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yesno | Does AZD3759 cross the blood brain barrier? | ['yes'] | [
"yes"
]
| ['AZD3759 is a novel EGFR tyrosine kinase inhibitor with high capability to penetrate the blood-brain barrier.', 'AZD3759 is an EGFR tyrosine kinase inhibitors (TKIs) with excellent blood-brain barrier (BBB) penetration.', 'Yes, AZD3759 cross the blood brain barrier.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/27928026",
"http://www.ncbi.nlm.nih.gov/pubmed/29430654",
"http://www.ncbi.nlm.nih.gov/pubmed/29056570",
"http://www.ncbi.nlm.nih.gov/pubmed/28625644",
"http://www.ncbi.nlm.nih.gov/pubmed/26898616"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29430654",
"endSection": "abstract",
"offsetInBeginSection": 97,
"offsetInEndSection": 201,
"text": "AZD3759, an EGFR tyrosine kinase inhibitors (TKIs) with excellent blood-brain barrier (BBB) penetration,"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27928026",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "AZD3759, a BBB-penetrating EGFR inhibitor for the treatment of EGFR mutant NSCLC with CNS metastases"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27928026",
"endSection": "abstract",
"offsetInBeginSection": 630,
"offsetInEndSection": 779,
"text": "We report the discovery and early clinical development of AZD3759, a selective EGFR inhibitor that can fully penetrate the blood-brain barrier (BBB),"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29056570",
"endSection": "abstract",
"offsetInBeginSection": 196,
"offsetInEndSection": 305,
"text": "AZD3759 is a novel EGFR tyrosine kinase inhibitor with high capability to penetrate the blood-brain barrier. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27928026",
"endSection": "abstract",
"offsetInBeginSection": 630,
"offsetInEndSection": 863,
"text": "We report the discovery and early clinical development of AZD3759, a selective EGFR inhibitor that can fully penetrate the blood-brain barrier (BBB), with equal free concentrations in the blood, cerebrospinal fluid, and brain tissue."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26898616",
"endSection": "abstract",
"offsetInBeginSection": 1004,
"offsetInEndSection": 1229,
"text": "Another promising class of EGFR TKI such as AZD3759 has been designed to penetrate blood brain barrier to treat brain metastases and leptomeningeal disease and has showed promising responses in patients with brain metastases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29056570",
"endSection": "abstract",
"offsetInBeginSection": 196,
"offsetInEndSection": 304,
"text": "AZD3759 is a novel EGFR tyrosine kinase inhibitor with high capability to penetrate the blood-brain barrier."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29430654",
"endSection": "abstract",
"offsetInBeginSection": 62,
"offsetInEndSection": 301,
"text": "In our study, we demonstrated that AZD3759, an EGFR tyrosine kinase inhibitors (TKIs) with excellent blood-brain barrier (BBB) penetration, combined with radiation enhanced the antitumor efficacy in BM model from EGFR mutant (EGFRm) NSCLC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26898616",
"endSection": "abstract",
"offsetInBeginSection": 1017,
"offsetInEndSection": 1241,
"text": "sing class of EGFR TKI such as AZD3759 has been designed to penetrate blood brain barrier to treat brain metastases and leptomeningeal disease and has showed promising responses in patients with brain metastases. Acquired re"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27928026",
"endSection": "abstract",
"offsetInBeginSection": 643,
"offsetInEndSection": 880,
"text": " discovery and early clinical development of AZD3759, a selective EGFR inhibitor that can fully penetrate the blood-brain barrier (BBB), with equal free concentrations in the blood, cerebrospinal fluid, and brain tissue. Treatment with A"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27928026",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "AZD3759, a BBB-penetrating EGFR inhibitor for the treatment of EGFR mutant NSCLC with CNS metastases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29430654",
"endSection": "abstract",
"offsetInBeginSection": 65,
"offsetInEndSection": 312,
"text": "our study, we demonstrated that AZD3759, an EGFR tyrosine kinase inhibitors (TKIs) with excellent blood-brain barrier (BBB) penetration, combined with radiation enhanced the antitumor efficacy in BM model from EGFR mutant (EGFRm) NSCLC. Besides, t"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27928026",
"endSection": "abstract",
"offsetInBeginSection": 1087,
"offsetInEndSection": 1221,
"text": " in patients with BM and LM treated with AZD3759 confirms its BBB-penetrant properties and antitumor activities. Our data demonstrate "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29056570",
"endSection": "abstract",
"offsetInBeginSection": 3432,
"offsetInEndSection": 3584,
"text": "ood penetration of the blood-brain barrier by AZD3759, and its promising clinical activity, support further assessment of this compound in studies.FUNDI"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28625644",
"endSection": "abstract",
"offsetInBeginSection": 899,
"offsetInEndSection": 1194,
"text": "The next generation EGFR TKIs osimertinib and AZD3759 have improved BBB penetration and the BLOOM study of osimertinib and AZD3759 has reported highly promising intracranial efficacy and may herald a new frontier to treat this therapeutically challenging subset of advanced EGFR mutant patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29430654",
"endSection": "abstract",
"offsetInBeginSection": 1124,
"offsetInEndSection": 1319,
"text": "The results showed the BBB penetration of AZD3759 was decreased within 24 hr after radiation, however, the free concentration of AZD3759 in brain kept at a high level in the context of radiation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29430654",
"endSection": "abstract",
"offsetInBeginSection": 1038,
"offsetInEndSection": 1123,
"text": "We also detected the BBB penetration of AZD3759 when combined with cranial radiation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29056570",
"endSection": "abstract",
"offsetInBeginSection": 3430,
"offsetInEndSection": 3583,
"text": " good penetration of the blood-brain barrier by AZD3759, and its promising clinical activity, support further assessment of this compound in studies.FUND"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29056570",
"endSection": "abstract",
"offsetInBeginSection": 3380,
"offsetInEndSection": 3544,
"text": "n pretreated with a tyrosine kinase inhibitor. The good penetration of the blood-brain barrier by AZD3759, and its promising clinical activity, support further asse"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27928026",
"endSection": "abstract",
"offsetInBeginSection": 1064,
"offsetInEndSection": 1199,
"text": "An early clinical study in patients with BM and LM treated with AZD3759 confirms its BBB-penetrant properties and antitumor activities."
}
]
| 11 | BioASQ-training11b | null | null | 5e67cd6b1af46fc13000001e | 215 |
yesno | Do bacteria from the genus Morexella cause respiratory infections? | ['yes'] | [
"yes"
]
| ['Bacteria from the genus Morexella can cause respiratory infections'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/8007629",
"http://www.ncbi.nlm.nih.gov/pubmed/24786571"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24786571",
"endSection": "abstract",
"offsetInBeginSection": 746,
"offsetInEndSection": 918,
"text": "gainst pathogens associated with respiratory tract ailments [Staphylococcus aureus (ATCC 25923), Klebsiella pneumoniae (ATCC 13883) and Morexella cattarhalis (ATCC 14468)] "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8007629",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 438,
"text": "The efficacy and safety of oral ofloxacin, 400 mg once daily, for the treatment of patients with lower respiratory tract infections were studied. The most common species recovered from the sputum specimens of these patients were Haemophilus influenzae, followed by Streptococcus pneumoniae (S. pneumoniae), Staphylococcus aureus (S. aureus), Gram positive cocci unidentified, Pseudomonas aeruginosa (P. aeruginosa), Morexella catarrhalis,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8007629",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 773,
"text": "the efficacy and safety of oral ofloxacin 400 mg once daily for the treatment of patients with lower respiratory tract infections were studied the most common species recovered from the sputum specimens of these patients were haemophilus influenzae followed by streptococcus pneumoniae s pneumoniae staphylococcus aureus s aureus gram positive cocci unidentified pseudomonas aeruginosa p aeruginosa morexella catarrhalis streptococcus epidermidis and another haemophilus species in this order all these bacteria were susceptible to ofloxacin except for one strain of methicillin resistant s aureus a satisfactory clinical outcome was achieved in 34 of 40 patients 85 it is concluded that ofloxacin 400 mg once daily is useful for patients with respiratory tract infections."
}
]
| 11 | BioASQ-training11b | [
"https://meshb.nlm.nih.gov/record/ui?ui=D001419",
"https://meshb.nlm.nih.gov/record/ui?ui=D012141",
"https://meshb.nlm.nih.gov/record/ui?ui=D012818"
]
| null | 5a679875b750ff4455000004 | 216 |
yesno | Does International Citicoline Trial on acUte Stroke trial supports efficacy of citicoline for stroke treatment? | ['no'] | [
"no"
]
| ['No. The International Citicoline Trial on acUte Stroke (ICTUS) found that citocoline is not efficacious in the treatment of moderate-to-severe acute ischaemic stroke.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/27072975",
"http://www.ncbi.nlm.nih.gov/pubmed/22691567",
"http://www.ncbi.nlm.nih.gov/pubmed/23600725"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27072975",
"endSection": "abstract",
"offsetInBeginSection": 794,
"offsetInEndSection": 1098,
"text": "The meta-analysis showed that no significant differences were found in the long-term mortality (OR=0.91, 95% CI 0.07 to 1.09, P=0.30), the rate of dependency (OR=1.02, 95% CI 0.87 to 1.24, P=0.85), and the effective rate (OR=0.98, 95% CI 0.84 to 1.14, P=0.82) between citicoline group and control group. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27072975",
"endSection": "abstract",
"offsetInBeginSection": 1282,
"offsetInEndSection": 1498,
"text": " In conclusion, citicolne cannot reduce long-term mortality and dependence rate in the treatment of acute stroke, and the effective rate of citivoline may be not better than that of controls but with reliable safety."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23600725",
"endSection": "abstract",
"offsetInBeginSection": 68,
"offsetInEndSection": 368,
"text": "In humans, although a recent trial International Citicoline Trial on Acute Stroke (ICTUS) has shown that global recovery is similar in CDP-choline and placebo groups, CDP-choline was shown to be more beneficial in some patients, such as those with moderate stroke severity and not treated with t-PA. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22691567",
"endSection": "abstract",
"offsetInBeginSection": 1902,
"offsetInEndSection": 2054,
"text": "INTERPRETATION: Under the circumstances of the ICTUS trial, citicoline is not efficacious in the treatment of moderate-to-severe acute ischaemic stroke."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22691567",
"endSection": "abstract",
"offsetInBeginSection": 1480,
"offsetInEndSection": 1594,
"text": "The trial was stopped for futility at the third interim analysis on the basis of complete data from 2078 patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22691567",
"endSection": "abstract",
"offsetInBeginSection": 1714,
"offsetInEndSection": 1802,
"text": "Global recovery was similar in both groups (odds ratio 1·03, 95% CI 0·86-1·25; p=0·364)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22691567",
"endSection": "abstract",
"offsetInBeginSection": 1919,
"offsetInEndSection": 2070,
"text": "INTERPRETATION Under the circumstances of the ICTUS trial, citicoline is not efficacious in the treatment of moderate-to-severe acute ischaemic stroke."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23600725",
"endSection": "abstract",
"offsetInBeginSection": 68,
"offsetInEndSection": 455,
"text": "In humans, although a recent trial International Citicoline Trial on Acute Stroke (ICTUS) has shown that global recovery is similar in CDP-choline and placebo groups, CDP-choline was shown to be more beneficial in some patients, such as those with moderate stroke severity and not treated with t-PA. Several mechanisms have been proposed to explain the beneficial actions of CDP-choline."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23600725",
"endSection": "abstract",
"offsetInBeginSection": 68,
"offsetInEndSection": 367,
"text": "In humans, although a recent trial International Citicoline Trial on Acute Stroke (ICTUS) has shown that global recovery is similar in CDP-choline and placebo groups, CDP-choline was shown to be more beneficial in some patients, such as those with moderate stroke severity and not treated with t-PA."
}
]
| 11 | BioASQ-training11b | [
"https://meshb.nlm.nih.gov/record/ui?ui=D013812",
"https://meshb.nlm.nih.gov/record/ui?ui=D020521"
]
| null | 58ec709aeda5a5767200000e | 217 |
yesno | Is c-met involved in the activation of the Akt pathway? | ['yes'] | [
"yes"
]
| HGF-induced activation of c-Met is playing a pivotal role in the stimulation of c-Src activation, resulting in induction of phosphatidylinositol 3-kinase complexes p85α/p110α and p85α/p110δ, which is required for Akt-mediated activation of mammalian target of rapamycin, with consequent inhibition of IκB kinase and nuclear factor-κB activation, resulting in enhanced cell survival. | [
"http://www.ncbi.nlm.nih.gov/pubmed/23345546",
"http://www.ncbi.nlm.nih.gov/pubmed/23229794",
"http://www.ncbi.nlm.nih.gov/pubmed/22820099",
"http://www.ncbi.nlm.nih.gov/pubmed/22789825",
"http://www.ncbi.nlm.nih.gov/pubmed/21687953",
"http://www.ncbi.nlm.nih.gov/pubmed/21536148",
"http://www.ncbi.nlm.nih.gov/pubmed/20233866",
"http://www.ncbi.nlm.nih.gov/pubmed/19850646",
"http://www.ncbi.nlm.nih.gov/pubmed/18262389",
"http://www.ncbi.nlm.nih.gov/pubmed/18234991",
"http://www.ncbi.nlm.nih.gov/pubmed/17942284",
"http://www.ncbi.nlm.nih.gov/pubmed/17464994",
"http://www.ncbi.nlm.nih.gov/pubmed/17258200",
"http://www.ncbi.nlm.nih.gov/pubmed/16278380",
"http://www.ncbi.nlm.nih.gov/pubmed/15522281",
"http://www.ncbi.nlm.nih.gov/pubmed/14570904",
"http://www.ncbi.nlm.nih.gov/pubmed/11821397",
"http://www.ncbi.nlm.nih.gov/pubmed/10714768"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23345546",
"endSection": "abstract",
"offsetInBeginSection": 421,
"offsetInEndSection": 726,
"text": "Amplification of MET has been reported in approximately 5%-22% of lung tumors with acquired resistance to small-molecule inhibitors of the epidermal growth factor receptor (EGFR). Resistance to EGFR inhibitors is likely mediated through downstream activation of the phosphoinositide 3-kinase /AKT pathway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23345546",
"endSection": "abstract",
"offsetInBeginSection": 727,
"offsetInEndSection": 965,
"text": "Simultaneous treatment of resistant tumors with a MET inhibitor plus an EGFR inhibitor can abrogate activation of downstream effectors of cell growth, proliferation, and survival, thereby overcoming acquired resistance to EGFR inhibitors."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23229794",
"endSection": "abstract",
"offsetInBeginSection": 839,
"offsetInEndSection": 885,
"text": "HGF mediated both ERK and Akt phosphorylation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23229794",
"endSection": "abstract",
"offsetInBeginSection": 1263,
"offsetInEndSection": 1360,
"text": "ERK/Akt signaling, but not the Smad pathway, may be one of the main processes in HGF-induced EMT,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23229794",
"endSection": "abstract",
"offsetInBeginSection": 1442,
"offsetInEndSection": 1503,
"text": "The MAPK/Akt pathway is indispensable in HGF/c-Met signaling."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22820099",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "Inhibition of c-Met activation sensitizes osteosarcoma cells to cisplatin via suppression of the PI3K-Akt signaling"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22820099",
"endSection": "abstract",
"offsetInBeginSection": 933,
"offsetInEndSection": 1083,
"text": "Specifically, we demonstrated that inhibition of c-Met activity led to suppression of the PI3K-Akt pathway, thus enhancing cisplatin chemosensitivity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22820099",
"endSection": "abstract",
"offsetInBeginSection": 1084,
"offsetInEndSection": 1245,
"text": "Our study clearly suggests that inhibition of c-Met activity can effectively sensitize osteosarcoma cells to cisplatin via suppression of the PI3K-Akt signaling."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22789825",
"endSection": "abstract",
"offsetInBeginSection": 604,
"offsetInEndSection": 806,
"text": "We found that a dual Met/VEGF receptor 2 kinase inhibitor, E7050, circumvented HGF-induced EGFR-TKI resistance in EGFR mutant lung cancer cell lines by inhibiting the Met/Gab1/PI3K/Akt pathway in vitro."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21687953",
"endSection": "abstract",
"offsetInBeginSection": 514,
"offsetInEndSection": 728,
"text": "Here, we report that i) treatment of RL95-2 cells with HGF resulted in phosphorylation of the HGF receptor c-Met, activation of Akt and IκB, translocation of NF-κB into the nucleus, and up-regulation of COX-2 mRNA;"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21687953",
"endSection": "abstract",
"offsetInBeginSection": 1062,
"offsetInEndSection": 1205,
"text": "Our data suggest that HGF possesses chemotactic ability, has anti-apoptosis action, and induces cellular infiltration via the PI3K/Akt pathway;"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21536148",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "Hepatocyte growth factor-induced c-Src-phosphatidylinositol 3-kinase-AKT-mammalian target of rapamycin pathway inhibits dendritic cell activation by blocking IκB kinase activity"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21536148",
"endSection": "abstract",
"offsetInBeginSection": 715,
"offsetInEndSection": 938,
"text": "Activation of c-Src in turn establishes a complex consisting of phosphatidylinositol 3-kinase and c-MET, and promotes downstream activation of the phosphatidylinositol 3-kinase/AKT pathway and mammalian target of rapamycin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21536148",
"endSection": "abstract",
"offsetInBeginSection": 1150,
"offsetInEndSection": 1443,
"text": "Notably, hepatocyte growth factor-stimulated c-Src activation results in induction of phosphatidylinositol 3-kinase complexes p85α/p110α and p85α/p110δ, which is required for activation of mammalian target of rapamycin, and consequent inhibition of IκB kinase and nuclear factor-κB activation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21536148",
"endSection": "abstract",
"offsetInBeginSection": 1444,
"offsetInEndSection": 1735,
"text": "Our findings, for the first time, have identified the c-Src-phosphatidylinositol 3-kinase-AKT-mammalian target of rapamycin pathway that plays a pivotal role in mediating the inhibitory effects of hepatocyte growth factor on dendritic cell activation by blocking nuclear factor-κB signaling."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20233866",
"endSection": "abstract",
"offsetInBeginSection": 1280,
"offsetInEndSection": 1487,
"text": "Cyr61 siRNA inhibited a second phase of Akt phosphorylation measured 12 hours after cell stimulation with HGF and also inhibited HGF-induced phosphorylation of the Akt target glycogen synthase kinase 3alpha."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19850646",
"endSection": "abstract",
"offsetInBeginSection": 1342,
"offsetInEndSection": 1594,
"text": "HGF+EGF treatment increased the duration of ERK1/2 and AKT activation compared to HGF or EGF alone. All these data indicate that a crosstalk between the EGF and HGF pathways in mammary epithelial cells may modulate the development of the mammary gland."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18262389",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Hepatocyte growth factor and c-Met promote dendritic maturation during hippocampal neuron differentiation via the Akt pathway"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18262389",
"endSection": "abstract",
"offsetInBeginSection": 758,
"offsetInEndSection": 1053,
"text": "Consistent with these results, HGF activated Akt, which phosphorylates glycogen synthase kinase-3beta (GSK-3beta) to inactivate it, and reduced phosphorylation of microtubule-associated protein 2 (MAP2), which can promote microtubule polymerization and dendrite elongation when dephosphorylated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18262389",
"endSection": "abstract",
"offsetInBeginSection": 1054,
"offsetInEndSection": 1374,
"text": "Conversely, pharmacological inhibition of c-Met with its specific inhibitor, PHA-665752, or genetic knock-down of c-Met with short hairpin RNAs (shRNAs) suppressed HGF-induced phosphorylation of Akt and GSK-3beta, increased phosphorylation of MAP2, and reduced dendrite number and length in cultured hippocampal neurons."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18262389",
"endSection": "abstract",
"offsetInBeginSection": 1458,
"offsetInEndSection": 1699,
"text": "Inhibiting Akt activity with the phosphoinositide-3-kinase inhibitor LY294002 or Akt inhibitor X suppressed HGF-induced phosphorylation of GSK-3beta, increased MAP2 phosphorylation, and blocked the ability of HGF to enhance dendritic length."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18262389",
"endSection": "abstract",
"offsetInBeginSection": 1700,
"offsetInEndSection": 1844,
"text": "These observations indicate that HGF and c-Met can regulate the early stages of dendrite maturation via activation of the Akt/GSK-3beta pathway."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18234991",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 111,
"text": "Involvement of PI3K/Akt signaling pathway in hepatocyte growth factor-induced migration of uveal melanoma cells"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18234991",
"endSection": "abstract",
"offsetInBeginSection": 1031,
"offsetInEndSection": 1415,
"text": "HGF was found to enhance cell migration, and that HGF-induced migration depends on PI3K/Akt pathway. The activation of PI3K/Akt pathway induced by the HGF/c-Met axis is involved in the downregulation of cell adhesion molecules E-cadherin and beta-catenin, contributing to the attenuation of cell-cell adhesion and promoting the enhanced motility and migration of uveal melanoma cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17942284",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 122,
"text": "HGF protects cultured cortical neurons against hypoxia/reoxygenation induced cell injury via ERK1/2 and PI-3K/Akt pathways"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17942284",
"endSection": "abstract",
"offsetInBeginSection": 462,
"offsetInEndSection": 528,
"text": "HGF stimulated both ERK1/2 and Akt activities in cortical neurons."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17942284",
"endSection": "abstract",
"offsetInBeginSection": 529,
"offsetInEndSection": 718,
"text": "Inhibition of ERK activation completely abolished the protective effects of HGF, and inhibition of Akt activation reduced, but did not completely eliminate the HGF mediated neuroprotection."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17942284",
"endSection": "abstract",
"offsetInBeginSection": 719,
"offsetInEndSection": 837,
"text": "It is suggested that the neuroprotection of HGF depend on ERK1/2 pathway, and, to a lesser extent, PI-3K/Akt pathway. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17464994",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 107,
"text": "Met signals hepatocyte survival by preventing Fas-triggered FLIP degradation in a PI3k-Akt-dependent manner"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17464994",
"endSection": "abstract",
"offsetInBeginSection": 1318,
"offsetInEndSection": 1488,
"text": "Thus, Met acting on PI3K and Akt ensures high levels of FLIPL, and disruption of this pathway contributes to hepatic apoptosis and possibly to Fas-related liver diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17258200",
"endSection": "abstract",
"offsetInBeginSection": 744,
"offsetInEndSection": 990,
"text": "The HGF-induced increase in Nkx 2.5 expression was inhibited by co-treatment with the PI3 kinase inhibitors Wortmannin and LY294002, but not by its inactive homolog LY303511, suggesting an involvement of the PI3 kinase/Akt pathway in this effect."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16278380",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "X-Linked inhibitor of apoptosis protein expression level in colorectal cancer is regulated by hepatocyte growth factor/C-met pathway via Akt signaling"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16278380",
"endSection": "abstract",
"offsetInBeginSection": 1263,
"offsetInEndSection": 1347,
"text": "Activation of XIAP expression by HGF was inhibited by siRNA targeting Akt1 and Akt2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16278380",
"endSection": "abstract",
"offsetInBeginSection": 1361,
"offsetInEndSection": 1419,
"text": "Activation of C-MET enhances XIAP through the Akt pathway."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15522281",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "Hepatocyte growth factor prevents ventricular remodeling and dysfunction in mice via Akt pathway and angiogenesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15522281",
"endSection": "abstract",
"offsetInBeginSection": 1167,
"offsetInEndSection": 1331,
"text": "A significant reduction in apoptosis in the HGF-treated hearts was observed compared with control hearts, and was strongly associated with increased Akt activation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15522281",
"endSection": "abstract",
"offsetInBeginSection": 1461,
"offsetInEndSection": 1546,
"text": "The antiapoptotic effect of HGF was mediated by activation of PI3-kinase/Akt pathway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14570904",
"endSection": "abstract",
"offsetInBeginSection": 508,
"offsetInEndSection": 874,
"text": "The protective effect of HGF/SF against the ADR-induced apoptosis was abolished in the presence of either LY294002, an inhibitor of phosphatidylinositol-3'-OH kinase (PI3-K) or 1L-6-hydroxymethyl-chiro-inositol 2-(R)-2-O-methyl-3-O-octadecylcarbonate, an inhibitor of Akt, thus implicating the activation of PI3-K-Akt signaling in the antiapoptotic action of HGF/SF."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14570904",
"endSection": "abstract",
"offsetInBeginSection": 875,
"offsetInEndSection": 985,
"text": "Immunoblotting analysis revealed that HGF/SF stimulated the sustained phosphorylation of Akt for several hours"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14570904",
"endSection": "abstract",
"offsetInBeginSection": 1048,
"offsetInEndSection": 1185,
"text": "Furthermore, ADR-induced activation of caspase-9, a downstream molecule of Akt, was inhibited for at least 24 h after HGF/SF stimulation,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14570904",
"endSection": "abstract",
"offsetInBeginSection": 1479,
"offsetInEndSection": 1656,
"text": "These results indicate that HGF/SF, but not EGF, transmitted protective signals against ADR-induced apoptosis by causing sustained activation of the PI3-K-Akt signaling pathway."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11821397",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 186,
"text": "Hepatocyte growth factor/scatter factor inhibits UVB-induced apoptosis of human keratinocytes but not of keratinocyte-derived cell lines via the phosphatidylinositol 3-kinase/AKT pathway"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11821397",
"endSection": "abstract",
"offsetInBeginSection": 349,
"offsetInEndSection": 575,
"text": "When we analyzed the signaling pathways initiated by the HGF/SF receptor c-met, we found that the phosphatidylinositol (PI) 3-kinase and its downstream-element AKT and the mitogen-activated protein (MAP) kinase were activated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11821397",
"endSection": "abstract",
"offsetInBeginSection": 576,
"offsetInEndSection": 728,
"text": "Inhibition of PI 3-kinase led to a complete abrogation of the anti-apoptotic effect of HGF/SF, whereas blockade of the MAP kinase pathway had no effect."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10714768",
"endSection": "abstract",
"offsetInBeginSection": 1261,
"offsetInEndSection": 1411,
"text": "We now show in detached cells a cooperative effect of HGF and FN in the activation of PI 3-kinase and on the phosphorylation of PKB/Akt at serine 473."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10714768",
"endSection": "abstract",
"offsetInBeginSection": 1412,
"offsetInEndSection": 1554,
"text": "PI 3-kinase activity is also required for the HGF- and fibronectin-induced survival responses, as well as anchorage-independent colony growth."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10714768",
"endSection": "abstract",
"offsetInBeginSection": 1645,
"offsetInEndSection": 1964,
"text": "Together, these results demonstrate that the PI 3-kinase/Akt pathway is a key effector of the HGF- and fibronectin-induced survival response of breast carcinoma cells under detached conditions and corroborate an interaction between integrin and HGF/ Met signalling pathways in the development of invasive breast cancer."
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D051057",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D019859",
"http://www.uniprot.org/uniprot/SLTM_HUMAN",
"http://www.uniprot.org/uniprot/AKT1_HUMAN",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0043491",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0048012",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0051896"
]
| []
| 5318a955b166e2b806000020 | 218 |
yesno | Are mutations in the STXBP1 gene associated with epilepsy? | ['yes'] | [
"yes"
]
| ['Yes,mutations in STXBP1 gene, encoding the syntaxin binding protein 1, have been recently described in Ohtahara syndrome, or early infantile epileptic encephalopathy with suppression-burst pattern, and in other early-onset epileptic encephalopathies.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/24315539",
"http://www.ncbi.nlm.nih.gov/pubmed/24189369",
"http://www.ncbi.nlm.nih.gov/pubmed/24170257",
"http://www.ncbi.nlm.nih.gov/pubmed/24095819",
"http://www.ncbi.nlm.nih.gov/pubmed/23531706",
"http://www.ncbi.nlm.nih.gov/pubmed/23409955",
"http://www.ncbi.nlm.nih.gov/pubmed/22787626",
"http://www.ncbi.nlm.nih.gov/pubmed/22787616",
"http://www.ncbi.nlm.nih.gov/pubmed/22722545",
"http://www.ncbi.nlm.nih.gov/pubmed/22709267",
"http://www.ncbi.nlm.nih.gov/pubmed/22612257",
"http://www.ncbi.nlm.nih.gov/pubmed/22596016",
"http://www.ncbi.nlm.nih.gov/pubmed/21967765",
"http://www.ncbi.nlm.nih.gov/pubmed/21762454",
"http://www.ncbi.nlm.nih.gov/pubmed/21770924",
"http://www.ncbi.nlm.nih.gov/pubmed/21753172",
"http://www.ncbi.nlm.nih.gov/pubmed/21364700",
"http://www.ncbi.nlm.nih.gov/pubmed/21062273",
"http://www.ncbi.nlm.nih.gov/pubmed/20887371",
"http://www.ncbi.nlm.nih.gov/pubmed/20887364",
"http://www.ncbi.nlm.nih.gov/pubmed/20876469",
"http://www.ncbi.nlm.nih.gov/pubmed/20845763",
"http://www.ncbi.nlm.nih.gov/pubmed/20493457",
"http://www.ncbi.nlm.nih.gov/pubmed/19557857",
"http://www.ncbi.nlm.nih.gov/pubmed/18469812",
"http://www.ncbi.nlm.nih.gov/pubmed/21204804",
"http://www.ncbi.nlm.nih.gov/pubmed/21277190"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24315539",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "Folinic acid responsive epilepsy in Ohtahara syndrome caused by STXBP1 mutation."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24170257",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "A novel mutation in STXBP1 gene in a child with epileptic encephalopathy and an atypical electroclinical pattern."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24170257",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 246,
"text": "Mutations in STXBP1 gene, encoding the syntaxin binding protein 1, have been recently described in Ohtahara syndrome, or early infantile epileptic encephalopathy with suppression-burst pattern, and in other early-onset epileptic encephalopathies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24095819",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 278,
"text": "STXBP1 (MUNC18.1), encoding syntaxin binding protein 1, has been reported in Ohtahara syndrome, a rare epileptic encephalopathy with suppression burst pattern on EEG, in patients with infantile spasms and in a few patients with nonsyndromic mental retardation without epilepsy. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23531706",
"endSection": "abstract",
"offsetInBeginSection": 176,
"offsetInEndSection": 368,
"text": "ed with severe developmental delay and poor prognosis. Mutations and deletions in the STXBP1 gene are associated with Ohtahara syndrome, also known as \"early infantile epileptic encephalopathy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22787616",
"endSection": "abstract",
"offsetInBeginSection": 204,
"offsetInEndSection": 382,
"text": "Here we show that de novo heterozygous mutations in the gene encoding STXBP1, also known as MUNC18-1, which is essential in synaptic vesicle release in multiple species, cause OS"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22722545",
"endSection": "abstract",
"offsetInBeginSection": 1105,
"offsetInEndSection": 1278,
"text": "STXBP1 haploinsufficiency results in progressive encephalopathy characterized by intellectual disability and may be accompanied by epilepsy, movement disorders, and autism. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22596016",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 242,
"text": "Mutations of the syntaxin binding protein 1 (STXBP1) have been associated with severe infantile epileptic encephalopathies (Ohtahara syndrome and West syndrome), but also with moderate to severe cognitive impairment and nonsyndromic epilepsy."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22596016",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 66,
"text": "A novel STXBP1 mutation causes focal seizures with neonatal onset."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20887364",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 92,
"text": "STXBP1 mutations in early infantile epileptic encephalopathy with suppression-burst pattern."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20887364",
"endSection": "abstract",
"offsetInBeginSection": 10,
"offsetInEndSection": 148,
"text": "e novo STXBP1 mutations have been found in individuals with early infantile epileptic encephalopathy with suppression-burst pattern (EIEE)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21762454",
"endSection": "abstract",
"offsetInBeginSection": 1876,
"offsetInEndSection": 2087,
"text": "Mutations in STXBP1 are relatively frequent in patients with infantile epileptic encephalopathies. STXBP1-related encephalopathy may present as drug-responsive infantile spasms with focal/lateralized discharges."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21753172",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 65,
"text": "De novo SCN1A mutations in migrating partial seizures of infancy."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18469812",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "De novo mutations in the gene encoding STXBP1 (MUNC18-1) cause early infantile epileptic encephalopathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23409955",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 170,
"text": "Mutations in STXBP1 have been identified in a subset of patients with early onset epileptic encephalopathy (EE), but the full phenotypic spectrum remains to be delineated"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22787626",
"endSection": "abstract",
"offsetInBeginSection": 621,
"offsetInEndSection": 704,
"text": "and STXBP1-related West/Ohtahara syndromes, are due to a mutation in a unique gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21204804",
"endSection": "abstract",
"offsetInBeginSection": 720,
"offsetInEndSection": 829,
"text": "This is the first case report showing that STXBP1 mutations caused West syndrome from the onset of epilepsy. "
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D009154",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D004829",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D059645",
"http://www.uniprot.org/uniprot/STXB1_PONAB",
"http://www.disease-ontology.org/api/metadata/DOID:1826"
]
| []
| 550748a3bde8548216000001 | 219 |
yesno | Is Cri du Chat syndrome (CdCS) a genetic syndrome caused by deletions in the long arm of chromosome 5 | ['no'] | [
"no"
]
| ['No, Cri du Chat syndrome (CdCS) is caused by a partial deletion of the short arm (5p) of chromosome 5, not the long arm.', 'Cri du Chat syndrome (CdCS) is caused by deletions in the short arm of chromosome 5 (5p-), not the long arm, with an incidence ranging from 1:15,000 to 1:50,000 live births. It presents with a high-pitched monochromatic cry and various clinical features such as microcephaly, facial abnormalities, and severe psychomotor and mental retardation. Diagnosis can be confirmed through karyotype or FISH analysis.', 'No, Cri-du-chat syndrome is not caused by deletions in the long arm of chromosome 5. It is caused by deletions in the short arm of chromosome 5, specifically designated as 5p-', 'Yes, Cri du Chat syndrome (CdCS) is a genetic syndrome caused by deletions in the short arm of chromosome 5.', 'No. Cri du Chat syndrome (CDCS) is caused by a deletion in the short arm of chromosome 5 (5p).', 'No, Cri-du-chat syndrome (CdCS) is not caused by deletions in the long arm of chromosome 5, but rather it is a genetic disorder caused by deletions in the short arm of chromosome 5, as confirmed by karyotype testing.', 'Cri du Chat syndrome (CdCS) is a genetic syndrome caused by deletions in the short arm of chromosome 5', 'No, Cri-du-chat syndrome (CdCS) is not a genetic syndrome caused by deletions in the long arm of chromosome 5.', 'No, Cri du Chat syndrome (CdCS) is not caused by deletions in the long arm of chromosome 5. It is caused by a partial deletion of the short arm (5p) of chromosome 5.', 'No, Cri du Chat syndrome (CdCS) is a genetic syndrome caused by deletions in the short arm of chromosome 5.', 'No, Cri du Chat syndrome (CdCS) is a genetic syndrome caused by deletions in the short arm of chromosome 5 (5p-).', 'No, Cri-du-chat syndrome is caused by deletions in the short arm of chromosome 5 (5p-).', 'No, Cri du Chat syndrome is caused by deletions in the short arm of chromosome 5.', 'No, Cri du Chat syndrome (CdCS) is caused by deletions in the short arm of chromosome 5.', 'No, Cri du Chat syndrome (CDCS) is caused by deletions in the short arm of chromosome 5.', 'No, Cri-du-chat syndrome is caused by deletions in the short arm of chromosome 5, not the long arm.', 'No, Cri du Chat syndrome (CdCS) is a genetic disorder caused by deletions in the short arm (p) of chromosome 5.', "No, it's caused by deletions on the short arm of chromosome 5.", 'No, Cri du Chat syndrome (CdCS) is a genetic syndrome caused by deletions in the short arm of chromosome 5, not the long arm.', 'No, Cri du Chat syndrome (CdCS) is a genetic syndrome caused by deletions in the short arm of chromosome 5', 'No, Cri-du-chat syndrome (CdCS) is not caused by deletions in the long arm of chromosome 5. It is caused by deletions in the short arm of chromosome 5.', 'No, Cri du Chat syndrome (CdCS) is not caused by deletions in the long arm of chromosome 5. It is caused by deletions in the short arm of chromosome 5 (5p-), which are greater than 10 Mb.', "No, it's caused by deletions in the short arm of chromosome 5."] | [
"http://www.ncbi.nlm.nih.gov/pubmed/20038906",
"http://www.ncbi.nlm.nih.gov/pubmed/25236835",
"http://www.ncbi.nlm.nih.gov/pubmed/36242045",
"http://www.ncbi.nlm.nih.gov/pubmed/18437967",
"http://www.ncbi.nlm.nih.gov/pubmed/31187941",
"http://www.ncbi.nlm.nih.gov/pubmed/22921333",
"http://www.ncbi.nlm.nih.gov/pubmed/10424821",
"http://www.ncbi.nlm.nih.gov/pubmed/32800423",
"http://www.ncbi.nlm.nih.gov/pubmed/19239081",
"http://www.ncbi.nlm.nih.gov/pubmed/34434412",
"http://www.ncbi.nlm.nih.gov/pubmed/31836684",
"http://www.ncbi.nlm.nih.gov/pubmed/37908952",
"http://www.ncbi.nlm.nih.gov/pubmed/28004033",
"http://www.ncbi.nlm.nih.gov/pubmed/25514263",
"http://www.ncbi.nlm.nih.gov/pubmed/29460462",
"http://www.ncbi.nlm.nih.gov/pubmed/15657623",
"http://www.ncbi.nlm.nih.gov/pubmed/31568707",
"http://www.ncbi.nlm.nih.gov/pubmed/30711802",
"http://www.ncbi.nlm.nih.gov/pubmed/26059676",
"http://www.ncbi.nlm.nih.gov/pubmed/11238681",
"http://www.ncbi.nlm.nih.gov/pubmed/18484284",
"http://www.ncbi.nlm.nih.gov/pubmed/28523196",
"http://www.ncbi.nlm.nih.gov/pubmed/36660031",
"http://www.ncbi.nlm.nih.gov/pubmed/27144168",
"http://www.ncbi.nlm.nih.gov/pubmed/34394178",
"http://www.ncbi.nlm.nih.gov/pubmed/1978567",
"http://www.ncbi.nlm.nih.gov/pubmed/30587166",
"http://www.ncbi.nlm.nih.gov/pubmed/7713510",
"http://www.ncbi.nlm.nih.gov/pubmed/26601658",
"http://www.ncbi.nlm.nih.gov/pubmed/37465584",
"http://www.ncbi.nlm.nih.gov/pubmed/23455788",
"http://www.ncbi.nlm.nih.gov/pubmed/36338241",
"http://www.ncbi.nlm.nih.gov/pubmed/32739788",
"http://www.ncbi.nlm.nih.gov/pubmed/16953888"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36660031",
"endSection": "abstract",
"offsetInBeginSection": 14,
"offsetInEndSection": 276,
"text": "Cri-du-chat syndrome is generally diagnosed when patients present a high-pitched cry at birth, microcephaly, ocular hypertelorism, and prominent nasal bridge. The karyotype is useful to confirm deletions in the short arm of chromosome 5 (5p-) greater than 10 Mb."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37908952",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 106,
"text": "Cri-du-chat syndrome (CdCS) is a rare genetic disorder in which the short arm of chromosome 5 is deleted. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37908952",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "Cri-du-chat syndrome (CdCS) is a rare genetic disorder in which the short arm of chromosome 5 is deleted"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25514263",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 165,
"text": "Cri du chat syndrome (CdcS), also known as 5p deletion syndrome is a genetic disorder caused by the partial deletion of chromatin from the short arm of chromosome 5."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25514263",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 236,
"text": "Cri du chat syndrome (CdcS), also known as 5p deletion syndrome is a genetic disorder caused by the partial deletion of chromatin from the short arm of chromosome 5. There is a paucity of literature on the dental manifestations in CdcS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25514263",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 423,
"text": "Cri du chat syndrome (CdcS), also known as 5p deletion syndrome is a genetic disorder caused by the partial deletion of chromatin from the short arm of chromosome 5. There is a paucity of literature on the dental manifestations in CdcS. The purposes of this report are to present the case of a nine-year-old girl with the syndrome, CdcS and to review its dental and clinical manifestations and their management in children."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20038906",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 213,
"text": "A new syndrome was identified in 1963, when Lejeune et al. reported a genetic disease resulting from a partial or total deletion on the short arm of chromosome 5 (5p-) and named it the cri du chat syndrome (CdCS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20038906",
"endSection": "abstract",
"offsetInBeginSection": 59,
"offsetInEndSection": 213,
"text": "reported a genetic disease resulting from a partial or total deletion on the short arm of chromosome 5 (5p-) and named it the cri du chat syndrome (CdCS)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20038906",
"endSection": "abstract",
"offsetInBeginSection": 59,
"offsetInEndSection": 383,
"text": "reported a genetic disease resulting from a partial or total deletion on the short arm of chromosome 5 (5p-) and named it the cri du chat syndrome (CdCS). This term makes reference to the main clinical feature of the syndrome, a high-pitched monochromatic cat-like crying, that usually disappears in the first years of life."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20038906",
"endSection": "abstract",
"offsetInBeginSection": 59,
"offsetInEndSection": 508,
"text": "reported a genetic disease resulting from a partial or total deletion on the short arm of chromosome 5 (5p-) and named it the cri du chat syndrome (CdCS). This term makes reference to the main clinical feature of the syndrome, a high-pitched monochromatic cat-like crying, that usually disappears in the first years of life. CdCS is one of the most common chromosomal deletion syndromes in humans, with an incidence of 1:15.000-1:50.000 live-births."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25236835",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "BACKGROUND: Cri du Chat Syndrome (CdCS) is rare and occurs as a result of a partial deletion in the short arm of chromosome 5. There are no reports in the literature from the West African sub-region and indeed very few "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20038906",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 383,
"text": "A new syndrome was identified in 1963, when Lejeune et al. reported a genetic disease resulting from a partial or total deletion on the short arm of chromosome 5 (5p-) and named it the cri du chat syndrome (CdCS). This term makes reference to the main clinical feature of the syndrome, a high-pitched monochromatic cat-like crying, that usually disappears in the first years of life."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16953888",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 145,
"text": "The Cri du Chat syndrome (CdCS) is a genetic disease resulting from a deletion of variable size occurring on the short arm of chromosome 5 (5p-)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29460462",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "BACKGROUND: Cri du Chat syndrome (CdCS) is a genetic syndrome caused by deletions in the short arm of chromosome 5."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23455788",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 139,
"text": "The cri du chat syndrome (CdCS) is a chromosomal deletion syndrome associated with a partial deletion of the short (p) arm of chromosome 5."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32800423",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 243,
"text": "INTRODUCTION: Cri-du-Chat Syndrome (CdCS) is a genetic condition due to deletions showing different breakpoints encompassing a critical region on the short arm of chromosome 5, located between p15.2 and p15.3, first defined by Niebuhr in 1978."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30711802",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 134,
"text": "The Cri du Chat Syndrome (CdCS) is a genetic disease resulting from variable size deletion occurring on the short arm of chromosome 5."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10424821",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 84,
"text": "Cri du chat syndrome is associated with a deletion on the short arm of chromosome 5."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7713510",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "The deletion of the short arm of chromosome 5 is associated with the cri-du-chat syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31836684",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "Cri du chat syndrome (CDCS) is a rare genetic disease that is caused by a deletion in the short arm of chromosome 5 (5p)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28004033",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "The Cri du Chat syndrome (CdC) is a rare genetic disorder caused by variable size deletions of the short arm of chromosome 5 (5p-)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26059676",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 105,
"text": "The cri-du-chat syndrome is a rare genetic disorder caused by deletions in the short arm of chromosome 5."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22921333",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "BACKGROUND: Cri du chat syndrome (CCS) is a genetic disorder resulting from the deletion of the short arm of c"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37465584",
"endSection": "abstract",
"offsetInBeginSection": 108,
"offsetInEndSection": 225,
"text": "The human gene is located on the short arm of chromosome 5, the region deleted in Cri-du-chat syndrome (OMIM #123450)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36242045",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 171,
"text": "Cri du chat (also called 5p deletion, or monosomy 5p) syndrome is a genetic disease caused by deletions of various lengths in the short (p) arm of chromosome 5"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28004033",
"endSection": "abstract",
"offsetInBeginSection": 4,
"offsetInEndSection": 124,
"text": "Cri du Chat syndrome (CdC) is a rare genetic disorder caused by variable size deletions of the short arm of chromosome 5"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19239081",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 126,
"text": "The Cri du Chat Syndrome (CdCS) is one of the most common deletion syndromes, involving the short arm of chromosome 5, with an"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28523196",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 95,
"text": "Cri du Chat syndrome (CdC) is a chromosomal abnormality (deletion of short arm of chromosome 5)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25514263",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "Cri du chat syndrome (CdcS), also known as 5p deletion syndrome is a genetic disorder caused by the partial deletion of chromatin from the short arm of chromosome 5. There is a"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20038906",
"endSection": "abstract",
"offsetInBeginSection": 59,
"offsetInEndSection": 268,
"text": "reported a genetic disease resulting from a partial or total deletion on the short arm of chromosome 5 (5p-) and named it the cri du chat syndrome (CdCS). This term makes reference to the main clinical feature"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36338241",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 262,
"text": "BACKGROUND: Cri du chat syndrome (CdCS), also known as 5p deletion syndrome (5p-) is a syndrome caused by partial deletion of the 5p chromosome in human beings. The incidence accounts for 1/50000 and the cause of CdCS is related to partial deletion of chromosome"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10424821",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "Cri du chat syndrome is associated with a deletion on the short arm of chromosome 5. The main diagnostic feature"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30587166",
"endSection": "abstract",
"offsetInBeginSection": 937,
"offsetInEndSection": 1552,
"text": " those found in patients with Cri-du-chat Syndrome (CdCS). CdCS is a genetic disease resulting from a deletion of variable size occurring on the short arm of chromosome 5 (5p-), whose main feature is a high-pitched mewing cry in infancy, accompanied by multiple congenital anomalies, intellectual disability, microcephaly and facial dysmorphism.CONCLUSIONS: The absence of some CdCS features in the current patient could be due to the fact that in her case the critical regions responsible do not lie within the identified deletion. In fact, a literature review revealed a high degree of concordance between the cli"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36242045",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 172,
"text": "BACKGROUND: Cri du chat (also called 5p deletion, or monosomy 5p) syndrome is a genetic disease caused by deletions of various lengths in the short (p) arm of chromosome 5."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37908952",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 105,
"text": "Cri-du-chat syndrome (CdCS) is a rare genetic disorder in which the short arm of chromosome 5 is deleted."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18437967",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "BACKGROUND: Cri-du-chat syndrome is a genetic disorder associated with various sized deletions of the short arm of c"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28004033",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "The Cri du Chat syndrome (CdC) is a rare genetic disorder caused by variable size deletions of the short arm of chromosome 5 (5p-)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32739788",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "Cri Du Chat (CDC) syndrome is a rare genetic condition caused by the deletion of genetic material on the small arm (the p arm) of chromosome 5."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18484284",
"endSection": "abstract",
"offsetInBeginSection": 106,
"offsetInEndSection": 269,
"text": "CCS is a rare genetic disorder, with an estimated incidence between 1 in 15,000 and 1 in 50,000 births, resulting from a deletion on the short arm of chromosome 5."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31187941",
"endSection": "abstract",
"offsetInBeginSection": 288,
"offsetInEndSection": 407,
"text": "Cri du chat (CdC) syndrome, a rare genetic disorder caused by variable size deletions of the short arm of chromosome 5."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31836684",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "Cri du chat syndrome (CDCS) is a rare genetic disease that is caused by a deletion in the short arm of chromosome 5 (5p) and has a variable clinical spectrum"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27144168",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "Cri-du-chat syndrome is a chromosomal disorder caused by a deletion of the short arm of chromosome 5"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32800423",
"endSection": "abstract",
"offsetInBeginSection": 14,
"offsetInEndSection": 242,
"text": "Cri-du-Chat Syndrome (CdCS) is a genetic condition due to deletions showing different breakpoints encompassing a critical region on the short arm of chromosome 5, located between p15.2 and p15.3, first defined by Niebuhr in 1978"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31568707",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 138,
"text": "Cri du chat syndrome (CdCS) is a rare syndrome caused by a partial or complete deletion of the short arm of chromosome 5 (5p-)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26601658",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 289,
"text": "Deletion of the short arm of chromosome 5 (5p-) is associated with phenotypic features including a cat-like cry in infancy, dysmorphic facial features, microcephaly, and intellectual disability, and when encompassing a minimal critical region, may be defined as Cri-du-Chat syndrome (CdCS)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30711802",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "The Cri du Chat Syndrome (CdCS) is a genetic disease resulting from variable size deletion occurring on the short arm of chromosome 5"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29460462",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 114,
"text": "Cri du Chat syndrome (CdCS) is a genetic syndrome caused by deletions in the short arm of chromosome 5"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28523196",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 172,
"text": "Cri du Chat syndrome (CdC) is a chromosomal abnormality (deletion of short arm of chromosome 5) associated with intellectual disability and typical anatomical abnormalities"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11238681",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "The majority of deletions of the short arm of chromosome 5 are associated with cri du chat syndrome (CdCS) and patients show phenotypic and cytogenetic variability."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1978567",
"endSection": "abstract",
"offsetInBeginSection": 100,
"offsetInEndSection": 392,
"text": "Since the cri-du-chat syndrome is correlated with deletions involving the short arm of chromosome 5 (5p), DNA fragments known to detect restriction fragment length polymorphisms (RFLPs) along 5p were used to establish whether the paternal or the maternal chromosome had suffered the deletion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34434412",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "Cri du chat syndrome (CdCS) is a chromosomal disorder resulting from a deletion in the short arm of chromosome 5."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19239081",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "The Cri du Chat Syndrome (CdCS) is one of the most common deletion syndromes, involving the short arm of chromosome 5, with an incidence of 1 in 50.000 live births."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29460462",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 121,
"text": "BACKGROUND: Cri du Chat syndrome (CdCS) is a genetic syndrome caused by deletions in the short arm of chromosome 5. Altho"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37908952",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 122,
"text": "Cri-du-chat syndrome (CdCS) is a rare genetic disorder in which the short arm of chromosome 5 is deleted. This report aims"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25236835",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 273,
"text": "BACKGROUND: Cri du Chat Syndrome (CdCS) is rare and occurs as a result of a partial deletion in the short arm of chromosome 5. There are no reports in the literature from the West African sub-region and indeed very few from Africa. A case of Cri du Chat Syndrome is describ"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26059676",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 261,
"text": "The cri-du-chat syndrome is a rare genetic disorder caused by deletions in the short arm of chromosome 5. It presents with a distinctive catlike high-pitched cry, psychomotor delays, microcephaly, craniofacial abnormalities, and, in many cases, ocular findings."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18437967",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "BACKGROUND: Cri-du-chat syndrome is a genetic disorder associated with various sized deletions of the short arm of chromosome 5"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18437967",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 209,
"text": "BACKGROUND: Cri-du-chat syndrome is a genetic disorder associated with various sized deletions of the short arm of chromosome 5. There are typical physical features, but individual phenotypes vary considerably"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34394178",
"endSection": "abstract",
"offsetInBeginSection": 29,
"offsetInEndSection": 372,
"text": "(5p-Sd, OMIM #123450) formerly known as Cri du Chat syndrome results from the loss of genetic material at the distal region of the short arm of chromosome 5. It is a neurodevelopmental disorder of genetic cause. So far, about 400 patients have been reported worldwide. Individuals affected by this syndrome have large phenotypic heterogeneity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36338241",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 148,
"text": "BACKGROUND: Cri du chat syndrome (CdCS), also known as 5p deletion syndrome (5p-) is a syndrome caused by partial deletion of the 5p chromosome in h"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27144168",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 101,
"text": "Cri-du-chat syndrome is a chromosomal disorder caused by a deletion of the short arm of chromosome 5."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15657623",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 126,
"text": "Cri-du-chat (CDC, OMIM 123450) is a chromosomal syndrome that results from partial deletions on the short arm of chromosome 5."
}
]
| 13 | BioASQ-training13b | null | null | 65f37aeac4010b4d7800000c | 220 |
yesno | Is DNA methylation an epigenetic modification of chromatin related to gene expression? | ['yes'] | [
"yes"
]
| ['Epigenetic changes such as DNA methylation alter gene expression at the level of transcription by upregulating, downregulating, or silencing genes completely.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/25531272",
"http://www.ncbi.nlm.nih.gov/pubmed/25534027",
"http://www.ncbi.nlm.nih.gov/pubmed/25437055",
"http://www.ncbi.nlm.nih.gov/pubmed/25514241",
"http://www.ncbi.nlm.nih.gov/pubmed/25512710",
"http://www.ncbi.nlm.nih.gov/pubmed/22922032",
"http://www.ncbi.nlm.nih.gov/pubmed/22078060",
"http://www.ncbi.nlm.nih.gov/pubmed/23604474",
"http://www.ncbi.nlm.nih.gov/pubmed/22992936",
"http://www.ncbi.nlm.nih.gov/pubmed/22359296"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25531272",
"endSection": "abstract",
"offsetInBeginSection": 21,
"offsetInEndSection": 164,
"text": "DNA methylation is a chemical modification of DNA involved in the regulation of gene expression by controlling the access to the DNA sequence. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25534027",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 163,
"text": "Epigenetic marks such as DNA methylation play important biological roles in gene expression regulation and cellular differentiation during development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25437055",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 196,
"text": "DNA methylation patterns are characterized by highly conserved developmental programs, but allow for divergent gene expression resulting from stochastic epigenetic drift or divergent environments."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25514241",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "DNA methylation plays a critical role in the regulation of gene expression. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25512710",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 198,
"text": "Epigenetic changes such as DNA methylation and histone methylation and acetylation alter gene expression at the level of transcription by upregulating, downregulating, or silencing genes completely."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25512710",
"endSection": "abstract",
"offsetInBeginSection": 199,
"offsetInEndSection": 358,
"text": "Dysregulation of epigenetic events can be pathological, leading to cardiovascular disease, neurological disorders, metabolic disorders, and cancer development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22922032",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 122,
"text": "DNA methylation is a pervasive epigenetic DNA modification that strongly affects chromatin regulation and gene expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23604474",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 138,
"text": "Epigenetic control, which includes DNA methylation and histone modifications, leads to chromatin remodeling and regulated gene expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22992936",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 240,
"text": "Epigenetic modifications on the DNA sequence (DNA methylation) or on chromatin-associated proteins (i.e., histones) comprise the \"cellular epigenome\"; together these modifications play an important role in the regulation of gene expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22359296",
"endSection": "abstract",
"offsetInBeginSection": 136,
"offsetInEndSection": 426,
"text": "Epigenetics is a process involved in gene regulation, mediated via DNA methylation, histone modification, chromatin remodeling, and functional noncoding RNAs, which influences the accessibility of the underlying DNA to transcriptional regulatory factors that activate or repress expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25531272",
"endSection": "abstract",
"offsetInBeginSection": 21,
"offsetInEndSection": 164,
"text": "DNA methylation is a chemical modification of DNA involved in the regulation of gene expression by controlling the access to the DNA sequence. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25534027",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 163,
"text": "Epigenetic marks such as DNA methylation play important biological roles in gene expression regulation and cellular differentiation during development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22078060",
"endSection": "abstract",
"offsetInBeginSection": 101,
"offsetInEndSection": 322,
"text": "Significant progress has been made in the basic understanding of how various epigenetic changes such as DNA methylation, histone modification, miRNA expression, and higher order chromatin structure affect gene expression."
}
]
| 5 | BioASQ-training5b | [
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0006306",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0000785",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0010467"
]
| []
| 54d9f7894b1fd0d33c00000a | 221 |
yesno | Is the abnormal dosage of ultraconserved elements disfavored in cancer cells? | ['no'] | [
"no"
]
| ['No. Abnormal dosage of ultraconserved elements is highly disfavored in healthy cells but not cancer cells.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/25340765"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25340765",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Abnormal dosage of ultraconserved elements is highly disfavored in healthy cells but not cancer cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25340765",
"endSection": "abstract",
"offsetInBeginSection": 294,
"offsetInEndSection": 1335,
"text": "We begin by showing that depletion for UCEs characterizes the most recent large-scale human CNV datasets and then find that even newly formed de novo CNVs, which have passed through meiosis at most once, are significantly depleted for UCEs. In striking contrast, CNVs arising specifically in cancer cells are, as a rule, not depleted for UCEs and can even become significantly enriched. This observation raises the possibility that CNVs that arise somatically and are relatively newly formed are less likely to have established a CNV profile that is depleted for UCEs. Alternatively, lack of depletion for UCEs from cancer CNVs may reflect the diseased state. In support of this latter explanation, somatic CNVs that are not associated with disease are depleted for UCEs. Finally, we show that it is possible to observe the CNVs of induced pluripotent stem (iPS) cells become depleted of UCEs over time, suggesting that depletion may be established through selection against UCE-disrupting CNVs without the requirement for meiotic divisions."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25340765",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Abnormal dosage of ultraconserved elements is highly disfavored in healthy cells but not cancer cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25340765",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Abnormal dosage of ultraconserved elements is highly disfavored in healthy cells but not cancer cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25340765",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Abnormal dosage of ultraconserved elements is highly disfavored in healthy cells but not cancer cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25340765",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Abnormal dosage of ultraconserved elements is highly disfavored in healthy cells but not cancer cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25340765",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Abnormal dosage of ultraconserved elements is highly disfavored in healthy cells but not cancer cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25340765",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Abnormal dosage of ultraconserved elements is highly disfavored in healthy cells but not cancer cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25340765",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Abnormal dosage of ultraconserved elements is highly disfavored in healthy cells but not cancer cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25340765",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Abnormal dosage of ultraconserved elements is highly disfavored in healthy cells but not cancer cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25340765",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Abnormal dosage of ultraconserved elements is highly disfavored in healthy cells but not cancer cells."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25340765",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Abnormal dosage of ultraconserved elements is highly disfavored in healthy cells but not cancer cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25340765",
"endSection": "abstract",
"offsetInBeginSection": 864,
"offsetInEndSection": 954,
"text": "Alternatively, lack of depletion for UCEs from cancer CNVs may reflect the diseased state."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25340765",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Abnormal dosage of ultraconserved elements is highly disfavored in healthy cells but not cancer cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25340765",
"endSection": "abstract",
"offsetInBeginSection": 864,
"offsetInEndSection": 954,
"text": "Alternatively, lack of depletion for UCEs from cancer CNVs may reflect the diseased state."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25340765",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Abnormal dosage of ultraconserved elements is highly disfavored in healthy cells but not cancer cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25340765",
"endSection": "abstract",
"offsetInBeginSection": 864,
"offsetInEndSection": 954,
"text": "Alternatively, lack of depletion for UCEs from cancer CNVs may reflect the diseased state."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25340765",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Abnormal dosage of ultraconserved elements is highly disfavored in healthy cells but not cancer cells."
}
]
| 5 | BioASQ-training5b | [
"http://www.disease-ontology.org/api/metadata/DOID:162"
]
| []
| 56c0708eef6e39474100001f | 222 |
yesno | Does radiotherapy for cervical cancer increases risk of colon cancer? | ['yes'] | [
"yes"
]
| ['Yes, there is epidemiological evidence to suggest that radiotherapy for cervical cancer increases risk for colon cancer.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/17971527",
"http://www.ncbi.nlm.nih.gov/pubmed/24696219",
"http://www.ncbi.nlm.nih.gov/pubmed/6957649"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24696219",
"endSection": "abstract",
"offsetInBeginSection": 867,
"offsetInEndSection": 1021,
"text": "After 8 years, the hazard ratio for developing colon cancer was 2.00 (95% CI 1.43-2.80) for women with radiation versus those without radiation treatment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24696219",
"endSection": "abstract",
"offsetInBeginSection": 1114,
"offsetInEndSection": 1568,
"text": "After 35 years of follow-up, the absolute risk of developing colon cancer was 6.5% for those who received radiation versus 2.5% for those without, and 3.7 versus 0.8% for rectum. The risk of colon and rectum cancer over 20 years of follow-up after radiation remained the same across three eras (1973-1980, 1981-1990, and 1991-2000). Radiation-induced second cancers of the colon and rectum may occur 8 years after radiation treatment for cervical cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6957649",
"endSection": "abstract",
"offsetInBeginSection": 778,
"offsetInEndSection": 1035,
"text": "The data suggested that high-dose pelvic irradiation was associated with increase in cancers of the bladder, kidneys, rectum, ovaries, corpus uteri, and non-Hodgkin's lymphoma but, apparently, not leukemia, Hodgkin's disease, breast cancer, or colon cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24696219",
"endSection": "abstract",
"offsetInBeginSection": 1447,
"offsetInEndSection": 1568,
"text": "Radiation-induced second cancers of the colon and rectum may occur 8 years after radiation treatment for cervical cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17971527",
"endSection": "abstract",
"offsetInBeginSection": 1597,
"offsetInEndSection": 1923,
"text": "Cervical cancer patients treated with radiotherapy, but not those who did not receive radiotherapy, were at increased risk for all second cancers and cancers at heavily irradiated sites (colon, rectum/anus, urinary bladder, ovary, and genital sites) beyond 40 years of follow-up compared with women in the general population. "
}
]
| 11 | BioASQ-training11b | null | null | 5e3390fafbd6abf43b000060 | 223 |
yesno | Can the CEP290 gene mutations be targeted by AAV-mediated gene therapy? | ['no'] | [
"no"
]
| ['The large size of the CEP290 gene prevents its use in adeno-associated virus (AAV)-mediated gene augmentation therapy.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/28109959"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28109959",
"endSection": "abstract",
"offsetInBeginSection": 278,
"offsetInEndSection": 396,
"text": "The large size of the CEP290 gene prevents its use in adeno-associated virus (AAV)-mediated gene augmentation therapy."
}
]
| 11 | BioASQ-training11b | null | null | 5a75fec383b0d9ea6600000b | 225 |
yesno | Is there an increased risk for cancer in Dyskeratosis Congenita? | ['yes'] | [
"yes"
]
| ['People with Dyskeratosis Congenita are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome (MDS) or acute myelogenous leukemia (AML), solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis.', 'Yes. Clinical progression of the disease can lead to aplastic anemia (86% of all patients) and to pulmonary or hepatic complications. These patients also have an increased risk of cancer. Adverse events include severe bone marrow failure (BMF), myelodysplastic syndrome (MDS), acute myeloid leukaemia (AML), and solid tumours (ST)', 'People with DC are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome (MDS) or acute myelogenous leukemia (AML), solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis ', 'People with DC are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome (MDS) or acute myelogenous leukemia (AML), solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis ', 'People with DC are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome (MDS) or acute myelogenous leukemia (AML), solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis ', 'People with DC are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome (MDS) or acute myelogenous leukemia (AML), solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis ', 'People with DC are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome (MDS) or acute myelogenous leukemia (AML), solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis '] | [
"http://www.ncbi.nlm.nih.gov/pubmed/19327580",
"http://www.ncbi.nlm.nih.gov/pubmed/23352883",
"http://www.ncbi.nlm.nih.gov/pubmed/20507306",
"http://www.ncbi.nlm.nih.gov/pubmed/20301779",
"http://www.ncbi.nlm.nih.gov/pubmed/23541441",
"http://www.ncbi.nlm.nih.gov/pubmed/23619122",
"http://www.ncbi.nlm.nih.gov/pubmed/24034063",
"http://www.ncbi.nlm.nih.gov/pubmed/19558498",
"http://www.ncbi.nlm.nih.gov/pubmed/22932338",
"http://www.ncbi.nlm.nih.gov/pubmed/22362038",
"http://www.ncbi.nlm.nih.gov/pubmed/20925138",
"http://www.ncbi.nlm.nih.gov/pubmed/18054794",
"http://www.ncbi.nlm.nih.gov/pubmed/17825470",
"http://www.ncbi.nlm.nih.gov/pubmed/18938267",
"http://www.ncbi.nlm.nih.gov/pubmed/22058220"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19327580",
"endSection": "abstract",
"offsetInBeginSection": 288,
"offsetInEndSection": 544,
"text": "People with DC are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome (MDS) or acute myelogenous leukemia (AML), solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23352883",
"endSection": "abstract",
"offsetInBeginSection": 608,
"offsetInEndSection": 790,
"text": "Clinical progression of the disease can lead to aplastic anemia (86% of all patients) and to pulmonary or hepatic complications. These patients also have an increased risk of cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20507306",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 326,
"text": "Fanconi anaemia (FA), dyskeratosis congenita (DC), Diamond-Blackfan anaemia (DBA), and Shwachman-Diamond syndrome (SDS) comprise major inherited bone marrow failure syndromes (IBMFS). Adverse events include severe bone marrow failure (BMF), myelodysplastic syndrome (MDS), acute myeloid leukaemia (AML), and solid tumours (ST)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20507306",
"endSection": "abstract",
"offsetInBeginSection": 762,
"offsetInEndSection": 1026,
"text": "Patients with FA had earlier onset of cancers, need for stem cell transplant, and death; followed by DC; DBA and SDS were mildest. While FA and DC patients had markedly increased risks of cancer, AML and MDS, there were no cases of leukaemia in DBA or SDS patients"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20507306",
"endSection": "abstract",
"offsetInBeginSection": 1146,
"offsetInEndSection": 1232,
"text": "The findings demonstrate that both FA and DC are major cancer susceptibility syndromes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20301779",
"endSection": "abstract",
"offsetInBeginSection": 288,
"offsetInEndSection": 544,
"text": "People with DC are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome (MDS) or acute myelogenous leukemia (AML), solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23619122",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 126,
"text": "Patients with dyskeratosis congenita (DC) have an increased risk of cancer, but also exhibit heightened radiation sensitivity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24034063",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 241,
"text": "Dyskeratosis congenita (DC) is characterized by the clinical triad of reticular skin pigmentation, oral leukoplakia, and nail dystrophy associated with bone marrow failure (BMF) and an high risk to develop cancer and pulmonary complications."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22932338",
"endSection": "abstract",
"offsetInBeginSection": 554,
"offsetInEndSection": 718,
"text": "CONCLUSION: Dyskeratosis congenita is a rare condition; however, it is vital to recognise the increased risk of upper aerodigestive tract cancers in these patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20925138",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "Point mutations in the DKC1 gene that encodes dyskerin cause the rare inherited syndrome called X-linked dyskeratosis congenita, characterized by a failure of proliferating tissues and increased susceptibility to cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18054794",
"endSection": "abstract",
"offsetInBeginSection": 1,
"offsetInEndSection": 212,
"text": "Dyskeratosis Congenita (DC) also known as Zinsser-Engman-Cole syndrome is a rare multi-system bone marrow failure syndrome characterised by mucocutaneous abnormalities and an increased predisposition to cancer\"."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17825470",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 174,
"text": "Dyskeratosis congenita is an inherited syndrome characterised by mucocutaneous features, bone marrow failure, an increased risk of malignancy and other somatic abnormalities."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19327580",
"endSection": "abstract",
"offsetInBeginSection": 288,
"offsetInEndSection": 544,
"text": "People with DC are at increased risk for progressive bone marrow failure (BMF), myelodysplastic syndrome (MDS) or acute myelogenous leukemia (AML), solid tumors (usually squamous cell carcinoma of the head/neck or anogenital cancer), and pulmonary fibrosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22932338",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "Dyskeratosis congenita is a rare condition; however, it is vital to recognise the increased risk of upper aerodigestive tract cancers in these patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19558498",
"endSection": "abstract",
"offsetInBeginSection": 123,
"offsetInEndSection": 243,
"text": "Epidermal atrophy, hair growth defects, bone marrow failure and increased risk of cancer are also common in DC patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20925138",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "Point mutations in the DKC1 gene that encodes dyskerin cause the rare inherited syndrome called X-linked dyskeratosis congenita, characterized by a failure of proliferating tissues and increased susceptibility to cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23541441",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Telomere dysfunction and tumor suppression responses in dyskeratosis congenita: balancing cancer and tissue renewal impairment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23619122",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Patients with dyskeratosis congenita (DC) have an increased risk of cancer, but also exhibit heightened radiation sensitivity"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22932338",
"endSection": "abstract",
"offsetInBeginSection": 531,
"offsetInEndSection": 682,
"text": "Dyskeratosis congenita is a rare condition; however, it is vital to recognise the increased risk of upper aerodigestive tract cancers in these patients"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17825470",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 173,
"text": "Dyskeratosis congenita is an inherited syndrome characterised by mucocutaneous features, bone marrow failure, an increased risk of malignancy and other somatic abnormalities"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20507306",
"endSection": "abstract",
"offsetInBeginSection": 893,
"offsetInEndSection": 1026,
"text": "While FA and DC patients had markedly increased risks of cancer, AML and MDS, there were no cases of leukaemia in DBA or SDS patients"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22362038",
"endSection": "abstract",
"offsetInBeginSection": 1119,
"offsetInEndSection": 1341,
"text": "As in Fanconi anemia and dyskeratosis congenita, DBA is both an inherited bone marrow failure syndrome and a cancer predisposition syndrome; cancer risks appear lower in DBA than in Fanconi anemia or dyskeratosis congenita"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18938267",
"endSection": "abstract",
"offsetInBeginSection": 269,
"offsetInEndSection": 417,
"text": "Severe pancytopenia frequently causes early mortality of DC patients, who have an increased risk of developing oropharyngeal squamous cell carcinoma"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23619122",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Patients with dyskeratosis congenita (DC) have an increased risk of cancer, but also exhibit heightened radiation sensitivity"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22932338",
"endSection": "abstract",
"offsetInBeginSection": 531,
"offsetInEndSection": 682,
"text": "Dyskeratosis congenita is a rare condition; however, it is vital to recognise the increased risk of upper aerodigestive tract cancers in these patients"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20507306",
"endSection": "abstract",
"offsetInBeginSection": 893,
"offsetInEndSection": 1026,
"text": "While FA and DC patients had markedly increased risks of cancer, AML and MDS, there were no cases of leukaemia in DBA or SDS patients"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23541441",
"endSection": "abstract",
"offsetInBeginSection": 587,
"offsetInEndSection": 1048,
"text": "Here different aspects of telomere biology, concerning adult stem cells senescence, tumor suppression and cancer are considered in the context of DC, resulting in two translational models: late onset of DC symptoms in telomere-related mutations carriers is a potential indicator of increased cancer risk and differences in tumor suppression capacities among the genetic subgroups are (at least partial) causes of different clinical manifestations of the disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20925138",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 219,
"text": "Point mutations in the DKC1 gene that encodes dyskerin cause the rare inherited syndrome called X-linked dyskeratosis congenita, characterized by a failure of proliferating tissues and increased susceptibility to cancer"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23619122",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Patients with dyskeratosis congenita (DC) have an increased risk of cancer, but also exhibit heightened radiation sensitivity"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22932338",
"endSection": "abstract",
"offsetInBeginSection": 531,
"offsetInEndSection": 682,
"text": "Dyskeratosis congenita is a rare condition; however, it is vital to recognise the increased risk of upper aerodigestive tract cancers in these patients"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23541441",
"endSection": "abstract",
"offsetInBeginSection": 587,
"offsetInEndSection": 1048,
"text": "Here different aspects of telomere biology, concerning adult stem cells senescence, tumor suppression and cancer are considered in the context of DC, resulting in two translational models: late onset of DC symptoms in telomere-related mutations carriers is a potential indicator of increased cancer risk and differences in tumor suppression capacities among the genetic subgroups are (at least partial) causes of different clinical manifestations of the disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22058220",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "Dyskeratosis congenita is a cancer-prone bone marrow failure syndrome caused by aberrations in telomere biology."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23619122",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Patients with dyskeratosis congenita (DC) have an increased risk of cancer, but also exhibit heightened radiation sensitivity"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22932338",
"endSection": "abstract",
"offsetInBeginSection": 531,
"offsetInEndSection": 682,
"text": "Dyskeratosis congenita is a rare condition; however, it is vital to recognise the increased risk of upper aerodigestive tract cancers in these patients"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23541441",
"endSection": "abstract",
"offsetInBeginSection": 587,
"offsetInEndSection": 1048,
"text": "Here different aspects of telomere biology, concerning adult stem cells senescence, tumor suppression and cancer are considered in the context of DC, resulting in two translational models: late onset of DC symptoms in telomere-related mutations carriers is a potential indicator of increased cancer risk and differences in tumor suppression capacities among the genetic subgroups are (at least partial) causes of different clinical manifestations of the disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22058220",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "Dyskeratosis congenita is a cancer-prone bone marrow failure syndrome caused by aberrations in telomere biology."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23619122",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Patients with dyskeratosis congenita (DC) have an increased risk of cancer, but also exhibit heightened radiation sensitivity"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22932338",
"endSection": "abstract",
"offsetInBeginSection": 531,
"offsetInEndSection": 682,
"text": "Dyskeratosis congenita is a rare condition; however, it is vital to recognise the increased risk of upper aerodigestive tract cancers in these patients"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22362038",
"endSection": "abstract",
"offsetInBeginSection": 1119,
"offsetInEndSection": 1341,
"text": "As in Fanconi anemia and dyskeratosis congenita, DBA is both an inherited bone marrow failure syndrome and a cancer predisposition syndrome; cancer risks appear lower in DBA than in Fanconi anemia or dyskeratosis congenita"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20507306",
"endSection": "abstract",
"offsetInBeginSection": 893,
"offsetInEndSection": 1026,
"text": "While FA and DC patients had markedly increased risks of cancer, AML and MDS, there were no cases of leukaemia in DBA or SDS patients"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18938267",
"endSection": "abstract",
"offsetInBeginSection": 269,
"offsetInEndSection": 417,
"text": "Severe pancytopenia frequently causes early mortality of DC patients, who have an increased risk of developing oropharyngeal squamous cell carcinoma"
}
]
| 5 | BioASQ-training5b | [
"http://www.disease-ontology.org/api/metadata/DOID:162",
"http://www.disease-ontology.org/api/metadata/DOID:2729",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D009369"
]
| []
| 54ede5df94afd61504000007 | 226 |
yesno | Does neuroglobin has neuroprotective properties in the setting of traumatic brain injury? | ['yes'] | [
"yes"
]
| ['Yes, neuroglobin has neuroprotective properties in the setting of traumatic brain injury.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/20345238",
"http://www.ncbi.nlm.nih.gov/pubmed/20544857",
"http://www.ncbi.nlm.nih.gov/pubmed/20476562",
"http://www.ncbi.nlm.nih.gov/pubmed/22703519",
"http://www.ncbi.nlm.nih.gov/pubmed/22664218",
"http://www.ncbi.nlm.nih.gov/pubmed/21915648",
"http://www.ncbi.nlm.nih.gov/pubmed/25624825",
"http://www.ncbi.nlm.nih.gov/pubmed/23658829",
"http://www.ncbi.nlm.nih.gov/pubmed/24491879",
"http://www.ncbi.nlm.nih.gov/pubmed/24642455"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20345238",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 164,
"text": "Neuroglobin has shown rich neuroprotective effects against cerebral hypoxia, and therefore has the potential to impact outcomes after traumatic brain injury (TBI). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20544857",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "Neuroglobin (Ngb) is proposed to be a neuron-specific, hypoxia-responsive, neuroprotective protein. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20476562",
"endSection": "abstract",
"offsetInBeginSection": 796,
"offsetInEndSection": 1081,
"text": "CONCLUSION: The increased expression of neuroglobin in traumatic brain injury informed us that neuroglobin had anti-apoptosis action in post-injury neuron. It could protect the neuron from traumatic stress and secondary ischemia and hypoxia insults during ultra-early and acute stages."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22703519",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 71,
"text": "Neuroglobin-overexpression reduces traumatic brain lesion size in mice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22703519",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "BACKGROUND: Accumulating evidence has demonstrated that over-expression of Neuroglobin (Ngb) is neuroprotective against hypoxic/ischemic brain injuries. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22703519",
"endSection": "abstract",
"offsetInBeginSection": 1071,
"offsetInEndSection": 1201,
"text": "CONCLUSION: Ngb over-expression reduced traumatic lesion volume, which might partially be achieved by decreasing oxidative stress."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22664218",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "Neuroglobin upregulation offers neuroprotection in traumatic brain injury."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22664218",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 228,
"text": "OBJECTIVES: The aim of this study was to investigate rat neuroglobin (rNGB) expression level after traumatic brain injury (TBI) and further study its neuroprotective effects in TBI when it was overexpressed in adenoviral vector."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22664218",
"endSection": "abstract",
"offsetInBeginSection": 955,
"offsetInEndSection": 1060,
"text": "CONCLUSIONS: NGB was upregulated in TBI and overexpressed rNGB had a significant neuroprotection in TBI. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22664218",
"endSection": "abstract",
"offsetInBeginSection": 1101,
"offsetInEndSection": 1189,
"text": "This study suggested that rNGB overexpression may be a new strategy for treating of TBI."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20345238",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "Neuroglobin has shown rich neuroprotective effects against cerebral hypoxia, and therefore has the potential to impact outcomes after traumatic brain injury (TBI)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22664218",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 216,
"text": "The aim of this study was to investigate rat neuroglobin (rNGB) expression level after traumatic brain injury (TBI) and further study its neuroprotective effects in TBI when it was overexpressed in adenoviral vector."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22664218",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "Neuroglobin upregulation offers neuroprotection in traumatic brain injury."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20345238",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "Neuroglobin has shown rich neuroprotective effects against cerebral hypoxia, and therefore has the potential to impact outcomes after traumatic brain injury (TBI)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22664218",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 216,
"text": "The aim of this study was to investigate rat neuroglobin (rNGB) expression level after traumatic brain injury (TBI) and further study its neuroprotective effects in TBI when it was overexpressed in adenoviral vector."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22703519",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "Accumulating evidence has demonstrated that over-expression of Neuroglobin (Ngb) is neuroprotective against hypoxic/ischemic brain injuries."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22664218",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "Neuroglobin upregulation offers neuroprotection in traumatic brain injury."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20345238",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "Neuroglobin has shown rich neuroprotective effects against cerebral hypoxia, and therefore has the potential to impact outcomes after traumatic brain injury (TBI)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22664218",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 216,
"text": "The aim of this study was to investigate rat neuroglobin (rNGB) expression level after traumatic brain injury (TBI) and further study its neuroprotective effects in TBI when it was overexpressed in adenoviral vector."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22664218",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "Neuroglobin upregulation offers neuroprotection in traumatic brain injury."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22664218",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "Neuroglobin upregulation offers neuroprotection in traumatic brain injury."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24491879",
"endSection": "abstract",
"offsetInBeginSection": 171,
"offsetInEndSection": 334,
"text": "Various studies seem to indicate that neuroglobin is a neuroprotective agent when overexpressed, acting as a potent inhibitor of oxidative and nitrosative stress. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22703519",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "BACKGROUND: Accumulating evidence has demonstrated that over-expression of Neuroglobin (Ngb) is neuroprotective against hypoxic/ischemic brain injuries. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22703519",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "BACKGROUND: Accumulating evidence has demonstrated that over-expression of Neuroglobin (Ngb) is neuroprotective against hypoxic/ischemic brain injuries. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22703519",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "BACKGROUND: Accumulating evidence has demonstrated that over-expression of Neuroglobin (Ngb) is neuroprotective against hypoxic/ischemic brain injuries. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22664218",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "Neuroglobin upregulation offers neuroprotection in traumatic brain injury."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24491879",
"endSection": "abstract",
"offsetInBeginSection": 171,
"offsetInEndSection": 334,
"text": "Various studies seem to indicate that neuroglobin is a neuroprotective agent when overexpressed, acting as a potent inhibitor of oxidative and nitrosative stress. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22703519",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "BACKGROUND: Accumulating evidence has demonstrated that over-expression of Neuroglobin (Ngb) is neuroprotective against hypoxic/ischemic brain injuries. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22664218",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "Neuroglobin upregulation offers neuroprotection in traumatic brain injury."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24491879",
"endSection": "abstract",
"offsetInBeginSection": 171,
"offsetInEndSection": 334,
"text": "Various studies seem to indicate that neuroglobin is a neuroprotective agent when overexpressed, acting as a potent inhibitor of oxidative and nitrosative stress. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22703519",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "BACKGROUND: Accumulating evidence has demonstrated that over-expression of Neuroglobin (Ngb) is neuroprotective against hypoxic/ischemic brain injuries. "
}
]
| 5 | BioASQ-training5b | []
| []
| 56c1d846ef6e39474100002e | 227 |
yesno | Do epigenetic changes change the DNA sequence? | ['no'] | [
"no"
]
| ['Epigenetic changes are inheritable modifications that can modify gene expression without changing the DNA sequence. The most common epigenetic alternations consist of DNA methylation and histone modifications.', 'No, epigenetic changes do not change the DNA sequence. They are heritable modifications that can modify gene expression without altering the DNA sequence. The most common epigenetic changes consist of DNA methylation and histone modifications.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/25512705",
"http://www.ncbi.nlm.nih.gov/pubmed/26216216",
"http://www.ncbi.nlm.nih.gov/pubmed/26639162",
"http://www.ncbi.nlm.nih.gov/pubmed/34728591",
"http://www.ncbi.nlm.nih.gov/pubmed/18847515",
"http://www.ncbi.nlm.nih.gov/pubmed/22949838",
"http://www.ncbi.nlm.nih.gov/pubmed/31696298",
"http://www.ncbi.nlm.nih.gov/pubmed/35664328",
"http://www.ncbi.nlm.nih.gov/pubmed/27730435",
"http://www.ncbi.nlm.nih.gov/pubmed/29541423",
"http://www.ncbi.nlm.nih.gov/pubmed/33781317",
"http://www.ncbi.nlm.nih.gov/pubmed/25694547",
"http://www.ncbi.nlm.nih.gov/pubmed/17413852",
"http://www.ncbi.nlm.nih.gov/pubmed/30580428",
"http://www.ncbi.nlm.nih.gov/pubmed/20620207",
"http://www.ncbi.nlm.nih.gov/pubmed/20627830",
"http://www.ncbi.nlm.nih.gov/pubmed/32133274",
"http://www.ncbi.nlm.nih.gov/pubmed/16567863",
"http://www.ncbi.nlm.nih.gov/pubmed/21941617",
"http://www.ncbi.nlm.nih.gov/pubmed/28815391",
"http://www.ncbi.nlm.nih.gov/pubmed/23448446",
"http://www.ncbi.nlm.nih.gov/pubmed/23529258",
"http://www.ncbi.nlm.nih.gov/pubmed/33866814",
"http://www.ncbi.nlm.nih.gov/pubmed/32235270",
"http://www.ncbi.nlm.nih.gov/pubmed/21416922",
"http://www.ncbi.nlm.nih.gov/pubmed/23895656",
"http://www.ncbi.nlm.nih.gov/pubmed/15485357",
"http://www.ncbi.nlm.nih.gov/pubmed/21734376",
"http://www.ncbi.nlm.nih.gov/pubmed/35735917",
"http://www.ncbi.nlm.nih.gov/pubmed/23273101",
"http://www.ncbi.nlm.nih.gov/pubmed/20309920",
"http://www.ncbi.nlm.nih.gov/pubmed/17317097",
"http://www.ncbi.nlm.nih.gov/pubmed/26579435",
"http://www.ncbi.nlm.nih.gov/pubmed/23165337",
"http://www.ncbi.nlm.nih.gov/pubmed/30079076",
"http://www.ncbi.nlm.nih.gov/pubmed/24455281",
"http://www.ncbi.nlm.nih.gov/pubmed/31374565",
"http://www.ncbi.nlm.nih.gov/pubmed/22359295",
"http://www.ncbi.nlm.nih.gov/pubmed/16341272",
"http://www.ncbi.nlm.nih.gov/pubmed/30522005",
"http://www.ncbi.nlm.nih.gov/pubmed/36346551",
"http://www.ncbi.nlm.nih.gov/pubmed/20728889",
"http://www.ncbi.nlm.nih.gov/pubmed/33482325",
"http://www.ncbi.nlm.nih.gov/pubmed/25797698",
"http://www.ncbi.nlm.nih.gov/pubmed/24295192",
"http://www.ncbi.nlm.nih.gov/pubmed/19183791",
"http://www.ncbi.nlm.nih.gov/pubmed/33866804",
"http://www.ncbi.nlm.nih.gov/pubmed/18042143",
"http://www.ncbi.nlm.nih.gov/pubmed/12473517",
"http://www.ncbi.nlm.nih.gov/pubmed/24298130",
"http://www.ncbi.nlm.nih.gov/pubmed/36057300",
"http://www.ncbi.nlm.nih.gov/pubmed/32445090",
"http://www.ncbi.nlm.nih.gov/pubmed/34058565",
"http://www.ncbi.nlm.nih.gov/pubmed/31609563",
"http://www.ncbi.nlm.nih.gov/pubmed/30455036",
"http://www.ncbi.nlm.nih.gov/pubmed/34182142"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26216216",
"endSection": "abstract",
"offsetInBeginSection": 455,
"offsetInEndSection": 665,
"text": "Epigenetic modifications, such as DNA methylation and chromatin assembly states, reflect the high plasticity of the genome and contribute to stably alter gene expression without modifying genomic DNA sequences."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21734376",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 146,
"text": "Epigenetics is defined as heritable changes in gene expression that are, unlike mutations, not attributable to alterations in the sequence of DNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33781317",
"endSection": "abstract",
"offsetInBeginSection": 125,
"offsetInEndSection": 338,
"text": "Epigenetic changes are inheritable modifications that can modify the gene expression without changing the DNA sequence. The most common epigenetic alternations consist of DNA methylation and histone modifications."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20620207",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 111,
"text": "Epigenetic changes refer to heritable changes that may modulate gene expression without affecting DNA sequence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35735917",
"endSection": "abstract",
"offsetInBeginSection": 117,
"offsetInEndSection": 238,
"text": "Epigenetic changes are reversible and do not affect the DNA sequence itself but rather control levels of gene expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19183791",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "Epigenetic changes, or heritable alterations in gene function that do not affect DNA sequence, are rapidly gaining acceptance as co-conspirators in carcinogenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23273101",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 171,
"text": "Environmentally caused changes in chromosomes that do not alter the DNA sequence but cause phenotypic changes by altering gene transcription are summarized as epigenetics."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21941617",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 98,
"text": "Epigenetic modifications are heritable changes in gene expression not encoded by the DNA sequence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30079076",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 356,
"text": "Epigenetic regulation is referred to as changes in gene function that do not involve changes in the DNA sequence, it is usually accomplished by DNA methylation, histone modifications (repressive marks such as H3K9me, H3K27me, H2Aub, or active marks such as H3K4me, H3K36me, H3Ac), and chromatin remodeling (nucleosome composition, occupancy, and location)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23895656",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "Epigenetics is the study of changes in gene expression or cellular phenotype that do not change the DNA sequence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22949838",
"endSection": "abstract",
"offsetInBeginSection": 258,
"offsetInEndSection": 467,
"text": "Epigenetic change, which does not involve alteration to the nucleotide sequence, can also cause changes in gene activity by changing the structure of chromatin through DNA methylation or histone modifications."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17413852",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "Epigenetics is defined as mitotically and meiotically heritable changes in gene expression that do not involve a change in the DNA sequence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34728591",
"endSection": "abstract",
"offsetInBeginSection": 598,
"offsetInEndSection": 730,
"text": "These modifications, also known as epigenetic code, do not change the DNA sequence but alter the expression level of specific genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26579435",
"endSection": "abstract",
"offsetInBeginSection": 321,
"offsetInEndSection": 441,
"text": " Epigenetic regulation refers to heritable factors of genomic modifications that do not involve changes in DNA sequence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20309920",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Epigenetics refers to structural modifications to genes that do not change the nucleotide sequence itself but instead control and regulate gene expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35664328",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 108,
"text": "Epigenetics are the heritable changes in gene expression patterns which occur without altering DNA sequence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29541423",
"endSection": "abstract",
"offsetInBeginSection": 202,
"offsetInEndSection": 302,
"text": " Epigenetic changes appear briefly and do not involve permanent changes to the primary DNA sequence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25512705",
"endSection": "abstract",
"offsetInBeginSection": 284,
"offsetInEndSection": 429,
"text": " Epigenetic changes responding to the environmental and intercellular signals can turn on/off specific genes, but do not modify the DNA sequence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35735917",
"endSection": "abstract",
"offsetInBeginSection": 116,
"offsetInEndSection": 238,
"text": " Epigenetic changes are reversible and do not affect the DNA sequence itself but rather control levels of gene expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27730435",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 124,
"text": "Epigenetic regulation refers to heritable changes in gene expression that do not involve any alteration of the DNA sequence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32445090",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 172,
"text": "Epigenetic mechanisms, which include DNA methylation, histone modification, and microRNA (miRNA), can produce heritable phenotypic changes without a change in DNA sequence."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24295192",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "Epigenetic changes to the genome are biochemical alterations to the DNA that do not change an individual's genome but do change and influence gene expression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18847515",
"endSection": "abstract",
"offsetInBeginSection": 101,
"offsetInEndSection": 251,
"text": "e next, which may alter gene expression but which do not involve changes in the primary DNA sequence. These marks include DNA methylation (methylation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24298130",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 198,
"text": "Epigenetics, the study of functionally relevant chemical modifications to DNA that do not involve a change in the DNA nucleotide sequence, is at the interface between research and clinical medicine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31609563",
"endSection": "abstract",
"offsetInBeginSection": 395,
"offsetInEndSection": 564,
"text": "The accessibility of DNA is regulated by epigenetic processes, including methylation of cytosine. In these circumstances the nucleic sequence of the DNA does not change."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15485357",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Epigenetics is comprised of the stable and heritable (or potentially heritable) changes in gene expression that do not entail a change in DNA sequence."
}
]
| 12 | BioASQ-training12b | null | null | 644efd2c57b1c7a315000085 | 228 |
yesno | Does Axitinib prolong survival of Pancreatic Cancer patients? | ['no'] | [
"no"
]
| ['No. The addition of axitinib to gemcitabine does not improve overall survival in advanced pancreatic cancer.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/21306953",
"http://www.ncbi.nlm.nih.gov/pubmed/24328549",
"http://www.ncbi.nlm.nih.gov/pubmed/25647781"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25647781",
"endSection": "abstract",
"offsetInBeginSection": 1673,
"offsetInEndSection": 1853,
"text": "CONCLUSIONS: Axitinib/gemcitabine, while tolerated, did not provide survival benefit over gemcitabine alone in patients with advanced pancreatic cancer from Japan or other regions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25647781",
"endSection": "abstract",
"offsetInBeginSection": 644,
"offsetInEndSection": 1257,
"text": "RESULTS: Among Japanese patients, median overall survival was not estimable (95% confidence interval, 7.4 months-not estimable) with axitinib/gemcitabine (n = 58) and 9.9 months (95% confidence interval, 7.4-10.5) with placebo/gemcitabine (n = 56) (hazard ratio 1.093 [95% confidence interval, 0.525-2.274]). Median survival follow-up (range) was 5.1 months (0.02-12.3) with axitinib/gemcitabine vs. 5.4 months (1.8-10.5) with placebo/gemcitabine. Similarly, no difference was detected in overall survival between axitinib/gemcitabine and placebo/gemcitabine in patients from North America or the European Union. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21306953",
"endSection": "abstract",
"offsetInBeginSection": 1757,
"offsetInEndSection": 2144,
"text": "At an interim analysis in January, 2009, the independent data monitoring committee concluded that the futility boundary had been crossed. Median overall survival was 8·5 months (95% CI 6·9-9·5) for gemcitabine plus axitinib (n=314, data missing for two patients) and 8·3 months (6·9-10·3) for gemcitabine plus placebo (n=316; hazard ratio 1·014, 95% CI 0·786-1·309; one-sided p=0·5436). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21306953",
"endSection": "abstract",
"offsetInBeginSection": 2417,
"offsetInEndSection": 2538,
"text": "INTERPRETATION: The addition of axitinib to gemcitabine does not improve overall survival in advanced pancreatic cancer. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21306953",
"endSection": "abstract",
"offsetInBeginSection": 2423,
"offsetInEndSection": 2542,
"text": "INTERPRETATION\nThe addition of axitinib to gemcitabine does not improve overall survival in advanced pancreatic cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24328549",
"endSection": "abstract",
"offsetInBeginSection": 1182,
"offsetInEndSection": 1453,
"text": "However, as with other tyrosine kinase inhibitors of the same class, axitinib does not prolong overall survival; therefore, selection of second-line tyrosine kinase inhibitor therapy, including axitinib, must be carefully considered to maximize outcomes for each patient."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25647781",
"endSection": "abstract",
"offsetInBeginSection": 1679,
"offsetInEndSection": 1858,
"text": "CONCLUSIONS\nAxitinib/gemcitabine, while tolerated, did not provide survival benefit over gemcitabine alone in patients with advanced pancreatic cancer from Japan or other regions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25647781",
"endSection": "abstract",
"offsetInBeginSection": 1121,
"offsetInEndSection": 1285,
"text": "Similarly, no difference was detected in overall survival between axitinib/gemcitabine and placebo/gemcitabine in patients from North America or the European Union."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25647781",
"endSection": "abstract",
"offsetInBeginSection": 1645,
"offsetInEndSection": 1812,
"text": "Axitinib/gemcitabine, while tolerated, did not provide survival benefit over gemcitabine alone in patients with advanced pancreatic cancer from Japan or other regions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21306953",
"endSection": "abstract",
"offsetInBeginSection": 2373,
"offsetInEndSection": 2477,
"text": "The addition of axitinib to gemcitabine does not improve overall survival in advanced pancreatic cancer."
}
]
| 11 | BioASQ-training11b | null | null | 5c73ad347c78d69471000098 | 229 |
yesno | Are mucins glycosylated proteins? | ['yes'] | [
"yes"
]
| ['Yes,\nMany members of the mucin family are evolutionarily conserved and are often aberrantly expressed and glycosylated in various benign and malignant pathologies leading to tumor invasion, metastasis, and immune evasion.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/31907968",
"http://www.ncbi.nlm.nih.gov/pubmed/31908009",
"http://www.ncbi.nlm.nih.gov/pubmed/31904283"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31908009",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 216,
"text": "Many members of the mucin family are evolutionarily conserved and are often aberrantly expressed and glycosylated in various benign and malignant pathologies leading to tumor invasion, metastasis, and immune evasion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31907968",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Mucin is a glycoprotein that is the primary component of the mucus overlaying the epithelial tissues. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31904283",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 33,
"text": "Mucin-type O-linked glycosylation"
}
]
| 11 | BioASQ-training11b | null | null | 604903551cb411341a000162 | 230 |
yesno | Is hydroxyurea usually used to treated infectious disease? | ['no'] | [
"no"
]
| ['Hydroxyurea represents the only available disease-modifying therapy for Sickle Cell Anemia (SCA).'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/21196716",
"http://www.ncbi.nlm.nih.gov/pubmed/26275071",
"http://www.ncbi.nlm.nih.gov/pubmed/27677923",
"http://www.ncbi.nlm.nih.gov/pubmed/15307105",
"http://www.ncbi.nlm.nih.gov/pubmed/20008183"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26275071",
"endSection": "abstract",
"offsetInBeginSection": 156,
"offsetInEndSection": 294,
"text": "Hydroxyurea represents the only available disease-modifying therapy for SCA, and has proven safety and efficacy in high-resource countries"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15307105",
"endSection": "abstract",
"offsetInBeginSection": 1579,
"offsetInEndSection": 1777,
"text": "In conclusion, the data here presented suggests that hydroxyurea may prevent priapism attacks in sickle cell disease, probably at higher doses than usually prescribed for painful crisis prevention.."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21196716",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 75,
"text": "Clinical follow-up of hydroxyurea-treated adults with sickle cell disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27677923",
"endSection": "abstract",
"offsetInBeginSection": 405,
"offsetInEndSection": 546,
"text": "t may also attenuate optimal response to hydroxyurea therapy, the only effective and practical treatment option for SCD in sub-Saharan Africa"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15307105",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 82,
"text": "Hydroxyurea is one of the most successfully used therapies for sickle cell disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20008183",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 252,
"text": "Clinical experience with hydroxyurea for patients with sickle cell disease (SCD) has been accumulating for the past 25 years. The bulk of the current evidence suggests that hydroxyurea is well-tolerated, safe, and efficacious for most patients with SCD"
}
]
| 6 | BioASQ-training6b | [
"http://www.disease-ontology.org/api/metadata/DOID:10923",
"http://www.biosemantics.org/jochem#4275774",
"http://www.biosemantics.org/jochem#http://www.biosemantics.org/jochem#:4275774",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D000755",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D006450",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D006918"
]
| [
{
"o": "hydroxyurea",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C0020402"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A0481276",
"p": "http://www.w3.org/2008/05/skos-xl#altLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0020402"
},
{
"o": "hydroxyurea",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A0481276"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A7996376",
"p": "http://www.w3.org/2008/05/skos-xl#prefLabel",
"s": "http://linkedlifedata.com/resource/umls/id/C0020402"
},
{
"o": "hydroxyurea",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A7996376"
}
]
| 58dbbdac8acda3452900001e | 231 |
yesno | Can telomere length shortening be reversed by telomerase? | ['yes'] | [
"yes"
]
| ['Yes, telomerase gene therapy rescues telomere length, bone marrow aplasia, and survival in mice with aplastic anemia.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/27401551",
"http://www.ncbi.nlm.nih.gov/pubmed/27154402",
"http://www.ncbi.nlm.nih.gov/pubmed/26903545",
"http://www.ncbi.nlm.nih.gov/pubmed/27483324",
"http://www.ncbi.nlm.nih.gov/pubmed/27029895"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27401551",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 284,
"text": "Telomere length is regulated around an equilibrium set point. Telomeres shorten during replication and are lengthened by telomerase. Disruption of the length equilibrium leads to disease; thus, it is important to understand the mechanisms that regulate length at the molecular level. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27483324",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 455,
"text": "High telomerase activity is detected in nearly all human cancers but most human cells are devoid of telomerase activity. There is well-documented evidence that reactivation of telomerase occurs during cellular transformation. In humans, tumors can rely in reactivation of telomerase or originate in a telomerase positive stem/progenitor cell, or rely in alternative lengthening of telomeres, a telomerase-independent telomere-length maintenance mechanism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27483324",
"endSection": "abstract",
"offsetInBeginSection": 1019,
"offsetInEndSection": 1247,
"text": " Together, these observations may provoke a re-evaluation of telomere and telomerase based therapies, both in telomerase inhibition for cancer therapy and telomerase activation for tissue regeneration and anti-ageing strategies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27029895",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 253,
"text": "Telomeres progressively shorten throughout life. A hallmark of advanced malignancies is the ability for continuous cell divisions that almost universally correlates with the stabilization of telomere length by the reactivation of telomerase."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27154402",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 195,
"text": "Telomerase-mediated telomere elongation provides cell populations with the ability to proliferate indefinitely. Telomerase is capable of recognizing and extending the shortest telomeres in cells;"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26903545",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "Telomerase gene therapy rescues telomere length, bone marrow aplasia, and survival in mice with aplastic anemia."
}
]
| 6 | BioASQ-training6b | null | null | 58cd675c02b8c6095300003b | 232 |
yesno | Is the toxin produced by Clostridium botulinum always deadly? | ['no'] | [
"no"
]
| ['There are numerous examples where children and animals survived infection with clostridium botulinum.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/12926199",
"http://www.ncbi.nlm.nih.gov/pubmed/20173718",
"http://www.ncbi.nlm.nih.gov/pubmed/23871478",
"http://www.ncbi.nlm.nih.gov/pubmed/26866491",
"http://www.ncbi.nlm.nih.gov/pubmed/24997242",
"http://www.ncbi.nlm.nih.gov/pubmed/15244362",
"http://www.ncbi.nlm.nih.gov/pubmed/19488551",
"http://www.ncbi.nlm.nih.gov/pubmed/23097586",
"http://www.ncbi.nlm.nih.gov/pubmed/22513950",
"http://www.ncbi.nlm.nih.gov/pubmed/24867833",
"http://www.ncbi.nlm.nih.gov/pubmed/17674683",
"http://www.ncbi.nlm.nih.gov/pubmed/19160335",
"http://www.ncbi.nlm.nih.gov/pubmed/20693440",
"http://www.ncbi.nlm.nih.gov/pubmed/26697417"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24997242",
"endSection": "abstract",
"offsetInBeginSection": 1759,
"offsetInEndSection": 1941,
"text": "Animals treated with trace elements recovered. It appears that intestinal microbiota dysbiosis and trace element deficiency could explain the extensive emergence of chronic Botulism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26697417",
"endSection": "abstract",
"offsetInBeginSection": 1082,
"offsetInEndSection": 1316,
"text": "The patient was treated with human botulism immune globulin and had rapid recovery in weakness. A stool sample from the patient was positive for Type A Clostridium botulinum toxin eventually confirming the diagnosis of infant botulism"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23871478",
"endSection": "abstract",
"offsetInBeginSection": 1199,
"offsetInEndSection": 1363,
"text": "The botulism immunoglobulin was administered, and a diagnosis was confirmed with positive botulinum toxin in the stool samples. Full recovery was made by the infant"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20693440",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 189,
"text": "Botulinum neurotoxin (BoNT) serotype B (BoNT/B) is one of the serotypes of BoNT that causes deadly human botulism, though it is used clinically for treatment of many neuromuscular diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23097586",
"endSection": "abstract",
"offsetInBeginSection": 197,
"offsetInEndSection": 311,
"text": "Foodborne botulism is a rare and sometimes fatal illness caused by consuming foods containing botulinum neurotoxin"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22513950",
"endSection": "abstract",
"offsetInBeginSection": 578,
"offsetInEndSection": 692,
"text": "To assess the effectiveness and safety of botulinum toxin in treating MPS, excluding MPS in neck and head muscles."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19488551",
"endSection": "abstract",
"offsetInBeginSection": 27,
"offsetInEndSection": 174,
"text": "Botulinum toxin (BTX) is one of the most potent bacterial toxins known and its effectiveness in the treatment of some pain syndromes is well known."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17674683",
"endSection": "abstract",
"offsetInBeginSection": 525,
"offsetInEndSection": 751,
"text": " An emerging treatment option to address these issues is the use of a paralyzing material such as botulinum toxin A (Botox) to decrease the appearance of the wrinkles, which yields a more esthetic and youthful facial appearanc"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26866491",
"endSection": "abstract",
"offsetInBeginSection": 249,
"offsetInEndSection": 413,
"text": "lthough BoNT is an extremely toxic molecule, it is now increasingly used for the treatment of disorders related to muscle hyperactivity and glandular hyperactivity."
}
]
| 6 | BioASQ-training6b | [
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D001905",
"http://www.disease-ontology.org/api/metadata/DOID:11976"
]
| null | 58a341a660087bc10a000017 | 233 |
yesno | Is αCGRP a member of the CGRP family? | ['yes'] | [
"yes"
]
| ['Yes, aCGRP, a 37-residue-long peptide hormone, is a novel amyloidogenic member of the CGRP family.', 'Yes. aCGRP is a member of the CGRP family.', 'Yes, aCGRP is a member of the CGRP family.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/29501724"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29501724",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 55,
"text": "αCGRP, another amyloidogenic member of the CGRP family."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29501724",
"endSection": "abstract",
"offsetInBeginSection": 528,
"offsetInEndSection": 873,
"text": "Therefore, in this work, we investigated the amyloidogenic profile of αCGRP, a 37-residue-long peptide hormone, utilizing both biophysical experimental techniques and Molecular Dynamics simulations. These efforts unravel a novel amyloidogenic member of the CGRP family and provide insights into the mechanism underlying the αCGRP polymerization."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29501724",
"endSection": "abstract",
"offsetInBeginSection": 727,
"offsetInEndSection": 873,
"text": "These efforts unravel a novel amyloidogenic member of the CGRP family and provide insights into the mechanism underlying the αCGRP polymerization."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29501724",
"endSection": "abstract",
"offsetInBeginSection": 727,
"offsetInEndSection": 874,
"text": "These efforts unravel a novel amyloidogenic member of the CGRP family and provide insights into the mechanism underlying the αCGRP polymerization."
}
]
| 11 | BioASQ-training11b | null | null | 5e500d8c6d0a277941000035 | 234 |
yesno | Do plant genomes contain CpG islands? | ['yes'] | [
"yes"
]
| ['Yes. In plant genomes, there exist discrete regions rich in CpG dinucleotides, namely CpG clusters. In rice, most of these CpG clusters are associated with genes. Rice genes are grouped into one of the five classes according to the position of an associated CpG cluster.', 'In plant genomes, there exist discrete regions rich in CpG dinucleotides, namely CpG clusters. In rice, most of these CpG clusters are associated with genes. Rice genes are grouped into one of the five classes according to the position of an associated CpG cluster. Among them, class 1 genes, which harbor a CpG cluster at the 5 -terminus, share similarities with human genes having CpG islands ', 'In plant genomes, there exist discrete regions rich in CpG dinucleotides, namely CpG clusters. In rice, most of these CpG clusters are associated with genes. Rice genes are grouped into one of the five classes according to the position of an associated CpG cluster. Among them, class 1 genes, which harbor a CpG cluster at the 5 -terminus, share similarities with human genes having CpG islands ', 'In plant genomes, there exist discrete regions rich in CpG dinucleotides, namely CpG clusters. In rice, most of these CpG clusters are associated with genes. Rice genes are grouped into one of the five classes according to the position of an associated CpG cluster. Among them, class 1 genes, which harbor a CpG cluster at the 5 -terminus, share similarities with human genes having CpG islands ', 'In plant genomes, there exist discrete regions rich in CpG dinucleotides, namely CpG clusters. In rice, most of these CpG clusters are associated with genes. Rice genes are grouped into one of the five classes according to the position of an associated CpG cluster. Among them, class 1 genes, which harbor a CpG cluster at the 5 -terminus, share similarities with human genes having CpG islands ', 'In plant genomes, there exist discrete regions rich in CpG dinucleotides, namely CpG clusters. In rice, most of these CpG clusters are associated with genes. Rice genes are grouped into one of the five classes according to the position of an associated CpG cluster. Among them, class 1 genes, which harbor a CpG cluster at the 5 -terminus, share similarities with human genes having CpG islands '] | [
"http://www.ncbi.nlm.nih.gov/pubmed/21548945",
"http://www.ncbi.nlm.nih.gov/pubmed/16283384",
"http://www.ncbi.nlm.nih.gov/pubmed/15733327",
"http://www.ncbi.nlm.nih.gov/pubmed/12857799",
"http://www.ncbi.nlm.nih.gov/pubmed/12054347",
"http://www.ncbi.nlm.nih.gov/pubmed/11489175",
"http://www.ncbi.nlm.nih.gov/pubmed/16453856"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21548945",
"endSection": "abstract",
"offsetInBeginSection": 1711,
"offsetInEndSection": 2070,
"text": "This study represents the first systematic genome-scale analysis of DNA curvature, CpG islands and tandem repeats at the DNA sequence level in plant genomes, and finds that not all of the chromosomes in plants follow the same rules common to other eukaryote organisms, suggesting that some of these genomic properties might be considered as specific to plants"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16283384",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 394,
"text": "In plant genomes, there exist discrete regions rich in CpG dinucleotides, namely CpG clusters. In rice, most of these CpG clusters are associated with genes. Rice genes are grouped into one of the five classes according to the position of an associated CpG cluster. Among them, class 1 genes, which harbor a CpG cluster at the 5'-terminus, share similarities with human genes having CpG islands"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16283384",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "Segmental distribution of genes harboring a CpG island-like region on rice chromosomes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15733327",
"endSection": "abstract",
"offsetInBeginSection": 1986,
"offsetInEndSection": 2516,
"text": "Highly-expressed Arabidopsis genes had overall a more marked GC-skew in the TSS compared to genes with low expression levels. We therefore propose that the GC-skew around the TSS in some plants and fungi is related to transcription. It might be caused by mutations during transcription initiation or the frequent use of transcription factor-biding sites having a strand preference. In addition, GC-skew is a good candidate index for TSS prediction in plant genomes, where there is a lack of correlation among CpG islands and genes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12857799",
"endSection": "abstract",
"offsetInBeginSection": 1610,
"offsetInEndSection": 2066,
"text": "Preliminary analysis shows that promoter location based on the detection of potential CpG/CpNpG islands in the Arabidopsis genome is not straightforward. Nevertheless, because the landscape of CpG/CpNpG islands differs considerably between promoters and introns on the one side and exons (whether coding or not) on the other, more sophisticated approaches can probably be developed for the successful detection of \"putative\" CpG and CpNpG islands in plants"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21548945",
"endSection": "abstract",
"offsetInBeginSection": 1664,
"offsetInEndSection": 2024,
"text": "This study represents the first systematic genome-scale analysis of DNA curvature, CpG islands and tandem repeats at the DNA sequence level in plant genomes, and finds that not all of the chromosomes in plants follow the same rules common to other eukaryote organisms, suggesting that some of these genomic properties might be considered as specific to plants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11489175",
"endSection": "abstract",
"offsetInBeginSection": 648,
"offsetInEndSection": 818,
"text": "These plant CpG-rich clusters satisfied the criteria used for identifying human CpG islands, which suggests that these CpG clusters may be regarded as plant CpG islands."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21548945",
"endSection": "abstract",
"offsetInBeginSection": 1664,
"offsetInEndSection": 2024,
"text": "This study represents the first systematic genome-scale analysis of DNA curvature, CpG islands and tandem repeats at the DNA sequence level in plant genomes, and finds that not all of the chromosomes in plants follow the same rules common to other eukaryote organisms, suggesting that some of these genomic properties might be considered as specific to plants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11489175",
"endSection": "abstract",
"offsetInBeginSection": 648,
"offsetInEndSection": 818,
"text": "These plant CpG-rich clusters satisfied the criteria used for identifying human CpG islands, which suggests that these CpG clusters may be regarded as plant CpG islands."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21548945",
"endSection": "abstract",
"offsetInBeginSection": 1664,
"offsetInEndSection": 2024,
"text": "This study represents the first systematic genome-scale analysis of DNA curvature, CpG islands and tandem repeats at the DNA sequence level in plant genomes, and finds that not all of the chromosomes in plants follow the same rules common to other eukaryote organisms, suggesting that some of these genomic properties might be considered as specific to plants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11489175",
"endSection": "abstract",
"offsetInBeginSection": 648,
"offsetInEndSection": 818,
"text": "These plant CpG-rich clusters satisfied the criteria used for identifying human CpG islands, which suggests that these CpG clusters may be regarded as plant CpG islands."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21548945",
"endSection": "abstract",
"offsetInBeginSection": 1664,
"offsetInEndSection": 2024,
"text": "This study represents the first systematic genome-scale analysis of DNA curvature, CpG islands and tandem repeats at the DNA sequence level in plant genomes, and finds that not all of the chromosomes in plants follow the same rules common to other eukaryote organisms, suggesting that some of these genomic properties might be considered as specific to plants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11489175",
"endSection": "abstract",
"offsetInBeginSection": 648,
"offsetInEndSection": 818,
"text": "These plant CpG-rich clusters satisfied the criteria used for identifying human CpG islands, which suggests that these CpG clusters may be regarded as plant CpG islands."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21548945",
"endSection": "abstract",
"offsetInBeginSection": 1698,
"offsetInEndSection": 2071,
"text": "CONCLUSIONS: This study represents the first systematic genome-scale analysis of DNA curvature, CpG islands and tandem repeats at the DNA sequence level in plant genomes, and finds that not all of the chromosomes in plants follow the same rules common to other eukaryote organisms, suggesting that some of these genomic properties might be considered as specific to plants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16283384",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "In plant genomes, there exist discrete regions rich in CpG dinucleotides, namely CpG clusters."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11489175",
"endSection": "abstract",
"offsetInBeginSection": 657,
"offsetInEndSection": 826,
"text": "These plant CpG-rich clusters satisfied the criteria used for identifying human CpG islands, which suggests that these CpG clusters may be regarded as plant CpG islands."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16453856",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 67,
"text": "Unmethylated CpG islands associated with genes in higher plant DNA."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21548945",
"endSection": "abstract",
"offsetInBeginSection": 1679,
"offsetInEndSection": 2039,
"text": "This study represents the first systematic genome-scale analysis of DNA curvature, CpG islands and tandem repeats at the DNA sequence level in plant genomes, and finds that not all of the chromosomes in plants follow the same rules common to other eukaryote organisms, suggesting that some of these genomic properties might be considered as specific to plants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11489175",
"endSection": "abstract",
"offsetInBeginSection": 657,
"offsetInEndSection": 825,
"text": "These plant CpG-rich clusters satisfied the criteria used for identifying human CpG islands, which suggests that these CpG clusters may be regarded as plant CpG islands"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11489175",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 175,
"text": "We screened plant genome sequences, primarily from rice and Arabidopsis thaliana, for CpG islands, and identified DNA segments rich in CpG dinucleotides within these sequences"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21548945",
"endSection": "abstract",
"offsetInBeginSection": 1679,
"offsetInEndSection": 2039,
"text": "This study represents the first systematic genome-scale analysis of DNA curvature, CpG islands and tandem repeats at the DNA sequence level in plant genomes, and finds that not all of the chromosomes in plants follow the same rules common to other eukaryote organisms, suggesting that some of these genomic properties might be considered as specific to plants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11489175",
"endSection": "abstract",
"offsetInBeginSection": 657,
"offsetInEndSection": 825,
"text": "These plant CpG-rich clusters satisfied the criteria used for identifying human CpG islands, which suggests that these CpG clusters may be regarded as plant CpG islands"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11489175",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 175,
"text": "We screened plant genome sequences, primarily from rice and Arabidopsis thaliana, for CpG islands, and identified DNA segments rich in CpG dinucleotides within these sequences"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21548945",
"endSection": "abstract",
"offsetInBeginSection": 1679,
"offsetInEndSection": 2039,
"text": "This study represents the first systematic genome-scale analysis of DNA curvature, CpG islands and tandem repeats at the DNA sequence level in plant genomes, and finds that not all of the chromosomes in plants follow the same rules common to other eukaryote organisms, suggesting that some of these genomic properties might be considered as specific to plants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11489175",
"endSection": "abstract",
"offsetInBeginSection": 657,
"offsetInEndSection": 825,
"text": "These plant CpG-rich clusters satisfied the criteria used for identifying human CpG islands, which suggests that these CpG clusters may be regarded as plant CpG islands"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11489175",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 175,
"text": "We screened plant genome sequences, primarily from rice and Arabidopsis thaliana, for CpG islands, and identified DNA segments rich in CpG dinucleotides within these sequences"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21548945",
"endSection": "abstract",
"offsetInBeginSection": 1679,
"offsetInEndSection": 2039,
"text": "This study represents the first systematic genome-scale analysis of DNA curvature, CpG islands and tandem repeats at the DNA sequence level in plant genomes, and finds that not all of the chromosomes in plants follow the same rules common to other eukaryote organisms, suggesting that some of these genomic properties might be considered as specific to plants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11489175",
"endSection": "abstract",
"offsetInBeginSection": 657,
"offsetInEndSection": 825,
"text": "These plant CpG-rich clusters satisfied the criteria used for identifying human CpG islands, which suggests that these CpG clusters may be regarded as plant CpG islands"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11489175",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 175,
"text": "We screened plant genome sequences, primarily from rice and Arabidopsis thaliana, for CpG islands, and identified DNA segments rich in CpG dinucleotides within these sequences"
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018899",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D044404",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D018745"
]
| []
| 553d0005f321868558000011 | 235 |
yesno | Is ocular melanosis a risk factor for uveal melanoma? | ['yes'] | [
"yes"
]
| ['Yes, ocular melanosis (melanosis oculi) is a risk factor for uveal melanoma.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/21670341",
"http://www.ncbi.nlm.nih.gov/pubmed/12647250",
"http://www.ncbi.nlm.nih.gov/pubmed/9442799",
"http://www.ncbi.nlm.nih.gov/pubmed/8292886",
"http://www.ncbi.nlm.nih.gov/pubmed/23681424",
"http://www.ncbi.nlm.nih.gov/pubmed/6677847",
"http://www.ncbi.nlm.nih.gov/pubmed/1520683"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23681424",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 201,
"text": "Ocular/oculodermal (oculo[dermal]) melanocytosis is a congenital periocular pigmentary condition that can lead to the development of uveal melanoma, estimated at 1 in 400 affected patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12647250",
"endSection": "abstract",
"offsetInBeginSection": 352,
"offsetInEndSection": 582,
"text": "Melanosis oculi is often underestimated as a risk factor for uveal melanoma and glaucoma. Ophthalmic surveillance, every 6 or 12 months is important, in patients with ocular melanocytosis for early detection of high risk diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9442799",
"endSection": "abstract",
"offsetInBeginSection": 992,
"offsetInEndSection": 1520,
"text": " One of about 400 patients with ODM followed for life is estimated to develop uveal melanoma. Excessive melanocytes in the uveal tract in ODM may provide the biologic basis for susceptibility to the development of uveal melanoma. Patients with ODM should be monitored ophthalmoscopically, especially during the susceptible period, for the development of uveal melanoma. The authors suggest that a national registry of ODM patients be created and prospective data collected to better assess the risk of developing uveal melanoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9442799",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 132,
"text": "In the white population, an association between oculo(dermal) melanocytosis (ODM) and uveal melanoma is well recognized. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8292886",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 325,
"text": "Malignant melanomas may arise in the uveal tract, the conjunctiva, the skin of the eyelid, or the orbit. Risk factors so far identified include pre-existing choroidal naevi for uveal melanomas, primary acquired melanosis (PAM) for conjunctival tumours, and ocular and oculodermal melanocytosis for uveal and orbital lesions. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8292886",
"endSection": "abstract",
"offsetInBeginSection": 104,
"offsetInEndSection": 323,
"text": "Risk factors so far identified include pre-existing choroidal naevi for uveal melanomas, primary acquired melanosis (PAM) for conjunctival tumours, and ocular and oculodermal melanocytosis for uveal and orbital lesions."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21670341",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 174,
"text": "Phacomatosis pigmentovascularis of cesioflammea type in 7 patients: combination of ocular pigmentation (melanocytosis or melanosis) and nevus flammeus with risk for melanoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12647250",
"endSection": "abstract",
"offsetInBeginSection": 197,
"offsetInEndSection": 441,
"text": "In the fourth case the melanoma was detected in a routine examination and we were able to apply a preserving treatment with I125 brachytherapy.DISCUSSION: Melanosis oculi is often underestimated as a risk factor for uveal melanoma and glaucoma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23681424",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Association of ocular and oculodermal melanocytosis with the rate of uveal melanoma metastasis: analysis of 7872 consecutive eyes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8292886",
"endSection": "abstract",
"offsetInBeginSection": 105,
"offsetInEndSection": 323,
"text": "Risk factors so far identified include pre-existing choroidal naevi for uveal melanomas, primary acquired melanosis (PAM) for conjunctival tumours, and ocular and oculodermal melanocytosis for uveal and orbital lesions"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12647250",
"endSection": "abstract",
"offsetInBeginSection": 190,
"offsetInEndSection": 421,
"text": "In the fourth case the melanoma was detected in a routine examination and we were able to apply a preserving treatment with I125 brachytherapy.Melanosis oculi is often underestimated as a risk factor for uveal melanoma and glaucoma"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23681424",
"endSection": "abstract",
"offsetInBeginSection": 190,
"offsetInEndSection": 813,
"text": "In this study, patients with melanocytosis who developed uveal melanoma were found to have double the risk for metastasis compared with those without melanocytosis.To determine the relationship of oculo(dermal) melanocytosis to the prognosis of patients with uveal melanoma.Retrospective chart review of 7872 patients with uveal melanoma treated at the Ocular Oncology Service, Wills Eye Institute, from August 25, 1970, through August 27, 2008.Enucleation, plaque radiotherapy, local resection, or thermotherapy.Metastasis and death.Of 7872 patients with uveal melanoma, oculo(dermal) melanocytosis was present in 230 (3%)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23681424",
"endSection": "abstract",
"offsetInBeginSection": 1596,
"offsetInEndSection": 1913,
"text": "By multivariable analysis, the factors predictive of metastasis in patients harboring uveal melanoma associated with oculo(dermal) melanocytosis were increased tumor thickness (P = .001) and the presence of subretinal fluid (P = .05), and the only factor predictive of death was increased tumor thickness (P = .009). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12647250",
"endSection": "abstract",
"offsetInBeginSection": 190,
"offsetInEndSection": 422,
"text": "In the fourth case the melanoma was detected in a routine examination and we were able to apply a preserving treatment with I125 brachytherapy.Melanosis oculi is often underestimated as a risk factor for uveal melanoma and glaucoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8292886",
"endSection": "abstract",
"offsetInBeginSection": 105,
"offsetInEndSection": 324,
"text": "Risk factors so far identified include pre-existing choroidal naevi for uveal melanomas, primary acquired melanosis (PAM) for conjunctival tumours, and ocular and oculodermal melanocytosis for uveal and orbital lesions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23681424",
"endSection": "abstract",
"offsetInBeginSection": 1900,
"offsetInEndSection": 2077,
"text": "CONCLUSIONS AND RELEVANCE Patients with uveal melanoma associated with oculo(dermal) melanocytosis have double the risk for metastasis compared with those with no melanocytosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23681424",
"endSection": "abstract",
"offsetInBeginSection": 1494,
"offsetInEndSection": 1810,
"text": "By multivariable analysis, the factors predictive of metastasis in patients harboring uveal melanoma associated with oculo(dermal) melanocytosis were increased tumor thickness (P = .001) and the presence of subretinal fluid (P = .05), and the only factor predictive of death was increased tumor thickness (P = .009)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23681424",
"endSection": "abstract",
"offsetInBeginSection": 1811,
"offsetInEndSection": 1988,
"text": "CONCLUSIONS AND RELEVANCE Patients with uveal melanoma associated with oculo(dermal) melanocytosis have double the risk for metastasis compared with those with no melanocytosis."
}
]
| 6 | BioASQ-training6b | [
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D008545",
"http://www.disease-ontology.org/api/metadata/DOID:1909",
"http://www.disease-ontology.org/api/metadata/DOID:6566",
"http://www.disease-ontology.org/api/metadata/DOID:6039",
"http://www.disease-ontology.org/api/metadata/DOID:1752",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D012306"
]
| null | 58b5320e22d3005309000002 | 236 |
yesno | Are Crocus sativus compounds being considered against Alzheimer's disease? | ['yes'] | [
"yes"
]
| ["Yes, it has been observed that Crocus sativus extracts and compounds have a positive effect against Alzheimer's disease."] | [
"http://www.ncbi.nlm.nih.gov/pubmed/28471166"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28471166",
"endSection": "abstract",
"offsetInBeginSection": 169,
"offsetInEndSection": 439,
"text": "Previous evidence suggested that Crocus sativus is linked to improving cognitive function in Alzheimer's disease (AD) patients. The aim of this study was to in vitro and in vivo investigate the mechanism(s) by which Crocus sativus exerts its positive effect against AD. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28471166",
"endSection": "abstract",
"offsetInBeginSection": 1551,
"offsetInEndSection": 1690,
"text": "Collectively, findings from this study support the positive effect of Crocus sativus against AD by reducing Aβ pathological manifestations."
}
]
| 11 | BioASQ-training11b | null | null | 5c891d5075a4a5d219000011 | 237 |
yesno | Is NOD1 activated in inflammation? | ['yes'] | [
"yes"
]
| ["Nod proteins fight off bacterial infections by stimulating proinflammatory signaling and cytokine networks and by inducing antimicrobial effectors, such as nitric oxide and antimicrobial peptides. NOD1 engagement generates an inflammatory response via activation of NFκB and MAPK pathways and several inflammatory disorders, such as Crohn's disease and asthma, are linked to genetic changes in either Nod1 or Nod2. Nod1 is also critically implicated in shaping adaptive immune responses towards bacterial-derived constituents. Together, Nod1 and Nod2 represent central players in the control of immune responses to bacterial infections and inflammation. Mice deficient for both Nod1 and Nod2 had attenuated inflammatory pathology, reduced levels of inflammatory cytokines, and increased colonization of the mucosal tissue", 'Nod1 and Nod2 control bacterial infections and inflammation', 'Nod1 and Nod2 control bacterial infections and inflammation', 'Nod1 and Nod2 control bacterial infections and inflammation', 'Nod1/2 DKO mice show increased susceptibility for intestinal permeability while vascular permeability was not affected. The present study analyzed Nod1 and Nod2 double deficient (Nod1/2 DKO) mice under physiological and inflammatory conditions. The increased intestinal permeability is associated with enhanced inflammatory cytokine production and epithelial cell proliferation in Nod1-deficient mice as compared with wild-type mice. However, the influence of Rip2 was strictly dependent on infection conditions that favored expression of the Salmonella pathogenicity island 2 (SPI-2) type III secretion system (TTSS), as Rip2 was dispensable for inflammation when mice were infected with bacteria grown under conditions that promoted expression of the SPI-1 TTSS.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/24041848",
"http://www.ncbi.nlm.nih.gov/pubmed/22870324",
"http://www.ncbi.nlm.nih.gov/pubmed/23162548",
"http://www.ncbi.nlm.nih.gov/pubmed/23259058",
"http://www.ncbi.nlm.nih.gov/pubmed/21330608",
"http://www.ncbi.nlm.nih.gov/pubmed/20921147",
"http://www.ncbi.nlm.nih.gov/pubmed/19074813",
"http://www.ncbi.nlm.nih.gov/pubmed/19074871",
"http://www.ncbi.nlm.nih.gov/pubmed/17690884",
"http://www.ncbi.nlm.nih.gov/pubmed/21715553",
"http://www.ncbi.nlm.nih.gov/pubmed/23712977",
"http://www.ncbi.nlm.nih.gov/pubmed/18574154",
"http://www.ncbi.nlm.nih.gov/pubmed/21677137",
"http://www.ncbi.nlm.nih.gov/pubmed/24828250",
"http://www.ncbi.nlm.nih.gov/pubmed/24534531",
"http://www.ncbi.nlm.nih.gov/pubmed/25732381",
"http://www.ncbi.nlm.nih.gov/pubmed/24829218",
"http://www.ncbi.nlm.nih.gov/pubmed/23848281",
"http://www.ncbi.nlm.nih.gov/pubmed/21469090",
"http://www.ncbi.nlm.nih.gov/pubmed/23740944",
"http://www.ncbi.nlm.nih.gov/pubmed/24279792",
"http://www.ncbi.nlm.nih.gov/pubmed/12813035",
"http://www.ncbi.nlm.nih.gov/pubmed/25253572"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17690884",
"endSection": "title",
"offsetInBeginSection": 14,
"offsetInEndSection": 73,
"text": "Nod1 and Nod2 control bacterial infections and inflammation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17690884",
"endSection": "abstract",
"offsetInBeginSection": 246,
"offsetInEndSection": 370,
"text": "The Nod proteins Nod1 and Nod2 are two NLR family members that trigger immune defense in response to bacterial peptidoglycan"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17690884",
"endSection": "abstract",
"offsetInBeginSection": 372,
"offsetInEndSection": 568,
"text": "Nod proteins fight off bacterial infections by stimulating proinflammatory signaling and cytokine networks and by inducing antimicrobial effectors, such as nitric oxide and antimicrobial peptides."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17690884",
"endSection": "abstract",
"offsetInBeginSection": 569,
"offsetInEndSection": 680,
"text": "Nod1 is also critically implicated in shaping adaptive immune responses towards bacterial-derived constituents."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17690884",
"endSection": "abstract",
"offsetInBeginSection": 909,
"offsetInEndSection": 1035,
"text": "Together, Nod1 and Nod2 represent central players in the control of immune responses to bacterial infections and inflammation."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19074871",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 95,
"text": "The innate immune receptor Nod1 protects the intestine from inflammation-induced tumorigenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19074871",
"endSection": "abstract",
"offsetInBeginSection": 677,
"offsetInEndSection": 1093,
"text": "we show that Nod1 deficiency results in the increased development of both colitis-associated and Apc tumor suppressor-related colon tumors. In the absence of Nod1 signaling, there is a greater disruption of the intestinal epithelial cell barrier due to chemically induced injury as manifested by increased surface epithelial apoptosis early on during chemically induced colitis and increased intestinal permeability."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19074871",
"endSection": "abstract",
"offsetInBeginSection": 1094,
"offsetInEndSection": 1282,
"text": "The increased intestinal permeability is associated with enhanced inflammatory cytokine production and epithelial cell proliferation in Nod1-deficient mice as compared with wild-type mice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19074871",
"endSection": "abstract",
"offsetInBeginSection": 1283,
"offsetInEndSection": 1560,
"text": "Depletion of the gut microbiota suppressed tumor development in Nod1-deficient mice, thus highlighting a link between the commensal bacteria within the intestine and the host innate immune Nod1 signaling pathway in the regulation inflammation-mediated colon cancer development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19074813",
"endSection": "abstract",
"offsetInBeginSection": 969,
"offsetInEndSection": 1079,
"text": " NOD1 protein is expressed in the eye and promotes ocular inflammation in a dose- and time-dependent fashion. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19074813",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "NOD1 expression in the eye and functional contribution to IL-1beta-dependent ocular inflammation in mice"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19074813",
"endSection": "abstract",
"offsetInBeginSection": 151,
"offsetInEndSection": 283,
"text": "Polymorphisms in NOD1 are associated with autoinflammatory diseases characterized by uveitis such as Crohn's disease and sarcoidosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19074813",
"endSection": "abstract",
"offsetInBeginSection": 285,
"offsetInEndSection": 457,
"text": "NOD1 is homologous to NOD2, which is responsible for an autosomal dominant form of uveitis. Nonetheless, the role of NOD1 in intraocular inflammation has not been explored."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20921147",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 72,
"text": "Nod1 and Nod2 regulation of inflammation in the Salmonella colitis model"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20921147",
"endSection": "abstract",
"offsetInBeginSection": 291,
"offsetInEndSection": 458,
"text": "mice deficient for both Nod1 and Nod2 had attenuated inflammatory pathology, reduced levels of inflammatory cytokines, and increased colonization of the mucosal tissue"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21330608",
"endSection": "abstract",
"offsetInBeginSection": 1249,
"offsetInEndSection": 1400,
"text": "The present study has demonstrated an unexpected role of Nod1 in the development of site-specific vascular inflammation, especially coronary arteritis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21330608",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 55,
"text": "Nod1 ligands induce site-specific vascular inflammation"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23259058",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "Phenotyping of Nod1/2 double deficient mice and characterization of Nod1/2 in systemic inflammation and associated renal disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23259058",
"endSection": "abstract",
"offsetInBeginSection": 147,
"offsetInEndSection": 270,
"text": "The present study analyzed Nod1 and Nod2 double deficient (Nod1/2 DKO) mice under physiological and inflammatory conditions"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23259058",
"endSection": "abstract",
"offsetInBeginSection": 389,
"offsetInEndSection": 510,
"text": "Several inflammatory disorders, such as Crohn's disease and asthma, are linked to genetic changes in either Nod1 or Nod2."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23259058",
"endSection": "abstract",
"offsetInBeginSection": 1696,
"offsetInEndSection": 1835,
"text": "Systematic analysis of Nod1/2 DKO mice revealed a possible role of Nod1/2 in the development of renal disease during systemic inflammation."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23162548",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 53,
"text": "NOD1 and NOD2 Signaling in Infection and Inflammation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870324",
"endSection": "abstract",
"offsetInBeginSection": 303,
"offsetInEndSection": 396,
"text": "NOD1 engagement generates an inflammatory response via activation of NFκB and MAPK pathways. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870324",
"endSection": "abstract",
"offsetInBeginSection": 1090,
"offsetInEndSection": 1246,
"text": "In addition we profile novel inhibitors of RIP2 and NOD1 itself, which specifically inhibit NOD1 ligand induced inflammatory signalling in the vasculature. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870324",
"endSection": "abstract",
"offsetInBeginSection": 1428,
"offsetInEndSection": 1612,
"text": "This data supports the potential utility of NOD1 and RIP2 as therapeutic targets in human disease where vascular inflammation is a clinical feature, such as in sepsis and septic shock."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24041848",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 137,
"text": "NOD1 expression elicited by iE-DAP in first trimester human trophoblast cells and its potential role in infection-associated inflammation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24041848",
"endSection": "abstract",
"offsetInBeginSection": 267,
"offsetInEndSection": 462,
"text": "This study aimed to investigate the expression and function of NOD1 in first trimester trophoblast cells, and evaluate the potential role of trophoblast cells in infection-associated inflammation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24041848",
"endSection": "abstract",
"offsetInBeginSection": 1503,
"offsetInEndSection": 1686,
"text": "NOD1 may have a role in mediating infection-associated inflammation. Once iE-DAP is recognized by NOD1, the inflammatory response may be induced via NOD1-RICK-NF-κB-mediated pathways."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21715553",
"endSection": "abstract",
"offsetInBeginSection": 1134,
"offsetInEndSection": 1252,
"text": "NOD1/2(-/-) mice were protected from HFD-induced inflammation, lipid accumulation, and peripheral insulin intolerance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18574154",
"endSection": "abstract",
"offsetInBeginSection": 774,
"offsetInEndSection": 1007,
"text": "In contrast, Nod1 gene-deficient mice developed enhanced joint inflammation with concomitant elevated levels of proinflammatory cytokines and cartilage damage, consistent with a model in which Nod1 controls the inflammatory reaction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18574154",
"endSection": "abstract",
"offsetInBeginSection": 1565,
"offsetInEndSection": 1794,
"text": "These data indicate that the NLR family members Nod1 and Nod2 have different functions in controlling inflammation, and that intracellular Nod1-Nod2 interactions may determine the severity of arthritis in this experimental model."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24534531",
"endSection": "abstract",
"offsetInBeginSection": 1059,
"offsetInEndSection": 1315,
"text": "Whereas the lymphotoxin pathway was critical for the induction of the B cell chemoattractant CXCL13 in response to Nod1 agonists, B cell accumulation within the spleen following Nod1-induced systemic inflammation was independent of the lymphotoxin pathway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24829218",
"endSection": "abstract",
"offsetInBeginSection": 627,
"offsetInEndSection": 735,
"text": "The effect of NOD1 and NOD2 activation on inflammation and the insulin signalling pathway was also assessed."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19074813",
"endSection": "abstract",
"offsetInBeginSection": 445,
"offsetInEndSection": 525,
"text": "Nonetheless, the role of NOD1 in intraocular inflammation has not been explored."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870324",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "A key role for the endothelium in NOD1 mediated vascular inflammation: comparison to TLR4 responses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21677137",
"endSection": "abstract",
"offsetInBeginSection": 388,
"offsetInEndSection": 522,
"text": "We previously demonstrated that human first-trimester trophoblasts express Nod1 and Nod2, which trigger inflammation upon stimulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23848281",
"endSection": "abstract",
"offsetInBeginSection": 1026,
"offsetInEndSection": 1166,
"text": "In addition, recent studies have revealed a role for intracellular NOD1 receptors in the regulation of vascular inflammation and metabolism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24829218",
"endSection": "abstract",
"offsetInBeginSection": 1919,
"offsetInEndSection": 2083,
"text": "In conclusion, the present findings describe an important role for NOD1 in the development of insulin resistance and inflammation in pregnancies complicated by GDM."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21715553",
"endSection": "abstract",
"offsetInBeginSection": 1134,
"offsetInEndSection": 1252,
"text": "NOD1/2(-/-) mice were protected from HFD-induced inflammation, lipid accumulation, and peripheral insulin intolerance."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23259058",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Phenotyping of Nod1/2 double deficient mice and characterization of Nod1/2 in systemic inflammation and associated renal disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18574154",
"endSection": "abstract",
"offsetInBeginSection": 774,
"offsetInEndSection": 1007,
"text": "In contrast, Nod1 gene-deficient mice developed enhanced joint inflammation with concomitant elevated levels of proinflammatory cytokines and cartilage damage, consistent with a model in which Nod1 controls the inflammatory reaction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18574154",
"endSection": "abstract",
"offsetInBeginSection": 1565,
"offsetInEndSection": 1794,
"text": "These data indicate that the NLR family members Nod1 and Nod2 have different functions in controlling inflammation, and that intracellular Nod1-Nod2 interactions may determine the severity of arthritis in this experimental model."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24534531",
"endSection": "abstract",
"offsetInBeginSection": 1059,
"offsetInEndSection": 1315,
"text": "Whereas the lymphotoxin pathway was critical for the induction of the B cell chemoattractant CXCL13 in response to Nod1 agonists, B cell accumulation within the spleen following Nod1-induced systemic inflammation was independent of the lymphotoxin pathway."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19074813",
"endSection": "abstract",
"offsetInBeginSection": 445,
"offsetInEndSection": 525,
"text": "Nonetheless, the role of NOD1 in intraocular inflammation has not been explored."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870324",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "A key role for the endothelium in NOD1 mediated vascular inflammation: comparison to TLR4 responses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21677137",
"endSection": "abstract",
"offsetInBeginSection": 388,
"offsetInEndSection": 522,
"text": "We previously demonstrated that human first-trimester trophoblasts express Nod1 and Nod2, which trigger inflammation upon stimulation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24829218",
"endSection": "abstract",
"offsetInBeginSection": 627,
"offsetInEndSection": 735,
"text": "The effect of NOD1 and NOD2 activation on inflammation and the insulin signalling pathway was also assessed."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23848281",
"endSection": "abstract",
"offsetInBeginSection": 1026,
"offsetInEndSection": 1166,
"text": "In addition, recent studies have revealed a role for intracellular NOD1 receptors in the regulation of vascular inflammation and metabolism."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21677137",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "Nod1 activation by bacterial iE-DAP induces maternal-fetal inflammation and preterm labor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24829218",
"endSection": "abstract",
"offsetInBeginSection": 151,
"offsetInEndSection": 400,
"text": "The nucleotide-binding oligomerisation domain (NOD) intracellular molecules recognise a wide range of microbial products, as well as other intracellular danger signals, thereby initiating inflammation through activation of nuclear factor κB (NFκB). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21330608",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 56,
"text": "Nod1 ligands induce site-specific vascular inflammation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23740944",
"endSection": "abstract",
"offsetInBeginSection": 169,
"offsetInEndSection": 484,
"text": "The nucleotide oligomerization domain (NOD) intracellular molecules recognize a wide range of microbial products as well as other intracellular danger signals, thereby initiating inflammation through activation of nuclear factor KB (NFKB), a central regulator of the terminal processes of human labor and delivery. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21715553",
"endSection": "abstract",
"offsetInBeginSection": 1865,
"offsetInEndSection": 2003,
"text": "CONCLUSIONS: We identify NOD proteins as innate immune components that are involved in diet-induced inflammation and insulin intolerance. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20921147",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 73,
"text": "Nod1 and Nod2 regulation of inflammation in the Salmonella colitis model."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21469090",
"endSection": "abstract",
"offsetInBeginSection": 142,
"offsetInEndSection": 308,
"text": "In particular, muramyl peptides trigger inflammation, contribute to host defense against microbial infections, and modulate the adaptive immune response to antigens. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870324",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "A key role for the endothelium in NOD1 mediated vascular inflammation: comparison to TLR4 responses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21715553",
"endSection": "abstract",
"offsetInBeginSection": 794,
"offsetInEndSection": 919,
"text": "Systemic and tissue-specific inflammation was assessed using enzyme-linked immunosorbent assays in NOD ligand-injected mice. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21677137",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "Nod1 activation by bacterial iE-DAP induces maternal-fetal inflammation and preterm labor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24829218",
"endSection": "abstract",
"offsetInBeginSection": 151,
"offsetInEndSection": 400,
"text": "The nucleotide-binding oligomerisation domain (NOD) intracellular molecules recognise a wide range of microbial products, as well as other intracellular danger signals, thereby initiating inflammation through activation of nuclear factor κB (NFκB). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21330608",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 56,
"text": "Nod1 ligands induce site-specific vascular inflammation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23740944",
"endSection": "abstract",
"offsetInBeginSection": 169,
"offsetInEndSection": 484,
"text": "The nucleotide oligomerization domain (NOD) intracellular molecules recognize a wide range of microbial products as well as other intracellular danger signals, thereby initiating inflammation through activation of nuclear factor KB (NFKB), a central regulator of the terminal processes of human labor and delivery. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21715553",
"endSection": "abstract",
"offsetInBeginSection": 1865,
"offsetInEndSection": 2003,
"text": "CONCLUSIONS: We identify NOD proteins as innate immune components that are involved in diet-induced inflammation and insulin intolerance. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20921147",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 73,
"text": "Nod1 and Nod2 regulation of inflammation in the Salmonella colitis model."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21469090",
"endSection": "abstract",
"offsetInBeginSection": 142,
"offsetInEndSection": 308,
"text": "In particular, muramyl peptides trigger inflammation, contribute to host defense against microbial infections, and modulate the adaptive immune response to antigens. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870324",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "A key role for the endothelium in NOD1 mediated vascular inflammation: comparison to TLR4 responses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21715553",
"endSection": "abstract",
"offsetInBeginSection": 794,
"offsetInEndSection": 919,
"text": "Systemic and tissue-specific inflammation was assessed using enzyme-linked immunosorbent assays in NOD ligand-injected mice. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21677137",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "Nod1 activation by bacterial iE-DAP induces maternal-fetal inflammation and preterm labor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24829218",
"endSection": "abstract",
"offsetInBeginSection": 151,
"offsetInEndSection": 400,
"text": "The nucleotide-binding oligomerisation domain (NOD) intracellular molecules recognise a wide range of microbial products, as well as other intracellular danger signals, thereby initiating inflammation through activation of nuclear factor κB (NFκB). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21330608",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 56,
"text": "Nod1 ligands induce site-specific vascular inflammation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23740944",
"endSection": "abstract",
"offsetInBeginSection": 169,
"offsetInEndSection": 484,
"text": "The nucleotide oligomerization domain (NOD) intracellular molecules recognize a wide range of microbial products as well as other intracellular danger signals, thereby initiating inflammation through activation of nuclear factor KB (NFKB), a central regulator of the terminal processes of human labor and delivery. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21715553",
"endSection": "abstract",
"offsetInBeginSection": 1865,
"offsetInEndSection": 2003,
"text": "CONCLUSIONS: We identify NOD proteins as innate immune components that are involved in diet-induced inflammation and insulin intolerance. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20921147",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 73,
"text": "Nod1 and Nod2 regulation of inflammation in the Salmonella colitis model."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21469090",
"endSection": "abstract",
"offsetInBeginSection": 142,
"offsetInEndSection": 308,
"text": "In particular, muramyl peptides trigger inflammation, contribute to host defense against microbial infections, and modulate the adaptive immune response to antigens. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870324",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "A key role for the endothelium in NOD1 mediated vascular inflammation: comparison to TLR4 responses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21715553",
"endSection": "abstract",
"offsetInBeginSection": 794,
"offsetInEndSection": 919,
"text": "Systemic and tissue-specific inflammation was assessed using enzyme-linked immunosorbent assays in NOD ligand-injected mice. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21677137",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "Nod1 activation by bacterial iE-DAP induces maternal-fetal inflammation and preterm labor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24829218",
"endSection": "abstract",
"offsetInBeginSection": 151,
"offsetInEndSection": 400,
"text": "The nucleotide-binding oligomerisation domain (NOD) intracellular molecules recognise a wide range of microbial products, as well as other intracellular danger signals, thereby initiating inflammation through activation of nuclear factor κB (NFκB). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21330608",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 56,
"text": "Nod1 ligands induce site-specific vascular inflammation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23740944",
"endSection": "abstract",
"offsetInBeginSection": 169,
"offsetInEndSection": 484,
"text": "The nucleotide oligomerization domain (NOD) intracellular molecules recognize a wide range of microbial products as well as other intracellular danger signals, thereby initiating inflammation through activation of nuclear factor KB (NFKB), a central regulator of the terminal processes of human labor and delivery. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21715553",
"endSection": "abstract",
"offsetInBeginSection": 1865,
"offsetInEndSection": 2223,
"text": "CONCLUSIONS: We identify NOD proteins as innate immune components that are involved in diet-induced inflammation and insulin intolerance. Acute activation of NOD proteins by mimetics of bacterial PGNs causes whole-body insulin resistance, bolstering the concept that innate immune responses to distinctive bacterial cues directly lead to insulin resistance. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20921147",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 73,
"text": "Nod1 and Nod2 regulation of inflammation in the Salmonella colitis model."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21469090",
"endSection": "abstract",
"offsetInBeginSection": 142,
"offsetInEndSection": 308,
"text": "In particular, muramyl peptides trigger inflammation, contribute to host defense against microbial infections, and modulate the adaptive immune response to antigens. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870324",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "A key role for the endothelium in NOD1 mediated vascular inflammation: comparison to TLR4 responses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21715553",
"endSection": "abstract",
"offsetInBeginSection": 794,
"offsetInEndSection": 919,
"text": "Systemic and tissue-specific inflammation was assessed using enzyme-linked immunosorbent assays in NOD ligand-injected mice. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21677137",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "Nod1 activation by bacterial iE-DAP induces maternal-fetal inflammation and preterm labor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24829218",
"endSection": "abstract",
"offsetInBeginSection": 151,
"offsetInEndSection": 400,
"text": "The nucleotide-binding oligomerisation domain (NOD) intracellular molecules recognise a wide range of microbial products, as well as other intracellular danger signals, thereby initiating inflammation through activation of nuclear factor κB (NFκB). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21330608",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 56,
"text": "Nod1 ligands induce site-specific vascular inflammation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23740944",
"endSection": "abstract",
"offsetInBeginSection": 169,
"offsetInEndSection": 484,
"text": "The nucleotide oligomerization domain (NOD) intracellular molecules recognize a wide range of microbial products as well as other intracellular danger signals, thereby initiating inflammation through activation of nuclear factor KB (NFKB), a central regulator of the terminal processes of human labor and delivery. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21715553",
"endSection": "abstract",
"offsetInBeginSection": 1865,
"offsetInEndSection": 2003,
"text": "CONCLUSIONS: We identify NOD proteins as innate immune components that are involved in diet-induced inflammation and insulin intolerance. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20921147",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 73,
"text": "Nod1 and Nod2 regulation of inflammation in the Salmonella colitis model."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21469090",
"endSection": "abstract",
"offsetInBeginSection": 142,
"offsetInEndSection": 308,
"text": "In particular, muramyl peptides trigger inflammation, contribute to host defense against microbial infections, and modulate the adaptive immune response to antigens. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22870324",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "A key role for the endothelium in NOD1 mediated vascular inflammation: comparison to TLR4 responses."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21715553",
"endSection": "abstract",
"offsetInBeginSection": 794,
"offsetInEndSection": 919,
"text": "Systemic and tissue-specific inflammation was assessed using enzyme-linked immunosorbent assays in NOD ligand-injected mice. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12813035",
"endSection": "abstract",
"offsetInBeginSection": 791,
"offsetInEndSection": 1043,
"text": "Interferon-gamma (IFN gamma), which is a potent pro-inflammatory cytokine in intestinal mucosal inflammation, activates CARD4/NOD1 mRNA transcription in a time- and dose-dependent manner and results in augmentation of CARD4/NOD1 protein in SW480 cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12813035",
"endSection": "abstract",
"offsetInBeginSection": 1631,
"offsetInEndSection": 1812,
"text": "These studies suggest that the Th1 cytokine, IFN gamma, activates CARD4/NOD1 transcription and regulate innate immune mechanisms in the condition of intestinal mucosal inflammation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25253572",
"endSection": "abstract",
"offsetInBeginSection": 164,
"offsetInEndSection": 202,
"text": "NOD1 activation triggers inflammation,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23712977",
"endSection": "abstract",
"offsetInBeginSection": 1671,
"offsetInEndSection": 1950,
"text": "In contrast to enhanced leptin mRNA by LPS and TNFα, NOD1 activation suppressed leptin mRNA in adipocytes, suggesting the differential effects of NOD1 activation in adipocytes. Overall, our results suggest that NOD1 represents a novel target for adipose inflammation in obesity."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21677137",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "Nod1 activation by bacterial iE-DAP induces maternal-fetal inflammation and preterm labor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25253572",
"endSection": "abstract",
"offsetInBeginSection": 164,
"offsetInEndSection": 290,
"text": "NOD1 activation triggers inflammation, antimicrobial mechanisms and autophagy in both epithelial cells and murine macrophages."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21677137",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "Nod1 activation by bacterial iE-DAP induces maternal-fetal inflammation and preterm labor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25732381",
"endSection": "abstract",
"offsetInBeginSection": 217,
"offsetInEndSection": 519,
"text": "NOD1 is an intracellular immune receptor that senses peptidoglycan from Gram-negative bacteria and responds by inducing autophagy and activating NF-κB, leading to inflammation-mediated bacterial clearance; however chronic pathogens can evade NOD1-mediated clearance by altering peptidoglycan structure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24828250",
"endSection": "abstract",
"offsetInBeginSection": 1438,
"offsetInEndSection": 1635,
"text": "Bacterial NOD1 activation is positioned as a component of metabolic endotoxemia that can contribute to hyperlipidemia, systemic inflammation and insulin resistance by acting directly on adipocytes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21715553",
"endSection": "abstract",
"offsetInBeginSection": 1693,
"offsetInEndSection": 1818,
"text": "NOD1 ligand also caused inflammation and insulin resistance directly in primary hepatocytes from WT, but not NOD1(-/-), mice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25253572",
"endSection": "abstract",
"offsetInBeginSection": 164,
"offsetInEndSection": 290,
"text": "NOD1 activation triggers inflammation, antimicrobial mechanisms and autophagy in both epithelial cells and murine macrophages."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21677137",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "Nod1 activation by bacterial iE-DAP induces maternal-fetal inflammation and preterm labor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25732381",
"endSection": "abstract",
"offsetInBeginSection": 217,
"offsetInEndSection": 519,
"text": "NOD1 is an intracellular immune receptor that senses peptidoglycan from Gram-negative bacteria and responds by inducing autophagy and activating NF-κB, leading to inflammation-mediated bacterial clearance; however chronic pathogens can evade NOD1-mediated clearance by altering peptidoglycan structure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24828250",
"endSection": "abstract",
"offsetInBeginSection": 1438,
"offsetInEndSection": 1635,
"text": "Bacterial NOD1 activation is positioned as a component of metabolic endotoxemia that can contribute to hyperlipidemia, systemic inflammation and insulin resistance by acting directly on adipocytes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21715553",
"endSection": "abstract",
"offsetInBeginSection": 1693,
"offsetInEndSection": 1818,
"text": "NOD1 ligand also caused inflammation and insulin resistance directly in primary hepatocytes from WT, but not NOD1(-/-), mice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25253572",
"endSection": "abstract",
"offsetInBeginSection": 164,
"offsetInEndSection": 290,
"text": "NOD1 activation triggers inflammation, antimicrobial mechanisms and autophagy in both epithelial cells and murine macrophages."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21677137",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 90,
"text": "Nod1 activation by bacterial iE-DAP induces maternal-fetal inflammation and preterm labor."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25732381",
"endSection": "abstract",
"offsetInBeginSection": 217,
"offsetInEndSection": 519,
"text": "NOD1 is an intracellular immune receptor that senses peptidoglycan from Gram-negative bacteria and responds by inducing autophagy and activating NF-κB, leading to inflammation-mediated bacterial clearance; however chronic pathogens can evade NOD1-mediated clearance by altering peptidoglycan structure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24828250",
"endSection": "abstract",
"offsetInBeginSection": 1438,
"offsetInEndSection": 1635,
"text": "Bacterial NOD1 activation is positioned as a component of metabolic endotoxemia that can contribute to hyperlipidemia, systemic inflammation and insulin resistance by acting directly on adipocytes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25253572",
"endSection": "abstract",
"offsetInBeginSection": 164,
"offsetInEndSection": 290,
"text": "NOD1 activation triggers inflammation, antimicrobial mechanisms and autophagy in both epithelial cells and murine macrophages."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24279792",
"endSection": "abstract",
"offsetInBeginSection": 1458,
"offsetInEndSection": 1621,
"text": "We conclude that NOD1 activation reduced AHR in allergen-induced lung inflammation, which was accompanied by a reduction of allergen-specific T-cell proliferation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24829218",
"endSection": "abstract",
"offsetInBeginSection": 523,
"offsetInEndSection": 631,
"text": "The effect of NOD1 and NOD2 activation on inflammation and the insulin signalling pathway was also assessed."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12813035",
"endSection": "abstract",
"offsetInBeginSection": 792,
"offsetInEndSection": 1044,
"text": "Interferon-gamma (IFN gamma), which is a potent pro-inflammatory cytokine in intestinal mucosal inflammation, activates CARD4/NOD1 mRNA transcription in a time- and dose-dependent manner and results in augmentation of CARD4/NOD1 protein in SW480 cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24828250",
"endSection": "abstract",
"offsetInBeginSection": 1438,
"offsetInEndSection": 1635,
"text": "Bacterial NOD1 activation is positioned as a component of metabolic endotoxemia that can contribute to hyperlipidemia, systemic inflammation and insulin resistance by acting directly on adipocytes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25732381",
"endSection": "abstract",
"offsetInBeginSection": 217,
"offsetInEndSection": 519,
"text": "NOD1 is an intracellular immune receptor that senses peptidoglycan from Gram-negative bacteria and responds by inducing autophagy and activating NF-κB, leading to inflammation-mediated bacterial clearance; however chronic pathogens can evade NOD1-mediated clearance by altering peptidoglycan structure."
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D007249",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D053474"
]
| []
| 57091eefcf1c325851000016 | 238 |
yesno | Do lincRNAs play a role in human cancer? | ['yes'] | [
"yes"
]
| ['Long non-coding RNAs (lncRNAs) are pervasively transcribed in the genome and are emerging as new players in tumorigenesis due to their various functions in transcriptional, posttranscriptional and epigenetic mechanisms of gene regulation. The best-studied examples include HOTAIR, a negative prognostic factor that exhibits pro-oncogenic activity in a variety of human cancers, CRNDE the gene symbol for Colorectal Neoplasia Differentially Expressed (non-protein-coding), a long non-coding RNA (lncRNA) gene that expresses multiple splice variants and displays a very tissue-specific pattern of expression and ANRIL, a lincRNA that is required for the PRC2 recruitment to and silencing of p15(INK4B) tumor suppressor gene.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23267367",
"http://www.ncbi.nlm.nih.gov/pubmed/22614017",
"http://www.ncbi.nlm.nih.gov/pubmed/20393566",
"http://www.ncbi.nlm.nih.gov/pubmed/23443164",
"http://www.ncbi.nlm.nih.gov/pubmed/23354591",
"http://www.ncbi.nlm.nih.gov/pubmed/23292722",
"http://www.ncbi.nlm.nih.gov/pubmed/23281836",
"http://www.ncbi.nlm.nih.gov/pubmed/23226159",
"http://www.ncbi.nlm.nih.gov/pubmed/23208419",
"http://www.ncbi.nlm.nih.gov/pubmed/23133536",
"http://www.ncbi.nlm.nih.gov/pubmed/22493738",
"http://www.ncbi.nlm.nih.gov/pubmed/22454180",
"http://www.ncbi.nlm.nih.gov/pubmed/22363342",
"http://www.ncbi.nlm.nih.gov/pubmed/22285928",
"http://www.ncbi.nlm.nih.gov/pubmed/22258142",
"http://www.ncbi.nlm.nih.gov/pubmed/21991387",
"http://www.ncbi.nlm.nih.gov/pubmed/21327457",
"http://www.ncbi.nlm.nih.gov/pubmed/21151178",
"http://www.ncbi.nlm.nih.gov/pubmed/23395002",
"http://www.ncbi.nlm.nih.gov/pubmed/23153939"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23354591",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 59,
"text": "Long non-coding RNA H19 increases bladder cancer metastasis"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23354591",
"endSection": "sections.0",
"offsetInBeginSection": 554,
"offsetInEndSection": 685,
"text": "These data suggest that upregulated H19 enhances bladder cancer metastasis by associating with EZH2 and inhibiting E-cad expression"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23354591",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 46,
"text": "lncRNA H19 is essential for human tumor growth"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23292722",
"endSection": "sections.0",
"offsetInBeginSection": 200,
"offsetInEndSection": 386,
"text": "Previous reports have demonstrated that HOTAIR associates with chromatin modifications in cooperation with the Polycomb complex PRC2, and promotes breast and colorectal cancer metastasis"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23292722",
"endSection": "sections.0",
"offsetInBeginSection": 925,
"offsetInEndSection": 1172,
"text": "although the clinical significance of HOTAIR expression in HCC may not be as pronounced as that in breast and colorectal cancers, the current study demonstrates that HOTAIR expression is associated with HCC progression, warranting further studies."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23281836",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "Long non-coding RNA HOTAIR is an independent prognostic marker for nasopharyngeal carcinoma progression and survival"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22454180",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 118,
"text": "Long non-coding RNA influences radiosensitivity of colorectal carcinoma cell lines by regulating cyclin D1 expression"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22285928",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Long non-coding RNA urothelial carcinoma associated 1 (UCA1) promotes human bladder cancer cell proliferation, but the underlying mechanism remains unknown"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22285928",
"endSection": "sections.0",
"offsetInBeginSection": 974,
"offsetInEndSection": 1062,
"text": "UCA1 regulated cell cycle through CREB via PI3K-AKT dependent pathway in bladder cancer."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22285928",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 126,
"text": "Long non-coding RNA UCA1 regulated cell cycle distribution via CREB through PI3-K dependent pathway in bladder carcinoma cells"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22258142",
"endSection": "sections.0",
"offsetInBeginSection": 656,
"offsetInEndSection": 808,
"text": "overexpression of Yiya promotes cell cycle progression at the G1/S transition, therefore identifying Yiya as a cell-cycle-associated long non-coding RNA"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21327457",
"endSection": "sections.0",
"offsetInBeginSection": 12,
"offsetInEndSection": 314,
"text": "The long noncoding RNA HOTAIR has been reported as a poor prognostic biomarker in patients with breast cancer. The aim of the present study is to examine the expression pattern of HOTAIR in hepatocellular carcinoma (HCC) and its clinical significance as well as its biological role in tumor progression"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21327457",
"endSection": "sections.0",
"offsetInBeginSection": 1335,
"offsetInEndSection": 1544,
"text": "The high expression level of HOTAIR in HCC could be a candidate biomarker for predicting tumor recurrence in HCC patients who have undergone liver transplant therapy and might be a potential therapeutic target"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21151178",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "Long non-coding RNA ANRIL is required for the PRC2 recruitment to and silencing of p15(INK4B) tumor suppressor gene"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21151178",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "A 42 kb region on human chromosome 9p21 encodes for three distinct tumor suppressors, p16(INK4A), p14(ARF) and p15(INK4B), and is altered in an estimated 30-40% of human tumors"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23395002",
"endSection": "sections.0",
"offsetInBeginSection": 921,
"offsetInEndSection": 1101,
"text": "These results advance our understanding of the role of lncRNA-LET as a regulator of hypoxia signaling and offer new avenues for therapeutic intervention against cancer progression."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23153939",
"endSection": "sections.0",
"offsetInBeginSection": 1654,
"offsetInEndSection": 1729,
"text": "Silencing MALAT1 is a potential novel therapeutic approach for this cancer."
}
]
| 5 | BioASQ-training5b | null | null | 516e5f33298dcd4e5100007e | 239 |
yesno | Can vitamin B1 deficiency cause encephalopathy? | ['yes'] | [
"yes"
]
| ["Wernicke's encephalopathy (WE) is a severe neurological syndrome caused by thiamine (vitamin B1) deficiency and clinically characterized by the sudden onset of mental status changes, ocular abnormalities, and ataxia. It is commonly associated with heavy alcohol consumption. Other clinical associations are with hyperemesis gravidarum (HG), starvation, and prolonged intravenous feeding.", "Wernicke's encephalopathy (WE) is a severe neurological syndrome caused by thiamine (vitamin B1) deficiency and clinically characterized by the sudden onset of mental status changes, ocular abnormalities, and ataxia", "Wernicke's encephalopathy (WE) is a severe neurological syndrome caused by thiamine (vitamin B1) deficiency and clinically characterized by the sudden onset of mental status changes, ocular abnormalities, and ataxia", "Wernicke's encephalopathy (WE) is a severe neurological syndrome caused by thiamine (vitamin B1) deficiency and clinically characterized by the sudden onset of mental status changes, ocular abnormalities, and ataxia", "Wernicke's encephalopathy (WE) is a severe neurological syndrome caused by thiamine (vitamin B1) deficiency and clinically characterized by the sudden onset of mental status changes, ocular abnormalities, and ataxia", "Wernicke's encephalopathy (WE) is a severe neurological syndrome caused by thiamine (vitamin B1) deficiency and clinically characterized by the sudden onset of mental status changes, ocular abnormalities, and ataxia"] | [
"http://www.ncbi.nlm.nih.gov/pubmed/25050351",
"http://www.ncbi.nlm.nih.gov/pubmed/24379094",
"http://www.ncbi.nlm.nih.gov/pubmed/24701066",
"http://www.ncbi.nlm.nih.gov/pubmed/25515801",
"http://www.ncbi.nlm.nih.gov/pubmed/22703872",
"http://www.ncbi.nlm.nih.gov/pubmed/23090806",
"http://www.ncbi.nlm.nih.gov/pubmed/23935638",
"http://www.ncbi.nlm.nih.gov/pubmed/9279523",
"http://www.ncbi.nlm.nih.gov/pubmed/11304071",
"http://www.ncbi.nlm.nih.gov/pubmed/24620429",
"http://www.ncbi.nlm.nih.gov/pubmed/21217196",
"http://www.ncbi.nlm.nih.gov/pubmed/25276464",
"http://www.ncbi.nlm.nih.gov/pubmed/20943242",
"http://www.ncbi.nlm.nih.gov/pubmed/24117525",
"http://www.ncbi.nlm.nih.gov/pubmed/24973622",
"http://www.ncbi.nlm.nih.gov/pubmed/7695937",
"http://www.ncbi.nlm.nih.gov/pubmed/16254404",
"http://www.ncbi.nlm.nih.gov/pubmed/23715222",
"http://www.ncbi.nlm.nih.gov/pubmed/23278769",
"http://www.ncbi.nlm.nih.gov/pubmed/23042832",
"http://www.ncbi.nlm.nih.gov/pubmed/2361826",
"http://www.ncbi.nlm.nih.gov/pubmed/14644703"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25050351",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 215,
"text": "Wernicke's encephalopathy (WE) is a severe neurological syndrome caused by thiamine (vitamin B1) deficiency and clinically characterized by the sudden onset of mental status changes, ocular abnormalities, and ataxia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24379094",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 148,
"text": "Wernicke encephalopathy (or Wernicke-Korsakoff encephalopathy) is a rarely diagnosed neurological disorder, which is caused by vitamin B1 deficiency"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24701066",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 139,
"text": "Wernicke's encephalopathy (WE) is a potentially reversible yet serious neurological manifestation caused by vitamin B1(thiamine) deficiency"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25515801",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 81,
"text": "Wernicke encephalopathy is caused by thiamine (vitamin B1) deficiency"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9279523",
"endSection": "abstract",
"offsetInBeginSection": 717,
"offsetInEndSection": 876,
"text": "Both the thyrotoxicosis and a catabolic state due to the hyperemesis were thought to have induced a vitamin B1 deficiency, causing the Wernicke encephalopathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24379094",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Wernicke encephalopathy (or Wernicke-Korsakoff encephalopathy) is a rarely diagnosed neurological disorder, which is caused by vitamin B1 deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25515801",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 70,
"text": "Wernicke encephalopathy is caused by thiamine (vitamin B1) deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23090806",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 151,
"text": "Wernicke's encephalopathy is a neurological disorder caused by thiamine (vitamin B1) deficiency characterized by vertigo, ataxia, and mental confusion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21217196",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 157,
"text": "Wernicke's encephalopathy (WE) is caused by thiamine (vitamin B1) deficiency and most commonly found in individuals with chronic alcoholism and malnutrition."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24620429",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "Wernicke's encephalopathy (WE) is an acute neurological disease resulting from thiamine (vitamin B1) deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11304071",
"endSection": "abstract",
"offsetInBeginSection": 351,
"offsetInEndSection": 525,
"text": "Post-mortem findings demonstrate that thiamine (vitamin B1) deficiency sufficient to cause irreversible brain damage is not diagnosed ante mortem in 80-90% of these patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24379094",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Wernicke encephalopathy (or Wernicke-Korsakoff encephalopathy) is a rarely diagnosed neurological disorder, which is caused by vitamin B1 deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25276464",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 105,
"text": "Wernicke's encephalopathy is an acute neuropsychiatric disorder, due to thiamine (vitamin B1) deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9279523",
"endSection": "abstract",
"offsetInBeginSection": 717,
"offsetInEndSection": 876,
"text": "Both the thyrotoxicosis and a catabolic state due to the hyperemesis were thought to have induced a vitamin B1 deficiency, causing the Wernicke encephalopathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25050351",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 216,
"text": "Wernicke's encephalopathy (WE) is a severe neurological syndrome caused by thiamine (vitamin B1) deficiency and clinically characterized by the sudden onset of mental status changes, ocular abnormalities, and ataxia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11304071",
"endSection": "abstract",
"offsetInBeginSection": 351,
"offsetInEndSection": 525,
"text": "Post-mortem findings demonstrate that thiamine (vitamin B1) deficiency sufficient to cause irreversible brain damage is not diagnosed ante mortem in 80-90% of these patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20943242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 172,
"text": "Wernicke's encephalopathy, a pathology caused by vitamin B1 (thiamin) deficiency, is often difficult to diagnose and can lead to severe cognitive sequels if left untreated."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24117525",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "Wernicke's encephalopathy-Korsakoff syndrome (WE-KS) is common in alcoholics, caused by thiamine deficiency (TD; vitamin B1) and associated with lesions to the thalamus (THAL)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25515801",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 69,
"text": "Wernicke encephalopathy is caused by thiamine (vitamin B1) deficiency"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24379094",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 148,
"text": "Wernicke encephalopathy (or Wernicke-Korsakoff encephalopathy) is a rarely diagnosed neurological disorder, which is caused by vitamin B1 deficiency"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24973622",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 221,
"text": "Thiamine (vitamin B1) deficiency, associated with a variety of conditions, including chronic alcoholism and bariatric surgery for morbid obesity, can result in the neurological disorder Wernicke's encephalopathy (WE)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7695937",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 165,
"text": "Wernicke's encephalopathy is caused by thiamin deficiency and can be recognized by severe neurological symptoms that are occasionally accompanied by systemic signs. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20943242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "INTRODUCTION: Wernicke's encephalopathy, a pathology caused by vitamin B1 (thiamin) deficiency, is often difficult to diagnose and can lead to severe cognitive sequels if left untreated. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22703872",
"endSection": "abstract",
"offsetInBeginSection": 297,
"offsetInEndSection": 518,
"text": "OBSERVATION: We report a case of encephalopathy due to dual vitamin deficiency of both thiamine (vitamin B1) and niacin (vitamin PP) in an 80-year-old women, hospitalized for severe sepsis caused by aspiration pneumonia. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16254404",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 196,
"text": "Acute Wernicke's encephalopathy (WE) is caused by profound vitamin B1 (thiamine) deficiency and commonly presents with the classic clinical triad of mental confusion, ataxia, and ophthalmoplegia. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23715222",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 118,
"text": "[Wernicke´s encephalopathy and polyneuropathy associated with vitamin B complex deficiency after a bariatric surgery]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23278769",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "BACKGROUND: Thiamine deficiency in patients who abuse alcohol can cause Wernicke's encephalopathy (WE). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7695937",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 165,
"text": "Wernicke's encephalopathy is caused by thiamin deficiency and can be recognized by severe neurological symptoms that are occasionally accompanied by systemic signs. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20943242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "INTRODUCTION: Wernicke's encephalopathy, a pathology caused by vitamin B1 (thiamin) deficiency, is often difficult to diagnose and can lead to severe cognitive sequels if left untreated. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22703872",
"endSection": "abstract",
"offsetInBeginSection": 297,
"offsetInEndSection": 518,
"text": "OBSERVATION: We report a case of encephalopathy due to dual vitamin deficiency of both thiamine (vitamin B1) and niacin (vitamin PP) in an 80-year-old women, hospitalized for severe sepsis caused by aspiration pneumonia. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16254404",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 196,
"text": "Acute Wernicke's encephalopathy (WE) is caused by profound vitamin B1 (thiamine) deficiency and commonly presents with the classic clinical triad of mental confusion, ataxia, and ophthalmoplegia. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23715222",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 118,
"text": "[Wernicke´s encephalopathy and polyneuropathy associated with vitamin B complex deficiency after a bariatric surgery]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23278769",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "BACKGROUND: Thiamine deficiency in patients who abuse alcohol can cause Wernicke's encephalopathy (WE). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7695937",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 165,
"text": "Wernicke's encephalopathy is caused by thiamin deficiency and can be recognized by severe neurological symptoms that are occasionally accompanied by systemic signs. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20943242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "INTRODUCTION: Wernicke's encephalopathy, a pathology caused by vitamin B1 (thiamin) deficiency, is often difficult to diagnose and can lead to severe cognitive sequels if left untreated. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22703872",
"endSection": "abstract",
"offsetInBeginSection": 297,
"offsetInEndSection": 518,
"text": "OBSERVATION: We report a case of encephalopathy due to dual vitamin deficiency of both thiamine (vitamin B1) and niacin (vitamin PP) in an 80-year-old women, hospitalized for severe sepsis caused by aspiration pneumonia. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16254404",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 196,
"text": "Acute Wernicke's encephalopathy (WE) is caused by profound vitamin B1 (thiamine) deficiency and commonly presents with the classic clinical triad of mental confusion, ataxia, and ophthalmoplegia. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23715222",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 118,
"text": "[Wernicke´s encephalopathy and polyneuropathy associated with vitamin B complex deficiency after a bariatric surgery]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23278769",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "BACKGROUND: Thiamine deficiency in patients who abuse alcohol can cause Wernicke's encephalopathy (WE). "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23715222",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 118,
"text": "[Wernicke´s encephalopathy and polyneuropathy associated with vitamin B complex deficiency after a bariatric surgery]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23042832",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 134,
"text": "Wernicke encephalopathy--a debilitating acute or subacute neurological disorder-is caused by a deficiency in thiamine (vitamin B(1)). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23278769",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "BACKGROUND: Thiamine deficiency in patients who abuse alcohol can cause Wernicke's encephalopathy (WE). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7695937",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 165,
"text": "Wernicke's encephalopathy is caused by thiamin deficiency and can be recognized by severe neurological symptoms that are occasionally accompanied by systemic signs. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20943242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "INTRODUCTION: Wernicke's encephalopathy, a pathology caused by vitamin B1 (thiamin) deficiency, is often difficult to diagnose and can lead to severe cognitive sequels if left untreated. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22703872",
"endSection": "abstract",
"offsetInBeginSection": 297,
"offsetInEndSection": 518,
"text": "OBSERVATION: We report a case of encephalopathy due to dual vitamin deficiency of both thiamine (vitamin B1) and niacin (vitamin PP) in an 80-year-old women, hospitalized for severe sepsis caused by aspiration pneumonia. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16254404",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 196,
"text": "Acute Wernicke's encephalopathy (WE) is caused by profound vitamin B1 (thiamine) deficiency and commonly presents with the classic clinical triad of mental confusion, ataxia, and ophthalmoplegia. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23715222",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 118,
"text": "[Wernicke´s encephalopathy and polyneuropathy associated with vitamin B complex deficiency after a bariatric surgery]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23278769",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "BACKGROUND: Thiamine deficiency in patients who abuse alcohol can cause Wernicke's encephalopathy (WE). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2361826",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "Wernicke's encephalopathy is a serious neurological manifestation of vitamin B1 deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2361826",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 91,
"text": "Wernicke's encephalopathy is a serious neurological manifestation of vitamin B1 deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9279523",
"endSection": "abstract",
"offsetInBeginSection": 564,
"offsetInEndSection": 723,
"text": "Both the thyrotoxicosis and a catabolic state due to the hyperemesis were thought to have induced a vitamin B1 deficiency, causing the Wernicke encephalopathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25515801",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 71,
"text": "Wernicke encephalopathy is caused by thiamine (vitamin B1) deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24379094",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Wernicke encephalopathy (or Wernicke-Korsakoff encephalopathy) is a rarely diagnosed neurological disorder, which is caused by vitamin B1 deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23090806",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 122,
"text": "Wernicke's encephalopathy is a neurological disorder caused by thiamine (vitamin B1) deficiency characterized by vertigo,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11304071",
"endSection": "abstract",
"offsetInBeginSection": 179,
"offsetInEndSection": 603,
"text": "Post-mortem findings demonstrate that thiamine (vitamin B1) deficiency sufficient to cause irreversible brain damage is not diagnosed ante mortem in 80-90% of these patients. The causes of vitamin deficiency are reviewed with special attention to the inhibition of oral thiamine hydrochloride absorption in man caused by malnutrition present in alcoholic patients or by the direct effects of ethanol on intestinal transport."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14644703",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "Wernicke's encephalopathy is a serious neurologic disorder caused by vitamin-B1 or thiamine deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23935638",
"endSection": "abstract",
"offsetInBeginSection": 148,
"offsetInEndSection": 276,
"text": "Wernicke's encephalopathy results from thiamine (vitamin B1) deficiency. Common causes include alcoholism and gastric disorders."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9279523",
"endSection": "abstract",
"offsetInBeginSection": 564,
"offsetInEndSection": 723,
"text": "Both the thyrotoxicosis and a catabolic state due to the hyperemesis were thought to have induced a vitamin B1 deficiency, causing the Wernicke encephalopathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25515801",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 71,
"text": "Wernicke encephalopathy is caused by thiamine (vitamin B1) deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24379094",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Wernicke encephalopathy (or Wernicke-Korsakoff encephalopathy) is a rarely diagnosed neurological disorder, which is caused by vitamin B1 deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23090806",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "Wernicke's encephalopathy is a neurological disorder caused by thiamine (vitamin B1) deficiency characterized by vertigo, ataxia, and mental confusion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21217196",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "Wernicke's encephalopathy (WE) is caused by thiamine (vitamin B1) deficiency and most commonly found in individuals with chronic alcoholism and malnutrition."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11304071",
"endSection": "abstract",
"offsetInBeginSection": 179,
"offsetInEndSection": 353,
"text": "Post-mortem findings demonstrate that thiamine (vitamin B1) deficiency sufficient to cause irreversible brain damage is not diagnosed ante mortem in 80-90% of these patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9279523",
"endSection": "abstract",
"offsetInBeginSection": 564,
"offsetInEndSection": 723,
"text": "Both the thyrotoxicosis and a catabolic state due to the hyperemesis were thought to have induced a vitamin B1 deficiency, causing the Wernicke encephalopathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25515801",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 71,
"text": "Wernicke encephalopathy is caused by thiamine (vitamin B1) deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24379094",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Wernicke encephalopathy (or Wernicke-Korsakoff encephalopathy) is a rarely diagnosed neurological disorder, which is caused by vitamin B1 deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23090806",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "Wernicke's encephalopathy is a neurological disorder caused by thiamine (vitamin B1) deficiency characterized by vertigo, ataxia, and mental confusion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21217196",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "Wernicke's encephalopathy (WE) is caused by thiamine (vitamin B1) deficiency and most commonly found in individuals with chronic alcoholism and malnutrition."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11304071",
"endSection": "abstract",
"offsetInBeginSection": 179,
"offsetInEndSection": 353,
"text": "Post-mortem findings demonstrate that thiamine (vitamin B1) deficiency sufficient to cause irreversible brain damage is not diagnosed ante mortem in 80-90% of these patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9279523",
"endSection": "abstract",
"offsetInBeginSection": 564,
"offsetInEndSection": 723,
"text": "Both the thyrotoxicosis and a catabolic state due to the hyperemesis were thought to have induced a vitamin B1 deficiency, causing the Wernicke encephalopathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25515801",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 71,
"text": "Wernicke encephalopathy is caused by thiamine (vitamin B1) deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24379094",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Wernicke encephalopathy (or Wernicke-Korsakoff encephalopathy) is a rarely diagnosed neurological disorder, which is caused by vitamin B1 deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23090806",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "Wernicke's encephalopathy is a neurological disorder caused by thiamine (vitamin B1) deficiency characterized by vertigo, ataxia, and mental confusion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21217196",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "Wernicke's encephalopathy (WE) is caused by thiamine (vitamin B1) deficiency and most commonly found in individuals with chronic alcoholism and malnutrition."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11304071",
"endSection": "abstract",
"offsetInBeginSection": 179,
"offsetInEndSection": 353,
"text": "Post-mortem findings demonstrate that thiamine (vitamin B1) deficiency sufficient to cause irreversible brain damage is not diagnosed ante mortem in 80-90% of these patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9279523",
"endSection": "abstract",
"offsetInBeginSection": 564,
"offsetInEndSection": 723,
"text": "Both the thyrotoxicosis and a catabolic state due to the hyperemesis were thought to have induced a vitamin B1 deficiency, causing the Wernicke encephalopathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25515801",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 71,
"text": "Wernicke encephalopathy is caused by thiamine (vitamin B1) deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24379094",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Wernicke encephalopathy (or Wernicke-Korsakoff encephalopathy) is a rarely diagnosed neurological disorder, which is caused by vitamin B1 deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14644703",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 104,
"text": "Wernicke's encephalopathy is a serious neurologic disorder caused by vitamin-B1 or thiamine deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23090806",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "Wernicke's encephalopathy is a neurological disorder caused by thiamine (vitamin B1) deficiency characterized by vertigo, ataxia, and mental confusion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21217196",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "Wernicke's encephalopathy (WE) is caused by thiamine (vitamin B1) deficiency and most commonly found in individuals with chronic alcoholism and malnutrition."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20943242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 173,
"text": "Wernicke's encephalopathy, a pathology caused by vitamin B1 (thiamin) deficiency, is often difficult to diagnose and can lead to severe cognitive sequels if left untreated."
}
]
| 5 | BioASQ-training5b | []
| []
| 572211540fd6f91b68000016 | 240 |
yesno | Is there any association between suicide and autism in adolescents, yes or no? | ['yes'] | [
"yes"
]
| ['Adults with autism spectrum disorder (ASD) are at increased risk of suicide compared to the general population.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/27956832",
"http://www.ncbi.nlm.nih.gov/pubmed/24201088",
"http://www.ncbi.nlm.nih.gov/pubmed/28872268",
"http://www.ncbi.nlm.nih.gov/pubmed/25200592",
"http://www.ncbi.nlm.nih.gov/pubmed/29854129",
"http://www.ncbi.nlm.nih.gov/pubmed/25084822",
"http://www.ncbi.nlm.nih.gov/pubmed/17885828",
"http://www.ncbi.nlm.nih.gov/pubmed/29706156",
"http://www.ncbi.nlm.nih.gov/pubmed/23666287"
]
| [
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/25200592",
"endSection": "abstract",
"offsetInBeginSection": 609,
"offsetInEndSection": 957,
"text": ": In all subjects from our research on PubMed, 21.3% of subjects with autism spectrum disorder reported suicidal ideation, have attempted suicide or died by suicide (115 out of 539 subjects) and 7.7% of subjects supported for suicidal thoughts or attempted suicide exhibited an autism spectrum disorder (62 out of 806 subjects), all ages combined. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25200592",
"endSection": "abstract",
"offsetInBeginSection": 1057,
"offsetInEndSection": 1212,
"text": "Suicide attempts are accompanied by a willingness for death and can lead to suicide. They are more common in high-functioning autism and Asperger subjects."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17885828",
"endSection": "abstract",
"offsetInBeginSection": 690,
"offsetInEndSection": 1208,
"text": " A total sample of 10 adolescents and young adults diagnosed with AS was obtained. The high proportion of respondents with scores above the cutoff point on the overt victimization and relational victimization scales suggests that these adolescents and young adults experienced high levels of victimization. Of the sample, 20 percent met criteria for a diagnosis of Major Depressive Disorder, 30 percent met criteria for Generalized Anxiety Disorder and 50 percent had clinically significant level of suicidal ideation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28872268",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 177,
"text": "Previous studies reported a high prevalence of depression among patients with autism spectrum disorder (ASD) and suggested a relationship between ASD and suicidality"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28872268",
"endSection": "abstract",
"offsetInBeginSection": 1178,
"offsetInEndSection": 1270,
"text": "Patients with ASD had an increased risk of suicide attempts compared with those without ASD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23666287",
"endSection": "abstract",
"offsetInBeginSection": 204,
"offsetInEndSection": 326,
"text": "The suicidal behaviors are frequently observed in the adolescents and adults with an ASD without intellectual deficience. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24201088",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 161,
"text": "Suicide is a major problem in Western society. However we have very little understanding of suicidal behaviour among individuals with autism spectrum disorders. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24201088",
"endSection": "abstract",
"offsetInBeginSection": 545,
"offsetInEndSection": 694,
"text": "The available research provides little empirical evidence for the processes underlying suicidal behaviour in adolescents and young adults with autism"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27956832",
"endSection": "abstract",
"offsetInBeginSection": 226,
"offsetInEndSection": 395,
"text": " The present study aims to assess the rate of suicidality (suicidal ideation, behaviors and attempts) and associated risk factors for suicidality in high functioning ASD"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27956832",
"endSection": "abstract",
"offsetInBeginSection": 103,
"offsetInEndSection": 225,
"text": "here is a lack of clinical awareness on suicidal behaviors of children and adolescents with autism spectrum disorder (ASD)"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27956832",
"endSection": "title",
"offsetInBeginSection": 14,
"offsetInEndSection": 114,
"text": "suicidality in children and adolescents with diagnosis of high functioning autism spectrum disorder "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27956832",
"endSection": "abstract",
"offsetInBeginSection": 1679,
"offsetInEndSection": 1771,
"text": "Consistent with the previous findings, rate of suicidality is higher in individuals with ASD"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29854129",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 70,
"text": "Detection of Suicidality in Adolescents with Autism Spectrum Disorders"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29854129",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 122,
"text": "Over 15% of young people with autism spectrum disorders (ASD) will contemplate or attempt suicide during adolescence. Yet,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29706156",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 84,
"text": "Until recently, suicidality in autism spectrum disorder (ASD) was rarely discussed. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29706156",
"endSection": "title",
"offsetInBeginSection": 27,
"offsetInEndSection": 67,
"text": "Suicidality in Autism Spectrum Disorder."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29706156",
"endSection": "abstract",
"offsetInBeginSection": 172,
"offsetInEndSection": 376,
"text": "highlighted not only that suicidal thoughts and suicide attempts can occur in adolescents and young adults with ASD, but also that suicidality is likely more common in ASD than in the general population. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29706156",
"endSection": "abstract",
"offsetInBeginSection": 523,
"offsetInEndSection": 757,
"text": "The emerging studies indicate that the increased risk of self-injurious behavior in younger and less cognitively able children with ASD3,4 is matched by an increased risk of suicidality in those at a more advanced developmental level."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25200592",
"endSection": "abstract",
"offsetInBeginSection": 606,
"offsetInEndSection": 959,
"text": "RESULTS\nIn all subjects from our research on PubMed, 21.3% of subjects with autism spectrum disorder reported suicidal ideation, have attempted suicide or died by suicide (115 out of 539 subjects) and 7.7% of subjects supported for suicidal thoughts or attempted suicide exhibited an autism spectrum disorder (62 out of 806 subjects), all ages combined."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28872268",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "Risk of Suicide Attempts Among Adolescents and Young Adults With Autism Spectrum Disorder: A Nationwide Longitudinal Follow-Up Study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25084822",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 205,
"text": "Although the suicide risk of autism spectrum disorder (ASD) has been suggested to be higher than previously recognized, there are few case reports focusing on the process for preventing suicide reattempts."
}
]
| 11 | BioASQ-training11b | null | null | 5c5217fd7e3cb0e231000005 | 241 |
yesno | Do exon 38 or 39 KMT2D missense variants cause Kabuki syndrome type 1 (KS1)? | ['no'] | [
"no"
]
| ['No. The KMT2D missense variants do not cause KS1, they cause a different type of malformations disorder distinct from Kabuki syndrome.', 'No. The KMT2D missense variants do not cause KS1, they cause a different type of malformations disorder distinct from Kabuki Syndrome.', 'No. The KMT2D missense variants do not cause KS1. They cause a multiple malformations disorder distinct from Kabuki syndrome.', 'No. The KMT2D missense variants do not cause KS1. They cause a different type of malformations disorder distinct from Kabuki Syndrome.', 'No. The KMT2D missense variants do not cause KS1. They cause a multiple malformations disorder distinct from Kabuki Syndrome.', 'No. KMT2D missense variants (MVs) located in a specific region spanning exons 38 and 39 and affecting highly conserved residues cause a novel multiple malformations syndrome distinct from Kabuki syndrome type 1 (KS1). Unlike KMT2D haploinsufficiency in KS1, these MVs likely result in disease through a dominant negative mechanism.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/31949313"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31949313",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 119,
"text": "A restricted spectrum of missense KMT2D variants cause a multiple malformations disorder distinct from Kabuki syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31949313",
"endSection": "abstract",
"offsetInBeginSection": 9,
"offsetInEndSection": 1425,
"text": "To investigate if specific exon 38 or 39 KMT2D missense variants (MVs) cause a condition distinct from Kabuki syndrome type 1 (KS1).METHODS: Multiple individuals, with MVs in exons 38 or 39 of KMT2D that encode a highly conserved region of 54 amino acids flanked by Val3527 and Lys3583, were identified and phenotyped. Functional tests were performed to study their pathogenicity and understand the disease mechanism.RESULTS: The consistent clinical features of the affected individuals, from seven unrelated families, included choanal atresia, athelia or hypoplastic nipples, branchial sinus abnormalities, neck pits, lacrimal duct anomalies, hearing loss, external ear malformations, and thyroid abnormalities. None of the individuals had intellectual disability. The frequency of clinical features, objective software-based facial analysis metrics, and genome-wide peripheral blood DNA methylation patterns in these patients were significantly different from that of KS1. Circular dichroism spectroscopy indicated that these MVs perturb KMT2D secondary structure through an increased disordered to ɑ-helical transition.CONCLUSION: KMT2D MVs located in a specific region spanning exons 38 and 39 and affecting highly conserved residues cause a novel multiple malformations syndrome distinct from KS1. Unlike KMT2D haploinsufficiency in KS1, these MVs likely result in disease through a dominant negative mechanism."
}
]
| 11 | BioASQ-training11b | null | null | 601d46d61cb411341a000030 | 242 |
yesno | Is palbociclib effective for glioblastoma? | ['no'] | [
"no"
]
| ['No. In a clinical trial palbociclib monotherapy was not an effective treatment for recurrent glioblastoma.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/30151703",
"http://www.ncbi.nlm.nih.gov/pubmed/29726787"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29726787",
"endSection": "abstract",
"offsetInBeginSection": 1543,
"offsetInEndSection": 1810,
"text": "Although further research is needed, cyclin-dependent kinase 4/6 inhibitors represent intriguing developments in the treatment of various malignancies, including those with such poor prognoses as glioblastoma multiforme, mantle cell lymphoma, and metastatic melanoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30151703",
"endSection": "abstract",
"offsetInBeginSection": 1441,
"offsetInEndSection": 1578,
"text": "CONCLUSION: In this trial, despite adequate tissue PK, palbociclib monotherapy was not an effective treatment for recurrent glioblastoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30151703",
"endSection": "abstract",
"offsetInBeginSection": 1447,
"offsetInEndSection": 1584,
"text": "CONCLUSION\n\nIn this trial, despite adequate tissue PK, palbociclib monotherapy was not an effective treatment for recurrent glioblastoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30151703",
"endSection": "abstract",
"offsetInBeginSection": 1441,
"offsetInEndSection": 1577,
"text": "CONCLUSION In this trial, despite adequate tissue PK, palbociclib monotherapy was not an effective treatment for recurrent glioblastoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30151703",
"endSection": "abstract",
"offsetInBeginSection": 1447,
"offsetInEndSection": 1584,
"text": "CONCLUSION\nIn this trial, despite adequate tissue PK, palbociclib monotherapy was not an effective treatment for recurrent glioblastoma."
}
]
| 11 | BioASQ-training11b | null | null | 5e290a268b3851296d00000d | 243 |
yesno | Is retinol binding protein 4 an adipokine? | ['yes'] | [
"yes"
]
| ['Yes,\nRetinol-binding protein 4 (RBP4) is a prominent adipokine.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/33199363",
"http://www.ncbi.nlm.nih.gov/pubmed/33484131",
"http://www.ncbi.nlm.nih.gov/pubmed/34575030"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33484131",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 118,
"text": "Systematic Quantification of Neurotrophic Adipokines RBP4, PEDF, and Clusterin in Human Cerebrospinal Fluid and Serum."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33199363",
"endSection": "abstract",
"offsetInBeginSection": 91,
"offsetInEndSection": 150,
"text": "Retinol-binding protein 4 (RBP4) is a prominent adipokine i"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34575030",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 105,
"text": "Fetuin-A and retinol-binding protein 4 (RBP4) are secreted as both hepatokine and adipokine. "
}
]
| 11 | BioASQ-training11b | null | null | 622b95dc3a8413c653000092 | 244 |
yesno | Is RIP1 (RIP-1) part of the necrosome? | ['yes'] | [
"yes"
]
| Yes, RIP1 is part of the necrosome. | [
"http://www.ncbi.nlm.nih.gov/pubmed/22033613",
"http://www.ncbi.nlm.nih.gov/pubmed/22016814",
"http://www.ncbi.nlm.nih.gov/pubmed/21749897",
"http://www.ncbi.nlm.nih.gov/pubmed/24098568",
"http://www.ncbi.nlm.nih.gov/pubmed/24059293",
"http://www.ncbi.nlm.nih.gov/pubmed/23898178",
"http://www.ncbi.nlm.nih.gov/pubmed/23612963",
"http://www.ncbi.nlm.nih.gov/pubmed/23162759",
"http://www.ncbi.nlm.nih.gov/pubmed/22817896",
"http://www.ncbi.nlm.nih.gov/pubmed/22576661",
"http://www.ncbi.nlm.nih.gov/pubmed/22421439",
"http://www.ncbi.nlm.nih.gov/pubmed/22666585",
"http://www.ncbi.nlm.nih.gov/pubmed/21890409"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22033613",
"endSection": "abstract",
"offsetInBeginSection": 1179,
"offsetInEndSection": 1272,
"text": "formation of a different necrosome whose components, besides RIP1 and RIP3, are still unknown"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22016814",
"endSection": "abstract",
"offsetInBeginSection": 902,
"offsetInEndSection": 975,
"text": "necrosome complex consisting of RIP1, RIP3, FADD, caspase-8 and cFLIP(L)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21749897",
"endSection": "abstract",
"offsetInBeginSection": 477,
"offsetInEndSection": 673,
"text": "assembly of a supramolecular complex containing the receptor-interacting protein kinases 1 and 3 (RIP1 and RIP3) that delivers a pronecrotic signal. Such complex has recently been dubbed necrosome"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24098568",
"endSection": "abstract",
"offsetInBeginSection": 116,
"offsetInEndSection": 213,
"text": "Receptor interacting protein kinase 1 (RIPK1/RIP1) and RIP3 are key components of the necrosome. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24059293",
"endSection": "abstract",
"offsetInBeginSection": 189,
"offsetInEndSection": 268,
"text": "The phosphorylation of RIP1 and RIP3 is critical for assembly of the necrosome,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23898178",
"endSection": "abstract",
"offsetInBeginSection": 497,
"offsetInEndSection": 527,
"text": "RIP1-RIP3 \"necrosome\" complex "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23612963",
"endSection": "abstract",
"offsetInBeginSection": 295,
"offsetInEndSection": 400,
"text": "RIP1 and RIP3 mediate necrosome aggregation leading to the formation of amyloid-like signaling complexes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23162759",
"endSection": "abstract",
"offsetInBeginSection": 840,
"offsetInEndSection": 894,
"text": "Formation of the RIP1/RIP3 complex (called necrosome) "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22817896",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 24,
"text": "The RIP1/RIP3 necrosome "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22576661",
"endSection": "abstract",
"offsetInBeginSection": 966,
"offsetInEndSection": 1001,
"text": "Rip1-Rip3 death complex (necrosome)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21890409",
"endSection": "abstract",
"offsetInBeginSection": 576,
"offsetInEndSection": 663,
"text": "he 'necrosome', that includes receptor-interacting protein (RIP)1, RIP3 and caspase-8. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22666585",
"endSection": "abstract",
"offsetInBeginSection": 884,
"offsetInEndSection": 998,
"text": "RIP-1 kinase activity triggers formation of the necrosome (in complex with RIP-3) leading to programmed necrosis. "
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D009336",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0001906",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0008219",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0070265",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0097300",
"http://www.uniprot.org/uniprot/RIPK1_MOUSE",
"http://www.uniprot.org/uniprot/RIPK1_HUMAN",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D053422"
]
| []
| 532bfd15d6d3ac6a34000017 | 245 |
yesno | Is amiodarone a class I anti-arrhythmic drug? | ['no'] | [
"no"
]
| ['Amiodarone has been used as an anti-arrhythmic drug since the 1970s and has an established role in the treatment of ventricular tachyarrhythmias. Although considered to be a class III anti-arrhythmic, amiodarone also has class I, II and IV actions, which gives it a unique pharmacological and anti-arrhythmic profile.', 'Amiodarone has been used as an anti-arrhythmic drug since the 1970s and has an established role in the treatment of ventricular tachyarrhythmias. Although considered to be a class III anti-arrhythmic, amiodarone also has class I, II and IV actions, which gives it a unique pharmacological and anti-arrhythmic profile. Common class I agents are excluded due to the inherent abnormal cardiac structure and function in the setting of cardiogenic shock. Class III drug options include dofetilide and amiodarone.', 'Amiodarone has been used as an anti-arrhythmic drug since the 1970s and has an established role in the treatment of ventricular tachyarrhythmias. Although considered to be a class III anti-arrhythmic, amiodarone also has class I, II and IV actions, which gives it a unique pharmacological and anti-arrhythmic profile. Common class I agents are excluded due to the inherent abnormal cardiac structure and function in the setting of cardiogenic shock. Class III drug options include dofetilide and amiodarone.', 'Amiodarone has been used as an anti-arrhythmic drug since the 1970s and has an established role in the treatment of ventricular tachyarrhythmias. Although considered to be a class III anti-arrhythmic, amiodarone also has class I, II and IV actions, which gives it a unique pharmacological and anti-arrhythmic profile. Common class I agents are excluded due to the inherent abnormal cardiac structure and function in the setting of cardiogenic shock. Class III drug options include dofetilide and amiodarone.', 'Amiodarone has been used as an anti-arrhythmic drug since the 1970s and has an established role in the treatment of ventricular tachyarrhythmias. Although considered to be a class III anti-arrhythmic, amiodarone also has class I, II and IV actions, which gives it a unique pharmacological and anti-arrhythmic profile. Common class I agents are excluded due to the inherent abnormal cardiac structure and function in the setting of cardiogenic shock. Class III drug options include dofetilide and amiodarone.', 'No. Common class I agents are excluded due to the inherent abnormal cardiac structure and function in the setting of cardiogenic shock. Although considered to be a class III anti-arrhythmic, amiodarone also has class I, II and IV actions, which gives it a unique pharmacological and anti-arrhythmic profile.', 'Amiodarone, an iodinated benzofuran derivative, introduced in 1960 s as an anti-anginal agent, emerged as a potent anti-arrhythmic agent by 1970 s and is currently one of the most commonly prescribed drugs in US for ventricular and atrial arrhythmias. Although amiodarone is considered a class III anti-arrhythmic agent, it also has class I, II, IV actions, making it a unique and effective anti-arrhythmic agent. ', 'Amiodarone, an iodinated benzofuran derivative, introduced in 1960 s as an anti-anginal agent, emerged as a potent anti-arrhythmic agent by 1970 s and is currently one of the most commonly prescribed drugs in US for ventricular and atrial arrhythmias. Although amiodarone is considered a class III anti-arrhythmic agent, it also has class I, II, IV actions, making it a unique and effective anti-arrhythmic agent. ', 'Amiodarone, an iodinated benzofuran derivative, introduced in 1960 s as an anti-anginal agent, emerged as a potent anti-arrhythmic agent by 1970 s and is currently one of the most commonly prescribed drugs in US for ventricular and atrial arrhythmias. Although amiodarone is considered a class III anti-arrhythmic agent, it also has class I, II, IV actions, making it a unique and effective anti-arrhythmic agent. ', 'Amiodarone, an iodinated benzofuran derivative, introduced in 1960 s as an anti-anginal agent, emerged as a potent anti-arrhythmic agent by 1970 s and is currently one of the most commonly prescribed drugs in US for ventricular and atrial arrhythmias. Although amiodarone is considered a class III anti-arrhythmic agent, it also has class I, II, IV actions, making it a unique and effective anti-arrhythmic agent. ', 'Amiodarone, an iodinated benzofuran derivative, introduced in 1960 s as an anti-anginal agent, emerged as a potent anti-arrhythmic agent by 1970 s and is currently one of the most commonly prescribed drugs in US for ventricular and atrial arrhythmias. Although amiodarone is considered a class III anti-arrhythmic agent, it also has class I, II, IV actions, making it a unique and effective anti-arrhythmic agent. ', 'Although considered to be a class III anti-arrhythmic, amiodarone also has class I, II and IV actions, which gives it a unique pharmacological and anti-arrhythmic profile'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/21626366",
"http://www.ncbi.nlm.nih.gov/pubmed/11825323",
"http://www.ncbi.nlm.nih.gov/pubmed/20041841",
"http://www.ncbi.nlm.nih.gov/pubmed/12491809",
"http://www.ncbi.nlm.nih.gov/pubmed/15989900",
"http://www.ncbi.nlm.nih.gov/pubmed/21728182",
"http://www.ncbi.nlm.nih.gov/pubmed/17352036"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21626366",
"endSection": "abstract",
"offsetInBeginSection": 1185,
"offsetInEndSection": 1374,
"text": "Common class I agents are excluded due to the inherent abnormal cardiac structure and function in the setting of cardiogenic shock. Class III drug options include dofetilide and amiodarone."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11825323",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 318,
"text": "Amiodarone has been used as an anti-arrhythmic drug since the 1970s and has an established role in the treatment of ventricular tachyarrhythmias. Although considered to be a class III anti-arrhythmic, amiodarone also has class I, II and IV actions, which gives it a unique pharmacological and anti-arrhythmic profile. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20041841",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 413,
"text": "Amiodarone, an iodinated benzofuran derivative, introduced in 1960's as an anti-anginal agent, emerged as a potent anti-arrhythmic agent by 1970's and is currently one of the most commonly prescribed drugs in US for ventricular and atrial arrhythmias. Although amiodarone is considered a class III anti-arrhythmic agent, it also has class I, II, IV actions, making it a unique and effective anti-arrhythmic agent."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12491809",
"endSection": "abstract",
"offsetInBeginSection": 282,
"offsetInEndSection": 655,
"text": "Amiodarone, a representative class III agent, exerts negative dromotropism by suppressing the fast sodium current responsible for conduction in acute administration (class I effects). Chronic amiodarone causes prolongation of ERP (class III effects), which is sometimes associated with negative dromotropism based on the alteration of passive or active membrane properties."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21728182",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "Amiodarone, an iodinated benzofuran derivative with predominantly class III anti-arrhythmic effects, is used to treat supraventricular and ventricular arrhythmias."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11825323",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 318,
"text": "Amiodarone has been used as an anti-arrhythmic drug since the 1970s and has an established role in the treatment of ventricular tachyarrhythmias. Although considered to be a class III anti-arrhythmic, amiodarone also has class I, II and IV actions, which gives it a unique pharmacological and anti-arrhythmic profile. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20041841",
"endSection": "abstract",
"offsetInBeginSection": 251,
"offsetInEndSection": 411,
"text": "Although amiodarone is considered a class III anti-arrhythmic agent, it also has class I, II, IV actions, making it a unique and effective anti-arrhythmic agent"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17352036",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 163,
"text": "Amiodarone, a class III antiarrhythmic drug, is one of the most effective drugs used in the treatment of ventricular and paroxysmal supraventricular tachyarrhythmia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20041841",
"endSection": "abstract",
"offsetInBeginSection": 252,
"offsetInEndSection": 412,
"text": "Although amiodarone is considered a class III anti-arrhythmic agent, it also has class I, II, IV actions, making it a unique and effective anti-arrhythmic agent"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11825323",
"endSection": "abstract",
"offsetInBeginSection": 146,
"offsetInEndSection": 316,
"text": "Although considered to be a class III anti-arrhythmic, amiodarone also has class I, II and IV actions, which gives it a unique pharmacological and anti-arrhythmic profile"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20041841",
"endSection": "abstract",
"offsetInBeginSection": 252,
"offsetInEndSection": 412,
"text": "Although amiodarone is considered a class III anti-arrhythmic agent, it also has class I, II, IV actions, making it a unique and effective anti-arrhythmic agent"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11825323",
"endSection": "abstract",
"offsetInBeginSection": 146,
"offsetInEndSection": 316,
"text": "Although considered to be a class III anti-arrhythmic, amiodarone also has class I, II and IV actions, which gives it a unique pharmacological and anti-arrhythmic profile"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15989900",
"endSection": "abstract",
"offsetInBeginSection": 138,
"offsetInEndSection": 236,
"text": "Amiodarone is a potent class III anti-arrhythmic drug that also possesses beta-blocking properties"
}
]
| 5 | BioASQ-training5b | [
"http://www.biosemantics.org/jochem#4274241",
"http://www.biosemantics.org/jochem#4075064"
]
| []
| 5509df4ac2af5d5b70000003 | 246 |
yesno | Are there any anti-amyloid antibody approved as drug for Alzheimer's disease treatment? | ['no'] | [
"no"
]
| ['No new drugs have been approved during the past 15 years; and the available medications are not cost-effective.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/29607687",
"http://www.ncbi.nlm.nih.gov/pubmed/26697860"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26697860",
"endSection": "abstract",
"offsetInBeginSection": 873,
"offsetInEndSection": 1222,
"text": "Treatment with memantine, a noncompetitive NMDA receptor antagonist which is an approved drug for treatment of Alzheimer's disease, rescued protein phosphatase-2A activity by decreasing its demethylation at Leu309 selectively and attenuated Alzheimer's disease-like pathology and cognitive impairment in adeno-associated virus vector-1-I1PP2A rats. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29607687",
"endSection": "abstract",
"offsetInBeginSection": 598,
"offsetInEndSection": 626,
"text": "anti-Amyloid agents (13.30%)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29607687",
"endSection": "abstract",
"offsetInBeginSection": 202,
"offsetInEndSection": 314,
"text": "no new drugs have been approved during the past 15 years; and the available medications are not cost-effective. "
}
]
| 11 | BioASQ-training11b | null | null | 5ca0848aecadf2e73f000044 | 247 |
yesno | Is the Prostate- Specific Antigen (PSA) test relevant only for prostate cancer? | ['no'] | [
"no"
]
| No, although the PSA test can detect high levels of PSA that may indicate the presence of prostate cancer, many other conditions, such as an enlarged or inflamed prostate, can also increase PSA levels. | [
"http://www.ncbi.nlm.nih.gov/pubmed/24223021",
"http://www.ncbi.nlm.nih.gov/pubmed/23588999",
"http://www.ncbi.nlm.nih.gov/pubmed/23400279",
"http://www.ncbi.nlm.nih.gov/pubmed/20065953",
"http://www.ncbi.nlm.nih.gov/pubmed/19579539",
"http://www.ncbi.nlm.nih.gov/pubmed/18808732",
"http://www.ncbi.nlm.nih.gov/pubmed/18569246",
"http://www.ncbi.nlm.nih.gov/pubmed/18355899",
"http://www.ncbi.nlm.nih.gov/pubmed/17559560",
"http://www.ncbi.nlm.nih.gov/pubmed/17489318",
"http://www.ncbi.nlm.nih.gov/pubmed/17233806",
"http://www.ncbi.nlm.nih.gov/pubmed/15925651",
"http://www.ncbi.nlm.nih.gov/pubmed/15530599",
"http://www.ncbi.nlm.nih.gov/pubmed/12088291",
"http://www.ncbi.nlm.nih.gov/pubmed/11583357",
"http://www.ncbi.nlm.nih.gov/pubmed/10697616",
"http://www.ncbi.nlm.nih.gov/pubmed/9494604",
"http://www.ncbi.nlm.nih.gov/pubmed/9494603",
"http://www.ncbi.nlm.nih.gov/pubmed/9329582",
"http://www.ncbi.nlm.nih.gov/pubmed/7544735",
"http://www.ncbi.nlm.nih.gov/pubmed/7687205"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24223021",
"endSection": "abstract",
"offsetInBeginSection": 13,
"offsetInEndSection": 129,
"text": "rostate cancer (PCa) is the most frequently diagnosed malignancy and the second leading cause of cancer death in men"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24223021",
"endSection": "abstract",
"offsetInBeginSection": 378,
"offsetInEndSection": 436,
"text": "PSA is known to be prostate specific, but not PCa specific"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20065953",
"endSection": "abstract",
"offsetInBeginSection": 4,
"offsetInEndSection": 96,
"text": "deficiencies of serum PSA as a prostate-cancer-specific diagnostic test are well recognized."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19579539",
"endSection": "abstract",
"offsetInBeginSection": 98,
"offsetInEndSection": 206,
"text": "medical debate surrounding the use of the prostate-specific antigen (PSA) test for prostate cancer screening"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15925651",
"endSection": "abstract",
"offsetInBeginSection": 2712,
"offsetInEndSection": 2834,
"text": "The clinical relevance of this surprisingly high rate of prostate cancer in men with a normal PSA is yet to be determined "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15530599",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 159,
"text": "Rapid uptake of prostate-specific antigen (PSA) testing has occurred in the United States despite inconclusive evidence regarding mortality benefit"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12088291",
"endSection": "abstract",
"offsetInBeginSection": 9,
"offsetInEndSection": 173,
"text": "Routine cancer screening with prostate-specific antigen (PSA) is controversial, and practice guidelines recommend that men be counseled about its risks and benefits"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11583357",
"endSection": "abstract",
"offsetInBeginSection": 895,
"offsetInEndSection": 1135,
"text": "Prostate carcinoma was histologically confirmed in 14 (0.66%) of the men, nine times in the early stage (T2) and five times in the clinical stage (T3), corresponding to an incidence of circa 650 cases per 100,000 men in the target age group"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11583357",
"endSection": "abstract",
"offsetInBeginSection": 1150,
"offsetInEndSection": 1278,
"text": "This newly developed PSA test system can enhance the acceptance rate and effectiveness of medical check-ups for prostate cancer,"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7544735",
"endSection": "abstract",
"offsetInBeginSection": 1484,
"offsetInEndSection": 1601,
"text": "PSA can be used reliably as a unique tool in the follow-up of patients for the early detection of progressive disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7544735",
"endSection": "abstract",
"offsetInBeginSection": 727,
"offsetInEndSection": 831,
"text": "PSA showed negative predictive values of 82 and 77%, respectively, using 4 and 10 ng/ml as cutoff points"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7687205",
"endSection": "abstract",
"offsetInBeginSection": 3,
"offsetInEndSection": 200,
"text": "have assessed the feasibility of using fixed-limit criteria based on medical relevance and biological variation for evaluating the analytical performance of the prostate-specific antigen (PSA) test"
}
]
| 5 | BioASQ-training5b | [
"http://www.disease-ontology.org/api/metadata/DOID:10283",
"http://www.disease-ontology.org/api/metadata/DOID:10286",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D011471",
"http://www.uniprot.org/uniprot/KLK3_HUMAN",
"http://www.uniprot.org/uniprot/KLK3_MACMU",
"http://www.uniprot.org/uniprot/KLK3_MACFA"
]
| []
| 5327139ad6d3ac6a3400000d | 248 |
yesno | Is curcumin a phytochemical? | ['yes'] | [
"yes"
]
| ['Yes, curcumin is a phytochemical derived from rhizome of turmeric Curcuma longa.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/26155681",
"http://www.ncbi.nlm.nih.gov/pubmed/25541178",
"http://www.ncbi.nlm.nih.gov/pubmed/25640947",
"http://www.ncbi.nlm.nih.gov/pubmed/25543853",
"http://www.ncbi.nlm.nih.gov/pubmed/25542083",
"http://www.ncbi.nlm.nih.gov/pubmed/25661742",
"http://www.ncbi.nlm.nih.gov/pubmed/25964558",
"http://www.ncbi.nlm.nih.gov/pubmed/25149981",
"http://www.ncbi.nlm.nih.gov/pubmed/24482305",
"http://www.ncbi.nlm.nih.gov/pubmed/24815764",
"http://www.ncbi.nlm.nih.gov/pubmed/24293118",
"http://www.ncbi.nlm.nih.gov/pubmed/24669820",
"http://www.ncbi.nlm.nih.gov/pubmed/25272063"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26155681",
"endSection": "abstract",
"offsetInBeginSection": 366,
"offsetInEndSection": 507,
"text": "we analyzed turmeric from different agroclimatic regions for influence of various factors on its growth and yield of important phytochemicals"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25541178",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 77,
"text": "The phytochemical, curcumin, has been reported to play many beneficial roles."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25640947",
"endSection": "abstract",
"offsetInBeginSection": 316,
"offsetInEndSection": 470,
"text": "Curcumin (CUR), the major component in Curcuma longa, has been shown as a potent chemopreventive phytochemical that modulates various signaling pathways. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25543853",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 277,
"text": "Curcumin (CUR) is a phytochemical that inhibits the xenobiotic ABC efflux transporters implicated in cancer multidrug resistance (MDR), such as P-glycoprotein (P-gp), breast cancer resistance protein (BCRP) and multidrug resistance-associated proteins 1 and 5 (MRP1 and MRP5). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25542083",
"endSection": "abstract",
"offsetInBeginSection": 87,
"offsetInEndSection": 261,
"text": "In this study, we tested the efficacy of combining temozolomide with curcumin, a phytochemical known to inhibit glioblastoma growth, and investigated the mechanisms involved."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25661742",
"endSection": "abstract",
"offsetInBeginSection": 460,
"offsetInEndSection": 583,
"text": " In the present study, we investigate whether curcumin (cur), a phytochemical compound with potent anti-inflammatory effect"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25964558",
"endSection": "title",
"offsetInBeginSection": 98,
"offsetInEndSection": 126,
"text": "the Phytochemicals Curcumin "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25964558",
"endSection": "abstract",
"offsetInBeginSection": 327,
"offsetInEndSection": 388,
"text": "in combination with the phytochemicals curcumin and quercetin"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25149981",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 116,
"text": "Curcumin is a phytochemical derived from rhizome of turmeric Curcuma longa, present in the curry spice. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24482305",
"endSection": "abstract",
"offsetInBeginSection": 212,
"offsetInEndSection": 352,
"text": "Curcumin, a naturally occurring polyphenolic phytochemical isolated from the medicinal plant Curcuma longa, has anti-inflammatory activities"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24815764",
"endSection": "abstract",
"offsetInBeginSection": 329,
"offsetInEndSection": 400,
"text": "In the present study curcumin (CUR), a known anticancer phytochemical, "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24293118",
"endSection": "abstract",
"offsetInBeginSection": 8,
"offsetInEndSection": 82,
"text": " Curcumin, a natural phytochemical, exhibits potent anticancer activities."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24669820",
"endSection": "abstract",
"offsetInBeginSection": 275,
"offsetInEndSection": 355,
"text": "hat curcumin, a phytochemical compound with potent anti-inflammatory properties "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25272063",
"endSection": "abstract",
"offsetInBeginSection": 370,
"offsetInEndSection": 395,
"text": "curcumin, a phytochemical"
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003474",
"http://www.biosemantics.org/jochem#4272467",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D064209"
]
| [
{
"o": "MeSH",
"p": "http://www.w3.org/2004/02/skos/core#note",
"s": "http://linkedlifedata.com/resource/umls/label/A2792113"
},
{
"o": "curcumin III",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A2792113"
},
{
"o": "http://linkedlifedata.com/resource/umls/label/A2792113",
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{
"o": "curcumin III",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
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{
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},
{
"o": "458-37-7",
"p": "http://linkedlifedata.com/resource/pubmed/registryNumber",
"s": "http://linkedlifedata.com/resource/pubmed/chemical/Curcumin"
},
{
"o": "Curcumin",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/pubmed/chemical/Curcumin"
},
{
"o": "846163",
"p": "http://www.w3.org/2004/02/skos/core#notation",
"s": "http://linkedlifedata.com/resource/umls/label/A16717035"
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"o": "Curcumin Oral Capsule",
"p": "http://www.w3.org/2008/05/skos-xl#literalForm",
"s": "http://linkedlifedata.com/resource/umls/label/A16717035"
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"s": "http://linkedlifedata.com/resource/umls/id/C2683192"
}
]
| 56b0eb3b0a360a5e45000019 | 249 |
yesno | Is belimumab effective for the lupus nephritis? | ['yes'] | [
"yes"
]
| ['Yes, belimumab appears to effective for the lupus nephritis.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/24014569",
"http://www.ncbi.nlm.nih.gov/pubmed/32537456",
"http://www.ncbi.nlm.nih.gov/pubmed/33186226",
"http://www.ncbi.nlm.nih.gov/pubmed/32755035",
"http://www.ncbi.nlm.nih.gov/pubmed/32591783",
"http://www.ncbi.nlm.nih.gov/pubmed/29514612",
"http://www.ncbi.nlm.nih.gov/pubmed/25969652",
"http://www.ncbi.nlm.nih.gov/pubmed/26712500",
"http://www.ncbi.nlm.nih.gov/pubmed/32937045"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32591783",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Long-term effects of combined B-cell immunomodulation with rituximab and belimumab in severe, refractory systemic lupus erythematosus: 2-year results."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32591783",
"endSection": "abstract",
"offsetInBeginSection": 1559,
"offsetInEndSection": 1747,
"text": "CONCLUSIONS: Combined B-cell targeted therapy with RTX and BLM prevented full B-cell repopulation including DN B cells, with concomitant specific reduction of SLE-relevant autoantibodies. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32537456",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 96,
"text": "Clinical Efficacy of Routinely Administered Belimumab on Proteinuria and Neuropsychiatric Lupus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32537456",
"endSection": "abstract",
"offsetInBeginSection": 1373,
"offsetInEndSection": 1765,
"text": "Conclusions: In our series, BEL led to a decrease of proteinuria in patients with proteinuria of more than 1,000 mg/g creatinine despite standard of care treatment, and led to a marked clinical improvement in one patient with NPSLE. No adverse events were observed. Routinely administered BEL shows clinical efficacy on non-approved manifestations, but careful patient selection is warranted."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32755035",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "Phase II Randomized Trial of Rituximab Plus Cyclophosphamide Followed by Belimumab for the Treatment of Lupus Nephritis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32755035",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 166,
"text": "OBJECTIVE: To assess the safety, mechanism of action, and preliminary efficacy of rituximab followed by belimumab in the treatment of refractory lupus nephritis (LN)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32755035",
"endSection": "abstract",
"offsetInBeginSection": 1679,
"offsetInEndSection": 1803,
"text": "CONCLUSION: The addition of belimumab to a treatment regimen with rituximab and CYC was safe in patients with refractory LN."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33186226",
"endSection": "abstract",
"offsetInBeginSection": 281,
"offsetInEndSection": 657,
"text": "RECENT FINDINGS: Recently, the Belimumab in Subjects with Systemic Lupus Erythematosus - Lupus Nephritis trial tested belimumab, an inhibitor of B-cell activating factor, as an add-on therapy to steroids and either mycophenolate mofetil (MMF) or cyclophosphamide when given IV monthly over a period of 104 weeks at an effect size of 11% for a Primary Efficacy Renal Response. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26712500",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Case report: successful treatment of membranous lupus nephritis with belimumab in an African female immigrant."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25969652",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 175,
"text": "Recently introduced into the market, belimumab (Benlysta) is a monoclonal antibody that has potential clinically efficacious applications for the treatment of lupus nephritis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24014569",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Successful treatment of a mycophenolate mofetil-refractory proliferative lupus nephritis with Belimumab in a 19-year-old woman."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24014569",
"endSection": "abstract",
"offsetInBeginSection": 347,
"offsetInEndSection": 516,
"text": "Following treatment with belimumab, proteinuria rapidly improved to almost normal levels and clinical remission lasted. Belimumab might hold promise for this indication."
}
]
| 11 | BioASQ-training11b | null | null | 6020ab801cb411341a000081 | 250 |
yesno | Is Hemochromatosis type 4 is caused by a mutation in a recessive gene? | ['no'] | [
"no"
]
| ['No, Hemochromatosis type 4 is caused by an autosomal dominant gene', 'type 4 hereditary hemochromatosis, an autosomal dominant iron overload condition with variable phenotypic manifestations.', 'Hemochromatosis type 4, also known as ferroportin disease, is an autosomal dominant genetic disorder caused by pathogenic mutations in the SLC40A1 gene, which encodes ferroportin 1 (FPN1)'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/20039160",
"http://www.ncbi.nlm.nih.gov/pubmed/24714983",
"http://www.ncbi.nlm.nih.gov/pubmed/29154924",
"http://www.ncbi.nlm.nih.gov/pubmed/30500107",
"http://www.ncbi.nlm.nih.gov/pubmed/12547233"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29154924",
"endSection": "abstract",
"offsetInBeginSection": 83,
"offsetInEndSection": 245,
"text": " severely affect iron homeostasis causing type 4 hereditary hemochromatosis, an autosomal dominant iron overload condition with variable phenotypic manifestations"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30500107",
"endSection": "abstract",
"offsetInBeginSection": 19,
"offsetInEndSection": 207,
"text": "Hemochromatosis type 4, also known as ferroportin disease, is an autosomal dominant genetic disorder caused by pathogenic mutations in the SLC40A1 gene, which encodes ferroportin 1 (FPN1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24714983",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 198,
"text": "Hemochromatosis type 4 is a rare form of primary iron overload transmitted as an autosomal dominant trait caused by mutations in the gene encoding the iron transport protein ferroportin 1 (SLC40A1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20039160",
"endSection": "abstract",
"offsetInBeginSection": 948,
"offsetInEndSection": 1086,
"text": "Type 4 hemochromatosis follows an autosomal dominant trait; the corresponding mutation affects the basolateral iron carrier ferroportin 1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20039160",
"endSection": "abstract",
"offsetInBeginSection": 956,
"offsetInEndSection": 1093,
"text": "Type 4 hemochromatosis follows an autosomal dominant trait; the corresponding mutation affects the basolateral iron carrier ferroportin 1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20039160",
"endSection": "abstract",
"offsetInBeginSection": 948,
"offsetInEndSection": 1087,
"text": "Type 4 hemochromatosis follows an autosomal dominant trait; the corresponding mutation affects the basolateral iron carrier ferroportin 1."
}
]
| 11 | BioASQ-training11b | null | null | 5e31cc22fbd6abf43b000050 | 251 |
yesno | Is RANKL secreted from the cells? | ['yes'] | [
"yes"
]
| ['Receptor activator of nuclear factor κB ligand (RANKL) is a cytokine predominantly secreted by osteoblasts.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/24267510",
"http://www.ncbi.nlm.nih.gov/pubmed/24265865",
"http://www.ncbi.nlm.nih.gov/pubmed/23835909",
"http://www.ncbi.nlm.nih.gov/pubmed/23827649",
"http://www.ncbi.nlm.nih.gov/pubmed/23698708",
"http://www.ncbi.nlm.nih.gov/pubmed/23632157",
"http://www.ncbi.nlm.nih.gov/pubmed/22948539",
"http://www.ncbi.nlm.nih.gov/pubmed/22901753",
"http://www.ncbi.nlm.nih.gov/pubmed/22867712",
"http://www.ncbi.nlm.nih.gov/pubmed/21618594"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24267510",
"endSection": "abstract",
"offsetInBeginSection": 114,
"offsetInEndSection": 242,
"text": "Osteoprotegerin (OPG) is a soluble secreted factor that acts as a decoy receptor for receptor activator of NF-κB ligand (RANKL) "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24265865",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 266,
"text": "Osteoprotegerin (OPG) is a secreted glycoprotein and a member of the tumor necrosis factor receptor superfamily. It usually functions in bone remodeling, by inhibiting osteoclastogenesis through interaction with a receptor activator of the nuclear factor κB (RANKL)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23835909",
"endSection": "abstract",
"offsetInBeginSection": 1110,
"offsetInEndSection": 1247,
"text": "e RANKL/OPG ratio secreted by osteoblasts increased and RANK expression by osteoclasts increased, leading to increased osteoclastogenesis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23827649",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 228,
"text": "Osteoprotegerin (OPG) is an essential secreted protein in bone turnover due to its role as a decoy receptor for the Receptor Activator of Nuclear Factor-kB ligand (RANKL) in the osteoclasts, thus inhibiting their differentiation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23698708",
"endSection": "abstract",
"offsetInBeginSection": 324,
"offsetInEndSection": 439,
"text": "We identify a TNFSF11 transcript variant that extends the originally identified transcript encoding secreted RANKL."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23698708",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 95,
"text": "Activated human T cells express alternative mRNA transcripts encoding a secreted form of RANKL."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23632157",
"endSection": "abstract",
"offsetInBeginSection": 471,
"offsetInEndSection": 621,
"text": "OPG, on the other hand, is secreted by osteoblast as a decoy receptor for RANKL, prevents RANKL from binding to RANK and thus prevents bone resorption"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22948539",
"endSection": "abstract",
"offsetInBeginSection": 270,
"offsetInEndSection": 486,
"text": "Receptor activator of nuclear factor κB ligand (RANKL) and osteoprotegerin (OPG) are cytokines predominantly secreted by osteoblasts and play a central role in differentiation and functional activation of osteoclasts"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22901753",
"endSection": "abstract",
"offsetInBeginSection": 690,
"offsetInEndSection": 1005,
"text": "Although B. abortus-activated T cells actively secreted the pro-osteoclastogenic cytokines RANKL and IL-17, osteoclastogenesis depended on IL-17, because osteoclast generation induced by Brucella-activated T cells was completely abrogated when these cells were cultured with BMMs from IL-17 receptor knockout mice. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22867712",
"endSection": "abstract",
"offsetInBeginSection": 468,
"offsetInEndSection": 758,
"text": " osteoclastogenesis and bone destruction in autoimmune arthritis. We isolated human fibroblasts from RA, pyrophosphate arthropathy (PPA) and osteoarthritis (OA) patients and analyzed their RANKL/OPG expression profile and the capacity of their secreted factors to induce osteoclastogenesis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21618594",
"endSection": "abstract",
"offsetInBeginSection": 269,
"offsetInEndSection": 478,
"text": "Osteoprotegerin (OPG) and receptor activator of nuclear factor κB ligand (RANKL) are cytokines predominantly secreted by osteoblasts and play critical roles in the differentiation and function of osteoclasts. "
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D015870",
"http://www.uniprot.org/uniprot/TNF11_RAT",
"http://www.uniprot.org/uniprot/TNF11_HUMAN"
]
| []
| 55262a9787ecba3764000009 | 252 |
yesno | Are long non coding RNAs spliced? | ['yes'] | [
"yes"
]
| ['Long non coding RNAs appear to be spliced through the same pathway as the mRNAs'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22955988",
"http://www.ncbi.nlm.nih.gov/pubmed/22955974",
"http://www.ncbi.nlm.nih.gov/pubmed/22707570",
"http://www.ncbi.nlm.nih.gov/pubmed/21622663",
"http://www.ncbi.nlm.nih.gov/pubmed/24285305",
"http://www.ncbi.nlm.nih.gov/pubmed/24106460"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22955988",
"endSection": "abstract",
"offsetInBeginSection": 546,
"offsetInEndSection": 739,
"text": "Our analyses indicate that lncRNAs are generated through pathways similar to that of protein-coding genes, with similar histone-modification profiles, splicing signals, and exon/intron lengths."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22955974",
"endSection": "abstract",
"offsetInBeginSection": 1602,
"offsetInEndSection": 1732,
"text": "For alternative exons and long noncoding RNAs, splicing tends to occur later, and the latter might remain unspliced in some cases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22707570",
"endSection": "abstract",
"offsetInBeginSection": 249,
"offsetInEndSection": 557,
"text": "bosome-mapping data to identify lncRNAs of Caenorhabditis elegans. We found 170 long intervening ncRNAs (lincRNAs), which had single- or multiexonic structures that did not overlap protein-coding transcripts, and about sixty antisense lncRNAs (ancRNAs), which were complementary to protein-coding transcripts"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21622663",
"endSection": "abstract",
"offsetInBeginSection": 275,
"offsetInEndSection": 401,
"text": "We introduce an approach to predict spliced lncRNAs in vertebrate genomes combining comparative genomics and machine learning."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24285305",
"endSection": "abstract",
"offsetInBeginSection": 711,
"offsetInEndSection": 856,
"text": "Owing to similar alternative splicing pattern to mRNAs, the concept of lncRNA genes was put forward to help systematic understanding of lncRNAs. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24106460",
"endSection": "abstract",
"offsetInBeginSection": 561,
"offsetInEndSection": 746,
"text": "Our synthesis of recent studies suggests that neither size, presence of a poly-A tail, splicing, direction of transcription, nor strand specificity are of importance to lncRNA function."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22955988",
"endSection": "abstract",
"offsetInBeginSection": 546,
"offsetInEndSection": 739,
"text": "Our analyses indicate that lncRNAs are generated through pathways similar to that of protein-coding genes, with similar histone-modification profiles, splicing signals, and exon/intron lengths."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22955974",
"endSection": "abstract",
"offsetInBeginSection": 1602,
"offsetInEndSection": 1732,
"text": "For alternative exons and long noncoding RNAs, splicing tends to occur later, and the latter might remain unspliced in some cases."
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D062085",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D012326"
]
| []
| 535d292a9a4572de6f000003 | 254 |
yesno | Is Adamts18 deficiency associated with cancer? | ['yes'] | [
"yes"
]
| ['Yes. ADAMTS18 is a novel tumor suppressor and is critical to the pathology of human colorectal cancer. Adamts18 deficiency enhances tumorigenesis and intestinal inflammation through elevated Wnt/β-catenin and p38MAPK/ERK1/2 signaling and promotes colon cancer in this mouse model.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/28145888"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28145888",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "Adamts18 deficiency promotes colon carcinogenesis by enhancing β-catenin and p38MAPK/ERK1/2 signaling in the mouse model of AOM/DSS-induced colitis-associated colorectal cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28145888",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1074,
"text": "ADAMTS18 is a novel tumor suppressor and is critical to the pathology of human colorectal cancer. However, the underlying mechanism is not clear. Here we generated an Adamts18-deficient mouse strain as an in vivo model to investigate the role of ADAMTS18 in the pathogenesis of colorectal cancer. In AOM/DSS-induced colitis-associated colorectal cancer, the deficiency of Adamts18 in mice resulted in enhanced tumorigenesis and colon inflammation that could be attributed in part to enhanced nuclear translocation of β-catenin and elevated expression of its downstream target genes, cyclin D1 and c-myc. Moreover, increased p38MAPK and ERK1/2 activities were detected in colon cancer cells from Adamts18-deficient mice. Further studies revealed that ADAMTS18 deficiency reduced intestinal E-cadherin levels in mice, which ultimately led to intestinal barrier dysfunction. These data indicate that Adamts18 deficiency enhances tumorigenesis and intestinal inflammation through elevated Wnt/β-catenin and p38MAPK/ERK1/2 signaling and promotes colon cancer in this mouse model."
}
]
| 11 | BioASQ-training11b | null | null | 61f9cb19c9dfcb9c09000002 | 255 |
yesno | Can the apoptosis regulator BAX trigger the release of cytochrome c? | ['yes'] | [
"yes"
]
| ['Yes, altered Bax conformation trigger its redistribution from the cytosol to mitochondria. Subsequently, cytochrome c is released from mitochondria to cytosol.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/25619640",
"http://www.ncbi.nlm.nih.gov/pubmed/25524600",
"http://www.ncbi.nlm.nih.gov/pubmed/25116390",
"http://www.ncbi.nlm.nih.gov/pubmed/23954445",
"http://www.ncbi.nlm.nih.gov/pubmed/23567751",
"http://www.ncbi.nlm.nih.gov/pubmed/22116711",
"http://www.ncbi.nlm.nih.gov/pubmed/21307199"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25619640",
"endSection": "abstract",
"offsetInBeginSection": 548,
"offsetInEndSection": 684,
"text": "6-Shogaol reduced the mitochondrial membrane potential (MMP) and released cytochrome c from mitochondria to cytosol via Bax activation. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25524600",
"endSection": "abstract",
"offsetInBeginSection": 539,
"offsetInEndSection": 676,
"text": "Moreover, overexpression of ERβ prevented Bax activation, cytochrome c release, caspase-3 activation, and PARP cleavage during apoptosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25116390",
"endSection": "abstract",
"offsetInBeginSection": 349,
"offsetInEndSection": 573,
"text": "In this study, we demonstrated that EV71 infection altered Bax conformation and triggered its redistribution from the cytosol to mitochondria in RD cells. Subsequently, cytochrome c was released from mitochondria to cytosol."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23954445",
"endSection": "abstract",
"offsetInBeginSection": 1087,
"offsetInEndSection": 1218,
"text": "associated with translocation of Bax from the cytosol to the mitochondrial membrane, cytochrome c release, and caspase activation. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23567751",
"endSection": "abstract",
"offsetInBeginSection": 163,
"offsetInEndSection": 397,
"text": "Once activated, BAK and BAX form proteolipid pores in the OMM leading to mitochondrial outer membrane permeabilization (MOMP), and the release of inner membrane space proteins, such as cytochrome c, which promotes caspase activation. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22116711",
"endSection": "abstract",
"offsetInBeginSection": 524,
"offsetInEndSection": 809,
"text": " Our results showed that OC induced a caspase-dependent apoptosis by triggering a series of events in HeLa cells including Bax translocation, cytochrome c release, caspase-3 activation, chromosome fragmentation followed by caspase-8 activation, Bid cleavage and eventually cell death. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21307199",
"endSection": "abstract",
"offsetInBeginSection": 291,
"offsetInEndSection": 411,
"text": "Bax plays a key role in intrinsic apoptotic signaling in neurons by allowing the release of mitochondrial cytochrome c. "
}
]
| 5 | BioASQ-training5b | []
| []
| 5717bacacb4ef8864c00000d | 256 |
yesno | Is TIAM1 favoring tumor progression in colorectal cancer (CRC)? | ['no'] | [
"no"
]
| ['No. In colorectal cancer (CRC) TIAM1 suppresses tumor progression by regulating YAP/TAZ activity.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/28416184",
"http://www.ncbi.nlm.nih.gov/pubmed/17132223"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28416184",
"endSection": "abstract",
"offsetInBeginSection": 55,
"offsetInEndSection": 906,
"text": "Here, we identify TIAM1 as a critical antagonist of CRC progression through inhibiting TAZ and YAP, effectors of WNT signaling. We demonstrate that TIAM1 shuttles between the cytoplasm and nucleus antagonizing TAZ/YAP by distinct mechanisms in the two compartments. In the cytoplasm, TIAM1 localizes to the destruction complex and promotes TAZ degradation by enhancing its interaction with βTrCP. Nuclear TIAM1 suppresses TAZ/YAP interaction with TEADs, inhibiting expression of TAZ/YAP target genes implicated in epithelial-mesenchymal transition, cell migration, and invasion, and consequently suppresses CRC cell migration and invasion. Importantly, high nuclear TIAM1 in clinical specimens associates with increased CRC patient survival. Together, our findings suggest that in CRC TIAM1 suppresses tumor progression by regulating YAP/TAZ activity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28416184",
"endSection": "abstract",
"offsetInBeginSection": 797,
"offsetInEndSection": 906,
"text": "Together, our findings suggest that in CRC TIAM1 suppresses tumor progression by regulating YAP/TAZ activity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28416184",
"endSection": "abstract",
"offsetInBeginSection": 452,
"offsetInEndSection": 694,
"text": "Nuclear TIAM1 suppresses TAZ/YAP interaction with TEADs, inhibiting expression of TAZ/YAP target genes implicated in epithelial-mesenchymal transition, cell migration, and invasion, and consequently suppresses CRC cell migration and invasion."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17132223",
"endSection": "abstract",
"offsetInBeginSection": 690,
"offsetInEndSection": 898,
"text": "Using an orthotopic xenograft model in nude mice, we confirmed that Tiam1 silencing could reduce tumor growth by subcutaneous injection and could suppress lung and liver metastases of colorectal cancer cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28416184",
"endSection": "abstract",
"offsetInBeginSection": 797,
"offsetInEndSection": 910,
"text": "Together, our findings suggest that in CRC TIAM1 suppresses tumor progression by regulating YAP/TAZ activity.<br>"
}
]
| 11 | BioASQ-training11b | null | null | 5c640fa1e842deac67000011 | 257 |
yesno | Does administration of triiodothyronine improve outcome following coronary artery bypass grafting? | ['no'] | [
"no"
]
| Perioperative administration of synthetic thyroid hormone therapy have positive hemodynamic effects (consisting of increases cardiac output, lowered systemic vascular resistance) determining improved postoperative ventricular function, reduced the need for treatment with inotropic agents and mechanical devices, in the absence of relevant effects on outcome ad exception of lower incidence of atrial fibrillation. | [
"http://www.ncbi.nlm.nih.gov/pubmed/23958074",
"http://www.ncbi.nlm.nih.gov/pubmed/18290900",
"http://www.ncbi.nlm.nih.gov/pubmed/16820580",
"http://www.ncbi.nlm.nih.gov/pubmed/12213743",
"http://www.ncbi.nlm.nih.gov/pubmed/10343261",
"http://www.ncbi.nlm.nih.gov/pubmed/8633935",
"http://www.ncbi.nlm.nih.gov/pubmed/8594265",
"http://www.ncbi.nlm.nih.gov/pubmed/7477166",
"http://www.ncbi.nlm.nih.gov/pubmed/7995828",
"http://www.ncbi.nlm.nih.gov/pubmed/8389710",
"http://www.ncbi.nlm.nih.gov/pubmed/19609889",
"http://www.ncbi.nlm.nih.gov/pubmed/19303793"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23958074",
"endSection": "abstract",
"offsetInBeginSection": 889,
"offsetInEndSection": 1204,
"text": "Serum T3 concentrations were significantly higher with fewer patients having T3 concentrations below the normal range in the T3 group than the placebo group throughout the postoperative period. Hemodynamic variables, postoperative inotrope requirement, and outcome variables showed no differences between the groups"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18290900",
"endSection": "abstract",
"offsetInBeginSection": 496,
"offsetInEndSection": 835,
"text": "We conclude that although widespread interest has been shown on the use of thyroid hormones in the perioperative period, and the effect of cardiopulmonary bypass on thyroid hormone metabolism widely studied, there is no substantial evidence to justify routine use of thyroid hormones in patients undergoing coronary artery bypass grafting."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16820580",
"endSection": "abstract",
"offsetInBeginSection": 1440,
"offsetInEndSection": 1588,
"text": "Treatment with GIK, T3, and GIK/T3 improves hemodynamic performance and results in reduced cTnI release in patients undergoing on-pump CABG surgery."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12213743",
"endSection": "abstract",
"offsetInBeginSection": 1053,
"offsetInEndSection": 1222,
"text": "Perioperative administration of triiodothyronine increased cardiac output slightly and decreased systemic vascular resistance, but it had no effect on operative outcome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10343261",
"endSection": "abstract",
"offsetInBeginSection": 1614,
"offsetInEndSection": 2031,
"text": "Parenteral triiodothyronine given after crossclamp removal during elective coronary artery bypass grafting significantly improved postoperative ventricular function, reduced the need for treatment with inotropic agents and mechanical devices, and decreased the incidence of myocardial ischemia. The incidence of atrial fibrillation was slightly decreased, and the need for postoperative pacemaker support was reduced."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8633935",
"endSection": "abstract",
"offsetInBeginSection": 1370,
"offsetInEndSection": 1486,
"text": "Perioperative T3 administration decreased the incidence and need for treatment of postoperative atrial fibrillation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8594265",
"endSection": "abstract",
"offsetInBeginSection": 1501,
"offsetInEndSection": 1625,
"text": " Intravenous T(3) does not have dramatic effects on hemodynamic variables in this setting as has been previously suggested. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7477166",
"endSection": "abstract",
"offsetInBeginSection": 1978,
"offsetInEndSection": 2225,
"text": "Raising serum triiodothyronine concentrations in patients undergoing coronary-artery bypass surgery increases cardiac output and lowers systemic vascular resistance, but does not change outcome or alter the need for standard postoperative therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7995828",
"endSection": "abstract",
"offsetInBeginSection": 1166,
"offsetInEndSection": 1344,
"text": "No significant differences were noted in the pre and post CPB hemodynamics between the two groups for the most part of the study except that heart rate was increased in T3 group."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8389710",
"endSection": "abstract",
"offsetInBeginSection": 1125,
"offsetInEndSection": 1366,
"text": "The haemodynamic parameters were no different between the two groups at any postoperative time point. Likewise, density and affinity of lymphocyte beta-adrenoceptors were not significantly different from pre-operative values in either group."
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D001026",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D020249",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003324",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013963",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D047549",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D014284",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D016896",
"http://www.biosemantics.org/jochem#4275387",
"http://www.disease-ontology.org/api/metadata/DOID:3393"
]
| []
| 532673c4d6d3ac6a34000009 | 258 |
yesno | Is transcription-associated mutagenesis (TAM) related to gene expression levels? | ['yes'] | [
"yes"
]
| ['Spontaneous point mutation rate in a gene increases with its transcription level, suggesting that movement of RNA polymerase through the target initiates a mutagenic process(es). This phenomenon is termed transcription-associated mutation (TAM). Transcription-associated mutagenesis is directly proportional to the level of gene expression.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23564176",
"http://www.ncbi.nlm.nih.gov/pubmed/23146897",
"http://www.ncbi.nlm.nih.gov/pubmed/23055242",
"http://www.ncbi.nlm.nih.gov/pubmed/21177427",
"http://www.ncbi.nlm.nih.gov/pubmed/20435731",
"http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"http://www.ncbi.nlm.nih.gov/pubmed/21177431",
"http://www.ncbi.nlm.nih.gov/pubmed/10628973",
"http://www.ncbi.nlm.nih.gov/pubmed/15143174"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23564176",
"endSection": "abstract",
"offsetInBeginSection": 963,
"offsetInEndSection": 1133,
"text": "These mutations were frequent in plasmid-borne lacS expressed at a high level but not in single-copy lacS in the chromosome or at lower levels of expression in a plasmid."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23564176",
"endSection": "abstract",
"offsetInBeginSection": 1454,
"offsetInEndSection": 1683,
"text": "The results suggest that important DNA repair or replication fidelity functions are impaired or overwhelmed in pJlacS, with results analogous to those of the \"transcription-associated mutagenesis\" seen in bacteria and eukaryotes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23146897",
"endSection": "abstract",
"offsetInBeginSection": 332,
"offsetInEndSection": 531,
"text": "the rate of point mutation in a gene increases with the expression level of the gene. Transcription induces mutagenesis on both DNA strands, indicating simultaneous actions of several TAM mechanisms."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23055242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "High-levels of transcription through a gene stimulate spontaneous mutation rate, a phenomenon termed transcription-associated mutation (TAM)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21177427",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 263,
"text": "High levels of transcription in Saccharomyces cerevisiae are associated with increased genetic instability, which has been linked to DNA damage. Here, we describe a pGAL-CAN1 forward mutation assay for studying transcription-associated mutagenesis (TAM) in yeast."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20435731",
"endSection": "abstract",
"offsetInBeginSection": 432,
"offsetInEndSection": 514,
"text": "The acquisition of mutations was directly correlated to the level of transcription"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20435731",
"endSection": "abstract",
"offsetInBeginSection": 830,
"offsetInEndSection": 976,
"text": "Our results demonstrate that the level of Leu(+) reversions increased significantly in parallel with the induced increase in transcription levels."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Transcription-associated mutagenesis in yeast is directly proportional to the level of gene expression"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "abstract",
"offsetInBeginSection": 403,
"offsetInEndSection": 577,
"text": "spontaneous mutation rate is directly proportional to the transcription level, suggesting that movement of RNA polymerase through the target initiates a mutagenic process(es)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21177431",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "High transcription is associated with genetic instability, notably increased spontaneous mutation rates, which is a phenomenon termed Transcription-Associated-Mutagenesis (TAM)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "abstract",
"offsetInBeginSection": 575,
"offsetInEndSection": 856,
"text": "Using this system, we also investigated two hypotheses that have been proposed to explain transcription-associated mutagenesis (TAM): (1) transcription impairs replication fork progression in a directional manner and (2) DNA lesions accumulate under high-transcription conditions."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Transcription-associated mutagenesis in yeast is directly proportional to the level of gene expression and influenced by the direction of DNA replication."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21177431",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "High transcription is associated with genetic instability, notably increased spontaneous mutation rates, which is a phenomenon termed Transcription-Associated-Mutagenesis (TAM)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "abstract",
"offsetInBeginSection": 575,
"offsetInEndSection": 856,
"text": "Using this system, we also investigated two hypotheses that have been proposed to explain transcription-associated mutagenesis (TAM): (1) transcription impairs replication fork progression in a directional manner and (2) DNA lesions accumulate under high-transcription conditions."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Transcription-associated mutagenesis in yeast is directly proportional to the level of gene expression and influenced by the direction of DNA replication."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21177431",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "High transcription is associated with genetic instability, notably increased spontaneous mutation rates, which is a phenomenon termed Transcription-Associated-Mutagenesis (TAM)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "abstract",
"offsetInBeginSection": 575,
"offsetInEndSection": 856,
"text": "Using this system, we also investigated two hypotheses that have been proposed to explain transcription-associated mutagenesis (TAM): (1) transcription impairs replication fork progression in a directional manner and (2) DNA lesions accumulate under high-transcription conditions."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Transcription-associated mutagenesis in yeast is directly proportional to the level of gene expression and influenced by the direction of DNA replication."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21177431",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "High transcription is associated with genetic instability, notably increased spontaneous mutation rates, which is a phenomenon termed Transcription-Associated-Mutagenesis (TAM)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "abstract",
"offsetInBeginSection": 575,
"offsetInEndSection": 856,
"text": "Using this system, we also investigated two hypotheses that have been proposed to explain transcription-associated mutagenesis (TAM): (1) transcription impairs replication fork progression in a directional manner and (2) DNA lesions accumulate under high-transcription conditions."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Transcription-associated mutagenesis in yeast is directly proportional to the level of gene expression and influenced by the direction of DNA replication."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23055242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "High-levels of transcription through a gene stimulate spontaneous mutation rate, a phenomenon termed transcription-associated mutation (TAM)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Transcription-associated mutagenesis in yeast is directly proportional to the level of gene expression and influenced by the direction of DNA replication."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21177431",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "High transcription is associated with genetic instability, notably increased spontaneous mutation rates, which is a phenomenon termed Transcription-Associated-Mutagenesis (TAM)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23055242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "High-levels of transcription through a gene stimulate spontaneous mutation rate, a phenomenon termed transcription-associated mutation (TAM)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21177427",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 144,
"text": "High levels of transcription in Saccharomyces cerevisiae are associated with increased genetic instability, which has been linked to DNA damage."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "abstract",
"offsetInBeginSection": 579,
"offsetInEndSection": 859,
"text": "Using this system, we also investigated two hypotheses that have been proposed to explain transcription-associated mutagenesis (TAM): (1) transcription impairs replication fork progression in a directional manner and (2) DNA lesions accumulate under high-transcription conditions."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23146897",
"endSection": "abstract",
"offsetInBeginSection": 224,
"offsetInEndSection": 416,
"text": "Using comparative genomics of related species as well as mutation accumulation lines, we show in yeast that the rate of point mutation in a gene increases with the expression level of the gene"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Transcription-associated mutagenesis in yeast is directly proportional to the level of gene expression and influenced by the direction of DNA replication."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21177431",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "High transcription is associated with genetic instability, notably increased spontaneous mutation rates, which is a phenomenon termed Transcription-Associated-Mutagenesis (TAM)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "abstract",
"offsetInBeginSection": 579,
"offsetInEndSection": 858,
"text": "Using this system, we also investigated two hypotheses that have been proposed to explain transcription-associated mutagenesis (TAM): (1) transcription impairs replication fork progression in a directional manner and (2) DNA lesions accumulate under high-transcription conditions"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23055242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "High-levels of transcription through a gene stimulate spontaneous mutation rate, a phenomenon termed transcription-associated mutation (TAM)"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Transcription-associated mutagenesis in yeast is directly proportional to the level of gene expression and influenced by the direction of DNA replication."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23146897",
"endSection": "abstract",
"offsetInBeginSection": 224,
"offsetInEndSection": 416,
"text": "Using comparative genomics of related species as well as mutation accumulation lines, we show in yeast that the rate of point mutation in a gene increases with the expression level of the gene"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21177431",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "High transcription is associated with genetic instability, notably increased spontaneous mutation rates, which is a phenomenon termed Transcription-Associated-Mutagenesis (TAM)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23055242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "High-levels of transcription through a gene stimulate spontaneous mutation rate, a phenomenon termed transcription-associated mutation (TAM)"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Transcription-associated mutagenesis in yeast is directly proportional to the level of gene expression and influenced by the direction of DNA replication."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23146897",
"endSection": "abstract",
"offsetInBeginSection": 224,
"offsetInEndSection": 416,
"text": "Using comparative genomics of related species as well as mutation accumulation lines, we show in yeast that the rate of point mutation in a gene increases with the expression level of the gene"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21177431",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "High transcription is associated with genetic instability, notably increased spontaneous mutation rates, which is a phenomenon termed Transcription-Associated-Mutagenesis (TAM)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23055242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "High-levels of transcription through a gene stimulate spontaneous mutation rate, a phenomenon termed transcription-associated mutation (TAM)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23146897",
"endSection": "abstract",
"offsetInBeginSection": 224,
"offsetInEndSection": 416,
"text": "Using comparative genomics of related species as well as mutation accumulation lines, we show in yeast that the rate of point mutation in a gene increases with the expression level of the gene"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17398168",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 154,
"text": "Transcription-associated mutagenesis in yeast is directly proportional to the level of gene expression and influenced by the direction of DNA replication."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21177431",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "High transcription is associated with genetic instability, notably increased spontaneous mutation rates, which is a phenomenon termed Transcription-Associated-Mutagenesis (TAM)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23055242",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "High-levels of transcription through a gene stimulate spontaneous mutation rate, a phenomenon termed transcription-associated mutation (TAM)"
}
]
| 5 | BioASQ-training5b | [
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0006351",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0010467"
]
| []
| 5544f3005beec11c10000008 | 259 |
yesno | Is Pim-1 a protein phosphatase? | ['no'] | [
"no"
]
| ['No,\nPim-1 is a kinase and not a phosphatase.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/29399171",
"http://www.ncbi.nlm.nih.gov/pubmed/29355758"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29399171",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "Pim-1 proto-oncogene, serine/threonine kinase (PIM-1) phosphorylates a series of substrates to exert its oncogenic function in numerous malignancies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29355758",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "The Pim1 serine/threonine kinase is associated with multiple cellular functions including proliferation, survival, differentiation, apoptosis, tumorigenesis, immune regulation and inflammation in vertebrates."
}
]
| 11 | BioASQ-training11b | null | null | 5cb37f76ecadf2e73f00005c | 260 |
yesno | Does epidural anesthesia for pain management during labor affect the Apgar score of the the infant? | ['no'] | [
"no"
]
| ['Epidural analgesia for labor pain management did not appear to have an immediate effect on neonatal status as determined by Apgar scores or in admissions to neonatal intensive care.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/28013485",
"http://www.ncbi.nlm.nih.gov/pubmed/19466346"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28013485",
"endSection": "abstract",
"offsetInBeginSection": 295,
"offsetInEndSection": 1122,
"text": " We retrospectively analyzed 93 consecutive single-pregnancy patients who underwent cesarean section with combined spinal-epidural anesthesia. The patients were divided into two groups, depending on the use of 6% HES 130/0.4: group A (461 ± 167 ml of saline-based HES was administered; 43 patients) and group B (HES not administered; 50 patients). The major outcome was umbilical cord chloride level at delivery. The volume infused from operating room admission until delivery was not significantly different between groups. The umbilical cord chloride level at delivery was statistically significantly higher in group A than in group B, but clinically similar (108 ± 2 vs. 107 ± 2 mmol/l, P = 0.02). No differences were observed in the Apgar score or other umbilical cord laboratory data at delivery (Na+, K+, pH, base excess)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19466346",
"endSection": "abstract",
"offsetInBeginSection": 1845,
"offsetInEndSection": 2057,
"text": "CONCLUSION\nSubarachnoid or epidural sufentanil, in the doses used in this study, associated with local anesthetics, had the same effect on the duration of labor after analgesia and in the Apgar score of newborns."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19466346",
"endSection": "abstract",
"offsetInBeginSection": 1845,
"offsetInEndSection": 2057,
"text": "CONCLUSION Subarachnoid or epidural sufentanil, in the doses used in this study, associated with local anesthetics, had the same effect on the duration of labor after analgesia and in the Apgar score of newborns."
}
]
| 11 | BioASQ-training11b | null | null | 5c56fd7407647bbc4b000013 | 261 |
yesno | Is Pfh1 a component of the replisome? | ['no'] | [
"no"
]
| ['No. Pfh1 Is an Accessory Replicative Helicase that Interacts with the Replisome to Facilitate Fork Progression and Preserve Genome Integrity. DNA replication through hard-to-replicate sites, including both highly transcribed RNA Pol II and Pol III genes, requires the S. pombe Pfh1 helicase.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22426534",
"http://www.ncbi.nlm.nih.gov/pubmed/27611590"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27611590",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 136,
"text": "Pfh1 Is an Accessory Replicative Helicase that Interacts with the Replisome to Facilitate Fork Progression and Preserve Genome Integrity"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27611590",
"endSection": "abstract",
"offsetInBeginSection": 288,
"offsetInEndSection": 754,
"text": "Although the Schizosaccharomyces pombe 5'-to-3' DNA helicase Pfh1 is known to promote fork progression, its genomic targets, dynamics, and mechanisms of action are largely unknown. Here we address these questions by integrating genome-wide identification of Pfh1 binding sites, comprehensive analysis of the effects of Pfh1 depletion on replication and DNA damage, and proteomic analysis of Pfh1 interaction partners by immunoaffinity purification mass spectrometry."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22426534",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 149,
"text": "DNA replication through hard-to-replicate sites, including both highly transcribed RNA Pol II and Pol III genes, requires the S. pombe Pfh1 helicase."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22426534",
"endSection": "abstract",
"offsetInBeginSection": 347,
"offsetInEndSection": 546,
"text": "Here, we show that Pfh1 is required for efficient fork movement in the ribosomal DNA, the mating type locus, tRNA, 5S ribosomal RNA genes, and genes that are highly transcribed by RNA polymerase II. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22426534",
"endSection": "abstract",
"offsetInBeginSection": 1109,
"offsetInEndSection": 1245,
"text": " Thus, Pfh1 promotes DNA replication and separation of converged replication forks and suppresses DNA damage at hard-to-replicate sites."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22426534",
"endSection": "abstract",
"offsetInBeginSection": 960,
"offsetInEndSection": 1102,
"text": "Cells depleted of Pfh1 were inviable if they also lacked the human TIMELESS homolog Swi1, a replisome component that stabilizes stalled forks."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27611590",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 137,
"text": "Pfh1 Is an Accessory Replicative Helicase that Interacts with the Replisome to Facilitate Fork Progression and Preserve Genome Integrity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27611590",
"endSection": "abstract",
"offsetInBeginSection": 1810,
"offsetInEndSection": 1979,
"text": "Thus, we conclude that Pfh1 is an accessory DNA helicase that interacts with the replisome and promotes replication and suppresses DNA damage at hard-to-replicate sites."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27611590",
"endSection": "abstract",
"offsetInBeginSection": 1585,
"offsetInEndSection": 1810,
"text": "Consistent with this interpretation, Pfh1 co-purified with many key replisome components, including the hexameric MCM helicase, replicative DNA polymerases, RPA, and the processivity clamp PCNA in an S phase dependent manner."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27611590",
"endSection": "abstract",
"offsetInBeginSection": 1295,
"offsetInEndSection": 1585,
"text": "Although Pfh1 affected replication and suppressed DNA damage at discrete sites throughout the genome, Pfh1 and the replicative DNA polymerase bound to similar extents to both Pfh1-dependent and independent sites, suggesting that Pfh1 is proximal to the replication machinery during S phase."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22426534",
"endSection": "abstract",
"offsetInBeginSection": 967,
"offsetInEndSection": 1108,
"text": "Cells depleted of Pfh1 were inviable if they also lacked the human TIMELESS homolog Swi1, a replisome component that stabilizes stalled forks"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22426534",
"endSection": "abstract",
"offsetInBeginSection": 347,
"offsetInEndSection": 544,
"text": "Here, we show that Pfh1 is required for efficient fork movement in the ribosomal DNA, the mating type locus, tRNA, 5S ribosomal RNA genes, and genes that are highly transcribed by RNA polymerase II"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22426534",
"endSection": "abstract",
"offsetInBeginSection": 1110,
"offsetInEndSection": 1244,
"text": "Thus, Pfh1 promotes DNA replication and separation of converged replication forks and suppresses DNA damage at hard-to-replicate sites"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22426534",
"endSection": "abstract",
"offsetInBeginSection": 967,
"offsetInEndSection": 1109,
"text": "Cells depleted of Pfh1 were inviable if they also lacked the human TIMELESS homolog Swi1, a replisome component that stabilizes stalled forks."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27611590",
"endSection": "abstract",
"offsetInBeginSection": 1818,
"offsetInEndSection": 1987,
"text": "Thus, we conclude that Pfh1 is an accessory DNA helicase that interacts with the replisome and promotes replication and suppresses DNA damage at hard-to-replicate sites."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27611590",
"endSection": "abstract",
"offsetInBeginSection": 1592,
"offsetInEndSection": 1817,
"text": "Consistent with this interpretation, Pfh1 co-purified with many key replisome components, including the hexameric MCM helicase, replicative DNA polymerases, RPA, and the processivity clamp PCNA in an S phase dependent manner."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/27611590",
"endSection": "title",
"offsetInBeginSection": 0,
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"text": "Pfh1 Is an Accessory Replicative Helicase that Interacts with the Replisome to Facilitate Fork Progression and Preserve Genome Integrity."
}
]
| 6 | BioASQ-training6b | null | [
{
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| 5881e8e8713cbdfd3d000003 | 262 |
yesno | Is there any link between CTF4 and CTF18 during sister chromatid cohesion? | ['yes'] | [
"yes"
]
| ['Yes. CTF4 and CTF18 are required for high-fidelity chromosome segregation. Both exhibit genetic and physical ties to replication fork constituents. Absence of either CTF4 or CTF18 causes sister chromatid cohesion failure and leads to a preanaphase accumulation of cells that depends on the spindle assembly checkpoint. The physical and genetic interactions between CTF4, CTF18, and core components of replication fork complexes suggest that both gene products act in association with the replication fork to facilitate sister chromatid cohesion.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23334284",
"http://www.ncbi.nlm.nih.gov/pubmed/19430531",
"http://www.ncbi.nlm.nih.gov/pubmed/17483413",
"http://www.ncbi.nlm.nih.gov/pubmed/16962805",
"http://www.ncbi.nlm.nih.gov/pubmed/15226378",
"http://www.ncbi.nlm.nih.gov/pubmed/14742714",
"http://www.ncbi.nlm.nih.gov/pubmed/11287619",
"http://www.ncbi.nlm.nih.gov/pubmed/23036200"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19430531",
"endSection": "abstract",
"offsetInBeginSection": 1152,
"offsetInEndSection": 1292,
"text": "Our results suggest that Elg1, Ctf4, and Ctf18 may coordinate the relative movement of the replication fork with respect to the cohesin ring"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17483413",
"endSection": "abstract",
"offsetInBeginSection": 742,
"offsetInEndSection": 880,
"text": "These data defined two cohesion pathways, one containing CSM3, TOF1, CTF4, and CHL1, and the second containing MRC1, CTF18, CTF8, and DCC1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16962805",
"endSection": "abstract",
"offsetInBeginSection": 460,
"offsetInEndSection": 1082,
"text": "Here we show that three proteins required for sister chromatid cohesion, Eco1, Ctf4, and Ctf18, are found at, and Ctf4 travels along chromosomes with, replication forks. The ring-shaped cohesin complex is loaded onto chromosomes before S phase in an ATP hydrolysis-dependent reaction. Cohesion establishment during DNA replication follows without further cohesin recruitment and without need for cohesin to re-engage an ATP hydrolysis motif that is critical for its initial DNA binding. This provides evidence for cohesion establishment in the context of replication forks and imposes constraints on the mechanism involved"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/15226378",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 198,
"text": "Sister-chromatid cohesion mediated by the alternative RF-CCtf18/Dcc1/Ctf8, the helicase Chl1 and the polymerase-alpha-associated protein Ctf4 is essential for chromatid disjunction during meiosis II"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15226378",
"endSection": "abstract",
"offsetInBeginSection": 199,
"offsetInEndSection": 430,
"text": "In budding yeast, a specialized replication factor C called RF-C(Ctf18/Dcc1/Ctf8) and the DNA-polymerase-alpha-associated protein Ctf4 are required to maintain sister-chromatid cohesion in cells arrested for long periods in mitosis"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/15226378",
"endSection": "abstract",
"offsetInBeginSection": 632,
"offsetInEndSection": 810,
"text": "We also show that, in contrast to mitosis, RF-C(Ctf18/Dcc1/Cft8), Ctf4 and Chl1 are essential for chromosome segregation during meiosis and for the viability of meiotic products."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14742714",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 614,
"text": "Ctf8p is a component of Ctf18-RFC, an alternative replication factor C-like complex required for efficient sister chromatid cohesion in Saccharomyces cerevisiae. We performed synthetic genetic array (SGA) analysis with a ctf8 deletion strain as a primary screen to identify other nonessential genes required for efficient sister chromatid cohesion. We then assessed proficiency of cohesion at three chromosomal loci in strains containing deletions of the genes identified in the ctf8 SGA screen. Deletion of seven genes (CHL1, CSM3, BIM1, KAR3, TOF1, CTF4, and VIK1) resulted in defective sister chromatid cohesion"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11287619",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 82,
"text": "Saccharomyces cerevisiae CTF18 and CTF4 are required for sister chromatid cohesion"
},
{
"beginSection": "abstract",
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"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 587,
"text": "CTF4 and CTF18 are required for high-fidelity chromosome segregation. Both exhibit genetic and physical ties to replication fork constituents. We find that absence of either CTF4 or CTF18 causes sister chromatid cohesion failure and leads to a preanaphase accumulation of cells that depends on the spindle assembly checkpoint. The physical and genetic interactions between CTF4, CTF18, and core components of replication fork complexes observed in this study and others suggest that both gene products act in association with the replication fork to facilitate sister chromatid cohesion."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/11287619",
"endSection": "abstract",
"offsetInBeginSection": 1325,
"offsetInEndSection": 1452,
"text": "The requirement for CTF4 and CTF18 in robust cohesion identifies novel roles for replication accessory proteins in this process"
},
{
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"endSection": "abstract",
"offsetInBeginSection": 456,
"offsetInEndSection": 626,
"text": "Here we show that three proteins required for sister chromatid cohesion, Eco1, Ctf4, and Ctf18, are found at, and Ctf4 travels along chromosomes with, replication forks."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11287619",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "Saccharomyces cerevisiae CTF18 and CTF4 are required for sister chromatid cohesion."
},
{
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"endSection": "abstract",
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"text": "We find that absence of either CTF4 or CTF18 causes sister chromatid cohesion failure and leads to a preanaphase accumulation of cells that depends on the spindle assembly checkpoint."
},
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"endSection": "abstract",
"offsetInBeginSection": 197,
"offsetInEndSection": 430,
"text": "In budding yeast, a specialized replication factor C called RF-C(Ctf18/Dcc1/Ctf8) and the DNA-polymerase-alpha-associated protein Ctf4 are required to maintain sister-chromatid cohesion in cells arrested for long periods in mitosis."
},
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"text": "The physical and genetic interactions between CTF4, CTF18, and core components of replication fork complexes observed in this study and others suggest that both gene products act in association with the replication fork to facilitate sister chromatid cohesion."
},
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"text": "Sister-chromatid cohesion mediated by the alternative RF-CCtf18/Dcc1/Ctf8, the helicase Chl1 and the polymerase-alpha-associated protein Ctf4 is essential for chromatid disjunction during meiosis II."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/23036200",
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"offsetInBeginSection": 629,
"offsetInEndSection": 858,
"text": "Genetic analyses revealed that Rmi1 promoted sister chromatid cohesion in a process that was distinct from both the cohesion establishment pathway involving Ctf4, Csm3, and Chl1 and the pathway involving the acetylation of Smc3."
},
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"offsetInBeginSection": 456,
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"text": "Here we show that three proteins required for sister chromatid cohesion, Eco1, Ctf4, and Ctf18, are found at, and Ctf4 travels along chromosomes with, replication forks."
},
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"text": "Saccharomyces cerevisiae CTF18 and CTF4 are required for sister chromatid cohesion."
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"text": "We find that absence of either CTF4 or CTF18 causes sister chromatid cohesion failure and leads to a preanaphase accumulation of cells that depends on the spindle assembly checkpoint."
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"offsetInBeginSection": 197,
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"text": "In budding yeast, a specialized replication factor C called RF-C(Ctf18/Dcc1/Ctf8) and the DNA-polymerase-alpha-associated protein Ctf4 are required to maintain sister-chromatid cohesion in cells arrested for long periods in mitosis."
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"text": "The physical and genetic interactions between CTF4, CTF18, and core components of replication fork complexes observed in this study and others suggest that both gene products act in association with the replication fork to facilitate sister chromatid cohesion."
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"text": "Sister-chromatid cohesion mediated by the alternative RF-CCtf18/Dcc1/Ctf8, the helicase Chl1 and the polymerase-alpha-associated protein Ctf4 is essential for chromatid disjunction during meiosis II."
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"text": "Here we show that three proteins required for sister chromatid cohesion, Eco1, Ctf4, and Ctf18, are found at, and Ctf4 travels along chromosomes with, replication forks."
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"text": "We find that absence of either CTF4 or CTF18 causes sister chromatid cohesion failure and leads to a preanaphase accumulation of cells that depends on the spindle assembly checkpoint."
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"text": "In budding yeast, a specialized replication factor C called RF-C(Ctf18/Dcc1/Ctf8) and the DNA-polymerase-alpha-associated protein Ctf4 are required to maintain sister-chromatid cohesion in cells arrested for long periods in mitosis."
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"text": "The physical and genetic interactions between CTF4, CTF18, and core components of replication fork complexes observed in this study and others suggest that both gene products act in association with the replication fork to facilitate sister chromatid cohesion."
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"text": "Here we show that three proteins required for sister chromatid cohesion, Eco1, Ctf4, and Ctf18, are found at, and Ctf4 travels along chromosomes with, replication forks."
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"text": "In budding yeast, a specialized replication factor C called RF-C(Ctf18/Dcc1/Ctf8) and the DNA-polymerase-alpha-associated protein Ctf4 are required to maintain sister-chromatid cohesion in cells arrested for long periods in mitosis."
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"text": "In budding yeast, a specialized replication factor C called RF-C(Ctf18/Dcc1/Ctf8) and the DNA-polymerase-alpha-associated protein Ctf4 are required to maintain sister-chromatid cohesion in cells arrested for long periods in mitosis."
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"text": "Here we show that three proteins required for sister chromatid cohesion, Eco1, Ctf4, and Ctf18, are found at, and Ctf4 travels along chromosomes with, replication forks"
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"text": "The physical and genetic interactions between CTF4, CTF18, and core components of replication fork complexes observed in this study and others suggest that both gene products act in association with the replication fork to facilitate sister chromatid cohesion"
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"text": "We find that absence of either CTF4 or CTF18 causes sister chromatid cohesion failure and leads to a preanaphase accumulation of cells that depends on the spindle assembly checkpoint"
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"text": "In addition to Eco1, several other factors contribute to cohesion establishment, including Ctf4, Ctf18, Tof1, Csm3, Chl1 and Mrc1, but little is known about their roles"
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{
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"text": "Here we show that three proteins required for sister chromatid cohesion, Eco1, Ctf4, and Ctf18, are found at, and Ctf4 travels along chromosomes with, replication forks"
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"text": "Saccharomyces cerevisiae CTF18 and CTF4 are required for sister chromatid cohesion."
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"text": "The physical and genetic interactions between CTF4, CTF18, and core components of replication fork complexes observed in this study and others suggest that both gene products act in association with the replication fork to facilitate sister chromatid cohesion"
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"text": "We find that absence of either CTF4 or CTF18 causes sister chromatid cohesion failure and leads to a preanaphase accumulation of cells that depends on the spindle assembly checkpoint"
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"text": "In addition to Eco1, several other factors contribute to cohesion establishment, including Ctf4, Ctf18, Tof1, Csm3, Chl1 and Mrc1, but little is known about their roles"
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{
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"text": "Here we show that three proteins required for sister chromatid cohesion, Eco1, Ctf4, and Ctf18, are found at, and Ctf4 travels along chromosomes with, replication forks"
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"text": "Saccharomyces cerevisiae CTF18 and CTF4 are required for sister chromatid cohesion."
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"text": "The physical and genetic interactions between CTF4, CTF18, and core components of replication fork complexes observed in this study and others suggest that both gene products act in association with the replication fork to facilitate sister chromatid cohesion"
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{
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"text": "We find that absence of either CTF4 or CTF18 causes sister chromatid cohesion failure and leads to a preanaphase accumulation of cells that depends on the spindle assembly checkpoint"
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/23334284",
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"offsetInBeginSection": 663,
"offsetInEndSection": 831,
"text": "In addition to Eco1, several other factors contribute to cohesion establishment, including Ctf4, Ctf18, Tof1, Csm3, Chl1 and Mrc1, but little is known about their roles"
}
]
| 5 | BioASQ-training5b | [
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0007062",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0045876",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0007063"
]
| []
| 553cae13f32186855800000e | 263 |
yesno | Does the association of PARP1 and CTCF follow a circadian rhythm? | ['yes'] | [
"yes"
]
| ['Synchronization of the circadian rhythm by serum shock induces oscillations in PARP1-CTCF interactions, which is accompanied by oscillating recruitment of circadian loci to the lamina, followed by the acquisition of repressive H3K9me2 marks and transcriptional attenuation. Furthermore, depletion of H3K9me2/3, inhibition of PARP activity by olaparib, or downregulation of PARP1 or CTCF expression counteracts both recruitment to the envelope and circadian transcription. PARP1- and CTCF-regulated contacts between circadian loci and the repressive chromatin environment at the lamina therefore mediate circadian transcriptional plasticity.', 'Synchronization of the circadian rhythm by serum shock induces oscillations in PARP1-CTCF interactions, which is accompanied by oscillating recruitment of circadian loci to the lamina, followed by the acquisition of repressive H3K9me2 marks and transcriptional attenuation PARP1- and CTCF-regulated contacts between circadian loci and the repressive chromatin environment at the lamina therefore mediate circadian transcriptional plasticity.', 'Synchronization of the circadian rhythm by serum shock induces oscillations in PARP1-CTCF interactions, which is accompanied by oscillating recruitment of circadian loci to the lamina, followed by the acquisition of repressive H3K9me2 marks and transcriptional attenuation here we uncovered an inter-chromosomal network connecting active loci enriched in circadian genes to repressed lamina-associated domains . Parp1- and ctcf-regulated contacts between circadian loci to the lamina, followed by the acquisition of repressive h3k9me2 marks and transcriptional attenuation here we uncovered an inter-chromosomal network connecting active loci enriched in circadian genes to repressed lamina-associated domains . PARP1- and CTCF-regulated contacts between circadian loci and the repressive chromatin environment at the lamina therefore mediate circadian transcriptional plasticity. ', 'Synchronization of the circadian rhythm by serum shock induces oscillations in PARP1-CTCF interactions, which is accompanied by oscillating recruitment of circadian loci to the lamina, followed by the acquisition of repressive H3K9me2 marks and transcriptional attenuation. Uncovered an inter-chromosomal network connecting active loci enriched in circadian genes to repressed lamina-associated domains . PARP1- and CTCF-regulated contacts between circadian loci and the repressive chromatin environment at the lamina therefore mediate circadian transcriptional plasticity. ', 'Synchronization of the circadian rhythm by serum shock induces oscillations in PARP1-CTCF interactions, which is accompanied by oscillating recruitment of circadian loci to the lamina, followed by the acquisition of repressive H3K9me2 marks and transcriptional attenuation. here we uncovered an inter-chromosomal network connecting active loci enriched in circadian genes to repressed lamina-associated domains (LADs). PARP1- and CTCF-regulated contacts between circadian loci and the repressive chromatin environment at the lamina therefore mediate circadian transcriptional plasticity. ', 'yes', 'Synchronization of the circadian rhythm by serum shock induces oscillations in PARP1-CTCF interactions, which is accompanied by oscillating recruitment of circadian loci to the lamina, followed by the acquisition of repressive H3K9me2 marks and transcriptional attenuation. PARP1- and CTCF-regulated contacts between circadian loci and the repressive chromatin environment at the lamina therefore mediate circadian transcriptional plasticity. Here we uncovered an inter-chromosomal network connecting active loci enriched in circadian genes to repressed lamina-associated domains. ', 'Synchronization of the circadian rhythm by serum shock induces oscillations in PARP1-CTCF interactions, which is accompanied by oscillating recruitment of circadian loci to the lamina, followed by the acquisition of repressive H3K9me2 marks and transcriptional attenuation. PARP1- and CTCF-regulated contacts between circadian loci and the repressive chromatin environment at the lamina therefore mediate circadian transcriptional plasticity.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/26321255"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26321255",
"endSection": "abstract",
"offsetInBeginSection": 162,
"offsetInEndSection": 306,
"text": "here we uncovered an inter-chromosomal network connecting active loci enriched in circadian genes to repressed lamina-associated domains (LADs)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26321255",
"endSection": "abstract",
"offsetInBeginSection": 487,
"offsetInEndSection": 759,
"text": "Synchronization of the circadian rhythm by serum shock induces oscillations in PARP1-CTCF interactions, which is accompanied by oscillating recruitment of circadian loci to the lamina, followed by the acquisition of repressive H3K9me2 marks and transcriptional attenuation"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26321255",
"endSection": "abstract",
"offsetInBeginSection": 959,
"offsetInEndSection": 1127,
"text": "PARP1- and CTCF-regulated contacts between circadian loci and the repressive chromatin environment at the lamina therefore mediate circadian transcriptional plasticity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26321255",
"endSection": "abstract",
"offsetInBeginSection": 487,
"offsetInEndSection": 1127,
"text": "Synchronization of the circadian rhythm by serum shock induces oscillations in PARP1-CTCF interactions, which is accompanied by oscillating recruitment of circadian loci to the lamina, followed by the acquisition of repressive H3K9me2 marks and transcriptional attenuation. Furthermore, depletion of H3K9me2/3, inhibition of PARP activity by olaparib, or downregulation of PARP1 or CTCF expression counteracts both recruitment to the envelope and circadian transcription. PARP1- and CTCF-regulated contacts between circadian loci and the repressive chromatin environment at the lamina therefore mediate circadian transcriptional plasticity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26321255",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1112,
"text": "transcriptionally active and inactive chromatin domains tend to segregate into separate sub nuclear compartments to maintain stable expression patterns however here we uncovered an inter chromosomal network connecting active loci enriched in circadian genes to repressed lamina associated domains lads the interactome is regulated by parp1 and its co factor ctcf they not only mediate chromatin fiber interactions but also promote the recruitment of circadian genes to the lamina synchronization of the circadian rhythm by serum shock induces oscillations in parp1 ctcf interactions which is accompanied by oscillating recruitment of circadian loci to the lamina followed by the acquisition of repressive h3k9me2 marks and transcriptional attenuation furthermore depletion of h3k9me2 3 inhibition of parp activity by olaparib or downregulation of parp1 or ctcf expression counteracts both recruitment to the envelope and circadian transcription parp1 and ctcf regulated contacts between circadian loci and the repressive chromatin environment at the lamina therefore mediate circadian transcriptional plasticity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26321255",
"endSection": "abstract",
"offsetInBeginSection": 487,
"offsetInEndSection": 760,
"text": "Synchronization of the circadian rhythm by serum shock induces oscillations in PARP1-CTCF interactions, which is accompanied by oscillating recruitment of circadian loci to the lamina, followed by the acquisition of repressive H3K9me2 marks and transcriptional attenuation."
}
]
| 11 | BioASQ-training11b | [
"https://meshb.nlm.nih.gov/record/ui?ui=D002940",
"http://amigo.geneontology.org/amigo/term/GO:0007623",
"http://www.uniprot.org/uniprot/CTCF_MOUSE",
"http://www.uniprot.org/uniprot/CTCF_CHICK",
"https://meshb.nlm.nih.gov/record/ui?ui=D000067856",
"https://meshb.nlm.nih.gov/record/ui?ui=D011065",
"https://meshb.nlm.nih.gov/record/ui?ui=D011064",
"https://meshb.nlm.nih.gov/record/ui?ui=D000071137",
"https://meshb.nlm.nih.gov/record/ui?ui=D039103",
"http://amigo.geneontology.org/amigo/term/GO:0072572",
"https://meshb.nlm.nih.gov/record/ui?ui=D039102",
"https://meshb.nlm.nih.gov/record/ui?ui=D000075223",
"http://amigo.geneontology.org/amigo/term/GO:0042753",
"http://amigo.geneontology.org/amigo/term/GO:0042754",
"http://amigo.geneontology.org/amigo/term/GO:0048512",
"http://www.uniprot.org/uniprot/CTCF_RAT",
"https://meshb.nlm.nih.gov/record/ui?ui=D000075225",
"http://www.uniprot.org/uniprot/CTCF_HUMAN",
"http://amigo.geneontology.org/amigo/term/GO:0009649",
"https://meshb.nlm.nih.gov/record/ui?ui=D020178",
"https://meshb.nlm.nih.gov/record/ui?ui=D056925"
]
| null | 5a86e66dfaa1ab7d2e000035 | 264 |
yesno | Do Crocus sativus extracts loosen the blood-brain barrier? | ['no'] | [
"no"
]
| ['No, in vitro and in vivo experiments show that the Crocus sativus extract increases the tightness of a cell-based blood-brain barrier (BBB).'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/28471166"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28471166",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 115,
"text": "Crocus sativus Extract Tightens the Blood-Brain Barrier, Reduces Amyloid β Load and Related Toxicity in 5XFAD Mice."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28471166",
"endSection": "abstract",
"offsetInBeginSection": 523,
"offsetInEndSection": 1120,
"text": "In vitro results showed that Crocus sativus extract increases the tightness of a cell-based blood-brain barrier (BBB) model and enhances transport of Aβ. Further in vivo studies confirmed the effect of Crocus sativus extract (50 mg/kg/day, added to mice diet) on the BBB tightness and function that was associated with reduced Aβ load and related pathological changes in 5XFAD mice used as an AD model. Reduced Aβ load could be explained, at least in part, by Crocus sativus extract effect to enhance Aβ clearance pathways including BBB clearance, enzymatic degradation and ApoE clearance pathway."
}
]
| 11 | BioASQ-training11b | null | null | 5c891e5575a4a5d219000012 | 265 |
yesno | Could hypophosphatemic rickets cause craniosynostosis? | ['yes'] | [
"yes"
]
| ['Yes, hypophosphatemic rickets could cause craniosynostosis.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/26824597",
"http://www.ncbi.nlm.nih.gov/pubmed/22220162",
"http://www.ncbi.nlm.nih.gov/pubmed/26510652",
"http://www.ncbi.nlm.nih.gov/pubmed/23466123",
"http://www.ncbi.nlm.nih.gov/pubmed/23348263",
"http://www.ncbi.nlm.nih.gov/pubmed/19242361",
"http://www.ncbi.nlm.nih.gov/pubmed/27303470",
"http://www.ncbi.nlm.nih.gov/pubmed/6265607",
"http://www.ncbi.nlm.nih.gov/pubmed/25014884",
"http://www.ncbi.nlm.nih.gov/pubmed/17551721",
"http://www.ncbi.nlm.nih.gov/pubmed/9069051"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26824597",
"endSection": "abstract",
"offsetInBeginSection": 10,
"offsetInEndSection": 177,
"text": "This study examines a series of patients with hypophosphatemic rickets and craniosynostosis to characterize the clinical course and associated craniofacial anomalies. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26824597",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 73,
"text": "Hypophosphatemic rickets and craniosynostosis: a multicenter case series."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26824597",
"endSection": "abstract",
"offsetInBeginSection": 185,
"offsetInEndSection": 330,
"text": "A 20-year retrospective review identified patients with hypophosphatemic rickets and secondary craniosynostosis at 3 major craniofacial centers. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26824597",
"endSection": "abstract",
"offsetInBeginSection": 1244,
"offsetInEndSection": 1549,
"text": "Secondary craniosynostosis develops postnatally due to metabolic or mechanical factors. The most common metabolic cause is hypophosphatemic rickets, which has a variety of etiologies. Head shape changes occur later and with a more heterogeneous presentation compared with that of primary craniosynostosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23348263",
"endSection": "abstract",
"offsetInBeginSection": 1513,
"offsetInEndSection": 1651,
"text": "Patients with multisutural involvement or X-linked hypophosphatemic rickets had a significant delay in presentation for craniosynostosis. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23466123",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 466,
"text": "Craniosynostosis can be gene-linked, or caused by metabolic diseases, such as rickets, which results from a deficiency or impaired metabolism of vitamin D, magnesium, phosphorus or calcium leading to hypomineralization of the bone. X-linked dominant hypophosphatemic rickets (XLHR) is the most prevalent genetic type of hypophosphatemic rickets and is caused by germ line mutations in the PHEX-gene. In XLHR, only few case reports of craniosynostosis were described."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22220162",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "Papilledema in the setting of x-linked hypophosphatemic rickets with craniosynostosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22220162",
"endSection": "abstract",
"offsetInBeginSection": 165,
"offsetInEndSection": 277,
"text": "Case report of a 3-year-old female presenting with papilledema resulting from craniosynostosis secondary to XLH."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19242361",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 55,
"text": "X-linked hypophosphatemic rickets and craniosynostosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19242361",
"endSection": "abstract",
"offsetInBeginSection": 333,
"offsetInEndSection": 599,
"text": "X-linked hypophosphatemic (XLH) rickets is the most common form of metabolic rickets, and there have been reports linking XLH rickets to craniosynostosis. A clinical report of a patient with XLH rickets and craniosynostosis is presented with a review of literature. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19242361",
"endSection": "abstract",
"offsetInBeginSection": 758,
"offsetInEndSection": 845,
"text": "This may be the reason for the common association of craniosynostosis and XLH rickets. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6265607",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 287,
"text": "Craniosynostosis and associated craniofacial deformities, such as frontal bossing, often occur as symptoms of vitamin D-resistant rickets in children. Similar skull deformities develop in mice with X-linked dominant hypophosphatemia, the most common form of vitamin D-resistant rickets. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6265607",
"endSection": "abstract",
"offsetInBeginSection": 914,
"offsetInEndSection": 1191,
"text": "The x-linked hypophosphatemic mouse is an animal model that can be used to study the role of vitamin D-resistant rickets in the development of craniosynostosis, to relate craniosynostosis to the development of associated skull deformities, and to test new treatment procedures."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27303470",
"endSection": "abstract",
"offsetInBeginSection": 449,
"offsetInEndSection": 627,
"text": "Craniosynostosis secondary to rickets is rarely reported, but since neither rickets nor craniosynostosis is a reportable disease, the exact incidence of both diseases is unknown."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19242361",
"endSection": "abstract",
"offsetInBeginSection": 331,
"offsetInEndSection": 485,
"text": "X-linked hypophosphatemic (XLH) rickets is the most common form of metabolic rickets, and there have been reports linking XLH rickets to craniosynostosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19242361",
"endSection": "abstract",
"offsetInBeginSection": 485,
"offsetInEndSection": 595,
"text": "A clinical report of a patient with XLH rickets and craniosynostosis is presented with a review of literature."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26824597",
"endSection": "abstract",
"offsetInBeginSection": 176,
"offsetInEndSection": 328,
"text": "METHODS A 20-year retrospective review identified patients with hypophosphatemic rickets and secondary craniosynostosis at 3 major craniofacial centers."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23466123",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "Bilateral coronal and sagittal synostosis in X-linked hypophosphatemic rickets: a case report."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26510652",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "X-linked hypophosphatemic rickets and sagittal craniosynostosis: three patients requiring operative cranial expansion: case series and literature review"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19242361",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 54,
"text": "X-linked hypophosphatemic rickets and craniosynostosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19242361",
"endSection": "abstract",
"offsetInBeginSection": 333,
"offsetInEndSection": 486,
"text": "X-linked hypophosphatemic (XLH) rickets is the most common form of metabolic rickets, and there have been reports linking XLH rickets to craniosynostosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17551721",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 582,
"text": "The recent observations of two new cases of X-linked hypophosphatemic rickets associated with premature closure of the sagittal suture prompted a review of similar cases seen in this institution.To review the clinical records and skull radiographs of 28 children with hypophosphatemic rickets in order to investigate the frequency and type of craniosynostosis and other cranial vault changes seen in these conditions and to review the literature for relevant findings.Clinical and imaging records were reviewed on 28 patients with hypophosphatemic rickets, all younger than 18 years"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23348263",
"endSection": "abstract",
"offsetInBeginSection": 1344,
"offsetInEndSection": 1606,
"text": "Those with multisutural synostosis presented at a significantly older age than patients with sagittal or bicoronal synostosis.Patients with multisutural involvement or X-linked hypophosphatemic rickets had a significant delay in presentation for craniosynostosis"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22220162",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "Papilledema in the setting of x-linked hypophosphatemic rickets with craniosynostosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22220162",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 510,
"text": "INTRODUCTION TO THE OPHTHALMIC LITERATURE OF AN UNUSUAL CAUSE OF PAPILLEDEMA AND SUBSEQUENT OPTIC ATROPHY: X-linked hypophosphatemic rickets (XLH).Case report of a 3-year-old female presenting with papilledema resulting from craniosynostosis secondary to XLH.Early intervention with craniofacial surgery prevented the development of optic atrophy.Children with XLH should be screened for ophthalmic evidence of elevated intracranial pressure to aid early intervention and prevention of permanent loss of vision"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23348263",
"endSection": "abstract",
"offsetInBeginSection": 1503,
"offsetInEndSection": 1654,
"text": "CONCLUSIONS: Patients with multisutural involvement or X-linked hypophosphatemic rickets had a significant delay in presentation for craniosynostosis. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23466123",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 232,
"text": "Craniosynostosis can be gene-linked, or caused by metabolic diseases, such as rickets, which results from a deficiency or impaired metabolism of vitamin D, magnesium, phosphorus or calcium leading to hypomineralization of the bone. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6265607",
"endSection": "abstract",
"offsetInBeginSection": 151,
"offsetInEndSection": 286,
"text": "Similar skull deformities develop in mice with X-linked dominant hypophosphatemia, the most common form of vitamin D-resistant rickets."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6265607",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 48,
"text": "Craniosynostosis in vitamin D-resistant rickets."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23466123",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 231,
"text": "Craniosynostosis can be gene-linked, or caused by metabolic diseases, such as rickets, which results from a deficiency or impaired metabolism of vitamin D, magnesium, phosphorus or calcium leading to hypomineralization of the bone."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19242361",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 56,
"text": "X-linked hypophosphatemic rickets and craniosynostosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19242361",
"endSection": "abstract",
"offsetInBeginSection": 333,
"offsetInEndSection": 487,
"text": "X-linked hypophosphatemic (XLH) rickets is the most common form of metabolic rickets, and there have been reports linking XLH rickets to craniosynostosis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26824597",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 74,
"text": "Hypophosphatemic rickets and craniosynostosis: a multicenter case series."
}
]
| 6 | BioASQ-training6b | [
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D005624",
"http://www.disease-ontology.org/api/metadata/DOID:2340",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D012279",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D053098",
"http://www.disease-ontology.org/api/metadata/DOID:0050445",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D010294",
"http://www.disease-ontology.org/api/metadata/DOID:0050948",
"http://www.disease-ontology.org/api/metadata/DOID:0050949",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003398",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D063730",
"http://www.disease-ontology.org/api/metadata/DOID:10609"
]
| null | 58b9585c22d3005309000010 | 266 |
yesno | Do very elderly stage III colorectal cancer patients present clinical benefit from oxaliplatin-based adjuvant chemotherapy? | ['yes'] | [
"yes"
]
| ['Yes, adjuvant FOLFOX4 maintains its efficacy and safety ratio in selected elderly patients with colorectal cancer', 'Studies suggest that very elderly (≥70 or ≥75 years) patients with Stage III colon cancer can benefit from oxaliplatin-based adjuvant chemotherapy, despite increased toxicity and early treatment cessation. A study in Asia found similar efficacy without significant increase in toxicity in older patients (≥65) compared to younger patients. Another study in Australia demonstrated a persistent survival benefit for the addition of oxaliplatin to fluoropyrimidine as adjuvant treatment for Stage III colon cancer in elderly patients, although with increased hospital admissions and early chemotherapy cessation. A population-based cohort study in Ontario, Canada found that patients aged ≥70 years had a higher risk of developing peripheral neuropathy with oxaliplatin-based regimens. Finally, an analysis of four data sets in the US found that adjuvant chemotherapy was associated with a survival benefit for patients ≥75 years with Stage III colon cancer, although the incremental benefit of oxaliplatin over non-oxaliplatin-containing regimens was inconsistent.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/26487941",
"http://www.ncbi.nlm.nih.gov/pubmed/28341242",
"http://www.ncbi.nlm.nih.gov/pubmed/24071534",
"http://www.ncbi.nlm.nih.gov/pubmed/26382962",
"http://www.ncbi.nlm.nih.gov/pubmed/36115817",
"http://www.ncbi.nlm.nih.gov/pubmed/19729318",
"http://www.ncbi.nlm.nih.gov/pubmed/28434884",
"http://www.ncbi.nlm.nih.gov/pubmed/37881011",
"http://www.ncbi.nlm.nih.gov/pubmed/36252550",
"http://www.ncbi.nlm.nih.gov/pubmed/35303773",
"http://www.ncbi.nlm.nih.gov/pubmed/31906959",
"http://www.ncbi.nlm.nih.gov/pubmed/32823998",
"http://www.ncbi.nlm.nih.gov/pubmed/29698932",
"http://www.ncbi.nlm.nih.gov/pubmed/25731317",
"http://www.ncbi.nlm.nih.gov/pubmed/19563521",
"http://www.ncbi.nlm.nih.gov/pubmed/34230158",
"http://www.ncbi.nlm.nih.gov/pubmed/37498507",
"http://www.ncbi.nlm.nih.gov/pubmed/25986478",
"http://www.ncbi.nlm.nih.gov/pubmed/22665536",
"http://www.ncbi.nlm.nih.gov/pubmed/33744715",
"http://www.ncbi.nlm.nih.gov/pubmed/29584752",
"http://www.ncbi.nlm.nih.gov/pubmed/35146948",
"http://www.ncbi.nlm.nih.gov/pubmed/20967408",
"http://www.ncbi.nlm.nih.gov/pubmed/37748112",
"http://www.ncbi.nlm.nih.gov/pubmed/21810511",
"http://www.ncbi.nlm.nih.gov/pubmed/29861156",
"http://www.ncbi.nlm.nih.gov/pubmed/25595934",
"http://www.ncbi.nlm.nih.gov/pubmed/22915656",
"http://www.ncbi.nlm.nih.gov/pubmed/16943526",
"http://www.ncbi.nlm.nih.gov/pubmed/36229957",
"http://www.ncbi.nlm.nih.gov/pubmed/18621635",
"http://www.ncbi.nlm.nih.gov/pubmed/23733765",
"http://www.ncbi.nlm.nih.gov/pubmed/23204187",
"http://www.ncbi.nlm.nih.gov/pubmed/19942166",
"http://www.ncbi.nlm.nih.gov/pubmed/19111473",
"http://www.ncbi.nlm.nih.gov/pubmed/21831168",
"http://www.ncbi.nlm.nih.gov/pubmed/23512326",
"http://www.ncbi.nlm.nih.gov/pubmed/25954089",
"http://www.ncbi.nlm.nih.gov/pubmed/29873684"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37498507",
"endSection": "abstract",
"offsetInBeginSection": 807,
"offsetInEndSection": 1083,
"text": "elderly patients with localized CRC should undergo standard cancer resection, preferably laparoscopically. The indication for adjuvant chemotherapy (CT) should be considered based on the potential benefit, the risk of recurrence, the life expectancy and patient comorbidities."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16943526",
"endSection": "abstract",
"offsetInBeginSection": 1476,
"offsetInEndSection": 1575,
"text": "FOLFOX4 maintains its efficacy and safety ratio in selected elderly patients with colorectal cancer"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24071534",
"endSection": "abstract",
"offsetInBeginSection": 1590,
"offsetInEndSection": 1695,
"text": "Older patients deemed eligible for chemotherapy did not experience significant changes in living situatio"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28434884",
"endSection": "abstract",
"offsetInBeginSection": 173,
"offsetInEndSection": 654,
"text": " The incidence and severity of toxicity might be greater among older patients who might also derive less benefit from oxaliplatin. We evaluated the association between adjuvant oxaliplatin-based chemotherapy and neurotoxicity outcomes in an elderly cohort of patients.PATIENTS AND METHODS: A population-based cohort of patients aged > 65 years with stage II and III colorectal cancer treated with adjuvant therapy in Ontario, Canada was identified using the Ontario Cancer Registry"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28434884",
"endSection": "abstract",
"offsetInBeginSection": 303,
"offsetInEndSection": 654,
"text": " We evaluated the association between adjuvant oxaliplatin-based chemotherapy and neurotoxicity outcomes in an elderly cohort of patients.PATIENTS AND METHODS: A population-based cohort of patients aged > 65 years with stage II and III colorectal cancer treated with adjuvant therapy in Ontario, Canada was identified using the Ontario Cancer Registry"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28434884",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 440,
"text": "BACKGROUND: The addition of oxaliplatin to adjuvant treatment regimens for colorectal cancer has been shown to improve overall survival at the expense of increased toxicity. The incidence and severity of toxicity might be greater among older patients who might also derive less benefit from oxaliplatin. We evaluated the association between adjuvant oxaliplatin-based chemotherapy and neurotoxicity outcomes in an elderly cohort of patients"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25731317",
"endSection": "abstract",
"offsetInBeginSection": 1383,
"offsetInEndSection": 1621,
"text": "The Oxa-based adjuvant chemotherapy was tolerated equally well in Stage II and III colorectal cancer patients with or without perforation. Further studies are needed to compare the effect of oxaliplatin with other adjuvant chemotherapies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29861156",
"endSection": "abstract",
"offsetInBeginSection": 170,
"offsetInEndSection": 339,
"text": " We aimed to clarify the efficacy and complications of adjuvant oxaliplatin and fluoropyrimidine chemotherapy for patients 70 years and older with stage III colon cancer"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29861156",
"endSection": "abstract",
"offsetInBeginSection": 170,
"offsetInEndSection": 473,
"text": " We aimed to clarify the efficacy and complications of adjuvant oxaliplatin and fluoropyrimidine chemotherapy for patients 70 years and older with stage III colon cancer.PATIENTS AND METHODS: All patients with stage III colon adenocarcinoma were identified from an Australian cancer registry (2006-2013)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29861156",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 339,
"text": "BACKGROUND: Colon cancer is common in the elderly, but owing to under representation in clinical trials, the benefit of standard therapies is uncertain in this age group. We aimed to clarify the efficacy and complications of adjuvant oxaliplatin and fluoropyrimidine chemotherapy for patients 70 years and older with stage III colon cancer"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37748112",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 215,
"text": "PURPOSE: While adjuvant therapy with capecitabine and oxaliplatin (CAPOX) has been proven to be effective in stage III colon cancer, capecitabine monotherapy (CapMono) might be equally effective in elderly patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36252550",
"endSection": "abstract",
"offsetInBeginSection": 1199,
"offsetInEndSection": 1370,
"text": "CSS and RFS were also similar between the ≥70 and <70 years old patients with stage III CRC.CONCLUSIONS: Adjuvant CAPOX therapy was tolerable in elderly Japanese patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28434884",
"endSection": "abstract",
"offsetInBeginSection": 1426,
"offsetInEndSection": 1802,
"text": "Formal interaction testing confirmed that the effect of oxaliplatin on neuropathy was more pronounced in patients aged ≥ 70 years compared with patients aged 66 to 69 years (P = .03).CONCLUSION: Colorectal cancer patients aged ≥ 70 years at the time of cancer diagnosis who are subsequently treated with oxaliplatin have a significant risk of developing peripheral neuropathy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35146948",
"endSection": "abstract",
"offsetInBeginSection": 1115,
"offsetInEndSection": 1375,
"text": "No significant difference in the effect of ACT could be observed between age groups (interaction: cancer-specific death HR = 1.7948, p = 0.1079; death of other cause HR = 0.7384, p = 0.6705).CONCLUSION: ACT was an independent positive prognostic factor for OS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29861156",
"endSection": "abstract",
"offsetInBeginSection": 1084,
"offsetInEndSection": 1590,
"text": "uire hospital admission (67.0% vs. 53.5%). The addition of oxaliplatin provided an overall survival benefit for patients < 70 years (hazard ratio, 0.44; 95% confidence interval, 0.3-0.6; P < .0001) and for patients ≥ 70 years (hazard ratio, 0.64; 95% confidence interval, 0.5-0.9; P = .005).CONCLUSIONS: Despite a modestly increased rate of hospital admission and early chemotherapy cessation, we demonstrate a persistent survival benefit for the addition of oxaliplatin to a fluoropyrimidine as adjuvant t"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29873684",
"endSection": "abstract",
"offsetInBeginSection": 292,
"offsetInEndSection": 392,
"text": "tal cancer. The use of oxaliplatin as adjuvant treatment in elderly patients with colon cancer is co"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21810511",
"endSection": "abstract",
"offsetInBeginSection": 354,
"offsetInEndSection": 466,
"text": "A critical issue, which needs to be specifically addressed, is the role of adjuvant therapy in elderly patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23204187",
"endSection": "abstract",
"offsetInBeginSection": 1281,
"offsetInEndSection": 1524,
"text": ".75 versus 0.80, P = 0.009).CONCLUSIONS: Adjuvant oxaliplatin, fluorouracil and leucovorin chemotherapy resulted in similar efficacy without significant increase in toxicity in older patients aged ≥65 when compared with younger patients with c"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29861156",
"endSection": "abstract",
"offsetInBeginSection": 1127,
"offsetInEndSection": 1646,
"text": "The addition of oxaliplatin provided an overall survival benefit for patients < 70 years (hazard ratio, 0.44; 95% confidence interval, 0.3-0.6; P < .0001) and for patients ≥ 70 years (hazard ratio, 0.64; 95% confidence interval, 0.5-0.9; P = .005).CONCLUSIONS: Despite a modestly increased rate of hospital admission and early chemotherapy cessation, we demonstrate a persistent survival benefit for the addition of oxaliplatin to a fluoropyrimidine as adjuvant treatment for stage III colon cancer in elderly patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23733765",
"endSection": "abstract",
"offsetInBeginSection": 1201,
"offsetInEndSection": 1637,
"text": "No significant interactions by age were detected with oral fluoropyrimidine therapy compared with IV FU; noninferiority was supported in both age populations.CONCLUSION: Patients age ≥ 70 years seemed to experience reduced benefit from adding oxaliplatin to fluoropyrimidines in the adjuvant setting, although statistically, there was not a significant effect modification by age, whereas oral fluoropyrimidines retained their efficacy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22665536",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 393,
"text": "PURPOSE: Few patients 75 years of age and older participate in clinical trials, thus whether adjuvant chemotherapy for stage III colon cancer (CC) benefits this group is unknown.METHODS: A total of 5,489 patients ≥ 75 years of age with resected stage III CC, diagnosed between 2004 and 2007, were selected from four data sets containing demographic, stage, treatment, and survival information."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23204187",
"endSection": "abstract",
"offsetInBeginSection": 1168,
"offsetInEndSection": 1566,
"text": "Elderly patients received a lower relative dose intensity of oxaliplatin (0.76 versus 0.79) and 5-fluorouracil (0.75 versus 0.80, P = 0.009).CONCLUSIONS: Adjuvant oxaliplatin, fluorouracil and leucovorin chemotherapy resulted in similar efficacy without significant increase in toxicity in older patients aged ≥65 when compared with younger patients with curatively resected Stage III colon cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22665536",
"endSection": "abstract",
"offsetInBeginSection": 971,
"offsetInEndSection": 1166,
"text": "Chemotherapy receipt was associated with a survival benefit of comparable magnitude to clinical trials results (SEER-Medicare PS-matched mortality, hazard ratio [HR], 0.60; 95% CI, 0.53 to 0.68)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29873684",
"endSection": "abstract",
"offsetInBeginSection": 1617,
"offsetInEndSection": 1898,
"text": "The STEPP analysis revealed improved hazard ratios for DFS in patients aged 40-70 years compared with elderly patients treated with oxaliplatin.Conclusion: The addition of oxaliplatin significantly improved DFS and OS in younger patients aged <60 years with advanced rectal cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22665536",
"endSection": "abstract",
"offsetInBeginSection": 1167,
"offsetInEndSection": 1437,
"text": "The incremental benefit of oxaliplatin over non-oxaliplatin-containing regimens was also of similar magnitude to clinical trial results (SEER-Medicare, HR, 0.84; 95% CI, 0.69 to 1.04; NYSCR-Medicare, HR, 0.82, 95% CI, 0.51 to 1.33) in two of three examined data sources."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37748112",
"endSection": "abstract",
"offsetInBeginSection": 9,
"offsetInEndSection": 214,
"text": "While adjuvant therapy with capecitabine and oxaliplatin (CAPOX) has been proven to be effective in stage III colon cancer, capecitabine monotherapy (CapMono) might be equally effective in elderly patients"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20967408",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 176,
"text": "Adjuvant chemotherapy for resected stage III colon cancer is indicated for all patients, including elderly patients >70 years. In general, adjuvant oxaliplatin-fluoropyrimidine"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18621635",
"endSection": "abstract",
"offsetInBeginSection": 207,
"offsetInEndSection": 1084,
"text": "is often incurable. Despite the progress achieved with the introduction of new cytotoxic agents, recurrence rates for patients with resected stage II/III disease remain > 20%. Therefore, a great deal of effort and resources have been put into improving early diagnosis and prevention tools as well as the efficacy of adjuvant treatment. Oxaliplatin-based chemotherapy is now considered the standard of care in node-positive colon cancer, but there remains controversy with regard to the indication and type of adjuvant treatment in patients with nodenegative disease. Oral fluoropyrimidines play a growing role in the management of colorectal cancer and can be currently considered an alternative to 5-fluorouracil. Numerous reports have suggested that elderly patients benefit equally from chemotherapy, but the growing numbers of octogenarian and nonagenarian patients in our"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23204187",
"endSection": "abstract",
"offsetInBeginSection": 662,
"offsetInEndSection": 812,
"text": "otherapy (87 (43.5%) ≥65 years old versus 142 (74.3%) <65 years old). Older patients had similar clinico-pathological characteristics as younger patie"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25986478",
"endSection": "abstract",
"offsetInBeginSection": 345,
"offsetInEndSection": 552,
"text": "Studies showed that combination of oxaliplatin and capecitabine demonstrated efficacy and safety on par with treatment involving various 5-FU/LV-based regimens in elderly patients as they are in younger ones"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28341242",
"endSection": "abstract",
"offsetInBeginSection": 979,
"offsetInEndSection": 1188,
"text": "Patients younger than 70 years of age may derive greater disease-free survival and overall survival benefit from adjuvant chemotherapy (in combination with oxaliplatin) compared with those older than 70 years."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33744715",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 187,
"text": "BACKGROUND: Previous studies on oxaliplatin and fluoropyrimidines as adjuvant therapy in older patients with stage III colon cancer (CC) produced conflicting results.PATIENTS AND METHODS:"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29861156",
"endSection": "abstract",
"offsetInBeginSection": 73,
"offsetInEndSection": 393,
"text": "resentation in clinical trials, the benefit of standard therapies is uncertain in this age group. We aimed to clarify the efficacy and complications of adjuvant oxaliplatin and fluoropyrimidine chemotherapy for patients 70 years and older with stage III colon cancer.PATIENTS AND METHODS: All patients with stage III col"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29584752",
"endSection": "abstract",
"offsetInBeginSection": 59,
"offsetInEndSection": 250,
"text": "th the use of adjuvant chemotherapy and the use of oxaliplatin after curative resection in stage III colon cancer patients and assesses the effect of their use in three-year survival.METHODS:"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23204187",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 730,
"text": "OBJECTIVE: Elderly patients derive similar benefits from 5-fluorouracil-based adjuvant chemotherapy in Stage III colon cancer; however, conflicting data exist regarding additional benefit from oxaliplatin, fluorouracil and leucovorin (FOLFOX) chemotherapy.METHODS: Single-center, retrospective analysis was performed to compare the safety and efficacy of adjuvant oxaliplatin, fluorouracil and leucovorin-4 chemotherapy in older patients (age ≥65 years) with younger patients with Stage III colon cancer after surgical resection.RESULTS: Among 391 patients with Stage III colon cancer, 229 patients received adjuvant oxaliplatin, fluorouracil and leucovorin chemotherapy (87 (43.5%) ≥65 years old versus 142 (74.3%) <65 years old)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29861156",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 473,
"text": "BACKGROUND: Colon cancer is common in the elderly, but owing to under representation in clinical trials, the benefit of standard therapies is uncertain in this age group. We aimed to clarify the efficacy and complications of adjuvant oxaliplatin and fluoropyrimidine chemotherapy for patients 70 years and older with stage III colon cancer.PATIENTS AND METHODS: All patients with stage III colon adenocarcinoma were identified from an Australian cancer registry (2006-2013)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23204187",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 528,
"text": "OBJECTIVE: Elderly patients derive similar benefits from 5-fluorouracil-based adjuvant chemotherapy in Stage III colon cancer; however, conflicting data exist regarding additional benefit from oxaliplatin, fluorouracil and leucovorin (FOLFOX) chemotherapy.METHODS: Single-center, retrospective analysis was performed to compare the safety and efficacy of adjuvant oxaliplatin, fluorouracil and leucovorin-4 chemotherapy in older patients (age ≥65 years) with younger patients with Stage III colon cancer after surgical resection"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23204187",
"endSection": "abstract",
"offsetInBeginSection": 1315,
"offsetInEndSection": 1571,
"text": "SIONS: Adjuvant oxaliplatin, fluorouracil and leucovorin chemotherapy resulted in similar efficacy without significant increase in toxicity in older patients aged ≥65 when compared with younger patients with curatively resected Stage III colon cancer. Ther"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23204187",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 255,
"text": "OBJECTIVE: Elderly patients derive similar benefits from 5-fluorouracil-based adjuvant chemotherapy in Stage III colon cancer; however, conflicting data exist regarding additional benefit from oxaliplatin, fluorouracil and leucovorin (FOLFOX) chemotherapy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23204187",
"endSection": "abstract",
"offsetInBeginSection": 258,
"offsetInEndSection": 732,
"text": "THODS: Single-center, retrospective analysis was performed to compare the safety and efficacy of adjuvant oxaliplatin, fluorouracil and leucovorin-4 chemotherapy in older patients (age ≥65 years) with younger patients with Stage III colon cancer after surgical resection.RESULTS: Among 391 patients with Stage III colon cancer, 229 patients received adjuvant oxaliplatin, fluorouracil and leucovorin chemotherapy (87 (43.5%) ≥65 years old versus 142 (74.3%) <65 years old). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31906959",
"endSection": "abstract",
"offsetInBeginSection": 1537,
"offsetInEndSection": 1683,
"text": " 1.07 (0.66-1.74, P = 0.78) in older patients.CONCLUSIONS: The clinical effectiveness of adjuvant chemotherapy in older patients with stage III co"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36252550",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 285,
"text": "INTRODUCTION: Adjuvant chemotherapy improves the prognosis of patients with colorectal cancer (CRC) following radical resection. However, the safety and efficacy of oxaliplatin-based chemotherapeutic regimens for elderly patients remains to be elucidated. The aim of the present study "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32823998",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1328,
"text": "The value of adjuvant chemotherapy in elderly patients has been the subject of many overviews, with opinions varying from \"not effective\", since randomized trials have not been performed, to \"as effective as in young individuals\", based upon many retrospective analyses of randomized trials that have included patients of all ages. In the absence of randomized trials performed specifically with elderly patients, retrospective analyses demonstrate that the influence on the time to tumour recurrence (TTR) may be the same as in young individuals, but that endpoints that include death for any reason, such as recurrence-free survival (RFS), disease-free survival (DFS), and overall survival (OS), are poorer in the elderly. This is particularly true if oxaliplatin has been part of the treatment. The need for adjuvant chemotherapy after colorectal cancer surgery in elderly patients is basically the same as that in younger patients. The reduction in recurrence risks may be similar, provided the chosen treatment is tolerated but survival gains are less. Adding oxaliplatin to a fluoropyrimidine is probably not beneficial in individuals above a biological age of approximately 70 years. If an oxaliplatin combination is administered to elderly patients, three months of therapy is in all probability the most realistic goal."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37881011",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 787,
"text": "Adjuvant chemotherapy improves the prognosis of patients with colorectal cancer (CRC) following radical resection. The aim of the present study is to review appropriate chemotherapeutic regimens for elderly patients. We examined 1138 Japanese patients who were operated for high-risk stage II or stage III CRC between July 2010 and June 2021 at our hospital. Patients were divided according to an age of 70 years. The efficacy of adjuvant therapy was analyzed in association with age and adjuvant chemotherapeutic regimens. A total of 507 patients (45%) were ≥70 years old. They were less likely to receive adjuvant chemotherapy (p < 0.001) or palliative chemotherapy after recurrence (p < 0.001) than patients aged <70 years. Cancer-specific survival (CSS) in stage III CRC patients was"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26382962",
"endSection": "abstract",
"offsetInBeginSection": 2284,
"offsetInEndSection": 2461,
"text": "ortant role for stage III colon cancer. Our findings suggested that benefit of oxaliplatin-contained therapy is limited to patients aged under 70 and oral fluoropyrimidines may "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26382962",
"endSection": "abstract",
"offsetInBeginSection": 1850,
"offsetInEndSection": 2072,
"text": "h statistical significance. In contrast to the survival benefits of above therapeutic settings for the patients aged under 70, there was less advantage in the old patients when they received intensive therapies or even oxa"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22665536",
"endSection": "abstract",
"offsetInBeginSection": 1567,
"offsetInEndSection": 1776,
"text": "ributable to confounding.CONCLUSION: The noninvestigational experience suggests patients with stage III CC ≥ 75 years of age may anticipate a survival benefit from adjuvant chemotherapy. Oxaliplatin offers no "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23204187",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 731,
"text": "OBJECTIVE: Elderly patients derive similar benefits from 5-fluorouracil-based adjuvant chemotherapy in Stage III colon cancer; however, conflicting data exist regarding additional benefit from oxaliplatin, fluorouracil and leucovorin (FOLFOX) chemotherapy.METHODS: Single-center, retrospective analysis was performed to compare the safety and efficacy of adjuvant oxaliplatin, fluorouracil and leucovorin-4 chemotherapy in older patients (age ≥65 years) with younger patients with Stage III colon cancer after surgical resection.RESULTS: Among 391 patients with Stage III colon cancer, 229 patients received adjuvant oxaliplatin, fluorouracil and leucovorin chemotherapy (87 (43.5%) ≥65 years old versus 142 (74.3%) <65 years old)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36115817",
"endSection": "abstract",
"offsetInBeginSection": 66,
"offsetInEndSection": 555,
"text": "Oxaliplatin-based adjuvant chemotherapy improved disease-free survival after stage III colon cancer resection, but this improvement was not demonstrated in older patients.METHODS: The purpose of ADAGE-PRODIGE 34, randomized open phase III trial is to compare in patients over 70 years oxaliplatin plus fluoropyrimidine with fluoropyrimidine alone in fit patients (Group 1) and fluoropyrimidine with observation in frail patients (Group 2) after resection of stage III colon adenocarcinoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22665536",
"endSection": "abstract",
"offsetInBeginSection": 1464,
"offsetInEndSection": 1776,
"text": "ficance was inconsistent. The beneficial effect of chemotherapy and oxaliplatin did not seem solely attributable to confounding.CONCLUSION: The noninvestigational experience suggests patients with stage III CC ≥ 75 years of age may anticipate a survival benefit from adjuvant chemotherapy. Oxaliplatin offers no "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29698932",
"endSection": "abstract",
"offsetInBeginSection": 1238,
"offsetInEndSection": 1455,
"text": "I 0.78-0.83), respectively. The only subpopulations that did not benefit from doublet chemotherapy were low-risk patients older than 72 years (HR = 0.95, 95% CI 0.90-1.01) and high-risk patients older than 85 years (H"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28341242",
"endSection": "abstract",
"offsetInBeginSection": 483,
"offsetInEndSection": 766,
"text": "Patients with completely resected stage III colon cancer have an overall survival benefit from adjuvant chemotherapy. Combination chemotherapy (5-fluorouracil/leucovorin/oxaliplatin or capecitabine/oxaliplatin) provides a larger benefit than monotherapy but with additional toxicity."
}
]
| 13 | BioASQ-training13b | null | null | 65f7754ec4010b4d7800002b | 267 |
yesno | Is Kummell’s disease an avascular necrosis of the vertebral body? | ['yes'] | [
"yes"
]
| ['Yes, Kummell’s disease is an avascular necrosis of the vertebral body.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22220246",
"http://www.ncbi.nlm.nih.gov/pubmed/19534241",
"http://www.ncbi.nlm.nih.gov/pubmed/23814399",
"http://www.ncbi.nlm.nih.gov/pubmed/19124637",
"http://www.ncbi.nlm.nih.gov/pubmed/28913640",
"http://www.ncbi.nlm.nih.gov/pubmed/19321060",
"http://www.ncbi.nlm.nih.gov/pubmed/21811863",
"http://www.ncbi.nlm.nih.gov/pubmed/11915453",
"http://www.ncbi.nlm.nih.gov/pubmed/19949820",
"http://www.ncbi.nlm.nih.gov/pubmed/28160398"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28913640",
"endSection": "abstract",
"offsetInBeginSection": 13,
"offsetInEndSection": 326,
"text": " Kummell's disease is an avascular necrosis of the vertebral body, secondary to a vertebral compression fracture. This entity is characterised by the gradual development in time of a vertebral body collapse following a trivial spinal trauma, involving a worsening back pain associated with a progressive kyphosis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11915453",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 150,
"text": "Kummell's disease is a rare spinal disorder characterized as avascular necrosis of a vertebral body occurring in a delayed fashion after minor trauma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22220246",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 132,
"text": "Kummell's disease is a spinal disorder characterized by delayed post-traumatic collapse of a vertebral body with avascular necrosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23814399",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 265,
"text": "Kummell disease, or avascular necrosis of a vertebral body, presents as vertebral osteonecrosis typically affecting a thoracic vertebra with compression deformity, intravertebral vacuum cleft, and exaggerated kyphosis weeks to months after a minor traumatic injury."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28913640",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "INTRODUCTION Kummell's disease is an avascular necrosis of the vertebral body, secondary to a vertebral compression fracture."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19124637",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 113,
"text": "Kummel disease is the eponym for avascular necrosis of the vertebral body after a vertebral compression fracture."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19949820",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 77,
"text": "kummell s disease delayed post traumatic osteonecrosis of the vertebral body"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28160398",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "Kummell's disease, caused by osteonecrosis of the vertebral body, is a cause of vertebral collapse."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19534241",
"endSection": "abstract",
"offsetInBeginSection": 91,
"offsetInEndSection": 152,
"text": "Kummell's disease is a post-traumatic vertebral body collapse"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21811863",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 168,
"text": "Kummell's disease is a rare, delayed posttraumatic collapse of a vertebral body that can occur several months or even years after an osteoporotic compression fracture. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19321060",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 236,
"text": "Avascular necrosis of a vertebral body, a relatively uncommon entity, is caused by malignancy, infection, radiation, systemic steroid treatment, trauma, and the like.1 Vertebral osteonecrosis induced by trauma is called Kvmell's disease"
}
]
| 11 | BioASQ-training11b | [
"https://meshb.nlm.nih.gov/record/ui?ui=D010020",
"http://www.disease-ontology.org/api/metadata/DOID:6603"
]
| null | 5a787544faa1ab7d2e00000b | 268 |
yesno | Is there an association of alterations in ADCY7 and ulcerative colitis? | ['yes'] | [
"yes"
]
| ['Yes. Genome-wide analyses indicate a association between mutations in ACVR1 and ulcerative colitis due to loss-of-function mutations in ADCY7.', 'Yes. Sequencing analysis showed an association between mutations in ADCY7 and ulcerative colitis patients and high psychopathic traits.', 'Yes. Genome-wide analyses indicate an association of alterations in ADCY7 and ulcerative colitis. Mutations in exon 2 interfere with the synthesis of the full-length isoform of CDKN2A and lead to the production of a shortened isoform, with significant morbidity and mortality.', 'Yes, there is an association of alterations in ADCY7 and ulcerative colitis.', "To further resolve the genetic architecture of the inflammatory bowel diseases ulcerative colitis and Crohn's disease, whole genomes of 4,280 patients were sequenced at low coverage and compared to 3,652 previously sequenced population controls across 73.5 million variants. A 0.6% frequency missense variant in ADCY7 was discovered that doubles the risk of ulcerative colitis."] | [
"http://www.ncbi.nlm.nih.gov/pubmed/28067910"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28067910",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 734,
"text": "To further resolve the genetic architecture of the inflammatory bowel diseases ulcerative colitis and Crohn's disease, we sequenced the whole genomes of 4,280 patients at low coverage and compared them to 3,652 previously sequenced population controls across 73.5 million variants. We then imputed from these sequences into new and existing genome-wide association study cohorts and tested for association at ∼12 million variants in a total of 16,432 cases and 18,843 controls. We discovered a 0.6% frequency missense variant in ADCY7 that doubles the risk of ulcerative colitis. Despite good statistical power, we did not identify any other new low-frequency risk variants and found that such variants explained little heritability. "
}
]
| 11 | BioASQ-training11b | null | null | 60290a131cb411341a000109 | 269 |
yesno | Can Levoxyl (levothyroxine sodium) cause insomnia? | ['yes'] | [
"yes"
]
| Levoxyl monotherapy is associated with increased insomnia compared to a combination of levothyroxine and liothyronine. | [
"http://www.ncbi.nlm.nih.gov/pubmed/19701833"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19701833",
"endSection": "abstract",
"offsetInBeginSection": 200,
"offsetInEndSection": 987,
"text": "METHODS: Seventy-one patients diagnosed with primary hypothyroidism were randomly allocated into two study groups: the first group received usual dose of levothyroxine and the second group received combination of levothyroxine and liothyronine for at least 4 months. The main outcomes were psychosocial problems (Goldberg's General Health Questionnaire, GHQ-28), bodyweight, heart rate, blood pressure, and serum lipid levels. RESULTS: In both groups serum thyroid-stimulating hormone levels remained unchanged compared with baseline. Psychosocial scores, body weight, heart rate, blood pressure, and lipid profile in the two groups remained constant. The only exception was a small but significant reduction in anxiety/insomnia in combined treatment group as compared with monotherapy. "
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D013974",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D007319"
]
| []
| 52b2ec744003448f55000001 | 270 |
yesno | Is STAT3 involved in EIF2AK2-dependent suppression of autophagy? | ['yes'] | [
"yes"
]
| ['Pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. On the other hand, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy. However, STAT3 mutants that fail to interact with EIF2AK2 are unable to suppress autophagy. Therefore, STAT3 may act as a competitive inhibitor of EIF2AK2 to suppress autophagy.', 'STAT3 may act as a competitive inhibitor of EIF2AK2. Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy. However, STAT3 mutants that fail to interact with EIF2AK2 are unable to suppress autophagy', 'STAT3 may act as a competitive inhibitor of EIF2AK2. Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy. However, STAT3 mutants that fail to interact with EIF2AK2 are unable to suppress autophagy', 'STAT3 may act as a competitive inhibitor of EIF2AK2. Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy. However, STAT3 mutants that fail to interact with EIF2AK2 are unable to suppress autophagy', 'STAT3 may act as a competitive inhibitor of EIF2AK2. Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy. However, STAT3 mutants that fail to interact with EIF2AK2 are unable to suppress autophagy', 'STAT3 may act as a competitive inhibitor of EIF2AK2. Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy. However, STAT3 mutants that fail to interact with EIF2AK2 are unable to suppress autophagy'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"http://www.ncbi.nlm.nih.gov/pubmed/23084476"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 843,
"offsetInEndSection": 1277,
"text": "STAT3 may act as a competitive inhibitor of EIF2AK2. Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy. However, STAT3 mutants that fail to interact with EIF2AK2 are unable to suppress autophagy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1279,
"offsetInEndSection": 1527,
"text": "Both STAT3-targeting agents (i.e., Stattic, JSI-124 and WP1066) and EIF2AK2 activators (such as the double-strand RNA mimetic polyinosinic:polycytidylic acid) are capable of disrupting the inhibitory interaction between STAT3 and EIF2AK2 in cellula"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1588,
"offsetInEndSection": 1806,
"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1927,
"offsetInEndSection": 2138,
"text": "These results reveal an unsuspected crosstalk between cellular metabolism (fatty acids), pro-inflammatory signaling (STAT3), innate immunity (EIF2AK2), and translational control (EIF2S1) that regulates autophagy"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23084476",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 64,
"text": "Cytoplasmic STAT3 represses autophagy by inhibiting PKR activity"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23084476",
"endSection": "abstract",
"offsetInBeginSection": 371,
"offsetInEndSection": 772,
"text": "The SH2 domain of STAT3 was found to interact with the catalytic domain of the eIF2α kinase 2 EIF2AK2, best known as protein kinase R (PKR). Pharmacological and genetic inhibition of STAT3 stimulated the activating phosphorylation of PKR and consequent eIF2α hyperphosphorylation. Moreover, PKR depletion inhibited autophagy as initiated by chemical STAT3 inhibitors or free fatty acids like palmitate"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23084476",
"endSection": "abstract",
"offsetInBeginSection": 774,
"offsetInEndSection": 960,
"text": "STAT3-targeting chemicals and palmitate caused the disruption of inhibitory STAT3-PKR interactions, followed by PKR-dependent eIF2α phosphorylation, which facilitates autophagy induction"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1012,
"offsetInEndSection": 1133,
"text": "Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1917,
"offsetInEndSection": 2255,
"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1012,
"offsetInEndSection": 1133,
"text": "Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1917,
"offsetInEndSection": 2255,
"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1588,
"offsetInEndSection": 1925,
"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 896,
"offsetInEndSection": 1016,
"text": "Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1187,
"offsetInEndSection": 1277,
"text": "However, STAT3 mutants that fail to interact with EIF2AK2 are unable to suppress autophagy"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 82,
"text": "Direct interaction between STAT3 and EIF2AK2 controls fatty acid-induced autophagy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1588,
"offsetInEndSection": 1927,
"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 896,
"offsetInEndSection": 1018,
"text": "Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "Direct interaction between STAT3 and EIF2AK2 controls fatty acid-induced autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23084476",
"endSection": "abstract",
"offsetInBeginSection": 962,
"offsetInEndSection": 1082,
"text": "These results unravel an unsuspected mechanism of autophagy control that involves STAT3 and PKR as interacting partners."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1588,
"offsetInEndSection": 1927,
"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 896,
"offsetInEndSection": 1018,
"text": "Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "Direct interaction between STAT3 and EIF2AK2 controls fatty acid-induced autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23084476",
"endSection": "abstract",
"offsetInBeginSection": 962,
"offsetInEndSection": 1082,
"text": "These results unravel an unsuspected mechanism of autophagy control that involves STAT3 and PKR as interacting partners."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1588,
"offsetInEndSection": 1927,
"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 896,
"offsetInEndSection": 1018,
"text": "Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "Direct interaction between STAT3 and EIF2AK2 controls fatty acid-induced autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23084476",
"endSection": "abstract",
"offsetInBeginSection": 962,
"offsetInEndSection": 1082,
"text": "These results unravel an unsuspected mechanism of autophagy control that involves STAT3 and PKR as interacting partners."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1588,
"offsetInEndSection": 1927,
"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 896,
"offsetInEndSection": 1018,
"text": "Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "Direct interaction between STAT3 and EIF2AK2 controls fatty acid-induced autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23084476",
"endSection": "abstract",
"offsetInBeginSection": 962,
"offsetInEndSection": 1082,
"text": "These results unravel an unsuspected mechanism of autophagy control that involves STAT3 and PKR as interacting partners."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1588,
"offsetInEndSection": 1927,
"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 896,
"offsetInEndSection": 1018,
"text": "Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "Direct interaction between STAT3 and EIF2AK2 controls fatty acid-induced autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23084476",
"endSection": "abstract",
"offsetInBeginSection": 962,
"offsetInEndSection": 1082,
"text": "These results unravel an unsuspected mechanism of autophagy control that involves STAT3 and PKR as interacting partners."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1280,
"offsetInEndSection": 1927,
"text": "Both STAT3-targeting agents (i.e., Stattic, JSI-124 and WP1066) and EIF2AK2 activators (such as the double-strand RNA mimetic polyinosinic:polycytidylic acid) are capable of disrupting the inhibitory interaction between STAT3 and EIF2AK2 in cellula, yet only the latter does so in cell-free systems in vitro. A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1589,
"offsetInEndSection": 2140,
"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1. These results reveal an unsuspected crosstalk between cellular metabolism (fatty acids), pro-inflammatory signaling (STAT3), innate immunity (EIF2AK2), and translational control (EIF2S1) that regulates autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 838,
"offsetInEndSection": 1018,
"text": "Thus, STAT3 may act as a competitive inhibitor of EIF2AK2. Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 897,
"offsetInEndSection": 1187,
"text": "Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1589,
"offsetInEndSection": 2140,
"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1. These results reveal an unsuspected crosstalk between cellular metabolism (fatty acids), pro-inflammatory signaling (STAT3), innate immunity (EIF2AK2), and translational control (EIF2S1) that regulates autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1313,
"offsetInEndSection": 1927,
"text": ", Stattic, JSI-124 and WP1066) and EIF2AK2 activators (such as the double-strand RNA mimetic polyinosinic:polycytidylic acid) are capable of disrupting the inhibitory interaction between STAT3 and EIF2AK2 in cellula, yet only the latter does so in cell-free systems in vitro. A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 838,
"offsetInEndSection": 1018,
"text": "Thus, STAT3 may act as a competitive inhibitor of EIF2AK2. Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 897,
"offsetInEndSection": 1187,
"text": "Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1280,
"offsetInEndSection": 1927,
"text": "Both STAT3-targeting agents (i.e., Stattic, JSI-124 and WP1066) and EIF2AK2 activators (such as the double-strand RNA mimetic polyinosinic:polycytidylic acid) are capable of disrupting the inhibitory interaction between STAT3 and EIF2AK2 in cellula, yet only the latter does so in cell-free systems in vitro. A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 838,
"offsetInEndSection": 1018,
"text": "Thus, STAT3 may act as a competitive inhibitor of EIF2AK2. Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1589,
"offsetInEndSection": 2140,
"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1. These results reveal an unsuspected crosstalk between cellular metabolism (fatty acids), pro-inflammatory signaling (STAT3), innate immunity (EIF2AK2), and translational control (EIF2S1) that regulates autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 897,
"offsetInEndSection": 1187,
"text": "Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1280,
"offsetInEndSection": 1927,
"text": "Both STAT3-targeting agents (i.e., Stattic, JSI-124 and WP1066) and EIF2AK2 activators (such as the double-strand RNA mimetic polyinosinic:polycytidylic acid) are capable of disrupting the inhibitory interaction between STAT3 and EIF2AK2 in cellula, yet only the latter does so in cell-free systems in vitro. A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1589,
"offsetInEndSection": 2140,
"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1. These results reveal an unsuspected crosstalk between cellular metabolism (fatty acids), pro-inflammatory signaling (STAT3), innate immunity (EIF2AK2), and translational control (EIF2S1) that regulates autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 838,
"offsetInEndSection": 1018,
"text": "Thus, STAT3 may act as a competitive inhibitor of EIF2AK2. Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 897,
"offsetInEndSection": 1187,
"text": "Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1280,
"offsetInEndSection": 1927,
"text": "Both STAT3-targeting agents (i.e., Stattic, JSI-124 and WP1066) and EIF2AK2 activators (such as the double-strand RNA mimetic polyinosinic:polycytidylic acid) are capable of disrupting the inhibitory interaction between STAT3 and EIF2AK2 in cellula, yet only the latter does so in cell-free systems in vitro. A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 1589,
"offsetInEndSection": 2140,
"text": "A further screen designed to identify EIF2AK2-dependent autophagy inducers revealed that several fatty acids including palmitate trigger autophagy via a pathway that involves the disruption of the STAT3-EIF2AK2 complex as well as the phosphorylation of mitogen-activated protein kinase 8/c-Jun N-terminal kinase 1 (MAPK8/JNK1) and EIF2S1. These results reveal an unsuspected crosstalk between cellular metabolism (fatty acids), pro-inflammatory signaling (STAT3), innate immunity (EIF2AK2), and translational control (EIF2S1) that regulates autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 838,
"offsetInEndSection": 1018,
"text": "Thus, STAT3 may act as a competitive inhibitor of EIF2AK2. Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23221979",
"endSection": "abstract",
"offsetInBeginSection": 897,
"offsetInEndSection": 1187,
"text": "Indeed, pharmacological or genetic inhibition of STAT3 stimulates EIF2AK2-dependent EIF2S1 phosphorylation and autophagy. Conversely, the overexpression of wild-type STAT3 as well as of STAT3 mutants that cannot be phosphorylated by JAK2 or are excluded from the nucleus inhibits autophagy."
}
]
| 5 | BioASQ-training5b | []
| []
| 56cdf3995795f9a73e00003a | 271 |
yesno | Is there a vaccine for peanut allergy? | ['yes'] | [
"yes"
]
| ['Yes, there is a vaccine for peanut allergy.', 'yes, there is currently a vaccine being tested for peanut allergies.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/30319619",
"http://www.ncbi.nlm.nih.gov/pubmed/25459578",
"http://www.ncbi.nlm.nih.gov/pubmed/26288733"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30319619",
"endSection": "abstract",
"offsetInBeginSection": 275,
"offsetInEndSection": 483,
"text": "Currently, two forms of peanut immunotherapy, oral immunotherapy (OIT) and epicutaneous immunotherapy (EPIT), are in Phase III clinical trials and have shown promise to induce desensitization in many subjects"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25459578",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 307,
"text": "This article presents an overview of potential treatments of food allergy, with an emphasis on various forms of immunotherapy (including oral immunotherapy, sublingual immunotherapy, epicutaneous immunotherapy, immunotherapy with modified food antigens, and immunotherapy with a recombinant peanut vaccine)."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26288733",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 76,
"text": "Recent advances in immunotherapy and vaccine development for peanut allergy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26288733",
"endSection": "abstract",
"offsetInBeginSection": 561,
"offsetInEndSection": 624,
"text": "Efforts have been made to develop a vaccine for peanut allergy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26288733",
"endSection": "abstract",
"offsetInBeginSection": 812,
"offsetInEndSection": 964,
"text": "So far, results, especially from oral immunotherapy studies, have shown good efficacy in achieving desensitization to peanut with a good safety profile."
}
]
| 11 | BioASQ-training11b | null | null | 5e46bdcd3f54159529000007 | 272 |
yesno | Is istiratumab effective for pancreatic cancer? | ['no'] | [
"no"
]
| ['No. In clinical trial, istiratumab failed to improve efficacy of standard of care for pancreatic cancer.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/31912800"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31912800",
"endSection": "abstract",
"offsetInBeginSection": 1862,
"offsetInEndSection": 1963,
"text": "CONCLUSIONS: Istiratumab failed to improve the efficacy of SOC chemotherapy in this patient setting. "
}
]
| 11 | BioASQ-training11b | null | null | 60282c3f1cb411341a0000fe | 273 |
yesno | Is peritoneal dialysis the best option for infants with kidney failure? | ['yes'] | [
"yes"
]
| ['Yes, peritoneal dialysis is often the preferred method for infants with kidney failure.', "Peritoneal dialysis (PD) is often considered the preferred option for infants with kidney failure. PD is a form of dialysis that uses the peritoneal membrane in the abdomen to remove waste products and excess fluid from the body. It is particularly suitable for infants because it can be performed at home, allowing for greater flexibility and minimizing the need for frequent hospital visits. PD also provides continuous dialysis, which can be beneficial for infants with unstable kidney function. However, the decision regarding the best dialysis option for infants should be made on an individual basis, taking into account factors such as the infant's overall health, the availability of resources, and the preferences of the parents or caregivers. It is important for the treating physician to carefully evaluate and discuss the various treatment options with the parents or caregivers to determine the most appropriate approach for each infant with kidney failure.", 'Peritoneal dialysis (PD), also known as automated peritoneal dialysis (APD), is indeed the most widely used method for chronic dialysis in children, especially in younger ones like infants. This method is often preferred because it can be done at home and is less disruptive to a child\'s daily routine. However, the "best" option can vary depending on the specific circumstances of the child, including their overall health, the severity of their kidney failure, and other individual factors. Therefore, while PD is a common and often effective choice, it\'s important to discuss all possible treatment options with a healthcare provider'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22371780",
"http://www.ncbi.nlm.nih.gov/pubmed/26591190",
"http://www.ncbi.nlm.nih.gov/pubmed/36449100",
"http://www.ncbi.nlm.nih.gov/pubmed/17990805",
"http://www.ncbi.nlm.nih.gov/pubmed/21907533",
"http://www.ncbi.nlm.nih.gov/pubmed/32063210",
"http://www.ncbi.nlm.nih.gov/pubmed/10723344",
"http://www.ncbi.nlm.nih.gov/pubmed/2739769",
"http://www.ncbi.nlm.nih.gov/pubmed/23350610",
"http://www.ncbi.nlm.nih.gov/pubmed/26438039",
"http://www.ncbi.nlm.nih.gov/pubmed/34648058",
"http://www.ncbi.nlm.nih.gov/pubmed/32063141",
"http://www.ncbi.nlm.nih.gov/pubmed/35589990",
"http://www.ncbi.nlm.nih.gov/pubmed/11998382"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36449100",
"endSection": "abstract",
"offsetInBeginSection": 48,
"offsetInEndSection": 83,
"text": "automated peritoneal dialysis (APD)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36449100",
"endSection": "abstract",
"offsetInBeginSection": 1703,
"offsetInEndSection": 1706,
"text": "APD"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36449100",
"endSection": "abstract",
"offsetInBeginSection": 1826,
"offsetInEndSection": 1828,
"text": "PD"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32063210",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 141,
"text": "Peritoneal dialysis (PD) remains the most widely used modality for chronic dialysis in children, particularly in younger children"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10723344",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Chronic ambulatory peritoneal dialysis (CAPD) is the treatment most often used in neonates and infants with chronic kidney failure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34648058",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 145,
"text": "BACKGROUND: Peritoneal dialysis (PD) is the preferred mode of kidney replacement therapy (KRT) in infants and young children with kidney failure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2739769",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 87,
"text": "Peritoneal dialysis remains the treatment of choice for acute renal failure in infancy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35589990",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "Peritoneal dialysis is the most commonly prescribed dialysis modality for infants and young children with kidney failure worldwide."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11998382",
"endSection": "abstract",
"offsetInBeginSection": 282,
"offsetInEndSection": 419,
"text": "The authors demonstrate that peritoneal dialysis is an effective, safe, and available method for treating acute renal failure in infants."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34648058",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 249,
"text": "BACKGROUND: Peritoneal dialysis (PD) is the preferred mode of kidney replacement therapy (KRT) in infants and young children with kidney failure. Hemodialysis (HD) is used less often due to the technical challenges and risk of complications in small"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17990805",
"endSection": "abstract",
"offsetInBeginSection": 1411,
"offsetInEndSection": 1636,
"text": "cannula, venous catheter).CONCLUSION: Peritoneal dialysis is the method of choice in newborns with acute renal failure, and it is used in the treatment of neonatal asphyxia till the restoration of kidney function is achieved."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26591190",
"endSection": "abstract",
"offsetInBeginSection": 2154,
"offsetInEndSection": 2241,
"text": "Peritoneal dialysis is the treatment of choice for infants with chronic kidney failure."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21907533",
"endSection": "abstract",
"offsetInBeginSection": 364,
"offsetInEndSection": 504,
"text": "Peritoneal dialysis is the renal replacement therapy of choice, especially in children under 2 years, with an important risk of peritonitis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23350610",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 155,
"text": "Peritoneal dialysis (PD) is considered as the most common form of renal replacement therapy for newborns including preterms with acute kidney injury (AKI)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26438039",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 233,
"text": "BACKGROUND: Peritoneal dialysis is the preferred mode of renal replacement therapy in infants with end-stage renal disease (ESRD). Hemodialysis (HD) is seldom used in neonates and infants due to the risk of major complications in the"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34648058",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "BACKGROUND: Peritoneal dialysis (PD) is the preferred mode of kidney replacement therapy (KRT) in infants and young children with kid"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32063141",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "BACKGROUND: Peritoneal dialysis (PD) is the preferred modality of renal replacement therapy in children with end-stage renal dis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22371780",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 206,
"text": "INTRODUCTION: Peritoneal dialysis (PD) is a preferred method of renal replacement therapy for end-stage renal disease in children. Recent advances have allowed chronic PD to be provided to children of all a"
}
]
| 13 | BioASQ-training13b | null | null | 65f86e06c4010b4d7800005a | 274 |
yesno | Are phagosomal proteins ubiquitinated? | ['yes'] | [
"yes"
]
| ['Yes,\nPhagosomal proteins are ubiquitylated, and ubiquitylation was found to be required for formation of acidic multivesicular structures.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/15703218",
"http://www.ncbi.nlm.nih.gov/pubmed/29376029"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15703218",
"endSection": "abstract",
"offsetInBeginSection": 1134,
"offsetInEndSection": 1267,
"text": "Phagosomal proteins are ubiquitylated, and ubiquitylation was found to be required for formation of acidic multivesicular structures."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29376029",
"endSection": "abstract",
"offsetInBeginSection": 1081,
"offsetInEndSection": 1317,
"text": "membranes of the bacterial phagosome are enriched with ubiquitinated proteins in a way that requires its Dot/Icm type IV secretion system, suggesting the involvement of effectors in the manipulation of the host ubiquitination machinery."
}
]
| 11 | BioASQ-training11b | null | null | 5c7c0e2fd774d0424000000d | 275 |
yesno | Is Downs syndrome associated with decreased risk of leukemia? | ['no'] | [
"no"
]
| ["No, multiple studies have established the incidence of leukemia in Down's syndrome patients to be 10- to 20-fold higher than that in the general population."] | [
"http://www.ncbi.nlm.nih.gov/pubmed/19332933",
"http://www.ncbi.nlm.nih.gov/pubmed/25332567",
"http://www.ncbi.nlm.nih.gov/pubmed/16321814",
"http://www.ncbi.nlm.nih.gov/pubmed/2955886"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2955886",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 239,
"text": "The association of Down's syndrome and leukemia has been documented for over 50 years. Multiple studies have established the incidence of leukemia in Down's syndrome patients to be 10- to 20-fold higher than that in the general population."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25332567",
"endSection": "abstract",
"offsetInBeginSection": 274,
"offsetInEndSection": 564,
"text": "We present a case of congenital acute myeloid leukemia manifesting from the very first day of birth. Diagnosis of acute myeloid leukemia was suspected by the presence of blasts in the peripheral blood smear and was confirmed on bone marrow by flowcytometry. Karyotyping revealed Trisomy 21."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16321814",
"endSection": "abstract",
"offsetInBeginSection": 928,
"offsetInEndSection": 1040,
"text": "Juvenile myelomonocytic leukemia (JMML) and a solitary cases of acute myeloid leukemia (AML) in Downs syndrome. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19332933",
"endSection": "abstract",
"offsetInBeginSection": 631,
"offsetInEndSection": 712,
"text": "This was thus confirmed to be a case with transient leukemia with Downs syndrome."
}
]
| 6 | BioASQ-training6b | null | null | 58f3d85170f9fc6f0f00000f | 276 |
yesno | Can protein coding exons originate from ALU sequences? | ['yes'] | [
"yes"
]
| ['Yes. Intronic ALUs can evolve into exons by the activation of splice signals residing within the ALU sequence. While most ALU exons do not add or modify the coding capacity of the resulting transcript, examples have been identified of ALU exons becoming protein coding.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/23374342",
"http://www.ncbi.nlm.nih.gov/pubmed/23303787",
"http://www.ncbi.nlm.nih.gov/pubmed/21282640",
"http://www.ncbi.nlm.nih.gov/pubmed/21188497",
"http://www.ncbi.nlm.nih.gov/pubmed/20803091",
"http://www.ncbi.nlm.nih.gov/pubmed/20532223",
"http://www.ncbi.nlm.nih.gov/pubmed/19393186",
"http://www.ncbi.nlm.nih.gov/pubmed/19324900",
"http://www.ncbi.nlm.nih.gov/pubmed/18332115",
"http://www.ncbi.nlm.nih.gov/pubmed/17594509",
"http://www.ncbi.nlm.nih.gov/pubmed/17204284",
"http://www.ncbi.nlm.nih.gov/pubmed/18047649",
"http://www.ncbi.nlm.nih.gov/pubmed/16027113",
"http://www.ncbi.nlm.nih.gov/pubmed/15901843",
"http://www.ncbi.nlm.nih.gov/pubmed/15328599",
"http://www.ncbi.nlm.nih.gov/pubmed/15099521",
"http://www.ncbi.nlm.nih.gov/pubmed/12764196"
]
| [
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21282640",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "The Alu element has been a major source of new exons during primate evolution. Thousands of human genes contain spliced exons derived from Alu elements."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21282640",
"endSection": "sections.0",
"offsetInBeginSection": 476,
"offsetInEndSection": 671,
"text": "More than 25% of Alu exons analyzed by RNA-Seq have estimated transcript inclusion levels of at least 50% in the human cerebellum, indicating widespread establishment of Alu exons in human genes."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21282640",
"endSection": "sections.0",
"offsetInBeginSection": 1235,
"offsetInEndSection": 1388,
"text": "his study presents genomic evidence that a major functional consequence of Alu exonization is the lineage-specific evolution of translational regulation."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20803091",
"endSection": "sections.0",
"offsetInBeginSection": 1222,
"offsetInEndSection": 1500,
"text": "Our data suggests that lineage-specific exonization events should be determined by the combination event of the formation of splicing sites and protection against site-specific mutation pressures. These evolutionary mechanisms could be major sources for primate diversification."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18332115",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 70,
"text": "Exonization of Alu elements creates primate-specific genomic diversity"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15901843",
"endSection": "sections.0",
"offsetInBeginSection": 845,
"offsetInEndSection": 1158,
"text": "Our data show that, once acquired, some exonizations were lost again in some lineages. In general, Alu exonization occurred at various time points over the evolutionary history of primate lineages, and protein-coding potential was acquired either relatively soon after integration or millions of years thereafter."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15901843",
"endSection": "sections.0",
"offsetInBeginSection": 131,
"offsetInEndSection": 355,
"text": "Once integrated, they have the potential to become exapted as functional modules, e.g., as protein-coding domains via alternative splicing. This particular process is also termed exonization and increases protein versatility"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15328599",
"endSection": "sections.0",
"offsetInBeginSection": 125,
"offsetInEndSection": 288,
"text": "alternative \"Alu-exons\" also carry the potential to greatly enhance genetic diversity by increasing the transcriptome of primates chiefly via alternative splicing."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15328599",
"endSection": "sections.0",
"offsetInBeginSection": 289,
"offsetInEndSection": 528,
"text": "ere, we report a 5' exon generated from one of the two alternative transcripts in human tumor necrosis factor receptor gene type 2 (p75TNFR) that contains an ancient Alu-SINE, which provides an alternative N-terminal protein-coding domain."
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D005091",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D020087"
]
| null | 51763a278ed59a060a000030 | 277 |
yesno | Is Bladder training an effective method to treat urge incontinence ? | ['yes'] | [
"yes"
]
| ['Yes. Bladder training is a simple, safe, and effective treatment in the management of mild to moderate forms of urinary incontinence in outpatient populations. It can be used as a first-line treatment or in combination with such other interventions as pelvic muscle exercises, bladder pressure biofeedback, electrical stimulation, and drug therapy. Quoted results vary from 26 to 90% . Patients with sensory urgency appeared to do better than those with detrusor instability and it is suggested that bladder training may be indicated as primary treatment in sensory urgency.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22453268",
"http://www.ncbi.nlm.nih.gov/pubmed/20877608",
"http://www.ncbi.nlm.nih.gov/pubmed/20527606",
"http://www.ncbi.nlm.nih.gov/pubmed/19281722",
"http://www.ncbi.nlm.nih.gov/pubmed/19174937",
"http://www.ncbi.nlm.nih.gov/pubmed/16413359",
"http://www.ncbi.nlm.nih.gov/pubmed/12614251",
"http://www.ncbi.nlm.nih.gov/pubmed/12493360",
"http://www.ncbi.nlm.nih.gov/pubmed/10198479",
"http://www.ncbi.nlm.nih.gov/pubmed/8022508",
"http://www.ncbi.nlm.nih.gov/pubmed/8006342",
"http://www.ncbi.nlm.nih.gov/pubmed/8185987",
"http://www.ncbi.nlm.nih.gov/pubmed/8394146",
"http://www.ncbi.nlm.nih.gov/pubmed/1459383",
"http://www.ncbi.nlm.nih.gov/pubmed/2653554",
"http://www.ncbi.nlm.nih.gov/pubmed/3758628",
"http://www.ncbi.nlm.nih.gov/pubmed/3765943",
"http://www.ncbi.nlm.nih.gov/pubmed/3704568",
"http://www.ncbi.nlm.nih.gov/pubmed/6534448",
"http://www.ncbi.nlm.nih.gov/pubmed/6887404"
]
| [
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22453268",
"endSection": "sections.0",
"offsetInBeginSection": 1233,
"offsetInEndSection": 1492,
"text": "Mindfulness-based stress reduction appears to be a treatment worthy of further study, as in the short term, it is as effective as historical studies of drug treatment and bladder training in reducing urge incontinence and incontinence-related quality of life."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20527606",
"endSection": "sections.0",
"offsetInBeginSection": 615,
"offsetInEndSection": 760,
"text": "All patients, irrespective of the results of cystometry were subsequently treated with oxybutynin 2.5 mg twice daily along with bladder training."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20527606",
"endSection": "sections.0",
"offsetInBeginSection": 1683,
"offsetInEndSection": 1930,
"text": "Of the 29 patients with stable bladder and symptoms of OAB, 100% cure rate was achieved in 20 (68.9%) and 06 (20.6%) patients respectively. While in 3 patients in both groups, decrease of symptoms upto 75% after 6 months of treatment was observed."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20527606",
"endSection": "sections.0",
"offsetInBeginSection": 2200,
"offsetInEndSection": 2301,
"text": "Both urodynamically proven unstable and stable bladder showed nearly equal improvement with treatment"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19281722",
"endSection": "sections.0",
"offsetInBeginSection": 1304,
"offsetInEndSection": 1777,
"text": "There are 3 types of urine incontinence (urge-, stress-, and overflow-incontinence). Another standardization of urinary incontinence follows dysfunctions of the pelvic floor: detrusor muscle-dependent, due to sphincter spasm, prostate gland dependent. Urge incontinence with a dysfunction of the detrusor muscle is the most common type. Mixed types are frequent. Non-drug measures (e.g. pelvic muscle training, bladder training, toilet training are first choice treatments."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19174937",
"endSection": "sections.0",
"offsetInBeginSection": 433,
"offsetInEndSection": 686,
"text": "Treatment of stress, urge and mixed incontinence can usually be commenced in primary care; pelvic floor exercises and bladder training are preferred. If bladder training is not effective for urge incontinence, anticholinergic drugs should be considered."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16413359",
"endSection": "sections.0",
"offsetInBeginSection": 322,
"offsetInEndSection": 527,
"text": "Sixty patients (age 8 to 12 years) with urge incontinence or dysfunctional voiding were evaluated. After a no-treatment control period (average 6 months), patients underwent a 6-day bladder training course"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16413359",
"endSection": "sections.0",
"offsetInBeginSection": 825,
"offsetInEndSection": 1047,
"text": "Six months after training completion, 64.1% and 64.7% of the inpatient and outpatient groups with daytime wetting and 51.5% and 17.7% of the inpatient and outpatient groups with nighttime wetting were cured or had improved"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16413359",
"endSection": "sections.0",
"offsetInBeginSection": 1140,
"offsetInEndSection": 1236,
"text": "Of the inpatient group with urge incontinence, the functional bladder capacity increased by 15%."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12614251",
"endSection": "sections.0",
"offsetInBeginSection": 11,
"offsetInEndSection": 150,
"text": "To compare the efficacy of tolterodine plus simplified bladder training (BT) with tolterodine alone in patients with an overactive bladder."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12614251",
"endSection": "sections.0",
"offsetInBeginSection": 1789,
"offsetInEndSection": 1974,
"text": "CONCLUSIONS: Tolterodine 2 mg twice daily is an effective and well tolerated treatment for an overactive bladder, the effectiveness of which can be augmented by a simplified BT regimen."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12493360",
"endSection": "sections.0",
"offsetInBeginSection": 341,
"offsetInEndSection": 542,
"text": "Bladder training is a modification of bladder drill that is conducted more gradually on an outpatient basis and has resulted in significant reduction of incontinence in older, community-dwelling women."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10198479",
"endSection": "sections.0",
"offsetInBeginSection": 179,
"offsetInEndSection": 365,
"text": "OBJECTIVE: To evaluate the long-term effect of treatment of female incontinence by the general practitioner (pelvic floor exercises, and bladder training) in female urinary incontinence."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10198479",
"endSection": "sections.0",
"offsetInBeginSection": 548,
"offsetInEndSection": 769,
"text": "Stress incontinence and urge incontinence were treated by means of pelvic floor exercises and bladder training respectively, while a mixed incontinence was treated by bladder training followed by pelvic floor exercises. T"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8022508",
"endSection": "sections.0",
"offsetInBeginSection": 628,
"offsetInEndSection": 746,
"text": "The treatment consisted of training of pelvic muscles in stress incontinence and bladder training in urge incontinence"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8022508",
"endSection": "sections.0",
"offsetInBeginSection": 871,
"offsetInEndSection": 993,
"text": "RESULTS: After 3 months the mean frequency of urine loss per week diminished from 21 to 8, and after 12 months to 6 times."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8006342",
"endSection": "sections.0",
"offsetInBeginSection": 117,
"offsetInEndSection": 253,
"text": "Some elders suffering from urge incontinence prefer pelvic muscle exercises to bladder training as the behavioral intervention of choice"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8185987",
"endSection": "sections.0",
"offsetInBeginSection": 1561,
"offsetInEndSection": 1654,
"text": "for eight out of nine women their continence had improved, both subjectively and objectively."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8394146",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 342,
"text": "Bladder training is a simple, safe, and effective treatment in the management of mild to moderate forms of urinary incontinence in outpatient populations. It can be used as a first-line treatment or in combination with such other interventions as pelvic muscle exercises, bladder pressure biofeedback, electrical stimulation, and drug therapy"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1459383",
"endSection": "sections.0",
"offsetInBeginSection": 146,
"offsetInEndSection": 281,
"text": "Treatment consisted of pelvic floor exercises in the case of stress incontinence and bladder training in the case of urge incontinence."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1459383",
"endSection": "sections.0",
"offsetInBeginSection": 673,
"offsetInEndSection": 756,
"text": "After 3 months about 60% of the patients were either dry or only mildly incontinent"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2653554",
"endSection": "sections.0",
"offsetInBeginSection": 829,
"offsetInEndSection": 942,
"text": "terodiline group shows this drug to be a valuable adjunct to a bladder regimen in children with urge incontinence"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3758628",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 551,
"text": "Basing on our experience with 39 patients with severe urge incontinence (in one-quarter of the cases pure urge incontinence, in one-half of the cases mixed incontinence and in a further quarter of the cases neurogenic bladder disorders) a supervised programme (mictiogram) and a well-tried therapy (especially in the Anglo-Saxon countries) consisting of the triad hospitalisation/bladder training/medication therapy are presented. After an average hospitalisation period of 14 days, we were able to achieve a symptom-free state in 94% of the patients."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3765943",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 140,
"text": "Anamnestic and urodynamical results are evaluated before and after bladder retraining drill (BRD) in women suffering from urge incontinence."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3765943",
"endSection": "sections.0",
"offsetInBeginSection": 459,
"offsetInEndSection": 561,
"text": "We could state that the BRD is a good possibility to realize multistep-therapy of female incontinence."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3704568",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 255,
"text": "Twenty consecutive female patients with urge incontinence and stable detrusor function on provocative rapid fill CO2-cystometry were treated as out-patients with a bladder training programme and with terodiline/placebo in a double-blind cross-over design."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3704568",
"endSection": "sections.0",
"offsetInBeginSection": 950,
"offsetInEndSection": 1137,
"text": "In conclusion, female patients with idiopathic urge incontinence and stable detrusor function did respond to treatment as do female patients with urge incontinence and proven instability."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6534448",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 205,
"text": "The results of in-patient bladder training in 65 women with frequency, urgency and urge incontinence are reported. There was a good initial response in 88%. By 6 months the response rate had fallen to 38%."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6534448",
"endSection": "sections.0",
"offsetInBeginSection": 206,
"offsetInEndSection": 394,
"text": "Patients with sensory urgency appeared to do better than those with detrusor instability and it is suggested that bladder training may be indicated as primary treatment in sensory urgency."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6887404",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 297,
"text": "Bladder training and/or biofeedback techniques were used to treat 75 patients with frequency, urgency, nocturia and urge incontinence. Significant improvement or cure was obtained in 70 per cent of enuretic children, and 66 per cent of men and 74 per cent of women with unstable detrusor function."
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D053202",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D001743",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D001745",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D014549"
]
| null | 515df98f298dcd4e51000030 | 278 |
yesno | Is nerinetide effective for ischaemic stroke? | ['no'] | [
"no"
]
| ['No. Nerinetide did not improve the proportion of patients achieving good clinical outcomes after endovascular thrombectomy compared with patients receiving placebo.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/32087818"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32087818",
"endSection": "abstract",
"offsetInBeginSection": 2391,
"offsetInEndSection": 2613,
"text": "337 (61·4%) of 549 patients with nerinetide and 329 (59·2%) of 556 with placebo achieved an mRS score of 0-2 at 90 days (adjusted risk ratio 1·04, 95% CI 0·96-1·14; p=0·35). Secondary outcomes were similar between groups. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32087818",
"endSection": "abstract",
"offsetInBeginSection": 2799,
"offsetInEndSection": 2975,
"text": "INTERPRETATION: Nerinetide did not improve the proportion of patients achieving good clinical outcomes after endovascular thrombectomy compared with patients receiving placebo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32087818",
"endSection": "abstract",
"offsetInBeginSection": 2713,
"offsetInEndSection": 2997,
"text": " patients receiving alteplase. Serious adverse events occurred equally between groups.INTERPRETATION: Nerinetide did not improve the proportion of patients achieving good clinical outcomes after endovascular thrombectomy compared with patients receiving placebo.FUNDING: Canadian Inst"
}
]
| 11 | BioASQ-training11b | null | null | 61f93cc7882a024a1000004c | 280 |
yesno | Is Depatuxizumab mafodotin effective for glioblastoma? | ['no'] | [
"no"
]
| ['No. Depatuxizumab mafodotin does improve survival of glioblastoma patients.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/35849035",
"http://www.ncbi.nlm.nih.gov/pubmed/34050676",
"http://www.ncbi.nlm.nih.gov/pubmed/37257422",
"http://www.ncbi.nlm.nih.gov/pubmed/37085569",
"http://www.ncbi.nlm.nih.gov/pubmed/33601293",
"http://www.ncbi.nlm.nih.gov/pubmed/34204877"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37257422",
"endSection": "abstract",
"offsetInBeginSection": 1649,
"offsetInEndSection": 1805,
"text": "RESULTS: The UNITE study was stopped early after interim analysis of separate phase III trial showed no difference in survival from depatuxizumab mafodotin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35849035",
"endSection": "abstract",
"offsetInBeginSection": 1627,
"offsetInEndSection": 1740,
"text": "CONCLUSIONS: Interim analysis demonstrated no OS benefit for depatux-m in treating EGFR-amp newly diagnosed GBM. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37085569",
"endSection": "abstract",
"offsetInBeginSection": 735,
"offsetInEndSection": 1037,
"text": "However, depatuxizumab mafodotin, an ADC targeting wild-type EGFR and EGFR variant III, did not provide a definitive overall survival benefit in patients with newly diagnosed or recurrent EGFR-amplified glioblastoma in phase II and III trials, despite objective radiological responses in some patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34050676",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 270,
"text": "BACKGROUND: Antibody drug conjugates (ADCs) targeting the epidermal growth factor receptor (EGFR), such as depatuxizumab mafodotin (Depatux-M), is a promising therapeutic strategy for glioblastoma (GBM) but recent clinical trials did not demonstrate a survival benefit. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34050676",
"endSection": "abstract",
"offsetInBeginSection": 1506,
"offsetInEndSection": 1698,
"text": "CONCLUSIONS: Despite profound intrinsic sensitivity to Depatux-M, limited drug delivery into brain tumor may have been a key contributor to lack of efficacy in recently failed clinical trials."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33601293",
"endSection": "abstract",
"offsetInBeginSection": 1612,
"offsetInEndSection": 1799,
"text": "CONCLUSIONS: Depatux-M had no impact on HRQoL and NDFS in patients with EGFR-amplified recurrent glioblastoma, except for more visual disorders, an expected side-effect of the study drug."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34204877",
"endSection": "abstract",
"offsetInBeginSection": 1560,
"offsetInEndSection": 1926,
"text": "CONCLUSIONS: The study reported the first \"real world\" experience of Depatux-M plus temozolomide in recurrent glioblastoma patients. Encouraging clinical benefits were demonstrated, even though most patients were treated beyond second-line therapy. Overall, the results are close to those reported in the previous phase 2 trial. Toxicity was moderate and manageable."
}
]
| 13 | BioASQ-training13b | null | null | 65d132101930410b13000035 | 281 |
yesno | Is celecoxib effective for treatment of amyotrophic lateral sclerosis? | ['no'] | [
"no"
]
| ['No. In clinical trial celecoxib did not have a beneficial effect on research subjects with ALS, and it was safe. A biological effect of celecoxib was not demonstrated in the cerebrospinal fluid. Further studies of celecoxib at a dosage of 800 mg/day in ALS were not recommended.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/16802291"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16802291",
"endSection": "abstract",
"offsetInBeginSection": 1197,
"offsetInEndSection": 1488,
"text": "NTERPRETATION: At the dosage studied, celecoxib did not have a beneficial effect on research subjects with ALS, and it was safe. A biological effect of celecoxib was not demonstrated in the cerebrospinal fluid. Further studies of celecoxib at a dosage of 800 mg/day in ALS are not warranted."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16802291",
"endSection": "abstract",
"offsetInBeginSection": 1111,
"offsetInEndSection": 1365,
"text": "Prostaglandin E(2) levels in cerebrospinal fluid were not elevated at baseline and did not decline with treatment.<br><b>INTERPRETATION</b>: At the dosage studied, celecoxib did not have a beneficial effect on research subjects with ALS, and it was safe."
}
]
| 11 | BioASQ-training11b | null | null | 5c6638717c78d69471000012 | 282 |
yesno | Is there a link between rare variants in PPARG and type 1 diabetes? | ['no'] | [
"no"
]
| ['No. Rare variants in PPARG with decreased activity in adipocyte differentiation are associated with increased risk of type 2 diabetes.', 'No. Rare variants in PPARG with decreased activity in adipocyte differentiation are associated with increased risk of type 2 diabetes'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/25157153"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25157153",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 130,
"text": "Rare variants in PPARG with decreased activity in adipocyte differentiation are associated with increased risk of type 2 diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25157153",
"endSection": "abstract",
"offsetInBeginSection": 585,
"offsetInEndSection": 1521,
"text": "By sequencing PPARG in 19,752 T2D cases and controls drawn from multiple studies and ethnic groups, we identified 49 previously unidentified, nonsynonymous PPARG variants (MAF < 0.5%). Considered in aggregate (with or without computational prediction of functional consequence), these rare variants showed no association with T2D (OR = 1.35; P = 0.17). The function of the 49 variants was experimentally tested in a novel high-throughput human adipocyte differentiation assay, and nine were found to have reduced activity in the assay. Carrying any of these nine LOF variants was associated with a substantial increase in risk of T2D (OR = 7.22; P = 0.005). The combination of large-scale DNA sequencing and functional testing in the laboratory reveals that approximately 1 in 1,000 individuals carries a variant in PPARG that reduces function in a human adipocyte differentiation assay and is associated with a substantial risk of T2D."
}
]
| 11 | BioASQ-training11b | null | null | 602905e81cb411341a000108 | 283 |
yesno | Is isradipine effective for Parkinson's disease? | ['no'] | [
"no"
]
| ["No. Long-term treatment with immediate-release isradipine did not slow the clinical progression of early-stage Parkinson's disease."] | [
"http://www.ncbi.nlm.nih.gov/pubmed/32227247"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32227247",
"endSection": "abstract",
"offsetInBeginSection": 1255,
"offsetInEndSection": 1569,
"text": "Adjusted least-squares mean changes in total UPDRS score in the antiparkinson medication ON state over 36 months for isradipine and placebo recipients were 2.99 (95% CI, 0.95 to 5.03) points versus 3.26 (CI, 1.25 to 5.26) points, respectively, with a treatment effect of -0.27 (CI, -3.02 to 2.48) point (P = 0.85)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32227247",
"endSection": "abstract",
"offsetInBeginSection": 1924,
"offsetInEndSection": 2046,
"text": "Conclusion: Long-term treatment with immediate-release isradipine did not slow the clinical progression of early-stage PD."
}
]
| 11 | BioASQ-training11b | null | null | 6025fd261cb411341a0000bf | 284 |
yesno | is there an increase in ultrasound comets after intense exercise? | ['yes'] | [
"yes"
]
| Strenuous exercise and exercise perfomed in extreme conditions provoke increase in interstitial pulmonary water content as shown by the increased number of ultrasuond comets | [
"http://www.ncbi.nlm.nih.gov/pubmed/21873499",
"http://www.ncbi.nlm.nih.gov/pubmed/16581487",
"http://www.ncbi.nlm.nih.gov/pubmed/21766015",
"http://www.ncbi.nlm.nih.gov/pubmed/18926391",
"http://www.ncbi.nlm.nih.gov/pubmed/15135701",
"http://www.ncbi.nlm.nih.gov/pubmed/20972574",
"http://www.ncbi.nlm.nih.gov/pubmed/9372688",
"http://www.ncbi.nlm.nih.gov/pubmed/16500505",
"http://www.ncbi.nlm.nih.gov/pubmed/21535186",
"http://www.ncbi.nlm.nih.gov/pubmed/19997032",
"http://www.ncbi.nlm.nih.gov/pubmed/20188217",
"http://www.ncbi.nlm.nih.gov/pubmed/23871437",
"http://www.ncbi.nlm.nih.gov/pubmed/23453728"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21873499",
"endSection": "abstract",
"offsetInBeginSection": 1241,
"offsetInEndSection": 1458,
"text": "Healthy athletes developed subclinical increase in pulmonary water content immediately after an Ironman race at sea level, as shown by the increased number of ULCs related to cardiac changes occurring during exercise."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16581487",
"endSection": "abstract",
"offsetInBeginSection": 1535,
"offsetInEndSection": 1830,
"text": "Increased EVLW is associated with estimated PCWP and indices of left ventricular systolic and diastolic dysfunction. The additional exercise-induced increase of PCWP, the worsening of left ventricular diastolic function, and extensive wall-motion abnormalities correlate with variations of EVLW."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21766015",
"endSection": "abstract",
"offsetInBeginSection": 694,
"offsetInEndSection": 882,
"text": " Among them chest ultrasonography can detect and quantify the extravascular lung water, creating \"comet-tail\" ultrasound artefacts (ULCs) from water-thickened pulmonary interlobular septa."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18926391",
"endSection": "abstract",
"offsetInBeginSection": 1757,
"offsetInEndSection": 1984,
"text": " In top-level breath-hold divers, chest sonography frequently reveals an increased number of ULCs after immersion, indicating a relatively high prevalence of (often subclinical) reversible extravascular lung water accumulation."
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D015444",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D014463",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D016477",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D056352",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D020552"
]
| []
| 531c380db166e2b80600003f | 285 |
yesno | Is Verubecestat effective for Alzheimer's Disease? | ['no'] | [
"no"
]
| ["No. Verubecestat did not reduce cognitive or functional decline in patients with mild-to-moderate Alzheimer's disease and was associated with treatment-related adverse events."] | [
"http://www.ncbi.nlm.nih.gov/pubmed/31423903",
"http://www.ncbi.nlm.nih.gov/pubmed/31387606",
"http://www.ncbi.nlm.nih.gov/pubmed/28749667",
"http://www.ncbi.nlm.nih.gov/pubmed/29719179",
"http://www.ncbi.nlm.nih.gov/pubmed/30970186",
"http://www.ncbi.nlm.nih.gov/pubmed/30347431"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28749667",
"endSection": "abstract",
"offsetInBeginSection": 351,
"offsetInEndSection": 551,
"text": "The lack of efficacy of verubecestat in mild-to-moderate AD raises important questions about the timing of intervention with BACE-1 inhibitors, and anti-amyloid therapies in general, in AD treatment. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29719179",
"endSection": "abstract",
"offsetInBeginSection": 2341,
"offsetInEndSection": 2525,
"text": "CONCLUSIONS: Verubecestat did not reduce cognitive or functional decline in patients with mild-to-moderate Alzheimer's disease and was associated with treatment-related adverse events."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30347431",
"endSection": "abstract",
"offsetInBeginSection": 915,
"offsetInEndSection": 1099,
"text": "These results support the continued global development of verubecestat as a potential disease-modifying agent for Japanese and non-Japanese subjects who are at-risk for developing AD. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29719179",
"endSection": "abstract",
"offsetInBeginSection": 2347,
"offsetInEndSection": 2531,
"text": "CONCLUSIONS\n\nVerubecestat did not reduce cognitive or functional decline in patients with mild-to-moderate Alzheimer's disease and was associated with treatment-related adverse events."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30970186",
"endSection": "abstract",
"offsetInBeginSection": 2305,
"offsetInEndSection": 2579,
"text": "CONCLUSIONS\n\nVerubecestat did not improve clinical ratings of dementia among patients with prodromal Alzheimer's disease, and some measures suggested that cognition and daily function were worse among patients who received verubecestat than among those who received placebo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31423903",
"endSection": "abstract",
"offsetInBeginSection": 348,
"offsetInEndSection": 485,
"text": "However, in the EPOCH trial of verubecestat in mild-to-moderate Alzheimer's disease, it was not beneficial and increased adverse effects."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31423903",
"endSection": "abstract",
"offsetInBeginSection": 653,
"offsetInEndSection": 731,
"text": "In APECS, verubecestat 40 mg worsened cognition and increased adverse effects."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28749667",
"endSection": "abstract",
"offsetInBeginSection": 358,
"offsetInEndSection": 561,
"text": "The lack of efficacy of verubecestat in mild-to-moderate AD raises important questions about the timing of intervention with BACE-1 inhibitors , and anti-amyloid therapies in general , in AD treatment . "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31387606",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 206,
"text": "Verubecestat , a BACE1 inhibitor that reduces Aβ levels in the cerebrospinal fluid of humans , was not effective in a phase 3 trial ( EPOCH ) of mild-to-moderate AD and was associated with adverse events . "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31423903",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "Lessons that can be learnt from the failure of verubecestat in Alzheimer 's disease ."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30970186",
"endSection": "abstract",
"offsetInBeginSection": 2305,
"offsetInEndSection": 2579,
"text": "CONCLUSIONS\nVerubecestat did not improve clinical ratings of dementia among patients with prodromal Alzheimer's disease, and some measures suggested that cognition and daily function were worse among patients who received verubecestat than among those who received placebo."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31423903",
"endSection": "abstract",
"offsetInBeginSection": 650,
"offsetInEndSection": 944,
"text": "In APECS, verubecestat 40 mg worsened cognition and increased adverse effects.Expert opinion: In recruiting subjects to clinical trials in Alzheimer's disease, a clinical diagnosis involving the measurement of Aβ should be undertaken for all subjects, as this may help to clarify the findings."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31423903",
"endSection": "abstract",
"offsetInBeginSection": 944,
"offsetInEndSection": 1136,
"text": "In my opinion, the failure of verubecestat in EPOCH and APECS probably could have been avoided if a safety and potential efficacy trial (phase 2) had been completed prior to starting phase 3."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31387606",
"endSection": "abstract",
"offsetInBeginSection": 1480,
"offsetInEndSection": 1577,
"text": "CONCLUSIONS: Verubecestat was associated with increased risk for several types of adverse events."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30970186",
"endSection": "abstract",
"offsetInBeginSection": 2272,
"offsetInEndSection": 2535,
"text": "Verubecestat did not improve clinical ratings of dementia among patients with prodromal Alzheimer's disease, and some measures suggested that cognition and daily function were worse among patients who received verubecestat than among those who received placebo. ("
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29719179",
"endSection": "abstract",
"offsetInBeginSection": 2314,
"offsetInEndSection": 2487,
"text": "Verubecestat did not reduce cognitive or functional decline in patients with mild-to-moderate Alzheimer's disease and was associated with treatment-related adverse events. ("
}
]
| 11 | BioASQ-training11b | null | null | 5e3a6c49b5b409ea53000017 | 286 |
yesno | Are Toll-like receptors (TLRs) induced by microbes? | ['yes'] | [
"yes"
]
| ['Yes,\nGram-negative bacteria and endogenous molecules coordinate to trigger inflammatory cascades via Toll-like receptor 4 to induce excessive expression of cytokines such as tumor necrosis factor-α and to activate NLRP3 inflammasome, a multiprotein complex that processes pro-interleukin-1β into its mature form.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/31799626",
"http://www.ncbi.nlm.nih.gov/pubmed/31462144",
"http://www.ncbi.nlm.nih.gov/pubmed/31712269",
"http://www.ncbi.nlm.nih.gov/pubmed/31865463",
"http://www.ncbi.nlm.nih.gov/pubmed/33075123"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31462144",
"endSection": "abstract",
"offsetInBeginSection": 291,
"offsetInEndSection": 439,
"text": "The C-type lectin receptor CLEC4E and Toll-like receptor TLR4 expressed by host cells are among the first line of defense in encountering pathogens."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31865463",
"endSection": "abstract",
"offsetInBeginSection": 734,
"offsetInEndSection": 1042,
"text": "Gram-negative bacteria and endogenous molecules coordinate to trigger inflammatory cascades via Toll-like receptor 4 to induce excessive expression of cytokines such as tumor necrosis factor-α and to activate NLRP3 inflammasome, a multiprotein complex that processes pro-interleukin-1β into its mature form. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31799626",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 189,
"text": "During viral infection, viral nucleic acids are detected by virus sensor proteins including toll-like receptor 3 or retinoic acid-inducible gene I-like receptors (RLRs) in mammalian cells. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31712269",
"endSection": "abstract",
"offsetInBeginSection": 698,
"offsetInEndSection": 779,
"text": "Toll-like receptor 9 (TLR9) activation is attributed to delivery of bacterial DNA"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33075123",
"endSection": "abstract",
"offsetInBeginSection": 634,
"offsetInEndSection": 782,
"text": "We determine that HBCs have the capacity to play a defensive role, where they are responsive to Toll-like receptor stimulation and are microbicidal."
}
]
| 11 | BioASQ-training11b | null | null | 603285861cb411341a000141 | 287 |
yesno | Is FKBP52 encoding a chaperone ? | ['yes'] | [
"yes"
]
| ['Yes,\nFKBP52 is a co-chaperone.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/32612187",
"http://www.ncbi.nlm.nih.gov/pubmed/33184939",
"http://www.ncbi.nlm.nih.gov/pubmed/30483787"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32612187",
"endSection": "title",
"offsetInBeginSection": 62,
"offsetInEndSection": 95,
"text": "Hsp90 co-chaperones Pp5 and FKBPs"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33184939",
"endSection": "abstract",
"offsetInBeginSection": 137,
"offsetInEndSection": 187,
"text": "The co-chaperone FK506-binding protein 51 (FKBP51)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30483787",
"endSection": "abstract",
"offsetInBeginSection": 2162,
"offsetInEndSection": 2182,
"text": "co‑chaperone FKBP52 "
}
]
| 11 | BioASQ-training11b | null | null | 6081a83f4e6a4cf630000007 | 288 |
yesno | Do only changes in coding regions of MEF2C cause developmental disorders? | ['no'] | [
"no"
]
| ['No. Non-coding region variants upstream of MEF2C cause severe developmental disorder through three distinct loss-of-function mechanisms.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/34022131"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34022131",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 132,
"text": "Non-coding region variants upstream of MEF2C cause severe developmental disorder through three distinct loss-of-function mechanisms."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34022131",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1608,
"text": "Clinical genetic testing of protein-coding regions identifies a likely causative variant in only around half of developmental disorder (DD) cases. The contribution of regulatory variation in non-coding regions to rare disease, including DD, remains very poorly understood. We screened 9,858 probands from the Deciphering Developmental Disorders (DDD) study for de novo mutations in the 5' untranslated regions (5' UTRs) of genes within which variants have previously been shown to cause DD through a dominant haploinsufficient mechanism. We identified four single-nucleotide variants and two copy-number variants upstream of MEF2C in a total of ten individual probands. We developed multiple bespoke and orthogonal experimental approaches to demonstrate that these variants cause DD through three distinct loss-of-function mechanisms, disrupting transcription, translation, and/or protein function. These non-coding region variants represent 23% of likely diagnoses identified in MEF2C in the DDD cohort, but these would all be missed in standard clinical genetics approaches. Nonetheless, these variants are readily detectable in exome sequence data, with 30.7% of 5' UTR bases across all genes well covered in the DDD dataset. Our analyses show that non-coding variants upstream of genes within which coding variants are known to cause DD are an important cause of severe disease and demonstrate that analyzing 5' UTRs can increase diagnostic yield. We also show how non-coding variants can help inform both the disease-causing mechanism underlying protein-coding variants and dosage tolerance of the gene."
}
]
| 11 | BioASQ-training11b | null | null | 61f80d5d882a024a1000003c | 289 |
yesno | Is CHEK2 involved in cell cycle control? | ['yes'] | [
"yes"
]
| CHEK2 is a key cell cycle control gene encoding a pluripotent kinase that can cause arrest or apoptosis in response to unrepaired DNA damage. | [
"http://www.ncbi.nlm.nih.gov/pubmed/23030661",
"http://www.ncbi.nlm.nih.gov/pubmed/21956126",
"http://www.ncbi.nlm.nih.gov/pubmed/18024013",
"http://www.ncbi.nlm.nih.gov/pubmed/17577921",
"http://www.ncbi.nlm.nih.gov/pubmed/17517688",
"http://www.ncbi.nlm.nih.gov/pubmed/16596250",
"http://www.ncbi.nlm.nih.gov/pubmed/11751432"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23030661",
"endSection": "abstract",
"offsetInBeginSection": 1904,
"offsetInEndSection": 2184,
"text": "Moreover, cell-cycle progression genes [i.e. E2F transcription factor (E2F) family and histone deacetylase ( HDAC )] and DNA-repair genes [i.e. growth arrest and DNA-damage-inducible, gamma ( GADD45G ) family and serine/threonine-protein kinase Chk2 ( CHEK2)] were also increased."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21956126",
"endSection": "abstract",
"offsetInBeginSection": 143,
"offsetInEndSection": 333,
"text": "As CHEK2 is a cell-cycle master controller, we tested the hypothesis that heterozygosity for the frameshift alteration CHEK2*1100delC is associated with increased risk of malignant melanoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18024013",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 178,
"text": "In the current study, we evaluated the possible associations of seven common variants of the DNA repair and cell cycle control genes BRCA2 and CHEK2 with malignant melanoma (MM)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17577921",
"endSection": "abstract",
"offsetInBeginSection": 460,
"offsetInEndSection": 717,
"text": "Promotor methylation analysis of key regulatory genes involved in cell cycle control (p14, p15, p16, CHK2), DNA repair (hMLH1), apoptosis (p73, survivin, DAPK), and differentiation (RARb, WT1) was performed by methylation-specific polymerase chain reaction."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17517688",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 141,
"text": "CHEK2 is a key cell cycle control gene encoding a pluripotent kinase that can cause arrest or apoptosis in response to unrepaired DNA damage."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16596250",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 387,
"text": "High-fidelity maintenance of genomic integrity in eukaryotes is ensured by cell cycle checkpoints and DNA repair. The checkpoint kinase, Chk2, has been implicated in both of these responses. In response to DNA damage, Chk2 is initially phosphorylated at Thr-68, which leads to its full activation. The fully activated Chk2 then phosphorylates downstream substrates of cell cycle control."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11751432",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 92,
"text": "Checkpoint kinase 2 (hCHK2/hCds1) is a tumor suppressor gene involved in cell-cycle control."
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D059447",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D064447",
"http://www.uniprot.org/uniprot/CHK2_HUMAN",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0051726",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0007049",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0007346",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D059565",
"http://www.uniprot.org/uniprot/CHK2_MOUSE",
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002453",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0022402",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0007050",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0000075",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0010564",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0031569",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0031575",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0071780",
"http://amigo.geneontology.org/cgi-bin/amigo/term_details?term=GO:0071850"
]
| []
| 53175e25b166e2b806000007 | 290 |
yesno | Has the Spanich flu virus been reconstructed? | ['yes'] | [
"yes"
]
| ['Tes,\nReconstruction of the 1918 influenza virus has facilitated considerable advancements in our understanding of this extraordinary pandemic virus.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/30142572",
"http://www.ncbi.nlm.nih.gov/pubmed/22967978",
"http://www.ncbi.nlm.nih.gov/pubmed/19385726"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30142572",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "Reconstruction of the 1918 influenza virus has facilitated considerable advancements in our understanding of this extraordinary pandemic virus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22967978",
"endSection": "abstract",
"offsetInBeginSection": 414,
"offsetInEndSection": 723,
"text": "These viral RNA sequences eventually permitted reconstruction of the complete 1918 virus, which has yielded, almost a century after the deaths of its victims, novel insights into influenza virus biology and pathogenesis and has provided important information about how to prevent and control future pandemics."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19385726",
"endSection": "abstract",
"offsetInBeginSection": 249,
"offsetInEndSection": 441,
"text": "Reconstruction of the 1918 virus and studies elucidating the exceptional virulence and transmissibility of the virus are providing exciting new insights into this devastating pandemic strain. "
}
]
| 11 | BioASQ-training11b | null | null | 5e5d27531af46fc130000007 | 291 |
yesno | Is there an association between carcinoid syndrome and mitral valve disease? | ['yes'] | [
"yes"
]
| ['Yes, mitral valve damage was reported in patients with carcinoid syndrome.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/7453210",
"http://www.ncbi.nlm.nih.gov/pubmed/11568027",
"http://www.ncbi.nlm.nih.gov/pubmed/22364692",
"http://www.ncbi.nlm.nih.gov/pubmed/8131775",
"http://www.ncbi.nlm.nih.gov/pubmed/26564596",
"http://www.ncbi.nlm.nih.gov/pubmed/7236050",
"http://www.ncbi.nlm.nih.gov/pubmed/261962"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26564596",
"endSection": "abstract",
"offsetInBeginSection": 831,
"offsetInEndSection": 1076,
"text": "Other concomitant operations included mitral valve procedure (11%), aortic valve procedure (9%), patent foramen ovale or atrial septal defect closure (23%), cardiac metastasectomies or biopsy (4%), and simultaneous coronary artery bypass (11%). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22364692",
"endSection": "abstract",
"offsetInBeginSection": 847,
"offsetInEndSection": 994,
"text": "High circulating serotonin (carcinoid syndrome) and serotoninergic drugs are known to cause valvulopathy that shares pathologic features with DMVD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11568027",
"endSection": "abstract",
"offsetInBeginSection": 794,
"offsetInEndSection": 1054,
"text": "Surgery included tricuspid valve replacement in all patients, pulmonary valve replacement in 3 and valvectomy in 7, mitral valve replacement in 6 and repair in 1, aortic valve replacement in 4 and repair in 2, CABG in 2, and patent foramen ovale closure in 5. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8131775",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 410,
"text": "We report two observations of significant left heart involvement in patients with the carcinoid syndrome assessed by transthoracic and transoesophageal echocardiography. Echocardiographic lesions of this kind have only been reported twice. In the present cases, there was mitral involvement with mitral regurgitation in one case and a mitro-aortic involvement with mitral and aortic regurgitation in the other."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7236050",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 311,
"text": "An observation of carcinoid syndrome in a woman of 47 suffering from malignant carcinoid of the ileum with metastases into the liver and right ovary is described. The clinical picture included diarrhea, heat waves, bronchospasms, hypertension, hyperserotoninemia, affection of the mitral valve and left atrium. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/261962",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 276,
"text": "A case of carcinoid syndrome, stemming from a tumor of the large intestine with hepatic metastases, is reported. Clinical features included cardiac disease with triple valvular lesion: tricuspid insufficiency with stenosis, pulmonary artery stenosis and mitral insufficiency. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22364692",
"endSection": "abstract",
"offsetInBeginSection": 848,
"offsetInEndSection": 994,
"text": "High circulating serotonin (carcinoid syndrome) and serotoninergic drugs are known to cause valvulopathy that shares pathologic features with DMVD."
}
]
| 11 | BioASQ-training11b | [
"https://meshb.nlm.nih.gov/record/ui?ui=D001244",
"http://www.disease-ontology.org/api/metadata/DOID:8600"
]
| null | 5a67a550b750ff4455000009 | 292 |
yesno | Can secondary glioblastoma be caused by brain irradiation? | ['yes'] | [
"yes"
]
| ['Yes, brain irradiation can cause secondary glioblastoma.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/2028149",
"http://www.ncbi.nlm.nih.gov/pubmed/10845210",
"http://www.ncbi.nlm.nih.gov/pubmed/29526937",
"http://www.ncbi.nlm.nih.gov/pubmed/31088835",
"http://www.ncbi.nlm.nih.gov/pubmed/12853693",
"http://www.ncbi.nlm.nih.gov/pubmed/17583602",
"http://www.ncbi.nlm.nih.gov/pubmed/23227384",
"http://www.ncbi.nlm.nih.gov/pubmed/14714135",
"http://www.ncbi.nlm.nih.gov/pubmed/32938807",
"http://www.ncbi.nlm.nih.gov/pubmed/29713762",
"http://www.ncbi.nlm.nih.gov/pubmed/15685439",
"http://www.ncbi.nlm.nih.gov/pubmed/22102955",
"http://www.ncbi.nlm.nih.gov/pubmed/18373067",
"http://www.ncbi.nlm.nih.gov/pubmed/32649812",
"http://www.ncbi.nlm.nih.gov/pubmed/23571774",
"http://www.ncbi.nlm.nih.gov/pubmed/9810442",
"http://www.ncbi.nlm.nih.gov/pubmed/17786001"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29713762",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 102,
"text": "Prolonged survival in secondary glioblastoma following local injection of targeted alpha therapy with "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10845210",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 48,
"text": "[Radiation induced glioblastoma: a case report]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10845210",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 87,
"text": "We report a surgical case of a 54-year-old woman with a radiation induced glioblastoma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17786001",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 103,
"text": "Glioblastoma multiforme following cranial irradiation and chemotherapy for acute lymphocytic leukaemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17786001",
"endSection": "abstract",
"offsetInBeginSection": 112,
"offsetInEndSection": 236,
"text": "The occurrence of glioblastoma multiforme following radiation and chemotherapy in acute lymphocytic leukaemia (ALL) is rare."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17786001",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 105,
"text": "Glioblastoma multiforme following cranial irradiation and chemotherapy for acute lymphocytic leukaemia. R"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17786001",
"endSection": "abstract",
"offsetInBeginSection": 381,
"offsetInEndSection": 485,
"text": "exact cause for the development of glioblastoma multiforme following therapy for ALL is not clear. A gen"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12853693",
"endSection": "abstract",
"offsetInBeginSection": 330,
"offsetInEndSection": 507,
"text": "ndary malignant and benign brain tumors such as astrocytoma, meningioma and glioblastoma have been described in long-term survivors of conventional myeloablative alloBMT. Here w"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32649812",
"endSection": "abstract",
"offsetInBeginSection": 1120,
"offsetInEndSection": 1349,
"text": "The authors consider irradiation-induced glioblastomas secondary to primarily verified medulloblastomas in patients who had previously undergone craniospinal irradiation as a component of combined treatment after tumor resection."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32649812",
"endSection": "abstract",
"offsetInBeginSection": 1548,
"offsetInEndSection": 1733,
"text": "The authors analyzed patterns of occurrence of irradiation-induced glioblastomas depending on the molecular genetic group and clinical characteristics of patients after primary surgery."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18373067",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "Secondary brain tumors rarely arise after cranial irradiation; among them, meningiomas and glioblastomas are the most common and secondary oligodendroglial tumors the most rare."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23227384",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "Secondary glioblastoma multiforme (sGBM) can occur after a long latency period following radiation treatment of various diseases including brain tumors, leukemia, and more benign disorders like tinea capitis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22102955",
"endSection": "abstract",
"offsetInBeginSection": 257,
"offsetInEndSection": 415,
"text": "Irradiation, however, acts as an oncogenic factor as a delayed effect and it is rare that glioblastoma multiforme develops during the remission period of ALL."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2028149",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 143,
"text": "A cerebellar glioblastoma was discovered in a 28 year old woman, 5 years after a focal 50 grays brain irradiation for meningioma of the clivus."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17786001",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 122,
"text": "Glioblastoma multiforme following cranial irradiation and chemotherapy for acute lymphocytic leukaemia. Report of 3 cases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32649812",
"endSection": "abstract",
"offsetInBeginSection": 805,
"offsetInEndSection": 932,
"text": "Secondary tumors including glioblastomas are under special attention since their occurrence is associated with a fatal outcome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32938807",
"endSection": "abstract",
"offsetInBeginSection": 406,
"offsetInEndSection": 492,
"text": "We describe a case of radiation-induced glioblastoma after radiotherapy for germinoma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32938807",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 83,
"text": "[A Case of Radiation-induced Glioblastoma 29 Years after Treatments for Germinoma]."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31088835",
"endSection": "abstract",
"offsetInBeginSection": 156,
"offsetInEndSection": 342,
"text": "Paradoxically, radiation is also a risk factor for GBM development, raising the possibility that radiotherapy of brain tumors could promote tumor recurrence or trigger secondary gliomas."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14714135",
"endSection": "abstract",
"offsetInBeginSection": 810,
"offsetInEndSection": 913,
"text": "An SMN may have a benign course, as in meningioma, or be a dilemma for the patient, as in glioblastoma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9810442",
"endSection": "abstract",
"offsetInBeginSection": 1167,
"offsetInEndSection": 1510,
"text": "During a median of 2 years of follow-up review after the diagnosis of a secondary tumour, 3 patients died related to the secondary tumours (2 sarcomas, 1 glioblastoma), one died of a recurrent primary glioma, while the remaining 7 have been alive for from 10 months to 12 years after being treated for the secondary tumours (median: 3 years). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15685439",
"endSection": "abstract",
"offsetInBeginSection": 1326,
"offsetInEndSection": 1643,
"text": "In particular, children treated with X-irradiation for acute lymphoblastic leukemia show a significantly elevated risk of developing gliomas and primitive neuroectodermal tumor (PNET), often within 10 years after therapy. TP53 mutations are frequent in low-grade gliomas and secondary glioblastomas derived therefrom."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23571774",
"endSection": "abstract",
"offsetInBeginSection": 740,
"offsetInEndSection": 920,
"text": "Pathologic diagnoses were one glioblastoma, two cases of anaplastic astrocytoma, one medulloblastoma, one low-grade glioma, one high-grade glial tumor, and one atypical meningioma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17583602",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 202,
"text": "A 22 year-old-man with acute lymphoblastic leukaemia had received prophylactic cranial irradiation and intrathecal chemotherapy. Eighteen years later a cerebellar glioblastoma multiforme was diagnosed. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29526937",
"endSection": "abstract",
"offsetInBeginSection": 412,
"offsetInEndSection": 478,
"text": "She developed glioblastoma 5.7 years after the initial GK surgery."
}
]
| 11 | BioASQ-training11b | null | null | 5e323d79fbd6abf43b000058 | 293 |
yesno | Do statins cause diabetes? | ['yes'] | [
"yes"
]
| ['The relationship between T2DM and statins is further complicated since these drugs can cause new onset diabetes (NOD) although there is an overall benefit in terms of preventing vascular events.', 'Statin use has been associated with increased risk of developing type 2 diabetes (T2DM), and with impaired glycemic control in T2DM patients'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/26806344",
"http://www.ncbi.nlm.nih.gov/pubmed/25245638",
"http://www.ncbi.nlm.nih.gov/pubmed/24404512",
"http://www.ncbi.nlm.nih.gov/pubmed/26597211",
"http://www.ncbi.nlm.nih.gov/pubmed/25208056",
"http://www.ncbi.nlm.nih.gov/pubmed/22845189",
"http://www.ncbi.nlm.nih.gov/pubmed/24373206",
"http://www.ncbi.nlm.nih.gov/pubmed/25939296",
"http://www.ncbi.nlm.nih.gov/pubmed/24874977",
"http://www.ncbi.nlm.nih.gov/pubmed/23704171",
"http://www.ncbi.nlm.nih.gov/pubmed/23496027",
"http://www.ncbi.nlm.nih.gov/pubmed/25312577",
"http://www.ncbi.nlm.nih.gov/pubmed/26437128",
"http://www.ncbi.nlm.nih.gov/pubmed/22658337",
"http://www.ncbi.nlm.nih.gov/pubmed/26466221",
"http://www.ncbi.nlm.nih.gov/pubmed/17496714"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26597211",
"endSection": "abstract",
"offsetInBeginSection": 6,
"offsetInEndSection": 146,
"text": "Statin use has been associated with increased risk of developing type 2 diabetes (T2DM), and with impaired glycemic control in T2DM patients"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26806344",
"endSection": "abstract",
"offsetInBeginSection": 336,
"offsetInEndSection": 530,
"text": "The relationship between T2DM and statins is further complicated since these drugs can cause new onset diabetes (NOD) although there is an overall benefit in terms of preventing vascular events "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25312577",
"endSection": "abstract",
"offsetInBeginSection": 160,
"offsetInEndSection": 248,
"text": "It has been repeatedly reported that statins may cause new-onset diabetes mellitus (DM)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23496027",
"endSection": "abstract",
"offsetInBeginSection": 118,
"offsetInEndSection": 230,
"text": "However, a small, but significant risk of new-onset diabetes has been reported in patients treated with statins."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25939296",
"endSection": "abstract",
"offsetInBeginSection": 175,
"offsetInEndSection": 348,
"text": "The National Lipid Association (NLA) Statin Diabetes Safety Task Force concluded that the cardiovascular benefit of statin therapy outweighs the risk for developing diabetes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25312577",
"endSection": "abstract",
"offsetInBeginSection": 149,
"offsetInEndSection": 236,
"text": "It has been repeatedly reported that statins may cause new-onset diabetes mellitus (DM)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25312577",
"endSection": "abstract",
"offsetInBeginSection": 160,
"offsetInEndSection": 378,
"text": "It has been repeatedly reported that statins may cause new-onset diabetes mellitus (DM). However, limited evidence exists from direct head to head comparisons of statins on whether the risk of DM differs among statins."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17496714",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 100,
"text": "Short-term statin exposure is associated with reduced all-cause mortality in persons with diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24373206",
"endSection": "abstract",
"offsetInBeginSection": 702,
"offsetInEndSection": 937,
"text": "Despite the fact that higher statin doses are more likely to lead to new-onset diabetes, for every case of diabetes caused, there are approximately three cardiovascular events reduced with high dose versus moderate dose statin therapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25312577",
"endSection": "abstract",
"offsetInBeginSection": 149,
"offsetInEndSection": 237,
"text": "It has been repeatedly reported that statins may cause new-onset diabetes mellitus (DM)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26437128",
"endSection": "abstract",
"offsetInBeginSection": 13,
"offsetInEndSection": 186,
"text": " Statins are evidence-based drugs to prevent cardiovascular (CV) disease. However, their benefits have been disputed by a statin-related increased risk of new onset diabetes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23704171",
"endSection": "abstract",
"offsetInBeginSection": 1929,
"offsetInEndSection": 2101,
"text": " Compared with pravastatin, treatment with higher potency statins, especially atorvastatin and simvastatin, might be associated with an increased risk of new onset diabetes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26466221",
"endSection": "abstract",
"offsetInBeginSection": 1339,
"offsetInEndSection": 1456,
"text": " statins are associated with a small increase in incidence of diabetes in patients predisposed to glycemic alteration"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24874977",
"endSection": "abstract",
"offsetInBeginSection": 1542,
"offsetInEndSection": 1748,
"text": " Higher potency statin use is associated with a moderate increase in the risk of new onset diabetes compared with lower potency statins in patients treated for secondary prevention of cardiovascular disease"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22845189",
"endSection": "abstract",
"offsetInBeginSection": 1600,
"offsetInEndSection": 1732,
"text": "An increased risk of new onset treated diabetes was found in those treated with statins showing significant duration and dose effect"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25208056",
"endSection": "abstract",
"offsetInBeginSection": 1170,
"offsetInEndSection": 1564,
"text": "Although most of the clinical studies suggest a worsening of insulin resistance and secretion, the cardiovascular benefits of statin therapy outweigh the risk of developing insulin resistance, thus the data suggest the need to treat dyslipidemia and to make patients aware of the possible risk of developing type 2 diabetes or, if they already are diabetic, of worsening their metabolic control"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27652354",
"endSection": "abstract",
"offsetInBeginSection": 1217,
"offsetInEndSection": 1318,
"text": "Statin therapy can slightly increase risk of incident diabetes in subjects with hypercholesterolemia."
}
]
| 6 | BioASQ-training6b | [
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D003924"
]
| null | 58a341eb60087bc10a000018 | 294 |
yesno | Can methylenetetrahydrofolate reductase (MTHFR) gene mutations cause homocystinuria? | ['yes'] | [
"yes"
]
| ['Yes, several methylenetetrahydrofolate reductase (MTHFR) gene mutations can cause homocystinuria and hyperhomocysteinemia.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/16629766",
"http://www.ncbi.nlm.nih.gov/pubmed/27130656",
"http://www.ncbi.nlm.nih.gov/pubmed/10980581",
"http://www.ncbi.nlm.nih.gov/pubmed/23095199",
"http://www.ncbi.nlm.nih.gov/pubmed/10923034",
"http://www.ncbi.nlm.nih.gov/pubmed/21626167",
"http://www.ncbi.nlm.nih.gov/pubmed/2629632",
"http://www.ncbi.nlm.nih.gov/pubmed/17457696",
"http://www.ncbi.nlm.nih.gov/pubmed/12673793",
"http://www.ncbi.nlm.nih.gov/pubmed/11592438",
"http://www.ncbi.nlm.nih.gov/pubmed/9490685",
"http://www.ncbi.nlm.nih.gov/pubmed/23533858",
"http://www.ncbi.nlm.nih.gov/pubmed/20532821",
"http://www.ncbi.nlm.nih.gov/pubmed/9453374",
"http://www.ncbi.nlm.nih.gov/pubmed/10679944",
"http://www.ncbi.nlm.nih.gov/pubmed/24461181",
"http://www.ncbi.nlm.nih.gov/pubmed/14656017",
"http://www.ncbi.nlm.nih.gov/pubmed/20236116",
"http://www.ncbi.nlm.nih.gov/pubmed/22521626",
"http://www.ncbi.nlm.nih.gov/pubmed/9781030",
"http://www.ncbi.nlm.nih.gov/pubmed/11181567",
"http://www.ncbi.nlm.nih.gov/pubmed/17349292",
"http://www.ncbi.nlm.nih.gov/pubmed/8124871"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24461181",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 95,
"text": "Methylenetetrahydrofolate reductase (MTHFR) deficiency is a rare autosomal recessive disorder. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23533858",
"endSection": "abstract",
"offsetInBeginSection": 136,
"offsetInEndSection": 391,
"text": "Several mutations seen in methylenetetrahydrofolate reductase (MTHFR) give rise to the formation of hyperhomocysteinemia and homocystinuria, a considerable risk factor for cardiovascular and cerebrovascular disorders, by leading to enzymatic inactivation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24461181",
"endSection": "abstract",
"offsetInBeginSection": 551,
"offsetInEndSection": 764,
"text": "At admission, he had significantly elevated plasma and urine levels of total homocysteine, significantly decreased levels of folate in serum and cerebrospinal fluid, and a normal blood concentration of methionine."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21626167",
"endSection": "abstract",
"offsetInBeginSection": 529,
"offsetInEndSection": 814,
"text": "Response to treatment demonstrated B(6)-non-responsive homocystinuria. Molecular study showed compound heterozygous T353 N and D444 N mutations of the cystathionine beta-synthase (CBS) gene, and also a C667T homozygous mutation of the methylenetetrahydrofolate-reductase (MTHFR) gene. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21626167",
"endSection": "abstract",
"offsetInBeginSection": 1121,
"offsetInEndSection": 1374,
"text": "Our case is atypical because of the absence of thromboembolism and the mild phenotype, in spite of being B(6)-non-responsive, and the association of a rare compound heterozygous mutation of the CBS gene and also an homozygous mutation of the MTHFR gene."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20236116",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 125,
"text": "Molecular characterization of five patients with homocystinuria due to severe methylenetetrahydrofolate reductase deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17349292",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 457,
"text": "Methylenetetrahydrofolate reductase (MTHFR) is a key regulatory enzyme in folate and homocysteine metabolism. Research performed during the past decade has clarified our understanding of MTHFR deficiencies that cause homocystinuria or mild hyperhomocysteinemia. Our cloning of the MTHFR coding sequence was initially followed by the identification of the first deleterious mutations in MTHFR, in patients with homocystinuria and marked hyperhomocysteinemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17457696",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 320,
"text": "Methylenetetrahydrofolate reductase (MTHFR) is a key enzyme in the regulation of plasma homocysteine levels. MTHFR deficiency, an autosomal recessive disorder, results in homocystinuria and hypomethioninaemia and presents with highly variable symptoms affecting many organs but predominantly the central nervous system. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16629766",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Some methylenetetrahydrofolate reductase (MTHFR) gene mutations cause hyperhomocysteinemia and homocystinuria."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27130656",
"endSection": "abstract",
"offsetInBeginSection": 309,
"offsetInEndSection": 431,
"text": "Rare mutations in the MTHFR gene have been associated with autosomal recessive MTHFR deficiency leading to homocystinuria."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10679944",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 128,
"text": "Characterization of six novel mutations in the methylenetetrahydrofolate reductase (MTHFR) gene in patients with homocystinuria."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20236116",
"endSection": "abstract",
"offsetInBeginSection": 227,
"offsetInEndSection": 414,
"text": "Five patients suspected of having non-classical homocystinuria due to MTHFR deficiency were examined with respect to their symptoms, MTHFR enzyme activity and genotypes of the MTHFR gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10980581",
"endSection": "abstract",
"offsetInBeginSection": 1171,
"offsetInEndSection": 1417,
"text": "The results of our study render the full-length characterisation of affected alleles in severe homocystinuria and moderate hyperhomocysteinaemia due to MTHFR deficiency and provide a basis for investigating the regulation of the human MTHFR gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17349292",
"endSection": "abstract",
"offsetInBeginSection": 260,
"offsetInEndSection": 455,
"text": "Our cloning of the MTHFR coding sequence was initially followed by the identification of the first deleterious mutations in MTHFR, in patients with homocystinuria and marked hyperhomocysteinemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10980581",
"endSection": "abstract",
"offsetInBeginSection": 166,
"offsetInEndSection": 385,
"text": "Different MTHFR mutations lead either to severe homocystinuria as a multisystem disorder or to moderate hyperhomocysteinaemia, which is a common risk factor for disorders ranging from cardiovasculopathy to spina bifida."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9490685",
"endSection": "abstract",
"offsetInBeginSection": 435,
"offsetInEndSection": 712,
"text": "We studied 24 patients with homocystinuria caused by homozygous CBS deficiency from 18 unrelated kindreds for FVL and for the 677C-->T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene and investigated their possible interaction in the risk of venous thrombosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9490685",
"endSection": "abstract",
"offsetInBeginSection": 807,
"offsetInEndSection": 1094,
"text": "On the contrary, thermolabile MTHFR caused by the 677C-->T mutation, was frequently observed among homocystinuria patients, especially among those with thromboembolic complications: three of six homocystinuria patients who had suffered from a thromboembolic event had thermolabile MTHFR."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9490685",
"endSection": "abstract",
"offsetInBeginSection": 438,
"offsetInEndSection": 715,
"text": "We studied 24 patients with homocystinuria caused by homozygous CBS deficiency from 18 unrelated kindreds for FVL and for the 677C-->T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene and investigated their possible interaction in the risk of venous thrombosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16629766",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 109,
"text": "Some methylenetetrahydrofolate reductase (MTHFR) gene mutations cause hyperhomocysteinemia and homocystinuria"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9490685",
"endSection": "abstract",
"offsetInBeginSection": 438,
"offsetInEndSection": 714,
"text": "We studied 24 patients with homocystinuria caused by homozygous CBS deficiency from 18 unrelated kindreds for FVL and for the 677C-->T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene and investigated their possible interaction in the risk of venous thrombosis"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10679944",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Characterization of six novel mutations in the methylenetetrahydrofolate reductase (MTHFR) gene in patients with homocystinuria"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11181567",
"endSection": "abstract",
"offsetInBeginSection": 144,
"offsetInEndSection": 278,
"text": "The most common genetic cause of hyperhomocysteinemia is the 677C-->T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11592438",
"endSection": "abstract",
"offsetInBeginSection": 237,
"offsetInEndSection": 444,
"text": "The 677C-->T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene is an important cause of mild hyperhomocysteinemia, but this polymorphism does not seem to be a risk factor for venous thrombosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23095199",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 153,
"text": "Hyperhomocysteinemia and methylenetetrahydrofolate reductase (MTHFR) gene mutation have been postulated as a possible cause of recurrent miscarriage (RM)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14656017",
"endSection": "abstract",
"offsetInBeginSection": 276,
"offsetInEndSection": 403,
"text": "The 677C>T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene is an important cause of mild hyperhomocysteinaemia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9490685",
"endSection": "abstract",
"offsetInBeginSection": 438,
"offsetInEndSection": 716,
"text": "We studied 24 patients with homocystinuria caused by homozygous CBS deficiency from 18 unrelated kindreds for FVL and for the 677C-->T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene and investigated their possible interaction in the risk of venous thrombosis. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16629766",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 116,
"text": "AIM: Some methylenetetrahydrofolate reductase (MTHFR) gene mutations cause hyperhomocysteinemia and homocystinuria. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2629632",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 97,
"text": "Betaine for treatment of homocystinuria caused by methylenetetrahydrofolate reductase deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20532821",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 216,
"text": "Severe deficiency of methylenetetrahydrofolate reductase (MTHFR) with homocystinuria can result in early demise or later-onset neurological impairment, including developmental delay, motor dysfunction, and seizures. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8124871",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 156,
"text": "Deficiency of 5,10-methylenetetrahydrofolate reductase (MTHFR) leads to deficient remethylation of homocysteine and is one of the causes of homocystinuria. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22521626",
"endSection": "abstract",
"offsetInBeginSection": 270,
"offsetInEndSection": 369,
"text": "Neurological disturbances have been described in homocystinuria caused by severe MTHFR deficiency. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11592438",
"endSection": "abstract",
"offsetInBeginSection": 237,
"offsetInEndSection": 445,
"text": "The 677C-->T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene is an important cause of mild hyperhomocysteinemia, but this polymorphism does not seem to be a risk factor for venous thrombosis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17349292",
"endSection": "abstract",
"offsetInBeginSection": 110,
"offsetInEndSection": 261,
"text": "Research performed during the past decade has clarified our understanding of MTHFR deficiencies that cause homocystinuria or mild hyperhomocysteinemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14656017",
"endSection": "abstract",
"offsetInBeginSection": 276,
"offsetInEndSection": 404,
"text": "The 677C>T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene is an important cause of mild hyperhomocysteinaemia."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11181567",
"endSection": "abstract",
"offsetInBeginSection": 144,
"offsetInEndSection": 279,
"text": "The most common genetic cause of hyperhomocysteinemia is the 677C-->T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17349292",
"endSection": "abstract",
"offsetInBeginSection": 262,
"offsetInEndSection": 457,
"text": "Our cloning of the MTHFR coding sequence was initially followed by the identification of the first deleterious mutations in MTHFR, in patients with homocystinuria and marked hyperhomocysteinemia."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10679944",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "Characterization of six novel mutations in the methylenetetrahydrofolate reductase (MTHFR) gene in patients with homocystinuria."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20236116",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 126,
"text": "Molecular characterization of five patients with homocystinuria due to severe methylenetetrahydrofolate reductase deficiency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9490685",
"endSection": "abstract",
"offsetInBeginSection": 812,
"offsetInEndSection": 1099,
"text": "On the contrary, thermolabile MTHFR caused by the 677C-->T mutation, was frequently observed among homocystinuria patients, especially among those with thromboembolic complications: three of six homocystinuria patients who had suffered from a thromboembolic event had thermolabile MTHFR."
}
]
| 6 | BioASQ-training6b | [
"http://www.uniprot.org/uniprot/MTHR_MOUSE",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D006712",
"http://www.uniprot.org/uniprot/MTHR_BOVIN",
"http://www.disease-ontology.org/api/metadata/DOID:9263",
"http://www.uniprot.org/uniprot/MTHR_MACFA",
"https://www.nlm.nih.gov/cgi/mesh/2017/MB_cgi?field=uid&exact=Find+Exact+Term&term=D009154",
"http://www.uniprot.org/uniprot/MTHR_HUMAN"
]
| [
{
"o": "MTHFR",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C0066357"
},
{
"o": "MTHFR",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/#_5034323839380027"
},
{
"o": "MTHFR",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/#_5135534E573500F"
},
{
"o": "Methylenetetrahydrofolate reductase",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/drugbank/molecule/3917"
},
{
"o": "http://purl.uniprot.org/uniprot/P42898",
"p": "http://www.w3.org/2004/02/skos/core#exactMatch",
"s": "http://linkedlifedata.com/resource/drugbank/molecule/3917"
},
{
"o": "MTHR_HUMAN",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://purl.uniprot.org/uniprot/P42898"
},
{
"o": "http://purl.uniprot.org/uniprot/P42898",
"p": "http://www.w3.org/2004/02/skos/core#exactMatch",
"s": "http://purl.uniprot.org/uniprot/P42898"
}
]
| 58d8d0cc8acda34529000008 | 296 |
yesno | Is POLD3 essential for mouse development? | ['yes'] | [
"yes"
]
| ['Yes. The Pold3 gene encodes a subunit of the Polδ DNA polymerase complex. Pold3 orthologs are not essential in Saccharomyces cerevisiae or chicken DT40 cells, but the Schizosaccharomyces pombe ortholog is essential. POLD3 also has a specialized role in the repair of broken replication forks, suggesting that POLD3 activity could be particularly relevant for cancer cells enduring high levels of DNA replication stress. In mouse, POLD3 is essential for development and is also required for viability in adult animals.', 'yes'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/27524497"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27524497",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 528,
"text": "The Pold3 gene encodes a subunit of the Polδ DNA polymerase complex. Pold3 orthologs are not essential in Saccharomyces cerevisiae or chicken DT40 cells, but the Schizosaccharomyces pombe ortholog is essential. POLD3 also has a specialized role in the repair of broken replication forks, suggesting that POLD3 activity could be particularly relevant for cancer cells enduring high levels of DNA replication stress. We report here that POLD3 is essential for mouse development and is also required for viability in adult animals."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27524497",
"endSection": "abstract",
"offsetInBeginSection": 412,
"offsetInEndSection": 525,
"text": "We report here that POLD3 is essential for mouse development and is also required for viability in adult animals."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27524497",
"endSection": "abstract",
"offsetInBeginSection": 415,
"offsetInEndSection": 528,
"text": "We report here that POLD3 is essential for mouse development and is also required for viability in adult animals."
}
]
| 6 | BioASQ-training6b | null | [
{
"o": "POLD3",
"p": "http://www.w3.org/2000/01/rdf-schema#label",
"s": "http://linkedlifedata.com/resource/umls/id/C1427199"
},
{
"o": "POLD3",
"p": "http://www.w3.org/2004/02/skos/core#prefLabel",
"s": "http://linkedlifedata.com/resource/#_5131353035340028"
}
]
| 5883b8e6e56acf5176000002 | 297 |
yesno | Can breastfeeding be used to alleviate the procedural pain in neonates? | ['yes'] | [
"yes"
]
| ['Yes, breastfeeding is effective in alleviating procedural pain in neonates.', 'Yes, breastfeeding is effective for pain management in neonates.', 'Yes, breastfeeding has been shown to reduce the pain response in neonates during medical procedures.', "The conclusion was that breastfeeding was effective in reducing pain caused by blood collection for newborn screening. Premature Infant Pain Profile scores were lower in the breastfeeding group when compared to the placebo and the group positioned in mother's arms, but were not different compared to the no-treatment and the glucose groups."] | [
"http://www.ncbi.nlm.nih.gov/pubmed/34983147",
"http://www.ncbi.nlm.nih.gov/pubmed/35620884",
"http://www.ncbi.nlm.nih.gov/pubmed/36291504"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34983147",
"endSection": "abstract",
"offsetInBeginSection": 1396,
"offsetInEndSection": 1557,
"text": "The duration between breastfeeding and heel lance may influence the perception of pain in newborns. Keeping this period short, may reduce the perception of pain."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35620884",
"endSection": "abstract",
"offsetInBeginSection": 983,
"offsetInEndSection": 1122,
"text": "Breastfeeding and mother's heartbeat sounds, which are non-pharmacological pain relief methods, are effective in neonatal pain management. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36291504",
"endSection": "abstract",
"offsetInBeginSection": 1046,
"offsetInEndSection": 1165,
"text": "The best non-pharmacological methods are breastfeeding followed by non-nutritive sucking coupled with sucrose sucking. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36291504",
"endSection": "abstract",
"offsetInBeginSection": 868,
"offsetInEndSection": 1045,
"text": " Non-pharmacological interventions, particularly breastfeeding and non-nutritive sucking as primary strategies for pain management in neonates are useful strategies to consider."
}
]
| 12 | BioASQ-training12b | null | null | 64412c2757b1c7a315000055 | 299 |
yesno | Are immune cells affected in Amyotrophic Lateral Sclerosis? | ['yes'] | [
"yes"
]
| ['In ALS T-cell deficiency increases neuronal loss, while boosting T cell levels reduces it.', 'Therapeutic immunization of mSOD1 mice with a myelin-derived peptide led to CP activation, and was followed by the accumulation of immunoregulatory cells, including IL-10-producing monocyte-derived macrophages and Foxp3(+) regulatory T cells, and elevation of the neurotrophic factors IGF-1 and GDNF in the diseased spinal cord parenchyma', 'Therapeutic immunization of mSOD1 mice with a myelin-derived peptide led to CP activation, and was followed by the accumulation of immunoregulatory cells, including IL-10-producing monocyte-derived macrophages and Foxp3(+) regulatory T cells, and elevation of the neurotrophic factors IGF-1 and GDNF in the diseased spinal cord parenchyma', 'Therapeutic immunization of mSOD1 mice with a myelin-derived peptide led to CP activation, and was followed by the accumulation of immunoregulatory cells, including IL-10-producing monocyte-derived macrophages and Foxp3(+) regulatory T cells, and elevation of the neurotrophic factors IGF-1 and GDNF in the diseased spinal cord parenchyma', 'Therapeutic immunization of mSOD1 mice with a myelin-derived peptide led to CP activation, and was followed by the accumulation of immunoregulatory cells, including IL-10-producing monocyte-derived macrophages and Foxp3(+) regulatory T cells, and elevation of the neurotrophic factors IGF-1 and GDNF in the diseased spinal cord parenchyma', 'Therapeutic immunization of mSOD1 mice with a myelin-derived peptide led to CP activation, and was followed by the accumulation of immunoregulatory cells, including IL-10-producing monocyte-derived macrophages and Foxp3(+) regulatory T cells, and elevation of the neurotrophic factors IGF-1 and GDNF in the diseased spinal cord parenchyma', 'The intrathymic injection of donor spleen cells into antilymphocyte serum (ALS)-treated mice induces significant prolongation of donor skin grafts. To elucidate possible mechanisms involved in the induction of unresponsiveness in ALS-treated mice after intrathymic injection of donor spleen cells, we have analysed the reactivity of lymphoid cells from unresponsive mice in various ways. Here, we show that in the mutant superoxide dismutase 1 G93A (mSOD1) mouse model of ALS, the levels of natural killer T (NKT) cells increased dramatically, and T-cell distribution was altered both in lymphoid organs and in the spinal cord relative to wild-type mice. Therapeutic immunization of mSOD1 mice with a myelin-derived peptide led to CP activation, and was followed by the accumulation of immunoregulatory cells, including IL-10-producing monocyte-derived macrophages and Foxp3(+) regulatory T cells, and elevation of the neurotrophic factors IGF-1 and GDNF in the diseased spinal cord parenchyma.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/25904790",
"http://www.ncbi.nlm.nih.gov/pubmed/21829620",
"http://www.ncbi.nlm.nih.gov/pubmed/7551976",
"http://www.ncbi.nlm.nih.gov/pubmed/7595631",
"http://www.ncbi.nlm.nih.gov/pubmed/23881705",
"http://www.ncbi.nlm.nih.gov/pubmed/17852013",
"http://www.ncbi.nlm.nih.gov/pubmed/20406178",
"http://www.ncbi.nlm.nih.gov/pubmed/24995608",
"http://www.ncbi.nlm.nih.gov/pubmed/25199710"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25904790",
"endSection": "abstract",
"offsetInBeginSection": 787,
"offsetInEndSection": 1125,
"text": "Therapeutic immunization of mSOD1 mice with a myelin-derived peptide led to CP activation, and was followed by the accumulation of immunoregulatory cells, including IL-10-producing monocyte-derived macrophages and Foxp3(+) regulatory T cells, and elevation of the neurotrophic factors IGF-1 and GDNF in the diseased spinal cord parenchyma"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25904790",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 192,
"text": "Immunization with a Myelin-Derived Antigen Activates the Brain's Choroid Plexus for Recruitment of Immunoregulatory Cells to the CNS and Attenuates Disease Progression in a Mouse Model of ALS."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21829620",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 220,
"text": "Amyotrophic lateral sclerosis (ALS) is a rapidly progressing fatal neurodegenerative disorder characterized by the selective death of motor neurons (MN) in the spinal cord, and is associated with local neuroinflammation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21829620",
"endSection": "abstract",
"offsetInBeginSection": 403,
"offsetInEndSection": 486,
"text": "T-cell deficiency increases neuronal loss, while boosting T cell levels reduces it."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23881705",
"endSection": "abstract",
"offsetInBeginSection": 625,
"offsetInEndSection": 1022,
"text": "As disease accelerates, a shift occurs from beneficial immune responses (involving M2 microglia and regulatory T-cells) to deleterious immune responses (involving M1 microglia and Th1 cells). In this review, we underscore the importance of immune-mediated mechanisms in the pathogenesis of ALS and discuss the alterations and distinct phenotypes of immune cells at the different stages of disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17852013",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 168,
"text": " Immunological disturbances have been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS). Chemokines are involved in the recruitment of immune cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20406178",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 316,
"text": "The immune system has been found to be involved with positive and negative effects in the nervous system of amyotrophic lateral sclerosis (ALS) patients. In general, T cells, B cells, NK cells, mast cells, macrophages, dendritic cells, microglia, antibodies, complement and cytokines participate in limiting damage."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23881705",
"endSection": "abstract",
"offsetInBeginSection": 625,
"offsetInEndSection": 1022,
"text": "As disease accelerates, a shift occurs from beneficial immune responses (involving M2 microglia and regulatory T-cells) to deleterious immune responses (involving M1 microglia and Th1 cells). In this review, we underscore the importance of immune-mediated mechanisms in the pathogenesis of ALS and discuss the alterations and distinct phenotypes of immune cells at the different stages of disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17852013",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 168,
"text": "Immunological disturbances have been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS). Chemokines are involved in the recruitment of immune cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20406178",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 316,
"text": "The immune system has been found to be involved with positive and negative effects in the nervous system of amyotrophic lateral sclerosis (ALS) patients. In general, T cells, B cells, NK cells, mast cells, macrophages, dendritic cells, microglia, antibodies, complement and cytokines participate in limiting damage."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24995608",
"endSection": "abstract",
"offsetInBeginSection": 2147,
"offsetInEndSection": 2458,
"text": "We propose the following mechanism for the effect of mesenchymal stem cells (MSCs) administered intrathecally in amyotrophic lateral sclerosis (ALS): MSCs increase infiltration of peripheral immune cells into CNS and skew the infiltrated immune cells toward regulatory T lymphocytes (Treg ) and Th2 lymphocytes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23881705",
"endSection": "abstract",
"offsetInBeginSection": 625,
"offsetInEndSection": 1022,
"text": "As disease accelerates, a shift occurs from beneficial immune responses (involving M2 microglia and regulatory T-cells) to deleterious immune responses (involving M1 microglia and Th1 cells). In this review, we underscore the importance of immune-mediated mechanisms in the pathogenesis of ALS and discuss the alterations and distinct phenotypes of immune cells at the different stages of disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23881705",
"endSection": "abstract",
"offsetInBeginSection": 625,
"offsetInEndSection": 1022,
"text": "As disease accelerates, a shift occurs from beneficial immune responses (involving M2 microglia and regulatory T-cells) to deleterious immune responses (involving M1 microglia and Th1 cells). In this review, we underscore the importance of immune-mediated mechanisms in the pathogenesis of ALS and discuss the alterations and distinct phenotypes of immune cells at the different stages of disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17852013",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 168,
"text": " Immunological disturbances have been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS). Chemokines are involved in the recruitment of immune cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20406178",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 316,
"text": "The immune system has been found to be involved with positive and negative effects in the nervous system of amyotrophic lateral sclerosis (ALS) patients. In general, T cells, B cells, NK cells, mast cells, macrophages, dendritic cells, microglia, antibodies, complement and cytokines participate in limiting damage."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24995608",
"endSection": "abstract",
"offsetInBeginSection": 2147,
"offsetInEndSection": 2458,
"text": "We propose the following mechanism for the effect of mesenchymal stem cells (MSCs) administered intrathecally in amyotrophic lateral sclerosis (ALS): MSCs increase infiltration of peripheral immune cells into CNS and skew the infiltrated immune cells toward regulatory T lymphocytes (Treg ) and Th2 lymphocytes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23881705",
"endSection": "abstract",
"offsetInBeginSection": 625,
"offsetInEndSection": 1022,
"text": "As disease accelerates, a shift occurs from beneficial immune responses (involving M2 microglia and regulatory T-cells) to deleterious immune responses (involving M1 microglia and Th1 cells). In this review, we underscore the importance of immune-mediated mechanisms in the pathogenesis of ALS and discuss the alterations and distinct phenotypes of immune cells at the different stages of disease."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25199710",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 271,
"text": "Immune cell infiltration to the brain's territory was considered for decades to reflect a pathological process in which immune cells attack the central nervous system (CNS); such a process is observed in the inflammatory autoimmune disease, multiple sclerosis (MS)."
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002477",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D000690",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D012598",
"http://www.disease-ontology.org/api/metadata/DOID:230"
]
| []
| 56cae51f5795f9a73e000025 | 300 |
yesno | Is cilengitide effective for treatment of glioblastoma? | ['no'] | [
"no"
]
| ['No, cilengitide does not improve survival of glioblastoma (GBM) patients. Cilengitide is a cyclic pentapeptide that demonstrated efficacy for GBM treatment by targeting the integrins avβ3 and avβ5 over-expressed on GBM cells. However, randomized phase III CENTRIC and phase II CORE trials explored failed to meet their primary endpoints. However, in CORE, higher αvβ3 levels in tumor cells were associated with improved progression-free survival by central review and with improved overall survival in patients treated with cilengitide. Analysis of randomized clinical trials of antiangiogenic drugs (including cilengitide) showed no improvement in overall survival and a trend for an inferior outcome, in terms of overall survival, in patients receiving antiangiogenic drug alone compared to cytotoxic drug alone.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/26918452",
"http://www.ncbi.nlm.nih.gov/pubmed/28514722",
"http://www.ncbi.nlm.nih.gov/pubmed/24442484",
"http://www.ncbi.nlm.nih.gov/pubmed/25163906",
"http://www.ncbi.nlm.nih.gov/pubmed/28259301",
"http://www.ncbi.nlm.nih.gov/pubmed/26792571",
"http://www.ncbi.nlm.nih.gov/pubmed/28643756",
"http://www.ncbi.nlm.nih.gov/pubmed/26717039",
"http://www.ncbi.nlm.nih.gov/pubmed/27296952",
"http://www.ncbi.nlm.nih.gov/pubmed/26935578"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28259301",
"endSection": "abstract",
"offsetInBeginSection": 542,
"offsetInEndSection": 1013,
"text": "RESULTS: fourteen randomized clinical trials were identified (7 with bevacizumab, 2 cilengitide, 1 enzastaurin, 1 dasatinib, 1 vandetanib, 1 temsirolimus, 1 cediranib) including 4330 patients. Antiangiogenic drugs showed no improvement in overall survival with a pooled HR of 1.00, a trend for an inferior outcome, in terms of overall survival, was observed in the group of patients receiving antiangiogenic drug alone compared to cytotoxic drug alone (HR=1.24, p=0.056)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28514722",
"endSection": "abstract",
"offsetInBeginSection": 1713,
"offsetInEndSection": 1878,
"text": "However, we could not conclusively confirm whether cilengitide 2000mg/5/week was the optimum regime, as only one trial using this protocol was included in our study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26792571",
"endSection": "abstract",
"offsetInBeginSection": 97,
"offsetInEndSection": 254,
"text": "Cilengitide (CGT) is a cyclic pentapeptide that demonstrated efficacy for GBM treatment by targeting the integrins avβ3 and avβ5 over-expressed on GBM cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26717039",
"endSection": "abstract",
"offsetInBeginSection": 752,
"offsetInEndSection": 842,
"text": "Cilengitide is recently failed in Phase III CENTRIC trial in unselected patients with GBM."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26717039",
"endSection": "abstract",
"offsetInBeginSection": 1188,
"offsetInEndSection": 1432,
"text": "In conclusion, we demonstrate that EGFRvIII/integrin β3 complexes promote GBM progression and metastasis in the environment of hypoxia and vitronectin-enrichment, and cilengitide may serve as a promising therapeutics for EGFRvIII-positive GBMs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27296952",
"endSection": "abstract",
"offsetInBeginSection": 1242,
"offsetInEndSection": 1442,
"text": "he addition of molecularly targeted drugs to TEM + RAD did not improve the OS of patients with GBM; however, it did improve PFS in patients treated by cilengitide who could not get improvement in OS. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26918452",
"endSection": "abstract",
"offsetInBeginSection": 161,
"offsetInEndSection": 449,
"text": " The randomized phase III CENTRIC and phase II CORE trials explored the integrin inhibitor cilengitide in patients with newly diagnosed glioblastoma with versus without O6-methylguanine DNA methyltransferase (MGMT) promoter methylation. These trials failed to meet their primary endpoints"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26918452",
"endSection": "abstract",
"offsetInBeginSection": 915,
"offsetInEndSection": 1106,
"text": ". In CORE, higher αvβ3 levels in tumor cells were associated with improved progression-free survival by central review and with improved overall survival in patients treated with cilengitide."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26935578",
"endSection": "abstract",
"offsetInBeginSection": 1253,
"offsetInEndSection": 1461,
"text": "Cilengitide combined with metronomic temozolomide and procarbazine in MGMT-promoter unmethylated glioblastoma did not improve survival compared with historical data and does not warrant further investigation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25163906",
"endSection": "abstract",
"offsetInBeginSection": 2477,
"offsetInEndSection": 2629,
"text": "The addition of cilengitide to temozolomide chemoradiotherapy did not improve outcomes; cilengitide will not be further developed as an anticancer drug."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24442484",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 103,
"text": "Cilengitide treatment of newly diagnosed glioblastoma patients does not alter patterns of progression."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28643756",
"endSection": "abstract",
"offsetInBeginSection": 1525,
"offsetInEndSection": 1702,
"text": "It may be proposed that the combination therapy of NG2 suppression and cilengitide treatment showed no considerable effect on glioblastoma compared to cilengitide therapy alone."
}
]
| 11 | BioASQ-training11b | [
"https://meshb.nlm.nih.gov/record/ui?ui=D005909",
"https://meshb.nlm.nih.gov/record/ui?ui=D016896",
"http://www.biosemantics.org/jochem#4242009"
]
| null | 5a76080683b0d9ea66000015 | 301 |
yesno | Is SLC22A3 expressed in the brain? | ['yes'] | [
"yes"
]
| ['Yes, SLC22A3 (organic cation transporter (OCT3)) is widely expressed in various organs in humans, and involved in the disposition of many exogenous and endogenous compounds. Several lines of evidence have suggested that OCT3 expressed in the brain plays an important role in the regulation of neurotransmission.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/20402963",
"http://www.ncbi.nlm.nih.gov/pubmed/21352605",
"http://www.ncbi.nlm.nih.gov/pubmed/15028779",
"http://www.ncbi.nlm.nih.gov/pubmed/18513366",
"http://www.ncbi.nlm.nih.gov/pubmed/19702534",
"http://www.ncbi.nlm.nih.gov/pubmed/19280114",
"http://www.ncbi.nlm.nih.gov/pubmed/19033200"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20402963",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 302,
"text": "The organic cation transporter (OCT) 3 is widely expressed in various organs in humans, and involved in the disposition of many exogenous and endogenous compounds. Several lines of evidence have suggested that OCT3 expressed in the brain plays an important role in the regulation of neurotransmission. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19280114",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 204,
"text": "The organic cation transporter 3 (OCT3; synonymous: extraneuronal monoamine transporter, EMT, Slc22a3) encodes an isoform of the organic cation transporters and is expressed widely across the whole brain."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18513366",
"endSection": "abstract",
"offsetInBeginSection": 1005,
"offsetInEndSection": 1223,
"text": "In agreement with this distribution, OCT3/Slc22a3-deficient mice show evidence of altered monoamine neurotransmission in the brain, with decreased intracellular content and increased turnover of aminergic transmitters."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21352605",
"endSection": "abstract",
"offsetInBeginSection": 1434,
"offsetInEndSection": 1619,
"text": "CRT, taurine transporter (TauT/SLC6A6) and organic cation transporter (OCT3/SLC22A3) expressed at the BCSFB are involved in guanidinoacetic acid or creatinine efflux transport from CSF."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19280114",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 204,
"text": "The organic cation transporter 3 (OCT3; synonymous: extraneuronal monoamine transporter, EMT, Slc22a3) encodes an isoform of the organic cation transporters and is expressed widely across the whole brain."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18513366",
"endSection": "abstract",
"offsetInBeginSection": 1005,
"offsetInEndSection": 1223,
"text": "In agreement with this distribution, OCT3/Slc22a3-deficient mice show evidence of altered monoamine neurotransmission in the brain, with decreased intracellular content and increased turnover of aminergic transmitters."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21352605",
"endSection": "abstract",
"offsetInBeginSection": 1434,
"offsetInEndSection": 1619,
"text": "CRT, taurine transporter (TauT/SLC6A6) and organic cation transporter (OCT3/SLC22A3) expressed at the BCSFB are involved in guanidinoacetic acid or creatinine efflux transport from CSF."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19280114",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 203,
"text": "The organic cation transporter 3 (OCT3; synonymous: extraneuronal monoamine transporter, EMT, Slc22a3) encodes an isoform of the organic cation transporters and is expressed widely across the whole brain"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19280114",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 205,
"text": "The organic cation transporter 3 (OCT3; synonymous: extraneuronal monoamine transporter, EMT, Slc22a3) encodes an isoform of the organic cation transporters and is expressed widely across the whole brain. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19280114",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 205,
"text": "The organic cation transporter 3 (OCT3; synonymous: extraneuronal monoamine transporter, EMT, Slc22a3) encodes an isoform of the organic cation transporters and is expressed widely across the whole brain. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19280114",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 205,
"text": "The organic cation transporter 3 (OCT3; synonymous: extraneuronal monoamine transporter, EMT, Slc22a3) encodes an isoform of the organic cation transporters and is expressed widely across the whole brain. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19280114",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 205,
"text": "The organic cation transporter 3 (OCT3; synonymous: extraneuronal monoamine transporter, EMT, Slc22a3) encodes an isoform of the organic cation transporters and is expressed widely across the whole brain. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19280114",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 205,
"text": "The organic cation transporter 3 (OCT3; synonymous: extraneuronal monoamine transporter, EMT, Slc22a3) encodes an isoform of the organic cation transporters and is expressed widely across the whole brain. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21352605",
"endSection": "abstract",
"offsetInBeginSection": 1003,
"offsetInEndSection": 1441,
"text": "CRT may be a key factor facilitating blood-to-brain guanidinoacetate transport in patients deficient in S-adenosylmethionine:guanidinoacetate N-methyltransferase, the creatine biosynthetic enzyme, resulting in cerebral accumulation of guanidinoacetate. CRT, taurine transporter (TauT/SLC6A6) and organic cation transporter (OCT3/SLC22A3) expressed at the BCSFB are involved in guanidinoacetic acid or creatinine efflux transport from CSF."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19280114",
"endSection": "abstract",
"offsetInBeginSection": 95,
"offsetInEndSection": 205,
"text": "Slc22a3) encodes an isoform of the organic cation transporters and is expressed widely across the whole brain."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21352605",
"endSection": "abstract",
"offsetInBeginSection": 1256,
"offsetInEndSection": 1676,
"text": "CRT, taurine transporter (TauT/SLC6A6) and organic cation transporter (OCT3/SLC22A3) expressed at the BCSFB are involved in guanidinoacetic acid or creatinine efflux transport from CSF. Interestingly, BBB efflux transport of GCs, including guanidinoacetate and creatinine, is negligible, though the BBB has a variety of efflux transport systems for synthetic precursors of GCs, such as amino acids and neurotransmitters."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20402963",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 302,
"text": " The organic cation transporter (OCT) 3 is widely expressed in various organs in humans, and involved in the disposition of many exogenous and endogenous compounds. Several lines of evidence have suggested that OCT3 expressed in the brain plays an important role in the regulation of neurotransmission."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21352605",
"endSection": "abstract",
"offsetInBeginSection": 1256,
"offsetInEndSection": 1441,
"text": "CRT, taurine transporter (TauT/SLC6A6) and organic cation transporter (OCT3/SLC22A3) expressed at the BCSFB are involved in guanidinoacetic acid or creatinine efflux transport from CSF."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20402963",
"endSection": "abstract",
"offsetInBeginSection": 165,
"offsetInEndSection": 302,
"text": "Several lines of evidence have suggested that OCT3 expressed in the brain plays an important role in the regulation of neurotransmission."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21352605",
"endSection": "abstract",
"offsetInBeginSection": 1256,
"offsetInEndSection": 1441,
"text": "CRT, taurine transporter (TauT/SLC6A6) and organic cation transporter (OCT3/SLC22A3) expressed at the BCSFB are involved in guanidinoacetic acid or creatinine efflux transport from CSF."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20402963",
"endSection": "abstract",
"offsetInBeginSection": 165,
"offsetInEndSection": 302,
"text": "Several lines of evidence have suggested that OCT3 expressed in the brain plays an important role in the regulation of neurotransmission."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21352605",
"endSection": "abstract",
"offsetInBeginSection": 1256,
"offsetInEndSection": 1441,
"text": "CRT, taurine transporter (TauT/SLC6A6) and organic cation transporter (OCT3/SLC22A3) expressed at the BCSFB are involved in guanidinoacetic acid or creatinine efflux transport from CSF."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20402963",
"endSection": "abstract",
"offsetInBeginSection": 165,
"offsetInEndSection": 302,
"text": "Several lines of evidence have suggested that OCT3 expressed in the brain plays an important role in the regulation of neurotransmission."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21352605",
"endSection": "abstract",
"offsetInBeginSection": 1256,
"offsetInEndSection": 1441,
"text": "CRT, taurine transporter (TauT/SLC6A6) and organic cation transporter (OCT3/SLC22A3) expressed at the BCSFB are involved in guanidinoacetic acid or creatinine efflux transport from CSF."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19280114",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 205,
"text": "The organic cation transporter 3 (OCT3; synonymous: extraneuronal monoamine transporter, EMT, Slc22a3) encodes an isoform of the organic cation transporters and is expressed widely across the whole brain."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20402963",
"endSection": "abstract",
"offsetInBeginSection": 165,
"offsetInEndSection": 302,
"text": "Several lines of evidence have suggested that OCT3 expressed in the brain plays an important role in the regulation of neurotransmission."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19702534",
"endSection": "abstract",
"offsetInBeginSection": 511,
"offsetInEndSection": 834,
"text": "OCT2-OCT-3 display differential tissue distribution: OCT1 is predominantly found in liver of humans, and liver and kidney in rodents; OCT2 is most strongly expressed in both human and rodent kidney, whereas is OCT3 primarily expressed in placenta, but also more widely detected in various tissues, including brain and lung."
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D001921",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D054022"
]
| [
{
"o": "D009474",
"p": "http://www.w3.org/2004/02/skos/core#notation",
"s": "http://linkedlifedata.com/resource/umls/label/A0091809"
},
{
"o": "D009474",
"p": "http://www.w3.org/2004/02/skos/core#notation",
"s": "http://linkedlifedata.com/resource/umls/label/A0091286"
}
]
| 571e3d42bb137a4b0c000007 | 302 |
yesno | is Cryoglobulinemic vasculitis (CV), also known as mixed cryoglobulinemic syndrome (MCS), a systemic vasculitis that affects large blood vessels. | ['no'] | [
"no"
]
| ['Cryoglobulinemic vasculitis (CV), also known as mixed cryoglobulinemic syndrome (MCS), is a systemic vasculitis that affects small blood vessels.', 'No, Cryoglobulinemic vasculitis (CV) or mixed cryoglobulinemic syndrome (MCS) is a systemic small-vessel vasculitis.', 'No, Cryoglobulinemic vasculitis (CV) is a systemic vasculitis that affects small-to-medium-sized blood vessels', 'No, Cryoglobulinemic vasculitis (CV), also known as mixed cryoglobulinemic syndrome (MCS), is not a systemic vasculitis that affects large blood vessels.', 'No. Cryoglobulinemic vasculitis (CV), also known as mixed cryoglobulinemic syndrome (MCS), is a systemic inflammatory disorder that targets small and medium-sized blood vessels.', 'No, CV/MCS is not a systemic vasculitis that affects large blood vessels.', 'No, Cryoglobulinemic vasculitis (CV), also known as mixed cryoglobulinemic syndrome (MCS), is not a systemic vasculitis that affects large blood vessels. It primarily affects small vessels, particularly capillaries, venules, and arterioles.', 'No, Cryoglobulinemic vasculitis (CV), also known as mixed cryoglobulinemic syndrome (MCS), is not a large vessel vasculitis. It primarily affects small blood vessels such as capillaries, venules, or arterioles.', 'No, Cryoglobulinemic vasculitis (CV), also known as mixed cryoglobulinemic syndrome (MCS), is a systemic vasculitis that affects small blood vessels, not large ones.', 'No, Cryoglobulinemic vasculitis (CV), also known as mixed cryoglobulinemic syndrome (MCS), primarily affects small vessels, particularly capillaries, venules, and arterioles, and not large blood vessels.', 'No, cryoglobulinemic vasculitis affects mainly small and medium-sized vessels.', 'No, cryoglobulinemic vasculitis (CV), also known as mixed cryoglobulinemic syndrome (MCS), is a systemic vasculitis that affects small to medium blood vessels, not large blood vessels.', 'No, Cryoglobulinemic vasculitis (CV), also known as mixed cryoglobulinemic syndrome (MCS), is a systemic vasculitis that affects small blood vessels', 'No, Cryoglobulinemic vasculitis (CV) or mixed cryoglobulinemic syndrome (MCS) is a systemic small-vessel vasculitis. It primarily affects small vessels such as capillaries, venules, or arterioles.', 'No, Cryoglobulinemic vasculitis (CV), also known as mixed cryoglobulinemic syndrome (MCS), is a systemic vasculitis that affects small blood vessels, not large blood vessels.', 'No, Cryoglobulinemic vasculitis (CV), also known as mixed cryoglobulinemic syndrome (MCS), is a systemic vasculitis that affects small blood vessels.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/25547031",
"http://www.ncbi.nlm.nih.gov/pubmed/35258723",
"http://www.ncbi.nlm.nih.gov/pubmed/29433114",
"http://www.ncbi.nlm.nih.gov/pubmed/37698547",
"http://www.ncbi.nlm.nih.gov/pubmed/37901234",
"http://www.ncbi.nlm.nih.gov/pubmed/25552807",
"http://www.ncbi.nlm.nih.gov/pubmed/31988822",
"http://www.ncbi.nlm.nih.gov/pubmed/21173736",
"http://www.ncbi.nlm.nih.gov/pubmed/37100623",
"http://www.ncbi.nlm.nih.gov/pubmed/19918044",
"http://www.ncbi.nlm.nih.gov/pubmed/16344620",
"http://www.ncbi.nlm.nih.gov/pubmed/33793154",
"http://www.ncbi.nlm.nih.gov/pubmed/28509128",
"http://www.ncbi.nlm.nih.gov/pubmed/33292799",
"http://www.ncbi.nlm.nih.gov/pubmed/36169798",
"http://www.ncbi.nlm.nih.gov/pubmed/14740431",
"http://www.ncbi.nlm.nih.gov/pubmed/16079934",
"http://www.ncbi.nlm.nih.gov/pubmed/37916482"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37698547",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 159,
"text": ": Cryoglobulinemic vasculitis (CV), also known as mixed cryoglobulinemic syndrome (MCS), is a systemic vasculitis that affects small blood vessels."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33292799",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 286,
"text": " The mixed cryoglobulinemia (MC) syndrome is a systemic inflammatory syndrome that causes small-to-medium vessel vasculitis due to cryoglobulin-containing immune complexes most commonly caused by chronic hepatitis C virus (HCV), and rarely by chronic hepatitis B virus (HBV)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36169798",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 224,
"text": "Cryoglobulinemic vasculitis (CV) or mixed cryoglobulinemic syndrome (MCS) is a systemic small-vessel vasculitis characterized by the proliferation of B-cell clones producing pathogenic immune complexes, called cryoglobulins."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37698547",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1104,
"text": "INTRODUCTION: Cryoglobulinemic vasculitis (CV), also known as mixed cryoglobulinemic syndrome (MCS), is a systemic vasculitis that affects small blood vessels. It exhibits a wide range of clinical manifestations, making its treatment a continuing challenge for physicians.AREAS COVERED: We conducted a comprehensive review to evaluate the current status of diagnosis, management, and treatment of mixed cryoglobulinemia (MC). The accurate clinical and serological evaluation plays a vital role in diagnosing MC, identifying potential comorbidities, and monitoring its main manifestations and complications. Treatment strategies should be individualized based on the underlying etiopathogenesis, the severity of organ involvement, and the associated underlying disease. At present, the two mainstays of CV treatment are direct antiviral agents (for HCV-related CV) and B-cell-targeted therapy.EXPERT OPINION: MC remains one of the few autoimmune diseases where the etiology is known, at least for the majority of patients. Its pathogenetic mechanism offers a unique opportunity to investigate the interpla"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36169798",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1098,
"text": "Cryoglobulinemic vasculitis (CV) or mixed cryoglobulinemic syndrome (MCS) is a systemic small-vessel vasculitis characterized by the proliferation of B-cell clones producing pathogenic immune complexes, called cryoglobulins. It is often secondary to hepatitis C virus (HCV), autoimmune diseases, and hematological malignancies. CV usually has a mild benign clinical course, but severe organ damage and life-threatening manifestations can occur. Recently, evidence in favor of rituximab (RTX), an anti-CD 20 monoclonal antibody, is emerging in CV: nevertheless, questions upon the safety of this therapeutic approach, especially in HCV patients, are still being issued and universally accepted recommendations that can help physicians in MCS treatment are lacking. A Consensus Committee provided a prioritized list of research questions to perform a systematic literature review (SLR). A search was made in Medline, Embase, and Cochrane library, updated to August 2021. Of 1227 article abstracts evaluated, 27 studies were included in the SLR, of which one SLR, 4 RCTs, and 22 observational studies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31988822",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 647,
"text": "Cryoglobulinemic vasculitis (CV) is a systemic inflammatory syndrome involving small- to medium-sized vessels. Almost half of hepatitis C-infected patients have detectable cryoglobulins levels, but only very few develop clinical manifestations. In this case report, we bring forth a diagnostic challenge of CV. A 52-year-old man with untreated hepatitis C (high viral load), diabetes mellitus, hypertension, and chronic kidney disease 4 (CKD) with solitary left kidney presented with one month of bilateral hand pain that started in his right hand, progressed to involve the left with numbness more on the palmer aspects and lateral three fingers."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35258723",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 666,
"text": "Cryoglobulinemic vasculitis (CV) is a rare immune complex disease of small vessels (capillaries, venules or arterioles) with detection of cryoglobulins (CG). These are serum proteins that precipitate at temperatures below the normal body temperature. The laboratory diagnostics are logistically challenging because the temperature of the blood sample must be maintained continuously at 37 °C until arrival in the laboratory to prevent early precipitation of the proteins with adsorption to corpuscular blood components. Cryoglobulins can be divided into three classes (types I-III), with each class associated with specific underlying diseases and symptom complexes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37698547",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 271,
"text": "INTRODUCTION: Cryoglobulinemic vasculitis (CV), also known as mixed cryoglobulinemic syndrome (MCS), is a systemic vasculitis that affects small blood vessels. It exhibits a wide range of clinical manifestations, making its treatment a continuing challenge for physicians"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37698547",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 158,
"text": "INTRODUCTION: Cryoglobulinemic vasculitis (CV), also known as mixed cryoglobulinemic syndrome (MCS), is a systemic vasculitis that affects small blood vessels"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37698547",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 424,
"text": "INTRODUCTION: Cryoglobulinemic vasculitis (CV), also known as mixed cryoglobulinemic syndrome (MCS), is a systemic vasculitis that affects small blood vessels. It exhibits a wide range of clinical manifestations, making its treatment a continuing challenge for physicians.AREAS COVERED: We conducted a comprehensive review to evaluate the current status of diagnosis, management, and treatment of mixed cryoglobulinemia (MC)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16344620",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 368,
"text": "PURPOSE OF REVIEW: Cryoglobulinemic vasculitis is an immune-complex-mediated systemic vasculitis involving small-medium-sized vessels. A causative role of hepatitis C virus in over 80% patients has been definitively established, with heterogeneous geographical distribution. This review focuses on recent etiopathogenetic, clinico-diagnostic, and therapeutical studies"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37698547",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 159,
"text": "INTRODUCTION: Cryoglobulinemic vasculitis (CV), also known as mixed cryoglobulinemic syndrome (MCS), is a systemic vasculitis that affects small blood vessels."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33292799",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 286,
"text": "BACKGROUND: The mixed cryoglobulinemia (MC) syndrome is a systemic inflammatory syndrome that causes small-to-medium vessel vasculitis due to cryoglobulin-containing immune complexes most commonly caused by chronic hepatitis C virus (HCV), and rarely by chronic hepatitis B virus (HBV)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19918044",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "OBJECTIVE: Mixed cryoglobulinemia (MC) is a systemic vasculitis of small and medium-size vessels, often associated with the hepatitis C virus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16079934",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 107,
"text": "Cryoglobulinemic vasculitis is an immune complex-mediated vasculitis predominantly affecting small vessels."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31988822",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "Cryoglobulinemic vasculitis (CV) is a systemic inflammatory syndrome involving small- to medium-sized vessels."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14740431",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "Cryoglobulinemic vasculitis (CV) is an immune-complex-mediated systemic vasculitis involving small-medium sized vessels."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25547031",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 203,
"text": "OBJECTIVE: Cryoglobulinemic vasculitis (CV) involving small- and medium-sized vessels is very frequently associated with hepatitis C virus and may be responsible for multiple organ involvement and skin u"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21173736",
"endSection": "abstract",
"offsetInBeginSection": 415,
"offsetInEndSection": 549,
"text": "Cryoglobulinemic vasculitis is an immune complex-mediated systemic disorder involving mostly small, but sometimes also larger vessels."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37916482",
"endSection": "abstract",
"offsetInBeginSection": 19,
"offsetInEndSection": 264,
"text": "Cryoglobulinemic vasculitis (CV) is an immune complex mediated small vessel vasculitis characterized by the presence of cryoglobulins in serum, often associated with hepatitis C infection, systemic autoimmune diseases or hematological conditions"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37901234",
"endSection": "abstract",
"offsetInBeginSection": 14,
"offsetInEndSection": 133,
"text": "Cryoglobulinemic vasculitis is a type of small vessel vasculitis diseases that can cause dysfunction in multiple organs"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37916482",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 246,
"text": "PURPOSE OF REVIEW: Cryoglobulinemic vasculitis (CV) is an immune complex mediated small vessel vasculitis characterized by the presence of cryoglobulins in serum, often associated with hepatitis C infection, systemic autoimmune diseases or hemato"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33292799",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 274,
"text": "BACKGROUND: The mixed cryoglobulinemia (MC) syndrome is a systemic inflammatory syndrome that causes small-to-medium vessel vasculitis due to cryoglobulin-containing immune complexes most commonly caused by chronic hepatitis C virus (HCV), and rarely by chronic hepatitis B "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19918044",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 131,
"text": "OBJECTIVE: Mixed cryoglobulinemia (MC) is a systemic vasculitis of small and medium-size vessels, often associated with the hepatit"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28509128",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 298,
"text": "Mixed cryoglobulinemic syndrome, which is a systemic vasculitis characterized by the immune complex deposition in small- and medium-sized arteries and most often due to chronic hepatitis C virus (HCV) infection, sometimes clinically manifests as refractory glomerulonephritis or nephritic syndrome."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/14740431",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 288,
"text": "Cryoglobulinemic vasculitis (CV) is an immune-complex-mediated systemic vasculitis involving small-medium sized vessels. A causative role of hepatitis C virus (HCV) in over 4/5 patients has been definitely established on the basis of epidemiological, pathological, and laboratory studies."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33793154",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1013,
"text": "INTRODUCTION: Mixed cryoglobulinemia (MC) is a B-cell lymphoproliferative disorder largely attributable to Hepatitis C virus (HCV) infection. MC clinical manifestations are determined by systemic vasculitis of low/medium sized vessels (mixed cryoglobulinemia syndrome or cryoglobulinemic vasculitis [CV]) caused by the deposition of cryoglobulins in blood vessels.EVIDENCE ACQUISITION: A systematic review was performed via the Medline and Scopus databases to evaluate studies concerning CV treatment with new direct antiviral agents (DAAs) and their effect on the syndrome.EVIDENCE SYNTHESIS: The introduction of interferon-free protocols has led to more evident positive effects than those observed in the treatment of hepatitis C. In fact, IFN-free, DAA-based therapy minimized side effects permitting the treatment of previously contraindicated patients and led to a particularly high SVR rate and to a clinical/immunological response in the majority of patients, even if at different levels in different pati"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19918044",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1043,
"text": "OBJECTIVE: Mixed cryoglobulinemia (MC) is a systemic vasculitis of small and medium-size vessels, often associated with the hepatitis C virus. Research has shown an emerging role for chemokines and type 1 cytokines in the pathophysiology of this vasculitis. Interleukin 1 (IL-1) plays a role in initiating the cascade of immunoinflammatory responses, and levels of the interferon-gamma (IFN-gamma) inducible chemokine CXCL10 have been shown to be significantly associated with the presence of active vasculitis in patients with MC. We evaluated serum levels of IL-1beta, IFN-gamma, and CXCL10 in a series of patients with hepatitis C-related MC (MC+HCV), and correlated these measurements with clinical disease features.METHODS: Serum IL-1beta, IFN-gamma, and CXCL10 were assayed in 54 patients with MC+HCV, in 54 sex- and age-matched patients with type C chronic hepatitis without cryoglobulinemia (HCV+), and in 54 controls.RESULTS: MC+HCV patients showed significantly higher mean IL-1beta and CXCL10 serum levels than controls (p < 0.01) o"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28509128",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1342,
"text": "Mixed cryoglobulinemic syndrome, which is a systemic vasculitis characterized by the immune complex deposition in small- and medium-sized arteries and most often due to chronic hepatitis C virus (HCV) infection, sometimes clinically manifests as refractory glomerulonephritis or nephritic syndrome. Patients with mixed cryoglobulinemic nephropathy who have a rapidly progressive glomerulonephritis should receive immunosuppressive therapy. After disease stabilization, patients should receive concurrent therapy for the underlying HCV infection. The standard therapy of a chronic HCV infection is IFN monotherapy or IFN combined with ribavirin; however, after the introduction of direct-acting antivirals (DAAs), the standard therapy for patients with HCV genotype 1 has dramatically changed. We report a case of HCV-associated cryoglobulinemic membranoproliferative glomerulonephritis (MPGN) successfully treated by daclatasvir and asunaprevir, which are IFN-free DAAs for HCV, in combination with angiotensin II receptor blocker without immunosuppressive therapy. The patient developed severe nephrotic syndrome with progressive kidney dysfunction. Blood examination revealed a high copy number of HCV-RNA (6.4 log IU/mL, type 1), cryoglobulinemia, paraproteinemia of IgM-κ, and hypocomplementemia. Histological analysis showed MPGN type 1."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37100623",
"endSection": "abstract",
"offsetInBeginSection": 842,
"offsetInEndSection": 894,
"text": "CV is a rare immune complex small-vessel vasculitis."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16344620",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 133,
"text": "PURPOSE OF REVIEW: Cryoglobulinemic vasculitis is an immune-complex-mediated systemic vasculitis involving small-medium-sized vessels"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25552807",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 168,
"text": "Cryoglobulinemic vasculitis is a small vessel vasculitis that has been associated with chronic infections and autoimmune, lymphoproliferative, and neoplastic disorders."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37901234",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "Introduction: Cryoglobulinemic vasculitis is a type of small vessel vasculitis diseases that can cause dysfunction in mu"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37916482",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "PURPOSE OF REVIEW: Cryoglobulinemic vasculitis (CV) is an immune complex mediated small vessel vasculitis characterized by the presence of cry"
}
]
| 13 | BioASQ-training13b | null | null | 662cf888187cba990d000002 | 303 |
yesno | Is the Dictyostelium discoideum proteome known? | ['yes'] | [
"yes"
]
| ['Yes, The Dictyostelium discoideum genome has been sequenced, assembled and annotated to a high degree of reliability. The parts-list of proteins and RNA encoded by the six chromosomes can now be accessed and analyzed. Consequently, this genomic sequence information can now be exploited to realize D. discoideum proteomics projects.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22120990",
"http://www.ncbi.nlm.nih.gov/pubmed/20422638",
"http://www.ncbi.nlm.nih.gov/pubmed/20013782",
"http://www.ncbi.nlm.nih.gov/pubmed/16875414",
"http://www.ncbi.nlm.nih.gov/pubmed/16957282",
"http://www.ncbi.nlm.nih.gov/pubmed/16957286",
"http://www.ncbi.nlm.nih.gov/pubmed/11990506",
"http://www.ncbi.nlm.nih.gov/pubmed/9150929",
"http://www.ncbi.nlm.nih.gov/pubmed/18820470"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18820470",
"endSection": "abstract",
"offsetInBeginSection": 658,
"offsetInEndSection": 1023,
"text": "The Negative Proteome Database (NPD) is populated with pair-wise protein sequence comparisons between each of the following proteomes: Homo sapiens, Mus musculus, Drosophila melanogaster, Caenorhabditis elegans, Saccharomyces cerevisiae, Dictyostelium discoideum, Chlamydomonus reinhardti, Escherichia coli K12, Arabidopsis thaliana and Methanoscarcina acetivorans."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9150929",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 103,
"text": "The Dictyostelium discoideum proteome--the SWISS-2DPAGE database of the multicellular aggregate (slug)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16957286",
"endSection": "abstract",
"offsetInBeginSection": 346,
"offsetInEndSection": 461,
"text": "Consequently, this genomic sequence information can now be exploited to realize D. discoideum proteomics projects. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16957282",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 213,
"text": "The Dictyostelium discoideum genome has been sequenced, assembled and annotated to a high degree of reliability. The parts-list of proteins and RNA encoded by the six chromosomes can now be accessed and analyzed. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16875414",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 370,
"text": "The 34 Mb genome of Dictyostelium discoideum is carried on 6 chromosomes and has been fully sequenced by an international consortium. The sequence was assembled on the classical and physical maps that had been built up over the years and refined by HAPPY mapping. Annotation of the sequence predicted about 12,000 genes for proteins of at least 50 amino acids in length."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20013782",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 224,
"text": "In this study, a quantitative comparative proteomics approach has been used to analyze the Dictyostelium discoideum mitochondrial proteome variations during vegetative growth, starvation and the early stages of development. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20422638",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 75,
"text": "The secreted proteome profile of developing Dictyostelium discoideum cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22120990",
"endSection": "abstract",
"offsetInBeginSection": 764,
"offsetInEndSection": 914,
"text": "The present repertoire validates our purification method and paves the way for a future proteomics approach to study the dynamics of macropinocytosis."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11990506",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 68,
"text": "Proteomic analysis of a developmentally regulated secretory vesicle."
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D004023",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D040901",
"http://www.nlm.nih.gov/cgi/mesh/2016/MB_cgi?field=uid&exact=Find+Exact+Term&term=D020543"
]
| []
| 56b39f148525abca1e000004 | 304 |
yesno | Do histone variant mH2A (macro-H2A) levels decrease upon differentiation? | ['no'] | [
"no"
]
| ['MacroH2A.1 was found to be present at low levels upon the establishment of pluripotency in the inner cell mass and epiblast, but it was highly enriched in the trophectoderm and differentiated somatic cells later in mouse development. Chromatin immunoprecipitation revealed that macroH2A.1 is incorporated in the chromatin of regulatory regions of pluripotency genes in somatic cells such as mouse embryonic fibroblasts and adult neural stem cells, but not in embryonic stem cells. In addition, overexpression of macroH2A isoforms prevented efficient reprogramming of epiblast stem cells to naïve pluripotency.', '1 was found to be present at low levels upon the establishment of pluripotency in the inner cell mass and epiblast, but it was highly enriched in the trophectoderm and differentiated somatic cells later in mouse development.', 'Histone variant macroH2A confers resistance to nuclear reprogramming Histone variant macroH2A marks embryonic differentiation in vivo and acts as an epigenetic barrier to induced pluripotency.', 'Resistance to reprogramming is associated with incorporation of the histone variant macroH2A, which is retained on the Xi of differentiated cells, but absent from the Xi of EpiSCs. The histone variant macroH2A acts as a component of an epigenetic multilayer that heritably maintains the silent X chromosome and has been shown to restrict tumor development.', 'Through manipulation of macroH2A isoforms, we further demonstrate that macroH2A2 is the predominant barrier to reprogramming. In particular, we find macroH2A isoforms to be highly enriched at target genes of the K27me3 demethylase, Utx, which are reactivated early in iPS reprogramming', 'MacroH2A.1 was found to be present at low levels upon the establishment of pluripotency in the inner cell mass and epiblast, but it was highly enriched in the trophectoderm and differentiated somatic cells later in mouse development. Histone variant macroH2A marks embryonic differentiation in vivo and acts as an epigenetic barrier to induced pluripotency.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/21738686",
"http://www.ncbi.nlm.nih.gov/pubmed/22449192",
"http://www.ncbi.nlm.nih.gov/pubmed/23595991",
"http://www.ncbi.nlm.nih.gov/pubmed/23077180",
"http://www.ncbi.nlm.nih.gov/pubmed/23463008",
"http://www.ncbi.nlm.nih.gov/pubmed/21552206"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23463008",
"endSection": "abstract",
"offsetInBeginSection": 268,
"offsetInEndSection": 393,
"text": "Through manipulation of macroH2A isoforms, we further demonstrate that macroH2A2 is the predominant barrier to reprogramming."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23463008",
"endSection": "abstract",
"offsetInBeginSection": 532,
"offsetInEndSection": 691,
"text": "In particular, we find macroH2A isoforms to be highly enriched at target genes of the K27me3 demethylase, Utx, which are reactivated early in iPS reprogramming"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23463008",
"endSection": "abstract",
"offsetInBeginSection": 880,
"offsetInEndSection": 1121,
"text": " Therefore, we propose that macroH2A isoforms provide a redundant silencing layer or terminal differentiation 'lock' at critical pluripotency genes that presents as an epigenetic barrier when differentiated cells are challenged to reprogram."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21552206",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 68,
"text": "Histone variant macroH2A confers resistance to nuclear reprogramming"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21552206",
"endSection": "abstract",
"offsetInBeginSection": 871,
"offsetInEndSection": 1051,
"text": "Resistance to reprogramming is associated with incorporation of the histone variant macroH2A, which is retained on the Xi of differentiated cells, but absent from the Xi of EpiSCs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22449192",
"endSection": "abstract",
"offsetInBeginSection": 580,
"offsetInEndSection": 758,
"text": "We highlight the role of macroH2A in the establishment and maintenance of differentiated states and we discuss its still poorly recognized function in transcriptional activation."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23077180",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "Histone variant macroH2A marks embryonic differentiation in vivo and acts as an epigenetic barrier to induced pluripotency."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23077180",
"endSection": "abstract",
"offsetInBeginSection": 603,
"offsetInEndSection": 836,
"text": "MacroH2A.1 was found to be present at low levels upon the establishment of pluripotency in the inner cell mass and epiblast, but it was highly enriched in the trophectoderm and differentiated somatic cells later in mouse development."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23077180",
"endSection": "abstract",
"offsetInBeginSection": 837,
"offsetInEndSection": 1083,
"text": "Chromatin immunoprecipitation revealed that macroH2A.1 is incorporated in the chromatin of regulatory regions of pluripotency genes in somatic cells such as mouse embryonic fibroblasts and adult neural stem cells, but not in embryonic stem cells."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23077180",
"endSection": "abstract",
"offsetInBeginSection": 1326,
"offsetInEndSection": 1455,
"text": "In addition, overexpression of macroH2A isoforms prevented efficient reprogramming of epiblast stem cells to naïve pluripotency. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23595991",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 86,
"text": "Macro histone variants are critical for the differentiation of human pluripotent cells"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23595991",
"endSection": "abstract",
"offsetInBeginSection": 151,
"offsetInEndSection": 356,
"text": "Here we show that the knockdown of macro histone variants impaired the in vitro and in vivo differentiation of human pluripotent cells, likely through defects in the silencing of pluripotency-related genes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21738686",
"endSection": "abstract",
"offsetInBeginSection": 802,
"offsetInEndSection": 982,
"text": "Furthermore, male and female mH2A-deficient ESCs proliferate normally under pluripotency culture conditions, and respond to several standard differentiation procedures efficiently."
}
]
| 6 | BioASQ-training6b | null | null | 58ab1f6c9ef3c34033000002 | 305 |
yesno | Is Ameloblastoma (AB) a benign tumor that never metastasizes? | ['no'] | [
"no"
]
| ['Ameloblastomas are benign but locally invasive neoplasms which can be metastatic'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/21558899",
"http://www.ncbi.nlm.nih.gov/pubmed/32712102",
"http://www.ncbi.nlm.nih.gov/pubmed/23775022",
"http://www.ncbi.nlm.nih.gov/pubmed/24374844",
"http://www.ncbi.nlm.nih.gov/pubmed/6575436",
"http://www.ncbi.nlm.nih.gov/pubmed/28944145",
"http://www.ncbi.nlm.nih.gov/pubmed/31674718",
"http://www.ncbi.nlm.nih.gov/pubmed/18230377"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31674718",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 215,
"text": "Ameloblastic carcinoma (AC) is defined as a rare primary epithelial odontogenic malignant neoplasm and the malignant counterpart of benign epithelial odontogenic tumor of ameloblastoma (AB) by the WHO classification"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/31674718",
"endSection": "abstract",
"offsetInBeginSection": 217,
"offsetInEndSection": 313,
"text": "AC develops pulmonary metastasis in about one third of the patients and reveals a poor prognosis"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32712102",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 313,
"text": "Ameloblastomas are benign but locally invasive neoplasms which may grow to massive proportions and cause significant morbidity. Although some types of ameloblastoma can be treated predictably with aggressive surgical treatment, recurrent ameloblastoma and metastasising ameloblastoma are still difficult to treat."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21558899",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 82,
"text": "Ameloblastoma of the maxilla is a rare odontogenic tumor that rarely metastasizes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18230377",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 99,
"text": "Ameloblastoma is an odontogenic tumor, usually benign, which rarely metastasizes to distant organs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24374844",
"endSection": "abstract",
"offsetInBeginSection": 73,
"offsetInEndSection": 218,
"text": "Although ameloblastomas rarely metastasise, recurrences together with radical surgery often result in facial deformity and significant morbidity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28944145",
"endSection": "abstract",
"offsetInBeginSection": 74,
"offsetInEndSection": 224,
"text": "The World Health Organization (WHO) has defined malignant ameloblastoma (MA) as a histologically benign-appearing ameloblastoma that has metastasized."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23775022",
"endSection": "abstract",
"offsetInBeginSection": 102,
"offsetInEndSection": 250,
"text": "Distant metastasis is a very rare condition and is designated as metastasizing (malignant) ameloblastoma despite its benign histological appearance."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6575436",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 127,
"text": "Ameloblastoma is a locally invasive, histologically nonmalignant tumor that may on very rare occasions give rise to metastases."
}
]
| 11 | BioASQ-training11b | null | null | 622901d23a8413c65300008c | 306 |
yesno | Does Uc.160 promote cancer? | ['no'] | [
"no"
]
| ['No. Uc.160+ is a T-UCR reported to be downregulated in human cancer. In addition, Uc.160+ could possibly have a tumor suppressive role in gastric cancer.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/28382457",
"http://www.ncbi.nlm.nih.gov/pubmed/20802525"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28382457",
"endSection": "abstract",
"offsetInBeginSection": 245,
"offsetInEndSection": 1592,
"text": "We previously discovered the downregulation of T-UCR expression in gastric cancer (GC), indicating that T-UCRs could play an important role in GC biology. Uc.160+, a T-UCR reported to be downregulated in human cancer, has not been examined in GC.METHODS: We analyzed the expression pattern of Uc.160+ in nonneoplastic and tumor tissues of the stomach by using uantitative reverse transcription polymerase chain reaction (qRT-PCR) and in situ hybridization (ISH), specifically focusing on the mechanism of transcriptional regulation and target genes that are regulated by T-UCRs. We also attempted to determine the effect of Uc.160+ expression on biological features of GC cell lines by Western blotting.RESULTS: On the basis of the qRT-PCR and ISH results, Uc.160+ expression in adenoma and GC tissues was clearly downregulated compared with that in nonneoplastic mucosa tissues of the stomach. Cancer-specific DNA methylation in the promoter region of Uc.160 was observed by bisulfite genomic DNA sequencing analysis. The effect of DNA methylation on Uc.160+ expression was further confirmed by reporter gene assay. We also revealed that Uc.160+ inhibited the phosphorylation of Akt by regulating phosphatase and tensin homolog (PTEN) expression.CONCLUSIONS: These results indicate that Uc.160+ could possibly have a tumor suppressive role in GC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28382457",
"endSection": "abstract",
"offsetInBeginSection": 407,
"offsetInEndSection": 841,
"text": "Uc.160+, a T-UCR reported to be downregulated in human cancer, has not been examined in GC.<br><b>METHODS</b>: We analyzed the expression pattern of Uc.160+ in nonneoplastic and tumor tissues of the stomach by using uantitative reverse transcription polymerase chain reaction (qRT-PCR) and in situ hybridization (ISH), specifically focusing on the mechanism of transcriptional regulation and target genes that are regulated by T-UCRs."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28382457",
"endSection": "abstract",
"offsetInBeginSection": 1391,
"offsetInEndSection": 1636,
"text": "We also revealed that Uc.160+ inhibited the phosphorylation of Akt by regulating phosphatase and tensin homolog (PTEN) expression.<br><b>CONCLUSIONS</b>: These results indicate that Uc.160+ could possibly have a tumor suppressive role in GC.<br>"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28382457",
"endSection": "abstract",
"offsetInBeginSection": 842,
"offsetInEndSection": 1168,
"text": "We also attempted to determine the effect of Uc.160+ expression on biological features of GC cell lines by Western blotting.<br><b>RESULTS</b>: On the basis of the qRT-PCR and ISH results, Uc.160+ expression in adenoma and GC tissues was clearly downregulated compared with that in nonneoplastic mucosa tissues of the stomach."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28382457",
"endSection": "abstract",
"offsetInBeginSection": 1498,
"offsetInEndSection": 1597,
"text": "CONCLUSIONS These results indicate that Uc.160+ could possibly have a tumor suppressive role in GC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28382457",
"endSection": "abstract",
"offsetInBeginSection": 399,
"offsetInEndSection": 490,
"text": "Uc.160+, a T-UCR reported to be downregulated in human cancer, has not been examined in GC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20802525",
"endSection": "abstract",
"offsetInBeginSection": 1280,
"offsetInEndSection": 1494,
"text": "Among the T-UCRs that were reactivated upon drug treatment, Uc.160+, Uc283+A and Uc.346+ were found to undergo specific CpG island hypermethylation-associated silencing in cancer cells compared with normal tissues."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28382457",
"endSection": "abstract",
"offsetInBeginSection": 388,
"offsetInEndSection": 479,
"text": "Uc.160+, a T-UCR reported to be downregulated in human cancer, has not been examined in GC."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28382457",
"endSection": "abstract",
"offsetInBeginSection": 1465,
"offsetInEndSection": 1553,
"text": "These results indicate that Uc.160+ could possibly have a tumor suppressive role in GC.."
}
]
| 11 | BioASQ-training11b | [
"http://www.disease-ontology.org/api/metadata/DOID:162",
"https://meshb.nlm.nih.gov/record/ui?ui=D009369"
]
| null | 5a6d2558b750ff4455000036 | 307 |
yesno | Is Apelin usually decreased in diabetes? | ['no'] | [
"no"
]
| ['Different studies in both animals and humans have shown that plasma apelin concentrations are usually increased during obesity and type 2 diabetes.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/19756893",
"http://www.ncbi.nlm.nih.gov/pubmed/25914650",
"http://www.ncbi.nlm.nih.gov/pubmed/29229313",
"http://www.ncbi.nlm.nih.gov/pubmed/24721640"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25914650",
"endSection": "abstract",
"offsetInBeginSection": 558,
"offsetInEndSection": 816,
"text": "Apelin has been shown to act on glucose and lipid metabolism but also to modulate insulin secretion. Moreover, different studies in both animals and humans have shown that plasma apelin concentrations are usually increased during obesity and type 2 diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29229313",
"endSection": "abstract",
"offsetInBeginSection": 630,
"offsetInEndSection": 791,
"text": "Upregulated expression of resistin, vaspin, apelin and TNF-α plays a significant role in induction of insulin resistance linked with obesity and type 2 diabetes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25914650",
"endSection": "abstract",
"offsetInBeginSection": 659,
"offsetInEndSection": 816,
"text": "Moreover, different studies in both animals and humans have shown that plasma apelin concentrations are usually increased during obesity and type 2 diabetes."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19756893",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 85,
"text": "Apelin levels are increased in morbidly obese subjects with type 2 diabetes mellitus."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24721640",
"endSection": "abstract",
"offsetInBeginSection": 1217,
"offsetInEndSection": 1593,
"text": "In men at risk for diabetes (HbA1c 5.7-6.4%, FPG 100-125mg/dl, or OGTT-2h-PG 140-199mg/dl), the risk for developing diabetes was higher in those with higher plasma apelin concentration than in those with lower plasma apelin concentrations (10.6%/year vs. 5.1%/year, p<0.001).<br><b>CONCLUSIONS</b>: Plasma apelin is a novel biomarker for predicting type 2 diabetes in men.<br>"
}
]
| 11 | BioASQ-training11b | null | null | 5caa0806ecadf2e73f000057 | 308 |
yesno | Are psammoma bodies characteristic to meningiomas? | ['yes'] | [
"yes"
]
| ['Yes, psammoma bodies are commonly seen and are characteristic to meningiomas. However, they can be also present in other types of tumors or non-neoplastic tissues.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/19373908",
"http://www.ncbi.nlm.nih.gov/pubmed/10396741",
"http://www.ncbi.nlm.nih.gov/pubmed/8712177",
"http://www.ncbi.nlm.nih.gov/pubmed/8727067",
"http://www.ncbi.nlm.nih.gov/pubmed/8629394",
"http://www.ncbi.nlm.nih.gov/pubmed/7487408",
"http://www.ncbi.nlm.nih.gov/pubmed/8162148",
"http://www.ncbi.nlm.nih.gov/pubmed/8336812",
"http://www.ncbi.nlm.nih.gov/pubmed/1492779",
"http://www.ncbi.nlm.nih.gov/pubmed/1630573",
"http://www.ncbi.nlm.nih.gov/pubmed/2168257",
"http://www.ncbi.nlm.nih.gov/pubmed/3736772",
"http://www.ncbi.nlm.nih.gov/pubmed/3776472",
"http://www.ncbi.nlm.nih.gov/pubmed/3020860",
"http://www.ncbi.nlm.nih.gov/pubmed/7015802",
"http://www.ncbi.nlm.nih.gov/pubmed/6699695"
]
| [
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19373908",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 267,
"text": "Psammoma bodies (PBs) are concentric lamellated calcified structures, observed most commonly in papillary thyroid carcinoma (PTC), meningioma, and papillary serous cystadenocarcinoma of ovary but have rarely been reported in other neoplasms and nonneoplastic lesions."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19373908",
"endSection": "sections.0",
"offsetInBeginSection": 668,
"offsetInEndSection": 863,
"text": "Studies on serous cystadenocarcinoma of ovary and meningioma, however, revealed that collagen production by neoplastic cells and subsequent calcification was responsible for the formation of PBs."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19373908",
"endSection": "sections.0",
"offsetInBeginSection": 864,
"offsetInEndSection": 1163,
"text": "The existence of some precursor forms of PBs was reported in meningiomas and more recently in PTC, which were mostly in the form of extracellular hyaline globules surrounded by well-preserved neoplastic cells or in a smaller number of cases intracytoplasmic bodies liberated from intact tumor cells."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/10396741",
"endSection": "sections.0",
"offsetInBeginSection": 1315,
"offsetInEndSection": 1677,
"text": "Light microscopy revealed abundant microcysts of varied size throughout the tumor tissue with the presence of whorl formation and psammoma body, but no malignancy was indicated. Electron microscopy further demonstrated interdigitation of the neighboring cell membranes, desmosomes, and intracytoplasmic filaments, which are pathognomonic findings of meningiomas."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8712177",
"endSection": "sections.0",
"offsetInBeginSection": 1197,
"offsetInEndSection": 1531,
"text": "Unlike SFT, FMs were glycogen-containing and variously exhibited a storiform pattern (13 of 20), psammoma body formation (9 of 20), and calcification of collagen (4 of 20). Immunoreactivities included vimentin (100%), focal to patchy EMA (80%), S-100 protein (80%), collagen IV (25%), and patchy, mild-to-moderate CD34 staining (60%)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8727067",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 118,
"text": "In contrast to the inner structure, three-dimensional structure of psammona bodies in meningiomas is not well defined."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8727067",
"endSection": "sections.0",
"offsetInBeginSection": 119,
"offsetInEndSection": 337,
"text": "This study examined three cultured meningiomas, in which surface observation of psammoma bodies might be easier than in the tumor tissues since influence of interposing connective tissue is minimized in tissue culture."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8727067",
"endSection": "sections.0",
"offsetInBeginSection": 941,
"offsetInEndSection": 1284,
"text": "The results suggest that psammoma bodies in meningiomas arise in part from meningothelial whorls due to collagen production by tumor cells followed by obliteration and disappearance of tumor cell processes, although some of the alternative pathways for psammoma body formation proposed by other investigators cannot be ruled out by this study."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8629394",
"endSection": "sections.0",
"offsetInBeginSection": 11,
"offsetInEndSection": 105,
"text": "To demonstrate that psammoma bodies in human meningiomas contain type VI collagen and laminin."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8629394",
"endSection": "sections.0",
"offsetInBeginSection": 690,
"offsetInEndSection": 818,
"text": "This is the first report to describe the involvement of type VI collagen in psammoma bodies and whorl formations in meningiomas."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8162148",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 152,
"text": "Calcification such as psammoma body is sometimes found especially in spinal cord meningioma but ossification of the meningeal tumor was rarely observed."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8336812",
"endSection": "sections.0",
"offsetInBeginSection": 603,
"offsetInEndSection": 673,
"text": "Histological diagnosis was transitional meningioma with psammoma body."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1492779",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 386,
"text": "In this study we analyzed the morphologic and ultrastructural characteristics of the psammoma bodies in ten meningiomas of different histologic subtypes, characterizing the components of the psammoma body and the elements of the tumor, such as the capillaries and degenerative cells that have been classically considered as initiators of the formation of these calcareous is structures."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1492779",
"endSection": "sections.0",
"offsetInBeginSection": 735,
"offsetInEndSection": 979,
"text": "It is concluded that the mineralization of the psammoma bodies is induced principally by the collagen fibers synthesized by the meningocytes and that the form of mineralization is spherical and growth is radial, controlled by the tumoral cells."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/1630573",
"endSection": "sections.0",
"offsetInBeginSection": 495,
"offsetInEndSection": 610,
"text": "CSF cytology revealed benign fibroblastic or meningotheliomatous meningioma with whorl formation and psammoma body."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/2168257",
"endSection": "sections.0",
"offsetInBeginSection": 568,
"offsetInEndSection": 743,
"text": "Electron microscopic examination of the calculi showed membrane-bound vesicles and radially precipitated crystals that simulated hydroxyapatite of psammoma body in meningioma."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3736772",
"endSection": "sections.0",
"offsetInBeginSection": 1215,
"offsetInEndSection": 1291,
"text": "Psammoma bodies in meningiomas resembled those in the choroid plexus stroma."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3736772",
"endSection": "sections.0",
"offsetInBeginSection": 1431,
"offsetInEndSection": 1626,
"text": "The results of this study suggest that psammoma bodies in the choroid plexus, as in meningiomas, form by a process of dystrophic calcification associated with arachnoid cells and collagen fibres."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3776472",
"endSection": "sections.0",
"offsetInBeginSection": 257,
"offsetInEndSection": 384,
"text": "An early stage of psammoma body formation was seen more frequently in these villous microcores than in the meningocytic whorls."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3020860",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 80,
"text": "Psammoma bodies in meningocytic whorls were investigated by electron microscopy."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/3020860",
"endSection": "sections.0",
"offsetInBeginSection": 800,
"offsetInEndSection": 1011,
"text": "Psammoma body formation in the meningocytic whorls may represent degeneration in some whorls of the central cells which contain connective tissue fibers, producing cell debris such as membrane invested vesicles."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7015802",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 293,
"text": "Twenty human meningiomas were examined for IgG and IgM by the direct immunofluorescence of immunoperoxidase methods, or both. IgG was conspicuously found in and around the blood vessels, whorls, and psammoma bodies. It was also clearly present on the cytoplasmic membranes of the tumour cells."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7015802",
"endSection": "sections.0",
"offsetInBeginSection": 357,
"offsetInEndSection": 514,
"text": "Significance of these findings is briefly discussed including possible humoral immune reactions in regard to whorl and psammoma body formation in meningioma."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6699695",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 92,
"text": "The fine structure of psammoma bodies was examined in four cases of fibroblastic meningioma."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6699695",
"endSection": "sections.0",
"offsetInBeginSection": 93,
"offsetInEndSection": 216,
"text": "In general, large numbers of various-sized calcified bodies (psammoma bodies) were scattered among the interstitial fibers."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/6699695",
"endSection": "sections.0",
"offsetInBeginSection": 1130,
"offsetInEndSection": 1293,
"text": "These findings suggest that both matrix giant bodies and matrix vesicles may serve as initial nidus of calcification of psammoma bodies in fibroblastic meningioma."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/7487408",
"endSection": "sections.0",
"offsetInBeginSection": 987,
"offsetInEndSection": 1114,
"text": "Psammoma body formation or dystrophic mineralization and gliosis of the intervening parenchyma was observed in all three cases."
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D008579",
"http://www.disease-ontology.org/api/metadata/DOID:3565",
"http://www.disease-ontology.org/api/metadata/DOID:7210",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D002479"
]
| null | 514a4679d24251bc0500005b | 309 |
yesno | Is imatinib an antidepressant drug? | ['no'] | [
"no"
]
| ['No. Imatinib is a tyrosine-kinase inhibitor used in the treatment of multiple cancers, most notably Chronic myelogenous leukemia (CML) and Gastrointestinal stromal tumor (GIST).'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22678007",
"http://www.ncbi.nlm.nih.gov/pubmed/22593820",
"http://www.ncbi.nlm.nih.gov/pubmed/22484890",
"http://www.ncbi.nlm.nih.gov/pubmed/22460758",
"http://www.ncbi.nlm.nih.gov/pubmed/22135725",
"http://www.ncbi.nlm.nih.gov/pubmed/22110503",
"http://www.ncbi.nlm.nih.gov/pubmed/22035758",
"http://www.ncbi.nlm.nih.gov/pubmed/21938530",
"http://www.ncbi.nlm.nih.gov/pubmed/21087500",
"http://www.ncbi.nlm.nih.gov/pubmed/21073206",
"http://www.ncbi.nlm.nih.gov/pubmed/20726677",
"http://www.ncbi.nlm.nih.gov/pubmed/20676553",
"http://www.ncbi.nlm.nih.gov/pubmed/20442314",
"http://www.ncbi.nlm.nih.gov/pubmed/20407930",
"http://www.ncbi.nlm.nih.gov/pubmed/19628568",
"http://www.ncbi.nlm.nih.gov/pubmed/19110398",
"http://www.ncbi.nlm.nih.gov/pubmed/18506179",
"http://www.ncbi.nlm.nih.gov/pubmed/17554495",
"http://www.ncbi.nlm.nih.gov/pubmed/16566359",
"http://www.ncbi.nlm.nih.gov/pubmed/16403813",
"http://www.ncbi.nlm.nih.gov/pubmed/15966213",
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"text": "Gastrointestinal stromal tumor (GIST) is the most common mesenchymal tumor of the gastrointestinal tract. Surgery remains the elective treatment. We retrospectively compared two group of patients, who underwent surgery for GIST before and after Imatinib advent in order to analyze the recurrence and survival rate."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/22831984",
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"text": "Adjuvant imatinib 400 mg/day for 3 years duration is a standard treatment in all patients with significant risk of recurrence following resection of primary GISTs"
},
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"text": "R1 surgery (versus R0) alone is not an indication for adjuvant imatinib in low-risk GIST."
},
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"text": "Treatment is not recommended in an imatinib-insensitive D842V-mutated GIST"
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"text": "Prognostic factors such as tumor size, mitotic rate and presence of metastases may provide an indication for adjuvant imatinib mesylate (IM) treatment. Here we present a young patient with a large GIST with high-risk features who is in complete remission after surgical excision and adjuvant IM treatment. This patient is the only colon-located CD117-positive case where IM was administered."
},
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/22460758",
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"text": "Imatinib mesylate is the sole BCR-ABL tyrosine kinase inhibitor approved as first-line treatment of accelerated-phase (AP) chronic myeloid leukemia (CML)."
},
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"text": "imatinib mesylate could be a therapeutic target of strategies against osteosarcoma tumors."
},
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"text": "Allogeneic hematopoietic stem cell transplantation (HSCT) is well-established as a potentially curative treatment for patients who have chronic myeloid leukemia. The success of imatinib and other tyrosine kinase inhibitors (TKI) as initial therapy has changed the treatment paradigm for this disease."
},
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"text": "Imatinib plus hydroxyurea is well tolerated among patients with meningioma but has modest anti-tumor activity for this indication."
},
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"text": "Ki67 correlated with time to recurrence (p=0.022). Ki67 >11% was taken as the indication to start imatinib chemotherapy (sensitivity 61.5%, specificity 92.0%, p=0.022)."
},
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"text": "Significant pharmacokinetic interactions have already been shown between St. John's Wort (SJW) and the anticancer drugs imatinib and irinotecan."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/21073206",
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"text": "for CML we analysed imatinib, dasatinib and nilotinib."
},
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"endSection": "sections.0",
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"text": "Imatinib mesylate, an orally administered kinase inhibitor that targets the Kit (CD117) protein, currently has 10 approved indications including treatment of chronic myelogenous leukemia and metastatic gastrointestinal stromal tumors (GIST)."
},
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"offsetInBeginSection": 539,
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"text": "The drugs were assessed according to clinical evidence on efficacy and safety, based on Micromedex categorization, on systematic reviews and meta-analyses. Indications present in the legal documentation were compared to the indications approved by regulatory agencies. RESULTS: Bevacizumab, capecitabine, cetuximab, erlotinib, rituximab, imatinib, and temozolomide"
},
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/20442314",
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"offsetInBeginSection": 540,
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"text": "Bcr-Abl, an oncogene responsible for CML"
},
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"text": "Bcr-Abl-expressing cells showed resistance to death activated by spindle defects, reversed by imatinib."
},
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"text": "Imatinib, an oral tyrosine kinase inhibitor (TKI), is first-line treatment in patients with metastatic or unresectable GIST."
},
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"text": "Surgical indication for metastatic gastrointestinal stromal tumor (GIST) treated with imatinib is not yet established."
},
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"text": "Surgery of residual disease upon best clinical response seems associated with survival benefit compared with historical controls in similar patient collectives treated with imatinib alone."
},
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"text": "To explore the effect of preoperative imatinib mesylate (IM) in patients with unresectable or locally advanced primary gastrointestinal stromal tumor (GIST)"
},
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"text": "The patient had been diagnosed 14 months earlier and had been submitted to surgery, followed by adjuvant radiotherapy and temozolomide-based chemotherapy. On clinical suspicion of recurrence 5 months later, magnetic resonance imaging (MRI) revealed a lesion at the site of preceded surgery, which was treated by imatinib mesylate"
},
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"text": "Radical surgery remains the most effective method of GIST treatment. In inoperable/metastatic lesion the treatment of choice is tyrosinase kinase inhibitor--imatinib."
},
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"text": "Imatinib mesylate (STI571), a specific Bcr-Abl inhibitor, has shown a potent antileukemic activity in clinical studies of chronic myeloid leukemia (CML) patients."
},
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"text": "Imatinib, an inhibitor of the tyrosine kinase activity of c-kit, was used as an adjuvant chemotherapy in two patients who underwent curative surgery for recurrent gastrointestinal stromal tumors."
},
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"text": "Gastrointestinal stromal tumor (GIST) is the most common mesenchymal tumor of the gastrointestinal tract. Surgery remains the elective treatment. We retrospectively compared two group of patients, who underwent surgery for GIST before and after Imatinib advent in order to analyze the recurrence and survival rate."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22831984",
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"text": "Adjuvant imatinib 400 mg/day for 3 years duration is a standard treatment in all patients with significant risk of recurrence following resection of primary GISTs."
}
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| 51542e84d24251bc05000083 | 311 |
yesno | Should UGT1A1 alteration be routinely determined in colorectal cancer patients? | ['yes'] | [
"yes"
]
| ['Yes, UGT1A1 alteration should be routinely determined in colorectal cancer patients.The UGT1A1 gene is a potential biomarker for colorectal cancer diagnosis and prognosis.The UGT1A1 gene is a potential biomarker for colorectal cancer diagnosis and prognosis.The UGT1A1 gene is a potential biomarker for colorectal cancer diagnosis and prognosis.The UGT1A1 gene is a potential biomarker for colorectal cancer diagnosis and prognosis.The UGT1A1 gene is a potential biomarker for colorectal cancer diagnosis and prognosis.The UGT1A1 gene is a potential biomarker for colorectal cancer diagnosis and prognosis.The UGT1A1 gene is a potential biomarker for colorectal cancer diagnosis and prognosis.The UGT1A1 gene is a potential biomarker for colorectal cancer diagnosis and prognosis.The UGT1A1 gene is a potential biomarker for colorectal cancer diagnosis and prognosis.The UGT1A1 gene is a potential biomarker for colorectal cancer diagnosis and prognosis.The UGT1A1 gene is a potential biomarker for colorectal cancer diagnosis and prognosis.The UGT1A1 gene is a potential biomarker for colorectal cancer diagnosis and prognosis.The UGT1A1 gene is a potential biomarker for colorectal cancer diagnosis and prognosis.The UGT1A1 gene is a potential biomarker for colorectal cancer diagnosis and prognosis.The UGT1A1 gene is a potential biomarker for colorectal cancer diagnosis and prognosis.The UGT1A1 gene is a potential biomarker for colorectal cancer diagnosis and prognosis.The UGT1', 'Yes, determining UGT1A1 alterations should be considered routinely in colorectal cancer patients, especially before administering irinotecan-based chemotherapy. This is because variations in the UGT1A1 gene, particularly UGT1A1*28, can significantly affect how a patient metabolizes irinotecan, potentially leading to increased toxicity. Testing for these genetic variations can help tailor treatment plans to individual patients, enhancing both the efficacy and safety of the therapy', 'Yes, determining UGT1A1 alterations should be routinely done in colorectal cancer patients, especially considering the impact of UGT1A1*6 and UGT1A1*28 on the toxicity and efficacy of irinotecan-based treatments. The examination of other UGT1A loci beyond these two does not significantly improve the predictive value for these outcomes.', 'Based on the provided snippet, routine determination of UGT1A1 alterations beyond UGT1A1*6 and UGT1A1*28 may not significantly improve the prediction of irinotecan-based toxicity and efficacy in colorectal cancer patients. This suggests that testing for these specific alleles could be sufficient for risk stratification and personalized treatment planning. However, it is important to note that this conclusion is based on the examination of certain UGT1A loci only and may not exclude the potential relevance of other UGT1A alterations. Therefore, further research is needed to comprehensively evaluate the clinical utility of UGT1A1 genotyping in colorectal cancer management.', 'The question of whether UGT1A1 alteration should be routinely determined in colorectal cancer patients is a complex one. On the one hand, identifying patients with the UGT1A1*28 allele could help prevent severe neutropenia and potentially life-threatening side effects associated with irinotecan treatment. This could lead to improved outcomes and reduced healthcare costs. However, the cost of genetic testing and the potential for false negatives or false positives must also be considered. Additionally, the clinical utility of UGT1A1 genotyping is still uncertain, and there is a lack of prospective studies examining the effectiveness of modifying irinotecan regimens based on UGT1A1 genotype. Therefore, it is unclear whether UGT1A1 alteration should be routinely determined in colorectal cancer patients. Further research is needed to determine the benefits and harms of UGT1', 'Yes, UGT1A1 alteration should be routinely determined in colorectal cancer patients.', "According to the American Society of Clinical Oncology (ASCO) and the National Comprehensive Cancer Network (NCCN), no, UGT1A1 alteration should not be routinely determined in colorectal cancer patients. However, some healthcare providers and institutions may offer this testing on a case-by-case basis for patients with a history of severe toxicity or those receiving high-dose irinotecan. It is recommended to consult with a healthcare provider or a genetic counselor to determine if UGT1A1 genotyping is appropriate for a specific patient's situation.", 'Yes, a UGT1A1 test should be performed in colorectal cancer patients prior to treatment with irinotecan.', 'The decision of whether to routinely determine UGT1A1 alterations in colorectal cancer patients for predicting irinotecan-based toxicity and efficacy is still a subject of debate in the medical community. While the UGT1A1*6 and UGT1A1*28 variants have been associated with irinotecan-induced toxicity, the clinical utility of routinely testing for these variants is not yet clear.\n\nA meta-analysis published in the Journal of Clinical Oncology in 2019 found that UGT1A1*6 and UGT1A1*28 variants were significantly associated with increased risk of irinotecan-induced neutropenia and diarrhea, but the clinical significance of this finding is still uncertain. The authors', 'UGT1A1 alteration should be routinely determined in colorectal cancer patients, especially those undergoing treatment with irinotecan, as it can help predict the risk of severe toxicity such as neutropenia. Identifying UGT1A1 alterations can guide personalized dosing strategies and improve treatment outcomes by reducing the likelihood of adverse reactions to irinotecan therapy.', "The UGT1A1*6 and UGT1A1*28 alterations have been shown to be predictive of irinotecan-based toxicity and efficacy in colorectal cancer patients. However, an examination of other UGT1A loci did not improve the predictive value. Therefore, it may not be necessary to routinely determine UGT1A1 alterations other than *6 and *28 in colorectal cancer patients. It is important to note that this is a complex issue and the decision to test for UGT1A1 alterations should be individualized based on the patient's specific circumstances and the availability of alternative treatment options.", 'Yes, UGT1A1 alteration should be routinely determined in colorectal cancer patients.UGT1A1 is a critical enzyme involved in the metabolism of many drugs, including chemotherapeutics, and genetic variations in UGT1A1 have been associated with altered drug metabolism and response. Therefore, determining UGT1A1 alterations in colorectal cancer patients may help guide personalized medicine approaches, including drug selection and dosing.Additionally, UGT1A1 has been implicated in the development and progression of colorectal cancer, and alterations in UGT1A1 may be associated with poorer prognosis. Therefore, determining UGT1A1 alterations in colorectal cancer patients may help identify patients at high risk of recurrence or metastasis.In summary, UGT1A1 alteration should be routinely determined in colorectal cancer patients to help guide personalized medicine approaches and improve patient outcomes.', 'Yes, UGT1A1 alteration should be routinely determined in colorectal cancer patients. The presence of the UGT1A1*28 allele is associated with a higher risk of adverse effects and reduced efficacy of irinotecan-based therapy. Routine genotyping of UGT1A1 can help to identify patients who are at risk of adverse effects and optimize their treatment.', 'Based on the current evidence, routine determination of UGT1A1 alteration in colorectal cancer patients is recommended. UGT1A1 polymorphisms, such as UGT1A1*28 and UGT1A1*6, have been associated with increased risk of irinotecan-induced toxicity, including severe hematological toxicity. Several studies have shown that patients with the UGT1A1*28 7/7 genotype have a higher risk of hematological toxicity, increased hospitalization rates, and lower overall survival when treated with irinotecan. Therefore, determining UGT1A1 alteration can help identify patients who may be at higher risk of adverse effects from irinotecan therapy and guide personalized treatment decisions.', 'No, UGT1A1 alteration should not be routinely determined in colorectal cancer patients.', "Yes, routine determination of UGT1A1 alterations is recommended for colorectal cancer patients who are candidates for treatment with irinotecan-based chemotherapy. This is because genetic polymorphisms in the UGT1A1 gene can significantly affect a patient's ability to metabolize and tolerate irinotecan, leading to increased toxicity or reduced efficacy of the drug. The most common polymorphism, UGT1A1*28, has been associated with decreased glucuronidation activity and an increased risk of severe neutropenia when standard doses of irinotecan are used. Patients who are heterozygous for this allele or have other variants known to affect drug metabolism may benefit from dose reduction or alternative treatment strategies to optimize safety and efficacy.", 'The decision of whether to routinely determine UGT1A1 alterations in colorectal cancer patients for predicting irinotecan-based toxicity and efficacy is still a subject of debate in the medical community. While the UGT1A1*6 and UGT1A1*28 variants have been associated with increased risk of irinotecan-induced toxicity, particularly neutropenia and diarrhea, the clinical utility of routine UGT1A1 genotyping is not yet established.\n\nA meta-analysis published in the Journal of Clinical Oncology in 2019 found that UGT1A1 genotyping could improve the prediction of irinotecan-induced toxicity, particularly in Asian populations. However, the authors noted that the clinical significance of this finding is still uncertain, as the majority of studies included in the meta-analysis were retrospective and had small sample sizes.\n\nIn a 2020 review published in the Journal of Gastrointestinal Oncology, the authors concluded that UGT1A1 genotyping should be considered in patients with a history of severe ir', "According to the current guidelines from the Food and Drug Administration (FDA) of the United States, UGT1A1 alteration should be routinely determined in colorectal cancer patients receiving irinotecan, a chemotherapy drug commonly used in the treatment of colorectal cancer. However, the clinical significance of UGT1A1 testing in colorectal cancer patients receiving other chemotherapy agents, such as 5-fluorouracil (5-FU), is less clear and requires further investigation. Therefore, it is recommended to consult with a healthcare provider or a genetic counselor to determine if UGT1A1 genotyping is appropriate for a specific patient's situation. In summary, UGT1A1 alteration should be routinely determined in colorectal cancer patients receiving irinotecan, but the decision to test for UGT1A1 alteration in patients receiving other chemotherapy agents is still a subject of debate among healthcare professionals.", 'no, examining more UGT1A loci beyond UGT1A1*6 and UGT1A1*28 does not improve the predictive value of irinotecan-based toxicity and efficacy in colorectal cancer patients.', 'The determination of UGT1A1 alteration in colorectal cancer patients is not currently a routine test. However, it may be considered in certain cases, such as patients with metastatic disease who are being considered for irinotecan-based chemotherapy. This is because UGT1A1 alterations can lead to an increased risk of irinotecan-induced toxicity. However, the clinical utility of UGT1A1 testing in colorectal cancer patients is still a topic of ongoing research and debate. It is important to consult with a healthcare provider to determine the most appropriate course of action for an individual patient.', 'Yes, UGT1A1 alteration should be routinely determined in colorectal cancer patients because it is associated with aggressive behavior and poor outcome.', 'Yes, UGT1A1 alteration should be routinely determined in colorectal cancer patients because it is associated with aggressive behavior of the cancer and it is a marker of poor prognosis.', 'Yes, UGT1A1 alteration should be routinely determined in colorectal cancer patients. UGT1A1 is a critical enzyme involved in the metabolism of many chemotherapeutic agents, including capecitabine and oxaliplatin, which are commonly used in the treatment of colorectal cancer. UGT1A1 alterations have been associated with altered drug metabolism and response, and may impact treatment outcomes. Therefore, determining UGT1A1 status in colorectal cancer patients may help guide personalized treatment strategies and improve patient outcomes.', 'No. The Evaluation of Genomic Applications in Practice and Prevention (EGAPP) Working Group found that the evidence is currently insufficient to recommend for or against the routine use of UGT1A1 genotyping in patients with metastatic colorectal cancer who are to be treated with irinotecan, with the intent of modifying the dose as a way to avoid adverse drug reactions (severe neutropenia).', 'The study suggests that UGT1A1*6 and UGT1A1*28 are associated with an increased risk of severe neutropenia in Chinese patients with metastatic colorectal cancer (mCRC) treated with irinotecan-based chemotherapy. However, the study also found that examining more UGT1A loci did not improve the predictive value of irinotecan-based toxicity and efficacy. Therefore, it is unclear whether UGT1A1 alteration should be routinely determined in colorectal cancer patients. Further research is needed to confirm these findings and determine the clinical utility of UGT1A1 genotyping in this patient population.', 'Determining UGT1A1 alterations might be helpful in predicting irinotecan toxicity in colorectal cancer patients, but their clinical relevance in gastric cancer patients is currently unclear.', 'yes, determining UGT1A1 alterations should be routinely done in colorectal cancer patients, especially considering the impact of UGT1A1*6 and UGT1A1*28 on the toxicity and efficacy of irinotecan-based treatments. The examination of additional UGT1A loci beyond these two does not significantly improve the predictive value for irinotecan-related outcomes.', 'No, UGT1A1 alteration should not be routinely determined in colorectal cancer patients, as it does not significantly improve the predictive value of irinotecan-based toxicity and efficacy.', 'Yes, UGT1A1 alteration should be determined in all coloreectal cancer patients. This is because UGTP is an essential co-factor for the synthesis of viral hemagens, which are used as a proxy for viral infection. UGTP is also involved in the metabolism of various drugs, including those used in the treatment of coloreectal cancer. ', 'Based on the provided information, it appears that examining additional UGT1A loci beyond UGT1A1*6 and UGT1A1*28 does not significantly improve the predictive value of irinotecan-based toxicity and efficacy in colorectal cancer patients. Therefore, routine determination of UGT1A1 alterations may not be necessary for all colorectal cancer patients receiving irinotecan treatment. However, it is important to note that this conclusion is based on the specific studies mentioned and does not rule out the potential value of genetic testing in certain clinical contexts or patient populations. For personalized medicine approaches, further research is needed to determine if other genetic markers or combinations thereof could provide more accurate predictions of irinotecan response and toxicity.', 'Based on the provided information, examining more UGT1A loci beyond UGT1A1*6 and UGT1A1*28 was not helpful in improving the predictive value of irinotecan-based toxicity and efficacy in colorectal cancer patients. Therefore, routine determination of UGT1A1 alterations beyond *6 and *28 does not appear to be beneficial for guiding irinotecan therapy in this patient population. The abstract suggests focusing on UGT1A1*6 and *28 variants is sufficient. However, more context and additional studies would be needed to make a definitive recommendation on routine UGT1A1 testing in colorectal cancer.', 'An examination of more UGT1A loci, except for UGT1A1*6 and UGT1A1*28, was not helpful to improve the predictive value of irinotecan-based toxicity and efficacy.', 'Based on the available evidence, it is recommended that UGT1A1 alteration should be routinely determined in colorectal cancer patients receiving irinotecan-based therapy. This can help to determine the optimal dose of irinotecan and prevent hematologic and digestive toxicities, especially in patients who are homozygous for the UGT1A1*28 allele. However, it is important to note that testing for UGT1A1 alteration does not improve treatment efficacy, and its clinical utility remains uncertain due to the lack of prospective studies examining treatment options based on UGT1A1 genotype. Nevertheless, given the potential benefits and minimal harm associated with UGT1A1 testing, it is recommended as a routine practice in colorectal cancer patients receiving irinotecan-based therapy.', 'Yes, routine determination of UGT1A1 alteration should be considered in colorectal cancer patients. Although additional UGT1A loci beyond UGT1A1*6 and UGT1A1*28 do not improve the predictive value of irinotecan-based toxicity and efficacy, UGT1A1 alterations can still have clinical implications. UGT1A1 polymorphisms are associated with variable drug metabolism and can affect the response to irinotecan, a commonly used chemotherapy drug in colorectal cancer. Therefore, determining UGT1A1 alterations can help guide treatment decisions and optimize patient outcomes.', 'Yes, determining UGT1A1 alterations should be a standard practice for colorectal cancer patients.', 'Answer: The routine determination of UGT1A1 alteration in colorectal cancer patients is recommended to assess the risk of irinotecan-induced toxicities and guide personalized treatment decisions.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/25285015",
"http://www.ncbi.nlm.nih.gov/pubmed/25545261",
"http://www.ncbi.nlm.nih.gov/pubmed/16982469",
"http://www.ncbi.nlm.nih.gov/pubmed/25782327",
"http://www.ncbi.nlm.nih.gov/pubmed/35822291",
"http://www.ncbi.nlm.nih.gov/pubmed/21486535",
"http://www.ncbi.nlm.nih.gov/pubmed/33125947",
"http://www.ncbi.nlm.nih.gov/pubmed/25817555",
"http://www.ncbi.nlm.nih.gov/pubmed/24642571",
"http://www.ncbi.nlm.nih.gov/pubmed/19770637",
"http://www.ncbi.nlm.nih.gov/pubmed/21287524",
"http://www.ncbi.nlm.nih.gov/pubmed/34327766",
"http://www.ncbi.nlm.nih.gov/pubmed/19125128",
"http://www.ncbi.nlm.nih.gov/pubmed/19125129",
"http://www.ncbi.nlm.nih.gov/pubmed/30550693",
"http://www.ncbi.nlm.nih.gov/pubmed/33090402",
"http://www.ncbi.nlm.nih.gov/pubmed/23686699",
"http://www.ncbi.nlm.nih.gov/pubmed/33619631",
"http://www.ncbi.nlm.nih.gov/pubmed/37470120",
"http://www.ncbi.nlm.nih.gov/pubmed/18437170",
"http://www.ncbi.nlm.nih.gov/pubmed/28637434",
"http://www.ncbi.nlm.nih.gov/pubmed/17090741",
"http://www.ncbi.nlm.nih.gov/pubmed/25981652",
"http://www.ncbi.nlm.nih.gov/pubmed/26098842",
"http://www.ncbi.nlm.nih.gov/pubmed/36183220",
"http://www.ncbi.nlm.nih.gov/pubmed/37257181",
"http://www.ncbi.nlm.nih.gov/pubmed/30585257",
"http://www.ncbi.nlm.nih.gov/pubmed/16551870",
"http://www.ncbi.nlm.nih.gov/pubmed/23840132",
"http://www.ncbi.nlm.nih.gov/pubmed/37932443",
"http://www.ncbi.nlm.nih.gov/pubmed/32264830",
"http://www.ncbi.nlm.nih.gov/pubmed/26591441",
"http://www.ncbi.nlm.nih.gov/pubmed/22559977",
"http://www.ncbi.nlm.nih.gov/pubmed/33877904",
"http://www.ncbi.nlm.nih.gov/pubmed/35356222",
"http://www.ncbi.nlm.nih.gov/pubmed/26830078",
"http://www.ncbi.nlm.nih.gov/pubmed/24439671",
"http://www.ncbi.nlm.nih.gov/pubmed/16641252",
"http://www.ncbi.nlm.nih.gov/pubmed/27072236",
"http://www.ncbi.nlm.nih.gov/pubmed/36308049",
"http://www.ncbi.nlm.nih.gov/pubmed/36239106",
"http://www.ncbi.nlm.nih.gov/pubmed/23386248",
"http://www.ncbi.nlm.nih.gov/pubmed/28502040",
"http://www.ncbi.nlm.nih.gov/pubmed/16965601",
"http://www.ncbi.nlm.nih.gov/pubmed/18594531",
"http://www.ncbi.nlm.nih.gov/pubmed/32829105",
"http://www.ncbi.nlm.nih.gov/pubmed/19450125",
"http://www.ncbi.nlm.nih.gov/pubmed/15280927",
"http://www.ncbi.nlm.nih.gov/pubmed/37802427",
"http://www.ncbi.nlm.nih.gov/pubmed/23236239",
"http://www.ncbi.nlm.nih.gov/pubmed/32357899",
"http://www.ncbi.nlm.nih.gov/pubmed/19859999",
"http://www.ncbi.nlm.nih.gov/pubmed/30538568",
"http://www.ncbi.nlm.nih.gov/pubmed/30583998",
"http://www.ncbi.nlm.nih.gov/pubmed/17184208",
"http://www.ncbi.nlm.nih.gov/pubmed/17510208",
"http://www.ncbi.nlm.nih.gov/pubmed/34860573",
"http://www.ncbi.nlm.nih.gov/pubmed/28474802",
"http://www.ncbi.nlm.nih.gov/pubmed/26692528",
"http://www.ncbi.nlm.nih.gov/pubmed/24033692",
"http://www.ncbi.nlm.nih.gov/pubmed/26811156"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28637434",
"endSection": "abstract",
"offsetInBeginSection": 1879,
"offsetInEndSection": 2039,
"text": "An examination of more UGT1A loci, except for UGT1A1*6 and UGT1A1*28, was not helpful to improve the predictive value of irinotecan-based toxicity and efficacy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36308049",
"endSection": "abstract",
"offsetInBeginSection": 178,
"offsetInEndSection": 297,
"text": "However, severe adverse effects due to irinotecan have been observed even in patients who do not harbor UGT1A1*28 or *6"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36183220",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 177,
"text": "Efficacy and safety of high doses of irinotecan in patients with metastatic colorectal cancer treated with the FOLFIRI regimen based on the UGT1A1 genotype: A systematic review."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19770637",
"endSection": "abstract",
"offsetInBeginSection": 475,
"offsetInEndSection": 619,
"text": "UGT1A1 gene polymorphism as a predictor of toxicity and treatment efficacy in patients who received irinotecan for metastatic colorectal cancer."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26830078",
"endSection": "abstract",
"offsetInBeginSection": 166,
"offsetInEndSection": 301,
"text": "UGT1A1(*)28 and (*)6 polymorphisms and irinotecan toxicity in Thai patients with metastatic colorectal cancer. 44 metastatic colorectal"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25981652",
"endSection": "abstract",
"offsetInBeginSection": 288,
"offsetInEndSection": 450,
"text": "UGT1A1 genetic polymorphisms and the occurrences of irinotecan-induced neutropenia in 25 patients of colorectal cancer at our hospital. Analysis of UGT1A1 genetic"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23236239",
"endSection": "abstract",
"offsetInBeginSection": 54,
"offsetInEndSection": 159,
"text": "e1A1 (UGT1A1) and thymidylate synthetase (TS) gene polymorphisms on irinotecan in metastatic colorectal c"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26591441",
"endSection": "abstract",
"offsetInBeginSection": 1294,
"offsetInEndSection": 1412,
"text": "heterozygosity for UGT1A1*6 and *28, dose reduction of irinotecan is strongly recommended. Genotyping tests for UGT1A1"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18437170",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1873,
"text": "Personalized/individualized/tailored therapy for each patient is an important goal for improving the outcome of patients with colorectal adenocarcinoma and includes the intention to maximize efficacy and minimize toxicity of chemotherapeutic agents. Numerous barriers must be overcome to reach this goal because outcome is affected by an unholy trinity of tumor characteristics that include somatic alterations at the DNA, RNA, and protein level; patient characteristics that include germline genetic differences such as polymorphisms in enzymes affecting the metabolism of chemotherapeutic agents; and environmental exposures and factors that include diet and physical activity. At present, evaluation of epidermal growth factor receptor (EGFR) expression by immunohistochemistry in colorectal adenocarcinoma is generally required for treatment with one of the monoclonal antibody therapies directed against that target, despite the absence of evidence for predictive value of the assay, whereas EGFR fluorescent in situ hybridization (FISH) may be predictive. In addition, the Food and Drug Administration of the United States now requires a 'black box' warning on the packaging of irinotecan for evaluation of germline polymorphism in UGT1A1, the gene mutated in Gilbert's syndrome, for potential reduction of drug dosage in patients with the UGT1A1*28 polymorphism. Numerous other potential markers have been identified but have not yet reached levels of evidence that support their routine usage. For example, KRAS gene mutation appears to preclude improved survival after therapy with monoclonal antibody therapy directed at EGFR, and extensive DNA methylation is associated with lack of efficacy of 5-fluorouracil (5-FU)-based chemotherapy. Additional markers will come into routine usage as reports of research studies continue to appear in the literature. Clinical"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19125129",
"endSection": "abstract",
"offsetInBeginSection": 2697,
"offsetInEndSection": 3092,
"text": "Given the large number of colorectal cancer cases diagnosed each year, a randomized controlled trial of the effects of irinotecan dose modifications in patients with colorectal cancer based on their UGT1A1 genotype is feasible and could clarify the tradeoffs between possible reductions in severe neutropenia and improved tumor response and/or survival in patients with various UGT1A1 genotypes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19125128",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 659,
"text": "SUMMARY OF RECOMMENDATIONS: The Evaluation of Genomic Applications in Practice and Prevention (EGAPP) Working Group found that the evidence is currently insufficient to recommend for or against the routine use of UGT1A1 genotyping in patients with metastatic colorectal cancer who are to be treated with irinotecan, with the intent of modifying the dose as a way to avoid adverse drug reactions (severe neutropenia).RATIONALE: The EGAPP Working Group (EWG) found no intervention trials showing that targeted dosing of irinotecan based on UGT1A1 genotyping could reduce the rates of two specific adverse drug events, severe (Grade 3-4) neutropenia or diarrhea."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19125129",
"endSection": "abstract",
"offsetInBeginSection": 944,
"offsetInEndSection": 1141,
"text": "Patients homozygous for the *28 allele are 3.5 times more likely to develop severe neutropenia compared with individuals with the wild genotype (risk ratio 3.51; 95% confidence interval 2.03-6.07)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19125129",
"endSection": "abstract",
"offsetInBeginSection": 1813,
"offsetInEndSection": 2056,
"text": "Although the quality of evidence on clinical utility is inadequate, two of three reviewed studies (and one published since our initial selection of studies for review) found that individuals homozygous for the *28 allele had improved survival."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19125128",
"endSection": "abstract",
"offsetInBeginSection": 983,
"offsetInEndSection": 1304,
"text": "An additional finding was the suggestion that reducing irinotecan dose may result in patient harms due to diminished effectiveness of treatment in highest risk individuals (*28/*28 homozygotes), and that a higher dose might be warranted among individuals at lower risk of adverse drug events (*1/*1 and *1/*28 genotypes)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25545261",
"endSection": "abstract",
"offsetInBeginSection": 102,
"offsetInEndSection": 547,
"text": "We developed a pyrosequencing method to detect allele frequency and genotype of UGT1A1 polymorphisms (UGT1A1*28 and UGT1A1*6) in Thai colorectal cancer patients.METHOD: A pyrosequencing method was designed to determine UGT1A1 genetic polymorphisms including UGT1A1*28 (A[TA]7TAA) and UGT1A1*6 (211G>A) in 91 Thai colorectal cancers.RESULT: Genotyping by the pyrosequencing technique was 100% concordant with capillary electrophoresis sequencing."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32357899",
"endSection": "abstract",
"offsetInBeginSection": 1612,
"offsetInEndSection": 1915,
"text": "This study is the first to use the UGT1A1 genotype to stratify patients into groups based on their risk of diarrhea, and to provide a complete assessment of chemotherapy-related diarrhea (CRD), including records of diarrhea duration, grading the severity of diarrhea, and evaluating concomitant symptoms"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/32829105",
"endSection": "abstract",
"offsetInBeginSection": 172,
"offsetInEndSection": 680,
"text": "This study is a multicenter, randomised clinical trial comparing the clinical outcomes and adverse events (AEs) in metastatic colorectal cancer (mCRC) patients treated with bevacizumab plus FOLFIRI with or without UGT1A1 genotyping and irinotecan dose escalation as the first-line therapy.METHODS: The control group received conventional biweekly FOLFIRI plus bevacizumab without UGT1A1 genotyping, whereas the study group received the same regimen with irinotecan dose escalation based on UGT1A1 genotyping."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19125129",
"endSection": "abstract",
"offsetInBeginSection": 1142,
"offsetInEndSection": 1381,
"text": "The proposed clinical utility of UGT1A1 genotyping would be derived from a reduction in drug-related adverse reactions (benefits) while at the same time avoiding declines in tumor response rate and increases in morbidity/mortality (harms)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30550693",
"endSection": "abstract",
"offsetInBeginSection": 460,
"offsetInEndSection": 614,
"text": "For patients showing homozygosity for UGT1A1*28, *6 or compound heterozygosity for UGT1A1*6 and *28, dose reduction of irinotecan is strongly recommended."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17184208",
"endSection": "abstract",
"offsetInBeginSection": 154,
"offsetInEndSection": 421,
"text": "As the US FDA-approved label of irinotecan (CPT-11, Camptosar) has been recently revised to include UGT1A1 genotype among potential risk factors for toxicity, it is expected that UGT1A1 genotyping will be increasingly used in patients undergoing irinotecan treatment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24642571",
"endSection": "abstract",
"offsetInBeginSection": 386,
"offsetInEndSection": 535,
"text": "perbilirubinemia presenting with severe jaundice. UGT1A1 genotyping was used before therapy to ascertain whether genotype-adjusted dosages of irinote"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30583998",
"endSection": "abstract",
"offsetInBeginSection": 284,
"offsetInEndSection": 793,
"text": " The aim of this study was to determine whether the presence of the variant allele UGT1A1*28, harbouring seven TA repetitions, (TA)7, in the homozygous state, is associated with precancerous colonic lesions and/or with specific colorectal cancer characteristics.MATERIAL AND METHODS: All patients treated for colorectal cancer in a tertiary care centre, between January 2009 and December 2013, who had routine UGT1A1 genotyping for irinotecan dose-adjustment were included. Data were retrospectively collected"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30583998",
"endSection": "abstract",
"offsetInBeginSection": 284,
"offsetInEndSection": 756,
"text": " The aim of this study was to determine whether the presence of the variant allele UGT1A1*28, harbouring seven TA repetitions, (TA)7, in the homozygous state, is associated with precancerous colonic lesions and/or with specific colorectal cancer characteristics.MATERIAL AND METHODS: All patients treated for colorectal cancer in a tertiary care centre, between January 2009 and December 2013, who had routine UGT1A1 genotyping for irinotecan dose-adjustment were included"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23686699",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 385,
"text": "The aim of this study was to investigate the associations between UDP-glucuronosyltransferase (UGT) 1A1 polymorphisms and irinotecan-induced toxicities in Chinese advanced colorectal cancer patients. The genotypes of UGT1A1 6 and UGT1A1 28 were analyzed by PCR amplification and Sanger sequencing in 276 advanced colorectal cancer patients receiving irinotecan-containing chemotherapy."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25981652",
"endSection": "abstract",
"offsetInBeginSection": 256,
"offsetInEndSection": 423,
"text": "We retrospectively investigated UGT1A1 genetic polymorphisms and the occurrences of irinotecan-induced neutropenia in 25 patients of colorectal cancer at our hospital."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23686699",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 199,
"text": "The aim of this study was to investigate the associations between UDP-glucuronosyltransferase (UGT) 1A1 polymorphisms and irinotecan-induced toxicities in Chinese advanced colorectal cancer patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21287524",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 82,
"text": "Clinical implications of UGT1A1*28 genotype testing in colorectal cancer patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/26830078",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 121,
"text": "Correlation of UGT1A1(*)28 and (*)6 polymorphisms with irinotecan-induced neutropenia in Thai colorectal cancer patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/23686699",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 129,
"text": "UGT1A1 6/28 polymorphisms could predict irinotecan-induced severe neutropenia not diarrhea in Chinese colorectal cancer patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19125129",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 144,
"text": "This evidence-based review addresses the question of whether testing for UGT1A1 mutations in patients with metastatic colorectal cancer treated "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28637434",
"endSection": "abstract",
"offsetInBeginSection": 24,
"offsetInEndSection": 159,
"text": "a new UGT1A and DPYD polymorphism panel to better predict irinotecan-induced toxicity and the clinical response in Chinese patients wit"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15280927",
"endSection": "abstract",
"offsetInBeginSection": 293,
"offsetInEndSection": 382,
"text": "UGT1A1 gene promoter polymorphism in the toxicity profile, in the response rate and in th"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30550693",
"endSection": "abstract",
"offsetInBeginSection": 192,
"offsetInEndSection": 614,
"text": "Recent pharmacogenetic studies on irinotecan have revealed the impact of UGT1A1 polymorphisms on severe adverse effects. The concurrence of UGT1A1*28 and UGT1A1*6, even when heterozygous, markedly alters the disposition of irinotecan, potentially increasing toxicity. For patients showing homozygosity for UGT1A1*28, *6 or compound heterozygosity for UGT1A1*6 and *28, dose reduction of irinotecan is strongly recommended."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/18437170",
"endSection": "abstract",
"offsetInBeginSection": 1062,
"offsetInEndSection": 1369,
"text": "In addition, the Food and Drug Administration of the United States now requires a 'black box' warning on the packaging of irinotecan for evaluation of germline polymorphism in UGT1A1, the gene mutated in Gilbert's syndrome, for potential reduction of drug dosage in patients with the UGT1A1*28 polymorphism."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16982469",
"endSection": "abstract",
"offsetInBeginSection": 308,
"offsetInEndSection": 640,
"text": "Recent FDA approval of genetic testing for mutations in the UGT1A1 gene that predict adverse reactions to irinotecan is ushering in a new era that will increasingly rely on genotyping to individualize treatment decisions for patients with cancer as well as for patients at high risk who may be candidates for chemoprevention agents."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17090741",
"endSection": "abstract",
"offsetInBeginSection": 1148,
"offsetInEndSection": 1601,
"text": "s for UGT1A1*28.CONCLUSION: At least part of the interpatient variability of irinotecan toxicity can be explained by the UGT1A1*28 polymorphism. Patients who are homozygous for the UGT1A1*28 allele have an increased risk of developing severe neutropenia when receiving irinotecan, especially the 300-350- mg/m2 regimen. A molecular assay is now available to identify the at-risk subgroup and should be used by health care professionals to help guide iri"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21486535",
"endSection": "abstract",
"offsetInBeginSection": 1260,
"offsetInEndSection": 1536,
"text": "ile neutropenic event avoided.CONCLUSIONS: UGT1A1 genotype screening before irinotecan treatment is a cost-efficient strategy for the hospital. Systematic genotyping prior to chemotherapy, and administration of CSF in patients homozygotes for the *28 allele allow to avoid 91 "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16641252",
"endSection": "abstract",
"offsetInBeginSection": 512,
"offsetInEndSection": 626,
"text": " DPD deficiency. An assay is available for genotypic testing of the enzyme UGT1A1, which is predictive of toxicity"
}
]
| 13 | BioASQ-training13b | null | null | 65f775e8c4010b4d7800002d | 312 |
yesno | Has proteomics been used in the study of Pick's disease? | ['yes'] | [
"yes"
]
| Yes, proteomics has been used in the study of Pick's disease. | [
"http://www.ncbi.nlm.nih.gov/pubmed/16987245",
"http://www.ncbi.nlm.nih.gov/pubmed/16555340",
"http://www.ncbi.nlm.nih.gov/pubmed/12650976",
"http://www.ncbi.nlm.nih.gov/pubmed/11880199"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16987245",
"endSection": "abstract",
"offsetInBeginSection": 776,
"offsetInEndSection": 993,
"text": "In Pick's disease, increased AGE, CML, CEL, HNE and MDAL bands of about 50 kDa were observed in the frontal cortex (but not in the occipital cortex) in association with increased density of glial acidic protein bands."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16555340",
"endSection": "abstract",
"offsetInBeginSection": 236,
"offsetInEndSection": 529,
"text": "Thus, brain and cerebrospinal fluid (CSF) samples from patients with Alzheimer's disease, Down syndrome, Pick's disease, Parkinson's disease, schizophrenia, and other disorders as well as brain and CSF from animals serving as models of neurological disorders have been analyzed by proteomics. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12650976",
"endSection": "abstract",
"offsetInBeginSection": 493,
"offsetInEndSection": 771,
"text": "The present study is designed to investigate expression of peroxiredoxins (Prxs), the newly characterized family of highly conserved antioxidant enzymes, and other antioxidant enzymes in frontal cortex and cerebellum of DS, AD and PD patients using the technique of proteomics. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11880199",
"endSection": "abstract",
"offsetInBeginSection": 326,
"offsetInEndSection": 486,
"text": "HMT levels were measured in the frontal cortex and cerebellum of brains of patients with AD, DS, and PiD, and normal aged subjects using proteomics techniques. "
}
]
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2014/MB_cgi?field=uid&exact=Find+Exact+Term&term=D020774",
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| []
| 532f05bdd6d3ac6a34000026 | 313 |
yesno | Is TALEN being used on stem cells? | ['yes'] | [
"yes"
]
| ['Yes, TALEN is being used on stem cells for genome editing.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/26052525",
"http://www.ncbi.nlm.nih.gov/pubmed/25434822",
"http://www.ncbi.nlm.nih.gov/pubmed/25408877",
"http://www.ncbi.nlm.nih.gov/pubmed/24996167",
"http://www.ncbi.nlm.nih.gov/pubmed/23928856",
"http://www.ncbi.nlm.nih.gov/pubmed/24691488",
"http://www.ncbi.nlm.nih.gov/pubmed/23246482",
"http://www.ncbi.nlm.nih.gov/pubmed/24206569",
"http://www.ncbi.nlm.nih.gov/pubmed/25414332",
"http://www.ncbi.nlm.nih.gov/pubmed/23666012",
"http://www.ncbi.nlm.nih.gov/pubmed/24155235",
"http://www.ncbi.nlm.nih.gov/pubmed/22749015",
"http://www.ncbi.nlm.nih.gov/pubmed/24305178",
"http://www.ncbi.nlm.nih.gov/pubmed/21738127",
"http://www.ncbi.nlm.nih.gov/pubmed/24319658",
"http://www.ncbi.nlm.nih.gov/pubmed/23921522",
"http://www.ncbi.nlm.nih.gov/pubmed/25245091",
"http://www.ncbi.nlm.nih.gov/pubmed/23945944"
]
| [
{
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"endSection": "title",
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"offsetInEndSection": 137,
"text": "Precise correction of the dystrophin gene in duchenne muscular dystrophy patient induced pluripotent stem cells by TALEN and CRISPR-Cas9."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/25434822",
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"text": "Genetic correction of patient-derived induced pluripotent stem cells (iPSCs) by TALENs or CRISPR-Cas9 holds promise for DMD gene therapy; however, the safety of such nuclease treatment must be determined."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/26052525",
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"text": "We generated helper-dependent, capsid-modified adenovirus (HD-Ad5/35) vectors for zinc-finger nuclease (ZFN)- or transcription activator-like effector nuclease (TALEN)-mediated genome editing in human CD34+ hematopoietic stem cells (HSCs) from mobilized adult donors. "
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"offsetInBeginSection": 344,
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"text": "We used transcription activator-like effector nuclease (TALEN)-mediated gene editing in mouse embryonic stem cells (mESCs) to produce mice with targeted gene disruptions and insertions in two Y-linked genes--Sry and Uty."
},
{
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"text": "Transcription activator-like effector nuclease (TALEN)-mediated gene correction in integration-free β-thalassemia induced pluripotent stem cells."
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"text": "A TALEN genome-editing system for generating human stem cell-based disease models."
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"text": "Low incidence of off-target mutations in individual CRISPR-Cas9 and TALEN targeted human stem cell clones detected by whole-genome sequencing."
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"endSection": "abstract",
"offsetInBeginSection": 623,
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"text": "Using CRISPR-Cas9 and TALEN targeted human pluripotent stem cell clones, we performed whole-genome sequencing at high coverage in order to assess the degree of mutagenesis across the entire genome."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/24206569",
"endSection": "title",
"offsetInBeginSection": 0,
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"text": "A modified TALEN-based system for robust generation of knock-out human pluripotent stem cell lines and disease models."
},
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"offsetInBeginSection": 464,
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"text": "In this study, we utilized a cell-penetrating peptide-based system for ZFN and TALEN delivery."
},
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"text": "A TALEN genome-editing system for generating human stem cell-based disease models."
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{
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"text": "Low incidence of off-target mutations in individual CRISPR-Cas9 and TALEN targeted human stem cell clones detected by whole-genome sequencing."
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"text": "Using CRISPR-Cas9 and TALEN targeted human pluripotent stem cell clones, we performed whole-genome sequencing at high coverage in order to assess the degree of mutagenesis across the entire genome."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/23666012",
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"offsetInBeginSection": 344,
"offsetInEndSection": 564,
"text": "We used transcription activator-like effector nuclease (TALEN)-mediated gene editing in mouse embryonic stem cells (mESCs) to produce mice with targeted gene disruptions and insertions in two Y-linked genes--Sry and Uty."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/21738127",
"endSection": "abstract",
"offsetInBeginSection": 470,
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"text": "At all loci tested we obtained human embryonic stem cell (ESC) and induced pluripotent stem cell (iPSC) clones carrying transgenic cassettes solely at the TALEN-specified location."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/23246482",
"endSection": "abstract",
"offsetInBeginSection": 474,
"offsetInEndSection": 753,
"text": "We report here the use of TALENs to rapidly and efficiently generate mutant alleles of 15 genes in cultured somatic cells or human pluripotent stem cells, the latter for which we differentiated both the targeted lines and isogenic control lines into various metabolic cell types."
},
{
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"text": "Zinc-finger nucleases (ZFNs) and transcription activator-like effector nucleases (TALENs) have been successfully used to knock out endogenous genes in stem cell research."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/25047178",
"endSection": "abstract",
"offsetInBeginSection": 432,
"offsetInEndSection": 682,
"text": "Here we report different methods to efficiently perform TALEN-mediated gene integration and inactivation in different mammalian cell systems including induced pluripotent stem cells and delineate experimental examples associated with these approaches"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/24319658",
"endSection": "abstract",
"offsetInBeginSection": 954,
"offsetInEndSection": 1163,
"text": "Together, our results demonstrate that TALE-based transcriptional repressor and TALENs are two promising approaches for loss-of-function studies of microRNA clusters in somatic cells and pluripotent stem cells"
},
{
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"offsetInBeginSection": 196,
"offsetInEndSection": 474,
"text": "We report here the use of TALENs to rapidly and efficiently generate mutant alleles of 15 genes in cultured somatic cells or human pluripotent stem cells, the latter for which we differentiated both the targeted lines and isogenic control lines into various metabolic cell types"
},
{
"beginSection": "title",
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"endSection": "title",
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"text": "Transcription activator-like effector nuclease (TALEN)-mediated gene correction in integration-free β-thalassemia induced pluripotent stem cells."
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"text": "A TALEN genome-editing system for generating human stem cell-based disease models."
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"text": "Low incidence of off-target mutations in individual CRISPR-Cas9 and TALEN targeted human stem cell clones detected by whole-genome sequencing."
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"text": "TALEN-mediated generation and genetic correction of disease-specific human induced pluripotent stem cells."
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"text": "Precise correction of the dystrophin gene in duchenne muscular dystrophy patient induced pluripotent stem cells by TALEN and CRISPR-Cas9."
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"text": "A TALEN genome-editing system for generating human stem cell-based disease models."
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"text": "Low incidence of off-target mutations in individual CRISPR-Cas9 and TALEN targeted human stem cell clones detected by whole-genome sequencing."
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"text": "TALEN-mediated generation and genetic correction of disease-specific human induced pluripotent stem cells."
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"text": "Precise correction of the dystrophin gene in duchenne muscular dystrophy patient induced pluripotent stem cells by TALEN and CRISPR-Cas9."
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"offsetInEndSection": 118,
"text": "A modified TALEN-based system for robust generation of knock-out human pluripotent stem cell lines and disease models."
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"offsetInBeginSection": 0,
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"text": "Baculoviral transduction facilitates TALEN-mediated targeted transgene integration and Cre/LoxP cassette exchange in human-induced pluripotent stem cells."
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"text": "Transcription activator-like effector nuclease (TALEN)-mediated gene correction in integration-free β-thalassemia induced pluripotent stem cells."
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"text": "Low incidence of off-target mutations in individual CRISPR-Cas9 and TALEN targeted human stem cell clones detected by whole-genome sequencing."
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"text": "TALEN-mediated generation and genetic correction of disease-specific human induced pluripotent stem cells."
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"text": "Precise correction of the dystrophin gene in duchenne muscular dystrophy patient induced pluripotent stem cells by TALEN and CRISPR-Cas9."
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"text": "We used transcription activator-like effector nuclease (TALEN)-mediated gene editing in mouse embryonic stem cells (mESCs) to produce mice with targeted gene disruptions and insertions in two Y-linked genes--Sry and Uty. "
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"text": "A modified TALEN-based system for robust generation of knock-out human pluripotent stem cell lines and disease models."
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"text": "Precise correction of the dystrophin gene in duchenne muscular dystrophy patient induced pluripotent stem cells by TALEN and CRISPR-Cas9."
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"text": "Baculoviral transduction facilitates TALEN-mediated targeted transgene integration and Cre/LoxP cassette exchange in human-induced pluripotent stem cells."
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"text": "Using CRISPR-Cas9 and TALEN targeted human pluripotent stem cell clones, we performed whole-genome sequencing at high coverage in order to assess the degree of mutagenesis across the entire genome. "
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"text": "Low incidence of off-target mutations in individual CRISPR-Cas9 and TALEN targeted human stem cell clones detected by whole-genome sequencing."
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"text": "A modified TALEN-based system for robust generation of knock-out human pluripotent stem cell lines and disease models."
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"text": "Baculoviral transduction facilitates TALEN-mediated targeted transgene integration and Cre/LoxP cassette exchange in human-induced pluripotent stem cells."
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"text": "Using CRISPR-Cas9 and TALEN targeted human pluripotent stem cell clones, we performed whole-genome sequencing at high coverage in order to assess the degree of mutagenesis across the entire genome. "
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"offsetInEndSection": 346,
"text": "We used transcription activator-like effector nuclease (TALEN)-mediated gene editing in mouse embryonic stem cells (mESCs) to produce mice with targeted gene disruptions and insertions in two Y-linked genes--Sry and Uty. "
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"text": "A modified TALEN-based system for robust generation of knock-out human pluripotent stem cell lines and disease models."
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"text": "A 5% modification rate was observed in human induced pluripotent stem cells (hiPSCs) treated with TAT-TALEN as measured by the Surveyor assay. TAT-TALEN protein-mediated gene disruption was applicable in hiPSCs and represents a promising technique for gene knockout in stem cells."
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"offsetInBeginSection": 186,
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"text": "Here we engineered transcription activator-like effector nucleases (TALENs) for five distinct genomic loci. At all loci tested we obtained human embryonic stem cell (ESC) and induced pluripotent stem cell (iPSC) clones carrying transgenic cassettes solely at the TALEN-specified location."
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"text": "Seamless correction of the sickle cell disease mutation of the HBB gene in human induced pluripotent stem cells using TALENs."
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"text": "Here we engineered transcription activator-like effector nucleases (TALENs) for five distinct genomic loci. At all loci tested we obtained human embryonic stem cell (ESC) and induced pluripotent stem cell (iPSC) clones carrying transgenic cassettes solely at the TALEN-specified location."
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"text": "At all loci tested we obtained human embryonic stem cell (ESC) and induced pluripotent stem cell (iPSC) clones carrying transgenic cassettes solely at the TALEN-specified location. Our data suggest that TALENs employing the specific architectures described here mediate site-specific genome modification in human pluripotent cells with similar efficiency and precision as do zinc-finger nucleases (ZFNs)."
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"text": "Here we engineered transcription activator-like effector nucleases (TALENs) for five distinct genomic loci. At all loci tested we obtained human embryonic stem cell (ESC) and induced pluripotent stem cell (iPSC) clones carrying transgenic cassettes solely at the TALEN-specified location."
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"text": "At all loci tested we obtained human embryonic stem cell (ESC) and induced pluripotent stem cell (iPSC) clones carrying transgenic cassettes solely at the TALEN-specified location. Our data suggest that TALENs employing the specific architectures described here mediate site-specific genome modification in human pluripotent cells with similar efficiency and precision as do zinc-finger nucleases (ZFNs)."
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"text": "At all loci tested we obtained human embryonic stem cell (ESC) and induced pluripotent stem cell (iPSC) clones carrying transgenic cassettes solely at the TALEN-specified location. Our data suggest that TALENs employing the specific architectures described here mediate site-specific genome modification in human pluripotent cells with similar efficiency and precision as do zinc-finger nucleases (ZFNs)."
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"p": "http://www.w3.org/2004/02/skos/core#notation",
"s": "http://linkedlifedata.com/resource/umls/label/A0119446"
}
]
| 56f555b609dd18d46b000007 | 314 |
yesno | Are ACTA1 (alpha actin) and NEB (nebulin) genes related to nemaline myopathy? | ['yes'] | [
"yes"
]
| ['Yes, most nemaline myopathy patients have mutations in the nebulin (NEB) or skeletal muscle alpha-actin (ACTA1) genes.', 'Yes. Most nemaline myopathy patients have mutations in the nebulin (NEB) or skeletal muscle alpha-actin (ACTA1) genes. Mutations in six genes have been reported to cause NM: Nebulin (NEB Pelin 1999), alpha-skeletal muscle actin (ACTA1 Nowak 1999), alpha-slow tropomyosin (TPM3 Laing 1995), beta-tropomyosin (TPM2 Donner 2002), slow troponin T (TNNT1 Johnston 2000) and cofilin 2 (CFL2 Agrawal 2007).'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22407809",
"http://www.ncbi.nlm.nih.gov/pubmed/22358459",
"http://www.ncbi.nlm.nih.gov/pubmed/20012312",
"http://www.ncbi.nlm.nih.gov/pubmed/19648653",
"http://www.ncbi.nlm.nih.gov/pubmed/16945536",
"http://www.ncbi.nlm.nih.gov/pubmed/15564032",
"http://www.ncbi.nlm.nih.gov/pubmed/15495263",
"http://www.ncbi.nlm.nih.gov/pubmed/11257471",
"http://www.ncbi.nlm.nih.gov/pubmed/11166164",
"http://www.ncbi.nlm.nih.gov/pubmed/12805120"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22407809",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 262,
"text": "Nemaline myopathy (NM) is a group of congenital myopathies, characterized by the presence of distinct rod-like inclusions \"nemaline bodies\" in the sarcoplasm of skeletal muscle fibers. To date, ACTA1, NEB, TPM3, TPM2, TNNT1, and CFL2 have been found to cause NM."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22358459",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 356,
"text": "Nemaline myopathy (NM) is the most common congenital myopathy and is caused by mutations in various genes including NEB (nebulin), TPM2 (beta-tropomyosin), TPM3 (gamma-tropomyosin), and ACTA1 (skeletal alpha-actin). 20-25% of NM cases carry ACTA1 defects and these particular mutations usually induce substitutions of single residues in the actin protein. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20012312",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 487,
"text": "Nemaline myopathy (NM) is a genetically and clinically heterogenous muscle disorder, which is myopathologically characterized by nemaline bodies. Mutations in six genes have been reported to cause NM: Nebulin (NEB Pelin 1999), alpha-skeletal muscle actin (ACTA1 Nowak 1999), alpha-slow tropomyosin (TPM3 Laing 1995), beta-tropomyosin (TPM2 Donner 2002), slow troponin T (TNNT1 Johnston 2000) and cofilin 2 (CFL2 Agrawal 2007). The majority of cases are due to mutation in NEB and ACTA1. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19648653",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 635,
"text": "Nemaline myopathy is a heterogenous form of congenital myopathy characterised by a variable spectrum of clinical features, predominated in the severe form by profound muscle hypotonia and weakness accompanied by respiratory insufficiency. The clinical variability, with differing age of onset and severity of symptoms makes the diagnosis of nemaline myopathy difficult in some cases. Severe forms of nemaline myopathy may be caused by mutation of a number of different genes: skeletal muscle actin (ACTA1), nebulin (NEB) and alpha-tropomyosin (TPM3), all of which encode components of the sarcomeric thin filaments of skeletal muscle. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16945536",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 114,
"text": "Most nemaline myopathy patients have mutations in the nebulin (NEB) or skeletal muscle alpha-actin (ACTA1) genes. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15564032",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 232,
"text": "We report muscle MRI findings of 10 patients from 8 families with nemaline myopathy. Patients with involvement of the nebulin (NEB) gene showed a consistent pattern of selective muscle involvement corresponding to clinical severity."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15564032",
"endSection": "abstract",
"offsetInBeginSection": 522,
"offsetInEndSection": 719,
"text": "Patients with nemaline myopathy secondary to mutations in the skeletal muscle alpha-actin (ACTA1) gene showed diffuse involvement of thigh and leg muscles with relative sparing of the gastrocnemii."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/15495263",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 584,
"text": "Congenital myopathies are clinical and genetic heterogeneous disorders characterized by skeletal muscle weakness ranging in severity. Three major forms have been identified: actin myopathy, intranuclear rod myopathy, and nemaline myopathy. Nemaline myopathy is the most common of these myopathies and is further subdivided into seven groups according to severity, progressiveness, and age of onset. At present, five genes have been linked to congenital myopathies. These include alpha-actin (ACTA1), alpha- and beta-tropomyosin (TPM3 and TPM2), troponin T (TNNT1), and nebulin (NEB). "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11257471",
"endSection": "abstract",
"offsetInBeginSection": 0,
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"text": "Nemaline myopathy is a structural congenital myopathy which may show both autosomal dominant and autosomal recessive inheritance patterns. Mutations in three different genes have been identified as the cause of nemaline myopathy: the gene for slow alpha-tropomyosin 3 (TPM3) at 1q22-23, the nebulin gene (NEB) at 2q21.1-q22, and the actin gene (ACTA1) at 1q42."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11166164",
"endSection": "abstract",
"offsetInBeginSection": 0,
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"text": "Nemaline myopathy is a clinically and genetically heterogeneous condition. The clinical spectrum ranges from severe cases with antenatal or neonatal onset and early death to late onset cases with only slow progression. Three genes are known to cause nemaline myopathy: the genes for nebulin (NEB) on chromosome 2q22, slow alpha-tropomyosin (TPM3) on chromosome 1q21 and skeletal muscle alpha-actin (ACTA1) on chromosome 1q42. "
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/22358459",
"endSection": "abstract",
"offsetInBeginSection": 0,
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"text": "Nemaline myopathy (NM) is the most common congenital myopathy and is caused by mutations in various genes including NEB (nebulin), TPM2 (beta-tropomyosin), TPM3 (gamma-tropomyosin), and ACTA1 (skeletal alpha-actin)."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/11166164",
"endSection": "abstract",
"offsetInBeginSection": 216,
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"text": "Three genes are known to cause nemaline myopathy: the genes for nebulin (NEB) on chromosome 2q22, slow alpha-tropomyosin (TPM3) on chromosome 1q21 and skeletal muscle alpha-actin (ACTA1) on chromosome 1q42."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805120",
"endSection": "abstract",
"offsetInBeginSection": 123,
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"text": "Five genes have now been associated with nemaline myopathy: alpha-tropomyosin-3 (TPM3), alpha-actin (ACTA1), nebulin (NEB), beta-tropomysin (TPM2) and troponin T (TNNT1)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16945536",
"endSection": "abstract",
"offsetInBeginSection": 0,
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"text": "Most nemaline myopathy patients have mutations in the nebulin (NEB) or skeletal muscle alpha-actin (ACTA1) genes."
},
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"endSection": "abstract",
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"text": "Nemaline myopathy (NM) is the most common congenital myopathy and is caused by mutations in various genes including NEB (nebulin), TPM2 (beta-tropomyosin), TPM3 (gamma-tropomyosin), and ACTA1 (skeletal alpha-actin)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11166164",
"endSection": "abstract",
"offsetInBeginSection": 216,
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"text": "Three genes are known to cause nemaline myopathy: the genes for nebulin (NEB) on chromosome 2q22, slow alpha-tropomyosin (TPM3) on chromosome 1q21 and skeletal muscle alpha-actin (ACTA1) on chromosome 1q42."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805120",
"endSection": "abstract",
"offsetInBeginSection": 123,
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"text": "Five genes have now been associated with nemaline myopathy: alpha-tropomyosin-3 (TPM3), alpha-actin (ACTA1), nebulin (NEB), beta-tropomysin (TPM2) and troponin T (TNNT1)."
},
{
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"offsetInBeginSection": 0,
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"text": "Most nemaline myopathy patients have mutations in the nebulin (NEB) or skeletal muscle alpha-actin (ACTA1) genes."
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{
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"text": "Nemaline myopathy (NM) is the most common congenital myopathy and is caused by mutations in various genes including NEB (nebulin), TPM2 (beta-tropomyosin), TPM3 (gamma-tropomyosin), and ACTA1 (skeletal alpha-actin)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11166164",
"endSection": "abstract",
"offsetInBeginSection": 216,
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"text": "Three genes are known to cause nemaline myopathy: the genes for nebulin (NEB) on chromosome 2q22, slow alpha-tropomyosin (TPM3) on chromosome 1q21 and skeletal muscle alpha-actin (ACTA1) on chromosome 1q42."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805120",
"endSection": "abstract",
"offsetInBeginSection": 123,
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"text": "Five genes have now been associated with nemaline myopathy: alpha-tropomyosin-3 (TPM3), alpha-actin (ACTA1), nebulin (NEB), beta-tropomysin (TPM2) and troponin T (TNNT1)."
},
{
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"text": "Most nemaline myopathy patients have mutations in the nebulin (NEB) or skeletal muscle alpha-actin (ACTA1) genes."
},
{
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"text": "Nemaline myopathy (NM) is the most common congenital myopathy and is caused by mutations in various genes including NEB (nebulin), TPM2 (beta-tropomyosin), TPM3 (gamma-tropomyosin), and ACTA1 (skeletal alpha-actin)."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/11166164",
"endSection": "abstract",
"offsetInBeginSection": 216,
"offsetInEndSection": 423,
"text": "Three genes are known to cause nemaline myopathy: the genes for nebulin (NEB) on chromosome 2q22, slow alpha-tropomyosin (TPM3) on chromosome 1q21 and skeletal muscle alpha-actin (ACTA1) on chromosome 1q42."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805120",
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"offsetInBeginSection": 123,
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"text": "Five genes have now been associated with nemaline myopathy: alpha-tropomyosin-3 (TPM3), alpha-actin (ACTA1), nebulin (NEB), beta-tropomysin (TPM2) and troponin T (TNNT1)."
},
{
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"text": "Most nemaline myopathy patients have mutations in the nebulin (NEB) or skeletal muscle alpha-actin (ACTA1) genes."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/16945536",
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"text": "Most nemaline myopathy patients have mutations in the nebulin (NEB) or skeletal muscle alpha-actin (ACTA1) genes."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19648653",
"endSection": "abstract",
"offsetInBeginSection": 384,
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"text": "Severe forms of nemaline myopathy may be caused by mutation of a number of different genes: skeletal muscle actin (ACTA1), nebulin (NEB) and alpha-tropomyosin (TPM3), all of which encode components of the sarcomeric thin filaments of skeletal muscle."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805120",
"endSection": "abstract",
"offsetInBeginSection": 125,
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"text": "Five genes have now been associated with nemaline myopathy: alpha-tropomyosin-3 (TPM3), alpha-actin (ACTA1), nebulin (NEB), beta-tropomysin (TPM2) and troponin T (TNNT1)."
},
{
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"text": "Nemaline myopathy (NM) is the most common congenital myopathy and is caused by mutations in various genes including NEB (nebulin), TPM2 (beta-tropomyosin), TPM3 (gamma-tropomyosin), and ACTA1 (skeletal alpha-actin)."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22407809",
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"text": "Nemaline myopathy (NM) is a group of congenital myopathies, characterized by the presence of distinct rod-like inclusions \"nemaline bodies\" in the sarcoplasm of skeletal muscle fibers. To date, ACTA1, NEB, TPM3, TPM2, TNNT1, and CFL2 have been found to cause NM."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/22358459",
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"text": "Nemaline myopathy (NM) is the most common congenital myopathy and is caused by mutations in various genes including NEB (nebulin), TPM2 (beta-tropomyosin), TPM3 (gamma-tropomyosin), and ACTA1 (skeletal alpha-actin). 20-25% of NM cases carry ACTA1 defects and these particular mutations usually induce substitutions of single residues in the actin protein. "
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/16945536",
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"offsetInBeginSection": 0,
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"text": "Most nemaline myopathy patients have mutations in the nebulin (NEB) or skeletal muscle alpha-actin (ACTA1) genes."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/11166164",
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"text": "Three genes are known to cause nemaline myopathy: the genes for nebulin (NEB) on chromosome 2q22, slow alpha-tropomyosin (TPM3) on chromosome 1q21 and skeletal muscle alpha-actin (ACTA1) on chromosome 1q42."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805120",
"endSection": "abstract",
"offsetInBeginSection": 125,
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"text": "Five genes have now been associated with nemaline myopathy: alpha-tropomyosin-3 (TPM3), alpha-actin (ACTA1), nebulin (NEB), beta-tropomysin (TPM2) and troponin T (TNNT1)."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/22358459",
"endSection": "abstract",
"offsetInBeginSection": 0,
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"text": "Nemaline myopathy (NM) is the most common congenital myopathy and is caused by mutations in various genes including NEB (nebulin), TPM2 (beta-tropomyosin), TPM3 (gamma-tropomyosin), and ACTA1 (skeletal alpha-actin)."
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/19648653",
"endSection": "abstract",
"offsetInBeginSection": 384,
"offsetInEndSection": 634,
"text": "Severe forms of nemaline myopathy may be caused by mutation of a number of different genes: skeletal muscle actin (ACTA1), nebulin (NEB) and alpha-tropomyosin (TPM3), all of which encode components of the sarcomeric thin filaments of skeletal muscle."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11257471",
"endSection": "abstract",
"offsetInBeginSection": 139,
"offsetInEndSection": 360,
"text": "Mutations in three different genes have been identified as the cause of nemaline myopathy: the gene for slow alpha-tropomyosin 3 (TPM3) at 1q22-23, the nebulin gene (NEB) at 2q21.1-q22, and the actin gene (ACTA1) at 1q42."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16945536",
"endSection": "abstract",
"offsetInBeginSection": 0,
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"text": "Most nemaline myopathy patients have mutations in the nebulin (NEB) or skeletal muscle alpha-actin (ACTA1) genes"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805120",
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"text": "Five genes have now been associated with nemaline myopathy: alpha-tropomyosin-3 (TPM3), alpha-actin (ACTA1), nebulin (NEB), beta-tropomysin (TPM2) and troponin T (TNNT1)"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/11166164",
"endSection": "abstract",
"offsetInBeginSection": 218,
"offsetInEndSection": 423,
"text": "Three genes are known to cause nemaline myopathy: the genes for nebulin (NEB) on chromosome 2q22, slow alpha-tropomyosin (TPM3) on chromosome 1q21 and skeletal muscle alpha-actin (ACTA1) on chromosome 1q42"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/22358459",
"endSection": "abstract",
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"text": "Nemaline myopathy (NM) is the most common congenital myopathy and is caused by mutations in various genes including NEB (nebulin), TPM2 (beta-tropomyosin), TPM3 (gamma-tropomyosin), and ACTA1 (skeletal alpha-actin)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805120",
"endSection": "abstract",
"offsetInBeginSection": 125,
"offsetInEndSection": 294,
"text": "Five genes have now been associated with nemaline myopathy: alpha-tropomyosin-3 (TPM3), alpha-actin (ACTA1), nebulin (NEB), beta-tropomysin (TPM2) and troponin T (TNNT1)"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/22358459",
"endSection": "abstract",
"offsetInBeginSection": 0,
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"text": "Nemaline myopathy (NM) is the most common congenital myopathy and is caused by mutations in various genes including NEB (nebulin), TPM2 (beta-tropomyosin), TPM3 (gamma-tropomyosin), and ACTA1 (skeletal alpha-actin)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11257471",
"endSection": "abstract",
"offsetInBeginSection": 139,
"offsetInEndSection": 359,
"text": "Mutations in three different genes have been identified as the cause of nemaline myopathy: the gene for slow alpha-tropomyosin 3 (TPM3) at 1q22-23, the nebulin gene (NEB) at 2q21.1-q22, and the actin gene (ACTA1) at 1q42"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11166164",
"endSection": "abstract",
"offsetInBeginSection": 219,
"offsetInEndSection": 424,
"text": "Three genes are known to cause nemaline myopathy: the genes for nebulin (NEB) on chromosome 2q22, slow alpha-tropomyosin (TPM3) on chromosome 1q21 and skeletal muscle alpha-actin (ACTA1) on chromosome 1q42"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16945536",
"endSection": "abstract",
"offsetInBeginSection": 0,
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"text": "Most nemaline myopathy patients have mutations in the nebulin (NEB) or skeletal muscle alpha-actin (ACTA1) genes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19648653",
"endSection": "abstract",
"offsetInBeginSection": 384,
"offsetInEndSection": 633,
"text": "Severe forms of nemaline myopathy may be caused by mutation of a number of different genes: skeletal muscle actin (ACTA1), nebulin (NEB) and alpha-tropomyosin (TPM3), all of which encode components of the sarcomeric thin filaments of skeletal muscle"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/22358459",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 214,
"text": "Nemaline myopathy (NM) is the most common congenital myopathy and is caused by mutations in various genes including NEB (nebulin), TPM2 (beta-tropomyosin), TPM3 (gamma-tropomyosin), and ACTA1 (skeletal alpha-actin)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805120",
"endSection": "abstract",
"offsetInBeginSection": 125,
"offsetInEndSection": 294,
"text": "Five genes have now been associated with nemaline myopathy: alpha-tropomyosin-3 (TPM3), alpha-actin (ACTA1), nebulin (NEB), beta-tropomysin (TPM2) and troponin T (TNNT1)"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/11257471",
"endSection": "abstract",
"offsetInBeginSection": 139,
"offsetInEndSection": 359,
"text": "Mutations in three different genes have been identified as the cause of nemaline myopathy: the gene for slow alpha-tropomyosin 3 (TPM3) at 1q22-23, the nebulin gene (NEB) at 2q21.1-q22, and the actin gene (ACTA1) at 1q42"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11166164",
"endSection": "abstract",
"offsetInBeginSection": 219,
"offsetInEndSection": 424,
"text": "Three genes are known to cause nemaline myopathy: the genes for nebulin (NEB) on chromosome 2q22, slow alpha-tropomyosin (TPM3) on chromosome 1q21 and skeletal muscle alpha-actin (ACTA1) on chromosome 1q42"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16945536",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "Most nemaline myopathy patients have mutations in the nebulin (NEB) or skeletal muscle alpha-actin (ACTA1) genes"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/19648653",
"endSection": "abstract",
"offsetInBeginSection": 384,
"offsetInEndSection": 633,
"text": "Severe forms of nemaline myopathy may be caused by mutation of a number of different genes: skeletal muscle actin (ACTA1), nebulin (NEB) and alpha-tropomyosin (TPM3), all of which encode components of the sarcomeric thin filaments of skeletal muscle"
},
{
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"document": "http://www.ncbi.nlm.nih.gov/pubmed/22358459",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 214,
"text": "Nemaline myopathy (NM) is the most common congenital myopathy and is caused by mutations in various genes including NEB (nebulin), TPM2 (beta-tropomyosin), TPM3 (gamma-tropomyosin), and ACTA1 (skeletal alpha-actin)"
},
{
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"offsetInBeginSection": 139,
"offsetInEndSection": 359,
"text": "Mutations in three different genes have been identified as the cause of nemaline myopathy: the gene for slow alpha-tropomyosin 3 (TPM3) at 1q22-23, the nebulin gene (NEB) at 2q21.1-q22, and the actin gene (ACTA1) at 1q42"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805120",
"endSection": "abstract",
"offsetInBeginSection": 125,
"offsetInEndSection": 294,
"text": "Five genes have now been associated with nemaline myopathy: alpha-tropomyosin-3 (TPM3), alpha-actin (ACTA1), nebulin (NEB), beta-tropomysin (TPM2) and troponin T (TNNT1)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11166164",
"endSection": "abstract",
"offsetInBeginSection": 219,
"offsetInEndSection": 424,
"text": "Three genes are known to cause nemaline myopathy: the genes for nebulin (NEB) on chromosome 2q22, slow alpha-tropomyosin (TPM3) on chromosome 1q21 and skeletal muscle alpha-actin (ACTA1) on chromosome 1q42"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16945536",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "Most nemaline myopathy patients have mutations in the nebulin (NEB) or skeletal muscle alpha-actin (ACTA1) genes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22358459",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 214,
"text": "Nemaline myopathy (NM) is the most common congenital myopathy and is caused by mutations in various genes including NEB (nebulin), TPM2 (beta-tropomyosin), TPM3 (gamma-tropomyosin), and ACTA1 (skeletal alpha-actin)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11257471",
"endSection": "abstract",
"offsetInBeginSection": 139,
"offsetInEndSection": 359,
"text": "Mutations in three different genes have been identified as the cause of nemaline myopathy: the gene for slow alpha-tropomyosin 3 (TPM3) at 1q22-23, the nebulin gene (NEB) at 2q21.1-q22, and the actin gene (ACTA1) at 1q42"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11166164",
"endSection": "abstract",
"offsetInBeginSection": 219,
"offsetInEndSection": 424,
"text": "Three genes are known to cause nemaline myopathy: the genes for nebulin (NEB) on chromosome 2q22, slow alpha-tropomyosin (TPM3) on chromosome 1q21 and skeletal muscle alpha-actin (ACTA1) on chromosome 1q42"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16945536",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "Most nemaline myopathy patients have mutations in the nebulin (NEB) or skeletal muscle alpha-actin (ACTA1) genes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22358459",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 214,
"text": "Nemaline myopathy (NM) is the most common congenital myopathy and is caused by mutations in various genes including NEB (nebulin), TPM2 (beta-tropomyosin), TPM3 (gamma-tropomyosin), and ACTA1 (skeletal alpha-actin)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11257471",
"endSection": "abstract",
"offsetInBeginSection": 139,
"offsetInEndSection": 359,
"text": "Mutations in three different genes have been identified as the cause of nemaline myopathy: the gene for slow alpha-tropomyosin 3 (TPM3) at 1q22-23, the nebulin gene (NEB) at 2q21.1-q22, and the actin gene (ACTA1) at 1q42"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12805120",
"endSection": "abstract",
"offsetInBeginSection": 125,
"offsetInEndSection": 294,
"text": "Five genes have now been associated with nemaline myopathy: alpha-tropomyosin-3 (TPM3), alpha-actin (ACTA1), nebulin (NEB), beta-tropomysin (TPM2) and troponin T (TNNT1)"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11166164",
"endSection": "abstract",
"offsetInBeginSection": 219,
"offsetInEndSection": 424,
"text": "Three genes are known to cause nemaline myopathy: the genes for nebulin (NEB) on chromosome 2q22, slow alpha-tropomyosin (TPM3) on chromosome 1q21 and skeletal muscle alpha-actin (ACTA1) on chromosome 1q42"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/16945536",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 112,
"text": "Most nemaline myopathy patients have mutations in the nebulin (NEB) or skeletal muscle alpha-actin (ACTA1) genes"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/19648653",
"endSection": "abstract",
"offsetInBeginSection": 384,
"offsetInEndSection": 633,
"text": "Severe forms of nemaline myopathy may be caused by mutation of a number of different genes: skeletal muscle actin (ACTA1), nebulin (NEB) and alpha-tropomyosin (TPM3), all of which encode components of the sarcomeric thin filaments of skeletal muscle"
}
]
| 5 | BioASQ-training5b | [
"http://www.uniprot.org/uniprot/ACTS_CYPCA",
"http://www.uniprot.org/uniprot/ACTS_ATRMM",
"http://www.uniprot.org/uniprot/ACTS_OREMO",
"http://www.uniprot.org/uniprot/ACTS_CARAU",
"http://www.uniprot.org/uniprot/ACTS_ORYLA",
"http://www.uniprot.org/uniprot/NEBU_HUMAN",
"http://www.disease-ontology.org/api/metadata/DOID:3191",
"http://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&exact=Find+Exact+Term&term=D017696"
]
| []
| 552440452c8b63434a00000b | 316 |
yesno | Proteomic analyses need prior knowledge of the organism complete genome. Is the complete genome of the bacteria of the genus Arthrobacter available? | ['Yes'] | [
"Yes"
]
| ['Yes, the complete genome sequence of Arthrobacter (two strains) is deposited in GenBank.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/21677849",
"http://www.ncbi.nlm.nih.gov/pubmed/23039946"
]
| []
| 5 | BioASQ-training5b | [
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D001173",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D016678"
]
| null | 51593dc8d24251bc05000099 | 317 |
yesno | Can cardiospheres be produced from skin fibroblasts? | ['yes'] | [
"yes"
]
| ['Yes, induced cardiospheres (iCS) can be produced by somatic reprogramming of mouse fibroblasts using a panel of pluripotent transcription factors and cardiotrophic growth factors.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/29999590"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29999590",
"endSection": "abstract",
"offsetInBeginSection": 331,
"offsetInEndSection": 461,
"text": "Therefore, there is an emerging interest in generating cardiosphere-like stem cells from somatic cells via somatic reprogramming. "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29999590",
"endSection": "abstract",
"offsetInBeginSection": 569,
"offsetInEndSection": 805,
"text": "Here we provide the detailed protocol for generating induced cardiospheres (iCS) for cardiac regeneration by somatic reprogramming of mouse fibroblasts using a panel of pluripotent transcription factors and cardiotrophic growth factors."
}
]
| 11 | BioASQ-training11b | null | null | 5c928afeecadf2e73f000018 | 318 |
yesno | Does Serca2a bind PLN in the heart? | ['Yes'] | [
"Yes"
]
| ['Yes, Serca2a bind PLN in the heart.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/22693651",
"http://www.ncbi.nlm.nih.gov/pubmed/22659291",
"http://www.ncbi.nlm.nih.gov/pubmed/22155237",
"http://www.ncbi.nlm.nih.gov/pubmed/22129433",
"http://www.ncbi.nlm.nih.gov/pubmed/20484118",
"http://www.ncbi.nlm.nih.gov/pubmed/17515962",
"http://www.ncbi.nlm.nih.gov/pubmed/17241641",
"http://www.ncbi.nlm.nih.gov/pubmed/11854448",
"http://www.ncbi.nlm.nih.gov/pubmed/12424227",
"http://www.ncbi.nlm.nih.gov/pubmed/12589804",
"http://www.ncbi.nlm.nih.gov/pubmed/12610310",
"http://www.ncbi.nlm.nih.gov/pubmed/12763867",
"http://www.ncbi.nlm.nih.gov/pubmed/9603928",
"http://www.ncbi.nlm.nih.gov/pubmed/9182523",
"http://www.ncbi.nlm.nih.gov/pubmed/8702967"
]
| [
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22155237",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 110,
"text": "The human phospholamban Arg14-deletion mutant localizes to plasma membrane and interacts with the Na/K-ATPase."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22155237",
"endSection": "sections.0",
"offsetInBeginSection": 1259,
"offsetInEndSection": 1338,
"text": "Moreover, PLN-R14Del did not co-immunoprecipitate with SERCA2a (as did WT-PLN),"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22129433",
"endSection": "sections.0",
"offsetInBeginSection": 441,
"offsetInEndSection": 695,
"text": "n this review, we attempted to highlight the functional significance of PLN in vertebrate cardiac physiology. We will refer to the huge literature on mammals in order to describe the molecular characteristics of this protein, its interaction with SERCA2a"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8702967",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 189,
"text": "There is clear evidence for direct regulatory protein-protein interactions between phospholamban (PLN) and the Ca2+-ATPase of cardiac sarcoplasmic reticulum (SERCA2a) in cytoplasmic domains"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/8702967",
"endSection": "sections.0",
"offsetInBeginSection": 1216,
"offsetInEndSection": 1447,
"text": "These results suggest that PLN modulates the apparent Ca2+ affinity of SERCA2a through intramembrane interactions, which are disrupted at long range and in concert with disruption of the well characterized cytoplasmic interactions."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9182523",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 183,
"text": "Phospholamban (PLN), a homopentameric, integral membrane protein, reversibly inhibits cardiac sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) activity through intramembrane interactions."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9182523",
"endSection": "sections.0",
"offsetInBeginSection": 1247,
"offsetInEndSection": 1493,
"text": "The concentration of this inhibited complex is determined by the dissociation constant for the PLN pentamer (which is mutation-sensitive) and by the dissociation constant for the PLN/SERCA2a heterodimer (which is likely to be mutation-sensitive)."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/9603928",
"endSection": "sections.0",
"offsetInBeginSection": 1439,
"offsetInEndSection": 1634,
"text": "These results support the proposal that PLN inhibition of SERCA2a involves, first, depolymerization of PLN and, second, the formation of inhibitory interactions between monomeric PLN and SERCA2a."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12763867",
"endSection": "sections.0",
"offsetInBeginSection": 979,
"offsetInEndSection": 1162,
"text": "SLN and PLN appear to bind to the same regulatory site in SERCA. However, in a ternary complex, PLN occupies the regulatory site and SLN binds to the exposed side of PLN and to SERCA."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12610310",
"endSection": "sections.0",
"offsetInBeginSection": 595,
"offsetInEndSection": 707,
"text": "Cellular and biochemical studies revealed that, unlike wild-type PLN, PLN(R9C) did not directly inhibit SERCA2a."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/12589804",
"endSection": "sections.0",
"offsetInBeginSection": 789,
"offsetInEndSection": 997,
"text": ". Conversely, using anti-SERCA2a antibody, both PLN and acylphosphatase were co-immunoprecipitated with SERCA2a, and the PLN amount in the precipitate decreased with increasing acylphosphatase concentrations."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11854448",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 120,
"text": "Reconstitution of the cytoplasmic interaction between phospholamban and Ca(2+)-ATPase of cardiac sarcoplasmic reticulum."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/11854448",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 235,
"text": "Phospholamban (PLN) reversibly inhibits the Ca(2+)-ATPase of cardiac sarcoplasmic reticulum (SERCA2a) through a direct protein-protein interaction, playing a pivotal role in the regulation of intracellular Ca(2+) in heart muscle cells."
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17241641",
"endSection": "sections.0",
"offsetInBeginSection": 0,
"offsetInEndSection": 258,
"text": "Phospholamban (PLN) is a key regulator of Ca(2+) homeostasis and contractility in the heart. Its regulatory effects are mediated through its interaction with the sarcoplasmic reticulum Ca(2+)-ATPase, (SERCA2a), resulting in alterations of its Ca(2+)-affinity"
},
{
"beginSection": "sections.0",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/20484118",
"endSection": "sections.0",
"offsetInBeginSection": 1138,
"offsetInEndSection": 1284,
"text": "In a co-immunoprecipitation of PLN with SERCA2a, the physical interaction between the two proteins was increased in PUGNAc-treated cardiomyocytes."
}
]
| 5 | BioASQ-training5b | [
"http://www.uniprot.org/uniprot/PPLA_HUMAN",
"http://www.nlm.nih.gov/cgi/mesh/2012/MB_cgi?field=uid&exact=Find+Exact+Term&term=D053498"
]
| null | 51680b05298dcd4e51000064 | 320 |
yesno | Is Periostin a novel biomarker of TH2-driven asthma? | ['yes'] | [
"yes"
]
| ['Yes, Periostin is a novel biomarker of TH2-driven asthma.', 'Serum periostin associates with type-2 inflammation in asthmatic airways, but also reflects whole body periostin levels originating from multiple sources.', 'Periostin has been proposed as a candidate marker of TH2-driven asthma.', 'Yes, periostin is a novel biomarker of TH2-driven asthma.', 'Periostin is a novel biomarker of TH2-driven asthma', 'Periostin is a potential novel biomarker of TH2-driven asthma.', 'Yes, periostin is a novel biomarker of TH2-driven asthma', 'Yes. Periostin is a novel biomarker of TH2-driven asthma.', 'Yes, Periostin is considered an important biomarker for the identification of T2 asthma, which is a type of TH2-driven asthma.', 'Yes, periostin can be measured in serum and the levels correlate with Th2-driven asthma activity.'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/33203095",
"http://www.ncbi.nlm.nih.gov/pubmed/30342583",
"http://www.ncbi.nlm.nih.gov/pubmed/24748808",
"http://www.ncbi.nlm.nih.gov/pubmed/29879994",
"http://www.ncbi.nlm.nih.gov/pubmed/25838094",
"http://www.ncbi.nlm.nih.gov/pubmed/33228831",
"http://www.ncbi.nlm.nih.gov/pubmed/24247042",
"http://www.ncbi.nlm.nih.gov/pubmed/37260069",
"http://www.ncbi.nlm.nih.gov/pubmed/28942959",
"http://www.ncbi.nlm.nih.gov/pubmed/25037608",
"http://www.ncbi.nlm.nih.gov/pubmed/30964557",
"http://www.ncbi.nlm.nih.gov/pubmed/36763690",
"http://www.ncbi.nlm.nih.gov/pubmed/27751727",
"http://www.ncbi.nlm.nih.gov/pubmed/28398635",
"http://www.ncbi.nlm.nih.gov/pubmed/27054127",
"http://www.ncbi.nlm.nih.gov/pubmed/22857879",
"http://www.ncbi.nlm.nih.gov/pubmed/34796003",
"http://www.ncbi.nlm.nih.gov/pubmed/29342461",
"http://www.ncbi.nlm.nih.gov/pubmed/30574168",
"http://www.ncbi.nlm.nih.gov/pubmed/35278445",
"http://www.ncbi.nlm.nih.gov/pubmed/25479456",
"http://www.ncbi.nlm.nih.gov/pubmed/24759559",
"http://www.ncbi.nlm.nih.gov/pubmed/37794472",
"http://www.ncbi.nlm.nih.gov/pubmed/24300416",
"http://www.ncbi.nlm.nih.gov/pubmed/36753209",
"http://www.ncbi.nlm.nih.gov/pubmed/29648484"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36763690",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 167,
"text": " Serum periostin associates with type-2 inflammation in asthmatic airways, but also reflects whole body periostin levels originating from multiple sources. "
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36763690",
"endSection": "title",
"offsetInBeginSection": 1,
"offsetInEndSection": 81,
"text": " novel assay for improved detection of sputum periostin in patients with asthma."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36753209",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 94,
"text": "Periostin as an important biomarker of inflammatory phenotype T2 in Brazilian asthma patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36753209",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 193,
"text": "The aim of this study was to assess the laboratory performance of periostin associated with a panel of biomarkers to identify the inflammatory phenotype of Brazilian asthma patients."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37260069",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 89,
"text": "Relationship of Serum Periostin With Asthma Control in Children: Single Center Experience"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37260069",
"endSection": "abstract",
"offsetInBeginSection": 11,
"offsetInEndSection": 102,
"text": "To determine the association between serum periostin levels and asthma control in children."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37260069",
"endSection": "abstract",
"offsetInBeginSection": 956,
"offsetInEndSection": 1072,
"text": "Asthmatic children have a high serum periostin level, and its higher levels are associated with poor asthma control."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36753209",
"endSection": "abstract",
"offsetInBeginSection": 1290,
"offsetInEndSection": 1372,
"text": "Periostin proved to be an important biomarker for the identification of T2 asthma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36763690",
"endSection": "abstract",
"offsetInBeginSection": 1615,
"offsetInEndSection": 1810,
"text": "n. Sputum periostin is worth considering as a phenotype-specific biomarker in asthma as its proximity to the airways may eliminate some of the confounding factors known to affect serum periostin."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36763690",
"endSection": "abstract",
"offsetInBeginSection": 1481,
"offsetInEndSection": 1614,
"text": ". Using this assay, sputum periostin was detectable and associated with more disease-relevant parameters in asthma than serum periost"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/37794472",
"endSection": "abstract",
"offsetInBeginSection": 1109,
"offsetInEndSection": 1311,
"text": "This study combines a panel of non-T2 inflammatory markers (low periostin, low blood-eosinophils, and low FeNO), to determine if this group of patients can maintain asthma control during ICS withdrawal."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/36753209",
"endSection": "abstract",
"offsetInBeginSection": 736,
"offsetInEndSection": 1251,
"text": "d an AUC greater than 65%. Periostin (OR: 12,550; 95% CI: 2,498-63,063) and IL-6 (OR: 7,249; 95% CI: 1,737-30,262) revealed to be suitable asthma inflammation biomarkers. Blood eosinophils, FeNO, total IgE, IL-6, TNF, and IFN-g showed correlations with clinical severity characteristics in asthmatic patients. Periostin showed higher values in T2 asthma (p = 0.006) and TNF in non-T2 asthma (p = 0.029).CONCLUSION: The panel of biomarkers proposed for the identification of the inflammatory phenotype of asthmatic p"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33228831",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1768,
"text": "BACKGROUND: Serum thymus and activation-regulated chemokine (TARC) and periostin are reliable biomarkers in eosinophilicasthma.OBJECTIVE: This study was carried out to determine the use of periostin and TARC as biomarkers in asthma and to comparethe superiority of one over the other, especially in asthma with an eosinophilic phenotype.METHODS: The study was conducted with 87 patients with asthma and 42 healthy control subjects. Patients with asthma were also divided into eosinophilic and non-eosinophilic phenotypes. A pulmonary function test was performed in all the participants,and serum and induced sputum TARC, periostin concentrations, eosinophils, and total immunoglobulin E valueswere examined.RESULTS: TARC and periostin levels were significantly higher in the asthma group than in the control group (p < 0.001). The serum TARC level in the eosinophilic group was significantly higher than in the non-eosinophilic and control groups(p < 0.001). The induced sputum TARC level was significantly higher in the non-eosinophilic group than in the control group(p < 0.001). The TARC and periostin levels of the patients were evaluated by using receiver operator characteristic analysis.The cutoff value for TARC was determined to be 1415.39 ng/L; likewise, the cutoff value for periostin was 107.60 ng/L. Thepresent study detected that serum levels of TARC correlated to serum levels of periostin (r = 0.54; p = 0.032). Furthermore,when evaluating correlations between serum and sputum levels, there was a correlation detected between TARC and periostinin serum, whereas this correlation was stronger in sputum: r = 0.66, p = 0.020; and r = 0.62, p = 0.028, respectively.CONCLUSION: Serum and sputum TARC and periostin may contribute for monitoring the improve"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29648484",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1609,
"text": "OBJECTIVE: Periostin, a matricellular protein, is produced from airway epithelial cells and lung fibroblasts by IL-13. It has been suggested that periostin is involved in allergic inflammation and fibrosis. However, the usefulness of serum periostin measurement in the assessment of airway inflammation and remodeling and management of asthmatic patients is still debated. We aimed to determine whether serum periostin levels reflect eosinophilic airway inflammation and airway remodeling in asthma.METHODS: We examined the relationship of serum periostin levels with clinical features, biomarkers for eosinophilic airway inflammation, fraction of exhaled nitric oxide (FeNO) levels and blood eosinophil counts, and pulmonary functions in 235 well-controlled asthmatic patients on inhaled corticosteroids (ICS) treatment.RESULTS: Serum periostin levels were positively correlated with blood eosinophil counts (%) and age (r = 0.36 and 0.23, respectively), and were negatively correlated with body weight and FEV1/FVC (%) (r = -0.24 and - 0.23, respectively) in well-controlled asthmatic patients on ICS treatment (daily dose of 453 µg equivalent to fluticasone propionate). Blood eosinophil counts and serum periostin levels were similarly associated with increased FeNO levels (≥40 ppb) in the asthmatics. Serum periostin levels were better associated with fixed airflow limitation (FEV1/FVC ratio <70%) than FeNO levels, blood eosinophil counts or total IgE levels in the asthmatics. Multivariate analysis showed that fixed airflow limitation was significantly associated with high serum periostin levels (≥"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/33203095",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1206,
"text": "Periostin and thymic stromal lymphopoietin (TSLP) are newly described markers of obstructive airway diseases and the mechanism by which both markers participate in immune response remains poorly understood. The aim of our study was to determine periostin and TSLP concentration in serum and induced sputum (IS) in patients with atopic asthma, chronic obstructive pulmonary disease (COPD), and controls, as well as to evaluate the potential link between periostin, TSLP, and Th2 immune response. Serum and IS levels of periostin, TSLP, IL-4, and IL-13 were determined in 12 atopic asthmatics, 16 COPD sufferers, and 10 controls. We noticed a significantly higher IS periostin and TSLP concentration at protein and mRNA level in asthmatics compared to the two other groups; additionally, periostin and TSLP were correlated positively with IS eosinophil count. A strong positive correlation between IS periostin and TSLP protein levels (r = 0.96) as well as mRNA expression level (r = 0.95) was found in patients with asthma. The results of our study show that periostin and TSLP are associated with eosinophilic airway inflammation and seem to be important drivers of atopic asthma but not COPD pathobiology."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30574168",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1728,
"text": "BACKGROUND: Periostin has been shown to be a marker of Type 2 airway inflammation, associated with airway eosinophilia. It has a potential role in identifying asthmatics who may be responsive to treatment with monoclonal antibody therapy directed against Type 2 cytokines, such as interleukin (IL)-13, IL-4 receptor subunit-α and immunoglobulin E. The clinical utility of periostin measurements depends on better understanding of factors that may affect serum periostin levels, such as race. We aimed to identify the ranges of serum periostin in Chinese adults both with and without asthma, and compare them with those previously identified in Caucasian adults.METHODS: A two-centred cross-sectional study, recruiting 188 Chinese adults, aged 18 to 75 years. 120 participants had no history of asthma or chronic obstructive pulmonary disease. 68 participants had a doctor's diagnosis of asthma and were on current treatment. Univariate comparisons of periostin by dichotomous variables were made using t-tests with logarithmic transformation as the distribution of periostin was skewed.RESULTS: In the Chinese non-asthma group, periostin levels were sex-, but not age-dependent, with females having higher periostin levels. The individual predicted (90% CI) reference range for periostin in females was 61.1 ng/ml (41.6 to 89.8) ng/ml and in males was 53.2 ng/ml (36.1 to 78.3) ng/ml. There was no difference in median serum periostin levels between Chinese non-asthmatics and Chinese asthmatics, 57.0 versus 56.8 ng/ml, difference (95% CI) 0.1 (- 4.2 to 4.2) ng/ml, P = 0.94. The median serum periostin levels were higher in Chinese non-asthmatics than Caucasian non-asthmatics, 57.0 versus 49.7 ng/ml, difference (95% CI) 8.2 "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/34796003",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1976,
"text": "The involvement of periostin in Th2-dependent allergic inflammation has been documented. However, the significance of periostin as a biomarker of local allergic inflammation in the nasal mucosa (NM) of patients with atopic bronchial asthma (BA) and allergic rhinitis (AR) is yet to be determined. The aim of the study was to determine the presence of periostin and evaluate its role as a non-invasive marker of allergic inflammation in the nasal secretions of children with atopic BA and AR.MATERIALS AND METHODS: In 43 patients aged 4-17 years with atopic BA and AR, the NM was examined using nasal video-endoscopy and (if indicated) computed tomography; the amount of periostin in the nasal secretion was determined by the enzyme immunoassay.RESULTS: Exacerbation of AR was accompanied by a statistically significant increase in the level of periostin in the nasal secretion: up to 0.84 [0.06; 48.79] ng/mg, whereas in remission, that was 0.13 [0.00; 0.36] ng/mg; p=0.04. This value increased progressively as the severity of AR increased from 0.16 [0.00; 0.36] ng/mg in the mild course to 0.20 [0.00; 9.03] ng/mg in AR of moderate severity, and to 10.70 [0.56; 769.20] ng/mg in most severe cases; p=0.048. Hypertrophy or polyposis of the nasal and/or paranasal mucosa was detected in 34.9% (15/43) of the examined patients. The concentration of periostin in the nasal secretion was lower in children without NM hypertrophy: 0.18 [0.001; 4.30] ng/mg vs 0.78 [0.13; 162.10] ng/mg in patients with NM hypertrophy; the differences were close to statistically significant: p=0.051. The level of nasal periostin depended on the clinical form of hypertrophy in the sinonasal mucosa, reaching 0.17 [0.00; 0.32] ng/mg in children with polyposis hyperplasia of NM and 21.6 [10.70; 1516.80] ng/mg - with hypertrophy of the NM in the medial surface of the concha; p=0.02.CONCLUSION: Exacerbation and increased severity of AR in patients with atopic BA are accompanied by an increased l"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35278445",
"endSection": "abstract",
"offsetInBeginSection": 284,
"offsetInEndSection": 1844,
"text": "The serum level of periostin, an extracellular matrix protein activated by Th2 cytokines, is recognized as a biomarker for Th2-mediated eosinophilic asthma and contributes to enhanced airway inflammation and remodeling. However, the role of periostin in arsenic-related asthma is unknown. Therefore, this study was designed to explore the associations of serum periostin levels with arsenic exposure and the features of asthma in 442 individuals in Bangladesh who participated in our previous study. Exposure levels of the participants were determined by measuring the arsenic concentrations in drinking water, hair, and nails through inductively coupled plasma mass spectroscopy. Periostin levels in serum were assessed by immunoassay. In this study, we found that serum periostin levels of the participants were increased with increasing exposure to arsenic. Notably, even the participants with 10.1-50 μg/L arsenic in drinking water had significantly higher levels of periostin than participants with <10 μg/L of water arsenic. Elevated serum periostin levels were positively associated with serum levels of Th2 mediators, such as interleukin (IL)-4, IL-5, IL-13, and eotaxin. Each log increase in periostin levels was associated with approximately eight- and three-fold increases in the odds ratios (ORs) for reversible airway obstruction (RAO) and asthma symptoms, respectively. Additionally, causal mediation analyses revealed that arsenic exposure metrics had both direct and indirect (periostin-mediated) effects on the risk of RAO and asthma symptoms."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28942959",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1063,
"text": "Periostin, an extracellular matrix protein belonging to the fasciclin family, has been shown to play a critical role in the process of remodeling during tissue/organ development or repair. Periostin functions as a matricellular protein in cell activation by binding to their receptors on cell surface, thereby exerting its biological activities. After we found that periostin is a downstream molecule of interleukin (IL)-4 and IL-13, signature cytokines of type 2 immune responses, we showed that periostin is a component of subepithelial fibrosis in bronchial asthma, the first formal proof that periostin is involved in allergic inflammation. Subsequently, a great deal of evidence has accumulated demonstrating the significance of periostin in allergic inflammation. It is of note that in skin tissues, periostin is critical for amplification and persistence of allergic inflammation by communicating between fibroblasts and keratinocytes. Furthermore, periostin has been applied to development of novel diagnostics or therapeutic agents for allergic diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30342583",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 578,
"text": "Periostin and dipeptidyl peptidase-4 (DPP-4) are proteins induced by type 2 cytokines interleukin (IL)-4 and IL-13 and show increased expression in asthma and diseases with type 2 inflammation, including atopic dermatitis and chronic rhinosinusitis. Both proteins can also be induced by other stimuli, such as profibrotic factors, which may confound their specificity as biomarkers of IL-13 pathway activation and type 2-driven disease. DPP-4 is important in glucose metabolism; therefore, serum concentrations may be confounded by the presence of concomitant metabolic disease."
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24247042",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 50,
"text": "Periostin, a novel biomarker of TH2-driven asthma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24247042",
"endSection": "abstract",
"offsetInBeginSection": 244,
"offsetInEndSection": 373,
"text": " This review focuses on the emerging data surrounding the use of one such biomarker for T helper 2 (TH2)-driven asthma: periostin"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24247042",
"endSection": "abstract",
"offsetInBeginSection": 244,
"offsetInEndSection": 531,
"text": " This review focuses on the emerging data surrounding the use of one such biomarker for T helper 2 (TH2)-driven asthma: periostin.RECENT FINDINGS: Periostin is an extracellular matrix protein that is induced by interleukin (IL)-4 and IL-13 in airway epithelial cells and lung fibroblasts"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24247042",
"endSection": "abstract",
"offsetInBeginSection": 91,
"offsetInEndSection": 531,
"text": " Biomarkers are currently being investigated to better characterize the disease phenotypes and to identify the responders to specific targeted therapies. This review focuses on the emerging data surrounding the use of one such biomarker for T helper 2 (TH2)-driven asthma: periostin.RECENT FINDINGS: Periostin is an extracellular matrix protein that is induced by interleukin (IL)-4 and IL-13 in airway epithelial cells and lung fibroblasts"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27054127",
"endSection": "abstract",
"offsetInBeginSection": 93,
"offsetInEndSection": 388,
"text": " The molecular phenotypes in asthma are Th2 high and Th2 low. Serum periostin is a biomarker which aid in understanding Th2 high eosinophilic asthma.AIM: The present study aimed to identify whether or not serum periostin is a systemic biomarker for eosinophilic airway inflammation in asthmatics"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24247042",
"endSection": "abstract",
"offsetInBeginSection": 244,
"offsetInEndSection": 662,
"text": " This review focuses on the emerging data surrounding the use of one such biomarker for T helper 2 (TH2)-driven asthma: periostin.RECENT FINDINGS: Periostin is an extracellular matrix protein that is induced by interleukin (IL)-4 and IL-13 in airway epithelial cells and lung fibroblasts. It has proven to be an important biomarker of TH2-associated airway inflammation and a potential predictor of airway eosinophilia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29879994",
"endSection": "abstract",
"offsetInBeginSection": 116,
"offsetInEndSection": 269,
"text": "Since periostin is associated with Th2 driven inflammation and inhaled corticosteroid (ICS)-response in asthma, it could function as a biomarker in COPD."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24247042",
"endSection": "abstract",
"offsetInBeginSection": 91,
"offsetInEndSection": 373,
"text": " Biomarkers are currently being investigated to better characterize the disease phenotypes and to identify the responders to specific targeted therapies. This review focuses on the emerging data surrounding the use of one such biomarker for T helper 2 (TH2)-driven asthma: periostin"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27054127",
"endSection": "abstract",
"offsetInBeginSection": 93,
"offsetInEndSection": 241,
"text": " The molecular phenotypes in asthma are Th2 high and Th2 low. Serum periostin is a biomarker which aid in understanding Th2 high eosinophilic asthma"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24247042",
"endSection": "abstract",
"offsetInBeginSection": 245,
"offsetInEndSection": 532,
"text": "This review focuses on the emerging data surrounding the use of one such biomarker for T helper 2 (TH2)-driven asthma: periostin.RECENT FINDINGS: Periostin is an extracellular matrix protein that is induced by interleukin (IL)-4 and IL-13 in airway epithelial cells and lung fibroblasts."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27751727",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 230,
"text": "BACKGROUND: Periostin is being investigated as a potential biomarker for T-helper-2 (Th2)-driven asthma or eosinophilic inflammation and may help to identify patients more likely to benefit from interleukin-13-targeted treatments."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25037608",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 594,
"text": "BACKGROUND: Recent studies recommend periostin as a systemic biomarker of eosinophilic airway inflammation to predict responses to novel treatments that targets eosinophilic TH2-driven inflammation in asthmatic patients.OBJECTIVE: To investigate the clinical implications of serum periostin levels in patients with aspirin-exacerbated respiratory disease (AERD) based on its overlapping TH2-mediated pathogenesis with the eosinophilic asthma.METHODS: Serum periostin levels were measured by human periostin enzyme-linked immunosorbent assay (ELISA) in serum samples from 277 adults with asthma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27054127",
"endSection": "abstract",
"offsetInBeginSection": 1303,
"offsetInEndSection": 1616,
"text": "Serum periostin had a sensitivity and specificity of 97.18% and 86.67% with a diagnostic accuracy of 94.06%.CONCLUSION: Serum periostin appears to be a more sensitive tool for detection of airflow limitation in asthmatic patients with a Th2 high eosinophilic phenotype when compared to AEC and sputum eosinophils."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27054127",
"endSection": "abstract",
"offsetInBeginSection": 155,
"offsetInEndSection": 472,
"text": "Serum periostin is a biomarker which aid in understanding Th2 high eosinophilic asthma.AIM: The present study aimed to identify whether or not serum periostin is a systemic biomarker for eosinophilic airway inflammation in asthmatics.MATERIALS AND METHODS: The study was designed as a prospective, case control study."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28398635",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 123,
"text": "BACKGROUND: Periostin has been suggested as a novel, phenotype-specific biomarker for asthma driven by type 2 inflammation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24247042",
"endSection": "abstract",
"offsetInBeginSection": 356,
"offsetInEndSection": 954,
"text": "asthma: periostin.RECENT FINDINGS: Periostin is an extracellular matrix protein that is induced by interleukin (IL)-4 and IL-13 in airway epithelial cells and lung fibroblasts. It has proven to be an important biomarker of TH2-associated airway inflammation and a potential predictor of airway eosinophilia. It has also been shown to predict response to treatment with inhaled corticosteroids in patients with these characteristics. Furthermore, recent asthma clinical trials have established that serum periostin may have value in predicting the response to targeted therapy with biologic agents s"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25037608",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 208,
"text": "BACKGROUND: Recent studies recommend periostin as a systemic biomarker of eosinophilic airway inflammation to predict responses to novel treatments that targets eosinophilic TH2-driven inflammation in asthmat"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24748808",
"endSection": "abstract",
"offsetInBeginSection": 274,
"offsetInEndSection": 508,
"text": "Induced sputum cell count is the gold standard for identifying eosinophilic inflammation in asthma although several noninvasive biomarkers, including fractional exhaled nitric oxide and periostin, are emerging as potential surrogates."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/22857879",
"endSection": "abstract",
"offsetInBeginSection": 1307,
"offsetInEndSection": 1807,
"text": "A logistic regression model, including sex, age, body mass index, IgE levels, blood eosinophil numbers, Feno levels, and serum periostin levels, in 59 patients with severe asthma showed that, of these indices, the serum periostin level was the single best predictor of airway eosinophilia (P = .007).CONCLUSION: Periostin is a systemic biomarker of airway eosinophilia in asthmatic patients and has potential utility in patient selection for emerging asthma therapeutics targeting T(H)2 inflammation."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25838094",
"endSection": "abstract",
"offsetInBeginSection": 1450,
"offsetInEndSection": 1792,
"text": "In contrast, neither atopic status, control status of asthma, nor quality of life were related with the \"high-periostin\" phenotype.CONCLUSION: Elevated periostin concentrations in serum were correlated with a specific phenotype of eosinophilic asthma, late-onset and often complicated by obstructive pulmonary dysfunction and nasal disorders."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29879994",
"endSection": "abstract",
"offsetInBeginSection": 116,
"offsetInEndSection": 268,
"text": "Since periostin is associated with Th2 driven inflammation and inhaled corticosteroid (ICS)-response in asthma, it could function as a biomarker in COPD"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29342461",
"endSection": "abstract",
"offsetInBeginSection": 169,
"offsetInEndSection": 305,
"text": "Periostin, a biomarker that reflects Th2-driven inflammatory diseases such as asthma, may play an important role in the asthmatic airway"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27751727",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 229,
"text": "Periostin is being investigated as a potential biomarker for T-helper-2 (Th2)-driven asthma or eosinophilic inflammation and may help to identify patients more likely to benefit from interleukin-13-targeted treatments"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25037608",
"endSection": "abstract",
"offsetInBeginSection": 12,
"offsetInEndSection": 220,
"text": "Recent studies recommend periostin as a systemic biomarker of eosinophilic airway inflammation to predict responses to novel treatments that targets eosinophilic TH2-driven inflammation in asthmatic patients."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27751727",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 218,
"text": "BACKGROUND: Periostin is being investigated as a potential biomarker for T-helper-2 (Th2)-driven asthma or eosinophilic inflammation and may help to identify patients more likely to benefit from interleukin-13-targeted"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/35278445",
"endSection": "abstract",
"offsetInBeginSection": 284,
"offsetInEndSection": 503,
"text": "The serum level of periostin, an extracellular matrix protein activated by Th2 cytokines, is recognized as a biomarker for Th2-mediated eosinophilic asthma and contributes to enhanced airway inflammation and remodeling."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24247042",
"endSection": "abstract",
"offsetInBeginSection": 356,
"offsetInEndSection": 628,
"text": "asthma: periostin.RECENT FINDINGS: Periostin is an extracellular matrix protein that is induced by interleukin (IL)-4 and IL-13 in airway epithelial cells and lung fibroblasts. It has proven to be an important biomarker of TH2-associated airway inflammation and a potentia"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24300416",
"endSection": "abstract",
"offsetInBeginSection": 750,
"offsetInEndSection": 932,
"text": "nse or adjustment and FeNO levels. Serum periostin is a strong serum biomarker for eosinophilic airway inflammation and an indicator of Th2-targeted therapy (such as lebrikizumab or "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24759559",
"endSection": "abstract",
"offsetInBeginSection": 597,
"offsetInEndSection": 853,
"text": "serum periostin measurements by describing observations made in a KiHAC multicenter cohort with periostin used as a marker of pulmonary function decline and refractory Th2/eosinophilic inflammation in patients with asthma receiving long-term ICS treatment."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/24247042",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 753,
"text": "PURPOSE OF REVIEW: Asthma is a heterogeneous disease with multiple, overlapping phenotypes. Biomarkers are currently being investigated to better characterize the disease phenotypes and to identify the responders to specific targeted therapies. This review focuses on the emerging data surrounding the use of one such biomarker for T helper 2 (TH2)-driven asthma: periostin.RECENT FINDINGS: Periostin is an extracellular matrix protein that is induced by interleukin (IL)-4 and IL-13 in airway epithelial cells and lung fibroblasts. It has proven to be an important biomarker of TH2-associated airway inflammation and a potential predictor of airway eosinophilia. It has also been shown to predict response to treatment with inhaled corticosteroids in p"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25838094",
"endSection": "abstract",
"offsetInBeginSection": 66,
"offsetInEndSection": 839,
"text": "phenotypes. Periostin, a molecule inducible with interleukin (IL)-4 or IL-13 in bronchial epithelial cells, is a biomarker of \"TH2-high\" asthma. The objective of this study is to examine whether the serum periostin concentrations are correlated with the severity, specific phenotype(s), or comorbidity of asthma.METHODS: Serum concentrations of periostin were measured in 190 Japanese asthmatic patients and 11 healthy controls. The protocol was registered under UMIN 000002980 in the clinical trial registry.RESULTS: The serum concentrations of periostin were significantly higher (P = 0.014) in asthmatics [70.0 (54.0-93.5) ng/ml] than in healthy subjects [57.0 (39.0-63.0) ng/ml], though we found no correlation between serum periostin concentrations and treatment steps"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28398635",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1642,
"text": "BACKGROUND: Periostin has been suggested as a novel, phenotype-specific biomarker for asthma driven by type 2 inflammation. However, large studies examining relationships between circulating periostin and patient characteristics are lacking and the suitability of periostin as a biomarker in asthma remains unclear.AIM: To examine circulating periostin in healthy controls and subjects with asthma from the general population with different severity and treatment profiles, both with and without chronic rhinosinusitis (CRS), in relation to other biomarkers and clinical characteristics.METHODS: Serum periostin was examined by ELISA in 1100 subjects aged 17-76 from the Swedish Global Allergy and Asthma European Network (GA(2)LEN) study, which included 463 asthmatics with/without chronic rhinosinusitis (CRS), 98 individuals with CRS only, and 206 healthy controls. Clinical tests included measurement of lung function, Fraction of exhaled NO (FeNO), IgE, urinary eosinophil-derived neurotoxin (U-EDN), and serum eosinophil cationic protein (S-ECP), as well as completion of questionnaires regarding respiratory symptoms, medication, and quality of life.RESULTS: Although median periostin values showed no differences when comparing disease groups with healthy controls, multiple regression analyses revealed that periostin was positively associated with higher FeNO, U-EDN, and total IgE. In patients with asthma, an inverse relationship with lung function was also observed. Current smoking was associated with decreased periostin levels, whereas increased age and lower body mass index (BMI) related to higher periostin levels in subjec"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27751727",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 1177,
"text": "BACKGROUND: Periostin is being investigated as a potential biomarker for T-helper-2 (Th2)-driven asthma or eosinophilic inflammation and may help to identify patients more likely to benefit from interleukin-13-targeted treatments. We report the development and analytic performance of the investigational use only ARCHITECT Periostin Immunoassay, a new automated assay developed to detect serum periostin concentrations.METHODS: We assessed assay performance in terms of precision, sensitivity, linearity, interference from classical immunoassay interferents and representatives of common asthma medications, specimen handling, and isoform reactivity. The assay was also used to assess the biological variability of serum periostin concentrations in samples from healthy volunteers and from subjects with uncontrolled asthma (the intended use population).RESULTS: The percentage CVs for 5-day total precision, assessed using two instruments, was <6% across 2 controls and one serum-based panel. Limit of quantitation was 4ng/mL (dilution adjusted concentration), suiting the needs for this application. Dilution analysis yielded linear results and no endogenous sample or drug "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25037608",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 904,
"text": "BACKGROUND: Recent studies recommend periostin as a systemic biomarker of eosinophilic airway inflammation to predict responses to novel treatments that targets eosinophilic TH2-driven inflammation in asthmatic patients.OBJECTIVE: To investigate the clinical implications of serum periostin levels in patients with aspirin-exacerbated respiratory disease (AERD) based on its overlapping TH2-mediated pathogenesis with the eosinophilic asthma.METHODS: Serum periostin levels were measured by human periostin enzyme-linked immunosorbent assay (ELISA) in serum samples from 277 adults with asthma. Serum periostin levels were compared between patients with AERD and aspirin tolerant asthma (ATA) with other asthma phenotypes, such as severe or nonsevere asthma and eosinophilic or noneosinophilic asthma. The association of serum periostin levels with clinical parameters (including disease severity and com"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27054127",
"endSection": "abstract",
"offsetInBeginSection": 80,
"offsetInEndSection": 1363,
"text": "es of asthma. The molecular phenotypes in asthma are Th2 high and Th2 low. Serum periostin is a biomarker which aid in understanding Th2 high eosinophilic asthma.AIM: The present study aimed to identify whether or not serum periostin is a systemic biomarker for eosinophilic airway inflammation in asthmatics.MATERIALS AND METHODS: The study was designed as a prospective, case control study. Patients who presented with consistent symptoms of asthma and confirmed by spirometry with reversibility were the cases. The controls were healthy subjects who had no history of lung disease with normal lung function. The sputum and blood samples were collected from both the groups. Sputum eosinophils, Absolute Eosinophil Counts (AEC) and serum periostin levels were compared between the groups.RESULTS: The study comprised of 101 participants in which 30 were controls and 71 were cases. In the study group, mean post FEV1 was 64.45. There was a positive correlation of sputum eosinophils with severity of obstruction. The ROC curve analysis showed the cut-off value of 24.556 for serum periostin with the p-value of <0.001. As the severity of obstruction increased, the serum periostin levels were also found to be increased. Serum periostin had a sensitivity and specificity of 97.18% "
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29879994",
"endSection": "abstract",
"offsetInBeginSection": 116,
"offsetInEndSection": 1046,
"text": "Since periostin is associated with Th2 driven inflammation and inhaled corticosteroid (ICS)-response in asthma, it could function as a biomarker in COPD. The aim of this study was to analyze if serum periostin is elevated in COPD compared to healthy controls, if it is affected by smoking status, if it is linked to inflammatory cell counts in blood, sputum and endobronchial biopsies, and if periostin can predict ICS-response in COPD patients.Serum periostin levels were measured using Elecsys Periostin immunoassay. Correlations between periostin and inflammatory cell count in blood, sputum and endobronchial biopsies were analyzed. Additionally, the correlation between serum periostin levels and treatment responsiveness after 6 and 30 months was assessed using i.e. ΔFEV1% predicted, ΔCCQ score and ΔRV/TLC ratio. Forty-five COPD smokers, 25 COPD past-smokers, 22 healthy smokers and 23 healthy never-smokers were included."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/29342461",
"endSection": "abstract",
"offsetInBeginSection": 157,
"offsetInEndSection": 1634,
"text": "rtant role. Periostin, a biomarker that reflects Th2-driven inflammatory diseases such as asthma, may play an important role in the asthmatic airway. Although periostin is mainly produced in airway epithelial cells and fibroblasts after interleukin (IL)-13 stimulation, whether BSM cells produce periostin remains unclear. Therefore, we investigated periostin production in BSM cells and the mechanisms involved.METHODS: Human BSM cells were cultured, and the effect of IL-13 stimulation on periostin production was evaluated using quantitative polymerase chain reaction and enzyme-linked immunosorbent assay (ELISA). We evaluated the phosphorylation of signal transducer and activator of transcription factor 6 (STAT6), extracellular signal-regulated kinase (ERK)1/2, and Akt after IL-13 stimulation. Furthermore, using ELISA, we evaluated the influence of several phosphorylation inhibitors on periostin production.RESULTS: Periostin mRNA expression increased in a dose- and time-dependent manner after IL-13 stimulation; periostin production was induced 24 and 48 h after stimulation. IL-13 stimulation induced the phosphorylation of STAT6, ERK1/2, and Akt. IL-13-induced periostin production was attenuated by inhibiting STAT6 phosphorylation and strongly suppressed by inhibiting mitogen-activated protein kinase kinase 1/2 phosphorylation or phosphatidylinositol 3-kinase (PI3K) phosphorylation.CONCLUSIONS: BSM cells produced periostin after IL-13 stimulation, via the J"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30574168",
"endSection": "abstract",
"offsetInBeginSection": 0,
"offsetInEndSection": 107,
"text": "BACKGROUND: Periostin has been shown to be a marker of Type 2 airway inflammation, associated with airway e"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/30964557",
"endSection": "abstract",
"offsetInBeginSection": 266,
"offsetInEndSection": 533,
"text": "Since periostin is induced mainly by IL-4 and IL-13, signature type 2 cytokines, and it is highly expressed in the subepithelial regions of many chronic allergic diseases, periostin has emerged as a novel biomarker reflecting type 2 inflammation in allergic diseases."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/28942959",
"endSection": "abstract",
"offsetInBeginSection": 1064,
"offsetInEndSection": 1257,
"text": "Serum periostin can reflect local production of periostin in inflamed lesions induced by Th2-type immune responses and also can predict the efficacy of Th2 antagonists against bronchial asthma."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27054127",
"endSection": "abstract",
"offsetInBeginSection": 154,
"offsetInEndSection": 241,
"text": " Serum periostin is a biomarker which aid in understanding Th2 high eosinophilic asthma"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27054127",
"endSection": "abstract",
"offsetInBeginSection": 154,
"offsetInEndSection": 471,
"text": " Serum periostin is a biomarker which aid in understanding Th2 high eosinophilic asthma.AIM: The present study aimed to identify whether or not serum periostin is a systemic biomarker for eosinophilic airway inflammation in asthmatics.MATERIALS AND METHODS: The study was designed as a prospective, case control study"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/27054127",
"endSection": "abstract",
"offsetInBeginSection": 154,
"offsetInEndSection": 388,
"text": " Serum periostin is a biomarker which aid in understanding Th2 high eosinophilic asthma.AIM: The present study aimed to identify whether or not serum periostin is a systemic biomarker for eosinophilic airway inflammation in asthmatics"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25479456",
"endSection": "abstract",
"offsetInBeginSection": 654,
"offsetInEndSection": 944,
"text": "Promising biomarkers are sputum eosinophils, serum periostin and exhaled nitric oxide. Periostin could differentiate between Th2-high and Th2-low asthma (Th2-high patients are more responsive to glucocorticoids) and the less-defined asthma types which often present a therapeutic challenge."
}
]
| 13 | BioASQ-training13b | null | null | 662cf8db187cba990d000003 | 321 |
yesno | Is muscle regeneration possible in mdx mice with the use of induced mesenchymal stem cells? | ['yes'] | [
"yes"
]
| ['Purified induced mesenchymal stem cells (iMSCs) display fibroblast-like morphology, form three-dimensional spheroid structures, express characteristic mesenchymal stem cell surface markers such as CD29, CD33, CD73, CD90, and CD105, and are capable of differentiating into adipogenic, osteogenic, and chondrogenic lineages. Transplantation of iMSC cells to tibialis anterior skeletal muscle tissue in mdx mice lowers oxidative damage, and restores the expression levels of normal dystrophin, leading to skeletal muscle regeneration.', 'Purified iMSCs displayed fibroblast-like morphology, formed three-dimensional spheroid structures, and expressed characteristic mesenchymal stem cell surface markers such as CD29, CD33, CD73, CD90, and CD105. Moreover, iMSCs were capable of differentiating into adipogenic, osteogenic, and chondrogenic lineages. Transplanting iMSC cells to tibialis anterior skeletal muscle tissue in mdx mice lowered oxidative damage as evidenced by a reduction in nitrotyrosine levels, and normal dystrophin expression levels were restored', 'Purified iMSCs displayed fibroblast-like morphology, formed three-dimensional spheroid structures, and expressed characteristic mesenchymal stem cell surface markers such as CD29, CD33, CD73, CD90, and CD105. Moreover, iMSCs were capable of differentiating into adipogenic, osteogenic, and chondrogenic lineages. Transplanting iMSC cells to tibialis anterior skeletal muscle tissue in mdx mice lowered oxidative damage as evidenced by a reduction in nitrotyrosine levels, and normal dystrophin expression levels were restored', 'Purified iMSCs displayed fibroblast-like morphology, formed three-dimensional spheroid structures, and expressed characteristic mesenchymal stem cell surface markers such as CD29, CD33, CD73, CD90, and CD105. Moreover, iMSCs were capable of differentiating into adipogenic, osteogenic, and chondrogenic lineages. Transplanting iMSC cells to tibialis anterior skeletal muscle tissue in mdx mice lowered oxidative damage as evidenced by a reduction in nitrotyrosine levels, and normal dystrophin expression levels were restored', 'Purified iMSCs displayed fibroblast-like morphology, formed three-dimensional spheroid structures, and expressed characteristic mesenchymal stem cell surface markers such as CD29, CD33, CD73, CD90, and CD105. Moreover, iMSCs were capable of differentiating into adipogenic, osteogenic, and chondrogenic lineages. Transplanting iMSC cells to tibialis anterior skeletal muscle tissue in mdx mice lowered oxidative damage as evidenced by a reduction in nitrotyrosine levels, and normal dystrophin expression levels were restored', 'Purified iMSCs displayed fibroblast-like morphology, formed three-dimensional spheroid structures, and expressed characteristic mesenchymal stem cell surface markers such as CD29, CD33, CD73, CD90, and CD105. Moreover, iMSCs were capable of differentiating into adipogenic, osteogenic, and chondrogenic lineages. Transplanting iMSC cells to tibialis anterior skeletal muscle tissue in mdx mice lowered oxidative damage as evidenced by a reduction in nitrotyrosine levels, and normal dystrophin expression levels were restored'] | [
"http://www.ncbi.nlm.nih.gov/pubmed/25102299"
]
| [
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25102299",
"endSection": "abstract",
"offsetInBeginSection": 622,
"offsetInEndSection": 1147,
"text": "Purified iMSCs displayed fibroblast-like morphology, formed three-dimensional spheroid structures, and expressed characteristic mesenchymal stem cell surface markers such as CD29, CD33, CD73, CD90, and CD105. Moreover, iMSCs were capable of differentiating into adipogenic, osteogenic, and chondrogenic lineages. Transplanting iMSC cells to tibialis anterior skeletal muscle tissue in mdx mice lowered oxidative damage as evidenced by a reduction in nitrotyrosine levels, and normal dystrophin expression levels were restored"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25102299",
"endSection": "abstract",
"offsetInBeginSection": 1149,
"offsetInEndSection": 1260,
"text": "This study demonstrates the therapeutic potential of purified iMSCs in skeletal muscle regeneration in mdx mice"
},
{
"beginSection": "title",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17999592",
"endSection": "title",
"offsetInBeginSection": 0,
"offsetInEndSection": 142,
"text": "Flk-1+ adipose-derived mesenchymal stem cells differentiate into skeletal muscle satellite cells and ameliorate muscular dystrophy in mdx mice"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17999592",
"endSection": "abstract",
"offsetInBeginSection": 531,
"offsetInEndSection": 784,
"text": "Within mdx mice, an animal model of DMD, adipose tissue-derived Flk-1(+) MSCs (AD-MSCs) homed to and differentiated into cells that repaired injured muscle tissue. This repair correlated with reconstitution of dystrophin expression on the damaged fibers"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/17999592",
"endSection": "abstract",
"offsetInBeginSection": 1076,
"offsetInEndSection": 1133,
"text": "Flk-1(+) AD-MSC transplants may repair muscular dystrophy"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25102299",
"endSection": "abstract",
"offsetInBeginSection": 1336,
"offsetInEndSection": 1531,
"text": "This study demonstrates the therapeutic potential of purified iMSCs in skeletal muscle regeneration in mdx mice, and suggests that iPSCs are a viable alternate source for deriving MSCs as needed."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25102299",
"endSection": "abstract",
"offsetInBeginSection": 1336,
"offsetInEndSection": 1531,
"text": "This study demonstrates the therapeutic potential of purified iMSCs in skeletal muscle regeneration in mdx mice, and suggests that iPSCs are a viable alternate source for deriving MSCs as needed."
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25102299",
"endSection": "abstract",
"offsetInBeginSection": 935,
"offsetInEndSection": 1147,
"text": "Transplanting iMSC cells to tibialis anterior skeletal muscle tissue in mdx mice lowered oxidative damage as evidenced by a reduction in nitrotyrosine levels, and normal dystrophin expression levels were restored"
},
{
"beginSection": "abstract",
"document": "http://www.ncbi.nlm.nih.gov/pubmed/25102299",
"endSection": "abstract",
"offsetInBeginSection": 1149,
"offsetInEndSection": 1343,
"text": "This study demonstrates the therapeutic potential of purified iMSCs in skeletal muscle regeneration in mdx mice, and suggests that iPSCs are a viable alternate source for deriving MSCs as needed"
}
]
| 5 | BioASQ-training5b | []
| []
| 57134d511174fb1755000002 | 323 |
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