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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAlcohol exposure during pregnancy results in an array of structural and functional abnormalities called fetal alcohol spectrum disorders (FASD). Alcohol dysregulates the exquisite coordination and regulation of gestational adaptations at the level of the uterine vasculature. We herein hypothesized that chronic binge-like alcohol results in uterine vascular dysfunction and impairs maternal uterine artery reactivity to vasoconstrictors and dilators. We utilized a once-daily binge alcohol (4.5 g/kg body weight) exposure paradigm (gestational day 7 to 17) in a pregnant rat model system and investigated primary uterine artery function in response to vasoconstrictors and vasodilators utilizing wire myography. Alcohol (peak blood alcohol concentration, 216 mg/dl) produced uterine vascular dysfunction. Alcohol did not produce altered uterine vascular reactivity to α1 adrenergic agonist phenylephrine or the prostanoid thromboxane. However, alcohol specifically impaired acetylcholine (ACh)-mediated uterine artery vasodilation but exogenous endothelium-independent vasodilators like sodium nitroprusside exhibited no alcohol effect; ACh significantly decreased vessel relaxation (p = 0.003; ↓pD2 [negative log molar ACh concentration producing the half maximum response], -7.004 ± 0.215 vs. -6.310 ± 0.208; EMax [maximal ACh response], 92% vs. 75%).\n\nQuestion:\nDoes chronic binge alcohol exposure during pregnancy impair rat maternal uterine vascular function?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo examine the relationship of knee malalignment to the occurrence of knee osteoarthritis (OA) among subjects without radiographic OA at baseline to determine whether malalignment is a risk factor for incident disease or simply a marker of increasing disease severity. We selected 110 incident tibiofemoral (TF) OA case knees (76 subjects) and 356 random control knees (178 subjects) from among participants in the Framingham Osteoarthritis Study. Case knees did not have OA at baseline (1992-1994 examination) but had developed OA (Kellgren/Lawrence grade>or=2) at followup (2002-2005 examination) (mean of 8.75 years between examinations). Control knees did not have OA at baseline. Standardized digital radiographs of the fully extended knee with weight-bearing were read using a standard protocol and eFilm viewing software. We measured the anatomic axis, the condylar angle, the tibial plateau angle, and the condylar tibial plateau angle. The interobserver intraclass correlation coefficient (ICC) ranged from 0.93 to 0.96 and the intraobserver ICC from 0.94 to 0.97. In a knee-specific analysis, we examined the relationship of each alignment measurement to the risk of TF OA using generalized estimating equations, adjusting for age, sex, and body mass index (BMI). We used the same approach to assess the association between each alignment measurement and the risk of medial TF OA. Subjects in the case population were older and had a higher BMI than the controls. The alignment values were normally distributed and were not different between the cases and the controls. After adjustment for age, sex and BMI, there was no significant increase in incident OA in the highest quartile compared with the lowest quartile category for any of the alignment measures (P for trend for anatomic axis and condylar tibial plateau angle was 0.83 and 0.80, respectively). Similar results were also observed for medial compartment OA.\n\nQuestion:\nDoes knee alignment predict incident osteoarthritis : the Framingham osteoarthritis study?\n\nAnswer:",
"role": "user"
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{
"content": "no",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHypoxic pulmonary vasoconstriction (HPV) is impaired during inflammatory lung processes such as pneumonia or the acute respiratory distress syndrome. Voltage-gated potassium channels play a central role in mediating HPV. The aim of this study was to determine whether 4-aminopyridine (4-AP), a known voltage-gated potassium channel inhibitor, may restore HPV in sepsis. The effects of 0.01, 0.1, and 1.0 mm 4-AP on HPV responsiveness were assessed in isolated lungs of untreated mice and of mice 18 h after lipopolysaccharide injection (20 mg/kg intraperitoneal Escherichia coli 0111:B4 lipopolysaccharide). HPV was quantified as the increase in perfusion pressure in response to hypoxic ventilation in percent of baseline perfusion pressure. Intrinsic pulmonary vascular resistance (R0) and pulmonary vascular distensibility (alpha) were determined by nonlinear regression analysis of pulmonary vascular pressure-flow curves generated during normoxic and hypoxic ventilation, respectively. HPV was impaired in lungs isolated from lipopolysaccharide-challenged mice. Addition of 4-AP to the perfusate did not alter HPV responsiveness in untreated mice but dose dependently restored HPV in endotoxemic mice. Analysis of pulmonary vascular pressure-flow curves revealed that 4-AP (1) counteracted the observed lipopolysaccharide-induced changes in alpha and R0 under normoxic conditions and (2) augmented the hypoxia-induced increase in R0 in lungs of endotoxemic mice.\n\nQuestion:\nDoes 4-Aminopyridine restore impaired hypoxic pulmonary vasoconstriction in endotoxemic mice?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe objective of this study was to determine if hypertriglyceridemia is associated with isolated impaired glucose tolerance in subjects without insulin resistance. A total of 365 apparently healthy individuals aged 20-65 years were enrolled in a population-based cross-sectional study. Subjects were allocated into the groups with and without hypertriglyceridemia. Age, gender, body mass index, and waist circumference were matched criteria. Individuals with impaired fasting glucose, impaired fasting glucose+impaired glucose tolerance, diabetes, homeostasis model assessment of insulin resistance index ≥ 2.5, and/or chronic illnesses such as renal disease or malignancy were excluded. Hypertriglyceridemia was defined by triglycerides levels ≥ 150 mg/dL. Impaired glucose tolerance was defined by plasma glucose concentration 2-h post-load glucose ≥ 140 mg/dL <200 mg/dL. Subjects with impaired glucose tolerance were required to have fasting plasma glucose levels <100 mg/dL. Logistic regression analysis was used to compute the odds ratio between hypertriglyceridemia (independent variable) and impaired glucose tolerance (dependent variable). A total of 132 and 233 subjects were allocated into the groups with and without hypertriglyceridemia, respectively. The frequency of impaired glucose tolerance was 13.6% and 5.6% in the individuals with and without hypertriglyceridemia, p = 0.01. The logistic regression analysis adjusted by gender, blood pressure, and high-density lipoprotein cholesterol showed that hypertriglyceridemia is significantly associated with impaired glucose tolerance (OR 2.34; 95% CI: 1.02-5.32, p = 0.04).\n\nQuestion:\nIs the hypertriglyceridemia associated with isolated impaired glucose tolerance in subjects without insulin resistance?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nChronic allograft nephropathy represents the principal cause of graft loss after the first year of transplantation. Transforming growth factor-beta1 (TGF-beta1) is a key factor in fibrogenesis and has been involved in the pathogenesis of chronic allograft nephropathy and other chronic nephropathies. Experimental studies have demonstrated that the angiotensin II receptor antagonist (losartan) could decrease the synthesis of TGF-beta1. The aim of this study was to determine the plasma levels of TGF-beta1 in transplant patients with chronic allograft nephropathy, and to evaluate the effect of losartan on TGF-beta1 plasma levels and other vasoactive peptides (angiotensin II, plasma renin activity, aldosterone, endothelin-1, and nitrites and nitrates). Angiotensin-converting enzyme genotypes were also determined in all patients. Fourteen transplant patients with chronic allograft nephropathy were included. Treatment with losartan (50 mg) was introduced. Consecutive determinations of TGF-beta1 and other vasoactive peptides were performed during follow-up. Patients with chronic allograft nephropathy presented higher plasma levels of TGF-beta1 than the control groups. The treatment with losartan significantly decreased the plasma levels of TGF-beta1 (P < 0.05) and endothelin (P < 0.05) in all patients. The decrease of TGF-beta1 was statistically correlated with the blockade of the angiotensin II receptor (P < 0.05). No significant correlation could be demonstrated between angiotensin-converting enzyme genotypes and TGF-beta, endothelin-1, and nitrite-nitrate serum levels.\n\nQuestion:\nDoes losartan decrease plasma levels of TGF-beta1 in transplant patients with chronic allograft nephropathy?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCD46 molecule (complement regulatory protein [CD46]), known as a human cell surface receptor, plays an important role in complement and T-cell regulation for organ transplantation. This study was performed to evaluate the association of promoter polymorphism (rs2796267, -496 A/G) of the CD46 gene with acute renal allograft rejection (AR), late acute rejection (LAR), and graft loss (GL) in Korean patients. A total of 334 patients with kidney transplants were recruited. Transplantation outcomes were determined in terms of AR, LAR, and GL criteria. The promoter single nucleotide polymorphism (SNP) of CD46 was genotyped by direct sequencing. The rs2796267 SNP exhibited significant differences between the AR group and non-AR group (codominant1 model, P = .012; odds ratio [OR], 0.47 [95% confidence interval, 0.26-0.84]; dominant model, P = .012; OR, 0.50 [95% CI, 0.29-0.86]; and allele distribution, P = .034; OR, 0.64 [95% CI, 0.43-0.94]). In addition, the SNP also exhibited significant associations with LAR (codominant2 model, P = .041; OR, 0.12 [95% CI, 0.02-0.92]; recessive model, P = .005; OR, 0.13 [95% CI, 0.02-0.94]; and allele distribution, P = .038; OR, 0.58 [95% CI, 0.35-0.97]).\n\nQuestion:\nDoes a Promoter Polymorphism in the CD46 Complement Regulatory Protein Gene be Associated With Acute Renal Allograft Rejection?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nLaparoscopic adrenalectomy has surpassed open adrenalectomy as the gold standard for excision of benign adrenal lesions. The size threshold for offering laparoscopic adrenalectomy is controversial as the prevalence of adrenocortical carcinoma increases with increasing tumour size. The aim of this paper was to assess the safety of laparoscopic adrenalectomy for large adrenal tumours (tumours > or = 60 mm). A retrospective cohort study of patients who underwent adrenalectomy in a single unit during the period 1995-2005 was undertaken. One hundred and seventy patients with 173 tumours were included in this study. Of these, 29 were > or = 60 mm in size, and 16 of these patients underwent laparoscopic adrenalectomy. There were 8 adrenocortical carcinomas in the group with tumours > or = 60 mm in size. Five of these patients underwent an open adrenalectomy, while 2 and 1 patients had laparoscopic and laparoscopic converted to open adrenalectomy respectively. Four of the patients undergoing open adrenalectomy died of their disease while 1 is alive with recurrence 3 years later. The 3 patients who underwent either laparoscopic or laparoscopic converted to open adrenalectomy are alive without evidence of disease after 18 months follow up.\n\nQuestion:\nIs laparoscopic surgery safe for large adrenal lesions?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe investigated the effects of photodynamic therapy (PDT) combined with low-dose chemotherapy on breast cancer cells. Photodynamic treatment was administered by irradiating indocyanine green-preloaded MCF-7 cells with an IR diode laser source at 805 nm; cisplatin was used for chemotherapy. The dose-response phenomena associated with the two treatments administered individually and together were evaluated with the following tests: trypan blue dye exclusion, 3-(4,5-dimethylthiazol)-2,5-diphenyltetrazolium bromide (MTT) assay, clonogenic survival, thymidine and methionine incorporation, and insulin-dependent and insulin-independent glucose transport. Viability and metabolic data demonstrated mutual reinforcement of therapeutic efficacy. However, isobolographic analysis of quantal and variable data indicated that reinforcement was additive according to trypan blue data and synergistic according to MTT data. To investigate the molecular mechanisms underlying alterations in cell proliferation and apoptosis, we evaluated (by Western blotting) the expression of proteins Bcl-2, Bax, Bcl-X(L), p21, p53, and poly(ADP-ribose) polymerase. Photodynamic treatment caused transient selective destruction of Bcl-2 and up-regulation of Bax. It also induced apoptosis in a limited fraction of cells (10-12%). Flow cytometry data showed that PDT killed mostly G(1)-phase cells, whereas cisplatin killed mostly S-phase cells. This disjointed phase-related effect may account for the favorable effects exerted by combined treatment.\n\nQuestion:\nDoes photodynamic therapy with indocyanine green complement and enhances low-dose cisplatin cytotoxicity in MCF-7 breast cancer cells?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe thrombogenicity of a disrupted atherosclerotic lesion is dependent on the nature and extent of the plaque components exposed to flowing blood together with local rheology and a variety of systemic factors. We previously reported on the different thrombogenicity of the various types of human atherosclerotic lesions when exposed to flowing blood in a well-characterized perfusion system. This study examines the role of tissue factor in the thrombogenicity of different types of atherosclerotic plaques and their components. Fifty human arterial segments (5 foam cell-rich, 9 collagen-rich, and 10 lipid-rich atherosclerotic lesions and 26 normal, nonatherosclerotic segments) were exposed to heparinized blood at high shear rate conditions in the Badimon perfusion chamber. The thrombogenicity of the arterial specimens was assessed by 111In-labeled platelets. After perfusion, specimens were stained for tissue factor by use of an in situ binding assay for factor VIIa. Tissue factor in specimens was semiquantitatively assessed on a scale of 0 to 3. Platelet deposition on the lipid-rich atheromatous core was significantly higher than on all other substrates (P = .0002). The lipid-rich core also exhibited the most intense tissue factor staining (3 +/- 0.1 arbitrary units) compared with other arterial components. Comparison of all specimens showed a positive correlation between quantitative platelet deposition and tissue factor staining score (r = .35, P < .01).\n\nQuestion:\nDoes tissue factor modulate the thrombogenicity of human atherosclerotic plaques?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nras oncogenic activation has long been demonstrated in thyroid carcinomas of follicular cell derivation, but no consistent relationship has been shown between mutations and clinicopathologic features. We analyzed H-, K-, and N-ras mutations by polymerase chain reaction-single-strand conformational polymorphism followed by DNA sequencing in 125 thyroid carcinoma specimens from 107 patients, to include tumors covering the entire spectrum of thyroid tumor differentiation. Mutations were identified in four (8.2%) of 49 well-differentiated carcinomas (WDCs; two [6.7%] of 30 of the tumors were papillary carcinomas, two [10.5%] of 19 of them were follicular carcinomas), in 16 (55.2%) of 29 poorly differentiated carcinomas (PDCs), and in 15 (51.7%) of 29 undifferentiated carcinomas, with a significant association between ras mutation and poorly or undifferentiated tumors (P <.001). Twenty-six (74.3%) of 35 patients with ras-mutated tumors died as a result of disease as opposed to 23 (31.9%) of 72 patients with tumors lacking the mutations. Among patients with differentiated thyroid carcinomas (WDC and PDC), 11 (55.0%) of 20 patients with mutated tumors died as a result of disease as opposed to nine (15.5%) of 58 patients with wild-type ras tumors, and the correlation was independent of tumor differentiation and stage (P =.016). K-ras codon 13 mutations (all with G-A nucleotide transitions resulting in Gly>Asp substitution) and single activating mutations in any of the ras genes were also independent predictors of poor survival in differentiated thyroid carcinomas (P =.027 and P =.007, respectively).\n\nQuestion:\nAre ras mutations associated with aggressive tumor phenotypes and poor prognosis in thyroid cancer?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIt is well known that most neurodegenerative diseases are associated with microglia-mediated inflammation. Our previous research demonstrates that the CD40 signaling is critically involved in microglia-related immune responses in the brain. For example, it is well known that the activation of the signal transducer and activator of transcription (STAT) signaling pathway plays a central role in interferon-gamma (IFN-gamma)-induced microglial CD40 expression. We and others have previously reported that microglial CD40 expression is significantly induced by IFN-gamma and amyloid-beta (A beta) peptide. Recent studies have shown that certain flavonoids possess anti-inflammatory and neuroprotective properties distinct from their well-known anti-oxidant effects. In particular, flavonoids, apigenin and luteolin have been found to be effective CD40 immunomodulators. Cultured microglia, both N9 and primary derived lines, were treated with flavonoids in the presence of IFN-gamma and/or CD40 ligation to assess any anti-inflammatory effects and/or mechanisms. CD40 expression on microglia was analyzed by fluorescence activated cell sorting (FACS). Anti-inflammatory effects and mechanisms were confirmed by ELISA for interleukin-6 (IL-6) and TNF-alpha, lactate dehydrogenase (LDH) assay, and STAT1 Western blotting. Apigenin and luteolin concentration-dependently suppressed IFN-gamma-induced CD40 expression. Apigenin and luteolin also suppressed microglial TNF-alpha and IL-6 production stimulated by IFN-gamma challenge in the presence of CD40 ligation. In addition, apigenin and luteolin markedly inhibited IFN-gamma-induced phosphorylation of STAT1 with little impact on cell survival.\n\nQuestion:\nDo apigenin and luteolin modulate microglial activation via inhibition of STAT1-induced CD40 expression?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo provide a comprehensive simultaneous relation of various semiquantitative knee OA MRI features as well as the presence of baseline radiographic osteoarthritis (OA) to quantitative longitudinal cartilage loss. We studied Multicenter OA Study (MOST) participants from a longitudinal observational study that included quantitative MRI measurement of cartilage thickness. These subjects also had Whole Organ MRI Score (WORMS) scoring of cartilage damage, bone marrow lesions (BMLs), meniscal pathology, and synovitis, as well as baseline radiographic evaluation for Kellgren and Lawrence (KL) grading. Knee compartments were classified as progressors when exceeding thresholds of measurement variability in normal knees. All potential risk factors of cartilage loss were dichotomized into \"present\" (score ≥2 for cartilage, ≥1 for others) or \"absent\". Differences in baseline scores of ipsi-compartmental risk factors were compared between progressor and non-progressor knees by multivariable logistic regression, adjusting for age, sex, body mass index, alignment axis (degrees) and baseline KL grade. Odds ratios (OR) and 95% CIs were calculated for medial femorotibial compartment (MFTC) and lateral femorotibial compartment (LFTC) cartilage loss. Cartilage loss across both compartments was studied using Generalized Estimating Equations. 196 knees of 196 participants were included (age 59.8 ± 6.3 years [mean ± SD], BMI 29.5 ± 4.6, 62% women). For combined analyses of MFTC and LFTC, baseline factors related to cartilage loss were radiographic OA (KL grade ≥2: aOR 4.8 [2.4-9.5], cartilage damage (aOR 2.3 [1.2-4.4])), meniscal damage (aOR 3.9 [2.1-7.4]) and extrusion (aOR 2.9 [1.6-5.3]), all in the ipsilateral compartment, but not BMLs or synovitis.\n\nQuestion:\nIs baseline radiographic osteoarthritis and semi-quantitatively assessed meniscal damage and extrusion and cartilage damage on MRI related to quantitatively defined cartilage thickness loss in knee osteoarthritis : the Multicenter Osteoarthritis Study?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe Trauma Related Injury Severity Score (TRISS) has been previously validated to predict outcomes in nonintubated, nonparalyzed trauma patients. The purpose of this study was to assess the impact of scene vital signs on predicting survival in intubated trauma patients. Our Trauma Registry of the American College of Surgeons was reviewed for all trauma patients admitted between 10/01/04 and 09/30/06, arriving by aeromedical transport. TRISS was evaluated for each patient based on their (1) scene vital signs and (2) arrival vital signs. Additionally, the \"TRISS-like\" score was calculated for each patient. Expected mortality for each score was measured against observed mortality. Four thousand four hundred ninety-nine Trauma Registry of the American College of Surgeons patients were admitted during the study period; 695 (15%) were transported by air; 163 patients (23%) arrived intubated; 480 arrived nonintubated. Observed survival in the intubated group was 76%. Observed survival in the nonintubated group was 100%. TRISS using scene vital signs more closely predicted mortality among intubated patients than the other scoring systems (69% versus 39% using TRISS-arrival versus 80% using TRISS-like). Scene vital signs with TRISS also resulted in fewer \"unexpected\" outcomes (survivors and deaths).\n\nQuestion:\nDoes use of scene vital signs improve TRISS predicted survival in intubated trauma patients?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe hypothesis that earlier menarche is associated with higher non alcoholic fatty liver disease (NAFLD) and ectopic adiposity, independent of young adult body mass index (BMI), was tested. The data from 1,214 black and white women in the Coronary Artery Risk Development in Young Adults (CARDIA) study who reliably reported menarche age at exam years 0 and 2, who had multiple-slice abdominal computed tomography (CT) at exam year 25, and who had no known liver disease or secondary causes of steatosis were included. Women were aged 18-30 at year 0 and 43-55 at year 25. Liver attenuation, visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), and inter-muscular adipose tissue (IMAT) were derived from CT. NAFLD was defined as liver attenuation less than 51 Hounsfield units. One-year earlier menarche was associated with higher NAFLD (RR = 1.15; 95% CI: 1.07, 1.24), and VAT (6.7 cc; 95% CI: 4.3, 9.0 cc), IMAT (1.0 cc; 95% CI: 0.6, 1.4 cc), and SAT (19.6 cc; 95% CI: 13.2, 26.0 cc) after confounder adjustment. Associations remained significant (P < 0.05) after further adjustment for year 0 BMI. Only VAT remained significant (P = 0.047) after adjustment for weight gain between years 0 and 25.\n\nQuestion:\nIs earlier menarche associated with fatty liver and abdominal ectopic fat in midlife , independent of young adult BMI : The CARDIA study?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nFunctional preload parameters such as stroke-volume variation (SVV) and pulse-pressure variation (PPV) are superior to filling pressures when assessing volume responsiveness in mechanically ventilated patients. This investigation studied their application in the setting of acute myocardial ischemia and reperfusion (I/R). Experimental animal study in a university laboratory. Twenty anesthetized and ventilated pigs. A temporary reduction of preload was obtained by ventilation with a positive end-expiratory pressure of 10 cmH(2)O. Ischemia was induced by temporary occlusion of the left anterior descending coronary artery for 60 minutes and was followed by 30 minutes of reperfusion. Animals were instrumented with an ultrasonic aortic flow probe to monitor stroke volume (SV) and SVV. Arterial pressure and PPV were recorded with a microtip catheter; left ventricular volume and pressure were registered by a conductance catheter. Respective hemodynamic measurements were made before, during, and after PEEP; before and after the induction of I/R. Eleven animals survived I/R and were analyzed. Before I/R, SVV (r = 0.87, p < 0.001) and PPV (r = 0.75, p < 0.05) during PEEP correlated significantly with relative changes in SV caused by the release of PEEP. Changes in SVV (r = 0.82, p < 0.01) and PPV (r = 0.67, p < 0.05) correlated significantly with relative changes in SV. After I/R, neither the relations between changes in SV to SVV or PPV during PEEP nor the relations between changes in SVV or PPV to changes in SV reached significance.\n\nQuestion:\nDo functional hemodynamic parameters reflect volume responsiveness in the immediate phase after acute myocardial ischemia and reperfusion?\n\nAnswer:",
"role": "user"
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{
"content": "no",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nElevated serum alkaline phosphatase (ALP) in infants with intestinal failure (IF) can be due to parenteral nutrition-associated liver disease (PNALD) or metabolic bone disease (MBD). The purpose of the study was to determine the utility of serum ALP in the diagnostic criteria for PNALD by measuring tissue-specific levels in infants with IF and PNALD. A retrospective review of patient data for 15 infants diagnosed with PNALD between December 2012 and August 2013 was performed. PNALD was defined as the presence of 2 consecutive direct bilirubin (DB) levels >2 mg/dL. Fractionated serum alkaline phosphatase was measured in each patient, while the DB was >2 mg/dL. Parathyroid hormone (PTH), vitamin D3, calcium, and phosphate levels were recorded where available. In 15 infants with PNALD, elevation in total ALP was due to marked elevations in bone-specific ALP. The median liver-specific ALP remained within the normal range. PTH, vitamin D3, calcium, and phosphate levels were within normal limits.\n\nQuestion:\nDoes elevated Alkaline Phosphatase in Infants With Parenteral Nutrition-Associated Liver Disease reflect Bone Rather Than Liver Disease?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPeople with chronic obstructive pulmonary disease (COPD) have frequent hospitalizations and emergency department visits, often due to COPD exacerbations which worsen disease status. Recognizing exacerbations is challenging; patients must distinguish between day-to-day COPD symptom variations and exacerbation symptoms. Self-regulation theory (Bandura, 1999) is useful for understanding symptom recognition, interpretation, and response. In this article a qualitative study of self-regulation use by 28 older adults with COPD (Brandt, 2005) is summarized. Twenty-eight community-dwelling older adults were interviewed. Data were analyzed using the interpretive description method.\n\nQuestion:\nDoes study of older adults ' use of self-regulation for COPD self-management inform an evidence-based patient teaching plan?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nZinc finger RNA binding protein (ZFR) is involved in the regulation of growth and cancer development. However, little is known about ZFR function in pancreatic cancer. Herein, to investigate whether ZFR is involved in tumor growth, Oncomine microarray data was firstly used to evaluate ZFR gene expression in human pancreatic tumors. Then short hairpin RNA (shRNA) targeting ZFR was designed and delivered into PANC-1 pancreatic cancer cells to knock down ZFR expression. Cell viability, cell proliferation and cell cycle analysis after ZFR knockdown were determined by MTT, colony forming and FACS, respectively. In addition, cell migration and invasion were assessed using the Transwell system. The expression of ZFR was significantly higher in pancreatic tumors than normal pancreas tissues by Oncomine database analysis. Knockdown of ZFR by shRNA-expressing lentivirus significantly decreased the viability and invasion ability of pancreatic cancer cells. Moreover, FACS analysis showed that knockdown of ZFR in PANC-1 cells caused a significant cell cycle arrest at G0/G1 phase. Furthermore, knockdown of ZFR decreased the levels of CDK2, CDK4, CyclinA and CyclinD1 and enhanced the expression of p27, which has evidenced by qRT-PCR and Western blot analysis.\n\nQuestion:\nDoes knockdown of ZFR suppress cell proliferation and invasion of human pancreatic cancer?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nNADPH oxidase is believed to modulate arterial tone, but its role in humans is still unclear. The objective of this study was to evaluate whether NADPH oxidase is involved in flow-mediated arterial dilation (FMD). Twenty-five patients with hereditary deficiency of gp91(phox), the catalytic core of NADPH oxidase, (X-CGD), 25 healthy subjects, and 25 obese patients matched for sex and age were recruited. FMD, platelet gp91(phox), serum levels of nitrite and nitrate as markers of nitric oxide generation, oxidized low-density lipoprotein, and urinary excretion of isoprostanes as markers of oxidative stress were determined. Platelet gp91(phox) expression was downregulated in X-CGD patients (1.0+/-0.8 mean fluorescence; P<0.001) and upregulated in obese patients (4.1+/-2.2 mean fluorescence; P=0.01) compared with healthy subjects (2.9+/-1.7 mean fluorescence). Urinary excretion of isoprostanes was reduced in X-CGD patients (41.7+/-33.3 pg/mg creatinine; P=0.04) and increased in obese patients (154.4+/-91 pg/mg creatinine; P<0.001) compared with healthy subjects (69.5+/-52.4 pg/mg creatinine). Obese patients had higher serum oxidized low-density lipoprotein than healthy subjects (35.3+/-6.7 versus 24.8+/-9.8 U/L; P<0.001) and X-CGD patients (28.5+/-7.2 U/L; P<0.001). X-CGD patients had significantly higher FMD (14.7+/-5.9%) compared with healthy subjects (7.9+/-2.5%; P<0.001); obese patients had lower FMD (5.3+/-3.0%; P=0.028) compared with healthy subjects. Serum nitrite and nitrate levels were significantly higher in patients with X-CGD (36.0+/-10.8 micromol/L; P=0.016) and lower in obese patients (9.3+/-11.0 micromol/L; P=0.001) compared with healthy subjects (27.1+/-19.1 micromol/L). Serum nitrite and nitrate levels significantly correlated with FMD (R(s)=0.403, P<0.001) and platelet gp91(phox) (R(s)=-0.515, P<0.001). FMD inversely correlated with platelet gp91(phox) (R(s)=-0.502, P<0.001) and isoprostanes (R(s)=-0.513, P<0.001).\n\nQuestion:\nIs hereditary deficiency of gp91 ( phox ) associated with enhanced arterial dilatation : results of a multicenter study?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPosttraumatic stress disorder (PTSD) is common among veterans of the military, with sleep disturbance as a hallmark manifestation. A growing body of research has suggested a link between obstructive sleep apnea and PTSD, potentially due to obstructive sleep apnea (OSA) related sleep disruption, or via other mechanisms. We examined the hypothesis that treatment of OSA with positive airway pressure would reduce PTSD symptoms over 6 months. A prospective study of Veterans with confirmed PTSD and new diagnosis of OSA not yet using PAP therapy were recruited from a Veteran's Affairs sleep medicine clinic. All subjects were instructed to use PAP each night. Assessments were performed at 3 and 6 months. The primary outcome was a reduction in PTSD symptoms at 6 months. Fifty-nine subjects were enrolled; 32 remained in the study at 6 months. A significant reduction in PTSD symptoms, measured by PCL-S score was observed over the course of the study (60.6±2.7 versus 52.3±3.2 points; p < 0.001). Improvement was also seen in measures of sleepiness, sleep quality, and daytime functioning, as well as depression and quality of life. Percentage of nights in which PAP was used, but not mean hours used per night, was predictive of improvement.\n\nQuestion:\nIs treatment of OSA with CPAP Associated with Improvement in PTSD Symptoms among Veterans?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAtherosclerosis is a major cause of cerebrovascular disease. Matrix metalloproteinases (MMPs) play an important role in matrix degradation within the atherosclerotic lesion leading to plaque destabilization and ischemic stroke. We hypothesized that MMP-7 could be involved in this process. Plasma levels of MMP-7 were measured in 182 consecutive patients with moderate (50-69%) or severe (≥70%) internal carotid artery stenosis, and in 23 healthy controls. The mRNA levels of MMP-7 were measured in atherosclerotic carotid plaques with different symptomatology, and based on its localization to macrophages, the in vitro regulation of MMP-7 in primary monocytes was examined. Our major findings were (i) Patients with carotid atherosclerosis had markedly increased plasma levels of MMP-7 compared to healthy controls, with particularly high levels in patients with recent symptoms (i.e., within the last 2 months). (ii) A similar pattern was found within carotid plaques with markedly higher mRNA levels of MMP-7 than in non-atherosclerotic vessels. Particularly high protein levels of MMP-7 levels were found in those with the most recent symptoms. (iii) Immunhistochemistry showed that MMP-7 was localized to macrophages, and in vitro studies in primary monocytes showed that the inflammatory cytokine tumor necrosis factor-α in combination with hypoxia and oxidized LDL markedly increased MMP-7 expression. (iv) During the follow-up of patients with carotid atherosclerosis, high plasma levels of MMP-7 were independently associated with total mortality.\n\nQuestion:\nIs matrix metalloproteinase 7 associated with symptomatic lesions and adverse events in patients with carotid atherosclerosis?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
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] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTrichorhinophalangeal syndrome 1 (Trps1) gene is a member of GATA transcription factor family and has an important function in tumorigenesis and progression. However, there are rare studies on its roles in carcinogenesis and prognostic significance in human osteosarcoma. The expression of Trps1 was detected by immunohistochemistry, and MVD was evaluated to determine the amounts of microvessels by counting CD31-positive endothelial cells. Of the 74 cases that underwent study, Trps1-positive cases were 24. And it was associated with MVD significantly (P = 0.008). The data also exhibited more cases of remote metastasis (P = 0.013) and higher Enneking stage (P = 0.017) in Trps1-positive group compared to Trps1-negative group. Univariate analysis revealed that distant metastasis, MVD and Trps1 expression were associated with a lower 3-year overall survival rate and disease-free survival rate (P = 0.003, and P = 0.012 respectively). Furthermore, Trps1 and distant metastasis retained their significant prognostic effects on patients survival rate by multivariate analysis (P < 0.05).\n\nQuestion:\nDoes overexpression of Trps1 contribute to tumor angiogenesis and poor prognosis of human osteosarcoma?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nChronic rhinosinusitis (CRS) is a common inflammatory disease of the upper airways that is often categorized into subtypes including \"with\" and \"without\" nasal polyps. However, the influence of multiple important epidemiologic factors, including race, on CRS has not been investigated. The present study assessed various phenotypic characteristics of CRS in patients, living in the United States, with different racial backgrounds. We performed a large retrospective cohort study of patients with CRS treated at a large urban tertiary care referral center in Chicago. African American (AA) patients with CRS living in Chicago were more likely to report hyposmia as a symptom of CRS. Furthermore, AA patients with CRS who failed medical therapy and required surgical intervention had a significantly higher frequency of nasal polyposis and aspirin-exacerbated respiratory disease, and a higher disease severity index on computed tomography imaging than did white patients with CRS. The increased polyposis in AAs was associated with increased hospitalization for asthma. There were no differences in the prevalence of atopy, asthma, atopic dermatitis, food allergy, duration of disease, or number of surgeries between different races.\n\nQuestion:\nDo african American Patients with Chronic Rhinosinusitis Have a Distinct Phenotype of Polyposis Associated with Increased Asthma Hospitalization?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nInfarcts in the brain can be divided into larger cortical and smaller deep lacunar infarcts. The pathogenesis differs between these two types of infarctions. This study aims to investigate the relationship between measures of endothelium-dependent vasodilation (EDV) and occurrence of cortical and lacunar infarcts in a population-based sample. In the Prospective Study of the Vasculature in Uppsala Seniors (PIVUS) study, 1016 subjects aged 70 were evaluated by the invasive forearm technique with acetylcholine (EDV) and brachial artery ultrasound to assess flow-mediated vasodilation (FMD). Six to seven years later MRI of the brain was performed, and the prevalence of cortical and lacunar infarcts was visually assessed in 407 randomly selected subjects. Lacunar infarcts were found in 22% and cortical infarcts in 5·9% of the subjects. EDV and FMD were both significantly related to the occurrence of cortical, but not lacunar infarcts. In a model adjusting for gender, waist circumference, body mass index, fasting blood glucose, systolic and diastolic blood pressure, HDL and LDL cholesterol, serum triglycerides, smoking, antihypertensive treatment and statin use, both EDV and FMD were independent predictors of cortical infarcts (P = 0·035 and P = 0·008, respectively).\n\nQuestion:\nIs endothelium-dependent vasodilation related to the occurrence of cortical brain infarcts at MR imaging : The Prospective Investigation of the Vasculature in Uppsala Seniors ( PIVUS ) study?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nOverweight and obesity are becoming more widespread with alarming projections for the coming years. Obesity may increase susceptibility to the adverse effects of PM exposure, exacerbating the effects on cardiovascular diseases and altering the biomarkers of vascular inflammation. The associated biological mechanisms have not been fully understood yet; the common denominator in the pathogenesis of the co-morbidities of obesity is the presence of an active, low-grade inflammatory process. DNA methylation has been shown to regulate inflammatory pathways that are responsible for the development of cardiovascular diseases. The aim of the study was to investigate, in a population of overweight/obese subjects, the effects of PM on blood DNA methylation in genes associated to inflammatory response. Using bisulfite pyrosequencing, we measured DNA methylation in peripheral blood mononuclear cells from 186 overweighted/obese subjects. In particular, we quantified DNA methylation in a set of 3 candidate genes, including CD14, TLR4 and TNF-α, because of the important roles that these genes play in the inflammatory pathway. Personal exposure to PM We found an inverse association between the daily PM\n\nQuestion:\nIs particulate matter exposure associated with inflammatory gene methylation in obese subjects?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThrombocytopenia is a common side effect of tumor chemotherapy, the main management approach to which is based on platelet (PLT) transfusion. However, PLTs, containing angiogenesis regulators, play a major role in boosting tumor growth and metastasis. The purpose of the study was to determine whether PLTs have the capacity to overexpress tumstatin by modified megakaryocyte (MK) and PLT precursors using lentivirus-mediated gene transfer, which might lead to alteration in proangiogenic effect of PLTs. CD34+ hematopoietic stem cells (HSCs) were transduced with recombinant lentivirus carrying tumstatin and induced to produce MKs and PLTs in the culture medium containing a cytokine cocktail. Flow cytometry and aggregation test were used to detect the generation and function of MKs and PLTs. Western blot analysis and confocal microscopy were applied to examine the expression and distribution of tumstatin in transgenic MKs and PLTs. Capillary tube formation of human umbilical vein endothelial cells (HUVECs) was used to evaluate the inhibitory effect of transgenic PLTs. CD34+ HSCs can be efficiently transduced with lentivirus vectors and successfully differentiated into MKs and PLTs. Large amounts of functional MKs and PLTs could be generated and had correct biologic characteristics. The tests demonstrated the feasibility of tumstatin expression in MKs and PLTs under control of the cytomegalovirus promoter, that thus tumstatin was stored in the α-granules of PLTs, and that the releasate of thrombin or A543 cell-stimulated transgenic PLTs obviously inhibited the growth of capillary tube network structures of HUVECs.\n\nQuestion:\nDoes overexpression of tumstatin in genetically modified megakaryocytes change the proangiogenic effect of platelets?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nFluoropyrimidines, oxaliplatin, irinotecan and targeted therapies represent the standard treatment of metastatic colorectal cancer. After failure of all these treatments, few options are available. In such chemorefractory patients the effect of triplet chemotherapy with bevacizumab (FOLFIRINOX bevacizumab) has never been investigated. 49 consecutive patients bearing unresectable metastatic colorectal cancer and who experienced failure to oxaliplatin- and irinotecan-based chemotherapy were treated with oxaliplatin (85 mg/m(2)), irinotecan (180 mg/m(2)), leucovorin (400 mg/m(2)), and fluorouracil (400 mg/m(2) bolus then 2,400 mg/m(2)) repeated every 2 weeks. Median age was 63 (range 36-82) years. After a median follow-up of 12 months, the median progression-free survival was 5.8 months (95% CI 3.4-6.8) and the median overall survival was 11.9 months (95% CI 8-18). The response rate after the cycle was evaluable for 36 patients, whereby we observed 18% (95% CI 8-35) partial or complete response, 45% (95% CI 28-68) stable disease of more than 2 months, and 37% (95% CI 21-58) progression.\n\nQuestion:\nIs fOLFIRINOX bevacizumab a promising therapy for chemorefractory metastatic colorectal cancer?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo assess changes in the prevalence of overweight and obesity among adolescents in urban districts of Ho Chi Minh City between 2002 and 2004. Two surveys were conducted among high school students (11-16 years) in 2002 (n = 1003 students) and 2004 (n = 2684). International Obesity Taskforce (IOTF) sex and age specific BMI cut-offs were used to define overweight and obesity. Underweight was defined as a BMI-for-age z-score <-2, based on the US Centers for Disease Control and Prevention (CDC) 2000 growth reference. In 2002, students completed a questionnaire about household assets. In 2004, parents answered questions about their weight, height, education, occupation, and ownership of 14 household assets. The prevalence of overweight and obesity increased from 5.0% and 0.6% in 2002, to 11.7% and 2.0% in 2004, respectively (p<0.001), while the prevalence of underweight decreased from 13.1% to 6.7%. There was a significant increase in prevalence of overweight and obesity by gender over the two years: the 113% increase in prevalence of overweight and obesity in boys was significantly greater than the 39% increase in girls (p<0.001). The percentage increase in overweight and obesity was considerably lower in adolescents from the poorest households (33%), than from the other quintiles of wealthier households (ranging from 77% to 124%) (p<0.001).\n\nQuestion:\nAre overweight and obesity rapidly emerging among adolescents in Ho Chi Minh City , Vietnam , 2002-2004?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo determine the effectiveness of a multidisciplinary, outpatient pulmonary rehabilitation (PR) program in patients with severe and very severe chronic obstructive pulmonary disease (COPD). PR is recommended in advanced COPD, but there is limited evidence on the effectiveness of PR in reducing health care resources when applied in outpatients. Before and after intervention, a prospective research trial of patients enrolled in a PR program. Outpatient respiratory department in a specialized hospital. We considered prospectively 82 consecutive patients with advanced COPD and finally studied 72 patients who completed the PR intensive phase. PR program. The effectiveness of this PR program was assessed by comparing health resources use from the year before and the year after PR. Clinical variables including dyspnea; the body mass index, obstruction, dyspnea, exercise capacity (BODE) index; and the Chronic Respiratory Questionnaire and health resources use including the number of exacerbations, the number of hospitalizations, and days of hospitalization. Patients had a forced expiratory volume in the first second percentage predicted (mean +/- SD) of 33.0+/-9.8 and a BODE index of 5.0+/-2.0. Significant improvements after PR were found in dyspnea, exercise capacity, and quality of life and on the BODE index (P<.05). Compared with the 12 months before PR, there were also significant reductions during the year after PR on exacerbations (3.4+/-3.5 vs 1.9+/-2.0, P=.002), hospitalizations (2.4+/-2.0 vs 0.9+/-1.2, P<.001), and days of hospitalization (36.1+/-32.7 vs 16.1+/-31.3, P<.001) (ie, a reduction of 44%, 63%, and 55%, respectively; all P<.05).\n\nQuestion:\nDo effectiveness of pulmonary rehabilitation in reducing health resources use in chronic obstructive pulmonary disease?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHypercholesterolemia is an important risk factor for the development of coronary artery disease. Some dietary polyphenols, such as coffee polyphenols (CPPs), reduce cholesterol levels. The mechanism of this cholesterol-lowering effect is not fully understood, although 5-CQA, a major component of CPPs, reportedly inhibits cholesterol biosynthesis. Here, we investigated the mechanism of the cholesterol-lowering effect of CPPs on the basis of cholesterol metabolism-related gene expression in the liver. We also examined the effects of CPPs on vascular lipid accumulation in zebrafish with high cholesterol diet-induced hypercholesterolemia. Over 14 weeks, adult zebrafish were fed a control diet, a high-cholesterol diet, or the latter diet supplemented with CPPs. To measure the extent of vascular lipid accumulation, for 10 days larval zebrafish (which are optically transparent) were fed these same diets with the addition of a fluorescent cholesteryl ester. In adult zebrafish, addition of CPPs to a high-cholesterol diet significantly suppressed the increase in plasma and liver cholesterol levels seen when fish ingested the same diet lacking CPPs. Transcription levels of the liver genes hmgcra (encoding 3-hydroxy-3-methylglutaryl-coenzyme A reductase A, a rate-limiting enzyme in cholesterol biosynthesis) and mtp (encoding microsomal triglyceride transfer protein, a lipid transfer protein required for assembly and secretion of lipoproteins) were significantly lower in fish fed the CPP-containing diet than in fish fed the unsupplemented high-cholesterol diet. In contrast, the expression level of the liver gene cyp7a1a (encoding the cytochrome P450 polypeptide 1a of subfamily A of family 7, a rate-limiting enzyme for bile acid biosynthesis) increased significantly upon consumption of the CPP-containing diet. In larval fish, accumulation of fluorescently labeled cholesterol in the caudal artery was greatly reduced on the CPP-containing diet.\n\nQuestion:\nDo coffee polyphenols exert hypocholesterolemic effects in zebrafish fed a high-cholesterol diet?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe present investigation examines the effects of increasing central nervous system (CNS) levels of nitric oxide (NO), via the administration of L-arginine, on the development of experimental allergic encephalomyelitis (EAE). EAE was induced in male Lewis rats (200-250 g). Normal rats were orally dosed with L-arginine (300 mg/kg body weight) once daily for 12 days. EAE-sensitised animals received L-arginine (300 mg/kg body weight) once daily from day 1 to 12 post-inoculation. Neurological and histological development of EAE were assessed. In addition, CNS cytosol levels of nitrite, superoxide and hydrogen peroxide were measured. Results were analysed using the Mann Whitney U-test and Chi-squared test. L-arginine administration significantly delayed disease onset (p < 0.05) and reduced the severity of neurological (p < 0.05) and histological (p < 0.001) signs of EAE. Treatment with L-arginine caused a significant elevation in CNS nitrite concentrations (p < 0.05) which in EAE-sensitised animals was associated with a concomitant and dramatic decrease in superoxide (p < 0.05) and hydrogen peroxide (p < 0.05) levels.\n\nQuestion:\nDoes l-arginine modify free radical production and the development of experimental allergic encephalomyelitis?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHypoparathyroidism-retardation-dysmorphism (HRD) syndrome, an autosomal recessive disorder characterized by distinct clinical, biochemical, and genetic abnormalities, is characterized by severe short stature, the etiology of which is unclear. Homozygous mutation of the tubulin cofactor E (TBCE) gene leading to loss of four amino acids (c.155-166del12; p.del 52-55) in the TBCE protein has been associated with the syndrome. The aim of the study was to describe the clinical, biochemical, and neuroradiological features of children with genetically proven HRD syndrome. Six children from four independent Middle Eastern pedigrees with clinical features of HRD syndrome were confirmed to have the previously reported homozygous mutation in TBCE (c.155-166del12) and were investigated with magnetic resonance imaging (MRI) of the brain and standard pituitary function testing. Cranial MRI in all children showed severe hypoplasia of the anterior pituitary and corpus callosum, with decreased white matter bulk. Four of five children tested had subnormal GH and cortisol responses to glucagon, and plasma IGF-I concentration was low in all six children. Cortisol response to synacthen was suboptimal in one of three patients tested. Male children (n = 3) had clinical features suggestive of hypogonadotropic hypogonadism.\n\nQuestion:\nIs mutation in the TBCE gene associated with hypoparathyroidism-retardation-dysmorphism syndrome featuring pituitary hormone deficiencies and hypoplasia of the anterior pituitary and the corpus callosum?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nNocturnal hypoxemia is important in precapillary pulmonary hypertension (pPH) as it worsens pulmonary hemodynamics. Whether daytime oxygen saturation (SpO(2)) predicts nocturnal hypoxemia in pPH patients has not been conclusively studied. To investigate the prevalence of nocturnal hypoxemia in comparison to daytime SpO(2) and disease severity in ambulatory patients with pulmonary hypertension. Consecutive patients diagnosed with pPH classified as either pulmonary arterial (PAH) or chronic thromboembolic pPH (CTEPH) had daytime resting and exercise SpO(2) (at the end of a 6-min walk test); thereafter, they underwent overnight pulse oximetry at home. Functional class, pro-brain natriuretic peptide (pro-BNP) and the tricuspid pressure gradient were assessed. Sixty-three patients [median (quartiles) age 62 (53; 71), 43 females] with PAH (n = 44) and CTEPH (n = 19) were included. The resting SpO(2), exercise SpO(2), and mean nocturnal SpO(2) were 95% (92; 96), 88% (81; 95), and 89% (85; 92), respectively. Forty-nine patients (77%) spent >10% of the night with SpO(2) <90% (desaturators), and 33 (52%) spent >50% of the night with SpO(2) <90% (sustained desaturators). The positive predictive values of daytime SpO(2) >90% for being a nocturnal nondesaturator or sustained nondesaturator were 25 and 53%, respectively. Nocturnal SpO(2) was negatively correlated with the tricuspid pressure gradient, but not with functional class, 6-min walk test, or pro-BNP.\n\nQuestion:\nDo daytime measurements underestimate nocturnal oxygen desaturations in pulmonary arterial and chronic thromboembolic pulmonary hypertension?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTumor cells use aerobic glycolysis to rapidly generate ATP and growth substrate which expenses a large amount of glucose. However, how tumor cells take in enough glucose from the tumor microenvironment of insufficient blood supply remains poorly understood. The cellular FLICE-like inhibitory protein (FLIP), a cell apoptosis inhibiting molecule, is highly expressed in hepatocellular carcinoma (HCC) and is implicated in HCC development. The effects of FLIPL (the long form of FLIP) on aerobic glycolysis and glucose uptake were assessed in HCC cells and xenograft tumors. The correlations between FLIPL expression and sodium/glucose cotransporter 1 (SGLT1) expression in clinical HCC tissues were analyzed. The consequences of FLIPL-induced regulation of SGLT1 at the transcription and translation levels and the interaction between FLIPL and SGLT1 were examined. FLIPL-mediated tolerance upon glucose limitation and its mechanism were detected. We report a novel role for FLIPL in promoting the aerobic glycolysis of HCC cells. FLIPL overexpression induced a significant increase in cell aerobic glycolysis indexes including glucose uptake, glucose consumption, and lactate production. FLIPL co-localized and interacted with SGLT1, a major active glucose transporter in HCC cells. FLIPL increased the stability of SGLT1 protein by inhibiting its ubiquitination and degradation. The expression level of FLIPL was positively correlated with the expression level of SGLT1 in 79 HCC tissues from surgical operation. Furthermore, FLIPL increased cell tolerance ability and decreased cell apoptosis to low glucose by regulating SGLT1.\n\nQuestion:\nIs fLIP ( L ) critical for aerobic glycolysis in hepatocellular carcinoma?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCutaneous melanoma represents the most lethal form of skin cancer and remains refractory to current therapies. Failure of treatment has been attributed to the over-expression of ABC transporters which efflux the drugs, below their cytotoxic threshold within cells. Therefore, this study set to investigate; the efficacy of a combinatorial approach comprising chemotherapy (Dacarbazine) and photodynamic therapy (PDT) to overcome resistance in pigmented and unpigmented metastatic melanoma and potentially identify resistant mechanisms. The cytotoxic effect of the chemotherapy, PDT and combination therapy treatment (Dacarbazine+PDT) was determined using a cell viability XTT assay. Thereafter, melanoma cells morphology, self-renewal capacity and ABCG2 protein expression, were determined using fluorescence microscopy, clonogenic assay, western blot and flow cytometry. All results were analyzed by t-test and ANOVA, followed by individual comparisons with post-tests. This study describes possible synergism of PDT+DTIC in reducing melanoma cell viability in vitro. At 24h post-treatment, only the unpigmented melanomas were sensitive to DTIC treatment (20-25% death at 1.25mM). At 48h, a lethal dose of 50% was reached in these cells in contrast to the pigmented melanoma (20% at 48h). The same trend was observed with the combination therapy (DTIC+PDT) at both time points. Furthermore, complete morphological disruption could be observed upon PDT only and PDT+DTIC treatments. Moreover, PDT and DTIC+PDT suppressed the self-renewal capacity of both melanoma cell lines. No significant differences in ABCG2 protein expression was found at 24h post-treatment.\n\nQuestion:\nDoes a combination of photodynamic therapy and chemotherapy display a differential cytotoxic effect on human metastatic melanoma cells?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAlthough foot process effacement is a characteristic alteration of podocytes in the proteinuric state, whether this is the cause or the result of proteinuria is not understood. We studied the morphology and molecular background of foot process effacement in relation to proteinuria, using the passive Heymann nephritis (PHN) model. Foot process effacement was evaluated by electron microscopy. C3 deposition and the expression of alpha 3-integrin, a major adhesion molecule of podocytes, and actin cytoskeleton were examined by immunofluorescent staining. alpha 3-Integrin was also evaluated by immunoelectron microscopy. Western blotting was performed to examine whether anti-Fx1A recognizes alpha 3 beta 1-integrin. Foot process effacement accompanied by decreased expression of alpha 3-integrin was already observed from day 1 after the injection of anti-Fx1A, but albuminuria was not observed until day 5. Complement activation, a key pathogenesis in PHN, was estimated to occur from day 2 after the appearance of foot process effacement. The degree of foot process effacement had not changed before the onset of albuminuria, while after the onset of albuminuria it significantly deteriorated with increased expression of actin. By immunoelectron microscopy, alpha 3-integrin decreased exclusively at the site of deposits. Western blotting showed anti-Fx1A recognizing beta1-integrin.\n\nQuestion:\nIs podocyte foot process effacement in very early phase of passive Heymann nephritis a prerequisite for proteinuria?\n\nAnswer:",
"role": "user"
},
{
"content": "no",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe objective of this study was to assess the efficacy and safety of an alternative surgical incision for bilateral sequential lung transplantation. The vast majority of these operations worldwide have been performed through an anterolateral thoracosternotomy known as the \"clamshell\" incision. Recently, we have undertaken most of these operations through bilateral anterolateral thoracotomies without sternal division. Our medical center performed 262 bilateral sequential single lung transplantations from 1989 to April 1998. Between July 1996 and April 1998 we performed 69 bilateral sequential single lung transplantations on 68 recipients with 52 transplantations being conducted without initial sternal division. We retrospectively reviewed the results of these operations to assess the safety of the altered exposure and the efficacy in avoiding sternal wound complications such as malunion, dehiscence, osteomyelitis, and migrating hardware. Comparison was made to a historical control group composed of the last 50 patients in whom the full clamshell incision was used. Of the 68 patients who underwent transplantations, 52 patients underwent the initial exploratory procedure without sternal division. Two patients required emergency sternal division for institution of cardiopulmonary bypass to control life-threatening bleeding. Eleven of 68 patients were placed on bypass electively to permit transplantation, and the lack of a sternotomy in 8 patients did not present an obstacle to ascending aortic and right atrial cannulation. There were no wound healing complications in the 50 patients for whom the sternum was left intact. In a historical control group of 50 patients who underwent transplantation with sternal division, 34% experienced morbidity or mild disability as a direct result of poor sternal healing.\n\nQuestion:\nDoes bilateral sequential lung transplantation without sternal division eliminate posttransplantation sternal complications?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCytotoxic T-lymphocyte-associated protein 4 (CTLA4) is a strong candidate gene in autoimmunity susceptibility. In particular, the CTLA4 CT60 A/G dimorphism has been associated with celiac disease (CD) and was reported to be strongly associated with autoimmune thyroid disease (AITD). This study aimed to investigate the possible influences of the CTLA4 CT60 A/G polymorphism in the susceptibility of Italian children to CD and in the predisposition to develop AITD in children with CD. We genotyped 317 Italian celiac children, including 44 patients (13.9%) who developed AITD after CD diagnosis and 350 controls. The CTLA4 CT60 GG genotype distribution did not show any significant difference between children with CD and control population (p=0.4). On the contrary, the frequency of the GG genotype was significantly higher in patients with CD complicated with AITD than in control subjects (p=0.002) and CD patients without AITD (p=0.02).\n\nQuestion:\nDoes a common CTLA4 polymorphism confer susceptibility to autoimmune thyroid disease in celiac children?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nNeural crest cells emerge by delamination from the dorsal neural tube and give rise to various components of the peripheral nervous system in vertebrate embryos. These cells change from non-motile into highly motile cells migrating to distant areas before further differentiation. Mechanisms controlling delamination and subsequent migration of neural crest cells are not fully understood. Slit2, a chemorepellant for axonal guidance that repels and stimulates motility of trunk neural crest cells away from the gut has recently been suggested to be a tumor suppressor molecule. The goal of this study was to further investigate the role of Slit2 in trunk neural crest cell migration by constitutive expression in neural crest cells. We found that Slit gain-of-function significantly impaired neural crest cell migration while Slit loss-of-function favored migration. In addition, we observed that the distribution of key cytoskeletal markers was disrupted in both gain and loss of function instances.\n\nQuestion:\nDo slits affect the timely migration of neural crest cells via Robo receptor?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe recently have reported the first randomized, controlled study on the effects of short-term recombinant human growth hormone (rhGH|| therapy on the nutritional status of a group of malnourished adult dialysis patients. In order to evaluate whether rhGH administration exerts any influence on GH, thyrotropin (TSH|| and prolactin (PRL|| responses to TSH-releasing hormone (TRH||, we assessed these responses before and after rhGH therapy. GH, PRL and TSH responses to TRH before and 1 month after rhGH therapy in a group of adult dialysis patients were evaluated. Seventeen dialysis patients (11 on continuous ambulatory peritoneal dialysis/six on haemodialysis|| were studied (rhGH group, n=8; control group, n=9||. In the rhGH group, 0.2 IU/kg/day rhGH was administered subcutaneously. Each patient was tested with TRH (400 microg bolus i.v.|| on two separate occasions, just before and immediately after the treatment period. rhGH treatment did not modify baseline serum GH concentrations (6.6+/-2.7 vs 4.1+/-1.1 microg/l||, paradoxical GH responses to TRH (six out of eight patients||, GH peak (11.9+/-4.6 vs 11.2+/-5.3 microg/l, NS|| or area under the secretory curve of GH (GH AUC; 19.1+/-4.5 vs 12.1+/-3.1 microg/h/l||. Both basal PRL (35.5+/-7.1 vs 36.7+/-8.6 microg/l|| and TSH (2.3+/-1.1 vs 2.8+/-1.7 mU/l|| concentrations, as well as their responses to TRH stimulation (PRL peak, 59.9+/-16.6 vs 59. 5+/-11.8 microg/l; TSH peak, 6.2+/-2.6 vs 7.1+/-3.9 mU/l||, were also unaffected by rhGH therapy.\n\nQuestion:\nDoes short-term recombinant human growth hormone therapy modify growth hormone , thyrotropin and prolactin responses to thyrotropin-releasing hormone in adult dialysis patients?\n\nAnswer:",
"role": "user"
},
{
"content": "no",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMatrix-assisted laser desorption/ionization (MALDI) mass spectrometry (MS) has been demonstrated to be useful for molecular profiling of common solid tumors. Using recently developed MALDI matrices for lipid profiling, we evaluated whether direct tissue MALDI MS analysis on proteins and lipids may classify human breast cancer samples according to the intrinsic subtype. Thirty-four pairs of frozen, resected breast cancer and adjacent normal tissue samples were analyzed using histology-directed, MALDI MS analysis. Sinapinic acid and 2,5-dihydroxybenzoic acid/α-cyano-4-hydroxycinnamic acid were manually deposited on areas of each tissue section enriched in epithelial cells to identify lipid profiles, and mass spectra were acquired using a MALDI-time of flight instrument. Protein and lipid profiles distinguish cancer from adjacent normal tissue samples with the median prediction accuracy of 94.1%. Luminal, HER2+, and triple-negative tumors demonstrated different protein and lipid profiles, as evidenced by permutation P values less than 0.01 for 0.632+ bootstrap cross-validated misclassification rates with all classifiers tested. Discriminatory proteins and lipids were useful for classifying tumors according to the intrinsic subtype with median prediction accuracies of 80.0-81.3% in random test sets.\n\nQuestion:\nDo protein and lipid MALDI profiles classify breast cancers according to the intrinsic subtype?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe investigated the ability of In-111-capromab pendetide to separate patients who have failed radical prostatectomy into categories of those who would versus those who would not respond to salvage radiotherapy. Prostate-specific antigen (PSA) levels in 32 men with prostate cancer who had failed radical prostatectomy and had undergone a whole-body In-111-capromab pendetide scan were followed-up for 13 months (median) after salvage radiotherapy to the pelvis. A logistic regression model was used to determine whether the scan findings, as well as other clinical variables, were associated with a durable complete response (DCR), a nondurable response (NDR), or no response (NR). Sixteen of 23 (70%) men with a normal scan outside the prostatic fossa achieved a DCR after salvage radiotherapy versus two of nine (22%) who had a positive scan outside the prostate fossa and pelvis (P = .0225, Fisher's exact test). Predicted probability (95% confidence interval [CI]) that a DCR would be obtained with a normal scan was 0.88 (0.55 to 0.98); for men with a positive scan limited to the prostatic fossa it was 0.62 (0.42 to 0.79); and for men with a positive scan outside the pelvis it was 0.27 (0.09 to 0.58). No other variables before radiotherapy showed a significant association with the DCR rate.\n\nQuestion:\nDoes radioimmunoscintigraphy with In-111-labeled capromab pendetide predict prostate cancer response to salvage radiotherapy after failed radical prostatectomy?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\n4-Methylumbelliferone (4-MU), a hyaluronan (HA) synthesis inhibitor, has antitumor activity in cancer cells. However, few studies have focused on its effects on ovarian cancer. The aim of this study was to investigate the effects of 4-MU on ovarian cancer and to elucidate its mechanism of action. The HRA human ovarian serous adenocarcinoma cell line was used in this study. The effects of 4-MU on cell proliferation, migration, and invasion were determined by using in vitro assays as well as an in vivo rat peritoneal carcinomatosis model. The expression of HA synthase (HAS), CD44 HA receptor, vascular endothelial growth factor (VEGF), and thymidine phosphorylase (TP) mRNA in HRA cells was analyzed by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). 4-MU administration inhibited the growth of peritoneal tumors and significantly prolonged survival. In vitro experiments showed that 4-MU inhibited HRA cell proliferation in a dose-dependent manner, while it did not affect HRA cell invasion and migration. 4-MU significantly decreased TP mRNA expression in HRA cells. On the other hand, since HAS2, CD44, and VEGF endogenous mRNA expression levels were very low in HRA cells, it was impossible to evaluate the effect of 4-MU treatment.\n\nQuestion:\nDoes 4-Methylumbelliferone inhibit ovarian cancer growth by suppressing thymidine phosphorylase expression?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nChronic skin inflammation in atopic dermatitis (AD) is associated with elevated expression of proinflammatory genes and activation of innate immune responses in keratinocytes. microRNAs (miRNAs) are short, single-stranded RNA molecules that silence genes via the degradation of target mRNAs or inhibition of translation. The aim of this study was to investigate the role of miR-146a in skin inflammation in AD. RNA and protein expression was analyzed using miRNA and mRNA arrays, RT-quantitative PCR, Western blotting, and immunonohistochemistry. Transfection of miR-146a precursors and inhibitors into human primary keratinocytes, luciferase assays, and MC903-dependent mouse model of AD were used to study miR-146a function. We show that miR-146a expression is increased in keratinocytes and chronic lesional skin of patients with AD. miR-146a inhibited the expression of numerous proinflammatory factors, including IFN-γ-inducible and AD-associated genes CCL5, CCL8, and ubiquitin D (UBD) in human primary keratinocytes stimulated with IFN-γ, TNF-α, or IL-1β. In a mouse model of AD, miR-146a-deficient mice developed stronger inflammation characterized by increased accumulation of infiltrating cells in the dermis, elevated expression of IFN-γ, CCL5, CCL8, and UBD in the skin, and IFN-γ, IL-1β, and UBD in draining lymph nodes. Both tissue culture and in vivo experiments in mice demonstrated that miR-146a-mediated suppression in allergic skin inflammation partially occurs through direct targeting of upstream nuclear factor kappa B signal transducers caspase recruitment domain-containing protein 10 and IL-1 receptor-associated kinase 1. In addition, human CCL5 was determined as a novel, direct target of miR-146a.\n\nQuestion:\nDoes microRNA-146a alleviate chronic skin inflammation in atopic dermatitis through suppression of innate immune responses in keratinocytes?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIn recent years, obesity has become a global epidemic, highlighting the necessity for basic research into mechanisms underlying growth of adipose tissue and differentiation of stem cells into adipocytes, in humans. For better understanding of cell signalling in adipogenesis, the role of DNER (delta/Notch-like EGF-related receptor) in adipogenic differentiation of human adipose tissue-derived mesenchymal stem cells (hAMSC) was investigated. To assess the role of DNER in hAMSC adipogenesis, hAMSCs were transfected with DNER small interfering RNA (siDNER). Real-time quantitative reverse transcriptase polymerase chain reactions to assess expression levels of adipogenesis-related genes regulated by siDNER, cell cycle and immunoblot analyses were performed. First, it was determined that DNER mRNA was profoundly expressed in hAMSCs and reduced during adipogenic differentiation. Knockdown of DNER altered cell morphology, inhibited proliferation and increased frequency and efficiency of adipogenesis in hAMSC. Expression of CCAAT/enhancer-binding protein delta increased and proportion of cells in S phase decreased by knockdown of DNER, using specific siRNA. Moreover, adipocyte-specific genes including peroxisome proliferator-activated receptor gamma, fatty acid binding protein 4 and perilipin were up-regulated in siDNER compared to the siControl group during adipogenesis in hAMSC.\n\nQuestion:\nDoes dNER modulate adipogenesis of human adipose tissue-derived mesenchymal stem cells via regulation of cell proliferation?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nOur purpose was to determine whether patients prefer immediate or delayed results of screening mammography and to determine the cost of immediate reporting at our institution. A survey was anonymously and randomly distributed to 129 women who were 35-70 years old during a visit to their primary care physician, asking the women's preference for receiving mammography results by one of two systems: by letter with a return visit for any additional tests; or by speaking at once with the radiologist, with the option of additional tests being performed during the same visit. Patients' willingness to pay for the latter service was also determined. A cost identification model was constructed using commercially available software. We considered the impact on radiologists' and technologists' time and the need for additional equipment and space, and we analyzed the effect on the cost of immediate reporting. One hundred twenty (93%) surveys were completed. Eighty women (67%) preferred immediate reporting, and 62 (78%) of these 80 patients would wait 30-60 min. The additional cost of immediate reporting is $28.22 per patient. Only 11% of patients were willing to pay this additional cost. When new equipment and space were not required, the cost would increase by $4.38. This cost was most influenced by the time required to give patients normal results.\n\nQuestion:\nIs patient expectations and costs of immediate reporting of screening mammography : talk n't cheap?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nInterferon alfa has been suggested as a possible treatment for choroidal neovascularization. However, retinal complications following interferon therapy have been reported. To evaluate the effects of interferon alfa on leukocyte dynamics in the rat retinal microcirculation. Interferon alfa of different doses was intravenously administered in rats. Leukocyte dynamics were observed with acridine orange digital fluorography, which uses a nuclear fluorescent dye of acridine orange and scanning laser ophthalmoscopy. This technique allows visualization of leukocyte movements in the retinal microcirculation in vivo. After interferon alfa was administered, leukocytes adhered to vascular walls and became trapped in the retinal microcirculation. Leukocyte trapping was dose-dependent.\n\nQuestion:\nDoes interferon alfa induce leukocyte capillary trapping in rat retinal microcirculation?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nNo therapy for fibrotic disease is available. The proadhesive matricellular protein connective tissue growth factor CCN2 is a marker of fibrotic cells; however, the specific role of CCN2 in connective tissue biology in general and in fibrogenesis in particular is unclear. The aim of this study was to assess whether adult mice bearing a smooth muscle cell/fibroblast-specific deletion of CCN2 are resistant to bleomycin-induced skin scleroderma. Cutaneous fibrosis was induced in mice by subcutaneous injection of bleomycin. Untreated control groups were injected with phosphate buffered saline. Mice bearing a fibroblast/smooth muscle cell-specific deletion of CCN2 were investigated for changes in dermal thickness, collagen content, and the number of α-smooth muscle actin (α-SMA)-positive cells. Dermal fibroblasts were isolated to assess whether the induction of collagen and α-SMA messenger RNA in response to transforming growth factor β (TGFβ) was impaired. The loss of CCN2 resulted in resistance to bleomycin-induced skin fibrosis. In response to bleomycin, wild-type mice possessed, but CCN2-deficient mice lacked, abundant α-SMA-expressing myofibroblasts within fibrotic lesions. Fibroblast responses to TGFβ, a potent inducer of myofibroblast differentiation, were not affected. Collectively, these results indicate that CCN2 is essential for bleomycin-induced skin fibrosis, likely due to a defect in myofibroblast recruitment.\n\nQuestion:\nIs cCN2 required for bleomycin-induced skin fibrosis in mice?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe cardiac biomarkers cardiac Troponin T (cTNT) and NT-proBNP tend to be elevated in nearly all hemodialysis patients. The high percentage and magnitude of these increased molecules is associated with cardiovascular morbidity and mortality in hemodialysis patients. This study investigates the impact of the dialysis procedure itself on cardiac biomarkers. Standard chronic hemodialysis lasting 4-5 hs 3 times weekly and using polysulfone dialyzers (high-flux and low-flux) was performed. Blood flow rates varied between 250-350 ml/min. The cTNT levels of 49 chronic hemodialysis patients were measured twice (interval of 6 weeks) before and after a hemodialysis session by a third-generation assay (Elecsys Analyzer, Roche Diagnostics, Mannheim, Germany). NT-proBNP levels were measured with polyclonal antibodies capable of recognizing the N-terminal fragment of BNP. In a follow-up period of 42 months, cardiovascular events and death were assessed. The median concentration of cTNT prior to hemodialysis was 0.024 ng/ml (< 0.001-0.703). All dialysis patients presented high plasma levels of NT-proBNP (median 4,885 pg/ml). Oligoanuric patients had significantly higher cTNT and NT-proBNP levels prior to dialysis compared to patients with normal diuresis (p < 0.0001). cTNT and NT-proBNP levels increased significantly during the hemodialysis sessions in which a low-flux dialyzer was used (p < 0.0001) but remained unchanged when a high-flux dialyzer was utilized. Neither the predialytic nor the interdialytic changes in cTNT and NT-proBNP levels were influenced by blood flow. NT-proBNP levels increased markedly during hemodialysis sessions (p < 0.005) utilizing the low-flux dialyzer. Patients with a non-native fistula had significantly higher predialysis cTNT and NT-proBNP levels (p < 0.05). Patients with cardiovascular events had a significantly higher cTNT and NT-proBNP at the beginning of the study.\n\nQuestion:\nAre cardiac biomarkers influenced by dialysis characteristics?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nRecent studies have demonstrated the overexpression of cyclooxygenase-2 (COX-2) in endometriosis. The aim of this study was to investigate the correlation between COX-2 expression and the clinical outcome rate in a homogeneous series of patients undergoing fertility-sparing complete laparoscopic ablation for severe endometriosis. COX-2 expression was analysed by immunohistochemistry in 103 samples, 71 endometriomas (group 1) and 32 peritoneal implants and or recto-vaginal nodules (group 2) of endometriotic tissue from 85 patients submitted to complete laparoscopic ablation of severe endometriosis. At median follow-up of 54 months, a recurrence rate of 24.7% (n = 21) was observed. Patients with COX-2-positive endometriotic cysts showed a lower relapse rate than COX-2-negative cases (16.7 versus 41.2%; P = 0.036). Patients with COX-2-positive peritoneal implant and or recto-vaginal nodule showed a similar trend. Taking the two groups of patients together, we found a significantly lower relapse rate in COX-2-positive patients in comparison to COX-2-negative patients (16.4 versus 40%; P = 0.0152). Moreover, COX-2-positive patients showed a longer relapse-free survival in comparison to COX-2-negative patients (P = 0.016).\n\nQuestion:\nIs increased cyclooxygenase-2 expression associated with better clinical outcome in patients submitted to complete ablation for severe endometriosis?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMonocyte chemoattractant protein-1 (MCP-1) is a chemokine that has various roles in tumor development and progression. We previously reported that expression of MCP-1 is associated with macrophage infiltration and tumor vessel density in human gastric carcinomas. The present study was undertaken to obtain direct evidence that MCP-1 participates in recruitment of macrophages and induction of angiogenesis. We did transfection experiments to analyze the role of MCP-1 in tumorigenicity and angiogenesis in gastric carcinoma in nude mice. The human MCP-1 gene cloned into the BCMGS-Neo expression vector was transfected into the human gastric carcinoma TMK-1 cell line. We examined tumor volumes with the ectopic s.c. xenograft model and tumorigenicity with the orthotopic gastric xenograft model. We determined intratumor microvessel counts and tumor-infiltrating macrophage counts by immunohistochemical staining. There was no difference in in vitro proliferation between MCP-1-transfected TMK-1 cells and mock-transfected (control) cells; however, MCP-1 transfectants induced tumor growth in ectopic xenografts and increased tumorigenicity and induced lymph node metastases and ascites in orthotopic xenografts. In both ectopic and orthotopic xenograft models, strong infiltration of macrophages was observed within and around the tumors after implantation of MCP-1 transfectants whereas fewer macrophages were seen after inoculation of control cells. The microvessel density was significantly higher in tumors produced by MCP-1 transfectants than in control tumors.\n\nQuestion:\nDoes monocyte chemoattractant protein-1 transfection induce angiogenesis and tumorigenesis of gastric carcinoma in nude mice via macrophage recruitment?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nDevelopmental language disorder is a heterogeneous diagnostic category. Little research has compared the long-term outcomes of children with different subtypes of language impairment. To determine whether the pattern of language impairment in childhood related to language and literacy outcomes in adulthood. Adults who took part in previous studies as children were traced. There were four groups of participants, each with a different childhood diagnosis: specific language impairment (SLI; n = 19, mean age at follow-up = 24;8), pragmatic language impairment (PLI; n = 7, mean age at follow-up = 22;3), autism spectrum disorder (ASD; n = 11; mean age at follow-up = 21;9), and no childhood diagnosis (typical; n = 12; mean age at follow-up = 21;6). Participants were administered a battery of language and literacy tests. Adults with a history of SLI had persisting language impairment as well as considerable literacy difficulties. Pragmatic deficits also appeared to develop over time in these individuals. The PLI group had enduring difficulties with language use, but presented with relatively intact language and literacy skills. Although there were some similarities in the language profile of the PLI and ASD groups, the ASD group was found to have more severe pragmatic deficits and parent-reported linguistic difficulties in conversational speech.\n\nQuestion:\nDo qualitative aspects of developmental language impairment relate to language and literacy outcome in adulthood?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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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:\nEpratuzumab, a humanized anti-CD22 monoclonal antibody, is under investigation as a therapeutic antibody in non-Hodgkin's lymphoma and systemic lupus erythematosus (SLE), but its mechanism of action on B-cells remains elusive. Treatment of SLE patients with epratuzumab leads to a reduction of circulating CD27(negative) B-cells, although epratuzumab is weakly cytotoxic to B-cells in vitro. Therefore, potential effects of epratuzumab on adhesion molecule expression and the migration of B-cells have been evaluated. Epratuzumab binding specificity and the surface expression of adhesion molecules (CD62L, β7 integrin and β1 integrin) after culture with epratuzumab was studied on B-cell subsets of SLE patients by flow cytometry. In addition, in vitro transwell migration assays were performed to analyze the effects of epratuzumab on migration towards different chemokines such as CXCL12, CXCL13 or to CXCR3 ligands, and to assess the functional consequences of altered adhesion molecule expression. Epratuzumab binding was considerably higher on B-cells relative to other cell types assessed. No binding of epratuzumab was observed on T-cells, while weak non-specific binding of epratuzumab on monocytes was noted. On B-cells, binding of epratuzumab was particularly enhanced on CD27(negative) B-cells compared to CD27(positive) B-cells, primarily related to a higher expression of CD22 on CD27(negative) B-cells. Moreover, epratuzumab binding led to a decrease in the cell surface expression of CD62L and β7 integrin, while the expression of β1 integrin was enhanced. The effects on the pattern of adhesion molecule expression observed with epratuzumab were principally confined to a fraction of the CD27(negative) B-cell subpopulation and were associated with enhanced spontaneous migration of B-cells. Furthermore, epratuzumab also enhanced the migration of CD27(negative) B-cells towards the chemokine CXCL12.\n\nQuestion:\nDoes epratuzumab targeting of CD22 affect adhesion molecule expression and migration of B-cells in systemic lupus erythematosus?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAllopregnanolone is a neurosteroid produced in the brain that can alter the excitability of the CNS. Neurosteroids have neuroprotective properties, and their elevation in response to stress may protect the newborn brain following infection or hypoxia. Infection, particularly of the respiratory tract, may lead to episodes of hypoxia. Infection and hypoxia have been identified as factors contributing to neonatal morbidity and mortality. To determine the effect of acute episodes of hypoxia alone or in combination with lipopolysaccharide (LPS) exposure on plasma and brain allopregnanolone concentrations in lambs 10-21 days old. Also, to examine plasma levels of cortisol and the cytokines, tumour necrosis factor-alpha and interleutkin-6 after these challenges. Allopregnanolone concentrations in the brain were markedly increased after hypoxia. Hypoxia following prior LPS treatment resulted in greater increases in brain allopregnanolone concentrations compared to either the LPS or hypoxia treatment alone. Importantly, brain regions unaffected by LPS or hypoxia alone (thalamus/hypothalamus, cerebellum) showed significant increases of allopregnanolone content following the combined LPS and hypoxia treatments. Plasma tumour necrosis factor-alpha and interleukin-6 concentrations were increased after LPS treatment with and without hypoxia, but not by hypoxia alone. In contrast, plasma cortisol concentrations were increased after both stressors.\n\nQuestion:\nDoes hypoxia potentiate endotoxin-induced allopregnanolone concentrations in the newborn brain?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMagnesium supplementation is an effective protective method against cisplatin-induced nephrotoxicity (CIN); however, there are few reports regarding the mechanism of its nephroprotective effect. The aim of this study was to determine whether premedication with intravenous magnesium prevents CIN and to determine the relationship between its nephroprotective effect and serum magnesium level. Fifty-eight patients with head and neck cancer who received cisplatin, docetaxel, and 5-fluorouracil (DCF) were retrospectively investigated. Grade 2 or more serum creatinine elevation was defined as CIN. The incidence of CIN was compared between a magnesium sulfate (20 mEq, 2.46 g) premedication group and a non-magnesium group during the first cycle and in all cycles. CIN did not occur in any patients receiving magnesium premedication but did occur in 5 of 29 patients during the first cycle and in 6 patients during all subsequent cycles in patients who did not receive magnesium premedication. Furthermore, the variation of creatinine clearance was significantly worse in the non-magnesium group than in the magnesium premedication group from baseline. There was no difference in adverse effects or response rate between the two groups. Univariate analysis suggested that magnesium premedication significantly reduced the risk of CIN. On the other hand, serum magnesium depletion was seen in both groups to equal degrees despite supplementation.\n\nQuestion:\nDoes premedication with intravenous magnesium have a protective effect against cisplatin-induced nephrotoxicity?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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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:\nClinically evident renal disease (dialysis, history of renal insufficiency, or serum creatinine >2.0 mg/dL) is a known risk factor for mortality after thoracoabdominal aortic aneurysm repair. We extended this concept to the questions of whether subclinical renal disease is also a risk factor and how best to identify subclinical disease. We hypothesized that the glomerular filtration rate (GFR) would be a more sensitive determinant of renal function than serum creatinine alone. Between 1991 and 2004, we repaired 1106 thoracoabdominal aortic aneurysms and descending thoracic aortic aneurysms. The median age was 67 years. There were 400 (36%) women and 706 (64%) men. We estimated GFR by using the Cockcroft-Gault equation. We divided baseline serum creatinine and baseline GFR into quartiles and estimated the association of the quartiles with 30-day postoperative mortality by chi2 testing. We further subdivided the population into patients with and without clinically evident renal disease and repeated the analysis in the patients without clinically apparent disease (n = 869). Clinically apparent renal disease was highly associated with 30-day mortality (odds ratio, 3.2; P < .0001). In all patients, serum creatinine quartile and GFR quartile were also both highly significantly associated with 30-day mortality (P < .0001). In patients without clinically apparent renal disease, both creatinine and GFR predicted additional mortality, but GFR was a much stronger predictor (P < .02 for creatinine vs < .0001 for GFR). In these patients, mortality ranged from 5% in the best GFR quartile to 27% in the worst. Taken as continuous variables in logistic regression equations, serum creatinine had no discrimination in patients without clinical disease (P = .73), whereas GFR remained strong (P < .0001).\n\nQuestion:\nIs glomerular filtration rate superior to serum creatinine for prediction of mortality after thoracoabdominal aortic surgery?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe use data from rural Nepal and South India to compare the prevalence of small-for-gestational-age (SGA) and neonatal mortality risk associated with SGA using different birth-weight-for-gestation reference populations. We identified 46 reference populations in low-, middle-, and high-income countries, of which 26 met the inclusion criteria of being commonly cited and having numeric 10th percentile cut points published. Those reference populations were then applied to populations from two community-based studies to determine SGA prevalence and its relative risk of neonatal mortality. The prevalence of SGA ranged from 10.5% to 72.5% in Nepal, and 12.0% to 78.4% in India, depending on the reference population. Females had higher rates of SGA than males using reference populations that were not sex specific. SGA prevalence was lowest when using reference populations from low-income countries. Infants who were both preterm and SGA had much higher mortality risk than those who were term and appropriate-for-gestational-age. Risk ratios for those who are both preterm and SGA ranged from 7.34-17.98 in Nepal and 5.29-11.98 in India, depending on the reference population.\n\nQuestion:\nDoes prevalence of small-for-gestational-age and its mortality risk vary by choice of birth-weight-for-gestation reference population?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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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:\nSplenomegaly is a characteristic symptom of schistosome infection. Unlike the well known hepatic pathology of schistosomiasis, splenomegaly has received little scientific research and is generally considered to be a non-specific congestion caused by increased blood pressure within the venous sinuses. Moreover, to date, few studies have reported the deposition of schistosome eggs in the spleen. In a previous study, however, we observed that prolonged S. japonicum infections destroyed the structure of the lymphoid follicles in the spleen of mice at 8 weeks post-infection and found that eggs were frequently deposited in the spleen. These prior observations suggested a relationship between granulomas and splenic morphology which we investigate further in this study. C57BL/6 mice were infected percutaneously with twenty cercariae of S. japonicum and sacrificed at different times post-infection. The number of eggs present in the homogenates of spleens and livers was quantified by light microscopy. Splenic pathology was observed by immunohistochemistry staining of paraffin-embedded sections. At 18 weeks post-infection the infected mice were divided into two groups (granulomatous spleens and non-granulomatous spleens). Serum antibodies and cytokines in the antigen- or mitogen-stimulated lymphocyte cultures were then determined by ELISA. We found that eggs deposition in the spleens of infected mice occurred frequently but only occasionally led to granulomas formation. The lymphoid follicles within the granulomatous spleens maintained their structural integrity until 20 weeks post-infection, unlike the lymphoid follicles in spleens without egg granulomas. Mice with granulomatous spleens accompanied by lymphoid follicles exhibited a germinal center (GC)-like structure and had enhanced humoral immune responses. Splenocytes from granulomatous spleens also showed significantly elevated levels of Th2 cytokines during late infection stages.\n\nQuestion:\nDoes the formation of egg granulomas in the spleens of mice with late Schistosoma japonicum infection alter splenic morphology?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCD26, a multifunctional T cell surface glycoprotein, is a type II transmembrane protein containing only six amino acid residues in its cytoplasmic region. In addition to its membrane form, CD26 exists in plasma in a soluble form (sCD26), which is thought to be the extracellular domain of the molecule cleaved from the cell surface. Recent studies indicated CD26 have an important role in the pathogenesis of asthma, known as Th2 like disease. The function of CD26 in the esosinophlic lung disease is not well understood. Serum sCD26 was determined by enzyme-linked immunosorbent assay in patients with acute eosinophilic pneumonia, chronic eosinophilic pneumonia (CEP), and sarcoidosis, and in healthy volunteers, to establish its value for discriminating between disease entities and as marker of disease activity. Soluble CD26 was significantly reduced in CEP and was related to disease severity. In particular, sCD26 was inversely correlated with arterial oxygen tension in CEP.\n\nQuestion:\nIs soluble CD26 inversely Associated with Disease Severity in Patients with Chronic Eosinophilic Pneumonia?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTransforming growth factor beta is recognized as a major cytokine in extracellular matrix (ECM) pathobiology as occurs in diabetic nephropathy. While experimental studies have advanced a protective role of carnosine for diabetic complications, a link between carnosine, TGF-β and matrix accumulation remains to be elucidated. In the present study, we tested the hypothesis that L-carnosine inhibits TGF-β production and signalling, thereby reducing hyperglycaemia-associated ECM accumulation. Human mesangial cells (MC) were cultured in high-glucose (HG, 25 mM D-glucose) medium alone or in HG medium to which 20 mM L-carnosine was added. Collagen VI (Col6) and fibronectin (FN) deposition and messenger RNA expression were studied. In addition, TGF-β production and activation of Smad1/5/8 (ALK1) and Smad2/3 (ALK5) pathways were assessed. Under HG conditions, deposition of Col6 and FN were increased 1.4- and 1.6-fold. This was significantly inhibited on the protein and messenger RNA level by L-carnosine. TGF-β production increased under HG conditions but was completely normalized by addition of L-carnosine. Addition of exogenous TGF-β could not overcome the effect of L-carnosine on Col6 and FN expression, indicating additionally interference with TGF-β downstream signalling. Along the same line, L-carnosine reduced TGF-β-mediated Smad2 phosphorylation, suggesting an inhibitory effect on ALK5 signalling. ALK1 signalling remained unchanged. Under HG conditions, pharmacologic inhibition of ALK5 prevented Col6 accumulation but did not change FN deposition.\n\nQuestion:\nDoes l-carnosine inhibit high-glucose-mediated matrix accumulation in human mesangial cells by interfering with TGF-β production and signalling?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe optimal therapy for adult steroid-resistant nephrotic syndrome (SRNS) remains a therapeutic challenge. We investigated the efficacy and safety of tacrolimus as a promising regimen in Chinese adult patients. A prospective, multicenter trial was conducted in 9 nephrology centers from 2006 to 2008, in patients with SRNS (defined as failure to respond to 1 mg/kg/day of prednisone for 8, and 16 weeks, in focal segmental glomerulosclerosis). Patients were treated with tacrolimus (TAC) plus prednisone for 12 months. TAC dose was titrated to achieve a target trough blood concentration of 5-10 ng/ml for the first 6 months and 4-6 ng/ml for the subsequent 6 months. The primary outcomes included complete or partial remission [complete remission (CR): proteinuria <0.3 g/24 h, with serum albumin ≥ 3.5 g/dl and stable renal function; partial remission (PR): proteinuria between 0.3 and 3.5 g/24 h and a decrease of at least 50 % from the baseline level, with serum albumin ≥ 3.0 g/dl and stable renal function]. Secondary end-points included relapse rate, changes of clinical parameters (proteinuria, serum albumin, and lipid profile) and adverse events. Twenty-four patients with SRNS were enrolled. After 6 months of therapy, CR was achieved in 58.3 % of patients and PR in 16.7 %, yielding a final response rate of 75.0 %. The decrease in proteinuria was 43.1 ± 17.5 % after the first month of treatment (P < 0.001). Complete or PR was achieved in 6 of 8 patients with minimal change disease, 4 of 6 patients with mesangioproliferative glomerulonephritis (MsPGN), 6 of 7 patients with focal segmental glomerulosclerosis (FSGS), and all 2 patients with IgA nephropathy. Two patients (1 with MsPGN and 1 with FSGS) experienced relapses during the subsequent 6 months of follow-up. Adverse events included infection, hand tremor, diarrhea, acute reversible or persistent nephrotoxicity.\n\nQuestion:\nIs tacrolimus an alternative therapy option for the treatment of adult steroid-resistant nephrotic syndrome : a prospective , multicenter clinical trial?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nVitamin D is important in normal brain development. In animals low vitamin D level is associated with brain morphological alterations including enlargement of the brain. Whether a similar association exists in humans is unknown. Here we investigated the relationship between vitamin D and total intracranial volume as well as total volume of the cortical grey and cerebral white matter and that of the ventricles in young healthy women. To assess volumes we applied semi-automatic user-independent MR volumetry. For the vitamin D measurements automated electrochemiluminescence immunoassay was used. We found a significant negative correlation between vitamin D and total intracranial volume as well as total cortical grey and cerebral white matter volumes.\n\nQuestion:\nDoes intracranial volume inversely correlate with serum 25 ( OH ) D level in healthy young women?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nLiposuction-curettage (LC) is an effective surgical therapy option for axillary hyperhidrosis, with less scarring compared with radical excision of axillary skin. Although this method has proven to be effective, the treatment of nonresponders to minimally invasive surgery has not been previously defined. Whether these patients benefit from a second surgical procedure has not been evaluated so far. To investigate efficacy and side-effects of a second LC with an aggressive rasping cannula in patients with insufficient prior surgery. Nineteen nonresponders to prior LC (13 female and six male) underwent a second LC with a rasping cannula. Gravimetry was performed before and 8 months after surgery. Side-effects, patient satisfaction, the surgeons' intraoperative evaluation and the Vancouver Scar Scale (VSS) before and after surgery were documented. Sweat rates showed a reduction of 69% in 17 (89%) patients. Two patients (11%) did not respond to surgery. Eighty-four per cent of all patients were completely satisfied or satisfied with postoperative results. No severe side-effects were observed. The surgeon reported slightly increased difficulties during dissection of dermis from subcutaneous fat in three patients. Assessment of scars showed an excellent aesthetic outcome (mean VSS 0.79 before vs. 1.1 after surgery).\n\nQuestion:\nIs repeat liposuction-curettage treatment of axillary hyperhidrosis safe and effective?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThickening and reduplication of the tubular basement membrane have been reported as early events in diabetic nephropathy. In this study, we have examined the polar requirements of proximal tubular cells for the d-glucose-stimulated accumulation of fibronectin and the mechanism by which this occurred, with particular emphasis on the polyol pathway. To determine the polarity of fibronectin generation in response to glucose, LLC-PK1 cells were grown on porous tissue culture inserts. Monolayer confluence was determined by serial measurement of transepithelial resistance. Confluent cells were growth arrested by serum deprivation, and all experiments were performed under serum-free conditions. Application of 25 mm d-glucose to either the apical or basolateral aspect of LLC-PK1 cells led to fibronectin accumulation in the basolateral compartment. This reached statistical significance 24 hours following apical addition of glucose (2.6-fold increase compared with 5 mm d-glucose, P = 0.0025, N = 6 vs. N = 4 controls) and 12 hours after the basolateral addition of glucose (2.5-fold increase compared with 5 mm d-glucose, P = 0.03, N = 6 vs. N = 4 controls). Exposure of cells to glucose at either their apical or basolateral aspect leads to accumulation of intracellular glucose and polyol pathway activation, as assessed by sorbitol accumulation. The increase in fibronectin concentration in response to glucose was inhibited by the aldose reductase inhibitor sorbinil. At a dose of 100 micron sorbinil, there was a 59% inhibition of fibronectin accumulation in response to apical glucose (P = 0.004, N = 3 sorbinil vs. N = 4 controls) and a 66% inhibition in response to basolateral glucose (P = 0.008, N = 3 sorbinil vs. N = 4 controls) 48 hours after the addition of the inhibitor. Furthermore, fibronectin accumulation was also demonstrated following both the apical and basolateral addition of 1 mm sorbitol, but not following the addition of 25 mm galactose to either aspect of the cells. Following the addition of sorbitol, there was a 2. 8-fold increase in fibronectin 48 hours after apical stimulation (P = 0.01, N = 3 treated vs. N = 4 control) and a 2.27-fold increase following basolateral stimulation (P = 0.04, N = 3 treated vs. N = 4 control) at 24 hours.\n\nQuestion:\nIs renal proximal tubular cell fibronectin accumulation in response to glucose polyol pathway dependent?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nExperimental animal study. To investigate the neuroprotective efficacy of this magnesium in polyethylene glycol (PEG) formulation in a contusive model of cervical spinal cord injury (SCI). Intravenously administered magnesium has been extensively investigated as a neuroprotective agent in animal models of SCI, stroke, and traumatic brain injuries, and has been evaluated in large scale clinical trials for the latter 2 indications. We have developed a novel formulation of magnesium chloride (MgCl₂) within PEG, and have previously demonstrated the neuroprotective benefit of this formulation in animal models of thoracic SCI. Twenty-two Sprague Dawley rats underwent a unilateral cervical hemicontusion at C4-C5 and were randomized 2 hours later to either the MgCl₂ in PEG formulation, or normal saline. Each treatment was administered in 5 intravenous infusions spaced 6 hours apart. Behavioral recovery was assessed over 6 weeks, after which the cord was analyzed to measure the extent of gray matter and white matter sparing through the injury site. In the horizontal ladder test, the percentage of forelimb errors made by the animals treated with MgCl₂ in PEG formulation was significantly lower than the saline-treated controls. Histologic analysis also revealed a significantly higher cumulative white matter sparing through the injury site in the MgCl₂ in PEG group.\n\nQuestion:\nDoes magnesium in a polyethylene glycol formulation provide neuroprotection after unilateral cervical spinal cord injury?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nFrequent beta-catenin mutations have been detected in juvenile angiofibromas, but the tumor pathogenesis remains unknown. Metaphase-comparative genomic hybridization (CGH) was used to identify chromosomal aberrations in 29 tumor specimens. Two tumors were investigated using genome DNA microarrays. Three hundred eleven chromosomal gains and losses were detected by metaphase-CGH. Frequent chromosomal gains were detected at 4q, 6, 12, and X, while frequent chromosomal losses affected regions of chromosomes 8, 16, 17, 22, and Y. Genome DNA microarray analysis in 2 tumors of the series confirmed chromosomal aberrations, detected by metaphase-CGH, and indicated genes such as AURKA (20q13.2) not being recognized by metaphase-CGH.\n\nQuestion:\nDoes comprehensive genomic analysis identify MDM2 and AURKA as novel amplified genes in juvenile angiofibromas?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nRecent studies demonstrating a role for plasminogen activator inhibitor (PAI)-1 in cholestatic liver disease in mice suggested that tissue-type plasminogen activator (tPA) or urokinase plasminogen activator (uPA) might be important after biliary tract obstruction. We now demonstrate that blocking tPA exacerbates liver injury after bile duct ligation (BDL). tPA deficient mice have increased bile infarcts, increased TUNEL positive cells, increased neutrophil infiltration, reduced hepatocyte proliferation and reduced ductular reaction 72 hours after BDL compared to wild type mice. In addition, the protective and proliferative effects of plasminogen activator inhibitor 1 (PAI-1) deficiency after BDL are dramatically blocked by the tPA inhibitor tPA-STOP. One potential mechanism for these effects is that both tPA deficiency and tPA-STOP reduce hepatocyte growth factor (HGF) activation and c-Met phosphorylation in the liver after BDL. In support of this hypothesis, HGF treatment reverses the effects of tPA deficiency in mice. Furthermore, preferential tPA activation in areas of injury after BDL might occur because fibrin accumulates in bile infarcts and activates tPA.\n\nQuestion:\nDoes tissue-type plasminogen activator deficiency exacerbate cholestatic liver injury in mice?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nParental distress following the birth of a premature infant diminishes the parent's ability to be sensitive to the infant's cues, and this may affect infant developmental outcomes. The present study examined the effects of maternal anxiety during infant hospitalization in the Neonatal Intensive Care Unit (NICU) on the interactive behavior of mothers with their very low birthweight (VLBW) children in toddlerhood. A sample of 56 mothers and their VLBW infants were recruited in the NICU. During the infant's NICU stay, mothers completed a self-report measure of trait anxiety. These mothers and their infants were followed when the infants were 24 months corrected age, when mothers and their children were videotaped during free play at home. These videotapes were then coded using the Emotional Availability Scales. Maternal anxiety was not found to be related to severity of neonatal illness. Maternal anxiety in the NICU was associated with less sensitivity and less structure in interaction with their toddlers at 24 months corrected age, even controlling for maternal education and child birthweight. Children of mothers with higher anxiety scores in the NICU were less likely to involve their mothers in their play at 24 months corrected age.\n\nQuestion:\nDoes persistent maternal anxiety affect the interaction between mothers and their very low birthweight children at 24 months?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHip dislocation after arthroplasty for femoral neck fractures remains a serious complication. The aim of our study was to investigate the dislocation rate in acute femoral neck fracture patients operated with a posterior approach with cemented conventional or dual articulation acetabular components. We compared the dislocation rate in 56 consecutive patients operated with conventional (single mobility) cemented acetabular components to that in 42 consecutive patients operated with dual articulation acetabular components. All the patients were operated via posterior approach and were followed up to one year postoperatively. There were 8 dislocations in the 56 patients having conventional components as compared to no dislocations in those 42 having dual articulation components (p = 0.01). The groups were similar with respect to age and gender distribution.\n\nQuestion:\nDoes dual mobility cup reduce dislocation rate after arthroplasty for femoral neck fracture?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIn this study, we sought to address changes in blood lymphocyte subpopulations and labial salivary gland (LSG) inflammation after belimumab treatment in patients with primary Sjögren's syndrome (pSS) and to identify predictors of response to treatment. Sequential blood lymphocyte subsets and LSG biopsies were analysed between week 0 (W0) and W28 in 15 patients with pSS treated with belimumab. Systemic response to treatment was defined as a decrease in the European League Against Rheumatism Sjögren's Syndrome Disease Activity Index score of ≥3 points at W28. After belimumab, we observed a decrease in blood B lymphocytes primarily involving CD27-negative/immunoglobulin D-positive naïve B cells (p=0.008). Lymphocytic sialadenitis (focus score >1) that was present in 12 patients (80.0 %) before belimumab treatment became negative in 5 of them after treatment (p=0.03). The median (interquartile range) LSG B-cell/T-cell ratio decreased from 0.58 (0.5-0.67) to 0.50 (0.5-0.5) (p=0.06). B-cell activating factor (BAFF) staining was detected in 11 (78.6 %) of 14 patients before belimumab treatment compared with 7 (50.0 %) of 14 after belimumab therapy (p=0.10). The median percentage of BAFF-positive cells in foci significantly decreased from 27.5 % (10-40) to 5 % (0-20) (p=0.03). A systemic response was achieved in six patients (40 %). The only predictor of response was the presence of a low number of natural killer (NK) cells, both in blood (8.5 % [7-10] vs 11 % [9-21]; p=0.04) and in LSG (20.6/mm(3) [20.0-21.4] vs 30.0/mm(3) [25.0-100.0], p=0.003). Serum BAFF levels did not influence response to treatment.\n\nQuestion:\nAre low numbers of blood and salivary natural killer cells associated with a better response to belimumab in primary Sjögren 's syndrome : results of the BELISS study?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAdded transforming growth factor beta (TGFbeta) inhibits the proliferation of immature cardiomyocytes. We have now examined the hypothesis that suppression of endogenous TGFbeta signaling will boost the proliferative response (DNA synthesis) of cardiac myocytes to serum and/or to the mitogenic factor fibroblast growth factor-2 (FGF-2). Overexpression of a kinase-deficient TGFbeta type II receptor (TGFbetaRIIDeltaKD) resulted in a 2.8-fold increase in cardiomyocyte DNA synthesis in serum-rich cultures, an effect requiring active FGFR-1 since it was not observed in the presence of excess kinase-deficient FGFR-1. This finding suggested that endogenous TGFbeta-TGFbetaRII suppressed endogenous FGFR-1-mediated signals that stimulate or are permissive for DNA synthesis. TGFbeta had no effect, however, on the FGF-2-induced acute stimulation of extracellular signal regulated kinase1/2. FGF-2, added in the absence or presence of TGFbeta inhibition, elicited a 3- or a 13-fold stimulation of DNA synthesis, respectively, pointing to a synergistic effect.\n\nQuestion:\nDoes inhibition of TGFbeta signaling potentiate the FGF-2-induced stimulation of cardiomyocyte DNA synthesis?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe study aimed to determine the risk of death or urgent transplant for patients who survived an initial 6 months on the outpatient heart transplant waiting list when criteria emphasizing reduced peak oxygen consumption are used for transplant candidate selection. Waiting time is a key criterion for heart donor allocation. A recent single-center investigation described decreasing survival benefit from transplant for patients who survived an initial 6 months on the outpatient waiting list. Kaplan-Meier survival analyses were performed for 80 patients from the Hospital of the University of Pennsylvania (HUP) listed from July 1986 to January 1991, and 132 patients from Columbia-Presbyterian Medical Center (CPMC) listed from September 1993 to September 1995. Survival from the time of outpatient listing for the entire group (ALL) was compared to subsequent survival from 6 months onward for those patients who survived the initial 6 months after placement on the outpatient list (6M). Both urgent transplant and left ventricular assist device implantation were considered equivalent to death; elective transplant was censored. RESULTS Survival for 6M was not significantly better than ALL at HUP (subsequent 12 months: 60+/-7 vs. 60+/-6% [mean+/-SD]; p = 0.89) nor at CPMC (subsequent 12 months: 60+/-6 vs. 48+/-5%; p = 0.35). Survival for 6M at both centers was substantially lower than survival following transplant from the outpatient list in the United States in 1995.\n\nQuestion:\nDoes mortality remain high for outpatient transplant candidates with prolonged ( > 6 months ) waiting list time?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nGlioblastoma (GBM) genomes feature recurrent genetic alterations that dysregulate core intracellular signaling pathways, including the G1/S cell cycle checkpoint and the MAPK and PI3K effector arms of receptor tyrosine kinase (RTK) signaling. Elucidation of the phenotypic consequences of activated RTK effectors is required for the design of effective therapeutic and diagnostic strategies. Genetically defined, G1/S checkpoint-defective cortical murine astrocytes with constitutively active Kras and/or Pten deletion mutations were used to systematically investigate the individual and combined roles of these 2 RTK signaling effectors in phenotypic hallmarks of glioblastoma pathogenesis, including growth, migration, and invasion in vitro. A novel syngeneic orthotopic allograft model system was used to examine in vivo tumorigenesis. Constitutively active Kras and/or Pten deletion mutations activated both MAPK and PI3K signaling. Their combination led to maximal growth, migration, and invasion of G1/S-defective astrocytes in vitro and produced progenitor-like transcriptomal profiles that mimic human proneural GBM. Activation of both RTK effector arms was required for in vivo tumorigenesis and produced highly invasive, proneural-like GBM.\n\nQuestion:\nIs cooperativity between MAPK and PI3K signaling activation required for glioblastoma pathogenesis?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIntravesical electrical stimulation (IVES) has been used clinically to treat patients with voiding disorders. The aim of the present experimental study was to obtain objective evidence of a modulation of the micturition reflex by intravesical electrical stimulation (IVES). Forty-one female rats, anesthetized by alpha-chloralose were used for the experiments. Intravesical electrical stimulation was given by a catheter electrode in the bladder (5 minutes of continuous stimulation at 20 Hz, 7 to 11 mA). The effect was evaluated by the change in cystometric micturition threshold volume. The threshold volume of the micturition reflex decreased significantly to 82% of controls after IVES (p<0.001; n=31). The effect was reversible and lasted for about 1 hour. The decrease was prevented by a transient blockade of the bladder nerves during IVES.\n\nQuestion:\nDoes intravesical electrical stimulation induce a prolonged decrease in micturition threshold volume in the rat?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPost-menopausal osteoporosis (PO) affecting a large fraction of elderly women, is triggered by the decline in 17β-estradiol (E2) level. Experimental studies in animal models and cell cultures have suggested that the fall in E2 might contribute to developing oxidative stress (OS) which in turn is believed to play an important role in PO pathogenesis. The scarcity of human studies focusing on this issue prompted us to investigate the effects of the reproductive and post-reproductive phase of women's life on OS and bone health. Serum parameters of oxidative challenge (lipid hydroperoxides and protein advanced oxidation products) and antioxidant defence (total serum antioxidants levels) along with bone mineral density (BMD) at femoral neck and lumbar spine were assessed in a sample of 191 women (98 pre- and 93 post-menopausal, of whom 30 osteoporotic). Pearson's correlation analysis unveiled that spinal BMD was negatively correlated with lipid hydroperoxides in overall postmenopausal subsample (r=-0.251, p=0.012), while no significant link between these two variables was detected in women in reproductive age (r=-0.022, p=0.833). Noteworthy, stepwise multiple regression analysis showed that the association found in post-menopausal women retained significance after adjusting for potential confounding factors (p=0.001).\n\nQuestion:\nDoes bone mass density selectively correlate with serum markers of oxidative damage in post-menopausal women?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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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:\nSynchronous activation of the Wnt signaling pathway, mostly because of loss of function of the APC tumor suppressor, and of the oncogenic KRAS-signaling pathway is very frequent in colorectal cancer and is associated with poor prognosis. We have generated a compound transgenic mouse model, KRAS(V12G)/Apc(+/1638N), to recapitulate the human disease and compared it with single transgenic littermates. Compound mutant mice are characterized by a 10-fold increase in tumor multiplicity and by accelerated tumor progression, resulting in strongly enhanced morbidity and mortality. Tumors from compound mutant mice proliferate faster and show decreased levels of apoptosis. Several lines of evidence indicate that the observed increase in tumor multiplicity and malignant transformation is caused by the synergistic activation of Wnt signaling in cells with oncogenic KRAS and loss-of-function Apc mutations. Activated KRAS is known to induce tyrosine phosphorylation of beta-catenin, leading to its release from E-cadherin at the adherens junction. This results in an increased beta-catenin pool in the cytoplasma, its subsequent translocation to the nucleus, and the transcriptional activation of Wnt downstream target genes. Accordingly, intestinal tumors from KRAS(V12G)/Apc(+/1638N) mice show a significant increase in cells with nuclear accumulation of beta-catenin when compared with Apc(+/1638N) animals. Moreover, Apc/KRAS-mutant embryonic stem cells show a significantly enhanced beta-catenin/T-cell factor-mediated transcriptional activation, accompanied by increased beta-catenin nuclear localization.\n\nQuestion:\nAre aPC and oncogenic KRAS synergistic in enhancing Wnt signaling in intestinal tumor formation and progression?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe study of faeces offers a unique opportunity to observe cooperation between the microbiome and the metabolism of mammalian hosts, an essential element in the study of the human metabolome. In the present study, a global metabolomics approach was used to identify metabolites differentially excreted in the faeces of cirrhotic patients compared to controls. Seventeen cirrhotic patients and 24 healthy individuals were recruited. Faecal metabolites were detected through non-targeted reversed-phase ultra-performance liquid chromatography coupled to electrospray ionization quadrupole time-of-flight mass spectrometry. A total of 9215 peaks were detected. Using unequal variance t-tests, 2393 peaks were observed with P≤0.05, approximately 74.0% of which were due to decreased faecal metabolite concentrations in liver cirrhosis vs. healthy controls. Integrating multivariate data analyses, we identified six major groups of metabolites. Relative levels of identified metabolites were as follows: strong increase in lysophosphatidylcholines, aromatic amino acids, fatty acids, and acylcarnitines, and a dramatic decrease in bile acids and bile pigments.\n\nQuestion:\nDoes metabolomic analyses of faeces reveal malabsorption in cirrhotic patients?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo investigate YBX2 gene alterations in men with severe defects in spermatogenesis, including azoospermia or severe oligozoospermia, and protamine deregulation. MSY2 has been identified as a central component in the regulation of spermatogenesis in mice, but the potential role of its human orthologue, YBX2 or \"Contrin,\" in human infertility is not known. A prospective cohort study. University infertility clinic and associated research laboratory. A total of 288 men were evaluated. Diagnoses were made of complete azoospermia, severe oligozoospermia, and protamine deregulation, or men were of known paternity. Deoxyribonucleic acid (from peripheral blood) and semen samples were collected and analyzed for gene mutations and semen parameters respectively. YBX2 gene alterations. YBX2 sequence analysis revealed 15 polymorphic sites, of which seven polymorphisms were present at a statistically higher frequency in one or both of the patient populations than in controls. Of these seven, two resulted in an amino acid substitution in the highly conserved cold shock domain and one resulted in a highly significant synonymous change in exon 8 of infertile patients. The frequency of single nucleotide polymorphisms was significantly elevated in patients with infertility, particularly in men with abnormal protamine expression.\n\nQuestion:\nAre sequence alterations in the YBX2 gene associated with male factor infertility?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo determine if melanoma cells secrete chemotactic factors that result in the migration of multipotent stem cells. In vitro cell culture. Chemotaxis and invasion of human mesenchymal stem cells (hMSCs) was determined using the modified Boyden chamber assay. Quantification of growth factors secreted by melanoma cells (A375) was determined using enzyme-linked immunosorbent assay. Conditioned A375 melanoma media caused significant migration and invasion of hMSCs compared to serum-free controls and conditioned media from normal melanocytes (P < .0001). The migratory effect appeared maximal after the A375 media was conditioned for 48 hours. Physiologically relevant concentrations of fibroblast growth factor-2 (FGF2) (90 pg/mL) secreted by A375 melanoma cells caused significant migration of hMSCs (P < .001) compared to serum-free and normal melanocyte controls. Neutralization of FGF2 inhibited the migration of hMSCs to that of the negative controls (conditioned media from normal melanocytes).\n\nQuestion:\nDoes malignant melanoma induce migration and invasion of adult mesenchymal stem cells?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIn order to validate immature granulocytes as a universal biomarker, we have compared the clinical relevance of the proportion of immature granulocytes (IG%), measured using Sysmex XE-2100, with other biomarkers (white blood cell, C-reactive protein, lactate and procalcitonin). This single center, retrospective study included 184 patients with sepsis admitted to an emergency department. Patients were classified into two groups: Uncomplicated sepsis and complicated sepsis (severe sepsis and septic shock). IG% and other biomarkers were evaluated and compared for predicting sepsis severity, overt disseminated intravascular coagulation (DIC) and 28 day mortality. In multivariate analysis, only IG% (odd ratio [OR] 2.530, p = 0.004) and lactate (OR 4.500, p < 0.001) could discriminate between complicated and uncomplicated sepsis. The optimal cut-off value for IG% and lactate was 0.5% and 2.0 mmol/L, respectively. In subgroup analyses of complicated sepsis, IG% was related to overt DIC. However, no single biomarker could predict 28-day mortality.\n\nQuestion:\nDoes fraction of immature granulocytes reflect severity but not mortality in sepsis?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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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:\nX-linked adrenoleukodystrophy (ALD) is a metabolic, peroxisomal disease that results from a mutation in the ABCD1 gene. The most severe course of ALD progression is the cerebral inflammatory and demyelinating form of the disease, cALD. To date there is very little information on the cytokine mediators in the cerebral spinal fluid (CSF) of these boys. Measurement of 23 different cytokines was performed on CSF and serum of boys with cerebral ALD and patients without ALD. Significant elevations in CSF IL-8 (29.3±2.2 vs 12.8±1.1 pg/ml, p = 0.0001), IL-1ra (166±30 vs 8.6±6.5 pg/ml, p = 0.005), MCP-1 (610±47 vs 328±34 pg/ml, p = 0.002), and MIP-1b (14.2±1.3 vs 2.0±1.4 pg/ml, p<0.0001) were found in boys with cALD versus the control group. The only serum cytokine showing an elevation in the ALD group was SDF-1 (2124±155 vs 1175±125 pg/ml, p = 0.0001). The CSF cytokines of IL-8 and MCP-1b correlated with the Loes MRI severity score (p = 0.04 and p = 0.008 respectively), as well as the serum SDF-1 level (p = 0.002). Finally, CSF total protein was also significantly elevated in boys with cALD and correlated with both IL-8, MCP-1b (p = 0.0001 for both), as well as Loes MRI severity score (p = 0.0007).\n\nQuestion:\nDoes elevated cerebral spinal fluid cytokine levels in boys with cerebral adrenoleukodystrophy correlate with MRI severity?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nRheological blood properties were studied during storage. Blood viscosity, erythrocyte morphology and ATP levels were determined in filtered samples (Leukotrap WB filter system) and their unfiltered counterparts during storage with saline-adenine-glucose-mannitol (SAG-M) for 42 days. Prestorage leucocyte depletion decreased blood viscosity at a high shear rate and reduced the degree of anisocytosis of erythrocytes. During storage, erythrocytes underwent a time-dependent echinocytic shape transformation, which increased the suspension viscosity at high and low shear rates. On day 42, high shear viscosity in filtered units remained lower than in unfiltered counterparts, the mean cellular volume and red blood cell distribution width (RDW) were lower and erythrocytic ATP levels were higher.\n\nQuestion:\nDoes influence of prestorage leucocyte depletion and storage time on rheologic properties of erythrocyte concentrate?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe formation of cholesterol gallstones is a complex process involving contributions from genes and environmental factors. Although gallbladder inflammation is believed to be common during cholelithogenesis, the role of immunologic factors is unknown. The role of adaptive immunity in cholesterol cholelithogenesis was analyzed utilizing immunocompetent Helicobacter spp.-infected and -uninfected BALB/c and congenic immunodeficient Rag2(-/-) (Rag) mice. Lymphocyte transfer studies were performed to determine which cellular subset was responsible for cholesterol gallstone formation. Also, gallbladder inflammation was quantified to determine the nature of the inflammatory response associated with cholelilithogenesis. When fed a lithogenic diet for 8 weeks, wild-type mice developed significantly more cholesterol gallstones (27%-80% prevalence) than Rag mice ( approximately 5%, P < .05). Helicobacter spp.-infected BALB/cJ mice displayed statistically significant increases in cholesterol gallstone prevalence compared with uninfected mice (81% vs. 39%; P < .05). Transfer of splenocytes or T lymphocytes to Rag2(-/-) mice increased stone prevalence markedly (26% and 40% respectively; P < .05), whereas transfer of B cells was not appreciably cholelithogenic (13%). The adaptive immune response increased the expression of gallbladder Muc genes and accumulation of mucin gel. In addition, T cells and cholesterol monohydrate crystals induced proinflammatory gene expression in the gallbladder, which likely contributes to gallbladder dysfunction.\n\nQuestion:\nIs t-cell function critical for murine cholesterol gallstone formation?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe amount of clinical information that providers encounter daily creates an environment for information overload and medical error. To create a more efficient EMR human-computer interface, we aimed to understand clinical information needs among NICU providers. A web-based survey to evaluate 98 data items was created and distributed to NICU providers. Participants were asked to rate the importance of each data item in helping them make routine clinical decisions in the NICU. There were 23 responses (92% - response rate) with participants distributed among four clinical roles. The top 5 items with the highest mean score were daily weight, pH, pCO2, FiO2, and blood culture results. When compared by clinical role groupings, supervisory physicians gave individual data item ratings at the extremes of the scale when compared to providers more responsible for the daily clinical care of NICU patients.\n\nQuestion:\nDoes clinical data need in the neonatal intensive care unit electronic medical record?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPlacenta accreta is one of the most devastating pregnancy complications. We sought to compare outcomes between women with placenta accreta when diagnosed antenatally or intrapartum, and to define predictors of the antenatal diagnosis. Retrospective case-control study. University teaching hospital. Twenty-four women with placenta accreta diagnosed antenatally and 20 women discovered intrapartum. Chart review of historical and delivery-associated variables. Rates were compared between the groups. Placenta accreta diagnosed antenatally or intrapartum. Women with antenatal diagnosis had a lower estimated blood loss of a median of 4500ml (range 100-15000ml) compared with 7800ml (range 2500-17000ml, p=0.012) and required fewer units of packed red blood cells transfused (median 7; range 0-27 compared with 13.5; range 4-31, p=0.026). Nineteen (79%) women diagnosed antenatally had balloon catheter occlusion carried out during the cesarean section. Five (21%) had the entire placenta left in situ. There was no difference in the rate of surgical complications or duration of hospitalization. The clinical diagnosis among women with antenatal diagnosis was more often placenta percreta (p=0.013). The risk factor profile of women with antenatal diagnosis of placenta accreta included higher gravidity (p=0.014) and parity (p<0.0001), history of cesarean section (p=0.004), and placenta previa in the current pregnancy (p<0.001).\n\nQuestion:\nDoes antenatal diagnosis of placenta accreta lead to reduced blood loss?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nOsteoarthritis (OA) is a highly prevalent, disabling joint disease with no existing therapies to slow or halt its progression. Cartilage degeneration hallmarks OA pathogenesis, and pannexin 3 (Panx3), a member of a novel family of channel proteins, is upregulated during this process. The function of Panx3 remains poorly understood, but we consistently observed a strong increase in Panx3 immunostaining in OA lesions in both mice and humans. Here, we developed and characterized the first global and conditional Panx3 knockout mice to investigate the role of Panx3 in OA. Interestingly, global Panx3 deletion produced no overt phenotype and had no obvious effect on early skeletal development. Mice lacking Panx3 specifically in the cartilage and global Panx3 knockout mice were markedly resistant to the development of OA following destabilization of medial meniscus surgery. These data indicate a specific catabolic role of Panx3 in articular cartilage and identify Panx3 as a potential therapeutic target for OA. Lastly, while Panx1 has been linked to over a dozen human pathologies, this is the first in vivo evidence for a role of Panx3 in disease.\n\nQuestion:\nDoes deletion of Panx3 prevent the Development of Surgically Induced Osteoarthritis?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSeveral lines of evidence support the involvement of mannose-binding lectin (MBL) in stroke brain damage. The lectin pathway of the complement system facilitates thrombin activation and clot formation under certain experimental conditions. In the present study, we examine whether MBL promotes thrombosis after ischemia/reperfusion and influences the course and prognosis of ischemic stroke. Middle cerebral artery occlusion/reperfusion was performed in MBL-deficient (n=85) and wild-type (WT; n=83) mice, and the brain lesion was assessed by MRI at days 1 and 7. Relative cerebral blood flow was monitored up to 6 hours after middle cerebral artery occlusion with laser speckle contrast imaging. Fibrin(ogen) was analyzed in the brain vasculature and plasma, and the effects of thrombin inhibitor argatroban were evaluated to assess the role of MBL in thrombin activation. Infarct volumes and neurological deficits were smaller in MBL knockout mice than in WT mice. Relative cerebral blood flow values during middle cerebral artery occlusion and at reperfusion were similar in both groups, but decreased during the next 6 hours in the WT group only. Also, the WT mice showed more fibrin(ogen) in brain vessels and a better outcome after argatroban treatment. In contrast, argatroban did not improve the outcome in MBL knockout mice.\n\nQuestion:\nDoes mannose-binding lectin promote local microvascular thrombosis after transient brain ischemia in mice?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo evaluate the association between genetic variants in Ser-Arg (SR) protein-coding genes and the susceptibility of nonobstructive azoospermia (NOA) in Chinese men. Case-control study. State Key Laboratory of Reproductive Medicine in Nanjing Medical University conducted the genotyping and examined the expression levels of genes. The study included 962 NOA patients and 1,931 control subjects. None. Genotyping of 16 single-nucleotide polymorphisms (SNPs) of eight \"canonic\" SR protein-coding genes were performed with the use of the Illumina Infinium Beadchip platform. Odds ratios were calculated by logistic regression analysis in the additive model. Expression levels were measured by quantitative reverse-transcription polymerase chain reaction. Rs17431717 near SFRS9 and rs12046213 near SFRS4 were significantly associated with a decreased risk of NOA, whereas rs10849753 near SFRS9 and rs6103330 in SFRS6 were associated with an increased risk of NOA. Of the two SNPs in SFRS9, only rs17431717 remained significant after conditioning on another. Combined analysis of three promising SNPs (rs17431717, rs12046213, and rs6103330) showed that compared with individuals with \"0-2\" risk alleles, those carrying \"3,\" \"4,\" and \"≥ 5\" risk alleles had 1.22-, 1.38-, and 1.90-fold increased risk of NOA, respectively.\n\nQuestion:\nAre genetic variants in Ser-Arg protein-coding genes associated with the risk of nonobstructive azoospermia in Chinese men?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nA biomechanical study of facet joint pressure after total disc replacement using cadaveric human cervical spines during lateral bending and axial torsion. The goal was to measure the contact pressure in the facet joint in cadaveric human cervical spines subjected to physiologic lateral bending and axial torsion before and after implantation of a ProDisc-C implant. Changes in facet biomechanics can damage the articular cartilage in the joint, potentially leading to degeneration and painful arthritis. Few cadaveric and computational studies have evaluated the changes in facet joint loading during spinal loading with an artificial disc implanted. Computational models have predicted that the design and placement of the implant influence facet joint loading, but limited cadaveric studies document changes in facet forces and pressures during nonsagittal bending after implantation of a ProDisc. As such, little is known about the local facet joint mechanics for these complicated loading scenarios in the cervical spine. Seven osteoligamentous C2-T1 cadaveric cervical spines were instrumented with a transducer to measure the C5-C6 facet pressure profiles during physiological lateral bending and axial torsion, before and after implantation of a ProDisc-C at that level. Rotations at that level and global cervical spine motions and loads were also quantified. RESULT.: Global and segmental rotations were not altered by the disc implantation. Facet contact pressure increased after implantation during ipsilateral lateral bending and contralateral torsion, but that increase was not significant compared with the intact condition.\n\nQuestion:\nDoes proDisc cervical arthroplasty alter facet joint contact pressure during lateral bending or axial torsion?\n\nAnswer:",
"role": "user"
},
{
"content": "no",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo assess the intraocular pressure (IOP) lowering mechanism of deep sclerectomy with collagen implant (DSCI), a non-penetrating glaucoma surgery. Nine eyes of nine patients with medically uncontrolled open angle glaucoma underwent DSCI. Ultrasound biomicroscopy (UBM) of the sclerectomy site was performed 1 month after surgery. The following factors were assessed: length and height of collagen implant, and thickness of the residual trabeculocorneal membrane. Postoperative IOP decreased significantly in all nine eyes from a preoperative mean value of 25.8 (SD 4.8) mm Hg to a postoperative (1 month) mean value of 11.3 (6.3) mm Hg (p = 0.001). In all nine eyes, UBM at 1 month after surgery showed a subconjunctival filtration through the thin trabeculocorneal membrane and through the scleral flap around the collagen implant. In four cases, a hypoechoic area in the suprachoroidal space was observed and might represent ciliary body detachment or be due to suprachoroidal drainage of aqueous humour through the thin deep scleral wall. At 1 month after surgery the mean trabeculocorneal membrane thickness was 110.1 (16.8) microns, and the mean length and height of the collagen implant were 2.3 (0.1) mm and 1.1 (0.1) mm respectively.\n\nQuestion:\nDo ultrasound biomicroscopy of eyes undergoing deep sclerectomy with collagen implant?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nInterleukin 18 (IL-18) is a regulatory cytokine that degrades the disc matrix. Bone morphogenetic protein-2 (BMP-2) stimulates synthesis of the disc extracellular matrix. However, the combined effects of BMP-2 and IL-18 on human intervertebral disc degeneration have not previously been reported. The aim of this study was to investigate the effects of the anabolic cytokine BMP-2 and the catabolic cytokine IL-18 on human nucleus pulposus (NP) and annulus fibrosus (AF) cells and, therefore, to identify potential therapeutic and clinical benefits of recombinant human (rh)BMP-2 in intervertebral disc degeneration. Levels of IL-18 were measured in the blood of patients with intervertebral disc degenerative disease and in control patients. Human NP and AF cells were cultured in a NP cell medium and treated with IL-18 or IL-18 plus BMP-2. mRNA levels of target genes were measured by real-time polymerase chain reaction, and protein levels of aggrecan, type II collagen, SOX6, and matrix metalloproteinase 13 (MMP13) were assessed by western blot analysis. The serum level of patients (IL-18) increased significantly with the grade of IVD degeneration. There was a dramatic alteration in IL-18 level between the advanced degeneration (Grade III to V) group and the normal group (p = 0.008) Furthermore, IL-18 induced upregulation of the catabolic regulator MMP13 and downregulation of the anabolic regulators aggrecan, type II collagen, and SOX6 at 24 hours, contributing to degradation of disc matrix enzymes. However, BMP-2 antagonised the IL-18 induced upregulation of aggrecan, type II collagen, and SOX6, resulting in reversal of IL-18 mediated disc degeneration.\n\nQuestion:\nDoes bone morphogenetic protein-2 provoke interleukin-18-induced human intervertebral disc degeneration?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo asses the effects of seminal plasma on sperm function. Retrospective case-control study. University hospital. One hundred fourteen infertile men. Acrobeads Test scores (0-4) and measurement of interleukin (IL)-6, soluble IL-6 receptor, epidermal growth factor, insulin-like growth factor-I (IGF-I), transforming growth factor-beta I, superoxide dismutase, calcitonin, and macrophage migration inhibitory factor (MIF) levels in seminal plasma. Kruskal-Wallis test to compare the concentrations of substances as a nonparametric test for differences among Acrobeads Test scores and a multivariable logistic regression model to find independent risk factors associated with abnormal Acrobeads Test results. The Acrobeads Test score was 0 for 7 samples, 1 for 20 samples, 2 for 18 samples, 3 for 28 samples, and 4 for 41 samples. Age, abstinence period, and semen parameters, except for sperm motility and percentage of sperm with abnormal morphology, had no effect on the Acrobeads Test results. Concentrations of IGF-I and MIF were significantly higher in patients with abnormal Acrobeads Test results. Multivariate analysis indicated that MIF and IGF-I were significantly associated with abnormal Acrobeads Test results (scores 0 to 1).\n\nQuestion:\nDo relationship between substances in seminal plasma and Acrobeads Test results?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nDiabetic women are five times more likely to develop congestive heart failure compared with two fold for men. The underlying mechanism for this gender difference is not known. Here we investigate the molecular mechanisms responsible for this female disadvantage and attempt safeguarding cardiomyocytes viability and function through restoration of pro-survival Pim-1. Diabetes was induced by injection of streptozotocin in CD1 mice of both genders. Functional and dimensional parameters measurement using echocardiography revealed diastolic dysfunction in female diabetic mice within 8 weeks after STZ-induced diabetes. This was associated with significant downregulation of pro-survival Pim-1 and upregulation of pro-apoptotic Caspase-3, microRNA-1 and microRNA-208a. Male diabetic mice did not show any significant changes at this time point (P < 0.05 vs. female diabetic). Further, the onset of ventricular remodelling was quicker in female diabetic mice showing marked left ventricular dilation, reduced ejection fraction and poor contractility (P < 0.05 vs. male diabetic at 12 and 16 weeks of STZ-induced diabetes). Molecular analysis of samples from human diabetic hearts confirmed the results of pre-clinical studies, showing marked downregulation of Pim-1 in the female diabetic heart (P < 0.05 vs. male diabetic). Finally, in vitro restoration of Pim-1 reversed the female disadvantage in diabetic cardiomyocytes.\n\nQuestion:\nDoes rapid onset of cardiomyopathy in STZ-induced female diabetic mice involve the downregulation of pro-survival Pim-1?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nInfants of diabetic mothers have been characterized by macrosomia due to hyperinsulinism. A relation has been observed between circulating levels of leptin and the intrauterine growth pattern. We studied the leptin and insulin concentrations in the cord blood of 29 newborn infants of mothers with type 1 diabetes (iT1DM), 70 newborn infants of mothers with gestational diabetes and 105 newborn infants of nondiabetic mothers. There were significant differences (p < 0.001) between the 3 groups with the highest leptin levels 24.9 microg/l (range 1.7-94.1) in infants of mothers with iT1DM and the second-highest levels 14.0 microg/l (range 2.6-74.9) in infants of mothers with gestational diabetes (iGDM), whereas the control infants had the lowest leptin levels 10.0 microg/l (range 0.10-45.9). Girls had higher leptin concentrations than boys among the iT1DM and control infants. The insulin concentrations were 18.1 mU/l (range 1.9-123.3), 6.1 mU/l (range 1.1-51.4) and 3.6 mU/l (range 0.5-21.5) in the 3 groups (p < 0.001), respectively. A significant correlation was observed between leptin and insulin concentrations in iGDM and control infants (r = 0.51; p < 0.001 and r = 0.25; p < 0.05). Both absolute and relative birth weights correlated with leptin levels in all 3 groups (r = 0.60, p = 0.01 and r = 0.51, p = 0.05 in iT1DM; r = 0.51 and 0.56, p < 0.001 in iGDM and r = 0.42 and 0.59, p < 0.001 in control infants).\n\nQuestion:\nAre leptin concentrations elevated in newborn infants of diabetic mothers?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nFluvastatin is an agent of a new lipid lowering drug class, the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors, which seems to elicit direct effects on the vasculature. The effect of fluvastatin on endothelin secretion in endothelial cell cultures from human umbilical veins was investigated. Fluvastatin significantly reduced endothelin secretion by 13% at a concentration of 10(-8) M, by 41% at 10(-7) M and by 62% at 10(-6) M.\n\nQuestion:\nDoes fluvastatin reduce endothelin secretion of cultured human umbilical vein endothelial cells?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPatients with Parkinson disease (PD) are often profoundly slow in their performance of physical tasks, as well as in motor imagery (MI). This may limit the implementation and potential benefits of MI practice during rehabilitation. The authors investigated whether the quality of MI could be improved by external cueing. Fourteen patients with PD and 14 healthy controls physically executed and visually imagined a goal-directed aiming task and a box-and-block task, both in the presence and absence of visual and auditory cues. Mental chronometry and eye movement recording allowed objective evaluation of the temporal and spatial characteristics of MI when compared with physical execution. Visual analogue scales were used to assess imagery vividness. The presence of visual cues significantly reduced the patients' bradykinesia during MI and increased their imagery vividness.\n\nQuestion:\nDoes external cueing improve motor imagery quality in patients with Parkinson disease?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nKirsten-RAS (KRAS) mutations play an important role in the carcinogenesis of a subset of lung adenocarcinomas and are associated with poorer prognosis. To investigate the relationship of KRAS mutation status to the histologic subtype of adenocarcinoma according to the recent classification, patient demographics, tumor size, predominant histologic subtype, nodal status, and visceral pleural invasion, in an attempt to uncover the reason for the worse prognosis associated with KRAS mutation. A total of 187 consecutive resected lung adenocarcinomas from our institution from 2008 to 2011 that were diagnosed according to the new International Association for the Study of Lung Cancer/American Thoracic Society/European Respiratory Society classification and screened for KRAS mutations were included in the study. A total of 32% of the adenocarcinomas harbored the KRAS mutation. The median age in the KRAS mutation group was 69 years (range, 43-86 years), and male to female ratio was 1:2.3. The proportion of heavy smokers was significantly higher in tumors with KRAS mutation compared with wild type (83% versus 62%; P = .01). A total of 27% of tumors with KRAS mutation had pleural invasion versus 11% of tumors without KRAS mutation (P = .009). A total of 59 tumor samples were positive for KRAS mutation (25 for G12C, 14 for G12A, 8 for G12V, 7 for G12D, 3 for G12S, and 1 for G12T), and only 3 tumors harbored codon 13 mutations (G13C). Two tumors had double mutations.\n\nQuestion:\nAre peripheral lung adenocarcinomas with KRAS mutations more likely to invade visceral pleura?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nBiomarkers of endothelial dysfunction, inflammation and coagulation are associated with atherosclerosis and cardiovascular disease, but their association and possible predictive value remain controversial among HIV-1-infected individuals. We sought to investigate the association of seven biomarkers with first-time myocardial infarction (MI) in an HIV-1-infected population. A matched case-control study of 54 cases and 54 controls. We compared 54 HIV-1-infected patients with verified first-time MI and 54 HIV-1-infected controls matched for age, duration of antiretroviral therapy, sex, smoking and no known cardiovascular disease. Levels of high-sensitivity C-reactive protein, soluble endothelial selectin, soluble vascular cell adhesion molecule, soluble intercellular adhesion molecule, matrix metalloprotease 9, myeloperoxidase, and plasminogen activator inhibitor 1 (PAI-1) were measured using a Luminex assay in plasma samples from routine visits both 12 and 2 months prior to the case patient's MI. The two groups had similar HIV characteristics and traditional cardiovascular risk factors. In univariate analysis, PAI-1 levels were associated with MI, whereas none of the other markers showed any association.In multivariate analyses adjusting for the D:A:D risk score, HIV viral load and high-sensitivity C-reactive protein, PAI-1 levels in the highest quartile were associated with a six to seven-fold increased risk of MI in both samples.\n\nQuestion:\nDoes plasma plasminogen activator inhibitor-1 predict myocardial infarction in HIV-1-infected individuals?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nEndoscopic injection of stabilized nonanimal hyaluronic acid/dextranomer gel is an established treatment for vesicoureteral reflux in children. We performed a subgroup analysis to assess this treatment in reflux associated with bladder dysfunction. Of 308 consecutive children treated endoscopically with stabilized nonanimal hyaluronic acid/dextranomer gel for dilating vesicoureteral reflux 54 were observed retrospectively to have bladder dysfunction. Initial followup consisted of voiding cystourethrogram at 3 and 12 months after injection, with positive response defined as reflux grade 0 or I. At 7 to 12 years following treatment patient charts were checked for urinary tract infections and bladder dysfunction, and a followup survey (postal questionnaire) was administered. A positive response to therapy (cure) was observed in 45 children (83%) after 1 to 3 endoscopic treatments. Concurrently, bladder dysfunction had resolved in 32 patients (59%). After the last stabilized nonanimal hyaluronic acid/dextranomer gel implantation 45 patients (83%) were free of urinary tract infections. Questionnaire results were similar to chart based findings. Stabilized nonanimal hyaluronic acid/dextranomer gel implantation was well tolerated, with no associated complications.\n\nQuestion:\nIs endoscopic treatment with stabilized nonanimal hyaluronic acid/dextranomer gel effective in vesicoureteral reflux associated with bladder dysfunction?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPlant growth depends on both cell division and cell expansion. Plant hormones, including brassinosteroids (BRs), are central to the control of these two cellular processes. Despite clear evidence that BRs regulate cell elongation, their roles in cell division have remained elusive. Here, we report results emphasizing the importance of BRs in cell division. An Arabidopsis BR biosynthetic mutant, dwarf7-1, displayed various characteristics attributable to slower cell division rates. We found that the DWARF4 gene which encodes for an enzyme catalyzing a rate-determining step in the BR biosynthetic pathways, is highly expressed in the actively dividing callus, suggesting that BR biosynthesis is necessary for dividing cells. Furthermore, dwf7-1 showed noticeably slower rates of callus growth and shoot induction relative to wild-type control. Flow cytometric analyses of the nuclei derived from either calli or intact roots revealed that the cell division index, which was represented as the ratio of cells at the G2/M vs. G1 phases, was smaller in dwf7-1 plants. Finally, we found that the expression levels of the genes involved in cell division and shoot induction, such as PROLIFERATING CELL NUCLEAR ANTIGEN2 (PCNA2) and ENHANCER OF SHOOT REGENERATION2 (ESR2), were also lower in dwf7-1 as compared with wild type.\n\nQuestion:\nDoes arabidopsis brassinosteroid biosynthetic mutant dwarf7-1 exhibit slower rates of cell division and shoot induction?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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