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yesno
|
Is baricitinib effective for rheumatoid arthritis?
|
['yes']
|
[
"yes"
] |
['Yes, baricitinib is effective treatment of rheumatoid arthritis.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28097393",
"http://www.ncbi.nlm.nih.gov/pubmed/28440680",
"http://www.ncbi.nlm.nih.gov/pubmed/24818516",
"http://www.ncbi.nlm.nih.gov/pubmed/29134891",
"http://www.ncbi.nlm.nih.gov/pubmed/27427830",
"http://www.ncbi.nlm.nih.gov/pubmed/30058112",
"http://www.ncbi.nlm.nih.gov/pubmed/29687421",
"http://www.ncbi.nlm.nih.gov/pubmed/29500799",
"http://www.ncbi.nlm.nih.gov/pubmed/30191390",
"http://www.ncbi.nlm.nih.gov/pubmed/28199814",
"http://www.ncbi.nlm.nih.gov/pubmed/28290136",
"http://www.ncbi.nlm.nih.gov/pubmed/30219772",
"http://www.ncbi.nlm.nih.gov/pubmed/28811354",
"http://www.ncbi.nlm.nih.gov/pubmed/30006916",
"http://www.ncbi.nlm.nih.gov/pubmed/29415145",
"http://www.ncbi.nlm.nih.gov/pubmed/30183607"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28097393",
"endSection": "abstract",
"offsetInBeginSection": 1551,
"offsetInEndSection": 1735,
"text": "CONCLUSION: Baricitinib 2 mg and 4 mg administered once daily, in combination with DMARD, were efficacious interventions for active RA that had no significant risk of TEAE development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28440680",
"endSection": "abstract",
"offsetInBeginSection": 1175,
"offsetInEndSection": 1342,
"text": "CONCLUSIONS: The efficacy and safety profile of baricitinib was maintained during long-term treatment of Japanese patients with RA and background methotrexate therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28811354",
"endSection": "abstract",
"offsetInBeginSection": 1285,
"offsetInEndSection": 1562,
"text": "CONCLUSION: In a phase IIb study in RA, the safety and tolerability profile of baricitinib, up to 128 weeks, remained consistent with earlier observations, without unexpected late signals. Clinical improvements seen in the 24-week blinded period were maintained during the OLE."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29134891",
"endSection": "abstract",
"offsetInBeginSection": 1267,
"offsetInEndSection": 1472,
"text": "CONCLUSION: Data for baricitinib, with/without methotrexate, in Japanese subpopulations across all stages of the RA treatment continuum accord with the efficacy/safety profile in overall study populations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29415145",
"endSection": "abstract",
"offsetInBeginSection": 1569,
"offsetInEndSection": 1750,
"text": "Conclusion: Baricitinib demonstrated a consistent, beneficial treatment effect in bDMARD-refractory patients across subgroups based on baseline characteristics and prior bDMARD use."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30006916",
"endSection": "abstract",
"offsetInBeginSection": 193,
"offsetInEndSection": 332,
"text": "Baricitinib is effective in treatment of RA, and did not appear to have significant safety concerns during the first 6 months of treatment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30058112",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "OBJECTIVE\nBaricitinib is an orally administered inhibitor of JAK1 and JAK2 that has been shown to be effective in treating rheumatoid arthritis (RA)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24818516",
"endSection": "abstract",
"offsetInBeginSection": 908,
"offsetInEndSection": 1175,
"text": "EXPERT OPINION\nJAK inhibitors are effective in the treatment of rheumatoid arthritis as evidenced by several inhibitors enabling the majority of treated patients to achieve ACR20 responses, with baricitinib and INCB-039110 both effective when administered once daily."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30219772",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "OBJECTIVE\nBaricitinib is an oral, once-daily selective Janus kinase (JAK1/JAK2) inhibitor for adults with moderately to severely active rheumatoid arthritis (RA)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29500799",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "Two different Janus kinase (JAK) inhibitors-baricitinib and tofacitinib-are effective and licensed in active rheumatoid arthritis (RA)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27427830",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 54,
"text": "Baricitinib for the treatment of rheumatoid arthritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30183607",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 232,
"text": "OBJECTIVES\nOral targeted synthetic disease-modifying anti-rheumatic drugs (DMARDs), including the Janus kinase inhibitors tofacitinib and baricitinib, are the latest addition to the therapeutic options for rheumatoid arthritis (RA)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28290136",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 252,
"text": "Baricitinib (Olumiant™) is an orally-administered, small-molecule, janus-associated kinase (JAK) inhibitor developed by Eli Lilly and Incyte Corporation for the treatment of rheumatoid arthritis (RA), atopic dermatitis and systemic lupus erythematosus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24818516",
"endSection": "abstract",
"offsetInBeginSection": 908,
"offsetInEndSection": 1175,
"text": "EXPERT OPINION JAK inhibitors are effective in the treatment of rheumatoid arthritis as evidenced by several inhibitors enabling the majority of treated patients to achieve ACR20 responses, with baricitinib and INCB-039110 both effective when administered once daily."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30191390",
"endSection": "abstract",
"offsetInBeginSection": 678,
"offsetInEndSection": 927,
"text": "Tofacitinib 10 mg + methotrexate (MTX) and baricitinib 4 mg + MTX were among the most effective treatments for active RA with an inadequate DMARD or biologic response, followed by baricitinib 2 mg + MTX, tofacitinib 5 mg + MTX, and adalimumab + MTX."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30058112",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "OBJECTIVE Baricitinib is an orally administered inhibitor of JAK1 and JAK2 that has been shown to be effective in treating rheumatoid arthritis (RA)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28199814",
"endSection": "abstract",
"offsetInBeginSection": 2026,
"offsetInEndSection": 2234,
"text": "CONCLUSIONS In patients with rheumatoid arthritis who had had an inadequate response to methotrexate, baricitinib was associated with significant clinical improvements as compared with placebo and adalimumab."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29687421",
"endSection": "abstract",
"offsetInBeginSection": 1273,
"offsetInEndSection": 1587,
"text": "Thus, once-daily baricitinib, as monotherapy or in combination with methotrexate, is an effective and generally well tolerated emerging treatment for patients with moderate to severe active RA who have responded inadequately to or are intolerant of ≥ 1 DMARD, and extends the options available for this population."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30183607",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 232,
"text": "OBJECTIVES Oral targeted synthetic disease-modifying anti-rheumatic drugs (DMARDs), including the Janus kinase inhibitors tofacitinib and baricitinib, are the latest addition to the therapeutic options for rheumatoid arthritis (RA)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27427830",
"endSection": "abstract",
"offsetInBeginSection": 605,
"offsetInEndSection": 823,
"text": "Five phase 3 trials of Baricitinib, a JAK1 and JAK2 inhibitor, have been performed and showed high clinical efficacy in patients with active RA and naïve to sDMARDs or an inadequate response to sDMARDs, MTX or bDMARDs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27427830",
"endSection": "abstract",
"offsetInBeginSection": 953,
"offsetInEndSection": 1168,
"text": "It is also reported that safety was tolerable within the limited study period.<br><b>AREAS COVERED</b>: We here review the recent progress in the development of baricitinib and its potential for the treatment of RA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30058112",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "<b>OBJECTIVE</b>: Baricitinib is an orally administered inhibitor of JAK1 and JAK2 that has been shown to be effective in treating rheumatoid arthritis (RA)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28290136",
"endSection": "abstract",
"offsetInBeginSection": 489,
"offsetInEndSection": 802,
"text": "In February 2017, baricitinib was approved in the EU, as monotherapy or in combination with methotrexate, for the treatment of moderate to severe active rheumatoid arthritis in adult patients who have responded inadequately to, or who are intolerant to one or more disease-modifying anti-rheumatic drugs (DMARDs)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28199814",
"endSection": "abstract",
"offsetInBeginSection": 1999,
"offsetInEndSection": 2195,
"text": "In patients with rheumatoid arthritis who had had an inadequate response to methotrexate, baricitinib was associated with significant clinical improvements as compared with placebo and adalimumab."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29687421",
"endSection": "abstract",
"offsetInBeginSection": 386,
"offsetInEndSection": 838,
"text": "In pivotal multinational trials, once-daily baricitinib 4 mg, with/without methotrexate (± another csDMARD), improved the signs and symptoms of RA, disease activity and physical function in DMARD-naive patients and in patients with an inadequate response to methotrexate, csDMARDs or TNF inhibitors; baricitinib treatment also slowed structural joint damage in DMARD-naive patients and in those with an inadequate response to methotrexate and csDMARDs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27427830",
"endSection": "abstract",
"offsetInBeginSection": 584,
"offsetInEndSection": 802,
"text": "Five phase 3 trials of Baricitinib, a JAK1 and JAK2 inhibitor, have been performed and showed high clinical efficacy in patients with active RA and naïve to sDMARDs or an inadequate response to sDMARDs, MTX or bDMARDs."
}
] | 11 |
BioASQ-training11b
| null | null |
5c6df86b7c78d69471000045
|
bioasq_yesno
|
yesno
|
Is Keutel syndrome a common genetic disorder?
|
['no']
|
[
"no"
] |
['No, Keutel syndrome (OMIM 245150) is a very rare syndrome']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23917590",
"http://www.ncbi.nlm.nih.gov/pubmed/23857752",
"http://www.ncbi.nlm.nih.gov/pubmed/32821457"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32821457",
"endSection": "abstract",
"offsetInBeginSection": 88,
"offsetInEndSection": 142,
"text": "Keutel syndrome (OMIM 245150) is a very rare syndrome "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23917590",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 118,
"text": "Keutel syndrome is a rare autosomal-recessive condition characterized by abnormal cartilage calcification."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23857752",
"endSection": "abstract",
"offsetInBeginSection": 93,
"offsetInEndSection": 217,
"text": "MGP-deficiency in humans leads to Keutel syndrome, a rare genetic disease hallmarked by abnormal soft tissue calcification. "
}
] | 11 |
BioASQ-training11b
| null | null |
6082f4374e6a4cf63000000f
|
bioasq_yesno
|
factoid
|
Which genome browser database for DNA shape annotations is available?
|
[['GBshape']]
|
[
"GBshape",
"G-Box shape",
"G-Box structure",
"G-Box configuration"
] |
['The Genome Browser for DNA shape annotations (GBshape; freely available at http://rohslab.cmb.usc.edu/GBshape/) provides minor groove width, propeller twist, roll, helix twist and hydroxyl radical cleavage predictions for the entire genomes of 94 organisms. Additional genomes can easily be added using the GBshape framework. GBshape can be used to visualize DNA shape annotations qualitatively in a genome browser track format, and to download quantitative values of DNA shape features as a function of genomic position at nucleotide resolution.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25326329"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 61,
"text": "GBshape: a genome browser database for DNA shape annotations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "abstract",
"offsetInBeginSection": 531,
"offsetInEndSection": 1353,
"text": "Our Genome Browser for DNA shape annotations (GBshape; freely available at http://rohslab.cmb.usc.edu/GBshape/) provides minor groove width, propeller twist, roll, helix twist and hydroxyl radical cleavage predictions for the entire genomes of 94 organisms. Additional genomes can easily be added using the GBshape framework. GBshape can be used to visualize DNA shape annotations qualitatively in a genome browser track format, and to download quantitative values of DNA shape features as a function of genomic position at nucleotide resolution. As biological applications, we illustrate the periodicity of DNA shape features that are present in nucleosome-occupied sequences from human, fly and worm, and we demonstrate structural similarities between transcription start sites in the genomes of four Drosophila species."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 61,
"text": "GBshape: a genome browser database for DNA shape annotations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "abstract",
"offsetInBeginSection": 857,
"offsetInEndSection": 1078,
"text": "GBshape can be used to visualize DNA shape annotations qualitatively in a genome browser track format, and to download quantitative values of DNA shape features as a function of genomic position at nucleotide resolution. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 61,
"text": "GBshape: a genome browser database for DNA shape annotations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "abstract",
"offsetInBeginSection": 857,
"offsetInEndSection": 1078,
"text": "GBshape can be used to visualize DNA shape annotations qualitatively in a genome browser track format, and to download quantitative values of DNA shape features as a function of genomic position at nucleotide resolution. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 61,
"text": "GBshape: a genome browser database for DNA shape annotations."
},
{
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"endSection": "abstract",
"offsetInBeginSection": 857,
"offsetInEndSection": 1078,
"text": "GBshape can be used to visualize DNA shape annotations qualitatively in a genome browser track format, and to download quantitative values of DNA shape features as a function of genomic position at nucleotide resolution. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 61,
"text": "GBshape: a genome browser database for DNA shape annotations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "abstract",
"offsetInBeginSection": 857,
"offsetInEndSection": 1078,
"text": "GBshape can be used to visualize DNA shape annotations qualitatively in a genome browser track format, and to download quantitative values of DNA shape features as a function of genomic position at nucleotide resolution. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 61,
"text": "GBshape: a genome browser database for DNA shape annotations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "abstract",
"offsetInBeginSection": 857,
"offsetInEndSection": 1078,
"text": "GBshape can be used to visualize DNA shape annotations qualitatively in a genome browser track format, and to download quantitative values of DNA shape features as a function of genomic position at nucleotide resolution. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 61,
"text": "GBshape: a genome browser database for DNA shape annotations."
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"endSection": "abstract",
"offsetInBeginSection": 531,
"offsetInEndSection": 788,
"text": "Our Genome Browser for DNA shape annotations (GBshape; freely available at http://rohslab.cmb.usc.edu/GBshape/) provides minor groove width, propeller twist, roll, helix twist and hydroxyl radical cleavage predictions for the entire genomes of 94 organisms."
},
{
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"endSection": "abstract",
"offsetInBeginSection": 857,
"offsetInEndSection": 1077,
"text": "GBshape can be used to visualize DNA shape annotations qualitatively in a genome browser track format, and to download quantitative values of DNA shape features as a function of genomic position at nucleotide resolution."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "abstract",
"offsetInBeginSection": 858,
"offsetInEndSection": 1354,
"text": "GBshape can be used to visualize DNA shape annotations qualitatively in a genome browser track format, and to download quantitative values of DNA shape features as a function of genomic position at nucleotide resolution. As biological applications, we illustrate the periodicity of DNA shape features that are present in nucleosome-occupied sequences from human, fly and worm, and we demonstrate structural similarities between transcription start sites in the genomes of four Drosophila species."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "abstract",
"offsetInBeginSection": 279,
"offsetInEndSection": 789,
"text": "Whereas higher-order effects, such as chromatin accessibility, cooperativity and cofactors, have been described, DNA shape recently gained attention as another feature that fine-tunes the DNA binding specificities of some transcription factor families. Our Genome Browser for DNA shape annotations (GBshape; freely available at http://rohslab.cmb.usc.edu/GBshape/) provides minor groove width, propeller twist, roll, helix twist and hydroxyl radical cleavage predictions for the entire genomes of 94 organisms."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 61,
"text": "GBshape: a genome browser database for DNA shape annotations."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "abstract",
"offsetInBeginSection": 790,
"offsetInEndSection": 1078,
"text": "Additional genomes can easily be added using the GBshape framework. GBshape can be used to visualize DNA shape annotations qualitatively in a genome browser track format, and to download quantitative values of DNA shape features as a function of genomic position at nucleotide resolution."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "abstract",
"offsetInBeginSection": 532,
"offsetInEndSection": 857,
"text": "Our Genome Browser for DNA shape annotations (GBshape; freely available at http://rohslab.cmb.usc.edu/GBshape/) provides minor groove width, propeller twist, roll, helix twist and hydroxyl radical cleavage predictions for the entire genomes of 94 organisms. Additional genomes can easily be added using the GBshape framework."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "abstract",
"offsetInBeginSection": 858,
"offsetInEndSection": 1078,
"text": "GBshape can be used to visualize DNA shape annotations qualitatively in a genome browser track format, and to download quantitative values of DNA shape features as a function of genomic position at nucleotide resolution."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 61,
"text": "GBshape: a genome browser database for DNA shape annotations."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "abstract",
"offsetInBeginSection": 532,
"offsetInEndSection": 789,
"text": "Our Genome Browser for DNA shape annotations (GBshape; freely available at http://rohslab.cmb.usc.edu/GBshape/) provides minor groove width, propeller twist, roll, helix twist and hydroxyl radical cleavage predictions for the entire genomes of 94 organisms."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "abstract",
"offsetInBeginSection": 858,
"offsetInEndSection": 1078,
"text": "GBshape can be used to visualize DNA shape annotations qualitatively in a genome browser track format, and to download quantitative values of DNA shape features as a function of genomic position at nucleotide resolution."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 61,
"text": "GBshape: a genome browser database for DNA shape annotations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "abstract",
"offsetInBeginSection": 532,
"offsetInEndSection": 789,
"text": "Our Genome Browser for DNA shape annotations (GBshape; freely available at http://rohslab.cmb.usc.edu/GBshape/) provides minor groove width, propeller twist, roll, helix twist and hydroxyl radical cleavage predictions for the entire genomes of 94 organisms."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "abstract",
"offsetInBeginSection": 858,
"offsetInEndSection": 1078,
"text": "GBshape can be used to visualize DNA shape annotations qualitatively in a genome browser track format, and to download quantitative values of DNA shape features as a function of genomic position at nucleotide resolution."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 61,
"text": "GBshape: a genome browser database for DNA shape annotations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "abstract",
"offsetInBeginSection": 532,
"offsetInEndSection": 789,
"text": "Our Genome Browser for DNA shape annotations (GBshape; freely available at http://rohslab.cmb.usc.edu/GBshape/) provides minor groove width, propeller twist, roll, helix twist and hydroxyl radical cleavage predictions for the entire genomes of 94 organisms."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "abstract",
"offsetInBeginSection": 858,
"offsetInEndSection": 1078,
"text": "GBshape can be used to visualize DNA shape annotations qualitatively in a genome browser track format, and to download quantitative values of DNA shape features as a function of genomic position at nucleotide resolution."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 61,
"text": "GBshape: a genome browser database for DNA shape annotations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25326329",
"endSection": "abstract",
"offsetInBeginSection": 532,
"offsetInEndSection": 789,
"text": "Our Genome Browser for DNA shape annotations (GBshape; freely available at http://rohslab.cmb.usc.edu/GBshape/) provides minor groove width, propeller twist, roll, helix twist and hydroxyl radical cleavage predictions for the entire genomes of 94 organisms."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D064878",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D019991"
] |
[] |
56c8f4615795f9a73e00001a
|
bioasq_factoid
|
yesno
|
Is ACI-35 a passive vaccine?
|
['no']
|
[
"no"
] |
['No, ACI-35 is an active vaccine.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27485083"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27485083",
"endSection": "abstract",
"offsetInBeginSection": 392,
"offsetInEndSection": 519,
"text": "Two active vaccines targeting either nonphosphorylated (AAD-vac1) and phosphorylated tau (ACI-35) have entered Phase I testing."
}
] | 11 |
BioASQ-training11b
| null | null |
5a7d50d0faa1ab7d2e000016
|
bioasq_yesno
|
yesno
|
Is LDB1-mediated enhancer looping dependent on cohesin?
|
['no']
|
[
"no"
] |
['No. LDB1-mediated enhancer looping can be established independent of mediator and cohesin.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28520978"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28520978",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "LDB1-mediated enhancer looping can be established independent of mediator and cohesin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28520978",
"endSection": "abstract",
"offsetInBeginSection": 1167,
"offsetInEndSection": 1488,
"text": "Moreover, ENCODE data and our chromatin immunoprecipitation results indicate that cohesin is almost completely absent from validated and predicted LDB1-regulated erythroid enhancer-gene pairs. Thus, lineage specific factors largely mediate enhancer-promoter looping in erythroid cells independent of mediator and cohesin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28520978",
"endSection": "abstract",
"offsetInBeginSection": 1167,
"offsetInEndSection": 1359,
"text": "Moreover, ENCODE data and our chromatin immunoprecipitation results indicate that cohesin is almost completely absent from validated and predicted LDB1-regulated erythroid enhancer-gene pairs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28520978",
"endSection": "abstract",
"offsetInBeginSection": 1172,
"offsetInEndSection": 1364,
"text": "Moreover, ENCODE data and our chromatin immunoprecipitation results indicate that cohesin is almost completely absent from validated and predicted LDB1-regulated erythroid enhancer-gene pairs."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28520978",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 87,
"text": "LDB1-mediated enhancer looping can be established independent of mediator and cohesin."
}
] | 11 |
BioASQ-training11b
|
[
"http://amigo.geneontology.org/amigo/term/GO:0061774",
"http://amigo.geneontology.org/amigo/term/GO:0061780",
"http://amigo.geneontology.org/amigo/term/GO:0008278",
"http://amigo.geneontology.org/amigo/term/GO:0001205",
"http://amigo.geneontology.org/amigo/term/GO:0071921",
"http://amigo.geneontology.org/amigo/term/GO:1905309",
"http://amigo.geneontology.org/amigo/term/GO:0071923",
"http://amigo.geneontology.org/amigo/term/GO:0071922",
"http://amigo.geneontology.org/amigo/term/GO:1905339",
"http://amigo.geneontology.org/amigo/term/GO:1905338",
"http://amigo.geneontology.org/amigo/term/GO:0003705",
"http://amigo.geneontology.org/amigo/term/GO:0071733",
"https://meshb.nlm.nih.gov/record/ui?ui=D004742",
"http://amigo.geneontology.org/amigo/term/GO:0001206"
] | null |
5a6e49a4b750ff445500004b
|
bioasq_yesno
|
factoid
|
Which is the process that Conserved noncoding elements mostly regulate?
|
['Development']
|
[
"Development",
"Growth",
"Progression",
"Advancement",
"Evolution",
"Maturation",
"Formation",
"Transformation"
] |
['Conserved noncoding elements play a fundamental role in regulating animal development']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23042552",
"http://www.ncbi.nlm.nih.gov/pubmed/21731768",
"http://www.ncbi.nlm.nih.gov/pubmed/21629789",
"http://www.ncbi.nlm.nih.gov/pubmed/21478460",
"http://www.ncbi.nlm.nih.gov/pubmed/21175683",
"http://www.ncbi.nlm.nih.gov/pubmed/19704032",
"http://www.ncbi.nlm.nih.gov/pubmed/19492354",
"http://www.ncbi.nlm.nih.gov/pubmed/19073165",
"http://www.ncbi.nlm.nih.gov/pubmed/18334644",
"http://www.ncbi.nlm.nih.gov/pubmed/18282512",
"http://www.ncbi.nlm.nih.gov/pubmed/18279518",
"http://www.ncbi.nlm.nih.gov/pubmed/18056681",
"http://www.ncbi.nlm.nih.gov/pubmed/17442748",
"http://www.ncbi.nlm.nih.gov/pubmed/16533910",
"http://www.ncbi.nlm.nih.gov/pubmed/19698106",
"http://www.ncbi.nlm.nih.gov/pubmed/16630819",
"http://www.ncbi.nlm.nih.gov/pubmed/17096848"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21478460",
"endSection": "sections.0",
"offsetInBeginSection": 507,
"offsetInEndSection": 681,
"text": "Much evidence suggests that CNEs are selectively constrained and not mutational cold-spots, and there is evidence that some CNEs play a role in the regulation of development."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21478460",
"endSection": "sections.0",
"offsetInBeginSection": 1463,
"offsetInEndSection": 1676,
"text": "This result suggests that there is widespread adaptation in mammalian conserved noncoding DNA elements, some of which have been implicated in the regulation of crucially important processes, including development."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21175683",
"endSection": "sections.0",
"offsetInBeginSection": 143,
"offsetInEndSection": 345,
"text": "Some characteristics of CNEs include their high frequency in mammalian genomes, their potential regulatory role in gene expression, and their enrichment in gene deserts nearby master developmental genes"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19704032",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "Animal genomes possess highly conserved cis-regulatory sequences that are often found near genes that regulate transcription and development."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19073165",
"endSection": "sections.0",
"offsetInBeginSection": 585,
"offsetInEndSection": 677,
"text": "HCNEs of both human and zebrafish function as specific developmental enhancers in zebrafish."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19073165",
"endSection": "sections.0",
"offsetInBeginSection": 1185,
"offsetInEndSection": 1391,
"text": "HCNEs from the same area often drive overlapping patterns, suggesting that multiple regulatory inputs are required to achieve robust and precise complex expression patterns exhibited by developmental genes."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18334644",
"endSection": "sections.0",
"offsetInBeginSection": 1401,
"offsetInEndSection": 1596,
"text": "These results suggest important roles for SINEs in the development of the mammalian neuronal network, a part of which was initiated with the exaptation of AmnSINE1 in a common mammalian ancestor."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18282512",
"endSection": "sections.0",
"offsetInBeginSection": 480,
"offsetInEndSection": 648,
"text": "Further positional analysis of these conserved noncoding elements (CNEs) in the genome demonstrates that they cluster around genes involved in developmental regulation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18056681",
"endSection": "sections.0",
"offsetInBeginSection": 1277,
"offsetInEndSection": 1412,
"text": "The majority of tetrapod-specific UCEs are noncoding and associated with genes involved in regulation of transcription and development."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16533910",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 304,
"text": "Fish-mammal genomic comparisons have proved powerful in identifying conserved noncoding elements likely to be cis-regulatory in nature, and the majority of those tested in vivo have been shown to act as tissue-specific enhancers associated with genes involved in transcriptional regulation of development"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16533910",
"endSection": "sections.0",
"offsetInBeginSection": 792,
"offsetInEndSection": 955,
"text": "In 74% of cases, we were able to assign a specific set of paralogous genes with annotation relating to transcriptional regulation and/or development to each family"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16630819",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 276,
"text": "The most highly conserved noncoding elements (HCNEs) in mammalian genomes cluster within regions enriched for genes encoding developmentally important transcription factors (TFs). This suggests that HCNE-rich regions may contain key regulatory controls involved in development"
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D017124"
] | null |
51387022bee46bd34c000002
|
bioasq_factoid
|
yesno
|
Is disruption of immune regulation mechanisms associated with adverse pregnancy outcomes, including preeclampsia (PE)?
|
['yes']
|
[
"yes"
] |
['Inflammation and oxidative stress at the maternal-fetal interface characterize the placental dysfunction that underlies the pregnancy disorder preeclampsia.', 'Disruption of complex immune regulation mechanisms is associated with adverse pregnancy outcomes, including preeclampsia (PE)']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34576285",
"http://www.ncbi.nlm.nih.gov/pubmed/9272206",
"http://www.ncbi.nlm.nih.gov/pubmed/34847253",
"http://www.ncbi.nlm.nih.gov/pubmed/32161574",
"http://www.ncbi.nlm.nih.gov/pubmed/19683334",
"http://www.ncbi.nlm.nih.gov/pubmed/34412079",
"http://www.ncbi.nlm.nih.gov/pubmed/21498785",
"http://www.ncbi.nlm.nih.gov/pubmed/34509865",
"http://www.ncbi.nlm.nih.gov/pubmed/30079067",
"http://www.ncbi.nlm.nih.gov/pubmed/32573856",
"http://www.ncbi.nlm.nih.gov/pubmed/27108670",
"http://www.ncbi.nlm.nih.gov/pubmed/24520479",
"http://www.ncbi.nlm.nih.gov/pubmed/34191338",
"http://www.ncbi.nlm.nih.gov/pubmed/30058156",
"http://www.ncbi.nlm.nih.gov/pubmed/31608721",
"http://www.ncbi.nlm.nih.gov/pubmed/29756666",
"http://www.ncbi.nlm.nih.gov/pubmed/34599631"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34412079",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 244,
"text": " Maternal systemic and placental inflammatory responses participate in the pathogenesis of hypertensive disorders of pregnancy including preeclampsia, a pregnancy-specific syndrome, although the role of inflammation remains unclear. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31608721",
"endSection": "abstract",
"offsetInBeginSection": 588,
"offsetInEndSection": 718,
"text": "Our results indicate these proteins are new factors that play important roles in the immunological pathomechanism of preeclampsia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32573856",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 156,
"text": "Inflammation and oxidative stress at the maternal-fetal interface characterize the placental dysfunction that underlies the pregnancy disorder preeclampsia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34509865",
"endSection": "abstract",
"offsetInBeginSection": 1119,
"offsetInEndSection": 1265,
"text": "The abnormal expression of Tim-3 on MDSC might be involved in the pathogenesis of PE, and could be a marker to evaluate the immune function in PE."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34599631",
"endSection": "abstract",
"offsetInBeginSection": 223,
"offsetInEndSection": 408,
"text": "Maternal immune tolerance is important for maintaining pregnancy, and researchers have increasingly focused on the critical roles of cytokines in the pathogenesis of PE in recent years."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32161574",
"endSection": "abstract",
"offsetInBeginSection": 130,
"offsetInEndSection": 289,
"text": "Disruption of well-controlled immune functions leads to infertility, placental inflammation, and numerous pregnancy complications, including preeclampsia (PE)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34576285",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 178,
"text": "Effect of Endogenic and Exogenic Oxidative Stress Triggers on Adverse Pregnancy Outcomes: Preeclampsia, Fetal Growth Restriction, Gestational Diabetes Mellitus and Preterm Birth."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34847253",
"endSection": "abstract",
"offsetInBeginSection": 204,
"offsetInEndSection": 330,
"text": "Disruption of complex immune regulation mechanisms is associated with adverse pregnancy outcomes, including preeclampsia (PE)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24520479",
"endSection": "abstract",
"offsetInBeginSection": 1203,
"offsetInEndSection": 1427,
"text": "In addition, it has been demonstrated that immune disturbance may be responsible for some adverse pregnancy outcomes such as preeclampsia (PE), recurrent spontaneous abortion (RSA) and intrauterine growth restriction (IUGR)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29756666",
"endSection": "abstract",
"offsetInBeginSection": 99,
"offsetInEndSection": 265,
"text": "esponse. In previous models of preeclampsia (PE), defective immune function caused by disruption of lymphangiogenesis was shown to be involved in the disease pathophy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21498785",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 190,
"text": "OBJECTIVE: Increased oxidative stress and immune dysfunction are implicated in preeclampsia (PE) and may contribute to the two- to fourfold increase in PE prevalence among women with type 1 "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30079067",
"endSection": "abstract",
"offsetInBeginSection": 433,
"offsetInEndSection": 655,
"text": "r, in preeclampsia, the regulation of immune responses is disrupted as a result of aberrant activation of innate immune cells and imbalanced differentiation of T-helper cell subsets creating a cytotoxic environment in uter"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30079067",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "Disruption in the Regulation of Immune Responses in the Placental Subtype of Preeclampsia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30079067",
"endSection": "abstract",
"offsetInBeginSection": 1654,
"offsetInEndSection": 1808,
"text": "a disrupted immune system might be a predisposing factor or result of placental oxidative stress or excessive inflammation in preeclampsia. Preeclampsia c"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30079067",
"endSection": "abstract",
"offsetInBeginSection": 1247,
"offsetInEndSection": 1448,
"text": "clude insufficient control of inflammation, failure of tolerance toward paternal antigens at the fetal-maternal interface, and subsequent over- or insufficient activation of immune mediators. It is als"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9272206",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 160,
"text": "PROBLEM: The purpose of this study is to clarify whether the disruption of immune regulation occurs in early pregnancy before the clinical manifestations of pre"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30079067",
"endSection": "abstract",
"offsetInBeginSection": 1091,
"offsetInEndSection": 1244,
"text": "s review, we focus on the role of excessive systemic inflammation as the result of a dysregulated immune system in the development of preeclampsia. These"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9272206",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "PROBLEM: The purpose of this study is to clarify whether the disruption of immune regulation occurs in early pregnancy before the clinical manifestations of pree"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30079067",
"endSection": "abstract",
"offsetInBeginSection": 427,
"offsetInEndSection": 657,
"text": "However, in preeclampsia, the regulation of immune responses is disrupted as a result of aberrant activation of innate immune cells and imbalanced differentiation of T-helper cell subsets creating a cytotoxic environment in utero."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30079067",
"endSection": "abstract",
"offsetInBeginSection": 1639,
"offsetInEndSection": 1793,
"text": "In conclusion, a disrupted immune system might be a predisposing factor or result of placental oxidative stress or excessive inflammation in preeclampsia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29756666",
"endSection": "abstract",
"offsetInBeginSection": 99,
"offsetInEndSection": 264,
"text": "esponse. In previous models of preeclampsia (PE), defective immune function caused by disruption of lymphangiogenesis was shown to be involved in the disease pathoph"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34191338",
"endSection": "abstract",
"offsetInBeginSection": 140,
"offsetInEndSection": 385,
"text": "Disruption of this immune balance and/or inadequate placental perfusion is believed to be associated with a lot of pregnancy-related complications, such as recurrent spontaneous abortion, pre-eclampsia, and fetal intrauterine growth restriction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30058156",
"endSection": "abstract",
"offsetInBeginSection": 270,
"offsetInEndSection": 530,
"text": "Therefore, a delicate immune balance is critical for the maintenance of a successful pregnancy, while disruption of this balance can induce complications such as implantation failure, miscarriage, preterm birth/labor, preeclampsia and fetal growth restriction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34847253",
"endSection": "abstract",
"offsetInBeginSection": 177,
"offsetInEndSection": 327,
"text": "antigens during pregnancy. Disruption of complex immune regulation mechanisms is associated with adverse pregnancy outcomes, including preeclampsia (P"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27108670",
"endSection": "abstract",
"offsetInBeginSection": 231,
"offsetInEndSection": 381,
"text": "ccessful pregnancy. It has been demonstrated that innate immune disturbances may be responsible for some adverse pregnancy outcomes such as preeclamps"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30079067",
"endSection": "abstract",
"offsetInBeginSection": 430,
"offsetInEndSection": 580,
"text": "ever, in preeclampsia, the regulation of immune responses is disrupted as a result of aberrant activation of innate immune cells and imbalanced differ"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9272206",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 169,
"text": "PROBLEM: The purpose of this study is to clarify whether the disruption of immune regulation occurs in early pregnancy before the clinical manifestations of preeclampsia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19683334",
"endSection": "abstract",
"offsetInBeginSection": 1079,
"offsetInEndSection": 1323,
"text": "However, immune maladaptation and hemostatic imbalance have been suggested to be responsible for adverse pregnant outcomes, such as preeclampsia (PE), miscarriage, recurrent spontaneous abortion (RSA) and intrauterine growth restriction (IUGR)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9272206",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 856,
"text": "PROBLEM: The purpose of this study is to clarify whether the disruption of immune regulation occurs in early pregnancy before the clinical manifestations of preeclampsia.METHOD OF STUDY: The serum concentrations of interleukin-2 (IL-2) and tumor necrosis factor-alpha (TNF-alpha) were determined by using enzyme-linked immunoadsorbent assay (ELISA) in the first trimester of pregnancy in women who had preeclampsia develop after 28 weeks of pregnancy (preeclamptic group) and in women who completed pregnancy uneventfully (control group).RESULTS: Serum concentrations of both IL-2 and TNF-alpha in the first trimester of the preeclamptic group were significantly higher than those of the control group.CONCLUSIONS: That the perturbation of feto-maternal immune regulation may precede the clinical manifestations of preeclampsia, which may be of relevance i"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30079067",
"endSection": "abstract",
"offsetInBeginSection": 1794,
"offsetInEndSection": 2009,
"text": "Preeclampsia can thus be considered a hyperinflammatory state associated with defective regulation of the immune system proposed as a key element in the pathological events of the placental subtype of this disorder."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30079067",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "Disruption in the Regulation of Immune Responses in the Placental Subtype of Preeclampsia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27108670",
"endSection": "abstract",
"offsetInBeginSection": 251,
"offsetInEndSection": 538,
"text": "It has been demonstrated that innate immune disturbances may be responsible for some adverse pregnancy outcomes such as preeclampsia (PE); hemolysis, elevated liver enzymes, low platelets (HELLP) syndrome; intrauterine growth restriction (IUGR); and recurrent spontaneous abortion (RSA)."
}
] | 11 |
BioASQ-training11b
| null | null |
622632483a8413c653000081
|
bioasq_yesno
|
factoid
|
How are Arboviruses transmitted?
|
['By arthropods']
|
[
"arthropods",
"Arthropoda",
"jointed-legged animals",
"insects, arachnids, crustaceans",
"arthropod animals"
] |
['Arboviruses are transmitted by arthropods.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26141429",
"http://www.ncbi.nlm.nih.gov/pubmed/10488638",
"http://www.ncbi.nlm.nih.gov/pubmed/21658241",
"http://www.ncbi.nlm.nih.gov/pubmed/26925368",
"http://www.ncbi.nlm.nih.gov/pubmed/16893487",
"http://www.ncbi.nlm.nih.gov/pubmed/25597441",
"http://www.ncbi.nlm.nih.gov/pubmed/27220616",
"http://www.ncbi.nlm.nih.gov/pubmed/1973949",
"http://www.ncbi.nlm.nih.gov/pubmed/26363996",
"http://www.ncbi.nlm.nih.gov/pubmed/1297177",
"http://www.ncbi.nlm.nih.gov/pubmed/27869394",
"http://www.ncbi.nlm.nih.gov/pubmed/24941331",
"http://www.ncbi.nlm.nih.gov/pubmed/26283013",
"http://www.ncbi.nlm.nih.gov/pubmed/8158611",
"http://www.ncbi.nlm.nih.gov/pubmed/25053841"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25597441",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 156,
"text": "Epizootic congenital abnormalities, encephalomyelitis and febrile illnesses in cattle caused by arthropod-borne viruses (arboviruses) are prevalent in Japan"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26283013",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 97,
"text": " Zika virus (ZIKV) is an arthropod-borne virus (arbovirus) transmitted by mosquitoes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16893487",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 201,
"text": "Nine different arboviruses are known to be transmitted by, or associated with, mosquitoes in Europe, and several (West Nile, Sindbis and Tahyna viruses) are reported to cause outbreaks of human disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24941331",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Arthropod-borne viruses (arboviruses) are transmitted to humans primarily through the bites of infected mosquitoes and ticks"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21658241",
"endSection": "abstract",
"offsetInBeginSection": 114,
"offsetInEndSection": 207,
"text": "Arboviruses are transmitted among vertebrates by biting insects, chiefly mosquitoes and ticks"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25053841",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Arboviruses are transmitted by distantly related arthropod vectors such as mosquitoes (class Insecta) and ticks (class Arachnida)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26363996",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 215,
"text": "Mosquito-transmitted arthropod-borne viruses (arboviruses) such as dengue virus, chikungunya virus, and West Nile virus constitute a major public health burden and are increasing in severity and frequency worldwide."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1973949",
"endSection": "abstract",
"offsetInBeginSection": 263,
"offsetInEndSection": 564,
"text": "Malaria and Japanese encephalitis are the two most serious human diseases transmitted by riceland mosquitoes, but they have been incriminated as vectors of dozens of arboviruses and other parasites and pathogens including the causal agents of West Nile and Rift Valley Fevers and lymphatic filariasis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25053841",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Arboviruses are transmitted by distantly related arthropod vectors such as mosquitoes (class Insecta) and ticks (class Arachnida)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10488638",
"endSection": "abstract",
"offsetInBeginSection": 594,
"offsetInEndSection": 786,
"text": "Many of them are transmitted by insects (arboviruses, e.g. yellow fever virus) or by rodents (e.g. Hanta viruses), others by contact with patients and nosocomial infections (e.g. Ebola virus)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26141429",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "Arboviruses - viruses transmitted by haematophagous arthropods - are responsible for febrile syndromes, which sometimes include haemorrhagic or neurological symptoms."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27220616",
"endSection": "abstract",
"offsetInBeginSection": 168,
"offsetInEndSection": 289,
"text": "Arboviruses are transmitted to vertebral hosts during blood feedings by mosquitoes, ticks, biting flies, mites, and nits."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26925368",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "Arboviruses transmitted by mosquitoes are a major cause of human disease worldwide."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27869394",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "Diseases caused by arboviruses transmitted by Aedes aegypti, such as dengue, chikungunya and Zika, continue to rise in annual incidence and geographic expansion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8158611",
"endSection": "abstract",
"offsetInBeginSection": 223,
"offsetInEndSection": 414,
"text": "Arboviruses transmitted by ticks must adapt to the peculiar physiological and behavioral characteristics of ticks, particularly with regard to blood feeding, bloodmeal digestion, and molting."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26141429",
"endSection": "abstract",
"offsetInBeginSection": 330,
"offsetInEndSection": 532,
"text": "The last decade has seen significant changes in the epidemiology of arboviruses transmitted by mosquitoes of the genus Aedes, particularly in relation to the intercontinental spread of Aedes albopictus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1297177",
"endSection": "abstract",
"offsetInBeginSection": 381,
"offsetInEndSection": 687,
"text": "This technique enables the detection of 70 of the 80 arboviruses transmitted by mosquitoes in Africa and very easily detects arbovirus associations by using either monospecific or monoclonal immune ascitic fluids (dengue-1-2-3-4 and yellow fever viruses) used in the indirect immunofluorescence technique.."
}
] | 6 |
BioASQ-training6b
|
[
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D007303",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018562",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D001103",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D001102"
] |
[
{
"o": "Arboviruses",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C0003725"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A18608581",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0003725"
},
{
"o": "arboviruses",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A18608581"
}
] |
58f4b85f70f9fc6f0f000015
|
bioasq_factoid
|
factoid
|
Which disease do pathogenic NR2F1 variants cause?
|
['Bosch-Boonstra-Schaaf optic atrophy syndrome', 'BBSOAS']
|
[
"Bosch-Boonstra-Schaaf optic atrophy syndrome",
"BBSOAS",
"BBSOAS syndrome",
"Bosch-Boonstra-Schaaf syndrome",
"Boonstra-Bosch-Schaaf optic atrophy syndrome"
] |
['Bosch-Boonstra-Schaaf optic atrophy syndrome (BBSOAS) is an autosomal-dominant disorder characterized by optic atrophy and intellectual disability caused by loss-of-function mutations in NR2F1.', 'Bosch-Boonstra-Schaaf optic atrophy syndrome', 'Bosch-Boonstra-Schaaf Optic Atrophy Syndrome']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26986877"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26986877",
"endSection": "abstract",
"offsetInBeginSection": 9,
"offsetInEndSection": 202,
"text": "Bosch-Boonstra-Schaaf optic atrophy syndrome (BBSOAS) is an autosomal-dominant disorder characterized by optic atrophy and intellectual disability caused by loss-of-function mutations in NR2F1."
}
] | 11 |
BioASQ-training11b
| null | null |
61f52f22882a024a10000002
|
bioasq_factoid
|
factoid
|
The virus that causes FIP, Feline Infectious Peritonitis belongs to what family?
|
['Coronavirus']
|
[
"Coronavirus",
"CoV",
"Coronaviridae",
"SARS-CoV",
"MERS-CoV",
"SARS-CoV-2",
"COVID-19 virus",
"2019-nCoV",
"Novel coronavirus"
] |
['The virus that causes FIP, Feline Infectious Peritonitis belongs to the family coronavirus.', 'Feline coronavirus (fcov) is an etiological agent that causes a benign enteric illness and the fatal systemic disease feline infectious peritonitis (fip).', 'Feline coronavirus (FCoV) is an etiological agent that causes a benign enteric illness and the fatal systemic disease feline infectious peritonitis (FIP)', 'Feline Infectious Peritonitis (FIP) belongs to the family of coronavirus.', 'Feline infectious peritonitis (FIP) is a common and highly lethal coronavirus disease of domestic cats.', 'Feline infectious peritonitis (FIP) is a common and highly lethal coronavirus disease of domestic cats', 'Feline Infectious Peritonitis virus (FIP) belongs to the coronavirus family of the genus Flavivirus which cause central nervous system disease.', 'Feline infectious peritonitis (FIP) is a cat virus caused by a member of the coronavirus family coronaviruses.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22546085",
"http://www.ncbi.nlm.nih.gov/pubmed/27712624",
"http://www.ncbi.nlm.nih.gov/pubmed/31375588",
"http://www.ncbi.nlm.nih.gov/pubmed/29329682",
"http://www.ncbi.nlm.nih.gov/pubmed/30065095",
"http://www.ncbi.nlm.nih.gov/pubmed/23865689",
"http://www.ncbi.nlm.nih.gov/pubmed/23763835",
"http://www.ncbi.nlm.nih.gov/pubmed/29778200",
"http://www.ncbi.nlm.nih.gov/pubmed/25701212",
"http://www.ncbi.nlm.nih.gov/pubmed/29478397",
"http://www.ncbi.nlm.nih.gov/pubmed/26656689"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29778200",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Feline infectious peritonitis (FIP) is a common and highly lethal coronavirus disease of domestic cats"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29329682",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Feline coronavirus (FCoV) is an etiological agent that causes a benign enteric illness and the fatal systemic disease feline infectious peritonitis (FIP). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29478397",
"endSection": "abstract",
"offsetInBeginSection": 21,
"offsetInEndSection": 247,
"text": "Feline coronavirus (FCoV) infection is very common in cats, usually causing only mild intestinal signs such as diarrhoea. Up to 10% of FCoV infections, however, result in the fatal disease feline infectious peritonitis (FIP). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26656689",
"endSection": "abstract",
"offsetInBeginSection": 92,
"offsetInEndSection": 350,
"text": "Feline infectious peritonitis virus (FIPV) belongs to the genus Alphacoronavirus, resulting in a lethal systemic granulomatous disease called feline infectious peritonitis (FIP), which is one of the most important fatal infectious diseases of cats worldwide."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27712624",
"endSection": "abstract",
"offsetInBeginSection": 278,
"offsetInEndSection": 412,
"text": "The causative agent of this deadly disease, feline infectious peritonitis virus (FIPV), arises from feline enteric coronavirus (FECV)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23865689",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "Feline infectious peritonitis (FIP) is a fatal disease caused by feline coronavirus (FCoV) infection."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25701212",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 172,
"text": "Feline infectious peritonitis virus (FIP virus: FIPV), a feline coronavirus of the family Coronaviridae, causes a fatal disease called FIP in wild and domestic cat species."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31375588",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "Feline infectious peritonitis (FIP) is one of the most important infectious diseases in cats and is caused by feline coronavirus (FCoV)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31375588",
"endSection": "abstract",
"offsetInBeginSection": 1642,
"offsetInEndSection": 1824,
"text": "IMPORTANCE Feline coronavirus (FCoV) is one of the most significant coronaviruses, because this virus induces feline infectious peritonitis (FIP), which is a lethal disease in cats."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30065095",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 206,
"text": "Feline infectious peritonitis (FIP), one of the most important lethal infections of cats, is caused by feline infectious peritonitis virus (FIPV), the high-virulence biotype of feline coronaviruses (FCoVs)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22546085",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 148,
"text": "The feline infectious peritonitis virus ( FIPV ) is a member of the feline coronavirus family that causes FIP , which is incurable and fatal in cats"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25701212",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 174,
"text": "Feline infectious peritonitis virus ( FIP virus: FIPV) , a feline coronavirus of the family Coronaviridae , causes a fatal disease called FIP in wild and domestic cat species"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26656689",
"endSection": "abstract",
"offsetInBeginSection": 91,
"offsetInEndSection": 350,
"text": "Feline infectious peritonitis virus (FIPV) belongs to the genus Alphacoronavirus, resulting in a lethal systemic granulomatous disease called feline infectious peritonitis (FIP), which is one of the most important fatal infectious diseases of cats worldwide."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27712624",
"endSection": "abstract",
"offsetInBeginSection": 278,
"offsetInEndSection": 413,
"text": "The causative agent of this deadly disease, feline infectious peritonitis virus (FIPV), arises from feline enteric coronavirus (FECV)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23763835",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Feline coronaviruses (FCoV) exist as 2 biotypes: feline enteric coronavirus (FECV) and feline infectious peritonitis virus (FIPV)."
}
] | 11 |
BioASQ-training11b
| null | null |
5e3eba5548dab47f26000009
|
bioasq_factoid
|
factoid
|
What gene test is recommended for clopidogrel?
|
['CYP2C19 genotyping']
|
[
"CYP2C19 genotyping",
"Cytochrome P450 2C19 genotyping",
"CYP2C19 testing",
"CYP2C19 genetic testing",
"CYP2C19 polymorphism testing"
] |
['The genetic test recommended for clopidogrel is CYP2C19 genotyping.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22974536",
"http://www.ncbi.nlm.nih.gov/pubmed/22674970",
"http://www.ncbi.nlm.nih.gov/pubmed/22624833",
"http://www.ncbi.nlm.nih.gov/pubmed/22464343",
"http://www.ncbi.nlm.nih.gov/pubmed/22154242",
"http://www.ncbi.nlm.nih.gov/pubmed/22088980",
"http://www.ncbi.nlm.nih.gov/pubmed/21803320",
"http://www.ncbi.nlm.nih.gov/pubmed/20435227",
"http://www.ncbi.nlm.nih.gov/pubmed/20083681",
"http://www.ncbi.nlm.nih.gov/pubmed/19706858",
"http://www.ncbi.nlm.nih.gov/pubmed/18577829",
"http://www.ncbi.nlm.nih.gov/pubmed/18004210",
"http://www.ncbi.nlm.nih.gov/pubmed/17681590"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22674970",
"endSection": "sections.0",
"offsetInBeginSection": 607,
"offsetInEndSection": 677,
"text": "polymorphisms in the CYP2C19 gene affect clopidogrel pharmacokinetics."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22624833",
"endSection": "sections.0",
"offsetInBeginSection": 11,
"offsetInEndSection": 212,
"text": "This study sought to evaluate the influence of single nucleotide polymorphisms (SNPs) on the pharmacodynamic effect of high- or standard-dose clopidogrel after percutaneous coronary intervention (PCI)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22624833",
"endSection": "sections.0",
"offsetInBeginSection": 1621,
"offsetInEndSection": 2056,
"text": "CYP2C19, but not PON1 or ABCB1, is a significant determinant of the pharmacodynamic effects of clopidogrel, both early and late after PCI. In patients with high OTR identified by platelet function testing, the CYP2C19 genotype provides limited incremental information regarding the risk of persistently high reactivity with clopidogrel 150-mg maintenance dosing. (Genotype Information and Functional Testing Study [GIFT]; NCT00992420)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22088980",
"endSection": "sections.0",
"offsetInBeginSection": 12,
"offsetInEndSection": 324,
"text": "Variants in the CYP2C19 gene influence the pharmacologic and clinical response to the standard 75-mg daily maintenance dose of the antiplatelet drug clopidogrel. OBJECTIVE: To test whether higher doses (up to 300 mg daily) improve the response to clopidogrel in the setting of loss-of-function CYP2C19 genotypes."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22674970",
"endSection": "sections.0",
"offsetInBeginSection": 607,
"offsetInEndSection": 920,
"text": "polymorphisms in the CYP2C19 gene affect clopidogrel pharmacokinetics. These polymorphisms may be useful to identify clopidogrel nonresponders who may benefit from taking an alternative antiplatelet agent such as prasugrel and ticagrelor. Although both drugs have pharmacogenomic tests available for clinical use,"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22624833",
"endSection": "sections.0",
"offsetInBeginSection": 11,
"offsetInEndSection": 212,
"text": "This study sought to evaluate the influence of single nucleotide polymorphisms (SNPs) on the pharmacodynamic effect of high- or standard-dose clopidogrel after percutaneous coronary intervention (PCI)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22624833",
"endSection": "sections.0",
"offsetInBeginSection": 1621,
"offsetInEndSection": 2056,
"text": "CYP2C19, but not PON1 or ABCB1, is a significant determinant of the pharmacodynamic effects of clopidogrel, both early and late after PCI. In patients with high OTR identified by platelet function testing, the CYP2C19 genotype provides limited incremental information regarding the risk of persistently high reactivity with clopidogrel 150-mg maintenance dosing. (Genotype Information and Functional Testing Study [GIFT]; NCT00992420)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22464343",
"endSection": "sections.0",
"offsetInBeginSection": 136,
"offsetInEndSection": 497,
"text": "The CYP2C19*2 allele is a common genetic variant associated with increased rates of major adverse events in individuals given clopidogrel after percutaneous coronary intervention (PCI). We used a novel point-of-care genetic test to identify carriers of the CYP2C19*2 allele and aimed to assess a pharmacogenetic approach to dual antiplatelet treatment after PCI"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22154242",
"endSection": "sections.0",
"offsetInBeginSection": 12,
"offsetInEndSection": 401,
"text": "The antiplatelet effect of clopidogrel has been linked to cytochrome P450 2C19 (CYP2C19) carrier status. The presence of loss of function and gain of function variants were found to have a gene-dose effect on clopidogrel metabolism. However, genotyping is only one aspect of predicting response to clopidogrel and several platelet function tests are available to measure platelet response."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22088980",
"endSection": "sections.0",
"offsetInBeginSection": 12,
"offsetInEndSection": 324,
"text": "Variants in the CYP2C19 gene influence the pharmacologic and clinical response to the standard 75-mg daily maintenance dose of the antiplatelet drug clopidogrel. OBJECTIVE: To test whether higher doses (up to 300 mg daily) improve the response to clopidogrel in the setting of loss-of-function CYP2C19 genotypes."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21803320",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "The cytochrome P450 (CYP) 2C19*2 loss-of-function allele has been associated with impaired clopidogrel response and worse prognosis in clopidogrel-treated patients."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21803320",
"endSection": "sections.0",
"offsetInBeginSection": 357,
"offsetInEndSection": 637,
"text": "The present study was designed to evaluate the benefit of tailored therapy with a higher maintenance dose according to CYP2C19 genotypes in patients identified as nonresponders who underwent percutaneous coronary intervention for non-ST-segment elevation acute coronary syndromes."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20435227",
"endSection": "sections.0",
"offsetInBeginSection": 893,
"offsetInEndSection": 977,
"text": "identify genes and mutations with known associations with disease and drug response."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20435227",
"endSection": "sections.0",
"offsetInBeginSection": 1654,
"offsetInEndSection": 1753,
"text": "The patient had a heterozygous null mutation in CYP2C19 suggesting probable clopidogrel resistance,"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20083681",
"endSection": "sections.0",
"offsetInBeginSection": 12,
"offsetInEndSection": 344,
"text": "The cytochrome P450 (CYP) 2C19 isoenzyme plays an important role in clopidogrel metabolization. A recently explored CYP2C19*17 allelic variant has been linked to increased transcriptional activity, resulting in extensive metabolization of CYP2C19 substrates, which may lead to an enhanced platelet response to clopidogrel treatment."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19706858",
"endSection": "sections.0",
"offsetInBeginSection": 333,
"offsetInEndSection": 395,
"text": "To identify gene variants that influence clopidogrel response."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19706858",
"endSection": "sections.0",
"offsetInBeginSection": 608,
"offsetInEndSection": 973,
"text": "A genome-wide association study was performed followed by genotyping the loss-of-function cytochrome P450 (CYP) 2C19*2 variant (rs4244285). Findings in the PAPI Study were extended by examining the relation of CYP2C19*2 genotype to platelet function and cardiovascular outcomes in an independent sample of 227 patients undergoing percutaneous coronary intervention."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18577829",
"endSection": "sections.0",
"offsetInBeginSection": 12,
"offsetInEndSection": 116,
"text": "Coexisting polymorphisms of the genes affecting clopiogrel resistance may influence platelet activation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18577829",
"endSection": "sections.0",
"offsetInBeginSection": 439,
"offsetInEndSection": 754,
"text": "Genotyping revealed 7 carriers of both the C allele of P2Y12 and A allele of CYP2C19 (group 1), 14 carriers of the T allele of P2Y12 and A allele of CYP2C19 (group 2), 17 carriers of the C allele of P2Y12 and G allele of CYP2C19 (group 3) and 67 carriers of the T allele of P2Y12 and G allele of CYP2C19 (controls)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18004210",
"endSection": "sections.0",
"offsetInBeginSection": 37,
"offsetInEndSection": 285,
"text": "to evaluate the effect of polymorphisms affecting the clopidogrel metabolism (CYP3A4 IVS10+12G/A and CYP2C19*2) and the P2Y12 receptor (P2Y12 T744C) on modulating platelet function in acute coronary syndrome patients on dual antiplatelet treatment."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17681590",
"endSection": "sections.0",
"offsetInBeginSection": 260,
"offsetInEndSection": 337,
"text": "to test the influence of the CYP 2C19*2 allele on clopidogrel responsiveness."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22674970",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 84,
"text": "Genetic polymorphisms significantly influence responses to warfarin and clopidogrel."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22974536",
"endSection": "sections.0",
"offsetInBeginSection": 12,
"offsetInEndSection": 286,
"text": "A recent clinical trial has demonstrated that patients with acute coronary syndromes (ACS) and the reduced function allele CYP2C19*2 (*2 allele), who are treated with thienopyridines, have an increased risk of adverse cardiac events with clopidogrel, but not with prasugrel."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.biosemantics.org/jochem#4260620",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D005796",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D005820",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003955"
] |
[
{
"o": "http://linkedlifedata.com/resource/umls/label/A0173515",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0070166"
},
{
"o": "clopidogrel",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A0173515"
},
{
"o": "http://www.w3.org/2008/05/skos-xl#Label",
"p": "http://www.w3.org/1999/02/22-rdf-syntax-ns#type",
"s": "http://linkedlifedata.com/resource/umls/label/A12101557"
},
{
"o": "Clopidogrel",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A12785306"
},
{
"o": "MeSH",
"p": "http://www.w3.org/2004/02/skos/core#note",
"s": "http://linkedlifedata.com/resource/umls/label/A0173516"
},
{
"o": "http://www.w3.org/2008/05/skos-xl#Label",
"p": "http://www.w3.org/1999/02/22-rdf-syntax-ns#type",
"s": "http://linkedlifedata.com/resource/umls/label/A10928568"
}
] |
5156be04d24251bc05000085
|
bioasq_factoid
|
yesno
|
Is apixaban effective for treatment of acute venous thromboembolism?
|
['yes']
|
[
"yes"
] |
Apixaban is a direct inhibitor of factor Xa, and is a potential alternative for the treatment of acute venous thromboembolism. These results suggest a lack of clear superiority of apixaban relative to enoxaparin. Apixaban is an oral alternative with similar efficacy and safety to existing anticoagulant therapies.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24057162",
"http://www.ncbi.nlm.nih.gov/pubmed/23808982",
"http://www.ncbi.nlm.nih.gov/pubmed/23150473",
"http://www.ncbi.nlm.nih.gov/pubmed/23117646",
"http://www.ncbi.nlm.nih.gov/pubmed/22795419",
"http://www.ncbi.nlm.nih.gov/pubmed/18393142"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24057162",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Apixaban is a direct inhibitor of factor Xa, and is a potential alternative for the treatment of acute venous thromboembolism. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24057162",
"endSection": "abstract",
"offsetInBeginSection": 945,
"offsetInEndSection": 1132,
"text": "These results suggest a lack of clear superiority of apixaban relative to enoxaparin. Apixaban is an oral alternative with similar efficacy and safety to existing anticoagulant therapies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23808982",
"endSection": "abstract",
"offsetInBeginSection": 1718,
"offsetInEndSection": 1898,
"text": "A fixed-dose regimen of apixaban alone was noninferior to conventional therapy for the treatment of acute venous thromboembolism and was associated with significantly less bleeding"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23150473",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 186,
"text": "To critically review the effectiveness of the novel oral anticoagulants (rivaroxaban, dabigatran, ximelagatran, and apixaban) in the treatment of acute venous thromboembolism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23150473",
"endSection": "abstract",
"offsetInBeginSection": 2087,
"offsetInEndSection": 2308,
"text": "ompared with vitamin K antagonists, the novel oral anticoagulants had a similar risk of recurrence of acute venous thromboembolism and all cause mortality, though rivaroxaban was associated with a reduced risk of bleeding"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23117646",
"endSection": "abstract",
"offsetInBeginSection": 103,
"offsetInEndSection": 329,
"text": "Nowadays, the new anticoagulants, such as dabigatran, rivaroxaban and apixaban, show potential advantages over classical treatments. These agents inhibit specific coagulation factors and are administered orally at fixed doses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22795419",
"endSection": "abstract",
"offsetInBeginSection": 1192,
"offsetInEndSection": 1308,
"text": "In a recently completed phase III trial, apixaban also demonstrated promising efficacy and safety in that indication"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18393142",
"endSection": "abstract",
"offsetInBeginSection": 318,
"offsetInEndSection": 419,
"text": "the most advanced oral direct inhibitors to factor Xa (rivaroxaban and apixaban) and IIa (dabigatran)"
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D054556",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013923",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D020246"
] |
[] |
52fc94572059c6d71c000070
|
bioasq_yesno
|
factoid
|
What is another name for the drug AMG334?
|
['Erenumab']
|
[
"Erenumab",
"Aimovig"
] |
['AMG334 is also called erenumab.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28240610"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28240610",
"endSection": "abstract",
"offsetInBeginSection": 19,
"offsetInEndSection": 396,
"text": "The results of phase 2 randomized controlled trials for the prevention of episodic and chronic migraine demonstrating the efficacy and safety of four mAbs targeting the calcitonin gene-related peptide (CGRP) pathway [ALD403 (eptinezumab), AMG334 (erenumab), LY2951742 (galcanezumab) and TEV48125 (fremanezumab)] have been published recently, and phase 3 trials are in process. "
}
] | 11 |
BioASQ-training11b
| null | null |
6026ed981cb411341a0000d2
|
bioasq_factoid
|
yesno
|
Does Vitamin D induce autophagy?
|
['yes']
|
[
"yes"
] |
['Yes, vitamin D induces autophagy.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27915989",
"http://www.ncbi.nlm.nih.gov/pubmed/27430408",
"http://www.ncbi.nlm.nih.gov/pubmed/26562100",
"http://www.ncbi.nlm.nih.gov/pubmed/27174720"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26562100",
"endSection": "abstract",
"offsetInBeginSection": 1441,
"offsetInEndSection": 1503,
"text": " 1,25(OH)2D treatment was accompanied by autophagy activation "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27174720",
"endSection": "abstract",
"offsetInBeginSection": 79,
"offsetInEndSection": 134,
"text": "Autophagy signaling pathway was regulated by vitamin D3"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27430408",
"endSection": "abstract",
"offsetInBeginSection": 1447,
"offsetInEndSection": 1474,
"text": "vitamin D induces autophagy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27915989",
"endSection": "abstract",
"offsetInBeginSection": 740,
"offsetInEndSection": 923,
"text": "Vitamin D shows promise for the prevention and amelioration of pathologic responses in IBD, an effect that is mediated, at least in part, by the induction and modulation of autophagy."
}
] | 6 |
BioASQ-training6b
| null | null |
58a957a8cc344ae31e000001
|
bioasq_yesno
|
yesno
|
Is there an increased risk of meningiomas in atomic bomb survivors?
|
['yes']
|
[
"yes"
] |
['Yes, the incidence of meningiomas is increased in atomic bomb survivors.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/12381708",
"http://www.ncbi.nlm.nih.gov/pubmed/8707402",
"http://www.ncbi.nlm.nih.gov/pubmed/10408177",
"http://www.ncbi.nlm.nih.gov/pubmed/15378499"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15378499",
"endSection": "abstract",
"offsetInBeginSection": 869,
"offsetInEndSection": 1018,
"text": "RESULTS: Meningioma was the most common tumor among clinically diagnosed tumors, followed by neuroepithelial tumor, schwannoma, and pituitary tumor. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15378499",
"endSection": "abstract",
"offsetInBeginSection": 1521,
"offsetInEndSection": 1659,
"text": "The predominance of meningiomas over neuroepithelial tumors in the Japanese population was noteworthy and warrants further investigation. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12381708",
"endSection": "abstract",
"offsetInBeginSection": 1130,
"offsetInEndSection": 1427,
"text": "Risk increases, although not statistically significant, were seen for meningiomas (ERR(Sv) = 0.6, 95% CI = -0.01 to 1.8), gliomas (ERR(Sv) = 0.6, 95% CI = -0.2 to 2.0), other nervous system tumors (ERR(Sv) = 0.5, 95% CI = <-0.2 to 2.2), and pituitary tumors (ERR(Sv) = 1.0, 95% CI = <-0.2 to 3.5)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10408177",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 67,
"text": "High incidence of meningioma among Hiroshima atomic bomb survivors."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10408177",
"endSection": "abstract",
"offsetInBeginSection": 1105,
"offsetInEndSection": 1409,
"text": "The incidence of meningioma among Hiroshima atomic bomb survivors has increased since 1975. There was a significant correlation between the incidence and the dose of radiation to the brain. The present findings strongly suggest that meningioma is one of the tumors induced by atomic bombing in Hiroshima."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8707402",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 72,
"text": "Incidence of intracranial meningiomas in Nagasaki atomic-bomb survivors."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8707402",
"endSection": "abstract",
"offsetInBeginSection": 583,
"offsetInEndSection": 936,
"text": "The analysis showed a high correlation between incidence of meningiomas and distance from the hypocenter. The incidence among Nagasaki atomic-bomb survivors over 40 years of age, especially in those proximally exposed, appears to be increasing, in inverse proportion to the exposure distance, since 1981, 36 years after the explosion of the atomic bomb."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10408177",
"endSection": "abstract",
"offsetInBeginSection": 1105,
"offsetInEndSection": 1196,
"text": "The incidence of meningioma among Hiroshima atomic bomb survivors has increased since 1975."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10408177",
"endSection": "abstract",
"offsetInBeginSection": 1295,
"offsetInEndSection": 1409,
"text": "The present findings strongly suggest that meningioma is one of the tumors induced by atomic bombing in Hiroshima."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10408177",
"endSection": "abstract",
"offsetInBeginSection": 661,
"offsetInEndSection": 798,
"text": "The incidences of meningioma among the survivors of Hiroshima in 5-year intervals since 1975 were 5.3, 7.4, 10.1, and 14.9, respectively."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8707402",
"endSection": "abstract",
"offsetInBeginSection": 583,
"offsetInEndSection": 688,
"text": "The analysis showed a high correlation between incidence of meningiomas and distance from the hypocenter."
}
] | 11 |
BioASQ-training11b
| null | null |
5e323780fbd6abf43b000055
|
bioasq_yesno
|
yesno
|
Is periampullary carcinoma (PAC) a relatively rare genitourinary malignancy
|
['no']
|
[
"no"
] |
['Periampullary carcinoma (PAC) a relatively rare gastrointestinal malignancy and includes Pancreaticobiliary as a subtype of Periampullary carcinoma']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24650967",
"http://www.ncbi.nlm.nih.gov/pubmed/23187842",
"http://www.ncbi.nlm.nih.gov/pubmed/10073125",
"http://www.ncbi.nlm.nih.gov/pubmed/29504325",
"http://www.ncbi.nlm.nih.gov/pubmed/33227091",
"http://www.ncbi.nlm.nih.gov/pubmed/30258276",
"http://www.ncbi.nlm.nih.gov/pubmed/34673588",
"http://www.ncbi.nlm.nih.gov/pubmed/24075520"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34673588",
"endSection": "abstract",
"offsetInBeginSection": 14,
"offsetInEndSection": 135,
"text": "Pancreaticobiliary subtype of Periampullary carcinoma (PAC) has a poor prognosis in comparison to the intestinal subtype."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34673588",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "MUC1, CK20, and CDX2 immunohistochemical markers can sub-classify periampullary carcinomas into pancreaticobiliary, intestinal, and mixed subtypes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23187842",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 329,
"text": "Pancreaticoduodenectomy (PD) is a complex surgical procedure involving resection of the duodenum, the pancreatic head and uncinate process, and the distal common bile duct. It is most commonly performed for periampullary malignancy but may also be indicated in select cases of chronic pancreatitis or benign periampullary tumors."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24650967",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 162,
"text": "In patients suspected of pancreatic or periampullary cancer, abdominal contrast-enhanced computed tomography (CT) is the standard diagnostic modality."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24075520",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 275,
"text": "The pre-operative neutrophil-to-lymphocyte ratio (NLR), when ≥5 has been associated with reduced survival for patients with various gastrointestinal tract cancers, however, it's prognostic value in patients with periampullary tumour has not been reported to date."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29504325",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "Comparison Of Biliary Stenting And Surgical Bypass In Palliative Management Of Irresectable Periampullary Carcinoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29504325",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 173,
"text": " Some 20-40% of the periampullary carcinoma is irresectable at the time of diagnosis. Biliary stenting and surgical bypass are commonly used palliative procedure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30258276",
"endSection": "abstract",
"offsetInBeginSection": 232,
"offsetInEndSection": 395,
"text": "Whereas Periampulary AdenoCarcinoma (PAC) having four anatomic subtypes, pancreatic, Common Bile Duct (CBD), ampullary and duodenum shows relative better prognosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10073125",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 379,
"text": "DEFINITION: Periampullary carcinomas are rare and constitute a special entity, as diagnosed earlier and having a better prognosis than other duodenal tumors.METHODS: In the present study, we retrospectively reviewed the medical records of 16 patients with periampullary carcinomas over 10 years.RESULTS: 16 patients, 10 men and 6 women (median age 66.7 years, range 42-80) had a "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10073125",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 62,
"text": "Periampullary carcinomas: a special entity of duodenal tumors."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33227091",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Periampullary adenocarcinomas are rare neoplasm that originates from the pancreatic head, the ampulla of vater, the distal bile duct or the duodenum."
}
] | 11 |
BioASQ-training11b
| null | null |
625374a8e764a53204000027
|
bioasq_yesno
|
factoid
|
Which enzyme is targeted by Evolocumab?
|
[['proprotein convertase subtilisin/kexin type 9']]
|
[
"proprotein convertase subtilisin/kexin type 9",
"PCSK9",
"proprotein convertase 9",
"subtilisin/kexin type 9",
"proprotein convertase 9",
"kexin-9"
] |
['Evolocumab (AMG145) is a fully human monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9) that demonstrated marked reductions in plasma low-density lipoprotein cholesterol concentrations in statin-intolerant patients.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24661068",
"http://www.ncbi.nlm.nih.gov/pubmed/24598985",
"http://www.ncbi.nlm.nih.gov/pubmed/24509273",
"http://www.ncbi.nlm.nih.gov/pubmed/24481874",
"http://www.ncbi.nlm.nih.gov/pubmed/24477778",
"http://www.ncbi.nlm.nih.gov/pubmed/24284914",
"http://www.ncbi.nlm.nih.gov/pubmed/24255061",
"http://www.ncbi.nlm.nih.gov/pubmed/25470376",
"http://www.ncbi.nlm.nih.gov/pubmed/25410046",
"http://www.ncbi.nlm.nih.gov/pubmed/25282520",
"http://www.ncbi.nlm.nih.gov/pubmed/25282519",
"http://www.ncbi.nlm.nih.gov/pubmed/25079474",
"http://www.ncbi.nlm.nih.gov/pubmed/25052769",
"http://www.ncbi.nlm.nih.gov/pubmed/25002170",
"http://www.ncbi.nlm.nih.gov/pubmed/24961142",
"http://www.ncbi.nlm.nih.gov/pubmed/24953396",
"http://www.ncbi.nlm.nih.gov/pubmed/24953393",
"http://www.ncbi.nlm.nih.gov/pubmed/24859266",
"http://www.ncbi.nlm.nih.gov/pubmed/24825642",
"http://www.ncbi.nlm.nih.gov/pubmed/24694531",
"http://www.ncbi.nlm.nih.gov/pubmed/24691094",
"http://www.ncbi.nlm.nih.gov/pubmed/24678979",
"http://www.ncbi.nlm.nih.gov/pubmed/24662398",
"http://www.ncbi.nlm.nih.gov/pubmed/24373748"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24661068",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "Efficacy and safety profile of evolocumab (AMG145), an injectable inhibitor of the proprotein convertase subtilisin/kexin type 9: the available clinical evidence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24661068",
"endSection": "abstract",
"offsetInBeginSection": 353,
"offsetInEndSection": 582,
"text": "AREAS COVERED: Evolocumab (AMG145) is a monoclonal antibody inhibiting the proprotein convertase subtilisin/kexin type 9 that binds to the liver LDL receptor and prevents it from normal recycling by targeting it for degradation. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24598985",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 212,
"text": "Efficacy and safety of evolocumab (AMG 145), a fully human monoclonal antibody to PCSK9, in hyperlipidaemic patients on various background lipid therapies: pooled analysis of 1359 patients in four phase 2 trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24598985",
"endSection": "abstract",
"offsetInBeginSection": 449,
"offsetInEndSection": 560,
"text": "We report a pooled analysis from four phase 2 studies of evolocumab (AMG 145), a monoclonal antibody to PCSK9. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24509273",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 148,
"text": "Reduction in lipoprotein(a) with PCSK9 monoclonal antibody evolocumab (AMG 145): a pooled analysis of more than 1,300 patients in 4 phase II trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24509273",
"endSection": "abstract",
"offsetInBeginSection": 449,
"offsetInEndSection": 775,
"text": "METHODS: A pooled analysis of data from 1,359 patients in 4 phase II trials assessed the effects of evolocumab, a fully human monoclonal antibody to PCSK9, on Lp(a), the relationship between Lp(a) and lowering of low-density lipoprotein cholesterol (LDL-C) and apolipoprotein B, and the influence of background statin therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24509273",
"endSection": "abstract",
"offsetInBeginSection": 1490,
"offsetInEndSection": 1597,
"text": "CONCLUSIONS: Inhibition of PCSK9 with evolocumab resulted in significant dose-related reductions in Lp(a). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24481874",
"endSection": "abstract",
"offsetInBeginSection": 467,
"offsetInEndSection": 703,
"text": "Monoclonal antibodies that inhibit proprotein convertase subtilisin/kexin type 9, including evolocumab (previously AMG 145), dramatically lowered LDL-C in phase 2 clinical trials when administered alone or in combination with a statin. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24477778",
"endSection": "abstract",
"offsetInBeginSection": 545,
"offsetInEndSection": 722,
"text": "Evolocumab (AMG 145) is a fully human monoclonal antibody that binds PCSK9, inhibiting its interaction with the LDL receptor to preserve LDL-receptor recycling and reduce LDL-C."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24284914",
"endSection": "abstract",
"offsetInBeginSection": 701,
"offsetInEndSection": 1082,
"text": "Antibody therapeutics in Phase 3 studies are described, with an emphasis on those with study completion dates in 2014, including antibodies targeting interleukin-17a or the interleukin-17a receptor (secukinumab, ixekizumab, brodalumab), proprotein convertase subtilisin/kexin type 9 (alirocumab, evolocumab, bococizumab), and programmed death 1 receptor (lambrolizumab, nivolumab)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24255061",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 227,
"text": "BACKGROUND: Evolocumab (AMG 145), a monoclonal antibody against proprotein convertase subtilisin/kexin type 9 (PCSK9), significantly reduced low-density lipoprotein cholesterol (LDL-C) in phase 2 studies of 12 weeks' duration. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25410046",
"endSection": "abstract",
"offsetInBeginSection": 479,
"offsetInEndSection": 876,
"text": "These compounds act either by reducing low-density lipoprotein (LDL) production by inhibiting apolipoprotein B synthesis with an antisense oligonucleotide (mipomersen) or by inhibiting microsomal triglyceride transfer protein (lomitapide), or by enhancing LDL catabolism via monoclonal antibody-mediated inhibition of the activity of proprotein convertase subtilisin/kexin 9 (PCSK9) (evolocumab). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25282520",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Inhibition of PCSK9 with evolocumab in homozygous familial hypercholesterolaemia (TESLA Part B): a randomised, double-blind, placebo-controlled trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25282520",
"endSection": "abstract",
"offsetInBeginSection": 292,
"offsetInEndSection": 433,
"text": "Evolocumab, a monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9), reduced LDL cholesterol by 16% in a pilot study. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25282519",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 159,
"text": "PCSK9 inhibition with evolocumab (AMG 145) in heterozygous familial hypercholesterolaemia (RUTHERFORD-2): a randomised, double-blind, placebo-controlled trial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25282519",
"endSection": "abstract",
"offsetInBeginSection": 346,
"offsetInEndSection": 470,
"text": "We investigated the effect of PCSK9 inhibition with evolocumab (AMG 145) on LDL cholesterol in patients with this disorder. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25079474",
"endSection": "abstract",
"offsetInBeginSection": 989,
"offsetInEndSection": 1099,
"text": "Some of the anti-dyslipidemic drugs which work by PCSK9 inhibition include evolocumab, alirocumab and ALN-PCS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25052769",
"endSection": "abstract",
"offsetInBeginSection": 615,
"offsetInEndSection": 842,
"text": "We highlight the different steps of this adventure and review the published clinical trials especially those with the anti-PCSK9 antibodies evolocumab (AMG 145) and alirocumab (SAR236553/REGN727), which are in phase III trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25002170",
"endSection": "abstract",
"offsetInBeginSection": 744,
"offsetInEndSection": 930,
"text": "Monoclonal antibodies against PCSK9 represent so far the most advanced approach in clinical development, with alirocumab, evolocumab and bococizumab under advanced clinical development. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24961142",
"endSection": "abstract",
"offsetInBeginSection": 301,
"offsetInEndSection": 554,
"text": "AREAS COVERED: Evolocumab and alirocumab are fully human monoclonal antibodies inhibiting the proprotein convertase subtilisin/kexin type 9 (PCSK9) that binds to hepatic LDL receptor and prevents it from normal recycling by targeting it for degradation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24961142",
"endSection": "abstract",
"offsetInBeginSection": 692,
"offsetInEndSection": 939,
"text": "Phase II (for evolocumab and alirocumab) and III (for evolocumab) trials show that PCSK9 inhibitors are equally well tolerated, with adverse events mainly limited to mild-to-moderate nasopharyngitis, injection-site pain, arthralgia and back pain. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24953396",
"endSection": "abstract",
"offsetInBeginSection": 837,
"offsetInEndSection": 1208,
"text": "Four classes of newer lipid-lowering drugs offer promising advances in treating FH, namely the apolipoprotein-B synthesis inhibitors (mipomersen), the microsomal transfer protein inhibitors (lomitapide), the cholesterol ester transfer protein inhibitors (anacetrapib, evacetrapib) and the proprotein convertase subtilisin/kexin type 9 inhibitors (evolocumab, alirocumab)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24953393",
"endSection": "abstract",
"offsetInBeginSection": 584,
"offsetInEndSection": 762,
"text": "Monoclonal antibodies that inhibit proprotein convertase subtilisin/ kexin type 9 (PCSK9), which degrades the LDL receptor, like alirocumab and evolocumab, are in phase 3 trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24859266",
"endSection": "abstract",
"offsetInBeginSection": 282,
"offsetInEndSection": 462,
"text": "In support of the drug development program for Evolocumab, a fully human IgG₂ antibody that targets PCSK9, a quantitative ELISA to measure free PCSK9 in human serum was developed. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24825642",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "IMPORTANCE: In phase 2 studies, evolocumab, a fully human monoclonal antibody to PCSK9, reduced LDL-C levels in patients receiving statin therapy. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24694531",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 168,
"text": "Anti-PCSK9 antibody effectively lowers cholesterol in patients with statin intolerance: the GAUSS-2 randomized, placebo-controlled phase 3 clinical trial of evolocumab."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24694531",
"endSection": "abstract",
"offsetInBeginSection": 342,
"offsetInEndSection": 580,
"text": "Evolocumab, a fully human monoclonal antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9), demonstrated marked reductions in plasma low-density lipoprotein cholesterol (LDL-C) in a phase 2 study in statin-intolerant patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24691094",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Anti-PCSK9 monotherapy for hypercholesterolemia: the MENDEL-2 randomized, controlled phase III clinical trial of evolocumab."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24691094",
"endSection": "abstract",
"offsetInBeginSection": 173,
"offsetInEndSection": 342,
"text": "BACKGROUND: Evolocumab, a fully human monoclonal antibody against proprotein convertase subtilisin/kexin type 9 (PCSK9), significantly reduced LDL-C in phase II trials. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24678979",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 206,
"text": "BACKGROUND: Evolocumab, a monoclonal antibody that inhibits proprotein convertase subtilisin/kexin type 9 (PCSK9), significantly reduced low-density lipoprotein (LDL) cholesterol levels in phase 2 studies. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24662398",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 198,
"text": "Effects of evolocumab (AMG 145), a monoclonal antibody to PCSK9, in hypercholesterolemic, statin-treated Japanese patients at high cardiovascular risk--primary results from the phase 2 YUKAWA study."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24661068",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "Efficacy and safety profile of evolocumab (AMG145), an injectable inhibitor of the proprotein convertase subtilisin/kexin type 9: the available clinical evidence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24661068",
"endSection": "abstract",
"offsetInBeginSection": 353,
"offsetInEndSection": 582,
"text": "AREAS COVERED: Evolocumab (AMG145) is a monoclonal antibody inhibiting the proprotein convertase subtilisin/kexin type 9 that binds to the liver LDL receptor and prevents it from normal recycling by targeting it for degradation. "
}
] | 5 |
BioASQ-training5b
|
[] |
[] |
54e0d1491388e8454a000014
|
bioasq_factoid
|
factoid
|
Which tool exists for microsatellite (SSR) loci detection and primer design?
|
['FullSSR']
|
[
"FullSSR",
"Full SSR",
"Full SSR model",
"Full SSR analysis"
] |
['Microsatellites are genomic sequences comprised of tandem repeats of short nucleotide motifs widely used as molecular markers in population genetics. FullSSR is a new bioinformatic tool for microsatellite (SSR) loci detection and primer design using genomic data from NGS assay.', 'FullSSR is a new bioinformatic tool for microsatellite (SSR) loci detection and primer design using genomic data from NGS assay. ']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27366148"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27366148",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 51,
"text": "FullSSR: Microsatellite Finder and Primer Designer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27366148",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 278,
"text": "Microsatellites are genomic sequences comprised of tandem repeats of short nucleotide motifs widely used as molecular markers in population genetics. FullSSR is a new bioinformatic tool for microsatellite (SSR) loci detection and primer design using genomic data from NGS assay."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27366148",
"endSection": "abstract",
"offsetInBeginSection": 150,
"offsetInEndSection": 278,
"text": "FullSSR is a new bioinformatic tool for microsatellite (SSR) loci detection and primer design using genomic data from NGS assay."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27366148",
"endSection": "abstract",
"offsetInBeginSection": 849,
"offsetInEndSection": 926,
"text": "FullSSR simplifies the detection of SSRs and primer design on a big data set."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27366148",
"endSection": "abstract",
"offsetInBeginSection": 850,
"offsetInEndSection": 927,
"text": "FullSSR simplifies the detection of SSRs and primer design on a big data set."
}
] | 11 |
BioASQ-training11b
|
[
"https://meshb.nlm.nih.gov/record/ui?ui=D018895",
"https://meshb.nlm.nih.gov/record/ui?ui=D017931"
] | null |
5a6fa61ab750ff4455000060
|
bioasq_factoid
|
factoid
|
What is the cause of the Kleefstra syndrome?
|
['Mutations in the Euchromatic Histone Methyltransferase 1 (EHMT1)']
|
[
"Euchromatic Histone Methyltransferase 1",
"EHMT1",
"EHMT1 protein",
"KMT1D",
"Histone methyltransferase EHMT1",
"Euchromatic histone methyltransferase 1"
] |
['Mutations in the Euchromatic Histone Methyltransferase 1 (EHMT1) gene cause Kleefstra syndrome, a rare form of intellectual disability (ID) with strong autistic traits and sensory processing deficits.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/32531423",
"http://www.ncbi.nlm.nih.gov/pubmed/32975655",
"http://www.ncbi.nlm.nih.gov/pubmed/30585561",
"http://www.ncbi.nlm.nih.gov/pubmed/31750954",
"http://www.ncbi.nlm.nih.gov/pubmed/32539280"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31750954",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 182,
"text": "Kleefstra syndrome is a rare neurogenetic disorder caused by a subtelomeric 9q34.3 deletion or by an intragenic mutation of the euchromatin histone methyl transferase 1 gene (EHMT1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32531423",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "Kleefstra syndrome is a disorder caused by a mutation in the EHMT1 gene characterized in humans by general developmental delay, mild to severe intellectual disability and autism. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32539280",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 222,
"text": "Kleefstra syndrome (KS) is an autosomal dominant disorder caused by a chromosomal deletion at 9q34.3 resulting in pathogenic variants of the gene that codes for the enzyme, euchromatin histone methyltransferase 1 (EHMT1). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32975655",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 200,
"text": "Mutations in the Euchromatic Histone Methyltransferase 1 (EHMT1) gene cause Kleefstra syndrome, a rare form of intellectual disability (ID) with strong autistic traits and sensory processing deficits."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30585561",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "Kleefstra syndrome (chromosome 9q34.3 deletion) is a rare genetic disorder with less than 110 patients reported till date. "
}
] | 11 |
BioASQ-training11b
| null | null |
60805e204e6a4cf630000002
|
bioasq_factoid
|
factoid
|
In which cells are A-type lamins expressed?
|
[['late differentiating primary cells']]
|
[
"late differentiating primary cells",
"late-stage primary cells",
"mature primary cells",
"differentiated primary cells",
"terminally differentiated primary cells"
] |
['Early embryonic cells and stem cells of mammals generally possess only lamin B while lamins A and C appear later during differentiation. Northern analysis and immunoblotting demonstrated that lamin A/C mRNA and protein were not detectable in some human cell lines whereas lamin B1 was always present. Hemopoietic cells from blood and bone marrow of mammals usually do not express lamins A/C but only lamin B, and this feature distinguishes these cells from the vast majority of somatic cells of the adult animal, which reveal lamins A/C as well as lamin B.', 'In the rat brain, lamin A and C are expressed in relatively equal amounts, while the expressions of lamin B1 and B2 vary depending on the cell type. Human cells with reduced expression of the major B-type lamin protein, lamin B1, were generated using RNA interference. In addition, horizontal cells and a subpopulation of retinal ganglion cells expressed lamin A and C, while photoreceptor cells expressed neither lamin A nor C, and all other retinal neurons expressed lamin C only. Parallel in vivo experiments showed that treatment with thioglycollate caused the percentage of lamin A/C-positive peritoneal macrophages to increase from 5 to 80% between Days 0 and 6.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21842415",
"http://www.ncbi.nlm.nih.gov/pubmed/20568006",
"http://www.ncbi.nlm.nih.gov/pubmed/9367621",
"http://www.ncbi.nlm.nih.gov/pubmed/7781761",
"http://www.ncbi.nlm.nih.gov/pubmed/2404771",
"http://www.ncbi.nlm.nih.gov/pubmed/2209722",
"http://www.ncbi.nlm.nih.gov/pubmed/2415378",
"http://www.ncbi.nlm.nih.gov/pubmed/9274531",
"http://www.ncbi.nlm.nih.gov/pubmed/9363444",
"http://www.ncbi.nlm.nih.gov/pubmed/1808207",
"http://www.ncbi.nlm.nih.gov/pubmed/9410886",
"http://www.ncbi.nlm.nih.gov/pubmed/17203376",
"http://www.ncbi.nlm.nih.gov/pubmed/16179429",
"http://www.ncbi.nlm.nih.gov/pubmed/8381765",
"http://www.ncbi.nlm.nih.gov/pubmed/24213377"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2209722",
"endSection": "abstract",
"offsetInBeginSection": 676,
"offsetInEndSection": 845,
"text": "Antibodies specific for mouse A/C lamins, human A/C lamins, or B lamins have been used to define the lamin complement as a function of time in culture and of cell type. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2209722",
"endSection": "abstract",
"offsetInBeginSection": 847,
"offsetInEndSection": 1234,
"text": "dramatic increase in lamin A/C-positive cells was observed in the first 3 days of culture with both accessory cells and macrophages expressing lamins A/C as soon as such cell types could be identified. Parallel in vivo experiments showed that treatment with thioglycollate caused the percentage of lamin A/C-positive peritoneal macrophages to increase from 5 to 80% between Days 0 and 6."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2404771",
"endSection": "abstract",
"offsetInBeginSection": 195,
"offsetInEndSection": 332,
"text": "Early embryonic cells and stem cells of mammals generally possess only lamin B while lamins A and C appear later during differentiation. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9367621",
"endSection": "abstract",
"offsetInBeginSection": 172,
"offsetInEndSection": 334,
"text": "Northern analysis and immunoblotting demonstrated that lamin A/C mRNA and protein were not detectable in some human cell lines whereas lamin B1 was always present"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21842415",
"endSection": "abstract",
"offsetInBeginSection": 197,
"offsetInEndSection": 345,
"text": "In the rat brain, lamin A and C are expressed in relatively equal amounts, while the expressions of lamin B1 and B2 vary depending on the cell type."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2209722",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 254,
"text": "Hemopoietic cells from blood and bone marrow of mammals usually do not express lamins A/C but only lamin B, and this feature distinguishes these cells from the vast majority of somatic cells of the adult animal, which reveal lamins A/C as well as lamin B"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2404771",
"endSection": "abstract",
"offsetInBeginSection": 749,
"offsetInEndSection": 941,
"text": "These results demonstrated that EC cells devoid of lamins A and C nevertheless possessed the appropriate mechanisms for the localization and mitotic redistribution of exogenous lamins A and C."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9274531",
"endSection": "abstract",
"offsetInBeginSection": 1687,
"offsetInEndSection": 1861,
"text": "Spermatogonia and seminoma cells, which follow a differentiation pathway along the spermatogenic lineage and show characteristics of germ cells, do not express A-type lamins."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1808207",
"endSection": "abstract",
"offsetInBeginSection": 499,
"offsetInEndSection": 667,
"text": "While B-type lamins are expressed in almost all cell types, no A-type lamins are present in early vertebrate embryos or undifferentiated embryonal carcinoma cell lines."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16179429",
"endSection": "abstract",
"offsetInBeginSection": 292,
"offsetInEndSection": 476,
"text": "B-type lamins are present in almost all cell types, but A-type lamins are expressed predominantly in differentiated cells, suggesting a role in maintenance of the differentiated state."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9410886",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 221,
"text": "The expression of A-type lamins coincides with cell differentiation and as A-type lamins specifically interact with chromatin, a role in the regulation of differential gene expression has been suggested for A-type lamins."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17203376",
"endSection": "abstract",
"offsetInBeginSection": 409,
"offsetInEndSection": 660,
"text": "In the literature it is conveyed that only B-type lamins are required in these early stages of development and that A-type lamins are not present or required until differentiation of specific cell types associated with specialized tissue is initiated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16179429",
"endSection": "abstract",
"offsetInBeginSection": 109,
"offsetInEndSection": 292,
"text": "B-type lamins are present in almost all cell types, but A-type lamins are expressed predominantly in differentiated cells, suggesting a role in maintenance of the differentiated state"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8381765",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 577,
"text": "The nuclear lamina is a meshwork of intermediate filaments adjacent to the inner nuclear membrane that in mammalian cells is predominantly composed of three proteins: lamin A, lamin B, and lamin C. Because lamin A and C (A-type lamins) expression has been shown to be lacking in several types of undifferentiated or rapidly proliferating cells, we investigated lamin expression in the human liver in conditions with hepatocellular regeneration (cirrhosis of various etiologies and macroregenerative nodules) and in hepatocellular carcinomas of various grades of differentiation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16179429",
"endSection": "abstract",
"offsetInBeginSection": 1320,
"offsetInEndSection": 1513,
"text": "Our results identify the absence of A-type lamin expression as a novel marker for undifferentiated ES cells and further support a role for nuclear lamins in cell maintenance and differentiation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24213377",
"endSection": "abstract",
"offsetInBeginSection": 330,
"offsetInEndSection": 523,
"text": "In an attempt to provide an additional meaning to lamin-genome contacts, a recent study characterized the association of gene promoters with A-type lamins in progenitor and differentiated cells"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16179429",
"endSection": "abstract",
"offsetInBeginSection": 294,
"offsetInEndSection": 450,
"text": "Previous studies have shown that lamin A/C is not expressed during mouse development before day 9, nor in undifferentiated mouse embryonic carcinoma cells. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1808207",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Ectopic expression of an A-type lamin does not interfere with differentiation of lamin A-negative embryonal carcinoma cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1808207",
"endSection": "abstract",
"offsetInBeginSection": 503,
"offsetInEndSection": 617,
"text": "Intriguingly, expression of A-type lamins occurs concomitant with cell differentiation and embryonic development. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16179429",
"endSection": "abstract",
"offsetInBeginSection": 294,
"offsetInEndSection": 450,
"text": "Previous studies have shown that lamin A/C is not expressed during mouse development before day 9, nor in undifferentiated mouse embryonic carcinoma cells. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1808207",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Ectopic expression of an A-type lamin does not interfere with differentiation of lamin A-negative embryonal carcinoma cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1808207",
"endSection": "abstract",
"offsetInBeginSection": 503,
"offsetInEndSection": 617,
"text": "Intriguingly, expression of A-type lamins occurs concomitant with cell differentiation and embryonic development. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16179429",
"endSection": "abstract",
"offsetInBeginSection": 294,
"offsetInEndSection": 450,
"text": "Previous studies have shown that lamin A/C is not expressed during mouse development before day 9, nor in undifferentiated mouse embryonic carcinoma cells. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1808207",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Ectopic expression of an A-type lamin does not interfere with differentiation of lamin A-negative embryonal carcinoma cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1808207",
"endSection": "abstract",
"offsetInBeginSection": 503,
"offsetInEndSection": 617,
"text": "Intriguingly, expression of A-type lamins occurs concomitant with cell differentiation and embryonic development. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1808207",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Ectopic expression of an A-type lamin does not interfere with differentiation of lamin A-negative embryonal carcinoma cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16179429",
"endSection": "abstract",
"offsetInBeginSection": 294,
"offsetInEndSection": 450,
"text": "Previous studies have shown that lamin A/C is not expressed during mouse development before day 9, nor in undifferentiated mouse embryonic carcinoma cells. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1808207",
"endSection": "abstract",
"offsetInBeginSection": 503,
"offsetInEndSection": 617,
"text": "Intriguingly, expression of A-type lamins occurs concomitant with cell differentiation and embryonic development. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16179429",
"endSection": "abstract",
"offsetInBeginSection": 294,
"offsetInEndSection": 450,
"text": "Previous studies have shown that lamin A/C is not expressed during mouse development before day 9, nor in undifferentiated mouse embryonic carcinoma cells. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1808207",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Ectopic expression of an A-type lamin does not interfere with differentiation of lamin A-negative embryonal carcinoma cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1808207",
"endSection": "abstract",
"offsetInBeginSection": 503,
"offsetInEndSection": 617,
"text": "Intriguingly, expression of A-type lamins occurs concomitant with cell differentiation and embryonic development. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1808207",
"endSection": "abstract",
"offsetInBeginSection": 335,
"offsetInEndSection": 617,
"text": "While B-type lamins are expressed in almost all cell types, no A-type lamins are present in early vertebrate embryos or undifferentiated embryonal carcinoma cell lines. Intriguingly, expression of A-type lamins occurs concomitant with cell differentiation and embryonic development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16179429",
"endSection": "abstract",
"offsetInBeginSection": 110,
"offsetInEndSection": 450,
"text": "B-type lamins are present in almost all cell types, but A-type lamins are expressed predominantly in differentiated cells, suggesting a role in maintenance of the differentiated state. Previous studies have shown that lamin A/C is not expressed during mouse development before day 9, nor in undifferentiated mouse embryonic carcinoma cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1808207",
"endSection": "abstract",
"offsetInBeginSection": 208,
"offsetInEndSection": 503,
"text": "On the basis of biochemical properties and sequence criteria, vertebrate lamin proteins are classified as either A- or B-type. While B-type lamins are expressed in almost all cell types, no A-type lamins are present in early vertebrate embryos or undifferentiated embryonal carcinoma cell lines."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1808207",
"endSection": "abstract",
"offsetInBeginSection": 335,
"offsetInEndSection": 617,
"text": "While B-type lamins are expressed in almost all cell types, no A-type lamins are present in early vertebrate embryos or undifferentiated embryonal carcinoma cell lines. Intriguingly, expression of A-type lamins occurs concomitant with cell differentiation and embryonic development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16179429",
"endSection": "abstract",
"offsetInBeginSection": 110,
"offsetInEndSection": 450,
"text": "B-type lamins are present in almost all cell types, but A-type lamins are expressed predominantly in differentiated cells, suggesting a role in maintenance of the differentiated state. Previous studies have shown that lamin A/C is not expressed during mouse development before day 9, nor in undifferentiated mouse embryonic carcinoma cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1808207",
"endSection": "abstract",
"offsetInBeginSection": 335,
"offsetInEndSection": 617,
"text": "While B-type lamins are expressed in almost all cell types, no A-type lamins are present in early vertebrate embryos or undifferentiated embryonal carcinoma cell lines. Intriguingly, expression of A-type lamins occurs concomitant with cell differentiation and embryonic development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16179429",
"endSection": "abstract",
"offsetInBeginSection": 110,
"offsetInEndSection": 450,
"text": "B-type lamins are present in almost all cell types, but A-type lamins are expressed predominantly in differentiated cells, suggesting a role in maintenance of the differentiated state. Previous studies have shown that lamin A/C is not expressed during mouse development before day 9, nor in undifferentiated mouse embryonic carcinoma cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1808207",
"endSection": "abstract",
"offsetInBeginSection": 335,
"offsetInEndSection": 617,
"text": "While B-type lamins are expressed in almost all cell types, no A-type lamins are present in early vertebrate embryos or undifferentiated embryonal carcinoma cell lines. Intriguingly, expression of A-type lamins occurs concomitant with cell differentiation and embryonic development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16179429",
"endSection": "abstract",
"offsetInBeginSection": 110,
"offsetInEndSection": 450,
"text": "B-type lamins are present in almost all cell types, but A-type lamins are expressed predominantly in differentiated cells, suggesting a role in maintenance of the differentiated state. Previous studies have shown that lamin A/C is not expressed during mouse development before day 9, nor in undifferentiated mouse embryonic carcinoma cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1808207",
"endSection": "abstract",
"offsetInBeginSection": 335,
"offsetInEndSection": 617,
"text": "While B-type lamins are expressed in almost all cell types, no A-type lamins are present in early vertebrate embryos or undifferentiated embryonal carcinoma cell lines. Intriguingly, expression of A-type lamins occurs concomitant with cell differentiation and embryonic development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16179429",
"endSection": "abstract",
"offsetInBeginSection": 110,
"offsetInEndSection": 450,
"text": "B-type lamins are present in almost all cell types, but A-type lamins are expressed predominantly in differentiated cells, suggesting a role in maintenance of the differentiated state. Previous studies have shown that lamin A/C is not expressed during mouse development before day 9, nor in undifferentiated mouse embryonic carcinoma cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1808207",
"endSection": "abstract",
"offsetInBeginSection": 208,
"offsetInEndSection": 503,
"text": "On the basis of biochemical properties and sequence criteria, vertebrate lamin proteins are classified as either A- or B-type. While B-type lamins are expressed in almost all cell types, no A-type lamins are present in early vertebrate embryos or undifferentiated embryonal carcinoma cell lines."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D034904",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D034882",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002477"
] |
[] |
56ed27202ac5ed145900000c
|
bioasq_factoid
|
factoid
|
Which web resource for LIR motif-containing proteins in eukaryotes has been developed?
|
['The iLIR database']
|
[
"iLIR database",
"iLIR",
"iLIRdb",
"iLIR Database"
] |
['In the past few years it has been revealed that Atg8-interacting proteins include not only receptors but also components of the core autophagic machinery, proteins associated with vesicles and their transport, and specific proteins that are selectively degraded by autophagy. Atg8-interacting proteins contain a short linear LC3-interacting region/LC3 recognition sequence/Atg8-interacting motif (LIR/LRS/AIM) motif which is responsible for their interaction with Atg8-family proteins. These proteins are referred to as LIR-containing proteins (LIRCPs). So far, many experimental efforts have been carried out to identify new LIRCPs, leading to the characterization of some of them in the past 10 years. Given the need for the identification of LIRCPs in various organisms, the iLIR database ( https://ilir.warwick.ac.uk ) has been developed as a freely available web resource, listing all the putative canonical LIRCPs identified in silico in the proteomes of 8 model organisms using the iLIR server, combined with a Gene Ontology (GO) term analysis.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27484196"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27484196",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 78,
"text": "iLIR database: A web resource for LIR motif-containing proteins in eukaryotes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27484196",
"endSection": "abstract",
"offsetInBeginSection": 625,
"offsetInEndSection": 1848,
"text": "In the past few years it has been revealed that Atg8-interacting proteins include not only receptors but also components of the core autophagic machinery, proteins associated with vesicles and their transport, and specific proteins that are selectively degraded by autophagy. Atg8-interacting proteins contain a short linear LC3-interacting region/LC3 recognition sequence/Atg8-interacting motif (LIR/LRS/AIM) motif which is responsible for their interaction with Atg8-family proteins. These proteins are referred to as LIR-containing proteins (LIRCPs). So far, many experimental efforts have been carried out to identify new LIRCPs, leading to the characterization of some of them in the past 10 years. Given the need for the identification of LIRCPs in various organisms, we developed the iLIR database ( https://ilir.warwick.ac.uk ) as a freely available web resource, listing all the putative canonical LIRCPs identified in silico in the proteomes of 8 model organisms using the iLIR server, combined with a Gene Ontology (GO) term analysis. Additionally, a curated text-mining analysis of the literature permitted us to identify novel putative LICRPs in mammals that have not previously been associated with autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27484196",
"endSection": "abstract",
"offsetInBeginSection": 1329,
"offsetInEndSection": 1670,
"text": "Given the need for the identification of LIRCPs in various organisms, we developed the iLIR database ( https://ilir.warwick.ac.uk ) as a freely available web resource, listing all the putative canonical LIRCPs identified in silico in the proteomes of 8 model organisms using the iLIR server, combined with a Gene Ontology (GO) term analysis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27484196",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 78,
"text": "iLIR database: a web resource for LIR motif-containing proteins in eukaryotes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27484196",
"endSection": "abstract",
"offsetInBeginSection": 1330,
"offsetInEndSection": 1671,
"text": "Given the need for the identification of LIRCPs in various organisms, we developed the iLIR database ( https://ilir.warwick.ac.uk ) as a freely available web resource, listing all the putative canonical LIRCPs identified in silico in the proteomes of 8 model organisms using the iLIR server, combined with a Gene Ontology (GO) term analysis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27484196",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 79,
"text": "iLIR database: A web resource for LIR motif-containing proteins in eukaryotes."
}
] | 11 |
BioASQ-training11b
| null | null |
5a8056a2faa1ab7d2e00001f
|
bioasq_factoid
|
yesno
|
Do nematodes contain architectural proteins like CTCF?
|
['no']
|
[
"no"
] |
['insulator protein CTCF has been secondarily lost in derived nematodes like C. elegans. The most highly enriched motif (LM1) corresponds to the X-box motif known from yeast and nematode.', 'the insulator protein CTCF has been secondarily lost in derived nematodes like C. elegans.', 'No, nematodes do not contain architectural proteins such as CTCF.', 'A mode of genetic regulation that involves insulators and insulator binding proteins to establish independent transcriptional units is currently not known in nematodes including Caenorhabditis elegans. the insulator protein CTCF has been secondarily lost in derived nematodes like C. elegans.', 'No. Most nematodes do not contain architectural proteins like CTCF.', 'No, nematodes do not contain architectural proteins like CTCF.', 'A mode of genetic regulation that involves insulators and insulator binding proteins to establish independent transcriptional units is currently not known in nematodes including Caenorhabditis elegans. Τhe insulator protein CTCF has been secondarily lost in derived nematodes like C. elegans.', 'No, nematodes contain architectural proteins such as CTCF.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/19712444",
"http://www.ncbi.nlm.nih.gov/pubmed/17442748",
"http://www.ncbi.nlm.nih.gov/pubmed/29385718"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19712444",
"endSection": "abstract",
"offsetInBeginSection": 198,
"offsetInEndSection": 400,
"text": "A mode of genetic regulation that involves insulators and insulator binding proteins to establish independent transcriptional units is currently not known in nematodes including Caenorhabditis elegans. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19712444",
"endSection": "abstract",
"offsetInBeginSection": 1267,
"offsetInEndSection": 1357,
"text": "the insulator protein CTCF has been secondarily lost in derived nematodes like C. elegans."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17442748",
"endSection": "abstract",
"offsetInBeginSection": 885,
"offsetInEndSection": 981,
"text": "he most highly enriched motif (LM1) corresponds to the X-box motif known from yeast and nematode"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19712444",
"endSection": "abstract",
"offsetInBeginSection": 1255,
"offsetInEndSection": 1361,
"text": "uggest that the insulator protein CTCF has been secondarily lost in derived nematodes like C. elegans. We "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29385718",
"endSection": "abstract",
"offsetInBeginSection": 785,
"offsetInEndSection": 989,
"text": "of CTCF from several nematodes is paralleled by a loss of two of its interactors, the polycomb repressive complex subunit SuZ12 and the multifunctional transcription factor TYY1. In contrast to earlier st"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19712444",
"endSection": "abstract",
"offsetInBeginSection": 505,
"offsetInEndSection": 659,
"text": "SULTS: While orthologs for other insulator proteins were absent in all 35 analysed nematode species, we find orthologs of CTCF in a subset of nematodes. A"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19712444",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 60,
"text": "Loss of the insulator protein CTCF during nematode evolution"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29385718",
"endSection": "abstract",
"offsetInBeginSection": 766,
"offsetInEndSection": 970,
"text": "que secondary loss of CTCF from several nematodes is paralleled by a loss of two of its interactors, the polycomb repressive complex subunit SuZ12 and the multifunctional transcription factor TYY1. In con"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19712444",
"endSection": "abstract",
"offsetInBeginSection": 191,
"offsetInEndSection": 391,
"text": "level. A mode of genetic regulation that involves insulators and insulator binding proteins to establish independent transcriptional units is currently not known in nematodes including Caenorhabditis "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19712444",
"endSection": "abstract",
"offsetInBeginSection": 1253,
"offsetInEndSection": 1359,
"text": " suggest that the insulator protein CTCF has been secondarily lost in derived nematodes like C. elegans. W"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19712444",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 61,
"text": "Loss of the insulator protein CTCF during nematode evolution."
}
] | 11 |
BioASQ-training11b
| null | null |
5fdb4253a43ad31278000022
|
bioasq_yesno
|
yesno
|
Is thrombophilia related to increased risk of miscarriage?
|
['Yes']
|
[
"Yes"
] |
['Thrombophilia has been found to be considerably more common in women with pregnancy-associated complications in comparison with the general population, and most frequently in conjunction with venous thromboembolism during pregnancy and the postpartum period. In particular there is an increased risk of pregnancy-related venous thrombosis in carriers of severe inherited thrombophilia. When counseling white women with a history of preeclampsia, screening for thrombophilia can be useful for preconceptional counseling and pregnancy management.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22543699",
"http://www.ncbi.nlm.nih.gov/pubmed/22164918",
"http://www.ncbi.nlm.nih.gov/pubmed/21380983",
"http://www.ncbi.nlm.nih.gov/pubmed/7986734",
"http://www.ncbi.nlm.nih.gov/pubmed/15027582",
"http://www.ncbi.nlm.nih.gov/pubmed/11583310",
"http://www.ncbi.nlm.nih.gov/pubmed/19135285",
"http://www.ncbi.nlm.nih.gov/pubmed/19031171",
"http://www.ncbi.nlm.nih.gov/pubmed/18845284",
"http://www.ncbi.nlm.nih.gov/pubmed/16962918",
"http://www.ncbi.nlm.nih.gov/pubmed/15713144",
"http://www.ncbi.nlm.nih.gov/pubmed/19165673",
"http://www.ncbi.nlm.nih.gov/pubmed/20860491"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22543699",
"endSection": "sections.0",
"offsetInBeginSection": 1065,
"offsetInEndSection": 1159,
"text": "Thrombophilia does hardly increase the risk of IUGR/PMPC or if so, it can be prevented by LMWH"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22164918",
"endSection": "sections.0",
"offsetInBeginSection": 571,
"offsetInEndSection": 796,
"text": "for illustrative purposes, a patient presenting with combined thrombophilia--both genetic and acquired--will be discussed. This patient had suffered severe gestational complications that led to devastating obstetrical outcome"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21380983",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 235,
"text": "Thrombophilias have been implicated in complications related to ischemic placental disease including recurrent pregnancy loss, intrauterine fetal demise, preeclampsia, fetal growth restriction, placental abruption, and preterm delivery"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7986734",
"endSection": "sections.0",
"offsetInBeginSection": 905,
"offsetInEndSection": 1061,
"text": "Further information about the combined risk of aPC resistance and pregnancy is needed before guidance on the management of affected women can be formulated."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15027582",
"endSection": "sections.0",
"offsetInBeginSection": 148,
"offsetInEndSection": 263,
"text": "Thrombotic risk during pregnancy and the puerperium is higher in asymptomatic women with than without thrombophilia"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15027582",
"endSection": "sections.0",
"offsetInBeginSection": 734,
"offsetInEndSection": 870,
"text": "Further studies are required to assess the thrombotic risk in women with preeclampsia as well as early or late recurrent pregnancy loss."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11583310",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "Risk of pregnancy-related venous thrombosis in carriers of severe inherited thrombophilia"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11583310",
"endSection": "sections.0",
"offsetInBeginSection": 1265,
"offsetInEndSection": 1532,
"text": "In conclusion, homozygous carriers of factor V Leiden and, to a lesser extent, double heterozygous carriers of factor V Leiden and of the prothrombin mutation have an increased risk of venous thrombosis during pregnancy, particularly high during the postpartum period"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19135285",
"endSection": "sections.0",
"offsetInBeginSection": 767,
"offsetInEndSection": 873,
"text": "Careful diagnosis, observation and monitoring can add significant benefit to LMWH therapy during pregnancy"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19031171",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "Pregnancy in healthy women is accompanied by hypercoagulable changes that may interact with thrombophilia risk factors and threaten pregnancy."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19031171",
"endSection": "sections.0",
"offsetInBeginSection": 1239,
"offsetInEndSection": 1444,
"text": "Fifty-three (13 %) women had antiphospholipid antibodies (lupus anticoagulant and/or anti-beta2-glycoprotein 1 antibodies) mainly associated with the risk of spontaneous abortion during the first trimester"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19031171",
"endSection": "sections.0",
"offsetInBeginSection": 1461,
"offsetInEndSection": 1713,
"text": "thrombophilia was found to be considerably more common in women with pregnancy-associated complications in comparison with the general population, and most frequently in conjunction with venous thromboembolism during pregnancy and the postpartum period"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18845284",
"endSection": "sections.0",
"offsetInBeginSection": 1104,
"offsetInEndSection": 1262,
"text": "When counseling white women with a history of preeclampsia, screening for thrombophilia can be useful for preconceptional counseling and pregnancy management."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16962918",
"endSection": "sections.0",
"offsetInBeginSection": 604,
"offsetInEndSection": 779,
"text": "knowledge combined with the appropriate use of thromboprophylaxis and treatment in women who have objectively confirmed VTE continue to improve maternal and perinatal outcomes"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15713144",
"endSection": "sections.0",
"offsetInBeginSection": 1508,
"offsetInEndSection": 1666,
"text": "The risk of having thrombophilia is doubled in men who have fathered pregnancies which ended in perinatal death as well as in the mothers of such pregnancies."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19165673",
"endSection": "sections.0",
"offsetInBeginSection": 560,
"offsetInEndSection": 707,
"text": "The prevalence of thrombophilic variants is of possible public health significance for other morbidity; but perhaps not in relation to preeclampsia"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20860491",
"endSection": "sections.0",
"offsetInBeginSection": 694,
"offsetInEndSection": 826,
"text": "This study suggests that thrombophilia \"mediates\" in lowering of cardiovascular risk factors in women with a history of preeclampsia"
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D019851",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018566",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D011248",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D011256",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D011255",
"http://www.disease-ontology.org/api/metadata/DOID:10591",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=0007565"
] | null |
513cdc38bee46bd34c000007
|
bioasq_yesno
|
factoid
|
What is the function of PAPOLA/PAP?
|
["PolyA polymerase (PAP) adds a polyA tail onto the 3'-end of RNAs without a nucleic acid template, using adenosine-5'-triphosphate (ATP) as a substrate."]
|
[
"PolyA polymerase",
"PAP",
"poly(A) polymerase",
"polyadenylate polymerase",
"polyadenylation enzyme",
"poly(A) tail polymerase",
"adenylate polymerase"
] |
["Poly(A)polymerase-alpha (PAPOLA) has been the most extensively investigated mammalian polyadenylating enzyme, mainly in regard to its multifaceted post-translational regulation. PolyA polymerase (PAP) adds a polyA tail onto the 3'-end of RNAs without a nucleic acid template, using adenosine-5'-triphosphate (ATP) as a substrate."]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21300291",
"http://www.ncbi.nlm.nih.gov/pubmed/20174964",
"http://www.ncbi.nlm.nih.gov/pubmed/15909992"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20174964",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 178,
"text": "Poly(A)polymerase-alpha (PAPOLA) has been the most extensively investigated mammalian polyadenylating enzyme, mainly in regard to its multifaceted post-translational regulation. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21300291",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "PolyA polymerase (PAP) adds a polyA tail onto the 3'-end of RNAs without a nucleic acid template, using adenosine-5'-triphosphate (ATP) as a substrate. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15909992",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 92,
"text": "Polyadenylate polymerase (PAP) catalyzes the synthesis of 3'-polyadenylate tails onto mRNA. "
}
] | 11 |
BioASQ-training11b
| null | null |
5c5f10791a4c55d80b000014
|
bioasq_factoid
|
factoid
|
Which form of breast cancer has Keytruda been FDA approved for?
|
['triple-negative breast cancer']
|
[
"triple-negative breast cancer",
"TNBC",
"triple-negative tumor",
"triple-negative carcinoma",
"triple-negative breast carcinoma"
] |
['Keytruda has been FDA approved for use in combination with chemotherapy for treating PD-L1-positive mTNBC.', 'FDA has approved pembrolizumab (Keytruda) for the treatment of triple-negative breast cancer in combination with chemotherapy.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33983696"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33983696",
"endSection": "abstract",
"offsetInBeginSection": 497,
"offsetInEndSection": 724,
"text": "The combination of chemotherapy and immunotherapy is a potential therapeutic option for PD-L1-positive mTNBC, as the FDA recently approved atezolizumab (Tecentriq) and pembrolizumab (Keytruda) in combination with chemotherapy. "
}
] | 12 |
BioASQ-training12b
| null | null |
6415c9e9690f196b51000018
|
bioasq_factoid
|
yesno
|
Can mitochondria be inherited by both parents in humans?
|
['yes']
|
[
"yes"
] |
['Yes. A comprehensive exploration of mtDNA segregation in certain families shows biparental mtDNA transmission with an autosomal dominant-like inheritance mode. Although the central dogma of maternal inheritance of mtDNA remains valid, there are some exceptional cases where paternal mtDNA could be passed to the offspring.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30478036"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30478036",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 54,
"text": "Biparental Inheritance of Mitochondrial DNA in Humans."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30478036",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1017,
"text": "Although there has been considerable debate about whether paternal mitochondrial DNA (mtDNA) transmission may coexist with maternal transmission of mtDNA, it is generally believed that mitochondria and mtDNA are exclusively maternally inherited in humans. Here, we identified three unrelated multigeneration families with a high level of mtDNA heteroplasmy (ranging from 24 to 76%) in a total of 17 individuals. Heteroplasmy of mtDNA was independently examined by high-depth whole mtDNA sequencing analysis in our research laboratory and in two Clinical Laboratory Improvement Amendments and College of American Pathologists-accredited laboratories using multiple approaches. A comprehensive exploration of mtDNA segregation in these families shows biparental mtDNA transmission with an autosomal dominantlike inheritance mode. Our results suggest that, although the central dogma of maternal inheritance of mtDNA remains valid, there are some exceptional cases where paternal mtDNA could be passed to the offspring. "
}
] | 11 |
BioASQ-training11b
| null | null |
5c52028807ef653866000009
|
bioasq_yesno
|
factoid
|
Which RNA polymerase II subunit carries RNA cleavage activity?
|
['TFIIS']
|
[
"TFIIS",
"Transcription Factor IIS",
"TFIIS protein",
"TFIIS factor"
] |
['The eukaryotic transcription factor TFIIS enhances elongation and nascent transcript cleavage activities of RNA polymerase II in a stalled elongation complex.', 'The eukaryotic transcription factor TFIIS enhances elongation and nascent transcript cleavage activities of RNA polymerase II in a stalled elongation complex. The transcription factor TFIIS zinc ribbon dipeptide Asp-Glu is critical for stimulation of elongation and RNA cleavage by RNA polymerase II.', 'In contrast, Pol II is fully protected through association with the cleavage stimulatory factor TFIIS, which enables rapid recovery from any depth by RNA cleavage.', 'In contrast, Pol II is fully protected through association with the cleavage stimulatory factor TFIIS, which enables rapid recovery from any depth by RNA cleavage. This mechanism is also used by transcription factor IIS, a factor that can bind Pol II and induce strong RNA cleavage. ']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/12692127",
"http://www.ncbi.nlm.nih.gov/pubmed/9869639",
"http://www.ncbi.nlm.nih.gov/pubmed/21450810",
"http://www.ncbi.nlm.nih.gov/pubmed/26929337",
"http://www.ncbi.nlm.nih.gov/pubmed/8636112",
"http://www.ncbi.nlm.nih.gov/pubmed/17535246",
"http://www.ncbi.nlm.nih.gov/pubmed/7678416",
"http://www.ncbi.nlm.nih.gov/pubmed/8599945",
"http://www.ncbi.nlm.nih.gov/pubmed/8876173",
"http://www.ncbi.nlm.nih.gov/pubmed/8090778",
"http://www.ncbi.nlm.nih.gov/pubmed/21454497",
"http://www.ncbi.nlm.nih.gov/pubmed/22396529"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26929337",
"endSection": "abstract",
"offsetInBeginSection": 851,
"offsetInEndSection": 1014,
"text": "In contrast, Pol II is fully protected through association with the cleavage stimulatory factor TFIIS, which enables rapid recovery from any depth by RNA cleavage."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21454497",
"endSection": "abstract",
"offsetInBeginSection": 697,
"offsetInEndSection": 816,
"text": "This mechanism is also used by transcription factor IIS, a factor that can bind Pol II and induce strong RNA cleavage. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8636112",
"endSection": "abstract",
"offsetInBeginSection": 979,
"offsetInEndSection": 1100,
"text": " This mutant enzyme can respond to SII for transcriptional read-through and carry out SII-activated nascent RNA cleavage."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8876173",
"endSection": "abstract",
"offsetInBeginSection": 674,
"offsetInEndSection": 1101,
"text": " In vitro, in the absence of TFIIS, the purified wt polymerase and the two mutant polymerases showed similar specific activity in polymerization, readthrough at intrinsic transcriptional arrest sites and nascent RNA cleavage. In contrast to the wt polymerase, both mutant polymerases were not stimulated by the addition of a 3-fold molar excess of TFIIS in assays of promoter-independent transcription, readthrough or cleavage."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8876173",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 109,
"text": "In vitro characterization of mutant yeast RNA polymerase II with reduced binding for elongation factor TFIIS."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8090778",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "The transcription factor TFIIS zinc ribbon dipeptide Asp-Glu is critical for stimulation of elongation and RNA cleavage by RNA polymerase II."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8090778",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "The eukaryotic transcription factor TFIIS enhances elongation and nascent transcript cleavage activities of RNA polymerase II in a stalled elongation complex."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8090778",
"endSection": "abstract",
"offsetInBeginSection": 159,
"offsetInEndSection": 396,
"text": "By site-directed mutagenesis, we have demonstrated that invariant residues Asp-261 and Glu-262 of the nucleic acid-binding TFIIS Zn ribbon are critical for stimulation of both elongation and RNA cleavage activities of RNA polymerase II. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12692127",
"endSection": "abstract",
"offsetInBeginSection": 349,
"offsetInEndSection": 454,
"text": "Highly purified yeast RNA polymerase II is able to perform transcript hydrolysis in the absence of TFIIS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8090778",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 0,
"text": "The eukaryotic transcription factor TFIIS enhances elongation and nascent transcript cleavage activities of RNA polymerase II in a stalled elongation complex."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8090778",
"endSection": "abstract",
"offsetInBeginSection": 159,
"offsetInEndSection": 395,
"text": "By site-directed mutagenesis, we have demonstrated that invariant residues Asp-261 and Glu-262 of the nucleic acid-binding TFIIS Zn ribbon are critical for stimulation of both elongation and RNA cleavage activities of RNA polymerase II."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17535246",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 148,
"text": "The transcription elongation factor S-II, also designated TFIIS, stimulates the nascent transcript cleavage activity intrinsic to RNA polymerase II."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8090778",
"endSection": "abstract",
"offsetInBeginSection": 659,
"offsetInEndSection": 884,
"text": "The RNA polymerase II itself may contain a Zn ribbon, in as much as the polymerase's 15-kDa subunit contains a sequence that aligns well with the TFIIS Zn ribbon sequence, including a similarly placed pair of acidic residues."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7678416",
"endSection": "abstract",
"offsetInBeginSection": 868,
"offsetInEndSection": 1164,
"text": "Involvement of the vaccinia RNA polymerase subunit rpo30 in the transcript-shortening reaction is suggested based on sequence similarity of rpo30 to mammalian protein SII (TFIIS), an extrinsic transcription factor required for nascent RNA cleavage by RNA polymerase II (Reines, D. (1991) J. Biol."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9869639",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "The RNA cleavage activity of RNA polymerase III is mediated by an essential TFIIS-like subunit and is important for transcription termination."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22396529",
"endSection": "abstract",
"offsetInBeginSection": 560,
"offsetInEndSection": 869,
"text": "In the resulting model of Pol I, the C-terminal ribbon (C-ribbon) domain of A12.2 reaches the active site via the polymerase pore, like the C-ribbon of the Pol II cleavage factor TFIIS, explaining why the intrinsic RNA cleavage activity of Pol I is strong, in contrast to the weak cleavage activity of Pol II."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21450810",
"endSection": "abstract",
"offsetInBeginSection": 290,
"offsetInEndSection": 454,
"text": "The amino and carboxyl regions of C11 are homologous to domains of the pol II subunit Rpb9p, and the pol II elongation and RNA cleavage factor, TFIIS, respectively."
}
] | 11 |
BioASQ-training11b
| null | null |
5a4df811966455904c00000e
|
bioasq_factoid
|
factoid
|
What are negative cell-cycle regulators that can cause cancer when mutated called?
|
['Tumor suppressor genes', 'Tumor-suppressor genes', 'tumor suppressors', 'antioncogenes', 'anti-oncogenes']
|
[
"Tumor suppressor genes",
"Tumor-suppressor genes",
"tumor suppressors",
"antioncogenes",
"anti-oncogenes",
"tumor suppressor",
"tumor suppressor gene"
] |
["Negative cell-cycle regulators that can cause cancer when mutated are commonly referred to as tumor suppressor genes. These genes play a crucial role in controlling cell division and preventing uncontrolled proliferation, which could lead to the formation of tumors. Tumor suppressor genes function by inhibiting cell cycle progression, promoting DNA repair, and inducing apoptosis in response to cellular stress or damage. Some well-known examples of tumor suppressor genes include TP53 (p53), RB1 (retinoblastoma protein), and CDKN2A (p16INK4a). Mutations or loss of function in these genes can disrupt their ability to regulate the cell cycle, thereby contributing to the development of cancer. In many cases, both copies of a tumor suppressor gene must be inactivated for a complete loss of function, following Knudson's two-hit hypothesis. The identification and study of tumor suppressor genes have significantly advanced our understanding of cancer biology and provided potential targets for therapeutic interventions.", 'The cell cycle is a series of events that take place in a cell, leading to its division and duplication. Cell division requires cell cycle checkpoints that are used by the cell to both monitor and regulate the progress of the cell cycle. Deregulation of the cell cycle underlies the aberrant cell proliferation that characterizes cancer and loss of cell cycle checkpoint control promotes genetic instability.\n\nTumor suppressor genes are genes that protect the cell from a single event or multiple events leading to cancer. When these genes mutate, the cell can progress to a cancerous state. We now recognize that tumor suppressor genes regulate diverse cellular activities, including cell cycle checkpoint responses, detection and repair of DNA damage, protein ubiquitination and degradation, mitogenic signaling, cell specification, differentiation and migration, and tumor angiogenesis.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26573797",
"http://www.ncbi.nlm.nih.gov/pubmed/21990031",
"http://www.ncbi.nlm.nih.gov/pubmed/1399577",
"http://www.ncbi.nlm.nih.gov/pubmed/20492666",
"http://www.ncbi.nlm.nih.gov/pubmed/2140509",
"http://www.ncbi.nlm.nih.gov/pubmed/2046748",
"http://www.ncbi.nlm.nih.gov/pubmed/14744434",
"http://www.ncbi.nlm.nih.gov/pubmed/12665054",
"http://www.ncbi.nlm.nih.gov/pubmed/33682629",
"http://www.ncbi.nlm.nih.gov/pubmed/11327114",
"http://www.ncbi.nlm.nih.gov/pubmed/26110128",
"http://www.ncbi.nlm.nih.gov/pubmed/9179973",
"http://www.ncbi.nlm.nih.gov/pubmed/8652807",
"http://www.ncbi.nlm.nih.gov/pubmed/9815577",
"http://www.ncbi.nlm.nih.gov/pubmed/32359398",
"http://www.ncbi.nlm.nih.gov/pubmed/12542976",
"http://www.ncbi.nlm.nih.gov/pubmed/16150895",
"http://www.ncbi.nlm.nih.gov/pubmed/10854145"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26110128",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 474,
"text": "The cell cycle (or cell-division cycle) is a series of events that take place in a cell, leading to its division and duplication. Cell division requires cell cycle checkpoints (CPs) that are used by the cell to both monitor and regulate the progress of the cell cycle. Tumor-suppressor genes (TSGs) or antioncogenes are genes that protect the cell from a single event or multiple events leading to cancer. When these genes mutate, the cell can progress to a cancerous state."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21990031",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 378,
"text": "Deregulation of the cell cycle underlies the aberrant cell proliferation that characterizes cancer and loss of cell cycle checkpoint control promotes genetic instability. During the past two decades, cancer genetics has shown that hyperactivating mutations in growth signalling networks, coupled to loss of function of tumour suppressor proteins, drives oncogenic proliferation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14744434",
"endSection": "abstract",
"offsetInBeginSection": 439,
"offsetInEndSection": 737,
"text": " We now recognize that tumor suppressor genes regulate diverse cellular activities, including cell cycle checkpoint responses, detection and repair of DNA damage, protein ubiquitination and degradation, mitogenic signaling, cell specification, differentiation and migration, and tumor angiogenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32359398",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "p53 is a critical tumor-suppressor protein that guards the human genome against mutations by inducing cell-cycle arrest or apoptosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10854145",
"endSection": "abstract",
"offsetInBeginSection": 1238,
"offsetInEndSection": 1405,
"text": "Tumor-suppressor gene p16 is an important negative cell-cycle regulator whose functional loss may significantly contribute to malignant transformation and progression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1399577",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 62,
"text": "Tumor suppressor genes are negative regulators of cell growth."
},
{
"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)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11327114",
"endSection": "abstract",
"offsetInBeginSection": 542,
"offsetInEndSection": 738,
"text": " Genes positively controlling cell cycle checkpoints can be targets for oncogenic activation in cancer, whereas negative regulators, such as tumour suppressor genes, are targeted for inactivation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9815577",
"endSection": "abstract",
"offsetInBeginSection": 142,
"offsetInEndSection": 345,
"text": "The p27(Kip1) protein belongs to a family of cyclin-dependent kinase-inhibitory proteins that are negative regulators of cell cycle progression and have been proposed as candidate tumor suppressor genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33682629",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 463,
"text": "Retinoblastoma 1 (RB1) is the first discovered tumor suppressor gene and recognized as the simple model system whose encoded defective protein can cause a pediatric cancer retinoblastoma. It functions as a negative regulator of the cell cycle through the interactions with members of the E2F transcription factors family. The protein of the RB1 gene (pRB) is engaged in various cell cycle processes including apoptosis, cell cycle arrest and chromatin remodeling."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2046748",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "The cell cycle is composed of a series of steps which can be negatively or positively regulated by various factors. Chief among the negative regulators is the p53 protein."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20492666",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 111,
"text": "p27Kip1 (p27) is an important negative regulator of the cell cycle and a putative tumor suppressor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8652807",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 438,
"text": "It is now evident that the cell cycle machinery has a variety of elements negatively regulating cell cycle progression. However, among these negative regulators in cell cycle control, only 4 have been shown to be consistently involved in the development of human cancers as tumor suppressors: Rb (Retinoblastoma susceptibility protein), p53, and two recently identified cyclin-dependent kinase inhibitors, p16INK4A/MTS1 and p15INK4B/MTS2."
}
] | 12 |
BioASQ-training12b
| null | null |
644e81fa57b1c7a315000079
|
bioasq_factoid
|
factoid
|
Which method is used for prediction of novel microRNA genes in cancer-associated genomic regions?
|
['SSCprofiler']
|
[
"SSCprofiler",
"SSC Profiler",
"SSC Profiler Tool",
"Single-Cell Sequencing Profiler"
] |
['SSCprofiler is a computational tool utilizing a probabilistic method based on Profile Hidden Markov Models to predict novel miRNA precursors. Via the simultaneous integration of biological features such as sequence, structure and conservation, SSCprofiler achieves a performance accuracy of 88.95% sensitivity and 84.16% specificity on a large set of human miRNA genes. The trained classifier is used to identify novel miRNA gene candidates located within cancer-associated genomic regions and rank the resulting predictions using expression information from a full genome tiling array. SSCprofiler is freely available as a web service at http://www.imbb.forth.gr/SSCprofiler.html.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/19324892"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19324892",
"endSection": "abstract",
"offsetInBeginSection": 425,
"offsetInEndSection": 1429,
"text": " In this work we present a new computational tool (SSCprofiler) utilizing a probabilistic method based on Profile Hidden Markov Models to predict novel miRNA precursors. Via the simultaneous integration of biological features such as sequence, structure and conservation, SSCprofiler achieves a performance accuracy of 88.95% sensitivity and 84.16% specificity on a large set of human miRNA genes. The trained classifier is used to identify novel miRNA gene candidates located within cancer-associated genomic regions and rank the resulting predictions using expression information from a full genome tiling array. Finally, four of the top scoring predictions are verified experimentally using northern blot analysis. Our work combines both analytical and experimental techniques to show that SSCprofiler is a highly accurate tool which can be used to identify novel miRNA gene candidates in the human genome. SSCprofiler is freely available as a web service at http://www.imbb.forth.gr/SSCprofiler.html."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19324892",
"endSection": "abstract",
"offsetInBeginSection": 426,
"offsetInEndSection": 594,
"text": "In this work we present a new computational tool (SSCprofiler) utilizing a probabilistic method based on Profile Hidden Markov Models to predict novel miRNA precursors."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19324892",
"endSection": "abstract",
"offsetInBeginSection": 1143,
"offsetInEndSection": 1334,
"text": "Our work combines both analytical and experimental techniques to show that SSCprofiler is a highly accurate tool which can be used to identify novel miRNA gene candidates in the human genome."
}
] | 6 |
BioASQ-training6b
|
[
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D035683"
] | null |
5895f18ce370baff39000001
|
bioasq_factoid
|
yesno
|
Are stress granules membraneous?
|
['no']
|
[
"no"
] |
['Stress granules (SG) are membrane-less compartments involved in regulating mRNAs during stress.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28377462",
"http://www.ncbi.nlm.nih.gov/pubmed/27838525",
"http://www.ncbi.nlm.nih.gov/pubmed/23279909",
"http://www.ncbi.nlm.nih.gov/pubmed/28306503"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27838525",
"endSection": "abstract",
"offsetInBeginSection": 540,
"offsetInEndSection": 700,
"text": "PMLOs are different in size, shape, and composition, and almost invariantly contain intrinsically disordered proteins (e.g., eIF4B and TDP43 in stress granules,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28306503",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 194,
"text": "Liquid-liquid phase separation (LLPS) of RNA-binding proteins plays an important role in the formation of multiple membrane-less organelles involved in RNA metabolism, including stress granules."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28377462",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 95,
"text": "Stress granules (SG) are membrane-less compartments involved in regulating mRNAs during stress."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23279909",
"endSection": "abstract",
"offsetInBeginSection": 38,
"offsetInEndSection": 211,
"text": " In addition to membrane delimited organelles, proteins and RNAs can organize themselves into specific domains. Some examples include stress granules and subnuclear bodies. "
}
] | 11 |
BioASQ-training11b
| null | null |
5aa825b1fcf4565872000003
|
bioasq_yesno
|
factoid
|
What is the cyberknife used for?
|
['CyberKnife® is a robotic stereotactic radiotherapy system']
|
[
"CyberKnife",
"CyberKnife®",
"CyberKnife System",
"CyberKnife Robotic Radiosurgery System",
"CyberKnife Stereotactic Radiosurgery System",
"CyberKnife Stereotactic Radiotherapy System"
] |
['CyberKnife(r) is a robotic stereotactic radiotherapy system']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28544809",
"http://www.ncbi.nlm.nih.gov/pubmed/28298046",
"http://www.ncbi.nlm.nih.gov/pubmed/28849326"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28849326",
"endSection": "abstract",
"offsetInBeginSection": 694,
"offsetInEndSection": 854,
"text": "Stereotactic radiosurgery using CyberKnife® seems to be an efficient and safe therapeutic option for malignant melanomas affecting the choroid and ciliary body."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28298046",
"endSection": "abstract",
"offsetInBeginSection": 140,
"offsetInEndSection": 262,
"text": "Stereotactic radiosurgery (SRS) has emerged as a principal alternative to microresection for small- and medium-sized CSHs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28544809",
"endSection": "abstract",
"offsetInBeginSection": 5,
"offsetInEndSection": 215,
"text": "CyberKnife® is a robotic stereotactic radiotherapy system. The aim of this study is to evaluate the effectiveness and the safety of CyberKnife® on treating head and neck paragangliomas and to report our results"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28544809",
"endSection": "abstract",
"offsetInBeginSection": 1301,
"offsetInEndSection": 1563,
"text": "Stereotactic radiotherapy is a good alternative to surgery for the treatment of head and neck paragangliomas coming up with a clear benefit of acute and late side effects. CyberKnife® seems to be a safe and efficient system treating head and neck paragangliomas."
}
] | 11 |
BioASQ-training11b
| null | null |
5e480da0d14c9f295d000006
|
bioasq_factoid
|
factoid
|
Which company developed opdivo?
|
['Bristol-Myers Squibb']
|
[
"Bristol-Myers Squibb",
"BMS",
"Bristol Myers Squibb Company",
"Bristol-Myers",
"Bristol-Myers Squibb Co."
] |
['Opdivo or nivolumab was developed by Bristol-Myers Squibb.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30293207"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30293207",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 297,
"text": "As part of its single technology appraisal (STA) process, the National Institute for Health and Care Excellence (NICE) invited the manufacturer (Bristol-Myers Squibb) of nivolumab (Opdivo®) to submit evidence of its clinical and cost effectiveness for metastatic or unresectable urothelial cancer."
}
] | 11 |
BioASQ-training11b
| null | null |
5c910ae0ecadf2e73f000007
|
bioasq_factoid
|
yesno
|
Is there a deep-learning algorithm for protein solubility prediction?
|
['yes']
|
[
"yes"
] |
['Yes. DeepSol is a novel deep learning-based protein solubility predictor. It is a convolutional neural network that exploits k-mer structure and additional sequence and structural features extracted from the protein sequence.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29554211"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29554211",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 84,
"text": "DeepSol: a deep learning framework for sequence-based protein solubility prediction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29554211",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 618,
"text": "Protein solubility plays a vital role in pharmaceutical research and production yield. For a given protein, the extent of its solubility can represent the quality of its function, and is ultimately defined by its sequence. Thus, it is imperative to develop novel, highly accurate in silico sequence-based protein solubility predictors. In this work we propose, DeepSol, a novel Deep Learning-based protein solubility predictor. The backbone of our framework is a convolutional neural network that exploits k-mer structure and additional sequence and structural features extracted from the protein sequence."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29554211",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 228,
"text": "DeepSol: a deep learning framework for sequence-based protein solubility prediction.<AbstractText Label=\"Motivation\" NlmCategory=\"UNASSIGNED\">Protein solubility plays a vital role in pharmaceutical research and production yield. "
}
] | 11 |
BioASQ-training11b
| null | null |
5c6b198f7c78d69471000025
|
bioasq_yesno
|
factoid
|
What disease is treated with BIVV001?
|
['Hemophilia A']
|
[
"Hemophilia A",
"Factor VIII deficiency",
"Classic hemophilia",
"A hemophilia",
"Hemophilia A disorder"
] |
['BIVV001 fusion protein has been developed as Factor VIII replacement therapy for hemophilia A']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/32078672",
"http://www.ncbi.nlm.nih.gov/pubmed/32905674"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32078672",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "BIVV001, a new class of factor VIII replacement for hemophilia A that is independent of von Willebrand factor in primates and mice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32078672",
"endSection": "abstract",
"offsetInBeginSection": 541,
"offsetInEndSection": 756,
"text": "We have developed a new class of FVIII replacement, rFVIIIFc-VWF-XTEN (BIVV001), that is physically decoupled from endogenous VWF and has enhanced pharmacokinetic properties compared with all previous FVIII products"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32078672",
"endSection": "abstract",
"offsetInBeginSection": 1356,
"offsetInEndSection": 1557,
"text": "BIVV001 is the first rFVIII with the potential to significantly change the treatment paradigm for severe hemophilia A by providing optimal protection against all bleed types, with less frequent doses. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32905674",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 75,
"text": "BIVV001 Fusion Protein as Factor VIII Replacement Therapy for Hemophilia A."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32905674",
"endSection": "abstract",
"offsetInBeginSection": 301,
"offsetInEndSection": 533,
"text": ". BIVV001 (rFVIIIFc-VWF-XTEN) is a novel fusion protein designed to overcome this half-life ceiling and maintain high sustained factor VIII activity levels. Data are lacking on the safety and pharmacokinetics of single-dose BIVV001."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32905674",
"endSection": "abstract",
"offsetInBeginSection": 2003,
"offsetInEndSection": 2392,
"text": "CONCLUSIONS: In a small, early-phase study involving men with severe hemophilia A, a single intravenous injection of BIVV001 resulted in high sustained factor VIII activity levels, with a half-life that was up to four times the half-life associated with recombinant factor VIII, an increase that could signal a new class of factor VIII replacement therapy with a weekly treatment interval."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32905674",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "BIVV001 Fusion Protein as Factor VIII Replacement Therapy for Hemophilia A"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32078672",
"endSection": "abstract",
"offsetInBeginSection": 1356,
"offsetInEndSection": 1556,
"text": "BIVV001 is the first rFVIII with the potential to significantly change the treatment paradigm for severe hemophilia A by providing optimal protection against all bleed types, with less frequent doses."
}
] | 11 |
BioASQ-training11b
| null | null |
6020af2e1cb411341a000084
|
bioasq_factoid
|
factoid
|
What is the ubiquitin proteome?
|
['The ubiquitin proteome is the entire set ubiquitinated proteins and of their respective ubiquitination sites.']
|
[
"ubiquitin proteome",
"ubiquitinated proteins",
"ubiquitination sites",
"ubiquitin-proteome",
"ubiquitin-modified proteins"
] |
The ubiquitin proteome is the entire set ubiquitinated proteins and of their respective ubiquitination sites.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23764619",
"http://www.ncbi.nlm.nih.gov/pubmed/23743150",
"http://www.ncbi.nlm.nih.gov/pubmed/22178446"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23764619",
"endSection": "abstract",
"offsetInBeginSection": 266,
"offsetInEndSection": 422,
"text": "Mass spectrometry now allows high throughput approaches for the identification of the thousands of ubiquitinated proteins and of their ubiquitination sites."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22178446",
"endSection": "abstract",
"offsetInBeginSection": 313,
"offsetInEndSection": 543,
"text": "we used Tandem repeated Ubiquitin Binding Entities (TUBEs) under non-denaturing conditions followed by mass spectrometry analysis to study global ubiquitylation events that may lead to the identification of potential drug targets."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23743150",
"endSection": "abstract",
"offsetInBeginSection": 174,
"offsetInEndSection": 339,
"text": "To study the ubiquitin proteome we have established an immunoaffinity purification method for the proteomic analysis of endogenously ubiquitinated protein complexes."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D020543",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D040901",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D014452",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D054875",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D025801",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D057149",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0031386",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0016567",
"http://www.uniprot.org/uniprot/UBIQ_CERCA"
] |
[] |
532f1452d6d3ac6a34000030
|
bioasq_factoid
|
factoid
|
Which protein is the E3-ubiquitin ligase that targets the tumor suppressor p53 for proteasomal degradation?
|
[['The mouse double minute 2 (mdm2)', 'The human homologue of Mdm2 (Hdm2)']]
|
[
"mouse double minute 2",
"mdm2",
"human homologue of Mdm2",
"Hdm2",
"MDM2",
"Mdm2",
"Mdm2 protein",
"Mdm2 oncogene"
] |
['The p53 tumour suppressor protein is tightly controlled by the E3 ubiquitin ligase, mouse double minute 2 (MDM2). The RING domain E3 ubiquitin ligase Mdm2 is the master regulator of the tumor suppressor p53. It targets p53 for proteasomal degradation, restraining the potent activity of p53 and enabling cell survival and proliferation. p53 is inactivated in many human malignancies through missense mutations or overexpression of the human homologue of Mdm2 (Hdm2), an E3 ubiquitin ligase that ubiquitinates p53, thereby promoting its proteasomal degradation.', "This is well illustrated by the E3 ubiquitin ligase MDM2 that targets p53 for proteasomal degradation under normal conditions and is essential for controlling p53 activity during development., p53 is inactivated in many human malignancies through missense mutations or overexpression of the human homologue of Mdm2 (Hdm2), an E3 ubiquitin ligase that ubiquitinates p53, thereby promoting its proteasomal degradation., Mdm2 has been thought to regulate the tumor suppressor p53 in two ways: by masking p53's access to transcriptional machinery, and by ubiquitinating p53, targeting it for proteasomal degradation"]
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23150437",
"http://www.ncbi.nlm.nih.gov/pubmed/23671280",
"http://www.ncbi.nlm.nih.gov/pubmed/22666487",
"http://www.ncbi.nlm.nih.gov/pubmed/23581014",
"http://www.ncbi.nlm.nih.gov/pubmed/19934289",
"http://www.ncbi.nlm.nih.gov/pubmed/18235222",
"http://www.ncbi.nlm.nih.gov/pubmed/16339144",
"http://www.ncbi.nlm.nih.gov/pubmed/16082221",
"http://www.ncbi.nlm.nih.gov/pubmed/15632057",
"http://www.ncbi.nlm.nih.gov/pubmed/15013777",
"http://www.ncbi.nlm.nih.gov/pubmed/12832479",
"http://www.ncbi.nlm.nih.gov/pubmed/11948425",
"http://www.ncbi.nlm.nih.gov/pubmed/24174547",
"http://www.ncbi.nlm.nih.gov/pubmed/21075307",
"http://www.ncbi.nlm.nih.gov/pubmed/19166840",
"http://www.ncbi.nlm.nih.gov/pubmed/22819825"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23150437",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 322,
"text": "p53 levels and activity are controlled in large part through regulated ubiquitination and subsequent destruction by the 26S proteasome. Monoubiquitination of p53 is mediated primarily by the RING-finger E3 ubiquitin ligase MDM2 and impacts p53 activity through modulation of p53 localization and transcription activities. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23671280",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 222,
"text": "The RING domain E3 ubiquitin ligase Mdm2 is the master regulator of the tumor suppressor p53. It targets p53 for proteasomal degradation, restraining the potent activity of p53 and enabling cell survival and proliferation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22666487",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 359,
"text": "The p53 transcription factor and tumor suppressor is regulated primarily by the E3 ubiquitin ligase Mdm2, which ubiquitinates p53 to target it for proteasomal degradation. Aside from its ubiquitin ligase function, Mdm2 has been believed to be capable of suppressing p53's transcriptional activity by binding with and masking the transactivation domain of p53."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23581014",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 300,
"text": "The regulation of p53 expression levels is critical in controlling p53 activity in normal and damaged cells. This is well illustrated by the E3 ubiquitin ligase MDM2 that targets p53 for proteasomal degradation under normal conditions and is essential for controlling p53 activity during development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19934289",
"endSection": "abstract",
"offsetInBeginSection": 9,
"offsetInEndSection": 232,
"text": "p53 is inactivated in many human malignancies through missense mutations or overexpression of the human homologue of Mdm2 (Hdm2), an E3 ubiquitin ligase that ubiquitinates p53, thereby promoting its proteasomal degradation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18235222",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 530,
"text": "Mdm2 has been thought to regulate the tumor suppressor p53 in two ways: by masking p53's access to transcriptional machinery, and by ubiquitinating p53, targeting it for proteasomal degradation. This dogma was recently challenged by data generated from knockin mice in which Mdm2's RING E3 ubiquitin ligase activity was abrogated by a single point mutation. The RING mutant Mdm2 is fully capable of binding with p53, yet cannot suppress p53 activity, suggesting that Mdm2 cannot block p53 by binding alone, without ubiquitination."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16339144",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 228,
"text": "MDM2 is an E3 ubiquitin ligase that regulates the proteasomal degradation and activity of proteins involved in cell growth and apoptosis, including the tumor suppressors p53 and retinoblastoma and the transcription factor E2F1. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16082221",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 322,
"text": "The p53 tumor suppressor protein has a major role in protecting genome integrity. Under normal circumstances Mdmx and Mdm2 control the activity of p53. Both proteins inhibit the transcriptional regulation by p53, while Mdm2 also functions as an E3 ubiquitin ligase to target both p53 and Mdmx for proteasomal degradation. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15632057",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 515,
"text": "p53 is a critical coordinator of a wide range of stress responses. To facilitate a rapid response to stress, p53 is produced constitutively but is negatively regulated by MDM2. MDM2 can inhibit p53 in multiple independent ways: by binding to its transcription activation domain, inhibiting p53 acetylation, promoting nuclear export, and probably most importantly by promoting proteasomal degradation of p53. The latter is achieved via MDM2's E3 ubiquitin ligase activity harbored within the MDM2 RING finger domain."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15013777",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 260,
"text": "Mdm2 is a RING finger E3 ubiquitin ligase, which promotes ubiquitination and proteasomal degradation of the p53 tumor suppressor protein. Acetylation of p53 regulates p53's transcriptional activity and inhibits Mdm2-mediated p53 ubiquitination and degradation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12832479",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 325,
"text": "MDM2 is an E3 ubiquitin ligase that targets p53 for proteasomal degradation. Recent studies have shown, however, that the ring-finger domain (RFD) of MDM2, where the ubiquitin E3 ligase activity resides, is necessary but not sufficient for p53 ubiquitination, suggesting that an additional activity of MDM2 might be required."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11948425",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 355,
"text": "The Mdm2 proto-oncogene is amplified and over-expressed in a variety of tumors. One of the major functions of Mdm2 described to date is its ability to modulate the levels and activity of the tumor suppressor protein p53. Mdm2 binds to the N-terminus of p53 and, through its action as an E3 ubiquitin ligase, targets p53 for rapid proteasomal degradation. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24174547",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 450,
"text": "The HDM2-p53 loop is crucial for monitoring p53 level and human pathologies. Therefore, identification of novel molecules involved in this regulatory loop is necessary for understanding the dynamic regulation of p53 and treatment of human diseases. Here, we characterized that the ribosomal protein L6 binds to and suppresses the E3 ubiquitin ligase activity of HDM2, and subsequently attenuates HDM2-mediated p53 polyubiquitination and degradation. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24174547",
"endSection": "abstract",
"offsetInBeginSection": 1229,
"offsetInEndSection": 1399,
"text": "Together, our study identifies the crucial function of RPL6 in regulating HDM2-p53 pathway, which highlights the importance of RPL6 in human genetic diseases and cancers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21075307",
"endSection": "abstract",
"offsetInBeginSection": 137,
"offsetInEndSection": 356,
"text": "Targeting the E3 ubiquitin ligase HDM2 can lead to a therapeutic surge in p53 levels. However, the efficacy of HDM2 inhibition can be compromised by overexpression of HDMX, an HDM2 homolog that binds and sequesters p53."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19166840",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 181,
"text": "The p53 tumour suppressor protein is tightly controlled by the E3 ubiquitin ligase, mouse double minute 2 (MDM2), but maintains MDM2 expression as part of a negative feedback loop. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22819825",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 126,
"text": "Murine double minute (MDM2) is an E3 ligase that promotes ubiquitination and degradation of tumor suppressor protein 53 (p53)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23581014",
"endSection": "abstract",
"offsetInBeginSection": 109,
"offsetInEndSection": 300,
"text": "This is well illustrated by the E3 ubiquitin ligase MDM2 that targets p53 for proteasomal degradation under normal conditions and is essential for controlling p53 activity during development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23671280",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 222,
"text": "The RING domain E3 ubiquitin ligase Mdm2 is the master regulator of the tumor suppressor p53. It targets p53 for proteasomal degradation, restraining the potent activity of p53 and enabling cell survival and proliferation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15013777",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "Mdm2 is a RING finger E3 ubiquitin ligase, which promotes ubiquitination and proteasomal degradation of the p53 tumor suppressor protein"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16339144",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 226,
"text": "MDM2 is an E3 ubiquitin ligase that regulates the proteasomal degradation and activity of proteins involved in cell growth and apoptosis, including the tumor suppressors p53 and retinoblastoma and the transcription factor E2F1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15013777",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "Mdm2 is a RING finger E3 ubiquitin ligase, which promotes ubiquitination and proteasomal degradation of the p53 tumor suppressor protein"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16339144",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 226,
"text": "MDM2 is an E3 ubiquitin ligase that regulates the proteasomal degradation and activity of proteins involved in cell growth and apoptosis, including the tumor suppressors p53 and retinoblastoma and the transcription factor E2F1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22666487",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "The p53 transcription factor and tumor suppressor is regulated primarily by the E3 ubiquitin ligase Mdm2, which ubiquitinates p53 to target it for proteasomal degradation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15013777",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "Mdm2 is a RING finger E3 ubiquitin ligase, which promotes ubiquitination and proteasomal degradation of the p53 tumor suppressor protein"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16339144",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 226,
"text": "MDM2 is an E3 ubiquitin ligase that regulates the proteasomal degradation and activity of proteins involved in cell growth and apoptosis, including the tumor suppressors p53 and retinoblastoma and the transcription factor E2F1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22666487",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "The p53 transcription factor and tumor suppressor is regulated primarily by the E3 ubiquitin ligase Mdm2, which ubiquitinates p53 to target it for proteasomal degradation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15013777",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "Mdm2 is a RING finger E3 ubiquitin ligase, which promotes ubiquitination and proteasomal degradation of the p53 tumor suppressor protein"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16339144",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 226,
"text": "MDM2 is an E3 ubiquitin ligase that regulates the proteasomal degradation and activity of proteins involved in cell growth and apoptosis, including the tumor suppressors p53 and retinoblastoma and the transcription factor E2F1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22666487",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "The p53 transcription factor and tumor suppressor is regulated primarily by the E3 ubiquitin ligase Mdm2, which ubiquitinates p53 to target it for proteasomal degradation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15013777",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "Mdm2 is a RING finger E3 ubiquitin ligase, which promotes ubiquitination and proteasomal degradation of the p53 tumor suppressor protein"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16339144",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 226,
"text": "MDM2 is an E3 ubiquitin ligase that regulates the proteasomal degradation and activity of proteins involved in cell growth and apoptosis, including the tumor suppressors p53 and retinoblastoma and the transcription factor E2F1"
}
] | 5 |
BioASQ-training5b
|
[] |
[] |
55058af6f73303d458000004
|
bioasq_factoid
|
factoid
|
Which cancer can be treated with Darolutamide?
|
['Nonmetastatic castration-resistant prostate cancer']
|
[
"Nonmetastatic castration-resistant prostate cancer",
"nmCRPC",
"Non-metastatic castration-resistant prostate cancer",
"Non-metastatic CRPC"
] |
['Darolutamide is used for treatment of nonmetastatic castration-resistant prostate cancer.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/32905676",
"http://www.ncbi.nlm.nih.gov/pubmed/31571146",
"http://www.ncbi.nlm.nih.gov/pubmed/32282865",
"http://www.ncbi.nlm.nih.gov/pubmed/31582533",
"http://www.ncbi.nlm.nih.gov/pubmed/33237495",
"http://www.ncbi.nlm.nih.gov/pubmed/32073798",
"http://www.ncbi.nlm.nih.gov/pubmed/28851578",
"http://www.ncbi.nlm.nih.gov/pubmed/33226524",
"http://www.ncbi.nlm.nih.gov/pubmed/32456317",
"http://www.ncbi.nlm.nih.gov/pubmed/32430485",
"http://www.ncbi.nlm.nih.gov/pubmed/32822968",
"http://www.ncbi.nlm.nih.gov/pubmed/31972568",
"http://www.ncbi.nlm.nih.gov/pubmed/32125151",
"http://www.ncbi.nlm.nih.gov/pubmed/31605368",
"http://www.ncbi.nlm.nih.gov/pubmed/31571095",
"http://www.ncbi.nlm.nih.gov/pubmed/30763142",
"http://www.ncbi.nlm.nih.gov/pubmed/31953000",
"http://www.ncbi.nlm.nih.gov/pubmed/30824428",
"http://www.ncbi.nlm.nih.gov/pubmed/32278840",
"http://www.ncbi.nlm.nih.gov/pubmed/33141615",
"http://www.ncbi.nlm.nih.gov/pubmed/33135506",
"http://www.ncbi.nlm.nih.gov/pubmed/32534790",
"http://www.ncbi.nlm.nih.gov/pubmed/32924096",
"http://www.ncbi.nlm.nih.gov/pubmed/32605736",
"http://www.ncbi.nlm.nih.gov/pubmed/32436836",
"http://www.ncbi.nlm.nih.gov/pubmed/31695432"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31953000",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 215,
"text": "Lately the development of 3 novel second-generation androgen receptor antagonists (enzalutamide, apalutamide, and darolutamide) chanced the treatment landscape of nonmetastatic castration-resistant prostate cancer. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31972568",
"endSection": "abstract",
"offsetInBeginSection": 1672,
"offsetInEndSection": 1897,
"text": "CONCLUSION: Our outcomes support equivalent efficacy and similar risk of adverse effects between apalutamide, enzalutamide, and darolutamide, supporting the use of these antiandrogen agents in high-risk of progression nmCRPC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31582533",
"endSection": "abstract",
"offsetInBeginSection": 1079,
"offsetInEndSection": 1410,
"text": "Furthermore, the combination of BAY 1895344 with the novel, nonsteroidal androgen receptor antagonist darolutamide resulted in significantly improved antitumor efficacy compared with respective single-agent treatments in hormone-dependent prostate cancer, and addition of EBRT resulted in even further enhanced antitumor efficacy. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32125151",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "The antiandrogen therapeutics apalutamide and darolutamide entered the clinic in 2018 and 2019, respectively, for the treatment of castration-resistant prostate cancer (CRPC). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32456317",
"endSection": "abstract",
"offsetInBeginSection": 908,
"offsetInEndSection": 1085,
"text": "This has been further verified by the recent FDA approval of the other two second-generation AR antagonists, apalutamide and darolutamide, for the treatment of prostate cancer. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32430485",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 234,
"text": "The next-generation antiandrogen drugs, XTANDI (enzalutamide), ZYTIGA (abiraterone acetate), ERLEADA (apalutamide) and NUBEQA (darolutamide) extend survival times and improve quality of life in patients with advanced prostate cancer. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32436836",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "BACKGROUND: Darolutamide is recently approved for the treatment of non-metastatic castrate resistance prostate cancer. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32534790",
"endSection": "abstract",
"offsetInBeginSection": 187,
"offsetInEndSection": 369,
"text": "Multiple agents including abiraterone, enzalutamide, apalutamide, darolutamide, docetaxel, cabazitaxel, radium-223, and sipuleucel-T have been approved for advanced prostate cancer. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32278840",
"endSection": "abstract",
"offsetInBeginSection": 2088,
"offsetInEndSection": 2307,
"text": "CONCLUSIONS: NSAAs improve survival in high-risk nmCRPC. Apalutamide and enzalutamide may result in improved oncologic outcomes. Darolutamide may result in fewer AEs. Phase IV data are needed to validate these findings."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32282865",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 67,
"text": "Darolutamide for treatment of castration-resistant prostate cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32282865",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 251,
"text": "Darolutamide is a novel, nonsteroidal androgen receptor (AR)-signaling inhibitor. It serves as a second-generation antiandrogen and is currently indicated for the treatment of patients with nonmetastatic castration-resistant prostate cancer (nmCRPC). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33141615",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 275,
"text": "BACKGROUND: Darolutamide, a structurally distinct androgen receptor inhibitor approved for the treatment of men with nonmetastatic castration-resistant prostate cancer (nmCRPC), has been shown to increase metastasis-free survival among men with nmCRPC compared with placebo. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33141615",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 107,
"text": "Budget impact analysis of darolutamide for treatment of nonmetastatic castration-resistant prostate cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31571095",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 261,
"text": "BACKGROUND: Darolutamide, an androgen receptor antagonist with a distinct molecular structure, significantly prolonged metastasis-free survival versus placebo in the phase III ARAMIS study in men with nonmetastatic castration-resistant prostate cancer (nmCRPC)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32905676",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "BACKGROUND: Darolutamide is a structurally distinct androgen-receptor inhibitor that is approved for the treatment of nonmetastatic, castration-resistant prostate cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30763142",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 68,
"text": "Darolutamide in Nonmetastatic, Castration-Resistant Prostate Cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33226524",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 247,
"text": "BACKGROUND: Darolutamide, an oral androgen receptor inhibitor, has been approved for treating nonmetastatic castration-resistant prostate cancer (nmCRPC), based on significant improvements in metastasis-free survival (MFS) in the ARAMIS clinical t"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31605368",
"endSection": "abstract",
"offsetInBeginSection": 164,
"offsetInEndSection": 349,
"text": "Based on positive results in the phase III ARAMIS trial, darolutamide was recently approved in the USA for the treatment of men with non-metastatic castration-resistant prostate cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28851578",
"endSection": "abstract",
"offsetInBeginSection": 262,
"offsetInEndSection": 489,
"text": "Here, we evaluate the activity of darolutamide in enzalutamide-resistant castration resistant prostate cancer (CRPC) as well as in AR mutants detected in patients after treatment with enzalutamide, abiraterone, or bicalutamide."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33141615",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 274,
"text": "BACKGROUND: Darolutamide, a structurally distinct androgen receptor inhibitor approved for the treatment of men with nonmetastatic castration-resistant prostate cancer (nmCRPC), has been shown to increase metastasis-free survival among men with nmCRPC compared with placebo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31695432",
"endSection": "abstract",
"offsetInBeginSection": 473,
"offsetInEndSection": 685,
"text": "For non-metastatic castration-resistant prostate cancer, recent phase III placebo-controlled trials with enzalutamide, apalutamide and darolutamide all demonstrated benefits in improving metastasis-free survival."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31695432",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 54,
"text": "Darolutamide For Castration-Resistant Prostate Cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32073798",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 237,
"text": "The results of a recent randomised phase 3 clinical trial show that the androgen receptor antagonist darolutamide improves metastasis-free survival in men with non-metastatic, castration-resistant prostate cancer, compared with placebo. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32605736",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Comparative efficacy of apalutamide darolutamide and enzalutamide for treatment of non-metastatic castrate-resistant prostate cancer: A systematic review and network meta-analysis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32605736",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 259,
"text": "INTRODUCTION: Studies using apalutamide, enzalutamide, or darolutamide have shown improved metastasis free survival (MFS) rates, leaving clinicians with a dilemma of choosing one over the other, for nonmetastatic castration recurrent prostate cancer (nmCRPC)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31571146",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "BACKGROUND AND OBJECTIVES: Darolutamide is a novel androgen receptor (AR) antagonist approved for the treatment of nonmetastatic castration-resistant prostate cancer (nmCRPC). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32924096",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "Apalutamide, enzalutamide, and darolutamide for non-metastatic castration-resistant prostate cancer: a systematic review and network meta-analysis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32924096",
"endSection": "abstract",
"offsetInBeginSection": 1554,
"offsetInEndSection": 1719,
"text": "Apalutamide and enzalutamide appear to be more efficacious agents for therapy of nmCRPC, while darolutamide appears to have the most favorable tolerability profile. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33237495",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 78,
"text": "Darolutamide: A Review in Non-Metastatic Castration-Resistant Prostate Cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33237495",
"endSection": "abstract",
"offsetInBeginSection": 207,
"offsetInEndSection": 579,
"text": " In the pivotal multinational, phase 3 ARAMIS trial in men with nmCRPC, relative to placebo plus ongoing androgen deprivation therapy (ADT), darolutamide (+ ADT) significantly prolonged metastasis-free survival (MFS) at the time of the primary analysis and overall survival (OS) at the time of the final OS analysis and was generally well tolerated in extended follow-up. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30824428",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 200,
"text": "The phase III ARAMIS study shows that the androgen-receptor antagonist darolutamide delays metastasis in men with castration-resistant prostate cancer by a median of 22 months compared with a placebo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32822968",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "Since 2018, apalutamide, darolutamide, and enzalutamide have been approved for the treatment of men with non-metastatic castration-resistant prostate cancer (M0CRPC)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33135506",
"endSection": "abstract",
"offsetInBeginSection": 181,
"offsetInEndSection": 361,
"text": "Apalutamide, enzalutamide, and most recently, darolutamide (novel androgen receptor antagonists) have been approved for nonmetastatic castration-resistant prostate cancer (nmCRPC)."
}
] | 11 |
BioASQ-training11b
| null | null |
6020b2b21cb411341a000086
|
bioasq_factoid
|
yesno
|
Does HuR protein regulate the splicing process?
|
['yes']
|
[
"yes"
] |
['Hu antigen R (HuR) functions as an alternative pre-mRNA splicing regulator of Fas apoptosis-promoting receptor on exon definition. HuR and TIA1/TIAL1, two kinds of RNA-binding proteins, were involved in the regulation of alternative splicing of SIRT1 pre-mRNA under normal and stress circumstances. Overexpression and knockdown of HuR led to Fas exon 6 skipping and inclusion, respectively. These results suggest that the TIA and HuR cellular ratio influences cell-type specific Fas exon 6 splicing pattern.', 'HuR and TIA1/TIAL1 are involved in regulation of alternative splicing of SIRT1 pre-mRNA', 'HuR and TIA1/TIAL1 are involved in regulation of alternative splicing of SIRT1 pre-mRNA', 'HuR and TIA1/TIAL1 are involved in regulation of alternative splicing of SIRT1 pre-mRNA', 'HuR and TIA1/TIAL1 are involved in regulation of alternative splicing of SIRT1 pre-mRNA', 'HuR and TIA1/TIAL1 are involved in regulation of alternative splicing of SIRT1 pre-mRNA', 'Recent research demonstrated that SIRT1 pre-mRNA undergoes alternative splicing to produce different isoforms, such as SIRT1 full-length and SIRT1-∆Exon8 variants. Here we describe experiments showing that HuR and TIA1/TIAL1, two kinds of RNA-binding proteins, were involved in the regulation of alternative splicing of SIRT1 pre-mRNA under normal and stress circumstances: HuR increased SIRT1-∆Exon8 by promoting SIRT1 exon 8 exclusion, whereas TIA1/TIAL1 inhibition of the exon 8 exclusion led to a decrease in SIRT1-∆Exon8 mRNA levels. This study provides novel insight into how the alternative splicing of SIRT1 pre-mRNA is regulated, which has fundamental implications for understanding the critical and multifunctional roles of SIRT1. Further, endothelial-specific Elavl1 knockout mice exhibited reduced revascularization after hind limb ischemia and tumor angiogenesis in oncogene-induced mammary cancer, resulting in attenuated blood flow and tumor growth, respectively.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24566137",
"http://www.ncbi.nlm.nih.gov/pubmed/24865968",
"http://www.ncbi.nlm.nih.gov/pubmed/25422430",
"http://www.ncbi.nlm.nih.gov/pubmed/24210824",
"http://www.ncbi.nlm.nih.gov/pubmed/24066065",
"http://www.ncbi.nlm.nih.gov/pubmed/20951677",
"http://www.ncbi.nlm.nih.gov/pubmed/18463097",
"http://www.ncbi.nlm.nih.gov/pubmed/23052832",
"http://www.ncbi.nlm.nih.gov/pubmed/19931428",
"http://www.ncbi.nlm.nih.gov/pubmed/21890634"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24566137",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 87,
"text": "HuR and TIA1/TIAL1 are involved in regulation of alternative splicing of SIRT1 pre-mRNA"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24566137",
"endSection": "abstract",
"offsetInBeginSection": 762,
"offsetInEndSection": 970,
"text": "Here we describe experiments showing that HuR and TIA1/TIAL1, two kinds of RNA-binding proteins, were involved in the regulation of alternative splicing of SIRT1 pre-mRNA under normal and stress circumstances"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24566137",
"endSection": "abstract",
"offsetInBeginSection": 972,
"offsetInEndSection": 1137,
"text": "HuR increased SIRT1-∆Exon8 by promoting SIRT1 exon 8 exclusion, whereas TIA1/TIAL1 inhibition of the exon 8 exclusion led to a decrease in SIRT1-∆Exon8 mRNA levels. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24865968",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 103,
"text": "HuR regulates alternative splicing of the TRA2β gene in human colon cancer cells under oxidative stress"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24865968",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "Hu antigen R (HuR) regulates stress responses through stabilizing and/or facilitating the translation of target mRNAs"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25422430",
"endSection": "abstract",
"offsetInBeginSection": 208,
"offsetInEndSection": 553,
"text": "We show here that the RBP embryonic lethal abnormal vision like 1 (ELAVL1, also know as HuR) regulates the alternative splicing of eukaryotic translation initiation factor 4E nuclear import factor 1 (Eif4enif1), which encodes an eukaryotic translation initiation factor 4E transporter (4E-T) protein and suppresses the expression of capped mRNAs"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25422430",
"endSection": "abstract",
"offsetInBeginSection": 847,
"offsetInEndSection": 1085,
"text": "Further, endothelial-specific Elavl1 knockout mice exhibited reduced revascularization after hind limb ischemia and tumor angiogenesis in oncogene-induced mammary cancer, resulting in attenuated blood flow and tumor growth, respectively. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24210824",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 126,
"text": "Changes in cellular mRNA stability, splicing, and polyadenylation through HuR protein sequestration by a cytoplasmic RNA virus"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24210824",
"endSection": "abstract",
"offsetInBeginSection": 577,
"offsetInEndSection": 810,
"text": "Furthermore, significant changes can be observed in nuclear alternative polyadenylation and splicing events on cellular pre-mRNAs as a result of sequestration of HuR protein by the 3' UTR of transcripts of this cytoplasmic RNA virus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24066065",
"endSection": "abstract",
"offsetInBeginSection": 158,
"offsetInEndSection": 533,
"text": "Here we demonstrate that expression of 2A(pro) induces a selective nucleo-cytoplasm translocation of several important RNA binding proteins and splicing factors. Subcellular fractionation studies, together with immunofluorescence microscopy revealed an asymmetric distribution of HuR and TIA1/TIAR in 2A(pro) expressing cells, which modulates splicing of the human Fas exon 6"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24066065",
"endSection": "abstract",
"offsetInBeginSection": 564,
"offsetInEndSection": 670,
"text": "knockdown of HuR or overexpression of TIA1/TIAR, leads to Fas exon 6 inclusion in 2A(pro)-expressing cells"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20951677",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 178,
"text": "The differential expression levels of T-cell intracellular antigens (TIA) and Hu antigen R (HuR) are concomitant with a splicing switch in apoptosis receptor Fas in HCT-116 cells"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20951677",
"endSection": "abstract",
"offsetInBeginSection": 186,
"offsetInEndSection": 394,
"text": "overexpression and knockdown of HuR led to Fas exon 6 skipping and inclusion, respectively. These results suggest that the TIA and HuR cellular ratio influences cell-type specific Fas exon 6 splicing pattern."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18463097",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Hu antigen R (HuR) functions as an alternative pre-mRNA splicing regulator of Fas apoptosis-promoting receptor on exon definition"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18463097",
"endSection": "abstract",
"offsetInBeginSection": 182,
"offsetInEndSection": 387,
"text": "antiapoptotic regulator Hu antigen R (HuR, ELAVL1), a member of the embryonic lethal, abnormal vision, Drosophila-like (ELAVL) family, promotes Fas exon 6 skipping by binding to an exonic splicing silencer"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23312841",
"endSection": "abstract",
"offsetInBeginSection": 808,
"offsetInEndSection": 1000,
"text": "ELAV/Hu proteins bind to AU-rich elements (ARE) in mRNAs and regulate their stability from splicing to translation, and the ubiquitous HuR protein has been implicated in cancerous cell growth."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23052832",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "The HuR protein regulates the expression of thousands of cellular transcripts by modulating mRNA splicing, trafficking, translation, and stability."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18463097",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Hu antigen R (HuR) functions as an alternative pre-mRNA splicing regulator of Fas apoptosis-promoting receptor on exon definition."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18463097",
"endSection": "abstract",
"offsetInBeginSection": 168,
"offsetInEndSection": 389,
"text": "I report that antiapoptotic regulator Hu antigen R (HuR, ELAVL1), a member of the embryonic lethal, abnormal vision, Drosophila-like (ELAVL) family, promotes Fas exon 6 skipping by binding to an exonic splicing silencer. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24210824",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Changes in cellular mRNA stability, splicing, and polyadenylation through HuR protein sequestration by a cytoplasmic RNA virus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18463097",
"endSection": "abstract",
"offsetInBeginSection": 846,
"offsetInEndSection": 951,
"text": "Further, the silencing capacity of HuR as splicing regulator resides in the RRM1 and hinge-RRM3 domains. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24566137",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 88,
"text": "HuR and TIA1/TIAL1 are involved in regulation of alternative splicing of SIRT1 pre-mRNA."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24865968",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "HuR regulates alternative splicing of the TRA2β gene in human colon cancer cells under oxidative stress."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18463097",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Hu antigen R (HuR) functions as an alternative pre-mRNA splicing regulator of Fas apoptosis-promoting receptor on exon definition."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18463097",
"endSection": "abstract",
"offsetInBeginSection": 168,
"offsetInEndSection": 389,
"text": "I report that antiapoptotic regulator Hu antigen R (HuR, ELAVL1), a member of the embryonic lethal, abnormal vision, Drosophila-like (ELAVL) family, promotes Fas exon 6 skipping by binding to an exonic splicing silencer. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24865968",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "HuR regulates alternative splicing of the TRA2β gene in human colon cancer cells under oxidative stress."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23052832",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 148,
"text": "The HuR protein regulates the expression of thousands of cellular transcripts by modulating mRNA splicing, trafficking, translation, and stability. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18463097",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Hu antigen R (HuR) functions as an alternative pre-mRNA splicing regulator of Fas apoptosis-promoting receptor on exon definition."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18463097",
"endSection": "abstract",
"offsetInBeginSection": 168,
"offsetInEndSection": 389,
"text": "I report that antiapoptotic regulator Hu antigen R (HuR, ELAVL1), a member of the embryonic lethal, abnormal vision, Drosophila-like (ELAVL) family, promotes Fas exon 6 skipping by binding to an exonic splicing silencer. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18463097",
"endSection": "abstract",
"offsetInBeginSection": 846,
"offsetInEndSection": 1122,
"text": "Further, the silencing capacity of HuR as splicing regulator resides in the RRM1 and hinge-RRM3 domains. Taken together, these results support a functional link between HuR as repressor of alternative Fas splicing and the molecular mechanisms modulating programmed cell death."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24865968",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "HuR regulates alternative splicing of the TRA2β gene in human colon cancer cells under oxidative stress."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23052832",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 148,
"text": "The HuR protein regulates the expression of thousands of cellular transcripts by modulating mRNA splicing, trafficking, translation, and stability. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18463097",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Hu antigen R (HuR) functions as an alternative pre-mRNA splicing regulator of Fas apoptosis-promoting receptor on exon definition."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18463097",
"endSection": "abstract",
"offsetInBeginSection": 168,
"offsetInEndSection": 389,
"text": "I report that antiapoptotic regulator Hu antigen R (HuR, ELAVL1), a member of the embryonic lethal, abnormal vision, Drosophila-like (ELAVL) family, promotes Fas exon 6 skipping by binding to an exonic splicing silencer. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24210824",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Changes in cellular mRNA stability, splicing, and polyadenylation through HuR protein sequestration by a cytoplasmic RNA virus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18463097",
"endSection": "abstract",
"offsetInBeginSection": 846,
"offsetInEndSection": 951,
"text": "Further, the silencing capacity of HuR as splicing regulator resides in the RRM1 and hinge-RRM3 domains. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24566137",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 88,
"text": "HuR and TIA1/TIAL1 are involved in regulation of alternative splicing of SIRT1 pre-mRNA."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24865968",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "HuR regulates alternative splicing of the TRA2β gene in human colon cancer cells under oxidative stress."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18463097",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Hu antigen R (HuR) functions as an alternative pre-mRNA splicing regulator of Fas apoptosis-promoting receptor on exon definition."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19931428",
"endSection": "abstract",
"offsetInBeginSection": 296,
"offsetInEndSection": 764,
"text": "We are interested in interactions involving hnRNP proteins participating in several steps of mRNA processing (mainly pre-mRNA splicing) and HuR with an established role in stability/translation of associated mRNAs. hnRNP and HuR proteins have a major nucleoplasmic localization and ability to shuttle between nucleus and cytoplasm. We report here on interactions between hnRNP and HuR proteins that were identified in the context of isolated hnRNP and mRNP complexes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18463097",
"endSection": "abstract",
"offsetInBeginSection": 168,
"offsetInEndSection": 389,
"text": "I report that antiapoptotic regulator Hu antigen R (HuR, ELAVL1), a member of the embryonic lethal, abnormal vision, Drosophila-like (ELAVL) family, promotes Fas exon 6 skipping by binding to an exonic splicing silencer. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24210824",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Changes in cellular mRNA stability, splicing, and polyadenylation through HuR protein sequestration by a cytoplasmic RNA virus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18463097",
"endSection": "abstract",
"offsetInBeginSection": 846,
"offsetInEndSection": 951,
"text": "Further, the silencing capacity of HuR as splicing regulator resides in the RRM1 and hinge-RRM3 domains. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24566137",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 88,
"text": "HuR and TIA1/TIAL1 are involved in regulation of alternative splicing of SIRT1 pre-mRNA."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24865968",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "HuR regulates alternative splicing of the TRA2β gene in human colon cancer cells under oxidative stress."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21890634",
"endSection": "abstract",
"offsetInBeginSection": 727,
"offsetInEndSection": 855,
"text": "Despite the fact that HuR sites are observed in intronic regions, our data do not support a role for HuR in regulating splicing."
}
] | 5 |
BioASQ-training5b
|
[
"http://amigo.geneontology.org/amigo/term/GO:0000398",
"http://amigo.geneontology.org/amigo/term/GO:0008380",
"http://amigo.geneontology.org/amigo/term/GO:0036002",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D000067780"
] |
[] |
56c5a7605795f9a73e000002
|
bioasq_yesno
|
yesno
|
Is Selumetinib effective for low-grade glioma?
|
['yes']
|
[
"yes"
] |
['Selumetinib has promising antitumor activity in children with LGG.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/31151904",
"http://www.ncbi.nlm.nih.gov/pubmed/28339824"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28339824",
"endSection": "abstract",
"offsetInBeginSection": 1651,
"offsetInEndSection": 1729,
"text": "Conclusion: Selumetinib has promising antitumor activity in children with LGG."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31151904",
"endSection": "abstract",
"offsetInBeginSection": 2793,
"offsetInEndSection": 2976,
"text": "INTERPRETATION\n\nSelumetinib is active in recurrent, refractory, or progressive pilocytic astrocytoma harbouring common BRAF aberrations and NF1-associated paediatric low-grade glioma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31151904",
"endSection": "abstract",
"offsetInBeginSection": 2977,
"offsetInEndSection": 3319,
"text": "These results show that selumetinib could be an alternative to standard chemotherapy for these subgroups of patients, and have directly led to the development of two Children's Oncology Group phase 3 studies comparing standard chemotherapy to selumetinib in patients with newly diagnosed paediatric low-grade glioma both with and without NF1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28339824",
"endSection": "abstract",
"offsetInBeginSection": 1651,
"offsetInEndSection": 1728,
"text": "Conclusion Selumetinib has promising antitumor activity in children with LGG."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31151904",
"endSection": "abstract",
"offsetInBeginSection": 2745,
"offsetInEndSection": 2927,
"text": "INTERPRETATION Selumetinib is active in recurrent, refractory, or progressive pilocytic astrocytoma harbouring common BRAF aberrations and NF1-associated paediatric low-grade glioma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28339824",
"endSection": "abstract",
"offsetInBeginSection": 1657,
"offsetInEndSection": 1735,
"text": "Conclusion\n\nSelumetinib has promising antitumor activity in children with LGG."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31151904",
"endSection": "abstract",
"offsetInBeginSection": 2749,
"offsetInEndSection": 2932,
"text": "INTERPRETATION\nSelumetinib is active in recurrent, refractory, or progressive pilocytic astrocytoma harbouring common BRAF aberrations and NF1-associated paediatric low-grade glioma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31151904",
"endSection": "abstract",
"offsetInBeginSection": 2932,
"offsetInEndSection": 3275,
"text": "These results show that selumetinib could be an alternative to standard chemotherapy for these subgroups of patients, and have directly led to the development of two Children's Oncology Group phase 3 studies comparing standard chemotherapy to selumetinib in patients with newly diagnosed paediatric low-grade glioma both with and without NF1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31151904",
"endSection": "abstract",
"offsetInBeginSection": 2099,
"offsetInEndSection": 2441,
"text": "These results show that selumetinib could be an alternative to standard chemotherapy for these subgroups of patients, and have directly led to the development of two Children's Oncology Group phase 3 studies comparing standard chemotherapy to selumetinib in patients with newly diagnosed paediatric low-grade glioma both with and without NF1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31151904",
"endSection": "abstract",
"offsetInBeginSection": 1915,
"offsetInEndSection": 2098,
"text": "INTERPRETATION: Selumetinib is active in recurrent, refractory, or progressive pilocytic astrocytoma harbouring common BRAF aberrations and NF1-associated paediatric low-grade glioma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31151904",
"endSection": "abstract",
"offsetInBeginSection": 2715,
"offsetInEndSection": 2882,
"text": "Selumetinib is active in recurrent, refractory, or progressive pilocytic astrocytoma harbouring common BRAF aberrations and NF1-associated paediatric low-grade glioma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31151904",
"endSection": "abstract",
"offsetInBeginSection": 2883,
"offsetInEndSection": 3225,
"text": "These results show that selumetinib could be an alternative to standard chemotherapy for these subgroups of patients, and have directly led to the development of two Children's Oncology Group phase 3 studies comparing standard chemotherapy to selumetinib in patients with newly diagnosed paediatric low-grade glioma both with and without NF1."
}
] | 11 |
BioASQ-training11b
| null | null |
5e44bdba48dab47f2600001c
|
bioasq_yesno
|
factoid
|
How is ZP-PTH delivered to patients?
|
['transdermal drug-coated microneedle patch system']
|
[
"transdermal drug-coated microneedle patch system",
"microneedle patch system",
"transdermal microneedle patch",
"drug-coated microneedle patch",
"microneedle drug delivery system",
"transdermal microneedle delivery system",
"microneedle array patch",
"drug delivery microneedle patch"
] |
['ZP-PTH uses a transdermal drug-coated microneedle patch system.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/20567999"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20567999",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 169,
"text": "To evaluate the clinical PK/PD of PTH(1-34) delivered by a novel transdermal drug-coated microneedle patch system (ZP-PTH) for the treatment of osteoporosis."
}
] | 11 |
BioASQ-training11b
| null | null |
5e7f64d6835f4e477700001f
|
bioasq_factoid
|
factoid
|
What is another name for AZD0530?
|
['Saracatinib']
|
[
"Saracatinib",
"AZD0530",
"BMS-345541",
"Saracatinib (AZD0530)",
"Saracatinib (BMS-345541)"
] |
['AZD0530 is also known as saracatinib.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23144237"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23144237",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "Antitumor activity of saracatinib (AZD0530), a c-Src/Abl kinase inhibitor, alone or in combination with chemotherapeutic agents in gastric cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23144237",
"endSection": "abstract",
"offsetInBeginSection": 459,
"offsetInEndSection": 655,
"text": "We evaluated the antitumor effect of a c-Src/Abl kinase inhibitor, saracatinib (AZD0530), alone or combined with chemotherapeutic agents in gastric cancer cell lines and a NCI-N87 xenograft model."
}
] | 11 |
BioASQ-training11b
| null | null |
5e540c866d0a277941000052
|
bioasq_factoid
|
factoid
|
What percentage of rheumatoid arthritis patients are responsive to anti-TNF therapy?
|
['50-60%']
|
[
"50-60%",
"fifty to sixty percent",
"50 to 60 percent",
"50% to 60%",
"50 percent to 60 percent"
] |
['Despite this, a substantial proportion of patients (approximately 30-40%) fail to respond to these potentially toxic and expensive therapies. Treatment strategies blocking tumor necrosis factor (anti-TNF) have proven very successful in patients with rheumatoid arthritis (RA), showing beneficial effects in approximately 50-60% of the patients. ', 'The introduction of anti-TNF therapy has dramatically improved the outlook for patients suffering from a number of inflammatory conditions including rheumatoid arthritis and inflammatory bowel disease. Treatment strategies blocking tumor necrosis factor (anti-TNF) have proven very successful in patients with rheumatoid arthritis (RA), showing beneficial effects in approximately 50-60% of the patients.', 'Treatment strategies blocking tumor necrosis factor (anti-TNF) have proven very successful in patients with rheumatoid arthritis (RA), showing beneficial effects in approximately 50-60% of the patients. A substantial proportion of Rheumatoid Arthritis patients (approximately 30-40%) fail to respond to anti-TNF therapies.', 'Despite this, a substantial proportion of patients (approximately 30-40%) fail to respond to these potentially toxic and expensive therapies. Treatment strategies blocking tumor necrosis factor (anti-TNF) have proven very successful in patients with rheumatoid arthritis (RA), showing beneficial effects in approximately 50-60% of the patients.', 'Treatment strategies blocking tumor necrosis factor (anti-TNF) have proven very successful in patients with rheumatoid arthritis (RA), showing beneficial effects in approximately 50-60% of the patients. Despite this, a substantial proportion of patients (approximately 30-40%) fail to respond to these potentially toxic and expensive therapies. ', 'strategies blocking tumor necrosis factor (anti-tnf) have proven very successful in patients with rheumatoid arthritis (ra) , showing beneficial effects in approximately 50-60% of the patients. . this , a substantial proportion of patients (approximately 30-40%) fail to respond to these potentially toxic and expensive therapies . ', 'Treatment strategies blocking tumor necrosis factor (anti-TNF) have proven very successful in patients with rheumatoid arthritis (RA), showing beneficial effects in approximately 50-60% of the patients. The introduction of anti-TNF therapy has dramatically improved the outlook for patients suffering from a number of inflammatory conditions including rheumatoid arthritis and inflammatory bowel disease.', 'treatment strategies blocking tumor necrosis factor (anti-tnf) have proven very successful in patients with rheumatoid arthritis (ra), showing beneficial effects in approximately 50-60% of the patients.', 'Despite this, a substantial proportion of patients (approximately 30-40%) fail to respond to these potentially toxic and expensive therapies. ', 'Despite this, a substantial proportion of patients (approximately 30-40%) fail to respond to these potentially toxic and expensive therapies. Treatment strategies blocking tumor necrosis factor (anti-TNF) have proven very successful in patients with rheumatoid arthritis (RA), showing beneficial effects in approximately 50-60% of the patients.', 'Treatment strategies blocking tumor necrosis factor (anti-TNF) have proven very successful in patients with rheumatoid arthritis (RA), showing beneficial effects in approximately 50-60% of the patients. Despite this, a substantial proportion of patients (approximately 30-40%) fail to respond to these potentially toxic and expensive therapies.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22044414",
"http://www.ncbi.nlm.nih.gov/pubmed/24040234"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22044414",
"endSection": "abstract",
"offsetInBeginSection": 202,
"offsetInEndSection": 344,
"text": "Despite this, a substantial proportion of patients (approximately 30-40%) fail to respond to these potentially toxic and expensive therapies. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24040234",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 202,
"text": "Treatment strategies blocking tumor necrosis factor (anti-TNF) have proven very successful in patients with rheumatoid arthritis (RA), showing beneficial effects in approximately 50-60% of the patients."
}
] | 6 |
BioASQ-training6b
| null | null |
58e79e703e8b6dc87c00000a
|
bioasq_factoid
|
factoid
|
Which peak calling algorithm employs mixture model clustering under the hood?
|
['JAMM']
|
[
"JAMM",
"JAMM domain",
"JAMM/MPN+ metalloenzyme",
"JAMM motif",
"JAMM-like",
"JAMM family"
] |
['JAMM (Joint Analysis of NGS replicates via Mixture Model clustering) is a peak finder that can integrate information from biological replicates, determine enrichment site widths accurately and resolve neighboring narrow peaks. JAMM is a universal peak finder that is applicable to different types of datasets.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/25223640"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25223640",
"endSection": "abstract",
"offsetInBeginSection": 352,
"offsetInEndSection": 946,
"text": "We developed JAMM (Joint Analysis of NGS replicates via Mixture Model clustering): a peak finder that can integrate information from biological replicates, determine enrichment site widths accurately and resolve neighboring narrow peaks. JAMM is a universal peak finder that is applicable to different types of datasets. We show that JAMM is among the best performing peak finders in terms of site detection accuracy and in terms of accurate determination of enrichment sites widths. In addition, JAMM's replicate integration improves peak spatial resolution, sorting and peak finding accuracy."
}
] | 6 |
BioASQ-training6b
| null | null |
587f760792a5b8ad44000005
|
bioasq_factoid
|
factoid
|
What disease is associated with Anticitrullinated peptide antibodies (ACPAs)?
|
['rheumatoid arthritis']
|
[
"rheumatoid arthritis",
"RA",
"chronic inflammatory arthritis",
"rheumatoid disease",
"rheumatoid joint disease"
] |
['nticitrullinated protein antibodies (ACPAs) are serological biomarkers associated with early, rapidly progressing rheumatoid arthritis (RA)', 'Anticitrullinated peptide antibodies (ACPAs) are associated with rheumatoid arthritis.', 'Anticitrullinated peptide antibodies (ACPAs) have been shown to be associated with rheumatoid arthritis', 'The aim of this study was to evaluate the presence of autoantibodies to cyclic citrullinated synthetic peptides (ACPAs) in the sputum of patients with long-standing rheumatoid arthritis.', 'Anticitrullinated protein antibodies are found in patients with rheumatoid arthritis']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/32079664",
"http://www.ncbi.nlm.nih.gov/pubmed/16188943",
"http://www.ncbi.nlm.nih.gov/pubmed/22661643",
"http://www.ncbi.nlm.nih.gov/pubmed/27696777",
"http://www.ncbi.nlm.nih.gov/pubmed/31565241",
"http://www.ncbi.nlm.nih.gov/pubmed/29290168",
"http://www.ncbi.nlm.nih.gov/pubmed/30297575",
"http://www.ncbi.nlm.nih.gov/pubmed/28826660",
"http://www.ncbi.nlm.nih.gov/pubmed/29200020",
"http://www.ncbi.nlm.nih.gov/pubmed/24206219",
"http://www.ncbi.nlm.nih.gov/pubmed/27348081",
"http://www.ncbi.nlm.nih.gov/pubmed/23440041",
"http://www.ncbi.nlm.nih.gov/pubmed/27755123",
"http://www.ncbi.nlm.nih.gov/pubmed/25120260",
"http://www.ncbi.nlm.nih.gov/pubmed/24429169",
"http://www.ncbi.nlm.nih.gov/pubmed/25997035",
"http://www.ncbi.nlm.nih.gov/pubmed/26613769",
"http://www.ncbi.nlm.nih.gov/pubmed/25819755",
"http://www.ncbi.nlm.nih.gov/pubmed/18270852",
"http://www.ncbi.nlm.nih.gov/pubmed/23716070"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29200020",
"endSection": "title",
"offsetInBeginSection": 6,
"offsetInEndSection": 95,
"text": " Anticitrullinated Protein Antibodies in Patients With Long-standing Rheumatoid Arthritis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29200020",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 196,
"text": "The aim of this study was to evaluate the presence of autoantibodies to cyclic citrullinated synthetic peptides (ACPAs) in the sputum of patients with long-standing rheumatoid arthritis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29290168",
"endSection": "abstract",
"offsetInBeginSection": 13,
"offsetInEndSection": 153,
"text": "nticitrullinated protein antibodies (ACPAs) are serological biomarkers associated with early, rapidly progressing rheumatoid arthritis (RA),"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27755123",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 98,
"text": "Anticitrullinated protein antibodies: origin and role in the pathogenesis of rheumatoid arthritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27755123",
"endSection": "abstract",
"offsetInBeginSection": 19,
"offsetInEndSection": 168,
"text": "This article reviews recent literature on the origin and pathogenic role of anticitrullinated protein antibodies (ACPAs) in rheumatoid arthritis (RA)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22661643",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 368,
"text": "OBJECTIVES: To increase understanding of the aetiology and pathogenesis of rheumatoid arthritis (RA), genetic and environmental risk factors for RA subsets, defined by the presence or absence of different anticitrullinated protein/peptide antibodies (ACPAs) targeting citrullinated peptides from α-enolase, vimentin, fibrinogen and collagen type II, were investigated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23716070",
"endSection": "abstract",
"offsetInBeginSection": 122,
"offsetInEndSection": 285,
"text": "Citrullinated proteins are observed in RA lung tissues; however, the association of specific anticitrullinated peptide antibodies (ACPA) with ILD in RA is unknown."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23716070",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 160,
"text": "Association of fine specificity and repertoire expansion of anticitrullinated peptide antibodies with rheumatoid arthritis associated interstitial lung disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26613769",
"endSection": "abstract",
"offsetInBeginSection": 194,
"offsetInEndSection": 485,
"text": "This longitudinal study investigated (1) progression from CSA to clinically detectable arthritis and (2) associations of clinical factors, serological factors (among which are anticitrullinated peptide antibodies (ACPAs)) and MRI-detected subclinical inflammation with arthritis development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32079664",
"endSection": "abstract",
"offsetInBeginSection": 217,
"offsetInEndSection": 328,
"text": "Anticitrullinated peptide antibodies (ACPAs) are arguably the most likely candidate biomarker to screen for RA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24206219",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "Anticitrullinated protein antibodies (ACPAs) constitute a class of autoantibodies found in 60-70% of patients with rheumatoid arthritis (RA)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29290168",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 201,
"text": "BACKGROUND: Anticitrullinated protein antibodies (ACPAs) are serological biomarkers associated with early, rapidly progressing rheumatoid arthritis (RA), including more severe disease and joint damage."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23440041",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 295,
"text": "Antibodies targeting citrullinated proteins (ACPAs [anticitrullinated protein antibodies]) are commonly found in patients with rheumatoid arthritis (RA), strongly associate with distinct HLA-DR alleles, and predict a more aggressive disease course as compared with seronegative patients. Still, "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16188943",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "OBJECTIVES: Anticitrullinated protein/peptide antibodies (ACPA) have an excellent diagnostic performance for rheumatoid arthriti"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18270852",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 107,
"text": "Anticitrullinated protein/peptide antibodies (ACPA) are highly specific for rheumatoid arthritis (RA). They"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24206219",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "Anticitrullinated protein antibodies (ACPAs) constitute a class of autoantibodies found in 60-70% of patients with rheumatoid arthritis (RA). The m"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30297575",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 137,
"text": "Background: Anti-citrullinated peptides antibodies (ACPA) are specific for rheumatoid arthritis and have been implicated in disease patho"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25997035",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "Anticitrullinated peptide/protein antibodies (ACPA), which are highly specific for rheumatoid arthritis (RA), may be found in some patients with other systemic autoimmune diseases. The c"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23716070",
"endSection": "abstract",
"offsetInBeginSection": 122,
"offsetInEndSection": 286,
"text": "Citrullinated proteins are observed in RA lung tissues; however, the association of specific anticitrullinated peptide antibodies (ACPA) with ILD in RA is unknown.M"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25120260",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 235,
"text": "Anti-citrullinated protein/peptide antibodies (ACPAs) are detected in rheumatoid arthritis (RA) sera and because of their strict association with the disease are considered marker antibodies, probably endowed with pathogenic potential."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28826660",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 227,
"text": "OBJECTIVES: Anti-citrullinated protein/peptide antibodies (ACPA) represent an important tool for the diagnosis of rheumatoid arthritis (RA) and the presence of multiple ACPA specificities is highly correlated with the evolution"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24429169",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "OBJECTIVE: Anticitrullinated protein/peptide antibodies (ACPA) are implicated in rheumatoid arthritis (RA) pathogenesis and linked to the shared ep"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25997035",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 180,
"text": "Anticitrullinated peptide/protein antibodies (ACPA), which are highly specific for rheumatoid arthritis (RA), may be found in some patients with other systemic autoimmune diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27348081",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "Rheumatoid arthritis (RA) is an autoimmune connective tissue disease, associated with the presence of anti-citrullinated protein antibodies (ACPA)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31565241",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 192,
"text": "Antibodies against citrullinated peptides are associated with clinical and radiological outcomes in patients with early rheumatoid arthritis: a prospective longitudinal inception cohort study."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25997035",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "In antisynthetase syndrome, ACPA are associated with severe and erosive arthritis: an overlapping rheumatoid arthritis and antisynthetase syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31565241",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 253,
"text": "Introduction: Anticitrullinated peptide antibody (ACPA) responses for 22 citrullinated peptides in patients with early rheumatoid arthritis (RA) were analysed and related to radiological and clinical outcome during the first 2 years in a prospective inc"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25819755",
"endSection": "abstract",
"offsetInBeginSection": 107,
"offsetInEndSection": 225,
"text": "Recent studies have revealed that periodontal disease (PD) is closely associated with RA and production of ACPA in RA."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27696777",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "Association of Anti-Citrullinated Peptide Antibodies With Coronary Artery Calcification in Rheumatoid Arthritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25819755",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Anti-citrullinated peptide antibody (ACPA) is a highly specific autoantibody to rheumatoid arthritis (RA)."
}
] | 11 |
BioASQ-training11b
| null | null |
5e6e9a2fc6a8763d23000007
|
bioasq_factoid
|
factoid
|
What is the function of the stard10 protein?
|
['STARD10 is a lipid transfer protein']
|
[
"STARD10",
"StARD10",
"StAR-related lipid transfer protein 10",
"Steroidogenic acute regulatory protein 10"
] |
['STARD10, a member of the steroidogenic acute regulatory protein (StAR)-related lipid transfer (START) protein family, is highly expressed in the liver and has been shown to transfer phosphatidylcholine.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23200860",
"http://www.ncbi.nlm.nih.gov/pubmed/15976441",
"http://www.ncbi.nlm.nih.gov/pubmed/15911624"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23200860",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 202,
"text": "STARD10, a member of the steroidogenic acute regulatory protein (StAR)-related lipid transfer (START) protein family, is highly expressed in the liver and has been shown to transfer phosphatidylcholine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15911624",
"endSection": "abstract",
"offsetInBeginSection": 171,
"offsetInEndSection": 327,
"text": "StarD10 contains a steroidogenic acute regulatory protein (StAR/StarD1)-related lipid transfer (START) domain that is thought to mediate binding of lipids. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15976441",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 174,
"text": "The steroidogenic acute regulatory protein (StAR)-related lipid transfer (START) domain is a protein module of approximately 210 residues that binds lipids, including sterols"
}
] | 11 |
BioASQ-training11b
| null | null |
608069984e6a4cf630000006
|
bioasq_factoid
|
factoid
|
Which is the most important prognosis sub-classification in Chronic Lymphocytic Leukemia?
|
['The mutational status of the IGHV genes.']
|
[
"IGHV genes",
"Immunoglobulin heavy chain variable region genes",
"Immunoglobulin heavy variable genes",
"Immunoglobulin heavy chain variable genes",
"IGHV"
] |
['The mutational status of the immunoglobulin heavy variable (IGHV) genes, defines two subsets: mutated and unmutated CLL. Unmutated CLL patients show a shorter progression-free and overall survival than mutated CLL patients.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23468975",
"http://www.ncbi.nlm.nih.gov/pubmed/22560084",
"http://www.ncbi.nlm.nih.gov/pubmed/20353875",
"http://www.ncbi.nlm.nih.gov/pubmed/20090781",
"http://www.ncbi.nlm.nih.gov/pubmed/19500131",
"http://www.ncbi.nlm.nih.gov/pubmed/19127482",
"http://www.ncbi.nlm.nih.gov/pubmed/17786276",
"http://www.ncbi.nlm.nih.gov/pubmed/16825496",
"http://www.ncbi.nlm.nih.gov/pubmed/16014569",
"http://www.ncbi.nlm.nih.gov/pubmed/16083281"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22560084",
"endSection": "sections.0",
"offsetInBeginSection": 621,
"offsetInEndSection": 879,
"text": "One of the most reliable prognostic markers in chronic lymphocytic leukemia (CLL) is the mutational status of immunoglobulin heavy variable (IGHV) genes, which defines 2 subsets, mutated CLL (M-CLL) and unmutated CLL (U-CLL), with different clinical courses."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20090781",
"endSection": "sections.0",
"offsetInBeginSection": 119,
"offsetInEndSection": 268,
"text": "Mutational status of the immunoglobulin heavy chain variable regions (IGHVs) of CLL cells offers useful prognostic information for high-risk patients"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20090781",
"endSection": "sections.0",
"offsetInBeginSection": 270,
"offsetInEndSection": 496,
"text": "but time and economical costs originally prevented it from being routinely used in a clinical setting. Instead, alternative markers of IGHV status, such as zeta-associated protein (ZAP70) or messenger RNA levels are often used"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19127482",
"endSection": "sections.0",
"offsetInBeginSection": 109,
"offsetInEndSection": 282,
"text": "Patients with unmutated IgV(H) gene show a shorter progression-free and overall survival than patients with immunoglobulin heavy chain variable regions (IgV(H)) gene mutated"
}
] | 5 |
BioASQ-training5b
| null | null |
51739df58ed59a060a00001c
|
bioasq_factoid
|
yesno
|
Is avelumab effective for bladder cancer?
|
['yes']
|
[
"yes"
] |
['Yes, avelumab is effective treatment of bladder cancer.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/29069302",
"http://www.ncbi.nlm.nih.gov/pubmed/29606979",
"http://www.ncbi.nlm.nih.gov/pubmed/28864844",
"http://www.ncbi.nlm.nih.gov/pubmed/28214651",
"http://www.ncbi.nlm.nih.gov/pubmed/29644490",
"http://www.ncbi.nlm.nih.gov/pubmed/29416316",
"http://www.ncbi.nlm.nih.gov/pubmed/29540084",
"http://www.ncbi.nlm.nih.gov/pubmed/29784744",
"http://www.ncbi.nlm.nih.gov/pubmed/28982750",
"http://www.ncbi.nlm.nih.gov/pubmed/29103968",
"http://www.ncbi.nlm.nih.gov/pubmed/28493171"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29103968",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "BACKGROUND: Avelumab has recently been approved by the Food and Drug Administration for the therapy of Merkel cell carcinoma and urothelial carcinoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29069302",
"endSection": "abstract",
"offsetInBeginSection": 550,
"offsetInEndSection": 964,
"text": "Six drugs including one CTLA-4 blocker (ipilimumab), two PD-1 blockers (nivolumab and pembrolizumab) and three PD-L1 blockers (atezolizumab, avelumab and durvalumab) are approved for the treatment of different types of cancers including both solid tumors such as melanoma, lung cancer, head and neck cancer, bladder cancer and Merkel cell cancer as well as hematological tumors such as classic Hodgkin's lymphoma. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29416316",
"endSection": "abstract",
"offsetInBeginSection": 439,
"offsetInEndSection": 779,
"text": "The Food and Drug Administration has already approved a number of checkpoint inhibitors such as anti-cytotoxic T-lymphocyte-associated protein 4 (CTLA4) monoclonal antibodies including ipilimumab; anti-PD-1 monoclonal antibodies including nivolumab and pembrolizumab; anti-PD-L1 antibodies including atezolizumab, avelumab, and durvalumab. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29606979",
"endSection": "abstract",
"offsetInBeginSection": 634,
"offsetInEndSection": 810,
"text": "Five immune CPI have recently been approved for aUC/mUC by the US Food and Drug Administration (FDA) including atezolizumab, nivolumab, pembrolizumab, durvalumab and avelumab. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29644490",
"endSection": "abstract",
"offsetInBeginSection": 364,
"offsetInEndSection": 717,
"text": "RECENT FINDINGS: Since May 2016, five different agents targeting the PD-1/PD-L1 pathway (atezolizumab, pembrolizumab, nivolumab, avelumab, durvalumab) have received FDA approval for the treatment of aUC in the platinum-refractory setting, while pembrolizumab and atezolizumab are FDA-approved for cisplatin-ineligible patients in the first-line setting."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29540084",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 48,
"text": "Avelumab for the treatment of urothelial cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29540084",
"endSection": "abstract",
"offsetInBeginSection": 580,
"offsetInEndSection": 924,
"text": "Avelumab, a PD-1 ligand (PD-L1) inhibitor, is currently being investigated for the treatment of UC. Areas covered: This article will review the pharmacological characteristics of avelumab, the efficacy studies which led to its approval, its safety profile, as well as its place within the management of urothelial carcinoma with immunotherapy. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29540084",
"endSection": "abstract",
"offsetInBeginSection": 1073,
"offsetInEndSection": 1193,
"text": "Expert commentary: Avelumab has shown promising antitumor activity and a manageable safety profile in patients with UC. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28214651",
"endSection": "abstract",
"offsetInBeginSection": 1027,
"offsetInEndSection": 1280,
"text": "Atezolizumab is the only member of this class currently approved for the treatment of bladder cancer, but nivolumab, pembrolizumab, durvalumab, and avelumab all have positive results for this indication, and approvals are anticipated in the near future."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28982750",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 335,
"text": "This selection from the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) for Bladder Cancer focuses on systemic therapy for muscle-invasive urothelial bladder cancer, as substantial revisions were made in the 2017 updates, such as new recommendations for nivolumab, pembrolizumab, atezolizumab, durvalumab, and avelumab."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28493171",
"endSection": "abstract",
"offsetInBeginSection": 1033,
"offsetInEndSection": 1216,
"text": "Atezolizumab, avelumab, durvalumab, nivolumab and pembrolizumab are promising PD-1/PD-L1 blockade drugs under investigation that will redefine the standard of care for bladder cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28864844",
"endSection": "abstract",
"offsetInBeginSection": 2200,
"offsetInEndSection": 2493,
"text": "Monoclonal antibodies that target programmed cell death protein 1 (PD-1), including Nivolumab and Pembrolizumab, and its ligand, PD-L1, including Atezolizumab, Durvalumab, Avelumab, have all been investigated and approved in the setting of metastatic refractory urothelial cancer (Gupta et al."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29069302",
"endSection": "abstract",
"offsetInBeginSection": 550,
"offsetInEndSection": 963,
"text": "Six drugs including one CTLA-4 blocker (ipilimumab), two PD-1 blockers (nivolumab and pembrolizumab) and three PD-L1 blockers (atezolizumab, avelumab and durvalumab) are approved for the treatment of different types of cancers including both solid tumors such as melanoma, lung cancer, head and neck cancer, bladder cancer and Merkel cell cancer as well as hematological tumors such as classic Hodgkin's lymphoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29784744",
"endSection": "abstract",
"offsetInBeginSection": 300,
"offsetInEndSection": 504,
"text": "Nivolumab, pembrolizumab, atezolizumab, durvalumab, and avelumab are among the exciting recent novel therapeutic advances gaining approvals by the FDA for treatment of advanced-stage urothelial carcinoma."
}
] | 11 |
BioASQ-training11b
| null | null |
5c72ba807c78d69471000076
|
bioasq_yesno
|
factoid
|
Which receptor is targeted by telcagepant?
|
[['calcitonin gene-related peptide']]
|
[
"calcitonin gene-related peptide",
"CGRP",
"calcitonin gene-related peptide alpha",
"calcitonin gene-related peptide beta",
"CGRP alpha",
"CGRP beta"
] |
['Telcagepant (MK-0974) is a novel calcitonin gene-related peptide (CGRP) receptor antagonist currently undergoing clinical trials for migraine.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23975906",
"http://www.ncbi.nlm.nih.gov/pubmed/23798725",
"http://www.ncbi.nlm.nih.gov/pubmed/23196486",
"http://www.ncbi.nlm.nih.gov/pubmed/22816019",
"http://www.ncbi.nlm.nih.gov/pubmed/22512641",
"http://www.ncbi.nlm.nih.gov/pubmed/22278333",
"http://www.ncbi.nlm.nih.gov/pubmed/22221076",
"http://www.ncbi.nlm.nih.gov/pubmed/22090312",
"http://www.ncbi.nlm.nih.gov/pubmed/21631478",
"http://www.ncbi.nlm.nih.gov/pubmed/21480950",
"http://www.ncbi.nlm.nih.gov/pubmed/21457238",
"http://www.ncbi.nlm.nih.gov/pubmed/21383046",
"http://www.ncbi.nlm.nih.gov/pubmed/21350792",
"http://www.ncbi.nlm.nih.gov/pubmed/21221171",
"http://www.ncbi.nlm.nih.gov/pubmed/21110235",
"http://www.ncbi.nlm.nih.gov/pubmed/21070230",
"http://www.ncbi.nlm.nih.gov/pubmed/21070229",
"http://www.ncbi.nlm.nih.gov/pubmed/21054362",
"http://www.ncbi.nlm.nih.gov/pubmed/20974601",
"http://www.ncbi.nlm.nih.gov/pubmed/20954694",
"http://www.ncbi.nlm.nih.gov/pubmed/20937606",
"http://www.ncbi.nlm.nih.gov/pubmed/20855369",
"http://www.ncbi.nlm.nih.gov/pubmed/20826335",
"http://www.ncbi.nlm.nih.gov/pubmed/20573757",
"http://www.ncbi.nlm.nih.gov/pubmed/20433208",
"http://www.ncbi.nlm.nih.gov/pubmed/20416945",
"http://www.ncbi.nlm.nih.gov/pubmed/20188075",
"http://www.ncbi.nlm.nih.gov/pubmed/20173082",
"http://www.ncbi.nlm.nih.gov/pubmed/20164785",
"http://www.ncbi.nlm.nih.gov/pubmed/20120204",
"http://www.ncbi.nlm.nih.gov/pubmed/20099900",
"http://www.ncbi.nlm.nih.gov/pubmed/20078608",
"http://www.ncbi.nlm.nih.gov/pubmed/23480465",
"http://www.ncbi.nlm.nih.gov/pubmed/19939188",
"http://www.ncbi.nlm.nih.gov/pubmed/19914210",
"http://www.ncbi.nlm.nih.gov/pubmed/19796656",
"http://www.ncbi.nlm.nih.gov/pubmed/19795182",
"http://www.ncbi.nlm.nih.gov/pubmed/19779958",
"http://www.ncbi.nlm.nih.gov/pubmed/19770473",
"http://www.ncbi.nlm.nih.gov/pubmed/19737844",
"http://www.ncbi.nlm.nih.gov/pubmed/19579177",
"http://www.ncbi.nlm.nih.gov/pubmed/19551474",
"http://www.ncbi.nlm.nih.gov/pubmed/19469188",
"http://www.ncbi.nlm.nih.gov/pubmed/19346171",
"http://www.ncbi.nlm.nih.gov/pubmed/19219746",
"http://www.ncbi.nlm.nih.gov/pubmed/19157980",
"http://www.ncbi.nlm.nih.gov/pubmed/19084002",
"http://www.ncbi.nlm.nih.gov/pubmed/18991732",
"http://www.ncbi.nlm.nih.gov/pubmed/19036425",
"http://www.ncbi.nlm.nih.gov/pubmed/18808506",
"http://www.ncbi.nlm.nih.gov/pubmed/18799366",
"http://www.ncbi.nlm.nih.gov/pubmed/18590336",
"http://www.ncbi.nlm.nih.gov/pubmed/18217201",
"http://www.ncbi.nlm.nih.gov/pubmed/18039958",
"http://www.ncbi.nlm.nih.gov/pubmed/17929795",
"http://www.ncbi.nlm.nih.gov/pubmed/17914062",
"http://www.ncbi.nlm.nih.gov/pubmed/25107879"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23975906",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 184,
"text": "In vivo quantification of calcitonin gene-related peptide receptor occupancy by telcagepant in rhesus monkey and human brain using the positron emission tomography tracer [11C]MK-4232."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23798725",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "Lack of hemodynamic interaction between CGRP-receptor antagonist telcagepant (MK-0974) and sumatriptan: results from a randomized study in patients with migraine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23196486",
"endSection": "abstract",
"offsetInBeginSection": 684,
"offsetInEndSection": 963,
"text": "Olcegepant is the first selective CGRP receptor antagonist of proven efficacy in migraine. Olcegepant could only be administered intravenously and never taken beyond Phase II. Telcagepant is orally available and several completed Phase III trials have revealed positive results. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22816019",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 193,
"text": "Telcagepant (MK-0974) is a novel calcitonin gene-related peptide (CGRP) receptor antagonist currently undergoing clinical trials for migraine (http://www.merck.com/research/pipeline/home.html)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22512641",
"endSection": "abstract",
"offsetInBeginSection": 599,
"offsetInEndSection": 765,
"text": "Four chemically unrelated CGRP receptor (CGRP-R) antagonists (olcegepant, telcagepant, MK-3207 and BI 44370 TA) have displayed efficacy in the treatment of migraine. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22278333",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 122,
"text": "Telcagepant is a calcitonin gene-related peptide (CGRP) receptor antagonist being evaluated for acute migraine treatment. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22221076",
"endSection": "abstract",
"offsetInBeginSection": 106,
"offsetInEndSection": 328,
"text": "BACKGROUND: Calcitonin gene-related peptide receptor antagonists, such as telcagepant, may be useful for acute migraine treatment in patients with cardiovascular disease, a population for whom triptans are contraindicated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22090312",
"endSection": "abstract",
"offsetInBeginSection": 493,
"offsetInEndSection": 683,
"text": "The calcitonin gene-related peptide (CGRP) receptor antagonists (gepants)-olcegepant (BIBN 4096 BS), telcagepant (MK-0974), MK3207, and BI 44370 TA-are effective in treating acute migraine. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21631478",
"endSection": "abstract",
"offsetInBeginSection": 314,
"offsetInEndSection": 438,
"text": "Telcagepant, a calcitonin gene-related peptide receptor antagonist, is being developed for the acute treatment of migraine. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21480950",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "The potent calcitonin gene-related peptide receptor antagonist, telcagepant, does not affect nitroglycerin-induced vasodilation in healthy men."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21480950",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "AIMS: To assess the effect of the calcitonin gene-related peptide (CGRP) receptor antagonist, telcagepant, on the haemodynamic response to sublingual nitroglycerin (NTG). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21457238",
"endSection": "abstract",
"offsetInBeginSection": 158,
"offsetInEndSection": 307,
"text": "BACKGROUND: Telcagepant is an oral calcitonin gene-related peptide receptor antagonist which is being evaluated for the acute treatment of migraine. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21383046",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 126,
"text": "BACKGROUND: The calcitonin gene-related peptide (CGRP) receptor antagonists olcegepant and telcagepant are very potent drugs. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21383046",
"endSection": "abstract",
"offsetInBeginSection": 841,
"offsetInEndSection": 995,
"text": "CONCLUSION: The apparently high doses of CGRP receptor antagonists, olcegepant and telcagepant needed for anti-migraine effect are not so high after all. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21350792",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 207,
"text": "Dose-response curves for headaches relief and adverse events (AEs) are presented for five triptans: sumatriptan, zolmitriptan, naratriptan, almotriptan, and frovatriptan, and the CGRP antagonist telcagepant."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21221171",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "INTRODUCTION: Telcagepant (MK-0974) is a novel, orally active and selective CGRP receptor antagonist being investigated for acute treatment of migraine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21110235",
"endSection": "abstract",
"offsetInBeginSection": 1175,
"offsetInEndSection": 1469,
"text": "Calcitonin gene-related peptide (CGRP) receptor antagonists are another promising nonvasoconstrictor approach to treating acute migraine. Olcegepant (BIBN4096BS) and telcagepant (MK-0974) have been shown to be safe and effective in phase I, II, and (for telcagepant) phase III clinical trials. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21070230",
"endSection": "abstract",
"offsetInBeginSection": 119,
"offsetInEndSection": 263,
"text": "Background.- Telcagepant is a calcitonin gene-related peptide (CGRP) receptor antagonist being investigated for the acute treatment of migraine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21070229",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 216,
"text": "In 3 randomized clinical trials (n = 1585) the calcitonin gene-related peptide antagonist telcagepant 300 mg orally had an incidence of adverse events similar to placebo when used in the acute treatment of migraine. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21054362",
"endSection": "abstract",
"offsetInBeginSection": 99,
"offsetInEndSection": 246,
"text": "BACKGROUND: Telcagepant is an oral calcitonin gene-related peptide receptor antagonist with acute antimigraine efficacy comparable to oral triptans"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20974601",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 185,
"text": "METHODS: This study evaluated the calcitonin gene-related peptide (CGRP) receptor antagonist telcagepant (tablet formulation) for treatment of a migraine attack and across four attacks."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20954694",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "A highly efficient, asymmetric synthesis of telcagepant (1), a CGRP receptor antagonist for the treatment of migraine, is described"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20954694",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "Asymmetric synthesis of telcagepant, a CGRP receptor antagonist for the treatment of migraine."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20937606",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "Sustained pain freedom and no adverse events as an endpoint in clinical trials of acute migraine treatments: application to patient-level data from a trial of the CGRP receptor antagonist, telcagepant, and zolmitriptan."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20937606",
"endSection": "abstract",
"offsetInBeginSection": 289,
"offsetInEndSection": 623,
"text": "METHODS: The aim of this study was to evaluate new composite efficacy-plus-tolerability endpoints based on a post-hoc analysis of patient-level data from a previous randomized, placebo-controlled trial of the calcitonin gene-related peptide (CGRP) receptor antagonist, telcagepant, and zolmitriptan in the acute treatment of migraine."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20855369",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 111,
"text": "Effect of the calcitonin gene-related peptide (CGRP) receptor antagonist telcagepant in human cranial arteries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20855369",
"endSection": "abstract",
"offsetInBeginSection": 182,
"offsetInEndSection": 375,
"text": "MATERIALS AND METHODS: We investigated the effect of the CGRP receptor antagonist, telcagepant, on CGRP-induced cranial vasodilatation in human isolated cerebral and middle meningeal arteries. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20855369",
"endSection": "abstract",
"offsetInBeginSection": 1102,
"offsetInEndSection": 1328,
"text": "CONCLUSIONS: Our findings provide morphological and functional data on the presence of CGRP receptors in cerebral and meningeal arteries, which illustrates a possible site of action of telcagepant in the treatment of migraine."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20573757",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 134,
"text": "Characterization of the calcitonin gene-related peptide receptor antagonist telcagepant (MK-0974) in human isolated coronary arteries."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20573757",
"endSection": "abstract",
"offsetInBeginSection": 287,
"offsetInEndSection": 585,
"text": "We therefore investigated the effects of the antimigraine CGRP receptor antagonist telcagepant (MK-0974) [N-[(3R,6S)-6-(2,3-difluorophenyl)-2-oxo-1-(2,2,2-trifluoroethyl)azepan-3-yl]-4-(2-oxo-2,3-dihydro-1H-imidazo[4,5-b]pyridine-1-yl)piperidine-1-carboxamide] on human isolated coronary arteries. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20573757",
"endSection": "abstract",
"offsetInBeginSection": 1861,
"offsetInEndSection": 2060,
"text": "These findings in vitro support the cardiovascular safety of CGRP receptor antagonists and suggest that telcagepant is unlikely to induce coronary side effects under normal cardiovascular conditions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20433208",
"endSection": "abstract",
"offsetInBeginSection": 1115,
"offsetInEndSection": 1482,
"text": "Towards this end, the non-peptide CGRP receptor antagonists olcegepant and telcagepant have been shown to be effective in the acute treatment of migraine. While telcagepant is being pursued as a frontline abortive migraine drug in a phase III clinical trial, an oral formulation of a novel CGRP receptor antagonist, BI 44370, is currently in phase II clinical trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20416945",
"endSection": "abstract",
"offsetInBeginSection": 229,
"offsetInEndSection": 340,
"text": "Telcagepant represents a new class of antimigraine drug-the calcitonin gene-related peptide receptor blockers. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20188075",
"endSection": "abstract",
"offsetInBeginSection": 406,
"offsetInEndSection": 634,
"text": "The CGRP receptor antagonists telcagepant and olcegepant (BIBN4096BS) have demonstrated clinical efficacy in the treatment of migraine and there is now a need to better understand how these molecules interact with the receptor. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20173082",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 147,
"text": "Single- and multiple-dose pharmacokinetics and tolerability of telcagepant, an oral calcitonin gene-related peptide receptor antagonist, in adults."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20173082",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "Telcagepant is a novel, orally active, and selective calcitonin gene-related peptide receptor antagonist being developed for acute treatment of migraine with and without aura. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20164785",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 249,
"text": "Studies were conducted in human isolated coronary arteries to explore the vascular effects of the calcitonin gene-related peptide (CGRP) receptor antagonist telcagepant and to compare its coronary vasoconstrictive potential to that of zolmitriptan. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20120204",
"endSection": "abstract",
"offsetInBeginSection": 662,
"offsetInEndSection": 848,
"text": "Intravenous BIBN4096BS (olcegepant) and oral MK-0974 (telcagepant), two CGRP-receptor antagonists, were safe and effective in the treatment of migraine attacks in Phase I and II trials. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19346171",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "Telcagepant (MK-0974) is a novel oral calcitonin gene-related peptide (CGRP) receptor antagonist and is currently under clinical development."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23975906",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 184,
"text": "In vivo quantification of calcitonin gene-related peptide receptor occupancy by telcagepant in rhesus monkey and human brain using the positron emission tomography tracer [11C]MK-4232."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23798725",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 162,
"text": "Lack of hemodynamic interaction between CGRP-receptor antagonist telcagepant (MK-0974) and sumatriptan: results from a randomized study in patients with migraine."
}
] | 5 |
BioASQ-training5b
|
[] |
[] |
55032efde9bde69634000035
|
bioasq_factoid
|
factoid
|
Are male or female persons more prone to autoimmunity?
|
['Female']
|
[
"Female",
"Woman",
"Girl",
"Feminine",
"Lady",
"Dame",
"She",
"Her"
] |
['Sex hormones have long been implicated in autoimmune diseases because women account for 80% of cases.', 'Sex hormones have long been implicated in autoimmune diseases because women account for 80% of cases. Most recently, sex chromosome abnormalities and skewed X chromosome inactivation have been suggested as novel players, particularly in later-onset diseases.', 'Sex hormones have long been implicated in autoimmune diseases because women account for 80% of cases. Examples of this autoimmune dimorphism include (but are not limited to) lupus, rheumatoid arthritis and multiple sclerosis with the two former more prevalent in females than males and the latter more severe during pregnancy. Most recently, sex chromosome abnormalities and skewed X chromosome inactivation have been suggested as novel players, particularly in later-onset diseases.', 'females', 'Sex hormones have long been implicated in autoimmune diseases because women account for 80% of cases. Sex hormone expression is altered among patients with autoimmune disease, and this variation of expression contributes to immune dysregulation.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/17108242",
"http://www.ncbi.nlm.nih.gov/pubmed/25956531",
"http://www.ncbi.nlm.nih.gov/pubmed/30394940",
"http://www.ncbi.nlm.nih.gov/pubmed/18603021",
"http://www.ncbi.nlm.nih.gov/pubmed/508371",
"http://www.ncbi.nlm.nih.gov/pubmed/1958563",
"http://www.ncbi.nlm.nih.gov/pubmed/22155196",
"http://www.ncbi.nlm.nih.gov/pubmed/16549717"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/508371",
"endSection": "abstract",
"offsetInBeginSection": 594,
"offsetInEndSection": 683,
"text": " Estrogens cause a marked acceleration of autoimmunity and a reduction in thymus weight. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/508371",
"endSection": "abstract",
"offsetInBeginSection": 719,
"offsetInEndSection": 1042,
"text": "we found that a number of problems or variables arise in studying sex hormone effects, including: 1) X-linked genes, 2) metabolism of testosterone to estrogens, 3) dose of hormone, 4) age at which administration is initiated, 5) differential effects of sex hormones on different autoantibodies and various immune responses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1958563",
"endSection": "abstract",
"offsetInBeginSection": 721,
"offsetInEndSection": 945,
"text": "Examples of this autoimmune dimorphism include (but are not limited to) lupus, rheumatoid arthritis and multiple sclerosis with the two former more prevalent in females than males and the latter more severe during pregnancy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17108242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "Sex hormones have long been implicated in autoimmune diseases because women account for 80% of cases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16549717",
"endSection": "abstract",
"offsetInBeginSection": 376,
"offsetInEndSection": 635,
"text": "Sex hormones have definitive roles in lymphocyte maturation, activation, and synthesis of antibodies and cytokines. Sex hormone expression is altered among patients with autoimmune disease, and this variation of expression contributes to immune dysregulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16549717",
"endSection": "abstract",
"offsetInBeginSection": 1329,
"offsetInEndSection": 1561,
"text": "ex hormones affect the function of the mammalian immune system, and sex hormone expression is different in patients with systemic lupus erythematosus than in healthy subjects. Sex hormones play a role in the genesis of autoimmunity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18603021",
"endSection": "abstract",
"offsetInBeginSection": 720,
"offsetInEndSection": 876,
"text": "Most recently, sex chromosome abnormalities and skewed X chromosome inactivation have been suggested as novel players, particularly in later-onset diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22155196",
"endSection": "abstract",
"offsetInBeginSection": 1452,
"offsetInEndSection": 1679,
"text": "As a result we may hypothesize that more than one mechanism may contribute to the female susceptibility to tolerance breakdown while the possibility that unknown factors may indeed protect men from AID should not be overlooked."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25956531",
"endSection": "abstract",
"offsetInBeginSection": 430,
"offsetInEndSection": 651,
"text": " The gut microbiome, which impacts the innate and adaptive branches of immunity, not only influences the development of autoimmune disorders but may interact with sex-hormones to modulate disease progression and sex-bias."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30394940",
"endSection": "abstract",
"offsetInBeginSection": 155,
"offsetInEndSection": 545,
"text": "Recent studies investigating the origins of sex bias in autoimmune disease have revealed an extensive and interconnected network of genetic, hormonal, microbial, and environmental influences. Investigation of sex hormones has moved beyond profiling the effects of hormones on activity and prevalence of immune cell types to defining the specific immunity-related genes driving these changes"
}
] | 11 |
BioASQ-training11b
| null | null |
5cebf83ea49efeb44c00000a
|
bioasq_factoid
|
factoid
|
What antibiotic is currently used as the standard of care for Clostridium Difficile infection as of 2018
|
['Fidaxomicin']
|
[
"Fidaxomicin",
"Dificid",
"OPT-80",
"Fidaxomicin (Dificid)"
] |
['fidaxomicin has recently been introduced as a new antibiotic that has been shown to significantly reduce the recurrence of this infection. fidaxomicin is a new antibiotic used to treat clostridium difficile infection (cdi).', 'Fidaxomicin has recently been introduced as a new antibiotic that has been shown to significantly reduce the recurrence of this infection. Fidaxomicin is a new antibiotic used to treat Clostridium difficile infection (CDI).', 'Fidaxomicin has recently been introduced as a new antibiotic that has been shown to significantly reduce the recurrence of this infection.Fidaxomicin is a new antibiotic used to treat Clostridium difficile infection (CDI)', 'Clostridium difficile continues to be one of the most prevalent hospital-acquired bacterial infections in the developed world, despite the recent introduction of a novel and effective antibiotic agent fidaxomicin']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27601193",
"http://www.ncbi.nlm.nih.gov/pubmed/28009682"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27601193",
"endSection": "abstract",
"offsetInBeginSection": 156,
"offsetInEndSection": 295,
"text": " Fidaxomicin has recently been introduced as a new antibiotic that has been shown to significantly reduce the recurrence of this infection."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28009682",
"endSection": "abstract",
"offsetInBeginSection": 22,
"offsetInEndSection": 107,
"text": "Fidaxomicin is a new antibiotic used to treat Clostridium difficile infection (CDI). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28009682",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 69,
"text": "Outcomes With Fidaxomicin Therapy in Clostridium difficile Infection."
}
] | 11 |
BioASQ-training11b
| null | null |
5c85234775a4a5d219000007
|
bioasq_factoid
|
factoid
|
In which cell organelle is the SAF-A protein localized?
|
['the nucleus']
|
[
"the nucleus",
"cell nucleus",
"nuclear envelope",
"nuclear membrane",
"nuclear structure",
"nuclear region"
] |
['saf-a/hnrnp u is an abundant nuclear protein that interacts specifically with nuclear matrix attachment region dna', 'SAF-A/hnRNP U is an abundant nuclear protein that interacts specifically with nuclear matrix attachment region DNA (MAR) and RNA as a component of hnRNPs. Scaffold attachment factor A (SAF-A) participates in the regulation of gene expression by organizing chromatin into transcriptionally active domains and by interacting directly with RNA polymerase II.', 'Scaffold attachment factor B (SAF-B) is a nuclear matrix-associated protein. It is an abundant nuclear protein that interacts specifically with nuclear matrix attachment region DNA (MAR) and RNA as a component of hnRNPs.', 'TheSAF-A protein is localized to the nuclear matrix', 'SAF-A/hnRNP U is an abundant nuclear protein that interacts specifically with nuclear matrix attachment region DNA (MAR) and RNA as a component of hnRNPs. ', 'The SAF-A protein localizes to the nucleus where it promotes ribosome biogenesis', 'SAF-A is localized to the nucleus where it promotes ribosomal RNA (rRNA) transcription thereby stimulating cell growth.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/10933876",
"http://www.ncbi.nlm.nih.gov/pubmed/19556781",
"http://www.ncbi.nlm.nih.gov/pubmed/22162999"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19556781",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "SAF-A/hnRNP U is an abundant nuclear protein that interacts specifically with nuclear matrix attachment region DNA (MAR) and RNA as a component of hnRNPs. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22162999",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 212,
"text": "Scaffold attachment factor A (SAF-A) participates in the regulation of gene expression by organizing chromatin into transcriptionally active domains and by interacting directly with RNA polymerase II."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22162999",
"endSection": "abstract",
"offsetInBeginSection": 877,
"offsetInEndSection": 1074,
"text": "Functional analyses reveal that dual depletion of SAF-A and BRG1 abolishes global transcription by RNA polymerase II, while the nucleolar RNA polymerase I transcription machinery remains unaffected"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10933876",
"endSection": "abstract",
"offsetInBeginSection": 698,
"offsetInEndSection": 916,
"text": "Using this domain as a probe, we performed a yeast two-hybrid screening and we found that scaffold attachment factor B (SAF-B), a nuclear matrix-associated protein, exhibits protein-protein interaction to this region. "
}
] | 11 |
BioASQ-training11b
| null | null |
5d35e7ddb3a638076300000e
|
bioasq_factoid
|
factoid
|
What is the function of the gene MDA5?
|
['Sensing of non-self RNAs, especially viral RNA']
|
[
"Sensing of non-self RNAs, especially viral RNA",
"Recognition of foreign RNAs",
"Detection of non-self RNA",
"Viral RNA sensing",
"Non-self RNA detection",
"Viral RNA recognition"
] |
['Melanoma differentiation-associated gene 5 (MDA5) is a pattern recognition receptor that recognizes cytoplasmic viral double-stranded RNA (dsRNA) and initiates rapid innate antiviral responses. MDA5 forms a filament-like multimer along the dsRNA leading to oligomerization, which in turn activates the adaptor protein mitochondrial antiviral signaling protein (MAVS) to provide a signal platform for the induction of type I interferon (IFN) and proinflammatory cytokines. The conformational switch of MDA5 causes antiviral defense, but excessive activation of the MDA5-MAVS pathway may result in autoimmune diseases.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28530548",
"http://www.ncbi.nlm.nih.gov/pubmed/29117565",
"http://www.ncbi.nlm.nih.gov/pubmed/28250012",
"http://www.ncbi.nlm.nih.gov/pubmed/29069650",
"http://www.ncbi.nlm.nih.gov/pubmed/28374903"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28250012",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 144,
"text": "Sensing of viral RNA by the cytosolic receptors RIG-I and melanoma differentiation-associated gene 5 (MDA5) leads to innate antiviral response. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28530548",
"endSection": "abstract",
"offsetInBeginSection": 407,
"offsetInEndSection": 647,
"text": "The host innate immune response to RNA virus infection primarily involves pathogen-sensing toll-like receptors (TLRs) TLR3 and TLR7 and retinoic acid-inducible gene I-like receptor RIG-I and melanoma differentiation associated gene 5 (MDA5)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28374903",
"endSection": "abstract",
"offsetInBeginSection": 652,
"offsetInEndSection": 748,
"text": "RNA PRRs are comprised of TLR3, TLR7, TLR8, RIG-I, MDA5, NLRP3, NOD2, and some other minorities."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29069650",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 616,
"text": "Melanoma differentiation-associated gene 5 (MDA5) is a pattern recognition receptor that recognizes cytoplasmic viral double-stranded RNA (dsRNA) and initiates rapid innate antiviral responses. MDA5 forms a filament-like multimer along the dsRNA leading to oligomerization, which in turn activates the adaptor protein mitochondrial antiviral signaling protein (MAVS) to provide a signal platform for the induction of type I interferon (IFN) and proinflammatory cytokines. The conformational switch of MDA5 causes antiviral defense, but excessive activation of the MDA5-MAVS pathway may result in autoimmune diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29117565",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 206,
"text": "Retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs), including melanoma differentiation-associated gene 5 (MDA5) and RIG-I, are crucial for host recognition of non-self RNAs, especially viral RNA. "
}
] | 11 |
BioASQ-training11b
| null | null |
5a88370c61bb38fb24000014
|
bioasq_factoid
|
yesno
|
Is Trifluridine/Tipiracil a preferential treatment over Regorafenib in elderly colorectal cancer patients?
|
['yes']
|
[
"yes"
] |
["There is no definitive answer to this question, as the choice of treatment for elderly colorectal cancer patients should be individualized based on the patient's overall health, comorbidities, and personal preferences. Both Trifluridine/Tipiracil and Regorafenib are approved treatment options for patients with metastatic colorectal cancer who have been previously treated with fluoropyrimidine-, oxaliplatin- and irinotecan-based chemotherapy, an anti-VEGF therapy, and, if RAS wild type, an anti-EGFR therapy.\n\nA phase III clinical trial (RECOURSE) compared Trifluridine/Tipiracil to placebo in patients with metastatic colorectal cancer who had been previously treated with standard chemotherapy and found a significant improvement in overall survival and progression-free survival.\n\nAnother phase III clinical trial (CORRECT) compared Regorafenib to placebo in patients with metastatic colorectal cancer who had been previously treated with standard chemotherapy and found a significant improvement in overall survival.\n\nA retrospective study of 102 elderly patients with metastatic colorectal cancer who received Trifluridine/Tipiracil or Regorafenib as third-line treatment found that Trifluridine/Tipiracil was associated with a trend towards better overall survival compared to Regorafenib (median 7.1 vs 5.3 months, p=0.057). However, this study was not randomized and had a small sample size.\n\nTherefore, it is not possible to say that Trifluridine/Tipiracil is a preferential treatment over Regorafenib in elderly colorectal cancer patients based on the current evidence. It is important to consider the individual patient's characteristics and to discuss the potential benefits and risks of each treatment option with the patient.", 'Trifluridine/tipiracil (FTD/TPI) is not clearly preferable over regorafenib in older patients with metastatic colorectal cancer. Both have similar efficacy and tolerability.', 'Yes, Trifluridine/Tipiracil is a preferential treatment over Regorafenib in elderly colorectal cancer patients based on the favorable survival outcomes observed in patients aged ≥65 years.', 'Yes, trifluridine/tipiracil (FTD/TPI) is favored in patients aged ≥65 years for treating colorectal cancer, as indicated by the subgroup analysis showing better survival outcomes in this age group compared to regorafenib.', 'Regorafenib and trifluridine/tipiracil hydrochloride (TFTD) are novel antitumor agents for patients with refractory metastatic colorectal cancer. In this study, we report the survival benefits of TFTD and Regorafenib in elderly frail patients with metastatic colorectal cancer.', 'A recent study suggested that Trifluridine/Tipiracil and Regorafenib have comparable efficacy and safety in elderly patients with refractory metastatic colorectal cancer (mCRC)', 'Yes, Trifluridine/Tipiracil (FTD/TPI) appears to be a more favorable treatment option for elderly colorectal cancer patients, specifically those aged 65 years and older, as it showed better survival outcomes in this age group compared to Regorafenib', 'Yes, Trifluridine/Tipiracil (FTD/TPI) is a preferential treatment over Regorafenib in elderly colorectal cancer patients, as it has been shown to have better tumor response and disease control.', "According to a subgroup analysis of a clinical trial, Trifluridine/Tipiracil (FTD/TPI) was found to have better tumor response and disease control in elderly colorectal cancer patients (aged ≥65 years) compared to Regorafenib. However, in an adjusted analysis using propensity score, there was no significant difference in overall survival between the two drugs in the overall population. In the subgroup analysis, Regorafenib showed favorable survival in patients aged <65 years, while FTD/TPI was favored in patients aged ≥65 years. Therefore, the choice of treatment between FTD/TPI and Regorafenib may depend on the patient's age and other clinical factors. It is always recommended to consult with a healthcare provider for personalized treatment recommendations.", 'Trifluridine/tipiracil is a preferential treatment over regorafenib in elderly colorectal cancer patients, as shown in clinical trials and real-world studies. In a phase III randomized controlled trial, trifluridine/tipiracil demonstrated superior overall survival and progression-free survival compared to placebo in patients with metastatic colorectal cancer who had been previously treated with standard chemotherapies. Additionally, a cost-effectiveness analysis showed that trifluridine/tipiracil is more clinically and cost-effective than regorafenib, with better outcomes at reduced costs. In real clinical practice, a retrospective study found that the effectiveness results of standard clinical practice are lower than those described in clinical trials and the literature, but trifluridine/tipiracil has a better toxicity profile compared to regorafenib. Therefore, trifl', 'Yes, Trifluridine/Tipiracil is preferred for patients aged 65 and above.', 'Although no difference in overall survival was found between the two drugs in adjusted analysis using propensity score, regorafenib showed favorable survival in patients aged <65 years, whereas trifluridine/tipiracil was favored in patients aged ≥65 years in the subgroup analysis.', 'yes, Trifluridine/Tipiracil (FTD/TPI) appears to be a more favorable treatment option for elderly colorectal cancer patients aged 65 years and older. In the subgroup analysis, Trifluridine/Tipiracil showed better survival outcomes in this age group with a hazard ratio (HR) of 0.78, which suggests a lower risk of death compared to Regorafenib.', "Trifluridine/Tipiracil (TAS-102) is generally preferred over Regorafenib as a treatment option for elderly colorectal cancer patients due to its favorable safety profile and efficacy in this population. Clinical studies have shown that TAS-102 provides significant survival benefits and manageable side effects compared to Regorafenib, making it a more suitable choice for elderly patients with colorectal cancer. However, the choice between these two treatments should be individualized based on factors such as patient's overall health, treatment goals, and potential drug interactions.", 'Yes, patients treated with FTD/TPI had better tumor response and disease control than patients treated with regorafenib', 'Although no difference in overall survival was found between the two drugs in adjusted analysis using propensity score, regorafenib showed favorable survival in patients aged <65 years, whereas trifluridine/tipiracil was favored in patients aged ≥65 years in the subgroup analysis', 'Based on the subgroup analysis, Trifluridine/Tipiracil (FTD/TPI) is favored as a treatment option over Regorafenib in elderly colorectal cancer patients (aged ≥65 years). The analysis showed that FTD/TPI had better tumor response and disease control in this age group. Although there was no significant difference in overall survival between the two drugs in the adjusted analysis, FTD/TPI showed a favorable survival trend in elderly patients compared to Regorafenib. Therefore, FTD/TPI may be considered as a preferential treatment for elderly colorectal cancer patients.', 'Based on the available evidence, Trifluridine/Tipiracil (FTD/TPI) may be a preferential treatment over Regorafenib in elderly colorectal cancer patients. A retrospective cohort study showed that FTD/TPI had better tumor response and disease control rates compared to Regorafenib in patients with refractory metastatic colorectal cancer. Subgroup analysis also suggested that early use of FTD/TPI may have clinical benefits in second- or third-line therapy. However, further studies are needed to confirm these findings and identify predictive biomarkers to guide treatment selection.', 'yes, trifluridine/tipiracil is favored in patients aged ≥65 years for treating colorectal cancer, as it showed better survival rates in this age group compared to regorafenib.', 'Yes, Trifluridine/Tipiracil (FTD/TPI) is favored as a treatment over Regorafenib in elderly colorectal cancer patients aged ≥65 years. The subgroup analysis showed that Trifluridine/Tipiracil had a more favorable survival outcome in this age group, with a hazard ratio (HR) of 0.78 (95% CI, 0.59-1.03), indicating a lower risk of death compared to Regorafenib.', 'Yes, Trifluridine/Tipiracil (FTD/TPI) appears to be a preferential treatment over Regorafenib in elderly colorectal cancer patients aged ≥65 years. While regorafenib showed favorable survival in patients aged <65 years, FTD/TPI was favored in patients aged ≥65 years based on the subgroup analysis. Additionally, patients treated with FTD/TPI had better tumor response and disease control compared to those treated with regorafenib.', 'According to the retrospective study conducted at a tertiary oncology center, Trifluridine/Tipiracil (FTD/TPI) appears to be a preferential treatment over Regorafenib in elderly colorectal cancer patients. In the subgroup analysis of patients aged ≥65 years, FTD/TPI showed better overall survival compared to Regorafenib, with an adjusted hazard ratio of 0.78 (95% CI, 0.59-1.03). This suggests that in elderly patients with metastatic colorectal cancer refractory to standard chemotherapy, FTD/TPI may be a better treatment option than Regorafenib. However, it is important to note that this study has limitations as an observational study and further research is needed to confirm these findings.', 'According to a subgroup analysis of a clinical trial, in elderly colorectal cancer patients (aged ≥65 years), Trifluridine/Tipiracil (FTD/TPI) was found to have better disease control and tumor response compared to Regorafenib. However, in the adjusted analysis using propensity score, there was no significant difference in overall survival between the two drugs. In patients aged <65 years, Regorafenib showed favorable survival, while FTD/TPI was favored in patients aged ≥65 years. Therefore, the choice of treatment between FTD/TPI and Regorafenib in elderly colorectal cancer patients should be individualized based on factors such as age, overall health, and other clinical considerations.', 'Based on the available literature, Trifluridine/Tipiracil (FTD/TPI) appears to be a more cost-effective treatment option compared to Regorafenib in elderly patients with refractory metastatic colorectal cancer. The study showed that FTD/TPI had a lower expected cost per patient and a lower cost-effectiveness ratio compared to Regorafenib. Additionally, FTD/TPI can be safely administered while maintaining efficacy in patients who are ineligible for Regorafenib due to comorbidities. However, it is important to consider individual patient factors and preferences when making treatment decisions.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28894015",
"http://www.ncbi.nlm.nih.gov/pubmed/27900102",
"http://www.ncbi.nlm.nih.gov/pubmed/27487107",
"http://www.ncbi.nlm.nih.gov/pubmed/33952483",
"http://www.ncbi.nlm.nih.gov/pubmed/35289802",
"http://www.ncbi.nlm.nih.gov/pubmed/32653227",
"http://www.ncbi.nlm.nih.gov/pubmed/29452346",
"http://www.ncbi.nlm.nih.gov/pubmed/34406678",
"http://www.ncbi.nlm.nih.gov/pubmed/33597364",
"http://www.ncbi.nlm.nih.gov/pubmed/32912821",
"http://www.ncbi.nlm.nih.gov/pubmed/30344762",
"http://www.ncbi.nlm.nih.gov/pubmed/27670892",
"http://www.ncbi.nlm.nih.gov/pubmed/30350179",
"http://www.ncbi.nlm.nih.gov/pubmed/36990929",
"http://www.ncbi.nlm.nih.gov/pubmed/34718946",
"http://www.ncbi.nlm.nih.gov/pubmed/34199694"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34406678",
"endSection": "abstract",
"offsetInBeginSection": 1664,
"offsetInEndSection": 1778,
"text": "Patients treated with FTD/TPI had better tumor response and disease control than patients treated with regorafenib"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28894015",
"endSection": "abstract",
"offsetInBeginSection": 2180,
"offsetInEndSection": 2460,
"text": "Although no difference in overall survival was found between the two drugs in adjusted analysis using propensity score, regorafenib showed favorable survival in patients aged <65 years, whereas trifluridine/tipiracil was favored in patients aged ≥65 years in the subgroup analysis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28894015",
"endSection": "abstract",
"offsetInBeginSection": 1194,
"offsetInEndSection": 1372,
"text": "Regorafenib showed favorable survival in patients aged <65 years (HR, 1.29; 95% CI, 0.98-1.69), whereas TFTD was favored in patients aged ≥65 years (HR, 0.78; 95% CI, 0.59-1.03)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36990929",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "Trifluridine/tipiracil (FTD/TPI) and regorafenib in older patients with metastatic colorectal cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34718946",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 151,
"text": "Regorafenib and trifluridine/tipiracil are standard third-line chemotherapies for colorectal cancer patients, but their efficacy is limited"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34199694",
"endSection": "abstract",
"offsetInBeginSection": 10,
"offsetInEndSection": 1487,
"text": "project aimed to better understand practice patterns, identify drivers for treatment goals, and determine third- and fourth-line treatment choices for patients with metastatic colorectal cancer (mCRC). The survey was developed by an expert panel of gastrointestinal oncologists. Questions concerned general practice patterns, and treatment decisions for three hypothetical patient case scenarios. Participants had to routinely manage patients with mCRC. We present results from 629 participants who provided input on patient treatment scenarios (data cutoff: 17/01/2020). Prolonging overall survival (OS; 51%) was the main aim in first line. In third line, quality of life (QOL) was the primary goal (34%). Forty-three percent also cited efficacy-focused goals; 18% and 13% noted prolonging OS and improving progression-free survival as main aims, respectively. For fit and active patients, 89% of respondents considered trifluridine-tipiracil an appropriate third-line treatment; regorafenib (31%) or clinical trial enrollment (29%) were the fourth-line options. For patients with comorbidities and limited caregiver support, trifluridine-tipiracil was the preferred third-line treatment (70%). For KRAS-mutated patients with comorbidities and adverse events who received prior oxaliplatin, 90% considered oxaliplatin rechallenge an unsuitable third-line treatment, mainly due to the risk of cumulative toxicity (75%). In the third/fourth-line settings, trifluridine-tipiracil"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28894015",
"endSection": "abstract",
"offsetInBeginSection": 1194,
"offsetInEndSection": 1480,
"text": "Regorafenib showed favorable survival in patients aged <65 years (HR, 1.29; 95% CI, 0.98-1.69), whereas TFTD was favored in patients aged ≥65 years (HR, 0.78; 95% CI, 0.59-1.03).CONCLUSION: No significant difference in OS between regorafenib and TFTD was observed in patients with mCRC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34406678",
"endSection": "abstract",
"offsetInBeginSection": 1893,
"offsetInEndSection": 2281,
"text": "IONS FOR PRACTICE: In this retrospective cohort study, patients with refractory metastatic colorectal cancer treated with trifluridine/tipiracil (FTD/TPI) were significantly less likely than those treated with regorafenib to have dose modifications and more likely to have higher real-world objective response rate (rwORR) and real-world disease control rate (rwDCR) while treated. Patien"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33597364",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 273,
"text": "Although the effectiveness of trifluridine/tipiracil(TFTD)with bevacizumab for unresectable colorectal cancer that was refractory to previous standard chemotherapy was reported, its effectiveness as a first-line treatment, especially for elderly frail patients, is unclear."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36990929",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "Colorectal cancer is a disease of older patients, but few guidelines directly address age in their recommendations."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27900102",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 329,
"text": "Regorafenib and trifluridine/tipiracil combination tablet regimens are standard third-line or later treatments for advanced and recurrent colorectal cancer with no significant difference in efficacy. The present study aimed to compare the cost-effectiveness of using regorafenib vs. the trifluridine/tipiracil combination tablet."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36990929",
"endSection": "abstract",
"offsetInBeginSection": 327,
"offsetInEndSection": 453,
"text": "oral agents for third-line treatment in older patients with refractory metastatic colorectal cancer, regorafenib, and trifluri"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29452346",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1477,
"text": "Background: The optimal chemotherapeutic regimen for use beyond the second line for patients with metastatic colorectal cancer (mCRC) remains unclear.Materials and methods: We systematically searched the Cochrane Database of Systematic Reviews, EMBASE and Medline for records published between January 2002 and May 2017, and cancer congress databases for records published between January 2014 and June 2017. Eligible studies evaluated the efficacy, safety and patient-reported outcomes of monotherapies or combination therapies at any dose and number of treatment cycles for use beyond the second line in patients with mCRC. Studies were assessed for design and quality, and a qualitative data synthesis was conducted to understand the impact of treatment on overall survival and other relevant cancer-related outcomes.Results: The search yielded 938 references of which 68 were included for qualitative synthesis. There was limited evidence to support rechallenge with chemotherapy, targeted therapy or both. Compared with placebo, an overall survival benefit for trifluridine/tipiracil (also known as TAS-102) or regorafenib has been shown for patients previously treated with conventional chemotherapy and targeted therapy. There was no evidence to suggest a difference in efficacy between these treatments. Patient choice and quality of life at this stage of treatment should also be considered when choosing an appropriate therapy.Conclusions: These findings support the "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35289802",
"endSection": "abstract",
"offsetInBeginSection": 715,
"offsetInEndSection": 927,
"text": "The safety profile of each agent can help guide selection. Patients with metastatic colorectal cancer require an individualized treatment strategy that incorporates their age, comorbidities, and prior treatments."
}
] | 13 |
BioASQ-training13b
| null | null |
65f7778fc4010b4d78000031
|
bioasq_yesno
|
yesno
|
Has AZD9668 been tested in clinical trials?
|
['yes']
|
[
"yes"
] |
['Yes, AZD9668 has been tested in clinical trials.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/22458939",
"http://www.ncbi.nlm.nih.gov/pubmed/26043724"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22458939",
"endSection": "abstract",
"offsetInBeginSection": 152,
"offsetInEndSection": 450,
"text": "Efficacy, safety and tolerability of AZD9668 (5, 20 and 60 mg bid) were compared with placebo in a randomised, double-blind, placebo-controlled, 12-week, Phase IIb trial (NCT00949975: approved by an Investigational Review Board), in patients with symptomatic COPD receiving maintenance tiotropium. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22458939",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "A randomised, placebo-controlled, dose-finding study of AZD9668, an oral inhibitor of neutrophil elastase, in patients with chronic obstructive pulmonary disease treated with tiotropium."
}
] | 11 |
BioASQ-training11b
| null | null |
602c28551cb411341a000123
|
bioasq_yesno
|
yesno
|
Is nucleosome eviction ATP-dependent?
|
['yes']
|
[
"yes"
] |
Yes, nucleosome eviction and chromatin remodelling depends on ATP
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/24068556",
"http://www.ncbi.nlm.nih.gov/pubmed/24008565",
"http://www.ncbi.nlm.nih.gov/pubmed/23460895",
"http://www.ncbi.nlm.nih.gov/pubmed/22177115",
"http://www.ncbi.nlm.nih.gov/pubmed/20513433",
"http://www.ncbi.nlm.nih.gov/pubmed/19933844",
"http://www.ncbi.nlm.nih.gov/pubmed/19470761",
"http://www.ncbi.nlm.nih.gov/pubmed/19029894",
"http://www.ncbi.nlm.nih.gov/pubmed/17235287"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24068556",
"endSection": "abstract",
"offsetInBeginSection": 33,
"offsetInEndSection": 166,
"text": "ATP-dependent chromatin remodeling and nucleosome-depleted 'barriers' co-operate to determine the kinetics of nucleosome organization"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24008565",
"endSection": "abstract",
"offsetInBeginSection": 99,
"offsetInEndSection": 275,
"text": "ATP-dependent nucleosome-remodeling factors endow chromatin with structural flexibility by promoting assembly or disruption of nucleosomes and the exchange of histone variants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23460895",
"endSection": "abstract",
"offsetInBeginSection": 948,
"offsetInEndSection": 1164,
"text": "remodeling takes place in an ATP-independent manner. Binding of distamycin to the linker and nucleosomal DNA culminates in eviction of the linker histone and the formation of a population of off-centered nucleosomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22177115",
"endSection": "abstract",
"offsetInBeginSection": 574,
"offsetInEndSection": 735,
"text": "which promotes histone deposition onto DNA, and a novel activity, which prevents nucleosome eviction but not remodeling mediated by the ATP-dependent RSC complex"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20513433",
"endSection": "abstract",
"offsetInBeginSection": 4,
"offsetInEndSection": 134,
"text": "ATP-dependent chromatin remodeling complex SWI/SNF regulates transcription and has been implicated in promoter nucleosome eviction"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19933844",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 122,
"text": "ATP-dependent nucleosome-remodeling enzyme involved in transcription, replication, and the DNA damage response"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19933844",
"endSection": "abstract",
"offsetInBeginSection": 1361,
"offsetInEndSection": 1430,
"text": "Iec1-Ino80 complex promotes transcription through nucleosome eviction"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19933844",
"endSection": "abstract",
"offsetInBeginSection": 237,
"offsetInEndSection": 323,
"text": "Ino80 complex from fission yeast mediates ATP-dependent nucleosome remodeling in vitro"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19470761",
"endSection": "abstract",
"offsetInBeginSection": 969,
"offsetInEndSection": 1153,
"text": "reconstitution of nucleosome disassembly using the ATP-dependent chromatin remodeler Rsc and Vps75 revealed that these proteins can cooperate to remove H2A/H2B dimers from nucleosomes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19029894",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 106,
"text": "TP-dependent chromatin-remodeling complexes, such as RSC, can reposition, evict or restructure nucleosome"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17235287",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 87,
"text": "TP-dependent chromatin remodeling complexes play a critical role in chromatin dynamics"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17235287",
"endSection": "abstract",
"offsetInBeginSection": 348,
"offsetInEndSection": 418,
"text": " activity of SWI/SNF to histone eviction in trans from gene promoters."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D009707",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D000255",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0000786",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0006337"
] |
[] |
532ff558d6d3ac6a34000037
|
bioasq_yesno
|
factoid
|
What is another name for bimagrumab
|
['BYM338']
|
[
"BYM338",
"BYM 338",
"BYM-338"
] |
['Bimagrumab also goes by the name BYM338.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/32690797"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32690797",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 93,
"text": "Long-term safety and tolerability of bimagrumab (BYM338) in sporadic inclusion body myositis."
}
] | 11 |
BioASQ-training11b
| null | null |
602c1b141cb411341a00011c
|
bioasq_factoid
|
factoid
|
What part of the body is associated with Cauda equina
|
['spine']
|
[
"spine",
"vertebral column",
"backbone",
"spinal column",
"spinal cord",
"spinal vertebrae"
] |
['The cauda equina is the sack of nerve roots (nerves that leave the spinal cord between spaces in the bones of the spine to connect to other parts of the body) at the lower end of the spinal cord.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26442520",
"http://www.ncbi.nlm.nih.gov/pubmed/25495513",
"http://www.ncbi.nlm.nih.gov/pubmed/22254963",
"http://www.ncbi.nlm.nih.gov/pubmed/27753733",
"http://www.ncbi.nlm.nih.gov/pubmed/3356808",
"http://www.ncbi.nlm.nih.gov/pubmed/22996855",
"http://www.ncbi.nlm.nih.gov/pubmed/3806684",
"http://www.ncbi.nlm.nih.gov/pubmed/32541159",
"http://www.ncbi.nlm.nih.gov/pubmed/33261250",
"http://www.ncbi.nlm.nih.gov/pubmed/23101243",
"http://www.ncbi.nlm.nih.gov/pubmed/11311464",
"http://www.ncbi.nlm.nih.gov/pubmed/18664636",
"http://www.ncbi.nlm.nih.gov/pubmed/10797973",
"http://www.ncbi.nlm.nih.gov/pubmed/34321945",
"http://www.ncbi.nlm.nih.gov/pubmed/22764663"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33261250",
"endSection": "abstract",
"offsetInBeginSection": 218,
"offsetInEndSection": 346,
"text": "the right pedicle of L4, moved inside the vertebral canal (bridging the cauda equina) stopping just in front of the body of S2. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23101243",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 124,
"text": "Thermoesthesia-and-algesthesia status in the dermatomes of cauda equina roots in patients with lumbar spine osteochondrosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23101243",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "Thermoesthesia-and-algesthesia disorders have been registered in the dermatomes of cauda equina roots of patients with lumbar spine osteochondrosis in all the cases. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22764663",
"endSection": "abstract",
"offsetInBeginSection": 581,
"offsetInEndSection": 722,
"text": " Magnetic resonance images of the lumbar spine showed an intradural cystic lesion displacing and compressing the lower cord and cauda equina."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22996855",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 109,
"text": "Cauda equina syndrome is a well described state of neurologic compromise due to lumbosacral root compression."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22996855",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 63,
"text": "Acute cauda equina syndrome secondary to a lumbar synovial cyst"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25495513",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 296,
"text": "INTRODUCTION: Schwannoma is a relatively common benign spinal cord and/or cauda equina tumor; however, giant cauda equina schwannoma with extensive scalloping of the lumbar vertebral body is a rare pathology, and the treatment strategy, including the use of surgical procedures, is controversial."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25495513",
"endSection": "abstract",
"offsetInBeginSection": 297,
"offsetInEndSection": 509,
"text": "In this report, we present a rare case of a giant lumbar schwannoma of the cauda equina with extremely large scalloping of the vertebral body, and we discuss the surgical strategy we used to treat this pathology."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3356808",
"endSection": "abstract",
"offsetInBeginSection": 532,
"offsetInEndSection": 791,
"text": "In contrast, the caudal cord of Rana is reduced to a filum terminale consisting of little more than an ependymal tube; spinal nerves to all caudal myotomes leave the cord in the sacral region and reach their motor targets via a cauda equina and caudal plexus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3806684",
"endSection": "abstract",
"offsetInBeginSection": 662,
"offsetInEndSection": 791,
"text": "The spinal cords of other teleosts, the sun-fish and angler, also are abbreviated and possess a filum terminale and cauda equina."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10797973",
"endSection": "abstract",
"offsetInBeginSection": 993,
"offsetInEndSection": 1126,
"text": "Penetrating spinal cord injury with foreign body included or myelography stop or showing cauda equina syndrome should be operated on."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27753733",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "Cauda Equina Conduction Time Determined by F-Waves in Normal Subjects and Patients With Neurogenic Intermittent Claudication Caused by Lumbar Spinal Stenosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22254963",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 259,
"text": "After spinal cord injury, electrical stimulation of the roots inside the spinal column at the level of the cauda equina is a safe and effective way to regain some degree of control over lower body function, e.g. bladder and bowel management and leg movement. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32541159",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 167,
"text": "Malignant spinal cord compression(MSCC)is defined as a compression of the spinal cord or cauda equina with neuropathy caused by tumor spreading to the vertebral body. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26442520",
"endSection": "abstract",
"offsetInBeginSection": 37,
"offsetInEndSection": 187,
"text": "nction of the cauda equina, the collection of ventral and dorsal lumbar, sacral and coccygeal nerve roots that surround the filum terminale. This most"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25495513",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 295,
"text": "INTRODUCTION: Schwannoma is a relatively common benign spinal cord and/or cauda equina tumor; however, giant cauda equina schwannoma with extensive scalloping of the lumbar vertebral body is a rare pathology, and the treatment strategy, including the use of surgical procedures, is controversial"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18664636",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "Cauda equina syndrome is a relatively uncommon condition typically associated with a large, space-occupying lesion within the canal of the lumbosacral spine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26442520",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "Cauda equina syndrome refers to dysfunction of the cauda equina, the collection of ventral and dorsal lumbar, sacral and coccygeal nerve roots that surround the filum terminale."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11311464",
"endSection": "abstract",
"offsetInBeginSection": 1320,
"offsetInEndSection": 1510,
"text": "The involvement of intrinsic spinal cord neurons in the compression-induced cauda equina syndrome includes anterograde, retrograde and transneuronal degeneration in the lumbosacral segments."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11311464",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 179,
"text": "Single or double-level compression of the lumbosacral nerve roots located in the dural sac results in a polyradicular symptomatology clinically diagnosed as cauda equina syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34321945",
"endSection": "abstract",
"offsetInBeginSection": 329,
"offsetInEndSection": 470,
"text": "The cauda equina is an anatomic structure located in the lower part of the spinal canal consisting of multiple lumbar and sacral nerve roots."
}
] | 11 |
BioASQ-training11b
| null | null |
6238a0033a8413c6530000b8
|
bioasq_factoid
|
factoid
|
What is the role of cytidine deaminase in healthy cells?
|
['deamination of deoxycytidines']
|
[
"deamination of deoxycytidines",
"deoxycytidine deamination",
"deoxycytidine deaminase reaction",
"deamination of dC",
"deamination of 2'-deoxycytidine"
] |
['Activation-induced cytidine deaminase (AID) catalyses the deamination of deoxycytidines to deoxyuracils within immunoglobulin genes to induce somatic hypermutation and class-switch recombination.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/34819671",
"http://www.ncbi.nlm.nih.gov/pubmed/34819670",
"http://www.ncbi.nlm.nih.gov/pubmed/32729075",
"http://www.ncbi.nlm.nih.gov/pubmed/34528388",
"http://www.ncbi.nlm.nih.gov/pubmed/32729074"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32729074",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "The AID/APOBEC family of enzymes are cytidine deaminases that act upon DNA and RNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32729075",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 117,
"text": "APOBEC1 is a member of the AID/APOBECs, a group of deaminases responsible for the editing of C>U in both DNA and RNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34528388",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 281,
"text": "The human genome contains 11 APOBEC (apolipoprotein B mRNA editing catalytic polypeptide-like) cytidine deaminases classified into four families. These proteins function mainly in innate antiviral immunity and can also restrict endogenous retrotransposable element multiplication. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34819670",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 194,
"text": "Activation-induced cytidine deaminase (AID) catalyses the deamination of deoxycytidines to deoxyuracils within immunoglobulin genes to induce somatic hypermutation and class-switch recombination"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34819671",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 411,
"text": "Efficient humoral responses rely on DNA damage, mutagenesis and error-prone DNA repair. Diversification of B cell receptors through somatic hypermutation and class-switch recombination are initiated by cytidine deamination in DNA mediated by activation-induced cytidine deaminase (AID)1 and by the subsequent excision of the resulting uracils by uracil DNA glycosylase (UNG) and by mismatch repair proteins1-3. "
}
] | 11 |
BioASQ-training11b
| null | null |
6217d8973a8413c653000020
|
bioasq_factoid
|
factoid
|
Which disease is caused by repeat expansion in VWA1?
|
['Recessive hereditary motor neuropathy']
|
[
"Recessive hereditary motor neuropathy",
"Hereditary motor neuropathy type 1A",
"HMN type 1A",
"Recessive hereditary motor neuron disease",
"Recessive hereditary motor neuronopathy"
] |
['An ancestral 10-bp repeat expansion in VWA1 causes recessive hereditary motor neuropathy.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/33559681"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33559681",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "An ancestral 10-bp repeat expansion in VWA1 causes recessive hereditary motor neuropathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33559681",
"endSection": "abstract",
"offsetInBeginSection": 2510,
"offsetInEndSection": 3068,
"text": "In summary, we estimate that biallelic variants in VWA1 may be responsible for up to 1% of unexplained hereditary motor neuropathy cases in Europeans. The detailed clinical characterization provided here will facilitate targeted testing on suitable patient cohorts. This novel disease gene may have previously evaded detection because of high GC content, consequential low coverage and computational difficulties associated with robustly detecting repeat-expansions. Reviewing previously unsolved exomes using lower QC filters may generate further diagnoses."
}
] | 11 |
BioASQ-training11b
| null | null |
61f86c03882a024a10000044
|
bioasq_factoid
|
factoid
|
What is trichotillomania?
|
['Trichotillomania is a hair pulling disorder.']
|
[
"Trichotillomania",
"hair pulling disorder",
"trichotillomania disorder",
"compulsive hair pulling",
"trichotillomania syndrome"
] |
['Trichotillomania is a hair pulling disorder.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27137957",
"http://www.ncbi.nlm.nih.gov/pubmed/26001984",
"http://www.ncbi.nlm.nih.gov/pubmed/26580849"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26001984",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 190,
"text": "Trichotillomania (hair pulling disorder, HPD) is characterized by significant psychological distress, childhood-onset, and, in adults, certain cognitive deficits such as inhibitory control. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26580849",
"endSection": "title",
"offsetInBeginSection": 44,
"offsetInEndSection": 84,
"text": "TRICHOTILLOMANIA (HAIR PULLING DISORDER)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27137957",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "Hair pulling disorder (HPD; trichotillomania) is thought to be associated with significant psychiatric comorbidity and functional impairment. "
}
] | 6 |
BioASQ-training6b
| null | null |
58a8045860087bc10a000035
|
bioasq_factoid
|
factoid
|
What is the process that generates multiple transcripts from the same gene?
|
['Alternative splicing', 'Alternative splicing (AS)']
|
[
"Alternative splicing",
"Alternative splicing (AS)",
"AS",
"Alternative RNA splicing",
"Variable splicing",
"Differential splicing"
] |
['The process that generates multiple transcripts from the same gene is called alternative splicing (AS). AS is a post-transcriptional regulatory mechanism that allows for the production of different mRNA isoforms from a single gene. This process can increase proteome diversity and regulate mRNA levels, which is important for expanding proteomic complexity and functional diversity in higher eukaryotes. In plants, AS may also serve as a buffer against stress-responsive transcriptomes to reduce the metabolic cost of translating all AS transcripts. While the contribution of AS to proteome complexity remains elusive in plants, it is clear that this process plays an important role in regulating gene expression and generating protein isoforms with distinct functions.', 'Alternative splicing generates multiple transcripts and potentially more than one protein from the same gene. It markedly enhances the coding capacity of the genome and can increase protein diversity which plays a crucial role in controlling development and stress responses.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/18369186",
"http://www.ncbi.nlm.nih.gov/pubmed/30014301",
"http://www.ncbi.nlm.nih.gov/pubmed/2788825",
"http://www.ncbi.nlm.nih.gov/pubmed/16611169",
"http://www.ncbi.nlm.nih.gov/pubmed/28064309",
"http://www.ncbi.nlm.nih.gov/pubmed/20815140",
"http://www.ncbi.nlm.nih.gov/pubmed/30852095",
"http://www.ncbi.nlm.nih.gov/pubmed/33406240",
"http://www.ncbi.nlm.nih.gov/pubmed/34383135",
"http://www.ncbi.nlm.nih.gov/pubmed/35269461",
"http://www.ncbi.nlm.nih.gov/pubmed/26273603",
"http://www.ncbi.nlm.nih.gov/pubmed/21896509",
"http://www.ncbi.nlm.nih.gov/pubmed/18088312",
"http://www.ncbi.nlm.nih.gov/pubmed/16054339",
"http://www.ncbi.nlm.nih.gov/pubmed/24369421",
"http://www.ncbi.nlm.nih.gov/pubmed/32811430",
"http://www.ncbi.nlm.nih.gov/pubmed/22811948",
"http://www.ncbi.nlm.nih.gov/pubmed/22961303",
"http://www.ncbi.nlm.nih.gov/pubmed/18817741",
"http://www.ncbi.nlm.nih.gov/pubmed/31921258",
"http://www.ncbi.nlm.nih.gov/pubmed/35821097",
"http://www.ncbi.nlm.nih.gov/pubmed/26327458",
"http://www.ncbi.nlm.nih.gov/pubmed/32484809",
"http://www.ncbi.nlm.nih.gov/pubmed/34440445",
"http://www.ncbi.nlm.nih.gov/pubmed/33629774",
"http://www.ncbi.nlm.nih.gov/pubmed/28402429",
"http://www.ncbi.nlm.nih.gov/pubmed/25577379",
"http://www.ncbi.nlm.nih.gov/pubmed/25577391",
"http://www.ncbi.nlm.nih.gov/pubmed/29074233",
"http://www.ncbi.nlm.nih.gov/pubmed/35327956",
"http://www.ncbi.nlm.nih.gov/pubmed/28273663",
"http://www.ncbi.nlm.nih.gov/pubmed/35339647"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30852095",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Alternative splicing (AS) generates multiple transcripts from the same gene, however, AS contribution to proteome complexity remains elusive in plants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30852095",
"endSection": "abstract",
"offsetInBeginSection": 306,
"offsetInEndSection": 522,
"text": "We propose that plants employ AS not only to potentially increasing proteomic complexity, but also to buffer against the stress-responsive transcriptome to reduce the metabolic cost of translating all AS transcripts."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29074233",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "Alternative splicing, which generates multiple transcripts from the same gene, is an important modulator of gene expression that can increase proteome diversity and regulate mRNA levels."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22961303",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 253,
"text": "Alternative splicing, which generates multiple transcripts from the same gene and potentially different protein isoforms, is a key posttranscriptional regulatory mechanism for expanding proteomic diversity and functional complexity in higher eukaryotes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24369421",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "Alternative splicing (AS), in higher eukaryotes, is one of the mechanisms of post-transcriptional regulation that generate multiple transcripts from the same gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26273603",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 245,
"text": "Over the past decade, alternative splicing has been progressively recognized as a major mechanism regulating gene expression patterns in different tissues and disease states through the generation of multiple mRNAs from the same gene transcript."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35269461",
"endSection": "abstract",
"offsetInBeginSection": 317,
"offsetInEndSection": 497,
"text": "Alternative splicing is a physiological process by which cells generate several transcripts from one single gene and may in turn give rise to different proteins from the same gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16054339",
"endSection": "abstract",
"offsetInBeginSection": 274,
"offsetInEndSection": 490,
"text": "However, as well as conventional splicing, several genes have the inherent capacity to undergo alternative splicing, thus allowing synthesis of multiple gene transcripts, perhaps with different functional properties."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18088312",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 159,
"text": "Alternative splicing (AS) increases the proteomic and functional capacity of genomes through the generation of alternative mRNA transcripts from the same gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25577391",
"endSection": "abstract",
"offsetInBeginSection": 136,
"offsetInEndSection": 226,
"text": "Indeed, through AS individual gene loci can generate multiple RNAs from the same pre-mRNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26327458",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "Alternative splicing is an important biological process in the generation of multiple functional transcripts from the same genomic sequences."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33406240",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 222,
"text": "Alternative splicing generates multiple transcript and protein isoforms from a single gene and controls transcript intracellular localization and stability by coupling to mRNA export and nonsense-mediated mRNA decay (NMD)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31921258",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "Alternative Splicing (AS) is a mechanism that generates different mature transcripts from precursor mRNAs (pre-mRNAs) of the same gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16611169",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Alternative splicing is a widespread mechanism in mammals that generates several mRNAs from one gene, thereby creating genetic diversity of the genome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34440445",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 160,
"text": "Alternative pre-mRNA splicing plays a very important role in expanding protein diversity as it generates numerous transcripts from a single protein-coding gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32484809",
"endSection": "abstract",
"offsetInBeginSection": 378,
"offsetInEndSection": 534,
"text": " This task is complicated due to the complexity of alternative splicing - a mechanism by which the same gene may generate multiple distinct RNA transcripts."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28064309",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "Alternative splicing of pre-mRNA is one of the main mechanisms regulating gene expression that generates multiple transcripts from one gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28402429",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "Alternative splicing generates multiple transcript and protein isoforms from the same gene and thus is important in gene expression regulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34383135",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 103,
"text": "Alternative splicing is a widespread phenomenon, which generates multiple isoforms of the gene product."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18817741",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "Alternative splicing of messenger RNA (mRNA) precursors generates multiple transcripts from a single primary transcript."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32811430",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 223,
"text": "Among eukaryotic organisms, alternative splicing is an important process that can generate multiple transcripts from one same precursor messenger RNA, which greatly increase transcriptome and proteome diversity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21896509",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 156,
"text": " Alternative splicing (AS) is a pre-mRNA maturation process leading to the expression of multiple mRNA variants from the same primary transcript."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33629774",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 375,
"text": "Alternative splicing (AS) is a process that produces various mRNA splicing isoforms via different splicing patterns of mRNA precursors (pre-mRNAs). AS is the primary mechanism for increasing the types and quantities of proteins to improve biodiversity and influence multiple biological processes, including chromatin modification, signal transduction, and protein expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35821097",
"endSection": "abstract",
"offsetInBeginSection": 144,
"offsetInEndSection": 274,
"text": "Alternative splicing generates multiple transcripts from a single gene, enriching the diversity of proteins and phenotypic traits."
}
] | 12 |
BioASQ-training12b
| null | null |
6428da74690f196b51000052
|
bioasq_factoid
|
factoid
|
Which cyclin- dependent kinase inhibitor is regulated by Bmi-1?
|
['p16INK4']
|
[
"p16INK4",
"p16",
"p16INK4a",
"CDKN2A",
"cyclin-dependent kinase inhibitor 2A"
] |
p16INK4 (also known as CDKN2A)
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/20661663",
"http://www.ncbi.nlm.nih.gov/pubmed/20591222",
"http://www.ncbi.nlm.nih.gov/pubmed/20551323",
"http://www.ncbi.nlm.nih.gov/pubmed/19321450",
"http://www.ncbi.nlm.nih.gov/pubmed/18371338",
"http://www.ncbi.nlm.nih.gov/pubmed/18371328",
"http://www.ncbi.nlm.nih.gov/pubmed/18275833",
"http://www.ncbi.nlm.nih.gov/pubmed/17989730",
"http://www.ncbi.nlm.nih.gov/pubmed/17651940",
"http://www.ncbi.nlm.nih.gov/pubmed/17145810",
"http://www.ncbi.nlm.nih.gov/pubmed/17102614",
"http://www.ncbi.nlm.nih.gov/pubmed/16537449",
"http://www.ncbi.nlm.nih.gov/pubmed/16157028",
"http://www.ncbi.nlm.nih.gov/pubmed/16155021",
"http://www.ncbi.nlm.nih.gov/pubmed/14982841",
"http://www.ncbi.nlm.nih.gov/pubmed/14574365",
"http://www.ncbi.nlm.nih.gov/pubmed/12714971",
"http://www.ncbi.nlm.nih.gov/pubmed/12482990",
"http://www.ncbi.nlm.nih.gov/pubmed/9923679",
"http://www.ncbi.nlm.nih.gov/pubmed/21928107",
"http://www.ncbi.nlm.nih.gov/pubmed/18346113",
"http://www.ncbi.nlm.nih.gov/pubmed/21496667",
"http://www.ncbi.nlm.nih.gov/pubmed/21164364",
"http://www.ncbi.nlm.nih.gov/pubmed/19907431",
"http://www.ncbi.nlm.nih.gov/pubmed/19390085",
"http://www.ncbi.nlm.nih.gov/pubmed/19389366",
"http://www.ncbi.nlm.nih.gov/pubmed/17597110",
"http://www.ncbi.nlm.nih.gov/pubmed/17233832",
"http://www.ncbi.nlm.nih.gov/pubmed/16869752",
"http://www.ncbi.nlm.nih.gov/pubmed/16778197",
"http://www.ncbi.nlm.nih.gov/pubmed/15964994",
"http://www.ncbi.nlm.nih.gov/pubmed/15892997",
"http://www.ncbi.nlm.nih.gov/pubmed/14732230",
"http://www.ncbi.nlm.nih.gov/pubmed/14536079",
"http://www.ncbi.nlm.nih.gov/pubmed/11355949"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20661663",
"endSection": "abstract",
"offsetInBeginSection": 663,
"offsetInEndSection": 748,
"text": "the knockdown of BMI-1 expression could lead to significant up-regulation of p16INK4a"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20591222",
"endSection": "abstract",
"offsetInBeginSection": 1621,
"offsetInEndSection": 1694,
"text": "In EC9706 cells transfected by Bmi-1 siRNA, the expression levels of p16 "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20551323",
"endSection": "abstract",
"offsetInBeginSection": 270,
"offsetInEndSection": 392,
"text": "One important pathway regulated by Bmi-1 is that involving two cyclin-dependent kinase inhibitors, p16(Ink4a) and p19(Arf)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19321450",
"endSection": "abstract",
"offsetInBeginSection": 643,
"offsetInEndSection": 814,
"text": "We also observe that ROS-induced up-regulation of p16(Ink4a) occurs correlatively with ERK1/2-dependent down-regulation and subsequent dissociation from chromatin of Bmi-1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18371338",
"endSection": "abstract",
"offsetInBeginSection": 51,
"offsetInEndSection": 214,
"text": "Bmi-1 is important for postnatal, but not embryonic, neural stem cell (NSC) self-renewal and have identified the cell-cycle inhibitors p16/p19 as molecular targets"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18371328",
"endSection": "abstract",
"offsetInBeginSection": 180,
"offsetInEndSection": 307,
"text": "Bmi-1 function in stem cells during development that, surprisingly, seems to involve regulation of the cell-cycle inhibitor p21"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18371338",
"endSection": "abstract",
"offsetInBeginSection": 823,
"offsetInEndSection": 892,
"text": "Our data therefore implicate p21 as an important Bmi-1 target in NSCs"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18275833",
"endSection": "abstract",
"offsetInBeginSection": 628,
"offsetInEndSection": 663,
"text": "Bmi-1-mediated repression of Cdkn2A"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17989730",
"endSection": "abstract",
"offsetInBeginSection": 798,
"offsetInEndSection": 894,
"text": "decreased expression of proliferating cell nuclear antigen and Bmi-1; upregulation of p16(INK4a)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17651940",
"endSection": "abstract",
"offsetInBeginSection": 573,
"offsetInEndSection": 701,
"text": "BMI-1 promotes self-renewal of stem cells largely by interfering with two central cellular tumor suppressor pathways, p16(Ink4a)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17145810",
"endSection": "abstract",
"offsetInBeginSection": 104,
"offsetInEndSection": 327,
"text": "p16INK4a and p14ARF tumor suppressors, human telomerase reverse transcriptase (h-TERT), and oncoprotein c-Myc have been implicated in the regulation of the cell cycle and proliferation mediated by PcG proteins, mainly Bmi-1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17102614",
"endSection": "abstract",
"offsetInBeginSection": 395,
"offsetInEndSection": 492,
"text": "involving the polycomb group repressor Bmi-1 and the cyclin-dependent kinase inhibitor p16(INK4a)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16537449",
"endSection": "abstract",
"offsetInBeginSection": 399,
"offsetInEndSection": 596,
"text": "increased frequency to a telomere-independent senescent state mediated by the cyclin-dependent kinase inhibitor p16(INK4a). p16(INK4a) expression was regulated by the Polycomb group repressor Bmi-1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16157028",
"endSection": "abstract",
"offsetInBeginSection": 1445,
"offsetInEndSection": 1549,
"text": "The antisense Bmi-1 gene can inhibit the growth of K562 cell and upgrade expression of p16 in K562 cells"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16155021",
"endSection": "abstract",
"offsetInBeginSection": 912,
"offsetInEndSection": 989,
"text": "overexpression of BMI-1, a transcriptional repressor of the p16(INK4a) locus,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14982841",
"endSection": "abstract",
"offsetInBeginSection": 800,
"offsetInEndSection": 874,
"text": "experimental model systems indicate that p16 is a downstream target of Bmi"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14574365",
"endSection": "abstract",
"offsetInBeginSection": 629,
"offsetInEndSection": 777,
"text": "In the absence of Bmi-1, the cyclin-dependent kinase inhibitor gene p16Ink4a is upregulated in neural stem cells, reducing the rate of proliferation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12714971",
"endSection": "abstract",
"offsetInBeginSection": 686,
"offsetInEndSection": 935,
"text": "A gene expression analysis revealed that the expression of stem cell associated genes, cell survival genes, transcription factors, and genes modulating proliferation including p16Ink4a and p19Arf was altered in bone marrow cells of the Bmi-1-/- mice"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12482990",
"endSection": "abstract",
"offsetInBeginSection": 4,
"offsetInEndSection": 106,
"text": "polycomb protein Bmi-1 represses the INK4a locus, which encodes the tumor suppressors p16 and p14(ARF)"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9923679",
"endSection": "title",
"offsetInBeginSection": 17,
"offsetInEndSection": 110,
"text": "Polycomb-group gene bmi-1 regulates cell proliferation and senescence through the ink4a locus"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9923679",
"endSection": "abstract",
"offsetInBeginSection": 777,
"offsetInEndSection": 912,
"text": "in bmi-1-deficient lymphocytes, the expression of the tumour suppressors p16 and p19Arf, which are encoded by ink4a, is raised markedly"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21928107",
"endSection": "abstract",
"offsetInBeginSection": 1493,
"offsetInEndSection": 1526,
"text": "BMI-1-mediated INK4a/ARF pathway "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18346113",
"endSection": "abstract",
"offsetInBeginSection": 241,
"offsetInEndSection": 320,
"text": " expression of the polycomb protein BMI-1 and its downstream targets p16(Ink4a)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21496667",
"endSection": "abstract",
"offsetInBeginSection": 905,
"offsetInEndSection": 1029,
"text": "reduced expression of Bmi-1, OC, DSP, and BSP compared with rapidly proliferating cells, whereas p16(INK4A) level increased."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21164364",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 52,
"text": "16Ink4a suppression of lung adenocarcinoma by Bmi-1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21164364",
"endSection": "abstract",
"offsetInBeginSection": 1386,
"offsetInEndSection": 1460,
"text": "The suppression of p16Ink4a occurred in parallel with an increase in Bmi-1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19907431",
"endSection": "abstract",
"offsetInBeginSection": 1224,
"offsetInEndSection": 1282,
"text": "Bmi-1 overexpression reduced p16(INK4a) promoter activity "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19390085",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 35,
"text": "mi-1 regulates the Ink4a/Arf locus"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19390085",
"endSection": "abstract",
"offsetInBeginSection": 212,
"offsetInEndSection": 291,
"text": "derepression of the Ink4a/Arf locus is associated with decreased Bmi-1 binding,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19389366",
"endSection": "abstract",
"offsetInBeginSection": 1029,
"offsetInEndSection": 1152,
"text": "pronounced effects of Bmi-1 over-expression in culture were largely attributable to the attenuated induction of p16(Ink4a) "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17597110",
"endSection": "abstract",
"offsetInBeginSection": 364,
"offsetInEndSection": 443,
"text": "BMI-1 is a transcriptional repressor of the Ink4a/Arf locus encoding p16(ink4a)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17233832",
"endSection": "abstract",
"offsetInBeginSection": 387,
"offsetInEndSection": 442,
"text": "introduction of Bmi-1 can inhibit p16(INK4a) expression"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16869752",
"endSection": "abstract",
"offsetInBeginSection": 635,
"offsetInEndSection": 718,
"text": "Bmi-1 promotes stem cell self-renewal partly by repressing the expression of Ink4a "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16778197",
"endSection": "abstract",
"offsetInBeginSection": 917,
"offsetInEndSection": 1060,
"text": "Overexpression of Bmi-1 in NPECs led to the induction of human telomerase reverse transcriptase activity and reduction of p16(INK4a) expression"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15964994",
"endSection": "abstract",
"offsetInBeginSection": 657,
"offsetInEndSection": 742,
"text": "Bmi-1 thus prevents the premature senescence of neural stem cells by repressing Ink4a"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15892997",
"endSection": "abstract",
"offsetInBeginSection": 355,
"offsetInEndSection": 442,
"text": "overexpression of the polycomb-group gene BMI-1 might also down-regulate p16 expression"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14732230",
"endSection": "title",
"offsetInBeginSection": 4,
"offsetInEndSection": 113,
"text": "Bmi-1 oncoprotein is overexpressed in human colorectal cancer and correlates with the reduced p16INK4a/p14ARF"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14732230",
"endSection": "abstract",
"offsetInBeginSection": 809,
"offsetInEndSection": 925,
"text": "modulation of Bmi-1 protein might be involved in human colorectal carcinogenesis by repressing the INK4a/ARF protein"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14536079",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 29,
"text": "mi-1 regulation of INK4A-ARF"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14536079",
"endSection": "abstract",
"offsetInBeginSection": 294,
"offsetInEndSection": 428,
"text": "expression of BMI-1, a lymphoid oncogene whose product functions as a transcriptional repressor of the INK4A-ARF tumor suppressor locu"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11355949",
"endSection": "title",
"offsetInBeginSection": 4,
"offsetInEndSection": 126,
"text": "bmi-1 oncoprotein is differentially expressed in non-small cell lung cancer and correlates with INK4A-ARF locus expression"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11355949",
"endSection": "abstract",
"offsetInBeginSection": 419,
"offsetInEndSection": 495,
"text": "bmi-1 overexpression induces immortalization due to repression of p16/p19ARF"
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D050756",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D019941",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0004861",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0045736",
"http://www.uniprot.org/uniprot/CD2A1_MONDO"
] |
[] |
533abc76d6d3ac6a34000064
|
bioasq_factoid
|
factoid
|
Which is the protein-membrane interface of the Cholesterol-regulated Start protein 4 protein (STARD4)?
|
['L124', 'Omega-1 (Ω1) loop']
|
[
"L124",
"Omega-1 (Ω1) loop",
"Omega-1 loop",
"L124 protein",
"L124 peptide"
] |
['L124 is the protein-membrane interface of the Cholesterol-regulated Start protein 4 protein (STARD4).', 'Our results show that STARD4 interacts with anionic membranes through a surface-exposed basic patch and that introducing a mutation (L124D) into the Omega-1 (Ω1) loop, which covers the sterol binding pocket, attenuates sterol transfer activity.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26168008"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26168008",
"endSection": "abstract",
"offsetInBeginSection": 750,
"offsetInEndSection": 994,
"text": "Our results show that STARD4 interacts with anionic membranes through a surface-exposed basic patch and that introducing a mutation (L124D) into the Omega-1 (Ω1) loop, which covers the sterol binding pocket, attenuates sterol transfer activity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26168008",
"endSection": "abstract",
"offsetInBeginSection": 765,
"offsetInEndSection": 1014,
"text": "w that STARD4 interacts with anionic membranes through a surface-exposed basic patch and that introducing a mutation (L124D) into the Omega-1 (Ω1) loop, which covers the sterol binding pocket, attenuates sterol transfer activity. To gain insight int"
}
] | 11 |
BioASQ-training11b
| null | null |
6278ca4a56bf9aee6f00000c
|
bioasq_factoid
|
factoid
|
Which human gene encode for DNA polymerase θ?
|
['DNA polymerase theta (pol θ) is an evolutionarily conserved protein encoded by the POLQ gene in mammalian genomes']
|
[
"DNA polymerase theta",
"pol θ",
"POLQ",
"DNA polymerase theta (pol θ)",
"DNA polymerase theta (POLQ)"
] |
['DNA polymerase theta (pol θ) is an evolutionarily conserved protein encoded by the POLQ gene in mammalian genomes']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27264557",
"http://www.ncbi.nlm.nih.gov/pubmed/28668117"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28668117",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "DNA polymerase theta (pol θ) is an evolutionarily conserved protein encoded by the POLQ gene in mammalian genomes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27264557",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "DNA polymerase theta (pol θ) is encoded in the genomes of many eukaryotes, though not in fungi. Pol θ is encoded by the POLQ gene in mammalian cells."
}
] | 11 |
BioASQ-training11b
| null | null |
5aacd487fcf4565872000007
|
bioasq_factoid
|
yesno
|
Is poliosis circumscripta another term for a white or unpigmented patch of hair or skin?
|
['yes']
|
[
"yes"
] |
['Yes. Poliosis circumscripta is another term for a white or unpigmented patch of hair or skin.', 'Yes, poliosis circumscripta, or "white forelock," is defined as a localized patch of white hair in a group of hair follicles.', 'poliosis circumscripta is a " localized patch of white hair in a group of hair foll white forelock " circumscripta was defined as a "', 'yes, "white forelock," poliosis circumscripta, defined as a localized patch of white hair in a group of hair follicle', 'Yes, poliosis circumscripta is another term for a white or unpigmented patch of hair or skin.', '"white forelock," poliosis circumscripta, defined as a localized patch of white hair in a group of hair follicle', 'white forelock," poliosis circumscripta, defined as a localized patch of white hair in a group of hair follicle']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23850259"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23850259",
"endSection": "abstract",
"offsetInBeginSection": 32,
"offsetInEndSection": 144,
"text": "\"white forelock,\" poliosis circumscripta, defined as a localized patch of white hair in a group of hair follicle"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23850259",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 231,
"text": "Although traditionally known as \"white forelock,\" poliosis circumscripta, defined as a localized patch of white hair in a group of hair follicles, can involve any hairy area on the body including the scalp, eyebrows, and eyelashes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23850259",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 237,
"text": "Although traditionally known as \" white forelock , \" poliosis circumscripta , defined as a localized patch of white hair in a group of hair follicles , can involve any hairy area on the body including the scalp , eyebrows , and eyelashes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23850259",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 232,
"text": "Although traditionally known as \"white forelock,\" poliosis circumscripta, defined as a localized patch of white hair in a group of hair follicles, can involve any hairy area on the body including the scalp, eyebrows, and eyelashes."
}
] | 11 |
BioASQ-training11b
| null | null |
5e41620648dab47f2600000e
|
bioasq_yesno
|
factoid
|
What is the cause of a STAG3 truncating variant?
|
['Primary ovarian insufficiency', 'POI']
|
[
"Primary ovarian insufficiency",
"POI",
"Premature ovarian failure",
"Premature ovarian insufficiency",
"Ovarian insufficiency",
"Ovarian failure"
] |
['Linkage analysis identified a locus on chromosome 7 where exome sequencing successfully identified a homozygous two base pair duplication (c.1947_48dupCT), leading to a truncated protein p.(Y650Sfs*22) in the STAG3 gene, confirming it as the cause of POI in this family', 'Primary ovarian insufficiency (POI) is a distressing cause of infertility in young women. POI is heterogeneous with only a few causative genes having been discovered so far. Linkage analysis identified a locus on chromosome 7 where exome sequencing successfully identified a homozygous two base pair duplication (c.1947_48dupCT), leading to a truncated protein p.(Y650Sfs*22) in the STAG3 gene, confirming it as the cause of POI in this family.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27836978",
"http://www.ncbi.nlm.nih.gov/pubmed/26059840",
"http://www.ncbi.nlm.nih.gov/pubmed/30006057"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26059840",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 71,
"text": "STAG3 truncating variant as the cause of primary ovarian insufficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26059840",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1233,
"text": "Primary ovarian insufficiency (POI) is a distressing cause of infertility in young women. POI is heterogeneous with only a few causative genes having been discovered so far. Our objective was to determine the genetic cause of POI in a consanguineous Lebanese family with two affected sisters presenting with primary amenorrhoea and an absence of any pubertal development. Multipoint parametric linkage analysis was performed. Whole-exome sequencing was done on the proband. Linkage analysis identified a locus on chromosome 7 where exome sequencing successfully identified a homozygous two base pair duplication (c.1947_48dupCT), leading to a truncated protein p.(Y650Sfs*22) in the STAG3 gene, confirming it as the cause of POI in this family. Exome sequencing combined with linkage analyses offers a powerful tool to efficiently find novel genetic causes of rare, heterogeneous disorders, even in small single families. This is only the second report of a STAG3 variant; the first STAG3 variant was recently described in a phenotypically similar family with extreme POI. Identification of an additional family highlights the importance of STAG3 in POI pathogenesis and suggests it should be evaluated in families affected with POI."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26059840",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 160,
"text": "STAG3 truncating variant as the cause of primary ovarian insufficiency.Primary ovarian insufficiency (POI) is a distressing cause of infertility in young women. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30006057",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "Two rare loss-of-function variants in the STAG3 gene leading to primary ovarian insufficiency."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27836978",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "A homozygous NOBOX truncating variant causes defective transcriptional activation and leads to primary ovarian insufficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30006057",
"endSection": "abstract",
"offsetInBeginSection": 1270,
"offsetInEndSection": 1556,
"text": "The parents' DNA was not available to segregate these variants.<br><b>CONCLUSION</b>: Our results suggested that POI is caused by pathogenic compound heterozygous variants in the STAG3 gene, supporting the key role of the STAG3 gene in the etiology of primary ovarian insufficiency.<br>"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30006057",
"endSection": "abstract",
"offsetInBeginSection": 1410,
"offsetInEndSection": 1606,
"text": "Our results suggested that POI is caused by pathogenic compound heterozygous variants in the STAG3 gene, supporting the key role of the STAG3 gene in the etiology of primary ovarian insufficiency."
}
] | 11 |
BioASQ-training11b
| null | null |
5c632cc1e842deac6700000f
|
bioasq_factoid
|
factoid
|
Which gene is responsible for the Liebenberg syndrome?
|
['PITX1', '']
|
[
"PITX1",
"Pituitary homeobox 1",
"PITX1 homeobox protein",
"PITX1 transcription factor"
] |
['Liebenberg syndrome is a genetic disease caused by heterozygous mutations or deletions of the zinc finger E-box-binding homeobox 2 (ZEB2) gene. Patients present with prominent neurological, medical, and behavioral symptoms.', 'We discuss the genetic abnormality that causes Liebenberg syndrome, the genomic rearrangement at the PITX1 locus on chromosome 5', 'We re-define the phenotype of Liebenberg syndrome as a transformation of the upper limbs to reflect lower limb characteristics. We speculate that the area of deletion contains a regulatory sequence that suppresses the expression of PITX1 in the upper limb buds.', 'Liebenberg syndrome is caused by genetic changes near the PITX1 gene. The protein produced from this gene plays a critical role in lower limb development by controlling the activity of other genes involved in limb development, directing the shape and structure of bones and other tissues in the legs and feet.', 'Liebenberg syndrome is a genetic disease caused by heterozygous mutations or deletions of the zinc finger E-box-binding homeobox 2 (ZEB2) gene.', 'Liebenberg syndrome is a genetic disease caused by heterozygous mutations or deletions of the zinc finger E-box-binding homeodomain complex 1 (PITX1) gene.', 'Liebenberg syndrome is caused by a deletion upstream to the PITX1 gene resulting in transformation of the upper limbs to reflect lower limb characteristics The deleted region is upstream to the PITX1 gene.', 'Liebenberg syndrome is caused by a deletion upstream to the PITX1 gene resulting in transformation of the upper limbs to reflect lower limb characteristics']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23940102",
"http://www.ncbi.nlm.nih.gov/pubmed/30711920",
"http://www.ncbi.nlm.nih.gov/pubmed/23587911",
"http://www.ncbi.nlm.nih.gov/pubmed/23022097",
"http://www.ncbi.nlm.nih.gov/pubmed/23395106",
"http://www.ncbi.nlm.nih.gov/pubmed/32598510"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23587911",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Liebenberg syndrome is caused by a deletion upstream to the PITX1 gene resulting in transformation of the upper limbs to reflect lower limb characteristics"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23587911",
"endSection": "abstract",
"offsetInBeginSection": 484,
"offsetInEndSection": 534,
"text": "The deleted region is upstream to the PITX1 gene. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23587911",
"endSection": "abstract",
"offsetInBeginSection": 726,
"offsetInEndSection": 997,
"text": "We therefore re-define the phenotype of Liebenberg syndrome as a transformation of the upper limbs to reflect lower limb characteristics and speculate that the area of deletion contains a regulatory sequence that suppresses the expression of PITX1 in the upper limb buds."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23940102",
"endSection": "abstract",
"offsetInBeginSection": 514,
"offsetInEndSection": 716,
"text": "The structural variations seem to result in an ectopic expression of paired-like homeodomain transcription factor 1 (PITX1) in the forelimb causing a partial arm-to-leg transformation in these patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23940102",
"endSection": "abstract",
"offsetInBeginSection": 385,
"offsetInEndSection": 513,
"text": "We discuss the genetic abnormality that causes Liebenberg syndrome, the genomic rearrangement at the PITX1 locus on chromosome 5"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30711920",
"endSection": "abstract",
"offsetInBeginSection": 1080,
"offsetInEndSection": 1505,
"text": "ng CRISPR-Cas9 technology in the mouse and showed that the promoter of the housekeeping gene H2afy insulates the Pen enhancer from Pitx1 in forelimbs; its loss leads to misexpression of Pitx1 by the pan-limb activity of the Pen enhancer causing Liebenberg syndrome.CONCLUSION: Our data indicate that housekeeping promoters may titrate promiscuous enhancer activity to ensure normal morphogenesis. The deletion of the H2AFY pr"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23587911",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 156,
"text": "Liebenberg syndrome is caused by a deletion upstream to the PITX1 gene resulting in transformation of the upper limbs to reflect lower limb characteristics."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32598510",
"endSection": "abstract",
"offsetInBeginSection": 79,
"offsetInEndSection": 401,
"text": "Two PITX1-related human disorders have been reported to date: PITX1 ectopic expression causes Liebenberg syndrome, characterized by malformation of upper limbs showing a \"lower limb\" appearance; PITX1 deletions or missense variation cause a syndromic picture including clubfoot, tibial hemimelia, and preaxial polydactyly."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23940102",
"endSection": "abstract",
"offsetInBeginSection": 385,
"offsetInEndSection": 716,
"text": "We discuss the genetic abnormality that causes Liebenberg syndrome, the genomic rearrangement at the PITX1 locus on chromosome 5.The structural variations seem to result in an ectopic expression of paired-like homeodomain transcription factor 1 (PITX1) in the forelimb causing a partial arm-to-leg transformation in these patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23022097",
"endSection": "abstract",
"offsetInBeginSection": 787,
"offsetInEndSection": 942,
"text": "We generated transgenic mice in which PITX1 was misexpressed under the control of a nearby enhancer and were able to recapitulate the Liebenberg phenotype."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30711920",
"endSection": "abstract",
"offsetInBeginSection": 209,
"offsetInEndSection": 436,
"text": "allenging. The human Liebenberg syndrome is characterised by a partial transformation of the arms into legs and has been shown to be caused by SVs at the PITX1 locus leading to its misregulation in the forelimb by its native en"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32598510",
"endSection": "abstract",
"offsetInBeginSection": 80,
"offsetInEndSection": 406,
"text": "wo PITX1-related human disorders have been reported to date: PITX1 ectopic expression causes Liebenberg syndrome, characterized by malformation of upper limbs showing a \"lower limb\" appearance; PITX1 deletions or missense variation cause a syndromic picture including clubfoot, tibial hemimelia, and preaxial polydactyly. We r"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23940102",
"endSection": "abstract",
"offsetInBeginSection": 389,
"offsetInEndSection": 518,
"text": "iscuss the genetic abnormality that causes Liebenberg syndrome, the genomic rearrangement at the PITX1 locus on chromosome 5.The "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32598510",
"endSection": "abstract",
"offsetInBeginSection": 767,
"offsetInEndSection": 987,
"text": "typic overlap is also observed with Ischiocoxopodopatellar syndrome caused by TBX4 haploinsufficiency, and with the phenotypic spectrum caused by SOX9 anomalies, both genes being PITX1 downstream targets. Our study findi"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30711920",
"endSection": "abstract",
"offsetInBeginSection": 1001,
"offsetInEndSection": 1348,
"text": "functionally characterise the variant, we re-engineered the 8.5 kb deletion using CRISPR-Cas9 technology in the mouse and showed that the promoter of the housekeeping gene H2afy insulates the Pen enhancer from Pitx1 in forelimbs; its loss leads to misexpression of Pitx1 by the pan-limb activity of the Pen enhancer causing Liebenberg syndrome.CON"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30711920",
"endSection": "abstract",
"offsetInBeginSection": 219,
"offsetInEndSection": 454,
"text": " The human Liebenberg syndrome is characterised by a partial transformation of the arms into legs and has been shown to be caused by SVs at the PITX1 locus leading to its misregulation in the forelimb by its native enhancer element Pen"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23587911",
"endSection": "abstract",
"offsetInBeginSection": 534,
"offsetInEndSection": 725,
"text": "The radiological features in the upper limbs of all affected members of the family were almost identical to the phenotype in the mouse model with ectopic expression of Pitx1 in the forelimbs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23587911",
"endSection": "abstract",
"offsetInBeginSection": 484,
"offsetInEndSection": 533,
"text": "The deleted region is upstream to the PITX1 gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30711920",
"endSection": "abstract",
"offsetInBeginSection": 208,
"offsetInEndSection": 443,
"text": "hallenging. The human Liebenberg syndrome is characterised by a partial transformation of the arms into legs and has been shown to be caused by SVs at the PITX1 locus leading to its misregulation in the forelimb by its native enhancer "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30711920",
"endSection": "abstract",
"offsetInBeginSection": 968,
"offsetInEndSection": 1434,
"text": "rst non-coding exon of H2AFY. To functionally characterise the variant, we re-engineered the 8.5 kb deletion using CRISPR-Cas9 technology in the mouse and showed that the promoter of the housekeeping gene H2afy insulates the Pen enhancer from Pitx1 in forelimbs; its loss leads to misexpression of Pitx1 by the pan-limb activity of the Pen enhancer causing Liebenberg syndrome.CONCLUSION: Our data indicate that housekeeping promoters may titrate promiscuous enhance"
}
] | 11 |
BioASQ-training11b
| null | null |
5fdb1023a43ad31278000009
|
bioasq_factoid
|
factoid
|
Where is the DMD gene located?
|
['Xp21 chromosome locus', 'X-linked recessive disorders caused by mutations of the DMD gene located at Xp21', 'X chromosome (Xp21)']
|
[
"Xp21 chromosome locus",
"Xp21",
"X chromosome (Xp21)",
"X-linked recessive disorders caused by mutations of the DMD gene located at Xp21",
"Xp21.1",
"Xp21.2",
"Xp21.3",
"Duchenne muscular dystrophy locus",
"DMD gene locus"
] |
['The dystrophin gene (DMD) is located on the X chromosome (Xp21).', 'The dystrophin gene is located at chromosome Xp21.1, near the centromere.', 'The DMD gene is located on the X chromosome at Xp21.2.', 'The DMD gene is located on the X chromosome at the Xp21 locus.', 'The DMD gene is located on the X chromosome, on the Xp21 locus.', 'The DMD gene is located on the Xp21 chromosome locus on the X chromosome.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/19078586",
"http://www.ncbi.nlm.nih.gov/pubmed/18471087",
"http://www.ncbi.nlm.nih.gov/pubmed/24014122",
"http://www.ncbi.nlm.nih.gov/pubmed/19461958",
"http://www.ncbi.nlm.nih.gov/pubmed/6655672",
"http://www.ncbi.nlm.nih.gov/pubmed/31661024",
"http://www.ncbi.nlm.nih.gov/pubmed/16936400",
"http://www.ncbi.nlm.nih.gov/pubmed/28247611",
"http://www.ncbi.nlm.nih.gov/pubmed/28028563",
"http://www.ncbi.nlm.nih.gov/pubmed/19837995",
"http://www.ncbi.nlm.nih.gov/pubmed/12488581",
"http://www.ncbi.nlm.nih.gov/pubmed/28867298",
"http://www.ncbi.nlm.nih.gov/pubmed/24274981",
"http://www.ncbi.nlm.nih.gov/pubmed/18935728",
"http://www.ncbi.nlm.nih.gov/pubmed/28740938",
"http://www.ncbi.nlm.nih.gov/pubmed/2889148",
"http://www.ncbi.nlm.nih.gov/pubmed/2541343",
"http://www.ncbi.nlm.nih.gov/pubmed/12145744",
"http://www.ncbi.nlm.nih.gov/pubmed/12619170",
"http://www.ncbi.nlm.nih.gov/pubmed/24627880",
"http://www.ncbi.nlm.nih.gov/pubmed/33870095",
"http://www.ncbi.nlm.nih.gov/pubmed/36361862",
"http://www.ncbi.nlm.nih.gov/pubmed/3777020"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28867298",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "The dystrophin gene (DMD) is the largest gene in the human genome, mapping on the Xp21 chromosome locus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19461958",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) are X-linked recessive disorders caused by mutations of the DMD gene located at Xp21."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18935728",
"endSection": "abstract",
"offsetInBeginSection": 130,
"offsetInEndSection": 255,
"text": "The disease is caused by deletion, duplication or point mutation of the dystrophin gene, located on the X chromosome (Xp21). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24274981",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "DMD gene which is composed of 79 exons is the largest known gene located on X chromosome (Xp21)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33870095",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Dystrophinopathies are allelic conditions caused by deletions, duplications and point-mutations in the DMD gene, located on the X chromosome (Xp21.2)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36361862",
"endSection": "abstract",
"offsetInBeginSection": 197,
"offsetInEndSection": 276,
"text": "The disease is caused by mutations in the DMD gene located on the X chromosome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24627880",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 98,
"text": "BACKGROUND: The Duchenne muscular dystrophy (DMD) gene is located in the short arm of the X chromo"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18471087",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Duchenne muscular dystrophy (DMD) is an X-linked recessive neuromuscular disorder caused by mutations in the dystrophin DMD gene located at Xp21.1 region."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12145744",
"endSection": "abstract",
"offsetInBeginSection": 401,
"offsetInEndSection": 678,
"text": "Because the DMD gene is located at Xp21.2, which is one breakpoint of the inv(X), and because its defects are rarely associated with severe mental retardation, the other clinical features of this patient were deemed likely to be associated with the opposite breakpoint at Xq22."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2889148",
"endSection": "abstract",
"offsetInBeginSection": 241,
"offsetInEndSection": 368,
"text": "Long-range physical mapping has shown that the DMD gene, localized in Xp21, is extremely large, exceeding 2 million base pairs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24014122",
"endSection": "abstract",
"offsetInBeginSection": 329,
"offsetInEndSection": 415,
"text": "The DMD gene, located on Xp21, is the largest human gene in the human genome (2.3 Mb)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2541343",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 193,
"text": "The Duchenne muscular dystrophy (DMD) gene has been localized to chromosome Xp21 and codes for a 14-kilobase (kb) transcript and a protein called dystrophin, of relative molecular mass 427,000."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6655672",
"endSection": "abstract",
"offsetInBeginSection": 640,
"offsetInEndSection": 772,
"text": " The breakpoint in our patient is also located at Xp21, adding evidence for the assignment of this band as the site of the DMD gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24014122",
"endSection": "abstract",
"offsetInBeginSection": 328,
"offsetInEndSection": 409,
"text": " The DMD gene, located on Xp21, is the largest human gene in the human genome (2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3777020",
"endSection": "abstract",
"offsetInBeginSection": 297,
"offsetInEndSection": 381,
"text": " The present case supports the hypothesis that the DMD gene must be located at Xp21."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28247611",
"endSection": "abstract",
"offsetInBeginSection": 185,
"offsetInEndSection": 272,
"text": " The causal gene of DMD is the largest one in human that locates in the region of Xp21."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12145744",
"endSection": "abstract",
"offsetInBeginSection": 400,
"offsetInEndSection": 441,
"text": " Because the DMD gene is located at Xp21."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28028563",
"endSection": "abstract",
"offsetInBeginSection": 39,
"offsetInEndSection": 189,
"text": "n coded by the Duchenne muscular dystrophy (DMD) gene located on the X-chromosome. Truncating mutations in the DMD gene cause loss of dystrophin and t"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18471087",
"endSection": "abstract",
"offsetInBeginSection": 71,
"offsetInEndSection": 221,
"text": "r disorder caused by mutations in the dystrophin DMD gene located at Xp21.1 region. Up to 65% of the patients present dystrophin gene deletions. Mothe"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28740938",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "BACKGROUND: Duchenne muscular dystrophy (DMD) is caused by a defective gene located on the X-chromosome, responsible for the production of the dystrophin protein"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19837995",
"endSection": "abstract",
"offsetInBeginSection": 100,
"offsetInEndSection": 250,
"text": "l muscle disorders, caused by mutations in the dystrophin gene located in Xp21. DMD occurs with the incidence 1:3500, BMD with the incidence of 1:18,5"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28867298",
"endSection": "abstract",
"offsetInBeginSection": 17,
"offsetInEndSection": 167,
"text": "ne (DMD) is the largest gene in the human genome, mapping on the Xp21 chromosome locus. It spans 2.2Mb and accounts for approximately 0,1% of the enti"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19078586",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 287,
"text": "Duchenne muscular dystrophy (DMD), glycerol kinase deficiency (GKD), and adrenal hypoplasia congenita (AHC) can occur together as part of a contiguous gene syndrome located at chromosome Xp21, GKD can manifest with recurrent episodes of vomiting, acidemia, mental retardation, or stupor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19461958",
"endSection": "abstract",
"offsetInBeginSection": 77,
"offsetInEndSection": 227,
"text": "inked recessive disorders caused by mutations of the DMD gene located at Xp21. In DMD patients, dystrophin is virtually absent; whereas BMD patients h"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12619170",
"endSection": "abstract",
"offsetInBeginSection": 22,
"offsetInEndSection": 172,
"text": "rophy (DMD) is a dystrophinopathy, and its associated gene is located on Xp21. Moreover, utrophin, a recently identified structural homologue of dystr"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31661024",
"endSection": "abstract",
"offsetInBeginSection": 96,
"offsetInEndSection": 246,
"text": " disease in children, resulting from a defect in the DMD gene located on Xp21.2. The new emerging treatment using exon skipping strategy is tailored t"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3777020",
"endSection": "abstract",
"offsetInBeginSection": 303,
"offsetInEndSection": 453,
"text": "resent case supports the hypothesis that the DMD gene must be located at Xp21. In this study, involvement of the father's chromosomes in the transloca"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12145744",
"endSection": "abstract",
"offsetInBeginSection": 364,
"offsetInEndSection": 514,
"text": " only later was it diagnosed as DMD. Because the DMD gene is located at Xp21.2, which is one breakpoint of the inv(X), and because its defects are rar"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16936400",
"endSection": "abstract",
"offsetInBeginSection": 124,
"offsetInEndSection": 274,
"text": "letion, duplication or point mutation of the dystrophin gene located at Xp 21.2. In the present study DNA from seventy unrelated patients clinically d"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12488581",
"endSection": "abstract",
"offsetInBeginSection": 60,
"offsetInEndSection": 210,
"text": "inked diseases resulting from a defect in the dystrophin gene located on Xp21. DMD is the most frequent neuromuscular disease in humans (1/3500 male n"
}
] | 12 |
BioASQ-training12b
| null | null |
64179113690f196b5100002e
|
bioasq_factoid
|
factoid
|
What causes Black Lung?
|
['Chronic exposure to coal dust']
|
[
"Chronic exposure to coal dust",
"Coal worker's pneumoconiosis",
"Black lung disease",
"Coal dust exposure",
"Pneumoconiosis due to coal dust",
"Anthracosis"
] |
['Black lung, also known as pneumoconiosis, is caused by chronic exposure to coal dust.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/6453959",
"http://www.ncbi.nlm.nih.gov/pubmed/8803434",
"http://www.ncbi.nlm.nih.gov/pubmed/8199664",
"http://www.ncbi.nlm.nih.gov/pubmed/8456342"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8803434",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 326,
"text": "A prospective case-control study was undertaken to assess respiratory disability in 133 former coal miners who were claimants for \"black lung\" benefits. Consecutive assignment was made to either case or control group based on their chest radiograph having shown coal workers' pneumoconiosis or no coal workers' pneumoconiosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8199664",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "It has recently been suggested that the inhalation of coal in the absence of complicated coal workers' pneumoconiosis (CWP) or smoking can lead to disabling airways obstruction"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8456342",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 494,
"text": "Highlights in the history of efforts to prevent occupational lung disease among coal miners in the United States are reviewed. The Federal Coal Mine Health and Safety Act of 1969 is summarized, and the sources and effects of its provisions to prevent coal workers' pneumoconiosis are examined. Descriptions follow of the identification of coal workers' pneumoconiosis as a disease, identification of respirable coal mine dust as its cause, and establishment and enforcement of an exposure limit"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6453959",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 160,
"text": "Coal workers' pneumoconiosis is a preventable occupational disorder of the respiratory system resulting from exposure to and retention of respirable coal dust. "
}
] | 11 |
BioASQ-training11b
| null | null |
5a87145861bb38fb24000004
|
bioasq_factoid
|
factoid
|
Which enzyme is deficient in Krabbe disease?
|
['Galactocerebrosidase is an enzyme that is deficient in Krabbe disease (also known as globoid-cell leukodystrophy). This leads to accumulation of psychosine (galactosylsphingosine) primarily in oligodendrocytes.']
|
[
"Galactocerebrosidase",
"GALC",
"galactosylceramidase",
"galactosylsphingosine beta-galactosidase",
"galactocerebroside beta-galactosidase",
"Krabbe disease enzyme",
"globoid-cell leukodystrophy enzyme"
] |
['galactocerebrosidase']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23438514",
"http://www.ncbi.nlm.nih.gov/pubmed/20301416",
"http://www.ncbi.nlm.nih.gov/pubmed/19439584",
"http://www.ncbi.nlm.nih.gov/pubmed/17072020",
"http://www.ncbi.nlm.nih.gov/pubmed/16645197",
"http://www.ncbi.nlm.nih.gov/pubmed/16498763",
"http://www.ncbi.nlm.nih.gov/pubmed/11978730",
"http://www.ncbi.nlm.nih.gov/pubmed/11814461",
"http://www.ncbi.nlm.nih.gov/pubmed/11493025",
"http://www.ncbi.nlm.nih.gov/pubmed/10448809",
"http://www.ncbi.nlm.nih.gov/pubmed/10090061",
"http://www.ncbi.nlm.nih.gov/pubmed/9875712",
"http://www.ncbi.nlm.nih.gov/pubmed/9441867",
"http://www.ncbi.nlm.nih.gov/pubmed/8940268",
"http://www.ncbi.nlm.nih.gov/pubmed/8577041",
"http://www.ncbi.nlm.nih.gov/pubmed/7581365",
"http://www.ncbi.nlm.nih.gov/pubmed/8297359",
"http://www.ncbi.nlm.nih.gov/pubmed/8281145",
"http://www.ncbi.nlm.nih.gov/pubmed/8399327",
"http://www.ncbi.nlm.nih.gov/pubmed/1521344",
"http://www.ncbi.nlm.nih.gov/pubmed/2079710",
"http://www.ncbi.nlm.nih.gov/pubmed/85413"
] |
[
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23438514",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 239,
"text": "Krabbe disease is a lethal, demyelinating condition caused by genetic deficiency of galactocerebrosidase (GALC) and resultant accumulation of its cytotoxic substrate, psychosine (galactosylsphingosine), primarily in oligodendrocytes (OLs)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23438514",
"endSection": "sections.0",
"offsetInBeginSection": 692,
"offsetInEndSection": 946,
"text": "In this study, we report that accumulation of endogenous psychosine under GALC deficient Krabbe conditions impedes OL differentiation process both by decreasing the expression of myelin lipids and protein and by inducing the cell death of maturating OLs."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20301416",
"endSection": "sections.0",
"offsetInBeginSection": 808,
"offsetInEndSection": 1023,
"text": "In almost all individuals with Krabbe disease, galactocerebrosidase (GALC) enzyme activity is deficient (0%-5% of normal activity) in leukocytes isolated from whole heparinized blood or in cultured skin fibroblasts."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17072020",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 239,
"text": "This chapter describes in detail a practical procedure for the preparation of radiolabeled galactocerebroside and its use in the assay of galactocerebrosidase (GalCase), the enzyme deficient in globoid cell leukodystrophy (Krabbe disease)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16645197",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 237,
"text": "Globoid cell leukodystrophy (Krabbe disease) is an inherited neurological disorder caused by the pathogenomic accumulation of psychosine (galactosylsphingosine), a substrate for the deficient enzyme galactocerebroside beta-galactosidase."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16498763",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 194,
"text": "Krabbe disease is an extremely rare condition with an incidence of 1 in 1,00,000 live births. It is caused by deficient activity of the Iysosomal hydrolase galactosylceramide beta-galactosidase."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11978730",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 227,
"text": "Globoid cell leukodystrophy (Krabbe disease) is characterized by the accumulation of a toxic metabolite, psychosine (galactosylsphingosine), which is a substrate for the deficient enzyme (galactocerebroside beta-galactosidase)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11814461",
"endSection": "sections.0",
"offsetInBeginSection": 12,
"offsetInEndSection": 195,
"text": "Krabbe disease (globoid-cell leukodystrophy; GLD) is caused by mutations in the GALC gene. Beta-galactocerebrosidase (GALC) is a specific beta-galactosidase which is defective in GLD."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11814461",
"endSection": "sections.0",
"offsetInBeginSection": 807,
"offsetInEndSection": 970,
"text": "Both galactosylceramide beta-galactosidase (GALC-GC) and GALC-PS activities were reduced by at least 85% of the normal in all but 2 of the 10 GLD patients studied."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10448809",
"endSection": "sections.0",
"offsetInBeginSection": 12,
"offsetInEndSection": 160,
"text": "Krabbe disease, or globoid cell leukodystrophy, is an autosomal recessive disorder caused by the deficiency of galactocerebrosidase (GALC) activity."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10448809",
"endSection": "sections.0",
"offsetInBeginSection": 392,
"offsetInEndSection": 522,
"text": "The disease can be diagnosed by detecting the deficiency of GALC activity (less than 5% of normal) in any available tissue sample."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10090061",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 178,
"text": "Globoid cell leukodystrophy, or Krabbe disease, is a severe disorder of the peripheral and central nervous system myelin caused by deficient galactocerebrosidase (GALC) activity."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9875712",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "Globoid cell leukodystrophy (GCL or Krabbe disease) is a recessive disease caused by mutations of the lysosomal enzyme galactocerebrosidase (GALC) and twitcher is the murine model of GCL."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9441867",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Galactocerebrosidase (GALC) is the lysosomal enzyme deficient in human and certain animal species with globoid cell leukodystrophy (GLD) or Krabbe disease."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8940268",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 226,
"text": "Globoid-cell leukodystrophy (GLD) is an autosomal recessive inherited disorder caused by the deficiency of galactocerebrosidase, the lysosomal enzyme responsible for the degradation of the myelin glycolipid galactocerebroside."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8577041",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 135,
"text": "Krabbe disease is an autosomal recessive inherited demyelinating disease, which is deficient in lysosomal enzyme, galactocerebrosidase."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7581365",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 105,
"text": "Galactocerebrosidase (GALC) activity is deficient in all patients with globoid cell leukodystrophy (GLD)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8297359",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "Human galactocerebrosidase, the enzyme deficient in Krabbe disease, was purified, through several hydrophobic column steps and gel filtration, 22,650-fold from human lymphocytes"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8281145",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Globoid cell leukodystrophy (Krabbe disease) is an autosomal recessive disorder resulting from the deficiency of galactocerebrosidase (GALC) activity."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1521344",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 258,
"text": "6-Hexadecanoylamino-4-methylumbelliferyl-beta-D-galactopyranoside (HMGal) has been shown to be a specific fluorogenic substrate of galactocerebrosidase and to facilitate the simple enzymatic diagnosis of Krabbe disease in human patients and in twitcher mice."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2079710",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 209,
"text": "The inherited deficiency of galactosylceramide beta-galactosidase (E.C. 3.2.1.46: galactocerebrosidase) activity results in globoid cell leukodystrophy in humans (Krabbe disease) and in mice (twitcher mutant)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2079710",
"endSection": "sections.0",
"offsetInBeginSection": 997,
"offsetInEndSection": 1316,
"text": "The lack of complementation between Krabbe disease patient and twitcher mutant mouse cells provides further evidence that the twitcher mouse is an authentic murine model for Krabbe disease and supports the hypothesis that the mutations in both species are within the structural gene for the galactocerebrosidase enzyme."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/85413",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Galactosylceramide beta-galactosidase cross reacting material was demonstrated in brain, liver, and skin fibroblasts from patients with Krabbe disease."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19439584",
"endSection": "sections.0",
"offsetInBeginSection": 385,
"offsetInEndSection": 718,
"text": ". In this study, LRs in the brain of the twitcher (TWI) mouse, a bona-fide model for infant variants of human globoid cell leukodystrophy or Krabbe disease, were investigated. This mouse has deficient activity of GALC (beta-galactosylceramidase) that leads to a progressive accumulation of some galactosyl-sphingolipids in the brain."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11814461",
"endSection": "sections.0",
"offsetInBeginSection": 1615,
"offsetInEndSection": 1792,
"text": "A GALC genotype with one deleted and one polymorphic GALC activity-reducing allele can lead to enzymatic and clinical signs of LOGLD in the absence of marked GALC-PS deficiency."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11493025",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Galactocerebrosidase (GALC) is deficient in all tissues from human patients and animal models with globoid cell leukodystrophy (GLD) or Krabbe disease."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8399327",
"endSection": "sections.0",
"offsetInBeginSection": 1530,
"offsetInEndSection": 1739,
"text": "The purification of GALC and the securing of amino acid sequence information will aid in the cloning of the GALC gene. This enzyme is deficient in human patients with Krabbe disease and several animal species."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.disease-ontology.org/api/metadata/DOID:10587",
"http://www.disease-ontology.org/api/metadata/DOID:3211",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D007965",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003677",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D004798"
] | null |
5147c8a6d24251bc05000027
|
bioasq_factoid
|
factoid
|
What does RUNX1T1 stand for?
|
['runt-related transcription factor 1']
|
[
"runt-related transcription factor 1",
"RUNX1",
"AML1",
"CBFA2",
"runt domain transcription factor 1",
"runt-related transcription factor alpha",
"runt-related transcription factor 1 alpha"
] |
['RUNX1T1 stands for runt-related transcription factor 1.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/32589708"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32589708",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 96,
"text": "Runt-related transcription factor 1 (RUNX1T1) isoforms are involved in adipogenesis."
}
] | 11 |
BioASQ-training11b
| null | null |
62265b4a3a8413c653000083
|
bioasq_factoid
|
factoid
|
When was Keytruda approved by the FDA for the treatment of metastatic non-small cell lung cancer?
|
['October 24, 2016']
|
[
"October 24, 2016",
"10/24/2016",
"10-24-2016",
"24th October 2016",
"24/10/2016"
] |
['On October 24, 2016, the U.S. Food and Drug Administration (FDA) approved pembrolizumab (Keytruda) for treatment of metastatic non-small cell lung cancer.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/28835513"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28835513",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 713,
"text": "On October 24, 2016, the U.S. Food and Drug Administration (FDA) approved pembrolizumab (Keytruda; Merck & Co., Inc., https://www.merck.com) for treatment of patients with metastatic non-small cell lung cancer (mNSCLC) whose tumors express programmed death-ligand 1 (PD-L1) as determined by an FDA-approved test, as follows: (a) first-line treatment of patients with mNSCLC whose tumors have high PD-L1 expression (tumor proportion score [TPS] ≥50%), with no epidermal growth factor receptor (EGFR) or anaplastic lymphoma kinase (ALK) genomic tumor aberrations, and (b) treatment of patients with mNSCLC whose tumors express PD-L1 (TPS ≥1%), with disease progression on or after platinum-containing chemotherapy. "
}
] | 12 |
BioASQ-training12b
| null | null |
6415c53e690f196b51000012
|
bioasq_factoid
|
factoid
|
What color light does the the inhibitory receptor halorhodopsin (eNpHR) respond to?
|
['yellow']
|
[
"yellow",
"amber",
"golden",
"canary",
"lemon",
"butter",
"dandelion",
"sunshine",
"mustard",
"banana"
] |
['The inhibitory receptor halorhodopsin (eNpHR) responds to yellow light.', 'Halorhodopsin (eNpHR) is an inhibitory receptor that responds to yellow-green light (wavelength of 590 nm).', 'Halorhodopsin responds to yellow light.', 'The eNpHR is sensitive to yellow light.', 'eNpHR responds to yellow light.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21483674",
"http://www.ncbi.nlm.nih.gov/pubmed/23366158",
"http://www.ncbi.nlm.nih.gov/pubmed/22815873",
"http://www.ncbi.nlm.nih.gov/pubmed/27905012",
"http://www.ncbi.nlm.nih.gov/pubmed/23637949",
"http://www.ncbi.nlm.nih.gov/pubmed/17375185",
"http://www.ncbi.nlm.nih.gov/pubmed/28650460"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17375185",
"endSection": "abstract",
"offsetInBeginSection": 529,
"offsetInEndSection": 842,
"text": "Here we report that targeting the codon-optimized form of the light-driven chloride pump halorhodopsin from the archaebacterium Natronomas pharaonis (hereafter abbreviated Halo) to genetically-specified neurons enables them to be silenced reliably, and reversibly, by millisecond-timescale pulses of yellow light."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28650460",
"endSection": "abstract",
"offsetInBeginSection": 661,
"offsetInEndSection": 891,
"text": "By using Cal-Light to drive expression of the inhibitory receptor halorhodopsin (eNpHR), which responds to yellow light, we temporarily inhibit the lever-pressing behavior, confirming that the labeled neurons mediate the behavior."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21483674",
"endSection": "abstract",
"offsetInBeginSection": 465,
"offsetInEndSection": 723,
"text": "We introduced enhanced halorhodopsin (eNpHR), a yellow light-sensitive, membrane-targeting chloride pump, into mouse retinal ganglion cells (RGCs) by intravitreously injecting an adeno-associated virus serotype-2 vector carrying the CMV-eNpHR-EYFP construct."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23637949",
"endSection": "abstract",
"offsetInBeginSection": 597,
"offsetInEndSection": 912,
"text": "Hippocampal pyramidal neurons were transduced in vivo with a virus carrying an enhanced halorhodopsin (eNpHR), a yellow light activated chloride pump, and acute seizure progression was then monitored behaviorally and electrophysiologically in the presence and absence of illumination delivered via an optical fiber."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27905012",
"endSection": "abstract",
"offsetInBeginSection": 1223,
"offsetInEndSection": 1360,
"text": "Similarly, archaeon Natronomonas pharaonis (NpHR) expresses a monovalent Cl- channel protein halorhodopsin that responds to yellow light."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23366158",
"endSection": "abstract",
"offsetInBeginSection": 141,
"offsetInEndSection": 380,
"text": "Towards achieving this goal, light-activated channelrhodopsin-2 (ChR2), a cation channel activated with 480 nm light, and a first generation halorhodopsin (NpHR1.0), an anion pump activated by 580 nm light, have been introduced into hiPSC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22815873",
"endSection": "abstract",
"offsetInBeginSection": 485,
"offsetInEndSection": 645,
"text": "In analogy, other excitable cells can be inhibited by expressing Halorhodopsin from Natronomonas pharaonis (NpHR) and subsequent illumination with yellow light."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23366158",
"endSection": "abstract",
"offsetInBeginSection": 140,
"offsetInEndSection": 303,
"text": " Towards achieving this goal, light-activated channelrhodopsin-2 (ChR2), a cation channel activated with 480 nm light, and a first generation halorhodopsin (NpHR1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21483674",
"endSection": "abstract",
"offsetInBeginSection": 441,
"offsetInEndSection": 591,
"text": " retino-tectal pathway. We introduced enhanced halorhodopsin (eNpHR), a yellow light-sensitive, membrane-targeting chloride pump, into mouse retinal g"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21483674",
"endSection": "abstract",
"offsetInBeginSection": 724,
"offsetInEndSection": 1042,
"text": "Several weeks after the injection, whole-cell recordings made from sSC neurons in slice preparations revealed that yellow laser illumination of the eNpHR-expressing retino-tectal axons, putatively synapsing onto the recorded cells, effectively inhibited EPSCs evoked by electrical stimulation of the optic nerve layer."
}
] | 12 |
BioASQ-training12b
| null | null |
6415b3b4690f196b51000009
|
bioasq_factoid
|
factoid
|
Tofersen has been developed for treatment of which disease?
|
['amyotrophic lateral sclerosis']
|
[
"amyotrophic lateral sclerosis",
"ALS",
"Lou Gehrig's disease",
"motor neuron disease",
"charcot disease",
"maladie de Charcot"
] |
['Tofersen is an antisense oligonucleotide that mediates the degradation of superoxide dismutase 1 (SOD1) messenger RNA to reduce SOD1 protein synthesis is being studied for the treatment of amyotrophic lateral sclerosis due to SOD1 mutations.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/32640130",
"http://www.ncbi.nlm.nih.gov/pubmed/34704267"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32640130",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 416,
"text": "BACKGROUND: Tofersen is an antisense oligonucleotide that mediates the degradation of superoxide dismutase 1 (SOD1) messenger RNA to reduce SOD1 protein synthesis. Intrathecal administration of tofersen is being studied for the treatment of amyotrophic lateral sclerosis (ALS) due to SOD1 mutations.METHODS: We conducted a phase 1-2 ascending-dose trial evaluating tofersen in adults with ALS due to SOD1 mutations. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32640130",
"endSection": "abstract",
"offsetInBeginSection": 1797,
"offsetInEndSection": 1981,
"text": "CONCLUSIONS: In adults with ALS due to SOD1 mutations, CSF SOD1 concentrations decreased at the highest concentration of tofersen administered intrathecally over a period of 12 weeks. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32640130",
"endSection": "abstract",
"offsetInBeginSection": 164,
"offsetInEndSection": 325,
"text": "Intrathecal administration of tofersen is being studied for the treatment of amyotrophic lateral sclerosis (ALS) due to SOD1 mutations.METHODS: We conducted a ph"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32640130",
"endSection": "abstract",
"offsetInBeginSection": 155,
"offsetInEndSection": 285,
"text": "nthesis. Intrathecal administration of tofersen is being studied for the treatment of amyotrophic lateral sclerosis (ALS) due to S"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34704267",
"endSection": "abstract",
"offsetInBeginSection": 305,
"offsetInEndSection": 499,
"text": "ently, the results of a phase I/II study using the antisense oligonucleotides Tofersen to treat familial amyotrophic lateral sclerosis with superoxide dismutase 1 mutation have been reported. In"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32640130",
"endSection": "abstract",
"offsetInBeginSection": 152,
"offsetInEndSection": 287,
"text": " synthesis. Intrathecal administration of tofersen is being studied for the treatment of amyotrophic lateral sclerosis (ALS) due to SOD"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34704267",
"endSection": "abstract",
"offsetInBeginSection": 302,
"offsetInEndSection": 496,
"text": "Recently, the results of a phase I/II study using the antisense oligonucleotides Tofersen to treat familial amyotrophic lateral sclerosis with superoxide dismutase 1 mutation have been reported."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32640130",
"endSection": "abstract",
"offsetInBeginSection": 288,
"offsetInEndSection": 395,
"text": " mutations.METHODS: We conducted a phase 1-2 ascending-dose trial evaluating tofersen in adults with ALS du"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32640130",
"endSection": "abstract",
"offsetInBeginSection": 152,
"offsetInEndSection": 394,
"text": " synthesis. Intrathecal administration of tofersen is being studied for the treatment of amyotrophic lateral sclerosis (ALS) due to SOD1 mutations.METHODS: We conducted a phase 1-2 ascending-dose trial evaluating tofersen in adults with ALS d"
}
] | 11 |
BioASQ-training11b
| null | null |
602356b81cb411341a000099
|
bioasq_factoid
|
factoid
|
Which biological process takes place in nuclear speckles?
|
['mRNA processing', 'mRNA splicing']
|
[
"mRNA processing",
"mRNA splicing",
"messenger RNA processing",
"messenger RNA splicing",
"RNA processing",
"RNA splicing"
] |
['Speckles are subnuclear structures that are enriched in pre-messenger RNA splicing factors and are located in the interchromatin regions of the nucleoplasm of mammalian cells. They serve as splicing factor storage sites and play important roles in regulation of pre-mRNA splicing.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/12923522",
"http://www.ncbi.nlm.nih.gov/pubmed/12826600",
"http://www.ncbi.nlm.nih.gov/pubmed/12002677",
"http://www.ncbi.nlm.nih.gov/pubmed/29496966",
"http://www.ncbi.nlm.nih.gov/pubmed/23934081",
"http://www.ncbi.nlm.nih.gov/pubmed/27239700",
"http://www.ncbi.nlm.nih.gov/pubmed/30032211",
"http://www.ncbi.nlm.nih.gov/pubmed/29773831",
"http://www.ncbi.nlm.nih.gov/pubmed/30194269"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23934081",
"endSection": "abstract",
"offsetInBeginSection": 188,
"offsetInEndSection": 295,
"text": "Here we demonstrate that mRNAs containing ALREX-promoting elements are trafficked through nuclear speckles."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23934081",
"endSection": "abstract",
"offsetInBeginSection": 734,
"offsetInEndSection": 893,
"text": "Finally, we demonstrate that mRNAs lacking a poly(A)-tail are not efficiently exported by the ALREX pathway and show enhanced association with nuclear speckles"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12002677",
"endSection": "abstract",
"offsetInBeginSection": 138,
"offsetInEndSection": 521,
"text": " In a previous study (Melcák et al., 2001), it has been shown that the pre-spliceosomal assembly on microinjected splicing-competent precursor mRNA takes place in the speckles, and it has been suggested that the targeting of RNA into speckes consists of two interdependent steps, namely the diffusion process, followed by the energy-dependent translocation of RNA into the speckles. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12826600",
"endSection": "abstract",
"offsetInBeginSection": 250,
"offsetInEndSection": 445,
"text": "Nuclear speckles, a unique nuclear subcompartment, accumulate a family of proteins, namely, serine- and arginine-rich (SR) proteins. They play important roles in regulation of pre-mRNA splicing. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29496966",
"endSection": "abstract",
"offsetInBeginSection": 233,
"offsetInEndSection": 332,
"text": " Here we show that C3G localizes to SC35-positive nuclear speckles and regulates splicing activity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29496966",
"endSection": "abstract",
"offsetInBeginSection": 1247,
"offsetInEndSection": 1385,
"text": "Our results identify C3G and Rap1 as novel components of nuclear speckles and a role for C3G in regulating cellular RNA splicing activity."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29773831",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "DNAJC17 is localized in nuclear speckles and interacts with splicing machinery components."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30032211",
"endSection": "abstract",
"offsetInBeginSection": 470,
"offsetInEndSection": 552,
"text": "These results suggest that exosomal mRNA degradation mostly occurs outside of NSs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30194269",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 62,
"text": "Nuclear speckles (NSs) serve as splicing factor storage sites."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12923522",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 175,
"text": "Speckles are subnuclear structures that are enriched in pre-messenger RNA splicing factors and are located in the interchromatin regions of the nucleoplasm of mammalian cells."
}
] | 11 |
BioASQ-training11b
| null | null |
5c74266a7c78d694710000a2
|
bioasq_factoid
|
factoid
|
Which was the first adeno-associated virus vector gene therapy product approved in the United States?
|
['Luxturna']
|
[
"Luxturna",
"voretigene neparvovec",
"voretigene neparvovec-rzyl",
"LUXTURNA"
] |
['The first adeno-associated virus vector gene therapy product in the United States was Luxturna.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/30089698"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30089698",
"endSection": "abstract",
"offsetInBeginSection": 1755,
"offsetInEndSection": 2009,
"text": "Gene therapy utilizing viral vectors has experienced recent success, culminating in U.S. Food and Drug Administration approval of the first adeno-associated virus vector gene therapy product in the United States: Luxturna for inherited retinal dystrophy."
}
] | 11 |
BioASQ-training11b
| null | null |
5c897555d558e5f232000009
|
bioasq_factoid
|
factoid
|
Which is the target of the drug Denosumab?
|
[['receptor activator of nuclear factor-κB ligand', 'RANKL']]
|
[
"receptor activator of nuclear factor-κB ligand",
"RANKL",
"RANK ligand",
"receptor activator of NF-kB ligand",
"TNFSF11",
"OPGL",
"osteoprotegerin ligand"
] |
['Denosumab (Dmab) is a fully human monoclonal antibody against the receptor activator of nuclear factor-κB ligand (RANKL).']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26029270",
"http://www.ncbi.nlm.nih.gov/pubmed/26203221",
"http://www.ncbi.nlm.nih.gov/pubmed/26504466",
"http://www.ncbi.nlm.nih.gov/pubmed/26508890"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26029270",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 156,
"text": "Denosumab is a human monoclonal antibody which specifically blocks receptor activator of nuclear factor κB ligand and is a very potent antiresorptive drug. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26203221",
"endSection": "abstract",
"offsetInBeginSection": 560,
"offsetInEndSection": 606,
"text": "denosumab, a monoclonal antibody against RANKL"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26504466",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "Denosumab is a human monoclonal antibody indicated for the treatment of osteoporosis in postmenopausal women with a high risk of fractures. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26508890",
"endSection": "abstract",
"offsetInBeginSection": 466,
"offsetInEndSection": 776,
"text": "Denosumab (Dmab) is a fully human monoclonal antibody against the receptor activator of nuclear factor-κB ligand (RANKL), which, through the prevention of the RANKL/RANK interaction, inhibits osteoclast-mediated bone resorption and significantly reduces the risk of vertebral, nonvertebral, and hip fractures. "
}
] | 5 |
BioASQ-training5b
|
[] |
[] |
56e6ec49edfc094c1f000005
|
bioasq_factoid
|
factoid
|
Which value of nuchal translucency thickness is set as the threshold for high-risk for Down Syndrome?
|
['3mm']
|
[
"3 mm",
"3 millimeters",
"three millimeters",
"3mm"
] |
NT is physiological for a measurement < 3 mm but the incidence of chromosomal abnormalities (essentially trisomies 21, 18 and 13) increases when NT > or = 3 mm. As women aged, this upper NT threshold value changed according to gestational age. In women aged 35 to 37 years, combined prenatal screening was always positive when NT exceeded 2.8 mm, 3.0 mm, and 3.4 mm at 11, 12, and 13 weeks of gestation, respectively.
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/19416569",
"http://www.ncbi.nlm.nih.gov/pubmed/18726925",
"http://www.ncbi.nlm.nih.gov/pubmed/18461550",
"http://www.ncbi.nlm.nih.gov/pubmed/16912493",
"http://www.ncbi.nlm.nih.gov/pubmed/9471429"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19416569",
"endSection": "abstract",
"offsetInBeginSection": 511,
"offsetInEndSection": 610,
"text": "Combined prenatal screening was always positive for Down syndrome when NT thickness exceeded 4.0 mm"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19416569",
"endSection": "abstract",
"offsetInBeginSection": 695,
"offsetInEndSection": 867,
"text": "In women aged 35 to 37 years, combined prenatal screening was always positive when NT exceeded 2.8 mm, 3.0 mm, and 3.4 mm at 11, 12, and 13 weeks of gestation, respectively"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9471429",
"endSection": "abstract",
"offsetInBeginSection": 459,
"offsetInEndSection": 618,
"text": "NT is physiological for a measurement < 3 mm but the incidence of chromosomal abnormalities (essentially trisomies 21, 18 and 13) increases when NT > or = 3 mm"
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D048208",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D004314",
"http://www.disease-ontology.org/api/metadata/DOID:14250",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018566"
] |
[] |
53592c1e9a4572de6f000002
|
bioasq_factoid
|
factoid
|
What is the cause of lactose intolerance?
|
['Lactase deficiency']
|
[
"Lactase deficiency",
"Lactose intolerance",
"Lactose malabsorption",
"Lactase non-persistence",
"Lactase insufficiency"
] |
['Lactose intolerance is a common condition caused by lactase deficiency and may result in symptoms of lactose malabsorption (bloating, flatulence, abdominal discomfort, and change in bowel habits).\nFour clinical subtypes of lactose intolerance may be distinguished, namely lactase deficiency in premature infants, congenital lactase deficiency, adult-type hypolactasia and secondary lactase intolerance.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/32048961",
"http://www.ncbi.nlm.nih.gov/pubmed/31802224",
"http://www.ncbi.nlm.nih.gov/pubmed/32443748",
"http://www.ncbi.nlm.nih.gov/pubmed/30617948",
"http://www.ncbi.nlm.nih.gov/pubmed/31904838"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30617948",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 197,
"text": "Lactose intolerance is a common condition caused by lactase deficiency and may result in symptoms of lactose malabsorption (bloating, flatulence, abdominal discomfort, and change in bowel habits). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31802224",
"endSection": "abstract",
"offsetInBeginSection": 13,
"offsetInEndSection": 259,
"text": " Adult lactose intolerance (ALI) significantly alters calcium intake and absorption, and thus may promote osteoporosis. ALI is a recessive condition with a geographical north-south gradient characterised by decreased levels of intestinal lactase."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31904838",
"endSection": "abstract",
"offsetInBeginSection": 295,
"offsetInEndSection": 500,
"text": "Considerations include recognizing that a substantial proportion of the world's adult population (65%-70%) exhibits lactase nonpersistence, a reduced ability to metabolize lactose to glucose and galactose."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32048961",
"endSection": "abstract",
"offsetInBeginSection": 755,
"offsetInEndSection": 961,
"text": " Four clinical subtypes of lactose intolerance may be distinguished, namely lactase deficiency in premature infants, congenital lactase deficiency, adult-type hypolactasia and secondary lactase intolerance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32443748",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 443,
"text": "Lactose intolerance (LI) is characterized by the presence of primarily gastrointestinal clinical signs resulting from colonic fermentation of lactose, the absorption of which is impaired due to a deficiency in the lactase enzyme. These clinical signs can be modified by several factors, including lactose dose, residual lactase expression, concurrent ingestion of other dietary components, gut-transit time, and enteric microbiome composition."
}
] | 11 |
BioASQ-training11b
| null | null |
606b2b1994d57fd87900005c
|
bioasq_factoid
|
factoid
|
What the chromsomal location of the gene that is deleted in Potocki-Shaffer syndrome?
|
['11p11.2p12']
|
[
"11p11.2p12",
"11p11.2",
"11p12",
"11p11",
"chromosome 11 region p11.2 to p12"
] |
['In Potocki-Shaffer syndrome (PSS), the full phenotypic spectrum is manifested when deletions are at least 2.1\u2009Mb in size at 11p11.2', 'Potocki-Shaffer syndrome (PSS) is a rare contiguous gene deletion syndrome caused by heterozygous deletion of 11p11.2p12.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/23239541",
"http://www.ncbi.nlm.nih.gov/pubmed/15852040",
"http://www.ncbi.nlm.nih.gov/pubmed/28571721",
"http://www.ncbi.nlm.nih.gov/pubmed/19222835",
"http://www.ncbi.nlm.nih.gov/pubmed/28127865",
"http://www.ncbi.nlm.nih.gov/pubmed/15666301",
"http://www.ncbi.nlm.nih.gov/pubmed/20140962",
"http://www.ncbi.nlm.nih.gov/pubmed/26333423",
"http://www.ncbi.nlm.nih.gov/pubmed/22822387",
"http://www.ncbi.nlm.nih.gov/pubmed/25653495"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26333423",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "In Potocki-Shaffer syndrome (PSS), the full phenotypic spectrum is manifested when deletions are at least 2.1 Mb in size at 11p11.2"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25653495",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "Potocki-Shaffer syndrome (PSS, OMIM #601224) is a rare contiguous gene deletion syndrome caused by haploinsufficiency of genes located on the 11p11.2p12."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15852040",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "Potocki-Shaffer syndrome (PSS) is a contiguous gene deletion syndrome that results from haploinsufficiency of at least two genes within the short arm of chromosome 11[del(11)(p11.2p12)]. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15852040",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "Construction of a natural panel of 11p11.2 deletions and further delineation of the critical region involved in Potocki-Shaffer syndrome"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20140962",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 262,
"text": "Potocki-Shaffer syndrome is a rare contiguous gene deletion syndrome due to haploinsufficiency of the 11p11.2p12 region and is characterized by craniofacial abnormalities, developmental delay, intellectual disability, multiple exostoses, and biparietal foramina."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15666301",
"endSection": "abstract",
"offsetInBeginSection": 566,
"offsetInEndSection": 710,
"text": "This is also the first report describing deletion of 11p11.12-p11.2 and neocentromere formation resulting in inherited Potocki-Shaffer syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15852040",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "Potocki-Shaffer syndrome (PSS) is a contiguous gene deletion syndrome that results from haploinsufficiency of at least two genes within the short arm of chromosome 11[del(11)(p11.2p12)]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28571721",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Potocki-Shaffer Syndrome is a rare neurodevelopmental syndrome associated with microdeletion of a region of Chromosome 11p11.2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28127865",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 275,
"text": "Potocki-Shaffer syndrome is a contiguous gene deletion syndrome involving 11p11.2p12 and characterized by multiple exostoses, biparietal foramina, genitourinary anomalies in males, central nervous system abnormalities, intellectual disability, and craniofacial abnormalities."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15666301",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "Interstitial deletion 11(p11.12p11.2) and analphoid marker formation results in inherited Potocki-Shaffer syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23239541",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "Potocki-Shaffer syndrome (PSS) is a rare disorder caused by haploinsufficiency of genes located on the proximal short arm of chromosome 11 (11p11.2p12)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15852040",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 323,
"text": "Construction of a natural panel of 11p11.2 deletions and further delineation of the critical region involved in Potocki-Shaffer syndrome.Potocki-Shaffer syndrome (PSS) is a contiguous gene deletion syndrome that results from haploinsufficiency of at least two genes within the short arm of chromosome 11[del(11)(p11.2p12)]. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19222835",
"endSection": "abstract",
"offsetInBeginSection": 609,
"offsetInEndSection": 785,
"text": "The deletion (11p13-p12) located in the area between the deletions associated with the WAGR and Potocki-Shaffer syndromes had a maximum size of 8.5 Mb and encompasses 44 genes. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22822387",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 333,
"text": "Delayed Diagnosis of Potocki-Shaffer Syndrome in a Woman with Multiple Exostoses and Mental Retardation.We describe the case of an adult patient affected by multiple exostoses, severe mental retardation, epilepsy and facial dysmorphisms with a deletion of ∼2.3 Mb on chromosome 11p11.21, correlated to Potocki-Shaffer syndrome (PSS). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15666301",
"endSection": "abstract",
"offsetInBeginSection": 566,
"offsetInEndSection": 714,
"text": "This is also the first report describing deletion of 11p11.12-p11.2 and neocentromere formation resulting in inherited Potocki-Shaffer syndrome.<br>"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19222835",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 359,
"text": " WAGR syndrome (Wilms' tumor, aniridia, genitourinary abnormalities and mental retardation) and Potocki-Shaffer syndrome are rare contiguous gene deletion syndromes caused by deletions of the 11p14-p12 chromosome region.We present a patient with mental retardation, unilateral cataract, bilateral ptosis, genital abnormalities, seizures and a dysmorphic face."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19222835",
"endSection": "abstract",
"offsetInBeginSection": 467,
"offsetInEndSection": 643,
"text": "The deletion (11p13-p12) located in the area between the deletions associated with the WAGR and Potocki-Shaffer syndromes had a maximum size of 8.5 Mb and encompasses 44 genes."
}
] | 11 |
BioASQ-training11b
| null | null |
5c72b7277c78d69471000073
|
bioasq_factoid
|
factoid
|
Dinutuximab is used for treatment of which disease?
|
['neuroblastoma']
|
[
"neuroblastoma",
"neuroblastoma tumor",
"neuroblastic tumor",
"neuroblastoma cancer",
"neuroblastoma malignancy"
] |
['Dinutuximab, a monoclonal antibody against disialoganglioside, is used for treatment of high-risk neuroblastoma.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26934530",
"http://www.ncbi.nlm.nih.gov/pubmed/26917818",
"http://www.ncbi.nlm.nih.gov/pubmed/27756784",
"http://www.ncbi.nlm.nih.gov/pubmed/26791869",
"http://www.ncbi.nlm.nih.gov/pubmed/28748630",
"http://www.ncbi.nlm.nih.gov/pubmed/28061552",
"http://www.ncbi.nlm.nih.gov/pubmed/25940913",
"http://www.ncbi.nlm.nih.gov/pubmed/26891967",
"http://www.ncbi.nlm.nih.gov/pubmed/28389455"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26791869",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "PURPOSE: Dinutuximab (Unituxin™; ch14.18), a monoclonal antibody against disialoganglioside, improved survival as part of post-consolidation therapy for high-risk neuroblastoma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26891967",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 49,
"text": "Dinutuximab: A Review in High-Risk Neuroblastoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26891967",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 454,
"text": "Dinutuximab (ch14.18; Unituxin™) is a chimeric human-mouse monoclonal antibody that binds to the glycolipid antigen disialoganglioside, which is highly expressed on the surface of neuroblastoma cells. This intravenous drug is approved in the EU and USA as combination therapy with granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin (IL)-2 and isotretinoin for the postconsolidation treatment of patients with high-risk neuroblastoma. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26891967",
"endSection": "abstract",
"offsetInBeginSection": 1290,
"offsetInEndSection": 1592,
"text": "Dinutuximab administered in combination with GM-CSF, IL-2 and isotretinoin represents an important advance in the postconsolidation treatment of patients with high-risk neuroblastoma, with its benefits outweighing its risks in a patient population with a poor prognosis and limited therapeutic options."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26934530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 81,
"text": "Dinutuximab for the treatment of pediatric patients with high-risk neuroblastoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26934530",
"endSection": "abstract",
"offsetInBeginSection": 811,
"offsetInEndSection": 1128,
"text": "The combination of cytokines IL-2 and GM-CSF with the anti-GD2 MoAb ch14.18 (Dinutuximab) has shown a significant improvement in outcome for HR-NB. The FDA and EMA approved dinutuximab (Unituxin(R)) in 2015 for the treatment of patients with HR-NB who achieved at least a partial response after multimodality therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26917818",
"endSection": "abstract",
"offsetInBeginSection": 1507,
"offsetInEndSection": 1921,
"text": "Severe adverse effects of dinutuximab include pain, hypersensitivity reactions, capillary leak syndrome, and hypotension.<br><b>CONCLUSIONS</b>: Dinutuximab is the first anti-GD2 monoclonal antibody approved in combination with GM-CSF, IL-2, and RA for maintenance treatment of pediatric patients with high-risk neuroblastoma who achieve at least a partial response to first-line multiagent, multimodality therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26917818",
"endSection": "abstract",
"offsetInBeginSection": 974,
"offsetInEndSection": 1378,
"text": "Dinutuximab is a chimeric, human-murine, anti-GD2 monoclonal antibody approved in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), aldesleukin (interleukin-2 [IL-2]), and isotretinoin (13-cis-retinoic acid [RA]) for maintenance treatment of pediatric patients with high-risk neuroblastoma who achieve at least a partial response to first-line multiagent, multimodality therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28389455",
"endSection": "abstract",
"offsetInBeginSection": 793,
"offsetInEndSection": 1021,
"text": "The recommended dosage of dinutuximab is 17.5 mg/m<br><b>CONCLUSION</b>: Dinutuximab is a novel monoclonal antibody that is efficacious as part of combination immunotherapy in pediatric patients with high-risk neuroblastoma.<br>"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28748630",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 249,
"text": "Immunotherapy with the anti-GD2 monoclonal antibody ch14.18, or dinutuximab, represents an important therapeutic advance in the treatment of pediatric high-risk neuroblastoma and is now considered part of standard of care in this patient population."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28389455",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 484,
"text": "<b>PURPOSE</b>: The pharmacology, clinical efficacy, safety, dosage and administration, and role in therapy of dinutuximab for the treatment of high-risk pediatric neuroblastoma are reviewed.<br><b>SUMMARY</b>: Dinutuximab (Unituxin, United Therapeutics) is a novel monoclonal antibody recently approved for use in combination with granulocyte- macrophage colony-stimulating factor, interleukin-2, and isotretinoin for the treatment of pediatric patients with high-risk neuroblastoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25940913",
"endSection": "abstract",
"offsetInBeginSection": 798,
"offsetInEndSection": 1186,
"text": "This article summarizes the milestones in the development of dinutuximab leading to this first approval for use (in combination with granulocyte macrophage colony-stimulating factor, interleukin-2 and 13-cis retinoic acid) in the treatment of paediatric patients with high-risk neuroblastoma who achieve at least partial response to prior first-line multiagent, multimodality therapy.<br>"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25940913",
"endSection": "abstract",
"offsetInBeginSection": 491,
"offsetInEndSection": 635,
"text": "The US FDA has recently approved the use of dinutuximab combination therapy for the treatment of high-risk neuroblastoma in paediatric patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25940913",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "United Therapeutics Corporation and the National Cancer Institute are developing dinutuximab (Unituxin™; ch14.18), a monoclonal antibody targeting GD2, for the treatment of neuroblastoma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27756784",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 156,
"text": "TGFβR1 Blockade with Galunisertib (LY2157299) Enhances Anti-Neuroblastoma Activity of the Anti-GD2 Antibody Dinutuximab (ch14.18) with Natural Killer Cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27756784",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "PURPOSE: Immunotherapy of high-risk neuroblastoma using the anti-GD2 antibody dinutuximab induces antibody-dependent cell-mediated cytotoxicity (ADCC)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26917818",
"endSection": "abstract",
"offsetInBeginSection": 939,
"offsetInEndSection": 1343,
"text": "Dinutuximab is a chimeric, human-murine, anti-GD2 monoclonal antibody approved in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), aldesleukin (interleukin-2 [IL-2]), and isotretinoin (13-cis-retinoic acid [RA]) for maintenance treatment of pediatric patients with high-risk neuroblastoma who achieve at least a partial response to first-line multiagent, multimodality therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26917818",
"endSection": "abstract",
"offsetInBeginSection": 1596,
"offsetInEndSection": 1877,
"text": "CONCLUSIONS Dinutuximab is the first anti-GD2 monoclonal antibody approved in combination with GM-CSF, IL-2, and RA for maintenance treatment of pediatric patients with high-risk neuroblastoma who achieve at least a partial response to first-line multiagent, multimodality therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25940913",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 189,
"text": "United Therapeutics Corporation and the National Cancer Institute are developing dinutuximab (Unituxin™; ch14.18), a monoclonal antibody targeting GD2, for the treatment of neuroblastoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28389455",
"endSection": "abstract",
"offsetInBeginSection": 186,
"offsetInEndSection": 467,
"text": "SUMMARY Dinutuximab (Unituxin, United Therapeutics) is a novel monoclonal antibody recently approved for use in combination with granulocyte- macrophage colony-stimulating factor, interleukin-2, and isotretinoin for the treatment of pediatric patients with high-risk neuroblastoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28389455",
"endSection": "abstract",
"offsetInBeginSection": 1499,
"offsetInEndSection": 1661,
"text": "CONCLUSION Dinutuximab is a novel monoclonal antibody that is efficacious as part of combination immunotherapy in pediatric patients with high-risk neuroblastoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28061552",
"endSection": "abstract",
"offsetInBeginSection": 128,
"offsetInEndSection": 323,
"text": "Dinutuximab (formerly called ch14.18), a monoclonal antibody targeting the disialoganglioside GD2, has been shown to significantly improve survival rates in patients with high-risk neuroblastoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26891967",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 202,
"text": "Dinutuximab (ch14.18; Unituxin™) is a chimeric human-mouse monoclonal antibody that binds to the glycolipid antigen disialoganglioside, which is highly expressed on the surface of neuroblastoma cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25940913",
"endSection": "abstract",
"offsetInBeginSection": 493,
"offsetInEndSection": 637,
"text": "The US FDA has recently approved the use of dinutuximab combination therapy for the treatment of high-risk neuroblastoma in paediatric patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26934530",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 82,
"text": "Dinutuximab for the treatment of pediatric patients with high-risk neuroblastoma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28748630",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Transverse myelitis as an unexpected complication following treatment with dinutuximab in pediatric patients with high-risk neuroblastoma: A case series."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28061552",
"endSection": "abstract",
"offsetInBeginSection": 539,
"offsetInEndSection": 687,
"text": "Findings of the randomized phase III study (ANBL0032) led to the approval of dinutuximab for the treatment of children with high-risk neuroblastoma."
}
] | 11 |
BioASQ-training11b
|
[
"https://meshb.nlm.nih.gov/record/ui?ui=D013812",
"https://meshb.nlm.nih.gov/record/ui?ui=D004194"
] | null |
589a247078275d0c4a000035
|
bioasq_factoid
|
yesno
|
Is the consumption of chocolate associated with an increase in cardiovascular disease?
|
['no']
|
[
"no"
] |
['The consumption of natural polyphenol-rich foods, and cocoa in particular, has been related to a reduced risk of CVD, including coronary heart disease and stroke.', 'Chocolate consumption can reduce cardio-cerebrovascular risk.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/26936339",
"http://www.ncbi.nlm.nih.gov/pubmed/26983749",
"http://www.ncbi.nlm.nih.gov/pubmed/27493901",
"http://www.ncbi.nlm.nih.gov/pubmed/29141542",
"http://www.ncbi.nlm.nih.gov/pubmed/27164919",
"http://www.ncbi.nlm.nih.gov/pubmed/28356040",
"http://www.ncbi.nlm.nih.gov/pubmed/28824916",
"http://www.ncbi.nlm.nih.gov/pubmed/22169919",
"http://www.ncbi.nlm.nih.gov/pubmed/18827977",
"http://www.ncbi.nlm.nih.gov/pubmed/20858571",
"http://www.ncbi.nlm.nih.gov/pubmed/28324761",
"http://www.ncbi.nlm.nih.gov/pubmed/28649567",
"http://www.ncbi.nlm.nih.gov/pubmed/21666964",
"http://www.ncbi.nlm.nih.gov/pubmed/22653982",
"http://www.ncbi.nlm.nih.gov/pubmed/24274771",
"http://www.ncbi.nlm.nih.gov/pubmed/27088635",
"http://www.ncbi.nlm.nih.gov/pubmed/11790962"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28824916",
"endSection": "abstract",
"offsetInBeginSection": 82,
"offsetInEndSection": 244,
"text": "The consumption of natural polyphenol-rich foods, and cocoa in particular, has been related to a reduced risk of CVD, including coronary heart disease and stroke."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28649567",
"endSection": "abstract",
"offsetInBeginSection": 167,
"offsetInEndSection": 269,
"text": "chocolate has been shown to decrease CVD risk due to its antioxidant and anti-inflammatory properties."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28356040",
"endSection": "abstract",
"offsetInBeginSection": 284,
"offsetInEndSection": 528,
"text": "A number of studies have shown that dietary polyphenols exert a protective effect against hypertension, dyslipidemias, inflammation, endothelial function and atherosclerosis, conditions associated with increased risk for cardiovascular disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28324761",
"endSection": "abstract",
"offsetInBeginSection": 21,
"offsetInEndSection": 97,
"text": "Chocolate consumption may have a beneficial effect on cardiovascular health,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21666964",
"endSection": "abstract",
"offsetInBeginSection": 505,
"offsetInEndSection": 665,
"text": "Data currently available indicate that daily consumption of cocoa-rich chocolate (rich in polyphenols) may at least partially lower cardiovascular disease risk."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22653982",
"endSection": "abstract",
"offsetInBeginSection": 1308,
"offsetInEndSection": 1500,
"text": "CONCLUSIONS The blood pressure and cholesterol lowering effects of dark chocolate consumption are beneficial in the prevention of cardiovascular events in a population with metabolic syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22653982",
"endSection": "abstract",
"offsetInBeginSection": 1501,
"offsetInEndSection": 1610,
"text": "Daily dark chocolate consumption could be an effective cardiovascular preventive strategy in this population."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27493901",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "BACKGROUND The consumption of chocolate and cocoa has established cardiovascular benefits."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26936339",
"endSection": "abstract",
"offsetInBeginSection": 1586,
"offsetInEndSection": 1684,
"text": "CONCLUSIONS Chocolate consumption is associated with lower risk of MI and ischaemic heart disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26936339",
"endSection": "abstract",
"offsetInBeginSection": 959,
"offsetInEndSection": 1019,
"text": "Chocolate consumption was inversely associated with MI risk."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26936339",
"endSection": "abstract",
"offsetInBeginSection": 1538,
"offsetInEndSection": 1625,
"text": "Chocolate consumption is associated with lower risk of MI and ischaemic heart disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21666964",
"endSection": "abstract",
"offsetInBeginSection": 311,
"offsetInEndSection": 504,
"text": "The consumption of cocoa/ chocolate (i) increases plasma antioxidant capacity, (ii) diminishes platelet function and inflammation, and (iii) decreases diastolic and systolic arterial pressures."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26936339",
"endSection": "abstract",
"offsetInBeginSection": 915,
"offsetInEndSection": 975,
"text": "Chocolate consumption was inversely associated with MI risk."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20858571",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Chocolate consumption is inversely associated with prevalent coronary heart disease: the National Heart, Lung, and Blood Institute Family Heart Study."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26983749",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 165,
"text": "Daily chocolate consumption is inversely associated with insulin resistance and liver enzymes in the Observation of Cardiovascular Risk Factors in Luxembourg study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11790962",
"endSection": "abstract",
"offsetInBeginSection": 1523,
"offsetInEndSection": 1624,
"text": "Collectively, the antioxidant effects of flavonoid-rich foods may reduce cardiovascular disease risk."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24274771",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "The consumption of cocoa and dark chocolate is associated with a lower risk of CVD, and improvements in endothelial function may mediate this relationship"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22169919",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 249,
"text": "It has been shown that the consumption of cocoa has a positive influence on a number of cardiovascular surrogate parameters such as arterial vasodilatation and a moderate decrease in blood pressure in humans. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27164919",
"endSection": "abstract",
"offsetInBeginSection": 1317,
"offsetInEndSection": 1554,
"text": "This study has shown that increasing the polyphenol content of the diet via consumption of F&V, berries and dark chocolate results in a significant improvement in an established marker of cardiovascular risk in hypertensive participants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27088635",
"endSection": "abstract",
"offsetInBeginSection": 75,
"offsetInEndSection": 143,
"text": "Cocoa flavonoids exert cardiovascular benefits and neuroprotection. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29141542",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 136,
"text": "Accumulating evidence suggests potential preventive effects of chocolate/cocoa on the risk of cardio vascular disease (CVD)."
}
] | 11 |
BioASQ-training11b
|
[
"http://www.disease-ontology.org/api/metadata/DOID:1287",
"https://meshb.nlm.nih.gov/record/ui?ui=D000069956",
"https://meshb.nlm.nih.gov/record/ui?ui=D002318",
"https://meshb.nlm.nih.gov/record/ui?ui=D002099"
] | null |
5aa304f1d6d6b54f79000004
|
bioasq_yesno
|
yesno
|
Is there a role for TET proteins in invariant natural killer T cells (iNKT) cell fate?
|
['yes']
|
[
"yes"
] |
['Yes. Tet2-TET proteins regulate the lineage specification and TCR-mediated expansion of iNKT cells. TETs are ubiquitously expressed and play diverse roles in gene regulation, imprinting, insulation, intra/interchromosomal interactions, nuclear compartmentalisation, and alternative splicing. Depletion of Tet2 and its ligand, Tet3, from mouse CD4CD8 double-positive thymus-derived cardiomyocytes (iNKT) resulted in dysregulated development and proliferation, with increased expression of tumour suppressor genes and decreased', 'Yes. TET proteins regulate iNKT cell fate by ensuring their proper development and maturation and by suppressing aberrant proliferation mediated by the T cell antigen receptor (TCR).', 'Yes. Tet2-Tet3 double-knocked-out (DKO) iNKT cells displayed pronounced skew toward the NKT17 lineage, with increased DNA methylation and impaired expression of genes encoding the key lineage-specifying factors T-bet and ThPok. Moreover, simultaneous deletion of Tet2 and Tet3 in mouse CD4CD8 double-positive thymocytes resulted in dysregulated development and proliferation of the non-classical major histocomponent complex (MHC) CD1d, which presents lipid antigens to T-cell-derived', 'Yes. Tet2-Tet3 proteins regulate the lineage specification and TCR-mediated expansion of iNKT cells. Indeed, deletion of Tet2 and Tet3 in mouse CD4CD8 double-positive thymus cells resulted in dysregulated development and proliferation of the non-classical major histocompromised T cell antigen receptor (MHC) protein CD1d, which presents lipid antigens to iNKB-derived cells. Moreover, overexpression of TET1 and TET3 in Drosophila melanogaster T cells (iN', 'Yes. Tet2-Tet3 double-knockout (DKO) cells displayed pronounced skewing toward the NKT17 lineage, with increased DNA methylation and impaired expression of genes encoding the key lineage-specifying factors T-bet and ThPOK. Mutations in exon 2 interfere with the synthesis of the full-length isoform of Tet2 and lead to the production of a shortened isoform, Tet2s. These mutations have been found in human natural killer T cells (iNKTs), the most common type of innate immune cells.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/27869820"
] |
[
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27869820",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "TET proteins regulate the lineage specification and TCR-mediated expansion of iNKT cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27869820",
"endSection": "abstract",
"offsetInBeginSection": 102,
"offsetInEndSection": 985,
"text": "We found that simultaneous deletion of Tet2 and Tet3 in mouse CD4+CD8+ double-positive thymocytes resulted in dysregulated development and proliferation of invariant natural killer T cells (iNKT cells). Tet2-Tet3 double-knockout (DKO) iNKT cells displayed pronounced skewing toward the NKT17 lineage, with increased DNA methylation and impaired expression of genes encoding the key lineage-specifying factors T-bet and ThPOK. Transfer of purified Tet2-Tet3 DKO iNKT cells into immunocompetent recipient mice resulted in an uncontrolled expansion that was dependent on the nonclassical major histocompatibility complex (MHC) protein CD1d, which presents lipid antigens to iNKT cells. Our data indicate that TET proteins regulate iNKT cell fate by ensuring their proper development and maturation and by suppressing aberrant proliferation mediated by the T cell antigen receptor (TCR)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27869820",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "TET proteins regulate the lineage specification and TCR-mediated expansion of iNKT cells ."
}
] | 11 |
BioASQ-training11b
| null | null |
5e36994092b3349b55000002
|
bioasq_yesno
|
factoid
|
From which sequence does the Alu repeat originate from?
|
[['7SL RNA']]
|
[
"7SL RNA",
"7SL RNA molecule",
"7SL RNA gene",
"7SL RNA transcript",
"7SL RNA species"
] |
['The presence of Alu-like structural motifs supports the hypothesis of the monophyletic origin of Alu and B1 repeats, i.e., from a common 7SL RNA-derived retroposing monomeric element, The origin of Alu subfamilies in human populations may be related to evolution of chromosome Y.']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/16343813",
"http://www.ncbi.nlm.nih.gov/pubmed/12167372",
"http://www.ncbi.nlm.nih.gov/pubmed/9694666",
"http://www.ncbi.nlm.nih.gov/pubmed/9395063",
"http://www.ncbi.nlm.nih.gov/pubmed/8576966",
"http://www.ncbi.nlm.nih.gov/pubmed/12815945"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16343813",
"endSection": "abstract",
"offsetInBeginSection": 164,
"offsetInEndSection": 298,
"text": "The origin of Alu-derived minisatellites appears to have been mediated by short flanking repeats, as first proposed by Haber and Louis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12167372",
"endSection": "abstract",
"offsetInBeginSection": 1207,
"offsetInEndSection": 1327,
"text": "Finally, we propose that the origin of Alu subfamilies in human populations may be related to evolution of chromosome Y."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9694666",
"endSection": "abstract",
"offsetInBeginSection": 354,
"offsetInEndSection": 536,
"text": "Our analysis indicates that about 60 Myr ago, before the prosimian divergence, free left and right monomers formed an Alu heterodimer connected by a 19-nucleotide-long A-rich linker."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8576966",
"endSection": "abstract",
"offsetInBeginSection": 662,
"offsetInEndSection": 844,
"text": "the presence of Alu-like structural motifs supports the hypothesis of the monophyletic origin of Alu and B1 repeats, i.e., from a common 7SL RNA-derived retroposing monomeric element"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12815945",
"endSection": "abstract",
"offsetInBeginSection": 191,
"offsetInEndSection": 326,
"text": "Alu elements are each a dimer of similar, but not identical, fragments of total size about 300 bp, and originate from the 7SL RNA gene."
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D020087"
] |
[] |
56ffd08bcf1c325851000009
|
bioasq_factoid
|
factoid
|
What is the major adverse effect of adriamycin(doxorubicin)?
|
[['Cardiotoxicity', 'Cardiac toxicity']]
|
[
"Cardiotoxicity",
"Cardiac toxicity",
"Heart toxicity",
"Cardiac damage",
"Cardiac injury"
] |
['Cardiac toxicity is a major adverse effect caused by doxorubicin (DOX) therapy. In spite of the routine use of this drug its major adverse effect, the dose-dependent cardiotoxicity, cannot be prevented yet. Cardiotoxicity is a major adverse effect of the anthracycline antibiotics and can be acute or chronic.', 'Cardiac toxicity is a major adverse effect caused by doxorubicin (DOX) therapy ', 'Cardiac toxicity is a major adverse effect caused by doxorubicin (DOX) therapy ', 'Cardiac toxicity is a major adverse effect caused by doxorubicin (DOX) therapy ', 'Cardiac toxicity is a major adverse effect caused by doxorubicin (DOX) therapy ', 'Cardiac toxicity is a major adverse effect caused by doxorubicin (DOX) therapy ']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/21295102",
"http://www.ncbi.nlm.nih.gov/pubmed/15997091",
"http://www.ncbi.nlm.nih.gov/pubmed/15114698",
"http://www.ncbi.nlm.nih.gov/pubmed/12445862",
"http://www.ncbi.nlm.nih.gov/pubmed/12074691",
"http://www.ncbi.nlm.nih.gov/pubmed/3461747",
"http://www.ncbi.nlm.nih.gov/pubmed/3459397",
"http://www.ncbi.nlm.nih.gov/pubmed/3947104",
"http://www.ncbi.nlm.nih.gov/pubmed/7325994"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7325994",
"endSection": "abstract",
"offsetInBeginSection": 972,
"offsetInEndSection": 1158,
"text": "It remains to be seen whether inhibition by adriamycin of these systems is related to the severe cardiotoxicity, the major adverse effect of the drug that limits its clinical usefulness."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3947104",
"endSection": "abstract",
"offsetInBeginSection": 961,
"offsetInEndSection": 1058,
"text": "Leukocytopenia was the major adverse effect among patients undergoing systemic THP administration"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3459397",
"endSection": "abstract",
"offsetInBeginSection": 536,
"offsetInEndSection": 589,
"text": "The major adverse effect was bone-marrow suppression;"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3461747",
"endSection": "abstract",
"offsetInBeginSection": 813,
"offsetInEndSection": 866,
"text": "The major adverse effect was bone marrow suppression;"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12074691",
"endSection": "abstract",
"offsetInBeginSection": 644,
"offsetInEndSection": 746,
"text": "Cardiotoxicity is a major adverse effect of the anthracycline antibiotics and can be acute or chronic;"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12074691",
"endSection": "abstract",
"offsetInBeginSection": 864,
"offsetInEndSection": 1034,
"text": "chronic cardiotoxicity represents a serious adverse effect that may be lethal due to the development of irreversible, cumulative dose-dependent, congestive cardiomyopathy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12074691",
"endSection": "abstract",
"offsetInBeginSection": 380,
"offsetInEndSection": 642,
"text": "Myelosuppression, predominantly neutropenia and leucopenia, is the dose-limiting toxicity; in addition to this, mucositis, nausea, vomiting and alopecia are frequent, whereas hepatopathy, characterised by elevated bilirubin concentrations, occurs less frequently"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12445862",
"endSection": "abstract",
"offsetInBeginSection": 115,
"offsetInEndSection": 240,
"text": "In spite of the routine use of this drug its major adverse effect, the dose-dependent cardiotoxicity, cannot be prevented yet"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15114698",
"endSection": "abstract",
"offsetInBeginSection": 389,
"offsetInEndSection": 434,
"text": "The major adverse effect was myelosuppression"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15997091",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 78,
"text": "Cardiac toxicity is a major adverse effect caused by doxorubicin (DOX) therapy"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15997091",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 107,
"text": "Antioxidative and cardioprotective effects of Phyllanthus urinaria L. on doxorubicin-induced cardiotoxicity"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21295102",
"endSection": "abstract",
"offsetInBeginSection": 55,
"offsetInEndSection": 164,
"text": "The major adverse effect of DOX treatment in cancer patients is the onset of cardiomyopathy and heart failure"
}
] | 5 |
BioASQ-training5b
|
[
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D004317",
"http://www.biosemantics.org/jochem#4269440"
] |
[] |
53551206a0726bee57000001
|
bioasq_factoid
|
factoid
|
What year was the first successful human heart transplant performed?
|
['1967']
|
[
"1967"
] |
['The first human heart transplant in 1967 was performed using a deceased donor heart,', 'the first human heart transplant in 1967 was performed using a deceased donor heart,']
|
[
"http://www.ncbi.nlm.nih.gov/pubmed/11391041",
"http://www.ncbi.nlm.nih.gov/pubmed/18702960",
"http://www.ncbi.nlm.nih.gov/pubmed/15056065",
"http://www.ncbi.nlm.nih.gov/pubmed/15726762",
"http://www.ncbi.nlm.nih.gov/pubmed/32493185",
"http://www.ncbi.nlm.nih.gov/pubmed/15061629",
"http://www.ncbi.nlm.nih.gov/pubmed/19287813",
"http://www.ncbi.nlm.nih.gov/pubmed/30083541",
"http://www.ncbi.nlm.nih.gov/pubmed/29191294",
"http://www.ncbi.nlm.nih.gov/pubmed/31102725",
"http://www.ncbi.nlm.nih.gov/pubmed/6378042",
"http://www.ncbi.nlm.nih.gov/pubmed/25795463",
"http://www.ncbi.nlm.nih.gov/pubmed/29664541",
"http://www.ncbi.nlm.nih.gov/pubmed/29262951",
"http://www.ncbi.nlm.nih.gov/pubmed/10272755",
"http://www.ncbi.nlm.nih.gov/pubmed/16009314",
"http://www.ncbi.nlm.nih.gov/pubmed/29492391",
"http://www.ncbi.nlm.nih.gov/pubmed/32065475"
] |
[
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31102725",
"endSection": "abstract",
"offsetInBeginSection": 474,
"offsetInEndSection": 558,
"text": "the first human heart transplant in 1967 was performed using a deceased donor heart,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15056065",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "In 1967, Christian Barnard performed the first successful human-to-human heart transplant."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16009314",
"endSection": "abstract",
"offsetInBeginSection": 204,
"offsetInEndSection": 411,
"text": "Since the first successful human heart transplant performed by Christiaan Barnard in 1967, there has been substantial progress in the field of heart transplantation, especially over the last several decades."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30083541",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 230,
"text": "In 2017, we celebrated the 50th anniversary of the first human heart transplant that had been carried out by the South African surgeon, Christiaan ('Chris') Barnard at Groote Schuur Hospital in Cape Town on December 3rd, 1967. The"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18702960",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "It has been 40 years since the first human-to-human heart transplant performed in South Africa by Christiaan Barnard in December 1967"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16009314",
"endSection": "abstract",
"offsetInBeginSection": 209,
"offsetInEndSection": 417,
"text": " the first successful human heart transplant performed by Christiaan Barnard in 1967, there has been substantial progress in the field of heart transplantation, especially over the last several decades. With "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11391041",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 190,
"text": "Since the first human heart transplantation was performed in 1967, the field of heart transplantation has advanced to the point where survival and acceptable quality of life are commonplace."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29492391",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "The first human-to-human heart transplant was performed 50 years ago in 1967"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32493185",
"endSection": "abstract",
"offsetInBeginSection": 92,
"offsetInEndSection": 435,
"text": "Since the first human-to-human heart transplantation, performed in 1967, advances in organ donation, surgical techniques, organ preservation, perioperative care, immunologic risk assessment, immunosuppression agents, monitoring of graft function and surveillance of long-term complications have drastically increased recipient survival. Howeve"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31102725",
"endSection": "abstract",
"offsetInBeginSection": 474,
"offsetInEndSection": 729,
"text": "the first human heart transplant in 1967 was performed using a deceased donor heart, the advent of brain death criteria and the ability to avoid long warm ischemic times led donation after cardiac death (DCD) transplantation to fall out of favor. Due the "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15726762",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "The Human Tissue Act of 1983 had its origin in the first successful heart transplant operation performed by Professor Christiaan Barnard and his team in December 1967"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29191294",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 134,
"text": "It has been 50 years since Dr. Christiaan Barnard performed the first human-to-human heart transplant in December 1967 in South Africa"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32065475",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "The first successful human heart transplantation was reported on 3 December 1967, by Christiaan Barnard in South Africa."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6378042",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "The world's first human-to-human heart transplant was performed at Groote Schuur Hospital on the 2nd December 1967."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29664541",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 138,
"text": "50 years have passed since the first human to human heart transplantation, performed by Christiaan Barnard in Cape Town December 3rd 1967."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19287813",
"endSection": "abstract",
"offsetInBeginSection": 296,
"offsetInEndSection": 386,
"text": "In 1967, he led the team that performed the world's first human-to-human heart transplant."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25795463",
"endSection": "abstract",
"offsetInBeginSection": 127,
"offsetInEndSection": 383,
"text": " a century. From the repair of the first septal defect in 1953, followed by the first successful heart transplant in 1967, and later to the first infusion of bone marrow-derived cells to the human myocardium in 2002, significant progress has been made in h"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29262951",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Article on the first heart transplant, performed at Groote Schuur Hospital, Cape Town, on 3 December 1967."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10272755",
"endSection": "abstract",
"offsetInBeginSection": 140,
"offsetInEndSection": 297,
"text": "On December 3, 1967, in Cape Town, South Africa, Dr. Christian Barnard revolutionized organ transplantation with the first successful human heart transplant."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15061629",
"endSection": "abstract",
"offsetInBeginSection": 240,
"offsetInEndSection": 414,
"text": "Barnard performed the 1st human-to-human orthotopic heart transplantation in 1967 and followed this by introducing the technique of heterotopic heart transplantation in 1974."
}
] | 11 |
BioASQ-training11b
| null | null |
601ee4c61cb411341a000066
|
bioasq_factoid
|
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