Datasets:

YBXL
/

PubmedQA_train

Dataset card Data Studio Files Files and versions Community

Split (3)

train · 211k rows

Subsets and Splits

No community queries yet

The top public SQL queries from the community will appear here once available.

id stringlengths 9 14	conversations listlengths 2 2	text stringlengths 231 5.9k
PubmedQA74100	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Telemetry monitoring is a widely used, labor-intensive, and often-limited resource. Little is known of the effectiveness of methods to guide appropriate use. Our intervention for appropriate use included: (1) a hospitalist-led, daily review of bed utilization, (2) hospitalist-driven education module for trainees, (3) quarterly feedback of telemetry usage, and (4) financial incentives. Hospitalists were encouraged to discuss daily telemetry utilization on rounds. A module on appropriate telemetry usage was taught by hospitalists during the intervention period (January 2013-August 2013) on medicine wards. Pre- and post-evaluations measured changes regarding telemetry use. We compared hospital bed-use data between the baseline period (January 2012-December 2012), intervention period, and extension period (September 2014-March 2015). During the intervention period, hospital bed-use data were sent to the hospitalist group quarterly. Financial incentives were provided after a decrease in hospitalist telemetry utilization. Stanford Hospital, a 444-bed, academic medical center in Stanford, California. Hospitalists saw reductions for both length of stay (LOS) (2.75 vs 2.13 days, P = 0.005) and total cost (22.5% reduction) for telemetry bed utilization in the intervention period. Nonhospitalists telemetry bed utilization remained unchanged. We saw significant improvements in trainee knowledge of the most cost-saving action (P = 0.002) and the least cost-saving action (P = 0.003) in the pre- and post-evaluation analyses. Results were sustained in the hospitalist group, with telemetry LOS of 1.93 days in the extension period.\n Question: Does hospitalist intervention for appropriate use of telemetry reduce length of stay and cost?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Telemetry monitoring is a widely used, labor-intensive, and often-limited resource. Little is known of the effectiveness of methods to guide appropriate use. Our intervention for appropriate use included: (1) a hospitalist-led, daily review of bed utilization, (2) hospitalist-driven education module for trainees, (3) quarterly feedback of telemetry usage, and (4) financial incentives. Hospitalists were encouraged to discuss daily telemetry utilization on rounds. A module on appropriate telemetry usage was taught by hospitalists during the intervention period (January 2013-August 2013) on medicine wards. Pre- and post-evaluations measured changes regarding telemetry use. We compared hospital bed-use data between the baseline period (January 2012-December 2012), intervention period, and extension period (September 2014-March 2015). During the intervention period, hospital bed-use data were sent to the hospitalist group quarterly. Financial incentives were provided after a decrease in hospitalist telemetry utilization. Stanford Hospital, a 444-bed, academic medical center in Stanford, California. Hospitalists saw reductions for both length of stay (LOS) (2.75 vs 2.13 days, P = 0.005) and total cost (22.5% reduction) for telemetry bed utilization in the intervention period. Nonhospitalists telemetry bed utilization remained unchanged. We saw significant improvements in trainee knowledge of the most cost-saving action (P = 0.002) and the least cost-saving action (P = 0.003) in the pre- and post-evaluation analyses. Results were sustained in the hospitalist group, with telemetry LOS of 1.93 days in the extension period. Question: Does hospitalist intervention for appropriate use of telemetry reduce length of stay and cost? Output:
PubmedQA107403	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: HbA(1c) variability has been shown to be an independent risk factor for nephropathy in patients with type 1 diabetes. In this study, we aimed to explore the association between HbA(1c) variability and microalbuminuria development in patients with type 2 diabetes. We also intended to test the applicability of serially measured HbA(1c) over 2 years for this risk assessment. Between 2003 and 2005, we recruited 821 middle-aged normoalbuminuric individuals with type 2 diabetes and followed them through to the end of 2010. The average follow-up time was 6.2 years. We defined microalbuminuria as a urine albumin to creatinine ratio of 30 mg/g (3.4 mg/mmol) or higher. HbA(1c) variability was calculated by the SD of serially measured HbA(1c). The Cox proportional hazards model was used to evaluate the association between HbA(1c) SD quartile and development of microalbuminuria. The incidence of microalbuminuria for the overall population was 58.4, 58.6, 60.8 and 91.9 per 1,000 person-years for Q1- to Q4-adjusted HbA(1c) SD, respectively (p for trend = 0.042). Compared with patients in Q1, those in Q4 were about 37% more likely to develop microalbuminuria. The HR derived from a series of 2 year HbA(1c) measurements was similar to that from data collection for longer than 4 years.\n Question: Is hbA1c variability associated with microalbuminuria development in type 2 diabetes : a 7-year prospective cohort study?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: HbA(1c) variability has been shown to be an independent risk factor for nephropathy in patients with type 1 diabetes. In this study, we aimed to explore the association between HbA(1c) variability and microalbuminuria development in patients with type 2 diabetes. We also intended to test the applicability of serially measured HbA(1c) over 2 years for this risk assessment. Between 2003 and 2005, we recruited 821 middle-aged normoalbuminuric individuals with type 2 diabetes and followed them through to the end of 2010. The average follow-up time was 6.2 years. We defined microalbuminuria as a urine albumin to creatinine ratio of 30 mg/g (3.4 mg/mmol) or higher. HbA(1c) variability was calculated by the SD of serially measured HbA(1c). The Cox proportional hazards model was used to evaluate the association between HbA(1c) SD quartile and development of microalbuminuria. The incidence of microalbuminuria for the overall population was 58.4, 58.6, 60.8 and 91.9 per 1,000 person-years for Q1- to Q4-adjusted HbA(1c) SD, respectively (p for trend = 0.042). Compared with patients in Q1, those in Q4 were about 37% more likely to develop microalbuminuria. The HR derived from a series of 2 year HbA(1c) measurements was similar to that from data collection for longer than 4 years. Question: Is hbA1c variability associated with microalbuminuria development in type 2 diabetes : a 7-year prospective cohort study? Output:
PubmedQA191584	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Oligodeoxynucleotides (ODNs) containing the dinucleotide CpG in a specific sequence context (CpG-ODNs) have the ability to prevent the development of eosinophilic airway inflammation and bronchial hyperreactivity in a murine model of asthma. We have previously demonstrated that CpG-ODNs stimulate expression of the T(H1)-inducing cytokines IFN-gamma and IL-12 in a murine model of asthma and that this stimulation is associated with the protection against asthmatic inflammation. The purpose of this study was to examine whether the protection conferred by CpG-ODNs in a schistosome egg-egg antigen murine model of asthma is dependent on the induction of IFN-gamma, IL-12, or both. C57BL/6 mice were sensitized to schistosome eggs in the presence or absence of CpG-ODNs or control ODNs and then stimulated with soluble egg antigen in the airway. The protection offered by CpG-ODNs in these mice was compared with the protection induced by CpG-ODNs in IL-12 and IFN-gamma knockout mice and in mice treated with anticytokine blocking antibodies. Double-knockout mice (IL-12/IFN-gamma) were also generated and used in these studies. Determinations included airway eosinophilic inflammation and bronchial hyperreactivity to inhaled methacholine. We found that CpG-ODNs confer protection against both airway eosinophilia and bronchial hyperreactivity in the absence of IFN-gamma or IL-12 or in the presence of both cytokines together. However, in the absence of either IL-12 or IFN-gamma, mice require 10 times as much CpG-ODNs to be protected against the induction of airway eosinophilia. The T(H2) cytokines IL-4 and IL-5 were reduced in all of the CpG-treated mice, although less in the absence of IL-12 and IFN-gamma.\n Question: Do cpG oligodeoxynucleotides require TH1 cytokines to prevent eosinophilic airway inflammation in a murine model of asthma?\n Output: " }, { "role": "assistant", "content": "no" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Oligodeoxynucleotides (ODNs) containing the dinucleotide CpG in a specific sequence context (CpG-ODNs) have the ability to prevent the development of eosinophilic airway inflammation and bronchial hyperreactivity in a murine model of asthma. We have previously demonstrated that CpG-ODNs stimulate expression of the T(H1)-inducing cytokines IFN-gamma and IL-12 in a murine model of asthma and that this stimulation is associated with the protection against asthmatic inflammation. The purpose of this study was to examine whether the protection conferred by CpG-ODNs in a schistosome egg-egg antigen murine model of asthma is dependent on the induction of IFN-gamma, IL-12, or both. C57BL/6 mice were sensitized to schistosome eggs in the presence or absence of CpG-ODNs or control ODNs and then stimulated with soluble egg antigen in the airway. The protection offered by CpG-ODNs in these mice was compared with the protection induced by CpG-ODNs in IL-12 and IFN-gamma knockout mice and in mice treated with anticytokine blocking antibodies. Double-knockout mice (IL-12/IFN-gamma) were also generated and used in these studies. Determinations included airway eosinophilic inflammation and bronchial hyperreactivity to inhaled methacholine. We found that CpG-ODNs confer protection against both airway eosinophilia and bronchial hyperreactivity in the absence of IFN-gamma or IL-12 or in the presence of both cytokines together. However, in the absence of either IL-12 or IFN-gamma, mice require 10 times as much CpG-ODNs to be protected against the induction of airway eosinophilia. The T(H2) cytokines IL-4 and IL-5 were reduced in all of the CpG-treated mice, although less in the absence of IL-12 and IFN-gamma. Question: Do cpG oligodeoxynucleotides require TH1 cytokines to prevent eosinophilic airway inflammation in a murine model of asthma? Output:
PubmedQA200212	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Although perianal streptococcal dermatitis (PSD) is well known in children, it has only rarely been documented in adults. The incidence and necessity for treatment may be underestimated. We have retrospectively identified adult patients with perianal streptococcal dermatitis. Patients with streptococcal anal dermatitis were identified from a prospective office database. Treatment was with oral antibiotics according to the organism sensitivity. Additional concomitant anorectal disease was treated according to standard guidelines. Patients were compared with a control group, without eczema or erythema, for the presence of β-haemolysing Streptococci on perianal swab. Demographic and microbiological data were assessed and compared between and within treatment and control groups. Fifty-three (22 female) patients older than 20 (mean = 49) years of age were diagnosed with perianal streptococcal dermatitis between 2005 and 2009. In most cases group B β-haemolytic Streptococci were found. Fifty patients received antibiotics for 14 days. In 28 of 33 patients who had a post-treatment swab, the result was negative. Five patients showed Streptococci of different groups in the post-treatment swab. Of the 50 patients, 21 (42%) had no further anorectal complaint and 29 (58%) required continuing treatment for another anorectal condition. In the control group β-haemolysing Streptococcus was found in 34%. Men over 60 years of age more often required no further anorectal treatment compared with women (P < 0.05).\n Question: Is perianal streptococcal dermatitis in adults : its association with pruritic anorectal diseases mainly caused by group B Streptococci?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Although perianal streptococcal dermatitis (PSD) is well known in children, it has only rarely been documented in adults. The incidence and necessity for treatment may be underestimated. We have retrospectively identified adult patients with perianal streptococcal dermatitis. Patients with streptococcal anal dermatitis were identified from a prospective office database. Treatment was with oral antibiotics according to the organism sensitivity. Additional concomitant anorectal disease was treated according to standard guidelines. Patients were compared with a control group, without eczema or erythema, for the presence of β-haemolysing Streptococci on perianal swab. Demographic and microbiological data were assessed and compared between and within treatment and control groups. Fifty-three (22 female) patients older than 20 (mean = 49) years of age were diagnosed with perianal streptococcal dermatitis between 2005 and 2009. In most cases group B β-haemolytic Streptococci were found. Fifty patients received antibiotics for 14 days. In 28 of 33 patients who had a post-treatment swab, the result was negative. Five patients showed Streptococci of different groups in the post-treatment swab. Of the 50 patients, 21 (42%) had no further anorectal complaint and 29 (58%) required continuing treatment for another anorectal condition. In the control group β-haemolysing Streptococcus was found in 34%. Men over 60 years of age more often required no further anorectal treatment compared with women (P < 0.05). Question: Is perianal streptococcal dermatitis in adults : its association with pruritic anorectal diseases mainly caused by group B Streptococci? Output:
PubmedQA142491	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The ABCC8 gene encodes the sulfonylurea receptor 1 (SUR1) subunit of the pancreatic beta cell ATP-sensitive potassium (K(ATP)) channel. Inactivating mutations cause congenital hyperinsulinism (CHI) and activating mutations cause transient neonatal diabetes (TNDM) or permanent neonatal diabetes (PNDM) that can usually be treated with sulfonylureas. Sulfonylurea sensitivity is also a feature of HNF1A and HNF4A MODY, but patients referred for genetic testing with clinical features of these types of diabetes do not always have mutations in the HNF1A/4A genes. Our aim was to establish whether mutations in the ABCC8 gene cause MODY that is responsive to sulfonylurea therapy. We sequenced the ABCC8 gene in 85 patients with a BMI <30 kg/m², no family history of neonatal diabetes and who were deemed sensitive to sulfonylureas by the referring clinician or were sulfonylurea-treated. All had tested negative for mutations in the HNF1A and HNF4A genes. ABCC8 mutations were found in seven of the 85 (8%) probands. Four patients were heterozygous for previously reported mutations and four novel mutations, E100K, G214R, Q485R and N1245D, were identified. Only four probands fulfilled MODY criteria, with two diagnosed after 25 years and one patient, who had no family history of diabetes, as a result of a proven de novo mutation.\n Question: Are heterozygous ABCC8 mutations a cause of MODY?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The ABCC8 gene encodes the sulfonylurea receptor 1 (SUR1) subunit of the pancreatic beta cell ATP-sensitive potassium (K(ATP)) channel. Inactivating mutations cause congenital hyperinsulinism (CHI) and activating mutations cause transient neonatal diabetes (TNDM) or permanent neonatal diabetes (PNDM) that can usually be treated with sulfonylureas. Sulfonylurea sensitivity is also a feature of HNF1A and HNF4A MODY, but patients referred for genetic testing with clinical features of these types of diabetes do not always have mutations in the HNF1A/4A genes. Our aim was to establish whether mutations in the ABCC8 gene cause MODY that is responsive to sulfonylurea therapy. We sequenced the ABCC8 gene in 85 patients with a BMI <30 kg/m², no family history of neonatal diabetes and who were deemed sensitive to sulfonylureas by the referring clinician or were sulfonylurea-treated. All had tested negative for mutations in the HNF1A and HNF4A genes. ABCC8 mutations were found in seven of the 85 (8%) probands. Four patients were heterozygous for previously reported mutations and four novel mutations, E100K, G214R, Q485R and N1245D, were identified. Only four probands fulfilled MODY criteria, with two diagnosed after 25 years and one patient, who had no family history of diabetes, as a result of a proven de novo mutation. Question: Are heterozygous ABCC8 mutations a cause of MODY? Output:
PubmedQA99594	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Even with the improvements in surgical techniques and perioperative care, obesity is still a risk factor for occurrence of adverse events following cardiac surgery. In this observational, retrospective study, we aimed to document the effects of obesity on surgical outcomes in patients undergoing coronary artery bypass surgery and find out the effects of improvements in cardiac surgery. Between January 2011 and March 2013, isolated coronary artery bypass surgery was performed on 790 patients. The body mass index values of the patients were calculated and patients were divided into two groups; below 30 were classified as non-obese group whereas above 30 were classified as obese group. The odds ratio was obtained by using univariate analysis in order to document the effects of obesity on outcomes. There were 548 (69.3%) patients in non-obese group, whereas 242 (30.7%) patients in obese group. The cardiopulmonary bypass (80.47±23.58 vs. 80.89±28.46, p=0.449) and aortic clamp times (54.13±16.60 vs. 54.19±19.85, p=0.511) and number of bypass grafts (3.09±1.02 vs. 2.96±1.00, p=0.11) were comparable between the groups. The mean number of fresh frozen plasma used was higher in obese patients (1.37±1.75 vs. 1.48±4.63, p=0.02). Intubation time was higher in obese patients (10.57±6.87 vs. 12.71±35.31, p=0.014). Total amount of postoperative drainage was higher in non-obese patients (766.77±472.27 vs. 648.72±371.39, p<0.001). The superficial infection/mediastenitis (0.4% vs. 2.5%, p=0.012), dehiscence (0.2% vs. 3.7%, p<0.001) and postoperative renal failure rates (4.7% vs. 8.7%, p=0.031) were higher in obese patients. The incidence of atrial fibrillation was lower in obese patients (19.7% vs. 12.8%, p=0.019). The mortality (0.5% vs. 1.7%, p=0.210) and postoperative stroke rates (1.1% vs. 0.8%, p=1.000) were similar in both groups.\n Question: Is obesity still a risk factor in coronary artery bypass surgery?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Even with the improvements in surgical techniques and perioperative care, obesity is still a risk factor for occurrence of adverse events following cardiac surgery. In this observational, retrospective study, we aimed to document the effects of obesity on surgical outcomes in patients undergoing coronary artery bypass surgery and find out the effects of improvements in cardiac surgery. Between January 2011 and March 2013, isolated coronary artery bypass surgery was performed on 790 patients. The body mass index values of the patients were calculated and patients were divided into two groups; below 30 were classified as non-obese group whereas above 30 were classified as obese group. The odds ratio was obtained by using univariate analysis in order to document the effects of obesity on outcomes. There were 548 (69.3%) patients in non-obese group, whereas 242 (30.7%) patients in obese group. The cardiopulmonary bypass (80.47±23.58 vs. 80.89±28.46, p=0.449) and aortic clamp times (54.13±16.60 vs. 54.19±19.85, p=0.511) and number of bypass grafts (3.09±1.02 vs. 2.96±1.00, p=0.11) were comparable between the groups. The mean number of fresh frozen plasma used was higher in obese patients (1.37±1.75 vs. 1.48±4.63, p=0.02). Intubation time was higher in obese patients (10.57±6.87 vs. 12.71±35.31, p=0.014). Total amount of postoperative drainage was higher in non-obese patients (766.77±472.27 vs. 648.72±371.39, p<0.001). The superficial infection/mediastenitis (0.4% vs. 2.5%, p=0.012), dehiscence (0.2% vs. 3.7%, p<0.001) and postoperative renal failure rates (4.7% vs. 8.7%, p=0.031) were higher in obese patients. The incidence of atrial fibrillation was lower in obese patients (19.7% vs. 12.8%, p=0.019). The mortality (0.5% vs. 1.7%, p=0.210) and postoperative stroke rates (1.1% vs. 0.8%, p=1.000) were similar in both groups. Question: Is obesity still a risk factor in coronary artery bypass surgery? Output:
PubmedQA58307	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Albumin and prealbumin are associated with nutritional status and inflammatory status. Each has a residual effect on mortality outcomes when included in regression models that include the other. Prealbumin is increased in the obese mouse model as a consequence of stabilization of prealbumin by retinol binding protein 4 (RBP4) secreted by adipocytes. We carried out this study to establish the contribution of adiposity to prealbumin levels in prevalent patients receiving dialysis and the relationship of prealbumin to RBP4. We determined whether prealbumin was associated with adiposity in patients receiving hemodialysis (HD), controlling for the effects of inflammation and nutrition. We evaluated body composition in 48 prevalent patients receiving HD by magnetic resonance imaging (MRI), measuring total skeletal muscle mass (SM), visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), and serum albumin, prealbumin, RBP4, and interleukin-6 (IL-6) levels. We used normalized protein catabolic rate (nPCR) to report nutrition and separately analyzed the determinants of albumin and then of prealbumin by multiple stepwise regression. Thirty-two patients were women, 16 patients were diabetic, and median age and body mass index were 54.5 and 27.3 kg/m(2), respectively. Median total adipose tissue (TAT) was 24.3 kg and VAT was 3.25 kg. Prealbumin was positively associated with VAT, nPCR, and RBP4 and was negatively associated with IL-6; r(2) for the model was 0.64. By contrast, albumin was positively associated with nPCR and negatively associated with IL-6 but not with any measure of adiposity (r(2) for the model = 0.2).\n Question: Is prealbumin associated with visceral fat mass in patients receiving hemodialysis?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Albumin and prealbumin are associated with nutritional status and inflammatory status. Each has a residual effect on mortality outcomes when included in regression models that include the other. Prealbumin is increased in the obese mouse model as a consequence of stabilization of prealbumin by retinol binding protein 4 (RBP4) secreted by adipocytes. We carried out this study to establish the contribution of adiposity to prealbumin levels in prevalent patients receiving dialysis and the relationship of prealbumin to RBP4. We determined whether prealbumin was associated with adiposity in patients receiving hemodialysis (HD), controlling for the effects of inflammation and nutrition. We evaluated body composition in 48 prevalent patients receiving HD by magnetic resonance imaging (MRI), measuring total skeletal muscle mass (SM), visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), and serum albumin, prealbumin, RBP4, and interleukin-6 (IL-6) levels. We used normalized protein catabolic rate (nPCR) to report nutrition and separately analyzed the determinants of albumin and then of prealbumin by multiple stepwise regression. Thirty-two patients were women, 16 patients were diabetic, and median age and body mass index were 54.5 and 27.3 kg/m(2), respectively. Median total adipose tissue (TAT) was 24.3 kg and VAT was 3.25 kg. Prealbumin was positively associated with VAT, nPCR, and RBP4 and was negatively associated with IL-6; r(2) for the model was 0.64. By contrast, albumin was positively associated with nPCR and negatively associated with IL-6 but not with any measure of adiposity (r(2) for the model = 0.2). Question: Is prealbumin associated with visceral fat mass in patients receiving hemodialysis? Output:
PubmedQA151456	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Both oxidative stress and endoplasmic reticulum stress (ER stress) are causal events in diabetic embryopathy. We tested whether oxidative stress causes ER stress. Wild-type (WT) and superoxide dismutase 1 (SOD1)-overexpressing day 8.75 embryos from nondiabetic WT control with SOD1 transgenic male and diabetic WT female with SOD1 transgenic male were analyzed for ER stress markers: C/EBP-homologous protein (CHOP), calnexin, eukaryotic initiation factor 2α (eIF2α), protein kinase ribonucleic acid (RNA)-like ER kinase (PERK), binding immunoglobulin protein, protein disulfide isomerase family A member 3, kinases inositol-requiring protein-1α (IRE1α), and the X-box binding protein (XBP1) messenger RNA (mRNA) splicing. Maternal diabetes significantly increased the levels of CHOP, calnexin, phosphorylated (p)-eIF2α, p-PERK, and p-IRE1α; triggered XBP1 mRNA splicing; and enhanced ER chaperone gene expression in WT embryos. SOD1 overexpression blocked these diabetes-induced ER stress markers.\n Question: Does superoxide dismutase 1 overexpression in mice abolish maternal diabetes-induced endoplasmic reticulum stress in diabetic embryopathy?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Both oxidative stress and endoplasmic reticulum stress (ER stress) are causal events in diabetic embryopathy. We tested whether oxidative stress causes ER stress. Wild-type (WT) and superoxide dismutase 1 (SOD1)-overexpressing day 8.75 embryos from nondiabetic WT control with SOD1 transgenic male and diabetic WT female with SOD1 transgenic male were analyzed for ER stress markers: C/EBP-homologous protein (CHOP), calnexin, eukaryotic initiation factor 2α (eIF2α), protein kinase ribonucleic acid (RNA)-like ER kinase (PERK), binding immunoglobulin protein, protein disulfide isomerase family A member 3, kinases inositol-requiring protein-1α (IRE1α), and the X-box binding protein (XBP1) messenger RNA (mRNA) splicing. Maternal diabetes significantly increased the levels of CHOP, calnexin, phosphorylated (p)-eIF2α, p-PERK, and p-IRE1α; triggered XBP1 mRNA splicing; and enhanced ER chaperone gene expression in WT embryos. SOD1 overexpression blocked these diabetes-induced ER stress markers. Question: Does superoxide dismutase 1 overexpression in mice abolish maternal diabetes-induced endoplasmic reticulum stress in diabetic embryopathy? Output:
PubmedQA31556	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Sphingosine-1-phosphate (S1P) regulates the egress of T cells from lymphoid organs; levels of S1P in the tissues are controlled by S1P lyase (Sgpl1). Hence, Sgpl1 offers a target to block T cell-dependent inflammatory processes. However, the involvement of Sgpl1 in models of disease has not been fully elucidated yet, since Sgpl1 KO mice have a short life-span. We generated inducible Sgpl1 KO mice featuring partial reduction of Sgpl1 activity and analyzed them with respect to sphingolipid levels, T-cell distribution, and response in models of inflammation. The partially Sgpl1 deficient mice are viable but feature profound reduction of peripheral T cells, similar to the constitutive KO mice. While thymic T cell development in these mice appears normal, mature T cells are retained in thymus and lymph nodes, leading to reduced T cell numbers in spleen and blood, with a skewing towards increased proportions of memory T cells and T regulatory cells. The therapeutic relevance of Sgpl1 is demonstrated by the fact that the inducible KO mice are protected in experimental autoimmune encephalomyelitis (EAE). T cell immigration into the CNS was found to be profoundly reduced. Since S1P levels in the brain of the animals are unchanged, we conclude that protection in EAE is due to the peripheral effect on T cells, leading to reduced CNS immigration, rather than on local effects in the CNS.\n Question: Does partial deficiency of sphingosine-1-phosphate lyase confer protection in experimental autoimmune encephalomyelitis?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Sphingosine-1-phosphate (S1P) regulates the egress of T cells from lymphoid organs; levels of S1P in the tissues are controlled by S1P lyase (Sgpl1). Hence, Sgpl1 offers a target to block T cell-dependent inflammatory processes. However, the involvement of Sgpl1 in models of disease has not been fully elucidated yet, since Sgpl1 KO mice have a short life-span. We generated inducible Sgpl1 KO mice featuring partial reduction of Sgpl1 activity and analyzed them with respect to sphingolipid levels, T-cell distribution, and response in models of inflammation. The partially Sgpl1 deficient mice are viable but feature profound reduction of peripheral T cells, similar to the constitutive KO mice. While thymic T cell development in these mice appears normal, mature T cells are retained in thymus and lymph nodes, leading to reduced T cell numbers in spleen and blood, with a skewing towards increased proportions of memory T cells and T regulatory cells. The therapeutic relevance of Sgpl1 is demonstrated by the fact that the inducible KO mice are protected in experimental autoimmune encephalomyelitis (EAE). T cell immigration into the CNS was found to be profoundly reduced. Since S1P levels in the brain of the animals are unchanged, we conclude that protection in EAE is due to the peripheral effect on T cells, leading to reduced CNS immigration, rather than on local effects in the CNS. Question: Does partial deficiency of sphingosine-1-phosphate lyase confer protection in experimental autoimmune encephalomyelitis? Output:
PubmedQA1439	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Hypocalcemia is the most common complication after total thyroidectomy. Some patients need to stay in the hospital for monitoring of hypocalcemic symptoms and serum calcium levels for several days. We investigated the efficacy and safety of using early postoperative parathyroid hormone (PTH) results for early discharge after thyroidectomy. A retrospective cohort study of 2 sequential groups of patients undergoing total thyroidectomy between January 2010 and March 2013 was undertaken. Patients were divided into 2 groups. In Group 1 (before June 2011), patients had daily monitoring of serum calcium level and hypocalcemic symptoms. They were discharged when calcium level was static and asymptomatic. Postoperative PTH was not utilized for discharge plan. In Group 2 (after June 2011), postoperative PTH and calcium level on day 1 were utilized to dictate subsequent management and discharge plan. Of the 107 patients reviewed, 54 (50.5%) were in Group 1 and 53 (49.5%) were in Group 2. A total of 51 (47.7%) patients developed hypocalcemia. The two groups were comparable in demographic data, early postoperative PTH value, rate of hypocalcemia, the need for oral calcium and vitamin D supplements and rate of permanent hypoparathyroidism. Fewer patients in Group 2 experienced hypocalcemic symptoms, p=0.005. None of the patients in Group 2 needed intravenous calcium supplement (p=0.003). The median postoperative hospital stay for Group 1 was 4 days and for Group 2 was 1 day (p<0.0001).\n Question: Does postoperative PTH monitoring of hypocalcemia expedite discharge after thyroidectomy?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Hypocalcemia is the most common complication after total thyroidectomy. Some patients need to stay in the hospital for monitoring of hypocalcemic symptoms and serum calcium levels for several days. We investigated the efficacy and safety of using early postoperative parathyroid hormone (PTH) results for early discharge after thyroidectomy. A retrospective cohort study of 2 sequential groups of patients undergoing total thyroidectomy between January 2010 and March 2013 was undertaken. Patients were divided into 2 groups. In Group 1 (before June 2011), patients had daily monitoring of serum calcium level and hypocalcemic symptoms. They were discharged when calcium level was static and asymptomatic. Postoperative PTH was not utilized for discharge plan. In Group 2 (after June 2011), postoperative PTH and calcium level on day 1 were utilized to dictate subsequent management and discharge plan. Of the 107 patients reviewed, 54 (50.5%) were in Group 1 and 53 (49.5%) were in Group 2. A total of 51 (47.7%) patients developed hypocalcemia. The two groups were comparable in demographic data, early postoperative PTH value, rate of hypocalcemia, the need for oral calcium and vitamin D supplements and rate of permanent hypoparathyroidism. Fewer patients in Group 2 experienced hypocalcemic symptoms, p=0.005. None of the patients in Group 2 needed intravenous calcium supplement (p=0.003). The median postoperative hospital stay for Group 1 was 4 days and for Group 2 was 1 day (p<0.0001). Question: Does postoperative PTH monitoring of hypocalcemia expedite discharge after thyroidectomy? Output:
PubmedQA1612	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Progressive familial intrahepatic cholestasis type 2 (PFIC2) is an autosomal recessive disease due to mutations in ABCB11. ABCB11 encodes the bile salt export pump (BSEP), the major transporter responsible for biliary bile acid secretion, which expression is restricted to hepatocytes. In some patients, molecular analysis of ABCB11 revealed either exonic or intronic variations - including common polymorphisms - predicted to affect splicing according to in silico analysis or in vitro minigene studies. Transcript analysis in liver tissue is the best way to determine whether the variations predicted to affect splicing are deleterious or not. We performed ABCB11 transcript analysis in liver tissue from five PFIC2 patients who had variations which were predicted to either affect splicing or not. Among eleven variants tested, only the silent c.3003A>G variant and the intronic c.3213+4A>G variant led to abnormal splicing as suggested by in silico analysis.\n Question: Does liver transcript analysis reveal aberrant splicing due to silent and intronic variations in the ABCB11 gene?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Progressive familial intrahepatic cholestasis type 2 (PFIC2) is an autosomal recessive disease due to mutations in ABCB11. ABCB11 encodes the bile salt export pump (BSEP), the major transporter responsible for biliary bile acid secretion, which expression is restricted to hepatocytes. In some patients, molecular analysis of ABCB11 revealed either exonic or intronic variations - including common polymorphisms - predicted to affect splicing according to in silico analysis or in vitro minigene studies. Transcript analysis in liver tissue is the best way to determine whether the variations predicted to affect splicing are deleterious or not. We performed ABCB11 transcript analysis in liver tissue from five PFIC2 patients who had variations which were predicted to either affect splicing or not. Among eleven variants tested, only the silent c.3003A>G variant and the intronic c.3213+4A>G variant led to abnormal splicing as suggested by in silico analysis. Question: Does liver transcript analysis reveal aberrant splicing due to silent and intronic variations in the ABCB11 gene? Output:
PubmedQA120500	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The present study was designed to investigate the potential association between the 981C>T polymorphism in protein tyrosine phosphatase 1B (PTP-1B) and coronary artery disease (CAD). We conducted a hospital-based case-control study with 864 CAD patients and 1008 controls to explore the association between the PTP-1B 981C>T polymorphism and risk of CAD in Chinese Han population. Subjects with the variant genotypes (CT+TT) had a 52% decreased risk of CAD relative to CC carriers (adjusted odds ratio, 0.48; 95% confidence interval, 0.39-0.60). The 981C>T polymorphism was associated with a higher body mass index and serum triglyceride levels in both CAD patients and controls. Moreover, this polymorphism was found to be associated with a lower serum glucose levels in cases, but not in controls.\n Question: Is the 981C > T polymorphism in protein tyrosine phosphatase 1B associated with decreased risk of coronary artery disease in Chinese Han population?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The present study was designed to investigate the potential association between the 981C>T polymorphism in protein tyrosine phosphatase 1B (PTP-1B) and coronary artery disease (CAD). We conducted a hospital-based case-control study with 864 CAD patients and 1008 controls to explore the association between the PTP-1B 981C>T polymorphism and risk of CAD in Chinese Han population. Subjects with the variant genotypes (CT+TT) had a 52% decreased risk of CAD relative to CC carriers (adjusted odds ratio, 0.48; 95% confidence interval, 0.39-0.60). The 981C>T polymorphism was associated with a higher body mass index and serum triglyceride levels in both CAD patients and controls. Moreover, this polymorphism was found to be associated with a lower serum glucose levels in cases, but not in controls. Question: Is the 981C > T polymorphism in protein tyrosine phosphatase 1B associated with decreased risk of coronary artery disease in Chinese Han population? Output:
PubmedQA29983	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: One of the major tenets in breast cancer research is that early detection is vital for patient survival by increasing treatment options. To that end, we have previously used a novel unsupervised approach to identify a set of genes whose expression predicts prognosis of breast cancer patients. The predictive genes were selected in a well-defined three dimensional (3D) cell culture model of non-malignant human mammary epithelial cell morphogenesis as down-regulated during breast epithelial cell acinar formation and cell cycle arrest. Here we examine the ability of this gene signature (3D-signature) to predict prognosis in three independent breast cancer microarray datasets having 295, 286, and 118 samples, respectively. Our results show that the 3D-signature accurately predicts prognosis in three unrelated patient datasets. At 10 years, the probability of positive outcome was 52, 51, and 47 percent in the group with a poor-prognosis signature and 91, 75, and 71 percent in the group with a good-prognosis signature for the three datasets, respectively (Kaplan-Meier survival analysis, p<0.05). Hazard ratios for poor outcome were 5.5 (95% CI 3.0 to 12.2, p<0.0001), 2.4 (95% CI 1.6 to 3.6, p<0.0001) and 1.9 (95% CI 1.1 to 3.2, p = 0.016) and remained significant for the two larger datasets when corrected for estrogen receptor (ER) status. Hence the 3D-signature accurately predicts breast cancer outcome in both ER-positive and ER-negative tumors, though individual genes differed in their prognostic ability in the two subtypes. Genes that were prognostic in ER+ patients are AURKA, CEP55, RRM2, EPHA2, FGFBP1, and VRK1, while genes prognostic in ER- patients include ACTB, FOXM1 and SERPINE2 (Kaplan-Meier p<0.05). Multivariable Cox regression analysis in the largest dataset showed that the 3D-signature was a strong independent factor in predicting breast cancer outcome.\n Question: Does prognostic breast cancer signature identified from 3D culture model accurately predict clinical outcome across independent datasets?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: One of the major tenets in breast cancer research is that early detection is vital for patient survival by increasing treatment options. To that end, we have previously used a novel unsupervised approach to identify a set of genes whose expression predicts prognosis of breast cancer patients. The predictive genes were selected in a well-defined three dimensional (3D) cell culture model of non-malignant human mammary epithelial cell morphogenesis as down-regulated during breast epithelial cell acinar formation and cell cycle arrest. Here we examine the ability of this gene signature (3D-signature) to predict prognosis in three independent breast cancer microarray datasets having 295, 286, and 118 samples, respectively. Our results show that the 3D-signature accurately predicts prognosis in three unrelated patient datasets. At 10 years, the probability of positive outcome was 52, 51, and 47 percent in the group with a poor-prognosis signature and 91, 75, and 71 percent in the group with a good-prognosis signature for the three datasets, respectively (Kaplan-Meier survival analysis, p<0.05). Hazard ratios for poor outcome were 5.5 (95% CI 3.0 to 12.2, p<0.0001), 2.4 (95% CI 1.6 to 3.6, p<0.0001) and 1.9 (95% CI 1.1 to 3.2, p = 0.016) and remained significant for the two larger datasets when corrected for estrogen receptor (ER) status. Hence the 3D-signature accurately predicts breast cancer outcome in both ER-positive and ER-negative tumors, though individual genes differed in their prognostic ability in the two subtypes. Genes that were prognostic in ER+ patients are AURKA, CEP55, RRM2, EPHA2, FGFBP1, and VRK1, while genes prognostic in ER- patients include ACTB, FOXM1 and SERPINE2 (Kaplan-Meier p<0.05). Multivariable Cox regression analysis in the largest dataset showed that the 3D-signature was a strong independent factor in predicting breast cancer outcome. Question: Does prognostic breast cancer signature identified from 3D culture model accurately predict clinical outcome across independent datasets? Output:
PubmedQA114016	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Ethylene glycol monomethyl ether (EGME) exposure is associated with impaired reproductive function. The primary metabolite of EGME is methoxyacetic acid (MAA), a short-chain fatty acid that inhibits histone deacetylase activity and alters gene expression. Because estrogen signaling is necessary for normal reproductive function and modulates gene expression, the estrogen-signaling pathway is a likely target for MAA; however, little is known about the effects of MAA in this regard. We evaluated the mechanistic effects of MAA on estrogen receptor (ER) expression and estrogen signaling using in vitro and in vivo model systems. MAA potentiates 17beta-estradiol (E(2)) stimulation of an estrogen-responsive reporter plasmid in HeLa cells transiently transfected with either a human ERalpha or ERbeta expression vector containing a cytomegalovirus (CMV) promoter. This result is attributed to increased exogenous ER expression due to MAA-mediated activation of the CMV promoter. In contrast to its effects on exogenous ER, MAA decreases endogenous ERalpha expression and attenuates E(2)-stimulated endogenous gene expression in both MCF-7 cells and the mouse uterus.\n Question: Does the short-chain fatty acid methoxyacetic acid disrupt endogenous estrogen receptor-alpha-mediated signaling?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Ethylene glycol monomethyl ether (EGME) exposure is associated with impaired reproductive function. The primary metabolite of EGME is methoxyacetic acid (MAA), a short-chain fatty acid that inhibits histone deacetylase activity and alters gene expression. Because estrogen signaling is necessary for normal reproductive function and modulates gene expression, the estrogen-signaling pathway is a likely target for MAA; however, little is known about the effects of MAA in this regard. We evaluated the mechanistic effects of MAA on estrogen receptor (ER) expression and estrogen signaling using in vitro and in vivo model systems. MAA potentiates 17beta-estradiol (E(2)) stimulation of an estrogen-responsive reporter plasmid in HeLa cells transiently transfected with either a human ERalpha or ERbeta expression vector containing a cytomegalovirus (CMV) promoter. This result is attributed to increased exogenous ER expression due to MAA-mediated activation of the CMV promoter. In contrast to its effects on exogenous ER, MAA decreases endogenous ERalpha expression and attenuates E(2)-stimulated endogenous gene expression in both MCF-7 cells and the mouse uterus. Question: Does the short-chain fatty acid methoxyacetic acid disrupt endogenous estrogen receptor-alpha-mediated signaling? Output:
PubmedQA132404	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Interstitial cystitis is a highly prevalent pain condition estimated to affect 3% to 6% of women in the United States. Emerging data suggest there are central neurobiological components to the etiology of this disease. We report the first brain structural imaging findings from the MAPP network with data on more than 300 participants. We used voxel based morphometry to determine whether human patients with chronic interstitial cystitis display changes in brain morphology compared to healthy controls. A total of 33 female patients with interstitial cystitis without comorbidities and 33 age and gender matched controls taken from the larger sample underwent structural magnetic resonance imaging at 5 MAPP sites across the United States. Compared to controls, females with interstitial cystitis displayed significant increased gray matter volume in several regions of the brain including the right primary somatosensory cortex, the superior parietal lobule bilaterally and the right supplementary motor area. Gray matter volume in the right primary somatosensory cortex was associated with greater pain, mood (anxiety) and urological symptoms. We explored these correlations in a linear regression model, and found independent effects of these 3 measures on primary somatosensory cortex gray matter volume, namely clinical pain (McGill pain sensory total), a measure of urgency and anxiety (HADS).\n Question: Is increased brain gray matter in the primary somatosensory cortex associated with increased pain and mood disturbance in patients with interstitial cystitis/painful bladder syndrome?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Interstitial cystitis is a highly prevalent pain condition estimated to affect 3% to 6% of women in the United States. Emerging data suggest there are central neurobiological components to the etiology of this disease. We report the first brain structural imaging findings from the MAPP network with data on more than 300 participants. We used voxel based morphometry to determine whether human patients with chronic interstitial cystitis display changes in brain morphology compared to healthy controls. A total of 33 female patients with interstitial cystitis without comorbidities and 33 age and gender matched controls taken from the larger sample underwent structural magnetic resonance imaging at 5 MAPP sites across the United States. Compared to controls, females with interstitial cystitis displayed significant increased gray matter volume in several regions of the brain including the right primary somatosensory cortex, the superior parietal lobule bilaterally and the right supplementary motor area. Gray matter volume in the right primary somatosensory cortex was associated with greater pain, mood (anxiety) and urological symptoms. We explored these correlations in a linear regression model, and found independent effects of these 3 measures on primary somatosensory cortex gray matter volume, namely clinical pain (McGill pain sensory total), a measure of urgency and anxiety (HADS). Question: Is increased brain gray matter in the primary somatosensory cortex associated with increased pain and mood disturbance in patients with interstitial cystitis/painful bladder syndrome? Output:
PubmedQA59099	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The purpose of this study was to determine whether aqueous levels of vascular endothelial growth factor (VEGF) and pigment epithelium-derived factor (PEDF) are associated with developments of serous retinal detachment (SRD) secondary to branch retinal vein occlusion. We recruited 102 patients with branch retinal vein occlusion and 10 controls. We divided patients into two groups according to optical coherence tomography images of the macula. Forty-six of 102 patients showed SRD defined as being subretinal fluid accumulation with low reflectivity, and the remaining 56 patients presented only cystoid macular edema (CME) defined as being hyporeflective intraretinal cavities. We measured the extent of vascular leakage (disk areas) by digital fluorescein angiography and evaluated the retinal ischemia defined as capillary nonperfusion. Aqueous concentrations of VEGF and pigment epithelium-derived factor were measured by enzyme-linked immunosorbent assay and compared between the two groups. The incidence of major branch retinal vein occlusion was higher in the SRD group (38 of 46, 83%) than in the CME group (32 of 56, 66%, P = 0.01). The incidences of ischemic vein occlusion and macular ischemia was similar between the SRD group (18 of 46 and 20 of 46) and the CME group (20 of 56 and 24 of 56), whereas vascular leakage areas were larger in the SRD group than in the CME group (P = 0.02). Aqueous VEGF levels were higher in the SRD group than in the CME group (P < 0.001), whereas aqueous pigment epithelium-derived factor levels were similar. Vascular endothelial growth factor levels were positively correlated with pigment epithelium-derived factor levels (P < 0.001).\n Question: Are aqueous vascular endothelial growth factor levels associated with serous macular detachment secondary to branch retinal vein occlusion?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The purpose of this study was to determine whether aqueous levels of vascular endothelial growth factor (VEGF) and pigment epithelium-derived factor (PEDF) are associated with developments of serous retinal detachment (SRD) secondary to branch retinal vein occlusion. We recruited 102 patients with branch retinal vein occlusion and 10 controls. We divided patients into two groups according to optical coherence tomography images of the macula. Forty-six of 102 patients showed SRD defined as being subretinal fluid accumulation with low reflectivity, and the remaining 56 patients presented only cystoid macular edema (CME) defined as being hyporeflective intraretinal cavities. We measured the extent of vascular leakage (disk areas) by digital fluorescein angiography and evaluated the retinal ischemia defined as capillary nonperfusion. Aqueous concentrations of VEGF and pigment epithelium-derived factor were measured by enzyme-linked immunosorbent assay and compared between the two groups. The incidence of major branch retinal vein occlusion was higher in the SRD group (38 of 46, 83%) than in the CME group (32 of 56, 66%, P = 0.01). The incidences of ischemic vein occlusion and macular ischemia was similar between the SRD group (18 of 46 and 20 of 46) and the CME group (20 of 56 and 24 of 56), whereas vascular leakage areas were larger in the SRD group than in the CME group (P = 0.02). Aqueous VEGF levels were higher in the SRD group than in the CME group (P < 0.001), whereas aqueous pigment epithelium-derived factor levels were similar. Vascular endothelial growth factor levels were positively correlated with pigment epithelium-derived factor levels (P < 0.001). Question: Are aqueous vascular endothelial growth factor levels associated with serous macular detachment secondary to branch retinal vein occlusion? Output:
PubmedQA185007	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The aim of this study was to evaluate whether functional status is a predictor of outcomes after redo lung transplantation (LTx). Adults undergoing redo LTx after implementation of the Lung Allocation Score (May 2005 to December 2010) were identified in the United Network for Organ Sharing database. Patients were stratified into three groups based on functional status as measured before redo LTx by the Karnofsky scale: (1) no assistance required, (2) some assistance required, and (3) total assistance required. Outcomes after redo LTx were compared based on these preoperative functional cohorts. A total of 390 redo LTx were identified: 44 (11%) required no functional assistance, 176 (45%) required some assistance, and 170 (44%) required total assistance preoperatively. Overall survival at 1 year after redo LTx was significantly reduced in the total assistance group (56% versus 82% no assistance, versus 82% some assistance; p < 0.001). After risk adjustment, recipients requiring total assistance preoperatively were at significant risk for 1-year mortality (odds ratio 3.72, p = 0.02). Overall, the preoperative functional assessment outperformed the Lung Allocation Score in predicting 1-year survival after redo LTx (c-index: 0.68 versus 0.58). Transplant survivors who required total assistance before redo LTx were also at increased risk of requiring total assistance after redo LTx (26% versus 0% no assistance, versus 3% some assistance; p < 0.001).\n Question: Is functional status highly predictive of outcomes after redo lung transplantation : an analysis of 390 cases in the modern era?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The aim of this study was to evaluate whether functional status is a predictor of outcomes after redo lung transplantation (LTx). Adults undergoing redo LTx after implementation of the Lung Allocation Score (May 2005 to December 2010) were identified in the United Network for Organ Sharing database. Patients were stratified into three groups based on functional status as measured before redo LTx by the Karnofsky scale: (1) no assistance required, (2) some assistance required, and (3) total assistance required. Outcomes after redo LTx were compared based on these preoperative functional cohorts. A total of 390 redo LTx were identified: 44 (11%) required no functional assistance, 176 (45%) required some assistance, and 170 (44%) required total assistance preoperatively. Overall survival at 1 year after redo LTx was significantly reduced in the total assistance group (56% versus 82% no assistance, versus 82% some assistance; p < 0.001). After risk adjustment, recipients requiring total assistance preoperatively were at significant risk for 1-year mortality (odds ratio 3.72, p = 0.02). Overall, the preoperative functional assessment outperformed the Lung Allocation Score in predicting 1-year survival after redo LTx (c-index: 0.68 versus 0.58). Transplant survivors who required total assistance before redo LTx were also at increased risk of requiring total assistance after redo LTx (26% versus 0% no assistance, versus 3% some assistance; p < 0.001). Question: Is functional status highly predictive of outcomes after redo lung transplantation : an analysis of 390 cases in the modern era? Output:
PubmedQA137308	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: We compared the motor-unit number estimation (MUNE) findings in patients who presented with signs and/or findings associated with carpal tunnel syndrome (CTS) and healthy controls, with the aim of determining if motor-unit loss occurs during the clinically silent period and if there is a correlation between clinical and MUNE findings in CTS patients. The study investigated 60 hands of 35 patients with clinical CTS and 60 hands of 34 healthy controls. Routine median and ulnar nerve conduction studies and MUNE analysis according to the multipoint stimulation method were performed. The most common electrophysiological abnormality was reduced conduction velocity in the median sensory nerve (100% of the hands). The MUNE value was significantly lower for the patient group than for the control group (p=0.0001). ROC analysis showed that a MUNE value of 121 was the optimal cutoff for differentiating between patients and controls, with a sensitivity of 63.3% and a specificity of 68.3%. MUNE values were lower in patients with complaints of numbness, pain, and weakness in the median nerve territory (p<0.05, for all comparisons), and lower in patients with hypoesthesia than in patients with normal neurological findings (p=0.023).\n Question: Does motor-Unit Number Estimation be Sensitive in Detecting Motor Nerve Involvement in Patients with Carpal Tunnel Syndrome?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: We compared the motor-unit number estimation (MUNE) findings in patients who presented with signs and/or findings associated with carpal tunnel syndrome (CTS) and healthy controls, with the aim of determining if motor-unit loss occurs during the clinically silent period and if there is a correlation between clinical and MUNE findings in CTS patients. The study investigated 60 hands of 35 patients with clinical CTS and 60 hands of 34 healthy controls. Routine median and ulnar nerve conduction studies and MUNE analysis according to the multipoint stimulation method were performed. The most common electrophysiological abnormality was reduced conduction velocity in the median sensory nerve (100% of the hands). The MUNE value was significantly lower for the patient group than for the control group (p=0.0001). ROC analysis showed that a MUNE value of 121 was the optimal cutoff for differentiating between patients and controls, with a sensitivity of 63.3% and a specificity of 68.3%. MUNE values were lower in patients with complaints of numbness, pain, and weakness in the median nerve territory (p<0.05, for all comparisons), and lower in patients with hypoesthesia than in patients with normal neurological findings (p=0.023). Question: Does motor-Unit Number Estimation be Sensitive in Detecting Motor Nerve Involvement in Patients with Carpal Tunnel Syndrome? Output:
PubmedQA160406	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Gal-geun-dang-gwi-tang (GGDGT), an herbal medicine, is used to treat hypertension, stroke, and other inflammatory disorders in the clinical setting. Recently, GGDGT was recognized by the Korea Institute of Oriental Medicine. This study aimed to evaluate the effects of GGDGT in a diabetic atherosclerosis model using apolipoprotein E knockout (ApoE-/-) mice fed a Western diet. The mice were divided into four groups: control group, C57BL6J mice receiving a regular diet (RD); ApoE-/- group, ApoE-/- mice receiving a Western diet (WD); rosiglitazone group, ApoE-/- mice receiving rosiglitazone (WD + 10 mg · kg(-1) · day(-1)); GGDGT group, ApoE-/- mice receiving GGDGT (WD + 200 mg · kg(-1) · day(-1)). Treatment with GGDGT significantly improved glucose tolerance and plasma lipid levels. In addition, GGDGT ameliorated acetylcholine-induced vascular relaxation of the aortic rings. Immunohistochemical staining showed that GGDGT suppressed intercellular adhesion molecule (ICAM)-1 expression; however, expression of endothelial nitric oxide synthase (eNOS) and insulin receptor substrate (IRS)-1 were restored in the thoracic aorta and skeletal muscle, respectively.\n Question: Does gal-geun-dang-gwi-tang improve diabetic vascular complication in apolipoprotein E KO mice fed a western diet?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Gal-geun-dang-gwi-tang (GGDGT), an herbal medicine, is used to treat hypertension, stroke, and other inflammatory disorders in the clinical setting. Recently, GGDGT was recognized by the Korea Institute of Oriental Medicine. This study aimed to evaluate the effects of GGDGT in a diabetic atherosclerosis model using apolipoprotein E knockout (ApoE-/-) mice fed a Western diet. The mice were divided into four groups: control group, C57BL6J mice receiving a regular diet (RD); ApoE-/- group, ApoE-/- mice receiving a Western diet (WD); rosiglitazone group, ApoE-/- mice receiving rosiglitazone (WD + 10 mg · kg(-1) · day(-1)); GGDGT group, ApoE-/- mice receiving GGDGT (WD + 200 mg · kg(-1) · day(-1)). Treatment with GGDGT significantly improved glucose tolerance and plasma lipid levels. In addition, GGDGT ameliorated acetylcholine-induced vascular relaxation of the aortic rings. Immunohistochemical staining showed that GGDGT suppressed intercellular adhesion molecule (ICAM)-1 expression; however, expression of endothelial nitric oxide synthase (eNOS) and insulin receptor substrate (IRS)-1 were restored in the thoracic aorta and skeletal muscle, respectively. Question: Does gal-geun-dang-gwi-tang improve diabetic vascular complication in apolipoprotein E KO mice fed a western diet? Output:
PubmedQA6843	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To evaluate the efficacy of etanercept (ETN) on monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH) in rats. A PAH rat model was induced by intraperitoneal injection (i.p.) of MCT (60 mg/kg) once and ENT therapy (2.5 mg/kg twice a week i.p.) was initiated on the day following MCT injection (prevention protocol) or after PAH is established (remedial protocol) for 2 weeks. The mean pulmonary arterial pressure (mPAP) was measured using a right heart catheterization technique; quantitative determination of lung small artery blood wall thickening observed by hematoxylin and eosin staining; the expression of tumor necrosis factor (TNF)-α and interleukin (IL)-6 in the rat lung tissues were determined using immunohistochemistry. Both preventive (12.53 ± 3.8 vs. model control 28.67 ± 7.57 mmHg, P < 0.01) and remedial (35.95 ± 20.29 vs. model control 66.17 ± 24.29 mmHg, P < 0.01) applications of ETN could significantly reduce mPAP. We obtained similar results when using the R-value to assess the efficacy of ETN in two treatment groups (preventive groups, 0.273 ± 0.018 vs. 0.203 ± 0.036, P < 0.01; remedial groups, 0.227 ± 0.031 vs. 0.124 ± 0.008, P < 0.01). The immunohistochemistry staining showed that there were strong expressions of TNF-α and IL-6 in the lung tissues of model groups and decreased expression in both treatment groups.\n Question: Do preventive and remedial application of etanercept attenuate monocrotaline-induced pulmonary arterial hypertension?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To evaluate the efficacy of etanercept (ETN) on monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH) in rats. A PAH rat model was induced by intraperitoneal injection (i.p.) of MCT (60 mg/kg) once and ENT therapy (2.5 mg/kg twice a week i.p.) was initiated on the day following MCT injection (prevention protocol) or after PAH is established (remedial protocol) for 2 weeks. The mean pulmonary arterial pressure (mPAP) was measured using a right heart catheterization technique; quantitative determination of lung small artery blood wall thickening observed by hematoxylin and eosin staining; the expression of tumor necrosis factor (TNF)-α and interleukin (IL)-6 in the rat lung tissues were determined using immunohistochemistry. Both preventive (12.53 ± 3.8 vs. model control 28.67 ± 7.57 mmHg, P < 0.01) and remedial (35.95 ± 20.29 vs. model control 66.17 ± 24.29 mmHg, P < 0.01) applications of ETN could significantly reduce mPAP. We obtained similar results when using the R-value to assess the efficacy of ETN in two treatment groups (preventive groups, 0.273 ± 0.018 vs. 0.203 ± 0.036, P < 0.01; remedial groups, 0.227 ± 0.031 vs. 0.124 ± 0.008, P < 0.01). The immunohistochemistry staining showed that there were strong expressions of TNF-α and IL-6 in the lung tissues of model groups and decreased expression in both treatment groups. Question: Do preventive and remedial application of etanercept attenuate monocrotaline-induced pulmonary arterial hypertension? Output:
PubmedQA37605	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: While surgical resection is a cornerstone of cancer treatment, local and distant recurrences continue to adversely affect outcome in a significant proportion of patients. Evidence that an alternative debulking strategy involving radiofrequency ablation (RFA) induces antitumor immunity prompted the current investigation of the efficacy of performing RFA prior to surgical resection (pre-resectional RFA) in a preclinical mouse model. Therapeutic efficacy and systemic immune responses were assessed following pre-resectional RFA treatment of murine CT26 colon adenocarcinoma. Treatment with pre-resectional RFA significantly delayed tumor growth and improved overall survival compared to sham surgery, RFA, or resection alone. Mice in the pre-resectional RFA group that achieved a complete response demonstrated durable antitumor immunity upon tumor re-challenge. Failure to achieve a therapeutic benefit in immunodeficient mice confirmed that tumor control by pre-resectional RFA depends on an intact adaptive immune response rather than changes in physical parameters that make ablated tumors more amenable to a complete surgical excision. RFA causes a marked increase in intratumoral CD8+ T lymphocyte infiltration, thus substantially enhancing the ratio of CD8+ effector T cells: FoxP3+ regulatory T cells. Importantly, pre-resectional RFA significantly increases the number of antigen-specific CD8+ T cells within the tumor microenvironment and tumor-draining lymph node but had no impact on infiltration by myeloid-derived suppressor cells, M1 macrophages or M2 macrophages at tumor sites or in peripheral lymphoid organs (i.e., spleen). Finally, pre-resectional RFA of primary tumors delayed growth of distant tumors through a mechanism that depends on systemic CD8+ T cell-mediated antitumor immunity.\n Question: Does immune Adjuvant Activity of Pre-Resectional Radiofrequency Ablation protect against Local and Systemic Recurrence in Aggressive Murine Colorectal Cancer?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: While surgical resection is a cornerstone of cancer treatment, local and distant recurrences continue to adversely affect outcome in a significant proportion of patients. Evidence that an alternative debulking strategy involving radiofrequency ablation (RFA) induces antitumor immunity prompted the current investigation of the efficacy of performing RFA prior to surgical resection (pre-resectional RFA) in a preclinical mouse model. Therapeutic efficacy and systemic immune responses were assessed following pre-resectional RFA treatment of murine CT26 colon adenocarcinoma. Treatment with pre-resectional RFA significantly delayed tumor growth and improved overall survival compared to sham surgery, RFA, or resection alone. Mice in the pre-resectional RFA group that achieved a complete response demonstrated durable antitumor immunity upon tumor re-challenge. Failure to achieve a therapeutic benefit in immunodeficient mice confirmed that tumor control by pre-resectional RFA depends on an intact adaptive immune response rather than changes in physical parameters that make ablated tumors more amenable to a complete surgical excision. RFA causes a marked increase in intratumoral CD8+ T lymphocyte infiltration, thus substantially enhancing the ratio of CD8+ effector T cells: FoxP3+ regulatory T cells. Importantly, pre-resectional RFA significantly increases the number of antigen-specific CD8+ T cells within the tumor microenvironment and tumor-draining lymph node but had no impact on infiltration by myeloid-derived suppressor cells, M1 macrophages or M2 macrophages at tumor sites or in peripheral lymphoid organs (i.e., spleen). Finally, pre-resectional RFA of primary tumors delayed growth of distant tumors through a mechanism that depends on systemic CD8+ T cell-mediated antitumor immunity. Question: Does immune Adjuvant Activity of Pre-Resectional Radiofrequency Ablation protect against Local and Systemic Recurrence in Aggressive Murine Colorectal Cancer? Output:
PubmedQA151607	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Emerging evidence suggests that cardiac angiotensin-converting enzyme 2 (ACE2) may contribute to the regulation of heart function and hypertension-induced cardiac remodeling. We tested the hypothesis that inhibition of ACE2 in the hearts of (mRen2)27 hypertensive rats may accelerate progression of cardiac hypertrophy and fibrosis by preventing conversion of angiotensin II (Ang II) into the antifibrotic peptide, angiotensin-(1-7) (Ang-(1-7)). Fourteen male (mRen2)27 transgenic hypertensive rats (12 weeks old, 401 + or - 7 g) were administered either vehicle (0.9% saline) or the ACE2 inhibitor, MLN-4760 (30 mg/kg/day), subcutaneously via mini-osmotic pumps for 28 days. Although ACE2 inhibition had no effect on average 24-h blood pressures, left ventricular (LV) Ang II content increased 24% in rats chronically treated with the ACE2 inhibitor (P < 0.05). Chronic ACE2 inhibition had no effect on plasma Ang II or Ang-(1-7) levels. Increased cardiac Ang II levels were associated with significant increases in both LV anterior, posterior, and relative wall thicknesses, as well as interstitial collagen fraction area and cardiomyocyte hypertrophy in the transgenic animals chronically treated with the ACE2 inhibitor. Cardiac remodeling was not accompanied by any further alterations in LV function.\n Question: Does inhibition of angiotensin-converting enzyme 2 exacerbate cardiac hypertrophy and fibrosis in Ren-2 hypertensive rats?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Emerging evidence suggests that cardiac angiotensin-converting enzyme 2 (ACE2) may contribute to the regulation of heart function and hypertension-induced cardiac remodeling. We tested the hypothesis that inhibition of ACE2 in the hearts of (mRen2)27 hypertensive rats may accelerate progression of cardiac hypertrophy and fibrosis by preventing conversion of angiotensin II (Ang II) into the antifibrotic peptide, angiotensin-(1-7) (Ang-(1-7)). Fourteen male (mRen2)27 transgenic hypertensive rats (12 weeks old, 401 + or - 7 g) were administered either vehicle (0.9% saline) or the ACE2 inhibitor, MLN-4760 (30 mg/kg/day), subcutaneously via mini-osmotic pumps for 28 days. Although ACE2 inhibition had no effect on average 24-h blood pressures, left ventricular (LV) Ang II content increased 24% in rats chronically treated with the ACE2 inhibitor (P < 0.05). Chronic ACE2 inhibition had no effect on plasma Ang II or Ang-(1-7) levels. Increased cardiac Ang II levels were associated with significant increases in both LV anterior, posterior, and relative wall thicknesses, as well as interstitial collagen fraction area and cardiomyocyte hypertrophy in the transgenic animals chronically treated with the ACE2 inhibitor. Cardiac remodeling was not accompanied by any further alterations in LV function. Question: Does inhibition of angiotensin-converting enzyme 2 exacerbate cardiac hypertrophy and fibrosis in Ren-2 hypertensive rats? Output:
PubmedQA126170	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To determine sensitivity, specificity, predictive value of routine fecal occult blood (FOB) testing on the identification of Bell's Stage II or III necrotizing enterocolitis (NEC) in very low birth weight (VLBW) infants. Retrospective medical record review of VLBW infants from 2012- 2013 evaluating FOB results and clinical and demographic risk factors. We determined predictive values of positive FOB testing within 48 hours of definite NEC diagnosis. We performed logistic regression analyses for predictors of NEC and for predictors of having positive FOB during NICU admission. The incidence of NEC in our cohort of 203 infants was 3.9% (n = 8). None had positive FOB results within 48 hours of diagnosis, and only 12.5% had any positive FOB within 7 days. Sensitivity of positive FOB for predicting definite NEC = 0%, specificity = 34.4%, and positive predictive value = 0%. A majority of VLBWs (67.0%) had > one positive FOB result during their NICU course. On logistic regression, intrauterine growth restricted (IUGR) infants had significantly higher odds of both developing NEC and of having positive FOB. Positive FOB was not a significant predictor of NEC. Those with lower birth gestational ages had higher odds of positive FOB.\n Question: Does routine fecal occult blood testing predict necrotizing enterocolitis in very low birth weight neonates?\n Output: " }, { "role": "assistant", "content": "no" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To determine sensitivity, specificity, predictive value of routine fecal occult blood (FOB) testing on the identification of Bell's Stage II or III necrotizing enterocolitis (NEC) in very low birth weight (VLBW) infants. Retrospective medical record review of VLBW infants from 2012- 2013 evaluating FOB results and clinical and demographic risk factors. We determined predictive values of positive FOB testing within 48 hours of definite NEC diagnosis. We performed logistic regression analyses for predictors of NEC and for predictors of having positive FOB during NICU admission. The incidence of NEC in our cohort of 203 infants was 3.9% (n = 8). None had positive FOB results within 48 hours of diagnosis, and only 12.5% had any positive FOB within 7 days. Sensitivity of positive FOB for predicting definite NEC = 0%, specificity = 34.4%, and positive predictive value = 0%. A majority of VLBWs (67.0%) had > one positive FOB result during their NICU course. On logistic regression, intrauterine growth restricted (IUGR) infants had significantly higher odds of both developing NEC and of having positive FOB. Positive FOB was not a significant predictor of NEC. Those with lower birth gestational ages had higher odds of positive FOB. Question: Does routine fecal occult blood testing predict necrotizing enterocolitis in very low birth weight neonates? Output:
PubmedQA185602	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Oral daily ibandronate was investigated for the prevention of bone loss in postmenopausal women without osteoporosis (n = 653). BMD at the lumbar spine and hip were significantly increased (3.1% and 1.8%, respectively; p < or = 0.0001 versus placebo) with 2.5 mg ibandronate after 24 months. Oral ibandronate is a promising option for the prevention of postmenopausal bone loss. Further strategies to manage patients most at risk from developing postmenopausal osteoporosis are required. The objectives of this multicenter, double-blind, randomized, placebo-controlled study were to examine the efficacy, tolerability, and optimal dose of oral daily ibandronate in the prevention of bone loss in postmenopausal women. In total, 653 women (mean bone mineral density [BMD] T-score > -2.5 at the lumbar spine), who had been postmenopausal for at least 1 year, were allocated to one of four strata based on time since menopause and baseline lumbar spine BMD. Women were randomized to receive calcium (500 mg daily) plus either placebo (n = 162) or ibandronate 0.5 mg (n = 162), 1 mg (n = 166), or 2.5 mg (n = 163) as once-daily oral treatment for 2 years. The primary endpoint was the mean percent change in lumbar spine BMD with ibandronate versus placebo.\n Question: Does oral daily ibandronate prevent bone loss in early postmenopausal women without osteoporosis?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Oral daily ibandronate was investigated for the prevention of bone loss in postmenopausal women without osteoporosis (n = 653). BMD at the lumbar spine and hip were significantly increased (3.1% and 1.8%, respectively; p < or = 0.0001 versus placebo) with 2.5 mg ibandronate after 24 months. Oral ibandronate is a promising option for the prevention of postmenopausal bone loss. Further strategies to manage patients most at risk from developing postmenopausal osteoporosis are required. The objectives of this multicenter, double-blind, randomized, placebo-controlled study were to examine the efficacy, tolerability, and optimal dose of oral daily ibandronate in the prevention of bone loss in postmenopausal women. In total, 653 women (mean bone mineral density [BMD] T-score > -2.5 at the lumbar spine), who had been postmenopausal for at least 1 year, were allocated to one of four strata based on time since menopause and baseline lumbar spine BMD. Women were randomized to receive calcium (500 mg daily) plus either placebo (n = 162) or ibandronate 0.5 mg (n = 162), 1 mg (n = 166), or 2.5 mg (n = 163) as once-daily oral treatment for 2 years. The primary endpoint was the mean percent change in lumbar spine BMD with ibandronate versus placebo. Question: Does oral daily ibandronate prevent bone loss in early postmenopausal women without osteoporosis? Output:
PubmedQA133933	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Spontaneous immortalisation of cultured mammary epithelial cells (MECs) is an extremely rare event, and the molecular mechanism behind spontaneous immortalisation of MECs is unclear. Here, we report the establishment of a spontaneously immortalised bovine mammary epithelial cell line (BME65Cs) and the changes in gene expression associated with BME65Cs cells. BME65Cs cells maintain the general characteristics of normal mammary epithelial cells in morphology, karyotype and immunohistochemistry, and are accompanied by the activation of endogenous bTERT (bovine Telomerase Reverse Transcriptase) and stabilisation of the telomere. Currently, BME65Cs cells have been passed for more than 220 generations, and these cells exhibit non-malignant transformation. The expression of multiple genes was investigated in BME65Cs cells, senescent BMECs (bovine MECs) cells, early passage BMECs cells and MCF-7 cells (a human breast cancer cell line). In comparison with early passage BMECs cells, the expression of senescence-relevant apoptosis-related gene were significantly changed in BME65Cs cells. P16INK4a was downregulated, p53 was low expressed and Bax/Bcl-2 ratio was reversed. Moreover, a slight upregulation of the oncogene c-Myc, along with an undetectable level of breast tumor-related gene Bag-1 and TRPS-1, was observed in BME65Cs cells while these genes are all highly expressed in MCF-7. In addition, DNMT1 is upregulated in BME65Cs. These results suggest that the inhibition of both senescence and mitochondrial apoptosis signalling pathways contribute to the immortality of BME65Cs cells. The expression of p53 and p16INK4a in BME65Cs was altered in the pattern of down-regulation but not \"loss\", suggesting that this spontaneous immortalization is possibly initiated by other mechanism rather than gene mutation of p53 or p16INK4a.\n Question: Do spontaneously immortalised bovine mammary epithelial cells exhibit a distinct gene expression pattern from the breast cancer cells?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Spontaneous immortalisation of cultured mammary epithelial cells (MECs) is an extremely rare event, and the molecular mechanism behind spontaneous immortalisation of MECs is unclear. Here, we report the establishment of a spontaneously immortalised bovine mammary epithelial cell line (BME65Cs) and the changes in gene expression associated with BME65Cs cells. BME65Cs cells maintain the general characteristics of normal mammary epithelial cells in morphology, karyotype and immunohistochemistry, and are accompanied by the activation of endogenous bTERT (bovine Telomerase Reverse Transcriptase) and stabilisation of the telomere. Currently, BME65Cs cells have been passed for more than 220 generations, and these cells exhibit non-malignant transformation. The expression of multiple genes was investigated in BME65Cs cells, senescent BMECs (bovine MECs) cells, early passage BMECs cells and MCF-7 cells (a human breast cancer cell line). In comparison with early passage BMECs cells, the expression of senescence-relevant apoptosis-related gene were significantly changed in BME65Cs cells. P16INK4a was downregulated, p53 was low expressed and Bax/Bcl-2 ratio was reversed. Moreover, a slight upregulation of the oncogene c-Myc, along with an undetectable level of breast tumor-related gene Bag-1 and TRPS-1, was observed in BME65Cs cells while these genes are all highly expressed in MCF-7. In addition, DNMT1 is upregulated in BME65Cs. These results suggest that the inhibition of both senescence and mitochondrial apoptosis signalling pathways contribute to the immortality of BME65Cs cells. The expression of p53 and p16INK4a in BME65Cs was altered in the pattern of down-regulation but not "loss", suggesting that this spontaneous immortalization is possibly initiated by other mechanism rather than gene mutation of p53 or p16INK4a. Question: Do spontaneously immortalised bovine mammary epithelial cells exhibit a distinct gene expression pattern from the breast cancer cells? Output:
PubmedQA9658	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Acute intravascular hemolysis after exchange transfusion with glucose 6-phosphate dehydrogenase-deficient blood has been reported; however, it is not routine to screen donor blood for glucose 6-phosphate dehydrogenase deficiency while performing exchange transfusion. We hypothesized that exchange transfusion with glucose 6-phosphate dehydrogenase-deficient blood would lead to a less-than-expected decrease in total serum bilirubin. The objective of this study was to evaluate the effect of exchange transfusion with glucose 6-phosphate dehydrogenase-deficient blood in neonates with idiopathic hyperbilirubinemia on postexchange total serum bilirubin levels, duration of phototherapy, and need for repeat exchange transfusions. All neonates who were undergoing exchange transfusion for idiopathic hyperbilirubinemia were enrolled. A sample of donor blood was collected at the time of exchange transfusion for a glucose 6-phosphate dehydrogenase assay. The standard criteria for starting and stopping phototherapy and exchange transfusion were applied. During the 1-year study period, 21 infants underwent exchange with glucose 6-phosphate dehydrogenase-deficient blood, and 114 neonates with similar baseline characteristics underwent exchange transfusion with glucose 6-phosphate dehydrogenase-normal blood. From 6 to 60 hours after exchange transfusion, there was a significantly lesser drop in total serum bilirubin in the recipients of glucose 6-phosphate dehydrogenase-deficient donor blood compared with recipients of glucose 6-phosphate dehydrogenase-normal blood. The mean duration of phototherapy in the postexchange period and number of infants who underwent repeat exchange transfusions were significantly higher in recipients of glucose 6-phosphate dehydrogenase-deficient donor blood in comparison with control subjects. Concurrently, there was a significantly higher drop in hematocrit and rise in plasma hemoglobin in the glucose 6-phosphate dehydrogenase-deficient donor group.\n Question: Does donor blood glucose 6-phosphate dehydrogenase deficiency reduce the efficacy of exchange transfusion in neonatal hyperbilirubinemia?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Acute intravascular hemolysis after exchange transfusion with glucose 6-phosphate dehydrogenase-deficient blood has been reported; however, it is not routine to screen donor blood for glucose 6-phosphate dehydrogenase deficiency while performing exchange transfusion. We hypothesized that exchange transfusion with glucose 6-phosphate dehydrogenase-deficient blood would lead to a less-than-expected decrease in total serum bilirubin. The objective of this study was to evaluate the effect of exchange transfusion with glucose 6-phosphate dehydrogenase-deficient blood in neonates with idiopathic hyperbilirubinemia on postexchange total serum bilirubin levels, duration of phototherapy, and need for repeat exchange transfusions. All neonates who were undergoing exchange transfusion for idiopathic hyperbilirubinemia were enrolled. A sample of donor blood was collected at the time of exchange transfusion for a glucose 6-phosphate dehydrogenase assay. The standard criteria for starting and stopping phototherapy and exchange transfusion were applied. During the 1-year study period, 21 infants underwent exchange with glucose 6-phosphate dehydrogenase-deficient blood, and 114 neonates with similar baseline characteristics underwent exchange transfusion with glucose 6-phosphate dehydrogenase-normal blood. From 6 to 60 hours after exchange transfusion, there was a significantly lesser drop in total serum bilirubin in the recipients of glucose 6-phosphate dehydrogenase-deficient donor blood compared with recipients of glucose 6-phosphate dehydrogenase-normal blood. The mean duration of phototherapy in the postexchange period and number of infants who underwent repeat exchange transfusions were significantly higher in recipients of glucose 6-phosphate dehydrogenase-deficient donor blood in comparison with control subjects. Concurrently, there was a significantly higher drop in hematocrit and rise in plasma hemoglobin in the glucose 6-phosphate dehydrogenase-deficient donor group. Question: Does donor blood glucose 6-phosphate dehydrogenase deficiency reduce the efficacy of exchange transfusion in neonatal hyperbilirubinemia? Output:
PubmedQA76571	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Progesterone differently regulates TNFα-induced gene expression of cyclooxygenase-2 (COX-2) and manganese superoxide dismutase (Mn-SOD) in human endometrial stromal cells (ESC). The present study investigated the mechanisms by which TNFα and progesterone affect the expressions of COX-2 and Mn-SOD in ESC. ESC were incubated with TNFα and progesterone. COX-2 and Mn-SOD mRNA expression was determined by real-time RT-PCR. Nuclear factor (NF)-κB binding to the promoter region or histone acetylation status of the NF-κB response element was analyzed by a chromatin immunoprecipitation assay. TNFα increased COX-2 and Mn-SOD mRNA levels. Progesterone (10(-6) M) suppressed TNFα-induced COX-2 mRNA expression, whereas TNFα-induced Mn-SOD expression was not inhibited by progesterone. The inhibitory effect of progesterone was abolished by knockdown of progesterone receptors by small interfering RNA. Chromatin immunoprecipitation assay revealed that TNFα increased NF-κB binding at both the COX-2 promoter and the Mn-SOD enhancer and that progesterone inhibited only the NF-κB binding at the COX-2 promoter. The histone acetylation level of the NF-κB response element of the Mn-SOD enhancer was lower than that of the COX-2 promoter. However, when histone acetylation was induced by histone deacetylase inhibitors, progesterone inhibited the TNFα-induced NF-κB binding to the Mn-SOD enhancer.\n Question: Are differential effects of progesterone on COX-2 and Mn-SOD expressions associated with histone acetylation status of the promoter region in human endometrial stromal cells?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Progesterone differently regulates TNFα-induced gene expression of cyclooxygenase-2 (COX-2) and manganese superoxide dismutase (Mn-SOD) in human endometrial stromal cells (ESC). The present study investigated the mechanisms by which TNFα and progesterone affect the expressions of COX-2 and Mn-SOD in ESC. ESC were incubated with TNFα and progesterone. COX-2 and Mn-SOD mRNA expression was determined by real-time RT-PCR. Nuclear factor (NF)-κB binding to the promoter region or histone acetylation status of the NF-κB response element was analyzed by a chromatin immunoprecipitation assay. TNFα increased COX-2 and Mn-SOD mRNA levels. Progesterone (10(-6) M) suppressed TNFα-induced COX-2 mRNA expression, whereas TNFα-induced Mn-SOD expression was not inhibited by progesterone. The inhibitory effect of progesterone was abolished by knockdown of progesterone receptors by small interfering RNA. Chromatin immunoprecipitation assay revealed that TNFα increased NF-κB binding at both the COX-2 promoter and the Mn-SOD enhancer and that progesterone inhibited only the NF-κB binding at the COX-2 promoter. The histone acetylation level of the NF-κB response element of the Mn-SOD enhancer was lower than that of the COX-2 promoter. However, when histone acetylation was induced by histone deacetylase inhibitors, progesterone inhibited the TNFα-induced NF-κB binding to the Mn-SOD enhancer. Question: Are differential effects of progesterone on COX-2 and Mn-SOD expressions associated with histone acetylation status of the promoter region in human endometrial stromal cells? Output:
PubmedQA179095	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Reductions in cholinergic function occur in Alzheimer disease (AD) and dementia with Lewy bodies and correlate with cognitive decline. However, whether such alterations appear in early-stage disease is unclear. To examine the timing of cholinergic deficits in AD and dementia with Lewy bodies. Autopsy series of 89 patients with AD and 50 patients with the Lewy body variant of AD (LBV). Stage of disease was stratified according to results of the last Mini-Mental State Examination (MMSE) before death as mild, moderate, severe, or very severe. We analyzed choline acetyltransferase (ChAT) activity in the midfrontal, superior temporal, and inferior parietal cortices. Although compared with a normal control group ChAT activity was decreased in the AD and LBV cohorts, ChAT activity reduction for the LBV cohort was much greater. Moreover, although the decline in ChAT activity in the AD cohort compared with the normal control group was significant only for patients in later stages of the illness, the decline in the LBV cohort was significant for those who died with mild-stage disease. When less impaired patients in each cohort (MMSE, > or = 10) underwent separate analysis, the relationship of ChAT activity with the MMSE score was strong and significant for the LBV cohort alone.\n Question: Do early and widespread cholinergic losses differentiate dementia with Lewy bodies from Alzheimer disease?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Reductions in cholinergic function occur in Alzheimer disease (AD) and dementia with Lewy bodies and correlate with cognitive decline. However, whether such alterations appear in early-stage disease is unclear. To examine the timing of cholinergic deficits in AD and dementia with Lewy bodies. Autopsy series of 89 patients with AD and 50 patients with the Lewy body variant of AD (LBV). Stage of disease was stratified according to results of the last Mini-Mental State Examination (MMSE) before death as mild, moderate, severe, or very severe. We analyzed choline acetyltransferase (ChAT) activity in the midfrontal, superior temporal, and inferior parietal cortices. Although compared with a normal control group ChAT activity was decreased in the AD and LBV cohorts, ChAT activity reduction for the LBV cohort was much greater. Moreover, although the decline in ChAT activity in the AD cohort compared with the normal control group was significant only for patients in later stages of the illness, the decline in the LBV cohort was significant for those who died with mild-stage disease. When less impaired patients in each cohort (MMSE, > or = 10) underwent separate analysis, the relationship of ChAT activity with the MMSE score was strong and significant for the LBV cohort alone. Question: Do early and widespread cholinergic losses differentiate dementia with Lewy bodies from Alzheimer disease? Output:
PubmedQA163300	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Cannabinoid compounds are known to regulate feeding behavior by modulating the hedonic and/or the incentive properties of food. The aim of this work was to determine the involvement of the cannabinoid system in food reinforcement associated with a conflict situation generated by stress. Mice were trained on a fixed ratio 1 schedule of reinforcement to obtain standard, chocolate-flavored or fat-enriched pellets. Once the acquisition criteria were achieved, the reinforced lever press was paired with foot-shock exposure, and the effects of Delta(9)-tetrahydrocannabinol (THC; 1 mg/kg) were evaluated in this conflict paradigm. THC did not modify the operant response in mice trained with standard pellets. In contrast, THC improved the instrumental performance of mice trained with chocolate-flavored and fat-enriched pellets. However, the cannabinoid agonist did not fully restore the baseline responses obtained previous to foot-shock delivery. THC ameliorated the performance to obtain high palatable food in this conflict test in both food-restricted and sated mice. The effects of THC on food reinforcement seem to be long-lasting since mice previously treated with this compound showed a better recovery of the instrumental behavior after foot-shock exposure.\n Question: Does delta-9-tetrahydrocannabinol enhance food reinforcement in a mouse operant conflict test?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Cannabinoid compounds are known to regulate feeding behavior by modulating the hedonic and/or the incentive properties of food. The aim of this work was to determine the involvement of the cannabinoid system in food reinforcement associated with a conflict situation generated by stress. Mice were trained on a fixed ratio 1 schedule of reinforcement to obtain standard, chocolate-flavored or fat-enriched pellets. Once the acquisition criteria were achieved, the reinforced lever press was paired with foot-shock exposure, and the effects of Delta(9)-tetrahydrocannabinol (THC; 1 mg/kg) were evaluated in this conflict paradigm. THC did not modify the operant response in mice trained with standard pellets. In contrast, THC improved the instrumental performance of mice trained with chocolate-flavored and fat-enriched pellets. However, the cannabinoid agonist did not fully restore the baseline responses obtained previous to foot-shock delivery. THC ameliorated the performance to obtain high palatable food in this conflict test in both food-restricted and sated mice. The effects of THC on food reinforcement seem to be long-lasting since mice previously treated with this compound showed a better recovery of the instrumental behavior after foot-shock exposure. Question: Does delta-9-tetrahydrocannabinol enhance food reinforcement in a mouse operant conflict test? Output:
PubmedQA67301	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Although many studies have focused on the effects of the physical activity on plasma homocysteine (Hcy) levels, the data gathered up to now are contradictory. In fact, it is true that some researches highlighted an exercise-induced fall in Hcy concentrations, but there are many reports proving that the physical exercise does not contribute to depress plasma Hcy levels and/or that in some instances it would even produce an increase. As a result, the question about the nature of the relationship between Hcy and physical activity remains unanswered. In this study, we have investigated whether the modification in Hcy level after a moderate physical activity was explainable in the light of the common connection of physical activity and Hcy to creatine (Cn). In 16 young volunteers aged from 21 to 37, divided into sedentary (n=6) and athletes (n=10) sub-groups, before and after an incremental cycle ergometer stress test, performed every 30 days for 4 months, we measured the plasma levels of guanidino acetic acid (GAA), ornithine (Orn), glycine (Gly), arginine (Arg), methionine (Met) as well as the plasma levels of Cn and of total and reduced form of the homocysteine (tHcy, rHcy). By difference in the total proteins (tProt) amount between the pre- and post-exercise phases also the dehydration degree of the subjects was measured. After exercise rHcy decreased, tHcy was unchanged while Cn increased. Gly, Arg and Met at the end of exercise remained unaffected whereas, interestingly, GAA decreased in both sub-groups while Orn was significant diminished in athletes and, although not significantly, the same trend was observable in the sedentaries group.\n Question: Are acute variations in homocysteine levels related to creatine changes induced by physical activity?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Although many studies have focused on the effects of the physical activity on plasma homocysteine (Hcy) levels, the data gathered up to now are contradictory. In fact, it is true that some researches highlighted an exercise-induced fall in Hcy concentrations, but there are many reports proving that the physical exercise does not contribute to depress plasma Hcy levels and/or that in some instances it would even produce an increase. As a result, the question about the nature of the relationship between Hcy and physical activity remains unanswered. In this study, we have investigated whether the modification in Hcy level after a moderate physical activity was explainable in the light of the common connection of physical activity and Hcy to creatine (Cn). In 16 young volunteers aged from 21 to 37, divided into sedentary (n=6) and athletes (n=10) sub-groups, before and after an incremental cycle ergometer stress test, performed every 30 days for 4 months, we measured the plasma levels of guanidino acetic acid (GAA), ornithine (Orn), glycine (Gly), arginine (Arg), methionine (Met) as well as the plasma levels of Cn and of total and reduced form of the homocysteine (tHcy, rHcy). By difference in the total proteins (tProt) amount between the pre- and post-exercise phases also the dehydration degree of the subjects was measured. After exercise rHcy decreased, tHcy was unchanged while Cn increased. Gly, Arg and Met at the end of exercise remained unaffected whereas, interestingly, GAA decreased in both sub-groups while Orn was significant diminished in athletes and, although not significantly, the same trend was observable in the sedentaries group. Question: Are acute variations in homocysteine levels related to creatine changes induced by physical activity? Output:
PubmedQA155471	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Neutrophils are common cells of the inflammatory infiltrate and are predominantly enriched in many cancers. We recently found that neutrophils are accumulated in human hepatocellular carcinoma (HCC), where they promote disease progression by releasing matrix metalloproteinase-9 (MMP9). The underlying mechanisms, however, that allow tumour microenvironments to educate neutrophils are largely unknown. Neutrophils were purified from HCC patients and healthy donors. Immunohistochemistry and immunoblotting were used for the evaluation of autophagy in neutrophils. The regulation and function of increased neutrophil autophagy were assessed by both in vitro and ex vivo studies. Most neutrophils in HCC intratumoural regions, in contrast to those located in the paired non-tumoural areas and within tumour vessels, substantially expressed autophagy-specific protein LC3. Soluble factors derived from hepatoma, including hyaluronan fragments, triggered a considerable increase of functional LC3 and autophagosomes in neutrophils, but this was unrelated to the deactivation of mTOR signalling. Inhibiting the activation of Erk1/2, p38, and NF-κB signals could significantly attenuate such tumour-elicited autophagy. These neutrophils, undergoing autophagy, exhibited long-lived phenotypes with retained Mcl-1 and significantly more intact mitochondria as well as low cleaved caspase-3, which could be abolished by inhibiting the initiation of autophagy. Moreover, increased neutrophil autophagy also correlated with sustained production of pro-metastatic oncostatin M and MMP9 and advanced migration of cancer cells.\n Question: Does increased autophagy sustain the survival and pro-tumourigenic effects of neutrophils in human hepatocellular carcinoma?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Neutrophils are common cells of the inflammatory infiltrate and are predominantly enriched in many cancers. We recently found that neutrophils are accumulated in human hepatocellular carcinoma (HCC), where they promote disease progression by releasing matrix metalloproteinase-9 (MMP9). The underlying mechanisms, however, that allow tumour microenvironments to educate neutrophils are largely unknown. Neutrophils were purified from HCC patients and healthy donors. Immunohistochemistry and immunoblotting were used for the evaluation of autophagy in neutrophils. The regulation and function of increased neutrophil autophagy were assessed by both in vitro and ex vivo studies. Most neutrophils in HCC intratumoural regions, in contrast to those located in the paired non-tumoural areas and within tumour vessels, substantially expressed autophagy-specific protein LC3. Soluble factors derived from hepatoma, including hyaluronan fragments, triggered a considerable increase of functional LC3 and autophagosomes in neutrophils, but this was unrelated to the deactivation of mTOR signalling. Inhibiting the activation of Erk1/2, p38, and NF-κB signals could significantly attenuate such tumour-elicited autophagy. These neutrophils, undergoing autophagy, exhibited long-lived phenotypes with retained Mcl-1 and significantly more intact mitochondria as well as low cleaved caspase-3, which could be abolished by inhibiting the initiation of autophagy. Moreover, increased neutrophil autophagy also correlated with sustained production of pro-metastatic oncostatin M and MMP9 and advanced migration of cancer cells. Question: Does increased autophagy sustain the survival and pro-tumourigenic effects of neutrophils in human hepatocellular carcinoma? Output:
PubmedQA70652	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Endoscopic retrograde cholangiopancreatography (ERCP) is often unsuccessful in patients with Roux-en-Y anatomy. Augmented enteroscopy allows deep insertion into the small bowel and can be useful in patients with Roux-en-Y anatomy. The aim of this study was to compare single balloon assisted ERCP (SBE-ERCP) and spiral assisted ERCP (SE-ERCP) in patients with Roux-en-Y anatomy in terms of diagnostic and therapeutic yield, procedure time, and complications. This is a retrospective cohort study of consecutive patients with Roux-en-Y anatomy who underwent SBE-ERCP or SE-ERCP between October 2007 and March 2011. Diagnostic yield was defined as successful duct cannulation. Therapeutic yield was defined as the ability to successfully carry out endoscopic therapy in those cannulated. Procedure time and complications were assessed. Thirty-four consecutive patients with Roux-en-Y anatomy underwent 54 ERCP procedures. The overall diagnostic yield was 44.4% with no significant difference between the diagnostic yield of SBE-ERCP (48.3%) and SE-ERCP (40%). The diagnostic yield was lower in patients with gastric by-pass (38.9%) compared with other types of Roux-en-Y anatomy (47.2%) but this was not statistically significant (P = 0.772). The overall therapeutic yield was 93.8%, with a therapeutic yield of 100% for SBE-ERCP and 87.5% for SE-ERCP (P = 1.0). There was one perforation during SBE-ERCP, giving a complication rate of 3.5%. The mean procedure time did not differ between the two techniques.\n Question: Is spiral assisted ERCP equivalent to single balloon assisted ERCP in patients with Roux-en-Y anatomy?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Endoscopic retrograde cholangiopancreatography (ERCP) is often unsuccessful in patients with Roux-en-Y anatomy. Augmented enteroscopy allows deep insertion into the small bowel and can be useful in patients with Roux-en-Y anatomy. The aim of this study was to compare single balloon assisted ERCP (SBE-ERCP) and spiral assisted ERCP (SE-ERCP) in patients with Roux-en-Y anatomy in terms of diagnostic and therapeutic yield, procedure time, and complications. This is a retrospective cohort study of consecutive patients with Roux-en-Y anatomy who underwent SBE-ERCP or SE-ERCP between October 2007 and March 2011. Diagnostic yield was defined as successful duct cannulation. Therapeutic yield was defined as the ability to successfully carry out endoscopic therapy in those cannulated. Procedure time and complications were assessed. Thirty-four consecutive patients with Roux-en-Y anatomy underwent 54 ERCP procedures. The overall diagnostic yield was 44.4% with no significant difference between the diagnostic yield of SBE-ERCP (48.3%) and SE-ERCP (40%). The diagnostic yield was lower in patients with gastric by-pass (38.9%) compared with other types of Roux-en-Y anatomy (47.2%) but this was not statistically significant (P = 0.772). The overall therapeutic yield was 93.8%, with a therapeutic yield of 100% for SBE-ERCP and 87.5% for SE-ERCP (P = 1.0). There was one perforation during SBE-ERCP, giving a complication rate of 3.5%. The mean procedure time did not differ between the two techniques. Question: Is spiral assisted ERCP equivalent to single balloon assisted ERCP in patients with Roux-en-Y anatomy? Output:
PubmedQA150439	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Visceral leishmaniasis is a chronic protozoan disease caused by Leishmania donovani, an obligatory intracellular parasite that resides and multiplies within macrophages of the reticuloendothelial system. The aim of this study was to evaluate the efficacy of nine novel synthetic chromone derivatives as antileishmanial molecules in experimental murine visceral leishmaniasis. In vitro activity of the molecules (2, 5 and 10 μg/ml) was assessed against promastigotes of both pentavalent antimonial-responsive strain AG83 and pentavalent antimonial-resistant strain GE1F8R at days 2 (48 h), 4 (96 h) and 6 (144 h). The efficacy of the most efficient chromone derivative [C-(6-Methyl-4-oxo-4H-1-benzopyran-3-yl)-N-(p-tolyl) nitrone], designated here as NP1, was also tested against intracellular amastigotes in vitro and in vivo. NP1, 5 μg/ml, inhibited the growth of AG83 and GE1F8R promastigotes by 98.57% (day 4) and 75.75% (day 6), respectively, and also inhibited the growth of intracellular amastigotes by 85% (day 3), compared to DMSO control. Treatment of L. donovani-infected mice with NP1 resulted in a 70% significant decrease in parasite load in the spleen in the 7th week after infection (5 mice in each group), with associated induction of interferon-γ synthesis by dose 2 (37.5 mg/kg body weight) compared to DMSO control. Dose 2 was found efficient over dose 1 (25 mg/kg body weight).\n Question: Does protective therapy with novel chromone derivative against Leishmania donovani infection induce Th1 response in vivo?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Visceral leishmaniasis is a chronic protozoan disease caused by Leishmania donovani, an obligatory intracellular parasite that resides and multiplies within macrophages of the reticuloendothelial system. The aim of this study was to evaluate the efficacy of nine novel synthetic chromone derivatives as antileishmanial molecules in experimental murine visceral leishmaniasis. In vitro activity of the molecules (2, 5 and 10 μg/ml) was assessed against promastigotes of both pentavalent antimonial-responsive strain AG83 and pentavalent antimonial-resistant strain GE1F8R at days 2 (48 h), 4 (96 h) and 6 (144 h). The efficacy of the most efficient chromone derivative [C-(6-Methyl-4-oxo-4H-1-benzopyran-3-yl)-N-(p-tolyl) nitrone], designated here as NP1, was also tested against intracellular amastigotes in vitro and in vivo. NP1, 5 μg/ml, inhibited the growth of AG83 and GE1F8R promastigotes by 98.57% (day 4) and 75.75% (day 6), respectively, and also inhibited the growth of intracellular amastigotes by 85% (day 3), compared to DMSO control. Treatment of L. donovani-infected mice with NP1 resulted in a 70% significant decrease in parasite load in the spleen in the 7th week after infection (5 mice in each group), with associated induction of interferon-γ synthesis by dose 2 (37.5 mg/kg body weight) compared to DMSO control. Dose 2 was found efficient over dose 1 (25 mg/kg body weight). Question: Does protective therapy with novel chromone derivative against Leishmania donovani infection induce Th1 response in vivo? Output:
PubmedQA108402	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Ischemic postconditioning has been found to decrease brain infarct area and spinal cord ischemic injury. In this study, we tested the hypothesis that ischemic postconditioning reduces global cerebral ischemia/reperfusion-induced structural and functional injury in rats. Ten-minute global ischemia was induced by 4-vessel occlusion in male Sprague-Dawley rats. The animals underwent postconditioning consisting of 3 cycles of 15-second/15-second (Post-15/15), 30-second/30-second (Post-30/30), or 60-second/15-second (Post-60/15) reperfusion/reocclusion or 15-second/15-second reperfusion/reocclusion applied after a 45-second reperfusion (Post-45-15/15). Ten minutes of ischemia and 7 days of reperfusion destroyed 85.8% of CA1 hippocampal neurons and 64.1% of parietal cortical neurons. Three cycles of Post-15/15, Post-30/30, and Post-45-15/15 reperfusion/reocclusion markedly reduced neuronal loss after 7 days or 3 weeks of reperfusion and diminished the deficiency in spatial learning and memory. After reperfusion, a period of hyperperfusion followed by hypoperfusion was observed, both of which were blocked by postconditioning. The cytosolic level of cytochrome c increased significantly after 48 hours of reperfusion, and this was inhibited by Post-15/15, Post-30/30, and Post-45-15/15. However, 3 cycles of 60-second/15-second reperfusion/reocclusion failed to protect against neuronal damage, behavioral deficit, or cytochrome c translocation.\n Question: Does ischemic postconditioning protect against global cerebral ischemia/reperfusion-induced injury in rats?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Ischemic postconditioning has been found to decrease brain infarct area and spinal cord ischemic injury. In this study, we tested the hypothesis that ischemic postconditioning reduces global cerebral ischemia/reperfusion-induced structural and functional injury in rats. Ten-minute global ischemia was induced by 4-vessel occlusion in male Sprague-Dawley rats. The animals underwent postconditioning consisting of 3 cycles of 15-second/15-second (Post-15/15), 30-second/30-second (Post-30/30), or 60-second/15-second (Post-60/15) reperfusion/reocclusion or 15-second/15-second reperfusion/reocclusion applied after a 45-second reperfusion (Post-45-15/15). Ten minutes of ischemia and 7 days of reperfusion destroyed 85.8% of CA1 hippocampal neurons and 64.1% of parietal cortical neurons. Three cycles of Post-15/15, Post-30/30, and Post-45-15/15 reperfusion/reocclusion markedly reduced neuronal loss after 7 days or 3 weeks of reperfusion and diminished the deficiency in spatial learning and memory. After reperfusion, a period of hyperperfusion followed by hypoperfusion was observed, both of which were blocked by postconditioning. The cytosolic level of cytochrome c increased significantly after 48 hours of reperfusion, and this was inhibited by Post-15/15, Post-30/30, and Post-45-15/15. However, 3 cycles of 60-second/15-second reperfusion/reocclusion failed to protect against neuronal damage, behavioral deficit, or cytochrome c translocation. Question: Does ischemic postconditioning protect against global cerebral ischemia/reperfusion-induced injury in rats? Output:
PubmedQA106292	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To conduct a dose-finding trial using a single low dose and dose escalation of a higher dose of thalidomide in patients with metastatic renal cell carcinoma (RCC), and to evaluate the antineoplastic effectiveness of thalidomide as an anti-angiogenic agent on RCC. The 14 patients enrolled in the study had progressive measurable metastatic RCC and consented to participate. Patients were randomized to either a fixed low dose of 200 mg of thalidomide or to a high dose of 800 mg that was increased to a maximum dose of 1200 mg daily. Patients were evaluated for response after 8 weeks of therapy. Stable disease was achieved in six patients and was seen in both the low-dose and high-dose thalidomide groups. The median overall survival was 9 months. The low-dose thalidomide regimen was better tolerated and patients survived longer than those on the high-dose regimen (16 vs 6 months, P = 0.04)\n Question: Is a lower dose of thalidomide better than a high dose in metastatic renal cell carcinoma?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To conduct a dose-finding trial using a single low dose and dose escalation of a higher dose of thalidomide in patients with metastatic renal cell carcinoma (RCC), and to evaluate the antineoplastic effectiveness of thalidomide as an anti-angiogenic agent on RCC. The 14 patients enrolled in the study had progressive measurable metastatic RCC and consented to participate. Patients were randomized to either a fixed low dose of 200 mg of thalidomide or to a high dose of 800 mg that was increased to a maximum dose of 1200 mg daily. Patients were evaluated for response after 8 weeks of therapy. Stable disease was achieved in six patients and was seen in both the low-dose and high-dose thalidomide groups. The median overall survival was 9 months. The low-dose thalidomide regimen was better tolerated and patients survived longer than those on the high-dose regimen (16 vs 6 months, P = 0.04) Question: Is a lower dose of thalidomide better than a high dose in metastatic renal cell carcinoma? Output:
PubmedQA91896	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Down's syndrome patients express a neurodegenerative disorder and mental retardation. We studied the reactivity of EEG and its correlation with neuropsychological test score in Down's syndrome. We studied 32 patients with Down's syndrome and 31 controls for blocking of occipital EEG activity. The temporo-occipital EEG with eyes open (EO) was compared with resting EEG with eyes closed (EC), (EC/EO ratio). Both Down patients and controls showed significant diminution of alpha, beta and theta activity and decrease of EEG frequency with EO. However, there was a significant impairment in Down patients in the EC/EO ratio in alpha band, compared to controls. The controls had no correlation of the alpha EC/EO ratio with age or gender. The Down patients showed a significant correlation of this variable with age which is in accordance with a gradually progressing disease. They had also significant correlations of the alpha EC/EO ratio and neuropsychological test scores which indicates that this ratio may be a more general measure of cerebral or hemispherical dysfunction than a mere impairment of visual activation. Down patients also showed significant differences in resting EEG variables, compared to the controls, even if the conventional EEG showed normal or mildly slowed dominant occipital rhythm in most of the patients. The correlation analysis between resting EEG and EC/EO ratio variables pointed out that they are relatively independent, representing different factors in the regulation of EEG.\n Question: Does eEG reactivity correlate with neuropsychological test scores in Down 's syndrome?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Down's syndrome patients express a neurodegenerative disorder and mental retardation. We studied the reactivity of EEG and its correlation with neuropsychological test score in Down's syndrome. We studied 32 patients with Down's syndrome and 31 controls for blocking of occipital EEG activity. The temporo-occipital EEG with eyes open (EO) was compared with resting EEG with eyes closed (EC), (EC/EO ratio). Both Down patients and controls showed significant diminution of alpha, beta and theta activity and decrease of EEG frequency with EO. However, there was a significant impairment in Down patients in the EC/EO ratio in alpha band, compared to controls. The controls had no correlation of the alpha EC/EO ratio with age or gender. The Down patients showed a significant correlation of this variable with age which is in accordance with a gradually progressing disease. They had also significant correlations of the alpha EC/EO ratio and neuropsychological test scores which indicates that this ratio may be a more general measure of cerebral or hemispherical dysfunction than a mere impairment of visual activation. Down patients also showed significant differences in resting EEG variables, compared to the controls, even if the conventional EEG showed normal or mildly slowed dominant occipital rhythm in most of the patients. The correlation analysis between resting EEG and EC/EO ratio variables pointed out that they are relatively independent, representing different factors in the regulation of EEG. Question: Does eEG reactivity correlate with neuropsychological test scores in Down 's syndrome? Output:
PubmedQA86303	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Thrombin generation (TG) in plasma can be monitored continuously with a fluorogenic thrombin substrate using calibrated automated thrombinography (CAT). In the presence of low concentrations of a reversible direct thrombin inhibitor (DTI), CAT shows an unexpected effect: the endogenous thrombin potential (ETP) increases at low concentrations of the inhibitor to subsequently decrease concentration dependently at higher concentrations (> approximately 100 nm). To find an explanation for this phenomenon, we measured the concentrations of free thrombin and alpha(2)-macroglobulin-thrombin complex (alpha(2)MT) with a sub-sampling technique in the presence of AR-H067637, a selective DTI. At all concentrations of the DTI there was a gradual dose-dependent decrease in the concentration of free, not-inhibited thrombin but a transient increase in free alpha(2)MT due to competition of thrombin and alpha(2)MT for the inhibitor. Because the CAT technique uses an algorithm to subtract alpha(2)MT activity from the total amidolytic activity, this transient increase in alpha(2)MT activity is not subtracted and erroneously attributed to thrombin itself.\n Question: Is the paradoxical stimulation by a reversible thrombin inhibitor of thrombin generation in plasma measured with thrombinography caused by alpha-macroglobulin-thrombin?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Thrombin generation (TG) in plasma can be monitored continuously with a fluorogenic thrombin substrate using calibrated automated thrombinography (CAT). In the presence of low concentrations of a reversible direct thrombin inhibitor (DTI), CAT shows an unexpected effect: the endogenous thrombin potential (ETP) increases at low concentrations of the inhibitor to subsequently decrease concentration dependently at higher concentrations (> approximately 100 nm). To find an explanation for this phenomenon, we measured the concentrations of free thrombin and alpha(2)-macroglobulin-thrombin complex (alpha(2)MT) with a sub-sampling technique in the presence of AR-H067637, a selective DTI. At all concentrations of the DTI there was a gradual dose-dependent decrease in the concentration of free, not-inhibited thrombin but a transient increase in free alpha(2)MT due to competition of thrombin and alpha(2)MT for the inhibitor. Because the CAT technique uses an algorithm to subtract alpha(2)MT activity from the total amidolytic activity, this transient increase in alpha(2)MT activity is not subtracted and erroneously attributed to thrombin itself. Question: Is the paradoxical stimulation by a reversible thrombin inhibitor of thrombin generation in plasma measured with thrombinography caused by alpha-macroglobulin-thrombin? Output:
PubmedQA196120	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To test the hypothesis that primed PMNLs in blood of chronic kidney disease patients release the active form of elastase and cathepsin G causing degradation of vital proteins and promote tissue damage. RT-PCR, immunocytochemical staining, immunoblotting, and FACS analyses were used to study these enzymes in hemodialysis patients (HD) versus healthy normal controls (NC). Using PMNLs and endothelial cells cocultivation system we measure the effect of HD PMNLs on the endothelial VE-cadherin, an essential protein for maintaining endothelial integrity. Levels of elastase and cathepsin G were reduced in PMNLs of HD patients, while mRNA enzymes levels were not different. Elevated levels of the active form of these enzymes were found in blood of HD patients compared to NC.HD plasma had higher levels of soluble VE-cadherin present in three molecular forms: whole 140 kDa molecule and two fragments of 100 and 40 kDa. Cocultivation studies showed that primed PMNLs cleave the endothelial cadherin, resulting in a 100 kDa fragment.\n Question: Do elastase and cathepsin G from primed leukocytes cleave vascular endothelial cadherin in hemodialysis patients?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To test the hypothesis that primed PMNLs in blood of chronic kidney disease patients release the active form of elastase and cathepsin G causing degradation of vital proteins and promote tissue damage. RT-PCR, immunocytochemical staining, immunoblotting, and FACS analyses were used to study these enzymes in hemodialysis patients (HD) versus healthy normal controls (NC). Using PMNLs and endothelial cells cocultivation system we measure the effect of HD PMNLs on the endothelial VE-cadherin, an essential protein for maintaining endothelial integrity. Levels of elastase and cathepsin G were reduced in PMNLs of HD patients, while mRNA enzymes levels were not different. Elevated levels of the active form of these enzymes were found in blood of HD patients compared to NC.HD plasma had higher levels of soluble VE-cadherin present in three molecular forms: whole 140 kDa molecule and two fragments of 100 and 40 kDa. Cocultivation studies showed that primed PMNLs cleave the endothelial cadherin, resulting in a 100 kDa fragment. Question: Do elastase and cathepsin G from primed leukocytes cleave vascular endothelial cadherin in hemodialysis patients? Output:
PubmedQA15450	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The main problem of tremor is the damage caused to the quality of the life of patients, especially those at more advanced ages. There is not a consensus yet about the origins of this disorder, but it can be examined in the correlations between the biological signs of aging and the tremor characteristics. This work sought correlations between the osmotic fragility of erythrocytes and features extracted from electromyographic (EMG) activity resulting from physiological tremor in healthy patients (N = 44) at different ages (24-87 years). The osmotic fragility was spectrophotometrically evaluated by the dependence of hemolysis, provided by the absorbance in 540 nm (A54o), on the concentration of NaCl. The data were adjusted to curves of sigmoidal regression and characterized by the half transition point (H50), amplitude of lysis transition (dx) and values of A540 in the curve regions that characterize the presence of lysed (A1) and preserved erythrocytes (A2). The approximate entropy was estimated from EMG signals detected from the extensor carpi ulnaris muscle during the movement of the hand of subjects holding up a laser pen towards an Archimedes spiral, fixed in a whiteboard. The evaluations were carried out with the laser pen at rest, at the center of the spiral, and in movement from the center to the outside and from outside to the center. The correlations among the parameters of osmotic fragility, tremor and age were tested. Negative correlations with age were found for A1 and dx. With the hand at rest, a positive correlation with H50 was found for the approximate entropy. Negative correlations with H50 were found for the entropy with the hand in movement, as from the center to the outside or from the outside to the center of the spiral.\n Question: Does the approximate entropy of the electromyographic signals of tremor correlate with the osmotic fragility of human erythrocytes?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The main problem of tremor is the damage caused to the quality of the life of patients, especially those at more advanced ages. There is not a consensus yet about the origins of this disorder, but it can be examined in the correlations between the biological signs of aging and the tremor characteristics. This work sought correlations between the osmotic fragility of erythrocytes and features extracted from electromyographic (EMG) activity resulting from physiological tremor in healthy patients (N = 44) at different ages (24-87 years). The osmotic fragility was spectrophotometrically evaluated by the dependence of hemolysis, provided by the absorbance in 540 nm (A54o), on the concentration of NaCl. The data were adjusted to curves of sigmoidal regression and characterized by the half transition point (H50), amplitude of lysis transition (dx) and values of A540 in the curve regions that characterize the presence of lysed (A1) and preserved erythrocytes (A2). The approximate entropy was estimated from EMG signals detected from the extensor carpi ulnaris muscle during the movement of the hand of subjects holding up a laser pen towards an Archimedes spiral, fixed in a whiteboard. The evaluations were carried out with the laser pen at rest, at the center of the spiral, and in movement from the center to the outside and from outside to the center. The correlations among the parameters of osmotic fragility, tremor and age were tested. Negative correlations with age were found for A1 and dx. With the hand at rest, a positive correlation with H50 was found for the approximate entropy. Negative correlations with H50 were found for the entropy with the hand in movement, as from the center to the outside or from the outside to the center of the spiral. Question: Does the approximate entropy of the electromyographic signals of tremor correlate with the osmotic fragility of human erythrocytes? Output:
PubmedQA59760	[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Natalizumab is an efficacious agent for induction and maintenance of remission in patients with Crohn's disease (CD) who have failed anti-tumor necrosis factor agents. We aimed to assess the impact of endoscopic severity and mucosal healing on the long-term outcome of natalizumab treatment in CD. We retrospectively assessed endoscopic severity according to the Simple Endoscopic Score for Crohn's Disease in patients with CD who received natalizumab therapy. The degree of endoscopic severity before natalizumab treatment and mucosal healing after treatment and their correlation with long-term outcome were studied. Thirty-two patients with CD (15 male, median age 32.5 years) receiving natalizumab underwent at least 1 colonoscopy before or during natalizumab treatment. All patients had previously failed immunomodulator(s), and 31 failed anti-tumor necrosis factor agent(s). Mean duration of natalizumab treatment was 14.1 months. Baseline Simple Endoscopic Score for CD was categorized into quartiles, and those with a greater score were less likely to respond to treatment as assessed by Kaplan-Meier survival analysis (n = 32, log-rank test, P = 0.0055). Mucosal healing (decrease of Simple Endoscopic Score for CD of >70%) was achieved in 11 of 26 patients (42.3%), and this was correlated with an improved long-term outcome (log-rank test, P = 0.0063).\n Question: Is mucosal healing associated with improved long-term outcome of maintenance therapy with natalizumab in Crohn 's disease?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Natalizumab is an efficacious agent for induction and maintenance of remission in patients with Crohn's disease (CD) who have failed anti-tumor necrosis factor agents. We aimed to assess the impact of endoscopic severity and mucosal healing on the long-term outcome of natalizumab treatment in CD. We retrospectively assessed endoscopic severity according to the Simple Endoscopic Score for Crohn's Disease in patients with CD who received natalizumab therapy. The degree of endoscopic severity before natalizumab treatment and mucosal healing after treatment and their correlation with long-term outcome were studied. Thirty-two patients with CD (15 male, median age 32.5 years) receiving natalizumab underwent at least 1 colonoscopy before or during natalizumab treatment. All patients had previously failed immunomodulator(s), and 31 failed anti-tumor necrosis factor agent(s). Mean duration of natalizumab treatment was 14.1 months. Baseline Simple Endoscopic Score for CD was categorized into quartiles, and those with a greater score were less likely to respond to treatment as assessed by Kaplan-Meier survival analysis (n = 32, log-rank test, P = 0.0055). Mucosal healing (decrease of Simple Endoscopic Score for CD of >70%) was achieved in 11 of 26 patients (42.3%), and this was correlated with an improved long-term outcome (log-rank test, P = 0.0063). Question: Is mucosal healing associated with improved long-term outcome of maintenance therapy with natalizumab in Crohn 's disease? Output: