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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:\nExposure to violence predisposes youths to future violent behavior. Breaking the cycle of violence in inner cities is the primary objective of hospital-based violence intervention and prevention programs. An evaluation was undertaken to determine if a hospital-based, peer intervention program, \"Caught in the Crossfire,\" reduces the risk of criminal justice involvement, decreases hospitalizations from traumatic reinjury, diminishes death from intentional violent trauma, and is cost effective. We designed a retrospective cohort study conducted between January 1998 and June 2003 at a university-based urban trauma center. The duration of followup was 18 months. Patients were 12 to 20 years of age and were hospitalized for intentional violent trauma. The \"enrolled\" group had a minimum of five interactions with an intervention specialist. The control group was selected from the hospital database by matching age, gender, race or ethnicity, type of injury, and year of admission. All patients came from socioeconomically disadvantaged areas. The total sample size was 154 patients. Participation in the hospital-based peer intervention program lowered the risk of criminal justice involvement (relative risk=0.67; 95% CI, 0.45, 0.99; p=0.04). There was no effect on risks of reinjury and death. Subsequent violent criminal behavior was reduced by 7% (p=0.15). Logistic regression analysis showed age had a confounding effect on the association between program participation and criminal justice involvement (relative risk=0.71; p=0.043). When compared with juvenile detention center costs, the total cost reduction derived from the intervention program annually was $750,000 to $1.5 million.\n\nQuestion:\nDo benefits of a hospital-based peer intervention program for violently injured youth?\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:\nCytokine induction can occur routinely in cardiac surgery with cardiopulmonary bypass. We have studied the relationships between the kinetics of pro-inflammatory cytokine release and the postoperative organ function. Ten adult patients (6 men and 4 women) undergoing elective cardiac surgery with cardiopulmonary bypass, at Hiroshima University Hospital were studied. Patients with acute infection, insulin-dependent diabetes, acute or chronic respiratory failure, renal or hepatic failure, acute cardiogenic shock, and emergency patients were not included. The age of the patient ranged from 44 to 78 years (mean 69 +/- 2.0 years). The type of surgical intervention performed was coronary artery bypass grafting in four patients, mitral valve plasty or replacement with modified maze procedure in another five patients, and both procedures in the other one patient. Plasma cytokine levels until 48 hours after aortic declamping were measured in blood samples. The Respiratory Index and the serum levels of choline esterase and creatinine were also measured. The plasma levels of the pro-inflammatory cytokines (interleukin-6 and interleukin-8) were measured. The highest interleukin-6 levels were significantly correlated with hepatic dysfunction (r = -0.80, p = 0.006) and with renal dysfunction (r = 0.78, p = 0.009). The highest interleukin-8 levels were significantly correlated with respiratory dysfunction (r = 0.86, p = 0.001).\n\nQuestion:\nDo kinetics of pro-inflammatory cytokines release in cardiac surgery with cardiopulmonary bypass?\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:\nX-linked adrenoleukodystrophy is caused by a defective peroxisomal membrane transporter, ABCD1, responsible for transporting very-long-chain fatty acid substrate into peroxisomes for degradation. The main biochemical defect, which is also one of the major diagnostic hallmarks, of X-linked adrenoleukodystrophy is the accumulation of saturated very-long-chain fatty acids in all tissues and body fluids. Direct and reverse-transcribed polymerase chain reactions followed by DNA sequencing-based mutational analyses were performed on one Taiwanese and three Malaysian X-linked adrenoleukodystrophy families. A novel splicing donor site mutation (c.1272+1g>a) was identified in a Taiwanese X-linked adrenoleukodystrophy patient, resulting in a deletion of 121 bp and a premature stop codon (p.Val425fs*92) in messenger-RNA transcript. This deletion is caused by the activation of a cryptic splicing donor site in exon 4 of the ABCD1 gene, which is consistent with the prediction by several online algorithms. In addition, three previously described missense mutations (c.965T>C, c.1978C>T, and c.2006A>G), leading to aberrant ABCD1 of p.Leu322Pro, p.Arg660Trp, and p.His669Arg, were also identified in Malaysian probands.\n\nQuestion:\nDo mutational analyses on X-linked adrenoleukodystrophy reveal a novel cryptic splicing and three missense mutations in the ABCD1 gene?\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:\nKnown gene mutations account for approximately 50% of the hereditary risk for breast cancer. Moderate and low penetrance variants, discovered by genomic approaches, account for an as-yet-unknown proportion of the remaining heritability. A truncating mutation c.325C>T:p.Arg109* (R109X) in the ATP-dependent helicase ERCC3 was observed recurrently among exomes sequenced in BRCA wild-type, breast cancer-affected individuals of Ashkenazi Jewish ancestry. Modeling of the mutation in ERCC3-deficient or CRISPR/Cas9-edited cell lines showed a consistent pattern of reduced expression of the protein and concomitant hypomorphic functionality when challenged with UVC exposure or treatment with the DNA alkylating agent IlludinS. Overexpressing the mutant protein in ERCC3-deficient cells only partially rescued their DNA repair-deficient phenotype. Comparison of frequency of this recurrent mutation in over 6,500 chromosomes of breast cancer cases and 6,800 Ashkenazi controls showed significant association with breast cancer risk (OR\n\nQuestion:\nDoes a Recurrent ERCC3 Truncating Mutation confer Moderate Risk for Breast 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:\nRenal cell carcinoma (RCC) is the tenth most commonly diagnosed cancer in the United States. While it is usually lethal when metastatic, RCC is successfully treated with surgery when tumors are confined to the kidney and have low tumor volume. Because most early stage renal tumors do not result in symptoms, there is a strong need for biomarkers that can be used to detect the presence of the cancer as well as to monitor patients during and after therapy. We examined genome-wide DNA methylation alterations in renal cell carcinomas of diverse histologies and benign adjacent kidney tissues from 96 patients. We observed widespread methylation differences between tumors and benign adjacent tissues, particularly in immune-, G-protein coupled receptor-, and metabolism-related genes. Additionally, we identified a single panel of DNA methylation biomarkers that reliably distinguishes tumor from benign adjacent tissue in all of the most common kidney cancer histologic subtypes, and a second panel does the same specifically for clear cell renal cell carcinoma tumors. This set of biomarkers were validated independently with excellent performance characteristics in more than 1,000 tissues in The Cancer Genome Atlas clear cell, papillary, and chromophobe renal cell carcinoma datasets.\n\nQuestion:\nDoes dNA methylation profiling reveal novel diagnostic biomarkers in renal cell carcinoma?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nUremic pruritus (UP) is still a common tormenting symptom among patients on hemodialysis (HD). The pathogenesis of UP is complex and not fully clarified. Some preliminary studies indicate that UP is a systemic inflammatory disease with a deranged balance of T helper (TH) cell differentiation toward TH1 predominance. The aim of this study was to further elucidate the potential contribution of TH1 cytokines to the pathogenesis of UP. In this study, 112 HD patients were screened for UP. After meeting the required criteria, 31 HD patients with UP were included in the study as case group and 30 age- and sex-matched HD patients without UP were enrolled as controls. The serum levels of interleukin (IL)-2 and interferon-γ (as TH1 cytokines), IL-4 (as a TH-2 cytokine), high-sensitive C-reactive protein (as an inflammatory marker), parathyroid hormone, calcium, phosphate, albumin and ferritin were measured in all patients. Moreover, blood variables including hemoglobin and mean corpuscular volume were also determined. The correlations of measured factors with UP severity were determined as well. Except for the serum levels of IL-2, which were significantly higher in HD patients with itch versus those without it [0.544 ± 0.126 (U/mL) versus 0.318 ± 0.145 (U/mL); P < 0.0001], no statistically significant difference was observed in the levels of each of the above-mentioned factors between the two groups. Additionally, no correlation was detected between the levels of measured factors and UP severity.\n\nQuestion:\nAre interleukin-2 serum levels elevated in patients with uremic pruritus : a novel finding with practical implications?\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:\nHemostasis management has evolved to include sophisticated point-of-care systems that provide individualized dosing through heparin concentration-based anticoagulation. The Hepcon HMS Plus system (Medtronic, Minneapolis, MN) estimates heparin dose, activated clotting time (ACT), and heparin dose response (HDR). However, the accuracy of this test has not been systematically evaluated in large cohorts. We examined institutional databases for all patients who underwent cardiac surgery with cardiopulmonary bypass (CPB) at our institution from February 2005 to July 2008. During this period, the Hepcon HMS Plus was used exclusively for assessment of heparin dosing and coagulation monitoring. Detailed demographic, surgical, laboratory, and heparin dosing data were recorded. ACT, calculated and measured HDR, and heparin concentrations were recorded. Performance of the Hepcon HMS Plus was assessed by comparison of actual and target ACT values and calculated and measured HDR. In 3880 patients undergoing cardiac surgery, heparin bolus dosing to a target ACT resulted in wide variation in the postheparin ACT (r(2) = 0.03). The postheparin ACT did not reach the target ACT threshold in 7.4%(i.e., when target ACT was 300 s) and 16.9% (i.e., when target ACT was 350 s) of patients. Similarly, the target heparin level calculated from the HDR did not correlate with the postbolus heparin level, with 18.5% of samples differing by more than 2 levels of the assay. Calculated and measured HDR were not linearly related at any heparin level.\n\nQuestion:\nDoes heparin concentration-based anticoagulation for cardiac surgery fail to reliably predict heparin bolus dose requirements?\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:\nPaediatric low-grade gliomas (LGGs) encompass a heterogeneous set of tumours of different histologies, site of lesion, age and gender distribution, growth potential, morphological features, tendency to progression and clinical course. Among LGGs, Pilocytic astrocytomas (PAs) are the most common central nervous system (CNS) tumours in children. They are typically well-circumscribed, classified as grade I by the World Health Organization (WHO), but recurrence or progressive disease occurs in about 10-20% of cases. Despite radiological and neuropathological features deemed as classic are acknowledged, PA may present a bewildering variety of microscopic features. Indeed, tumours containing both neoplastic ganglion and astrocytic cells occur at a lower frequency. Gene expression profiling on 40 primary LGGs including PAs and mixed glial-neuronal tumours comprising gangliogliomas (GG) and desmoplastic infantile gangliogliomas (DIG) using Affymetrix array platform was performed. A biologically validated machine learning workflow for the identification of microarray-based gene signatures was devised. The method is based on a sparsity inducing regularization algorithm l₁l₂ that selects relevant variables and takes into account their correlation. The most significant genetic signatures emerging from gene-chip analysis were confirmed and validated by qPCR. We identified an expression signature composed by a biologically validated list of 15 genes, able to distinguish infratentorial from supratentorial LGGs. In addition, a specific molecular fingerprinting distinguishes the supratentorial PAs from those originating in the posterior fossa. Lastly, within supratentorial tumours, we also identified a gene expression pattern composed by neurogenesis, cell motility and cell growth genes which dichotomize mixed glial-neuronal tumours versus PAs. Our results reinforce previous observations about aberrant activation of the mitogen-activated protein kinase (MAPK) pathway in LGGs, but still point to an active involvement of TGF-beta signaling pathway in the PA development and pick out some hitherto unreported genes worthy of further investigation for the mixed glial-neuronal tumours.\n\nQuestion:\nDoes molecular fingerprinting reflect different histotypes and brain region in low grade gliomas?\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:\nValve sounds are thought to be useful in evaluating the functioning of prosthetic heart valves. In previous reports, two recording instruments have mainly been used, a condenser microphone (instrument A) and an accelerometer (instrument B), respectively. This study aimed to investigate the applicability of these conventional devices in recording mechanical heart valve sounds in daily clinical situations. In addition, two other instruments, namely, a stethoscope including a small microphone in its tube (instrument C) and an electrostethoscope (instrument D), were proposed and examined. Mechanical valve sounds were recorded from postoperative patients using each-device and the signal to noise ratio (SNR) of each was calculated. Frequency characteristics of the two newly proposed instruments were also investigated by recording a sweep signal in an anechoic chamber. The SNR values of the new instruments were significantly superior to those of conventional ones (A, sound signals were not defined from noises; B, 0.97 +/- 0.59 dB; C, 11.5 +/- 4.7 dB; and D, 9.4 +/- 3.5 dB, respectively p<0.05). The frequency characteristics of the two newly proposed instruments were also shown to be acceptable (under 10 kHz), though resonance frequency peaks were observed.\n\nQuestion:\nDoes the optimal method for recording prosthetic heart valve sound in clinical situations?\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:\nPhysiologic saline (NaCl 0.9%) is commonly used in treating acute and chronic rhinosinusitis. Moreover, physiologic saline is used as a control medium, vehicle, or solvent in studies on ciliary beat frequency (CBF). Hypertonic saline (NaCl 7% and 14.4%) has been applied in attempts to enhance mucociliary transport in patients with cystic fibrosis or asthma and in healthy subjects. Therefore the objective of this study is to document in vitro effects of saline solutions in different concentrations on CBF. Experimental, in vitro. The effects on CBF of cryopreserved mucosa of the sphenoidal sinus was measured by a photoelectrical method. Initial frequencies, measured in Locke-Ringer's solution (LR), were compared with CBF after exposure to NaCl in concentrations of 0.9%, 7.0%, and 14.4% (w/v). NaCl 0.9% has a moderately negative effect on CBF. The 7% solution leads to a complete ciliostasis within 5 minutes, although this effect turns out to be reversible after rinsing with LR. A hypertonic solution of 14.4% has an irreversible ciliostatic effect.\n\nQuestion:\nDo physiologic and hypertonic saline solutions impair ciliary activity in vitro?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe diagnosis of food allergy (FA) can be challenging because approximately half of food-sensitized patients are asymptomatic. Current diagnostic tests are excellent makers of sensitization but poor predictors of clinical reactivity. Thus oral food challenges (OFCs) are required to determine a patient's risk of reactivity. We sought to discover genomic biomarkers of clinical FA with utility for predicting food challenge outcomes. Genome-wide DNA methylation (DNAm) profiling was performed on blood mononuclear cells from volunteers who had undergone objective OFCs, concurrent skin prick tests, and specific IgE tests. Fifty-eight food-sensitized patients (aged 11-15 months) were assessed, half of whom were clinically reactive. Thirteen nonallergic control subjects were also assessed. Reproducibility was assessed in an additional 48 samples by using methylation data from an independent population of patients with clinical FA. Using a supervised learning approach, we discovered a DNAm signature of 96 CpG sites that predict clinical outcomes. Diagnostic scores were derived from these 96 methylation sites, and cutoffs were determined in a sensitivity analysis. Methylation biomarkers outperformed allergen-specific IgE and skin prick tests for predicting OFC outcomes. FA status was correctly predicted in the replication cohort with an accuracy of 79.2%.\n\nQuestion:\nDo blood DNA methylation biomarkers predict clinical reactivity in food-sensitized infants?\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 adults, hemodialysis (HD)-induced ischemia causes reversible myocardial dysfunction (myocardial stunning) that is progressive with raised attendant mortality. Children share an increased risk for death from a spectrum of uremia-related cardiovascular abnormalities but in the absence of significant classical atheromatous coronary artery disease; therefore, we elected to assess children who were on HD for the occurrence of myocardial stunning to investigate the relative importance of characteristic uremic cardiovascular abnormalities in the development of ischemic cardiac injury. We included all single-center long-term HD patients (n = 12; range 2 to 17 yr), excluding those with structural cardiac disease. Patients underwent conventional thrice-weekly HD for 4 h using high-flux membranes. We measured regional left ventricle wall motion using serial echocardiography (before HD, during HD, and 15 min after HD). Significant stunning was defined as a 20% reduction in regional wall motion (RRWM) in two or more segments and hyperkinesis as an either >20 or >50% increase in shortening fraction (SF). Eleven of 12 patients developed myocardial stunning with varying degrees of compensatory hyperkinesis in unaffected segments, maintaining left ventricular ejection fraction throughout HD. The mean segmental %SF([Overall]) and %SF([RRWM]) fell during HD (2.19 to 1.77 and 2.72 to 1.37, respectively). Intradialytic BP reduction was significantly associated with mean segmental %SF([RRWM]).\n\nQuestion:\nDoes pediatric myocardial stunning underscore the cardiac toxicity of conventional hemodialysis treatments?\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:\nVascular calcification is an active deposition process of calcium phosphate which resembles bone formation and is highly regulated by osteoblast-like cells. Existing studies demonstrate that advanced glycation end-products (AGEs) may play a pathogenic role in the vascular calcification process. However, their mechanism remains poorly understood. The aim of our current study is to investigate how non-cross-link and non-fluorescent N(ε)-carboxymethyl-Lysine (CML), a major immunogen of AGEs, affect the progression of atherosclerotic calcification in diabetes. The present study consisted of an in vivo investigation and two in vitro investigations. In study I, male apoE(-/-) mice were first rendered diabetic by the administration of 5 daily intraperitoneal injections of streptozotocin (STZ, 40 mg/kg), and then given a semi-synthetic high-fat diet (HFD) plus daily injections of CML (10mg/kg/day). The mice were euthanized and analyzed at 0 month (group 0M, n = 10), 2 months (group 2M, n = 10), and 4 months (group 4M, n = 10) after the triple administrations of STZ-CML-HFD. In study II, the effects of CML on the apoptosis in macrophages were investigated. RAW264.7 cells were incubated with or without 50 μg/mL oxLDL plus various concentrations of CML for 48 h. In study III, we investigated whether A7r5 aortic smooth muscle cells were induced into osteoblast-like phenotypes by incubation with or without 80 μg/mL of RAW264.7-derived-apoptotic bodies and 50 μg/mL of oxLDL plus various concentrations of CML (or high-glucose) for 7 days. Related analyses (i.e., H&E staining, Masson staining, von Kossa staining, TUNEL staining, immunohistochemical staining, calcium content assay, annexin V-FITC/PI double-staining, and Western blot) were performed. Morphological analysis showed that early atherosclerotic plaques appeared 2 months after the triple administrations of STZ-CML-HFD, and that typically advanced plaques with extensive calcification lesions, abundant cholesterol crystals, and proliferative collagen were formed 4 months after the triple administrations of STZ-CML-HFD. Furthermore, CML deposition signals and the expression of receptor for advanced glycation end-products (RAGE) in the aortic wall were mainly restricted in the atherosclerotic plaques. After the incubation of A7r5 smooth muscle cells with 10 μmol/L CML plus 50 μg/mL oxLDL, and 80 μg/mL apoptotic bodies (ABs) for 7 days, semi-quantitative analysis of bone morphogenetic protein 2 (BMP-2), core-binding factor α1 (cbfα1), and alkaline phosphatase (ALP) expression showed 5.0-, 2.0-, and 2.9-fold increases, respectively, compared with those in 50 μg/mL oxLDL and 80 μg/mL ABs. Subsequently, a similar trend was observed in the calcium deposition of the cell layer. However, high-glucose had no effects on the ALP activity and calcium deposition of A7r5 cell layer under high-lipid, apoptosis-coexisting conditions. Both animal and cell studies consistently demonstrated that the CML/RAGE axis may first initiate the apoptosis of macrophages in atherosclerotic lesions and then induce BMP-2-cbfα1-ALP-calcification cascade in a high-lipid, apoptosis-coexisting environment.\n\nQuestion:\nDoes advanced glycation end-product Nε-carboxymethyl-Lysine accelerate progression of atherosclerotic calcification in diabetes?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo evaluate insulin-like growth factor-1 receptor (IGF1R) expression in penile cancer and its association with oncologic outcomes. Tissue microarrays were constructed from 53 patients treated at our institution. Expression of IGF1R was evaluated using a Her2-like scoring system. Overexpression was defined as 1+ or greater membranous staining. Association of IGF1R expression with pathologic features was assessed with comparative statistics, and association with local recurrence, progression to nodal or distance metastases, or death was assessed with Kaplan-Meier survival analysis and Cox proportional hazard regression models. Overall, IGF1R overexpression was seen in 33 (62%) cases. With a median follow-up of 27.8 months, IGF1R overexpression was associated with inferior progression-free survival (PFS) (P  =  .003). In a multivariable model controlling for grade, T stage, perineural invasion, and lymphovascular invasion, IGF1R expression was independently associated with disease progression (hazard ratio 2.3, 95% confidence interval 1.1-5.1, P  =  .03. Comparing patients without IGF1R overexpression to those with overexpression, 5-year PFS was 94.1% vs 45.8%.\n\nQuestion:\nDoes overexpression of Insulin-like Growth Factor-1 Receptor be Associated With Penile Cancer Progression?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis study was conducted to estimate the incidence and clinical predictors of post-thoracotomy shoulder pain and to determine the effectiveness of thoracic epidural block in alleviating this pain. A prospective clinical trial. University teaching hospital. Thirty-two adult patients undergoing elective thoracic surgery consented to participate in the study. All operations were open thoracotomies done by the same team of surgeons and anesthesiologists. A thoracic (T6) epidural catheter was placed before induction of general anesthesia. Each patient received 7 mL of lidocaine 2% epidurally and repeated doses of 5 mL of lidocaine 2% every half hour during the operation. Postoperatively, the occurrence of incision or ipsilateral shoulder pain was observed and treated with a maximal dose of 5 mL of lidocaine 2%. If ineffective, indomethacin suppository (nonsteroidal anti-inflammatory drug [NSAID]) was given. Variables such as patient's age, sex, American Society of Anesthesiologists physical status, type, site and duration of surgery, duration of anesthesia, the resection of main bronchus, and the use of thoracostomy tubes were recorded. Postoperatively, 10 patients (31%) had shoulder pain, 4 patients (12.5%) complained of incision pain, and 2 (6.3%) complained of both incision and shoulder pain. A bolus of 5 mL of lidocaine 2% in the epidural catheter relieved incision pain in all the patients, but was ineffective for shoulder pain. Indomethacin suppository was effective in these patients. No correlation was found between any variable and the occurrence of shoulder pain.\n\nQuestion:\nAre thoracic epidural local anesthetics ineffective in alleviating post-thoracotomy ipsilateral shoulder pain?\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:\nDss1 (or Rpn15) is a recently identified subunit of the 26S proteasome regulatory particle. In addition to its function in the protein degradation machinery, it has been linked to BRCA2 (breast cancer susceptibility gene 2 product) and homologous DNA recombination, mRNA export, and exocytosis. While the fungal orthologues of Dss1 are not essential for viability, the significance of Dss1 in metazoans has remained unknown due to a lack of knockout animal models. In the current study deletion of dss-1 was studied in Caenorhabditis elegans with a dss-1 loss-of-function mutant and dss-1 directed RNAi. The analysis revealed an essential role for dss-1 in oogenesis. In addition, dss-1 RNAi caused embryonic lethality and larval arrest, presumably due to loss of the dss-1 mRNA maternal contribution. DSS-1::GFP fusion protein localised primarily in the nucleus. No apparent effect on proteasome function was found in dss-1 RNAi treated worms. However, expression of the C. elegans dss-1 in yeast cells deleted for its orthologue SEM1 rescued their temperature-sensitive growth phenotype, and partially rescued the accumulation of polyubiquitinated proteins in these cells.\n\nQuestion:\nIs c. elegans dss-1 functionally conserved and required for oogenesis and larval growth?\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:\nTranscranial alternating current stimulation (tACS), which is a novel technique for the manipulation of cortical oscillations, can generate subjective visual sensations (phosphenes). In this work, we computationally investigate the current that reaches the eyes from tACS electrodes in order to show that phosphenes induced by tACS are retinal in origin. The finite-element method is used for modelling the path of the current in an anatomically realistic model of the head for various electrode montages. The computational results are used for analysing previous experimental data to investigate the sensitivity of the eye to electrical stimulation. Depending on the locations of both the stimulating and reference electrodes, a small portion of the stimulation current chooses a path that goes through the eyes. Due to the sensitivity of the retina to electrical stimulation, even distant electrodes can produce a sufficiently strong current at the eyes for inducing retinal phosphenes.\n\nQuestion:\nDoes computational analysis shows why transcranial alternating current stimulation induce retinal phosphenes?\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:\nGenetic variation in leptin receptor (LEPR) gene has been reported to associate with insulin and glucose metabolism and adiposity in different study settings and various populations. We wanted to evaluate the association between LEPR polymorphisms, diabetes risk and body weight in Finnish subjects with impaired glucose tolerance (IGT). We investigated the associations of the three LEPR polymorphisms (Lys109Arg, Gln223Arg, 3'UTR Del/Ins) with the conversion to type 2 diabetes and the changes in body weight in 507 individuals with IGT participating in the Finnish Diabetes Prevention Study. Participants were randomized to either an intensive diet and exercise intervention group or a control group. After 3 years, the odds ratio for the development of type 2 diabetes in individuals in the control group with the Lys109Lys genotype was 2.38-fold higher than in individuals with other genotype combinations (P=0.016). Irrespective of group individuals with the Gln223Gln genotype had higher conversion to type 2 diabetes (OR 2.01 (95% CI 1.03-3.93)) than the Arg223 allele carriers (P=0.042). The risk was more pronounced in the control group than in the intervention group. Individuals having the 3'UTR Del/Del genotype had a slightly higher body weight throughout the study than those with the insertion allele (P=0.020), although no difference in weight change was observed.\n\nQuestion:\nIs genetic variation in leptin receptor gene associated with type 2 diabetes and body weight : The Finnish Diabetes Prevention Study?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe present study aimed to identify any relationship between existing access block occupancy (ABO) at the time of patient presentation and delay to definitive procedure. Retrospective descriptive cohort study of all patients aged over 50 years with an ED diagnosis of fractured neck of femur admitted through a tertiary ED over 2 years. The independent variable was the ABO at the start of the hour in which the patient presented, derived from existing ED records, and expressed as the quartile for that hour of the day. The dependent variable was start of surgery more than 24 h after arrival without a documented reason for delay. The data abstractor was blinded to the ABO. All 442 diagnoses of fractured neck of femur recorded in the ED were reviewed, 73 were excluded (16 age, 5 misdiagnosis, 31 no surgery, 21 documented medical reasons for delay). There was a significant relationship between ABO quartile and the rate of delay to surgery ranging from 54% (95% CI 43-63%) for those presenting in the lowest ABO quartile to 77% (68-85%) in the highest (P= 0.006, chi(2)). Subgroup analysis showed that arrival ABO predicted patient access block, and that patient access block was associated with delay to surgery and longer postoperative length of stay (geometric mean 12.9 vs 9.9 days, P < 0.01, t-test).\n\nQuestion:\nDoes emergency Department access block occupancy predict delay to surgery in patients with fractured neck of femur?\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:\nBecause of the heterogeneity in port-wine stains, a number of them prove resistant to treatment with the pulsed-dye laser (PDL). A new variable pulse-duration PDL improves a refractory port-wine stain. A 26-year-old man with a congenital port-wine stain underwent eight treatments with the 1.5-ms pulse-duration PDL resulting in minimal improvement. A single treatment was then administered with the 3-ms pulse-duration PDL. Initial results of treatment with the 3-ms pulse-duration PDL on this patient's port-wine stain show dramatic clearance in areas previously treated with significantly higher fluences, an identical spot size, but with a pulse duration half as long.\n\nQuestion:\nDo treatment of a resistant port-wine stain with a new variable pulse-duration pulsed-dye laser?\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 authors have previously reported on the relationship between activity and subsequent damage at the patient level for patients with psoriatic arthritis (PsA). The aim of this study was to identify key predictors of damage to individual joints in the hands and feet of patients with PsA, in particular those that capture previous activity. Data from patients followed prospectively at the University of Toronto PsA clinic between 1978 and 2006 were available for analysis. Logistic regression was used to relate the probability of a joint developing damage, within a specified time interval after the most recent clinic visit, to potential predictor variables. The predictor variables considered encompassed the history of disease activity of the joint and elsewhere, previous damage and the timing of clinical assessments. 511 patients with no hand damage at clinic entry and 552 patients with no foot damage at clinic entry were included in the analysis of the hand and foot joints, respectively. The analysis of the hand and foot joints demonstrated that the activity (tenderness and/or swelling) history of the specific joint is associated with subsequent damage. For the joints of the feet, activity observations elsewhere in the same foot, and in particular the same toe, were also shown to be associated with subsequent damage.\n\nQuestion:\nDoes inflammation in an individual joint predict damage to that joint in psoriatic arthritis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nRandomized, double-blind, crossover, sham-controlled trial. Repetitive transcranial magnetic stimulation (rTMS) over the primary motor cortex (M1) leads to a significant reduction of spasticity in subjects with spinal cord injury (SCI), but the physiological basis of this effect is still not well understood. The purpose of this study was to evaluate the disynaptic reciprocal Ia inhibition of soleus motoneurons in SCI patients. Department of Neurology, Merano, Italy and TMS Laboratory, Paracelsus Medical University, Salzburg, Austria. Nine subjects with incomplete cervical or thoracic SCI received 5 days of daily sessions of real or sham rTMS applied over the contralateral M1. We compared the reciprocal inhibition, the Modified Ashworth Scale and the Spinal Cord Injury Assessment Tool for Spasticity at baseline, after the last session and 1 week later in the real rTMS and sham stimulation groups. We found that real rTMS significantly reduced lower limb spasticity and restored the impaired excitability in the disynaptic reciprocal inhibitory pathway.\n\nQuestion:\nDoes rTMS modulate reciprocal inhibition in patients with traumatic spinal cord injury?\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 ovarian clear cell adenocarcinoma (OCCA) and ovarian endometrioid adenocarcinoma (EC) are considered to be closely related to endometriosis, the mechanisms of carcinogenesis of these two malignancies and malignant transformation of endometriosis are unclear. In this study, we examined the biology of OCCA and EC by performing large-scale analysis of K-ras activation and p53 mutation and overexpression in these malignancies. The results were subsequently analyzed for correlation with the clinicopathologic data. In the present study of OCCA and EC, we obtained clinicopathological data and analyzed frequency of mutations and overexpression of K-ras and p53. DNA was extracted from formalin-fixed, paraffin-embedded tissue, and target sequences were amplified in vitro by polymerase chain reaction. The DNA was analyzed for K-ras and p53 mutations by testing for single-strand conformation polymorphisms and by direct sequencing. Immunohistochemical staining was performed using p53 monoclonal antibody. Univariate analysis was performed using the Kaplan-Meier algorithm, and differences in survival were analyzed using the log rank test. The prognostic significance of the studied variables for survival was assessed using multivariate analysis with Cox regression analysis. K-ras mutation was detected in 16.2% (6/37) of OCCA patients and 3.7% (1/27) of EC patients. No evidence of p53 mutation was detected in OCCA patients, but p53 mutation was detected in 63.0% of EC patients; these findings are consistent with the results of p53 immunohistochemistry. No statistical significance was observed for K-ras mutation in OCCA or EC. In EC patients, the absence of endometriosis and p53 overexpression was associated with a poorer survival. In OCCA patients tubulocystic and papillary histotype as well as stage II correlated with a worse survival.\n\nQuestion:\nDo p53 mutations and overexpression affect prognosis of ovarian endometrioid cancer but not clear cell 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:\nAmyotrophic lateral sclerosis (ALS) is characterized by pronounced clinical heterogeneity in terms of onset and disease progression. Widespread changes in white matter fibres could be observed by diffusion tensor imaging (DTI), which detects alterations in the degree (diffusivity, ADC) and directedness (fractional anisotropy, FA) of proton movement. The aim of the current study was to determine whether different ALS onset types were reflected in different DTI brain patterns. Seventeen patients with a diagnosis of ALS (6 bulbar, 11 limb onset) and seventeen age-matched controls received 1.5T DTI, where FA and ADC were analyzed using statistical parametric mapping. In ALS patients, an increased diffusivity in the white matter was found below the precentral gyrus and along the corticospinal tract (CST) right into the internal capsule. The FA was decreased in the posterior limb of internal capsule and in the subcortical white matter in the precentral gyrus. In bulbar onset increased diffusivity was found in the CST, whilst in limb onset, frontal subcortical areas displayed an increased diffusivity.\n\nQuestion:\nDo diffusion tensor imaging patterns differ in bulbar and limb onset amyotrophic lateral sclerosis?\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:\nLoss of cognitive function is a common condition in the elderly population. Cognitive impairment is defined as the transitional stage of cognitive decline, between normal aging and early dementia. We tested whether arterial stiffness, evaluated as pulse wave velocity (PWV), is associated with cognitive impairment in older subjects, and whether PWV is increased at a comparable extent in older subjects with cortical or subcortical cerebral lesions when compared with age-matched controls referred for memory deficits. Eighty-four subjects (78 +/- 5 years, 30 men and 54 women) referred for memory deficit with no history of stroke or atrial fibrillation were studied. Carotid-femoral PWV was determined non-invasively with Complior. The Mini Mental State Examination was assessed as a measure of global cognitive function. The sum of the score on the Activities of Daily Living and Instrumental Activities of Daily Living scales was used as a measure of personal independency. Based upon brain imaging, subjects were classified as referred for memory deficits with normal brain imaging, or control, with subcortical microvascular lesions or with cortical atrophy. PWV, normalized for mean blood pressure, was inversely correlated with the Mini Mental State Examination (r = -0.26, P < 0.05), even after controlling for education, prevalent cardiovascular (CV) disease, CV risk factors, and medication use (beta coefficient = -0.28, P < 0.01). PWV was also inversely correlated with personal independency (r = -0.36, P < 0.01; beta coefficient = -0.38, P < 0.01, after multiple adjustment). In the presence of no significant differences in age, education, traditional CV risk factor levels, carotid plaques, or prevalence of CV disease, higher PWV values were more frequent in subjects with cortical atrophy than in patients with subcortical microvascular lesions or controls (P < 0.05).\n\nQuestion:\nIs arterial stiffness an independent risk factor for cognitive impairment in the elderly : a pilot study?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo investigate the production of type I interferon (IFN) by myoblasts and to identify its cell source and the link to Toll-like receptor (TLR) and C-type lectin receptor (CLR) expression and function in myositis biopsy sections. Production of IFNβ was assessed in cultured myoblasts after stimulation with the TLR-3 agonist poly(I-C) or with cytokines involved in Th1 and Th17 differentiation. Expression of HLA class I molecules by myoblasts was analyzed by fluorescence-activated cell sorting after activation of TLR-3 and IFNβ neutralization. In muscle biopsy samples from patients with polymyositis or dermatomyositis, expression of IFNβ, CD56 (a marker of immature muscle precursors), and HLA class I was analyzed using immunohistochemistry. Inflammatory infiltrates were characterized for the expression of myeloid dendritic cells (DCs), their associated CLRs, and the products of activated DCs, interleukin-12 (IL-12), and IL-23. In cultured myoblasts, stimulation of TLR-3 induced the production of IFNβ when combined with IFNγ and up-regulated the expression of HLA class I molecules, which was decreased after IFNβ blockade. In myositis biopsy tissues, immature muscle precursors overexpressing HLA class I were identified as a source of IFNβ. CLRs associated with myeloid DCs were broadly expressed in inflammatory infiltrates, in association with IL-12 and IL-23, and with immature muscle precursors.\n\nQuestion:\nAre immature muscle precursors a source of interferon-β in myositis : role of Toll-like receptor 3 activation and contribution to HLA class I up-regulation?\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 paraventricular nucleus (PVN) of the hypothalamus plays an important role in the progression of heart failure (HF). We investigated whether cyclooxygenase-2 (COX-2) inhibition in the PVN attenuates the activities of sympathetic nervous system (SNS) and renin-angiotensin system (RAS) in rats with adriamycin-induced heart failure. Heart failure was induced by intraperitoneal injection of adriamycin over a period of 2 weeks (cumulative dose of 15 mg/kg). On day 19, rats received intragastric administration daily with either COX-2 inhibitor celecoxib (CLB) or normal saline. Treatment with CLB reduced mortality and attenuated both myocardial atrophy and pulmonary congestion in HF rats. Compared with the HF rats, ventricle to body weight (VW/BW) and lung to body weight (LW/BW) ratios, heart rate (HR), left ventricular end-diastolic pressure (LVEDP), left ventricular peak systolic pressure (LVPSP) and maximum rate of change in left ventricular pressure (LV±dp/dtmax) were improved in HF+CLB rats. Angiotensin II (ANG II), norepinephrine (NE), COX-2 and glutamate (Glu) in the PVN were increased in HF rats. HF rats had higher levels of ANG II and NE in plasma, higher level of ANG II in myocardium, and lower levels of ANP in plasma and myocardium. Treatment with CLB attenuated these HF-induced changes. HF rats had more COX-2-positive neurons and more corticotropin releasing hormone (CRH) positive neurons in the PVN than did control rats. Treatment with CLB decreased COX-2-positive neurons and CRH positive neurons in the PVN of HF rats.\n\nQuestion:\nDoes inhibition of cyclooxygenase-2 reduce hypothalamic excitation in rats with adriamycin-induced heart failure?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo investigate the effect of anti-apoptotic agents on cartilage degradation after a single impact to ankle cartilage. Ten human normal tali were impacted with the impulse of 1 Ns generating peak forces in the range of 600 N using a 4 mm diameter indenter. Eight millimeter cartilage plugs containing the 4 mm diameter impacted core and a 4 mm adjacent ring were removed and cultured with or without P188 surfactant (8 mg/ml), caspase-3 (10 uM), or caspase-9 (2 uM) inhibitors for 48 h. Results were assessed in the superficial and middle-deep layers immediately after injury at day 0 and at 2, 7 and 14 days after injury by live/dead cell and Tunel assays and by histology with Safranin O/fast green staining. A single impact to human articular cartilage ex vivo resulted in cell death, cartilage degeneration, and radial progression of apoptosis to the areas immediately adjacent to the impact. The P188 was more effective in preventing cell death than the inhibitors of caspases. It reduced cell death by more than 2-fold (P<0.05) in the core and by about 30% in the ring in comparison with the impacted untreated control at all time points. P188 also prevented radial expansion of apoptosis in the ring region especially in the first 7 days post-impaction (7.5% Tunel-positive cells vs 46% in the untreated control; P<0.01). Inhibitors of caspase-3 or -9 were effective in reducing cell death in the impacted core only at early time points, but were ineffective in doing so in the ring. Mankin score was significantly improved in the P188 and caspase-3 treated groups.\n\nQuestion:\nDo anti-apoptotic treatments prevent cartilage degradation after acute trauma to human ankle cartilage?\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 preferentially develops at sites of disturbed blood flow. We tested the hypothesis that transglutaminase activity plays a role in plaque development at these locations. Exposure of endothelial cells to steady flow (7 dynes/cm(2)) was associated with relatively low transglutaminase activity, whereas under low oscillatory flow (1.3 ± 2.6 dynes/cm(2)) endothelial cells showed a >4-fold higher level of transglutaminase activity. Under oscillatory flow, transglutaminase activity increased the expression of the chemokine MCP-1 (CCL2). In vivo, oscillatory flow was induced by placement of a tapered perivascular cast around the carotid artery of type 2 transglutaminase (TGM2) knockout mice and WT counterparts. After 2 days, significantly less monocytes adhered to the endothelium in TGM2 knockout mice as compared to WT. In a more chronic setting, ApoE knockout mice that were equipped with the flow-modifying cast developed lesions proximal to the cast (low shear stress), and distal to the cast (oscillatory shear stress). Inhibition of transglutaminase induced a marked reduction in macrophage and fat content in distal lesions only. In addition, lesion size was increased in this area, which was attributed to an increase in smooth muscle content.\n\nQuestion:\nDoes transglutaminase activity regulate atherosclerotic plaque composition at locations exposed to oscillatory shear stress?\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 RNA-binding proteins are thought to play important roles in neural development and the functional regulation of postmitotic neurones by mediating post-transcriptional gene regulation. RNA-binding proteins belonging to the Musashi family are highly expressed in the nervous system; however, their roles are poorly understood. We identified a Caenorhabditis elegans Musashi homologue, MSI-1, whose RNA-recognition motifs show extensive similarity to those of Drosophila and vertebrate Musashi proteins. We isolated a msi-1 mutant and found males with this mutation to have a mating defect. C. elegans male mating behaviour includes a distinct series of steps: response to contact, backing, turning, vulva location, spicule insertion, and sperm transfer. msi-1 is required for the turning and vulva location steps. Like other Musashi family members, MSI-1 is expressed specifically in neural cells, including male-specific neurones required for turning and vulva location. However, msi-1 was not expressed in proliferating neural progenitors in C. elegans, unlike the Musashi family genes in other systems.\n\nQuestion:\nIs mSI-1 , a neural RNA-binding protein , involved in male mating behaviour in Caenorhabditis elegans?\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 activity of virus-specific T lymphocytes, among which those capable of a polyfunctional response against the viral protein gag, is crucial to control HIV infection. The objective of this study is to investigate the polyfunctionality of gag-specific T cells in different phases of HIV infection, analyzing markers related to T-helper cell 1 (Th1) and degranulation/cytotoxicity, and the production of Th1 cytokines in peripheral blood lymphocytes from patients experiencing an acute primary infection, long-term nonprogressors, patients naive for antiretroviral drugs, and patients taking HAART. Cells were stimulated with a pool of gag-derived peptides or with a superantigen (staphylococcal enterotoxin B). Using eight-color polychromatic flow cytometry, we analyzed the expression of interleukin-2, interferon-gamma, CD154, and CD107a by CD4 and CD8 T cells. The main finding was that in all HIV-positive patients, about half gag-specific CD4 T cells were CD107a, that is, able to degranulate. CD4CD154 cells unable to produce Th1 cytokines were the second most represented population. Truly polyfunctional CD4 T cells were very rare and present only in a few long-term nonprogressors. Superantigen stimulation showed that CD4 T lymphocytes from all patients displayed a typical Th response, including interleukin-2 and interferon-gamma production, lacking CD107a expression.\n\nQuestion:\nDoes cytotoxic granule release dominate gag-specific CD4+ T-cell response in different phases of HIV infection?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe aim of this study is to evaluate the long-term outcome of granulosa cell tumour (GCT) of the ovary in a large series of patients treated in MITO centres (Multicentre Italian Trials in Ovarian Cancer) and to define prognostic parameters for relapse and survival. A retrospective multi-institutional review of patients with GCTs of the ovary treated or referred to MITO centres was conducted. Surgical outcome, intraoperative and pathological findings and follow-up data were analysed. Kaplan-Meier and Cox proportional hazards analyses were used to determine the predictors for survival and recurrence. A total of 97 patients with primary GCT of the ovary were identified. The median follow-up period was 88 months (range 6-498). Of these, 33 patients had at least one episode of disease recurrence, with a median time to recurrence of 53 months (range 9-332). Also, 47% of recurrences occurred after 5 years from initial diagnosis. At multivariate analysis, age and stage were independent poor prognostic indicators for survival; surgical treatment outside MITO centres and incomplete surgical staging retained significant predictive value for recurrence in both univariate and multivariate analyses.\n\nQuestion:\nIs long-term follow-up crucial after treatment for granulosa cell tumours of the ovary?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo test the hypothesis that prophylactic treatment with the surfactant Curosurf (Chiesi Farmaceutici SPA, Parma, Italy) improves survival and respiratory problems more than rescue treatment. Meta-analysis of three prophylaxis versus rescue treatment trials, conducted in four countries. A meta-analysis was performed with the original, individual data of mortality, severe respiratory distress syndrome, and chronic lung disease of 671 newborns as outcomes. The random-effects logistic model (accounting for the trial-within-country structure) was applied and adjusted for imbalances in covariates. The probability of each outcome differed between the countries, but the actual treatment effect itself did not. The adjusted odds ratios (ORs) and confidence intervals (CIs) for prophylaxis versus rescue were as follows: mortality: OR, .47; 95% CI, .30 to .73; severe RDS: OR, .50; 95% CI, .33 to .74; and chronic lung disease of the newborn in the survivors at day 28 after birth: OR, .54; 95% CI, .34 to .86. Gender, birth weight, gestational age, and prenatal administration of glucocorticosteroids were significant confounding covariates.\n\nQuestion:\nAre mortality , severe respiratory distress syndrome , and chronic lung disease of the newborn reduced more after prophylactic than after therapeutic administration of the surfactant Curosurf?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo determine whether genetic influences account for individual differences in susceptibility to falls in older women. Prospective twin cohort study. Research laboratory and residential environment. Ninety-nine monozygotic (MZ) and 114 dizygotic (DZ) female twin pairs aged 63 to 76 from the Finnish Twin Cohort study. The participants recorded their falls on a calendar for an average+/-standard deviation of 344+/-41 days. Reported falls were verified via telephone interview, and circumstances, causes, and consequences of the fall were asked about. The total number of falls was 434, of which 188 were injurious; 91 participants had two or more falls. Casewise concordance was 0.61 (95% confidence interval (CI)=0.49-0.72) for MZ twins and 0.49 (95% CI=0.37-0.62) for DZ twins for at least one fall, 0.38 (95% CI=0.23-0.53) for MZ and 0.33 (95% CI=0.17-0.50) for DZ twins for at least one injurious fall, and 0.43 (95% CI=0.26-0.60) for MZ and 0.36 (95% CI=0.17-0.55) for DZ twins for recurrent falls. On average, the proportion of familial influences accounting for the individual differences in susceptibility to at least one fall was 30% and to recurrent falls was 40%; nongenetic familial and nonfamilial factors alone accounted for susceptibility to at least one injurious fall.\n\nQuestion:\nDoes genetic factors and susceptibility to fall in older women?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe have previously created a potent DNA vaccine encoding calreticulin linked to the human papillomavirus (HPV) oncogenic protein E7 (CRT/E7). While treatment with the CRT/E7 DNA vaccine generates significant tumor-specific immune responses in vaccinated mice, the potency with the DNA vaccine could potentially be improved by co-administration of a histone deacetylase inhibitor (HDACi) as HDACi has been shown to increase the expression of MHC class I and II molecules. Thus, we aimed to determine whether co-administration of a novel HDACi, AR-42, with therapeutic HPV DNA vaccines could improve the activation of HPV antigen-specific CD8(+) T cells, resulting in potent therapeutic antitumor effects. To do so, HPV-16 E7-expressing murine TC-1 tumor-bearing mice were treated orally with AR-42 and/or CRT/E7 DNA vaccine via gene gun. Mice were monitored for E7-specific CD8(+) T cell immune responses and antitumor effects. TC-1 tumor-bearing mice treated with AR-42 and CRT/E7 DNA vaccine experienced longer survival, decreased tumor growth, and enhanced E7-specific immune response compared to mice treated with AR-42 or CRT/E7 DNA vaccine alone. Additionally, treatment of TC-1 cells with AR-42 increased the surface expression of MHC class I molecules and increased the susceptibility of tumor cells to the cytotoxicity of E7-specific T cells. This study indicates the ability of AR-42 to significantly enhance the potency of the CRT/E7 DNA vaccine by improving tumor-specific immune responses and antitumor effects. Both AR-42 and CRT/E7 DNA vaccines have been used in independent clinical trials; the current study serves as foundation for future clinical trials combining both treatments in cervical cancer therapy.\n\nQuestion:\nDoes histone deacetylase inhibitor AR-42 enhance E7-specific CD8⁺ T cell-mediated antitumor immunity induced by therapeutic HPV DNA vaccination?\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:\nPlease see related commentary: http://www.biomedcentral.com/1741-7015/10/21/abstract Age-related macular degeneration (AMD) is a leading cause of blindness that affects the central region of the retinal pigmented epithelium (RPE), choroid, and neural retina. Initially characterized by an accumulation of sub-RPE deposits, AMD leads to progressive retinal degeneration, and in advanced cases, irreversible vision loss. Although genetic analysis, animal models, and cell culture systems have yielded important insights into AMD, the molecular pathways underlying AMD's onset and progression remain poorly delineated. We sought to better understand the molecular underpinnings of this devastating disease by performing the first comparative transcriptome analysis of AMD and normal human donor eyes. RPE-choroid and retina tissue samples were obtained from a common cohort of 31 normal, 26 AMD, and 11 potential pre-AMD human donor eyes. Transcriptome profiles were generated for macular and extramacular regions, and statistical and bioinformatic methods were employed to identify disease-associated gene signatures and functionally enriched protein association networks. Selected genes of high significance were validated using an independent donor cohort. We identified over 50 annotated genes enriched in cell-mediated immune responses that are globally over-expressed in RPE-choroid AMD phenotypes. Using a machine learning model and a second donor cohort, we show that the top 20 global genes are predictive of AMD clinical diagnosis. We also discovered functionally enriched gene sets in the RPE-choroid that delineate the advanced AMD phenotypes, neovascular AMD and geographic atrophy. Moreover, we identified a graded increase of transcript levels in the retina related to wound response, complement cascade, and neurogenesis that strongly correlates with decreased levels of phototransduction transcripts and increased AMD severity. Based on our findings, we assembled protein-protein interactomes that highlight functional networks likely to be involved in AMD pathogenesis.\n\nQuestion:\nDoes systems-level analysis of age-related macular degeneration reveal global biomarkers and phenotype-specific functional networks?\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:\nAcute-on-chronic liver failure (ACLF) is characterized by acute deterioration of cirrhosis, systemic inflammation and multi-organ failure. Inflammation is also key to the pathobiology of portal hypertension. This study aims to define the relationship between systemic and hepatic haemodynamics in patients with ACLF. Sixty patients with alcoholic cirrhosis were prospectively enrolled - stable cirrhosis (SC, n = 27), acute decompensation without ACLF (AD, n = 14) and ACLF (n = 19) - and managed with standard therapy. Systemic and hepatic haemodynamic studies were performed, and patients were followed up for 3 months. Plasma norepinephrine, cytokine profile, nitrate/nitrite and malondialdehyde levels were measured. Three-month mortality was as follows: SC - none; AD - 14%; ACLF - 47.2% (P < 0.001). Mean arterial pressure was lowest in the ACLF group (P < 0.001). ACLF patients had significantly higher hepatic vein pressure gradient (HVPG), while the hepatic blood flow was markedly reduced with an increase in intrahepatic resistance, which predicted mortality (AUROC: 0.87, P < 0.0001). In ACLF, the severity of intrahepatic resistance correlated with markers of inflammatory response, norepinephrine levels, creatinine levels and severity of encephalopathy. Modelling data showed that the high norepinephrine levels in ACLF may contribute to the right shift of the HVPG-hepatic blood flow relationship and its levels correlated with inflammatory markers and mortality (AUROC: 0.90; P < 0.0001).\n\nQuestion:\nIs systemic inflammation associated with increased intrahepatic resistance and mortality in alcohol-related acute-on-chronic liver failure?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThyroglobulin (Tg) levels measured at the time of remnant ablation after thyroid hormone withdrawal (THW) were shown to have prognostic value in predicting disease-free status. Our objectives were to determine whether stimulated Tg levels, measured at the time of remnant ablation performed under recombinant human TSH (rhTSH) stimulation, has value in predicting absence of detectable disease 1 year after radioiodine therapy and to compare the results obtained with this approach with a cohort of patients submitted to ablation after THW. This was a prospective observational study. The study included 293 consecutive patients treated for a differentiated thyroid carcinoma with no initial evidence of distant metastasis. All patients were submitted to a total or near-total thyroidectomy, followed by ablation either under rhTSH (n = 151) or endogenous TSH stimulation (n = 142). Patients with positive Tg antibodies were excluded. The predictive value of Tg at ablation was assessed by receiver operating characteristic curve analysis. In the rhTSH group, 96 patients (73.3%) were considered disease-free at 1 year. Stimulated Tg at ablation after rhTSH was found to be an independent prognostic indicator of disease persistence 12 months later. The highest-accuracy cutoff value for absence of detectable disease was defined as 7.2 ng/mL, with a negative predictive value of 90%. In the THW group, Tg at ablation also proved to have independent predictive value. Using the same threshold (7.2 ng/mL), the negative predictive value of Tg was 95% in the THW group.\n\nQuestion:\nDoes stimulated thyroglobulin at recombinant human TSH-aided ablation predict disease-free status one year later?\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:\nHeart and pulmonary involvement is a leading cause of systemic sclerosis (SSc)-related deaths. The six-minute walk test (6MWT) is a simple and reproducible test commonly used to evaluate exercise capacity. We tried to assess a potential relationship between exercise capacity assessed by 6MWT, echocardiographic parameters of right ventricular function and serum levels of endothelin-1 and NTproBNP. We prospectively studied 111 consecutive patients (101F, 10M, age 54.2±13.8 years) with diagnosed SSc (mean disease duration 9±12.4 years) and a group of 21 age-matched subjects (18F, 3M, age 49.3±10.5 years). In addition to routine evaluation, 6MWT and transthoracic echocardiography (Phillips iE 33) were performed. We also measured serum endothelin-1 (Human Endothelin-1 immunoassay R & D Systems) and NT-proBNP levels (Elecsys pro-BNP immunoassay; Roche Diagnostics). The mean 6MWT distance was significantly shorter in the SSc group than in the controls (562.8±60.3 vs. 514.7±102.5 m, p=0.03). In the SSc group 6MWT distance correlated with ET-1 (r=-0.5, p<0.0001), NTproBNP (r=-0.4, p=0.0008) levels, and echocardiographic indices AcT (r=0.4, p=0.0002) and TRPG (r=-0.4, p=0.0011). Moreover, in patients with 6MWT distance <450 m NTproBNP and endotothelin-1 levels were significantly higher than in patients with distance >450 m (311.2, 31.1-17237 vs. 105.3, 5-17670 pg/ml, p=0.0138 and 2.9±2.2 vs. 1.4±0.7 pg/ml, p=0.0032).\n\nQuestion:\nDoes six-minute walk test reflect neurohormonal activation and right ventricular function in systemic sclerosis patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPostoperative nausea and vomiting (PONV) remains the most common postoperative complication, and causes decreased patient satisfaction, prolonged postoperative hospital stays, and unanticipated admission. There are limited data that indicate that dextrose may reduce nausea and vomiting. In this trial, we attempted to determine whether the rate of PONV can be decreased by postoperative administration of IV dextrose bolus. To test the effect of postoperative dextrose administration on PONV rates, we conducted a double-blind, randomized, placebo-controlled trial. We enrolled 62 nondiabetic, ASA class I or II nonsmoking outpatients scheduled for gynecologic laparoscopic and hysteroscopic procedures. Patients were randomized into 2 groups: the treatment group received dextrose 5% in Ringer lactate solution, and the control (placebo) group received Ringer lactate solution given immediately after surgery. All patients underwent a standardized general anesthesia and received 1 dose of antiemetic a half hour before emergence from anesthesia. PONV scores, antiemetic rescue medications, narcotic consumption, and discharge time were recorded in the postanesthesia care unit (PACU) in half-hour intervals. The 2 groups were similar with regard to age, weight, anxiety scores, prior PONV, non per os status, presurgical glucose, anesthetic duration, intraoperative narcotic use, and total weight-based fluid volume received. Postoperative nausea scores were not significantly different in the dextrose group compared with the control group (P > 0.05) after Bonferroni correction for repeated measurements over time. However, patients who received dextrose 5% in Ringer lactate solution consumed less rescue antiemetic medications (ratio mean difference, 0.56; 95% confidence interval, 0.39-0.82; P = 0.02), and had a shorter length of stay in the PACU (ratio mean difference, 0.80; 95% confidence interval, 0.66-0.97; P = 0.03) compared with patients in the control group.\n\nQuestion:\nDoes intravenous dextrose administration reduce postoperative antiemetic rescue treatment requirements and postanesthesia care unit length of stay?\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:\nPolymorphism of rs2016520 in gene PPARD has been associated with lipid metabolism, obesity, metabolic syndrome and type 2 diabetes mellitus (T2DM). We aimed to study the association of rs2016520 with common metabolic traits in a large population of Han Chinese adults. The polymorphism was genotyped in 1409 subjects using Matrix-Assisted Laser Desorption/Ionization Time of Flight Mass Spectrometry (MALDI-TOF MS); all participants underwent standard clinical examination and a 75g oral glucose tolerance test (OGTT); associations between the polymorphism and metabolic traits and indices of insulin resistance and insulin sensitivity were analyzed. There was no significant difference in genotypes between the normal glucose tolerance (NGT) and the prediabetes group (χ(2)=3.17, P=0.2), except a nominal difference of allele frequency (χ(2)=3.07, P=0.07). The G carrier presented lower fasting plasma glucose (FPG, P=0.03), lower 2h plasma glucose (Pdom=0.04) and lower fasting insulin (P=0.02), lower systolic blood pressure (SBP, P=0.03), lower HOMA-IR (P=0.02) and higher QUICKI (P=0.01). Moreover, rs2016520 polymorphism was associated with FPG (β=-0.09, P=0.05), it was also associated with indices of insulin resistance (HOMA-IR, β=-0.06, Pdom=0.02; fasting insulin, β=-0.04, P=0.02) and indices of insulin sensitivity (QUICKI, β=-0.01, P=0.004). In addition, we observed that the allele G was also associated with lower SBP (β=-1.29, P=0.04) and diastolic blood pressure (DBP, β=-0.09, P=0.01). However, the minor allele G was not associated with risk of metabolic disorders including prediabetes, overweight, hypertension and metabolic syndrome.\n\nQuestion:\nIs pPARD rs2016520 polymorphism associated with metabolic traits in a large population of Chinese adults?\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:\nAdult-type hypolactasia (lactase non-persistence) is a common cause of gastrointestinal symptoms. Several DNA sequence variants have been identified for the lactase-persistence/non-persistence (LP/LNP), the most common being the C to T residing -13910 bp upstream of the lactase gene (LCT). We have analysed sequence variants of LP/LNP in subjects originating from Northern Russia. A total of 148 subjects with gastrointestinal complaints were genotyped covering about 400 bp around the -13910C/T variant using direct PCR-sequencing. All patients were interviewed about milk-related symptoms using the questionnaire. Disaccharidase activities were measured from intestinal biopsy specimens of the index person. The prevalence of the -13910C/C genotype among 148 patients was 28.4%. A G to A variant residing 13914 bp upstream from the LCT gene (-13914G>A) was identified in one participant carrying the -13910C/C genotype. In two biopsy specimens her lactase activity was above the generally accepted cut off level for adult-type hypolactasia, 10U/g protein. Three other family members also carried the -13914G>A genotype. Among eight family members five had the LNP genotype -13910C/C.\n\nQuestion:\nDoes the -13914G > A variant upstream of the lactase gene ( LCT ) is associate with lactase persistence/non-persistence?\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:\nAcute and chronic renal dysfunction (ARD, CRD) are common complications after liver transplantation and are associated with poor outcome. We reviewed the results of 181 liver transplants performed in our institution between January 1, 1998 and December 31, 2000 in which the recipients were alive with good liver function at the end of the follow-up period (mean 2.7 years). Renal dysfunction was defined as a serum creatinine (Cr) greater than or equal to 2 mg/dL in both acute and chronic settings. The incidence of ARD during the first posttransplant week was 39.2% (n=71), whereas late CRD occurred in 6.0% (n=11) of the patients by the end of the follow-up period. Among the variables we examined for association with CRD, five factors were found to be statistically significant in univariate analysis: pretransplant diabetes (PRTDM) (0.000), Cr greater than or equal to 2 during the first postoperative week (0.003), posttransplant diabetes (POTDM) (0.014), age greater than 50 (0.025), and tacrolimus level greater than 15 ng/mL at postoperative day 15 (0.058). In binary logistic regression analysis, PRTDM (odds ratio [OR]=5.7, 95% confidence interval [CI]) and early postoperative ARD (OR=10.2 95% CI) remained consistently significant. Nine of 11 patients with CRD also had a history of ARD during the first postoperative week. These patients progressed to CRD despite the fact that seven of nine had normalized their renal function by day 90 posttransplant.\n\nQuestion:\nDoes early kidney dysfunction post liver transplantation predict late chronic kidney 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:\nBloom's syndrome (BS) is an autosomal recessive disorder causing short stature, immunodeficiency, and an increased risk of cancer. Increased rates of sister chromatid exchange and chromosomal aberration have been observed in cells having defects in the BLM gene. Among five kinds of human RecQ helicases cloned, the mutations in WRN and RecQL4 have been known as the causes of premature ageing. Little is, however, known about the function of BLM helicase in ageing. We show that human BLM, but not WRN can prevent the premature ageing and the increased homologous recombination at the rDNA loci caused by sgs1 mutation. Unexpectedly, the levels of ERCs (extrachromosomal rDNA circles), the products of homologous recombination, formed in 7-generation cells of the wild-type or the sgs1:BLM strain were comparable with those of the sgs1 or the sgs1:WRN age-matched-old cells.\n\nQuestion:\nDoes bloom 's syndrome gene suppress premature ageing caused by Sgs1 deficiency in yeast?\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 explore (1) whether extremely low gestational age newborns exposed to inflammation-associated pregnancy disorders differ in retinopathy of prematurity (ROP) risk from infants exposed to placenta dysfunction-associated disorders, and (2) whether ROP risk associated with postnatal hyperoxemia and bacteremia differs among infants exposed to these disorders. Pregnancy disorders resulting in preterm birth include inflammation-associated: preterm labor, prelabor premature rupture of membranes (pPROM), cervical insufficiency, and abruption and placenta dysfunction-associated: preeclampsia and fetal indication. The risk of severe ROP associated with pregnancy disorders was evaluated by multivariable analyses in strata defined by potential effect modifiers, postnatal hyperoxemia and bacteremia. Compared to preterm labor, infants delivered after pPROM were at reduced risk of plus disease (Odds ratio = 0.4, 95% confidence interval: 0.2-0.8) and prethreshold/threshold ROP (0.5, 0.3-0.8). Infants delivered after abruption had reduced risk of zone I ROP (0.2, 0.1-0.8) and prethreshold/threshold ROP (0.3, 0.1-0.7). In stratified analyses, infants born after placenta dysfunction had higher risks of severe ROP associated with subsequent postnatal hyperoxemia and bacteremia than infants born after inflammation-associated pregnancy disorders.\n\nQuestion:\nDo pregnancy disorders appear to modify the risk for retinopathy of prematurity associated with neonatal hyperoxemia and bacteremia?\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 clinical use of paclitaxel is limited by variable responses and the potential for significant toxicity. To date, studies of associations between variants in candidate genes and paclitaxel effects have yielded conflicting results. We aimed to evaluate the relationships between global gene expression and paclitaxel sensitivity. We utilized well-genotyped lymphoblastoid cell lines derived from the International HapMap Project to evaluate the relationships between cellular susceptibility to paclitaxel and global gene expression. Cells were exposed to varying concentrations of paclitaxel to evaluate paclitaxel-induced cytotoxicity and apoptosis. Among the top genes, we identified solute carrier (SLC) genes associated with paclitaxel sensitivity and narrowed down the list to those that had single nucleotide polymorphisms associated with both the expression level of the SLC gene and also with paclitaxel sensitivity. We performed an independent validation in an independent set of cell lines and also conducted functional studies using RNA interference. Of all genes associated with paclitaxel-induced cytotoxicity at P less than 0.05 (1713 genes), there was a significant enrichment in SLC genes (31 genes). A subset of SLC genes, namely SLC31A2, SLC43A1, SLC35A5, and SLC41A2, was associated with paclitaxel sensitivity and had regulating single nucleotide polymorphisms that were also associated with paclitaxel-induced cytotoxicity. Multivariate modeling demonstrated that those four SLC genes together explained 20% of the observed variability in paclitaxel susceptibility. Using RNA interference, we demonstrated increased paclitaxel susceptibility with knockdown of three SLC genes, SLC31A2, SLC35A5, and SLC41A2.\n\nQuestion:\nDo whole-genome studies identify solute carrier transporters in cellular susceptibility to paclitaxel?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe goal of this study was to develop and implement methodology that would aid in the analysis of extended high-density single nucleotide polymorphism (SNP) major histocompatibility complex (MHC) haplotypes combined with human leucocyte antigen (HLA) alleles in relation to type 1 diabetes risk. High-density SNP genotype data (2918 SNPs) across the MHC from the Type 1 Diabetes Genetics Consortium (1240 families), in addition to HLA data, were processed into haplotypes using PedCheck and Merlin, and extended DR3 haplotypes were analysed. With this large dense set of SNPs, the conservation of DR3-B8-A1 (8.1) haplotypes spanned the MHC (>/=99% SNP identity). Forty-seven individuals homozygous for the 8.1 haplotype also shared the same homozygous genotype at four 'sentinel' SNPs (rs2157678 'T', rs3130380 'A', rs3094628 'C' and rs3130352 'T'). Conservation extended from HLA-DQB1 to the telomeric end of the SNP panels (3.4 Mb total). In addition, we found that the 8.1 haplotype is associated with lower risk than other DR3 haplotypes by both haplotypic and genotypic analyses [haplotype: p = 0.009, odds ratio (OR) = 0.65; genotype: p = 6.3 x 10(-5), OR = 0.27]. The 8.1 haplotype (from genotypic analyses) is associated with lower risk than the high-risk DR3-B18-A30 haplotype (p = 0.01, OR = 0.23), but the DR3-B18-A30 haplotype did not differ from other non-8.1 DR3 haplotypes relative to diabetes association.\n\nQuestion:\nDoes the frequent and conserved DR3-B8-A1 extended haplotype confer less diabetes risk than other DR3 haplotypes?\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:\nMajor depressive disorder has been associated with low serum levels of brain-derived neurotrophic factor (sBDNF), which is functionally involved in neuroplasticity. Although sBDNF levels tend to normalize following psychopathological improvement with antidepressant treatment, it is unclear how closely sBDNF changes are associated with treatment outcome. To examine whether baseline sBDNF or early changes in sBDNF are predictive of response to therapy. Twenty-five patients with major depressive disorder underwent standardized treatment with duloxetine. Severity of depression, measured by the Hamilton Depression Rating Scale, and sBDNF were assessed at baseline, and after 1, 2, and 6 weeks of treatment. Therapy outcome after 6 weeks was defined as response (≥50 % reduction in baseline Hamilton Depression Rating score) and remission (Hamilton Depression Rating score <8). The predictive values for treatment outcome of baseline sBDNF, and early (i.e., ≤2 weeks) changes in sBDNF and Hamilton Depression Rating score were also assessed. At baseline, sBDNF correlated with Hamilton Depression Rating scores. Treatment response was associated with a higher baseline sBDNF concentration, and a greater Hamilton Depression Rating score reduction after 1 and 2 weeks. A greater early rise in sBDNF correlated with a decreased early Hamilton Depression Rating score reduction.\n\nQuestion:\nAre high baseline BDNF serum levels and early psychopathological improvement predictive of treatment outcome in major depression?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nStudies suggest that inappropriate responses to proinflammatory stimuli might contribute to inflammation in cystic fibrosis (CF) lungs. However, technical challenges have made it difficult to distinguish whether altered responses in CF airways are an intrinsic defect or a secondary effect of chronic disease in their tissue of origin. The CF pig model provides an opportunity to study the inflammatory responses of CF airways at birth, before the onset of infection and inflammation. To test the hypothesis that acute inflammatory responses are perturbed in porcine CF airways. We investigated the inflammatory responses of newborn CF and non-CF pig airways following a 4-hour exposure to heat-killed Staphylococcus aureus, in vivo and in vitro. Following an in vivo S. aureus challenge, markers of inflammation were similar between CF and littermate control animals through evaluation of bronchoalveolar lavage and tissues. However, transcriptome analysis revealed genotype-dependent differences as CF pigs showed a diminished host defense response compared with their non-CF counterparts. Furthermore, CF pig airways exhibited an increase in apoptotic pathways and a suppression of ciliary and flagellar biosynthetic pathways. Similar differences were observed in cultured airway epithelia from CF and non-CF pigs exposed to the stimulus.\n\nQuestion:\nDo newborn Cystic Fibrosis Pigs Have a Blunted Early Response to an Inflammatory Stimulus?\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:\nAcute graft-versus-host disease (GVHD) remains a significant impediment to successful hematopoietic stem-cell transplantation (HSCT). Here, we examined the effectiveness of 2-amino-2-(2-[4-octylphenyl]ethyl)-1,3-propanediol hydrochloride (FTY720), an immunosuppressant that retraffics activated lymphocytes to secondary lymphoid organs, for the treatment of acute GVHD in an established dog leukocyte antigen-nonidentical unrelated canine HSCT model. Dogs were given HSCT after conditioning with 920 cGy total body irradiation. The dogs received methotrexate 0.4 mg/kg/day on days 1, 3, 6, and 11 and FTY720 (5 mg/kg/day orally) after developing GVHD. Five of six dogs achieved engraftment, developed acute GVHD, and were treated with FTY720. FTY720 resulted in a profound decrease in lymphocytes and a temporary mitigation of clinical GVHD; however, GVHD recurred in all dogs. Four of five dogs were euthanized because of severe GVHD and the fifth because of severe inanition associated with moderate GVHD.\n\nQuestion:\nDoes fTY720 abrogate acute graft-versus-host disease in the dog leukocyte antigen-nonidentical unrelated canine model?\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:\nNumerous epidemiological studies have reported the association between polymorphisms of Toll-like receptor 2 (TLR2) and susceptibility to tuberculosis (TB). However, the results remain inconclusive. Therefore, we performed a quantitative meta-analysis to evaluate associations between the polymorphism of Arg753Gln of the TLR2 gene and susceptibility to TB. Three databases (PubMed, CNKI and Embase) were systematically searched for eligible studies. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) as our index were used to assess the relation between the TLR2 gene Arg753Gln polymorphism and risk of TB. Overall and subgroup analyses were conducted according to the available information. With a detailed selection, 7 eligible studies with 1486 cases and 1322 controls were identified in our meta-analysis. There was a significant difference between TLR2 gene Arg753Gln polymorphism and the risk of TB (additive model: P<0.01, OR=2.89, 95% CI: 2.13-3.91; GA vs. GG: P<0.01, OR=2.92, 95% CI: 2.09-4.08). Interestingly, subgroup analysis based on ethnicity indicated that TB risk was significantly increased in Asians (additive model: P<0.01, OR=3.17, 95% CI: 2.31-4.35; GA vs. GG: P<0.01, OR=3.29, 95% CI: 2.32-4.68); by contrast, there was no association found in whites (additive model: P=0.40, OR=0.57, 95% CI: 0.15-2.13; GA vs. GG: P=0.40, OR=0.57, 95% CI: 0.15-2.13).\n\nQuestion:\nAre arg753Gln Polymorphisms in Toll-Like Receptor 2 Gene Associated with Tuberculosis Risk : A Meta-Analysis?\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:\nRepetitive Transcranial Magnetic Stimulation (rTMS) has been recently employed as a therapeutic strategy for stroke, although its effects on cerebral hemodynamics has been poorly investigated. This study aims to examine the impact of high frequency rTMS on cerebral vasomotor reactivity (VMR). Twenty-nine healthy subjects were randomly assigned to real (19) or sham 17-Hz rTMS, applied on primary motor cortex (M1) of the dominant hemisphere. All subjects underwent Transcranial Doppler of the middle cerebral arteries to evaluate mean flow velocity and VMR before (T(0)) and within 10 min (T(1)) following rTMS. Four subjects underwent further VMR evaluations at 2 (T(2)), 5 (T(3)) and 24 h (T(4)) after rTMS. As a control condition, 10 subjects underwent real (5) or sham rTMS on calcarine cortex. In addition, five acute stroke patients underwent five daily rTMS sessions on the affected hemisphere mimicking a therapeutic trial. Following real rTMS on M1 (p=0.002) and calcarine cortex (p<0.001) VMR decreased with respect to T(0) in both hemispheres, while no change was observed after sham rTMS (p>0.6). VMR tended to remain lower than T(0) until T(3.) Cerebral VMR decreased independently of the stimulated side also in the patients' group.\n\nQuestion:\nDoes high frequency repetitive transcranial magnetic stimulation decrease cerebral vasomotor reactivity?\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:\nCranial endplates of human vertebrae are injured more often than caudal, in both young and elderly spines. We hypothesise that cranial endplates are inherently vulnerable to compressive loading because of structural asymmetries in the vertebrae. Sixty-two \"motion segments\" (two vertebrae and the intervening disc and ligaments) were obtained post-mortem from thirty-five human spines (17F/18M, age 48-92 yrs, all spinal levels from T8-9 to L4-5). Specimens were compressed to failure while positioned in 2-6 degrees of flexion, and the resulting damage characterised from radiographs and at dissection. 2 mm-thick slices of 94 vertebral bodies (at least one from each motion segment) were cut in the mid-sagittal plane, and in a para-sagittal plane through the pedicles. Microradiographs of the slices were subjected to image analysis to determine the thickness of each endplate at 10 locations. Optical density of the endplates and adjacent trabecular bone was also measured. Measurements obtained in cranial and caudal regions, and in mid-sagittal and pedicle slices, were compared using repeated measures ANOVA with age, level and gender included as between-subject factors. Linear regression was used to determine significant predictors of compressive strength (failure stress). Fracture affected the cranial endplate in 55/62 specimens. Cranial endplates were thinner than caudal (p=0.003) by 14% and 11% on average, in mid-sagittal and pedicle slices respectively. Caudal but not cranial endplates were thicker at lower spinal levels (p=0.01). Optical density of trabecular bone adjacent to the endplates was 6% lower cranially than caudally (p=0.004), and the average optical density of trabecular bone in mid-sagittal slices was 10% lower in women than in men (p=0.025). Vertebral yield stress (mean 2.22 MPa, SD 0.77 MPa) was best predicted by the density of trabecular bone underlying the cranial endplate of the mid-sagittal slice of the fractured vertebra (r(2)=0.67, p=0.0006).\n\nQuestion:\nDo vertebral fractures usually affect the cranial endplate because it is thinner and supported by less-dense trabecular bone?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo study matrix metalloproteinases (MMP) and tissue inhibitors of metalloproteinases (TIMP) in the corneas from mice with ulcerative herpes stromal keratitis (HSK) treated with amniotic membrane transplantation (AMT). The corneas from BALB/c mice were infected with HSV-1. Mice with ulcerative HSK on postinfection (PI) day 14 were used for the experiments. In one group of mice, the corneas were treated with transplantation of amniotic membrane (AMT) that was secured with a tarsorrhaphy, and a control group underwent tarsorrhaphy alone. After 2 days, the appearance of corneal ulcers and stromal inflammation was judged clinically. Corneal sections were studied by immunohistochemistry for the expression of MMP-2, -8, and -9 and TIMP-1 and -2. MMP activity in the corneas was investigated by zymography, and the expression of the enzymes was measured by the Western blot technique. At day 14 PI, the ulcers stained intensely positive for MMP-2, -8, and -9 and TIMP-1 and -2. Ulceration (P < 0.001), stromal inflammation (P < 0.01) and inflammatory cell infiltration (P < 0.001) markedly improved by day 2 after AMT. This was associated with reduced expression (P < 0.01) and activity of MMP-8, and -9 and increased localization of TIMP-1 (P < 0.01), whereas TIMP-2 was not affected. In contrast, high levels of expression of MMP-8 and -9 remained in the cornea after tarsorrhaphy, and the TIMP-1 expression was only slightly upregulated.\n\nQuestion:\nDoes transplantation of amniotic membrane in murine herpes stromal keratitis modulate matrix metalloproteinases in the cornea?\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:\nMaspin is known as a tumor suppressor gene, but its significance has been questioned in various human cancers. The aim of this study was to investigate the expression pattern of Maspin in human gastric adenocarcinomas and its possible correlation with clinicopathological findings. The expression of Maspin mRNA was measured by nested RT-PCR using 60 frozen adenocarcinomas of the stomach and 31 noncancerous tissues from the proximal resection margin. Immunohistochemical study for Maspin protein expression was carried out using 62 paraffin-embedded tissues, composed of both cancer and noncancerous tissues. Maspin mRNA expression was detected in 80.0% (48 of 60) of the gastric adenocarcinomas, but in only 22.6% (7 of 31) of the normal gastric mucosa (p<0.001). The positive rate of Maspin protein expression was higher in the adenocarcinomas than the normal tissues (62.9% vs. 27.4%, p<0.05). In addition, the intestinal type of tumors showed significantly higher expression levels compared to the diffuse type of tumors (81.5% vs. 48.6%, p<0.05).\n\nQuestion:\nIs expression of maspin associated with the intestinal type of gastric adenocarcinoma?\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:\nHypoxia inducible factor-1 (HIF-1) promotes transitory neuronal survival suggesting that additional mechanisms such as the endoplasmic reticulum (ER) stress might be involved in determining neuronal survival or death. Here, we examined the involvement of ER stress in hypoxia-induced neuronal death and analysed the relationship between ER stress and the HIF-1 pathways. Cultures of rat cortical neurons were exposed to chemical hypoxia induced by 200 μM CoCl2 , and its effect on neuronal viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and counting apoptotic nuclei. Protein levels were determined by Western blot analysis. RT-PCR was performed to analyse the content and the t1/2 of HIF-1α mRNA. Chemical hypoxia induced neuronal apoptosis in a time-dependent manner and activated the ER stress PRK-like endoplasmic reticulum kinase (PERK)-dependent pathway. At later stages, chemical hypoxia increased the expression of the C/EBP homologous protein (CHOP) and caspase 12 activity. CoCl2 reduced HIF-1α mRNA t1/2 leading to a decrease in HIF-1α mRNA and protein content, simultaneously activating the ER stress PERK-dependent pathway. Salubrinal, a selective inhibitor of phospho-eIF2α phosphatase, protected neurons from chemical hypoxia by reducing CHOP levels and caspase 12 activity, and increasing the t1/2 of HIF-1α mRNA and the levels of HIF-1α protein. Knocking down HIF-1α blocked the neuroprotective effects of salubrinal.\n\nQuestion:\nAre the endoplasmic reticulum stress and the HIF-1 signalling pathways involved in the neuronal damage caused by chemical hypoxia?\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:\nVascular smooth muscle cells (VSMCs) can express heme-oxygenase (HO), a rate-limiting enzyme in the degradation of heme to bilirubin, ferritin and carbon monoxide (CO). VSMC-derived CO can suppress VSMC proliferation and may serve as an antiproliferation factor. The promoter region of HO-1 shows a polymorphism with different (GT) n repeats that has been reported to differently induce gene expression. The objective of this study was to examine the effect of this variation on the occurrence of restenosis after in-stent treatment in patients with coronary artery disease. Candidates who underwent coronary stent implantation were genotyped for the HO-1 promoter polymorphism using polymerase chain reaction (PCR) and automated DNA capillary sequencer. Serum levels of IL-6 and C-reactive protein (CRP) were obtained at baseline, 24 hours and 48 hours after stenting. The primary end point for the study was angiographic evidence of in-stent restenosis at 6 months. All parameters for evaluation of restenosis were analysed by quantitative computer-assisted angiographic analysis (QCA). One hundred and eighty-seven patients who underwent coronary stent implantation were studied of whom 27.8% showed > or = 50% restenosis after 6 months. The distribution of (GT) n repeats of all patients in the promoter region of HO-1 genotype ranged from 22 to 42, with (GT) 25 and (GT) 32 being the two most common alleles. The allelic repeats were divided into the short class (S) with 29 (GT) n, the middle class (M) with 30-37 (GT) n and the long class (L) with 38 (GT) n. There was no significant difference in the restenosis between the genotype groups or between post operation levels of inflammation markers, but carriers of the S allele (n = 120) had 33.3% lower baseline IL-6 compared with non-S carriers (n = 67, P = 0.0008).\n\nQuestion:\nIs the microsatellite polymorphism of heme oxygenase-1 associated with baseline plasma IL-6 level but not with restenosis after coronary in-stenting?\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:\nHalothane relaxes airway smooth muscle, in part, by decreasing the force produced for a given intracellular [Ca(2+)] (i.e., Ca(2+) sensitivity) during muscarinic stimulation, an effect produced by a decrease in regulatory myosin light-chain (rMLC) phosphorylation. The authors tested the hypothesis that halothane reduces rMLC phosphorylation during muscarinic stimulation at constant intracellular [Ca(2+)] by increasing smooth muscle protein phosphatase (SMPP) activity, without changing myosin light-chain kinase (MLCK) activity. Enzyme activities were assayed in beta-escin permeabilized strips of canine tracheal smooth muscle. Under conditions of constant intracellular [Ca(2+)], the rate of rMLC phosphorylation was measured by Western blotting during inhibition of SMPP with microcystin-LR (to assay MLCK activity) or during inhibition of MLCK by wortmannin and adenosine triphosphate depletion (to assay SMPP activity). The effect of halothane (0.8 mm) on enzyme activities and isometric force during stimulation with 0.6 microm Ca(2+) and 10 microm acetylcholine was determined. Halothane produced a 14 +/- 8% (mean +/- SD) decrease in isometric force by significantly reducing rMLC phosphorylation (from 32 +/- 9% to 28 +/- 9%). Halothane had no significant effect on any parameter of a monoexponential relation fit to the data for the MLCK activity assay. In contrast, halothane significantly decreased the half-time for rMLC dephosphorylation in the SMPP activity assay (from 0.74 +/- 0.28 min to 0.44 +/- 0.10 min), indicating that it increased SMPP activity.\n\nQuestion:\nDoes halothane increase smooth muscle protein phosphatase in airway smooth muscle?\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:\nMetastasis is a complex process involving loss of adhesion, migration, invasion and proliferation of cancer cells. Cell adhesion molecules play a pivotal role in this phenomenon by regulating cell-cell and cell-matrix interactions. CD146 (MCAM) is associated with an advanced tumor stage in melanoma, prostate cancer and ovarian cancer. Studies of CD146 expression and function in breast cancer remain scarce except for a report concluding that CD146 could act as a tumor suppressor in breast carcinogenesis. To resolve these apparent discrepancies in the role of CD146 in tumor cells, we looked at the association of CD146 expression with histoclinical features in human primary breast cancers using DNA and tissue microarrays. By flow cytometry, we characterized CD146 expression on different breast cancer cell lines. Using siRNA or shRNA technology, we studied functional consequences of CD146 downmodulation of MDA-MB-231 cells in migration assays. Wild-type, mock-transfected and downmodulated transfected cells were profiled using whole-genome DNA microarrays to identify genes whose expression was modified by CD146 downregulation. Microarray studies revealed the association of higher levels of CD146 with histoclinical features that belong to the basal cluster of human tumors. Expression of CD146 protein on epithelial cells was detected in a small subset of cancers with histoclinical features of basal tumors. CD146+ cell lines displayed a mesenchymal phenotype. Downmodulation of CD146 expression in the MDA-MB-231 cell line resulted in downmodulation of vimentin, as well as of a set of genes that include both genes associated with a poor prognosis in a variety of cancers and genes known to promote cell motility. In vitro functional assays revealed decreased migration abilities associated with decreased CD146 expression.\n\nQuestion:\nIs cD146 expression associated with a poor prognosis in human breast tumors and with enhanced motility in breast cancer cell lines?\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:\nSkeletal muscle wasting is an important comorbidity of Chronic Obstructive Pulmonary Disease (COPD) and is strongly correlated with morbidity and mortality. Patients who experience frequent acute exacerbations of COPD (AECOPD) have more severe muscle wasting and reduced recovery of muscle mass and function after each exacerbation. Serum levels of the pro-inflammatory acute phase protein Serum Amyloid A (SAA) can rise more than 1000-fold in AECOPD and are predictively correlated with exacerbation severity. The direct effects of SAA on skeletal muscle are poorly understood. Here we have examined SAA effects on pro-inflammatory cachectic cytokine expression (IL-6 and TNFα) and atrophy in C2C12 myotubes. SAA increased IL-6 (31-fold) and TNFα (6.5-fold) mRNA levels compared to control untreated cells after 3h of SAA treatment, and increased secreted IL-6 protein at 24h. OxPAPC, a dual TLR2 and TLR4 inhibitor, reduced the response to SAA by approximately 84% compared to SAA alone, and the TLR2 neutralising antibody T2.5 abolished SAA-induced expression of IL-6, indicating that SAA signalling in C2C12 myotubes is primarily via TLR2. SAA also reduced myotube width by 10-13% and induced a 2.5-fold increase in the expression of the muscle atrophy gene Atrogin-1, suggesting direct effects of SAA on muscle wasting. Blocking of TLR2 inhibited the SAA-induced decrease in myotube width and Atrogin-1 gene expression, indicating that SAA induces atrophy through TLR2.\n\nQuestion:\nDoes serum Amyloid A induce Toll-Like Receptor 2-Dependent Inflammatory Cytokine Expression and Atrophy in C2C12 Skeletal Muscle Myotubes?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nGlutamate mediated excitotoxicity of the hyperactive subthalamic nucleus (STN) has been reported to contribute to nigral degeneration in Parkinson's disease (PD). Deep brain stimulation of the STN (STN DBS), in its role as a highly effective treatment of severe PD motor complications, has been thought to inhibit STN hyperactivity and therefore decrease progression of PD. In a prospective two centre study, disease progression was determined by means of serial (18)F-fluorodopa (F-dopa) positron emission tomography (PET) in 30 patients with successful STN DBS over the first 16 (SD 6) months after surgery. Depending on the method of PET data analysis used in the two centres, annual progression rates relative to baseline were 9.5-12.4% in the caudate and 10.7-12.9% in the putamen.\n\nQuestion:\nDoes disease progression continue in patients with advanced Parkinson 's disease and effective subthalamic nucleus stimulation?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWorldwide, Caesarean sections are commonly done under regional anaesthesia which offers numerous advantages over general anesthesia. However there are still indications for the use of general anaesthesia in obstetric practice. This includes emergent Caesarean sections. This study sought to determine the factors that inform the decision on the choice of anaesthesia for Caesarean section in a tertiary institution in Nigeria. All patients scheduled for elective and emergency caesarean sections between January and December 2002 were prospectively studied. Study variables included age of mother, gestational age and parity. Urgency of surgery, indication for surgery, maternal pre-existing disease and the choice of anaesthetic technique were documented. Neonatal weight was recorded and outcome was assessed by Apgar score at 1 and 5 minutes, the presence of respiratory difficulties and the need for admission into the Neonatal unit. One hundred and ninety-six patients were studied. Elective surgery was performed for 17.3%, while 47.4% and 28.6% had urgent and emergency Caesarean sections respectively. Urgency of surgery was not documented in 6.7% of cases. Previous caesarean section was the commonest indication for elective procedures (47%), foetal distress for emergency (62.5%) and previous caesarean section in labour for urgent procedures (30.1%). General anaesthesia was employed in 33.2% of patients while regional anaesthesia was used in 66.8%. Fifty per cent of emergency cases had general anaesthesia. Regional anaesthesia was used in 72% of urgent and 85.3% of elective procedures. The commonest regional technique was spinal anaesthesia (60.7%). Nineteen per cent of our patients had a co-existing medical problem, and 73% of these received a spinal anaesthetic. More neonates delivered under general anaesthesia had respiratory difficulties at birth (p=0.002) and more were admitted to the Neonatal unit (p=0.031).\n\nQuestion:\nDo urgency of surgery and presence of maternal disease influence the choice of anaesthesia for Caesarean section at LUTH?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo determine which maternal glycaemic parameters in type 1 diabetes better predict large-for-gestational-age (LGA) infants. Maternal glycaemic parameters (mean overall, preprandial, and postprandial glucose; the percentage of glucose readings above and below target and HbA1c levels) of LGA (n=37) and appropriate-for-gestational-age (n=36) infants were compared during preconception and each trimester of pregnancy. Logistic regression was used to select predictive variables. Preconception glycaemic parameters were not different. Mean glucose and the percentage of glucose readings above target were higher in mothers of LGA infants in every trimester of pregnancy. Second and third trimesters mean postprandial glucose, third trimester mean preprandial glucose and third trimester HbA1c were also higher. Only third trimester glycaemic variables were risk indicators of LGA infants: mean glucose (OR: 3.45; 95% CI: 1.52-7.80), mean preprandial glucose (OR: 2.97; 95% CI: 1.34-6.60), mean postprandial glucose (OR: 2.09; 95% CI: 1.19-3.67) and the percentage of glucose readings above target (OR: 1.08; 95% CI: 1.03-1.14). The percentage of glucose readings above target was the best risk indicator.\n\nQuestion:\nDo maternal third trimester hyperglycaemic excursions predict large-for-gestational-age infants in type 1 diabetic pregnancy?\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 'cosmeceutical' agent 2-dimethylaminoethanol (DMAE) is a tertiary amine found in high concentration in numerous topical antiwrinkle preparations. We hypothesized that a 337 mmol L(-1) (3%) DMAE reservoir applied to the skin could reproduce the cytopathology induced by other amines by maintaining a millimolar drug concentration within a certain depth of the skin layers, and that vacuolar cell expansion could account for the very rapid effect on the apparent skin fullness. Morphological and functional assays were applied to cultured rabbit dermal fibroblasts treated with tertiary amines in vitro. A morphological verification of the vacuolization caused by topical DMAE was also attempted in vivo using the inner skin of the rabbit ear and in vitro using primary cultures of human cutaneous epithelial cells. Fibroblasts responded to DMAE (2.5-10 mmol L(-1)) by massive vacuolization (0.5-4 h; phase contrast observations). Triethanolamine, another chemical frequently used topically, was also active in this respect (10 mmol L(-1)). The vacuolar adenosine triphosphatase inhibitor bafilomycin A1 prevented DMAE- or triethanolamine-induced vacuolization; adding bafilomycin A1 or cell washout slowly reversed the established vacuolization induced by DMAE. Further effects of DMAE in cultured fibroblasts included a moderate cytotoxicity (10 mmol L(-1)) that was abated by bafilomycin A1 cotreatment, a concentration-dependent mitotic arrest (2.5 mmol L(-1)) and transient and mild effects on cell ploidy. The epidermis of the rabbit external ear was significantly thickened and exhibited clear perinuclear swelling indicative of vacuolization in response to 3% DMAE (1 h; paraffin tissue sections). Cultured human cutaneous epithelial cells responded to DMAE by vacuolization (inhibited by bafilomycin A1 cotreatment).\n\nQuestion:\nDoes the antiwrinkle effect of topical concentrated 2-dimethylaminoethanol involve a vacuolar cytopathology?\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 with short bowel syndrome (SBS) are at a high risk for infectious complications and liver failure. We hypothesized that SBS, independent of total parenteral nutrition, is a proinflammatory state that is magnified by sepsis. Sprague-Dawley rats were divided into 2 groups: sham laparotomy (SH, n = 10) or 75% small bowel resection (n = 10). After 14 days, each group underwent a second sham laparotomy (SH/SH and SBS/SH) or cecal ligation and puncture, followed 16 hours later by cecal excision and peritoneal washout (SH/sepsis and SBS/sepsis). Animals were killed 56 hours later. The SBS rats had higher serum levels of interleukin (IL) 6 vs SH (355 +/- 99 vs 104 +/- 71 pg/mL, P < .05). Liver injury scores were higher in SBS/sepsis compared with SBS/SH animals (3.7 +/- 0.7 vs 1.9 +/- 0.3, P < .05). Hepatic messenger RNA levels of IL-6 (12.8-fold change [FC]) and tumor necrosis factor alpha (5.65 FC) were elevated in SBS vs SH rats; and IL-6 (114 FC), tumor necrosis factor alpha (3.87 FC), and Toll-like receptor 4 (7.65 FC) were increased in SBS/sepsis compared with SH/sepsis animals.\n\nQuestion:\nIs two-hit rat model of short bowel syndrome and sepsis : independent of total parenteral nutrition , short bowel syndrome proinflammatory and injurious to the liver?\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:\nEvolutionary dynamics plays a central role in facilitating the mechanisms of species divergence among pathogenic and saprophytic mycobacteria. The ability of mycobacteria to colonize hosts, to proliferate and to cause diseases has evolved due to its predisposition to various evolutionary forces acting over a period of time. Mycobacterium indicus pranii (MIP), a taxonomically unknown 'generalist' mycobacterium, acts as an immunotherapeutic against leprosy and is approved for use as a vaccine against it. The large-scale field trials of this MIP based leprosy vaccine coupled with its demonstrated immunomodulatory and adjuvant property has led to human clinical evaluations of MIP in interventions against HIV-AIDS, psoriasis and bladder cancer. MIP, commercially available as 'Immuvac', is currently the focus of advanced phase III clinical trials for its antituberculosis efficacy. Thus a comprehensive analysis of MIP vis-à-vis evolutionary path, underpinning its immanent immunomodulating properties is of the highest desiderata. Genome wide comparisons together with molecular phylogenetic analyses by fluorescent amplified fragment length polymorphism (FAFLP), enterobacterial repetitive intergenic consensus (ERIC) based genotyping and candidate orthologues sequencing revealed that MIP has been the predecessor of highly pathogenic Mycobacterium avium intracellulare complex (MAIC) that did not resort to parasitic adaptation by reductional gene evolution and therefore, preferred a free living life-style. Further analysis suggested a shared aquatic phase of MAIC bacilli with the early pathogenic forms of Mycobacterium, well before the latter diverged as 'specialists'.\n\nQuestion:\nDoes molecular analysis of a leprosy immunotherapeutic bacillus provide insights into Mycobacterium evolution?\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:\nAntiretrovirals do not prevent anal intraepithelial neoplasia. However, the influence of antiretrovirals in the natural history of invasive anal cancer is less clear. The objective is to investigate the impact of antiretrovirals in the time to the development of anal cancer in HIV-positive MSM. A retrospective analysis of cases of anal cancer in a cohort of HIV-positive MSM receiving antiretrovirals between 1988 and 2008. Time from first CD4 cell count or HIV RNA viral load test to anal cancer diagnosis was analysed using Cox regression and Kaplan-Meier curves. Anal cancer cases treated in the era prior to HAART (<1996) were compared with those treated later (1996-2008). Anal cancer cases (n = 37) were compared with a cohort of 1654 HIV-positive MSM on antiretrovirals. Antiretrovirals were started in the pre-HAART era by 70% of cancer cases, and median CD4 cell count nadir was 70 cells/μl (10-130). Time to development of anal cancer was shorter for cases treated during the pre-HAART era [adjusted hazard ratio (AHR) 3.04, 95% confidence interval (95% CI) 1.48-6.24, P = 0.002], with a CD4 cell count nadir less than 100 cells/μl (AHR 2.21, 95% CI 1.06-4.62, P = 0.035) and longer duration of CD4 cell count less than 100 cells/μl (AHR 1.33, 95% CI 1.11-1.58, P = 0.002).\n\nQuestion:\nDoes hAART slow progression to anal cancer in HIV-infected MSM?\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:\nAnterior chamber (AC) inoculation of the KOS strain of herpes simplex virus type 1 (HSV-1) results in morphologic sparing of the ipsilateral retina, whereas the retina of the uninoculated contralateral eye becomes infected and undergoes acute retinal necrosis. Natural killer (NK) cells are an important component of the primary immune response to most virus infections. The purpose of this study was to determine whether NK cells are involved in preventing early direct anterior-to-posterior spread of HSV-1 after AC inoculation. Normal BALB/c mice were inoculated with 4 X 10(4) plaque-forming units (PFU) of the KOS strain of HSV-1 using the AC route. NK activity was measured in the spleen, the superficial cervical and submandibular lymph nodes, and the inoculated eye by lysis of chromium-labeled, NK-sensitive YAC-1 target cells. Histopathologic scoring and immunohistochemical staining for HSV-1 were performed in NK-depleted (injected intravenously with anti-asialo GM1) or mock-depleted (injected intravenously with normal rabbit serum) mice. In mock-depleted mice, NK activity in the spleens, superficial cervical and submandibular lymph nodes, and inoculated eyes peaked at postinoculation (pi) day 5 and declined by pi day 7. Treatment with anti-asialo GM1 eliminated NK activity in the eye and at nonocular sites. The histopathologic scores at pi day 5 indicated more damage to the retinas of NK-depleted mice than to those of mock-depleted mice, and immunohistochemical staining for HSV-1 showed spread of the virus to the sensory retina only in NK-depleted mice.\n\nQuestion:\nDo natural killer cells prevent direct anterior-to-posterior spread of herpes simplex virus type 1 in the eye?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nEvolutionary biologists want to explain the origin of novel features and functions. Two recent but separate lines of research address this question. The first describes one possible outcome of hybridization, called transgressive segregation, where hybrid offspring exhibit trait distributions outside of the parental range. The second considers the explicit mapping of form to function and illustrates manifold paths to similar function (called many to one mapping, MTOM) when the relationship between the two is complex. Under this scenario, functional novelty may be a product of the number of ways to elicit a functional outcome (i.e., the degree of MTOM). We fuse these research themes by considering the influence of MTOM on the production of transgressive jaw biomechanics in simulated hybrids between Lake Malawi cichlid species. We characterized the component links and functional output (kinematic transmission, KT) of the 4-bar mechanism in the oral jaws of Lake Malawi cichlids. We demonstrated that the input and output links, the length of the lower jaw and the length of the maxilla respectively, have consistent but opposing relationships with KT. Based on these data, we predicted scenarios in which species with different morphologies but similar KT (MTOM species) would produce transgressive function in hybrids. We used a simple but realistic genetic model to show that transgressive function is a likely outcome of hybridization among Malawi species exhibiting MTOM. Notably, F2 hybrids are transgressive for function (KT), but not the component links that contribute to function. In our model, transgression is a consequence of recombination and assortment among alleles specifying the lengths of the lower jaw and maxilla.\n\nQuestion:\nDoes hybridization produce novelty when the mapping of form to function is many to one?\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:\nMetabolic syndrome is associated with insulin resistance and increased future risk of type 2 diabetes. This study investigates the relationship between insulin secretion, insulin resistance and individual metabolic syndrome components in subjects without a prior diagnosis of diabetes. We assessed insulin secretion during hyperglycemic clamps by infusing dextrose to maintain hyperglycemia (200mg/dL), followed by L-arginine administration. Studies in 98 individuals (mean age 45.3±1.2years, 56% female, 22% African-American, 49% with metabolic syndrome) were analyzed. We tested the association between the number of metabolic syndrome components and individual outcome variables using linear mixed-effects models to adjust for potential confounding effects of age, sex, and race. Insulin sensitivity index was reduced in the presence of 1 or more metabolic syndrome components. Insulin sensitivity was independently associated with age, waist circumference, male gender and decreased HDL cholesterol. The acute insulin response was greater with two or more metabolic syndrome components, and late glucose-stimulated and L-arginine-stimulated insulin responses exhibited a similar trend. In contrast, the disposition index, a measure of beta cell compensation for insulin resistance, was linearly lower with the number of metabolic syndrome components, and was negatively associated with age, Caucasian race, waist circumference, fasting glucose, and decreased HDL cholesterol.\n\nQuestion:\nIs hyperglycemic clamp-derived disposition index negatively associated with metabolic syndrome severity in obese subjects?\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 ulcerative colitis and primary sclerosing cholangitis are at high risk for colonic dysplasia and cancer. This risk approaches 50% after 25 years of colitis. Ursodiol has been shown to protect against development of colorectal neoplasia in animal models. To assess the relationship between ursodiol use and colonic dysplasia, the precursor to colon cancer, in patients with ulcerative colitis and primary sclerosing cholangitis. Cross-sectional study. University medical center. 59 patients with ulcerative colitis and primary sclerosing cholangitis who were undergoing colonoscopic surveillance for colonic dysplasia. Use of ursodiol was assessed in all patients. The presence or absence of colonic dysplasia was evaluated by colonoscopic surveillance. Other variables assessed were age at onset and duration of ulcerative colitis; duration of primary sclerosing cholangitis; Child-Pugh classification; and use of sulfasalazine, other 5-aminosalicylic acid preparations, prednisone, cyclosporine, azathioprine, and methotrexate. Ursodiol use was strongly associated with decreased prevalence of colonic dysplasia (odds ratio, 0.18 [95% CI, 0.05 to 0.61]; P = 0.005). The association between dysplasia and ursodiol use remained after adjustment for sex, age at onset of colitis, duration of colitis, duration of sclerosing cholangitis, severity of liver disease, and sulfasalazine use (adjusted odds ratio, 0.14 [CI, 0.03 to 0.64]; P = 0.01). Younger age at onset of colitis was associated with an increased risk for dysplasia.\n\nQuestion:\nIs ursodiol use associated with lower prevalence of colonic neoplasia in patients with ulcerative colitis and primary sclerosing cholangitis?\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:\nObesity and insulin resistance are increasingly common problems in children. Tumor necrosis factor-alpha (TNF-alpha) has important effects on lipid and glucose metabolism. This effect may be mediated through soluble TNF-alpha receptor 2 (sTNFR2). To investigate the relationship between insulin resistance and the TNF-alpha system in childhood obesity. Twenty-one obese and six non-obese children were studied. Body mass index (BMI) z-scores, percent body fat (PBF) and waist to hip ratio (WHR) were determined. Fasting serum levels of total cholesterol, HDL-cholesterol, LDL-cholesterol, TNF-alpha and sTNFR2 were measured. A standard 2-hour oral glucose tolerance test (dose of glucose: 1.75 g/kg, max. 75 g) was done. Insulin resistance (IR) was estimated by fasting plasma insulin, plasma insulin at 120 min, homeostasis model assessment (HOMA) and insulin area under the curve (AUC) from OGTT. Insulin sensitivity was estimated by oral glucose insulin sensitivity (OGIS120). Among the obese participants, one child (5.2%) was found to have diabetes mellitus and four others (21.1%) impaired glucose tolerance (IGT). Obese children had significantly elevated sTNFR2 levels. Furthermore, the group of obese children with IGT and the patient with newly diagnosed diabetes mellitus together (n = 5) had significantly higher levels of serum sTNFR2 (2,865+/-320 pg/ml) than the rest of the obese (2,460+/-352 pg/ml; p = 0.016) or lean (1,969+/-362 pg/ml; p = 0.014) children. Serum sTNFR2 levels correlated positively with insulin AUC, HOMA IR, fasting plasma insulin, plasma insulin at 120 min, total cholesterol and LDL/ HDL ratio, and negatively with OGIS120. Multiple regression analysis revealed that age, WHR, sTNFR2 and LDL predicted 81% of the variability in glucose at 120 min.\n\nQuestion:\nAre serum levels of soluble tumor necrosis factor-alpha receptor 2 linked to insulin resistance and glucose intolerance in children?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nBone morphogenetic protein-9 (BMP9)/activin-like kinase-1 and delta-like 4 (DLL4)/Notch promote endothelial quiescence, and we aim to understand mechanistic interactions between the 2 pathways. We identify new targets that contribute to endothelial quiescence and test whether loss of Dll4(+/-) in adult vasculature alters BMP signaling. Human endothelial cells respond synergistically to BMP9 and DLL4 stimulation, showing complete quiescence and induction of HEY1 and HEY2. Canonical BMP9 signaling via activin-like kinase-1-Smad1/5/9 was disrupted by inhibition of Notch signaling, even in the absence of exogenous DLL4. Similarly, DLL4 activity was suppressed when the basal activin-like kinase-1-Smad1/5/9 pathway was inhibited, showing that these pathways are interdependent. BMP9/DLL4 required induction of P27(KIP1) for quiescence, although multiple factors are involved. To understand these mechanisms, we used proteomics data to identify upregulation of thrombospondin-1, which contributes to the quiescence phenotype. To test whether Dll4 regulates BMP/Smad pathways and endothelial cell phenotype in vivo, we characterized the vasculature of Dll4(+/-) mice, analyzing endothelial cells in the lung, heart, and aorta. Together with changes in endothelial structure and vascular morphogenesis, we found that loss of Dll4 was associated with a significant upregulation of pSmad1/5/9 signaling in lung endothelial cells. Because steady-state endothelial cell proliferation rates were not different in the Dll4(+/-) mice, we propose that the upregulation of pSmad1/5/9 signaling compensates to maintain endothelial cell quiescence in these mice.\n\nQuestion:\nDoes dLL4/Notch1 and BMP9 Interdependent Signaling induce Human Endothelial Cell Quiescence via P27KIP1 and Thrombospondin-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:\nInterleukin (IL)-17 and IL-23 play roles in inflammation and autoimmunity. The function of the IL-17/IL-23 pathway has not been completely evaluated in cancer patients. We aimed to investigate serum IL-17 and IL-23 levels and their relationship with clinicopathological and biochemical parameters in lung cancer patients. Forty-five lung cancer patients and 46 healthy volunteers were included in the study. IL-17 and IL-23 measurements were made with the ELISA method. The ages of patients (53-84 years) and healthy subjects (42-82 years) were similar. Serum IL-23 levels were higher in lung cancer patients than in healthy subjects (491.27 ±1263.38 pg/ml vs. 240.51 ±233.18 pg/ml; p = 0.032). IL-23 values were higher in small cell lung cancer (SCLC) patients than in non-small cell lung cancer (NSCLC) patients (1325.30 ±2478.06 pg/ml vs. 229.15 ±103.22 pg/ml; p = 0.043). Serum IL-17 levels were lower in the patients, but the difference was not statistically significant (135.94 ±52.36 pg/ml vs. 171.33 ±133.51 pg/ml; p = 0.124). Presence of comorbid disease (diabetes mellitus, hypertension or chronic obstructive lung disease) did not have any effect on the levels of IL-17 or IL-23. Erythrocyte sedimentation rate values were positively correlated with cytokine levels, but serum albumin levels were negatively correlated.\n\nQuestion:\nIs the inflammatory cytokine interleukin-23 elevated in lung cancer , particularly small cell type?\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:\nMetabolic syndrome is prevalently associated with stroke. Triglyceride-rich lipoproteins contribute to atherothrombotic complications in metabolic syndrome. This study examined whether high levels of remnant lipoprotein, atherogenic triglyceride-rich lipoprotein, may be associated with future ischemic stroke in metabolic syndrome. We followed up 292 consecutive patients with metabolic syndrome meeting ATP III criteria and mild carotid plaques for a period of </=24 months until occurrence of an ischemic stroke. Remnant lipoprotein (remnant-like lipoprotein particles cholesterol; RLP-C) were measured by an immunoseparation method. Twenty-two ischemic stroke events occurred during follow-up. A multivariate Cox proportional hazards models showed that high RLP-C levels were a significant and independent predictor of ischemic stroke events (p<0.01). Echolucent carotid plaques were also a significant predictor of ischemic stroke that was independent of other carotid ultrasound parameters in Cox proportional hazards models (p<0.01). High RLP-C levels were intimately and independently associated with carotid plaque echolucency (p<0.01).\n\nQuestion:\nDo high serum levels of remnant lipoproteins predict ischemic stroke in patients with metabolic syndrome and mild carotid atherosclerosis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo investigate the association between keratinized mucosa (KM) width and mucosal thickness (MTh) with clinical and immunological parameters around dental implants. Sixty-three functioning dental implants (3I osseotite) were examined. Clinical examinations included plaque index (PI), probing depth (PD), bleeding on probing (BOP), KM width, MTh and buccal mucosal recession (MR). Peri-implant crevicular fluid (PICF) samples were collected for PgE2 assay. KM width ranged from 0 to 7 mm (mean 2.5+/-2), MTh ranged from 0.38 to 2.46 mm (mean 1.11+/-0.4) and the mean MR was 0.62 mm, ranging from 0 to 3 mm. A negative correlation was found between MTh and MR (r=-0.32, P=0.01); Likewise, KM width showed a negative correlation with MR, periodontal attachment level (PAL) and PgE2 levels (r=-0.41, P<0.001; r=-0.26, P=0.04; r=-0.26, P=0.04, respectively). In contrast, a positive correlation was found between KM width and PD (r=0.27, P=0.03). When data were dichotomized by KM width, a wider mucosal band (>1 mm) was associated with less MR compared with narrow (<or=1 mm) band (0.27 and 0.9 mm, respectively, P=0.001). A wider KM band was also associated with a greater PD (3.13 mm) compared with a narrow band (2.66 mm, P=0.04). Similarly, a thick mucosa (>or=1 mm) was associated with lesser recession compared with a thin (<1 mm) mucosa (0.45 and 0.9 mm, respectively, P=0.04).\n\nQuestion:\nDo the dimensions of keratinized mucosa around implants affect clinical and immunological parameters?\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-23 (IL-23) has a role in inflammatory bowel diseases (IBD) as a condition of higher risk of colorectal carcinogenesis. Vascular endothelial growth factor (VEGF) is overexpressed in IBD and colorectal carcinoma. Therefore, we aimed at uncovering the relationship between serum level of IL-23 and expression of VEGF in colorectal cancer (CRC) patients and to establish the relationship between VEGF and p53 and serum levels of IL-23, as well as its possible role in carcinogenesis of colorectal carcinomas. Levels of IL-23 from serum samples of patients with colorectal carcinoma (n = 40) and healthy control samples (n = 37) were examined for IL-23-Ab using an ELISA assay. We also determined the expression of VEGF and p53 by immunohistochemistry in 59 cases of CRC. We found significantly higher serum levels of IL-23 in patients with CRC compared to control subjects (IL-23; mean 189.46 pg/mL vs. mean 34.77 pg/mL, p = 0.033). We also detected higher serum levels of IL-23 in patients with overexpressed VEGF (p = 0.028). Our results also showed that concomitant expression of VEGF and increased serum levels of IL-23 are in positive correlation with histological grade 2 (p <0.05).\n\nQuestion:\nDoes elevated serum level of IL-23 correlate with expression of VEGF in human colorectal carcinoma?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo use spectra acquired by matrix-assisted laser desorption/ionization (MALDI) mass spectrometry (MS) from pre- and post-digital rectal examination (DRE) urine samples to search for discriminating peaks that can adequately distinguish between benign and malignant prostate conditions, and identify the peaks' underlying biomolecules. Twenty-five participants with prostate cancer (PCa) and 27 participants with a variety of benign prostatic conditions as confirmed by a 10-core tissue biopsy were included. Pre- and post-DRE urine samples were prepared for MALDI MS profiling using an automated clean-up procedure. Following mass spectra collection and processing, peak mass and intensity were extracted and subjected to statistical analysis to identify peaks capable of distinguishing between benign and cancer. Logistic regression was used to combine markers to create a sensitive and specific test. A peak at m/z 10,760 was identified as β-microseminoprotein (β-MSMB) and found to be statistically lower in urine from PCa participants using the peak's average areas. By combining serum prostate-specific antigen (PSA) levels with MALDI MS-measured β-MSMB levels, optimum threshold values obtained from Receiver Operator characteristics curves gave an increased sensitivity of 96% at a specificity of 26%.\n\nQuestion:\nDoes mALDI MS profiling of post-DRE urine samples highlight the potential of β-microseminoprotein as a marker for prostatic diseases?\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:\nEven with the improvements in surgical techniques and perioperative care, obesity is still a risk factor for occurrence of adverse events following cardiac surgery. In this observational, retrospective study, we aimed to document the effects of obesity on surgical outcomes in patients undergoing coronary artery bypass surgery and find out the effects of improvements in cardiac surgery. Between January 2011 and March 2013, isolated coronary artery bypass surgery was performed on 790 patients. The body mass index values of the patients were calculated and patients were divided into two groups; below 30 were classified as non-obese group whereas above 30 were classified as obese group. The odds ratio was obtained by using univariate analysis in order to document the effects of obesity on outcomes. There were 548 (69.3%) patients in non-obese group, whereas 242 (30.7%) patients in obese group. The cardiopulmonary bypass (80.47±23.58 vs. 80.89±28.46, p=0.449) and aortic clamp times (54.13±16.60 vs. 54.19±19.85, p=0.511) and number of bypass grafts (3.09±1.02 vs. 2.96±1.00, p=0.11) were comparable between the groups. The mean number of fresh frozen plasma used was higher in obese patients (1.37±1.75 vs. 1.48±4.63, p=0.02). Intubation time was higher in obese patients (10.57±6.87 vs. 12.71±35.31, p=0.014). Total amount of postoperative drainage was higher in non-obese patients (766.77±472.27 vs. 648.72±371.39, p<0.001). The superficial infection/mediastenitis (0.4% vs. 2.5%, p=0.012), dehiscence (0.2% vs. 3.7%, p<0.001) and postoperative renal failure rates (4.7% vs. 8.7%, p=0.031) were higher in obese patients. The incidence of atrial fibrillation was lower in obese patients (19.7% vs. 12.8%, p=0.019). The mortality (0.5% vs. 1.7%, p=0.210) and postoperative stroke rates (1.1% vs. 0.8%, p=1.000) were similar in both groups.\n\nQuestion:\nIs obesity still a risk factor in coronary artery bypass surgery?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo investigate whether interactions of sulfasalazine (SSZ) with reduced folate carrier (RFC), the dominant cell membrane transporter for natural folates and methotrexate (MTX), may limit the efficacy of combination therapy with MTX and SSZ in patients with rheumatoid arthritis. Human RFC-(over)expressing CEM cells of T cell origin were used to analyze the effect of SSZ on the RFC-mediated cellular uptake of radiolabeled MTX and the natural folate leucovorin. Moreover, both cells with and those without acquired resistance to SSZ were used to assess the antiproliferative effects of MTX in combination with SSZ. Transport kinetic analyses revealed that SSZ was a potent noncompetitive inhibitor of RFC-mediated cellular uptake of MTX and leucovorin, with mean +/- SD K(i) (50% inhibitory concentration) values of 36 +/- 6 microM and 74 +/- 7 microM, respectively. Consistent with the inhibitory interaction of SSZ with RFC, a marked loss of MTX efficacy was observed when MTX was coadministered with SSZ: up to 3.5-fold for CEM cells in the presence of 0.25 mM of SSZ, and >400-fold for SSZ-resistant cells in the presence of 2.5 mM of SSZ. Importantly, along with diminished efficacy of MTX, evidence for cellular folate depletion was obtained by the demonstration of an SSZ dose-dependent decrease in leucovorin accumulation.\n\nQuestion:\nIs sulfasalazine a potent inhibitor of the reduced folate carrier : implications for combination therapies with methotrexate in rheumatoid arthritis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nElevated expression levels of monocytic-ACE have been found in haemodialysis patients. They are not only epidemiologically linked with increased mortality and cardiovascular disease, but may also directly participate in the initial steps of atherosclerosis. To further address this question we tested the role of monocytic-ACE in promotion of atherosclerotic events in vitro under conditions mimicking those of chronic renal failure. Treatment of human primary monocytes or THP-1 cells with uremic serum as well as PMA-induced differentiation led to significantly up-regulated expression of ACE, further increased by additional treatment with LPS. Functionally, these monocytes revealed significantly increased adhesion and transmigration through endothelial monolayers. Overexpression of ACE in transfected monocytes or THP-1 cells led to development of more differentiated, macrophage-like phenotype with up-regulated expression of Arg1, MCSF, MCP-1 and CCR2. Expression of pro-inflammatory cytokines TNFa and IL-6 were also noticeably up-regulated. ACE overexpression resulted in significantly increased adhesion and transmigration properties. Transcriptional screening of ACE-overexpressing monocytes revealed noticeably increased expression of Angiotensin II receptors and adhesion- as well as atherosclerosis-related ICAM-1 and VCAM1. Inhibition of monocyte ACE or AngII-receptor signalling led to decreased adhesion potential of ACE-overexpressing cells.\n\nQuestion:\nDo uremic conditions drive human monocytes to pro-atherogenic differentiation via an angiotensin-dependent mechanism?\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:\nPrevalence and risk factors for human papillomavirus (HPV) persistence in oral mucosa are largely unknown. Furthermore, the antiviral effects of saliva in the outcome of oral HPV infections are unexplored. To compare the levels of selected salivary defence proteins in women with a persistent oral HPV infection and in those without any signs of oral HPV. Lifestyle factors including the use of oral contraceptives, oral sex, smoking and alcohol drinking habits were also assessed. This nested case-control study of the Finnish Family HPV Study included 60 women with a persistent oral HPV infection and 117 women who remained HPV DNA negative throughout a 6-year follow-up. Whole saliva samples and oral scrapings for HPV testing were collected at the same visit. The oral HPV status was related to salivary concentrations of lactoferrin, lysozyme, IgA, IgG, total protein and sodium as well as to the use of oral contraceptives, oral sex, smoking and alcohol drinking habits. Women with a persistent oral HPV infection had higher salivary levels of IgG (p=0.007) and lysozyme (p=0.002, when adjusted to the total protein concentration), than those without an HPV infection. Lactoferrin and IgA concentrations were not related to the HPV-status. Smoking increased the risk of a persistent oral HPV infection (p=0.020), but the oral HPV status was not related to other life-style factors studied.\n\nQuestion:\nIs persistent oral human papillomavirus infection associated with smoking and elevated salivary immunoglobulin G concentration?\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:\nInward rectifier K+ currents (K(ir)) determine the resting membrane potential and thereby modulate essential Ca2+-dependent pathways, like cell growth and synthesis of vasoactive agents in endothelial cells. Basic fibroblast growth factor (bFGF) acts as a vasodilatator and angiogenic factor. Therefore, we investigated the effect of bFGF on K(ir) and assessed the role in proliferation and nitric oxide (NO) formation of endothelial cells. Using the patch-clamp technique, we found characteristic K(ir) in human umbilical cord vein endothelial cells (HUVEC), which were dose-dependently blocked by barium (10 to 100 micromol/L). Perfusion with bFGF (50 ng/mL) caused a significant increase of K(ir), which was blocked by 100 micromol/L barium (n=18, P<0.01). The bFGF-induced HUVEC proliferation was significantly inhibited when using 50 to 100 micromol/L barium (n=6; P<0.01). NO production was examined using a cGMP radioimmunoassay. bFGF caused a significant increase of cGMP levels (n=10; P<0.05), which were blocked by barium.\n\nQuestion:\nDoes basic fibroblast growth factor-induced endothelial proliferation and NO synthesis involve inward rectifier K+ current?\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:\nIdentification of fibroblast derived factors in tumor progression has the potential to provide novel molecular targets for modulating tumor cell growth and metastasis. Multiple matrix metalloproteases (MMPs) are expressed by both mesenchymal and epithelial cells within head and neck squamous cell carcinomas (HNSCCs), but the relative importance of these enzymes and the cell source is the subject of controversy. The invasive potential of HNSCC tumor cells were assessed in vitro atop type I collagen gels in coculture with wild-type (WT), MMP-2 null, MMP-9 null or MT1-MMP null fibroblasts. A floor of mouth mouse model of HNSCC was used to assess in vivo growth after co-injection of FaDu tumor cells with MMP null fibroblasts. Here we report changes in tumor phenotype when FaDu HNSCCs cells are cocultured with WT, MMP-2 null, MMP-9 null or MT1-MMP null fibroblasts in vitro and in vivo. WT, MMP-2 null and MMP-9 null fibroblasts, but not MT1-MMP null fibroblasts, spontaneously invaded into type I collagen gels. WT fibroblasts stimulated FaDu tumor cell invasion in coculture. This invasive phenotype was unaffected by combination with MMP-9 null fibroblasts, reduced with MMP-2 null fibroblasts (50%) and abrogated in MT1-MMP null fibroblasts. Co-injection of FaDu tumor cells with fibroblasts in an orthotopic oral cavity SCID mouse model demonstrated a reduction of tumor volume using MMP-9 and MMP-2 null fibroblasts (48% and 49%, respectively) compared to WT fibroblasts. Consistent with in vitro studies, MT1-MMP null fibroblasts when co-injected with FaDu cells resulted in a 90% reduction in tumor volume compared to FaDu cells injected with WT fibroblasts.\n\nQuestion:\nDoes fibroblast-derived MT1-MMP promote tumor progression in vitro and in vivo?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe aim of this study is to count the dentinal tubules in the coronal and middle-apical third of root dentin of teeth extracted due to the progression of periodontal disease, and to compare the Ultimate Tensile Strength (UTS) of the same areas. The research hypothesis was that root dentin areas with different densities of dentinal tubules would also show different UTS values. From 10 caries free maxillary central, lateral incisors and canines, extracted for periodontal reasons from three patients, cylindrical specimens approximately 10 mm long were prepared parallel to the long axis of the root and then divided into two parts using a low speed diamond saw one from the coronal third of the root, (Group 1) and one from the middle-apical third of the root (Group 2). The density of the dentinal tubules of the specimens of the two groups was measured by means of a scanning electron microscope and the UTS of the specimens was measured by a microtensile test. One way ANOVA was used to assess the effect of specimen location (coronal specimens vs. middle-apical specimens) on UTS. The differences in the density of dentinal tubules between coronal and middle-apical specimens were also subjected to statistical analysis using one-way ANOVA. UTS values of middle-apical specimens were found to be significantly (p < 0.05) higher than those of coronal specimens. The results of the one-way analysis of variance showed that the number of dentinal tubules of the samples from the coronal part of the root groups was significantly higher than that of samples from the middle-apical part (p < 0.05).\n\nQuestion:\nDoes density of dentinal tubules affect the tensile strength of root dentin?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPrevious reports of site-directed deletion analysis on gamma (gamma)-phage lysin protein (PlyG) have demonstrated that removal of a short amino acid sequence in the C-terminal region encompassing a 10-amino acid motif (190LKMTADFILQ199) abrogates its binding activity specific to the cell wall of Bacillus anthracis. Whether short synthetic peptides representing the10-amino acid PlyG putative binding motif flanked by surrounding N- and C-terminal residues also selectively bind to the bacterial cell wall has not been evaluated. If such peptides do demonstrate selective binding to the cell wall, they could serve as bio-probes towards developing detection technologies for B. anthracis. Furthermore, by using B. anthracis (Sterne, 34F2), an animal vaccine and B. cereus-4342, a gamma-phage susceptible rare strain as surrogates of B. anthracis, development of proof-of-concepts for B. anthracis are feasible. Using four different methods, we evaluated six synthetic peptides representing the putative binding motif including flanking sequences (PlyG-P1 through P6) for the bacterial cell wall binding capacity. Our analysis identified PlyG-P1, PlyG-P3 and PlyG-P5 to have binding capability to both B. anthracis (Sterne, 34F2) and B. cereus-4342. The peptides however did not bind to B. cereus-11778, B. thuringiensis, and B. cereus-10876 suggesting their specificity for B. anthracis-Sterne and B. cereus-4342. PlyG-P3 in combination with fluorescent light microscopy detected even a single bacterium in plasma spiked with the bacteria.\n\nQuestion:\nAre gamma-phage lysin PlyG sequence-based synthetic peptides coupled with Qdot-nanocrystals useful for developing detection methods for Bacillus anthracis by using its surrogates , B. anthracis-Sterne and B. cereus-4342?\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 have previously demonstrated that putaminal but not caudate volumes are associated with poor outcome in patients with chronic schizophrenia. Present longitudinal study was designed to investigate progressive differences in striatal volumes among chronic schizophrenia patients with different outcomes and healthy subjects. Structural MRI scans were acquired at baseline and at follow-up four years later to evaluate volumetric changes in 26 poor-outcome schizophrenia patients, 23 good-outcome patients and 16 healthy subjects. Schizophrenia patients with different outcomes entered the study with similar volumes of the caudate nucleus and putamen. The rate of decline in volumes of the putamen was greater in patients with poor outcome than in the good-outcome group, so that their putaminal but not caudate volumes were significantly smaller at the time of follow-up. There were no differences in baseline and follow-up volumes of the putamen or in the rate of their progression among patients with schizophrenia and healthy comparison subjects. The caudate volumes were lower in schizophrenia patients than healthy subjects at baseline and follow-up, but showed no differential patterns of progression between the groups.\n\nQuestion:\nIs poor outcome in chronic schizophrenia associated with progressive loss of volume of the putamen?\n\nAnswer:", "role": "user" }, { "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 apply independent component analysis (ICA) in intracranial recordings to analyze interactions during temporal lobe seizures. Seizures from 20 patients with bitemporal implantation were classified as unilateral or bilateral and analyzed with ICA. During the period preceding bilateral activity, correlation coefficients were calculated between ICA components having ictal activity during the unilateral seizure phase (early ICA components) and every channel of the original EEG. ICA components were classified as unilateral if the correlation was >0.2 exclusively with channels in one hemisphere; and bilateral if both hemispheres were involved. One hundred twenty-three seizures were analyzed. Thirty-two percent of visually classified unilateral seizures and 64% of bilateral seizures (during the unilateral phase) had bilateral ICA components. The proportion of early ICA components that were bilateral and the proportion of channels contralateral to the visually identified seizure with correlation higher than 0.2 with at least one early ICA component were significantly lower in seizures that stayed unilateral than in seizures that later became bilateral by visual inspection (11 and 10%, respectively, in unilateral seizures; 33 and 28% in bilateral seizures; P=0.001).\n\nQuestion:\nDoes independent component analysis identify ictal bitemporal activity in intracranial recordings at the time of unilateral discharges?\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:\nAsbestos exposure induces generation of reactive oxygen and nitrogen species. Nitric oxide is involved in asbestos-related lung toxicity in vitro and can be measured non-invasively in humans in exhaled breath. The authors hypothesized that fractional exhaled nitric oxide concentration (FENO) would be increased in subjects with asbestos-related lung disorders. FENO was measured in 56 subjects with asbestos-related disorders (asbestosis: 12; pleural plaques: 32; asbestos-related diffuse pleural thickening: 12) and in 35 normal subjects. The authors also measured exhaled carbon monoxide, another marker of lung inflammation. Median (25-75 percentile) FENO was increased in subjects with asbestosis (7.9 (6.6-15.7) p.p.b.; P=0.001) and pleural plaques (6.3 (5.3-9) p.p.b.; P=0.03) compared with normal controls (4.6 (3.5-6) p.p.b.). Subjects with DPT had a median FENO of 5.6 p.p.b., similar to controls. No significant differences in exhaled carbon monoxide were observed between controls (1.0+/-0.3 p.p.m.) and subjects with asbestosis (1.3+/-0.3 p.p.m.), pleural plaques (1.2+/-0.3 p.p.m.) or diffuse pleural thickening (1.1+/-0.3 p.p.m.).\n\nQuestion:\nIs fractional exhaled nitric oxide concentration increased in asbestosis and pleural plaques?\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 angiopoietins (Ang) comprise a family of growth factors mainly known for their role in blood vessel formation and remodeling. The best-studied member, Ang-1, exhibits antiapoptotic and antiinflammatory effects. Although the involvement of Ang-1 in angiogenesis is well recognized, little information exists about its role in respiratory physiology and disease. On the basis of its ability to inhibit vascular permeability, adhesion molecule expression, and cytokine production, we hypothesized that Ang-1 administration might exert a protective role in asthma. To determine changes in the expression of Ang and to assess the ability of Ang-1 to prevent the histologic, biochemical, and functional changes observed in an animal model of asthma. To test our hypothesis, a model of allergic airway disease that develops after ovalbumin (OVA) sensitization and challenge was used. Ang-1 expression was reduced at the mRNA and protein levels in lung tissue of mice sensitized and challenged with OVA, leading to reduced Tie2 phosphorylation. Intranasal Ang-1 treatment prevented the OVA-induced eosinophilic lung infiltration, attenuated the increase in IL-5 and IL-13, and reduced eotaxin and vascular cell adhesion molecule 1 expression. These antiinflammatory actions of Ang-1 coincided with higher levels of IkappaB and decreased nuclear factor-kappaB binding activity. More importantly, Ang-1 reversed the OVA-induced increase in tissue resistance and elastance, improving lung function.\n\nQuestion:\nDoes angiopoietin-1 protect against airway inflammation and hyperreactivity in asthma?\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:\nDuring a Florida red tide, brevetoxins (PbTxs) produced by Karenia brevis become aerosolized and can cause both immediate and prolonged airway symptoms in humans, especially in those with preexisting airway disease (e.g., asthma). Although environmental monitoring indicates that toxins remain airborne for up to 4 consecutive days, there is little information on airway responses after multiple-day exposures. To delineate putative mechanisms leading to pulmonary dysfunction after PbTx exposure, we studied airway responses before and after multiple exposures to aerosol PbTx-3, the most potent PbTx produced, in nonallergic (healthy) and in allergic sheep, which serve as a surrogate for patients with compromised airways. Both groups were exposed to 20 breaths of increasing concentrations of PbTx-3 (30-300 pg/mL) for 4 consecutive days. Airway responsiveness to carbachol (1 and 8 days after) and airway inflammation as assessed by bronchoalveolar lavage (0 and 7 days after) were measured. Both groups developed airway hyperresponsiveness (AHR) 1 day after challenge; the severity was concentration dependent and more severe in the allergic group. AHR remained after 8 days, but the difference in the severity between the groups was lost. Both groups developed an inflammatory response after exposure to 300 pg/mL PbTx-3. Immediately after exposure, lung neutrophilia was prominent. This neutrophilia persisted for 7 days in addition to increases in total cells and macrophages.\n\nQuestion:\nDoes repeated exposure to aerosolized brevetoxin-3 induce prolonged airway hyperresponsiveness and lung inflammation in sheep?\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 demonstrate the role of intrinsic hyaluronic acid (HA) in the entrapment of inflammatory cells by amniotic membrane (AM) in vitro. HA concentration in AM was analyzed by the sandwich protein binding assay, and the approximate molecular weight was measured by gel filtration chromatography. To localize HA in AM tissue, toluidine blue staining with and without hyaluronidase treatment was performed. Adhesion of the lymphocyte cell lines, Jurkat and Molt 4, and peripheral blood mononuclear cells (PBMC) to AM and HA-coated glass slides was analyzed in an in vitro binding assay. Flow cytometry was performed to quantify the expression of the HA receptor, CD44, in Jurkat, Molt 4, and PBMC. HA was present in high levels in the stroma of AM, also demonstrated by intense staining with toluidine blue. Staining was inhibited by both hyaluronidase treatment and acidic pH. Molt 4, which constitutively expressed CD44, bound to AM and HA-coated slides significantly more than Jurkat cells (CD44-). Adhesion of Molt 4 was inhibited by pretreatment with both soluble HA and anti-CD44 antibody. LPS- or TNF-alpha-treated PBMC also bound to AM and HA-coated slides and was inhibited by pretreatment with an anti-CD44 antibody.\n\nQuestion:\nDoes hyaluronic acid-CD44 interaction mediate the adhesion of lymphocytes by amniotic membrane stroma?\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:\nSpecialized electroencephalography (EEG) methods have been used to provide clues about stroke features and prognosis. However, the value of routine EEG in stroke patients without (suspected) seizures has been somewhat neglected. We aimed to assess this in a group of acute ischemic stroke patients in regard to short-term prognosis and basic stroke features. We assessed routine (10-20) EEG findings in 69 consecutive acute ischemic stroke patients without seizures. Associations between EEG abnormalities and NIHSS scores, clinical improvement or deterioration as well as MRI stroke characteristics were evaluated. Mean age was 69 ± 18 years, 43 of the patients (62.3%) were men. Abnormal EEG was found in 40 patients (58%) and was associated with higher age (p = 0.021). The most common EEG pathology was focal slowing (30; 43.5%). No epileptiform potentials were found. Abnormal EEG in general and generalized or focal slowing in particular was significantly associated with higher NIHSS score on admission and discharge as well as with hemorrhagic transformation of the ischemic lesion. Abnormal EEG and generalized (but not focal) slowing were associated with clinical deterioration ( p = 0.036, p = 0.003). Patients with lacunar strokes had no EEG abnormalities.\n\nQuestion:\nIs the use of routine EEG in acute ischemic stroke patients without seizures : generalized but not focal EEG pathology associated with clinical deterioration?\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:\nPostischemic ischemia reperfusion injury is a frequent and unpredictable problem in clinical lung transplantation. Pentoxifylline (PTX) has a number of effects that could decrease reperfusion injury: reduced neutrophil adhesion to endothelium, decreased production of tumor necrosis factor, decreased platelet aggregation, and increased production of vasodilatory prostaglandins by vascular endothelium. We have demonstrated previously that PTX administered before storage and again during reperfusion reduced lung reperfusion injury. The purpose of the present study was to determine whether these observations were storage or reperfusion effects. Fourteen canine left lung allotransplantations were performed. Donor lungs were flushed with modified Euro-Collins solution and stored for 24 hours at 1 degree C. Immediately after transplantation, the contralateral right main pulmonary artery and bronchus were ligated to assess isolated allograft function. Hemodynamic indices and arterial blood gas analysis (inspired oxygen fraction 1.0) were assessed for 6 hours before sacrifice. Allograft myeloperoxidase activity was assessed. Bronchoalveolar lavage fluid was obtained from the allograft middle lobe for neutrophil counts. The animals were divided into three groups based on the timing of PTX administration. Group 1 (n = 5) animals received no PTX. Group 2 (n = 4) animals received PTX (20 mg/kg) just before reperfusion as well as continuous infusion (0.1 mg x kg-1 x min-1) during the assessment period. In group 3 (n = 5), donor lungs received PTX (200mg/L) in the flush solution only. Superior gas exchange was noted in the lungs receiving PTX only in the flush solution (group 3). Myeloperoxidase activity in group-3 allografts was significantly reduced. In addition, protein levels and neutrophil counts in the bronchoalveolar lavage fluid were significantly reduced in group-3 allografts.\n\nQuestion:\nDoes pentoxifylline in flush solution improve early lung allograft function?\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:\nBranch arteries of the aortic arch have been a blind zone for transesophageal echocardiography. Information regarding blood flow, which is important in both planned and emergency operations on the aorta, has therefore been limited. We have established a technique for visualizing these arteries in nearly all cases. In 25 consecutive patients requiring either planned or emergency operations on the aorta, the branch arteries were visualized whenever cerebral malperfusion was suspected. Lateral flexion of the probe tip was used when the trachea interfered with visualization of the arteries. The left subclavian, left and right common carotid, right subclavian, innominate, and left and right vertebral arteries were visualized in 96% (24/25), 92% (23/25), 96% (24/25), 100% (25/25), 84% (21/25), 92% (22/24), and 88% (21/24), respectively. The origin of the innominate artery was visualized in 36% (9/25). In some cases, dissection extended into branch arteries during surgery or during conservative therapy. When the subclavian artery was clamped, retrograde flow was detected in the vertebral artery (steal flow). The cannula for selective cerebral perfusion occasionally was entered into the right common carotid or subclavian artery and obstructed the other branch with a balloon.\n\nQuestion:\nAre aortic arch branches no longer a blind zone for transesophageal echocardiography : a new eye for aortic surgeons?\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 hypothesized that there may be a correlation between the interleukin-7 (IL-7)/IL-7 receptor (IL-7R) regulatory system and parameters of T-cell homeostasis in HIV-infected long-term nonprogressors (LTNPs) as compared with patients with disease progression. The possibility of a correlation between T-cell homeostatic parameters and IL-7/IL-7R was investigated in 22 LTNPs (CD4 count > or =500 cells/microL for >10 years) vs. HIV-positive patients at different disease stages [12 early: CD4 count > or =400 cells/microL ; 15 late (AIDS-presenters): CD4 count < or =150 cells/microL ]. Compared with early-stage HIV-positive patients, LTNPs displayed a higher circulating IL-7 concentration (P=0.05), which was positively associated with higher IL-7Ralpha expression and a higher T-cell receptor excision circle (TREC) content specifically within CD4 cells (P<0.05). Compared with late-stage disease patients, early-stage disease patients displayed a lower IL-7 concentration (P<0.01) and higher percentages of IL-7Ralpha+ CD4 and CD8 cells (P=0.05). IL-7 was positively correlated with the percentage of TREC+ CD4 cells (P<0.01), which translated into a higher percentage of naïve CD4 cells in early-stage disease patients than in late-stage disease patients; however, the CD4 cells in early-stage disease patients were less enriched in recent thymic emigrants (RTEs) compared with LTNPs (P<0.05). In late-stage AIDS-developing patients, substantially increased IL-7 was correlated with a decreased percentage of IL-7Ralpha+ CD4 cells (P=0.01), which resulted in these patients having a significantly lower percentage of naïve T cells (P<0.01) and a significantly lower content of TREC (P<0.01) than the other patients.\n\nQuestion:\nDo hIV-infected long-term nonprogressors display a unique correlative pattern between the interleukin-7/interleukin-7 receptor circuit and T-cell homeostasis?\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:\nNitric oxide (NO), is a biological messenger molecule and a component of innate immunity, with important roles in the regulation of inflammation and in defense against bacterial biofilms. Polymorphisms in genes regulating NO production have the potential for a role in the development of chronic rhinosinusitis (CRS). The purpose of this study was to determine whether polymorphisms in genes regulating NO synthesis are associated with CRS. An established population of 206 individuals with severe CRS and 196 postal code-matched controls was previously screened using a pooling genome-wide associations study to estimate allelic frequency. Genes regulating NO synthesis with a maximal probability of association were identified. High-probability single nucleotide polymorphisms SNPs from the NO synthase (NOS1) and its ligand NOS1 adaptor protein (NOS1AP) genes were retained for individual genotyping. PLINK software was used to determine association. Sixteen SNPs were genotyped successfully with a genotype distribution in agreement with Hardy-Weinberg equilibrium. Two SNPs for NOS1 (rs1483757 and rs9658281) were significantly associated with CRS, with a protective effect. The severe subphenotype showed stronger associations. Subgroup analysis for the presence of nasal polyps, origin, and gender did not influence strength of associations.\n\nQuestion:\nAre polymorphisms in the nitric oxide synthase 1 gene associated with severe chronic rhinosinusitis?\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:\nWhile the neurotensin (NT) roles in pancreatic cancer growth are well documented, its effects on pancreatic cancer cell migration have not been described. The NT-induced effects on the migration process of human pancreatic ductal adenocarcinoma cells (PDACs) were characterized by means of various assays including computer-assisted video-microscopy, fluorescence microscopy, ELISA-based, small GTPase pull-down and phosphorylation assays. The NT-induced modifications on in vitro PDACs migration largely depended on the extra-cellular matrix environment and cell propensity to migrate collectively or individually. While NT significantly reduced the level of migration of collectively migrating PDACs on vitronectin, it significantly increased the level of individually migrating PDACs. These effects were mainly mediated through the sortilin/NTR3 receptor. Neurotensin both induced altered expression of alphaV and beta5 integrin subunits in PDACs cultured on vitronectin resulting in modified adhesion abilities, and caused modifications to the organization of the actin cytoskeleton through the NT-mediated activation of small Rho GTPases. While the NT effects on individually migrating PDACs were mediated at least through the EGFR/ERK signaling pathways, those on collectively migrating PDACs appeared highly dependent on the PI 3-kinase pathway.\n\nQuestion:\nIs neurotensin a versatile modulator of in vitro human pancreatic ductal adenocarcinoma cell ( PDAC ) migration?\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:\nBowel resection is required in the majority of patients with Crohn's disease (CD) during their lifetime. The Prognostic Nutritional Index (PNI) is a useful tool for predicting postoperative outcomes in patients undergoing cancer surgery. We examined the ability of the PNI to predict short-term outcomes in patients with CD-related bowel resection. Seventy-three patients who underwent bowel resection for CD were retrospectively enrolled in the study. The PNI was calculated as follows: 10 × serum albumin (g/dL) + 0.005 × total lymphocyte count (per mL). Patients were divided into 2 groups: PNI <40 (n = 30) and PNI ≥40 (n = 43). A significant difference was found in body mass index (17.9 ± 2.4 vs 19.2 ± 2.2, P = .018) between the 2 groups. Postoperative overall and infectious complications occurred more frequently in patients with PNI <40 than in those with PNI ≥40 (50.0% and 46.7% vs 23.3% and 16.3%, P = .018 and P = .005, respectively). In the univariate analysis, body mass index <18.5, penetrating behavior, open surgery, and PNI <40 were associated with an increased risk of overall complications and infectious complications. In the multivariate analysis, only PNI <40 was an independent prognostic factor for infectious complications (odds ratio: 3.846, 95% confidence interval: 1.145-12.821).\n\nQuestion:\nDoes prognostic Nutritional Index predict Short-Term Postoperative Outcomes After Bowel Resection for Crohn 's 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:\nOne of the hallmarks of cancer is the disruption of gene expression patterns. Many molecular lesions contribute to this phenotype, and the importance of aberrant DNA methylation profiles is increasingly recognized. Much of the research effort in this area has examined proximal promoter regions and epigenetic alterations at other loci are not well characterized. Using whole genome bisulfite sequencing to examine uncharted regions of the epigenome, we identify a type of far-reaching DNA methylation alteration in cancer cells of the distal regulatory sequences described as super-enhancers. Human tumors undergo a shift in super-enhancer DNA methylation profiles that is associated with the transcriptional silencing or the overactivation of the corresponding target genes. Intriguingly, we observe locally active fractions of super-enhancers detectable through hypomethylated regions that suggest spatial variability within the large enhancer clusters. Functionally, the DNA methylomes obtained suggest that transcription factors contribute to this local activity of super-enhancers and that trans-acting factors modulate DNA methylation profiles with impact on transforming processes during carcinogenesis.\n\nQuestion:\nDoes epigenomic analysis detect aberrant super-enhancer DNA methylation in human cancer?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]
0