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4.35k
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24
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|---|---|---|---|---|---|---|---|---|---|---|---|---|
factoid
|
How is the STING protein activated?
|
['By intracellular DNA']
|
[
"intracellular DNA",
"DNA within cells",
"cellular DNA",
"DNA in cells",
"By intracellular DNA"
] |
['During DNA virus infections, detection of cytosolic DNA by the cGAS-STING pathway leads to activation of IFN-β.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/31928996",
"http://www.ncbi.nlm.nih.gov/pubmed/31820985",
"http://www.ncbi.nlm.nih.gov/pubmed/31896590",
"http://www.ncbi.nlm.nih.gov/pubmed/31980485",
"http://www.ncbi.nlm.nih.gov/pubmed/31991682"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31820985",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 341,
"text": "Stimulator of interferon genes (STING) is an endoplasmic reticulum-localized adaptor protein (STING receptor) that has been shown to be activated by binding to natural cyclic dinucleotide (CDN) ligands and plays a vital role in innate immune sensing of exogenous or endogenous DNA, which then induces type I interferons and other cytokines. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31928996",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "During DNA virus infections, detection of cytosolic DNA by the cGAS-STING pathway leads to activation of IFN-β. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31896590",
"endSection": "abstract",
"offsetInBeginSection": 255,
"offsetInEndSection": 373,
"text": "Herpes simplex virus 1 (HSV-1) triggers both the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31980485",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Detection of intracellular DNA by the cGAS-STING pathway activates a type I interferon-mediated innate immune response that protects from virus infection. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31991682",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "Several DNA viruses have evolved antagonists to inhibit the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) DNA-sensing immune pathway."
}
] | 11 |
BioASQ-training11b
| null | null |
60490c421cb411341a000166
|
bioasq_factoid
|
factoid
|
On what chromosome would the MKKS gene for McKusick-Kaufman(AKA Kaufman-McKusick) syndrome be found?
|
['20', '20p12', 'mkks or bbs6 gene on chromosome 20p12', '20p12 between D20S162 and D20S894 markers']
|
[
"20",
"20p12",
"mkks",
"bbs6 gene",
"mkks or bbs6 gene on chromosome 20p12",
"20p12 between D20S162 and D20S894 markers"
] |
['The MKKS gene is mapped to chromosome 20']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/10973238",
"http://www.ncbi.nlm.nih.gov/pubmed/22090721",
"http://www.ncbi.nlm.nih.gov/pubmed/15266619",
"http://www.ncbi.nlm.nih.gov/pubmed/10802661"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22090721",
"endSection": "abstract",
"offsetInBeginSection": 235,
"offsetInEndSection": 353,
"text": "The syndrome is caused by mutations in the MKKS gene mapped onto chromosome 20p12 between D20S162 and D20S894 markers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15266619",
"endSection": "abstract",
"offsetInBeginSection": 869,
"offsetInEndSection": 1046,
"text": " Both MKS and BBS can be caused by mutations in the MKKS or BBS6 gene on chromosome 20p12 and BBS is also associated with mutations in other genes (BBS1, BBS2, BBS4, and BBS7). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15266619",
"endSection": "abstract",
"offsetInBeginSection": 870,
"offsetInEndSection": 1045,
"text": "Both MKS and BBS can be caused by mutations in the MKKS or BBS6 gene on chromosome 20p12 and BBS is also associated with mutations in other genes (BBS1, BBS2, BBS4, and BBS7)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15266619",
"endSection": "abstract",
"offsetInBeginSection": 887,
"offsetInEndSection": 1064,
"text": "can be caused by mutations in the MKKS or BBS6 gene on chromosome 20p12 and BBS is also associated with mutations in other genes (BBS1, BBS2, BBS4, and BBS7). To address this he"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22090721",
"endSection": "abstract",
"offsetInBeginSection": 244,
"offsetInEndSection": 361,
"text": "ome is caused by mutations in the MKKS gene mapped onto chromosome 20p12 between D20S162 and D20S894 markers. Mutatio"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10973238",
"endSection": "abstract",
"offsetInBeginSection": 1803,
"offsetInEndSection": 1909,
"text": "Genotyping with markers from the MKKS region confirmed homozygosity at 20p12 in both affected individuals."
}
] | 11 |
BioASQ-training11b
| null | null |
601eb56c1cb411341a000058
|
bioasq_factoid
|
factoid
|
What is detected by the UV-damaged DNA-binding protein (UV-DDB) complex?
|
['UV-DDB associates tightly with chromatin and is involved in global genomic nucleotide excision repair (NER)']
|
[
"UV-DDB",
"UV-DDB complex",
"UV-damaged DNA-binding protein",
"DNA repair protein UV-DDB",
"UV-DDB protein",
"UV-DDB heterodimer"
] |
['Upon UV irradiation of primate cells, UV-DDB associates tightly with chromatin and is involved in global genomic nucleotide excision repair (NER) in mammalian cells.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/12034848",
"http://www.ncbi.nlm.nih.gov/pubmed/12812979",
"http://www.ncbi.nlm.nih.gov/pubmed/16473935"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16473935",
"endSection": "abstract",
"offsetInBeginSection": 213,
"offsetInEndSection": 308,
"text": "UV-damaged DNA-binding protein complex (UV-DDB), involved in the damage recognition step of NER"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12034848",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "The UV-damaged DNA binding protein complex (UV-DDB) is implicated in global genomic nucleotide excision repair (NER) in mammalian cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12034848",
"endSection": "abstract",
"offsetInBeginSection": 316,
"offsetInEndSection": 394,
"text": "Upon UV irradiation of primate cells, UV-DDB associates tightly with chromatin"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12812979",
"endSection": "abstract",
"offsetInBeginSection": 357,
"offsetInEndSection": 516,
"text": " The cells of some XP-E patients are deficient in a protein complex (consisting of two subunits: p127/DDBI and p48/DDB2) which binds to UV-damaged DNA (UV-DDB)"
}
] | 11 |
BioASQ-training11b
| null | null |
5e46da9c3f5415952900000a
|
bioasq_factoid
|
factoid
|
What is measured with the Proseek panels?
|
['Differnet Proseek multiplex protein biomarker panels exists: CVD, inflammatory, neurology and oncology biomarker.']
|
[
"Proseek multiplex protein biomarker panels",
"Proseek multiplex panels",
"CVD biomarker panels",
"inflammatory biomarker panels",
"neurology biomarker panels",
"oncology biomarker panels",
"Proseek panels"
] |
['Differnet Proseek multiplex protein biomarker panels exists: CVD, inflammatory, neurology and oncology biomarker.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28734077",
"http://www.ncbi.nlm.nih.gov/pubmed/28930774",
"http://www.ncbi.nlm.nih.gov/pubmed/26475405",
"http://www.ncbi.nlm.nih.gov/pubmed/27383427",
"http://www.ncbi.nlm.nih.gov/pubmed/29026368",
"http://www.ncbi.nlm.nih.gov/pubmed/28083617",
"http://www.ncbi.nlm.nih.gov/pubmed/29050213",
"http://www.ncbi.nlm.nih.gov/pubmed/28948068",
"http://www.ncbi.nlm.nih.gov/pubmed/28586402",
"http://www.ncbi.nlm.nih.gov/pubmed/26204497",
"http://www.ncbi.nlm.nih.gov/pubmed/29051715",
"http://www.ncbi.nlm.nih.gov/pubmed/28437237"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28586402",
"endSection": "abstract",
"offsetInBeginSection": 215,
"offsetInEndSection": 360,
"text": "A total of 92 biomarkers were measured before a standardized meal as well as 30 and 120 minutes afterwards with the Proseek Multiplex CVD III kit"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28437237",
"endSection": "abstract",
"offsetInBeginSection": 877,
"offsetInEndSection": 926,
"text": " PROSEEK Multiplex CVD and PROSEEK Multiplex INF "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28437237",
"endSection": "abstract",
"offsetInBeginSection": 248,
"offsetInEndSection": 455,
"text": "A multiplex proximity extension assay allowed us to measure 157 cardiovascular disease (CVD) and inflammatory disease-related biomarkers in patients from the international, multicenter, and randomized trial;"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28734077",
"endSection": "abstract",
"offsetInBeginSection": 543,
"offsetInEndSection": 702,
"text": "Plasma concentrations of MMP12 were measured at baseline in 3394 subjects with high-risk for cardiovascular disease (CVD) using the Olink ProSeek CVD I array. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28930774",
"endSection": "abstract",
"offsetInBeginSection": 738,
"offsetInEndSection": 948,
"text": "The samples were analyzed with a multiplex proximity extension assay in which 92 inflammation-related proteins were measured simultaneously (Proseek Multiplex Inflammation I; Olink Bioscience, Uppsala, Sweden)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28948068",
"endSection": "abstract",
"offsetInBeginSection": 302,
"offsetInEndSection": 448,
"text": " A total of 92 biomarkers were measured before a standardized meal as well as 30 and 120 min afterward with the Proseek Multiplex Neurology I kit."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29026368",
"endSection": "abstract",
"offsetInBeginSection": 423,
"offsetInEndSection": 651,
"text": "We used proximity extension immunoassay (PEA, Proseek Multiplex, Olink) to assess the serum levels of ninety-two inflammation-related proteins in Czech patients with SLE (n = 75) and age-matched healthy control subjects (n = 23)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29050213",
"endSection": "abstract",
"offsetInBeginSection": 160,
"offsetInEndSection": 266,
"text": "Using highly-sensitive Proximity Extension ImmunoAssay on 92 cancer biomarkers (Proseek Multiplex, Olink),"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29051715",
"endSection": "abstract",
"offsetInBeginSection": 371,
"offsetInEndSection": 530,
"text": "This new technology (Proseek®Multiplex Oncology Plates) can simultaneously measure the expression of 92 proteins in serum based on a proximity extension assay."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26204497",
"endSection": "abstract",
"offsetInBeginSection": 439,
"offsetInEndSection": 539,
"text": "Levels of 82 proteins were assessed in plasma by a proximity extension assay (Proseek Multiplex CVD,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27383427",
"endSection": "abstract",
"offsetInBeginSection": 812,
"offsetInEndSection": 927,
"text": "92 inflammatory proteins were analysed with a multiplex system (Proseek Multiplex Inflammation I, Olink Bioscience)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28083617",
"endSection": "abstract",
"offsetInBeginSection": 544,
"offsetInEndSection": 829,
"text": "erum concentrations of 92 inflammation-associated proteins were measured in samples obtained from 80 aHSCT patients 14 days after transplantation and from 23 healthy control subjects by a novel sensitive proximity extension assay technology using Proseek Multiplex Inflammation I kit. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26475405",
"endSection": "abstract",
"offsetInBeginSection": 1055,
"offsetInEndSection": 1174,
"text": " Laboratory analyses were performed by Proximity Extension Assay (Proseek Multiplex CVD I(96 × 96)), ELISAs and RT-PCR."
}
] | 11 |
BioASQ-training11b
| null | null |
5a9d99ac4e03427e73000002
|
bioasq_factoid
|
factoid
|
What is the function of the protein Cuf1?
|
['Cuf1 is a copper-sensing transcription factor.']
|
[
"Cuf1",
"Copper-sensing transcription factor 1",
"Cuf1 protein",
"Cuf1 transcription factor"
] |
['Cuf1 is a copper-sensing transcription factor.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/11274192",
"http://www.ncbi.nlm.nih.gov/pubmed/21489137",
"http://www.ncbi.nlm.nih.gov/pubmed/18723604",
"http://www.ncbi.nlm.nih.gov/pubmed/17384198",
"http://www.ncbi.nlm.nih.gov/pubmed/12244050"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21489137",
"endSection": "abstract",
"offsetInBeginSection": 106,
"offsetInEndSection": 213,
"text": " CUF1 was involved both in copper acquisition and in copper detoxification in response to copper variation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18723604",
"endSection": "abstract",
"offsetInBeginSection": 961,
"offsetInEndSection": 990,
"text": "the transcription factor Cuf1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17384198",
"endSection": "abstract",
"offsetInBeginSection": 88,
"offsetInEndSection": 114,
"text": "transcription factor Cuf1 "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12244050",
"endSection": "abstract",
"offsetInBeginSection": 514,
"offsetInEndSection": 555,
"text": " copper-sensing transcription factor Cuf1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11274192",
"endSection": "abstract",
"offsetInBeginSection": 1004,
"offsetInEndSection": 1046,
"text": "copper-sensing transcription factor Cuf1, "
}
] | 11 |
BioASQ-training11b
| null | null |
60355c0f1cb411341a000156
|
bioasq_factoid
|
factoid
|
Which company produces Ruconest?
|
['Pharming']
|
[
"Pharming",
"Pharming technology",
"Pharming (pharmaceutical farming)",
"Pharming (genetic engineering)",
"Pharmaceutical farming"
] |
['Ruconest is produced by the company Pharming.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21426252"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21426252",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 194,
"text": "Recombinant human C1 esterase inhibitor (rhC1INH) (Ruconest(®), Pharming) is a new drug developed for the relief of symptoms occurring in patients with angioedema due to C1-inhibitor deficiency."
}
] | 12 |
BioASQ-training12b
| null | null |
643305b257b1c7a315000025
|
bioasq_factoid
|
factoid
|
Where is the respirasome located?
|
['In the inner mitochondrial membrane']
|
[
"inner mitochondrial membrane",
"IMM",
"mitochondrial inner membrane"
] |
['Respirasomes are macromolecular assemblies of the respiratory chain complexes I, III and IV in the inner mitochondrial membrane. The 4.0 Å cryo-EM structure of one of the most intricate enzyme systems, the respirasome, in the mitochondrial inner membrane is now available.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27830641",
"http://www.ncbi.nlm.nih.gov/pubmed/27912054"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27912054",
"endSection": "abstract",
"offsetInBeginSection": 181,
"offsetInEndSection": 305,
"text": "he 4.0 Å cryo-EM structure of one of the most intricate enzyme systems, the respirasome, in the mitochondrial inner membrane"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27830641",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "Respirasomes are macromolecular assemblies of the respiratory chain complexes I, III and IV in the inner mitochondrial membrane."
}
] | 6 |
BioASQ-training6b
| null | null |
58a9d8a1396a458e50000005
|
bioasq_factoid
|
factoid
|
Which tool has been developed for microRNA-target enrichment and network-based analysis?
|
['MIENTURNET']
|
[
"MIENTURNET",
"MIENTURNET Network",
"MIENTURNET Database"
] |
['MIENTURNET (MicroRNA ENrichment TURned NETwork) is a web tool that receives in input a list of miRNAs or mRNAs and tackles the problem of prioritizing miRNA-target interactions by performing a statistical analysis followed by a fully featured network-based visualization and analysis. The statistics is used to assess the significance of an over-representation of miRNA-target interactions and then MIENTURNET filters based on the statistical significance associated with each miRNA-target interaction. In addition, the holistic approach of the network theory is used to infer possible evidences of miRNA regulation by capturing emergent properties of the miRNA-target regulatory network that would be not evident through a pairwise analysis of the individual components.', 'MIENTURNET (MicroRNA ENrichment TURned NETwork) is an interactive web tool for microRNA-target enrichment and network-based analysis.', 'MIENTURNET is a web tool for microRNA-target enrichment and network-based analysis. MIENTURNET offers the possibility to consistently perform both statistical and network-based analyses.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/31684860"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31684860",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "MIENTURNET: an interactive web tool for microRNA-target enrichment and network-based analysis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31684860",
"endSection": "abstract",
"offsetInBeginSection": 563,
"offsetInEndSection": 2057,
"text": "We propose a new and easy-to-use web tool MIENTURNET (MicroRNA ENrichment TURned NETwork) that receives in input a list of miRNAs or mRNAs and tackles the problem of prioritizing miRNA-target interactions by performing a statistical analysis followed by a fully featured network-based visualization and analysis. The statistics is used to assess the significance of an over-representation of miRNA-target interactions and then MIENTURNET filters based on the statistical significance associated with each miRNA-target interaction. In addition, the holistic approach of the network theory is used to infer possible evidences of miRNA regulation by capturing emergent properties of the miRNA-target regulatory network that would be not evident through a pairwise analysis of the individual components.CONCLUSION: MIENTURNET offers the possibility to consistently perform both statistical and network-based analyses by using only a single tool leading to a more effective prioritization of the miRNA-target interactions. This has the potential to avoid researchers without computational and informatics skills to navigate multiple websites and thus to independently investigate miRNA activity in every cellular process of interest in an easy and at the same time exhaustive way thanks to the intuitive web interface. The web application along with a well-documented and comprehensive user guide are freely available at http://userver.bio.uniroma1.it/apps/mienturnet/ without any login requirement."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31684860",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 93,
"text": "MIENTURNET: an interactive web tool for microRNA-target enrichment and network-based analysis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31684860",
"endSection": "abstract",
"offsetInBeginSection": 554,
"offsetInEndSection": 875,
"text": "RESULTS: We propose a new and easy-to-use web tool MIENTURNET (MicroRNA ENrichment TURned NETwork) that receives in input a list of miRNAs or mRNAs and tackles the problem of prioritizing miRNA-target interactions by performing a statistical analysis followed by a fully featured network-based visualization and analysis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31684860",
"endSection": "abstract",
"offsetInBeginSection": 410,
"offsetInEndSection": 854,
"text": " processes. A reasonable solution is certainly to prioritize miRNA-target interactions to maximize the effectiveness of the downstream analysis.RESULTS: We propose a new and easy-to-use web tool MIENTURNET (MicroRNA ENrichment TURned NETwork) that receives in input a list of miRNAs or mRNAs and tackles the problem of prioritizing miRNA-target interactions by performing a statistical analysis followed by a fully featured network-based visual"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31684860",
"endSection": "abstract",
"offsetInBeginSection": 1073,
"offsetInEndSection": 1547,
"text": "-target interaction. In addition, the holistic approach of the network theory is used to infer possible evidences of miRNA regulation by capturing emergent properties of the miRNA-target regulatory network that would be not evident through a pairwise analysis of the individual components.CONCLUSION: MIENTURNET offers the possibility to consistently perform both statistical and network-based analyses by using only a single tool leading to a more effective prioritization "
}
] | 11 |
BioASQ-training11b
| null | null |
60579cb394d57fd87900002e
|
bioasq_factoid
|
factoid
|
Which heat shock protein is found to be upregulated during Hsp90 inhibition?
|
['HSP70']
|
[
"HSP70",
"Heat shock protein 70",
"HSP 70",
"HSP-70",
"HSP70 protein",
"HSP70A",
"HSPA1A",
"HSPA1B",
"HSPA1L"
] |
HSP90 inhibition was found to be associated with induction of HSP70 expression.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24100469",
"http://www.ncbi.nlm.nih.gov/pubmed/23023377",
"http://www.ncbi.nlm.nih.gov/pubmed/20015528"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24100469",
"endSection": "abstract",
"offsetInBeginSection": 935,
"offsetInEndSection": 1110,
"text": "HSP90 inhibition was associated with decreased neuroendocrine ErbB and IGF-I receptor expression, decreased Erk and Akt phospho-rylation and the induction of HSP70 expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23023377",
"endSection": "abstract",
"offsetInBeginSection": 896,
"offsetInEndSection": 1001,
"text": "Inhibition of Hsp90 upregulated the expression of Hsp70 and Hsp70-bound Nox2, 5 and promoted degradation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20015528",
"endSection": "abstract",
"offsetInBeginSection": 931,
"offsetInEndSection": 1080,
"text": "Conversely, inhibition of HSP90 significantly increased the expression of both VEGF and HGF mRNA, and induced HSP70 protein in PHH cultures in vitro."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018841",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D006360",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018840",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D015854",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018869",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0006986",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0042026",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0034620"
] |
[] |
534abe8aaeec6fbd07000013
|
bioasq_factoid
|
factoid
|
Which mutated gene is associated with Waardenburg and Tietz syndromes?
|
['microphthalmia-associated transcription factor gene', 'MITF']
|
[
"microphthalmia-associated transcription factor gene",
"MITF",
"Microphthalmia Transcription Factor",
"Microphthalmia-associated transcription factor",
"Microphthalmia gene",
"MITF gene"
] |
['Mutations in microphthalmia-associated transcription factor (MITF) gene cause Waardenburg and Tietz syndromes.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/10952390",
"http://www.ncbi.nlm.nih.gov/pubmed/22371403",
"http://www.ncbi.nlm.nih.gov/pubmed/24379252",
"http://www.ncbi.nlm.nih.gov/pubmed/23098757",
"http://www.ncbi.nlm.nih.gov/pubmed/22258527",
"http://www.ncbi.nlm.nih.gov/pubmed/23020089",
"http://www.ncbi.nlm.nih.gov/pubmed/19938076",
"http://www.ncbi.nlm.nih.gov/pubmed/23787126",
"http://www.ncbi.nlm.nih.gov/pubmed/20485200",
"http://www.ncbi.nlm.nih.gov/pubmed/9546825",
"http://www.ncbi.nlm.nih.gov/pubmed/10790403",
"http://www.ncbi.nlm.nih.gov/pubmed/10536986",
"http://www.ncbi.nlm.nih.gov/pubmed/23512835",
"http://www.ncbi.nlm.nih.gov/pubmed/10851256",
"http://www.ncbi.nlm.nih.gov/pubmed/27604145",
"http://www.ncbi.nlm.nih.gov/pubmed/22196401",
"http://www.ncbi.nlm.nih.gov/pubmed/26252099"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27604145",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "Tietz/Waardenburg type 2A syndrome associated with posterior microphthalmos in two unrelated patients with novel MITF gene mutations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27604145",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 97,
"text": "Tietz syndrome and Waardenburg syndrome type 2A are allelic conditions caused by MITF mutations. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24379252",
"endSection": "abstract",
"offsetInBeginSection": 953,
"offsetInEndSection": 1054,
"text": "For example, mutations of the MITF gene cause Waardenburg syndrome type 2A as well as Tietz syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24379252",
"endSection": "abstract",
"offsetInBeginSection": 1152,
"offsetInEndSection": 1346,
"text": "For example, mutations of MITF, SNAI2 and SOX10 genes are observed in Waardenburg syndrome type II and mutations of EDNRB, EDN3 and SOX10 genes are responsible for Waardenburg syndrome type IV. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24379252",
"endSection": "abstract",
"offsetInBeginSection": 480,
"offsetInEndSection": 636,
"text": "These disorders are represented by Waardenburg syndrome, piebaldism and Tietz syndrome, and are caused by different mutations of various or the same genes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23787126",
"endSection": "abstract",
"offsetInBeginSection": 163,
"offsetInEndSection": 344,
"text": "Mutations in the MITF have been found in patients with the dominantly inherited hypopigmentation and deafness syndromes Waardenburg syndrome type 2A (WS2A) and Tietz syndrome (TS). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23512835",
"endSection": "abstract",
"offsetInBeginSection": 1164,
"offsetInEndSection": 1342,
"text": "All patients with PAX3 mutations had typical phenotype of WS with dystopia canthorum (WS1), whereas patients with MITF gene mutations presented without dystopia canthorum (WS2). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23512835",
"endSection": "abstract",
"offsetInBeginSection": 1491,
"offsetInEndSection": 1676,
"text": "MITF 3-bp deletions at amino acid position 217 have previously been described in patients with Tietz syndrome (TS), a clinical entity with hearing loss and generalised hypopigmentation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23512835",
"endSection": "abstract",
"offsetInBeginSection": 1689,
"offsetInEndSection": 2048,
"text": "On the basis of these findings, we conclude that sequencing and copy number analysis of both PAX3 and MITF have to be recommended in the routine molecular diagnostic setting for patients, WS1 and WS2. Furthermore, our genotype-phenotype analyses indicate that WS2 and TS correspond to a clinical spectrum that is influenced by MITF mutation type and position."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22258527",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "Novel and recurrent non-truncating mutations of the MITF basic domain: genotypic and phenotypic variations in Waardenburg and Tietz syndromes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22258527",
"endSection": "abstract",
"offsetInBeginSection": 200,
"offsetInEndSection": 487,
"text": "A notable relationship has been described between non-truncating mutations of its basic domain and Tietz syndrome, which is characterized by albinoid-like hypopigmentation of the skin and hair, rather than the patchy depigmentation seen in Waardenburg syndrome, and severe hearing loss. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20485200",
"endSection": "abstract",
"offsetInBeginSection": 9,
"offsetInEndSection": 348,
"text": "Mutations in microphthalmia-associated transcription factor (MITF) lead to Waardenburg syndrome type 2 (WS2), a dominantly inherited disorder involving hearing loss and pigment disturbances caused by a lack of melanocytes. On rare occasions, mutations in MITF lead to Tietz syndrome (TS), which is characterized by a severe WS2 phenotype. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10952390",
"endSection": "abstract",
"offsetInBeginSection": 257,
"offsetInEndSection": 389,
"text": "In humans, haploinsufficiency of MITF causes Waardenburg syndrome type 2, while a dominant-negative mutation causes Tietz syndrome. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10851256",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 70,
"text": "Tietz syndrome (hypopigmentation/deafness) caused by mutation of MITF."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10851256",
"endSection": "abstract",
"offsetInBeginSection": 474,
"offsetInEndSection": 869,
"text": "This family was reascertained and a missense mutation was found in the basic region of the MITF gene in family members with Tietz syndrome. Mutations in other regions of this gene have been found to produce Waardenburg syndrome type 2 (WS2), which also includes pigmentary changes and hearing loss, but in contrast to Tietz syndrome, depigmentation is patchy and hearing loss is variable in WS2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10790403",
"endSection": "abstract",
"offsetInBeginSection": 266,
"offsetInEndSection": 427,
"text": "In humans, MITF mutations cause Waardenburg syndrome type 2A (WS2A) and Tietz syndrome, autosomal dominant disorders resulting in deafness and hypopigmentation. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9546825",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 73,
"text": "Mutation of the MITF gene in albinism-deafness syndrome (Tietz syndrome)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9546825",
"endSection": "abstract",
"offsetInBeginSection": 260,
"offsetInEndSection": 334,
"text": "MITF gene mutations account for 20% of Waardenburg syndrome (WS) type II. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23787126",
"endSection": "abstract",
"offsetInBeginSection": 163,
"offsetInEndSection": 343,
"text": "Mutations in the MITF have been found in patients with the dominantly inherited hypopigmentation and deafness syndromes Waardenburg syndrome type 2A (WS2A) and Tietz syndrome (TS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22258527",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 485,
"text": "The microphthalmia-associated transcription factor (MITF) is a basic helix-loop-helix leucine zipper transcription factor, which regulates melanocyte development and the biosynthetic melanin pathway. A notable relationship has been described between non-truncating mutations of its basic domain and Tietz syndrome, which is characterized by albinoid-like hypopigmentation of the skin and hair, rather than the patchy depigmentation seen in Waardenburg syndrome, and severe hearing loss"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22371403",
"endSection": "abstract",
"offsetInBeginSection": 1650,
"offsetInEndSection": 1750,
"text": "Mutations of the MITF gene may lead to hereditary diseases: Waardenburg type II and Tietz syndromes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23020089",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 236,
"text": "The human deafness-pigmentation syndromes, Waardenburg syndrome (WS) type 2a, and Tietz syndrome are characterized by profound deafness but only partial cutaneous pigmentary abnormalities. Both syndromes are caused by mutations in MITF."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10536986",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 265,
"text": "On some occasions, mutations of a gene cause different syndromes that may have similar phenotypes. For example, mutations of the MITF gene cause Waardenburg syndrome type 2 (Tassabehji et al, 1994; Nobukuni et al, 1996) as well as Tietz syndrome (Smith et al, 1997)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22371403",
"endSection": "abstract",
"offsetInBeginSection": 1638,
"offsetInEndSection": 1738,
"text": "Mutations of the MITF gene may lead to hereditary diseases: Waardenburg type II and Tietz syndromes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23787126",
"endSection": "abstract",
"offsetInBeginSection": 162,
"offsetInEndSection": 342,
"text": "Mutations in the MITF have been found in patients with the dominantly inherited hypopigmentation and deafness syndromes Waardenburg syndrome type 2A (WS2A) and Tietz syndrome (TS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24379252",
"endSection": "abstract",
"offsetInBeginSection": 947,
"offsetInEndSection": 1048,
"text": "For example, mutations of the MITF gene cause Waardenburg syndrome type 2A as well as Tietz syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10536986",
"endSection": "abstract",
"offsetInBeginSection": 98,
"offsetInEndSection": 265,
"text": "For example, mutations of the MITF gene cause Waardenburg syndrome type 2 (Tassabehji et al, 1994; Nobukuni et al, 1996) as well as Tietz syndrome (Smith et al, 1997)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23020089",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "Hearing dysfunction in heterozygous Mitf(Mi-wh) /+ mice, a model for Waardenburg syndrome type 2 and Tietz syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10536986",
"endSection": "abstract",
"offsetInBeginSection": 527,
"offsetInEndSection": 720,
"text": "By analyzing the genes for Waardenburg syndrome, we showed that PAX3, the gene responsible for Waardenburg syndrome type 1, regulates MITF, the gene responsible for Waardenburg syndrome type 2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9546825",
"endSection": "abstract",
"offsetInBeginSection": 260,
"offsetInEndSection": 333,
"text": "MITF gene mutations account for 20% of Waardenburg syndrome (WS) type II."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23787126",
"endSection": "abstract",
"offsetInBeginSection": 163,
"offsetInEndSection": 342,
"text": "Mutations in the MITF have been found in patients with the dominantly inherited hypopigmentation and deafness syndromes Waardenburg syndrome type 2A (WS2A) and Tietz syndrome (TS)"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22258527",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "Novel and recurrent non-truncating mutations of the MITF basic domain: genotypic and phenotypic variations in Waardenburg and Tietz syndromes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24379252",
"endSection": "abstract",
"offsetInBeginSection": 953,
"offsetInEndSection": 1053,
"text": "For example, mutations of the MITF gene cause Waardenburg syndrome type 2A as well as Tietz syndrome"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10851256",
"endSection": "abstract",
"offsetInBeginSection": 474,
"offsetInEndSection": 614,
"text": "This family was reascertained and a missense mutation was found in the basic region of the MITF gene in family members with Tietz syndrome. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20485200",
"endSection": "abstract",
"offsetInBeginSection": 232,
"offsetInEndSection": 348,
"text": "On rare occasions, mutations in MITF lead to Tietz syndrome (TS), which is characterized by a severe WS2 phenotype. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10536986",
"endSection": "abstract",
"offsetInBeginSection": 99,
"offsetInEndSection": 267,
"text": "For example, mutations of the MITF gene cause Waardenburg syndrome type 2 (Tassabehji et al, 1994; Nobukuni et al, 1996) as well as Tietz syndrome (Smith et al, 1997). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10536986",
"endSection": "abstract",
"offsetInBeginSection": 99,
"offsetInEndSection": 266,
"text": "For example, mutations of the MITF gene cause Waardenburg syndrome type 2 (Tassabehji et al, 1994; Nobukuni et al, 1996) as well as Tietz syndrome (Smith et al, 1997)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10790403",
"endSection": "abstract",
"offsetInBeginSection": 266,
"offsetInEndSection": 426,
"text": "In humans, MITF mutations cause Waardenburg syndrome type 2A (WS2A) and Tietz syndrome, autosomal dominant disorders resulting in deafness and hypopigmentation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10952390",
"endSection": "abstract",
"offsetInBeginSection": 257,
"offsetInEndSection": 388,
"text": "In humans, haploinsufficiency of MITF causes Waardenburg syndrome type 2, while a dominant-negative mutation causes Tietz syndrome."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27604145",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 134,
"text": "Tietz/Waardenburg type 2A syndrome associated with posterior microphthalmos in two unrelated patients with novel MITF gene mutations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27604145",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "Tietz syndrome and Waardenburg syndrome type 2A are allelic conditions caused by MITF mutations."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23020089",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Hearing dysfunction in heterozygous Mitf(Mi-wh) /+ mice, a model for Waardenburg syndrome type 2 and Tietz syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24379252",
"endSection": "abstract",
"offsetInBeginSection": 1152,
"offsetInEndSection": 1345,
"text": "For example, mutations of MITF, SNAI2 and SOX10 genes are observed in Waardenburg syndrome type II and mutations of EDNRB, EDN3 and SOX10 genes are responsible for Waardenburg syndrome type IV."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9546825",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "Mutation of the MITF gene in albinism-deafness syndrome (Tietz syndrome)."
}
] | 6 |
BioASQ-training6b
|
[
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D005796",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D051739",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013577",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D014849",
"http://www.uniprot.org/uniprot/MITF_HUMAN"
] | null |
58a57f9460087bc10a00001f
|
bioasq_factoid
|
factoid
|
What is the estimated cost reduction when using telegenetics?
|
['10-12%']
|
[
"10-12%",
"ten to twelve percent",
"10 to 12 percent",
"10% to 12%",
"10 percent to 12 percent"
] |
['The estimated cost reduction by online counseling is about 10-12%.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26785833"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26785833",
"endSection": "abstract",
"offsetInBeginSection": 1548,
"offsetInEndSection": 1644,
"text": "We estimated reduced time and costs by online counseling with about 8% and 10-12%, respectively."
}
] | 12 |
BioASQ-training12b
| null | null |
6415bb3c690f196b5100000e
|
bioasq_factoid
|
factoid
|
What was the predominant rotavirus genotype in the pre-vaccine era, in Australia?
|
['G1P[8]']
|
[
"G1P[8]",
"G1P8",
"G1P[8] enzyme",
"G1P[8] synthase",
"G1P[8] protein"
] |
['G1P[8] was the dominant genotype in Australia in the prevaccine era (1995-2006).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29790933",
"http://www.ncbi.nlm.nih.gov/pubmed/30755297",
"http://www.ncbi.nlm.nih.gov/pubmed/32060546"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29790933",
"endSection": "abstract",
"offsetInBeginSection": 789,
"offsetInEndSection": 867,
"text": "G1P[8] was the dominant genotype nationally in the prevaccine era (1995-2006)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29790933",
"endSection": "abstract",
"offsetInBeginSection": 436,
"offsetInEndSection": 638,
"text": "From 1995 to 2015, the Australian Rotavirus Surveillance Program conducted genotypic analysis on 13051 rotavirus-positive samples from children <5 years of age, hospitalized with acute gastroenteritis. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30755297",
"endSection": "abstract",
"offsetInBeginSection": 873,
"offsetInEndSection": 979,
"text": "In the pre-vaccine era, G1P[8] was most prevalent, ranging from 39% (411/1,057) to 74% (527/709) per year."
}
] | 11 |
BioASQ-training11b
| null | null |
5e7667b1835f4e4777000004
|
bioasq_factoid
|
factoid
|
What animal is thought to be the host for the Coronavirus causing MERS?
|
['camel']
|
[
"camel",
"dromedary",
"Bactrian camel",
"Arabian camel",
"Camelus dromedarius",
"Camelus bactrianus"
] |
['The animal thought to be the host for the Coronavirus causing MERS is camels.', 'The Virus causing MERS is though to have originated in dromedary camels']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29239118",
"http://www.ncbi.nlm.nih.gov/pubmed/30146782",
"http://www.ncbi.nlm.nih.gov/pubmed/25791336",
"http://www.ncbi.nlm.nih.gov/pubmed/29336306"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29239118",
"endSection": "abstract",
"offsetInBeginSection": 1260,
"offsetInEndSection": 1437,
"text": "hese data demonstrate a genetic link for each of these clusters to a camel and support the hypothesis that human MERS-CoV diversity results from multiple zoonotic introductions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30146782",
"endSection": "abstract",
"offsetInBeginSection": 563,
"offsetInEndSection": 821,
"text": "The exact origin of MERS-CoV remains unknown, but the transmission pattern and evidence from virological studies suggest that dromedary camels are the major reservoir host, from which human infections may sporadically occur through the zoonotic transmission."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29336306",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "Middle East respiratory syndrome coronavirus (MERS-CoV) is a zoonotic virus from camels causing significant mortality and morbidity in humans in the Arabian Peninsula"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29336306",
"endSection": "abstract",
"offsetInBeginSection": 401,
"offsetInEndSection": 528,
"text": " Here, we use existing MERS-CoV sequence data to explore its phylodynamics in two of its known major hosts, humans and camels. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29336306",
"endSection": "abstract",
"offsetInBeginSection": 581,
"offsetInEndSection": 704,
"text": "ong-term MERS-CoV evolution occurs exclusively in camels, whereas humans act as a transient, and ultimately terminal host. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29336306",
"endSection": "abstract",
"offsetInBeginSection": 811,
"offsetInEndSection": 926,
"text": " human outbreaks in the Arabian peninsula are driven by seasonally varying zoonotic transfer of viruses from camels"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25791336",
"endSection": "abstract",
"offsetInBeginSection": 72,
"offsetInEndSection": 291,
"text": "While bats may be the primary reservoir for both viruses, SARS coronavirus (SARS-CoV) likely crossed into humans from civets in China, and MERS coronavirus (MERS-CoV) has been transmitted from camels in the Middle East."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30146782",
"endSection": "abstract",
"offsetInBeginSection": 576,
"offsetInEndSection": 835,
"text": "The exact origin of MERS-CoV remains unknown , but the transmission pattern and evidence from virological studies suggest that dromedary camels are the major reservoir host , from which human infections may sporadically occur through the zoonotic transmission"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25791336",
"endSection": "abstract",
"offsetInBeginSection": 72,
"offsetInEndSection": 292,
"text": "While bats may be the primary reservoir for both viruses, SARS coronavirus (SARS-CoV) likely crossed into humans from civets in China, and MERS coronavirus (MERS-CoV) has been transmitted from camels in the Middle East."
}
] | 11 |
BioASQ-training11b
| null | null |
5e2f4a8bfbd6abf43b00002a
|
bioasq_factoid
|
yesno
|
Is pimavanserin effective for Parkinson's disease psychosis?
|
['yes']
|
[
"yes"
] |
["Yes. Pimavanserin is effective for treating Parkinson's disease psychosis. It is a highly selective serotonin 5-HT2A receptor inverse agonist/antagonist."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28493654",
"http://www.ncbi.nlm.nih.gov/pubmed/24183563",
"http://www.ncbi.nlm.nih.gov/pubmed/27609312",
"http://www.ncbi.nlm.nih.gov/pubmed/29497575",
"http://www.ncbi.nlm.nih.gov/pubmed/29185542",
"http://www.ncbi.nlm.nih.gov/pubmed/29047301",
"http://www.ncbi.nlm.nih.gov/pubmed/26908168",
"http://www.ncbi.nlm.nih.gov/pubmed/28385039",
"http://www.ncbi.nlm.nih.gov/pubmed/28622212",
"http://www.ncbi.nlm.nih.gov/pubmed/28375643",
"http://www.ncbi.nlm.nih.gov/pubmed/29452684",
"http://www.ncbi.nlm.nih.gov/pubmed/28880354",
"http://www.ncbi.nlm.nih.gov/pubmed/29098976",
"http://www.ncbi.nlm.nih.gov/pubmed/29185820",
"http://www.ncbi.nlm.nih.gov/pubmed/29105858",
"http://www.ncbi.nlm.nih.gov/pubmed/27262680",
"http://www.ncbi.nlm.nih.gov/pubmed/30298184",
"http://www.ncbi.nlm.nih.gov/pubmed/26744739",
"http://www.ncbi.nlm.nih.gov/pubmed/19907417",
"http://www.ncbi.nlm.nih.gov/pubmed/28817967",
"http://www.ncbi.nlm.nih.gov/pubmed/27830568",
"http://www.ncbi.nlm.nih.gov/pubmed/29955528"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29185820",
"endSection": "abstract",
"offsetInBeginSection": 587,
"offsetInEndSection": 791,
"text": "Two cases of Parkinson's disease with an unusual delusional misidentification, intermetamorphosis, are presented, along with their improvement with pimavanserin, a novel atypical antipsychotic medication."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29105858",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 144,
"text": "RATIONALE: Pimavanserin, a selective serotonin 2A receptor inverse agonist, is a promising candidate for treating Parkinson's disease psychosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29098976",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 349,
"text": "OBJECTIVE: Our aim was to describe the efficacy and tolerability of pimavanserin, a highly selective serotonin 5-HT2A receptor inverse agonist/antagonist indicated for the treatment of hallucinations and delusions associated with Parkinson's disease psychosis (PDP), using the metrics of number needed to treat (NNT) and number needed to harm (NNH)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29047301",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 70,
"text": "Pimavanserin: novel pharmacotherapy for Parkinson's disease psychosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29047301",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 192,
"text": "INTRODUCTION: Pimavanserin is the first FDA-approved atypical antipsychotic drug indicated for the treatment of hallucinations and delusions associated with Parkinson's disease psychosis (PDP)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29047301",
"endSection": "abstract",
"offsetInBeginSection": 1095,
"offsetInEndSection": 1256,
"text": "A pivotal phase III clinical trial demonstrated significant improvement in PDP symptoms in patients receiving pimavanserin compared to placebo-treated patients. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29047301",
"endSection": "abstract",
"offsetInBeginSection": 1332,
"offsetInEndSection": 1560,
"text": "Pimavanserin's mechanism of action might contribute to its unique psychopharmacological properties in the improved treatment of PDP, and perhaps psychosis in other diseases including schizophrenia and dementia-related psychosis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29955528",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "Pimavanserin (Nuplazid™) for the treatment of Parkinson disease psychosis: A review of the literature.Options for the treatment of Parkinson disease psychosis are limited. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27609312",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 299,
"text": "Pimavanserin for the treatment of Parkinson's disease psychosis.Pimavanserin is an antipsychotic with a unique mechanism of action (5-HT2A receptor inverse agonist) and no measurable dopaminergic activity; it has been demonstrated to be efficacious, well tolerated and safe for the treatment of PDP. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28622212",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 223,
"text": "A Retrospective Study of Pimavanserin Use in a Movement Disorders Clinic.Pimavanserin, a 5-HT2A inverse agonist, was commercially released in the United States in April 2016 for the treatment of Parkinson disease psychosis. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27830568",
"endSection": "abstract",
"offsetInBeginSection": 85,
"offsetInEndSection": 277,
"text": "receptor inverse agonist pimavanserin was recently approved by the US FDA for the treatment of PDP and may prove to be a more targeted therapy without the downsides of atypical antipsychotics."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28385039",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 242,
"text": "Evidence-Based Review of Pharmacotherapy Used for Parkinson's Disease Psychosis.Despite lack of rigor in study designs, published data to date suggest that clozapine and pimavanserin should be considered drugs of choice to treat PD psychosis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29185542",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 316,
"text": "Pimavanserin: A novel therapeutic option for Parkinson disease psychosis.While pimavanserin appears to be a safe, effective, and well-tolerated therapeutic option for PDP, additional clinical trials and open-label extension studies are needed to determine the long-term safety and efficacy of this promising therapy. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29497575",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 145,
"text": "Objective: Pimavanserin is the first United States Food and Drug Administration (FDA)-approved treatment for Parkinson's disease psychosis (PDP)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29497575",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 75,
"text": "Pimavanserin: A Novel Drug Approved to Treat Parkinson's Disease Psychosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28493654",
"endSection": "abstract",
"offsetInBeginSection": 1357,
"offsetInEndSection": 1509,
"text": "CONCLUSIONS\nPimavanserin is the only FDA-approved treatment for the hallucinations and delusions seen in patients with psychosis of Parkinson's disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28493654",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 249,
"text": "OBJECTIVE\nTo summarize the US Food and Drug Administration's (FDA's) review of the safety and effectiveness for pimavanserin, an atypical antipsychotic, for the treatment of hallucinations and delusions associated with Parkinson's disease psychosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28493654",
"endSection": "abstract",
"offsetInBeginSection": 897,
"offsetInEndSection": 1017,
"text": "RESULTS\nPimavanserin 34 mg/d was effective in treating hallucinations and delusions associated with Parkinson's disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29452684",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 202,
"text": "BACKGROUND\nPimavanserin is a selective 5-HT2A receptor inverse agonist and antagonist approved in the USA for the treatment of hallucinations and delusions associated with Parkinson's disease psychosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29047301",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "Pimavanserin is the first FDA-approved atypical antipsychotic drug indicated for the treatment of hallucinations and delusions associated with Parkinson's disease psychosis (PDP)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24183563",
"endSection": "abstract",
"offsetInBeginSection": 1944,
"offsetInEndSection": 2071,
"text": "INTERPRETATION\nPimavanserin may benefit patients with Parkinson's disease psychosis for whom few other treatment options exist."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26744739",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "Pimavanserin (ACP-103) is a selective inverse agonist of the 5-hydroxytryptamine 2A (5-HT2A) receptor intended to treat patients with Parkinson's disease psychosis (PDP)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29452684",
"endSection": "abstract",
"offsetInBeginSection": 2808,
"offsetInEndSection": 3013,
"text": "INTERPRETATION\nPimavanserin showed efficacy in patients with Alzheimer's disease psychosis at the primary endpoint (week 6) with an acceptable tolerability profile and without negative effect on cognition."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28880354",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 70,
"text": "[Pimavanserin: a new treatment for the Parkinson's disease psychosis]."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19907417",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 107,
"text": "Pimavanserin, a serotonin(2A) receptor inverse agonist, for the treatment of parkinson's disease psychosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30298184",
"endSection": "abstract",
"offsetInBeginSection": 264,
"offsetInEndSection": 444,
"text": "Pimavanserin, a selective 5-HT2A inverse agonist/antagonist, was approved in the U.S. for treating hallucinations and delusions associated with Parkinson's disease psychosis (PDP)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28375643",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 70,
"text": "Pimavanserin: A Novel Antipsychotic for Parkinson's Disease Psychosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28493654",
"endSection": "abstract",
"offsetInBeginSection": 1357,
"offsetInEndSection": 1509,
"text": "CONCLUSIONS Pimavanserin is the only FDA-approved treatment for the hallucinations and delusions seen in patients with psychosis of Parkinson's disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28493654",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 249,
"text": "OBJECTIVE To summarize the US Food and Drug Administration's (FDA's) review of the safety and effectiveness for pimavanserin, an atypical antipsychotic, for the treatment of hallucinations and delusions associated with Parkinson's disease psychosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28493654",
"endSection": "abstract",
"offsetInBeginSection": 897,
"offsetInEndSection": 1017,
"text": "RESULTS Pimavanserin 34 mg/d was effective in treating hallucinations and delusions associated with Parkinson's disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26908168",
"endSection": "abstract",
"offsetInBeginSection": 859,
"offsetInEndSection": 1050,
"text": "If this is granted, we believe the evidence of Pimavanserin efficacy, safety and tolerability will position this medication as the first choice for treatment of Parkinson's disease psychosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28817967",
"endSection": "abstract",
"offsetInBeginSection": 1158,
"offsetInEndSection": 1344,
"text": "The development of pimavanserin as an antipsychotic opened a new therapeutic avenue in the treatment of PDP as well as targeting psychosis in other disorders such as Alzheimer's disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28375643",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 200,
"text": "OBJECTIVE To review the pharmacology, pharmacokinetics, efficacy, safety, and place in therapy of pimavanserin for the treatment of hallucinations and delusions of Parkinson's disease psychosis (PDP)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24183563",
"endSection": "abstract",
"offsetInBeginSection": 1944,
"offsetInEndSection": 2071,
"text": "INTERPRETATION Pimavanserin may benefit patients with Parkinson's disease psychosis for whom few other treatment options exist."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28493654",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 257,
"text": "<b>OBJECTIVE</b>: To summarize the US Food and Drug Administration's (FDA's) review of the safety and effectiveness for pimavanserin, an atypical antipsychotic, for the treatment of hallucinations and delusions associated with Parkinson's disease psychosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28493654",
"endSection": "abstract",
"offsetInBeginSection": 677,
"offsetInEndSection": 1043,
"text": "Data were available from 616 patients with Parkinson's disease with hallucinations and delusions who received at least 1 dose of pimavanserin, with a total exposure of 825 patient-years in the Parkinson's disease psychosis population.<br><b>RESULTS</b>: Pimavanserin 34 mg/d was effective in treating hallucinations and delusions associated with Parkinson's disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28493654",
"endSection": "abstract",
"offsetInBeginSection": 1212,
"offsetInEndSection": 1544,
"text": "Pimavanserin did not worsen motor function, an adverse effect commonly observed with other antipsychotics, probably because of a lack of consequential dopamine binding.<br><b>CONCLUSIONS</b>: Pimavanserin is the only FDA-approved treatment for the hallucinations and delusions seen in patients with psychosis of Parkinson's disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27262680",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 290,
"text": "Pimavanserin (Nuplazid™) is a selective and potent serotonin 2A (5-HT2A) receptor inverse agonist and antagonist developed by ACADIA Pharmaceuticals that has been approved in the US as a treatment for patients with hallucinations and delusions associated with Parkinson's disease psychosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27262680",
"endSection": "abstract",
"offsetInBeginSection": 472,
"offsetInEndSection": 674,
"text": "This article summarizes the milestones in the development of pimavanserin leading to this first approval for the treatment of hallucinations and delusions in patients with Parkinson's disease psychosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30298184",
"endSection": "abstract",
"offsetInBeginSection": 900,
"offsetInEndSection": 1084,
"text": "In a Phase 2 study with pimavanserin in Alzheimer's disease psychosis, pimavanserin significantly (p=0.045) improved psychosis at Week 6 vs. placebo on the NPI-NH Psychosis Score (PS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28493654",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 239,
"text": "To summarize the US Food and Drug Administration's (FDA's) review of the safety and effectiveness for pimavanserin, an atypical antipsychotic, for the treatment of hallucinations and delusions associated with Parkinson's disease psychosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28493654",
"endSection": "abstract",
"offsetInBeginSection": 1320,
"offsetInEndSection": 1460,
"text": "Pimavanserin is the only FDA-approved treatment for the hallucinations and delusions seen in patients with psychosis of Parkinson's disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28493654",
"endSection": "abstract",
"offsetInBeginSection": 870,
"offsetInEndSection": 982,
"text": "Pimavanserin 34 mg/d was effective in treating hallucinations and delusions associated with Parkinson's disease."
}
] | 11 |
BioASQ-training11b
| null | null |
5c6f6d997c78d69471000055
|
bioasq_yesno
|
factoid
|
Which was the first cholera vaccine approved in the US?
|
['Vaxchora']
|
[
"Vaxchora",
"Cholera vaccine",
"Vaxchora oral cholera vaccine"
] |
['Vaxchora is the first vaccine approved by the Food and Drug Administration for the prophylaxis of cholera infection.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29018300"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29018300",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "Vaxchora: The First FDA-Approved Cholera Vaccination in the United States."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29018300",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Vaxchora is the first vaccine approved by the Food and Drug Administration for the prophylaxis of cholera infection. "
}
] | 11 |
BioASQ-training11b
| null | null |
5e7641a0c6a8763d23000011
|
bioasq_factoid
|
yesno
|
Are there small molecule CGRPs under development for the treatment of migraine?
|
['yes']
|
[
"yes"
] |
['Yes, there are several small molecule CGRPs under development for the treatment of migraine.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28644160"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28644160",
"endSection": "abstract",
"offsetInBeginSection": 500,
"offsetInEndSection": 643,
"text": "Meanwhile, 1 small-molecule CGRP receptor antagonist (ubrogepant, MK-1602) is currently in phase 3 studies for the acute treatment of migraine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28644160",
"endSection": "abstract",
"offsetInBeginSection": 753,
"offsetInEndSection": 890,
"text": "Several other small-molecular CGRP receptor antagonists are in earlier stages of development for acute migraine treatment or prevention. "
}
] | 11 |
BioASQ-training11b
| null | null |
6026de661cb411341a0000d1
|
bioasq_yesno
|
factoid
|
What happens to retrotransposons during ageing?
|
['Activation']
|
[
"Activation",
"Activating",
"Activation process",
"Activation mechanism",
"Stimulus",
"Triggering",
"Initiation"
] |
['Retrotransposons are activated as organisms age']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27692431",
"http://www.ncbi.nlm.nih.gov/pubmed/26581630"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27692431",
"endSection": "abstract",
"offsetInBeginSection": 249,
"offsetInEndSection": 570,
"text": "Senescent cells undergo dramatic alterations to their chromatin landscape that affect genome accessibility and their transcriptional program. These include the loss of DNA-nuclear lamina interactions, the distension of centromeres, and changes in chromatin composition that can lead to the activation of retrotransposons."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26581630",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "Retrotransposons are activated as organisms age, based on work from several model systems. "
}
] | 11 |
BioASQ-training11b
| null | null |
5c929094ecadf2e73f000019
|
bioasq_factoid
|
factoid
|
What is the role of the IRE1a-XBP1 pathway?
|
['Promotion of T helper cell differentiation by resolving secretory stress and accelerating proliferation']
|
[
"Promotion of T helper cell differentiation by resolving secretory stress and accelerating proliferation",
"T helper cell differentiation",
"Th cell differentiation",
"T helper cell maturation",
"T helper cell development",
"T helper cell activation"
] |
['The IRE1a-XBP1 pathway is a conserved adaptive mediator of the unfolded protein response, playing an important role in the regulation of cell differentiation.', 'The IRE1a-XBP1 pathway is a conserved adaptive mediator of the unfolded protein response, playing an important role in the regulation of cell proliferation and differentiation.', 'The inositol-requiring enzyme 1a (IRE1a)/X-box binding protein 1 (XBP1) pathway plays crucial roles in cell survival and cell death by upregulating UPR-associated genes involved in protein entry into the endoplasmic reticulum and ER-associated degradation (ERAD).', 'The IRE1a-XBP1 pathway is a conserved adaptive mediator of the unfold protein response.', 'The IRE1a-XBP1 pathway is a conserved adaptive mediator of the unfolded protein response. The pathway is indispensable for the development of secretory cells by facilitating protein folding and enhancing secretory capacity.', 'The IRE1a-XBP1 pathway is a conserved adaptive mediator of the unfolded protein response.', 'Genome-wide analyses reveal the IRE1a-XBP1 pathway promotes T helper cell differentiation by resolving secretory stress and accelerating proliferation.', 'The IRE1a-XBP1 pathway is a conserved adaptive mediator of the unfolded protein response. It is indispensable for the development of secretory cells by facilitating protein folding and enhancing secretory capacity.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30355343"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30355343",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Genome-wide analyses reveal the IRE1a-XBP1 pathway promotes T helper cell differentiation by resolving secretory stress and accelerating proliferation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30355343",
"endSection": "abstract",
"offsetInBeginSection": 1977,
"offsetInEndSection": 2352,
"text": "We confirm and detail the critical role of the IRE1a-XBP1 pathway during Th2 lymphocyte activation in regulating cytokine expression, secretion, and cell proliferation. Our high-quality genome-wide XBP1 ChIP and gene expression data provide a rich resource for investigating XBP1-regulated genes. We provide a browsable online database available at http://data.teichlab.org ."
}
] | 11 |
BioASQ-training11b
| null | null |
605cc21d94d57fd879000036
|
bioasq_factoid
|
factoid
|
In which cells does TLR7 escape X-chromosome inactivation?
|
['immune cells']
|
[
"immune cells",
"immune system cells",
"immunocytes",
"white blood cells",
"leukocytes",
"lymphocytes",
"T cells",
"B cells",
"natural killer cells",
"macrophages",
"dendritic cells",
"granulocytes"
] |
['The tlr7 gene encodes by an x chromosome locus. Tlr7 is encoded by an x-chromosome inactivation in immune cells from women and klinefelter syndrome patients.', 'TLR7 evades silencing by X chromosome inactivation in immune cells.', 'TLR7 escape X-chromosome inactivation by RNA polymerase II (ChIP-seq) DNA methylation to produce active TLR7 in immune cells', 'TLR7 escape X-chromosome inactivation by becoming activated in response to DNA damage caused by biallelic loss-of-function mutations on the X chromosome. In addition, TLR7 expression can also be observed in a dose-dependent manner in immune cells, such as epithelial cells, monocytes and macrophages.', 'immune cells', 'TLR7 is encoded by an X chromosome locus, and we examined here whether the TLR7 gene evades silencing by X chromosome inactivation in immune cells from women and Klinefelter syndrome males']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/16887967",
"http://www.ncbi.nlm.nih.gov/pubmed/29374079",
"http://www.ncbi.nlm.nih.gov/pubmed/30276444"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29374079",
"endSection": "abstract",
"offsetInBeginSection": 417,
"offsetInEndSection": 606,
"text": " TLR7 is encoded by an X chromosome locus, and we examined here whether the TLR7 gene evades silencing by X chromosome inactivation in immune cells from women and Klinefelter syndrome males"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16887967",
"endSection": "abstract",
"offsetInBeginSection": 995,
"offsetInEndSection": 1209,
"text": "X-inactivation escape of the TLR7 gene was investigated in monoclonal B cell lines and, independently, in pDCs after cell sorting and single-cell picking, indicating regular silencing of one TLR7 allele in females."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30276444",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 108,
"text": "Female predisposition to TLR7-driven autoimmunity: gene dosage and the escape from X chromosome inactivation"
}
] | 11 |
BioASQ-training11b
| null | null |
5d38767ca1e159510500000b
|
bioasq_factoid
|
factoid
|
Which disease can be categorized using the Koos grading system?
|
['vestibular schwannoma']
|
[
"vestibular schwannoma",
"acoustic neuroma",
"neuroma of the vestibular nerve",
"vestibular nerve schwannoma",
"schwannoma of the vestibular nerve"
] |
['Koos grading system is used for vestibular schwannoma.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26967786",
"http://www.ncbi.nlm.nih.gov/pubmed/25811349",
"http://www.ncbi.nlm.nih.gov/pubmed/26606668",
"http://www.ncbi.nlm.nih.gov/pubmed/25181431",
"http://www.ncbi.nlm.nih.gov/pubmed/27513938",
"http://www.ncbi.nlm.nih.gov/pubmed/24797568",
"http://www.ncbi.nlm.nih.gov/pubmed/15179293",
"http://www.ncbi.nlm.nih.gov/pubmed/21665381",
"http://www.ncbi.nlm.nih.gov/pubmed/23160632",
"http://www.ncbi.nlm.nih.gov/pubmed/27453796",
"http://www.ncbi.nlm.nih.gov/pubmed/24987677"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26967786",
"endSection": "abstract",
"offsetInBeginSection": 636,
"offsetInEndSection": 789,
"text": "The patients had Koos Grade I or II tumors and American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS) Class D hearing status preoperatively. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27513938",
"endSection": "abstract",
"offsetInBeginSection": 250,
"offsetInEndSection": 378,
"text": "METHODS: This is a retrospective review of 22 patients with VS Koos grade III and IV who were treated with STR followed by SRS. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25811349",
"endSection": "abstract",
"offsetInBeginSection": 483,
"offsetInEndSection": 585,
"text": " VS was characterized by its size (Koos classification) and the presence or not of a cystic component."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24797568",
"endSection": "abstract",
"offsetInBeginSection": 624,
"offsetInEndSection": 788,
"text": "MAIN OUTCOME MEASURES: All data recorded were reviewed to access age, sex, tumor type, and tumor size according to the Koos classification and presenting symptoms. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25181431",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "Facial nerve preservation surgery for koos grade 3 and 4 vestibular schwannomas."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26606668",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Safety and Efficacy of Gamma Knife Radiosurgery for the Management of Koos Grade 4 Vestibular Schwannomas."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24987677",
"endSection": "abstract",
"offsetInBeginSection": 368,
"offsetInEndSection": 509,
"text": "In all 333 patients microsurgical vestibular schwannoma (Koos grade 1: 12, grade 2: 34, grade 3: 62, and grade 4: 225) removal was performed."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25181431",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 81,
"text": "Facial nerve preservation surgery for koos grade 3 and 4 vestibular schwannomas."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25181431",
"endSection": "abstract",
"offsetInBeginSection": 195,
"offsetInEndSection": 293,
"text": "To report, in a retrospective study, outcomes for large Koos grade 3 and 4 vestibular schwannomas."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26606668",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 107,
"text": "Safety and Efficacy of Gamma Knife Radiosurgery for the Management of Koos Grade 4 Vestibular Schwannomas."
}
] | 6 |
BioASQ-training6b
|
[
"http://www.disease-ontology.org/api/metadata/DOID:4",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D004194",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=diseases_category"
] |
[
{
"o": "http://linkedlifedata.com/resource/umls/label/A0049608",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0012634"
},
{
"o": "Disease",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A0049608"
},
{
"o": "http://linkedlifedata.com/resource/rxnorm/label/3147522",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/rxnorm/id/1022004"
},
{
"o": "Disease",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/rxnorm/label/3147522"
}
] |
5886519c3b87a8a738000007
|
bioasq_factoid
|
factoid
|
What is the mode of delivery of the drug XIPERE?
|
['microneedle-based delivery in the suprachoroidal space']
|
[
"microneedle-based delivery in the suprachoroidal space",
"microneedle delivery in the suprachoroidal space",
"microneedle-assisted delivery in the suprachoroidal space",
"microneedle technology for suprachoroidal delivery",
"suprachoroidal microneedle delivery",
"microneedle-mediated delivery in the suprachoroidal space"
] |
['XIPERE is administered via a microneedle-based device, the SCS Microinjector, in the suprachoroidal space.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/35868358"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35868358",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 513,
"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®. Suprachoroidal (SC) delivery facilitates targeting, compartmentalization, and durability of small molecule suspensions, thereby potentially addressing some of the efficacy, safety, and treatment burden limitations of current retinal therapies. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35868358",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "Suprachoroidal delivery enables targeting, localization and durability of small molecule suspensions."
}
] | 12 |
BioASQ-training12b
| null | null |
6440396957b1c7a31500004b
|
bioasq_factoid
|
factoid
|
What is the difference between dermatillomania and skin picking disorder?
|
['None']
|
[
"None",
"null",
"naught",
"nothing",
"zero",
"nil",
"no one",
"not any"
] |
['Dermatillomania is also known as skin picking disorder (SPD).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33808008"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33808008",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 241,
"text": "Dermatillomania or skin picking disorder (SPD) is a chronic, recurrent, and treatment resistant neuropsychiatric disorder with an underestimated prevalence that has a concerning negative impact on an individual's health and quality of life. "
}
] | 12 |
BioASQ-training12b
| null | null |
6414c4cf690f196b51000006
|
bioasq_factoid
|
factoid
|
Which enzyme is involved in the maintenance of DNA (cytosine-5-)-methylation?
|
['DNMT1', 'MET1']
|
[
"DNMT1",
"DNA methyltransferase 1",
"Cytosine-5 DNA methyltransferase 1",
"MET1",
"Methyltransferase 1"
] |
['The mammalian DNA (cytosine-5) methyltransferase 1, DNMT1 is the major enzyme responsible for the maintenance of the DNA methylation patterns on the newly synthesized strand after DNA replication. DNMT1 prefers hemimethylated DNA and during DNA replication methylates hemimethylated CpG sites by copying methylation patterns from the parental DNA strand to the newly synthesized daughter strand. The equivalent of DNMT1 in plants is MET1.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23029374",
"http://www.ncbi.nlm.nih.gov/pubmed/22967183",
"http://www.ncbi.nlm.nih.gov/pubmed/22898819",
"http://www.ncbi.nlm.nih.gov/pubmed/22761581",
"http://www.ncbi.nlm.nih.gov/pubmed/22633409",
"http://www.ncbi.nlm.nih.gov/pubmed/22563479",
"http://www.ncbi.nlm.nih.gov/pubmed/22538524",
"http://www.ncbi.nlm.nih.gov/pubmed/7638194",
"http://www.ncbi.nlm.nih.gov/pubmed/22413869",
"http://www.ncbi.nlm.nih.gov/pubmed/22323818",
"http://www.ncbi.nlm.nih.gov/pubmed/22284370",
"http://www.ncbi.nlm.nih.gov/pubmed/22278882",
"http://www.ncbi.nlm.nih.gov/pubmed/22088914",
"http://www.ncbi.nlm.nih.gov/pubmed/22072770",
"http://www.ncbi.nlm.nih.gov/pubmed/22064703",
"http://www.ncbi.nlm.nih.gov/pubmed/22048250",
"http://www.ncbi.nlm.nih.gov/pubmed/21913078",
"http://www.ncbi.nlm.nih.gov/pubmed/22704242",
"http://www.ncbi.nlm.nih.gov/pubmed/21625467",
"http://www.ncbi.nlm.nih.gov/pubmed/21559294",
"http://www.ncbi.nlm.nih.gov/pubmed/21553025",
"http://www.ncbi.nlm.nih.gov/pubmed/21532572",
"http://www.ncbi.nlm.nih.gov/pubmed/21518897",
"http://www.ncbi.nlm.nih.gov/pubmed/21268065",
"http://www.ncbi.nlm.nih.gov/pubmed/20940144",
"http://www.ncbi.nlm.nih.gov/pubmed/20864525",
"http://www.ncbi.nlm.nih.gov/pubmed/20364115",
"http://www.ncbi.nlm.nih.gov/pubmed/20139415",
"http://www.ncbi.nlm.nih.gov/pubmed/20071334",
"http://www.ncbi.nlm.nih.gov/pubmed/20035856",
"http://www.ncbi.nlm.nih.gov/pubmed/22073356",
"http://www.ncbi.nlm.nih.gov/pubmed/19966177",
"http://www.ncbi.nlm.nih.gov/pubmed/19932585",
"http://www.ncbi.nlm.nih.gov/pubmed/19789556",
"http://www.ncbi.nlm.nih.gov/pubmed/19468253",
"http://www.ncbi.nlm.nih.gov/pubmed/19450230",
"http://www.ncbi.nlm.nih.gov/pubmed/19417133",
"http://www.ncbi.nlm.nih.gov/pubmed/19282482",
"http://www.ncbi.nlm.nih.gov/pubmed/19173286",
"http://www.ncbi.nlm.nih.gov/pubmed/18922972",
"http://www.ncbi.nlm.nih.gov/pubmed/19016755",
"http://www.ncbi.nlm.nih.gov/pubmed/18536530",
"http://www.ncbi.nlm.nih.gov/pubmed/18302924",
"http://www.ncbi.nlm.nih.gov/pubmed/18297739",
"http://www.ncbi.nlm.nih.gov/pubmed/17965600",
"http://www.ncbi.nlm.nih.gov/pubmed/17929180",
"http://www.ncbi.nlm.nih.gov/pubmed/17312023",
"http://www.ncbi.nlm.nih.gov/pubmed/16963560",
"http://www.ncbi.nlm.nih.gov/pubmed/17033890",
"http://www.ncbi.nlm.nih.gov/pubmed/16807237",
"http://www.ncbi.nlm.nih.gov/pubmed/17989773",
"http://www.ncbi.nlm.nih.gov/pubmed/16500889",
"http://www.ncbi.nlm.nih.gov/pubmed/15799776",
"http://www.ncbi.nlm.nih.gov/pubmed/17576694",
"http://www.ncbi.nlm.nih.gov/pubmed/20348135",
"http://www.ncbi.nlm.nih.gov/pubmed/18665914",
"http://www.ncbi.nlm.nih.gov/pubmed/23393137",
"http://www.ncbi.nlm.nih.gov/pubmed/22934696",
"http://www.ncbi.nlm.nih.gov/pubmed/21507353",
"http://www.ncbi.nlm.nih.gov/pubmed/21389349",
"http://www.ncbi.nlm.nih.gov/pubmed/21163962",
"http://www.ncbi.nlm.nih.gov/pubmed/20820192",
"http://www.ncbi.nlm.nih.gov/pubmed/20506537",
"http://www.ncbi.nlm.nih.gov/pubmed/20007090",
"http://www.ncbi.nlm.nih.gov/pubmed/19923434",
"http://www.ncbi.nlm.nih.gov/pubmed/19825994",
"http://www.ncbi.nlm.nih.gov/pubmed/19819843",
"http://www.ncbi.nlm.nih.gov/pubmed/19778587"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22967183",
"endSection": "sections.0",
"offsetInBeginSection": 969,
"offsetInEndSection": 1198,
"text": "his defect does not appear in mouse models with mutations in Dnmt3a and Mthfr genes and, therefore, it is specific for the Dnmt1 gene and is suggestive of a role of DNMT1 in imprint resetting or maintenance in the male germ line."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22633409",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 97,
"text": "Specificity of Dnmt1 for methylation of hemimethylated CpG sites resides in its catalytic domain."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7638194",
"endSection": "sections.0",
"offsetInBeginSection": 827,
"offsetInEndSection": 1110,
"text": "We obtained evidence that some 5-methylcytosine residues in these single-stranded DNAs can stimulate de novo methylation of adjacent sites by murine DNA 5-cytosine methyltransferase as effectively as 5-methylcytosine residues in double-stranded DNA stimulate maintenance methylation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22898819",
"endSection": "sections.0",
"offsetInBeginSection": 249,
"offsetInEndSection": 434,
"text": "We present in vitro evidence that the mammalian de novo DNA methyltransferases DNMT3A and DNMT3B, but not the maintenance enzyme DNMT1, are also redox-dependent DNA dehydroxymethylases."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22538524",
"endSection": "sections.0",
"offsetInBeginSection": 903,
"offsetInEndSection": 1035,
"text": "Direct comparison to met1 plants, deficient in maintenance methyltransferase MET1, showed higher sensitivity of ddm1 plants to NaCl."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7638194",
"endSection": "sections.0",
"offsetInBeginSection": 827,
"offsetInEndSection": 1110,
"text": "We obtained evidence that some 5-methylcytosine residues in these single-stranded DNAs can stimulate de novo methylation of adjacent sites by murine DNA 5-cytosine methyltransferase as effectively as 5-methylcytosine residues in double-stranded DNA stimulate maintenance methylation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22323818",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "DNMT1, the major maintenance DNA methyltransferase in animals, helps to regulate gene expression, genome imprinting, and X-chromosome inactivation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22088914",
"endSection": "sections.0",
"offsetInBeginSection": 634,
"offsetInEndSection": 805,
"text": "Correct establishment and maintenance of methylation patterns at imprinted genes has been associated with placental function and regulation of embryonic/fetal development."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22072770",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 107,
"text": "Contributions of CTCF and DNA methyltransferases DNMT1 and DNMT3B to Epstein-Barr virus restricted latency."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22072770",
"endSection": "sections.0",
"offsetInBeginSection": 1191,
"offsetInEndSection": 1301,
"text": "Thus, differential expression of CTCF and DNMT1 and -3B is not critical for maintenance of restricted latency."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22064703",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "Recent studies demonstrate that UHRF1 is required for DNA methylation maintenance by targeting DNMT1 to DNA replication foci, presumably through its unique hemi-methylated DNA-binding activity and interaction with DNMT1."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22048250",
"endSection": "sections.0",
"offsetInBeginSection": 134,
"offsetInEndSection": 476,
"text": "It is generally accepted that DNA methyltransferases carry out specific and non-overlapping functions, Dnmt3a and Dnmt3b being responsible for the establishment of methylation around the time of implantation and Dnmt1 ensuring that methylation is faithfully copied to daughter cells via what has come to be known as \"maintenance methylation.\""
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22048250",
"endSection": "sections.0",
"offsetInBeginSection": 622,
"offsetInEndSection": 768,
"text": "A new model is emerging that takes into account a contribution of the de novo enzymes Dnmt3a and Dnmt3b in the maintenance of the DNA methylation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22048250",
"endSection": "sections.0",
"offsetInBeginSection": 1089,
"offsetInEndSection": 1270,
"text": "We propose here observations in support of the hypothesis that the maintenance of methylation and subsequent silencing of a handful of germ line genes requires Dnmt3b but not Dnmt1."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21913078",
"endSection": "sections.0",
"offsetInBeginSection": 162,
"offsetInEndSection": 407,
"text": "DNA methyltransferase 1 (Dnmt1) is the enzyme responsible for maintaining the methylation marks through cell division. However, the de novo methyltransferases, Dnmt3a and Dnmt3b, can also contribute to the maintenance of the methylation pattern."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22704242",
"endSection": "sections.0",
"offsetInBeginSection": 569,
"offsetInEndSection": 780,
"text": "These new data support the notion that de novo DNMTs also have an important role in the maintenance of DNA methylation and suggest that, in addition to acting as oncogenes, they also behave as tumor suppressors."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21518897",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "Structural insight into maintenance methylation by mouse DNA methyltransferase 1 (Dnmt1)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21518897",
"endSection": "sections.0",
"offsetInBeginSection": 103,
"offsetInEndSection": 367,
"text": "The DNA methyltransferase Dnmt1 is responsible for the propagation of methylation patterns to the next generation via its preferential methylation of hemimethylated CpG sites in the genome; however, how Dnmt1 maintains methylation patterns is not fully understood."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21268065",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "Usp7 and Uhrf1 control ubiquitination and stability of the maintenance DNA methyltransferase Dnmt1."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21268065",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "In mammals Dnmt1 is the DNA methyltransferase chiefly responsible for maintaining genomic methylation patterns through DNA replication cycles, but how its maintenance activity is controlled is still not well understood."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20864525",
"endSection": "sections.0",
"offsetInBeginSection": 706,
"offsetInEndSection": 863,
"text": "DMAP1 is a potent activator of DNMT1 methylation in vitro, suggesting that DMAP1 is a co-repressor that supports the maintenance and de novo action of DNMT1."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20364115",
"endSection": "sections.0",
"offsetInBeginSection": 173,
"offsetInEndSection": 303,
"text": "A group of enzymes, the DNA methyltransferases (DNMTs) tightly regulate both the initiation and maintenance of these methyl marks."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20035856",
"endSection": "sections.0",
"offsetInBeginSection": 232,
"offsetInEndSection": 408,
"text": "Maintenance of DNA methylation depends on DNA methyltransferase 1 (Dnmt1) and intracellular S-adenosylmethionine (SAM) levels, and is inhibited by S-adenosylhomocysteine (SAH)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19468253",
"endSection": "sections.0",
"offsetInBeginSection": 314,
"offsetInEndSection": 416,
"text": "While DNMT3a is mostly involved in de novo methylation, DNMT1 acts as a maintenance methyltransferase."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19789556",
"endSection": "sections.0",
"offsetInBeginSection": 252,
"offsetInEndSection": 541,
"text": "We propose a new model that suggests that the maintenance of DNA methylation relies not only on the recognition of hemimethylated DNA by DNA methyltransferase 1 (DNMT1) but also on the localization of the DNMT3A and DNMT3B enzymes to specific chromatin regions that contain methylated DNA."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19450230",
"endSection": "sections.0",
"offsetInBeginSection": 130,
"offsetInEndSection": 321,
"text": "The maintenance methylase, DNMT1 (DNA methyltransferase 1), is a prominent enzyme in the process that is linked to DNA replication and drives the heritable nature of epigenetic modifications."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19417133",
"endSection": "sections.0",
"offsetInBeginSection": 181,
"offsetInEndSection": 341,
"text": "We have shown previously that these drugs selectively and rapidly induce degradation of the maintenance DNA methyltransferase (DNMT) 1 by a proteasomal pathway."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19282482",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 207,
"text": "Inheritance of epigenetic information encoded by cytosine DNA methylation patterns is crucial for mammalian cell survival, in large part through the activity of the maintenance DNA methyltransferase (DNMT1)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20940144",
"endSection": "sections.0",
"offsetInBeginSection": 295,
"offsetInEndSection": 500,
"text": "We and others have shown that DNA methyltransferase 1 (DNMT1), the maintenance methyltransferase, contributes to the cellular response to DNA damage, yet DNMT1's exact role in this process remains unclear."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19173286",
"endSection": "sections.0",
"offsetInBeginSection": 301,
"offsetInEndSection": 494,
"text": "The maintenance function of Dnmt1 is regulated by its large regulatory N-terminal domain that interacts with other chromatin factors and is essential for the recognition of hemi-methylated DNA."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18922972",
"endSection": "sections.0",
"offsetInBeginSection": 146,
"offsetInEndSection": 380,
"text": "In the absence of a human pituitary tumor cell line, small interfering RNA-mediated knockdown of the maintenance methyltransferase DNA methyltransferase (cytosine 5)-1 (Dnmt1) was used in the murine pituitary adenoma cell line AtT-20."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19016755",
"endSection": "sections.0",
"offsetInBeginSection": 806,
"offsetInEndSection": 962,
"text": "We found that DNA methylation was maintained only when exogenous DNA methyltransferase 1 (DNMT1) and S-adenosyl methionine (SAM) were added to the reaction."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18536530",
"endSection": "sections.0",
"offsetInBeginSection": 357,
"offsetInEndSection": 638,
"text": "We examined the expression of DNMT1 and DNMT3a, representative of a maintenance and de novo methyltransferase respectively, in response to in-vitro depolarization of cortical neurons, using standard techniques such as high potassium (KCl) or the sodium channel agonist veratridine."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18302924",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 349,
"text": "DNA methyltransferase-1 (DNMT1) has a higher specific activity on hemimethylated DNA than on unmethylated DNA, but this preference is too small to explain the faithful mitotic inheritance of genomic methylation patterns. New genetic studies in plants and mammals have identified a novel factor that increases the fidelity of maintenance methylation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18297739",
"endSection": "sections.0",
"offsetInBeginSection": 347,
"offsetInEndSection": 520,
"text": "Dnmt1 is the main maintenance methyltransferase in the mouse and its expression is regulated by a splicing mechanism that dictates the expression of stage-specific isoforms."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17965600",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "Phosphorylation of serine-515 activates the Mammalian maintenance methyltransferase Dnmt1."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17965600",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 93,
"text": "DNA methyltransferase 1 methylates hemi-methylated CG sites generated during DNA replication."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17929180",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "DNA methylation is catalyzed by a family of DNA methyltransferases (DNMTs) including the maintenance enzyme DNMT 1 and de novo methyltransferases DNMT 3a and DNMT 3b."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16963560",
"endSection": "sections.0",
"offsetInBeginSection": 1200,
"offsetInEndSection": 1327,
"text": "Our data suggest that DNMT1 might be essential for maintenance of DNA methylation, proliferation, and survival of cancer cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17033890",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 103,
"text": "Maintenance DNA methyltransferase (Met1) and silencing of CpG-methylated foreign DNA in Volvox carteri."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17033890",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "DNA methylation plays an important role in the gene-silencing network of higher eukaryotes. We have analyzed the 21.5-kb maintenance methyltransferase (M-MTase) gene, met1, of the multicellular green alga Volvox carteri."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16807237",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "DNA damage-induced down-regulation of human Cdc25C and Cdc2 is mediated by cooperation between p53 and maintenance DNA (cytosine-5) methyltransferase 1."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23393137",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 234,
"text": "Methylation at the 5-position of DNA cytosine on the vertebrate genomes is accomplished by the combined catalytic actions of three DNA methyltransferases (DNMTs), the de novo enzymes DNMT3A and DNMT3B and the maintenance enzyme DNMT1."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22934696",
"endSection": "sections.0",
"offsetInBeginSection": 433,
"offsetInEndSection": 613,
"text": "DNA methylation, the major form of epigenetic modifications, is catalyzed by the maintenance DNA methyltransferase (DNMT) 1 and/or the de novo methyltransferases DNMT3A and DNMT3B."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22633409",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "The maintenance methylation of hemimethylated CpG sites by the DNA methyltransferase Dnmt1 is the molecular basis of the inheritance of DNA methylation patterns."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21507353",
"endSection": "sections.0",
"offsetInBeginSection": 309,
"offsetInEndSection": 416,
"text": "The allosteric site(s) on Dnmt1 can regulate processes of de novo and maintenance DNA methylation in cells."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21389349",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "Dnmt1 (DNA methyltransferase 1) is the principal enzyme responsible for maintenance of cytosine methylation at CpG dinucleotides in the mammalian genome."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21163962",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "Maintenance of genomic methylation patterns is mediated primarily by DNA methyltransferase-1 (DNMT1)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20820192",
"endSection": "sections.0",
"offsetInBeginSection": 169,
"offsetInEndSection": 291,
"text": "In this study, we showed that DNMT1, which encodes a methylation maintenance enzyme, is a transcriptional target of BRCA1."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20506537",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 156,
"text": "DNA methyltransferases (DNMTs) are essential for maintenance of aberrant methylation in cancer cells and play important roles in the development of cancers."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20007090",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 139,
"text": "DNA methyltransferase-1 (Dnmt1) is involved in the maintenance of DNA methylation patterns and is crucial for normal mammalian development."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19966177",
"endSection": "sections.0",
"offsetInBeginSection": 990,
"offsetInEndSection": 1109,
"text": "DNMT1, which is important for maintenance of methylation, increased across development and stayed high in adult cortex."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19932585",
"endSection": "sections.0",
"offsetInBeginSection": 1087,
"offsetInEndSection": 1296,
"text": "Our results indicate that DNMT1 plays the main role in maintenance of methylation of CXCR4 promoter, while DNMT3B may function as an accessory DNA methyltransferase to modulate CXCR4 expression in AsPC1 cells."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19825994",
"endSection": "sections.0",
"offsetInBeginSection": 110,
"offsetInEndSection": 225,
"text": "DNA methylation patterns are established and maintained by three DNA methyltransferases: DNMT1, DNMT3A, and DNMT3B."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19819843",
"endSection": "sections.0",
"offsetInBeginSection": 285,
"offsetInEndSection": 514,
"text": "According to their structure and functions, DNA methyltransferases (Dnmts) are divided into two major families in mammalian cells: maintenance methyltransferase (Dnmt1) and de novo methyltransferases (Dnmt3a, Dnmt3b, and Dnmt3L)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19778587",
"endSection": "sections.0",
"offsetInBeginSection": 1154,
"offsetInEndSection": 1216,
"text": "The 5-LOX DNA methylation increased with the age of the cells."
}
] | 5 |
BioASQ-training5b
|
[
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=0010216",
"http://www.uniprot.org/uniprot/CMT1_MAIZE",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=0090116",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=0003886",
"http://www.uniprot.org/uniprot/DCM_ECOLI",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D019175",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D015257"
] | null |
51585b28d24251bc0500008d
|
bioasq_factoid
|
yesno
|
Is there a role for the cylindromatosis tumor suppressor (CYLD) in lung cancer?
|
['yes']
|
[
"yes"
] |
['Yes. Down-regulation of Cyld expression has been associated with the development of various types of human malignancies including lung cancer. Deletion of exon 9 would cause a carboxyl-terminal truncation of CYLD and inactivation of its deubiquitinating activity. Fibroblasts from Cyld(Delta 9/Delta 9) embryos had hyperactive nuclear factor kappaB and c-Jun kinase pathways compared with control fibroblasts. Cyld(Delta 9/Delta 9) newborn mice were smaller than wild-type littermates with a short and kinky tail and no major developmental defects. However, Cyld(Delta 9/Delta 9) mice died shortly after birth from apparent respiratory dysfunction. Histological examination of E18.5 Cyld(Delta 9/Delta 9) lungs demonstrated an immature phenotype characterized by hyperplasic mesenchyme but apparently normal epithelial, smooth muscle and endothelial structures. Thus, it is thought that CYLD has an important role in lung maturation, which may underlie the development of many cases of lung cancer.', 'To explore a correlation between CYLD expression and responsiveness to TRAIL in lung cancer cell lines, we established lung cancer cell lines that stably express CYLD. Our data provided the first evidence that increased expression of CYLD directly blocks TRAIL-induced NF - B activation, and consequently increases TRAIL-induced apoptosis in lung cancer cells. CYLD may act as a therapeutic target of lung cancer. Targeting CYLD, in combination with TRAIL, may be a new strategy to treat lung cancer with high NF - B activity. Cyld encodes a 956-amino acid deubiquitinating enzyme, which is a negative regulator of nuclear factor kappaB and mitogen-activated protein kinase pathways. Mutations that truncate and inactivate the carboxyl-terminal deubiquitinating domain of CYLD underlie the development of skin appendage tumors in humans, whereas down-regulation of Cyld expression has been associated with the development of various types of human malignancies including lung cancer. To establish an animal model of human CYLD inactivation and characterize the biological role of CYLD in vivo, we generated mice carrying a homozygous deletion of Cyld exon 9 mice ) using a conditional approach. Our study identifies an important role of CYLD in lung maturation, which may underlie the development of many cases of lung cancer. ', 'To explore a correlation between CYLD expression and responsiveness to TRAIL in lung cancer cell lines, we established lung cancer cell lines that stably express CYLD. Our data provided the first evidence that increased expression of CYLD directly blocks TRAIL-induced NF - B activation, and consequently increases TRAIL-induced apoptosis in lung cancer cells. CYLD may act as a therapeutic target of lung cancer. Targeting CYLD, in combination with TRAIL, may be a new strategy to treat lung cancer with high NF - B activity. Cyld encodes a 956-amino acid deubiquitinating enzyme, which is a negative regulator of nuclear factor kappaB and mitogen-activated protein kinase pathways. Mutations that truncate and inactivate the carboxyl-terminal deubiquitinating domain of CYLD underlie the development of skin appendage tumors in humans, whereas down-regulation of Cyld expression has been associated with the development of various types of human malignancies including lung cancer. To establish an animal model of human CYLD inactivation and characterize the biological role of CYLD in vivo, we generated mice carrying a homozygous deletion of Cyld exon 9 mice ) using a conditional approach. Our study identifies an important role of CYLD in lung maturation, which may underlie the development of many cases of lung cancer. ', 'To explore a correlation between CYLD expression and responsiveness to TRAIL in lung cancer cell lines, we established lung cancer cell lines that stably express CYLD. Our data provided the first evidence that increased expression of CYLD directly blocks TRAIL-induced NF - B activation, and consequently increases TRAIL-induced apoptosis in lung cancer cells. But studies have demonstrated that many tumor cells were resistant to TRAIL-induced apoptosis. CYLD is recognized as a negative regulator of nuclear factor-kappa B activity. Cyld encodes a 956-amino acid deubiquitinating enzyme, which is a negative regulator of nuclear factor kappaB and mitogen-activated protein kinase pathways. Mutations that truncate and inactivate the carboxyl-terminal deubiquitinating domain of CYLD underlie the development of skin appendage tumors in humans, whereas down-regulation of Cyld expression has been associated with the development of various types of human malignancies including lung cancer. To establish an animal model of human CYLD inactivation and characterize the biological role of CYLD in vivo, we generated mice carrying a homozygous deletion of Cyld exon 9 mice ) using a conditional approach. Our study identifies an important role of CYLD in lung maturation, which may underlie the development of many cases of lung cancer. ']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22017589",
"http://www.ncbi.nlm.nih.gov/pubmed/19412431"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22017589",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 121,
"text": "Over-expressing CYLD augments antitumor activity of TRAIL by inhibiting the NF-κB survival signaling in lung cancer cells"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22017589",
"endSection": "abstract",
"offsetInBeginSection": 521,
"offsetInEndSection": 834,
"text": "increased expression of CYLD directly blocks TRAIL-induced NF-κB activation, and consequently increases TRAIL-induced apoptosis in lung cancer cells. CYLD may act as a therapeutic target of lung cancer. Targeting CYLD, in combination with TRAIL, may be a new strategy to treat lung cancer with high NF-κB activity"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19412431",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 98,
"text": "Truncation of the catalytic domain of the cylindromatosis tumor suppressor impairs lung maturation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19412431",
"endSection": "abstract",
"offsetInBeginSection": 326,
"offsetInEndSection": 462,
"text": "down-regulation of Cyld expression has been associated with the development of various types of human malignancies including lung cancer"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19412431",
"endSection": "abstract",
"offsetInBeginSection": 697,
"offsetInEndSection": 1584,
"text": "Deletion of exon 9 would cause a carboxyl-terminal truncation of CYLD and inactivation of its deubiquitinating activity. In accordance with previous studies, fibroblasts from Cyld(Delta 9/Delta 9) embryos had hyperactive nuclear factor kappaB and c-Jun kinase pathways compared with control fibroblasts. Cyld(Delta 9/Delta 9) newborn mice were smaller than wild-type littermates with a short and kinky tail and no major developmental defects. However, Cyld(Delta 9/Delta 9) mice died shortly after birth from apparent respiratory dysfunction. Histological examination of E18.5 Cyld(Delta 9/Delta 9) lungs demonstrated an immature phenotype characterized by hyperplasic mesenchyme but apparently normal epithelial, smooth muscle. and endothelial structures. Our study identifies an important role of CYLD in lung maturation, which may underlie the development of many cases of lung cancer"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19412431",
"endSection": "abstract",
"offsetInBeginSection": 164,
"offsetInEndSection": 463,
"text": "Mutations that truncate and inactivate the carboxyl-terminal deubiquitinating domain of CYLD underlie the development of skin appendage tumors in humans, whereas down-regulation of Cyld expression has been associated with the development of various types of human malignancies including lung cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19412431",
"endSection": "abstract",
"offsetInBeginSection": 1454,
"offsetInEndSection": 1585,
"text": "Our study identifies an important role of CYLD in lung maturation, which may underlie the development of many cases of lung cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19412431",
"endSection": "abstract",
"offsetInBeginSection": 1454,
"offsetInEndSection": 1585,
"text": "Our study identifies an important role of CYLD in lung maturation, which may underlie the development of many cases of lung cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19412431",
"endSection": "abstract",
"offsetInBeginSection": 164,
"offsetInEndSection": 462,
"text": "Mutations that truncate and inactivate the carboxyl-terminal deubiquitinating domain of CYLD underlie the development of skin appendage tumors in humans, whereas down-regulation of Cyld expression has been associated with the development of various types of human malignancies including lung cancer"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19412431",
"endSection": "abstract",
"offsetInBeginSection": 1454,
"offsetInEndSection": 1585,
"text": "Our study identifies an important role of CYLD in lung maturation, which may underlie the development of many cases of lung cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19412431",
"endSection": "abstract",
"offsetInBeginSection": 164,
"offsetInEndSection": 462,
"text": "Mutations that truncate and inactivate the carboxyl-terminal deubiquitinating domain of CYLD underlie the development of skin appendage tumors in humans, whereas down-regulation of Cyld expression has been associated with the development of various types of human malignancies including lung cancer"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19412431",
"endSection": "abstract",
"offsetInBeginSection": 1454,
"offsetInEndSection": 1585,
"text": "Our study identifies an important role of CYLD in lung maturation, which may underlie the development of many cases of lung cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19412431",
"endSection": "abstract",
"offsetInBeginSection": 164,
"offsetInEndSection": 462,
"text": "Mutations that truncate and inactivate the carboxyl-terminal deubiquitinating domain of CYLD underlie the development of skin appendage tumors in humans, whereas down-regulation of Cyld expression has been associated with the development of various types of human malignancies including lung cancer"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19412431",
"endSection": "abstract",
"offsetInBeginSection": 1454,
"offsetInEndSection": 1585,
"text": "Our study identifies an important role of CYLD in lung maturation, which may underlie the development of many cases of lung cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19412431",
"endSection": "abstract",
"offsetInBeginSection": 164,
"offsetInEndSection": 462,
"text": "Mutations that truncate and inactivate the carboxyl-terminal deubiquitinating domain of CYLD underlie the development of skin appendage tumors in humans, whereas down-regulation of Cyld expression has been associated with the development of various types of human malignancies including lung cancer"
}
] | 5 |
BioASQ-training5b
|
[
"http://www.disease-ontology.org/api/metadata/DOID:1324",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D008175"
] |
[] |
5545e926d355485447000002
|
bioasq_yesno
|
factoid
|
Which eye condition is managed by the athens protocol?
|
[['Keratoconus', 'cornea blindness due to severe corneal scarring']]
|
[
"Keratoconus",
"conical cornea",
"keratoconus disease",
"keratoconus syndrome",
"corneal ectasia",
"corneal thinning",
"corneal deformation"
] |
['The athens protocol (transepithelial topography-guided PRK therapeutic remodeling, combined with same-day, collagen cross-linking) was developed for the management of cornea blindness due to severe corneal scarring.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24763473",
"http://www.ncbi.nlm.nih.gov/pubmed/22347790",
"http://www.ncbi.nlm.nih.gov/pubmed/25176050",
"http://www.ncbi.nlm.nih.gov/pubmed/21117539",
"http://www.ncbi.nlm.nih.gov/pubmed/24893359"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24763473",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "Keratoconus management: long-term stability of topography-guided normalization combined with high-fluence CXL stabilization (the Athens Protocol)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24763473",
"endSection": "abstract",
"offsetInBeginSection": 1624,
"offsetInEndSection": 1910,
"text": "The Athens Protocol to arrest keratectasia progression and improve corneal regularity demonstrates safe and effective results as a keratoconus management option. Progressive potential for long-term flattening validates using caution in the surface normalization to avoid overcorrection."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22347790",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 201,
"text": "The management of cornea blindness from severe corneal scarring, with the Athens Protocol (transepithelial topography-guided PRK therapeutic remodeling, combined with same-day, collagen cross-linking)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22347790",
"endSection": "abstract",
"offsetInBeginSection": 8,
"offsetInEndSection": 296,
"text": " To evaluate the safety and efficacy of combined transepithelial topography-guided photorefractive keratectomy (PRK) therapeutic remodeling, combined with same-day, collagen cross-linking (CXL). This protocol was used for the management of cornea blindness due to severe corneal scarring."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24763473",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "Keratoconus management: long-term stability of topography-guided normalization combined with high-fluence CXL stabilization (the Athens Protocol)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21117539",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "Management of corneal ectasia after LASIK with combined, same-day, topography-guided partial transepithelial PRK and collagen cross-linking: the athens protocol."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24893359",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Corneal refractive power and symmetry changes following normalization of ectasias treated with partial topography-guided PTK combined with higher-fluence CXL (the Athens Protocol)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25176050",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 199,
"text": "To compare epithelial remodeling in keratoconic eyes that had photorefractive keratectomy and corneal collagen crosslinking (Athens protocol) with that in untreated keratoconic eyes and healthy eyes."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22347790",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 201,
"text": "The management of cornea blindness from severe corneal scarring, with the Athens Protocol (transepithelial topography-guided PRK therapeutic remodeling, combined with same-day, collagen cross-linking)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21117539",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 307,
"text": "To evaluate a series of patients with corneal ectasia after LASIK that underwent the Athens Protocol: combined topography-guided photorefractive keratectomy (PRK) to reduce or eliminate induced myopia and astigmatism followed by sequential, same-day ultraviolet A (UVA) corneal collagen cross-linking (CXL)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24763473",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "Keratoconus management: long-term stability of topography-guided normalization combined with high-fluence CXL stabilization (the Athens Protocol)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21117539",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "Management of corneal ectasia after LASIK with combined, same-day, topography-guided partial transepithelial PRK and collagen cross-linking: the athens protocol."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24893359",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Corneal refractive power and symmetry changes following normalization of ectasias treated with partial topography-guided PTK combined with higher-fluence CXL (the Athens Protocol)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25176050",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 199,
"text": "To compare epithelial remodeling in keratoconic eyes that had photorefractive keratectomy and corneal collagen crosslinking (Athens protocol) with that in untreated keratoconic eyes and healthy eyes."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22347790",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 201,
"text": "The management of cornea blindness from severe corneal scarring, with the Athens Protocol (transepithelial topography-guided PRK therapeutic remodeling, combined with same-day, collagen cross-linking)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21117539",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 307,
"text": "To evaluate a series of patients with corneal ectasia after LASIK that underwent the Athens Protocol: combined topography-guided photorefractive keratectomy (PRK) to reduce or eliminate induced myopia and astigmatism followed by sequential, same-day ultraviolet A (UVA) corneal collagen cross-linking (CXL)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21117539",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "Management of corneal ectasia after LASIK with combined, same-day, topography-guided partial transepithelial PRK and collagen cross-linking: the athens protocol."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24763473",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "Keratoconus management: long-term stability of topography-guided normalization combined with high-fluence CXL stabilization (the Athens Protocol)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25176050",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 676,
"text": "PURPOSE: To compare epithelial remodeling in keratoconic eyes that had photorefractive keratectomy and corneal collagen crosslinking (Athens protocol) with that in untreated keratoconic eyes and healthy eyes.SETTING: Private clinical practice, Athens, Greece.DESIGN: Comparative case series.METHODS: Fourier-domain anterior segment optical coherence tomography (AS-OCT) was used to obtain in vivo 3-dimensional epithelial thickness maps and center, superior, inferior, maximum, minimum, mean, midperipheral, and variability data.RESULTS: Group A comprised 175 treated keratoconic eyes (Athens protocol); Group B, 193 untreated keratoconic eyes; and Group C, 160 healthy eyes. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24893359",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Corneal refractive power and symmetry changes following normalization of ectasias treated with partial topography-guided PTK combined with higher-fluence CXL (the Athens Protocol)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24763473",
"endSection": "abstract",
"offsetInBeginSection": 1614,
"offsetInEndSection": 1789,
"text": "CONCLUSIONS: The Athens Protocol to arrest keratectasia progression and improve corneal regularity demonstrates safe and effective results as a keratoconus management option. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21117539",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "Management of corneal ectasia after LASIK with combined, same-day, topography-guided partial transepithelial PRK and collagen cross-linking: the athens protocol."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24763473",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "Keratoconus management: long-term stability of topography-guided normalization combined with high-fluence CXL stabilization (the Athens Protocol)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25176050",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 676,
"text": "PURPOSE: To compare epithelial remodeling in keratoconic eyes that had photorefractive keratectomy and corneal collagen crosslinking (Athens protocol) with that in untreated keratoconic eyes and healthy eyes.SETTING: Private clinical practice, Athens, Greece.DESIGN: Comparative case series.METHODS: Fourier-domain anterior segment optical coherence tomography (AS-OCT) was used to obtain in vivo 3-dimensional epithelial thickness maps and center, superior, inferior, maximum, minimum, mean, midperipheral, and variability data.RESULTS: Group A comprised 175 treated keratoconic eyes (Athens protocol); Group B, 193 untreated keratoconic eyes; and Group C, 160 healthy eyes. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24893359",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Corneal refractive power and symmetry changes following normalization of ectasias treated with partial topography-guided PTK combined with higher-fluence CXL (the Athens Protocol)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24763473",
"endSection": "abstract",
"offsetInBeginSection": 1614,
"offsetInEndSection": 1789,
"text": "CONCLUSIONS: The Athens Protocol to arrest keratectasia progression and improve corneal regularity demonstrates safe and effective results as a keratoconus management option. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21117539",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "Management of corneal ectasia after LASIK with combined, same-day, topography-guided partial transepithelial PRK and collagen cross-linking: the athens protocol."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24763473",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "Keratoconus management: long-term stability of topography-guided normalization combined with high-fluence CXL stabilization (the Athens Protocol)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25176050",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 676,
"text": "PURPOSE: To compare epithelial remodeling in keratoconic eyes that had photorefractive keratectomy and corneal collagen crosslinking (Athens protocol) with that in untreated keratoconic eyes and healthy eyes.SETTING: Private clinical practice, Athens, Greece.DESIGN: Comparative case series.METHODS: Fourier-domain anterior segment optical coherence tomography (AS-OCT) was used to obtain in vivo 3-dimensional epithelial thickness maps and center, superior, inferior, maximum, minimum, mean, midperipheral, and variability data.RESULTS: Group A comprised 175 treated keratoconic eyes (Athens protocol); Group B, 193 untreated keratoconic eyes; and Group C, 160 healthy eyes. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24893359",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Corneal refractive power and symmetry changes following normalization of ectasias treated with partial topography-guided PTK combined with higher-fluence CXL (the Athens Protocol)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24763473",
"endSection": "abstract",
"offsetInBeginSection": 1614,
"offsetInEndSection": 1789,
"text": "CONCLUSIONS: The Athens Protocol to arrest keratectasia progression and improve corneal regularity demonstrates safe and effective results as a keratoconus management option. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21117539",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "Management of corneal ectasia after LASIK with combined, same-day, topography-guided partial transepithelial PRK and collagen cross-linking: the athens protocol."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24763473",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "Keratoconus management: long-term stability of topography-guided normalization combined with high-fluence CXL stabilization (the Athens Protocol)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25176050",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 676,
"text": "PURPOSE: To compare epithelial remodeling in keratoconic eyes that had photorefractive keratectomy and corneal collagen crosslinking (Athens protocol) with that in untreated keratoconic eyes and healthy eyes.SETTING: Private clinical practice, Athens, Greece.DESIGN: Comparative case series.METHODS: Fourier-domain anterior segment optical coherence tomography (AS-OCT) was used to obtain in vivo 3-dimensional epithelial thickness maps and center, superior, inferior, maximum, minimum, mean, midperipheral, and variability data.RESULTS: Group A comprised 175 treated keratoconic eyes (Athens protocol); Group B, 193 untreated keratoconic eyes; and Group C, 160 healthy eyes. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24893359",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Corneal refractive power and symmetry changes following normalization of ectasias treated with partial topography-guided PTK combined with higher-fluence CXL (the Athens Protocol)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24763473",
"endSection": "abstract",
"offsetInBeginSection": 1614,
"offsetInEndSection": 1789,
"text": "CONCLUSIONS: The Athens Protocol to arrest keratectasia progression and improve corneal regularity demonstrates safe and effective results as a keratoconus management option. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21117539",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "Management of corneal ectasia after LASIK with combined, same-day, topography-guided partial transepithelial PRK and collagen cross-linking: the athens protocol."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24763473",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "Keratoconus management: long-term stability of topography-guided normalization combined with high-fluence CXL stabilization (the Athens Protocol)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25176050",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 676,
"text": "PURPOSE: To compare epithelial remodeling in keratoconic eyes that had photorefractive keratectomy and corneal collagen crosslinking (Athens protocol) with that in untreated keratoconic eyes and healthy eyes.SETTING: Private clinical practice, Athens, Greece.DESIGN: Comparative case series.METHODS: Fourier-domain anterior segment optical coherence tomography (AS-OCT) was used to obtain in vivo 3-dimensional epithelial thickness maps and center, superior, inferior, maximum, minimum, mean, midperipheral, and variability data.RESULTS: Group A comprised 175 treated keratoconic eyes (Athens protocol); Group B, 193 untreated keratoconic eyes; and Group C, 160 healthy eyes. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24893359",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Corneal refractive power and symmetry changes following normalization of ectasias treated with partial topography-guided PTK combined with higher-fluence CXL (the Athens Protocol)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24763473",
"endSection": "abstract",
"offsetInBeginSection": 1614,
"offsetInEndSection": 1789,
"text": "CONCLUSIONS: The Athens Protocol to arrest keratectasia progression and improve corneal regularity demonstrates safe and effective results as a keratoconus management option. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21117539",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 307,
"text": "To evaluate a series of patients with corneal ectasia after LASIK that underwent the Athens Protocol: combined topography-guided photorefractive keratectomy (PRK) to reduce or eliminate induced myopia and astigmatism followed by sequential, same-day ultraviolet A (UVA) corneal collagen cross-linking (CXL)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25176050",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 243,
"text": "To compare epithelial remodeling in keratoconic eyes that had photorefractive keratectomy and corneal collagen crosslinking (Athens protocol) with that in untreated keratoconic eyes and healthy eyes. Private clinical practice, Athens, Greece."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25176050",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 200,
"text": "To compare epithelial remodeling in keratoconic eyes that had photorefractive keratectomy and corneal collagen crosslinking (Athens protocol) with that in untreated keratoconic eyes and healthy eyes."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.disease-ontology.org/api/metadata/DOID:10428",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D005123"
] |
[] |
56bdc79bef6e394741000001
|
bioasq_factoid
|
factoid
|
What is liquid liquid phase transition?
|
['membrane-free microcompartments']
|
[
"membrane-free microcompartments",
"membrane-less microcompartments",
"cytosolic microcompartments",
"biomolecular condensates",
"liquid-like microcompartments",
"non-membrane-bound microcompartments"
] |
['The influence of membrane-free microcompartments resulting from crowding-induced liquid/liquid phase separation (LLPS) on the dynamic spatial organization of FtsZ, the main component of the bacterial division machinery, has been studied using several LLPS systems.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27725777",
"http://www.ncbi.nlm.nih.gov/pubmed/28980860",
"http://www.ncbi.nlm.nih.gov/pubmed/25436423"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28980860",
"endSection": "abstract",
"offsetInBeginSection": 980,
"offsetInEndSection": 1190,
"text": "engaged in or are at least related to the physiological liquid-liquid phase transitions (LLPTs) leading to the formation of various proteinaceous membrane-less organelles (PMLOs), both normal and pathological. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27725777",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 264,
"text": "The influence of membrane-free microcompartments resulting from crowding-induced liquid/liquid phase separation (LLPS) on the dynamic spatial organization of FtsZ, the main component of the bacterial division machinery, has been studied using several LLPS systems."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25436423",
"endSection": "abstract",
"offsetInBeginSection": 6,
"offsetInEndSection": 193,
"text": "we hypothesize that intrinsically disordered proteins (IDPs) serve as important drivers of the intracellular liquid-liquid phase separations that generate various membrane-less organelles"
}
] | 11 |
BioASQ-training11b
| null | null |
5aa6c800d6d6b54f79000012
|
bioasq_factoid
|
factoid
|
Which is the primary protein component of Lewy bodies?
|
['alpha-synuclein', 'α-synuclein', 'αSyn']
|
[
"alpha-synuclein",
"α-synuclein",
"αSyn",
"SNCA",
"non-Aβ component of Alzheimer's disease amyloid",
"NACP",
"synuclein alpha"
] |
['The primary protein component of Lewy bodies are fibrils composed of alpha-synuclein.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23180276",
"http://www.ncbi.nlm.nih.gov/pubmed/11814405",
"http://www.ncbi.nlm.nih.gov/pubmed/10722726",
"http://www.ncbi.nlm.nih.gov/pubmed/20551689",
"http://www.ncbi.nlm.nih.gov/pubmed/24252509",
"http://www.ncbi.nlm.nih.gov/pubmed/12541013",
"http://www.ncbi.nlm.nih.gov/pubmed/23965852",
"http://www.ncbi.nlm.nih.gov/pubmed/10327208",
"http://www.ncbi.nlm.nih.gov/pubmed/18510319",
"http://www.ncbi.nlm.nih.gov/pubmed/22843682",
"http://www.ncbi.nlm.nih.gov/pubmed/24058647",
"http://www.ncbi.nlm.nih.gov/pubmed/26667592",
"http://www.ncbi.nlm.nih.gov/pubmed/23344955",
"http://www.ncbi.nlm.nih.gov/pubmed/18607609",
"http://www.ncbi.nlm.nih.gov/pubmed/10764738",
"http://www.ncbi.nlm.nih.gov/pubmed/11440819",
"http://www.ncbi.nlm.nih.gov/pubmed/23557146",
"http://www.ncbi.nlm.nih.gov/pubmed/22516611",
"http://www.ncbi.nlm.nih.gov/pubmed/9726379",
"http://www.ncbi.nlm.nih.gov/pubmed/16452621",
"http://www.ncbi.nlm.nih.gov/pubmed/24392030",
"http://www.ncbi.nlm.nih.gov/pubmed/26502720",
"http://www.ncbi.nlm.nih.gov/pubmed/10825478",
"http://www.ncbi.nlm.nih.gov/pubmed/17899395",
"http://www.ncbi.nlm.nih.gov/pubmed/11900526",
"http://www.ncbi.nlm.nih.gov/pubmed/19475665",
"http://www.ncbi.nlm.nih.gov/pubmed/12722831",
"http://www.ncbi.nlm.nih.gov/pubmed/18508479",
"http://www.ncbi.nlm.nih.gov/pubmed/10762166",
"http://www.ncbi.nlm.nih.gov/pubmed/20617407",
"http://www.ncbi.nlm.nih.gov/pubmed/26401513",
"http://www.ncbi.nlm.nih.gov/pubmed/11085897",
"http://www.ncbi.nlm.nih.gov/pubmed/23796501",
"http://www.ncbi.nlm.nih.gov/pubmed/12122208",
"http://www.ncbi.nlm.nih.gov/pubmed/14502650",
"http://www.ncbi.nlm.nih.gov/pubmed/16319716",
"http://www.ncbi.nlm.nih.gov/pubmed/24586691",
"http://www.ncbi.nlm.nih.gov/pubmed/9600990",
"http://www.ncbi.nlm.nih.gov/pubmed/22483285",
"http://www.ncbi.nlm.nih.gov/pubmed/26161848",
"http://www.ncbi.nlm.nih.gov/pubmed/25846226",
"http://www.ncbi.nlm.nih.gov/pubmed/11816795",
"http://www.ncbi.nlm.nih.gov/pubmed/11207422",
"http://www.ncbi.nlm.nih.gov/pubmed/16343531",
"http://www.ncbi.nlm.nih.gov/pubmed/20890676"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24058647",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 222,
"text": "Aggregation of α-synuclein (αSyn), the primary protein component in Lewy body inclusions of patients with Parkinson's disease, arises when the normally soluble intrinsically disordered protein converts to amyloid fibrils. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22483285",
"endSection": "abstract",
"offsetInBeginSection": 245,
"offsetInEndSection": 500,
"text": "The primary structural component of Lewy bodies are fibrils composed primarily of alpha-synuclein, a highly conserved 140 amino acid protein that is predominantly expressed in neurons and which may play a role in synaptic plasticity and neurotransmission."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22516611",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "Fibrillar α-synuclein (AS) is the major component of Lewy bodies, the pathological hallmark of Parkinson's disease. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19475665",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "Alpha-synuclein (alphaS) is the primary component of Lewy bodies, the pathological hallmark of Parkinson's Disease. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18510319",
"endSection": "abstract",
"offsetInBeginSection": 578,
"offsetInEndSection": 827,
"text": "For alpha-synuclein, the major protein component of Lewy bodies associated with Parkinson's disease, we have used a combination of ssNMR and biochemical data to identify the key region for self-aggregation of the protein as residues 77-82 (VAQKTV). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17899395",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 134,
"text": "The protein alpha-synuclein (AS) is the primary fibrillar component of Lewy bodies, the pathological hallmark of Parkinson's disease. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10327208",
"endSection": "abstract",
"offsetInBeginSection": 159,
"offsetInEndSection": 276,
"text": "Recently, the presynaptic protein alpha-synuclein was shown to be a major component of Lewy bodies and Lewy neurites."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9726379",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "Alpha-synuclein forms the major component of Lewy bodies and Lewy neurites, the defining neuropathological characteristics of Parkinson's disease and dementia with Lewy bodies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20617407",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "á-Synuclein is the major protein component of Lewy bodies--the pathological hallmark of Parkinson's disease (PD) and Dementia with Lewy bodies (DLB)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11085897",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "alpha-Synuclein and ubiquitin are two Lewy body protein components that may play antagonistic roles in the pathogenesis of Lewy bodies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11085897",
"endSection": "abstract",
"offsetInBeginSection": 926,
"offsetInEndSection": 1089,
"text": "The segregation of alpha-synuclein to Lewy body peripheral domain is consistent with the hypothesis that alpha-synuclein is continually deposited onto Lewy bodies."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22843682",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "Identification of protein interfaces between α-synuclein, the principal component of Lewy bodies in Parkinson disease, and the molecular chaperones human Hsc70 and the yeast Ssa1p"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18508479",
"endSection": "abstract",
"offsetInBeginSection": 374,
"offsetInEndSection": 634,
"text": "Whereas approximately 550 proteins were identified in the LB-enriched sample by mass spectrometry, quantitative comparison with the control sample revealed that approximately 40 proteins were co-enriched with alpha-synuclein, the major component in Lewy bodies"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24252509",
"endSection": "abstract",
"offsetInBeginSection": 509,
"offsetInEndSection": 1085,
"text": "This apparent conflict in protein levels might have arisen from examining Lewy body disease cases with coexisting Alzheimer-type pathologies.To assess whether ATP13A2 levels in Lewy body disease are modified by Alzheimer-type β-amyloid deposition, we evaluated cases of pure PD and pure dementia with Lewy bodies (DLB) for changes in ATP13A2, α-synuclein and β-amyloid protein levels in cortical regions with and without Lewy bodies.In all Lewy body disease cases, we identified decreased ATP13A2 protein levels that correlated with increases in both α-synuclein and β-amyloid"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24252509",
"endSection": "abstract",
"offsetInBeginSection": 1087,
"offsetInEndSection": 1444,
"text": "Partial colocalization was observed between ATP13A2 and α-synuclein in Lewy bodies, whereas ATP13A2 did not colocalize with pathological β-amyloid deposition.Our data show that patients with Lewy body diseases have an overall deficit in ATP13A2 protein levels, with the remaining protein being more insoluble and partially redistributing towards Lewy bodies"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22843682",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Identification of protein interfaces between α-synuclein, the principal component of Lewy bodies in Parkinson disease, and the molecular chaperones human Hsc70 and the yeast Ssa1p."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23557146",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 175,
"text": "Human α-synuclein is a small-sized, natively unfolded protein that in fibrillar form is the primary component of Lewy bodies, the pathological hallmark of Parkinson's disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20890676",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 308,
"text": "Parkinson's disease is the most common neurodegenerative movement disorder. α-Synuclein is a small synaptic protein that has been linked to familial Parkinson's disease (PD) and is also the primary component of Lewy bodies, the hallmark neuropathology found in the brain of sporadic and familial PD patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17899395",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "The protein alpha-synuclein (AS) is the primary fibrillar component of Lewy bodies, the pathological hallmark of Parkinson's disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23344955",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 107,
"text": "α-Synuclein is an abundant presynaptic protein and a primary component of Lewy bodies in Parkinson disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16343531",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 134,
"text": "The natively disordered protein alpha-synuclein is the primary component of Lewy bodies, the cellular hallmark of Parkinson's disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23965852",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 301,
"text": "Common cellular and molecular mechanisms including protein aggregation and inclusion body formation are involved in many neurodegenerative diseases. α-Synuclein is a major component of Lewy bodies in Parkinson's disease (PD) as well as in glial cytoplasmic inclusions in multiple system atrophy (MSA)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23796501",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Alpha-synuclein (α-Syn) is the principal protein component of Lewy bodies, a pathological hallmark of Parkinson's disease (PD)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10327208",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 276,
"text": "Lewy bodies and coarse Lewy neurites are the pathological hallmarks of degenerating neurons in the brains of patients suffering from Parkinson's disease (PD). Recently, the presynaptic protein alpha-synuclein was shown to be a major component of Lewy bodies and Lewy neurites."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10327208",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 433,
"text": "Lewy bodies and coarse Lewy neurites are the pathological hallmarks of degenerating neurons in the brains of patients suffering from Parkinson's disease (PD). Recently, the presynaptic protein alpha-synuclein was shown to be a major component of Lewy bodies and Lewy neurites. This study demonstrates for the first time that extensive and thin alpha-synuclein-immunoreactive inclusions are present in the axonal processes of neurons."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20617407",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 249,
"text": "á-Synuclein is the major protein component of Lewy bodies--the pathological hallmark of Parkinson's disease (PD) and Dementia with Lewy bodies (DLB). Its accumulation into intracellular aggregates is implicated in the process of Lewy body formation."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9726379",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "Filamentous alpha-synuclein inclusions link multiple system atrophy with Parkinson's disease and dementia with Lewy bodies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26667592",
"endSection": "abstract",
"offsetInBeginSection": 199,
"offsetInEndSection": 330,
"text": "Lewy bodies comprise of aggregated intracellular vesicles and proteins and α-synuclein is reported to be a major protein component."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10764738",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Microtubule-associated protein 1B is a component of cortical Lewy bodies and binds alpha-synuclein filaments."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9600990",
"endSection": "abstract",
"offsetInBeginSection": 1267,
"offsetInEndSection": 1384,
"text": "These findings indicate that alpha-synuclein forms the major filamentous component of Lewy bodies and Lewy neurites.."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11816795",
"endSection": "abstract",
"offsetInBeginSection": 1180,
"offsetInEndSection": 1405,
"text": "The protein alpha-synuclein appears to be an important structural component of Lewy bodies, an observation spurred by the discovery of point mutations in the alpha-synuclein gene linked to rare cases of autosomal dominant PD."
}
] | 6 |
BioASQ-training6b
|
[
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D016631",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D051844"
] | null |
58a2e5f760087bc10a000007
|
bioasq_factoid
|
factoid
|
Where, in what US state, was there a measles outbreak in an Amish community
|
['Ohio']
|
[
"Ohio",
"Buckeye State",
"OH"
] |
['The measles outbreak started an Amish community in Ohio']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28302434",
"http://www.ncbi.nlm.nih.gov/pubmed/26103154",
"http://www.ncbi.nlm.nih.gov/pubmed/27705270"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28302434",
"endSection": "abstract",
"offsetInBeginSection": 395,
"offsetInEndSection": 474,
"text": "Recent outbreaks in Amish communities include a 2014 measles outbreak in Ohio, "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26103154",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Measles outbreaks in the United States continue to occur in subpopulations with sufficient numbers of undervaccinated individuals, with a 2014 outbreak in Amish communities in Ohio"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27705270",
"endSection": "abstract",
"offsetInBeginSection": 1607,
"offsetInEndSection": 1874,
"text": "CONCLUSIONS\nThe key epidemiologic features of a measles outbreak in the Amish community in Ohio were transmission primarily within households, the small proportion of Amish people affected, and the large number of people in the Amish community who sought vaccination."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26103154",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 267,
"text": "Measles outbreaks in the United States continue to occur in subpopulations with sufficient numbers of undervaccinated individuals, with a 2014 outbreak in Amish communities in Ohio pushing the annual cases to the highest national number reported in the last 20 years."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28302434",
"endSection": "abstract",
"offsetInBeginSection": 394,
"offsetInEndSection": 505,
"text": "Recent outbreaks in Amish communities include a 2014 measles outbreak in Ohio, resulting in 368 cases reported."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27705270",
"endSection": "abstract",
"offsetInBeginSection": 1607,
"offsetInEndSection": 1874,
"text": "CONCLUSIONS The key epidemiologic features of a measles outbreak in the Amish community in Ohio were transmission primarily within households, the small proportion of Amish people affected, and the large number of people in the Amish community who sought vaccination."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26103154",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 359,
"text": "Modeling Measles Transmission in the North American Amish and Options for Outbreak Response.Measles outbreaks in the United States continue to occur in subpopulations with sufficient numbers of undervaccinated individuals, with a 2014 outbreak in Amish communities in Ohio pushing the annual cases to the highest national number reported in the last 20 years. "
}
] | 11 |
BioASQ-training11b
| null | null |
5c5312097e3cb0e231000011
|
bioasq_factoid
|
factoid
|
What is the genetic cause of Roberts syndrome?
|
['Roberts syndrome (RBS) is a human developmental disorder caused by mutations in the cohesin acetyltransferase ESCO2.']
|
[
"Roberts syndrome",
"RBS",
"Roberts syndrome (RBS)",
"Cohesin acetyltransferase ESCO2"
] |
['Roberts syndrome (RBS) is a human developmental disorder caused by mutations in the cohesin acetyltransferase ESCO2.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26729373",
"http://www.ncbi.nlm.nih.gov/pubmed/29084713",
"http://www.ncbi.nlm.nih.gov/pubmed/26710928",
"http://www.ncbi.nlm.nih.gov/pubmed/28934466",
"http://www.ncbi.nlm.nih.gov/pubmed/28422453"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28934466",
"endSection": "abstract",
"offsetInBeginSection": 163,
"offsetInEndSection": 318,
"text": " Mutations in Esco2 cause Roberts syndrome, a developmental disease characterized by severe prenatal retardation as well as limb and facial abnormalities. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28422453",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 190,
"text": "Genetic mapping studies reveal that mutations in cohesion pathways are responsible for multispectrum developmental abnormalities termed cohesinopathies. These include Roberts syndrome (RBS),"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26710928",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 202,
"text": "Roberts syndrome and SC phocomelia syndrome are rare autosomal recessive genetic disorders representing the extremes of the spectrum of severity of the same condition, caused by mutations in ESCO2 gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26729373",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 128,
"text": " Roberts syndrome (RBS) is a human developmental disorder caused by mutations in the cohesin acetyltransferase ESCO2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29084713",
"endSection": "abstract",
"offsetInBeginSection": 518,
"offsetInEndSection": 700,
"text": "RBS arises due to autosomal recessive mutations in cohesin auxiliary factorESCO2, the gene that encodes an N-acetyltransferase which targets the SMC3 subunit of the cohesin complex. "
}
] | 11 |
BioASQ-training11b
| null | null |
5ad35d01133db5eb78000003
|
bioasq_factoid
|
factoid
|
Idecabtagene vicleucel can be used for treatment of which disease?
|
['Multiple Myeloma']
|
[
"Multiple Myeloma",
"Plasma Cell Myeloma",
"Myeloma",
"Kahler's Disease",
"Myelomatosis"
] |
['Idecabtagene vicleucel was shown to be effective for Relapsed and Refractory Multiple Myeloma.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34461271",
"http://www.ncbi.nlm.nih.gov/pubmed/34256668",
"http://www.ncbi.nlm.nih.gov/pubmed/33896344",
"http://www.ncbi.nlm.nih.gov/pubmed/34527606",
"http://www.ncbi.nlm.nih.gov/pubmed/34625232",
"http://www.ncbi.nlm.nih.gov/pubmed/33626253",
"http://www.ncbi.nlm.nih.gov/pubmed/33598857",
"http://www.ncbi.nlm.nih.gov/pubmed/34854741",
"http://www.ncbi.nlm.nih.gov/pubmed/34104374",
"http://www.ncbi.nlm.nih.gov/pubmed/34145225"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34461271",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 342,
"text": "B-cell maturation antigen (BCMA) has become a key target for antibody-drug conjugates, bispecific antibodies, chimeric antigen receptor T-cell therapies, and other immunotherapies in multiple myeloma. Some of these agents such as belantamab mafodotin and idecabtagene vicleucel have already received regulatory approval in the United States. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34527606",
"endSection": "abstract",
"offsetInBeginSection": 1113,
"offsetInEndSection": 1321,
"text": "These include isatuximab (also anti-CD38) and, in the past year, the antibody-drug conjugate (ADC) belantamab mafodotin and the chimeric antigen receptor (CAR) T-cell product idecabtagene vicleucel (ide-cel)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34256668",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "Matching-adjusted indirect comparison of efficacy outcomes for ciltacabtagene autoleucel in CARTITUDE-1 versus idecabtagene vicleucel in KarMMa for the treatment of patients with relapsed or refractory multiple myeloma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34145225",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "KarMMa-RW: comparison of idecabtagene vicleucel with real-world outcomes in relapsed and refractory multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34145225",
"endSection": "abstract",
"offsetInBeginSection": 233,
"offsetInEndSection": 406,
"text": "Idecabtagene vicleucel (ide-cel, bb2121), a BCMA-directed CAR T-cell therapy, demonstrated efficacy in triple-class exposed RRMM patients in the KarMMa trial (NCT03361748). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33626253",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 67,
"text": "Idecabtagene Vicleucel in Relapsed and Refractory Multiple Myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33626253",
"endSection": "abstract",
"offsetInBeginSection": 1917,
"offsetInEndSection": 2100,
"text": "CONCLUSIONS: Ide-cel induced responses in a majority of heavily pretreated patients with refractory and relapsed myeloma; MRD-negative status was achieved in 26% of treated patients. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34104374",
"endSection": "abstract",
"offsetInBeginSection": 1633,
"offsetInEndSection": 1822,
"text": "Here, we will discuss the preclinical and clinical development of idecabtagene vicleucel and its future role in the changing treatment landscape of relapsed and refractory multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34104374",
"endSection": "abstract",
"offsetInBeginSection": 1207,
"offsetInEndSection": 1632,
"text": "After the recent publication of the results of a phase II trial confirming a notable efficacy and acceptable safety profile, idecabtagene vicleucel is the first CAR-T to gain regulatory US Food and Drug Administration approval to treat refractory multiple myeloma patients who have already been exposed to antibodies against CD38, proteasome inhibitors, and immunomodulatory agents and who are refractory to the last therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33598857",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 337,
"text": "BACKGROUND AND OBJECTIVE: Registrational trials for ciltacabtagene autoleucel [cilta-cel]) and idecabtagene vicleucel [ide-cel] chimeric antigen receptor T-cell (CAR-T) therapies were single-arm studies conducted with relapse refractory multiple myeloma (MM) patients who were triple-class-exposed (TCE) or triple-class-refractory (TCR)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33626253",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 276,
"text": "BACKGROUND: Idecabtagene vicleucel (ide-cel, also called bb2121), a B-cell maturation antigen-directed chimeric antigen receptor (CAR) T-cell therapy, has shown clinical activity with expected CAR T-cell toxic effects in patients with relapsed and refractory multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33896344",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 325,
"text": "Idecabtagene vicleucel (ide-cel, bb2121), a chimeric antigen receptor (CAR) T cell therapy, has been investigated in patients with relapsed and refractory multiple myeloma (RRMM) who have received an immunomodulatory drug, proteasome inhibitor, and anti-CD38 antibody in the single-arm phase 2 KarMMa clinical trial. Two ther"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33626253",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 269,
"text": "BACKGROUND: Idecabtagene vicleucel (ide-cel, also called bb2121), a B-cell maturation antigen-directed chimeric antigen receptor (CAR) T-cell therapy, has shown clinical activity with expected CAR T-cell toxic effects in patients with relapsed and refractory multiple m"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34104374",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 98,
"text": "The role of idecabtagene vicleucel in patients with heavily pretreated refractory multiple myeloma"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34104374",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "The role of idecabtagene vicleucel in patients with heavily pretreated refractory multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33896344",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 316,
"text": "Idecabtagene vicleucel (ide-cel, bb2121), a chimeric antigen receptor (CAR) T cell therapy, has been investigated in patients with relapsed and refractory multiple myeloma (RRMM) who have received an immunomodulatory drug, proteasome inhibitor, and anti-CD38 antibody in the single-arm phase 2 KarMMa clinical trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34854741",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 341,
"text": "Idecabtagene vicleucel (ide-cel), a novel chimeric antigen receptor (CAR) T-cell therapy targeting B-cell maturation antigen (BCMA), has recently gained approval by the US FDA for relapsed and refractory multiple myeloma (RRMM) after multicenter trials have demonstrated unprecedented results in this difficult-to-treat subgroup of patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34854741",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 97,
"text": "Idecabtagene vicleucel (ide-cel) CAR T-cell therapy for relapsed and refractory multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33626253",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 392,
"text": "BACKGROUND: Idecabtagene vicleucel (ide-cel, also called bb2121), a B-cell maturation antigen-directed chimeric antigen receptor (CAR) T-cell therapy, has shown clinical activity with expected CAR T-cell toxic effects in patients with relapsed and refractory multiple myeloma.METHODS: In this phase 2 study, we sought to confirm the efficacy and safety of ide-cel in patients with relapsed an"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34625232",
"endSection": "abstract",
"offsetInBeginSection": 499,
"offsetInEndSection": 886,
"text": "The bulk of CAR T-cell constructs currently in clinical development target the B-cell maturation antigen (BCMA) and to date only idecabtagene vicleucel (ide-cel) is approved by the Food and Drug Administration (FDA) for commercial use in adult patients with relapsed or refractory MM based on the promising clinical responses and positive safety record shown in the pivotal KarMMa study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34145225",
"endSection": "abstract",
"offsetInBeginSection": 233,
"offsetInEndSection": 405,
"text": "Idecabtagene vicleucel (ide-cel, bb2121), a BCMA-directed CAR T-cell therapy, demonstrated efficacy in triple-class exposed RRMM patients in the KarMMa trial (NCT03361748)."
}
] | 11 |
BioASQ-training11b
| null | null |
61f7ce26882a024a1000002d
|
bioasq_factoid
|
factoid
|
What is the aim of the "Radiogenomics Consortium"?
|
['Pre-identification of people who are at greatest risk for adverse effects resulting from cancer treatment using radiation.']
|
[
"Pre-identification of people who are at greatest risk for adverse effects resulting from cancer treatment using radiation",
"Radiation treatment risk assessment",
"Cancer treatment risk identification",
"Radiation therapy risk evaluation",
"Adverse effect prediction in cancer treatment",
"Risk stratification for radiation therapy"
] |
['A major aim of research in radiogenomics is the development of a predictive instrument to enable identification of people who are at greatest risk for adverse effects resulting from cancer treatment using radiation. An important effort to advance radiobiology in the genomic era was establishment of the Radiogenomics Consortium to enable the creation of the large radiotherapy cohorts required to exploit advances in genomics.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27515689",
"http://www.ncbi.nlm.nih.gov/pubmed/29888979",
"http://www.ncbi.nlm.nih.gov/pubmed/27979370",
"http://www.ncbi.nlm.nih.gov/pubmed/28865512"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29888979",
"endSection": "abstract",
"offsetInBeginSection": 1167,
"offsetInEndSection": 1378,
"text": "An important effort to advance radiobiology in the genomic era was establishment of the Radiogenomics Consortium to enable the creation of the large radiotherapy cohorts required to exploit advances in genomics."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28865512",
"endSection": "abstract",
"offsetInBeginSection": 977,
"offsetInEndSection": 1192,
"text": "A major aim of research in radiogenomics is the development of a predictive instrument to enable identification of people who are at greatest risk for adverse effects resulting from cancer treatment using radiation."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27979370",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 92,
"text": "Optimal design and patient selection for interventional trials using radiogenomic biomarkers"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27515689",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 311,
"text": "Nearly 50% of cancer patients undergo radiotherapy. Late radiotherapy toxicity affects quality-of-life in long-term cancer survivors and risk of side-effects in a minority limits doses prescribed to the majority of patients. Development of a test predicting risk of toxicity could benefit many cancer patients. "
}
] | 11 |
BioASQ-training11b
| null | null |
5e48efd9f8b2df0d49000004
|
bioasq_factoid
|
factoid
|
Which intermediate filament (IF) protein can be used as a non-specific marker of the neuronal precursor cells of the subventricular zone?
|
[['Nestin']]
|
[
"Nestin",
"Nestin protein",
"Nestin isoform",
"Nestin (NES)",
"Neuroepithelial stem cell protein Nestin"
] |
["Nestin can be used as a nonspecific marker protein for precursor cells in the subventricular zone (SVZ). Nestin is a unique intermediate filament protein. While it is robustly expressed in developing brain, postnatal expression is limited to the brain's SVZ."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23407958",
"http://www.ncbi.nlm.nih.gov/pubmed/20552272",
"http://www.ncbi.nlm.nih.gov/pubmed/21527990",
"http://www.ncbi.nlm.nih.gov/pubmed/15056462",
"http://www.ncbi.nlm.nih.gov/pubmed/11078926",
"http://www.ncbi.nlm.nih.gov/pubmed/14715941",
"http://www.ncbi.nlm.nih.gov/pubmed/15458607",
"http://www.ncbi.nlm.nih.gov/pubmed/23131160",
"http://www.ncbi.nlm.nih.gov/pubmed/12812760",
"http://www.ncbi.nlm.nih.gov/pubmed/10802345",
"http://www.ncbi.nlm.nih.gov/pubmed/16567040",
"http://www.ncbi.nlm.nih.gov/pubmed/17717696",
"http://www.ncbi.nlm.nih.gov/pubmed/22027098",
"http://www.ncbi.nlm.nih.gov/pubmed/11294470",
"http://www.ncbi.nlm.nih.gov/pubmed/16647786"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15056462",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 174,
"text": "Nestin is a unique intermediate filament protein. While it is robustly expressed in developing brain, postnatal expression is limited to the brain's subventricular zone (SVZ)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11078926",
"endSection": "abstract",
"offsetInBeginSection": 394,
"offsetInEndSection": 465,
"text": "nestin, a marker protein for precursor cells in the subventricular zone"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21527990",
"endSection": "abstract",
"offsetInBeginSection": 29,
"offsetInEndSection": 101,
"text": "adult subventricular zone (SVZ) stem and progenitor cells express nestin"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20552272",
"endSection": "abstract",
"offsetInBeginSection": 597,
"offsetInEndSection": 646,
"text": "the typical protein of neural progenitors, nestin"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23407958",
"endSection": "abstract",
"offsetInBeginSection": 631,
"offsetInEndSection": 675,
"text": "the nonspecific precursor cell marker Nestin"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14715941",
"endSection": "abstract",
"offsetInBeginSection": 969,
"offsetInEndSection": 1130,
"text": "In the subventricular zone, this effect was exerted selectively on a precursor subpopulation expressing nestin but not neuronal or glial cell-specific proteins."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23131160",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 172,
"text": "Nestin is an intermediate filament protein expressed in neuroepithelial stem cells during development and it is later replaced by cell specific neuronal or glial filaments."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11078926",
"endSection": "abstract",
"offsetInBeginSection": 221,
"offsetInEndSection": 485,
"text": "The results indicate that administration of thyroid hormone and retinoic acid increases the expression of Ki67, a nuclear antigen associated with cell proliferation, and of nestin, a marker protein for precursor cells in the subventricular zone of adult male rats."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16647786",
"endSection": "abstract",
"offsetInBeginSection": 584,
"offsetInEndSection": 668,
"text": "Only a minority of stem cells expressed nestin, a marker for neural precursor cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11294470",
"endSection": "abstract",
"offsetInBeginSection": 481,
"offsetInEndSection": 702,
"text": "In addition, bone marrow transplantation promoted proliferation of ependymal and subependymal cells, identified by nestin (a neuroepithelial stem cell marker), within the ventricular zone and subventricular zone (VZ/SVZ)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11078926",
"endSection": "abstract",
"offsetInBeginSection": 221,
"offsetInEndSection": 484,
"text": "The results indicate that administration of thyroid hormone and retinoic acid increases the expression of Ki67, a nuclear antigen associated with cell proliferation, and of nestin, a marker protein for precursor cells in the subventricular zone of adult male rats"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11078926",
"endSection": "abstract",
"offsetInBeginSection": 221,
"offsetInEndSection": 484,
"text": "The results indicate that administration of thyroid hormone and retinoic acid increases the expression of Ki67, a nuclear antigen associated with cell proliferation, and of nestin, a marker protein for precursor cells in the subventricular zone of adult male rats"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12812760",
"endSection": "abstract",
"offsetInBeginSection": 493,
"offsetInEndSection": 653,
"text": "In all animals, 20-40% of the newly generated cells in the dentate gyrus and subventricular zone expressed the neural progenitor cell markers Musashi1 or Nestin"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11078926",
"endSection": "abstract",
"offsetInBeginSection": 221,
"offsetInEndSection": 484,
"text": "The results indicate that administration of thyroid hormone and retinoic acid increases the expression of Ki67, a nuclear antigen associated with cell proliferation, and of nestin, a marker protein for precursor cells in the subventricular zone of adult male rats"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11078926",
"endSection": "abstract",
"offsetInBeginSection": 221,
"offsetInEndSection": 484,
"text": "The results indicate that administration of thyroid hormone and retinoic acid increases the expression of Ki67, a nuclear antigen associated with cell proliferation, and of nestin, a marker protein for precursor cells in the subventricular zone of adult male rats"
}
] | 5 |
BioASQ-training5b
|
[
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0005882",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0021849"
] |
[] |
5540ca8a0083d1bf0e000003
|
bioasq_factoid
|
factoid
|
Which is the cellular target of gefitinib?
|
['Epidermal growth factor receptor (EGFR)']
|
[
"Epidermal growth factor receptor (EGFR)",
"EGFR",
"ErbB-1",
"HER1",
"CD326",
"epidermal growth factor receptor",
"epidermal growth factor receptor 1"
] |
The specific cellular target of Gefitinib (Iressa) is the epidermal growth factor receptor (EGFR).
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23255952",
"http://www.ncbi.nlm.nih.gov/pubmed/19276163",
"http://www.ncbi.nlm.nih.gov/pubmed/18089711"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23255952",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 126,
"text": "Gefitinib, the specific inhibitor of the epidermal growth factor receptor (EGFR), may cause growth delay in cancer cell lines."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19276163",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "Gefitinib (Iressa) is a specific and effective epidermal growth factor receptor inhibitor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18089711",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 185,
"text": "Gefitinib is a specific inhibitor of the epidermal growth factor receptor (EGFR) that causes growth delay in cancer cell lines and human tumor xenografts expressing high levels of EGFR."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.biosemantics.org/jochem#4274201",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D016503",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D058990",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D011958",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0005006",
"http://www.uniprot.org/uniprot/EGFR_CHICK"
] |
[] |
53188480b166e2b806000018
|
bioasq_factoid
|
yesno
|
Is transcription-associated mutagenesis (TAM) related to gene expression levels?
|
['yes']
|
[
"yes"
] |
['Spontaneous point mutation rate in a gene increases with its transcription level, suggesting that movement of RNA polymerase through the target initiates a mutagenic process(es). This phenomenon is termed transcription-associated mutation (TAM). Transcription-associated mutagenesis is directly proportional to the level of gene expression.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23564176",
"http://www.ncbi.nlm.nih.gov/pubmed/23146897",
"http://www.ncbi.nlm.nih.gov/pubmed/23055242",
"http://www.ncbi.nlm.nih.gov/pubmed/21177427",
"http://www.ncbi.nlm.nih.gov/pubmed/20435731",
"http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"http://www.ncbi.nlm.nih.gov/pubmed/21177431",
"http://www.ncbi.nlm.nih.gov/pubmed/10628973",
"http://www.ncbi.nlm.nih.gov/pubmed/15143174"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23564176",
"endSection": "abstract",
"offsetInBeginSection": 963,
"offsetInEndSection": 1133,
"text": "These mutations were frequent in plasmid-borne lacS expressed at a high level but not in single-copy lacS in the chromosome or at lower levels of expression in a plasmid."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23564176",
"endSection": "abstract",
"offsetInBeginSection": 1454,
"offsetInEndSection": 1683,
"text": "The results suggest that important DNA repair or replication fidelity functions are impaired or overwhelmed in pJlacS, with results analogous to those of the \"transcription-associated mutagenesis\" seen in bacteria and eukaryotes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23146897",
"endSection": "abstract",
"offsetInBeginSection": 332,
"offsetInEndSection": 531,
"text": "the rate of point mutation in a gene increases with the expression level of the gene. Transcription induces mutagenesis on both DNA strands, indicating simultaneous actions of several TAM mechanisms."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23055242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "High-levels of transcription through a gene stimulate spontaneous mutation rate, a phenomenon termed transcription-associated mutation (TAM)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21177427",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 263,
"text": "High levels of transcription in Saccharomyces cerevisiae are associated with increased genetic instability, which has been linked to DNA damage. Here, we describe a pGAL-CAN1 forward mutation assay for studying transcription-associated mutagenesis (TAM) in yeast."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20435731",
"endSection": "abstract",
"offsetInBeginSection": 432,
"offsetInEndSection": 514,
"text": "The acquisition of mutations was directly correlated to the level of transcription"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20435731",
"endSection": "abstract",
"offsetInBeginSection": 830,
"offsetInEndSection": 976,
"text": "Our results demonstrate that the level of Leu(+) reversions increased significantly in parallel with the induced increase in transcription levels."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Transcription-associated mutagenesis in yeast is directly proportional to the level of gene expression"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "abstract",
"offsetInBeginSection": 403,
"offsetInEndSection": 577,
"text": "spontaneous mutation rate is directly proportional to the transcription level, suggesting that movement of RNA polymerase through the target initiates a mutagenic process(es)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21177431",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "High transcription is associated with genetic instability, notably increased spontaneous mutation rates, which is a phenomenon termed Transcription-Associated-Mutagenesis (TAM)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "abstract",
"offsetInBeginSection": 575,
"offsetInEndSection": 856,
"text": "Using this system, we also investigated two hypotheses that have been proposed to explain transcription-associated mutagenesis (TAM): (1) transcription impairs replication fork progression in a directional manner and (2) DNA lesions accumulate under high-transcription conditions."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Transcription-associated mutagenesis in yeast is directly proportional to the level of gene expression and influenced by the direction of DNA replication."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21177431",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "High transcription is associated with genetic instability, notably increased spontaneous mutation rates, which is a phenomenon termed Transcription-Associated-Mutagenesis (TAM)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "abstract",
"offsetInBeginSection": 575,
"offsetInEndSection": 856,
"text": "Using this system, we also investigated two hypotheses that have been proposed to explain transcription-associated mutagenesis (TAM): (1) transcription impairs replication fork progression in a directional manner and (2) DNA lesions accumulate under high-transcription conditions."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Transcription-associated mutagenesis in yeast is directly proportional to the level of gene expression and influenced by the direction of DNA replication."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21177431",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "High transcription is associated with genetic instability, notably increased spontaneous mutation rates, which is a phenomenon termed Transcription-Associated-Mutagenesis (TAM)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "abstract",
"offsetInBeginSection": 575,
"offsetInEndSection": 856,
"text": "Using this system, we also investigated two hypotheses that have been proposed to explain transcription-associated mutagenesis (TAM): (1) transcription impairs replication fork progression in a directional manner and (2) DNA lesions accumulate under high-transcription conditions."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Transcription-associated mutagenesis in yeast is directly proportional to the level of gene expression and influenced by the direction of DNA replication."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21177431",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "High transcription is associated with genetic instability, notably increased spontaneous mutation rates, which is a phenomenon termed Transcription-Associated-Mutagenesis (TAM)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "abstract",
"offsetInBeginSection": 575,
"offsetInEndSection": 856,
"text": "Using this system, we also investigated two hypotheses that have been proposed to explain transcription-associated mutagenesis (TAM): (1) transcription impairs replication fork progression in a directional manner and (2) DNA lesions accumulate under high-transcription conditions."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Transcription-associated mutagenesis in yeast is directly proportional to the level of gene expression and influenced by the direction of DNA replication."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23055242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "High-levels of transcription through a gene stimulate spontaneous mutation rate, a phenomenon termed transcription-associated mutation (TAM)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Transcription-associated mutagenesis in yeast is directly proportional to the level of gene expression and influenced by the direction of DNA replication."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21177431",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "High transcription is associated with genetic instability, notably increased spontaneous mutation rates, which is a phenomenon termed Transcription-Associated-Mutagenesis (TAM)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23055242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "High-levels of transcription through a gene stimulate spontaneous mutation rate, a phenomenon termed transcription-associated mutation (TAM)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21177427",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 144,
"text": "High levels of transcription in Saccharomyces cerevisiae are associated with increased genetic instability, which has been linked to DNA damage."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "abstract",
"offsetInBeginSection": 579,
"offsetInEndSection": 859,
"text": "Using this system, we also investigated two hypotheses that have been proposed to explain transcription-associated mutagenesis (TAM): (1) transcription impairs replication fork progression in a directional manner and (2) DNA lesions accumulate under high-transcription conditions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23146897",
"endSection": "abstract",
"offsetInBeginSection": 224,
"offsetInEndSection": 416,
"text": "Using comparative genomics of related species as well as mutation accumulation lines, we show in yeast that the rate of point mutation in a gene increases with the expression level of the gene"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Transcription-associated mutagenesis in yeast is directly proportional to the level of gene expression and influenced by the direction of DNA replication."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21177431",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "High transcription is associated with genetic instability, notably increased spontaneous mutation rates, which is a phenomenon termed Transcription-Associated-Mutagenesis (TAM)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "abstract",
"offsetInBeginSection": 579,
"offsetInEndSection": 858,
"text": "Using this system, we also investigated two hypotheses that have been proposed to explain transcription-associated mutagenesis (TAM): (1) transcription impairs replication fork progression in a directional manner and (2) DNA lesions accumulate under high-transcription conditions"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23055242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "High-levels of transcription through a gene stimulate spontaneous mutation rate, a phenomenon termed transcription-associated mutation (TAM)"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Transcription-associated mutagenesis in yeast is directly proportional to the level of gene expression and influenced by the direction of DNA replication."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23146897",
"endSection": "abstract",
"offsetInBeginSection": 224,
"offsetInEndSection": 416,
"text": "Using comparative genomics of related species as well as mutation accumulation lines, we show in yeast that the rate of point mutation in a gene increases with the expression level of the gene"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21177431",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "High transcription is associated with genetic instability, notably increased spontaneous mutation rates, which is a phenomenon termed Transcription-Associated-Mutagenesis (TAM)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23055242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "High-levels of transcription through a gene stimulate spontaneous mutation rate, a phenomenon termed transcription-associated mutation (TAM)"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Transcription-associated mutagenesis in yeast is directly proportional to the level of gene expression and influenced by the direction of DNA replication."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23146897",
"endSection": "abstract",
"offsetInBeginSection": 224,
"offsetInEndSection": 416,
"text": "Using comparative genomics of related species as well as mutation accumulation lines, we show in yeast that the rate of point mutation in a gene increases with the expression level of the gene"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21177431",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "High transcription is associated with genetic instability, notably increased spontaneous mutation rates, which is a phenomenon termed Transcription-Associated-Mutagenesis (TAM)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23055242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "High-levels of transcription through a gene stimulate spontaneous mutation rate, a phenomenon termed transcription-associated mutation (TAM)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23146897",
"endSection": "abstract",
"offsetInBeginSection": 224,
"offsetInEndSection": 416,
"text": "Using comparative genomics of related species as well as mutation accumulation lines, we show in yeast that the rate of point mutation in a gene increases with the expression level of the gene"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Transcription-associated mutagenesis in yeast is directly proportional to the level of gene expression and influenced by the direction of DNA replication."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21177431",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "High transcription is associated with genetic instability, notably increased spontaneous mutation rates, which is a phenomenon termed Transcription-Associated-Mutagenesis (TAM)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23055242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "High-levels of transcription through a gene stimulate spontaneous mutation rate, a phenomenon termed transcription-associated mutation (TAM)"
}
] | 5 |
BioASQ-training5b
|
[
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0006351",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0010467"
] |
[] |
5544f3005beec11c10000008
|
bioasq_yesno
|
yesno
|
Is myasthenia gravis associated with osteoporosis?
|
['yes']
|
[
"yes"
] |
['Myasthenia gravis (MG) is a neuromuscular disease which has been associated with an increased risk of glucocorticoid-induced osteoporosis. Thymectomy can also increase risk for osteoporosis. Appropriate osteoporosis preventive measures can reduce osteoporosis risk in MG patients.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23543381",
"http://www.ncbi.nlm.nih.gov/pubmed/22840813",
"http://www.ncbi.nlm.nih.gov/pubmed/22531999",
"http://www.ncbi.nlm.nih.gov/pubmed/16690366",
"http://www.ncbi.nlm.nih.gov/pubmed/15168159",
"http://www.ncbi.nlm.nih.gov/pubmed/15003307",
"http://www.ncbi.nlm.nih.gov/pubmed/11328209",
"http://www.ncbi.nlm.nih.gov/pubmed/2237235",
"http://www.ncbi.nlm.nih.gov/pubmed/24935165",
"http://www.ncbi.nlm.nih.gov/pubmed/25285145",
"http://www.ncbi.nlm.nih.gov/pubmed/25122205"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23543381",
"endSection": "abstract",
"offsetInBeginSection": 508,
"offsetInEndSection": 615,
"text": "We performed PVP in 4 patients with generalized MG associated with recent steroid-induced symptomatic VFs. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22840813",
"endSection": "abstract",
"offsetInBeginSection": 242,
"offsetInEndSection": 436,
"text": "In this case report, we used tacrolimus to successfully treat a 13-year-old boy with ocular MG who had suffered from severe steroid complications, including a failure of thrive and osteoporosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22531999",
"endSection": "abstract",
"offsetInBeginSection": 360,
"offsetInEndSection": 573,
"text": " INTRODUCTION: Myasthenia gravis (MG) is a neuromuscular disease which has been associated with an increased falls risk and glucocorticoid-induced osteoporosis, recognized determinants of increased fracture risk. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22531999",
"endSection": "abstract",
"offsetInBeginSection": 949,
"offsetInEndSection": 1462,
"text": "RESULTS: Compared to the control cohort, there was no statistically significant increased risk observed in patients with MG for any fracture (adjusted hazard ratio [AHR] 1.11; 95 % confidence interval [CI], 0.84-1.47) or osteoporotic fractures (AHR 0.98 [95 % CI 0.67-1.41]). Further, use of oral glucocorticoids up to a cumulative dose exceeding 5 g prednisolone equivalents did not increase risk of osteoporotic fracture (AHR 0.99 [95 % CI, 0.31-3.14]) compared with MG patients without glucocorticoid exposure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16690366",
"endSection": "abstract",
"offsetInBeginSection": 1271,
"offsetInEndSection": 1405,
"text": "The RANKL/OPG ratio and indices of bone metabolisms are also not affected by THX, although THX increases the levels of IL-7 and RANKL."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15168159",
"endSection": "abstract",
"offsetInBeginSection": 83,
"offsetInEndSection": 575,
"text": "Both disorders had been controlled for around 15 years by oral prednisolone and a cholinesterase inhibitor following surgical removal of invasive thymoma and radiotherapy, but muscular weakness due to myalgia and an increase in serum levels of myogenic enzymes, mainly ascribable to the recurrence of PM, reappeared immediately after cessation of these drugs, which was done because the patient had multiple bone fractures and severe osteoporosis due to the long-term corticosteroid therapy. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15003307",
"endSection": "abstract",
"offsetInBeginSection": 160,
"offsetInEndSection": 391,
"text": "We measured bone density in 36 patients (26 females and 10 males) who had undergone long-term prednisolone administration, and found a decrease in bone density in 31% of female patients and osteoporosis in only 11.5% (three cases)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15003307",
"endSection": "abstract",
"offsetInBeginSection": 533,
"offsetInEndSection": 681,
"text": "In conclusion, prednisolone-treated patients with myasthenia gravis have an acceptable risk of bone loss if prophylactic medication is administered."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22531999",
"endSection": "abstract",
"offsetInBeginSection": 361,
"offsetInEndSection": 572,
"text": "INTRODUCTION: Myasthenia gravis (MG) is a neuromuscular disease which has been associated with an increased falls risk and glucocorticoid-induced osteoporosis, recognized determinants of increased fracture risk."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23543381",
"endSection": "abstract",
"offsetInBeginSection": 508,
"offsetInEndSection": 615,
"text": "We performed PVP in 4 patients with generalized MG associated with recent steroid-induced symptomatic VFs. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22840813",
"endSection": "abstract",
"offsetInBeginSection": 242,
"offsetInEndSection": 436,
"text": "In this case report, we used tacrolimus to successfully treat a 13-year-old boy with ocular MG who had suffered from severe steroid complications, including a failure of thrive and osteoporosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24935165",
"endSection": "abstract",
"offsetInBeginSection": 901,
"offsetInEndSection": 1020,
"text": "Alendronate should be used with caution in patients with myasthenia gravis who have corticosteroid-induced osteoporosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25285145",
"endSection": "abstract",
"offsetInBeginSection": 399,
"offsetInEndSection": 614,
"text": "In this paper we present two cases of young women who developed severe PAO with vertebral fractures: a 42-year-old woman with a family history of osteoporosis, and a 21-year-old woman affected with myasthenia gravis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22531999",
"endSection": "abstract",
"offsetInBeginSection": 353,
"offsetInEndSection": 549,
"text": "Myasthenia gravis (MG) is a neuromuscular disease which has been associated with an increased falls risk and glucocorticoid-induced osteoporosis, recognized determinants of increased fracture risk"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22531999",
"endSection": "abstract",
"offsetInBeginSection": 353,
"offsetInEndSection": 549,
"text": "Myasthenia gravis (MG) is a neuromuscular disease which has been associated with an increased falls risk and glucocorticoid-induced osteoporosis, recognized determinants of increased fracture risk"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22531999",
"endSection": "abstract",
"offsetInBeginSection": 353,
"offsetInEndSection": 549,
"text": "Myasthenia gravis (MG) is a neuromuscular disease which has been associated with an increased falls risk and glucocorticoid-induced osteoporosis, recognized determinants of increased fracture risk"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22531999",
"endSection": "abstract",
"offsetInBeginSection": 353,
"offsetInEndSection": 549,
"text": "Myasthenia gravis (MG) is a neuromuscular disease which has been associated with an increased falls risk and glucocorticoid-induced osteoporosis, recognized determinants of increased fracture risk"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22531999",
"endSection": "abstract",
"offsetInBeginSection": 353,
"offsetInEndSection": 549,
"text": "Myasthenia gravis (MG) is a neuromuscular disease which has been associated with an increased falls risk and glucocorticoid-induced osteoporosis, recognized determinants of increased fracture risk"
}
] | 5 |
BioASQ-training5b
|
[
"http://www.disease-ontology.org/api/metadata/DOID:437",
"http://www.disease-ontology.org/api/metadata/DOID:11476"
] |
[] |
55032d8be9bde69634000033
|
bioasq_yesno
|
factoid
|
What is the effect induced by sympathetic nervous system on pupil size?
|
[['pupillary dilatation (increase of the pupil size)']]
|
[
"pupillary dilatation",
"pupil dilation",
"pupil enlargement",
"mydriasis",
"increase of the pupil size",
"pupillary expansion"
] |
['Pupil size is determined by the interaction of the parasympathetic and the sympathetic nervous system. The sympathetic nervous system acts either directly on the dilator muscle (peripherally) or centrally by inhibiting the Edinger-Westphal nucleus. Thus, the sympathetic nervous system mediates pupillary dilatation.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21601076",
"http://www.ncbi.nlm.nih.gov/pubmed/14639139",
"http://www.ncbi.nlm.nih.gov/pubmed/8873544",
"http://www.ncbi.nlm.nih.gov/pubmed/3604881",
"http://www.ncbi.nlm.nih.gov/pubmed/11306012",
"http://www.ncbi.nlm.nih.gov/pubmed/9247742",
"http://www.ncbi.nlm.nih.gov/pubmed/9357887",
"http://www.ncbi.nlm.nih.gov/pubmed/7697953",
"http://www.ncbi.nlm.nih.gov/pubmed/3423165",
"http://www.ncbi.nlm.nih.gov/pubmed/6499637",
"http://www.ncbi.nlm.nih.gov/pubmed/7188336",
"http://www.ncbi.nlm.nih.gov/pubmed/6881176",
"http://www.ncbi.nlm.nih.gov/pubmed/6413073",
"http://www.ncbi.nlm.nih.gov/pubmed/1619750"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21601076",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Pupil size is determined by the interaction of the parasympathetic and the sympathetic nervous system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21601076",
"endSection": "abstract",
"offsetInBeginSection": 204,
"offsetInEndSection": 349,
"text": "The sympathetic nervous system acts either directly on the dilator muscle (peripherally) or centrally by inhibiting the Edinger-Westphal nucleus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14639139",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 285,
"text": "The mechanism of reflex pupillary dilation was investigated in eight patients who were declared brain dead after rupture of intracranial vascular malformations and in eight awake volunteers. The authors hypothesized that the reflex was primarily a spinal sympathetic reflex"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14639139",
"endSection": "abstract",
"offsetInBeginSection": 1543,
"offsetInEndSection": 1704,
"text": "The authors conclude that pupillary reflex dilation, as it is clinically performed in awake subjects by stimulating somatic nociceptors, is a sympathetic reflex."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8873544",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 141,
"text": "Pupil size is determined by an interaction between the sympathetic and parasympathetic divisions of the autonomic nervous system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8873544",
"endSection": "abstract",
"offsetInBeginSection": 1083,
"offsetInEndSection": 1155,
"text": "Sympathetic nervous system activation, with reflex dilation of the pupil"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3604881",
"endSection": "abstract",
"offsetInBeginSection": 1388,
"offsetInEndSection": 1465,
"text": "reproducibly larger pupil size--indicative of increased sympathetic arousal--"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11306012",
"endSection": "abstract",
"offsetInBeginSection": 614,
"offsetInEndSection": 729,
"text": "activation of autonomic sympathetic preganglionic neurons in the thoracic spinal cord produces pupillary dilatation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9247742",
"endSection": "abstract",
"offsetInBeginSection": 591,
"offsetInEndSection": 661,
"text": "sympathetic responses (sweating, pupil dilatation, piloerection, etc.)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8873544",
"endSection": "abstract",
"offsetInBeginSection": 228,
"offsetInEndSection": 323,
"text": "In the absence of anesthesia, dilation is primarily mediated by the sympathetic nervous system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8873544",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Pupil size is determined by an interaction between the sympathetic and parasympathetic divisions of the autonomic nervous system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8873544",
"endSection": "abstract",
"offsetInBeginSection": 1052,
"offsetInEndSection": 1277,
"text": "Sympathetic nervous system activation, with reflex dilation of the pupil, was produced by noxious electrical stimulation during 4% and 8% end-tidal desflurane, and by a rapid 4%-to-8% step-up in the desflurane concentration."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8873544",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Pupil size is determined by an interaction between the sympathetic and parasympathetic divisions of the autonomic nervous system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8873544",
"endSection": "abstract",
"offsetInBeginSection": 1052,
"offsetInEndSection": 1277,
"text": "Sympathetic nervous system activation, with reflex dilation of the pupil, was produced by noxious electrical stimulation during 4% and 8% end-tidal desflurane, and by a rapid 4%-to-8% step-up in the desflurane concentration."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21601076",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Pupil size is determined by the interaction of the parasympathetic and the sympathetic nervous system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8873544",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Pupil size is determined by an interaction between the sympathetic and parasympathetic divisions of the autonomic nervous system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8873544",
"endSection": "abstract",
"offsetInBeginSection": 1052,
"offsetInEndSection": 1277,
"text": "Sympathetic nervous system activation, with reflex dilation of the pupil, was produced by noxious electrical stimulation during 4% and 8% end-tidal desflurane, and by a rapid 4%-to-8% step-up in the desflurane concentration."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21601076",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Pupil size is determined by the interaction of the parasympathetic and the sympathetic nervous system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8873544",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Pupil size is determined by an interaction between the sympathetic and parasympathetic divisions of the autonomic nervous system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8873544",
"endSection": "abstract",
"offsetInBeginSection": 1052,
"offsetInEndSection": 1277,
"text": "Sympathetic nervous system activation, with reflex dilation of the pupil, was produced by noxious electrical stimulation during 4% and 8% end-tidal desflurane, and by a rapid 4%-to-8% step-up in the desflurane concentration."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8873544",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "BACKGROUND: Pupil size is determined by an interaction between the sympathetic and parasympathetic divisions of the autonomic nervous system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6499637",
"endSection": "abstract",
"offsetInBeginSection": 902,
"offsetInEndSection": 1115,
"text": "Dark-adapted pupil size after topical PNS blockade (an index of iris sympathetic nervous system [SNS] activity) was also smaller in both groups of diabetic subjects (NIDD, P less than 0.01; IDD, P less than 0.05)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21601076",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Pupil size is determined by the interaction of the parasympathetic and the sympathetic nervous system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21601076",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Pupil size is determined by the interaction of the parasympathetic and the sympathetic nervous system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6881176",
"endSection": "abstract",
"offsetInBeginSection": 1224,
"offsetInEndSection": 1408,
"text": "However, dark-adapted pupil size during parasympathetic nervous system blockade, an index of iris sympathetic nervous system activity, declined with age (r = -0.81, p less than 0.001)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6881176",
"endSection": "abstract",
"offsetInBeginSection": 1224,
"offsetInEndSection": 1407,
"text": "However, dark-adapted pupil size during parasympathetic nervous system blockade, an index of iris sympathetic nervous system activity, declined with age (r = -0.81, p less than 0.001)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21601076",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "Pupil size is determined by the interaction of the parasympathetic and the sympathetic nervous system"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8873544",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "Pupil size is determined by an interaction between the sympathetic and parasympathetic divisions of the autonomic nervous system"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6881176",
"endSection": "abstract",
"offsetInBeginSection": 1224,
"offsetInEndSection": 1407,
"text": "However, dark-adapted pupil size during parasympathetic nervous system blockade, an index of iris sympathetic nervous system activity, declined with age (r = -0.81, p less than 0.001)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21601076",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "Pupil size is determined by the interaction of the parasympathetic and the sympathetic nervous system"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8873544",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "Pupil size is determined by an interaction between the sympathetic and parasympathetic divisions of the autonomic nervous system"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6881176",
"endSection": "abstract",
"offsetInBeginSection": 1224,
"offsetInEndSection": 1407,
"text": "However, dark-adapted pupil size during parasympathetic nervous system blockade, an index of iris sympathetic nervous system activity, declined with age (r = -0.81, p less than 0.001)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21601076",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "Pupil size is determined by the interaction of the parasympathetic and the sympathetic nervous system"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8873544",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "Pupil size is determined by an interaction between the sympathetic and parasympathetic divisions of the autonomic nervous system"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6881176",
"endSection": "abstract",
"offsetInBeginSection": 1224,
"offsetInEndSection": 1407,
"text": "However, dark-adapted pupil size during parasympathetic nervous system blockade, an index of iris sympathetic nervous system activity, declined with age (r = -0.81, p less than 0.001)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8873544",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "Pupil size is determined by an interaction between the sympathetic and parasympathetic divisions of the autonomic nervous system"
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013564",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D001342",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018373",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D009420"
] |
[] |
5547ec32f35db7552600000a
|
bioasq_factoid
|
yesno
|
Are Tregs CD4(+)CD25(+) regulatory T cells a positive regulator of the immune response?
|
['no']
|
[
"no"
] |
['CD4(+)CD25(+) regulatory T cells (Tregs) are negative regulators of the immune system that induce and maintain immune tolerance.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/19816193",
"http://www.ncbi.nlm.nih.gov/pubmed/18205702",
"http://www.ncbi.nlm.nih.gov/pubmed/21386770",
"http://www.ncbi.nlm.nih.gov/pubmed/17848162",
"http://www.ncbi.nlm.nih.gov/pubmed/23531479",
"http://www.ncbi.nlm.nih.gov/pubmed/17826781",
"http://www.ncbi.nlm.nih.gov/pubmed/24095986",
"http://www.ncbi.nlm.nih.gov/pubmed/16809644",
"http://www.ncbi.nlm.nih.gov/pubmed/17368474",
"http://www.ncbi.nlm.nih.gov/pubmed/23983771",
"http://www.ncbi.nlm.nih.gov/pubmed/20843956",
"http://www.ncbi.nlm.nih.gov/pubmed/17407195",
"http://www.ncbi.nlm.nih.gov/pubmed/22749847",
"http://www.ncbi.nlm.nih.gov/pubmed/34495808",
"http://www.ncbi.nlm.nih.gov/pubmed/16020508",
"http://www.ncbi.nlm.nih.gov/pubmed/18032693",
"http://www.ncbi.nlm.nih.gov/pubmed/20384869",
"http://www.ncbi.nlm.nih.gov/pubmed/23635849",
"http://www.ncbi.nlm.nih.gov/pubmed/27109178",
"http://www.ncbi.nlm.nih.gov/pubmed/18580479",
"http://www.ncbi.nlm.nih.gov/pubmed/19005268",
"http://www.ncbi.nlm.nih.gov/pubmed/24754976",
"http://www.ncbi.nlm.nih.gov/pubmed/25113439",
"http://www.ncbi.nlm.nih.gov/pubmed/19543397",
"http://www.ncbi.nlm.nih.gov/pubmed/15778406",
"http://www.ncbi.nlm.nih.gov/pubmed/16393984",
"http://www.ncbi.nlm.nih.gov/pubmed/21597299",
"http://www.ncbi.nlm.nih.gov/pubmed/17234458",
"http://www.ncbi.nlm.nih.gov/pubmed/24483245",
"http://www.ncbi.nlm.nih.gov/pubmed/21655351",
"http://www.ncbi.nlm.nih.gov/pubmed/22899644"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19816193",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "The immunosuppressive effects of CD4+ CD25 high regulatory T cells (Tregs) interfere with antitumor immune responses in cancer patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25113439",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 146,
"text": "Alteration of regulatory T cells (Tregs) may contribute to ineffective suppression of proinflammatory cytokines in type 1 diabetes.AIM"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24754976",
"endSection": "abstract",
"offsetInBeginSection": 110,
"offsetInEndSection": 179,
"text": "Regulatory T cells (Tregs) suppress excessive immune responses in IRI"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24095986",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "CD4(+)CD25(+) regulatory T cells (Tregs) are negative regulators of the immune system that induce and maintain immune tolerance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19005268",
"endSection": "abstract",
"offsetInBeginSection": 870,
"offsetInEndSection": 1022,
"text": "lar to chronic patients, Treg from patients with PHI inhibited the proliferation of purified tuberculin (PPD) and HIV p24 activated CD4CD25 T cells. CD4"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21386770",
"endSection": "abstract",
"offsetInBeginSection": 655,
"offsetInEndSection": 901,
"text": " demonstrate that aTregs are necessary for tolerance, DBA/2 skin was transplanted onto C57BL/6-RAG-1-deficient recipients adoptively transferred with purified sorted CD4CD25 T cells; half of the recipients undergo tolerance induction treatment.RE"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23635849",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "It is well established that CD4CD25 regulatory T cells (Tregs) downregulate inflammatory immune responses and help to maintain immune homeostasis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18580479",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "In vitro expanded human CD4+CD25+ regulatory T cells are potent suppressors of T-cell-mediated xenogeneic responses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19543397",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 81,
"text": "BACKGROUND: Regulatory T cells (Tregs) are essential in the control of tolerance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20384869",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "CD4(+)CD25(+) regulatory T cells (Tregs) are critical for the peripheral immune tolerance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27109178",
"endSection": "abstract",
"offsetInBeginSection": 114,
"offsetInEndSection": 287,
"text": "T regulatory cells (Tregs) have a role in immunosuppression and control of autoimmunity, and are currently an important topic in the study of immune response to tumor cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23635849",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "CD4+CD25+ regulatory T cells attenuate lipopolysaccharide-induced systemic inflammatory responses and promotes survival in murine Escherichia coli infection."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23531479",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "OBJECTIVES: CD4CD25 regulatory T cells (Tregs) play a key role in the prevention of various inflammatory and autoimmune disorders by suppressing immune responses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21655351",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 243,
"text": "CD25(High) CD4+ regulatory T cells (Treg cells) have been described as key players in immune regulation, preventing infection-induced immune pathology and limiting collateral tissue damage caused by vigorous anti-parasite immune response. In t"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22899644",
"endSection": "abstract",
"offsetInBeginSection": 240,
"offsetInEndSection": 521,
"text": "ic subset of T cells, currently recognized as FOXP3(+) CD25(+) CD4(+) regulatory T cells (Tregs), are pivotal in suppressing autoimmunity and maintaining immune homeostasis by mediating self-tolerance at the periphery as shown in autoimmune diseases and cancers. A growing body of "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16020508",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 92,
"text": "CD4+CD25+ regulatory T cells (Tregs) are essential negative regulators of immune responses. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22749847",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 255,
"text": "Accumulating evidence has demonstrated that naturally occurring CD4(+)CD25(+) regulatory T cells (Tregs) are critical for maintenance of immunological tolerance and have been shown to be important in regulating the immune responses in many diseases. Curcu"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24483245",
"endSection": "abstract",
"offsetInBeginSection": 280,
"offsetInEndSection": 426,
"text": "4+CD25+ Foxp3+ regulatory T cells (Tregs) are recognized as one of the major regulatory factors in immune tolerance and inflammatory responses. Si"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17826781",
"endSection": "abstract",
"offsetInBeginSection": 370,
"offsetInEndSection": 552,
"text": "lly occurring CD4(+)CD25(+) regulatory T cells (Tregs) have a key role in the prevention of various inflammatory and autoimmune disorders by suppressing immune responses. We tested t"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17368474",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "CD4(+)CD25(+) regulatory T cells (Tregs) are considered to play a key role as suppressors of immune mediated reactions. The a"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18205702",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "CD4+ CD25+ T regulatory cells (Tregs) are classified as a subset of T cells whose role is the suppression and regulation of immune responses to self and non-self. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18032693",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "CD4(+)CD25(+) regulatory T cells (Tregs) are potent modulators of immune responses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16393984",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 213,
"text": "CD4+ T cells naturally expressing CD25 molecules (natural T regulatory cells (Tregs)) have a role in maintaining self tolerance and in regulating responses to infectious agents, transplantation Ags, and tumor Ags."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20843956",
"endSection": "abstract",
"offsetInBeginSection": 157,
"offsetInEndSection": 275,
"text": "Naturally occurring CD4(+)CD25(+) regulatory T cells (Tregs) are essential for the active suppression of autoimmunity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16809644",
"endSection": "abstract",
"offsetInBeginSection": 260,
"offsetInEndSection": 489,
"text": "Amongst these, naturally occurring CD4(+)CD25(+) Treg cells (nTreg) represent a major lymphocyte population engaged in the dominant control of self-reactive T responses and maintaining tolerance in several models of autoimmunity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16020508",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "CD4+CD25+ regulatory T cells (Tregs) are essential negative regulators of immune responses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17407195",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 191,
"text": "Naturally occurring CD4(+)CD25(+)FoxP3(+) regulatory T cells (CD25(+) Tregs) constitute a specialized population of T cells that is essential for the maintenance of peripheral self-tolerance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34495808",
"endSection": "abstract",
"offsetInBeginSection": 68,
"offsetInEndSection": 394,
"text": "One of the subpopulations of CD4+ T cells that express CD25+ and the transcription factor FOXP3, known as Regulator T cells (TReg), plays an essential role in maintaining tolerance and immune homeostasis preventing autoimmune diseases, minimalize chronic inflammatory diseases by enlisting various immunoregulatory mechanisms."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15778406",
"endSection": "abstract",
"offsetInBeginSection": 128,
"offsetInEndSection": 240,
"text": "Regulatory T cells (Tregs) are CD4(+)CD25(bright)CD62L(high) cells that actively down-regulate immune responses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17234458",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 202,
"text": "CD4(+)CD25(+) regulatory T cells (Treg) play a central role in the prevention of autoimmunity and in the control of immune responses by down-regulating the function of effector CD4(+) or CD8(+) T cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23983771",
"endSection": "abstract",
"offsetInBeginSection": 124,
"offsetInEndSection": 389,
"text": "FoxP3(+)CD25(+)CD4(+) regulatory T cells (Tregs) suppress a variety of normal physiological and pathological immune responses via several pathways, such as inhibitory cytokine secretion, direct cytolysis induction, and antigen-presenting cell functional modulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17848162",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 236,
"text": "Regulatory CD4(+) CD25(+) T (Treg) cells with the ability to suppress host immune responses against self- or non-self antigens play important roles in the processes of autoimmunity, transplant rejection, infectious diseases and cancers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21597299",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 165,
"text": "BACKGROUND: Evidence indicating that CD4+CD25+ regulatory T (Treg) cells play a crucial role in the maintenance of peripheral T cell tolerance to allergens has been "
}
] | 11 |
BioASQ-training11b
| null | null |
621ed10f3a8413c653000062
|
bioasq_yesno
|
factoid
|
Clue cells are characteristics to which causative bacteria of vaginitis?
|
['Gardnerella vaginalis']
|
[
"Gardnerella vaginalis",
"Haemophilus vaginalis",
"Gardnerella",
"G. vaginalis"
] |
["Clue cells are characteristic to Gardnerella vaginalis vaginitis (bacterial vaginosis). Depopulation of lactobacilli from the normal vaginal flora and overgrowth of Gardnerella vaginalis and other anaerobic species are the presumed etiology. The diagnosis is confirmed when at least three of the following four findings are present (Amsel's criteria): 1) thin, homogenous discharge, 2) pH greater than 4.5, 3) positive amine test, and 4) presence of clue cell."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/11025268",
"http://www.ncbi.nlm.nih.gov/pubmed/18459549",
"http://www.ncbi.nlm.nih.gov/pubmed/10948822",
"http://www.ncbi.nlm.nih.gov/pubmed/20006195",
"http://www.ncbi.nlm.nih.gov/pubmed/11845812",
"http://www.ncbi.nlm.nih.gov/pubmed/22555524",
"http://www.ncbi.nlm.nih.gov/pubmed/20949462"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20949462",
"endSection": "abstract",
"offsetInBeginSection": 921,
"offsetInEndSection": 1030,
"text": "Most of these 290 smears contained clue cells (indicating Gardnerella infection) and a lack of lactobacilli. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22555524",
"endSection": "abstract",
"offsetInBeginSection": 292,
"offsetInEndSection": 487,
"text": "As part of the routine screening process, all smears were screened for the overgrowth of Gardnerella (i.e. smears with an abundance of clue cells) and for the presence of Trichomonas and Candida."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20006195",
"endSection": "abstract",
"offsetInBeginSection": 454,
"offsetInEndSection": 722,
"text": "Positive criteria for a Gram stain included greater than 10 white blood cells per high-power field, gram-negative intracellular/extracellular diplococci (suggesting N gonorrhoeae), clue cells (suggesting T vaginalis), or direct visualization of T vaginalis organisms. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18459549",
"endSection": "abstract",
"offsetInBeginSection": 249,
"offsetInEndSection": 373,
"text": "he appraised infectious agents were Coccobacilli, Candida sp, Trichomonas vaginalis, and clue cells (Gardnerella vaginalis)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11845812",
"endSection": "abstract",
"offsetInBeginSection": 417,
"offsetInEndSection": 540,
"text": "Smears deficient in lactobacilli and positive for clue cells were considered to indicate a diagnosis of bacterial vaginosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11025268",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 746,
"text": "Bacterial vaginosis is the most common cause of vaginitis, affecting over 3 million women in the United States annually. Depopulation of lactobacilli from the normal vaginal flora and overgrowth of Gardnerella vaginalis and other anaerobic species are the presumed etiology. To date, no scientific evidence shows that bacterial vaginosis is a sexually transmitted disease. Malodorous vaginal discharge is the most common symptom. Differential diagnoses include trichomoniasis, moniliasis, and allergic or chemical dermatitis. The diagnosis is confirmed when at least three of the following four findings are present (Amsel's criteria): 1) thin, homogenous discharge, 2) pH greater than 4.5, 3) positive amine test, and 4) presence of clue cells. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10948822",
"endSection": "abstract",
"offsetInBeginSection": 1010,
"offsetInEndSection": 1189,
"text": "Although the presence of clue cells and amine-like odor in KOH test have relationship with Gardnerella vaginalis, these tests could also suggest the presence of these mycoplasmas."
}
] | 11 |
BioASQ-training11b
|
[
"https://meshb.nlm.nih.gov/record/ui?ui=D014627",
"http://www.disease-ontology.org/api/metadata/DOID:2170"
] | null |
5a68f965b750ff445500001a
|
bioasq_factoid
|
factoid
|
Which R/Bioconductor package has been developed for cancer subtype identification?
|
['CancerSubtypes']
|
[
"Cancer Subtypes",
"Cancer Types",
"Cancer Classifications",
"Tumor Subtypes",
"Tumor Types",
"Oncological Subtypes",
"Oncological Classifications"
] |
['Identifying molecular cancer subtypes from multi-omics data is an important step in the personalized medicine. CancerSubtypes is an R/Bioconductor package for molecular cancer subtype identification, validation and visualization. CancerSubtypes integrates four main computational methods which are highly cited for cancer subtype identification and provides a standardized framework for data pre-processing, feature selection, and result follow-up analyses, including results computing, biology validation and visualization. The input and output of each step in the framework are packaged in the same data format, making it convenience to compare different methods.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28605519"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28605519",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "CancerSubtypes: an R/Bioconductor package for molecular cancer subtype identification, validation and visualization."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28605519",
"endSection": "abstract",
"offsetInBeginSection": 9,
"offsetInEndSection": 986,
"text": "Identifying molecular cancer subtypes from multi-omics data is an important step in the personalized medicine. We introduce CancerSubtypes, an R package for identifying cancer subtypes using multi-omics data, including gene expression, miRNA expression and DNA methylation data. CancerSubtypes integrates four main computational methods which are highly cited for cancer subtype identification and provides a standardized framework for data pre-processing, feature selection, and result follow-up analyses, including results computing, biology validation and visualization. The input and output of each step in the framework are packaged in the same data format, making it convenience to compare different methods. The package is useful for inferring cancer subtypes from an input genomic dataset, comparing the predictions from different well-known methods and testing new subtype discovery methods, as shown with different application scenarios in the Supplementary Material."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28605519",
"endSection": "abstract",
"offsetInBeginSection": 279,
"offsetInEndSection": 573,
"text": "CancerSubtypes integrates four main computational methods which are highly cited for cancer subtype identification and provides a standardized framework for data pre-processing, feature selection, and result follow-up analyses, including results computing, biology validation and visualization."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28605519",
"endSection": "abstract",
"offsetInBeginSection": 111,
"offsetInEndSection": 278,
"text": "We introduce CancerSubtypes, an R package for identifying cancer subtypes using multi-omics data, including gene expression, miRNA expression and DNA methylation data."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28605519",
"endSection": "abstract",
"offsetInBeginSection": 127,
"offsetInEndSection": 294,
"text": "We introduce CancerSubtypes, an R package for identifying cancer subtypes using multi-omics data, including gene expression, miRNA expression and DNA methylation data."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28605519",
"endSection": "abstract",
"offsetInBeginSection": 295,
"offsetInEndSection": 589,
"text": "CancerSubtypes integrates four main computational methods which are highly cited for cancer subtype identification and provides a standardized framework for data pre-processing, feature selection, and result follow-up analyses, including results computing, biology validation and visualization."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28605519",
"endSection": "abstract",
"offsetInBeginSection": 119,
"offsetInEndSection": 286,
"text": "We introduce CancerSubtypes, an R package for identifying cancer subtypes using multi-omics data, including gene expression, miRNA expression and DNA methylation data."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28605519",
"endSection": "abstract",
"offsetInBeginSection": 287,
"offsetInEndSection": 581,
"text": "CancerSubtypes integrates four main computational methods which are highly cited for cancer subtype identification and provides a standardized framework for data pre-processing, feature selection, and result follow-up analyses, including results computing, biology validation and visualization."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28605519",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 114,
"text": "cancersubtypes an r bioconductor package for molecular cancer subtype identification validation and visualization"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28605519",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1211,
"text": "identifying molecular cancer subtypes from multi omics data is an important step in the personalized medicine we introduce cancersubtypes an r package for identifying cancer subtypes using multi omics data including gene expression mirna expression and dna methylation data cancersubtypes integrates four main computational methods which are highly cited for cancer subtype identification and provides a standardized framework for data pre processing feature selection and result follow up analyses including results computing biology validation and visualization the input and output of each step in the framework are packaged in the same data format making it convenience to compare different methods the package is useful for inferring cancer subtypes from an input genomic dataset comparing the predictions from different well known methods and testing new subtype discovery methods as shown with different application scenarios in the supplementary material the package is implemented in r and available under gpl 2 license from the bioconductor website http bioconductor org packages cancersubtypes thuc le unisa edu au or jiuyong li unisa edu au supplementary data are available at bioinformatics online."
}
] | 11 |
BioASQ-training11b
| null | null |
5a6e3155b750ff445500003f
|
bioasq_factoid
|
factoid
|
Which bioconductor tool has been developed for accessing bacterial regulatory networks?
|
['regutools']
|
[
"regutools",
"ReguTools",
"Regulatory Tools"
] |
['The Regutools R package to facilitates programmatic access to RegulonDB data in computational biology. regutools gives researchers the possibility of writing reproducible workflows with automated queries to RegulonDB. The regutools package serves as a bridge between RegulonDB data and the Bioconductor ecosystem by reusing the data structures and statistical methods powered by other Bioconductor packages.', 'RegulonDB has collected, harmonized and centralized data from hundreds of experiments for nearly two decades and is considered a point of reference for transcriptional regulation in Escherichia coli K12. The regutools package serves as a bridge between RegulonDB data and the Bioconductor ecosystem by reusing the data structures and statistical methods powered by other Bioconductor packages.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/32573705"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32573705",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 68,
"text": "Programmatic access to bacterial regulatory networks with regutools."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32573705",
"endSection": "abstract",
"offsetInBeginSection": 9,
"offsetInEndSection": 1076,
"text": "RegulonDB has collected, harmonized and centralized data from hundreds of experiments for nearly two decades and is considered a point of reference for transcriptional regulation in Escherichia coli K12. Here, we present the regutools R package to facilitate programmatic access to RegulonDB data in computational biology. regutools gives researchers the possibility of writing reproducible workflows with automated queries to RegulonDB. The regutools package serves as a bridge between RegulonDB data and the Bioconductor ecosystem by reusing the data structures and statistical methods powered by other Bioconductor packages. We demonstrate the integration of regutools with Bioconductor by analyzing transcription factor DNA binding sites and transcriptional regulatory networks from RegulonDB. We anticipate that regutools will serve as a useful building block in our progress to further our understanding of gene regulatory networks.AVAILABILITY AND IMPLEMENTATION: regutools is an R package available through Bioconductor at bioconductor.org/packages/regutools."
}
] | 11 |
BioASQ-training11b
| null | null |
606081e594d57fd879000041
|
bioasq_factoid
|
yesno
|
Can parasite infections by Schistosoma japonicum prevent or improve asthma?
|
['yes']
|
[
"yes"
] |
['A peptide named as SJMHE1 from Schistosoma japonicum can suppress asthma in mice.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/31496071",
"http://www.ncbi.nlm.nih.gov/pubmed/34703270",
"http://www.ncbi.nlm.nih.gov/pubmed/34358648",
"http://www.ncbi.nlm.nih.gov/pubmed/26840774",
"http://www.ncbi.nlm.nih.gov/pubmed/28614408",
"http://www.ncbi.nlm.nih.gov/pubmed/17042799",
"http://www.ncbi.nlm.nih.gov/pubmed/18654798",
"http://www.ncbi.nlm.nih.gov/pubmed/18824533",
"http://www.ncbi.nlm.nih.gov/pubmed/34169075"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31496071",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "Helminths and their products can shape immune responses by modulating immune cells, which are dysfunctional in inflammatory diseases such as asthm"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31496071",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 95,
"text": "Schistosoma japonicum peptide SJMHE1 suppresses airway inflammation of allergic asthma in mice."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28614408",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 107,
"text": "Schistosoma japonicum infection downregulates house dust mite-induced allergic airway inflammation in mice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28614408",
"endSection": "abstract",
"offsetInBeginSection": 1091,
"offsetInEndSection": 1294,
"text": "To our knowledge, it is the first study to reveal the impact of S. japonicum infection on house dust mite induced severe asthma. More in depth investigation is need to elucidate the underlying mechanisms"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26840774",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "Novel T-cell epitopes on Schistosoma japonicum SjP40 protein and their preventive effect on allergic asthma in mice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26840774",
"endSection": "abstract",
"offsetInBeginSection": 845,
"offsetInEndSection": 1022,
"text": "hese results reveal a novel form of immune protective mechanism, which may play an important role in the modulating effect of helminth infection on allergic asthmatic reactions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26840774",
"endSection": "abstract",
"offsetInBeginSection": 597,
"offsetInEndSection": 843,
"text": "Using a panel of overlapping peptides, we identified T-cell epitopes on SjP40 protein of Schistosoma japonicum, which can induce Th1 cytokine and inhibit the production of Th2 cytokines and airway inflammation in a mouse model of allergic asthma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34703270",
"endSection": "abstract",
"offsetInBeginSection": 9,
"offsetInEndSection": 148,
"text": "Helminths and their products can regulate immune response and offer new strategies to control and alleviate inflammation, including asthma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34703270",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "SJMHE1 Peptide from Schistosoma japonicum Inhibits Asthma in Mice by Regulating Th17/Treg Cell Balance via miR-155."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34703270",
"endSection": "abstract",
"offsetInBeginSection": 149,
"offsetInEndSection": 254,
"text": "We previously found that a peptide named as SJMHE1 from Schistosoma japonicum can suppress asthma in mice"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26840774",
"endSection": "abstract",
"offsetInBeginSection": 608,
"offsetInEndSection": 855,
"text": "el of overlapping peptides, we identified T-cell epitopes on SjP40 protein of Schistosoma japonicum, which can induce Th1 cytokine and inhibit the production of Th2 cytokines and airway inflammation in a mouse model of allergic asthma. These resul"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18654798",
"endSection": "abstract",
"offsetInBeginSection": 150,
"offsetInEndSection": 268,
"text": "has been shown that helminth infections including Schistosoma mansoni may modulate atopic diseases including asthma. I"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28614408",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Schistosoma japonicum infection downregulates house dust mite-induced allergic airway inflammation in mice"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28614408",
"endSection": "abstract",
"offsetInBeginSection": 1109,
"offsetInEndSection": 1237,
"text": "it is the first study to reveal the impact of S. japonicum infection on house dust mite induced severe asthma. More in depth inv"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28614408",
"endSection": "abstract",
"offsetInBeginSection": 402,
"offsetInEndSection": 675,
"text": "s study, we investigated the impact of Schistosoma japonicum infection on the allergic airway inflammation induced by repeated intracheal inoculations of house dust mites (HDM), which is a Th17 and neutrophils dominant murine asthma model, mimicking severe asthma. We found"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34169075",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "Schistosoma japonicum infection showed protective effects against allergic airway inflammation (AAI)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17042799",
"endSection": "abstract",
"offsetInBeginSection": 152,
"offsetInEndSection": 384,
"text": "Therefore, we hypothesize that Schistosoma japonicum egg antigens, a type of native antigen, can induce production of CD4(+) CD25(+) T cells with regulatory activity, modulating airway inflammation and inhibiting asthma development."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18654798",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Schistosoma japonicum infection modulates the development of allergen-induced airway inflammation in mice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18654798",
"endSection": "abstract",
"offsetInBeginSection": 147,
"offsetInEndSection": 266,
"text": "It has been shown that helminth infections including Schistosoma mansoni may modulate atopic diseases including asthma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17042799",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "Schistosoma japonicum egg antigens stimulate CD4 CD25 T cells and modulate airway inflammation in a murine model of asthma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34169075",
"endSection": "abstract",
"offsetInBeginSection": 229,
"offsetInEndSection": 511,
"text": "Most previous studies focused on understanding the preventive effect of S. japonicum infection on asthma (infection before allergen sensitization), whereas the protective effects of S. japonicum infection (allergen sensitization before infection) on asthma were rarely investigated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34169075",
"endSection": "abstract",
"offsetInBeginSection": 1619,
"offsetInEndSection": 1739,
"text": "In conclusion, our data showed that lung-stage S. japonicum infection could relieve OVA-induced asthma in a mouse model."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34169075",
"endSection": "abstract",
"offsetInBeginSection": 512,
"offsetInEndSection": 641,
"text": "In this study, we investigated the protective effects of S. japonicum infection on AAI using a mouse model of OVA-induced asthma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18654798",
"endSection": "abstract",
"offsetInBeginSection": 972,
"offsetInEndSection": 1122,
"text": " prior to OVA immunization. These results suggest that both bisexual and male S. japonicum infections may modulate the development of allergic asthma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26840774",
"endSection": "abstract",
"offsetInBeginSection": 699,
"offsetInEndSection": 849,
"text": "aponicum, which can induce Th1 cytokine and inhibit the production of Th2 cytokines and airway inflammation in a mouse model of allergic asthma. These"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34358648",
"endSection": "abstract",
"offsetInBeginSection": 455,
"offsetInEndSection": 605,
"text": "ve found that Schistosoma infection or Schistosoma related products can improve or prevent some immune and inflammatory diseases, such as severe asthm"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28614408",
"endSection": "abstract",
"offsetInBeginSection": 904,
"offsetInEndSection": 1090,
"text": "Our findings indicated that S. japonicum infection was able to effectively inhibit host's allergic airway inflammation, which may be related to the upregulated Treg cells upon infection."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18654798",
"endSection": "abstract",
"offsetInBeginSection": 1000,
"offsetInEndSection": 1122,
"text": "These results suggest that both bisexual and male S. japonicum infections may modulate the development of allergic asthma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34169075",
"endSection": "abstract",
"offsetInBeginSection": 936,
"offsetInEndSection": 1069,
"text": "We found that lung-stage S. japonicum infection significantly ameliorated OVA-induced AAI, whereas post-lung-stage infection did not."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17042799",
"endSection": "abstract",
"offsetInBeginSection": 1201,
"offsetInEndSection": 1378,
"text": "In a murine model of asthma, S. japonicum egg antigens decreased the expression of Th2 cytokines, relieved antigen-induced airway inflammation, and inhibited asthma development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28614408",
"endSection": "abstract",
"offsetInBeginSection": 667,
"offsetInEndSection": 745,
"text": "We found that S. japonicum infection downregulated airway hyperresponsiveness."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34358648",
"endSection": "abstract",
"offsetInBeginSection": 419,
"offsetInEndSection": 655,
"text": "However, in recent years, studies have found that Schistosoma infection or Schistosoma related products can improve or prevent some immune and inflammatory diseases, such as severe asthma, inflammatory bowel disease, diabetes and so on."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18824533",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 159,
"text": "In areas where schistosomiasis is endemic, a negative correlation is observed between atopy and helminth infection, associated with a low prevalence of asthma."
}
] | 11 |
BioASQ-training11b
| null | null |
622f6ad13a8413c6530000aa
|
bioasq_yesno
|
factoid
|
Which antiepileptic drug is most strongly associated with spina bifida?
|
['Valproate']
|
[
"Valproate",
"Valproic acid",
"Divalproex sodium",
"Sodium valproate",
"Valproate sodium"
] |
['Phenytoin is not used in pregnancy as it is associated with a severe fetal deformation. From the other anticonvulsants most studies report the higher association between use during pregnancy and spin bifida to occur with Valproate.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23082254",
"http://www.ncbi.nlm.nih.gov/pubmed/22051200",
"http://www.ncbi.nlm.nih.gov/pubmed/21766433",
"http://www.ncbi.nlm.nih.gov/pubmed/19490036",
"http://www.ncbi.nlm.nih.gov/pubmed/17075842",
"http://www.ncbi.nlm.nih.gov/pubmed/11077457",
"http://www.ncbi.nlm.nih.gov/pubmed/10339792",
"http://www.ncbi.nlm.nih.gov/pubmed/8075508",
"http://www.ncbi.nlm.nih.gov/pubmed/2707392",
"http://www.ncbi.nlm.nih.gov/pubmed/3939491"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22051200",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 258,
"text": "The teratogenicity of antiepilepsy drug valproic acid (VPA) mostly is found in genetic and somatic levels, causing teratogenesis involving neurotubular defects (NTDs), anencephaly, lumbosacral meningomyelocele, and leg dysfunction due to spina bifida aperta."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21766433",
"endSection": "sections.0",
"offsetInBeginSection": 721,
"offsetInEndSection": 1062,
"text": "The summary odds ratio estimate for the association between valproic acid and spina bifida was 11.9 (95% uncertainty interval (UI): 4.0-21.2); for valproic acid and cleft palate 5.8 (95% UI: 3.3-9.5); for carbamazepine and spina bifida 3.6 (95% UI: 1.3-7.8); and for carbamazepine and cleft palate 2.4 (95% UI: 1.1-4.5) in the United States."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19490036",
"endSection": "sections.0",
"offsetInBeginSection": 1030,
"offsetInEndSection": 1307,
"text": "Increased risk for MCMs could be demonstrated only for exposure to valproate (5.6%, p = 0.005) and AED polytherapy (6.1%, p = 0.02). Neonatal spina bifida was not significantly increased, but was a major indication for elective pregnancy termination among women with epilepsy. "
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17075842",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 316,
"text": "Valproic acid, a drug commonly used to treat seizures and other psychiatric disorders, causes neural tube defects (NTDs) in exposed fetuses at a rate 20 times higher than in the general population. Failure of the neural tube to close during development results in exencephaly or anencephaly, as well as spina bifida."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11077457",
"endSection": "sections.0",
"offsetInBeginSection": 1034,
"offsetInEndSection": 1095,
"text": "Associations were found for spina bifida with valproic acid. "
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10339792",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 95,
"text": "Fetal exposure to valproic acid or carbamazepine increases the risk of neural tube defect (NTD)"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8075508",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 684,
"text": "Women with epilepsy giving birth during 1973 to 1991 were identified by record linkage of Swedish health registries. Among 3,625 identified infants, 9 had spina bifida. A nested case-control study was performed, comparing drugs used in early pregnancy in the 9 cases and in 18 controls, matched for year of delivery, maternal age, and parity. Six of the spina bifida mothers had used carbamazepine and two had used valproic acid. Among the controls, 5 women used carbamazepine and one valproic acid. There is an apparent excess risk for spina bifida after use of either of these two drugs, but it is not statistically significant when the analysis is restricted to drug-using women. T"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2707392",
"endSection": "sections.0",
"offsetInBeginSection": 459,
"offsetInEndSection": 623,
"text": "A significant association was seen between maternal use of valproic acid and spina bifida, and a weaker, non-significant one between carbamazepine and spina bifida."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3939491",
"endSection": "sections.0",
"offsetInBeginSection": 768,
"offsetInEndSection": 988,
"text": "A statistically significant association between Spina Bifida and Valproic Acid (odds ratio 22.7; Fisher p value = 0.0364) was observed: no other anticonvulsant tested showed any association with any type of malformation."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.disease-ontology.org/api/metadata/DOID:0080016",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D000927"
] | null |
51588bb2d24251bc05000091
|
bioasq_factoid
|
factoid
|
What is the function of calcium-sensing receptor (CaSR)?
|
['The calcium-sensing receptor (CaSR) is a G-protein-coupled receptor that plays an essential role in maintaining calcium homeostasis.']
|
[
"calcium-sensing receptor",
"CaSR",
"calcium-sensing receptor (CaSR)",
"Ca2+ sensing receptor",
"calcium receptor"
] |
['The calcium-sensing receptor (CaSR) is a G-protein-coupled receptor that plays an essential role in maintaining calcium homeostasis.\nThe CaSR is a key regulator for such diverse processes as hormone secretion, gene expression, inflammation, proliferation, differentiation, and apoptosis. Due to this pleiotropy, the CaSR is able to regulate cell fate and is implicated in the development of many types of benign or malignant tumours of the breast, prostate, parathyroid, and colon.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21566074",
"http://www.ncbi.nlm.nih.gov/pubmed/26386835",
"http://www.ncbi.nlm.nih.gov/pubmed/23856267",
"http://www.ncbi.nlm.nih.gov/pubmed/26608608",
"http://www.ncbi.nlm.nih.gov/pubmed/26261299"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26386835",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "The calcium-sensing receptor (CaSR) is a G-protein-coupled receptor that plays an essential role in maintaining calcium homeostasis. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26608608",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 261,
"text": "The calcium-sensing receptor (CaSR) plays a pivotal role in systemic calcium metabolism by regulating parathyroid hormone secretion and urinary calcium excretion. The CaSR is ubiquitously expressed, implying a wide range of functions regulated by this receptor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26608608",
"endSection": "abstract",
"offsetInBeginSection": 689,
"offsetInEndSection": 1037,
"text": "The CaSR is a key regulator for such diverse processes as hormone secretion, gene expression, inflammation, proliferation, differentiation, and apoptosis. Due to this pleiotropy, the CaSR is able to regulate cell fate and is implicated in the development of many types of benign or malignant tumours of the breast, prostate, parathyroid, and colon."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26261299",
"endSection": "abstract",
"offsetInBeginSection": 168,
"offsetInEndSection": 326,
"text": "Extracellular calcium-sensing receptor (CaSR) and ovarian cancer gene receptor 1 (OGR1) are two GPCRs that sense extracellular Ca(2+) and H(+), respectively. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21566074",
"endSection": "abstract",
"offsetInBeginSection": 91,
"offsetInEndSection": 179,
"text": " The calcium-sensing receptor (CASR) plays a key role in maintaining calcium homeostasis"
}
] | 6 |
BioASQ-training6b
| null | null |
58cd7fed02b8c6095300003f
|
bioasq_factoid
|
factoid
|
What is the first-line treatment for BRAF mutated advanced colorectal cancer patients?
|
['FOLFOXIRI plus Bevacizumab', 'FOLFOXIRI + Bevacizumab']
|
[
"FOLFOXIRI plus Bevacizumab",
"FOLFOXIRI + Bevacizumab",
"FOLFOXIRI with Bevacizumab",
"FOLFOXIRI and Bevacizumab"
] |
['The first-line treatment for BRAF mutated advanced colorectal cancer patients is chemotherapy with bevacizumab as well as 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab in patients with a good performance status.', 'The first-line treatment for BRAF mutated advanced colorectal cancer patients has been a subject of intense debate and research. A triplet regimen, which consists of BRAF inhibitor, MEK inhibitor and EGFR inhibitor has shown to provide promising results for patients with BRAF-mutant advanced colorectal cancer in comparison to conventional doublet chemotherapy.', 'The first-line treatment for BRAF mutated advanced colorectal cancer typically involves chemotherapy with bevacizumab, as well as 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab in patients with a good performance status. However, recent clinical research has shown promising results for combination strategies involving mitogen-activated protein kinase (MAPK) pathway blockade, such as the Binimetinib, Encorafenib, And Cetuximab cOmbiNed to treat BRAF-mutant Colorectal Cancer (BEACON CRC) study. This study provided strong clinical evidence to support BRAF and epidermal growth factor receptor inhibition with the combination of encorafenib plus cetuximab in BRAF V600E-mutated mCRC. As', 'The first-line treatment for BRAF mutated advanced colorectal cancer patients includes bevacizumab, chemotherapy, and chemotherapy\u2009+\u2009bevacizumab.', 'The first-line treatment for BRAF mutated advanced colorectal cancer patients is chemotherapy, which includes cytotoxic chemotherapy plus bevacizumab.', 'The first-line treatment for BRAF-mutated advanced colorectal cancer includes chemotherapy with bevacizumab, and specifically the regimen of 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab for patients with good performance status.', 'The first-line treatment for BRAF-mutated advanced colorectal cancer includes chemotherapy with bevacizumab and a regimen of 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan, known as FOLFOXIRI, particularly for patients with good performance status.', 'The current standard first-line treatment for BRAF-mutated advanced colorectal cancer patients is chemotherapy with bevacizumab, as well as 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab in patients with a good performance status.', 'Chemotherapy with bevacizumab, 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab is the first-line treatment for BRAF mutated advanced colorectal cancer patients.', 'The first-line treatment for BRAF mutated advanced colorectal cancer patients is chemotherapy with bevacizumab, as well as 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab in patients with a good performance status.', 'Chemotherapy with bevacizumab as well as 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab is the first-line treatment for BRAF mutated advanced colorectal cancer patients.', 'The first-line treatment for BRAF-mutated advanced colorectal cancer patients typically involves a combination of chemotherapy with bevacizumab, such as the FOLFOXIRI regimen, which includes 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan, along with bevacizumab. This treatment approach has shown efficacy in improving outcomes for these patients, regardless of their RAS and BRAF mutational status. Additionally, FOLFOXIRI plus bevacizumab is considered a preferred first-line treatment option for clinically selected patients with right-sided metastatic colorectal cancer.', 'The current standard first-line treatment options for BRAF-mutated metastatic colorectal cancer (mCRC) are:\n\n1. Chemotherapy with bevacizumab \n2. FOLFOXIRI (5-fluorouracil, leucovorin, oxaliplatin, and irinotecan) plus bevacizumab in patients with a good performance status\n\nFOLFOXIRI plus bevacizumab is a feasible treatment option for eligible patients irrespective of baseline clinical characteristics and RAS or BRAF mutational status. However, patients with BRAF mutations have worse overall survival compared to those with RAS mutations or RAS/BRAF wild-type.', 'The first-line treatment for BRAF-mutated advanced colorectal cancer patients typically involves a combination of cytotoxic chemotherapy and an antiangiogenic antibody, such as bevacizumab.', 'The first-line treatment for advanced colorectal cancer patients with a BRAF mutation includes FOLFOXIRI combined with bevacizumab, or chemotherapy alongside bevacizumab, incorporating drugs like 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan.', 'The current standard therapies for first-line treatment of BRAF-mutated mCRC include chemotherapy with bevacizumab and 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab in patients with a good performance status.', 'The first-line treatment for BRAF-mutated advanced colorectal cancer (mCRC) typically includes chemotherapy combined with bevacizumab. Specifically, regimens such as 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab are used, especially in patients who have a good performance status. This approach is feasible for patients who meet specific study inclusion criteria, regardless of their RAS or BRAF mutational status.', 'The first-line treatment for BRAF mutated advanced colorectal cancer patients is a fluoropyrimidine-based cytotoxic regimen in combination with bevacizumab.', 'The current standard first-line treatment for BRAF-mutated advanced colorectal cancer patients involves chemotherapy with bevacizumab, along with a combination of 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab, especially in patients with a good performance status. FOLFOXIRI plus bevacizumab is considered a feasible treatment option for eligible patients, regardless of baseline clinical characteristics and RAS or BRAF mutational status.', 'The current standard therapies for first-line treatment of BRAF-mutated mCRC are chemotherapy with bevacizumab as well as 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab in patients with a good performance status. FOLFOXIRI plus bevacizumab is a feasible treatment option for those patients who meet the inclusion criteria of the present study, irrespective of baseline clinical characteristics and RAS or BRAF mutational status', 'The first-line treatment for BRAF-mutated advanced colorectal cancer typically includes chemotherapy combined with bevacizumab, specifically using regimens like FOLFOXIRI (5-fluorouracil, leucovorin, oxaliplatin, and irinotecan) plus bevacizumab, especially in patients with good performance status', 'The standard first-line treatment for BRAF mutated advanced colorectal cancer (mCRC) typically involves combination chemotherapy with or without targeted therapy, such as bevacizumab or cetuximab. For patients with wild-type RAS and BRAF mutations, the addition of anti-EGFR antibodies like cetuximab to standard chemotherapy has shown improved outcomes compared to chemotherapy alone. However, for those with BRAF V600E mutation specifically, response rates to these treatments are generally lower, and more recent data suggest that a combination therapy including BRAF inhibitors (e.g., encorafenib) along with anti-EGFR antibodies may provide better outcomes in the first-line setting. It is important to note that treatment options can vary based on individual patient characteristics, disease stage, and molecular profiling results.', 'The first-line treatment for BRAF mutated advanced colorectal cancer patients typically involves a combination of chemotherapy and targeted therapy. The current standard therapies include fluoropyrimidine-based cytotoxic regimen with bevacizumab, or FOLFOXIRI plus bevacizumab in patients with good performance status. Recently, combination strategies involving mitogen-activated protein kinase (MAPK) pathway blockade have shown promising results for the treatment of patients with BRAF V600E-mutated mCRC. The largest study to date is the Binimetinib, Encorafenib, And Cetuximab cOmbiNed to treat BRAF-mutant ColoRectal Cancer (BEACON CRC) study, which has provided strong clinical evidence for BRAF and epidermal growth factor receptor inhibition with the combination of encorafenib plus cetuximab.', 'The current standard first-line treatment for BRAF-mutated metastatic colorectal cancer (mCRC) patients is FOLFOXIRI (5-fluorouracil, leucovorin, oxaliplatin, and irinotecan) plus bevacizumab, especially for patients with a good performance status. Triplet chemotherapy (FOLFOXIRI) plus bevacizumab is indicated as a preferred option for these patients, irrespective of their RAS mutational status.', "The current standard first-line treatment for BRAF mutated advanced colorectal cancer patients is a combination of chemotherapy with bevacizumab (a monoclonal antibody that targets vascular endothelial growth factor) and either 5-fluorouracil, leucovorin, and oxaliplatin (FOLFOX) or 5-fluorouracil, leucovorin, and irinotecan (FOLFIRI), depending on the patient's performance status and other factors. This treatment is recommended for patients with a good performance status, as FOLFOXIRI plus bevacizumab is a feasible treatment option for those who meet the inclusion criteria, irrespective of baseline clinical characteristics and RAS or BRAF mutational status. However, the median overall survival is shorter in patients with RAS-mutation-positive or BRAF-mutation-positive tumors compared to those with RAS and BRAF wild-type tumors (25.6 months vs. 37.1 months vs. 13.4 months, respectively).", 'Triplet chemotherapy (FOLFOXIRI) + bevacizumab regimen is indicated as first-line treatment of BRAF-mutated metastatic colorectal cancer (mCRC).', 'The first-line treatment for BRAF-mutated advanced colorectal cancer (mCRC) typically includes chemotherapy combined with bevacizumab, specifically using regimens like 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab, especially in patients with good performance status. This approach is feasible for patients who meet specific study inclusion criteria, regardless of their RAS or BRAF mutational status.', 'The first-line treatment for BRAF mutated advanced colorectal cancer patients is chemotherapy with bevacizumab, FOLFOXIRI plus bevacizumab, and bevacizumab.', 'The first-line treatment for BRAF mutated advanced colorectal cancer patients is not well established, as there are limited data and no consensus on the optimal approach. However, a phase II study known as NIVACOR is currently investigating the combination of triplet chemotherapy (FOLFOXIRI) with bevacizumab and nivolumab in patients with mCRC RAS/BRAF mutated, regardless of microsatellite status. The primary endpoint of the study is the overall response rate, and secondary endpoints include overall survival, safety, time to progression, and duration of response. Additionally, translational studies are being conducted to evaluate tumor mutational burden and genetic alterations by circulating free DNA (cfDNA) obtained from plasma samples. The trial is currently open to enrollment.', 'The first-line treatment for BRAF mutated advanced colorectal cancer (mCRC) patients includes chemotherapy with bevacizumab and 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab. This combination therapy has been found to be a feasible treatment option for mCRC patients with a good performance status, regardless of their baseline clinical characteristics or RAS or BRAF mutational status. However, it is important to note that the median overall survival (OS) for BRAF-mutation-positive subgroups is shorter compared to RAS and BRAF wild-type subgroups. The OS for BRAF-mutation-positive patients is 13.4 months (95% CI 8.2-24.1), while for RAS and BRAF wild-type subgroups,', 'The first-line treatment for BRAF mutated advanced colorectal cancer patients would be a combination of BRAF, MEK, and EGFR inhibitors.', 'The current standard first-line treatment for BRAF-mutated advanced colorectal cancer patients is chemotherapy with bevacizumab, as well as 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab. This treatment regimen has shown improved overall survival compared to other treatment options.', "The current standard first-line treatment for BRAF mutated advanced colorectal cancer (mCRC) patients is chemotherapy with either 5-fluorouracil, leucovorin, and irinotecan (FOLFIRI) or capecitabine and irinotecan (XELOXI), both in combination with the anti-EGFR antibody panitumumab or cetuximab. However, patients with BRAF mutations should not receive anti-EGFR therapy as it has been shown to be ineffective and may even worsen outcomes. Therefore, the choice of chemotherapy regimen and anti-EGFR antibody should be based on other factors such as patient's performance status, prior chemotherapy, and RAS mutational status. Bevacizum", '1. Chemotherapy with bevacizumab and 2. FOLFOXIRI plus bevacizumab in patients with good performance status are the first-line treatment options for BRAF-mutated metastatic colorectal cancer.', 'The first-line treatment for BRAF mutated advanced colorectal cancer patients is chemotherapy with bevacizumab as well as 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab.', 'chemotherapy with bevacizumab as well as 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/37352476",
"http://www.ncbi.nlm.nih.gov/pubmed/30120161",
"http://www.ncbi.nlm.nih.gov/pubmed/24390240",
"http://www.ncbi.nlm.nih.gov/pubmed/35130499",
"http://www.ncbi.nlm.nih.gov/pubmed/23666916",
"http://www.ncbi.nlm.nih.gov/pubmed/32326305",
"http://www.ncbi.nlm.nih.gov/pubmed/33734401",
"http://www.ncbi.nlm.nih.gov/pubmed/36475784",
"http://www.ncbi.nlm.nih.gov/pubmed/33914242",
"http://www.ncbi.nlm.nih.gov/pubmed/30592501",
"http://www.ncbi.nlm.nih.gov/pubmed/31661924",
"http://www.ncbi.nlm.nih.gov/pubmed/35649231",
"http://www.ncbi.nlm.nih.gov/pubmed/36849918",
"http://www.ncbi.nlm.nih.gov/pubmed/27943689",
"http://www.ncbi.nlm.nih.gov/pubmed/37971411",
"http://www.ncbi.nlm.nih.gov/pubmed/28214977",
"http://www.ncbi.nlm.nih.gov/pubmed/33108877",
"http://www.ncbi.nlm.nih.gov/pubmed/37815847",
"http://www.ncbi.nlm.nih.gov/pubmed/33836264",
"http://www.ncbi.nlm.nih.gov/pubmed/26338525",
"http://www.ncbi.nlm.nih.gov/pubmed/31455117",
"http://www.ncbi.nlm.nih.gov/pubmed/33987088",
"http://www.ncbi.nlm.nih.gov/pubmed/37455182",
"http://www.ncbi.nlm.nih.gov/pubmed/34761599",
"http://www.ncbi.nlm.nih.gov/pubmed/37639010",
"http://www.ncbi.nlm.nih.gov/pubmed/32867715",
"http://www.ncbi.nlm.nih.gov/pubmed/37760573",
"http://www.ncbi.nlm.nih.gov/pubmed/32318348",
"http://www.ncbi.nlm.nih.gov/pubmed/24138831",
"http://www.ncbi.nlm.nih.gov/pubmed/37369457"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33836264",
"endSection": "abstract",
"offsetInBeginSection": 883,
"offsetInEndSection": 1132,
"text": "The current standard therapies for first-line treatment of BRAF-mutated mCRC are chemotherapy with bevacizumab as well as 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab in patients with a good performance status"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26338525",
"endSection": "abstract",
"offsetInBeginSection": 2733,
"offsetInEndSection": 2947,
"text": "FOLFOXIRI plus bevacizumab is a feasible treatment option for those patients who meet the inclusion criteria of the present study, irrespective of baseline clinical characteristics and RAS or BRAF mutational status"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26338525",
"endSection": "abstract",
"offsetInBeginSection": 2292,
"offsetInEndSection": 2621,
"text": "Median overall survival was 37·1 months (95% CI 29·7-42·7) in the RAS and BRAF wild-type subgroup compared with 25·6 months (22·4-28·6) in the RAS-mutation-positive subgroup (HR 1·49, 95% CI 1·11-1·99) and 13·4 months (8·2-24·1) in the BRAF-mutation-positive subgroup (HR 2·79, 95% CI 1·75-4·46; likelihood-ratio test p<0·0001). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32326305",
"endSection": "abstract",
"offsetInBeginSection": 49,
"offsetInEndSection": 329,
"text": "the most frequently used first-line treatments for patients with BRAF-mutant colorectal cancer (CRC), while second-line treatment requires extensive further research. In this pooled analysis, we evaluate the impact of anti-angiogenics in patients with pre-treated BRAF-mutant CRC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35649231",
"endSection": "abstract",
"offsetInBeginSection": 579,
"offsetInEndSection": 822,
"text": "for patients with BRAFV600E-mutated metastatic colorectal cancer include first-line cytotoxic chemotherapy plus bevacizumab and subsequent therapy with the BRAF inhibitor encorafenib and antiepidermal growth factor receptor antibody cetuximab."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36475784",
"endSection": "abstract",
"offsetInBeginSection": 131,
"offsetInEndSection": 300,
"text": "However, there are no clear recommendations regarding first-line therapy for patients with early recurrent BRAF V600E-mutated CRC, during or after adjuvant chemotherapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33836264",
"endSection": "abstract",
"offsetInBeginSection": 1313,
"offsetInEndSection": 1730,
"text": "The Binimetinib, Encorafenib, And Cetuximab cOmbiNed to treat BRAF-mutant ColoRectal Cancer (BEACON CRC) study represents the largest study in this population to date and has given strong clinical evidence to support BRAF and epidermal growth factor receptor inhibition with the combination of encorafenib plus cetuximab.CONCLUSIONS: The treatment of BRAF-mutated mCRC has evolved rapidly over the last several years."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36849918",
"endSection": "abstract",
"offsetInBeginSection": 1635,
"offsetInEndSection": 1959,
"text": "Surgical treatment of the primary tumor (P = 0.041; HR, 0.523; 95% CI, 0.280-0.974) was significantly associated with PFS too.CONCLUSION: For patients with BRAF V600E-mutated advanced CRC, chemotherapy alone did not differ significantly in OS and PFS compared with chemotherapy + bevacizumab for advanced first-line therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35649231",
"endSection": "abstract",
"offsetInBeginSection": 504,
"offsetInEndSection": 822,
"text": "On the basis of recent clinical trials, current standard-of-care therapies for patients with BRAFV600E-mutated metastatic colorectal cancer include first-line cytotoxic chemotherapy plus bevacizumab and subsequent therapy with the BRAF inhibitor encorafenib and antiepidermal growth factor receptor antibody cetuximab."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33836264",
"endSection": "abstract",
"offsetInBeginSection": 855,
"offsetInEndSection": 1105,
"text": "es in this setting.RESULTS: The current standard therapies for first-line treatment of BRAF-mutated mCRC are chemotherapy with bevacizumab as well as 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab in patients wit"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24138831",
"endSection": "abstract",
"offsetInBeginSection": 1571,
"offsetInEndSection": 1685,
"text": "domised trials in this specific molecular subgroup, FOLFOXIRI plus bevacizumab might be a reasonable option for th"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26338525",
"endSection": "abstract",
"offsetInBeginSection": 2659,
"offsetInEndSection": 2874,
"text": " different across molecular subgroups (pinteraction=0·52).INTERPRETATION: FOLFOXIRI plus bevacizumab is a feasible treatment option for those patients who meet the inclusion criteria of the present study, irrespecti"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28214977",
"endSection": "abstract",
"offsetInBeginSection": 1037,
"offsetInEndSection": 1276,
"text": "Despite the lack of a randomized phase 3 study dedicated to BRAF-mutated CRC, chemotherapy intensification combining a quadruple association of 5-fluorouracil, oxaliplatin, irinotecan (FOLFOXIRI), and bevacizumab seems like a valid option."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32867715",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 201,
"text": "BACKGROUND: FOLFOXIRI (fluorouracil, leucovorin, oxaliplatin, and irinotecan) plus bevacizumab has shown to be one of the therapeutic regimens in first line with the highest activity in patients (pts.)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37639010",
"endSection": "abstract",
"offsetInBeginSection": 770,
"offsetInEndSection": 1282,
"text": "This article reviews the progress of clinical research on molecularly targeted drugs, immune checkpoint inhibitors, first-line chemotherapeutic agents, and different combination therapy regimens (including different targeted drug combinations, immune combination targeting, and chemotherapy combination targeting) for colorectal cancer patients with BRAF V600E mutation, which provides a reference for further in-depth clinical exploration of the treatment of colorectal cancer patients with BRAF V600E mutation."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36475784",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "TRESBIEN (OGSG 2101): encorafenib, binimetinib and cetuximab for early recurrent stage II/III "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37352476",
"endSection": "abstract",
"offsetInBeginSection": 1458,
"offsetInEndSection": 1763,
"text": "Median OS analyzed at an event rate of 64.5% showed a trend toward shorter survival in cetuximab-treated patients (12.9 months v 17.1 months; HR, 1.4; P = .20).CONCLUSION: To our knowledge, FIRE-4.5 is the first prospective and randomized study investigating first-line treatment of BRAFV600E-mutant mCRC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37352476",
"endSection": "abstract",
"offsetInBeginSection": 1914,
"offsetInEndSection": 2028,
"text": "Bevacizumab-based chemotherapy remains the preferable first-line treatment of patients with BRAFV600E-mutant mCRC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31661924",
"endSection": "abstract",
"offsetInBeginSection": 429,
"offsetInEndSection": 657,
"text": "Chemotherapy plus bevacizumab is the current standard therapy in first-line treatment of BRAF-mutated metastatic CRC (mCRC), with triplet (FOLFOXIRI) plus bevacizumab as a valid option in patients with a good performance status."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35130499",
"endSection": "abstract",
"offsetInBeginSection": 1147,
"offsetInEndSection": 1353,
"text": "95% CI, 0.41-0.56; P<.001). Only 3% of patients with BRAF mutations received first-line FOLFOXIRI ± bevacizumab, with a median OS of 13.8 months compared with 15.5 months in those treated with doublet chemo"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35130499",
"endSection": "abstract",
"offsetInBeginSection": 1354,
"offsetInEndSection": 1629,
"text": "herapy ± bevacizumab (P=.38). In patients with BRAF mutations, propensity-weighted analysis did not detect a significant improvement in OS with FOLFIRI + bevacizumab (HR, 0.90; 95% CI, 0.58-1.39; P=.63) or FOLFOX/CAPEOX + bevacizumab (HR, 0.81; 95% CI, 0.52-1.26; P=.35) vers"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27943689",
"endSection": "abstract",
"offsetInBeginSection": 1009,
"offsetInEndSection": 1318,
"text": "Currently, three biologic agents-bevacizumab, cetuximab, and panitumumab-are approved for first-line treatment of metastatic colorectal cancer. For patients with mutant RAS and likely mutant BRAF V600E tumors, bevacizumab is the only biologic agent that can be used in conjunction with cytotoxic chemotherapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27943689",
"endSection": "abstract",
"offsetInBeginSection": 1153,
"offsetInEndSection": 1318,
"text": "For patients with mutant RAS and likely mutant BRAF V600E tumors, bevacizumab is the only biologic agent that can be used in conjunction with cytotoxic chemotherapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34761599",
"endSection": "abstract",
"offsetInBeginSection": 1049,
"offsetInEndSection": 1377,
"text": "Multivariate analysis indicated that age (HR:0.41,p=0.045), primary tumor resection (HR:0.41,p=0.037) and primary tumor localization (HR:0.38,p=0.021) for PFS and age (HR:0.39, p=0.09), the presence of BRAF mutation (HR:0.59,p=0.019) and the type of targeted therapy (HR:3.16,p=0.025) for OS were independent prognostic factors."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35649231",
"endSection": "abstract",
"offsetInBeginSection": 499,
"offsetInEndSection": 1208,
"text": "ing. On the basis of recent clinical trials, current standard-of-care therapies for patients with BRAFV600E-mutated metastatic colorectal cancer include first-line cytotoxic chemotherapy plus bevacizumab and subsequent therapy with the BRAF inhibitor encorafenib and antiepidermal growth factor receptor antibody cetuximab. Treatment regimens currently under exploration in BRAFV600E-mutant metastatic colorectal cancer include combinatorial options of various pathway-targeted therapies, cytotoxic chemotherapy, and/or immune checkpoint blockade, among others. Circumvention of adaptive and acquired resistance to BRAF-targeted therapies is a significant challenge to be overcome in BRAF-mutated advanced col"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35649231",
"endSection": "abstract",
"offsetInBeginSection": 499,
"offsetInEndSection": 1045,
"text": "ing. On the basis of recent clinical trials, current standard-of-care therapies for patients with BRAFV600E-mutated metastatic colorectal cancer include first-line cytotoxic chemotherapy plus bevacizumab and subsequent therapy with the BRAF inhibitor encorafenib and antiepidermal growth factor receptor antibody cetuximab. Treatment regimens currently under exploration in BRAFV600E-mutant metastatic colorectal cancer include combinatorial options of various pathway-targeted therapies, cytotoxic chemotherapy, and/or immune checkpoint blockade"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35649231",
"endSection": "abstract",
"offsetInBeginSection": 499,
"offsetInEndSection": 812,
"text": "ing. On the basis of recent clinical trials, current standard-of-care therapies for patients with BRAFV600E-mutated metastatic colorectal cancer include first-line cytotoxic chemotherapy plus bevacizumab and subsequent therapy with the BRAF inhibitor encorafenib and antiepidermal growth factor receptor antibody "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33108877",
"endSection": "abstract",
"offsetInBeginSection": 216,
"offsetInEndSection": 562,
"text": " BRAF mutated colorectal cancer define specific challenging subgroup associated with dismal prognosis, lower rate of response rate, shorter progression free survival and overall survival. Current treatment choices are associated with poor outcomes. For the first line treatment doublet or triplet chemotherapy plus antiangiogenic antibody is used"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30120161",
"endSection": "abstract",
"offsetInBeginSection": 2023,
"offsetInEndSection": 2173,
"text": "utated mCRC with progression following first-line with FOLFOXIRI plus bevacizumab, although tolerability was acceptable. Our trial suggests that explo"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33836264",
"endSection": "abstract",
"offsetInBeginSection": 802,
"offsetInEndSection": 1852,
"text": "mCRC, with a focus on recent clinical research advances in this setting.RESULTS: The current standard therapies for first-line treatment of BRAF-mutated mCRC are chemotherapy with bevacizumab as well as 5-fluorouracil, leucovorin, oxaliplatin, and irinotecan (FOLFOXIRI) plus bevacizumab in patients with a good performance status. Combination strategies involving mitogen-activated protein kinase (MAPK) pathway blockade have shown promising results for the treatment of patients with BRAF V600E-mutated mCRC. The Binimetinib, Encorafenib, And Cetuximab cOmbiNed to treat BRAF-mutant ColoRectal Cancer (BEACON CRC) study represents the largest study in this population to date and has given strong clinical evidence to support BRAF and epidermal growth factor receptor inhibition with the combination of encorafenib plus cetuximab.CONCLUSIONS: The treatment of BRAF-mutated mCRC has evolved rapidly over the last several years. Recently, combination strategies involving MAPK pathway blockade have shown promising results in BRAF V600E-mutated mCRC,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32318348",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1528,
"text": "Colorectal cancer (CRC) is a highly lethal disease worldwide. The majority of patients receiving targeted therapy or chemotherapy develop drug resistance, while its molecular mechanism remains to be elucidated. The plasma circulating tumor DNA (ctDNA) exhibited the potential in identifying gene variations and monitoring drug resistance in CRC treatment. In this study, we monitored the ctDNA mutational changes in advanced CRC patients underwent first-line therapy with bevacizumab and cetuximab combined with chemotherapy. The mutation spectrum of 43 patients was established by a 605-gene next-generation sequencing (NGS) panel. The baseline measurement shows that genes with the highest mutation frequency were TP53 (74%), APC (58%), KRAS (40%), SYNE1 (33%), LRP1B (23%), TOP1 (23%), and PIK3CA (21%). Mutations in TP53, APC, and KRAS were detected in 29 paired plasma and tissue samples with the consistency of 81, 67, and 42%, respectively. Clinically targetable gene mutations, such as APC, RNF43, SMAD4, BRAD1, KRAS, RAF1, and TP53, were also identified in ctDNA. The overall consistency between ctDNA and tissue samples was 54.6%. Alleviation of mutational burden in BRAF, KRAS, AMER1, and other major driving genes was observed following the first-line therapy. Patients with KRAS and TP53 mutations in tissues appeared to benefit more than the wild-type counterpart. The dynamic change of plasma mutation status was consistent with the tissue tumor burden and was closely correlated with disease progression. In conc"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33108877",
"endSection": "abstract",
"offsetInBeginSection": 453,
"offsetInEndSection": 845,
"text": "r outcomes. For the first line treatment doublet or triplet chemotherapy plus antiangiogenic antibody is used. To date, there were no reasonable treatment options in the second line settings. Recently published BEACON trial sets new standard of treatment with combination of encorafenib plus cetuximab, which led to significantly longer overall survival and overall response compared to stand"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24138831",
"endSection": "abstract",
"offsetInBeginSection": 292,
"offsetInEndSection": 473,
"text": " trial that FOLFOXIRI (5-FU/LV+Oxaliplatin+Irinotecan) plus bevacizumab might allow to achieve remarkable results in terms of PFS and Overall Survival (OS) also in this poor-prognos"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24138831",
"endSection": "abstract",
"offsetInBeginSection": 1508,
"offsetInEndSection": 1685,
"text": "rol rate were 72% and 88%, respectively.CONCLUSION: Lacking randomised trials in this specific molecular subgroup, FOLFOXIRI plus bevacizumab might be a reasonable option for th"
}
] | 13 |
BioASQ-training13b
| null | null |
66099a25fdcbea915f00001e
|
bioasq_factoid
|
factoid
|
Cilta-cel was developed for treatment of which disease?
|
['multiple myeloma']
|
[
"multiple myeloma",
"plasma cell myeloma",
"myeloma",
"Kahler's disease",
"myelomatosis"
] |
['Cilta-cel, a BCMA-targeting chimeric antigen receptor T-cell therapy for multiple myeloma.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/37014590",
"http://www.ncbi.nlm.nih.gov/pubmed/34175021",
"http://www.ncbi.nlm.nih.gov/pubmed/37716872",
"http://www.ncbi.nlm.nih.gov/pubmed/37913909",
"http://www.ncbi.nlm.nih.gov/pubmed/37497629",
"http://www.ncbi.nlm.nih.gov/pubmed/36271807",
"http://www.ncbi.nlm.nih.gov/pubmed/37272512",
"http://www.ncbi.nlm.nih.gov/pubmed/36411210",
"http://www.ncbi.nlm.nih.gov/pubmed/37750399",
"http://www.ncbi.nlm.nih.gov/pubmed/36720180",
"http://www.ncbi.nlm.nih.gov/pubmed/36269898",
"http://www.ncbi.nlm.nih.gov/pubmed/34885106",
"http://www.ncbi.nlm.nih.gov/pubmed/35764490",
"http://www.ncbi.nlm.nih.gov/pubmed/34840088",
"http://www.ncbi.nlm.nih.gov/pubmed/37704875",
"http://www.ncbi.nlm.nih.gov/pubmed/35900317"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36411210",
"endSection": "abstract",
"offsetInBeginSection": 1174,
"offsetInEndSection": 1407,
"text": " Additional indirect treatment comparisons conducted separately for ide-cel and cilta-cel have demonstrated that these CAR-T therapies hold promise for substantial clinical benefit relative to currently available treatments for RRMM."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36271807",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 607,
"text": "OBJECTIVE: This study used the latest available data cuts from the CARTITUDE-1 and KarMMa clinical trials to update previously published matching-adjusted indirect treatment comparisons (MAICs) assessing the comparative efficacy of ciltacabtagene autoleucel (cilta-cel) versus the FDA-approved idecabtagene vicleucel (ide-cel) dose range of 300 to 450 × 106 CAR-positive T-cells in the treatment of patients with relapsed or refractory multiple myeloma (RRMM) who were previously treated with a proteasome inhibitor, an immunomodulatory drug, and an anti-CD38 monoclonal antibody (i.e. triple-class exposed)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36271807",
"endSection": "abstract",
"offsetInBeginSection": 1645,
"offsetInEndSection": 1850,
"text": "CONCLUSIONS: These analyses demonstrate improved efficacy with cilta-cel versus ide-cel for all outcomes over longer follow-up and highlight its therapeutic potential in triple-class exposed RRMM patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36269898",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 253,
"text": "PURPOSE: CARTIFAN-1 aimed to evaluate the efficacy and safety of ciltacabtagene autoleucel (cilta-cel), a B-cell maturation antigen-targeting chimeric antigen receptor T-cell therapy, in Chinese patients with relapsed/refractory multiple myeloma (RRMM)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36269898",
"endSection": "abstract",
"offsetInBeginSection": 1776,
"offsetInEndSection": 1978,
"text": "CONCLUSION: These data demonstrate a favorable risk-benefit profile for a single infusion of cilta-cel, resulting in early, deep, and durable responses in heavily pretreated patients with RRMM in China."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37497629",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "Cilta-cel, a BCMA-targeting CAR-T therapy for heavily pretreated patients with relapsed/refractory multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37497629",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 323,
"text": "Cilta-cel, a BCMA-targeting chimeric antigen receptor T-cell therapy for multiple myeloma, was approved in USA on 28 February 2022, for patients with relapsed or refractory disease who have received ≥4 prior lines of therapy, including a proteasome inhibitor, an immunomodulatory drug, and an anti-CD38 monoclonal antibody."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37913909",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 432,
"text": "Since 2021, 2 B cell maturation antigen (BCMA)-directed chimeric antigen receptor T cell (CAR-T) therapies-idecabtagene vicleucel (ide-cel), and ciltacabtagene autoleucel (cilta-cel)-have been approved by the US Food and Drug Administration (FDA) for treating relapsed or refractory multiple myeloma (RRMM) after 4 or more prior lines of therapy, including an immunomodulatory drug, a proteasome inhibitor, and an anti-CD38 antibody"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34840088",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 602,
"text": "BACKGROUND: In the single-arm, phase 1b/2 CARTITUDE-1 study, ciltacabtagene autoleucel (cilta-cel), an anti-B-cell maturation antigen chimeric antigen receptor T-cell (CAR-T) therapy, showed encouraging efficacy in US patients with multiple myeloma (MM) who previously received an immunomodulatory drug, proteasome inhibitor, and anti-CD38 monoclonal antibody (triple-class exposed).PATIENTS AND METHODS: A dataset of US patients refractory to an anti-CD38 monoclonal antibody (MAMMOTH) was used to identify patients who would meet eligibility for CARTITUDE-1 and received subsequent non-CAR-T therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37272512",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 204,
"text": "BACKGROUND: Ciltacabtagene autoleucel (cilta-cel), a B-cell maturation antigen (BCMA)-directed CAR T-cell therapy, is effective in heavily pretreated patients with relapsed or refractory multiple myeloma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34175021",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 765,
"text": "BACKGROUND: CARTITUDE-1 aimed to assess the safety and clinical activity of ciltacabtagene autoleucel (cilta-cel), a chimeric antigen receptor T-cell therapy with two B-cell maturation antigen-targeting single-domain antibodies, in patients with relapsed or refractory multiple myeloma with poor prognosis.METHODS: This single-arm, open-label, phase 1b/2 study done at 16 centres in the USA enrolled patients aged 18 years or older with a diagnosis of multiple myeloma and an Eastern Cooperative Oncology Group performance status score of 0 or 1, who received 3 or more previous lines of therapy or were double-refractory to a proteasome inhibitor and an immunomodulatory drug, and had received a proteasome inhibitor, immunomodulatory drug, and anti-CD38 antibody."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34885106",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 214,
"text": "Ciltacabtagene autoleucel (cilta-cel) is a Chimeric antigen receptor T-cell therapy with the potential for long-term disease control in heavily pre-treated patients with relapsed/refractory multiple myeloma (RRMM)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37014590",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 410,
"text": "INTRODUCTION: Ciltacabtagene autoleucel (cilta-cel), is a B-cell maturation antigen-directed, genetically modified autologous chimeric antigen receptor T-cell (CAR-T) immunotherapy. It is indicated for treatment for adult patients with relapsed or refractory multiple myeloma (RRMM) after four or more prior lines of therapy, including a proteasome inhibitor, an immunomodulatory agent, and an anti-CD38 monocl"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35764490",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 557,
"text": "INTRODUCTION: This study estimated the comparative efficacy of ciltacabtagene autoleucel (cilta-cel; CARTITUDE-1), a chimeric antigen receptor (CAR)-T-cell therapy, versus 3 non-CAR-T therapies (belantamab mafodotin [DREAMM-2], selinexor plus dexamethasone [STORM Part 2], and melphalan flufenamide plus dexamethasone [HORIZON]), each with distinct mechanisms of action, for the treatment of patients with relapsed or refractory multiple myeloma (RRMM) who were triple-class exposed to an immunomodulatory drug, proteasome inhibitor, and an anti-CD38 monocl"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37750399",
"endSection": "abstract",
"offsetInBeginSection": 159,
"offsetInEndSection": 528,
"text": "Two BCMA-directed CAR T-cell products - idecabtagene vicleucel (ide-cel) and ciltacabtagene autoleucel (cilta-cel) - have received US Food and Drug Administration (FDA) approval for patients with relapsed/refractory MM who underwent four or more prior lines of therapy (including an immunomodulatory agent, a proteasome inhibitor, and an anti-CD38 monoclonal antibody)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37913909",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 433,
"text": "Since 2021, 2 B cell maturation antigen (BCMA)-directed chimeric antigen receptor T cell (CAR-T) therapies-idecabtagene vicleucel (ide-cel), and ciltacabtagene autoleucel (cilta-cel)-have been approved by the US Food and Drug Administration (FDA) for treating relapsed or refractory multiple myeloma (RRMM) after 4 or more prior lines of therapy, including an immunomodulatory drug, a proteasome inhibitor, and an anti-CD38 antibody."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36720180",
"endSection": "abstract",
"offsetInBeginSection": 118,
"offsetInEndSection": 402,
"text": "nancies. Ciltacabtagene autoleucel (cilta-cel), a second-generation CAR-T cell with double B cell maturation antigen (BCMA) targeting binding domains, showed an 88% overall response rate (ORR) in patients with relapsed/refractory multiple myeloma (MM), which were carried out in our i"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37704875",
"endSection": "abstract",
"offsetInBeginSection": 712,
"offsetInEndSection": 935,
"text": "The US Food and Drug Administration (FDA) and European Medicines Agency (EMA) has approved two BCMA-targeting CAR T cell products, idecabtagene vicleucel (Ide-cel) and ciltacabtagene autoleucel (Cilta-cel), for use in RRMM."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35900317",
"endSection": "abstract",
"offsetInBeginSection": 803,
"offsetInEndSection": 975,
"text": "The autologous CAR-T cell therapy against BCMA (ide-cel and cilta-cel) shows the best efficacy with an overall response rate and a median progression-free survival in RRMM."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37716872",
"endSection": "abstract",
"offsetInBeginSection": 132,
"offsetInEndSection": 413,
"text": "eptor (CAR) T cell therapies, because their engineered cells may include allogeneic T cells. Ciltacabtagene autoleucel (cilta-cel) demonstrated early, deep, durable responses and manageable safety in heavily pretreated relapsed/refractory multiple myeloma patients. We retrospectiv"
}
] | 13 |
BioASQ-training13b
| null | null |
65cfd4b21930410b13000020
|
bioasq_factoid
|
factoid
|
DX-88 is investigational name of which drug?
|
[['Ecallantide']]
|
[
"Ecallantide",
"DX-88",
"Ecallantide (DX-88)",
"Ecallantide injection"
] |
['DX-88 is investigational name of a drug Ecallantide, a 60-amino acid recombinant protein discovered through phage display technology, that is a highly specific, potent inhibitor of human plasma kallikrein that has been used successfully in the treatment of patients experiencing acute hereditary angioedema attacks.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21760740",
"http://www.ncbi.nlm.nih.gov/pubmed/21481442",
"http://www.ncbi.nlm.nih.gov/pubmed/19093699",
"http://www.ncbi.nlm.nih.gov/pubmed/18613770",
"http://www.ncbi.nlm.nih.gov/pubmed/18467921",
"http://www.ncbi.nlm.nih.gov/pubmed/18220151",
"http://www.ncbi.nlm.nih.gov/pubmed/16916274",
"http://www.ncbi.nlm.nih.gov/pubmed/14572819"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21760740",
"endSection": "abstract",
"offsetInBeginSection": 505,
"offsetInEndSection": 635,
"text": "Ecallantide (known as DX-88 previously), a potent and specific inhibitor of plasma kallikrein is an innovative medicinal product. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21481442",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "Ecallantide (DX-88) for acute hereditary angioedema attacks: integrated analysis of 2 double-blind, phase 3 studies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19093699",
"endSection": "abstract",
"offsetInBeginSection": 661,
"offsetInEndSection": 992,
"text": "Several novel therapies have completed phase III trials in the US, including: (i) plasma-derived C1-INH replacement therapies (Berinert P and Cinryze); (ii) a recombinant C1-INH replacement therapy (conestat alfa; Rhucin); (iii) a kallikrein inhibitor (ecallantide [DX-88]); and (iv) a bradykinin-2-receptor antagonist (icatibant)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18613770",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "Ecallantide (DX-88), a plasma kallikrein inhibitor for the treatment of hereditary angioedema and the prevention of blood loss in on-pump cardiothoracic surgery."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18613770",
"endSection": "abstract",
"offsetInBeginSection": 315,
"offsetInEndSection": 403,
"text": "OBJECTIVE: Ecallantide (DX-88) is a potent and specific inhibitor of plasma kallikrein. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18467921",
"endSection": "abstract",
"offsetInBeginSection": 277,
"offsetInEndSection": 537,
"text": "DX-88 (ecallantide), a 60-amino acid recombinant protein discovered through phage display technology, is a highly specific, potent inhibitor of human plasma kallikrein that has been used successfully in the treatment of patients experiencing acute HAE attacks."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18220151",
"endSection": "abstract",
"offsetInBeginSection": 983,
"offsetInEndSection": 1204,
"text": "DX-88 or ecallantide, a potent and specific inhibitor of plasma kallikrein, achieved all primary and secondary efficacy end points in a placebo-controlled, double-blind, phase 3 study, with a second phase 3 study ongoing."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16916274",
"endSection": "abstract",
"offsetInBeginSection": 387,
"offsetInEndSection": 552,
"text": "DX-88 (ecallantide, Dyax Corp.) is a highly specific recombinant plasma kallikrein inhibitor that halts the production of bradykinin and can be dosed subcutaneously."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21760740",
"endSection": "abstract",
"offsetInBeginSection": 505,
"offsetInEndSection": 635,
"text": "Ecallantide (known as DX-88 previously), a potent and specific inhibitor of plasma kallikrein is an innovative medicinal product. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21481442",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "Ecallantide (DX-88) for acute hereditary angioedema attacks: integrated analysis of 2 double-blind, phase 3 studies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16916274",
"endSection": "abstract",
"offsetInBeginSection": 387,
"offsetInEndSection": 551,
"text": "DX-88 (ecallantide, Dyax Corp.) is a highly specific recombinant plasma kallikrein inhibitor that halts the production of bradykinin and can be dosed subcutaneously"
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D015507"
] |
[] |
54f1e031c409818c32000001
|
bioasq_factoid
|
factoid
|
What is drug target for olaparib?
|
['poly ADP ribose polymerase (PARP)']
|
[
"poly ADP ribose polymerase (PARP)",
"PARP",
"poly(ADP-ribose) polymerase",
"poly(ADP-ribose) polymerase 1",
"PARP1",
"poly(ADP-ribose) polymerase 2",
"PARP2",
"ADP-ribosyltransferase",
"ADP-ribose polymerase"
] |
['Olaparib(Lynparza) is a PARP inhibitor, inhibiting poly ADP ribose polymerase (PARP), an enzyme involved in DNA repair.', 'Olaparib is a Poly(ADP-ribose) Polymerase (PARP) Inhibitor']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29129088",
"http://www.ncbi.nlm.nih.gov/pubmed/30660828",
"http://www.ncbi.nlm.nih.gov/pubmed/30486888"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29129088",
"endSection": "abstract",
"offsetInBeginSection": 1409,
"offsetInEndSection": 1471,
"text": "PARP inhibition with olaparib, warrants further investigation,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30660828",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 37,
"text": "Olaparib is a PARP inhibitor (PARPi)."
}
] | 11 |
BioASQ-training11b
| null | null |
5e42d1a748dab47f26000010
|
bioasq_factoid
|
yesno
|
Does triiodothyronine (T3) has cardiac angiogenic effects?
|
['Yes']
|
[
"Yes"
] |
['T3-induced cardiac sprouting angiogenesis in adult hypothyroid mice was associated with PDGF-BB, PDGFR-β and downstream activation of Akt.\nT(3) administration restored TRbeta mRNA expression level in AAC hearts to the control level.\nTRbeta in the coronary ECs regulates capillary density during cardiac development, and down-regulation of TRbeta results in coronary microvascular rarefaction during pathological hypertrophy.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22681587",
"http://www.ncbi.nlm.nih.gov/pubmed/20100314",
"http://www.ncbi.nlm.nih.gov/pubmed/19286941",
"http://www.ncbi.nlm.nih.gov/pubmed/19074585",
"http://www.ncbi.nlm.nih.gov/pubmed/2530972"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22681587",
"endSection": "sections.0",
"offsetInBeginSection": 1664,
"offsetInEndSection": 1802,
"text": "T3-induced cardiac sprouting angiogenesis in adult hypothyroid mice was associated with PDGF-BB, PDGFR-β and downstream activation of Akt."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20100314",
"endSection": "sections.0",
"offsetInBeginSection": 916,
"offsetInEndSection": 1073,
"text": "L-T3 significantly increased angiogenesis and cell survival and enhanced the expression of nuclear-encoded transcription factors involved in these processes."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19074585",
"endSection": "sections.0",
"offsetInBeginSection": 761,
"offsetInEndSection": 854,
"text": "T(3) administration restored TRbeta mRNA expression level in AAC hearts to the control level."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19074585",
"endSection": "sections.0",
"offsetInBeginSection": 907,
"offsetInEndSection": 1049,
"text": "Rbeta knockout and TRalpha/TRbeta double-knockout mice both exhibited significantly less capillary density in LV compared with wild-type mice."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19074585",
"endSection": "sections.0",
"offsetInBeginSection": 1406,
"offsetInEndSection": 1597,
"text": "TRbeta in the coronary ECs regulates capillary density during cardiac development, and down-regulation of TRbeta results in coronary microvascular rarefaction during pathological hypertrophy."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D014284",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=0045766",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=0045765",
"http://www.biosemantics.org/jochem#4275389",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D043925",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018919",
"http://www.biosemantics.org/jochem#4005955",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D043924",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D011988",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=0002040"
] | null |
513f4892bee46bd34c000014
|
bioasq_yesno
|
yesno
|
Is phospholamban phosphorylated by Protein kinase A?
|
['yes']
|
[
"yes"
] |
['Phospholamban (PLB) is a sarcoplasmic reticulum (SR) protein that is phosphorylated at Ser16 by PKA. Phosphorylation of PLB by PKA reverses the inhibitory action of PLB.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/19191503",
"http://www.ncbi.nlm.nih.gov/pubmed/16226237",
"http://www.ncbi.nlm.nih.gov/pubmed/15909986",
"http://www.ncbi.nlm.nih.gov/pubmed/15524173",
"http://www.ncbi.nlm.nih.gov/pubmed/15362510",
"http://www.ncbi.nlm.nih.gov/pubmed/15229104",
"http://www.ncbi.nlm.nih.gov/pubmed/15049694",
"http://www.ncbi.nlm.nih.gov/pubmed/14577598",
"http://www.ncbi.nlm.nih.gov/pubmed/12962492",
"http://www.ncbi.nlm.nih.gov/pubmed/11502581",
"http://www.ncbi.nlm.nih.gov/pubmed/3730367",
"http://www.ncbi.nlm.nih.gov/pubmed/7857766",
"http://www.ncbi.nlm.nih.gov/pubmed/17548345",
"http://www.ncbi.nlm.nih.gov/pubmed/16600289",
"http://www.ncbi.nlm.nih.gov/pubmed/11812163",
"http://www.ncbi.nlm.nih.gov/pubmed/10330247"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19191503",
"endSection": "abstract",
"offsetInBeginSection": 456,
"offsetInEndSection": 514,
"text": "cAMP-dependent protein kinase (PKA) phosphorylation of PLB"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16226237",
"endSection": "abstract",
"offsetInBeginSection": 197,
"offsetInEndSection": 246,
"text": "phosphorylation of PLN, at either Ser(16) by PKA "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15909986",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 222,
"text": "Activation of cardiac muscle sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) by beta1-agonists involves cAMP- and PKA-dependent phosphorylation of phospholamban (PLB), which relieves the inhibitory effects of PLB on SERCA2a. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15524173",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "Phospholamban (PLB) is a sarcoplasmic reticulum (SR) protein that when phosphorylated at Ser16 by PKA"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15362510",
"endSection": "abstract",
"offsetInBeginSection": 1044,
"offsetInEndSection": 1163,
"text": "phosphorylation of PLB by the Ca2+-calmodulin-dependent protein kinase (CaMK) and cAMP-dependent protein kinase (PKA). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15229104",
"endSection": "abstract",
"offsetInBeginSection": 897,
"offsetInEndSection": 990,
"text": "cAMP-dependent protein kinase (PKA)-mediated phospholamban (PLB) phosphorylation at serine-16"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15049694",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 404,
"text": "Phospholamban (PLB) is a major target of the beta-adrenergic cascade in the heart, functioning to modulate contractile force by altering the rate of calcium re-sequestration by the Ca-ATPase. Functionally, inhibition by PLB binding is manifested by shifts in the calcium dependence of Ca-ATPase activation toward higher calcium levels; phosphorylation of PLB by PKA reverses the inhibitory action of PLB."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14577598",
"endSection": "abstract",
"offsetInBeginSection": 134,
"offsetInEndSection": 213,
"text": "phosphorylation of both PLB residues (Ser16, PKA site, and Thr17, CaMKII site) "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12962492",
"endSection": "abstract",
"offsetInBeginSection": 1401,
"offsetInEndSection": 1434,
"text": "Phosphorylation of Ser(16) by PKA"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12962492",
"endSection": "abstract",
"offsetInBeginSection": 2296,
"offsetInEndSection": 2370,
"text": "stabilization of the structure of PLB following phosphorylation of Ser(16)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11502581",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 173,
"text": "Phospholamban (PLB) inhibits the sarcoplasmic reticulum (SR) Ca(2+)-ATPase, and this inhibition is relieved by cAMP-dependent protein kinase (PKA)-mediated phosphorylation. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3957897",
"endSection": "abstract",
"offsetInBeginSection": 1023,
"offsetInEndSection": 1341,
"text": "Two-dimensional tryptic peptide maps of phosphorylated phospholamban indicated that cAMP-dependent protein kinase phosphorylates at a single site, A, and Ca2+-calmodulin-dependent protein kinase phosphorylates at sites C1 and C2 in the low molecular weight form, where A is different from C1 but may be the same as C2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19191503",
"endSection": "abstract",
"offsetInBeginSection": 456,
"offsetInEndSection": 514,
"text": "cAMP-dependent protein kinase (PKA) phosphorylation of PLB"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16226237",
"endSection": "abstract",
"offsetInBeginSection": 197,
"offsetInEndSection": 246,
"text": "phosphorylation of PLN, at either Ser(16) by PKA "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11812163",
"endSection": "abstract",
"offsetInBeginSection": 117,
"offsetInEndSection": 455,
"text": "Because SR function is regulated by phosphorylation of phospholamban (PLB), a SR protein phosphorylated by cAMP-dependent protein kinase (PKA) at Ser(16)and Ca(2+)-calmodulin-dependent protein kinase (CaMKII) at Thr(17), the phosphorylation of these residues during ischemia and reperfusion was examined in Langendorff-perfused rat hearts"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16600289",
"endSection": "abstract",
"offsetInBeginSection": 680,
"offsetInEndSection": 908,
"text": "These changes were associated with reduced protein expression of sarcoplasmic reticulum Ca(2+)-ATPase (SERCA2a) and protein kinase A phosphorylated phospholamban (PLB), which was reduced in HF, but essentially abolished in VD-HF"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10330247",
"endSection": "abstract",
"offsetInBeginSection": 1127,
"offsetInEndSection": 1499,
"text": "The data indicate that 1) phosphorylation of phospholamban at Ser16 by cAMP-dependent protein kinase is the main regulator of beta-adrenergic-induced cardiac relaxation definitely preceding Thr17 phosphorylation and 2) the beta-adrenergic-mediated phosphorylation of Thr17 by Ca2+-calmodulin-dependent protein kinase required influx of Ca2+ through the L-type Ca2+ channel"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17548345",
"endSection": "abstract",
"offsetInBeginSection": 407,
"offsetInEndSection": 654,
"text": "Here we extend this model to explain the reversal of SERCA2a inhibition that occurs after phosphorylation of PLB at Ser(16) by protein kinase A (PKA) and after binding of the anti-PLB monoclonal antibody 2D12, which recognizes residues 7-13 of PLB"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7857766",
"endSection": "abstract",
"offsetInBeginSection": 191,
"offsetInEndSection": 421,
"text": "Phospholamban is phosphorylated in heart by cAMP-dependent protein kinase, cGMP-dependent protein kinase and calcium/calmodulin-dependent protein kinase II (CM-kinase-II) and in smooth muscle cells by cGMP-dependent protein kinase"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3730367",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 268,
"text": "Phospholamban, the cardiac sarcoplasmic reticulum proteolipid, is phosphorylated by cAMP-dependent protein kinase, by Ca2+/phospholipid-dependent protein kinase, and by an endogenous Ca2+/calmodulin-dependent protein kinase, the identity of which remains to be defined"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3730367",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 268,
"text": "Phospholamban, the cardiac sarcoplasmic reticulum proteolipid, is phosphorylated by cAMP-dependent protein kinase, by Ca2+/phospholipid-dependent protein kinase, and by an endogenous Ca2+/calmodulin-dependent protein kinase, the identity of which remains to be defined"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7857766",
"endSection": "abstract",
"offsetInBeginSection": 191,
"offsetInEndSection": 421,
"text": "Phospholamban is phosphorylated in heart by cAMP-dependent protein kinase, cGMP-dependent protein kinase and calcium/calmodulin-dependent protein kinase II (CM-kinase-II) and in smooth muscle cells by cGMP-dependent protein kinase"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3730367",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 268,
"text": "Phospholamban, the cardiac sarcoplasmic reticulum proteolipid, is phosphorylated by cAMP-dependent protein kinase, by Ca2+/phospholipid-dependent protein kinase, and by an endogenous Ca2+/calmodulin-dependent protein kinase, the identity of which remains to be defined"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7857766",
"endSection": "abstract",
"offsetInBeginSection": 191,
"offsetInEndSection": 421,
"text": "Phospholamban is phosphorylated in heart by cAMP-dependent protein kinase, cGMP-dependent protein kinase and calcium/calmodulin-dependent protein kinase II (CM-kinase-II) and in smooth muscle cells by cGMP-dependent protein kinase"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3730367",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 268,
"text": "Phospholamban, the cardiac sarcoplasmic reticulum proteolipid, is phosphorylated by cAMP-dependent protein kinase, by Ca2+/phospholipid-dependent protein kinase, and by an endogenous Ca2+/calmodulin-dependent protein kinase, the identity of which remains to be defined"
}
] | 5 |
BioASQ-training5b
|
[] |
[] |
54da0c524b1fd0d33c00000b
|
bioasq_yesno
|
yesno
|
Is TNF-α an activator of pancreatic stellate cells?
|
['yes']
|
[
"yes"
] |
['Yes,\nTNF-α is the prime factor responsible for the activation of pancreatic stellate cells.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24089530",
"http://www.ncbi.nlm.nih.gov/pubmed/20689058"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24089530",
"endSection": "abstract",
"offsetInBeginSection": 825,
"offsetInEndSection": 910,
"text": "TNF-α is the prime factor responsible for the activation of pancreatic stellate cells"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20689058",
"endSection": "abstract",
"offsetInBeginSection": 602,
"offsetInEndSection": 735,
"text": "Activated PSCs expressed IL-33 in the nucleus, and the expression was increased by IL-1β, TNF-α, PDGF-BB, and IFN-γ, but not TGF-β1. "
}
] | 11 |
BioASQ-training11b
| null | null |
5c9f0dabecadf2e73f00003b
|
bioasq_yesno
|
factoid
|
What is the ChIP-exo method used for?
|
['location of DNA binding proteins at high resolution']
|
[
"location of DNA binding proteins at high resolution",
"high-resolution location of DNA binding proteins",
"DNA binding protein localization at high resolution",
"high-resolution DNA binding protein location",
"DNA binding protein positioning at high resolution"
] |
['Precise Identification of DNA-Binding Proteins Genomic Location by Exonuclease Coupled Chromatin Immunoprecipitation (ChIP-exo).', 'ChIP-exo method for identifying genomic location of DNA-binding proteins with near-single-nucleotide accuracy. ', 'ChIP-exo method for identifying genomic location of DNA-binding proteins with near-single-nucleotide accuracy. ChIP-exo allows identification of a nearly complete set of the binding locations of DNA-binding proteins at near-single-nucleotide resolution with almost no background. Precise Identification of DNA-Binding Proteins Genomic Location by Exonuclease Coupled Chromatin Immunoprecipitation (ChIP-exo).', 'ChIP-exo method for identifying genomic location of DNA-binding proteins with near-single-nucleotide accuracy.', 'ChIP-exo is a molecular biology method for identifying genomic location of DNA-binding proteins with near-single-nucleotide accuracy.', 'ChIP-exo method for identifying genomic location of DNA-binding proteins with near-single-nucleotide accuracy. ChIP-exo allows identification of a nearly complete set of the binding locations of DNA-binding proteins at near-single-nucleotide resolution with almost no background.', "ChIP-exo allows identification of a nearly complete set of the binding locations of DNA-binding proteins at near-single-nucleotide resolution with almost no background. The key distinction of the ChIP-exo methodology is the incorporation of lambda exonuclease digestion in the library preparation workflow to effectively footprint the left and right 5' DNA borders of the protein-DNA crosslink site. "]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23026909",
"http://www.ncbi.nlm.nih.gov/pubmed/28060339",
"http://www.ncbi.nlm.nih.gov/pubmed/26404150"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23026909",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "ChIP-exo method for identifying genomic location of DNA-binding proteins with near-single-nucleotide accuracy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23026909",
"endSection": "abstract",
"offsetInBeginSection": 172,
"offsetInEndSection": 340,
"text": "ChIP-exo allows identification of a nearly complete set of the binding locations of DNA-binding proteins at near-single-nucleotide resolution with almost no background."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26404150",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "Precise Identification of DNA-Binding Proteins Genomic Location by Exonuclease Coupled Chromatin Immunoprecipitation (ChIP-exo)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26404150",
"endSection": "abstract",
"offsetInBeginSection": 531,
"offsetInEndSection": 870,
"text": "A significant improvement of the ChIP-seq technique results from the addition of an exonuclease treatment during the immunoprecipitation step (ChIP-exo) that lowers background noise and more importantly increases the identification of binding sites to a level near to single-base resolution by effectively footprinting DNA-bound proteins. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28060339",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 88,
"text": "The ChIP-exo Method: Identifying Protein-DNA Interactions with Near Base Pair Precision."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28060339",
"endSection": "abstract",
"offsetInBeginSection": 545,
"offsetInEndSection": 776,
"text": "The key distinction of the ChIP-exo methodology is the incorporation of lambda exonuclease digestion in the library preparation workflow to effectively footprint the left and right 5' DNA borders of the protein-DNA crosslink site. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23026909",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 111,
"text": "ChIP-exo method for identifying genomic location of DNA-binding proteins with near-single-nucleotide accuracy."
}
] | 11 |
BioASQ-training11b
| null | null |
5ac24c9495d0062724000002
|
bioasq_factoid
|
yesno
|
Is P. gingivalis bacteria found in brain?
|
['yes']
|
[
"yes"
] |
['Yes']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28800332",
"http://www.ncbi.nlm.nih.gov/pubmed/30281647"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30281647",
"endSection": "abstract",
"offsetInBeginSection": 185,
"offsetInEndSection": 439,
"text": "studies using animal model of periodontitis and human post-mortem brain tissues from subjects with AD strongly suggest that a gram-negative periodontal pathogen, Porphyromonas gingivalis (Pg) and/or its product gingipain is/are translocated to the brain."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28800332",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 182,
"text": "The polymicrobial dysbiotic subgingival biofilm microbes associated with periodontal disease appear to contribute to developing pathologies in distal body sites, including the brain."
}
] | 11 |
BioASQ-training11b
| null | null |
5c5f2b771a4c55d80b000020
|
bioasq_yesno
|
factoid
|
Centor criteria are used for which disease?
|
['streptococcal pharyngitis']
|
[
"streptococcal pharyngitis",
"strep throat",
"streptococcal sore throat",
"streptococcal infection of the throat",
"acute streptococcal pharyngitis"
] |
['Centor criteria were developed to diagnose streptococcal pharyngitis.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27618925",
"http://www.ncbi.nlm.nih.gov/pubmed/11719744",
"http://www.ncbi.nlm.nih.gov/pubmed/26934845",
"http://www.ncbi.nlm.nih.gov/pubmed/23613571",
"http://www.ncbi.nlm.nih.gov/pubmed/19054454",
"http://www.ncbi.nlm.nih.gov/pubmed/26141740",
"http://www.ncbi.nlm.nih.gov/pubmed/27358410",
"http://www.ncbi.nlm.nih.gov/pubmed/27573720",
"http://www.ncbi.nlm.nih.gov/pubmed/29045629",
"http://www.ncbi.nlm.nih.gov/pubmed/27493985",
"http://www.ncbi.nlm.nih.gov/pubmed/23783139",
"http://www.ncbi.nlm.nih.gov/pubmed/28469911",
"http://www.ncbi.nlm.nih.gov/pubmed/15231926",
"http://www.ncbi.nlm.nih.gov/pubmed/28991775",
"http://www.ncbi.nlm.nih.gov/pubmed/27439523",
"http://www.ncbi.nlm.nih.gov/pubmed/22432746"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29045629",
"endSection": "abstract",
"offsetInBeginSection": 292,
"offsetInEndSection": 486,
"text": "Methods: MEDLINE was searched for prospective studies that reported throat culture for both GAS and non-GAS as a reference standard, and reported at least one sign, symptom, or the Centor score."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27439523",
"endSection": "abstract",
"offsetInBeginSection": 356,
"offsetInEndSection": 616,
"text": "METHODS: Trained pharmacy staff assessed patients presenting with a sore throat using the Centor scoring system and patients meeting three or all four of the criteria were offered a throat swab test for Streptococcus pyogenes, Lancefield group A streptococci. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26934845",
"endSection": "abstract",
"offsetInBeginSection": 1464,
"offsetInEndSection": 1605,
"text": "CONCLUSION: Clinician judgement and Centor score are inadequate tools for clinical decision-making for children presenting with sore throat. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27493985",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "A Study to Determine if Addition of Palatal Petechiae to Centor Criteria Adds More Significance to Clinical Diagnosis of Acute Strep Pharyngitis in Children."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27493985",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 445,
"text": "Objective. A study to determine if addition of palatal petechiae to Centor criteria adds more value for clinical diagnosis of acute strep pharyngitis in children. Hypothesis. In children, Centor Criteria does not cover all the symptoms and signs of acute strep pharyngitis. We hypothesize that addition of palatal petechiae to Centor Criteria will increase the possibility of clinical diagnosis of group A streptococcal pharyngitis in children. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27493985",
"endSection": "abstract",
"offsetInBeginSection": 1831,
"offsetInEndSection": 2021,
"text": "Conclusion. Our study concludes that addition of petechiae over the palate to Centor Criteria will increase the possibility of diagnosing acute group A streptococcal pharyngitis in children."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27573720",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Appropriateness of diagnosis of streptococcal pharyngitis among Thai community pharmacists according to the Centor criteria."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27573720",
"endSection": "abstract",
"offsetInBeginSection": 220,
"offsetInEndSection": 428,
"text": "Objective To ascertain the appropriateness of diagnosis of streptococcal pharyngitis among Thai community pharmacists according to the Centor criteria and to identify factors related to antibiotic dispensing."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27573720",
"endSection": "abstract",
"offsetInBeginSection": 858,
"offsetInEndSection": 1178,
"text": "Main outcome measure The appropriateness of diagnosis of streptococcal pharyngitis according to the original and modified Centor criteria and determinants of antibiotic dispensing including demographic characteristics of pharmacists, knowledge on pharyngitis, and attitudes and control beliefs on antibiotic dispensing. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27573720",
"endSection": "abstract",
"offsetInBeginSection": 2289,
"offsetInEndSection": 2478,
"text": "Conclusion Pharmacists who are knowledgeable on the Centor criteria are more likely to appropriately diagnose streptococcal pharyngitis and less likely to dispense antibiotics in such case."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27618925",
"endSection": "abstract",
"offsetInBeginSection": 841,
"offsetInEndSection": 1078,
"text": "Adult men and women, youth and children ≥6 years of age who consult for sore throat and is judged to have a pharyngotonsillitis, with 3-4 Centor criteria and a positive rapid test for group A streptococci, will be included in the study. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26141740",
"endSection": "abstract",
"offsetInBeginSection": 72,
"offsetInEndSection": 273,
"text": "Previous studies have shown that the Centor score combined with Rapid Antigen Detection Test (RADT) for Group A Streptococci can reduce unnecessary antibiotic prescribing in patients with sore throat. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15231926",
"endSection": "abstract",
"offsetInBeginSection": 1711,
"offsetInEndSection": 2095,
"text": "Spectrum bias was present, inasmuch as RADT sensitivity increased with Centor scores, ie, 47% sensitivity among children with 0 Centor criteria, 65% among those with 1 criterion, 82% among those with 2 criteria, and 90% among those with 3 or 4 criteria.<br><b>CONCLUSIONS</b>: The sensitivity of RADT for GABHS pharyngitis is not a fixed value but varies with the severity of disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15231926",
"endSection": "abstract",
"offsetInBeginSection": 1519,
"offsetInEndSection": 1710,
"text": "The prevalence of GABHS pharyngitis was 18% among patients with 0 Centor criteria, 16% among those with 1 criterion, 32% among those with 2 criteria, and 50% among those with 3 or 4 criteria."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15231926",
"endSection": "abstract",
"offsetInBeginSection": 2096,
"offsetInEndSection": 2308,
"text": "However, even among pediatric patients with > or =3 Centor criteria for GABHS pharyngitis, the sensitivity of RADT is still too low to support the use of RADT without culture confirmation of negative results.<br>"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27493985",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 162,
"text": "A study to determine if addition of palatal petechiae to Centor criteria adds more value for clinical diagnosis of acute strep pharyngitis in children."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27493985",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "if Addition of Palatal Petechiae to Centor Criteria Adds More Significance to Clinical Diagnosis of Acute Strep Pharyngitis in Children."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27493985",
"endSection": "abstract",
"offsetInBeginSection": 1844,
"offsetInEndSection": 2022,
"text": "Our study concludes that addition of petechiae over the palate to Centor Criteria will increase the possibility of diagnosing acute group A streptococcal pharyngitis in children."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22432746",
"endSection": "abstract",
"offsetInBeginSection": 311,
"offsetInEndSection": 435,
"text": "The Centor scoring system can help to identify those patients who have higher likelihood of group A streptococcal infection."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27493985",
"endSection": "abstract",
"offsetInBeginSection": 274,
"offsetInEndSection": 444,
"text": "We hypothesize that addition of palatal petechiae to Centor Criteria will increase the possibility of clinical diagnosis of group A streptococcal pharyngitis in children."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23613571",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 274,
"text": "INTRODUCTION Centor criteria (fever >38.5°C, swollen, tender anterior cervical lymph nodes, tonsillar exudate and absence of cough) are an algorithm to assess the probability of group A β haemolytic Streptococcus (GABHS) as the origin of sore throat, developed for adults."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27573720",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "appropriateness of diagnosis of streptococcal pharyngitis among thai community pharmacists according to the centor criteria"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23783139",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 951,
"text": "Diagnosing GABHS (Group A-beta Hemolytic Streptococcus) tonsillopharyngitis by clinical scoring is a recommended approach in developed countries, but there is still much controversy for low resource settings.We aimed to assess the impact of Centor criteria with the support of practical laboratory tests.We prospectively included patients complaining sore throat (N = 282). We evaluated them in terms of Centor scoring and performed white blood cell count (WBC), C-reactive protein (CRP), rapid antigen detecting test, and throat culture.In GABHS cases (N = 32, 11·3%), two of the criteria were observed to be positive in more than half of the cases (N = 19, 59·3%), while 13 (40·7%) cases met three/four criteria. The specificity of having two criteria was found to be 65·5% and increased to 91·5% after including CRP and WBC.Centor criteria could be safely used to reduce unnecessary antibiotic usage for tonsillopharyngitis in developing countries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15231926",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 2198,
"text": "Rapid antigen detection testing (RADT) is often performed for diagnosis of group A beta-hemolytic streptococcal (GABHS) pharyngitis among children. Among adults, the sensitivity of this test varies on the basis of disease severity (spectrum bias). A similar phenomenon may occur when this test is used in a pediatric population, which may affect the need for culture confirmation of all negative RADT results.To assess the performance of a clinical scoring system and to determine whether RADT spectrum bias is present among children who are evaluated for GABHS pharyngitis.Laboratory and clinical records for a consecutive series of pediatric patients who underwent RADT at the Marshfield Clinic between January 2002 and March 2002 were reviewed retrospectively. Patients were stratified according to the number of clinical features present by using modified Centor criteria, ie, history of fever, absence of cough, presence of pharyngeal exudates, and cervical lymphadenopathy. The sensitivity of the RADT was defined as the number of patients with positive RADT results divided by the number of patients with either positive RADT results or negative RADT results but positive throat culture results.RADT results were positive for 117 of 561 children (21%), and culture results were positive for 35 of 444 children (8%) with negative RADT results. The overall prevalence of GABHS pharyngitis was 27% (95% confidence interval: 23-31%). The prevalence of GABHS pharyngitis was 18% among patients with 0 Centor criteria, 16% among those with 1 criterion, 32% among those with 2 criteria, and 50% among those with 3 or 4 criteria. Spectrum bias was present, inasmuch as RADT sensitivity increased with Centor scores, ie, 47% sensitivity among children with 0 Centor criteria, 65% among those with 1 criterion, 82% among those with 2 criteria, and 90% among those with 3 or 4 criteria.The sensitivity of RADT for GABHS pharyngitis is not a fixed value but varies with the severity of disease. However, even among pediatric patients with > or =3 Centor criteria for GABHS pharyngitis, the sensitivity of RADT is still too low to support the use of RADT without culture confirmation of negative results."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23613571",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1833,
"text": "Centor criteria (fever >38.5°C, swollen, tender anterior cervical lymph nodes, tonsillar exudate and absence of cough) are an algorithm to assess the probability of group A β haemolytic Streptococcus (GABHS) as the origin of sore throat, developed for adults. We wanted to evaluate the correlation between Centor criteria and presence of GABHS in children with sore throat admitted to our paediatric emergency department (PED).Retrospective cohort study.The emergency department of a large tertiary university hospital in Brussels, with over 20 000 yearly visits for children below age 16.All medical records (from 2008 to 2010) of children between ages 2 and 16, who were diagnosed with pharyngitis, tonsillitis or sore throat and having a throat swab culture for GABHS. Children with underlying chronic respiratory, cardiac, haematological or immunological diseases and children who had already received antibiotics (AB) prior to the PED consult were excluded. Only records with a full disease history were selected. Out of a total 2118 visits for sore throats, 441 met our criteria. The children were divided into two age groups, 2-5 and 5-16 years.The prevalence of GABHS was higher in the older children compared to the preschoolers (38.7 vs 27.6; p=0.01), and the overall prevalence was 32%. There was no significant difference in the prevalence of GABHS for all different Centor scores within an age group. Likelihood ratios (LR) demonstrate that none of the individual symptoms or a Centor score of ≥3 seems to be effective in ruling in or ruling out GABHS. Pooled LR (CI) for Centor ≥3 was 0.67 (CI 0.50 to 0.90) for the preschoolers and 1.37 (CI 1.04 to 1.79) for the older children.Our results confirm the ineffectiveness of Centor criteria as a predicting factor for finding GABHS in a throat swab culture in children."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22432746",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1643,
"text": "The European Society for Clinical Microbiology and Infectious Diseases established the Sore Throat Guideline Group to write an updated guideline to diagnose and treat patients with acute sore throat. In diagnosis, Centor clinical scoring system or rapid antigen test can be helpful in targeting antibiotic use. The Centor scoring system can help to identify those patients who have higher likelihood of group A streptococcal infection. In patients with high likelihood of streptococcal infections (e.g. 3-4 Centor criteria) physicians can consider the use of rapid antigen test (RAT). If RAT is performed, throat culture is not necessary after a negative RAT for the diagnosis of group A streptococci. To treat sore throat, either ibuprofen or paracetamol are recommended for relief of acute sore throat symptoms. Zinc gluconate is not recommended to be used in sore throat. There is inconsistent evidence of herbal treatments and acupuncture as treatments for sore throat. Antibiotics should not be used in patients with less severe presentation of sore throat, e.g. 0-2 Centor criteria to relieve symptoms. Modest benefits of antibiotics, which have been observed in patients with 3-4 Centor criteria, have to be weighed against side effects, the effect of antibiotics on microbiota, increased antibacterial resistance, medicalisation and costs. The prevention of suppurative complications is not a specific indication for antibiotic therapy in sore throat. If antibiotics are indicated, penicillin V, twice or three times daily for 10 days is recommended. At the present, there is no evidence enough that indicates shorter treatment length."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27493985",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1952,
"text": "A study to determine if addition of palatal petechiae to Centor criteria adds more value for clinical diagnosis of acute strep pharyngitis in children.In children, Centor Criteria does not cover all the symptoms and signs of acute strep pharyngitis. We hypothesize that addition of palatal petechiae to Centor Criteria will increase the possibility of clinical diagnosis of group A streptococcal pharyngitis in children.One hundred patients with a complaint of sore throat were enrolled in the study. All the patients were examined clinically using the Centor Criteria. They were also examined for other signs and symptoms like petechial lesions over the palate, abdominal pain, and skin rash. All the patients were given rapid strep tests, and throat cultures were sent. No antibiotics were given until culture results were obtained.The sample size was 100 patients. All 100 had fever, sore throat, and erythema of tonsils. Twenty of the 100 patients had tonsillar exudates, 85/100 had tender anterior cervical lymph nodes, and 86/100 had no cough. In total, 9 out of the 100 patients had positive throat cultures. We observed that petechiae over the palate, a very significant sign, is not included in the Centor Criteria. Palatal petechiae were present in 8 out of the 100 patients. Six out of these 8 with palatal petechiae had positive throat culture for strep (75%). Only 7 out of 20 with exudates had positive strep culture. Sixteen out of the 100 patients had rapid strep test positive. Those 84/100 who had negative rapid strep also had negative throat culture.We used Fisher's exact test, comparing throat culture positive and negative versus presence of exudates and palatal hemorrhages with positive and negative throat cultures and the resultant P value <.0001.Our study concludes that addition of petechiae over the palate to Centor Criteria will increase the possibility of diagnosing acute group A streptococcal pharyngitis in children."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11719744",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1597,
"text": "we evaluate the test characteristics and test for spectrum bias of a rapid antigen test for group a beta hemolytic streptococcal gabhs pharyngitis among adults medical record and laboratory results of consecutive adult patients receiving a rapid antigen test for gabhs in the emergency department or urgent care clinic of an urban teaching hospital between august 1999 and december 1999 were analyzed patients were stratified according to the number of clinical features present using the following modified centor criteria history of fever absence of cough presence of pharyngeal exudate and cervical lymphadenopathy the sensitivity of the rapid antigen test was defined as the number of patients with positive rapid antigen test results divided by the number of patients with either positive rapid antigen test results or negative rapid antigen test results and positive throat culture results in the study sample of 498 patient visits the prevalence of gabhs pharyngitis was 28 95 confidence interval ci 24 to 32 the prevalence of gabhs pharyngitis increased as modified centor scores increased 0 or 1 14 2 20 3 43 and 4 52 an increased number of modified centor criteria 0 or 1 2 3 4 was associated with increased rapid antigen test sensitivity 61 76 90 and 97 respectively mantel haenszel trend test p 001 the sensitivity of the rapid antigen test for gabhs is not a fixed value but varies with the spectrum of disease among adults with 3 or 4 clinical criteria for gabhs pharyngitis further study may reveal that culture confirmation of negative rapid antigen test results are not necessary."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19054454",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1301,
"text": "to determine the validity of the rapid antigen test rat osom strepa genzyme for the diagnosis of acute pharyngitis caused by group a beta haemolytic strep gabhs diagnostic techniques survey urban primary care centre spain all patients over 14 years old seen in 6 surgeries with sore throat and 2 or more centor criteria pharyngotonsillar exudate tender laterocervical nodes absence of coughing and or history or presence of fever pharyngeal swabs were taken from all the patients one for rat and another to send for culture in the microbiology department a total of 182 patients were evaluable with a mean age of 30 6 12 1 years of which 116 were women 63 7 63 patients had 2 centor criteria 83 had 3 and 36 the 4 criteria the culture was positive in 102 patients 56 with gabhs showing infection in forty 22 95 confidence interval ci 21 2 22 8 group c streptococcus was isolated in 26 patients 14 3 gabhs was higher among patients with four centor criteria 38 9 vs 25 3 observed among those with 3 criteria and 7 9 with 2 criteria p 001 sensitivity of rat was 95 with a specificity of 93 a positive predictive value of 79 2 and a negative predictive value of 98 5 these results show the usefulness of rat for diagnosing streptococcal pharyngitis its use should be spread to all primary care practices."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28469911",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 2339,
"text": "acute sore throat is a common presentation in primary care settings we aimed to improve our compliance with national antibiotic guidelines for sore throat symptoms to 90 in 3 months time period the national guidelines are based on centor criteria a retrospective audit of 102 patient records with sore throat symptoms presenting between 1 january to 30 december 2015 showed that over 50 were given antibiotics those who were prescribed antibiotics 27 did not meet nice criteria and 85 of patients were given immediate antibiotic prescription centor criteria was documented in just 2 of cases compliance with correct antibiotic course length was 15 antibiotic choice and dose was correct in 94 and 92 of cases respectively antibiotic frequency was correctly prescribed in 100 of patients we introduced interventions that included oral and poster presentations to multidisciplinary team dissemination of guidelines through internal e mail and systemic changes to gp electronic patient record system emis this involved creating an automated sore throat template and information page on re auditing of 71 patients after two pdsa cycles compliance with nice criteria was 87 with a significant reduction in immediate prescribing 66 centor criteria documentation was 42 correct antibiotic course length was prescribed in over 30 of cases other antibiotic regimen parameters choice dose and frequency were correct in 100 of cases the initial results demonstrated that significant changes were needed in particular reducing the amount of antibiotics prescribed by increasing compliance with nice criteria and ensuring all parameters of antibiotic prescription were correct we showed that significant sustainable improvement is achievable through carefully devised automated systemic changes that provides critical information in readily accessible format and does not solely rely on prescribers knowledge and initiative the outcome of these interventions are a decrease in immediate antibiotic prescription significant increase in centor criteria documentation and an increase in compliance with the correct course length of antibiotics all these measures would contribute to reduction in antimicrobial resistance and improvement in patient care in the community future work must focus on improving compliance with correct antibiotic course length."
}
] | 11 |
BioASQ-training11b
| null | null |
5a6f960fb750ff445500005c
|
bioasq_factoid
|
factoid
|
What is the prevalence of intellectual developmental disorders in Becker Muscular Dystrophy?
|
['8%']
|
[
"8 percent",
"eight percent",
"0.08",
"0.08 fraction",
"8/100"
] |
['The global prevalence of intellectual developmental disorder (IDD) is 8% in Becker muscular dystrophy.', 'The global prevalence of intellectual developmental disorder (IDD) in Becker muscular dystrophy (BMD) is 8%.', 'The prevalence of intellectual developmental disorders in Becker Muscular Dystrophy is 8%.', 'The global prevalence of intellectual developmental disorder (IDD) was 8% in Becker muscular dystrophy.', 'The global prevalence of intellectual developmental disorder (IDD) in Becker muscular dystrophy is 8%.', 'The prevalence of intellectual developmental disorders in Becker Muscular Dystrophy is 8%', 'The prevalence of intellectual developmental disorders in Becker Muscular Dystrophy is estimated to be 8.3%.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/36440509"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36440509",
"endSection": "abstract",
"offsetInBeginSection": 1369,
"offsetInEndSection": 1471,
"text": "The global prevalence of intellectual developmental disorder (IDD) was 8% in Becker muscular dystrophy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36440509",
"endSection": "abstract",
"offsetInBeginSection": 655,
"offsetInEndSection": 727,
"text": "dies were included. The prevalence of IDD in BMD was 8.0% (95% confidenc"
}
] | 13 |
BioASQ-training13b
| null | null |
66300d3e187cba990d00001b
|
bioasq_factoid
|
yesno
|
Are there any DNMT3 proteins present in plants?
|
['Yes.']
|
[
"Yes."
] |
['Yes. The plant DOMAINS REARRANGED METHYLTRANSFERASE2 (DRM2) is a homolog of the mammalian de novo methyltransferase DNMT3. DRM2 contains a novel arrangement of the motifs required for DNA methyltransferase catalytic activity.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21150311",
"http://www.ncbi.nlm.nih.gov/pubmed/21060858",
"http://www.ncbi.nlm.nih.gov/pubmed/10781108",
"http://www.ncbi.nlm.nih.gov/pubmed/15946751",
"http://www.ncbi.nlm.nih.gov/pubmed/20505370",
"http://www.ncbi.nlm.nih.gov/pubmed/23021223",
"http://www.ncbi.nlm.nih.gov/pubmed/22058406",
"http://www.ncbi.nlm.nih.gov/pubmed/18488247",
"http://www.ncbi.nlm.nih.gov/pubmed/17660570",
"http://www.ncbi.nlm.nih.gov/pubmed/11487702",
"http://www.ncbi.nlm.nih.gov/pubmed/11459824",
"http://www.ncbi.nlm.nih.gov/pubmed/15282033",
"http://www.ncbi.nlm.nih.gov/pubmed/12151602",
"http://www.ncbi.nlm.nih.gov/pubmed/12121623",
"http://www.ncbi.nlm.nih.gov/pubmed/9584105"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21150311",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "De novo DNA methylation in Arabidopsis thaliana is catalyzed by the methyltransferase DRM2, a homolog of the mammalian de novo methyltransferase DNMT3."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10781108",
"endSection": "sections.0",
"offsetInBeginSection": 387,
"offsetInEndSection": 851,
"text": "Here we describe DNA methyltransferase genes from both Arabidopsis and maize that show a high level of sequence similarity to Dnmt3, suggesting that they encode plant de novo methyltransferases. Relative to all known eukaryotic methyltransferases, these plant proteins contain a novel arrangement of the motifs required for DNA methyltransferase catalytic activity. The N termini of these methyltransferases contain a series of ubiquitin-associated (UBA) domains. "
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15946751",
"endSection": "sections.0",
"offsetInBeginSection": 365,
"offsetInEndSection": 519,
"text": "BLASTX searches and phylogenetic analysis suggested that five cDNAs belonged to four classes (Dnmt1, Dnmt2, CMT and Dnmt3) of DNA methyltransferase genes."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.uniprot.org/uniprot/CMT1_ARATH",
"http://www.uniprot.org/uniprot/CMT2_ARATH",
"http://www.uniprot.org/uniprot/CMT3_ARATH"
] | null |
511a16f9df1ebcce7d000005
|
bioasq_yesno
|
factoid
|
Which R/bioconductor package is used for integrative genomics visualizations?
|
[['Sushi.R']]
|
[
"Sushi.R",
"Sushi R",
"SushiR",
"Sushi R package",
"Sushi R software"
] |
['Sushi.R is a flexible, quantitative and integrative genomic visualizations for publication-quality multi-panel figures using common genomic data formats including Browser Extensible Data (BED), bedGraph and Browser Extensible Data Paired-End (BEDPE). Sushi.R is open source and made publicly available through GitHub (https://github.com/dphansti/Sushi) and Bioconductor (http://bioconductor.org/packages/release/bioc/html/Sushi.html).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24903420"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24903420",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "Sushi.R: flexible, quantitative and integrative genomic visualizations for publication-quality multi-panel figures."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24903420",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 785,
"text": "Interpretation and communication of genomic data require flexible and quantitative tools to analyze and visualize diverse data types, and yet, a comprehensive tool to display all common genomic data types in publication quality figures does not exist to date. To address this shortcoming, we present Sushi.R, an R/Bioconductor package that allows flexible integration of genomic visualizations into highly customizable, publication-ready, multi-panel figures from common genomic data formats including Browser Extensible Data (BED), bedGraph and Browser Extensible Data Paired-End (BEDPE). Sushi.R is open source and made publicly available through GitHub (https://github.com/dphansti/Sushi) and Bioconductor (http://bioconductor.org/packages/release/bioc/html/Sushi.html)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24903420",
"endSection": "abstract",
"offsetInBeginSection": 260,
"offsetInEndSection": 588,
"text": "To address this shortcoming, we present Sushi.R, an R/Bioconductor package that allows flexible integration of genomic visualizations into highly customizable, publication-ready, multi-panel figures from common genomic data formats including Browser Extensible Data (BED), bedGraph and Browser Extensible Data Paired-End (BEDPE)"
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D016678",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D023281"
] |
[] |
56b330bb39c782df06000001
|
bioasq_factoid
|
factoid
|
Which type of distance is used in the R-package XenofilteR?
|
['Edit-distance']
|
[
"Edit-distance",
"Levenshtein distance",
"String edit distance",
"Minimum edit distance",
"Edit distance metric"
] |
['The R-package XenofilteR separates mouse from human sequence reads based on the edit-distance between a sequence read and reference genome.', 'XenofilteR separates mouse from human sequence reads based on the edit-distance between a sequence read and reference genome.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30286710"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30286710",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 98,
"text": "XenofilteR: computational deconvolution of mouse and human reads in tumor xenograft sequence data."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30286710",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 1391,
"text": "Mouse xenografts from (patient-derived) tumors (PDX) or tumor cell lines are widely used as models to study various biological and preclinical aspects of cancer. However, analyses of their RNA and DNA profiles are challenging, because they comprise reads not only from the grafted human cancer but also from the murine host. The reads of murine origin result in false positives in mutation analysis of DNA samples and obscure gene expression levels when sequencing RNA. However, currently available algorithms are limited and improvements in accuracy and ease of use are necessary.RESULTS: We developed the R-package XenofilteR, which separates mouse from human sequence reads based on the edit-distance between a sequence read and reference genome. To assess the accuracy of XenofilteR, we generated sequence data by in silico mixing of mouse and human DNA sequence data. These analyses revealed that XenofilteR removes > 99.9% of sequence reads of mouse origin while retaining human sequences. This allowed for mutation analysis of xenograft samples with accurate variant allele frequencies, and retrieved all non-synonymous somatic tumor mutations.CONCLUSIONS: XenofilteR accurately dissects RNA and DNA sequences from mouse and human origin, thereby outperforming currently available tools. XenofilteR is open source and available at https://github.com/PeeperLab/XenofilteR ."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30286710",
"endSection": "abstract",
"offsetInBeginSection": 595,
"offsetInEndSection": 763,
"text": "RESULTS\n\nWe developed the R-package XenofilteR, which separates mouse from human sequence reads based on the edit-distance between a sequence read and reference genome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30286710",
"endSection": "abstract",
"offsetInBeginSection": 593,
"offsetInEndSection": 760,
"text": "RESULTS We developed the R-package XenofilteR, which separates mouse from human sequence reads based on the edit-distance between a sequence read and reference genome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30286710",
"endSection": "abstract",
"offsetInBeginSection": 595,
"offsetInEndSection": 763,
"text": "RESULTS\nWe developed the R-package XenofilteR, which separates mouse from human sequence reads based on the edit-distance between a sequence read and reference genome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30286710",
"endSection": "abstract",
"offsetInBeginSection": 593,
"offsetInEndSection": 761,
"text": "RESULTS: We developed the R-package XenofilteR, which separates mouse from human sequence reads based on the edit-distance between a sequence read and reference genome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30286710",
"endSection": "abstract",
"offsetInBeginSection": 582,
"offsetInEndSection": 741,
"text": "We developed the R-package XenofilteR, which separates mouse from human sequence reads based on the edit-distance between a sequence read and reference genome."
}
] | 11 |
BioASQ-training11b
| null | null |
5e52be146d0a27794100004a
|
bioasq_factoid
|
factoid
|
Which cancer is associated with increased levels of Serum alpha fetoprotein (AFP) ?
|
['HCC', 'hepatocelluar carcinoma']
|
[
"HCC",
"hepatocellular carcinoma",
"hepatocellular cancer",
"hepatoma",
"liver cancer",
"liver cell carcinoma"
] |
['Serum alpha fetoprotein (AFP) is a marker of germ cell neoplasms,\r\nSerum α-Fetoprotein (AFP) is a widely used diagnostic biomarker, but it has limited sensitivity and is not elevated in all HCC cases.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28989060",
"http://www.ncbi.nlm.nih.gov/pubmed/28750141",
"http://www.ncbi.nlm.nih.gov/pubmed/29052791",
"http://www.ncbi.nlm.nih.gov/pubmed/28582340",
"http://www.ncbi.nlm.nih.gov/pubmed/28482112"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28989060",
"endSection": "abstract",
"offsetInBeginSection": 1624,
"offsetInEndSection": 1864,
"text": "In the competing-risk regression, the sum of tumor number and size and of log10 level of AFP were significantly associated with HCC-specific death (P < .001), returning an average c-statistic of 0.780 (95% confidence interval, 0.763-0.798)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28582340",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 224,
"text": "Ovarian Sertoli-Leydig cell tumors (SLCTs) are uncommon neoplasms that are occasionally associated with an elevated level of serum alpha fetoprotein (AFP), a marker of germ cell neoplasms, particularly yolk sac tumor (YST). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28482112",
"endSection": "abstract",
"offsetInBeginSection": 337,
"offsetInEndSection": 610,
"text": "Serum α-Fetoprotein (AFP) is a widely used diagnostic biomarker, but it has limited sensitivity and is not elevated in all HCC cases so, we incorporate a second blood-based biomarker, des'γ carboxy-prothrombin (DCP), that has shown potential as a screening marker for HCC. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28750141",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 182,
"text": "Cirrhosis in patients with chronic hepatitis C increases the risk of hepatocellular carcinoma (HCC), and surveillance with ultrasound (US) and alpha-fetoprotein (AFP) is recommended."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29052791",
"endSection": "abstract",
"offsetInBeginSection": 1861,
"offsetInEndSection": 2036,
"text": " The combination of enhancement patterns on CEUS and serum tumor markers (AFP and CA19-9) may be a potentially specific diagnostic method to differentiate CHC from HCC and CC."
}
] | 11 |
BioASQ-training11b
| null | null |
5c89623bf9c2ba6b28000005
|
bioasq_factoid
|
factoid
|
Which is the major symptom of the Doose syndrome?
|
[['myoclonic astatic epilepsy']]
|
[
"myoclonic astatic epilepsy",
"myoclonic astatic epilepsy syndrome",
"MAE",
"myoclonic astatic seizures",
"myoclonic astatic epilepsy type 1",
"myoclonic astatic epilepsy type 2"
] |
['Myoclonic astatic epilepsy is the major symptom of the Doose syndrome, which is a difficult to treat idiopathic generalized epilepsy of early childhood.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23941843",
"http://www.ncbi.nlm.nih.gov/pubmed/23159713",
"http://www.ncbi.nlm.nih.gov/pubmed/22780699",
"http://www.ncbi.nlm.nih.gov/pubmed/22322415",
"http://www.ncbi.nlm.nih.gov/pubmed/22266062",
"http://www.ncbi.nlm.nih.gov/pubmed/21396429",
"http://www.ncbi.nlm.nih.gov/pubmed/21351810",
"http://www.ncbi.nlm.nih.gov/pubmed/20722665",
"http://www.ncbi.nlm.nih.gov/pubmed/20472190",
"http://www.ncbi.nlm.nih.gov/pubmed/20301494",
"http://www.ncbi.nlm.nih.gov/pubmed/19049588",
"http://www.ncbi.nlm.nih.gov/pubmed/18990309",
"http://www.ncbi.nlm.nih.gov/pubmed/17105462",
"http://www.ncbi.nlm.nih.gov/pubmed/12073789",
"http://www.ncbi.nlm.nih.gov/pubmed/10768159",
"http://www.ncbi.nlm.nih.gov/pubmed/9184597",
"http://www.ncbi.nlm.nih.gov/pubmed/8753132",
"http://www.ncbi.nlm.nih.gov/pubmed/8891396",
"http://www.ncbi.nlm.nih.gov/pubmed/8214350",
"http://www.ncbi.nlm.nih.gov/pubmed/8243377",
"http://www.ncbi.nlm.nih.gov/pubmed/1396420",
"http://www.ncbi.nlm.nih.gov/pubmed/2115971",
"http://www.ncbi.nlm.nih.gov/pubmed/24696509"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23941843",
"endSection": "abstract",
"offsetInBeginSection": 816,
"offsetInEndSection": 1011,
"text": "KD is particularly effective in myoclonic astatic epilepsy (MAE; Doose Syndrome) and West syndrome with 100% and 81.25% of the patients having a greater than 50% seizure reduction, respectively. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23159713",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "Myoclonic astatic epilepsy (Doose syndrome) - a lamotrigine responsive epilepsy?"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23159713",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "PURPOSE: Myoclonic astatic epilepsy (MAE, Doose syndrome) is a difficult to treat idiopathic generalized epilepsy of early childhood."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22780699",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 175,
"text": "Herman Doose first described the generalized childhood epilepsy syndrome of myoclonic astatic epilepsy (MAE) in 1970, attributing a genetic cause from this first description. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22322415",
"endSection": "abstract",
"offsetInBeginSection": 410,
"offsetInEndSection": 704,
"text": "RECENT FINDINGS: In the past several years, neurologists are finding new indications to use these dietary treatments, perhaps even as first-line therapy, including infantile spasms, myoclonic-astatic epilepsy (Doose syndrome), Dravet syndrome, and status epilepticus (including FIRES syndrome)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22266062",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "First long-term experience with the orphan drug rufinamide in children with myoclonic-astatic epilepsy (Doose syndrome)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22266062",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "INTRODUCTION: We evaluated the long-term efficacy and tolerability of the orphan drug rufinamide (RUF) in children with pharmacoresistant myoclonic-astatic epilepsy (MAE, Doose syndrome)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21396429",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 251,
"text": "Mutations in SCN1A gene, encoding the voltage-gated sodium channel α1-subunit, are found to be associated with severe myoclonic epilepsy in infancy or Dravet syndrome (DS), but only rarely with the myoclonic astatic epilepsy (MAE, or Doose syndrome). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21351810",
"endSection": "abstract",
"offsetInBeginSection": 1022,
"offsetInEndSection": 1305,
"text": "The difficulty early in the course of Lennox-Gastaut syndrome is distinguishing this diagnosis from severe myoclonic epilepsy of infancy (Dravet syndrome) or from myoclonic-astatic epilepsy (Doose syndrome), as the seizure patterns in these three syndromes may overlap at the onset. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20722665",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 66,
"text": "Doose syndrome (myoclonic-astatic epilepsy): 40 years of progress."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20722665",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Doose syndrome, otherwise traditionally known as myoclonic-astatic epilepsy, was first described as a unique epilepsy syndrome by Dr Hermann Doose in 1970."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20472190",
"endSection": "abstract",
"offsetInBeginSection": 536,
"offsetInEndSection": 769,
"text": "Of 38 patients, 22 had Lennox-Gastaut syndrome (58%); 6 had myoclonic-astatic epilepsy of Doose (16%); 5 had symptomatic generalized epilepsy, not otherwise specified (13%); and 5 had symptomatic localization-related epilepsy (13%). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20472190",
"endSection": "abstract",
"offsetInBeginSection": 872,
"offsetInEndSection": 1080,
"text": "With felbamate treatment, 6 patients (16%) became seizure free, including 4 of the 6 patients with myoclonic-astatic epilepsy of Doose; 24 patients (63%) had a greater than 50% reduction in seizure frequency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20301494",
"endSection": "abstract",
"offsetInBeginSection": 547,
"offsetInEndSection": 738,
"text": "Less commonly observed phenotypes include myoclonic-astatic epilepsy (MAE or Doose syndrome), Lennox-Gastaut syndrome (LGS), infantile spasms, and vaccine-related encephalopathy and seizures."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19049588",
"endSection": "abstract",
"offsetInBeginSection": 87,
"offsetInEndSection": 343,
"text": "This includes syndromes with multiple etiologies, including Lennox-Gastaut syndrome and infantile spasms; developmental syndromes of unknown etiology, such as Landau-Kleffner syndrome; and idiopathic epilepsies, such as myoclonic-astatic (Doose) epilepsy. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18990309",
"endSection": "abstract",
"offsetInBeginSection": 188,
"offsetInEndSection": 303,
"text": "It should be considered early in the treatment of Dravet syndrome and myoclonic-astatic epilepsy (Doose syndrome). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17105462",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "The purpose of this article is to present a short review of the natural history of myoclonic astatic epilepsy (MAE; Doose syndrome) and the Lennox-Gastaut syndrome (LGS). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12073789",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 98,
"text": "[Clinical case of the month. Myoclonic-astatic epilepsy in a young child (MAE) or Doose syndrome]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10768159",
"endSection": "abstract",
"offsetInBeginSection": 601,
"offsetInEndSection": 771,
"text": "His refractory epilepsy which started 7 years ago shares symptoms and signs of both epilepsy with myoclonic-astatic seizures (Doose Syndrome) and Lennox-Gastaut Syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9184597",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 224,
"text": "PURPOSE: Before 1986, the spectrum of childhood epilepsies, including Lennox-Gastaut syndrome (LGS) and Doose syndrome (DS), known collectively as \"epilepsia myoclonica astatica,\" was believed to represent a single disease. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8753132",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "We reported a 7-year-old girl with myoclonic-astatic epilepsy of early childhood (Doose syndrome). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8891396",
"endSection": "abstract",
"offsetInBeginSection": 451,
"offsetInEndSection": 1005,
"text": "Other myoclonic epilepsy syndromes with onset in the first year of life (Aicardi's Neonatal (Early) Myoclonic Encephalopathy, West's Syndrome, Dravet's Severe Myoclonic Epilepsy, and Dravet's Benign Myoclonic Epilepsy of Infancy), in early childhood (Lennox-Gastaut-Dravet Syndrome, Myoclonic Variant of Lennox Gastaut Dravet Syndrome, Myoclonic-Astatic Epilepsy of Doose, Benign Myoclonic Epilepsies (BME), or even in late childhood (Childhood Absence Epilepsy with myoclonias, vs. Myoclonic Absence Epilepsy) are probably genetically complex diseases. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8214350",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "A study of epileptic drop attacks (EDA) by simultaneous video-polygraphic recordings was carried out in one epileptic patient with myoclonic astatic seizures (Doose syndrome). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8243377",
"endSection": "abstract",
"offsetInBeginSection": 627,
"offsetInEndSection": 981,
"text": "A number of variants or atypical forms have been proposed. As a result, differential diagnosis presents a major challenge and includes specific generalized epilepsies, i.e., metabolic or inflammatory; secondarily generalized epilepsies, i.e., those arising from the frontal lobe; and severe forms of idiopathic generalized epilepsy, i.e., Doose syndrome."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1396420",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Video-EEG analysis of drop seizures in myoclonic astatic epilepsy of early childhood (Doose syndrome)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2115971",
"endSection": "abstract",
"offsetInBeginSection": 972,
"offsetInEndSection": 1204,
"text": " The clinical and EEG pattern, the high familial incidence are shared by the Doose syndrome, of which the present series seems to be a subgroup, as are other well-defined syndromes: benign and severe myoclonic epilepsies of infancy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21351810",
"endSection": "abstract",
"offsetInBeginSection": 1022,
"offsetInEndSection": 1304,
"text": "The difficulty early in the course of Lennox-Gastaut syndrome is distinguishing this diagnosis from severe myoclonic epilepsy of infancy (Dravet syndrome) or from myoclonic-astatic epilepsy (Doose syndrome), as the seizure patterns in these three syndromes may overlap at the onset."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23941843",
"endSection": "abstract",
"offsetInBeginSection": 816,
"offsetInEndSection": 1011,
"text": "KD is particularly effective in myoclonic astatic epilepsy (MAE; Doose Syndrome) and West syndrome with 100% and 81.25% of the patients having a greater than 50% seizure reduction, respectively. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23159713",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "Myoclonic astatic epilepsy (Doose syndrome) - a lamotrigine responsive epilepsy?"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21351810",
"endSection": "abstract",
"offsetInBeginSection": 1021,
"offsetInEndSection": 1302,
"text": "The difficulty early in the course of Lennox-Gastaut syndrome is distinguishing this diagnosis from severe myoclonic epilepsy of infancy (Dravet syndrome) or from myoclonic-astatic epilepsy (Doose syndrome), as the seizure patterns in these three syndromes may overlap at the onset"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10768159",
"endSection": "abstract",
"offsetInBeginSection": 601,
"offsetInEndSection": 770,
"text": "His refractory epilepsy which started 7 years ago shares symptoms and signs of both epilepsy with myoclonic-astatic seizures (Doose Syndrome) and Lennox-Gastaut Syndrome"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20722665",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Doose syndrome, otherwise traditionally known as myoclonic-astatic epilepsy, was first described as a unique epilepsy syndrome by Dr Hermann Doose in 1970"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10768159",
"endSection": "abstract",
"offsetInBeginSection": 601,
"offsetInEndSection": 770,
"text": "His refractory epilepsy which started 7 years ago shares symptoms and signs of both epilepsy with myoclonic-astatic seizures (Doose Syndrome) and Lennox-Gastaut Syndrome"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10768159",
"endSection": "abstract",
"offsetInBeginSection": 601,
"offsetInEndSection": 770,
"text": "His refractory epilepsy which started 7 years ago shares symptoms and signs of both epilepsy with myoclonic-astatic seizures (Doose Syndrome) and Lennox-Gastaut Syndrome"
}
] | 5 |
BioASQ-training5b
|
[] |
[] |
550342a8f8aee20f27000002
|
bioasq_factoid
|
factoid
|
What is the mode of action of filgotinib?
|
['JAK1 inhibitor']
|
[
"JAK1 inhibitor",
"Janus kinase 1 inhibitor",
"JAK1 antagonist",
"JAK1 blocker"
] |
["Filgotinib is an oral selective Janus kinase 1 (JAK1) inhibitor. It has been tested in patients with rheumatoid arthritis and Chroni's disease, and has been shown to be effective.", "Filgotinib (GLPG0634) is a selective inhibitor of Janus kinase 1 (JAK1) currently in development for the treatment of rheumatoid arthritis and Crohn's disease.", 'Filgotinib is an oral selective JAK inhibitor. It works by inhibiting JAK1.', 'Filgotinib (GLPG0634) is a selective inhibitor of Janus kinase 1 (JAK1).', "Filgotinib (GS-6034, formerly GLPG0634) is an oral, selective Janus kinase 1 (JAK1) inhibitor that showed early response and sustained efficacy in patients with rheumatoid arthritis and with Crohn's disease. Effect of filgotinib, a selective JAK 1 inhibitor, with and without methotrexate in patients with rheumatoid arthritis: patient-reported outcomes.", "Filgotinib is an oral selective JAK1 inhibitor. It has been tested in patients with rheumatoid arthritis and Chroni's disease, and has been shown to be safe and efficacious.", 'Efficacy and safety of filgotinib, a selective Janus kinase 1 inhibitor,', 'Selective inhibition of JAK-1 with filgotinib shows initial efficacy in RA with an encouraging safety profile in these exploratory studies. The selectivity of filgotinib for JAK1 may have theoretical advantages in terms of limiting toxicity.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30088677",
"http://www.ncbi.nlm.nih.gov/pubmed/30360969",
"http://www.ncbi.nlm.nih.gov/pubmed/27993829",
"http://www.ncbi.nlm.nih.gov/pubmed/27993828",
"http://www.ncbi.nlm.nih.gov/pubmed/28622463",
"http://www.ncbi.nlm.nih.gov/pubmed/30360970",
"http://www.ncbi.nlm.nih.gov/pubmed/27988142",
"http://www.ncbi.nlm.nih.gov/pubmed/25681059",
"http://www.ncbi.nlm.nih.gov/pubmed/28838249",
"http://www.ncbi.nlm.nih.gov/pubmed/29566740",
"http://www.ncbi.nlm.nih.gov/pubmed/26693854"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25681059",
"endSection": "abstract",
"offsetInBeginSection": 27,
"offsetInEndSection": 187,
"text": "Filgotinib (GLPG0634) is a selective inhibitor of Janus kinase 1 (JAK1) currently in development for the treatment of rheumatoid arthritis and Crohn's disease. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26693854",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Clinical Confirmation that the Selective JAK1 Inhibitor Filgotinib (GLPG0634) has a Low Liability for Drug-drug Interactions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26693854",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 284,
"text": "The selective Janus kinase 1 inhibitor filgotinib (GLPG0634), which is currently in clinical development for the treatment of rheumatoid arthritis (RA) and Crohn's disease, demonstrated encouraging safety and efficacy profiles in RA patients after 4 weeks of daily dosing. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26693854",
"endSection": "abstract",
"offsetInBeginSection": 1125,
"offsetInEndSection": 1577,
"text": " In vitro, filgotinib and its active metabolite at clinically relevant concentrations did not interact with cytochrome P450 enzymes and uridine 5'-diphospho-glucuronosyltransferases, and did not inhibit key drug transporters. In the clinic, a lack of relevant pharmacokinetic drug interactions by filgotinib and its active metabolite with substrates of CYP3A4, as well as with organic anion transporters involved in methotrexate elimination were found."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28622463",
"endSection": "abstract",
"offsetInBeginSection": 1903,
"offsetInEndSection": 2042,
"text": "Selective inhibition of JAK-1 with filgotinib shows initial efficacy in RA with an encouraging safety profile in these exploratory studies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28838249",
"endSection": "abstract",
"offsetInBeginSection": 551,
"offsetInEndSection": 690,
"text": "Here we review the pharmacology and clinical trial data for efficacy and safety of filgotinib, an investigational selective JAK1 inhibitor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28838249",
"endSection": "abstract",
"offsetInBeginSection": 808,
"offsetInEndSection": 909,
"text": "The selectivity of filgotinib for JAK1 may have theoretical advantages in terms of limiting toxicity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27988142",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 123,
"text": "Filgotinib (GLPG0634, GS-6034) is a once-daily, orally administered, Janus kinase 1 (JAK1)-selective inhibitor."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27993829",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 63,
"text": "Filgotinib (GLPG0634/GS-6034), an oral JAK1 selective inhibitor"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27993829",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 127,
"text": "To evaluate the efficacy and safety of different doses and regimens of filgotinib, an oral Janus kinase 1 inhibitor"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27993828",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 63,
"text": "Filgotinib (GLPG0634/GS-6034), an oral selective JAK1 inhibitor"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27993828",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 235,
"text": "To evaluate the efficacy and safety of different doses of filgotinib, an oral Janus kinase 1 inhibitor, as monotherapy in patients with active rheumatoid arthritis (RA) and previous inadequate response to methotrexate (MTX)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30360970",
"endSection": "abstract",
"offsetInBeginSection": 259,
"offsetInEndSection": 378,
"text": "The TORTUGA trial investigated the efficacy and safety of filgotinib, an oral selective Janus kinase 1 (JAK1) inhibitor"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30360969",
"endSection": "abstract",
"offsetInBeginSection": 110,
"offsetInEndSection": 241,
"text": "We aimed to investigate the efficacy and safety of filgotinib, a selective JAK1 inhibitor, for the treatment of psoriatic arthritis"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30360969",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "Efficacy and safety of filgotinib, a selective Janus kinase 1 inhibitor, in patients with active psoriatic arthritis"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30088677",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Influence of age and renal impairment on the steady state pharmacokinetics of filgotinib, a selective JAK1 inhibitor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30088677",
"endSection": "abstract",
"offsetInBeginSection": 6,
"offsetInEndSection": 214,
"text": "Filgotinib (GS-6034, formerly GLPG0634) is an oral, selective Janus kinase 1 (JAK1) inhibitor that showed early response and sustained efficacy in patients with rheumatoid arthritis and with Crohn's disease. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29566740",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "Effect of filgotinib, a selective JAK 1 inhibitor, with and without methotrexate in patients with rheumatoid arthritis: patient-reported outcomes."
}
] | 11 |
BioASQ-training11b
| null | null |
5cd96f33a49efeb44c000004
|
bioasq_factoid
|
factoid
|
What is the life expectancy of professional athletes in respect to the general population?
|
['longer than the general population']
|
[
"longer than average",
"longer than typical",
"longer than the general population",
"greater than the general population",
"above average length"
] |
Elite endurance (aerobic) athletes and mixed-sports (aerobic and anaerobic) athletes show higher longevity than the general population, but results about power (anaerobic) athletes are inconsistent.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21435018",
"http://www.ncbi.nlm.nih.gov/pubmed/18369530",
"http://www.ncbi.nlm.nih.gov/pubmed/19574095",
"http://www.ncbi.nlm.nih.gov/pubmed/17436206",
"http://www.ncbi.nlm.nih.gov/pubmed/9177584",
"http://www.ncbi.nlm.nih.gov/pubmed/8164540",
"http://www.ncbi.nlm.nih.gov/pubmed/8450727",
"http://www.ncbi.nlm.nih.gov/pubmed/2253729",
"http://www.ncbi.nlm.nih.gov/pubmed/16389882",
"http://www.ncbi.nlm.nih.gov/pubmed/17214401",
"http://www.ncbi.nlm.nih.gov/pubmed/21618162"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21435018",
"endSection": "abstract",
"offsetInBeginSection": 655,
"offsetInEndSection": 791,
"text": "In all 13 intervals, cumulative observed survival was smaller than cumulative expected survival, resulting in cumulative RSRs being <1. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21435018",
"endSection": "abstract",
"offsetInBeginSection": 890,
"offsetInEndSection": 1086,
"text": "This impaired survival experience of the internationals translates into a loss of median residual lifetime of 1.9 years [95% confidence interval: 0.6, 3.2] years at the entry time into the cohort."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18369530",
"endSection": "abstract",
"offsetInBeginSection": 1130,
"offsetInEndSection": 1350,
"text": "All the obtained results proved that high level physical activity in youth positively influenced men's mortality, what was observed for the former athletes even after 40 years since the end of their professional carrier."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19574095",
"endSection": "abstract",
"offsetInBeginSection": 645,
"offsetInEndSection": 844,
"text": "It appears that elite endurance (aerobic) athletes and mixed-sports (aerobic and anaerobic) athletes survive longer than the general population, as indicated by lower mortality and higher longevity. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19574095",
"endSection": "abstract",
"offsetInBeginSection": 945,
"offsetInEndSection": 1039,
"text": "On the other hand, there are inconsistent results among studies of power (anaerobic) athletes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19574095",
"endSection": "abstract",
"offsetInBeginSection": 1040,
"offsetInEndSection": 1171,
"text": "When elite athletes engaging in various sports are analysed together, their mortality is lower than that of the general population."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17436206",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "Moderate exercise and intense physical training are associated with increased life expectancy (LE)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9177584",
"endSection": "abstract",
"offsetInBeginSection": 1324,
"offsetInEndSection": 1524,
"text": "We found that former aerobic sports athletes (endurance and mixed sports) in particular have high total and active life expectancy and low risk for ischemic heart disease and diabetes in later years. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8164540",
"endSection": "abstract",
"offsetInBeginSection": 1245,
"offsetInEndSection": 1381,
"text": "Higher leisure aerobic activity and less frequent smoking after athletic years might explain higher life expectancy of Finnish athletes."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8450727",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 55,
"text": "Increased life expectancy of world class male athletes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8450727",
"endSection": "abstract",
"offsetInBeginSection": 913,
"offsetInEndSection": 1659,
"text": "The mean LE adjusted for occupational group, marital status, and the age at entry to the cohort (and its 95% confidence limits) was in endurance sports (long distance running and cross-country skiing) 75.6 (73.6, 77.5) yr; in team games (soccer, ice hockey, basketball, as well as jumpers and short-distance runners from track and field (73.9 (72.7, 75.1) yr; in power sports (boxing, wrestling, weight lifting, and throwers from field athletics) 71.5 (70.4, 72.2) yr; and in the reference group 69.9 (69.0, 70.9) yr. The increased mean life expectancies were mainly explained by decreased cardiovascular mortality (endurance sports mortality odds ratio OR = 0.49 (95% CL 0.26, 0.93), team sports OR = 0.61 (0.41, 0.92) compared with referents). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2253729",
"endSection": "abstract",
"offsetInBeginSection": 422,
"offsetInEndSection": 722,
"text": "Thirty-four deaths were observed among males (vs 46.6 expected) with a O/E ratio of 0.73, while 3 deaths were observed among women (vs 6.2 expected) with a O/E ratio of 0.48. Neither of these differences was significant, but the O/E ratio for the group as a whole was quite significant (p = 0.0296). "
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D008017",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D056352"
] |
[] |
52efc016c8da89891000001a
|
bioasq_factoid
|
factoid
|
What is the mode of inheritance of nemaline myopathy?
|
['autosomal dominant', 'autosomal recessive']
|
[
"autosomal dominant",
"autosomal recessive",
"AD",
"AR",
"dominant inheritance",
"recessive inheritance",
"autosomal inheritance"
] |
['Nemaline myopathy has a autosomal dominant or recessive mode of inheritance.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/17846275",
"http://www.ncbi.nlm.nih.gov/pubmed/15336686",
"http://www.ncbi.nlm.nih.gov/pubmed/2213842"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17846275",
"endSection": "sections.0",
"offsetInBeginSection": 879,
"offsetInEndSection": 1010,
"text": "The results indicate that mutations in TPM2 may cause nemaline myopathy as well as cap disease with a dominant mode of inheritance."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15336686",
"endSection": "sections.0",
"offsetInBeginSection": 346,
"offsetInEndSection": 435,
"text": "Autosomal recessive inheritance had been verified or appeared likely in all nebulin cases"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15336686",
"endSection": "sections.0",
"offsetInBeginSection": 664,
"offsetInEndSection": 850,
"text": "Most cases were sporadic, but in addition there were instances of both autosomal dominant and autosomal recessive inheritance, while two families showed mosaicism for dominant mutations."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15336686",
"endSection": "sections.0",
"offsetInBeginSection": 1046,
"offsetInEndSection": 1114,
"text": "Finding the causative mutation(s) determines the mode of inheritance"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2213842",
"endSection": "sections.0",
"offsetInBeginSection": 751,
"offsetInEndSection": 967,
"text": "We conclude that in the Finnish CNM patients, the mode of inheritance appears to be recessive. Apart from a few instances of dominant inheritance, most cases published also seem compatible with recessive inheritance."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.disease-ontology.org/api/metadata/DOID:3191",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D017696",
"http://www.disease-ontology.org/api/metadata/DOID:423",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D020914",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D020512"
] | null |
516be1d6298dcd4e5100006a
|
bioasq_factoid
|
factoid
|
What cellular process is the gene product of NANOG involved in?
|
['regulation of transcription']
|
[
"regulation of transcription",
"transcription regulation",
"transcriptional regulation",
"control of transcription",
"transcription control"
] |
['NANOG is a transcription factor and a biomarker of cancer and pluripotent stem cells.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26339994",
"http://www.ncbi.nlm.nih.gov/pubmed/29177763",
"http://www.ncbi.nlm.nih.gov/pubmed/29414604",
"http://www.ncbi.nlm.nih.gov/pubmed/29243835",
"http://www.ncbi.nlm.nih.gov/pubmed/29486740",
"http://www.ncbi.nlm.nih.gov/pubmed/29204746",
"http://www.ncbi.nlm.nih.gov/pubmed/28866747"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28866747",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 187,
"text": "The objective of this study was to explore the prognostic value of cancer stem cell markers, namely CD133, NANOG, and NOTCH1, in early stage oral squamous cell carcinoma (OSCC)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29177763",
"endSection": "abstract",
"offsetInBeginSection": 320,
"offsetInEndSection": 378,
"text": " transcription factors (TFs) such as Oct4, Sox2, and Nanog"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29243835",
"endSection": "abstract",
"offsetInBeginSection": 569,
"offsetInEndSection": 636,
"text": "expression of breast CSCs markers (CD44, ALDH1A1, Nanog, and Oct4),"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29204746",
"endSection": "abstract",
"offsetInBeginSection": 1266,
"offsetInEndSection": 1310,
"text": "pluripotency markers OCT-4, SOX-2 and NANOG "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29414604",
"endSection": "abstract",
"offsetInBeginSection": 232,
"offsetInEndSection": 377,
"text": "The obtained induced pluripotent stem cell (iPSC) line showed pluripotency verified by the expression of pluripotency markers, NANOG, SOX2, OCT4,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26339994",
"endSection": "abstract",
"offsetInBeginSection": 128,
"offsetInEndSection": 226,
"text": "Nanog is one of the transcription factors that are essential for stem cellular physiology process."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29486740",
"endSection": "abstract",
"offsetInBeginSection": 975,
"offsetInEndSection": 1069,
"text": "CONCLUSIONS\nNanog has been recognized as a critical pluripotency gene in stem cell regulation."
}
] | 11 |
BioASQ-training11b
| null | null |
5c9789a9ecadf2e73f000024
|
bioasq_factoid
|
factoid
|
Which brain tumors does neuroligin-3 promote?
|
['high-grade gliomas']
|
[
"high-grade gliomas",
"high-grade glioma",
"malignant gliomas",
"malignant glioma",
"grade III gliomas",
"grade IV gliomas",
"anaplastic gliomas",
"glioblastoma",
"glioblastoma multiforme"
] |
['Neuroligin-3 promotes the growth of high-grade gliomas.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28959975"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28959975",
"endSection": "abstract",
"offsetInBeginSection": 605,
"offsetInEndSection": 1576,
"text": "An important mechanism that mediates this neural regulation of brain cancer is activity-dependent cleavage and secretion of the synaptic adhesion molecule neuroligin-3 (NLGN3), which promotes glioma proliferation through the PI3K-mTOR pathway. However, the necessity of NLGN3 for glioma growth, the proteolytic mechanism of NLGN3 secretion, and the further molecular consequences of NLGN3 secretion in glioma cells remain unknown. Here we show that HGG growth depends on microenvironmental NLGN3, identify signalling cascades downstream of NLGN3 binding in glioma, and determine a therapeutically targetable mechanism of secretion. Patient-derived orthotopic xenografts of paediatric GBM, DIPG and adult GBM fail to grow in Nlgn3 knockout mice. NLGN3 stimulates several oncogenic pathways, such as early focal adhesion kinase activation upstream of PI3K-mTOR, and induces transcriptional changes that include upregulation of several synapse-related genes in glioma cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28959975",
"endSection": "abstract",
"offsetInBeginSection": 1794,
"offsetInEndSection": 1913,
"text": "This work defines a promising strategy for targeting NLGN3 secretion, which could prove transformative for HGG therapy."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28959975",
"endSection": "title",
"offsetInBeginSection": -1,
"offsetInEndSection": 81,
"text": "Targeting neuronal activity-regulated neuroligin-3 dependency in high-grade glioma"
}
] | 11 |
BioASQ-training11b
| null | null |
5a9ac4e81d1251d03b000011
|
bioasq_factoid
|
yesno
|
Have machine learning methods been used to predict the severity of major depressive disorder(MDD)?
|
['yes']
|
[
"yes"
] |
['Machine-learning (ML) models developed from self-reports can be used to predict persistence and severity of major depressive disorder(MDD)']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26821982",
"http://www.ncbi.nlm.nih.gov/pubmed/29879133",
"http://www.ncbi.nlm.nih.gov/pubmed/25066141",
"http://www.ncbi.nlm.nih.gov/pubmed/30286415",
"http://www.ncbi.nlm.nih.gov/pubmed/27551669",
"http://www.ncbi.nlm.nih.gov/pubmed/28702811",
"http://www.ncbi.nlm.nih.gov/pubmed/26728563",
"http://www.ncbi.nlm.nih.gov/pubmed/22544901",
"http://www.ncbi.nlm.nih.gov/pubmed/29682732"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30286415",
"endSection": "abstract",
"offsetInBeginSection": 300,
"offsetInEndSection": 484,
"text": "Here, we conduct a meta-review to identify predictors of response to antidepressant therapy in order to select robust input features for machine learning models of treatment response. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28702811",
"endSection": "title",
"offsetInBeginSection": 2,
"offsetInEndSection": 117,
"text": "machine learning framework involving EEG-based functional connectivity to diagnose major depressive disorder (MDD)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29879133",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 412,
"text": "Identification of risk factors of treatment resistance may be useful to guide treatment selection, avoid inefficient trial-and-error, and improve major depressive disorder (MDD) care. We extended the work in predictive modeling of treatment resistant depression (TRD) via partition of the data from the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) cohort into a training and a testing dataset."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26728563",
"endSection": "title",
"offsetInBeginSection": 52,
"offsetInEndSection": 132,
"text": "persistence and severity of major depressive disorder from baseline self-reports"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26728563",
"endSection": "abstract",
"offsetInBeginSection": 1572,
"offsetInEndSection": 1778,
"text": " These results confirm that clinically useful MDD risk-stratification models can be generated from baseline patient self-reports and that ML methods improve on conventional methods in developing such models"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22544901",
"endSection": "abstract",
"offsetInBeginSection": 2017,
"offsetInEndSection": 2189,
"text": "Furthermore, machine learning weighting factors may reflect an objective biomarker of major depressive disorder illness severity, based on abnormalities of brain structure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22544901",
"endSection": "abstract",
"offsetInBeginSection": 1474,
"offsetInEndSection": 1813,
"text": "Notably, while the only information provided for training the classifiers was T(1)-weighted scans plus a categorical label (major depressive disorder versus controls), both relevance vector machine and support vector machine 'weighting factors' (used for making predictions) correlated strongly with subjective ratings of illness severity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25066141",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 248,
"text": "BACKGROUND\nAlthough variation in the long-term course of major depressive disorder (MDD) is not strongly predicted by existing symptom subtype distinctions, recent research suggests that prediction can be improved by using machine learning methods."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25066141",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 248,
"text": "BACKGROUND Although variation in the long-term course of major depressive disorder (MDD) is not strongly predicted by existing symptom subtype distinctions, recent research suggests that prediction can be improved by using machine learning methods."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27551669",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "BACKGROUND Growing evidence documents the potential of machine learning for developing brain based diagnostic methods for major depressive disorder (MDD)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26821982",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "OBJECTIVE We aimed to integrate neural data and an advanced machine learning technique to predict individual major depressive disorder (MDD) patient severity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22544901",
"endSection": "abstract",
"offsetInBeginSection": 2145,
"offsetInEndSection": 2317,
"text": "Furthermore, machine learning weighting factors may reflect an objective biomarker of major depressive disorder illness severity, based on abnormalities of brain structure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25066141",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 256,
"text": "<b>BACKGROUND</b>: Although variation in the long-term course of major depressive disorder (MDD) is not strongly predicted by existing symptom subtype distinctions, recent research suggests that prediction can be improved by using machine learning methods."
}
] | 11 |
BioASQ-training11b
| null | null |
5c5215e67e3cb0e231000004
|
bioasq_yesno
|
factoid
|
What is the target of Selpercatinib?
|
['rearranged during transfection (RET) kinase']
|
[
"rearranged during transfection (RET) kinase",
"RET kinase",
"rearranged during transfection kinase",
"rearranged during transfection receptor tyrosine kinase",
"REarranged during Transfection kinase"
] |
['Selpercatinib is an orally-administered, selective inhibitor of rearranged during transfection (RET) kinase approved for the treatment of advanced RET fusion-positive non-small cell lung cancer (NSCLC).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/37265026",
"http://www.ncbi.nlm.nih.gov/pubmed/36122315",
"http://www.ncbi.nlm.nih.gov/pubmed/32703767",
"http://www.ncbi.nlm.nih.gov/pubmed/32493697",
"http://www.ncbi.nlm.nih.gov/pubmed/37718634",
"http://www.ncbi.nlm.nih.gov/pubmed/37070927",
"http://www.ncbi.nlm.nih.gov/pubmed/37317595",
"http://www.ncbi.nlm.nih.gov/pubmed/37131086",
"http://www.ncbi.nlm.nih.gov/pubmed/32416592",
"http://www.ncbi.nlm.nih.gov/pubmed/36996322",
"http://www.ncbi.nlm.nih.gov/pubmed/33239432",
"http://www.ncbi.nlm.nih.gov/pubmed/31988000",
"http://www.ncbi.nlm.nih.gov/pubmed/37565829",
"http://www.ncbi.nlm.nih.gov/pubmed/36825106",
"http://www.ncbi.nlm.nih.gov/pubmed/33007380",
"http://www.ncbi.nlm.nih.gov/pubmed/32083997",
"http://www.ncbi.nlm.nih.gov/pubmed/35582449",
"http://www.ncbi.nlm.nih.gov/pubmed/36626081",
"http://www.ncbi.nlm.nih.gov/pubmed/37795873",
"http://www.ncbi.nlm.nih.gov/pubmed/36469155",
"http://www.ncbi.nlm.nih.gov/pubmed/36108661",
"http://www.ncbi.nlm.nih.gov/pubmed/37360768",
"http://www.ncbi.nlm.nih.gov/pubmed/32557397",
"http://www.ncbi.nlm.nih.gov/pubmed/36632846",
"http://www.ncbi.nlm.nih.gov/pubmed/35726802",
"http://www.ncbi.nlm.nih.gov/pubmed/37603207",
"http://www.ncbi.nlm.nih.gov/pubmed/34099825",
"http://www.ncbi.nlm.nih.gov/pubmed/37059058",
"http://www.ncbi.nlm.nih.gov/pubmed/37425604",
"http://www.ncbi.nlm.nih.gov/pubmed/34649088",
"http://www.ncbi.nlm.nih.gov/pubmed/35799394",
"http://www.ncbi.nlm.nih.gov/pubmed/35647935",
"http://www.ncbi.nlm.nih.gov/pubmed/33150799",
"http://www.ncbi.nlm.nih.gov/pubmed/33314236",
"http://www.ncbi.nlm.nih.gov/pubmed/36422787",
"http://www.ncbi.nlm.nih.gov/pubmed/34832869",
"http://www.ncbi.nlm.nih.gov/pubmed/33161056",
"http://www.ncbi.nlm.nih.gov/pubmed/34713870",
"http://www.ncbi.nlm.nih.gov/pubmed/35969032",
"http://www.ncbi.nlm.nih.gov/pubmed/34505490",
"http://www.ncbi.nlm.nih.gov/pubmed/37972337",
"http://www.ncbi.nlm.nih.gov/pubmed/35425116",
"http://www.ncbi.nlm.nih.gov/pubmed/38050583",
"http://www.ncbi.nlm.nih.gov/pubmed/37525669",
"http://www.ncbi.nlm.nih.gov/pubmed/36568522",
"http://www.ncbi.nlm.nih.gov/pubmed/34237031",
"http://www.ncbi.nlm.nih.gov/pubmed/36729098",
"http://www.ncbi.nlm.nih.gov/pubmed/33771190",
"http://www.ncbi.nlm.nih.gov/pubmed/35704797",
"http://www.ncbi.nlm.nih.gov/pubmed/33489819",
"http://www.ncbi.nlm.nih.gov/pubmed/36657661",
"http://www.ncbi.nlm.nih.gov/pubmed/36075388",
"http://www.ncbi.nlm.nih.gov/pubmed/32846061",
"http://www.ncbi.nlm.nih.gov/pubmed/35304457",
"http://www.ncbi.nlm.nih.gov/pubmed/37274265",
"http://www.ncbi.nlm.nih.gov/pubmed/36481304",
"http://www.ncbi.nlm.nih.gov/pubmed/36198171",
"http://www.ncbi.nlm.nih.gov/pubmed/35950566",
"http://www.ncbi.nlm.nih.gov/pubmed/33455880",
"http://www.ncbi.nlm.nih.gov/pubmed/36572992",
"http://www.ncbi.nlm.nih.gov/pubmed/33082208",
"http://www.ncbi.nlm.nih.gov/pubmed/35007206",
"http://www.ncbi.nlm.nih.gov/pubmed/37051304",
"http://www.ncbi.nlm.nih.gov/pubmed/37265412",
"http://www.ncbi.nlm.nih.gov/pubmed/31768065",
"http://www.ncbi.nlm.nih.gov/pubmed/32846060",
"http://www.ncbi.nlm.nih.gov/pubmed/37870973",
"http://www.ncbi.nlm.nih.gov/pubmed/34402300",
"http://www.ncbi.nlm.nih.gov/pubmed/33169506",
"http://www.ncbi.nlm.nih.gov/pubmed/36416226"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36729098",
"endSection": "abstract",
"offsetInBeginSection": 359,
"offsetInEndSection": 486,
"text": "More recently, two selective RET inhibitors, selpercatinib and pralsetinib, demonstrated higher efficacy and good tolerability."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36568522",
"endSection": "abstract",
"offsetInBeginSection": 1515,
"offsetInEndSection": 1641,
"text": "Drug exposure of RET inhibitors is expected to increase with CYP 3A4 inhibition, with selpercatinib being the least affected. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36572992",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "An overview of the role of selpercatinib and pralsetinib in RET-fusion-positive non-small cell lung cancer (NSCLC)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36572992",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "OBJECTIVE: Selpercatinib and pralsetinib are new targeted therapies used to treat patients with non-small cell lung cancer (NSCLC) due to RET gene rearrangements."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36626081",
"endSection": "abstract",
"offsetInBeginSection": 1606,
"offsetInEndSection": 1671,
"text": "Three RET-mutant patients received selpercatinib; all showed PR. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36632846",
"endSection": "abstract",
"offsetInBeginSection": 828,
"offsetInEndSection": 981,
"text": "Rapid translation and regulatory approval of selective RET inhibitors, selpercatinib and pralsetinib, have opened up the field of RET precision oncology."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36422787",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 62,
"text": "Selpercatinib: A Review in Advanced RET Fusion-Positive NSCLC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36422787",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 223,
"text": "Selpercatinib (Retevmo®/Retsevmo®) is an orally-administered, selective inhibitor of rearranged during transfection (RET) kinase approved for the treatment of advanced RET fusion-positive non-small cell lung cancer (NSCLC)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36422787",
"endSection": "abstract",
"offsetInBeginSection": 927,
"offsetInEndSection": 1090,
"text": "Thus, currently available evidence suggests that selpercatinib is a promising new RET-targeted therapy option for patients with advanced RET fusion-positive NSCLC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36416226",
"endSection": "abstract",
"offsetInBeginSection": 74,
"offsetInEndSection": 169,
"text": "Selpercatinib is a highly selective RET inhibitor for treatment of metastatic RET-altered MTC. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32557397",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 191,
"text": "Selpercatinib (RETEVMO™) is a receptor tyrosine kinase RET (rearranged during transfection) inhibitor being developed by Loxo Oncology for the treatment of cancers harbouring RET alterations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37603207",
"endSection": "abstract",
"offsetInBeginSection": 1663,
"offsetInEndSection": 1824,
"text": "Conclusions Selective RET inhibitors Pralsetinib and Selpercatinib have shown a good effect on RET fusion-positive NSCLC, with a low incidence of adverse events."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34832869",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 172,
"text": "Selpercatinib is a targeted, FDA-approved, oral, small-molecule inhibitor for the treatment of rearranged during transfection (RET) proto-oncogene mutation-positive cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32557397",
"endSection": "abstract",
"offsetInBeginSection": 192,
"offsetInEndSection": 443,
"text": "Based on results from the phase I/II LIBRETTO-001 trial, selpercatinib was recently approved by the US FDA for the treatment of RET fusion-positive non-small-cell lung cancer, RET fusion-positive thyroid cancer and RET-mutant medullary thyroid cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33771190",
"endSection": "abstract",
"offsetInBeginSection": 629,
"offsetInEndSection": 815,
"text": "Selpercatinib (LOXO-292) and pralsetinib (BLU-667) are potent and selective inhibitors that target RET alterations, including fusions and mutations, irrespective of the tissue of origin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37795873",
"endSection": "abstract",
"offsetInBeginSection": 117,
"offsetInEndSection": 232,
"text": "Selpercatinib is a highly selective RET inhibitor that has demonstrated anti-tumor activity in RET-mutated cancers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37059058",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 75,
"text": "Selpercatinib is a small molecule that binds at the RET kinase active site."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33489819",
"endSection": "abstract",
"offsetInBeginSection": 620,
"offsetInEndSection": 871,
"text": "In 2020, the US Food and Drug Administration approved selpercatinib, a selective RET inhibitor, for adults with lung and thyroid cancers with RET rearrangements or mutations, making it the first targeted therapy to be approved for RET-altered cancers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36469155",
"endSection": "abstract",
"offsetInBeginSection": 267,
"offsetInEndSection": 449,
"text": "Here, we describe a case of a sarcoma, associated with a RET::TRIM33-fusion gene with an exceptional response to a neoadjuvant therapy with the selective RET inhibitor selpercatinib."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37131086",
"endSection": "abstract",
"offsetInBeginSection": 80,
"offsetInEndSection": 466,
"text": "Oncogenic RET fusions or mutations are found most often in non-small cell lung cancer (NSCLC) and in thyroid cancer, but also increasingly in various types of cancers at low rates. In the last few years, two potent and selective RET protein tyrosine kinase inhibitors (TKIs), pralsetinib (BLU-667) and selpercatinib (LOXO-292, LY3527723) were developed and received regulatory approval."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31988000",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 279,
"text": "INTRODUCTION: Novel rearranged in transfection (RET)-specific tyrosine kinase inhibitors (TKIs) such as selpercatinib (LOXO-292) have shown unprecedented efficacy in tumors positive for RET fusions or mutations, notably RET fusion-positive NSCLC and RET-mutated medullary thyroid"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34832869",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "P-Glycoprotein (ABCB1/MDR1) and BCRP (ABCG2) Limit Brain Accumulation and Cytochrome P450-3A (CYP3A) Restricts Oral Exposure of the RET Inhibitor Selpercatinib (RETEVMO)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34505490",
"endSection": "abstract",
"offsetInBeginSection": 145,
"offsetInEndSection": 383,
"text": "Selpercatinib and pralsetinib are tyrosine kinase inhibitors selectively targeting RET and with clinical activity in RET-positive NSCLC.CASE PRESENTATION: A male never-smoker in his forties was diagnosed with advanced lung adenocarcinoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37718634",
"endSection": "abstract",
"offsetInBeginSection": 314,
"offsetInEndSection": 504,
"text": "Fortunately, two selective RET inhibitors (sRETi), namely pralsetinib and selpercatinib, have been approved for treating RET fusion NSCLC due to their remarkable efficacy and safety profiles"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37565829",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "Sustained Response with Dose-reduced Selpercatinib in a Pediatric Patient with Metastatic NCOA4-RET Fusion Papillary Thyroid Carcinoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37317595",
"endSection": "abstract",
"offsetInBeginSection": 308,
"offsetInEndSection": 558,
"text": "In addition to these approvals, dostarlimab for mismatch repair deficiency(dMMR), dabrafenib and trametinib for BRAF V600E, and selpercatinib for RET fusion gene have been approved in the United States as tumor agnostic biomarkers and their treatment"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33455880",
"endSection": "abstract",
"offsetInBeginSection": 410,
"offsetInEndSection": 643,
"text": "To overcome these issues, new selective RET inhibitors such as pralsetinib (BLU-667) and selpercatinib (LOXO-292) have been developed in clinical trials, with selpercatinib recently approved by the Food and Drug Administration (FDA)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33007380",
"endSection": "abstract",
"offsetInBeginSection": 112,
"offsetInEndSection": 389,
"text": "er (NSCLC). RET-selective inhibitors selpercatinib (LOXO-292) and pralsetinib (BLU-667) recently demonstrated favorable antitumor activity and safety profiles in advanced RET fusion-positive NSCLC, and both have received approval by the US Food and Drug Administration for this"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32083997",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1634,
"text": "Activating receptor tyrosine kinase RET (rarranged during transfection) gene alterations have been identified as oncogenic in multiple malignancies. RET gene rearrangements retaining the kinase domain are oncogenic drivers in papillary thyroid cancer, non-small-cell lung cancer, and multiple other cancers. Activating RET mutations are associated with different phenotypes of multiple endocrine neoplasia type 2 as well as sporadic medullary thyroid cancer. RET is thus an attractive therapeutic target in patients with oncogenic RET alterations. Multikinase inhibitors with RET inhibitor activity, such as cabozantinib and vandetanib, have been explored in the clinic for tumors with activating RET gene alterations with modest clinical efficacy. As a result of the nonselective nature of these multikinase inhibitors, patients had off-target adverse effects, such as hypertension, rash, and diarrhea. This resulted in a narrow therapeutic index of these drugs, limiting ability to dose for clinically effective RET inhibition. In contrast, the recent discovery and clinical validation of highly potent selective RET inhibitors (pralsetinib, selpercatinib) demonstrating improved efficacy and a more favorable toxicity profile are poised to alter the landscape of RET-dependent cancers. These drugs appear to have broad activity across tumors with activating RET alterations. The mechanisms of resistance to these next-generation highly selective RET inhibitors is an area of active research. This review summarizes the current understanding of RET alterations and the state-of-the-art treatment strategies in RET-dependent cancers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36198171",
"endSection": "abstract",
"offsetInBeginSection": 185,
"offsetInEndSection": 465,
"text": "o carcinomas. Six inhibitors have been approved for the treatment of RET-driven cancers: vandetanib, cabozantinib, lenvatinib, sorafenib, selpercatinib, and pralsetinib. Only selpercatinib and pralsetinib have been developed specifically for RET, while the remaining are multikina"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35969032",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "Selpercatinib is a first-in-class, highly selective and potent, central nervous system-active RET kinase inhibitor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35582449",
"endSection": "abstract",
"offsetInBeginSection": 603,
"offsetInEndSection": 715,
"text": "Recently, two potent and selective RET TKIs, pralsetinib (BLU-667) and selpercatinib (LOXO-292), were developed."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37603207",
"endSection": "abstract",
"offsetInBeginSection": 250,
"offsetInEndSection": 404,
"text": "nt benefit. Selective RET inhibitors Pralsetinib and Selpercatinib are targeted drugs approved by the US Food and Drug Administration for treating RET-mut"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36198171",
"endSection": "abstract",
"offsetInBeginSection": 185,
"offsetInEndSection": 340,
"text": "o carcinomas. Six inhibitors have been approved for the treatment of RET-driven cancers: vandetanib, cabozantinib, lenvatinib, sorafenib, selpercatinib, an"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37525669",
"endSection": "abstract",
"offsetInBeginSection": 356,
"offsetInEndSection": 550,
"text": "Recent advancements in targeted therapies have led to the development of ret proto-oncogene (RET) inhibitors, such as selpercatinib and pralsetinib, which have been approved for the treatment of"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36572992",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "OBJECTIVE: Selpercatinib and pralsetinib are new targeted therapies used to treat patients with non-small cell lung cancer (NSCLC) due to RET gene rear"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33082208",
"endSection": "abstract",
"offsetInBeginSection": 173,
"offsetInEndSection": 229,
"text": "r types. Selpercatinib is a highly selective RET kinase "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35726802",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 114,
"text": "INTRODUCTION: Selpercatinib is a RET selective tyrosine kinase inhibitor with nanomolar potency against diverse RE"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37131086",
"endSection": "abstract",
"offsetInBeginSection": 299,
"offsetInEndSection": 436,
"text": "selective RET protein tyrosine kinase inhibitors (TKIs), pralsetinib (BLU-667) and selpercatinib (LOXO-292, LY3527723) were developed and"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33314236",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 65,
"text": "Selpercatinib (LOXO-292) is a selective and potent RET inhibitor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32557397",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 192,
"text": "Selpercatinib (RETEVMO™) is a receptor tyrosine kinase RET (rearranged during transfection) inhibitor being developed by Loxo Oncology for the treatment of cancers harbouring RET alterations. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35007206",
"endSection": "abstract",
"offsetInBeginSection": 197,
"offsetInEndSection": 311,
"text": "er treatment. Selpercatinib (LOXO-292) is a highly selective RET kinase inhibitor indicated in advanced RET-mutant"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34099825",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 243,
"text": "Recently Food and Drug Administration (FDA)-approved pralsetinib (BLU-667) and selpercatinib (LOXO-292) are RET-selective protein tyrosine kinase inhibitors for treating RET-altered cancers, but whether they have distinct activity was unknown."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33161056",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 214,
"text": "BACKGROUND: Selpercatinib (LOXO-292) and pralsetinib (BLU-667) are highly potent RET-selective protein tyrosine kinase inhibitors (TKIs) for treating advanced RET-altered thyroid cancers and non-small-cell lung can"
}
] | 13 |
BioASQ-training13b
| null | null |
65cfa22b1930410b1300000c
|
bioasq_factoid
|
factoid
|
Which is the most known bacterium responsible for botulism (sausage-poisoning)?
|
[['Clostridium botulinum']]
|
[
"Clostridium botulinum",
"C. botulinum",
"botulinum toxin-producing Clostridium",
"Clostridium botulinum type A",
"Clostridium botulinum type B",
"Clostridium botulinum type E",
"Clostridium botulinum type F"
] |
['Botulism is a severe neuroparalytic disease caused by botulinum neurotoxin (BoNT), and affects humans, all warm-blooded animals, birds, and some fishes. Botulinum toxin is produced under anaerobic conditions by the bacterium Clostridium botulinum, which is the most known etiological agent of the disease, and some other clostridia, and is one of the most dangerous toxin in the world.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24253240",
"http://www.ncbi.nlm.nih.gov/pubmed/24252701",
"http://www.ncbi.nlm.nih.gov/pubmed/24252222",
"http://www.ncbi.nlm.nih.gov/pubmed/24246230",
"http://www.ncbi.nlm.nih.gov/pubmed/24206405",
"http://www.ncbi.nlm.nih.gov/pubmed/23971808",
"http://www.ncbi.nlm.nih.gov/pubmed/23971806",
"http://www.ncbi.nlm.nih.gov/pubmed/21130733",
"http://www.ncbi.nlm.nih.gov/pubmed/15839401",
"http://www.ncbi.nlm.nih.gov/pubmed/23421373",
"http://www.ncbi.nlm.nih.gov/pubmed/23239346",
"http://www.ncbi.nlm.nih.gov/pubmed/23523511",
"http://www.ncbi.nlm.nih.gov/pubmed/21747146",
"http://www.ncbi.nlm.nih.gov/pubmed/15027048",
"http://www.ncbi.nlm.nih.gov/pubmed/20961439",
"http://www.ncbi.nlm.nih.gov/pubmed/11153358",
"http://www.ncbi.nlm.nih.gov/pubmed/24997242",
"http://www.ncbi.nlm.nih.gov/pubmed/18388640",
"http://www.ncbi.nlm.nih.gov/pubmed/21171846",
"http://www.ncbi.nlm.nih.gov/pubmed/21975066",
"http://www.ncbi.nlm.nih.gov/pubmed/20569065",
"http://www.ncbi.nlm.nih.gov/pubmed/17458494",
"http://www.ncbi.nlm.nih.gov/pubmed/24961027",
"http://www.ncbi.nlm.nih.gov/pubmed/19573697",
"http://www.ncbi.nlm.nih.gov/pubmed/23971804",
"http://www.ncbi.nlm.nih.gov/pubmed/16080379",
"http://www.ncbi.nlm.nih.gov/pubmed/23025151"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24253240",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "Botulism is a serious foodborne neuroparalytic disease, caused by botulinum neurotoxin (BoNT), produced by the anaerobic bacterium Clostridium botulinum."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24252701",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Cattle botulism is a fatal intoxication caused by botulinum neurotoxins (BoNTs) produced by Clostridium botulinum serotypes C and D"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24252222",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "Botulism in horses in the USA is attributed to Clostridium botulinum types A, B or C."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24246230",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 178,
"text": "Clostridium botulinum is the etiological agent of botulism. Due to food-borne poisoning and the potential use of the extremely toxic botulinum neurotoxin (BoNT) from C. botulinum"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24206405",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 207,
"text": "Botulism is a serious neuroparalytic disease caused by toxins of Clostridium botulinum. Botulinum toxin is produced under anaerobic conditions and is one of the most dangerous toxin in the world."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23971808",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 307,
"text": "Botulism is a neuroparalytic disease that can occur in all warm-blooded animals, birds, and fishes. The disease in animals is mainly caused by toxins produced by Clostridium botulinum strains belonging to group III, although outbreaks due to toxins produced by group I and II organisms have been recognized."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23971806",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 233,
"text": "Botulism is a severe neuroparalytic disease that affects humans, all warm-blooded animals, and some fishes. The disease is caused by exposure to toxins produced by Clostridium botulinum and other botulinum toxin-producing clostridia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21130733",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 295,
"text": "The botulinum neurotoxins (BoNTs) produced by different strains of the bacterium Clostridium botulinum are responsible for the disease botulism and include a group of immunologically distinct serotypes (A, B, E, and F) that are considered to be the most lethal natural proteins known for humans."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11153358",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Botulinumtoxin (BTX) is a neurotoxin produced from Clostridium botulinum under anaerobic conditions and is responsible for botulism, a notifiable, bacterial form of food poisoning."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21130733",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 295,
"text": "The botulinum neurotoxins (BoNTs) produced by different strains of the bacterium Clostridium botulinum are responsible for the disease botulism and include a group of immunologically distinct serotypes (A, B, E, and F) that are considered to be the most lethal natural proteins known for humans."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21130733",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 295,
"text": "The botulinum neurotoxins (BoNTs) produced by different strains of the bacterium Clostridium botulinum are responsible for the disease botulism and include a group of immunologically distinct serotypes (A, B, E, and F) that are considered to be the most lethal natural proteins known for humans."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11153358",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Botulinumtoxin (BTX) is a neurotoxin produced from Clostridium botulinum under anaerobic conditions and is responsible for botulism, a notifiable, bacterial form of food poisoning."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21130733",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 295,
"text": "The botulinum neurotoxins (BoNTs) produced by different strains of the bacterium Clostridium botulinum are responsible for the disease botulism and include a group of immunologically distinct serotypes (A, B, E, and F) that are considered to be the most lethal natural proteins known for humans."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21975066",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "Botulism is a disease characterized by neuromuscular paralysis and is produced from botulinum neurotoxins (BoNTs) found within the Gram positive bacterium Clostridium botulinum."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11153358",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Botulinumtoxin (BTX) is a neurotoxin produced from Clostridium botulinum under anaerobic conditions and is responsible for botulism, a notifiable, bacterial form of food poisoning."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20569065",
"endSection": "abstract",
"offsetInBeginSection": 78,
"offsetInEndSection": 248,
"text": "An epidemiological investigation and laboratory detection studies showed that sausage contaminated by type A Clostridium botulinum caused this outbreak of food poisoning."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23025151",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "Botulism is caused by botulinum neurotoxin produced by the bacterium Clostridium botulinum."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11153358",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "Botulinumtoxin (BTX) is a neurotoxin produced from Clostridium botulinum under anaerobic conditions and is responsible for botulism, a notifiable, bacterial form of food poisoning"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11153358",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "Botulinumtoxin (BTX) is a neurotoxin produced from Clostridium botulinum under anaerobic conditions and is responsible for botulism, a notifiable, bacterial form of food poisoning"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11153358",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "Botulinumtoxin (BTX) is a neurotoxin produced from Clostridium botulinum under anaerobic conditions and is responsible for botulism, a notifiable, bacterial form of food poisoning"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11153358",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "Botulinumtoxin (BTX) is a neurotoxin produced from Clostridium botulinum under anaerobic conditions and is responsible for botulism, a notifiable, bacterial form of food poisoning"
}
] | 5 |
BioASQ-training5b
|
[
"http://www.disease-ontology.org/api/metadata/DOID:11976"
] |
[] |
55475dc2f35db75526000001
|
bioasq_factoid
|
factoid
|
Which protein pathway is regulating SGK1-mediated phosphorylation of FOXO3a to control cell proliferation?
|
[['The mTOR pathway']]
|
[
"mTOR pathway",
"mechanistic target of rapamycin pathway",
"mammalian target of rapamycin pathway",
"mTOR signaling pathway",
"mTORC1 pathway",
"mTORC2 pathway"
] |
['mTORC1, in coordination with mTORC2, controls cell proliferation by regulating FoxO3a gene expression and SGK1-mediated phosphorylation of FOXO3a at Ser314.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24558442"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24558442",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "The mTOR pathway controls cell proliferation by regulating the FoxO3a transcription factor via SGK1 kinase"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24558442",
"endSection": "abstract",
"offsetInBeginSection": 289,
"offsetInEndSection": 427,
"text": "the FoxO3a transcription factor is coordinately regulated by mTORC1 and mTORC2, and plays a crucial role in controlling cell proliferation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24558442",
"endSection": "abstract",
"offsetInBeginSection": 1370,
"offsetInEndSection": 1525,
"text": "mTORC1, in coordination with mTORC2, controls cell proliferation by regulating FoxO3a gene expression and SGK1-mediated phosphorylation of FoxO3a at Ser314"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24558442",
"endSection": "abstract",
"offsetInBeginSection": 1343,
"offsetInEndSection": 1525,
"text": "These results suggest that mTORC1, in coordination with mTORC2, controls cell proliferation by regulating FoxO3a gene expression and SGK1-mediated phosphorylation of FoxO3a at Ser314"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24558442",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "The mTOR pathway controls cell proliferation by regulating the FoxO3a transcription factor via SGK1 kinase"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24558442",
"endSection": "abstract",
"offsetInBeginSection": 1154,
"offsetInEndSection": 1527,
"text": "SGK1 overexpression suppressed CDKI expression in p18-deficient cells, whereas SGK1 knockdown induced CDKI expression in wild-type cells, resulting in the suppression of cell proliferation. These results suggest that mTORC1, in coordination with mTORC2, controls cell proliferation by regulating FoxO3a gene expression and SGK1-mediated phosphorylation of FoxO3a at Ser314."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24558442",
"endSection": "abstract",
"offsetInBeginSection": 1154,
"offsetInEndSection": 1527,
"text": "SGK1 overexpression suppressed CDKI expression in p18-deficient cells, whereas SGK1 knockdown induced CDKI expression in wild-type cells, resulting in the suppression of cell proliferation. These results suggest that mTORC1, in coordination with mTORC2, controls cell proliferation by regulating FoxO3a gene expression and SGK1-mediated phosphorylation of FoxO3a at Ser314."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24558442",
"endSection": "abstract",
"offsetInBeginSection": 1154,
"offsetInEndSection": 1527,
"text": "SGK1 overexpression suppressed CDKI expression in p18-deficient cells, whereas SGK1 knockdown induced CDKI expression in wild-type cells, resulting in the suppression of cell proliferation. These results suggest that mTORC1, in coordination with mTORC2, controls cell proliferation by regulating FoxO3a gene expression and SGK1-mediated phosphorylation of FoxO3a at Ser314."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24558442",
"endSection": "abstract",
"offsetInBeginSection": 1154,
"offsetInEndSection": 1527,
"text": "SGK1 overexpression suppressed CDKI expression in p18-deficient cells, whereas SGK1 knockdown induced CDKI expression in wild-type cells, resulting in the suppression of cell proliferation. These results suggest that mTORC1, in coordination with mTORC2, controls cell proliferation by regulating FoxO3a gene expression and SGK1-mediated phosphorylation of FoxO3a at Ser314."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24558442",
"endSection": "abstract",
"offsetInBeginSection": 1154,
"offsetInEndSection": 1527,
"text": "SGK1 overexpression suppressed CDKI expression in p18-deficient cells, whereas SGK1 knockdown induced CDKI expression in wild-type cells, resulting in the suppression of cell proliferation. These results suggest that mTORC1, in coordination with mTORC2, controls cell proliferation by regulating FoxO3a gene expression and SGK1-mediated phosphorylation of FoxO3a at Ser314."
}
] | 5 |
BioASQ-training5b
|
[] |
[] |
56cafa845795f9a73e00002e
|
bioasq_factoid
|
factoid
|
Which is the phenotype of the disease fibrodysplasia ossificans progressiva?
|
['3.\tFibrodysplasia ossificans progressiva (FOP), a congenital heterotopic ossification (HO) syndrome caused by gain-of-function mutations of bone morphogenetic protein (BMP) type I receptor ACVR1, manifests with progressive ossification of skeletal muscles, tendons, ligaments, and joints.']
|
[
"Fibrodysplasia ossificans progressiva",
"FOP",
"myositis ossificans progressiva",
"congenital heterotopic ossification syndrome",
"ossification of soft tissues",
"ACVR1-related fibrodysplasia ossificans progressiva"
] |
['Fibrodysplasia ossificans progressiva (FOP), a congenital heterotopic ossification (HO) syndrome caused by gain-of-function mutations of bone morphogenetic protein (BMP) type I receptor ACVR1, manifests with progressive ossification of skeletal muscles, tendons, ligaments, and joints.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29033382",
"http://www.ncbi.nlm.nih.gov/pubmed/26049728",
"http://www.ncbi.nlm.nih.gov/pubmed/27881824"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29033382",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 142,
"text": "Fibrodysplasia ossificans progressiva (FOP) is an ultra-rare genetic disorder in which heterotopic bone forms in the soft tissues. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26049728",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "Metaphyseal bony outgrowths are a well-recognized feature of fibrodysplasia ossificans progressiva (FOP) phenotype, "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27881824",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 285,
"text": "Fibrodysplasia ossificans progressiva (FOP), a congenital heterotopic ossification (HO) syndrome caused by gain-of-function mutations of bone morphogenetic protein (BMP) type I receptor ACVR1, manifests with progressive ossification of skeletal muscles, tendons, ligaments, and joints."
}
] | 11 |
BioASQ-training11b
| null | null |
5e5b8b4e752ebcdc7a000001
|
bioasq_factoid
|
yesno
|
Can Diabetes be caused by a defect in a potassium chanel?
|
['yes']
|
[
"yes"
] |
['Mutations in the KATP channel can lead to neonatal diabetes.', 'Mutations in KATP channel genes can result in hypo- or hypersecretion of insulin, as in neonatal diabetes mellitus and congenital hyperinsulinism, respectively.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25931474",
"http://www.ncbi.nlm.nih.gov/pubmed/27118464",
"http://www.ncbi.nlm.nih.gov/pubmed/15746700",
"http://www.ncbi.nlm.nih.gov/pubmed/24827651"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27118464",
"endSection": "abstract",
"offsetInBeginSection": 146,
"offsetInEndSection": 306,
"text": "Mutations in KATP channel genes can result in hypo- or hypersecretion of insulin, as in neonatal diabetes mellitus and congenital hyperinsulinism, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27118464",
"endSection": "abstract",
"offsetInBeginSection": 307,
"offsetInEndSection": 472,
"text": "To date, all patients affected by neonatal diabetes due to a mutation in the pore-forming subunit of the channel (Kir6.2, KCNJ11) are heterozygous for the mutation. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27118464",
"endSection": "abstract",
"offsetInBeginSection": 479,
"offsetInEndSection": 571,
"text": "e report the first clinical case of neonatal diabetes caused by a homozygous KCNJ11 mutation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25931474",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Diffuse congenital hyperinsulinism in infancy (CHI-D) arises from mutations inactivating the KATP channel;"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24827651",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 178,
"text": "We report a case of a 6-week-old infant with diabetes mellitus based on a genetic defect in the sulfonylurea receptor 1 (SUR1), an ATP-sensitive potassium (KATP) channel protein."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15746700",
"endSection": "abstract",
"offsetInBeginSection": 1094,
"offsetInEndSection": 1150,
"text": "In diabetes, vascular KATP channel function is impaired."
}
] | 6 |
BioASQ-training6b
|
[
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D016640",
"http://www.disease-ontology.org/api/metadata/DOID:11717",
"http://www.disease-ontology.org/api/metadata/DOID:9351",
"http://www.biosemantics.org/jochem#4277521",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D011188",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D011189",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003921",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003923",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003922",
"http://www.biosemantics.org/jochem#http://www.biosemantics.org/jochem#:4277521",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003920",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D024681",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003924",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D015221"
] | null |
58a0a28a78275d0c4a000051
|
bioasq_yesno
|
yesno
|
Is there a vaccine for rotavirus?
|
['yes']
|
[
"yes"
] |
['yes, rotavirus pentavalent vaccine (RotaTeq(r)) as a sole vaccine', 'Effectiveness of rotavirus pentavalent vaccine rotavirus pentavalent vaccine (RotaTeq(r)) as a sole vaccine', 'safety and immunogenicity of pentavalent rotavirus vaccine (rv5 )', 'Yes, there is a vaccine against rotavirus infection that is approved for Europe, Canada and Australia.', 'Yes, there is a human neonatal rotavirus vaccine against serogroup B Rotavirus.', 'Effectiveness of rotavirus pentavalent vaccine', 'Yes, there is a 4-component vaccine against capsular rotavirus vaccine.', 'Yes, there is a pentavalent vaccine for Rotavirus', 'Yes, there is a human neonatal rotavirus vaccine.', 'High effectiveness of RotaTeq as the sole rotavirus vaccine in a universal immunization programme was demonstrated in a high-income country.', ' rotavirus pentavalent vaccine (RotaTeq(r)) as a sole vaccine']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22423021",
"http://www.ncbi.nlm.nih.gov/pubmed/2851185",
"http://www.ncbi.nlm.nih.gov/pubmed/7707626",
"http://www.ncbi.nlm.nih.gov/pubmed/22796685",
"http://www.ncbi.nlm.nih.gov/pubmed/16397431",
"http://www.ncbi.nlm.nih.gov/pubmed/8920706",
"http://www.ncbi.nlm.nih.gov/pubmed/24422678",
"http://www.ncbi.nlm.nih.gov/pubmed/28442435",
"http://www.ncbi.nlm.nih.gov/pubmed/27443593",
"http://www.ncbi.nlm.nih.gov/pubmed/19995190",
"http://www.ncbi.nlm.nih.gov/pubmed/15502699",
"http://www.ncbi.nlm.nih.gov/pubmed/22702319",
"http://www.ncbi.nlm.nih.gov/pubmed/26263200",
"http://www.ncbi.nlm.nih.gov/pubmed/22119590",
"http://www.ncbi.nlm.nih.gov/pubmed/9015114",
"http://www.ncbi.nlm.nih.gov/pubmed/22431803",
"http://www.ncbi.nlm.nih.gov/pubmed/19931717",
"http://www.ncbi.nlm.nih.gov/pubmed/21504245",
"http://www.ncbi.nlm.nih.gov/pubmed/8752295",
"http://www.ncbi.nlm.nih.gov/pubmed/11389295",
"http://www.ncbi.nlm.nih.gov/pubmed/27522178",
"http://www.ncbi.nlm.nih.gov/pubmed/25680314",
"http://www.ncbi.nlm.nih.gov/pubmed/20661105",
"http://www.ncbi.nlm.nih.gov/pubmed/30046133",
"http://www.ncbi.nlm.nih.gov/pubmed/28340179",
"http://www.ncbi.nlm.nih.gov/pubmed/29102168",
"http://www.ncbi.nlm.nih.gov/pubmed/9949951",
"http://www.ncbi.nlm.nih.gov/pubmed/31023829",
"http://www.ncbi.nlm.nih.gov/pubmed/28369477"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28340179",
"endSection": "title",
"offsetInBeginSection": 38,
"offsetInEndSection": 102,
"text": "Safety and Immunogenicity of Pentavalent Rotavirus Vaccine (RV5)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28340179",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 88,
"text": "This study compares the safety and immunogenicity of pentavalent rotavirus vaccine (RV5)"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28442435",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 46,
"text": "Effectiveness of rotavirus pentavalent vaccine"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28442435",
"endSection": "abstract",
"offsetInBeginSection": 22,
"offsetInEndSection": 81,
"text": " rotavirus pentavalent vaccine (RotaTeq®) as a sole vaccine"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31023829",
"endSection": "abstract",
"offsetInBeginSection": 285,
"offsetInEndSection": 375,
"text": "We describe rotavirus vaccine coverage and missed opportunities for rotavirus vaccination."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31023829",
"endSection": "abstract",
"offsetInBeginSection": 1877,
"offsetInEndSection": 2048,
"text": "CONCLUSIONS\n\nAddressing missed opportunities for rotavirus vaccination is essential to achieving the 80% rotavirus vaccine coverage target outlined by Healthy People 2020."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31023829",
"endSection": "abstract",
"offsetInBeginSection": 1734,
"offsetInEndSection": 1875,
"text": "Complete rotavirus vaccine coverage could be improved to 81% if all missed opportunities within the ACIP-recommended schedule were addressed."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27522178",
"endSection": "abstract",
"offsetInBeginSection": 1045,
"offsetInEndSection": 1194,
"text": "RESULTS\n\nThe national coverage for rotavirus vaccine achieved a year after the introduction was 89% for one dose and 82% for two doses, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27522178",
"endSection": "abstract",
"offsetInBeginSection": 1747,
"offsetInEndSection": 1989,
"text": "CONCLUSIONS\n\nNorway achieved a high national coverage and excellent adherence with the strict age limits for rotavirus vaccine administration during the first year of introduction, indicating robustness of the national immunisation programme."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26263200",
"endSection": "abstract",
"offsetInBeginSection": 1563,
"offsetInEndSection": 1679,
"text": "Upper age limit recommendations for rotavirus vaccine administration contributed to suboptimal vaccination coverage."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26263200",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 111,
"text": "Catching-up with pentavalent vaccine: Exploring reasons behind lower rotavirus vaccine coverage in El Salvador."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7707626",
"endSection": "title",
"offsetInBeginSection": 95,
"offsetInEndSection": 131,
"text": "US Rotavirus Vaccine Efficacy Group."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31023829",
"endSection": "abstract",
"offsetInBeginSection": 284,
"offsetInEndSection": 374,
"text": "We describe rotavirus vaccine coverage and missed opportunities for rotavirus vaccination."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25680314",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 39,
"text": "Rotavirus vaccines: a story of success."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2851185",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 57,
"text": "Clinical and immunological studies of rotavirus vaccines."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29102168",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 92,
"text": "Impact of rotavirus vaccine on rotavirus diarrhoea in countries of East and Southern Africa."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8920706",
"endSection": "abstract",
"offsetInBeginSection": 1079,
"offsetInEndSection": 1133,
"text": "Rotavirus diarrheal episodes were identified by ELISA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29102168",
"endSection": "abstract",
"offsetInBeginSection": 2032,
"offsetInEndSection": 2170,
"text": "The decrease in rotavirus positivity was inversely related to increase in rotavirus vaccine coverage showing impact of rotavirus vaccines."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29102168",
"endSection": "abstract",
"offsetInBeginSection": 1050,
"offsetInEndSection": 1169,
"text": "We described trends in rotavirus positivity among tested stool samples before and after rotavirus vaccine introduction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2851185",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "The RIT 4237 bovine rotavirus vaccine has served as a useful model for rotavirus vaccination, but the vaccine will not be further developed or tested."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8920706",
"endSection": "abstract",
"offsetInBeginSection": 2156,
"offsetInEndSection": 2272,
"text": "Only the RRV vaccine induced a low level of protection against rotavirus diarrhea mainly of serotype G1 specificity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22119590",
"endSection": "abstract",
"offsetInBeginSection": 2543,
"offsetInEndSection": 2719,
"text": "It is recommended that new rotavirus vaccine candidates be developed at cheaper price to speed up the introduction of rotavirus immunization in the developing world in general."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8752295",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 46,
"text": "Review of rotavirus vaccine trials in Finland."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24422678",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 63,
"text": "Risk of intussusception after monovalent rotavirus vaccination."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31023829",
"endSection": "abstract",
"offsetInBeginSection": 213,
"offsetInEndSection": 283,
"text": "Rotavirus vaccines are underused compared with other routine vaccines."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22796685",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 261,
"text": "With rotavirus vaccines now available globally , it will be useful to assemble the available evidence on the epidemiology and burden of rotavirus gastroenteritis in India , in order to weigh the urgency of introducing a vaccine to help control rotavirus disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22423021",
"endSection": "abstract",
"offsetInBeginSection": 183,
"offsetInEndSection": 328,
"text": "Is there evidence that rotavirus vaccines are effective in preventing acute gastroenteritis complications such as dehydration and hospitalization"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16397431",
"endSection": "abstract",
"offsetInBeginSection": 1325,
"offsetInEndSection": 1506,
"text": "With the introduction of new rotavirus vaccines in sight , rotavirus gastroenteritis may be regarded as the single most frequent vaccine-preventable disease among children in the EU"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19995190",
"endSection": "abstract",
"offsetInBeginSection": 374,
"offsetInEndSection": 658,
"text": "With the recent introduction of the two rotavirus vaccines , RotaTeq and Rotarix , in many countries , it appears that the total number of hospitalizations due to rotavirus infections is being reduced , at least in developed countries that implemented a universal immunization program"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20661105",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 97,
"text": "Change in rotavirus epidemiology in northeast Florida after the introduction of rotavirus vaccine"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22431803",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 265,
"text": "With the recent postlicensure identification of an increased risk of intussusception with rotavirus vaccine , the 14 Latin American countries currently using rotavirus vaccine must now weigh the health benefits versus risks to assess whether to continue vaccination"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22702319",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 49,
"text": "Impact of rotavirus vaccines on rotavirus disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19931717",
"endSection": "abstract",
"offsetInBeginSection": 457,
"offsetInEndSection": 630,
"text": "With safe and efficacious rotavirus vaccines now on the verge of widespread adoption , researchers can be vital advocates for their uptake into routine immunization programs"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21504245",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 145,
"text": "Rotavirus vaccine RIX4414 (Rotarix™): a pharmacoeconomic review of its use in the prevention of rotavirus gastroenteritis in developed countries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21504245",
"endSection": "abstract",
"offsetInBeginSection": 450,
"offsetInEndSection": 633,
"text": "In addition, various naturalistic studies have demonstrated 'real-world' effectiveness after the introduction of widespread rotavirus vaccination programmes in the community setting."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21504245",
"endSection": "abstract",
"offsetInBeginSection": 238,
"offsetInEndSection": 450,
"text": "The monovalent rotavirus vaccine RIX4414 (Rotarix™) is administered as a two-dose oral series in infants and has demonstrated protective efficacy against RVGE in clinical trials conducted in developed countries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21504245",
"endSection": "abstract",
"offsetInBeginSection": 633,
"offsetInEndSection": 844,
"text": "Numerous cost-effectiveness analyses have been conducted in developed countries in which a universal rotavirus vaccination programme using RIX4414 was compared with no universal rotavirus vaccination programme."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21504245",
"endSection": "abstract",
"offsetInBeginSection": 1507,
"offsetInEndSection": 1716,
"text": "It is also difficult to draw conclusions regarding the cost effectiveness of rotavirus vaccine RIX4414 relative to that of the pentavalent rotavirus vaccine, which is administered as a three-dose oral series."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21504245",
"endSection": "abstract",
"offsetInBeginSection": 1716,
"offsetInEndSection": 1995,
"text": "Although indirect comparisons in cost-effectiveness analyses indicate that RIX4414 provided more favourable incremental cost-effectiveness ratios when each vaccine was compared with no universal rotavirus vaccination programme, results were generally sensitive to vaccine costs."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15502699",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 81,
"text": "A rotavirus vaccine for prophylaxis of infants against rotavirus gastroenteritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15502699",
"endSection": "abstract",
"offsetInBeginSection": 138,
"offsetInEndSection": 307,
"text": "A live attenuated monovalent rotavirus vaccine (Rotarix) containing human rotavirus strain RIX4414 of G1P1A P[8] specificity is being developed to meet the global need."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15502699",
"endSection": "abstract",
"offsetInBeginSection": 814,
"offsetInEndSection": 985,
"text": "Rotarix significantly reduced rotavirus gastroenteritis episodes and rotavirus-related hospitalizations in vaccinated infants compared with placebo recipients (P < 0.05)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30046133",
"endSection": "abstract",
"offsetInBeginSection": 99,
"offsetInEndSection": 364,
"text": "We describe the intussusception epidemiology prior to rotavirus vaccine, temporal association of intussusception cases to administration of rotavirus vaccine, and estimate the additional number of intussusception cases that may be associated with rotavirus vaccine."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30046133",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 88,
"text": "Epidemiology of intussusception before and after rotavirus vaccine introduction in Fiji."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30046133",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 98,
"text": "In 2012, Fiji introduced rotavirus vaccine (Rotarix, GSK) into the national immunisation schedule."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9015114",
"endSection": "abstract",
"offsetInBeginSection": 414,
"offsetInEndSection": 635,
"text": "Four trials of RIT 4237 bovine rotavirus vaccine, one trial of group A RRV-1 rhesus rotavirus vaccine, and one trial of rhesus-human reassortant rotavirus vaccines D x RRV and DS1 x RRV were carried out between 1983-1989."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9015114",
"endSection": "abstract",
"offsetInBeginSection": 1009,
"offsetInEndSection": 1248,
"text": "Problems associated with the use of any oral rotavirus vaccine include acid lability of the vaccine virus, which requires buffering, and a slight but significant interference of oral poliovirus vaccine with the uptake of rotavirus vaccine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9015114",
"endSection": "abstract",
"offsetInBeginSection": 1249,
"offsetInEndSection": 1374,
"text": "In the near future, oral heterologous rotavirus vaccines may be available for prevention of severe rotavirus gastroenteritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9015114",
"endSection": "abstract",
"offsetInBeginSection": 856,
"offsetInEndSection": 1008,
"text": "There was no apparent difference between bovine and rhesus-based rotavirus vaccines in the protective efficacy against severe rotavirus gastroenteritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9015114",
"endSection": "abstract",
"offsetInBeginSection": 148,
"offsetInEndSection": 413,
"text": "Efficacy studies of this vaccine in 6-12 month-old children gave results characteristic of the performance of oral rotavirus vaccines in general: 58% protective efficacy against any rotavirus gastroenteritis and 82% against \"clinically significant\" gastroenteritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9015114",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "Live oral rotavirus vaccine strain RIT 4237, derived from group A bovine rotavirus NCDV, was given to human volunteers in Tampere, Finland in 1982."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27443593",
"endSection": "abstract",
"offsetInBeginSection": 683,
"offsetInEndSection": 881,
"text": "Targeted efforts to evaluate indirect effects of rotavirus vaccine in low income countries are required to understand the total impact of rotavirus vaccine on the global burden of rotavirus disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27443593",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Widespread introduction of rotavirus vaccines has led to major reductions in the burden of rotavirus gastroenteritis worldwide."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27443593",
"endSection": "abstract",
"offsetInBeginSection": 451,
"offsetInEndSection": 682,
"text": "While rotavirus vaccine indirect effects have been demonstrated in high and middle income countries, there are very little data from low income countries where force of infection, population structures and vaccine schedules differ."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27443593",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 72,
"text": "Measuring indirect effects of rotavirus vaccine in low income countries."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11389295",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 109,
"text": "Intussusception among recipients of rotavirus vaccine: reports to the vaccine adverse event reporting system."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11389295",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Rotavirus vaccine was licensed on August 31, 1998, and subsequently recommended for routine use among infants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11389295",
"endSection": "abstract",
"offsetInBeginSection": 184,
"offsetInEndSection": 355,
"text": "To describe the cases of intussusception among rotavirus vaccine recipients reported to the Vaccine Adverse Event Reporting System from October 1998 through December 1999."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11389295",
"endSection": "abstract",
"offsetInBeginSection": 356,
"offsetInEndSection": 419,
"text": "Infants vaccinated with rotavirus vaccine in the United States."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11389295",
"endSection": "abstract",
"offsetInBeginSection": 569,
"offsetInEndSection": 785,
"text": "There were 98 confirmed cases of intussusception after vaccination with rotavirus vaccine reported to the Vaccine Adverse Event Reporting System; 60 of these developed intussusception within 1 week after vaccination."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11389295",
"endSection": "abstract",
"offsetInBeginSection": 1011,
"offsetInEndSection": 1222,
"text": "Using a passive surveillance system for vaccine adverse events, we observed at least a fourfold increase over the expected number of intussusception cases occurring within 1 week of receipt of rotavirus vaccine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11389295",
"endSection": "abstract",
"offsetInBeginSection": 1223,
"offsetInEndSection": 1333,
"text": "Other studies were initiated to further define the relationship between rotavirus vaccine and intussusception."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11389295",
"endSection": "abstract",
"offsetInBeginSection": 1334,
"offsetInEndSection": 1548,
"text": "In light of these and other data, the rotavirus vaccine manufacturer voluntarily removed its product from the market, and the recommendation for routine use of rotavirus vaccine among US infants has been withdrawn."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9949951",
"endSection": "abstract",
"offsetInBeginSection": 86,
"offsetInEndSection": 255,
"text": "To review the biology, immunology, and virology of rotavirus infections and describe the efforts towards the construction of vaccines using human and animal rotaviruses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9949951",
"endSection": "abstract",
"offsetInBeginSection": 396,
"offsetInEndSection": 511,
"text": "In August 1998 the Food and Drug Administration in the United States approved the licensure of a rotavirus vaccine."
}
] | 11 |
BioASQ-training11b
| null | null |
5e64f1921af46fc130000018
|
bioasq_yesno
|
factoid
|
What part of the cell is mitophagy associated with?
|
['mitochondria']
|
[
"mitochondria",
"mitochondrion",
"powerhouse of the cell",
"cellular power plant",
"mitochondrial organelle"
] |
['Mitophagy is a specific type of autophagy that involves the selective elimination of damaged or dysfunctional mitochondria via autophagosomes and lysosomes, a process that is critical for mitochondrial quality control.', 'Mitophagy is associated with the mitochondria, which are critical cellular energy resources and central to the life of the neuron. Mitophagy selectively clears damaged or dysfunctional mitochondria through autophagic machinery to maintain mitochondrial quality control and homeostasis.', 'Mitophagy is a selective form of autophagy, where damaged or dysfunctional mitochondria are targeted and degraded by the autophagosome.', 'Mitophagy is associated with mitochondria.', 'Mitophagy is associated with mitochondria, involving their encapsulation into autophagosomes for delivery to lysosomes for degradation.', 'Mitophagy is associated with "mitochondria".', ' Mitophory are primarily associated with the organelle membrane of eukaryotes, where they play a crucial role in the degradation of misfolded proteins and the maintenance of cellular integrity. ', 'Mitophagy is associated with mitochondria, the part of the cell responsible for energy production. It specifically targets damaged or dysfunctional mitochondria for degradation to maintain cellular health', 'Mitophagy is a selective autophagy of mitochondria, can efficiently degrade, remove and recycle the malfunctioning or damaged mitochondria, and is crucial for quality control.', 'Mitophagy, or selective autophagy of mitochondria, is an essential pathway to preserve mitochondrial homeostasis by clearing up damaged mitochondria', 'Mitophagy is associated with the lysosomes, which are responsible for the degradation of damaged or superfluous mitochondria.', 'Mitophagy is associated with the mitochondria, which are the powerhouses of the cell.', 'Mitophagy is a process by which cells selectively remove and burn their own mitochondria. It is a conserved mechanism that all eukaryotes use to remove damaged mitochondria.', 'Mitophagy is associated with the clearance of damaged mitochondria via lysosomes.', 'Mitophagy is associated with mitochondria. It is the selective autophagy of damaged or dysfunctional mitochondria to maintain mitochondrial homeostasis and quality control.', 'Mitophagy is a selective form of autophagy that specifically targets damaged or dysfunctional mitochondria for degradation and recycling. It is a quality control mechanism associated with maintaining a healthy mitochondrial pool within the cell.', 'Mitophagy is associated with mitochondria, which are organelles within eukaryotic cells. Mitophagy is a process by which cells selectively remove and recycle damaged or dysfunctional mitochondria through the autophagy-lysosome pathway. This helps to maintain mitochondrial quality control and homeostasis.', 'Mitophagy is an essential physiological process that eliminates damaged mitochondria via lysosomes.', 'Mitophagy is associated with the outer mitochondrial membrane 20 (Tomm20), a mitochondrial translocase that, when ubiquitinated, promotes mitophagy.', 'Mitophagy is an essential pathway responsible for preserving mitochondrial homeostasis through the clearance of damaged mitochondria.', 'Mitophagy refers to selective autophagy of mitochondria, which plays a crucial role in preserving mitochondrial homeostasis by clearing up damaged or dysfunctional mitochondria.', 'Mitophagy is associated with the mitochondria, targeting them for degradation.', 'Mitophagy is associated with the elimination of damaged mitochondria and maintenance of mitochondrial homeostasis. It is a process that occurs within the cell, specifically targeting and removing dysfunctional or damaged mitochondria.', 'Mitophagy is associated with the selective autophagic clearance of flawed or damaged mitochondria within the cell, ensuring the maintenance of a healthy mitochondrial pool and cellular homeostasis.', 'Mitochondrial autophagy is associated with the removal of defective mitochondria from the cell by internalisation into autophagosomes which fuse with lysosomes.', 'Mitophagy is associated with mitochondria, the part of the cell responsible for energy production. It specifically targets damaged or dysfunctional mitochondria, clearing them out to maintain cellular health and efficiency.', 'Mitophagy is associated with the process of selectively clearing damaged or dysfunctional mitochondria through autophagic machinery to maintain mitochondrial quality control and homeostasis within the cell.', 'Mitophagy is associated with lysosomes, where defective mitochondria are internalized into autophagosomes that fuse with lysosomes for degradation.', "Mitophagy is a process associated with the elimination of damaged or dysfunctional mitochondria through autophagic machinery, which is a part of the cell's quality control and homeostasis maintenance mechanism.", 'Mitophagy is associated with mitochondria, which are organelles within eukaryotic cells. Mitophagy is a process by which cells selectively remove and recycle damaged or dysfunctional mitochondria through the autophagy-lysosome pathway. This process helps to maintain mitochondrial quality control and homeostasis.', 'Mitophagy is associated with the mitochondria.', 'Mitophagy is associated with mitochondria, specifically targeting damaged or dysfunctional mitochondria for degradation to maintain cellular health.', 'Mitophagy is associated with the lysosomes, which are responsible for the degradation of damaged or dysfunctional mitochondria.', 'Mitophagy is associated with mitochondria through autophagic machinery to maintain mitochondrial quality control and homeostasis.', 'Mitophagy is associated with lysosomes.', 'Mitophagy is associated with the outer membrane of mitochondria (OMM).', 'Mitochondrial dysfunction is targeted for degradation in the lysosomes by mitophagy.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25753537",
"http://www.ncbi.nlm.nih.gov/pubmed/29311991",
"http://www.ncbi.nlm.nih.gov/pubmed/37488884",
"http://www.ncbi.nlm.nih.gov/pubmed/25634658",
"http://www.ncbi.nlm.nih.gov/pubmed/36740450",
"http://www.ncbi.nlm.nih.gov/pubmed/32131138",
"http://www.ncbi.nlm.nih.gov/pubmed/32587855",
"http://www.ncbi.nlm.nih.gov/pubmed/36860818",
"http://www.ncbi.nlm.nih.gov/pubmed/26223426",
"http://www.ncbi.nlm.nih.gov/pubmed/36625039",
"http://www.ncbi.nlm.nih.gov/pubmed/34975548",
"http://www.ncbi.nlm.nih.gov/pubmed/21126205",
"http://www.ncbi.nlm.nih.gov/pubmed/31956306",
"http://www.ncbi.nlm.nih.gov/pubmed/34291135",
"http://www.ncbi.nlm.nih.gov/pubmed/28976890",
"http://www.ncbi.nlm.nih.gov/pubmed/33922020",
"http://www.ncbi.nlm.nih.gov/pubmed/37678420",
"http://www.ncbi.nlm.nih.gov/pubmed/33570005",
"http://www.ncbi.nlm.nih.gov/pubmed/33239048",
"http://www.ncbi.nlm.nih.gov/pubmed/30113005",
"http://www.ncbi.nlm.nih.gov/pubmed/36982862",
"http://www.ncbi.nlm.nih.gov/pubmed/25470007",
"http://www.ncbi.nlm.nih.gov/pubmed/29115402",
"http://www.ncbi.nlm.nih.gov/pubmed/36974405",
"http://www.ncbi.nlm.nih.gov/pubmed/28368777",
"http://www.ncbi.nlm.nih.gov/pubmed/32820310",
"http://www.ncbi.nlm.nih.gov/pubmed/36283334",
"http://www.ncbi.nlm.nih.gov/pubmed/31776996",
"http://www.ncbi.nlm.nih.gov/pubmed/37862201",
"http://www.ncbi.nlm.nih.gov/pubmed/31550441",
"http://www.ncbi.nlm.nih.gov/pubmed/34099564",
"http://www.ncbi.nlm.nih.gov/pubmed/31704095",
"http://www.ncbi.nlm.nih.gov/pubmed/34229552",
"http://www.ncbi.nlm.nih.gov/pubmed/35850516",
"http://www.ncbi.nlm.nih.gov/pubmed/25437922",
"http://www.ncbi.nlm.nih.gov/pubmed/37192628",
"http://www.ncbi.nlm.nih.gov/pubmed/34060004",
"http://www.ncbi.nlm.nih.gov/pubmed/36909283",
"http://www.ncbi.nlm.nih.gov/pubmed/33476770",
"http://www.ncbi.nlm.nih.gov/pubmed/35096821",
"http://www.ncbi.nlm.nih.gov/pubmed/37993864",
"http://www.ncbi.nlm.nih.gov/pubmed/38093134",
"http://www.ncbi.nlm.nih.gov/pubmed/28324490",
"http://www.ncbi.nlm.nih.gov/pubmed/26085571",
"http://www.ncbi.nlm.nih.gov/pubmed/23985961",
"http://www.ncbi.nlm.nih.gov/pubmed/32454052",
"http://www.ncbi.nlm.nih.gov/pubmed/28576471",
"http://www.ncbi.nlm.nih.gov/pubmed/34688664",
"http://www.ncbi.nlm.nih.gov/pubmed/35691026",
"http://www.ncbi.nlm.nih.gov/pubmed/36092697",
"http://www.ncbi.nlm.nih.gov/pubmed/37549565"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37488884",
"endSection": "abstract",
"offsetInBeginSection": 360,
"offsetInEndSection": 510,
"text": "Mitophagy, or selective autophagy of mitochondria, is an essential pathway to preserve mitochondrial homeostasis by clearing up damaged mitochondria. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37549565",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "Mitophagy is an essential physiological process that eliminates damaged mitochondria via lysosomes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37862201",
"endSection": "abstract",
"offsetInBeginSection": 95,
"offsetInEndSection": 250,
"text": "Mitophagy selectively clears damaged or dysfunctional mitochondria through autophagic machinery to maintain mitochondrial quality control and homeostasis. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34229552",
"endSection": "abstract",
"offsetInBeginSection": 9,
"offsetInEndSection": 133,
"text": "increasing evidence that mitophagy, a specialized form of autophagy to degrade and clear long-lived or damaged mitochondria,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26223426",
"endSection": "abstract",
"offsetInBeginSection": 1080,
"offsetInEndSection": 1298,
"text": "(I) turnover of mitochondria via mitophagy (II) turnover of several vesicular structures via macroautophagy or chaperone-mediated autophagy or (III) general lysosome function. This article is part of a special issue on"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36860818",
"endSection": "abstract",
"offsetInBeginSection": 491,
"offsetInEndSection": 671,
"text": "Mitochondrial autophagy (mitophagy) is the process through which defective mitochondria are removed from the cell by internalisation into autophagosomes which fuse with a lysosome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36092697",
"endSection": "abstract",
"offsetInBeginSection": 129,
"offsetInEndSection": 309,
"text": "Through mitophagy (a selective type of autophagy that promotes mitochondrial proteostasis) cells keep a healthy pool of mitochondria, and prevent oxidative stress and inflammation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34688664",
"endSection": "abstract",
"offsetInBeginSection": 340,
"offsetInEndSection": 429,
"text": "Clearance of bulk mitochondria occurs via a selective form of autophagy termed mitophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33922020",
"endSection": "abstract",
"offsetInBeginSection": 378,
"offsetInEndSection": 492,
"text": "Excessive and dysfunctional/damaged mitochondria are degraded by selective autophagic pathways known as mitophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32587855",
"endSection": "abstract",
"offsetInBeginSection": 431,
"offsetInEndSection": 604,
"text": "Mitophagy, a selective autophagy of mitochondria, can efficiently degrade, remove and recycle the malfunctioning or damaged mitochondria, and is crucial for quality control."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33570005",
"endSection": "abstract",
"offsetInBeginSection": 243,
"offsetInEndSection": 424,
"text": "Selective autophagic clearance of flawed mitochondria, a process termed mitophagy, is one of the most prominent mechanisms through which cells maintain a healthy mitochondrial pool."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32454052",
"endSection": "abstract",
"offsetInBeginSection": 197,
"offsetInEndSection": 323,
"text": "Selective autophagy of mitochondria, id est mitophagy, is one of the cellular mechanisms controlling mitochondria homeostasis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36625039",
"endSection": "abstract",
"offsetInBeginSection": 163,
"offsetInEndSection": 282,
"text": "Mitophagy is a mechanism by which cells selectively wrap and degrade damaged mitochondria to maintain cell homeostasis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28976890",
"endSection": "abstract",
"offsetInBeginSection": 464,
"offsetInEndSection": 568,
"text": "One critical level of mitochondrial quality control is the removal of damaged mitochondria by mitophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35850516",
"endSection": "abstract",
"offsetInBeginSection": 615,
"offsetInEndSection": 778,
"text": "Mitophagy and mitochondrial-specific autophagy play an important role in maintenance of neuronal health through the removal of dysfunctional and aged mitochondria."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36740450",
"endSection": "abstract",
"offsetInBeginSection": 1664,
"offsetInEndSection": 1740,
"text": "Colocalization of mitochondria and lysosomes indirectly indicated mitophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33476770",
"endSection": "abstract",
"offsetInBeginSection": 348,
"offsetInEndSection": 493,
"text": "As a part of mitochondrial quality control, the aged and damaged mitochondria are removed through a selective mode of autophagy called mitophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25470007",
"endSection": "abstract",
"offsetInBeginSection": 706,
"offsetInEndSection": 947,
"text": "This unique sensing property was successfully applied to the ratiometric fluorescence imaging of autolysosome formation in selective mitochondrial autophagy (mitophagy), which highlights the utility of this novel probe in autophagy research."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30113005",
"endSection": "abstract",
"offsetInBeginSection": 283,
"offsetInEndSection": 445,
"text": "ys including autophagy. Mitochondria and mitochondrial autophagy play a vital role in cellular health and failure of these pathways can have a devastating effect "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36974405",
"endSection": "abstract",
"offsetInBeginSection": 144,
"offsetInEndSection": 317,
"text": "Mitophagy is the process by which autophagy causes disruption inside mitochondria and the total removal of damaged or stressed mitochondria, hence enhancing cellular health."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37192628",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "Mitophagy plays an important role in mitochondrial homeostasis by selective degradation of mitochondria."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36283334",
"endSection": "abstract",
"offsetInBeginSection": 225,
"offsetInEndSection": 390,
"text": "It interacts with the Atg11 protein to initiate mitophagy and with the Atg8 protein to ensure the engulfment of mitochondria into the autophagosomes for elimination."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37993864",
"endSection": "abstract",
"offsetInBeginSection": 1700,
"offsetInEndSection": 1981,
"text": "Rescue experiments using an AMPK pathway inhibitor (compound C) and an autophagy inhibitor (3-methyladenine) revealed that excessive mitophagy was induced through AMPK/ULK1 pathway activation, worsening mitochondrial damage and subsequent cell death in differentiated SH-SY5Y cells"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37678420",
"endSection": "abstract",
"offsetInBeginSection": 1539,
"offsetInEndSection": 1628,
"text": "Mitochondria were reduced, and mitophagy was inhibited in aortic cells of the model group"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37192628",
"endSection": "abstract",
"offsetInBeginSection": 579,
"offsetInEndSection": 798,
"text": "In mitofissin-deficient cells, a part of the mitochondria is recognized by the mitophagy machinery as cargo but cannot be enwrapped by the autophagosome precursor, the phagophore, due to a lack of mitochondrial fission."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37192628",
"endSection": "abstract",
"offsetInBeginSection": 105,
"offsetInEndSection": 260,
"text": "During mitophagy, mitochondria should be fragmented to allow engulfment within autophagosomes, whose capacity is exceeded by the typical mitochondria mass."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/38093134",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "Mitophagy, a form of selective autophagy, plays an essential role to maintain a population of healthy and functional mitochondria for normal cellular metabolism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34975548",
"endSection": "abstract",
"offsetInBeginSection": 280,
"offsetInEndSection": 400,
"text": "Damaged or unwanted mitochondria are selectively removed by mitophagy, which is a crucial determinant of cell viability."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29311991",
"endSection": "abstract",
"offsetInBeginSection": 1018,
"offsetInEndSection": 1211,
"text": "Mitochondria are eliminated by mitophagy. This is a macroautophagy pathway consisting in the engulfment of mitochondria into a double-membrane structure called autophagosome before degradation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34099564",
"endSection": "abstract",
"offsetInBeginSection": 419,
"offsetInEndSection": 499,
"text": "mitophagy (a specific form of autophagy that removes dysfunctional mitochondria)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31704095",
"endSection": "abstract",
"offsetInBeginSection": 1028,
"offsetInEndSection": 1261,
"text": " Mitochondria may represent a proximal target of HO-1/CO action. HO-1 may localize to mitochondria in response to stress, while CO can moderate mitochondrial dysfunction and regulate mitochondrial autophagy (mitophagy) and biogenesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31776996",
"endSection": "abstract",
"offsetInBeginSection": 445,
"offsetInEndSection": 536,
"text": "Mitophagy is a process for selective degradation of mitochondria, which is well documented."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33239048",
"endSection": "abstract",
"offsetInBeginSection": 375,
"offsetInEndSection": 511,
"text": "The elimination of dysfunctional mitochondria may function as an effective way employed by mitophagy to keep the immune system in check."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36982862",
"endSection": "abstract",
"offsetInBeginSection": 707,
"offsetInEndSection": 918,
"text": "In contrast, fission segregates damaged mitochondria from intact and healthy counterparts and is followed by selective clearance of the damaged mitochondria via mitochondrial specific autophagy, i.e., mitophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32131138",
"endSection": "abstract",
"offsetInBeginSection": 412,
"offsetInEndSection": 573,
"text": "To maintain its quantity and quality, mitochondria undergo multiple processes such as fission, fusion, and mitophagy to eliminate or replace damaged mitochondria"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28368777",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 245,
"text": "Mitophagy is a highly specialized process to remove dysfunctional or superfluous mitochondria through the macroautophagy/autophagy pathway, aimed at protecting cells from the damage of disordered mitochondrial metabolism and apoptosis induction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25634658",
"endSection": "abstract",
"offsetInBeginSection": 98,
"offsetInEndSection": 195,
"text": "Damaged mitochondria can be degraded by a selective type of autophagy, which is termed mitophagy."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28368777",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "PINK1 and BECN1 relocalize at mitochondria-associated membranes during mitophagy and promote ER-mitochondria tethering and autophagosome formation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28324490",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 335,
"text": "Aberrant mitochondrial function is associated with many neurological diseases. Mitophagy is a key mechanism for the elimination of damaged mitochondria and maintenance of mitochondrial homeostasis. Induced pluripotent stem (iPS) cell technologies developed over the last decade have allowed us to analyze functions of the human neuron."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28324490",
"endSection": "abstract",
"offsetInBeginSection": 79,
"offsetInEndSection": 335,
"text": "Mitophagy is a key mechanism for the elimination of damaged mitochondria and maintenance of mitochondrial homeostasis. Induced pluripotent stem (iPS) cell technologies developed over the last decade have allowed us to analyze functions of the human neuron."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36909283",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 265,
"text": "Mitochondrial dysfunction is associated with ototoxicity, which is caused by external factors. Mitophagy plays a key role in maintaining mitochondrial homeostasis and function and is regulated by a series of key mitophagy regulatory proteins and signaling pathways."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36909283",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 371,
"text": "Mitochondrial dysfunction is associated with ototoxicity, which is caused by external factors. Mitophagy plays a key role in maintaining mitochondrial homeostasis and function and is regulated by a series of key mitophagy regulatory proteins and signaling pathways. The results of ototoxicity models indicate the importance of this process in the etiology of ototoxicity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36860818",
"endSection": "abstract",
"offsetInBeginSection": 407,
"offsetInEndSection": 551,
"text": "this paper is on the quality control processes involved in and around mitochondria. Mitochondrial autophagy (mitophagy) is the process through w"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31550441",
"endSection": "abstract",
"offsetInBeginSection": 92,
"offsetInEndSection": 216,
"text": "the autophagic removal of depolarized mitochondria (mitophagy). Parkin-mediated protein ubiquitinations may be counteracted "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21126205",
"endSection": "abstract",
"offsetInBeginSection": 373,
"offsetInEndSection": 499,
"text": "both insufficient and excessive mitophagy have been linked to neurodegeneration. Kinases implicated in regulating mammalian mi"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26085571",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Mitophagy is a critical regulator of mitochondrial quality control and is necessary for elimination of dysfunctional mitochon"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34975548",
"endSection": "abstract",
"offsetInBeginSection": 280,
"offsetInEndSection": 621,
"text": "Damaged or unwanted mitochondria are selectively removed by mitophagy, which is a crucial determinant of cell viability. Mitochondria-associated Endoplasmic Reticulum Membranes (MAMs) are the cellular structures that connect the ER and mitochondria and are involved in calcium signaling, lipid transfer, mitochondrial dynamic, and mitophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34099564",
"endSection": "abstract",
"offsetInBeginSection": 419,
"offsetInEndSection": 500,
"text": "mitophagy (a specific form of autophagy that removes dysfunctional mitochondria)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35691026",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Parkin is an E3 ubiquitin ligase mostly known for its role in regulating the removal of defective mitochondria via mitophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34060004",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1049,
"text": "Autophagy is a mechanism responsible for the degradation of cellular components to maintain their homeostasis. However, autophagy is commonly altered and compromised in several diseases, including neurodegenerative disorders. Parkinson's disease (PD) can be considered a multifactorial disease because environmental factors, genetic factors, and aging are involved. Several genes are involved in PD pathology, among which the LRRK2 gene and its mutations, inherited in an autosomal dominant manner, are responsible for most genetic PD cases. The R1441G LRRK2 mutation is, after G2019S, the most important in PD pathogenesis. Our results demonstrate a relationship between the R1441G LRRK2 mutation and a mechanistic dysregulation of autophagy that compromises cell viability. This altered autophagy mechanism is associated with organellar stress including mitochondrial (which induces mitophagy) and endoplasmic reticulum (ER) stress, consistent with the fact that patients with this mutation are more vulnerable to toxins related to PD, such as MPP"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31956306",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "Mitochondria are linked with various radiation responses, including mitophagy, genomic instability, apoptosis, and the bystander effect."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28576471",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 737,
"text": "Mitochondrial biogenesis and function depend on the intensive exchange of molecules with other cellular compartments. The mitochondrial outer membrane plays a central role in this communication process. It is equipped with a number of specific protein machineries that enable the transport of proteins and metabolites. Furthermore, the outer membrane forms molecular contact sites with other cell organelles like the endoplasmic reticulum (ER), thus integrating mitochondrial function in cellular physiology. The best-studied mitochondrial organelle contact site, the ER-mitochondria encounter structure (ERMES) has been linked to many vital processes including mitochondrial division, inheritance, mitophagy, and phospholipid transport."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36982862",
"endSection": "abstract",
"offsetInBeginSection": 595,
"offsetInEndSection": 918,
"text": "Fusion connects and unites neighboring depolarized mitochondria to derive a healthy and distinct mitochondrion. In contrast, fission segregates damaged mitochondria from intact and healthy counterparts and is followed by selective clearance of the damaged mitochondria via mitochondrial specific autophagy, i.e., mitophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32820310",
"endSection": "abstract",
"offsetInBeginSection": 114,
"offsetInEndSection": 433,
"text": "Mitochondrial fusion-fission dynamics are critical to maintain normal morphology, distribution and quantity of mitochondria, and ensure the normal activity of cells. In addition, mitochondrial autophagy (mitophagy) plays an important role in maintaining mitochondrial quality by degrading aging or damaged mitochondria."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35096821",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "Mitochondrial autophagy (or mitophagy) regulates the mitochondrial network and function to contribute to multiple cellular processes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29115402",
"endSection": "abstract",
"offsetInBeginSection": 234,
"offsetInEndSection": 414,
"text": "Mitochondrial autophagy, also known as mitophagy, which selectively eliminates dysfunctional and unwanted mitochondria, is the most important type of mitochondrial quality control."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23985961",
"endSection": "abstract",
"offsetInBeginSection": 117,
"offsetInEndSection": 283,
"text": "Mitochondrial autophagy (mitophagy) refers to selective sequestration of mitochondria by autophagosomes, which subsequently deliver them to lysosomes for destruction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25753537",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 64,
"text": "Mitochondrial autophagy (mitophagy) is a core cellular activity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25437922",
"endSection": "abstract",
"offsetInBeginSection": 501,
"offsetInEndSection": 570,
"text": "Mitochondria are eliminated via mitochondrial autophagy or mitophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34291135",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 216,
"text": "Mitochondrial autophagy (mitophagy) is the selective clearance of damaged or incomplete mitochondria by autophagy, which is critical for the functional integrity of the entire mitochondrial network and cell survival."
}
] | 13 |
BioASQ-training13b
| null | null |
660877c8fdcbea915f000008
|
bioasq_factoid
|
factoid
|
Which kinase does PD98059 inhibit?
|
['MEK']
|
[
"MEK",
"MAPK/ERK kinase",
"Mitogen-activated protein kinase kinase",
"MAP kinase kinase",
"MAPKK",
"MEK1",
"MEK2"
] |
['PD98059 is a specific, reversible MEK inhibitor.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/32378175"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32378175",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "An injectable microparticle formulation for the sustained release of the specific MEK inhibitor PD98059: in vitro evaluation and pharmacokinetics."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32378175",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 181,
"text": "PD98059 is a reversible MEK inhibitor that we are investigating as a potential treatment for neurochemical changes in the brain that drive neurohumoral excitation in heart failure. "
}
] | 11 |
BioASQ-training11b
| null | null |
6206bf3cc9dfcb9c0900003d
|
bioasq_factoid
|
factoid
|
Which is the major clinical feature observed in FDXR-associated disease?
|
['Retinal dystrophy']
|
[
"Retinal dystrophy",
"Retinitis pigmentosa",
"Rod-cone dystrophy",
"Retinal degeneration",
"Inherited retinal dystrophy",
"Retinal degeneration dystrophy"
] |
['FDXR-associated disease is a phenotypically heterogeneous disorder with retinal dystrophy being a major clinical feature observed in this cohort.', 'Retinal dystrophy is a major clinical feature observed in FDXR-associated disease.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33938912"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33938912",
"endSection": "abstract",
"offsetInBeginSection": 1204,
"offsetInEndSection": 1531,
"text": "FDXR-associated disease is a phenotypically heterogeneous disorder with retinal dystrophy being a major clinical feature observed in this cohort. In addition, we hypothesize that a number of factors are likely to drive the pathogenesis of optic atrophy, retinal degeneration, and perhaps the associated systemic manifestations."
}
] | 11 |
BioASQ-training11b
| null | null |
61f81857882a024a10000040
|
bioasq_factoid
|
factoid
|
What is the cause of episodic ataxia type 6?
|
[['EAAT1 mutations']]
|
[
"EAAT1 mutations",
"excitatory amino acid transporter 1 mutations",
"GLT-1 mutations",
"SLC1A2 mutations"
] |
['Episodic ataxia type 6, is caused by mutations in the gene encoding a glial glutamate transporter, the excitatory amino acid transporter-1. Reduced glutamate uptake by mutant excitatory amino acid transporter-1 (EAAT1) has been thought to be the main pathophysiological process in episodic ataxia type 6.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23107647"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23107647",
"endSection": "abstract",
"offsetInBeginSection": 98,
"offsetInEndSection": 497,
"text": "There are several genetically and clinically distinct forms of this disease, and one of them, episodic ataxia type 6, is caused by mutations in the gene encoding a glial glutamate transporter, the excitatory amino acid transporter-1. So far, reduced glutamate uptake by mutant excitatory amino acid transporter-1 has been thought to be the main pathophysiological process in episodic ataxia type 6. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23107647",
"endSection": "abstract",
"offsetInBeginSection": 1645,
"offsetInEndSection": 1934,
"text": "Episodic ataxia type 6 represents the first human disease found to be associated with altered function of excitatory amino acid transporter anion channels and illustrates possible physiological and pathophysiological impacts of this functional mode of this class of glutamate transporters."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23107647",
"endSection": "abstract",
"offsetInBeginSection": 99,
"offsetInEndSection": 497,
"text": "There are several genetically and clinically distinct forms of this disease, and one of them, episodic ataxia type 6, is caused by mutations in the gene encoding a glial glutamate transporter, the excitatory amino acid transporter-1. So far, reduced glutamate uptake by mutant excitatory amino acid transporter-1 has been thought to be the main pathophysiological process in episodic ataxia type 6."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23107647",
"endSection": "abstract",
"offsetInBeginSection": 99,
"offsetInEndSection": 332,
"text": "There are several genetically and clinically distinct forms of this disease, and one of them, episodic ataxia type 6, is caused by mutations in the gene encoding a glial glutamate transporter, the excitatory amino acid transporter-1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23107647",
"endSection": "abstract",
"offsetInBeginSection": 99,
"offsetInEndSection": 332,
"text": "There are several genetically and clinically distinct forms of this disease, and one of them, episodic ataxia type 6, is caused by mutations in the gene encoding a glial glutamate transporter, the excitatory amino acid transporter-1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23107647",
"endSection": "abstract",
"offsetInBeginSection": 99,
"offsetInEndSection": 332,
"text": "There are several genetically and clinically distinct forms of this disease, and one of them, episodic ataxia type 6, is caused by mutations in the gene encoding a glial glutamate transporter, the excitatory amino acid transporter-1."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.disease-ontology.org/api/metadata/DOID:963"
] |
[] |
571e4293bb137a4b0c00000b
|
bioasq_factoid
|
factoid
|
Which cells produce Interleukin 17A?
|
['T helper type 17 (TH17) cells.']
|
[
"T helper type 17 (TH17) cells",
"TH17 cells",
"T helper 17 cells",
"T17 cells",
"CD4+ T helper 17 cells"
] |
['Interleukin (IL)-17A is secreted from T helper type 17 (TH17) cells.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28930285",
"http://www.ncbi.nlm.nih.gov/pubmed/28941323",
"http://www.ncbi.nlm.nih.gov/pubmed/28935156"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28935156",
"endSection": "abstract",
"offsetInBeginSection": 207,
"offsetInEndSection": 306,
"text": "Several studies have shown an increased expression/release of Th17 related cytokine, IL-17A in ASD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28930285",
"endSection": "abstract",
"offsetInBeginSection": 256,
"offsetInEndSection": 323,
"text": " interleukin (IL)-17A, secreted from T helper type 17 (TH17) cells,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28930285",
"endSection": "abstract",
"offsetInBeginSection": 766,
"offsetInEndSection": 806,
"text": " IL-17A, markedly produced by TH17 cells"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28941323",
"endSection": "abstract",
"offsetInBeginSection": 643,
"offsetInEndSection": 764,
"text": "IL-22 and IL-17A derive from both independent and overlapping lineages, defined as T helper (Th)22 and IL-22+ Th17 cells."
}
] | 11 |
BioASQ-training11b
| null | null |
5c5f30c91a4c55d80b000025
|
bioasq_factoid
|
factoid
|
Is the long non- coding RNA malat-1 up or downregulated in cancer?
|
['upregulated']
|
[
"upregulated",
"up-regulated",
"increased expression",
"enhanced expression",
"stimulated expression"
] |
Malat-1 expression is upregulated in several tumor types
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22722759",
"http://www.ncbi.nlm.nih.gov/pubmed/22088988",
"http://www.ncbi.nlm.nih.gov/pubmed/24163781",
"http://www.ncbi.nlm.nih.gov/pubmed/23845456",
"http://www.ncbi.nlm.nih.gov/pubmed/23726266",
"http://www.ncbi.nlm.nih.gov/pubmed/23104528",
"http://www.ncbi.nlm.nih.gov/pubmed/22858678",
"http://www.ncbi.nlm.nih.gov/pubmed/21678027",
"http://www.ncbi.nlm.nih.gov/pubmed/16878148",
"http://www.ncbi.nlm.nih.gov/pubmed/16441420",
"http://www.ncbi.nlm.nih.gov/pubmed/15552795",
"http://www.ncbi.nlm.nih.gov/pubmed/12970751",
"http://www.ncbi.nlm.nih.gov/pubmed/21266177",
"http://www.ncbi.nlm.nih.gov/pubmed/18006640"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22722759",
"endSection": "abstract",
"offsetInBeginSection": 132,
"offsetInEndSection": 188,
"text": "lncRNA MALAT-1 expression is upregulated in some tumors."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22088988",
"endSection": "abstract",
"offsetInBeginSection": 98,
"offsetInEndSection": 225,
"text": "Metastasis-Associated-in-Lung-Adenocarcinoma-Transcript-1 (MALAT-1) is an ncRNA that is highly expressed in several tumor types"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24163781",
"endSection": "abstract",
"offsetInBeginSection": 21,
"offsetInEndSection": 158,
"text": "metastasis-associated lung adenocarcinoma transcript (MALAT)-1 is known to be consistently upregulated in several epithelial malignancies"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23845456",
"endSection": "abstract",
"offsetInBeginSection": 975,
"offsetInEndSection": 1048,
"text": "MALAT-1 was up-regulated in human prostate cancer tissues and cell lines."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23726266",
"endSection": "abstract",
"offsetInBeginSection": 933,
"offsetInEndSection": 1043,
"text": "Genome-wide profiling revealed that MALAT-1 and prostate cancer gene 3 (PCA3) are overexpressed in PCa tissues"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23104528",
"endSection": "abstract",
"offsetInBeginSection": 1015,
"offsetInEndSection": 1131,
"text": "The level of MALAT-1 in LSCC was significantly higher than that in the corresponding adjacent non-neoplastic tissues"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22858678",
"endSection": "abstract",
"offsetInBeginSection": 4,
"offsetInEndSection": 189,
"text": "metastasis-associated lung adenocarcinoma transcript 1, MALAT1, is a long non-coding RNA (lncRNA) that has been discovered as a marker for lung cancer metastasis. It is highly abundant,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21678027",
"endSection": "abstract",
"offsetInBeginSection": 54,
"offsetInEndSection": 185,
"text": "(MALAT1), a long non-coding RNA (lncRNA), is up-regulated in many solid tumors and associated with cancer metastasis and recurrence"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16878148",
"endSection": "abstract",
"offsetInBeginSection": 619,
"offsetInEndSection": 715,
"text": " Quantitative analyses indicated a 6-7-fold increased RNA level in HCCs versus uninvolved liver,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16878148",
"endSection": "abstract",
"offsetInBeginSection": 205,
"offsetInEndSection": 335,
"text": "(hcn), encoding a 7-kb mRNA-like transcript. The gene appears to be the murine ortholog of the human alpha gene, that is, MALAT-1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16441420",
"endSection": "abstract",
"offsetInBeginSection": 330,
"offsetInEndSection": 532,
"text": "After suppression subtractive hybridization and differential screening, we detected the metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1) gene as one of the major genes upregulated in ESS"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15552795",
"endSection": "abstract",
"offsetInBeginSection": 961,
"offsetInEndSection": 1117,
"text": "a novel non-coding RNA (MALAT-1) to be expressed at significantly higher levels in stage-I and stage-II NSCLC primary tumours that subsequently metastasised"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12970751",
"endSection": "abstract",
"offsetInBeginSection": 388,
"offsetInEndSection": 635,
"text": "quantitative RT-PCR verified overexpression in metastasizing samples. Several of the identified genes (eIF4A1, thymosin beta4 and a novel transcript named MALAT-1) were demonstrated to be significantly associated with metastasis in NSCLC patients "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21266177",
"endSection": "abstract",
"offsetInBeginSection": 177,
"offsetInEndSection": 289,
"text": "Σ RNA is a class of conserved large non-coding RNAs (murine Hepcarcin; human MALAT-1) up-regulated in carcinomas"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18006640",
"endSection": "abstract",
"offsetInBeginSection": 242,
"offsetInEndSection": 415,
"text": "To date, most known NCTs studied have been relatively short, but several important regulatory NCTs, including XIST, MALAT-1, BC1 and BC200, are considerably larger in length"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18006640",
"endSection": "abstract",
"offsetInBeginSection": 1292,
"offsetInEndSection": 1364,
"text": "These NCTs were among the most abundantly expressed transcripts detected"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22858678",
"endSection": "abstract",
"offsetInBeginSection": 440,
"offsetInEndSection": 642,
"text": "The nuclear transcript MALAT-1 has been functionally associated with gene regulation and alternative splicing and its regulation has been shown to impact proliferation, apoptosis, migration and invasion"
}
] | 5 |
BioASQ-training5b
|
[
"http://www.disease-ontology.org/api/metadata/DOID:162",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D022661",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D062085"
] |
[] |
53440d2caeec6fbd07000004
|
bioasq_factoid
|
factoid
|
For which type of diabetes can empagliflozin be used?
|
[['type 2 diabetes mellitus']]
|
[
"type 2 diabetes",
"type II diabetes",
"non-insulin-dependent diabetes mellitus",
"adult-onset diabetes",
"diabetes mellitus type 2",
"T2DM",
"diabetes type 2",
"insulin resistance diabetes",
"type 2 DM",
"type 2 diabetes mellitus"
] |
['The oral antidiabetes agent, empagliflozin, can be used as monotherapy or alongside other glucose-lowering treatments, including insulin, to treat T2DM.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25712444",
"http://www.ncbi.nlm.nih.gov/pubmed/25274537",
"http://www.ncbi.nlm.nih.gov/pubmed/24795251",
"http://www.ncbi.nlm.nih.gov/pubmed/24948511",
"http://www.ncbi.nlm.nih.gov/pubmed/23906374",
"http://www.ncbi.nlm.nih.gov/pubmed/25775379",
"http://www.ncbi.nlm.nih.gov/pubmed/23398530",
"http://www.ncbi.nlm.nih.gov/pubmed/24991224",
"http://www.ncbi.nlm.nih.gov/pubmed/24463454",
"http://www.ncbi.nlm.nih.gov/pubmed/24843716",
"http://www.ncbi.nlm.nih.gov/pubmed/24746173",
"http://www.ncbi.nlm.nih.gov/pubmed/26557225",
"http://www.ncbi.nlm.nih.gov/pubmed/25598831",
"http://www.ncbi.nlm.nih.gov/pubmed/25644093",
"http://www.ncbi.nlm.nih.gov/pubmed/24943000",
"http://www.ncbi.nlm.nih.gov/pubmed/23940010",
"http://www.ncbi.nlm.nih.gov/pubmed/25332189",
"http://www.ncbi.nlm.nih.gov/pubmed/25941565",
"http://www.ncbi.nlm.nih.gov/pubmed/25692841",
"http://www.ncbi.nlm.nih.gov/pubmed/24964723",
"http://www.ncbi.nlm.nih.gov/pubmed/24944269",
"http://www.ncbi.nlm.nih.gov/pubmed/22268612",
"http://www.ncbi.nlm.nih.gov/pubmed/24007456",
"http://www.ncbi.nlm.nih.gov/pubmed/24186878",
"http://www.ncbi.nlm.nih.gov/pubmed/25301180",
"http://www.ncbi.nlm.nih.gov/pubmed/24622369"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25712444",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Empagliflozin, an SGLT2 inhibitor for the treatment of type 2 diabetes mellitus: a review of the evidence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25712444",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 257,
"text": "To review available studies of empagliflozin, a sodium glucose co-transporter-2 (SGLT2) inhibitor approved in 2014 by the European Commission and the United States Food and Drug Administration for the treatment of type 2 diabetes mellitus (T2DM)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24991224",
"endSection": "abstract",
"offsetInBeginSection": 1149,
"offsetInEndSection": 1422,
"text": "In Phase II trials in patients with type 2 diabetes, empagliflozin provided improvements in glycosylated hemoglobin (HbA1c) and other measures of glycemic control when given as monotherapy or add-on to metformin, as well as reductions in weight and systolic blood pressure."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25274537",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 77,
"text": "Empagliflozin: a review of its use in patients with type 2 diabetes mellitus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25274537",
"endSection": "abstract",
"offsetInBeginSection": 1655,
"offsetInEndSection": 1774,
"text": "This article reviews the pharmacological properties and clinical use of empagliflozin in patients with type 2 diabetes."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24991224",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 108,
"text": "Empagliflozin: a new sodium-glucose co-transporter 2 (SGLT2) inhibitor for the treatment of type 2 diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24843716",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 144,
"text": "To evaluate the pharmacodynamics, pharmacokinetics, safety and tolerability of empagliflozin in Japanese patients with type 2 diabetes mellitus."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23398530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "A Phase IIb, randomized, placebo-controlled study of the SGLT2 inhibitor empagliflozin in patients with type 2 diabetes."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24843716",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "Pharmacokinetics, pharmacodynamics, safety and tolerability of 4 weeks' treatment with empagliflozin in Japanese patients with type 2 diabetes mellitus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24795251",
"endSection": "abstract",
"offsetInBeginSection": 364,
"offsetInEndSection": 481,
"text": "We assessed the efficacy and safety of empagliflozin as an add-on treatment in patients with type 2 diabetes and CKD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24991224",
"endSection": "abstract",
"offsetInBeginSection": 1149,
"offsetInEndSection": 1422,
"text": "In Phase II trials in patients with type 2 diabetes, empagliflozin provided improvements in glycosylated hemoglobin (HbA1c) and other measures of glycemic control when given as monotherapy or add-on to metformin, as well as reductions in weight and systolic blood pressure."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25274537",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 77,
"text": "Empagliflozin: a review of its use in patients with type 2 diabetes mellitus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25274537",
"endSection": "abstract",
"offsetInBeginSection": 1655,
"offsetInEndSection": 1774,
"text": "This article reviews the pharmacological properties and clinical use of empagliflozin in patients with type 2 diabetes."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24991224",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 108,
"text": "Empagliflozin: a new sodium-glucose co-transporter 2 (SGLT2) inhibitor for the treatment of type 2 diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24843716",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 144,
"text": "To evaluate the pharmacodynamics, pharmacokinetics, safety and tolerability of empagliflozin in Japanese patients with type 2 diabetes mellitus."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23398530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "A Phase IIb, randomized, placebo-controlled study of the SGLT2 inhibitor empagliflozin in patients with type 2 diabetes."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24843716",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "Pharmacokinetics, pharmacodynamics, safety and tolerability of 4 weeks' treatment with empagliflozin in Japanese patients with type 2 diabetes mellitus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24795251",
"endSection": "abstract",
"offsetInBeginSection": 364,
"offsetInEndSection": 481,
"text": "We assessed the efficacy and safety of empagliflozin as an add-on treatment in patients with type 2 diabetes and CKD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24943000",
"endSection": "abstract",
"offsetInBeginSection": 306,
"offsetInEndSection": 499,
"text": "The SGLT-2 inhibitor empagliflozin improves glucose control, body weight and blood pressure when used as monotherapy or add-on to other antihyperglycemic agents in patients with type 2 diabetes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23940010",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 253,
"text": "Data from five randomized, placebo-controlled, multiple oral dose studies of empagliflozin in patients with type 2 diabetes mellitus (T2DM; N = 974; 1-100 mg q.d.; ≤12 weeks) were used to develop a population pharmacokinetic (PK) model for empagliflozin"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25332189",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 214,
"text": "Empagliflozin, (2S,3R,4R,5S,6R)-2-[4-chloro-3-[[4-[(3S)-oxolan-3-yl]oxyphenyl]methyl]phenyl]-6-(hydroxymethyl)oxane-3,4,5-triol was recently approved by the FDA for the treatment of chronic type 2 diabetes mellitus"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25941565",
"endSection": "abstract",
"offsetInBeginSection": 288,
"offsetInEndSection": 456,
"text": "The SGLT2 inhibitor empagliflozin has gained approval in the EU and in the USA for the treatment of adults with T2DM (there is no current indication in type 1 diabetes)"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24843716",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 156,
"text": "Pharmacokinetics, pharmacodynamics, safety and tolerability of 4 weeks' treatment with empagliflozin in Japanese patients with type 2 diabetes mellitus"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24943000",
"endSection": "abstract",
"offsetInBeginSection": 318,
"offsetInEndSection": 513,
"text": "The SGLT-2 inhibitor empagliflozin improves glucose control, body weight and blood pressure when used as monotherapy or add-on to other antihyperglycemic agents in patients with type 2 diabetes. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23906374",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "Efficacy and safety of empagliflozin, a sodium glucose cotransporter 2 (SGLT2) inhibitor, as add-on to metformin in type 2 diabetes with mild hyperglycaemia."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23906374",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "Efficacy and safety of empagliflozin, a sodium glucose cotransporter 2 (SGLT2) inhibitor, as add-on to metformin in type 2 diabetes with mild hyperglycaemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24943000",
"endSection": "abstract",
"offsetInBeginSection": 318,
"offsetInEndSection": 513,
"text": "The SGLT-2 inhibitor empagliflozin improves glucose control, body weight and blood pressure when used as monotherapy or add-on to other antihyperglycemic agents in patients with type 2 diabetes. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23906374",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "Efficacy and safety of empagliflozin, a sodium glucose cotransporter 2 (SGLT2) inhibitor, as add-on to metformin in type 2 diabetes with mild hyperglycaemia."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23906374",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "Efficacy and safety of empagliflozin, a sodium glucose cotransporter 2 (SGLT2) inhibitor, as add-on to metformin in type 2 diabetes with mild hyperglycaemia."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24944269",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "The SGLT2 inhibitor empagliflozin ameliorates early features of diabetic nephropathy in BTBR ob/ob type 2 diabetic mice with and without hypertension."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24007456",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 243,
"text": "Rationale, design and baseline characteristics of a 4-year (208-week) phase III trial of empagliflozin, an SGLT2 inhibitor, versus glimepiride as add-on to metformin in patients with type 2 diabetes mellitus with insufficient glycemic control."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24964723",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 132,
"text": "Exposure-response modelling for empagliflozin, a sodium glucose cotransporter 2 (SGLT2) inhibitor, in patients with type 2 diabetes."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23906374",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "Efficacy and safety of empagliflozin, a sodium glucose cotransporter 2 (SGLT2) inhibitor, as add-on to metformin in type 2 diabetes with mild hyperglycaemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25274537",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 118,
"text": "This article reviews the pharmacological properties and clinical use of empagliflozin in patients with type 2 diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25274537",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 240,
"text": "With its insulin-independent mechanism of action, empagliflozin monotherapy or combination therapy with other antidiabetic drugs, including insulin, provides a useful addition to the therapeutic options for the management of type 2 diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25274537",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 340,
"text": "In several phase III trials (104weeks' duration; typically 24weeks' duration) and extension studies (typically76weeks' treatment), empagliflozin monotherapy or add-on therapy to other antihyperglycaemics, including insulin, improved glycaemic control and reduced bodyweight and systolic blood pressure in adult patients with type 2 diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25274537",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "Oral empagliflozin (Jardiance()), a sodium glucose cotransporter-2 (SGLT2) inhibitor, is a convenient once-daily treatment for adult patients with type 2 diabetes mellitus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25301180",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 675,
"text": "Sodium glucose cotransporter 2 (SGLT2) inhibitors are a new class of treatment for T2DM that reduce hyperglycemia by reducing renal glucose reabsorption and thereby increasing urinary glucose excretion.This paper reviews the pharmacokinetic and pharmacodynamic properties of the SGLT2 inhibitor empagliflozin , the results of clinical trials investigating the efficacy of empagliflozin given as monotherapy or as add-on therapy on glycemic control, body weight, and blood pressure in patients with T2DM, and the safety and tolerability profile of empagliflozin.Empagliflozin offers good glycemic efficacy, weight loss, blood pressure reduction, and a low risk of hypoglycemia."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25301180",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 51,
"text": "Empagliflozin for the treatment of type 2 diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25301180",
"endSection": "abstract",
"offsetInBeginSection": 596,
"offsetInEndSection": 955,
"text": "This paper reviews the pharmacokinetic and pharmacodynamic properties of the SGLT2 inhibitor empagliflozin , the results of clinical trials investigating the efficacy of empagliflozin given as monotherapy or as add-on therapy on glycemic control, body weight, and blood pressure in patients with T2DM, and the safety and tolerability profile of empagliflozin."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25301180",
"endSection": "title",
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"text": "Empagliflozin for the treatment of type 2 diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24795251",
"endSection": "abstract",
"offsetInBeginSection": 2286,
"offsetInEndSection": 2519,
"text": "In patients with type 2 diabetes and stage 2 or 3 CKD, empagliflozin reduced HbA1c and was well tolerated. However, our findings might not be applicable to the general population of patients with type 2 diabetes and renal impairment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25274537",
"endSection": "abstract",
"offsetInBeginSection": 1302,
"offsetInEndSection": 1663,
"text": "With its insulin-independent mechanism of action, empagliflozin monotherapy or combination therapy with other antidiabetic drugs, including insulin, provides a useful addition to the therapeutic options for the management of type 2 diabetes. This article reviews the pharmacological properties and clinical use of empagliflozin in patients with type 2 diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23398530",
"endSection": "abstract",
"offsetInBeginSection": 1469,
"offsetInEndSection": 1715,
"text": "In patients with type 2 diabetes, empagliflozin resulted in dose-dependent, clinically meaningful reductions in HbA1c and FPG, and reductions in body weight compared with placebo. Empagliflozin was well-tolerated with a favourable safety profile."
},
{
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"endSection": "abstract",
"offsetInBeginSection": 1405,
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"text": "No UTIs or genital infections led to premature discontinuation. In patients with type 2 diabetes, empagliflozin resulted in dose-dependent, clinically meaningful reductions in HbA1c and FPG, and reductions in body weight compared with placebo."
},
{
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"text": "In patients with type 2 diabetes, empagliflozin resulted in dose-dependent, clinically meaningful reductions in HbA1c and FPG, and reductions in body weight compared with placebo."
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"text": "In Phase II trials in patients with type 2 diabetes, empagliflozin provided improvements in glycosylated hemoglobin (HbA1c) and other measures of glycemic control when given as monotherapy or add-on to metformin, as well as reductions in weight and systolic blood pressure."
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"text": "A Phase IIb, randomized, placebo-controlled study of the SGLT2 inhibitor empagliflozin in patients with type 2 diabetes."
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"text": "In Phase II trials in patients with type 2 diabetes, empagliflozin provided improvements in glycosylated hemoglobin (HbA1c) and other measures of glycemic control when given as monotherapy or add-on to metformin, as well as reductions in weight and systolic blood pressure."
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"text": "In Phase II trials in patients with type 2 diabetes, empagliflozin provided improvements in glycosylated hemoglobin (HbA1c) and other measures of glycemic control when given as monotherapy or add-on to metformin, as well as reductions in weight and systolic blood pressure."
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"offsetInBeginSection": 1469,
"offsetInEndSection": 1648,
"text": "In patients with type 2 diabetes, empagliflozin resulted in dose-dependent, clinically meaningful reductions in HbA1c and FPG, and reductions in body weight compared with placebo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24463454",
"endSection": "abstract",
"offsetInBeginSection": 1846,
"offsetInEndSection": 2116,
"text": "In patients with type 2 diabetes, empagliflozin-induced glycosuria improved β cell function and insulin sensitivity, despite the fall in insulin secretion and tissue glucose disposal and the rise in EGP after one dose, thereby lowering fasting and postprandial glycemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24991224",
"endSection": "abstract",
"offsetInBeginSection": 882,
"offsetInEndSection": 1155,
"text": "In Phase II trials in patients with type 2 diabetes, empagliflozin provided improvements in glycosylated hemoglobin (HbA1c) and other measures of glycemic control when given as monotherapy or add-on to metformin, as well as reductions in weight and systolic blood pressure."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25775379",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "Single-pill combination therapy for type 2 diabetes mellitus: linagliptin plus empagliflozin."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003924",
"http://www.disease-ontology.org/api/metadata/DOID:9352"
] |
[] |
571e14fbbb137a4b0c000001
|
bioasq_factoid
|
factoid
|
Which molecule is targeted by Fenebrutinib?
|
["Bruton's tyrosine kinase"]
|
[
"Bruton's tyrosine kinase",
"BTK",
"Bruton tyrosine kinase",
"Bruton's kinase",
"Bruton's lymphocyte tyrosine kinase"
] |
["Fenebrutinib is a noncovalent, oral, and highly selective inhibitor of Bruton's tyrosine kinase (BTK)."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34750553",
"http://www.ncbi.nlm.nih.gov/pubmed/31494233",
"http://www.ncbi.nlm.nih.gov/pubmed/32832028",
"http://www.ncbi.nlm.nih.gov/pubmed/32270926",
"http://www.ncbi.nlm.nih.gov/pubmed/33806595",
"http://www.ncbi.nlm.nih.gov/pubmed/31907670",
"http://www.ncbi.nlm.nih.gov/pubmed/31446134",
"http://www.ncbi.nlm.nih.gov/pubmed/34042314",
"http://www.ncbi.nlm.nih.gov/pubmed/33777941",
"http://www.ncbi.nlm.nih.gov/pubmed/31371481",
"http://www.ncbi.nlm.nih.gov/pubmed/33689480"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33689480",
"endSection": "abstract",
"offsetInBeginSection": 600,
"offsetInEndSection": 898,
"text": "These inhibitors include four Syk inhibitors, Bay 61-3606, R406 (fostamatinib), entospletinib, TAK-659; four irreversible BTK inhibitors, ibrutinib, acalabrutinib, ONO-4059 (tirabrutinib), AVL-292 (spebrutinib); and four reversible BTK inhibitors, CG-806, BMS-935177, BMS-986195, and fenebrutinib. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33777941",
"endSection": "abstract",
"offsetInBeginSection": 782,
"offsetInEndSection": 1103,
"text": "However, an increasing number of trials instead addresses autoimmunity and inflammation in multiple sclerosis, rheumatoid arthritis, pemphigus and systemic lupus erythematosus with the use of either irreversibly binding inhibitors, e.g., evobrutinib and tolebrutinib, or reversibly binding inhibitors, like fenebrutinib. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34042314",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "OBJECTIVE: Fenebrutinib (GDC-0853) is a noncovalent, oral, and highly selective inhibitor of Bruton's tyrosine kinase (BTK)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33806595",
"endSection": "abstract",
"offsetInBeginSection": 607,
"offsetInEndSection": 1013,
"text": "In contrast, no bleeding has been reported in clinical trials of other BTKi. These include the brain-penetrant irreversible tolebrutinib and evobrutinib (against multiple sclerosis), the irreversible branebrutinib, the reversible BMS-986142 and fenebrutinib (targeting rheumatoid arthritis and lupus erythematodes), and the reversible covalent rilzabrutinib (against pemphigus and immune thrombocytopenia)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34750553",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 290,
"text": "Bruton's tyrosine kinase (BTK) is crucial for FcεRI-mediated mast cell activation and essential for autoantibody production by B cells in chronic spontaneous urticaria (CSU). Fenebrutinib, an orally administered, potent, highly selective, reversible BTK inhibitor, may be effective in CSU. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31494233",
"endSection": "abstract",
"offsetInBeginSection": 973,
"offsetInEndSection": 1311,
"text": "New therapeutics under investigation include IgG1 anti-IgE monoclonal antibodies (ligelizumab), chemoattractant rector-homologous molecule expressed on TH2 cells antagonists (AZD1981), Bruton tyrosine kinase inhibitors (fenebrutinib), anti-siglec-8 monoclonal antibody (AK002), and topical spleen tyrosine kinase inhibitors (GSK2646264). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31371481",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "Fenebrutinib (GDC-0853) is an orally administered small molecule inhibitor of Bruton's tyrosine kinase being investigated for treatment of rheumatoid arthritis in patients with inadequate responses to methotrexate (MTX)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31371481",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Absence of Pharmacokinetic Interactions between the Bruton's Tyrosine Kinase Inhibitor Fenebrutinib and Methotrexate."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32832028",
"endSection": "abstract",
"offsetInBeginSection": 285,
"offsetInEndSection": 560,
"text": "In efforts to develop additional series of reversible Btk inhibitors for chronic immune diseases, we sought to differentiate from our clinical stage inhibitor fenebrutinib using cyclopropyl amide isosteres of the 2-aminopyridyl group to occupy the flat, lipophilic H2 pocket."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31494233",
"endSection": "abstract",
"offsetInBeginSection": 979,
"offsetInEndSection": 1338,
"text": "erapeutics under investigation include IgG1 anti-IgE monoclonal antibodies (ligelizumab), chemoattractant rector-homologous molecule expressed on TH2 cells antagonists (AZD1981), Bruton tyrosine kinase inhibitors (fenebrutinib), anti-siglec-8 monoclonal antibody (AK002), and topical spleen tyrosine kinase inhibitors (GSK2646264). We review the mechanisms of"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31446134",
"endSection": "abstract",
"offsetInBeginSection": 1103,
"offsetInEndSection": 1430,
"text": "promising drugs that are currently under development for CU are a chemoattractant receptor-homologous molecule expressed on TH2 cell antagonist, a monoclonal antibody to Siglec-8 (AK002), Bruton tyrosine kinase inhibitors (fenebrutinib and Lou064), a spleen tyrosine kinase inhibitor, and dupilumab. Promising targets of future"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33689480",
"endSection": "abstract",
"offsetInBeginSection": 600,
"offsetInEndSection": 897,
"text": "These inhibitors include four Syk inhibitors, Bay 61-3606, R406 (fostamatinib), entospletinib, TAK-659; four irreversible BTK inhibitors, ibrutinib, acalabrutinib, ONO-4059 (tirabrutinib), AVL-292 (spebrutinib); and four reversible BTK inhibitors, CG-806, BMS-935177, BMS-986195, and fenebrutinib."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34042314",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "OBJECTIVE: Fenebrutinib (GDC-0853) is a noncovalent, oral, and highly selective inhibitor of Bruton's tyrosine kinase"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32270926",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "OBJECTIVE: To evaluate fenebrutinib, an oral and highly selective non-covalent inhibitor of Bruton's tyrosine kinase (BTK), in patients with active rheumatoid arthrit"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31907670",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 160,
"text": "PURPOSE: Fenebrutinib (GDC-0853), a Bruton's tyrosine kinase (BTK) inhibitor was investigated in a Phase 2 clinical trial in patients with rheumatoid arthritis "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31371481",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 222,
"text": "Fenebrutinib (GDC-0853) is an orally administered small molecule inhibitor of Bruton's tyrosine kinase being investigated for treatment of rheumatoid arthritis in patients with inadequate responses to methotrexate (MTX). T"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34042314",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "OBJECTIVE: Fenebrutinib (GDC-0853) is a noncovalent, oral, and highly selective inhibitor of Bruton's tyrosine ki"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31907670",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 156,
"text": "PURPOSE: Fenebrutinib (GDC-0853), a Bruton's tyrosine kinase (BTK) inhibitor was investigated in a Phase 2 clinical trial in patients with rheumatoid arthri"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32270926",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "OBJECTIVE: To evaluate fenebrutinib, an oral and highly selective non-covalent inhibitor of Bruton's tyrosine kinase (BTK), in patients with active rheumatoid arth"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34042314",
"endSection": "abstract",
"offsetInBeginSection": 1370,
"offsetInEndSection": 1610,
"text": "utinib 200 mg twice daily. By week 48, patients treated with fenebrutinib had reduced levels of a BTK-dependent plasmablast RNA signature, anti-double-stranded DNA autoantibodies, total IgG, and IgM, as well as increased complement C4 level"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32270926",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 375,
"text": "OBJECTIVE: To evaluate fenebrutinib, an oral and highly selective non-covalent inhibitor of Bruton's tyrosine kinase (BTK), in patients with active rheumatoid arthritis (RA).METHODS: Patients with RA and inadequate response to methotrexate (cohort 1, n=480) were randomized to fenebrutinib (50 mg once daily, 150 mg once daily, 200 mg twice daily), 40 mg adalimumab every oth"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34750553",
"endSection": "abstract",
"offsetInBeginSection": 175,
"offsetInEndSection": 289,
"text": "Fenebrutinib, an orally administered, potent, highly selective, reversible BTK inhibitor, may be effective in CSU."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34042314",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "Efficacy, Safety, and Pharmacodynamic Effects of the Bruton's Tyrosine Kinase Inhibitor Fenebrutinib (GDC-0853) in Systemic Lupus Erythematosus: Results of a Phase II, Randomized, Double-Blind, Placebo-Controlled Trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31494233",
"endSection": "abstract",
"offsetInBeginSection": 921,
"offsetInEndSection": 1258,
"text": "essants; however, additional treatments are needed. New therapeutics under investigation include IgG1 anti-IgE monoclonal antibodies (ligelizumab), chemoattractant rector-homologous molecule expressed on TH2 cells antagonists (AZD1981), Bruton tyrosine kinase inhibitors (fenebrutinib), anti-siglec-8 monoclonal antibody (AK002), and top"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34042314",
"endSection": "abstract",
"offsetInBeginSection": 1368,
"offsetInEndSection": 1758,
"text": "brutinib 200 mg twice daily. By week 48, patients treated with fenebrutinib had reduced levels of a BTK-dependent plasmablast RNA signature, anti-double-stranded DNA autoantibodies, total IgG, and IgM, as well as increased complement C4 levels, all relative to placebo.CONCLUSION: While fenebrutinib had an acceptable safety profile, the primary end point, SRI-4 response, was not met despi"
}
] | 11 |
BioASQ-training11b
| null | null |
61f7d5a0882a024a10000035
|
bioasq_factoid
|
factoid
|
Lucio’s Phenomenon is characteristic to which disease?
|
['leprosy']
|
[
"leprosy",
"Hansen's disease",
"Mycobacterium leprae infection",
"lepromatous leprosy",
"tuberculoid leprosy",
"borderline leprosy"
] |
["Lucio's phenomenon is a rare but distinctive skin eruption seen in patients with diffuse lepromatous leprosy."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24863848",
"http://www.ncbi.nlm.nih.gov/pubmed/34672479",
"http://www.ncbi.nlm.nih.gov/pubmed/22475236",
"http://www.ncbi.nlm.nih.gov/pubmed/31783808",
"http://www.ncbi.nlm.nih.gov/pubmed/15985035",
"http://www.ncbi.nlm.nih.gov/pubmed/19702985",
"http://www.ncbi.nlm.nih.gov/pubmed/25509720",
"http://www.ncbi.nlm.nih.gov/pubmed/22570037",
"http://www.ncbi.nlm.nih.gov/pubmed/24346890",
"http://www.ncbi.nlm.nih.gov/pubmed/19078473",
"http://www.ncbi.nlm.nih.gov/pubmed/31114260",
"http://www.ncbi.nlm.nih.gov/pubmed/17544965",
"http://www.ncbi.nlm.nih.gov/pubmed/29048291",
"http://www.ncbi.nlm.nih.gov/pubmed/17506277",
"http://www.ncbi.nlm.nih.gov/pubmed/26566619"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31114260",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 184,
"text": "Diffuse multibacillary leprosy patient with Lucio's phenomenon and positive anticardiolipin antibody misdiagnosed as lupus erythematosus panniculitis in the People's Republic of China."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31114260",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "Lucio's phenomenon (LP) is a special reactional state associated with diffuse multibacillary leprosy; both exhibit a limitative global distribution mainly in Mexico and Central America. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29048291",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 81,
"text": "Diffuse Multibacillary Leprosy of Lucio and Latapí with Lucio's Phenomenon, Peru."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29048291",
"endSection": "abstract",
"offsetInBeginSection": 148,
"offsetInEndSection": 302,
"text": "He also had Lucio's phenomenon, characterized by vascular thrombosis and invasion of blood vessel walls by leprosy bacilli, causing extensive skin ulcers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24863848",
"endSection": "abstract",
"offsetInBeginSection": 213,
"offsetInEndSection": 323,
"text": "Lucio's phenomenon is a rare but distinctive skin eruption seen in patients with diffuse lepromatous leprosy. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22570037",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 70,
"text": "Lucio's phenomenon is defined as a variant of type 2 leprosy reaction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34672479",
"endSection": "abstract",
"offsetInBeginSection": 203,
"offsetInEndSection": 326,
"text": "Lucio's phenomenon is a rare manifestation among lepromatous patients with a rapid and severe evolution and high mortality."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24863848",
"endSection": "abstract",
"offsetInBeginSection": 213,
"offsetInEndSection": 322,
"text": "Lucio's phenomenon is a rare but distinctive skin eruption seen in patients with diffuse lepromatous leprosy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19078473",
"endSection": "abstract",
"offsetInBeginSection": 428,
"offsetInEndSection": 537,
"text": " Lucio's phenomenon is a rare but distinctive skin eruption seen in patients with diffuse lepromatous leprosy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31114260",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "Lucio's phenomenon (LP) is a special reactional state associated with diffuse multibacillary leprosy; both exhibit a limitative global distribution mainly in Mexico and Central America. W"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26566619",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 139,
"text": "BACKGROUND: Lucio's phenomenon is a rare manifestation of untreated leprosy which is seen almost exclusively in regions surrounding the Gul"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17506277",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "O Lucio's phenomenon is an uncommon type 2 reactional state occurring exclusively in patients with diffuse lepromatous leprosy (Lucio-Latapi leprosy)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24346890",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "Lucio's phenomenon represents a serious cutaneous necrotizing reaction, which can occur with Lucio's leprosy and also in other forms of lepromatous leprosy. T"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22475236",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "BACKGROUND: Lucio's phenomenon is a rare leprosy reaction characterised by bizarrely-shaped, purpuric skin lesions and "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25509720",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 199,
"text": "Lucio's phenomenon (LPh) is considered a necrotizing panvasculitis and a variant of leprosy Type 2 reaction, clinically characterised by necrotic-haemorrhagic lesions on the extremities and trunk. LP"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31783808",
"endSection": "abstract",
"offsetInBeginSection": 164,
"offsetInEndSection": 306,
"text": "estations. Ulcer is not a common feature in leprosy patients, except during reactional states, Lucio's phenomenon (LP), or secondary to neurop"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17544965",
"endSection": "abstract",
"offsetInBeginSection": 688,
"offsetInEndSection": 1019,
"text": "to the clinical and histopathological manifestations, leprosy reactions may be separated in 2 or 3 different variants: reverse reaction (type I), erythema nodosum leprosum (type II), erythema polymorphous (type II) and Lucio's phenomenon, mainly considered a type II reaction, but sometimes designated type III. Type I leprosy reac"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19078473",
"endSection": "abstract",
"offsetInBeginSection": 429,
"offsetInEndSection": 538,
"text": "Lucio's phenomenon is a rare but distinctive skin eruption seen in patients with diffuse lepromatous leprosy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17506277",
"endSection": "abstract",
"offsetInBeginSection": 245,
"offsetInEndSection": 412,
"text": "Lucio's phenomenon is characterized by necrotic ulcerations of the skin preferentially on the lower extremities usually in association with ongoing Lucio lepromatosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15985035",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 210,
"text": "Lucio's phenomenon/erythema necroticans is a peculiar reaction pattern that occurs in untreated pure primitive diffuse lepromatous leprosy (PPDL) and/or relapsing leprosy recognized as spotted leprosy of Lucio."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19702985",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "BACKGROUND: Lucio's phenomenon is a rare and aggressive necrotising variant of erythema nodosum leprosum that classically occur in patients with undiagnosed, diffuse non-nodular lepromat"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26566619",
"endSection": "abstract",
"offsetInBeginSection": 1010,
"offsetInEndSection": 1230,
"text": "io's phenomenon was suspected. A clinical diagnosis of Lucio's phenomenon occurring in the backdrop of lepromatous leprosy was made.CONCLUSION: Though leprosy is still a prevalent disease, it has manifestations that are "
}
] | 11 |
BioASQ-training11b
| null | null |
61f7c9ac882a024a10000028
|
bioasq_factoid
|
yesno
|
Is Prasinezumab effective for Parkinson’s Disease?
|
['no']
|
[
"no"
] |
['No, Prasinezumab is not effective for Parkinson’s Disease.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/35921451"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35921451",
"endSection": "abstract",
"offsetInBeginSection": 2015,
"offsetInEndSection": 2208,
"text": "CONCLUSIONS: Prasinezumab therapy had no meaningful effect on global or imaging measures of Parkinson's disease progression as compared with placebo and was associated with infusion reactions. "
}
] | 12 |
BioASQ-training12b
| null | null |
63eef9b6f36125a426000011
|
bioasq_yesno
|
factoid
|
What is the prognostic role of alterred thyroid profile after cardiosurgery?
|
['Altered thyroid profile after cardiosurgery is associated with several events in adults and in children']
|
[
"altered thyroid profile",
"thyroid dysfunction",
"thyroid hormone imbalance",
"thyroid profile changes",
"thyroid profile alterations",
"thyroid profile after surgery",
"thyroid profile after cardiosurgery",
"thyroid profile in adults",
"thyroid profile in children"
] |
Altered thyroid profile after cardiosurgery is associated with high incidence of atrial fibrillation e delay in recovery (prolonged hospitalisation) in adults and higher score on The Pediatric Risk of Mortality (PRISM; P < 0.042) and a longer duration of ventilation in children.Impportantly in transplanted patients altered thyroid metabolism,low T3 syndrome, is characterized by highest mortality, highest incidence of acute rejection or reoperations and infections
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21959513",
"http://www.ncbi.nlm.nih.gov/pubmed/19463607",
"http://www.ncbi.nlm.nih.gov/pubmed/19303793",
"http://www.ncbi.nlm.nih.gov/pubmed/14500064",
"http://www.ncbi.nlm.nih.gov/pubmed/1929631",
"http://www.ncbi.nlm.nih.gov/pubmed/21097430",
"http://www.ncbi.nlm.nih.gov/pubmed/16677263",
"http://www.ncbi.nlm.nih.gov/pubmed/15868525",
"http://www.ncbi.nlm.nih.gov/pubmed/12475369"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21959513",
"endSection": "abstract",
"offsetInBeginSection": 919,
"offsetInEndSection": 1161,
"text": " Patients with fT3 syndrome had the highest mortality (16.7%, NS), highest incidence of acute rejection (38.9%, NS), highest number of reoperations (27.8%, NS), and highest incidence of bacterial (16.7%, NS) and fungal infections (11.1%, NS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19463607",
"endSection": "abstract",
"offsetInBeginSection": 1415,
"offsetInEndSection": 1546,
"text": "SCH appears to influence the postoperative outcome for patients by increasing the development of postoperative atrial fibrillation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19303793",
"endSection": "abstract",
"offsetInBeginSection": 1244,
"offsetInEndSection": 1338,
"text": "There was a significant inverse relationship between fT3 levels and global oxygen consumption."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16677263",
"endSection": "abstract",
"offsetInBeginSection": 637,
"offsetInEndSection": 869,
"text": "However, in the high inotropic support group, FT4 was lower for a longer time. This group also had a significantly higher score on The Pediatric Risk of Mortality (PRISM; P < 0.042) and a longer duration of ventilation (P < 0.014). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15868525",
"endSection": "abstract",
"offsetInBeginSection": 1878,
"offsetInEndSection": 2059,
"text": " In a group of elderly patients undergoing cardiac surgery, there was a strong association between a postoperative decrease of serum triiodothyronine levels and atrial fibrillation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14500064",
"endSection": "abstract",
"offsetInBeginSection": 1474,
"offsetInEndSection": 1575,
"text": "Low basal fT3 concentration can reliably predict the occurrence of postoperative AF in CABG patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1929631",
"endSection": "abstract",
"offsetInBeginSection": 1359,
"offsetInEndSection": 1488,
"text": "Those with an uneventful recovery had a higher serum free T4 level on the sixth day after operation than those with complications"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21097430",
"endSection": "abstract",
"offsetInBeginSection": 1312,
"offsetInEndSection": 1488,
"text": "Enhancement of T3 levels after mitral valve replacement may increase the probability of early spontaneous cardioversion of AF, but can not affect the duration of sinus rhythm. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12475369",
"endSection": "abstract",
"offsetInBeginSection": 945,
"offsetInEndSection": 1294,
"text": "A relevant finding was that the days of post-operative hospitalization (10+/-3 days, means+/-S.D.) was inversely correlated with the slope of the recovery of T3 concentration (P<0.001) or with the area under the plasma curves of T3 (P=0.024, time range 72-144 h) and the FT3/FT4 ratio (P=0.037, time range 72-144 h) during the post-operative period."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013903",
"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=D010361",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013959",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D011379"
] |
[] |
53265dd4d6d3ac6a34000007
|
bioasq_factoid
|
factoid
|
Which technique is used for detection of EWS/FLI1 fusion transcripts?
|
[['Reverse transcription - polymerase chain reaction (RT-PCR)']]
|
[
"Reverse transcription - polymerase chain reaction (RT-PCR)",
"RT-PCR",
"Reverse transcription PCR",
"Reverse transcriptase PCR",
"RT-PCR assay",
"RT-PCR technique"
] |
['Molecular detection of EWS-FLI1 chimeric transcripts in Ewing family tumors is carried out by reverse transcription-polymerase chain reaction (RT-PCR).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/20231617",
"http://www.ncbi.nlm.nih.gov/pubmed/10379685",
"http://www.ncbi.nlm.nih.gov/pubmed/15565546",
"http://www.ncbi.nlm.nih.gov/pubmed/9552022",
"http://www.ncbi.nlm.nih.gov/pubmed/17154184",
"http://www.ncbi.nlm.nih.gov/pubmed/15363317",
"http://www.ncbi.nlm.nih.gov/pubmed/24293381",
"http://www.ncbi.nlm.nih.gov/pubmed/23475435"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20231617",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 520,
"text": "We evaluated the feasibility and usefulness of reverse transcriptase-polymerase chain reaction (RT-PCR) on fine-needle aspirates for categorization of small blue round cell tumors (SBRCTs). A total of 51 cases, including 25 Ewing sarcoma/peripheral primitive neuroectodermal tumors (PNETs), 11 rhabdomyosarcomas, 13 neuroblastomas, and 2 desmoplastic small round cell tumors (DSRCTs) were analyzed. The detection of the EWS-FLI1 (20/25) and EWS-ERG (4/25) fusion transcripts resolved 24 of 25 cases of Ewing sarcoma/PNET"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10379685",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "Molecular detection of EWS-FLI1 chimeric transcripts in Ewing family tumors by nested reverse transcription-polymerase chain reaction"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10379685",
"endSection": "abstract",
"offsetInBeginSection": 374,
"offsetInEndSection": 1042,
"text": "To assess the feasibility and reliability of the molecular detection of the transcript originating from the chimeric gene in paraffin-embedded tumor specimens, we performed a nested reverse transcription-polymerase chain reaction (RT-PCR)-based assay to detect the EWS-FLI1 chimeric message in a series of Ewing family tumors. Of 24 paraffin-embedded tumor specimens from 23 cases analyzed, the chimeric message was detectable in 20 (83%) specimens from 20 cases (87%) by this nested RT-PCR assay, whereas none of 7 small round cell tumors not from this family (3 alveolar rhabdomyosarcomas, 2 neuroblastomas, 2 malignant lymphomas) showed detectable chimeric messages"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15565546",
"endSection": "abstract",
"offsetInBeginSection": 3113,
"offsetInEndSection": 3359,
"text": "Using our different sets of exon specific primer pairs, it was possible to detect 4 different breakpoints of ews/fli1 fusion transcripts and the ews/erg fusion by RT-PCR in RNA isolates from formalin-fixed, paraffin-embedded Ewing's tumor tissue."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16157025",
"endSection": "abstract",
"offsetInBeginSection": 1814,
"offsetInEndSection": 2011,
"text": "Molecular detection of EWS-Fli1 fusion transcripts in formalin-fixed paraffin-embedded material by nested RT-PCR is feasible and is useful for the diagnosis and differential diagnosis of ES/pPNETs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15565546",
"endSection": "abstract",
"offsetInBeginSection": 1729,
"offsetInEndSection": 2045,
"text": "We established a novel RT-PCR method, using 3 different exon specific sets of PCR primer pairs, selected according to the coding ews and fli1 nucleotide sequences (NCBI database), suitable for RT-PCR identification of variant ews/fli1 fusion transcripts in RNA isolated from formalin-fixed, paraffin-embedded tissue."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9135495",
"endSection": "abstract",
"offsetInBeginSection": 236,
"offsetInEndSection": 393,
"text": "In this study, we evaluated reverse transcriptase-polymerase chain (RT-PCR) for EWS-FLI1 fusion transcripts in 18 neurally derived small round cell tumours."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15565546",
"endSection": "abstract",
"offsetInBeginSection": 3113,
"offsetInEndSection": 3359,
"text": "Using our different sets of exon specific primer pairs, it was possible to detect 4 different breakpoints of ews/fli1 fusion transcripts and the ews/erg fusion by RT-PCR in RNA isolates from formalin-fixed, paraffin-embedded Ewing's tumor tissue."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16157025",
"endSection": "abstract",
"offsetInBeginSection": 1814,
"offsetInEndSection": 2011,
"text": "Molecular detection of EWS-Fli1 fusion transcripts in formalin-fixed paraffin-embedded material by nested RT-PCR is feasible and is useful for the diagnosis and differential diagnosis of ES/pPNETs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15565546",
"endSection": "abstract",
"offsetInBeginSection": 1729,
"offsetInEndSection": 2045,
"text": "We established a novel RT-PCR method, using 3 different exon specific sets of PCR primer pairs, selected according to the coding ews and fli1 nucleotide sequences (NCBI database), suitable for RT-PCR identification of variant ews/fli1 fusion transcripts in RNA isolated from formalin-fixed, paraffin-embedded tissue."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15565546",
"endSection": "abstract",
"offsetInBeginSection": 3113,
"offsetInEndSection": 3359,
"text": "Using our different sets of exon specific primer pairs, it was possible to detect 4 different breakpoints of ews/fli1 fusion transcripts and the ews/erg fusion by RT-PCR in RNA isolates from formalin-fixed, paraffin-embedded Ewing's tumor tissue."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16157025",
"endSection": "abstract",
"offsetInBeginSection": 1814,
"offsetInEndSection": 2011,
"text": "Molecular detection of EWS-Fli1 fusion transcripts in formalin-fixed paraffin-embedded material by nested RT-PCR is feasible and is useful for the diagnosis and differential diagnosis of ES/pPNETs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15565546",
"endSection": "abstract",
"offsetInBeginSection": 1729,
"offsetInEndSection": 2045,
"text": "We established a novel RT-PCR method, using 3 different exon specific sets of PCR primer pairs, selected according to the coding ews and fli1 nucleotide sequences (NCBI database), suitable for RT-PCR identification of variant ews/fli1 fusion transcripts in RNA isolated from formalin-fixed, paraffin-embedded tissue."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15565546",
"endSection": "abstract",
"offsetInBeginSection": 3113,
"offsetInEndSection": 3359,
"text": "Using our different sets of exon specific primer pairs, it was possible to detect 4 different breakpoints of ews/fli1 fusion transcripts and the ews/erg fusion by RT-PCR in RNA isolates from formalin-fixed, paraffin-embedded Ewing's tumor tissue."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16157025",
"endSection": "abstract",
"offsetInBeginSection": 1814,
"offsetInEndSection": 2011,
"text": "Molecular detection of EWS-Fli1 fusion transcripts in formalin-fixed paraffin-embedded material by nested RT-PCR is feasible and is useful for the diagnosis and differential diagnosis of ES/pPNETs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15565546",
"endSection": "abstract",
"offsetInBeginSection": 1729,
"offsetInEndSection": 2045,
"text": "We established a novel RT-PCR method, using 3 different exon specific sets of PCR primer pairs, selected according to the coding ews and fli1 nucleotide sequences (NCBI database), suitable for RT-PCR identification of variant ews/fli1 fusion transcripts in RNA isolated from formalin-fixed, paraffin-embedded tissue."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9552022",
"endSection": "abstract",
"offsetInBeginSection": 684,
"offsetInEndSection": 869,
"text": "We performed a clinical and pathologic analysis of 112 patients with ES in which EWS-FLI1 fusion transcripts were identified by reverse-transcriptase polymerase chain reaction (RT-PCR)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20231617",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 520,
"text": "We evaluated the feasibility and usefulness of reverse transcriptase-polymerase chain reaction (RT-PCR) on fine-needle aspirates for categorization of small blue round cell tumors (SBRCTs). A total of 51 cases, including 25 Ewing sarcoma/peripheral primitive neuroectodermal tumors (PNETs), 11 rhabdomyosarcomas, 13 neuroblastomas, and 2 desmoplastic small round cell tumors (DSRCTs) were analyzed. The detection of the EWS-FLI1 (20/25) and EWS-ERG (4/25) fusion transcripts resolved 24 of 25 cases of Ewing sarcoma/PNET"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10379685",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "Molecular detection of EWS-FLI1 chimeric transcripts in Ewing family tumors by nested reverse transcription-polymerase chain reaction"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16157025",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 197,
"text": "Molecular detection of EWS-Fli1 fusion transcripts in formalin-fixed paraffin-embedded material by nested RT-PCR is feasible and is useful for the diagnosis and differential diagnosis of ES/pPNETs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17154184",
"endSection": "abstract",
"offsetInBeginSection": 467,
"offsetInEndSection": 677,
"text": "RT-PCR confirmed that SK-NEP-1 expresses EWS-FLI1 gene fusion transcripts characteristic of Ewing sarcoma, and DNA sequencing demonstrated the joining of exon 7 of EWS with exon 5 of FLI1 for these transcripts."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23475435",
"endSection": "abstract",
"offsetInBeginSection": 834,
"offsetInEndSection": 937,
"text": "Reverse transcriptase-polymerase chain reaction confirmed the expression of EWS-FLI1 fusion transcripts"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24293381",
"endSection": "abstract",
"offsetInBeginSection": 199,
"offsetInEndSection": 626,
"text": "The aims of this study were (1) to present the diverse clinicopathological and molecular profile of EFTs in our settings, (2) to identify a pragmatic approach for diagnosing EFTs, especially for application of ancillary techniques, namely RT-PCR for specific transcripts (EWS-FLI1, EWS-ERG) and FISH for EWSR1 gene rearrangement, in certain cases and (3) to show the utility of tissue microarray in establishing a new FISH test"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15363317",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 156,
"text": "[Detection of EWS-FLI1 fusion transcript in Ewing's sarcoma/peripheral primitive neuroectodermal tumors by one-step RT-PCR using paraffin-embedded tissues]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16157025",
"endSection": "abstract",
"offsetInBeginSection": 1835,
"offsetInEndSection": 2032,
"text": "Molecular detection of EWS-Fli1 fusion transcripts in formalin-fixed paraffin-embedded material by nested RT-PCR is feasible and is useful for the diagnosis and differential diagnosis of ES/pPNETs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15565546",
"endSection": "abstract",
"offsetInBeginSection": 1751,
"offsetInEndSection": 2066,
"text": "We established a novel RT-PCR method, using 3 different exon specific sets of PCR primer pairs, selected according to the coding ews and fli1 nucleotide sequences (NCBI database), suitable for RT-PCR identification of variant ews/fli1 fusion transcripts in RNA isolated from formalin-fixed, paraffin-embedded tissue"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15363317",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 156,
"text": "[Detection of EWS-FLI1 fusion transcript in Ewing's sarcoma/peripheral primitive neuroectodermal tumors by one-step RT-PCR using paraffin-embedded tissues]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16157025",
"endSection": "abstract",
"offsetInBeginSection": 1835,
"offsetInEndSection": 2032,
"text": "Molecular detection of EWS-Fli1 fusion transcripts in formalin-fixed paraffin-embedded material by nested RT-PCR is feasible and is useful for the diagnosis and differential diagnosis of ES/pPNETs."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10379685",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 191,
"text": "Molecular detection of EWS-FLI1 chimeric transcripts in Ewing family tumors by nested reverse transcription-polymerase chain reaction: application to archival paraffin-embedded tumor tissues."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15363317",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 156,
"text": "[Detection of EWS-FLI1 fusion transcript in Ewing's sarcoma/peripheral primitive neuroectodermal tumors by one-step RT-PCR using paraffin-embedded tissues]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16157025",
"endSection": "abstract",
"offsetInBeginSection": 1835,
"offsetInEndSection": 2032,
"text": "Molecular detection of EWS-Fli1 fusion transcripts in formalin-fixed paraffin-embedded material by nested RT-PCR is feasible and is useful for the diagnosis and differential diagnosis of ES/pPNETs."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15363317",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 156,
"text": "[Detection of EWS-FLI1 fusion transcript in Ewing's sarcoma/peripheral primitive neuroectodermal tumors by one-step RT-PCR using paraffin-embedded tissues]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16157025",
"endSection": "abstract",
"offsetInBeginSection": 1835,
"offsetInEndSection": 2032,
"text": "Molecular detection of EWS-Fli1 fusion transcripts in formalin-fixed paraffin-embedded material by nested RT-PCR is feasible and is useful for the diagnosis and differential diagnosis of ES/pPNETs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15565546",
"endSection": "abstract",
"offsetInBeginSection": 1751,
"offsetInEndSection": 2066,
"text": "We established a novel RT-PCR method, using 3 different exon specific sets of PCR primer pairs, selected according to the coding ews and fli1 nucleotide sequences (NCBI database), suitable for RT-PCR identification of variant ews/fli1 fusion transcripts in RNA isolated from formalin-fixed, paraffin-embedded tissue"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15363317",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 156,
"text": "[Detection of EWS-FLI1 fusion transcript in Ewing's sarcoma/peripheral primitive neuroectodermal tumors by one-step RT-PCR using paraffin-embedded tissues]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16157025",
"endSection": "abstract",
"offsetInBeginSection": 1835,
"offsetInEndSection": 2032,
"text": "Molecular detection of EWS-Fli1 fusion transcripts in formalin-fixed paraffin-embedded material by nested RT-PCR is feasible and is useful for the diagnosis and differential diagnosis of ES/pPNETs."
}
] | 5 |
BioASQ-training5b
|
[] |
[] |
553653a5bc4f83e828000007
|
bioasq_factoid
|
factoid
|
Which database exists that contains regulatory SNPs which affect predicted transcription factor binding site affinity?
|
['SNP2TFBS']
|
[
"SNP2TFBS",
"SNP2TFBS database",
"SNP to Transcription Factor Binding Site"
] |
["SNP2TFBS is a computational resource intended to support researchers investigating the molecular mechanisms underlying regulatory variation in the human genome. The database essentially consists of a collection of text files providing specific annotations for human single nucleotide polymorphisms (SNPs), namely whether they are predicted to abolish, create or change the affinity of one or several transcription factor (TF) binding sites. A SNP's effect on TF binding is estimated based on a position weight matrix (PWM) model for the binding specificity of the corresponding factor.", 'SNP2TFBS is a computational resource intended to support researchers investigating the molecular mechanisms underlying regulatory variation in the human genome. The database essentially consists of a collection of text files providing specific annotations for human single nucleotide polymorphisms (SNPs), namely whether they are predicted to abolish, create or change the affinity of one or several transcription factor (TF) binding sites.', "SN2TFBS is a computational resource intended to support researchers investigating the molecular mechanisms underlying regulatory variation in the human genome. The database essentially consists of a collection of text files providing specific annotations for human single nucleotide polymorphisms (SNPs), namely whether they are predicted to abolish, create or change the affinity of one or several transcription factor (TF) binding sites. A SNP's effect on TF binding is estimated based on a position weight matrix (PWM) model for the binding specificity of the corresponding factor.", "SNP2TFBS is a computational resource intended to support researchers investigating the molecular mechanisms underlying regulatory variation in the human genome. The database essentially consists of a collection of text files providing specific annotations for human single nucleotide polymorphisms (SNPs), namely whether they are predicted to abolish, create or change the affinity of one or several transcription factor (TF) binding sites. A SNP's effect on TF binding is estimated based on a position weight matrix (PWM) model for the binding specificity of the corresponding factor. These data files are regenerated at regular intervals by an automatic procedure that takes as input a reference genome, a comprehensive SNP catalogue and a collection of PWMs. SNP2TFBS is also accessible over a web interface, enabling users to view the information provided for an individual SNP, to extract SNPs based on various search criteria, to annotate uploaded sets of SNPs or to display statistics about the frequencies of binding sites affected by selected SNPs."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27899579"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27899579",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "SNP2TFBS - a database of regulatory SNPs affecting predicted transcription factor binding site affinity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27899579",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1101,
"text": "SNP2TFBS is a computational resource intended to support researchers investigating the molecular mechanisms underlying regulatory variation in the human genome. The database essentially consists of a collection of text files providing specific annotations for human single nucleotide polymorphisms (SNPs), namely whether they are predicted to abolish, create or change the affinity of one or several transcription factor (TF) binding sites. A SNP's effect on TF binding is estimated based on a position weight matrix (PWM) model for the binding specificity of the corresponding factor. These data files are regenerated at regular intervals by an automatic procedure that takes as input a reference genome, a comprehensive SNP catalogue and a collection of PWMs. SNP2TFBS is also accessible over a web interface, enabling users to view the information provided for an individual SNP, to extract SNPs based on various search criteria, to annotate uploaded sets of SNPs or to display statistics about the frequencies of binding sites affected by selected SNPs. Homepage: http://ccg.vital-it.ch/snp2tfbs/."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27899579",
"endSection": "abstract",
"offsetInBeginSection": 762,
"offsetInEndSection": 1057,
"text": "SNP2TFBS is also accessible over a web interface, enabling users to view the information provided for an individual SNP, to extract SNPs based on various search criteria, to annotate uploaded sets of SNPs or to display statistics about the frequencies of binding sites affected by selected SNPs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27899579",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 160,
"text": "SNP2TFBS is a computational resource intended to support researchers investigating the molecular mechanisms underlying regulatory variation in the human genome."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27899579",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 103,
"text": "SNP2TFBS - a database of regulatory SNPs affecting predicted transcription factor binding site affinity"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27899579",
"endSection": "abstract",
"offsetInBeginSection": 762,
"offsetInEndSection": 1058,
"text": "SNP2TFBS is also accessible over a web interface, enabling users to view the information provided for an individual SNP, to extract SNPs based on various search criteria, to annotate uploaded sets of SNPs or to display statistics about the frequencies of binding sites affected by selected SNPs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27899579",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "SNP2TFBS is a computational resource intended to support researchers investigating the molecular mechanisms underlying regulatory variation in the human genome."
}
] | 11 |
BioASQ-training11b
| null | null |
5e49c2356d0a277941000010
|
bioasq_factoid
|
factoid
|
What is the target of the drug Olmesartan?
|
['angiotensin II receptor']
|
[
"angiotensin II receptor",
"AT1 receptor",
"Angiotensin II type 1 receptor",
"Angiotensin receptor",
"Angiotensin II type 1 angiotensin receptor",
"AGTR1"
] |
['Olmesartan (OL) is the pharmacologically active metabolite of Olmesartan medoxomil (OM), an FDA-approved angiotensin II receptor antagonist for administrating cardiovascular diseases']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29872491",
"http://www.ncbi.nlm.nih.gov/pubmed/29414040",
"http://www.ncbi.nlm.nih.gov/pubmed/30217371"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29414040",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 183,
"text": "Olmesartan (OL) is the pharmacologically active metabolite of Olmesartan medoxomil (OM), an FDA-approved angiotensin II receptor antagonist for administrating cardiovascular diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29872491",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 376,
"text": "Either angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor 1 blocker (ARB) attenuates cardiac remodeling. However, the overall molecular modulation of the reversing remodeling process in response to the ACEI or ARB treatment is not yet well determined. In this study, we examined whether gene expressions are modulated by ACEI (temocapril), ARB (olmesartan)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30217371",
"endSection": "abstract",
"offsetInBeginSection": 241,
"offsetInEndSection": 262,
"text": " ARB olmesartan (OLM)"
}
] | 11 |
BioASQ-training11b
| null | null |
5e808ef4835f4e477700002a
|
bioasq_factoid
|
factoid
|
Are most driver gene mutations synonymous or non-synonymous?
|
[['non-synonymous']]
|
[
"non-synonymous",
"non-synonymous mutation",
"non-synonymous substitution",
"missense mutation"
] |
['A common goal of tumor sequencing projects is finding genes whose mutations are selected for during tumor development. This is accomplished by choosing genes that have more non-synonymous mutations than expected from an estimated background mutation frequency.', 'A common goal of tumor sequencing projects is finding genes whose mutations are selected for during tumor development. This is accomplished by choosing genes that have more non-synonymous mutations than expected from an estimated background mutation frequency. ', 'A common goal of tumor sequencing projects is finding genes whose mutations are selected for during tumor development. This is accomplished by choosing genes that have more non-synonymous mutations than expected from an estimated background mutation frequency. ', 'A common goal of tumor sequencing projects is finding genes whose mutations are selected for during tumor development. This is accomplished by choosing genes that have more non-synonymous mutations than expected from an estimated background mutation frequency. ', 'A common goal of tumor sequencing projects is finding genes whose mutations are selected for during tumor development. This is accomplished by choosing genes that have more non-synonymous mutations than expected from an estimated background mutation frequency. ']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24147068",
"http://www.ncbi.nlm.nih.gov/pubmed/23935863",
"http://www.ncbi.nlm.nih.gov/pubmed/23819581",
"http://www.ncbi.nlm.nih.gov/pubmed/23799614",
"http://www.ncbi.nlm.nih.gov/pubmed/23704925",
"http://www.ncbi.nlm.nih.gov/pubmed/23694700",
"http://www.ncbi.nlm.nih.gov/pubmed/23450047",
"http://www.ncbi.nlm.nih.gov/pubmed/23015295",
"http://www.ncbi.nlm.nih.gov/pubmed/22893128",
"http://www.ncbi.nlm.nih.gov/pubmed/22649506",
"http://www.ncbi.nlm.nih.gov/pubmed/22072984",
"http://www.ncbi.nlm.nih.gov/pubmed/19633228",
"http://www.ncbi.nlm.nih.gov/pubmed/15946860"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24147068",
"endSection": "abstract",
"offsetInBeginSection": 1649,
"offsetInEndSection": 1869,
"text": "Therefore, this study highlights the need for multiple biopsies and sequencing during progression of a cancer and combinatorial DNA and RNA sequencing approach for systematic identification of expressed driver mutations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24147068",
"endSection": "abstract",
"offsetInBeginSection": 703,
"offsetInEndSection": 934,
"text": "Whole genome sequencing of the index liver metastasis identified 44 non-synonymous somatic mutations in 42 genes (0.85 mutation/MB) and a large hemizygous deletion in the ATRX gene which has been recently reported in neuroblastoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23935863",
"endSection": "abstract",
"offsetInBeginSection": 543,
"offsetInEndSection": 650,
"text": "In addition, we show that NetDiseaseSNP discriminates cancer driver and passenger mutations satisfactorily."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23935863",
"endSection": "abstract",
"offsetInBeginSection": 651,
"offsetInEndSection": 913,
"text": "Our method outperforms other state-of-the-art methods on several disease/neutral datasets as well as on cancer driver/passenger mutation datasets and can thus be used to pinpoint and prioritize plausible disease candidates among nsSNPs for further investigation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23819581",
"endSection": "abstract",
"offsetInBeginSection": 1411,
"offsetInEndSection": 1704,
"text": "Moreover, we find that a large fraction of the driver mutations are neither located in conserved functional sites, nor responsible for structural stability, but rather regulate protein activity through allosteric transitions, protein-protein interactions, or protein-nucleic acid interactions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23799614",
"endSection": "abstract",
"offsetInBeginSection": 128,
"offsetInEndSection": 239,
"text": "We used whole-exome sequencing to identify novel non-synonymous somatic mutations in squamous cell lung cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23799614",
"endSection": "abstract",
"offsetInBeginSection": 240,
"offsetInEndSection": 399,
"text": "We identified 101 single-nucleotide variants (SNVs) including 77 non-synonymous SNVs (67 missense and 10 nonsense mutations) and 11 INDELs causing frameshifts."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23704925",
"endSection": "abstract",
"offsetInBeginSection": 781,
"offsetInEndSection": 1066,
"text": "Besides confirming the presence of known melanoma driver mutations (BRAF(V600E), NRAS(Q61R) ), we identified novel mutated genes involved in signalling pathways crucial for melanoma pathogenesis and already addressed by current targeted therapies (such as MAPK and glutamate pathways)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23694700",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 260,
"text": "A common goal of tumor sequencing projects is finding genes whose mutations are selected for during tumor development. This is accomplished by choosing genes that have more non-synonymous mutations than expected from an estimated background mutation frequency."
}
] | 5 |
BioASQ-training5b
|
[
"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=D009369",
"http://www.disease-ontology.org/api/metadata/DOID:162"
] |
[] |
534427f8aeec6fbd07000009
|
bioasq_factoid
|
factoid
|
Which disease can be diagnosed with the "probe to bone" test?
|
['diabetic foot osteomyelitis']
|
[
"diabetic foot osteomyelitis",
"diabetic osteomyelitis",
"diabetic foot infection",
"osteomyelitis in diabetic foot",
"diabetic foot bone infection"
] |
['Probe-to-bone test is used for the diagnosis of diabetic foot osteomyelitis. The test has good sensitivity and specificity. Other diagnostic tests of diabetic foot osteomyelitis are plain films and magnetic resonance imaging.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28440774",
"http://www.ncbi.nlm.nih.gov/pubmed/20622159",
"http://www.ncbi.nlm.nih.gov/pubmed/27369321",
"http://www.ncbi.nlm.nih.gov/pubmed/17259493",
"http://www.ncbi.nlm.nih.gov/pubmed/26804367",
"http://www.ncbi.nlm.nih.gov/pubmed/18285592",
"http://www.ncbi.nlm.nih.gov/pubmed/21219428",
"http://www.ncbi.nlm.nih.gov/pubmed/26009740",
"http://www.ncbi.nlm.nih.gov/pubmed/24857262",
"http://www.ncbi.nlm.nih.gov/pubmed/23001730"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28440774",
"endSection": "abstract",
"offsetInBeginSection": 552,
"offsetInEndSection": 698,
"text": "Clinical inflammatory signs, probe-to-bone test, and plain X-rays are postulated as the basic tests for clinical diagnosis when DFO is suspected. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26804367",
"endSection": "abstract",
"offsetInBeginSection": 1596,
"offsetInEndSection": 1773,
"text": "In patients with a new DFU, we recommend probe to bone test and plain films to be followed by magnetic resonance imaging if a soft tissue abscess or osteomyelitis is suspected. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27369321",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 103,
"text": "Diagnostic Accuracy of Probe to Bone to Detect Osteomyelitis in the Diabetic Foot: A Systematic Review."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27369321",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 279,
"text": "The probe-to-bone (PTB) test is a commonly used clinical test for osteomyelitis (OM), but its utility has been questioned in clinical settings where the prevalence of OM is low. This article aims to systematically review the accuracy of the PTB test to diagnose diabetic foot OM."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27369321",
"endSection": "abstract",
"offsetInBeginSection": 602,
"offsetInEndSection": 878,
"text": "Pooled sensitivity and specificity for the PTB test was 0.87 (95% confidence interval [CI], .75-.93) and 0.83 (95% CI, .65-.93), respectively. We conclude that the PTB test can accurately rule in diabetic foot OM in the high-risk patients and rule out OM in low-risk patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24857262",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "Inter-observer reproducibility of diagnosis of diabetic foot osteomyelitis based on a combination of probe-to-bone test and simple radiography."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24857262",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 340,
"text": "Probe-to-bone test and simple X-rays are both standard tests for the diagnosis of diabetic foot osteomyelitis. This study demonstrates the importance of considering jointly clinical information (probe-to-bone test) and diagnostic tests (simple radiography) to increase agreement among clinicians on diagnosis of diabetic foot osteomyelitis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26009740",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 473,
"text": "Magnetic resonance imaging (MRI) has a higher sensitivity and specificity (90% and 79%) than plain radiography (54% and 68%) for diagnosing diabetic foot osteomyelitis. MRI performs somewhat better than any of several common tests--probe to bone (PTB), erythrocyte sedimentation rate (ESR)>70 mm/hr, C-reactive protein (CRP)>14 mg/L, procalcitonin>0.3 ng/mL, and ulcer size>2 cm²--although PTB has the highest specificity of any test and is commonly used together with MRI."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21219428",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 174,
"text": "AIMS: To investigate the accuracy of the sequential combination of the probe-to-bone test and plain X-rays for diagnosing osteomyelitis in the foot of patients with diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21219428",
"endSection": "abstract",
"offsetInBeginSection": 935,
"offsetInEndSection": 1149,
"text": "RESULTS: Overall, 72.4% of patients had histologically proven osteomyelitis, 85.2% of whom had positive bone culture. The performance characteristics of both the probe-to-bone test and plain X-rays were excellent. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21219428",
"endSection": "abstract",
"offsetInBeginSection": 1464,
"offsetInEndSection": 1745,
"text": "CONCLUSIONS: Clinicians seeing patients in a setting similar to ours (specialized diabetic foot unit with a high prevalence of osteomyelitis) can confidently diagnose diabetic foot osteomyelitis when either the probe-to-bone test or a plain X-ray, or especially both, are positive."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20622159",
"endSection": "abstract",
"offsetInBeginSection": 192,
"offsetInEndSection": 469,
"text": "The tests assessed were probe-to-bone (PTB), clinical signs of infection, radiography signs of osteomyelitis, and ulcer specimen culture.<br><b>RESEARCH DESIGN AND METHODS</b>: A prospective study was performed on patients with foot ulcers referred to our diabetic foot clinic."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20622159",
"endSection": "abstract",
"offsetInBeginSection": 1135,
"offsetInEndSection": 1720,
"text": "Among the tests compared, the best results were yielded by the PTB test including an efficiency of 94%, sensitivity of 98%, specificity of 78%, positive predictive value of 95%, and negative predictive value of 91% (P < 0.001, κ 0.803); the positive likelihood ratio was 4.41, and the negative likelihood ratio was 0.02 (95% CI).<br><b>CONCLUSIONS</b>: In our outpatient population with a high prevalence of osteomyelitis, the PTB test was of greatest diagnostic value, especially for neuropathic ulcers, and proved to be efficient for detecting osteomyelitis in the diabetic foot.<br>"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17259493",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 81,
"text": "Probe-to-bone test for diagnosing diabetic foot osteomyelitis: reliable or relic?"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27369321",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 82,
"text": "Diagnostic Accuracy of Probe to Bone to Detect Osteomyelitis in the Diabetic Foot:"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17259493",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 175,
"text": "OBJECTIVE: We sought to assess the accuracy of the probe-to-bone (PTB) test in diagnosing foot osteomyelitis in a cohort of diabetic patients with bone culture proven disease."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20622159",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 108,
"text": "Validating the probe-to-bone test and other tests for diagnosing chronic osteomyelitis in the diabetic foot."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18285592",
"endSection": "abstract",
"offsetInBeginSection": 2757,
"offsetInEndSection": 3022,
"text": "An ulcer area larger than 2 cm2, a positive probe-to-bone test result, an erythrocyte sedimentation rate of more than 70 mm/h, and an abnormal plain radiograph result are helpful in diagnosing the presence of lower extremity osteomyelitis in patients with diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27369321",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "The probe-to-bone (PTB) test is a commonly used clinical test for osteomyelitis (OM), but its utility has been questioned in clinical settings where the prevalence of OM is low."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21219428",
"endSection": "abstract",
"offsetInBeginSection": 1470,
"offsetInEndSection": 1750,
"text": "CONCLUSIONS Clinicians seeing patients in a setting similar to ours (specialized diabetic foot unit with a high prevalence of osteomyelitis) can confidently diagnose diabetic foot osteomyelitis when either the probe-to-bone test or a plain X-ray, or especially both, are positive."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21219428",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 173,
"text": "AIMS To investigate the accuracy of the sequential combination of the probe-to-bone test and plain X-rays for diagnosing osteomyelitis in the foot of patients with diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17259493",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 174,
"text": "OBJECTIVE We sought to assess the accuracy of the probe-to-bone (PTB) test in diagnosing foot osteomyelitis in a cohort of diabetic patients with bone culture proven disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23001730",
"endSection": "abstract",
"offsetInBeginSection": 1286,
"offsetInEndSection": 1681,
"text": "Wound area and depth were not found to be statistically significantly different between groups.<br><b>CONCLUSIONS</b>: Positive probe-to-bone test results and erythrocyte sedimentation rates greater than 70 mm/h provide some support for the diagnosis of diabetic foot osteomyelitis, but it is not strong; magnetic resonance imaging or bone biopsy will probably be required in cases of doubt.<br>"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23001730",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 629,
"text": "<b>BACKGROUND</b>: We investigated the validity of probe-to-bone testing in the diagnosis of osteomyelitis in a selected subgroup of patients clinically suspected of having diabetic foot osteomyelitis.<br><b>METHODS</b>: Between January 1, 2007, and December 31, 2008, inpatients and outpatients with a diabetic foot ulcer were prospectively evaluated, and those having a clinical diagnosis of foot infection and at least one of the osteomyelitis clinical suspicion criteria were consecutively included in this study.<br><b>RESULTS</b>: Sixty-five patients met the inclusion criteria and were prospectively enrolled in the study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17259493",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "We sought to assess the accuracy of the probe-to-bone (PTB) test in diagnosing foot osteomyelitis in a cohort of diabetic patients with bone culture proven disease."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17259493",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 82,
"text": "Probe-to-bone test for diagnosing diabetic foot osteomyelitis: reliable or relic?"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20622159",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 109,
"text": "Validating the probe-to-bone test and other tests for diagnosing chronic osteomyelitis in the diabetic foot."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21219428",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "Diagnosing diabetic foot osteomyelitis: is the combination of probe-to-bone test and plain radiography sufficient for high-risk inpatients?"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21219428",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 168,
"text": "To investigate the accuracy of the sequential combination of the probe-to-bone test and plain X-rays for diagnosing osteomyelitis in the foot of patients with diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21219428",
"endSection": "abstract",
"offsetInBeginSection": 1443,
"offsetInEndSection": 1712,
"text": "Clinicians seeing patients in a setting similar to ours (specialized diabetic foot unit with a high prevalence of osteomyelitis) can confidently diagnose diabetic foot osteomyelitis when either the probe-to-bone test or a plain X-ray, or especially both, are positive.."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24857262",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Probe-to-bone test and simple X-rays are both standard tests for the diagnosis of diabetic foot osteomyelitis."
}
] | 11 |
BioASQ-training11b
|
[
"https://meshb.nlm.nih.gov/record/ui?ui=D003933",
"https://meshb.nlm.nih.gov/record/ui?ui=D004194"
] | null |
5a6f853ab750ff4455000055
|
bioasq_factoid
|
factoid
|
What is the administration route of IVIG in Alzheimer's disease patients?
|
['Intravenous']
|
[
"Intravenous",
"IV",
"intra-venous",
"IV administration",
"intravenous therapy",
"intravenous injection"
] |
['IVIG is administered intravenously.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24760109"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24760109",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 138,
"text": "ntravenous immunoglobulin (IVIG) treatment exerts antioxidant and neuropreservatory effects in preclinical models of Alzheimer's disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24760109",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 271,
"text": "Intravenous immunoglobulin (IVIG) has shown limited promise so far in human clinical studies on Alzheimer's disease (AD), yet overwhelmingly positive preclinical work in animals and human brain cultures support the notion that the therapy remains potentially efficacious."
}
] | 11 |
BioASQ-training11b
| null | null |
5a7d51dafaa1ab7d2e000017
|
bioasq_factoid
|
factoid
|
What is evaluated with the SAD PERSONS scale?
|
['suicide risk']
|
[
"suicide risk",
"risk of suicide",
"suicidal risk",
"risk for suicide",
"suicidal ideation risk",
"risk of self-harm",
"self-harm risk"
] |
['SAD PERSONS scale was developed to evaluate suicide risk.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22795212",
"http://www.ncbi.nlm.nih.gov/pubmed/21546092",
"http://www.ncbi.nlm.nih.gov/pubmed/29699523",
"http://www.ncbi.nlm.nih.gov/pubmed/26346049",
"http://www.ncbi.nlm.nih.gov/pubmed/24533537",
"http://www.ncbi.nlm.nih.gov/pubmed/29665120",
"http://www.ncbi.nlm.nih.gov/pubmed/28471534",
"http://www.ncbi.nlm.nih.gov/pubmed/28302702",
"http://www.ncbi.nlm.nih.gov/pubmed/28723978",
"http://www.ncbi.nlm.nih.gov/pubmed/24884399"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29699523",
"endSection": "abstract",
"offsetInBeginSection": 330,
"offsetInEndSection": 582,
"text": "METHOD: We compared the predictive accuracy of the Manchester Self-Harm Rule (MSHR), ReACT Self-Harm Rule (ReACT), SAD PERSONS Scale (SPS) and Modified SAD PERSONS Scale (MSPS) in an unselected sample of patients attending hospital following self-harm."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29665120",
"endSection": "abstract",
"offsetInBeginSection": 359,
"offsetInEndSection": 653,
"text": "Clinicians completed a standard suicide risk instrument (modified SAD PERSONS scale), a 10-point Likert scale assessment of judgment of patient suicide risk (Clinician Prediction Scale), and a measure of their emotional responses to the patient (Therapist Response Questionnaire-Suicide Form). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28302702",
"endSection": "abstract",
"offsetInBeginSection": 133,
"offsetInEndSection": 412,
"text": "AimsTo evaluate the performance of risk scales (Manchester Self-Harm Rule, ReACT Self-Harm Rule, SAD PERSONS scale, Modified SAD PERSONS scale, Barratt Impulsiveness Scale); and patient and clinician estimates of risk in identifying patients who repeat self-harm within 6 months."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28471534",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 46,
"text": "Predicting suicide with the SAD PERSONS scale."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28471534",
"endSection": "abstract",
"offsetInBeginSection": 128,
"offsetInEndSection": 382,
"text": "The SAD PERSONS suicide risk assessment scale is widely implemented in clinical settings despite limited supporting evidence. This article aims to determine the ability of the SAD PERSONS scale (SPS) to predict future suicide in the emergency department."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28471534",
"endSection": "abstract",
"offsetInBeginSection": 1379,
"offsetInEndSection": 1603,
"text": "CONCLUSIONS: Although widely used in educational and clinical settings, these findings do not support the use of the SPS and Modified SPS to predict suicide in adults seen by psychiatric services in the emergency department."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28723978",
"endSection": "abstract",
"offsetInBeginSection": 867,
"offsetInEndSection": 1206,
"text": " For the outcome suicide attempt SAD PERSONS Scale had a sensitivity of 15% (95% CI 8-24) and specificity of 97% (96-98), and the Manchester Self-Harm Rule (MSHR) a sensitivity of 97% (97-97) and a specificity of 20% (20-21). ReACT, which is a modification of MSHR, had a similar low specificity, as did the Sodersjukhuset Self Harm Rule. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22795212",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "OBJECTIVE\nThe SAD PERSONS scale is a widely used risk assessment tool for suicidal behavior despite a paucity of supporting data."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22795212",
"endSection": "abstract",
"offsetInBeginSection": 1283,
"offsetInEndSection": 1442,
"text": "SAD PERSONS did not predict suicide attempts better than chance (area under the curve =0.572; 95% confidence interval [CI], 0.51-0.64; P value nonsignificant)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22795212",
"endSection": "abstract",
"offsetInBeginSection": 1780,
"offsetInEndSection": 1885,
"text": "CONCLUSION\nIn their current form, SAD PERSONS and MSPS do not accurately predict future suicide attempts."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24533537",
"endSection": "abstract",
"offsetInBeginSection": 1767,
"offsetInEndSection": 1896,
"text": "CONCLUSIONS\nThe Chinese SAD PERSONS Scale is a brief instrument with acceptable psychometric properties for self-harm prediction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28471534",
"endSection": "abstract",
"offsetInBeginSection": 127,
"offsetInEndSection": 252,
"text": "The SAD PERSONS suicide risk assessment scale is widely implemented in clinical settings despite limited supporting evidence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22795212",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "OBJECTIVE The SAD PERSONS scale is a widely used risk assessment tool for suicidal behavior despite a paucity of supporting data."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24533537",
"endSection": "abstract",
"offsetInBeginSection": 1767,
"offsetInEndSection": 1896,
"text": "CONCLUSIONS The Chinese SAD PERSONS Scale is a brief instrument with acceptable psychometric properties for self-harm prediction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24884399",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 108,
"text": "The SAD PERSONS scale (SPS) is widely used for suicide risk assessment in clinical and educational settings."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21546092",
"endSection": "abstract",
"offsetInBeginSection": 765,
"offsetInEndSection": 929,
"text": "Beck's Medical Lethality Scale (BMLS) was administered to assess the degree of medical injury, and the SAD PERSONS mnemonic scale was used to evaluate suicide risk."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24884399",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "The SAD PERSONS scale for suicide risk assessment: a systematic review.The SAD PERSONS scale (SPS) is widely used for suicide risk assessment in clinical and educational settings. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28471534",
"endSection": "abstract",
"offsetInBeginSection": 195,
"offsetInEndSection": 320,
"text": "The SAD PERSONS suicide risk assessment scale is widely implemented in clinical settings despite limited supporting evidence. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24533537",
"endSection": "abstract",
"offsetInBeginSection": 2048,
"offsetInEndSection": 2225,
"text": "<AbstractText Label=\"CONCLUSIONS\" NlmCategory=\"CONCLUSIONS\">The Chinese SAD PERSONS Scale is a brief instrument with acceptable psychometric properties for self-harm prediction. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22795212",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 255,
"text": "Predicting suicide attempts with the SAD PERSONS scale: a longitudinal analysis.<AbstractText Label=\"OBJECTIVE\" NlmCategory=\"OBJECTIVE\">The SAD PERSONS scale is a widely used risk assessment tool for suicidal behavior despite a paucity of supporting data. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28471534",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 194,
"text": "Predicting suicide with the SAD PERSONS scale.<AbstractText Label=\"BACKGROUND\">Suicide is a major public health issue, and a priority requirement is accurately identifying high-risk individuals. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26346049",
"endSection": "abstract",
"offsetInBeginSection": 528,
"offsetInEndSection": 720,
"text": "Subjects completed a series of depression/suicide screening tools: the Columbia Suicide Severity Scale, SAD PERSONS scale, Patient Health Questionnaire 9, and Beck Scale for Suicidal Ideation. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22795212",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 137,
"text": "<b>OBJECTIVE</b>: The SAD PERSONS scale is a widely used risk assessment tool for suicidal behavior despite a paucity of supporting data."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22795212",
"endSection": "abstract",
"offsetInBeginSection": 1051,
"offsetInEndSection": 1136,
"text": "Both SAD PERSONS and MSPS showed poor predictive ability for future suicide attempts."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22795212",
"endSection": "abstract",
"offsetInBeginSection": 1309,
"offsetInEndSection": 1468,
"text": "SAD PERSONS did not predict suicide attempts better than chance (area under the curve =0.572; 95% confidence interval [CI], 0.51-0.64; P value nonsignificant)."
}
] | 11 |
BioASQ-training11b
| null | null |
5c73ad027c78d6947100008d
|
bioasq_factoid
|
yesno
|
Is peritoneal dialysis the best option for infants with kidney failure?
|
['yes']
|
[
"yes"
] |
['Yes, peritoneal dialysis is often the preferred method for infants with kidney failure.', "Peritoneal dialysis (PD) is often considered the preferred option for infants with kidney failure. PD is a form of dialysis that uses the peritoneal membrane in the abdomen to remove waste products and excess fluid from the body. It is particularly suitable for infants because it can be performed at home, allowing for greater flexibility and minimizing the need for frequent hospital visits. PD also provides continuous dialysis, which can be beneficial for infants with unstable kidney function. However, the decision regarding the best dialysis option for infants should be made on an individual basis, taking into account factors such as the infant's overall health, the availability of resources, and the preferences of the parents or caregivers. It is important for the treating physician to carefully evaluate and discuss the various treatment options with the parents or caregivers to determine the most appropriate approach for each infant with kidney failure.", 'Peritoneal dialysis (PD), also known as automated peritoneal dialysis (APD), is indeed the most widely used method for chronic dialysis in children, especially in younger ones like infants. This method is often preferred because it can be done at home and is less disruptive to a child\'s daily routine. However, the "best" option can vary depending on the specific circumstances of the child, including their overall health, the severity of their kidney failure, and other individual factors. Therefore, while PD is a common and often effective choice, it\'s important to discuss all possible treatment options with a healthcare provider']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22371780",
"http://www.ncbi.nlm.nih.gov/pubmed/26591190",
"http://www.ncbi.nlm.nih.gov/pubmed/36449100",
"http://www.ncbi.nlm.nih.gov/pubmed/17990805",
"http://www.ncbi.nlm.nih.gov/pubmed/21907533",
"http://www.ncbi.nlm.nih.gov/pubmed/32063210",
"http://www.ncbi.nlm.nih.gov/pubmed/10723344",
"http://www.ncbi.nlm.nih.gov/pubmed/2739769",
"http://www.ncbi.nlm.nih.gov/pubmed/23350610",
"http://www.ncbi.nlm.nih.gov/pubmed/26438039",
"http://www.ncbi.nlm.nih.gov/pubmed/34648058",
"http://www.ncbi.nlm.nih.gov/pubmed/32063141",
"http://www.ncbi.nlm.nih.gov/pubmed/35589990",
"http://www.ncbi.nlm.nih.gov/pubmed/11998382"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36449100",
"endSection": "abstract",
"offsetInBeginSection": 48,
"offsetInEndSection": 83,
"text": "automated peritoneal dialysis (APD)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36449100",
"endSection": "abstract",
"offsetInBeginSection": 1703,
"offsetInEndSection": 1706,
"text": "APD"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36449100",
"endSection": "abstract",
"offsetInBeginSection": 1826,
"offsetInEndSection": 1828,
"text": "PD"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32063210",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 141,
"text": "Peritoneal dialysis (PD) remains the most widely used modality for chronic dialysis in children, particularly in younger children"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10723344",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Chronic ambulatory peritoneal dialysis (CAPD) is the treatment most often used in neonates and infants with chronic kidney failure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34648058",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 145,
"text": "BACKGROUND: Peritoneal dialysis (PD) is the preferred mode of kidney replacement therapy (KRT) in infants and young children with kidney failure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2739769",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 87,
"text": "Peritoneal dialysis remains the treatment of choice for acute renal failure in infancy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35589990",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Peritoneal dialysis is the most commonly prescribed dialysis modality for infants and young children with kidney failure worldwide."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11998382",
"endSection": "abstract",
"offsetInBeginSection": 282,
"offsetInEndSection": 419,
"text": "The authors demonstrate that peritoneal dialysis is an effective, safe, and available method for treating acute renal failure in infants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34648058",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 249,
"text": "BACKGROUND: Peritoneal dialysis (PD) is the preferred mode of kidney replacement therapy (KRT) in infants and young children with kidney failure. Hemodialysis (HD) is used less often due to the technical challenges and risk of complications in small"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17990805",
"endSection": "abstract",
"offsetInBeginSection": 1411,
"offsetInEndSection": 1636,
"text": "cannula, venous catheter).CONCLUSION: Peritoneal dialysis is the method of choice in newborns with acute renal failure, and it is used in the treatment of neonatal asphyxia till the restoration of kidney function is achieved."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26591190",
"endSection": "abstract",
"offsetInBeginSection": 2154,
"offsetInEndSection": 2241,
"text": "Peritoneal dialysis is the treatment of choice for infants with chronic kidney failure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21907533",
"endSection": "abstract",
"offsetInBeginSection": 364,
"offsetInEndSection": 504,
"text": "Peritoneal dialysis is the renal replacement therapy of choice, especially in children under 2 years, with an important risk of peritonitis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23350610",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Peritoneal dialysis (PD) is considered as the most common form of renal replacement therapy for newborns including preterms with acute kidney injury (AKI)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26438039",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 233,
"text": "BACKGROUND: Peritoneal dialysis is the preferred mode of renal replacement therapy in infants with end-stage renal disease (ESRD). Hemodialysis (HD) is seldom used in neonates and infants due to the risk of major complications in the"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34648058",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "BACKGROUND: Peritoneal dialysis (PD) is the preferred mode of kidney replacement therapy (KRT) in infants and young children with kid"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32063141",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "BACKGROUND: Peritoneal dialysis (PD) is the preferred modality of renal replacement therapy in children with end-stage renal dis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22371780",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 206,
"text": "INTRODUCTION: Peritoneal dialysis (PD) is a preferred method of renal replacement therapy for end-stage renal disease in children. Recent advances have allowed chronic PD to be provided to children of all a"
}
] | 13 |
BioASQ-training13b
| null | null |
65f86e06c4010b4d7800005a
|
bioasq_yesno
|
factoid
|
What are positive cell-cycle regulators that can cause cancer when mutated called?
|
['Proto-oncogenes']
|
[
"Proto-oncogenes",
"Proto-oncogene",
"Oncogenes",
"Oncogene",
"Cancer genes",
"Tumorigenic genes"
] |
['Proto-oncogenes are normal regulatory genes that can be transformed - by gain-of-function mutations - to oncogenes which are important contributors to human carcinogenesis.', 'Positive cell-cycle regulators that can cause cancer when mutated are called oncogenes. These genes are gain-of-function mutations of normal regulatory genes or proto-oncogenes, which are altered by point mutation, amplification or rearrangement. Oncogenes were originally discovered in retroviruses initiating a variety of animal and avian cancers, and they are believed to be important contributors to human carcinogenesis. When activated, oncogenes promote cell proliferation and inhibit apoptosis, leading to uncontrolled growth and tumor formation. Some examples of well-known oncogenes include HER2/neu, KRAS, BRAF, and MYC. Mutations in these genes have been implicated in various types of cancer such as breast cancer, lung cancer, melanoma, and leukemia. Understanding the role of oncogenes in cancer development is crucial for the development of targeted therapies aimed at inhibiting their activity and preventing tumor growth.', 'Oncogenes are gain-of-function mutations of normal regulatory genes or proto-oncogenes. Originally discovered in retroviruses initiating a variety of animal and avian cancers, oncogenes are believed to be important contributors to human carcinogenesis.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/12665054",
"http://www.ncbi.nlm.nih.gov/pubmed/1546217",
"http://www.ncbi.nlm.nih.gov/pubmed/8143345",
"http://www.ncbi.nlm.nih.gov/pubmed/10697588"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10697588",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 331,
"text": "Oncogenes are gain-of-function mutations of normal regulatory genes or proto-oncogenes. Originally discovered in retroviruses initiating a variety of animal and avian cancers, oncogenes are believed to be important contributors to human carcinogenesis. Proto-oncogenes are altered by point mutation, amplification or rearrangement."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12665054",
"endSection": "abstract",
"offsetInBeginSection": 340,
"offsetInEndSection": 599,
"text": "Aberrant proteolysis with oncogenic potential is elicited by two major mechanisms: defective degradation of positive cell cycle regulators (i.e., proto-oncoproteins) and enhanced degradation of negative cell cycle regulators (i.e., tumor suppressor proteins)."
}
] | 12 |
BioASQ-training12b
| null | null |
644ef46557b1c7a315000083
|
bioasq_factoid
|
factoid
|
What is targeted by CIS43LS?
|
['Plasmodium falciparum']
|
[
"Plasmodium falciparum",
"P. falciparum",
"malaria parasite",
"falciparum malaria",
"Plasmodium species",
"P. falciparum malaria"
] |
['CIS43LS is a monoclonal antibody that targets Plasmodium falciparum.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34379916",
"http://www.ncbi.nlm.nih.gov/pubmed/36317783",
"http://www.ncbi.nlm.nih.gov/pubmed/33332286"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36317783",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "BACKGROUND: CIS43LS is a monoclonal antibody that was shown to protect against controlled Plasmodium falciparum infection in a phase 1 clinical trial. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36317783",
"endSection": "abstract",
"offsetInBeginSection": 281,
"offsetInEndSection": 485,
"text": "METHODS: We conducted a phase 2 trial to assess the safety and efficacy of a single intravenous infusion of CIS43LS against P. falciparum infection in healthy adults in Mali over a 6-month malaria season."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36317783",
"endSection": "abstract",
"offsetInBeginSection": 1748,
"offsetInEndSection": 1887,
"text": "CONCLUSIONS: CIS43LS was protective against P. falciparum infection over a 6-month malaria season in Mali without evident safety concerns. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33332286",
"endSection": "abstract",
"offsetInBeginSection": 1150,
"offsetInEndSection": 1306,
"text": "Based on these data, CIS43LS has advanced to phase I clinical trials, and AAV delivery provides a potential next-generation approach for malaria prevention."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34379916",
"endSection": "abstract",
"offsetInBeginSection": 104,
"offsetInEndSection": 342,
"text": "METHODS: We conducted a two-part, phase 1 clinical trial to assess the safety and pharmacokinetics of CIS43LS, an antimalarial monoclonal antibody with an extended half-life, and its efficacy against infection with Plasmodium falciparum. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34379916",
"endSection": "abstract",
"offsetInBeginSection": 1910,
"offsetInEndSection": 2095,
"text": "CONCLUSIONS: Among adults who had never had malaria infection or vaccination, administration of the long-acting monoclonal antibody CIS43LS prevented malaria after controlled infection."
}
] | 12 |
BioASQ-training12b
| null | null |
63eeefc5f36125a426000009
|
bioasq_factoid
|
yesno
|
Is Iron deficiency anemia a common complication of chronic kidney disease?
|
['yes']
|
[
"yes"
] |
['iron deficiency anemia is common in patients with chronic kidney disease (CKD).', 'Iron deficiency anemia is a common complication of chronic kidney disease', 'Yes, Iron deficiency anemia is a common complication of chronic kidney disease.', 'Yes, iron deficiency anemia is a common complication in patients with chronic kidney disease, especially those requiring dialysis.', 'Yes, iron deficiency anemia is a common complication of chronic kidney disease due to reduced erythropoietin production and decreased red blood cell lifespan, leading to decreased hemoglobin levels.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/18824288",
"http://www.ncbi.nlm.nih.gov/pubmed/35644772",
"http://www.ncbi.nlm.nih.gov/pubmed/20630409",
"http://www.ncbi.nlm.nih.gov/pubmed/19325171",
"http://www.ncbi.nlm.nih.gov/pubmed/28682026",
"http://www.ncbi.nlm.nih.gov/pubmed/22935483",
"http://www.ncbi.nlm.nih.gov/pubmed/24432707",
"http://www.ncbi.nlm.nih.gov/pubmed/17533016",
"http://www.ncbi.nlm.nih.gov/pubmed/30970355",
"http://www.ncbi.nlm.nih.gov/pubmed/28372549",
"http://www.ncbi.nlm.nih.gov/pubmed/29533917",
"http://www.ncbi.nlm.nih.gov/pubmed/31614529",
"http://www.ncbi.nlm.nih.gov/pubmed/16198278",
"http://www.ncbi.nlm.nih.gov/pubmed/31464252",
"http://www.ncbi.nlm.nih.gov/pubmed/17804903",
"http://www.ncbi.nlm.nih.gov/pubmed/26342303",
"http://www.ncbi.nlm.nih.gov/pubmed/22303745",
"http://www.ncbi.nlm.nih.gov/pubmed/29336855",
"http://www.ncbi.nlm.nih.gov/pubmed/16949463",
"http://www.ncbi.nlm.nih.gov/pubmed/16164657",
"http://www.ncbi.nlm.nih.gov/pubmed/36166211",
"http://www.ncbi.nlm.nih.gov/pubmed/34514189",
"http://www.ncbi.nlm.nih.gov/pubmed/20126670",
"http://www.ncbi.nlm.nih.gov/pubmed/29696955",
"http://www.ncbi.nlm.nih.gov/pubmed/33123967",
"http://www.ncbi.nlm.nih.gov/pubmed/35058395",
"http://www.ncbi.nlm.nih.gov/pubmed/32762831",
"http://www.ncbi.nlm.nih.gov/pubmed/27236129",
"http://www.ncbi.nlm.nih.gov/pubmed/34860142",
"http://www.ncbi.nlm.nih.gov/pubmed/28412770",
"http://www.ncbi.nlm.nih.gov/pubmed/28403561",
"http://www.ncbi.nlm.nih.gov/pubmed/33516607",
"http://www.ncbi.nlm.nih.gov/pubmed/29481308",
"http://www.ncbi.nlm.nih.gov/pubmed/33842503",
"http://www.ncbi.nlm.nih.gov/pubmed/19833421",
"http://www.ncbi.nlm.nih.gov/pubmed/36165109",
"http://www.ncbi.nlm.nih.gov/pubmed/17106764",
"http://www.ncbi.nlm.nih.gov/pubmed/31477258",
"http://www.ncbi.nlm.nih.gov/pubmed/28153964",
"http://www.ncbi.nlm.nih.gov/pubmed/25468387",
"http://www.ncbi.nlm.nih.gov/pubmed/30675430",
"http://www.ncbi.nlm.nih.gov/pubmed/16470356",
"http://www.ncbi.nlm.nih.gov/pubmed/19776721",
"http://www.ncbi.nlm.nih.gov/pubmed/16893403",
"http://www.ncbi.nlm.nih.gov/pubmed/32556307",
"http://www.ncbi.nlm.nih.gov/pubmed/21684231"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36165109",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Intravenous iron therapy is increasingly being used worldwide to treat anemia in chronic kidney disease and more recently iron deficiency in heart failure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36166211",
"endSection": "abstract",
"offsetInBeginSection": 49,
"offsetInEndSection": 145,
"text": " iron deficiency in patients with chronic kidney disease (CKD), either with or without anaemia. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28153964",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "Iron deficiency, both functional and absolute, is common in patients with chronic kidney disease (CKD), especially those requiring dialysis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29533917",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "Treatment with iron preparations remains one of the main directions in the treatment of anemia in patients with chronic kidney disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33516607",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "This work presents an update on the management of iron deficiency in patients with chronic renal failure (CRF), either with or without anaemia."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33516607",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 101,
"text": "ron replacement therapy in the management of anaemia in non-dialysis chronic renal failure patients:"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30970355",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "Iron deficiency anemia is a common complication of chronic kidney disease (CKD)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30970355",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 49,
"text": "Iron Deficiency Anemia in Chronic Kidney Disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28372549",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "BACKGROUND: Iron deficiency anemia (IDA) is a common manifestation of chronic kidney disease (CKD), affecting most patients on hemodialysis and imposing a substantial clin"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21684231",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "Anemia is a common complication of chronic kidney disease (CKD) in predialysis stage."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27236129",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 88,
"text": "Anemia is a common and clinically important consequence of chronic kidney disease (CKD)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30970355",
"endSection": "abstract",
"offsetInBeginSection": 775,
"offsetInEndSection": 1022,
"text": "Among CKD patients, absolute iron deficiency is defined when the transferrin saturation (TSAT) is ≤20% and the serum ferritin concentration is ≤100 ng/mL among predialysis and peritoneal dialysis patients or ≤200 ng/mL among hemodialysis patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18824288",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "BACKGROUND: Iron deficiency anemia is a common complication in patients with chronic kidney di"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31477258",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "Iron deficiency anemia (IDA) is a frequent complication of chronic kidney disease (CKD) and is associated with adverse outcomes in these patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19776721",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Iron deficiency anemia is a common complication in end-stage renal disease (ESRD) and impairs the therapeutic efficacy of recombinant erythropoietin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30970355",
"endSection": "abstract",
"offsetInBeginSection": 424,
"offsetInEndSection": 502,
"text": "Anemia in CKD is associated with an increased risk of morbidity and mortality."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25468387",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 528,
"text": "BACKGROUND: Iron deficiency anemia and serum phosphate levels > 4.0mg/dL are relatively common in chronic kidney disease stages 3 to 5 and are associated with higher risks of progressive loss of kidney function, cardiovascular events, and mortality.STUDY DESIGN: Double-blind, placebo-controlled, randomized trial.SETTING & PARTICIPANTS: 149 patients with estimated glomerular filtration rates < 60 mL/min/1.73 m(2), iron deficiency anemia (hemoglobin, 9.0-12.0 g/dL; transferrin saturation [TSAT]≤ 30%, serum ferritin ≤ 300 ng/"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20630409",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Anemia resulting from iron and erythropoietin deficiencies is a common complication of advanced chronic kidney disease (CKD)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34514189",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 121,
"text": "Iron deficiency is common in individuals with chronic kidney disease and plays a major role in the development of anemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20126670",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "Iron deficiency anemia is a common occurrence in patients with chronic kidney disease and many patients do not respond well to supplementation with oral iron."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27236129",
"endSection": "abstract",
"offsetInBeginSection": 392,
"offsetInEndSection": 740,
"text": "However, the diagnosis of iron-deficiency anemia in CKD patients is complicated by the relatively poor predictive ability of easily obtained routine serum iron indices (eg, ferritin and transferrin saturation) and more invasive gold standard measures of iron deficiency (eg, bone marrow iron stores) or erythropoietic response to supplemental iron."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17106764",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Iron deficiency in patients with chronic kidney disease: potential role for intravenous iron therapy independent of erythropoietin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17804903",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 198,
"text": "Iron deficiency anemia is common in people with chronic kidney disease (CKD) and its importance in supporting erythropoiesis is unquestioned especially in those patients treated with erythropoietin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17533016",
"endSection": "abstract",
"offsetInBeginSection": 209,
"offsetInEndSection": 380,
"text": " Limited data suggest that iron deficiency is common in patients with chronic kidney disease with anemia; this lack of iron can hinder the effectiveness of erythropoiesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32556307",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 52,
"text": "Anemia is a frequent complication of kidney disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16949463",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 58,
"text": "Anemia is a common complication of chronic kidney disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29481308",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "Severe anemia and iron deficiency are common complications in chronic kidney disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17804903",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Iron deficiency anemia is common in people with chronic kidney disease (CKD) and its importance in supporting erythropoiesis is unquestioned especiall"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30970355",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Iron deficiency anemia is a common complication of chronic kidney disease (CKD). CKD patients suffer from both absolute and functional iron deficiency"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22303745",
"endSection": "abstract",
"offsetInBeginSection": 58,
"offsetInEndSection": 208,
"text": " diabetic nephropathy is a leading cause of CKD. One of the most common complications of CKD is anemia, the frequency and severity of which increase a"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16470356",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Anemia is as a frequent complication in patients with chronic kidney disease, which gains in importance in the treatment of patients with renal diseas"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29481308",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Severe anemia and iron deficiency are common complications in chronic kidney disease. The cause of renal anemia is multifactorial and includes decreas"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26342303",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Anemia is a common complication in patients with chronic kidney disease (CKD), mainly due to inadequate renal production of erythropoietin. In hemodia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19325171",
"endSection": "abstract",
"offsetInBeginSection": 316,
"offsetInEndSection": 466,
"text": "o anemia. The other cause of anemia is deficiency of iron. Iron deficiency anemia is common in people with CKD and its importance in supporting erythr"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16470356",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "Anemia is as a frequent complication in patients with chronic kidney disease, which gains in importance in the treatment of patients with renal disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35058395",
"endSection": "abstract",
"offsetInBeginSection": 223,
"offsetInEndSection": 373,
"text": " development and treat complications including anemia. Anemia is one of the common complication of chronic kidney disease (CKD), which is a significan"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35058395",
"endSection": "abstract",
"offsetInBeginSection": 748,
"offsetInEndSection": 1006,
"text": "The diagnosis of iron deficiency anemia in patients with CKD is complicated due to the relatively low predictive ability of routine serum iron markers (e.g., ferritin and transferrin saturation) and more invasive measurements such as bone marrow iron stores."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28682026",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Anemia is a frequent complication in chronic kidney disease (CKD), and it is often accompanied by various clinical symptoms. The primary cause of anem"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30970355",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Iron deficiency anemia is a common complication of chronic kidney disease (CKD). CKD patients suffer from both absolute and functional iron deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29336855",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 84,
"text": "Anemia is a frequent complication during the later stages of chronic kidney disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28403561",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "Anemia in chronic kidney disease is common and iron deficiency is an important cause."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28412770",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 32,
"text": "nemia in chronic kidney disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28412770",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 98,
"text": "nemia is common and associated with adverse outcomes in children with chronic kidney disease (CKD"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20126670",
"endSection": "title",
"offsetInBeginSection": 18,
"offsetInEndSection": 66,
"text": "e treatment of anemia in chronic kidney disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17106764",
"endSection": "abstract",
"offsetInBeginSection": 13,
"offsetInEndSection": 279,
"text": "he prevalence of iron deficiency and its contribution to the anemia of end stage renal disease has been extensively studied, but much less is known about the role of iron deficiency in the pathogenesis of the anemia of chronic kidney disease in predialysis patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19833421",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 47,
"text": "nemia in renal disease: diagnosis and manageme"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19325171",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "Anemia is a very common clinical problem in patients with chronic kidney disease (CKD) and is associated with increased morbidity and mortality in these patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19325171",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "Safety issues with intravenous iron products in the management of anemia in chronic kidney disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27236129",
"endSection": "abstract",
"offsetInBeginSection": 195,
"offsetInEndSection": 264,
"text": " Deciding on the appropriate treatment for anemia associated with CKD"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20630409",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 32,
"text": "nemia in chronic kidney disease"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29336855",
"endSection": "title",
"offsetInBeginSection": 10,
"offsetInEndSection": 50,
"text": "Anemia in ESRD and Earlier Stages of CKD"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28372549",
"endSection": "title",
"offsetInBeginSection": 3,
"offsetInEndSection": 40,
"text": " Ferumoxytol for Anemia of CKD Trial "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25468387",
"endSection": "title",
"offsetInBeginSection": 104,
"offsetInEndSection": 165,
"text": " anemia and reduction of serum phosphate in patients with CKD"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19833421",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 108,
"text": "Chronic kidney disease (CKD) is a widespread health problem in the world and anemia is a common complication"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29696955",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 89,
"text": "nemia in diabetic kidney disease - underappreciated but still clinically relevant proble"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16198278",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 46,
"text": "Anemia in children with chronic kidney disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16198278",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 112,
"text": "nemia in children with chronic kidney disease (CKD) is common secondary to inadequate erythropoietin production"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22935483",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 27,
"text": "echanisms of anemia in CKD"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22935483",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 64,
"text": "Anemia is a common feature of CKD associated with poor outcomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22935483",
"endSection": "abstract",
"offsetInBeginSection": 66,
"offsetInEndSection": 150,
"text": "he current management of patients with anemia in CKD is controversial, with recent c"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22935483",
"endSection": "abstract",
"offsetInBeginSection": 259,
"offsetInEndSection": 346,
"text": "Here, we examine recent insights into the molecular mechanisms underlying anemia of CKD"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31614529",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 65,
"text": "nemia of Inflammation with An Emphasis on Chronic Kidney Disease"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32762831",
"endSection": "title",
"offsetInBeginSection": 33,
"offsetInEndSection": 93,
"text": " Treatment of Anemia in Patients with Chronic Kidney Disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32762831",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 135,
"text": "nemia is a common complication of chronic kidney disease (CKD), and its prevalence has shown a tendency to increase in many countries."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16893403",
"endSection": "title",
"offsetInBeginSection": 2,
"offsetInEndSection": 81,
"text": "ythropoietin resistance in the treatment of the anemia of chronic renal failure"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16893403",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 122,
"text": "esistance to erythropoietin therapy is a common complication of the modern management of anemia in chronic kidney disease"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31464252",
"endSection": "title",
"offsetInBeginSection": 12,
"offsetInEndSection": 79,
"text": "spectrum of anemia in non-dialysis-dependent chronic kidney disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31464252",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 152,
"text": " retrospective study was conducted over seven years and it aimed to find out various causes of anemia among patients with chronic kidney disease (CKD)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16164657",
"endSection": "title",
"offsetInBeginSection": 4,
"offsetInEndSection": 89,
"text": "safety and efficacy of ferumoxytol therapy in anemic chronic kidney disease patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30675430",
"endSection": "title",
"offsetInBeginSection": 4,
"offsetInEndSection": 53,
"text": "options for the anemia of chronic kidney disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30675430",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 57,
"text": "nemia is a common complication of chronic kidney disease"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24432707",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 64,
"text": "Urology and nephrology update: anemia of chronic kidney disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24432707",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "Anemia is associated with chronic kidney disease (CKD) at all stages, and it is nearly universal among patients with stage 5 CKD"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33842503",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 34,
"text": "nemia in Chronic Kidney Disease: "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33842503",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 114,
"text": "nemia is a common complication in chronic kidney disease (CKD), and is associated with a reduced quality of life,"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34860142",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Anemia and its predictors among adult non-dialysis chronic kidney disease patients in Southern Ethiopia: a cross-sectional study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34860142",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 98,
"text": "Anemia is an adverse outcome and common complication in chronic kidney disease patient"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35644772",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 162,
"text": "Prevalence of malnutrition and absolute and functional iron deficiency anemia in nondialysis-dependent chronic kidney disease and hemodialysis Algerian patients]"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35644772",
"endSection": "abstract",
"offsetInBeginSection": 2,
"offsetInEndSection": 178,
"text": " chronic kidney disease, anemia and malnutrition coupled with inflammation as malnutrition-inflammation complex syndrom are common and considered as morbidity-mortality factors"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33123967",
"endSection": "title",
"offsetInBeginSection": 8,
"offsetInEndSection": 65,
"text": "f Anemia in Chronic Kidney Disease: Beyond Erythropoietin"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33123967",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 65,
"text": "nemia is a frequent comorbidity of chronic kidney disease (CKD) "
}
] | 12 |
BioASQ-training12b
| null | null |
641365f6201352f04a00003a
|
bioasq_yesno
|
factoid
|
Which enzyme is inhibited by Orteronel?
|
[['CYP17A1']]
|
[
"CYP17A1",
"Cytochrome P450 17A1",
"Steroid 17-alpha-hydroxylase",
"17-alpha-hydroxylase/17,20-lyase",
"CYP17",
"CYP17A",
"P450c17"
] |
['Orteronel inhibits the 17,20 lyase activity of the enzyme CYP17A1, which is important for androgen synthesis in the testes, adrenal glands and prostate cancer cells. Orteronel is used for treatment for castration-resistant prostate cancer.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25537627",
"http://www.ncbi.nlm.nih.gov/pubmed/25533464",
"http://www.ncbi.nlm.nih.gov/pubmed/25297456",
"http://www.ncbi.nlm.nih.gov/pubmed/25264242",
"http://www.ncbi.nlm.nih.gov/pubmed/24965748",
"http://www.ncbi.nlm.nih.gov/pubmed/24844235",
"http://www.ncbi.nlm.nih.gov/pubmed/24799061",
"http://www.ncbi.nlm.nih.gov/pubmed/24759590",
"http://www.ncbi.nlm.nih.gov/pubmed/24418642",
"http://www.ncbi.nlm.nih.gov/pubmed/24314737",
"http://www.ncbi.nlm.nih.gov/pubmed/24276076",
"http://www.ncbi.nlm.nih.gov/pubmed/23880851",
"http://www.ncbi.nlm.nih.gov/pubmed/23856460",
"http://www.ncbi.nlm.nih.gov/pubmed/23788266",
"http://www.ncbi.nlm.nih.gov/pubmed/23371447",
"http://www.ncbi.nlm.nih.gov/pubmed/23146910",
"http://www.ncbi.nlm.nih.gov/pubmed/22249003",
"http://www.ncbi.nlm.nih.gov/pubmed/21978946"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25537627",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "PURPOSE: Orteronel (TAK-700) is a non-steroidal, selective, reversible inhibitor of 17,20-lyase."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25533464",
"endSection": "abstract",
"offsetInBeginSection": 883,
"offsetInEndSection": 984,
"text": "The drug orteronel selectively blocked the lyase reaction of P450 17A1 but only in the case of Prog. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25297456",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 75,
"text": "Preclinical assessment of Orteronel(®), a CYP17A1 enzyme inhibitor in rats."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25297456",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "Orteronel (TAK-700) is a novel and selective inhibitor of CYP17A1, which is expressed in testicular, adrenal and prostate tumor tissues."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25264242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "Orteronel is a nonsteroidal, selective inhibitor of 17,20-lyase that was recently in phase 3 clinical development as a treatment for castration-resistant prostate cancer. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25264242",
"endSection": "abstract",
"offsetInBeginSection": 244,
"offsetInEndSection": 480,
"text": "Human liver microsomal studies indicated that orteronel weakly inhibits CYP1A2, 2C8, 2C9 and 2C19, with IC50 values of 17.8, 27.7, 30.8 and 38.8 µm, respectively, whereas orteronel does not inhibit CYP2B6, 2D6 or 3A4/5 (IC50 > 100 µm)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24965748",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "PURPOSE: Orteronel (TAK-700) is an investigational, nonsteroidal, oral, inhibitor of androgen synthesis with greater specificity for 17,20-lyase than for 17α-hydroxylase."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24844235",
"endSection": "abstract",
"offsetInBeginSection": 425,
"offsetInEndSection": 705,
"text": "Based on these observations, potent agents targeting the AR axis were developed: 1) inhibitors of CYP17 (a key enzyme in the production of androgens), such as abiraterone and orteronel; 2) AR antagonists that bind to AR and impair AR activation, such as enzalutamide and ARN-509. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24799061",
"endSection": "abstract",
"offsetInBeginSection": 129,
"offsetInEndSection": 295,
"text": "Orteronel inhibits the 17,20 lyase activity of the enzyme CYP17A1, which is important for androgen synthesis in the testes, adrenal glands and prostate cancer cells. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24759590",
"endSection": "abstract",
"offsetInBeginSection": 908,
"offsetInEndSection": 1309,
"text": "Inhibition of 17α-hydroxylase by abiraterone results in accumulation of upstream mineralocorticoids due to loss of cortisol-mediated suppression of pituitary adrenocorticotropic hormone (ACTH), providing a rationale for development of CYP17 inhibitors with increased specificity for 17,20-lyase (orteronel, galeterone and VT-464) that can potentially be administered without exogenous corticosteroids."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24418642",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 148,
"text": "Phase I/II trial of orteronel (TAK-700)--an investigational 17,20-lyase inhibitor--in patients with metastatic castration-resistant prostate cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24418642",
"endSection": "abstract",
"offsetInBeginSection": 153,
"offsetInEndSection": 319,
"text": "Orteronel (TAK-700) is an investigational, oral, nonsteroidal, selective, reversible inhibitor of 17,20-lyase, a key enzyme in the production of androgenic hormones. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24314737",
"endSection": "abstract",
"offsetInBeginSection": 688,
"offsetInEndSection": 833,
"text": "Hence, some molecules target the androgen biosynthesis, as abiraterone acetate and orteronel, which are selective inhibitors of the enzyme CYP17."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24276076",
"endSection": "abstract",
"offsetInBeginSection": 1274,
"offsetInEndSection": 1667,
"text": "To achieve enhanced clinical benefits, new strategies are being explored that include selective inhibition of the C17,20-lyase activity of CYP17 and multi-targeting strategies that affect androgen synthesis and signalling at different points. Some of these strategies-including the drugs orteronel, VT-464 and galeterone--are supported by preclinical data and are being explored in the clinic."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23880851",
"endSection": "abstract",
"offsetInBeginSection": 559,
"offsetInEndSection": 943,
"text": "Besides further CYP17 inhibitors (Orteronel, Galeterone, VT-464 and CFG920), androgen receptor antagonists (ARN-509, ODM-201, AZD-3514 and EZN-4176) and vaccine Prostvac, more drug candidates with various mechanisms or new indications of launched drugs are currently under evaluation in different stages of clinical trials, including various kinase inhibitors and platinum complexes. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23856460",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 211,
"text": "Effect of an investigational CYP17A1 inhibitor, orteronel (TAK-700), on estrogen- and corticoid-synthesis pathways in hypophysectomized female rats and on the serum estradiol levels in female cynomolgus monkeys."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23856460",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "Orteronel (TAK-700) is an investigational, non-steroidal inhibitor of CYP17A1 with preferential inhibition of 17,20-lyase in NCI-H295 cells. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23856460",
"endSection": "abstract",
"offsetInBeginSection": 1896,
"offsetInEndSection": 2171,
"text": "In summary, orteronel can suppress serum estradiol concentrations in hypophysectomized female rats and monkeys through selective inhibition of CYP17A1 activity, suggesting that orteronel might be effective for hormone-dependent breast cancers and estrogen-dependent diseases."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23788266",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 182,
"text": "Development and validation of an RP-HPLC method for the quantitation of Orteronel (TAK-700), a CYP17A1 enzyme inhibitor, in rat plasma and its application to a pharmacokinetic study."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23371447",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 132,
"text": "Targeting the adrenal gland in castration-resistant prostate cancer: a case for orteronel, a selective CYP-17 17,20-lyase inhibitor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23371447",
"endSection": "abstract",
"offsetInBeginSection": 769,
"offsetInEndSection": 966,
"text": "A new CYP17 inhibitor, with more selective inhibition of 17,20-lyase over 17α-hydroxylase, orteronel (TAK-700), is currently undergoing phase III clinical trials in pre- and postchemotherapy CRPC. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23146910",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 97,
"text": "Effect of a novel 17,20-lyase inhibitor, orteronel (TAK-700), on androgen synthesis in male rats."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23146910",
"endSection": "abstract",
"offsetInBeginSection": 181,
"offsetInEndSection": 472,
"text": "Orteronel (TAK-700), 6-[(7S)-7-hydroxy-6,7-dihydro-5H-pyrrolo[1,2-c]imidazol-7-yl]-N-methyl-2-naphthamide, is a novel, non-steroidal, selective inhibitor of the 17,20-lyase activity of CYP17A--a key enzyme in the production of steroidal hormones--and is being developed as a therapy for PC. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23146910",
"endSection": "abstract",
"offsetInBeginSection": 703,
"offsetInEndSection": 890,
"text": "Orteronel inhibited 17,20-lyase activity in rats with an IC(50) of 1200 nM but did not inhibit 17α-hydroxylase or 11β-hydroxylase (CYP11B1) activity in rats at concentrations up to 10 μM."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22249003",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "Orteronel (TAK-700), a novel non-steroidal 17,20-lyase inhibitor: effects on steroid synthesis in human and monkey adrenal cells and serum steroid levels in cynomolgus monkeys."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22249003",
"endSection": "abstract",
"offsetInBeginSection": 989,
"offsetInEndSection": 1532,
"text": "Orteronel (TAK-700), a novel, selective, and potent inhibitor of 17,20-lyase is under development as a drug to inhibit androgen synthesis. In this study, we quantified the inhibitory activity and specificity of orteronel for testicular and adrenal androgen production by evaluating its effects on CYP17A1 enzymatic activity, steroid production in monkey adrenal cells and human adrenal tumor cells, and serum levels of dehydroepiandrosterone (DHEA), cortisol, and testosterone after oral dosing in castrated and intact male cynomolgus monkeys."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22249003",
"endSection": "abstract",
"offsetInBeginSection": 2589,
"offsetInEndSection": 2738,
"text": " In summary, orteronel potently inhibited the 17,20-lyase activity of monkey and human CYP17A1 and reduced serum androgen levels in vivo in monkeys. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21978946",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 175,
"text": "Discovery of orteronel (TAK-700), a naphthylmethylimidazole derivative, as a highly selective 17,20-lyase inhibitor with potential utility in the treatment of prostate cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23146910",
"endSection": "abstract",
"offsetInBeginSection": 181,
"offsetInEndSection": 702,
"text": "Orteronel (TAK-700), 6-[(7S)-7-hydroxy-6,7-dihydro-5H-pyrrolo[1,2-c]imidazol-7-yl]-N-methyl-2-naphthamide, is a novel, non-steroidal, selective inhibitor of the 17,20-lyase activity of CYP17A--a key enzyme in the production of steroidal hormones--and is being developed as a therapy for PC. The purpose of this study was to elucidate the inhibitory activity of orteronel, in particular its specificity for androgen synthesis enzymes, in male rats--an androgen-synthesis model that largely reflects this pathway in humans."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22249003",
"endSection": "abstract",
"offsetInBeginSection": 2195,
"offsetInEndSection": 2587,
"text": "In terms of human CYP17A1 and human adrenal tumor cells, orteronel inhibited 17,20-lyase activity 5.4 times more potently than 17-hydroxylase activity in cell-free enzyme assays and DHEA production 27 times more potently than cortisol production in human adrenal tumor cells, suggesting greater specificity of inhibition between 17,20-lyase and 17-hydroxylase activities in humans vs monkeys."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22249003",
"endSection": "abstract",
"offsetInBeginSection": 2588,
"offsetInEndSection": 2735,
"text": "In summary, orteronel potently inhibited the 17,20-lyase activity of monkey and human CYP17A1 and reduced serum androgen levels in vivo in monkeys."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25537627",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "PURPOSE: Orteronel (TAK-700) is a non-steroidal, selective, reversible inhibitor of 17,20-lyase."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25297456",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 134,
"text": "Orteronel (TAK-700) is a novel and selective inhibitor of CYP17A1, which is expressed in testicular, adrenal and prostate tumor tissues"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24799061",
"endSection": "abstract",
"offsetInBeginSection": 128,
"offsetInEndSection": 292,
"text": "Orteronel inhibits the 17,20 lyase activity of the enzyme CYP17A1, which is important for androgen synthesis in the testes, adrenal glands and prostate cancer cells"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22249003",
"endSection": "abstract",
"offsetInBeginSection": 988,
"offsetInEndSection": 1125,
"text": "Orteronel (TAK-700), a novel, selective, and potent inhibitor of 17,20-lyase is under development as a drug to inhibit androgen synthesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22249003",
"endSection": "abstract",
"offsetInBeginSection": 2590,
"offsetInEndSection": 2736,
"text": "In summary, orteronel potently inhibited the 17,20-lyase activity of monkey and human CYP17A1 and reduced serum androgen levels in vivo in monkeys"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23146910",
"endSection": "abstract",
"offsetInBeginSection": 703,
"offsetInEndSection": 889,
"text": "Orteronel inhibited 17,20-lyase activity in rats with an IC(50) of 1200 nM but did not inhibit 17α-hydroxylase or 11β-hydroxylase (CYP11B1) activity in rats at concentrations up to 10 μM"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22249003",
"endSection": "abstract",
"offsetInBeginSection": 2197,
"offsetInEndSection": 2588,
"text": "In terms of human CYP17A1 and human adrenal tumor cells, orteronel inhibited 17,20-lyase activity 5.4 times more potently than 17-hydroxylase activity in cell-free enzyme assays and DHEA production 27 times more potently than cortisol production in human adrenal tumor cells, suggesting greater specificity of inhibition between 17,20-lyase and 17-hydroxylase activities in humans vs monkeys"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23856460",
"endSection": "abstract",
"offsetInBeginSection": 1896,
"offsetInEndSection": 2170,
"text": "In summary, orteronel can suppress serum estradiol concentrations in hypophysectomized female rats and monkeys through selective inhibition of CYP17A1 activity, suggesting that orteronel might be effective for hormone-dependent breast cancers and estrogen-dependent diseases"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22249003",
"endSection": "abstract",
"offsetInBeginSection": 2590,
"offsetInEndSection": 2736,
"text": "In summary, orteronel potently inhibited the 17,20-lyase activity of monkey and human CYP17A1 and reduced serum androgen levels in vivo in monkeys"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23146910",
"endSection": "abstract",
"offsetInBeginSection": 703,
"offsetInEndSection": 889,
"text": "Orteronel inhibited 17,20-lyase activity in rats with an IC(50) of 1200 nM but did not inhibit 17α-hydroxylase or 11β-hydroxylase (CYP11B1) activity in rats at concentrations up to 10 μM"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22249003",
"endSection": "abstract",
"offsetInBeginSection": 2197,
"offsetInEndSection": 2588,
"text": "In terms of human CYP17A1 and human adrenal tumor cells, orteronel inhibited 17,20-lyase activity 5.4 times more potently than 17-hydroxylase activity in cell-free enzyme assays and DHEA production 27 times more potently than cortisol production in human adrenal tumor cells, suggesting greater specificity of inhibition between 17,20-lyase and 17-hydroxylase activities in humans vs monkeys"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24314737",
"endSection": "abstract",
"offsetInBeginSection": 644,
"offsetInEndSection": 788,
"text": "Hence, some molecules target the androgen biosynthesis, as abiraterone acetate and orteronel, which are selective inhibitors of the enzyme CYP17"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24418642",
"endSection": "abstract",
"offsetInBeginSection": 144,
"offsetInEndSection": 309,
"text": "Orteronel (TAK-700) is an investigational, oral, nonsteroidal, selective, reversible inhibitor of 17,20-lyase, a key enzyme in the production of androgenic hormones."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23788266",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 182,
"text": "Development and validation of an RP-HPLC method for the quantitation of Orteronel (TAK-700), a CYP17A1 enzyme inhibitor, in rat plasma and its application to a pharmacokinetic study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23856460",
"endSection": "abstract",
"offsetInBeginSection": 1896,
"offsetInEndSection": 2170,
"text": "In summary, orteronel can suppress serum estradiol concentrations in hypophysectomized female rats and monkeys through selective inhibition of CYP17A1 activity, suggesting that orteronel might be effective for hormone-dependent breast cancers and estrogen-dependent diseases"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22249003",
"endSection": "abstract",
"offsetInBeginSection": 2590,
"offsetInEndSection": 2736,
"text": "In summary, orteronel potently inhibited the 17,20-lyase activity of monkey and human CYP17A1 and reduced serum androgen levels in vivo in monkeys"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23146910",
"endSection": "abstract",
"offsetInBeginSection": 703,
"offsetInEndSection": 889,
"text": "Orteronel inhibited 17,20-lyase activity in rats with an IC(50) of 1200 nM but did not inhibit 17α-hydroxylase or 11β-hydroxylase (CYP11B1) activity in rats at concentrations up to 10 μM"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22249003",
"endSection": "abstract",
"offsetInBeginSection": 2197,
"offsetInEndSection": 2588,
"text": "In terms of human CYP17A1 and human adrenal tumor cells, orteronel inhibited 17,20-lyase activity 5.4 times more potently than 17-hydroxylase activity in cell-free enzyme assays and DHEA production 27 times more potently than cortisol production in human adrenal tumor cells, suggesting greater specificity of inhibition between 17,20-lyase and 17-hydroxylase activities in humans vs monkeys"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24314737",
"endSection": "abstract",
"offsetInBeginSection": 644,
"offsetInEndSection": 788,
"text": "Hence, some molecules target the androgen biosynthesis, as abiraterone acetate and orteronel, which are selective inhibitors of the enzyme CYP17"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24418642",
"endSection": "abstract",
"offsetInBeginSection": 144,
"offsetInEndSection": 309,
"text": "Orteronel (TAK-700) is an investigational, oral, nonsteroidal, selective, reversible inhibitor of 17,20-lyase, a key enzyme in the production of androgenic hormones."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23788266",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 182,
"text": "Development and validation of an RP-HPLC method for the quantitation of Orteronel (TAK-700), a CYP17A1 enzyme inhibitor, in rat plasma and its application to a pharmacokinetic study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23856460",
"endSection": "abstract",
"offsetInBeginSection": 1896,
"offsetInEndSection": 2170,
"text": "In summary, orteronel can suppress serum estradiol concentrations in hypophysectomized female rats and monkeys through selective inhibition of CYP17A1 activity, suggesting that orteronel might be effective for hormone-dependent breast cancers and estrogen-dependent diseases"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22249003",
"endSection": "abstract",
"offsetInBeginSection": 2590,
"offsetInEndSection": 2736,
"text": "In summary, orteronel potently inhibited the 17,20-lyase activity of monkey and human CYP17A1 and reduced serum androgen levels in vivo in monkeys"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23146910",
"endSection": "abstract",
"offsetInBeginSection": 703,
"offsetInEndSection": 889,
"text": "Orteronel inhibited 17,20-lyase activity in rats with an IC(50) of 1200 nM but did not inhibit 17α-hydroxylase or 11β-hydroxylase (CYP11B1) activity in rats at concentrations up to 10 μM"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24314737",
"endSection": "abstract",
"offsetInBeginSection": 644,
"offsetInEndSection": 788,
"text": "Hence, some molecules target the androgen biosynthesis, as abiraterone acetate and orteronel, which are selective inhibitors of the enzyme CYP17"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24418642",
"endSection": "abstract",
"offsetInBeginSection": 144,
"offsetInEndSection": 309,
"text": "Orteronel (TAK-700) is an investigational, oral, nonsteroidal, selective, reversible inhibitor of 17,20-lyase, a key enzyme in the production of androgenic hormones."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22249003",
"endSection": "abstract",
"offsetInBeginSection": 2197,
"offsetInEndSection": 2588,
"text": "In terms of human CYP17A1 and human adrenal tumor cells, orteronel inhibited 17,20-lyase activity 5.4 times more potently than 17-hydroxylase activity in cell-free enzyme assays and DHEA production 27 times more potently than cortisol production in human adrenal tumor cells, suggesting greater specificity of inhibition between 17,20-lyase and 17-hydroxylase activities in humans vs monkeys"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23788266",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 182,
"text": "Development and validation of an RP-HPLC method for the quantitation of Orteronel (TAK-700), a CYP17A1 enzyme inhibitor, in rat plasma and its application to a pharmacokinetic study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23856460",
"endSection": "abstract",
"offsetInBeginSection": 1896,
"offsetInEndSection": 2170,
"text": "In summary, orteronel can suppress serum estradiol concentrations in hypophysectomized female rats and monkeys through selective inhibition of CYP17A1 activity, suggesting that orteronel might be effective for hormone-dependent breast cancers and estrogen-dependent diseases"
}
] | 5 |
BioASQ-training5b
|
[] |
[] |
54e0c3e71388e8454a000013
|
bioasq_factoid
|
factoid
|
Which molecule is targeted by Upadacitinib?
|
['Janus kinase 1']
|
[
"Janus kinase 1",
"JAK1",
"JAK-1",
"Janus kinase-1",
"Janus kinase 1 (JAK1)"
] |
['Upadacitinib is a Janus kinase 1 inhibitor developed for treatment of moderate to severe rheumatoid arthritis.', 'Upadacitinib is a Janus kinase 1 inhibitor under development for the treatment of several inflammatory disorders including rheumatoid arthritis.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/31287230",
"http://www.ncbi.nlm.nih.gov/pubmed/31781755",
"http://www.ncbi.nlm.nih.gov/pubmed/31867699",
"http://www.ncbi.nlm.nih.gov/pubmed/29688617",
"http://www.ncbi.nlm.nih.gov/pubmed/31130260",
"http://www.ncbi.nlm.nih.gov/pubmed/30973649",
"http://www.ncbi.nlm.nih.gov/pubmed/31654328",
"http://www.ncbi.nlm.nih.gov/pubmed/31448433",
"http://www.ncbi.nlm.nih.gov/pubmed/31692920",
"http://www.ncbi.nlm.nih.gov/pubmed/31317509",
"http://www.ncbi.nlm.nih.gov/pubmed/31378969",
"http://www.ncbi.nlm.nih.gov/pubmed/32648334",
"http://www.ncbi.nlm.nih.gov/pubmed/32776305",
"http://www.ncbi.nlm.nih.gov/pubmed/32044319",
"http://www.ncbi.nlm.nih.gov/pubmed/31786154",
"http://www.ncbi.nlm.nih.gov/pubmed/28762476",
"http://www.ncbi.nlm.nih.gov/pubmed/30633369",
"http://www.ncbi.nlm.nih.gov/pubmed/29908670",
"http://www.ncbi.nlm.nih.gov/pubmed/28503781",
"http://www.ncbi.nlm.nih.gov/pubmed/31401212",
"http://www.ncbi.nlm.nih.gov/pubmed/33129109",
"http://www.ncbi.nlm.nih.gov/pubmed/30725185",
"http://www.ncbi.nlm.nih.gov/pubmed/31327403",
"http://www.ncbi.nlm.nih.gov/pubmed/30394138",
"http://www.ncbi.nlm.nih.gov/pubmed/29672874",
"http://www.ncbi.nlm.nih.gov/pubmed/29908669",
"http://www.ncbi.nlm.nih.gov/pubmed/29076110",
"http://www.ncbi.nlm.nih.gov/pubmed/30886973",
"http://www.ncbi.nlm.nih.gov/pubmed/28765121",
"http://www.ncbi.nlm.nih.gov/pubmed/30500075",
"http://www.ncbi.nlm.nih.gov/pubmed/32530345"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28765121",
"endSection": "abstract",
"offsetInBeginSection": 1255,
"offsetInEndSection": 1554,
"text": "We summarise the development and recent application of Janus kinase (JAK) inhibitors in the treatment of IMIDs, including first-generation pan-JAK inhibitors (tofacitinib, baricitinib, ruxolitinib, peficitinib) and second-generation selective JAK inhibitors (decernotinib, filgotinib, upadacitinib)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28762476",
"endSection": "abstract",
"offsetInBeginSection": 353,
"offsetInEndSection": 463,
"text": "Upadacitinib is a Janus kinase 1 inhibitor currently being evaluated in phase III rheumatoid arthritis trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29076110",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "BACKGROUND AND OBJECTIVES: Upadacitinib is a janus kinase (JAK) 1 inhibitor being developed for the treatment of rheumatoid arthritis (RA) and other inflammatory diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29672874",
"endSection": "abstract",
"offsetInBeginSection": 932,
"offsetInEndSection": 1163,
"text": "RESULTS: In randomised controlled trials primary efficacy endpoints were met for tofacitinib (JAK 1/3 inhibitor-phase III), upadacitinib (JAK 1 inhibitor-phase II) and AJM300 (α4-integrin antagonist-phase II) in ulcerative colitis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29688617",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Upadacitinib is a Janus kinase 1 inhibitor under development for the treatment of several inflammatory disorders including rheumatoid arthritis (RA). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30394138",
"endSection": "abstract",
"offsetInBeginSection": 249,
"offsetInEndSection": 371,
"text": "Upadacitinib selectively inhibits Janus Kinase 1 (JAK1) which could potentially reduce JAK2 and JAK3-related side effects. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29908670",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 184,
"text": "BACKGROUND\nPhase 2 studies with upadacitinib, a selective Janus kinase 1 (JAK1) inhibitor, have shown safety and efficacy in the treatment of patients with active rheumatoid arthritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29908669",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "BACKGROUND\nUpadacitinib is a selective inhibitor of Janus kinase 1 and was efficacious in phase 2 studies in patients with moderate-to-severe rheumatoid arthritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30500075",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "Upadacitinib is a novel selective oral Janus kinase 1 (JAK) inhibitor being developed for treatment of several inflammatory diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29076110",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "BACKGROUND AND OBJECTIVES\nUpadacitinib is a janus kinase (JAK) 1 inhibitor being developed for the treatment of rheumatoid arthritis (RA) and other inflammatory diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28503781",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "AIMS\nUpadacitinib (ABT-494) is a selective Janus kinase 1 inhibitor being developed for treatment of auto-immune inflammatory disorders."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29672874",
"endSection": "abstract",
"offsetInBeginSection": 938,
"offsetInEndSection": 1168,
"text": "RESULTS\nIn randomised controlled trials primary efficacy endpoints were met for tofacitinib (JAK 1/3 inhibitor-phase III), upadacitinib (JAK 1 inhibitor-phase II) and AJM300 (α4-integrin antagonist-phase II) in ulcerative colitis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28503781",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "AIMS Upadacitinib (ABT-494) is a selective Janus kinase 1 inhibitor being developed for treatment of auto-immune inflammatory disorders."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29908669",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "BACKGROUND Upadacitinib is a selective inhibitor of Janus kinase 1 and was efficacious in phase 2 studies in patients with moderate-to-severe rheumatoid arthritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30394138",
"endSection": "abstract",
"offsetInBeginSection": 194,
"offsetInEndSection": 316,
"text": "Upadacitinib selectively inhibits Janus Kinase 1 (JAK1) which could potentially reduce JAK2 and JAK3-related side effects."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30394138",
"endSection": "abstract",
"offsetInBeginSection": 1117,
"offsetInEndSection": 1321,
"text": "Expert commentary: Upadacitinib has displayed a rapid and favorable efficacy profile in RA but despite being a selective JAK1 inhibitor appears to have a similar safety profile to less-selective Jakinibs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29076110",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "BACKGROUND AND OBJECTIVES Upadacitinib is a janus kinase (JAK) 1 inhibitor being developed for the treatment of rheumatoid arthritis (RA) and other inflammatory diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29688617",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Upadacitinib is a Janus kinase 1 inhibitor under development for the treatment of several inflammatory disorders including rheumatoid arthritis (RA)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30394138",
"endSection": "abstract",
"offsetInBeginSection": 338,
"offsetInEndSection": 463,
"text": "Areas covered: In this paper, we review a newly developed oral selective JAK inhibitor, upadacitinib for the treatment of RA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30394138",
"endSection": "abstract",
"offsetInBeginSection": 215,
"offsetInEndSection": 337,
"text": "Upadacitinib selectively inhibits Janus Kinase 1 (JAK1) which could potentially reduce JAK2 and JAK3-related side effects."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28503781",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 144,
"text": "<b>AIMS</b>: Upadacitinib (ABT-494) is a selective Janus kinase 1 inhibitor being developed for treatment of auto-immune inflammatory disorders."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30394138",
"endSection": "abstract",
"offsetInBeginSection": 1138,
"offsetInEndSection": 1342,
"text": "Expert commentary: Upadacitinib has displayed a rapid and favorable efficacy profile in RA but despite being a selective JAK1 inhibitor appears to have a similar safety profile to less-selective Jakinibs."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28503781",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Assessment of effect of CYP3A inhibition, CYP induction, OATP1B inhibition, and high-fat meal on pharmacokinetics of the JAK1 inhibitor upadacitinib."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28503781",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Upadacitinib (ABT-494) is a selective Janus kinase 1 inhibitor being developed for treatment of auto-immune inflammatory disorders."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30394138",
"endSection": "abstract",
"offsetInBeginSection": 317,
"offsetInEndSection": 442,
"text": "Areas covered: In this paper, we review a newly developed oral selective JAK inhibitor, upadacitinib for the treatment of RA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30725185",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 193,
"text": "OBJECTIVES: We assessed the relative efficacy and safety of once-daily administration of 15 and 30 mg upadacitinib (a JAK1-selective inhibitor) in patients with active rheumatoid arthritis (RA)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31781755",
"endSection": "abstract",
"offsetInBeginSection": 533,
"offsetInEndSection": 797,
"text": " In contrast, efficacy of filgotinib, a selective JAK1 inhibitor, in CD patients was demonstrated in the randomized, double-blinded, placebo-controlled phase II FITZROY study. Upadacitinib also showed promising results in a phase II trial in moderate to severe CD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31867699",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 278,
"text": "Upadacitinib is a Janus kinase 1 inhibitor developed for treatment of moderate to severe rheumatoid arthritis (RA) and was recently approved by the US Food and Drug Administration for this indication in adults who have had an inadequate response or intolerance to methotrexate. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31786154",
"endSection": "abstract",
"offsetInBeginSection": 109,
"offsetInEndSection": 292,
"text": "BJECTIVE: We sought to evaluate the safety and efficacy of multiple doses of the selective Janus kinase 1 inhibitor upadacitinib in patients with moderate to severe atopic dermatitis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31378969",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 189,
"text": "The aim of this study was to characterize the effects of upadacitinib, a Janus kinase 1 inhibitor, on in vivo activity of different cytochrome P450 (CYP) enzymes using a cocktail approach. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30886973",
"endSection": "abstract",
"offsetInBeginSection": 990,
"offsetInEndSection": 1088,
"text": "thods: Structure-based hypotheses were used to design the JAK1 selective inhibitor upadacitinib. J"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29672874",
"endSection": "abstract",
"offsetInBeginSection": 938,
"offsetInEndSection": 1169,
"text": "S: In randomised controlled trials primary efficacy endpoints were met for tofacitinib (JAK 1/3 inhibitor-phase III), upadacitinib (JAK 1 inhibitor-phase II) and AJM300 (α4-integrin antagonist-phase II) in ulcerative colitis. Ozani"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31692920",
"endSection": "abstract",
"offsetInBeginSection": 1115,
"offsetInEndSection": 1459,
"text": "Both these new compounds are active on the majority of four JAK family members (JAK1, JAK2, JAK3, and TYK2), whereas the most recent emerging approach is directed toward the development of JAK1 selective inhibitors (upadacitinib and filgotinib) with the aim to improve the safety profile by minimizing the effects on JAK3 and, especially, JAK2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30886973",
"endSection": "abstract",
"offsetInBeginSection": 540,
"offsetInEndSection": 757,
"text": "Upadacitinib (ABT-494) is a selective JAK1 inhibitor that was engineered to address the hypothesis that greater JAK1 selectivity over other JAK family members will translate into a more favorable benefit:risk profile."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32530345",
"endSection": "abstract",
"offsetInBeginSection": 369,
"offsetInEndSection": 516,
"text": "Upadacitinib is a JAK inhibitor engineered to be selective for JAK1, and has recently been approved for use in patients with moderate-to-severe RA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30886973",
"endSection": "abstract",
"offsetInBeginSection": 755,
"offsetInEndSection": 990,
"text": "e. Upadacitinib selectively targets JAK1 dependent disease drivers such as IL-6 and IFNγ, while reducing effects on reticulocytes and natural killer (NK) cells, which potentially contributed to the tolerability issues of tofacitinib.Me"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30886973",
"endSection": "abstract",
"offsetInBeginSection": 535,
"offsetInEndSection": 755,
"text": "mia. Upadacitinib (ABT-494) is a selective JAK1 inhibitor that was engineered to address the hypothesis that greater JAK1 selectivity over other JAK family members will translate into a more favorable benefit:risk profil"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30886973",
"endSection": "abstract",
"offsetInBeginSection": 998,
"offsetInEndSection": 1087,
"text": "tructure-based hypotheses were used to design the JAK1 selective inhibitor upadacitinib. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32044319",
"endSection": "abstract",
"offsetInBeginSection": 19,
"offsetInEndSection": 178,
"text": "We evaluated the efficacy and safety of upadacitinib, an oral selective Janus kinase 1 inhibitor, in a randomized trial of patients with Crohn's disease (CD).M"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30886973",
"endSection": "abstract",
"offsetInBeginSection": 746,
"offsetInEndSection": 1065,
"text": "sk profile. Upadacitinib selectively targets JAK1 dependent disease drivers such as IL-6 and IFNγ, while reducing effects on reticulocytes and natural killer (NK) cells, which potentially contributed to the tolerability issues of tofacitinib.Methods: Structure-based hypotheses were used to design the JAK1 selective in"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28503781",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "AIMS: Upadacitinib (ABT-494) is a selective Janus kinase 1 inhibitor being developed for treatment of auto-immune inflammatory diso"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31448433",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "Upadacitinib is a selective Janus kinase (JAK) 1 inhibitor being developed for treatment of rheumatoid arthritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30886973",
"endSection": "abstract",
"offsetInBeginSection": 1727,
"offsetInEndSection": 1837,
"text": "o physiological consequences. Upadacitinib is ~ 60 fold selective for JAK1 over JAK2, and > 100 fold selective"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31448433",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "Preferential Inhibition of JAK1 Relative to JAK3 by Upadacitinib: Exposure-Response Analyses of Ex Vivo Data From 2 Phase 1 Clinical Trials and Comparison to Tofacitinib."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33129109",
"endSection": "abstract",
"offsetInBeginSection": 804,
"offsetInEndSection": 959,
"text": "Here, we demonstrated that Upadacitinib, a JAK-1 inhibitor, inhibited the proliferation of cytokine-dependent ATL cell lines and the expression of p-STAT5."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32776305",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "Selective JAK1 Inhibitors for the Treatment of Atopic Dermatitis: Focus on Upadacitinib and Abrocitinib."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32776305",
"endSection": "abstract",
"offsetInBeginSection": 892,
"offsetInEndSection": 1010,
"text": "Upadacitinib and abrocitinib are oral small molecules that inhibit the JAK/STAT pathway by selectively blocking JAK1. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31317509",
"endSection": "abstract",
"offsetInBeginSection": 1515,
"offsetInEndSection": 1711,
"text": "Several more selective JAK-1 inhibitors, including filgotinib and upadacitinib, have also shown positive results in phase II studies and are currently enrolling in phase III development programs. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31401212",
"endSection": "abstract",
"offsetInBeginSection": 627,
"offsetInEndSection": 720,
"text": "Emerging data with selective JAK1 inhibitors upadacitinib and filgotinib looks very promising"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31287230",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 302,
"text": "OBJECTIVE: To evaluate the efficacy, including capacity for inhibition of radiographic progression, and safety of upadacitinib, a JAK1-selective inhibitor, as compared to placebo or adalimumab in patients with rheumatoid arthritis (RA) who have experienced an inadequate response to methotrexate (MTX)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29908670",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "BACKGROUND: Phase 2 studies with upadacitinib, a selective Janus kinase 1 (JAK1) inhibitor, have shown safety and efficacy in the treatment of patients with active rheumatoid arthritis. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29908669",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 165,
"text": "BACKGROUND: Upadacitinib is a selective inhibitor of Janus kinase 1 and was efficacious in phase 2 studies in patients with moderate-to-severe rheumatoid arthritis. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30394138",
"endSection": "abstract",
"offsetInBeginSection": 208,
"offsetInEndSection": 330,
"text": "Upadacitinib selectively inhibits Janus Kinase 1 (JAK1) which could potentially reduce JAK2 and JAK3-related side effects."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31654328",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 160,
"text": "Upadacitinib is a selective Janus Kinase 1 inhibitor which is being developed for the treatment of several inflammatory diseases including rheumatoid arthritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30633369",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 137,
"text": "Upadacitinib is a novel selective Janus kinase 1 inhibitor developed for treatment of rheumatoid arthritis and other autoimmune diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30973649",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "Upadacitinib is a selective Janus kinase 1 inhibitor being developed for the treatment of several inflammatory autoimmune diseases, including rheumatoid arthritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31130260",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 280,
"text": "BACKGROUND: Upadacitinib, an oral Janus kinase (JAK)1-selective inhibitor, showed efficacy in combination with stable background conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) in patients with rheumatoid arthritis who had an inadequate response to DMARDs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32648334",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 201,
"text": "This phase 1 study characterized the effect of multiple doses of upadacitinib, an oral Janus kinase 1 selective inhibitor, on the pharmacokinetics of the cytochrome P450 (CYP) 2B6 substrate bupropion. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31327403",
"endSection": "abstract",
"offsetInBeginSection": 249,
"offsetInEndSection": 431,
"text": "To date, three JAK inhibitors have been tested in patients with moderate-to-severe CD: tofacitinib (pan-JAK inhibitor), filgotinib (JAK1 inhibitor) and upadacitinib (JAK1 inhibitor)."
}
] | 11 |
BioASQ-training11b
| null | null |
601c317a1cb411341a000014
|
bioasq_factoid
|
factoid
|
What is disrupted by ALS- and FTD-associated missense mutations in TBK1?
|
['mitophagy']
|
[
"mitophagy",
"mitochondrial autophagy",
"mitochondrial degradation",
"mitochondrial turnover",
"mitochondrial quality control"
] |
['ALS- and FTD-associated missense mutations in TBK1 differentially disrupt mitophagy.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34099552"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34099552",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 84,
"text": "ALS- and FTD-associated missense mutations in TBK1 differentially disrupt mitophagy."
}
] | 11 |
BioASQ-training11b
| null | null |
62190ca03a8413c653000035
|
bioasq_factoid
|
yesno
|
Are there negative enhancers?
|
['yes']
|
[
"yes"
] |
['Yes, negative enhancers are also called gene silencers.', 'Yes, there are. There is a gene called the CANP mL gene, which is responsible for muscle type regulation. It is a negative enhancer.', 'Yes, they are genomic regions that are dense in negative regulatory elements.', 'Yes. Negative enhancers are enhancers that negatively regulate gene expression by physically blocking transcription of a subset of genes, often immobilizing transcriptional machinery.', 'Yes. Numerous studies suggest that negative enhancers are present in eukaryotic genomes and play key roles in gene expression.', 'Yes, there are. There is a gene called the CANP mL gene, which is responsible for muscle type regulation. It has a positive and a negative enhancer. The positive enhancer gene controls muscle type, while the negative one controls muscle growth.', 'Yes. There are numerous studies of gene regulation in which enhancers are found to be negative enhancers, either because they negatively regulate transcription, or are absent or have a limited function.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/1883358",
"http://www.ncbi.nlm.nih.gov/pubmed/8405675",
"http://www.ncbi.nlm.nih.gov/pubmed/25605944",
"http://www.ncbi.nlm.nih.gov/pubmed/8770895",
"http://www.ncbi.nlm.nih.gov/pubmed/2481227",
"http://www.ncbi.nlm.nih.gov/pubmed/9038208",
"http://www.ncbi.nlm.nih.gov/pubmed/2539381",
"http://www.ncbi.nlm.nih.gov/pubmed/2968500"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9038208",
"endSection": "title",
"offsetInBeginSection": 103,
"offsetInEndSection": 150,
"text": "Role of a YY-1 factor-binding negative enhancer"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9038208",
"endSection": "abstract",
"offsetInBeginSection": 988,
"offsetInEndSection": 1156,
"text": "Mutations targeted to the CArG-like motif abolished the suppressive effect of the negative enhancer and the inducibility of the promoter during myogenic differentiation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9038208",
"endSection": "abstract",
"offsetInBeginSection": 1158,
"offsetInEndSection": 1299,
"text": "Our results suggest that the activity of the negative enhancer may determine the level of expression of the COX Vb gene in different tissues."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8405675",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Coordinate regulation of Drosophila tropomyosin gene expression is controlled by multiple muscle-type-specific positive and negative enhancer elements."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8405675",
"endSection": "abstract",
"offsetInBeginSection": 375,
"offsetInEndSection": 534,
"text": "enhancer regions contain multiple muscle-type-specific positive and negative cis-acting elements which together contribute toward full expression of the gene. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8405675",
"endSection": "abstract",
"offsetInBeginSection": 1050,
"offsetInEndSection": 1286,
"text": "We also show that this somatic/visceral muscle element(s) can be repressed through an adjacent negative control region, suggesting that the regulation of expression in these muscles is under dual control during both phases of myogenesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8405675",
"endSection": "abstract",
"offsetInBeginSection": 1288,
"offsetInEndSection": 1544,
"text": "We propose a model in which transcriptional regulation of the Drosophila TmI gene is controlled by the cooperative interaction of multiple positive and negative cis-acting regulatory elements that control the temporal and muscle-type pattern of expression."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2539381",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "Tandemly reiterated negative enhancer-like elements regulate transcription of a human gene for the large subunit of calcium-dependent protease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2539381",
"endSection": "abstract",
"offsetInBeginSection": 865,
"offsetInEndSection": 1143,
"text": "Upstream of the promoter region are tandemly reiterated multiple regulatory regions (-2.5k to -690, -690 to -460, -460 to -260, and -260 to -202), each of which negatively regulates the CANP mL gene promoter as well as heterologous promoters in an orientation-independent manner"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2539381",
"endSection": "abstract",
"offsetInBeginSection": 1313,
"offsetInEndSection": 1494,
"text": "he negative regulation of transcription mediated by these reiterated cis-acting elements and trans-acting factor(s) may play an essential role in the expression of the CANP mL gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25605944",
"endSection": "abstract",
"offsetInBeginSection": 779,
"offsetInEndSection": 1208,
"text": "Although LDB1-dependent activated genes are regulated at the level of transcriptional initiation, the LDB1-dependent repressed transcription units appear to be regulated primarily at the level of promoter pausing, with LDB1 regulating recruitment of metastasis-associated 1 family, member 2, a component of the nucleosome remodeling deacetylase complex, on these negative enhancers, required for the repressive enhancer function."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2481227",
"endSection": "abstract",
"offsetInBeginSection": 1410,
"offsetInEndSection": 1640,
"text": "The site was similar to silencers, or negative enhancers, in that it acted to repress transcription from outside the transcribed region, but was distinct in that the function of a canonical silencer was independent of orientation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8770895",
"endSection": "abstract",
"offsetInBeginSection": 1114,
"offsetInEndSection": 1249,
"text": "Clones in which the transgene was down-regulated by dexamethasone survived and were designated AtT-20/NET (for negative enhancer trap)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2968500",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 290,
"text": "The E1a gene of adenovirus encodes two proteins, 289 and 243 amino acids long, which have positive (transactivator) and negative (enhancer repressor) RNA polymerase II transcriptional regulatory properties and cell transformation activities including cooperation with an activated ras gene."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2539381",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "Tandemly reiterated negative enhancer-like elements regulate transcription of a human gene for the large subunit of calcium-dependent protease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2539381",
"endSection": "abstract",
"offsetInBeginSection": 865,
"offsetInEndSection": 1144,
"text": "Upstream of the promoter region are tandemly reiterated multiple regulatory regions (-2.5k to -690, -690 to -460, -460 to -260, and -260 to -202), each of which negatively regulates the CANP mL gene promoter as well as heterologous promoters in an orientation-independent manner."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2539381",
"endSection": "abstract",
"offsetInBeginSection": 1145,
"offsetInEndSection": 1311,
"text": "The presence of a cellular factor(s) mediating the action of these positive (promoter) and negative regulatory elements was suggested by an in vivo competition assay."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1883358",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "We have previously identified a silencer (negative enhancer) in glutathione transferase P (GST-P) gene which is strongly and specifically induced during hepatocarcinogenesis of the rat. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1883358",
"endSection": "abstract",
"offsetInBeginSection": 692,
"offsetInEndSection": 795,
"text": "The possibility that SF-B/LAP/IL6-DBP functions as a dual positive and negative regulator is discussed."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8405675",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Coordinate regulation of Drosophila tropomyosin gene expression is controlled by multiple muscle-type-specific positive and negative enhancer elements"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8405675",
"endSection": "abstract",
"offsetInBeginSection": 360,
"offsetInEndSection": 533,
"text": "Together these enhancer regions contain multiple muscle-type-specific positive and negative cis-acting elements which together contribute toward full expression of the gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8405675",
"endSection": "abstract",
"offsetInBeginSection": 1050,
"offsetInEndSection": 1544,
"text": "We also show that this somatic/visceral muscle element(s) can be repressed through an adjacent negative control region, suggesting that the regulation of expression in these muscles is under dual control during both phases of myogenesis. We propose a model in which transcriptional regulation of the Drosophila TmI gene is controlled by the cooperative interaction of multiple positive and negative cis-acting regulatory elements that control the temporal and muscle-type pattern of expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9038208",
"endSection": "abstract",
"offsetInBeginSection": 988,
"offsetInEndSection": 1297,
"text": "Mutations targeted to the CArG-like motif abolished the suppressive effect of the negative enhancer and the inducibility of the promoter during myogenic differentiation. Our results suggest that the activity of the negative enhancer may determine the level of expression of the COX Vb gene in different tissue"
}
] | 11 |
BioASQ-training11b
| null | null |
5d35eb01b3a638076300000f
|
bioasq_yesno
|
factoid
|
What gene is mutated in Huntington's disease?
|
['HTT or IT-15 gene or HD gene']
|
[
"HTT",
"IT-15 gene",
"HD gene",
"Huntingtin",
"Huntingtin protein",
"Huntingtin gene"
] |
["Huntington disease (HD; OMIM 143100), a progressive neurodegenerative disorder, is caused by an expanded trinucleotide CAG (polyQ) motif in the HTT gene. Mutations of the huntingtin protein (HTT) gene underlie both adult-onset and juvenile forms of Huntington's disease (HD).", 'Huntington disease is a progressive neurodegenerative disorder and is caused by an expanded trinucleotide CAG (polyQ) motif in the HTT gene.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25993131",
"http://www.ncbi.nlm.nih.gov/pubmed/1839672",
"http://www.ncbi.nlm.nih.gov/pubmed/25254119",
"http://www.ncbi.nlm.nih.gov/pubmed/26863614",
"http://www.ncbi.nlm.nih.gov/pubmed/18651325",
"http://www.ncbi.nlm.nih.gov/pubmed/19059613",
"http://www.ncbi.nlm.nih.gov/pubmed/26160070",
"http://www.ncbi.nlm.nih.gov/pubmed/16109169",
"http://www.ncbi.nlm.nih.gov/pubmed/15651335",
"http://www.ncbi.nlm.nih.gov/pubmed/11723754",
"http://www.ncbi.nlm.nih.gov/pubmed/19816846",
"http://www.ncbi.nlm.nih.gov/pubmed/26079385",
"http://www.ncbi.nlm.nih.gov/pubmed/12805114",
"http://www.ncbi.nlm.nih.gov/pubmed/9392570",
"http://www.ncbi.nlm.nih.gov/pubmed/25931812",
"http://www.ncbi.nlm.nih.gov/pubmed/12523115",
"http://www.ncbi.nlm.nih.gov/pubmed/16847693",
"http://www.ncbi.nlm.nih.gov/pubmed/27400454",
"http://www.ncbi.nlm.nih.gov/pubmed/26466780",
"http://www.ncbi.nlm.nih.gov/pubmed/8985734",
"http://www.ncbi.nlm.nih.gov/pubmed/24196395",
"http://www.ncbi.nlm.nih.gov/pubmed/11494364"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25993131",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "Huntington disease (HD; OMIM 143100), a progressive neurodegenerative disorder, is caused by an expanded trinucleotide CAG (polyQ) motif in the HTT gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25931812",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 138,
"text": "Huntington's disease (HD) is caused by a genetic mutation that results in polyglutamine expansion in the N-terminal regions of huntingtin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26863614",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 121,
"text": "Mutations of the huntingtin protein (HTT) gene underlie both adult-onset and juvenile forms of Huntington's disease (HD)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9392570",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 201,
"text": "Huntington's disease is an inherited disorder caused by expansion of a CAG trinucleotide repeat in the IT15 gene, which leads to expansion of a polyglutamine tract within the protein called huntingtin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24196395",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 267,
"text": "Huntington disease is a monogenic, autosomal dominant, progressive neurodegenerative disorder caused by a trinucleotide CAG repeat expansion in exon 1 of the huntingtin (HTT) gene; age of onset of clinical symptoms inversely correlates with expanded CAG repeat length"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26466780",
"endSection": "abstract",
"offsetInBeginSection": 170,
"offsetInEndSection": 446,
"text": "The causative gene (mutated HTT) is widely expressed outside the CNS and several peripheral signs of disease, including weight loss and increased proinflammatory signalling, are often seen; however, their importance in the pathophysiology of Huntington's disease is not clear."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26160070",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 248,
"text": "Huntington's disease (HD) is an inherited, neurodegenerative disorder caused by a single-gene mutation: a CAG expansion in the huntingtin (HTT) gene that results in production of a mutated protein, mutant HTT, with a polyglutamine tail (polyQ-HTT)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9392570",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 666,
"text": "Huntington's disease is an inherited disorder caused by expansion of a CAG trinucleotide repeat in the IT15 gene, which leads to expansion of a polyglutamine tract within the protein called huntingtin. Despite the characterization of the IT15 gene and the mutation involved in the disease, the normal function of huntingtin and the effects of the mutation on its function and on its neuronal location remain unknown. To study whether mutated huntingtin has the same neuronal distribution and intracellular location as normal huntingtin, we analyzed immunohistochemically both forms of this protein in the brain of 5 controls and 5 patients with Huntington's disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9392570",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 416,
"text": "Huntington's disease is an inherited disorder caused by expansion of a CAG trinucleotide repeat in the IT15 gene, which leads to expansion of a polyglutamine tract within the protein called huntingtin. Despite the characterization of the IT15 gene and the mutation involved in the disease, the normal function of huntingtin and the effects of the mutation on its function and on its neuronal location remain unknown."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1839672",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "Huntingtons disease (HD) is a hereditary disorder involving the central nervous system. Its effects are devastating, to the affected person as well as his family."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17941857",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Huntington disease (HD) is a neurodegenerative disorder due to an excessive number of CAG repeats in the IT15 gene on chromosome 4."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19059613",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 138,
"text": "Huntington disease in subjects from an Israeli Karaite community carrying alleles of intermediate and expanded CAG repeats in the HTT gene"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25254119",
"endSection": "abstract",
"offsetInBeginSection": 79,
"offsetInEndSection": 176,
"text": "The causative mutation is an expansion of more than 36 CAG repeats in the first exon of IT15 gene"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12523115",
"endSection": "title",
"offsetInBeginSection": 35,
"offsetInEndSection": 124,
"text": "Huntington's disease in relation to the number of trinucleotide CAG repeats in IT-15 gene"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12523115",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 178,
"text": "Huntington's disease (HD) is a neurological condition of progressive course that results from abnormally increased number of CAG repeats within IT-15 gene, coding for huntington."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11494364",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "Huntington's disease (HD) is a neurodegenerative disorder characterized by the expansion of CAG repeats in exon 1 of the HD gene"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27400454",
"endSection": "abstract",
"offsetInBeginSection": 141,
"offsetInEndSection": 268,
"text": "However, not all patients with an HD phenotype carry the pathological expansion in HTT, and the positive diagnosis rate is poor"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16847693",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 217,
"text": "The expansion of a polymorphic CAG repeat in the HD gene encoding huntingtin has been identified as the major cause of Huntington's disease (HD) and determines 42-73% of the variance in the age-at-onset of the disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26079385",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 248,
"text": "Huntington disease (HD) is a progressive autosomal dominant neurodegenerative disorder, characterized by abnormal movements, cognitive decline, and psychiatric symptoms, caused by a CAG repeat expansion in the huntingtin (HTT) gene on chromosome 4p"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19816846",
"endSection": "abstract",
"offsetInBeginSection": 125,
"offsetInEndSection": 245,
"text": "The disorder is caused by mutation in the gene encoding the huntingtin protein (Htt), producing intracellular aggregates"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11723754",
"endSection": "abstract",
"offsetInBeginSection": 480,
"offsetInEndSection": 700,
"text": "HD is less common in other ethnic groups. Huntington's disease is caused by an expanded trinucleotide CAG repeat in the HD gene on chromosome 4. The gene encodes for the protein huntingtin, with an as yet unknown functio"
}
] | 6 |
BioASQ-training6b
|
[
"http://www.disease-ontology.org/api/metadata/DOID:1289",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D006816",
"http://www.disease-ontology.org/api/metadata/DOID:12858"
] | null |
58a3428d60087bc10a00001b
|
bioasq_factoid
|
factoid
|
Which disease has been associated to a disruptive ALX1 protein?
|
[['frontonasal dysplasia']]
|
[
"frontonasal dysplasia",
"frontonasal malformation",
"frontonasal syndrome",
"frontonasal dysostosis"
] |
['Disruption of ALX1 causes extreme microphthalmia and severe facial clefting: expanding the spectrum of autosomal-recessive ALX-related frontonasal dysplasia.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/20451171",
"http://www.ncbi.nlm.nih.gov/pubmed/20627960",
"http://www.ncbi.nlm.nih.gov/pubmed/19598128",
"http://www.ncbi.nlm.nih.gov/pubmed/15728667",
"http://www.ncbi.nlm.nih.gov/pubmed/12559496",
"http://www.ncbi.nlm.nih.gov/pubmed/12390248",
"http://www.ncbi.nlm.nih.gov/pubmed/8673125",
"http://www.ncbi.nlm.nih.gov/pubmed/25686609",
"http://www.ncbi.nlm.nih.gov/pubmed/24376213"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20451171",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "Disruption of ALX1 causes extreme microphthalmia and severe facial clefting: expanding the spectrum of autosomal-recessive ALX-related frontonasal dysplasia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20451171",
"endSection": "abstract",
"offsetInBeginSection": 650,
"offsetInEndSection": 882,
"text": "In the second family we identified a homozygous donor-splice-site mutation (c.531+1G>A) in the ALX1 gene, providing evidence that complete loss of function of ALX1 protein causes severe disruption of early craniofacial development. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20627960",
"endSection": "abstract",
"offsetInBeginSection": 975,
"offsetInEndSection": 1070,
"text": "expression of Alx1, an effector of scapula blade patterning, is absent in all compound mutants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19598128",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 137,
"text": "Mutations in each of the transcriptional co-activator genes - CBP, p300, Cited2, Cart1 and Carm1 - result in neural tube defects in mice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15728667",
"endSection": "abstract",
"offsetInBeginSection": 1021,
"offsetInEndSection": 1168,
"text": "Scapular truncation in triple mutants of Tbx15, Alx4 and Cart1 indicates essential functions for Alx4 and Cart1 in the anterior part of the scapula"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12559496",
"endSection": "abstract",
"offsetInBeginSection": 637,
"offsetInEndSection": 854,
"text": " Ectopic expression of Cart1 in transgenic mice does not disturb development, whereas expression of a Cart1 form from which the aristaless domain has been deleted results in severe cranial and vertebral malformations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12559496",
"endSection": "abstract",
"offsetInBeginSection": 431,
"offsetInEndSection": 502,
"text": "Cart1, is essential for correct morphogenesis of the limbs and cranium."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12390248",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 196,
"text": "Cart1 encodes the paired-like homeodomain in the central portion of the gene, and plays a crucial role in the developmental lineage of bone and cartilage, especially in head formation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8673125",
"endSection": "abstract",
"offsetInBeginSection": 159,
"offsetInEndSection": 382,
"text": "we show that Cart1-homozygous mutant mice are born alive with acrania and meroanencephaly but die soon after birth-a phenotype that strikingly resembles a corresponding human syndrome caused by a neural tube closure defect."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25686609",
"endSection": "abstract",
"offsetInBeginSection": 528,
"offsetInEndSection": 649,
"text": " 240 kilobase haplotype encompassing the ALX1 gene that encodes a transcription factor affecting craniofacial development"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24376213",
"endSection": "abstract",
"offsetInBeginSection": 382,
"offsetInEndSection": 492,
"text": "ALX3, ALX4, and ALX1, which have been related with distinct phenotypes named FND1, FND2, and FND3 respectively"
}
] | 5 |
BioASQ-training5b
|
[] |
[] |
56cf36263975bb303a000007
|
bioasq_factoid
|
yesno
|
Is Wilson's disease described as an iron storage disease?
|
['no']
|
[
"no"
] |
["No, Wilson's disease is an autosomal recessive disorder caused by a mutation in the ATP7B gene, which leads to an accumulation of copper in the body. It is not an iron storage disease.", "Wilson's disease is a genetic copper storage disorder that causes hepatic and neurologic symptoms.", "No, Wilson's disease is a copper storage disorder, not an iron storage disorder.", "No, Wilson's disease is not an iron storage disease. It is a copper storage disorder that affects the liver and brain.", 'Yes. Wilson disease is a copper storage disease caused by mutations in ATP7B, which leads to excessive copper accumulation throughout the body. This excess metal results in damage to various organs such as the liver and brain, causing severe neurological problems and ultimately requiring lifelong chelation therapy.', "No, Wilson's disease is not described as an iron storage disease. It is an inherited disorder that affects the body's ability to regulate copper.", "Wilson's disease is a rare inherited disorder that causes copper to accumulate in your liver, brain and other vital organs.", 'Wilson disease is a genetic copper storage disorder that causes hepatic and neurologic symptoms.', "Yes, Wilson's Disease is characterized by excessive accumulation of copper due to impaired transport or decreased metabolism of Cu2+. This results in disruption of vital organs such as the liver and brain leading to symptoms like neurological damage, pigment abnormalities, pancytopenia and even death if left untreated."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23583003",
"http://www.ncbi.nlm.nih.gov/pubmed/34289020",
"http://www.ncbi.nlm.nih.gov/pubmed/35322347",
"http://www.ncbi.nlm.nih.gov/pubmed/8984578",
"http://www.ncbi.nlm.nih.gov/pubmed/25704483",
"http://www.ncbi.nlm.nih.gov/pubmed/14738953",
"http://www.ncbi.nlm.nih.gov/pubmed/34341141",
"http://www.ncbi.nlm.nih.gov/pubmed/9093597",
"http://www.ncbi.nlm.nih.gov/pubmed/23542331",
"http://www.ncbi.nlm.nih.gov/pubmed/30646728",
"http://www.ncbi.nlm.nih.gov/pubmed/36381061",
"http://www.ncbi.nlm.nih.gov/pubmed/30271060",
"http://www.ncbi.nlm.nih.gov/pubmed/21886393",
"http://www.ncbi.nlm.nih.gov/pubmed/31345362",
"http://www.ncbi.nlm.nih.gov/pubmed/16466879",
"http://www.ncbi.nlm.nih.gov/pubmed/33175593",
"http://www.ncbi.nlm.nih.gov/pubmed/8114295",
"http://www.ncbi.nlm.nih.gov/pubmed/8229372",
"http://www.ncbi.nlm.nih.gov/pubmed/17505988",
"http://www.ncbi.nlm.nih.gov/pubmed/11787982",
"http://www.ncbi.nlm.nih.gov/pubmed/24266916",
"http://www.ncbi.nlm.nih.gov/pubmed/32738633",
"http://www.ncbi.nlm.nih.gov/pubmed/33555495",
"http://www.ncbi.nlm.nih.gov/pubmed/22774841",
"http://www.ncbi.nlm.nih.gov/pubmed/33573009",
"http://www.ncbi.nlm.nih.gov/pubmed/1306026",
"http://www.ncbi.nlm.nih.gov/pubmed/12508671",
"http://www.ncbi.nlm.nih.gov/pubmed/22098612",
"http://www.ncbi.nlm.nih.gov/pubmed/8757902",
"http://www.ncbi.nlm.nih.gov/pubmed/28168129"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35322347",
"endSection": "abstract",
"offsetInBeginSection": 155,
"offsetInEndSection": 261,
"text": "Wilson's disease (WD), an inherited disorder of copper metabolism that mostly affects the liver and brain;"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8757902",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 111,
"text": "Wilsons disease is a rare autosomal recessive disorder of copper transportation, which is fatal if not treated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30646728",
"endSection": "abstract",
"offsetInBeginSection": 398,
"offsetInEndSection": 570,
"text": "Wilsons disease and idiopathic toxicosis are examples of severe chronic liver diseases that are the results of genetic predisposition to the hepatic accumulation of copper."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23542331",
"endSection": "abstract",
"offsetInBeginSection": 19,
"offsetInEndSection": 116,
"text": "Wilson disease is a genetic copper storage disorder that causes hepatic and neurologic symptoms. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8984578",
"endSection": "abstract",
"offsetInBeginSection": 483,
"offsetInEndSection": 536,
"text": "Wilson's disease represents a copper storage disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24266916",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Hereditary hemochromatosis and Wilson disease are autosomal recessive storage disorders of iron and copper overload, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17505988",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 224,
"text": "Hereditary deposition of iron (primary haemochromatosis) or copper (Wilson's disease) are autosomal recessive metabolic disease characterized by progressive liver pathology and subsequent involvement of various other organs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31345362",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "OBJECTIVES: Wilson's disease (WD) is a metabolic disorder leading to hepatic and extrahepatic copper"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33555495",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 73,
"text": "Wilson's disease (WD) is a rare hereditary disorder of copper metabolism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12508671",
"endSection": "abstract",
"offsetInBeginSection": 748,
"offsetInEndSection": 884,
"text": "Wilson's disease, a copper storage disorder, in which biliary copper excretion is reduced, is inherited as an autosomal recessive trait."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23542331",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "BACKGROUND & AIMS: Wilson disease is a genetic copper storage disorder that causes hepatic and n"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22098612",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 156,
"text": "UNLABELLED: Wilson disease (WD) is a rare inherited disorder of copper metabolism, which can lead to severe liver failure and to a variety of neuropsychiatr"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33573009",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 206,
"text": "Wilson disease (WD) (OMIM# 277900) is an autosomal recessive inherited disorder characterized by excess copper (Cu) storage in different human tissues, such as the brain, liver, and the corneas of the eyes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22774841",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 159,
"text": "UNLABELLED: Wilson's disease (WND) and hereditary hemochromatosis (HH) are two metal loading diseases of copper and iron, respectively, and are both recessivel"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36381061",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "Wilson's disease is an autosomal recessive inherited disease with congenital copper metabolism disorder, characterized by decreased ceruloplasmin and increased urine copper, which can involve multiple organs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8229372",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "Wilson's disease is an autosomal recessive disease of copper metabolism which is widely recognized as a disease occurring clinically in children, adolescents, and young adults."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23583003",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Hereditary copper-associated hepatitis in dogs resembles Wilson's disease, a copper storage disease in humans."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21886393",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 105,
"text": "Wilson's disease is a rare inherited disorder of copper metabolism causing severe damage to vital organs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9093597",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "Inherited copper toxic disease, Wilson's disease, is an autosomal recessive disorder arising from a defect in biliary copper excretion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14738953",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Wilson's disease is a genetic disorder of copper metabolism with a hepatic or neurologic presentation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30271060",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 81,
"text": "Wilson's disease is an autosomal recessive disease of abnormal copper metabolism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8114295",
"endSection": "abstract",
"offsetInBeginSection": 579,
"offsetInEndSection": 683,
"text": " Hemochromatosis and Wilson's disease are known as iron and copper accumulation disorders, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8984578",
"endSection": "abstract",
"offsetInBeginSection": 482,
"offsetInEndSection": 536,
"text": " Wilson's disease represents a copper storage disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16466879",
"endSection": "abstract",
"offsetInBeginSection": 796,
"offsetInEndSection": 904,
"text": " In the new paradigm, Wilson's disease is seen as a hereditary disorder associated with copper intoxication."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8984578",
"endSection": "abstract",
"offsetInBeginSection": 434,
"offsetInEndSection": 584,
"text": "ve determination of elevated liver iron content. Wilson's disease represents a copper storage disease. Prominent clinical features are hepatomegaly an"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25704483",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "Wilson's disease is an autosomal recessive disorder in which the liver does not properly release copper into bile, resulting in prominent copper accumulation in various tissues."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28168129",
"endSection": "abstract",
"offsetInBeginSection": 337,
"offsetInEndSection": 498,
"text": "Wilson's disease is one such hereditary disease that creates chaos in tissues, usually the brain and liver, via deposition of abnormal amounts of copper in them."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1306026",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 111,
"text": "Wilson's disease is rare autosomal-recessive disorder originated on the basis of metabolic copper over-storage."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34341141",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 193,
"text": "Wilson's disease is an autosomal-recessive disorder of copper metabolism caused by mutations in ATP7B and associated with neurological, psychiatric, ophthalmological and hepatic manifestations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11787982",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "PROJECT: Wilson's disease (WD) is an inherited disorder of copper metabolism characterised by juvenile liver cirrhosis and by neurological symptoms"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33175593",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 78,
"text": "OBJECTIVE: Wilson's disease (WD) is a hereditary disorder of copper metabolism"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34289020",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Wilson's disease is an autosomal-recessive disorder of copper metabolism with neurological and hepatic presentations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32738633",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 121,
"text": "Wilson's disease is an inherited disorder associated with copper accumulation in the liver, brain and other vital organs."
}
] | 12 |
BioASQ-training12b
| null | null |
640c821c201352f04a000023
|
bioasq_yesno
|
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