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[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe standard treatment for cervical cancer in developed countries includes surgery and chemoradiation, with standard of care lagging in developing countries. Even in the former case, treatment frequently yields recalcitrant tumors and women succumb to disease. Here we examine the impact of nelfinavir, an off-patent viral protease inhibitor, which has shown promise as an antineoplastic agent. We evaluated the morphological and proliferative effects of the autophagy-stressing drug nelfinavir in normal and cisplatin-resistant cervical cancer cells. Immunofluorescent validation of autophagy markers was performed and the impact of nelfinavir in an in vivo model of tumor growth was determined. Nelfinavir exhibits cytotoxicity against both cisplatin-sensitive and -resistant ME-180 human cervical cancer cells in vitro and in vivo. Immunoblotting and immunofluorescence showed an expression of the autophagy marker LC3-II in response to nelfinavir treatment.\n\nQuestion:\nIs nelfinavir effective against human cervical cancer cells in vivo : a potential treatment modality in resource-limited settings?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSmooth muscle cells (SMC) of the bladder undergo hypertrophy and hyperplasia following exposure to sustained mechanical overload. Although superficial similarities in the response of the heart and bladder to hypertrophic stimuli suggest that similar molecular mechanisms may be involved, this remains to be demonstrated. In this study we compared signal transduction pathway activation in primary culture bladder SMC and cardiac myofibroblasts in response to cyclic stretch. The effects of growth factor stimulation on pathway activation in bladder SMC were also investigated. Primary culture rodent bladder SMC or cardiac myofibroblasts were subjected to cyclic stretch-relaxation in the absence or presence of pharmacologic inhibitors of the phosphoinositide-3-kinase, (PI3K)/Akt, extracellular signal-regulated kinase-mitogen activated protein kinase (Erk-MAPK) or the p38 stress-activated protein kinase-2 (SAPK2) pathways. In parallel experiments human bladder SMC were treated with platelet-derived growth factor-BB (PDGF-BB), heparin-binding EGF-like growth factor (HB-EGF) or fibroblast growth factor-2 (FGF-2). In each case the extent of DNA synthesis was determined by uptake of tritiated thymidine, and activation of specific signaling intermediates was determined by immunoblot analysis using antibodies to the non-phosphorylated and phosphorylated (activated) forms of Akt, p38 and Erk1/2. Akt and p38 were rapidly phosphorylated in stretched bladder SMC and cardiac myofibroblasts, and stretch-induced DNA synthesis in these cells was ablated with inhibitors of PI3K or p38 but not Erk-MAPK. Similarly, PDGF-BB up-regulated DNA synthesis in bladder SMC in a p38 and Akt-dependent manner.\n\nQuestion:\nDoes signaling through PI3K/Akt mediate stretch and PDGF-BB-dependent DNA synthesis in bladder smooth muscle cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nStage II rectal cancers comprise a heterogeneous group, and there is significant variability in practise with regards to adjuvant chemotherapy; the survival benefit of chemotherapy is perceived to be <4% in these patients. However, in recent years, the emergence of additional prognostic factors such as extramural venous invasion (EMVI) suggests that there may be sub-stratification of stage II tumours and, further, we may be under-estimating the benefit adjuvant chemotherapy provides in high-risk patients. This study examined the outcomes of patients with stage II and III rectal cancer to determine whether EMVI status influences disease-free survival (DFS). An analysis of a prospectively maintained database was conducted of patients presenting with rectal cancer between 2006 and 2012. All patients underwent curative surgery and had no evidence of metastases at presentation. Clinicopathological factors were compared between stage II and III disease. The primary end point was 3-year DFS; univariate and multivariate analysis was carried out using Cox proportional hazards regression models; hazard ratios (HR) with 95% confidence intervals (CIs) were calculated. Four hundred and seventy-eight patients were included: 233 stage II; 245 stage III. The prevalence of EMVI was 34.9%; 57 stage II patients (24.5%) and 110 stage III patients (44.9%). On multivariate analysis, only EMVI status was a significant factor for DFS. The adjusted HR for EMVI either alone or in combination with nodal involvement was 2.08 (95% CI 1.10-2.95) and 2.74 (95% CI 1.66-4.52), respectively.\n\nQuestion:\nDoes eMVI-positive stage II rectal cancer have similar clinical outcomes as stage III disease following pre-operative chemoradiotherapy?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nInfection with Helicobacter pylori is the main risk factor for development of gastric cancer. CD44 overexpression, especially that of variant 9 (CD44v9), has also been implicated in the local inflammatory response and metaplasia-carcinoma sequence in human stomach. We recently identified miR-328 as one of the microRNAs targeting CD44 in gastric cancer. The aim of the current study was to determine the relationship between miR-328 and CD44v9 expression in H. pylori-infected gastric mucosa during the development of preneoplastic lesions. Immunohistochemical staining of myeloperoxidase and CD44v9 was performed using paraffin-embedded tissue sections obtained from 54 patients who underwent gastric resection without preoperative treatment. The levels of miR-328 expression in the gastric mucosa were measured in the same patients using quantitative reverse transcription polymerase chain reaction. Both infiltration of myeloperoxidase-positive inflammatory cells and expression of proinflammatory cytokines closely correlated with H. pylori infection in the cancer-afflicted gastric mucosa. High CD44v9 expression levels, identified in the gastric mucosa in 61 % of samples (33/54), correlated significantly with H. pylori infection in the gastric mucosa. Notably, high CD44v9 expression was significantly associated with low miR-328 expression, whereas low CD44v9 expression was significantly associated with high miR-328 expression.\n\nQuestion:\nIs chronic inflammation with Helicobacter pylori infection implicated in CD44 overexpression through miR-328 suppression in the gastric mucosa?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIt can be clinically difficult to distinguish depressed individuals with bipolar disorder (BD) and major depressive disorder (MDD). To examine potential biomarkers of difference between the two disorders, the current study examined differences in the functioning of emotion-processing neural regions during a dynamic emotional faces task. During functional magnetic resonance imaging, healthy control adults (HC) (n = 29) and depressed adults with MDD (n = 30) and BD (n = 22) performed an implicit emotional-faces task in which they identified a color label superimposed on neutral faces that dynamically morphed into one of four emotional faces (angry, fearful, sad, happy). We compared neural activation between the groups in an amygdala region-of-interest and at the whole-brain level. Adults with MDD showed significantly greater activity than adults with BD in the left amygdala to the anger condition (p = 0.01). Results of whole-brain analyses (at p < 0.005, k ≥ 20) revealed that adults with BD showed greater activity to sad faces in temporoparietal regions, primarily in the left hemisphere, whereas individuals with MDD demonstrated greater activity than those with BD to displays of anger, fear, and happiness. Many of the observed BD-MDD differences represented abnormalities in functioning compared to HC.\n\nQuestion:\nDoes amygdala and whole-brain activity to emotional faces distinguish major depressive disorder and bipolar disorder?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo develop a theoretically informed and empirically validated survey instrument for assessing prescribers' perception of computerized drug-drug interaction (DDI) alerts. The survey is grounded in the unified theory of acceptance and use of technology and an adapted accident causation model. Development of the instrument was also informed by a review of the extant literature on prescribers' attitude toward computerized medication safety alerts and common prescriber-provided reasons for overriding. To refine and validate the survey, we conducted a two-stage empirical validation study consisting of a pretest with a panel of domain experts followed by a field test among all eligible prescribers at our institution. The resulting survey instrument contains 28 questionnaire items assessing six theoretical dimensions: performance expectancy, effort expectancy, social influence, facilitating conditions, perceived fatigue, and perceived use behavior. Satisfactory results were obtained from the field validation; however, a few potential issues were also identified. We analyzed these issues accordingly and the results led to the final survey instrument as well as usage recommendations.\n\nQuestion:\nDoes development and validation of a survey instrument for assessing prescribers ' perception of computerized drug-drug interaction alert?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIt has been shown that the expression of the receptor for advanced glycation end products (RAGE) is closely associated with invasion and metastasis in gastric cancer. A Gly82Ser polymorphism in exon 3 of RAGE gene was identified and thought to have an effect on the functions of its protein. Therefore, the goal of the present study was to investigate whether the polymorphism is involved in the development or progression of gastric cancer. In the hospital-based case-control study, the RAGE genotypes were determined using PCR-RFLP in 566 individuals (283 gastric cancer patients and 283 age- and sex-matched controls). The distribution of genotype was significantly different between cases and controls (P = 0.038). Compared with the wild-type 82Gly/Gly carriers, subjects with the variant genotypes (82Gly/Ser and 82Ser/Ser) had a significantly higher risk of gastric cancer (adjusted odds ratio, 1.47; 95% confidence interval, 1.05-2.06). Moreover, the elevated gastric cancer risk was especially evident in younger individuals (ages < or =58 years), nonsmokers, and rural subjects. Further analyses revealed that the variant genotypes were associated with adjacent organ invasion in the subanalysis of gastric cancer patients.\n\nQuestion:\nIs gly82Ser polymorphism of the receptor for advanced glycation end products associated with an increased risk of gastric cancer in a Chinese population?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis study investigates the effect of pravastatin on blood pressure, cardiovascular remodelling and impaired endothelial function induced as early signs of cardiovascular disease in young spontaneously hypertensive rats (SHR). Eight-week-old SHR were treated for 4 weeks with pravastatin (20 mg kg(-1) day(-1)). Systolic blood pressure was measured periodically during the study using the tail-cuff method. At the end of the study, the left ventricular weight /body weight ratio was used as an index of left ventricular hypertrophy (LVH). Vascular function, superoxide (O(2)(-*)) production and structure were studied in aortic rings. Lipid peroxidation was measured in plasma (thiobarbituric acid reactive substances assay). Systolic blood pressure was lower in treated SHR than in control SHR, at the end of the study (171 +/- 1 vs. 159 +/- 2 mmHg, P < 0.05), and LVH was significantly reduced by pravastatin (2.7 +/- 0.02 vs. 2.5 +/- 0.01 mg g(-1), P < 0.05). Vascular responses to sodium nitroprusside and phenylephrine were similar in both groups; nevertheless, the relaxation response to acetylcholine was higher in the treated rats (45.6 +/- 2.6 vs. 58.1 +/- 3.2 %, P < 0.05). Vascular O(2)(-*) and plasma thiobarbituric acid reactive substances were reduced by pravastatin treatment, and urinary nitrites was elevated. Finally aortic wall became thinner after pravastatin treatment.\n\nQuestion:\nDoes chronic treatment with pravastatin prevent early cardiovascular changes in spontaneously hypertensive rats?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe aimed to evaluate the prognostic significance of the preoperative tumor-marker cancer antigen (CA) 15.3 in Saudi patients with breast cancer and to find out whether any correlation exists between preoperative CA 15.3 and tumor size and nodal status. Preoperative blood samples for serum CA 15.3 levels were taken in 112 breast cancer patients who underwent breast-conserving surgery or modified radical mastectomy between February 1988 and August 2008. Serum levels of CA 15.3 below 35 U/mL were considered normal. The correlation between pre- and postoperative CA 15.3 levels with tumor size and nodal status was calculated using Pearson correlative coefficients. Kaplan-Meier curves were used to determine disease-free survival (DFS) according to CA 15.3 groups (<35, 36-100 and above >100 U/mL). The mean age of the cohort was 47.0 years (range 23-76, standard deviation 10.3). According to menopausal status, 93 patients (83.0%) were premenopausal, and 19 patients (17.0%) were postmenopausal. Mean preoperative CA 15.3 levels were 43.69 U/mL (1.0-209.87). Ten-year DFS rates were 100%, 84%, and 57.7% for CA 15.3 <35 U/mL, 36-100 U/mL, and >100 U/mL, respectively (P = 0.003). Preoperative CA 15.3 levels showed positive correlation with primary tumor size (R = 0.43, R (2) = 0.83, P = 0.03) and nodal status (R = 0.59, R (2) = 0.28, P < 0.0001), respectively.\n\nQuestion:\nAre elevated preoperative serum cancer antigen 15.3 levels associated with reduced disease-free survival : a single-institution experience?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe investigated the relationship between iodine-123-metaiodobenzylguanidine (123I-MIBG) findings and myocardial contractile reserve in patients with mild to moderate dilated cardiomyopathy (DCM). Little is known regarding the relationship between cardiac sympathetic nervous function and myocardial contractile reserve in DCM. Twenty-four DCM patients who showed sinus rhythm underwent echocardiography, biventricular catheterization, and myocardial 123I-MIBG scintigraphy. Left ventricular (LV) pressures were measured using a micromanometer-tipped catheter. The myocardial contractile function (LV dP/dt(max)) was determined at rest and during atrial pacing. The messenger ribonucleic acid (mRNA) expressions of intracellular Ca2+-regulatory proteins were analyzed by real-time quantitative reverse transcription-polymerase chain reaction. Myocardial 123I-MIBG accumulation was quantified as a heart-mediastinum ratio (HMR). A significant correlation was observed between the delayed 123I-MIBG HMR and the percentage change in LV dP/dt(max) from the baseline to the peak or critical heart rate (r = 0.64; p < 0.001). The delayed 123I-MIBG HMR was significantly lower in patients showing a worsening change in LV dP/dt(max) than in those showing a favorable change (p < 0.005). The maximum LV dP/dt(max) during pacing and the sarcoplasmic reticulum Ca2+-ATPase (SERCA2) mRNA levels were significantly more reduced in patients with a delayed HMR < or =1.8 than in those with a delayed HMR >1.8 (p < 0.05, respectively).\n\nQuestion:\nDoes cardiac sympathetic dysfunction correlate with abnormal myocardial contractile reserve in dilated cardiomyopathy patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nEnvironmental factors affect the dissemination and distribution of intestinal parasites in human communities. To comprehend the prevalence of parasitic infestation and to examine whether geographical location and age also influence the prevalence of infection, fecal samples from 195 school children (rural = 95; male = 39; female = 56) (urban = 100; male = 60; female = 40) of five age groups ranging from 5 to 11 years in two different socio-economic zones (rural and urban) were screened for specific intestinal parasites using standard histological techniques. Percentage incidences of parasitic species found in fecal wet mounts and concentrates in rural children were Entamoeba coli (25.3%), Giardia lamblia (17.9%), Blastocystis hominis (14.7%), Entamoeba histolytica (4.2%), Iodamoeba butschlii (1.1%), Hymenolepis nana (1.1%) and Ascaris lumbricoides (1.1%). Whereas the percentage incidences among urban children were E. coli (26%), A. lumbricoides (21%), B. hominis (18%), G. lamblia (14%), T. trichiura (8%), I. butschlii (4%) and A. duodenale (1%). Such findings may be related to dietary differences, living conditions and the greater use of natural anti-helminthic medicinal plants in rural communities. These results are important for both epidemiological data collection and for correlating dietary differences to intestinal parasitic diseases. We chose to investigate whether geographical location and age affect the prevalence and distribution of intestinal parasites among school children from two separate regions (rural and urban) in areas surrounding, Chennai, Tamil Nadu, India. A study of the prevalence of parasitic infestations was undertaken among primary school children, in rural and urban communities around Chennai, Tamil Nadu, India. Faecal sample collection, direct microscopic techniques, macroscopic examination and concentration techniques for identifying the parasites. Percentage incidences of parasitic species found in faecal wet mounts and concentrates were done instead of statistical analyses. Both macroscopic and microscopic examinations of faecal samples revealed that the overall percentage prevalence of parasite species encountered in rural children were Entamoeba coli (25.3%), G. lamblia (17.9%), B. hominis (14.7%), Entamoeba histolytica (4.2%), I. butschlii (1.1%), H. nana (1.1%), Ascaris lumbricoides (1.1%). The prevalence among urban children were E. coli (26%), A. lumbricoides (21%), B. hominis (18%), G. lamblia (14%), T. trichiura (8%), I. butschlii (4%) and A. duodenale (1%). Overall, comparative significant differences were noted between rural and urban children for E. histolytica (4.2 vs. 14%), G. lamblia (17.9 vs. 14%), A. lumbricoides (1.1 vs. 21%) and T. trichiura (0 vs. 8%), with the major difference being the much higher occurrence of A. lumbricoides and T. trichiura infections in urban children.\n\nQuestion:\nDoes geographical location and age affect the incidence of parasitic infestations in school children?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCholangiocarcinoma (CCA) is an aggressive disease with limited effective treatment options. The PI3K/Akt/mTOR pathway represents an attractive therapeutic target due to its frequent dysregulation in CCA. MK2206, an allosteric Akt inhibitor, has been shown to reduce cellular proliferation in other cancers. We hypothesized that MK2206 mediated inhibition of Akt would impact CCA cellular viability. Post treatment with MK2206 (0-2 μM), cellular viability was assessed in two human CCA cell lines-CCLP-1 and SG231-using an MTT assay. Lysates from the MK2206 treated CCA cells were then examined for apoptotic marker expression levels using Western blot analysis. Additionally, the effect on cellular proliferation of MK2206 treatment on survivin depleted cells was determined. CCLP-1 and SG231 viability was significantly reduced at MK2206 concentrations of 0.5, 1, and 2 μM by approximately 44%, 53%, and 64% (CCLP-1; p = 0.01) and 32%, 32%, and 42% (SG231; p < 0.00005) respectively. Western analysis revealed a decrease in AKT(Ser473), while AKT(Thr308) expression was unchanged. In addition, cleaved PARP as well as survivin expression increased while pro-caspase 3 and 9 levels decreased with treatment. Depletion of survivin in CCLP-1 cells resulted in apoptosis as evidenced by increased cleaved PARP. In addition, survivin siRNA further enhanced the antitumor activity of MK2206.\n\nQuestion:\nDoes inhibition of the AKT pathway in cholangiocarcinoma by MK2206 reduce cellular viability via induction of apoptosis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nChronic drug use has been associated with increased impulsivity and maladaptive behaviour, but the underlying mechanisms of this impairment remain unclear. We investigated the ability to adapt behaviour according to changes in reward contingencies, using a probabilistic reversal-learning task, in chronic drug users and controls. Five groups were compared: chronic amphetamine users (n = 30); chronic cocaine users (n = 27); chronic opiate users (n = 42); former drug users of psychostimulants and opiates (n = 26); and healthy non-drug-taking control volunteers (n = 25). Participants had to make a forced choice between two alternative stimuli on each trial to acquire a stimulus-reward association on the basis of degraded feedback and subsequently to reverse their responses when the reward contingencies changed. Chronic cocaine users demonstrated little behavioural change in response to the change in reward contingencies, as reflected by perseverative responding to the previously rewarded stimulus. Perseverative responding was observed in cocaine users regardless of whether they completed the reversal stage successfully. Task performance in chronic users of amphetamines and opiates, as well as in former drug users, was not measurably impaired.\n\nQuestion:\nIs chronic cocaine but not chronic amphetamine use associated with perseverative responding in humans?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nQuality of life (QoL) in valvular surgery may differ according to the underlying pathology and surgical technique used. 82 adults undergoing their first elective surgery for valve repair (VP; n = 9) or valve replacement (VR) with a mechanical valve (MVR; n = 57) or bioprosthesis (BVR; n = 16) were assessed before surgery and three months afterwards. delta scores (postoperative-preoperative) on QoL measures (Quality of Life Systemic Inventory (QLSI) and SF-36). Paired t tests and ANCOVAs with age and preoperative QoL scores as covariates. QoL improves after surgery according to most subscales. According to group comparisons, patients with an MVR improve more than those with a BVR on the mental health subscale. In physical roles, patients with an MVR improve while those with a BVR deteriorate. In emotional roles, patients with a VR improve while those with a VP deteriorate. However, they are similar on all other subscales. Women improve more than men on leisure, affectivity and social functioning while the opposite holds true for mental health.\n\nQuestion:\nIs quality of life before and after heart valve surgery influenced by gender and type of valve?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAtrial fibrillation (AF) is a common cardiac arrhythmia characterized by disorganized cardiac electrical activity. Defibrillation electrode placement has been shown to affect the amount of energy and number of shocks required to defibrillate. The objective of this study was to investigate the relationship between esophageal electric fields (EEFs) and atrial defibrillation thresholds (ADFTs) to determine the feasibility of using EEFs during a low-strength shock to predict patient-specific defibrillation electrode placements. AF was induced and defibrillated according to a Bayesian four-shock protocol for 12-electrode placements in six pigs. EEFs were measured during each of the four shocks of the protocol and during a 1-J shock for each electrode placement. Squared EEFs (EEF(2) s) during all shocks were compared to the ADFTs using a linear regression. There was a negative relationship between EEF(2) s during the 1-J shocks and ADFTs, with median R(2) values of 0.863 and 0.840 for anterior-anterior (AA) and anterior-posterior (AP) electrode placements, respectively. There was a strong, positive relationship between applied energy and EEF(2) s, with median R(2) values of at least 0.866 for all animals. The placement with the highest EEF(2) resulted in the lowest ADFT for both AA and AP placements in four of six pigs. In the other two animals, this held for one electrode set but not both.\n\nQuestion:\nAre esophageal electric fields predictive of atrial defibrillation thresholds?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe origin of congenital diaphragmatic hernia (CDH) is considered to lie in a malformation of the nonmuscular primordial diaphragm. It is known that fetal diaphragmatic development requires the structural integrity of its underlying mesenchymal tissue. Developmental mutations that inhibit the formation of normal diaphragmatic mesenchyme have been shown to cause CDH. FRAS1-related extracellular matrix 1 (FREM1) plays a critical role in the development of the fetal diaphragm. It has been demonstrated that a deficiency of FREM1 can lead to CDH both in humans and mice. Furthermore, FREM1-deficient fetuses exhibit a decreased level of mesenchymal cell proliferation in their developing diaphragms. We hypothesized that FREM1 expression is decreased in developing diaphragms of fetal rats with nitrofen-induced CDH. Timed-pregnant rats were exposed to either nitrofen or vehicle on gestational day 9 (D9), and fetuses were harvested on selected time-points D13, D15, and D18. Dissected diaphragms (n = 72) were divided into control and nitrofen-exposed samples (n = 12 per time-point and experimental group). Diaphragmatic gene expression levels of FREM1 were analyzed by quantitative polymerase chain reaction. Immunofluorescence staining for FREM1 was combined with the mesenchymal marker GATA4 to localize FREM1 protein expression and tissue distribution in fetal diaphragms. In nitrofen-exposed fetuses, relative mRNA expression of FREM1 was significantly reduced in pleuroperitoneal folds on D13 (0.30 ± 0.23 vs. 0.83 ± 0.19; p < 0.05), developing diaphragms on D15 (0.54 ± 0.22 vs. 1.19 ± 0.28; p < .05) and fully muscularized diaphragms on D18 (0.49 ± 0.37 vs. 0.97 ± 0.53; p < 0.05) in comparison with controls. Confocal laser scanning microscopy revealed markedly diminished diaphragmatic FREM1 immunofluorescence, which was associated with reduced proliferation of diaphragmatic mesenchymal cells in nitrofen-exposed fetuses on D13, D15, and D18 compared to controls.\n\nQuestion:\nDoes gene Expression of FRAS1-Related Extracellular Matrix 1 be Decreased in Nitrofen-Induced Congenital Diaphragmatic Hernia?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAutonomic dysfunction (AD) is a significant problem in primary biliary cirrhosis (PBC) and is equally present in early disease stages. Currently, AD in PBC is considered to be central in origin. The aim of this study was to examine peripheral mechanisms in the pathogenesis of AD in PBC using novel microvascular optical assessments for this patient group. Twenty-four early stage PBC patients and 24 age-matched controls attended for two microvascular optical-based measurement techniques. Firstly, the regulation of microvascular blood volume to the periphery was assessed using multisite photoplethysmography (PPG) by examining the degree of correlation between the right and left sides of the body, with reduced correlation consistent with peripheral AD. Secondly, the peripheral vasomotor reflex response to standing was dynamically tested using laser Doppler flowmetry to quantify the degree of autonomic tone in peripheral vasoconstriction. PBC patients had a significantly reduced right to left side blood volume multisite PPG correlation compared with controls when corrected for age, body mass index, heart rate and systolic blood pressure [impaired synchronization between pulse wave amplitude between right and left fingers and right and left ears (both P<0.05)]. The veno-arteriolar reflex on standing in PBC patients was significantly lower than for the controls, consistent with poorer autonomic tone for vasoconstriction in PBC (P<0.01).\n\nQuestion:\nDoes microvascular optical assessment confirm the presence of peripheral autonomic dysfunction in primary biliary cirrhosis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nChanges in plant diversity may induce distinct changes in soil food web structure and accompanying soil feedbacks to plants. However, knowledge of the long-term consequences of plant community simplification for soil animal food webs and functioning is scarce. Nematodes, the most abundant and diverse soil Metazoa, represent the complexity of soil food webs as they comprise all major trophic groups and allow calculation of a number of functional indices. We studied the functional composition of nematode communities three and five years after establishment of a grassland plant diversity experiment (Jena Experiment). In response to plant community simplification common nematode species disappeared and pronounced functional shifts in community structure occurred. The relevance of the fungal energy channel was higher in spring 2007 than in autumn 2005, particularly in species-rich plant assemblages. This resulted in a significant positive relationship between plant species richness and the ratio of fungal-to-bacterial feeders. Moreover, the density of predators increased significantly with plant diversity after five years, pointing to increased soil food web complexity in species-rich plant assemblages. Remarkably, in complex plant communities the nematode community shifted in favour of microbivores and predators, thereby reducing the relative abundance of plant feeders after five years.\n\nQuestion:\nDo changes in plant species richness induce functional shifts in soil nematode communities in experimental grassland?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe antimalarial agent, artemisinin, also confers cancer-specific cytotoxic effects by reacting with ferrous iron atoms to form free radicals. Here, we investigated the radiosensitizing effects of dihydroartemisinin on glioma cells and assessed some possible mechanisms for these effects. U373MG glioma cells treated with various concentrations of dihydroartemisinin plus radiation, and efficiency of radiosensitization was assessed by clonogenic survival assay. Expression and activity of antioxidant enzymes, glutathione-S-transferase (GST) were quantified by western blot and enzymatic activity analyses, respectively. Dihydroartemisinin showed higher cytotoxicity in the glioma cell lines than in the liver, breast or cervical cancer cell lines. In clonogenic survival assays, treatment with dihydroartemisinin alone dose-dependently reduced the number of U373MG colonies, while treatment with dihydroartemisinin plus gamma-irradiation showed far lower clonal survival than cultures treated with radiation or dihydroartemisinin alone. The radiosensitizing effect of dihydroartemisinin was blocked significantly by the free radical scavengers, NAC and TIRON, indicating association with dihydroartemisinin-induced ROS generation. In addition, the radiation-induced expression of endogenous GST was suppressed by treatment with dihydroartemisinin. The radiosensitizing effect of dihydroartemisinin was also markedly enhanced by the addition of holotransferrin\n\nQuestion:\nDoes dihydroartemisinin enhance radiosensitivity of human glioma cells in vitro?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThere is a sparsity of data on the impact of cachexia on human muscle function. This study examined the relationship between cachexia, quality of life and the mass/function/mechanical quality of lower limb skeletal muscle in gastrointestinal cancer patients. Quadriceps strength and lower limb power were measured in 54 patients with gastrointestinal cancer (n = 24 ≥ 10% weight-loss) and 18 healthy controls. Quadriceps cross-sectional area was measured in 33/54 patients and in all controls using MRI. Muscle mechanical quality was defined as quadriceps strength/unit quadriceps cross-sectional area. Quality of life was assessed using the EORTC QLQ-C30. Patients with weight-loss ≥ 10% were classified as cachectic. In male cachectic patients, quadriceps strength (p = 0.003), lower limb power (p = 0.026), quadriceps cross-sectional area (p = 0.019) and muscle quality (p = 0.008) were reduced compared with controls. In female cachectic patients, quadriceps strength (p = 0.001) and muscle quality (p = 0.001) were reduced compared with controls. Physical function (p = 0.013) and fatigue (p = 0.004) quality of life scores were reduced in male cachectic compared with non-cachectic patients, but not in females.\n\nQuestion:\nDoes sexual dimorphism modulate the impact of cancer cachexia on lower limb muscle mass and function?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nDevices for rapid induction of mild hypothermia after cardiac arrest are needed. We hypothesized that the Life Recovery Systems' ThermoSuit System provides effective core cooling by pumping ice water over the skin surface and improves neurologic outcome after prolonged cardiac arrest. Prospective experimental study. University research laboratory. Large White breed pigs (29 to 35 kg). Swine were anesthetized and mechanically ventilated. Ten minutes of untreated ventricular fibrillation, 3 mins of basic life support, and 5 mins of advanced cardiac life support, including two 0.4 IU/kg doses of vasopressin, were followed by up to three countershocks. After restoration of spontaneous circulation, swine were randomized to two groups (normothermic control, hypothermia). The hypothermia group was cooled from a pulmonary artery temperature of 38.5 +/- 0.5 degrees C to 33.0 degrees C and kept for 14 hrs. At day 9 of the experiment, overall performance categories scores (1, normal; 2, slightly disabled; 3, severely disabled; 4, comatose; 5, dead, brain dead) and neurologic deficit scores (0%, normal; 100%, brain dead) were assessed. Data are presented as median and interquartile range; group comparison was done with a Mann-Whitney U test. In total, 16 of 22 animals were randomized. Time to target temperature in the hypothermia group (n = 8) was 9.0 (5.3-11.9) mins (cooling rate 0.4 [0.3-0.8] degrees C/min), and all animals achieved an overall performance categories score of 1. In the control group, one swine achieved an overall performance categories score of 1, three achieved a score of 2, and four achieved a score of 3 (p = .002). Neurologic deficit score was 0% (0%-4%) in the hypothermia group and 39% (19%-55%) in the control group (p = .001). No harmful side effects could be observed.\n\nQuestion:\nDoes therapeutic hypothermia with a novel surface cooling device improve neurologic outcome after prolonged cardiac arrest in swine?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe have investigated the effects of BRCA1 over-expression and knockdown on 5F-203-induced gene expression and cytotoxicity in human breast cancer cells. 5F-203 is a chemotherapeutic prodrug that both induces a p450 enzyme, CYP1A1, and is metabolically activated by CYP1A1. We used several molecular biological techniques to confirm our findings. BRCA1 regulates sensitivity to 5F-203 by regulating the expression of CYP1A1 mRNA and its EROD activity. XRE-Luc reporter assays, semi-quantitative RT-PCR, Western blot analysis, EROD activity measurements, gene knockdown and MTT cell survival assays were used for this study. Our results show that the ability of 5F-203 treatments to increase CYP1A1 mRNA level and CYP1A1 enzymatic activity (EROD activity) are affected by BRCA1 protein levels. In addition, the ability of 5F-203 treatments to induce proteins, P53 and P53 target genes such as P21, is significantly decreased in BRCA1 knockdown cells, suggesting that BRCA1-related effects could at least partially explain why BRCA1 knockdown increases resistance to 5F-203-mediated cytotoxicity. We also observed altered expression of the two major transcription factors (AhR and ARNT) that affect CYP1A1 expression when BRCA1 protein levels are altered.\n\nQuestion:\nDoes bRCA1 modulate sensitivity to 5F-203 by regulating xenobiotic stress-inducible protein levels and EROD activity?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMitofilin was originally described as a heart muscle protein because of its abundance in the heart tissue; however, its function in the heart is still to be elucidated. Thus, this study aims at investigating the role of mitofilin in the heart in response to hypertrophic stimuli. In this study, a significant increase in mitofilin expression was observed in the hearts of patients with hypertrophic cardiomyopathy. Transgenic (TG) mice with cardiomyocyte-specific overexpression of mitofilin were generated, and cardiac hypertrophy was introduced by transverse aortic constriction (TAC) or chronic infusion of isoproterenol (ISO). In TG mice overexpressing mitofilin, the level of cardiac hypertrophy was significantly greater than that in wild-type (WT) mice after TAC and ISO stimulation. A detailed analysis showed that compared with WT mice, the level of reactive oxygen species was increased after TAC and ISO induction and mitochondrial oxidative phosphorylation (OXPHOS) activity in the TG hearts was lower. These alterations may contribute to the aggravated cardiac hypertrophy observed in response to TAC and ISO stimulation.\n\nQuestion:\nDoes overexpression of mitofilin in the mouse heart promote cardiac hypertrophy in response to hypertrophic stimuli?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo examine the relationship between intuitive eating (IE), which includes eating in response to hunger and satiety cues rather than emotional cues and without having forbidden foods, and weight status in a large sample of adults. A total of 11,774 men and 40,389 women aged ≥18 years participating in the NutriNet-Santé cohort were included in this cross-sectional analysis. Self-reported weight and height were collected as well as IE levels using the validated French version of the Intuitive Eating Scale-2. The association between IE and weight status was assessed using multinomial logistic regression models. A higher IE score was strongly associated with lower odds of overweight or obesity in both men and women. The strongest associations were observed in women for both overweight [quartile 4 vs. 1 of IE: odds ratio, 95% confidence interval: (0.19, 0.17-0.20)] and obesity (0.09, 0.08-0.10). Associations in men were as follows: for overweight (0.43, 0.38-0.48) and obesity (0.14, 0.11-0.18).\n\nQuestion:\nIs intuitive eating inversely associated with body weight status in the general population-based NutriNet-Santé study?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe aim of this study was to demonstrate bacterial translocation after experimentally induced intestinal obstruction as well as investigate the preventive effects of hyperbaric oxygen on obstruction-induced bacterial translocation in rats. Forty Wistar-albino male and female rats were used. Although no procedure was done in the control group (n = 8), hyperbaric oxygen treatment under 2.5 atm absolute for 90 minutes daily was applied for two days in the hyperbaric oxygen group (n = 8). In the sham group (n = 8), after laparotomy the small bowel was only handled gently, and tissue sampling was done 48 hours later. In the obstruction group (n = 8) the ileum was ligated by 5-0 polypropylene just 5 cm proximal to the ileocecal valve. In the obstruction and hyperbaric oxygen group (n = 8), after obstruction hyperbaric oxygen treatment was applied. Forty-eight hours after the procedures, tissue samples from small bowel, mesenteric lymph nodes, spleen, and liver were taken and 1 ml of blood from the portal vein was withdrawn. All samples were cultured for microbiologic examination. Hyperbaric oxygen treatment significantly reduced the endogenous bacterial overgrowth in the small intestine of normal rats. Endogenous bacteria in the small intestine were significantly increased in the obstruction group, and the presence of bacterial overgrowth was proven by bacterial presence on mesenteric lymph nodes, spleen, liver, and blood. Hyperbaric oxygen treatment significantly reduced the endogenous bacterial overgrowth in the small intestine and prevented the bacterial translocation almost completely in obstruction-induced rats.\n\nQuestion:\nDoes hyperbaric oxygen ameliorate bacterial translocation in rats with mechanical intestinal obstruction?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis study tests the hypothesis that complexation between a cationic polymer, poly-L-arginine (PLA), and an anionic drug, low molecular weight heparin (LMWH), enhances pulmonary absorption and reduces the epithelial toxicity. Enoxaparin, a LMWH, was complexed with PLAs of different molecular weights at varying concentrations. The resulting complexes were characterized by measuring particle size and zeta potential, and by quantitating the interactions between PLA and enoxaparin using an azure A assay. Changes in transepithelial electrical resistance (TEER) and cytotoxicity induced by enoxaparin-PLA complex were investigated in Calu-3 cells. Pulmonary absorption of LMWH was determined by measuring plasma anti-factor Xa levels. A bronchoalveolar lavage (BAL) study was performed to investigate if the PLA-based formulations caused any cellular or biochemical changes in the lungs. The particle size of enoxaparin-PLA complexes decreased and the zeta potential values of the complex became less negative as the concentration of positively charged PLA in the complex increased. In vitro experiments suggest that addition of enoxaparin-PLA complex to the apical side of a polarized cell monolayer results in a significant increase in permeability to 14C-mannitol and a decrease in TEER. Pulmonary formulations of enoxaparin plus 0.0125% or 0.0625% PLA of molecular weight 93 kDa led to a twofold increase in the relative bioavailability of LMWH compared to the control (enoxaparin plus normal saline). The BAL study showed that the enoxaparin-PLA complex formulation did not elicit any significant increases in marker enzyme activities compared to the normal saline-treated or untreated control groups.\n\nQuestion:\nDoes complexation of a poly-L-arginine with low molecular weight heparin enhance pulmonary absorption of the drug?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSalvage therapy based on foscarnet plus a thymidine analog is effective in patients with advanced-stage HIV disease and viruses harbouring multiple drug-resistance mutations. To identify viral genetic determinants associated with the virological efficacy of foscarnet salvage therapy. Thirteen patients received foscarnet at a fixed dose of 80 mg/kg twice daily for 14 days, in combination with zidovudine or stavudine. The baseline median HIV viral load and CD4 cell count were 5.10log(10) copies/ml and 23 cells/mm(3), respectively. Following foscarnet therapy, viral load fell by a median of 1.84log(10)copies/ml (range: -0.29 to -2.82), and by at least 1log(10)copies/ml in 11 patients, all of whom harboured viruses with at least three thymidine-associated mutations (TAMs). The two patients with smaller declines in viral load (<0.50log(10)copies/ml) harboured viruses with only one or zero TAMs.\n\nQuestion:\nIs foscarnet salvage therapy efficacy associated with the presence of thymidine-associated mutations ( TAMs ) in HIV-infected patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMyocardial fibrosis is a hallmark of hypertrophic cardiomyopathy (HCM) and a potential substrate for arrhythmias and heart failure. Sarcomere mutations seem to induce profibrotic changes before left ventricular hypertrophy (LVH) develops. To further evaluate these processes, we used cardiac magnetic resonance with T1 measurements on a genotyped HCM population to quantify myocardial extracellular volume (ECV). Sarcomere mutation carriers with LVH (G+/LVH+, n=37) and without LVH (G+/LVH-, n=29), patients with HCM without mutations (sarcomere-negative HCM, n=11), and healthy controls (n=11) underwent contrast cardiac magnetic resonance, measuring T1 times pre- and postgadolinium infusion. Concurrent echocardiography and serum biomarkers of collagen synthesis, hemodynamic stress, and myocardial injury were also available in a subset. Compared with controls, ECV was increased in patients with overt HCM, as well as G+/LVH- mutation carriers (ECV=0.36±0.01, 0.33±0.01, 0.27±0.01 in G+/LVH+, G+/LVH-, controls, respectively; P≤0.001 for all comparisons). ECV correlated with N-terminal probrain natriuretic peptide levels (r=0.58; P<0.001) and global E' velocity (r=-0.48; P<0.001). Late gadolinium enhancement was present in >60% of overt patients with HCM but absent from G+/LVH- subjects. Both ECV and late gadolinium enhancement were more extensive in sarcomeric HCM than sarcomere-negative HCM.\n\nQuestion:\nDo t1 measurements identify extracellular volume expansion in hypertrophic cardiomyopathy sarcomere mutation carriers with and without left ventricular hypertrophy?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPostoperative cognitive dysfunction is a clinical entity that is associated with poor outcome. We determined the effectiveness of amantadine in reducing surgery-induced cognitive impairment and the role of glial cell line-derived neurotrophic factor (GDNF) in this effect. Four-month old male Fischer 344 rats were subjected to right carotid exposure under intravenous anesthesia. Some rats received intraperitoneal injection of 25 mg/kg/day amantadine for 3 days with the first dose at 15 min before the surgery or intracerebroventricular injection of GDNF or an anti-GDNF antibody at the end of surgery. One week later, rats were started to be tested by Barnes maze and fear conditioning. Hippocampus was harvested at 6 h, 24 h or 10 days after the surgery for biochemical analysis. C8-B4 cells, a microglial cell line, were pretreated with 1 ng/ml GDNF for 30 min before being exposed to 5 ng/ml lipopolysaccharide for 2 h. Surgery increased the time to identify the target box in the Barnes maze when tested 1 day [22 (median) (11-66) (interquartile range) of control group vs. 158 (29-180) of surgery group, n = 15, P = 0.022) or 8 days after the training sessions and reduced context-related freezing behavior in the fear conditioning test. These effects were attenuated by amantadine (25 (14-90), n = 15, P = 0.029 compared with surgery group at 1 day after the training sessions in Barnes maze) and intracerebroventricular GDNF. Amantadine increased GDNF that was co-localized with glial fibrillary acidic protein, an astrocytic marker, in the hippocampus. Intracerebroventricular injection of an anti-GDNF antibody but not the denatured antibody blocked the effects of amantadine on cognition. Surgery induced neuroinflammation that was inhibited by amantadine. Lipopolysaccharide increased interleukin 1β production from C8-B4 cells. This effect was inhibited by GDNF.\n\nQuestion:\nDoes amantadine alleviate postoperative cognitive dysfunction possibly by increasing glial cell line-derived neurotrophic factor in rats?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe aim of this study is to determine whether caspase activity and oxidative stress of granulosa cells are associated with the viability and developmental potential of vitrified immature oocytes. Oocytes from mice were exposed to genistein or/and Z-VAD-FMK with or without vitrification. Ultrastructural alterations of granulosa cells in vitrified immature oocytes were observed. Moreover, the level of superoxide dismutase (SOD) in granulosa cells, incidence of apoptotic follicles, the viability of vitrified-warmed oocytes and their subsequent developmental competence were measured. Ultrastructural alterations of granulosa cells vitrified in the presence of genistein or Z-VAD-FMK were slighter than that of granulosa cells vitrified in the absence of genistein or Z-VAD-FMK. The incidence of apoptotic follicles vitrified in the presence of genistein or Z-VAD-FMK was significantly lower than that of immature oocytes vitrified in the absence of genistein or Z-VAD-FMK, whereas, the level of SOD in granulosa cells, the viability and developmental competence of immature oocytes vitrified in the presence of genistein or Z-VAD-FMK were significantly higher than that of immature oocytes vitrified in the absence of genistein or Z-VAD-FMK.\n\nQuestion:\nAre caspase activity and oxidative stress of granulosa cells associated with the viability and developmental potential of vitrified immature oocytes?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTumor cell invasion into adjacent normal brain is a mesenchymal feature of GBM and a major factor contributing to their dismal outcomes. Therefore, better understandings of mechanisms that promote mesenchymal change in GBM are of great clinical importance to address invasion. We previously showed that the bHLH transcription factor TWIST1 which orchestrates carcinoma metastasis through an epithelial mesenchymal transition (EMT) is upregulated in GBM and promotes invasion of the SF767 GBM cell line in vitro. To further define TWIST1 functions in GBM we tested the impact of TWIST1 over-expression on invasion in vivo and its impact on gene expression. We found that TWIST1 significantly increased SNB19 and T98G cell line invasion in orthotopic xenotransplants and increased expression of genes in functional categories associated with adhesion, extracellular matrix proteins, cell motility and locomotion, cell migration and actin cytoskeleton organization. Consistent with this TWIST1 reduced cell aggregation, promoted actin cytoskeletal re-organization and enhanced migration and adhesion to fibronectin substrates. Individual genes upregulated by TWIST1 known to promote EMT and/or GBM invasion included SNAI2, MMP2, HGF, FAP and FN1. Distinct from carcinoma EMT, TWIST1 did not generate an E- to N-cadherin \"switch\" in GBM cell lines. The clinical relevance of putative TWIST target genes SNAI2 and fibroblast activation protein alpha (FAP) identified in vitro was confirmed by their highly correlated expression with TWIST1 in 39 human tumors. The potential therapeutic importance of inhibiting TWIST1 was also shown through a decrease in cell invasion in vitro and growth of GBM stem cells.\n\nQuestion:\nDoes tWIST1 promote invasion through mesenchymal change in human glioblastoma?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nActive smoking increases the risk of developing community-acquired pneumonia (CAP) and invasive pneumococcal disease, although its impact on mortality in pneumococcal CAP outcomes remains unclear. The aim of this study was to investigate the influence of current smoking status on pneumococcal CAP mortality. We performed a multicenter, prospective, observational cohort study in 4,288 hospitalized patients with CAP. The study group consisted of 892 patients with pneumococcal CAP: 204 current smokers (22.8%), 387 nonsmokers (43.4%), and 301 exsmokers (33.7%). Mortality at 30 days was 3.9%: 4.9% in current smokers vs 4.3% in nonsmokers and 2.6% in exsmokers. Current smokers with CAP were younger (51 years vs 74 years), with more alcohol abuse and fewer cardiac, renal, and asthma diseases. Current smokers had lower CURB-65 (confusion, uremia, respiratory rate, BP, age ≥ 65 years) scores, although 40% had severe sepsis at diagnosis. Current smoking was an independent risk factor (OR, 5.0; 95% CI, 1.8-13.5; P = .001) for 30-day mortality of pneumococcal CAP after adjusting for age (OR, 1.06; P = .001), liver disease (OR, 4.5), sepsis (OR, 2.3), antibiotic adherence to guidelines, and first antibiotic dose given < 6 h. The independent risk effect of current smokers remained when compared only with nonsmokers (OR, 4.0; 95% CI, 1.3-12.6; P = .015) or to exsmokers (OR, 3.9; 95% CI, 1.09-4.95; P = .02).\n\nQuestion:\nDoes tobacco smoking increase the risk for death from pneumococcal pneumonia?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSeveral recent reports demonstrated the usefulness of new biomarkers in early prediction of delayed graft function (DGF) and graft recovery after kidney transplantation (KT). It is unknown, however, whether these biomarkers would predict long-term graft outcome. In this study, we examined whether the biomarkers including neutrophil gelatinase-associated lipocalin (NGAL) and liver-type fatty acid-binding protein (L-FABP) can predict 1-year graft outcome as well as short-term graft function especially in patients with early graft function (EGF). This was a single-center, prospective observational study. Urine samples at 0 hours and 2 and 6 days were obtained and the level of NGAL and L-FABP were measured. Of the 69 KT recipients enrolled, seven developed DGF, and the remaining 62 patients were finally enrolled as EGF recipients. EGF recipients were additionally divided into immediate graft function (IGF, n = 48) and slow graft function (SGF, n = 14) groups. Urinary NGAL (u-NGAL) level on day 2, but not L-FABP nor serum creatinine, was significantly higher in SGF compared to IGF group. Higher day 2 u-NGAL level was associated with more frequent development of SGF and, in addition, with significantly lower 1-year estimated glomerular filtration rate (eGFR). In multivariate logistic regression analysis, day 2 u-NGAL was a significant, independent factor for predicting poor long-term graft function (1-year eGFR < 60 mL/min/1.73 m(2)).\n\nQuestion:\nDoes urine neutrophil gelatinase-associated lipocalin predict graft outcome up to 1 year after kidney transplantation?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo assess dynamic cerebral autoregulation (CA) in patients with acute ischaemic stroke of undetermined aetiology, within 72h of stroke onset. In 6 patients with ischaemic stroke of undetermined aetiology (aged 66±9 years, National Institutes of Health Stroke Scale [NIHSS] score on admission: 4.0, range: 4-11), selected based on screening of 118 consecutive ischaemic stroke patients and in 14 volunteers (aged 62±10 years), we continuously monitored RR intervals (RRI), mean arterial pressure (MAP) by means of photoplethysmography, mean cerebral blood flow velocity (CBFV) using transcranial Doppler ultrasonography, end-tidal CO2 (ETCO2) and respiration during 2-min deep breathing paced at 6min(-1) (0.1Hz). To assess CA, we evaluated the impact of breathing-induced MAP oscillations on fluctuations of CBFV in the hemispheres with stroke, the non-involved hemispheres and randomly selected hemispheres of controls by applying cross-spectral analysis and calculating coherence, transfer function gain (CBFV-MAP gain) and phase shift angle between the two oscillating signals. Phase shift angle between MAP and CBFV oscillations showed values >0 and was significantly reduced in the hemispheres without stroke as compared to controls (0.39±0.95 vs. -1.59±0.33rad, p=0.015), whereas in the hemispheres with stroke, phase shift angle did not differ significantly from that observed in the control hemispheres. Clinical status of stroke patients significantly improved at discharge from the hospital (NIHSS: 2.0, range: 1-8, p=0.028).\n\nQuestion:\nIs dynamic cerebral autoregulation compromised in ischaemic stroke of undetermined aetiology only in the non-affected hemisphere?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nLoratadine, a novel histamine H1-receptor antagonist, is effective in the treatment of patients with seasonal and perennial rhinitis and some allergic skin disorders. Histamine and other chemical mediators are synthesized and immunologically released by human peripheral blood basophils and tissue mast cells (Fc epsilon RI+ cells). To evaluate the effects of loratadine and its main metabolite, desethoxylcarbonyl-loratadine (des-loratadine), on the immunological release of preformed (histamine and tryptase) and de novo synthesized mediators (leukotriene C4: LTC4 and prostaglandin D2:PGD2) from human Fc epsilon RI+ cells. Human Fc epsilon RI+ cells purified from peripheral blood and from skin (HSMC) and lung tissue (HLMC) were preincubated with loratadine and des-loratadine before immunological challenge with Der p 1 antigen or anti-Fc epsilon RI. The release of preformed mediators (histamine and tryptase) and de novo synthesized eicosanoids was evaluated in the supernatants of human Fc epsilon RI+ cells. Preincubation (15 min, 37 degrees C) of purified (36-74%) basophils with loratadine (3 x 10(-6)-10(-4)M) and des-loratadine before Der p 1 antigen or anti-Fc epsilon RI challenge concentration-dependently (5-40%) inhibited the release of histamine and LTC4. Loratadine (3 x 10(-6)-10(-4)M) and des-loratadine also inhibited (10-40%) histamine, LTC4, and PGD2 release from purified HLMC (16-68%) activated by anti-Fc epsilon RI. Loratadine (3 x 10(-6)-10(-4)M) and des-loratadine caused concentration-dependent inhibition (10-40%) of histamine, tryptase, LTC4, and PGD2 release from purified HSMC (24-72%) immunologically challenged with anti-Fc epsilon RI.\n\nQuestion:\nDo loratadine and desethoxylcarbonyl-loratadine inhibit the immunological release of mediators from human Fc epsilon RI+ cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe Living Well With Stroke study has demonstrated effectiveness of a brief psychosocial treatment in reducing depressive symptoms after stroke. The purpose of this analysis was to determine whether key variables associated with prevalence of poststroke depression also predicted treatment response. Response to a brief psychosocial/behavioral intervention for poststroke depression was measured with the Hamilton Rating Scale for Depression. Analysis of covariance models tested for interaction of potential predictor variables with treatment group on percent change in Hamilton Rating Scale for Depression from pre- to post-treatment as an outcome. Initial depression severity, hemispheric location, level of social support, age, gender, and antidepressant adherence did not interact with the treatment with respect to percent change in Hamilton Rating Scale for Depression when considered 1 at a time. Participants who carried 1 or 2 s-alleles at the 5-HTTLPR serotonin transporterpolymorphism or 1 or 2 9- or 12-repeats of the STin2 VNTR polymorphism had significantly better response to psychosocial treatment than those with no s-alleles or no 9- or 12-repeats.\n\nQuestion:\nIs response to psychosocial treatment in poststroke depression associated with serotonin transporter polymorphisms?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis study investigates the effects of statin treatment on experimental intracerebral hemorrhage (ICH) using behavioral, histological, and MRI measures of recovery. Primary ICH was induced in rats. Simvastatin (2 mg/kg), atorvastatin (2 mg/kg), or phosphate-buffered saline (n=6 per group) was given daily for 1 week. MRI studies were performed 2 to 3 days before ICH, and at 1 to 2 hours and 1, 2, 7, 14, and 28 days after ICH. The ICH evolution was assessed via hematoma volume measurements using susceptibility-weighted imaging (SWI) and tissue loss using T2 maps and hematoxylin and eosin (H&E) histology. Neurobehavioral tests were done before ICH and at various time points post-ICH. Additional histological measures were performed with doublecortin neuronal nuclei and bromodeoxyuridine stainings. Initial ICH volumes determined by SWI were similar across all groups. Simvastatin significantly reduced hematoma volume at 4 weeks (P=0.002 versus control with acute volumes as baseline), whereas that for atorvastatin was marginal (P=0.09). MRI estimates of tissue loss (% of contralateral hemisphere) for treated rats were significantly lower (P=0.0003 and 0.001, respectively) than for control at 4 weeks. Similar results were obtained for H&E histology (P=0.0003 and 0.02, respectively). Tissue loss estimates between MRI and histology were well correlated (R2=0.764, P<0.0001). Significant improvement in neurological function was seen 2 to 4 weeks post-ICH with increased neurogenesis observed.\n\nQuestion:\nDo simvastatin and atorvastatin improve neurological outcome after experimental intracerebral hemorrhage?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCombination of polyamine and prostaglandin E2 (PGE2)-synthesis inhibitors reduced the risk of colorectal adenoma (CRA) by 70% in patients who received polypectomies. We studied effects of the combination of difluoromethylornithine (DFMO) and sulindac on biomarkers and investigated factors that modify their efficacy. We analyzed rectal mucosal levels of polyamines (spermidine, spermine, and putrescine) and PGE2, treatment regimens, and risk of CRA in 267 participants of a phase IIb/III chemoprevention trial of DFMO/sulindac. In the group that received DFMO/sulindac, spermidine-to-spermine ratio (Spd:Spm) in rectal mucosa decreased between baseline and 12- and 36-month follow-up examinations (0.30, 0.23, and 0.24, respectively; P < .001 for both comparisons to baseline). Putrescine levels decreased between baseline and 12 months (0.46 vs 0.15 nmol/mg protein; P < .001) but rebounded between 12 and 36 months (0.15 vs 0.36 nmol/mg protein; P = .001). PGE2 levels did not change, although aspirin use was significantly associated with lower baseline levels of PGE2. No significant associations were observed between changes in biomarker levels and efficacy. However, drug efficacy was greatest in subjects with low Spd:Spm and high PGE2 at baseline; none of these subjects, versus 39% of those given placebo, developed CRA (P < .001). Efficacy was lowest in subjects with high Spd:Spm and low PGE2 at baseline; 28% developed CRA, compared with 36% of patients given placebo (P = .563).\n\nQuestion:\nDo levels of rectal mucosal polyamines and prostaglandin E2 predict ability of DFMO and sulindac to prevent colorectal adenoma?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nModulation of endogenous epoxide levels by soluble epoxide hydrolase (sEH) in the endothelium represents an important mechanism in the regulation of cardiovascular function. We examined the relationship between a common, functional polymorphism of the human sEH gene and coronary artery calcification (CAC) in young, largely asymptomatic African-American and non-Hispanic white subjects. Multiple logistic regression and Tobit regression models were used to assess the relationship between the sEH Arg287Gln polymorphism and presence and quantity of CAC. Models adjusting for race (except in race-specific analyses), age, sex, smoking, body mass index, systolic blood pressure, LDL cholesterol, and HDL cholesterol were estimated. Allele and genotype frequency distributions were not significantly different between the 2 ethnic groups (P=0.22; P=0.17, respectively). The Arg287Gln polymorphism of the sEH gene was a significant predictor of CAC status in African-American participants, either alone or after adjusting for other risk factors. African-American subjects with at least 1 copy of the Gln287 allele had a 2-fold greater risk of having CAC compared with those not carrying this allele (95% CI, 1.1 to 2.9; P=0.02). There was no relationship between Arg287Gln polymorphism and the probability of having CAC in white participants (OR, 0.8; 95% CI, 0.5 to 1.3; P=0.49). Inferences from multivariable Tobit regression were similar to those obtained in the logistic regression models, indicating that the Arg287Gln polymorphism was a significant independent predictor of both presence and quantity of CAC in African-American but not white subjects.\n\nQuestion:\nIs polymorphism of the soluble epoxide hydrolase associated with coronary artery calcification in African-American subjects : The Coronary Artery Risk Development in Young Adults ( CARDIA ) study?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPsychopathy is a personality disorder associated with impairments in decision-making, empathy, and impulsivity. Recent brain imaging studies suggest that psychopathy is associated with abnormalities in limbic/paralimbic brain regions. To date, no studies have examined functional brain connectivity measures using independent component analyses (ICA) in adults with psychopathy. Here, we test hypotheses regarding paralimbic connectivity in adult incarcerated individuals stratified by psychopathy scores. One hundred and two prison inmates were rated using the Hare Psychopathy Checklist-Revised (PCL-R). FMRI data were collected while subjects performed an auditory target detection \"oddball\" task. FMRI data were analyzed using group ICA to identify functional networks responding to the oddball task correlating with psychopathy scores. Components demonstrating significant correlations with psychopathy included a default mode network, a frontoparietal component, and a visual/posterior cingulate component. Modulation trends correlated strongly with factor 2 (impulsivity) and total PCL-R scores in the frontoparietal and visual/posterior cingulate networks, and with factor 1 (affective) scores within the default mode network. The posterior cingulate region factored significantly in the modulation trends observed.\n\nQuestion:\nAre intrinsic limbic and paralimbic networks associated with criminal psychopathy?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo investigate the cell cycle regulator role of the third gaseous transmitter hydrogen sulfide (H2 S) in three oral SCC cell lines by using NaHS, a donor of H2 S. The synchronized oral squamous cell carcinoma cell lines (Cal27, GNM, and WSU-HN6) were treated with different concentrations of NaHS and then subjected to cell proliferation, cell cycle, and Western blot analyses. The CCK-8 assay results showed that the exogenously administered H2 S donor, NaHS, induced CAL-27, and GNM cell proliferation in a concentration-dependent manner, and the cell cycle analysis indicated that NaHS accelerated cell cycle progression of the synchronized CAL-27, GNM, and WSU-HN6 cells. Western blot analysis revealed that the cell cycle regulatory genes RPA70 and RB1 were significantly down-regulated and that proliferating cell nuclear antigen (PCNA) and CDK4 were markedly up-regulated by NaHS at specific time points in the cell cycle. In addition, our results indicated that the phosphorylation of Akt and Erk1/2 was involved in exogenous H2 S-induced oral SCC cell proliferation.\n\nQuestion:\nDoes hydrogen sulfide accelerate cell cycle progression in oral squamous cell carcinoma cell lines?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPreclinical data suggest that overexpression of Her2/neu confers cellular radioresistance. We retrospectively studied whether Her2/neu-positive disease was associated with locoregional recurrence (LRR) after postmastectomy radiotherapy (RT) for breast cancer. Data from 337 patients treated in four institutional prospective clinical trials neoadjuvant doxorubicin-based chemotherapy, mastectomy, and RT were reviewed. The trials were conducted between 1989 and 2000. Of the 337 patients, 108 (32%) had tumors that were tested for Her2/neu, with positivity defined by 3+ immunohistochemistry staining or gene amplification detected by fluorescence in situ hybridization. RT was delivered to the chest wall and draining lymphatics (median dose, 50 Gy) followed by a chest wall boost (median dose, 10 Gy). Thirty-two patients had Her2/neu-positive disease and 76 patients had Her2/neu-negative disease. The Her2/neu-positive tumors were associated with a greater rate of estrogen receptor-negative disease (p = 0.03), the presence of supraclavicular disease at diagnosis (p = 0.027), and a greater number of positive lymph nodes after chemotherapy (p = 0.026). Despite these adverse features, the actuarial overall LRR rate was roughly equivalent for the patients with Her2/neu-positive tumors vs. those with Her2/neu-negative tumors (5-year rate 17.5% vs. 13.9%, respectively; 10-year rate 17.5% vs. 18.9%, respectively; p = 0.757). On Cox regression analysis of LRR adjusted for N stage and estrogen receptor status, the hazard ratio for Her2/neu positivity was 0.89 (95% confidence interval, 0.31-2.59; p = 0.83).\n\nQuestion:\nDoes her2/neu-positive disease increase risk of locoregional recurrence for patients treated with neoadjuvant doxorubicin-based chemotherapy , mastectomy , and radiotherapy?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPatients with borderline personality disorder (BPD) frequently report unresolved life events but it is still poorly understood, how these experiences are represented in the brain. Using functional magnetic resonance imaging (fMRI), the present study aimed at investigating the neural correlates of the recall of unresolved life events in patients with BPD and healthy controls. Twenty female BPD patients and 21 healthy control subjects underwent fMRI. During measurement subjects recalled unresolved and resolved negative life events. Individual cue words were used to stimulate autobiographical memory. After scanning, subjects rated their emotional states during the recall of both types of memories. When contrasting unresolved and resolved life events, patients showed significant bilateral activation of frontotemporal areas including the insula, amygdala, and the anterior cingulate cortex, the left posterior cingulate cortex, right occipital cortex, the bilateral cerebellum and the midbrain. In healthy subjects, no differential brain activation was related to these conditions. The 2 x 2 factorial analysis (DeltaBPD - Deltacontrols) revealed similar results with bilateral activation of the frontal cortex including parts of the insula and of the orbitofrontal cortex, temporal activation including the amygdala, activation of the right occipital cortex, and parts of the cerebellum. Patients but not controls reported higher levels of anxiety and helplessness during the unresolved versus resolved memory condition.\n\nQuestion:\nDoes functional MRI correlate of the recall of unresolved life events in borderline personality disorder?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo assess the accuracy of antenatal ultrasound in the diagnosis of craniofacial malformations and to compare two-dimensional with three-dimensional ultrasound. This was a retrospective study in which the archives of our ultrasound laboratory were searched for cases with an ultrasound diagnosis of craniofacial malformation in the period 1986-2001. No attempt was made to look for false-negative diagnoses. Sixty cases with an antenatal diagnosis of a craniofacial malformation were found: 37 with cleft lip/palate; 17 with heterogeneous dysmorphisms (including mostly micrognathia and craniosynostosis) and 6 with miscellaneous craniofacial malformations. Associated anomalies were present in 48/60 (80%) cases, and holoprosencephaly (25 cases) was the most frequent of these. In 43 (72%) cases the diagnosis was made before 24 weeks' gestation. Postnatal follow-up was available for 43 cases and there was always complete correlation between antenatal and postnatal diagnoses. Cleft lip/palate was always accurately differentiated from cleft lip. Three-dimensional ultrasound was performed in 12 cases and was successful in 11. However, it did not provide further diagnostic information with regard to the two-dimensional scan.\n\nQuestion:\nIs two-dimensional ultrasound accurate in the diagnosis of fetal craniofacial malformation?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCoronary artery angioplasty triggers healing that causes constrictive remodeling. Because collagen accumulation correlates with constrictive remodeling and aldosterone has been implicated in collagen accumulation, we examined how aldosterone and the mineralocorticoid receptor antagonists spironolactone and eplerenone affect remodeling and collagen in porcine coronary and iliac arteries after angioplasty. Twenty-four pigs were allocated into 4 treatment groups: oral eplerenone (100 mg/d), oral spironolactone (200 mg/d), subcutaneous aldosterone (400 microgram/d), or no treatment. Twenty-eight days after angioplasty of the coronary arteries, eplerenone increased total vessel area by 30% (P<0.05) and luminal area by nearly 60% (P<0.05) compared with the no-treatment group, without affecting neointima size. These effects were accompanied by a 65% reduction in neointimal and medial collagen density (both P<0.05). Spironolactone was less effective, and aldosterone tended to exert opposite effects on coronary artery structure after angioplasty. These effects were not observed in angioplastied iliac arteries.\n\nQuestion:\nDoes eplerenone suppress constrictive remodeling and collagen accumulation after angioplasty in porcine coronary arteries?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAlthough blood pressure reduction has been postulated to result in a fall in cerebral perfusion pressure in patients with intracerebral hemorrhage, the latter is rarely measured. We assessed regional cerebral perfusion pressure in patients with intracerebral hemorrhage by using CT perfusion source data. Patients with acute primary intracerebral hemorrhage were randomized to target systolic blood pressures of <150 mm Hg (n = 37) or <180 mm Hg (n = 36). Regional maps of cerebral blood flow, cerebral perfusion pressure, and cerebrovascular resistance were generated by using CT perfusion source data, obtained 2 hours after randomization. Perihematoma cerebral blood flow (38.7 ± 11.9 mL/100 g/min) was reduced relative to contralateral regions (44.1 ± 11.1 mL/100 g/min, P = .001), but cerebral perfusion pressure was not (14.4 ± 4.6 minutes(-1) versus 14.3 ± 4.8 minutes(-1), P = .93). Perihematoma cerebrovascular resistance (0.34 ± 0.11 g/mL) was higher than that in the contralateral region (0.30 ± 0.10 g/mL, P < .001). Ipsilateral and contralateral cerebral perfusion pressure in the external (15.0 ± 4.6 versus 15.6 ± 5.3 minutes(-1), P = .15) and internal (15.0 ± 4.8 versus 15.0 ± 4.8 minutes(-1), P = .90) borderzone regions were all similar. Borderzone cerebral perfusion pressure was similar to mean global cerebral perfusion pressure (14.7 ± 4.7 minutes(-1), P ≥ .29). Perihematoma cerebral perfusion pressure did not differ between blood pressure treatment groups (13.9 ± 5.5 minutes(-1) versus 14.8 ± 3.4 minutes(-1), P = .38) or vary with mean arterial pressure (r = -0.08, [-0.10, 0.05]).\n\nQuestion:\nIs cerebral Perfusion Pressure Maintained in Acute Intracerebral Hemorrhage : A CT Perfusion Study?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nNonsecretor status of blood type antigen has been associated with higher risk of urinary tract infection (UTI) in women. However its implication in the modern management for pediatric UTI remains unclear. We evaluate the impact of secretor status on clinical course in children with primary vesicoureteral reflux (VUR). From 1998 to 2002, 382 cases of primary VUR presented to our institute and were treated either surgically or nonoperatively in accordance with the American Urological Association guideline. Of these potential candidates 128 patients and their guardians volunteered to be entered into the study. Antiseptic swabs to collect saliva were sent to them. The secretor status was determined using the hemagglutination inhibition assay from the eluted saliva on the swabs and medical records of responders were evaluated retrospectively. Secretor status was not associated with gender, VUR grade, presentation, history of breakthrough UTI, laterality of VUR and conservative vs surgical treatment. However, nonsecretor status weakly correlated with decreased split renal function and significantly correlated with the presence of focal renal scarring (40.9% vs 21.7% for children with and without scarring, respectively) as determined by technetium dimercapto-succinic acid renal scan.\n\nQuestion:\nIs renal scarring associated with nonsecretion of blood type antigen in children with primary vesicoureteral reflux?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAutophagy has been shown to be crucial in the regulation of the intracellular lipid stores in hepatocytes. We hypothesize that immunity-related GTPase family M (IRGM) gene (an autophagy-related gene) variants confer the susceptibility to non-alcoholic fatty liver disease (NAFLD) development. 832 obese children and adolescents aged 6-18years were recruited. NAFLD was determined by liver ultrasonography. We genotyped PNPLA3 rs738409, GCKR rs780094, TM6SF2 rs58542926, six IRGM single nucleotide polymorphisms (rs13361189, rs9637876, rs72553867, rs10065172, rs1000113, and rs11747270). To understand the molecular mechanism, we examined the effects of IRGM knockdown and overexpression on autophagic flux and lipid droplet metabolism in human hepatoma cells. 22.8% of recruited obese children and adolescents had NAFLD. Multiple logistic regression analysis revealed that after controlling for the effects of age- and gender-adjusted body mass index, gender, PNPLA3, GCKR, and TM6SF2 polymorphisms, variant IRGM rs10065172 TT genotype independently increased the odds ratio of NAFLD by 2.04 (95% confidence interval 1.22-3.42; p=0.007), as compared to the CC genotype. The predictive model was validated by means of 10-fold cross validation. Functional assay revealed that IRGM knockdown inhibited autophagic flux and increased lipid droplet content in HepG2 and PLC/PRF/5 cells, which were reversed by the autophagy inducer rapamycin administration. Similarly, wortmannin (an autophagy inhibitor) increased intracellular lipid droplet content. In contrast, overexpression of IRGM caused decreased lipid droplet content in HepG2 cells.\n\nQuestion:\nDo variants in the autophagy-related gene IRGM confer susceptibility to non-alcoholic fatty liver disease by modulating lipophagy?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIn order to predict long-term prognosis and define individual treatment modalities for patients with oral squamous cell carcinoma (OSCC), more reliable tumor biomarkers are needed during the pretreatment workup period. The present study aimed to identify more reliable immunohistochemical tumor prognostic markers in the pretreatment biopsy specimens of patients with OSCC. We selected 57 patients who were diagnosed with primary OSCC through histopathological analysis. Pretreatment biopsy specimens were immunohistochemically analyzed for the transcription factor NANOG, cancer stem cell marker CD44, and mutant tumor protein 53 (mutant p53). The immunostaining patterns were assessed for their association with the clinicopathological features of OSCC and overall survival rates. Late tumor stage, positive neck node metastasis, and high-grade differentiation were associated with significantly poorer survival rates. Enhanced expression of NANOG and mutant p53 positivity were significantly associated with clinically late-stage tumors, positive neck node metastasis, histologically high-grade tumors, and poor overall survival rates. OSCCs with strong co-detection of NANOG and mutant p53 were linked to significantly lower survival rates than those with both weak NANOG expression and p53 negativity. Increased expression of CD44 had a limited correlation with unfavorable clinicopathological features.\n\nQuestion:\nIs positive expression of NANOG , mutant p53 , and CD44 directly associated with clinicopathological features and poor prognosis of oral squamous cell carcinoma?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMalignant melanoma is an exceptionally aggressive, drug-resistant and heterogeneous cancer. Recently it has been shown that melanoma cells with high clonogenic and tumourigenic abilities are common, but markers distinguishing such cells from cells lacking these abilities have not been identified. There is therefore no definite evidence that an exclusive cell subpopulation, i.e. cancer stem cells (CSC), exists in malignant melanoma. Rather, it is suggested that multiple cell populations are implicated in initiation and progression of the disease, making it of importance to identify subpopulations with elevated aggressive properties. In several other cancer forms, Aldehyde Dehydrogenase (ALDH), which plays a role in stem cell biology and resistance, is a valuable functional marker for identification of cells that show enhanced aggressiveness and drug-resistance. Furthermore, the presence of ALDH(+) cells is linked to poor clinical prognosis in these cancers. By analyzing cell cultures, xenografts and patient biopsies, we showed that aggressive melanoma harboured a large, distinguishable ALDH(+) subpopulation. In vivo, ALDH(+) cells gave rise to ALDH(-) cells, while the opposite conversion was rare, indicating a higher abilities of ALDH(+) cells to reestablish tumour heterogeneity with respect to the ALDH phenotype. However, both ALDH(+) and ALDH(-) cells demonstrated similarly high abilities for clone formation in vitro and tumour initiation in vivo. Furthermore, both subpopulations showed similar sensitivity to the anti-melanoma drugs, dacarbazine and lexatumumab.\n\nQuestion:\nDoes aldehyde dehydrogenase ( ALDH ) activity select for cells with enhanced aggressive properties in malignant melanoma?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAlthough invasive management of ST segment elevation myocardial infarction has improved the clinical outcome, cardiogenic shock (CS) remains an important issue. Our purpose was to asses the utility of the initial electrocardiogram in detecting patients who are at increased risk of CS after percutaneous coronary intervention for acute myocardial infarction. We evaluated 508 consecutive patients admitted in our Coronary Unit and treated by primary angioplasty within 12 h of an ST segment elevation myocardial infarction. Patients with cardiogenic shock at admission were excluded. Two groups were defined according to the presence of distortion of the terminal portion of the QRS in two or more adjacent leads (group 1) or the absence of this pattern (group 2). There were 99 patients (20%) in group 1 and 409 (80%) in group 2. CS developed in 38 patients, 18 in group 1 (18%) and 20 in group 2 (5%), p<0.001. Seventeen patients died in hospital, 6 in group 1 (6%) and 11 in group 2 (3%), p 0.094. Multivariate analysis including clinical, electrocardiographic and angiographic variables showed distortion of the QRS as an independent predictor of cardiogenic shock (odds ratio 3.17, 95% confidence interval 1.44 to 6.96, p 0.004), together with Killip class at admission and TIMI 3 flow after revascularization.\n\nQuestion:\nIs distortion of the terminal portion of the QRS predictor of shock after primary percutaneous coronary intervention for acute myocardial infarction?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCardiac hypertrophy is a common response to pressure overload and is associated with increased mortality. Mechanical stress in the heart results in the activation of the small GTPase ras and the Raf-1/MEK/ERK signaling cascade in addition to other signaling pathways. In an attempt to determine the requirement for the serine/threonine kinase Raf-1 in the pathogenesis of cardiac hypertrophy, we generated transgenic mice with cardiac-specific expression of a dominant negative form of Raf-1 (DN-Raf). DN-Raf mice appeared normal at birth, were fertile, and had normal cardiac structure and function in the absence of provocative stimulation. In response to pressure overload, cardiac extracellular signal-regulated kinase (ERK) activation was inhibited, but c-Jun N-terminal kinase (JNK) activation and p38 mitogen-activated protein kinase (MAPK) activation were normal. DN-Raf mice were sensitized to pressure overload and the development of cardiomyocyte apoptosis, and >35% of animals died within 7 days of aortic banding. Surviving DN-Raf animals were markedly resistant to the development of cardiac hypertrophy and hypertrophic gene induction in response to transverse aortic constriction.\n\nQuestion:\nIs raf-1 kinase required for cardiac hypertrophy and cardiomyocyte survival in response to pressure overload?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIn bone remodeling, the expression and turnover of the proteoglycans versican and aggrecan are poorly understood. We report changes in adult mouse bone contents of versican and aggrecan associated with both age and treatment with the drug zoledronate. The data may have implications for experimental animal models of osteoporosis and related conditions. Versican and aggrecan are large, aggregating proteoglycans involved in skeletal development, but little is known about their roles in bone remodeling. The purpose of this study was to investigate versican and aggrecan contents in adult mouse bones, and changes in their contents in response to the bisphosphonate zoledronate (ZOL). Mice (9 weeks old) were treated with 125 μg/kg ZOL or vehicle for 3 or 15 weeks. Versican and aggrecan were isolated from tibial bones for Western blotting, automated integrated densitometry, and analysis (two-way ANOVA, α = 0.05). In ZOL-treated mouse bones, compared to vehicle, 340 and 60 kDa versican content decreased significantly, and 100 and 60 kDa aggrecan content decreased significantly (drug effect). In 24-week-old mouse bones, compared to 12 weeks, statistically significant decreases were observed in 340, 80, 60, and 11 kDa versican, and in 100, 70, and 40 kDa aggrecan (age effect). There was a statistically significant ZOL-age interaction for 330 kDa aggrecan.\n\nQuestion:\nDoes tibial bone versican content decrease with zoledronate treatment in adult mice?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCigarette smoking is associated with an increased risk to develop myocardial infarction and ischemic stroke. However, the mechanisms responsible for these effects are still poorly understood. To investigate whether nicotine, the major component of cigarette smoking, and its main metabolite, cotinine, might induce a pro-thrombotic state via stimulation of tissue factor (TF) expression in two cell population widely represented in the arterial wall such as endothelial cells (ECs), and smooth muscle cells (SMCs). Incubation of ECs and SMCs with nicotine and cotinine induced TF expression in both cell types in a dose-dependent fashion, exerting its effect at the transcriptional level, as demonstrated by semiquantitative and by real-time PCR. Nicotine- and cotinine-induced TF expression was mediated by the activation of the transcription factor, nuclear factor-kappa B (NF-kappaB), as demonstrated by electrophoretic mobility shift assay and by the suppression of TF expression by the NF-kappaB inhibitor, pyrrolidine dithio carbamate ammonium.\n\nQuestion:\nDoes nicotine induce tissue factor expression in cultured endothelial and smooth muscle cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCerebral hemodynamic derangement is well known in patients with fulminant hepatic failure. The advent of transcranial Doppler sonography (TCD) enabled noninvasive observation of cerebral hemodynamics. To evaluate its clinical usefulness, we examined longitudinal cerebral hemodynamic parameters in patients with fulminant hepatic failure and severe acute hepatitis. The six subjects were four patients with fulminant hepatic failure, one with severe acute hepatitis and one with severe acute exacerbation on chronic hepatitis. The pulsatility indices of the right middle cerebral artery were used as parameters of cerebral hemodynamics. The pulsatility indices of the two patients with a deteriorating course had elevated to >1.00, whereas those of the two patients undergoing recovery were within normal limits, as well as of the patients with acute hepatitis or acute exacerbation on chronic hepatitis.\n\nQuestion:\nDoes cerebral pulsatility index by transcranial Doppler sonography predict the prognosis of patients with fulminant hepatic failure?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo assess relative expression levels of mRNA for EP3 isoforms EP3-2, EP3-3, and EP3-6 in human myometrium in various physiologic states. Using semiquantitative reverse transcriptase-polymerase chain reaction, we analyzed myometrial samples from 46 women (ten menopausal, ten nongravid premenopausal, 19 gravidas, seven premenopausal misoprostol-treated nongravid women) for the specific expression of mRNA messages for the EP3 receptor isoforms EP3-2, EP3-3, and EP3-6. We found that the expression of EP3-2 was significantly lower in gravid than nongravid myometrium (P < .0001). Levels of the EP3-6 message were higher in gravid samples than in nongravid specimens (P < .02). EP3-3 mRNA was present in higher levels in menopausal samples compared with the other groups.\n\nQuestion:\nIs eP3-2 receptor mRNA expression reduced and EP3-6 receptor mRNA expression is increased in gravid human myometrium?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTiming of assessment of psychological construct is controversial and results differ based on the model of pain induction. Previous studies have not used an exercise-induced injury model to investigate timing of psychological assessment. Exercise-induced injury models may be appropriate for these investigations because they approximate clinical pain conditions better than other experimental stimuli. In this study we examined the changes of psychological constructs over time and determined whether timing of assessment affected the construct's association with reports of pain intensity and disability. One-hundred twenty-six healthy volunteers completed the Fear of Pain Questionnaire (FPQ-III), Pain Catastrophizing Scale (PCS), and Tampa Scale of Kinesiophobia (TSK) prior to inducing muscle injury to the shoulder. The PCS and TSK were measured again 48 and 96 hours postinjury induction. Pain intensity and disability were collected at 48 and 96 hours and served as dependent variables in separate regression models. Results indicated that the FPQ-III had the strongest prediction of pain intensity from baseline to 96 hours. After baseline the PCS and TSK were stronger predictors of pain intensity and disability, respectively. These data provide support for the use of psychological constructs in predicting outcomes from shoulder pain. However, they deviate from the current theoretical model indicating that fear of pain is a consequence of injury and instead suggests that fear of pain before injury may influence reports of pain intensity.\n\nQuestion:\nDo pain-related fear and catastrophizing predict pain intensity and disability independently using an induced muscle injury model?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMany patients with acute stroke are excluded from receiving thrombolysis agents within the necessary time limit (3 or 6 hours from stroke onset) because they or their family members are unable provide the time of stroke onset. Brain tissue sodium concentration ([Na(+)]) increases gradually and incessantly during the initial hours of experimental focal cerebral ischemia but only in severely damaged brain regions. We propose that this steady increase in [Na(+)] can be used to estimate the time after arterial occlusion in the rat middle cerebral artery occlusion model of ischemic stroke. Sixteen anesthetized Sprague-Dawley rats underwent permanent middle cerebral artery occlusion combined with bilateral common artery occlusion. After 100 to 450 minutes, diffusion-weighted MRI was used to generate apparent diffusion coefficient (ADC) maps, cerebral blood flow (CBF) was determined with (14)C-iodoantipyrine (in a subset of 7 animals), and the brain was frozen. Autoradiographic CBF sections and punch samples for Na(+) analysis were obtained from the brain at the same level of the MR image. Severely at risk regions were identified with an ADC of <520 microm(2)/s and, in the subset, with both ADC of <520 microm(2)/s and CBF of <40 mL. 100 g(-1). min(-1). Both CBF and the ADC dropped quickly and remained stable in the initial hours after ischemic onset. Linear regression revealed strong linearity between [Na(+)] and time after onset, with a slope of 0.95 or 1.00 (mEq/kg DW)/min, with both ADC and ADC-plus-CBF criteria, respectively. The 95% CIs at 180 and 360 minutes were between 41 and 52 minutes.\n\nQuestion:\nIs brain tissue sodium a ticking clock telling time after arterial occlusion in rat focal cerebral ischemia?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nDiabetic nephropathy (DN) is a serious complication that commonly confronted by diabetic patients. A common theory for the pathogenesis of this renal dysfunction in diabetes is cell injury, inflammation as well as oxidative stress. In this content, the detailed molecular mechanism underlying high glucose induced renal tubular epithelial injury was elaborated. An in vivo rat model of diabetes by injecting streptozotocin (STZ) and an in vitro high glucose incubated renal tubular epithelial cell (HK-2) model were used. Expression levels of Keap1, nuclear Nrf2 and p65 were determined by western blotting. Level of microR-29 (miR-29) was assessed using quantitative RT-PCR. Combination of p65 and miR-29 promotor was assessed using chromatin immunoprecipitation. Keap1 3'-UTR activity was detected using luciferase reporter gene assay. Cell viability was determined using MTT assay. In diabetic rat, miR-29 was downregulated and its expression is negatively correlated with both of serum creatinine and creatinine clearance. In high glucose incubated HK-2 cell, deacetylases activity of Sirt1 was attenuated that leads to decreased activity of nuclear factor kappa B (NF-κB). NF-κB was demonstrated to regulate miR-29 expression by directly binding to its promotor. The data of luciferase assay showed that miR-29 directly targets to Keap1 mRNA. While high glucose induced down regulation of miR-29 contributed to enhancement of Keap1 expression that finally reduced Nrf2 content by ubiquitinating Nrf2. Additionally, overexpression of miR-29 effectively relieved high glucose-reduced cell viability.\n\nQuestion:\nDoes high glucose induce renal tubular epithelial injury via Sirt1/NF-kappaB/microR-29/Keap1 signal pathway?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe aim of the study was to evaluate the association between sedentary lifestyle and the severity of menopausal symptoms and obesity in middle-aged women. The Menopause Rating Scale, the Goldberg Anxiety and Depression Scale, and the Athens Insomnia Scale were administered to 6,079 Latin American women aged 40 to 59 years. Sedentary lifestyle was defined as fewer than three weekly, 30-minute periods of physical activity. Sedentary women had more severe menopausal symptoms (total Menopause Rating Scale score: 9.57 ± 6.71 vs 8.01 ± 6.27 points, P < 0.0001) and more depressive symptoms (Goldberg), anxiety (Goldberg), and insomnia (Athens Scale) compared with non-sedentary women. They also had greater mean waist circumference (86.2 ± 12.3 vs 84.3 ± 1.8 cm, P < 0.0001) and a higher prevalence of obesity (20.9% vs 14.3%, P < 0.0001). Logistic regression analysis showed that both obesity (odds ratio [OR] 1.52; 95% CI, 1.32-1.76) and severe menopausal symptoms (OR 1.28; 95% CI, 1.06-1.53), including insomnia and depressive mood, were positively associated with a sedentary lifestyle. Having a stable partner (OR 0.85; 95% CI, 0.76-0.96), using hormone therapy (OR 0.75; 95% CI, 0.64-0.87) and having a higher educational level (OR 0.66; 95% CI, 0.60-0.74) were negatively related to sedentary lifestyle.\n\nQuestion:\nIs sedentary lifestyle in middle-aged women associated with severe menopausal symptoms and obesity?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo investigate the association of a calcium-sensing receptor (CaSR) gene missense polymorphism, 986Ala/Ser (A986S), with bone mineral density (BMD) and bone size in healthy Chinese premenopausal women. A total of 285 healthy Chinese premenopausal women (20.0 to 41.9 years of age) of Han nationality in the urban area of Shanghai were recruited for this study. The BMD and bone size of the spine and hip were measured by dual-energy X-ray absorptiometry. All the subjects were genotyped at the CaSR A986S site in exon 7 with polymerase chain reaction followed by restriction enzyme BsaHI digestion. The presence of the restriction fragment site was represented by alanine (A), while its absence by serine (S), rendering the genotypes AA, AS, and SS. The genotype AS was rare and SS absent in these Chinese women, and no significant differences in the BMD or bone size of either the spine or hip were found between the two genotypes.\n\nQuestion:\nIs [ A986S polymorphism of calcium-sensing receptor gene related to bone mineral density or bone size in premenopausal Chinese women ]?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMany patients with focal cortical dysplasia (FCD) continue to have seizures after surgical treatment. The usual explanation for the poor surgical outcome is the presence of residual dysplastic tissue missed by the preoperative neuroimaging investigation and therefore not resected during surgery. We apply a voxel-based morphometry (VBM) analysis to the magnetic resonance imaging (MRI) scans from patients with epilepsy and visually detected FCD to investigate whether (a) VBM is able to detect gray-matter concentration (GMC) abnormalities in patients with FCD, and (b) whether the extent of GMC abnormalities in the brain of these patients differs from the regions observed by using visual inspection. We studied 11 patients with visually detected FCD (eight of them with histologic confirmation of FCD). The GMC from each one of these patients was compared with the mean GMC from a control group of 96 normal healthy subjects by using an optimized VBM protocol. Ten of 11 patients showed statistically significant GMC excess, and among patients with GMC excess, only one showed GMC excess that was not exactly correspondent to the visually detected FCD. Seven patients exhibited excess in GMC extending beyond the area of visually detected FCD.\n\nQuestion:\nDoes voxel-based morphometry reveal excess gray matter concentration in patients with focal cortical dysplasia?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMyotonic dystrophy type 1 (DM1) is known to affect mainly the musculoskeletal system. Early mortality is related to respiratory disease and possibly additional cardiovascular complications. To identify possible cardiovascular disturbances that could predict survival of DM1 patients. We studied 30 DM1 patients (mean age 41 +/- 13.5 years, range 16-71, 15 women) who were cardiovascularly stable and compared them with 29 controls (mean age 55 +/- 7.8 years, range 42-66, 14 women) using electrocardiography (ECG) and conventional transthoracic echocardiography. The subgroup that survived a follow-up period of 17 years was re-examined using the same protocol. Of the 30 patients, 10 died of a documented respiratory cause and three of acute myocardial incidents. Compared with controls, left ventricular cavity size, corrected to body surface area, was slightly enlarged at end systole (P < 0.05) and hence fractional shortening was reduced (P < 0.01). Nine patients had first-degree heart block and 15 had a QRS duration >90 ms. Of all ECG and echocardiographic measurements, the sum of QRS duration + PR interval was the best predictor of mortality as shown by the area under the receiver operating characteristic curve of 85%, sensitivity of 70% and specificity of 84%.\n\nQuestion:\nDoes profound cardiac conduction delay predict mortality in myotonic dystrophy type 1?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCounseling for pyelectasis in the late 2nd trimester is usually based only upon assessing the antero-posterior (AP) width of the renal pelvis. We hypothesized that checking additional features would better predict postnatal outcome. Ultrasound (<24 weeks gestational age (GA)) and newborn outcome data collected prospectively since 1986 were analyzed retrospectively. We determined if outcome predictions in kidneys with a sonographically evident renal pelvis (SERP), which had evaluation of additional features (e.g., renal and bladder lengths, presence of a dilated ureter or dilated calyces) are more accurate than those that did not have these features. There were 286 fetuses studied with pediatric follow-up of an average of 6.5 years. There were 338 exams providing 459 ultrasound images with SERP. Additional features were not assessed in 183 fetuses; however 103 fetuses did have evaluation of additional features. These features were categorized as abnormal (92) or as normal (11). Fetuses with SERP and abnormal additional features required extensive urological care or died 6.1 times more often than fetuses in which additional features were not examined (p < 0.001) and 12.9 times more often when additional features were normal (p < 0.001).\n\nQuestion:\nIs late second trimester assessment of pyelectasis ( SERP ) to predict pediatric urological outcome improved by checking additional features?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe host immune response against mucosally acquired pathogens may be influenced by the mucosal immune milieu during acquisition. As Neisseria gonorrhoeae can impair dendritic cell and T-cell immune function, we hypothesized that coinfection during HIV acquisition would impair subsequent systemic T-cell responses. Monthly screening for sexually transmitted infections was performed in high risk, HIV seronegative Kenyan female sex workers as part of an HIV prevention trial. Early HIV-specific CD8 T-cell responses and subsequent HIV viral load set point were assayed in participants acquiring HIV, and were correlated with the presence of prior genital infections during HIV acquisition. Thirty-five participants acquired HIV during follow-up, and 16 out of 35 (46%) had a classical sexually transmitted infection at the time of acquisition. N. gonorrhoeae coinfection was present during HIV acquisition in 6 out of 35 (17%), and was associated with an increased breadth and magnitude of systemic HIV-specific CD8 T-cell responses, using both interferon-gamma gamma and MIP-1 beta as an output. No other genital infections were associated with differences in HIV-specific CD8 T-cell response, and neither N. gonorrhoeae nor other genital infections were associated with differences in HIV plasma viral load at set point.\n\nQuestion:\nIs mucosal Neisseria gonorrhoeae coinfection during HIV acquisition associated with enhanced systemic HIV-specific CD8 T-cell responses?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nRibavirin-induced anemia is one of the major causes of discontinuation and dose reduction during anti-hepatitis C virus therapy. Factors influencing this anemia, especially host genetic factors, are poorly understood. In this study we investigated predictive factors in hepatitis C virus patients treated with combination therapy. We performed a 2-step genome-wide screening followed by replication analysis and fine-mapping using a total of 923 Japanese hepatitis C virus 1b-infected patients treated with pegylated-interferon plus ribavirin. We also applied logistic regression analysis to search for possible independent associations of clinical parameters and genetic variants with treatment-induced hemoglobin (Hb) decline as well as treatment outcomes. We identified a variant, located upstream of the inosine triphosphate pyrophosphatase gene on chromosome 20p13 that is significantly associated with treatment-induced anemia (combined P = 6.0 × 10(-14)). Resequencing and fine-mapping revealed several single nucleotide polymorphisms (SNPs) strongly associated with Hb decline, including the nonsynonymous SNP rs1127354 (P = 3.5 × 10(-44)), which was recently reported for other ethnic groups. Another reported SNP, the splicing variant-related SNP rs7270101, was not polymorphic in the Japanese population. Stratified analysis based on rs1127354 genotype revealed that inosine triphosphate pyrophosphatase expression is not correlated with Hb decline, suggesting that rs1127354 is a direct causal variant in the Japanese population. Multivariate analysis demonstrated that age, baseline Hb, baseline platelet count, and rs1127354 were independently associated with severe anemia (Hb <10 g/dL).\n\nQuestion:\nDoes iTPA polymorphism affect ribavirin-induced anemia and outcomes of therapy -- a genome-wide study of Japanese HCV virus patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHippocampal sclerosis is a common finding in patients with temporal lobe epilepsy (TLE), and magnetic resonance imaging (MRI) studies associate the reduction of hippocampal volume with the neuron loss seen on histologic evaluation. Astrogliosis and increased levels of chondroitin sulfate, a major component of brain extracellular matrix, are also seen in hippocampal sclerosis. Our aim was to evaluate the association between hippocampal volume and chondroitin sulfate, as well as neuronal and astroglial populations in the hippocampus of patients with TLE. Patients with drug-resistant TLE were subdivided, according to hippocampal volume measured by MRI, into two groups: hippocampal atrophy (HA) or normal volume (NV) cases. Hippocampi from TLE patients and age-matched controls were submitted to immunohistochemistry to evaluate neuronal population, astroglial population, and chondroitin sulfate expression with antibodies against neuron nuclei protein (NeuN), glial fibrillary acidic protein (GFAP), and chondroitin sulfate (CS-56) antigens, respectively. Both TLE groups were clinically similar. NV cases had higher hippocampal volume, both ipsilateral and contralateral, when compared to HA. Compared to controls, NV and HA patients had reduced neuron density, and increased GFAP and CS-56 immunopositive area. There was no statistical difference between NV and HA groups in neuron density or immunopositive areas for GFAP and CS-56. Hippocampal volume correlated positively with neuron density in CA1 and prosubiculum, and with immunopositive areas for CS-56 in CA1, and negatively with immunopositive area for GFAP in CA1. Multiple linear regression analysis indicated that both neuron density and CS-56 immunopositive area in CA1 were statistically significant predictors of hippocampal volume.\n\nQuestion:\nAre temporal lobe epilepsy patients with severe hippocampal neuron loss but normal hippocampal volume : Extracellular matrix molecules important for the maintenance of hippocampal volume?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nA third of the population are estimated to have NAFLD of varying severity. Serum immunoglobulins are frequently elevated in patients with chronic liver disease, but little is known about serum immunoglobulin levels in patients with NAFLD. Aim of this study was to evaluate serum immunoglobulin levels (IgA, IgG, and IgM) in a large cohort of patients with biopsy-proven NAFLD and determine if immunoglobulin levels are associated with clinical or histological features. Patients seen in a tertiary fatty liver clinic between 1999 and 2009 were included. Liver biopsies were assessed using the Kleiner score. Immunoglobulin levels and other blood tests were taken at time of biopsy. 285 patients (110 simple steatosis and 175 NASH) had serum immunoglobulins measured within 6months of liver biopsy. 130 (46%) patients had elevated (>1× upper limit of normal) serum IgA levels, 28 (10%) patients had elevated IgG and 22 (8%) raised IgM. Serum IgA levels were elevated more frequently in patients with NASH compared with subjects with simple steatosis (55% vs. 31%, p<0.001). Overall, 55 (19%) patients had advanced liver fibrosis (Kleiner stage 3-4). There was a significant positive association between serum IgA levels and the stage of fibrosis (p<0.001). Serum IgA, age, platelets, AST/ALT ratio and BMI were all independently with advanced fibrosis following multivariate analysis. A model constructed from these independent predictors accurately predicted advanced fibrosis (AUROC 0.87).\n\nQuestion:\nDo serum immunoglobulin levels predict fibrosis in patients with non-alcoholic fatty liver disease?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nProhibitin 3' untranslated region 1630 C>T (rs6917) polymorphism creates a variant T allele that lacks the antiproliferative activity of the more common functional C allele. Previous studies indicate that women carrying the prohibitin T allele have an increased susceptibility to breast cancer. However, the role of 1630 C>T polymorphism in mRNA expression of prohibitin and its contribution to carcinogenesis in the breast remains controversial. Using mRNA expression data from the HapMap online database, we sought an association between prohibitin 1630 C>T polymorphism and its mRNA expression, then conducted a meta-analysis of prohibitin 1630 C>T polymorphism and risk of breast cancer. Although no significant association was found between prohibitin 1630 C>T polymorphism and mRNA expression in lymphoblastoid cell lines from the HapMap database (P trend = 0.543), the present meta-analysis involving 5072 cases and 4796 controls demonstrated that prohibitin 1630 C>T polymorphism was significantly correlated with breast cancer risk in allele contrast model T versus C (odds ratio [OR] 1.09, 95% confidence interval [CI] 1.01-1.18), the homozygote codominant model TT versus CC (OR 1.47, 95% CI 1.12-1.92), and the recessive model TT versus CC/CT (OR 1.45, 95% CI 1.10-1.89).\n\nQuestion:\nDoes 3 ' untranslated region 1630 C > T polymorphism of prohibitin increase risk of breast cancer?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe Human Natural Killer-1 carbohydrate (HNK-1) is involved in neurodevelopment and synaptic plasticity. Extracellular matrix structures called perineuronal nets, condensed around subsets of neurons and proximal dendrites during brain maturation, regulate synaptic transmission and plasticity. Ten genes of importance for HNK-1 biosynthesis (B3GAT1, B3GAT2, and CHST10) or for the formation of perineuronal nets (TNR, BCAN, NCAN, HAPLN1, HAPLN2, HAPLN3, and HAPLN4) were investigated for potential involvement in schizophrenia (SCZ) susceptibility, by genotyping 104 tagSNPs in the Scandinavian Collaboration on Psychiatric Etiology sample (849 cases; 1602 control subjects). Genome-wide association study imputation data from the European SGENE-plus sample (2663 cases; 13,498 control subjects) were used for comparison. The effect of SCZ risk alleles on brain structure was investigated in a Norwegian subset (98 cases; 177 control subjects) with structural magnetic resonance imaging data. Five single nucleotide polymorphisms (SNPs), located in two adjacent estimated linkage disequilibrium blocks in the first intron of β-1,3-glucuronyltransferase 2 (B3GAT2), were nominally associated with SCZ (.004 ≤ P(empirical) ≤ .05). The rs2460691 was significantly associated in the comparison sample and in the meta-analysis after correction for all 121 SNP/haplotype tests (P(raw) = 1 × 10(-4); P(corrected) = .018). Increased dosage of the rs2460691 SCZ risk allele was associated with decreased cortical area (p = .002) but not thickness or hippocampal volume. A second SNP (r(2) = .24 with rs10945275), which conferred the highest SCZ risk effect in the Norwegian subset, was also associated with cortical area.\n\nQuestion:\nIs candidate gene analysis of the human natural killer-1 carbohydrate pathway and perineuronal nets in schizophrenia : B3GAT2 associated with disease risk and cortical surface area?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSeizures are common after intracerebral hemorrhage (ICH) but their impact on outcome is uncertain and prophylactic anti-convulsant use is controversial. We hypothesized that seizures would not increase the risk of in-hospital mortality in a large administrative database. The study population included patients in the 2006 Nationwide Inpatient Sample over the age of 18 with a principal diagnosis of ICH (ICD9 = 431). Subjects with a secondary diagnosis of aneurysm, arterio-venous malformation, brain tumor, or traumatic brain injury were excluded. Seizures were defined by ICD9 codes (345.0x-345.5x, 345.7x-345.9x, 780.39). Logistic regression was used to quantify the relationship between seizures and in-hospital mortality. Pre-specified subgroups included age strata, length of stay, and invasive procedures. 13,033 subjects met all eligibility criteria, of which 1,430 (11.0 %) had a secondary diagnosis of seizure. Subjects with seizure were younger (64 vs. 70 years, p < 0.001), more likely to get craniectomy (2.1 vs. 1.2 %, p = 0.006), ventriculostomy (8.5 vs. 6.0 %, p < 0.001), intubation (32.2 vs. 25.9 %, p < 0.001), and tracheostomy (6.4 vs. 4.2 %, p < 0.001). Seizure patients had lower in-hospital mortality (24.3 vs. 28.0 %, p = 0.003). In a multivariable model incorporating patient and hospital level variables, seizures were associated with reduced odds of in-hospital death (OR = 0.62, 95 % CI 0.52-0.75).\n\nQuestion:\nDo seizures increase in-hospital mortality after intracerebral hemorrhage in the nationwide inpatient sample?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nBesides mechanical damage done by the enlarging ventricles, biochemical impairment in the periventricular tissue represents an important factor resulting from or contributing to the pathogenesis of hydrocephalus. In this study the changes in periventricular region total sialic acid levels in the early stage of experimentally induced hydrocephalus were evaluated. Hydrocephalus was induced in 3-week-old rat pups by kaolin injection into the cisterna magna. Ten days after hydrocephalus induction rats were sacrificed and total sialic acid levels in the periventricular area were determined by the thiobarbituric acid method.\n\nQuestion:\nDo total sialic acid levels decrease in the periventricular area of infantile rats with hydrocephalus?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo investigate the mechanism of cell death in laser-induced choroidal neovascularization (CNV) after photodynamic therapy (PDT). PDT was performed in Brown-Norway rats using laser light at a wavelength of 689 nm, irradiance of 600 mW/cm(2), and fluence of 25 J/cm(2) after intravenous injection of verteporfin at the doses of 3, 6, and 12 mg/m(2). Apoptotic cells in CNV were detected by TUNEL assay at 1, 3, 6, 15, 24, and 48 hours after PDT. Caspase activation at 1, 3, 6, 15, and 24 hours after PDT was determined by immunohistochemistry (IHC) with a cleaved caspase-3 or -9 antibody. Akt activity was determined by Western blot and IHC with a phosphorylated-Akt (pAkt) antibody. To investigate the roles of Akt in PDT-induced apoptosis, insulin-like growth factor (IGF)-1, an Akt activator, with or without wortmannin, an inhibitor of PI3K-Akt pathway, was injected into the vitreous before PDT. The number of TUNEL-positive cells in CNV increased at 3 hours after PDT and peaked at 6 hours, showing a dose dependence of verteporfin. Caspase activation was detected in TUNEL-positive cells. Dephosphorylation of Akt in CNV occurred within 1 hour. IGF-1 significantly activated Akt and suppressed the number of TUNEL-positive cells in CNV, and the effects of IGF-1 were diminished by wortmannin.\n\nQuestion:\nDoes photodynamic therapy induce caspase-dependent apoptosis in rat CNV model?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo examine the relationship of glucose and insulin levels during the 1-hour gestational diabetes screening test to determine their relation to gestational diabetes mellitus (GDM) and possible resulting pregnancy complications. This is a prospective observational study of the delivery records of 784 patients who obtained third trimester screening for both glucose and insulin levels during routine 1-hour 50 g oral glucose load. Insulin levels were positively correlated with glucose levels (p < 0.001). GDM was diagnosed in 17 patients (2.2%). Mean birth weight was not significantly different with glucose levels < 130 pmol/L, 130-140 pmol/L, or > 140 pmol/L (3,282 g, 3,409 g, and 3,310 g, respectively, p = 0.13), nor were 5-minute Apgar scores (p = 0.66). No difference in mean fetal birth weight was found in insulin ranges < 30 pmol/L, 30-60 pmol/L, and > 60 pmol/L (3,330 g, 3,306 g, and 3,276 g, respectively, p = 0.56). Moreover, no significant differences in 5-minute Apgar scores were observed between those groups (p = 0.05). Women who underwent cesarean section (n = 230) had significantly higher glucose and insulin levels than did those who had vaginal deliveries (n = 554) (p = 0.01 and p = 0.003, respectively).\n\nQuestion:\nAre third trimester insulin levels correlated with fetal macrosomia or delivery complications?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nOf the various biological activities ascribed to extracts from Casearia sylvestris (guaçatonga), its facilitatory activity, i.e., ability to increase skeletal muscle contractile amplitude, has promising therapeutic applications. In this work, we investigated the components responsible for the previously described neurofacilitation caused by C. sylvestris leaves. The methanolic fraction of C. sylvestris leaves was initially fractionated by column chromatography and partitioned in a MeOH:H2O gradient. The resulting fractions were analyzed by analytical HPLC and yielded fraction 5:5 (F55) that was subjected to solid phase extraction and preparative HPLC. Of the seven resulting subfractions, only F55-6 caused muscle facilitation. Subfractions F55-6 and F55-7 (similar in composition to F55-6 by TLC analysis, but inactive) were analyzed by 1H-NMR to identify their constituents. This analysis identified a rutin-glycoside phytocomplex that caused neurofacilitation, a property that commercial rutin alone did not exhibit.\n\nQuestion:\nIs a highly polar phytocomplex involving rutin responsible for the neuromuscular facilitation caused by Casearia sylvestris ( guaçatonga )?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAlthough morbidity and mortality rates from asthma are highest in patients > 65 years of age, the effect of older age on airway inflammation in asthma is not well established. To investigate age-related differences in the promotion of allergic inflammation after influenza A viral respiratory infection on antigen-specific IgE production, antigen-induced airway inflammation and airway hyperresponsiveness in mice. To accomplish this objective, the following model system was used. Young (6 week) and aged (18 months) BALB/c mice were first infected with a non-lethal dose of influenza virus A (H/HKx31). Mice were then ovalbumin (OVA)-sensitized during the acute infection (3-days post inoculation) and then chronically underwent challenge to the airways with OVA. Forty-eight hours after the final OVA challenge, airway hyperresponsiveness (AHR), bronchoalveolar fluid (BALF) cellular and cytokine profile, antigen-specific IgE and IgG1, and lung tissue inflammation were measured. Age-specific differences were noted on the effect of a viral infection, allergic sensitization, airway inflammation and airway hyperresponsiveness. Serum OVA-specific IgE was significantly increased in only the aged mice infected with influenza virus. Despite greater morbidity (e.g. weight loss and sickness scores) during the acute infection in the 18-month old mice that were OVA-sensitized, there was little effect on the AHR and BALF cellular differential. In contrast, BALF neutrophils and AHR increased, but eosinophils decreased in 6-week mice that were OVA-sensitized during an acute influenza infection.\n\nQuestion:\nDoes influenza A infection enhance antigen-induced airway inflammation and hyperresponsiveness in young but not aged mice?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nEpstein-Barr virus (EBV) infection has been associated with Richter transformation in patients with chronic lymphocytic leukemia (CLL). A direct isothermal mRNA amplification method was developed for detection of EBV latent membrane protein 1 (LMP1) mRNA transcriptional activity in the peripheral blood of 135 chronic lymphocytic leukemia patients and 98 hematologically healthy control subjects. EBV LMP1 mRNA transcripts were found in 19 of 135 (14%) of the CLL cases, but only 1% of the healthy controls (P < .0001). In contrast, 23 solid tumor patients tested negative for EBV LMP1 transcripts. In a later cohort of patients after hematopoietic stem cell transplantation, 4 of 7 patients with Hodgkin lymphoma or Burkitt lymphoma had EBV LMP1 detected. In a preliminary analysis, outcome data were available for 88 of the 135 patients with CLL. EBV LMP1 mRNA positivity was associated with a significantly increased degree of histologically demonstrated bone marrow involvement by CLL (P = .003, Mann-Whitney U test).\n\nQuestion:\nIs epstein-Barr virus latent membrane protein 1 mRNA expressed in a significant proportion of patients with chronic lymphocytic leukemia?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPositive affect has been associated with better prognosis in patients with ischemic heart disease, but the underlying mechanisms remain unclear. We examined whether positive affect predicted time to first cardiac-related hospitalization and all-cause mortality, and whether exercise mediated this relationship in patients with established ischemic heart disease. The sample comprised 607 patients with ischemic heart disease from Holbæk Hospital, Denmark. In 2005, patients completed the Global Mood Scale (GMS) to assess positive affect and a purpose-designed question on exercise. Data on mortality and hospitalization were collected from Danish national registers for the period 2006-2010. Adjusted Cox and logistic regression were used to analyze the mediation model. Because no significant association between positive affect and cardiac-related hospitalization was found, we constructed no mediation model for hospitalization. Importantly, patients with high positive affect had a significantly reduced risk of all-cause mortality (hazard ratio, 0.58; 95% confidence interval, 0.37-0.92; unadjusted analysis) and were more likely to exercise (odds ratio, 1.99; 95% confidence interval, 1.44-2.76; unadjusted analysis; odds ratio, 1.48; 95% confidence interval, 1.03-2.13; adjusted analysis). When controlling for positive affect and other relevant variables, patients engaged in exercise were less likely to die during follow-up (hazard ratio, 0.50; 95% confidence interval, 0.31-0.80; P=0.004). Importantly, exercise acted as a mediator in the relationship between positive affect and mortality.\n\nQuestion:\nDoes exercise mediate the association between positive affect and 5-year mortality in patients with ischemic heart disease?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe activation of spinal cord microglia and astrocytes after peripheral nerve injury or inflammation contributes to behavioral hypersensitivity. The contribution of spinal cord glia to mechanical hypersensitivity after hind paw incision has not been investigated previously. Male Sprague-Dawley rats underwent a unilateral plantar hind paw incision, and the development of mechanical hypersensitivity was assessed by using von Frey filaments. The activation of spinal cord microglia and astrocytes was measured 1, 2, 3, and 5 days after hind paw incision by using immunohistochemistry. The glial activation inhibitor, fluorocitrate, was administered intrathecally 24 hours after hind paw incision to determine glial involvement in mechanical hypersensitivity. Hind paw incision induced an activation of spinal astrocytes ipsilateral to incision within 24 hours. Both microglia and astrocytes reached a maximum activation 3 days after hind paw incision. Fluorocitrate produced a dose-dependent reduction in mechanical hypersensitivity when administered 24 hours after hind paw incision. Spinal cord glial activation contributes to the mechanical hypersensitivity that develops after hind paw incision.\n\nQuestion:\nDoes spinal glial activation contribute to postoperative mechanical hypersensitivity in the rat?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe mechanisms regulating basal uteroplacental blood flow (UBF) and the greater than 30-fold increase observed in normal pregnancy remain unclear. Although vascular growth contributes in early gestation, vasodilation accounts for the exponential rise seen in the last third of pregnancy. Large conductance potassium channels (BK(Ca)) are expressed in uterine vascular smooth muscle (VSM), but the extent of their role in regulating UBF in pregnancy is unclear. Therefore, we determined if BK(Ca) regulate basal UBF during ovine pregnancy. Studies were performed at 113 to 127 days and 135 to 150 days of gestation in eight pregnant ewes instrumented with uterine artery flow probes and uterine arterial and venous catheters. Tetraethylammonium chloride (TEA), a BK(Ca)-specific inhibitor at less than 1.0 mM, was infused intra-arterially into the pregnant uterine horn over 60 minutes to achieve levels of 0.001-0.35 mM while continuously monitoring UBF, arterial pressure (MAP), and heart rate (HR). Uterine arterial and venous blood was collected simultaneously to measure uterine cyclic guanosine monophosphate (cGMP) synthesis. Intra-arterial TEA dose-dependently decreased basal UBF in the early (R = 0.81, n = 36, P <.001) and late (R = 0.72, n = 31, P <.001) study periods without altering contralateral UBF, MAP, and HR. The IC(50) was 0.2 mM and basal UBF decreased >or=80% at 0.35 mM in both periods. Although UBF fell greater than 40% at estimated plasma TEA levels of 0.3 mM, uterine arterial cGMP was unchanged, uterine venous cGMP rose, and uterine cGMP synthesis was unchanged; therefore, upstream events associated with BK(Ca) activation were unaffected by blockade.\n\nQuestion:\nDo large-conductance Ca2+-dependent K+ channels regulate basal uteroplacental blood flow in ovine pregnancy?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe object of this study was to investigate the genotoxic effect of acute overexposure to combustion products originating from coal or wood stoves in patients presenting with acute carbon monoxide intoxication. In a prospective study, we analyzed the frequency of sister chromatid exchange and the carboxyhemoglobin concentration in 20 consecutive patients without a history of smoking or drug use who had been treated in the Emergency Care Unit of Istanbul Medical Faculty due to acute carbon monoxide intoxication. All of these cases were domestic accidents due to dysfunctioning coal or wood stoves. The results were compared with a control group of 20 nonsmoking, nondrug-using healthy individuals matched for age, sex, and absence of other chemical exposure. The mean sister chromatid exchange frequency per metaphase was significantly higher in the study group compared to the control group: 8.11 +/- 2.39 vs. 6.33 +/- 1.60 (p = 0.008). We found that there was no positive correlation between the blood carboxyhemoglobin concentration and sister chromatid exchange frequency.\n\nQuestion:\nDoes acute wood or coal exposure with carbon monoxide intoxication induce sister chromatid exchange?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo evaluate whether selective decontamination of the digestive tract (SDD) attenuates organ dysfunction in critically ill burn patients. The effect of SDD on the development and progression of organ dysfunction, as an important determinant of mortality in burned patients, is still unknown. We asked whether organ dysfunction is mitigated by treatment with SDD. Patients with burns >20% of total body surface or suspected inhalation injury from a randomized placebo-controlled trial were analyzed to determine the relationship between treatment received (placebo or SDD) and the severity of organ dysfunction as measured by the area under the curve of the Sequential Organ Failure Assessment (SOFA) score (and its individual components) from day 1 to day 7 of admission. One hundred seven patients (53 in the SDD group and 54 in the placebo group) were included. Survival was significantly higher in SDD-treated patients (48 of 53, 90.6%) than in placebo-treated patients (39 of 54, 72.2%, P = 0.013). Total (P < 0.01) and respiratory (P < 0.01), cardiovascular (P = 0.04) and hematological (not reaching statistical significance, P = 0.07) organ dysfunction was associated with mortality after adjusting for predicted mortality. In multivariate logistic regression, SDD treatment was independently associated with total (P < 0.01), respiratory (P = 0.02), and hematological (P < 0.01) dysfunction over the first week postinjury.\n\nQuestion:\nDoes selective Digestive Decontamination attenuate Organ Dysfunction in Critically Ill Burn Patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe aim of the study was to evaluate the effect of β-catenin immunohistochemical expression on the prognosis of lung cancer. We searched Pubmed and Embase to identify eligible studies. The enrolled references were between January 1985 and January, 2015, with no lower date limit. The citation lists associated with the studies were used to identify additional eligible studies. The data of β-catenin immunohistochemical expression, clinical features and survival in each eligible article were recorded and analyzed as hazard ratio (HR) and odd ratio (OR). A total of 15 studies were identified and comprised 3404 cases. β-catenin expression was not significantly correlated with poor overall survival (OS) in lung cancer patients (HR 0.79, 95 % CI 0.47-1.34), but showed a significant degree of heterogeneity (I (2) = 95 %, P < 0.0001). Subgroup analysis indicated that accumulation in the nucleus or loss of membrane significantly influences the survival of lung cancer patients independently. But, the result indicated that β-catenin expression was not associated with clinicopathological features such as TNM stage (OR 1.22, 95 % CI 0.69-2.14), T stage (OR 0.86, 95 % CI 0.63-1.17), lymph node metastasis (0.85, 95 % CI 0.41-1.78), distant metastasis (OR 0.82, 95 % CI 0.31-2.18), grade of differentiation (OR 0.92, 95 % CI 0.47-1.80), or vascular invasion (OR 0.99, 95 % CI 0.04-24.10).\n\nQuestion:\nIs a meta-analysis of abnormal β-catenin immunohistochemical expression as a prognostic factor in lung cancer : location more important?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIncreased intestinal epithelial permeability is associated with intestinal inflammation and dysfunction. The aim of the present study was to investigate the role of long-term oral melatonin administration on ethanol-induced increases in duodenal mucosal permeability and hypermotility. Male Sprague-Dawley rats were administered melatonin in their tap water (0.1 mg mL(-1) or 0.5 mg mL(-1) ) for 2 or 4 weeks. After the treatment period, the rats were anaesthetized with Inactin(®) , and a 30-mm duodenal segment was perfused in situ. The effects on duodenal mucosal paracellular permeability, bicarbonate secretion, fluid flux and motor activity were studied. The expression levels of the tight junction components, zona occludens (ZO)-1, ZO-2, and ZO-3, claudin-2, claudin-3, claudin-4, occludin, and myosin light chain kinase and of the melatonin receptors MT1 and MT2 were assessed using qRT-PCR. Melatonin administration for 2 weeks significantly reduced the basal paracellular permeability, an effect that was absent after 4 weeks. Perfusing the duodenal segment with 15% ethanol induced marked increases in duodenal paracellular permeability, bicarbonate secretion and motor activity. Melatonin for 2 weeks dose-dependently reduced ethanol-induced increases in permeability and motor activity. Four weeks of melatonin administration reduced the ethanol-induced increases in duodenal motility and bicarbonate secretion but had no effect on the increases in permeability. Two weeks of melatonin administration upregulated the expression of MT1 and MT2 , although both were downregulated after 4 weeks. Melatonin downregulated the expression of ZO-3 and upregulated the expression of claudin-2, even as all other mRNA-levels investigated were unaffected.\n\nQuestion:\nDoes long-term oral melatonin administration reduce ethanol-induced increases in duodenal mucosal permeability and motility in rats?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTopoisomerase I (Top I) is referred as the cellular target of the camptothecins (CPTs) which are now being explored as potential pesticides for insect control. Three amino acid substitutions, including L530P, A653T and S729T, in Top Is of insects were found in our previous studies. In order to investigate the effect of these three substitutions, a comparative analysis was conducted between the wild-type and mutant Top Is in Spodoptera exigua Hübner. The optimal salt concentration of A653T and S729T was 150 mm, which is consistent with that of the wild-type Top I, while the mutant L530P showed maximum relaxation activity at a lower KCl concentration (100 mm). The mutated L530P and A653T Top Is showed a higher relaxation efficiency owing to an increased relaxation velocity toward the negatively supercoiled plasmid pBR322 DNA, which rendered L530P and A653T resistant to CPTs, whereas mutant S729T exhibited sensitivity to CPTs as a result of a decreased relaxation activity toward plasmid pBR322 DNA.\n\nQuestion:\nDo substitutions in Spodoptera exigua topoisomerase I modulate its relaxation activity and camptothecin sensitivity?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo investigated the effects of Src family kinases on the expression of mRNA and protein of Nav1.1 in spiral ganglion neurons. RT-PCR and Western blot techniques respectively explored the level of expression of mRNA and protein of Nav1.1 in spiral ganglion neurons by Src family kinases inhibitor. An application of the inhibitor of Src family kinases which was PP2 (10 micromol/L) and SU6656 (2 micromol/L) gived rise to the mRNA decreasing to 26% +/- 0.8% and 36% +/- 1.5% respectively (P < 0.05), and protein reducing to 39% +/- 12.5% and 53% +/- 1.7% severally (P < 0.05).\n\nQuestion:\nDo [ Src family kinases affect the expression of Nav1.1 in spiral ganglion neurons ]?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCYP2D6, a member of the cytochrome P450 superfamily, is responsible for the metabolism of about 25% of the commonly prescribed drugs. Its activity ranges from complete deficiency to excessive activity, potentially causing toxicity of medication or therapeutic failure with recommended drug dosages. This study aimed to describe the CYP2D6 diversity at the global level. A total of 1060 individuals belonging to 52 worldwide-distributed populations were genotyped at 12 highly informative variable sites, as well as for gene deletion and duplications. Phenotypes were predicted on the basis of haplotype combinations.\n\nQuestion:\nDoes cYP2D6 worldwide genetic variation show high frequency of altered activity variants and no continental structure?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nA family history of appendicitis has been reported to increase the likelihood of the diagnosis in children and in a retrospective study of adults. We compare positive family history with the diagnosis of acute appendicitis in a prospective sample of adults. We conducted a prospective observational study of a convenience sample of 428 patients. We compared patients with surgically proven appendicitis to a group without appendicitis. The latter were further grouped by their presenting symptoms: those presenting with a chief complaint of abdominal pain and those with other chief complaints. Participants answered questions regarding their family history of appendicitis. Family history was then compared for the appendicitis group versus the nonappendicitis group as a whole, and then versus the subgroup of patients without appendicitis but with abdominal pain. The primary analysis was a χ(2) test of proportions and the calculation of odds ratio (OR) for the relationship between final diagnosis of appendicitis and family history. Of 428 patients enrolled, 116 had appendicitis. Of those with other diagnoses, 158 had abdominal pain and 154 had other complaints. Of all patients with appendicitis, 37.9% (confidence interval [Cl] = 29.1-46.8) had positive family history. Of those without appendicitis, 23.7% (Cl = 19.0-28.4) had positive family history. In the subgroup without appendicitis but with abdominal pain, 25.9% (Cl = 19.1-32.8) had positive family history. Both comparisons were significant (P = 0.003; OR = 1.97; 95% Cl = 1.2-3.1; and P=0.034; OR = 1.74; 95% Cl = 1.04-2.9, respectively). By multivariate logistic regression analysis across the full sample, family history was a significant independent predictor (P = 0.011; OR = 1.883) of appendicitis.\n\nQuestion:\nIs family history a predictor for appendicitis in adults in the emergency department?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nC-peptide increases forearm blood flow (FBF) in patients with Type 1 diabetes, probably by interaction with insulin, but not in healthy subjects. It is unclear if the vasodilating effect is sealed at normal fasting insulin concentrations. The effects of C-peptide alone and during local hyperinsulinaemia were studied in healthy young men. Subjects received intra-arterial insulin at 6 pmol min-1 (low dose) or placebo for 60 min with subsequent coinfusion of C-peptide at increasing doses of 2-60 pmol min-1 in a double-blind crossover study (n = 8). In control experiments insulin at 30 pmol min-1 (high dose) was coinfused with C-peptide (n = 3). FBF was measured by strain-gauge plethysmography. Placebo had no effect on FBF (mean percentage change from baseline at 50 min -3.1%, 95% confidence interval [CI]-14.9, + 8.7). Insulin infusion slightly enhanced FBF by + 10.2% (95% CI -6.8, + 27.2; low dose) and + 17.6% (95% CI -38.8, + 74.0; high dose), respectively. The mean individual difference of the change in FBF between low-dose insulin and placebo was + 13.3% (95% CI -6.0, + 32.7; P = NS). Infusion of C-peptide increased local C-peptide concentrations from 1.8 +/- 0.1 ng ml-1 to 6.1 +/- 2.8 ng ml-1, but had no effect on FBF during placebo or hyperinsulinaemia (mean difference vs low dose insulin -16.0%, 95% CI -38.9, + 6.9).\n\nQuestion:\nDoes c-peptide have no effect on forearm blood flow during local hyperinsulinaemia in healthy humans?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo explore the genetic and molecular events that control subclones exhibiting distinct invasive/migratory capacities derived from human epithelial ovarian cancer (EOC) cell line A2780 and SKOV3. Single-cell subclones were isolated and established that were derived from the SKOV3 and A2780 cell lines through limiting dilution methodology. Transwell insert assays and MTT assays were performed to screen and identify the subclones exhibiting the highest and the lowest invasive/migratory capacities, and the selected subclones were renamed as A-H (A2780 high), A-L (A2780 low), S-H (SKOV3 high), and S-L (SKOV3 low). Their biological characteristics were evaluated. RNA-Seq was conducted on the targeted subclones. Compared with their corresponding counterparts, A-H/S-H cells exhibited significantly higher invasive/migratory capacities (P < 0.001 and = 0.001, respectively). A-H/S-H cells displayed a clear reduction in doubling time (P = 0.004 and 0.001, respectively), and a significant increase in the percentage of cells in S phase (P = 0.004 and 0.022, respectively). Additionally, the apoptotic rates of A-H/S-H cells were significantly lower than those of A-L/S-L cells (P = 0.002 and 0.026, respectively). At both mRNA and protein levels, caspase-3 and caspase-7 expression were reduced but Bcl-2 expression was increased in A-H/S-H cells. The TrkB (anoikis-related) and Beclin1 (autophagy-related) levels were consistently high and low, respectively, in both A-H/S-H cells. Resistance to chemotherapy in vitro and higher capacities on tumor formation in vivo was presented in both A-H/S-H cells. PI3K/AKT/mTOR pathway components, PIK3CA, PIK3CD, AKT3, ECM1, GPCR, mTOR and PRKCB were increased but that the Nur77 and PTEN were decreased in A-H/S-H cells, identified by RNA-Seq and consistently confirmed by RT-PCR and Western blot analyses.\n\nQuestion:\nIs the PI3K/AKT/mTOR pathway a potential predictor of distinct invasive and migratory capacities in human ovarian cancer cell lines?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nDespite its small size, New Caledonia is characterized by a very diverse flora and striking environmental gradients, which make it an ideal setting to study species diversification. Thirteen of the 19 Araucaria species are endemic to the territory and form a monophyletic group, but patterns and processes that lead to such a high species richness are largely unexplored. We used 142 polymorphic AFLP markers and performed analyses based on Bayesian clustering algorithms, genetic distances, and cladistics on 71 samples representing all New Caledonian Araucaria species. We examined correlations between the inferred evolutionary relationships and shared morphological, ecological, or geographic parameters among species, to investigate evolutionary processes that may have driven speciation. We showed that genetic divergence among the present New Caledonian Araucaria species is low, suggesting recent diversification rather than pre-existence on Gondwana. We identified three genetic groups that included small-leaved, large-leaved, and coastal species, but detected no association with soil preference, ecological habitat, or rainfall. The observed patterns suggested that speciation events resulted from both differential adaptation and vicariance. Last, we hypothesize that speciation is ongoing and/or there are cryptic species in some genetically (sometimes also morphologically) divergent populations.\n\nQuestion:\nDo aFLP markers provide insights into the evolutionary relationships and diversification of New Caledonian Araucaria species ( Araucariaceae )?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nGata6 is required to complete and maintain acinar differentiation in the mouse pancreas. Pancreas-specific Gata6 ablation during development causes extensive and persistent acinar-ductal metaplasia, which is considered an initial step of mutant KRas-driven carcinogenesis. Therefore, the Gata6-null pancreas might represent a tumour-prone environment. We investigated whether Gata6 plays a role during pancreatic tumorigenesis. We analysed genetically engineered mouse models and human pancreatic ductal adenocarcinoma (PDAC) cell lines, using a combination of histopathological studies, genome-wide expression and chromatin immunoprecipitation experiments to understand the role of Gata6 in the initiation and progression of KRas(G12V)-driven tumours We show that Gata6 maintains the acinar differentiation programme, both directly and indirectly, and it concomitantly suppresses ectopic programmes in the pancreas. Gata6 ablation renders acinar cells more sensitive to KRas(G12V), thereby accelerating tumour development. Gata6 expression is spontaneously lost in a mouse model of KRas(G12V)-driven PDAC, in association with altered cell differentiation. Using a combination of ChIP-Seq and RNA-Seq, we show that Gata6 exerts its tumour-suppressive effect through the promotion of cell differentiation, the suppression of inflammatory pathways, and the direct repression of cancer-related pathways. Among them is the epidermal growth factor receptor (EGFR) pathway, the activity of which is upregulated in the normal and preneoplastic Gata6-null pancreas. Accordingly, GATA6-silencing in human PDAC cells leads to an upregulation of EGFR.\n\nQuestion:\nDoes the acinar regulator Gata6 suppress KrasG12V-driven pancreatic tumorigenesis in mice?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nLiver stellate cells are transdifferentiated to collagen-producing myofibroblast-like cells in vivo during liver injury or when placed in culture. The purpose of this study was to determine the presence of retinoids and the expression of the immediate early genes as they relate to the transdifferentiation of liver stellate cells in culture. Rat liver stellate cells were studied immediately after isolation or sequentially after culture for varying periods of time. RNA was isolated and specific messages were determined by RT-PCR. Cells were also isolated for determination of retinoid autofluorescence and immunofluorescent staining with specific antibodies by laser confocal microscopy. c-fos message and immunoprotein were high in the freshly isolated cells prior to culture, while c-myc expression increased markedly after one day of culture. Both c-fos and c-myc gene expression decreased prior to the transdifferentiation of the cells to myofibroblast-like cells and to the increase in alpha 1(I) and alpha 2(I) collagen messages and collagen production. The presence of retinoid autofluorescence and retinoic acid receptor (RAR-alpha and RAR-beta) messages and RAR-beta immunoprotein persisted during initial transdifferentiation of the stellate cells.\n\nQuestion:\nDoes a transient increase in c-myc precede the transdifferentiation of hepatic stellate cells to myofibroblast-like cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMolecular diagnosis for cystic fibrosis (CF) is based on the direct identification of mutations in the CFTR gene [cystic fibrosis transmembrane conductance regulator (ATP-binding cassette sub-family C, member 7)] (detection rate about 90% with scanning procedures) and on segregation analysis of intragenic polymorphisms for carrier and prenatal diagnosis in about 20% of CF families in which 1 or both causal mutations are unknown. We identified 3 novel intragenic polymorphic repeats (IVS3polyA, IVS4polyA, and IVS10CA repeats) in the CFTR gene and developed and validated a procedure based on the PCR followed by capillary electrophoresis for large-scale analysis of these polymorphisms and the 4 previously identified microsatellites (IVS1CA, IVS8CA, IVS17bTA, and IVS17bCA repeats) in a single run. We validated the procedure for both single- and 2-cell samples (for a possible use in preimplantation diagnosis), and on a large number of CF patients bearing different genotypes and non-CF controls. The allelic distribution and heterozygosity results suggest that the 3 novel polymorphisms strongly contribute to carrier and prenatal diagnosis of CF in families in which 1 or both causal mutations have not been identified. At least 1 of the 4 previously identified microsatellites was informative in 78 of 100 unrelated CF families; at least 1 of all 7 polymorphisms was informative in 98 of the families. Finally, the analysis of haplotypes for the 7 polymorphisms revealed that most CF mutations are associated with different haplotypes, suggesting multiple slippage events but a single origin for most CFTR mutations.\n\nQuestion:\nDo three novel CFTR polymorphic repeats improve segregation analysis for cystic fibrosis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIschemia-reperfusion (IR) is one of the strongest nonimmune factors associated with the development of chronic allograft nephropathy (CAN). This effect is often exacerbated by immunosuppressive medications, most notably cyclosporine. Although traditionally the macrophage was thought to stimulate fibroblast activity in CAN, recent evidence supports a role for lymphocytes. FTY720 is a new immunosuppressant that promotes lymphocyte sequestration into lymph nodes and Peyer's patches. This study investigated the effect of FTY720 on renal fibrosis in the rat following an IR insult (IRI). A rat model of IRI was used in which male Sprague-Dawley rats (under isoflurane anaesthesia) underwent bilateral flank incision with removal of the right kidney and clamping of the left renal hilum for 45 minutes. Five groups of animals were studied (n=4): nephrectomy only, IRI only, IRI+FTY720 (1 mg/kg/d), IRI+cyclosporine (15 mg/kg/d), and IRI+FTY 720 (1 mg/kg/d) and cyclosporine (15 mg/kg/d). Animals were humanely killed at 30 days. Serum creatinine (SCr) level was significantly reduced in the FTY720-treated animals. IRI alone produced a significant increase in SCr level compared with neprectomized animals (138 micromol/L vs 55 micromol/L; P<.05). This effect was potentiated by treatment with cyclosporine (173 micromol/L vs 55 micromol/L; P<.05). Treatment with FTY720 significantly reduced SCr level in rats following IRI alone (81 micromol/L vs 138 micromol/L; P<.01) and in rats following IRI + cyclosporine (98 micromol/L vs 173 micromol/L; P<.014). Parallel changes were seen in the levels of proteinuria. Fibrosis was assessed using Masson's trichrome (MT) staining. IRI alone produced a significant increase in MT staining compared with nephrectomized animals (0.92 vs 0.03; P<.05). This effect was potentiated by treatment with cyclosporine (1.12 vs 0.92; P=.022). Treatment with FTY720 reduced the level of MT staining in rats following IRI alone (0.34 vs 0.92; P<.05) and in rats following IRI+cyclosporine (70.34 vs 1.12; P<.05). Levels of TGF-beta1 were considerably reduced in FTY720-treated animals (compared with cyclosporine+IRI and IRI only), either alone (196+/-31 pg/mL vs 1105+/-59 pg/mL and 611+/-38; P<.05) or in conjunction with cyclosporine (423+/-26 pg/mL vs 1105+/-59 pg/mL and 611+/-38; P<.05).\n\nQuestion:\nDoes fTY720 reduce extracellular matrix expansion associated with ischemia-reperfusion induced injury?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTrehalose, naturally occurring disaccharide, has been reported to prevent postoperative abdominal adhesions in animal models. We investigated whether trehalose affects the function of human polymorphonuclear neutrophils (PMNs) in vitro to assess the feasibility of its clinical application as an anti-adhesive barrier. Human PMNs were obtained from 17 healthy volunteers. Escherichia coli and Staphylococcus aureus were used for the bacterial infection model, whereas lipopolysaccharide (LPS) and interleukin (IL)-1β were used for inflammation induction model. The PMN phagocytosis rates of bacteria and apoptosis/necrosis were assessed on trehalose, maltose, and control media. Cytokines; namely, tumor necrosis factor-α, IL-1α, IL-1Ra, IL-6, and IL-8; and PMN-elastase were measured on each medium in both models. There were no significant differences in the phagocytosis rates, apoptosis/necrosis rates, or levels of all cytokines or PMN-elastase among the three media in the bacterial infection model. There were also no significant differences in the levels of all cytokines and PMN-elastase among the three media in the IL-1β inflammation induction model. PMN-elastase was lower in trehalose and maltose medium after LPS stimulation, at 3 and 24 h.\n\nQuestion:\nDoes trehalose affect the functions of human neutrophils in vitro?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis study aimed to clarify the correlation between the myocardial washout rate (WR) of technetium-99m hexakis 2-methoxy-isobutyl-isonitrile ((99m)Tc-sestamibi) and cardiac enzyme levels in patients with acute myocardial infarction (AMI) 6 months after the onset. Sixty-one consecutive AMI patients (mean age, 66.2 ± 9.7 years) who underwent percutaneous coronary intervention (PCI) on admission were enrolled. Creatinine kinase MB isoenzyme (CK-MB) levels were measured every 3 h. (99m)Tc-sestamibi myocardial scintigraphic images were obtained at the early (30 min) and delayed (4 h) phases after tracer injection for calculating heart-to-mediastinum (H/M) ratios and global WRs at 2 weeks (0 M) and 6 months (6 M) after the onset of AMI. Regional WRs in the culprit lesions (culprit WR) and the extent score (ES) and severity score (SS) of myocardial damage were also calculated. PCI was performed 8.3 ± 7.7 h after AMI onset. At 6 M, the early H/M ratio (p = 0.04), delayed H/M ratio (p = 0.02), global WR (p = 0.01), culprit WR (p = 0.002), and delayed ES (p = 0.008) were alleviated. At 0 M, the peak CK-MB level correlated with the delayed H/M ratio (p = 0.003), global WR (p = 0.003), culprit WR (p < 0.001), early ES (p = 0.03), delayed ES (p = 0.01), early SS (p = 0.001), and delayed SS (p < 0.001). At 6 M, the peak CK-MB level correlated with the delayed H/M ratio (p < 0.001), global WR (p = 0.005), culprit WR (p = 0.001), early ES (p = 0.001), delayed ES (p < 0.001), early SS (p < 0.001), and delayed SS (p < 0.001).\n\nQuestion:\nDoes myocardial washout rate of technetium-99m-sestamibi in the chronic phase predict myocardial damage in patients with previous myocardial infarction?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMurine Leukemia Virus (MLV) is a rodent gammaretrovirus that serves as the backbone for common gene delivery tools designed for experimental and therapeutic applications. Recently, an infectious gammaretrovirus designated XMRV has been identified in prostate cancer patients. The similarity between the MLV and XMRV genomes suggests a possibility that the two viruses may interact when present in the same cell. We tested the ability of XMRV to complement replication-deficient MLV vectors upon co-infection of cultured human cells. We observed that XMRV can facilitate the spread of these vectors from infected to uninfected cells. This functional complementation occurred without any gross rearrangements in the vector structure, and the co-infected cells produced as many as 10(4) infectious vector particles per milliliter of culture medium.\n\nQuestion:\nDoes a natural human retrovirus efficiently complement vectors based on murine leukemia virus?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo evaluate the performance of an extubation readiness test based on a spontaneous breathing trial using pressure support. Retrospective chart review. Pediatric intensive care unit. All infants and children admitted to the pediatric intensive care unit requiring intubation from July 2007 to December 2008 were eligible for this study. Routine use of an extubation readiness test using pressure support set according to endotracheal tube size to determine completion of weaning and readiness for extubation. A total of 755 extubation readiness tests were performed in 538 patients with a pass rate of 83%. Of 500 children who passed the extubation readiness test and were extubated without planned noninvasive ventilation use, the extubation failure rate was 11.2% (5.8% required reintubation). Extubation failure was defined as need for noninvasive ventilation or reintubation within 24 hrs of planned extubation. Logistic regression analysis revealed a significant association between duration of mechanical ventilation and extubation failure. Children ventilated for over 48 hrs had an 18.5% failure rate despite passing an extubation readiness test before extubation and the extubation readiness test was not a significant predictor of extubation success. Most extubation failures were the result of inadequate gas exchange attributable to lower respiratory tract dysfunction.\n\nQuestion:\nDoes a spontaneous breathing trial with pressure support overestimate readiness for extubation in children?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe Affymetrix Drug Metabolizing Enzymes and Transporters (DMET) Plus Premier Pack has been designed to genotype 1936 gene variants thought to be essential for screening patients in personalized drug therapy. These variants include the cytochrome P450s (CYP450s), the key metabolizing enzymes, many other enzymes involved in phase I and phase II pharmacokinetic reactions, and signaling mediators associated with variability in clinical response to numerous drugs not only among individuals, but also between ethnic populations. We genotyped 600 Saudi individuals for 1936 variants on the DMET platform to evaluate their clinical potential in personalized medicine in ethnic Arabs. Approximately 49% each of the 437 CYP450 variants, 56% of the 581 transporters, 56% of 419 transferases, 48% of the 104 dehydrogenases, and 58% of the remaining 390 variants were detected. Several variants, such as rs3740071, rs6193, rs258751, rs6199, rs11568421, and rs8187797, exhibited significantly either higher or lower minor allele frequencies (MAFs) than those in other ethnic groups.\n\nQuestion:\nDoes the Affymetrix DMET Plus platform reveal unique distribution of ADME-related variants in ethnic Arabs?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]