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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 determine the phylogenetic group and the production of different virulence factors (VFs) of a collection of Escherichia coli strains overproducing their chromosomal AmpC cephalosporinase. Fifty-five E. coli strains, isolated over a 12 year period, and previously identified as AmpC overproducers by increased MICs of third-generation cephalosporins without extended-spectrum beta-lactamase production (negative double-disc synergy test), were phylogrouped by multiplex PCR. As a comparison, 100 E. coli clinical isolates, susceptible to all beta-lactams, were also tested by the same method. The ampC promoter sequence was determined for all these isolates. ERIC-2 PCR (where ERIC stands for enterobacterial repetitive intergenic consensus) was used to compare the isolates. Search for virulence-associated genes (papG alleles, sfa/foc, hly and iucC) was performed by multiplex PCR for the 55 AmpC overproducers. Most of the AmpC overproducers (47/55) belonged to phylogenetic group A, correlated with a low prevalence of the main VFs in these strains. The - 32, -42 and - 11 mutations, responsible for AmpC overproduction, were usually associated with DNA polymorphisms at positions - 88, - 82, -18, +1 and + 58 in the ampC promoter. In the control susceptible isolates, these polymorphisms were detected in 13 ampC promoters (9 group B1 and 4 group A). These polymorphisms were never associated with the main phylogenetic group B2, representing 66% of the susceptible isolates.\n\nQuestion:\nDo most Escherichia coli strains overproducing chromosomal AmpC beta-lactamase belong to phylogenetic group A?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMiR-198 has been considered as an inhibitor of cell proliferation, invasion, migration and a promoter of apoptosis in most cancer cells, while its effect on non-cancer cells is poorly understood. The effect of miR-198 transfection on HaCaT cell proliferation was firstly detected using Cell Count Kit-8 and the cell cycle progression was analyzed by flow cytometry. Using bioinformatics analyses and luciferase assay, a new target of miR-198 was searched and identified. Then, the effect of the new target gene of miR-198 on cell proliferation and cell cycle was also detected. Here we showed that miR-198 directly bound to the 3'-UTR of CCND2 mRNA, which was a key regulator in cell cycle progression. Overexpressed miR-198 repressed CCND2 expression at mRNA and protein levels and subsequently led to cell proliferation inhibition and cell cycle arrest in the G1 phase. Transfection ofSiCCND2 in HaCaT cells showed similar inhibitory effects on cell proliferation and cell cycle progression.\n\nQuestion:\nDoes miR-198 repress the Proliferation of HaCaT Cells by Targeting Cyclin D2?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nEosinophilic pleural effusion (EPE) is characterized by greater than 10% eosinophilia and is frequently associated with air and/or blood in the pleural cavity. Primary spontaneous pneumothorax (PSP), defined as the spontaneous presence of air in the pleural space, is one of the most common causes of EPE. Recent studies have shown that type 2 immune responses play important roles in eosinophilic airway inflammation resulting in pleural pathology. To determine the predominant immune responses associated with PSP in humans, and to examine whether IL-33, thymic stromal lymphopoietin (TSLP), or type 2 innate lymphoid cell (ILC2)-mediated immune responses are associated factors. Eosinophil-associated cytokines were measured in the pleural fluid of patients with PSP and control subjects. Th2 cell and ILC2 responses in the pleural cavity and peripheral blood were also evaluated by in vitro restimulation and intracellular cytokine staining of T cells and ILC2s in patients with PSP (n = 62) and control subjects (n = 33). IL-33-mediated IL-5 production by ILC2s was also evaluated. Significantly higher concentrations of IL-5 and eotaxin-3 were detected in the pleural fluid of patients with PSP, in addition to significantly higher concentrations of IL-33 and TSLP. Although IL-5 production was induced by IL-33 treatment of ILC2s, other Th2 cell-mediated immune responses were not detected.\n\nQuestion:\nIs innate type 2 immunity associated with eosinophilic pleural effusion in primary spontaneous pneumothorax?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPhysician counseling on the risks of tobacco smoking and the benefits of cessation has been shown to be an effective method of increasing the rate of smoking cessation. Using the \"Help Your Patients Quit Smoking: A Coaching Guide\" also referred to as the \"7A's of Smoking Cessation\" guideline from the New York City Department of Health and Mental Hygiene is thought to be effective to convey the importance of smoking cessation. To study the efficacy of the \"7A's of Smoking Cessation\" guideline counseling conducted by osteopathic medical students. Osteopathic medical students were trained to counsel smokers for 3-10 min based on New York City Department of Health's \"7A's of Smoking Cessation\" guidelines by a licensed physician. Students then counseled health fair participants who were cigarette smokers for 3-10 min. Postcounseling, participants were administered an 4 question survey to evaluate the effect counseling had on their desire to quit smoking. Survey data were collected and analyzed. Institutional Review Board approval was obtained for this study. A total of 13 anonymous health fair participants who were also smokers were administered both counseling sessions and surveys. 11/13 (84.6%) participants stated that the session motivated them to quit smoking. 9/13 (69.2%) participants responded that they were now motivated to discuss smoking cessation with their doctor after being counseled. Of these participants 12/13 (92.3%) had previously attempted to quit smoking without success.\n\nQuestion:\nIs osteopathic Medical Student Administered Smoking Cessation Counseling an Effective Tool?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 examine the hypothesis that induction of heat shock proteins in human endothelial cells (ECs) by either heat shock or sodium arsenite could prevent subsequent EC necrosis induced by activated human polymorphonuclear neutrophil leukocytes (PMNs). Cultures of ECs were exposed to heat shock (42 degrees C, 30 to 60 minutes) or sodium arsenite (40 to 320 mumol/L) for 6 hours to induce the expression of a heat shock protein of 72-kd molecular weight (HSP-72). Activated PMNs were subsequently added to these ECs for 24 hours to evaluate the ability of HSP-72 to prevent activated PMN-mediated EC necrosis. Neither EC necrosis nor apoptosis was induced by heat shock. Sodium arsenite (40 to 80 mumol/L) did not induce EC necrosis, although 320-mumol/L sodium arsenite caused a significant increase in EC necrosis. Sodium arsenite (80 to 320 mumol/L) also induced dose-dependent EC apoptosis. Endothelial cells exposed to heat shock and sodium arsenite (40 and 80 mumol/L) significantly attenuated subsequent EC necrosis induced by activated PMNs. However, sodium arsenite at 320 mumol/L aggravated activated PMN-mediated EC necrosis. Expression of HSP-72 was detected after ECs were treated both with heat shock and sodium arsenite (40 to 320 mumol/L) for 6 hours.\n\nQuestion:\nDoes induction of heat shock protein 72 prevent neutrophil-mediated human endothelial cell necrosis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 attempted to determine the molecular mechanism of fluid shear stress-induced lipocalin-type prostaglandin D synthase (l-PGDS) expression in vascular endothelial cells. We examined the promoter region of the l-PGDS gene by loading laminar shear stress (20 dyne/cm2), using a parallel-plate flow chamber, on endothelial cells transfected with luciferase reporter vectors containing the 5'-flanking regions of the human l-PGDS gene. A deletion mutant analysis revealed that a shear stress-responsive element resided in the region between -2607 and -2523 bp. A mutation introduced into the putative binding site for activator protein-1 (AP-1) within this region eliminated the response to shear stress. In an electrophoretic mobility shift assay, shear stress stimulated nuclear protein binding to the AP-1 binding site, which was supershifted by antibodies to c-Fos and c-Jun. Shear stress elevated the c-Jun phosphorylation level in a time-dependent manner, similar to that of l-PGDS gene expression. SP600125, a c-Jun N-terminal kinase inhibitor, decreased the c-Jun phosphorylation, DNA binding of AP-1, and l-PGDS expression induced by shear stress. Additionally, an mRNA chase experiment using actinomycin D demonstrated that shear stress did not stabilize l-PGDS mRNA.\n\nQuestion:\nDoes activator protein-1 mediate shear stress-induced prostaglandin d synthase gene expression in vascular endothelial cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWhile a relationship between alcohol and cardiovascular risk factors is well established, data suggest that the type of alcoholic beverage could modulate this relationship. To determine whether drinking patterns modulate the relationship between alcohol and cardiovascular risk factors. We tested the relationship between preference of alcoholic beverages and atherosclerotic risk factors in a cross-sectional study of 2,126 men. A hierarchical clustering method determined six drinking patterns, 'low drinkers', 'high quality wines', 'beer and cider', 'digestives', 'local wines', and 'table wines', according to the preferential intake of alcoholic beverages. Logistic models estimated the relative risk of abnormal markers in the drinking patterns compared with low drinkers. Unadjusted estimates investigated the relationship with the cluster as a group, while adjustment on alcohol, nutritional and socio-demographic factors investigated the relationship with the preference of alcoholic beverage in itself. Abstainers had high total plasma homocysteine (tHcy), even after full adjustment (odds ratio (OR) = 1.6, 95% confidence interval (CI): 1.0, 2.8). Drinkers of high quality wine had low lipoprotein( a), high tHcy and high body mass index; beer and cider drinkers had high tHcy and waist circumference. Drinkers of digestives had high triacylglycerol; after adjustment they were at risk of low apolipoprotein A-I (OR = 3.1, 95% CI: 1.2, 7.3), and high tHcy (OR = 4.9, 95% CI: 1.2, 33.3). Local wines drinkers were similar to low drinkers. Table wine drinkers had high apolipoprotein B, high triacylglycerol, and high waist-to-hip ratio.\n\nQuestion:\nAre drinking patterns associated with variations in atherosclerotic risk factors in French men?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo investigate whether granulocyte-colony stimulating factor (G-CSF) can decrease the extent of ovarian follicle loss caused by cisplatin treatment. Twenty-one adult female Sprague-Dawley rats were used. Fourteen rats were administered 2 mg/kg/day cisplatin by intraperitoneal injection twice per week for five weeks (total of 20 mg/kg). Half of the rats (n=7) were treated with 1 mL/kg/day physiological saline, and the other half (n=7) were treated with 100 μg/kg/day G-CSF. The remaining rats (n=7, control group) received no therapy. The animals were then euthanized, and both ovaries were obtained from all animals, fixed in 10% formalin, and stored at 4°C for paraffin sectioning. Blood samples were collected by cardiac puncture and stored at -30°C for hormone assays. All follicle counts (primordial, primary, secondary, and tertiary) and serum anti-Müllerian hormone levels were significantly increased in the cisplatin+G-CSF group compared to the cisplatin+physiological saline group.\n\nQuestion:\nDoes granulocyte-colony stimulating factor decrease the extent of ovarian damage caused by cisplatin in an experimental rat model?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nGalectin-3 (gal-3) participates in a variety of biological events, including cell adhesion, proliferation, differentiation and apoptosis. The aim of this study was to determine the relationship of gal-3 expression with clinicopathological findings and prognosis in patients with gastric cancer. Gal-3 and Ki-67 expressions were assessed by immunohistochemistry in 115 patients with gastric cancer. PCR-single strand conformation polymorphism (SSCP)-sequence analysis and the levels of gal-3 mRNA were also examined. The present study demonstrated that gal-3 expression was correlated with nodal status, lymphatic inivasion, pathological stage and histological parameters. On the other hand, gal-3 expression did not correlate with the expression of Ki-67. Reduced expression of gal-3 was significantly associated with a poor prognosis and multivariate analysis showed that gal-3 expression was an independent prognostic factor. On PCR-SSCP-sequence analysis, 2 single nucleotide polymorphisms (SNPs) were detected in the gal-3 gene, but none showed mutations.\n\nQuestion:\nIs reduced galectin-3 expression an indicator of unfavorable prognosis in gastric cancer?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nExchange transfusion (ET) has remained a controversial adjunct therapy for the treatment of severe malaria. In order to assess the relative contribution of ET to parasite clearance in severe malaria, all patients receiving ET as an adjunct treatment to parenteral quinine or to artesunate were compared with patients treated with parenteral treatment with quinine or artesunate but who did not receive ET. ET was executed using a standardized manual isovolumetric exchange protocol. All patients in the Rotterdam Malaria Cohort treated for severe P. falciparum malaria at the Institute for Tropical Diseases of the Harbour Hospital between 1999 and 2011 were included in this retrospective follow-up study. Both a two-stage approach and a log-linear mixed model approach were used to estimate parasite clearance times (PCTs) in patients with imported malaria. Severe malaria was defined according to WHO criteria. A total of 87 patients with severe malaria was included; 61 received intravenous quinine, whereas 26 patients received intravenous artesunate. Thirty-nine patients received ET as an adjunct treatment to either quinine (n = 23) or artesunate (n = 16). Data from 84 of 87 patients were suitable for estimation of parasite clearance rates. PCTs were significantly shorter after administration of artesunate as compared with quinine. In both models, ET did not contribute significantly to overall parasite clearance.\n\nQuestion:\nDoes manual blood exchange transfusion significantly contribute to parasite clearance in artesunate-treated individuals with imported severe Plasmodium falciparum malaria?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHepatocellular carcinoma (HCC) frequently arises in the context of chronic injury that promotes DNA damage and chromosomal aberrations. The cyclin-dependent kinase inhibitor p21 is an important transcriptional target of several tumor suppressors, which promotes cell cycle arrest in response to many stimuli. The aim of this study was to further delineate the role of p21 in the liver during moderate and severe injury and to specify its role in the initiation and progression of HCC. Deletion of p21 led to continuous hepatocyte proliferation in mice with severe injury allowing animal survival but also facilitated rapid tumor development, suggesting that control of compensatory proliferation by high levels of p21 is critical to the prevention of tumor development. Unexpectedly, however, liver regeneration and hepatocarcinogenesis was impaired in p21-deficient mice with moderate injury. Mechanistically, loss of p21 was compensated by activation of Sestrin2, which impaired mitogenic mammalian target of rapamycin (mTOR) signaling and activated cytoprotective Nrf2 signaling.\n\nQuestion:\nDoes the degree of liver injury determine the role of p21 in liver regeneration and hepatocarcinogenesis in mice?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo determine whether field photodynamic therapy (PDT) of actinic keratoses using a novel preparation of 5-aminolevulonic acid (novel ALA) results in fewer subsequent invasive skin cancers developing on the face of individuals with previous facial cutaneous malignancy in a prospective randomized controlled trial. Intervention patients received two treatments of novel ALA 2 weeks apart. Controls were observed. Patients were followed up with biopsy of any suspicious lesions for 3 years. The trial was suspended early because of problems with trial governance and the reporting of severe adverse events. Sixty-four patients who were recruited at that time at one center were monitored. Their average age was 71, and 57% were male. Patients were randomized to intervention (n = 34) or observation (n = 29). Over the subsequent 3 years, 13 intervention patients (38%) developed 30 new cutaneous malignancies in the field treated, and 11 control patients (38%) developed 22 new malignancies. Some intervention patients experienced prolonged adverse events, including permanent scarring.\n\nQuestion:\nDoes novel photodynamic therapy prevent new skin cancers -- randomized controlled trial?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis study investigated whether kinesthetic and/or visual imagery could alter the contingent negative variation (CNV) for patients with Parkinson's disease (PD). The CNV was recorded in six patients with PD and seven controls before and after a 10min block of imagery. There were two types of imagery employed: kinesthetic and visual, which were evaluated on separate days. The global field power (GFP) of the late CNV did not change after the visual imagery for either group, nor was there a significant difference between the groups. In contrast, kinesthetic imagery resulted in significant group differences pre-, versus post-imagery GFPs, which was not present prior to performing the kinesthetic imagery task. In patients with PD, the CNV amplitudes post-, relative to pre-kinesthetic imagery, increased over the dorsolateral prefrontal regions and decreased in the ipsilateral parietal regions. There were no such changes in controls.\n\nQuestion:\nDoes kinesthetic but not visual imagery assist in normalizing the CNV in Parkinson 's disease?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nChildren and adolescents are encouraged to maintain a habitually active lifestyle because of the known health benefits associated with regular physical activity, but there are some reports that a high level of activity may be associated with increased fracture risk. This prospective controlled exercise intervention study in prepubertal children evaluated if a school-based exercise intervention could enhance growth-related gains in muscle strength and muscular function without affecting fracture risk. Fractures were registered in 417 girls and 500 boys age 7-9 yr in the intervention and in 836 age-matched girls and 872 boys. The intervention included 40 min·d of school physical education for 2 yr, whereas the controls achieved 60 min·wk. In a subsample consisting of 49 girls and 80 boys in the intervention and 50 girls and 53 boys in the control group, body composition was measured by dual-energy x-ray absorptiometry, muscle strength by isokinetic peak torque (PT) of the knee extensors, and flexors at 60 and 180°·s by a computerized dynamometer and neuromuscular performance by vertical jump height. The rate ratio (95% confidence interval) for children in the intervention group to sustain a fracture was 1.07 (0.66-1.68). The annual gain in knee extensor PT at 180°·s was significantly higher for both girls (P < 0.001) and boys (P < 0.01) in the intervention compared with the control group. Boys in the intervention group also had a greater annual gain in knee flexion PT at 180°·s (P < 0.001), and girls had a greater gain in vertical jump height (P < 0.05).\n\nQuestion:\nDoes an increase in school-based physical education increase muscle strength in children?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 effect of Ac-hE-18A-NH2 on TNF-α secretion and mRNA expression in ox-LDL-stimulated RAW264.7 macrophages and to elucidate the possible mechanisms. Macrophages were incubated in the medium containing various concentrations of Ac-hE18A-NH2 (1-50 μg/mL) with ox-LDL (50 μg/mL) stimulated. The TNF-α level and intracellular cholesterol content were measured by commercially available quantitation kits following the manufacturer's instructions. TNF-α and ATP-binding cassette transporter A1 (ABCA1) mRNA expression were detected by real-time PCR. ABCA1 and IκB protein -expression in the macrophages were determined by Western blot. NF-κB activity was evaluated by electrophoretic mobility shift assay (EMSA). Ox-LDL stimulation induced a significant increase in TNF-α secretion, mRNA expression, cholesterol accumulation and nuclear factor-κB (NF-κB) activity in RAW264.7 macrophages. Ac-hE-18A-NH2 reduced TNF-α secretion and mRNA expression, up-regulated the ABCA1 mRNA and protein expression, reduced the intracellular cholesterol content, and inhibited NF- κB activation in a dose-dependent manner. Under the same condition and the same concentration, Ac-hE-18A-NH2 was more efficient than D-4F (apoA-I mimetic peptide) in inhibiting the inflammatory response induced by ox-LDL in the macrophages.\n\nQuestion:\nDoes [ Ac-hE-18A-NH2 inhibit the inflammatory response induced by ox-LDL via inhibiting NF-κB activation in RAW264.7 macrophages ]?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCrohn's disease frequency has increased in recent years in Iran. Genetic and environmental factors predispose people to this disease. Mutation in Caspase Recruitment Domain 15 (CARD15) gene is the most well known genetic predisposing factor to this disease. Frequency of three common CARD15 mutations has been studied in different ethnic groups. We aimed to study the frequency of these mutations in Iranian patients affected with Crohn's Disease. One hundred fifteen proved cases of Crohn Disease and 115 age and sex matched normal controls were recruited in this study. Lf1007fs, R702W and G908R mutations were studied by Polymerase Chain Reaction-Restriction Fragment Length Polymorphims (PCR-RFLP) followed by sequencing the positive cases. Lf1007fs and G908R mutations were not found in either patients or age-sex matched controls. Just in two patients, R702W mutation was proved by Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) and sequencing. None of these patients had illeal or fibrostenotic type of disease while 14.7% of total patients had stricturing type of disease. No complication was seen in these two patients while 50.4% of patients had acquired complications during the course of disease.\n\nQuestion:\nAre three common CARD15 mutations responsible for the pathogenesis of Crohn 's disease in Iranians?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nGrowth arrest-specific gene 7 (Gas7) has previously been shown to be involved in neurite outgrowth in vitro; however, its actual role has yet to be determined. To investigate the physiological function of Gas7 in vivo, here we generated a Gas7-deficient mouse strain with a labile Gas7 mutant protein whose functions are similar to wild-type Gas7. Our data show that aged Gas7-deficient mice have motor activity defects due to decreases in the number of spinal motor neurons and in muscle strength, of which the latter may be caused by changes in muscle fiber composition as shown in the soleus. In cross sections of the soleus of Gas7-deficient mice, gross morphological features and levels of myosin heavy chain I (MHC I) and MHC II markers revealed significantly fewer fast fibers. In addition, we found that nerve terminal sprouting, which may be associated with slow and fast muscle fiber composition, was considerably reduced at neuromuscular junctions (NMJ) during aging.\n\nQuestion:\nDoes gas7-deficient mouse reveal roles in motor function and muscle fiber composition during aging?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 protocols used for the preparation of human pancreatic islets immediately induce a sustained and massive activation of the c-Jun-N-terminal kinase (JNK). JNK, which participates in apoptosis of insulin-secreting cells, is activated by mechanical stresses, as well as by exposure to pro-inflammatory cytokines. Here, we investigated whether the delivery of a protease-resistant JNK inhibitory peptide (D-JNKI) through a protein transduction system during pancreatic digestion might impair JNK signalling throughout the transplantation procedure. Rat pancreases were treated with D-JNKI through the pancreatic duct and cells then isolated by enzymatic digestion. Protein extracts were prepared to determine JNK activity by kinase assays and total RNA was extracted to measure gene expressions by a Light-Cycler technique. Cell apoptosis rate was determined by terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) assay and by scoring cells displaying pycnotic nuclei. Our data establish that the peptide transduction system used here efficiently transfects islets, allowing for stable in vivo (up to 2 days) transfection of human islets transplanted under the kidney capsule. Further, D-JNKI decreases intracellular JNK signalling during isolation and following cytokine exposure in both human and rat islets, as measured by kinase assays and reduced c-fos expression; D-JNKI also confers protection against apoptosis induced during the rat islet preparation and subsequent to IL-1beta exposure.\n\nQuestion:\nDoes the c-Jun N-terminal kinase JNK participate in cytokine- and isolation stress-induced rat pancreatic islet apoptosis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 effect of Helicobacter pylori infection on non-steroidal anti-inflammatory drug-induced gastric mucosal injury is controversial. To examine the effect of the interaction between H. pylori and non-steroidal anti-inflammatory drugs on gastric mucosal injury. Mongolian gerbils infected with H. pylori were treated with indometacin at 8 mg/kg for 2 days or 7 days. Mucosal damage was assessed by macroscopic and histological examination, and myeloperoxidase activity was measured as an index of neutrophil infiltration. The expression levels of cyclo-oxygenase proteins were determined by Western blot analysis and cyclo-oxygenase activity. A 2-day course of indometacin did not cause an increase in gastric damage in H. pylori-infected Mongolian gerbils compared to uninfected gerbils, while a 7-day course of indometacin caused additive gastric damage in H. pylori-infected animals. H. pylori infection induced cyclo-oxygenase-2 expression in the stomach. Treatment with indometacin for 2 days did not significantly affect cyclo-oxygenase activity in H. pylori-infected animals, while treatment for 7 days inhibited both cyclo-oxygenase-1 and cyclo-oxygenase-2 activities. Pre-treatment with a selective cyclo-oxygenase-2 inhibitor aggravated mucosal injury in H. pylori-infected animals treated or not treated with indometacin for 2 days.\n\nQuestion:\nDoes inhibition of Helicobacter pylori-induced cyclo-oxygenase-2 aggravate NSAID-caused gastric damage in Mongolian gerbils?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 purpose of this study was to investigate why low-risk nulliparae were not willing to participate in a randomised controlled trial (RCT) of place of birth. Prospective study. The Netherlands. All low-risk nulliparous women starting their pregnancy under midwife. A questionnaire for 107 nulliparae who were willing to participate in a cohort study on place of birth, but at an earlier stage in their pregnancy declined to participate in a RCT of place of birth. This questionnaire included 12 items on a 4-point Likert scale but was not subjected to formal validation. Reasons why nulliparae did not accept randomisation of place of birth. The most important reason why women refused participation in the trial was that they had already chosen their place of birth before they were asked to participate at 12 weeks of pregnancy. From their answers, it became clear that pregnant women strongly value their autonomy of choice. The decision not to participate in the trial was not influenced by the information given by the midwife and the additional written information.\n\nQuestion:\nDo why women accept randomisation for place of birth : feasibility of a RCT in The Netherlands?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 RHO C110Y mutation has been recently reported to cause a phenotypically unspecified form of autosomal dominant retinitis pigmentosa (adRP). The study of a family affected with this mutation allowed us to hereby describe the genotype/phenotype correlation associated with the RHO C110Y mutation. A six-generation pedigree cosegregating adRP and RHO C110Y in ten accessible individuals was ophthalmologically investigated. All family members affected with RP went through complete eye examination and ERG testing. The disease first manifested with nyctalopia during adulthood and slowly progressed over the next decades towards tubular visual field defects and relatively preserved central vision. Ophthalmoscopically, the fundus remained almost unaltered until the end of the third decade of life, and then slowly progressed towards typical RP changes with minimal macular involvement by the eighth decade. Color vision remained unaltered. Earliest ERG alteration was limited to the rod system followed by a rod-cone pattern. Scotopic and photopic ERG were recordable until the fourth and sixth decades, respectively.\n\nQuestion:\nDoes rhodopsin C110Y mutation cause a type 2 autosomal dominant retinitis pigmentosa?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 cellular mechanisms involved in the regression of diabetic nephropathy, bone marrow-derived cells must be identified. The aim of this study was to obtain a diabetic chimeric model with bone marrow cells expressing enhanced green fluorecence protein (EGFP), without modifying the course of diabetic nephropathy. Bone marrow transplantation (BMT) was performed in an obese type 2 diabetic murine model (db/db) owing to a mutation in the leptin receptor gene. Whole bone marrow from female donor C57BL/6 EGFP+ mice was transplanted into 8-week-old C57BL/6 mice and into 8- and 24-week-old female C57BLKS (db/db) EGFP- mice. Recipient mice received total body irradiation (TBI) followed by bone marrow (BM) cell infusion. We tested various irradiation doses (Gy) and numbers of BM cells. When a low TBI dose and a small number of BM cells were administered, only syngeneic C57BL/6 mice became chimeric, whereas allogeneic db/db mice showed rejection. When Gy dose and BM cells were increased, db/db mice became chimeric. However, 8-week-old db/db mice lost the obese phenotype and became normoglycemic, probably due to peripheral BM cell infiltration. Conversely, 24-week-old db/db mice remained obese showing similar blood glucose values, body weights, albuminuria, and glomerular lesions at nontransplanted db/db mice.\n\nQuestion:\nDoes bone marrow transplantation induce normoglycemia in a type 2 diabetes mellitus murine model?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIGF-1 and the IGF-1 receptor (IGF-1R) have been implicated in the regulation of adipocyte differentiation and lipid accumulation in vitro. To investigate the role of IGF-1 receptor in vivo, we have inactivated the Igf-1r gene in adipose tissue (IGF-1R(aP2Cre) mice) using conditional gene targeting strategies. Conditional IGF-1R inactivation resulted in increased adipose tissue mass with a predominantly increased lipid accumulation in epigonadal fat pads. However, insulin-stimulated glucose uptake into adipocytes was unaffected by the deletion of the IGF-1R. Surprisingly, IGF-1R(aP2Cre) mice exhibited markedly increased somatic growth in the presence of elevated IGF-1 serum concentrations, and IGF-1 mRNA expression was significantly increased in liver and adipose tissue. IGF-1 stimulation of wild-type adipocytes significantly decreased IGF-1 mRNA expression, whereas the opposite effect was observed in IGF-1R-deficient adipocytes.\n\nQuestion:\nDoes autocrine IGF-1 action in adipocytes control systemic IGF-1 concentrations and growth?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 update our previous reports on the use of hypofractionated proton beam radiation therapy for early-stage lung cancer patients. Eligible subjects had biopsy-proven non-small cell carcinoma of the lung and were medically inoperable or refused surgery. Clinical workup required staging of T1 or T2, N0, M0. Subjects received hypofractionated proton beam therapy to the primary tumor only. The dose delivered was sequentially escalated from 51 to 60 Gy, then to 70 Gy in 10 fractions over 2 weeks. Endpoints included toxicity, pulmonary function, overall survival (OS), disease-specific survival (DSS), and local control (LC). One hundred eleven subjects were analyzed for treatment outcomes. The patient population had the following average characteristics; age 73.2 years, tumor size 3.6 cm, and 1.33 L forced expiratory volume in 1 second. The entire group showed improved OS with increasing dose level (51, 60, and 70 Gy) with a 4-year OS of 18%, 32%, and 51%, respectively (P=.006). Peripheral T1 tumors exhibited LC of 96%, DSS of 88%, and OS of 60% at 4 years. Patients with T2 tumors showed a trend toward improved LC and survival with the 70-Gy dose level. On multivariate analysis, larger tumor size was strongly associated with increased local recurrence and decreased survival. Central versus peripheral location did not correlate with any outcome measures. Clinical radiation pneumonitis was not found to be a significant complication, and no patient required steroid therapy after treatment for radiation pneumonitis. Pulmonary function was well maintained 1 year after treatment.\n\nQuestion:\nIs high-dose hypofractionated proton beam radiation therapy safe and effective for central and peripheral early-stage non-small cell lung cancer : results of a 12-year experience at Loma Linda University Medical Center?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPrior research suggests that difficulties in emotion regulation are associated with elevations in panic symptoms. The present study aimed to extend this work by prospectively examining the relation between difficulties in emotion regulation and panic symptoms over the course of a self-guided cannabis cessation attempt. One hundred and four cannabis-dependent military veterans participated in the study. Difficulties in emotion regulation and panic symptoms were assessed at baseline and at each week during a four-week cessation attempt for a total of five time-points. Fewer difficulties in emotion regulation were associated with a greater reduction in panic symptoms during the self-guided cannabis cessation period. RESULTS remained significant after statistically adjusting for mean substance use (i.e., cannabis, alcohol, and tobacco) during the study period.\n\nQuestion:\nAre difficulties in emotion regulation associated with panic symptom severity following a quit attempt among cannabis dependent veterans?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 resveratrol, a nontoxic plant product, in the treatment of uveal melanoma. The effect of oral administration and peritumor injection of resveratrol was tested on tumor growth in two animal models of uveal melanoma. The mechanism of resveratrol action on uveal melanoma cells was studied in vitro in a cell-viability assay: with JC-1 dye, to measure mitochondrial membrane potential; by Western blot analysis, to analyze the cellular redistribution of cytochrome c and Smac/diablo; and in a fluorescence assay with specific substrates, to measure activation of different caspases. Resveratrol treatment inhibited tumor growth in animal models of uveal melanoma. Since oral administration resulted in relatively low bioavailability of resveratrol, the effect of increased local levels was tested by peritumor injection of the drug. This method resulted in tumor cell death and tumor regression. In vitro experiments with multiple uveal melanoma cell lines demonstrate that resveratrol causes a decrease in cell viability, resulting at least in part from an increase in apoptosis through a mitochondrial pathway. An early event in drug action is the direct targeting of mitochondria by resveratrol, which leads to a decrease in mitochondrial membrane potential and the eventual activation of caspase-3.\n\nQuestion:\nDoes resveratrol inhibit uveal melanoma tumor growth via early mitochondrial dysfunction?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nEvaluate the addition of long-distance heart procurement on a heart transplant program and the status of heart transplant recipients waiting list. Between September 2006 and October 2012, 72 patients were listed as heart transplant recipients. Heart transplant was performed in 41 (57%), death on the waiting list occurred in 26 (36%) and heart recovery occurred in 5 (7%). Initially, all transplants were performed with local donors. Long-distance, interstate heart procurement initiated in February 2011. Thirty (73%) transplants were performed with local donors and 11 (27%) with long-distance donors (mean distance=792 km±397). Patients submitted to interstate heart procurement had greater ischemic times (212 min ± 32 versus 90 min±18; P<0.0001). Primary graft dysfunction (distance 9.1% versus local 26.7%; P=0.23) and 1 month and 12 months actuarial survival (distance 90.1% and 90.1% versus local 90% and 86.2%; P=0.65 log rank) were similar among groups. There were marked incremental transplant center volume (64.4% versus 40.7%, P=0.05) with a tendency on less waiting list times (median 1.5 month versus 2.4 months, P=0.18). There was a tendency on reduced waiting list mortality (28.9% versus 48.2%, P=0.09).\n\nQuestion:\nDoes addition of long-distance heart procurement promote changes in heart transplant waiting list status?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIs the length of the anogenital distance (AGD), a biomarker of the in-utero prenatal hormonal environment, associated with the presence of endometriomas and deep infiltrating endometriosis (DIE)?\n\nQuestion:\nAre endometriomas and deep infiltrating endometriosis in adulthood strongly associated with anogenital distance , a biomarker for prenatal hormonal environment?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSystemic treatment of endometrial carcinoma with distant metastases is currently performed, inter alia, with anthracyclines, platinum, paclitaxel, if osfamid or progestins. This is the first report presenting experience in treatment of metastatic endometrial carcinoma with docetaxel. A 69-year-old women with adenocarcinoma of the endometrium was treated with primary combined radiotherapy. Two years later disseminated bilateral pulmonary metastases were detected and the patient was submitted to chemotherapy with epirubicin. After three cycles of chemotherapy with epirubicin examinations revealed metastatic progression. Thus, chemotherapy was changed to docetaxel. After three cycles of chemotherapy with docetaxel examinations revealed remission of the described pulmonary metastases more than 50%. A further three cycles of chemotherapy with docetaxel lead to continuing shrinkage of the detectable metastases to less than 25% of the original size. Because of various side effects, like increasing fatigue and asthenia, uncomfortable acral paresthesia and allergic skin reactions, the patient refused to continue chemotherapy.\n\nQuestion:\nIs docetaxel effective in the treatment of metastatic endometrial cancer?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis study was aimed at deciphering the secretome of adipose-derived mesenchymal stromal cells (ADSCs) cultured in standard and hypoxic conditions to reveal proteins, which may be responsible for regenerative action of these cells. Human ADSCs were isolated from 10 healthy donors and cultured for 3-4 passages. Cells were serum deprived and cell purity was assessed using multiple cell surface markers. Conditioned media was collected and analyzed using LC-MS with a focus on characterizing secreted proteins. Purity of the ADSC assessed as CD90+/CD73+/CD105+/CD45-/CD31- cells was greater than 99 % and viability was greater than 97 %. More than 600 secreted proteins were detected in conditioned media of ADSCs. Of these 100 proteins were common to all cultures and included key molecules involved in tissue regeneration such as collagens and collagen maturation enzymes, matrix metalloproteases, matricellular proteins, macrophage-colony stimulating factor and pigment epithelium derived factor. Common set of proteins also included molecules, which contribute to regenerative processes but were not previously associated with ADSCs. These included olfactomedin-like 3, follistatin-like 1 and prosaposin. In addition, ADSCs from the different subjects secreted proteins, which were variable between different cultures. These included proteins with neurotrophic activities, which were not previously associated with ADSCs, such as mesencephalic astrocyte-derived neurotrophic factor, meteorin and neuron derived neurotrophic factor. Hypoxia resulted in secretion of 6 proteins, the most prominent included EGF-like repeats and discoidin I-like domains 3, adrenomedullin and ribonuclease 4 of RNase A family. It also caused the disappearance of 8 proteins, including regulator of osteogenic differentiation cartilage-associated protein.\n\nQuestion:\nDoes characterization of secretomes provide evidence for adipose-derived mesenchymal stromal cells subtypes?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 biomass structure of Epimedium acuminatum Franch in the different ecological environments for the development and protection. Through the scientific investigation in four typical habitats, the sampling spots were set up, the functional modules' biomass structure and relationship of E. acuminatum were researched. The average of rhizome, as the largest biomass, and the average total biomass had the same pattern: the open areas of forest edge > shrub lumber > shrub-weed > stream drains. The ratio of the functional modules' biomass had different rates under different habitat conditions. By analyzing and combining investigation, the aerial part of E. acuminatum in the shrub-weed were comparative advantage, and the roots of nutrient accumulation of E. acuminatum in the open areas of forest edge were the highest efficient. Under different ecological condition, the distribution of water metabolism was different strategies.\n\nQuestion:\nDo [ Study on modules biomass structure of Epimedium acuminatum in different habitats ]?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIschemic preconditioning (PC) is a powerful mechanism in reducing infarct size of the heart. Protection can be performed either by an ischemic stimulus of the heart itself or by ischemia of an organ distant to the heart (remote PC). We have previously shown that remote PC by infrarenal occlusion of the aorta [IOA] in the rat is as powerful as classical ischemic PC. This protection may be transmitted by humoral factors, and protein kinase C is a mediator in the signal transduction mechanism. Focus of the present study was to address the question whether remote preconditioning is dependent on the activation of the delta1-opioid receptor and/or free radicals, the infarct size was determined after either inhibition of the delta1-opioid receptor or scavenging free radicals. IOA was performed in rats by occlusion of the infrarenal aorta for 15 min followed by a 10-min reperfusion period. Infarction of the heart was induced by 30 min regional ischemia followed by 30 min of reperfusion. The area of infarct was determined by propidium iodide and the risk zone was demarcated by zinc cadmium sulfide fluorescent particles. Control hearts (30 min regional ischemia of the heart followed by 30 min of reperfusion; no IOA) had an infarct size of 54 +/- 3%, whereas classical preconditioning by three ischemia/reperfusion [I/R] cycles, 5 min each, reduced it to 12 +/- 1% of the risk zone (p<0.05). Fifteen minutes IOA with 10 min of reperfusion was highly protective and reduced the infarct size to 20 +/- 5% (p<0.05 vs. control). Inhibition of the delta1-opioid receptors by 7-benzylidenenaltrexone [BNTX] blocked the protection obtained by PC and IOA (41 +/- 4% and 44 +/- 2%, respectively; p<0.05 vs. the group without BNTX). BNTX in control hearts had no influence on infarct size (52 +/- 2%). Inhibition of endogenously released radicals by N-2-mercaptopropionyl glycine [MPG] blocked the infarct size reduction of IOA (46 +/- 3%; p<0.05 vs. IOA), but had no influence on the protection in classically preconditioned hearts protected by three cycles I/R (13 +/- 4%). Only if the number of the preconditioning stimuli was reduced to one was MPG able to overcome the protection (43 +/- 4%, p<0.05 vs. PC with one I/R cycle (21 +/- 4%)).\n\nQuestion:\nIs remote preconditioning by infrarenal aortic occlusion operative via delta1-opioid receptors and free radicals in vivo in the rat heart?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nExcess adiposity is associated with greater systemic inflammation. Whether visceral adiposity is more proinflammatory than subcutaneous abdominal adiposity is unclear. We examined the relations of abdominal subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT), assessed by multidetector computerized tomography, to circulating inflammatory and oxidative stress biomarkers in 1250 Framingham Heart Study participants (52% women; age 60+/-9 years). Biomarkers were examined in relation to increments of SAT and VAT after adjustment for age, sex, smoking, physical activity, menopause, hormone replacement therapy, alcohol, and aspirin use; additional models included body mass index and waist circumference. SAT and VAT were positively and similarly (with respect to strength of association) related to C-reactive protein, fibrinogen, intercellular adhesion molecule-1, interleukin-6, P-selectin, and tumor necrosis factor receptor-2 (multivariable model R2 0.06 to 0.28 [SAT] and 0.07 to 0.29 [VAT]). However, compared with SAT, VAT was more highly associated with urinary isoprostanes and monocyte chemoattractant protein-1 (SAT versus VAT comparison: isoprostanes, R2 0.07 versus 0.10, P=0.002; monocyte chemoattractant protein-1, R2 0.07 versus 0.08, P=0.04). When body mass index and waist circumference were added to the models, VAT remained significantly associated with only C-reactive protein (P=0.0003 for women; P=0.006 for men), interleukin-6 (P=0.01), isoprostanes (P=0.0002), and monocyte chemoattractant protein-1 (P=0.008); SAT only remained associated with fibrinogen (P=0.01).\n\nQuestion:\nAre visceral and subcutaneous adipose tissue volumes cross-sectionally related to markers of inflammation and oxidative stress : the Framingham Heart Study?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 which of the standard cardiovascular risk factors have the strongest associations with prevalent coronary artery calcification (CAC). A cross-sectional study of 6086 consecutive subjects who underwent electron beam computed tomography for CAC at a private, university-affiliated disease prevention center in San Diego, CA. The correlation between age and coronary calcium score in men (r=0.463) was twice that of the next highest correlation (0.218) for percent body fat. A similar relationship was found for women (0.413 vs. 0.238). Calcium scores increased incrementally by age category in both men and women. This pattern of increase was not present for LDL cholesterol. Men and women over the age of 74 had highly elevated risks for the presence of any calcified coronary atherosclerosis compared to those under the age of 45 (OR [95% CI]: 11.08 [6.186-19.859] and 11.81 [6.718-20.746], respectively). Addition of the other traditional cardiovascular risk factors did not significantly increase the discriminatory power beyond that provided by age on ROC analysis.\n\nQuestion:\nAre age and gender the strongest clinical correlates of prevalent coronary calcification ( R1 )?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAdenocarcinoma arises in Barrett's esophagus by progression from metaplasia to cancer through grades of dysplasia. Our aim in this exploratory study was to characterize the broad changes in gene expression that underlie this histologic progression to cancer and assess the potential for using these gene expression changes as a marker predictive of malignant progression in Barrett's epithelium. Microarray analysis was used to obtain individual gene expression profiles from endoscopic biopsies of nine esophageal adenocarcinomas and the Barrett's epithelia from which three of the cancers had arisen. Pooled samples from the Barrett's epithelia of six patients without cancer or dysplasia served as a reference. Barrett's epithelia from which cancer had arisen differed from the reference Barrett's epithelia primarily by underexpression of genes, many of which function in governing cell differentiation. These changes in gene expression were found even in those specimens of Barrett's epithelia from which cancer had arisen that lacked dysplasia. Each cancer differed from the Barrett's epithelium from which it had arisen primarily by an overexpression of genes, many of which were associated with tissue remodeling and invasiveness. Cancers without identifiable Barrett's epithelium differed from cancers that had arisen from a Barrett's epithelium by having an even greater number of these overexpressed genes.\n\nQuestion:\nDoes dedifferentiation precede invasion in the progression from Barrett 's metaplasia to esophageal adenocarcinoma?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nLocal ablation therapy has been shown to be effective for small hepatocellular carcinoma (HCC); however, HCC recurrence is very frequent even after apparently curative treatment. In particular, recurrent HCC may be more prone to subsequent recurrence, although quantitative data are lacking. The aim of this study was to evaluate the difference in the risk for subsequent recurrence, if any, between primary and recurrent cases. A retrospective analysis was conducted of 376 patients with HCC (uninodular and <or=5 cm, or 2-3 nodules each <or=3 cm) who underwent local ablation therapy. There were 207 primary cases (group I), 100 with first recurrence (group II), and 69 with second or later recurrence (group III). After confirming complete ablation, each patient was followed up for recurrence. Risk factors for recurrence-free survival were analyzed using proportional hazard regression. The median time to recurrence, as estimated by Kaplan-Meier method, was 30 months in group I, 23 months in group II, and 11 months in group III (P < 0.001). Multivariate proportional hazard regression analysis reveled that group (i.e. previous recurrence) was the strongest predictor of subsequent recurrence; compared to group I, group II showed a hazard ratio of 1.456 (P = 0.015) and group III, 3.011 (P < 0.0001). alpha-Fetoprotein level >100 ng/mL, treatment other than radiofrequency ablation, HCV antibody positivity, and tumor multinodularity also remained as significant predictors.\n\nQuestion:\nDoes recurrent hepatocellular carcinoma have an increased risk of subsequent recurrence after curative treatment?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 parental occupation such as anesthesia care provider can involve exposure of the parent to various chemicals in the work environment and has been correlated to skewed offspring sex ratios. The objective was to conduct a nation-wide survey to observe (a) whether firstborn offspring sex ratio (OSR) in anesthesia providers is skewed towards increased female offspring, and (b) to identify potential factors influencing firstborn OSR, particularly those relating to the peri-conceptional practice of inhalational anesthesia induction among anesthesia providers. After institutional review board approval, a questionnaire was uploaded on SurveyMonkey and sent to anesthesia providers through their program coordinators in United States (US) to complete the survey. The current US national total-population sex ratio is 0.97 male (s)/female with an at-birth sex ratio of 1.05 male (s)/female; comparatively, the results from anesthesia providers' survey respondents (n = 314) were a total OSR of 0.93 male (s)/female (P = 0.61) with firstborn OSR 0.82 male (s)/female (a 6% increase in female offspring; P = 0.03), respectively. The only significant peri-conceptional factor related to anesthesia providers' firstborn OSR's skew was inhalational induction practice by anesthesia care provider favoring female offspring (P < 0.01).\n\nQuestion:\nIs firstborn offspring sex ratio skewed towards female offspring in anesthesia care providers : A questionnaire-based nationwide study from United States?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 high frequency of thrombocytopenia in post-cardiac surgery patients makes it challenging to diagnose heparin-induced thrombocytopenia (HIT). Two platelet count profiles are reported as indicating possible HIT in these patients: profile 1 describes a platelet count fall that begins between postoperative days 5 and 10, whereas profile 2 denotes early-onset thrombocytopenia that persists beyond day 5. To examine how these platelet count profiles correlate with antibody status and HIT post-cardiac surgery. We prospectively screened 581 cardiac surgery patients for heparin-dependent antibodies by platelet factor 4 (PF4)-heparin immunoassay and platelet-activation test, and performed daily platelet counts (until day 10) with 30-day follow-up. All three patients with platelet count profile 1 tested positive for platelet-activating anti-PF4-heparin IgG antibodies [odds ratio (OR) 521.7, 95% confidence interval (CI) 3.9-34,000, P = 0.002], and were judged to have HIT. In contrast, none of 25 patients with early-onset and persisting thrombocytopenia (profile 2) was judged to have HIT, including five patients testing positive for platelet-activating anti-PF4-heparin IgG antibodies. In these patients, the frequency of heparin-dependent antibodies did not differ from that in non-thrombocytopenic controls, either for anti-PF4-heparin IgG (OR 1.7, 95% CI 0.7-4.1, P = 0.31) or for platelet-activating antibodies (OR 1.9, 95% CI 0.6-5.7, P = 0.20). Multivariate analysis revealed that type of cardiac surgery, but not HIT antibody status, predicted early-onset and persisting thrombocytopenia. Together, these findings show that HIT was uncommon in this study population [overall frequency, 3/581 (0.5%), 95% CI 0.1-1.5%].\n\nQuestion:\nIs early-onset and persisting thrombocytopenia in post-cardiac surgery patients rarely due to heparin-induced thrombocytopenia , even when antibody tests are positive?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCalciphylaxis is associated with a poor prognosis in dialysis patients, and its pathogenesis remains incompletely understood. Although the use of vitamin K antagonists (VKA) has been implicated, previous reports are conflicting. We aimed to determine if vitamin K antagonists conferred an increased risk of calciphylaxis in patients on dialysis. We performed a single-centre, retrospective cohort study of 2,234 patients receiving dialysis, and compared the characteristics of those with and without calciphylaxis. We identified 5 cases of calciphylaxis (all female) between January 2009 and December 2013. Overall, 142 patients (6.4%) were treated with VKA during the study period. Calciphylaxis was more common in the VKA group (4 of 142 patients, OR = 61, 95% CI 6.7-546, p = 0.0001). VKA was withdrawn in all cases and treatment instituted with sodium thiosulphate, cinacalcet and supportive measures. All patients recovered, although there was one sudden cerebrovascular death during follow-up.\n\nQuestion:\nDo vitamin K antagonists predispose to calciphylaxis in patients with end-stage renal disease?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 purpose of this study is to evaluate the levels of psychological distress in head and neck cancer patients using a validated screening tool. We aim to characterize distress in this cancer population and understand the factors driving distress levels. Review of prospectively gathered data. A review of prospectively gathered data was undertaken from 89 head and neck cancer patients (HNC) who completed the Distress Thermometer and Problem List (DT) from the National Comprehensive Cancer Network (NCCN). Distress levels were high in the overall population. The level of distress was significantly greater in patients with a self-reported history of depression (P <.001), family concerns (P = .030), emotional concerns (P = .001) and physical concerns (P = .014).\n\nQuestion:\nIs psychosocial distress prevalent in head and neck cancer patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 use of chromium-containing dietary supplements is widespread among patients with type 2 diabetes. Chromium's effects in patients at high risk for developing diabetes, especially those with metabolic syndrome, is unknown. The objective of this study was to determine the effects of chromium picolinate (CrPic) on glucose metabolism in patients with metabolic syndrome. A double-blind, placebo-controlled, randomized trial was conducted at a U.S. academic medical center. Sixty three patients with National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III)-defined metabolic syndrome were included. The primary end point was a change in the insulin sensitivity index derived from a frequently sampled intravenous glucose tolerance test. Prespecified secondary end points included changes in other measurements of glucose metabolism, oxidative stress, fasting serum lipids, and high sensitivity C-reactive protein. After 16 weeks of CrPic treatment, there was no significant change in insulin sensitivity index between groups (P = 0.14). However, CrPic increased acute insulin response to glucose (P 0.02). CrPic had no significant effect on other measures of glucose metabolism, body weight, serum lipids, or measures of inflammation and oxidative stress.\n\nQuestion:\nDoes chromium picolinate improve key features of metabolic syndrome in obese nondiabetic adults?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nGuidelines recommend collecting urine with suprapubic aspiration or urethral catheterisation in infants with a suspected urinary tract infection (UTI), but the invasiveness of these methods continues to drive research on new urine collection devices. We studied children with a suspected UTI, who had not been toilet trained, to compare a new midstream urine collector and catheterisation. During this prospective controlled diagnosis study of 94 children, urine collection was performed using the midstream collector and then controlled via catheterisation when the urine dipstick was positive. When end stream samples collected by the midstream collector were compared to catheter samples, the results were inconsistent in 23.4% of cases, similar to the inconsistent results between first stream samples discarded by the device and the catheter samples (21.3%). Interestingly, the overall rate of sample contamination in the bag of the midstream collector was lower than that reported in previously published studies and there were no false positive bag results.\n\nQuestion:\nIs a midstream urine collector a good alternative to a sterile collection method during the diagnosis of urinary tract infection?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWhile psychosocial factors have been associated with poorer outcomes after knee and hip arthroplasty, we hypothesized that augmented pain perception, as occurs in conditions such as fibromyalgia, may account for decreased responsiveness to primary knee and hip arthroplasty. A prospective, observational cohort study was conducted. Preoperative phenotyping was conducted using validated questionnaires to assess pain, function, depression, anxiety, and catastrophizing. Participants also completed the 2011 fibromyalgia survey questionnaire, which addresses the widespread body pain and comorbid symptoms associated with characteristics of fibromyalgia. Of the 665 participants, 464 were retained 6 months after surgery. Since individuals who met criteria for being classified as having fibromyalgia were expected to respond less favorably, all primary analyses excluded these individuals (6% of the cohort). In the multivariate linear regression model predicting change in knee/hip pain (primary outcome), a higher fibromyalgia survey score was independently predictive of less improvement in pain (estimate -0.25, SE 0.044; P < 0.00001). Lower baseline joint pain scores and knee (versus hip) arthroplasty were also predictive of less improvement (R(2) = 0.58). The same covariates were predictive in the multivariate logistic regression model for change in knee/hip pain, with a 17.8% increase in the odds of failure to meet the threshold of 50% improvement for every 1-point increase in fibromyalgia survey score (P = 0.00032). The fibromyalgia survey score was also independently predictive of change in overall pain and patient global impression of change.\n\nQuestion:\nDo characteristics of fibromyalgia independently predict poorer long-term analgesic outcomes following total knee and hip arthroplasty?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 previously demonstrated that nuclear and cytoplasmic accumulation of the intracellular domain (Ep-ICD) of epithelial cell adhesion molecule (EpCAM) accompanied by a reciprocal reduction of its extracellular domain (EpEx), occurs in aggressive thyroid cancers. This study was designed to determine whether similar accumulation of Ep-ICD is a common event in other epithelial cancers. Ten epithelial cancers were immunohistochemically analyzed using Ep-ICD and EpEx domain-specific antibodies. The subcellular localization of EpEx and Ep-ICD in the human colon adenocarcinoma cell line CX-1 was observed using immunofluorescence. Nuclear and cytoplasmic Ep-ICD expression was increased in cancers of the breast (31 of 38 tissues, 82%), prostate (40 of 49 tissues, 82%), head and neck (37 of 57 tissues, 65%) and esophagus (17 of 46 tissues, 37%) compared to their corresponding normal tissues that showed membrane localization of the protein. Importantly, Ep-ICD was not detected in the nuclei of epithelial cells in most normal tissues. High nuclear and cytoplasmic Ep-ICD accumulation also occurred in the other six epithelial cancer types analyzed - lung, colon, liver, bladder, pancreatic, and ovarian. A concomitant reduction in membrane EpEx expression was observed in a subset of all cancer types. Receiver operating characteristic curve analysis revealed nuclear Ep-ICD distinguished breast cancers with 82% sensitivity and 100% specificity and prostate cancers with 82% sensitivity and 78% specificity. Similar findings were observed for cytoplasmic accumulation of Ep-ICD in these cancers. We provide clinical evidence of increased nuclear and cytoplasmic Ep-ICD accumulation and a reduction in membranous EpEx in these cancers.\n\nQuestion:\nIs nuclear and cytoplasmic accumulation of Ep-ICD frequently detected in human epithelial cancers?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAtopic dermatitis is an inflammatory skin disease that is characterized by a reduced skin barrier function, reduced filaggrin (FLG) expression as well as increased colonization by Staphylococcus aureus. This study focused on the possible involvement of FLG in epidermal colonization by S. aureus and/or whether it affects the epidermal defence mechanisms, including the expression of antimicrobial peptides (AMPs) and enzymes involved in stratum corneum barrier lipid synthesis. Furthermore, IL-31 has been shown to reduce FLG expression, but its effects on bacterial colonization and on the expression of AMPs and enzymes involved in the barrier lipid synthesis are not known. We established N/TERT-based epidermal models (NEMs), after FLG knockdown (FLG-KD) and/or cultured with IL-31, that were colonized with S. aureus for 24 h. Both FLG-KD and IL-31 supplementation resulted in significantly increased epidermal S. aureus colonization, as well as in an up-regulation of S. aureus-induced IL-8 expression. IL-31, but not FLG-KD, prevented S. aureus-induced up-regulation of mRNA expression for the AMPs human β-defensin 2 and -3 and RNAse7, whereas psoriasin expression remained unchanged. Furthermore, the S. aureus colonization induced changes in mRNA expression of ELOVL4 was not affected by FLG-KD, but was blocked by IL-31. Expression of SCD-1 and Gcase mRNA was reduced by IL-31, but not by FLG-KD.\n\nQuestion:\nIs reduced filaggrin expression accompanied by increased Staphylococcus aureus colonization of epidermal skin models?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 prognostic value of epidermal growth factor receptor (EGFR) molecular characteristics of head and neck squamous cell carcinoma (HNSCC). HNSCC tumors from patients prospectively enrolled in either an Early Detection Research Network (EDRN) study and treated with surgery without an EGFR-targeted agent (N = 154) or enrolled in a chemoradiation trial involving the EGFR-targeted antibody cetuximab (N = 39) were evaluated for EGFR gene amplification by FISH and EGFR protein by immunohistochemical staining. Fresh-frozen tumors (EDRN) were also evaluated for EGFR protein and site-specific phosphorylation at Y992 and Y1068 using reverse-phase protein array (n = 67). Tumor (n = 50) EGFR and EGFRvIII mRNA levels were quantified using real-time PCR. EGFR expression by immunohistochemistry (IHC) was significantly higher in the EDRN tumors with EGFR gene amplification (P < 0.001), and a similar trend was noted in the cetuximab-treated cohort. In the EDRN and cetuximab-treated cohorts elevated EGFR by IHC was associated with reduced survival (P = 0.019 and P = 0.06, respectively). Elevated expression of total EGFR and EGFR PY1068 were independently significantly associated with reduced progression-free survival in the EDRN cohort [HR = 2.75; 95% confidence interval (CI) = 1.26-6.00 and HR = 3.29; 95% CI = 1.34-8.14, respectively].\n\nQuestion:\nAre tumor epidermal growth factor receptor and EGFR PY1068 independent prognostic indicators for head and neck squamous cell carcinoma?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAs adults lose strength with age and an increasing proportion of older adults are overweight or obese, this study was undertaken to examine the contribution of strength and adiposity to mobility difficulties among community-dwelling men and women at least 65 years of age. The National Health and Nutrition Examination Survey (NHANES) 2001-2002 provided complete demographic, anthropometric, strength, and self-reported mobility data for 687 men and women. Spearman correlations of adiposity (.024-.149) and knee extension strength (-.120-.234) with mobility difficulty were mostly significant but not strong. Multiple regression showed that together, body mass index, knee extension force, and age offered the best explanation of mobility difficulty.\n\nQuestion:\nDo knee extension strength and adiposity explain some of older adults ' self-reported difficulty with mobility?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nGenome-wide dense markers have been used to detect genes and estimate relative genetic values. Among many methods, Bayesian techniques have been widely used and shown to be powerful in genome-wide breeding value estimation and association studies. However, computation is known to be intensive under the Bayesian framework, and specifying a prior distribution for each parameter is always required for Bayesian computation. We propose the use of hierarchical likelihood to solve such problems. Using double hierarchical generalized linear models, we analyzed the simulated dataset provided by the QTLMAS 2010 workshop. Marker-specific variances estimated by double hierarchical generalized linear models identified the QTL with large effects for both the quantitative and binary traits. The QTL positions were detected with very high accuracy. For young individuals without phenotypic records, the true and estimated breeding values had Pearson correlation of 0.60 for the quantitative trait and 0.72 for the binary trait, where the quantitative trait had a more complicated genetic architecture involving imprinting and epistatic QTL.\n\nQuestion:\nDoes hierarchical likelihood open a new way of estimating genetic values using genome-wide dense marker maps?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nColorectal cancer (CRC) incidence and mortality are highest among African Americans. African Americans lag behind whites in CRC screening rates. Research has examined the role of CRC screening knowledge and beliefs and their relationship to CRC screening adherence. However, studies have not examined the effect cultural identity, social support, CRC beliefs, an informed decision, and having a chronic disease has on CRC screening among African Americans. This study examined CRC screening adherence among African Americans within the context of sociocultural variables, an informed decision, and health factors. A secondary data analysis was performed on survey data collected from 129 African American men and women. Social support and family influence were related to having a colonoscopy. Having diabetes was negatively related to having a colonoscopy. There was no relationship between having a primary care provider and making an informed decision about CRC screening. Religiosity and having a primary care provider predicted colonoscopy.\n\nQuestion:\nDoes sociocultural and health correlate related to colorectal cancer screening adherence among urban African Americans?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 possible existence of a genetically determined innate factor that could exert a profound influence on the development of analgesic overuse in chronic tension-type headache (CTTH). Many patients with CTTHs report the regular use of analgesics. Continuous use of analgesics results in the ultimate worsening of headaches. The factors related to development of analgesic overuse, however, remain poorly understood. The genetic factors for serotonin metabolism and the harm avoidance (HA) personality dimension are known to be associated with various substance abuse patterns. We performed serotonin transporter protein (5-HTT) gene-linked polymorphic region (5-HTTLPR) genotype polymorphism analyses, and investigated serotonin-related personality traits by assessing the HA dimension using tridimensional personality questionnaire, given to 48 patients with CTTHs and reported analgesic overuse (CTTH-AO), in 50 patients with CTTHs without analgesic overuse (CTTH-NO), and in 100 healthy controls. We compared their headache characteristics using standardized questionnaires. We discovered an excess frequency of 5-HTTLPR short allele and a different genotypic distribution in patients with CTTH-AO. The S/S genotype frequency was significantly higher in patients with CTTH-AO (83%) than in CTTH-NO (72%) and control (59%; P= .010) groups. Patients with CTTH-AO exhibited the highest HA scores (23.3 +/- 5.4), as compared to CTTH-NO (19.9 +/- 6.7) and control (16.3 +/- 6.1) groups. Individuals with the S/S genotype showed a greater tendency toward analgesic overuse (13.3 +/- 11.3 days per month) than did those with the non-S/S genotype (7.0 +/- 8.6 days per month: P= .02).\n\nQuestion:\nDoes serotonergic activity contribute to analgesic overuse in chronic tension-type headache?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis study tested the hypothesis that gestational age and agonist concentration are important determinants of beta-adrenergic-dependent myometrial contraction inhibition. In vitro concentration-response curves for ritodrine and terbutaline were generated with myometrial strips collected from 21-day-pregnant rats. The in vitro efficacy of ritodrine (0.1 mumol/L) was evaluated in tissue from 15-, 18-, and 21-day animals. Contractile responses were analyzed by computer and normalized to a control potassium response. The degree of the inhibitory effects of both drugs was concentration dependent over the range of 0.01 to 10 mumol/L. The duration of contraction inhibition progressively decreased from 15 to 21 days of pregnancy.\n\nQuestion:\nDoes contraction inhibition by beta-agonists progressively decrease before labor in the rat myometrium?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nGenetic variation in the serotonin-2C receptor encoded by the HTR2C gene is one of the genetic determinants of antipsychotic-induced weight gain. Peroxisome proliferator-activated receptors are nuclear receptors regulating the expression of genes involved in lipid and glucose metabolism. In this cross-sectional study, we investigated whether HTR2C-759C/T, HTR2C-697G/C, PPARα V227A, and PPARγ 161C/T genotypes were associated with metabolic syndrome (MetS) in patients with schizophrenia taking clozapine. One hundred forty-six Korean patients using clozapine for more than one year were genotyped for the HTR2C-759C/T, HTR2C-697G/C, PPARα V227A, and PPARγ 161C/T polymorphisms, and their weight, waist circumference, blood pressure, triglycerides, high-density lipoprotein-cholesterol, total cholesterol, and glucose were measured. We used the criteria for MetS proposed by the National Cholesterol Education Program-adapted Adult Treatment Panel III. The prevalence of MetS was 47.3% and was similar among men (49%) and women (42.9%). We found no significant differences between patients with and without MetS in terms of genotypes or allele frequencies. Logistic regression analyses also revealed no association between MetS and each genotype.\n\nQuestion:\nAre genetic Polymorphisms in the HTR2C and Peroxisome Proliferator-Activated Receptors Associated with Metabolic Syndrome in Patients with Schizophrenia Taking Clozapine?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nBlood transfusion can result in survival of donor leukocyte subpopulations in the recipient. Persistence of donor leukocytes in the transfusion recipient is termed microchimerism. Microchimerism likely reflects engraftment of the recipient with donor hematopoietic stem cells and is very uncommon with transfusion for elective surgery, sickle cell anemia, thalassemia, and HIV. We have found, however, that microchimerism may be more common in trauma patients. To determine how frequently transfusion after trauma is associated with microchimerism. We prospectively enrolled 45 trauma patients who were transfused > or =2 units of PRBCs. We sampled blood before hospital discharge and determined microchimerism by polymerase chain reaction (PCR) analysis of specimens using quantitative allele-specific HLA DR assays to detect non-recipient alleles. Data are expressed as median with interquartile range. Patients had a median age of 38 (interquartile range 25, 58) years, ISS of 19 (13, 29), and mortality of 7%. Seventy-eight percent were men, and 84% had blunt trauma. Patients received a median of 6 (4, 16) (range 2, 87) units of PRBCs. Of the 45 patients, 24 (53%) had evidence of microchimerism. Compared with patients without evidence of microchimerism, these patients had no difference in mean age, gender, ISS, units of PRBCs transfused, time from transfusion to blood sampling, or proportion that underwent splenectomy. Twenty-one of the 24 patients with microchimerism had only 1 or 2 non-recipient DR alleles identified by PCR.\n\nQuestion:\nIs blood transfusion associated with donor leukocyte microchimerism in trauma patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 hypothesized that without the analgesic effects of volatile anesthetics, caudal 0.20% ropivacaine would be less effective during surgical stimulation than 0.20% bupivacaine or 0.20% levobupivacaine. This trial was designed to examine whether the combination of a caudal block with 0.20% ropivacaine and i.v. anesthesia resulted in reduced analgesic efficacy during surgery compared with caudal 0.20% levobupivacaine or 0.20% bupivacaine in children. Ninety ASA I-II children between 1 and 7 years old, scheduled for inguinal hernia repair or orchidopexy under propofol anesthesia were randomized to receive a caudal block with 1 ml x kg(-1) of 0.2% bupivacaine, 0.2% ropivacaine or 0.2% levobupivacaine. The primary outcome measure of the study was the clinical efficacy of the caudal block during surgery. Secondary outcome measures were postoperative pain relief and residual motor blockade. Four children were excluded and 86 were analyzed. The proportion of children with effective caudal block during surgery was significantly higher in children receiving levobupivacaine (26/28) or bupivacaine (27/29) compared with patients receiving ropivacaine (21/29) (P = 0.03). There were no significant differences among groups in the analgesic onset time (P = 0.1), incidence of residual motor blockade (P = 0.4), number of patients requiring analgesia after operation or in the time from caudal injection to the first administration of analgesic medication (P = 0.3).\n\nQuestion:\nIs caudal 0.2 % ropivacaine less effective during surgery than 0.2 % levobupivacaine and 0.2 % bupivacaine : a double-blind , randomized , controlled trial?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAnalgesic effects of oxytocin and it's the other physiological effects were well-known. The aim of present study was determination of nitric oxide role on analgesic effects of oxytocin in mice. 216 male Albino mice were divided randomly into two experimental groups, tail flick and formalin test. Each experimental group consists of three main groups including: saline, L-arginine (50 mg/kg) and L-NAME (10 mg/kg) intraperitoneal (IP) injection. 15 min after injection in each of the following groups, the animals in each groups divided to the three subgroups including: saline (n=12), oxytocin (1 mg/kg) (n=12) and oxytocin (1 mg/kg) + atosiban (1 mg/kg) (n=12) was injected IP and then after 30 min of use the formalin test and tail flick were to evaluate the response to pain. Area under the curve (AUC) in the late phase of the formalin test, in sub-groups oxytocin + saline and L-NAME were significantly decreased compared with saline + saline group (P<0.05 to P< 0.001), and AUC in L-arginine + saline and atosiban + saline + oxytocin were significantly increased compared with oxytocin + saline group (P<0.05). Tail flick tests as well as a significant reduction in the AUC in oxytocin + L-arginine and atosiban + saline + oxytocin groups were compared with Oxytocin + Saline group (P<0.001).\n\nQuestion:\nDo the role of nitric oxide on the oxytocin induce analgesia in mice?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 examine whether emotion regulation predicts change of perceived health in patients with rheumatoid arthritis (RA). Sixty six patients (44 female, 22 male; mean (SD) age 57.7 (11.6) years) participated in a prospective study. Hierarchical regression analysis was used to predict change of perceived health between study entry and follow up (1(1/2) years later) from the emotion regulation styles ambiguity, control, orientation, and expression at study entry. Valuing and intensely experiencing emotions (emotional orientation) predicted a decrease of positive affect. Difficulty recognising and expressing emotions (ambiguity) predicted an increase of perceived disease activity. Emotion regulation showed no associations with change of negative affect and social and physical functioning.\n\nQuestion:\nDoes emotion regulation predict change of perceived health in patients with rheumatoid arthritis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 analyze the correlation between dose-volume parameters of the corpora cavernosa and erectile dysfunction (ED) after external beam radiotherapy (EBRT) for prostate cancer. Between June 1997 and February 2003, a randomized dose-escalation trial comparing 68 Gy and 78 Gy was conducted. Patients at our institute were asked to participate in an additional part of the trial evaluating sexual function. After exclusion of patients with less than 2 years of follow-up, ED at baseline, or treatment with hormonal therapy, 96 patients were eligible. The proximal corpora cavernosa (crura), the superiormost 1-cm segment of the crura, and the penile bulb were contoured on the planning computed tomography scan and dose-volume parameters were calculated. Two years after EBRT, 35 of the 96 patients had developed ED. No statistically significant correlations between ED 2 years after EBRT and dose-volume parameters of the crura, the superiormost 1-cm segment of the crura, or the penile bulb were found. The few patients using potency aids typically indicated to have ED.\n\nQuestion:\nDo dose-volume parameters of the corpora cavernosa correlate with erectile dysfunction after external beam radiotherapy for prostate cancer : results from a dose-escalation trial?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 high cost, coupled with the need for continuous infusion, renders Desferrioxamine (DFO), a non-feasible option for iron-chelation in a large majority of patients with β-thalassemia major in developing countries. Monotherapy with deferiprone (DFP) or deferasirox (DFX) may not always attain optimal control, particularly in heavily iron-loaded patients. Combination of DFP and DFX is a potential alternative. A prospective, single-center, open-label, uncontrolled study was conducted to evaluate the safety and efficacy of the combination in patients with β-thalassemia major. Patients who had received either DFP or DFX for >1 year and a serum ferritin >2,000 μg/L were enrolled. Blood counts, liver/renal functions, and serum ferritin were monitored during the 1-year study period. Facilities for cardiac T2*-MRI were unavailable. Thirty-six patients with a mean age of 13 ± 6.9 years (range: 4-29) and a ferritin of 6,768 ± 4,145 μg/L formed the study cohort. Eight (22%) patients had transient gastrointestinal adverse effects. DFX was discontinued in one patient for persistent abdominal pain/diarrhea. Eight (22%) had joint symptoms; DFP was discontinued in two. Four (11%) patients had elevation in AST/ALT levels, managed with temporary interruption of DFX. Nine (25%) had an inconsistent elevation of creatinine to >33% of baseline; no intervention was done. One had transient proteinuria. None had neutropenia. At the end of 1 year, the serum ferritin reduced by a mean value of 3,275.3 ± 618.2 μg/L (P < 0.001).\n\nQuestion:\nIs the deferiprone and deferasirox combination efficacious in iron overloaded patients with β-thalassemia major : A prospective , single center , open-label study?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nExtracellular matrix alterations are important elements in the arterial changes seen in diabetes, being associated with increased vascular stiffness and the development of cardiovascular diseases. However, no biomarkers for diabetes-related arterial changes have been defined. Mammary artery specimens from 17 men with type 2 diabetes and 18 nondiabetic individuals were used for microarray expression profiling, quantitative real-time PCR, immunoassay, and immunohistochemical analyses. A derived candidate marker, fibulin-1, which is an elastin-associated matrix molecule, was measured immunochemically in plasma from (a) 70 patients scheduled for vascular surgery, (b) 305 patients with type 2 diabetes examined with carotid ultrasonography and echocardiography, and (c) 308 patients with type 2 diabetes, followed for 15 years. The most upregulated transcript in nonatherosclerotic arterial tissue from patients with type 2 diabetes encoded the extracellular matrix protein, fibulin-1. Higher concentrations of fibulin-1-protein were present in artery extracts from patients with diabetes than extracts from individuals without diabetes, and increased fibulin-1 immunostaining was apparent around the external elastic lamina of diabetic arteries. Patients with diabetes displayed increased plasma concentrations of fibulin-1 (P = 0.006). Plasma fibulin-1 concentrations correlated with hemoglobin A(1c) (P < 0.001), arterial stiffness indices including pulse pressure (P < 0.001), and carotid compliance (P = 0.004), as well as plasma N-terminal pro-B-type natriuretic peptide concentrations (P < 0.001) and were predictive of 15-year mortality (P = 0.013).\n\nQuestion:\nIs fibulin-1 a marker for arterial extracellular matrix alterations in type 2 diabetes?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIdentifying a limitless source of β-cells that survive transplantation into a neovascularised site and provide normal blood glucose control remains an important goal in the development of pancreatic islet xenotransplantation. It was our hypothesis that fetal porcine pancreas fragments could achieve these objectives, and this was tested in a large preclinical animal model. Inbred \"Westran Pig\" fetal porcine pancreas fragments were transplanted beneath the splenic capsule into syngeneic Westran Pig recipients without immunosuppression, and 3 months later, a total native pancreatectomy was performed to demonstrate function. Histologic analysis showed appropriate development of islet-like structures up to and beyond 120 days after transplantation. After native pancreatectomy, recipients survived more than 100 days without exogenous insulin and with normal glucose homeostasis as assessed by normal glucose tolerance tests, K values, and normal glucagon secretion.\n\nQuestion:\nDoes subcapsular fetal pig pancreas fragment transplantation provide normal blood glucose control in a preclinical model of diabetes?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAutism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD) both have psychiatric comorbidities and distinctive profiles of executive dysfunction. Although there is evidence that executive function (EF) plays a role in the expression of specific behaviors and psychiatric symptoms, it is not known whether specific EF deficits in ASD and ADHD may be pathways to comorbidities in the disorders. This study examines whether parent reported problems with flexibility in ASD and inhibition in ADHD mediate the disorders' associations with anxiety/depression and oppositional/aggressive behavior, respectively. Parent report data from the Behavior Rating Inventory of Executive Function (BRIEF) and the Child Behavior Checklist (CBCL) were obtained for 125 children (70 ASD, 55 ADHD Hyperactive/Impulsive or Combined type) as part of a neuropsychological assessment. Diagnostic status, BRIEF Shift (shifting/flexibility) and Inhibit (behavioral inhibition) scale scores, and CBCL Anxious/Depressed (anxiety/depression) and Aggressive Behavior (oppositionality/aggression) scale scores were analyzed with a path analysis to investigate the relation of flexibility and inhibition to comorbid symptoms in children with ASD and ADHD. In a path model with good fit ASD predicted greater inflexibility which predicted greater anxiety/depression, while ADHD predicted greater disinhibition that predicted greater aggression, consistent with our mediational hypotheses. Unexpectedly, the greater inflexibility associated with ASD also predicted greater aggression.\n\nQuestion:\nDo everyday executive function impairments predict comorbid psychopathology in autism spectrum and attention deficit hyperactivity disorders?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 purpose of this study was to test whether a short-course treatment with ACE inhibitors may restore endothelium-dependent and/or -independent vasodilation in the femoral artery of microalbuminuric patients with type 1 diabetes and normal arterial pressure. We studied nine normotensive microalbuminuric type 1 diabetic patients and two groups of control subjects matched for femoral artery diameter to type 1 diabetic patients after placebo (control group A, n = 17) and ACE inhibitor (control group B, n = 18) treatment, respectively. The patients were enrolled in a double-blind cross-over study with a 1-week trial of either placebo, captopril (25 mg t.i.d.), or enalapril (10 mg/day) in randomized order to ascertain whether short-term ACE inhibition obtained with (captopril) or without (enalapril) a sulfhydryl donor molecule ameliorates vessel wall function. Endothelium-mediated flow-dependent vasodilation and endothelium-independent vasodilation were evaluated in the right common femoral artery by echo Doppler. Both captopril and enalapril normalized (control group B 22.9+/-3.2% per 8 min) endothelium-dependent response (19.6+/-7.5 and 18.0+/-5.3 vs. -10.4+/-4.1% per 8 min, P < 0.01, for both captopril and enalapril versus placebo, respectively) in the type 1 diabetic patients. Captopril (28.4+/-3.5 vs. 17.1+/-3.5% per 5 min during placebo, P < 0.05) but not enalapril (20.1+/-3.0 vs. 31.7+/-2.8% per 5 min, P < 0.05 for enalapril versus control group B, and NS for captopril vs. control group B) ameliorated endothelium-independent vasodilation in type 1 diabetic patients.\n\nQuestion:\nDo aCE inhibitors improve endothelial function in type 1 diabetic patients with normal arterial pressure and microalbuminuria?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 influence of body mass index (BMI) on postoperative death in patients undergoing surgery for HCC. Three hundred forty-two patients were enrolled, and divided into three groups: Group A, BMI <22.5; Group B, BMI ≥22.5 to <25; Group C, BMI ≥25. Univariate and multivariate analyses of postoperative death were performed to compare BMI with clinical factors. Kaplan-Meier analysis and log rank test were used to compare such outcome in Groups A, B, and C. Kaplan-Meier analysis and log rank test revealed that Group A had a higher rate of postoperative death than Group B or C (P = 0.010). Univariate and multivariate analyses selected being underweight (Group B, C/Group A) (odds ratio, 1.829; 95% C.I., 1.091-3.068; P = 0.022) as one of the factors predictive of postoperative death, together with aspartate aminotransferase level (P = 0.042) and HCC growth pattern (P = 0.032).\n\nQuestion:\nDo underweight patients show an increased rate of postoperative death after surgery for hepatocellular carcinoma?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nStudies have proposed that mesenchymal stem cells (MSCs) improve the hematopoietic engraftment in allogeneic or xenogeneic transplants and this is probably due to the MSCs' immunosuppressive properties. Our study aimed to discern, for the first time, whether MSC infusion could facilitate the engraftment of hematopoietic stem cells (HSCs) in autologous transplantations models, where no immune rejection of donor HSCs is expected. Recipient mice (CD45.2) mice, conditioned with moderate doses of radiation (5-7 Gy), were transplanted with low numbers of HSCs (CD45.1/CD45.2) either as a sole population or co-infused with increasing numbers of adipose-derived-MSCs (Ad-MSCs). The influence of Ad-MSC infusion on the short-term and long-term engraftment of donor HSCs was investigated. Additionally, homing assays and studies related with the administration route and with the Ad-MSC/HSC interaction were conducted. Our data show that the co-infusion of Ad-MSCs with low numbers of purified HSCs significantly improves the short-term and long-term hematopoietic reconstitution of recipients conditioned with moderate irradiation doses. This effect was Ad-MSC dose-dependent and associated with an increased homing of transplanted HSCs in recipients' bone marrow. In vivo and in vitro experiments also indicate that the Ad-MSC effects observed in this autologous transplant model are not due to paracrine effects but rather are related to Ad-MSC and HSC interactions, allowing us to propose that Ad-MSCs may act as HSC carriers, facilitating the migration and homing of the HSCs to recipient bone marrow niches.\n\nQuestion:\nDo mesenchymal stromal cells enhance the engraftment of hematopoietic stem cells in an autologous mouse transplantation model?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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-induced excitotoxicity has been implicated as a causative factor for selective neuronal loss in ischemia and hypoxia. Toxic exposure of neurons to glutamate results in an extended neuronal depolarization that precedes delayed neuronal death. Because both delayed neuronal death and extended neuronal depolarization are dependent on calcium, we examined the effect of glutamate exposure on extended neuronal depolarization and calcium/calmodulin-dependent protein kinase II (CaM kinase II) activity. Three-week-old cortical cell cultures from embryonic rats were exposed to 500 microM glutamate and 10 microM glycine or to control medium for 10 minutes. Cells were examined for neuronal toxicity, electrophysiology, and biochemical alterations. In one set of experiments, whole-cell current clamp recording was performed throughout the experiment. In a parallel experiment, cortical cultures were allowed to recover from glutamate exposure for 1 hour, at which time the cells were homogenized and CaM kinase II activity was assayed using standard techniques. Excitotoxic exposure to glutamate resulted in extended neuronal depolarization, which remained after removal of the glutamate. Glutamate exposure also resulted in delayed neuronal death, which was preceded by significant inhibition of CaM kinase II activity. The excitotoxic inhibition of CaM kinase II correlated with neuronal loss, was N-methyl-D-aspartate receptor-mediated, and was not due to autophosphorylation of the enzyme.\n\nQuestion:\nDoes excitotoxicity affect membrane potential and calmodulin kinase II activity in cultured rat cortical neurons?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHypoxia can induce autophagy, which plays an important role in cardioprotection. The present study tested the hypothesis that patients with congenital heart disease living at a high altitude could resist ischemia-reperfusion injury better than those at a low altitude, through elevated basal autophagy by chronic hypoxia. Twelve Tibetan patients residing at a high altitude of >3000 m and 12 Han patients residing at a low altitude of <500 m with simple atrial or ventricular septal defects were prospectively recruited. All patients underwent cardiopulmonary bypass, maintaining a flow rate of approximately 2.4 to 2.8 L/min/m2 and mean arterial pressure of ≥40 to 60 mm Hg. Myocardial ischemia-reperfusion injury between the 2 groups was compared using cardiac troponin I, brain natriuretic peptide, hematoxylin eosin staining, and the terminal deoxynucleotidyl transferase dUTP nick end labeling test. Autophagy-related proteins microtubule-associated protein 1 light chain 3 II (LC3II), Beclin1, and lysosomal-associated membrane protein 2 (LAMP2) and their upstream protein BCL2/adenovirus E1B 19-kDa protein-interacting protein 3 (Bnip3) were evaluated with Western blotting. The maximal cardiac troponin I concentration and increasing x-fold of brain natriuretic peptide in the high-altitude group were obviously lower than those in the low-altitude group (3.10±0.77 vs 7.10±2.28 ng/mL and 2.51±0.94 vs 14.66±6.83, respectively). The preoperative and postoperative levels of LC3II, LAMP2, and upstream Bnip3 in the high-altitude group were obviously greater. No difference was found in the Beclin1 level between the 2 groups at baseline or ischemia-reperfusion.\n\nQuestion:\nDoes high basal level of autophagy in high-altitude residents attenuate myocardial ischemia-reperfusion injury?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nVariation in the reaction wood (RW) response has been shown to be a principle component driving differences in lignocellulosic sugar yield from the bioenergy crop willow. The phenotypic cause(s) behind these differences in sugar yield, beyond their common elicitor, however, remain unclear. Here we use X-ray micro-computed tomography (μCT) to investigate RW-associated alterations in secondary xylem tissue patterning in three dimensions (3D). Major architectural alterations were successfully quantified in 3D and attributed to RW induction. Whilst the frequency of vessels was reduced in tension wood tissue (TW), the total vessel volume was significantly increased. Interestingly, a delay in programmed-cell-death (PCD) associated with TW was also clearly observed and readily quantified by μCT.\n\nQuestion:\nDoes x-ray micro-computed tomography in willow reveal tissue patterning of reaction wood and delay in programmed cell death?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 occurrence of speech disfluencies during narrative production in children with specific language impairment (SLI) and their age-matched peers. The study included 60 children aged between 7 and 10 years, 40 with typical language development and 20 with SLI. For data collection, a series of 15 stories was used, each one represented by pictures composed of four scenes. Narratives were transcripted and the speech disfluencies presented on them were classified as stuttering-like disfluencies (part-word repetition, single-syllable word repetition, and dysrhythmic phonation - prolongations, blocks and broken words) or other disfluencies (interjection, revision/abandoned utterances, and multisyllable/phrase repetition). The disfluency categories were compared in each group and its occurrence was also compared between groups. The occurrence of stuttering-like and other disfluencies did not differ among children with typical language development, whereas children with SLI produced other disfluencies. Between-group comparison showed that children with SLI produced more disfluencies of both types than their age-matched peers.\n\nQuestion:\nDo school-age children with specific language impairment produce more speech disfluencies than their peers?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 no effective therapeutic intervention developed targeting cerebrovascular toxicity of drugs of abuse, including methamphetamine (METH). We hypothesize that exercise protects against METH-induced disruption of the blood-brain barrier (BBB) by enhancing the antioxidant capacity of cerebral microvessels and modulating caveolae-associated signaling. Mice were subjected to voluntary wheel running for 5 weeks resembling the voluntary pattern of human exercise, followed by injection with METH (10 mg/kg). The frequency, duration, and intensity of each running session were monitored for each mouse via a direct data link to a computer and the running data are analyzed by Clock lab™ Analysis software. Controls included mice sedentary that did not have access to running wheels and/or injections with saline. METH induced oxidative stress in brain microvessels, resulting in up regulation of caveolae-associated NAD(P)H oxidase subunits, and phosphorylation of mitochondrial protein 66Shc. Treatment with METH disrupted also the expression and colocalization of tight junction proteins. Importantly, exercise markedly attenuated these effects and protected against METH-induced disruption of the BBB integrity.\n\nQuestion:\nDoes voluntary exercise protect against methamphetamine-induced oxidative stress in brain microvasculature and disruption of the blood-brain barrier?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nEvolutionarily conserved sequences within or adjoining orthologous genes often serve as critical cis-regulatory regions. Recent studies have identified long, non-coding genomic regions that are perfectly conserved between human and mouse, termed ultra-conserved regions (UCRs). Here, we focus on UCRs that cluster around genes involved in early vertebrate development; genes conserved over 450 million years of vertebrate evolution. Based on a high resolution detection procedure, our UCR set enables novel insights into vertebrate genome organization and regulation of developmentally important genes. We find that the genomic positions of deeply conserved UCRs are strongly associated with the locations of genes encoding key regulators of development, with particularly strong positional correlation to transcription factor-encoding genes. Of particular importance is the observation that most UCRs are clustered into arrays that span hundreds of kilobases around their presumptive target genes. Such a hallmark signature is present around several uncharacterized human genes predicted to encode developmentally important DNA-binding proteins.\n\nQuestion:\nDo arrays of ultraconserved non-coding regions span the loci of key developmental genes in vertebrate genomes?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 CD40/CD40 ligand system is involved in atherogenesis. Activated T lymphocytes and platelets, which express high amounts of CD40 ligand (CD40L) on their surface, contribute significantly to plaque instability with ensuing thrombus formation, leading to acute coronary syndromes. Because reendothelialization may play a pivotal role for plaque stabilization, we investigated a potential role of CD40L on endothelial cell (EC) migration. Stimulation of ECs with recombinant CD40L prevented vascular endothelial growth factor (VEGF)-induced EC migration, as determined by a \"scratched wound assay.\" In addition, activated T lymphocytes and platelets significantly inhibited VEGF-induced EC migration and tube formation in vitro. Because the activation of endothelial nitric oxide (NO) synthase and the release of NO are required for EC migration and angiogenesis, we analyzed the effect of NO. Coincubation with the NO donor S-nitroso-N-acetyl-penicillamine (SNAP) did not reverse the inhibitory effect of CD40L on VEGF-induced EC migration and tube formation. In addition, EC migration induced by SNAP was completely inhibited by CD40L. CD40L, however, induced the production of reactive oxygen species and reduced endothelial NO bioavailability. This reactive oxygen species-dependent effect of CD40L stimulation was reversed with vitamin C or N-acetylcysteine.\n\nQuestion:\nDoes cD40 ligand inhibit endothelial cell migration by increasing production of endothelial reactive oxygen species?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIncreased electrical activity in peripheral sensory neurons including dorsal root ganglia (DRG) and trigeminal ganglia neurons is an important mechanism underlying pain. Voltage gated sodium channels (VGSC) contribute to the excitability of sensory neurons and are essential for the upstroke of action potentials. A unique type of VGSC current, resurgent current (INaR), generates an inward current at repolarizing voltages through an alternate mechanism of inactivation referred to as open-channel block. INaRs are proposed to enable high frequency firing and increased INaRs in sensory neurons are associated with pain pathologies. While Nav1.6 has been identified as the main carrier of fast INaR, our understanding of the mechanisms that contribute to INaR generation is limited. Specifically, the open-channel blocker in sensory neurons has not been identified. Previous studies suggest Navβ4 subunit mediates INaR in central nervous system neurons. The goal of this study was to determine whether Navβ4 regulates INaR in DRG sensory neurons. Our immunocytochemistry studies show that Navβ4 expression is highly correlated with Nav1.6 expression predominantly in medium-large diameter rat DRG neurons. Navβ4 knockdown decreased endogenous fast INaR in medium-large diameter neurons as measured with whole-cell voltage clamp. Using a reduced expression system in DRG neurons, we isolated recombinant human Nav1.6 sodium currents in rat DRG neurons and found that overexpression of Navβ4 enhanced Nav1.6 INaR generation. By contrast neither overexpression of Navβ2 nor overexpression of a Navβ4-mutant, predicted to be an inactive form of Navβ4, enhanced Nav1.6 INaR generation. DRG neurons transfected with wild-type Navβ4 exhibited increased excitability with increases in both spontaneous activity and evoked activity. Thus, Navβ4 overexpression enhanced INaR and excitability, whereas knockdown or expression of mutant Navβ4 decreased INaR generation.\n\nQuestion:\nDoes navβ4 regulate fast resurgent sodium currents and excitability in sensory neurons?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 glucocorticoid receptors (GR) increases expression of the mitogen-activated protein kinase (MAPK) pathway leading to increased expression of Zif/268, an effector immediate early gene involved in cellular growth, intracellular signaling, and synaptic modification. Glucocorticoids induce expression of Zif/268 through two distinct mechanisms: a rapid-onset, MAPK-independent pathway and a slower-onset, MAPK-dependent mechanism. This study investigated both rapid and long-term expression of GR protein in the cytosolic extract, its translocation to the nucleus, and expression of mRNA for the Zif/268 gene in selected brain areas, associated with circulating levels of corticosterone, in an animal model of PTSD. Trauma cue-triggered Zif/268 expression was assessed eight days after stress exposure. The results demonstrated a pattern of response that was common to all exposed individuals at 30 min after exposure, characterized by a significant elevation in GR translocation to the nucleus and elevated levels of Zif/268 mRNA in the hippocampus. A distinct pattern associated with extreme behavioral response (EBR) was revealed upon further bioassay of behavioral response groups, classified according to their individual patterns of behavioral response at seven days. These EBR individuals displayed significantly higher circulating corticosterone and nuclear GR levels, compared to minimal behavioral responders and controls. No difference in Zif/268 mRNA levels was observed between the exposed and naïve animals.\n\nQuestion:\nIs a distinct pattern of intracellular glucocorticoid-related responses associated with extreme behavioral response to stress in an animal model of post-traumatic stress disorder?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAlthough functional status, as assessed by the New York Heart Association classification, is known to be a powerful prognostic marker in chronic heart failure (CHF), the significance of individual symptoms such as breathlessness and fatigue are unknown. To assess the relative importance of self-reported severity of symptoms as predictors of outcomes in CHF. All 3029 patients randomized in the Carvedilol or Metoprolol European Trial (ie, COMET) study were included in the analysis. Mean follow-up was 58 months. Symptoms were assessed by 5-point scales. In a univariate analysis, worse scores for breathlessness, orthopnea and fatigue were all significantly related to increased mortality (all P < .0001) and development of worsening heart failure. In a multivariate Cox regression analysis including 16 baseline covariates, only the symptom of breathlessness remained significantly related to mortality (risk ratio [RR] 1.14 per unit: 95% CI 1.04-1.26; P = .01). Fatigue, but not breathlessness, remained a significant predictor for developing worsening heart failure (RR 1.09 per unit; 95% CI 1.02-1.18; P = .02).\n\nQuestion:\nAre symptoms in patients with heart failure prognostic predictors : insights from COMET?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 clinical outcome after repair of zone I flexor tendon injuries using either the pullout button technique or suture anchors placed in the distal phalanx. Between 1998 and 2002 we treated 26 consecutive zone I flexor tendon injuries. Thirteen patients had repairs from 1998 to 2000 using a modified pullout button technique (group A) and 13 patients had repair using suture anchors placed in the distal phalanx (group B). Patient characteristics were similar for both groups. The same postoperative flexor tendon rehabilitation protocol and follow-up schedule were used for both groups. Evaluation included range of motion, sensibility and grip strength, failure, complications, and return to work. The Student t test was used to determine significant differences. All patients completed 1 year of follow-up evaluation. There were 2 infections in group A that resolved with oral antibiotics and no infections in group B. There were no tendon repair failures and no repeat surgeries in either group. At final follow-up evaluation there were no statistically significant differences for the following end points: sensibility (Semmes-Weinstein monofilament testing and 2-point discrimination), active range of motion (at the proximal interphalangeal joint, distal interphalangeal joint, or their combined motion), flexion contracture (at the proximal interphalangeal joint, distal interphalangeal joint, or their combined contracture), and grip strength (injured tendon as a percent of the contralateral uninjured tendon). The suture anchor group had a statistically significant improvement for time to return to work.\n\nQuestion:\nDo comparison of pullout button versus suture anchor for zone I flexor tendon repair?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\ncGMP-degrading phosphodiesterase 6 (PDE6) mutations cause around 4 to 5% of retinitis pigmentosa (RP), a rare form of retinal dystrophy. Growing evidence suggests that inflammation is involved in the progression of RP. The aims of this study were to corroborate the presence of high TNFα concentration in the eyes of RP patients and to evaluate whether the blockade of TNFα with Infliximab, a monoclonal anti-TNFα antibody, prevented retinal degeneration induced by PDE6 inhibition in cultures of porcine retina. Aqueous humor from 30 patients with RP and 13 healthy controls were used to quantify the inflammatory mediators IL-6, TNFα, IL-1β, IL-10 by a multiplex enzyme-linked immunosorbent assay (ELISA) system. Retinal explants from pig were exposed to Zaprinast, a PDE6 inhibitor, for 24 hours in the absence or the presence of Infliximab. Cell death was evaluated by TUNEL assay. The number and distribution of caspase-3 positive cells, indirect poly(ADP)ribose polymerase (PARP) activation and glial fibrillary acidic protein (GFAP) content were visualized by immunolabeling. Antioxidant total capacity, nitrites and thiobarbituric acid reactive substances (TBARS) formation were determined to evaluate antioxidant-oxidant status. IL-6 and TNFα concentrations were higher in the aqueous humor of RP patients than in controls. Infliximab prevented retinal degeneration, as judging by the reduced presence of TUNEL-positive cells, the reduction of caspase-3 activation and also reduction of glial activation, in an ex vivo model of porcine retina. Additionally, Infliximab partially reduced oxidative stress in retinal explants exposed to Zaprinast.\n\nQuestion:\nDoes infliximab reduce Zaprinast-induced retinal degeneration in cultures of porcine retina?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 studied retrospectively the interaction between c-erbB2 overexpression and adjuvant tomoxifen in node-negative breast cancer patients enrolled in the Gruppo Universitario Napoletano 1 (GUN-1) trial. c-erbB2, evaluated by immunohistochemistry in 145 of 173 patients randomly assigned to 2-year adjuvant tamoxifen or no further therapy, was considered overexpressed if greater than 10% of the cells showed specific membrane staining. The role of each prognostic variable and their independent effect were studied using the Cox model. Disease-free (DFS) and overall (OAS) survival curves were estimated by the Kaplan-Meier method. As of November 30, 1994, the median follow-up period was 12 years. c-erbB2 was overexpressed in 43 of 145 patients (29.7%), which directly correlated with tumor size and inversely with estrogen receptor (ER) level. At univariate analysis, overexpression of c-erbB2 did not affect either DFS or OAS; tamoxifen had a greater effect on reducing the risk of recurrence than of death. Addition of c-erbB2 to a multivariate Cox model that contained menopausal status, tumor size, nuclear grade, and treatment as covariates did not affect the significance of the model for DSF or OAS, whereas addition of the first-order interaction between c-erbB2 and tamoxifen was statistically significant both for DFS and OAS. The same result was obtained when the model contained ER status and ER-tamoxifen interaction. Indeed, adjuvant tamoxifen significantly prolonged DFS and OAS in c-erbB2-negative cases, whereas it had no effect on DFS and OAS in c-erbB2-positive patients.\n\nQuestion:\nDoes c-erb B2 overexpression decrease the benefit of adjuvant tamoxifen in early-stage breast cancer without axillary lymph node metastases?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIschemia time is a risk factor for mortality and right ventricular (RV) failure after heart transplantation. The purpose of this study was to determine the effect of ischemia time on known transesophageal echocardiography (TEE) parameters of RV function and on a novel quantitative measurement of RV circumferential shortening. Right and left ventricular (LV) function was evaluated retrospectively in 20 consecutive patients after heart transplant using known TEE parameters as well as a quantitative measurement of circumferential contraction. The control group consisted of 20 patients undergoing coronary artery bypass grafting (CABG) with no documented RV dysfunction. Posttransplant TEE parameters of RV function were depressed compared with post-cardiopulmonary bypass CABG patients. Significant correlation was observed between tricuspid annular planar systolic excursion, basal, mid, and global circumferential shortening and total ischemia time.\n\nQuestion:\nDoes total ischemia time alter the longitudinal and circumferential shortening of the right ventricle in transplanted hearts?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCardiac resynchronization therapy (CRT) was shown to improve heart failure (HF) prognosis. But many patients do not benefit from CRT. Optimization of left ventricular (LV) lead position to the latest activated LV area is important to increase CRT response. We aimed to detect the relationship between LV lead sensing delay and echocardiographic and electrocardiographic response to CRT treatment. We prospectively included 156 consecutive patients with HF diagnosis, QRS ≥ 120 ms, left bundle branch block, New York Heart Association II-IV, LV ejection fraction (LVEF) < 35%, and scheduled for CRT (100 male, 56 female; mean age 65.8 ± 10.06 years). Echocardiographic CRT response was defined as ≥15% reduction in LV end-systolic volume (LVESV). LV lead sensing delay was calculated as the time interval from the onset of surface QRS wave to the onset of depolarization wave recorded from the LV lead by using the LV pacing lead as a bipolar electrode. LVESV reduction was associated with baseline QRS width (r = 0.292, P = 001), QRS narrowing (r = 0.332, P < 001), and LV lead sensing delay (r = 0.454, P < 001) in bivariate analysis. In logistic regression analysis, LV lead sensing delay was found to be the only independent parameter for predicting significant LVESV reduction (β = 0.423, P < 0.001). LV lead sensing delay was also found to be significantly associated with LVEF increase (r = 0.320, P < 0.001) and QRS narrowing (r = 0.345, P < 0.001).\n\nQuestion:\nDoes high Left Ventricular Lead Sensing Delay predict QRS Narrowing and Good Response to Cardiac Resynchronization Therapy?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 investigated whether glucosamine sulfate modulates the production of ICAM-1 induced by proinflammatory cytokines and whether glucosamine sulfate inhibits leukocyte adhesion to a monolayer of human conjunctival epithelial cells stimulated with proinflammatory cytokines. We used flow cytometry and either primary cultured human conjunctival cells or the Chang conjunctival cell model to determine the effects of glucosamine sulfate on the production of ICAM-1 in response to tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, interleukin (IL)-1beta, IL-6, TNF-alpha plus IFN-gamma, or TNF-alpha plus IL-1beta. The effects of glucosamine sulfate on the expression of the ICAM-1 gene, upregulated by various cytokines, were determined by semiquantitative reverse transcription-polymerase chain reaction. The activation and nuclear translocation of the nuclear factors NF-kappaB and STAT1 were evaluated by the transient transfection of reporter gene systems and immunocytochemistry. The influence of glucosamine-sulfate-modulated ICAM-1 on neutrophil adhesion was demonstrated in a model that measures the adherence of conjunctival cells and neutrophils. TNF-alpha, IFN-gamma, and IL-1beta significantly increased the production of ICAM-1 by both primary cultured human conjunctival cells and Chang conjunctival cells. Glucosamine sulfate effectively downregulated the production of ICAM-1 induced by TNF-alpha, IFN-gamma, IL-1beta, TNF-alpha plus IFN-gamma, or TNF-alpha plus IL-1beta. This downregulation occurred through the interferon-stimulated response element, IFN-gamma activation sequence, and binding sequence of NF-kappaB at the mRNA and protein levels. Glucosamine sulfate further inhibited the nuclear translocation of p65 protein in TNF-alpha- and IL-1beta-stimulated Chang conjunctival cells and phosphorylated STAT1 in IFN-gamma-stimulated Chang conjunctival cells. Glucosamine sulfate also significantly reduced the number of neutrophils adhering to a conjunctival monolayer in response to TNF-alpha, IFN-gamma, or IL-1beta.\n\nQuestion:\nDoes glucosamine sulfate inhibit proinflammatory cytokine-induced icam-1 production in human conjunctival cells in vitro?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAlthough most women with gestational diabetes mellitus (GDM) return to normal glucose tolerance after delivery, they have increased risk of cardiometabolic diseases. This study aimed to evaluate the relationships between plasma levels of Lp-pla2 and AGEs and cardiometabolic risk factors in women with GDM. 190 women with GDM (cases) and 80 healthy women (controls) were enrolled. Demographic and clinical data were collected and analyzed about 2 years after the delivery. Of the 190 cases, 19 (10%), 38 (20%) and 10 (5%) had type 2 diabetes mellitus, metabolic syndrome and hypertension after delivery, respectively. There were significant differences in variables between cases and controls: Lp-pla2 (pg/mL) 1991.5 ± 905.3 versus 1527.0 ± 799.8; AGEs (ng/mL) 403.0 ± 208.6 versus 321.8 ± 150.3. The plasma Lp-pla2 and AGEs levels were positively correlated with metabolic indexes in women with previous GDM.\n\nQuestion:\nAre lipoprotein-associated phospholipase A2 and AGEs associated with cardiovascular risk factors in women with history of gestational diabetes mellitus?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSporadic-onset ataxia is common in a tertiary care setting but a significant percentage remains unidentified despite extensive evaluation. Rare genetic ataxias, reported only in specific populations or families, may contribute to a percentage of sporadic ataxia. Patients with adult-onset sporadic ataxia, who tested negative for common genetic ataxias (SCA1, SCA2, SCA3, SCA6, SCA7, and/or Friedreich ataxia), were evaluated using a stratified screening approach for variants in 7 rare ataxia genes. We screened patients for published mutations in SYNE1 (n = 80) and TGM6 (n = 118), copy number variations in LMNB1 (n = 40) and SETX (n = 11), sequence variants in SACS (n = 39) and PDYN (n = 119), and the pentanucleotide insertion of spinocerebellar ataxia type 31 (n = 101). Overall, we identified 1 patient with a LMNB1 duplication, 1 patient with a PDYN variant, and 1 compound SACS heterozygote, including a novel variant.\n\nQuestion:\nAre mutations in rare ataxia genes uncommon causes of sporadic cerebellar ataxia?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 accelerated sarcopenia in older persons with high interleukin (IL)-6 serum levels plays a role in the prospective association between inflammation and disability found in many studies. Cohort study of older women with moderate to severe disability. Six hundred twenty older women from the Women's Health and Aging Study in whom information on baseline IL-6 serum level was available. Self-report of functional status, objective measures of walking performance, and knee extensor strength were assessed at baseline and over six semiannual follow-up visits. Potential confounders were baseline age, race, body mass index, smoking, depression, and medical conditions. At baseline, women with high IL-6 were more often disabled and had lower walking speed. After adjusting for confounders, women in the highest IL-6 tertile (IL-6>3.10 pg/mL) were at higher risk of developing incident mobility disability (risk ratio (RR) = 1.50, 95% confidence interval (CI) = 1.01-2.27), disability in activities of daily living (RR = 1.41, 95% CI = 1.01-1.98), and severe limitation in walking (RR = 1.61, 95% CI = 1.09-2.38) and experienced steeper declines in walking speed (P <.001) than women in the lowest IL-6 tertile (IL-6 < or =1.78 pg/mL). Decline in knee extensor strength was also steeper, but differences across IL-6 tertiles were not significant. After adjusting for change over time in knee extensor strength, the association between high IL-6 and accelerated decline of physical function was no longer statistically significant.\n\nQuestion:\nDoes change in muscle strength explain accelerated decline of physical function in older women with high interleukin-6 serum levels?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 clinical spectrum and frequency of acute care revisits after tonsillectomy in a population-based sample from a single state in the US. We used California state discharge databases from 2009 to 2011 to retrospectively identify retrospectively routine tonsillectomy discharges in residents <25 years of age and to establish record linkage to revisits within 30 days at ambulatory surgery, inpatient, and emergency department facilities statewide. Percentages and descriptive statistics were sample-weighted, and revisit rates were adjusted for demographic factors, expected payer, chronic conditions, surgical indication, facility type, and clustering. Records were available for 35 085 index tonsillectomies, most of which were performed at hospital-owned ambulatory and inpatient facilities. There were 4944 associated revisits: 3761 (75.9%) treat-and-release emergency room visits, 816 (17.1%) inpatient admissions, and 367 (7.0%) ambulatory surgery visits. Most revisits (3225 [67.7%]) were unrelated to bleeding; these typically occurred early (mode, day 2) and were commonly associated with diagnosis codes indicating pain, nausea/vomiting, or dehydration. Crude all-cause revisit and readmission rates were 10.5% and 2.1%, respectively. Adjusted all-cause revisit rates (range, 8.6%-24.5%) were lowest in young children, increased in adolescents, and peaked in young adults. Adjusted bleeding-related revisit rates increased abruptly in adolescents and reached 13.9% in males (6.8% in females, P < .001) ages 20-24 years.\n\nQuestion:\nDoes a population-based study of acute care revisit following tonsillectomy?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nObsessive compulsive disorder (OCD) is one of the most disabling and highly prevalent anxiety disorders (ADs). Current cognitive models of OCD implicate views about the self and world in the maintenance of the disorder. However, little research has focused on issues that may lead to vulnerability to such views. In particular, a person's attachment insecurities (attachment anxiety, avoidance) may be important risk factors increasing the likelihood of such non-adaptive perceptions (Doron & Kyrios, 2005). Participants meeting criteria for OCD were compared with cohorts meeting criteria for other ADs and healthy controls on a range of measures including adult attachment, OC symptoms, cognitions, and mood. Diagnosis of the clinical groups was established using the Anxiety Disorders Interview Schedule for DSM-IV (Brown, Di Nardo, & Barlow, 1994). The clinical relevance of attachment insecurities was ascertained by comparing their prevalence in an OCD sample (N = 30), an ADs sample (N = 20), and a community sample (N = 32). Attachment anxiety was significantly higher in individuals with OCD, even when controlling for depression.\n\nQuestion:\nAre adult attachment insecurities associated with obsessive compulsive disorder?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIslet transplantation is an effective way of reversing type I diabetes. However, islet transplantation is hampered by issues such as immune rejection and shortage of donor islets. Mesenchymal stem cells can differentiate into insulin-producing cells. However, the potential of human umbilical cord mesenchymal stem cells (huMSCs) to become insulin-producing cells remains undetermined. We isolated and induced cultured huMSCs under islet cell culture conditions. The response of huMSCs were monitored under an inverted phase contrast microscope. Immunocytochemical and immunofluorescence staining methods were used to measure insulin and glucagon protein levels. Reverse transcription-polymerase chain reaction (RT-PCR) was performed to detect gene expression of human insulin and PDX-1. Dithizone-staining was employed to determine the zinc contents in huMSCs. Insulin secretion was also evaluated through radioimmunoassay. HuMSCs induced by nicotinamide and β-mercaptoethanol or by neurogenic differentiation 1 gene (NeuroD1) transfection gradually changed morphology from typically elongated fibroblast-shaped cells to round cells. They had a tendency to form clusters. Immunocytochemical studies showed positive expression of human insulin and glucagon in these cells in response to induction. RT-PCR experiments found that huMSCs expressed insulin and PDX-1 genes following induction and dithizone stained the cytoplasm of huMSCs a brownish red color after induction. Insulin secretion in induced huMSCs was significantly elevated compared with the control group (t = 6.183, P < 0.05).\n\nQuestion:\nDo human umbilical cord mesenchymal stem cells derived from Wharton 's jelly differentiate into insulin-producing cells in vitro?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nLatent tuberculosis infection is detected by the tuberculin skin test before treating with anti-Tumour-Necrosis factor alpha (anti TNFα) reagents. More accurate are Interferon gamma release assays (IFNγ release assays) to identify patients with latent tuberculosis. Because of a positive control in this assay, it is possible to identify those patients in which a result of tuberculosis testing is not available due to a lack of stimulation capacity of lymphocytes (indeterminate result). Patients suffering from IBD are often treated with immunosuppressive agents, which may influence the results of tuberculosis testing. The aim is to investigate the influence of immunosuppressive agents on the outcome of IFNγ-release assay. 50 consecutive patients were documented before introducing anti-TNF-treatment in this single centre study between April 2009 and April 2010. Data of INFγ release assay for latent tuberculosis, skin test and laboratory data and current medication were enrolled. For the period of one year data of 45 consecutive patients was available for statistical analysis. 24 patients out of 45 (corresponding to 53.3%) received at least low doses of corticoid treatment and 27 patients out of 45 (corresponding to 60.0%) received immunosuppressive agents. 13 patients out of 45 (corresponding to 28.9%) had an indeterminate result of the QuantiFERON test. A correlation between the indeterminate result and combination therapy of corticosteroids was found. The concomitant therapy of immunosuppressive agents lead to a lower IFN release but no significance was found.\n\nQuestion:\nDo corticosteroids and immunosuppressive therapy influence the result of QuantiFERON TB Gold testing in inflammatory bowel disease patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe (pro)renin receptor [(P)RR] is implicated in the pathogenesis of cardiovascular disease. We investigated the effects of (P)RR blockade after myocardial infarction (MI) in a mouse coronary-ligation model. Mice underwent sham control surgeries (n = 8) or induction of MI followed by 28 days' treatment with a vehicle control (n = 8) or (P)RR antagonist (n = 8). Compared with sham control subjects, MI + vehicle mice demonstrated reduced left ventricular (LV) ejection fraction (LVEF: P < .001) and fractional shortening (P < .001), and increased LV end-systolic and -diastolic volumes (LVESV: P < .001; LVEDV: P < .001) 28 days after MI. In addition, MI decreased LV posterior wall and septal diameters (both P < .001), increased heart weight-body weight ratios (P < .05), LV collagen deposition, and cardiomyocyte diameter (both P < .001), and up-regulated collagen 1 (P < .01) and β-myosin heavy chain (β-MHC: P < .05) mRNA. Compared with MI + vehicle mice, (P)RR antagonism after MI reduced infarct size (P < .01), improved LVEF (P < .001), fractional shortening (P < .001), and stroke volume (P < .05), and decreased LVESV (P < .001) and LVEDV (P < .001). (P)RR antagonism also reversed MI-induced transmural thinning (P < .001) and reduced LV fibrosis (P < .01), cardiomyocyte size (P < .001), and ventricular collagen 1 (P < .01), β-MHC (P = .06), transforming growth factor β1 (P < .01), and angiotensin-converting enzyme (P < .05) expression.\n\nQuestion:\nDoes ( Pro ) renin Receptor Blockade ameliorate Cardiac Injury and Remodeling and Improves Function After Myocardial Infarction?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSocial stress induces sexual dysfunction and reduces serum testosterone (T) level in rats. Stressful events exert an influence on a variety of behaviors and physiology through hormonal changes. The mechanism of stress-induced sexual dysfunction is unknown. To investigate the role of dehydroepiandrosterone (DHEA) in copulatory behavior induced by social stress in rats. Stress-induced male rats were subjected to social stress in which the males lived in a wire-mesh siege located in a colony of male and female rats and were exposed daily to a brief defeat by the colony of males for five consecutive days. After the stress period, copulatory behavior and serum concentrations of DHEA and T were measured. The effects of DHEA, T, and NE-100, a selective sigma 1 receptor antagonist, on copulatory behavior following social stress were examined. The males exhibited a marked suppression of copulatory behavior (elongation of intromission and ejaculation latencies). Serum concentrations of DHEA and T were significantly lower than those in nonstressed control males. Another three groups of social stressed males were injected daily with DHEA, T, or DHEA + NE-100 during the stress period. Injections of DHEA attenuated the stress-induced suppression of copulatory behavior, whereas T had no effect. The combined treatment of NE-100 made DHEA ineffective at restoring copulatory behavior.\n\nQuestion:\nDoes dehydroepiandrosterone alleviate copulatory disorder induced by social stress in male rats?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAsymmetric dimethylarginine (ADMA) plays role in the pathogenesis of coronary artery disease and related mortality and morbidity through a number of mechanisms. We hypothesized that plasma ADMA levels would be increased in the presence of reversible ischemia as measured by GATED single photon emission computed tomography (SPECT) myocardial perfusion scintigraphy (MPS). Fasting i.v. blood samples were drawn before testing. All patients underwent 99mTc-sestamibi GATED SPECT MPS with a one-day stress-rest protocol; the images were visually analyzed. Post-stress GATED parameters, including ejection fraction, end systolic and end diastolic volumes, and automatic stress defect scores, were recorded. The plasma ADMA levels were higher in the ischemic group than in the non-ischemic group (0.46 ± 0.19 vs. 0.40 ± 0.15; P = 0.016). Plasma ADMA levels (odds ratio [OR] = 13.5; 95% confidence interval [CI] = 1.7-109.01; P = 0.015) and sex (OR = 2.49, 95% CI = 1.18-5.26; P = 0.017) were independent predictors of ischemia. There was no linear correlation between plasma ADMA levels and both the GATED SPECT and stress test parameters.\n\nQuestion:\nIs asymmetric dimethylarginine a good predictor of ischemia using myocardial perfusion scintigraphy?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMetaplastic breast cancer is a rare histologic variant among breast cancers. We sought to investigate the impact of hormone receptor status in metaplastic breast cancer and compare outcomes with common histologic variants of breast cancer. The study was performed utilizing the Surveillance, Epidemiology, and End Results database. A query was made for patients with metaplastic breast cancer from 2000 to 2010. A separate query identified all patients with infiltrating ductal (IDC) or lobular (ILC) carcinoma during the same period. Effect of hormone receptor status was evaluated using Cox regression analysis. Significance was assessed for p < 0.05. A total of 2,338 patients with metaplastic breast cancer were available for study. Most tumors were hormone receptor negative (79.0 %) and greater than or equal to grade 3 (82.9 %). For comparison, 382,667 and 44,813 patients with IDC and ILC, respectively, were obtained. Overall 5-year survival for metaplastic breast cancer was 62.2 % compared with 81.2 % for IDC (p < 0.001) and 80.2 % for ILC (p < 0.001). For metaplastic cases, no difference in 5-year survival was found between hormone-positive and hormone-negative tumors (65.7 vs. 63.5 %; p = 0.70). Multivariate analysis demonstrated metaplastic histology as an independent risk factor for cancer-related mortality both among hormone-positive (hazard ratio [HR] 2.4; 95 % confidence interval [CI] 1.8-3.0; p < 0.001) and hormone-negative (HR 1.7; 95 % CI 1.5-1.9; p < 0.001) breast cancers.\n\nQuestion:\nDoes hormone receptor status affect prognosis in metaplastic breast cancer : a population-based analysis with comparison to infiltrating ductal and lobular carcinomas?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nFatigue contributes directly to anterior cruciate ligament (ACL) injury via promotion of high risk biomechanics. The potential for central fatigue to dominate this process, however, remains unclear. With centrally mediated movement behaviors being trainable, establishing this link seems critical for improved injury prevention. We thus determined whether fatigue-induced landing biomechanics were governed by a centrally fatiguing mechanism. Twenty female NCAA athletes had initial contact (IC) and peak stance (PS) three-dimensional hip and knee biomechanics quantified during anticipated and unanticipated single-leg landings, before and during unilateral fatigue accumulation. To induce fatigue, subjects performed repetitive (n = 3) single-leg squats and randomly ordered landings, until squats were no longer possible. Subject-based dependent factors were calculated across prefatigue trials and for those denoting 100%, 75%, 50%, and 25% fatigue and were submitted to three-way mixed-design analyses of covariance to test for decision, fatigue time, and limb effects. Fatigue produced significant (P < 0.01) decreases in IC knee flexion angle and PS knee flexion moment and increases in PS hip internal rotation and knee abduction angles and moments, with differences maintained from 50% fatigue through to maximum. Fatigue-induced increases in PS hip internal rotation angles and PS knee abduction angles and loads were also significantly (P < 0.01) greater during unanticipated landings. Apart from PS hip moments, significant limb differences in fatigued landing biomechanics were not observed.\n\nQuestion:\nDoes fatigue-induced ACL injury risk stem from a degradation in central control?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nBoth facilitatory and inhibitory effects of the sympathetic nervous system (SNS) on experimental arthritis have been reported. It is unknown whether such bidirectional effects are inherent to all experimental arthritis models and/or whether critical time windows exist for influences of the SNS on inflammation. To assess the effect of sympathectomy at different time points on the course and severity of murine antigen-induced arthritis (AIA). AIA was induced in mice. Chemical sympathectomy with 6-hydroxydopamine was carried out either neonatally, in the immunisation phase, or immediately before AIA elicitation, or during the chronic phase. In sympathectomised and non-sympathectomised AIA mice the inflammatory process (joint swelling, histopathology of inflammation and joint destruction), pain-related behaviour and cellular and humoral immune responses were analysed. Sympathectomy during AIA induction or neonatal sympathectomy significantly reduced the severity of acute AIA. Neither sympathectomy in the immunisation phase nor in the chronic phase influenced AIA. Flare-up reactions were reduced by sympathectomy just before flare-up or during the initial acute AIA stage. Sympathectomised AIA mice showed less hyperalgesia. Sympathectomy significantly reduced interleukin (IL) 2, IL-17 and transforming growth factor β in supernatants from lymph nodes and/or spleen cells and antigen-specific Th1-associated IgG2a in serum; IgG1 titres were unaffected. The ß blocker, propranolol, and the norepinephrine reuptake inhibitor bupropion produced similar anti-inflammatory effects, whereas the ß-adrenergic agonist isoproterenol increased AIA severity in neonatally sympathectomised mice.\n\nQuestion:\nAre the anti-inflammatory effects of sympathectomy in murine antigen-induced arthritis associated with a reduction of Th1 and Th17 responses?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nNeisseria meningitidis are common colonizers of the human nasopharynx. In some circumstances, N. meningitidis becomes an opportunistic pathogen that invades tissues and causes meningitis. While a vaccine against a number of serogroups has been in effective use for many years, a vaccine against N. meningitidis group B has not yet been universally adopted. Bacterial heat shock protein complex (HSPC) vaccines comprise bacterial HSPs, purified with their chaperoned protein cargo. HSPC vaccines use the intrinsic adjuvant activity of their HSP, thought to act via Toll-like receptors (TLR), to induce an immune response against their cargo antigens. This study evaluated HSPC vaccines from N. meningitidis and the closely related commensal N. lactamica. The protein composition of N. lactamica and N. meningitidis HSPCs were similar. Using human HEK293 cells we found that both HSPCs can induce an innate immune response via activation of TLR2. However, stimulation of TLR2 or TLR4 deficient murine splenocytes revealed that HSPCs can activate an innate immune response via multiple receptors. Vaccination of wildtype mice with the Neisseria HSPC induced a strong antibody response and a Th1-restricted T helper response. However, vaccination of mice deficient in the major TLR adaptor protein, MyD88, revealed that while the Th1 response to Neisseria HSPC requires MyD88, these vaccines unexpectedly induced an antigen-specific antibody response via a MyD88-independent mechanism.\n\nQuestion:\nDo heat shock protein complex vaccines induce antibodies against Neisseria meningitidis via a MyD88-independent mechanism?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 incidence of retained products of conception (RPOC) in relation to transvaginal ultrasound performed after first-trimester uterine evacuation. This was a prospective randomized study involving 809 women undergoing first-trimester uterine evacuation. The study group included 404 women in whom transvaginal sonography was performed at the end of the surgical procedure and the control group contained 405 women who did not undergo ultrasound examination. Initially, in the study group, recurettage was immediately performed if the endometrium appeared irregular but latterly only if endometrial thickness was > or = 8 mm. The patients were followed up by gynecological and ultrasound examinations 5-8 days following the surgical procedure. The total complication rate was 4.3%. RPOC presented in three women in the study group (0.7%) and in 15 women in the control group (3.7%, P < 0.05). Vaginal bleeding requiring hospitalization occurred in two women in the study group (0.5%) vs. seven in the control group (1.7%, P = 0.2). Endometritis was diagnosed in one woman in the study group (0.2%) vs. six in the control group (1.5%) and uterine perforation occurred in one woman in the control group vs. none in the study group. There were no cases of RPOC in women who had an endometrial thickness of < 8 mm as demonstrated by ultrasound at the end of the surgical procedure.\n\nQuestion:\nDoes transvaginal ultrasound after first-trimester uterine evacuation reduce the incidence of retained products of conception?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCancer of the exocrine pancreas is the fifth leading cause of cancer death in the United States. Neoadjuvant chemoradiation has been investigated in several trials as a strategy for downstaging locally advanced disease to resectability. The aim of the present study is to examine the effect of neoadjuvant radiation therapy (RT) vs. other treatments on long-term survival for patients with resectable pancreatic cancer in a large population-based sample group. The Surveillance, Epidemiology, and End Results (SEER) registry database (1994-2003) was queried for cases of surgically resected pancreatic cancer. Retrospective analysis was performed. The endpoint of the study was overall survival. Using Kaplan-Meier analysis we found that the median overall survival of patients receiving neoadjuvant RT was 23 months vs. 12 months with no RT and 17 months with adjuvant RT. Using Cox regression and controlling for independent covariates (age, sex, stage, grade, and year of diagnosis), we found that neoadjuvant RT results in significantly higher rates of survival than other treatments (hazard ratio [HR], 0.55; 95% confidence interval, 0.38-0.79; p = 0.001). Specifically comparing adjuvant with neoadjuvant RT, we found a significantly lower HR for death in patients receiving neoadjuvant RT rather than adjuvant RT (HR, 0.63; 95% confidence interval, 0.45-0.90; p = 0.03).\n\nQuestion:\nIs neoadjuvant radiation associated with improved survival in patients with resectable pancreatic cancer : an analysis of data from the surveillance , epidemiology , and end results ( SEER ) registry?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 anatomic resection of Couinaud's segments is one of the key techniques in liver surgery. However, the territories and volumes of the eight segments are not adequately assessed based on portal branching. Three-dimensional (3D) perfusion-based volumetry was performed in 107 normal livers. Based on Couinaud classification, the portal branches were identified and the volumes of each segment were calculated. The relationships between branching patterns of the portal veins and segmental volumes were assessed. In descending order of volume, median volumes of segments VIII, VII, IV, V, III, VI, II and I were recorded. Segment VIII was the largest, accounting for a median of 26.1% (range: 11.1-38.0%) of total liver volume (TLV), whereas segments II and III each represented <10% of TLV. In 69.2% of subjects, the portal branches of segment V diverged from the trunk of the branches of segment VIII. No relationship was found between branching type and segment volume.\n\nQuestion:\nDoes three-dimensional volumetry in 107 normal livers reveal clinically relevant inter-segment variation in size?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 care physical therapists contribute to the complex process of patient discharge planning. As physical therapists are experts at evaluating functional abilities and are able to incorporate various other factors relevant to discharge planning, it was expected that physical therapists' recommendations of patient discharge location would be both accurate and appropriate. This study determined how often the therapists' recommendations for patient discharge location and services were implemented, representing the accuracy of the recommendations. The impact of unimplemented recommendations on readmission rate was examined, reflecting the appropriateness of the recommendations. This retrospective study included the discharge recommendations of 40 acute care physical therapists for 762 patients in a large academic medical center. The frequency of mismatch between the physical therapist's recommendation and the patient's actual discharge location and services was calculated. The mismatch variable had 3 levels: match, mismatch with services lacking, or mismatch with different services. Regression analysis was used to test whether mismatch status, patient age, length of admission, or discharge location predicted patient readmittance. Overall, physical therapists' discharge recommendations were implemented 83% of the time. Patients were 2.9 times more likely to be readmitted when the therapist's discharge recommendation was not implemented and recommended follow-up services were lacking (mismatch with services lacking) compared with patients with a match. Limitations This study was limited to one facility. Limited information about the patients was collected, and data on patient readmission to other facilities were not collected.\n\nQuestion:\nDo physical therapists make accurate and appropriate discharge recommendations for patients who are acutely ill?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, 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 ActivPAL device is a well-established physical activity monitor for assessment of physical activity. To investigate test-retest reliability of step counts and establish minimal detectable changes (MDC) in step count to account for intra device error over time in various physical activities. Healthy participants (n=24, age range, 19-28 years) performed activities on two occasions, 1 week apart, in a laboratory setting; self-paced floor walking, treadmill walking at three different speeds (3.2 km/h, 4.5 km/h and 4.5 km/h with incline), treadmill jogging (8.0 km/h), stair walking and cycling on an exercise bike at three speeds (45 rpm, 60 rpm and 75 rpm). Relative reliability was calculated using intraclass correlation coefficient (ICC) and Spearman correlation. Absolute reliability was assessed using standard error of measurement (SEM) and coefficient of repeatability (CR). The ActivPAL showed high to very high relative reliability for treadmill walking at all speeds and stair walking, while self-paced normal floor walking showed moderate reliability. The absolute reliability was the best for treadmill walking activities, slightly increased for self-paced walking, followed by stair walking and jogging. The use of activity monitors during cycling has been questioned and our results confirm a low absolute and relative reliability. MDC values varied according to the type of activity e.g. treadmill walking 4.5 km/h (10 steps), walking on the floor (45 steps). Data loss in this study (10-13%) was higher than previously reported.\n\nQuestion:\nDoes test-retest reliability of step count with the ActivPAL™ device in common daily activities?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSummay: Insulin resistance is an important pathogenic factor in type 2 diabetes patents. An easy and efficiency measurement predicting insulin resistance; which can be done easily by type 2 patients is desired. To examine whether waist circumference is a better predictor of insulin resistance in type 2 diabetes than body mass index (BMI). From a population of 1356 registered diabetic patients, 144 who met (1) aged between 30 and 75 years, (2) being Chinese, (3) having had type 2 diabetes for more than one year, and (4) having been taking gliclazide and metformin for more than 6 months were enrolled in this study. The main outcome evaluated is the associations of HOMA insulin resistance index (HOMA index); which were assessed using multiple linear regression analysis. The coefficients of multiple regression analysis with stepwise model showed that waist circumference (β = 0.35, p < 0.001) but not BMI (β = 0.01, p = 0.94), adiponectin (β = -0.25, p = 0.04) and hemoglobulin A1c% (HbA1c) (β = 0.25, p = 0.01) were the main predictors of HOMA index.\n\nQuestion:\nIs waist circumference a better predictor than body mass index of insulin resistance in type 2 diabetes?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]