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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:\nDespite the effective use of antibiotics, occurrences of mortality and neurological sequelae following Streptococcus pneumoniae meningitis remain high. We investigated the neurogenesis of endogenous neural stem cells (NSCs) after inoculation with exogenous brain-derived neurotrophic factor (BDNF) in the hippocampus dentate gyrus following experimental S. pneumoniae meningitis using a double-labeling immunofluorescence analysis with 5-bromo-2'-deoxyuridine (BrdU), Nestin, DCX and NeuN. Our results showed that 7days after inoculation, the number of BrdU & Nestin co-labeled cells increased in the hippocampus in meningitis rats compared with control rats (p<0.05). But the number of DCX-positive cells decreased in the dentate gyrus of infected rats treated with saline (p<0.05). However, these cell numbers returned to close to normal-control levels in infected rats treated with BDNF (p>0.05). After treatment with exogenous BDNF, the number of BrdU & Nestin co-labeled cells increased in the hippocampus in both the meningitis rats and normal control rats (p<0.05), but this increase was more significant in the former (p<0.05). We found that the percentage of BrdU & DCX/BrdU co-labeled cells increased in infected rats treated with BDNF both 7days and 14days after inoculation in a greater proportion compared to other groups (p<0.05). No significant differences were found in the percentage of BrdU & NeuN/BrdU 28days after inoculation among all of the groups (p>0.05).\n\nQuestion:\nDoes exogenous BDNF increase neurogenesis in the hippocampus in experimental Streptococcus pneumoniae meningitis?\n\nAnswer:",
"role": "user"
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"content": "yes",
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe incidence of colorectal cancer increases with vitamin D deficiency as shown in recently published studies. In addition, prospective investigations have indicated that low vitamin D levels may be associated with increased mortality of colorectal cancer, especially in stage III and IV cases. However, the exact incidence of vitamin D deficiency and the relation between vitamin D deficiency and osteopenia/osteporosis is still not known. The aim of this study is to identify severity of vitamin D deficiency and absolute risk factors of osteopenia/osteoporosis in colorectal cancer survivors. A total of 113 colorectal cancer survivors treated with surgery and/or chemotherapy ± radiotherapy were recruited from medical oncology outpatient clinics during routine follow-up visits in 2012-2013. Bone mineral densitometry (BMD) was performed, and serum 25-OH vitamin D levels were also checked on the same day of the questionnaire. The patients was divided into 2 groups, group A with normal BMD and group B with osteopenia/osteoporosis. The median age of the study population was 58 (40-76). Thirty (30.0%) were female, whereas 79 (70.0%) were male. The median follow-up was 48 months (14-120 months). Vitamin D deficiency was found in 109 (96.5%); mild deficiency (20-30 ng/ml) in 19 (16.8%), moderate deficiency (10-20 ng/ml) in 54 (47.8%) and severe deficiency (<10 ng/ml) in 36 (31.9%). Osteopenia was evident in 58 (51.4%) patients whereas osteoporosis was noted in 17 (15.0%) . Normal BMD was observed in 38 (33.6%). No apparent effects of type of surgery, presence of stoma, chemotherapy, radiotherapy and TNM stage were found regarding the risk of osteopenia and osteoporosis. Also, the severity of the vitamin D deficiency had no effect in the risk of osteopenia and osteporosis (p=0.93). In female patients, osteopenia/osteoporosis were observed in 79.5% patients as compared to 60.7% of male patients (p=0.04).\n\nQuestion:\nIs serum 25-hydroxy vitamin D status related to osteopenia/osteoporosis risk in colorectal cancer survivors?\n\nAnswer:",
"role": "user"
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{
"content": "no",
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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:\nAcute hypotension may be implicated in cognitive dysfunction. L-type calcium channel blockers in the setting of hypoxia are protective of learning and memory. We tested the hypothesis that hypotension induced by nimodipine (NIMO) and nicardipine (NICA) would be protective of long- and short-term memory compared to hypotension induced by nitroglycerin (NTG). Forty Swiss-Webster mice (30 to 35 g, 6 to 8 weeks) were randomized into 4 groups for i.p. injection immediately after passive avoidance (PA) learning on day 0: (1) NTG (30 mg/kg); (2) NICA (40 mg/kg); (3) NIMO (40 mg/kg); and (4) saline. PA training latencies (seconds) were recorded for entry from a suspended platform into a Plexiglas tube where a shock (0.3 mA; 2-second duration) was automatically delivered. On day 2 latencies were recorded during a testing trial during which no shock was delivered. Latencies >900 seconds were assigned this value. Lower testing latency is indicative of an impairment of long-term associative memory. Forty-nine additional mice were randomized into similar groups for object recognition testing (ORT) and given i.p. injections on day 0. ORT measures short-term memory by exploiting the tendency of mice to prefer novel objects where a familiar object is present. On day 5 during training, 2 identical objects were placed in a circular arena and mice explored both for 15 minutes. A testing trial was conducted 1 hour later for 3 minutes after a novel object replaced a familiar one. Mice with intact memory spend about 65% of the time exploring the novel object. Mice with impaired memory devote equal time to each object. Recognition index (RI) is defined as the ratio of time spent exploring the novel object to time spent exploring both objects was the measure of memory. Mean arterial blood pressure (MAP), cerebral bloodflow, and body and brain oxygenation (PO(2)) studies were done in separate groups of mice to determine the dosages for matched degrees of hypotension and the physiological profile of each treatment. The median PA latencies for the different conditions were as follows: NTG (219.5 ± 93.5 second semi-interquartile range [SIQR]), NICA (372.5 ± 75.5 second SIQR), NIMO (540 ± 200 second SIQR) and saline (804 ± 257.5 second SIQR). Rank methods were used to analyze the PA latencies for significant differences. NTG latency was significantly shorter than NIMO latency (P = 0.012) and saline latency (P = 0.006), but not NICA latency (P = 0.126). ORT RI values showed a similar pattern. We found that NTG RI (47.2 ± 5.9% SEM) was different from NIMO RI (60.2 ± 4.6% SEM, P = 0.031) and different from saline RI (66.9 + 3.7% SEM, P = 0.006). Physiological experiments showed that MAP decreased to 45 to 50 mm Hg in all animals who became minimally responsive to external stimuli within 10 to 15 minutes of injection. Intergroup differences for MAP, body and brain oxygenation, and cerebral bloodflow were not statistically significant.\n\nQuestion:\nDoes nimodipine-induced hypotension but not nitroglycerin-induced hypotension preserve long- and short-term memory in adult 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:\nWe have developed a transgenic mouse with cardiac-restricted overexpression of tumor necrosis factor-alpha (TNF-alpha). These mice develop a heart failure phenotype characterized by left ventricular dysfunction and remodeling, pulmonary edema, and elevated levels of TNF-alpha in the peripheral circulation from cardiac spillover. Given that TNF-alpha causes atrophy and loss of function in respiratory muscle, we asked whether transgenic mice developed diaphragm dysfunction and whether contractile losses were caused by oxidative stress or tissue remodeling. muscles excised from transgenic mice and littermate controls were studied in vitro with direct electrical stimulation. Cytosolic oxidant levels were measured with 2', 7'-dichlorofluorescin diacetate; emissions of the oxidized product were detected by fluorescence microscopy. Force generation by the diaphragm of transgenic animals was 47% less than control (13.2+/-0. 8 [+/-SEM] versus 25.1+/-0.6 N/cm(2); P:<0.001); this weakness was associated with greater intracellular oxidant levels (P:<0.025) and was partially reversed by 30-minute incubation with the antioxidant N:-acetylcysteine 10 mmol/L (P:<0.01). Exogenous TNF-alpha 500 micromol/L increased oxidant production in diaphragm of wild-type mice and caused weakness that was inhibited by N:-acetylcysteine, suggesting that changes observed in the diaphragm of transgenic animals were mediated by TNF-alpha. There were no differences in body or diaphragm weights between transgenic and control animals, nor was there evidence of muscle injury or apoptosis.\n\nQuestion:\nDoes cardiac-specific overexpression of tumor necrosis factor-alpha cause oxidative stress and contractile dysfunction in mouse diaphragm?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe etiology and pathogenesis of angiogenesis in idiopathic pulmonary fibrosis (IPF) is poorly understood. Inter-alpha-trypsin inhibitor (IaI) is a serum protein that can bind to hyaluronan (HA) and may contribute to the angiogenic response to tissue injury. To determine whether IaI promotes HA-mediated angiogenesis in tissue injury. An examination was undertaken of angiogenesis in IaI-sufficient and -deficient mice in the bleomycin model of pulmonary fibrosis and in angiogenesis assays in vivo and in vitro. IaI and HA in patients with IPF were examined. IaI significantly enhances the angiogenic response to short-fragment HA in vivo and in vitro. lal deficiency Ieads to decreased angiogenesis in the matrigel model, and decreases lung angiogenesis after bleomycin exposure in mice. IaI is found in fibroblastic foci in IPF, where it colocalizes with HA. The colocalization is particularly strong in vascular areas around fibroblastic foci. Serum levels of IaI and HA are significantly elevated in patients with IPF compared with control subjects. High serum IaI and HA levels are associated with decreased lung diffusing capacity, but not FVC.\n\nQuestion:\nDo serum inter-alpha-trypsin inhibitor and matrix hyaluronan promote angiogenesis in fibrotic lung injury?\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:\nAllergen-specific TH2 responses contribute to the development of allergic asthma. Their increase may be due to a reduced early exposure to environmental pathogens, which induces a TH1 response, and thereby suppresses the allergic TH2 response. QbG10 (bacteriophage Qbeta-derived virus-like particle with CpG-motif G10 inside), a novel Toll-like receptor 9 agonist packaged into virus-like particles, was designed to stimulate the immune system toward a TH1-mediated protective response. We examined clinical efficacy, safety, and tolerability of QbG10 with patient-reported and objective clinical outcome parameters in patients with mild-to-moderate persistent allergic asthma. In this proof-of-concept parallel-group, double-blind, randomized trial, 63 asthmatic patients followed conversion to a standardized inhaled steroid and were treated with 7 injections of either QbG10 or placebo. Incorporating a controlled steroid withdrawal, the effects on patient-reported (day- and nighttime asthma symptoms, salbutamol usage, and 7-item-Asthma Control Questionnaire scores) and objective clinical outcome measures (FEV1, fraction of exhaled nitric oxide, and blood eosinophils) were assessed over 12 weeks (ClinicalTrials.gov number, NCT00890734). All patient-reported parameters improved overall between week 0 and 12 in QbG10-treated patients (n = 33) despite steroid withdrawal, compared with deteriorations observed under placebo (n = 30, P < .05). At week 12, two thirds of the QbG10-treated patients had their asthma \"well controlled\" (Asthma Control Questionnaire score ≤0.75) compared with one third under placebo. FEV1 had worsened to a clinically significant extent in patients on placebo, while it remained stable in QbG10 patients. Adverse events were mostly injection site reactions occurring after QbG10 administration.\n\nQuestion:\nDoes the novel TLR-9 agonist QbG10 show clinical efficacy in persistent allergic asthma?\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:\nFusarium head blight (FHB) caused by Fusarium graminearum not only causes severe losses in yield, but also reduces quality of wheat grain by accumulating mycotoxins. Breeding for host plant resistance is considered as the best strategy to manage FHB. Resistance in wheat to FHB is quantitative in nature, involving cumulative effects of many genes governing resistance. The poor understanding of genetics and lack of precise phenotyping has hindered the development of FHB resistant cultivars. Though more than 100 QTLs imparting FHB resistance have been reported, none discovered the specific genes localized within the QTL region, nor the underlying mechanisms of resistance. In our study recombinant inbred lines (RILs) carrying resistant (R-RIL) and susceptible (S-RIL) alleles of QTL-Fhb2 were subjected to metabolome and transcriptome profiling to discover the candidate genes. Metabolome profiling detected a higher abundance of metabolites belonging to phenylpropanoid, lignin, glycerophospholipid, flavonoid, fatty acid, and terpenoid biosynthetic pathways in R-RIL than in S-RIL. Transcriptome analysis revealed up-regulation of several receptor kinases, transcription factors, signaling, mycotoxin detoxification and resistance related genes. The dissection of QTL-Fhb2 using flanking marker sequences, integrating metabolomic and transcriptomic datasets, identified 4-Coumarate: CoA ligase (4CL), callose synthase (CS), basic Helix Loop Helix (bHLH041) transcription factor, glutathione S-transferase (GST), ABC transporter-4 (ABC4) and cinnamyl alcohol dehydrogenase (CAD) as putative resistance genes localized within the QTL-Fhb2 region.\n\nQuestion:\nDoes integrated Metabolo-Transcriptomics reveal Fusarium Head Blight Candidate Resistance Genes in Wheat QTL-Fhb2?\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:\nAssociation between lymphocyte-sensitivity to immunosuppressants in transplant recipients in vitro and clinical outcomes has been demonstrated. In general, renal transplant recipients are treated with a combination of immunosuppressants such as either glucocorticoid/cyclosporin A (CsA) or glucocorticoid/tacrolimus (FK506) but the pharmacological complementarity of these drugs is still controversial. We examined relationships between the lymphocyte-sensitivities to these immunosuppressants. We examined lymphocyte-sensitivities to prednisolone (PSL), CsA, and FK506 in vitro in a total of 190 chronic renal failure (CRF) patients and 140 healthy subjects. The lymphocyte-sensitivity was evaluated from the IC50 value against mitogen-stimulated lymphocyte-blastogenesis in vitro. Statistically significant correlations of the IC50 values in CRF patients between the following pairs of drugs were observed: PSL and CsA (P<0.0001; n=129, r=0.419), PSL and FK506 (P<0.001; n=54, r=0. 441), and CsA and FK506 (P<0.0001; n=45, r=0.608). Similar correlations were also observed in lymphocytes from healthy subjects. The population of CRF patients who exhibited high IC50 values (low sensitivities) to PSL and FK506 was significantly larger than that of healthy subjects (P<0.05).\n\nQuestion:\nDoes lymphocyte-sensitivity to glucocorticoid correlate with the sensitivity to cyclosporin A and tacrolimus in chronic renal failure 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:\nIn liver regeneration, quiescent hepatocytes need to be primed before they can fully respond to growth factors such as hepatocyte growth factor (HGF). Recently, interleukin-6 (IL-6) has been shown to play an important role in initiating liver regeneration via activating signal transducer and activator of transcription 3 (STAT3). We therefore investigated the effect of IL-6 on liver regeneration and examined STAT3 activation following IL-6 and/or HGF treatment in rats. The animals underwent portal branch ligation (PBL) of the left lateral and median branches. They were intravenously treated with either IL-6 (500 microg/kg), HGF (50 microg/kg), both, or vehicle alone on and every 12 h after PBL. The degree of compensatory hypertrophy in unoccluded lobes was examined by measuring the wet weight ratios of the unoccluded lobes to the whole liver and the 5-bromo-2'-deoxyuridine labeling index of hepatocytes in each group. STAT3 expression in regenerating liver was examined by Western blotting and immunohistochemistry. Coadministration of IL-6 and HGF most effectively increased both the wet weight of the unoccluded lobes and the hepatocellular DNA synthesis. HGF as well as IL-6-treated animals showed moderate STAT3 activation in hepatocytes throughout the experiment.\n\nQuestion:\nDoes interleukin-6 augment hepatocyte growth factor-induced liver regeneration ; involvement of STAT3 activation?\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 signs and symptoms of ischemia and no obstructive coronary artery disease often have coronary microvascular dysfunction (CMD), diagnosed by invasive coronary reactivity testing (CRT). Although traditional noninvasive stress imaging is often normal in CMD, cardiac MRI may be able to detect CMD in this population. Vasodilator stress cardiac MRI was performed in 118 women with suspected CMD who had undergone CRT and 21 asymptomatic reference subjects. Semi-quantitative evaluation of the first-pass perfusion images was completed to determine myocardial perfusion reserve index (MPRI). The relationship between CRT findings and MPRI was examined by Pearson correlations, logistic regression, and sensitivity/specificity. Symptomatic women had lower mean pharmacological stress MPRI compared with reference subjects (1.71±0.43 versus 2.23±0.37; P<0.0001). Lower MPRI was predictive of ≥1 abnormal CRT variables (odds ratio =0.78 [0.70, 0.88], P<0.0001, c-statistic 0.78 [0.68, 0.88]). An MPRI threshold of 1.84 predicted CRT abnormality with sensitivity 73% and specificity 74%.\n\nQuestion:\nIs cardiac magnetic resonance myocardial perfusion reserve index reduced in women with coronary microvascular dysfunction . A National Heart , Lung , and Blood Institute-sponsored study from the Women 's Ischemia Syndrome Evaluation?\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 study the adaptive potential of the right ventricular myocardium after 30 days of mechanical-induced overload in rats from two different age groups. We banded the pulmonary trunk, so as to increase the systolic work load of the right ventricle, in 19 adult Sprague-Dawley rats at the age of 10 weeks, and 16 weanlings when they were 3 weeks-old, using 10 adults and 10 weanlings as controls. We analysed the functional adaptation and structural changes of the right ventricular myocardium, blood vessels and interstitial tissue after 30 days of increased afterload. The increased workload induced an increase of the right ventricular weight and free wall thickness in animals from both age groups when compared to controls. These changes were mostly related to cardiomyocytic hypertrophy, as confirmed by the expression of myocardial hypertrophic markers, without any apparent increase of their number, a \"reactive\" fibrosis especially evident in the adult rats, with p-value less than 0.0001, and a more extensive neocapillary network in the weanlings compared to the adults aubsequent to banding, the p-value being less than 0.0001.\n\nQuestion:\nIs age a risk factor for maladaptive changes in rats exposed to increased pressure loading of the right ventricular myocardium?\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:\nRodents express two isoforms of the angiotensin II type 1 (AT(1)) receptor: AT(1A) and AT(1B). It is unclear which receptor subtype mediates contraction in response to angiotensin II in various arteries. We tested the hypothesis that the AT(1B) receptor is the predominant receptor that mediates contraction in the abdominal aorta in response to angiotensin II. Isometric tension responses to angiotensin II were determined in abdominal aortic rings obtained from male wild-type and AT(1B) receptor knockout mice. The rings were suspended in an organ bath of a wire myograph and contractions to angiotensin II and other vasoconstrictors were determined. Angiotensin II contracted aortic segments from wild-type mice; however, this response was virtually absent in rings obtained from AT(1B) receptor knockout mice. Contractions in response to K(+) and U46619 (thromboxane A(2) mimetic) were not different between rings obtained from wild-type and AT(1B) receptor knockout mice.\n\nQuestion:\nDo knockout mice reveal that the angiotensin II type 1B receptor links to smooth muscle contraction?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe aim of this study was to compare the effects of pulmonary rehabilitation (PR) on six-minute walk test (6mWT) between chronic obstructive pulmonary disease (COPD) patients with moderate or severe carbon monoxide diffusion defects. We also evaluated dyspnea sensation, pulmonary functions, blood gases analysis, quality of life parameters and psychological symptoms in both groups before and after pulmonary rehabilitation. Patients with COPD underwent a comprehensive 8-week out-patient PR program participated in this study. Patients grouped according to diffusion capacity as moderate or severe. Outcome measures were exercise capacity (6mWT), dyspnea sensation, pulmonary function tests, blood gases analysis, quality of life (QoL) and psychological symptoms. A total of 68 patients enrolled in the study. Thirty-two (47%) of them had moderate diffusion defect [Tl\n\nQuestion:\nDo cOPD patients with severe diffusion defect in carbon monoxide diffusing capacity predict a better outcome for pulmonary rehabilitation?\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:\nGlutamine (GLN) treatment prior to gut ischemia-reperfusion (I/R) reportedly preserves gut glutathione levels and gut barrier function. We hypothesized that intraluminal GLN during ischemia would also protect against gut I/R. After randomization to control and GLN groups, mice were exposed to 75 min (Exp 1) or 50 min (Exp 2 and 3) gut I/R. One mL of 2% GLN solution was injected into the duodenal lumen at the onset of ischemia in the GLN group, whereas controls were given normal saline. In experiment 1, survival was monitored for 120 h (n = 38). In experiment 2, blood, small intestine, and liver samples were collected at 4 h after reperfusion (n = 13). Expressions of CD11a and CD11b on myeloid cells were measured. Reactive oxygen intermediate production by myeloid cells was determined with or without phorbol myristate acetate stimulation. Glutathione levels in the small intestine and liver were also evaluated. In experiment 3, hemodynamic parameters were measured before and after I/R (n = 6). In experiment 1, survival time in the GLN group was reduced compared with the control group. In experiment 2, GLN increased expression of CD11b and reactive oxygen intermediate with phorbol myristate acetate, compared with controls. There were no significant differences in gut or liver glutathione levels between the two groups. In experiment 3, the GLN group showed a transient but significant reduction in systolic blood pressure after reperfusion compared with the control group.\n\nQuestion:\nDoes intraluminal glutamine administration during ischemia worsen survival after gut ischemia-reperfusion?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe decline of proteasomal activity is known to be associated with the age-related disorders but the early events involved in this process are not apparent. To address this, we investigated the early-age-related (pediatric vs. adult) mechanisms that augment immunopathogenesis of sepsis and acute lung injury. The 3-weeks (pediatric) and 6-months (adult) old C57BL/6 mice were selected as the study groups. Mice were subjected to 1×20 cecal ligation and puncture (CLP) mediated sepsis or intratracheal Psuedomonas aeruginosa (Pa)-LPS induced acute lung injury (ALI).We observed a significant increase in basal levels of pro-inflammatory cytokine, IL-6 and neutrophil activity marker, myeloperoxidase (MPO) in the adult mice compared to the pediatric indicating the age-related constitutive increase in inflammatory response. Next, we found that age-related decrease in PSMB6 (proteasomal subunit) expression in adult mice results in accumulation of ubiquitinated proteins that triggers the unfolded protein response (UPR). We identified that Pa-LPS induced activation of UPR modifier, p97/VCP (valosin-containing protein) in the adult mice lungs correlates with increase in Pa-LPS induced NFκB levels. Moreover, we observed a constitutive increase in p-eIF2α indicating a protective ER stress response to accumulation of ubiquitinated-proteins. We used MG-132 treatment of HBE cells as an in vitro model to standardize the efficacy of salubrinal (inhibitor of eIF2α de-phosphorylation) in controlling the accumulation of ubiquitinated proteins and the NFκB levels. Finally, we evaluated the therapeutic efficacy of salubrinal to correct proteostasis-imbalance in the adult mice based on its ability to control CLP induced IL-6 secretion or recruitment of pro-inflammatory cells.\n\nQuestion:\nDo early-age-related changes in proteostasis augment immunopathogenesis of sepsis and acute lung injury?\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 compare the effects of massage therapy (moderate pressure stroking) and exercise (flexion and extension of limbs) on preterm infants' weight gain and to explore potential underlying mechanisms for those effects. Weight gain and parasympathetic nervous system activity were assessed in 30 preterm infants randomly assigned to a massage therapy group or to an exercise group. Infants received 10min of moderate pressure massage or passive flexion and extension of the limbs 3 times per day for 5days, and EKGs were collected during the first session to assess vagal activity. Both massage and exercise led to increased weight gain. However, while exercise was associated with increased calorie consumption, massage was related to increased vagal activity.\n\nQuestion:\nIs preterm infant weight gain increased by massage therapy and exercise via different underlying 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:\nLow-power helium-neon (He-Ne) lasers have been increasingly widely applied in the treatment of cardiovascular diseases, and its vasodilation effect has been proven. The aim of this study was to determine the effects of low-power He-Ne laser irradiation directed at the precardial region of Wistar rats on capillary permeability in the myocardium and the expression of myocardial vascular endothelial growth factor (VEGF). Sixteen rats were divided randomly into control and irradiated groups (n = 8, each). A He-Ne laser (632.8 nm) was applied to the irradiated group with a dose of 60.5 J/cm(2). Ferritin was perfused into the left femoral vein and capillary permeability was examined under an electron microscope. VEGF expression in the myocardium was investigated by immunohistochemical methods, RT-PCR, and image analysis. The ultrastructures of the myocardial capillaries were examined. Compared to the control group, more high-density granules (ferritin), which were present within the capillary endothelium and the mitochondrions of myocardial cells in the internal layer of the myocardium, were observed in the irradiated group. VEGF staining of the myocardium was stronger in the irradiated group than that in the control group. The optic density of the irradiated group (0.246 +/- 0.015) was significantly higher than that of the control group (0.218 +/- 0.012, P < 0.05). Finally, the levels of RT-PCR products of VEGF165 mRNA were 2.79 times higher in irradiated rats than in the control rats.\n\nQuestion:\nDoes low-power Helium-Neon laser irradiation enhance the expression of VEGF in murine myocardium?\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:\nFluid resuscitation can contribute to postshock inflammation and the development of end organ injury. We have previously observed an attenuation in pulmonary and ileal inflammation when hypertonic saline and pentoxifylline (HSPTX) were concomitantly administered after hemorrhage. We hypothesized that the attenuation in hepatic injury observed with HSPTX is associated with the reduction of transcription factor activation and proinflammatory mediator production when compared with Ringer's lactate (RL). Male Sprague-Dawley rats were resuscitated with racemic RL (32 mL/kg) or HSPTX (4 mL/kg 7.5% NaCl + PTX 25 mg/kg) and killed at 4 hours and 24 hours after resuscitation. Liver injury was determined by histology and serum aminotransferases. Nitrite, tumor necrosis factor-alpha, interleukin (IL)-1beta, and IL-6 were measured with enzyme-linked immunosorbent assay. High mobility group box 1, inducible nitric oxide synthase, nuclear factor (NF)-kappaB phosphorylation, and signal transducers and activators of transcription-3 phosphorylation were determined by Western blot. Transcription factor activation was verified with Electrophoretic Mobility Shift Assay. RL resuscitation led to significant increases all measured parameters when compared with control. In contrast, HSPTX did not induce elevations in histologic liver injury or alanine aminotransferase levels. HSPTX attenuated inducible nitric oxide synthase by 23% (p < 0.01), nitrite by 25% (p < 0.05), tumor necrosis factor-alpha by 25% (p < 0.05), IL-1 by 63% (p < 0.01), IL-6 by 35% (p < 0.05), and high mobility group box 1 by 39% (p < 0.05) when compared with RL. HSPTX reduced IkappaB-alpha phosphorylation by 34% (p < 0.05), NF-kappaB p65 phosphorylation by 75% (p < 0.01), and signal transducers and activators of transcription-3 phosphorylation by 52% (p < 0.01).\n\nQuestion:\nIs hepatic transcription factor activation and proinflammatory mediator production attenuated by hypertonic saline and pentoxifylline resuscitation after hemorrhagic shock?\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:\nNeonatal hypoxia-ischemia (HI) is a major cause of perinatal brain injury and is associated with a spectrum of neuropsychiatric disorders. Although very few treatment options are currently available, doxycycline (DOXY) has been reported to be neuroprotective in neontatal HI. Our objective was to investigate the effects of DOXY on neonatal brain development in normal and HI rat pups. We hypothesized that DOXY would inhibit microglial activation but that developmentally important processes, including cytogenesis and trophic responses, would not be impaired. To investigate the putative neurodevelopmental consequences of DOXY administration in a clinically relevant animal model of HI, we performed a time-course analysis such that postnatal rat pups received DOXY (10mg/kg) or vehicle immediately before HI (n >or= 6). We then assessed cytogenesis, proinflammatory cytokines, brain-derived neurotrophic factor (BDNF) and matrix metalloproteinases regionally and longitudinally. We found that DOXY significantly inhibits neuroinflammation in the frontal cortex, striatum and hippocampus; decreases interleukin-1Beta (IL-1Beta) and tumour necrosis factor-alpha (TNF-alpha); and augments BDNF following HI. In addition, DOXY-treated pups have significantly fewer 2-bromo-5-deoxyuridine (BrdU)-positive cells in the subventricular zone 6 hours post-HI. However, DOXY does not persistently affect cytogenesis in the subventricular zone or dentate gyrus up to 7 days post-HI. The BrdU-positive cells not expressing markers for mature neurons colabel with nestin, an intermediate filament protein typical of neuronal precursors.\n\nQuestion:\nDoes doxycycline inhibit proinflammatory cytokines but not acute cerebral cytogenesis after hypoxia-ischemia in neonatal rats?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 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:\nIndividuals with ulcerative colitis (UC) are at increased risk for colorectal cancer. The standard method of surveillance for neoplasia in UC by colonoscopy is invasive and can miss flat lesions. We sought to identify a gene expression signature in nondysplastic mucosa without active inflammation that could serve as a marker for remote neoplastic lesions. Gene expression was analyzed by complementary DNA microarray in 5 normal controls, 4 UC patients without dysplasia, and 11 UC patients harboring remote neoplasia. Common gene ontology pathways of significantly differentially expressed genes were identified. Expression of genes which were progressively and significantly upregulated from controls to UC without neoplasia, to UC with remote neoplasia were evaluated by real-time polymerase chain reaction. Several gene products were also examined by immunohistochemistry. Four hundred and sixty-eight genes were significantly upregulated, and 541 genes were significantly downregulated in UC patients with neoplasia compared with UC patients without neoplasia. Nine genes (ACSL1, BIRC3, CLC, CREM, ELTD1, FGG, S100A9, THBD, and TPD52L1) were progressively and significantly upregulated from controls to nondysplastic UC to UC with neoplasia. Immunostaining of proteins revealed increased expression of S100A9 and REG1α in UC-associated cancer and in nondysplastic tissue from UC patients harboring remote neoplasia compared with UC patients without neoplasia and controls.\n\nQuestion:\nDoes gene signature distinguish patients with chronic ulcerative colitis harboring remote neoplastic lesions?\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:\nTo evaluate the combined contribution of UCP3-55CT and PPARγ2 Pro12Ala polymorphisms as correlates of BMI, energy expenditure (REE) and substrate oxidation in people with type 2 diabetes. Two independent population with type 2 diabetes were studied: population A, n = 272; population B, n = 269. Based on both UCP3 and PPARγ2 genotypes three groups were created. Carriers of the PPARγ2 Pro12Ala in combination with the CC genotype of UCP3 (ProAla/CC, group 1); carriers of only one of these genotypes (either CC/ProPro or CT-TT/ProAla, group 2); people with neither variants (CT-TT/ProPro, group 3). In both populations BMI (kg/m(2)) was highest in group 1, intermediate in group 2 and lowest in group 3, independent of energy intake (i.e 35.3 ± 6.7 vs 33.4 ± 5.4 vs 31.8 ± 3, p < 0.02, population A; 32.4 ± 4.2 vs 31.7 ± 3.8 vs 30.1 ± 2.7; p < 0.03, population B). People with the ProAla/CC genotype (group 1) showed similar REE, but lower lipid oxidation (10.9 vs 13.9 g/kg fat free mass/day; p = 0.04) and higher carbohydrate oxidation (23.6 vs 15.6 g/kg fat free mass/day; p = 0.02) than carriers of other genotypes.\n\nQuestion:\nDoes the combination of UCP3-55CT and PPARγ2Pro12Ala polymorphisms affect BMI and substrate oxidation in two diabetic populations?\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:\nGraft survival in transplant recipients depends on pharmacokinetics and on individual susceptibility towards immunosuppressive drugs. Nevertheless, pharmacodynamic changes in T-cell functionality in response to drugs and in relation to pharmacokinetics are poorly characterized. We therefore investigated the immunosuppressive effect of calcineurin inhibitors and steroids on general T-cell functionality after polyclonal stimulation of whole blood samples. General T-cell functionality in the absence or presence of immunosuppressive drugs was determined in vitro directly from whole blood based on cytokine induction after stimulation with the polyclonal stimulus Staphylococcus aureus enterotoxin B. In addition, diurnal changes in leukocyte and lymphocyte subsets, and on T-cell function after intake of immunosuppressive drugs were analyzed in 19 patients during one day and compared to respective kinetics in six immunocompetent controls. Statistical analysis was performed using non-parametric and parametric tests. Susceptibility towards calcineurin inhibitors showed interindividual differences. When combined with steroids, tacrolimus led to more pronounced increase in the inhibitory activity as compared to cyclosporine A. While circadian alterations in leukocyte subpopulations and T-cell function in controls were related to endogenous cortisol levels, T-cell functionality in transplant recipients decreased after intake of the morning medication, which was more pronounced in patients with higher drug-dosages. Interestingly, calcineurin inhibitors differentially affected circadian rhythm of T-cell function, as patients on cyclosporine A showed a biphasic decrease in T-cell reactivity after drug-intake in the morning and evening, whereas T-cell reactivity in patients on tacrolimus remained rather stable.\n\nQuestion:\nDo calcineurin inhibitors differentially alter the circadian rhythm of T-cell functionality in transplant recipients?\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:\nExtrinsic innervation mediates a proabsorptive effect in small intestine. Our aim was to determine whether extrinsic neural input modulates similar effects in the proximal colon in vivo. Ten adult dogs underwent enteric isolation of a 50-cm proximal colon loop; five each were randomized to undergo extrinsic denervation (Ext Den) of the isolated colonic segment or to serve as neurally innervated controls. After recovery, a 38 degrees C electrolyte solution (Na(+) 125 meq/L, K(+) 9 meq/L, Cl(-) 75 meq/L, HC03(-) 65 meq/L) was infused at 4 ml/min into the segment. Effluent was collected in 30-min intervals for 2 h after achieving steady state (determined by 14C nonabsorbable marker recovery); four studies were conducted at 1 and 12 weeks postoperatively. Net flux of H20, Na(+), K(+), and Cl(-) was determined. Colon morphometry was evaluated at 0 and 14 weeks. Data are presented as mean +/- SEM. Unpaired t test was applied for comparisons. Net absorptive flux of H20 (microL/min/cm) was decreased in Ext Den vs controls at 1 week (4.40 +/- 0.63 vs 7.92 +/- 0.92, P = 0.03) but was not different at 12 weeks (4.70 +/- 1.20 vs 5.97 +/- 0.69; P > 0.05). Na(+) and Cl(-) followed the trends in H20 absorption (P < or = 0.05). Crypt depth (microm) decreased in controls at 14 weeks vs 0 week (915 +/- 20 vs 740 +/- 07, P = 0.01) but remained unchanged in Ext Den.\n\nQuestion:\nDoes extrinsic neural innervation mediate absorption of water and electrolytes in canine proximal colon in vivo?\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:\nSerotonin is a platelet agonist and potent vasoconstrictor that has recently received attention concerning its potential role in acute coronary artery thrombosis. Selective serotonin-reuptake inhibitors, such as paroxetine, are widely used antidepressant agents. We sought to characterize the potential inhibitory effect of paroxetine on platelet function. Healthy male volunteers received 20 mg/d paroxetine for 2 weeks in a randomized, double-blind, placebo-controlled, two-way cross-over trial. Paroxetine decreased intraplatelet serotonin concentrations by -83% (P < .01). This inhibited platelet plug formation as reflected by a 31% prolongation of closure time measured with the platelet function analyzer-100 (P < .05). Furthermore, paroxetine lowered expression of the platelet activation marker CD63 in response to two different concentrations of thrombin receptor-activating peptide (P < .01). Plasma concentrations of prothrombin fragment, von Willebrand factor antigen, and circulating P-selectin remained unchanged in either period, indicating that paroxetine does not increase activation of coagulation, endothelium, or platelets in vivo, underlining a favorable safety profile.\n\nQuestion:\nDoes paroxetine decrease platelet serotonin storage and platelet function in human beings?\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:\nThe Fat family of atypical cadherins, originally identified in Drosophila, play diverse roles during embryogenesis and adult tissue maintenance. Among four mammalian members, Fat1 is essential for kidney and muscle organization, and is also essential for eye development; Fat1 knockout causes partial penetrant microphthalmia or anophthalmia. To account for the partial penetrance of the Fat1 phenotype, involvement of Fat4 in eye development was assessed. Lens phenotypes in Fat1 and 4 knockouts were also examined. Fat1 and Fat4 mRNA expression was examined by in situ hybridization. Knockout phenotypes of Fat1 and Fat4 were analyzed by hematoxylin and eosin (H&E) and immunofluorescent staining. We found Fat4 knockout did not affect eye induction or enhance severity of Fat1 eye defects. Although Fat1 and Fat4 mRNAs are similarly expressed in the lens epithelial cells, only Fat1 knockout caused a fully penetrant lens epithelial cell defect, which was apparent at embryonic day 14.5 (E14.5). The columnar structure of the lens epithelial cells was disrupted and in some regions cell aggregates were formed. In these multilayered regions, apical cell junctions were fragmented and the apical-basal polarity was lost. EdU incorporation assay also showed enhanced proliferation in the lens epithelial cells. Interestingly, these defects were found mainly in the central zone of the epithelial layer. The lens epithelial cells of the germinative zone maintained their normal morphology and fiber differentiation occurred normally at the equator.\n\nQuestion:\nDoes atypical Cadherin Fat1 be Required for Lens Epithelial Cell Polarity and Proliferation but Not for Fiber Differentiation?\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:\nTo test the efficacy of maternal skin-to-skin contact, or kangaroo care (KC), on diminishing the pain response of preterm neonates to heel lancing. A crossover design was used, in which the neonates served as their own controls. Subjects Preterm neonates (n = 74), between 32 and 36 weeks' postmenstrual age and within 10 days of birth, who were breathing without assistance and who were not receiving sedatives or analgesics in 3 level II to III neonatal intensive care units in Canada. In the experimental condition, the neonate was held in KC for 30 minutes before the heel-lancing procedure and remained in KC for the duration of the procedure. In the control condition, the neonate was in the prone position in the isolette. The ordering of conditions was random. The primary outcome was the Premature Infant Pain Profile, which is composed of 3 facial actions, maximum heart rate, and minimum oxygen saturation changes from baseline in 30-second blocks. Videotapes, taken with the camera positioned on the neonate's face so that an observer could not tell whether the neonate was being held or was in the isolette, were coded by research assistants who were naïve to the purpose of the study. Heart rate and oxygen levels were continuously monitored into a computer for later analysis. A repeated-measures analysis of covariance was used, with order of condition and site as factors and severity of illness as a covariate. Premature Infant Pain Profile scores across the first 90 seconds from the heel-lancing procedure were significantly (.002<P<.04) lower by 2 points in the KC condition.\n\nQuestion:\nIs kangaroo care effective in diminishing pain response in preterm neonates?\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:\nPatients with persistently active hepatitis B virus (HBV) replication are at high risk for progression to liver cirrhosis and hepatocellular carcinoma (HCC). The influence of the viral load of HBV on intrahepatic recurrence after local ablation therapy in patients with HBV-related HCC has not been elucidated. We aimed to evaluate predictors of intrahepatic recurrence and clarify the correlation between viral load and intrahepatic recurrence after percutaneous ablation. Patients with HBV-related, solitary HCC undergoing radiofrequency ablation (RFA) or percutaneous ethanol injection (PEI), between October 2004 and December 2008 were prospectively enrolled. Statistical analyses were performed using the Kaplan-Meier method and Cox regression model to identify risk factors for intrahepatic recurrence. A total of 145 patients (male, 81.4%; mean age, 55.3 years) were included. Ninety patients (62.1%) had serum HBV DNA ≥2000 IU/mL. The median follow-up duration was 28.9 months (range, 12.0-57.0) and 63 patients (43.4%) experienced intrahepatic tumor recurrence. Multivariate analysis indicated that seropositivity for hepatitis B envelope antigen (HBeAg) was an independent negative predictor of intrahepatic recurrence (hazard ratio, 0.473; P=0.026) and late (≥1 year) recurrence (HR, 0.288; P=0.012). The serum alpha fetoprotein (AFP) level also significantly predicted late recurrence (HR, 1.001; P=0.005). However, neither the ablation method nor serum HBV DNA titers were correlated with intrahepatic recurrence.\n\nQuestion:\nDoes negative hepatitis B envelope antigen predict intrahepatic recurrence in hepatitis B virus-related hepatocellular carcinoma after ablation therapy?\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:\nA small decrease in the serum albumin from the normal level is a common condition in preoperative laboratory tests of colorectal surgery patients; however, there is limited data examining these patients. We sought to identify outcomes of such patients. The National Surgical Quality Improvement Program database was used to evaluate all patients who had modest levels of hypoalbuminemia (3 ≤ serum albumin < 3.5 g/dL) before colorectal resection from 2005 to 2012. Multivariate analysis using logistic regression was performed to quantify complications associated with modest hypoalbuminemia. A total of 108,898 patients undergoing colorectal resection were identified, of which 16,962 (15.6%) had modest levels of preoperative hypoalbuminemia. Postsurgical complications significantly associated (P < .05) with modest hypoalbuminemia were as follows: hospitalization more than 30 days (adjusted odds ratio [AOR], 1.77), deep vein thrombosis (AOR, 1.64), unplanned intubation (AOR, 1.42), ventilator dependency for more than 48 hours (AOR, 1.30), and wound disruption (AOR, 1.22).\n\nQuestion:\nDoes even modest hypoalbuminemia affect outcomes of colorectal surgery 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:\nQT dispersion has been used in stratifying risk for sudden death in adults with dilated cardiomyopathy, but its role in the pediatric population has not been delineated. We reviewed electrocardiograms in pediatric patients with dilated cardiomyopathy referred for heart transplantation, to evaluate the role of QT dispersion in predicting malignant arrhythmias in these patients. Three groups were defined: Group I (n = 13) had dilated cardiomyopathy and malignant ventricular arrhythmias, Group II (n = 13) had dilated cardiomyopathy with no ventricular arrhythmias and Group III (n = 30) consisted of normals. QT dispersion was defined as the duration of the shortest QT subtracted from that of the longest. In addition, the standard deviation of the QT intervals was calculated for each ECG, using 12 leads. QT dispersion was significantly prolonged in Group I (97 +/- 33 msec) compared to Group II (74 +/- 19 msec) and Group III (42 +/- 17 msec). QT standard deviation was also prolonged in Group I (30 +/- 11 msec) vs Group II (22 +/- 5 msec) and Group III (13 +/- 4 msec). Using a threshold value of 90 msec for QT dispersion or 25 msec for QT standard deviation, a sensitivity of 78% and a specificity of 70% was obtained for identifying patients who would subsequently develop ventricular arrhythmias.\n\nQuestion:\nDoes qT dispersion predict ventricular arrhythmia in pediatric cardiomyopathy patients referred for heart transplantation?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 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:\nEthanol (EtOH) affects glutamatergic neurotransmission and this may underlie craving in alcoholics. The present study aimed to further elucidate the EtOH-induced modulation of glutamatergic neurotransmission in a model for alcoholism: the alcohol-preferring cAA rat. Glutamate transporter binding and function was assessed in membrane and synaptosomal preparations from the cerebral cortex of alcohol-preferring cAA rats and alcohol-naive cAA rats. [3H]L-glutamate transport activity (Vmax) was 699 pmol.min-1.mg-1 in alcohol-naive cAA rats and 487 pmol.min-1.mg-1 in alcohol-preferring cAA rats. The specific binding sites (Bmax) for [3H]D-aspartate were markedly decreased in alcohol-preferring cAA rats (2059 pmol/mg) as compared to alcohol-naive cAA rats (4275 pmol/mg).\n\nQuestion:\nIs glutamate transport downregulated in the cerebral cortex of alcohol-preferring rats?\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 investigate the 30-day and 12-month mortality risks among hospitalized stroke patients according to compliance with guideline-based process indicators. We used data from the Second Stroke Audit and the Mortality Register of Catalonia (Spain). The audit retrospectively explored quality of stroke care based on compliance with indicators among patients discharged from all public hospitals in Catalonia in 2007; they were identified and selected through a pre-established sampling method. The magnitude of the independent association of each indicator with 30-day and 12-month mortality was assessed using logistic regression with generalized estimating equations to account for clustering of patients within hospitals. Generalized estimating equations modeling was initially restricted to patients alive >72 hours poststroke to control for confounding by severity. Analyses were also run in 3 other samples (all patients, patients alive >7 days, and patients alive >14 days). Of 1767 stroke admissions in the Second Stroke Audit, 1697 patients survived >72 hours poststroke. Within this sample, the adjusted 30-day mortality risk was negatively associated with nonadherence to different indicators, of which only antithrombotics at discharge (OR, 4.3; 95% CI, 1.72-10.78) remained significant in all data sets. At 12 months, the adjusted mortality risk was negatively associated with management of hypertension (OR, 1.87; 95% CI, 1.22-2.86) and antithrombotics at discharge (OR, 2.79; 95% CI, 1.41-5.54). Both remained unchanged across different samples.\n\nQuestion:\nIs noncompliance with certain quality indicators associated with risk-adjusted mortality after stroke?\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:\nStatin therapy reduces coronary heart disease (CHD) and mortality in individuals with elevated C-reactive protein (CRP) but low-density lipoprotein cholesterol below the threshold at which statin therapy is recommended. We determined the proportion of individuals with elevated CRP in whom statin therapy was not indicated, and examined predictors for elevated CRP in a multi-ethnic Asian population. We studied 3404 participants (Chinese, Malays and Asian-Indians) without a history of hypercholesterolemia living in Singapore (mean age±s.d.: 48.9±11.2 years). Eligibility for statin therapy was determined based on the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III (ATPIII)) guideline. CRP was measured by high-sensitivity enzyme-linked immunosorbent assay method. CRP level greater than 2 mg l(-1) was considered as elevated. Elevated CRP was found in 29.3% participants who were not eligible for statin therapy (n=2974). Elevated CRP was more common in females and amongst those of Malay or Asian-Indian ethnicity. Compared with participants with low CRP, those with elevated CRP were shown to have higher levels of obesity, blood pressure, triglyceride and insulin resistance (IR), but lower high-density lipoprotein cholesterol levels (all Ps<0.001). After multivariate analysis, gender (odds ratio (OR) 3.34 for females), ethnicity (Malay OR 1.57, 95% confidence interval (CI) 1.25-1.96; Asian-Indian OR 1.97, 95% CI 1.55-2.50), waist circumference (OR 1.06, 95% CI 1.05-1.07), smoking (OR 1.49, 95% CI 1.08-2.05) and IR (OR 1.14, 95% CI 1.07-1.22) were significant predictors of CRP (all Ps--values<0.05).\n\nQuestion:\nAre central obesity and smoking key modifiable risk factors for elevated C-reactive protein in Asian individuals who are not eligible for statin therapy?\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:\nInsulin is proposed as a therapy for suppressing muscle wasting after burn trauma although the long-term effects of this therapy on wound healing are not yet known. The present study was designed to investigate the effect of systemically administered insulin therapy on burn wound healing. Young rats weighing 80-150 g were subjected to 15-20% total body surface area burn injury on their shaved dorsum. The insulin dosage was increased over the first 3 days in each rat from 0.25 U (Day 1), 0.5 U (Day 2), and 1.0 U (Day 3) per 100 g body wt. The rats were euthanized at the fourth or fifteenth day postinjury. Skin sections were analyzed by histochemistry and quantitative polarization microscopy. Histology showed a decreased number of inflammatory cells and increased vasodilation in the insulin-treated animals at Day 4 relative to untreated rats; at Day 15 there was increased reepithelialization. Quantitative analysis using polarization microscopy and picrosirius red staining showed an increased collagen deposition in wounds by Day 4 in insulin-treated rats relative to untreated burn controls.\n\nQuestion:\nDo influence of insulin therapy on burn wound healing in rats?\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:\nUnderstanding of the neuropathology leading to migraine pain has centered on either a vascular or neuronal origin. Sildenafil, a specific inhibitor of phosphodiesterase 5 (PDE5), induces migraine-like headache in a human headache model without concomitant artery dilation. The presence and activity of PDE3 and PDE5 is known in cerebral arteries. However, the presence in the neuronal part of the trigeminovascular pathway, i.e. the trigeminal ganglion and the possible co-localization with calcitonin gene-related peptide (CGRP), is not known. Rat trigeminal ganglia were isolated and immunohistochemistry and in situ hybridization was applied. Evaluations of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) hydrolysis were performed using scintillation proximity assays. PDE3 and PDE5 were present and active in the trigeminal ganglia. A subset of PDE3- and PDE5-positive neurons contained CGRP. In contrast to cGMP, both sildenafil and cilostazol influenced cAMP hydrolysis.\n\nQuestion:\nDo phosphodiesterases 3 and 5 express activity in the trigeminal ganglion and co-localize with calcitonin gene-related peptide?\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:\nAt one time, it was expected that if an individual reached young adulthood without smoking, his/her risk for initiation was minimal. However, recent data suggest that smoking initiation among young adults may be increasing. One particularly vulnerable population of young adults for smoking initiation is military recruits. This study examined whether a modified version of the Pierce Susceptibility Questionnaire (PSQ) might be useful for identifying military recruits who are vulnerable for the initiation of tobacco use. Active duty recruits entering the U.S. Air Force over a 1-year period (n=31,107) were assessed upon entry into basic military training (BMT), and a subsample was also assessed at 12 months following training. The modified PSQ predicted initiation of cigarette use for all categories of baseline smokers (never, experimenters, former smokers, and regular users). The likelihood of initiating smoking after BMT was substantially higher among those identified as susceptible than among those identified as not susceptible.\n\nQuestion:\nDoes prediction of adult-onset smoking initiation among U.S. Air force recruit using the pierce susceptibility questionnaire?\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 survival rate of lung cancer is low, thus new methods for treating this form of cancer must be explored. This study applies immune therapy with metronomic chemotherapy to observe the effect of combined therapy on suppressing tumor. Mice were inoculated with Lewis lung carcinoma cells. Different treatments, namely, saline, metronomic chemotherapy, dendritic cell (DC) vaccine, and metronomic chemotherapy with DC vaccine were administered to corresponding mice groups. Basic fibroblast growth factor and vascular endothelial growth factor (VEGF) were detected via microdialysis and Luminex. The median survival time of mice in the metronomic chemotherapy with DC vaccine group was (27.6±3.2) days, whereas that in the saline group was (13.5±2.7) days (P=0.008), that in the DC) vaccine group was (13.1±2.3) days (P=0.01), and that in the metronomic chemotherapy group was (11.8±3.0) days (P=0.01). The mice in the metronomic chemotherapy with DC vaccine group exhibited longer survival time than the mice in the other groups. This result could be related to the downregulation of VEGF secretion in the tumor-bearing mice groups within 48 h to 72 h.\n\nQuestion:\nDoes [ Metronomic chemotherapy combined with dendritic cell vaccine inhibit VEGF secretion ]?\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:\nSmall duct primary sclerosing cholangitis (PSC) is phenotypically a mild version of large duct PSC, but it is unknown whether these phenotypes share aetiology. We aimed to characterize their relationship by investigating genetic associations in the human leucocyte antigen (HLA) complex, which represent the strongest genetic risk factors in large duct PSC. Four classical HLA loci (HLA-A, HLA-B, HLA-C and HLA-DRB1) were genotyped in 87 small duct PSC patients, 485 large duct PSC patients and 1117 controls across three geographical regions. HLA-DRB1*13:01 (OR = 2.0, 95% CI 1.2-3.4, P = 0.01) and HLA-B*08 (OR = 1.6, 95% CI 1.1-2.4, P = 0.02) were significantly associated with small duct PSC compared with healthy controls. Based on the observed frequency of HLA-B*08 in small duct PSC, the strongest risk factor in large duct PSC, an estimated 32% (95% CI 4-65%) of this population can be hypothesized to represent early stages or mild variants of large duct PSC. This subgroup may be constituted by small duct PSC patients with inflammatory bowel disease (IBD), which greatly resembled large duct PSC in its HLA association. In contrast, small duct PSC without IBD was only associated with HLA-DRB1*13:01(P = 0.03) and was otherwise distinctly dissimilar from large duct PSC.\n\nQuestion:\nIs small duct primary sclerosing cholangitis without inflammatory bowel disease genetically different from large duct 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:\nThe role of inflammation in mood disorders has received increased attention. There is substantial evidence that cytokine therapies, such as interferon alpha (IFN-alpha), can induce depressive symptoms. Indeed, proinflammatory cytokines change brain function in several ways, such as altering neurotransmitters, the glucocorticoid axis, and apoptotic mechanisms. This study aimed to evaluate the impact on mood of initiating IFN-alpha and ribavirin treatment in a cohort of patients with chronic hepatitis C. We investigated clinical, personality, and functional genetic variants associated with cytokine-induced depression. We recruited 344 Caucasian outpatients with chronic hepatitis C, initiating IFN-alpha and ribavirin therapy. All patients were euthymic at baseline according to DSM-IV-R criteria. Patients were assessed at baseline and 4, 12, 24, and 48 weeks after treatment initiation using the Patient Health Questionnaire (PHQ), the Hospital Anxiety and Depression Scale (HADS), and the Temperament and Character Inventory (TCI). We genotyped several functional polymorphisms of interleukin-28 (IL28B), indoleamine 2,3-dioxygenase (IDO-1), serotonin receptor-1A (HTR1A), catechol-O-methyl transferase (COMT), glucocorticoid receptors (GCR1 and GCR2), brain-derived neurotrophic factor (BDNF), and FK506 binding protein 5 (FKBP5) genes. A survival analysis was performed, and the Cox proportional hazards model was used for the multivariate analysis. The cumulative incidence of depression was 0.35 at week 24 and 0.46 at week 48. The genotypic distributions were in Hardy-Weinberg equilibrium. Older age (p = 0.018, hazard ratio [HR] per 5 years = 1.21), presence of depression history (p = 0.0001, HR = 2.38), and subthreshold depressive symptoms at baseline (p = 0.005, HR = 1.13) increased the risk of IFN-induced depression. So too did TCI personality traits, with high scores on fatigability (p = 0.0037, HR = 1.17), impulsiveness (p = 0.0200 HR = 1.14), disorderliness (p = 0.0339, HR = 1.11), and low scores on extravagance (p = 0.0040, HR = 0.85). An interaction between HTR1A and COMT genes was found. Patients carrying the G allele of HTR1A plus the Met substitution of the COMT polymorphism had a greater risk for depression during antiviral treatment (HR = 3.83) than patients with the CC (HTR1A) and Met allele (COMT) genotypes. Patients carrying the HTR1A CC genotype and the COMT Val/Val genotype (HR = 3.25) had a higher risk of depression than patients with the G allele (HTR1A) and the Val/Val genotype. Moreover, functional variants of the GCR1 (GG genotype: p = 0.0436, HR = 1.88) and BDNF genes (Val/Val genotype: p = 0.0453, HR = 0.55) were associated with depression.\n\nQuestion:\nAre glucocorticoid Receptors , Brain-Derived Neurotrophic Factor , Serotonin and Dopamine Neurotransmission Associated with Interferon-Induced 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:\nCryoablation is an effective treatment for children with supraventricular tachycardias (SVT). The present study documents the effect of two different cryoablation protocols on acute and chronic success rates. Fifty-three consecutive patients (age range, 5-20 years) were treated; patients 1 to 17 were treated by a standard ablation protocol and patients 18 to 53 were treated by a modified ablation protocol that required lengthier cryoablations plus delivery of a bonus cryoapplication to consolidate the acutely successful irreversible lesion created at intervention. Electrophysiological study (EPS) was performed with diagnostic catheters and cryoablations were performed with a 7FR 4 mm tip catheter (CryoCath Technologies). Acute endpoints for non-inducibility of atrioventricular nodal re-entrant tachycardia (AVNRT) by programmed atrial stimulation at baseline or during isoproterenol performed 30 min post procedure, as well as non-inducibility and conduction block over the accessory pathway (AP). The chronic endpoint was arrhythmia recurrence post intervention. No permanent cryo-related complications or adverse outcomes were reported. Acute success rates for patients 1 to 17 and 18 to 53 were 88 and 100%, respectively. The cumulative percentage of patients without arrhythmia recurrence at 12 month follow-up was significantly different at 73 and 90%, respectively.\n\nQuestion:\nIs lengthier cryoablation and a bonus cryoapplication associated with improved efficacy for cryothermal catheter ablation of supraventricular tachycardias in children?\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:\nPrevention of rectal HIV transmission is a high-priority goal for vaccines and topical microbicides because a large fraction of HIV transmissions occurs rectally. Yet, little is known about the specific target-cell milieu in the human rectum other than inferences made from the colon. We conducted a comprehensive comparative in situ fluorescence study of HIV target cells (CCR5-expressing T cells, macrophages, and putative dendritic cells) at 4 and 30 cm proximal of the anal canal in 29 healthy individuals, using computerized analysis of digitized combination stains. Most strikingly, we find that more than 3 times as many CD68 macrophages express the HIV coreceptor CCR5 in the rectum than in the colon (P = 0.0001), and as such rectal macrophages seem biologically closer to the HIV-susceptible CCR5 phenotype in the vagina than the mostly HIV-resistant CCR5 phenotype in the colon. Putative CD209 dendritic cells are generally enriched in the colon compared with the rectum (P = 0.0004), though their CCR5 expression levels are similar in both compartments. CD3 T-cell densities and CCR5 expression levels are comparable in the colon and rectum.\n\nQuestion:\nDoes comprehensive assessment of HIV target cells in the distal human gut suggest increasing HIV susceptibility toward the anus?\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:\nHazardous drinking has been associated with risk taking and alcohol priming effects. However, the potential relationship between risk taking and priming has not been investigated. The Balloon Analogue Risk Task (BART) is a behavioural measure of risk taking which appears to be associated with drinking behaviour. However, alcohol's acute effects on BART performance are not clear, and the potentially mediating effect of alcohol-induced risk taking on priming has not been tested. To assess the effects of a priming dose of alcohol on BART performance; to determine the predictive utility of the BART on drinking habits; and to identify whether alcohol-induced risk taking mediates alcohol priming (urge to drink). A total of 142 participants provided data on drinking habits and trait-like impulsivity and sensation seeking. The BART was then completed after consuming alcohol (0.6 g/kg) or placebo (between-subjects design). Baseline and post-drink measures of alcohol urge were also taken. Alcohol consumption increased urge to drink (priming) and risk taking on the BART. In the alcohol group only, risk taking on the BART predicted unique variance in weekly alcohol consumption and bingeing. Mediation analysis showed that risk taking following alcohol consumption mediated alcohol priming.\n\nQuestion:\nDoes alcohol-induced risk taking on the BART mediate alcohol priming?\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:\nN-[(4-trifluoromethyl) benzyl] 4-methoxybutyramide (GET73) may be considered a promising therapeutic agent for the treatment of alcohol use disorders. The compound displayed anti-alcohol and anxiolytic properties in rat. In the present study, an in vitro experimental model of chronic ethanol treatment was used to investigate the ability of the compound to counteract the ethanol-induced neurotoxicity. Primary cultures of rat hippocampal neurons were exposed to ethanol (75 mM; 4 days) and the neuroprotective effects of GET73 were assessed by evaluating cell viability, cell morphology, glutamate levels and reactive oxygen species production. The exposure to ethanol induced a reduction of cell viability, an alteration of cytoskeleton, a decrease in extracellular glutamate levels and an increase of reactive oxygen species production. The addiction of GET73 (1 and 10 µM) 1 h before and during chronic ethanol exposure prevented all the above ethanol-induced effects. Based on the proposed GET73 mechanism of action, the effects of mGlu5 receptor negative allosteric modulator, 2-methyl-6-(phenylethynyl)-pyridine (MPEP), on ethanol-induced reduction of cell viability were also assessed. The results indicated that the addiction of MPEP (100 µM) 1 h before and during chronic ethanol exposure prevented the ethanol-induced cell viability reduction.\n\nQuestion:\nDoes gET73 prevent Ethanol-Induced Neurotoxicity in Primary Cultures of Rat Hippocampal Neurons?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPrevious studies have shown that the nuclear Ro/SSA autoantigens involved in photosensitive cutaneous lupus manifestations are regulated by ultraviolet B (UVB) irradiation. UVB exposure triggers the release of tumor necrosis factor alpha (TNFalpha) from keratinocytes in the epidermis and from mast cells in the dermis. The present study aimed to characterize the effect of TNFalpha on messenger RNA (mRNA) and protein expression of the intracellular 52-kd Ro/SSA autoantigen in primary human keratinocytes and to elucidate the TNFalpha receptor (TNFR) signaling pathways mediating this effect. Expression of 52-kd Ro/SSA mRNA in primary human keratinocytes was investigated by quantitative real-time polymerase chain reaction (LightCycler system) using GAPDH as the housekeeping gene. Expression of 52-kd Ro/SSA protein was studied by flow cytometry after staining intracellular protein with IgG purified from an anti-52-kd Ro/SSA-positive serum. TNFR function was assessed by culturing cells in the presence and absence of neutralizing antibodies directed against the TNFR subunits TNFRI and TNFRII. TNFalpha-induced up-regulation of 52-kd Ro/SSA mRNA expression peaked at 4 hours, followed by up-regulation of intracellular 52-kd Ro/SSA protein expression at 24 hours, independently of apoptosis. Between different donors, a high variability of both constitutive expression levels and TNFalpha-induced changes in 52-kd Ro/SSA mRNA and protein expression was observed. The up-regulatory effect of TNFalpha on 52-kd Ro/SSA mRNA and protein expression was inhibited by anti-TNFRI antibodies but enhanced by anti-TNFRII antibodies.\n\nQuestion:\nIs the intracellular 52-kd Ro/SSA autoantigen in keratinocytes up-regulated by tumor necrosis factor alpha via tumor necrosis factor receptor I?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo establish the association between airway inflammation and severity of obstructive sleep apnoea (OSA) in children. Consecutive children presenting with symptoms suggestive of OSA were recruited. They completed a sleep apnoea symptom questionnaire, underwent physical examination, spirometry, sputum induction and an overnight polysomnography. Adequate sputum contained <50% squamous epithelial cells, and OSA was diagnosed if the obstructive apnoea index was >1. 73 children with a median (interquartile range (IQR)) age of 11.3 (10.0-13.2) years were recruited. There were 21 girls and the median body mass index of the group was 24.0 (18.0-27.0) kg/m2. The most common presenting symptoms were habitual snoring, mouth breathing and prone sleeping position. Sputum induction was successful in 43 (59%) children, of whom 14 were found to have OSA. Children with OSA had significantly greater percentage sputum neutrophil than those without OSA (18.5 (IQR 8.0-42.0) v 4 (IQR 3.0-11.3), p = 0.006). On multiple regression analysis, percentage sputum neutrophil was significantly associated with OSA (odds ratio = 1.1, p = 0.013).\n\nQuestion:\nDo induced sputum inflammatory measures correlate with disease severity in children with obstructive sleep apnoea?\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:\nDopaminergic compounds have been targeted as potential treatments for cocaine abuse because of the known role of dopamine systems in drug reinforcement. Recent preclinical and human data have focused on the D1/5 antagonist, SCH 39166 (ecopipam), as a potential therapeutic agent. The objective of the present study was to determine whether treatment with chronic ecopipam can blunt or block the subjective effects of cocaine in the absence of significant behavioral impairment or toxic physiological effects. Four doses of ecopipam (0, 10, 25, and 100 mg p.o.) were administered daily for 1 week each in double-blind, random order to inpatient cocaine-dependent volunteers (n = 10). Cocaine challenge doses (0, 25, and 50 mg/70 kg i.v.) were administered on the 7th day in ascending order, 1 h apart. Ecopipam alone produced reliable dose-dependent deficits in performance on the digit symbol substitution task (DSST) and the circular lights task, but not a balance task. Impairment on the DSST waned with repeated dosing suggesting the development of tolerance. Ecopipam resulted in few direct subjective effects. Cocaine alone produced dose-dependent changes in prototypic subjective and physiological measures, however, ecopipam largely failed to alter either cocaine's direct effects or the desire for cocaine.\n\nQuestion:\nDoes repeated administration of the D1/5 antagonist ecopipam fail to attenuate the subjective effects of cocaine?\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:\nHearing restoration through hair cell regeneration will require revealing the dynamic interactions between proliferation and differentiation during development to avoid the limited viability of regenerated hair cells. Pax2-Cre N-Myc conditional knockout (CKO) mice highlighted the need of N-Myc for proper neurosensory development and possible redundancy with L-Myc. The late-onset hair cell death in the absence of early N-Myc expression could be due to mis-regulation of genes necessary for neurosensory formation and maintenance, such as Neurod1, Atoh1, Pou4f3, and Barhl1. Pax2-Cre N-Myc L-Myc double CKO mice show that proliferation and differentiation are linked together through Myc and in the absence of both Mycs, altered proliferation and differentiation result in morphologically abnormal ears. In particular, the organ of Corti apex is re-patterned into a vestibular-like organization and the base is truncated and fused with the saccule.\n\nQuestion:\nIs correct timing of proliferation and differentiation necessary for normal inner ear development and auditory hair cell viability?\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 a strong correlation between plasma C-reactive protein (CRP) concentration and risk of cardiovascular death. Low-fat diets have been recommended for maintenance of cardiovascular health, and it is known that a low-fat diet associated with weight loss lowers CRP concentration. However, it remains unclear whether dietary fat has an effect independent from weight change on markers of inflammation. Sixteen overweight subjects who were 46 +/- 14 y old were placed on a weight-maintaining baseline diet consisting of 35% fat, 45% carbohydrate, and 20% energy as protein. After 2 wk, subjects were switched to an isocaloric low-fat diet consisting of 15% fat, 65% carbohydrate, and 20% protein for another 2 wk. For the final 12 wk of the study, subjects consumed the same 15% fat diet ad libitum. At the end of each diet phase, CRP was measured by a high-sensitivity CRP assay. The weight of subjects remained stable during the first 4 wk of isocaloric diets. Plasma CRP concentrations after 2 wk on the weight-maintaining 35% fat diet and 2 wk on the isocaloric 15% fat diet were not significantly different (median +/- interquartile range 1.42 +/- 3.30 and 1.59 +/- 3.29 mg/L, respectively). Three months of ad libitum low-fat diet consumption resulted in a 4.1 +/- 0.7 kg weight loss associated with a decrease in CRP concentration to 1.17 +/- 2.03 mg/L (P = 0.03).\n\nQuestion:\nIs plasma C-reactive protein concentration affected by isocaloric dietary fat reduction?\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:\nIonizing irradiation is an effective treatment for malignant glioma (MG); however, a higher rate of recurrence with more aggressive phenotypes is a vital issue. Although epithelial-mesenchymal transition (EMT) is involved in irradiation-induced cancer progression, the role for such phenotypic transition in MG remains unknown. To investigate the mechanism of irradiation-dependent tumor progression in MG, we performed immunohistochemistry (IHC) and qRT-PCR using primary and recurrent MG specimens, MG cell lines, and primary culture cells of MG. siRNA technique was used for MG cell lines. In 22 cases of clinically recurrent MG, the expression of the mesenchymal markers vimentin and CD44 was found to be increased by IHC. In paired identical MG of 7 patients, the expression of collagen, MMPs, and YKL-40 were also elevated in the recurrent MGs, suggesting the The Cancer Genome Atlas-based mesenchymal subtype. Among EMT regulators, sustained elevation of Snail was observed in MG cells at 21 days after irradiation. Cells exhibited an upregulation of migration, invasion, numbers of focal adhesion, and MMP-2 production, and all of these mesenchymal features were abrogated by Snail knockdown. Intriguingly, phosphorylation of ERK1/2 and GSK-3β were increased after irradiation in a Snail-dependent manner, and TGF-β was elevated in both fibroblasts and macrophages but not in MG cells after irradiation. It was noteworthy that irradiated cells also expressed stemness features such as SOX2 expression and tumor-forming potential in vivo.\n\nQuestion:\nDoes sustained elevation of Snail promote glial-mesenchymal transition after irradiation in malignant glioma?\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 data in mice have identified de novo ceramide synthesis as the key mediator of hepatic insulin resistance (IR) that in humans characterizes increases in liver fat due to IR ('Metabolic NAFLD' but not that due to the I148M gene variant in PNPLA3 ('PNPLA3 NAFLD'). We determined which bioactive lipids co-segregate with IR in the human liver. Liver lipidome was profiled in liver biopsies from 125 subjects that were divided into equally sized groups based on median HOMA-IR ('High and Low HOMA-IR', n=62 and n=63) or PNPLA3 genotype (PNPLA3(148MM/MI), n=61 vs. PNPLA3(148II), n=64). The subjects were also divided into 4 groups who had either IR, the I148M gene variant, both of the risk factors or neither. Steatosis and NASH prevalence were similarly increased in 'High HOMA-IR' and PNPLA3(148MM/MI) groups compared to their respective control groups. The 'High HOMA-IR' but not the PNPLA3(148MM/MI) group had features of IR. The liver in 'High HOMA-IR' vs. 'Low HOMA-IR' was markedly enriched in saturated and monounsaturated triacylglycerols and free fatty acids, dihydroceramides (markers of de novo ceramide synthesis) and ceramides. Markers of other ceramide synthetic pathways were unchanged. In PNPLA3(148MM/MI)vs. PNPLA3(148II), the increase in liver fat was due to polyunsaturated triacylglycerols while other lipids were unchanged. Similar changes were observed when data were analyzed using the 4 subgroups.\n\nQuestion:\nDo hepatic ceramides dissociate steatosis and insulin resistance in patients with non-alcoholic fatty liver 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:\nGene expression profiling is a promising approach to better estimate patient prognosis; however, there are still unresolved problems, including little overlap among similarly developed gene sets and poor performance of a developed gene set in other datasets. We applied a gene sets approach to develop a prognostic gene set from multiple gene expression datasets. By analyzing 12 independent breast cancer gene expression datasets comprising 1,756 tissues with 2,411 pre-defined gene sets including gene ontology categories and pathways, we found many gene sets that were prognostic in most of the analyzed datasets. Those prognostic gene sets were related to biological processes such as cell cycle and proliferation and had additional prognostic values over conventional clinical parameters such as tumor grade, lymph node status, estrogen receptor (ER) status, and tumor size. We then estimated the prediction accuracy of each gene set by performing external validation using six large datasets and identified a gene set with an average prediction accuracy of 67.55%.\n\nQuestion:\nDoes a gene set approach for identifying prognostic gene signatures for outcome prediction?\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 main aim of our study was to assess the cerebrovascular thrombolytic efficacy of different tissue plasminogen activator treatment protocols with Doppler ultrasound. We occluded one internal carotid artery in 48 New Zealand White rabbits with whole blood emboli. Five minutes later the rabbits were assigned to receive one of the following tissue plasminogen activator protocols: 1) intravenous square-wave infusion in a total dose of 10 mg/kg, 2) intravenous constant infusion in a total dose of 10 mg/kg, 3) intravenous square-wave infusion in a total dose of 3 mg/kg, or 4) regional intra-arterial square-wave infusion in a total dose of 3 mg/kg. Blood flow velocities in the internal carotid arteries were continuously monitored during the study with Doppler ultrasound. In all 12 animals treated with a 10-mg/kg square-wave intravenous tissue plasminogen infusion, internal carotid artery blood flow was reestablished within 2 hours (57.9 +/- 33.3 minutes) after the initiation of treatment, whereas this was the case for only six (50%) of the 12 animals treated with a constant 10-mg/kg intravenous tissue plasminogen activator infusion (p less than 0.05, Fisher's exact test). Internal carotid artery blood flow was restored within 2 hours (33.5 +/- 40.4 minutes) in all animals treated with a regional intra-arterial tissue plasminogen infusion in a total dose of 3 mg/kg and in only three (50%) of the six animals treated with the same dosage intravenously (p less than 0.05, signed rank test).\n\nQuestion:\nIs tissue plasminogen activator cerebrovascular thrombolysis in rabbits dependent on the rate and route of administration?\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 prognostic value of multiple cell cycle-associated proteins in a large series of stage II and III colon cancers. From formalin-fixed, paraffin-embedded tumor samples of 386 patients with stage II and III colon cancer, DNA was isolated and tissue microarrays were constructed. Tissue microarray slides were immunohistochemically stained for p21, p27, p53, epidermal growth factor receptor, Her2/Neu, β-catenin, cyclin D1, Ki-67, thymidylate synthase, and Aurora kinase A (AURKA). Polymerase chain reaction-based microsatellite instability analysis was performed to allow for stratification of protein expression by microsatellite instability status. Overall, low p21, high p53, low cyclin D1, and high AURKA expression were significantly associated with recurrence (P = 0.01, P < 0.01, P = 0.04, and P < 0.01, respectively). In stage II patients who did not receive adjuvant chemotherapy (n = 190), significantly more recurrences were observed in case of low-p21 and high-p53-expressing tumors (P < 0.01 and P = 0.03, respectively). In stage III patients who did not receive chemotherapy, high p53 expression was associated with recurrence (P = 0.02), and in patients who received chemotherapy, high AURKA expression was associated with relapse (P < 0.01). In patients with microsatellite stable tumors, high levels of p53 and AURKA were associated with recurrence (P = 0.01 and P < 0.01, respectively). Multivariate analysis showed p21 (odds ratio 1.6, 95% confidence interval 0.9-2.8) and AURKA (odds ratio 2.7, 95% confidence interval 1.3-5.6) to be independently associated with disease recurrence.\n\nQuestion:\nDo cell cycle proteins predict recurrence in stage II and III colon 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:\nOur goal was to demonstrate that microparticles (MPs) are the endogenous signal leading to neovessel formation through CD40 ligation in human atherosclerotic plaques. Vulnerable atherosclerotic plaques prone to rupture are characterized by an increased number of vasa vasorum and frequent intraplaque hemorrhage. Although inflammatory cytokines, growth factors, or CD40/CD40 ligand (CD40L) are possible candidates, the mechanism of atherosclerotic plaque neovascularization remains unknown. Atherosclerotic plaques contain large amounts of membrane-shed submicron MPs released after cell activation or apoptosis. Microparticles were isolated from endarterectomy specimens surgically obtained from 26 patients and characterized by phosphatidylserine exposure and specific markers of cellular origin. Plaque MPs increased both endothelial proliferation assessed by (3)H-thymidine incorporation and cell number and stimulated in vivo angiogenesis in Matrigel (BD Biosciences, San Diego, California) assays performed in wild-type and BalbC/Nude mice, whereas circulating MPs had no effect. Microparticles from symptomatic patients expressed more CD40L and were more potent in inducing endothelial proliferation, when compared with asymptomatic plaque MPs. Most of CD40L+ MPs (93%) isolated from human plaques were of macrophage origin. Microparticle-induced endothelial proliferation was impaired by CD40L or CD40-neutralizing antibodies and abolished after endothelial CD40-ribonucleic acid silencing. In addition, the proangiogenic effect of plaque MPs was abolished in Matrigel assays performed in the presence of CD40L-neutralizing antibodies or in CD40-deficient mice.\n\nQuestion:\nDo cD40 ligand+ microparticles from human atherosclerotic plaques stimulate endothelial proliferation and angiogenesis a potential mechanism for intraplaque neovascularization?\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 peptidyl prolyl isomerase Pin1 frequently is overexpressed in hepatocellular carcinoma (HCC). Hepatitis B virus (HBV) is the most common etiologic agent in HCC, and its encoded X-protein (HBx) is oncogenic and possesses a serine-proline motif that may bind Pin1. The role of Pin1 in hepatocarcinogenesis, particularly in HBV-related HCC, was investigated. Immunohistochemical staining was performed to evaluate the prevalence of Pin1 overexpression in HCCs of different etiologies. Glutathione S-transferase pull-down and co-immunoprecipitation experiments were used to validate the physical interaction between Pin1 and HBx. Reporter assay, cell proliferation assay, and xenotransplantation experiments were used to show the functional consequence and importance of Pin1-HBx interaction in hepatocarcinogenesis. We showed preferential Pin1 overexpression in HBV-related tumors and confirmed the interaction between Pin1 and HBx at the specific serine-proline motif. Pin1 overexpression increased the protein stability of HBx. Furthermore, HBx-mediated transactivation was enhanced by co-expression of Pin1. HepG2 expressing Pin1 and HBx showed a synergistic increase in cellular proliferation, as compared with cells expressing Pin1 or HBx alone. Furthermore, concomitant expression of Pin1 and HBx in the nontumorigenic human hepatocyte cell line MIHA led to a synergistic increase in tumor growth. Finally, in Hep3B cells with suppressed Pin1 expression, HBx-enhanced tumor growth in nude mice was abrogated.\n\nQuestion:\nDoes pin1 interact with a specific serine-proline motif of hepatitis B virus X-protein to enhance hepatocarcinogenesis?\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:\nNutritional requirements are increased during pregnancy and lactation. The aim of this study was to compare the food intake and prevalence of inadequate nutrient intake among pregnant, lactating and reproductive-age women. Two-day dietary records of 322 pregnant and 751 lactating women were compared to those of 6837 non-pregnant and non-lactating women aged 19 to 40 years from a nationwide representative sample. The usual nutrient intake was estimated using the National Cancer Institute method, and compared to nutritional goals to estimate prevalence of inadequate intake. Pregnant, lactating and reproductive-age women did not differ in their average consumption of 18 food groups, except for rice, with greatest intake among lactating women. The prevalence of nutrient inadequacy in pregnant women was higher than in reproductive-age women for folate (78% versus 40%) and vitamin B6 (59% versus 33%). In lactating women, prevalence was higher than in reproductive-age women for vitamin A (95% versus 72%), vitamin C (56% versus 37%), vitamin B6 (75% vs. 33%), folate (72% versus 40%) and zinc (64% versus 20%). The percentage of sodium intake above the upper limit was greater than 70% in the three groups.\n\nQuestion:\nDo brazilian pregnant and lactating women change their food intake to meet nutritional goals?\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:\nInvestigate effects of aspirin/dipyridamole and aspirin on blood viscosity (BV) in subjects with hyperhomocystememia (>14 micromol/L) and stable cardiovascular disease (CVD) or >or= 20% risk for CVD were the aims of this study. Forty-seven subjects were treated with 14 days of either aspirin/dipyridamole (25 mg/200 mg twice-daily) or aspirin (81 mg daily). BV was measured from fasting specimens at 37 degrees C from whole blood at shear rates ranging from 1,000 to 1s(-1) by using a scanning capillary viscometer (Rheolog; Rheologics Inc., Exton, Pennsylvania, USA). Aspirin/dipyridamole was more effective than aspirin therapy in reducing BV at shear rates of 1 s(-1) (-3.03 [-3.88, -2.17] mPas vs. -0.07 [-1.06, 0.92] mPas; P<0.0001) and 2 s(-1) (-1.86 [-2.72, -1.01] mPas vs. -0.21 [-1.20, 0.79] mPas; P=0.0136); however, there were no significant differences in blood viscosity at shear rates of 5 s(-1) to 1000 s(-1). Changes in hematocrit, a major determinant of whole BV, were greater in the aspirin/dipyridamole group than the aspirin group (P=0.043). After hematocrit adjustment, differences in BV between aspirin/dipyridamole and aspirin remained significant at 1s(-1) (-2.78 [-3.68, -1.88] mPas vs. -0.04 [-1.05, 0.98] mPas; P<0.0001) and 2 s(-1) (-1.62 [-2.52, -0.72] mPas vs. -0.17 [-1.19, 0.85] mPas; P=0.0315).\n\nQuestion:\nIs treatment with aspirin and dipyridamole more effective than aspirin in reducing low shear blood viscosity?\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:\nHepatic iron deposition has been reported in chronic hepatitis C (CH-C), and iron-induced lipid peroxidation may be involved in the pathogenesis of CH-C. The aims of the present study were: 1) to determine whether patients with CH-C have evidence of enhanced hepatic lipid peroxidation and to evaluate its relation to iron status, compared with that in patients with chronic hepatitis B (CH-B); and 2) to assess the effect of interferon (IFN) therapy on hepatic iron and lipid peroxidation. In the liver biopsies of 40 patients with CH-C and 26 patients with CH-B, immunohistochemical detection of 4-hydroxy-2-nonenal (HNE)-protein adducts for evaluation of lipid peroxidation was performed, and hepatic iron status was biochemically and histologically assessed. In 16 CH-C patients with normal serum transaminases and undetectable serum HCV-RNA >6 months after the end of IFN treatment (responders) and in 11 nonresponders, hepatic HNE-protein adducts and siderosis were evaluated in pre- and posttreatment liver biopsies. Hepatocytic HNE-protein adducts and iron deposits were more abundant in the patients with CH-C than in those with CH-B. No correlation was found between the levels of hepatocytic HNE-protein adducts and hepatic iron status in either of the two groups. In the responders to IFN treatment for CH-C, hepatocytic HNE-protein adducts disappeared or attenuated with improvement of hepatic siderosis after the treatment, whereas IFN treatment did not improve hepatocytic expression of HNE-protein adducts and hepatic siderosis in the nonresponders.\n\nQuestion:\nDoes successful interferon therapy reverse enhanced hepatic iron accumulation and lipid peroxidation in chronic hepatitis C?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIt is postulated that peroxisome proliferator-activated receptor alpha agonists confer cardiovascular benefits in diabetes, independently of their effects on lipid metabolism. We investigated putative mechanisms responsible for these anti-atherogenic effects in an in vivo model of diabetes-associated atherosclerosis. Control and streptozotocin-induced diabetic apolipoprotein-deficient mice received gemfibrozil (100 mg kg(-1) day(-1)) or no treatment for 20 weeks. Aortic plaque deposition was assessed by Sudan IV staining and subsequent en face quantification. Superoxide production was measured using lucigenin-enhanced chemiluminescence. Markers of pathways including inflammation and oxidative stress were measured using real-time RT-PCR. No significant effect of gemfibrozil was observed on glycated haemoglobin, cholesterol or insulin in diabetic mice. Diabetes was associated with a three-fold increase in plaque area and a significant increase in NADPH-dependent superoxide compared with control mice. Gemfibrozil significantly attenuated plaque area and superoxide production in diabetic mice. In addition, gemfibrozil reduced the expression of the genes encoding the NADPH oxidase subunits p47phox, gp91phox and Rac-1. In addition, gemfibrozil reduced the expression of the genes encoding nuclear factor kappa B (NF-kappaB) subunit, p65, the NF-kappaB-dependent chemokine monocyte chemoattractant protein-1, and tissue factor.\n\nQuestion:\nDoes gemfibrozil decrease atherosclerosis in experimental diabetes in association with a reduction in oxidative stress and inflammation?\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:\nIsolated limb perfusion (ILP) with melphalan is an accepted treatment for intransit melanoma of the extremities. Using an ILP human melanoma xenograft model, we tested the hypothesis that acidosis augments the antitumor effect of melphalan and that nitric oxide (NO) induction mediates tumor regression. NIH1286 human melanoma tumor bearing athymic nude rats underwent a 10-minute ILP. Group C was perfused at physiologic pH without acid or melphalan, group M received melphalan at physiologic pH (7.2), group A received 0.2 N of HCl at pH 6.8, and group A/M received melphalan and HCl at pH 6.8. Groups 1400W + A and 1400W + A/M were injected with 1400W, a specific inhibitor of inducible NO synthase, 1 hour pre-ILP. Tumor response was followed for up to 60 days in all survival experiments. In 4 to 6 animals from groups C, M, A, and A/M, tumor NO was measured pre- and post-ILP, and tumor and thigh muscle from 2 additional animals in each group were collected at 20 minutes and 24 hours post-ILP and processed for terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Maximum mean reduction in tumor size after ILP in the different groups was as follows: C = 0%, M = 55%, A = 99.6% (3 of 4 complete responses), A/M = 100% (all complete responses), 1400W + A = 0%, and 1400W + A/M = 25%. Median tumor NO was 0.87 +/- 0.74 (SD) micromol/L before ILP and increased significantly (Mann-Whitney rank sum test, P <.001) after ILP (C = +6.9%, n = 4; M = +7.5%, n = 5; A = +66.0%, n = 6; A/M = +35.9%, n = 6). Also, minimal apoptotic cell death was seen in C and M, whereas A and A/M showed evidence of widespread apoptosis.\n\nQuestion:\nDoes acidosis plus melphalan induce nitric oxide-mediated tumor regression in an isolated limb perfusion human melanoma xenograft 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:\nCementum is a mineralized tissue that facilitates the attachment of periodontal ligament to the root and surrounding alveolar bone and plays a key role in the regeneration of periodontal tissues. The molecular mechanisms that regulate the proliferation and differentiation of cementoblasts, however, have not been elucidated to date. Enamel molecules are believed to regulate cementoblast differentiation and to initiate the formation of acellular extrinsic fiber cementum. The purpose of this study was therefore to isolate and culture human root-derived cells (HRDC) in order to determine whether they are able to express both cementum and specific enamel proteins and subsequently to confirm these findings in vivo. Human root-derived cells were isolated and expanded in vitro. Cells were characterized using RT-PCR, immunostaining, western blotting and by examination of total mRNA to determine the expression of cementum and enamel markers. Human periodontal tissues were also examined for the expression of enamel-related proteins by immunostaining. We showed that HRDC express mRNA corresponding to ameloblastin (AMBN), amelogenin (AMEL), enamelin (ENAM), tuftelin (TUFT) and cementum-associated molecules such as cementum protein 1 (CEMP1) and cementum attachment protein (CAP). Western blotting revealed that HRDC express both AMEL and AMBN gene products, as well as the cementum markers CEMP1 and CAP. In vivo, we have showed that AMBN and AMEL are expressed by cementoblasts lining cementum, paravascular cells and periodontal ligament cells.\n\nQuestion:\nDo human cementoblasts express enamel-associated molecules in vitro and in vivo?\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 growing evidence that the intrauterine environment can impact the neurodevelopment of the fetus through alterations in the functional epigenome of the placenta. In the placenta, the HSD11B2 gene encoding the 11-beta hydroxysteroid dehydrogenase enzyme, which is responsible for the inactivation of maternal cortisol, is regulated by DNA methylation, and has been shown to be susceptible to stressors from the maternal environment. We examined the association between DNA methylation of the HSD11B2 promoter region in the placenta of 185 healthy newborn infants and infant and maternal characteristics, as well as the association between this epigenetic variability and newborn neurobehavioral outcome assessed with the NICU Network Neurobehavioral Scales. Controlling for confounders, HSD11B2 methylation extent is greatest in infants with the lowest birthweights (P = 0.04), and this increasing methylation was associated with reduced scores of quality of movement (P = 0.04).\n\nQuestion:\nIs placental 11-beta hydroxysteroid dehydrogenase methylation associated with newborn growth and a measure of neurobehavioral outcome?\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 reason for cognitive deterioration in diabetes mellitus (DM) remains unknown. One suggestion is that despite elevated glucose levels, patients with DM generally have difficulty utilizing glucose during cognitive tasks. This assumption was tested in the present study. Male outpatients with DM (n = 46; age 52-85 years) were administered a series of standard neuropsychological and cognitive tests. In addition to assessing the time to complete the series of tests, peripheral blood glucose levels were measured prior to and following testing. The rate at which peripheral blood glucose levels changed was examined in relation to cognitive performance. Multiple linear regression analyses revealed significant relationships between the rate of glucose change and performance on tests measuring psychomotor skills, attention, visuoperceptual abilities, sequencing skills, mental flexibility, and planning. Higher rates of decline in peripheral blood glucose levels were associated with better performance on all cognitive measures, except verbal fluency.\n\nQuestion:\nDoes rate of peripheral glucose change during cognitive testing predict performance in diabetes mellitus?\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 the role of extracellular signal-regulated kinase (ERK) in cerebral ischemia and the mechanism of protective effects of U0126 (1,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio] butadiene) on ischemic brain. Mice underwent left middle cerebral artery occlusion (MCAO) by introducing a suture in the lumen. U0126 was injected intravenously through the internal jugular vein. The immuno-activity of phosphorylated ERK1/2 (pERK1/2), phosphorylated mitogen activated protein kinase kinase (pMEK), and phosphorylated Elk-1 (pElk-1) was assessed by Western blot analysis and immunohistochemistry. Interleukin (IL)-1beta mRNA level was measured by ribonuclease protection assay. Phosphorylated ERK1/2 in 2 hours MCAO mice was down-regulated after intravenous injection of U0126. The inhibition was dose dependent and treatment time related. pMEK and pElk-1 were also reduced in a similar fashion after U0126 treatment. IL-1beta mRNA increased after 1 and 2 hours of MCAO. After injection of U0126, it was down-regulated during 1 to 4 hours after MCAO.\n\nQuestion:\nDoes u0126 prevent ERK pathway phosphorylation and interleukin-1beta mRNA production after cerebral ischemia?\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:\nAzaspiracids (AZAs) are marine phycotoxins with an unknown mechanism of action, recently implicated in human intoxications. The predominant analog in nature, AZA-1 targets several organs in vivo, including the central nervous system and exhibits high neurotoxicity in vitro. We used pharmacological tools to inhibit the cytotoxic effect of the toxin in primary cultured neurons. Immunocytochemical techniques in combination with confocal microscopy were employed to examine the cellular mechanisms involved in the neurotoxic effect of AZA-1. Several targets for azaspiracid-induced neurotoxicity, specifically the cAMP pathway, or protein kinase C and phosphatidylinositol 3-kinase activation were excluded. Interestingly, the specific c-Jun-N-terminal protein kinase (JNK) inhibitor SP 600125 protected cultured neurons against AZA-induced cytotoxicity. Immunocytochemistry experiments showed that AZA-1 increased the amount of phosphorylated JNK and caused nuclear translocation of the active protein that was prevented by SP 600125.\n\nQuestion:\nIs the c-Jun-N-terminal kinase involved in the neurotoxic effect of azaspiracid-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:\nA recent study of obesity in Swedish men found that polymorphisms in the type 3 adenylyl cyclase (AC3) are associated with obesity, suggesting the interesting possibility that AC3 may play a role in weight control. Therefore, we examined the weight of AC3 mice over an extended period of time. We discovered that AC3(-/-) mice become obese as they age. Adult male AC3(-/-) mice are about 40% heavier than wild type male mice while female AC3(-/-) are 70% heavier. The additional weight of AC3(-/-) mice is due to increased fat mass and larger adipocytes. Before the onset of obesity, young AC3(-/-) mice exhibit reduced physical activity, increased food consumption, and leptin insensitivity. Surprisingly, the obesity of AC3(-/-) mice is not due to a loss of AC3 from white adipose and a decrease in lipolysis.\n\nQuestion:\nAre adult type 3 adenylyl cyclase-deficient mice obese?\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:\nGlutamate is a major signaling molecule that binds to glutamate receptors including the ionotropic glutamate receptors; kainate (KA) receptor (KAR), the N-methyl-d-aspartate receptor, and the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor. Each is well characterized in the central nervous system, but glutamate has important signaling roles in peripheral tissues as well, including a role in regulating platelet function. Our previous work has demonstrated that glutamate is released by platelets in high concentrations within a developing thrombus and increases platelet activation and thrombosis. We now show that platelets express a functional KAR that drives increased agonist induced platelet activation. KAR induced increase in platelet activation is in part the result of activation of platelet cyclooxygenase in a mitogen-activated protein kinase-dependent manner. Platelets derived from KAR subunit knockout mice (GluR6(-/-)) are resistant to KA effects and have a prolonged time to thrombosis in vivo. Importantly, we have also identified polymorphisms in KAR subunits that are associated with phenotypic changes in platelet function in a large group of whites and blacks.\n\nQuestion:\nDoes platelet kainate receptor signaling promote thrombosis by stimulating cyclooxygenase 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:\nActivation of Toll-like receptors (TLRs) is widely accepted as an essential event for defence against infection. Many TLRs utilize a common signalling pathway that relies on activation of the kinase IRAK4 and the transcription factor NFkappaB for the rapid expression of immunity genes. 21 K DNA microarray technology was used to evaluate LPS-induced (TLR4) gene responses in blood monocytes from a child with an IRAK4-deficiency. In vitro responsiveness to LPS was confirmed by real-time PCR and ELISA and compared to the clinical predisposition of the child and IRAK4-deficient mice to Gram negative infection. We demonstrated that the vast majority of LPS-responsive genes in IRAK4-deficient monocytes were greatly suppressed, an observation that is consistent with the described role for IRAK4 as an essential component of TLR4 signalling. The severely impaired response to LPS, however, is inconsistent with a remarkably low incidence of Gram negative infections observed in this child and other children with IRAK4-deficiency. This unpredicted clinical phenotype was validated by demonstrating that IRAK4-deficient mice had a similar resistance to infection with Gram negative S. typhimurium as wildtype mice. A number of immunity genes, such as chemokines, were expressed at normal levels in human IRAK4-deficient monocytes, indicating that particular IRAK4-independent elements within the repertoire of TLR4-induced responses are expressed.\n\nQuestion:\nAre robust TLR4-induced gene expression patterns an accurate indicator of human immunity?\n\nAnswer:",
"role": "user"
},
{
"content": "no",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAtrial fibrillation is the most common significant cardiac arrhythmia in clinical practice, but its risk factors remain to be clarified. We have hypothesized that left ventricular posterior wall thickness is an independent risk factor for paroxysmal atrial fibrillation (PAF). A total of 166 consecutive patients with paroxysmal atrial fibrillation were included in this study. Another 166 healthy check-up people, strictly age and sex-matched, were enrolled as controls in the same period. Univariable analysis and multivariable conditional logistic stepwise regression analysis were conducted. Receiver operating characteristic (ROC) curve analysis was performed on those significant indices obtained from the multivariable logistic regression analysis. The multivariable stepwise analysis identified left ventricular posterior wall thickness, left atrial diameter tricuspid insufficiency and residence (countryside) as independent predictors for paroxysmal atrial fibrillation. Receiver operating characteristic curve analysis demonstrated the cutoff values of those risk factors aforementioned.\n\nQuestion:\nIs left ventricular posterior wall thickness an independent risk factor for paroxysmal 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:\nPrevious studies of the effect of granulocyte-macrophage colony-stimulating factor (GM-CSF) on HIV-1 replication in macrophages have had inconsistent results, variously reporting no effect, augmentation or inhibition of viral replication. To investigate the regulation of HIV-1 in monocyte-derived macrophages (MDM) by GM-CSF in vitro. The role of GM-CSF on HIV-1 replication was assessed as supernatant and intracellular p24 antigen concentrations and by HIV-1 DNA and mRNA production under different culture conditions. Expression of CD4 and CCR5 receptors was examined. The effect of GM-CSF with an E21R mutation, which binds only to the alpha-chain of GM-CSF receptor, was used as an additional control. GM-CSF consistently suppressed HIV-1 replication in human MDM in vitro, as assessed by supernatant and intracellular p24 antigen concentrations and HIV-1 gag mRNA expression. The inhibitory effect of GM-CSF on HIV-1 replication was observed regardless of HIV-1 strain, source of GM-CSF, stage of MDM maturation or timing of GM-CSF exposure in relation to HIV-1 infection. The effect was dose dependent and reversed by addition of a neutralizing monoclonal antibody (4D4). Flow cytometric analysis of surface expression of CD4 and CCR5 indicates that GM-CSF does not affect HIV-1 entry into MDM. Analysis of intracellular HIV-1 DNA and mRNA suggests that HIV-1 replication is inhibited at or before transcription. E21R GM-CSF had no effect on HIV-1 replication in MDM.\n\nQuestion:\nDoes granulocyte-macrophage colony-stimulating factor inhibit HIV-1 replication in monocyte-derived macrophages?\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 observer faciolingual depth and vertical depth reading errors when using various X-ray beam array geometries to make basis images for tomosynthetic reconstruction using tuned aperture computed tomography (TACT). Tissue-equivalent models were constructed to replicate the position of dental implants in relation to simulated mandibular canals. X-ray beam geometries used to acquire the basis images for TACT(TM) integration included horizontal linear, vertical linear, and symmetric and asymmetric conical arrays. Twenty-one dentists trained in the use of TACT acted independently as observers. Tasks included: (1) determination of the relative position of the implant in relation to the simulated canal; and (2) measurement of the vertical depth and faciolingual (lateral) depth dimensions between these two structures. As the study did not involve repeated measures (only one measure was obtained from each observer on each of the two dependent variables), data for faciolingual depth and vertical depth reading errors were analysed using a one-way analysis of variance (ANOVA) with Tukey's honestly significant different (HSD) procedure. Errors in determining the relative position of the implant to the simulated canal were most frequent when the linear horizontal projection geometry was employed for producing basis images (57% error for model #2 where the implant was lingually placed). The mean measurement errors for TACT images constructed using the various different projection arrays depended both on the structural relationship of anatomic features and the employed beam array geometry.\n\nQuestion:\nDo array geometry for assessment of mandibular implant position using tuned aperture computed tomography ( TACT )?\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 intima-media thickness (IMT) of the carotid artery is dependent on the risk factor load during life and correlates well with the degree of atherosclerosis, also in other vascular beds. We reviewed our database of IMT measurements, from January 2002 to February 2007. We compared the mean IMT values of patients without a history of coronary artery disease (group 1) with those with a history of coronary artery disease (group 2). For both groups we divided the results of measurements according to age. We compared the IMT between both groups and looked for a correlation with increasing age. The IMT was measured with high-resolution echography at the posterior wall of the common carotid artery, using an automated edge-tracking method. The database contained 598 IMT measurements in group 1 and 672 in group 2. In both groups we observed a significant increase in IMT with increasing age. Within a certain age group, a significant difference in IMT between group 1 and 2 occurred at an age of 40 years or above (age 40-65: IMT 645.54 versus 671.71 microm, respectively, P = 0.04, and age > 65 years: IMT 715.2 versus 772.91 microm, respectively, P = 0.01).\n\nQuestion:\nIs carotid artery intima-media thickness associated with coronary artery 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:\nTo determine how frequent inflow stenosis is a contributing factor in the etiology of arteriovenous access-induced steal (AVAIS). A retrospective review of hemodialysis patients who underwent interventions from October 1998 to December 2011 for AVAIS was conducted at Mount Sinai Hospital. Patients with grade 3 AVAIS and complete arch and upper extremity vascular imaging were included. Demographics, access history, time to AVAIS, preoperative angiographic imaging and interventions performed were analyzed. A total of 52 patients were diagnosed with grade 3 (severe) AVAIS requiring intervention over the study period. Forty-seven percent of the patients were male, average age was 62 years, 47% were of African American race and 88% were diabetic. Seventeen consecutive patients, with imaging, were included in this study. The average time to presentation of steal symptoms was 147±228 days. All of the accesses were proximal, and 65.7% were autogenous. Imaging studies consisted of angiography (14) and computed tomography angiography (3). Five patients had imaging evidence of >50% luminal inflow stenosis (29.4%). The location of stenosis was the subclavian (3 cases) and brachial (2 cases) arteries. Patients underwent distal revascularization and interval ligation (3), ligation (1) and angioplasty/stenting (1).\n\nQuestion:\nDo inflow stenosis as a contributing factor in the etiology of AV access-induced ischemic steal?\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 current surgical cervical cancer treatment in Sweden 2008-12. Analysis of data in the Swedish National Quality Register for Gynecological Surgery (GynOP). A total of 249 cervical cancer patients undergoing surgery. Analysis of prospectively gathered preoperative and postoperative data including patient-reported information. Mean operating time, blood loss/transfusion, length of hospital stay, return to activities of daily living. The patients undergoing laparoscopic robot-assisted surgery (n = 64) or laparotomy (n = 185) did not differ in age, body mass index, American Society of Anesthesiologists score, International Federation of Gynecology and Obstetrics (FIGO) stage or mean operating time. Blood loss was higher in the laparotomy group (p < 0.001). Thirteen patients in the laparotomy group (7%) received a blood transfusion, but none in the robot group. Intraoperative complications were more common in the laparotomy group (p = 0.03). Re-admission or operations did not differ between the groups. The number of pelvic lymph nodes removed was significantly higher in the laparotomy group (median 31 vs. 24, p < 0.001). There was no difference regarding the number of patients with lymph node metastases in the two groups. The postoperative length of hospital stay was longer in the laparotomy group compared with the robot group (6.1 days vs. 2.1 days, p = 0.01). The patient-reported time to resume normal activities of daily living was longer in the laparotomy than the robot group (13.4 days vs. 9.7 days, p = 0.04).\n\nQuestion:\nDoes robot-assisted surgery in cervical cancer patients reduce the time to normal activities of daily living?\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:\nMucosal addressin cell adhesion molecule 1 (MAdCAM-1) is a cell adhesion molecule that is expressed on the endothelium in mucosa, and guides the specific homing of lymphocytes into mucosal tissues. MAdCAM-1 belongs to a subclass of the immunoglobulin superfamily (IgSF), the members of which are ligands for integrins. Human MAdCAM-1 has a unique dual function compared to other members in the same subclass in that it binds both the integrin alpha4beta7, through its two IgSF domains, and a selectin expressed on leukocytes, via carbohydrate sidechains. The structure determination of the two IgSF domains and comparison to the N-terminal two-domain structures of vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecules (ICAM-1 and ICAM-2) allow us to assess the molecular basis of the interactions between integrins and their preferred ligands. The crystal structure of a fragment containing the two IgSF domains of human MAdCAM-1 has been determined to 2.2 A resolution. The structure of MAdCAM-1 reveals two separate integrin-recognition motifs. The key integrin-binding residue, Asp42, resides in the CD loop of domain 1; a buried arginine residue (Arg70) plays a critical role in maintaining the conformation of this loop. The second binding site is associated with an unusual long D strand in domain 2. The D and E strands extend beyond the main body of the domain, forming a negatively charged beta ribbon unique to MAdCAM-1. This ribbon is located on the same face as the key aspartate residue in domain 1, consistent with evidence that it is involved in integrin binding.\n\nQuestion:\nDoes the structure of immunoglobulin superfamily domains 1 and 2 of MAdCAM-1 reveal novel features important for integrin recognition?\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 western corn rootworm (WCR) is economically the most important pest of maize in Croatia. To predict WCR adult population abundance and variability, traditional, genetic and morphometric monitoring of populations was conducted over time through each phase of the WCR invasion process in Croatia. Through traditional monitoring it was shown that WCR established their current population and reached economic densities after 14 years persisting in the study area. Regression-tree-based modelling showed that the best predictor of WCR adult abundance was the total amount of rainfall. Genetic monitoring indicated that genetic differentiation increased over time at the intrapopulation level, and morphometric monitoring indicated that wing morphotypes varied according to edaphic landscape changes.\n\nQuestion:\nAre monitoring techniques of the western corn rootworm the precursor to effective IPM strategies?\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 biological effects of passage through clinically relevant needles on the viability and metabolic activity of culture-expanded, human adipose tissue-derived mesenchymal stromal/stem cells (AMSCs). Prospective observational pilot study. Academic medical center. Patient-derived clinical-grade culture expanded AMSCs. AMSCs were passed through syringes without a needle attached (control), with an 18-gauge (25.4-mm) needle attached and with a 30-gauge (19-mm) needle attached at a constant injection flow rate and constant cell concentrations. Each injection condition was completed in triplicate. Cell number and viability, proliferative capacity, metabolic activity, and acute gene expression as measured by cell counts, mitochondrial activity, and quantitative real time reverse-transcription polymerase chain reaction on day 0 (immediately), day 1, and day 4 after injection. AMSC viability was not significantly affected by injection, and cells proliferated normally regardless of study group. Postinjection, AMSCs robustly expressed both proliferation markers and extracellular matrix proteins. Stress-response mRNAs were markedly but transiently increased independently of needle size within the first day in culture postinjection.\n\nQuestion:\nDo human Adipose-Derived Mesenchymal Stromal/Stem Cells Remain Viable and Metabolically Active Following Needle Passage?\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:\nPropacetamol is widely used in the management of postoperative pain. It decreases morphine requirements but its effect on the incidence of morphine-related adverse effects remains unknown. Patients (550) were randomly assigned to receive propacetamol or a placebo over the first 24 h after operation in a blinded study. Intravenous morphine titration was performed, after which morphine was administered s.c. every 4 h according to their pain score. Pain was assessed using a visual analogue scale (VAS). The primary end-point was the incidence of morphine-related adverse effects. The main secondary end-points were morphine requirements and VAS score. After morphine titration, the VAS score and the number of patients with pain relief did not differ between groups. Morphine requirements were decreased in the propacetamol group (21 vs 14.5 mg, P<0.001) but the incidence of morphine-related adverse effects did not differ between groups (42 vs 46%, not significant). In patients with moderate pain (n=395), morphine requirements decreased by 37% (P<0.001) and the percentage of patients requiring no morphine was greater (21 vs 8%, P=0.002) in the propacetamol group. In patients with severe pain (n=155), morphine requirements decreased by 18% (P=0.04) in the propacetamol group and the number of patients who did not require morphine (3 vs 8%) did not differ significantly.\n\nQuestion:\nDoes adjunctive analgesia with intravenous propacetamol reduce morphine-related adverse effects?\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:\nTrans-2-hexenal (2-hexenal) is an alpha,beta-unsaturated carbonyl compound protecting plants against harmful substances. Since humans have a permanent intake of 2-hexenal via vegetable products, this genotoxic and mutagenic compound is considered to play a role in human carcinogenicity. Ha-ras and p53 gene expression changes and tumor development were investigated in mice and rats after 2-hexenal administration. 2-Hexenal exposure did not result in gene expression alterations 24, 48 or 72 hours after administration while 10 out of the 72 mice and rats included in the long-term study developed a malignancy by the end of the 18-month follow-up.\n\nQuestion:\nIs carcinogenic potential of trans-2-hexenal based on epigenetic effect?\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:\nAdiposity has been thought to be related to colorectal carcinogenesis. The aim of this study was to explore any association between obesity factors and the presence of colorectal adenoma, a potential precancerous lesion. Two hundred and six consecutive patients undergoing colonoscopy without colorectal cancer were enrolled in the study. Anthropometric measures and other adiposity-related laboratory variables including insulin resistance and serum adiponectin levels were recorded and correlated with the presence of adenoma. Colorectal adenoma was detected in 68/206 patients (33%), tubular adenoma(s) in 38 patients, and tubulovillous or villous in 30 patients. Twenty-one patients (10.2%) had at least one proximal polyp. The size of the largest adenoma was ≤10 mm in 40 patients and >10 mm in 28 patients. No statistically significant difference was observed in body mass index, waist circumference, fasting plasma glucose concentration, insulin, homeostatic metabolic assessment, cholesterol, low-density lipoproteins, high-density lipoprotein, or triglycerides between patients with and without adenoma. In addition, there was no difference in plasma adiponectin between patients with adenoma (11.1 ± 6 μg/mL) and controls (10.2 ± 7.8 μg/mL). Furthermore, no significant difference in any parameter was found between patients with advanced adenoma and no advanced adenoma, nor between patients with proximal or distal tumors.\n\nQuestion:\nAre adiposity factors related to the presence of colorectal adenomas?\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:\nhPTTG1 (human pituitary tumor-transforming gene 1) is an oncogene overexpressed in breast cancer and several other types of cancer. Increased hPTTG1 expression has been shown to be associated with poor patient outcomes in breast cancer. Although hPTTG1 overexpression plays important roles in promoting the proliferation, invasion, and metastasis of cancer cells, it also has been suggested to induce cellular senescence. Deciphering the mechanism by which hPTTG1 overexpression induces these contradictory actions in breast cancer cells is critical to our understanding of the role of hPTTG1 in breast cancer development. MCF-10A and MCF-7 cells were used to identify the mechanism of hPTTG1-induced senescence. The interplay between hPTTG1 overexpression and chemokine C-X-C motif receptor 2 (CXCR2)/p21-dependent senescence in tumor growth and metastasis of MCF-7 cells was investigated by orthotopic transplantation of severe combined immunodeficiency (SCID) mice. Additionally, human invasive ductal carcinoma (IDC) tissue arrays were used to confirm the hPTTG1/CXCR2/p21 axis established in vitro. In this study, we investigated the mechanism of hPTTG1-induced senescence as well as its role in breast cancer progression and metastasis. Herein, we showed that hPTTG1 overexpression reinforced senescence through the CXCR2/p21 signaling. Furthermore, hPTTG1 overexpression activated NF-κB signaling to transactivate the expression of interleukin (IL)-8 and growth-regulated oncogene alpha (GROα) to execute CXCR2 signaling in MCF-7 cells. When CXCR2 expression was knocked down in hPTTG1-overexpressing MCF-7 cells, hPTTG1-induced senescence was abrogated by alleviating CXCR2-induced p21 expression. In a mouse model, CXCR2-mediated senescence limited hPTTG1-induced tumor growth and metastasis. Moreover, CXCR2 knockdown in hPTTG1-overexpressing MCF-7 tumors dramatically accelerated tumor growth and metastasis. Our in vitro and in vivo results demonstrated that hPTTG1 overexpression reinforces senescence through CXCR2 signaling, and the evasion of CXCR2/p21-dependent senescence was critical to hPTTG1 exerting its oncogenic potential. Interestingly, although CXCR2-dependent senescence restrained hPTTG1-induced tumor progression, when MCF-7 cells and hPTTG1-overexpressing MCF-7 cells were co-transplanted into the mammary fat pads of SCID mice, hPTTG1-overexpressing senescent cells created a metastasis-promoting microenvironment that promoted lung metastasis of the MCF-7 cells. Immunohistochemical analysis of human breast tumor samples also confirmed the importance of the hPTTG1/CXCR2 axis in promoting breast cancer metastasis.\n\nQuestion:\nDoes human pituitary tumor-transforming gene 1 overexpression reinforce oncogene-induced senescence through CXCR2/p21 signaling in breast cancer cells?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo test whether the pulmonary risk of repeated volume recruitment is greater or less than the risk associated with unreversed atelectasis during 6 hrs of high-frequency oscillatory ventilation in the atelectasis-prone rabbit lung. Prospective, controlled, randomized comparison over 6 hrs of ventilator management. Laboratory. Twenty-eight adult New Zealand white male rabbits (weight 2.3 to 2.8 kg). Controversy exists over whether high-frequency oscillatory ventilation should be used with volume recruitment maneuvers in the atelectasis-prone lung, or be used at low mean and peak pressures without volume recruitment to avoid the risks of even transient pulmonary overdistention. Potential risks and benefits accompany both alternatives. We evaluated the pulmonary effects of three high-frequency oscillatory ventilation protocols in anesthetized rabbits made surfactant deficient by saline lavage, using animals ventilated with conventional positive-pressure ventilation with positive end-expiratory pressure as a reference group; n = 5 in each group. The three high-frequency oscillatory ventilation groups were ventilated for 6 hrs at 15 Hz (900 breaths/min), FIO2 = 1.0. The repeated stretch group received 15-sec sustained inflations at 30 cm H2O mean airway pressure every 20 mins, with maintenance mean airway pressure sufficient to keep PaO2 > 350 torr (46.7 kPa). The repeated deflation group was maintained at levels that produced PaO2 70 to 120 torr (9.3 to 16 kPa), with the endotracheal tube opened to atmospheric pressure for 15 secs every 20 mins. Animals in the repeated stretch after deflations group were managed as in the repeated stretch protocol but each sustained inflation was preceded by a 15-sec deflation to functional residual capacity. The conventional positive-pressure ventilation group was ventilated at rates of 30 to 100 breaths/min, keeping PaO2 70 to 120 torr (9.3 to 16 kPa). End-points included terminal functional residual capacity and a compliance index computed from respiratory system pressure-volume curves. After 6 hrs of ventilation, respiratory system compliance in the repeated stretch group had returned to control values (1.35 +/- 0.18 [SD] mL/kg/cm H2O). Respiratory system compliance was significantly less than this number in both the repeated deflation (0.89 +/- 0.08) and repeated stretch after deflations (1.24 +/- 0.22) groups (p < .05). Respiratory system compliance after 3 hrs of conventional positive-pressure ventilation decreased to 0.34 +/- 0.10 mL/kg/cm H2O. Functional residual capacity changes paralleled these changes of respiratory system compliance.\n\nQuestion:\nAre volume recruitment maneuvers less deleterious than persistent low lung volumes in the atelectasis-prone rabbit lung during high-frequency oscillation?\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:\nThe aim of this study was to evaluate in vitro and in vivo effects of a unique high-butyrate-producing bacterial strain from human colonic flora, Enterococcus durans, in prevention and treatment of intestinal inflammation. A compartmentalized Caco-2/leukocyte coculture model was used to examine the in vitro effects of E durans and its metabolite butyrate on basal and Escherichia coli-stimulated secretion of proinflammatory immune factors (IL-8, IL-6, and TNF-α) and the anti-inflammatory cytokine IL-10. A murine model of dextran sodium sulfate-induced colitis was used to examine in vivo effects of prevention and therapy with E durans on clinical, biochemical, and histologic parameters of inflammation. In the coculture model, treatment with E durans and with butyrate reduced basal as well as E coli stimulated secretion of IL-8, IL-6, and TNF-α and increased secretion of IL-10. In the in vivo murine model, preventive administration of E durans significantly ameliorated clinical disease activity index (weight loss, fecal bleeding, and stool consistency), reduced myeloperoxidase concentration in colon tissue extracts, improved histologic scores of colonic inflammation, and inhibited colonic transcription of proinflammatory immune factors. The effect of therapeutic treatment alone on these parameters was more moderate but still significant.\n\nQuestion:\nDoes e durans strain M4-5 isolated from human colonic flora attenuate intestinal inflammation?\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:\nApoptosis is known to play a key role in cell death after retinal ischemia. However, little is known about the kinetics of the signaling pathways involved and their contribution to this process. The aim of this study was to determine whether changes in the expression of molecules in the mitochondrial apoptotic pathway might explain the progression of retinal damage following ischemia/reperfusion. Retinal ischemia was induced by elevating intraocular pressure in the vitreous cavity to 150 mmHg for a period of 60 min. At time 0, 3 h (early phase), and 24 h (late phase) after reperfusion, the retinas were harvested and modifications in the expression of Bax, Bak, Bcl-2, and Bcl-x(L) as well as caspase-3 and -7, were examined by qPCR and, in some cases, by western blot. qPCR analysis performed at the early phase after ischemia revealed a time dependent decrease in Bax, Bak, and Bcl-x(L) and no alteration in Bcl-2 mRNA expression in response to retinal ischemia. At the protein level, proapoptotic Bax and Bak were not modulated while Bcl-2 and Bcl-x(L) were significantly upregulated. At this stage, the Bax per Bcl-2 and Bax:Bcl-x(L) ratios were not modified. At the late phase of recovery, Bax and Bcl-x(L) mRNAs were downregulated while Bak was increased. Increased Bax:Bcl-2 and Bax:Bcl-x(L) ratios at both the mRNA and protein levels were observed 24 h after the ischemic insult. Analysis of caspases associated with mitochondria-mediated apoptosis revealed a specific increase in the expression of caspase-3 in the ischemic retinas 24 h after reperfusion, and a decrease in the expression of caspase-7.\n\nQuestion:\nIs retinal ischemia-induced apoptosis associated with alteration in Bax and Bcl-x ( L ) expression rather than modifications in Bak and Bcl-2?\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:\nLaser Doppler flowmetry (LDF) is increasingly used to assess adequate occlusion after embolic stroke (ES) in rats. Employing LDF, relative regional cerebral blood flow (rCBF) was continuously monitored during the first 2 h following ES and correlated with 24 h 2,3,5-triphenyltetrazolium chloride (TTC)-staining of corrected infarct volume. In a preliminary experiment (n=18), it was demonstrated that rCBF-reduction to 37% or less of baseline correctly identified occlusion success in the suture middle cerebral artery occlusion (sMCAO) model. Using the same methodology, we then assessed whether LDF allowed for identification of animals with successful ES (experiment 2, n=26) and tissue plasminogen activator (tPA)-mediated reperfusion following ES (experiment 3, n=28). In ES rats, 3 infarct patterns were identified: small (<150 mm(3)), medium ( approximately 250 mm(3)), and large (>400 mm(3)). Rats with an rCBF below 45% of preocclusion values had an 80% probability of developing medium to large infarcts, whereas rats with an rCBF above the 45%-threshold had a 100% chance of developing small infarcts. LDF did not reliably detect reperfusion in tPA-treated animals (sensitivity=40%), because it apparently occurred within brain areas remote from the LDF-monitoring site as indicated by TTC-staining and magnetic resonance angiography in a subset of animals.\n\nQuestion:\nDoes laser Doppler flowmetry predict occlusion but not tPA-mediated reperfusion success after rat embolic stroke?\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:\nPatients with gastroesophageal reflux disease (GERD) are advised to avoid alcoholic beverages since alcohol consumption induces gastroesophageal reflux in healthy volunteers and increases it in patients with GERD. Proton-pump inhibitors (PPIs) are frequently administered for reflux symptoms but their effect on gastroesophageal reflux after alcohol consumption has not yet been fully studied. The aim of the present study was therefore to investigate the effect of esomeprazole, an S-enantiomer of omeprazole, on gastroesophageal reflux after beer consumption. In this placebo-controlled, double-blind, crossover study, 16 healthy male volunteers received 20 mg esomeprazole daily for one week. On day 7, in an acute experiment, the subjects then consumed 500 ml beer within 5 min. Subsequently, gastroesophageal reflux was monitored by pH-metry over a period of 3 h. In addition, gastric emptying was measured by ultrasonography and blood concentrations of ethanol, cholecystokinin and gastrin were determined. Gastroesophageal reflux was significantly (p=0.001) reduced by 93% after treatment with esomeprazole (0.2%, median percentage of time pH<4) as compared to placebo (2.6%), but gastric emptying, blood ethanol and cholecystokinin concentrations were not significantly different after esomeprazole treatment. Plasma gastrin levels were significantly (p=0.0003) higher after esomeprazole (98.6+/-19.7 pg/ml) than after placebo (22.7+/-3.8 pg/ml) before beer consumption. However, there was no difference in the increase in plasma gastrin after beer consumption between the esomeprazole treatment and placebo.\n\nQuestion:\nDoes esomeprazole reduce gastroesophageal reflux after beer consumption in healthy volunteers?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe aim of this exploratory analysis was to evaluate if a combination of MR angiography (MRA) and diffusion-weighted imaging (DWI) selection criteria can be used to identify patients with acute stroke who are likely to benefit from early reperfusion. Data from DEFUSE, a study of 74 patients with stroke who received intravenous tissue plasminogen activator in the 3- to 6-hour time window and underwent MRIs before and approximately 4 hours after treatment were analyzed. The MRA-DWI mismatch model was defined as (1) a DWI lesion volume less than 25 mL in patients with a proximal vessel occlusion; or (2) a DWI lesion volume less than 15 mL in patients with proximal vessel stenosis or an abnormal finding of a distal vessel. Favorable clinical response was defined as an improvement on the National Institutes of Health Stroke Scale score of at least 8 points between baseline and 30 days or a National Institutes of Health Stroke Scale score </=1 at 30 days. Twenty-seven of 62 patients (44%) had an MRA-DWI mismatch. There was a differential response to early reperfusion based on MRA-DWI mismatch status. Reperfusion was associated with an increased rate of a favorable clinical response in patients with an MRA-DWI mismatch (OR, 12.5; 95% CI, 1.8 to 83.9) and a lower rate in patients without mismatch (OR, 0.2; 95% CI, 0.0 to 0.8).\n\nQuestion:\nDoes the MRA-DWI mismatch identify patients with stroke who are likely to benefit from reperfusion?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe aim of this study was to estimate relations between sputum neutrophilia and the chemotactic activity of peripheral blood neutrophils after the bronchial allergen challenge in asthma patients. Fifteen patients with allergic asthma (AA), 13 patients with allergic rhinitis (AR), all sensitized to Dermatophagoides pteronyssinus, and 8 healthy subjects (HS) underwent bronchial challenge with D. pteronyssinus. Sputum and peripheral blood collection were performed 24 h before, 7 and 24 h after the bronchial challenge. Cell counts were determined by the May-Grünwald-Giemsa method. Neutrophil chemotaxis was analyzed by a flow cytometer; IL-8 levels were measured by ELISA. Sputum neutrophil count and peripheral blood neutrophil chemotaxis of patients with AA were greater 7 and 24 h after the challenge compared with the baseline values and patients with AR and HS (P < 0.05). Moreover, a significant correlation was found between the neutrophil count in sputum and IL-8 levels, and the chemotactic activity of peripheral blood neutrophils 24 h after the bronchial challenge only the patients with AA (P < 0.05).\n\nQuestion:\nIs sputum neutrophil count after bronchial allergen challenge related to peripheral blood neutrophil chemotaxis in asthma 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:\nThe prolactin response to serotonergic stimulation has been used as an index of central nervous system serotonin function. We evaluated the prolactin response to d,l-fenfluramine to determine whether subtypes of alcoholics differed in prolactin responsivity compared with nonalcoholics and whether cigarette smoking affected prolactin response. One hundred ten healthy, abstinent men across four groups (controls [23% smokers]; alcoholics [72% smokers]; alcoholics with antisocial personality disorder [94% smokers]; nonalcoholic antisocials [88% smokers]) received d,l-fenfluramine (100 mg orally) in a randomized, double-blind, placebo-controlled study. Plasma prolactin levels were obtained at baseline and at half-hour intervals for 5 hr after fenfluramine/placebo administration. Plasma fenfluramine and norfenfluramine levels were obtained hourly. Smokers had a blunted prolactin response to fenfluramine compared with nonsmokers without any alcoholism or antisocial personality effects. Using a cutoff point of delta peak prolactin < 10 ng/ml, more smokers (41/76, 54%) had a dampened response to fenfluramine than did nonsmokers (7/34, 21%) [chi2(1) = 10.6, p < 0.003]. The percentage of low responders was greatest among smokers regardless of whether they were healthy controls, alcoholics, or antisocial. Multiple regression revealed that three variables--(1) number of pack-years of smoking, (2) actual dosage of fenfluramine received, and (3) plasma norfenfluramine level obtained--explained 43% of the variance (R2 = 0.43) in delta prolactin area under the curve. Variables that included alcoholism diagnostic status, antisocial personality diagnostic status, and impulsive aggressive personality, depressive, and suicidal traits failed to explain any additional unique variance.\n\nQuestion:\nDoes cigarette smoking decrease the prolactin response to serotonergic stimulation in subgroups of alcoholics and controls?\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 reported that sorafenib sensitizes hepatocellular carcinoma (HCC) cells to TRAIL through the inhibition of signal transducer and activator of transcription 3 (STAT3). Here, we report that sorafenib inhibits HCC via a kinase-independent mechanism: SHP-1 dependent STAT3 inactivation. SC-1 is a sorafenib derivative that closely resembles sorafenib structurally but with no kinase inhibition activity. HCC cell lines (PLC5, Huh-7, Hep3B, and Sk-Hep1) were treated with sorafenib or SC-1 and apoptosis and signal transduction were analyzed. In vivo efficacy was determined in nude mice with Huh-7 xenografts. SC-1 showed similar effects to sorafenib on growth inhibition and apoptosis in all tested HCC cell lines. SC-1 down-regulated phosphorylation of phospho-STAT3 (p-STAT3) at tyrosine 705 in all tested HCC cells. Expression of STAT3-driven genes, including Cyclin D1 and Survivin, was also repressed by SC-1. Luciferase reporter assay confirmed the inhibition of transcriptional activity of STAT3 in both sorafenib-treated and SC-1-treated cells. Ectopic expression of STAT3 in PLC5 cells abolished apoptosis in SC-1-treated cells. Sorafenib and SC-1 up-regulated SHP-1 activity. Knockdown of SHP-1, but not SHP-2 or PTP-1B, by small interference RNA reduced apoptosis induced by SC-1. Finally, SC-1 reduced Huh-7 tumor growth significantly in vivo, which was associated with down-regulation of p-STAT3 and up-regulation of SHP-1 activity.\n\nQuestion:\nIs signal transducer and activator of transcription 3 a major kinase-independent target of sorafenib in hepatocellular carcinoma?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo describe the operative procedure and report the clinical outcomes of articular surface reconstruction for various hand joint disorders using autologous osteochondral grafts from the knee. Ten patients underwent articular surface reconstruction for hand joint disorders with autologous osteochondral grafts from the patellofemoral joint. Mean patient age was 35 years (range, 15-52 y). The patients were followed for an average of 48 months (range, 16-89 mo). Arthroplasty was performed on the metacarpophalangeal joint in 4 cases, and on the proximal interphalangeal joint in 6 cases. The patients' clinical outcomes were evaluated with joint range of motion, visual analog scale (0-10 points), and Disabilities of the Arm, Shoulder, and Hand (DASH) score. Histological examination was performed in 3 cases after surgery. Graft union was confirmed in all cases without radiographic evidence of resorption or necrosis. Follow-up radiographic examinations showed good graft incorporation without signs of osteoarthritis such as joint space narrowing. The finger flexion-extension arc improved significantly from an average of 21° to 61°. The mean visual analog scale also improved significantly from 7.0 to 1.5. The mean total active motion showed a significant improvement from 151° before surgery to 201° after surgery, and the mean DASH score improved significantly from 33 to 12. There were no significant differences for the arc of finger motion and DASH score between metacarpophalangeal and proximal interphalangeal joint disorders or between hemiarthroplasty and total joint arthroplasty. Histological examination revealed viable chondrocytes in the implanted cartilage.\n\nQuestion:\nDo joint Arthroplasty With Osteochondral Grafting From the Knee for Posttraumatic or Degenerative Hand Joint Disorders?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo bring further understanding to the relationship between hormonal therapy (HT) and breast arterial calcification (BAC). Of women arriving for breast cancer screening mammography, 1995 consented to complete a survey and have their mammograms analyzed for the presence of BAC. The survey assessed HT use and major risk factors for CAD. Of the 1919 women with complete data, there were 268 with BAC (14%). When categorized into three age groups, BAC was present in 40.7% of the women > or =65, 10.9% of those 55-64 and 3.0% of those <55. The > or =65 year-old group showed a nearly 50%-point lower prevalence of BAC among HT users compared with women who were not on HT (25.8% versus 74.2%, respectively, p=0.006). With age included as a continuous variable, past use of HT was significantly associated with a lower prevalence of BAC (p<0.03), while the presence of diabetes or a history of stroke were significantly associated with a higher prevalence of BAC (p<0.002).\n\nQuestion:\nIs hormonal therapy associated with a lower prevalence of breast arterial calcification on mammography?\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:\nOsteosarcoma arises predominantly in the metaphyseal growth plate of children during the growth spurt years. These tumors develop during physiological growth from an expanding cell population, suggesting that the transformed cell is a bone-forming progenitor. An absence of the p53 oncogene has been implicated in the origin and progression of osteosarcoma, and because mesenchymal stem cells (MSCs) are the physiological osteogenic progenitor cell population, we hypothesized that a p53-/- mutation would enhance bone differentiation of MSC in a mouse model of in vitro osteogenesis. Clonal MSC populations were derived from p53-/- mice. P53-/- and wild-type cells were placed in osteogenic culture and assessed via Alizarin Red quantification and alkaline phosphatase staining. The osteogenic marker genes Cbfa1, osteopontin, and osteocalcin were assessed by quantitative real time polymerase chain reaction during differentiation. Bone nodule formation and alkaline phosphatase staining was accelerated and enhanced in the p53-/- cells. The early and intermediate osteogenic markers, Cbfa1 and osteopontin, were upregulated in p53-/- MSCs compared with wild-type cells during osteogenesis. The terminal osteogenic marker gene osteocalcin was paradoxically lower in p53-/- MSCs indicating impaired terminal differentiation.\n\nQuestion:\nDoes absence of the p53 tumor suppressor gene promote osteogenesis in mesenchymal stem cells?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nLycopene β-cyclase (LCYB) is a key enzyme catalyzing the biosynthesis of β-carotene, the main source of provitamin A. However, there is no documented research about this key cyclase gene's function and relationship with β-carotene content in wheat. Therefore, the objectives of this study were to clone TaLCYB and characterize its function and relationship with β-carotene biosynthesis in wheat grains. We also aimed to obtain more information about the endogenous carotenoid biosynthetic pathway and thus provide experimental support for carotenoid metabolic engineering in wheat. In the present study, a lycopene β-cyclase gene, designated TaLCYB, was cloned from the hexaploid wheat cultivar Chinese Spring. The cyclization activity of the encoded protein was demonstrated by heterologous complementation analysis. The TaLCYB gene was expressed differentially in different tissues of wheat. Although TaLCYB had a higher expression level in the later stages of grain development, the β-carotene content still showed a decreasing tendency. The expression of TaLCYB in leaves was dramatically induced by strong light and the β-carotene content variation corresponded with changes of TaLCYB expression. A post-transcriptional gene silencing strategy was used to down-regulate the expression of TaLCYB in transgenic wheat, resulting in a decrease in the content of β-carotene and lutein, accompanied by the accumulation of lycopene to partly compensate for the total carotenoid content. In addition, changes in TaLCYB expression also affected the expression of several endogenous carotenogenic genes to varying degrees.\n\nQuestion:\nDoes the lycopene β-cyclase play a significant role in provitamin A biosynthesis in wheat endosperm?\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:\nSPECT/CT is a hybrid imaging modality, which combines a 3D scintigraphy (SPECT) and a conventional computerised tomography (CT). SPECT/CT allows accurate anatomical localisation of metabolic tracer activity. It allows the correlation of surgical factors such as tunnel position and orientation with mechanical alignment, clinical outcome and biological factors. The purpose of this study was to investigate whether the SPECT/CT tracer uptake (intensity and distribution) correlates with the stability and laxity of the knee joint and the position and orientation of the tibial and femoral tunnels in patients after anterior cruciate ligament (ACL) reconstruction. A consecutive series of knees (n=66), with symptoms of pain and/or instability after ACL reconstruction were prospectively evaluated using clinical examination and 99mTc-HDP-SPECT/CT. Clinical laxity testing was performed using the Rolimeter (Ormed, Freiburg, Germany) including Lachman testing (0-2 mm, 3-5 mm, 6-10 mm, >10 mm), anterior drawer test (0-2 mm, 3-5 mm, 6-10 mm, >10 mm), pivot shift test (positive versus negative) and patient-based subjective instability (yes versus no). For analysis of SPECT/CT tracer uptake a previously validated SPECT/CT localisation scheme consisting of 17 tibial, nine femoral and four patellar regions on standardised axial, coronal, and sagittal slices was used. The tracer activity on SPECT/CT was localised and recorded using a 3D volumetric and quantitative analysis software. Mean, standard deviation, minimum and maximum of grading for each area of the localisation scheme were recorded. The position and orientation of the tibial and femoral tunnel was assessed using a previously published method on 3D-CT. Correlation of instability, pivot shift as well as clinical laxity testing with 99mTc-HDP-SPECT/CT tracer uptake intensity and distribution showed no significant correlation. 99mTc-HDP-SPECT/CT tracer uptake correlated significantly with the position and orientation of the ACL graft. A more horizontal femoral graft position showed significantly increased tracer uptake within the superior and posterior femoral regions. A more posteriorly-placed femoral insertion site showed significantly more tracer uptake within the femoral and tibial tunnel regions. A more vertical or a less medial tibial tunnel orientation showed significant increased uptake within the tibial and femoral tunnel regions. A more anterior tibial tunnel position showed significantly more tracer uptake in the femoral and tibial tunnel regions as well as the entire tibiofemoral joint.\n\nQuestion:\nIs sPECT/CT tracer uptake influenced by tunnel orientation and position of the femoral and tibial ACL graft insertion site?\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 plays an important role in the pathophysiology of vascular disease. In this study, we aimed to evaluate the associations of neutrophil to lymphocyte ratio (NLR; an indicator of inflammation) with left ventricular ejection fraction and ascending aorta diameter in patients with a bicuspid aortic valve (BAV). One hundred and thirty-nine consecutive patients with the diagnosis of BAV were enrolled in the study. Complete blood counts were analyzed for neutrophil and lymphocyte levels and NLR. The subjects were separated into two groups based on their ascending aorta diameter. The patients with ascending aorta diameter equal to or above 3.9 cm were included in group 1 whereas those with ascending aorta diameter below 3.9 cm were included in group 2. When the results were compared, it was demonstrated that there was a positive correlation between NLR and ascending aorta diameter (r: 0.485, P = 0.026), whereas there was a negative correlation between NLR and left ventricular end-diastolic diameter (r: 0.475, P = 0.030), left ventricular end-systolic diameter (r: 0.482, P = 0.027), and left ventricular ejection fraction (r: -0.467, P = 0.033) in BAV patients with ascending aorta dilatation (group 1).\n\nQuestion:\nIs higher neutrophil to lymphocyte ratio related to a lower ejectionfraction in bicuspid aortic valve 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:\nThe major side-effects of bevacizumab in glioma treatment are venous thromboembolic events (VTE). We retrospectively evaluated factors potentially predictive of thromboembolic events. Bevacizumab, alone or in combination with chemotherapy was used as salvage therapy for recurrence in malignant glioma every two weeks. None but one patient received anti-coagulants. Before each bevacizumab cycle differential blood cell count, kidney and liver parameters, D-dimers, neurological status, body-mass index, vital signs and signs of venous thrombosis were assessed. Thirty-eight patients received 428 cycles of bevacizumab. In five patients (13%), six VTE were observed. These complications were preceded four weeks before the onset of symptoms by D-dimer elevation above 0.865 mg/l [p<0.0001; sensitivity=89% (95% confidence interval=83-93%); specificity=89% (95% CI=52-100%)]. An existing hemiparesis constituted a 27-fold risk elevation for thrombotic complication (p<0.0001, χ(2)-test).\n\nQuestion:\nDo d-dimer elevation and paresis predict thromboembolic events during bevacizumab therapy for recurrent malignant glioma?\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 non-canonical NF-κB activating kinase IKKα, encoded by CHUK (conserved-helix-loop-helix-ubiquitous-kinase), has been reported to modulate pro- or anti- inflammatory responses, cellular survival and cellular differentiation. Here, we have investigated the mechanism of action of IKKα as a novel effector of human and murine chondrocyte extracellular matrix (ECM) homeostasis and differentiation towards hypertrophy. IKKα expression was ablated in primary human osteoarthritic (OA) chondrocytes and in immature murine articular chondrocytes (iMACs) derived from IKKα(f/f):CreERT2 mice by retroviral-mediated stable shRNA transduction and Cre recombinase-dependent Lox P site recombination, respectively. MMP-10 was identified as a major target of IKKα in chondrocytes by mRNA profiling, quantitative RT-PCR analysis, immunohistochemistry and immunoblotting. ECM integrity, as assessed by type II collagen (COL2) deposition and the lack of MMP-dependent COL2 degradation products, was enhanced by IKKα ablation in mice. MMP-13 and total collagenase activities were significantly reduced, while TIMP-3 (tissue inhibitor of metalloproteinase-3) protein levels were enhanced in IKKα-deficient chondrocytes. IKKα deficiency suppressed chondrocyte differentiation, as shown by the quantitative inhibition of.Alizarin red staining and the reduced expression of multiple chondrocyte differentiation effectors, including Runx2, Col10a1 and Vegfa,. Importantly, the differentiation of IKKα-deficient chondrocytes was rescued by a kinase-dead IKKα protein mutant.\n\nQuestion:\nDoes iKKα/CHUK regulate extracellular matrix remodeling independent of its kinase activity to facilitate articular chondrocyte differentiation?\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:\nAdverse environmental conditions elicit dry eye (DE)-related signs and symptoms. The purpose of this work is to determine whether these conditions can alter a normal-to-borderline ocular surface in subjects with DE symptoms. Ten minimally symptomatic contact lens (CL)-wearing subjects were exposed, without (WO-) and with (W-)CLs, to a controlled adverse environment (CAE) of 22.0 +/- 2.0 degrees C and 19.0% +/- 4.0% relative humidity (RH) for 2 hours in an environmental chamber (EC). One month later, the same subjects were placed in an indoor normal environment (INE) of 24.2 +/- 1.3 degrees C and 34.8% +/- 2.9% RH for 2 hours. DE-related signs and symptoms were evaluated before and after each exposure. The reversibility of changes provoked by CAE or INE was also evaluated. Without CL wear, significant changes were found in DE signs (noninvasive tear break-up time [NIBUT], conjunctival hyperemia and phenol red thread test) after CAE exposure, but not found after INE exposure. However with CL wear, the same tests were altered after both CAE and INE exposure. Most of these changes returned to normal values within 1 month after environmental exposure.\n\nQuestion:\nDoes exposure to a controlled adverse environment impair the ocular surface of subjects with minimally symptomatic dry eye?\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:\nAdolescent idiopathic scoliosis (characterized by a morphological deformation of the trunk) prompts the development of new postural control strategies. This adaptation has an influence on the dynamics of motor behaviour. The present study analysed ground reaction forces during lateral stepping in order to highlight the dynamic consequences of idiopathic scoliosis. Ten adolescents suffering from idiopathic scoliosis with right thoracic curvature (Cobb angle>or=15 degrees) and 15 healthy adolescents participated in the study. We used two force platforms to record ground reaction forces for the right and left legs during large and small lateral steps (LSs). Our results revealed intergroup and interlimb differences for both types of step. For small LSs, right-side (i.e. convexity side) initiation induced a significant increase in the ground reaction force impulse during the postural phase for the scoliotic group, when compared with the control group. For large LSs, left-side (i.e. concavity side) initiation induced a significant increase in ground reaction force impulse during the landing phase only. Patients always displayed slower dynamic behaviour than healthy controls. For both stepping sides, the asymmetry index (AI) was higher in the scoliotic group than in the control group (0.2<or=AI>or=85 in the scoliotic group versus 0.1<AI>24.4 in the control group). Furthermore, the scoliotic group showed a significant increase in the variability of the dynamic parameters (>8%).\n\nQuestion:\nDo lateral steps reveal adaptive biomechanical strategies in adolescent idiopathic scoliosis?\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:\nWorldwide, asthma and COPD are common causes of disability or death. Few studies have been made concerning the association with socioeconomic status (SES) and these diseases. The aim of this nationwide population-based study was to determine the association with educational and income levels (SES) and chronic airway diseases (CAD), i.e., asthma or COPD (FEV1/FVC < 0.70). Univariate and multivariate logistic regression were used to estimate odds ratios in relation to education and household income, using age, gender, smoking in lifetime and body mass index as possible confounders. In this population-based cohort aged ≥30 years the prevalence of asthma was 9% (588/6525). COPD was observed in 5% (338/6525) of research subjects. In the multivariate logistic regression analysis when adjusted for gender, age, smoking history and BMI, the basic educational level remained an independent risk factor for COPD (OR 1.8, 95% CI 1.2-2.6) and the low household income for asthma (OR 1.4, 95% CI 1.0-1.9).\n\nQuestion:\nIs low socioeconomic status associated with chronic obstructive airway diseases?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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