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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:\nIn Brugada syndrome, ventricular fibrillation (VF) occurs mainly during sleep, and Brugada ECG signs are intensified by parasympathomimetic drugs; therefore, vagal activity could be a precipitating factor of VF. The aim of the present study was to elucidate the relation between spontaneous augmentation of ST elevation and changes in autonomic nervous activities in the daily life of patients with Brugada syndrome. Twenty-three consecutive patients with Brugada syndrome were studied. Group VF(+) consisted of 7 symptomatic patients and 3 asymptomatic patients with inducible VF; group VF(-) consisted of 13 asymptomatic patients without documented or inducible VF. Two-channel unipolar lead (V(1) and V(2)) Holter ECG was recorded. Heart rate variability was analyzed by the maximum entropy method. Spontaneous augmentation of ST elevation (>/=1.5 mm/20 min) occurred more frequently during 24 hours in group VF(+) than in group VF(-) (5.7 +/- 2.5 times vs 2.3 +/- 2.4 times, P < 0.01). ST elevation was significantly greater in group VF(+) than in group VF(-) (2.1 +/- 0.2 mm vs 1.8 +/- 0.2 mm, P < 0.05). Power of the high-frequency component (HF: 0.15-0.4 Hz) and RR interval increased progressively, and the ratio of low-frequency component (LF; 0.04- 0.15 Hz) to high-frequency component (LF/HF) gradually decreased toward the time of maximum ST elevation. During an entire day, daytime (0-5 P.M.), and nighttime (0-5 A.M.), both HF and LF/HF were not different between groups VF(+) and VF(-).\n\nQuestion:\nDoes vagal activity modulate spontaneous augmentation of ST elevation in the daily life of patients with Brugada syndrome?\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:\nProgesterone receptor (PR) expression assessment in early invasive breast cancer remains controversial. This study sought to re-evaluate PR expression as a potential therapeutic guide in early breast cancer; particularly in oestrogen receptor (ER)-positive, lymph node (LN)-negative disease. A population cohort of 1074 patients presenting to a single Cancer Centre over 4 years (2000-2004) underwent surgery for primary invasive breast cancer with curative intent. Prospective data collection included patient demographics, pathology, ER and PR expression, HER2 status, adjuvant chemotherapy and endocrine therapy. Progesterone receptor expression was compared with (all causes) overall survival (OS), breast cancer-specific survival (BCSS) and disease-free survival (DFS). Overall survival was 71.0% and BCSS was 83.0% at median follow-up of 8.34 years. Absent PR expression was significantly associated with poorer prognosis for OS, BCSS and DFS (P<0.0001, log-rank), even within the ER-positive, LN-negative group (hazard ratio for BCSS 3.17, 95% CI 1.43-7.01) and was not influenced by endocrine therapy. Cox's regression analysis demonstrated that PR expression was an independent prognostic variable.\n\nQuestion:\nIs progesterone receptor expression an independent prognostic variable in early breast cancer : a population-based study?\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:\nIn a prospective observational study, we investigated whether patients with active systemic lupus erythematosus (SLE) had higher indices of endothelial damage and dysfunction than healthy controls and whether improved disease control was associated with improvement in these indices. Twenty-seven patients with active SLE (four or more American College of Rheumatology (ACR) criteria) and 22 age-matched controls were assessed. Endothelial microparticles (EMPs; CD31+/annexin V+/CD42b-) were quantified using flow cytometry. Brachial artery flow-mediated dilatation (FMD) was measured using automated edge-tracking software. Twenty-two patients had a second assessment at a median (IQR) of 20 (16, 22) weeks after initiating new immunosuppressive therapy. SLE patients had a median (IQR) baseline global British Isles Lupus Assessment Group Disease Activity Index (BILAG-2004) score of 14 (12, 22). CD31+/annexin V+/CD42b- EMPs were higher (157 548/ml (59 906, 272 643) vs 41 025(30 179, 98 082); p=0.003) and endothelial-dependent FMD was lower (1.63% (-1.22, 5.32) vs 5.40% (3.02, 8.57); p=0.05) in SLE patients than controls. CD31+/annexin V+/CD42b- EMPs correlated inversely with FMD (%) (r(2) -0.40; p=0.006). At follow-up, the median (IQR) change in global BILAG-2004 score was -11 (-18, -3). CD31+/annexin V+/CD42b- EMP levels were reduced (166 982/ml (59 906, 278 775 vs 55 655(29 475, 188 659; p=0.02) and FMD had improved (0.33% (-2.31, 4.1) vs 3.19% (0.98, 5.09); p=0.1) at the second visit.\n\nQuestion:\nDoes suppression of inflammation reduce endothelial microparticles in active systemic lupus erythematosus?\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:\nEndoscopic retrograde cholangiopancreatography (ERCP) performed on the weekend requires significant effort from the endoscopist, nursing staff, and anesthesia services. These factors often result in delaying the procedure until the following Monday. No data exist on whether performing weekend ERCP reduces length of stay (LOS) and total cost to justify the additional physician and nursing burden. In this single tertiary academic center, institutional review board-approved study, we retrospectively reviewed all hospitalized patients in whom an ERCP had been completed from May 2010 to September 2011. Demographic and clinical information, procedure details as well as total hospitalization charges (USD) were compared between patients who had an ERCP either on the weekend or weekday holiday (WE ERCP) or Monday (MON ERCP). Statistical comparisons were made using χ(2) and Fischer's exact test. A logistic regression model adjusted for propensity scores (PSs) was used to estimate the risk in prolonged LOS and high total charges associated with WE ERCPs vs. MON ERCPs. A total of 1,114 ERCP's were performed during the time period, 123 of which met inclusion criteria (52 WE, 71 MON). Mean patient age was 56.3±16.7 years (54.5% female, 60.2% Caucasian). There were no significant demographic differences between the two groups. The most common procedure indications were choledocholithiasis (34.9%) and elevated liver enzymes after liver transplantation (25.2%). The analysis showed a significantly decreased LOS (P=0.010) and a trend towards decreased cost (P=0.050) associated with WE ERCP. In the multivariate analysis adjusted for PS, WE ERCP had a significantly decreased odds ratio of LOS>3 days (odds ratio: 0.37 (0.16-0.85); P=0.019).\n\nQuestion:\nIs inpatient weekend ERCP associated with a reduction in patient length of stay?\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:\nCarbohydrate malabsorption causes more symptoms in patients with functional gastrointestinal disorders than in healthy individuals. The purpose of this study was to investigate whether this could be explained by differences in ileal brake hormone secretion. Eighteen consecutive patients with functional abdominal complaints, referred to our clinic for investigation of self-reported food hypersensitivity, were included in the study and compared with 15 healthy volunteers. All subjects ingested a mixture of 25 g fructose and 5 g sorbitol. Pulmonary hydrogen and methane excretion and plasma glucagon-like peptide 1 (GLP-1) and peptide YY (PYY) levels were measured during the next 3 h. Both habitual and post-test symptoms were assessed. Malabsorption of fructose and sorbitol was present in 61% of the patients and 73% of the controls. Nevertheless, the patients experienced significantly more symptoms following carbohydrate challenge, and 78% of the patients claimed that the challenge replicated their habitual gastrointestinal complaints. No significant differences in gas excretion or GLP-1 and PYY levels were found between patients and controls or between symptomatic and asymptomatic carbohydrate malabsorbers. A weak correlation between hydrogen excretion and PYY levels was demonstrated in non-producers of methane.\n\nQuestion:\nAre plasma glucagon-like peptide 1 and peptide YY levels altered in symptomatic fructose-sorbitol malabsorption?\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:\nNonalcoholic fatty liver disease (NAFLD) is closely associated with the metabolic syndrome. We evaluated the association among the metabolic syndrome, visceral fat accumulation, and the severity of fatty liver with a new scoring system of ultrasonographic findings in apparently healthy Japanese adults. Subjects consisted of 94 patients who received liver biopsy and 4,826 participants who were selected from the general population. Two hepatologists scored the ultrasonographic findings from 0 to 6 points. We calculated Cohen's kappa of within-observer reliability and between-observer reliability. We evaluated the predictive value of the score by the area under a conventional receiver operating characteristic curve (AUC). Within-observer reliability was 0.95 (95% CI 0.93-0.97, P<0.001) and between-observer reliability was 0.95 (95% CI 0.93-0.97, P<0.001). The AUC to diagnose NAFLD was 0.980. The sensitivity was 91.7% (95% CI 87.0-95.1, P<0.001) and the specificity was 100% (95% CI 95.4-100.0, P<0.001). The AUC to diagnose visceral obesity was 0.821. The sensitivity was 68.3% (95% CI 51.9-81.9, P=0.028) and the specificity was 95.1% (95% CI 86.3-99.0, P<0.001). Adjusted odds ratio of the score for the metabolic syndrome was 1.37 (95% CI 1.26-1.49, P<0.001).\n\nQuestion:\nDoes the severity of ultrasonographic findings in nonalcoholic fatty liver disease reflect the metabolic syndrome and visceral fat accumulation?\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:\nOsteosarcoma is the main malignant primary bone tumor in children and adolescents for whom the prognosis remains poor, especially when metastasis is present at diagnosis. Because transforming growth factor-β (TGFβ) has been shown to promote metastasis in many solid tumors, we investigated the effect of the natural TGFβ/Smad signaling inhibitor Smad7 and the TβRI inhibitor SD-208 on osteosarcoma behavior. By using a mouse model of osteosarcoma induced by paratibial injection of cells, we assessed the impact of Smad7 overexpression or SD-208 on tumor growth, tumor microenvironment, bone remodeling, and metastasis development. First, we demonstrated that TGFβ levels are higher in serum samples from patients with osteosarcoma compared with healthy volunteers and that TGFβ/Smad3 signaling pathway is activated in clinical samples. Second, we showed that Smad7 slows the growth of the primary tumor and increases mice survival. We furthermore demonstrated that Smad7 expression does not affect in vitro osteosarcoma cell proliferation but affects the microarchitectural parameters of bone. In addition, Smad7-osteosarcoma bone tumors expressed lower levels of osteolytic factors such as RANKL, suggesting that Smad7 overexpression affects the \"vicious cycle\" established between tumor cells and bone cells by its ability to decrease osteoclast activity. Finally, we showed that Smad7 overexpression in osteosarcoma cells and the treatment of mice with SD208 inhibit the development of lung metastasis.\n\nQuestion:\nDoes overexpression of smad7 block primary tumor growth and lung metastasis development in osteosarcoma?\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:\nOur purpose was to evaluate the mechanisms of cocaine's effect on both spontaneous and agonist-induced contractility of pregnant human myometrium. Myometrium was obtained from 42 women at term who were undergoing cesarean section. Myometrial strips were suspended in contraction baths and isometric contractions were measured. Tissue was exposed to various combinations of cocaine, prazosin, desipramine, benzoylecgonine, and procaine. Spontaneous contractility and the contractile responses to increasing concentrations of methoxamine and oxytocin were measured and compared. Cocaine increased spontaneous myometrial contractility by more than threefold. Prazosin, an alpha-adrenergic antagonist, blocked this effect only for the first 35 minutes of exposure. The cumulative concentration-response to the alpha-adrenergic agonist methoxamine was increased by cocaine in terms of both sensitivity and maximal response. The maximal response to oxytocin, but not the sensitivity, was increased by cocaine by an effect that could not be blocked by prazosin.\n\nQuestion:\nDoes cocaine augment contractility of the pregnant human uterus by both adrenergic and nonadrenergic mechanisms?\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 investigate whether corneal stiffness affects the elevation of intraocular pressure after an acute increase in the volume of ocular fluid. Saline (200 microL total) was infused into porcine globes before and after corneal stiffening. Intraocular pressure (IOP) was continuously monitored by a pressure sensor that was cannulated to the vitreous chamber. Corneal stiffening was achieved by immersing the corneas in a 1% or 4% glutaraldehyde solution for 20 minutes. Corneal strips were dissected from the globes, and the stress-strain relationships were measured. The mean secant modulus of each group of corneas at 5% strain was calculated. Control eyes with no corneal stiffening were also tested. A significantly higher IOP elevation was observed in the globes after the corneas were stiffened (mean +/- SD, 14.9 +/- 1.9 mm Hg before stiffening vs. 19.1 +/- 2.6 mm Hg after 1% glutaraldehyde treatment and 24.3 +/- 1.9 mm Hg after 4% glutaraldehyde treatment at 200 microL infusion; P < 0.001). The control group showed no change in IOP elevation. The 5% secant modulus was 0.46 +/- 0.24 MPa, 1.63 +/- 0.41 MPa, and 2.78 +/- 1.04 MPa (mean +/- SD), respectively for the original corneal tissue and tissue with 1% or 4% glutaraldehyde treatment.\n\nQuestion:\nDoes corneal stiffness affect IOP elevation during rapid volume change in the eye?\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:\n(1) To determine chronic illness costs for large cohort of primary care patients, (2) to develop prospective model predicting total costs over one year, using demographic and clinical information including widely used comorbidity index. Data including diagnostic, medication, and resource utilization were obtained for 5,861 patients from practice-based computer system over a 1-year period beginning December 1, 1993, for retrospective analysis. Hospital cost data were obtained from hospital cost accounting system. Average annual per patient cost was $2,655. Older patients and those with Medicare or Medicaid had higher costs. Hospital costs were $1,558, accounting for 58.7% of total costs. In the predictive model, individuals with higher comorbidity incurred exponentially higher annual costs, from $4,317 with comorbidity score of two, to $5,986 with score of three, to $13,326 with scores greater than seven. To use an adapted comorbidity index to predict total yearly costs, four conditions should be added to the index: hypertension, depression, and use of warfarin with a weight of one, skin ulcers/cellulitis, a weight of two.\n\nQuestion:\nIs the Charlson comorbidity index adapted to predict costs of chronic disease in primary care 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:\nC-reactive protein (CRP) is a sensitive marker of inflammation that has been linked with prognosis in various solid tumours. In the present study, we analysed the prognostic relevance of elevated plasma CRP levels in prostate cancer patients treated with radiotherapy. A total of 261 prostate cancer patients treated with 3D-conformal radiotherapy were evaluated retrospectively. Cancer specific survival (CSS), overall survival (OS) and clinical disease-free survival (DFS) were assessed using Kaplan-Meier analysis. To evaluate the independent prognostic significance of CRP plasma levels, multivariate Cox regression models were applied. The median follow-time was 80months. Applying receiver operating characteristics (ROC) analysis, the optimal cut-off level for the plasma CRP was 8.6mgl(-1). An elevated CRP level was associated with decreased CSS in univariate (hazard ratio (HR) 3.36, 95% confidence interval (CI) 1.42-7.91; p=0.006) and multivariate analysis (HR 4.31, 95% CI 1.22-15.1; p=0.023). Furthermore, a significant association with OS was detected in univariate (HR 2.69, 95% CI 1.57-4.59; p<0.001) and multivariate analyses (HR 3.24, 95% CI 1.84-5.71, p<0.001). Multivariate analysis also showed a significant association between plasma CRP and clinical DFS (HR 2.07, 95% CI 1.02-4.17; p=0.043).\n\nQuestion:\nIs the elevated C-reactive protein level associated with poor prognosis in prostate cancer patients treated with radiotherapy?\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:\nCyclic adenosine monophosphate (cAMP) is an important regulator of neuronal excitability. The effects of barbiturates on cAMP production in intact neurons are not known. This study used cultures of cortical neurons, cultures of glia, and slices of cerebral cortex from the rat to study the effects of barbiturates on cAMP regulation in the brain. Primary cultures of cortical neurons or glia were prepared from 17-day gestational Sprague-Dawley rat fetuses and were used after 12-16 days in culture. Cross-cut slices (300 microns) were prepared from cerebral cortex of adult rats. Cyclic AMP accumulation was determined by measuring the conversion of [3H]adenosine triphosphate (ATP) to [3H]cAMP in cells preloaded with [3H]adenine. Pentobarbital enhanced isoproterenol- and forskolin-stimulated, but not basal, cAMP accumulation in cultures of cerebral neurons. Cyclic AMP production was enhanced by pentobarbital in a dose-dependent fashion up to a concentration of 250 microM; This concentration of pentobarbital increased cAMP production by 40-50% relative to that in controls without pentobarbital. At 500 microM pentobarbital, the magnitude of the enhancement was less. Pentobarbital had no effect on isoproterenol-stimulated cAMP production in cultures containing only glia. Pentobarbital also enhanced isoproterenol-stimulated, but not basal, cAMP production in slices of cerebral cortex by approximately 30% at concentrations of 62.5-250 microM and by almost 100% at 500 microM.\n\nQuestion:\nDoes pentobarbital enhance cyclic adenosine monophosphate production in the brain by effects on neurons but not glia?\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:\nThis article will describe the impact of prehospital electrocardiogram (ECG) use on emergency department (ED) processes of care for non-ST-segment elevation myocardial infarction (NSTEMI) patients and assess the characteristics associated with prehospital ECG use. This is a retrospective, multicenter, observational analysis of NSTEMI patients captured by the National Cardiovascular Data Registry-Acute Coronary Treatment and Intervention Outcomes Network Registry-Get with the Guidelines (NCDR ACTION-GWTG) in 2007. Patient and hospital data were stratified by documentation of a prehospital ECG (pECG). Hospitals were stratified into tertiles of pECG use by higher pECG (>5.6%, n 91), lower pECG (< or = 5.6%, n = 83), or no pECG (n = 100). Statistical evaluation was done via Wilcoxon rank sum and chi(2) tests. There were 21 251 patients eligible for analysis. A pECG was documented in 1609 (7.6%) patients. Of 274 hospitals, 100 (36.5%) had no pECGs recorded. Median ED length of stay (LOS) was shorter at no pECG hospitals vs lower pECG hospitals (3.97 h vs 4.12 h, P < 0.05), but not higher pECG hospitals vs no pECG hospitals (3.85 h vs 3.97 h, P = not significant [NS]). A pECG was not associated with an improvement in ED performance metrics (use of aspirin, beta-blocker, any heparin) in the higher pECG hospitals vs no pECG hospitals or the lower pECG hospitals vs no pECG hospitals.\n\nQuestion:\nDo prehospital electrocardiograms ( ECGs ) improve the process of emergency department care in hospitals with higher usage of ECGs in non-ST-segment elevation myocardial infarction 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:\nWith the introduction of a self-expanding, memory-containing, circular hernia patch, surgeons have been enthusiastic about its use to repair ventral hernias smaller than 3 cm in diameter. The aim of this study was to evaluate the efficiency, reliability, and safety of the device laparoscopically with respect to adequate deployment of the patch. During 1 year all patients with small ventral hernias were treated with this memory-containing patch and were inspected by laparoscopy. Just prior to insertion of the patch, remaining adhesions on top of the peritoneum were analyzed, as was the interference of the umbilical ligament. The final position of the patch was monitored, identifying the cupping phenomenon, exposure of the polypropylene to the viscera, and the amount of tension on the straps. All patients were followed for 2 years and postoperative complications and recurrence rate were monitored. Twenty-eight patients were operated on for repair of a small ventral hernia with laparoscopic control. Adhesions, not digitally palpable, that interfered with adequate patch deployment were observed in more than 80% of the cases. After a median follow-up of 25 months a 14.8% recurrence rate was observed.\n\nQuestion:\nDoes laparoscopic evaluation show deficiencies in memory ring deployment during small ventral hernia repair?\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:\nWomen with polycystic ovary syndrome (PCOS) are prone for coronary artery disease (CAD), and hyperhomocysteinemia is an independent risk factor for CAD. MTHFR deficiency is the most common cause of hyperhomocysteinemia, thereby provoking a possible association between PCOS and MTHFR C677T polymorphism. The aim of this study was to investigate an association of MTHFR C677T polymorphism with PCOS. 92 women with PCOS (Rotterdam criteria) and 95 age-matched controls were compared with respect to MTHFR C677T polymorphism. The 2 genotypes (CC and CT) obtained were compared with clinical and laboratory parameters in women with PCOS. In a case-control study, clinical, biochemical, hormonal and genetic analysis (PCR-RFLP of peripheral leucocytes) was carried out on all women with PCOS as well as controls. Student \"t\" test for quantitative and Chi-square test for nominal variables was used. For estimation of risk, odds ratio and 95% confidence interval were calculated. The odds ratio of bearing a heterozygous genotype (CT) was 1.32 in women with PCOS as compared to controls (P = 0.48). No homozygous mutation (TT) was found in the study population. Serum cholesterol was more in heterozygous (CT) genotype (215.48 ± 25.56 mg/dl) as compared to normal (CC) genotype (203.29 ± 16.35 mg/dl) in women with PCOS (P = 0.01). Similarly, serum triglyceride was more in heterozygous (CT) genotype (95.86 ± 37.34 mg/dl) as compared to normal (CC) genotype (82.36 ± 20.88 mg/dl) in women with PCOS (P = 0.04).\n\nQuestion:\nIs mTHFR C677T polymorphism associated with hyperlipidemia in women with polycystic ovary syndrome?\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:\nPrevious structure-activity relationship studies with analogues of the CB1 receptor antagonist rimonabant have demonstrated that a subset of these analogues with 3-substituent replacements of rimonabant's pyrazole core displayed cannabimimetic profiles seemingly independent of CB1 receptors. We sought to further evaluate these analogues in several behavioural models sensitive to detecting THC-like abuse liability. Selected analogues were tested in a battery of tests in mice to replicate previous findings. Cross-generalization tests were conducted in mice trained to discriminate either THC or O-6629 from vehicle. Rimonabant and its analogues were also evaluated in substitution and challenge tests. Finally, development of cross-tolerance between THC and O-6211 in the mouse test battery was assessed. O-6629 and O-6658 produced dose-dependent acute cannabimimetic activity in mice, but neither substituted for nor antagonized THC's discriminative stimulus. Cross-substitution was observed with O-6658 in mice discriminating O-6629, whereas rimonabant neither substituted for nor attenuated the O-6629 discriminative stimulus. THC and morphine did not generate O-6629-like responding. Cross-tolerance did not develop in mice repeatedly treated with THC when tested with O-6211 in the mouse test battery.\n\nQuestion:\nDo novel 3-substituted rimonabant analogues lack Δ ( 9 ) -tetrahydrocannabinol-like abuse-related behavioural effects in mice?\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:\nHead and neck squamous cell carcinoma (HNSCC) is usually fatal, and innovative approaches targeting growth pathways are necessary to effectively treat this disease. Both the epidermal growth factor receptor (EGFR) and the hepatocyte growth factor (HGF)/c-Met pathways are overexpressed in HNSCC and initiate similar downstream signaling pathways. c-Met may act in consort with EGFR and/or be activated as a compensatory pathway in the presence of EGFR blockade. Expression levels of EGFR and c-Met were determined by Western analysis in HNSCC cell lines and correlated with antitumor responses to inhibitors of these pathways. Combining the c-Met inhibitor PF2341066 with the EGFR inhibitor gefitinib abrogated HNSCC cell proliferation, invasion, and wound healing significantly more than inhibition of each pathway alone in HNSCC cell lines. When both HGF and the EGFR ligand, TGF-α, were present in vitro, P-AKT and P-MAPK expression were maximally inhibited by targeting both EGFR and c-Met pathways, suggesting that c-Met or EGFR can compensate when phosphorylation of the other receptor is inhibited. We also showed that TGF-α can induce phosphorylation of c-Met over sixfold by 8 hours in the absence of HGF, supporting a ligand-independent mechanism. Combined targeting of c-Met and EGFR resulted in an enhanced inhibition of tumor volumes accompanied by a decreased number of proliferating cells and increased apoptosis compared with single agent treatment in vivo.\n\nQuestion:\nDoes dual blockade of EGFR and c-Met abrogate redundant signaling and proliferation in head and neck carcinoma cells?\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:\nActivation of glucagon-like peptide-1 (GLP-1) receptor exerts a range of cardioprotective effects. Geniposide is an agonist of GLP-1 receptor, but its role in cardiac hypertrophy remains completely unknown. Here, we have investigated its protective effects and clarified the underlying molecular mechanisms. The transverse aorta was constricted in C57/B6 mice and then geniposide was given orally for 7 weeks. Morphological changes, echocardiographic parameters, histological analyses and hypertrophic markers were used to evaluate hypertrophy. Geniposide inhibited the hypertrophic response induced by constriction of the transverse aorta or by isoprenaline. Activation of 5'-AMP-activated protein kinase-α (AMPKα) and inhibition of mammalian target of rapamycin, ERK and endoplasmic reticulum stress were observed in hypertrophic hearts that were treated with geniposide. Furthermore, Compound C (CpC) or knock-down of AMPKα restricted protection of geniposide against cell hypertrophy and activation of mammalian target of rapamycin and ERK induced by hypertrophic stimuli. CpC or shAMPKα also abolished the protection of geniposide against endoplasmic reticulum stress induced by thapsigargin or dihtiothreitol. The cardio-protective effects of geniposide were ablated in mice subjected to CpC. GLP-1receptor blockade counteracted the anti-hypertrophic response and activation of AMPKα by geniposide. Knock-down of GLP-1 receptor also offset the inhibitory effects of geniposide on cardiac hypertrophy in vivo.\n\nQuestion:\nDoes protection against cardiac hypertrophy by geniposide involve the GLP-1 receptor / AMPKα signalling pathway?\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:\nRecently, we have shown that intraplaque mast cell numbers are associated with atherosclerotic plaque vulnerability and with future cardiovascular events, which renders inhibition of mast cell activation of interest for future therapeutic interventions. However, the endogenous triggers that activate mast cells during the progression and destabilization of atherosclerotic lesions remain unidentified. Mast cells can be activated by immunoglobulins and in the present study, we aimed to establish whether specific immunoglobulins in plasma of patients scheduled for carotid endarterectomy were related to (activated) intraplaque mast cell numbers and plasma tryptase levels. In addition, the levels were related to other vulnerable plaque characteristics and baseline clinical data. OxLDL-IgG, total IgG and total IgE levels were measured in 135 patients who underwent carotid endarterectomy. No associations were observed between the tested plasma immunoglobulin levels and total mast cell numbers in atherosclerotic plaques. Furthermore, no associations were found between IgG levels and the following plaque characteristics: lipid core size, degree of calcification, number of macrophages or smooth muscle cells, amount of collagen and number of microvessels. Interestingly, statin use was negatively associated with plasma IgE and oxLDL-IgG levels.\n\nQuestion:\nAre circulating immunoglobulins associated with intraplaque mast cell number and other vulnerable plaque characteristics in patients with carotid artery stenosis?\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:\nPrevious animal data suggest that aspiration of activated charcoal is associated with pulmonary microvascular injury that may be related to excessive ventilator-induced airway pressures. The purpose of this study was to test the hypothesis that ventilator-induced airway trauma contributes to the lung vascular injury observed following activated charcoal aspiration. Capillary filtration coefficient (Kf,c), a sensitive measure of lung microvascular permeability, was determined isogravimetrically prior to and after intratracheal instillation of 0.4 ml/kg (12% weight/vol. solution, pH 7.4) activated charcoal oran equal volume of sterile water in isolated, perfused rat lungs in which ventilation was either pressure-controlled at 10cm H2O or volume-controlled at 5 ml/kg. There was significant lung injury in both activated charcoal groups regardless of ventilation method compared to control lungs or lungs administered sterile water (p < 0.05 ANOVA). However, injury to pressure-controlled ventilated lungs was significantly less than lungs ventilated with traditional, volume-controlled ventilation.\n\nQuestion:\nDoes pressure-controlled ventilation attenuate lung microvascular injury in a rat model of activated charcoal aspiration?\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:\nAcitretin has replaced etretinate in the treatment of various disorders of keratinization due to a considerably shorter terminal half-life. Possible esterification of acitretin to etretinate in the presence of ethanol has been reported. To determine the plasma concentrations of etretinate as a metabolite in patients with various disorders of keratinization after multiple acitretin dosing, and to assess the influence of alcohol consumption using a questionnaire. In addition, to study the influence of alcohol consumption on the risk of metabolic formation of etretinate. Eighty-six acitretin (Neotigason(R), Roche)-treated outpatients from three centres provided pre-dose (trough) samples for determining plasma concentrations of acitretin and its metabolites 13-cis-acitretin and etretinate. Patients received acitretin doses of between 0.1 and 1.3 mg kg-1 daily. The concentrations of etretinate, acitretin and 13-cis-acitretin were determined by reverse-phase high-performance liquid chromatography. Of the 86 patients, 30 had detectable plasma etretinate levels. No etretinate was found in 20 patients who reported that they never drank alcohol, while etretinate was found in all 16 patients with an average weekly alcohol consumption of > 200 g ethanol, corresponding to about 15 U (1 U equals half a pint of standard beer or a wine glass of non-fortified wine). Etretinate was detected in 14 of 50 patients with a moderate weekly alcohol intake of up to 200 g ethanol. A trend linking higher alcohol intake with both higher risk of etretinate formation and higher etretinate levels was observed. The study also revealed that the ethylesterification only relates to acitretin (13-trans-) and not to the main metabolite 13-cis-acitretin, although the latter compound showed higher plasma trough concentration levels at steady state.\n\nQuestion:\nIs acitretin converted to etretinate only during concomitant alcohol intake?\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 partial meniscectomy, the remaining meniscus is exposed to an altered loading environment. In vitro 20% dynamic compressive strains on meniscal tissue explants has been shown to lead to an increase in release of glycosaminoglycans from the tissue and increased expression of interleukin-1alpha (IL-1alpha). The goal of this study was to determine if compressive loading which induces endogenously expressed IL-1 results in downstream changes in gene expression of anabolic and catabolic molecules in meniscal tissue, such as MMP expression. Relative changes in gene expression of MMP-1, MMP-3, MMP-9, MMP-13, A Disintegrin and Metalloproteinase with ThromboSpondin 4 (ADAMTS4), ADAMTS5, TNFalpha, TGFbeta, COX-2, Type I collagen (COL-1) and aggrecan and subsequent changes in the concentration of prostaglandin E(2) released by meniscal tissue in response to varying levels of dynamic compression (0%, 10%, and 20%) were measured. Porcine meniscal explants were dynamically compressed for 2h at 1Hz. 20% dynamic compressive strains upregulated MMP-1, MMP-3, MMP-13 and ADAMTS4 compared to no dynamic loading. Aggrecan, COX-2, and ADAMTS5 gene expression were upregulated under 10% strain compared to no dynamic loading while COL-1, TIMP-1, and TGFbeta gene expression were not dependent on the magnitude of loading.\n\nQuestion:\nDoes meniscal tissue explants response depend on level of dynamic compressive strain?\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:\nBiomarkers may be helpful in screening patients with psoriasis for PsA. Our purpose was to identify serum biomarkers for psoriasis and PsA. Fifty-two patients with psoriasis (26 satisfying CASPAR classification criteria for PsA) and 26 healthy controls were recruited for our study. Patients with psoriasis and PsA were group matched for age, sex and psoriasis duration, whereas controls were matched for age and sex. Blood samples were drawn at the time of assessment and serum was analysed for the following: IL-12, IL-12p40, IL-17, TNF super family member 14 (TNFSF14), MMP-3, RANK ligand (RANKL), osteoprotegerin (OPG), cartilage oligomeric matrix protein (COMP), C-propeptide of Type II collagen (CPII), collagen fragment neoepitopes Col2-3/4(long mono) (C2C) and Col2-3/4(short) (C1-2C) and highly sensitive CRP (hsCRP). Data were analysed using logistic regression and receiver operating characteristic curves were plotted. Fifty-two patients with psoriatic disease had a mean age of 46 years and psoriasis duration of 16.8 years. Compared with controls, increased serum levels of RANKL, TNFSF14, MMP-3 and COMP independently associated with psoriatic disease (P < 0.05). Twenty-six PsA patients (mean swollen and/or tender joint count 16, swollen joint count 5) were then compared with 26 patients who had psoriasis alone. Increased levels of hsCRP, OPG, MMP-3 and the CPII : C2C ratio were independently associated with PsA (P < 0.03).\n\nQuestion:\nDo soluble biomarkers differentiate patients with psoriatic arthritis from those with psoriasis without arthritis?\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:\nHLA-G is a major histocompatibility complex (MHC), class Ib molecule that is selectively expressed at the fetal-maternal interface. It is thought to play a role in protecting the fetus from the maternal immune response. Interestingly, the preimplantation embryo development (Ped) gene product Qa-2 is also a mouse MHC class Ib protein that affects cleavage and division of preimplantation mouse embryos and subsequent embryonic survival. Data from many human in vitro fertilization (IVF) clinics suggest that the mouse Ped phenomenon also exists in human because embryos fertilized at the same time have different cleavage rates and consequently different IVF outcomes. As HLA-G is expressed in human early embryos, it is highly regarded as the functional homologue of Qa-2. Whether HLA-G expression is correlated with the cleavage rate of human embryos has great potential clinical value. In this study, 45 human early abnormal fertilized embryos (3 PN) from patients undergoing in vitro fertilization were used to test the effects of HLA-G knock-down via infection with adenovirus carrying its specific siRNA on the cleavage rate in a 2-day culture period. One-way ANOVA, Post hoc and Chi-square were used to compare groups. A p-value smaller than 0.05 was considered statistically significant. Knocking-down HLA-G in human pre-implantation stage embryos resulted in a higher cell arrest rate and a slower cleavage rate.\n\nQuestion:\nDoes down-regulation of HLA-G attenuate Cleavage Rate in Human Triploid Embryos?\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 influence of anisoosmolarity on the activation of the extracellular signal-regulated kinases-1 and -2 and on interleukin-6 release was studied in lipopolysaccharide-stimulated rat liver macrophages. Experiments were performed with rat liver macrophages. Activation of the extracellular signal-regulated kinases was determined by kinase shift assay and immune complex kinase assay. Interleukin-6 mRNA was measured by Northern blot analysis and interleukin-6 production by enzyme-linked immunosorbent assay. Lipopolysaccharide-induced activation of the extracellular signal-regulated kinases-1 and -2 was enhanced in hypoosmotic media (205 mosm/l) and diminished by hyperosmotic (405 mosm/l) exposure when compared to normoosmotic (305 mosm/l) conditions. These effects were paralleled by changes in lipopolysaccharide-stimulated interleukin-6 mRNA expression, when determined after 4 h and interleukin-6 release after 18 h. The mitogen-activated protein kinase-kinase inhibitor PD 098059 abolished phosphorylation of the extracellular signal-regulated kinases-1 and -2 in response to lipopolysaccharide, irrespective of the medium osmolarity, and diminished lipopolysaccharide-induced interleukin-6 mRNA expression and interleukin-6 production under normo- and hypoosmotic conditions by about 50%; it also resulted under hyperosmotic conditions in an about 80% inhibition. SB 203580, a specific inhibitor of p38 largely abolished interleukin-6 mRNA expression and interleukin-6 production, irrespective of medium osmolarity, whereas phosphorylation of the extracellular signal-regulated kinases was not affected.\n\nQuestion:\nIs activation of mitogen-activated protein kinases and IL-6 release in response to lipopolysaccharides in Kupffer cells modulated by anisoosmolarity?\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:\nMembers of the Burkholderia cepacia complex (Bcc) cause considerable morbidity and mortality in patients with chronic granulomatous disease and cystic fibrosis. Many Bcc strains are antibiotic resistant, which requires the exploration of novel antimicrobial approaches, including antisense technologies such as phosphorodiamidate morpholino oligomers (PMOs). Peptide-conjugated PMOs (PPMOs) were developed to target acpP, which encodes an acyl carrier protein (AcpP) that is thought to be essential for growth. Their antimicrobial activities were tested against different strains of Bcc in vitro and in infection models. PPMOs targeting acpP were bactericidal against clinical isolates of Bcc (>4 log reduction), whereas a PPMO with a scrambled base sequence (scrambled PPMO) had no effect on growth. Human neutrophils were infected with Burkholderia multivorans and treated with AcpP PPMO. AcpP PPMO augmented killing, compared with neutrophils alone and compared with neutrophils alone plus scrambled PPMO. Mice with chronic granulomatous disease that were infected with B. multivorans were treated with AcpP PPMO, scrambled PPMO, or water at 0, 3, and 6 h after infection. Compared with water-treated control mice, the AcpP PPMO-treated mice showed an approximately 80% reduction in the risk of dying by day 30 of the experiment and relatively little pathology.\n\nQuestion:\nDo antisense phosphorodiamidate morpholino oligomers targeted to an essential gene inhibit Burkholderia cepacia complex?\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 goal of this investigation was to use Raman spectroscopy to study the chemical interactions between 4-methacryloxyethyltrimellitic acid (4-MET), a hydrolized form of 4-methacryloxyethyltrimellitate anhydride (4-META) and powdered substrates such as bovine enamel powder and synthetic carbonate-containing apatite. Powdered samples were prepared by immersing them in 4-MET/methylmethacrylate (MMA) solution for 15 min, 3 h and 24 h. They were then dried for spectroscopy. An experimental Raman microprobe equipped with a cryogenically-cooled camera was employed to acquire spectra of the samples. Spectra of samples wetted for 24 h strongly indicate that there is strong ionic interaction between Ca2+ ions on the powdered sample surface and 4-MET. Spectra of the 15-min samples, however, suggest only some degree of hydrogen bonding. The spectrum of the 3-h 4-MET/enamel powder sample showed features intermediate between the two.\n\nQuestion:\nDo characterization of the chemical interactions betwen 4-MET and enamel by Raman spectroscopy?\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:\nEstrogen deficiency increases body weight or total and central adiposity and decreases energy expenditure. Hypothalamic neuropeptide Y (NPY) expression is altered by estrogen deficiency in rodents, but the long-term consequences on energy homeostasis are unknown. To investigate the role of NPY in the changes in energy expenditure and physical activity, as well as the associated changes in body weight and composition in response to short-term and long-term estrogen deficiency. Sham and ovariectomy (OVX) operations were performed at 8 weeks of age in wild-type (WT) and NPY(-/-) mice. Energy expenditure, physical activity, body composition and weight, as well as food intake were measured at 10-18 days (short-term) and 46-54 days (long-term) after OVX. OVX influences energy homeostasis differently at early compared with later time-points. At the early but not the late time point, OVX in WT mice reduced oxygen consumption and energy expenditure and tended to reduce resting metabolic rate. Interestingly, these effects of short-term estrogen deficiency were ablated by NPY deletion, with NPY(-/-) mice exhibiting significant increases in energy expenditure and resting metabolic rate. In addition to these hypermetabolic effects, OVX NPY(-/-) mice exhibited significantly lower body weight and whole-body fat mass relative to OVX WT controls at the short-term but not the long-term time point. Food intake and physical activity were unaltered by OVX, but NPY(-/-) mice exhibited significant reductions in these parameters relative to WT.\n\nQuestion:\nDoes neuropeptide Y mediate the short-term hypometabolic effect of estrogen deficiency 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:\nMammographic density is a strong risk factor for breast cancer, but it is unknown whether density at first breast cancer diagnosis and changes during follow-up influences risk of non-simultaneous contralateral breast cancer (CBC). We collected mammograms for CBC-patients (cases, N = 211) and unilateral breast cancer patients (controls, N = 211), individually matched on age and calendar period of first breast cancer diagnosis, type of adjuvant therapy and length of follow-up (mean follow-up time: 8.25 years). The odds of CBC as a function of changes of density during follow-up were investigated using conditional logistic regression, adjusting for non-dense area at diagnosis. Patients who experienced ≥10% absolute decrease in percent density had a 55% decreased odds of CBC (OR = 0.45 95% CI: 0.24 to 0.84) relative to patients who had little or no change in density from baseline to first follow-up mammogram (mean = 1.6 (SD = 0.6) years after diagnosis), whereas among those who experienced an absolute increase in percent density we could not detect any effect on the odds of CBC (OR = 0.83 95% CI: 0.24 to 2.87).\n\nQuestion:\nDoes change of mammographic density predict the risk of contralateral breast cancer -- a case-control 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:\nPostprandial hyperlipidemia (PPHL) is an independent risk factor for coronary heart disease (CHD) which is based on the accumulation of chylomicrons (CM) and CM remnants containing apolipoprotein B-48 (apoB-48). Since atherosclerotic cardiovascular diseases are frequently observed even in subjects with normal serum triglyceride (TG) level, the correlation between fasting apoB-48 containing lipoproteins and carotid intima-media thickness (IMT) was analyzed in subjects with normal TG levels. From subjects who took their annual health check at the Osaka Police Hospital (n=245, male), one-hundred and sixty-four male subjects were selected to take part in this study; the excluding factors were: systolic blood pressure ≥ 140 mmHg, intake of antihypertensive or antihyperlipidemic drugs, or age >65 years. The association between biochemical markers and IMT was analyzed and independent predictors of max-IMT were determined by multiple regression analysis in all subjects and in groups N-1 (TG<100mg/dl, n=58), N-2 (100 ≤ TG<150 mg/dl, n=53) and H (150 ≤ TG mg/dl, n=53), respectively. Fasting total cholesterol, LDL-cholesterol, HDL-cholesterol, apoB-100 and lnRemL-C (remnant lipoprotein-cholesterol) levels were not correlated with max-IMT, but lnTG and lnapoB-48 were significantly correlated with max-IMT in all subjects. LnapoB-48 and apoB-48/TG ratio were significantly correlated with max-IMT in group N-2. By multiple regression analysis, age and lnapoB-48 were independent variables associated with max-IMT in group N-2.\n\nQuestion:\nAre serum apolipoprotein B-48 levels correlated with carotid intima-media thickness in subjects with normal serum triglyceride levels?\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:\nParticipants in a phase I study were interviewed in order to establish the incidence and variability of subjective symptoms and changes in quality of life during phase I trials. The healthy subjects were randomized to receive a single dose of either 0.5 mg digoxin or an equivalent amount of each of four digitaloid mixtures every 14 days. The trial involved five 24-h monitoring periods. The duration of the study was 57 days. Wellbeing, subjective symptoms and quality of life were measured before, during and after the trial using the Freiburg Symptoms List (FSL), Wellbeing Scales (WBS), and Life Satisfaction Questionnaire (LSQ). Eight healthy subjects (25 years) were enrolled in the study. Their subjective symptoms were below the reference values for healthy subjects for each test but above the theoretical minimum and maximum values for total wellbeing, indicating that healthy subjects-not just patients-display subjective symptoms and impairment of wellbeing to a greater or lesser extent prior to a clinical trial. In terms of the total study population, comparison of the questionnaire scores before, during and after the study disclosed no significant changes in wellbeing or quality of life. However, some participants displayed marked intraindividual fluctuation.\n\nQuestion:\nDo subjective symptoms and quality of life in healthy subjects during a phase I 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:\nMitral annular calcification (MAC) has been associated with adverse cardiovascular disease outcomes and stroke in longitudinal and community-based cohorts. Prospective data are limited on its association with atrial fibrillation (AF). We examined the association between MAC and the long-term risk of AF over 16 years of follow-up in participants in the original cohort of the Framingham Heart Study who attended a routine examination between 1979 and 1981. MAC was assessed by M-mode echocardiography. cox proportional-hazards models were used to estimate hazard ratios (hr) for incident af. Of 1126 subjects who had adequate echocardiographic assessment and were AF-free at baseline, 149 (13%) had MAC. There were 217 cases of incident AF (42 in subjects with MAC). The age- and sex-adjusted incidence rate was 362 per 10,000 person-years in subjects with MAC compared with 185 per 10,000 person-years in those without MAC. In multivariable-adjusted analyses, MAC was associated with an increased risk of AF (HR 1.6, 95% CI 1.1-2.2). This association was attenuated upon further adjustment for left atrial size (HR 1.4, 95% CI 0.9-2.0).\n\nQuestion:\nIs mitral annular calcification a predictor for incident atrial fibrillation?\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:\nAlcoholic hepatitis (AH) frequently progresses to multiple organ failure (MOF) and death. However, the driving factors are largely unknown. At admission, patients with AH often show criteria of systemic inflammatory response syndrome (SIRS) even in the absence of an infection. We hypothesize that the presence of SIRS may predispose to MOF and death. To test this hypothesis, we studied a cohort including 162 patients with biopsy-proven AH. The presence of SIRS and infections was assessed in all patients, and multivariate analyses identified variables independently associated with MOF and 90-day mortality. At admission, 32 (19.8%) patients were diagnosed with a bacterial infection, while 75 (46.3%) fulfilled SIRS criteria; 58 patients (35.8%) developed MOF during hospitalization. Short-term mortality was significantly higher among patients who developed MOF (62.1% versus 3.8%, P < 0.001). The presence of SIRS was a major predictor of MOF (odds ratio = 2.69, P = 0.025) and strongly correlated with mortality. Importantly, the course of patients with SIRS with and without infection was similar in terms of MOF development and short-term mortality. Finally, we sought to identify serum markers that differentiate SIRS with and without infection. We studied serum levels of high-sensitivity C-reactive protein, procalcitonin, and lipopolysaccharide at admission. All of them predicted mortality. Procalcitonin, but not high-sensitivity C-reactive protein, serum levels identified those patients with SIRS and infection. Lipopolysaccharide serum levels predicted MOF and the response to prednisolone.\n\nQuestion:\nDo systemic inflammatory response and serum lipopolysaccharide levels predict multiple organ failure and death in alcoholic hepatitis?\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:\nFocal brain cooling is effective for suppression of epileptic seizures, but it is unclear if seizures can be suppressed without a substantial influence on normal neurologic function. To address the issue, a thermoelectrically driven cooling system was developed and applied in free-moving rat models of focal seizure and epilepsy. Focal seizures limited to the unilateral forelimb were induced by local application of a penicillin G solution or cobalt powder to the unilateral sensorimotor cortex. A proportional integration and differentiation (PID)-controlled, thermoelectrically driven cooling device (weight of 11 g) and bipolar electrodes were chronically implanted on the eloquent area (on the epileptic focus) and the effects of cooling (20, 15, and 10°C) on electrocorticography, seizure frequency, and neurologic changes were investigated. Cooling was associated with a distinct reduction of the epileptic discharges. In both models, cooling of epileptic foci significantly improved both seizure frequency and neurologic functions from 20°C down to 15°C. Cooling to 10°C also suppressed seizures, but with no further improvement in neurologic function. Subsequent investigation of sensorimotor function revealed significant deterioration in foot-fault tests and the receptive field size at 15°C.\n\nQuestion:\nDoes cooling of the epileptic focus suppress seizures with minimal influence on neurologic functions?\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:\nTwo reports suggested that vitamin D2 is less effective than vitamin D3 in maintaining vitamin D status. Our objective was to determine whether vitamin D2 was less effective than vitamin D3 in maintaining serum 25-hydroxyvitamin D levels or increased the catabolism of 25-hydroxyvitamin D3. This was a randomized, placebo-controlled, double-blinded study of healthy adults ages 18-84 yr who received placebo, 1000 IU vitamin D3, 1000 IU vitamin D2, or 500 IU vitamin D2 plus 500 IU vitamin D3 daily for 11 wk at the end of the winter. Sixty percent of the healthy adults were vitamin D deficient at the start of the study. The circulating levels of 25-hydroxyvitamin D (mean+/-sd) increased to the same extent in the groups that received 1000 IU daily as vitamin D2 (baseline 16.9+/-10.5 ng/ml; 11 wk 26.8+/-9.6 ng/ml), vitamin D3 (baseline 19.6+/-11.1 ng/ml; 11 wk 28.9+/-11.0 ng/ml), or a combination of 500 IU vitamin D2 and 500 IU vitamin D3 (baseline 20.2+/-10.4 ng/ml; 11 wk 28.4+/-7.7 ng/ml). The 25-hydroxyvitamin D3 levels did not change in the group that received 1000 IU vitamin D2 daily. The 1000 IU dose of vitamin D2 or vitamin D3 did not raise 25-hydroxyvitamin D levels in vitamin D-deficient subjects above 30 ng/ml.\n\nQuestion:\nIs vitamin D2 as effective as vitamin D3 in maintaining circulating concentrations of 25-hydroxyvitamin D?\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:\nGhrelin was recently identified as a specific endogenous ligand for the growth hormone secretagogue receptor (GHS-R). This new hormone was isolated from rat and human stomach and was reported to circulate in human plasma, but the regulation and physiological significance of ghrelin in humans have not been clarified. The present study was undertaken to test the following hypotheses: (1) prolonged fasting, which is known to stimulate GH secretion, is associated with changes in ghrelin immunoreactivity; (2) somatostatin in the systemic circulation regulates ghrelin secretion; and (3) GH affects ghrelin levels. The study population included normal subjects investigated on three occasions (fasting alone, fasting and somatostatin infusion +/- GH); GH-deficient adults investigated after 12 and 36 h of fasting +/- GH, as well as patients with active acromegaly before and after somatostatin analogue treatment. Somatostatin infusion lowered ghrelin levels 70-80% (P < 0.0001), whereas continued fasting +/- GH did not significantly affect ghrelin levels. In active acromegaly, suppression of plasma ghrelin levels was recorded after a single subcutaneous octreotide injection as well as during prolonged administration of slow-release octreotide.\n\nQuestion:\nIs ghrelin immunoreactivity in human plasma suppressed by somatostatin?\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 surgical approach of neonates with a functionally univentricular heart, transposition of the great arteries and excessive pulmonary bloodflow remains a challenge. Pulmonary artery banding remains a valuable option, but may induce ventricular hypertrophy, restriction of the bulboventricular foramen and dysplastic changes of the pulmonary valve. These secondary changes might compromise a later Damus-Kaye-Stansel connection because of pulmonary regurgitation but also a subsequent Fontan repair because of ventricular hypertrophy. The aim of this study is to investigate whether a previous pulmonary artery banding might compromise the function of a Damus-Kaye-Stansel connection. Thirteen neonates underwent pulmonary artery banding for functionally univentricular heart, transposition of the great arteries and pulmonary hypertension. Coarctation repair was associated in seven patients. All but one survived the operation. The twelve survivors underwent at a second stage a Damus-Kaye-Stansel connection after a mean interval of 1.1 years. The length of this interval was dictated by the degree of ventricular hypertrophy, the restriction of the bulboventricular foramen and by the degree of cyanosis. The Damus-Kaye-Stansel connection was constructed without any foreign material and with resorbable sutures. Associated procedures were: Glenn/hemi-Fontan (8 pts), Blalock-shunt (2 pts), biventricular correction with a homograft (1 pt), Fontan repair (1 pt). Four patients underwent successfully a Fontan repair at a third stage; seven patients are waiting for such repair. All patients survived the second and third stage of this surgical approach. The mean follow-up after the Damus-Kaye-Stansel connection was 2.5 years. Echocardiography at the last follow-up revealed: PR grade 0 (1 pt), grade 1 (8 pts), and grade 2 (3 pts). All patients - except one patient with a systolic gradient of 24 mmHg - had laminar flow without any gradient in the ascending aorta. All patients, including those who underwent a definitive repair, are doing extremely well.\n\nQuestion:\nDoes neonatal pulmonary artery banding compromise the short-term function of a Damus-Kaye-Stansel connection?\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 investigate whether inhalation of ethyl pyruvate (EP) encapsulated with poly(ethylene glycol)-block-lactide/glycolide copolymer nanoparticles (EP-NPs) can prevent the development of shunt-flow-induced hyperkinetic pulmonary arterial hypertension (PAH) in a rat model. Rats were separated into five groups: blank (ie, no treatment after shunt flow), normal control (ie, no shunt flow or treatment), EP-NP instillation, EP-only instillation, and vehicle. The animals received intratracheal instillation of EP-NPs or other treatments immediately after a shunt flow, and treatment continued weekly until the end of the experiment. Hemodynamic data were recorded, pulmonary arterial remodeling was assessed, and levels of inflammatory mediators and ET1 expression in the lung and serum were analyzed. In addition, retention of EP in the lungs of rats in the EP-NP and EP-only groups was measured using high-performance liquid chromatography. After 12 weeks, hemodynamic abnormalities and pulmonary arterial remodeling were improved in the EP-NP instillation group, compared with the blank, EP-only, and vehicle groups (P<0.05). In addition, the EP-NP group showed significantly decreased levels of HMGB1, IL-6, TNFα, reactive oxygen species, and ET1 in the lung during PAH development (P<0.05). Furthermore, EP-NP instillation was associated with reduced serum levels of inflammatory factors and ET1. High-performance liquid-chromatography measurement indicated that EP retention was greater in the lungs of the EP-NP group than in the EP-only group.\n\nQuestion:\nDoes intratracheal instillation of ethyl pyruvate nanoparticles prevent the development of shunt-flow-induced pulmonary arterial hypertension 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 combination of anti-cancer drugs with nutritional factors is a potential strategy for improving the efficacy and decreasing the toxicity of chemotherapy. However, whether nutritional factors enhance the effect of trichostatin A (TSA), a novel anti-cancer drug, is unclear. We investigated the individual enhancing effect and its possible mechanisms of genistein, daidzein, beta-carotene, retinoic acid, and alpha-tocopherol on the cell-growth-inhibitory effect of TSA in a human lung carcinoma cell line, A549. A549 cells were incubated with TSA (50 ng/mL) alone or in combination with the various nutritional factors for various times, and cell growth was measured. IMR90 cells, human lung fibroblasts, were also incubated with TSA alone or in combination with genistein or beta-carotene to determine the selectivity of these treatments. In addition, we studied effects on the cell cycle, caspase-3 activity, and DNA damage (by comet assay) in A549 cells. After treatment for 72 h, 10-microM genistein or beta-carotene significantly enhanced the growth-inhibitory effect of TSA in A549 cells. Daidzein, retinoic acid, and alpha-tocopherol at the same concentration had no significant effect. However, genistein and beta-carotene failed to enhance the cell-growth-arrest effect of TSA in IMR90 cells. Flow cytometric analysis showed that both genistein and beta-carotene significantly increased the TSA-induced apoptosis in A549 cells. Genistein significantly enhanced TSA-induced caspase-3 activity in A549 cells by 34% at 24 h, and the caspase-3 inhibitor partly inhibited the enhancing effect of genistein on TSA-induced apoptosis. beta-Carotene did not significantly affect TSA-induced caspase-3 activity. However, beta-carotene rather than genistein enhanced TSA-induced DNA damage.\n\nQuestion:\nDo genistein and beta-carotene enhance the growth-inhibitory effect of trichostatin A in A549 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:\nCeliac disease is a diet-induced, T cell-mediated enteropathy. The HLA variant DQ2.5 increases risk of the disease, and the homologous DQ2.2 confers a lower level of risk. As many as 5% of patients with celiac disease carry DQ2.2 without any other risk alleles. Epitopes commonly recognized by T cells of patients with HLA-DQ2.5 bind stably to DQ2.5 but unstably to DQ2.2. We investigated the response to gluten in patients with HLA-DQ2.2. We generated intestinal T-cell lines and clones from 7 patients with HLA-DQ2.2 (but not DQ2.5) and characterized the responses of the cells to gluten. The epitope off-rate was evaluated by gel filtration and T cell-based assays. Peptide binding to DQ2.2 was studied with peptide substitutes and DQ2 mutants. Patients with DQ2.2 and no other risk alleles had gluten-reactive T cells that did not respond to the common DQ2.5-restricted T-cell epitopes. Instead, many of the T cells responded to a distinct epitope that was not recognized by those from patients with HLA-DQ2.5. This immunodominant epitope bound stably to DQ2.2. A serine residue at P3 was required for the stable binding. The effect of this residue related to a polymorphism at DQα22 that was previously shown to determine stable binding of peptides to DQ2.5.\n\nQuestion:\nDoes t-cell response to gluten in patients with HLA-DQ2.2 reveal requirement of peptide-MHC stability in celiac 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:\nChanges in neurocognitive function after cardiopulmonary bypass (CPB) are difficult to assess in children with congenital cardiovascular malformations in part because identification of a suitable control group of children is difficult. We evaluated neurocognitive function in subjects aged 3 to 17 years both before and after surgical repair of an atrial septal defect (ASD). Eighteen subjects underwent testing within a median of 3 days (range, 1 to 27) before surgery and 5.8 months (range, 5.5 to 9) after surgery. The Differential Ability Scales was administered to subjects in a single testing session. All subjects were considered to be healthy, and they had no activity limitations. The mean General Conceptual Ability (GCA) scores (analogous to IQ) for the group were in the normal range before and after ASD repair. No significant difference was detected between the GCA scores before and after surgery. The GCA score was 90.8+/-18.6 before surgery and 93.1+/-16.3 after surgery.\n\nQuestion:\nDoes cardiopulmonary bypass to repair an atrial septal defect affect cognitive function in children?\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 identify prognostic factors in stage III and IV endometrial cancer with special attention to pretreatment platelet count. 59 patients with FIGO stage III or IV disease operated on between 1983 and 1993 were analyzed. Patients with preoperative thrombocytosis were compared with those without thrombocytosis. Prognostic factors were analyzed with a Cox proportional hazard model. With the exception of age, there were no significant differences between patients with or without thrombocytosis. At multivariate analysis, five-year disease-free survival was influenced significantly by FIGO stage (stage III vs stage IV; p = 0.009), thrombocytosis (p = 0.02) and cervical involvement (p = 0.024). Similarly, overall five-year survival was significantly influenced by stage (p < 0.001), cervical involvement (p = 0.005) and thrombocytosis (p = 0.01). Age, histology, grade, myometrial invasion, lymph-vascular space involvement or spread to adnexae were not significantly associated with survival.\n\nQuestion:\nIs preoperative thrombocytosis an independent prognostic factor in stage III and IV endometrial 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:\nMiR-375 has been implicated in insulin secretion and exocytosis through incompletely understood mechanisms. Here we aimed to investigate the role of miR-375 in the regulation of voltage-gated Na(+) channel properties and glucose-stimulated insulin secretion in insulin-secreting cells. MiR-375 was overexpressed using double-stranded mature miR-375 in INS-1 832/13 cells (OE375) or downregulated using locked nucleic acid (LNA)-based anti-miR against miR-375 (LNA375). Insulin secretion was determined using RIA. Exocytosis and ion channel properties were measured using the patch-clamp technique in INS-1 832/13 cells and beta-cells from miR-375KO mice. Gene expression was analysed by RT-qPCR, and protein levels were determined by Western blot. Voltage-gated Na(+) channels were found to be regulated by miR-375. In INS-1 832/13 cells, steady-state inactivation of the voltage-gated Na(+) channels was shifted by approx. 6 mV to a more negative membrane potential upon down-regulation of miR-375. In the miR-375 KO mouse, voltage-gated Na(+) channel inactivation was instead shifted by approx. 14 mV to a more positive membrane potential. Potential targets differed among species and expression of suggested targets Scn3a and Scn3b in INS-1 832/13 cells was only slightly moderated by miR-375. Modulation of miR-375 levels in INS-1-832/13 cells did not significantly affect insulin release. However, Ca(2+) dependent exocytosis was significantly reduced in OE375 cells.\n\nQuestion:\nDoes modulation of microRNA-375 expression alter voltage-gated Na ( + ) channel properties and exocytosis in insulin-secreting 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:\nCurrent single drug treatments for rheumatoid arthritis have problems of limited efficacy and/or high toxicity. This study investigates the benefits of individual and combined treatments with dexamethasone and substance P and glutamate receptor antagonists in a rat model of arthritis. Arthritis was induced in rats by unilateral intra-articular injection of Freund's complete adjuvant. Separate groups of rats were subjected to the following treatments 15 min before induction of arthritis: (i) control with no drug treatment; (ii) single intra-articular injection of a NK(1) receptor antagonist RP67580; (iii) single intra-articular injection of a NMDA receptor antagonist AP7 plus a non-NMDA receptor antagonist CNQX; (iv) daily oral dexamethasone; and (v) combined treatment with dexamethasone and all of the above receptor antagonists. Knee joint allodynia, swelling, hyperaemia and histological changes were examined over a period of 7 days. Treatment with dexamethasone suppressed joint swelling, hyperaemia and histological changes that include polymorphonuclear cell infiltration, synovial tissue proliferation and cartilage erosion in the arthritic rat knees. Treatment with RP67580 or AP7 plus CNQX did not attenuate hyperaemia or histological changes, but reduced joint allodynia and swelling. Co-administration of dexamethasone with these receptor antagonists produced greater inhibition on joint allodynia and swelling than their individual effects.\n\nQuestion:\nDo substance P and glutamate receptor antagonists improve the anti-arthritic actions of dexamethasone 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:\nIs chloride channel-3 (ClC-3) involved in regulating the biological behavior of endometrial stromal cells (ESCs)?\n\nQuestion:\nIs overexpression of chloride channel-3 associated with the increased migration and invasion ability of ectopic endometrial cells from patients with endometriosis?\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:\nIntracerebral hemorrhage (ICH) at high altitude is not well understood to date. This study investigates the effects of high altitude on ICH, and examines the acute neuroprotection of hyperbaric oxygen (HBO) therapy against high-altitude ICH. Minipigs were placed in a hypobaric chamber for 72 h before the operation. ICH was induced by an infusion of autologous arterial blood (3 ml) into the right basal ganglia. Animals in the high-altitude ICH group received HBO therapy (2.5 ATA for 60 min) 30 min after ICH. Blood gas, blood glucose and brain tissue oxygen partial pressure (PbtO2) were monitored continuously for animals from all groups, as were microdialysis products including glucose, lactate, pyruvate and glutamate in perihematomal tissue from 3 to 12 h post-ICH. High-altitude ICH animals showed significantly lower PbtO2, higher lactate/pyruvate ratio (LPR) and glutamate levels than low-altitude ICH animals. More severe neurological deficits, brain edema and neuronal damage were also observed in high-altitude ICH. After HBO therapy, PbtO2 was significantly increased and LPR and glutamate levels were significantly decreased. Brain edema, neurological deficits and neuronal damage were also ameliorated.\n\nQuestion:\nDoes hyperbaric oxygen therapy ameliorate acute brain injury after porcine intracerebral hemorrhage at high altitude?\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:\nCirculating endothelial progenitor cells (EPCs) contribute to postnatal angiogenesis. The number of circulating EPCs has an inverse correlation with coronary risk scores. However, the effect of smoking on the number of circulating EPCs is not well-known. We examined the effects of chronic smoking and of smoking cessation on EPC levels. Circulating EPCs were quantified by flow cytometry as CD45lowCD34+CD133+ (progenitor cells [PCs]) or CD45lowCD34+CD133+VEGFR2+ (EPCs) in 14 nonsmokers and in 15 smokers. All smokers quit smoking. Eight quit smoking with nicotine patch and 7 without nicotine patch. PC/EPC levels were inversely correlated with the number of cigarettes smoked. Circulating PCs/EPCs increased rapidly after cessation (P<0.0001) and decreased again after resumption of smoking to the level similar to that before cessation (P=0.0031). The magnitude of increase in EPCs was greater in light smokers than in heavy smokers.\n\nQuestion:\nDoes smoking cessation rapidly increase circulating progenitor cells in peripheral blood in chronic smokers?\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 present study examined the effect of C-type natriuretic peptide (CNP) on the anabolic and catabolic activities in chondrocyte/agarose constructs subjected to dynamic compression. Constructs were cultured under free-swelling conditions or subjected to dynamic compression with low (0.1 to 100 pM) or high concentrations (1 to 1,000 nM) of CNP, interleukin-1β (IL-1β), and/or KT-5823 (inhibits cyclic GMP-dependent protein kinase II (PKGII)). Anabolic and catabolic activities were assessed as follows: nitric oxide (NO) and prostaglandin E2 (PGE2) release, and [3H]-thymidine and 35SO4 incorporation were quantified by using biochemical assays. Gene expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), aggrecan, and collagen type II were assessed with real-time quantitative PCR (qPCR). Two-way ANOVA and the post hoc Bonferroni-corrected t tests were used to examine data. CNP reduced NO and PGE2 release and partially restored [3H]-thymidine and 35SO4 incorporation in constructs cultured with IL-1β. The response was dependent on the concentration of CNP, such that 100 pM increased [3H]-thymidine incorporation (P < 0.001). This is in contrast to 35SO4 incorporation, which was enhanced with 100 or 1000 nM CNP in the presence and absence of IL-1β (P < 0.001). Stimulation by both dynamic compression and CNP and/or the PKGII inhibitor further reduced NO and PGE2 release and restored [3H]-thymidine and 35SO4 incorporation. In the presence and absence of IL-1β, the magnitude of stimulation for [3H]-thymidine and 35SO4 incorporation by dynamic compression was dependent on the concentration of CNP and the response was inhibited with the PKGII inhibitor. In addition, stimulation by CNP and/or dynamic compression reduced IL-1β-induced iNOS and COX-2 expression and restored aggrecan and collagen type II expression. The catabolic response was not further influenced with the PKGII inhibitor in IL-1β-treated constructs.\n\nQuestion:\nDo biomechanical signals and the C-type natriuretic peptide counteract catabolic activities induced by IL-1β in chondrocyte/agarose constructs?\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:\nTextiles used to make clothing can represent a source, often ignored, of chemicals potentially noxious to both skin and the whole organism. Among the most frequently produced potentially noxious chemical manufacturing by-products are formaldehyde (FA), nickel (Ni) and hexavalent chromium (Cr); they are of potential clinical interest as all are known to be carcinogenic to humans and to be potent skin sensitizers. The aim of this study was to investigate, in vitro, effects of these potentially dangerous compounds on two different melanoma cell lines. In particular, attention was focused on A375P, a poorly metastatic and low invasive cell line and SK-MEL-28, a highly metastatic cell line. Effects of these compounds was evaluated on A375P and SK-MEL-28 cells. FA (1-5 × 10(-5) m), NiSO4 (10(-6) -10(-3) m), K2 Cr2 O7 (10(-7) -10(-6) m) effects on cell proliferation were evaluated by cell counting, while ERK pathway involvement was evaluated by Western blot analysis. Low concentrations of the chemicals, covering a range that corresponds to commonly accepted limits in textile production, induced a significant increase in cell proliferation concomitant with transient activation of phosphorylated ERK expression.\n\nQuestion:\nDo textile industry manufacturing by-products induce human melanoma cell proliferation via 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:\nA higher serum phosphate level is associated with worse outcome. Energy-demanding intracellular transport of phosphate is needed to secure anion bioavailability. In heart failure (HF), energy starvation may modify intracellular and serum levels of phosphate. We analysed determinants of serum phosphates in HF and assessed if catabolic/anabolic balance (CAB) was associated with elevation of serum phosphate. We retrospectively reviewed data from 1029 stable patients with HF and have calculated negative (loss) and positive (gain) components of weight change from the onset of HF till index date. The algebraic sum of these components was taken as CAB. The univariate and multivariable predictors of serum phosphorus were calculated. In quintiles of CAB, we have estimated odds ratios for serum phosphorus above levels previously identified to increase risk of mortality. As a reference, we have selected a CAB quintile with similar loss and gain. Apart from sex, age, and kidney function, we identified serum sodium, N-terminal fragment of pro-brain-type natriuretic peptide, and CAB as independent predictors of serum phosphorus. The odds for serum phosphorus above thresholds found in literature to increase risk were highest in more catabolic patients. In most catabolic quintile relative to neutral balance, the odds across selected phosphorus thresholds rose, gradually peaking at 1.30 mmol/L with a value of 3.29 (95% confidence interval: 2.00-5.40, P < 0.0001) in an unadjusted analysis and 2.55 (95% confidence interval: 1.38-2.72, P = 0.002) in a fully adjusted model.\n\nQuestion:\nIs higher serum phosphorus associated with catabolic/anabolic imbalance in 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:\nTo evaluate and compare the functional results of an established technique, laparoscopic radical prostatectomy(LRP), and the initial learning curve of robot assisted laparoscopic radical prostatectomy (RALRP). This is a transversal case-control hybrid studio including all patients undergoing RALRP (39 ) and similar number of patients undergoing LRP (37) from November 2009 to June 2011. We used a transversal phone interrogatory to evaluate functional outcome. The groups were comparable for IMC, age, serum PSA, prostatic ultrasound volume, biopsy Gleason, following time and clinical stage. For operative variables, there was no difference in estimated blood loss, hospital stay, days of drainage, time to catheter removal, transfusion rate and surgical margins. Median operative time was 216 min for RALRP, and 153 min for LRP (p < 0,001). There were no differences in erectile function or continence at 12 months. Mean time to continence was 5.7 weeks in RALRP and 8.9 week in LRP (p < 0,001). There was no difference in time to normal erectile function.\n\nQuestion:\nDoes comparison of the initial robot-assisted radical prostatectomy result with laparoscopic radical prostatectomy?\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:\nMelatonin is a molecule with antioxidative properties including direct free radical scavenging and indirect stimulatory actions on a variety of antioxidative enzymes which further promote its ability to reduce the toxicity of radicals and their associated reactants. Beer is an integral element of the diet of numerous people and is rich in antioxidants. We analyzed if melatonin is present in beer and if so, at what concentration. It further determines whether the moderate consumption of beer has an effect on the total antioxidant status (TAS) of human serum. We analyzed 18 brands of beer with different percentage of alcohol content in order to determine the concentration of melatonin. Serum samples were collected from 7 healthy volunteers. These samples were used to measure melatonin and TAS on basal conditions and after drinking beer. Showed that all the beer analyzed did indeed contain melatonin and the more they have got, the greater was its degree of alcohol. Both melatonin and TAS in human serum increased after drinking beer.\n\nQuestion:\nDoes melatonin present in beer contribute to increase the levels of melatonin and antioxidant capacity of the human serum?\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:\nCalcium intake is known to be associated with the risk of having metabolic syndrome. However, the previous studies did not take into account the fact that intestinal absorption and urinary excretion of calcium are estrogen dependent, and intestinal absorption efficiency and renal conservation of calcium deteriorate after menopause. Therefore, we performed a menopause status-specific analysis of the association between calcium intake and metabolic syndrome. A total of 9,341 participants (4,118 men, 3,359 premenopausal women, and 1,864 postmenopausal women) from the Korean National Health and Nutrition Examination Survey 2001 and 2005 were included in the study. Calcium and energy intake were significantly higher in men than in women and were lowest in postmenopausal women. On multivariate logistic regression analysis, postmenopausal women with calcium intake in the fourth quartile had a lower risk of having metabolic syndrome (odds ratio, 0.637; 95% CI, 0.452-0.898) compared with women with intake in the first quartile after adjustment for age, body mass index, marital status, education level, alcohol intake, smoking history, exercise, hormone therapy use, and energy intake. However, no association was detected in men and premenopausal women.\n\nQuestion:\nIs calcium intake inversely associated with metabolic syndrome in postmenopausal women : Korea National Health and Nutrition Survey , 2001 and 2005?\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:\nInflammation and oxidative stress is considered to have a crucial role in induction of nephropathy. Curcuma longa (C. longa) and Nigella sativa (N. sativa) have anti-inflammatory and antioxidant effects. This study was designed to investigate the effect of mixed hydro-alcoholic extract of N.sativa and C. longa on the oxidative stress induced by Adriamycin (ADR) in rat kidney. The animals were divided into 6 groups: control (CO), ADR, Adriamycin+ Vitamin C (ADR+VIT C), C. longa extract+ Adriamycin (C.LE+ADR), N. sativa extract+ Adriamycin (N.SE+ADR) and C. longa extract+ N. sativa extract + Adriamycin (N.S+C.L+ADR). ADR (5mg/kg) was injected intravenously, whereas VITC (100mg/kg) and extract of C. longa (1000mg/kg) and N. sativa (200mg/kg) were administrated orally. Finally, the renal tissue, urine and blood samples were collected and submitted to measure of redox markers, osmolarity and renal index. The renal content of total thiol and superoxide dismutase (SOD) activity significantly decreased and Malondialdehyde (MDA) concentration increased in Adriamycin group compared to control group. The renal content of total thiol and SOD activity significantly enhanced and MDA concentration reduced in treated-mixed extract of C. longa and N. sativa along with ADR group compared to ADR group. The mixed extract did not restore increased renal index percentage induced by ADR. There also was no significant difference in urine and serum osmolarity between the groups.\n\nQuestion:\nIs adriamycin-induced oxidative stress prevented by mixed hydro-alcoholic extract of Nigella sativa and Curcuma longa in rat kidney?\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:\nCanonical and noncanonical Wnt signaling pathways both play pivotal roles in bone development. Wntless/GPR177 is a chaperone protein that is required for secretion of all Wnt ligands. We previously showed that deletion of Wntless within mature osteoblasts severely impaired postnatal bone homeostasis. In this study, we systemically evaluated how deletion of Wntless in different stages of osteochondral differentiation affected embryonic bone development, by crossing Wntless (Wls)-flox/flox mice with strains expressing cre recombinase behind the following promoters: Osteocalcin, Collagen 2a1, or Dermo1. Ex vivo µCT and whole-mount skeletal staining were performed to examine skeletal mineralization. Histology and immunohistochemistry were used to evaluate cellular differentiation and alterations in Wnt signaling. In this work, we found that Wntless regulated chondrogenesis and osteogenesis through both canonical and noncanonical Wnt signaling.\n\nQuestion:\nDoes wntless spatially regulate bone development through β-catenin-dependent and independent mechanisms?\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:\nBlood cultures (BCs) are commonly performed on children admitted to hospital for skin and soft tissue infections (SSTIs). In recent years, this practice has been questioned in patients with uncomplicated SSTIs because of its low yield. At the same time, however, an increase in community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) infections has been described; its influence on rates of bacteremia in patients with SSTIs is unclear. The aims of the study were to describe the performance and the yield of BC in immunocompetent patients with uncomplicated SSTIs and to determine the prevalence of CA-MRSA as a causative agent in our area. Retrospective study: immunocompetent patients younger than 18 years evaluated in the emergency department and admitted for uncomplicated SSTIs (cellulitis, abscess, impetigo or erysipelas) from July 1, 2010 to June 31, 2014 were included. Patients referred from other hospitals who were receiving parenteral antibiotics and patients with complicated SSTIs (surgical or traumatic wound infection, need for surgical intervention and infected ulcers or burns) were excluded. We included 445 cases: 348 (78.2%) cellulitis, 78 (17.5%) abscess and 19 (4.3%) impetigo. BCs were performed on 353 (79.3%) patients. Two (0.6%; 95% confidence interval: 0.2-2.0%) were positive and 10 (2.8%; 95% confidence interval: 1.5-5.1%) contaminated. The positive BCs grew S. aureus and Streptococcus pyogenes. Wound cultures were performed on 148 (33.3%) patients; 98 (66.2%) were positive. In 22 (22.4%) patients CA-MRSA grew, accounting for 14.9% of overall wound cultures.\n\nQuestion:\nAre blood Cultures Useful in the Evaluation of Children with Uncomplicated Superficial Skin and Soft Tissue Infections?\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 aim of the study was to examine the relationship between apolipoprotein E4 allele (ApoE4) and depression among an older Japanese population. Mild cognitive impairment (MCI) was taken into consideration. This is a community-based cross-sectional study. We assessed the mood and cognitive function of Japanese community-dwelling individuals aged 65 years or older. In the first phase of the study, we evaluated the mood and cognitive function. In the second phase, face-to-face structured interviews were conducted. Individuals with dementia and other mental diseases were excluded on the basis of a consensus meeting of psychiatrists and neuropsychologists; 738 subjects with full data were included in the analyses. We subdivided depression into major depressive episode (MDE) and depressive symptoms cases (DSCs). DSC was defined as a score of 6 or more on the Geriatric Depression Scale but not having a diagnosis of MDE. The relationship between depression (MDE and DSC) and ApoE4 was examined by multivariate logistic regression. The adjusted odds ratio (OR) of ApoE4 on DSC was not significant (OR = 0.82, 95%CI = 0.48-1.39, p < 0.46). Sex (OR = 2.53, 95%CI = 1.33-4.79, p < 0.01), MCI (1.95, 1.21-3.14, p < 0.01), years of education (0.87, 0.79-0.95, p < 0.01), and Nishimura's activities of daily living scores (0.75, 0.63-0.89, p < 0.01) significantly correlated with prevalence of DSC. There were no significant risk factors for MDE.\n\nQuestion:\nIs apoE4 associated with depression when mild cognitive impairment is considered?\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:\nAngiogenesis is a critical factor in the progression of solid tumors and metastasis. The aim of this study was to characterise the roles of angiogenic and anti-angiogenic factors on ovarian cancer. The expression levels of vascular endothelial growth factor (VEGF, angiogenic factor) and pigment epithelial growth factor (PEDF, anti-angiogenic factor) were measured by real-time polymerase chain reaction and Western blotting in ovarian tumors. Microvessel density (MVD) was evaluated by the total microvessel length in high-power field of tumor tissue preparations. MVD correlated with tumor malignancy. The tissues with the highest expression levels of VEGF (VEGF-H) were malignant tumors. The VEGF expression levels in some malignant tumors (VEGF-L) were as low as that in benign tumors. Therefore, the expression of PEDF was examined. The PEDF expression levels in VEGF-L malignant tumors were significantly lower than those in benign tumors. On the other hand, the PEDF expression levels in VEGF-H malignant tumor tissues were not significantly different from those in benign tumors.\n\nQuestion:\nIs the reduction in pigment epithelium-derived factor a sign of malignancy in ovarian cancer expressing low-level of vascular endothelial growth factor?\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:\nViruses may contribute to RA. This prompted us to monitor viral load and response to anti-CD20 therapy in RA patients. Blood and bone marrow from 35 RA patients were analysed for CMV, EBV, HSV-1, HSV-2, parvovirus B19 and polyomavirus using real-time PCR before and 3 months after rituximab (RTX) treatment and related to the levels of autoantibodies and B-cell depletion. Clinical response to RTX was defined as decrease in the 28-joint disease activity score (DAS-28) >1.3 at 6 months. Before RTX treatment, EBV was identified in 15 out of 35 patients (EBV-positive group), of which 4 expressed parvovirus. Parvovirus was further detected in eight patients (parvo-positive group). Twelve patients were negative for the analysed viruses. Following RTX, EBV was cleared, whereas parvovirus was unaffected. Eighteen patients were responders, of which 12 were EBV positive. The decrease in the DAS-28 was significantly higher in EBV-positive group compared with parvo-positive group (P = 0.002) and virus-negative patients (P = 0.04). Most of EBV-negative patients that responded to RTX (75%) required retreatment within the following 11 months compared with only 8% of responding EBV-positive patients. A decrease of RF, Ig-producing cells and CD19(+) B cells was observed following RTX but did not distinguish between viral infections. However, EBV-infected patients had significantly higher levels of Fas-expressing B cells at baseline as compared with EBV-negative groups.\n\nQuestion:\nDoes epstein-Barr virus in bone marrow of rheumatoid arthritis patients predict response to rituximab treatment?\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 reaction time (RT) paradigms, in which a variable preparation interval preceded the imperative stimulus, RT become shorter as a function of increasing time from the start of a trial until presentation of the imperative stimulus. The shortening of RT as the preparatory foreperiod elapses reflects increasing motor readiness; however, the underlying neurochemical mechanisms are still poorly defined. The present study investigated in rats whether signals transmitted via the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors and via dopamine D2 receptors in the caudate-putamen (CPu) are involved in motor readiness. A simple RT task demanding conditioned lever release was used, in which the upcoming reward magnitude (5 pellets or 1 pellet) was signalled in advance by discriminative stimuli and the imperative stimulus was subsequently presented after a variable foreperiod (200, 500 or 800 ms). In intact rats, RT of conditioned responses was shortened with foreperiod lengthening and with expectancy of the high reward magnitude, but there was no interaction between both factors. Bilateral infusion of the competitive NMDA antagonist DL-2-amino-5-phosphonovaleric acid (APV) (2, 10 micrograms in 0.5 microliter/side), of the preferential dopamine D2 antagonist haloperidol (5, 12.5 micrograms in 0.5 microliter/side) or infusion of vehicle (0.5 microliter/side) into the central subregion of the CPu had no effect on progressive RT shortening with increasing foreperiod.\n\nQuestion:\nAre nMDA and dopamine D2 receptors in the caudate-putamen involved in control of motor readiness in rats?\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.
| [
{
"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:\nNuclear factor-κB (NF-κB) activation in hepatocytes and macrophages appeared as a double-edged-sword in hepatic ischemia reperfusion (IR) injury. Protein tyrosine phosphatase receptor type O (PTPRO) was recently identified as a potential activator of c-Src, which can in turn activate the NF-κB pathway. In this study, we aimed to determine the change and function of PTPRO in hepatocytes and macrophages during IR. Clinical patients with benign liver condition undergoing liver surgery were recruited in our study. Wild type (WT) and ptpro(-/-) C57BL/6 mice were processed to construct hepatic IR models. Isolated mouse hepatocytes and macrophages were treated with peroxide or TNFα in vitro. In human and mouse IR models, PTPRO level was decreased in the early phase but reversed in the late phase. In vitro studies demonstrated that NF-κB up-regulated PTPRO transcription. Using ptpro(-/-) mice and primary cells, we found that PTPRO deficiency resulted in reduction of NF-κB activation in both hepatocytes and macrophages and was correlated to c-Src phosphorylation; PTPRO in hepatocytes alleviated, but PTPROt in macrophages exacerbated IR injury.\n\nQuestion:\nDoes pTPRO play a dual role in hepatic ischemia reperfusion injury through feedback activation of NF-κB?\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:\nActivation of receptor tyrosine kinases is common in Malignancies. FGFR3 fusion with TACC3 has been reported to have transforming effects in primary glioblastoma and display oncogenic activity in vitro and in vivo. We set out to investigate the role of FGFR3 in glioma through transcriptomic analysis. FGFR3 increased in Classical subtype and Neural subtype consistently in CGGA and TCGA cohort. Similar patterns of FGFR3 distribution through subtypes were observed in CGGA and TCGA samples. Gene ontology analysis was performed with genes that were significantly correlated with FGFR3 expression. We found that positively associated biological processes of FGFR3 were focused on differentiated cellular functions and neuronal activities, while negatively correlated biological processes focused on mitosis and cell cycle phase. Clinical investigation showed that higher FGFR3 expression predicted improved survival for glioma patients, especially in Proneural subtype. Moreover, FGFR3 showed very limited relevance with other receptor tyrosine kinases in glioma at transcriptome level. FGFR3 expression data of glioma was obtained from Chinese Glioma Genome Atlas (CGGA) and TCGA (The Cancer Genome Atlas). In total, RNA sequencing data of 325 glioma samples and mRNA microarray data of 301 samples from CGGA dataset were enrolled into this study. To consolidate the findings that we have revealed in CGGA dataset, RNA-seq data of 672 glioma samples from TCGA dataset were used as a validation cohort. R language was used as the main tool to perform statistical analysis and graphical work.\n\nQuestion:\nIs fGFR3 , as a receptor tyrosine kinase , associated with differentiated biological functions and improved survival of glioma patients?\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:\nStereotactic body radiation therapy (SBRT) is a treatment option for patients with localized prostate cancer, with reported clinical and health-related quality-of-life (QOL) outcomes comparable to standard fractionation radiation therapy. The goal of this study was to evaluate correlations between short-term QOL outcomes and dosimetric parameters to guide future prostate SBRT planning. From 2010 to 2013, QOL data were prospectively collected from 75 patients enrolled in a prostate SBRT clinical trial. A comparison was made between Expanded Prostate Cancer Index Composite scores for patients with the top 25th percentile versus the bottom 75th percentile of the following dose-volume histogram parameters: planning target volume V100; bladder V50 and V100; and rectum V50, V80, V90, and V100. A linear mixed-effect model was used to estimate the difference between the 2 strata for each parameter. Median follow-up was 12 months. Patients with planning target volume V100 volumes >120 cm(3) had the worst reduction in urinary QOL. Urinary QOL was also decreased significantly in patients with bladder V100 volumes >5.5 cm(3). Bowel QOL was decreased significantly in patients with rectal V90 and V100 volumes >4.2 and >1.5 cm(3), respectively.\n\nQuestion:\nDo dosimetric parameters predict short-term quality-of-life outcomes for patients receiving stereotactic body radiation therapy for prostate 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:\nSystemic exposure to amphetamine (AMPH) leads to a number of long-lasting neuroadaptations including changes in dendritic morphology in rat forebrain. It remains unknown whether these changes relate to associative drug conditioning or to nonassociative drug sensitization, two forms of plasticity produced by systemic exposure to AMPH. We compared the behavioral, neuronal, and morphologic consequences of exposing rats to intraperitoneal (IP) AMPH to those of exposure to AMPH applied to the ventral tegmental area (VTA), infusions that sensitize AMPH-induced locomotion and nucleus accumbens (NAcc) DA overflow but do not produce drug conditioning. Both IP and VTA AMPH exposure sensitized locomotion and NAcc DA overflow, but only IP AMPH exposure produced conditioned locomotion. Importantly, whereas IP AMPH exposure increased spine density and dendritic length and branching in the NAcc, exposure to VTA AMPH produced the opposite effects. A similar differentiation of effects was observed in cortical areas.\n\nQuestion:\nDo amphetamine-induced changes in dendritic morphology in rat forebrain correspond to associative drug conditioning rather than nonassociative drug sensitization?\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:\nAlbuminuria and elevated C-reactive protein (CRP) levels are common manifestations of many inflammatory diseases. Cardiovascular-based drugs, with secondary anti-inflammatory actions, such as angiotensin-converting enzyme-inhibitors are able to reduce both proteinuria and CRP levels, raising the question of whether CRP directly influences the processes that result in proteinuria. As proteinuria is thought to be induced as a result of podocyte dysfunction, we investigated whether there is a pathomechanistic link with CRP. Podocytes were analysed for evidence of endogenous CRP production in response to inflammatory agents. In addition, they were incubated in the presence of various concentrations of exogenous CRP and analysed for evidence of a response to treatment. Our results demonstrated that inflammatory agents such as macrophage-conditioned medium and interleukin-1β induced the expression of CRP messenger RNA in podocytes. However, they were unable to induce CRP protein. Stimulation of podocytes with exogenous CRP demonstrated that 10 μg/mL CRP induced a low but significant level of interleukin-6 secretion. Tumour necrosis factor α, however, was not detected. CRP did up-regulate the expression of the slit diaphragm proteins nephrin and CD2AP, as well as the structural proteins ezrin and podocalyxin-like protein-1, proteins known to be involved in signalling via the phosphotidylinositol-3 (PI-3) kinase pathway. CRP exposure reduced caspase-3 enzyme activity and up-regulated the expression of the anti-apoptotic protein Bcl-2. In the presence of the PI-3 kinase inhibitor LY294002, the ability of CRP to suppress caspase-3 activity was significantly reduced.\n\nQuestion:\nDo low-level C-reactive protein levels exert cytoprotective actions on human podocytes?\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 work has shown that the gap junction protein connexin43 (Cx43) is upregulated in cells of the joint during osteoarthritis (OA). Here we examined if the OA-associated increase in Cx43 expression impacts the function of synovial fibroblasts by contributing to the production of catabolic and inflammatory factors that exacerbate joint destruction in arthritic disease. Using rabbit and human synovial fibroblast cell lines, we examined the effects of Cx43 overexpression and Cx43 siRNA-mediated knockdown on the gene expression of OA-associated matrix metalloproteinases (MMP1 and MMP13), aggrecanases (ADAMTS4 and ADAMTS5), and inflammatory factors (IL1, IL6 and PTGS2) by quantitative real time RT-PCR. We examined collagenase activity in conditioned media of cultured synovial cells following Cx43 overexpression. Lastly, we assessed the interplay between Cx43 and the NFκB cascade by western blotting and gene expression studies. Increasing Cx43 expression enhanced the gene expression of MMP1, MMP13, ADAMTS4, ADAMTS5, IL1, IL6 and PTGS2 and increased the secretion of collagenases into conditioned media of cultured synovial fibroblasts. Conversely, knockdown of Cx43 decreased expression of many of these catabolic and inflammatory genes. Modulation of Cx43 expression altered the phosphorylation of the NFκB subunit, p65, and inhibition of NFκB with chemical inhibitors blocked the effects of increased Cx43 expression on the mRNA levels of a subset of these catabolic and inflammatory genes.\n\nQuestion:\nDoes connexin43 enhance the expression of osteoarthritis-associated genes in synovial fibroblasts in culture?\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 describe the intra and postoperative frequency of complications in vaginal hysterectomies for benign disorders in patients with a history of caesarean section. Since 1996, 963 hysterectomies have been performed in our institution. 76.94% were performed exclusively by vaginal route (n = 741), 10.1% (n = 98) were by laparoscopic-assisted vaginal route and 12.9%, by pure abdominal route. We compared two groups of patients who underwent vaginal hysterectomy, with or without history of caesarean section. In each group we recorded the characteristics of the population and compared the intra and postoperative data, such as bladder or digestive tract wounds and haemorrhages. We used analysis of variance tests to compare means, chi2-tests and Fisher's exact tests for comparisons of numbers. A probability of P < 0.05 was adopted as the limit of significance. The frequency of haemorrhages was significantly higher in the patients with a history of caesareans. Bladder and intestine injury rates are significantly higher in the previous caesarean section group, but not significant for the bowel injuries. We compared the cumulative frequency of complications between the two groups. In the group with previous caesarean section, we recorded 18.3% of intra operative complications. In the group without history of caesarean section, we recorded 3.58% of complications. There is a significant difference between the cumulative frequency of complications in the two populations of patients in favour of the sub group without a history of caesarean scar (P < 0.0001).\n\nQuestion:\nIs [ Previous caesarean section an operative risk factor in vaginal hysterectomy ]?\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:\nHuman obesity is characterized by high levels of leptin, and it has been suggested that obese patients may be leptin resistant. The aim of our study was to investigate the influence of Lys656Asn polymorphism in the leptin receptor gene on leptin response and weight loss secondary to a lifestyle modification (Mediterranean hypocaloric diet and exercise) in obese patients. A population of 67 obese (body mass index >30) nondiabetic outpatients was analyzed in a prospective way. Before and after 3 months of lifestyle modification program, bipolar electrical bioimpedance, blood pressure, and a serial assessment of nutritional intake with 3 days written food records and biochemical analysis were performed. The lifestyle modification program consisted of a hypocaloric diet (1520 kcal, 52% carbohydrates, 25% lipids and 23% proteins). The exercise program consisted of aerobic exercise for at least three times per week (60 min each). Statistical analysis was performed for the combined Lys656/Asn656 and Asn656/Asn656 as mutant group and type Lys656/Lys 656 as wild-type second group. Sixty seven patients gave informed consent and were enrolled in the study. The mean age was 45.7 +/- 16.6 years and the mean BMI 34.1 +/- 5.1, with 18 males (26.9%) and 49 females (73.1%). Thirty six patients (10 males/26 females) (46.8%) had the genotype Lys656/Lys 656 (wild-type group) and 31 patients (8 males/23 females) (46.3%) Lys656/Asn656 (n = 28, 41.8%) or Asn656/Asn656 (n = 3, 4.5%) (mutant group). The percentage of responders (weight loss) was similar in both groups (91.7 vs. 87.1%). In wild-type group (responders and nonresponders), BMI, weight, fat mass, systolic blood pressure and waist circumference decreased. In mutant group, BMI, weight and waist circumference decreased. No differences were detected between basal values in both groups. Only leptin levels decreased significantly in wild-type group (11.5%; p <0.05) (57.3 +/- 31.5 ng/mL vs. 45.8 +/- 29.3 ng/mL; p <0.05). In mutant group, leptin increased without statistical differences (0.44%; ns).\n\nQuestion:\nIs leptin receptor Lys656Asn polymorphism associated with decreased leptin response and weight loss secondary to a lifestyle modification in obese patients?\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:\nOxidative stress markers are thought to be related to nociception. Because thiolic compounds are important antioxidants, we investigated the relationship between thiols, endogenous or exogenous, and nociception. Systemic or spinal, but not peripheral, administration of the exogenous thiolic compound N-acetyl-L-cysteine (NAC) reduced nociception induced by intraplantar capsaicin injection. Moreover, we detected an increase in lipid peroxidation and 3-nitrotyrosine and a decrease in nonprotein thiolic levels in the lumbar spinal cord of capsaicin-injected animals. All these effects were prevented by NAC treatment (i.p. and i.t.). Our findings confirm a role for the spinal cord in NAC actions because systemic NAC administration also reduced the nociception trigged by intrathecal injection of capsaicin. Moreover, adjuvant-induced arthritis, but not paw incision, also -decreases nonprotein thiol levels in the spinal cord. Similarly, NAC produced antinociception in adjuvant-treated animals, but not in paw-incised animals. Finally, we investigated the role of endogenous thiol compounds in the nociceptive process administrating buthionine-suphoxamine (BSO), an inhibitor of glutathione-synthesis. Intrathecal BSO treatment decreased nonprotein thiol levels in the spinal cord, as well as induced mechanical allodynia and chemical and thermal hyperalgesia. In conclusion, our results indicate a critical role for nonprotein thiols in nociception at the level of the spinal cord.\n\nQuestion:\nAre spinal levels of nonprotein thiols related to nociception in mice?\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 common cold is a major cause of asthma exacerbation and chronic obstructive lung disease. Rhinovirus is reported to be responsible for more than 50% of cases of the common cold. In a previous study, we reported that rhinovirus infection of cultured airway cells induced MUC5AC mucin overproduction and hypersecretion by activating the p44/42 mitogen-activated protein kinase (p44/42 MAPK) pathway. The aim of this study was to examine the effect of erythromycin on RV14-induced airway mucin overproduction and hypersecretion. RV14-infected human tracheal epithelial cells were treated with erythromycin. Erythromycin blocked RV14-induced MUC5AC protein overproduction and hypersecretion, and also blocked RV14-induced p44/42 MAPK activation in the cells.\n\nQuestion:\nDoes erythromycin attenuate MUC5AC synthesis and secretion in cultured human tracheal cells infected with RV14?\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:\nIFITM3, an IFN-inducible gene, is overexpressed in human colorectal cancer. In this study, we sought to determine the clinical significance and underlying mechanisms of its dysregulated expression in human colon tumor specimens and murine models of this disease. IFITM3 expression in a tissue microarray of tumor and matched normal colon tissue specimens and lymph node metastasis specimens obtained from 203 patients with colon cancer was measured immunohistochemically. IFITM3 was expressed at higher levels in colon tumors and, particularly, nodal metastases than in normal colon tissue. A Cox proportional hazards model showed that IFITM3 expression was an independent prognostic factor for disease-free survival in patients with colon cancer. Knockdown of IFITM3 expression by a specific siRNA significantly suppressed the proliferation, colony formation, migration, and invasion of colon cancer cells in vitro and tumor growth and metastasis in a xenograft model. Restored expression of KLF4, a putative tumor suppressor, downregulated IFITM3 expression in colon cancer cells in vitro. Two KLF4-binding sites in the IFITM3 promoter bound specifically to KLF4 protein in a chromatin immunoprecipitation assay and promoter mutagenesis analyses. Specific deletion of KLF4 led to IFITM3 overexpression in colon mucosa in Villin-Cre(+);Klf4(fl/fl) mice. An inverse correlation between loss of KLF4 expression and IFITM3 overexpression was evident in human colon tumors.\n\nQuestion:\nDoes kLF4-mediated negative regulation of IFITM3 expression play a critical role in colon cancer pathogenesis?\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:\nThere is intense interest in the interaction between microbial compounds and allergy. Although Toll-like receptor (TLR)-2 ligands derived from Gram-positive bacteria alter allergic sensitization in animal models, it is not clear what effect TLR2 ligands have on allergen-specific T-cell memory in human beings. To determine whether in vitro exposure to TLR2 ligands modifies the immune response to house dust mite allergen (HDM). Blood mononuclear cells were obtained from individuals both allergic (n = 23) and not allergic (n = 22) to HDM, and stimulated with HDM in the presence or absence of TLR2 ligands. In subjects allergic to HDM, IL-5 and IL-13 responses to HDM were inhibited by heat-killed Staphylococcus aureus, staphylococcal lipoteichoic acid, and the synthetic lipoprotein Pam3CSK4 (P < .005; all stimuli). Although the whole staphylococcal bacteria increased IFN-gamma responses, the purified TLR2 ligands lipoteichoic acid and Pam3CSK4 inhibited HDM-specific IFN-gamma synthesis. In contrast, TLR2 ligands had minimal effects on responses to HDM in subjects without allergy. TLR2 ligands induced upregulation of HLA-DR expression but did not inhibit antigen uptake or processing by antigen-presenting cells.\n\nQuestion:\nDo toll-like receptor 2 ligands inhibit TH2 responses to mite allergen?\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:\nDeterministic dynamic models of complex biological systems contain a large number of parameters and state variables, related through nonlinear differential equations with various types of feedback. A metamodel of such a dynamic model is a statistical approximation model that maps variation in parameters and initial conditions (inputs) to variation in features of the trajectories of the state variables (outputs) throughout the entire biologically relevant input space. A sufficiently accurate mapping can be exploited both instrumentally and epistemically. Multivariate regression methodology is a commonly used approach for emulating dynamic models. However, when the input-output relations are highly nonlinear or non-monotone, a standard linear regression approach is prone to give suboptimal results. We therefore hypothesised that a more accurate mapping can be obtained by locally linear or locally polynomial regression. We present here a new method for local regression modelling, Hierarchical Cluster-based PLS regression (HC-PLSR), where fuzzy C-means clustering is used to separate the data set into parts according to the structure of the response surface. We compare the metamodelling performance of HC-PLSR with polynomial partial least squares regression (PLSR) and ordinary least squares (OLS) regression on various systems: six different gene regulatory network models with various types of feedback, a deterministic mathematical model of the mammalian circadian clock and a model of the mouse ventricular myocyte function. Our results indicate that multivariate regression is well suited for emulating dynamic models in systems biology. The hierarchical approach turned out to be superior to both polynomial PLSR and OLS regression in all three test cases. The advantage, in terms of explained variance and prediction accuracy, was largest in systems with highly nonlinear functional relationships and in systems with positive feedback loops.\n\nQuestion:\nIs hierarchical cluster-based partial least squares regression ( HC-PLSR ) an efficient tool for metamodelling of nonlinear dynamic models?\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:\nIntracortical microstimulation (ICMS) is a technique used for a number of purposes including the derivation of cortical movement representations (motor maps). Its application can activate the output layer 5 of motor cortex and can result in the elicitation of body movements depending upon the stimulus parameters used. The extent to which pyramidal tract projection neurons of the motor cortex are activated transsynaptically or directly by ICMS remains an open question. Given this uncertainty in the mode of activation, we used a preparation that combined patch clamp whole-cell recordings from single layer 5 pyramidal neurons and extracellular ICMS in slices of motor cortex as well as a standard in vivo mapping technique to ask how ICMS activated motor cortex pyramidal neurons. We measured changes in synaptic spike threshold and spiking rate to ICMS in vitro and movement threshold in vivo in the presence or absence of specific pharmacological blockers of glutamatergic (AMPA, NMDA and Kainate) receptors and GABAA receptors. With major excitatory and inhibitory synaptic transmission blocked (with DNQX, APV and bicuculline methiodide), we observed a significant increase in the ICMS current intensity required to elicit a movement in vivo as well as to the first spike and an 85% reduction in spiking responses in vitro. Subsets of neurons were still responsive after the synaptic block, especially at higher current intensities, suggesting a modest direct activation.\n\nQuestion:\nDoes intracortical Microstimulation ( ICMS ) activate Motor Cortex Layer 5 Pyramidal Neurons Mainly Transsynaptically?\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:\nSorafenib and S-1 (one mixed formulation containing 5-FU prodrug and dihydropyrimidine dehydrogenase inhibitor) were two effective agents against hepatocellular carcinoma (HCC), but whether they had synergistic effects remained unclear. The present study aimed at evaluating their synergistic effects against HCC and its mechanisms. Inhibitory effects of sorafenib, 5-FU and their combination on HCC cells PLC/PRF/5 and SK-HEP-1 were evaluated. Expressions of transcription factor E2F-1 and its downstream thymidylate synthetase (TS) in the treated cells were determined using real-time PCR and Western blot. In vivo anti-tumoral efficacy of S-1 plus sorafenib on HCC was evaluated in NOD/SCID mice. E2F-1 and TS expressions in tumors were determined by immunohistochemical staining. Sorafenib inhibited growth of HCC cells in dose-dependent manner, with IC50 of 5.4 ± 0.3 μmol/L for PLC/PRF/5 and 5.3 ± 0.5 μmol/L for SK-HEP-1. Sorafenib (1 μmol/L) enhanced inhibitory efficacy of 5-FU on HCC cells in vitro, dropping IC50 of 5-FU from 167.7 ± 12.1 to 105.4 ± 8.4 μmol/L for PLC/PRF/5 and 115 ± 10.2 to 82 ± 7.4 μmol/L for SK-HEP-1 (both p < 0.01). Sorafenib downregulated E2F-1 and TS expressions on HCC cells, and its combination with 5-FU yielded a synergistic downregulation of TS expression on HCC cells. In NOD/SCID mice with subcutaneously inoculated HCC, sorafenib combined with S-1 yielded greater inhibition on tumor growth and remarkable TS suppression when compared with sorafenib or S-1 alone (all p < 0.05).\n\nQuestion:\nDoes sorafenib enhance the chemotherapeutic efficacy of S-1 against hepatocellular carcinoma through downregulation of transcription factor E2F-1?\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 aims to investigate what factors predict the development of postoperative bloodstream infection (BSI) in patients transplanted electively for chronic liver disease and compare outcomes in infected transplant recipients (BCLD) with noninfected patients (CLD). A retrospective cohort study of 218 patients who had elective liver transplantation (LT) between January 2003 and July 2005 and admitted to a specialist intensive care unit (ICU) was done. Fifteen patients had BSI post-LT (BCLD, 29 isolates) while in the ICU, and 203 patients did not (CLD). Thirty-eight percent of isolates were gram negatives; 55%, gram positives; and 7%, fungemia. Median time to first BSI post-LT was 11 days (range, 3-16 days). On admission post-LT to the ICU, patients with BCLD had higher Acute Physiology and Chronic Health Evaluation II scores (23 vs 10, P < .001). While in the ICU, patients with BCLD had greater requirements for renal replacement therapy (73% vs 8%) and days on mechanical ventilation (17 vs 2 days) and longer median ICU stay (21 vs 3 days, P < .001 for all). One-year survival was worse in the BCLD group (40% vs 94%, P < .001). On multivariate analysis, Acute Physiology and Chronic Health Evaluation II score (odds ratio, 1.36) post-LT was independently associated with subsequent BSI. Bloodstream infection (hazards ratio, 8.7) was independently associated with mortality.\n\nQuestion:\nIs bloodstream infection after elective liver transplantation associated with increased mortality 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:\nIntraspinal administration of neostigmine has been shown to prevent induction of hypotension in rats by bupivacaine spinal block, and thus to provide greater hemodynamic stability. This study was undertaken to determine whether subarachnoid neostigmine would prevent bupivacaine spinal anesthesia from causing hypotension or bradycardia in patients undergoing abdominal hysterectomy. Of 40 patients scheduled for abdominal hysterectomy under spinal anesthesia, 20 were randomly assigned to each of two groups. The control group (CG) received 1.5 mL subarachnoid saline followed by 15 mg (3 mL) of hyperbaric bupivacaine 0.5%. The neostigmine group (NG) received 75 micrograms (1.5 mL) of subarachnoid neostigmine followed by 15 mg (3 mL) of hyperbaric bupivacaine 0.5%. No preload was given. Hypotension was treated with 4-mg intravenous boluses of ephedrine to keep blood pressure above 75% of the baseline value. The skin body temperature was measured with probes at the suprascapular region and at the foot. Spinal neostigmine (75 micrograms) failed to prevent bupivacaine-induced hypotension. There was no statistical difference in the incidence of brady-cardia between the groups (NG, 2/20; CG 1/20), although the bradycardia appeared to be qualitatively different, being somewhat delayed in the NG. Spinal neostigmine did not alter the onset or duration of sensory block and did not affect skin body temperature in either anesthetized or unanesthetized sites. The incidence of intraoperative nausea was 20% in the NG and 5% in the CG.\n\nQuestion:\nDoes subarachnoid neostigmine affect blood pressure or heart rate during bupivacaine spinal anesthesia?\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:\nIn the United States, the use of polytertraflouroethylene (PTFE) graft compared with native arteriovenous fistula (AVF) for haemodialysis vascular access has been increasing despite a greater than twofold higher incidence of thrombosis and infection associated with PTFE grafts. We studied 214 haemodialysis patients with not more than two revisions of their vascular access, to determine whether any relationship exists between the type of haemodialysis vascular access and dialysis dose assessed primarily by urea reduction ratio (per cent reduction in blood urea nitrogen concentration after a dialysis session). Serum albumin concentration was used as a secondary outcome measure of dialysis adequacy. Urea reduction ratio and predialysis serum albumin concentration were measured at onset of study and at 4-week intervals and mean values were calculated for each subject. The 214 patients (118 males, 96 females) included 173 Blacks (81%), 26 Whites (15%), and 15 Hispanics (7%), of mean (+/-SD) age 55.6+/-15.5 years. Of these 214 subjects, 111 (52%) had a native AVF, while 103 (48%) had a PTFE graft. Both mean urea reduction ratio (native AVF=69 +/-6.7% vs PTFE graft=70+/-7.3%; P=0.31), and mean serum albumin concentration (native AVF=4.02+/-0.39 g/dl vs PTFE graft=4+/-0.33 g/dl; P= 0.59) were equivalent in both groups. Separate multiple logistic regression analyses with type of vascular access as one of the independent variables, found no significant relationship between type of vascular access and either a urea reduction ratio > 65% (P= 0.67), or a serum albumin concentration >4g/dl (P=0.89), after adjustment for age of vascular access, access revision, location of access, dialyser urea clearance, length of dialysis treatment, body weight, and age.\n\nQuestion:\nIs haemodialysis dose independent of type of surgically-created vascular access?\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:\nMultipotent mesenchymal stromal cells suppress T-cell function in vitro, a property that has underpinned their use in treating clinical steroid-refractory graft-versus-host disease after allogeneic hematopoietic stem cell transplantation. However the potential of mesenchymal stromal cells to resolve graft-versus-host disease is confounded by a paucity of pre-clinical data delineating their immunomodulatory effects in vivo. We examined the influence of timing and dose of donor-derived mesenchymal stromal cells on the kinetics of graft-versus-host disease in two murine models of graft-versus-host disease (major histocompatibility complex-mismatched: UBI-GFP/BL6 [H-2(b)]→BALB/c [H-2(d)] and the sibling transplant mimic, UBI-GFP/BL6 [H-2(b)]→BALB.B [H-2(b)]) using clinically relevant conditioning regimens. We also examined the effect of mesenchymal stromal cell infusion on bone marrow and spleen cellular composition and cytokine secretion in transplant recipients. Despite T-cell suppression in vitro, mesenchymal stromal cells delayed but did not prevent graft-versus-host disease in the major histocompatibility complex-mismatched model. In the sibling transplant model, however, 30% of mesenchymal stromal cell-treated mice did not develop graft-versus-host disease. The timing of administration and dose of the mesenchymal stromal cells influenced their effectiveness in attenuating graft-versus-host disease, such that a low dose of mesenchymal stromal cells administered early was more effective than a high dose of mesenchymal stromal cells given late. Compared to control-treated mice, mesenchymal stromal cell-treated mice had significant reductions in serum and splenic interferon-γ, an important mediator of graft-versus-host disease.\n\nQuestion:\nDo mesenchymal stromal cells transiently alter the inflammatory milieu post-transplant to delay graft-versus-host 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:\nOsteonecrosis of the jaw (ONJ) is a rare but serious adverse drug effect linked to long-term and/or high-dose exposure to nitrogen-bisphosphonates (N-BP), the standard of care for the treatment of bone fragility disorders. The mechanism leading to bisphosphonate-associated ONJ (BAONJ) is unclear and optimal treatment strategies are lacking. Recent evidence suggests that BAONJ may be linked to drug-induced immune dysfunction, possibly associated with increased susceptibility to infections in the oral cavity. The objective of this investigation was to comprehensively assess the relationship linking immune function, N-BP exposure, the oral microbiome and ONJ susceptibility. Leukocyte gene expression of factors important for immunity, wound healing and barrier function were assessed by real-time quantitative PCR and the oral microbiome was characterized by 454 pyrosequencing of the 16S rRNA gene in 93 subjects stratified by N-BP exposure and a history of ONJ. There were marked differences in the systemic expression of genes regulating immune and barrier functions including RANK (p = 0.007), aryl hydrocarbon receptor (AHR, p < 0.001), and FGF9 (p < 0.001), which were collectively up-regulated in individuals exposed to N-BP without ONJ relative to treatment controls. In contrast, the expression levels of these same genes were significantly down-regulated in those who had experienced BAONJ. Surprisingly, the oral microbiome composition was not directly linked to either BAONJ or N-BP exposure, rather the systemic leukocyte expression levels of RANK, TNFA and AHR each explained 9% (p = 0.04), 12% (p = 0.01), and 7% (p = 0.03) of the oral bacterial beta diversity.\n\nQuestion:\nDoes systemic immunity shape the oral microbiome and susceptibility to bisphosphonate-associated osteonecrosis of the jaw?\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 combined effect of disease phenotype, smoking and medical therapy [steroid, azathioprine (AZA), AZA/biological therapy] on the probability of disease behavior change in a Caucasian cohort of patients with Crohn's disease (CD). Three hundred and forty well-characterized, unrelated, consecutive CD patients were analyzed (M/F: 155/185, duration: 9.4 +/- 7.5 years) with a complete clinical follow-up. Medical records including disease phenotype according to the Montreal classification, extraintestinal manifestations, use of medications and surgical events were analyzed retrospectively. Patients were interviewed on their smoking habits at the time of diagnosis and during the regular follow-up visits. A change in disease behavior was observed in 30.8% of patients with an initially non-stricturing, non-penetrating disease behavior after a mean disease duration of 9.0 +/- 7.2 years. In a logistic regression analysis corrected for disease duration, perianal disease, smoking, steroid use, early AZA or AZA/biological therapy use were independent predictors of disease behavior change. In a subsequent Kaplan-Meier survival analysis and a proportional Cox regression analysis, disease location (P = 0.001), presence of perianal disease (P < 0.001), prior steroid use (P = 0.006), early AZA (P = 0.005) or AZA/biological therapy (P = 0.002), or smoking (P = 0.032) were independent predictors of disease behavior change.\n\nQuestion:\nAre perianal disease , small bowel disease , smoking , prior steroid or early azathioprine/biological therapy predictors of disease behavior change in patients with Crohn 's 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:\nDysregulated signaling of the JAK/STAT pathway is a common feature of chronic myeloproliferative neoplasms (MPN), usually associated with JAK2V617F mutation. Recent clinical trials with JAK2 inhibitors showed significant improvements in splenomegaly and constitutional symptoms in patients with myelofibrosis but meaningful molecular responses were not documented. Accordingly, there remains a need for exploring new treatment strategies of MPN. A potential additional target for treatment is represented by the PI3K/AKT/mammalian target of rapamycin (mTOR) pathway that has been found constitutively activated in MPN cells; proof-of-evidence of efficacy of the mTOR inhibitor RAD001 has been obtained recently in a Phase I/II trial in patients with myelofibrosis. The aim of the study was to characterize the effects in vitro of mTOR inhibitors, used alone and in combination with JAK2 inhibitors, against MPN cells. Mouse and human JAK2V617F mutated cell lines and primary hematopoietic progenitors from MPN patients were challenged with an allosteric (RAD001) and an ATP-competitive (PP242) mTOR inhibitor and two JAK2 inhibitors (AZD1480 and ruxolitinib). mTOR inhibitors effectively reduced proliferation and colony formation of cell lines through a slowed cell division mediated by changes in cell cycle transition to the S-phase. mTOR inhibitors also impaired the proliferation and prevented colony formation from MPN hematopoietic progenitors at doses significantly lower than healthy controls. JAK2 inhibitors produced similar antiproliferative effects in MPN cell lines and primary cells but were more potent inducers of apoptosis, as also supported by differential effects on cyclinD1, PIM1 and BcLxL expression levels. Co-treatment of mTOR inhibitor with JAK2 inhibitor resulted in synergistic activity against the proliferation of JAK2V617F mutated cell lines and significantly reduced erythropoietin-independent colony growth in patients with polycythemia vera.\n\nQuestion:\nDo mTOR inhibitors alone and in combination with JAK2 inhibitors effectively inhibit cells of myeloproliferative neoplasms?\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 most important clinical significance of an isolated high-grade prostatic intraepithelial neoplasia (HGPIN) diagnosis is the risk of missed prostate cancer (PCa) in subsequent biopsies. Because most patients with HGPIN do not harbor or develop PCa, clinical, pathological, or molecular markers that predict of PCa risk are of clinical significance. Overall, 155 men with a diagnosis of isolated HGPIN, which was based on the results of extended biopsy, and who underwent at least one repeat biopsy were analyzed for ERG oncoprotein (ERG) expression and clinicopathological parameters to determine the risk of finding PCa in subsequent biopsies. Of 155 patients diagnosed with HGPIN on initial biopsy, 39 (25%) had PCa on subsequent biopsies. For men with only one repeat biopsy, the cancer detection rate was 22%. Most (54%) PCas were detected in≤6 months of rebiopsy. ERG expression was present in 15 patients with HGPIN (9.6%). Patients with ERG expression in HGPIN were more likely to have PCa in repeat biopsy, with 9 (60%) ERG-positive and 30 (21%) of ERG-negative patients having PCa (P = 0.001). Multifocal involvement (P = 0.0001), cribriform morphology (P = 0.004), and bilaterality (P = 0.0075) of HGPIN were other significant risk factors. On multivariable analysis, only the presence of ERG positivity and multifocality remained significant parameters in detecting PCa on a repeat biopsy. The presence of ERG-negative focal HGPIN involving one core, which accounted for 46% of patients, had minimal (16%) PCa risk on subsequent biopsy. In total, 8 patients (89%) ERG-positive HGPIN had PCa identified at identical sites on subsequent biopsy, of which 5 (71%) were ERG positive.\n\nQuestion:\nDo eRG overexpression and multifocality predict prostate cancer in subsequent biopsy for patients with high-grade prostatic intraepithelial neoplasia?\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 horse is a valuable species to assess the effect of allogeneic mesenchymal stromal cells (MSCs) in regenerative treatments. No studies to date have examined recipient response to major histocompatibility complex (MHC)-mismatched equine MSCs. The purposes of this study were to immunophenotype MSCs from horses of known MHC haplotype and to compare the immunogenicity of MSCs with differing MHC class II expression. MSCs and peripheral blood leukocytes (PBLs) were obtained from Thoroughbred horses (n=10) of known MHC haplotype (ELA-A2, -A3, and -A9 homozygotes). MSCs were cultured through P8; cells from each passage (P2 to P8) were cryopreserved until used. Immunophenotyping of MHC class I and II, CD44, CD29, CD90, LFA-1, and CD45RB was performed by using flow cytometry. Tri-lineage differentiation assays were performed to confirm MSC multipotency. Recombinant equine IFN-γ was used to stimulate MHC class II negative MSCs in culture, after which expression of MHC class II was re-examined. To assess the ability of MHC class II negative or positive MSCs to stimulate an immune response, modified one-way mixed leukocyte reactions (MLRs) were performed by using MHC-matched and mismatched responder PBLs and stimulator PBLs or MSCs. Proliferation of gated CFSE-labeled CD3+ responder T cells was evaluated via CFSE attenuation by using flow cytometry and reported as the number of cells in the proliferating T-cell gate. MSCs varied widely in MHC class II expression despite being homogenous in terms of \"stemness\" marker expression and ability to undergo trilineage differentiation. Stimulation of MHC class II negative MSCs with IFN-γ resulted in markedly increased expression of MHC class II. MLR results revealed that MHC-mismatched MHC class II-positive MSCs caused significantly increased responder T-cell proliferation compared with MHC-mismatched MHC class II-negative and MHC-matched MSCs, and equivalent to that of the positive control of MHC-mismatched leukocytes.\n\nQuestion:\nAre equine bone marrow-derived mesenchymal stromal cells heterogeneous in MHC class II expression and capable of inciting an immune response in vitro?\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:\nTo describe the circumstances and consequences of falls reported by community-dwelling older women. This prospective study collected data for approximately 2 years for women aged>or=70 years at risk for falling who were enrolled in the Fall Evaluation and Prevention Program. Participants (263) completed a median of 24 months of follow-up. A total of 143 participants reported 341 falls; 70 reported 1 fall, and 73 reported 2 or more. A majority of falls (62%) occurred in/around the home, primarily during the daytime, and in living rooms or kitchens/dining rooms. Falls frequently occurred while walking, carrying objects, or reaching/leaning. Many falls did not result in injury (53%); however, 31% resulted in minor injuries, 10% in moderate injuries, and 6% in major injuries. Soft tissue injuries were common, and 5% of falls resulted in fractures. Nine falls resulted in hospitalization.\n\nQuestion:\nDoes circumstances and consequences of fall in community-dwelling older women?\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 evaluate the effects of moderate-intensity regular exercise on serum levels of tumor necrosis factor-alpha (TNF-alpha) and glucose and lipid metabolism parameters. Longitudinal intervention study of a 5 month exercise training program (30-45 min/day, 4-5 days/week). Forty-one healthy Japanese women aged 41-69 y at baseline; 27 participants in the exercise program. Body mass index (BMI), waist-to-hip ratio (WHR), percentage body fat, and fasting levels for serum TNF-alpha, serum soluble TNF receptor p55 (TNF-RI) and TNF receptor p75 (TNF-RII), serum lipids, HbA1c, and serum insulin before and after exercise. In overweight to obese subjects, serum levels of TNF-alpha, TNF-RI and TNF-RII were significantly higher than those in lean subjects. There were significant correlations between log serum TNF-alpha and BMI, percentage body fat, WHR, HbA1c and log insulin. TNF-RI was significantly correlated with BMI, percentage body fat, WHR and HbA1c. TNF-RII was also associated with BMI, percentage body fat and WHR. However, the correlation between TNF-RII and HbA1c did not reach statistical significance. Neither TNF-RI nor TNF-RII was correlated with log insulin. In contrast, TNF-alpha, TNF-RI and TNF-RII were negatively correlated with HDL cholesterol. Regular exercise decreased BMI, percentage body fat, HbA1c, serum TNF-alpha, TNF-RI and TNF-RII and increased HDL cholesterol levels. In addition, exercise-induced change in serum TNF-alpha was independently correlated with changes in HbA1c and serum insulin, after being adjusted for the change in fat-free mass.\n\nQuestion:\nDoes moderate-intensity regular exercise decrease serum tumor necrosis factor-alpha and HbA1c levels in healthy women?\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 frequency of chromosomal aberrations (CA) in peripheral blood lymphocytes of healthy individuals has been associated with cancer risk. It is presently unclear whether this association is influenced by individual susceptibility factors such as genetic polymorphisms of xenobiotic-metabolizing enzymes. To evaluate the role of polymorphisms in glutathione S-transferase (GST) M1 (GSTM1) and theta 1 (GSTT1) as effect modifiers of the association between CA and cancer risk. A case-control study was performed pooling data from cytogenetic studies carried out in 1974-1995 in three laboratories in Italy, Norway, and Denmark. A total of 107 cancer cases were retrieved from national registries and matched to 291 controls. The subjects were classified as low, medium, and high by tertile of CA frequency. The data were analyzed by setting up a Bayesian model that included prior information about cancer risk by CA frequency. The association between CA frequency and cancer risk was confirmed [OR(medium) (odds ratio)(medium) = 1.5, 95% credibility interval (CrI), 0.9-2.5; OR(high) = 2.8, 95% CrI, 1.6-4.6], whereas no effect of the genetic polymorphism was observed. A much stronger association was seen in the Italian subset (OR(high)= 9.4, 95% CrI, 2.6-28.0), which was characterized by a lower technical variability of the cytogenetic analysis. CA level was particularly associated with cancer of the respiratory tract (OR(high)= 6.2, 95% CrI, 1.5-20.0), the genitourinary tract (OR(high) = 4.0, 95% CrI, 1.4-10.0), and the digestive tract (OR(high) = 2.8, 95% CrI, 1.2-5.8).\n\nQuestion:\nIs association between frequency of chromosomal aberrations and cancer risk influenced by genetic polymorphisms in GSTM1 and GSTT1?\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:\nQUESTION UNDER STUDY/PRINCIPLES: Dimethylfumarate (DMF) had been reported to reduce asthma symptoms and to improve the quality of life of asthma patients. Therefore, we assessed the anti-inflammatory and anti-remodeling effect of DMF on isolated lung fibroblasts, which are relevant to inflammatory lung diseases. We determined the effect of DMF on platelet derived growth factor (PDGF)-BB induced proliferation, as well as on PDGF-BB and tumor necrosis factor (TNF)-α induced interleukin (IL)-6 secretion and on activation of activated protein (AP)-1 and nuclear factor kappaB (NF-ĸB). Confluent lung fibroblasts were incubated with DMF (0.1-100 μM) 1 hour before stimulation with PDGF-BB or TNF-α (both 10 ng/ml). IL-6 secretion was measured by ELISA. NF-ĸB and AP-1 activation was determined by immuno-blotting and EMSA. Cell proliferation was assessed by [3H]-thymidine incorporation in subconfluent fibroblasts. PDGF-BB but not TNF-α induced fibroblast proliferation. This was dose dependently reduced by DMF in a concentration range of 10-100 μM. PDGF-BB and TNF-α induced IL-6 secretion by lung fibroblasts and this was inhibited by DMF in a dose-dependent manner. However, PDGF-BB induced IL-6 secretion did not correlate with NF-ĸB activity, while TNF-α did. DMF inhibited the TNF-α induced NF-ĸB-DNA binding, but had neither an inhibitory effect on NF-ĸB nuclear entry nor on the degradation of IκB-α. PDGF-BB and TNF-α activated AP-1, which was also inhibited by DMF.\n\nQuestion:\nDoes inhibition of NF-κB and AP-1 by dimethylfumarate correlate with down-regulated IL-6 secretion and proliferation in human lung fibroblasts?\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 predictors of lightweight in 11-year-olds and how weight changes between ages 9-11 years affected selected cardiovascular risk factors. Cohort study among an ethnically and geographically diverse group of 5098 nine-year-olds who participated in the Child and Adolescent Trial for Cardiovascular Health (CATCH) and were followed from 1991 to 1994 until age 11 years. Lightweight (body mass index [BMI] <15th percentile) was defined from gender- and age-adjusted data on the total population in the National Health and Nutrition Examination Survey I of 1971 to 1973. Weight (BMI) category at follow-up (age 11 years) was the dependent variable in the logistic regression. Gender, race/ethnicity, school site, weight category at baseline, and participation in the CATCH (intervention or control group) were examined for possible predictors. The prevalence of lightweight was much lower than the 15% expected at both ages 9 and 11 years; 4.7% for males (M) and 7.4% for females (F) and at age 11 years; 5.9% for M and 8.3% for F. Lightweight at age 9 years was the best predictor of lightweight at age 11 years (OR = 56.8; CI 41.3, 78.2). Normal-weight children who entered the overweight category exhibited striking adverse percent changes in serum cholesterol and in both serum high-density cholesterol and apolipoprotein B cholesterol levels. Among children in each weight group at age 9 years, the heavier children at age 11 years had higher percent changes in systolic blood pressure, and lower times on the 9-min run. Maintenance of lightweight was associated with the most favorable pattern of cardiovascular risk factors. Differences between groups were not found for percent change in total calorie intake or percentage of calories from fat. Normal-weight children who became overweight exhibited striking percentage increases in levels of serum cholesterol and in serum apolipoprotein B cholesterols.\n\nQuestion:\nDoes maintenance of lightweight correlate with decreased cardiovascular risk factors in early adolescence?\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:\nHelicobacter pylori is an important etiologic factor in the development of gastric cancer. The aim of this study was to analyze the role of H. pylori infections in the induction of mutagenic events in gastric epithelial cells. The effect of a high-salt diet as a genotoxic risk factor was also investigated. Big Blue transgenic male mice (C57Bl/6) were inoculated with H. pylori (strain SS1) or Helicobacter felis (strain CS1) for 6 and 12 months. The frequency and spectrum of mutations at the stomach level were assessed. Inflammatory host response and inducible nitric oxide synthase (iNOS) expression by reverse-transcription polymerase chain reaction and immunohistochemistry analysis were also performed. After 6 months, the gastric mutant frequency was 4-fold and 1.7-fold higher in mice infected with H. pylori and H. felis, respectively, than in uninfected mice. It was associated with a high frequency of transversions (AT --> CG and GC --> TA) known to result from oxidative damages. The Helicobacter-infected mice exhibited severe gastritis and a high level of iNOS messenger RNA expression. Hyperplasia developed 12 months after inoculation, and both the mutagenic effects and iNOS expression decreased in H. pylori- and H. felis-infected mice. No synergistic effects of a high-salt diet and Helicobacter infection were observed regarding the frequency of gastric mutation.\n\nQuestion:\nDo chronic Helicobacter pylori infections induce gastric mutations 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:\nThe lifespan of red blood cells is terminated when macrophages remove senescent red blood cells by erythrophagocytosis. This puts macrophages at the center of systemic iron recycling in addition to their functions in tissue remodeling and innate immunity. Thus far, erythrophagocytosis has been studied by evaluating phagocytosis of erythrocytes that were damaged to mimic senescence. These studies have demonstrated that acquisition of some specific individual senescence markers can trigger erythrophagocytosis by macrophages, but we hypothesized that the mechanism of erythrophagocytosis of such damaged erythrocytes might differ from erythrophagocytosis of physiologically aged erythrocytes. To test this hypothesis we generated an erythrocyte population highly enriched in senescent erythrocytes by a hypertransfusion procedure in mice. Various erythrocyte-aging signals were analyzed and erythrophagocytosis was evaluated in vivo and in vitro. The large cohort of senescent erythrocytes from hypertransfused mice carried numerous aging signals identical to those of senescent erythrocytes from control mice. Phagocytosis of fluorescently-labeled erythrocytes from hypertransfused mice injected into untreated mice was much higher than phagocytosis of labeled erythrocytes from control mice. However, neither erythrocytes from hypertransfused mice, nor those from control mice were phagocytosed in vitro by primary macrophage cultures, even though these cultures were able to phagocytose oxidatively damaged erythrocytes.\n\nQuestion:\nDo physiologically aged red blood cells undergo erythrophagocytosis in vivo but not in vitro?\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:\nLead was one of the most dangerous environmental toxic substances for a long time in western countries, and this is still the case for many places on earth today. Its neurotoxic potential is highly significant but its secure blood level concentration remains unknown. The aim of this study was to approach the above issue from the perspective of social psychiatry. A systematic search was made of Dialog and Datastar interfaces for data regarding the neuropsychiatric complications of direct or chronic exposure to lead, and a review of the relevant literature was conducted using the databases Medline, Embase, CAB Global Health and Cochrane. Lead affects the cholinergic, dopaminergic and gloutamergic systems, thus intervening in the normal function of neurotransmion. The consequence of neurotoxicity in the central nervous system includes apoptosis and excitotoxicity. Direct as well as chronic exposure causes serious neurological symptoms and possibly constant cognitive impairment. Acute encephalopathy, the most serious expression of lead poisoning, occurs in blood level concentrations over 100 μg/dL in adults and 80-100 μg/dL in children. Early symptoms of lead neurotoxicity include irritability, headaches and difficulties in concentration in both children and adults. Continuous exposure in children produces neurobehavioral symptoms, such as decreased concentration, inability to follow instructions, difficulty to play games and low IQ, which are associated with concentrations of 10-35 μg/dL. However, some studies claim that cognitive decline and low IQ can occur in concentrations <10 μg/dL. The commonest symptom in adults is peripheral neuropathy with foot drop. Prenatal exposure to lead has been correlated with antisocial behavior and schizophrenia. Long-term lead exposure causing low and medium lead concentration in blood has been linked to depression as well as generalized anxiety disorder and other behavioral disorders. High blood level concentrations correlate with psychotic symptoms like delusions and hallucinations but more rarely with psychotic syndromes. Despite the fact that lead has been banned from gasoline, paint and water pipes, quite significant quantities of lead still exist, particularly in deprived areas of modern cities, in transition zones and city centers, and there are also great concentrations around lead mines and in developing countries, but even for the remaining areas there is no safe threshold.\n\nQuestion:\nIs there no safe threshold for lead exposure : Α literature review?\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 determine whether LR11 (low-density lipoprotein receptor with 11 binding repeats) is a potential key regulator of smooth muscle cell (SMC) proliferation during the progression of hypoxia-induced medial thickening in mice and whether sLR11 (soluble LR11) can serve as a biomarker in patients with pulmonary arterial hypertension. The role of LR11 in pulmonary arterial hypertension was investigated using mouse and cell models of induced hypoxia. The expression of LR11 and of hypoxia-inducible factor-1α was significantly increased in lung tissues from C57Bl/6 mice after 3 weeks of exposure to hypoxia compared with normoxia. Serum sLR11 levels were also increased. Physiological and histochemical analyses showed that increased right ventricular systolic pressure, right ventricular hypertrophy, and medial thickening induced under hypoxia in wild-type mice were attenuated in LR11(-/-) mice. The proliferation rates stimulated by hypoxia or platelet-derived growth factor-BB were attenuated in SMC derived from LR11(-/-) mice, compared with those from wild-type mice. Exogenous sLR11 protein increased the proliferation rates of SMC from wild-type mice. The expression of LR11 and hypoxia-inducible factor-1α was increased in cultured SMC under hypoxic conditions, and hypoxia-inducible factor-1α knockdown almost abolished the induction of LR11. Serum sLR11 levels were significantly higher in patients with, rather than without, pulmonary arterial hypertension. sLR11 levels positively correlated with pulmonary vascular resistance and mean pulmonary arterial pressure.\n\nQuestion:\nDoes deletion of LR11 attenuate Hypoxia-Induced Pulmonary Arterial Smooth Muscle Cell Proliferation With Medial Thickening 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:\nTreatment with TNF inhibitors is very efficient in the majority of the patients with rheumatoid arthritis (RA), but it does not achieve a sufficient treatment response in 40-50% of the cases. Goal of the study was to assess functional ex vivo-tests of RA monocytes as prognostic parameters of the subsequent treatment response. 20 anti-TNF naïve RA patients were enrolled in a prospective, open-label trial, and Etanercept therapy was initiated. Prior to treatment, reverse signaling was induced in peripheral blood monocytes by tmTNF crosslinking via TNFR2:Ig construct Etanercept in a standardized ex vivo-assay. Released cytokine and cytokine receptor concentrations were determined as parameters of the monocyte response. Crosslinking of tmTNF and consecutive reverse signaling led to production of pro- and anti-inflammatory cytokines and of soluble cytokine decoy receptors such as sTNFR1 and sIL-1R2. Several of the measured concentrations were found to correlate with the treatment response according to the EULAR criteria. The correlation was most pronounced in sTNFR1 concentrations (r = -0.657, p = 0.0031), which also predicted a good clinical response with the highest sensitivity and specificity according to EULAR criteria.\n\nQuestion:\nDoes in vitro response pattern of monocytes after tmTNF reverse signaling predict response to anti-TNF therapy in rheumatoid arthritis?\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 role of intracerebroventricular (icv) injection substance P(SP) in cardiovascular regulation and the relationship with noradrenergic system. Rabbits anesthetized with urethane were intracerebroventricularly given SP in presence or absence of phentolamine, prazosin, yohimbine. Cardiovascular responses including heart rate (HR), mean arterial blood pressure (MAP), left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP), the maximum velocity of ascending or descending in intraventricular pressure (+/- dp/dt(max)) and the maximum shortening velocity(Vpm) of myocardial contractile element were recorded, and changes of NA content in cerebrospinal fluid (CSF) were determined in rabbits with icy injection of SP. (1) icv SP elicited significant increased of HR, MAP, LVSP, LVEDP, + dp/dt(max), -dp/dt(max), Vpm and the levels of NA in intracisternal CSF 30 min after injection. (2) Pretreatment with phentolamine, prazosin, but not yohimbine, attenuated icv SP-induced cardiovascular responses compared with controls (P < 0.05).\n\nQuestion:\nIs [ Noradrenaline involved in cardiovascular responses induced by intracerebroventricular injection substance P in rabbits ]?\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:\nHypertension induces end-organ damage through inflammation, and autophagy plays a crucial role in the regulation of cellular homeostasis. In the present study, we aimed to define the role of autophagy in the development of inflammation and cardiac injury induced by angiotensin II (Ang II). Autophagy protein 5 (Atg5) haplodeficiency (Atg5(+/-)) and age-matched wild-type (WT) C57BL/6J mice were infused with Ang II (1500 ng/kg/min) or saline for 7 days. Heart sections were stained with hematoxylin and eosin (H&E), Masson's trichrome, and immunohistochemical stains. Cytokine and LC3 levels were measured using real-time PCR or western blot analysis. After Ang II infusion, the WT mice exhibited marked macrophage accumulation, cytokine expression, and reactive oxygen species (ROS) production compared with saline-infused controls. However, these effects induced by Ang II infusion were aggravated in Atg5(+/-) mice. These effects were associated with Atg5-mediated impaired autophagy, accompanied by increased production of ROS and activation of nuclear factor-κB (NF-κB) in macrophages. Finally, increased cardiac inflammation in Atg5 haplodeficient mice was associated with increased cardiac fibrosis.\n\nQuestion:\nDoes atg5 deficiency-mediated mitophagy aggravate cardiac inflammation and injury in response to angiotensin II?\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:\np27(Kip1)(p27) is a universal cyclin-dependent kinase inhibitor that inhibits cell cycle transition from G(1) to S phase and is primarily regulated at the post-transcriptional level via the ubiquitin-proteasome pathway. In vitro data suggest that p27 degradation may be accelerated by the c-Jun activation domain binding protein-1 (JAB1), originally identified as a coactivator of the gene regulatory AP-1 proteins. We assessed p27 and JAB1 in systemic anaplastic large cell lymphoma (ALCL), a group of tumors in which a substantial subset overexpresses anaplastic lymphoma kinase (ALK). The study included 5 ALK-positive ALCL cell lines, namely Karpas 299, JB-6, SR-786, SU-DHL1, and TG-S1, and 66 ALCL tumors (24 ALK positive and 42 ALK negative). The cell lines were analyzed by Western blot methods, and the tumors were assessed immunohistochemically. SU-DHL1 and TG-S1 cells were positive for p27 and negative for JAB1, whereas SR-786 and JB-6 cells were positive for JAB-1 but negative for p27. Karpas 299 expressed p27 at relatively low levels and JAB1 at high levels. Using a 10% cutoff, p27 was positive in 12 of 66 (18.2%) ALCL tumors (5 ALK positive and 7 ALK negative), whereas JAB1 was detected in 47 of 53 (88.7%) tumors (15 ALK positive and 32 ALK negative) assessed. p27 and JAB1 expression were inversely correlated (Spearman r = -0.27, P = 0.03). For 54 ALCL patients with complete follow-up, and in separate analyses of patients with ALK-positive or -negative tumors, p27 expression correlated with poorer prognosis.\n\nQuestion:\nAre expression of p27 ( Kip1 ) and c-Jun activation binding protein 1 inversely correlated in systemic anaplastic large cell lymphoma?\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:\nSuccessful treatment of melanoma depends on early diagnosis, but its varied clinical presentation means that no single noninvasive method or criterion can provide reliable detection in all cases. To determine whether combining sequential dermoscopy imaging with reflectance confocal microscopy (RCM) can improve melanoma detection and reduce the burden of unnecessary excisions. We conducted a retrospective study with median follow-up of 25 months. We included equivocal pigmented lesions that lacked clear dermoscopy criteria for melanoma at baseline but were excised subsequently because of changes during digital monitoring. RCM imaging was performed before excision. Main melanoma dermoscopy features, seven-point checklist score at baseline, and changes in structure and/or colour, and development of new melanoma-specific criteria at follow-up (scored as major, moderate or minor) were considered. Main melanoma RCM criteria were evaluated and diagnosis was made. Histopathological diagnosis was the reference standard for defining parameter frequency and diagnostic accuracy. Seventy lesions were included. Major changes were more frequently correlated with melanoma diagnosis, although one-third (four of 12) of melanomas showed moderate or minor changes. Cytological atypia and architectural disarrangement on RCM were correlated with melanoma diagnosis. A correct melanoma diagnosis was achieved with RCM in almost all cases (11 of 12, 92%). Referring for excision only those lesions with RCM-positive features and/or presenting major changes at digital dermoscopy follow-up, theoretically 27 of 58 naevi could be saved from surgery.\n\nQuestion:\nDoes integration of reflectance confocal microscopy in sequential dermoscopy follow-up improve melanoma detection accuracy?\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 study how common personality disorders (PDs) are among employed subjects with first-episode depression. Depression is the single most common cause of working disability in Finland. Personality disorders are associated with depression. Subjects were screened using the Beck Depression Inventory scale, with a cutoff point greater than 9. The structured clinical interview for Diagnostic and Statistical Manual, fourth revision, was used to assess mental disorders. Inclusion criterion was major depressive disorder. Most of the 272 participants were female (83%) and the majority (74%) were older than 40 years. The main finding was that one third of the participants had obsessive-compulsive PD. The prevalence of obsessive-compulsive PD was 50% among men and 28% in women.\n\nQuestion:\nIs obsessive-compulsive personality disorder common among occupational health care clients with depression?\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 local delivery of paclitaxel onto a graft has been reported to prevent neointimal hyperplasia. Because more than half of vascular stenoses occur within 3 cm of the venous anastomosis, this study tested the effectiveness of a paclitaxel coating restricted to both ends of the expanded polytetrafluoroethylene (ePTFE) graft to reduce the amount of drug delivered. Both ends of ePTFE grafts were coated with paclitaxel at a dose of 0.58 μg/mm(2); the total amount of paclitaxel per graft was 0.66 mg. Paclitaxel-coated hemodialysis grafts 15 cm in length were surgically implanted between the common carotid artery and external jugular vein in female Landrace pigs. The animals were sacrificed 6 weeks after graft placement. Cross sections of the anastomosis sites were analyzed histomorphometrically to measure the ratio of neointimal hyperplasia to the graft area (H/G ratio) and the percentage of luminal stenosis. The experimental results were compared between grafts coated with paclitaxel at the ends only (n = 8), grafts coated over the entire length (n = 6), and uncoated control grafts (n = 6). The mean ± standard error values of the H/G ratios for the arterial anastomosis were 0.82 ± 0.13 (control), 0.41 ± 0.09 (terminal coating), and 0.21 ± 0.04 (whole coating). The values for the venous anastomosis were 0.82 ± 0.12 (control), 0.39 ± 0.11 (terminal coating), and 0.12 ± 0.03 (whole coating). Compared with the uncoated grafts, neointimal hyperplasia was suppressed effectively in the vascular grafts coated terminally with paclitaxel (artery, P = 050; vein, P < .001). However, the suppressive effect was less than that of grafts coated with paclitaxel over the entire length. The percentages of luminal stenosis showed similar tendency to the H/G ratios.\n\nQuestion:\nDoes paclitaxel coating on the terminal portion of hemodialysis grafts effectively suppress neointimal hyperplasia in a porcine model?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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