInEndSection": 1186,
"text": "Current therapy for CD in the UK is less likely than previously to involve the use of long-term glucocorticoids.WHAT THIS STUDY ADDS: Despite advances in therapy, short stature and slow growth continue to be encountered in children with CD. There is a need for simple and consistent definitions of growth that can identify poor growth in children with chronic disease.METHODS: The anthropometric and treatment details of 116 children (68 male) with a mean (range) age at diagnosis of 10.8 years (4.9-15.5) and a mean age at maximum follow-up (MF) of 15.4 years (9.4-19.3) were studied retrospectively at diagnosis (T0), at 1 (T1), 2 (T2) and 3 years (T3) after diagnosis and at MF.RESULTS: At T0, mean height SD score (HtSDS) was -0.5 (-3.3 to 2.6) compared to a mid-parental HtSDS of 0.2 (-2.0 to 01.4) (p=0.002). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16534420",
"endSection": "abstract",
"offsetInBeginSection": 694,
"offsetInEndSection": 927,
"text": "White patients were significantly more likely to have ileal disease, whereas African American patients were significantly more likely to have ileocolonic and colonic disease. Age at diagnosis younger than 40 years (odds ratio [OR] 4."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16534420",
"endSection": "abstract",
"offsetInBeginSection": 694,
"offsetInEndSection": 927,
"text": "White patients were significantly more likely to have ileal disease, whereas African American patients were significantly more likely to have ileocolonic and colonic disease. Age at diagnosis younger than 40 years (odds ratio [OR] 4."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16534420",
"endSection": "abstract",
"offsetInBeginSection": 694,
"offsetInEndSection": 927,
"text": "White patients were significantly more likely to have ileal disease, whereas African American patients were significantly more likely to have ileocolonic and colonic disease. Age at diagnosis younger than 40 years (odds ratio [OR] 4."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19107777",
"endSection": "abstract",
"offsetInBeginSection": 1153,
"offsetInEndSection": 1419,
"text": "Both age at diagnosis and site of CD involvement were independently associated with expression of ASCA and anti-CBir1.Compared to children 8-15 years of age at diagnosis, those 0-7 years are more likely to express anti-CBir1 but only half as likely to express ASCA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16534420",
"endSection": "abstract",
"offsetInBeginSection": 694,
"offsetInEndSection": 927,
"text": "White patients were significantly more likely to have ileal disease, whereas African American patients were significantly more likely to have ileocolonic and colonic disease. Age at diagnosis younger than 40 years (odds ratio [OR] 4."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16534420",
"endSection": "abstract",
"offsetInBeginSection": 694,
"offsetInEndSection": 927,
"text": "White patients were significantly more likely to have ileal disease, whereas African American patients were significantly more likely to have ileocolonic and colonic disease. Age at diagnosis younger than 40 years (odds ratio [OR] 4."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.disease-ontology.org/api/metadata/DOID:4",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003424"
] |
[] |
56cae3eb5795f9a73e000021
|
bioasq_factoid
|
yesno
|
Can bergapten cross the blood-brain barrier?
|
['yes']
|
[
"yes"
] |
['Yes, bergapten can cross the blood-brain barrier.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34347307"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34347307",
"endSection": "abstract",
"offsetInBeginSection": 449,
"offsetInEndSection": 739,
"text": "Moreover, pharmacokinetic studies showed that bergapten has higher absolute bioavailability and can cross the blood-brain barrier and has a great potential for treating brain disease, but the mechanism needs further clarification to make greater use of its ability to treat brain diseases. "
}
] | 11 |
BioASQ-training11b
| null | null |
620586a8c9dfcb9c09000032
|
bioasq_yesno
|
factoid
|
Mutation of which gene is implicated in the Christianson syndrome?
|
['SLC9A6']
|
[
"SLC9A6",
"solute carrier family 9 member A6",
"sodium/hydrogen exchanger 6",
"NHE6"
] |
['Christianson syndrome is caused by mutations in SLC9A6 and is characterized by severe intellectual disability, absent speech, microcephaly, ataxia, seizures, and behavioral abnormalities.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24630051",
"http://www.ncbi.nlm.nih.gov/pubmed/18342287",
"http://www.ncbi.nlm.nih.gov/pubmed/26421989",
"http://www.ncbi.nlm.nih.gov/pubmed/25044251",
"http://www.ncbi.nlm.nih.gov/pubmed/25273398",
"http://www.ncbi.nlm.nih.gov/pubmed/27142213",
"http://www.ncbi.nlm.nih.gov/pubmed/26515654",
"http://www.ncbi.nlm.nih.gov/pubmed/27256868",
"http://www.ncbi.nlm.nih.gov/pubmed/20949524",
"http://www.ncbi.nlm.nih.gov/pubmed/25002837",
"http://www.ncbi.nlm.nih.gov/pubmed/27590723",
"http://www.ncbi.nlm.nih.gov/pubmed/24839169",
"http://www.ncbi.nlm.nih.gov/pubmed/24285247",
"http://www.ncbi.nlm.nih.gov/pubmed/24779060",
"http://www.ncbi.nlm.nih.gov/pubmed/21964919",
"http://www.ncbi.nlm.nih.gov/pubmed/21932316",
"http://www.ncbi.nlm.nih.gov/pubmed/22541666"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26515654",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "X-linked Christianson syndrome: heterozygous female Slc9a6 knockout mice develop mosaic neuropathological changes and related behavioral abnormalities."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26515654",
"endSection": "abstract",
"offsetInBeginSection": 251,
"offsetInEndSection": 434,
"text": "CS is caused by mutations in the SLC9A6 gene, which encodes a multipass transmembrane sodium (potassium)-hydrogen exchanger 6 (NHE6) protein, functional in early recycling endosomes. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27590723",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "A Christianson syndrome-linked deletion mutation (∆(287)ES(288)) in SLC9A6 disrupts recycling endosomal function and elicits neurodegeneration and cell death."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27590723",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 213,
"text": "BACKGROUND: Christianson Syndrome, a recently identified X-linked neurodevelopmental disorder, is caused by mutations in the human gene SLC9A6 encoding the recycling endosomal alkali cation/proton exchanger NHE6. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26421989",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 286,
"text": "BACKGROUND: Mutations of SLC9A6 may cause an X-linked clinical syndrome first described by Christianson in 1999 in which affected males exhibited profound intellectual disability, autism, drug-resistant epilepsy, ophthalmoplegia, mild craniofacial dysmorphism, microcephaly, and ataxia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25044251",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "OBJECTIVE: Recently, Christianson syndrome (CS) has been determined to be caused by mutations in the X-linked Na(+) /H(+) exchanger 6 (NHE6). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25044251",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "Genetic and phenotypic diversity of NHE6 mutations in Christianson syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24630051",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 583,
"text": "Mutations in the solute carrier family 9, subfamily A member 6 (SLC9A6) gene, encoding the endosomal Na+/H+ exchanger 6 (NHE6) are associated with Christianson syndrome, a syndromic form of X-linked intellectual disability characterized by microcephaly, severe global developmental delay, autistic behavior, early onset seizures and ataxia. In a 7-year-old boy with characteristic clinical and neuroimaging features of Christianson syndrome and epileptic encephalopathy with continuous spikes and waves during sleep, we identified a novel splice site mutation (IVS10-1G>A) in SLC9A6."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24285247",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 193,
"text": "Christianson syndrome (CS) is caused by mutations in SLC9A6 and is characterized by severe intellectual disability, absent speech, microcephaly, ataxia, seizures, and behavioral abnormalities. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24285247",
"endSection": "abstract",
"offsetInBeginSection": 342,
"offsetInEndSection": 481,
"text": "We report on two children with CS and confirmed mutations in SLC9A6 focusing on neuroimaging findings and review the available literature. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22541666",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 65,
"text": "Mutations in the SLC9A6 gene cause Christianson syndrome in boys."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22541666",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "Novel mutation in SLC9A6 gene in a patient with Christianson syndrome and retinitis pigmentosum."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21932316",
"endSection": "abstract",
"offsetInBeginSection": 1308,
"offsetInEndSection": 1432,
"text": "This patient broadens the spectrum of SLC9A6 mutations and contributes to the clinical delineation of Christianson syndrome."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22541666",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 95,
"text": "Novel mutation in SLC9A6 gene in a patient with Christianson syndrome and retinitis pigmentosum"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22541666",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 66,
"text": "Mutations in the SLC9A6 gene cause Christianson syndrome in boys. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24630051",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 159,
"text": "A novel mutation in the endosomal Na+/H+ exchanger NHE6 (SLC9A6) causes Christianson syndrome with electrical status epilepticus during slow-wave sleep (ESES)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24630051",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 341,
"text": "Mutations in the solute carrier family 9, subfamily A member 6 (SLC9A6) gene, encoding the endosomal Na+/H+ exchanger 6 (NHE6) are associated with Christianson syndrome, a syndromic form of X-linked intellectual disability characterized by microcephaly, severe global developmental delay, autistic behavior, early onset seizures and ataxia. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21932316",
"endSection": "abstract",
"offsetInBeginSection": 224,
"offsetInEndSection": 443,
"text": "Mutations in SLC9A6 are associated with Christianson syndrome (OMIM 300243), a syndromic form of X-linked mental retardation (XLMR) characterized by microcephaly, severe global developmental delay, ataxia and seizures. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21932316",
"endSection": "abstract",
"offsetInBeginSection": 1308,
"offsetInEndSection": 1433,
"text": "This patient broadens the spectrum of SLC9A6 mutations and contributes to the clinical delineation of Christianson syndrome. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24779060",
"endSection": "abstract",
"offsetInBeginSection": 792,
"offsetInEndSection": 972,
"text": "The single-gene disorders include Pitt–Hopkins syndrome (TCF4), Christianson syndrome (SLC9A6), Mowat–Wilson syndrome (ZEB2), Kleefstra syndrome (EHMT1), and Rett (MECP2) syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24630051",
"endSection": "abstract",
"offsetInBeginSection": 341,
"offsetInEndSection": 583,
"text": "In a 7-year-old boy with characteristic clinical and neuroimaging features of Christianson syndrome and epileptic encephalopathy with continuous spikes and waves during sleep, we identified a novel splice site mutation (IVS10-1G>A) in SLC9A6."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24630051",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 340,
"text": "Mutations in the solute carrier family 9, subfamily A member 6 (SLC9A6) gene, encoding the endosomal Na+/H+ exchanger 6 (NHE6) are associated with Christianson syndrome, a syndromic form of X-linked intellectual disability characterized by microcephaly, severe global developmental delay, autistic behavior, early onset seizures and ataxia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21932316",
"endSection": "abstract",
"offsetInBeginSection": 224,
"offsetInEndSection": 442,
"text": "Mutations in SLC9A6 are associated with Christianson syndrome (OMIM 300243), a syndromic form of X-linked mental retardation (XLMR) characterized by microcephaly, severe global developmental delay, ataxia and seizures."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27590723",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 200,
"text": "Christianson Syndrome, a recently identified X-linked neurodevelopmental disorder, is caused by mutations in the human gene SLC9A6 encoding the recycling endosomal alkali cation/proton exchanger NHE6."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27256868",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 97,
"text": "A new family with an SLC9A6 mutation expanding the phenotypic spectrum of Christianson syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26515654",
"endSection": "abstract",
"offsetInBeginSection": 251,
"offsetInEndSection": 433,
"text": "CS is caused by mutations in the SLC9A6 gene, which encodes a multipass transmembrane sodium (potassium)-hydrogen exchanger 6 (NHE6) protein, functional in early recycling endosomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26515654",
"endSection": "abstract",
"offsetInBeginSection": 1674,
"offsetInEndSection": 2010,
"text": "Our studies in heterozygous Slc9a6 KO female mice provide important clues for understanding the likely phenotypic range of Christianson syndrome among females heterozygous for SLC9A6 mutations and might improve diagnostic practice and genetic counseling by helping to characterize this presumably underappreciated patient/carrier group."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24630051",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 160,
"text": "A novel mutation in the endosomal Na+/H+ exchanger NHE6 (SLC9A6) causes Christianson syndrome with electrical status epilepticus during slow-wave sleep (ESES)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26515654",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "X-linked Christianson syndrome: heterozygous female Slc9a6 knockout mice develop mosaic neuropathological changes and related behavioral abnormalities."
}
] | 6 |
BioASQ-training6b
|
[
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D009154"
] | null |
5895bc397d9090f35300000b
|
bioasq_factoid
|
yesno
|
Can secondary glioblastoma be caused by brain irradiation?
|
['yes']
|
[
"yes"
] |
['Yes, brain irradiation can cause secondary glioblastoma.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/2028149",
"http://www.ncbi.nlm.nih.gov/pubmed/10845210",
"http://www.ncbi.nlm.nih.gov/pubmed/29526937",
"http://www.ncbi.nlm.nih.gov/pubmed/31088835",
"http://www.ncbi.nlm.nih.gov/pubmed/12853693",
"http://www.ncbi.nlm.nih.gov/pubmed/17583602",
"http://www.ncbi.nlm.nih.gov/pubmed/23227384",
"http://www.ncbi.nlm.nih.gov/pubmed/14714135",
"http://www.ncbi.nlm.nih.gov/pubmed/32938807",
"http://www.ncbi.nlm.nih.gov/pubmed/29713762",
"http://www.ncbi.nlm.nih.gov/pubmed/15685439",
"http://www.ncbi.nlm.nih.gov/pubmed/22102955",
"http://www.ncbi.nlm.nih.gov/pubmed/18373067",
"http://www.ncbi.nlm.nih.gov/pubmed/32649812",
"http://www.ncbi.nlm.nih.gov/pubmed/23571774",
"http://www.ncbi.nlm.nih.gov/pubmed/9810442",
"http://www.ncbi.nlm.nih.gov/pubmed/17786001"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29713762",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Prolonged survival in secondary glioblastoma following local injection of targeted alpha therapy with "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10845210",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 48,
"text": "[Radiation induced glioblastoma: a case report]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10845210",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 87,
"text": "We report a surgical case of a 54-year-old woman with a radiation induced glioblastoma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17786001",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 103,
"text": "Glioblastoma multiforme following cranial irradiation and chemotherapy for acute lymphocytic leukaemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17786001",
"endSection": "abstract",
"offsetInBeginSection": 112,
"offsetInEndSection": 236,
"text": "The occurrence of glioblastoma multiforme following radiation and chemotherapy in acute lymphocytic leukaemia (ALL) is rare."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17786001",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 105,
"text": "Glioblastoma multiforme following cranial irradiation and chemotherapy for acute lymphocytic leukaemia. R"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17786001",
"endSection": "abstract",
"offsetInBeginSection": 381,
"offsetInEndSection": 485,
"text": "exact cause for the development of glioblastoma multiforme following therapy for ALL is not clear. A gen"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12853693",
"endSection": "abstract",
"offsetInBeginSection": 330,
"offsetInEndSection": 507,
"text": "ndary malignant and benign brain tumors such as astrocytoma, meningioma and glioblastoma have been described in long-term survivors of conventional myeloablative alloBMT. Here w"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32649812",
"endSection": "abstract",
"offsetInBeginSection": 1120,
"offsetInEndSection": 1349,
"text": "The authors consider irradiation-induced glioblastomas secondary to primarily verified medulloblastomas in patients who had previously undergone craniospinal irradiation as a component of combined treatment after tumor resection."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32649812",
"endSection": "abstract",
"offsetInBeginSection": 1548,
"offsetInEndSection": 1733,
"text": "The authors analyzed patterns of occurrence of irradiation-induced glioblastomas depending on the molecular genetic group and clinical characteristics of patients after primary surgery."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18373067",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "Secondary brain tumors rarely arise after cranial irradiation; among them, meningiomas and glioblastomas are the most common and secondary oligodendroglial tumors the most rare."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23227384",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "Secondary glioblastoma multiforme (sGBM) can occur after a long latency period following radiation treatment of various diseases including brain tumors, leukemia, and more benign disorders like tinea capitis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22102955",
"endSection": "abstract",
"offsetInBeginSection": 257,
"offsetInEndSection": 415,
"text": "Irradiation, however, acts as an oncogenic factor as a delayed effect and it is rare that glioblastoma multiforme develops during the remission period of ALL."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2028149",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "A cerebellar glioblastoma was discovered in a 28 year old woman, 5 years after a focal 50 grays brain irradiation for meningioma of the clivus."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17786001",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 122,
"text": "Glioblastoma multiforme following cranial irradiation and chemotherapy for acute lymphocytic leukaemia. Report of 3 cases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32649812",
"endSection": "abstract",
"offsetInBeginSection": 805,
"offsetInEndSection": 932,
"text": "Secondary tumors including glioblastomas are under special attention since their occurrence is associated with a fatal outcome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32938807",
"endSection": "abstract",
"offsetInBeginSection": 406,
"offsetInEndSection": 492,
"text": "We describe a case of radiation-induced glioblastoma after radiotherapy for germinoma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32938807",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "[A Case of Radiation-induced Glioblastoma 29 Years after Treatments for Germinoma]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31088835",
"endSection": "abstract",
"offsetInBeginSection": 156,
"offsetInEndSection": 342,
"text": "Paradoxically, radiation is also a risk factor for GBM development, raising the possibility that radiotherapy of brain tumors could promote tumor recurrence or trigger secondary gliomas."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14714135",
"endSection": "abstract",
"offsetInBeginSection": 810,
"offsetInEndSection": 913,
"text": "An SMN may have a benign course, as in meningioma, or be a dilemma for the patient, as in glioblastoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9810442",
"endSection": "abstract",
"offsetInBeginSection": 1167,
"offsetInEndSection": 1510,
"text": "During a median of 2 years of follow-up review after the diagnosis of a secondary tumour, 3 patients died related to the secondary tumours (2 sarcomas, 1 glioblastoma), one died of a recurrent primary glioma, while the remaining 7 have been alive for from 10 months to 12 years after being treated for the secondary tumours (median: 3 years). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15685439",
"endSection": "abstract",
"offsetInBeginSection": 1326,
"offsetInEndSection": 1643,
"text": "In particular, children treated with X-irradiation for acute lymphoblastic leukemia show a significantly elevated risk of developing gliomas and primitive neuroectodermal tumor (PNET), often within 10 years after therapy. TP53 mutations are frequent in low-grade gliomas and secondary glioblastomas derived therefrom."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23571774",
"endSection": "abstract",
"offsetInBeginSection": 740,
"offsetInEndSection": 920,
"text": "Pathologic diagnoses were one glioblastoma, two cases of anaplastic astrocytoma, one medulloblastoma, one low-grade glioma, one high-grade glial tumor, and one atypical meningioma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17583602",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 202,
"text": "A 22 year-old-man with acute lymphoblastic leukaemia had received prophylactic cranial irradiation and intrathecal chemotherapy. Eighteen years later a cerebellar glioblastoma multiforme was diagnosed. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29526937",
"endSection": "abstract",
"offsetInBeginSection": 412,
"offsetInEndSection": 478,
"text": "She developed glioblastoma 5.7 years after the initial GK surgery."
}
] | 11 |
BioASQ-training11b
| null | null |
5e323d79fbd6abf43b000058
|
bioasq_yesno
|
factoid
|
What is the effect of CRD-BP on the stability of c-myc mRNA?
|
[['To protect c-myc CRD from endonucleolytic attack.']]
|
[
"c-myc",
"MYC",
"c-Myc",
"c-Myc protein",
"c-Myc transcription factor",
"c-myc proto-oncogene"
] |
['The c-myc mRNA coding region determinant-binding protein (CRD-BP) has high affinity for the coding region determinant (CRD) of c-myc mRNA. Such affinity is believed to protect c-myc CRD from endonucleolytic attack.', 'The coding region determinant-binding protein (CRD-BP) binds in vitro to c-myc mRNA and is thought to stabilize the mRNA and increase c-Myc protein abundance ', 'The coding region determinant-binding protein (CRD-BP) binds in vitro to c-myc mRNA and is thought to stabilize the mRNA and increase c-Myc protein abundance ', 'The coding region determinant-binding protein (CRD-BP) binds in vitro to c-myc mRNA and is thought to stabilize the mRNA and increase c-Myc protein abundance ', 'The coding region determinant-binding protein (CRD-BP) binds in vitro to c-myc mRNA and is thought to stabilize the mRNA and increase c-Myc protein abundance ', 'The coding region determinant-binding protein (CRD-BP) binds in vitro to c-myc mRNA and is thought to stabilize the mRNA and increase c-Myc protein abundance ']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/17264115",
"http://www.ncbi.nlm.nih.gov/pubmed/16778892",
"http://www.ncbi.nlm.nih.gov/pubmed/12894594",
"http://www.ncbi.nlm.nih.gov/pubmed/12024010",
"http://www.ncbi.nlm.nih.gov/pubmed/11745432",
"http://www.ncbi.nlm.nih.gov/pubmed/10850408",
"http://www.ncbi.nlm.nih.gov/pubmed/10692488",
"http://www.ncbi.nlm.nih.gov/pubmed/9801297",
"http://www.ncbi.nlm.nih.gov/pubmed/9178888"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17264115",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "CRD-BP shields c-myc and MDR-1 RNA from endonucleolytic attack by a mammalian endoribonuclease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17264115",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 213,
"text": "The c-myc mRNA coding region determinant-binding protein (CRD-BP) has high affinity for the coding region determinant (CRD) of c-myc mRNA. Such affinity is believed to protect c-myc CRD from endonucleolytic attack"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17264115",
"endSection": "abstract",
"offsetInBeginSection": 1061,
"offsetInEndSection": 1192,
"text": " These results provide the first direct evidence that CRD-BP can indeed protect c-myc CRD cleavage initiated by an endoribonuclease"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12894594",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "CRD-BP: a c-Myc mRNA stabilizing protein with an oncofetal pattern of expression"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12894594",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 206,
"text": "The Coding Region Determinant-Binding Protein (CRD-BP) is an RRM and KH-domain-containing protein that recognizes specifically at least three RNAs. It binds to one of the two c-myc mRNA instability elements"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12894594",
"endSection": "abstract",
"offsetInBeginSection": 302,
"offsetInEndSection": 402,
"text": "CRD-BP has been assigned a role in stabilizing c-myc mRNA by preventing its endonucleolytic cleavage"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12024010",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 207,
"text": "A 249-nucleotide coding region instability determinant (CRD) destabilizes c-myc mRNA. Previous experiments identified a CRD-binding protein (CRD-BP) that appears to protect the CRD from endonuclease cleavage"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12024010",
"endSection": "abstract",
"offsetInBeginSection": 968,
"offsetInEndSection": 1118,
"text": "These data suggest that c-myc mRNA is rapidly degraded unless it is (i) translated without pausing or (ii) protected by the CRD-BP when pausing occurs"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11745432",
"endSection": "abstract",
"offsetInBeginSection": 243,
"offsetInEndSection": 303,
"text": "Here, we confirm that human CRD-BP/IMP-1 binds to c-myc mRNA"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10850408",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "The coding region determinant-binding protein (CRD-BP) binds in vitro to c-myc mRNA and is thought to stabilize the mRNA and increase c-Myc protein abundance"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9801297",
"endSection": "abstract",
"offsetInBeginSection": 97,
"offsetInEndSection": 521,
"text": "Two regions within c- myc mRNA determine its short half-life. One is in the 3'-untranslated region, the other is in the coding region. A cytoplasmic protein, the coding region determinant-binding protein (CRD-BP), binds in vitro to the c- myc coding region instability determinant. We have proposed that the CRD-BP, when bound to the mRNA, shields the mRNA from endonucleolytic attack and thereby prolongs the mRNA half-life"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9178888",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "Developmental regulation of CRD-BP, an RNA-binding protein that stabilizes c-myc mRNA in vitro"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9178888",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "We previously isolated and characterized a coding region determinant-binding protein (CRD-BP) that might regulate c-myc mRNA post-transcriptionally"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9178888",
"endSection": "abstract",
"offsetInBeginSection": 149,
"offsetInEndSection": 296,
"text": "CRD-BP binds specifically to the coding region of c-myc mRNA and might stabilize c-myc mRNA in vitro by protecting it from endonucleolytic cleavage"
}
] | 5 |
BioASQ-training5b
|
[
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0070934",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0070937",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0048255",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0043488"
] |
[] |
55390901bc4f83e828000014
|
bioasq_factoid
|
yesno
|
Are microtubules marked by glutamylation?
|
['yes']
|
[
"yes"
] |
['Yes, glutamylation is the most prevalent tubulin posttranslational modification and marks stable microtubules.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26227334",
"http://www.ncbi.nlm.nih.gov/pubmed/19700636",
"http://www.ncbi.nlm.nih.gov/pubmed/23973077",
"http://www.ncbi.nlm.nih.gov/pubmed/26000474",
"http://www.ncbi.nlm.nih.gov/pubmed/25959773",
"http://www.ncbi.nlm.nih.gov/pubmed/25030760"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26227334",
"endSection": "abstract",
"offsetInBeginSection": 1220,
"offsetInEndSection": 1385,
"text": "Together with detyrosination, glutamylation and other modifications, tubulin acetylation may form a unique 'language' to regulate microtubule structure and function."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25959773",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "Glutamylation, the most prevalent tubulin posttranslational modification, marks stable microtubules and regulates recruitment and activity of microtubule- interacting proteins."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26000474",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "Enzymes of the tubulin tyrosine ligase-like (TTLL) family posttranslationally modify and thereby mark microtubules by glutamylation, generating specific recognition sites for microtubule-interacting proteins."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25030760",
"endSection": "abstract",
"offsetInBeginSection": 705,
"offsetInEndSection": 942,
"text": " PTMs of the cytoskeleton, including phosphorylation, glycosylation, ubiquitination, detyrosination/tyrosination, (poly)glutamylation and (poly)glycylation, acetylation, sumoylation, and palmitoylation, will be addressed in this chapter."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23973077",
"endSection": "abstract",
"offsetInBeginSection": 250,
"offsetInEndSection": 408,
"text": "The tubulin posttranslational modifications: acetylation, detyrosination, polyglutamylation, and polyglycylation play important roles in microtubule functions"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19700636",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "In most eukaryotic cells, tubulin is subjected to posttranslational glutamylation, a conserved modification of unclear function."
}
] | 6 |
BioASQ-training6b
| null | null |
58aa0a62396a458e50000007
|
bioasq_yesno
|
factoid
|
The drug JTV519 is derivative of which group of chemical compounds?
|
[['1,4-benzothiazepine', 'benzothiazepine']]
|
[
"1,4-benzothiazepine",
"benzothiazepine",
"benzothiazepine derivative",
"benzothiazepine compound"
] |
['JTV519 (K201), is a 1,4-benzothiazepine derivative and multi-channel blocker, which has been found to stabilize RyR2s and decrease SR Ca²⁺ leak.', 'The 1,4-benzothiazepine derivative JTV-519 is a new type of calcium ion channel modulator.JTV-519, which has potential use as an antiarrhythmic [285800]. The drug is a novel cardioprotectant derivative of 1,4-benzothiazepine for which phase I trials were completed in the third quarter of 1998', 'The 1,4-benzothiazepine derivative JTV-519 is a new type of calcium ion channel modulator.JTV-519, which has potential use as an antiarrhythmic [285800]. The drug is a novel cardioprotectant derivative of 1,4-benzothiazepine for which phase I trials were completed in the third quarter of 1998']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22509897",
"http://www.ncbi.nlm.nih.gov/pubmed/23349825",
"http://www.ncbi.nlm.nih.gov/pubmed/21989257",
"http://www.ncbi.nlm.nih.gov/pubmed/17313373",
"http://www.ncbi.nlm.nih.gov/pubmed/17112502",
"http://www.ncbi.nlm.nih.gov/pubmed/15073377",
"http://www.ncbi.nlm.nih.gov/pubmed/12551874",
"http://www.ncbi.nlm.nih.gov/pubmed/12433661",
"http://www.ncbi.nlm.nih.gov/pubmed/12359358",
"http://www.ncbi.nlm.nih.gov/pubmed/11757794",
"http://www.ncbi.nlm.nih.gov/pubmed/11429046",
"http://www.ncbi.nlm.nih.gov/pubmed/11101196",
"http://www.ncbi.nlm.nih.gov/pubmed/10864882",
"http://www.ncbi.nlm.nih.gov/pubmed/10789707",
"http://www.ncbi.nlm.nih.gov/pubmed/10683355"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22509897",
"endSection": "abstract",
"offsetInBeginSection": 202,
"offsetInEndSection": 341,
"text": "In these conditions, JTV519 (K201), a 1,4-benzothiazepine derivative and multi-channel blocker, stabilizes RyR2s and decrease SR Ca²⁺ leak."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23349825",
"endSection": "abstract",
"offsetInBeginSection": 284,
"offsetInEndSection": 514,
"text": "The 1,4-benzothiazepine derivative JTV519, and the more specific derivative S107 (2,3,4,5,-tetrahydro-7-methoxy-4-methyl-1,4-benzothiazepine), are thought to improve skeletal muscle function by stabilizing the RyR1-FKBP12 complex."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21989257",
"endSection": "abstract",
"offsetInBeginSection": 198,
"offsetInEndSection": 491,
"text": "In this article, we synthesize derivatives of the channel activator 4-chloro-3-methyl phenol (4-CmC) and the 1,4-benzothiazepine channel inhibitor 4-[-3{1-(4-benzyl) piperidinyl}propionyl]-7-methoxy-2,3,4,5-tetrahydro-1,4-benzothiazepine (K201, JTV519) with enhanced electron donor properties."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17313373",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "K201 (JTV519), a benzothiazepine derivative, has been shown to possess anti-arrhythmic and cardioprotective properties, but the mechanism of its action is both complex and controversial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17112502",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "K201 (JTV519) is a 1,4-benzothiazepine derivative that exhibits a strong cardioprotective action and acts as a multiple-channel blocker, including as a K+ channel blocker."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15073377",
"endSection": "abstract",
"offsetInBeginSection": 456,
"offsetInEndSection": 644,
"text": "A derivative of 1,4-benzothiazepine (JTV519) increased the affinity of calstabin2 for RyR2, which stabilized the closed state of RyR2 and prevented the Ca2+ leak that triggers arrhythmias."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12551874",
"endSection": "abstract",
"offsetInBeginSection": 200,
"offsetInEndSection": 396,
"text": "We report that a new drug, the 1,4-benzothiazepine derivative JTV519, reverses this pathogenic process. JTV519 is known to have a protective effect against Ca2+ overload-induced myocardial injury."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12433661",
"endSection": "abstract",
"offsetInBeginSection": 863,
"offsetInEndSection": 1066,
"text": "In conclusion, JTV519, a new 1,4-benzothiazepine derivative, corrected the defective channel gating in RyR (increase in both the rapid conformational change and the subsequent Ca(2+) release rate) in HF."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12359358",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 353,
"text": "A newly synthesized 1,4-benzothiazipine derivate, 4-[3-(4-benzylpiperidin-1-yl) propionyl]-7-methoxy-2,3,4,5-tetrahydro-1, 4-benzothiazepine monohydrochloride (JTV-519) was examined for its ability to reverse P-glycoprotein (P-gp) and multidrug resistance protein 1 (MRP1) mediated multidrug resistance (MDR) in K562/MDR and KB/MRP cells, respectively. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11757794",
"endSection": "abstract",
"offsetInBeginSection": 66,
"offsetInEndSection": 269,
"text": "JTV-519, which has potential use as an antiarrhythmic [285800]. The drug is a novel cardioprotectant derivative of 1,4-benzothiazepine for which phase I trials were completed in the third quarter of 1998"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11429046",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "The 1,4-benzothiazepine derivative JTV-519 is a new type of calcium ion channel modulator."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11101196",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "A new 1,4-benzothiazepine derivative, JTV519 (JTV), has strong protective effects against isoproterenol-induced myocardial injury. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10864882",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "A newly synthesized benzothiazepine derivative, JTV-519 (JT) has been reported to be cardioprotective."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10789707",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 103,
"text": "Protective effect of JTV519, a new 1,4-benzothiazepine derivative, on prolonged myocardial preservation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10683355",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 139,
"text": "A new 1,4-benzothiazepine derivative, JTV519, has a strong protective effect against Ca(2+) overload-induced myocardial injury."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12551874",
"endSection": "abstract",
"offsetInBeginSection": 185,
"offsetInEndSection": 289,
"text": " We report that a new drug, the 1,4-benzothiazepine derivative JTV519, reverses this pathogenic process."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10789707",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "Protective effect of JTV519, a new 1,4-benzothiazepine derivative, on prolonged myocardial preservation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11101196",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "A new 1,4-benzothiazepine derivative, JTV519 (JTV), has strong protective effects against isoproterenol-induced myocardial injury."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10683355",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "A new 1,4-benzothiazepine derivative, JTV519, has a strong protective effect against Ca(2+) overload-induced myocardial injury."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22509897",
"endSection": "abstract",
"offsetInBeginSection": 175,
"offsetInEndSection": 315,
"text": " In these conditions, JTV519 (K201), a 1,4-benzothiazepine derivative and multi-channel blocker, stabilizes RyR2s and decrease SR Ca?⁺ leak."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11101196",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "The cardioprotective effects of a new 1,4-benzothiazepine derivative, JTV519, on ischemia/reperfusion-induced Ca2+ overload in isolated rat hearts."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22509897",
"endSection": "abstract",
"offsetInBeginSection": 202,
"offsetInEndSection": 341,
"text": "In these conditions, JTV519 (K201), a 1,4-benzothiazepine derivative and multi-channel blocker, stabilizes RyR2s and decrease SR Ca²⁺ leak."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10789707",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "Protective effect of JTV519, a new 1,4-benzothiazepine derivative, on prolonged myocardial preservation."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11101196",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "The cardioprotective effects of a new 1,4-benzothiazepine derivative, JTV519, on ischemia/reperfusion-induced Ca2+ overload in isolated rat hearts."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11101196",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "A new 1,4-benzothiazepine derivative, JTV519 (JTV), has strong protective effects against isoproterenol-induced myocardial injury."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17112502",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "K201 (JTV519) is a 1,4-benzothiazepine derivative that exhibits a strong cardioprotective action and acts as a multiple-channel blocker, including as a K+ channel blocker."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15073377",
"endSection": "abstract",
"offsetInBeginSection": 456,
"offsetInEndSection": 644,
"text": "A derivative of 1,4-benzothiazepine (JTV519) increased the affinity of calstabin2 for RyR2, which stabilized the closed state of RyR2 and prevented the Ca2+ leak that triggers arrhythmias."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17313373",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "K201 (JTV519), a benzothiazepine derivative, has been shown to possess anti-arrhythmic and cardioprotective properties, but the mechanism of its action is both complex and controversial."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10789707",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "Protective effect of JTV519, a new 1,4-benzothiazepine derivative, on prolonged myocardial preservation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12551874",
"endSection": "abstract",
"offsetInBeginSection": 188,
"offsetInEndSection": 290,
"text": "We report that a new drug, the 1,4-benzothiazepine derivative JTV519, reverses this pathogenic process"
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=chemicals_and_drugs_category",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D004339"
] |
[] |
54f9b74306d9727f76000004
|
bioasq_factoid
|
factoid
|
Which molecular does daratumumab target?
|
['CD38']
|
[
"CD38",
"T10",
"ADP-ribosyl cyclase 1",
"NAD+-glycohydrolase",
"NAD+-glycohydrolase 1",
"NAD+-cyclase",
"NAD+-glycohydrolase CD38",
"NAD+-cyclase CD38"
] |
['Daratumumab is an anti-CD38 antibody.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29500635"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29500635",
"endSection": "abstract",
"offsetInBeginSection": 875,
"offsetInEndSection": 1076,
"text": "The addition of daratumumab (anti-CD38 antibody) augmented NK-cell cytotoxicity against target cells expressing high CD38, but not against CD38 low or negative target cells also in the presence of TME."
}
] | 11 |
BioASQ-training11b
| null | null |
5c6545bae842deac6700001d
|
bioasq_factoid
|
factoid
|
Which is the E3 ubiquitin ligase of Hsp90?
|
['Carboxyl terminus of hsc70-interacting protein (CHIP)']
|
[
"Carboxyl terminus of hsc70-interacting protein (CHIP)",
"C-terminus of Hsc70-interacting protein",
"C terminus of Hsc70-interacting protein",
"C terminus of CHIP",
"CHIP",
"C-HIP"
] |
Carboxyl terminus of hsc70-interacting protein (CHIP) can mediate ubiquitination of the 90 kDa heat-shock protein (hsp90) in vitro, with subsequent proteasomal degradation of the chaperone.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23429937",
"http://www.ncbi.nlm.nih.gov/pubmed/23344957",
"http://www.ncbi.nlm.nih.gov/pubmed/20618441",
"http://www.ncbi.nlm.nih.gov/pubmed/17209571"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23429937",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 232,
"text": "C-terminal Hsp-interacting protein (CHIP) is an HSP70 and HSP90 interacting co-chaperone and an E3 ubiquitin ligase. Previous studies have reported the role of CHIP in cancer progression by targeting protein degradation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23344957",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 209,
"text": "The U-box E3 ubiquitin ligase CHIP (C terminus of Hsc70-interacting protein) binds Hsp90 and/or Hsp70 via its tetratricopeptide repeat (TPR), facilitating ubiquitination of the chaperone-bound client proteins."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23344957",
"endSection": "abstract",
"offsetInBeginSection": 882,
"offsetInEndSection": 1055,
"text": "In vitro ubiquitination assays indicated that Ca(2+)/S100A2 and S100P are efficient and specific inhibitors of CHIP-mediated ubiquitination of Hsp70, Hsp90, HSF1, and Smad1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20618441",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 247,
"text": "The E3 ubiquitin ligase CHIP (C-terminus of Hsc70-interacting protein) is believed to be a central player in the cellular triage decision, as it links the molecular chaperones Hsp70/Hsc70 and Hsp90 to the ubiquitin proteasomal degradation pathway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20618441",
"endSection": "abstract",
"offsetInBeginSection": 596,
"offsetInEndSection": 675,
"text": "We found that CHIP has a sixfold higher affinity for Hsp90 compared with Hsc70."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17209571",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "Carboxyl terminus of hsc70-interacting protein (CHIP) can remodel mature aryl hydrocarbon receptor (AhR) complexes and mediate ubiquitination of both the AhR and the 90 kDa heat-shock protein (hsp90) in vitro"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17209571",
"endSection": "abstract",
"offsetInBeginSection": 619,
"offsetInEndSection": 864,
"text": "The analysis of the sucrose-gradient-fractionated in vitro translated AhR complexes revealed that CHIP can mediate hsp90 ubiquitination while cooperating with unidentified factors to promote the ubiquitination of mature unliganded AhR complexes."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D044767",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D043743",
"http://www.uniprot.org/uniprot/UB2E3_HUMAN",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0004842",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0044389",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0000151",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0051879",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018841"
] |
[] |
5319a7d2b166e2b806000029
|
bioasq_factoid
|
factoid
|
Mutations in which gene determine response to both erlotinib and gefitinib?
|
['epidermal growth factor receptor (EGFR) gene']
|
[
"epidermal growth factor receptor",
"EGFR",
"epidermal growth factor receptor (EGFR)",
"ErbB-1",
"HER1",
"CD326"
] |
['Patients who carry somatic activating mutations in the tyrosine kinase domain of the epidermal growth factor receptor (EGFR) gene, respond well to erlotinib and gefitinib.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23332287",
"http://www.ncbi.nlm.nih.gov/pubmed/22738915",
"http://www.ncbi.nlm.nih.gov/pubmed/22263058",
"http://www.ncbi.nlm.nih.gov/pubmed/21904575",
"http://www.ncbi.nlm.nih.gov/pubmed/21777765",
"http://www.ncbi.nlm.nih.gov/pubmed/21430269",
"http://www.ncbi.nlm.nih.gov/pubmed/20948254",
"http://www.ncbi.nlm.nih.gov/pubmed/20705455",
"http://www.ncbi.nlm.nih.gov/pubmed/20007486",
"http://www.ncbi.nlm.nih.gov/pubmed/19808904",
"http://www.ncbi.nlm.nih.gov/pubmed/18997733",
"http://www.ncbi.nlm.nih.gov/pubmed/16730855",
"http://www.ncbi.nlm.nih.gov/pubmed/16705038",
"http://www.ncbi.nlm.nih.gov/pubmed/16049312",
"http://www.ncbi.nlm.nih.gov/pubmed/15737014",
"http://www.ncbi.nlm.nih.gov/pubmed/23507588",
"http://www.ncbi.nlm.nih.gov/pubmed/22920167",
"http://www.ncbi.nlm.nih.gov/pubmed/22806307",
"http://www.ncbi.nlm.nih.gov/pubmed/20647703",
"http://www.ncbi.nlm.nih.gov/pubmed/20512075",
"http://www.ncbi.nlm.nih.gov/pubmed/19063875",
"http://www.ncbi.nlm.nih.gov/pubmed/18799900",
"http://www.ncbi.nlm.nih.gov/pubmed/18726117",
"http://www.ncbi.nlm.nih.gov/pubmed/17575237",
"http://www.ncbi.nlm.nih.gov/pubmed/17145836",
"http://www.ncbi.nlm.nih.gov/pubmed/16199108",
"http://www.ncbi.nlm.nih.gov/pubmed/16009451",
"http://www.ncbi.nlm.nih.gov/pubmed/15329413"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23332287",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Mutations in the epidermal growth factor receptor gene (EGFR) are frequently observed in non-small-cell lung cancer (NSCLC),"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23332287",
"endSection": "sections.0",
"offsetInBeginSection": 223,
"offsetInEndSection": 445,
"text": "EGFR tyrosine kinase inhibitors (TKIs), such as gefitinib and erlotinib, have transformed therapy for patients with EGFR-mutant NSCLC and have proved superior to chemotherapy as first-line treatment for this patient group."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22738915",
"endSection": "sections.0",
"offsetInBeginSection": 53,
"offsetInEndSection": 361,
"text": "Adenocarcinomas, the most common histologic subtype of non-small cell lung cancer (NSCLC), are frequently associated with activating mutations in the epidermal growth factor receptor (EGFR) gene. Although these patients often respond clinically to the EGFR tyrosine kinase inhibitors erlotinib and gefitinib,"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22263058",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 341,
"text": "Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) such as gefitinib and erlotinib are promising therapies for patients with advanced non-small-cell lung cancer (NSCLC). Patients with somatic activating mutations in the EGFR gene have dramatic response initially, but would eventually develop resistance to these TKIs."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21904575",
"endSection": "sections.0",
"offsetInBeginSection": 242,
"offsetInEndSection": 546,
"text": "NSCLCs with EGFR mutations (exon 19 deletions or the exon 21 L858R) attain responses to EGFR tyrosine kinase inhibitors (TKIs) gefitinib and erlotinib, with improved response rate (RR), progression-free survival (PFS) and in some reports overall survival (OS) when compared with EGFR wildtype (WT) cases."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21777765",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 216,
"text": "Patients presenting with non-small cell lung cancer (NSCLC) and active EGFR mutation have a high response rate (60-70%) to EGFR tyrosine kinase inhibitors (TKI) with little immediate progression (primary resistance)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21430269",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "Lung cancers harboring mutations in the epidermal growth factor receptor (EGFR) respond to EGFR tyrosine kinase inhibitors, but drug resistance invariably emerges."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20948254",
"endSection": "sections.0",
"offsetInBeginSection": 12,
"offsetInEndSection": 141,
"text": "EGFR-TKI yields a long survival period in cases of non-small cell lung cancer (NSCLC), especially those with EGFR gene mutations,"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20948254",
"endSection": "sections.0",
"offsetInBeginSection": 582,
"offsetInEndSection": 706,
"text": "Efficacy of erlotinib was recognized in the cases in which disease control was obtained by initial treatment with gefitinib."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20705455",
"endSection": "sections.0",
"offsetInBeginSection": 12,
"offsetInEndSection": 205,
"text": "Patients with lung adenocarcinoma who carry epidermal growth factor receptor (EGFR) gene mutations respond remarkably well to EGFR tyrosine kinase inhibitor (EGFR-TKI), gefitinib, or erlotinib."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20007486",
"endSection": "sections.0",
"offsetInBeginSection": 24,
"offsetInEndSection": 188,
"text": "lung adenocarcinomas with epidermal growth factor receptor (EGFR) mutations respond to treatment with the tyrosine kinase inhibitors (TKIs) gefitinib and erlotinib;"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19808904",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 204,
"text": "The development of resistance to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKI) seems almost inevitable, even in patients with lung cancer that initially respond well to EGFR-TKIs."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19808904",
"endSection": "sections.0",
"offsetInBeginSection": 425,
"offsetInEndSection": 823,
"text": "Gefitinib- or erlotinib-resistant sublines were established by exposing the parental PC-9 cell line to chronic, repeated treatments with these drugs. These resistant sublines showed more than 100-fold more resistance to gefitinib and erlotinib and acquired cross-resistance to other EGFR-TKIs. The T790M EGFR mutation was found by pyrosequencing, and this seemed to be the cause of drug resistance."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18997733",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 229,
"text": "Patients with advanced pulmonary adenocarcinoma exhibiting overexpression or mutation of epidermal growth factor receptor tend to respond better to targeted therapy with tyrosine kinase inhibitors such as gefitinib and erlotinib."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16730855",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 496,
"text": "Mutations of the epidermal growth factor receptor (EGFR) gene have been reported in non-small-cell lung cancer (NSCLC), especially in patients with adenocarcinoma and never smokers. Some common somatic mutations in EGFR, including deletion mutations in exon 19 and leucine-to-arginine substitution at amino acid position 858 (L858R) in exon 21, have been examined for their ability to predict sensitivity to gefitinib or erlotinib, which are selective EGFR tyrosine kinase inhibitors (EGFR-TKIs)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16705038",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 249,
"text": "Somatic mutations in exons encoding the tyrosine kinase domain of the epidermal growth factor receptor (EGFR) gene are found in human lung adenocarcinomas and are associated with sensitivity to the tyrosine kinase inhibitors gefitinib and erlotinib."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16049312",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 196,
"text": "Somatic mutations in the tyrosine kinase domain of the epidermal growth factor receptor (EGFR) gene are present in lung adenocarcinomas that respond to the EGFR inhibitors gefitinib and erlotinib."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23507588",
"endSection": "sections.0",
"offsetInBeginSection": 325,
"offsetInEndSection": 523,
"text": "Epidermal growth factor receptor(EGFR)-tyrosine kinase inhibitor(TKI)(such as gefitinib or erlotinib)treatment of lung cancer harboring EGFR gene mutation is one of the prototypes of such therapies."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22806307",
"endSection": "sections.0",
"offsetInBeginSection": 380,
"offsetInEndSection": 630,
"text": "patients with NSCLC and CNS metastases with epidermal growth factor receptor gene mutations who received CSF examinations during epidermal growth factor receptor-tyrosine kinase inhibitors treatment (250 mg daily gefitinib or 150 mg daily erlotinib)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20647703",
"endSection": "sections.0",
"offsetInBeginSection": 491,
"offsetInEndSection": 707,
"text": "The evidence of epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) such as gefitinib and erlotinib was first confirmed as the second-line treatment for non-selective patients with advanced NSCLC."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20647703",
"endSection": "sections.0",
"offsetInBeginSection": 927,
"offsetInEndSection": 1402,
"text": "patients with EGFR-mutated advanced NSCLC, the first-line treatment with gefitinib had achieved a significant prolongation of progression-free survival compared with standard platinum doublet chemotherapy in a few phase III trials, and became a new standard of care. Gefitinib is highly effective for patients with advanced NSCLC with EGFR mutation even if their performance status is poor, although one should always pay careful attention to fatal interstitial lung disease."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20512075",
"endSection": "sections.0",
"offsetInBeginSection": 11,
"offsetInEndSection": 187,
"text": "The tyrosine kinase inhibitors (TKIs) gefitinib and erlotinib are effective in non-small cell lung cancers (NSCLCs) with epidermal growth factor receptor (EGFR) gene mutations."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19063875",
"endSection": "sections.0",
"offsetInBeginSection": 12,
"offsetInEndSection": 226,
"text": "Somatic mutations in the epidermal growth factor receptor (EGFR) gene are associated with the responses to the tyrosine kinase inhibitors gefitinib and erlotinib in patients with non-small-cell lung cancer (NSCLC)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18799900",
"endSection": "sections.0",
"offsetInBeginSection": 1051,
"offsetInEndSection": 1393,
"text": "EGFR tyrosine kinase inhibitors (gefitinib, erlotinib), which are molecularly targeted drugs, and it has now become possible to select treatment methods by choosing from a number of anticancer drugs. EGFR tyrosine kinase inhibitors have been demonstrated to have a very high cytoreductive effect on lung cancers that have EGFR gene mutations."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18726117",
"endSection": "sections.0",
"offsetInBeginSection": 224,
"offsetInEndSection": 385,
"text": "EGFR gene mutations at kinase domain in non-small cell lung cancer (NSCLC) have been examined for their ability to predict sensitivity to gefitinib or erlotinib."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17575237",
"endSection": "sections.0",
"offsetInBeginSection": 214,
"offsetInEndSection": 386,
"text": "responsive patients can relapse as a result of selection for EGFR gene mutations that confer resistance to ATP competitive EGFR inhibitors, such as erlotinib and gefitinib."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17145836",
"endSection": "sections.0",
"offsetInBeginSection": 28,
"offsetInEndSection": 254,
"text": "the epidermal growth factor receptor (EGFR) was a therapeutic target in non-small cell lung cancer (NSCLC) and other cancers led to development of the small-molecule receptor tyrosine kinase inhibitors gefitinib and erlotinib."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17145836",
"endSection": "sections.0",
"offsetInBeginSection": 1387,
"offsetInEndSection": 1501,
"text": "There was a significant correlation between EGFR gene copy number, EGFR gene mutations, and gefitinib sensitivity."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16199108",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "Epidermal growth factor receptor (EGFR) gene mutations have been found in a subset of non-small cell lung cancer (NSCLC) with good clinical response to gefitinib therapy."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16009451",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 262,
"text": "Mutations in the tyrosine kinase (TK) domain of the epidermal growth factor receptor (EGFR) gene in non-small cell lung cancers are associated with increased sensitivity of these cancers to drugs that inhibit EGFR kinase activity such as gefitinib and erlotinib."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15329413",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 204,
"text": "Somatic mutations in the tyrosine kinase (TK) domain of the epidermal growth factor receptor (EGFR) gene are reportedly associated with sensitivity of lung cancers to gefitinib (Iressa), kinase inhibitor."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15329413",
"endSection": "sections.0",
"offsetInBeginSection": 1567,
"offsetInEndSection": 1689,
"text": "frequently containing mutations within the TK domain of EGFR that are associated with gefitinib and erlotinib sensitivity."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.biosemantics.org/jochem#4274201",
"http://www.biosemantics.org/jochem#4241662",
"http://www.biosemantics.org/jochem#4241661"
] |
[
{
"o": "Gene Mutation",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A7647895"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A7850263",
"p": "http://linkedlifedata.com/resource/umls/prefMetaMap",
"s": "http://linkedlifedata.com/resource/umls/id/C0596611"
},
{
"o": "Gene Mutation",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A7850263"
}
] |
51542e44d24251bc05000081
|
bioasq_factoid
|
yesno
|
Is eptinezumab a small molecule?
|
['no']
|
[
"no"
] |
['No, eptinezumab is a humanized monoclonal antibody.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/32266704"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32266704",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 193,
"text": "Eptinezumab-jjmr (referred to as eptinezumab hereafter; Vyepti™) is a humanised monoclonal antibody that binds to calcitonin gene-related peptide (CGRP) and blocks its binding to the receptor. "
}
] | 11 |
BioASQ-training11b
| null | null |
6026ee821cb411341a0000d3
|
bioasq_yesno
|
yesno
|
Can simvastatin alleviate depressive symptoms?
|
['yes']
|
[
"yes"
] |
['Yes, simvastatin decreases depressive symptoms.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25827645"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25827645",
"endSection": "abstract",
"offsetInBeginSection": 712,
"offsetInEndSection": 1091,
"text": "Simvastatin-treated patients experienced significantly more reductions in HDRS scores compared to the placebo group by the end of the trial (p=0.02). Early improvement and response rates were significantly greater in the simvastatin group than the placebo group (p=0.02 and p=0.01, respectively) but remission rate was not significantly different between the two groups (p=0.36)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25827645",
"endSection": "abstract",
"offsetInBeginSection": 1149,
"offsetInEndSection": 1280,
"text": "In conclusion, simvastatin seems to be a safe and effective adjuvant therapy for patients suffering from major depressive disorder."
}
] | 11 |
BioASQ-training11b
| null | null |
5c010e09133db5eb78000024
|
bioasq_yesno
|
factoid
|
PDQ39 questionnaires is design for which disease?
|
["Parkinson's Disease"]
|
[
"Parkinson's Disease",
"Parkinson disease",
"PD",
"Shaking Palsy",
"Parkinson's",
"Parkinson's syndrome",
"idiopathic Parkinson's disease"
] |
["PDQ39 is Parkinson's Disease Questionnaire that is used for assessment of quality of life in patients with Parkinson's Disease."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29670566",
"http://www.ncbi.nlm.nih.gov/pubmed/24035927",
"http://www.ncbi.nlm.nih.gov/pubmed/30363378",
"http://www.ncbi.nlm.nih.gov/pubmed/18543333",
"http://www.ncbi.nlm.nih.gov/pubmed/23346238",
"http://www.ncbi.nlm.nih.gov/pubmed/28805568",
"http://www.ncbi.nlm.nih.gov/pubmed/28122431",
"http://www.ncbi.nlm.nih.gov/pubmed/30108543",
"http://www.ncbi.nlm.nih.gov/pubmed/29542093",
"http://www.ncbi.nlm.nih.gov/pubmed/15778909",
"http://www.ncbi.nlm.nih.gov/pubmed/28980176",
"http://www.ncbi.nlm.nih.gov/pubmed/28770096",
"http://www.ncbi.nlm.nih.gov/pubmed/29644334",
"http://www.ncbi.nlm.nih.gov/pubmed/28290191",
"http://www.ncbi.nlm.nih.gov/pubmed/17702633",
"http://www.ncbi.nlm.nih.gov/pubmed/21163736",
"http://www.ncbi.nlm.nih.gov/pubmed/16258207",
"http://www.ncbi.nlm.nih.gov/pubmed/29215823",
"http://www.ncbi.nlm.nih.gov/pubmed/23323136",
"http://www.ncbi.nlm.nih.gov/pubmed/20347841",
"http://www.ncbi.nlm.nih.gov/pubmed/16763974"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28980176",
"endSection": "abstract",
"offsetInBeginSection": 752,
"offsetInEndSection": 1065,
"text": "The outcomes assessed were motor symptoms with Unified PD Rating Scale III (UPDRSIII), functional mobility with Timed Up and Go Test (TUG), endurance with 6 min walking test (6MWT), freezing of gait with Freezing of Gait Questionnaire (FOG_Q), walking velocity with GAITRite and QL with PD Questionnaire (PDQ39). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29215823",
"endSection": "abstract",
"offsetInBeginSection": 549,
"offsetInEndSection": 968,
"text": " They were assessed using SCOPA, Hoehn and Yahr Scale (HYS), Unified Parkinson's Disease Rating Scale (UPDRS), Parkinson's Disease Sleep Scale 2nd version (PDSS-2), Non-motor Symptoms Scale (NMSS), Montgomery Asberg Depression Scale (MADS), 39-item Parkinson's Disease Questionnaire (PDQ39), Neurogenic Orthostatic Hypotension Questionnaire (NOHQ), and Rapid Eye Movement Sleep Behaviour Disorder Questionnaire (RBDQ). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29670566",
"endSection": "abstract",
"offsetInBeginSection": 1463,
"offsetInEndSection": 1576,
"text": "The median PD questionnaire 39-score index (PDQ39-SI) was 23.22% and the most affected dimension was \"mobility.\" "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29644334",
"endSection": "abstract",
"offsetInBeginSection": 1179,
"offsetInEndSection": 1543,
"text": "In the 43% of cases in whom oral therapy was changed, total UPDRS improved significantly (effect size = 8) as did the PDQ39 in cases reaching target. NMS Quest and MOCA scores also improved significantly. This study shows that many people in a representative cohort of PD would benefit from objective assessment and treatment of their PD features against a target."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29542093",
"endSection": "abstract",
"offsetInBeginSection": 137,
"offsetInEndSection": 551,
"text": "Here, we applied a novel diffusion-weighted imaging approach, diffusion MRI connectometry, to investigate the correlation of quality of life, evaluated by Parkinson's Disease Questionnaire (PDQ39) with the white matter structural connectivity in 27 non-demented PD patients (disease duration of 5.3 ± 2.9 years, H and Y stage = 1.5 ± 0.6, UPDRS-III = 13.7 ± 6.5, indicating unilateral and mild motor involvement). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30108543",
"endSection": "abstract",
"offsetInBeginSection": 141,
"offsetInEndSection": 690,
"text": "The present study aimed to assess the beneficial and side effects of STN DBS in Moroccan Parkinsonian patients. Material and Methods: Thirty five patients underwent bilateral STN DBS from 2008 to 2016 in the Rabat University Hospital. Patients were assessed preoperatively and followed up for 6 to 12 months using the Unified Parkinson's Disease Rating Scale in four conditions (stimulation OFF and ON and medication OFF and ON), the levodopa-equivalent daily dose (LEDD), dyskinesia and fluctuation scores and PDQ39 scale for quality of life (QOL)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28122431",
"endSection": "abstract",
"offsetInBeginSection": 1235,
"offsetInEndSection": 1552,
"text": "The total K-SCOPA-AUT score showed a positive correlation with other non-motor symptoms [the Korean version of non-motor symptom scale (K-NMSS)], activities of daily living (Unified Parkinson's Disease Rating Scale part II) and quality of life [the Korean version of Parkinson's Disease Quality of Life 39 (K-PDQ39)]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28290191",
"endSection": "abstract",
"offsetInBeginSection": 726,
"offsetInEndSection": 1147,
"text": "METHODS: Static posturography (Centre of Pressure -CoP- parameters), gait (the Ten-Meter Walk Test [TMWT]), freezing of gait (the Freezing of Gait Questionnaire [FOG-Q]), the motor portion of the Movement Disorders Society-Unified Parkinson's Disease Rating Scale (MDS-UPDRS) and patient-perceived quality of life (the 39-item Parkinson's disease Questionnaire [PDQ39]), were assessed at pre-test, post-test, and re-test."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28805568",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 647,
"text": "The use of complementary and alternative medicine (CAM) therapy in nonmotor symptoms (NMS) for Parkinson disease (PD) is growing worldwide. Well-performed, systematic evidence-based research is largely lacking in this area and many studies include various forms of CAM with small patient numbers and a lack of standardization of the approaches studied. Taichi, Qigong, dance, yoga, mindfulness, acupuncture, and other CAM therapies are reviewed and there is some evidence for the following: Taichi in sleep and PDQ39; dance in cognition, apathy, and a mild trend to improved fatigue; yoga in PDQ39; and acupuncture in depression, PDQ39, and sleep."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18543333",
"endSection": "abstract",
"offsetInBeginSection": 401,
"offsetInEndSection": 641,
"text": "One hundred thirty patients with PD completed a booklet of questionnaires, which included the PDQ39 as a disease-specific measure of QoL, a symptom checklist, a mobility checklist, as well as patient ratings of disease stage and disability."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24035927",
"endSection": "abstract",
"offsetInBeginSection": 1024,
"offsetInEndSection": 1181,
"text": "At 70% sensitivity, the specificity for PDQ39 score and PD Symptoms Questionnaire score for the prediction of parkinsonism was 73.1% and 80.1%, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24035927",
"endSection": "abstract",
"offsetInBeginSection": 601,
"offsetInEndSection": 709,
"text": "Workers completed a health status questionnaire (PDQ39) and a Parkinson disease (PD) Symptoms Questionnaire."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23346238",
"endSection": "abstract",
"offsetInBeginSection": 753,
"offsetInEndSection": 917,
"text": "As for specific questionnaires: the Parkinson`s Disease Questionnaire (PDQ-39) and the Parkinson's Disease Quality of Life Questionnaire (PDQL) have been described."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21163736",
"endSection": "abstract",
"offsetInBeginSection": 728,
"offsetInEndSection": 841,
"text": "HRQOL was assessed with the EuroQol-5D and the specific questionnaire Parkinson's Disease Questionnaire-39 items."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18543333",
"endSection": "abstract",
"offsetInBeginSection": 410,
"offsetInEndSection": 656,
"text": "One hundred thirty patients with PD completed a booklet of questionnaires , which included the PDQ39 as a disease-specific measure of QoL , a symptom checklist , a mobility checklist , as well as patient ratings of disease stage and disability . "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29542093",
"endSection": "abstract",
"offsetInBeginSection": 140,
"offsetInEndSection": 566,
"text": "Here , we applied a novel diffusion-weighted imaging approach , diffusion MRI connectometry , to investigate the correlation of quality of life , evaluated by Parkinson 's Disease Questionnaire ( PDQ39 ) with the white matter structural connectivity in 27 non-demented PD patients ( disease duration of 5.3 ± 2.9 years , H and Y stage = 1.5 ± 0.6 , UPDRS-III = 13.7 ± 6.5 , indicating unilateral and mild motor involvement) . "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17702633",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 169,
"text": "The psychometric properties of the Dutch version of the Parkinson 's disease questionnaire 39 ( PDQ39-DV ) were tested in 177 patients with Parkinson 's disease ( PD) . "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20347841",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 201,
"text": "This study explored whether reflexology could improve or sustain the wellbeing of people with Parkinosn's Disease [PD] using the PDQ39 wellbeing tool designed specifically for use with people with PD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15778909",
"endSection": "abstract",
"offsetInBeginSection": 479,
"offsetInEndSection": 741,
"text": "METHODS\nThe results of 27 patients for the Unified Parkinson's disease Rating Scale (UPDRS), Parkinson's Disease Questionnaire 39 (PDQ39) and Short Form 36 health survey questionnaire (SF36) were compared before surgery and after 12 months of bilateral STN DBS."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17702633",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "Evaluation of the Dutch version of the Parkinson's Disease Questionnaire 39."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17702633",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "The psychometric properties of the Dutch version of the Parkinson's disease questionnaire 39 (PDQ39-DV) were tested in 177 patients with Parkinson's disease (PD)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15778909",
"endSection": "abstract",
"offsetInBeginSection": 475,
"offsetInEndSection": 737,
"text": "METHODS: The results of 27 patients for the Unified Parkinson's disease Rating Scale (UPDRS), Parkinson's Disease Questionnaire 39 (PDQ39) and Short Form 36 health survey questionnaire (SF36) were compared before surgery and after 12 months of bilateral STN DBS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16258207",
"endSection": "abstract",
"offsetInBeginSection": 290,
"offsetInEndSection": 530,
"text": "Both disease-specific motor disabilities and quality of life (QOL) in the patients were evaluated using the Unified Parkinson's Disease Rating Scale (UPDRS) and the Parkinson's Disease 39 Quality of Life Questionnaire (PDQ39), respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28290191",
"endSection": "abstract",
"offsetInBeginSection": 729,
"offsetInEndSection": 1150,
"text": "METHODS: Static posturography (Centre of Pressure -CoP- parameters), gait (the Ten-Meter Walk Test [TMWT]), freezing of gait (the Freezing of Gait Questionnaire [FOG-Q]), the motor portion of the Movement Disorders Society-Unified Parkinson's Disease Rating Scale (MDS-UPDRS) and patient-perceived quality of life (the 39-item Parkinson's disease Questionnaire [PDQ39]), were assessed at pre-test, post-test, and re-test."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15778909",
"endSection": "abstract",
"offsetInBeginSection": 477,
"offsetInEndSection": 739,
"text": "METHODS: The results of 27 patients for the Unified Parkinson's disease Rating Scale (UPDRS), Parkinson's Disease Questionnaire 39 (PDQ39) and Short Form 36 health survey questionnaire (SF36) were compared before surgery and after 12 months of bilateral STN DBS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30363378",
"endSection": "abstract",
"offsetInBeginSection": 431,
"offsetInEndSection": 815,
"text": "Methods: A pilot study was conducted in which laptops were distributed to 50 patients for 1 year to see whether such a service was feasible (in terms of patient participation and compliance) and whether this intervention affected the patient's condition, measured in UPDRS, Mini-Mental Status Examination (MMSE), 39-item Parkinson's Disease Questionnaire (PDQ39), and H & Y Scale."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23323136",
"endSection": "abstract",
"offsetInBeginSection": 522,
"offsetInEndSection": 843,
"text": "They were assessed using the K-NMSS, the Unified Parkinson's Disease Rating Scale (UPDRS), the Korean version of the Mini-Mental Status Examination (K-MMSE), the Korean version of the Montgomery-Asberg Depression Rating Scale (K-MADS), the Epworth Sleepiness Scale (ESS), and Parkinson's Disease Questionnaire 39 (PDQ39)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28770096",
"endSection": "abstract",
"offsetInBeginSection": 780,
"offsetInEndSection": 1003,
"text": "Patients were also evaluated by using the Parkinson Disease Questionnaire -39 (PDQ39), the Unified Parkinson's Disease Rating Scale (UPDRS), the Mini Mental State Examination (MMSE) and the Frontal Assessment Battery (FAB)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16763974",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 259,
"text": "We investigated the impact of subthalamic nucleus (STN) deep brain stimulation (DBS) on quality of life (QOL) in patients with advanced Parkinson's disease, as self-assessed before and after surgery by completing the Parkinson's Disease Questionnaire (PDQ39)."
}
] | 11 |
BioASQ-training11b
| null | null |
5e2b1ed9fbd6abf43b000005
|
bioasq_factoid
|
yesno
|
Can oleuropein aglycone interfere with amyloid aggregation?
|
['yes']
|
[
"yes"
] |
['Yes, oleuropein aglycone interferes in vitro and in vivo with amyloid aggregates.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29571746"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29571746",
"endSection": "abstract",
"offsetInBeginSection": 285,
"offsetInEndSection": 684,
"text": "Oleuropein, a phenolic secoiroid glycoside, is the main polyphenol in the olive oil. It has been reported that the aglycone form of Oleuropein (OleA) interferes in vitro and in vivo with amyloid aggregation of a number of proteins/peptides involved in amyloid, particularly neurodegenerative, diseases avoiding the growth of toxic oligomers and displaying protection against cognitive deterioration."
}
] | 11 |
BioASQ-training11b
| null | null |
5c890c3375a4a5d21900000e
|
bioasq_yesno
|
yesno
|
Is the Miller-Fisher syndrome considered to be a variant of Guillain-Barré?
|
['yes']
|
[
"yes"
] |
['Miller-Fisher syndrome is a variant of Guillain-Barré syndrome, characterized by the classic triad of ophthalmoplegia, ataxia, and areflexia.', 'Miller Fisher syndrome is a variant of Guillain-Barre syndrome characterized by the classic triad of ophthalmoplegia, ataxia, and areflexia', 'Miller Fisher syndrome is a variant of Guillain-Barre syndrome characterized by the classic triad of ophthalmoplegia, ataxia, and areflexia', 'Miller Fisher syndrome is a variant of Guillain-Barre syndrome characterized by the classic triad of ophthalmoplegia, ataxia, and areflexia', 'Miller Fisher syndrome is a variant of Guillain-Barre syndrome characterized by the classic triad of ophthalmoplegia, ataxia, and areflexia', 'Miller Fisher syndrome is a variant of Guillain-Barre syndrome characterized by the classic triad of ophthalmoplegia, ataxia, and areflexia']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26380131",
"http://www.ncbi.nlm.nih.gov/pubmed/26366317",
"http://www.ncbi.nlm.nih.gov/pubmed/24513384",
"http://www.ncbi.nlm.nih.gov/pubmed/25072194",
"http://www.ncbi.nlm.nih.gov/pubmed/9703176",
"http://www.ncbi.nlm.nih.gov/pubmed/16645971",
"http://www.ncbi.nlm.nih.gov/pubmed/16155441",
"http://www.ncbi.nlm.nih.gov/pubmed/21325125",
"http://www.ncbi.nlm.nih.gov/pubmed/19810856",
"http://www.ncbi.nlm.nih.gov/pubmed/10511801",
"http://www.ncbi.nlm.nih.gov/pubmed/22447677",
"http://www.ncbi.nlm.nih.gov/pubmed/15909003",
"http://www.ncbi.nlm.nih.gov/pubmed/16049921",
"http://www.ncbi.nlm.nih.gov/pubmed/11155543",
"http://www.ncbi.nlm.nih.gov/pubmed/18428104",
"http://www.ncbi.nlm.nih.gov/pubmed/3612209",
"http://www.ncbi.nlm.nih.gov/pubmed/15012892",
"http://www.ncbi.nlm.nih.gov/pubmed/10965158",
"http://www.ncbi.nlm.nih.gov/pubmed/1667714",
"http://www.ncbi.nlm.nih.gov/pubmed/19374296",
"http://www.ncbi.nlm.nih.gov/pubmed/8437011",
"http://www.ncbi.nlm.nih.gov/pubmed/11521055",
"http://www.ncbi.nlm.nih.gov/pubmed/19263690"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26380131",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 139,
"text": "Miller Fisher syndrome is a variant of Guillain-Barre syndrome characterized by the classic triad of ophthalmoplegia, ataxia, and areflexia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26366317",
"endSection": "abstract",
"offsetInBeginSection": 346,
"offsetInEndSection": 496,
"text": "We are reporting a rare case of Miller-Fisher (MFS) variant of Guillain-Barré syndrome (GBS) as the first manifestation of SLE in a 41-year-old female"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24513384",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 204,
"text": "Miller-Fisher syndrome is defined as ophthalmoplegia, ataxia and areflexia. Considered as a variant of Guillain-Barré syndrome, it differs in its clinical presentation and by anti-GQ1b antibody positivity"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25072194",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "Guillain-Barré syndrome (GBS) and its variant, Miller Fisher syndrome (MFS), exist as several clinical subtypes with different neurological features and presentations"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16049921",
"endSection": "abstract",
"offsetInBeginSection": 608,
"offsetInEndSection": 945,
"text": "Using in vitro and in vivo models of the Guillain-Barré syndrome variant, Miller Fisher syndrome, we have shown previously that anti-GQ1b ganglioside antibodies target the presynaptic motor nerve terminal axon and surrounding perisynaptic Schwann cells, thereby mediating destructive injury through deposition of membrane attack complex."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19810856",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Miller Fisher syndrome is a variant of Guillain-Barré syndrome, characterized by ophthalmoplegia, ataxia and areflexia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16155441",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Miller Fisher syndrome is a localized variant of Guillain-Barré syndrome, characterized by ophthalmoplegia, areflexia and ataxia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10511801",
"endSection": "abstract",
"offsetInBeginSection": 346,
"offsetInEndSection": 460,
"text": "Miller Fisher syndrome, a variant of Guillain-Barré syndrome, is associated with IgG antibody to GQ1b ganglioside."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22447677",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "Miller Fisher syndrome (MFS), a variant of Guillain-Barré syndrome, is a rare disorder typically characterized by a triad of ataxia, areflexia, and ophthalmoplegia, which may have a highly variable clinical presentation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21325125",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 222,
"text": "Miller Fisher syndrome is an acute inflammatory polyradiculoneuropathy that is generally considered a variant of Guillain-Barré syndrome and is characterized by the clinical triad of ataxia, areflexia, and ophthalmoplegia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16645971",
"endSection": "abstract",
"offsetInBeginSection": 362,
"offsetInEndSection": 548,
"text": "The objective of this study was to review the occurrence and clinical features of Guillain-Barré syndrome and its variant, the Miller Fisher syndrome, during TNFalpha antagonist therapy."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22447677",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Miller Fisher variant of Guillain-Barré syndrome masquerading as acute sphenoid sinusitis with orbital apex syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11155543",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 314,
"text": "Controversy exists concerning whether Miller Fisher syndrome (MFS) is the result of a predominantly axonal or demyelinating polyneuropathy and whether the Guillain-Barré syndrome variant of acute ataxia and areflexia without ophthalmoplegia, ataxic Guillain-Barré syndrome (atxGBS), has a distinct pathophysiology."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16049921",
"endSection": "abstract",
"offsetInBeginSection": 608,
"offsetInEndSection": 945,
"text": "Using in vitro and in vivo models of the Guillain-Barré syndrome variant, Miller Fisher syndrome, we have shown previously that anti-GQ1b ganglioside antibodies target the presynaptic motor nerve terminal axon and surrounding perisynaptic Schwann cells, thereby mediating destructive injury through deposition of membrane attack complex."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19810856",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "Miller Fisher syndrome is a variant of Guillain-Barré syndrome, characterized by ophthalmoplegia, ataxia and areflexia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16155441",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Miller Fisher syndrome is a localized variant of Guillain-Barré syndrome, characterized by ophthalmoplegia, areflexia and ataxia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10511801",
"endSection": "abstract",
"offsetInBeginSection": 346,
"offsetInEndSection": 460,
"text": "Miller Fisher syndrome, a variant of Guillain-Barré syndrome, is associated with IgG antibody to GQ1b ganglioside."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22447677",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "Miller Fisher syndrome (MFS), a variant of Guillain-Barré syndrome, is a rare disorder typically characterized by a triad of ataxia, areflexia, and ophthalmoplegia, which may have a highly variable clinical presentation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21325125",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 222,
"text": "Miller Fisher syndrome is an acute inflammatory polyradiculoneuropathy that is generally considered a variant of Guillain-Barré syndrome and is characterized by the clinical triad of ataxia, areflexia, and ophthalmoplegia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18428104",
"endSection": "abstract",
"offsetInBeginSection": 265,
"offsetInEndSection": 485,
"text": "Miller Fisher syndrome is characterised by the triad ophthalmoparesis, ataxia and areflexia and is considered to be a variant of Guillain-Barré syndrome; its differential diagnosis includes Wernicke's encephalopathy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21325125",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 221,
"text": "Miller Fisher syndrome is an acute inflammatory polyradiculoneuropathy that is generally considered a variant of Guillain-Barré syndrome and is characterized by the clinical triad of ataxia, areflexia, and ophthalmoplegia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15909003",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "Miller-Fisher syndrome is characterised by the clinical triad of ophthalmoplegia, ataxia and areflexia and is considered a variant form of Guillain-Barré syndrome"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3612209",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 203,
"text": "The syndrome of ataxia, areflexia and ophthalmoplegia, or Miller-Fisher syndrome, has been considered to be a variant of Guillain-Barré syndrome with pathology restricted to the peripheral nervous system"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15012892",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 183,
"text": "Miller-Fisher syndrome (MFS) is considered the most common variant of Guillain-Barré syndrome (GBS) and is characterized by the clinical triad of ophthalmoplegia, ataxia and areflexia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10965158",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Miller Fisher syndrome (MFS), characterized as ataxia, areflexia and ophthalmoplegia, is generally considered as a variant of Guillain-Barré syndrome (GBS)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1667714",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 174,
"text": "Miller Fisher Syndrome (MFS), which is characterized by ophthalmoplegia, ataxia and tendon areflexia, is generally considered as a clinical variant of Guillain-Barré Syndrome"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19374296",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "Miller-Fisher syndrome (MFS), a variant of Guillain-Barré syndrome (GBS) is a self-limiting demyelinating disease of the peripheral nervous system"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15909003",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "BACKGROUND: Miller-Fisher syndrome is characterised by the clinical triad of ophthalmoplegia, ataxia and areflexia and is considered a variant form of Guillain-Barré syndrome. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15012892",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 211,
"text": "BACKGROUND AND OBJECTIVE: Miller-Fisher syndrome (MFS) is considered the most common variant of Guillain-Barré syndrome (GBS) and is characterized by the clinical triad of ophthalmoplegia, ataxia and areflexia. "
},
{
"beginSection": "abstract",
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"endSection": "abstract",
"offsetInBeginSection": 274,
"offsetInEndSection": 491,
"text": "Miller Fisher syndrome is characterised by the triad ophthalmoparesis, ataxia and areflexia and is considered to be a variant of Guillain-Barré syndrome; its differential diagnosis includes Wernicke's encephalopathy. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22447677",
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"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Miller Fisher variant of Guillain-Barré syndrome masquerading as acute sphenoid sinusitis with orbital apex syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15909003",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "BACKGROUND: Miller-Fisher syndrome is characterised by the clinical triad of ophthalmoplegia, ataxia and areflexia and is considered a variant form of Guillain-Barré syndrome. "
},
{
"beginSection": "abstract",
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"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 211,
"text": "BACKGROUND AND OBJECTIVE: Miller-Fisher syndrome (MFS) is considered the most common variant of Guillain-Barré syndrome (GBS) and is characterized by the clinical triad of ophthalmoplegia, ataxia and areflexia. "
},
{
"beginSection": "abstract",
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"endSection": "abstract",
"offsetInBeginSection": 274,
"offsetInEndSection": 491,
"text": "Miller Fisher syndrome is characterised by the triad ophthalmoparesis, ataxia and areflexia and is considered to be a variant of Guillain-Barré syndrome; its differential diagnosis includes Wernicke's encephalopathy. "
},
{
"beginSection": "title",
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"offsetInEndSection": 117,
"text": "Miller Fisher variant of Guillain-Barré syndrome masquerading as acute sphenoid sinusitis with orbital apex syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15909003",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "BACKGROUND: Miller-Fisher syndrome is characterised by the clinical triad of ophthalmoplegia, ataxia and areflexia and is considered a variant form of Guillain-Barré syndrome. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15012892",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 211,
"text": "BACKGROUND AND OBJECTIVE: Miller-Fisher syndrome (MFS) is considered the most common variant of Guillain-Barré syndrome (GBS) and is characterized by the clinical triad of ophthalmoplegia, ataxia and areflexia. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18428104",
"endSection": "abstract",
"offsetInBeginSection": 274,
"offsetInEndSection": 491,
"text": "Miller Fisher syndrome is characterised by the triad ophthalmoparesis, ataxia and areflexia and is considered to be a variant of Guillain-Barré syndrome; its differential diagnosis includes Wernicke's encephalopathy. "
},
{
"beginSection": "title",
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"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Miller Fisher variant of Guillain-Barré syndrome masquerading as acute sphenoid sinusitis with orbital apex syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15909003",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "BACKGROUND: Miller-Fisher syndrome is characterised by the clinical triad of ophthalmoplegia, ataxia and areflexia and is considered a variant form of Guillain-Barré syndrome. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15012892",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 211,
"text": "BACKGROUND AND OBJECTIVE: Miller-Fisher syndrome (MFS) is considered the most common variant of Guillain-Barré syndrome (GBS) and is characterized by the clinical triad of ophthalmoplegia, ataxia and areflexia. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22447677",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Miller Fisher variant of Guillain-Barré syndrome masquerading as acute sphenoid sinusitis with orbital apex syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15909003",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "BACKGROUND: Miller-Fisher syndrome is characterised by the clinical triad of ophthalmoplegia, ataxia and areflexia and is considered a variant form of Guillain-Barré syndrome. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18428104",
"endSection": "abstract",
"offsetInBeginSection": 274,
"offsetInEndSection": 491,
"text": "Miller Fisher syndrome is characterised by the triad ophthalmoparesis, ataxia and areflexia and is considered to be a variant of Guillain-Barré syndrome; its differential diagnosis includes Wernicke's encephalopathy. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22447677",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Miller Fisher variant of Guillain-Barré syndrome masquerading as acute sphenoid sinusitis with orbital apex syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8437011",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "A recent report described serum anti-GQ1b ganglioside antibodies in Miller Fisher syndrome (MFS), a clinical variant of Guillain-Barré syndrome (GBS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8437011",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "A recent report described serum anti-GQ1b ganglioside antibodies in Miller Fisher syndrome (MFS), a clinical variant of Guillain-Barré syndrome (GBS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3612209",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 204,
"text": "The syndrome of ataxia, areflexia and ophthalmoplegia, or Miller-Fisher syndrome, has been considered to be a variant of Guillain-Barré syndrome with pathology restricted to the peripheral nervous system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11521055",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 279,
"text": "Guillain-Barré syndrome (GBS), an acute inflammatory polyneuropathy, is preceded in most cases by an infectious illness, and Campylobacter jejuni, a leading cause of acute gastroenteritis, is the most common antecedent to GBS and its ocular variant, Miller Fisher syndrome (MFS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15909003",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "Miller-Fisher syndrome is characterised by the clinical triad of ophthalmoplegia, ataxia and areflexia and is considered a variant form of Guillain-Barré syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15909003",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "Miller-Fisher syndrome is characterised by the clinical triad of ophthalmoplegia, ataxia and areflexia and is considered a variant form of Guillain-Barré syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3612209",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 357,
"text": " The syndrome of ataxia, areflexia and ophthalmoplegia, or Miller-Fisher syndrome, has been considered to be a variant of Guillain-Barré syndrome with pathology restricted to the peripheral nervous system. A patient with Miller-Fisher syndrome and bilateral demyelinating optic neuropathy suggesting associated central nervous system pathology is presented."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21325125",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 191,
"text": "Miller Fisher syndrome is an acute inflammatory polyradiculoneuropathy that is generally considered a variant of Guillain-Barré syndrome and is characterized by the clinical triad of ataxia,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19263690",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": " Miller Fisher syndrome is an uncommon disease and it is a variant of Guillain-Barre syndrome. Miller Fisher syndrome also has rarer variants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18428104",
"endSection": "abstract",
"offsetInBeginSection": 261,
"offsetInEndSection": 477,
"text": "Miller Fisher syndrome is characterised by the triad ophthalmoparesis, ataxia and areflexia and is considered to be a variant of Guillain-Barré syndrome; its differential diagnosis includes Wernicke's encephalopathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15909003",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "Miller-Fisher syndrome is characterised by the clinical triad of ophthalmoplegia, ataxia and areflexia and is considered a variant form of Guillain-Barré syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21325125",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 223,
"text": "Miller Fisher syndrome is an acute inflammatory polyradiculoneuropathy that is generally considered a variant of Guillain-Barré syndrome and is characterized by the clinical triad of ataxia, areflexia, and ophthalmoplegia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9703176",
"endSection": "abstract",
"offsetInBeginSection": 636,
"offsetInEndSection": 737,
"text": "Data were separately analysed for Miller Fisher syndrome and other Guillain-Barré syndrome variants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9703176",
"endSection": "abstract",
"offsetInBeginSection": 1099,
"offsetInEndSection": 1208,
"text": "Guillain-Barré syndrome variants alone (excluding Miller Fisher syndrome) accounted for 10.5% of total cases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15909003",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "Miller-Fisher syndrome is characterised by the clinical triad of ophthalmoplegia, ataxia and areflexia and is considered a variant form of Guillain-Barré syndrome."
},
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"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21325125",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 223,
"text": "Miller Fisher syndrome is an acute inflammatory polyradiculoneuropathy that is generally considered a variant of Guillain-Barré syndrome and is characterized by the clinical triad of ataxia, areflexia, and ophthalmoplegia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9703176",
"endSection": "abstract",
"offsetInBeginSection": 636,
"offsetInEndSection": 737,
"text": "Data were separately analysed for Miller Fisher syndrome and other Guillain-Barré syndrome variants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9703176",
"endSection": "abstract",
"offsetInBeginSection": 1099,
"offsetInEndSection": 1208,
"text": "Guillain-Barré syndrome variants alone (excluding Miller Fisher syndrome) accounted for 10.5% of total cases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15909003",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "Miller-Fisher syndrome is characterised by the clinical triad of ophthalmoplegia, ataxia and areflexia and is considered a variant form of Guillain-Barré syndrome."
},
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"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21325125",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 223,
"text": "Miller Fisher syndrome is an acute inflammatory polyradiculoneuropathy that is generally considered a variant of Guillain-Barré syndrome and is characterized by the clinical triad of ataxia, areflexia, and ophthalmoplegia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9703176",
"endSection": "abstract",
"offsetInBeginSection": 636,
"offsetInEndSection": 737,
"text": "Data were separately analysed for Miller Fisher syndrome and other Guillain-Barré syndrome variants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9703176",
"endSection": "abstract",
"offsetInBeginSection": 1099,
"offsetInEndSection": 1208,
"text": "Guillain-Barré syndrome variants alone (excluding Miller Fisher syndrome) accounted for 10.5% of total cases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15909003",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "Miller-Fisher syndrome is characterised by the clinical triad of ophthalmoplegia, ataxia and areflexia and is considered a variant form of Guillain-Barré syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3612209",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 205,
"text": "The syndrome of ataxia, areflexia and ophthalmoplegia, or Miller-Fisher syndrome, has been considered to be a variant of Guillain-Barré syndrome with pathology restricted to the peripheral nervous system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21325125",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 223,
"text": "Miller Fisher syndrome is an acute inflammatory polyradiculoneuropathy that is generally considered a variant of Guillain-Barré syndrome and is characterized by the clinical triad of ataxia, areflexia, and ophthalmoplegia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18428104",
"endSection": "abstract",
"offsetInBeginSection": 261,
"offsetInEndSection": 477,
"text": "Miller Fisher syndrome is characterised by the triad ophthalmoparesis, ataxia and areflexia and is considered to be a variant of Guillain-Barré syndrome; its differential diagnosis includes Wernicke's encephalopathy."
}
] | 5 |
BioASQ-training5b
|
[] |
[] |
571f59cd0fd6f91b68000008
|
bioasq_yesno
|
factoid
|
Against which protein is the antibody used for immonostaining of Lewy bodies raised?
|
['alpha-Synuclein']
|
[
"alpha-Synuclein",
"SNCA",
"non-A-beta component of Alzheimer's disease amyloid",
"NACP",
"synuclein alpha",
"alpha-synuclein protein",
"alpha-synuclein precursor",
"Parkinsonism associated protein"
] |
alpha-Synuclein is a presynaptic protein, which was identified as a specific component of Lewy bodies (LB) and Lewy neurites. Therefore, immunostaining for detecting the presence of Lewy bodies is carried out using antibodies against alpha-synuclein.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22370907",
"http://www.ncbi.nlm.nih.gov/pubmed/19272424",
"http://www.ncbi.nlm.nih.gov/pubmed/16691119",
"http://www.ncbi.nlm.nih.gov/pubmed/15854770",
"http://www.ncbi.nlm.nih.gov/pubmed/12722831",
"http://www.ncbi.nlm.nih.gov/pubmed/12536227",
"http://www.ncbi.nlm.nih.gov/pubmed/11207422",
"http://www.ncbi.nlm.nih.gov/pubmed/11005264",
"http://www.ncbi.nlm.nih.gov/pubmed/10967182",
"http://www.ncbi.nlm.nih.gov/pubmed/10867800",
"http://www.ncbi.nlm.nih.gov/pubmed/10822429",
"http://www.ncbi.nlm.nih.gov/pubmed/10787032",
"http://www.ncbi.nlm.nih.gov/pubmed/9759660",
"http://www.ncbi.nlm.nih.gov/pubmed/9600226"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22370907",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "α-Synuclein is the major protein associated with Lewy body dementia, Parkinson's disease and multiple system atrophy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22370907",
"endSection": "abstract",
"offsetInBeginSection": 310,
"offsetInEndSection": 518,
"text": "With the aim to develop antibodies showing high specificity and sensitivity for disease-associated α-synuclein, synthetic peptides containing different amino acid sequences were used for immunization of mice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19272424",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 387,
"text": "Parkinson's disease and dementia with Lewy bodies are very frequent neurological disorders of the elderly. Mutations in the alpha-synuclein (alphaSYN) gene cause Parkinson's disease, often associated with dementia. Neuropathologically these diseases are characterized by the presence of Lewy bodies and Lewy neurites, intraneuronal inclusions mostly composed of alphaSYN protein fibrils."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16691119",
"endSection": "abstract",
"offsetInBeginSection": 594,
"offsetInEndSection": 677,
"text": "Immunohistochemistry for alpha-synuclein revealed LBs in 31 of 290 PSP cases (11%)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15854770",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 294,
"text": "We immunohistochemically investigated the degeneration processes of the nigro-striatal and nigro-amygdaloid pathways and the relationship between the loss of dopaminergic neurons and Lewy bodies (LB) formation in the substantia nigra using 15 autopsied cases of dementia with Lewy bodies (DLB)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15854770",
"endSection": "abstract",
"offsetInBeginSection": 459,
"offsetInEndSection": 650,
"text": "The substantia nigra possessed alpha-synuclein-positive LB-bearing neurons that were almost evenly distributed, while the putamen exhibited diffuse or granular alpha-synuclein-immunostaining."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12722831",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "The major protein constituent of Lewy bodies (LBs), the pathological hallmark of Parkinson disease and dementia with Lewy bodies, is considered to be alpha-synuclein,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12536227",
"endSection": "abstract",
"offsetInBeginSection": 167,
"offsetInEndSection": 251,
"text": "Recently, alpha-synuclein (alphaS) has been found to be a central constituent of LB."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11207422",
"endSection": "abstract",
"offsetInBeginSection": 456,
"offsetInEndSection": 824,
"text": "By having the antibody AFshp raised specifically to alpha-synuclein to label Parkinson disease-specific Lewy bodies and Lewy neurites as well as synaptic boutons containing the unaltered protein, an initial attempt is made to map the overall distribution pattern and describe the staining behavior of the immunoreactive punctae in select regions of the prosencephalon."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11005264",
"endSection": "abstract",
"offsetInBeginSection": 680,
"offsetInEndSection": 880,
"text": "Notably, carboxy-terminal alpha-syn epitopes were immunodominant in GCIs, but the entire panel of antibodies immunostained cortical Lewy bodies (LBs) in dementia with LBs brain with similar intensity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10967182",
"endSection": "abstract",
"offsetInBeginSection": 994,
"offsetInEndSection": 1165,
"text": "Discrete immunostaining was demonstrated in NFTs and neuropil threads with various antibodies against phosphorylated tau, and in LBs with antibody against alpha-synuclein."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10867800",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 223,
"text": "The identification of the alpha-synuclein gene on chromosome 4q as a locus for familial Lewy-body parkinsonism and of alpha-synuclein as a component of Lewy bodies has heralded a new era in the study of Parkinson's disease."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10822429",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "Alpha-synuclein cortical Lewy bodies correlate with dementia in Parkinson's disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10822429",
"endSection": "abstract",
"offsetInBeginSection": 358,
"offsetInEndSection": 524,
"text": "recent advances in immunostaining of alpha-synuclein have suggested the possible importance of cortical Lewy bodies (CLBs) in the brains of demented patients with PD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10822429",
"endSection": "abstract",
"offsetInBeginSection": 1012,
"offsetInEndSection": 1133,
"text": "CLBs positive for alpha-synuclein are highly sensitive (91%) and specific (90%) neuropathologic markers of dementia in PD"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10822429",
"endSection": "abstract",
"offsetInBeginSection": 1314,
"offsetInEndSection": 1433,
"text": "CLBs detected by alpha-synuclein antibodies in patients with PD are a more sensitive and specific correlate of dementia"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10787032",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 61,
"text": "alpha-Synuclein immunoreactivity in dementia with Lewy bodies"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10787032",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "alpha-Synuclein is a presynaptic protein recently identified as a specific component of Lewy bodies (LB) and Lewy neurites."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10787032",
"endSection": "abstract",
"offsetInBeginSection": 609,
"offsetInEndSection": 738,
"text": "alpha-Synuclein immunostaining was more specific than ubiquitin immunostaining in that it differentiated LB from globose tangles."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9759660",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 325,
"text": "The precursor of the non-Abeta component of Alzheimer's disease amyloid (NACP) (also known as alpha-synuclein) is a presynaptic terminal molecule that abnormally accumulates in the plaques of Alzheimer's disease (AD) and in the Lewy bodies (LBs) of Lewy body variant of AD, diffuse Lewy body disease, and Parkinson's disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9759660",
"endSection": "abstract",
"offsetInBeginSection": 326,
"offsetInEndSection": 725,
"text": "To better understand the distribution of NACP/alpha-synuclein and its fragments in the LB-bearing neurons and neurites, as well as to clarify the patterns of NACP/alpha-synuclein compartmentalization, we studied NACP/alpha-synuclein immunoreactivity using antibodies against the C-terminal, N-terminal, and NAC regions after Proteinase K and formic acid treatment in the cortex of patients with LBs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9759660",
"endSection": "abstract",
"offsetInBeginSection": 1656,
"offsetInEndSection": 1872,
"text": "Ultrastructural analysis revealed that NACP/alpha-synuclein immunoreactivity was diffusely distributed within the amorphous electrodense material in the LBs and as small clusters in the filaments of LBs and neurites."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9759660",
"endSection": "abstract",
"offsetInBeginSection": 1873,
"offsetInEndSection": 2023,
"text": "These results support the view that aggregated NACP/alpha-synuclein might play an important role in the pathogenesis of disorders associated with LBs."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9600226",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "Nigral and cortical Lewy bodies and dystrophic nigral neurites in Parkinson's disease and cortical Lewy body disease contain alpha-synuclein immunoreactivity"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9600226",
"endSection": "abstract",
"offsetInBeginSection": 341,
"offsetInEndSection": 453,
"text": "PD brain demonstrated alpha-synuclein immunoreactivity in nigral Lewy bodies, pale bodies and abnormal neurites."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9600226",
"endSection": "abstract",
"offsetInBeginSection": 526,
"offsetInEndSection": 651,
"text": "DLB cases demonstrated these findings as well as alpha-synuclein immunoreactivity in cortical Lewy bodies and CA2-3 neurites."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9600226",
"endSection": "abstract",
"offsetInBeginSection": 652,
"offsetInEndSection": 833,
"text": "These results suggest that, even in sporadic cases, there is an early and direct role for alpha-synuclein in the pathogenesis of PD and the neuropathologically related disorder DLB."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D016631",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D010300",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D020961",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D000906",
"http://www.disease-ontology.org/api/metadata/DOID:12217",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0003823",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D051844",
"http://www.uniprot.org/uniprot/SYUA_SERCA"
] |
[] |
53189656b166e2b80600001c
|
bioasq_factoid
|
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
|
bioasq_yesno
|
factoid
|
What is another name for the plant Sideritis scardica?
|
['Mountain tea', 'Ironwort']
|
[
"Mountain tea",
"Ironwort",
"Sideritis",
"Sideritis scardica",
"Greek mountain tea",
"Shepherd's tea",
"Tea of the shepherds"
] |
['Sideritis scardica is also known as ironwort or mountain tea.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22274814"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22274814",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 221,
"text": "Sideritis scardica Griseb. (ironwort, mountain tea), an endemic plant of the Balkan Peninsula, has been used in traditional medicine in the treatment of gastrointestinal complaints, inflammation, and rheumatic disorders. "
}
] | 11 |
BioASQ-training11b
| null | null |
5c890e6d75a4a5d21900000f
|
bioasq_factoid
|
factoid
|
What is the cause of the Diamond Blackfan Anemia?
|
['Diamond Blackfan Anemia (DBA) is a congenital bone marrow failure syndrome associated with ribosomal gene mutations that lead to ribosomal insufficiency.']
|
[
"Diamond Blackfan Anemia",
"DBA",
"Diamond-Blackfan anemia",
"Diamond-Blackfan syndrome",
"Diamond-Blackfan disorder"
] |
['Diamond Blackfan Anemia (DBA) is a congenital bone marrow failure syndrome associated with ribosomal gene mutations that lead to ribosomal insufficiency.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/32643123",
"http://www.ncbi.nlm.nih.gov/pubmed/32630050",
"http://www.ncbi.nlm.nih.gov/pubmed/32620751"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32620751",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "Diamond Blackfan Anemia (DBA) is a congenital bone marrow failure syndrome associated with ribosomal gene mutations that lead to ribosomal insufficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32643123",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 284,
"text": "Diamond-Blackfan anemia is an autosomal dominant syndrome, characterized by anemia and a predisposition for malignancies. Ribosomal proteins are responsible for this syndrome, and the incidence of colorectal cancer in patients with this syndrome is higher than the general population."
}
] | 11 |
BioASQ-training11b
| null | null |
622d17b83a8413c6530000a2
|
bioasq_factoid
|
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