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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:\nDiabetes mellitus is gradually becoming a global health burden leading to an increase in the search for herbal hypoglycemic agents as alternatives to synthetic ones. Asystasia gangetica is one of the herbs used in folklore system of medicine for managing hypoglycaemia associated with diabetes. The influence of the juice of A. gangetica leaf on alloxan-induced diabetic rats was assessed by treating diabetic rats with 25%, 50% and 75% fresh juice and glibenclamide for 5 weeks. Afterwards, the plasma concentrations of glucose, triacylglycerols, total cholesterol, high-density lipoprotein (HDL) cholesterol, thiobarbituric acid reactive substances and bicarbonate were assayed spectrophotometrically. Treatment of the diabetic rats with the juice significantly (P < 0.05) reduced the elevated plasma levels of glucose to a level not significantly (P > 0.05) different from that of glibenclamide. The juice also significantly (P < 0.05) reduced the plasma lipid peroxidation and improved the lipid profile, as indicated by a significant (P < 0.05) reduction in the total cholesterol: HDL cholesterol ratio. However, there was a significant (P < 0.05) rise in the level of bicarbonate as result of the juice treatment from 28.15 ± 2.82 mmol/l in normal control to 60.83 ± 17.46 mmol/l in diabetic control and to 122.20 ± 34.68 mmol/l, 120.95 ± 35.09 mmol/l and 115.85 ± 11.79 mmol/l in 25%, 50% and 75% juice, respectively.\n\nQuestion:\nDoes persistence of acidosis in alloxan-induced diabetic rats treated with the juice of Asystasia gangetica leave?\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:\nIn Danish health care, secondary prevention after stroke is currently handled mainly by general practitioners using office blood pressure (OBP) assessment of hypertension. The aim of this study was to compare the OBP approach to 24-hour assessment by ambulatory blood pressure (ABP) monitoring. Furthermore, we aimed to record the degree of adherence to recommended therapy goals for blood pressure and plasma lipids. In a prospective observational study, 45 stroke patients aged 25-64 years who were participating in specialized intensive outpatient rehabilitation were monitored by OBP and ABP on average 1.3 (0.14-4.3) years post stroke. Furthermore, data on additional risk factors and medication for secondary prevention were collected. OBP and daytime ABP exceeded the therapy goal of 130/80 mmHg in 71% and 44% of the patients, respectively. ABP exceeded the night-time therapy goal of 115/65 in 57% of cases. Normal dipping at night was found in only 41% (systolic) and 32% (diastolic) of the patients. Considering both day- and night-time blood pressure, antihypertensive medication was absent or inadequate in 60%. Low density lipid (LDL) levels exceeded the recommended limit of 2.5 mmol/l in 49%.\n\nQuestion:\nAre treatment goals for ambulatory blood pressure and plasma lipids after stroke often not reached?\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:\nPoly (ADP-ribose) polymerase (PARP) inhibitors have shown promising results in Breast Cancer (BRCA) deficient breast cancer, but not in molecularly unselected patient populations. Two lines of research in this field are needed: the identification of novel subsets of patients that could potentially benefit from PARP inhibitors and the discovery of suitable targeted therapies for combination strategies. We tested PARP inhibition, alone or combined with the anti-HER2 antibody trastuzumab on HER2+ breast cancer. We used two PARP inhibitors in clinical development, olaparib and rucaparib, as well as genetic downmodulation of PARP-1 for in vitro studies. DNA damage was studied by the formation of γH2AX foci and comet assay. Finally, the in vivo anti-tumour effect of olaparib and trastuzumab was examined in nude mice subcutaneously implanted with BT474 cells. In a panel of four HER2 overexpressing breast cancer cell lines, both olaparib and rucaparib significantly decreased cell growth and enhanced anti-tumour effects of trastuzumab. Cells exposed to olaparib and trastuzumab had greater DNA damage than cells exposed to each agent alone. Mechanistic exploratory assays showed that trastuzumab downmodulated the homologous recombination protein proliferating cell nuclear antigen (PCNA). Combination treatment in the BT474 xenograft model resulted in enhanced growth inhibition, reduced tumour cell proliferation, and increased DNA damage and apoptosis.\n\nQuestion:\nDoes poly ( ADP-ribose ) polymerase inhibition enhance trastuzumab antitumour activity in HER2 overexpressing breast 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:\nPost-cardiac arrest management has seen significant advances with profound improvements in survival and neurologic outcome. However, early prognostication after return of spontaneous circulation remains most challenging. Biomarkers have evolved as helpful tools in identifying patients who are at increased risk of adverse outcome. While fibroblast growth factor 23 (FGF-23) has recently emerged as a promising predictor of mortality in patients with cardiogenic shock, its role in risk stratification in post-resuscitation management remains unresolved. This study included 90 patients who had been resuscitated and transferred to the ICU of the University Hospital Heidelberg. Survivors and non-survivors were retrospectively analyzed for known prognostic biomarkers as well as FGF-23 serum levels 24h and 72 h post cardiac arrest (CA). FGF-23 levels were significantly elevated in non-survivors compared to survivors. ROC analysis of FGF-23 levels at 24h and 72 h post CA yielded an AUC of 0.759 and 0.726, respectively, for prediction of overall survival after 6 months. FGF-23 levels remained as significant prognosticators after adjusting for age, renal function, and initial cardiac rhythm. FGF-23 levels did not show significant differences in patient outcome after stratification for cardiac origin of CA or left ventricular dysfunction. Furthermore, FGF-23 levels were moderately predictive of poor neurologic outcome in ROC analysis on day 1 and day 3 post CA with an AUC of 0.738 and 0.687, respectively.\n\nQuestion:\nIs fibroblast growth factor 23 ( FGF-23 ) an early predictor of mortality in patients with cardiac arrest?\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:\nCocaine and alcohol are frequently used simultaneously and this combination is associated with enhanced toxicity. We recently showed that active cocaine abusers have a markedly enhanced sensitivity to benzodiazepines. Because both benzodiazepines and alcohol facilitate GABAergic neurotransmission we questioned whether cocaine abusers would also have an enhanced sensitivity to alcohol that could contribute to the toxicity. In this study we compared the effects of alcohol (0.75 g/kg) on regional brain glucose metabolism between cocaine abusers (n = 9) and controls (n = 10) using PET and FDG. Alcohol significantly decreased whole brain metabolism and this effect was greater in controls (26+/-6%) than in abusers (17+/-10%) even though they had equivalent levels of alcohol in plasma. Analysis of the regional measures showed that cocaine abusers had a blunted response to alcohol in limbic regions, cingulate gyrus, medial frontal and orbitofrontal cortices.\n\nQuestion:\nDo cocaine abusers show a blunted response to alcohol intoxication in limbic brain regions?\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:\nStretching is a widely accepted standard-of-care therapy following spinal cord injury (SCI) that has not been systematically studied in animal models. To investigate the influence of a daily stretch-based physical therapy program on locomotor recovery in adult rats with moderate T9 contusive SCI. A randomized treatment and control study of stretching in an animal model of acute SCI. Moderate SCIs were delivered with the NYU Impactor. Daily stretching (30 min/day, 5 days/wk for 8 weeks) was provided by a team of animal handlers. Hindlimb function was assessed using the BBB Open Field Locomotor Scale and kinematically. Passive range-of-motion for each joint was determined weekly using a goniometer. Declines in hindlimb function during overground stepping were observed for the first 4 weeks for stretched animals. BBB scores improved weeks 5 to 10 but remained below the control group. Stretched animals had significant deficits in knee passive range of motion starting at week 4 and for the duration of the study. Kinematic assessment showed decreased joint excursion during stepping that partially recovered beginning at week 5.\n\nQuestion:\nDoes hindlimb stretching alter locomotor function after spinal cord injury in the adult rat?\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:\nTransient receptor potential melastatin 2 (TRPM2) highly expressed in immunocytes is a Ca(2+)-permeable non-selective cation channel activated by oxidative stress. Myocardial ischaemia/reperfusion (I/R) injury is characterized by acute inflammation associated with the augmentation of oxidative stress. We hypothesized that TRPM2 is implicated in the exacerbation of myocardial I/R injury. Wild-type (Trpm2(+/+)) and Trpm2 knockout (Trpm2(-/-)) mice were subjected to ligation of the left main coronary artery followed by reperfusion. Myocardial infarction following I/R, but not ischaemia alone, was reduced more in Trpm2(-/-)mice than in Trpm2(+/+) mice and cardiac contractile functions were also improved in Trpm2(-/-)mice. TRPM2 was highly expressed in the polymorphonuclear leucocytes (PMNs) rather than in the heart. The number of neutrophils and myeloperoxidase (MPO) activity in the reperfused area following ischaemia was lowered in Trpm2(-/-) mice. When Trpm2(+)(/+) or Trpm2(-/-) PMNs were administered to the Trpm2(-/-) heart ex vivo through the perfusate or in vivo by iv injection, Trpm2(+)(/+) PMNs produced enlargement of the infarct size. Following in vitro regional I/R, a pharmacological inhibitor of TRPM2 reduced the infarct size. The combination of H(2)O(2) and leukotriene B(4) (LTB(4)) increased intracellular Ca(2+) concentration and their adhesion to endothelial cells in Trpm2(+)(/+) but not in Trpm2(-/-)PMNs.\n\nQuestion:\nAre neutrophil TRPM2 channels implicated in the exacerbation of myocardial ischaemia/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:\nDense, vision-obscuring calcification on the posterior aspect of silicone intraocular lenses (IOLs) is often not amenable to neodymium:yttrium-aluminum-garnet capsulotomy, and, in prior reports, has required IOL exchange. We report the successful removal of dense calcium deposition on the posterior surface of a three-piece silicone lens using pars plana vitrectomy (PPV). A 23-gauge PPV was performed using the Stellaris(®) vitrectomy system. A light pipe was used to retroilluminate the IOL, and a dense fibrous tissue setting with a low cut-rate and high aspiration rate was able to clear the visual axis of the dystrophic calcification without damaging the IOL optic. Visual acuity improved from 20/100 to 20/25.\n\nQuestion:\nDo treatment of dystrophic calcification on a silicone intraocular lens with pars plana vitrectomy?\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 aim of this study was to investigate if ischemic stroke final infarction volume and location can be used to predict the associated functional outcome using a multi-class support vector machine (SVM). Sixty-eight follow-up MR FLAIR datasets of ischemic stroke patients with known modified Rankin Scale (mRS) functional outcome after 30 days were used. The infarct regions were segmented and used to calculate the percentage of lesioned voxels in the predefined MNI, Harvard-Oxford cortical and subcortical atlas regions as well as using four problem-specific VOIs, which were identified from the database using voxel-based lesion symptom mapping. An overall of 12 SVM classification models for predicting the corresponding mRS score were generated using the lesion overlap values from the different brain region definitions, stroke laterality information, and the optional parameters infarct volume, admission NIHSS, and patient age. Leave-one-out cross validations revealed that including information about the stroke location in terms of lesion overlap measurements led to improved mRS prediction results compared to classification models not utilizing the stroke location information. Furthermore, integration of the optional features led to improved mRS prediction results in all cases tested. The problem-specific brain regions and additional integration of the optional features led to the best mRS predictions with a precise multi-value mRS prediction accuracy of 56%, sliding window multi-value mRS prediction accuracy (mRS±1) of 82%, and binary mRS (0-2 vs. 3-5) prediction accuracy of 85%.\n\nQuestion:\nDoes multiclass Support Vector Machine-Based Lesion Mapping predict Functional Outcome in Ischemic Stroke 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:\nIt is well recognized that the beta-adrenergic receptor-adenylylcyclase system is altered during myocardial ischemia/hypoxia. However, there are no data regarding either regulation of beta-adrenergic receptors, particularly at the mRNA level, or adenylylcyclase activity in isolated cardiac myocytes exposed to chronic hypoxia. In a chronic hypoxia model in which neonatal rat ventricular myocytes were exposed to a 1% O2 environment for 72 hours, we investigated (1) beta 1-mRNA and receptor expression and adenylylcyclase activity and (2) beta 1-mRNA and receptor downregulation and adenylylcyclase desensitization induced by prolonged norepinephrine incubation. We found that hypoxia for 72 hours increased myocardial membrane beta 1-adrenergic receptor density by 44%. This increase was not associated with a corresponding decrease in cytosolic beta 1-adrenergic receptors. RNase protection assays demonstrated that hypoxia increased the steady-state levels of beta 1-mRNA by 109%. Adenylylcyclase activity stimulated by isoproterenol, sodium fluoride, guanyl-5'-imidodiphosphate, and forskolin in hypoxic membranes was not altered compared with normoxic controls. Hypoxia for 72 hours also did not affect norepinephrine-induced beta 1-mRNA and receptor downregulation and adenylylcyclase desensitization in response to isoproterenol, guanyl-5'-imidodiphosphate, or forskolin.\n\nQuestion:\nDoes chronic hypoxia increase beta 1-adrenergic receptor mRNA and density but not signaling in neonatal rat cardiac myocytes?\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:\nCollagen, as a component of the extracellular matrix, has been linked to atherosclerotic plaque formation and stability. Activation of LOX-1, a lectin-like oxidized low-density lipoprotein (LDL) receptor-1, exerts a significant role in collagen formation. We examine the hypothesis that LOX-1 deletion may inhibit collagen accumulation in atherosclerotic arteries in LDL receptor (LDLR) knockout (KO) mice. We generated LOX-1 KO and LOX-1/LDLR double KO mice on a C57BL/6 (wild-type mice) background and fed a 4% cholesterol/10% cocoa butter diet for 18 weeks. Vessel wall collagen accumulation was increased in association with atherogenesis in the LDLR KO mice (P < 0.01 vs. wild-type mice), but much less so in the double KO mice (P < 0.01 vs. LDLR KO mice). Collagen accumulation data were corroborated with pro-collagen I measurements. Expression/activity of osteopontin, fibronectin, and matrix metalloproteinases (MMP-2 and MMP-9) was also increased in the LDLR KO mice (P < 0.01 vs. wild-type mice), but not in the mice with LOX-1 deletion (P < 0.01 vs. LDLR KO mice). The expression of NADPH oxidase (p47(phox), p22(phox), gp91(phox), and Nox-4 subunits) and nitrotyrosine was increased in the LDLR KO mice (P < 0.01 vs. wild-type mice) and not in mice with LOX-1 deletion (P < 0.01 vs. LDLR KO mice). Phosphorylation of Akt-1 and endothelial nitric oxide synthase and expression of haem-oxygenase-1 were found to be reduced in the LDLR KO mice (P < 0.01 vs. wild-type mice), but not in the mice with LOX-1 deletion (P < 0.01 vs. LDLR KO mice).\n\nQuestion:\nDoes lOX-1 deletion decrease collagen accumulation in atherosclerotic plaque in low-density lipoprotein receptor knockout mice fed a high-cholesterol diet?\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:\nBesides the long-leg standing X-ray film focusing on static standing mechanical alignment of the lower extremity, dynamic alignment from full extension to 90° flexion after total knee arthroplasty (TKA) is rarely mentioned. Computer-assisted surgical technology enables surgeons to measure and assess knee behaviour during surgery. This study was designed to analyse the influences of femoral rotation on dynamic alignment of the lower extremity in TKA. Seventy-six consecutive patients with end-stage knee osteoarthritis were enrolled. External rotation osteotomy of the distal femur during TKA was completed according to the pre-operative external rotation angle (ERA), intra-operative transepicondylar axis (TEA) and anteroposterior (AP) line. Passive dynamic alignment of the lower extremity during knee flexion was recorded. The variation trend of hip-knee-ankle (HKA) alignment and the influences of femoral external rotation osteotomy were analysed. Postoperative deviation of HKA alignment from 0° to 90° flexion was associated with the rotational alignment of the femoral component (r = -0.769, p < 0.001). Variation trend of HKA alignment during knee flexion tended to be varus, valgus and neutral according to the selected angle of external rotation osteotomy of the distal femur.\n\nQuestion:\nDoes femoral rotation influence dynamic alignment of the lower extremity in total knee 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:\nAtherosclerosis is a chronic and progressive inflammatory disease of the arteries that is characterized by subendothelial accumulation of lipid-rich macrophages, called foam cells. We sought to identify the molecular details of cross-talk between liver X receptor α (LXRα) and hypoxia-inducible factor 1α (HIF-1α) for the formation of triglyceride-rich foam cells under hypoxic conditions. We first observed that expression of LXRα and its target lipogenic genes was time-dependently induced in human primary macrophages and RAW 264.7 cells under hypoxia. Similarly, TO901317, an activator of LXRα, enhanced the expression level and the transcriptional activity of HIF-1α. Second, we demonstrated that LXRα increased HIF-1α protein stability through a physical interaction between the ligand binding domain of LXRα and the oxygen-dependent degradation domain of HIF-1α. Third, we found that the activation of HIF-1α or LXRα synergistically induced triglyceride accumulation in macrophages. Finally, we showed that LXRα and HIF-1α were codistributed in the macrophages of atherosclerotic lesions of patients.\n\nQuestion:\nDoes positive cross-talk between hypoxia inducible factor-1α and liver X receptor α induce formation of triglyceride-loaded foam 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:\nThe development of Tuber melanosporum mycorrhizal symbiosis is associated with the production of an area devoid of vegetation (commonly referred to by the French word 'brûlé') around the symbiotic plants and where the fruiting bodies of T. melanosporum are usually collected. The extent of the ecological impact of such an area is still being discovered. While the relationship between T. melanosporum and the other fungi present in the brûlé has been assessed, no data are available on the relationship between this fungus and the bacteria inhabiting the brûlé. We used DGGE and DNA microarrays of 16S rRNA gene fragments to compare the bacterial and archaeal communities inside and outside of truffle brûlés. Soil samples were collected in 2008 from four productive T. melanosporum/Quercus pubescens truffle-grounds located in Cahors, France, showing characteristic truffle brûlé. All the samples were analyzed by DGGE and one truffle-ground was analyzed also using phylogenetic microarrays. DGGE profiles showed differences in the bacterial community composition, and the microarrays revealed a few differences in relative richness between the brûlé interior and exterior zones, as well as differences in the relative abundance of several taxa.\n\nQuestion:\nDo truffle brûlés have an impact on the diversity of soil bacterial communities?\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:\nIt has been reported that Th2 cytokines down-regulate antitumor immunity, while activation of Th1 cells promotes such immunity. The aim of this study was to assess changes of host immunity in relation to efficacy in patients with liver cirrhosis (LC) and advanced hepatocellular carcinoma (aHCC) treated by combined intra-arterial chemotherapy (CIAC). Forty-three adult Japanese LC patients who had aHCC received CIAC. Blood samples were collected before and after CIAC. Eleven of the 43 patients showed a partial response (group PR) and 21 patients had stable disease (group SD), but 11 patients showed no response (group PD). There were no significant differences of Th1 or Th2 cells between before and after CIAC in each group. However, groups SD and PD had higher levels of Th2 cells than in group PR before and after CIAC. The percentage of regulatory T (Treg) cells in group PD was significantly increased after CIAC compared with before CIAC, whereas groups PR and SD showed significant decrease after CIAC.\n\nQuestion:\nDoes host Immunity influence the Efficacy of Combined Intra-Arterial Chemotherapy for Advanced Hepatocellular Carcinoma in Liver Cirrhosis 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:\nIncisional hernia repair with prosthetic material is followed by fewer recurrences than primary repair. Polypropylene is the most commonly used prosthetic material but may cause entero- cutaneous fistulas. The aim of this study was to determine whether enterocutaneous fistulas developed after incisional hernia repair with polypropylene mesh and to evaluate clinical outcome after incisional hernia repair. A retrospective analysis of the outcome of incisional hernia repair with polypropylene mesh between 1982 and 1998 was conducted. Follow-up data were obtained from medical records and questionnaires. Polypropylene incisional hernia repair was performed in 136 patients. Median follow-up was 34 months. No enterocutaneous fistulas developed. Wound infection occurred in 6 per cent. Wound sinus formation occurred in two patients. No mesh was removed because of infection and no persisting infection of the mesh occurred.\n\nQuestion:\nIs intraperitoneal polypropylene mesh repair of incisional hernia associated with enterocutaneous fistula?\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:\nTo examine the influence of stimulus motion on measured visual field extent of 3.5- to 30-month-old children and adults. Each subject was tested with LED-hybrid and LED-kinetic perimetry procedures, using a black double-arc perimeter. Targets in both procedures were identical in size, color, luminance, contrast, and flicker rate. However, in the LED-hybrid procedure, peripheral targets were sequentially illuminated from more peripheral to more central locations, whereas in the LED-kinetic procedure, a peripheral target on a black wand was manually moved centrally along the perimeter arm. A subset of subjects was also tested with white sphere kinetic perimetry (WSKP). The LED-kinetic procedure produced larger measured visual field extent than the LED-hybrid procedure in 3.5-, 11-, 17-, and 30-month-olds, but not in 7-month-olds or adults. Data from subjects tested with WSKP indicated that both stimulus motion and discrepancies in scoring methods contributed to the difference reported previously between visual field measurements obtained with WSKP vs. LED-hybrid perimetry.\n\nQuestion:\nDoes stimulus motion increase measured visual field extent in children 3.5 to 30 months of age?\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 authors noted a significant increase in the diagnosis of atypical squamous cells of undetermined significance (ASCUS) in premenopausal women using oral contraceptive pills (OCP) (9%) versus women not on OCP (4%) using ThinPrep Pap smears (P = 0.02). The purpose of this study was to correlate these morphologic changes with human papillomavirus (HPV) DNA detection by in situ hybridization and clinical follow-up. Eighty-four ThinPrep Pap smears diagnosed as ASCUS or ASCUS favor low-grade squamous intraepithelial lesions (LGSIL) in young women receiving OCP were studied by HPV in situ hybridization. This information was correlated with colposcopic follow-up and AutoCyte Pap smear results. The authors also studied 80 ThinPreps from young women with a Pap smear diagnosis of unequivocal LGSIL where there was a corresponding biopsy (positive controls) and 40 ThinPreps diagnosed as within normal limits and that rescreened as such (negative controls). The detection rate of HPV DNA by in situ hybridization was 33% (28 of 84) in ASCUS cases versus 90% (72 of 80) for cases of unequivocal LGSIL. A blinded review of the 29 ASCUS Pap smears performed by AutoCyte showed that 66% (19 of 29) were diagnosed as within normal limits. The majority of the cervical biopsies in the women with ASCUS by ThinPrep Pap smears were negative for dysplasia (29 of 39 [74%]) whereas 71 of 80 biopsies (88%) showed dysplasia in women with Pap smears diagnosed as unequivocal LGSIL. The periodic acid-Schiff (PAS) stain demonstrated that many of the cells with halos in the ThinPrep Pap smears that mimicked LGSIL contained glycogen.\n\nQuestion:\nAre oral contraceptive pills associated with artifacts in ThinPrep Pap smears that mimic low-grade squamous intraepithelial lesions?\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:\nHenoch-Schönlein purpura nephritis (HSPN) is the most serious long-term complication of Henoch-Schönlein purpura and aberrant galactosylation of IgA1 plays a role in its development. However, the precise role of genetic factors contributing to the abnormal IgA1 galactosylation remains unknown. In order to examine the effects of C1GALT1 gene encoding core 1 β1,3-galactosyltransferase, an important role in the β1,3 glycosylation of IgA1, on HSPN susceptibility, we conducted a case-control association genetic study in 269 HSP and 61 HSPN in China. Five tagging SNPs, SNP1(-734 C/T), SNP4(-465A/G), SNP6(-330 G/T), SNP7(-292 C/-), and SNP8(1365 G/A) in C1GALT1 were studied using single-locus and haplotype-based multilocus analysis. Our results demonstrated that 1365 G allele frequency was significantly higher in HSPN patients than in HSP patients without nephritis (0.459 vs 0.331, p = 0.0008, adjusted p' = 0.004) with an odds ratio (OR) = 1.716, 95%CI 1.151-2.560). The GG genotype of 1,365 G/A was significantly different in HSP without nephritis and HSPN (p = 0.008, adjusted p'' = 0.04). We did not observe statistically significant differences in haplotype frequencies between HSPN and HSP patients.\n\nQuestion:\nAre c1GALT1 polymorphisms associated with Henoch-Schönlein purpura nephritis?\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 short (S) allele of the serotonin transporter gene promoter polymorphism (5-HTTLPR) contributes to the risk of alcohol dependence and co-occurring clinical features. We studied the putative link between this allele and relapse. 48 alcohol-dependent male patients were recruited and genotyped for the 5-HTTLPR. Relapse to alcohol drinking was monitored during 3 months after standardized withdrawal. The S allele was significantly associated with relapse (p = 0.008) while no other factor that was measured played a significant role.\n\nQuestion:\nDoes the short allele of the serotonin transporter promoter polymorphism influence relapse in alcohol dependence?\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:\nDuring early HIV-1 infection of CD4 T-lymphocytes, many host protein tyrosine kinases become activated within minutes, including phosphoprotein pp60 (c-Src) and the focal adhesion kinase family member, proline-rich tyrosine kinase 2 (Pyk2). Whether their activation facilitates or impedes infection remains to be determined. c-Src kinase inhibitors (SU6656, PP1, and PP2), adenovectors [wild-type and dominant-negative (DN) c-src] or siRNA (targeting c-src or pyk2) were used to inhibit, compete with or knockdown c-Src in Jurkat C, Jurkat E6-1, Hut 78 or Kit225 T-cell lines. Cells were then infected with HIV-1 luciferase reporter virus expressing VSV-G or HXB2(X4) envelope, and luciferase activity was measured after 2 days. Reverse transcriptase activity and viral cDNA were measured 1 hour after infection, whereas integrated virus was measured 12 hours after infection. Pretreating Jurkat T-cells with SU6656 led to increased VSV-G luciferase activity. In the adenovector experiments, T-cells overexpressing dominant-negative c-Src, but not wild-type c-Src, showed increased luciferase activity after VSV-G infection. siRNA knockdown of c-Src or Pyk2, followed by HXB2 infection in Jurkat T-cells, lead to increased reverse transcriptase activity, viral cDNA, integrated virus, and increased luciferase activity.\n\nQuestion:\nDo c-Src and Pyk2 protein tyrosine kinases play protective roles in early HIV-1 infection of CD4+ T-cell lines?\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:\nChildhood overweight and obesity have increased substantially in the past two decades, raising concerns about their psychosocial and cognitive consequences. We examined the associations between academic performance (AP), cognitive functioning (CF), and increased BMI in a nationally representative sample of children. Participants were 2,519 children aged 8-16 years, who completed a brief neuropsychological battery and measures of height and weight as a part of the Third National Health and Nutrition Examination Survey, a cross-sectional survey conducted between 1988 and 1994. Z-scores were calculated for each neuropsychological test, and poor performance was defined as z-score <2. The association between BMI and AP was not significant after adjusting for parental/familial characteristics. However, the associations between CF remained significant after adjusting for parental/familial characteristic, sports participation, physical activity, hours spent watching TV, psychosocial development, blood pressure, and serum lipid profile. Z-scores on block design (a measure of visuospatial organization and general mental ability) among overweight children and children at risk of overweight were below those of normal-weight children by 0.22 (s.e. = 0.16) and 0.10 (s.e. = 0.10) unit, respectively (P for trend <0.05). The odds of poor performance on block design were 1.97 (95% confidence interval: 1.01-3.83) and 2.80 (1.16-6.75), respectively, among children at risk or overweight compared to normal-weight peers.\n\nQuestion:\nIs overweight associated with decreased cognitive functioning among school-age children and adolescents?\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:\nIntraoperative nerve lesions can lead to chronic postoperative pain. There are conflicting data as to whether or not anaesthetics administered intraoperatively are beneficial. We investigated if remifentanil administered at the time of nerve injury was able to attenuate neuropathic hypersensitivity. Rats were anaesthetized with isoflurane, endotracheally intubated, and a tail vein catheter was inserted. Rats received an i.v. infusion of either saline or low- or high-dose remifentanil (2 or 20 μg kg(-1) min(-1), respectively) for 20 min. During this time, rats received a spinal nerve L5 transection to induce neuropathic pain or a sham procedure. Behavioural tests to assess mechanical and cold allodynia and heat hyperalgesia were performed on postoperative days 1, 3, 7, 14, 21, and 28. Sham-operated animals exhibited no hypersensitivity regardless of the intraoperative remifentanil dose. In rats which received spinal nerve L5 transection, mechanical and cold allodynia developed with no significant differences between treatment groups. However, thermal hyperalgesia was reduced in rats given high-dose remifentanil: mean (standard deviation) area under the curve 426 (53) compared with 363 (34) and 342 (24) in saline or low-dose remifentanil treated rats, respectively (P<0.05).\n\nQuestion:\nDoes high-dose remifentanil prevent development of thermal hyperalgesia in a neuropathic pain 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:\nIron-deficiency anemia is the most common systemic complication of inflammatory bowel diseases (IBD). Iron-deficiency anemia recurs frequently and rapidly after iron-replacement therapy in patients with IBD. We performed a randomized, placebo-controlled trial to determine if administration of ferric carboxymaltose (FCM) prevents anemia in patients with IBD and low levels of serum ferritin. We performed a single-blind, multicenter study of nonanemic patients who had completed the FERGIcor study. Serum levels of ferritin were assessed every second month, and patients were given FCM (total iron dose, 1181 ± 662 mg; n = 105) or placebo (n = 99) when levels decreased to less than 100 μg/L. The primary end point was time to recurrence of anemia within 8 months. Secondary end points included changes of quality of life, disease activity, results from laboratory tests, and adverse events. Anemia recurred in 26.7% of subjects given FCM and in 39.4% given placebo. The time to anemia recurrence was longer in the FCM group (hazard ratio, 0.62; 95% confidence interval, 0.38-1.00; P = .049). Markers of body levels of iron increased or remained at normal levels in subjects given FCM (ferritin increased by 30.3 μg/L, transferrin saturation increased by 0.6%) but decreased in the group given placebo (ferritin decreased by 36.1 μg/L, transferrin saturation decreased by 4.0%). Changes in quality of life and disease activity were comparable between groups. Adverse events were reported in 59.0% of the FCM group and 50.5% of the placebo group, and serious adverse events were reported in 6.7% and 8.1%, respectively.\n\nQuestion:\nDoes ferric carboxymaltose prevent recurrence of anemia in patients with inflammatory bowel 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:\nConventional quality control studies of the shelf life of RBC units do not consider cold chain interruptions that occur during cross-matching or between the release of RBCs from the blood bank and their return from the ward. These interruptions may, however, lead to a considerable loss of quality. On the other hand, differences in the quality of RBCs may derive from the different manufacturing processes employed in various blood centres. One day after the expiry date of the RBC unit, we analysed complete blood count, blood gas, potassium, LDH, hydroxybutyrate dehydrogenase, glucose, lactate, total and free haemoglobin (Hb) and ATP and compared the results with regard to the frequency of storage interruptions and to two manufacturers of these RBCs. We could not find any correlations between the frequency of interruptions (0-11) and these parameters in any of the data sets. However, we found significant differences when comparing the two suppliers. RBCs of manufacturer A ('A', inline filtration of whole blood) contained 25% more Hb than those of manufacturer B ('B', inline filtration after buffy coat reduction). Sixteen percentage of 'A'-RBC, but none of 'B'-RBC, exceeded a haemolysis of 0.8%.\n\nQuestion:\nDoes transitory interruption of recommended storage conditions cause significant changes in in vitro parameters of leucocyte-depleted red blood cells?\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:\nTo investigate whether electroacupuncture (EA) produced analgesic effect and whether nuclear factor kappa B (NF-κB) and cystathionine β synthase (CBS) involved in EA-mediated analgesia in painful diabetic neuropathy in rats. Diabetes was induced by an intraperitoneal injection of streptozotocin (STZ) in adult female rats. Mechanical pain threshold was measured by von Frey filaments. EA was applied at acupoint Zu-San-Li (ST-36) in both hindlimbs. Western blot analysis was employed to detect changes in protein levels of NF-κB and CBS in spinal dorsal root ganglion (DRGs). Mechanical allodynia was developed 2 weeks after STZ injection and lasted for another 4 weeks. STZ injection significantly enhanced expression of p65 and CBS in lumbar L4-6 DRGs when compared with age-matched controls. EA markedly attenuated mechanical allodynia. Importantly, EA treatment remarkably inhibited p65 and CBS expression in DRGs. Additionally, intrathecal injection of the p65 antagonist pyrrolidine dithiocarbamate attenuated mechanical allodynia and markedly inhibited CBS expression in DRGs in STZ rats.\n\nQuestion:\nDoes electroacupuncture suppress mechanical allodynia and nuclear factor κ B signaling in streptozotocin-induced diabetic 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:\nThis study aimed to report falls and identify factors that might predict a fall in women aged between 40 and 80 years and thus provide evidence of earlier falls and need for morbidity preventive intervention. A prospective cohort study design over 5 years. Personal demographic data of age, co-morbidities, number of prescribed medications, falls, activity level and living situation were obtained at face-to-face interview. Height, weight, body mass index and postural stability were measured in participating women living independently in the community. Women were categorized into age decade cohorts, with 463 remaining at the year 5 assessment. At baseline, 8% of the women in their forties, 14% in their fifties, 25% in their sixties and 40% in their seventies had fallen in the previous 12 months. Over the 5-year study period, 21% of women in their forties and fifties, 31% of women in their sixties and 47% in their seventies had fallen. Multiple fallers mostly comprised women in their sixties and seventies. Parametric modeling and the classification tree approach revealed age and number of co-morbidities to be most predictive of a fall. Women < 60 years old had an increased risk of a fall by 8% and women > 60 years an increased risk of a fall by 35% with every additional co-morbidity. Stability and other demographics were not predictive of falling.\n\nQuestion:\nIs falling just for older women : support for pre-emptive prevention intervention before 60?\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:\nA negative relationship between anemia before coronary artery bypass graft (CABG) surgery and the perioperative mortality has been shown. We tried to clarify whether anemia only expresses an increased perioperative risk or is a risk factor per se in a two-institution database. In the years 2005 and 2006, 185 of 3,311 patients undergoing isolated first-time CABG surgery had anemia defined as hematocrit less than 33% or Hb≤11 g/dL. Preoperative and postoperative data of patients having anemia and patients having normal hematocrit were compared using χ2-tests or Fisher's exact tests regarding structural group differences. To determine factors influencing perioperative mortality, methods of logistic regression were used. The 30-day mortality of anemic patients (12.9%) was significantly higher (p<0.001) than the mortality of nonanemic patients (2.2%). Patients having anemia, though, had a worse risk profile before surgery: high European System for Cardiac Operative Risk Evaluation values (median, 7 in anemic patients versus 4 in nonanemic patients), acute myocardial infarction (9.7% in anemic versus 2% in nonanemic patients), diabetes mellitus (45.4% in anemic versus 33.3% in nonanemic patients), and cardiogenic shock (5.4% in anemic versus 0.8% in nonanemic patients) were significantly more frequent in the anemic group. However, taking these risks in account, the logistic regression revealed preoperative anemia still to be a mortality-increasing factor in patients undergoing CABG surgery (odds ratio 3.727, confidence interval: 2.196 to 6.324). Furthermore, anemia was a risk factor for perioperative morbidity (major adverse cardiovascular events) after CABG surgery (odds ratio 2.199, confidence interval: 1.423 to 3.397).\n\nQuestion:\nDoes anemia before coronary artery bypass surgery as additional risk factor increase the perioperative risk?\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:\nGranulocyte colony stimulating factor (G-CSF) is a growth factor essential for generation of neutrophilic granulocytes. Apart from this hematopoietic function, we have recently uncovered potent neuroprotective and regenerative properties of G-CSF in the central nervous system (CNS). The G-CSF receptor and G-CSF itself are expressed in alpha motoneurons, G-CSF protects motoneurons, and improves outcome in the SOD1(G93A) transgenic mouse model for amyotrophic lateral sclerosis (ALS). In vitro, G-CSF acts anti-apoptotically on motoneuronal cells. Due to the pleiotrophic effects of G-CSF and the complexity of the SOD1 transgenic ALS models it was however not possible to clearly distinguish between directly mediated anti-apoptotic and indirectly protective effects on motoneurons. Here we studied whether G-CSF is able to protect motoneurons from purely apoptotic cell death induced by a monocausal paradigm, neonatal sciatic nerve axotomy. We performed sciatic nerve axotomy in neonatal mice overexpressing G-CSF in the CNS and found that G-CSF transgenic mice displayed significantly higher numbers of surviving lumbar motoneurons 4 days following axotomy than their littermate controls. Also, surviving motoneurons in G-CSF overexpressing animals were larger, suggesting additional trophic effects of this growth factor.\n\nQuestion:\nDoes g-CSF protect motoneurons against axotomy-induced apoptotic death in neonatal 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:\nThe authors previously described the complete regression of established neuroblastoma (NB) by the adoptive transfer of syngeneic interleukin-12 transduced dendritic cells (DC) from naive mice. However, some malignancies, like NB, abrogate DC immunostimulation. The authors hypothesize that IL-12 transduction of DC from NB-bearing mice will have the same antitumor properties. A/J mice (n = 32) with established NB received peritumoral injection of 1 x 10(6) DC (DC, IL-12 DC, day 7 IL-12 DC or day 14 IL-12 DC) on day 7. Tumor growth, phenotype, and ability to induce NK and T cell activity were measured. Vaccination with naive admIL-12 DC resulted in 100% tumor regression and prolonged survival. Transduced DC induced only partial responses in 75% (day 7) and 25% (day 14) of animals. No differences in phenotype or effector cell activation were noted between admIL-12DC in tumor-bearing or naive mice.\n\nQuestion:\nDoes advanced neuroblastoma impair dendritic cell function in adoptive immunotherapy?\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:\nTwin studies have shown that age at menarche may be subject to hereditary influences but the specific determinants are unknown. Estrogens are known to have an important role in menarche. Since the enzyme aromatase is responsible for the conversion of androgens to estrogens, the aromatase (CYP19) gene could be a candidate gene for the regulation of menarche. The aim of this study was to investigate the possible association of the CYP19(TTTA)(n) polymorphism with age at menarche. We studied 130 healthy adolescent females from a closed community in North-Western Greece. Information on menarche was obtained through interviews. The BMI was recorded. The CYP19(TTTA)(n) polymorphism was genotyped. The mean age at menarche was 12.9 ± 1.2 years and the BMI = 19.8 ± 2.3 kg/m(2). Genotype analysis revealed 5 CYP19(TTTA)(n) alleles containing 7-11 TTTA repeats. Girls homozygous for the allele with 7 TTTA repeats had earlier menarche (12.45 ± 0.9 years) than girls carrying other genotypes (13.0 ± 1.2 years, P = 0.025), whereas the BMI was not different between these two subgroups. Carriers of the allele with 11 TTTA repeats had later menarche compared with non-carriers (14.1 ± 0.75 versus 12.8 ± 1.2 years, P< 0.001), whereas no difference was found in BMI values. Comparing girls with early menarche (<12 years, 25th percentile) with girls with late menarche (>13.75 years, 75th percentile), we found that 31% of the girls with early menarche were homozygous for the (TTTA)(7) allele compared with 6.9% among girls with late menarche (P = 0.018). In addition, none of the girls carrying the (TTTA)(11) allele was found among the subgroup with early menarche, whereas 24.1% of girls with late menarche had the (TTTA)(11) allele (P = 0.001). No association between other alleles and age at menarche was found.\n\nQuestion:\nIs the ( TTTA ) n polymorphism of aromatase ( CYP19 ) gene associated with age at menarche?\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:\nBIM is essential for the response to tyrosine-kinase inhibitors (TKI) in chronic myeloid leukaemia (CML) patients. Recently, a deletion polymorphism in intron 2 of the BIM gene was demonstrated to confer an intrinsic TKI resistance in Asian patients. The present study aimed at identifying mutations in the BIM sequence that could lead to imatinib resistance independently of BCR-ABL mutations. BIM coding sequence analysis was performed in 72 imatinib-treated CML patients from a French population of our centre and in 29 healthy controls (reference population) as a case-control study. Real-time quantitative PCR (RT qPCR) was performed to assess Bim expression in our reference population. No mutation with amino-acid change was found in the BIM coding sequence. However, we observed a silent single nucleotide polymorphism (SNP) c465C>T (rs724710). A strong statistical link was found between the presence of the T allele and the high Sokal risk group (p = 0.0065). T allele frequency was higher in non responsive patients than in the reference population (p = 0.0049). Similarly, this T allele was associated with the mutation frequency on the tyrosine kinase domain of BCR-ABL (p<0.001) and the presence of the T allele significantly lengthened the time to achieve a major molecular response (MMR). Finally, the presence of the T allele was related to a decreased basal expression of the Bim mRNA in the circulating mononuclear cells of healthy controls.\n\nQuestion:\nIs a single nucleotide polymorphism in cBIM associated with a slower achievement of major molecular response in chronic myeloid leukaemia treated with imatinib?\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 significant prognostic difference exists among metastatic colorectal cancer (CRC) patients despite of any treatments. We identify the specific cytokines related to prognosis of metastatic CRC and assess their prognostic significance. Stage IV CRC patients were divided into two groups according to their prognosis. Difference in serum cytokine level between these groups was determined by the cytokine array. Among the specific cytokines, macrophage inflammatory protein-3 alpha (MIP-3a) was measured using an enzyme-linked immunosorbent assay (ELISA) in the sera of 242 CRC patients. Several cytokines related to prognostic difference in stage IV CRC were identified. The median MIP-3a level (28.2 pg/ml) was used as a cut-off value. Increased MIP-3a was significantly associated with synchronous liver metastases and age. In univariate analysis, high MIP-3a was correlated with poor prognosis (P < 0.001). Multivariate analysis showed that high MIP-3a was an independent prognostic factor in all CRC patients (P < 0.001). In subgroup analysis, high MIP-3a was significantly associated with poor survival in patients with stage II, II/III, and IV CRC, respectively.\n\nQuestion:\nIs macrophage inflammatory protein-3 alpha ( MIP-3a ) a novel serum prognostic marker in patients with colorectal 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:\nWe investigated whether a reduced estimated glomerular filtration rate (eGFR) was associated with cardiovascular disease (CVD) prevalence, independent of the effect of microalbuminuria in patients with diabetes. In a multicentre, large-scale cohort including 3002 Japanese patients with Type 2 diabetes without macroalbuminuria, the relationship of a reduced eGFR and microalbuminuria with CVD was investigated. Of those patients, 4.8% had a reduced eGFR and microalbuminuria, 12.7% had a reduced eGFR without microalbuminuria and 18.7% had microalbuminuria but normal eGFR. A reduced eGFR and microalbuminuria were each associated with a doubling of the prevalence of CVD. Compared with patients with no microalbuminuria/normal eGFR [odds ratio (OR) 1.0], the OR for CVD was significantly higher in those with a reduced eGFR without microalbuminuria (OR 1.97) and similarly higher in those with microalbuminuria without a reduced eGFR (OR 1.85). The OR was highest in those with both a reduced eGFR and microalbuminuria (OR 3.97, 95% confidence interval 2.55-6.20). The OR for CVD remained significant after adjustments for age, sex, hypertension, dyslipidaemia, smoking, body mass index, glycated haemoglobin and the duration of diabetes, and remained significant if the cut-off point for microalbuminuria was set at the median albumin : creatinine ratio (13.7 mg/g creatinine). In patients without microalbuminuria, a reduced eGFR was associated with CVD only in the older and male groups.\n\nQuestion:\nAre reduced GFR and microalbuminuria independently associated with prevalent cardiovascular disease in Type 2 diabetes : JDDM study 16?\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:\nDNA methylation is a heritable covalent modification that is developmentally regulated and is critical in tissue-type definition. Although genotype-phenotype correlations have been described for different subtypes of renal cell carcinoma (RCC), it is unknown if DNA methylation profiles correlate with morphological or ontology based phenotypes. Here, we test the hypothesis that DNA methylation signatures can discriminate between putative precursor cells in the nephron. We performed deep profiling of DNA methylation and transcriptome in diverse histopathological RCC subtypes and validated DNA methylation in an independent dataset as well as in The Cancer Genome Atlas Clear Cell and Chromophobe Renal Cell Carcinoma Datasets. Our data provide the first mapping of methylome epi-signature and indicate that RCC subtypes can be grouped into two major epi-clusters: C1, which encompasses clear-cell RCC, papillary RCC, mucinous and spindle cell carcinomas and translocation RCC; C2, which comprises oncocytoma and chromophobe RCC. Interestingly, C1 epi-cluster displayed 3-fold more hypermethylation as compared with C2 epi-cluster. Of note, differentially methylated regions between C1 and C2 epi-clusters occur in gene bodies and intergenic regions, instead of gene promoters. Transcriptome analysis of C1 epi-cluster suggests a functional convergence on Polycomb targets, whereas C2 epi-cluster displays DNA methylation defects. Furthermore, we find that our epigenetic ontogeny signature is associated with worse outcomes of patients with clear-cell RCC.\n\nQuestion:\nDoes dNA Methylation Signature reveal Cell Ontogeny of Renal Cell Carcinomas?\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 Krd mouse has a deletion in chromosome 19 that includes the Pax2 gene locus. The aim of this study was to characterize in detail how these retinas differ from normal. Both electroretinographic and anatomic methods were used to assess visual function. Full-field flash electroretinograms (ERGs) and planimetric densities were obtained from Krd and control animals. Measurements of the ERG show that in the Krd mice, both a- and b-wave amplitudes are attenuated relative to control by amounts that vary from animal to animal. The b-wave of the ERG generally is affected more severely than the a-wave. However, there is little or no shift of the curves relating the b-wave and a-wave amplitude to the intensity of the stimulus. Also, no change in the response kinetics seems to be associated with the attenuated responses. Estimates of planimetric cell density in the outer nuclear, inner nuclear, and ganglion cell layers show significant cell losses in affected animals that are more pronounced proportionally in the inner layers. Comparisons between electrophysiological and histologic measurements made on each eye show good correlation between the reduction in the ERG components and the magnitude of cell losses.\n\nQuestion:\nDoes electrophysiology and density of retinal neurons in mice with a mutation that include the Pax2 locus?\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 sought to assess whether pharmacological inhibition of hypoxia-inducible transcription factor (HIF)-prolyl hydroxylase enzymes (PHD1, PHD2, and PHD3) is a suitable strategy to stimulate liver regeneration after partial hepatectomy for colorectal liver metastases (CRLM). Liver regeneration occurs in a hypoxic environment. PHD1 to PHD3 are molecular oxygen sensors and increasingly considered as putative therapeutic targets. However, little is known about the effect of pharmacological PHD inhibition on tumor expansion, and on liver regeneration after surgical resection. Various mouse models of liver regeneration after extended partial hepatectomy and portal vein ligation for multiple bilobar CRLM were applied to assess the effect of the small molecule pan-PHD inhibitor ethyl-3,4-dihydroxybenzoate (EDHB) on liver regeneration and metastatic tumor growth. Metabolism and biodistribution of EDHB were analyzed using liquid chromatography coupled to tandem mass spectrometry. EDHB selectively augmented liver regeneration after partial hepatectomy and portal vein ligation, and increased the expression of cell cycle-promoting cyclin proteins, without enhancing metastatic tumor growth. Systemically administered EDHB and its active metabolite 3,4-dihydroxybenzoic acid accumulated in the liver to selectively induce hepatoprotective effects in the liver, but not in tumor tissue, without humoral adverse effects.\n\nQuestion:\nDoes prolyl Hydroxylase Inhibition enhance Liver Regeneration Without Induction of Tumor 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:\nMore than one third of energy intake in Iran is provided from bread. Therefore, improving bread mineral bioavailability through dephytinization can play an important role in decreasing the prevalence of many mineral deficiencies. In this study, effect of phytase supplementation on zinc, iron and calcium status in growing rats fed with a diet containing high phytate Iranian bread (Sangak) was assessed. Thirty weanling Wistar male rats were assigned to phytase (Aspergillus niger) or control group for 6 weeks. The diet was designed based on Iranian's food pattern and 34.2% of the energy was supplied from Sangak bread. Food intake, body and organ weight and body height were measured. Zinc was measured in blood, liver and femur. Iron was assessed in blood and liver and calcium was titrated from femur bone. Statistical analyses were performed using SPSS software. Paired sample t-test, Wilcoxon signed-rank test and repeated measurement ANOVA were used for proper analysis of data. Although weekly weight gain was not different between groups, final weight was in favor of control group. Food intakes, liver and femur bone weight did not differ between the two groups. However, the blood zinc was higher in the phytase group (26.2 ± 7.4 vs. 19.2 ± 5.2, P = 0.03). Thus positive effects of phytase supplementation on zinc, independent of growth was found. Other variables did not show any differences between groups.\n\nQuestion:\nDoes phytase supplementation improve blood zinc in rats fed with high phytate Iranian bread?\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 pathophysiology of heart failure with preserved ejection fraction (HFpEF) is complex but increased left ventricular (LV) diastolic stiffness plays a key role. A load-independent, non-invasive, direct measure of diastolic stiffness is lacking. The diastolic wall strain (DWS) index is based on the linear elastic theory, which predicts that impaired diastolic wall thinning reflects resistance to deformation in diastole and thus, increased diastolic myocardial stiffness. The objectives of this community-based study were to determine the distribution of this novel index in consecutive HFpEF patients and healthy controls, define the relationship between DWS and cardiac structure and function and determine whether increased diastolic stiffness as assessed by DWS is predictive of the outcome in HFpEF. Consecutive HFpEF patients (n = 327, EF ≥ 50%) and controls (n = 528) from the same community were studied. Diastolic wall strain was lower in HFpEF (0.33 ± 0.08) than in controls (0.40 ± 0.07, P < 0.001). Within HFpEF, those with DWS ≤ median (0.33) had higher LV mass index, relative wall thickness, E/e', Doppler-estimated LV end-diastolic pressure to LV end-diastolic volume ratio, left atrial volume index, and brain natriuretic peptide (BNP) levels than those with DWS > median. Heart failure with preserved ejection fraction patients with DWS ≤ median had higher rate of death or HF hospitalization than those with DWS > median (P = 0.003) even after the adjustment for age, gender, log BNP, LV geometry, or log E/e' (P < 0.01).\n\nQuestion:\nIs diastolic stiffness as assessed by diastolic wall strain associated with adverse remodelling and poor outcomes in heart failure with preserved ejection fraction?\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 resistance to activated protein C (aPCR), the most common known inherited thrombophilic disorder, on the risk of intestinal operation of fibrostenosis in patients with Crohn's disease (CD). In a previous study, we assessed the prevalence of aPCR in CD. In a retrospective case-controlled study, 8 of these CD patients with aPCR were now compared with 24 CD patients without aPCR, matched by gender, age at diagnosis and duration of disease in a 1:3 fashion. The primary end point was the occurrence of an intestinal CD-related operation with evidence of fibrostenosis in the bowel resection specimen. The Kaplan-Meier analysis revealed that patients with aPCR had a lower probability of remaining free of operation with fibrostenosis than patients without aPCR (P = 0.0372; exact log-rank test) resulting in a significantly shorter median time interval from diagnosis of CD to the first operation with fibrostenosis (32 vs 160 mo). At 10 years, the likelihood of remaining free of operation with fibrostenosis was 25% for patients with aPCR and 57.8% for patients without aPCR.\n\nQuestion:\nIs resistance to activated protein C a risk factor for fibrostenosis in Crohn '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:\nOur aim was to determine whether sildenafil citrate (Viagra) unfavorably alters coronary perfusion in canine models of coronary artery stenosis. Concern has been raised that sildenafil may exacerbate ischemia in patients with coronary artery disease. However, the effects of sildenafil on coronary perfusion are largely unexplored. Using anesthetized dogs, a micromanometer constrictor was applied to either an intact coronary artery (model of stable hypoperfusion: Protocol 1) or a site of arterial injury (model of recurrent platelet-mediated thrombosis: Protocol 2). After monitoring coronary flow for 1 h, dogs received two escalating, clinically relevant doses of sildenafil or placebo. Perfusion was assessed during the initial hour pretreatment, for 1 h following dose 1 and 1 h following dose 2 by measuring the area of the flow-time profile, normalized to baseline flow x 60 min. Interaction between sildenafil and adenosine-mediated inhibition of platelet aggregation was evaluated by in vitro platelet aggregometry (Protocol 3). In Protocol 1, flow-time area was maintained at 50% to 60% of baseline in both placebo- and sildenafil-treated groups. In Protocol 2, controls exhibited an expected modest, temporal adenosine-mediated improvement in flow-time area (from 40 +/- 5% to 61 +/- 7%; p < .05) while in contrast, perfusion in sildenafil-treated dogs remained unchanged (37 +/- 6% vs. 33% to 35% before vs. after treatment). In vitro aggregometry confirmed that sildenafil rendered platelets refractory to the inhibitory effects of adenosine receptor stimulation.\n\nQuestion:\nDoes sildenafil citrate ( Viagra ) exacerbate myocardial ischemia in canine models of coronary artery stenosis?\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:\nContextual fear memory depends on the hippocampus, but the role of unilateral hippocampus in this type of memory remains unclear. Herein, pharmacological inactivation or excitotoxic lesions were used to study the role of unilateral hippocampus in the stages of contextual fear memory. The pharmacological experiments revealed that compared with the control groups, unilateral hippocampal blockade did not impair 1-day recent memory following learning, whereas bilateral hippocampal blockade significantly impaired this memory. The lesion experiments showed that compared with the control groups, the formed contextual fear memory was retained for 7 days and that 30-day remote memory was markedly reduced in unilateral hippocampal lesion groups.\n\nQuestion:\nDoes unilateral hippocampal inactivation or lesion selectively impair remote contextual fear memory?\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:\nIt is not fully elucidated whether obesity enhances hepatocarcinogenesis in patients with chronic hepatitis C. The aim of this study was to investigate the relationship between body weight and risk of hepatocarcinogenesis in chronic hepatitis C patients. We enrolled 1431 patients with chronic hepatitis C who visited our liver clinic between 1994 and 2004, excluding those with hepatocellular carcinoma (HCC) at their visit or with a previous history of HCC. They were divided into 4 groups according to body mass index (BMI): underweight (< or =18.5 kg/m(2), N = 112); normal (18.5 to less than 25 kg/m(2), N = 1023); overweight (25 to less than 30 kg/m(2), N = 265); and obese (>30 kg/m(2), N = 31). We assessed the impact of obesity on the hepatocarcinogenesis adjusted by multivariate Cox proportional hazard regression with other risk factors found significant in univariate analysis. During the follow-up period (mean, 6.1 y), HCC developed in 340 patients, showing cumulative incidence rates of 10.5%, 19.7%, and 36.8% at 3, 5, and 10 years, respectively. The incidence differed significantly among the BMI groups (P = .007). Adjusting for other significant factors, overweight and obesity were shown to be an independent risk factor of HCC, with a hazard ratio of 1.86 (95% confidence interval, 1.09-3.16; P = .022) and 3.10 (95% confidence interval, 1.41-6.81; P = .005) as compared with the underweight patients.\n\nQuestion:\nIs obesity an independent risk factor for hepatocellular carcinoma development in chronic hepatitis C 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:\nStromal-epithelial interactions play a fundamental role in tissue homeostasis, controlling cell proliferation and differentiation. Not surprisingly, aberrant stromal-epithelial interactions contribute to malignancies. Studies of the cellular and molecular mechanisms underlying these interactions require ex vivo experimental model systems that recapitulate the complexity of human tissue without compromising the differentiation and proliferation potentials of human primary cells. We isolated and characterized human breast epithelial and mesenchymal precursors from reduction mammoplasty tissue and tagged them with lentiviral vectors. We assembled heterotypic co-cultures and compared mesenchymal and epithelial cells to cells in corresponding monocultures by analyzing growth, differentiation potentials, and gene expression profiles. We show that heterotypic culture of non-immortalized human primary breast epithelial and mesenchymal precursors maintains their proliferation and differentiation potentials and constrains their growth. We further describe the gene expression profiles of stromal and epithelial cells in co-cultures and monocultures and show increased expression of the tumor growth factor beta (TGFβ) family member inhibin beta A (INHBA) in mesenchymal cells grown as co-cultures compared with monocultures. Notably, overexpression of INHBA in mesenchymal cells increases colony formation potential of epithelial cells, suggesting that it contributes to the dynamic reciprocity between breast mesenchymal and epithelial cells.\n\nQuestion:\nDo mesenchymal precursor cells maintain the differentiation and proliferation potentials of breast epithelial 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:\nCerebral and flank near-infrared spectroscopy are used to monitor tissue oxygenation during cardiopulmonary bypass in pediatric patients. We sought to validate these noninvasive measurements as predictors of oxygen saturation in the superior and inferior venae cavae during cardiopulmonary bypass. Eight patients underwent elective repair of congenital heart defects with bicaval cannulation. Ultrasonic flow probes and oximetric catheters were placed in the superior and inferior venae cavae limbs of the perfusion circuit. Cerebral and flank near-infrared spectroscopy and 12 additional variables were recorded each minute on cardiopulmonary bypass. Relationships between these variables and superior and inferior venae cavae oxygen saturation were analyzed by linear mixed modeling. The regression of superior vena cava oxygen saturation by current cerebral near-infrared spectroscopy and 1-minute lag cerebral near-infrared spectroscopy, which are equivalent to the regression of the superior vena cava saturation by the current cerebral near-infrared spectroscopy and the 1-minute change in cerebral near-infrared spectroscopy, were used to assess cerebral near-infrared spectroscopy as a trend monitor. The mean number of observation time points per patient was 86 (median 72, range 34-194) for 690 total observations. The root mean square percentage error was 6.39% for the prediction model of superior vena cava saturation by single-factor cerebral near-infrared spectroscopy. The root mean square percentage error was 10.8% for the prediction model of inferior vena cava saturation by single-factor flank near-infrared spectroscopy.\n\nQuestion:\nDoes cerebral near-infrared spectroscopy during cardiopulmonary bypass predict superior vena cava oxygen saturation?\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 the in vitro production of metal-chelating compounds by ectomycorrhizal fungi collected from pine plantations in southern Chile. Scleroderma verrucosum, Suillus luteus and two isolates of Rhizopogon luteolus were grown in solid and liquid modified Melin-Norkans (MMN) media with and without iron addition and the production of iron-chelating compounds was determined by Chrome Azurol S (CAS) assay. The presence of hydroxamate and catecholate-type compounds and organic acids was also investigated in liquid medium. All isolates produced iron-chelating compounds as detected by CAS assay, and catecholates, hydroxamates as well as oxalic, citric and succinic acids were also detected in all fungal cultures. Scleroderma verrucosum produced the greatest amounts of catecholates and hydroxamates whereas the highest amounts of organic acids were detected in S. luteus. Nevertheless, the highest catecholate, hydroxamate and organic acid concentrations did not correlate with the highest CAS reaction which was observed in R. luteolus (Yum isolate).\n\nQuestion:\nDo metal-chelating compounds produced by ectomycorrhizal fungi collected from pine plantations?\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 aim of this study was to evaluate whether sildenafil, used for treatment of erectile dysfunction (ED), affects the exercise tolerance and ischaemic threshold in men with exercise-induced angina not taking nitrates. This was a double-blind placebo-controlled study in men with ED and chronic stable angina, assessing the effect of sildenafil on time to limiting angina during incremental treadmill exercise. Patients remained on their antianginal therapy and received a 100-mg dose of sildenafil or placebo 1h prior to treadmill exercise. Other measurements included times to onset of angina, 1-mm ST-segment depression, and total exercise time. Adjusted treatment differences for the time to limiting angina, time to onset of angina, total exercise time, and time to 1-mm ST-segment depression were (mean+/-SE) 20+/-10s (95% CI, 1-39; P=0.040), 32+/-11s (95% CI, 11-53; P=0.004), 20+/-10s (95% CI, 0-39; P=0.049), and 12+/-17s (95% CI, -21 to 45, P=0.48), respectively, in favour of sildenafil. There were no serious treatment-related adverse events.\n\nQuestion:\nDoes sildenafil citrate reduce exercise tolerance in men with erectile dysfunction and chronic stable angina?\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:\nColorectal cancer (CRC) is highly metastatic. Metastases spread directly into local tissue or invade distant organs via blood and lymphatic vessels, but the role of lymphangiogenesis in CRC progression has not been determined. Lymphangiogenesis is induced via vascular endothelial growth factor C (VEGFC) activation of its receptor, VEGFR3; high levels of VEGFC have been measured in colorectal tumors undergoing lymphangiogenesis and correlated with metastasis. We investigated VEGFC signaling and lymphatic barriers in human tumor tissues and mice with orthotopic colorectal tumors. We performed immunohistochemical, immunoblot, and real-time polymerase chain reaction analyses of colorectal tumor specimens collected from patients; healthy intestinal tissues collected during operations of patients without CRC were used as controls. CT26 CRC cells were injected into the distal posterior rectum of BALB/c-nude mice. Mice were given injections of an antibody against VEGFR3 or an adenovirus encoding human VEGFC before orthotopic tumors and metastases formed. Lymph node, lung, and liver tissues were collected and evaluated by flow cytometry. We measured expression of vascular endothelial cadherin (CDH5) on lymphatic vessels in mice and in human intestinal lymphatic endothelial cells. Levels of podoplanin (a marker of lymphatic vessels), VEGFC, and VEGFR3 were increased in colorectal tumor tissues, compared with controls. Mice that expressed VEGFC from the adenoviral vector had increased lymphatic vessel density and more metastases in lymph nodes, lungs, and livers, compared with control mice. Anti-VEGFR3 antibody reduced numbers of lymphatic vessels in colons and prevented metastasis. Expression of VEGFC compromised the lymphatic endothelial barrier in mice and endothelial cells, reducing expression of CDH5, increasing permeability, and increasing trans-endothelial migration by CRC cells. Opposite effects were observed in mice and cells when VEGFR3 was blocked.\n\nQuestion:\nDoes vascular endothelial growth factor C disrupt the endothelial lymphatic barrier to promote colorectal cancer invasion?\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:\nPeripheral serotonin is involved in tumorigenesis and induces a pro-proliferative effect in hepatocellular carcinoma (HCC) cells; however, the intracellular mechanisms by which serotonin exerts a mitogenic effect remain unclear. In this research, we examined whether FOXO3a, a transcription factor at the interface of crucial cellular processes, plays a role downstream of serotonin in HCC cells. The cell viability and expression of FOXO3a was assessed in three HCC cell lines (Huh7, HepG2 and Hep3B) during serum deprivation in the presence or absence of serotonin. Serum free media significantly inhibited HCC proliferation and led to reduced expression and nuclear accumulation of FOXO3a. Knockdown of FOXO3a enhanced the ability of serum deprivation to inhibit HCC cells proliferation. And overexpression of non-phosphorylated FOXO3a in HCC cells reversed serum-deprivation-induced growth inhibition. Serotonin reversed the serum-deprivation-induced inhibition of cell proliferation and upregulated FOXO3a in Huh7 cells; however, serotonin had no effect on the proliferation of serum-deprived HepG2 or Hep3B cells. In addition to proliferation, serotonin also induced phosphorylation of AKT and FOXO3a in serum-deprived Huh7 cells but not in HepG2 and Hep3B cells. However, the phosphorylation of FOXO3a induced by serotonin did not export FOXO3a from nucleus to cytoplasm in serum-deprived Huh7 cells. Consequently, we demonstrated that serotonin promoted the proliferation of Huh7 cells by increasing the expression of FOXO3a. We also provide preliminary evidence that different expression levels of the 5-HT2B receptor (5-HT2BR) may contribute to the distinct effects of serotonin in different serum-deprived HCC cells.\n\nQuestion:\nDoes serotonin promote the proliferation of serum-deprived hepatocellular carcinoma cells via upregulation of FOXO3a?\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 the fundamental nature of calcium release events (Ca2+ \"sparks\") evoked in rat ventricular myocytes during excitation-contraction (E-C) coupling. High-resolution line-scan confocal imaging with the fluorescent calcium indicator and patch-clamp techniques were used to study the spontaneous Ca2+ sparks and sparks evoked by depolarization. 1) Line scans oriented along the length of the cell showed that both spontaneous sparks and sparks evoked by depolarization to -35 mV appeared to arise at single sites spacing about 1.8 microm apart (ie, the sarcomere length), and measurements of their longitudinal spread (full-width at half-maximal amplitude: FWHM) followed single Gaussian distributions with means of 2.6 microm. 2) Different to this, transverse line scans often revealed spontaneous and evoked sparks that appeared to arise near-synchronously from paired sites. Measurements of transverse FWHM of both spontaneous and evoked sparks showed bimodal distributions, which were fit well by the sums of two Gaussian curves with means of 1.8 and 2.9 microm for spontaneous sparks and with means of 1.9 and 3.1 microm for evoked sparks. Relative areas under the two Gaussian curves were 1.73:1 and 1.85:1, respectively, for spontaneous and evoked sparks.\n\nQuestion:\nDoes ca2+ sparks evoke by depolarization of rat ventricular myocytes involve multiple release sites?\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:\nHypoactive sexual desire disorder (HSDD) is one of the most common sexual problems reported by women, but few studies have been conducted to evaluate treatments for this condition. The objective of this study was to evaluate the efficacy and safety of a testosterone patch in surgically menopausal women with HSDD. The design was a randomized, double-blind, parallel-group, placebo-controlled, 24-wk study (the Intimate SM 1 study). The study was performed at private or institutional practices. The subjects studied were women, aged 26-70 yr, with HSDD after bilateral salpingo-oophorectomy who were receiving concomitant estrogen therapy. Placebo (n = 279) or testosterone 300 microg/d (n = 283) was administered. There were 19 patients who withdrew due to adverse events in the placebo group and 24 in the 300 mug/d testosterone group. Testosterone (300 microg/d) or placebo patches were applied twice weekly. The primary end point was the change in the frequency of total satisfying sexual activity at 24 wk. Secondary end points included other sexual functioning end points and safety assessments. At 24 wk, there was an increase from baseline in the frequency of total satisfying sexual activity of 2.10 episodes/4 wk in the testosterone group, which was significantly greater than the change of 0.98 episodes/4 wk in the placebo group (P = 0.0003). The testosterone group also experienced statistically significant improvements in sexual desire and a decrease in distress. The overall safety profile was similar in both treatment groups.\n\nQuestion:\nDoes testosterone patch increase sexual activity and desire in surgically menopausal women with hypoactive sexual desire 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:\nPancreatic cancer is the fourth leading cause of cancer death in the U.S. Highly infectious Newcastle disease virus (NDV) strains are known to be very cytotoxic for an array of human tumor cell types in vitro and in vivo but the effects of these and avirulent NDV strains on pancreatic neoplasms are little known. Here, the direct cytolytic effects of the avirulent Hitchner-B1 (B1) and Ulster (U) NDV strains on 7 human pancreatic tumor cell lines and 4 normal human cell lines were studied. Cytotoxicity assays used serially diluted NDV to determine minimum cytotoxic plaque forming unit (PFU) doses. For NDV-B1, normal human cells were killed only by relatively high doses (range: 471-3,724 PFU) whereas NDV-U killed these cells at low PFU (range: 0.32-1.60 PFU). Most pancreatic cancer cell types were killed by much lower NDV-B1 doses (range: 0.40-2.60 PFU) while NDV-U killed Capan-1 and SU.86.86 cultures at very low doses (0.00041 PFU and 0.0034 PFU, respectively).\n\nQuestion:\nAre two avirulent , lentogenic strains of Newcastle disease virus cytotoxic for some human pancreatic tumor lines 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:\nBehçet's disease is associated with an increased risk of thrombosis, although the prothrombotic mechanisms are unclear. Alterations in blood rheology, particularly increased erythrocyte aggregation, might play a role in the development of such thrombotic events. We measured plasma lipids, fibrinogen, haematocrit, erythrocite aggregation, erythrocyte deformability, blood viscosity, plasma viscosity and erythrocyte indexes in patients with a nonactive disease at sampling, and in a well-matched control group. The patient group comprised 42 patients with BD (21 male, 21 female aged 43+/-12 years) and the control group comprised 46 healthy volunteers (23 male, 23 female aged 45+/-13 years). Twelve of the 42 patients with BD had a previous documented history of deep vein thrombosis at least 6 months before entering the study, and the other 30 did not. Compared with controls, patients showed statistically higher fibrinogen concentrations (P=0.001), plasma viscosity (P=0.002), blood viscosity (P=0.006) and erythrocyte aggregation, both at stasis (P=0.001) and at a low shear rate (P=0.002): the other rheological parameters were not statistically significant. No differences were observed in the rheological parameters when patients with and without previous thrombotic episodes were compared.\n\nQuestion:\nAre haemorheological alterations in Behçet 's disease related to a tendency for venous thrombosis?\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:\nHypoxia in the portal vein may compromise the survival of intraportally transplanted pancreatic islets. We therefore examined the effect of inspired oxygen on the outcome of islet transplantation. Blood glucose concentrations, glucose tolerance, and the size and number of surviving islets were measured in diabetic rats housed for 48 hr under hyperoxic (100% O(2)), hypoxic (11% O(2)), or normoxic (21%O(2)) conditions after intraportal transplantation of 350, 500, 700, or 1,000 syngeneic islets. In normoxic diabetic rats, the smallest graft size to consistently restore normoglycemia was 1,000 islets. A graft size of 700 islets was effective in only three of nine animals, whereas 500 islets were ineffective in all eight animals undergoing transplantation. In contrast, in hyperoxically housed rats, graft sizes of 700 or 500 islets restored normoglycemia in eight of nine or five of eight animals, respectively. In those animals that became normoglycemic, the glucose tolerance of the hyperoxically treated rats receiving 700 islets was almost identical to that of normoxically housed animals receiving 1,000 islets. The average size of the islets 6 weeks after transplantation was the same in livers of hyperoxic and control rats. However, the total islet area and number of islets engrafted in hyperoxic rats was significantly increased when compared with livers from normoxic animals receiving the same graft size, so the area in hyperoxic rats receiving 700 islets was not significantly different from normoxic recipients of 1,000 islets.\n\nQuestion:\nDoes hyperoxia improve the survival of intraportally transplanted syngeneic pancreatic islets?\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 serum levels of calprotectin (S100A8/S100A9) and S100A12 as markers of disease activity or distinct clinical or radiographic features in patients with psoriatic arthritis (PsA). Serum levels of calprotectin and S100A12, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) were determined in 119 patients with PsA. Correlations to clinical variables were calculated, and subgroups of patients were compared. The correlations to clinical disease activity measures were stronger for CRP than for ESR and calprotectin. In the regression analysis, calprotectin was identified as an independently associated factor for presence of peripheral radiographic features of arthritis (OR 1.33, 95% CI 1.01-1.76). S100A12 levels were also elevated in those with peripheral radiographic features (p = 0.036), but did not correlate with clinical variables of disease activity.\n\nQuestion:\nAre s100 proteins calprotectin and S100A12 related to radiographic changes rather than disease activity in psoriatic arthritis with low disease activity?\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:\nComputed tomography (CT) substitute images can be generated from ultrashort echo time (UTE) MRI sequences with radial k-space sampling. These CT substitutes can be used as ordinary CT images for PET attenuation correction and radiotherapy dose calculations. Parallel imaging allows faster acquisition of magnetic resonance (MR) images by exploiting differences in receiver coil element sensitivities. This study investigates whether non-Cartesian parallel imaging reconstruction can be used to improve CT substitutes generated from shorter examination times. The authors used gridding as well as two non-Cartesian parallel imaging reconstruction methods, SPIRiT and CG-SENSE, to reconstruct radial UTE and gradient echo (GE) data into images of the head for 23 patients. For each patient, images were reconstructed from the full dataset and from a number of subsampled datasets. The subsampled datasets simulated shorter acquisition times by containing fewer radial k-space spokes (1000, 2000, 3000, 5000, and 10,000 spokes) than the full dataset (30,000 spokes). For each combination of patient, reconstruction method, and number of spokes, the reconstructed UTE and GE images were used to generate a CT substitute. Each CT substitute image was compared to a real CT image of the same patient. The mean absolute deviation between the CT number in CT substitute and CT decreased when using SPIRiT as compared to gridding reconstruction. However, the reduction was small and the CT substitute algorithm was insensitive to moderate subsampling (≥ 5000 spokes) regardless of reconstruction method. For more severe subsampling (≤ 3000 spokes), corresponding to acquisition times less than a minute long, the CT substitute quality was deteriorated for all reconstruction methods but SPIRiT gave a reduction in the mean absolute deviation of down to 25 Hounsfield units compared to gridding.\n\nQuestion:\nDoes cT substitute derived from MR images reconstructed with parallel imaging?\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 evaluated whether ultrasound improves myocardial tissue perfusion in 14 animals with coronary artery occlusion. A recent study demonstrated that low-frequency ultrasound improves tissue perfusion in the rabbit ischemic limb, but there are no data on ultrasound enhancement of myocardial perfusion. Fourteen animals (9 dogs, 5 pigs) underwent thoracotomy and occlusion of a diagonal branch of the left anterior descending coronary artery. Myocardial tissue perfusion units (TPUs) and pH were measured before coronary occlusion, after occlusion, and after direct exposure of the ischemic myocardium in the presence of fixed occlusion to low-frequency ultrasound (27 kHz). The TPU decreased from 100.9 +/- 13 at baseline to 71.1 +/- 13 (p < 0.01) after 60 min occlusion but rose by 19.7% to 85.1 +/- 8 (p < 0.01) after ultrasound exposure for 60 min. After 60-min coronary occlusion, myocardial pH fell from 7.43 +/- 14 to 7.05 +/- 0.15 (p < 0.01) but then improved to normal (7.46 +/- 0.32) after ultrasound for 60 min. Administration of L-Nomega-nitro-arginine methyl esther (L-NAME), an inhibitor of nitric oxide synthase, before ultrasound exposure, blocked improvement in myocardial tissue perfusion and pH by ultrasound. Quantitative histomorphology showed a significant increase in the capillary area of myocardium exposed to ultrasound versus non-exposed myocardium (16.2 +/- 7.9 vs. 8.2 +/- 2.1, p < 0.02).\n\nQuestion:\nDoes ultrasound energy improve myocardial perfusion in the presence of coronary occlusion?\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 mechanisms involved in cardiac cachexia remain poorly understood. We examined the association of right ventricular (RV) and hepatic dysfunction with cardiac cachexia. We prospectively enrolled 118 patients with left ventricular ejection fraction (LVEF) ≤40%, which were subgrouped as follows: New York Heart Association (NYHA) class II (n=59), NYHA class III without cachexia (n=41) and NYHA class III with cachexia (n=18). All patients underwent blood collection, echocardiography and exercise testing. Reduced systolic RV function (tricuspid annular plane systolic excursion [TAPSE] ≤15 mm), was present in 80% of cachectic patients. When comparing NYHA class II patients vs. non-cachectic and cachectic NYHA class III patients we found a stepwise decrease in systolic RV function (TAPSE 19 [16-23] vs. 16 [13-19] vs. 14 [9-15] mm, respectively; p<0.001) and an increase in right atrial pressure (RAP; >10 mm Hg: 6.8 vs. 27.5 vs. 75.0%, respectively; p<0.001), indicating a higher degree of congestive right HF in cardiac cachexia. Systolic and diastolic function of the left ventricle did not differ between non-cachectic and cachectic patients in NYHA class III. Serum alkaline phosphatase and direct bilirubin correlated with TAPSE and RAP, and were highest in cachectic patients (all p ≤ 0.002), suggesting cholestatic dysfunction due to liver congestion. In multivariable regression analysis, RV dysfunction, cholestatic liver parameters and albumin were independently associated with the presence of cardiac cachexia.\n\nQuestion:\nIs cardiac cachexia associated with right ventricular failure and liver 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:\nTo determine whether alpha 1 adrenergic receptor mediated myocyte contractility and growth are depressed acutely after non-occlusive coronary artery narrowing, the left coronary artery was constricted in rats and mechanical behaviour, cytosolic calcium, and regulation of alpha 1 adrenergic receptors were examined in myocytes seven days later. Coronary artery stenosis was surgically induced in rats and following the estimation of global cardiac performance myocytes were enzymatically dissociated and radioligand binding studies were performed. In addition, the isotonic contractile performance, cytosolic calcium transients and noradrenaline stimulated inositol phosphate generation in myocytes were measured in the presence of WB 4101 or after chlorethylclonidine treatment. Estimations of cell mechanics in vitro established that peak shortening was decreased by 36% and 18% in left and right ventricular myocytes of coronary stenosed rats. Time to peak shortening was prolonged by 29% in left and 20% in right myocytes, whereas velocity of shortening was decreased by 27% in left myocytes. These alterations were associated with increases in cell length and width, indicative of myocyte hypertrophy. In addition, coronary stenosis was accompanied by reductions in the expression of alpha 1a and alpha 1b receptor subtypes in myocytes. alpha 1 Adrenergic receptor density and noradrenaline stimulated phosphoinositol turnover were decreased by 30% and 34% in left myocytes. alpha 1a Adrenergic receptor subtype mediated cytosolic calcium concentration and myocyte mechanical performance were also impaired in left myocytes only. The alpha 1a adrenergic receptor subtype antagonist WB 4101 abolished noradrenaline stimulated inositol phosphate generation in myocytes, whereas chlorethylclonidine at large doses only partially inhibited this response.\n\nQuestion:\nDoes coronary artery constriction in rats affect the activation of alpha 1 adrenergic receptors in cardiac myocytes?\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 tuberization mechanism of sweet potato (Ipomoea batatas) has long been studied using various approaches. Morphological data have revealed that the tuberizing events result from the activation of the cambium, followed by cell proliferation. However, uncertainties still remain regarding the regulators participating in this signal-transduction pathway. An attempt was made to characterize the role of one MADS-box transcription factor, which was preferentially expressed in sweet potato roots at the early tuberization stage. A differential expression level of IbMADS1 (Ipomoea batatas MADS-box 1) was detected temporally and spatially in sweet potato tissues. IbMADS1 responses to tuberization-related hormones were assessed. In order to identify the evolutionary significance, the expression pattern of IbMADS1 was surveyed in two tuber-deficient Ipomoea relatives, I. leucantha and I. trifida, and compared with sweet potato. In functional analyses, potato (Solanum tuberosum) was employed as a heterologous model. The resulting tuber morphogenesis was examined anatomically in order to address the physiological function of IbMADS1, which should act similarly in sweet potato. IbMADS1 was preferentially expressed as tuberous root development proceeded. Its expression was inducible by tuberization-related hormones, such as jasmonic acid and cytokinins. In situ hybridization data showed that IbMADS1 transcripts were specifically distributed around immature meristematic cells within the stele and lateral root primordia. Inter-species examination indicated that IbMADS1 expression was relatively active in sweet potato roots, but undetectable in tuber-deficient Ipomoea species. IbMADS1-transformed potatoes exhibited tuber morphogenesis in the fibrous roots. The partial swellings along fibrous roots were mainly due to anomalous proliferation and differentiation in the xylem.\n\nQuestion:\nIs ibMADS1 ( Ipomoea batatas MADS-box 1 gene ) involved in tuberous root initiation in sweet potato ( Ipomoea batatas )?\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:\nNear-infrared spectroscopy combined with a vascular occlusion test (VOT) could indicate an impairment of microvascular reactivity (MVR) in septic patients by detecting changes in dynamic variables of muscle O2 saturation (StO2). However, in the perioperative context the consequences of surgical trauma on dynamic variables of muscle StO2 as indicators of MVR are still unknown. This study is a sub-analysis of a randomised controlled trial in patients with metastatic primary ovarian cancer undergoing debulking surgery, during which a goal-directed haemodynamic algorithm was applied using oesophageal Doppler. During a 3 min VOT, near-infrared spectroscopy was used to assess dynamic variables arising from changes in muscle StO2. At the beginning of surgery, values of desaturation and recovery slope were comparable to values obtained in healthy volunteers. During the course of surgery, both desaturation and recovery slope showed a gradual decrease. Concomitantly, the study population underwent a transition to a surgically induced systemic inflammatory response state shown by a gradual increase in norepinephrine administration, heart rate, and Interleukin-6, with a peak immediately after the end of surgery. Higher rates of norepinephrine and a higher heart rate were related to a faster decline in StO2 during vascular occlusion.\n\nQuestion:\nIs dynamic muscle O2 saturation response impaired during major non-cardiac surgery despite goal-directed haemodynamic 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:\nCharacteristics of surgeons and their hospitals have been associated with cancer treatments and outcomes. However, little is known about factors that are associated with referral pathways. We analyzed tumor registry and survey data from women with breast cancer diagnosed in 2002 and reported to the Detroit and Los Angeles Surveillance, Epidemiology, and End Results registries (n = 1,844; response rate, 77.4%) and their attending surgeons (n = 365; response rate 80.0%). About half of the patients (54.3%) reported that they were referred to the surgeon by another provider or health plan; 20.3% reported that they selected the surgeon; and 21.9% reported that they both were referred and were involved in selecting the surgeon. Patients who selected the surgeon based on reputation were more likely to have received treatment from a high-volume surgeon (adjusted odds ratio [OR], 2.2; 95% CI, 1.5 to 3.4) and more likely to have been treated in an American College of Surgeons-approved cancer program or a National Cancer Institute (NCI) -designated cancer center (adjusted OR, 2.0; 95% CI, 1.3 to 3.1; adjusted OR, 3.4; 95% CI, 1.9 to 6.2, respectively). Patients who were referred to the surgeon were less likely to be treated in an NCI-designated cancer center (adjusted OR, 0.5; 95% CI, 0.3 to 0.9).\n\nQuestion:\nDoes patterns and correlate of patient referral to surgeons for treatment of breast 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:\nAutoimmune hepatitis (AIH) is historically classified into type 1 and type 2 on the basis of the autoantibody profile, anti-nuclear and/or anti-smooth muscle antibodies being the serological markers of type 1 AIH, whereas anti-liver/kidney microsomal antibody type 1 and/or anti-liver cytosol antibody type 1 characterise type 2 AIH. To evaluate whether such a distinction is justified on the basis of different expression of the disease in adults. Twenty-six adult patients with type 2 AIH and 52 age- and sex-matched patients with type 1 AIH, representative of the entire cohort of adults with type 1 AIH, were compared at onset and during follow-up. At diagnosis, median age was 26 years (range 17-53), female sex 86%, acute presentation 43%, severe liver histology 54%, cirrhosis 14%, complete response to treatment 52%, progression of the disease 17%, and median disease duration 72 months (range 12-280). HLA-DRB1*0301 was present in 26%, HLA-DRB1*0401 in 23% and HLA-DRB1*0701 in 25%. Clinical presentation, biochemical parameters, severe liver histology, genetic profile, response rate and progression of the disease were identical between type 1 and type 2 AIH.\n\nQuestion:\nDo type 1 and type 2 autoimmune hepatitis in adults share the same clinical phenotype?\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:\nHIV-1 reverse transcriptase (RT) is a heterodimer composed of p66 and p51 subunits and is responsible for reverse transcription of the viral RNA genome into DNA. RT can be post-translationally modified in vitro which may be an important mechanism for regulating RT activity. Here we report detection of different p66 and p51 RT isoforms by 2D gel electrophoresis in virions and infected cells. Major isoforms of the p66 and p51 RT subunits were observed, with pI's of 8.44 and 8.31 respectively (p66(8.44) and p51(8.31)). The same major isoforms were present in virions, virus-infected cell lysates and intracellular reverse transcription complexes (RTCs), and their presence in RTCs suggested that these are likely to be the forms that function in reverse transcription. Several minor RT isoforms were also observed. The observed pIs of the RT isoforms differed from the pI of theoretical unmodified RT (p66(8.53) and p51(8.60)), suggesting that most of the RT protein in virions and cells is post-translationally modified. The modifications of p66(8.44) and p51(8.31) differed from each other indicating selective modification of the different RT subunits. The susceptibility of RT isoforms to phosphatase treatment suggested that some of these modifications were due to phosphorylation. Dephosphorylation, however, had no effect on in vitro RT activity associated with virions, infected cells or RTCs suggesting that the phospho-isoforms do not make a major contribution to RT activity in an in vitro assay.\n\nQuestion:\nDoes human immunodeficiency virus type-1 reverse transcriptase exist as post-translationally modified forms in virions and 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:\nIt has been hypothesized that people with subjective hypersensitivity to chemicals may indeed suffer from neuronal damage due to widely distributed environmental toxins and that such deficits of diagnostic importance can be demonstrated with the help of functional neuroimaging even in single cases. In this study, a small group of well-characterized patients with idiopathic environmental intolerance were examined in order to identify such changes. Twelve patients with idiopathic environmental intolerance were investigated neuropsychologically and underwent cerebral F-18 fluorodeoxyglucose (F-18 FDG) positron emission tomography (PET). The imaging results were compared with findings from 17 healthy controls. Six patients showed deficits in verbal learning and memory, three of them also had a reduced information processing speed. In the individual analyses, 11 patients showed normal cerebral glucose metabolism. In the group analysis of the patients, no areas with significantly reduced glucose metabolism could be found.\n\nQuestion:\nDoes neuropsychological and positron emission tomography correlate in idiopathic environmental intolerances?\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 investigated the correlation between the connective tissue graft size and the percentage of root coverage. Fifteen patients with Miller Class I or II recession defects (one tooth/defect per patient) were treated using an envelope connective tissue graft procedure. Clinical parameters including gingival recession depth (RD), clinical attachment level (CAL), keratinized tissue width (KW), and the probing depth (PD) were measured. Visible denuded area (VDA) and graft tissue area (GTA) were indirectly measured in mm2 using computer software. Graft tissue thickness (GTT) and graft tissue width (GTW) were also measured. All clinical parameters and VDA were recorded at baseline and 3 and 6 months. The RD, CAL, KW, PD, and VDA were evaluated by Friedman test. The correlation between the percentage of root coverage (PRC) and factors related to graft size were determined by Spearman rank correlation and nonparametric regression analysis. The percent of root coverage at 3 and 6 months postoperatively was statistically significantly associated with the GTA:VDA ratio (P<0.01); it did not correlate with GTA, GTT, or RD, and was inconsistently correlated to GTW and VDA. In patients who had 100% root coverage, the GTA:VDA ratio ranged between 10.92:1 and 21.95:1; in patients with <100% root coverage, the ratio was between 4.54:1 and 11.06:1.\n\nQuestion:\nDoes relative connective tissue graft size affect root coverage treatment outcome in the envelope procedure?\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 have developed a new method for chemically measuring blood low-density-lipoprotein (LDL) cholesterol. In the present study, we simulated guidelines of the National Cholesterol Education Program (NCEP) using our LDL cholesterol measurements. Blood samples were collected from 1,069 individuals (519 males, 550 females) who were referred to our laboratory at Niigata University Hospital for lipoprotein analysis. LDL cholesterol levels were determined according to our assay protocol, which has been published previously. Subjects were categorized by NCEP guidelines and identified \"false positives\" and \"false negatives\" on the basis of LDL cholesterol levels measured by our method. The sensitivity of the NCEP guidelines is 87.5% and the specificity is 87.1%, provided we assume that every individual has fewer than two risk factors for coronary heart disease. If we assume that every individual has two or more risk factors, the sensitivity and specificity of the guidelines are 99 and 56.8%, respectively.\n\nQuestion:\nIs direct measurement of low-density-lipoprotein cholesterol more effective than total cholesterol for the purpose of lipoprotein screening?\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 implant survival rates after total hip arthroplasty with Exeter matte or polished stems and to determine the relationship of synovitis/joint effusion to signs of implant loosening and stem type. The first part of the study included retrospective revision rate analysis of 118 primary hip replacements performed during 1991-1995. Two different designs of Exeter stems were used: matte surface stems during 1991-1995 (matte surface group--47 cases), and polished stems during 1992-1995 (polished stem group--71 cases). During the second part of the study, 24 patients (11 in polished stem group and 13 in matte stem group) were prospectively examined with radiography and sonography. Sonography was performed in order to evaluate capsular distension, i.e. the distance between prosthetic femoral neck and anterior capsule. Capsular distension depends on synovitis and/or synovia in prosthetic hip. The relationship between capsular distension, stem type, and radiographic signs of loosening was assessed. For the first part of our study, total implant survival was 78% with matte stems and 61% with polished stems 13 years postoperatively (P=0.27). Stem survival was 82% for matte stems, and 88% for polished stems (P=0.54). In the second part of study, a significant relationship between increased capsular distension and cup loosening was determined (P=0.04). We did not find significant difference in capsular distension when compared matte and polished stems.\n\nQuestion:\nDoes exeter total hip arthroplasty with matte or polished stem?\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:\nBayesian random-effects meta-analyses require the analyst to specify the prior distribution for between-study variance of the treatment effect. We assessed the sensitivity of prediction and other outputs of the meta-analysis to the choice of this prior. We reanalyzed 7 published meta-analyses (5-14 trials) with rare (event rates <5%), moderate (15%-50%), and frequent binary outcomes (>50%). We examined 10 noninformative priors: inverse gamma on between-study variance (τ (2)), 2 uniforms on each of the between-study standard deviation (τ) and τ (2), uniform shrinkage on τ (2), DuMouchel shrinkage on τ, half-normal on τ (2), and half-normal priors on τ with large and small variances. For each analysis, we calculated the posterior distributions for τ, the population treatment effect in current studies, and the predicted treatment effect in a future study. We assessed goodness of fit using total residual deviance, the deviance information criterion, and predictive deviance (by cross-validations). According to total residual deviance, the best-fitting priors were uniform on τ (2). According to predictive deviance, half-normal on τ (2) and the shrinkage priors were optimal. Across analyses with the 10 priors, there were no important differences in the posteriors for the population treatment effect, but there were substantial differences in the posteriors for τ and predictions. The priors that fitted best according to predictive deviance resulted in less uncertainty around predictions of future treatment effect.\n\nQuestion:\nDoes the choice of a noninformative prior on between-study variance strongly affect predictions of future treatment effect?\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:\nSmoking has been associated with low serum levels of adiponectin, an adipocytokine with insulin-sensitizing, anti-inflammatory and anti-atherogenic properties. The objective of this study was to assess the early effect on adiponectin levels of smoking cessation supported by bupropion. Apparently healthy smokers of both sexes with no additional cardiovascular risk factors were administered 150mg sustained-release bupropion twice daily for 9 weeks. Quitters constituted the active group and non-quitters the control group. Sandwich enzyme-linked immunosorbent assays were employed for the measurement of serum adiponectin and cotinine, the latter used for validation of self-reported abstinence. Among the 106 participants (mean age 44.5+/-11.3 years, 57 females, Brinkman index 512.2+/-98.4, basal adiponectin 7.2+/-1.5mg/L), 45 (42.5%) had quitted smoking at week 9. Quitters' post-cessation adiponectin levels were significantly increased (mean difference with baseline 1.9+/-0.8mg/L, 95% CI 1.2, 2.3; p<0.001), while non-quitters' adiponectin remained unaltered. A multiple regression model including female gender (standardized beta coefficient=0.480, p=0.002), age (0.355, p=0.003), body mass index (BMI) (-0.308, p=0.005), waist circumference (-0.276, p=0.008), smoking status (-0.255, p=0.010), and cotinine levels (-0.233, p=0.021) explained about two thirds of the variation in adiponectin levels (adjusted R(2)=0.656).\n\nQuestion:\nDoes smoking cessation increase serum adiponectin levels in an apparently healthy Greek population?\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:\nCardiovascular disease (CVD) is increasing in HIV-infected patients. N-terminal pro-B-type natriuretic peptide (NT-proBNP) is a significant predictor of CVD in the general population. We aimed to quantify the risk of CVD events associated with NT-proBNP at baseline in the Strategies for Management of Anti-Retroviral Therapy study. In a nested case-control study, NT-proBNP was measured at baseline in 186 patients who experienced a CVD event over an average of 2.8 years of follow-up and in 329 matched controls. Odds ratios (ORs) associated with baseline levels of NT-proBNP for CVD were estimated using conditional logistic regression. At baseline median NT-proBNP [interquartile range (IQR)] was 48.1 (18.5, 112.9) pg/ml in patients who developed a CVD event and 25.7 (12.4, 50.2) pg/ml in controls. The unadjusted OR for the highest versus the lowest quartile was 3.7 [95% confidence interval (CI) 2.1-6.5, P < 0.0001]. After adjustment for baseline covariates and CVD risk factors, OR was 2.8 (95% CI 1.4-5.6, P = 0.003); with additional adjustment for IL-6, high-sensitivity C-reactive protein and D-dimer, OR was 2.3 (95% CI 1.1-4.9, P = 0.02).\n\nQuestion:\nDoes n-terminal-proB-type natriuretic peptide predict cardiovascular disease events in HIV-infected 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:\nUrotensin (U)-II receptor (UTR) has been previously reported to be over-expressed in a number of tumours. Whether UTR-related pathway plays a role in colon carcinogenesis is unknown. We evaluated UTR protein and mRNA expression in human epithelial colon cancer cell lines and in normal colon tissue, adenomatous polyps and colon cancer. U-II protein expression was assessed in cancer cell lines. Moreover, we evaluated the effects of U-II(4-11) (an UTR agonist), antagonists and knockdown of UTR protein expression through a specific shRNA, on proliferation, invasion and motility of human colon cancer cells. Cancer cell lines expressed U-II protein and UTR protein and mRNA. By immunohistochemistry, UTR was expressed in 5-30% of epithelial cells in 45 normal controls, in 30-48% in 21 adenomatous polyps and in 65-90% in 48 colon adenocarcinomas. UTR mRNA expression was increased by threefold in adenomatous polyps and eightfold in colon cancer, compared with normal colon. U-II(4-11) induced a 20-40% increase in cell growth while the blockade of the receptor with specific antagonists caused growth inhibition of 20-40%. Moreover, the knock down of UTR with a shRNA or the inhibition of UTR with the antagonist urantide induced an approximately 50% inhibition of both motility and invasion.\n\nQuestion:\nIs urotensin-II receptor over-expressed in colon cancer cell lines and in colon carcinoma in humans?\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 the surgical methods and outcome of reshaping the nose by using autologous cartilage grafting-silicone gel complex combined with trimming the lower lateral cartilages and thinning the superfluous tissue of the tip. Between May 2006 and July 2008, 36 patients with ugly nose shape received open nasal plasty by thinning the superfluous tissue and trimming the lower lateral cartilages combined with implant of auto-cartilage and silicone gel complex. There were 3 males and 33 females with an average age of 23 years (range, 18-36 years), including 20 cases of hypertrophy and obtuse round of nasal tip, 10 cases of flat of nasal tip, 2 cases of slight nostril exposure, and 4 cases of small whole nose with hypertrophy of nasal tip. Among them, 8 cases received 2-time operations. All incisions achieved healing by first intention. No deformation and complication occurred at donor sites of cartilage. The appearance, contour, color, and touch sensation of the nose were satisfactory and no complications of prosthesis exposure and skin redness of the nasal tip occurred. At 3-5 months after operation, the appearance of the nasal tip was satisfactory when part of the soft tissue was absorbed. Thirty-two patients were followed up 3-12 months (6 months on average), who were satisfied with the appearance of nose with good correct rate.\n\nQuestion:\nDo [ Complex of auto-cartilage grafting and silicone implant for open nasal plasty ]?\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:\nIn our previous studies, we found that intraglomerular deposition of fibrin and its metabolites was related to glomerular sclerosis and reduced renal function. It has been reported that both overlying and underlying fibrin may induce specific morphological changes of cultured endothelial cells from large blood vessels. The dependency of these morphological changes on the integrin alphavbeta3-arginyl-glycyl-aspartyl-serine (RGDS) interaction is still controversial. We hypothesized that glomerular endothelial cells (GECs) stimulated by fibrin might undergo morphological changes through an integrin alphavbeta3-RGDS interaction. Methods. In vitro studies were performed to examine the growing status of GECs stimulated by overlying and underlying fibrin gels in the presence or absence of the following: 50 microg/ml anti-alphavbeta3 integrin monoclonal antibody 23C6 or nonimmune mouse IgG, 1 mg/ml synthetic RGDS or arginyl-glycyl-glycyl-serine (RGGS) peptide, 10 mg/ml sodium heparin, 100 microg/ml cycloheximide, and 10 microM actinomycin D. Fast protein liquid chromatography (FPLC)-purified fibrinogen and the third to fifth passages of human GECs were also used in this study. GECs developed capillary tube structure after 60 hours of culturing on fibrin gels, and GECs cultured on gelatin-coated plates displayed a monolayer of cobblestone-like cells in the presence or absence of 23C6 and synthetic RGDS peptide. Fibrin-induced capillary tube formation was promoted by 23C6 and inhibited by RGDS peptide, cycloheximide, and actinomycin D. Disorganization of the GEC monolayer was induced by overlying fibrin, but was not induced by overlying agarose gels and glass cover slips or culturing in fibrinogen, 0.05 NIH U/ml thrombin, fibrin supernatants, as well as in fibrin degradation products. Disorganization of GEC monolayer can be induced by both des-AA-fibrin and des-AABB-fibrin and was unaffected by heparin. Furthermore, both 23C6 and synthetic RGDS peptide prevented disorganization of GECs induced by overlying fibrin, whereas nonimmune mouse IgG, synthetic RGGS peptide, cycloheximide, and actinomycin D had no similar effect.\n\nQuestion:\nDoes integrin alphavbeta3-RGDS interaction mediate fibrin-induced morphological changes of glomerular 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:\nTo identify the major difficulties nephrologists in the US face in providing adequate dialysis. To identify the perceived obstacles to achieving adequate dialysis in the US, 30 clinical support specialists responsible for nursing education and training were polled. Their responses together with those found in the recent literature were summarized and analyzed. The obstacles identified fell into the following major categories: (1) economic; (2) personnel shortage; (3) education, and (4) cultural. The principal specific difficulties identified in providing adequate dialysis were the provision of sufficient time and frequency of dialysis, adequate volume control and vascular and peritoneal access.\n\nQuestion:\nDoes major difficulties the US nephrologist face in providing adequate dialysis?\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:\nInterleukin-27 (IL-27) has been proposed to be useful for diagnosing tuberculous pleural effusion (TPE). Adenosine deaminase (ADA) has been long used for the same purpose. The aim of this study was to compare the performance of IL-27, ADA, and their product (IL-27 • ADA) in the diagnosis of TPE. Pleural fluid samples from patients with exudative pleural effusions were assessed for IL-27 and ADA levels. Receiver operating characteristic (ROC) curves were constructed to compare the overall diagnostic accuracy of IL-27, ADA, and IL-27 • ADA. Curves of false-positive (FPR) and false-negative (FNR) rates as a function of TPE prevalence were also constructed, and mean rates of false results in low (1-10%), intermediate (11-40%), and high (41-70%) prevalences were estimated to evaluate the ability of the three markers in ruling in or ruling out TPE. We studied 121 exudates. IL-27 and ADA were higher in TPEs compared with non-TPEs and they presented similar accuracies for the diagnosis of TPE. The product of IL-27 and ADA (IL-27 • ADA) was more accurate than ADA for the same purpose. IL-27 and IL-27 • ADA presented the lowest overall FPR and FNR, respectively. The FPR of IL-27, ADA and IL-27 • ADA was > 9%, even in high prevalence settings. Although their FNR was < 2% in low prevalence settings, only IL-27 • ADA exhibited sufficiently low FNR (< 1%) in intermediate and high prevalences.\n\nQuestion:\nDoes interleukin-27 improve the ability of adenosine deaminase to rule out tuberculous pleural effusion regardless of pleural tuberculosis prevalence?\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:\nPaternal age at childbirth has been increasing worldwide, and we assessed whether this increase affects growth, body composition and metabolism in their children. We studied 277 children (aged 3-12 years) born to fathers aged 19·8-51·8 years. Clinical assessments were height and weight adjusted for parental measurements, DEXA-derived body composition, fasting lipids, glucose homoeostasis and hormonal profiles. Children born to fathers aged 31-35 (P = 0·009) and >35 years (P = 0·021) were 2 cm taller than those of fathers aged ≤30 years. Children of fathers aged >35 years at childbirth had a lower body mass index (BMI) (-0·32 SDS) than offspring of fathers aged 31-35 (-0·01 SDS; P = 0·043) and ≤30 (0·22 SDS; P = 0·019). There were marked effects of paternal age at childbirth on childhood blood lipids. LDL-C concentrations in children born to fathers aged >35 years were 11% and 21% higher than in children of fathers aged 31-35 and ≤30 years, respectively (P < 0·01). Total cholesterol to HDL-C ratio was also higher among the children of fathers aged 31-35 (12%; P = 0·014) and >35 (16%; P = 0·004) years at childbirth compared with the ≤30 group. In addition, HOMA-IR in girls (but not boys) born of fathers aged 31-35 (0·99) and >35 years (1·11) indicated better insulin sensitivity compared with offspring in the ≤30 group (1·63; P < 0·05).\n\nQuestion:\nIs increasing paternal age at childbirth associated with taller stature and less favourable lipid profiles in their 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:\nPlatelet-derived growth factor (PDGF) is a potent mitogen for vascular smooth muscle cells and is implicated in the vascular response to injury and the pathogenesis of atherosclerosis. It is also a potent vasoconstrictor. To examine whether acute myocardial ischemia increases the level of PDGF in the coronary circulation, we measured plasma levels of PDGF in the coronary sinus and the aortic root simultaneously in 14 patients with coronary spastic angina. These measurements were performed before and after the left coronary artery spasm induced by intracoronary injection of acetylcholine, and measurements were also taken in 15 patients with stable exertional angina before and after acute myocardial ischemia induced by rapid atrial pacing. Eleven patients with chest pain but normal coronary arteries and no coronary spasm served as controls. Plasma PDGF levels increased significantly (P < 0.01) from 274 +/- 28 pg/mL to 364 +/- 27 pg/mL only in coronary sinus after anginal attacks in the patients with coronary spastic angina. However, plasma PDGF levels in coronary sinus remained unchanged after these attacks in the patients with stable exertional angina (from 230 +/- 27 pg/ml to 247 +/- 28 pg/mL) and after intracoronary injection of acetylcholine in the control subjects. Plasma PDGF levels in aortic root remained unchanged in all three patient groups.\n\nQuestion:\nIs platelet-derived growth factor released into the coronary circulation after coronary spasm?\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 aim of this study was to test whether orosomucoid like 3 (ORMDL3) and 17q21 variants are associated with susceptibility to ankylosing spondylitis (AS) in a Chinese population. A total of 753 unrelated AS patients and 1120 ethnically matched healthy controls were recruited. Seven single nucleotide polymorphisms (SNPs: rs7216389, rs12603332, rs12936231, rs9303277, rs11557467, rs1007654, and rs17608925), which were selected from chromosome 17q21 containing the genes ORMDL3, GSDMB, ZPBP2, and IKZF3, were genotyped by the Taqman SNP genotyping assay. Five of the SNPs (rs7216389, rs12603332, rs12936231, rs9303277, and rs11557467) were associated with AS (all p ≤ 0.01), especially in males (all p < 0.001). Of these, rs7216389, rs12603332, rs12936231, and rs11557467 were strongly associated with severity of the disease based on radiographic findings (p < 0.05).\n\nQuestion:\nAre genetic variants on 17q21 associated with ankylosing spondylitis susceptibility and severity in a Chinese Han population?\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:\nOxidative stress is an important causative factor in atherosclerosis. Isoprostanes are derivatives of arachidonate oxidized by reactive oxygen species (ROS). Oxidized lipids are markers of oxidative stress, important mediators of atherosclerosis, and activators of platelets. 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha) is a stable isoprostane and reliable marker of oxidative stress in vivo. The aim of the study was to determine the level of oxidative stress in acute coronary syndromes (ACS) and its correlations with the para meters of hemo stasis. Fourty-nine patients aged 46 to 76 years, including 28 with ACS and 25 with stable coronary artery disease (CAD), were enrolled to the study. The levels of 8-iso-PGF2alpha, soluble CD40 ligand (sCD40L), P-selectin (P-sel), beta-thromboglobulin, and the thrombin-antithrombin complex (TAT) in the plasma of venous blood were determined. A microvascular injury model was also used to evaluate TAT generation and sCD40L levels in blood collected every 60 seconds at the site of standardized microvascular injury. 8-iso-PGF2alpha levels were significantly higher in ACS compared to CAD patients (363.2 +/-45.94 vs. 328.2 -/+31.96 pg/ml, P = 0.011) and correlated with venous plasma levels of P-sel and beta-thromboglobulin in the ACS (r = 0.66; P = 0.0005 and r = 0.62; P = 0.001, respectively) and CAD groups (r = 0.46; P = 0.02 and r = 0.49; P = 0.01, respectively). In the microvascular injury model, the maximum concentrations of sCD40L in the ACS group were associated with plasma 8-iso-PGF2alpha levels (r = 0.50, P = 0.01). No correlations between 8-iso-PGF2alpha and markers of thrombin generation in venous blood and microvascular injury model were observed.\n\nQuestion:\nAre elevated levels of 8-iso-prostaglandin F2alpha in acute coronary syndromes associated with systemic and local platelet activation?\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:\nAnimal models have demonstrated that maternal undernutrition or early gestation glucocorticoid exposure induces endothelial dysfunction in the offspring. We sought to determine whether early gestation dexamethasone (DEX) exposure is further associated with increased vascular superoxide anion production. DEX (0.28 mg/kg/day i.v. for 48 h) was administered to pregnant ewes at 27-28 days' gestation (term 145 days). Tissues were harvested from DEX-exposed and control lambs at 125 days' gestation (n = 6 for each group) and 4 months following delivery (n = 9 and 12, respectively). By lucigenin-enhanced chemiluminescence, coronary and mesenteric arteries from DEX-exposed fetuses exhibited diminished basal superoxide production (both p < 0.01). Similarly, DEX-exposed carotid arteries from 4-month-old lambs had decreased superoxide production (p < 0.01) that localized to the endothelium by endothelial cell culture and dihydroethidium fluorescence. In contrast, DEX-exposed coronary arteries from the 4-month-old sheep had increased superoxide production (p < 0.05). Although early gestation DEX exposure did not alter lipid peroxidation, DEX exposure was associated with significantly increased renal and cerebral cortex aconitase activity (consistent with decreased protein oxidation). These changes occurred in the absence of alterations in renal cortex superoxide dismutase activity.\n\nQuestion:\nIs endothelial superoxide production altered in sheep programmed by early gestation dexamethasone exposure?\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:\nHigh frequency oscillatory ventilation (HFOV) improves gas exchange while providing lung protective effects during the ventilation of patients with the acute respiratory distress syndrome (ARDS). The purpose of this study was to review our experience with HFOV in adult burn patients with oxygenation failure secondary to ARDS. Retrospective cohort review of all burn patients treated with HFOV at a regional adult burn center. All values are reported as the mean +/- standard deviation (S.D.). HFOV was used on 28 occasions in 25 patients (age 44 +/- 16 years, %TBSA burns 40 +/- 15, and a 28% incidence of inhalation injury) who had severe oxygenation failure from ARDS (PaO2/FiO2 ratio 98 +/- 26, and oxygenation index (OI) (FiO2 x 100 x mean airway pressure/PaO2) 27 +/- 10) following 4.8 +/- 4.4 days of conventional mechanical ventilation (CMV). After switching from CMV to HFOV, there were significant improvements in the PaO(2)/FiO2 ratio within 1h and in the oxygenation index within 24 h. The duration of HFOV was 6.1 +/- 5.8 days. HFOV was continued during 26 surgeries for 14 patients where a mean of 18 +/- 9% TBSA burns were excised and closed. The only complications related to HFOV were three episodes of severe hypercapnia. In-hospital mortality was 32%.\n\nQuestion:\nDo high frequency oscillatory ventilation in burn patients with the acute respiratory distress syndrome?\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:\nTeeth are often included in the radiation field during head and neck radiotherapy, and recent clinical evidence suggests that dental pulp is negatively affected by the direct effects of radiation, leading to impaired sensitivity of the dental pulp. Therefore, this study aimed to investigate the direct effects of radiation on the microvasculature, innervation, and extracellular matrix of the dental pulp of patients who have undergone head and neck radiotherapy. Twenty-three samples of dental pulp from patients who finished head and neck radiotherapy were analyzed. Samples were histologically processed and stained with hematoxylin-eosin for morphologic evaluation of the microvasculature, innervation, and extracellular matrix. Subsequently, immunohistochemical analysis of proteins related to vascularization (CD34 and smooth muscle actin), innervation (S-100, NCAM/CD56, and neurofilament), and extracellular matrix (vimentin) of the dental pulp was performed. The morphologic study identified preservation of the microvasculature, nerve bundles, and components of the extracellular matrix in all studied samples. The immunohistochemical analysis confirmed the morphologic findings and showed a normal pattern of expression for the studied proteins in all samples.\n\nQuestion:\nIs micromorphology of the dental pulp highly preserved in cancer patients who underwent head and neck radiotherapy?\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:\nRetrograde coronary venous infusion is a promising delivery method for cellular cardiomyoplasty. Poor cell retention is the major obstacle to the establishment of this method as the preferred route for cell delivery. Here, we explored whether magnetic targeting could enhance retrograde cell retention in a rat model of myocardial infarction. Rat mesenchymal stem cells were labeled with superparamagnetic oxide nanoparticles. The magnetic responsiveness of MSCs was observed while cells flowed through a tube that served as a model of blood vessels in a 0.6-Tesla magnetic field. In a Sprague–Dawley rat model of acute myocardial infarction, 1 × 106 magnetic mesenchymal stem cells were transjugularly injected into the left cardiac vein while a 0.6-Tesla magnet was placed above the heart. The cardiac retention of transplanted cells was assessed by using quantitative Y chromosome-specific polymerase chain reaction, cardiac magnetic resonance imaging, and optical imaging. Cardiac function was measured by using echocardiography, and histologic analyses of infarct morphology and angiogenesis were obtained. The flowing iron oxide-labeled mesenchymal stem cells were effectively attracted to the area where the magnet was positioned. Twenty-four hours after cellular retrocoronary delivery, magnetic targeting significantly increased the cardiac retention of transplanted cells by 2.73- to 2.87-fold. Histologic analyses showed that more transplanted cells were distributed in the anterior wall of the left ventricle. The enhanced cell engraftment persisted for at least 3 weeks, at which time, left ventricular remodeling was attenuated, and cardiac function benefit was improved.\n\nQuestion:\nDoes magnetic targeting enhance retrograde cell retention in a rat model of 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:\nHyaluronic acid-binding protein 1 (HABP1/gC1qR/p32) has been recently implicated in oncogenesis and cancer progression in various malignancies; however, its clinical role in gastric cancer (GC) is still unclear. First, HABP1 expression was determined by Western blot analysis and immunohistochemistry. Then, we evaluated the expression of HABP1 and its clinical significance in tumor tissues from 181 patients with GC. Expression of HABP1 protein in GC tissues was noticeably higher than that in adjacent nonneoplastic tissues (\n\nQuestion:\nDoes elevated HABP1 protein expression correlate with progression and poor survival in patients with 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:\nRenal cell carcinoma in a renal graft is a rare condition whose incidence will increase in the future. To our knowledge no standardized treatment has been established for this disease. We performed a prospective study of nephron sparing surgery for small renal cell carcinoma in renal grafts. From January 2002 to December 2006, 2,050 renal graft recipients were followed at our transplantation center. Of these patients 7 were diagnosed with histologically confirmed renal cell carcinoma in the renal graft, 5 of whom presented with T1a renal cell carcinoma and prospectively underwent nephron sparing surgery. Five patients with 15 to 30 mm (median 20) renal cell carcinoma were included in the study and were treated with nephron sparing surgery. Median operative time was 110 minutes (range 60 to 150). Blood loss was less than 200 ml in each case. All tumors were pT1aN0M0 with negative margins. No postoperative complications were observed (hemorrhage, urinary fistulas, renal failure). Preoperative immunosuppressive treatment was not modified postoperatively. At 3 months after nephron sparing surgery and at a mean of 17.4 months of followup (range 5 to 54) no significant impairment of renal function or recurrence was observed.\n\nQuestion:\nIs nephron sparing surgery a feasible and efficient treatment of T1a renal cell carcinoma in kidney transplant : a prospective series from a single 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:\nThe management of type A intramural hematoma (IMH) is controversial. Although most Western countries still recommend immediate surgical repair, some centers in Asia have shown good results recently with medical treatment alone. Here, we present a case of type A IMH which was discovered during the operation to be a thrombosed type A dissection. An 83-year-old female patient presented with acute chest pain. After diagnostic exclusion of myocardial infarction, computed tomography was performed, which showed an IMH from the ascending to the descending aorta. No intimal flap could be detected. The ascending aorta was replaced surgically with a prosthesis. During the operation, we found a ruptured intimal plaque, which had caused dissection of the aorta with thrombosis of the false lumen. The true diagnosis-thrombosed type A dissection and not IMH-was revealed neither by computed tomography nor by transesophageal echocardiography.\n\nQuestion:\nDoes type A intramural hematoma often turn out to be a type A dissection?\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:\nCommencing antiretroviral therapy (ART) in human immunodeficiency virus-infected patients with treated or unrecognized Mycobacterium tuberculosis disease may trigger tuberculosis-associated immune reconstitution inflammatory syndrome (TB-IRIS) or ART-associated tuberculosis (ART-TB). We have shown that whole-blood interferon-gamma release assays may aid in the prediction and diagnosis of ART-TB. Here, we investigate interferon-gamma-inducible chemokines CXCL9 and CXCL10. CXCL9 and CXCL10 responses to region of difference 1 (RD1) antigens and purified protein derivative (PPD) were assayed in plasma from whole-blood cultures collected before and after 4, 12, and 24 weeks of ART from 15 TB-IRIS cases, 11 ART-TB cases, and matched controls. Relative to matched controls, ART-TB cases had elevated CXCL10 responses to RD1 antigens pre-ART (P = 0.02) and to PPD and RD1 antigens over 24 weeks of ART (P ≤ 0.02 and P ≤ 0.03). In contrast, TB-IRIS cases had higher CXCL10 responses to RD1 antigens before and after 4 weeks of ART only (P = 0.04 for both). CXCL9 responses to PPD and RD1 antigens were similar but less pronounced in ART-TB cases and did not differ between TB-IRIS cases and controls. CXCL10 responses to RD1 antigens performed as well as, or better than, IFN-γ responses in the prediction and diagnosis of ART-TB.\n\nQuestion:\nIs tuberculosis after commencing antiretroviral therapy for HIV infection associated with elevated CXCL9 and CXCL10 responses to Mycobacterium tuberculosis antigens?\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 demonstrate that occipital nerve injury is associated with chronic postoperative headache in patients who have undergone acoustic neuroma excision and to determine whether occipital nerve excision is an effective treatment for these headaches. Few previous reports have discussed the role of occipital nerve injury in the pathogenesis of the postoperative headache noted to commonly occur following the retrosigmoid approach to acoustic neuroma resection. No studies have supported a direct etiologic link between the two. The authors report on a series of acoustic neuroma patients with postoperative headache presenting as occipital neuralgia who were found to have occipital nerve injuries and were treated for chronic headache by excision of the injured nerves. Records were reviewed to identify patients who had undergone surgical excision of the greater and lesser occipital nerves for refractory chronic postoperative headache following acoustic neuroma resection. Primary outcomes examined were change in migraine headache index, change in number of pain medications used, continued use of narcotics, patient satisfaction, and change in quality of life. Follow-up was in clinic and via telephone interview. Seven patients underwent excision of the greater and lesser occipital nerves. All met diagnostic criteria for occipital neuralgia and failed conservative management. Six of 7 patients experienced pain reduction of greater than 80% on the migraine index. Average pain medication use decreased from 6 to 2 per patient; 3 of 5 patients achieved independence from narcotics. Six patients experienced 80% or greater improvement in quality of life at an average follow-up of 32 months. There was one treatment failure. Occipital nerve neuroma or nerve entrapment was identified during surgery in all cases where treatment was successful but not in the treatment failure.\n\nQuestion:\nAre postoperative headache following acoustic neuroma resection : occipital nerve injuries associated with a treatable occipital neuralgia?\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:\nHepatocellular carcinoma (HCC) has high mortality and no adequate treatment. Endocannabinoids interact with hepatic cannabinoid 1 receptors (CB1Rs) to promote hepatocyte proliferation in liver regeneration by inducing cell cycle proteins involved in mitotic progression, including Forkhead Box M1. Because this protein is highly expressed in HCC and contributes to its genesis and progression, we analyzed the involvement of the endocannabinoid/CB1R system in murine and human HCC. Postnatal diethylnitrosamine treatment induced HCC within 8 months in wild-type mice but fewer and smaller tumors in CB1R(-/-) mice or in wild-type mice treated with the peripheral CB1R antagonist JD5037, as monitored in vivo by serial magnetic resonance imaging. Genome-wide transcriptome analysis revealed CB1R-dependent, tumor-induced up-regulation of the hepatic expression of CB1R, its endogenous ligand anandamide, and a number of tumor-promoting genes, including the GRB2 interactome as well as Forkhead Box M1 and its downstream target, the tryptophan-catalyzing enzyme indoleamine 2,3-dioxygenase. Increased indoleamine 2,3-dioxygenase activity and consequent induction of immunosuppressive T-regulatory cells in tumor tissue promote immune tolerance.\n\nQuestion:\nDoes cannabinoid receptor 1 promote hepatocellular carcinoma initiation and progression through multiple mechanisms?\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:\nWell-controlled studies have demonstrated that inpatient hyperglycemia is an indicator of poor clinical outcomes, but the use of diabetes-specific enteral formulas in hospitalized patients remains a topic of great debate. In two different protocols, postprandial glycemia and insulinemia were measured in 22 subjects with diabetes fed a diabetes-specific or standard formula (protocol 1). Continuous glucose monitoring was used to assess glucose levels in 12 enterally fed patients with diabetes receiving the standard formula followed by the diabetes-specific formula continuously for 5 days each (protocol 2). End points included postprandial glycemia and insulinemia, glycemic variability (mean amplitude of glycemic excursions [MAGE]), mean glucose, and insulin use. In the postprandial response protocol, the diabetes-specific formula resulted in lower positive areas under the postprandial curve (P < 0.001) and peak glucose (P < 0.001) and insulin (P = 0.017) levels. In the protocol using continuous glucose monitoring, glycemic variability (as measured by MAGE) was lower with continuous administration of the diabetes-specific than the standard formula (64.6 +/- 6.8 mg/dL vs. 110.6 +/-15.3 mg/dL, P = 0.003). Also, administration of the diabetes-specific formula resulted in lower mean glucose concentrations during feeding (171.1 +/- 16.1 vs. 202.1 +/- 17.4 mg/dL, P = 0.024) and insulin requirements (7.8 +/- 2.3 vs. 10.9 +/- 3.3 units/day, P = 0.039) than the standard formula.\n\nQuestion:\nDoes a diabetes-specific enteral formula improve glycemic variability in patients with 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:\nMany complications have been reported to occur with surgery for scoliosis in Prader-Willi Syndrome (PWS). However, growth hormone (GH) treatment has contributed to improvements in height, body composition, bone density and breathing functions in PWS patients. The purpose of this study was to investigate patients who underwent surgery for scoliosis in PWS. There were 136 PWS patients being followed-up by the Pediatrics Department of our hospital. Among these, we investigated nine patients who had undergone surgery. Their mean age was 11 years. The mean follow-up period was 6 years 10 months. The mean body mass index was 22.5 kg/m(2). GH therapy was administered to eight patients. Brace treatment was performed in two patients. Spinal correction and fusion were performed in six patients, and the growing rod method was performed in three patients. Necessary reoperations were performed in two patients. For the total 11 surgeries in the nine patients, the mean blood loss was 397 ml and the mean operation time was 4 h and 20 min. The mean Cobb angles were 76.0 degrees preoperatively and 35.8 degrees at follow-up. Regarding complications, one patient experienced early dislodgment of the hook and one patient experienced a superior wound infection.\n\nQuestion:\nDoes growth hormone supplement treatment reduce the surgical risk for Prader-Willi Syndrome 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:\nNew-onset diabetes mellitus (DM) may herald pancreatic cancer (PaC). We determined whether changes in body weight distinguished PaC-associated DM (PaCDM) from type 2 DM. Among Olmsted County residents, we identified 29 PaCDM and 43 type 2 DM subjects who had serial fasting blood glucose measurements, new-onset DM, and no cancer-specific symptoms at DM onset. We compared body weight (kg) and fasting blood glucose (mg/dL) at DM onset, 1 to 2 years before and at index date in the 2 groups. Fasting blood glucose values were similar before and at the onset of DM. Before onset of DM, PaCDM and type 2 DM subjects had similar body weight (P = 0.80). However, at onset of DM, 59% of PaCDM subjects lost weight versus 30% of type 2 DM subjects (P = 0.02). At onset of DM, 56% of type 2 DM subjects gained weight versus 31% of PaCDM subjects (P = 0.04). By index date, PaCDM subjects lost more weight than type 2 DM subjects did (8.3 ± 8.3 vs 0.8 ± 4.8 kg, P < 0.01).\n\nQuestion:\nDoes weight loss precede cancer-specific symptoms in pancreatic cancer-associated 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:\nActivated Stat3 is an important mediator of oncogenesis in the colon. To test the hypothesis that select Stat activation and/or the pattern of Stat activation serves as a marker for early neoplastic transformation, we examined the distribution of activated Stat1(pStat1), Stat6(pStat6), and Stat3(pStat3) in colitis along the continuum of inactive disease to colitis-associated cancer. Tissue microarrays were constructed using colonoscopy biopsy and surgical specimens from 67 patients with ulcerative colitis or Crohn's colitis and 11 controls. In all, 111 sets of samples were analyzed representing normal tissue, active disease, low-grade dysplasia, high-grade dysplasia, and colitis-associated cancer. Immunohistochemistry to detect pStat1, pStat6, and pStat3 in colonic epithelial and mucosal immune cells was then correlated with clinical and pathological data (tumor location, histologic type, grade, and lymph node involvement). In 50% of colitis-associated cancer samples, pStat3 was detected prominently in epithelial cells, where it was routinely associated with intense pStat3 staining in surrounding immune cells. Stat3 activation was greater in low-grade tumors than in high-grade ones (P < 0.05). pStat6 expression was more common in normal tissues than in colitis-associated cancer (P < 0.05). pStat1 was detected in a small subset of immune cells in patients with chronic inactive and active colitis, low- and high-grade dysplasia, but not in colitis-associated cancer.\n\nQuestion:\nIs shift from pStat6 to pStat3 predominance associated with inflammatory bowel disease-associated dysplasia?\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 production of aggrecanase 1 (ADAM-TS4) in monolayer chondrocytes, capsular fibroblasts, and cartilage. Bovine nasal and articular cartilage, monolayer chondrocytes, and capsular fibroblasts were incubated in the absence and presence of interleukin-1 (IL-1). ADAM-TS4 production was evaluated by immunofluorescence or by Western blot analysis. Aggrecanase activity was measured in cells grown on an immobilized peptide substrate, and peptide cleavage was monitored by enzyme-linked immunosorbent assay. There was constitutive production of ADAM-TS4 in both cells and tissue. The protein was associated with the extracellular matrix based on the observation that the staining could be reduced following treatment of chondrocytes with heparin or exposure to chondroitinase ABC. Interestingly, there was no detectable change in the abundance of ADAM-TS4 in response to IL-1. Western blot analysis of cell lysates from IL-1-stimulated chondrocytes showed no evidence of increased ADAM-TS4 production, but resulted in activation of ADAM-TS4. The activation was associated with an increased generation in the aggrecanase neoepitope NITEGE in nasal cartilage in response to IL-1. These data suggest that induction of aggrecanase activity both in cells and in cartilage by IL-1 may involve the stimulation of an activator of ADAM-TS4. Consistent with this observation, culture of chondrocytes on a solid support containing a peptide substrate resulted in the generation of aggrecanase-mediated cleavage that could be blocked by selective inhibitors of ADAM-TS4.\n\nQuestion:\nDoes induction of aggrecanase 1 ( ADAM-TS4 ) by interleukin-1 occur through activation of constitutively produced protein?\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:\nAngelica Sinensis (AS), a folk medicine, has long been used in ergogenic aids for athletes, but there is little scientific evidence supporting its effects. We investigated whether AS induces hypertrophy in myotubes through the phosphatidylinositol 3-kinase (PI3K)/Akt (also termed PKB)/mammalian target of the rapamycin (mTOR) pathway. An in vitro experiment investigating the induction of hypertrophy in myotubes was conducted. To investigate whether AS promoted the hypertrophy of myotubes, an established in vitro model of myotube hypertrophy with and without AS was used and examined using microscopic images. The role of the PI3K/Akt/mTOR signaling pathway in AS-induced myotube hypertrophy was evaluated. Two inhibitors, wortmannin (an inhibitor of PI3K) and rapamycin (an inhibitor of mTOR), were used. The results revealed that the myotube diameters in the AS-treated group were significantly larger than those in the untreated control group (P < 0.05). Wortmannin and rapamycin inhibited AS-induced hypertrophy. Furthermore, AS increased Akt and mTOR phosphorylation through the PI3K pathway and induced myotube hypertrophy.\n\nQuestion:\nDoes angelica Sinensis promote myotube hypertrophy through the PI3K/Akt/mTOR pathway?\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:\nCytomegalovirus establishes lifelong persistency in the host and leads to life threatening situations in immunocompromised patients. FoxP3+ T regulatory cells (Tregs) critically control and suppress innate and adaptive immune responses. However, their specific role during MCMV infection, especially pertaining to their interaction with NK cells, remains incompletely defined. To understand the contribution of Tregs on NK cell function during acute MCMV infection, we infected Treg depleted and undepleted DEREG mice with WT MCMV and examined Treg and NK cell frequency, number, activation and effector function in vivo. Our results reveal an increased frequency of activated Tregs within the CD4+ T cell population shortly after MCMV infection. Specific depletion of Tregs in DEREG mice under homeostatic conditions leads to an increase in NK cell number as well as to a higher activation status of these cells as compared with non-depleted controls. Interestingly, upon infection this effect on NK cells is completely neutralized in terms of cell frequency, CD69 expression and functionality with respect to IFN-γ production. Furthermore, composition of the NK cell population with regard to Ly49H expression remains unchanged. In contrast, absence of Tregs still boosts the general T cell response upon infection to a level comparable to the enhanced activation seen in uninfected mice. CD4+ T cells especially benefit from Treg depletion exhibiting a two-fold increase of CD69+ cells 40 h and IFN-γ+ cells 7 days p.i. while, MCMV infection per se induces robust CD8+ T cell activation which is also further augmented in Treg-depleted mice. Nevertheless, the viral burden in the liver and spleen remain unaltered upon Treg ablation during the course of infection.\n\nQuestion:\nDoes mouse cytomegalovirus infection overrule T regulatory cell suppression on natural killer 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:\nRecent studies have shown that human papillomavirus (HPV) is associated with a certain subset of head and neck squamous cell carcinoma (HNSCC)-namely, those arising in the oropharynx. The objective of this study is to determine the efficacy, detection, and genotype of high-risk (HR) HPV using the Roche cobas 4800 system (Roche Molecular System, Pleasanton, CA). Forty-two fine-needle aspirate (FNA) specimens from 37 patients with cervical (n = 36) or mediastinal (n = 5) lymphadenopathy or a left parapharyngeal mass (n =1) were included in this prospective study. HR-HPV testing was performed on residual FNA material after direct smear preparation and, if positive, was further delineated into HPV 16/18 genotypes using the Roche cobas 4800 system. Follow-up included review of histologic material and/or electronic health records. Among those HNSCCs that were positive for HR-HPV, 18 (100%) of 18 originated from the oropharynx, whereas only two (13%) of 15 HR-HPV-negative HNSCCs originated from the oropharynx (χ(2) test, P < .05). p16 immunohistochemical assay and HPV 16 in situ hybridization on corresponding histologic specimens were concordant with cytologic HR-HPV results.\n\nQuestion:\nIs detection and genotype of high-risk human papillomavirus in fine-needle aspirates of patients with metastatic squamous cell carcinoma helpful in determining tumor origin?\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:\nViral load testing for cytomegalovirus (CMV) is an important diagnostic tool for the management of transplant recipients and immunocompromised individuals; however, inconsistency among laboratories in quantitative measurements of viral load limits interinstitutional comparisons. These inconsistencies stem from the lack of assays cleared by the US Food and Drug Administration, the absence of international standards, the wide variety of CMV-extraction and -detection methods, and differences in materials used for calibration. A critical component of standardization is the use of calibrators that are traceable and commutable. Bland-Altman plots and prediction ellipses were used to test the commutability of 2 CMV calibrators for 2 different quantification methods. Tests with 2 methods showed 1 calibrator to be commutable and the other to be noncommutable. The results for the commutable calibrator were within the 95% prediction interval of the clinical samples in the Bland-Altman plot and within the 95% prediction ellipse for a simulated commutable calibrator, whereas the results for the noncommutable calibrator were not within these prediction intervals. When used to calibrate patient results, only the commutable calibrator, the OptiQuant CMV(tc) Calibration Panel, significantly improved the comparability of viral loads for the 2 different measurement methods.\n\nQuestion:\nIs a commutable cytomegalovirus calibrator required to improve the agreement of viral load values between laboratories?\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:\nADRB3 DNA hypermethylation was recently associated with dyslipidemia in familial hypercholesterolemia (FH). In this study, we verified whether ADRB3 DNA methylation in blood and visceral adipose tissue (VAT) was associated with obesity and its related complications. DNA methylation levels were measured in the blood of 61 FH men, and the blood and VAT of 30 severely obese men. Common ADRB3 polymorphisms were genotyped in all subjects. Higher ADRB3 DNA methylation levels were significantly associated with lower low-density lipoprotein cholesterol levels (r = -0.40; p = 0.01) in FH, and with a lower waist-to-hip ratio (r = -0.55; p = 0.01) and higher blood pressure (r = 0.43; p = 0.05) in severely obese men. ADRB3 g.-843C>T and p.W64R polymorphisms were found to be strongly associated (p < 0.001) with ADRB3 DNA methylation and mRNA levels.\n\nQuestion:\nIs aDRB3 gene promoter DNA methylation in blood and visceral adipose tissue associated with metabolic disturbances in men?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]