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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIschemia/reperfusion (I/R) injury is frequently encountered during hepatic surgery. We recently showed that I/R accelerates the outgrowth of pre-established colorectal micrometastases. The aim of this study was to assess the influence of ischemia time, gender, age, and liver steatosis on the accelerated outgrowth of colorectal metastases following I/R. Five days after tumor cell inoculation, mice were subjected to 20, 30 or 45 min of left lobar I/R. To assess the influence of age, gender, and liver steatosis on I/R-accelerated tumor growth, we compared old with young mice, male with female mice, and mice with healthy livers with mice with steatotic livers. Endpoints were extent of tissue necrosis and tumor growth. With increasing ischemia times, tissue necrosis and I/R-accelerated tumor growth increased, with a significant stimulatory effect at 30 and 45 min of ischemia. I/R-stimulated outgrowth of micrometastases was further increased by 33% in aged mice and by 42% in steatotic livers and was associated with increased tissue necrosis. In female mice tissue necrosis had decreased by 47% and tumor growth was reduced in both control and clamped liver lobes. The stimulatory effect of I/R on metastasis outgrowth was similar in male and female mice.\n\nQuestion:\nDo ageing and hepatic steatosis exacerbate ischemia/reperfusion-accelerated outgrowth of colorectal micrometastases?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nNitrous oxide (N(2)O) can initially lower core temperature (T (core)), but hypothermic tolerance develops with chronic administration. Therefore, one or both of T (core)'s controlling determinants, heat production (HP) and heat loss (HL), must adapt across repeated N(2)O administrations. Simultaneous measurements of HP, HL, and T (core) during chronic N(2)O administrations will elucidate this adaptive process and constitute a rigorous model for studying the systems-level dynamics of tolerance in both mature and young animals. This approach is justified by the need to better understand the increased vulnerability to addiction associated with adolescent drug use. The objective of the study was to measure HL and HP across repeated steady-state administrations of 60% N(2)O in young and mature rats. Synchronous measurements of HP (indirect calorimetry), HL (direct calorimetry), and T (core) (telemetry) were obtained during 60% N(2)O administrations in adolescent (28-45 days, n = 11) and mature rats (>90 days, n = 8). Rats received five 90-min drug exposures (every other day). Compared to mature rats, adolescents initially exhibited greater hypothermia, but acquired tolerance more rapidly and actually developed hyperthermia during the fifth administration. In both groups, N(2)O consistently increased HL, but progressive increases of intrasessional HP over repeated administrations prevented hypothermia and subsequently promoted hyperthermia in adolescent rats.\n\nQuestion:\nDo systems-level adaptations explain chronic tolerance development to nitrous oxide hypothermia in young and mature rats?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo evaluate immunohistochemical expression of phosphatase and tensin homolog (PTEN) and mammalian target of rapamycin (mTOR) pathway members in pT1 urothelial carcinomas treated by transurethral resection and to determine if immunohistochemistry can be used to predict prognosis. Formalin-fixed, paraffin-embedded tissue samples from 156 patients with pT1 urothelial carcinoma treated by transurethral resection were used to build 5 tissue microarrays. Tissue microarray sections were stained for PTEN, phosphorylated (phos)-AKT, phos-mTOR, phos-S6, eukaryotic translation initiation factor 4E-binding protein 1 (4EBP1), and phos-4EBP1. Patients were monitored after initial treatment (mean, 22.5; median, 16; range, 3-108 months) to detect tumor recurrence, tumor progression, or systemic metastases. During follow-up, 101 patients (65%) showed tumor recurrence, 57 showed tumor progression (37%), and 18 showed systemic metastases (12%). Patients with ≥2 lesions at the initial workup had higher proportions and higher hazard ratios of tumor recurrence, tumor progression, and systemic metastases. Complete loss of PTEN expression was observed in 6 patients (4%), and >80% of the mTOR pathway members showed at least focal positivity. Proportions of tumors with higher levels of PTEN immunohistochemical expression were higher in patients with tumor recurrence (P=.001), tumor progression (P=.05), and systemic metastases (P=.001). Proportions of tumors with lower phos-S6 and low phos-4EBP1 levels were higher in patients with tumor recurrence (P≤.05). Proportions were similar for the remaining biomarkers.\n\nQuestion:\nAre high levels of phosphatase and tensin homolog expression associated with tumor progression , tumor recurrence , and systemic metastases in pT1 urothelial carcinoma of the bladder : a tissue microarray study of 156 patients treated by transurethral resection?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo evaluate the effects of nitrous oxide on automated air tonometry in the clinical setting. With approval of the Hospital Ethical Committee and after obtaining informed parental consent, an 8-F tonometry catheter was inserted orogastrically in ten children aged one to three years scheduled for elective surgery with combined regional and general anesthesia. A standardized general anesthesia technique with tracheal intubation was used in all patients and consisted of sevoflurane in oxygen/nitrous oxide (30%/70%; n = 5 patients) or in oxygen/air (FIO(2) 0.3; n = 5 patients). After obtaining steady state gastric CO(2) values (PrCO(2)), fresh gas mixtures were rapidly changed from oxygen/nitrous oxide to oxygen/air (A) or vice versa (B). In addition, balloon pressures were recorded using a pressure transducer. Measurements were performed at intervals of ten minutes with recording of balloon pressures, end-tidal CO(2) (PETCO(2)) and PrCO(2) values. Pr-ETCO(2)-gap were calculated to eliminate influences of changes in PaCO(2). Changing the fresh gas mixture from N(2)O/O(2) to O(2)/air resulted in a decrease of balloon pressure of -10.4% (113.4 +/- 14.7 mmHg to 101.6 +/- 25.0 mmHg). Changing the fresh gas mixture from O(2)/air to N(2)O/O(2) resulted in an increase of balloon pressures of 6.4% (107.6 +/- 19.3 mmHg to 114.0 +/- 20.3 mmHg). During both fresh gas exchange experiments no significant changes (> 0.2 kPa) in calculated Pr-ETCO(2)-gaps were observed.\n\nQuestion:\nDoes nitrous oxide affect automated air tonometry in children?\n\nAnswer:",
"role": "user"
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{
"content": "no",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nUlcerative colitis (UC) is a chronic inflammatory bowel disease characterized by dense infiltration of lymphocytes, plasma cells, neutrophils, and monocyte-macrophages into the colonic mucosa. Leukocytapheresis is a procedure for selectively removing white blood cells from withdrawn blood. It is used for the treatment of several autoimmune diseases. This study was performed to evaluate the effectiveness of leukocytapheresis for inducing and maintaining remission in corticosteroid-resistant UC, as compared with corticosteroid-responsive UC. Forty-five patients with active UC who were treated with a dose of 1 mg/kg per day or more of prednisolone given systemically for at least 2 weeks were evaluated. Twenty patients (6 males, 14 females) in whom improvement was induced only by high doses of prednisolone were allocated as the corticosteroid-responsive group. The other 25 patients (11 males, 14 females) who did not respond to the above-mentioned dose of prednisolone therapy were allocated as the corticosteroid-resistant group and received leukocytapheresis therapy once a week for 5 weeks. Of patients who had a remission, the corticosteroid-responsive group continued to have the conventional therapy and the corticosteroid-resistant group were given leukocytapheresis once every 4 weeks for at least 2 years as maintenance therapy. Remission was induced by 5 weeks of leukocytapheresis in 23 of the 25 (92%) patients with corticosteroid-resistant active UC. The number of days required to achieve remission of UC was fewer in patients who received leukocytapheresis than in those who did not. Follow-up study of the patients who had remission showed similar relapse rates at 2 years in the patients who received leukocytapheresis and those given high doses of prednisolone alone.\n\nQuestion:\nIs leukocytapheresis effective in inducing but not in maintaining remission in ulcerative colitis?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nA recent study suggested that high concentrations of leptin enhance platelet aggregations. Therefore, the aim of this study was to investigate whether platelet aggregation is altered in patients with leptin gene mutations compared with obese subjects or controls. Four men (one homozygous man and his three heterozygous brothers) carrying a leptin gene mutation; 20 age-matched, healthy, unrelated men; and 18 age-matched obese men were enrolled in the study. Adenosine diphosphate (ADP)-, collagen-, and epinephrine-induced platelet aggregation were evaluated in all individuals. Our results show that patients with the leptin gene mutation (both the homozygous and heterozygous patients) had significantly higher ADP-induced (78.3 +/- 3.4% vs. 57.9 +/- 9.3%, p = 0.001), collagen-induced (78.1 +/- 2.9% vs. 56.7 +/- 9.3%, p = 0.007), and epinephrine-induced (76.5 +/- 9.2% vs. 59.5 +/- 7.70%, p = 0.003) platelet aggregation compared with controls. However, ADP-, collagen-, or epinephrine-induced platelet aggregations were similar to those in obese patients. Platelet aggregation responses to a combination of pretreatment with leptin at concentrations of 20, 50, 100, or 500 ng/mL for 5 minutes and ADP at concentrations of 2 micromol/liter also were evaluated. However, we did not find significant increases in platelet aggregation even at high concentrations of leptin (100 or 500 ng/mL) in leptin-deficient patients, obese subjects, or controls.\n\nQuestion:\nDoes leptin play a major role in platelet aggregation in obesity and leptin deficiency?\n\nAnswer:",
"role": "user"
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{
"content": "no",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAnastomotic leakage is a major cause of morbidity after colorectal surgery. Epidural analgesia is the most effective method for postoperative pain relief after major abdominal surgery. Anyhow, its effect on anastomotic leakage rate is still controversial. This study aimed to compare epidural versus intravenous analgesia as risk factor for anastomotic leakage requiring reoperation in patients undergoing open colorectal surgery for cancer. A retrospective study on 1,474 patients was performed. The Cox proportional hazards model was used to study the relation between primary and secondary factors of risk and anastomotic leakage occurrence within 30 days after elective operation. Overall 30-day anastomotic leakage requiring reoperation was 4.9% (95%CI: 3.8-6.0%). No difference in anastomotic leakage occurrence was observed between the epidural analgesia group and the intravenous analgesia group (Hazard ratio: 0.94; 95%CI: 0.53-1.67%; P = 0.8338). Females had a rate of anastomotic leakage 43% lower than males (P = 0.0301). The diverting stoma resulted to be protective for anastomotic leakage occurrence (P = 0.0052). AL significantly increased postoperative median length of stay but not in-hospital mortality.\n\nQuestion:\nDoes epidural analgesia influence anastomotic leakage incidence after open colorectal surgery for cancer : A retrospective study on 1,474 patients?\n\nAnswer:",
"role": "user"
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{
"content": "no",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe aim of the study was to test if plasma levels of thrombomodulin could predict mortality in 209 patients on long-term anticoagulant treatment followed up for 3.8 years. The thrombomodulin level was 60.9 +/- 29.8 micrograms.l-1 for all 45 patients who died and 60.5 +/- 30.5 micrograms.l-1 for the 38 vascular deaths, compared to 52.3 +/- 20.7 micrograms.l-1 for the 164 survivors. We found that, in Cox regression analyses, all-cause (P = 0.025) and vascular mortality (P = 0.042) was significantly and independently associated with increased levels of thrombomodulin.\n\nQuestion:\nAre increased levels of plasma thrombomodulin associated with vascular and all-cause mortality in patients on long-term anticoagulant treatment?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMetabolic complications, including type 2 diabetes mellitus and metabolic syndrome, are increasingly recognized among HIV-infected individuals. Low vitamin D levels increase the risk of type 2 diabetes mellitus, and vitamin D supplementation has been shown to decrease the risk of type 2 diabetes mellitus in patients without HIV infection. The primary objective was to determine whether vitamin D deficiency (serum 25-hyrdoxyvitamin D <20 ng/ml) was associated with type 2 diabetes mellitus among HIV-infected patients. Our secondary objective was to determine whether vitamin D deficiency was associated with metabolic syndrome in HIV. We conducted a cross-sectional study among participants enrolled in the prospective Modena (Italy) HIV Metabolic Clinic Cohort. Clinical and laboratory data, including history of type 2 diabetes mellitus, fasting blood glucose, components of metabolic syndrome, and 25-hydroxyvitamin D levels, were obtained for all participants. After adjusting for vitamin D supplementation, sex, age, body mass index, and hepatitis C virus co-infection, vitamin D deficiency was associated with type 2 diabetes mellitus [adjusted odds ratio (OR) 1.85; 95% confidence interval (CI) 1.03-3.32; P = 0.038]. The association between vitamin D deficiency and metabolic syndrome was not significant after adjusting for vitamin D supplementation, sex, age and body mass index (adjusted OR 1.32; 95% CI 1.00-1.75; P = 0.053).\n\nQuestion:\nIs vitamin D deficiency associated with type 2 diabetes mellitus in HIV infection?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nUlcerative colitis (UC) is an inflammatory bowel disease with an unknown pathophysiological background. To identify possible regeneration or proliferation factors in colorectal mucosa of UC patients, we screened receptor-type protein tyrosine kinases in human colorectal mucosa. Total RNA was isolated from biopsy specimens of normal and UC patients. After reverse transcription, polymerase chain reaction (PCR) amplification was carried out with cDNA using degenerative primers designed to correspond to stretches of amino acids preserved in the kinase domain. This was followed by subcloning into a plasmid vector. A total of 297 clones were determined by automated sequencing and database homology searches. The analyses revealed that Ron (Recepteur d'Origine Nantals) is highly expressed in the mucosa of UC patients compared with normal mucosa. Subsequently, to investigate in vivo expression of Ron, immunohistological detection was performed with the normal and UC colorectal specimens. Ron was expressed in crypt cells, especially in the bottom of the crypta in normal colonic mucosa, though expression in active UC was distributed widely and strongly in the whole crypta.\n\nQuestion:\nIs receptor protein tyrosine kinase Ron highly expressed in colorectal mucosa of ulcerative colitis patients?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe Mediterranean-style diet is widely advocated for the prevention of cardiovascular diseases (CVD). Meanwhile, blood pressure variability (BPV) is a novel risk factor for CVD. It is unknown whether dietary pattern plays a role in modulating BPV. We prospectively followed-up 274 consecutive patients with stable coronary artery disease (CAD). The Mediterranean diet score (MDS) was derived for all individuals upon recruitment, blood pressure (BP) was measured during each subsequent clinic visit and the visit-to-visit BPV was calculated. The occurrence of major adverse cardiovascular events (MACEs) and all-cause mortality was monitored. After a mean follow-up of 77±12 months, 16.1% of the study population developed MACEs. About 11.3% died from all causes. Patients who developed MACEs or all-cause mortality had a greater systolic BPV compared to those who did not develop an adverse event. Patients who developed a MACE had a lower MDS and further analysis revealed those who developed a stroke had a lower MDS compared with those who did not develop a stroke, but there were no significant differences in MDS between CAD patients with or without subsequent acute coronary syndrome, cardiovascular, or all-cause mortality. After adjusting for confounding variables, a high MDS was an independent predictor for low systolic BPV (B -0.74, 95% confidence interval -1.27 to -0.21, P < 0.01) and was noted to be protective against subsequent development of stroke (hazards ratio 0.48, 95% confidence interval 0.24 to 0.94, P = 0.03).\n\nQuestion:\nIs mediterranean-style diet associated with reduced blood pressure variability and subsequent stroke risk in patients with coronary artery disease?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPapillary muscle displacement is an important element in the pathogenesis of ischemic mitral regurgitation (IMR). The effects of standard ring annuloplasty on subvalvular geometry are incompletely understood. The hypothesis was tested that annular reduction with a Panethtype suture annuloplasty would correct both annular and papillary muscle geometric abnormalities during acute left ventricular (LV) ischemia. Eight adult sheep underwent insertion of an adjustable, double-suture Paneth-type mitral annuloplasty and radiopaque markers on the left ventricle, mitral annulus, leaflet edges, and anterior (APM) and posterior (PPM) papillary muscle tips. Immediately after surgey, 3-D marker coordinates were determined during Control conditions and during proximal left circumflex occlusion before and after tightening the annuloplasty suture. Acute IMR (MR grade 0.3 +/- 0.3 to 2.1 +/- 0.4, Control versus Ischemia) was associated with end-systolic LV dilatation (+27 +/- 16 ml, change relative to Control), greater septal-lateral (+4.6 +/- 3.1 cm) and commissure-commissure (+3.3 +/- 1.6 cm) mitral annular diameters, longer anterior (+1.5 +/- 0.9 cm) and posterior (+0.6 +/- 0.9 cm) papillary muscle tethering distances, greater distance from the APM to the anterior commissure (+0.9 +/- 0.8 cm), and shorter distance from the PPM to the poslerior commissure (-1.3 +/- 1.5 cm). Suture annuloplasty corrected the annular and subvalvular changes, and IMR returned to Control levels (0.5 +/- 0.5); only LV end-systolic volume (ESV) was different from Control (+25 +/- 18 ml) (mean +/- SD, p < 0.05 versus Control by RMANOVA and Dunnett's test).\n\nQuestion:\nDoes mitral suture annuloplasty correct both annular and subvalvular geometry in acute ischemic mitral regurgitation?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo assess the effect of postsurgical exposure of peritoneal cavity to glove powders, Hydrocote, latex proteins, and lipopolysaccharide (LPS) on eicosanoid production in peritoneal fluid and cellular distribution of eicosanoid enzymes in peritoneal wound during healing. Randomised experimental study. Institute for Wound Research, USA. 360 mice randomised into six groups of 60 each. Abrasion of peritoneal cavity followed by instillation of 500 microl of sterile phosphate buffered saline (PBS) alone (Control) or containing 100 microg/ml of Biosorb, Keoflo, Hydrocote, 1 mg/ml of latex proteins, or 12.5 microg/ml of LPS. Mice were killed at 1, 2, 4, 7, 14 and 28 days, and the peritoneal washing obtained from each animal and concentration of eicosanoids measured. Tissue were immunostained for cyclooxygenases and 5-lipoxygenase and thromboxane A2 (TXA2) synthetase. Peritoneal fluid from uninjured controls contained 3.9 (0.8), 5.2 (0.3) and 0.2 (0.02) ng/ml of thromboxane B2 (TXB2), prostaglandin E2 (PGE2) and leukotriene B4 (LTB4), respectively. These increased significantly during the first week to 6.3 (0.3), 11.7 (0.8) and 2.6 (0.1) ng/ml, p<0.05, before returning to baseline by day 14. In all the treated groups the values were significantly higher than in controls (p<0.05). Immunoreactive cyclo-oxygenases, 5-lipoxygenase and TXA2 synthetase proteins were present in various cell types in uninjured skin and peritoneum, incisional and peritoneal wounds and adhesion tissues. Staining was more intense at the site of wounds and paralleled eicosanoid concentrations during healing. There was no difference between exposed and unexposed groups.\n\nQuestion:\nDoes postoperative exposure to glove powders modulate production of peritoneal eicosanoids during peritoneal wound healing?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nA 50% reduction in pain intensity difference (50%PID) between baseline and follow-up evaluation is commonly accepted as adequate pain relief in emergency departments (EDs). However, 50%PID seems to be problematic with the 11-point numerical rating scale (NRS) since even baseline values are more divisible by 2 (50% reduction) than odd baseline values. This study evaluated the impact of this bias and integrated time between baseline and follow-up measurements, hypothesizing that the slope of relative pain intensity difference (SRPID) is a more accurate gauge of pain relief that can decrease bias and incorporate the time component of pain relief. A post-hoc analysis of real-time data on an adult population from an urban ED identified 3199 consecutive patients who received an analgesic, had baseline NRS > 3 and a follow-up NRS within 2 h. Primary outcome was the percentage of patients with pain relieved from the 50%PID and the 50%SRPID criteria. Results showed that with 50%PID, even pain intensity levels on baseline NRS comprised a higher percentage of patients [60.7%; 95% confidence interval (CI): 58.8-63.0] with pain relief compared to odd pain intensity levels (51.7%; 95% CI: 48.8-54.6; p < 0.001), underestimating pain-relieved patients by 9% [95% CI: 0.05-0.13; effect size (ES) = 0.09]. The percentage of pain-relieved subjects with the 50%SRPID criteria was not affected by baseline NRS values (59.7% for whole sample; 95% CI: 58.0-61.4; ES = 0.02).\n\nQuestion:\nDoes percentage of pain intensity difference on an 11-point numerical rating scale underestimate acute pain resolution?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nA careful endoscopic surveillance of Barrett's oesophagus is warranted to prevent esophageal cancer. To identify the preferred location of non-circumferential Barrett's oesophagus and associated dysplasia within the esophageal circumference. We retrospectively reviewed a prospectively maintained database of patients with non-circumferential lesions. The location of metaplastic lesions and dysplastic lesions within the esophageal circumference was identified as on a clock face, and their distribution in the 4 quadrants was compared. Of overall 443 patients with Barrett's oesophagus, 192 (43%) were eligible for our study. Multiple lesions were diagnosed in 110 (57%) of them, for a total amount of 352 metaplastic areas. Barrett's oesophagus lesions were located significantly more in the posterior wall of the oesophagus (38.4%), rather than in the right wall (28.8%), the anterior wall (22.6%), or the left wall (10.2%) (P<0.0001). Among all metaplastic lesions, 28 were associated with dysplasia (7.9%), and one with adenocarcinoma (0.3%). Dysplastic lesions were significantly more common in the posterior wall (39.3%) than, respectively, in the anterior wall (35.8%), the right wall (21.4%) or the left wall (3.5%) (P=0.03).\n\nQuestion:\nAre barrett 's oesophagus and associated dysplasia equally distributed within the esophageal circumference?\n\nAnswer:",
"role": "user"
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{
"content": "no",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThiazolidinedione drugs (TZDs) such as pioglitazone are approved by the U.S. Food and Drug Administration for the treatment of insulin resistance in type 2 diabetes. However, whether TZDs reduce painful diabetic neuropathy (PDN) remains unknown. Therefore, we tested the hypothesis that chronic administration of pioglitazone would reduce PDN in Zucker Diabetic Fatty (ZDF(fa/fa) [ZDF]) rats. Compared with Zucker Lean (ZL(fa/+)) controls, ZDF rats developed: (1) increased blood glucose, hemoglobin A1c, methylglyoxal, and insulin levels; (2) mechanical and thermal hyperalgesia in the hind paw; (3) increased avoidance of noxious mechanical probes in a mechanical conflict avoidance behavioral assay, to our knowledge, the first report of a measure of affective-motivational pain-like behavior in ZDF rats; and (4) exaggerated lumbar dorsal horn immunohistochemical expression of pressure-evoked phosphorylated extracellular signal-regulated kinase. Seven weeks of pioglitazone (30 mg/kg/d in food) reduced blood glucose, hemoglobin A1c, hyperalgesia, and phosphorylated extracellular signal-regulated kinase expression in ZDF. To our knowledge, this is the first report to reveal hyperalgesia and spinal sensitization in the same ZDF animals, both evoked by a noxious mechanical stimulus that reflects pressure pain frequently associated with clinical PDN. Because pioglitazone provides the combined benefit of reducing hyperglycemia, hyperalgesia, and central sensitization, we suggest that TZDs represent an attractive pharmacotherapy in patients with type 2 diabetes-associated pain.\n\nQuestion:\nDoes pioglitazone inhibit the Development of Hyperalgesia and Sensitization of Spinal Nociresponsive Neurons in Type 2 Diabetes?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAlterations in cellular survival and plasticity are implicated in the neurobiology of depression, based primarily on the characterization of antidepressant efficacy in naïve rodents rather than on models that capture the debilitating and protracted feelings of anhedonia and loss of motivation that are core features of depression. In adult male mice, we evaluated persistent effects of oral corticosterone (CORT) exposure on anhedonic-like behavior, immobility in the forced swim test (FST), motivational performance in the progressive ratio task, and later endogenous CORT secretion. After verifying long-term decreases in hippocampal brain-derived neurotrophic factor (BDNF) and cAMP Response Element Binding protein phosphorylation (pCREB), the ability of direct hippocampal BDNF microinfusion after CORT exposure to reverse deficits was investigated. Prior CORT exposure decreased sucrose consumption, appetitive responding, and FST mobility without long-term effects on water/quinine discrimination and endogenous CORT secretion. Critically, BDNF replacement mimicked chronic antidepressant treatment (ADT) by reversing CORT-induced reductions in instrumental performance and FST mobility.\n\nQuestion:\nDoes acute hippocampal brain-derived neurotrophic factor restore motivational and forced swim performance after corticosterone?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis study was designed to examine the effects of verapamil and aspirin, which decrease thromboxane A2 and serotonin release, on the modulation of vascular tone by platelets. Aggregating platelets cause constriction of de-endothelialized arterial segments through thromboxane A2 and serotonin release. These cells cause relaxation of arterial segments with intact endothelium through release of the endothelium-derived relaxing factor. Healthy subjects were given either no drug, verapamil or aspirin for > or = 5 days before their platelets were obtained. The effects of platelets obtained from subjects before and after treatment with aspirin or verapamil on the tone of rat aortic rings were determined. As expected, control platelets (before verapamil or aspirin treatment) induced concentration-dependent relaxation of rat aortic rings with intact endothelium and a concentration-dependent contraction of de-endothelialized rings. Verapamil treatment enhanced (p < 0.02) the platelet-mediated relaxation in rings with intact endothelium and abolished platelet-mediated constriction (p < 0.01) in the de-endothelialized rings. Aspirin treatment also abolished (p < 0.05) platelet-mediated constriction of the de-endothelialized rings. The de-endothelialized rings contracted normally in response to the synthetic thromboxane A2 analogue U46,619, as well as to serotonin, indicating that the vascular smooth muscle response to thromboxane A2 and serotonin was intact.\n\nQuestion:\nDo verapamil and aspirin modulate platelet-mediated vasomotion in arterial segments with intact or disrupted endothelium?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe ability of antiinflammatory strategies to alter cardiovascular risk has not been rigorously examined. Colchicine is an antiinflammatory agent that affects macrophages, neutrophils, and endothelial cells, all of which are implicated in the pathogenesis of cardiovascular disease. We examined whether colchicine use was associated with a reduced risk of myocardial infarction (MI) in patients with gout. We conducted a retrospective, cross-sectional study of all patients with an International Classification of Diseases, 9th ed, code for gout in the electronic medical record (EMR) of the New York Harbor Healthcare System Veterans Affairs network and ≥ 1 hospital visit between August 2007 and August 2008. Hospital pharmacy data were used to identify patients who had filled at least 1 colchicine prescription versus those who had not. Demographics and CV comorbidities were collected by EMR review. The primary outcome was diagnosis of MI. Secondary outcomes included all-cause mortality and C-reactive protein (CRP) level. In total, 1288 gout patients were identified. Colchicine (n = 576) and no colchicine (n = 712) groups had similar baseline demographics and serum urate levels. Prevalence of MI was 1.2% in the colchicine versus 2.6% in the no-colchicine group (p = 0.03). Colchicine users also had fewer deaths and lower CRP levels, although these did not achieve statistical significance. Colchicine effects persisted when allopurinol users were excluded from the analysis.\n\nQuestion:\nIs colchicine use associated with decreased prevalence of myocardial infarction in patients with gout?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo determine whether controlling parental feeding practices are associated with children's adiposity and test the hypothesis that any associations are mediated by maternal perception of their child's weight. Children aged 7-9 years (n=405) were weighed and measured at school as part of the Physical Exercise and Appetite in CHildren Study (PEACHES). Adiposity was indexed with body mass index s.d. scores. The Child Feeding Questionnaire was completed by 53% of mothers of participating children (n=213). Mothers reported whether they thought their child was overweight, normal weight or underweight, and rated their concern about future overweight on a 5-point scale. Higher child adiposity was associated with lower 'pressure to eat' and higher 'restriction' scores. Restriction increased linearly with maternal concern about overweight, and maternal concern about overweight fully mediated the association between child adiposity and restriction. Use of pressure increased as mothers perceived their child to be thinner, but perceived weight did not mediate the association between child weight status and maternal pressure to eat. Monitoring was not associated with child adiposity, maternal perception of weight or concern about overweight.\n\nQuestion:\nAre associations between child weight and maternal feeding styles mediated by maternal perceptions and concerns?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTea infused with the seed of Cassia obtusifolia has been traditionally used as an herbal remedy for liver, eye, and acute inflammatory diseases. Recent pharmacological reports have indicated that Cassiae semen has neuroprotective effects, attributable to its anti-inflammatory actions, in ischemic stroke and Parkinson's disease models. Previously, the ethanol extract of C. obtusifolia seeds (COE) was reported to have memory enhancing properties. However, the effects of COE in an Alzheimer's disease (AD) model are currently unknown. In this study, we investigated the effect(s) of COE on aberrant synaptic plasticity and memory impairment induced by amyloid β (Aβ), a key toxic component found in the AD brain. To determine the effect of COE on Aβ-induced aberrant synaptic plasticity, we used acute mouse hippocampal slices and delivered theta burst stimulation to induce long-term potentiation (LTP). Western blots were used to detect Aβ- and/or COE-induced changes in signaling proteins. The novel object location recognition test was conducted to determine the effect of COE on Aβ-induced recognition memory impairment. COE was found to ameliorate Aβ-induced LTP impairment in the acute hippocampal slices. Glycogen synthase kinase-3β (GSK-3β), a key molecule in LTP impairment, was activated by Aβ. However, this process was inhibited by COE via Akt signaling. Moreover, COE was found to attenuate Aβ-induced microglia, inducible nitric oxide synthase (iNOS), and cyclooxygenase (COX) activation. In the in vivo studies performed, COE ameliorated the Aβ-induced object recognition memory impairment.\n\nQuestion:\nDoes cassia obtusifolia seed ameliorate amyloid β-induced synaptic dysfunction through anti-inflammatory and Akt/GSK-3β pathways?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHigh-fat, high-sucrose diet (HF)-induced reactive oxygen species (ROS) levels are implicated in skeletal muscle insulin resistance and mitochondrial dysfunction. Here we investigated whether mitochondrial ROS sequestering can circumvent HF-induced oxidative stress; we also determined the impact of any reduced oxidative stress on muscle insulin sensitivity and mitochondrial function. The Skulachev ion (plastoquinonyl decyltriphenylphosphonium) (SkQ), a mitochondria-specific antioxidant, was used to target ROS production in C2C12 muscle cells as well as in HF-fed (16 weeks old) male C57Bl/6 mice, compared with mice on low-fat chow diet (LF) or HF alone. Oxidative stress was measured as protein carbonylation levels. Glucose tolerance tests, glucose uptake assays and insulin-stimulated signalling were determined to assess muscle insulin sensitivity. Mitochondrial function was determined by high-resolution respirometry. SkQ treatment reduced oxidative stress in muscle cells (-23% p < 0.05), but did not improve insulin sensitivity and glucose uptake under insulin-resistant conditions. In HF mice, oxidative stress was elevated (56% vs LF p < 0.05), an effect completely blunted by SkQ. However, HF and HF+SkQ mice displayed impaired glucose tolerance (AUC HF up 33%, p < 0.001; HF+SkQ up 22%; p < 0.01 vs LF) and disrupted skeletal muscle insulin signalling. ROS sequestering did not improve mitochondrial function.\n\nQuestion:\nDoes targeting of mitochondrial reactive oxygen species production avert lipid-induced insulin resistance in muscle tissue from mice?\n\nAnswer:",
"role": "user"
},
{
"content": "no",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nGinsenosides are used widely for medicinal purposes, but the mechanisms of their action are still unclear, although there is some evidence that these effects are mediated by nuclear receptors. Here we examined whether two metabolites of ginsenoside, protopanaxadiol (g-PPD) and protopanaxatriol (g-PPT), could modulate endothelial cell functions through the glucocorticoid receptor (GR) and oestrogen receptor (ER). EXPERIMENT APPROACHES: The effects of g-PPD and g-PPT on intracellular calcium ion concentration ([Ca(2+)](i)) and nitric oxide (NO) production in human umbilical vein endothelial cells (HUVECs) were measured using Fura-2-acetoxymethyl ester, 4-amino-5-methylamino-2',7'-difluorofluorescein and Griess reagent. Effects on expression of GR and ER isoforms in HUVECs were determined using reverse transcriptase-/real-time PCR and immunocytochemistry. Phosphorylation of endothelial NO synthase (eNOS) was assessed by Western blotting. Ginsenoside protopanaxadiol and g-PPT increased [Ca(2+)](i), eNOS phosphorylation and NO production in HUVECs, which were inhibited by the GR antagonist, RU486, the ER antagonist, ICI 182,780 and siRNA targeting GR or ERbeta. The NO production was Ca(2+)-dependent and the [Ca(2+)](i) elevation in HUVECs resulted from both intracellular Ca(2+) release and extracellular Ca(2+) influx.\n\nQuestion:\nDo protopanaxadiol and protopanaxatriol bind to glucocorticoid and oestrogen receptors in endothelial cells?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSeipin is a protein that resides in endoplasmic reticulum, and involved in both lipid metabolic disorders and motor neuropathy. The aim of this study was to investigate the effects of mutant seipin on autophagy system and the morphology of lipid droplets in vitro. HEK-293, H1299 and MES23.5 cells were transfected with the plasmids of mutated seipin at glycosylation sites (N88S or S90L) and GFP-LC3 plasmids. The cells were subjected to immunofluorescence and flow cytometry assays, and the cell lysates were subjected to immunoblot analysis. Nile Red was used to stain the lipid droplets in the cells. Overexpression of the mutated seipin proteins N88S or S90L activated autophagy in the 3 cell lines, and substantially altered the sub-cellular distribution of the autophagosome marker GFP-LC3, leading to a number of large vacuoles appearing in the cytoplasm. The sub-cellular location of GFP-LC3 and mutated seipin proteins highly overlapped. Moreover, and the mutated seipin proteins caused diffuse small lipid droplets to fuse into larger lipid droplets. Treatment of mutated seipin-transfected cells with the autophagy inhibitor 3-MA (5 mmol/L) facilitated the fusion of mutated seipin-induced large vacuoles. The protein glycosylation inhibitor tunicamycin could mimic the mutated seipin-induced effects, and treatment of the wild-type seipin-transfected cells with tunicamycin (2.5 μg/mL) produced similar morphological and biochemical properties as in the mutated seipin-transfected cells.\n\nQuestion:\nDoes seipin mutation at glycosylation sites activate autophagy in transfected cells via abnormal large lipid droplets generation?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo characterize novel single-nucleotide polymorphisms (SNPs) in the human FSH receptor (FSHR) promoter region. Retrospective and basic research study. University hospital. Women (202 from Germany and 55 from Indonesia) with male or tubal factor infertility undergoing controlled ovarian stimulation for IVF treatment. None. Frequency, distribution, and correlation with clinical data of the SNPs. Dual luciferase assays and electrophoretic mobility shift assays (EMSA). We identified two SNPs and three mutations in the promoter region of the human FSHR which could be allocated to positions -29, -37, -114, -123, and -138 upstream of the translational initiation codon. One SNP showed a high incidence (-29: 44%, n = 202), but no correlation with basal FSH serum levels or ovarian response with the SNP at position -29 was found. Luciferase reporter assays, using pGL3 vector constructs, showed that mutations at positions -37 and -138 lead to significantly higher promoter activity. EMSA indicate that putative binding sites for transcription factors are affected by the SNPs.\n\nQuestion:\nDo single-nucleotide polymorphisms in the promoter region influence the expression of the human follicle-stimulating hormone receptor?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nVernal keratoconjunctivitis (VKC) is a severe though transient form of ocular allergy, predominant in young males, which requires careful management. Corticosteroids are effective but also cause serious topical side-effects in the eye, such as glaucoma and cataracts. The safer, mast cell stabilizing anti-inflammatories (commonly sodium cromoglycate) therefore have an important role. This parallel group study compared efficacy, tolerability and safety of sodium cromoglycate 2% with nedocromil sodium 2%, administered as one drop per eye four times daily for a period of 5 months. Children aged 4-17 years, with a diagnosis of mostly limbal VKC in the last 12 months, entered a 2-week baseline during which they used only artificial tears, and were then randomized to treatment, in groups of 18, on an investigator single-masked basis. Daily symptom diary cards were kept by patients/guardians, and VKC was assessed by the clinician at approximately monthly intervals. Dexamethasone was provided for rescue control of severe symptoms, if needed. A total of 34 patients completed the study. Both trial treatments produced rapid improvements and many ocular signs and symptoms, including Trantas' dots, chemosis, itching, soreness and sticky discharge, were fully controlled by the end of the study. However, nedocromil sodium took effect more quickly, with a significant reduction compared to sodium cromoglycate for itching, grittiness, hyperaemia and keratitis within 6 weeks. In addition, nedocromil sodium was the more efficacious overall (significant vs sodium cromoglycate for hyperaemia, keratitis, papillae and pannus at 22 weeks). Both treatments were well tolerated and without serious adverse effects. Final opinions favoured nedocromil sodium, with full control of VKC recorded for 94% (patient opinion) and 100% (clinician opinion) of this treatment group, compared with 29% and 0%, respectively, in the sodium cromoglycate group.\n\nQuestion:\nAre nedocromil sodium eye drops more effective than sodium cromoglycate eye drops for the long-term management of vernal keratoconjunctivitis?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe characteristic clinical symptoms of collagenous colitis are non-bloody diarrhoea, urgency and abdominal pain. Treatment is aimed at reducing the symptom burden and the disease impact on patients' health-related quality of life. The objective of this study was to analyse health-related quality of life in patients with collagenous colitis. In a cross-sectional, postal HRQL survey, 116 patients with collagenous colitis at four Swedish hospitals completed four health-related quality of life questionnaires, two disease-specific (Inflammatory Bowel Disease Questionnaire and Rating Form of IBD Patient Concerns), and two generic (Short Form 36, SF-36, and Psychological General Well-Being, PGWB), and a one-week symptom diary. Demographic and disease-related data were collected. Results for the collagenous colitis population were compared with a background population controlled for age and gender (n = 8931). Compared with a Swedish background population, patients with collagenous colitis scored significantly worse in all Short Form 36 dimensions (p < 0.01), except physical function. Patients with active disease scored worse health-related quality of life than patients in remission. Co-existing disease had an impact on health-related quality of life measured with the generic measures. Lower education level and shorter disease duration were associated with decreased well-being.\n\nQuestion:\nIs health-related quality of life impaired in active collagenous colitis?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nRecent studies suggest that 3-hydroxy-3-methylglutaryl co-enzyme A reductase inhibitors (statins) exert their protective effects against cardiovascular diseases independently of their cholesterol-decreasing effects. To clarify the effect of a statin on hypertensive nephrosclerosis. We treated stroke-prone spontaneously hypertensive rats (spSHRs) chronically, starting at the age of 4 weeks, with cerivastatin (2 mg/kg per day by gavage) or vehicle. Physiological parameters, plasma chemistry and urine protein excretion were analysed. At 14 weeks of age, the rats had their kidneys removed for use in assays. Compared with vehicle treatment, statin treatment reduced proteinuria and renal injury independently of blood pressure and cholesterol concentrations in spSHRs. Although expression of adhesion molecules and infiltration of inflammatory cells were not different whether or not cerivastatin treatment was used, renal fibrosis was significantly reduced in statin-treated spSHRs. We also found that expression of transforming growth factor-beta1 in kidneys was significantly inhibited in statin-treated spSHRs.\n\nQuestion:\nDoes a 3-hydroxy-3-methylglutaryl co-enzyme A reductase inhibitor reduce hypertensive nephrosclerosis in stroke-prone spontaneously hypertensive rats?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSelective visual attention is the process by which the visual system enhances behaviorally relevant stimuli and filters out others. Visual attention is thought to operate through a cortical mechanism known as biased competition. Representations of stimuli within cortical visual areas compete such that they mutually suppress each others' neural response. Competition increases with stimulus proximity and can be biased in favor of one stimulus (over another) as a function of stimulus significance, salience, or expectancy. Though there is considerable evidence of biased competition within the human visual system, the dynamics of the process remain unknown. Here, we used scalp-recorded electroencephalography (EEG) to examine neural correlates of biased competition in the human visual system. In two experiments, subjects performed a task requiring them to either simultaneously identify two targets (Experiment 1) or discriminate one target while ignoring a decoy (Experiment 2). Competition was manipulated by altering the spatial separation between target(s) and/or decoy. Both experimental tasks should induce competition between stimuli. However, only the task of Experiment 2 should invoke a strong bias in favor of the target (over the decoy). The amplitude of two lateralized components of the event-related potential, the N2pc and Ptc, mirrored these predictions. N2pc amplitude increased with increasing stimulus separation in Experiments 1 and 2. However, Ptc amplitude varied only in Experiment 2, becoming more positive with decreased spatial separation.\n\nQuestion:\nDo event-related potentials dissociate effects of salience and space in biased competition for visual representation?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCancer stem cells (CSCs) play an important role in the development and recurrence of malignant tumors including glioma. Notch signaling, an evolutionarily conserved pathway mediating direct cell-cell interaction, has been shown to regulate neural stem cells (NSCs) and glioma stem cells (GSCs) in normal neurogenesis and pathological carcinogenesis, respectively. However, how Notch signaling regulates the proliferation and differentiation of GSCs has not been well elucidated. We isolated and cultivate human GSCs from glioma patient specimens. Then on parallel comparison with NSCs, we inhibited Notch signaling using γ-secretase inhibitors (GSI) and assessed the potential functions of Notch signaling in human GSCs. Similar to the GSI-treated NSCs, the number of the primary and secondary tumor spheres from GSI-treated GSCs decreased significantly, suggesting that the proliferation and self-renewal ability of GSI-treated GSCs were attenuated. GSI-treated GSCs showed increased differentiation into mature neural cell types in differentiation medium, similar to GSI-treated NSCs. Next, we found that GSI-treated tumor spheres were composed of more intermediate progenitors instead of CSCs, compared with the controls. Interestingly, although inhibition of Notch signaling decreased the ratio of proliferating NSCs in long term culture, we found that the ratio of G2+M phase-GSCs were almost undisturbed on GSI treatment within 72 h.\n\nQuestion:\nDoes notch signaling contribute to the maintenance of both normal neural stem cells and patient-derived glioma stem cells?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis study examined visual and verbal learning in the early phase of recovery for 48 Veterans with alcohol use (AUD) and substance use disorders (SUD, primarily cocaine and opiate abusers). Previous studies have demonstrated visual and verbal learning deficits in AUD, however little is known about the differences between AUD and SUD on these domains. Since the DSM-5 specifically identifies problems with learning in AUD and not in SUD, and problems with visual and verbal learning have been more prevalent in the literature for AUD than SUD, we predicted that people with AUD would be more impaired on measures of visual and verbal learning than people with SUD. Participants were enrolled in a comprehensive rehabilitation program and were assessed within the first 5 weeks of abstinence. Verbal learning was measured using the Hopkins Verbal Learning Test (HVLT) and visual learning was assessed using the Brief Visuospatial Memory Test (BVMT). Results indicated significantly greater decline in verbal learning on the HVLT across the three learning trials for AUD participants but not for SUD participants (F=4.653, df=48, p=0.036). Visual learning was less impaired than verbal learning across learning trials for both diagnostic groups (F=0.197, df=48, p=0.674); there was no significant difference between groups on visual learning (F=0.401, df=14, p=0.538).\n\nQuestion:\nDo visual and verbal learning deficits in Veterans with alcohol and substance use disorders?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nChronic alcohol intake affects liver function and causes hepatic pathological changes. It has been shown that peroxisome proliferator-activated receptor α (PPARα)-null mice developed more pronounced hepatic changes than wild-type (WT) mice after chronic exposure to a diet containing 4% alcohol. The remarkable similarity between the histopathology of alcoholic liver disease (ALD) in Ppara-null model and in humans, and the fact that PPARα expression and activity in human liver are less than one-tenth of those in WT mouse liver make Ppara-null a good system to investigate ALD. In this study, the Ppara-null model was used to elucidate the dynamic regulation of PPARα activity during chronic alcohol intake. Hepatic transcriptomic and metabolomic analyses were used to examine alterations of gene expression and metabolites associated with pathological changes. The changes triggered by alcohol consumption on gene expression and metabolites in Ppara-null mice were compared with those in WT mice. The results showed that in the presence of PPARα, 3 major metabolic pathways in mitochondria, namely the fatty acid β-oxidation, the tricarboxylic acid cycle, and the electron transfer chain, were induced in response to a 2-month alcohol feeding, while these responses were greatly reduced in the absence of PPARα. In line with the transcriptional modulations of these metabolic pathways, a progressive accumulation of triglycerides, a robust increase in hepatic cholic acid and its derivatives, and a strong induction of fibrogenesis genes were observed exclusively in alcohol-fed Ppara-null mice.\n\nQuestion:\nDoes modulation of fatty acid and bile acid metabolism by peroxisome proliferator-activated receptor α protect against alcoholic liver disease?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe small actin-binding protein destrin is one of the key regulators involved in remodeling of the actin cytoskeleton, a process crucial for cytokinesis, cell migration and polarized cell growth as well as for cancer cell migration and invasion. A novel ex vivo nerve invasion model mirroring perineural cancer cell invasion as a key feature of pancreatic ductal adenocarcinoma has been previously established. Using this model, highly nerve-invasive clones of human pancreatic cancer cell lines have been obtained. Genome-wide transcriptional analyses of these cells revealed up-regulation of destrin in highly versus lowly nerve-invasive pancreatic cancer cells. Increased expression of destrin in these nerve-invasive cells was validated using quantitative RT-PCR and immunoblotting; concomitant changes in cell morphology were demonstrated using immunofluorescence analysis. Silencing of destrin by two specific siRNA oligonucleotides in Panc-1 pancreatic cancer cells decreased invasiveness and migration, and reduced proliferation of these cells.\n\nQuestion:\nIs the actin binding protein destrin associated with growth and perineural invasion of pancreatic cancer?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nFollowing chronic liver injury or when hepatocyte proliferation is impaired, ductular reactions containing hepatic progenitor cells (HPCs) appear in the periportal regions and can regenerate the liver parenchyma. HPCs exist in a niche composed of myofibroblasts, macrophages and laminin matrix. Galectin-3 (Gal-3) is a β-galactoside-binding lectin that binds to laminin and is expressed in injured liver in mice and humans. We examined the role of Gal-3 in HPC activation. HPC activation was studied following dietary induced hepatocellular (choline-deficient ethionine-supplemented diet) and biliary (3,5-diethoxycarbonyl-1,4-dihydrocollidine supplemented diet) injury in wild type and Gal-3(-/-) mice. HPC proliferation was significantly reduced in Gal-3(-/-) mice. Gal-3(-/-) mice failed to form a HPC niche, with reduced laminin formation. HPCs isolated from wild type mice secrete Gal-3 which enhanced adhesion and proliferation of HPCs on laminin in an undifferentiated form. These effects were attenuated in Gal3(-/-) HPCs and in wild type HPCs treated with the Gal-3 inhibitor lactose. Gal-3(-/-) HPCs in vitro showed increased hepatocyte function and prematurely upregulated both biliary and hepatocyte differentiation markers and regulated cell cycle genes leading to arrest in G0/G1.\n\nQuestion:\nDoes galectin-3 regulate hepatic progenitor cell expansion during liver injury?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe aim of this study was to discover whether the heavy use of alcohol in adolescence is associated with earlier psychiatric symptoms and deviance, gender, family structure and socio-economic situation of the family (SES). Questionnaires designed to reveal psychiatric symptoms and deviance were filled in by parents (Rutter A2 Scale), teachers (Rutter B2 Scale) and the children themselves (CDI) at the age of 12 years. The Rutter scales are behaviourally orientated questionnaires, and the CDI is a self-report of depression. Information concerning alcohol use was obtained from the children at the age of 15 years. Both male and female heavy users of alcohol had more commonly displayed externalizing behaviour and hyperactivity at school 3 years earlier than had their same-sex peers. Furthermore, female heavy users in particular had displayed hyperactivity at home. The probability that a boy who used alcohol excessively at the age of 15 years had already been deviant 3 years earlier was increased on the teachers' scale, and that of a girl was increased on the CDI. Logistic regression analysis using parent-assessed symptoms and self-reported depressive symptoms showed that externalizing behaviours and depression were the factors predicting the heavy use of alcohol in adolescence when gender, SES and family structure were controlled. When teacher-assessed symptoms and self-reported symptoms were used, externalizing behaviour predicted heavy alcohol use at the age of 15 years when gender, SES and family structure were controlled.\n\nQuestion:\nDo psychiatric symptoms and deviance in early adolescence predict heavy alcohol use 3 years later?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis retrospective, single-center study was designed to distinguish severe diabetic foot infection (DFI) from moderate DFI based on the presence or absence of systemic inflammatory response syndrome (SIRS). The database of a single academic foot and ankle program was reviewed and 119 patients were identified. Severe DFI was defined as local infection associated with manifestation of two or more objective findings of systemic toxicity using SIRS criteria. Patients with severe DFI experienced a 2.55-fold higher risk of any amputation (95% CI 1.21-5.36) and a 7.12-fold higher risk of major amputation (1.83-41.05) than patients with moderate DFI. The risk of minor amputations was not significantly different between the two groups (odds ratio 1.02 [95% CI 0.51-2.28]). The odds of having a severe DFI was 7.82 times higher in patients who presented with gangrene (2.03-44.81) and five times higher in patients who reported symptoms of anorexia, chills, nausea, or vomiting (2.22-11.25). The mean hospital length of stay for patients with severe DFI was ∼4 days longer than for patients with moderate DFI, and this difference was statistically significant.\n\nQuestion:\nIs sIRS valid in discriminating between severe and moderate diabetic foot infections?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nYoung adults with type 1 diabetes mellitus (T1DM) have increased glomerular filtration rate (GFR), which may mediate progressive renal disease and microalbuminuria. This may be secondary to low concentrations of insulin-like growth factor (IGF)-I and GH hypersecretion. We tested the hypothesis that restoration of circulating IGF-I concentrations in young adults with T1DM might suppress GH secretion, GFR and urinary albumin excretion. In a randomized double blind crossover study six young adults with T1DM (three men, 19-24 years) received 7 days treatment with rhIGF-I/insulin-like growth factor binding protein (IGFBP)-3 complex (SomatoKine) 0.4 mg/kg/day and placebo. Subjects underwent overnight insulin infusion for euglycaemia, followed by determination of GFR and albumin excretion rate. Following IGF-I/IGFBP-3 complex, overnight insulin requirements (0.15 vs placebo 0.21 mU/kg/min, P < 0.04), plasma insulin (77 vs placebo 152 pmol/l, P < 0.01) and mean overnight GH (2.6 vs placebo 4.8 mU/l, P < 0.04) fell. IGF-I (492 vs placebo 218 ng/ml, P < 0.01) and IGFBP-3 (4.5 vs placebo 3.9 microg/ml, P < 0.05) increased. GFR did not change (145.5 (23.9) ml/min/1.73 m(2) post-IGF-I/IGFBP-3 complex vs 152.2 (19.8) post placebo). Albumin excretion rate did not change 9.5 (5.5-16.6)mg/24 h pre- vs 11.5 (9.9-20.2) post-IGF-I/IGFBP-3 complex and 10.7 (8.1-21.2) pre- vs 11.5 (8.7-29.9) post placebo. Plasma creatinine levels were lower following IGF-I/IGFBP-3 complex (mean +/- SD, 56.2 +/- 16.8 micromol/l) vs placebo (61.5, 45.0, P < 0.02).\n\nQuestion:\nDoes short-term suppression of elevated growth hormone concentrations following insulin-like growth factor 1 administration in young adults with type 1 diabetes alter glomerular filtration or albumin excretion rates?\n\nAnswer:",
"role": "user"
},
{
"content": "no",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAtrial leads are often implanted in paediatric patients needing a pacemaker (PM). The aim of this study is the evaluation of their outcome in young patients. We evaluated transvenous atrial leads outcome in children and young adults from a single centre, with a retrospective analysis. A P< 0.05 was considered significant. Between 1992 and 2008, 110 patients, 75 with congenital heart defects (d-transposition of great arteries status/post, s/p, Mustard 41%, atrioventricular septal defect 11%, tetralogy 9%, ventricular septal defect 8%), aged 13.3 ± 5.3 years, underwent PM implantation with bipolar atrial transvenous leads for sinus node dysfunction (50%), atrioventricular block (38%), cardiomyopathies, and primary ventricular arrhythmias (12%). Leads are steroid-eluting (98%), tined (59%), screw-in (41%), polyurethane-insulated (72%), silicone-insulated (28%), and have been positioned by transcutaneous puncture of subclavian vein into right atrial appendage/remnant (RAA, 50%), right atrial free wall/septum (25%), left atrium (s/p Mustard, 25%). Follow-up duration is 6.4 ± 4.8 (range 0.1-18) years. At multivariate analysis, younger age at implant was a risk factor for lead failure (4 leads, 3.5%) (P= 0.03); 16 leads (14%) dislodged post-implantation and 12 were successfully repositioned, the others extracted or abandoned. Dislocation occurred more frequently with screw-in leads (P= 0.03) positioned outside RAA (P= 0.02). Atrial threshold showed a small but significant increase, 0.002 V/month (P< 0.001), impedance showed a decrease (0.6 Ω/month, P< 0.001), P-wave showed no significant difference.\n\nQuestion:\nDoes long-term outcome of transvenous bipolar atrial lead implanted in children and young adults with congenital heart disease?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPortal endotoxaemia has been speculated to be crucially involved in the pathogenesis of chronic hepatic inflammation, which is highly associated with the development of type 2 diabetes mellitus. This study tests whether portal endotoxaemia is a pathogenic link between chronic subacute hepatic inflammation and pancreatic beta-cell dysfunction. Rats were randomly assigned into two groups: rats with intraportal saline or low-dose lipopolysaccharide (LPS) infusion for 4 weeks. Pathological changes in the liver were evaluated via histological and biochemical examination. Pancreatic insulin secretion was evaluated by in vivo hyperglycaemic clamp study. White blood cell count was significantly increased after intraportal LPS infusion for 4 weeks. Plasma amylase and chemoluminescence counts indicating superoxide levels were significantly increased after LPS treatments for 2 and 4 weeks. Intraportal low-dose LPS infusion significantly increased tumour necrosis factor-alpha and interleukin-6 contents in liver and pancreas. Circulating C-reactive protein, thiobarbituric acid reactive substances (TBARS) and endotoxin levels were not different among groups. The first- and second-phase insulin secretions in hyperglycaemic clamp were significantly decreased in LPS-treated rats. The histopathological scores, de novo production of reactive oxygen substrate and TBARS contents in the liver and pancreas were significantly increased in LPS-infused rats. Leucocyte infiltration was clearly visible in pancreatic islets of LPS-treated rats.\n\nQuestion:\nDoes mild portal endotoxaemia induce subacute hepatic inflammation and pancreatic beta-cell dysfunction in rats?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe transcriptional complexity of mammalian cells suggests that they have broad abilities to respond to specific environmental stimuli and physiologic contexts. These abilities were not apparent a priori from the structure of mammalian genomes, but have been identified through detailed transcriptome analyses. In this study, we examined the transcriptomes of cells of the innate immune system, human neutrophils, using RNA sequencing (RNAseq). We sequenced poly-A RNA from nine individual samples corresponding to specific phenotypes: three children with active, untreated juvenile idiopathic arthritis (JIA)(AD), three children with the same disease whose disease was inactive on medication (CRM), and three children with cystic fibrosis (CF). We demonstrate that transcriptomes of neutrophils, typically considered non-specific in their responses and functions, display considerable specificity in their transcriptional repertoires dependent on the pathologic context, and included genes, gene isoforms, and long non-coding RNA transcripts. Furthermore, despite the small sample numbers, these findings demonstrate the potential of RNAseq approaches to biomarker development in rheumatic diseases.\n\nQuestion:\nDoes rNA sequencing from human neutrophils reveal distinct transcriptional differences associated with chronic inflammatory states?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nDNA supercoiling factor (SCF) was first identified in the silkworm as a protein capable of generating negative supercoils into a relaxed DNA in conjunction with eukaryotic topoisomerase II. Drosophila melanogaster SCF localizes to puffs on polytene chromosomes, implicating its role in gene expression. The factor is a Ca2+-binding protein with four EF-hand domains and possesses a tetrapeptide sequence HDEF at its C-terminus. To clarify the roles of the domains of SCF, we carried out a functional dissection of the factor. A glutamic acid to glutamine substitution at the end of the loop in EF-hand domain II or III reduced both the Ca2+ binding and supercoiling activities; simultaneous substitutions at both sites abolished these activities. During native polyacrylamide gel electrophoresis, SCF migrated more rapidly in the presence of Ca2+ than in the presence of Mg2+ or EGTA. SCF binds directly to topoisomerase II. Deletion of the C-terminal HDEF sequence destroyed the binding and supercoiling activity.\n\nQuestion:\nAre functional dissection of DNA supercoiling factor : EF-hand domains and C-terminal HDEF motif essential for its activity?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo investigate the underlying mechanism of ghrelin-induced gastro-protection in a cell culture model of ethanol-induced gastric epithelial cell injury. The human gastric epithelial cell line GES-1 was incubated with ghrelin (0.01-1 µM), 1 µM ghrelin and 1 µM D-Lys3-growth hormone releasing peptide-6 (GHRP-6), or 1 µM ghrelin and 400 nM antagomiR-21 for 24 h, followed by treatment with 8% ethanol for 3 h to induce apoptosis. Cell viability was determined by MTT assays and flow cytometry was used for detection of apoptosis rates. miR-21 transcription was analyzed by qRT-PCR and Akt, Bcl-2, Bax and caspase 3 expressions were measured by Western blot. Flow cytometry and a quantitative RT-PCR analysis of the expression of miR-21 showed that ghrelin inhibited apoptosis in a dose dependent manner through a signaling pathway that was both growth hormone secretagogue receptor (GHS-R) and miR-21 dependent, as the antiapoptotic effect of ghrelin was blocked by both D-Lys3-GHRP-6 and antagomiR-21, respectively. Western blotting of Akt, Bcl-2, Bax, and caspase 3 showed that the levels of the antiapoptotic proteins, Akt and Bcl-2, in the cells pretreated with ghrelin alone were higher than those in the cells pretreated with D-Lys3-GHRP-6 or antagomiR-21. By contrast, the levels of the proapoptotic proteins, Bax and caspase 3, in the cells pretreated with ghrelin alone were lower than those in the cells pretreated with D-Lys3-GHRP-6 or antagomiR-21.\n\nQuestion:\nIs ghrelin inhibition of ethanol-induced gastric epithelial cell apoptosis mediated by miR-21?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nStaphylococcus aureus evades host defense through releasing several virulence proteins, such as chemotaxis inhibitory protein of staphylococcus aureus (CHIPS). It has been shown that extracellular N terminus of C5a receptor (C5aR) forms the binding domain for CHIPS, and tyrosine sulfation is emerging as a key factor in determining protein-protein interaction. The aim of this study was to evaluate the role of tyrosine sulfation of N-terminal of C5aR in its binding with CHIPS. Expression plasmids encoding C5aR and its mutants were prepared using PCR and site-directed mutagenesis and were used to transfect HEK 293T cells using calcium phosphate. Recombinant CHIPS protein was purified. Western blotting was used to examine the binding efficiency of CHIPS to C5aR or its mutants. CHIPS exclusively binds to C5aR, but not to C5L2 or C3aR. A nonspecific sulfation inhibitor, sodium chlorate (50 nmol/L), diminishes the binding ability of C5aR with CHIPS. Blocking sulfation by mutation of tyrosine to phenylalanine at positions 11 and 14 of C5aR N terminus, which blocked sulfation, completely abrogates CHIPS binding. When tyrosine 14 alone was mutated to phenylalanine, the binding efficiency of recombinant CHIPS was substantially decreased.\n\nQuestion:\nIs tyrosine sulfation in N-terminal domain of human C5a receptor necessary for binding of chemotaxis inhibitory protein of Staphylococcus aureus?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIt is well established that smooth muscle contractility is regulated by an elevation of cytosolic Ca(2+) via myosin light chain phosphorylation, which is activated by myosin light chain kinase (MLCK). Recently, MLCK has been demonstrated to play an important role in smooth muscle contraction and normal gastrointestinal motility. The aim of our study is to investigate whether MLCK is involved in the mechanism of gastrointestinal dysfunction and the ameliorating effects of insulin on gastrointestinal dysfunction in diabetic rats. A diabetic rat model was established by an intravenous injection with streptozotocin. Rats were randomized into three groups: control group, diabetic group, and insulin-treated group. The gastrointestinal functions were assessed in terms of gastric emptying and intestinal transit. The expression of MLCK in the pylorus and ileum of the three groups was determined by real-time polymerase chain reaction (PCR) and Western blot methods. The diabetic group exhibited a significant delay in gastric emptying and intestinal transit than the control group. Insulin treatment significantly ameliorated the gastric emptying and intestinal transit in diabetic rats. The expression levels of MLCK in the pylorus and ileum of the diabetic group were both significantly decreased compared with the control group, and the changes of MLCK expression in these tissues of diabetic rats were partially reversed after treatment with insulin.\n\nQuestion:\nIs myosin light chain kinase involved in the mechanism of gastrointestinal dysfunction in diabetic rats?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCD8+ T-cells and interleukin-2 play an important role during organ rejection in kidney transplant recipients. Numerous studies showed increased interleukin-2 levels during acute rejection. The aim of our study is to show an association between intracellular interleukin-2 in CD8+ T-cells and the incidence of those who underwent organ rejection in kidney transplant recipients. 407 transplant recipients were included into this study. The rejection incidence was investigated from the patient records. White blood cells from recipients were separated using a ficoll gradient. The cells were double-gated (CD3+ and CD8+) for the analysis of cellular percentage for intracellular interleukin-2 with a flow cytometer. The percentage of CD8+ cells with detectable intracellular interleukin-2 was significantly higher in renal transplant recipients with a documented rejection compared to recipients without any history of rejection (9.06±0.50, N=133 vs. 4.28±0.24, N=274, p<0.0001, t-test). Further, there was a significant increase in patients with one (8.02±0.54, N=80, p<0.0001, t-test), two (10.40±1.17, N=33, p<0.0001, t-test) or three (11.82±1.58, N=18, p<0.0001, t-test) rejection events.\n\nQuestion:\nIs rejection quantity in kidney transplant recipients associated with increasing intracellular interleukin-2 in CD8+ T-cells?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo describe the natural history of subchondral bone marrow lesions (BMLs) in a sample of subjects with knee osteoarthritis (OA) or at risk of developing it. Additionally, to examine the association of change in BMLs from baseline to 30-month follow-up with the risk of cartilage loss in the same subregion at follow-up. 1.0 T MRI was performed using proton density-weighted, fat-suppressed sequences. BML size and cartilage status were scored in the same subregions according to the WORMS system. Subregions were categorised based on comparison of baseline and follow-up BML status. A logistic regression model was used to assess the association of change in BML status with cartilage loss over 30 months using stable BMLs as the reference group. 395 knees were included. 66% of prevalent BMLs changed in size; 50% showed either regression or resolution at follow-up. The adjusted odds ratios (95% confidence intervals) of cartilage loss in the same subregion at follow-up for the different groups were 1.2 (0.5 to 1.6) for regressing BMLs, 0.9 (0.5 to 1.6) for resolving BMLs, 2.8 (1.5 to 5.2) for progressing BMLs, 0.2 (0.1 to 0.3) for subregions with no BMLs at baseline and follow-up and 3.5 (2.1 to 5.9) for newly developing BMLs. BML size at baseline was associated with risk of subsequent cartilage loss.\n\nQuestion:\nIs change in MRI-detected subchondral bone marrow lesions associated with cartilage loss : the MOST Study . A longitudinal multicentre study of knee osteoarthritis?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nNocturnal hypoglycemia is a significant problem for children and adolescents with type 1 diabetes. The counterregulatory hormone response to hypoglycemia is blunted in both patients with type 1 diabetes and healthy subjects during sleep. It is not known whether the threshold for arousal from sleep is also modified by hypoglycemia. To address this question we compared the acoustic arousal threshold from sleep during hypoglycemia and euglycemia in adolescents with type 1 diabetes. Adolescents with type 1 diabetes were studied on two occasions: under hypoglycemic and euglycemic conditions. During the hypoglycemia night, subjects underwent a hyperinsulinemic hypoglycemic clamp with nadir glucose level of 2.8 mmol/L. Hypoglycemia was initiated during stage 2 sleep and maintained during slow-wave sleep. During the euglycemia night, blood glucose was maintained at 5.5 mmol/L using the same clamp technique. The acoustic arousal threshold was determined during the first cycle of slow-wave sleep. Seven subjects (mean±SE, 14.2±0.8 years old, mean glycosylated hemoglobin 8.1±0.3%, duration of diagnosis 2.5±0.5 years) completed both study nights. Arousal was only noted during acoustic testing and did not occur during hypoglycemia alone. The acoustic arousal threshold during slow-wave sleep was similar under both conditions: 79±8 dB during euglycemia and 71±6 dB (P=0.353) during hypoglycemia.\n\nQuestion:\nDoes hypoglycemia change the threshold for arousal from sleep in adolescents with type 1 diabetes?\n\nAnswer:",
"role": "user"
},
{
"content": "no",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe incidence of non-tuberculous mycobacteria (NTM) isolation from humans is increasing worldwide. In England, Wales and Northern Ireland (EW&NI) the reported rate of NTM more than doubled between 1996 and 2006. Although NTM infection has traditionally been associated with immunosuppressed individuals or those with severe underlying lung damage, pulmonary NTM infection and disease may occur in people with no overt immune deficiency. Here we report the incidence of NTM isolation in EW&NI between 2007 and 2012 from both pulmonary and extra-pulmonary samples obtained at a population level. All individuals with culture positive NTM isolates between 2007 and 2012 reported to Public Health England by the five mycobacterial reference laboratories serving EW&NI were included. Between 2007 and 2012, 21,118 individuals had NTM culture positive isolates. Over the study period the incidence rose from 5.6/100,000 in 2007 to 7.6/100,000 in 2012 (p < 0.001). Of those with a known specimen type, 90 % were pulmonary, in whom incidence increased from 4.0/100,000 to 6.1/100,000 (p < 0.001). In extra-pulmonary specimens this fell from 0.6/100,000 to 0.4/100,000 (p < 0.001). The most frequently cultured organisms from individuals with pulmonary isolates were within the M. avium-intracellulare complex family (MAC). The incidence of pulmonary MAC increased from 1.3/100,000 to 2.2/100,000 (p < 0.001). The majority of these individuals were over 60 years old.\n\nQuestion:\nIs pulmonary Mycobacterium avium-intracellulare the main driver of the rise in non-tuberculous mycobacteria incidence in England , Wales and Northern Ireland , 2007-2012?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPrevious studies have demonstrated that piromelatine (a melatonin and serotonin 5-HT1A and 5-HT1D agonist) exerts an antidepressant activity in rodent models of acute stress and improves cognitive impairments in a rat model of Alzheimer's disease (AD). However, the role of piromelatine in chronic stress-induced memory dysfunction remains unclear. The aim of this study was to determine whether piromelatine ameliorates chronic mild stress (CMS)-induced memory deficits and explore the underlying mechanisms. Rats were exposed randomly to chronic mild stressors for 7 weeks to induce anhedonia (reflected by a significant decrease in sucrose intake), which was used to select rats vulnerable (CMS-anhedonic, CMSA) or resistant (CMS-resistant, CMSR) to stress. Piromelatine (50 mg/kg) was administered daily during the last 2 weeks of CMS. The tail suspension and forced swimming tests were adopted to further characterize vulnerable and resilient rats. The Y-maze and novel object recognition (NOR) tests were used to evaluate memory performance. Brain-derived neurotrophic factor (BDNF), cAMP response element-binding protein (CREB), phosphorylated CREB (pCREB), and cytogenesis were measured in the hippocampus. We found that only CMSA rats displayed significant increases in immobility time in the tail suspension and forced swimming tests; memory deficits in the Y-maze and NOR tests; significant decreases in hippocampal BDNF, CREB, and pCREB expression; and cytogenesis. All these anhedonia-associated effects were reversed by piromelatine.\n\nQuestion:\nDoes piromelatine ameliorate memory deficits associated with chronic mild stress-induced anhedonia in rats?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nDeficiency of vitamin B-6, vitamin B-12, folate, folic acid, or methionine may lead to dysregulation of DNA methylation, which might lead to disturbed energy and lipid metabolism. We aimed to explore whether intakes of vitamin B-6, vitamin B-12, folate, folic acid, and methionine at 1 y are associated with measures of growth and body composition at the age of 6 y. This study was performed in 2922 children participating in The Generation R Study, a population-based prospective cohort study. Dietary intakes of vitamins B-6 and B-12, folate, folic acid, and methionine were assessed at a median age of 12.9 mo by using a validated food-frequency questionnaire. At the age of 6 y, height and weight were measured, and body mass index (BMI; in kg/m(2)) was calculated. Body fat was measured with dual-energy X-ray absorptiometry, and body fat percentage and the ratio of android fat mass to gynoid fat mass (android:gynoid) were calculated. In models adjusted for maternal and child characteristics, children with folic acid intakes in the highest tertile had a 0.16 SD score (SDS) lower weight (95% CI: -0.31, -0.02 SDS) and a 0.14 SDS lower BMI (95% CI: -0.26, -0.01 SDS) than children in the lowest tertile. Children with vitamin B-12 intakes in the highest tertile had a 0.13 SDS higher android:gynoid (95% CI: 0.00, 0.25 SDS) than children in the lowest tertile. In addition, children with intakes in the highest tertile of methionine had a 0.09 SDS higher BMI (95% CI: 0.01, 0.17) and a 0.12 SDS higher android:gynoid (95% CI: 0.02, 0.22) than children in the lowest tertile. Vitamin B-6 and folate intakes were not associated with any of the body composition outcomes measured.\n\nQuestion:\nDo dietary Intakes of Folic Acid and Methionine in Early Childhood Are Associated with Body Composition at School Age?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe pro-inflammatory proteins calprotectin (a heterocomplex of S100A8/A9) and S100A12 have been associated with disease activity in rheumatoid arthritis (RA). The aim of this study was to compare their potential as biomarkers in a prospective study of RA patients starting with infliximab as their first biological disease-modifying anti-rheumatic drug (DMARD). Thirty-nine RA patients were examined and serum samples collected when starting with infliximab and after 3, 6, and 12 months. Calprotectin and S100A12 were analysed by enzyme-linked immunosorbent assays (ELISAs) and, together with C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), measured at all time points. A disease activity score of 28 joints (DAS28) was calculated. Radiographs of the hands, wrists, and feet were taken at baseline and after 3 years, and assessed according to the modified Sharp/van der Heijde (SvH) score. Responsiveness was evaluated according to the European League of Associations for Rheumatology (EULAR) response criteria based on 28 joints. Both S100 proteins were significantly higher in seropositive than in seronegative patients (p = 0.01). Calprotectin correlated significantly with CRP (ρ = 0.51-0.75), ESR (ρ = 0.32-0.52), and DAS28 (ρ = 0.32-0.62). S100A12 correlated with calprotectin (ρ = 0.62-0.77) and CRP (ρ = 0.32-0.63). The S100 proteins, and especially calprotectin (ρ = 0.23-0.39), showed weak associations with radiographic progression, unlike CRP/ESR. None of the S100 proteins could predict responsiveness.\n\nQuestion:\nAre calprotectin ( S100A8/A9 ) and S100A12 associated with measures of disease activity in a longitudinal study of patients with rheumatoid arthritis treated with infliximab?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPerioperative optimization of spatially resolved near-infrared spectroscopy determined cerebral frontal lobe oxygenation (scO2) may reduce postoperative morbidity. Norepinephrine is routinely administered to maintain cerebral perfusion pressure and, thereby, cerebral blood flow, but norepinephrine reduces the scO2. We hypothesized that norepinephrine-induced reduction in scO2 is influenced by cutaneous vasoconstriction. Fifteen healthy male subjects (25 ± 5 yr, mean ± SD) were studied during: hyperventilation (1.5 kPa end-tidal PcO2 reduction), whole-body heating, administration of norepinephrine (0.15 μg · kg · min; with and without end-tidal carbon dioxide correction), and hypoxia (FiO2: 0.12%). Arterial (saO2), skin, and internal jugular venous oxygen saturations (sjO2) were recorded, and the average cerebral capillary oxygen saturation (scapO2) was calculated. This study indicates that scO2 is influenced by skin oxygen saturation because whole-body heating increased scO2 by 3.6% (2.1-5.1%; 95% CI) and skin oxygen saturation by 3.1% (1.3-4.9%), whereas scapO2 remained unaffected. Conversely, hyperventilation decreased scO2 by 2.1% (0.4-3.7%) and scapO2 by 5.3% (3.8-6.9%), whereas skin oxygen saturation increased 1.8% (0.5-3.1%). In response to hypoxia, scO2 (10.2%; 6.6-13.7%), scapO2 (7.9%; 6.4-9.4%), and skin oxygen saturation (8.9%; 6.3-11.6%) all decreased. With administration of norepinephrine there was a 2.2% (1.0-4.3%) decrease in skin oxygen saturation and scO2 decreased 6.2% (4.2-8.0%), with scapO2 remaining unaffected.\n\nQuestion:\nDoes cutaneous vasoconstriction affect near-infrared spectroscopy determined cerebral oxygen saturation during administration of norepinephrine?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMucosal mast cells (MMCs) play a central role in the development of symptoms associated with IgE-mediated food allergy. Recently, Notch2-mediated signaling was shown to be involved in proper MMC distribution in the intestinal tract. This study aimed to clarify the mechanism by which Notch signaling regulates MMC distribution in the intestinal mucosa. Furthermore, pharmacologic inhibition of Notch signaling was evaluated as a treatment for symptoms associated with experimental food allergy. Bone marrow-derived mast cells generated from mice were cultured with Notch ligands, and then expression of genes associated with MMCs was measured in the cells. In addition, the effect of an inhibitor of Notch signaling on food antigen-induced allergic reactions was examined in a mouse model of food allergy. Notch signaling induced MMC differentiation through upregulation of expression of genes characteristic of MMCs in the presence of IL-3. Some lamina propria cells isolated from the mouse small intestine expressed Notch ligands and were able to upregulate MMC markers in bone marrow-derived mast cells through Notch signaling. In a mouse model of food allergy, administration of a Notch signaling inhibitor led to suppression of food antigen-induced hyperplasia of intestinal MMCs, resulting in alleviation of allergic diarrhea and systemic anaphylaxis.\n\nQuestion:\nDoes pharmacologic inhibition of Notch signaling suppress food antigen-induced mucosal mast cell hyperplasia?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo assess the analgesic effect of a handheld forced cold air device during fractional photothermolysis. Twenty patients who were being treated with full-face fractional photothermolysis were asked to rate their pain level with and without the handheld air-cooling device. Pain was rated on a scale of 1 to 10, with 10 being the worst. Nineteen of 20 patients noted decreased pain with the addition of handheld cooling. The mean level of pain without air-cooling was 6.95 +/- 2.0. The mean level of discomfort with air cooling was 4.0 +/- 1.8. The mean decrease in pain with the addition of air-cooling was 2.9 +/- 1.8.\n\nQuestion:\nDoes concurrent use of a handheld forced cold air device minimize patient discomfort during fractional photothermolysis?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPrevious studies have observed decreased serum CRP levels in patients with established Alzheimer's disease (AD) compared to controls or other diagnostic groups of elderly patients with mental illness. We have investigated the relation between CRP level and the severity of AD as assessed by cognitive function, brain imaging and survival time. Patients with AD showed overall lower CRP levels than other patients with mental illness, but elevated CRP levels in these patients were associated with lower cognitive function and shorter survival time.\n\nQuestion:\nIs c-reactive protein level decreased in patients with Alzheimer 's disease and related to cognitive function and survival time?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe principal nutrient artery to the femur demonstrates an increase in nitric oxide-mediated vasodilation in rats after treadmill exercise training. The present study sought to determine whether exercise training improves hindlimb bone and marrow blood flow distribution at rest and during exercise. Six 8-month old male Sprague-Dawley rats were exercise trained (ET) with treadmill walking at 15 m · min(-1) up a 15° incline for 60 min · d(-1) over a 10- to 12-wk period. Sedentary (SED) control animals were acclimated to treadmill exercise for 5 min · d(-1) during the week preceding the blood flow measurements. Blood flow to nine distinct regions of the femur, tibia, and fibula was determined at rest and during low-intensity exercise (15 m · min(-1) walking, 0° incline) using the reference sample microsphere method. The results demonstrate an augmentation of exercise hyperemia above that observed in SED rats during exercise in only one region of the bone, the femoral diaphysis, of ET rats. However, whereas exercise hyperemia occurred in three of the nine hindlimb bone regions measured in SED rats, exercise hyperemia occurred in seven of nine regions in ET rats.\n\nQuestion:\nDoes exercise training augment regional bone and marrow blood flow during exercise?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo investigate pregnancy outcome in relation to red blood cell (RBC) level of long-chain n-3 polyunsaturated fatty acids (PUFA) in the first trimester of pregnancy and the influence of lifestyle factors on the RBC level of long-chain n-3 PUFA. Observational study in a community with traditional fish and cod liver oil consumption. Seventy-seven healthy pregnant women. The PUFA composition of RBC was measured in the 11th to 15th week of pregnancy. The women answered food frequency and lifestyle questionnaires. Information on pregnancy outcome was collected from birth records. Placental weight, long-chain n-3 PUFA in diet and RBC, smoking. Of all the pregnancy outcome variables tested, placental weight was the only one associated with long-chain n-3 PUFA in RBC. Inverse association was found between the proportion of long-chain n-3 PUFA in RBC and placental weight, adjusted for birthweight (p=0.035). The proportion of long-chain n-3 PUFA in RBC was positively related to long-chain n-3 PUFA intake (p<0.001) and negatively related to smoking (p=0.011).\n\nQuestion:\nAre red blood cell n-3 polyunsaturated fatty acids in first trimester of pregnancy inversely associated with placental weight?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTreatment of cancer patients with anthracycline antibiotic doxorubicin (DOX) may be complicated by development of acute and chronic congestive heart failure (CHF), malignant arrhythmias and death. The aim of this study was to test whether an aqueous low molecular weight (LMW) extract from cod muscle decreases acute mortality in the mouse model of acute CHF caused by DOX. A LMW fraction (<500 Da) of the aqueous phase of cod light muscle (AOX) was used for treatment of male BALB/c mice (approximately 25 g, n = 70). The animals were divided into four groups, DOX + AOX (n = 20), DOX + saline (NaCl) (n = 30), NaCl + AOX (n = 10) and NaCl only (n = 10). Echocardiography was performed in the separate subgroups (DOX treated n = 6 and controls n = 6) to verify the presence and the grade of acute CHF. The cod extract was delivered by subcutaneously implanted osmotic minipumps over the period of 2 weeks. High-dose injection of DOX was administered to randomly selected animals. The animals received single intraperitoneal injection of DOX (25 mg/kg) and were followed over two weeks for mortality. Mortality rate was 68% lower (p < 0.05) in the mice treated with the extract. The analyses of cod extract have shown strong antioxidative effect in vitro.\n\nQuestion:\nDoes aqueous fish extract increase survival in the mouse model of cytostatic toxicity?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nActivating length mutations in the juxtamembrane domain (FLT3-LM) and mutations in the tyrosine kinase domain (FLT3-TKD) of FLT3 represent the most frequent genetic alterations in acute myeloid leukemia (AML). However, the functional role of active FLT3 mutants in primary AML blast cells is not well characterized. We analyzed the transforming potential and the signaling of FLT3-ITD mutants in Ba/F3 cells and in primary AML blasts. FLT3-ITD mutants induce an autophosphorylation of the receptor, interleukin 3-independent growth in Ba/F3 cells, and a strong STAT5 and mitogen-activated protein kinase (MAPK) activation. In contrast to the FLT3-ITD mutants, the ligand-stimulated FLT3-WT receptor was unable to transduce a fully proliferative response in Ba/F3 and monocytic OCI-AML5 cells. The ligand-stimulated FLT3-WT receptor activated AKT and MAPK, but not STAT5. In primary blast cells from 60 patients with AML, FLT3 was expressed in 91.9% of patients carrying a FLT3-LM/TKD mutation compared with 77.8% in FLT3-LM/TKD-negative patients. STAT3 and STAT5 were constitutively activated in 76 and 63% of patients, respectively. In accordance with the results in Ba/F3 cells, a high FLT3 expression and the presence of a FLT3-LM was strongly associated with the STAT5 but not with the STAT3 activation in primary AML blast cells. Moreover, the constitutive tyrosine phosphorylation of STAT5 was efficiently down-regulated by a FLT3 protein tyrosine kinase inhibitor in AML cells expressing an active FLT3 mutant.\n\nQuestion:\nDoes overexpression and constitutive activation of FLT3 induce STAT5 activation in primary acute myeloid leukemia blast cells?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe aim of this prospective study conducted at a tertiary referral center was to evaluate the efficacy of high-frequency duplex scanning in the preoperative evaluation of potential pedal target vessels. Material and methods The study population consisted of thirty-three consecutive diabetics suffering critical limb ischemia, with indications of infra-popliteal occlusive disease. Duplex ultrasound was performed by an angiologist unaware of any prior imaging procedures. The pedal vessels were divided into four segments. The inner diameter-, the grade of calcification (on a scale from 1-to-3), the maximal systolic velocity, and the resistance index ([V.max syst-V min syst]/V max syst), were assessed by using a 13-MHz probe, and the pedal target vessel best suited for surgery was identified. Results of duplex scanning were compared to (1) the results of selective digital subtraction angiography (DSA) and contrast-enhanced magnetic resonance angiography (CE-MRA) studies interpreted by two radiologists, (2) the site of distal anastomosis predicted by a vascular surgeon according to DSA and CE-MRA studies, (3) the definitive site of distal anastomosis, and (4) early postoperative results (patency at three months). Duplex scanning depicted significantly more pedal vascular segments than selective DSA- (P =.004, McNemar test). Agreement in predicting the site of distal anastomosis expressed as kappa value as follows: duplex versus DSA/CE-MRA, kappa 0.71;-DSA/CE-MRA versus definitive anastomosis, kappa 0.67; -and duplex versus definitive anastomosis kappa 0.82. Two patients were excluded from surgery as all three imaging modalities failed to demonstrate a pedal target vessel. Two patients had exploratory dissection of a pedal vessel (according to CE-MRA findings) that turned out to be occluded (as predicted by duplex scanning). In one patient the operation had to be terminated due to lack of autologous bypass material. In 31 patients who underwent pedal artery bypass, the resistance index could not be correlated to the run-off as assessed by intra-operative angiography.\n\nQuestion:\nDo preoperative high-frequency duplex scanning of potential pedal target vessels?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMicrodialysis is a method used to monitor hepatic tissue metabolism. Membranes with a molecular cut-off of 20 kilodalton (kDa) are currently used to measure the small metabolites glucose, glycerol, lactate and pyruvate. Using membranes with higher cut-off such as 100 kDa allows the possibility of measuring larger molecules but may affect results regarding small molecules. The aim was to compare microdialysis catheters with a cut-off of 20 and 100 kDa in the measurement of small molecules in a pig liver model. Four microdialysis catheters were inserted into the liver of each pig used in the experiment (n = 6). Two catheters with cut-off of 20 kDa were perfused with Ringer acetate, and two catheters with cut-off of 100 kDa: one perfused with Ringer acetate and one with hydroxyethyl starch (Voluven) at a flow rate of 0·3 μl min(-1). Dialysate samples were collected at 40-min intervals and analysed for glucose, glycerol, lactate and pyruvate. Compared to the other catheters, the 100-kDa catheters perfused with Ringer acetate tended to measure higher dialysate concentrations of the small molecules, the difference reaching statistical significance in the case of pyruvate. Concentrations measured by the 100-kDa catheters perfused with Voluven were, however, comparable to the 20-kDa catheters.\n\nQuestion:\nDoes membrane cut-off influence results regarding the measurement of small molecules - a comparative study between 20- and 100-kDa catheters in hepatic microdialysis?\n\nAnswer:",
"role": "user"
},
{
"content": "no",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo test the hypothesis that fluid resuscitation with Ringer's solution enriched with pyruvate (PR), a physiological antioxidant and energy substrate, affords protection of myocardial metabolism and electrophysiological performance superior to lactated Ringer's (LR) during hypovolemia and hindlimb ischemia-reperfusion. Male domestic goats (25-30 kg) were exsanguinated to a mean arterial pressure of 48 ± 1 mmHg. Right hindlimb ischemia was imposed for 90 min by applying a tourniquet and femoral crossclamp. LR or PR, infused iv, delivered 0.05 mmol/kg per minute L-lactate or pyruvate, respectively, from 30 min hindlimb ischemia until 30 min post-ischemia. Time controls (TC) underwent neither hemorrhage, hindlimb ischemia nor resuscitation. Goats were sacrificed and left ventricular myocardium biopsied at 90 min fluid resuscitation (n = 6 per group) or 3.5 h later (n = 9 LR, 10 PR, 8 TC). Myocardial 8-isoprostane content, phosphocreatine phosphorylation potential, creatine kinase activity, and heart rate-adjusted QT interval (QTc) variability were evaluated at 90 min resuscitation and 3.5 h post-resuscitation. PR sharply lowered pro-arrhythmic QTc variability vs LR (P < 0.05); this effect persisted 3.5 h post-resuscitation. PR lowered myocardial 8-isoprostane content, a product of oxidative stress, by 39 and 37% during and 3.5 h after resuscitation, respectively, vs LR. Creatine kinase activity fell 42% post-LR vs TC (P < 0.05), but was stable post-PR (P < 0.02 vs post-LR). PR doubled phosphocreatine phosphorylation potential, a measure of ATP free energy state, vs TC and LR (P < 0.05); this energetic enhancement persisted 3.5 h post-resuscitation.\n\nQuestion:\nDoes pyruvate-fortified resuscitation stabilize cardiac electrical activity and energy metabolism during hypovolemia?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIncreasing evidence suggests that Nigella sativa oil (NSO) and its principal bioactive constituents, thymoquinone (TQ), exhibit antioxidant, antihyperglycemic and renoprotective effects in streptozotocin (STZ)-induced diabetes in rats. However, the potential molecular mechanisms by which NSO and TQ may exert their actions in the diabetic kidney are still poorly characterized. This study was designed to investigate the effect of NSO and TQ treatment on the albuminuria, podocyte injury and the complex systems controlling the extracellular matrix proteins accumulation and angiogenesis in the STZ-induced model of diabetic nephropathy. Adult female Wistar rats were divided into four experimental groups (control, untreated STZ-diabetic, and NSO or TQ treated STZ-diabetic rats). The treated rats received 2 mL/kg NSO or 50 mg/kg TQ via oral gavage once a day for 10 weeks. The results showed that the albuminuria and the kidney weight/body weight ratio were increased in the diabetic rats compared with the control animals and they were significantly ameliorated by the treatment with NSO or TQ. The real-time PCR showed that the NSO and TQ treatment prevented diabetes-induced downregulation of mRNA expression of the podocyte-specific marker (podocin) as well as the mRNA overexpressions of collagen IV, transforming growth factor-β1 (TGF-β1) and vascular endothelial growth factor-A (VEGF-A) in the diabetic kidney. These results were also confirmed by immunohistochemistry.\n\nQuestion:\nDo nigella sativa oil and thymoquinone ameliorate albuminuria and renal extracellular matrix accumulation in the experimental diabetic rats?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe aimed to investigate the correlation between ECG QRS voltage changes, N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels and clinical improvement in decompensated heart failure (DHF). DHF patients (n=56) with a mean age of 67.5±12.6 years showed limb QRS amplitude increase and NT-proBNP level decrease with clinical improvement (p<0.001). Significant correlation was found between percent changes (Δ%) in body weight and Δ% in QRS voltages of aVR, aVF, DII, ΣQRSI+II and ΣQRS (all limb-leads) (r = -0.40; r = -0.35; r = -0.32; r = -0.30; r = -0.30 respectively, p<0.05). No correlation was found between Δ% in NT-proBNP and body weight (r = -0.23, p=0.09). Δ% NT-proBNP was correlated with Δ% QRS voltage only in aVR (r = -0.312, p=0.019). In ROC analysis, ≥0.5 mm increase in aVR QRS voltage was found to predict ≥5 kg weight loss with a sensitivity of 74% and specificity of 62% (p=0.013, AUC: 0.699).\n\nQuestion:\nIs increase in QRS amplitudes better than N-terminal pro-B-type natriuretic peptide to predict clinical improvement in decompensated heart failure?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nLiver cirrhosis is associated with increased prevalence of gastrointestinal symptoms, insulin resistance, and altered gut transit. We aimed to assess the prevalence of gut transit abnormalities in patients with cirrhosis, compared with healthy controls, and to evaluate the relation of gut transit with gastrointestinal symptoms and postprandial glucose and hormone profiles. Half gastric emptying, small bowel residence, and colonic filling times were measured with a validated radiologic procedure in 42 consecutive patients with cirrhosis. In a subgroup of 25 patients, gastrointestinal symptoms were evaluated by using a validated questionnaire and a caloric satiation test. Postprandial glucose, insulin, leptin, ghrelin, glucagon-like peptide 1, and PYY responses were also studied. Eighty-three healthy subjects served as controls for the transit studies and 10 for the hormone analyses. Of patients with cirrhosis, 24% had delayed gastric emptying and 38% had prolonged small bowel transit (P < .05 compared with controls). Delayed gastric emptying was related to postprandial fullness and prolonged small bowel transit to diarrhea and abdominal pain (P < .05 for all). The patients with cirrhosis had increased postprandial glucose, insulin, and glucagon-like peptide 1 responses and reduced postprandial ghrelin. Delayed gastric emptying was related to increased postprandial glucose and reduced postprandial ghrelin. Prolonged small bowel transit was related to increased postprandial glucose and insulin and reduced postprandial ghrelin.\n\nQuestion:\nIs gut transit associated with gastrointestinal symptoms and gut hormone profile in patients with cirrhosis?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe extent to which the developmental transcription factor SOX9 functions as an oncogene or tumor suppressor in colorectal carcinoma (CRC) is debatable. We aimed to clarify the effect of SOX9 mutations on SOX9 protein expression and their association with known molecular subtypes and clinical characteristics in advanced CRC. Next generation sequencing data (MSK-IMPACT) from CRC patients was used to interrogate SOX9, KRAS, NRAS, BRAF, TP53, APC, and PIK3CA. Mutant and wild type (WT) SOX9 cases underwent immunohistochemical (IHC) staining to assess protein expression. SOX9 allele-specific copy number was assessed by Affymetrix Oncoscan array. SOX9 was mutated in 38 of 353 (10.7%) CRC, of which 82% were frameshift or nonsense. Compared to SOX9 WT, SOX9 mutation was strongly associated with coexistent mutant KRAS (p=0.0001) and WT TP53 (p=0.0004). SOX9 was overexpressed in both SOX9 mutant and WT CRC. Among SOX9 mutants, the highest expression was noted for truncating exon 3 mutants (mean H scores 239±105 versus 147±119, p value=0.02). Further, SOX9 truncating mutants with loss of the WT allele demonstrated protein overexpression indicating the WT protein was not required for protein stabilization.\n\nQuestion:\nAre recurrent , truncating Sox9 mutations associated with sox9 overexpression , KRAS mutation , and TP53 wild type status in colorectal carcinoma?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nLung cancer mortality rates are higher in more deprived populations. This may simply reflect higher incidence of the disease, or additionally delayed presentation and worse outcomes amongst more deprived patients. Low socio-economic status (SES) has also been linked to cancer fatalism which might account for such differences. We determined the interaction between SES, patient's characteristics at presentation with lung cancer, and disease outcome at a large UK teaching hospital. Stage, PS at presentation, treatment and survival data, index of multiple deprivation score and ACORN group (geo-demographic segmentation tool) were analysed for 1432 patients. There were no significant differences in stage or PS distribution by IMD quintile or ACORN group. When patients with stage I/II disease were considered, there were no differences in IMD or ACORN group for those undergoing or not undergoing surgical resection. Similarly when the whole cohort was considered, there were no differences in these parameters between those receiving and not receiving any anti-cancer therapy. There was a non-significant trend to lower IMD score (i.e. less deprivation) in the stage IIIb/IV patients receiving palliative chemotherapy compared to those not receiving chemotherapy. There was no significant difference in median survival or one-year survival according to IMD quintile or ACORN group.\n\nQuestion:\nDoes social deprivation affect lung cancer stage at presentation or disease outcome?\n\nAnswer:",
"role": "user"
},
{
"content": "no",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPhosphatidylethanolamine N-methyltransferase (PEMT) catalyses the synthesis of phosphatidylcholine from phosphatidylethanolamine. The aim of this study was to evaluate the effect of chronic ethanol ingestion on PEMT activity in the jejunal brush-border membrane (BBM) of adequately nourished rats. For this purpose, rats were fed a liquid diet containing ethanol [ethanol-fed group (EFG)] or an isocaloric liquid diet without ethanol [pair-fed group (PFG)] for 4 weeks. Diet ingestion, body weight, nitrogen balance and urinary creatinine excretion were monitored during the experimental period, and serum transferrin levels were determined at the end. BBM was isolated for the determination of PEMT activity. PEMT activity was significantly increased in the jejunal BBM of the EFG. Nutritional parameters, however, did not differ between groups.\n\nQuestion:\nIs phosphatidylethanolamine N-methyltransferase activity increased in rat intestinal brush-border membrane by chronic ethanol ingestion?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCCR5 antagonists block HIV cell entry through competitive binding to the CCR5 receptor present on the surface of CD4(+) cells. The CCR5 receptor is also present on CD8(+) cells involved in clearing hepatitis C virus (HCV). The goal of the present study was to examine the short-term safety of a CCR5 antagonist, vicriviroc, in patients with HIV/HCV coinfection. A randomized, double-blind trial was conducted in 28 HIV/HCV-coinfected subjects with compensated liver disease and plasma HIV RNA below 400 copies/mL. All subjects were receiving a ritonavir-enhanced protease inhibitor regimen, to which vicriviroc (5, 10, or 15 mg/day) or placebo was added for 28 days. Clinical and laboratory evaluations were performed 21 days beyond the treatment period. Treatment with vicriviroc resulted in no clinically meaningful changes in HCV or HIV viral load or any immune parameters. Adverse events were equally distributed among placebo and vicriviroc groups. Transaminase elevations of grade 1 or more were reported as AEs in 1 subject receiving 10-mg vicriviroc and 1 placebo subject. Vicriviroc plasma concentrations were similar to those observed in healthy subjects.\n\nQuestion:\nIs short-term administration of the CCR5 antagonist vicriviroc to patients with HIV and HCV coinfection safe and tolerable?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nEvidence accumulates that the neuropeptide oxytocin plays an important role in mediating social interaction among humans and that a dysfunction in oxytocin-modulated brain mechanisms might lie at the core of disturbed social behavior in neuropsychiatric disease. Explanatory models suggest that oxytocin guides social approach and avoidance by modulating the perceived salience of socially meaningful cues. Animal data point toward the ventral tegmental area (VTA) as the brain site where this modulation takes place. We used functional magnetic resonance imaging and a social incentive delay task to test the hypothesis that oxytocin modulates the neural processing of socially relevant cues in the VTA, hereby facilitating behavioral response. Twenty-eight nulliparous women (not taking any hormones) received intranasal oxytocin or placebo in a double-blind randomized clinical trial with a parallel-group design. Oxytocin significantly enhanced VTA activation in response to cues signaling social reward (friendly face) or social punishment (angry face). Oxytocin effects on behavioral performance were modulated by individual differences in sociability with enhanced performance in women scoring low but decreased performance in women scoring high on self-reported measures of agreeableness.\n\nQuestion:\nDoes oxytocin influence processing of socially relevant cues in the ventral tegmental area of the human brain?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nExtended warm ischemia time during partial nephrectomy leads to considerable renal injury. Using a rat model of renal ischemia, we examined the ability of a unique renoprotective cocktail to ameliorate warm ischemia-reperfusion injury and extend warm ischemia time. A warm renal ischemia model was developed using Sprague-Dawley rats, clamping the left renal artery for 40, 50, 60, and 70 minutes, followed by 48 hours of reperfusion. An improved renoprotective cocktail referred to as I-GPM (a mixture of specific renoprotective growth factors, porphyrins, and mitochondria-protecting amino acids) was administered -24 hours, 0 hours, and +24 hours after surgery. At 48 hours, both kidneys were harvested and examined with hematoxylin and eosin and periodic acid-Schiff stains for the analysis of renal tubular necrosis. Creatinine, protein, and gene expression levels were also analyzed to evaluate several ischemia-specific and antioxidant response markers. I-GPM treated kidneys showed significant reversal of morphologic changes and a significant reduction in specific ischemic markers lipocalin-2, galectin-3, GRP-78, and HMGB1 compared with ischemic controls. These experiments also showed an upregulation of the stress response protein, heat shock protein (HSP)-70, as well as the phosphorylated active form of the transcription factor, heat shock factor (HSF)-1. In addition, quantitative RT-PCR analyses revealed a robust upregulation of several antioxidant pathway response genes in I-GPM treated animals.\n\nQuestion:\nDoes the administration of renoprotective agents extend warm ischemia in a rat model?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe rationale for recanalization therapy in acute ischemic stroke is to preserve brain through penumbral salvage and thus improve clinical outcomes. We sought to determine the relationship between recanalization, clinical outcomes, and final infarct volumes in acute ischemic stroke patients presenting with middle cerebral artery occlusion who underwent endovascular therapy and post-procedure magnetic resonance imaging. We identified 201 patients with middle cerebral artery occlusion. Patients with other occlusive lesions were excluded. Baseline clinical/radiological characteristics, procedural outcomes (including thrombolysis in cerebral infarction scores), clinical outcome scores (modified Rankin scores), and final infarct volumes on diffusion weighted imaging were retrospectively analyzed from a prospectively collected database. Favorable outcome is defined as 90-day modified Rankin score≤2. Successful recanalization (thrombolysis in cerebral infarction grade 2b or 3) was achieved in 63.2% and favorable outcomes in 46% of cases. Mean infarct volume was 50.1 mL in recanalized versus 133.9 mL in non-recanalized patients (P<0.01) and 40.4 mL in patients with favorable outcomes versus 111.8 in patients with unfavorable outcomes (P<0.01). In multivariate analysis, thrombolysis in cerebral infarction≥2b, baseline National Institute of Health Stroke Scale, Alberta Stroke Program Early Computed Tomography scores, and age were identified as independent predictors of outcome. However, when infarct volumes were included in the analysis only final infarct volume and age remained significantly associated.\n\nQuestion:\nIs final infarct volume a stronger predictor of outcome than recanalization in patients with proximal middle cerebral artery occlusion treated with endovascular therapy?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe elevation of triglycerides is strongly linked with insulin resistance, but it has not been evaluated in relationship to insulin secretion. The aim of this study was to determine whether hypertriglyceridaemia is associated with abnormal insulin secretion. A cross-sectional study was carried out. Eligible subjects, apparently healthy men and non-pregnant women aged 20-65 years were recruited. According to the triglyceride levels, subjects were allocated in the groups with hypertriglyceridaemia and normotriglyceridaemia. Hypertriglyceridaemia was defined by serum triglyceride levels ≥150 mg/dL. Insulin secretion was evaluated by the first phase of insulin secretion (1st PIS) and the second phase of insulin secretion (2nd PIS). A regression linear analysis was performed to evaluate the association between hypertriglyceridaemia (independent variable) and the first and second phase insulin secretion (dependent variables). A total of 247 apparently healthy subjects were enrolled; 113 (45.7%) with hypertriglyceridaemia and 134 (54.3%) in the control group. The simple regression linear analysis showed a significant association between hypertriglyceridaemia and the 1st PIS [B = 207.0; 95% confidence interval (CI) 33.5-380.5, p = 0.02] and the 2nd PIS (B = 48.7; 95% CI 9.2-88.2, p = 0.01). A multiple regression linear analysis adjusted by age, sex, body mass index and waist circumference was performed showing that fasting hypertriglyceridaemia remained significantly associated with the 1st PIS (B = 184.3; 95% CI 13.0-355.7, p = 0.03) and the 2nd PIS (B = 43.1; 95% CI 4.2-81.9, p = 0.03).\n\nQuestion:\nIs insulin secretion increased in non-diabetic subjects with fasting hypertriglyceridaemia?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nNeointimal hyperplasia limits the longevity of vascular interventions. Nitric oxide (NO) is well known to inhibit neointimal hyperplasia. However, delivery of NO to the vasculature is challenging. Our study aims to evaluate the efficacy of delivering NO to the site of injury using a permeable balloon catheter. Our hypothesis is that ultra-short duration NO delivery using a permeable balloon catheter will inhibit neointimal hyperplasia. Ten-week-old male Sprague-Dawley rats underwent carotid artery balloon injury. Groups included: (1) control, (2) injury, (3) injury + periadventitial NO, and (4) injury + endoluminal NO via permeable balloon catheter. The catheter was inflated to 5 atm pressure for 5 min. Arteries were harvested 2 wk following injury. Morphometric assessment for neointimal hyperplasia and immunohistochemical staining for inflammatory markers were performed. Injury increased neointimal hyperplasia compared with control (intima/media area [I/M] ratio 1.07 versus 0.11, respectively, P < 0.001). Periadventitial delivery of NO reduced the I/M area ratio compared with injury alone (55% decrease, P < 0.001). Endoluminal delivery of NO also reduced the I/M area ratio compared with injury alone (65% decrease; P < 0.001). Both endoluminal and periadventitial NO affected the I/M ratio by reducing the intimal area (64% and 46%, respectively, P < 0.001) whereas neither affected the medial area. Periadventitial NO delivery increased lumen area (P < 0.05), whereas endoluminal NO delivery increased circumference (P < 0.05). Periadventitial NO delivery inhibited macrophage intimal infiltration compared with injury alone (P < 0.05).\n\nQuestion:\nDoes nitric oxide delivery via a permeable balloon catheter inhibit neointimal growth after arterial injury?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nNot all women with patent tubes develop clinically manifest endometriosis. Quality and quantity of endometrium in retrograde menstruation may be the determining factor in the development of the disease. We hypothesize that retrograde shedding of endometrial fragments with preserved integrity facilitates implantation of endometrium in ectopic locations, resulting in endometriotic lesion development. We evaluate the impact of tissue integrity on the success of endometriosis-like lesion development in the chicken embryo chorioallantoic membrane (CAM) model. Menstrual and non-menstrual (cyclic) endometrium were collected by biopsy, and either minced or enzymatically dispersed. Spontaneously shed menstrual effluent was collected by a menstrual cup, and cells and tissue were isolated. We evaluated whether infiltration or lesion formation in the CAM occurred after transplantation of endometrium onto the CAM. Transplantation of biopsied menstrual and cyclic endometrium fragments, and of endometrium fragments >1 mm(3) isolated from menstrual effluent, resulted in lesion formation. Transplantation of endometrial cells isolated from menstrual effluent did not lead to lesion formation. After transplantation of digested biopsied cyclic endometrium, infiltration in the CAM but no lesions were observed.\n\nQuestion:\nIs tissue integrity essential for ectopic implantation of human endometrium in the chicken chorioallantoic membrane?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAn emerging paradigm for understanding how anesthetics induce altered arousal is relating receptor targeting in specific neural circuits to electroencephalogram (EEG) activity. Enhanced gamma amino-butyric acid A (GABAA) inhibitory post-synaptic currents (IPSCs) manifest with large-amplitude slow (0.1-1Hz) and frontally coherent alpha (8-12Hz) EEG oscillations during general anesthesia. Therefore, we investigated the EEG signatures of modern day derivatives of ether (MDDE) anesthesia to assess the extent to which we could obtain insights into MDDE anesthetic mechanisms. We retrospectively studied cases from our database in which patients received isoflurane anesthesia vs. isoflurane/ketamine anesthesia (n=10 each) or desflurane anesthesia vs. desflurane/ketamine anesthesia (n=9 each). We analyzed the EEG recordings with spectral power and coherence methods. Similar to known GABAA circuit level mechanisms, we found that MDDE anesthesia induced large amplitude slow and frontally coherent alpha oscillations. Additionally, MDDE anesthesia also induced frontally coherent theta (4-8Hz) oscillations. Reduction of GABAergic IPSCs with ketamine resulted in beta/gamma (13-40Hz) oscillations, and significantly reduced MDDE anesthesia-induced slow, theta and alpha oscillation power.\n\nQuestion:\nAre gABAA circuit mechanisms associated with ether anesthesia-induced unconsciousness?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPatients with colitis have an increased risk of colorectal cancer, compared with persons without colitis. Many studies have shown chromoendoscopy (CE) to be superior to standard methods of detecting dysplasia in patients with colitis at index examination. We performed a prospective, longitudinal study to compare standard colonoscopy vs CE in detecting dysplasia in patients with inflammatory bowel diseases in a surveillance program. We analyzed data from 68 patients (44 men, 24 women) diagnosed with ulcerative colitis (n = 55) or Crohn's disease (n = 13) at Mount Sinai Medical Center from September 2005 through October 2011. The patients were followed from June 2006 through October 2011 (median, 27.8 months); each patient was analyzed by random biopsy, targeted white light examination (WLE), and CE. Specimens were reviewed by a single blinded pathologist. The 3 methods were compared by using the generalized estimating equations method, and the odds ratios (ORs) for detection of dysplasia were calculated (primary outcome). Time to colectomy was analyzed by using the Cox model. In the 208 examinations conducted, 44 dysplastic lesions were identified in 24 patients; 6 were detected by random biopsy, 11 by WLE, and 27 by CE. Ten patients were referred for colectomy, and no carcinomas were found. At any time during the study period, CE (OR, 5.4; 95% confidence interval [CI], 2.9-9.9) and targeted WLE (OR, 2.3; 95% CI, 1.0-5.3) were more likely than random biopsy analysis to detect dysplasia. CE was superior to WLE (OR, 2.4; 95% CI, 1.4-4.0). Patients identified as positive for dysplasia were more likely to need colectomy (hazard ratio, 12.1; 95% CI, 3.2-46.2).\n\nQuestion:\nDoes chromoendoscopy be More Effective Than Standard Colonoscopy in Detecting Dysplasia During Long-term Surveillance of Patients With Colitis?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTreatment of inflammatory bowel disease would benefit from specific targeting of therapeutics to the intestine. We developed a strategy for localized delivery of the immunosuppressive cytokine interleukin (IL)-27, which is synthesized actively in situ by the food-grade bacterium Lactococcus lactis (LL-IL-27), and tested its ability to reduce colitis in mice. The 2 genes encoding mouse IL-27 were synthesized with optimal codon use for L lactis and joined with a linker; a signal sequence was added to allow for product secretion. The construct was introduced into L lactis. Colitis was induced via transfer of CD4(+)CD45RB(hi) T cells into Rag(-/-) mice to induce colitis; 7.5 weeks later, LL-IL-27 was administered to mice via gavage. Intestinal tissues were collected and analyzed. LL-IL-27 administration protected mice from T-cell transfer-induced enterocolitis and death. LL-IL-27 reduced disease activity scores, pathology features of large and small bowel, and levels of inflammatory cytokines in colonic tissue. LL-IL-27 also reduced the numbers of CD4(+) and IL-17(+) T cells in gut-associated lymphoid tissue. The effects of LL-IL-27 required production of IL-10 by the transferred T cells. LL-IL-27 was more effective than either LL-IL-10 or systemic administration of recombinant IL-27 in reducing colitis in mice. LL-IL-27 also reduced colitis in mice after administration of dextran sodium sulfate.\n\nQuestion:\nDoes oral delivery of IL-27 recombinant bacteria attenuate immune colitis in mice?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe observed the relationship between the expression of thymidylate synthase protein (pTS) and cell cycle regulators in gastric and colorectal adenocarcinoma tissues. This study included 80 gastric and 50 colorectal adenocarcinomas. Immunohistochemical staining was performed using a polyclonal antibody to recombinant human pTS, and monoclonal antibodies to p53, p21/WAF1CIP1, p16/INK4, cyclin D1 and pRB. Each staining was quantified using computerized image analysis on a CAS 200 system. We selected the mean expression values as the cutoff values to distinguish between high and low expression of these substances. There was no relationship between pTS expression and p21/WAF1CIP1, cyclin D1, or pRB expression in gastric and colorectal carcinomas. In both gastric and colorectal carcinomas, the pTS expression was significantly low in the high p16/INK4 expression subgroup compared with the low p16/INK4 expression subgroup (P < 0.05). Further, the pTS expression was significantly high in the high p53 expression subgroup compared with the low p53 expression subgroup in colorectal adenocarcinomas (P < 0.05).\n\nQuestion:\nIs expression of thymidylate synthase in human gastric and colorectal adenocarcinomas upregulated by p16/INK4?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nLung cancer, predominantly non-small-cell lung cancer (NSCLC), is the leading cause of cancer deaths worldwide. There is a great need to identify critical effectors involved in metastasis of NSCLC that will facilitate the development of new therapeutic strategies. Here we evaluated the potential role of miR-125b in the metastasis of NSCLC cells. Human NSCLC cells were isolated from surgical tissues with Cancer Cell Isolation Kit. Expressions of miR-125b and TP53INP1 were detected with real-time PCR and western blot. Human miR-125b mimics, miR-125b inhibitor, TP53INP1 expression plasmid and TP53INP1 siRNA were transfected into NSCLC cells with nucleofector transfection kit. NSCLC metastasis was determined with adhesion assay, invasive assay and lung tumor metastasis model. The expression of miR-125b was significantly higher in poorly differentiated NSCLC cells that are endowed with high metastatic potentials. Up-regulation of miR-125b could enhance the metastatic potential of NSCLC cells in vitro and in vivo, while down-regulation of miR-125b resulted in decreased metastatic potentials in vitro and in vivo. Further, tumor protein 53-induced nuclear protein 1 (TP53INP1) was an important target of miR-125b involved in metastasis of NSCLC cells. TP53INP1 served as a negative regulator of NSCLC metastasis. Decreased expression of TP53INP1 in tumor tissues was inversely associated with their expression of miR-125b, significantly lower in poorly differentiated tumors and inversely correlated with the clinical stages in patients with NSCLC.\n\nQuestion:\nDoes microRNA-125b promote tumor metastasis through targeting tumor protein 53-induced nuclear protein 1 in patients with non-small-cell lung cancer?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nNeutrophil extracellular traps (NETs) are mesh-like DNA fibers clad with intracellular proteins that are cast out from neutrophils in response to certain stimuli. The process is thought to depend on reactive oxygen species (ROS) generated by the phagocyte NADPH-oxidase and the ROS-modulating granule enzyme myeloperoxidase (MPO), but when, how, and where these factors contribute is so far uncertain. The neutrophil NADPH-oxidase can be activated at different cellular sites and ROS may be produced and processed by MPO within intracellular granules, even in situations where a phagosome is not formed, e.g., upon stimulation with phorbol myristate acetate (PMA). We investigated the subcellular location of ROS production and processing by MPO in the context of PMA-induced NET formation. Complete neutralization of extracellular ROS was not sufficient to block NET formation triggered by PMA, indicating that intragranular ROS are critical for NETosis. Employing a set of novel MPO-inhibitors, inhibition of NET formation correlated with inhibition of intragranular MPO activity. Also, extracellular addition of MPO was not sufficient to rescue NET formation in completely MPO-deficient neutrophils and specific neutralization by luminol of MPO-processed ROS within intracellular granules led to a complete block of PMA-triggered NET formation.\n\nQuestion:\nIs neutrophil NET formation regulated from the inside by myeloperoxidase-processed reactive oxygen species?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe tested the hypothesis that treatment of embolic stroke with recombinant human tissue plasminogen activator (rhtPA) alters cerebral expression of adhesion molecules. Male Wistar rats were subjected to middle cerebral artery occlusion by a single fibrin-rich clot. P-selectin, E-selectin, and intercellular adhesion molecule-1 (ICAM-1) immunoreactivity was measured at 6 or 24 hours after embolic stroke in control rats and in rats treated with rhtPA at 1 or 4 hours after stroke. To examine the therapeutic efficacy of combined rhtPA and anti-ICAM-1 antibody treatment at 4 hours after embolization, ischemic lesion volumes were measured in rats treated with rhtPA alone, rats treated with rhtPA and anti-ICAM-1 antibody, and nontreated rats. Administration of rhtPA at 1 hour after embolization resulted in a significant reduction of adhesion molecule vascular immunoreactivity after embolization in the ipsilateral hemisphere compared with corresponding control rats. However, when rhtPA was administered to rats at 4 hours after embolization, significant increases of adhesion molecule immunoreactivity in the ipsilateral hemisphere were detected. A significant increase of ICAM-1 immunoreactivity was also detected in the contralateral hemisphere at 24 hours after ischemia. A significant reduction in lesion volume was found in rats treated with the combination of rhtPA and anti-ICAM-1 antibody compared with rats treated only with rhtPA.\n\nQuestion:\nDoes thrombolysis with tissue plasminogen activator alter adhesion molecule expression in the ischemic rat brain?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nDespite the recent advances in bypass surgery and catheter interventional therapy for peripheral artery disease (PAD), the long-term outcome of revascularization therapy for infrapopliteal lesions remains unsatisfactory. We have previously demonstrated that low-energy extracorporeal shock wave (SW) therapy effectively induces neovascularization through upregulation of angiogenic factors and improves myocardial ischemia in pigs and humans and in hindlimb ischemia in rabbits. In this study, we thus examined whether our SW therapy also improves the walking ability of patients with PAD and intermittent claudication. We treated 12 patients (19 limbs) in Fontaine II stage (males/females, 10/2; 60-86 years old) with low-energy SW therapy to their ischemic calf muscle 3 times/week for 3 consecutive weeks. After 24 weeks, the pain and distance subscale scores of the walking impairment questionnaire were significantly improved (33±25 vs. 64±26, 27±16 vs. 64±23, respectively, both P<0.01). Maximum walking distance was also significantly improved at 4 weeks (151±37% from baseline, P<0.01) and was maintained at 24 weeks (180±74% from baseline, P<0.01). Moreover, the recovery time of the tissue oxygenation index in the calf muscle during a treadmill test, which reflects local O<inf>2</inf> supply, was significantly shortened (295±222s vs. 146±137s, P<0.01). Importantly, no adverse effects were noted.\n\nQuestion:\nDoes extracorporeal shock wave therapy improve the walking ability of patients with peripheral artery disease and intermittent claudication?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIn anteroposterior (AP)-gliding mobile-bearing total knee arthroplasty (TKA), the femoral component can theoretically slide forward resulting in a more anterior contact point, causing pain due to impingement. A lower lever arm of the extensor apparatus can also attribute to higher patella pressures and pain. The goal of this study was to determine the contact point in a cohort of mobile- and fixed-bearing TKAs, to determine whether the contact point lies more anteriorly in mobile-bearing TKA and to confirm whether this results in anterior knee pain. We used 38 fixed-bearing TKA and 40 mobile-bearing TKA from a randomized trial with straight lateral knee X-rays and measured the contact point. The functional outcome was measured by Knee Society Score at 12 months postoperatively. Pain scores were analysed using a VAS score (0-100 mm) in all patients at rest and when moving. Difficulty at rising up out of a chair was also assessed using a VAS score. The contact point in mobile-bearing TKA was situated at 59.5 % of the AP distance of the tibia and in the fixed-bearing TKA group at 66.1 % (P< 0.05). Patients with mobile- and fixed-bearing TKAs had similar knee scores, pain scores and difficulty in chair rise. No significant correlation was found between contact point and knee pain.\n\nQuestion:\nDo different femorotibial contact points between fixed- and mobile-bearing TKAs do not show clinical impact?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSleep is regulated by circadian and homeostatic processes. The circadian pacemaker, located in the suprachiasmatic nuclei (SCN), regulates the timing and consolidation of the sleep-wake cycle, while a homeostatic mechanism governs the accumulation of sleep debt and sleep recovery. Recent studies using mice with deletions or mutations of circadian genes show that components of the circadian pacemaker can influence the total amount of baseline sleep and recovery from sleep deprivation, indicating a broader role for the SCN in sleep regulation. To further investigate the role of the circadian pacemaker in sleep regulation in mice, we recorded sleep in sham and SCN-lesioned mice under baseline conditions and following sleep deprivation. Compared to sham controls, SCN-lesioned mice exhibited a decrease in sleep consolidation and a decrease in wakefulness during the dark phase. Following sleep deprivation, SCN-lesioned mice exhibited an attenuated increase in non-rapid eye movement sleep time but an increase in non-rapid eye movement sleep electroencephalographic delta power that was similar to that of the sham controls.\n\nQuestion:\nDoes the suprachiasmatic nucleus regulate sleep timing and amount in mice?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nNitrogen-containing bisphosphonates have been shown to be effective for the treatment of osteoporosis and Paget's disease of bone. Unfortunately, these drugs also have the capacity to irritate the upper gastrointestinal mucosa. In this study we investigated the ability of alendronate and pamidronate to directly damage the gastric epithelium and attempted to determine whether these drugs caused injury through gastric microcirculatory alterations. An ex vivo gastric chamber model was used. Effects of topically applied alendronate and pamidronate on transmucosal potential difference and epithelial integrity (histology) were determined. Also, the effects of agents capable of preventing microvascular injury in the stomach (PGE2 and two nitric oxide donors) were examined for their ability to prevent gastric injury induced by the two N-bisphosphonates. Alendronate and pamidronate caused a concentration-dependent decrease in transmucosal potential difference, widespread epithelial injury and infiltration of neutrophils into the mucosa. PGE2 and the two nitric oxide donors did not prevent the changes in potential difference or the epithelial injury, but did reduce neutrophil infiltration. Significant release of PGE2 into the lumen was observed following application of the two bisphosphonates, but neither drug altered mucosal blood flow.\n\nQuestion:\nDo n-bisphosphonates cause gastric epithelial injury independent of effects on the microcirculation?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nFarnesoid X Receptor (FXR) and its co-partners Retinoid X Receptors (RXRs) are considered to participate in crucial biochemical and cellular processes, being involved in the pathogenesis of several diseases, including cancer. The present study aimed to evaluate the clinical significance of FXR alone and in conjunction with RXRs expression, in pancreatic adenocarcinoma. FXR, RXR-α, -β and -γ protein expression was assessed immunohistochemically on tumoral samples of 55 pancreatic adenocarcinoma cases and was statistically analyzed with clinicopathological characteristics, tumor proliferative capacity and patients' survival. Enhanced FXR expression was borderline associated with earlier histopathological stage (p=0.054). Concomitant elevated FXR/RXR-α expression was significantly associated with decreased tumor histological grade (p=0.017), while concomitant enhanced FXR/RXR-β and FXR/RXR-γ expression with earlier histopathological stage (p=0.017 and p=0.004, respectively) and smaller tumor size (p=0.037 and p=0.005, respectively). Concomitant enhanced FXR/RXR-γ expression was additionally significantly associated with the absence of lymph node metastases (p=0.018). Pancreatic adenocarcinoma patients with enhanced FXR, FXR/RXR-β or -γ expression showed significantly longer survival times compared to those with low expression (p=0.013, p=0.021 and p<0.001, respectively). In multivariate analysis, FXR and FXR/RXR-γ expression were identified as independent prognostic factors (p=0.044 and p=0.001, respectively).\n\nQuestion:\nIs elevated Farnesoid X Receptor ( FXR ) and Retinoid X Receptors ( RXRs ) expression associated with less tumor aggressiveness and favourable prognosis in patients with pancreatic adenocarcinoma?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMidazolam has been shown to have an analgesic effect by single shot epidural administration. In this study, the effect of midazolam on continuous epidural infusion of bupivacaine was investigated to find a better combination for postoperative analgesia. Sixty patients scheduled for gastrectomy were divided into three groups of 20. The following mixtures, in 40 ml, were infused continuously over 12 hr after surgery; 40 ml bupivacaine 0.5% in Group C, bupivacaine 0.5% 38 ml + 10 mg midazolam in Group M10, and bupivacaine 0.5% 36 ml + 20 mg midazolam in Group M20. If necessary, 50 mg indomethacin suppository was administered. Blood pressure, heart rate, respiratory rate, analgesia score, and sedation score were monitored for 12 hr after surgery. Amnesia and frequency of the administration of indomethacin suppository were also noted. Blood pressure, heart rate and respiratory rate showed no differences among the groups. Greater sedation was seen in Groups M10 and M20 compared with Group C during first 120 min (P < 0.05). The number of patients with memory was larger in Group C (18) than in Group M10 (10, P = 0.006) and Group M20 (6, P < 0.001). Better analgesia was obtained in patients receiving midazolam than in Group C (P < 0.05). The frequency of the indomethacin administration was 2.0 +/- 1.1 (SD) in Group C, which was larger than in Group M10 (1.1 +/- 0.9, P = 0.035) and Group M20 (1.2 +/- 0.7, P = 0.039).\n\nQuestion:\nDoes midazolam improve postoperative epidural analgesia with continuous infusion of local anaesthetics?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSoybean [Glycine max (L.) Merr.] is one of the most important crops for oil and protein resource. Improvement of stress tolerance will be beneficial for soybean seed production. Six GmPHD genes encoding Alfin1-type PHD finger protein were identified and their expressions differentially responded to drought, salt, cold and ABA treatments. The six GmPHDs were nuclear proteins and showed ability to bind the cis-element \"GTGGAG\". The N-terminal domain of GmPHD played a major role in DNA binding. Using a protoplast assay system, we find that GmPHD1 to GmPHD5 had transcriptional suppression activity whereas GmPHD6 did not have. In yeast assay, the GmPHD6 can form homodimer and heterodimer with the other GmPHDs except GmPHD2. The N-terminal plus the variable regions but not the PHD-finger is required for the dimerization. Transgenic Arabidopsis plants overexpressing the GmPHD2 showed salt tolerance when compared with the wild type plants. This tolerance was likely achieved by diminishing the oxidative stress through regulation of downstream genes.\n\nQuestion:\nDo soybean GmPHD-type transcription regulators improve stress tolerance in transgenic Arabidopsis plants?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis study sought to determine the association of high ankle brachial index (ABI) measurements with left ventricular (LV) mass, and to compare its strength with that of low ABI with LV mass. Arterial stiffness leads to LV mass through nonatherosclerotic pathways in mice. In humans, a high ABI indicates stiff peripheral arteries and is associated with cardiovascular disease (CVD) events. Whether high ABI is associated with LV mass in humans and whether this might reflect consequences of arterial stiffness, atherosclerosis, or both is unknown. Among 4,972 MESA (Multi-Ethnic Study of Atherosclerosis) participants without clinical CVD, we used linear regression to evaluate the association of low (<0.90) and high (>1.40 or incompressible) ABI with LV mass by cardiac magnetic resonance imaging (MRI). Intermediate ABIs served as the reference category. To determine the effect of subclinical atherosclerosis, models were adjusted for common and internal carotid intima media thickness (cIMT) and natural log-transformed coronary artery calcification. Compared with subjects with intermediate ABI, LV mass was higher with either low (2.70 g/m(2) higher, 95% confidence interval: 0.65 to 4.75) or high ABI (6.84 g/m(2) higher, 95% confidence interval: 3.2 to 10.47) after adjustment for traditional CVD risk factors, kidney function, and C-reactive protein. However, further adjustment for cIMT and CAC substantially attenuated the association of low ABI with LV mass index (1.24 g/m(2) higher, 95% confidence interval: -0.84 to 3.33), whereas the association of high ABI was minimally altered (6.01 g/m(2) higher, 95% confidence interval: 2.36 to 9.67).\n\nQuestion:\nIs a high ankle brachial index associated with greater left ventricular mass MESA ( Multi-Ethnic Study of Atherosclerosis )?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nRadiotherapy can induce severe skin responses that may limit the clinically acceptable radiation dose. The responses include erythema, dry and moist desquamation, erosions and dermal-epidermal blister formation. These effects reflect injury to, and reproductive failure of, epidermal cells and may also be due to dysregulation of the tissue remodelling process caused by excessive proteolytic activity. Calcitriol, the hormonally active vitamin D metabolite, protects keratinocytes from programmed cell death induced by various noxious stimuli. To examine whether calcitriol protects proliferating keratinocytes from the damage inflicted by ionizing radiation under conditions similar to those employed during radiotherapy. Autonomously proliferating HaCaT keratinocytes, used as a model for basal layer keratinocytes, were irradiated using a linear accelerator. Cell death was monitored by vital staining, executioner caspase activation, lactic dehydrogenase release and colony formation assay. Induction of matrix metalloproteinase-9 was assessed by gelatinase activity assay and mRNA determination. Levels of specific proteins were determined by immunoblotting. Treatment with calcitriol inhibited both caspase-dependent and -independent programmed cell death occurring within 48 h of irradiation and increased the colony formation capacity of irradiated cells. These effects may be attributable to inhibition of the c-Jun NH(2)-terminal kinase cascade and to upregulation of the truncated antiapoptotic isoform of p63. Treatment with the hormone also attenuated radiation-induced increase in matrix metalloproteinase-9 protein and mRNA levels.\n\nQuestion:\nDoes vitamin D protect keratinocytes from deleterious effects of ionizing radiation?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHigh sensitivity C-reactive protein (hsCRP) is more sensitive than standard C-reactive protein (CRP) assay in evaluating the risk of coronary heart disease and other atherosclerotic events. By this time, there are several reports that type 2 diabetic subjects have higher serum levels of hsCRP than those of non-diabetic subjects. However, there are few reports about factors which have influence upon the level of serum hsCRP in type 2 diabetic subjects. We had evaluated the association of serum hsCRP level with risk factors of cardiovascular diseases and carotid intima-media thickness (IMT) in type 2 diabetic subjects. One hundred and five patients (59 men and 46 women) with type 2 diabetes were recruited. Subjects with severe cardiovascular diseases were excluded. All subjects were undergone carotid ultrasonography for evaluation of carotid IMT. Serum hsCRP concentrations were measured. Serum hsCRP level was correlated with mean left IMT (r = 0.366, P = 0.003), maximal left IMT (r = 0.370, P = 0.002), mean right IMT (r = 0.281, P = 0.023) and maximal right IMT (r = 0.370, P = 0.002), body mass index (r = 0.377, P < 0.001), waist circumference (r = 0.342, P < 0.001), waist-hip ratio (r = 0.229, P = 0.020), serum total cholesterol (r = 0.202, P = 0.024), serum triglyceride (r = 0.292, P = 0.022) and serum low-density lipoprotein (r = 0.133, P = 0.044).\n\nQuestion:\nIs serum high sensitivity C-reactive protein associated with carotid intima-media thickness in type 2 diabetes?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo establish a journal club for librarians, which aimed to develop appraisal skills and assist in the application of research to practice. Fourteen health librarians were invited to attend a journal club. Each month a librarian was responsible for preparing a scenario, choosing a research paper, and selecting a checklist. The paper was appraised by the club, and a critically appraised topic (CAT) prepared. Six months later, a questionnaire was sent to all librarians. Six out of 14 librarians attended the journal club and five out of six returned the questionnaire. All five agreed that attending the journal club helped them develop appraisal skills, write a CAT and be more critical of research. Four agreed they always identified a research paper first, then formulated a question. One librarian agreed that applying results to their own practice was difficult, one disagreed and three were neutral.\n\nQuestion:\nIs a journal club an effective tool for assisting librarians in the practice of evidence-based librarianship : a case study?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nBreast cancer is highly resistant to chemotherapeutic approach and hence, alternative strategies have been developed to fight against this heterogeneous group of disease. In particular, many studies have demonstrated about various drugs for the treatment of breast cancer. In our study, we assessed the anti-angiogenenic activities of Bisindole-PBD (5b) in MCF-7 and MDA-MB-231 cell lines. In vitro Endothelial Cell (HUVEC) Tube Formation Assay was performed to show inhibitory role of 5b along with its role upon wound healing process in breast cancer cells in vitro. Semi-quantitative reverse transcription PCR (RT-PCR) was also done to examine the expression of VEGF in response to 5b in breast cancer cells and in HUVEC cells. siRNA transfection study explored STAT3 mediated VEGF transcription in breast cancer cells MCF-7 and MDA-MB-231. CAM assay was performed to see the role of 5b on vessel formation in chicken embryo. From in vitro data we have demonstrated that 5b played a role in regulation of breast cancer cell proliferation by inhibiting angiogenesis. Test drug 5b suppressed the expression VEGF at both transcriptional and post transcriptional levels. Apart from this, there was significant down regulation in STAT3 level after drug treatment, which was found to be involved in the VEGF transcription. Metastasis related MMP-2 and MMP-9 expressions were also modulated by 5b. In vivo study by Chick Chorioallantoic Membrane (CAM) Assay also showed anti-angiogenesis role of the test drug which was consistent with the in vitro data.\n\nQuestion:\nDoes a novel bisindole-PBD conjugate inhibit angiogenesis by regulating STAT3 and VEGF in breast cancer cells?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThromboxane A2 (TXA2) is a positive feedback lipid mediator that is generated upon stimulation of platelets with various agonists. Aspirin works as an antithrombotic drug by blocking the generation of TXA2. The aim of this study was to evaluate the role of the purinergic P2Y receptors in thrombin-induced TXA2 generation. PAR1-activating peptide (SFLLRN), PAR4-activating peptide (AYPGKF), and thrombin, induced the activation of cytosolic phospholipase A2 (cPLA2), release of arachidonic acid (AA) from membrane-bound phospholipids, and subsequent TXA2 generation in human platelets. The actions of these agonists were significantly inhibited in the presence of the P2Y12 receptor antagonist, AR-C69931MX, but not the P2Y1 receptor antagonist, MRS2179. In addition, AYPGKF- and thrombin-induced TXA2 generation was significantly reduced in platelets from mice dosed with clopidogrel, confirming the results obtained with the human platelets. Also, Pearl mouse platelets that lack releasable nucleotides generated significantly less TXA2 when compared with the wild-type littermates in response to PAR stimulation. Inhibition of extracellular signal-regulated protein kinase 1/2 (Erk 1/2) activation using U0126, an inhibitor of MAP kinase kinase (MEK), suppressed PAR-mediated cPLA2 phosphorylation and TXA2 generation. Further, platelets that were pretreated with AR-C69931MX, as well as Pearl mouse platelets, displayed the reduced levels of Erk1/2 phosphorylation upon stimulation with the PAR agonists.\n\nQuestion:\nDoes p2Y12 receptor-mediated potentiation of thrombin-induced thromboxane A2 generation in platelets occur through regulation of Erk1/2 activation?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe aortic valve interstitial cell (AVIC) has been implicated in the pathogenesis of aortic stenosis. In response to proinflammatory stimulation, the AVIC undergoes a phenotypic change from that of a myofibroblast phenotype to that of osteoblast-like cell. Matrix Gla-protein (MGP) has been identified as an important inhibitor of vascular calcification. We therefore hypothesized that MGP expression is reduced in diseased AVICs, and loss of this protective protein contributes to calcification of the aortic valve. Our purpose was to compare MGP expression in normal versus diseased AVICs. Human AVICs were isolated from normal aortic valves from explanted hearts (n = 6) at the time of heart transplantation. AVICs were also isolated from calcified, diseased valves of patients (n = 6) undergoing aortic valve replacement. AVICs were grown in culture until they reached passages 2-6 before experimentation. Immunofluorescent staining, reverse transcriptase-polymerase chain reaction, immunoblotting, and enzyme-linked immunosorbent assay were used to compare levels of MGP in normal and diseased AVICs. Statistics were performed using the Mann-Whitney U test (P < 0.05). MGP expression was significantly decreased in diseased AVICs relative to normal AVICs by immunofluorescent staining, reverse transcriptase-polymerase chain reaction, immunoblotting, and enzyme-linked immunosorbent assay.\n\nQuestion:\nDoes matrix Gla protein regulate calcification of the aortic valve?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe relationship between smoking and pancreatic cancer biology, particularly in the context of the heterogeneous microenvironment, remains incompletely defined. We hypothesized that nicotine exposure would lead to the augmentation of paracrine growth factor signaling between tumor-associated stroma (TAS) and pancreatic cancer cells, ultimately resulting in accelerated tumor growth and metastasis. The effect of tobacco use on overall survival was analyzed using a prospectively maintained database of surgically resected patients with pancreatic cancer. Nicotine exposure was evaluated in vitro using primary patient-derived TAS and pancreatic cancer cells independently and in coculture. Nicotine administration was then assessed in vivo using a patient-derived pancreatic cancer xenograft model. Continued smoking was associated with reduced overall survival after surgical resection. In culture, nicotine-stimulated hepatocyte growth factor (HGF) secretion in primary patient-derived TAS and nicotine stimulation was required for persistent pancreatic cancer cell c-Met activation in a coculture model. c-Met activation in this manner led to the induction of inhibitor of differentiation-1 (Id1) in pancreatic cancer cells, previously established as a mediator of growth, invasion and chemoresistance. HGF-induced Id1 expression was abrogated by both epigenetic and pharmacologic c-Met inhibition. In patient-derived pancreatic cancer xenografts, nicotine treatment augmented tumor growth and metastasis; tumor lysates from nicotine-treated mice demonstrated elevated HGF expression by qRT-PCR and phospho-Met levels by ELISA. Similarly, elevated levels of phospho-Met in surgically resected pancreatic cancer specimens correlated with reduced overall survival.\n\nQuestion:\nDoes nicotine reduce Survival via Augmentation of Paracrine HGF-MET Signaling in the Pancreatic Cancer Microenvironment?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCurrent contact lenses (CLs) when worn on an extended wear basis cause corneal epithelial alterations. The aim of this study was to evaluate changes in corneal epithelial cell morphology and physiology following short term (3 months) wear of highly oxygen permeable CLs and to compare this with disposable CLs. Subjects were wearers of highly oxygen permeable CLs (n=11, wearing CLs on a 30 night schedule), disposable CL users (n=6, wearing CLs on a 6 night schedule), and non-CL wearers (n=20). Mean CL wear experience was 3 months. Epithelial cells were harvested using corneal cytology and were stained using acridine orange and ethidium bromide. Epithelial cell size and viability were determined. The majority of epithelial cells recovered were non-viable (71%), and the mean longest cell diameter was 38 (SD 8) microm. Disposable CLs caused an increase in cell size (42 (7) microm) compared with both non-wear (39 (7) microm, p=0.01) and wear of highly oxygen permeable CLs (37 (10) microm, p=0.0049). There was no difference in cell viability between groups.\n\nQuestion:\nDoes short term wear of high Dk soft contact lenses alter corneal epithelial cell size or viability?\n\nAnswer:",
"role": "user"
},
{
"content": "no",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe pine wood nematode (PWN), Bursaphlenchus xylophilus, which collaborates with its associated bacteria to form ecosystem and has interaction among them, is the pathogen of pine wilt disease. This study focused on revealing the bacterial diversity of ecosystem of pine wood nematode and its associated bacteria. The metagenome of ecosystem of bacteria associated with the PWN was analyzed by 16S rRNA gene library and 454 sequencing. The results showed that 25 OTUs (Operational Taxonomic Units) were obtained from the library according to sequences similarity of 97%, which affiliated to Alphaproteobacteria, Betaproteobacteria, Gammaproteobacteria and Bacteroidetes. The dominant bacteria were belonged to Gammaproteobacteria, especially Stenotrophomonas maltophilia in this class dominated the library. In terms of dominant bacteria, the results revealed by metagenome were similar to that of 16S rRNA gene library.\n\nQuestion:\nDo [ Diversity of bacteria associated with pine wood nematode revealed by metagenome ]?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nDecreased ankle mobility is associated with delayed healing of venous ulcers. The aim of this study was to assess the efficacy of a 24-week home-based exercise programme in increasing ankle range of motion and increasing the strength and endurance of the calf muscle. The secondary aim was to see whether subjects with venous ulcers were able to maintain a consistent exercise programme. Eleven patients with long-standing venous ulcers were encouraged to undertake a thrice-weekly 5-10 min ankle exercise programme using elastic resistance bands and stretching in a 24-week single-arm pilot study. Ankle range of motion was measured monthly using a bi-plane ankle goniometer. Pain scores and participation levels were also recorded. There were significant improvements in ankle range of motion achieved at 12 and 24 weeks. Median pain scores (scale of 1-10) were reduced from 5.2 at baseline to 2.0 at weeks 12 and 24.\n\nQuestion:\nDoes a home-based exercise programme improve ankle range of motion in long-term venous ulcer patients?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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