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PubmedQA204198
|
[
{
"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: Butanol isomers are regarded as more suitable fuel substitutes than bioethanol. n-Butanol is naturally produced by some Clostridia species, but due to inherent problems with clostridial fermentations, industrially more relevant organisms have been genetically engineered for n-butanol production. Although the yeast Saccharomyces cerevisiae holds significant advantages in terms of scalable industrial fermentation, n-butanol yields and titers obtained so far are only low. Here we report a thorough analysis and significant improvements of n-butanol production from glucose with yeast via the acetoacetyl-CoA-derived pathway. First, we established an improved n-butanol pathway by testing various isoenzymes of different pathway reactions. This resulted in n-butanol titers around 15 mg/L in synthetic medium after 74 h. As the initial substrate of the n-butanol pathway is acetyl-coenzyme A (acetyl-CoA) and most intermediates are bound to coenzyme A (CoA), we increased CoA synthesis by overexpression of the pantothenate kinase coaA gene from Escherichia coli. Supplementation with pantothenate increased n-butanol production up to 34 mg/L. Additional reduction of ethanol formation by deletion of alcohol dehydrogenase genes ADH1-5 led to n-butanol titers of 71 mg/L. Further expression of a mutant form of an ATP independent acetylating acetaldehyde dehydrogenase, adhE(A267T/E568K), converting acetaldehyde into acetyl-CoA, resulted in 95 mg/L n-butanol. In the final strain, the n-butanol pathway genes, coaA and adhE (A267T/E568K), were stably integrated into the yeast genome, thereby deleting another alcohol dehydrogenase gene, ADH6, and GPD2-encoding glycerol-3-phosphate dehydrogenase. This led to a further decrease in ethanol and glycerol by-product formation and elevated redox power in the form of NADH. With the addition of pantothenate, this strain produced n-butanol up to a titer of 130 ± 20 mg/L and a yield of 0.012 g/g glucose. These are the highest values reported so far for S. cerevisiae in synthetic medium via an acetoacetyl-CoA-derived n-butanol pathway.\n Question: Is n-Butanol production in Saccharomyces cerevisiae limited by the availability of coenzyme A and cytosolic acetyl-CoA?\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: Butanol isomers are regarded as more suitable fuel substitutes than bioethanol. n-Butanol is naturally produced by some Clostridia species, but due to inherent problems with clostridial fermentations, industrially more relevant organisms have been genetically engineered for n-butanol production. Although the yeast Saccharomyces cerevisiae holds significant advantages in terms of scalable industrial fermentation, n-butanol yields and titers obtained so far are only low. Here we report a thorough analysis and significant improvements of n-butanol production from glucose with yeast via the acetoacetyl-CoA-derived pathway. First, we established an improved n-butanol pathway by testing various isoenzymes of different pathway reactions. This resulted in n-butanol titers around 15 mg/L in synthetic medium after 74 h. As the initial substrate of the n-butanol pathway is acetyl-coenzyme A (acetyl-CoA) and most intermediates are bound to coenzyme A (CoA), we increased CoA synthesis by overexpression of the pantothenate kinase coaA gene from Escherichia coli. Supplementation with pantothenate increased n-butanol production up to 34 mg/L. Additional reduction of ethanol formation by deletion of alcohol dehydrogenase genes ADH1-5 led to n-butanol titers of 71 mg/L. Further expression of a mutant form of an ATP independent acetylating acetaldehyde dehydrogenase, adhE(A267T/E568K), converting acetaldehyde into acetyl-CoA, resulted in 95 mg/L n-butanol. In the final strain, the n-butanol pathway genes, coaA and adhE (A267T/E568K), were stably integrated into the yeast genome, thereby deleting another alcohol dehydrogenase gene, ADH6, and GPD2-encoding glycerol-3-phosphate dehydrogenase. This led to a further decrease in ethanol and glycerol by-product formation and elevated redox power in the form of NADH. With the addition of pantothenate, this strain produced n-butanol up to a titer of 130 ± 20 mg/L and a yield of 0.012 g/g glucose. These are the highest values reported so far for S. cerevisiae in synthetic medium via an acetoacetyl-CoA-derived n-butanol pathway.
Question: Is n-Butanol production in Saccharomyces cerevisiae limited by the availability of coenzyme A and cytosolic acetyl-CoA?
Output:
|
PubmedQA99116
|
[
{
"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 bacterial rhinosinusitis (ABRS) is a common illness that is routinely managed by physicians from several different specialties. However, the actual diagnostic and treatment preferences of physicians from these different specialties are not known. To determine whether the radiographic evaluation and management of community-acquired ABRS differs according to medical specialty. Randomized survey of 450 board-certified physicians in the United States from family medicine, general internal medicine, and otolaryngology. Responding physicians' use of diagnostic radiography as well as choice and duration of antimicrobial and adjunctive treatments of ABRS. Otolaryngologists were more likely to use supportive diagnostic radiography (P =.04). They were also more likely to treat patients with adjunctive therapy, such as topical decongestants (P =.01), guaifenesin (P =.01), and saline nasal irrigation (P =.01), in addition to antibiotics. Otolaryngologists prescribed more medications to treat patients with ABRS than primary care physicians (P =.01). There were no significant differences in diagnosis and management by family physicians and general internists.\n Question: Is physician specialty associated with differences in the evaluation and management of acute bacterial rhinosinusitis?\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 bacterial rhinosinusitis (ABRS) is a common illness that is routinely managed by physicians from several different specialties. However, the actual diagnostic and treatment preferences of physicians from these different specialties are not known. To determine whether the radiographic evaluation and management of community-acquired ABRS differs according to medical specialty. Randomized survey of 450 board-certified physicians in the United States from family medicine, general internal medicine, and otolaryngology. Responding physicians' use of diagnostic radiography as well as choice and duration of antimicrobial and adjunctive treatments of ABRS. Otolaryngologists were more likely to use supportive diagnostic radiography (P =.04). They were also more likely to treat patients with adjunctive therapy, such as topical decongestants (P =.01), guaifenesin (P =.01), and saline nasal irrigation (P =.01), in addition to antibiotics. Otolaryngologists prescribed more medications to treat patients with ABRS than primary care physicians (P =.01). There were no significant differences in diagnosis and management by family physicians and general internists.
Question: Is physician specialty associated with differences in the evaluation and management of acute bacterial rhinosinusitis?
Output:
|
PubmedQA42691
|
[
{
"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 investigate the cause of increased incidence of impaired glucose tolerance and diabetes mellitus in patients with alpha-thalassaemia major and chronic hepatitis C virus (HCV) infection without cirrhosis of the liver. The study included 28 alpha-thalassaemic multi-transfused patients (14 females and 14 males; age, 25.7 +/- 6.3 years) with normal fasting glucose levels. Sixteen were seropositive for HCV and they had biopsy proven chronic hepatitis C without cirrhosis. An oral glucose tolerance test (OGTT) was performed. Glucose, insulin and C-peptide levels were measured every 30 min for 2 h. Fasting insulin resistance index (FIRI) was calculated according to the formula: FIRI = (fasting glucose x fasting insulin)/25. All patients had a normal OGTT except for two HCV positive and two HCV negative patients who had impaired glucose tolerance. HCV positive patients had higher fasting insulin levels (P = 0.02), higher fasting insulin/fasting glucose ratio (P = 0.017) and higher FIRI (P = 0.016) than HCV negative patients. During the OGTT, peak insulin levels occurred at 30 min in HCV negative patients but at 60 min in HCV positive. HCV infected patients had higher mean value of insulin at 60 (P = 0.017), 90 (P = 0.04), and 120 min (P = 0.04), and higher mean increment above basal at 60 (P = 0.015), 90 (P = 0.018) and 120 min (P = 0.05). The area under the curve (AUC) of insulin was also greater in HCV positive patients as compared to HCV negative (P = 0.04), although the AUC of glucose and the glucose levels at all time points of the OGTT were similar in both groups.\n Question: Does chronic hepatitis C virus infection without cirrhosis induce insulin resistance in patients with alpha-thalassaemia major?\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 investigate the cause of increased incidence of impaired glucose tolerance and diabetes mellitus in patients with alpha-thalassaemia major and chronic hepatitis C virus (HCV) infection without cirrhosis of the liver. The study included 28 alpha-thalassaemic multi-transfused patients (14 females and 14 males; age, 25.7 +/- 6.3 years) with normal fasting glucose levels. Sixteen were seropositive for HCV and they had biopsy proven chronic hepatitis C without cirrhosis. An oral glucose tolerance test (OGTT) was performed. Glucose, insulin and C-peptide levels were measured every 30 min for 2 h. Fasting insulin resistance index (FIRI) was calculated according to the formula: FIRI = (fasting glucose x fasting insulin)/25. All patients had a normal OGTT except for two HCV positive and two HCV negative patients who had impaired glucose tolerance. HCV positive patients had higher fasting insulin levels (P = 0.02), higher fasting insulin/fasting glucose ratio (P = 0.017) and higher FIRI (P = 0.016) than HCV negative patients. During the OGTT, peak insulin levels occurred at 30 min in HCV negative patients but at 60 min in HCV positive. HCV infected patients had higher mean value of insulin at 60 (P = 0.017), 90 (P = 0.04), and 120 min (P = 0.04), and higher mean increment above basal at 60 (P = 0.015), 90 (P = 0.018) and 120 min (P = 0.05). The area under the curve (AUC) of insulin was also greater in HCV positive patients as compared to HCV negative (P = 0.04), although the AUC of glucose and the glucose levels at all time points of the OGTT were similar in both groups.
Question: Does chronic hepatitis C virus infection without cirrhosis induce insulin resistance in patients with alpha-thalassaemia major?
Output:
|
PubmedQA56284
|
[
{
"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: There are several treatment modalities available for diabetes; however, the effects of the different medications on coronary artery disease are less understood. The purpose of this study was to evaluate the correlation of insulin-sensitizing therapy with the outcome of stress myocardial perfusion testing and to compare it with conventional therapy. Of 417 patients referred to stress testing for evaluation of chest pain, 222 were identified as being treated with conventional therapy only (insulin and insulin secretagogues) and 195 as being treated with insulin sensitizers (metformin and thiazolidinediones (TZD)). Multivariate logistic regression models were used to correct for confounding factors and to determine the independent relation between treatment type and stress-test outcome. Ischaemia, infarction and the composite outcome were less frequent in the insulin-sensitizer group than in the conventional therapy group (odds ratio (OR) = 0.39, P = 0.025; OR = 0.32, P = 0.021 and OR = 0.38, P = 0.009, respectively). The subgroup analysis showed that treatment with metformin (n = 125) compared with conventional therapy was associated with less infarction or the composite outcome of ischaemia and/or ischaemia (OR = 0.18 (95% confidence interval (CI): 0.05-0.66), P = 0.010; OR = 0.34 (95%CI: 0.15-0.80), P = 0.014, respectively). Treatment with TZD (n = 43) was associated with a trend to less frequent ischaemia (OR = 0.18 (95%CI: 0.03-1.01), P = 0.051).\n Question: Are insulin-sensitizing antihyperglycaemic medications associated with better outcome in patients with diabetes undergoing cardiac stress testing?\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: There are several treatment modalities available for diabetes; however, the effects of the different medications on coronary artery disease are less understood. The purpose of this study was to evaluate the correlation of insulin-sensitizing therapy with the outcome of stress myocardial perfusion testing and to compare it with conventional therapy. Of 417 patients referred to stress testing for evaluation of chest pain, 222 were identified as being treated with conventional therapy only (insulin and insulin secretagogues) and 195 as being treated with insulin sensitizers (metformin and thiazolidinediones (TZD)). Multivariate logistic regression models were used to correct for confounding factors and to determine the independent relation between treatment type and stress-test outcome. Ischaemia, infarction and the composite outcome were less frequent in the insulin-sensitizer group than in the conventional therapy group (odds ratio (OR) = 0.39, P = 0.025; OR = 0.32, P = 0.021 and OR = 0.38, P = 0.009, respectively). The subgroup analysis showed that treatment with metformin (n = 125) compared with conventional therapy was associated with less infarction or the composite outcome of ischaemia and/or ischaemia (OR = 0.18 (95% confidence interval (CI): 0.05-0.66), P = 0.010; OR = 0.34 (95%CI: 0.15-0.80), P = 0.014, respectively). Treatment with TZD (n = 43) was associated with a trend to less frequent ischaemia (OR = 0.18 (95%CI: 0.03-1.01), P = 0.051).
Question: Are insulin-sensitizing antihyperglycaemic medications associated with better outcome in patients with diabetes undergoing cardiac stress testing?
Output:
|
PubmedQA104695
|
[
{
"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: AMPK was shown to negatively regulate FcεRI activation, and FcεR-mediated Fyn activation can counteract the LKB1/AMPK axis in mast cells. However, the relationship between the major Src family kinase Lyn and AMPK remains poorly defined. Here, we investigate the molecular mechanism for AMPK inhibition by FcεRI-Lyn signaling in rat RBL-2H3 cells. We found that FcεRI activation could rapidly inhibit AMPK activation through increased AMPK phosphorylation at the inhibitory Ser485/491 residues without a change at the activating Th172 residue, and this was accompanied by a reduction of ACC phosphorylation. Using specific inhibitors and gene silencing, we found that such AMPK inhibition involved a signaling cascade through Lyn-Syk-Akt. When AMPK was activated by AICAR, A769662 and metformin, FcεRI-mediated Syk, ERK, JNK and p38 activation, and TNFα release were all inhibited. Consistently, AMPK inhibition by compound C increased FcεRI-mediated Lyn activation. Moreover, AMPK activation dominantly impaired IgE-induced recruitment of signal proteins to the FcεRI by blocking the formation of FcεRIβ-Lyn-Syk, FcεRIγ-Lyn-Syk, and AMPK-FcεRIβ complexes. In vitro kinase assay further revealed the ability of AMPKα2 to phosphorylate FcεRIβ in the complex. In vivo, AMPK activation by metformin could readily reduce vascular permeability and ear swelling in a mouse model of passive cutaneous anaphylaxis mediated by IgE. In summary, our findings demonstrate that IgE-mediated FcεRI activation results in AMPK inhibition through activation of Lyn-Syk-Akt pathway, and as such FcεRI receptor can efficiently propagate Lyn-mediated allergic signaling and response. These results provide important insights into the use of AMPK activators for the treatment of allergic diseases.\n Question: Does inhibition of AMPK through Lyn-Syk-Akt enhance FcεRI signal pathways for allergic response?\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: AMPK was shown to negatively regulate FcεRI activation, and FcεR-mediated Fyn activation can counteract the LKB1/AMPK axis in mast cells. However, the relationship between the major Src family kinase Lyn and AMPK remains poorly defined. Here, we investigate the molecular mechanism for AMPK inhibition by FcεRI-Lyn signaling in rat RBL-2H3 cells. We found that FcεRI activation could rapidly inhibit AMPK activation through increased AMPK phosphorylation at the inhibitory Ser485/491 residues without a change at the activating Th172 residue, and this was accompanied by a reduction of ACC phosphorylation. Using specific inhibitors and gene silencing, we found that such AMPK inhibition involved a signaling cascade through Lyn-Syk-Akt. When AMPK was activated by AICAR, A769662 and metformin, FcεRI-mediated Syk, ERK, JNK and p38 activation, and TNFα release were all inhibited. Consistently, AMPK inhibition by compound C increased FcεRI-mediated Lyn activation. Moreover, AMPK activation dominantly impaired IgE-induced recruitment of signal proteins to the FcεRI by blocking the formation of FcεRIβ-Lyn-Syk, FcεRIγ-Lyn-Syk, and AMPK-FcεRIβ complexes. In vitro kinase assay further revealed the ability of AMPKα2 to phosphorylate FcεRIβ in the complex. In vivo, AMPK activation by metformin could readily reduce vascular permeability and ear swelling in a mouse model of passive cutaneous anaphylaxis mediated by IgE. In summary, our findings demonstrate that IgE-mediated FcεRI activation results in AMPK inhibition through activation of Lyn-Syk-Akt pathway, and as such FcεRI receptor can efficiently propagate Lyn-mediated allergic signaling and response. These results provide important insights into the use of AMPK activators for the treatment of allergic diseases.
Question: Does inhibition of AMPK through Lyn-Syk-Akt enhance FcεRI signal pathways for allergic response?
Output:
|
PubmedQA167223
|
[
{
"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: Parental support interventions have shown some effectiveness in improving children's dietary and physical activity habits and preventing overweight and obesity. To date, there is limited research on barriers and facilitators of school-based parental support interventions targeting overweight and obesity. This study aimed to describe barriers and facilitators influencing implementation of the Healthy School Start (HSS) intervention in disadvantaged areas in Stockholm, Sweden, from the perspective of parents and teachers. Focus groups and individual interviews with teachers (n = 10) and focus groups with parents (n = 14) in the intervention group of the HSS were undertaken, guided by the Consolidated Framework for Implementation Research (CFIR). Transcriptions were analysed using qualitative content analysis in two steps: deductive sorting in two domains of the CFIR (intervention characteristics and process), and subsequent inductive analysis. The overarching theme \"tailoring the intervention to increase participant engagement\" was found. Among teachers, barriers and facilitators were related to how the intervention was introduced, perceptions of the usefulness of the classroom material, preparation ahead of the start of the intervention, cooperation between home and school and children's and parents' active engagement in the intervention activities. For parents, barriers and facilitators were related to the perceived relevance of the intervention, usefulness of the material, experiences of the Motivational Interviewing (MI) sessions, the family member targeted by the intervention, cooperation between home and school and parents' ability to act as good role models.\n Question: Does one size fit all-qualitative process evaluation of the Healthy School Start parental support programme to prevent overweight and obesity among children in disadvantaged areas in Sweden?\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: Parental support interventions have shown some effectiveness in improving children's dietary and physical activity habits and preventing overweight and obesity. To date, there is limited research on barriers and facilitators of school-based parental support interventions targeting overweight and obesity. This study aimed to describe barriers and facilitators influencing implementation of the Healthy School Start (HSS) intervention in disadvantaged areas in Stockholm, Sweden, from the perspective of parents and teachers. Focus groups and individual interviews with teachers (n = 10) and focus groups with parents (n = 14) in the intervention group of the HSS were undertaken, guided by the Consolidated Framework for Implementation Research (CFIR). Transcriptions were analysed using qualitative content analysis in two steps: deductive sorting in two domains of the CFIR (intervention characteristics and process), and subsequent inductive analysis. The overarching theme "tailoring the intervention to increase participant engagement" was found. Among teachers, barriers and facilitators were related to how the intervention was introduced, perceptions of the usefulness of the classroom material, preparation ahead of the start of the intervention, cooperation between home and school and children's and parents' active engagement in the intervention activities. For parents, barriers and facilitators were related to the perceived relevance of the intervention, usefulness of the material, experiences of the Motivational Interviewing (MI) sessions, the family member targeted by the intervention, cooperation between home and school and parents' ability to act as good role models.
Question: Does one size fit all-qualitative process evaluation of the Healthy School Start parental support programme to prevent overweight and obesity among children in disadvantaged areas in Sweden?
Output:
|
PubmedQA33371
|
[
{
"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: Exposure for open cholecystectomy entails lateral, caudal traction on the gallbladder infundibulum, which results in opening the angle between the cystic and hepatic ducts. Laparoscopic cholecystectomy (LC), as initially described, is done with cephalad traction on the gallbladder. We hypothesized LC exposure technique narrows the angle between the cystic and hepatic ducts, placing them at increased risk of injury. Twenty-three patients had routine LC. Cystic duct cholangiography (IOC) was done with a flexible 5-Fr catheter via a percutaneous introducer placed anterior to the gallbladder. Exposure of Calot's triangle was maintained with cephalad traction on the gallbladder fundus. IOC was repeated after allowing the organ to assume the anatomic position. The cholangiograms were inspected for significant differences, and the angle of the cystic to the hepatic duct (CDHD) was measured by a blinded radiologist. The mean angle of the cystic to hepatic duct was 30 degrees +/- 19 degrees in the IOCs taken with cephalad traction on the gallbladder fundus vs 59 degrees +/- 22 degrees, P < 0.001, in the cholangiograms taken without traction. A filling defect at the cystic-hepatic duct junction was present in 39% of IOC taken with traction vs none without traction. The intrahepatic ducts were seen in all films without traction, whereas the intrahepatic ducts were not visualized in 13% of IOCs taken with traction.\n Question: Does exposure for laparoscopic cholecystectomy dissection adversely alter biliary ductal 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: Exposure for open cholecystectomy entails lateral, caudal traction on the gallbladder infundibulum, which results in opening the angle between the cystic and hepatic ducts. Laparoscopic cholecystectomy (LC), as initially described, is done with cephalad traction on the gallbladder. We hypothesized LC exposure technique narrows the angle between the cystic and hepatic ducts, placing them at increased risk of injury. Twenty-three patients had routine LC. Cystic duct cholangiography (IOC) was done with a flexible 5-Fr catheter via a percutaneous introducer placed anterior to the gallbladder. Exposure of Calot's triangle was maintained with cephalad traction on the gallbladder fundus. IOC was repeated after allowing the organ to assume the anatomic position. The cholangiograms were inspected for significant differences, and the angle of the cystic to the hepatic duct (CDHD) was measured by a blinded radiologist. The mean angle of the cystic to hepatic duct was 30 degrees +/- 19 degrees in the IOCs taken with cephalad traction on the gallbladder fundus vs 59 degrees +/- 22 degrees, P < 0.001, in the cholangiograms taken without traction. A filling defect at the cystic-hepatic duct junction was present in 39% of IOC taken with traction vs none without traction. The intrahepatic ducts were seen in all films without traction, whereas the intrahepatic ducts were not visualized in 13% of IOCs taken with traction.
Question: Does exposure for laparoscopic cholecystectomy dissection adversely alter biliary ductal anatomy?
Output:
|
PubmedQA176490
|
[
{
"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: Metabolic syndrome (MetS) is a health disorder that increases the risk for cardiovascular complications such as heart disease and type 2 diabetes. Some drugs used in patients with MetS are substrates of intestinal P-glycoprotein (P-gp), one of the most important efflux pumps that limit the absorption of xenobiotics. Thus, their bioavailability could be affected by changes in this transporter. Because one of the major causes of MetS in humans is excessive sugar intake, the aim of this study was to evaluate the effect of a fructose-rich diet on intestinal P-gp activity and protein expression in male Sprague-Dawley rats. Fructose-drinking animals received standard chow and 15% (w/v) fructose in the drinking water over 8 wk; control rats were fed on standard chow and tap water. Ileal protein expression of P-gp was 50% lower in fructose-drinking rats than in control animals. This reduction was confirmed by immunofluorescence microscopy. These results correlated well with the decrease of about 50% in the transport rate of the substrate rhodamine 123 in everted intestinal sacs. Finally, an increase of 62% in the intestinal absorption of digoxin, a P-gp substrate used as therapeutic drug, was observed in vivo, in fructose-drinking animals.\n Question: Does fructose-induced metabolic syndrome decrease protein expression and activity of intestinal P-glycoprotein?\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: Metabolic syndrome (MetS) is a health disorder that increases the risk for cardiovascular complications such as heart disease and type 2 diabetes. Some drugs used in patients with MetS are substrates of intestinal P-glycoprotein (P-gp), one of the most important efflux pumps that limit the absorption of xenobiotics. Thus, their bioavailability could be affected by changes in this transporter. Because one of the major causes of MetS in humans is excessive sugar intake, the aim of this study was to evaluate the effect of a fructose-rich diet on intestinal P-gp activity and protein expression in male Sprague-Dawley rats. Fructose-drinking animals received standard chow and 15% (w/v) fructose in the drinking water over 8 wk; control rats were fed on standard chow and tap water. Ileal protein expression of P-gp was 50% lower in fructose-drinking rats than in control animals. This reduction was confirmed by immunofluorescence microscopy. These results correlated well with the decrease of about 50% in the transport rate of the substrate rhodamine 123 in everted intestinal sacs. Finally, an increase of 62% in the intestinal absorption of digoxin, a P-gp substrate used as therapeutic drug, was observed in vivo, in fructose-drinking animals.
Question: Does fructose-induced metabolic syndrome decrease protein expression and activity of intestinal P-glycoprotein?
Output:
|
PubmedQA101673
|
[
{
"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: Leptin-induced cardiomyocyte hypertrophy is dependent on both RhoA and p38 mitogen-activated protein kinase (p38 MAPK) activation. The present study investigated the role of lipid raft/caveolae in these responses and assessed the nature of p38 MAPK activation in mediating leptin-induced hypertrophy. Studies were carried out using cultured neonatal rat ventricular myocytes. Pharmacological, molecular, microscopy, and confocal imaging techniques were used to assess the role of caveolae in leptin-induced hypertrophy and to study the underlying cellular mechanisms. Leptin (3.1 nmol/L) treatment for 24 h significantly increased caveolae number two-fold and increased expression of caveolin-3 to 278 +/- 14% of control values. These effects were associated with increased cell surface area by 29 +/- 5% and leucine incorporation by 40 +/- 6%. The hypertrophic effect of leptin was associated with significant activation of RhoA (422 +/- 26%) and a decrease in the G-actin-to-F-actin ratio from 3.1 +/- 0.2 to 0.9 +/- 0.1. Caveolae disruption with methyl-beta-cyclodextrin (MbetaCD) potently attenuated leptin-induced cell hypertrophy and the associated signalling. RhoA was detected in caveolae fraction of a sucrose gradient after treatment with leptin for 5 min, indicating subcellular translocation of RhoA: this effect was inhibited by MbetaCD, the RhoA inhibitor C3 exoenzyme, and by disruption of actin filaments with latrunculin B. Furthermore, leptin-induced hypertrophy was associated with p38 MAPK but not with extracellular signal-regulated kinase (ERK1/2) translocation to nuclei, which was inhibited by MbetaCD, C3 exoenzyme, and the Rho kinase inhibitor Y-27632.\n Question: Does leptin-induced cardiomyocyte hypertrophy involve selective caveolae and RhoA/ROCK-dependent p38 MAPK translocation to nuclei?\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: Leptin-induced cardiomyocyte hypertrophy is dependent on both RhoA and p38 mitogen-activated protein kinase (p38 MAPK) activation. The present study investigated the role of lipid raft/caveolae in these responses and assessed the nature of p38 MAPK activation in mediating leptin-induced hypertrophy. Studies were carried out using cultured neonatal rat ventricular myocytes. Pharmacological, molecular, microscopy, and confocal imaging techniques were used to assess the role of caveolae in leptin-induced hypertrophy and to study the underlying cellular mechanisms. Leptin (3.1 nmol/L) treatment for 24 h significantly increased caveolae number two-fold and increased expression of caveolin-3 to 278 +/- 14% of control values. These effects were associated with increased cell surface area by 29 +/- 5% and leucine incorporation by 40 +/- 6%. The hypertrophic effect of leptin was associated with significant activation of RhoA (422 +/- 26%) and a decrease in the G-actin-to-F-actin ratio from 3.1 +/- 0.2 to 0.9 +/- 0.1. Caveolae disruption with methyl-beta-cyclodextrin (MbetaCD) potently attenuated leptin-induced cell hypertrophy and the associated signalling. RhoA was detected in caveolae fraction of a sucrose gradient after treatment with leptin for 5 min, indicating subcellular translocation of RhoA: this effect was inhibited by MbetaCD, the RhoA inhibitor C3 exoenzyme, and by disruption of actin filaments with latrunculin B. Furthermore, leptin-induced hypertrophy was associated with p38 MAPK but not with extracellular signal-regulated kinase (ERK1/2) translocation to nuclei, which was inhibited by MbetaCD, C3 exoenzyme, and the Rho kinase inhibitor Y-27632.
Question: Does leptin-induced cardiomyocyte hypertrophy involve selective caveolae and RhoA/ROCK-dependent p38 MAPK translocation to nuclei?
Output:
|
PubmedQA135990
|
[
{
"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 investigated the influence of type one cannabinoid receptor (CB1) deficiency on acute heart failure (AHF) and the underlying mechanism. Acute heart failure syndrome is an important clinical problem because of its high morbidity and mortality rates. Activation of CB1 induces vascular dilation and reinforces the properties of morphine, long-standing therapies for AHF syndrome, but the effect of endogenous CB1 activation on AHF is largely unknown. Acute heart failure mouse model characterized by hypertension and pulmonary oedema was created by using transverse aortic constriction (TAC). Mortality, echocardiography, haemodynamic, morphology, and circulatory catecholamine levels in response to TAC were evaluated in CB1 knockout (KO) and wild-type mice. Type one cannabinoid receptor KO mice had a much higher mortality rate at 1 week after TAC attributable to AHF (65 vs. 11%, P< 0.001). One hour after TAC, CB1 KO mice had significant larger lung weight to body weight ratio (LW/BW, 14.53 + 1.09 mg/g in KO vs. 10.42 + 0.36 mg/g in WT, P < 0.01) and higher plasma epinephrine levels (9720 + 1226 pg/mL vs. 6378 + 832 pg/mL, P < 0.05). Pharmacological activation of CB1 reduced LW/BW in wild-type mice. Administration of epinephrine to wild-type TAC mice significantly increased left ventricular end-diastolic pressure and LW/BW, while CB1 agonists reduced the LW/BW and the plasma levels of catecholamine and increased myocardial activity of AMP-activated protein kinase.\n Question: Does deficiency of type 1 cannabinoid receptors worsen acute heart failure induced by pressure overload in mice?\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 investigated the influence of type one cannabinoid receptor (CB1) deficiency on acute heart failure (AHF) and the underlying mechanism. Acute heart failure syndrome is an important clinical problem because of its high morbidity and mortality rates. Activation of CB1 induces vascular dilation and reinforces the properties of morphine, long-standing therapies for AHF syndrome, but the effect of endogenous CB1 activation on AHF is largely unknown. Acute heart failure mouse model characterized by hypertension and pulmonary oedema was created by using transverse aortic constriction (TAC). Mortality, echocardiography, haemodynamic, morphology, and circulatory catecholamine levels in response to TAC were evaluated in CB1 knockout (KO) and wild-type mice. Type one cannabinoid receptor KO mice had a much higher mortality rate at 1 week after TAC attributable to AHF (65 vs. 11%, P< 0.001). One hour after TAC, CB1 KO mice had significant larger lung weight to body weight ratio (LW/BW, 14.53 + 1.09 mg/g in KO vs. 10.42 + 0.36 mg/g in WT, P < 0.01) and higher plasma epinephrine levels (9720 + 1226 pg/mL vs. 6378 + 832 pg/mL, P < 0.05). Pharmacological activation of CB1 reduced LW/BW in wild-type mice. Administration of epinephrine to wild-type TAC mice significantly increased left ventricular end-diastolic pressure and LW/BW, while CB1 agonists reduced the LW/BW and the plasma levels of catecholamine and increased myocardial activity of AMP-activated protein kinase.
Question: Does deficiency of type 1 cannabinoid receptors worsen acute heart failure induced by pressure overload in mice?
Output:
|
PubmedQA13437
|
[
{
"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 trophoblast Kunitz domain proteins (TKDPs) constitute a highly expressed, placenta-specific, multigene family restricted to ruminant ungulates and characterized by a C-terminal \"Kunitz\" domain, preceded by one or more unique N-terminal domains. TKDP-1 shares an almost identical expression pattern with interferon-tau, the \"maternal recognition of pregnancy protein\" in ruminants. Our goal here has been to determine whether the ovine (ov) Tkdp-1 and IFNT genes possess a similar transcriptional code. The ovTkdp-1 promoter has been cloned and characterized. As with the IFNT promoter, the Tkdp-1 promoter is responsive to Ets-2, and promoter-driven reporter activity can be increased over 700-fold in response to over-expression of Ets-2 and a constitutively active form of protein Kinase A (PKA). Unexpectedly, the promoter element of Tkdp-1 responsible for this up-regulation, unlike that of the IFNT, does not bind Ets-2. However, mutation of a CCAAT/enhancer binding element within this control region not only reduced basal transcriptional activity, but prevented Ets-2 as well as cyclic adenosine 5'-monophosphate (cAMP)/PKA and Ras/mitogen-activated protein kinase (MAPK) responsiveness. In vitro binding experiments and in vivo protein-protein interaction assays implicated CCAAT/enhancer binding protein-beta (C/EBP-beta) as involved in up-regulating the Tkdp-1 promoter activity. A combination of Ets-2 and C/EBP-beta can up-regulate expression of the minimal Tkdp-1 promoter as much as 930-fold in presence of a cAMP analog. An AP-1-like element adjacent to the CCAAT enhancer, which binds Jun family members, is required for basal and cAMP/ C/EBP-beta-dependent activation of the gene, but not for Ets-2-dependent activity.\n Question: Are ets-2 and C/EBP-beta important mediators of ovine trophoblast Kunitz domain protein-1 gene expression in trophoblast?\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 trophoblast Kunitz domain proteins (TKDPs) constitute a highly expressed, placenta-specific, multigene family restricted to ruminant ungulates and characterized by a C-terminal "Kunitz" domain, preceded by one or more unique N-terminal domains. TKDP-1 shares an almost identical expression pattern with interferon-tau, the "maternal recognition of pregnancy protein" in ruminants. Our goal here has been to determine whether the ovine (ov) Tkdp-1 and IFNT genes possess a similar transcriptional code. The ovTkdp-1 promoter has been cloned and characterized. As with the IFNT promoter, the Tkdp-1 promoter is responsive to Ets-2, and promoter-driven reporter activity can be increased over 700-fold in response to over-expression of Ets-2 and a constitutively active form of protein Kinase A (PKA). Unexpectedly, the promoter element of Tkdp-1 responsible for this up-regulation, unlike that of the IFNT, does not bind Ets-2. However, mutation of a CCAAT/enhancer binding element within this control region not only reduced basal transcriptional activity, but prevented Ets-2 as well as cyclic adenosine 5'-monophosphate (cAMP)/PKA and Ras/mitogen-activated protein kinase (MAPK) responsiveness. In vitro binding experiments and in vivo protein-protein interaction assays implicated CCAAT/enhancer binding protein-beta (C/EBP-beta) as involved in up-regulating the Tkdp-1 promoter activity. A combination of Ets-2 and C/EBP-beta can up-regulate expression of the minimal Tkdp-1 promoter as much as 930-fold in presence of a cAMP analog. An AP-1-like element adjacent to the CCAAT enhancer, which binds Jun family members, is required for basal and cAMP/ C/EBP-beta-dependent activation of the gene, but not for Ets-2-dependent activity.
Question: Are ets-2 and C/EBP-beta important mediators of ovine trophoblast Kunitz domain protein-1 gene expression in trophoblast?
Output:
|
PubmedQA188854
|
[
{
"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: Recent studies have identified macrophage-mediated injury as an important component in the development of diabetic nephropathy. The aim of this study was to investigate the correlations between serum allograft inflammatory factor-1 (AIF-1) concentration, which is a marker of activated macrophages, and diabetic nephropathy. Serum AIF-1 concentrations were measured in 284 patients with type 2 diabetes. We evaluated relationships of serum AIF-1 concentrations to degree of urinary albumin excretion (UAE) or estimated glomerular filtration rate (eGFR) in univariate and multivariate linear regression analyses. Serum AIF-1 concentrations positively correlated with logarithm of UAE (r=0.260, P<0.0001), whereas serum AIF-1 concentrations inversely correlated with eGFR (r=-0.312, P<0.0001). Mean serum AIF-1 concentration was higher in patients with macroalbuminuria than that in patients with normoalbuminuria (P=0.0001) or that in patients with microalbuminuria (P=0.0093). In multivariate linear regression analyses, serum AIF-1 concentrations were independently correlated with logarithm of UAE (β=0.213, P=0.0120) and with eGFR (β=-0.286, P=0.0011).\n Question: Is serum allograft inflammatory factor-1 a novel marker for diabetic nephropathy?\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: Recent studies have identified macrophage-mediated injury as an important component in the development of diabetic nephropathy. The aim of this study was to investigate the correlations between serum allograft inflammatory factor-1 (AIF-1) concentration, which is a marker of activated macrophages, and diabetic nephropathy. Serum AIF-1 concentrations were measured in 284 patients with type 2 diabetes. We evaluated relationships of serum AIF-1 concentrations to degree of urinary albumin excretion (UAE) or estimated glomerular filtration rate (eGFR) in univariate and multivariate linear regression analyses. Serum AIF-1 concentrations positively correlated with logarithm of UAE (r=0.260, P<0.0001), whereas serum AIF-1 concentrations inversely correlated with eGFR (r=-0.312, P<0.0001). Mean serum AIF-1 concentration was higher in patients with macroalbuminuria than that in patients with normoalbuminuria (P=0.0001) or that in patients with microalbuminuria (P=0.0093). In multivariate linear regression analyses, serum AIF-1 concentrations were independently correlated with logarithm of UAE (β=0.213, P=0.0120) and with eGFR (β=-0.286, P=0.0011).
Question: Is serum allograft inflammatory factor-1 a novel marker for diabetic nephropathy?
Output:
|
PubmedQA203368
|
[
{
"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: Dissection and rupture of the ascending aorta are life-threatening conditions resulting in 80% mortality. Ascending aortic replacement in patients presenting with thoracic aortic aneurysm (TAA) is determined by metric measurement. However, a significant number of dissections occur outside of the parameters suggested by the current guidelines. We investigate the correlation among altered haemodynamic condition, oxidative stress, and vascular smooth muscle cell (VSMC) phenotype in controlling tissue homoeostasis. We demonstrate using finite element analysis (FEA) based on computed tomography geometries that TAA patients have higher wall stress in the ascending aorta than non-dilated patients. We also show that altered haemodynamic conditions are associated with increased levels of reactive oxygen species (ROS), direct regulators of the VSMC phenotype in the microregional area of the ascending aorta. Using in vitro and ex vivo studies on human tissues, we show that ROS accumulation correlates with media layer degeneration and increased connective tissue growth factor (CTGF) expression, which modulate the synthetic VSMC phenotype. Results were validated by a murine model of TAA (C57BL/6J) based on Angiotensin II infusion showing that medial thickening and luminal expansion of the proximal aorta is associated with the VSMC synthetic phenotype as seen in human specimens.\n Question: Does oxidative stress modulate vascular smooth muscle cell phenotype via CTGF in thoracic aortic aneurysm?\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: Dissection and rupture of the ascending aorta are life-threatening conditions resulting in 80% mortality. Ascending aortic replacement in patients presenting with thoracic aortic aneurysm (TAA) is determined by metric measurement. However, a significant number of dissections occur outside of the parameters suggested by the current guidelines. We investigate the correlation among altered haemodynamic condition, oxidative stress, and vascular smooth muscle cell (VSMC) phenotype in controlling tissue homoeostasis. We demonstrate using finite element analysis (FEA) based on computed tomography geometries that TAA patients have higher wall stress in the ascending aorta than non-dilated patients. We also show that altered haemodynamic conditions are associated with increased levels of reactive oxygen species (ROS), direct regulators of the VSMC phenotype in the microregional area of the ascending aorta. Using in vitro and ex vivo studies on human tissues, we show that ROS accumulation correlates with media layer degeneration and increased connective tissue growth factor (CTGF) expression, which modulate the synthetic VSMC phenotype. Results were validated by a murine model of TAA (C57BL/6J) based on Angiotensin II infusion showing that medial thickening and luminal expansion of the proximal aorta is associated with the VSMC synthetic phenotype as seen in human specimens.
Question: Does oxidative stress modulate vascular smooth muscle cell phenotype via CTGF in thoracic aortic aneurysm?
Output:
|
PubmedQA192970
|
[
{
"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 investigate the effect of vanillin, a dietary component, on adipocyte differentiation and the mechanism involved in the process using 3T3-L1 murine preadipocytes. The effect of vanillin on adipocyte differentiation was detected by Oil Red O analysis. The activation of extracellular signal regulated kinase 42/44 (ERK 42/44), Akt, expression of the key regulator of adipocyte differentiation peroxisome proliferators-activated receptor (PPARγ) and its target gene glucose transporter 4 (GLUT4) were detected by western blotting. Glucose uptake assay was used to determine the insulin sensitivity of adipocytes differentiated by vanillin treatment. To confirm the role of ERK 42/44 and Akt, Oil Red O analysis was performed with cells differentiated in the presence or absence of ERK inhibitor U0126 or Akt kinase 1/2 inhibitor. Vanillin induced adipocyte differentiation in 3T3-L1 cells in a dose dependent manner and also increased the expression levels of PPARγ and its target gene GLUT4. The adipocytes differentiated by vanillin exhibited insulin sensitivity as demonstrated by a significant increase in glucose uptake. Vanillin treatment activated the phosphorylation of ERK 42/44 during the initial phase of adipocyte differentiation but there was no significant change in the Akt phosphorylation status.\n Question: Does vanillin induce adipocyte differentiation in 3T3-L1 cells by activating extracellular signal regulated kinase 42/44?\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 investigate the effect of vanillin, a dietary component, on adipocyte differentiation and the mechanism involved in the process using 3T3-L1 murine preadipocytes. The effect of vanillin on adipocyte differentiation was detected by Oil Red O analysis. The activation of extracellular signal regulated kinase 42/44 (ERK 42/44), Akt, expression of the key regulator of adipocyte differentiation peroxisome proliferators-activated receptor (PPARγ) and its target gene glucose transporter 4 (GLUT4) were detected by western blotting. Glucose uptake assay was used to determine the insulin sensitivity of adipocytes differentiated by vanillin treatment. To confirm the role of ERK 42/44 and Akt, Oil Red O analysis was performed with cells differentiated in the presence or absence of ERK inhibitor U0126 or Akt kinase 1/2 inhibitor. Vanillin induced adipocyte differentiation in 3T3-L1 cells in a dose dependent manner and also increased the expression levels of PPARγ and its target gene GLUT4. The adipocytes differentiated by vanillin exhibited insulin sensitivity as demonstrated by a significant increase in glucose uptake. Vanillin treatment activated the phosphorylation of ERK 42/44 during the initial phase of adipocyte differentiation but there was no significant change in the Akt phosphorylation status.
Question: Does vanillin induce adipocyte differentiation in 3T3-L1 cells by activating extracellular signal regulated kinase 42/44?
Output:
|
PubmedQA136797
|
[
{
"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: Smokers are at risk for pancreatic cancer (PC) and other pancreatic diseases. Cigarette smoking also aggravates the risk of PC in patients with hereditary and chronic pancreatitis (CP) and results in a higher incidence of acute pancreatitis and relapses in CP. Both PC and CP are characterized by a progressive fibrosis. Recently, two studies on rats reported that tobacco smoking is associated with chronic pancreatic inflammation with fibrosis and scarring of pancreatic acinar structures. In this study, we aimed to confirm a relationship between cigarette smoking and pancreatic fibrosis (PF) in humans. In this retrospective study, pancreatic and liver tissue acquired during autopsy was collected and analyzed. PF was scored by assessing severity of intralobular, extralobular, and total PF: grade 0 (normal or mild; 0-25% PF), grade 1 (moderate; 25-50% PF), and grade 2 (severe; >50%). Information on smoking habits was extracted from (electronic) medical records. Of 900 autopsies performed from January 2005 to December 2007, a minority of patients (n=111) met all inclusion criteria for analysis. Grade 2-3 total PF and intralobular PF was significantly more present in smokers vs. \"never-smokers\" (total: 42.9 vs. 26.5%, P=0.027 and intralobular: 39.3 vs. 15.6%, P=0.013), whereas no differences could be found between never-smokers and ex-smokers and between ex-smokers and smokers. When we took into account interlobular PF, no differences between all groups were observed. No relationship between PF and age (P=0.893), body mass index (P=0.707), and pancreatic lipomatosis (P=0.916) was observed.\n Question: Is smoking related to pancreatic fibrosis in humans?\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: Smokers are at risk for pancreatic cancer (PC) and other pancreatic diseases. Cigarette smoking also aggravates the risk of PC in patients with hereditary and chronic pancreatitis (CP) and results in a higher incidence of acute pancreatitis and relapses in CP. Both PC and CP are characterized by a progressive fibrosis. Recently, two studies on rats reported that tobacco smoking is associated with chronic pancreatic inflammation with fibrosis and scarring of pancreatic acinar structures. In this study, we aimed to confirm a relationship between cigarette smoking and pancreatic fibrosis (PF) in humans. In this retrospective study, pancreatic and liver tissue acquired during autopsy was collected and analyzed. PF was scored by assessing severity of intralobular, extralobular, and total PF: grade 0 (normal or mild; 0-25% PF), grade 1 (moderate; 25-50% PF), and grade 2 (severe; >50%). Information on smoking habits was extracted from (electronic) medical records. Of 900 autopsies performed from January 2005 to December 2007, a minority of patients (n=111) met all inclusion criteria for analysis. Grade 2-3 total PF and intralobular PF was significantly more present in smokers vs. "never-smokers" (total: 42.9 vs. 26.5%, P=0.027 and intralobular: 39.3 vs. 15.6%, P=0.013), whereas no differences could be found between never-smokers and ex-smokers and between ex-smokers and smokers. When we took into account interlobular PF, no differences between all groups were observed. No relationship between PF and age (P=0.893), body mass index (P=0.707), and pancreatic lipomatosis (P=0.916) was observed.
Question: Is smoking related to pancreatic fibrosis in humans?
Output:
|
PubmedQA207368
|
[
{
"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 kidney injury (AKI) is a common complication after cardiac surgery. Associations between the time interval (TI) from preoperative coronary angiography (CAG) to cardiac surgery have been investigated, although with conflicting results. We evaluated data collected from a retrospective review of consecutive patients who underwent preoperative CAG and heart valve surgery at our institution between September 2008 and February 2013. A total of 426 patients met the study criteria. Patients were divided into two groups according to the length of time between preoperative CAG and valve surgery: within one day (group A) or longer than one day (group B). Logistic regression was applied to analyze the relationships between TI and postoperative AKI. Of 426 patients, 140 (33%) underwent CAG on preoperative day 1, while 286 (67%) underwent CAG on preoperative day 2 or sooner. AKI occurred in 19 (13.6%) patients in group A and in 35 (12.2%) patients in group B (p = 0.70). CAG on preoperative day 1 was not associated an increased risk of AKI relative to CAG on preoperative day 2 or sooner (p = 0.49; odds ratio, 1.26; 95% CI, 0.66 to 2.41).\n Question: Is preoperative coronary angiography within one day of valve surgery associated with postoperative acute kidney injury in patients with preserved renal function?\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: Acute kidney injury (AKI) is a common complication after cardiac surgery. Associations between the time interval (TI) from preoperative coronary angiography (CAG) to cardiac surgery have been investigated, although with conflicting results. We evaluated data collected from a retrospective review of consecutive patients who underwent preoperative CAG and heart valve surgery at our institution between September 2008 and February 2013. A total of 426 patients met the study criteria. Patients were divided into two groups according to the length of time between preoperative CAG and valve surgery: within one day (group A) or longer than one day (group B). Logistic regression was applied to analyze the relationships between TI and postoperative AKI. Of 426 patients, 140 (33%) underwent CAG on preoperative day 1, while 286 (67%) underwent CAG on preoperative day 2 or sooner. AKI occurred in 19 (13.6%) patients in group A and in 35 (12.2%) patients in group B (p = 0.70). CAG on preoperative day 1 was not associated an increased risk of AKI relative to CAG on preoperative day 2 or sooner (p = 0.49; odds ratio, 1.26; 95% CI, 0.66 to 2.41).
Question: Is preoperative coronary angiography within one day of valve surgery associated with postoperative acute kidney injury in patients with preserved renal function?
Output:
|
PubmedQA42337
|
[
{
"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: In this study, our aim was to investigate how different immunohistochemical techniques may influence the result of BCL6 positivity and categorization in germinal center (GC) and non-GC derived diffuse large B-cell lymphoma (DLBCL), as it has been proposed that classification of DLBCL according to cell-of-origin by immunohistochemistry may be performed as a routine procedure in the diagnostic work-up. However, a number of technical issues need to be solved before introducing this as a standard technique. Tumor specimens from 122 patients with de novo stage II-IV disease, adequately treated with anthracycline-containing chemotherapy regimens were collected. Immunohistochemical expression of BCL6, CD10, and MUM-1/IRF4 was examined using a tissue microarray (TMA) technique. BCL6 and CD10 were also evaluated on whole tissue sections. Due to profound tissue heterogeneity, BCL6 showed a wide range of positivity, with a high number of false negative results by TMA (25% positive), compared to 53% on whole tissue sections (WTS). CD10 was more homogeneously expressed, and TMA results corresponded better to WTS. Consequently, the results from categorization into GC and non-GC DLBCL differed considerably by use of the two methods, and resulted in very different outcome in terms of overall survival.\n Question: Is tissue microarray inappropriate for analysis of BCL6 expression in diffuse large B-cell lymphoma?\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: In this study, our aim was to investigate how different immunohistochemical techniques may influence the result of BCL6 positivity and categorization in germinal center (GC) and non-GC derived diffuse large B-cell lymphoma (DLBCL), as it has been proposed that classification of DLBCL according to cell-of-origin by immunohistochemistry may be performed as a routine procedure in the diagnostic work-up. However, a number of technical issues need to be solved before introducing this as a standard technique. Tumor specimens from 122 patients with de novo stage II-IV disease, adequately treated with anthracycline-containing chemotherapy regimens were collected. Immunohistochemical expression of BCL6, CD10, and MUM-1/IRF4 was examined using a tissue microarray (TMA) technique. BCL6 and CD10 were also evaluated on whole tissue sections. Due to profound tissue heterogeneity, BCL6 showed a wide range of positivity, with a high number of false negative results by TMA (25% positive), compared to 53% on whole tissue sections (WTS). CD10 was more homogeneously expressed, and TMA results corresponded better to WTS. Consequently, the results from categorization into GC and non-GC DLBCL differed considerably by use of the two methods, and resulted in very different outcome in terms of overall survival.
Question: Is tissue microarray inappropriate for analysis of BCL6 expression in diffuse large B-cell lymphoma?
Output:
|
PubmedQA67774
|
[
{
"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 farnesoid X receptor (FXR) is a member of the nuclear hormone receptor superfamily, which plays an essential role in the regulation of enterohepatic circulation and lipid homeostasis. Here we investigated whether WAY-362450, a synthetic potent FXR agonist, could protect against non-alcoholic steatohepatitis (NASH) in mice fed a methionine and choline-deficient (MCD) diet. Male C57BL/6 mice on the MCD diet were treated with or without WAY-362450 (30 mg/kg) for 4 weeks. The elevations of serum ALT and AST activities induced by the MCD diet were decreased with WAY-362450 treatment. In terms of liver histology, while WAY-362450 treatment showed no impact on hepatic triglyceride accumulation, it significantly reduced inflammatory cell infiltration and hepatic fibrosis. The reduction in inflammatory cell infiltration correlated with deceased serum levels of keratinocyte derived chemokine (mKC) and MCP 1 and decreased hepatic gene expression of MCP-1 and VCAM-1. The reduction of hepatic fibrosis by WAY-362450 treatment corresponded to a reduction in hepatic gene expression of fibrosis markers. The positive effects of WAY-362450 were FXR-dependent since no protection was observed in MCD diet-fed FXR deficient mice.\n Question: Does farnesoid X receptor agonist WAY-362450 attenuate liver inflammation and fibrosis in murine model of non-alcoholic steatohepatitis?\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 farnesoid X receptor (FXR) is a member of the nuclear hormone receptor superfamily, which plays an essential role in the regulation of enterohepatic circulation and lipid homeostasis. Here we investigated whether WAY-362450, a synthetic potent FXR agonist, could protect against non-alcoholic steatohepatitis (NASH) in mice fed a methionine and choline-deficient (MCD) diet. Male C57BL/6 mice on the MCD diet were treated with or without WAY-362450 (30 mg/kg) for 4 weeks. The elevations of serum ALT and AST activities induced by the MCD diet were decreased with WAY-362450 treatment. In terms of liver histology, while WAY-362450 treatment showed no impact on hepatic triglyceride accumulation, it significantly reduced inflammatory cell infiltration and hepatic fibrosis. The reduction in inflammatory cell infiltration correlated with deceased serum levels of keratinocyte derived chemokine (mKC) and MCP 1 and decreased hepatic gene expression of MCP-1 and VCAM-1. The reduction of hepatic fibrosis by WAY-362450 treatment corresponded to a reduction in hepatic gene expression of fibrosis markers. The positive effects of WAY-362450 were FXR-dependent since no protection was observed in MCD diet-fed FXR deficient mice.
Question: Does farnesoid X receptor agonist WAY-362450 attenuate liver inflammation and fibrosis in murine model of non-alcoholic steatohepatitis?
Output:
|
PubmedQA204116
|
[
{
"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: Urban minority girls are at risk for summertime weight gain, and may also experience insufficient summertime sleep. Few studies have objectively measured sleep in this population or examined correlates, including physical activity (PA). This study is the first to objectively describe summertime sleep among urban minority girls. Data were collected at a community-based summer program that promoted PA (n = 60 girls, ages 10-14 years), at two time points: before beginning programming (T1; unstructured context) and during the final week of programming (T2; structured context). At both time points, participants experienced shorter nighttime sleep than the recommended amount for girls their age. African American girls recorded significantly less sleep than Latina girls in the unstructured context. Findings also suggest that sleep schedules have an influential role in youths' abilities to obtain adequate sleep. \n Question: Is sleep in for Summer : Patterns of Sleep and Physical Activity in Urban Minority Girls?\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: Urban minority girls are at risk for summertime weight gain, and may also experience insufficient summertime sleep. Few studies have objectively measured sleep in this population or examined correlates, including physical activity (PA). This study is the first to objectively describe summertime sleep among urban minority girls. Data were collected at a community-based summer program that promoted PA (n = 60 girls, ages 10-14 years), at two time points: before beginning programming (T1; unstructured context) and during the final week of programming (T2; structured context). At both time points, participants experienced shorter nighttime sleep than the recommended amount for girls their age. African American girls recorded significantly less sleep than Latina girls in the unstructured context. Findings also suggest that sleep schedules have an influential role in youths' abilities to obtain adequate sleep.
Question: Is sleep in for Summer : Patterns of Sleep and Physical Activity in Urban Minority Girls?
Output:
|
PubmedQA208807
|
[
{
"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 study aim was to determine whether supraphysiological estradiol (E(2)) levels reduce oocyte/embryo quality in oocyte donation cycles. A retrospective analysis of 330 consecutive fresh oocyte donation cycles was performed in an assisted reproductive treatment programme between January 1996 and December 2000. Throughout the study period, oocyte donors and recipients followed a standard synchronization regimen that did not vary. A serum E(2) level (peak E(2)) was obtained from all oocyte donors on the morning of HCG administration. Peak E(2) values were grouped by 33rd percentile (group I, <1500 pg/ml; group II, 1500-3000 pg/ml; and group III, >3000 pg/ml). All embryo transfers were performed on day 3 after oocyte recovery. Comparisons between groups revealed no significant differences in the quality of oocytes retrieved, and in fertilization rates. Higher peak E(2) levels were directly correlated with a greater number of oocytes retrieved, embryos available for transfer and cryopreservation, and higher average embryo quality scores (P < 0.005). Compared with group I, group III had significantly higher embryo implantation rates (P < 0.05).\n Question: Do supraphysiological estradiol levels affect oocyte and embryo quality in oocyte donation cycles?\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: The study aim was to determine whether supraphysiological estradiol (E(2)) levels reduce oocyte/embryo quality in oocyte donation cycles. A retrospective analysis of 330 consecutive fresh oocyte donation cycles was performed in an assisted reproductive treatment programme between January 1996 and December 2000. Throughout the study period, oocyte donors and recipients followed a standard synchronization regimen that did not vary. A serum E(2) level (peak E(2)) was obtained from all oocyte donors on the morning of HCG administration. Peak E(2) values were grouped by 33rd percentile (group I, <1500 pg/ml; group II, 1500-3000 pg/ml; and group III, >3000 pg/ml). All embryo transfers were performed on day 3 after oocyte recovery. Comparisons between groups revealed no significant differences in the quality of oocytes retrieved, and in fertilization rates. Higher peak E(2) levels were directly correlated with a greater number of oocytes retrieved, embryos available for transfer and cryopreservation, and higher average embryo quality scores (P < 0.005). Compared with group I, group III had significantly higher embryo implantation rates (P < 0.05).
Question: Do supraphysiological estradiol levels affect oocyte and embryo quality in oocyte donation cycles?
Output:
|
PubmedQA16553
|
[
{
"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: Does constraint-induced movement therapy (CIMT) improve hand function in children with congenital hemiplegia compared to bimanual therapy? Randomised trial with concealed allocation and blinded outcome assessment. 6 CIMT and bimanual therapy day camps were conducted at a University in the United States. Children with congenital hemiplegia aged 3.5 to 10 years, with basic movement and grasp in their paretic hand, and who attended mainstream school. Health problems not associated with cerebral palsy, severe hypertonia, and recent surgery or botulinum toxin therapy were exclusion criteria. Randomisation of 44 participants allocated 22 to the CIMT group and 22 to the bimanual therapy group. The groups were matched for age and hand function. Both groups received 90 hours of therapy, delivered in day-camps with 2-5 children in each group. Participants completed 6 hours of therapy a day for 15 consecutive weekdays. Treatment was delivered by physiotherapists, occupational therapists, and students enrolled in health related courses. Participants worked individually and in groups. The CIMT group had their less affected hand restrained in a sling and performed age appropriate fine and gross motor unimanual activities The bimanual therapy group engaged in age appropriate fine and gross motor bimanual activities. The primary outcomes were the Jebsen-Taylor Test of Hand Function (JTTHF) to assess unimanual capacity and the Assisting Hand Assessment (AHA) to assess bimanual performance. Secondary outcome measures were Goal Attainment Scale, Quality of Upper Extremity Skills Test (QUEST), and physical activity (percentage time each hand was used during the AHA assessment). Assessments were completed before treatment, 2 days after treatment, and 1 and 6 months after treatment. 42 participants completed the study. At the end of the 15-day intervention period, the groups did not significantly differ on the primary outcome measures and on two secondary outcome measures (QUEST, physical activity). There were significant within group changes for both groups on each primary outcome (mean change score JTTHF -137 s, 95% CI -174 to -99; mean change score AHA -0.49 logits, 95% CI 0.25 to 0.73) which were maintained at the 6 month follow-up. There were also significant within group changes for both groups for the QUEST and physical activity assessments. The bimanual therapy group made greater progress than the CIMT group on their Goal Attainment Scale scores (mean difference between groups 8.1 T-score, 95% CI 0.7 to 15.5).\n Question: Are bimanual therapy and constraint-induced movement therapy equally effective in improving hand function in children with congenital hemiplegia?\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: Does constraint-induced movement therapy (CIMT) improve hand function in children with congenital hemiplegia compared to bimanual therapy? Randomised trial with concealed allocation and blinded outcome assessment. 6 CIMT and bimanual therapy day camps were conducted at a University in the United States. Children with congenital hemiplegia aged 3.5 to 10 years, with basic movement and grasp in their paretic hand, and who attended mainstream school. Health problems not associated with cerebral palsy, severe hypertonia, and recent surgery or botulinum toxin therapy were exclusion criteria. Randomisation of 44 participants allocated 22 to the CIMT group and 22 to the bimanual therapy group. The groups were matched for age and hand function. Both groups received 90 hours of therapy, delivered in day-camps with 2-5 children in each group. Participants completed 6 hours of therapy a day for 15 consecutive weekdays. Treatment was delivered by physiotherapists, occupational therapists, and students enrolled in health related courses. Participants worked individually and in groups. The CIMT group had their less affected hand restrained in a sling and performed age appropriate fine and gross motor unimanual activities The bimanual therapy group engaged in age appropriate fine and gross motor bimanual activities. The primary outcomes were the Jebsen-Taylor Test of Hand Function (JTTHF) to assess unimanual capacity and the Assisting Hand Assessment (AHA) to assess bimanual performance. Secondary outcome measures were Goal Attainment Scale, Quality of Upper Extremity Skills Test (QUEST), and physical activity (percentage time each hand was used during the AHA assessment). Assessments were completed before treatment, 2 days after treatment, and 1 and 6 months after treatment. 42 participants completed the study. At the end of the 15-day intervention period, the groups did not significantly differ on the primary outcome measures and on two secondary outcome measures (QUEST, physical activity). There were significant within group changes for both groups on each primary outcome (mean change score JTTHF -137 s, 95% CI -174 to -99; mean change score AHA -0.49 logits, 95% CI 0.25 to 0.73) which were maintained at the 6 month follow-up. There were also significant within group changes for both groups for the QUEST and physical activity assessments. The bimanual therapy group made greater progress than the CIMT group on their Goal Attainment Scale scores (mean difference between groups 8.1 T-score, 95% CI 0.7 to 15.5).
Question: Are bimanual therapy and constraint-induced movement therapy equally effective in improving hand function in children with congenital hemiplegia?
Output:
|
PubmedQA7945
|
[
{
"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: A close relationship exists between hyperglycaemia, oxidative stress, and diabetic complications. In fact, high glucose (HG) determines the overproduction of reactive oxygen species (ROS) by the mitochondria. p66ShcA is a gene that regulates the apoptotic responses to oxidative stress. Indeed, p66ShcA knockout (ko) mice display decreased ROS production and increased resistance to ROS-induced cell death in a variety of pathophysiological settings. Reduced endothelial progenitor cell (EPC) number, differentiation, and function are relevant components of the angiogenesis impairment observed in diabetic patients. We examined the role of p66ShcA in the EPC deficit induced by HG. Mouse bone marrow-derived c-kit+ cells differentiate in endothelial-like cells when plated on fibronectin (BM-derived EPCs). We found that cell culture in the presence of HG up-regulated p66ShcA protein expression and that HG exposure markedly decreased the number of BM-derived EPCs. Conversely, p66ShcA ko BM-derived EPCs were not sensitive to HG inhibition. Indeed, the resistance of p66ShcA ko BM-derived EPCs to HG was associated with reduced levels of both apoptosis and oxidative stress. To functionally link the HG response to ROS production, p66ShcA ko BM-derived EPCs were reconstituted either with p66ShcA wild-type (wt) or with a p66ShcA allele (p66ShcA qq) that was devoid of its ROS-generating function. We found that only p66ShcA wt and not the qq mutant rescued p66ShcA ko cell sensitivity to HG. One major feature of oxidative stress is its ability to reduce the bio-availability of nitric oxide (NO) that, in turn, plays a crucial role in endothelial differentiation and function. We found that the p66ShcA deletion prevented the HG-induced increase of nitrotyrosine, and that the resistance to HG of p66ShcA ko BM-derived EPCs was prevented by NO synthase inhibition. With a reciprocal approach, the treatment of p66ShcA wt cells with a NO donor prevented the HG-induced deficit. Finally, using a Matrigel plug angiogenesis assay, we demonstrated that p66ShcA ko prevented diabetic impairment of angiogenesis in vivo.\n Question: Does p66ShcA modulate oxidative stress and survival of endothelial progenitor cells in response to high glucose?\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: A close relationship exists between hyperglycaemia, oxidative stress, and diabetic complications. In fact, high glucose (HG) determines the overproduction of reactive oxygen species (ROS) by the mitochondria. p66ShcA is a gene that regulates the apoptotic responses to oxidative stress. Indeed, p66ShcA knockout (ko) mice display decreased ROS production and increased resistance to ROS-induced cell death in a variety of pathophysiological settings. Reduced endothelial progenitor cell (EPC) number, differentiation, and function are relevant components of the angiogenesis impairment observed in diabetic patients. We examined the role of p66ShcA in the EPC deficit induced by HG. Mouse bone marrow-derived c-kit+ cells differentiate in endothelial-like cells when plated on fibronectin (BM-derived EPCs). We found that cell culture in the presence of HG up-regulated p66ShcA protein expression and that HG exposure markedly decreased the number of BM-derived EPCs. Conversely, p66ShcA ko BM-derived EPCs were not sensitive to HG inhibition. Indeed, the resistance of p66ShcA ko BM-derived EPCs to HG was associated with reduced levels of both apoptosis and oxidative stress. To functionally link the HG response to ROS production, p66ShcA ko BM-derived EPCs were reconstituted either with p66ShcA wild-type (wt) or with a p66ShcA allele (p66ShcA qq) that was devoid of its ROS-generating function. We found that only p66ShcA wt and not the qq mutant rescued p66ShcA ko cell sensitivity to HG. One major feature of oxidative stress is its ability to reduce the bio-availability of nitric oxide (NO) that, in turn, plays a crucial role in endothelial differentiation and function. We found that the p66ShcA deletion prevented the HG-induced increase of nitrotyrosine, and that the resistance to HG of p66ShcA ko BM-derived EPCs was prevented by NO synthase inhibition. With a reciprocal approach, the treatment of p66ShcA wt cells with a NO donor prevented the HG-induced deficit. Finally, using a Matrigel plug angiogenesis assay, we demonstrated that p66ShcA ko prevented diabetic impairment of angiogenesis in vivo.
Question: Does p66ShcA modulate oxidative stress and survival of endothelial progenitor cells in response to high glucose?
Output:
|
PubmedQA176150
|
[
{
"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: It has been suggested that measurement of continuous cardiac output (CCO) is an advancement in the management of critically ill patients. Our objective was to determine the accuracy of CCO during the rapid hemodynamic changes induced by hemorrhage and resuscitation. In 12 anesthetized dogs (20.2+/-0.9 kg), pulmonary artery blood flow, our \"gold standard\" cardiac output, was measured with an sonographic flowprobe, whereas CCO, intermittent bolus cardiac output (ICO), and mixed venous oxygen saturation were measured with a thermodilution fiberoptic pulmonary artery catheter with a thermal filament. A graded hemorrhage (20 mL/min) was produced to a mean arterial pressure of 40 mm Hg, which was maintained at this level for 30 minutes. Total shed blood volume (701+/-53 mL) was retransfused at a rate of 40 mL/min, over 30 minutes, after which a massive hemorrhage (100 mL/min) was produced over 10 minutes. Hemorrhage induced significant decreases in mean arterial pressure, mixed venous oxygen saturation, and oxygen delivery, which were all restored during early resuscitation. However, CCO showed a delayed response after hemorrhage and resuscitation, compared with pulmonary blood flow, throughout the study (r = 0.549), matching only at baseline and at the end of both graded hemorrhage and resuscitation periods. There was a good correlation between ICO and pulmonary artery blood flow (r = 0.964) and no significant differences between them throughout the study.\n Question: Does thermal filament continuous thermodilution cardiac output delayed response limit its value during acute hemodynamic instability?\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: It has been suggested that measurement of continuous cardiac output (CCO) is an advancement in the management of critically ill patients. Our objective was to determine the accuracy of CCO during the rapid hemodynamic changes induced by hemorrhage and resuscitation. In 12 anesthetized dogs (20.2+/-0.9 kg), pulmonary artery blood flow, our "gold standard" cardiac output, was measured with an sonographic flowprobe, whereas CCO, intermittent bolus cardiac output (ICO), and mixed venous oxygen saturation were measured with a thermodilution fiberoptic pulmonary artery catheter with a thermal filament. A graded hemorrhage (20 mL/min) was produced to a mean arterial pressure of 40 mm Hg, which was maintained at this level for 30 minutes. Total shed blood volume (701+/-53 mL) was retransfused at a rate of 40 mL/min, over 30 minutes, after which a massive hemorrhage (100 mL/min) was produced over 10 minutes. Hemorrhage induced significant decreases in mean arterial pressure, mixed venous oxygen saturation, and oxygen delivery, which were all restored during early resuscitation. However, CCO showed a delayed response after hemorrhage and resuscitation, compared with pulmonary blood flow, throughout the study (r = 0.549), matching only at baseline and at the end of both graded hemorrhage and resuscitation periods. There was a good correlation between ICO and pulmonary artery blood flow (r = 0.964) and no significant differences between them throughout the study.
Question: Does thermal filament continuous thermodilution cardiac output delayed response limit its value during acute hemodynamic instability?
Output:
|
PubmedQA192768
|
[
{
"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: Nutrition affects milk composition thus influencing its nutritional properties. Nutrition also modifies the expression of mammary genes, whose regulation is not fully understood. MicroRNAs (miRNA) are small non coding RNA which are important post-transcriptional regulators of gene expression by targeting messenger RNAs. Our goal was to characterize miRNA whose expression is regulated by nutrition in the lactating goat mammary gland, which may provide clues to deciphering regulations of the biosynthesis and secretion of milk components. Using high-throughput sequencing technology, miRNomes of the lactating mammary gland were established from lactating goats fed ad libitum or deprived of food for 48 h affecting milk production and composition. High throughput miRNA sequencing revealed 30 miRNA with an expression potentially modulated by food deprivation; 16 were down-regulated and 14 were up-regulated. Diana-microT predictive tools suggested a potential role for several nutriregulated miRNA in lipid metabolism. Among the putative targets, 19 were previously identified as differently expressed genes (DEG). The functions of these 19 DEG revealed, notably, their involvement in tissue remodelling.\n Question: Does food Deprivation affect the miRNome in the Lactating Goat Mammary Gland?\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: Nutrition affects milk composition thus influencing its nutritional properties. Nutrition also modifies the expression of mammary genes, whose regulation is not fully understood. MicroRNAs (miRNA) are small non coding RNA which are important post-transcriptional regulators of gene expression by targeting messenger RNAs. Our goal was to characterize miRNA whose expression is regulated by nutrition in the lactating goat mammary gland, which may provide clues to deciphering regulations of the biosynthesis and secretion of milk components. Using high-throughput sequencing technology, miRNomes of the lactating mammary gland were established from lactating goats fed ad libitum or deprived of food for 48 h affecting milk production and composition. High throughput miRNA sequencing revealed 30 miRNA with an expression potentially modulated by food deprivation; 16 were down-regulated and 14 were up-regulated. Diana-microT predictive tools suggested a potential role for several nutriregulated miRNA in lipid metabolism. Among the putative targets, 19 were previously identified as differently expressed genes (DEG). The functions of these 19 DEG revealed, notably, their involvement in tissue remodelling.
Question: Does food Deprivation affect the miRNome in the Lactating Goat Mammary Gland?
Output:
|
PubmedQA6507
|
[
{
"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: In nonalcoholic fatty liver disease (NAFLD), increased alanine aminotransferase (ALT) concentrations are considered to be a consequence of hepatocyte damage. We performed a prospective study to examine the association between ALT within its reference interval and risk for subsequent development of NAFLD. The study cohort comprised 5237 healthy men without diagnosed NAFLD and without increases of either ALT (> or =35 U/L) or gamma-glutamyltransferase (GGT; > or =40 U/L) above the reference intervals. We assessed alcohol intake via self-reporting (questionnaire) and performed biochemical tests for liver and metabolic function and abdominal ultrasonography. We used the Cox proportional hazards model to calculate the adjusted hazard ratios (aHRs) in the model for NAFLD. During 13 276.6 person-years of follow-up over a 4-year period, 984 new incident cases of NAFLD developed. We adjusted for age, weight change, body mass index, glucose, blood pressure, triglycerides, HDL cholesterol, smoking, alcohol consumption, regular exercise, homeostasis model assessment of insulin resistance, C-reactive protein, and incident diabetes. Compared with an ALT concentration of <16 U/L, aHR values (95% confidence intervals) for ALT concentrations were 1.53 (1.18-1.98), 1.66 (1.29-2.13), 1.62 (1.26-2.08), and 2.21 (1.73-2.81) for ALT concentrations of 16-18, 19-21, 22-25, and 26-34 U/L, respectively. This relationship remained significant even among normal-weight participants who were still within the reference interval of ALT and GGT at all follow-up examinations.\n Question: Do higher concentrations of alanine aminotransferase within the reference interval predict nonalcoholic fatty liver 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: In nonalcoholic fatty liver disease (NAFLD), increased alanine aminotransferase (ALT) concentrations are considered to be a consequence of hepatocyte damage. We performed a prospective study to examine the association between ALT within its reference interval and risk for subsequent development of NAFLD. The study cohort comprised 5237 healthy men without diagnosed NAFLD and without increases of either ALT (> or =35 U/L) or gamma-glutamyltransferase (GGT; > or =40 U/L) above the reference intervals. We assessed alcohol intake via self-reporting (questionnaire) and performed biochemical tests for liver and metabolic function and abdominal ultrasonography. We used the Cox proportional hazards model to calculate the adjusted hazard ratios (aHRs) in the model for NAFLD. During 13 276.6 person-years of follow-up over a 4-year period, 984 new incident cases of NAFLD developed. We adjusted for age, weight change, body mass index, glucose, blood pressure, triglycerides, HDL cholesterol, smoking, alcohol consumption, regular exercise, homeostasis model assessment of insulin resistance, C-reactive protein, and incident diabetes. Compared with an ALT concentration of <16 U/L, aHR values (95% confidence intervals) for ALT concentrations were 1.53 (1.18-1.98), 1.66 (1.29-2.13), 1.62 (1.26-2.08), and 2.21 (1.73-2.81) for ALT concentrations of 16-18, 19-21, 22-25, and 26-34 U/L, respectively. This relationship remained significant even among normal-weight participants who were still within the reference interval of ALT and GGT at all follow-up examinations.
Question: Do higher concentrations of alanine aminotransferase within the reference interval predict nonalcoholic fatty liver disease?
Output:
|
PubmedQA171478
|
[
{
"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 management of knee osteoarthritis (OA) focuses on reducing the levels of pain and disability. Recently, a novel biomechanical device and treatment methodology (AposTherapy) was shown to reduce the knee adduction moment while simultaneously challenging the neuromuscular control system through perturbation. The purpose of the study was to investigate the changes in gait patterns and clinical measurements following treatment with a novel biomechanical device on patients with knee OA. A total of 745 patients with bilateral knee OA were analyzed. Patients completed a gait test, Western Ontario and McMaster Osteoarthritis Index (WOMAC) questionnaire and SF-36 Health Survey at baseline and after 12 weeks. The biomechanical device was individually calibrated to each patient. Shifting the center of pressure, through changes in the location of the biomechanical elements causes realignment and reduction in the knee adduction moment. Furthermore the configuration of the biomechanical element allows training under controlled perturbation. A significant decrease was found in WOMAC pain (28.6%) and WOMAC function (25.2%) following three months of therapy (p<0.001). A significant increase was found in the patients' physical quality of life (17.8%) and mental quality of life (11.0%) (p<0.001). Gait velocity, cadence step length, stance phase and single limb support phase improved significantly following three months of therapy (7.6%, 4%, 3.7% and 1.6%, respectively).\n Question: Does [ A new non-invasive biomechanical therapy for knee osteoarthritis improve clinical symptoms and gait patterns ]?\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 management of knee osteoarthritis (OA) focuses on reducing the levels of pain and disability. Recently, a novel biomechanical device and treatment methodology (AposTherapy) was shown to reduce the knee adduction moment while simultaneously challenging the neuromuscular control system through perturbation. The purpose of the study was to investigate the changes in gait patterns and clinical measurements following treatment with a novel biomechanical device on patients with knee OA. A total of 745 patients with bilateral knee OA were analyzed. Patients completed a gait test, Western Ontario and McMaster Osteoarthritis Index (WOMAC) questionnaire and SF-36 Health Survey at baseline and after 12 weeks. The biomechanical device was individually calibrated to each patient. Shifting the center of pressure, through changes in the location of the biomechanical elements causes realignment and reduction in the knee adduction moment. Furthermore the configuration of the biomechanical element allows training under controlled perturbation. A significant decrease was found in WOMAC pain (28.6%) and WOMAC function (25.2%) following three months of therapy (p<0.001). A significant increase was found in the patients' physical quality of life (17.8%) and mental quality of life (11.0%) (p<0.001). Gait velocity, cadence step length, stance phase and single limb support phase improved significantly following three months of therapy (7.6%, 4%, 3.7% and 1.6%, respectively).
Question: Does [ A new non-invasive biomechanical therapy for knee osteoarthritis improve clinical symptoms and gait patterns ]?
Output:
|
PubmedQA105625
|
[
{
"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 the rate and causes of inappropriate rhythm detection, and to compare adequacy of ventricular arrhythmia detection by single-chamber and dual-chamber cardioverter-defibrillators (ICD). We evaluated 190 patients (age 57.2 +/- 11.2 years) with ICD. 34.3 +/- +/- 22 months. Dual-chamber ICD was used in 54 patients. We evaluated 2244 arrhythmia events recognized as of ventricular origin, including ventricular tachycardia and ventricular fibrillation. 431 events (19.2%) were recognized erroneously and resulted in an inappropriate ICD discharge. Most cases of inappropriate therapies (182 events, 42.23%) were due to atrial fibrillation or flutter. Overall, inappropriate arrhythmia detection was found in 64 (33.6%) of 190 patients. In terms of the number of affected patients, the most common cause of inappropriate ICD discharge was sinus tachycardia - 23 (12.1%) patients, followed by atrial fibrillation - 16 (8.4%) patients. Among 54 patients with dual-chamber ICD, inappropriate therapy was noted in 21 (38.8%) patients, (T wave oversensing, sinus tachycardia and atrial fibrillation etc.). No significant difference was seen in the rate of inappropriate therapy due to a rapid supraventricular rhythm between patients with single-chamber versus dual-chamber ICD. In contrast, patients with single-chamber ICD more often experienced inappropriate therapy due to atrial fibrillation (155 vs. 28 patients) and sinus tachycardia (66 vs. 9 patients).\n Question: Does inappropriate cardioverter-defibrillator discharge continue to be a major problem in clinical practice?\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 the rate and causes of inappropriate rhythm detection, and to compare adequacy of ventricular arrhythmia detection by single-chamber and dual-chamber cardioverter-defibrillators (ICD). We evaluated 190 patients (age 57.2 +/- 11.2 years) with ICD. 34.3 +/- +/- 22 months. Dual-chamber ICD was used in 54 patients. We evaluated 2244 arrhythmia events recognized as of ventricular origin, including ventricular tachycardia and ventricular fibrillation. 431 events (19.2%) were recognized erroneously and resulted in an inappropriate ICD discharge. Most cases of inappropriate therapies (182 events, 42.23%) were due to atrial fibrillation or flutter. Overall, inappropriate arrhythmia detection was found in 64 (33.6%) of 190 patients. In terms of the number of affected patients, the most common cause of inappropriate ICD discharge was sinus tachycardia - 23 (12.1%) patients, followed by atrial fibrillation - 16 (8.4%) patients. Among 54 patients with dual-chamber ICD, inappropriate therapy was noted in 21 (38.8%) patients, (T wave oversensing, sinus tachycardia and atrial fibrillation etc.). No significant difference was seen in the rate of inappropriate therapy due to a rapid supraventricular rhythm between patients with single-chamber versus dual-chamber ICD. In contrast, patients with single-chamber ICD more often experienced inappropriate therapy due to atrial fibrillation (155 vs. 28 patients) and sinus tachycardia (66 vs. 9 patients).
Question: Does inappropriate cardioverter-defibrillator discharge continue to be a major problem in clinical practice?
Output:
|
PubmedQA203629
|
[
{
"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 presence of Epstein-Barr virus latent membrane protein-1 (LMP-1) gene in nasopharyngeal swabs indicates the presence of nasopharyngeal carcinoma (NPC) mucosal tumor cells. This study was undertaken to investigate whether the time taken for LMP-1 to disappear after initiation of primary radiotherapy (RT) was inversely associated with NPC local control. During July 1999 and October 2002, there were 127 nondisseminated NPC patients receiving serial examinations of nasopharyngeal swabbing with detection of LMP-1 during the RT course. The time for LMP-1 regression was defined as the number of days after initiation of RT for LMP-1 results to turn negative. The primary outcome was local control, which was represented by freedom from local recurrence. The time for LMP-1 regression showed a statistically significant influence on NPC local control both univariately (p < 0.0001) and multivariately (p = 0.004). In multivariate analysis, the administration of chemotherapy conferred a significantly more favorable local control (p = 0.03). Advanced T status (> or = T2b), overall treatment time of external photon radiotherapy longer than 55 days, and older age showed trends toward being poor prognosticators. The time for LMP-1 regression was very heterogeneous. According to the quartiles of the time for LMP-1 regression, we defined the pattern of LMP-1 regression as late regression if it required 40 days or more. Kaplan-Meier plots indicated that the patients with late regression had a significantly worse local control than those with intermediate or early regression (p = 0.0129).\n Question: Is the time frame of Epstein-Barr virus latent membrane protein-1 gene to disappear in nasopharyngeal swabs after initiation of primary radiotherapy an independently significant prognostic factor predicting local control for patients with nasopharyngeal 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: The presence of Epstein-Barr virus latent membrane protein-1 (LMP-1) gene in nasopharyngeal swabs indicates the presence of nasopharyngeal carcinoma (NPC) mucosal tumor cells. This study was undertaken to investigate whether the time taken for LMP-1 to disappear after initiation of primary radiotherapy (RT) was inversely associated with NPC local control. During July 1999 and October 2002, there were 127 nondisseminated NPC patients receiving serial examinations of nasopharyngeal swabbing with detection of LMP-1 during the RT course. The time for LMP-1 regression was defined as the number of days after initiation of RT for LMP-1 results to turn negative. The primary outcome was local control, which was represented by freedom from local recurrence. The time for LMP-1 regression showed a statistically significant influence on NPC local control both univariately (p < 0.0001) and multivariately (p = 0.004). In multivariate analysis, the administration of chemotherapy conferred a significantly more favorable local control (p = 0.03). Advanced T status (> or = T2b), overall treatment time of external photon radiotherapy longer than 55 days, and older age showed trends toward being poor prognosticators. The time for LMP-1 regression was very heterogeneous. According to the quartiles of the time for LMP-1 regression, we defined the pattern of LMP-1 regression as late regression if it required 40 days or more. Kaplan-Meier plots indicated that the patients with late regression had a significantly worse local control than those with intermediate or early regression (p = 0.0129).
Question: Is the time frame of Epstein-Barr virus latent membrane protein-1 gene to disappear in nasopharyngeal swabs after initiation of primary radiotherapy an independently significant prognostic factor predicting local control for patients with nasopharyngeal carcinoma?
Output:
|
PubmedQA133541
|
[
{
"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 risk of developing esophageal adenocarcinoma (EAC) for patients with Barrett's esophagus (BE) is approximately 0.5% per year. To investigate how patients with BE estimate and perceive their risk of developing EAC. Questionnaire study. Patients with BE who were undergoing surveillance endoscopy based on histologic and flow cytometric results. A total of 192 patients with BE were included. Individual patients were asked to estimate the numerical risk to develop EAC for patients with BE in general and for themselves. How patients perceived their own risk was measured on a scale from \"very small\" to \"very large.\" At least 1 question was filled out by 169 patients (88% response). Sixty percent of respondents underestimated the numerical risk for patients with BE, in general, to develop EAC, while even more patients (69%) underestimated their own risk. Most respondents perceived their own risk as very small or small (63%).\n Question: Do patients with Barrett 's esophagus perceive their risk of developing esophageal adenocarcinoma as low?\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 risk of developing esophageal adenocarcinoma (EAC) for patients with Barrett's esophagus (BE) is approximately 0.5% per year. To investigate how patients with BE estimate and perceive their risk of developing EAC. Questionnaire study. Patients with BE who were undergoing surveillance endoscopy based on histologic and flow cytometric results. A total of 192 patients with BE were included. Individual patients were asked to estimate the numerical risk to develop EAC for patients with BE in general and for themselves. How patients perceived their own risk was measured on a scale from "very small" to "very large." At least 1 question was filled out by 169 patients (88% response). Sixty percent of respondents underestimated the numerical risk for patients with BE, in general, to develop EAC, while even more patients (69%) underestimated their own risk. Most respondents perceived their own risk as very small or small (63%).
Question: Do patients with Barrett 's esophagus perceive their risk of developing esophageal adenocarcinoma as low?
Output:
|
PubmedQA164099
|
[
{
"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: This study was designed to examine the hypothesis that gender differences in I/R injury are associated with endothelial cell nitric oxide synthase (eNOS)-derived nitric oxide (NO). Wistar rats were randomized into seven experimental groups (12 animals per group). Except for the sham operated groups, all rats were subjected to total liver ischemia for 40 min followed by reperfusion. All experimental groups received different treatments 45 min before the laparotomy. For each group, half of the animals (six) were used to investigate the survival; blood samples and liver tissues were obtained in the remaining six animals after 3 h of reperfusion to assess serum NO, alanine aminotransferase (ALT) and TNF-alpha levels, liver tissue malondialdehyde (MDA) content, and severity of hepatic I/R injury. Basal serum NO levels in female sham operated (FS) group were nearly 1.5-fold of male sham operated (MS) group (66.7+/-11.0 micromol/L vs 45.3+/-10.1 micromol/L, P<0.01). Although serum NO levels decreased significantly after hepatic I/R (P<0.01, vs sham operated groups), they were still significantly higher in female rat (F) group than in male rat (M) group (47.8+/-8.6 micromol/L vs 23.8+/-4.7 micromol/L, P<0.01). Serum ALT and TNF-alpha levels, and liver tissue MDA content were significantly lower in F group than in M group (370.5+/-46.4 U/L, 0.99+/-0.11 microg/L and 0.57+/-0.10 micromol/g vs 668.7+/-78.7 U/L, 1.71+/-0.18 microg/L and 0.86+/-0.11 micromol/g, respectively, P<0.01). I/R induced significant injury to the liver both in M and F groups (P<0.01 vs sham operated groups). But the degree of hepatocyte injury was significantly milder in F group than in M group (P<0.05 and P<0.01). The median survival time was six days in F group and one day in M group. The overall survival rate was significantly higher in F group than in M group (P<0.05). When compared with male rats pretreated with saline (M group), pretreatment of male rats with 17-beta-estradiol (E2) (M+E2 group) significantly increased serum NO levels and significantly decreased serum ALT and TNF-alpha levels, and liver tissue MDA content after I/R (P<0.01). The degree of hepatocyte injury was significantly decreased and the overall survival rate was significantly improved in M+E2 group than in M group (P<0.01 and P<0.05). The NOS inhibitor N(w) -nitro-L-arginine methyl ester (L-NAME) treatment could completely abolish the protective effects of estrogen in both male and female rats.\n Question: Are gender differences in hepatic ischemic reperfusion injury in rats associated with endothelial cell nitric oxide synthase-derived nitric oxide?\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: This study was designed to examine the hypothesis that gender differences in I/R injury are associated with endothelial cell nitric oxide synthase (eNOS)-derived nitric oxide (NO). Wistar rats were randomized into seven experimental groups (12 animals per group). Except for the sham operated groups, all rats were subjected to total liver ischemia for 40 min followed by reperfusion. All experimental groups received different treatments 45 min before the laparotomy. For each group, half of the animals (six) were used to investigate the survival; blood samples and liver tissues were obtained in the remaining six animals after 3 h of reperfusion to assess serum NO, alanine aminotransferase (ALT) and TNF-alpha levels, liver tissue malondialdehyde (MDA) content, and severity of hepatic I/R injury. Basal serum NO levels in female sham operated (FS) group were nearly 1.5-fold of male sham operated (MS) group (66.7+/-11.0 micromol/L vs 45.3+/-10.1 micromol/L, P<0.01). Although serum NO levels decreased significantly after hepatic I/R (P<0.01, vs sham operated groups), they were still significantly higher in female rat (F) group than in male rat (M) group (47.8+/-8.6 micromol/L vs 23.8+/-4.7 micromol/L, P<0.01). Serum ALT and TNF-alpha levels, and liver tissue MDA content were significantly lower in F group than in M group (370.5+/-46.4 U/L, 0.99+/-0.11 microg/L and 0.57+/-0.10 micromol/g vs 668.7+/-78.7 U/L, 1.71+/-0.18 microg/L and 0.86+/-0.11 micromol/g, respectively, P<0.01). I/R induced significant injury to the liver both in M and F groups (P<0.01 vs sham operated groups). But the degree of hepatocyte injury was significantly milder in F group than in M group (P<0.05 and P<0.01). The median survival time was six days in F group and one day in M group. The overall survival rate was significantly higher in F group than in M group (P<0.05). When compared with male rats pretreated with saline (M group), pretreatment of male rats with 17-beta-estradiol (E2) (M+E2 group) significantly increased serum NO levels and significantly decreased serum ALT and TNF-alpha levels, and liver tissue MDA content after I/R (P<0.01). The degree of hepatocyte injury was significantly decreased and the overall survival rate was significantly improved in M+E2 group than in M group (P<0.01 and P<0.05). The NOS inhibitor N(w) -nitro-L-arginine methyl ester (L-NAME) treatment could completely abolish the protective effects of estrogen in both male and female rats.
Question: Are gender differences in hepatic ischemic reperfusion injury in rats associated with endothelial cell nitric oxide synthase-derived nitric oxide?
Output:
|
PubmedQA161695
|
[
{
"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: Job strain has been associated with depressive symptoms, and depression has been associated with low bone mineral density (BMD). The associations between BMD and job strain have not been studied. We examined the relations between BMD, job strain, and depressive symptoms in a population-based group of young adults in Finland. Ultrasonic measurement of BMD at the calcaneus was performed on 777 participants (men 45 %, aged 30-45) drawn from the Cardiovascular Risk in Young Finns Study. Job strain was assessed by self-administered questionnaires by the combination of job demands and job control. Depressive symptoms were assessed with a modified Beck Depression Inventory. The effects of job strain on BMD were studied with multivariable analyses with age, sex, BMI, vitamin D, and calcium intake, physical activity, cigarette smoking, alcohol use, and depressive symptoms as covariates. Depressive symptoms were independently associated with lower BMD T score in participants with high job strain (β = -0.241, p = 0.02), but depressive symptoms were not significantly associated with BMD in the low (β = -0.160, p = 0.26) and intermediate (β = -0.042, p = 0.66) job strain categories.\n Question: Are depressive symptoms associated with lower bone mineral density in young adults with high job strain . The Cardiovascular Risk in Young Finns 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: Job strain has been associated with depressive symptoms, and depression has been associated with low bone mineral density (BMD). The associations between BMD and job strain have not been studied. We examined the relations between BMD, job strain, and depressive symptoms in a population-based group of young adults in Finland. Ultrasonic measurement of BMD at the calcaneus was performed on 777 participants (men 45 %, aged 30-45) drawn from the Cardiovascular Risk in Young Finns Study. Job strain was assessed by self-administered questionnaires by the combination of job demands and job control. Depressive symptoms were assessed with a modified Beck Depression Inventory. The effects of job strain on BMD were studied with multivariable analyses with age, sex, BMI, vitamin D, and calcium intake, physical activity, cigarette smoking, alcohol use, and depressive symptoms as covariates. Depressive symptoms were independently associated with lower BMD T score in participants with high job strain (β = -0.241, p = 0.02), but depressive symptoms were not significantly associated with BMD in the low (β = -0.160, p = 0.26) and intermediate (β = -0.042, p = 0.66) job strain categories.
Question: Are depressive symptoms associated with lower bone mineral density in young adults with high job strain . The Cardiovascular Risk in Young Finns Study?
Output:
|
PubmedQA11749
|
[
{
"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: Visible light irradiation after application of a photosensitizer (topical photodynamic therapy; PDT) is increasingly used to treat nonmelanoma skin cancers and premalignant actinic keratoses. PDT can provide a cosmetically superior alternative to surgery, but carries failure rates of 10-40%. While some murine studies have suggested immune enhancement by PDT, others reported immunosuppressive effects, which may indicate impaired antitumour immunity and thus compromised tumour clearance. This study aimed to determine the in vivo immune effects of PDT in humans. Using healthy, Mantoux-positive volunteers, we irradiated discrete areas of the back with narrowband red light (630 nm; 37 J cm(-2)), with and without prior application of 5-aminolaevulinic acid (ALA) or methyl aminolaevulinate (MAL). Adjacent, untreated areas served as immunologically intact control sites. Delayed-type hypersensitivity responses to tuberculin purified protein derivative (Mantoux reactions) were then elicited in each of the irradiated, unirradiated and control sites, and the intensity of the reactions was quantitated with an erythema meter and by measurement of Mantoux diameter. By comparing Mantoux intensity at treated and control sites, immunosuppression was determined in each volunteer for each intervention. We found that both MAL-PDT and ALA-PDT significantly suppressed Mantoux erythema (by 30% and 50%, respectively) and diameter (41% and 38%). Red light alone significantly suppressed diameter (22%) but not erythema (13%).\n Question: Is topical photodynamic therapy immunosuppressive in humans?\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: Visible light irradiation after application of a photosensitizer (topical photodynamic therapy; PDT) is increasingly used to treat nonmelanoma skin cancers and premalignant actinic keratoses. PDT can provide a cosmetically superior alternative to surgery, but carries failure rates of 10-40%. While some murine studies have suggested immune enhancement by PDT, others reported immunosuppressive effects, which may indicate impaired antitumour immunity and thus compromised tumour clearance. This study aimed to determine the in vivo immune effects of PDT in humans. Using healthy, Mantoux-positive volunteers, we irradiated discrete areas of the back with narrowband red light (630 nm; 37 J cm(-2)), with and without prior application of 5-aminolaevulinic acid (ALA) or methyl aminolaevulinate (MAL). Adjacent, untreated areas served as immunologically intact control sites. Delayed-type hypersensitivity responses to tuberculin purified protein derivative (Mantoux reactions) were then elicited in each of the irradiated, unirradiated and control sites, and the intensity of the reactions was quantitated with an erythema meter and by measurement of Mantoux diameter. By comparing Mantoux intensity at treated and control sites, immunosuppression was determined in each volunteer for each intervention. We found that both MAL-PDT and ALA-PDT significantly suppressed Mantoux erythema (by 30% and 50%, respectively) and diameter (41% and 38%). Red light alone significantly suppressed diameter (22%) but not erythema (13%).
Question: Is topical photodynamic therapy immunosuppressive in humans?
Output:
|
PubmedQA79853
|
[
{
"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: Thyroid hormones and progesterone both influence core temperature, metabolism and are crucial during pregnancy. Our objective was to discover whether progesterone therapy caused changes in thyroid physiology compared with placebo. Post hoc analysis from a randomized (1:1) placebo-controlled 12-week trial of oral micronized progesterone (Progesterone, 300 mg/d at bedtime) for hot flushes (vasomotor symptoms, VMS) conducted in an academic medical centre. Postmenopausal euthyroid, healthy (without cardiovascular diseases or risks) women, 1-11 years since last flow on no thyroid or ovarian hormone therapy with VMS participated. Primary outcomes were final and 12-week changes in TSH, FreeT3 and FreeT4 on progesterone vs placebo. Women with thyroid data (69 of 133 in original trial) were randomized to progesterone (n = 39) or placebo (n = 30)-baseline thyroid values were normal. There were no VMS-thyroid interactions-VMS Score (number × intensity) did not correlate with TSH, FreeT3 or FreeT4 (Spearman's rank correlations: -0.03 to -0.19, respectively; all P > 0.15). At 12 weeks on progesterone, TSH levels tended to be lower (1.7 mU) than on placebo (2.2), P = 0.06; FreeT4 levels were higher (16.4 pmol/l) than on placebo (15.3), P = 0.02. FreeT3 was unchanged throughout. Analysis of covariance showed a significant increase in FreeT4 on progesterone (+2.5 pmol/l; 1.9-3.0) vs on placebo (+1.7; 1.1-2.4) with 95% CI of difference = 0.8 pmol/l [0.0, 1.6], P = 0.04.\n Question: Does progesterone therapy increase free thyroxine levels -- data from a randomized placebo-controlled 12-week hot flush trial?\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: Thyroid hormones and progesterone both influence core temperature, metabolism and are crucial during pregnancy. Our objective was to discover whether progesterone therapy caused changes in thyroid physiology compared with placebo. Post hoc analysis from a randomized (1:1) placebo-controlled 12-week trial of oral micronized progesterone (Progesterone, 300 mg/d at bedtime) for hot flushes (vasomotor symptoms, VMS) conducted in an academic medical centre. Postmenopausal euthyroid, healthy (without cardiovascular diseases or risks) women, 1-11 years since last flow on no thyroid or ovarian hormone therapy with VMS participated. Primary outcomes were final and 12-week changes in TSH, FreeT3 and FreeT4 on progesterone vs placebo. Women with thyroid data (69 of 133 in original trial) were randomized to progesterone (n = 39) or placebo (n = 30)-baseline thyroid values were normal. There were no VMS-thyroid interactions-VMS Score (number × intensity) did not correlate with TSH, FreeT3 or FreeT4 (Spearman's rank correlations: -0.03 to -0.19, respectively; all P > 0.15). At 12 weeks on progesterone, TSH levels tended to be lower (1.7 mU) than on placebo (2.2), P = 0.06; FreeT4 levels were higher (16.4 pmol/l) than on placebo (15.3), P = 0.02. FreeT3 was unchanged throughout. Analysis of covariance showed a significant increase in FreeT4 on progesterone (+2.5 pmol/l; 1.9-3.0) vs on placebo (+1.7; 1.1-2.4) with 95% CI of difference = 0.8 pmol/l [0.0, 1.6], P = 0.04.
Question: Does progesterone therapy increase free thyroxine levels -- data from a randomized placebo-controlled 12-week hot flush trial?
Output:
|
PubmedQA186725
|
[
{
"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: It has been shown that antagonism of the glutamatergic N-methyl-D-aspartate (NMDA) receptor with subanesthetic doses of ketamine perturbs the perception of elapsed time. Anticipatory eye movements are based on an internal representation of elapsed time. Therefore, the occurrence of anticipatory saccades could be a particularly sensitive indicator of abnormal time perception due to NMDA receptors blockade. The objective of this study was to determine whether the occurrence of anticipatory saccades could be selectively altered by a subanesthetic dose of ketamine. Three Rhesus monkeys were trained in a simple visually guided saccadic task with a variable delay. Monkeys were rewarded for making a visually guided saccade at the end of the delay. Premature anticipatory saccades to the future position of the eccentric target initiated before the end of the delay were not rewarded. A subanesthetic dose of ketamine (0.25 mg/kg) or a saline solution of the same volume was injected i.m. during the task. We found that the injected dose of ketamine did not induce sedation or abnormal behavior. However, in ∼4 min, ketamine induced a strong reduction of the occurrence of anticipatory saccades but did not reduce the occurrence of visually guided saccades.\n Question: Does a subanesthetic dose of ketamine in the Rhesus monkey reduce the occurrence of anticipatory saccades?\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: It has been shown that antagonism of the glutamatergic N-methyl-D-aspartate (NMDA) receptor with subanesthetic doses of ketamine perturbs the perception of elapsed time. Anticipatory eye movements are based on an internal representation of elapsed time. Therefore, the occurrence of anticipatory saccades could be a particularly sensitive indicator of abnormal time perception due to NMDA receptors blockade. The objective of this study was to determine whether the occurrence of anticipatory saccades could be selectively altered by a subanesthetic dose of ketamine. Three Rhesus monkeys were trained in a simple visually guided saccadic task with a variable delay. Monkeys were rewarded for making a visually guided saccade at the end of the delay. Premature anticipatory saccades to the future position of the eccentric target initiated before the end of the delay were not rewarded. A subanesthetic dose of ketamine (0.25 mg/kg) or a saline solution of the same volume was injected i.m. during the task. We found that the injected dose of ketamine did not induce sedation or abnormal behavior. However, in ∼4 min, ketamine induced a strong reduction of the occurrence of anticipatory saccades but did not reduce the occurrence of visually guided saccades.
Question: Does a subanesthetic dose of ketamine in the Rhesus monkey reduce the occurrence of anticipatory saccades?
Output:
|
PubmedQA127137
|
[
{
"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: Endothelin-1 (ET-1) has deleterious effects on water homeostasis, cerebral edema, and blood-brain barrier (BBB) integrity. Highly expressed ET-1 was observed after intracerebral hemorrhage (ICH); however, ET-1 changes and their relationship with BBB disruption within 24 hours of ICH have not been thoroughly investigated. The aim of the present study was to observe the changes in perihematomal ET-1 levels in various phases of ICH and their correlation with the BBB integrity in a rabbit model of ICH. Twenty-five rabbits (3.2-4.3 kg body weight) were randomly divided into a normal control group (five rabbits) and a model group (20 rabbits). Animals in the model group were equally divided into four subgroups (five rabbits each to be sacrificed at 6, 12, 18, and 24 hours following ICH establishment). An ICH model was prepared in the model group by infusing autologous arterial blood into the rabbit brain. ET-1 expression in perihematomal brain tissues was determined using immunohistochemistry and color image analysis, and the permeability of the BBB was assayed using the Evan's Blue (EB) method. A repeated measures analysis of variance was used to make comparisons of the ET-1 and EB content across the entire time series. The number of perihematomal endothelial cells with ET-1 positive expressions following 6, 12, 18, and 24 hours ICH model establishment was 9.32, 13.05, 15.90, and 20.44, respectively, but as low as 6.67 in the control group. The average transmittance of ET-1-positive cell bodies at 6, 12, 18, and 24 hours after ICH was 99.10, 97.40, 85.70, and 80.80, respectively, but 100.12 in the control group. These data reveal that the expression of ET-1 was significantly increased at 6, 12, 18, and 24 hours after ICH compared with the control group, and a marked decrease in the average transmittance of ET-1-positive cell bodies was noted (P < 0.05). Similarly, the perihematomal EB content at 6, 12, 18, and 24 hours after ICH was 29.39 ± 1.16, 32.20 ± 0.73, 33.63 ± 1.08, and 35.26 ± 1.12, respectively, in the model group and 28.06 ± 0.80 in the control group. The results indicate that a significant increase in the EB content in the model group was observed compared with that of the control group (P < 0.05). Moreover, a positive correlation between the number of ET-1-positive endothelial cells and BBB permeability was observed (r = 0.883, P < 0.05).\n Question: Is perihematomal endothelin-1 level associated with an increase in blood-brain barrier permeability in a rabbit model of intracerebral hematoma?\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: Endothelin-1 (ET-1) has deleterious effects on water homeostasis, cerebral edema, and blood-brain barrier (BBB) integrity. Highly expressed ET-1 was observed after intracerebral hemorrhage (ICH); however, ET-1 changes and their relationship with BBB disruption within 24 hours of ICH have not been thoroughly investigated. The aim of the present study was to observe the changes in perihematomal ET-1 levels in various phases of ICH and their correlation with the BBB integrity in a rabbit model of ICH. Twenty-five rabbits (3.2-4.3 kg body weight) were randomly divided into a normal control group (five rabbits) and a model group (20 rabbits). Animals in the model group were equally divided into four subgroups (five rabbits each to be sacrificed at 6, 12, 18, and 24 hours following ICH establishment). An ICH model was prepared in the model group by infusing autologous arterial blood into the rabbit brain. ET-1 expression in perihematomal brain tissues was determined using immunohistochemistry and color image analysis, and the permeability of the BBB was assayed using the Evan's Blue (EB) method. A repeated measures analysis of variance was used to make comparisons of the ET-1 and EB content across the entire time series. The number of perihematomal endothelial cells with ET-1 positive expressions following 6, 12, 18, and 24 hours ICH model establishment was 9.32, 13.05, 15.90, and 20.44, respectively, but as low as 6.67 in the control group. The average transmittance of ET-1-positive cell bodies at 6, 12, 18, and 24 hours after ICH was 99.10, 97.40, 85.70, and 80.80, respectively, but 100.12 in the control group. These data reveal that the expression of ET-1 was significantly increased at 6, 12, 18, and 24 hours after ICH compared with the control group, and a marked decrease in the average transmittance of ET-1-positive cell bodies was noted (P < 0.05). Similarly, the perihematomal EB content at 6, 12, 18, and 24 hours after ICH was 29.39 ± 1.16, 32.20 ± 0.73, 33.63 ± 1.08, and 35.26 ± 1.12, respectively, in the model group and 28.06 ± 0.80 in the control group. The results indicate that a significant increase in the EB content in the model group was observed compared with that of the control group (P < 0.05). Moreover, a positive correlation between the number of ET-1-positive endothelial cells and BBB permeability was observed (r = 0.883, P < 0.05).
Question: Is perihematomal endothelin-1 level associated with an increase in blood-brain barrier permeability in a rabbit model of intracerebral hematoma?
Output:
|
PubmedQA122039
|
[
{
"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 the study was to evaluate the efficacy of preoperative intravenous (IV) ferric carboxymaltose (FCM) administration vs. no-IV iron in colon cancer (CC) anemic patients undergoing elective surgery with curative intention. This was a multicenter, observational study including two cohorts of consecutive CC anemic patients: the no-IV iron treatment group was obtained retrospectively while FCM-treated patients were recorded prospectively. A total of 266 patients were included: 111 received FCM (median dose 1000 mg) and 155 were no-IV iron subjects. Both groups were similar in terms of demographic characteristics, tumor location, surgical approach, and intra-operative bleeding severity. The FCM group showed a significant lower need for red blood cell (RBC) transfusion during the study (9.9 vs. 38.7%; OR: 5.9, p < 0.001). In spite of lower hemoglobin levels at baseline diagnosis and lower transfusion rates in the FCM group, the proportion of responders was significantly higher with respect to the no-IV group both at hospital admission (48.1 vs. 20.0%, p < 0.0001) and at 30 days post-surgery (80.0 vs. 48.9%, p < 0.0001). The percentage of patients with normalized hemoglobin levels was also higher in the FCM group (40.0 vs. 26.7% at 30 days, p < 0.05). A lower number of reinterventions and post-surgery complications were seen in the FCM group (20.7 vs. 26.5%; p = 0.311). The FCM group presented a significant shorter hospital stay (8.4 ± 6.8 vs. 10.9 ± 12.4 days to discharge; p < 0.001).\n Question: Does ferric carboxymaltose reduce transfusions and hospital stay in patients with colon cancer and anemia?\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 the study was to evaluate the efficacy of preoperative intravenous (IV) ferric carboxymaltose (FCM) administration vs. no-IV iron in colon cancer (CC) anemic patients undergoing elective surgery with curative intention. This was a multicenter, observational study including two cohorts of consecutive CC anemic patients: the no-IV iron treatment group was obtained retrospectively while FCM-treated patients were recorded prospectively. A total of 266 patients were included: 111 received FCM (median dose 1000 mg) and 155 were no-IV iron subjects. Both groups were similar in terms of demographic characteristics, tumor location, surgical approach, and intra-operative bleeding severity. The FCM group showed a significant lower need for red blood cell (RBC) transfusion during the study (9.9 vs. 38.7%; OR: 5.9, p < 0.001). In spite of lower hemoglobin levels at baseline diagnosis and lower transfusion rates in the FCM group, the proportion of responders was significantly higher with respect to the no-IV group both at hospital admission (48.1 vs. 20.0%, p < 0.0001) and at 30 days post-surgery (80.0 vs. 48.9%, p < 0.0001). The percentage of patients with normalized hemoglobin levels was also higher in the FCM group (40.0 vs. 26.7% at 30 days, p < 0.05). A lower number of reinterventions and post-surgery complications were seen in the FCM group (20.7 vs. 26.5%; p = 0.311). The FCM group presented a significant shorter hospital stay (8.4 ± 6.8 vs. 10.9 ± 12.4 days to discharge; p < 0.001).
Question: Does ferric carboxymaltose reduce transfusions and hospital stay in patients with colon cancer and anemia?
Output:
|
PubmedQA39432
|
[
{
"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: Pathways of L-arginine metabolism including nitric oxide, agmatine and polyamine synthesis are upregulated during glomerular inflammation in experimental glomerulonephritis. In anti-Thy-1-glomerulonephritis L-arginine-deficient diets ameliorate the disease course in this model. However, it is unclear which metabolic pathway is affected by this substrate depletion. Since polyamines are important proproliferative molecules, we studied the effect of specific polyamine synthesis blockade in vivo on mesangial cell proliferation and glomerular fibrosis in this model. Anti-Thy-1-glomerulonephritis was induced in male Sprague-Dawley rats by single-bolus injection of monoclonal ER4-antibodies. Rats were treated with difluoromethylornithine (0.5-2% in the drinking water), a selective inhibitor of the rate-limiting enzyme of polyamine synthesis, ornithine decarboxylase (ODC). Mesangial cell proliferation and matrix expansion were evaluated in PAS-stained kidney tissues. Glomerular TGF-beta and biglycan-mRNA-expression were determined by Northern blot analysis and albuminuria was measured using a competitive ELISA. Data were compared to untreated controls. Though complete inhibition of ODC activity was achieved at any time point, difluoromethlornithine treatment had no significant effect on albuminuria, glomerular matrix protein expression and mesangial cell count in this model.\n Question: Is acute glomerular upregulation of ornithine decarboxylase essential for mesangial cell proliferation and matrix expansion in anti-Thy-1-nephritis?\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: Pathways of L-arginine metabolism including nitric oxide, agmatine and polyamine synthesis are upregulated during glomerular inflammation in experimental glomerulonephritis. In anti-Thy-1-glomerulonephritis L-arginine-deficient diets ameliorate the disease course in this model. However, it is unclear which metabolic pathway is affected by this substrate depletion. Since polyamines are important proproliferative molecules, we studied the effect of specific polyamine synthesis blockade in vivo on mesangial cell proliferation and glomerular fibrosis in this model. Anti-Thy-1-glomerulonephritis was induced in male Sprague-Dawley rats by single-bolus injection of monoclonal ER4-antibodies. Rats were treated with difluoromethylornithine (0.5-2% in the drinking water), a selective inhibitor of the rate-limiting enzyme of polyamine synthesis, ornithine decarboxylase (ODC). Mesangial cell proliferation and matrix expansion were evaluated in PAS-stained kidney tissues. Glomerular TGF-beta and biglycan-mRNA-expression were determined by Northern blot analysis and albuminuria was measured using a competitive ELISA. Data were compared to untreated controls. Though complete inhibition of ODC activity was achieved at any time point, difluoromethlornithine treatment had no significant effect on albuminuria, glomerular matrix protein expression and mesangial cell count in this model.
Question: Is acute glomerular upregulation of ornithine decarboxylase essential for mesangial cell proliferation and matrix expansion in anti-Thy-1-nephritis?
Output:
|
PubmedQA210764
|
[
{
"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 aetiology and pathogenesis of heterotopic ossification (HO) are still obscure. We evaluated the impact of necrotic gluteus minimus muscle (GMM) debridement on the formation of HO after operative treatment of posterior wall (PW) and associated transverse-posterior wall acetabular fracture (Tr/PW) fixations utilizing a Kocher-Langenbeck surgical exposure. Thirty-one consecutive patients with displaced PW or associated Tr/PW acetabular fracture-dislocations were operatively treated by a single surgeon using a Kocher-Langenbeck surgical exposure. Strict soft tissue technique was observed and self-retaining retractors were not used. Necrotic GMM was debrided in an attempt to diminish ectopic bone formation. Twenty-nine patients were available for post-operative clinical and radiographic evaluations. HO occurred in 12 patients. Significant HO (Brooker class III or IV) was noted in only three patients (10%). There were no complications associated with debridement of necrotic GMM.\n Question: Does gluteus minimus necrotic muscle debridement diminish heterotopic ossification after acetabular fracture fixation?\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 aetiology and pathogenesis of heterotopic ossification (HO) are still obscure. We evaluated the impact of necrotic gluteus minimus muscle (GMM) debridement on the formation of HO after operative treatment of posterior wall (PW) and associated transverse-posterior wall acetabular fracture (Tr/PW) fixations utilizing a Kocher-Langenbeck surgical exposure. Thirty-one consecutive patients with displaced PW or associated Tr/PW acetabular fracture-dislocations were operatively treated by a single surgeon using a Kocher-Langenbeck surgical exposure. Strict soft tissue technique was observed and self-retaining retractors were not used. Necrotic GMM was debrided in an attempt to diminish ectopic bone formation. Twenty-nine patients were available for post-operative clinical and radiographic evaluations. HO occurred in 12 patients. Significant HO (Brooker class III or IV) was noted in only three patients (10%). There were no complications associated with debridement of necrotic GMM.
Question: Does gluteus minimus necrotic muscle debridement diminish heterotopic ossification after acetabular fracture fixation?
Output:
|
PubmedQA2878
|
[
{
"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: Older adults often show sustained attention toward positive information and an improved memory for positive events. Little is known about the neural changes that may underlie these effects, although recent research has suggested that older adults may show differential recruitment of prefrontal regions during the successful encoding of emotional information. In the present study, effective connectivity analyses examined the network of regions that college-age and older adults recruited during the encoding of positive and negative images. Participants viewed positive and negative images while undergoing a functional magnetic resonance imaging (fMRI) scan. Structural equation modeling was used to compare young and older adults' connectivity among regions of the emotional memory network while they encoded negative or positive items. Aging did not impact the connectivity among regions engaged during the encoding of negative information, but age differences did arise during the encoding of positive information. Most notably, in older adults, the ventromedial prefrontal cortex and amygdala strongly influenced hippocampal activity during the encoding of positive information. By contrast, in young adults, a strong thalamic influence on hippocampal activity was evident during encoding.\n Question: Are there age-related changes in neural connectivity during the encoding of positive , but not negative , information?\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: Older adults often show sustained attention toward positive information and an improved memory for positive events. Little is known about the neural changes that may underlie these effects, although recent research has suggested that older adults may show differential recruitment of prefrontal regions during the successful encoding of emotional information. In the present study, effective connectivity analyses examined the network of regions that college-age and older adults recruited during the encoding of positive and negative images. Participants viewed positive and negative images while undergoing a functional magnetic resonance imaging (fMRI) scan. Structural equation modeling was used to compare young and older adults' connectivity among regions of the emotional memory network while they encoded negative or positive items. Aging did not impact the connectivity among regions engaged during the encoding of negative information, but age differences did arise during the encoding of positive information. Most notably, in older adults, the ventromedial prefrontal cortex and amygdala strongly influenced hippocampal activity during the encoding of positive information. By contrast, in young adults, a strong thalamic influence on hippocampal activity was evident during encoding.
Question: Are there age-related changes in neural connectivity during the encoding of positive , but not negative , information?
Output:
|
PubmedQA112687
|
[
{
"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: Many participants in microbicide trials remain uninfected despite ongoing exposure to HIV-1. Determining the emergence and nature of mucosal HIV-specific immune responses in such women is important, since these responses may contribute to protection and could provide insight for the rational design of HIV-1 vaccines. We first conducted a pilot study to compare three sampling devices (Dacron swabs, flocked nylon swabs and Merocel sponges) for detection of HIV-1-specific IgG and IgA antibodies in vaginal secretions. IgG antibodies from HIV-1-positive women reacted broadly across the full panel of eight HIV-1 envelope (Env) antigens tested, whereas IgA antibodies only reacted to the gp41 subunit. No Env-reactive antibodies were detected in the HIV-negative women. The three sampling devices yielded equal HIV-1-specific antibody titers, as well as total IgG and IgA concentrations. We then tested vaginal Dacron swabs archived from 57 HIV seronegative women who participated in a microbicide efficacy trial in Southern Africa (HPTN 035). We detected vaginal IgA antibodies directed at HIV-1 Env gp120/gp140 in six of these women, and at gp41 in another three women, but did not detect Env-specific IgG antibodies in any women.\n Question: Are hIV-1 specific IgA detected in vaginal secretions of HIV uninfected women participating in a microbicide trial in Southern Africa primarily directed toward gp120 and gp140 specificities?\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: Many participants in microbicide trials remain uninfected despite ongoing exposure to HIV-1. Determining the emergence and nature of mucosal HIV-specific immune responses in such women is important, since these responses may contribute to protection and could provide insight for the rational design of HIV-1 vaccines. We first conducted a pilot study to compare three sampling devices (Dacron swabs, flocked nylon swabs and Merocel sponges) for detection of HIV-1-specific IgG and IgA antibodies in vaginal secretions. IgG antibodies from HIV-1-positive women reacted broadly across the full panel of eight HIV-1 envelope (Env) antigens tested, whereas IgA antibodies only reacted to the gp41 subunit. No Env-reactive antibodies were detected in the HIV-negative women. The three sampling devices yielded equal HIV-1-specific antibody titers, as well as total IgG and IgA concentrations. We then tested vaginal Dacron swabs archived from 57 HIV seronegative women who participated in a microbicide efficacy trial in Southern Africa (HPTN 035). We detected vaginal IgA antibodies directed at HIV-1 Env gp120/gp140 in six of these women, and at gp41 in another three women, but did not detect Env-specific IgG antibodies in any women.
Question: Are hIV-1 specific IgA detected in vaginal secretions of HIV uninfected women participating in a microbicide trial in Southern Africa primarily directed toward gp120 and gp140 specificities?
Output:
|
PubmedQA163856
|
[
{
"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 adult human brain contains neural stem/progenitor cells (AHNPCs) that can survive transplantation into the adult rat brain, migrate toward a lesion, and display limited neuronal differentiation in vivo. To investigate the effect of manipulating AHNPCs before grafting by predifferentiation, ie, initiating neuronal differentiation before transplantation, and to determine whether this cell priming would affect their ability to migrate in vivo. AHNPCs were prepared from temporal lobe resections for epilepsy. Seven days after global brain ischemia, predifferentiated AHNPCs (exposed to basic fibroblast growth factor, heparin, and laminin) were transplanted to the left hippocampus. Four and 10 weeks after transplantation, brain sections were analyzed by immunohistochemistry. Transplanted primed cells expressed committed neuronal markers at a much earlier stage compared with nonprimed AHNPCs and were found colabeled with human markers within the damaged CA1 region 4 weeks after grafting. Furthermore, predifferentiated AHNPCs migrated preferentially into an ischemic lesion, similar to their undifferentiated counterparts. The chemoattractant effect from the expression of stromal cell-derived factor-1α (SDF-1α) in ischemic CA1 on AHNPCs expressing CXC chemokine receptor 4 (CXCR4) may explain this preference in migration in vivo.\n Question: Do predifferentiated brain-derived adult human progenitor cells migrate toward ischemia after transplantation to the adult rat brain?\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 adult human brain contains neural stem/progenitor cells (AHNPCs) that can survive transplantation into the adult rat brain, migrate toward a lesion, and display limited neuronal differentiation in vivo. To investigate the effect of manipulating AHNPCs before grafting by predifferentiation, ie, initiating neuronal differentiation before transplantation, and to determine whether this cell priming would affect their ability to migrate in vivo. AHNPCs were prepared from temporal lobe resections for epilepsy. Seven days after global brain ischemia, predifferentiated AHNPCs (exposed to basic fibroblast growth factor, heparin, and laminin) were transplanted to the left hippocampus. Four and 10 weeks after transplantation, brain sections were analyzed by immunohistochemistry. Transplanted primed cells expressed committed neuronal markers at a much earlier stage compared with nonprimed AHNPCs and were found colabeled with human markers within the damaged CA1 region 4 weeks after grafting. Furthermore, predifferentiated AHNPCs migrated preferentially into an ischemic lesion, similar to their undifferentiated counterparts. The chemoattractant effect from the expression of stromal cell-derived factor-1α (SDF-1α) in ischemic CA1 on AHNPCs expressing CXC chemokine receptor 4 (CXCR4) may explain this preference in migration in vivo.
Question: Do predifferentiated brain-derived adult human progenitor cells migrate toward ischemia after transplantation to the adult rat brain?
Output:
|
PubmedQA177510
|
[
{
"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: There are few data about predictors of cardiovascular mortality and rehospitalization rate in patients with left ventricular systolic dysfunction (LVSD) after myocardial revascularization and optimization of pharmacological treatment. 1,346 consecutive patients with left ventricular ejection fraction (LVEF) < 45% (64 + or - 10 years, 73% male, LVEF 36.3% + or - 8%), who were referred for inpatient cardiac rehabilitation, were followed prospectively for 731 + or - 215 days in a unicentric prospective longitudinal registry. Multivariate logistic regression Cox models were used to analyze demographic, echocardiographic and exercise variables in order to determine independent predictors of cardiovascular mortality and rehospitalization. LVEF failed to show prognostic power (hazard ratio [HR] 0.99 [95% confidence interval, CI, 0.94-1.03]; p = not significant), whereas moderate to severe mitral regurgitation (HR, 5.71 [95% CI 1.75-18.6]; p = 0.004) and atrial fibrillation (HR 1.67 [95% CI 1.15-2.44]; p = 0.008) were associated with a poorer prognosis. In an optimized multivariate model, 6-min walk test (HR 0.93 [95% CI 0.86-1.00] per 50 m; p = 0.049) and symptom-limited maximum exercise capacity test (HR 0.83 [95% CI 0.76-0.91] per 10 W; p < 0.001) as well as female gender (HR 0.58 [95% CI 0.39-0.84]; p = 0.005) were strong predictors for reduced overall mortality.\n Question: Is exercise capacity the most powerful predictor of 2-year mortality in patients with left ventricular systolic dysfunction?\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: There are few data about predictors of cardiovascular mortality and rehospitalization rate in patients with left ventricular systolic dysfunction (LVSD) after myocardial revascularization and optimization of pharmacological treatment. 1,346 consecutive patients with left ventricular ejection fraction (LVEF) < 45% (64 + or - 10 years, 73% male, LVEF 36.3% + or - 8%), who were referred for inpatient cardiac rehabilitation, were followed prospectively for 731 + or - 215 days in a unicentric prospective longitudinal registry. Multivariate logistic regression Cox models were used to analyze demographic, echocardiographic and exercise variables in order to determine independent predictors of cardiovascular mortality and rehospitalization. LVEF failed to show prognostic power (hazard ratio [HR] 0.99 [95% confidence interval, CI, 0.94-1.03]; p = not significant), whereas moderate to severe mitral regurgitation (HR, 5.71 [95% CI 1.75-18.6]; p = 0.004) and atrial fibrillation (HR 1.67 [95% CI 1.15-2.44]; p = 0.008) were associated with a poorer prognosis. In an optimized multivariate model, 6-min walk test (HR 0.93 [95% CI 0.86-1.00] per 50 m; p = 0.049) and symptom-limited maximum exercise capacity test (HR 0.83 [95% CI 0.76-0.91] per 10 W; p < 0.001) as well as female gender (HR 0.58 [95% CI 0.39-0.84]; p = 0.005) were strong predictors for reduced overall mortality.
Question: Is exercise capacity the most powerful predictor of 2-year mortality in patients with left ventricular systolic dysfunction?
Output:
|
PubmedQA63972
|
[
{
"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: Obesity can lead to cognitive dysfunction including poor performance in memory tasks. However, poor memory is not seen in all obese humans and takes several months to develop in animal models, indicating the adult brain is relatively resistant to obesity's cognitive effects. We have seen that, in the rat, overfeeding for as little as 3 weeks in early life leads to lasting obesity and microglial priming in the hypothalamus. Here we hypothesized that microglial hyper-sensitivity in the neonatally overfed rats extends beyond the hypothalamus into memory-associated brain regions, resulting in cognitive deficits. We tested this idea by manipulating Wistar rat litter sizes to suckle pups in litters of 4 (overfed) or 12 (control). Neonatally overfed rats had microgliosis in the hippocampus after only 14 days overfeeding, and this persisted into adulthood. These changes were coupled with poor performance in radial arm maze and novel object recognition tests relative to controls. In controls, the experience of the radial arm maze reduced cell proliferation in the dentate gyrus and neuron numbers in the CA3. The learning task also suppressed microglial number and density in hippocampus and retrosplenial cortex. Neonatally overfed brains had impaired sensitivity to learning, with no neuronal or cell proliferative effects and less effective microglial suppression.\n Question: Does early life overfeeding impair spatial memory performance by reducing microglial sensitivity to learning?\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: Obesity can lead to cognitive dysfunction including poor performance in memory tasks. However, poor memory is not seen in all obese humans and takes several months to develop in animal models, indicating the adult brain is relatively resistant to obesity's cognitive effects. We have seen that, in the rat, overfeeding for as little as 3 weeks in early life leads to lasting obesity and microglial priming in the hypothalamus. Here we hypothesized that microglial hyper-sensitivity in the neonatally overfed rats extends beyond the hypothalamus into memory-associated brain regions, resulting in cognitive deficits. We tested this idea by manipulating Wistar rat litter sizes to suckle pups in litters of 4 (overfed) or 12 (control). Neonatally overfed rats had microgliosis in the hippocampus after only 14 days overfeeding, and this persisted into adulthood. These changes were coupled with poor performance in radial arm maze and novel object recognition tests relative to controls. In controls, the experience of the radial arm maze reduced cell proliferation in the dentate gyrus and neuron numbers in the CA3. The learning task also suppressed microglial number and density in hippocampus and retrosplenial cortex. Neonatally overfed brains had impaired sensitivity to learning, with no neuronal or cell proliferative effects and less effective microglial suppression.
Question: Does early life overfeeding impair spatial memory performance by reducing microglial sensitivity to learning?
Output:
|
PubmedQA16000
|
[
{
"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 follow up smokers to examine whether the likelihood of quitting smoking varied by area deprivation, and whether smoking history, health status, personality characteristics, social support and stressful situations contributed to differences in area deprivation in quit rates. Longitudinal data with a 6-year follow-up period were analysed using multilevel logistic regression. Area-level deprivation was characterised by a composite measure that was the sum of the proportion of unemployed residents, the percentage of residents in blue-collar occupations and the proportion with only elementary-level education. Previously established predictors of smoking cessation, including education, age at smoking initiation, self-assessed health, chronic illness, locus of control, neuroticism, negative life events, longlasting relationship difficulties, emotional social support and negative neighbourhood conditions were examined separately and in a combined model to assess whether they contributed to neighbourhood deprivation differences in quitting. 404 participants (residing in 83 areas) identified as smokers at baseline and who did not change their residential address over the follow-up period. Being a non-smoker at follow-up. Odds ratios of quitting decreased with greater area-level deprivation, but differences reached significance only between the most and least deprived quartiles. Smoking history, health status, personality characteristics, social support and stressful situations did not contribute to the lower quitting rates seen among smokers in deprived areas.\n Question: Are smokers living in deprived areas less likely to quit : a longitudinal follow-up?\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 follow up smokers to examine whether the likelihood of quitting smoking varied by area deprivation, and whether smoking history, health status, personality characteristics, social support and stressful situations contributed to differences in area deprivation in quit rates. Longitudinal data with a 6-year follow-up period were analysed using multilevel logistic regression. Area-level deprivation was characterised by a composite measure that was the sum of the proportion of unemployed residents, the percentage of residents in blue-collar occupations and the proportion with only elementary-level education. Previously established predictors of smoking cessation, including education, age at smoking initiation, self-assessed health, chronic illness, locus of control, neuroticism, negative life events, longlasting relationship difficulties, emotional social support and negative neighbourhood conditions were examined separately and in a combined model to assess whether they contributed to neighbourhood deprivation differences in quitting. 404 participants (residing in 83 areas) identified as smokers at baseline and who did not change their residential address over the follow-up period. Being a non-smoker at follow-up. Odds ratios of quitting decreased with greater area-level deprivation, but differences reached significance only between the most and least deprived quartiles. Smoking history, health status, personality characteristics, social support and stressful situations did not contribute to the lower quitting rates seen among smokers in deprived areas.
Question: Are smokers living in deprived areas less likely to quit : a longitudinal follow-up?
Output:
|
PubmedQA170353
|
[
{
"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: Cerebral arteriovenous malformation (AVM) is a vascular disease that disrupts normal blood flow and leads to serious neurological impairment or death. Aberrant functions of AVM-derived brain endothelial cells (AVM-BECs) are a disease hallmark. Our aim was to use microRNA-18a (miR-18a) as a therapeutic agent to improve AVM-BEC function. Human AVM-BECs were tested for growth factor production and proliferation under different shear flow conditions and evaluated for tubule formation. Thrombospondin-1, inhibitor of DNA-binding protein 1, and vascular endothelial growth factor (VEGF) isotype mRNA levels were quantified by quantitative real-time polymerase chain reaction. Thrombospondin-1, VEGF-A, and VEGF-D protein expression was measured using enzyme-linked immunosorbent assay. Proliferation and tubule formation were evaluated using bromodeoxyuridine incorporation and growth factor-reduced Matrigel assays, respectively. miR-18a increased thrombospondin-1 production but decreased inhibitor of DNA-binding protein 1, a transcriptional repressor of thrombospondin-1. miR-18a reduced VEGF-A and VEGF-D levels, both overexpressed in untreated AVM-BECs. This is the first study reporting VEGF-D overexpression in AVM. These effects were most prominent under arterial shear flow conditions. miR-18a also reduced AVM-BEC proliferation, improved tubule formation, and was effectively internalized by AVM-BECs in the absence of extraneous transfection reagents.\n Question: Does microRNA-18a improve human cerebral arteriovenous malformation endothelial cell function?\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: Cerebral arteriovenous malformation (AVM) is a vascular disease that disrupts normal blood flow and leads to serious neurological impairment or death. Aberrant functions of AVM-derived brain endothelial cells (AVM-BECs) are a disease hallmark. Our aim was to use microRNA-18a (miR-18a) as a therapeutic agent to improve AVM-BEC function. Human AVM-BECs were tested for growth factor production and proliferation under different shear flow conditions and evaluated for tubule formation. Thrombospondin-1, inhibitor of DNA-binding protein 1, and vascular endothelial growth factor (VEGF) isotype mRNA levels were quantified by quantitative real-time polymerase chain reaction. Thrombospondin-1, VEGF-A, and VEGF-D protein expression was measured using enzyme-linked immunosorbent assay. Proliferation and tubule formation were evaluated using bromodeoxyuridine incorporation and growth factor-reduced Matrigel assays, respectively. miR-18a increased thrombospondin-1 production but decreased inhibitor of DNA-binding protein 1, a transcriptional repressor of thrombospondin-1. miR-18a reduced VEGF-A and VEGF-D levels, both overexpressed in untreated AVM-BECs. This is the first study reporting VEGF-D overexpression in AVM. These effects were most prominent under arterial shear flow conditions. miR-18a also reduced AVM-BEC proliferation, improved tubule formation, and was effectively internalized by AVM-BECs in the absence of extraneous transfection reagents.
Question: Does microRNA-18a improve human cerebral arteriovenous malformation endothelial cell function?
Output:
|
PubmedQA206870
|
[
{
"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: Recent studies have shown that ghrelin exhibits gastroprotective effects. The aim of present study was to examine the influence of ghrelin administration on the healing of chronic gastric and duodenal ulcers and to evaluate the role of growth hormone (GH) and insulin-like growth factor-1 (IGF-1) in this process. In pituitary-intact or hypophysectomized rats, chronic gastric and duodenal ulcers were induced by acetic acid. After induction of ulcers, rats were treated intraperitoneally twice a day with saline, ghrelin (4, 8 or 16 nmol/kg/dose) or IGF-1 (20 nmol/kg/dose) for six or ten days. In animals with intact pituitary, treatment with ghrelin increased serum level of GH and IGF-1. These effects were accompanied by the increase in mucosal cell proliferation, mucosal blood flow and healing rate of gastric and duodenal ulcers. After hypophysectomy, the significant increase in serum level of endogenous ghrelin was observed, but the healing of gastric and duodenal ulcers was delayed. This effect was accompanied by a significant decrease in serum concentration of endogenous GH and IGF-1, and reduction in mucosal blood flow and DNA synthesis. In hypophysectomized rats, administration of exogenous ghrelin was without any effect on serum level of GH and IGF-1, healing rate of gastroduodenal ulcers or mucosal cell proliferation. In contrast to this effect, administration of IGF-1 increased mucosal cell proliferation, healing rate of gastroduodenal ulcers and mucosal blood flow in hypophysectomized rats.\n Question: Does treatment with ghrelin accelerate the healing of acetic acid-induced gastric and duodenal ulcers 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: Recent studies have shown that ghrelin exhibits gastroprotective effects. The aim of present study was to examine the influence of ghrelin administration on the healing of chronic gastric and duodenal ulcers and to evaluate the role of growth hormone (GH) and insulin-like growth factor-1 (IGF-1) in this process. In pituitary-intact or hypophysectomized rats, chronic gastric and duodenal ulcers were induced by acetic acid. After induction of ulcers, rats were treated intraperitoneally twice a day with saline, ghrelin (4, 8 or 16 nmol/kg/dose) or IGF-1 (20 nmol/kg/dose) for six or ten days. In animals with intact pituitary, treatment with ghrelin increased serum level of GH and IGF-1. These effects were accompanied by the increase in mucosal cell proliferation, mucosal blood flow and healing rate of gastric and duodenal ulcers. After hypophysectomy, the significant increase in serum level of endogenous ghrelin was observed, but the healing of gastric and duodenal ulcers was delayed. This effect was accompanied by a significant decrease in serum concentration of endogenous GH and IGF-1, and reduction in mucosal blood flow and DNA synthesis. In hypophysectomized rats, administration of exogenous ghrelin was without any effect on serum level of GH and IGF-1, healing rate of gastroduodenal ulcers or mucosal cell proliferation. In contrast to this effect, administration of IGF-1 increased mucosal cell proliferation, healing rate of gastroduodenal ulcers and mucosal blood flow in hypophysectomized rats.
Question: Does treatment with ghrelin accelerate the healing of acetic acid-induced gastric and duodenal ulcers in rats?
Output:
|
PubmedQA121576
|
[
{
"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: Monocyte ingress into the brain during progressive human immunodeficiency virus (HIV-1) infection parallels the severity of cognitive impairments. Although activated monocyte phenotypes emerge in disease, the functional correlates of these cells remain unresolved. To this end, we studied the proteome of blood-derived monocytes obtained from Hispanic women with the most severe form of HIV-associated neurocognitive disorders, HIV-associated dementia (HAD). Monocytes isolated from peripheral blood mononuclear cells by CD14+ immunoaffinity column chromatography were >95% pure. Cells were recovered from four patients without evidence of cognitive impairment and five with HAD and analyzed by 2-D DIGE and tandem MS. Importantly, ADP ribosylhydrolase, myeloperoxidase, thioredoxin, peroxiredoxin 3, NADPH, and GTPase-activating protein were all downregulated in HAD. In regards to myeloperoxidase, thioredoxin, and peroxiredoxin 3, these changes were validated in an additional cohort of 30 patients by flow cytometry.\n Question: Do proteomic analyses of monocytes obtained from Hispanic women with HIV-associated dementia show depressed antioxidants?\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: Monocyte ingress into the brain during progressive human immunodeficiency virus (HIV-1) infection parallels the severity of cognitive impairments. Although activated monocyte phenotypes emerge in disease, the functional correlates of these cells remain unresolved. To this end, we studied the proteome of blood-derived monocytes obtained from Hispanic women with the most severe form of HIV-associated neurocognitive disorders, HIV-associated dementia (HAD). Monocytes isolated from peripheral blood mononuclear cells by CD14+ immunoaffinity column chromatography were >95% pure. Cells were recovered from four patients without evidence of cognitive impairment and five with HAD and analyzed by 2-D DIGE and tandem MS. Importantly, ADP ribosylhydrolase, myeloperoxidase, thioredoxin, peroxiredoxin 3, NADPH, and GTPase-activating protein were all downregulated in HAD. In regards to myeloperoxidase, thioredoxin, and peroxiredoxin 3, these changes were validated in an additional cohort of 30 patients by flow cytometry.
Question: Do proteomic analyses of monocytes obtained from Hispanic women with HIV-associated dementia show depressed antioxidants?
Output:
|
PubmedQA174933
|
[
{
"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: Ceramides are precursors of complex sphingolipids (SLs), which are important for normal functioning of both the developing and mature brain. Altered SL levels have been associated with many neurodegenerative disorders, including epilepsy, although few direct links have been identified between genes involved in SL metabolism and epilepsy. We used quantitative real-time PCR, Western blotting, and enzymatic assays to determine the mRNA, protein, and activity levels of ceramide synthase 2 (CERS2) in fiibroblasts isolated from parental control subjects and from a patient diagnosed with progressive myoclonic epilepsy (PME). Mass spectrometry and fluorescence microscopy were used to examine the effects of reduced CERS2 activity on cellular lipid composition and plasma membrane functions. We identify a novel 27 kb heterozygous deletion including the CERS2 gene in a proband diagnosed with PME. Compared to parental controls, levels of CERS2 mRNA, protein, and activity were reduced by ˜50% in fibroblasts isolated from this proband, resulting in significantly reduced levels of ceramides and sphingomyelins containing the very long-chain fatty acids C24:0 and C26:0. The change in SL composition was also reflected in a reduction in cholera toxin B immunofluorescence, indicating that membrane composition and function are altered.\n Question: Does reduced ceramide synthase 2 activity cause progressive myoclonic epilepsy?\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: Ceramides are precursors of complex sphingolipids (SLs), which are important for normal functioning of both the developing and mature brain. Altered SL levels have been associated with many neurodegenerative disorders, including epilepsy, although few direct links have been identified between genes involved in SL metabolism and epilepsy. We used quantitative real-time PCR, Western blotting, and enzymatic assays to determine the mRNA, protein, and activity levels of ceramide synthase 2 (CERS2) in fiibroblasts isolated from parental control subjects and from a patient diagnosed with progressive myoclonic epilepsy (PME). Mass spectrometry and fluorescence microscopy were used to examine the effects of reduced CERS2 activity on cellular lipid composition and plasma membrane functions. We identify a novel 27 kb heterozygous deletion including the CERS2 gene in a proband diagnosed with PME. Compared to parental controls, levels of CERS2 mRNA, protein, and activity were reduced by ˜50% in fibroblasts isolated from this proband, resulting in significantly reduced levels of ceramides and sphingomyelins containing the very long-chain fatty acids C24:0 and C26:0. The change in SL composition was also reflected in a reduction in cholera toxin B immunofluorescence, indicating that membrane composition and function are altered.
Question: Does reduced ceramide synthase 2 activity cause progressive myoclonic epilepsy?
Output:
|
PubmedQA194472
|
[
{
"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: A combination of PPIs and corticosteroids is the pharmacotherapy mostly used to treat eosinophilic esophagitis (EoE), while dietetic manipulations consist also an efficient option. The aim of this study was to compare the efficacy of allergy-test-driven elimination diet in children with mild symptoms of EoE to a group of children with moderate/severe symptoms. Thirty-five children, aged 7 months to 12 yr, with EoE were enrolled in the study. They had a clinical history of GERD-like (21 children, Group A) or more severe symptoms (14 children, Group B). The diagnosis had been confirmed after two preliminary months of therapy with PPIs and an esophagogastroduodenoscopy. Soon after diagnosis, they were allergy-tested, using IgE detection (SPT and serum-specific IgE) and atopy patch tests (APTs). A 12-month tailor-made diet was prescribed according to the tests. Patients of Group B continued PPIs for two more months, while swallowed topical steroids were also prescribed to them for the first 5 months after diagnosis, followed by an 'as-needed' use of them for the rest of the study. Endoscopy was repeated at the end of the study. Milk and egg were the most common APT-positive allergens. Thirty-two patients were instructed to follow an elimination diet, which was completed by 15/18 of Group A and 12/14 of Group B. An improvement of symptoms was reported by 26/27 patients that completed the study. The use of swallowed corticosteroids was noticeably decreased during the as-needed period, in Group B. A remarkable reduce of eosinophils was noticed in biopsies; from 42.84 ± 18.08, they decreased to 6.41 ± 3.20, a year after.\n Question: Is allergy-test-driven elimination diet useful in children with eosinophilic esophagitis , regardless of the severity of symptoms?\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: A combination of PPIs and corticosteroids is the pharmacotherapy mostly used to treat eosinophilic esophagitis (EoE), while dietetic manipulations consist also an efficient option. The aim of this study was to compare the efficacy of allergy-test-driven elimination diet in children with mild symptoms of EoE to a group of children with moderate/severe symptoms. Thirty-five children, aged 7 months to 12 yr, with EoE were enrolled in the study. They had a clinical history of GERD-like (21 children, Group A) or more severe symptoms (14 children, Group B). The diagnosis had been confirmed after two preliminary months of therapy with PPIs and an esophagogastroduodenoscopy. Soon after diagnosis, they were allergy-tested, using IgE detection (SPT and serum-specific IgE) and atopy patch tests (APTs). A 12-month tailor-made diet was prescribed according to the tests. Patients of Group B continued PPIs for two more months, while swallowed topical steroids were also prescribed to them for the first 5 months after diagnosis, followed by an 'as-needed' use of them for the rest of the study. Endoscopy was repeated at the end of the study. Milk and egg were the most common APT-positive allergens. Thirty-two patients were instructed to follow an elimination diet, which was completed by 15/18 of Group A and 12/14 of Group B. An improvement of symptoms was reported by 26/27 patients that completed the study. The use of swallowed corticosteroids was noticeably decreased during the as-needed period, in Group B. A remarkable reduce of eosinophils was noticed in biopsies; from 42.84 ± 18.08, they decreased to 6.41 ± 3.20, a year after.
Question: Is allergy-test-driven elimination diet useful in children with eosinophilic esophagitis , regardless of the severity of symptoms?
Output:
|
PubmedQA161188
|
[
{
"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: Dermatologists have greater accuracy than nondermatologists for diagnosis of skin disease. However, it is not clear whether this affects medical outcome. We tested the hypothesis that nondermatologists would be more likely than dermatologists to prescribe combination products for the treatment of common fungal skin infections. We analyzed office-based physician visits for fungal skin infections recorded in the 1990-1994 National Ambulatory Medical Care Survey. There were 4.1 million visits for cutaneous fungal disease of which 82% were to nondermatologists. Nondermatologists were more likely to prescribe combination agents (34.1%) than dermatologists (4.8%, p=0.001). If the percentage of combination agents used by nondermatologists was reduced to that of dermatologists, an estimated $24.9 million or $10.3 million would be saved if clotrimazole or ketoconazole, respectively, were the substituted drug for the combination agent clotrimazole/betamethasone dipropionate.\n Question: Are nondermatologists more likely than dermatologists to prescribe antifungal/corticosteroid products : an analysis of office visits for cutaneous fungal infections , 1990-1994?\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: Dermatologists have greater accuracy than nondermatologists for diagnosis of skin disease. However, it is not clear whether this affects medical outcome. We tested the hypothesis that nondermatologists would be more likely than dermatologists to prescribe combination products for the treatment of common fungal skin infections. We analyzed office-based physician visits for fungal skin infections recorded in the 1990-1994 National Ambulatory Medical Care Survey. There were 4.1 million visits for cutaneous fungal disease of which 82% were to nondermatologists. Nondermatologists were more likely to prescribe combination agents (34.1%) than dermatologists (4.8%, p=0.001). If the percentage of combination agents used by nondermatologists was reduced to that of dermatologists, an estimated $24.9 million or $10.3 million would be saved if clotrimazole or ketoconazole, respectively, were the substituted drug for the combination agent clotrimazole/betamethasone dipropionate.
Question: Are nondermatologists more likely than dermatologists to prescribe antifungal/corticosteroid products : an analysis of office visits for cutaneous fungal infections , 1990-1994?
Output:
|
PubmedQA202724
|
[
{
"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: Cytokines are central regulators of the immune response but the workings of this complex network in systemic lupus erythematosus (SLE) are not fully understood. We investigated a range of inflammatory and immune-modulating cytokines to determine their value as biomarkers for disease subsets in SLE. This was a cross-sectional study in 102 patients with SLE (87% women, disease duration 10.6 yrs). Circulating concentrations of interleukin 1β (IL-1β), IL-4, IL-6, IL-10, IL-12, IL-17, monocyte chemotactic protein 1 (MCP-1), macrophage inflammatory protein 1 (MIP-1α), MIP-1β, interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), and total transforming growth factor-β1 (TGF-β1) were related to disease activity (SLE Disease Activity Index; SLEDAI), lymphocyte subsets, autoantibody levels, accrued damage (Systemic Lupus International Collaborating Clinics/ACR Damage Index; SDI), and concomitant treatment. Patients with SLE had lower levels of TGF-β1 (p = 0.01) and IL-1β (p = 0.0004) compared to controls. TGF-β1 levels were lower in patients with SLEDAI scores 1-10 and SDI > 3; and were correlated with CD4+, CD8+, and natural killer cell counts; and were independent of steroid or cytotoxic drug use. Treatment with cardiovascular drugs was associated with lower IL-12 levels. No consistent disease associations existed for the other cytokines investigated.\n Question: Are levels of transforming growth factor-beta low in systemic lupus erythematosus patients with active 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: Cytokines are central regulators of the immune response but the workings of this complex network in systemic lupus erythematosus (SLE) are not fully understood. We investigated a range of inflammatory and immune-modulating cytokines to determine their value as biomarkers for disease subsets in SLE. This was a cross-sectional study in 102 patients with SLE (87% women, disease duration 10.6 yrs). Circulating concentrations of interleukin 1β (IL-1β), IL-4, IL-6, IL-10, IL-12, IL-17, monocyte chemotactic protein 1 (MCP-1), macrophage inflammatory protein 1 (MIP-1α), MIP-1β, interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), and total transforming growth factor-β1 (TGF-β1) were related to disease activity (SLE Disease Activity Index; SLEDAI), lymphocyte subsets, autoantibody levels, accrued damage (Systemic Lupus International Collaborating Clinics/ACR Damage Index; SDI), and concomitant treatment. Patients with SLE had lower levels of TGF-β1 (p = 0.01) and IL-1β (p = 0.0004) compared to controls. TGF-β1 levels were lower in patients with SLEDAI scores 1-10 and SDI > 3; and were correlated with CD4+, CD8+, and natural killer cell counts; and were independent of steroid or cytotoxic drug use. Treatment with cardiovascular drugs was associated with lower IL-12 levels. No consistent disease associations existed for the other cytokines investigated.
Question: Are levels of transforming growth factor-beta low in systemic lupus erythematosus patients with active disease?
Output:
|
PubmedQA157037
|
[
{
"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: Decreased concentrations of circulating soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) were recently reported to be associated with atherosclerosis, but there are still no data concerning its predictive performance. The current cross-sectional study investigates the potential of the novel atherosclerotic biomarker for the prediction of coronary artery disease (CAD). Serum sTWEAK was measured by ELISA in 76 CAD patients and 82 CAD-free subjects. Serum sTWEAK concentrations were significantly lower in the patients (534.5+/-110.9 microg/L) than in the controls (688.1+/-150.0 microg/L, p<0.001), even after adjusting for different confounders (p<0.001). The areas under ROC curves (AUC)s calculated for logistic regression models that included different known risk factors were significantly increased when sTWEAK was added to the corresponding model (p=0.011-0.035).\n Question: Does circulating sTWEAK improve the prediction of coronary artery 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: Decreased concentrations of circulating soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) were recently reported to be associated with atherosclerosis, but there are still no data concerning its predictive performance. The current cross-sectional study investigates the potential of the novel atherosclerotic biomarker for the prediction of coronary artery disease (CAD). Serum sTWEAK was measured by ELISA in 76 CAD patients and 82 CAD-free subjects. Serum sTWEAK concentrations were significantly lower in the patients (534.5+/-110.9 microg/L) than in the controls (688.1+/-150.0 microg/L, p<0.001), even after adjusting for different confounders (p<0.001). The areas under ROC curves (AUC)s calculated for logistic regression models that included different known risk factors were significantly increased when sTWEAK was added to the corresponding model (p=0.011-0.035).
Question: Does circulating sTWEAK improve the prediction of coronary artery disease?
Output:
|
PubmedQA69055
|
[
{
"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: Using non-selective and selective protein kinase C (PKC) epsilon and delta isoform inhibitors, we tested the hypothesis that the cardioprotective phenotype invoked by postconditioning (postcon) is dependent on PKC signalling. Furthermore, we determined whether postconditioning alters pPKCepsilon and/or pPKCdelta in cytosolic and mitochondrial fractions. Male Sprague-Dawley rats underwent 30 min left coronary artery (LCA) occlusion followed by 3 h of reperfusion. Rats were randomised to the following groups: Untreated, no intervention either before or after LCA occlusion; Postcon, 3 cycles of 10-s full reperfusion and 10-s re-occlusion, initiated immediately at the onset of reperfusion; Chelerythrine (non-selective PKC inhibitor, 5 mg/kg)+/-postcon; Rottlerin (PKCdelta inhibitor, 0.3 mg/kg)+/-postcon; KIE1-1 (PKCepsilon inhibitor, 3.8 mg/kg)+/-postcon. A subset of rats was employed to assess pPKCepsilon and/or pPKCdelta in sham, Isch/RP (30-min LCA occlusion followed by 30-min reperfusion), and postcon-treated hearts. Infarct size, expressed as area of necrosis as a percentage of the area at risk, AN/AAR (%), was significantly reduced by postcon compared to control (untreated) rats (39+/-2% vs. 53+/-1% in control, P<0.001). Treatment with chelerythrine alone or the PKCepsilon antagonist KIE1-1 alone at reperfusion had no effect on infarct size compared to control. In contrast, the infarct-sparing effect of postcon was abrogated by non-selective PKC inhibition and PKCepsilon antagonism (50+/-2% and 50+/-1%, respectively, P<0.002). Inhibition of PKCdelta reduced infarct size to values comparable to that in postcon group (36+/-3% vs. 39+/-2%). However, postcon in the presence of PKCdelta inhibitor did not enhance the infarct-sparing effects (38+/-2%). In addition, pPKCepsilon in postcon hearts was significantly higher in the total cell homogenate (10338+/-1627 vs. 4165+/-608 in Isch/RP, arbitrary units), and pPKCdelta translocation to mitochondria was significantly less (>2-fold decrease) compared to Isch/RP.\n Question: Is infarct-sparing effect of myocardial postconditioning dependent on protein kinase C signalling?\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: Using non-selective and selective protein kinase C (PKC) epsilon and delta isoform inhibitors, we tested the hypothesis that the cardioprotective phenotype invoked by postconditioning (postcon) is dependent on PKC signalling. Furthermore, we determined whether postconditioning alters pPKCepsilon and/or pPKCdelta in cytosolic and mitochondrial fractions. Male Sprague-Dawley rats underwent 30 min left coronary artery (LCA) occlusion followed by 3 h of reperfusion. Rats were randomised to the following groups: Untreated, no intervention either before or after LCA occlusion; Postcon, 3 cycles of 10-s full reperfusion and 10-s re-occlusion, initiated immediately at the onset of reperfusion; Chelerythrine (non-selective PKC inhibitor, 5 mg/kg)+/-postcon; Rottlerin (PKCdelta inhibitor, 0.3 mg/kg)+/-postcon; KIE1-1 (PKCepsilon inhibitor, 3.8 mg/kg)+/-postcon. A subset of rats was employed to assess pPKCepsilon and/or pPKCdelta in sham, Isch/RP (30-min LCA occlusion followed by 30-min reperfusion), and postcon-treated hearts. Infarct size, expressed as area of necrosis as a percentage of the area at risk, AN/AAR (%), was significantly reduced by postcon compared to control (untreated) rats (39+/-2% vs. 53+/-1% in control, P<0.001). Treatment with chelerythrine alone or the PKCepsilon antagonist KIE1-1 alone at reperfusion had no effect on infarct size compared to control. In contrast, the infarct-sparing effect of postcon was abrogated by non-selective PKC inhibition and PKCepsilon antagonism (50+/-2% and 50+/-1%, respectively, P<0.002). Inhibition of PKCdelta reduced infarct size to values comparable to that in postcon group (36+/-3% vs. 39+/-2%). However, postcon in the presence of PKCdelta inhibitor did not enhance the infarct-sparing effects (38+/-2%). In addition, pPKCepsilon in postcon hearts was significantly higher in the total cell homogenate (10338+/-1627 vs. 4165+/-608 in Isch/RP, arbitrary units), and pPKCdelta translocation to mitochondria was significantly less (>2-fold decrease) compared to Isch/RP.
Question: Is infarct-sparing effect of myocardial postconditioning dependent on protein kinase C signalling?
Output:
|
PubmedQA36563
|
[
{
"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: Ischemia-reperfusion injury (IRI) is responsible for primary liver dysfunction and failure after transplantation. The mitochondrial pathway appears to be involved in liver ischemia-reperfusion injury. Mitochondrial ATP-sensitive K (mitoK(ATP)) channels play a central role in protecting the heart from injury in ischemic preconditioning. The selective mitoK(ATP) channel agonist diazoxide potently reduced mitochondrial injury by preventing cytochrome c loss from the intermembrane space. Therefore, this study sought to determine whether diazoxide can attenuate ischemia-reperfusion injury induced by orthotopic liver transplantation (OLT) in mice. Furthermore, it was found that up-regulation of the Bcl-2 gene is a mechanism of diazoxide cytoprotection. Donors were treated with diazoxide, Bcl-2 siRNA, or diazoxide + Bcl-2 siRNA and vehicle 10 min or 24 h before liver harvesting. Liver grafts were then orthotopically transplanted into their corresponding recipients. Liver injury, as judged by transaminase level and histologic examination, was significantly lower in the diazoxide group compared with vehicle controls. The percentage of apoptotic cells and the amount of cytochrome c in the cytosol 6 h after transplant were also markedly reduced in diazoxide-treated grafts compared with vehicle-treated controls. Diazoxide notably up-regulated expression of Bcl-2, while siRNA knockdown of Bcl-2 abolished the cytoprotective effects of diazoxide.\n Question: Does diazoxide suppress hepatic ischemia/reperfusion injury after mouse liver transplantation by a BCL-2-dependent mechanism?\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: Ischemia-reperfusion injury (IRI) is responsible for primary liver dysfunction and failure after transplantation. The mitochondrial pathway appears to be involved in liver ischemia-reperfusion injury. Mitochondrial ATP-sensitive K (mitoK(ATP)) channels play a central role in protecting the heart from injury in ischemic preconditioning. The selective mitoK(ATP) channel agonist diazoxide potently reduced mitochondrial injury by preventing cytochrome c loss from the intermembrane space. Therefore, this study sought to determine whether diazoxide can attenuate ischemia-reperfusion injury induced by orthotopic liver transplantation (OLT) in mice. Furthermore, it was found that up-regulation of the Bcl-2 gene is a mechanism of diazoxide cytoprotection. Donors were treated with diazoxide, Bcl-2 siRNA, or diazoxide + Bcl-2 siRNA and vehicle 10 min or 24 h before liver harvesting. Liver grafts were then orthotopically transplanted into their corresponding recipients. Liver injury, as judged by transaminase level and histologic examination, was significantly lower in the diazoxide group compared with vehicle controls. The percentage of apoptotic cells and the amount of cytochrome c in the cytosol 6 h after transplant were also markedly reduced in diazoxide-treated grafts compared with vehicle-treated controls. Diazoxide notably up-regulated expression of Bcl-2, while siRNA knockdown of Bcl-2 abolished the cytoprotective effects of diazoxide.
Question: Does diazoxide suppress hepatic ischemia/reperfusion injury after mouse liver transplantation by a BCL-2-dependent mechanism?
Output:
|
PubmedQA187195
|
[
{
"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: Septins are well known to form a boundary between mother and daughter cells in mitosis, but their role in other morphogenic states is poorly understood. Using microfluidics and live-cell microscopy, coupled with new computational methods for image analysis, we investigated septin function during pheromone-dependent chemotropic growth in yeast. We show that septins colocalize with the regulator of G protein signaling (RGS) Sst2, a GTPase-activating protein that dampens pheromone receptor signaling. We show further that the septin structure surrounds the polar cap, ensuring that cell growth is directed toward the source of pheromone. When RGS activity is abrogated, septins are partially disorganized. Under these circumstances, the polar cap travels toward septin structures and away from sites of exocytosis, resulting in a loss of gradient tracking.\n Question: Do rGS proteins and septins cooperate to promote chemotropism by regulating polar cap mobility?\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: Septins are well known to form a boundary between mother and daughter cells in mitosis, but their role in other morphogenic states is poorly understood. Using microfluidics and live-cell microscopy, coupled with new computational methods for image analysis, we investigated septin function during pheromone-dependent chemotropic growth in yeast. We show that septins colocalize with the regulator of G protein signaling (RGS) Sst2, a GTPase-activating protein that dampens pheromone receptor signaling. We show further that the septin structure surrounds the polar cap, ensuring that cell growth is directed toward the source of pheromone. When RGS activity is abrogated, septins are partially disorganized. Under these circumstances, the polar cap travels toward septin structures and away from sites of exocytosis, resulting in a loss of gradient tracking.
Question: Do rGS proteins and septins cooperate to promote chemotropism by regulating polar cap mobility?
Output:
|
PubmedQA60082
|
[
{
"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: It has been suggested that talc and doxycycline might be acting through different pathways in creating pleurodesis. We hypothesized that combining doxycycline and talc in half the usual doses would be synergistic in inducing pleurodesis. Thirty-two rabbits were equally allocated into four groups: group 1, half-dose combination (5 mg/kg of doxycycline and 200 mg/kg of talc slurry); group 2, quarter-dose combination (2.5 mg/kg of doxycycline and 100 mg/kg of talc slurry); group 3, half-dose doxycycline (5 mg/kg of doxycycline); and group 4, half-dose talc (100 mg/kg of talc slurry). The pleurodesis scores from historical groups that received a full dose of talc (400 mg/kg) or doxycycline (10 mg/kg) were also compared to those obtained in the current study. Pleural fluid lactate dehydrogenase and protein levels were measured 24 h after the injection. Pleurodesis was graded from 1 (none) to 8 (> 50% symphysis) by two observers blinded to treatment groups. All rabbits underwent an ultrasonic examination on each side of their chest for the evaluation of pleurodesis. The mean pleurodesis score in the half-dose combination group was significantly higher than that in the half-dose talc group, half-dose doxycycline group, and the historical full-dose talc group (p = 0.009, p = 0.01, and p < 0.05, respectively). The quarter-dose combination group also had a significantly higher mean pleurodesis score compared to the half-dose talc group (p = 0.013). The difference between the historical full-dose doxycycline and the half-dose combination or quarter-dose combination groups was not significant (p > 0.05). A significantly positive correlation existed between the pleurodesis score and the ultrasound scores (r = 0.876, p = 0.000000005).\n Question: Is combination therapy with intrapleural doxycycline and talc in reduced doses effective in producing pleurodesis in rabbits?\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: It has been suggested that talc and doxycycline might be acting through different pathways in creating pleurodesis. We hypothesized that combining doxycycline and talc in half the usual doses would be synergistic in inducing pleurodesis. Thirty-two rabbits were equally allocated into four groups: group 1, half-dose combination (5 mg/kg of doxycycline and 200 mg/kg of talc slurry); group 2, quarter-dose combination (2.5 mg/kg of doxycycline and 100 mg/kg of talc slurry); group 3, half-dose doxycycline (5 mg/kg of doxycycline); and group 4, half-dose talc (100 mg/kg of talc slurry). The pleurodesis scores from historical groups that received a full dose of talc (400 mg/kg) or doxycycline (10 mg/kg) were also compared to those obtained in the current study. Pleural fluid lactate dehydrogenase and protein levels were measured 24 h after the injection. Pleurodesis was graded from 1 (none) to 8 (> 50% symphysis) by two observers blinded to treatment groups. All rabbits underwent an ultrasonic examination on each side of their chest for the evaluation of pleurodesis. The mean pleurodesis score in the half-dose combination group was significantly higher than that in the half-dose talc group, half-dose doxycycline group, and the historical full-dose talc group (p = 0.009, p = 0.01, and p < 0.05, respectively). The quarter-dose combination group also had a significantly higher mean pleurodesis score compared to the half-dose talc group (p = 0.013). The difference between the historical full-dose doxycycline and the half-dose combination or quarter-dose combination groups was not significant (p > 0.05). A significantly positive correlation existed between the pleurodesis score and the ultrasound scores (r = 0.876, p = 0.000000005).
Question: Is combination therapy with intrapleural doxycycline and talc in reduced doses effective in producing pleurodesis in rabbits?
Output:
|
PubmedQA45902
|
[
{
"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: Measuring children's dietary behavior is central to evaluating interventions and identifying predictors and outcomes of dietary behaviors. Systematic biases may obscure or inflate associations with self-reported intakes. To identify cognitive, behavioral, and social correlates of bias in children's reporting of breakfast items on a self-completion questionnaire. Cross-sectional survey. Children completed standardized tests of episodic memory, working memory, and attention, and a questionnaire assessing attitudes toward breakfast. Teachers completed a classroom behavior measure. Associations between measures and children's underreporting of breakfast foods (ie, cereals, bread, milk, fruits, sweet items, and potato chips) on a self-completion questionnaire relative to validated 24-hour recall were examined. Subjects were aged 9 to 11 years (n=678). Data were collected from 111 schools throughout Wales in 2005. A larger percentage of less-healthful breakfast items (ie, sweet snacks and potato chips) than more healthful items (ie, fruit, cereals, bread, and milk) were omitted from questionnaire self-reports. Children from lower socioeconomic status schools omitted more items than those from wealthier schools (Kruskal-Wallis H=12.51, P<0.01), with omissions twice as high for less-healthful items than for more-healthful items within the lowest socioeconomic status schools. Those with positive attitudes (H=23.85, P<0.001), better classroom behavior (H=6.26, P<0.05), and better episodic memory (H=8.42, P<0.05) omitted fewer items than those with negative attitudes, poorer behavior, and poorer episodic memory. Children who ate more items omitted more than those who ate fewer (H=47.65, P<0.001). No differences were observed in terms of attention and working memory.\n Question: Are cognitive , behavioral , and social factors associated with bias in dietary questionnaire self-reports by schoolchildren aged 9 to 11 years?\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: Measuring children's dietary behavior is central to evaluating interventions and identifying predictors and outcomes of dietary behaviors. Systematic biases may obscure or inflate associations with self-reported intakes. To identify cognitive, behavioral, and social correlates of bias in children's reporting of breakfast items on a self-completion questionnaire. Cross-sectional survey. Children completed standardized tests of episodic memory, working memory, and attention, and a questionnaire assessing attitudes toward breakfast. Teachers completed a classroom behavior measure. Associations between measures and children's underreporting of breakfast foods (ie, cereals, bread, milk, fruits, sweet items, and potato chips) on a self-completion questionnaire relative to validated 24-hour recall were examined. Subjects were aged 9 to 11 years (n=678). Data were collected from 111 schools throughout Wales in 2005. A larger percentage of less-healthful breakfast items (ie, sweet snacks and potato chips) than more healthful items (ie, fruit, cereals, bread, and milk) were omitted from questionnaire self-reports. Children from lower socioeconomic status schools omitted more items than those from wealthier schools (Kruskal-Wallis H=12.51, P<0.01), with omissions twice as high for less-healthful items than for more-healthful items within the lowest socioeconomic status schools. Those with positive attitudes (H=23.85, P<0.001), better classroom behavior (H=6.26, P<0.05), and better episodic memory (H=8.42, P<0.05) omitted fewer items than those with negative attitudes, poorer behavior, and poorer episodic memory. Children who ate more items omitted more than those who ate fewer (H=47.65, P<0.001). No differences were observed in terms of attention and working memory.
Question: Are cognitive , behavioral , and social factors associated with bias in dietary questionnaire self-reports by schoolchildren aged 9 to 11 years?
Output:
|
PubmedQA29954
|
[
{
"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: It is normally thought that deep corolla tubes evolve when a plant's successful reproduction is contingent on having a corolla tube longer than the tongue of the flower's pollinators, and that pollinators evolve ever-longer tongues because individuals with longer tongues can obtain more nectar from flowers. A recent model shows that, in the presence of pollinators with long and short tongues that experience resource competition, coexisting plant species can diverge in corolla-tube depth, because this increases the proportion of pollen grains that lands on co-specific flowers. We have extended the model to study whether resource competition can trigger the co-evolution of tongue length and corolla-tube depth. Starting with two plant and two pollinator species, all of them having the same distribution of tongue length or corolla-tube depth, we show that variability in corolla-tube depth leads to divergence in tongue length, provided that increasing tongue length is not equally costly for both species. Once the two pollinator species differ in tongue length, divergence in corolla-tube depth between the two plant species ensues.\n Question: Does resource competition trigger the co-evolution of long tongues and deep corolla tubes?\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: It is normally thought that deep corolla tubes evolve when a plant's successful reproduction is contingent on having a corolla tube longer than the tongue of the flower's pollinators, and that pollinators evolve ever-longer tongues because individuals with longer tongues can obtain more nectar from flowers. A recent model shows that, in the presence of pollinators with long and short tongues that experience resource competition, coexisting plant species can diverge in corolla-tube depth, because this increases the proportion of pollen grains that lands on co-specific flowers. We have extended the model to study whether resource competition can trigger the co-evolution of tongue length and corolla-tube depth. Starting with two plant and two pollinator species, all of them having the same distribution of tongue length or corolla-tube depth, we show that variability in corolla-tube depth leads to divergence in tongue length, provided that increasing tongue length is not equally costly for both species. Once the two pollinator species differ in tongue length, divergence in corolla-tube depth between the two plant species ensues.
Question: Does resource competition trigger the co-evolution of long tongues and deep corolla tubes?
Output:
|
PubmedQA62359
|
[
{
"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: There has recently been increasing interest in pharmacological manipulations that could potentially enhance exposure-based cognitive behaviour therapy for anxiety disorders. One such medication is the partial NMDA agonist d-cycloserine. It has been suggested that d-cycloserine enhances cognitive behaviour therapy by making learning faster. While animal studies have supported this view of the drug accelerating learning, evidence in human studies has been mixed. We therefore designed an experiment to measure the effects of d-cycloserine on human motor learning. Fifty-four healthy human volunteers were randomly assigned to a single dose of 250mg d-cycloserine versus placebo in a double-blind design. They then performed a motor sequence learning task. D-cycloserine did not increase the speed of motor learning or the overall amount learnt. However, we noted that participants on d-cycloserine tended to respond more carefully (shifting towards slower, but more correct responses).\n Question: Does the NMDA receptor partial agonist d-cycloserine enhance motor learning?\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: There has recently been increasing interest in pharmacological manipulations that could potentially enhance exposure-based cognitive behaviour therapy for anxiety disorders. One such medication is the partial NMDA agonist d-cycloserine. It has been suggested that d-cycloserine enhances cognitive behaviour therapy by making learning faster. While animal studies have supported this view of the drug accelerating learning, evidence in human studies has been mixed. We therefore designed an experiment to measure the effects of d-cycloserine on human motor learning. Fifty-four healthy human volunteers were randomly assigned to a single dose of 250mg d-cycloserine versus placebo in a double-blind design. They then performed a motor sequence learning task. D-cycloserine did not increase the speed of motor learning or the overall amount learnt. However, we noted that participants on d-cycloserine tended to respond more carefully (shifting towards slower, but more correct responses).
Question: Does the NMDA receptor partial agonist d-cycloserine enhance motor learning?
Output:
|
PubmedQA118459
|
[
{
"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: Prenylation is essential for membrane localization and participation of proteins in various signaling pathways. The following study was conducted to examine the importance of protein farnesylation and geranylgeranylation for the regulation of lymphoma cell survival and proliferation. Lymphoma cells were treated with the beta-hydroxy-beta-methylglutaryl-CoA reductase inhibitor lovastatin, which inhibits protein farnesylation and geranylgeranylation by the depletion of intracellular pools of farnesylpyrophosphate and geranylgeranylpyrophosphate. In addition, farnesyl transferase and geranylgeranyl transferase activities were specifically inhibited by FTI-277 and GGTI-298, respectively. Only inhibition of geranylgeranylation by lovastatin led to reduction of cell viability in lymphoma cell lines and purified tumor cells from lymphoma patients in a time- and dose-dependent way. Reduction in the number of viable cells was mediated by both induction of apoptosis and inhibition of proliferation. In addition, GGTI-298 was more effective in induction of apoptosis and inhibition of proliferation than FTI-277. Apoptosis induced by inhibition of protein geranylgeranylation was associated with a reduction of Mcl-1 protein levels, collapse of the mitochondrial transmembrane potential, and caspase-3 activation. Inhibition of proliferation resulted from the induction of G(1) arrest. Furthermore, lovastatin at low concentrations sensitized lymphoma cells to dexamethasone, including cells resistant to this drug.\n Question: Is protein geranylgeranylation critical for the regulation of survival and proliferation of lymphoma tumor 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: Prenylation is essential for membrane localization and participation of proteins in various signaling pathways. The following study was conducted to examine the importance of protein farnesylation and geranylgeranylation for the regulation of lymphoma cell survival and proliferation. Lymphoma cells were treated with the beta-hydroxy-beta-methylglutaryl-CoA reductase inhibitor lovastatin, which inhibits protein farnesylation and geranylgeranylation by the depletion of intracellular pools of farnesylpyrophosphate and geranylgeranylpyrophosphate. In addition, farnesyl transferase and geranylgeranyl transferase activities were specifically inhibited by FTI-277 and GGTI-298, respectively. Only inhibition of geranylgeranylation by lovastatin led to reduction of cell viability in lymphoma cell lines and purified tumor cells from lymphoma patients in a time- and dose-dependent way. Reduction in the number of viable cells was mediated by both induction of apoptosis and inhibition of proliferation. In addition, GGTI-298 was more effective in induction of apoptosis and inhibition of proliferation than FTI-277. Apoptosis induced by inhibition of protein geranylgeranylation was associated with a reduction of Mcl-1 protein levels, collapse of the mitochondrial transmembrane potential, and caspase-3 activation. Inhibition of proliferation resulted from the induction of G(1) arrest. Furthermore, lovastatin at low concentrations sensitized lymphoma cells to dexamethasone, including cells resistant to this drug.
Question: Is protein geranylgeranylation critical for the regulation of survival and proliferation of lymphoma tumor cells?
Output:
|
PubmedQA168684
|
[
{
"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: Laparoscopic adrenalectomy (LA) has become the established procedure for adrenal masses less than 6 cm. The role of LA for large adrenal masses is well defined to a lesser extent. Thirty-six LAs were performed in 32 patients (including four patients with single stage bilateral adrenalectomies) over a period of 3 years, from May 2002 to 2005. Patients were divided into two groups based on the tumour size, i.e. masses less than 6 cm (group I) and masses 6 cm or more (group II).The results with respect to mean (95% confidence interval) operative time, blood loss, postoperative course and complications were compared. Group II included 11 LAs performed in 10 patients including one bilateral LA for bilateral phaeochromocytomas in multiple endocrine neoplasia 2A. The mean size (+/-standard deviation) of masses was 8 cm (+/-1.47). In comparison, 22 patients in group I underwent 25 adrenalectomies (including three bilateral single stage procedures for Cushing's syndrome). The mean size of masses was 4.1 cm (+/-1.27). There were eight and six phaeochromocytomas in groups I and II, respectively. By comparing groups I and II, only minimal increase in blood loss and operating time was noted with no significant difference in hospital stay and morbidity. Two cases required conversion to hand assistance towards the end of the procedure in view of their large size.\n Question: Is laparoscopic adrenalectomy feasible for large adrenal masses > 6 cm?\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: Laparoscopic adrenalectomy (LA) has become the established procedure for adrenal masses less than 6 cm. The role of LA for large adrenal masses is well defined to a lesser extent. Thirty-six LAs were performed in 32 patients (including four patients with single stage bilateral adrenalectomies) over a period of 3 years, from May 2002 to 2005. Patients were divided into two groups based on the tumour size, i.e. masses less than 6 cm (group I) and masses 6 cm or more (group II).The results with respect to mean (95% confidence interval) operative time, blood loss, postoperative course and complications were compared. Group II included 11 LAs performed in 10 patients including one bilateral LA for bilateral phaeochromocytomas in multiple endocrine neoplasia 2A. The mean size (+/-standard deviation) of masses was 8 cm (+/-1.47). In comparison, 22 patients in group I underwent 25 adrenalectomies (including three bilateral single stage procedures for Cushing's syndrome). The mean size of masses was 4.1 cm (+/-1.27). There were eight and six phaeochromocytomas in groups I and II, respectively. By comparing groups I and II, only minimal increase in blood loss and operating time was noted with no significant difference in hospital stay and morbidity. Two cases required conversion to hand assistance towards the end of the procedure in view of their large size.
Question: Is laparoscopic adrenalectomy feasible for large adrenal masses > 6 cm?
Output:
|
PubmedQA135656
|
[
{
"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 examine the relationship of total cholesterol and high-density lipoprotein cholesterol (HDL-C) with coronary heart disease (CHD) mortality and with occurrence of new CHD events in persons aged 71 years and older. Prospective cohort study with a median of 4.4 years of follow-up. East Boston, Mass; New Haven, Conn; and Iowa and Washington counties, Iowa. A total of 2527 women and 1377 men who completed an interview, had serum lipid determinations, and survived at least 1 year. New CHD events were evaluated in persons with no CHD history or hospitalization. Death due to CHD (ICD-9 codes 410 through 414 as underlying cause of death); new occurrence of CHD events (fatal CHD or hospitalization with CHD [ICD-9 codes 410 through 414]). After adjustment for established CHD risk factors, the relative risk (RR) of death due to CHD for those with low HDL-C (< 0.90 mmol/L [< 35 mg/dL]) compared with the reference group (HDL-C > or = 1.55 mmol/L [> or = 60 mg/dL]) was 2.5 (95% confidence interval [CI], 1.6 to 4.0). Elevated risk was present in subgroups aged 71 through 80 years (RR, 4.1; 95% CI, 1.9 to 8.8) and over 80 years (RR, 1.8; 95% CI, 0.99 to 3.4), and in men and women. Low HDL-C predicted an increased risk of occurrence of new CHD events (RR, 1.4; 95% CI, 1.1 to 2.0), with similar but nonsignificant results in subgroups of men and women. Total cholesterol was less consistently associated with CHD mortality than HDL-C. When we compared individuals with total cholesterol of at least 6.20 mmol/L (240 mg/dL) with the reference group with total cholesterol of 4.16 to 5.19 mmol/L (161 to 199 mg/dL), a significant risk of CHD mortality was seen for women (RR 1.8; 95% CI, 1.03 to 3.0) but not for men (RR, 1.0; 95% CI, 0.5 to 2.0). In the total population, for each 1-unit increase in the total cholesterol/HDL-C ratio there was a 17% increase in the risk of CHD death that was statistically significant.\n Question: Does hDL cholesterol predict coronary heart disease mortality in older persons?\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 examine the relationship of total cholesterol and high-density lipoprotein cholesterol (HDL-C) with coronary heart disease (CHD) mortality and with occurrence of new CHD events in persons aged 71 years and older. Prospective cohort study with a median of 4.4 years of follow-up. East Boston, Mass; New Haven, Conn; and Iowa and Washington counties, Iowa. A total of 2527 women and 1377 men who completed an interview, had serum lipid determinations, and survived at least 1 year. New CHD events were evaluated in persons with no CHD history or hospitalization. Death due to CHD (ICD-9 codes 410 through 414 as underlying cause of death); new occurrence of CHD events (fatal CHD or hospitalization with CHD [ICD-9 codes 410 through 414]). After adjustment for established CHD risk factors, the relative risk (RR) of death due to CHD for those with low HDL-C (< 0.90 mmol/L [< 35 mg/dL]) compared with the reference group (HDL-C > or = 1.55 mmol/L [> or = 60 mg/dL]) was 2.5 (95% confidence interval [CI], 1.6 to 4.0). Elevated risk was present in subgroups aged 71 through 80 years (RR, 4.1; 95% CI, 1.9 to 8.8) and over 80 years (RR, 1.8; 95% CI, 0.99 to 3.4), and in men and women. Low HDL-C predicted an increased risk of occurrence of new CHD events (RR, 1.4; 95% CI, 1.1 to 2.0), with similar but nonsignificant results in subgroups of men and women. Total cholesterol was less consistently associated with CHD mortality than HDL-C. When we compared individuals with total cholesterol of at least 6.20 mmol/L (240 mg/dL) with the reference group with total cholesterol of 4.16 to 5.19 mmol/L (161 to 199 mg/dL), a significant risk of CHD mortality was seen for women (RR 1.8; 95% CI, 1.03 to 3.0) but not for men (RR, 1.0; 95% CI, 0.5 to 2.0). In the total population, for each 1-unit increase in the total cholesterol/HDL-C ratio there was a 17% increase in the risk of CHD death that was statistically significant.
Question: Does hDL cholesterol predict coronary heart disease mortality in older persons?
Output:
|
PubmedQA8963
|
[
{
"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: Breast cancer is the leading cause of cancer deaths in women world-wide. In low and middle income countries, where there are no population-based mammographic screening programmes, late presentation is common, and because of inadequate access to optimal treatment, survival rates are poor. Mammographic screening is well-studied in high-income countries in western populations, and because it has been shown to reduce breast cancer mortality, it has become part of the healthcare systems in such countries. However the performance of mammographic screening in a developing country is largely unknown. This study aims to evaluate the performance of mammographic screening in Malaysia, a middle income country, and to compare the stage and surgical treatment of screen-detected and symptomatic breast cancer. A retrospective review of 2510 mammograms performed from Jan to Dec 2010 in a tertiary medical centre is carried out. The three groups identified are the routine (opportunistic) screening group, the targeted (high risk) screening group and the diagnostic group. The performance indicators of each group is calculated, and stage at presentation and treatment between the screening and diagnostic group is analyzed. The cancer detection rate in the opportunistic screening group, targeted screening group, and the symptomatic group is 0.5 %, 1.25 % and 26 % respectively. The proportion of ductal carcinoma in situ is 23.1 % in the two screening groups compared to only 2.5 % in the diagnostic group. Among the opportunistic screening group, the cancer detection rate was 0.2 % in women below 50 years old compared to 0.65 % in women 50 years and above. The performance indicators are within international standards. Early-staged breast cancer (Stage 0-2) were 84.6 % in the screening groups compared to 61.1 % in the diagnostic group.\n Question: Does opportunistic mammography screening provide effective detection rates in a limited resource healthcare system?\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: Breast cancer is the leading cause of cancer deaths in women world-wide. In low and middle income countries, where there are no population-based mammographic screening programmes, late presentation is common, and because of inadequate access to optimal treatment, survival rates are poor. Mammographic screening is well-studied in high-income countries in western populations, and because it has been shown to reduce breast cancer mortality, it has become part of the healthcare systems in such countries. However the performance of mammographic screening in a developing country is largely unknown. This study aims to evaluate the performance of mammographic screening in Malaysia, a middle income country, and to compare the stage and surgical treatment of screen-detected and symptomatic breast cancer. A retrospective review of 2510 mammograms performed from Jan to Dec 2010 in a tertiary medical centre is carried out. The three groups identified are the routine (opportunistic) screening group, the targeted (high risk) screening group and the diagnostic group. The performance indicators of each group is calculated, and stage at presentation and treatment between the screening and diagnostic group is analyzed. The cancer detection rate in the opportunistic screening group, targeted screening group, and the symptomatic group is 0.5 %, 1.25 % and 26 % respectively. The proportion of ductal carcinoma in situ is 23.1 % in the two screening groups compared to only 2.5 % in the diagnostic group. Among the opportunistic screening group, the cancer detection rate was 0.2 % in women below 50 years old compared to 0.65 % in women 50 years and above. The performance indicators are within international standards. Early-staged breast cancer (Stage 0-2) were 84.6 % in the screening groups compared to 61.1 % in the diagnostic group.
Question: Does opportunistic mammography screening provide effective detection rates in a limited resource healthcare system?
Output:
|
PubmedQA140645
|
[
{
"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: Gene transfer to experimental lung grafts has been shown to reduce ischemia-reperfusion injury and acute rejection. The optimal delivery route should produce high lung expression with no inflammation and minimal systemic expression. The goal of this study was to determine the optimal gene transfer route for use in experimental lung transplantation. F344 rats were injected with 2.9 x 10(10) plaque-forming units of adenovirus vector encoding beta-galactosidase through intratracheal, intravenous, intraperitoneal, or intramuscular delivery routes and killed 48 hours later. Gene expression was measured by means of enzyme-linked immunosorbent assay. Intratracheal delivery produces significantly greater gene expression in the lung (75,350 +/- 47,288 pg/100 microg of protein, P <.001 vs intravenous, intraperitoneal, and intramuscular routes) and minimal systemic expression (nonsignificant in serum, kidney, liver, spleen, and muscle vs that seen in control animals, P =.016 for heart). Immunohistochemistry staining showed beta-galactosidase expression in the bronchial epithelium of lungs transfected through the intratracheal route with mild inflammation.\n Question: Is intratracheal adenovirus-mediated gene transfer optimal in experimental lung transplantation?\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: Gene transfer to experimental lung grafts has been shown to reduce ischemia-reperfusion injury and acute rejection. The optimal delivery route should produce high lung expression with no inflammation and minimal systemic expression. The goal of this study was to determine the optimal gene transfer route for use in experimental lung transplantation. F344 rats were injected with 2.9 x 10(10) plaque-forming units of adenovirus vector encoding beta-galactosidase through intratracheal, intravenous, intraperitoneal, or intramuscular delivery routes and killed 48 hours later. Gene expression was measured by means of enzyme-linked immunosorbent assay. Intratracheal delivery produces significantly greater gene expression in the lung (75,350 +/- 47,288 pg/100 microg of protein, P <.001 vs intravenous, intraperitoneal, and intramuscular routes) and minimal systemic expression (nonsignificant in serum, kidney, liver, spleen, and muscle vs that seen in control animals, P =.016 for heart). Immunohistochemistry staining showed beta-galactosidase expression in the bronchial epithelium of lungs transfected through the intratracheal route with mild inflammation.
Question: Is intratracheal adenovirus-mediated gene transfer optimal in experimental lung transplantation?
Output:
|
PubmedQA145930
|
[
{
"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 investigate potential associations of the ICAM-1 gene polymorphisms and Fuchs uveitis in a cohort of Italian patients. Seventy-one consecutive Italian patients affected by Fuchs uveitis were observed at the Ocular Immunology Unit, Arcispedale S. Maria Nuova (Reggio Emilia, Italy) from 2002 to 2008. Two hundred twenty-six healthy Italian blood donors from the same geographic area were selected as the control group. All Fuchs uveitis patients and control subjects were genotyped by polymerase chain reaction (PCR) and allele-specific oligonucleotide techniques for ICAM-1 polymorphisms at codon 241 (exon 4). The frequency of the ICAM-1 G/R 241 polymorphism was significantly higher in Fuchs uveitis than in the control subjects (16.9% vs. 5.8%; P=0.006, Pcorr=0.012; odds ratio, 3.3; 95% confidence interval, 1.4-7.7). No significant association between clinical features and ICAM-1 polymorphisms was found.\n Question: Is g/R 241 polymorphism of intercellular adhesion molecule 1 ( ICAM-1 ) associated with Fuchs uveitis?\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 investigate potential associations of the ICAM-1 gene polymorphisms and Fuchs uveitis in a cohort of Italian patients. Seventy-one consecutive Italian patients affected by Fuchs uveitis were observed at the Ocular Immunology Unit, Arcispedale S. Maria Nuova (Reggio Emilia, Italy) from 2002 to 2008. Two hundred twenty-six healthy Italian blood donors from the same geographic area were selected as the control group. All Fuchs uveitis patients and control subjects were genotyped by polymerase chain reaction (PCR) and allele-specific oligonucleotide techniques for ICAM-1 polymorphisms at codon 241 (exon 4). The frequency of the ICAM-1 G/R 241 polymorphism was significantly higher in Fuchs uveitis than in the control subjects (16.9% vs. 5.8%; P=0.006, Pcorr=0.012; odds ratio, 3.3; 95% confidence interval, 1.4-7.7). No significant association between clinical features and ICAM-1 polymorphisms was found.
Question: Is g/R 241 polymorphism of intercellular adhesion molecule 1 ( ICAM-1 ) associated with Fuchs uveitis?
Output:
|
PubmedQA99251
|
[
{
"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: Falls are frequent among older people living in residential care facilities. The aim of this study was to investigate the prediction accuracy of the Downton fall risk index among older people living in residential care facilities at 3, 6 and 12 months, and with two different definitions of falls. Seventy-eight residents in one residential care facility, 56 women and 22 men, mean +/- SD age 81 +/- 6 years, participated in this study. Forty-seven percent of participants had dementia, 45% depression, and 32% previous stroke. Forty-one percent of participants used a walking device indoors, and the median score of the Barthel ADL Index was 16. At baseline, the Downton fall risk index was scored for each individual. A score of 3 or more was taken to indicate high risk of falls. Participants were followed up prospectively for 12 months, with regard to falls indoors. At 3, 6 and 12 months, and using a fall definition including all indoor falls, sensitivity ranged from 81 to 95% with the highest value at 3 months, and specificity ranged from 35 to 40%. The prognostic separation values ranged from 0.26 to 0.37. Within 3 months, the risk of falling was 36% in the high-risk group (index score > or = 3) and 5% in the low-risk group. The accuracy of predictions did not improve when applying a fall definition in which falls precipitated by acute illness, acute disease, or drug side-effects were excluded.\n Question: Does prediction of fall among older people in residential care facilities by the Downton index?\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: Falls are frequent among older people living in residential care facilities. The aim of this study was to investigate the prediction accuracy of the Downton fall risk index among older people living in residential care facilities at 3, 6 and 12 months, and with two different definitions of falls. Seventy-eight residents in one residential care facility, 56 women and 22 men, mean +/- SD age 81 +/- 6 years, participated in this study. Forty-seven percent of participants had dementia, 45% depression, and 32% previous stroke. Forty-one percent of participants used a walking device indoors, and the median score of the Barthel ADL Index was 16. At baseline, the Downton fall risk index was scored for each individual. A score of 3 or more was taken to indicate high risk of falls. Participants were followed up prospectively for 12 months, with regard to falls indoors. At 3, 6 and 12 months, and using a fall definition including all indoor falls, sensitivity ranged from 81 to 95% with the highest value at 3 months, and specificity ranged from 35 to 40%. The prognostic separation values ranged from 0.26 to 0.37. Within 3 months, the risk of falling was 36% in the high-risk group (index score > or = 3) and 5% in the low-risk group. The accuracy of predictions did not improve when applying a fall definition in which falls precipitated by acute illness, acute disease, or drug side-effects were excluded.
Question: Does prediction of fall among older people in residential care facilities by the Downton index?
Output:
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PubmedQA134729
|
[
{
"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: Neuropsychological functioning of individuals with attention-deficit/hyperactivity disorder (ADHD) or heavy prenatal alcohol exposure has been well documented independently. This study examined the interaction between both factors on cognitive performance in children. As part of a multisite study, 344 children (8-16 y, M = 12.28, SD = 2.52) completed a comprehensive neuropsychological battery. Four subject groups were tested: children with histories of heavy prenatal alcohol exposure (AE) and ADHD (AE+, n = 90), alcohol-exposed without ADHD, (AE-, n = 38), nonexposed with ADHD (ADHD, n = 80), and nonexposed without ADHD (CON, n = 136). Separate 2(AE) × 2(ADHD) MANCOVAs revealed significant main and interactive effects of ADHD and AE on overall WISC-IV, D-KEFS, and CANTAB performance. Individual ANOVAs revealed significant interactions on 2 WISC-IV indices [Verbal Comprehension (VCI), Perceptual Reasoning (PRI)], and four D-KEFS and CANTAB subtests [Design Fluency, Verbal Fluency, Trail Making, Spatial Working Memory]. Follow-up analyses demonstrated no difference between AE+ and AE- groups on these measures. The combined AE+/- group demonstrated more severe impairment than the ADHD group on VCI and PRI, but there were no other differences between clinical groups.\n Question: Are neuropsychological deficits associated with heavy prenatal alcohol exposure exacerbated by ADHD?\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: Neuropsychological functioning of individuals with attention-deficit/hyperactivity disorder (ADHD) or heavy prenatal alcohol exposure has been well documented independently. This study examined the interaction between both factors on cognitive performance in children. As part of a multisite study, 344 children (8-16 y, M = 12.28, SD = 2.52) completed a comprehensive neuropsychological battery. Four subject groups were tested: children with histories of heavy prenatal alcohol exposure (AE) and ADHD (AE+, n = 90), alcohol-exposed without ADHD, (AE-, n = 38), nonexposed with ADHD (ADHD, n = 80), and nonexposed without ADHD (CON, n = 136). Separate 2(AE) × 2(ADHD) MANCOVAs revealed significant main and interactive effects of ADHD and AE on overall WISC-IV, D-KEFS, and CANTAB performance. Individual ANOVAs revealed significant interactions on 2 WISC-IV indices [Verbal Comprehension (VCI), Perceptual Reasoning (PRI)], and four D-KEFS and CANTAB subtests [Design Fluency, Verbal Fluency, Trail Making, Spatial Working Memory]. Follow-up analyses demonstrated no difference between AE+ and AE- groups on these measures. The combined AE+/- group demonstrated more severe impairment than the ADHD group on VCI and PRI, but there were no other differences between clinical groups.
Question: Are neuropsychological deficits associated with heavy prenatal alcohol exposure exacerbated by ADHD?
Output:
|
PubmedQA120147
|
[
{
"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: Various studies have reported that the administration of adenosine (ADO) in cardioplegia reduces myocardial ischemic injury, but this timing may not utilize ADO's potential against myocardial reperfusion injury. This study tested the hypothesis that ADO-supplemented blood cardioplegia (BCP) or ADO administered during reperfusion reduces postischemic dysfunction after severe regional ischemia. After 75 minutes of left anterior descending coronary artery occlusion, total cardiopulmonary bypass was initiated; cold (4 degrees C) antegrade BCP (8:1 blood:crystalloid) was delivered every 20 minutes for the first 3 doses, and 27 degrees C BCP was delivered for the terminal infusion. Dogs (n=6 per group) received unsupplemented BCP, ADO (100 micromol/L/L) supplemented in all infusions of BCP (ADO-CP), or ADO (100 micromol x L(-1) x L(-1)) supplemented only in the terminal infusion of BCP followed by intravenous ADO (140 microg x kg(-1) x min(-1)) infusion for the first 30 minutes of reperfusion (ADO-R). Postischemic regional systolic shortening was significantly greater in the ADO-R group (5+/-2.0%) than in the BCP group (-3+/-1.0%), but not in the ADO-CP group (2+/-0.2%). Postischemic regional diastolic stiffness in the area at risk during end reperfusion was lower with ADO-R (1.8+/-0.3%) than with ADO-CP (2.7+/-0.3%) or BCP (4.4+/-0.5%). Infarct size was reduced in the ADO-CP (29+/-2%) and ADO-R (21+/-2%) groups compared with the BCP group (42+/-4%). Edema in the myocardial area at risk was decreased in the ADO-CP (82+/-0.2%) and ADO-R (80+/-0.4%) groups compared with the BCP group (86+/-0.7%). Adherence of fluorescently labeled neutrophils (PMNs) to postischemic coronary artery endothelium was attenuated by ADO-R (55+/-2 PMNs/mm(2)), but not by ADO-CP (114+/-5 PMNs/mm(2)), compared with BCP (118+/-3 PMNs/mm(2)).\n Question: Does adenosine-supplemented blood cardioplegia attenuate postischemic dysfunction after severe regional ischemia?\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: Various studies have reported that the administration of adenosine (ADO) in cardioplegia reduces myocardial ischemic injury, but this timing may not utilize ADO's potential against myocardial reperfusion injury. This study tested the hypothesis that ADO-supplemented blood cardioplegia (BCP) or ADO administered during reperfusion reduces postischemic dysfunction after severe regional ischemia. After 75 minutes of left anterior descending coronary artery occlusion, total cardiopulmonary bypass was initiated; cold (4 degrees C) antegrade BCP (8:1 blood:crystalloid) was delivered every 20 minutes for the first 3 doses, and 27 degrees C BCP was delivered for the terminal infusion. Dogs (n=6 per group) received unsupplemented BCP, ADO (100 micromol/L/L) supplemented in all infusions of BCP (ADO-CP), or ADO (100 micromol x L(-1) x L(-1)) supplemented only in the terminal infusion of BCP followed by intravenous ADO (140 microg x kg(-1) x min(-1)) infusion for the first 30 minutes of reperfusion (ADO-R). Postischemic regional systolic shortening was significantly greater in the ADO-R group (5+/-2.0%) than in the BCP group (-3+/-1.0%), but not in the ADO-CP group (2+/-0.2%). Postischemic regional diastolic stiffness in the area at risk during end reperfusion was lower with ADO-R (1.8+/-0.3%) than with ADO-CP (2.7+/-0.3%) or BCP (4.4+/-0.5%). Infarct size was reduced in the ADO-CP (29+/-2%) and ADO-R (21+/-2%) groups compared with the BCP group (42+/-4%). Edema in the myocardial area at risk was decreased in the ADO-CP (82+/-0.2%) and ADO-R (80+/-0.4%) groups compared with the BCP group (86+/-0.7%). Adherence of fluorescently labeled neutrophils (PMNs) to postischemic coronary artery endothelium was attenuated by ADO-R (55+/-2 PMNs/mm(2)), but not by ADO-CP (114+/-5 PMNs/mm(2)), compared with BCP (118+/-3 PMNs/mm(2)).
Question: Does adenosine-supplemented blood cardioplegia attenuate postischemic dysfunction after severe regional ischemia?
Output:
|
PubmedQA204826
|
[
{
"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 objective of this study was to determine whether Emergency Medical Services (EMS) records can identify bars that serve a disproportionate number of minors, and if government officials will use this data to direct underage drinker enforcement efforts. Emergency Medical Services call logs to all bars in the study area were cross-referenced with a local hospital's records. The records of patients with alcohol-related complaints were analyzed. Outlier bars were identified, and presented to government officials who completed a survey to assess if this information would prompt new enforcement efforts. Emergency Medical Services responded to 149 establishments during the study period. Eighty-four responses were distributed across six bars, and 78 were matched with the hospital's records. Fifty-one patients, 18 (35%) of whom were underage, were treated for alcohol intoxication, with 46% of the cases originating from four bars. Government officials found the information useful, and planned to initiate new operations based on the information.\n Question: Do a public health enforcement initiative to combat underage drinking using Emergency Medical Services call data?\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 objective of this study was to determine whether Emergency Medical Services (EMS) records can identify bars that serve a disproportionate number of minors, and if government officials will use this data to direct underage drinker enforcement efforts. Emergency Medical Services call logs to all bars in the study area were cross-referenced with a local hospital's records. The records of patients with alcohol-related complaints were analyzed. Outlier bars were identified, and presented to government officials who completed a survey to assess if this information would prompt new enforcement efforts. Emergency Medical Services responded to 149 establishments during the study period. Eighty-four responses were distributed across six bars, and 78 were matched with the hospital's records. Fifty-one patients, 18 (35%) of whom were underage, were treated for alcohol intoxication, with 46% of the cases originating from four bars. Government officials found the information useful, and planned to initiate new operations based on the information.
Question: Do a public health enforcement initiative to combat underage drinking using Emergency Medical Services call data?
Output:
|
PubmedQA64102
|
[
{
"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: Early recognition of acute kidney injury (AKI) is important. It frequently develops first in the community. KDIGO-based AKI e-alert criteria may help clinicians recognize AKI in hospitals, but their suitability for application in the community is unknown. In a large renal cohort (n = 50 835) in one UK health authority, we applied the NHS England AKI 'e-alert' criteria to identify and follow three AKI groups: hospital-acquired AKI (HA-AKI), community-acquired AKI admitted to hospital within 7 days (CAA-AKI) and community-acquired AKI not admitted within 7 days (CANA-AKI). We assessed how AKI criteria operated in each group, based on prior blood tests (number and time lag). We compared 30-day, 1- and 5-year mortality, 90-day renal recovery and chronic renal replacement therapy (RRT). In total, 4550 patients met AKI e-alert criteria, 61.1% (2779/4550) with HA-AKI, 22.9% (1042/4550) with CAA-AKI and 16.0% (729/4550) with CANA-AKI. The median number of days since last blood test differed between groups (1, 52 and 69 days, respectively). Thirty-day mortality was similar for HA-AKI and CAA-AKI, but significantly lower for CANA-AKI (24.2, 20.2 and 2.6%, respectively). Five-year mortality was high in all groups, but followed a similar pattern (67.1, 64.7 and 46.2%). Differences in 5-year mortality among those not admitted could be explained by adjusting for comorbidities and restricting to 30-day survivors (hazard ratio 0.91, 95% confidence interval 0.80-1.04, versus hospital AKI). Those with CANA-AKI (versus CAA-AKI) had greater non-recovery at 90 days (11.8 versus 3.5%, P < 0.001) and chronic RRT at 5 years (3.7 versus 1.2%, P < 0.001).\n Question: Do kDIGO-based acute kidney injury criteria operate differently in hospitals and the community-findings from a large population cohort?\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: Early recognition of acute kidney injury (AKI) is important. It frequently develops first in the community. KDIGO-based AKI e-alert criteria may help clinicians recognize AKI in hospitals, but their suitability for application in the community is unknown. In a large renal cohort (n = 50 835) in one UK health authority, we applied the NHS England AKI 'e-alert' criteria to identify and follow three AKI groups: hospital-acquired AKI (HA-AKI), community-acquired AKI admitted to hospital within 7 days (CAA-AKI) and community-acquired AKI not admitted within 7 days (CANA-AKI). We assessed how AKI criteria operated in each group, based on prior blood tests (number and time lag). We compared 30-day, 1- and 5-year mortality, 90-day renal recovery and chronic renal replacement therapy (RRT). In total, 4550 patients met AKI e-alert criteria, 61.1% (2779/4550) with HA-AKI, 22.9% (1042/4550) with CAA-AKI and 16.0% (729/4550) with CANA-AKI. The median number of days since last blood test differed between groups (1, 52 and 69 days, respectively). Thirty-day mortality was similar for HA-AKI and CAA-AKI, but significantly lower for CANA-AKI (24.2, 20.2 and 2.6%, respectively). Five-year mortality was high in all groups, but followed a similar pattern (67.1, 64.7 and 46.2%). Differences in 5-year mortality among those not admitted could be explained by adjusting for comorbidities and restricting to 30-day survivors (hazard ratio 0.91, 95% confidence interval 0.80-1.04, versus hospital AKI). Those with CANA-AKI (versus CAA-AKI) had greater non-recovery at 90 days (11.8 versus 3.5%, P < 0.001) and chronic RRT at 5 years (3.7 versus 1.2%, P < 0.001).
Question: Do kDIGO-based acute kidney injury criteria operate differently in hospitals and the community-findings from a large population cohort?
Output:
|
PubmedQA7816
|
[
{
"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 whether KRAS mutations occur in primary bladder adenocarcinoma. Twenty-six cases of primary urinary bladder adenocarcinoma were analysed. DNA was extracted from formalin-fixed, paraffin-embedded tissue and amplified with shifted termination assay technology, which recognizes wild-type or mutant target sequences and selectively extends detection primers with labelled nucleotides. A mutation in KRAS was found in three (11.5%) of 26 primary bladder adenocarcinomas. Two of these three cases exhibited a G13D mutation, whereas the remaining case contained a mutation in G12V. None of the ten cases of urothelial carcinoma with glandular differentiation displayed KRAS mutation. Colonic adenocarcinoma contained a KRAS mutation in 18 (33%) of 55 cases. There was no distinct difference with regard to grade, stage or outcome according to the limited clinicopathological data available. However, the two youngest patients, aged 32 and 39 years, in our study group, with a mean population age of 61 years, were found to have mutations in KRAS.\n Question: Is kRAS mutation present in a small subset of primary urinary bladder adenocarcinomas?\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 determine whether KRAS mutations occur in primary bladder adenocarcinoma. Twenty-six cases of primary urinary bladder adenocarcinoma were analysed. DNA was extracted from formalin-fixed, paraffin-embedded tissue and amplified with shifted termination assay technology, which recognizes wild-type or mutant target sequences and selectively extends detection primers with labelled nucleotides. A mutation in KRAS was found in three (11.5%) of 26 primary bladder adenocarcinomas. Two of these three cases exhibited a G13D mutation, whereas the remaining case contained a mutation in G12V. None of the ten cases of urothelial carcinoma with glandular differentiation displayed KRAS mutation. Colonic adenocarcinoma contained a KRAS mutation in 18 (33%) of 55 cases. There was no distinct difference with regard to grade, stage or outcome according to the limited clinicopathological data available. However, the two youngest patients, aged 32 and 39 years, in our study group, with a mean population age of 61 years, were found to have mutations in KRAS.
Question: Is kRAS mutation present in a small subset of primary urinary bladder adenocarcinomas?
Output:
|
PubmedQA165620
|
[
{
"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: Many inhaled anesthetics potentiate the effect of glycine on inhibitory strychnine-sensitive glycine receptors in vitro, supporting the view that this receptor could mediate the immobility produced by inhaled anesthetics during noxious stimulation (i.e., would underlie minimum alveolar anesthetic concentration [MAC]). There are quantitative differences between anesthetics in their capacity to potentiate glycine's effect in receptor expression systems: halothane (most potentiation), isoflurane (intermediate), and cyclopropane (minimal). If glycine receptors mediate MAC, then their blockade in the spinal cord should increase the MAC of halothane more than that of isoflurane and isoflurane MAC more than cyclopropane MAC; the increases in MAC should be proportional to the receptor potentiation produced in vitro. Rats with chronically implanted intrathecal catheters were anesthetized with halothane, isoflurane, or cyclopropane. During intrathecal infusion of artificial cerebrospinal fluid, MAC was determined. Then MAC was re-determined during an infusion of 3, 12, 24, or 48 (isoflurane only) micro g/min of strychnine (strychnine blocks glycine receptors) in artificial cerebrospinal fluid. Strychnine infusion increased MAC in proportion to the enhancement of glycine receptors found in vitro. The maximum effect was with an infusion of 12 micro g/min. For the combined results at 12 and 24 micro g/min of strychnine, the increase in MAC correlated with the extent of in vitro potentiation (r(2) = 0.82). These results support the hypothesis that glycine receptors mediate part of the immobilization produced by inhaled anesthetics.\n Question: Do glycine receptors mediate part of the immobility produced by inhaled anesthetics?\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: Many inhaled anesthetics potentiate the effect of glycine on inhibitory strychnine-sensitive glycine receptors in vitro, supporting the view that this receptor could mediate the immobility produced by inhaled anesthetics during noxious stimulation (i.e., would underlie minimum alveolar anesthetic concentration [MAC]). There are quantitative differences between anesthetics in their capacity to potentiate glycine's effect in receptor expression systems: halothane (most potentiation), isoflurane (intermediate), and cyclopropane (minimal). If glycine receptors mediate MAC, then their blockade in the spinal cord should increase the MAC of halothane more than that of isoflurane and isoflurane MAC more than cyclopropane MAC; the increases in MAC should be proportional to the receptor potentiation produced in vitro. Rats with chronically implanted intrathecal catheters were anesthetized with halothane, isoflurane, or cyclopropane. During intrathecal infusion of artificial cerebrospinal fluid, MAC was determined. Then MAC was re-determined during an infusion of 3, 12, 24, or 48 (isoflurane only) micro g/min of strychnine (strychnine blocks glycine receptors) in artificial cerebrospinal fluid. Strychnine infusion increased MAC in proportion to the enhancement of glycine receptors found in vitro. The maximum effect was with an infusion of 12 micro g/min. For the combined results at 12 and 24 micro g/min of strychnine, the increase in MAC correlated with the extent of in vitro potentiation (r(2) = 0.82). These results support the hypothesis that glycine receptors mediate part of the immobilization produced by inhaled anesthetics.
Question: Do glycine receptors mediate part of the immobility produced by inhaled anesthetics?
Output:
|
PubmedQA135983
|
[
{
"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: Platelet additive solutions (PASs) facilitate improved recovery of plasma and may reduce the severity and/or frequency of plasma-associated transfusion reactions. Current apheresis platelet (PLT) PAS products contain approximately 30 to 40% residual plasma. In an effort to further decrease the residual plasma, two in vitro studies were conducted with PLTs suspended in 5% plasma and a reformulated PAS-3, named PAS-5, that contains additional salts, glucose, and bicarbonate. In Study 1, PLTs suspended in 5% plasma/95% PAS-5 were prepared directly on a separator (Amicus, Fenwal, Inc.) without additional centrifugation or washing. In Study 2, a double unit of hyperconcentrated Amicus PLTs in plasma was collected, divided, and centrifuged to prepare a control unit in 100% plasma and a paired test unit in 5% plasma/95% PAS-5. The in vitro properties of PLTs were assessed in both studies during 7-day storage at 20 to 24°C with continuous agitation. In Study 1, PLT concentration, pH, mean PLT volume (MPV), HCO(3)(-), pCO(2), pO(2), lactate dehydrogenase, and hypotonic shock response (HSR) did not significantly change during storage. By Day 7, glucose levels and morphology scores modestly decreased (17.6 and 14.4%, respectively) and lactate levels modestly increased (to 7.2 mmol/L). In Study 2, MPV, pH, glucose, pO(2), HSR, and morphology were comparable in control and test PLTs during 7-day storage. Glucose consumption and lactate production were significantly less in test versus control PLTs (p≤0.0015). Extent of shape change and %CD62P-positive test PLTs were less than those of controls (p<0.001).\n Question: Are in vitro variables of apheresis platelets stably maintained for 7 days with 5 % residual plasma in a glucose and bicarbonate salt solution , PAS-5?\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: Platelet additive solutions (PASs) facilitate improved recovery of plasma and may reduce the severity and/or frequency of plasma-associated transfusion reactions. Current apheresis platelet (PLT) PAS products contain approximately 30 to 40% residual plasma. In an effort to further decrease the residual plasma, two in vitro studies were conducted with PLTs suspended in 5% plasma and a reformulated PAS-3, named PAS-5, that contains additional salts, glucose, and bicarbonate. In Study 1, PLTs suspended in 5% plasma/95% PAS-5 were prepared directly on a separator (Amicus, Fenwal, Inc.) without additional centrifugation or washing. In Study 2, a double unit of hyperconcentrated Amicus PLTs in plasma was collected, divided, and centrifuged to prepare a control unit in 100% plasma and a paired test unit in 5% plasma/95% PAS-5. The in vitro properties of PLTs were assessed in both studies during 7-day storage at 20 to 24°C with continuous agitation. In Study 1, PLT concentration, pH, mean PLT volume (MPV), HCO(3)(-), pCO(2), pO(2), lactate dehydrogenase, and hypotonic shock response (HSR) did not significantly change during storage. By Day 7, glucose levels and morphology scores modestly decreased (17.6 and 14.4%, respectively) and lactate levels modestly increased (to 7.2 mmol/L). In Study 2, MPV, pH, glucose, pO(2), HSR, and morphology were comparable in control and test PLTs during 7-day storage. Glucose consumption and lactate production were significantly less in test versus control PLTs (p≤0.0015). Extent of shape change and %CD62P-positive test PLTs were less than those of controls (p<0.001).
Question: Are in vitro variables of apheresis platelets stably maintained for 7 days with 5 % residual plasma in a glucose and bicarbonate salt solution , PAS-5?
Output:
|
PubmedQA84775
|
[
{
"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: Danqi Pill (DQP), which contains Chinese herbs Salvia miltiorrhiza Bunge and Panax notoginseng, is widely used in the treatment of myocardial ischemia (MI) in China. Its regulatory effects on MI-associated lipid metabolism disorders haven't been comprehensively studied so far. We aimed to systematically investigate the regulatory mechanism of DQP on myocardial ischemia-induced lipid metabolism disorders. Myocardial ischemia rat model was induced by left anterior descending coronary artery ligation. The rat models were divided into three groups: model group with administration of normal saline, study group with administration of DanQi aqueous solution (1.5 mg/kg) and positive-control group with administration of pravastatin aqueous solution (1.2 mg/kg). In addition, another sham-operated group was set as negative control. At 28 days after treatment, cardiac function and degree of lipid metabolism disorders in rats of different groups were measured. Plasma lipid disorders were induced by myocardial ischemia, with manifestation of up-regulation of triglyceride (TG), low density lipoprotein (LDL), Apolipoprotein B (Apo-B) and 3-hydroxy-3-methyl glutaryl coenzyme A reductase (HMGCR). DQP could down-regulate the levels of TG, LDL, Apo-B and HMGCR. The Lipid transport pathway, fatty acids transport protein (FATP) and Carnitine palmitoyltransferase I (CPTI) were down-regulated in model group. DQP could improve plasma lipid metabolism by up-regulating this lipid transport pathway. The transcription factors peroxisome proliferator-activated receptor α (PPARα) and retinoid X receptors (RXRs), which regulate lipid metabolism, were also up-regulated by DQP. Furthermore, DQP was able to improve heart function and up-regulate ejection fraction (EF) by increasing the cardiac diastolic volume.\n Question: Does danqi Pill regulate lipid metabolism disorder induced by myocardial ischemia through FATP-CPTI pathway?\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: Danqi Pill (DQP), which contains Chinese herbs Salvia miltiorrhiza Bunge and Panax notoginseng, is widely used in the treatment of myocardial ischemia (MI) in China. Its regulatory effects on MI-associated lipid metabolism disorders haven't been comprehensively studied so far. We aimed to systematically investigate the regulatory mechanism of DQP on myocardial ischemia-induced lipid metabolism disorders. Myocardial ischemia rat model was induced by left anterior descending coronary artery ligation. The rat models were divided into three groups: model group with administration of normal saline, study group with administration of DanQi aqueous solution (1.5 mg/kg) and positive-control group with administration of pravastatin aqueous solution (1.2 mg/kg). In addition, another sham-operated group was set as negative control. At 28 days after treatment, cardiac function and degree of lipid metabolism disorders in rats of different groups were measured. Plasma lipid disorders were induced by myocardial ischemia, with manifestation of up-regulation of triglyceride (TG), low density lipoprotein (LDL), Apolipoprotein B (Apo-B) and 3-hydroxy-3-methyl glutaryl coenzyme A reductase (HMGCR). DQP could down-regulate the levels of TG, LDL, Apo-B and HMGCR. The Lipid transport pathway, fatty acids transport protein (FATP) and Carnitine palmitoyltransferase I (CPTI) were down-regulated in model group. DQP could improve plasma lipid metabolism by up-regulating this lipid transport pathway. The transcription factors peroxisome proliferator-activated receptor α (PPARα) and retinoid X receptors (RXRs), which regulate lipid metabolism, were also up-regulated by DQP. Furthermore, DQP was able to improve heart function and up-regulate ejection fraction (EF) by increasing the cardiac diastolic volume.
Question: Does danqi Pill regulate lipid metabolism disorder induced by myocardial ischemia through FATP-CPTI pathway?
Output:
|
PubmedQA92082
|
[
{
"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 chemokines CCL19 and CCL21 bind CCR7, which is involved in the organization of secondary lymphoid tissue and is expressed during chronic tissue inflammation. We investigated the expression of CCL21 and CCR7 in chronic hepatitis C. The effects of CCL21 on hepatic stellate cells (HSCs) were also studied. Expression of CCL21 was assessed by in situ hybridization and immunohistochemistry. CCR7 on T cells was analyzed by flow cytometry. Cultured human HSCs were studied in their activated phenotype. In patients with chronic hepatitis C, expression of CCL21 and CCR7 was up-regulated. CCL21 was detected in the portal tracts and around inflammatory lymphoid follicles, in proximity to T lymphocytes and dendritic cells, which contributed to expression of this chemokine. Expression of CCR7 was also increased in patients with primary biliary cirrhosis. Intrahepatic CD8(+) T lymphocytes isolated from patients with chronic hepatitis C had a significantly higher percentage of positivity for CCR7 than those from healthy controls, and the expression of CCR7 was associated with that of CXCR3. Cultured HSCs expressed functional CCR7, the activation of which stimulated cell migration and accelerated wound healing in an in vitro model. Exposure of HSCs to CCL21 triggered several signaling pathways, including extracellular signal-regulated kinase, Akt, and nuclear factor kappaB, resulting in induction of proinflammatory genes.\n Question: Does the chemokine CCL21 modulate lymphocyte recruitment and fibrosis in chronic hepatitis C?\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 chemokines CCL19 and CCL21 bind CCR7, which is involved in the organization of secondary lymphoid tissue and is expressed during chronic tissue inflammation. We investigated the expression of CCL21 and CCR7 in chronic hepatitis C. The effects of CCL21 on hepatic stellate cells (HSCs) were also studied. Expression of CCL21 was assessed by in situ hybridization and immunohistochemistry. CCR7 on T cells was analyzed by flow cytometry. Cultured human HSCs were studied in their activated phenotype. In patients with chronic hepatitis C, expression of CCL21 and CCR7 was up-regulated. CCL21 was detected in the portal tracts and around inflammatory lymphoid follicles, in proximity to T lymphocytes and dendritic cells, which contributed to expression of this chemokine. Expression of CCR7 was also increased in patients with primary biliary cirrhosis. Intrahepatic CD8(+) T lymphocytes isolated from patients with chronic hepatitis C had a significantly higher percentage of positivity for CCR7 than those from healthy controls, and the expression of CCR7 was associated with that of CXCR3. Cultured HSCs expressed functional CCR7, the activation of which stimulated cell migration and accelerated wound healing in an in vitro model. Exposure of HSCs to CCL21 triggered several signaling pathways, including extracellular signal-regulated kinase, Akt, and nuclear factor kappaB, resulting in induction of proinflammatory genes.
Question: Does the chemokine CCL21 modulate lymphocyte recruitment and fibrosis in chronic hepatitis C?
Output:
|
PubmedQA209511
|
[
{
"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: Assess the impact of the reduction or loss of autonomy of the elderly in the nosocomial infection risk. Using Karnosfsky scale (KPS). This study involved 163 patients aged 65 and over hospitalized for medical reasons. KPS index, body mass index, Index Norton, bladder's drainage system at the entrance and during hospitalization, colonization of resistant bacteria (BMR) at entry and during hospitalization, antibiotic use at entry and during hospitalization, infection at entry and during hospitalization. There is a statistically significant relationship between the degree of autonomy and the index of risk of pressure ulcers (Norton), between the degree of autonomy and the use of bladder's drainage system, between the degree of autonomy and risk acquisition of BMR, between the degree of autonomy and the nosocomial infection risk.\n Question: Does [ The dependence level of the elderly person influence the risk of infection ]?\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: Assess the impact of the reduction or loss of autonomy of the elderly in the nosocomial infection risk. Using Karnosfsky scale (KPS). This study involved 163 patients aged 65 and over hospitalized for medical reasons. KPS index, body mass index, Index Norton, bladder's drainage system at the entrance and during hospitalization, colonization of resistant bacteria (BMR) at entry and during hospitalization, antibiotic use at entry and during hospitalization, infection at entry and during hospitalization. There is a statistically significant relationship between the degree of autonomy and the index of risk of pressure ulcers (Norton), between the degree of autonomy and the use of bladder's drainage system, between the degree of autonomy and risk acquisition of BMR, between the degree of autonomy and the nosocomial infection risk.
Question: Does [ The dependence level of the elderly person influence the risk of infection ]?
Output:
|
PubmedQA67238
|
[
{
"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: This study investigated whether higher body mass index (BMI) is associated with more adverse lower extremity muscle characteristics at baseline and more adverse changes in muscle over time among participants with lower extremity peripheral arterial disease (PAD). This was a longitudinal, observational study of 425 men and women with PAD and 261 without PAD. Computed tomography was used to measure calf muscle characteristics at baseline and every 2 years. Knee extension isometric strength, power, and 6-minute walk distance were measured at baseline and annually. Baseline BMI (kg/m(2)) categories were ideal (20-25), overweight (>25-30), and obese (>30). Analyses adjust for age, race, sex, ankle brachial index, comorbidities, and other covariates. At baseline, higher BMI among participants with PAD was associated with greater calf muscle area (ideal BMI: 5181 mm(2); overweight: 5513 mm(2); obese: 5695 mm(2); P = .0009 for trend), higher calf muscle percentage of fat (6.38%, 10.28%, 17.44%, respectively, P < .0001 for trend), lower calf muscle density (P < .0001 for trend), and higher isometric knee extension strength (P = .015 for trend). Among participants with PAD, higher BMI was associated with greater declines in calf muscle area (P = .030 for trend) and greater increases in calf muscle percentage of fat (P = .023 for trend). Among participants without PAD, there were no significant associations of baseline BMI with changes in lower extremity muscle outcomes over time.\n Question: Is higher body mass index associated with more adverse changes in calf muscle characteristics in peripheral arterial 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: This study investigated whether higher body mass index (BMI) is associated with more adverse lower extremity muscle characteristics at baseline and more adverse changes in muscle over time among participants with lower extremity peripheral arterial disease (PAD). This was a longitudinal, observational study of 425 men and women with PAD and 261 without PAD. Computed tomography was used to measure calf muscle characteristics at baseline and every 2 years. Knee extension isometric strength, power, and 6-minute walk distance were measured at baseline and annually. Baseline BMI (kg/m(2)) categories were ideal (20-25), overweight (>25-30), and obese (>30). Analyses adjust for age, race, sex, ankle brachial index, comorbidities, and other covariates. At baseline, higher BMI among participants with PAD was associated with greater calf muscle area (ideal BMI: 5181 mm(2); overweight: 5513 mm(2); obese: 5695 mm(2); P = .0009 for trend), higher calf muscle percentage of fat (6.38%, 10.28%, 17.44%, respectively, P < .0001 for trend), lower calf muscle density (P < .0001 for trend), and higher isometric knee extension strength (P = .015 for trend). Among participants with PAD, higher BMI was associated with greater declines in calf muscle area (P = .030 for trend) and greater increases in calf muscle percentage of fat (P = .023 for trend). Among participants without PAD, there were no significant associations of baseline BMI with changes in lower extremity muscle outcomes over time.
Question: Is higher body mass index associated with more adverse changes in calf muscle characteristics in peripheral arterial disease?
Output:
|
PubmedQA156203
|
[
{
"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: There is evidence that populations living close to the coast have improved health and wellbeing. Coastal environments are linked to promotion of physical activity through provision of safe, opportune, aesthetic and accessible spaces for recreation. Exposure to coastal environments may also reduce stress and induce positive mood. We hypothesised that coastal climate may influence the vitamin D status of residents and thus partly explain benefits to health. Ecological and cross-sectional analyses were designed to elucidate the connection between coastal residence and vitamin D status. We divided residential data, from developed land use areas and the Lower Super Output Areas or Data Zones (Scotland) of the 1958 Birth Cohort participants, into the following coastal bands: <1 km, 1-5 km, 5-20 km, 20-50 km and over 50 km. In the ecological analysis we used a multiple regression model to describe the relationship between UV vitd and coastal proximity adjusted for latitude. Subsequently, using the residential information of the participants of the 1958 Birth Cohort we developed a multiple regression model to understand the relationship between serum 25(OH)D (a marker of vitamin D status) and coastal proximity adjusted for several factors related to vitamin D status (e.g. diet, outdoor activity). We found that coastal proximity was associated with solar irradiance; on average a 99.6 (96.1-103.3)J/m(2)/day regression coefficient was recorded for settlements <1 km from the coast compared with those at >50 km. This relationship was modified by latitude with settlements at a lower latitude exhibiting a greater effect. Individuals living closer to the coast in England had higher vitamin D levels than those inland, particularly in autumn.\n Question: Is coastal climate associated with elevated solar irradiance and higher 25 ( OH ) D level?\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: There is evidence that populations living close to the coast have improved health and wellbeing. Coastal environments are linked to promotion of physical activity through provision of safe, opportune, aesthetic and accessible spaces for recreation. Exposure to coastal environments may also reduce stress and induce positive mood. We hypothesised that coastal climate may influence the vitamin D status of residents and thus partly explain benefits to health. Ecological and cross-sectional analyses were designed to elucidate the connection between coastal residence and vitamin D status. We divided residential data, from developed land use areas and the Lower Super Output Areas or Data Zones (Scotland) of the 1958 Birth Cohort participants, into the following coastal bands: <1 km, 1-5 km, 5-20 km, 20-50 km and over 50 km. In the ecological analysis we used a multiple regression model to describe the relationship between UV vitd and coastal proximity adjusted for latitude. Subsequently, using the residential information of the participants of the 1958 Birth Cohort we developed a multiple regression model to understand the relationship between serum 25(OH)D (a marker of vitamin D status) and coastal proximity adjusted for several factors related to vitamin D status (e.g. diet, outdoor activity). We found that coastal proximity was associated with solar irradiance; on average a 99.6 (96.1-103.3)J/m(2)/day regression coefficient was recorded for settlements <1 km from the coast compared with those at >50 km. This relationship was modified by latitude with settlements at a lower latitude exhibiting a greater effect. Individuals living closer to the coast in England had higher vitamin D levels than those inland, particularly in autumn.
Question: Is coastal climate associated with elevated solar irradiance and higher 25 ( OH ) D level?
Output:
|
PubmedQA45405
|
[
{
"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: In neonatal rodents, serotonin (5-HT) neurons are critical for successful autoresuscitation. We hypothesized that caffeine, a respiratory stimulant, would hasten the onset of gasping and improve autoresuscitation in 5-HT-deficient, Pet-1(-/-) mice. Using a head-out system and electrocardiogram, we measured respiratory and heart rate (HR) responses of Pet-1(-/-) rodents and their littermates during episodic asphyxia at postnatal days 8-9 (P8-9). After a baseline recording, we injected either vehicle or caffeine (i.p.) at doses of 1, 5, or 10 mg/kg. We then induced 10 brief (~30 s) episodes of asphyxia, each interspersed with 5 min of room air to allow autoresuscitation. In addition to measuring survival, we measured the duration of hypoxic apnea (time to initiate gasping) and time to recover eupnea and HR. Caffeine had a dose-dependent effect of hastening the onset of gasping, recovery of breathing, and restoration of HR in Pet-1(-/-) (but not in wild-type) rodents, thereby improving survival across asphyxic episodes. Increased survival was strongly correlated with hastened onset of gasping.\n Question: Does caffeine improve the ability of serotonin-deficient ( Pet-1-/- ) mice to survive episodic asphyxia?\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: In neonatal rodents, serotonin (5-HT) neurons are critical for successful autoresuscitation. We hypothesized that caffeine, a respiratory stimulant, would hasten the onset of gasping and improve autoresuscitation in 5-HT-deficient, Pet-1(-/-) mice. Using a head-out system and electrocardiogram, we measured respiratory and heart rate (HR) responses of Pet-1(-/-) rodents and their littermates during episodic asphyxia at postnatal days 8-9 (P8-9). After a baseline recording, we injected either vehicle or caffeine (i.p.) at doses of 1, 5, or 10 mg/kg. We then induced 10 brief (~30 s) episodes of asphyxia, each interspersed with 5 min of room air to allow autoresuscitation. In addition to measuring survival, we measured the duration of hypoxic apnea (time to initiate gasping) and time to recover eupnea and HR. Caffeine had a dose-dependent effect of hastening the onset of gasping, recovery of breathing, and restoration of HR in Pet-1(-/-) (but not in wild-type) rodents, thereby improving survival across asphyxic episodes. Increased survival was strongly correlated with hastened onset of gasping.
Question: Does caffeine improve the ability of serotonin-deficient ( Pet-1-/- ) mice to survive episodic asphyxia?
Output:
|
PubmedQA208480
|
[
{
"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: Organic dust is a complex mixture of particulate matter from microbial, plant or animal origin. Occupations with exposure to animal products have been associated with an increased lung cancer risk, while exposure to microbial components (eg, endotoxin) has been associated with a decreased risk. To date there has not been a comprehensive evaluation of the possible association between occupational organic dust exposure (and its specific constituents) and lung cancer risk in the general population. The SYNERGY project has pooled information on lifetime working and smoking from 13 300 lung cancer cases and 16 273 controls from 11 case-control studies conducted in Europe and Canada. A newly developed general population job-exposure matrix (assigning no, low or high exposure to organic dust, endotoxin, and contact with animals or fresh animal products) was applied to determine level of exposure. ORs for lung cancer were estimated by logistic regression, adjusted for age, sex, study, cigarette pack-years, time since quitting smoking, and ever employment in occupations with established lung cancer risk. Occupational organic dust exposure was associated with increased lung cancer risk. The second to the fourth quartile of cumulative exposure showed significant risk estimates ranging from 1.12 to 1.24 in a dose-dependent manner (p<0.001). This association remained in the highest quartile after restricting analyses to subjects without chronic obstructive pulmonary disease or asthma. No association was observed between lung cancer and exposure to endotoxin or contact with animals or animal products.\n Question: Does occupational exposure to organic dust increase lung cancer risk in the general 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: Organic dust is a complex mixture of particulate matter from microbial, plant or animal origin. Occupations with exposure to animal products have been associated with an increased lung cancer risk, while exposure to microbial components (eg, endotoxin) has been associated with a decreased risk. To date there has not been a comprehensive evaluation of the possible association between occupational organic dust exposure (and its specific constituents) and lung cancer risk in the general population. The SYNERGY project has pooled information on lifetime working and smoking from 13 300 lung cancer cases and 16 273 controls from 11 case-control studies conducted in Europe and Canada. A newly developed general population job-exposure matrix (assigning no, low or high exposure to organic dust, endotoxin, and contact with animals or fresh animal products) was applied to determine level of exposure. ORs for lung cancer were estimated by logistic regression, adjusted for age, sex, study, cigarette pack-years, time since quitting smoking, and ever employment in occupations with established lung cancer risk. Occupational organic dust exposure was associated with increased lung cancer risk. The second to the fourth quartile of cumulative exposure showed significant risk estimates ranging from 1.12 to 1.24 in a dose-dependent manner (p<0.001). This association remained in the highest quartile after restricting analyses to subjects without chronic obstructive pulmonary disease or asthma. No association was observed between lung cancer and exposure to endotoxin or contact with animals or animal products.
Question: Does occupational exposure to organic dust increase lung cancer risk in the general population?
Output:
|
PubmedQA4562
|
[
{
"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 chest radiography is quick and inexpensive, previous research suggests that it is often misleading in emergency department (ED) patients with decompensated heart failure, resulting in misdiagnosis and inappropriate treatment. This study determines the rate of negative chest radiography results in patients found to have disease and the potential contribution of negative findings to a diagnosis discordant with heart failure by an emergency physician. We used data from the Acute Decompensated Heart Failure National Registry (ADHERE), a registry of patients with a primary hospital discharge diagnosis of heart failure. We compared initial ED admitting diagnosis to the criterion standard of a hospital discharge diagnosis of heart failure and related these to radiographic findings of heart failure (interstitial edema, pulmonary edema, or vascular congestion, as determined by a staff radiologist) for patients first treated in the ED. The proportion of patients with a non-heart failure ED diagnosis and the diagnostic sensitivity of radiographic findings of heart failure are calculated. There were 85,376 patients with chest radiograph results and an ED admitting diagnosis. Overall, there were 15,937 patients with no signs of congestion on ED chest radiography, giving a negative rate of 18.7% (95% confidence interval [CI] 18.4% to 18.9%). The proportion of patients with an ED non-heart failure admitting diagnosis was higher in patients with a negative chest radiograph result (23.3%; 95% CI 22.6% to 23.9%) than in patients with a positive chest radiograph result (13.0%; 95% CI 12.7% to 13.2%).\n Question: Does prevalence of negative chest radiography result in the emergency department patient with decompensated heart failure?\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 chest radiography is quick and inexpensive, previous research suggests that it is often misleading in emergency department (ED) patients with decompensated heart failure, resulting in misdiagnosis and inappropriate treatment. This study determines the rate of negative chest radiography results in patients found to have disease and the potential contribution of negative findings to a diagnosis discordant with heart failure by an emergency physician. We used data from the Acute Decompensated Heart Failure National Registry (ADHERE), a registry of patients with a primary hospital discharge diagnosis of heart failure. We compared initial ED admitting diagnosis to the criterion standard of a hospital discharge diagnosis of heart failure and related these to radiographic findings of heart failure (interstitial edema, pulmonary edema, or vascular congestion, as determined by a staff radiologist) for patients first treated in the ED. The proportion of patients with a non-heart failure ED diagnosis and the diagnostic sensitivity of radiographic findings of heart failure are calculated. There were 85,376 patients with chest radiograph results and an ED admitting diagnosis. Overall, there were 15,937 patients with no signs of congestion on ED chest radiography, giving a negative rate of 18.7% (95% confidence interval [CI] 18.4% to 18.9%). The proportion of patients with an ED non-heart failure admitting diagnosis was higher in patients with a negative chest radiograph result (23.3%; 95% CI 22.6% to 23.9%) than in patients with a positive chest radiograph result (13.0%; 95% CI 12.7% to 13.2%).
Question: Does prevalence of negative chest radiography result in the emergency department patient with decompensated heart failure?
Output:
|
PubmedQA98950
|
[
{
"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 investigate the contribution of inflammation to postangioplasty lumen loss, we used an adenoviral gene therapy approach to inhibit the central inflammatory mediator nuclear factor-kappaB (NF-kappaB) by overexpression of its natural inhibitor, IkappaBalpha. The adenovirus carrying human IkappaBalpha was applied immediately after balloon dilatation by a double-balloon catheter in a rabbit iliac artery restenosis model. Immunohistochemistry of IkappaBalpha revealed that mainly smooth muscle cells of the media but also cells of the adventitia were transduced and expressed the transgene IkappaB alpha for >/= 8 days. At this time point, intercellular adhesion molecule-1 (30%) and monocyte chemotactic protein-1 (50%) expression, as well as recruitment of macrophages into the wounded area (90%), were significantly reduced in IkappaB alpha-treated vessels. In addition, expression of inhibitor of apoptosis proteins was reduced and the percentage of apoptotic cells was increased compared with control-treated contralateral vessels. Animals killed 5 weeks after treatment exhibited a significantly reduced degree of lumen narrowing (P<0.02) on the side treated with adenovirus IkappaBalpha. The lumen gain of approximately 40% was due to positive remodeling.\n Question: Does activation of nuclear factor-kappa B significantly contribute to lumen loss in a rabbit iliac artery balloon angioplasty model?\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 investigate the contribution of inflammation to postangioplasty lumen loss, we used an adenoviral gene therapy approach to inhibit the central inflammatory mediator nuclear factor-kappaB (NF-kappaB) by overexpression of its natural inhibitor, IkappaBalpha. The adenovirus carrying human IkappaBalpha was applied immediately after balloon dilatation by a double-balloon catheter in a rabbit iliac artery restenosis model. Immunohistochemistry of IkappaBalpha revealed that mainly smooth muscle cells of the media but also cells of the adventitia were transduced and expressed the transgene IkappaB alpha for >/= 8 days. At this time point, intercellular adhesion molecule-1 (30%) and monocyte chemotactic protein-1 (50%) expression, as well as recruitment of macrophages into the wounded area (90%), were significantly reduced in IkappaB alpha-treated vessels. In addition, expression of inhibitor of apoptosis proteins was reduced and the percentage of apoptotic cells was increased compared with control-treated contralateral vessels. Animals killed 5 weeks after treatment exhibited a significantly reduced degree of lumen narrowing (P<0.02) on the side treated with adenovirus IkappaBalpha. The lumen gain of approximately 40% was due to positive remodeling.
Question: Does activation of nuclear factor-kappa B significantly contribute to lumen loss in a rabbit iliac artery balloon angioplasty model?
Output:
|
PubmedQA39823
|
[
{
"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: Some pediatric centers perform flexible bronchoscopy (FB) routinely when bronchiectasis is suspected. However, there are no published data evaluating this practice. To evaluate the contribution of FB and bronchoalveolar lavage (BAL) to the initial management of children newly diagnosed with non-cystic fibrosis (CF) bronchiectasis. We examined FB and BAL data collected prospectively in 56 children aged 0.8-9.8 years during initial investigations for bronchiectasis. Investigations contributed to management if any of the following were identified: (1) airway obstruction requiring additional intervention, (2) lower airway eosinophilia (BAL eosinophils >2.5%), or (3) BAL fluid culture >10(4) colony-forming units/ml of a respiratory bacterial pathogen requiring change from usual empiric antibiotics. Of the 56 children undergoing FB, there were 25 occasions in 23 children where these procedures altered empiric treatment. Lower airway eosinophilia was identified in 19 (34%) children, BAL microbiology results led to antibiotic changes in 5 (9%) and an unsuspected foreign body was found in another (2%). Strongyloides serology was performed in 38 children, including 12 of the 19 with airway eosinophilia, and was positive in 5 of these 12 children (42%).\n Question: Does bronchoscopy contribute to the clinical management of indigenous children newly diagnosed with bronchiectasis?\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: Some pediatric centers perform flexible bronchoscopy (FB) routinely when bronchiectasis is suspected. However, there are no published data evaluating this practice. To evaluate the contribution of FB and bronchoalveolar lavage (BAL) to the initial management of children newly diagnosed with non-cystic fibrosis (CF) bronchiectasis. We examined FB and BAL data collected prospectively in 56 children aged 0.8-9.8 years during initial investigations for bronchiectasis. Investigations contributed to management if any of the following were identified: (1) airway obstruction requiring additional intervention, (2) lower airway eosinophilia (BAL eosinophils >2.5%), or (3) BAL fluid culture >10(4) colony-forming units/ml of a respiratory bacterial pathogen requiring change from usual empiric antibiotics. Of the 56 children undergoing FB, there were 25 occasions in 23 children where these procedures altered empiric treatment. Lower airway eosinophilia was identified in 19 (34%) children, BAL microbiology results led to antibiotic changes in 5 (9%) and an unsuspected foreign body was found in another (2%). Strongyloides serology was performed in 38 children, including 12 of the 19 with airway eosinophilia, and was positive in 5 of these 12 children (42%).
Question: Does bronchoscopy contribute to the clinical management of indigenous children newly diagnosed with bronchiectasis?
Output:
|
PubmedQA163037
|
[
{
"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: Increased proinflammatory cytokines after myocardial infarction augment the progression of heart failure (HF) and are of prognostic significance. Recently, we demonstrated that increased proinflammatory cytokines in the brains of HF rats increased paraventricular nucleus (PVN) superoxide and down-regulated neuronal nitric oxide synthase (nNOS), contributing to sympathoexcitation. In this study, we explored the possible roles of brain proinflammatory cytokines and their effects on modulating PVN neurotransmitters in the exaggerated sympathetic activity in HF. Sprague-Dawley rats with HF or sham-operated control (SHAM) rats were treated for 4 weeks with a continuous intracerebroventricular (ICV) infusion of the cytokine blockers-pentoxifylline (PTX, 10 microg/h and 40 microg/h), etanercept (ETN, 5 microg/h and 10 microg/h), or vehicle. Another set of HF and SHAM rats were treated with intraperitoneal (ip) infusion of a similar dose of PTX or ETN. HF rats had increased neuronal excitation accompanied by higher levels of glutamate, norepinephrine (NE), and tyrosine hydroxylase (TH), and lower levels of gamma-aminobutyric acid (GABA), nNOS, and 67-kDa isoform of glutamate decarboxylase (GAD67) in the PVN when compared with SHAM rats. Plasma cytokines, NE, epinephrine, angiotensin II, and renal sympathetic nerve activity (RSNA) were also increased in HF rats. ICV treatment with low doses of PTX or ETN attenuated, and high doses prevented, increases in levels of glutamate, NE, and TH, and decreases in levels of GABA, nNOS, and GAD67 in the PVN in HF rats. The same ICV treatments also attenuated the increased RSNA seen in HF rats. IP treatment with similar doses of PTX or ETN did not affect glutamate, NE, TH, GABA, nNOS, and GAD67 in the PVN and had no effect on RSNA of HF rats.\n Question: Does brain tumour necrosis factor-alpha modulate neurotransmitters in hypothalamic paraventricular nucleus in heart failure?\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: Increased proinflammatory cytokines after myocardial infarction augment the progression of heart failure (HF) and are of prognostic significance. Recently, we demonstrated that increased proinflammatory cytokines in the brains of HF rats increased paraventricular nucleus (PVN) superoxide and down-regulated neuronal nitric oxide synthase (nNOS), contributing to sympathoexcitation. In this study, we explored the possible roles of brain proinflammatory cytokines and their effects on modulating PVN neurotransmitters in the exaggerated sympathetic activity in HF. Sprague-Dawley rats with HF or sham-operated control (SHAM) rats were treated for 4 weeks with a continuous intracerebroventricular (ICV) infusion of the cytokine blockers-pentoxifylline (PTX, 10 microg/h and 40 microg/h), etanercept (ETN, 5 microg/h and 10 microg/h), or vehicle. Another set of HF and SHAM rats were treated with intraperitoneal (ip) infusion of a similar dose of PTX or ETN. HF rats had increased neuronal excitation accompanied by higher levels of glutamate, norepinephrine (NE), and tyrosine hydroxylase (TH), and lower levels of gamma-aminobutyric acid (GABA), nNOS, and 67-kDa isoform of glutamate decarboxylase (GAD67) in the PVN when compared with SHAM rats. Plasma cytokines, NE, epinephrine, angiotensin II, and renal sympathetic nerve activity (RSNA) were also increased in HF rats. ICV treatment with low doses of PTX or ETN attenuated, and high doses prevented, increases in levels of glutamate, NE, and TH, and decreases in levels of GABA, nNOS, and GAD67 in the PVN in HF rats. The same ICV treatments also attenuated the increased RSNA seen in HF rats. IP treatment with similar doses of PTX or ETN did not affect glutamate, NE, TH, GABA, nNOS, and GAD67 in the PVN and had no effect on RSNA of HF rats.
Question: Does brain tumour necrosis factor-alpha modulate neurotransmitters in hypothalamic paraventricular nucleus in heart failure?
Output:
|
PubmedQA155449
|
[
{
"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: Few studies have focused on cardiac ventricular diastolic function in preterm neonates in the immediate post-natal period. This study evaluated Doppler-derived parameters of diastolic ventricular function in infants with birth weights of <1250 g during the transitional period. This was a prospective observational study conducted in the Coombe Women and Infants University Hospital in Dublin, Ireland. Flow patterns on the mitral and tricuspid valve, isovolumic relaxation time (IVRT), left and right ventricular output and superior vena cava flow were measured in 22 infants with a birth weight of below 1250 g at six, 12, 24 and 48 h of age. Early filling peak velocity of the left and right ventricle increased significantly from 30.3 to 39.5 cm/sec and 26.6 to 32.1 cm/sec, respectively. IVRT of the right ventricle decreased from 70 to 57 ms, and there was a nonsignificant decrease in IVRT of the left ventricle from 61.6 to 54 ms over the first 48 h.\n Question: Does diastolic ventricular function improve during the first 48-hours-of-life in infants weighting < 1250 g?\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: Few studies have focused on cardiac ventricular diastolic function in preterm neonates in the immediate post-natal period. This study evaluated Doppler-derived parameters of diastolic ventricular function in infants with birth weights of <1250 g during the transitional period. This was a prospective observational study conducted in the Coombe Women and Infants University Hospital in Dublin, Ireland. Flow patterns on the mitral and tricuspid valve, isovolumic relaxation time (IVRT), left and right ventricular output and superior vena cava flow were measured in 22 infants with a birth weight of below 1250 g at six, 12, 24 and 48 h of age. Early filling peak velocity of the left and right ventricle increased significantly from 30.3 to 39.5 cm/sec and 26.6 to 32.1 cm/sec, respectively. IVRT of the right ventricle decreased from 70 to 57 ms, and there was a nonsignificant decrease in IVRT of the left ventricle from 61.6 to 54 ms over the first 48 h.
Question: Does diastolic ventricular function improve during the first 48-hours-of-life in infants weighting < 1250 g?
Output:
|
PubmedQA91060
|
[
{
"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 investigate arousal from sleep in infants before and after triple antigen immunization (DTP). Arousal thresholds were determined in both active sleep (AS) and quiet sleep (QS) the day before and the day following the first DTP immunisation in 14 infants. Arousal was induced using a pulsatile puff of air delivered alternately to the nostrils of the infant. Arousal threshold was significantly higher in QS compared to AS in both studies (P < 0.001). Mean arousal threshold in the pre immunization study was not different from that in the post immunization study in either sleep state. Core temperature and heart rate measured at the time of stimulus delivery were both significantly elevated in the post immunisation study (P < 0.001). Sleep duration and number of awakenings from sleep were unaffected by immunization.\n Question: Does immunization have no effect on arousal from sleep in the newborn infant?\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 investigate arousal from sleep in infants before and after triple antigen immunization (DTP). Arousal thresholds were determined in both active sleep (AS) and quiet sleep (QS) the day before and the day following the first DTP immunisation in 14 infants. Arousal was induced using a pulsatile puff of air delivered alternately to the nostrils of the infant. Arousal threshold was significantly higher in QS compared to AS in both studies (P < 0.001). Mean arousal threshold in the pre immunization study was not different from that in the post immunization study in either sleep state. Core temperature and heart rate measured at the time of stimulus delivery were both significantly elevated in the post immunisation study (P < 0.001). Sleep duration and number of awakenings from sleep were unaffected by immunization.
Question: Does immunization have no effect on arousal from sleep in the newborn infant?
Output:
|
PubmedQA33274
|
[
{
"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: Using an animal model, we have previously shown that preeclampsia results in long-term adverse neuromotor outcomes in the offspring, and this phenotype was prevented by antenatal treatment with pravastatin. This study aims to localize the altered neuromotor programming in this animal model and to evaluate the role of pravastatin in its prevention. For the preeclampsia model, pregnant CD-1 mice were randomly allocated to injection of adenovirus carrying sFlt-1 or its control virus carrying mFc into the tail vein. Thereafter they received pravastatin (sFlt-1-pra \"experimental group\") or water (sFlt-1 \"positive control\") until weaning. The mFc group (\"negative control\") received water. Offspring at 6 months of age were sacrificed, and whole brains underwent magnetic resonance imaging (MRI). MRIs were performed using an 11.7 Tesla vertical bore MRI scanner. T2 weighted images were acquired to evaluate the volumes of 28 regions of interest, including areas involved in adaptation and motor, spatial and sensory function. Cytochemistry and cell quantification was performed using neuron-specific Nissl stain. One-way ANOVA with multiple comparison testing was used for statistical analysis. Compared with control offspring, male sFlt-1 offspring have decreased volumes in the fimbria, periaquaductal gray, stria medullaris, and ventricles and increased volumes in the lateral globus pallidus and neocortex; however, female sFlt-1 offspring showed increased volumes in the ventricles, stria medullaris, and fasciculus retroflexus and decreased volumes in the inferior colliculus, thalamus, and lateral globus pallidus. Neuronal quantification via Nissl staining exhibited decreased cell counts in sFlt-1 offspring neocortex, more pronounced in males. Prenatal pravastatin treatment prevented these changes.\n Question: Does maternal pravastatin prevent altered fetal brain development in a preeclamptic CD-1 mouse model?\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: Using an animal model, we have previously shown that preeclampsia results in long-term adverse neuromotor outcomes in the offspring, and this phenotype was prevented by antenatal treatment with pravastatin. This study aims to localize the altered neuromotor programming in this animal model and to evaluate the role of pravastatin in its prevention. For the preeclampsia model, pregnant CD-1 mice were randomly allocated to injection of adenovirus carrying sFlt-1 or its control virus carrying mFc into the tail vein. Thereafter they received pravastatin (sFlt-1-pra "experimental group") or water (sFlt-1 "positive control") until weaning. The mFc group ("negative control") received water. Offspring at 6 months of age were sacrificed, and whole brains underwent magnetic resonance imaging (MRI). MRIs were performed using an 11.7 Tesla vertical bore MRI scanner. T2 weighted images were acquired to evaluate the volumes of 28 regions of interest, including areas involved in adaptation and motor, spatial and sensory function. Cytochemistry and cell quantification was performed using neuron-specific Nissl stain. One-way ANOVA with multiple comparison testing was used for statistical analysis. Compared with control offspring, male sFlt-1 offspring have decreased volumes in the fimbria, periaquaductal gray, stria medullaris, and ventricles and increased volumes in the lateral globus pallidus and neocortex; however, female sFlt-1 offspring showed increased volumes in the ventricles, stria medullaris, and fasciculus retroflexus and decreased volumes in the inferior colliculus, thalamus, and lateral globus pallidus. Neuronal quantification via Nissl staining exhibited decreased cell counts in sFlt-1 offspring neocortex, more pronounced in males. Prenatal pravastatin treatment prevented these changes.
Question: Does maternal pravastatin prevent altered fetal brain development in a preeclamptic CD-1 mouse model?
Output:
|
PubmedQA171910
|
[
{
"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: Sentinel lymph node (SLN) biopsy is an important independent prognostic factor for invasive cutaneuos melanoma, although its role is strongly debated. In clinical practice SLN leads to complete lymph node dissection of basin draining melanoma site. However only 7-30% of positive sentinel node patients present additional non SLN metastasis. Melanoma cells diffusion through SLN and extranodal spreading depends upon biological features, such as cell chemokine receptors and adhesion molecules. CXCR4 has been proposed in melanoma patients as prognostic marker. Therefore we have analyzed both histopathological parameters and CXCR4 expression in melanoma infiltrate of SLN, in order to evaluate its potential prognostic role. Micrometastases were detected in 23 cases (48.93%); metastases >2 mm in 23 cases (48.93%) and isolated metastatic cells in one case (2.01%). High CXCR4 expression was observed in 21 nodal metastases. Node metastases in complete dissection were associated to >10% relative tumor area (RTA) in all lymph nodes (p = 0.006). Extranodal invasion (p = 0.006) and >2 mm centripetal metastasis thickness (p = 0.01), while shorter Disease Free Survival (DFS) was significantly associated to high CXCR4 expression (p = 0.02). Forty-seven positive lymph node metastases were collected and analysed for both histopathological parameters and CXCR4 expression.\n Question: Are histomorphologic parameters and CXCR4 mRNA and protein expression in sentinel node melanoma metastasis correlated to clinical outcome?\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: Sentinel lymph node (SLN) biopsy is an important independent prognostic factor for invasive cutaneuos melanoma, although its role is strongly debated. In clinical practice SLN leads to complete lymph node dissection of basin draining melanoma site. However only 7-30% of positive sentinel node patients present additional non SLN metastasis. Melanoma cells diffusion through SLN and extranodal spreading depends upon biological features, such as cell chemokine receptors and adhesion molecules. CXCR4 has been proposed in melanoma patients as prognostic marker. Therefore we have analyzed both histopathological parameters and CXCR4 expression in melanoma infiltrate of SLN, in order to evaluate its potential prognostic role. Micrometastases were detected in 23 cases (48.93%); metastases >2 mm in 23 cases (48.93%) and isolated metastatic cells in one case (2.01%). High CXCR4 expression was observed in 21 nodal metastases. Node metastases in complete dissection were associated to >10% relative tumor area (RTA) in all lymph nodes (p = 0.006). Extranodal invasion (p = 0.006) and >2 mm centripetal metastasis thickness (p = 0.01), while shorter Disease Free Survival (DFS) was significantly associated to high CXCR4 expression (p = 0.02). Forty-seven positive lymph node metastases were collected and analysed for both histopathological parameters and CXCR4 expression.
Question: Are histomorphologic parameters and CXCR4 mRNA and protein expression in sentinel node melanoma metastasis correlated to clinical outcome?
Output:
|
PubmedQA88518
|
[
{
"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: Daunorubicin (DNR)-induced cardiotoxicity, which is closely associated with cardiomyocyte apoptosis, limits the drug's clinical application. The activation of the extracellular regulated protein kinases (ERKs) pathway is responsible for the pro-apoptosis effect of DNR Sodium ferulate (SF) has recently been found to attenuate both DNR-induced cardiotoxicity and mitochondrial apoptosis in juvenile rats. Nonetheless, the precise mechanism underlying SF-induced cardio-protection remains unclear. The DNR-injured H9c2 cell model was prepared by incubating the cells in 1 µM DNR for 24 h. Amounts of 15.6, 31.3 or 62.5 µM SF were simultaneously added to the cells. The effect of SF on the cytotoxic and apoptotic parameters of the cells was studied by monitoring apoptosis regulation via the ERKs pathway. SF attenuated DNR-induced cell death (particularly apoptotic death), cTnI and β-tubulin degradation, and cellular morphological changes. SF reduced mitochondrial membrane potential depolarization, cytochrome c leakage, and caspase-9 and caspase-3 activation. SF also decreased ERK1/2, phospho-ERK1/2, p53 and Bax expression and increased Bcl-2 expression. These effects were similar to the results observed when using the pharmacological ERKs phosphorylation inhibitor, AZD6244.\n Question: Does sodium Ferulate prevent Daunorubicin -- Induced Apoptosis in H9c2 Cells via Inhibition of the ERKs Pathway?\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: Daunorubicin (DNR)-induced cardiotoxicity, which is closely associated with cardiomyocyte apoptosis, limits the drug's clinical application. The activation of the extracellular regulated protein kinases (ERKs) pathway is responsible for the pro-apoptosis effect of DNR Sodium ferulate (SF) has recently been found to attenuate both DNR-induced cardiotoxicity and mitochondrial apoptosis in juvenile rats. Nonetheless, the precise mechanism underlying SF-induced cardio-protection remains unclear. The DNR-injured H9c2 cell model was prepared by incubating the cells in 1 µM DNR for 24 h. Amounts of 15.6, 31.3 or 62.5 µM SF were simultaneously added to the cells. The effect of SF on the cytotoxic and apoptotic parameters of the cells was studied by monitoring apoptosis regulation via the ERKs pathway. SF attenuated DNR-induced cell death (particularly apoptotic death), cTnI and β-tubulin degradation, and cellular morphological changes. SF reduced mitochondrial membrane potential depolarization, cytochrome c leakage, and caspase-9 and caspase-3 activation. SF also decreased ERK1/2, phospho-ERK1/2, p53 and Bax expression and increased Bcl-2 expression. These effects were similar to the results observed when using the pharmacological ERKs phosphorylation inhibitor, AZD6244.
Question: Does sodium Ferulate prevent Daunorubicin -- Induced Apoptosis in H9c2 Cells via Inhibition of the ERKs Pathway?
Output:
|
PubmedQA157881
|
[
{
"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: Stored red blood cells (RBCs) release hemoglobin (Hb) that leads to oxidative damage, which may contribute to thrombosis in susceptible transfusion recipients. Oxidative stress stimulates the generation of a new class of lipid mediators called F2 -isoprostanes (F2 -IsoPs) and isofurans (IsoFs) that influence cellular behavior. This study investigated RBC-derived F2 -IsoPs and IsoFs during storage and their influence on human platelets (PLTs). F2 -IsoP and IsoF levels in RBC supernatants were measured by mass spectrometry during storage and after washing. The effects of stored supernatants, cell-free Hb, or a key F2 -IsoP, 8-iso-prostaglandin F2α (PGF2α ), on PLT function were examined in vitro. F2 -IsoPs, IsoFs, and Hb accumulated in stored RBC supernatants. Prestorage leukoreduction reduced supernatant F2 -IsoPs and IsoFs levels, which increased again over storage time. Stored RBC supernatants and 8-iso-PGF2α induced PLT activation marker CD62P (P-selectin) expression and prothrombotic thromboxane A2 release. Cell-free Hb did not alter PLT mediator release, but did inhibit PLT spreading. Poststorage RBC washing reduced F2 -IsoP and IsoF levels up to 24 hours.\n Question: Do isoprostane and isofuran lipid mediators accumulate in stored red blood cells and influence platelet function in vitro?\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: Stored red blood cells (RBCs) release hemoglobin (Hb) that leads to oxidative damage, which may contribute to thrombosis in susceptible transfusion recipients. Oxidative stress stimulates the generation of a new class of lipid mediators called F2 -isoprostanes (F2 -IsoPs) and isofurans (IsoFs) that influence cellular behavior. This study investigated RBC-derived F2 -IsoPs and IsoFs during storage and their influence on human platelets (PLTs). F2 -IsoP and IsoF levels in RBC supernatants were measured by mass spectrometry during storage and after washing. The effects of stored supernatants, cell-free Hb, or a key F2 -IsoP, 8-iso-prostaglandin F2α (PGF2α ), on PLT function were examined in vitro. F2 -IsoPs, IsoFs, and Hb accumulated in stored RBC supernatants. Prestorage leukoreduction reduced supernatant F2 -IsoPs and IsoFs levels, which increased again over storage time. Stored RBC supernatants and 8-iso-PGF2α induced PLT activation marker CD62P (P-selectin) expression and prothrombotic thromboxane A2 release. Cell-free Hb did not alter PLT mediator release, but did inhibit PLT spreading. Poststorage RBC washing reduced F2 -IsoP and IsoF levels up to 24 hours.
Question: Do isoprostane and isofuran lipid mediators accumulate in stored red blood cells and influence platelet function in vitro?
Output:
|
PubmedQA32931
|
[
{
"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: Activating transcription factor-3 (ATF3) is known as a suppressor of cytokine production after exposure to lipopolysaccharide or during gram-negative bacterial infection. However, the mechanism by which ATF3 regulates innate immunity against gram-positive bacterial infection, particularly Streptococcus pneumoniae, remains unknown. The wild-type and ATF3 knock-out (KO) mice were infected intranasally (i.n) or intraperitoneally with S. pneumoniae, and bacterial colonization or survival rate was determined. Pneumococcal pneumonia was induced by i.n infection, and ATF3 level was determined by Western blot. ATF3 KO cells or ATF3 siRNA transfection were used to determine expression of ATF3 downstream genes. Enzyme-linked immunosorbent assay was used to examine cytokines levels. ATF3 was highly expressed in various cell lines in vitro and in many organs in vivo. Pneumolysin was a novel inducer of ATF3. Pneumococcal infection induced ATF3, which subsequently stimulated production of cytokines (tumor necrosis factor [TNF]-α, interleukin [IL]-1β, and interferon [IFN]-γ). ATF3-mediated cytokine induction protected the host from pneumococcal infection. In the pneumonia infection model, the bacterial clearance of wild-type mice was more efficient than those of ATF3 KO mice.\n Question: Does aTF3 confer resistance to pneumococcal infection through positive regulation of cytokine production?\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: Activating transcription factor-3 (ATF3) is known as a suppressor of cytokine production after exposure to lipopolysaccharide or during gram-negative bacterial infection. However, the mechanism by which ATF3 regulates innate immunity against gram-positive bacterial infection, particularly Streptococcus pneumoniae, remains unknown. The wild-type and ATF3 knock-out (KO) mice were infected intranasally (i.n) or intraperitoneally with S. pneumoniae, and bacterial colonization or survival rate was determined. Pneumococcal pneumonia was induced by i.n infection, and ATF3 level was determined by Western blot. ATF3 KO cells or ATF3 siRNA transfection were used to determine expression of ATF3 downstream genes. Enzyme-linked immunosorbent assay was used to examine cytokines levels. ATF3 was highly expressed in various cell lines in vitro and in many organs in vivo. Pneumolysin was a novel inducer of ATF3. Pneumococcal infection induced ATF3, which subsequently stimulated production of cytokines (tumor necrosis factor [TNF]-α, interleukin [IL]-1β, and interferon [IFN]-γ). ATF3-mediated cytokine induction protected the host from pneumococcal infection. In the pneumonia infection model, the bacterial clearance of wild-type mice was more efficient than those of ATF3 KO mice.
Question: Does aTF3 confer resistance to pneumococcal infection through positive regulation of cytokine production?
Output:
|
PubmedQA78613
|
[
{
"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: Whether IGF-1 has a protective or a detrimental role in vascular homeostasis remains unsettled. There is evidence that the C/T polymorphism rs35767 near the promoter region of the IGF1 gene located in chromosome 12 is associated with plasma IGF-1 levels. We investigated the effects of this polymorphism on circulating IGF-1 levels, carotid intima media thickness (cIMT) and endothelial-dependent vasodilation. Two samples of adult nondiabetic Whites were studied. Sample 1 comprised 1124 individuals in whom cIMT was measured by ultrasonography. Sample 2 included 162 drug-naïve hypertensive individuals in whom endothelium-dependent and endothelium-independent vasodilation were assessed by intra-arterial infusion of acetylcholine (ACh), and sodium nitroprusside (SNP), respectively. IGF-1 was determined by chemiluminescent immunoassay. rs35767 polymorphism was screened using a TaqMan allelic discrimination assay. In sample 1, IGF-1 levels were higher in subjects carrying the T allele compared with CC carriers (178 ± 78 vs. 166 ± 60 ng/mL, respectively; P = 0.007 adjusted for age, gender, and BMI). cIMT was lower in subjects carrying the T allele compared with CC carriers (0.71 ± 0.20 vs. 0.76 ± 0.22 mm, respectively; P < 0.0001 adjusted for age, gender, and BMI). In sample 2, maximally ACh-stimulated forearm blood flow was higher in subjects carrying the T allele compared with CC carriers (343 ± 191 vs. 281 ± 125%, respectively; P = 0.02 adjusted for age, gender, and BMI).\n Question: Is a polymorphism at IGF1 locus associated with carotid intima media thickness and endothelium-dependent vasodilatation?\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: Whether IGF-1 has a protective or a detrimental role in vascular homeostasis remains unsettled. There is evidence that the C/T polymorphism rs35767 near the promoter region of the IGF1 gene located in chromosome 12 is associated with plasma IGF-1 levels. We investigated the effects of this polymorphism on circulating IGF-1 levels, carotid intima media thickness (cIMT) and endothelial-dependent vasodilation. Two samples of adult nondiabetic Whites were studied. Sample 1 comprised 1124 individuals in whom cIMT was measured by ultrasonography. Sample 2 included 162 drug-naïve hypertensive individuals in whom endothelium-dependent and endothelium-independent vasodilation were assessed by intra-arterial infusion of acetylcholine (ACh), and sodium nitroprusside (SNP), respectively. IGF-1 was determined by chemiluminescent immunoassay. rs35767 polymorphism was screened using a TaqMan allelic discrimination assay. In sample 1, IGF-1 levels were higher in subjects carrying the T allele compared with CC carriers (178 ± 78 vs. 166 ± 60 ng/mL, respectively; P = 0.007 adjusted for age, gender, and BMI). cIMT was lower in subjects carrying the T allele compared with CC carriers (0.71 ± 0.20 vs. 0.76 ± 0.22 mm, respectively; P < 0.0001 adjusted for age, gender, and BMI). In sample 2, maximally ACh-stimulated forearm blood flow was higher in subjects carrying the T allele compared with CC carriers (343 ± 191 vs. 281 ± 125%, respectively; P = 0.02 adjusted for age, gender, and BMI).
Question: Is a polymorphism at IGF1 locus associated with carotid intima media thickness and endothelium-dependent vasodilatation?
Output:
|
PubmedQA25490
|
[
{
"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: This study compares the efficacy of sequential clomiphene citrate (CC) + Gonadotropin to that of Gonadotropin alone with ultrasound monitoring. It is a retrospective analytic study done on a total of 100 couples to compare two groups receiving CC + Gonadotropin and Gonadotropin alone for ovarian stimulation followed by intrauterine Insemination (IUI). We studied the cycle performance parameters. Cumulative pregnancy rates and ovulation rates were the primary outcomes. Results were analyzed following the intention-to-treat principle. There were no significant differences with respect to indications and the numbers of dominant follicles recruited. The endometrial thickness was significantly better in Gonadotropin-alone group (P < 0.05). Ovulation rate was better for CC + Gonadotropin at 95.91 %. Nine pregnancies were in the CC + Gonadotropin group (18.36 %) and 17 in Gonadotropin-alone group (33.3 %).\n Question: Is gonadotropin Alone a Better Drug for Ovarian Stimulation than in Combination with Clomiphene in Intrauterine Insemination?\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: This study compares the efficacy of sequential clomiphene citrate (CC) + Gonadotropin to that of Gonadotropin alone with ultrasound monitoring. It is a retrospective analytic study done on a total of 100 couples to compare two groups receiving CC + Gonadotropin and Gonadotropin alone for ovarian stimulation followed by intrauterine Insemination (IUI). We studied the cycle performance parameters. Cumulative pregnancy rates and ovulation rates were the primary outcomes. Results were analyzed following the intention-to-treat principle. There were no significant differences with respect to indications and the numbers of dominant follicles recruited. The endometrial thickness was significantly better in Gonadotropin-alone group (P < 0.05). Ovulation rate was better for CC + Gonadotropin at 95.91 %. Nine pregnancies were in the CC + Gonadotropin group (18.36 %) and 17 in Gonadotropin-alone group (33.3 %).
Question: Is gonadotropin Alone a Better Drug for Ovarian Stimulation than in Combination with Clomiphene in Intrauterine Insemination?
Output:
|
PubmedQA23931
|
[
{
"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: Substantial literature documents that persistent postsurgical pain is a possible outcome of many common surgical procedures. As fracture-related surgery implies a risk of developing neuropathic pain and complex regional pain syndrome (CRPS), further studies investigating the prevalence and pain characteristics are required. All patients undergoing primary surgery because of ankle or wrist fracture at Hvidovre and Odense University Hospitals, Denmark, between April 15, 2013 and April 15, 2014, were identified from the Danish Fracture Database. A questionnaire regarding pain characteristics was sent to patients 1 yr after primary surgery. Replies were received from 328 patients, of whom 18.9% experienced persistent postsurgical pain defined as pain daily or constantly at a level that interfered much or very much with daily activities, 42.8% reported symptoms suggestive of neuropathic pain, and 4.0% fulfilled the diagnostic patient-reported research criteria for CRPS.\n Question: Is persistent pain common 1 year after ankle and wrist fracture surgery : a register-based questionnaire 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: Substantial literature documents that persistent postsurgical pain is a possible outcome of many common surgical procedures. As fracture-related surgery implies a risk of developing neuropathic pain and complex regional pain syndrome (CRPS), further studies investigating the prevalence and pain characteristics are required. All patients undergoing primary surgery because of ankle or wrist fracture at Hvidovre and Odense University Hospitals, Denmark, between April 15, 2013 and April 15, 2014, were identified from the Danish Fracture Database. A questionnaire regarding pain characteristics was sent to patients 1 yr after primary surgery. Replies were received from 328 patients, of whom 18.9% experienced persistent postsurgical pain defined as pain daily or constantly at a level that interfered much or very much with daily activities, 42.8% reported symptoms suggestive of neuropathic pain, and 4.0% fulfilled the diagnostic patient-reported research criteria for CRPS.
Question: Is persistent pain common 1 year after ankle and wrist fracture surgery : a register-based questionnaire study?
Output:
|
PubmedQA32063
|
[
{
"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 participation of microRNAs (miRNAs) in cardiovascular diseases suggests them as potential targets for novel preventive and therapeutic strategies. In this study, the key myocardial miRNA, miR-21, was identified in the murine coxsackievirus B3 (CVB3)-induced myocarditis model and its contribution to disease progression was explored. Myocardial microRNA expression changes in CVB3-infected mice were analyzed by real-time PCR and miR-21 was found to be the miRNA whose expression was significantly reduced. Mice were injected with plasmid encoding miR-21 (pMDH-miR-21) at day 1 post CVB3 infection and myocarditis severity was evaluated 7 days post-infection. The underlying mechanism of miR-21 in viral myocarditis was also investigated. Myocardial miR-21 expression was negatively related to viral myocarditis severity. Recovery of miR-21 expression, by injecting with pMDH-miR-21, significantly relieved CVB3-induced myocarditis as shown by increased body weight, reduced myocardial injury, lowered myocarditis score and increased survival rate. Further study showed that miR-21 could protect myocardial apoptosis by specifically inhibiting its target programmed cell death 4 (PDCD4) expression.\n Question: Does miR-21 confer resistance against CVB3-induced myocarditis by inhibiting PDCD4-mediated apoptosis?\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 participation of microRNAs (miRNAs) in cardiovascular diseases suggests them as potential targets for novel preventive and therapeutic strategies. In this study, the key myocardial miRNA, miR-21, was identified in the murine coxsackievirus B3 (CVB3)-induced myocarditis model and its contribution to disease progression was explored. Myocardial microRNA expression changes in CVB3-infected mice were analyzed by real-time PCR and miR-21 was found to be the miRNA whose expression was significantly reduced. Mice were injected with plasmid encoding miR-21 (pMDH-miR-21) at day 1 post CVB3 infection and myocarditis severity was evaluated 7 days post-infection. The underlying mechanism of miR-21 in viral myocarditis was also investigated. Myocardial miR-21 expression was negatively related to viral myocarditis severity. Recovery of miR-21 expression, by injecting with pMDH-miR-21, significantly relieved CVB3-induced myocarditis as shown by increased body weight, reduced myocardial injury, lowered myocarditis score and increased survival rate. Further study showed that miR-21 could protect myocardial apoptosis by specifically inhibiting its target programmed cell death 4 (PDCD4) expression.
Question: Does miR-21 confer resistance against CVB3-induced myocarditis by inhibiting PDCD4-mediated apoptosis?
Output:
|
PubmedQA145227
|
[
{
"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: Pogostemon cablin is a medicinal herb widely used to treat gastrointestinal diseases in many Asian countries. Pogostone is an important constituent of Pogostemon cablin, and possesses various bioactivitys. In this study, we performed to investigate the anti-colorectal tumor property of Pogostone by inducing aurophagy and apoptosis in human colorectal cancer cells, and to define the potential molecular mechanisms. In vitro,The anti-tumor activity of pogostone was assessed using MTT assay. Autophagy was monitored by transmission electron microscopy observation and mRFP-GFP-LC3 fluorescence analysis in colorectal tumor cell line. Apoptosis was measured by flow cytometry and annexinV-FITC/PI staining. The protein expressions or activition of LC3-Ⅱ, AKT, mTOR, caspase-3 and caspase-7 were detected through western blotting. In vivo, the anti-tumor effect of pogostone was tested with HCT116 colorectal tumor cells transplantation tumor model. The expression of Ki-67 was determed by Immunohistochemistry staining and the apoptosis was evaluated using TUNEL assay. In vitro, pogostone exhibits significant anti-tumor activity against human cancer cell lines, especially for HCT116 (18.7±1.93μg/ml). Transmission electron microscopy observation, mRFP-GFP-LC3 fluorescence analysis, flow cytometryand assay and western blotting detection revealed that the anti-colorectal tumor activity of pogostone was dependent on inducing autophagy and apoptosis through up-regulating the expression of LC3-Ⅱ, cleaved caspase-7 and caspase-3, and decreasing the phosphorylation of AKT/mTOR. In vivo, 150mg/kg pogostone inhibited the HCT116 tumor growth in immunodeficient mice with an inhibitory rate of 43.3%, decreased the expression of Ki67, and induced apoptosis in three days.\n Question: Does pogostone induce Autophagy and Apoptosis Involving PI3K/Akt/mTOR Axis in Human Colorectal Carcinoma HCT116 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: Pogostemon cablin is a medicinal herb widely used to treat gastrointestinal diseases in many Asian countries. Pogostone is an important constituent of Pogostemon cablin, and possesses various bioactivitys. In this study, we performed to investigate the anti-colorectal tumor property of Pogostone by inducing aurophagy and apoptosis in human colorectal cancer cells, and to define the potential molecular mechanisms. In vitro,The anti-tumor activity of pogostone was assessed using MTT assay. Autophagy was monitored by transmission electron microscopy observation and mRFP-GFP-LC3 fluorescence analysis in colorectal tumor cell line. Apoptosis was measured by flow cytometry and annexinV-FITC/PI staining. The protein expressions or activition of LC3-Ⅱ, AKT, mTOR, caspase-3 and caspase-7 were detected through western blotting. In vivo, the anti-tumor effect of pogostone was tested with HCT116 colorectal tumor cells transplantation tumor model. The expression of Ki-67 was determed by Immunohistochemistry staining and the apoptosis was evaluated using TUNEL assay. In vitro, pogostone exhibits significant anti-tumor activity against human cancer cell lines, especially for HCT116 (18.7±1.93μg/ml). Transmission electron microscopy observation, mRFP-GFP-LC3 fluorescence analysis, flow cytometryand assay and western blotting detection revealed that the anti-colorectal tumor activity of pogostone was dependent on inducing autophagy and apoptosis through up-regulating the expression of LC3-Ⅱ, cleaved caspase-7 and caspase-3, and decreasing the phosphorylation of AKT/mTOR. In vivo, 150mg/kg pogostone inhibited the HCT116 tumor growth in immunodeficient mice with an inhibitory rate of 43.3%, decreased the expression of Ki67, and induced apoptosis in three days.
Question: Does pogostone induce Autophagy and Apoptosis Involving PI3K/Akt/mTOR Axis in Human Colorectal Carcinoma HCT116 cells?
Output:
|
PubmedQA155658
|
[
{
"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: Astrocytomas are the most common and aggressive brain tumors characterized by their highly invasive growth. Gain of chromosome 7 with a hot spot at 7q32 appears to be the most prominent aberration in astrocytoma. Previously reports have shown that microRNA-335 (miR-335) resided on chromosome 7q32 is deregulated in many cancers; however, the biological function of miR-335 in astrocytoma has yet to be elucidated. We report that miR-335 acts as a tumor promoter in conferring tumorigenic features such as growth and invasion on malignant astrocytoma. The miR-335 level is highly elevated in C6 astrocytoma cells and human malignant astrocytomas. Ectopic expression of miR-335 in C6 cells dramatically enhances cell viability, colony-forming ability and invasiveness. Conversely, delivery of antagonist specific for miR-335 (antagomir-335) to C6 cells results in growth arrest, cell apoptosis, invasion repression and marked regression of astrocytoma xenografts. Further investigation reveals that miR-335 targets disheveled-associated activator of morphogenesis 1(Daam1) at posttranscriptional level. Moreover, silencing of endogenous Daam1 (siDaam1) could mimic the oncogenic effects of miR-335 and reverse the growth arrest, proapoptotic and invasion repression effects induced by antagomir-335. Notably, the oncogenic effects of miR-335 and siDAAM1 together with anti-tumor effects of antagomir-335 are also confirmed in human astrocytoma U87-MG cells.\n Question: Does targeting oncogenic miR-335 inhibit growth and invasion of malignant astrocytoma 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: Astrocytomas are the most common and aggressive brain tumors characterized by their highly invasive growth. Gain of chromosome 7 with a hot spot at 7q32 appears to be the most prominent aberration in astrocytoma. Previously reports have shown that microRNA-335 (miR-335) resided on chromosome 7q32 is deregulated in many cancers; however, the biological function of miR-335 in astrocytoma has yet to be elucidated. We report that miR-335 acts as a tumor promoter in conferring tumorigenic features such as growth and invasion on malignant astrocytoma. The miR-335 level is highly elevated in C6 astrocytoma cells and human malignant astrocytomas. Ectopic expression of miR-335 in C6 cells dramatically enhances cell viability, colony-forming ability and invasiveness. Conversely, delivery of antagonist specific for miR-335 (antagomir-335) to C6 cells results in growth arrest, cell apoptosis, invasion repression and marked regression of astrocytoma xenografts. Further investigation reveals that miR-335 targets disheveled-associated activator of morphogenesis 1(Daam1) at posttranscriptional level. Moreover, silencing of endogenous Daam1 (siDaam1) could mimic the oncogenic effects of miR-335 and reverse the growth arrest, proapoptotic and invasion repression effects induced by antagomir-335. Notably, the oncogenic effects of miR-335 and siDAAM1 together with anti-tumor effects of antagomir-335 are also confirmed in human astrocytoma U87-MG cells.
Question: Does targeting oncogenic miR-335 inhibit growth and invasion of malignant astrocytoma cells?
Output:
|
PubmedQA156190
|
[
{
"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: Attentional control (AC) is defined as the ability to voluntarily shift and disengage attention and is thought to moderate the relationship between preexisting risk factors for fear and the actual experience of fear. This longitudinal study elaborates on current models of AC by examining whether AC moderates or mediates effects of an ecologically valid stressor (a college examination) and also whether AC is predictive of state-like fear over longer timescales than previously reported. Based on previous findings, we hypothesized that AC would moderate the relationship between trait anxiety and affective distress in response to the examination stressor. We also tested a competing mediational model based on AC theory. These models were tested in two separate samples (sample 1, N = 219; sample 2, N = 129; Total N = 348) at two time points, at the beginning of a college semester in a large undergraduate class and 5 minutes prior to a college examination. Mediation but not moderation of anxiety by AC was supported in both samples using multiple dependent measures.\n Question: Does attentional control mediate fearful responding to an ecologically valid stressor?\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: Attentional control (AC) is defined as the ability to voluntarily shift and disengage attention and is thought to moderate the relationship between preexisting risk factors for fear and the actual experience of fear. This longitudinal study elaborates on current models of AC by examining whether AC moderates or mediates effects of an ecologically valid stressor (a college examination) and also whether AC is predictive of state-like fear over longer timescales than previously reported. Based on previous findings, we hypothesized that AC would moderate the relationship between trait anxiety and affective distress in response to the examination stressor. We also tested a competing mediational model based on AC theory. These models were tested in two separate samples (sample 1, N = 219; sample 2, N = 129; Total N = 348) at two time points, at the beginning of a college semester in a large undergraduate class and 5 minutes prior to a college examination. Mediation but not moderation of anxiety by AC was supported in both samples using multiple dependent measures.
Question: Does attentional control mediate fearful responding to an ecologically valid stressor?
Output:
|
PubmedQA95103
|
[
{
"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: Gradients of inducing molecules, or morphogens, could impose pattern on early embryos. Although there are candidates for morphogens in several systems, it is not well understood how cells might translate differences in extracellular inducer concentration into an orderly arrangement of cell types. With this question in mind, we have re-examined mesodermal patterning in Xenopus in response to the secreted growth factor activin. Previous work has shown that activin can initiate the formation of a variety of mesodermal tissues in a concentration-dependent fashion. We have sought to disentangle the roles played by individual cell responses to activin and subsequent interactions among induced cells in producing this outcome. We find that the initial response of dispersed cells to activin concentration is unexpectedly simple, showing neither the thresholds of activin concentration nor the distinct domains of gene expression that characterize the later response. The eventual emergence of an ordered series of coherent differentiation steps requires the reaggregation of the induced cells, implying that secondary interactions occur. Furthermore, when cells induced at different doses of activin are mixed, the final response apparently represents a consensus, rather than a mosaic, of the mixed populations.\n Question: Does mesodermal patterning by an inducer gradient depend on secondary cell-cell communication?\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: Gradients of inducing molecules, or morphogens, could impose pattern on early embryos. Although there are candidates for morphogens in several systems, it is not well understood how cells might translate differences in extracellular inducer concentration into an orderly arrangement of cell types. With this question in mind, we have re-examined mesodermal patterning in Xenopus in response to the secreted growth factor activin. Previous work has shown that activin can initiate the formation of a variety of mesodermal tissues in a concentration-dependent fashion. We have sought to disentangle the roles played by individual cell responses to activin and subsequent interactions among induced cells in producing this outcome. We find that the initial response of dispersed cells to activin concentration is unexpectedly simple, showing neither the thresholds of activin concentration nor the distinct domains of gene expression that characterize the later response. The eventual emergence of an ordered series of coherent differentiation steps requires the reaggregation of the induced cells, implying that secondary interactions occur. Furthermore, when cells induced at different doses of activin are mixed, the final response apparently represents a consensus, rather than a mosaic, of the mixed populations.
Question: Does mesodermal patterning by an inducer gradient depend on secondary cell-cell communication?
Output:
|
PubmedQA19215
|
[
{
"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: Leptin regulates appetite through the long isoform of its receptor in the hypothalamus. Although leptin regulates immune responses, it is still unknown whether a direct effect of leptin on lymphocytes is required. To clarify whether expression of leptin receptors on T lymphocytes modulates intestinal inflammation in mice. The model of colitis induced by transfer of CD4(+)CD45RB(high) (RB(high)) cells into scid mice was used. Wild-type (WT) or leptin receptor deficient (db/db) RB(high) cells were transferred into scid mice and development of colitis evaluated. Leptin receptors were expressed on both RB(high) and RB(low) cells. Intestinal lymphocytes of mice with colitis expressed high leptin levels compared with healthy controls whereas the opposite was true for serum leptin levels. Transfer of RB(high) cells from db/db mice induced delayed disease compared with transfer of WT cells. A high rate of apoptosis in lamina propria lymphocytes and reduced cytokine production were observed early on in scid mice receiving db/db RB(high) cells. These effects were not due to the high levels of glucocorticoids present in db/db mice as administration of corticosterone to WT mice failed to reproduce this phenomenon. High expression of peroxisome proliferator activated receptor gamma was observed in the colon of recipients of db/db compared with WT cells. Freshly isolated db/db RB(high) cells produced low levels of interferon gamma. Despite delayed onset of colitis, as disease progressed differences between mice receiving WT or db/db cells were no longer apparent.\n Question: Does leptin receptor expression on T lymphocytes modulate chronic intestinal inflammation in mice?\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: Leptin regulates appetite through the long isoform of its receptor in the hypothalamus. Although leptin regulates immune responses, it is still unknown whether a direct effect of leptin on lymphocytes is required. To clarify whether expression of leptin receptors on T lymphocytes modulates intestinal inflammation in mice. The model of colitis induced by transfer of CD4(+)CD45RB(high) (RB(high)) cells into scid mice was used. Wild-type (WT) or leptin receptor deficient (db/db) RB(high) cells were transferred into scid mice and development of colitis evaluated. Leptin receptors were expressed on both RB(high) and RB(low) cells. Intestinal lymphocytes of mice with colitis expressed high leptin levels compared with healthy controls whereas the opposite was true for serum leptin levels. Transfer of RB(high) cells from db/db mice induced delayed disease compared with transfer of WT cells. A high rate of apoptosis in lamina propria lymphocytes and reduced cytokine production were observed early on in scid mice receiving db/db RB(high) cells. These effects were not due to the high levels of glucocorticoids present in db/db mice as administration of corticosterone to WT mice failed to reproduce this phenomenon. High expression of peroxisome proliferator activated receptor gamma was observed in the colon of recipients of db/db compared with WT cells. Freshly isolated db/db RB(high) cells produced low levels of interferon gamma. Despite delayed onset of colitis, as disease progressed differences between mice receiving WT or db/db cells were no longer apparent.
Question: Does leptin receptor expression on T lymphocytes modulate chronic intestinal inflammation in mice?
Output:
|
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