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PubmedQA64639	[ { "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 elucidate the genetic basis for the pronounced resistance that the oral pathogen, Porphyromonas gingivalis (P. gingivalis), exhibits towards the cationic antimicrobial peptide, polymyxin B. A genetic screen of P. gingivalis clones generated by a Tn4400'-based random insertion mutagenesis strategy was performed to identify bacteria harboring novel genetic mutations that render P. gingivalis susceptible to killing by the cationic antimicrobial peptide, polymyxin B (PMB, 50 microg x mL(-1)). P. gingivalis (ATCC 33277) is unusually resistant to the cationic antimicrobial peptide, PMB at relatively high concentrations (200 microg x mL(-1)). Approximately 2,700 independent Tn4400'-derived mutants of P. gingivalis were examined for increased sensitivity to PMB killing at a relatively low dose (50 microg x mL(-1)). A single PMB-sensitive mutant was obtained in this phenotypic screen. We determined that the Tn4400' transposon was integrated into the gene encoding the lipid A 4'-phosphatase, PGN_0524, demonstrating that this insertion event was responsible for its increased susceptibility of this clone to PMB-dependent killing. The resulting mutant strain, designated 0524-Tn4400', was highly sensitive to PMB killing relative to wild-type P. gingivalis, and exhibited the same sensitivity as the previously characterized strain, 0524KO, which bears a genetically engineered deletion in the PGN_0524 locus. Positive ion mass spectrometric structural (MALDI-TOF MS) analyses revealed that lipid A isolates from 0524-Tn4400' and 0524KO strains displayed strikingly similar MALDI-TOF MS spectra that were substantially different from the wildtype P. gingivalis lipid A spectrum. Finally, intact 0524-Tn4400' and 0524KO mutant bacteria, as well as their corresponding LPS isolates, were significantly more potent in stimulating Toll-like receptor 4 (TLR4)-dependent E-selectin expression in human endothelial cells relative to intact wild-type P. gingivalis or its corresponding LPS isolate.\n Question: Is porphyromonas gingivalis resistance to polymyxin B determined by the lipid A 4'-phosphatase , PGN_0524?\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 elucidate the genetic basis for the pronounced resistance that the oral pathogen, Porphyromonas gingivalis (P. gingivalis), exhibits towards the cationic antimicrobial peptide, polymyxin B. A genetic screen of P. gingivalis clones generated by a Tn4400'-based random insertion mutagenesis strategy was performed to identify bacteria harboring novel genetic mutations that render P. gingivalis susceptible to killing by the cationic antimicrobial peptide, polymyxin B (PMB, 50 microg x mL(-1)). P. gingivalis (ATCC 33277) is unusually resistant to the cationic antimicrobial peptide, PMB at relatively high concentrations (200 microg x mL(-1)). Approximately 2,700 independent Tn4400'-derived mutants of P. gingivalis were examined for increased sensitivity to PMB killing at a relatively low dose (50 microg x mL(-1)). A single PMB-sensitive mutant was obtained in this phenotypic screen. We determined that the Tn4400' transposon was integrated into the gene encoding the lipid A 4'-phosphatase, PGN_0524, demonstrating that this insertion event was responsible for its increased susceptibility of this clone to PMB-dependent killing. The resulting mutant strain, designated 0524-Tn4400', was highly sensitive to PMB killing relative to wild-type P. gingivalis, and exhibited the same sensitivity as the previously characterized strain, 0524KO, which bears a genetically engineered deletion in the PGN_0524 locus. Positive ion mass spectrometric structural (MALDI-TOF MS) analyses revealed that lipid A isolates from 0524-Tn4400' and 0524KO strains displayed strikingly similar MALDI-TOF MS spectra that were substantially different from the wildtype P. gingivalis lipid A spectrum. Finally, intact 0524-Tn4400' and 0524KO mutant bacteria, as well as their corresponding LPS isolates, were significantly more potent in stimulating Toll-like receptor 4 (TLR4)-dependent E-selectin expression in human endothelial cells relative to intact wild-type P. gingivalis or its corresponding LPS isolate. Question: Is porphyromonas gingivalis resistance to polymyxin B determined by the lipid A 4'-phosphatase , PGN_0524? Output:
PubmedQA110194	[ { "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: What are the associations between the dietary intake of antioxidant nutrients and semen parameters in young men?\n Question: Is dietary intake of antioxidant nutrients associated with semen quality in young university students?\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: What are the associations between the dietary intake of antioxidant nutrients and semen parameters in young men? Question: Is dietary intake of antioxidant nutrients associated with semen quality in young university students? Output:
PubmedQA54024	[ { "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: Hypoxia-inducible factor 1 (HIF-1) regulates the expression of angiogenic growth factors. We analyzed the effect of intramuscular (i.m.) delivery of AdCA5, an adenovirus encoding a constitutively active form of the HIF-1alpha subunit, in a novel model of limb ischemia. AdCa5 or AdLacZ (6 x 10(8) pfu) was injected into male New Zealand White rabbits that were untreated or subjected to occlusion of the left superficial femoral artery by endovascular coils. Expression of mRNAs was quantified 1, 3, and 7 days after adenovirus injection into rabbits without occlusion. Calf blood pressure (BP), angiography, and immunohistochemical analyses were performed 14 days after arterial occlusion and adenovirus injection. AdCA5 increased the expression of HIF-1alpha, monocyte chemotactic protein-1, placental growth factor, platelet-derived growth factor B, stromal-derived factor 1alpha, and vascular endothelial growth factor (VEGF) mRNA as well as HIF-1alpha and VEGF protein. On day 14, AdCA5-injected limbs showed improved calf BP ratios (0.89+/-0.13 vs. 0.51+/-0.05, p=0.02), angiographic perfusion scores (3.50+/-0.56 vs. 8.33+/-1.31, p=0.007), and distal deep femoral artery diameter ratio (1.84+/-0.25 vs. 0.93+/-0.22, p=0.02) relative to those receiving AdLacZ. The capillary/myocyte ratio (0.93+/-0.03 vs. 0.78+/-0.06, p=0.04) and arterial luminal area (0.32+/-0.05 mm2 vs. 0.21+/-0.03 mm2, p=0.04) were significantly increased in the AdCA5 group.\n Question: Does constitutively active HIF-1alpha improve perfusion and arterial remodeling in an endovascular model of limb 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: Hypoxia-inducible factor 1 (HIF-1) regulates the expression of angiogenic growth factors. We analyzed the effect of intramuscular (i.m.) delivery of AdCA5, an adenovirus encoding a constitutively active form of the HIF-1alpha subunit, in a novel model of limb ischemia. AdCa5 or AdLacZ (6 x 10(8) pfu) was injected into male New Zealand White rabbits that were untreated or subjected to occlusion of the left superficial femoral artery by endovascular coils. Expression of mRNAs was quantified 1, 3, and 7 days after adenovirus injection into rabbits without occlusion. Calf blood pressure (BP), angiography, and immunohistochemical analyses were performed 14 days after arterial occlusion and adenovirus injection. AdCA5 increased the expression of HIF-1alpha, monocyte chemotactic protein-1, placental growth factor, platelet-derived growth factor B, stromal-derived factor 1alpha, and vascular endothelial growth factor (VEGF) mRNA as well as HIF-1alpha and VEGF protein. On day 14, AdCA5-injected limbs showed improved calf BP ratios (0.89+/-0.13 vs. 0.51+/-0.05, p=0.02), angiographic perfusion scores (3.50+/-0.56 vs. 8.33+/-1.31, p=0.007), and distal deep femoral artery diameter ratio (1.84+/-0.25 vs. 0.93+/-0.22, p=0.02) relative to those receiving AdLacZ. The capillary/myocyte ratio (0.93+/-0.03 vs. 0.78+/-0.06, p=0.04) and arterial luminal area (0.32+/-0.05 mm2 vs. 0.21+/-0.03 mm2, p=0.04) were significantly increased in the AdCA5 group. Question: Does constitutively active HIF-1alpha improve perfusion and arterial remodeling in an endovascular model of limb ischemia? Output:
PubmedQA174254	[ { "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 relation between ghrelin responses and meal initiation and the effects of BMI and energy status on this. The experiment had a randomised, cross-over design. Nine normal-weight (age: 33.2+/-4.8 y, BMI: 23.2+/-0.5 kg/m2) and eleven obese (age: 40.8+/- 4.7 y, BMI: 33.2+/-0.8 kg/m2) healthy men were recruited from a pool of volunteers and by advertisements. Subjects followed a three-day energy restrictive and a three-day energy balanced diet separated by one month. Each diet was followed by a time-blinded (overnight) stay at the research facility. Subjects received a breakfast (preload) and were instructed to ask for lunch when they felt hungry. Ghrelin, insulin, glucose, free fatty acids, appetite, IMI and energy intake during lunch were assessed. Postprandial decreases in ghrelin (r=-0.54; p<0.05) and the AUC of the ghrelin response (r=-0.57, p=0.01) were associated with the intermeal interval, independent of diet, but in normal weight subjects only. Lunch request was preceded by an increase in ghrelin, reaching at least 93% of fasting values. These preprandial increases in ghrelin were correlated with IMI, after energy restriction only. Ghrelin concentrations but not changes in ghrelin were correlated with appetite.\n Question: Are postprandial ghrelin responses associated with the intermeal interval in time-blinded normal weight men , but not in obese men?\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 relation between ghrelin responses and meal initiation and the effects of BMI and energy status on this. The experiment had a randomised, cross-over design. Nine normal-weight (age: 33.2+/-4.8 y, BMI: 23.2+/-0.5 kg/m2) and eleven obese (age: 40.8+/- 4.7 y, BMI: 33.2+/-0.8 kg/m2) healthy men were recruited from a pool of volunteers and by advertisements. Subjects followed a three-day energy restrictive and a three-day energy balanced diet separated by one month. Each diet was followed by a time-blinded (overnight) stay at the research facility. Subjects received a breakfast (preload) and were instructed to ask for lunch when they felt hungry. Ghrelin, insulin, glucose, free fatty acids, appetite, IMI and energy intake during lunch were assessed. Postprandial decreases in ghrelin (r=-0.54; p<0.05) and the AUC of the ghrelin response (r=-0.57, p=0.01) were associated with the intermeal interval, independent of diet, but in normal weight subjects only. Lunch request was preceded by an increase in ghrelin, reaching at least 93% of fasting values. These preprandial increases in ghrelin were correlated with IMI, after energy restriction only. Ghrelin concentrations but not changes in ghrelin were correlated with appetite. Question: Are postprandial ghrelin responses associated with the intermeal interval in time-blinded normal weight men , but not in obese men? Output:
PubmedQA125188	[ { "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: Chronic kidney disease (CKD) is an irreversible disease that diminishes length and quality of life. Emerging evidence suggests CKD progression and genomic integrity are inversely and causally related. To reduce health complications related to CKD progression, chronic aerobic exercise is often recommended. To date, appraisals of differing modes of exercise, along with postulations regarding the mechanisms responsible for observed effects, are lacking. In order to examine the ability of aerobic exercise to encourage improvements in genomic integrity, we evaluated the effects of 8 weeks of high-intensity interval training (HIIT; 85 % VO To assess genomic integrity, we examined kidney-specific messenger RNA (mRNA) expression of genes related to genomic repair and stability: Fan1, Mre11a, and telomere length as measured by T/S ratio. Following HIIT, mRNA expression of Fan1 was significantly up-regulated, compared to SED (p = 0.026) and T/S ratio was significantly increased, compared to SED (p < 0.001) and LIT (p = 0.002).\n Question: Does genomic Integrity be Favourably Affected by High-Intensity Interval Training in an Animal Model of Early-Stage Chronic Kidney 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: Chronic kidney disease (CKD) is an irreversible disease that diminishes length and quality of life. Emerging evidence suggests CKD progression and genomic integrity are inversely and causally related. To reduce health complications related to CKD progression, chronic aerobic exercise is often recommended. To date, appraisals of differing modes of exercise, along with postulations regarding the mechanisms responsible for observed effects, are lacking. In order to examine the ability of aerobic exercise to encourage improvements in genomic integrity, we evaluated the effects of 8 weeks of high-intensity interval training (HIIT; 85 % VO To assess genomic integrity, we examined kidney-specific messenger RNA (mRNA) expression of genes related to genomic repair and stability: Fan1, Mre11a, and telomere length as measured by T/S ratio. Following HIIT, mRNA expression of Fan1 was significantly up-regulated, compared to SED (p = 0.026) and T/S ratio was significantly increased, compared to SED (p < 0.001) and LIT (p = 0.002). Question: Does genomic Integrity be Favourably Affected by High-Intensity Interval Training in an Animal Model of Early-Stage Chronic Kidney Disease? Output:
PubmedQA109817	[ { "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: Primary open-angle glaucoma (POAG) is a common but complex disease with a strong genetic component. Notably, few genes have been robustly associated with POAG. An obvious group of genes to test as susceptibility factors for POAG are the developmental genes forkhead box C1 (FOXC1), transforming growth factor-beta 2 (TGFβ2), and bone morphogenic protein 4 (BMP4). These genes are known to play important roles in the normal morphogenesis of the anterior segment and/or have been implicated in intra-ocular pressure (IOP) regulation and trabecular meshwork function. This study investigates the role of FOXC1, TGFβ2, and BMP4 in POAG. The contribution of common genetic variation at the FOXC1, TGFβ2, and BMP4 loci to risk of POAG was investigated in a case-control association study in 330 British Caucasian individuals comprised of 272 high-tension glaucoma (HTG) and 58 ocular hypertension (OHT), and 276 matched controls. All the single nucleotide polymorphisms (SNPs) were in Hardy-Weinberg equilibrium and genotyping success rate was >92% for all SNPs. With the exception of a weak association between the BMP4 tagging SNP rs2761884 and the combined patient group HTG+OHT that did not withstand permutation testing (uncorrected p=0.0400, corrected p=0.1320), no associations (p<0.05) were identified between the patient groups (HTG and OHT) and FOXC1, TGFβ2, and BMP4 alleles and haplotypes compared to the control group.\n Question: Are common TGFβ2 , BMP4 , and FOXC1 variants associated with primary open-angle glaucoma?\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: Primary open-angle glaucoma (POAG) is a common but complex disease with a strong genetic component. Notably, few genes have been robustly associated with POAG. An obvious group of genes to test as susceptibility factors for POAG are the developmental genes forkhead box C1 (FOXC1), transforming growth factor-beta 2 (TGFβ2), and bone morphogenic protein 4 (BMP4). These genes are known to play important roles in the normal morphogenesis of the anterior segment and/or have been implicated in intra-ocular pressure (IOP) regulation and trabecular meshwork function. This study investigates the role of FOXC1, TGFβ2, and BMP4 in POAG. The contribution of common genetic variation at the FOXC1, TGFβ2, and BMP4 loci to risk of POAG was investigated in a case-control association study in 330 British Caucasian individuals comprised of 272 high-tension glaucoma (HTG) and 58 ocular hypertension (OHT), and 276 matched controls. All the single nucleotide polymorphisms (SNPs) were in Hardy-Weinberg equilibrium and genotyping success rate was >92% for all SNPs. With the exception of a weak association between the BMP4 tagging SNP rs2761884 and the combined patient group HTG+OHT that did not withstand permutation testing (uncorrected p=0.0400, corrected p=0.1320), no associations (p<0.05) were identified between the patient groups (HTG and OHT) and FOXC1, TGFβ2, and BMP4 alleles and haplotypes compared to the control group. Question: Are common TGFβ2 , BMP4 , and FOXC1 variants associated with primary open-angle glaucoma? Output:
PubmedQA202108	[ { "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: Abscission zones (AZ) are sites where leaves and other organs are shed. Investigating the AZ by classical biochemical techniques is difficult due to its small size and because the surrounding tissue is not involved in abscission. The goals of this study were to determine whether AZ cell walls are chemically unique from the other cells of the petiole, perhaps making them more susceptible to enzymatic degradation during abscission and to identify which cell wall polysaccharides are degraded during abscission. A battery of antibodies that recognize a large number of cell wall polysaccharide and glycoprotein epitopes was used to probe sections of the Impatiens leaf AZ at several time points in the abscission process. Prior to abscission, the walls of the AZ cells were found to be similar in composition to the walls of the cells both proximal and distal to the AZ. Of all the epitopes monitored, only the highly de-esterified homogalacturonans (HG) of the middle lamellae were found to be reduced post-abscission and only at the plane of separation. More highly esterified homogalacturonans, as well as other pectin and xyloglucan epitopes were not affected. Furthermore, cellulose, as detected by an endoglucanase-gold probe and cellulose-binding module staining, was unaffected, even on the walls of the cells facing the separation site.\n Question: Is leaf abscission in Impatiens ( Balsaminaceae ) due to loss of highly de-esterified homogalacturonans in the middle lamellae?\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: Abscission zones (AZ) are sites where leaves and other organs are shed. Investigating the AZ by classical biochemical techniques is difficult due to its small size and because the surrounding tissue is not involved in abscission. The goals of this study were to determine whether AZ cell walls are chemically unique from the other cells of the petiole, perhaps making them more susceptible to enzymatic degradation during abscission and to identify which cell wall polysaccharides are degraded during abscission. A battery of antibodies that recognize a large number of cell wall polysaccharide and glycoprotein epitopes was used to probe sections of the Impatiens leaf AZ at several time points in the abscission process. Prior to abscission, the walls of the AZ cells were found to be similar in composition to the walls of the cells both proximal and distal to the AZ. Of all the epitopes monitored, only the highly de-esterified homogalacturonans (HG) of the middle lamellae were found to be reduced post-abscission and only at the plane of separation. More highly esterified homogalacturonans, as well as other pectin and xyloglucan epitopes were not affected. Furthermore, cellulose, as detected by an endoglucanase-gold probe and cellulose-binding module staining, was unaffected, even on the walls of the cells facing the separation site. Question: Is leaf abscission in Impatiens ( Balsaminaceae ) due to loss of highly de-esterified homogalacturonans in the middle lamellae? Output:
PubmedQA30668	[ { "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 the present phase II randomized study, two different schedules of ondansetron were investigated as rescue antiemetic treatment for delayed emesis related to moderately emetogenic chemotherapy (MEC). Patients scheduled to receive a first course of MEC were randomized to ondansetron 8 mg intramuscularly (arm A) or ondansetron 16 mg orally (arm B) as rescue antiemetic treatment for delayed emesis. Efficacy and safety evaluation was performed from days 2 to 6 through the administration of a diary plus a questionnaire in which the emetic episodes and the use of the assigned rescue treatment were recorded. All patients received standard prophylaxis for delayed emesis with oral dexamethasone 8 mg daily for 4 days starting on day 2. Eighty-nine patients were enrolled into the study, of whom 44 were randomized to arm A and 45 to arm B. Twenty-two patients in each arm developed grade 1-2 delayed nausea/vomiting, all of which recurred to the rescue study treatment. Oral ondansetron resulted superior to intramuscular ondansetron in terms of complete response for nausea (77.3% vs 40.9%, respectively, p = 0.01) and vomiting (81.8% vs 31.8%, respectively, p = 0.001). Both schedules resulted to be very well tolerated, and no differences in toxicity were observed between the two arms of treatment. Furthermore, personal satisfaction about the use of the assigned rescue study medication was significantly higher in arm B.\n Question: Is oral ondansetron highly active as rescue antiemetic treatment for moderately emetogenic chemotherapy : results of a randomized phase II 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: In the present phase II randomized study, two different schedules of ondansetron were investigated as rescue antiemetic treatment for delayed emesis related to moderately emetogenic chemotherapy (MEC). Patients scheduled to receive a first course of MEC were randomized to ondansetron 8 mg intramuscularly (arm A) or ondansetron 16 mg orally (arm B) as rescue antiemetic treatment for delayed emesis. Efficacy and safety evaluation was performed from days 2 to 6 through the administration of a diary plus a questionnaire in which the emetic episodes and the use of the assigned rescue treatment were recorded. All patients received standard prophylaxis for delayed emesis with oral dexamethasone 8 mg daily for 4 days starting on day 2. Eighty-nine patients were enrolled into the study, of whom 44 were randomized to arm A and 45 to arm B. Twenty-two patients in each arm developed grade 1-2 delayed nausea/vomiting, all of which recurred to the rescue study treatment. Oral ondansetron resulted superior to intramuscular ondansetron in terms of complete response for nausea (77.3% vs 40.9%, respectively, p = 0.01) and vomiting (81.8% vs 31.8%, respectively, p = 0.001). Both schedules resulted to be very well tolerated, and no differences in toxicity were observed between the two arms of treatment. Furthermore, personal satisfaction about the use of the assigned rescue study medication was significantly higher in arm B. Question: Is oral ondansetron highly active as rescue antiemetic treatment for moderately emetogenic chemotherapy : results of a randomized phase II study? Output:
PubmedQA189473	[ { "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 report the long-term outcomes in patients with multiple myeloma (MM) who receive dialysis treatment for acute kidney injury (AKI) due to myeloma cast nephropathy and subsequently recover renal function. Patients presenting with dialysis-dependent AKI secondary to myeloma cast nephropathy and subsequently recovering independent renal function between January 2005 and December 2012 were included in this study. Both renal and haematological parameters were collected at multiple time points as part of routine clinic practice. Factors associated with renal function and overall survival (OS) were determined. Twenty-four patients fulfilled the criteria for inclusion. Mean age was 62.1 years; 75% were male and 75% were of White ethnicity. The median OS was 64.1 months (95% confidence interval [CI] 34.8-93.3). Twenty-three (95.8%) patients remained dialysis-independent until death or end of follow-up; one patient required further haemodialysis treatment during the follow-up period. The independent determinant of worse OS was a known history of chronic kidney disease (CKD) at presentation. Shorter length of time on haemodialysis and higher percentage reduction in clonal serum FLC at day 21 from baseline predicted better excretory renal function (estimated glomerular filtration rate) at 6 months.\n Question: Do patients with multiple myeloma have excellent long-term outcomes after recovery from dialysis-dependent acute kidney injury?\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 report the long-term outcomes in patients with multiple myeloma (MM) who receive dialysis treatment for acute kidney injury (AKI) due to myeloma cast nephropathy and subsequently recover renal function. Patients presenting with dialysis-dependent AKI secondary to myeloma cast nephropathy and subsequently recovering independent renal function between January 2005 and December 2012 were included in this study. Both renal and haematological parameters were collected at multiple time points as part of routine clinic practice. Factors associated with renal function and overall survival (OS) were determined. Twenty-four patients fulfilled the criteria for inclusion. Mean age was 62.1 years; 75% were male and 75% were of White ethnicity. The median OS was 64.1 months (95% confidence interval [CI] 34.8-93.3). Twenty-three (95.8%) patients remained dialysis-independent until death or end of follow-up; one patient required further haemodialysis treatment during the follow-up period. The independent determinant of worse OS was a known history of chronic kidney disease (CKD) at presentation. Shorter length of time on haemodialysis and higher percentage reduction in clonal serum FLC at day 21 from baseline predicted better excretory renal function (estimated glomerular filtration rate) at 6 months. Question: Do patients with multiple myeloma have excellent long-term outcomes after recovery from dialysis-dependent acute kidney injury? Output:
PubmedQA28866	[ { "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 examined cardiomyocyte apoptosis in chronic heart failure (HF) and its possible link to elevated wall stress. Moderate HF was produced in sheep by sequential coronary microembolization. Six months later, the animals remained in a stable compensated haemodynamic state of HF. Apoptosis of cardiomyocytes in left ventricles was verified using Western blotting based on increased expression of: the apoptosis-associated death receptor Fas (1.5-fold); its ligand (FasL, 2.0-fold); and an upstream protease caspase-8 (2.7-fold) as well as its active cleavage peptide, p20 (5.6-fold). Previously we have reported the elevated expression of caspase-3 in the same animal model. The occurrence of apoptotic cardiomyocytes (0.3%) was quantified by TUNEL assays. Haemodynamic analysis indicated that ventricular dilatation, without wall thickening, caused a 2-fold increase in LV wall stress which, together with LV end-diastolic pressure, was linearly correlated with expression of Fas/FasL. Immunohistochemical studies localized FasL and caspase-8 to intercalated discs, suggesting that wall stress may play a role in initiating cardiomyocyte apoptosis.\n Question: Is cardiomyocyte apoptosis associated with increased wall stress in chronic failing left ventricle?\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 examined cardiomyocyte apoptosis in chronic heart failure (HF) and its possible link to elevated wall stress. Moderate HF was produced in sheep by sequential coronary microembolization. Six months later, the animals remained in a stable compensated haemodynamic state of HF. Apoptosis of cardiomyocytes in left ventricles was verified using Western blotting based on increased expression of: the apoptosis-associated death receptor Fas (1.5-fold); its ligand (FasL, 2.0-fold); and an upstream protease caspase-8 (2.7-fold) as well as its active cleavage peptide, p20 (5.6-fold). Previously we have reported the elevated expression of caspase-3 in the same animal model. The occurrence of apoptotic cardiomyocytes (0.3%) was quantified by TUNEL assays. Haemodynamic analysis indicated that ventricular dilatation, without wall thickening, caused a 2-fold increase in LV wall stress which, together with LV end-diastolic pressure, was linearly correlated with expression of Fas/FasL. Immunohistochemical studies localized FasL and caspase-8 to intercalated discs, suggesting that wall stress may play a role in initiating cardiomyocyte apoptosis. Question: Is cardiomyocyte apoptosis associated with increased wall stress in chronic failing left ventricle? Output:
PubmedQA185983	[ { "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 evaluated the ability of flexible instruments compared with rigid instruments to place anatomic femoral tunnels in anterior cruciate ligament reconstructions by use of both transtibial drilling and anteromedial drilling without hyperflexion. Rigid and flexible pins were placed in 12 matched pairs of cadaveric knees with transtibial drilling (6 pairs) and anteromedial drilling (6 pairs) at 110° of flexion. Intraosseous pin lengths, femoral exit locations, and tunnel alignment were measured. Transtibial drilling with rigid pins placed relatively vertical femoral tunnels 5.8 ± 1.0 mm superior to the central anterior cruciate ligament insertion. Transtibial drilling with flexible pins placed tunnels in the center of the femoral attachment, but the tunnels were relatively close to the posterior femoral cortex, with a mean distance of 8.0 ± 5.9 mm (P < .05), compared with transtibial drilling with rigid pins. Anteromedial drilling resulted in central anatomic pin placements with rigid and flexible instruments. Tunnel lengths with flexible pins were longer (42.0 ± 7.2 mm) compared with tunnel lengths with rigid pins (32.5 ± 7.1 mm) (P < .01). Flexible pins exited farther from the posterior cortex compared with rigid pins (P < .01). In 3 of 6 knees with rigid pins, the exit point was at the posterior border of the femoral cortex. All flexible pins exited a safe distance from the posterior femoral cortex.\n Question: Do flexible instruments outperform rigid instruments to place anatomic anterior cruciate ligament femoral tunnels without hyperflexion?\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 evaluated the ability of flexible instruments compared with rigid instruments to place anatomic femoral tunnels in anterior cruciate ligament reconstructions by use of both transtibial drilling and anteromedial drilling without hyperflexion. Rigid and flexible pins were placed in 12 matched pairs of cadaveric knees with transtibial drilling (6 pairs) and anteromedial drilling (6 pairs) at 110° of flexion. Intraosseous pin lengths, femoral exit locations, and tunnel alignment were measured. Transtibial drilling with rigid pins placed relatively vertical femoral tunnels 5.8 ± 1.0 mm superior to the central anterior cruciate ligament insertion. Transtibial drilling with flexible pins placed tunnels in the center of the femoral attachment, but the tunnels were relatively close to the posterior femoral cortex, with a mean distance of 8.0 ± 5.9 mm (P < .05), compared with transtibial drilling with rigid pins. Anteromedial drilling resulted in central anatomic pin placements with rigid and flexible instruments. Tunnel lengths with flexible pins were longer (42.0 ± 7.2 mm) compared with tunnel lengths with rigid pins (32.5 ± 7.1 mm) (P < .01). Flexible pins exited farther from the posterior cortex compared with rigid pins (P < .01). In 3 of 6 knees with rigid pins, the exit point was at the posterior border of the femoral cortex. All flexible pins exited a safe distance from the posterior femoral cortex. Question: Do flexible instruments outperform rigid instruments to place anatomic anterior cruciate ligament femoral tunnels without hyperflexion? Output:
PubmedQA87816	[ { "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: Programmed cell death (PCD) is an important process for the development and maintenance of multicellular eukaryotes. In animals, there are three morphologically distinct cell death types: apoptosis, autophagic cell death, and necrosis. The search for an all-encompassing classification system based on plant cell death morphology continues. The lace plant is a model system for studying PCD as leaf perforations form predictably via this process during development. This study induced death in cells that do not undergo developmental PCD using various degrees and types of stress (heat, salt, acid and base). Cell death was observed via live cell imaging and compared to the developmental PCD pathway. Morphological similarities between developmental and induced PCD included: disappearance of anthocyanin from the vacuole, increase in vesicle formation, nuclear condensation, and fusing of vesicles containing organelles to the vacuole prior to tonoplast collapse. Plasma membrane retraction was a key feature of developmental PCD but did not occur in all induced modes of cell death.\n Question: Does a comparison of induced and developmental cell death morphologies in lace plant ( Aponogeton madagascariensis ) leave?\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: Programmed cell death (PCD) is an important process for the development and maintenance of multicellular eukaryotes. In animals, there are three morphologically distinct cell death types: apoptosis, autophagic cell death, and necrosis. The search for an all-encompassing classification system based on plant cell death morphology continues. The lace plant is a model system for studying PCD as leaf perforations form predictably via this process during development. This study induced death in cells that do not undergo developmental PCD using various degrees and types of stress (heat, salt, acid and base). Cell death was observed via live cell imaging and compared to the developmental PCD pathway. Morphological similarities between developmental and induced PCD included: disappearance of anthocyanin from the vacuole, increase in vesicle formation, nuclear condensation, and fusing of vesicles containing organelles to the vacuole prior to tonoplast collapse. Plasma membrane retraction was a key feature of developmental PCD but did not occur in all induced modes of cell death. Question: Does a comparison of induced and developmental cell death morphologies in lace plant ( Aponogeton madagascariensis ) leave? Output:
PubmedQA107414	[ { "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: Transcription factor 7-like 2 (TCF7L2) is a Wnt-signalling-associated transcription factor. Genetic studies have clearly demonstrated that DNA polymorphisms within TCF7L2 confer the strongest known association with increased risk of type 2 diabetes. However, the impact of the TCF7L2 type-2-diabetes-associated rs7903146 T allele on biological function and morphology of human pancreatic islets is unknown. Paraffin sections of pancreases from 187 brain-deceased donors (HbA(1c) <6.5% [48 mmol/mol]) were used to genotype the TCF7L2 variant rs7903146 and evaluate its impact on islet morphology and alpha and beta cell subpopulations following immunostaining for glucagon and C-peptide. Following islet isolation, we investigated the correlation between TCF7L2 genotype and in vitro islet functional variables from our in-house pancreatic database. TCF7L2 rs7903146 (T/T) was associated with reduced basal and glucose-stimulated insulin secretion in isolated human islets, and reduced islet density in whole pancreas. Morphological analysis demonstrated islet size was increased in T/T carriers. Furthermore, rs7903146 was associated with an increased glucagon/C-peptide ratio, especially in bigger islets.\n Question: Does tCF7L2 rs7903146 impair islet function and morphology in non-diabetic individuals?\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: Transcription factor 7-like 2 (TCF7L2) is a Wnt-signalling-associated transcription factor. Genetic studies have clearly demonstrated that DNA polymorphisms within TCF7L2 confer the strongest known association with increased risk of type 2 diabetes. However, the impact of the TCF7L2 type-2-diabetes-associated rs7903146 T allele on biological function and morphology of human pancreatic islets is unknown. Paraffin sections of pancreases from 187 brain-deceased donors (HbA(1c) <6.5% [48 mmol/mol]) were used to genotype the TCF7L2 variant rs7903146 and evaluate its impact on islet morphology and alpha and beta cell subpopulations following immunostaining for glucagon and C-peptide. Following islet isolation, we investigated the correlation between TCF7L2 genotype and in vitro islet functional variables from our in-house pancreatic database. TCF7L2 rs7903146 (T/T) was associated with reduced basal and glucose-stimulated insulin secretion in isolated human islets, and reduced islet density in whole pancreas. Morphological analysis demonstrated islet size was increased in T/T carriers. Furthermore, rs7903146 was associated with an increased glucagon/C-peptide ratio, especially in bigger islets. Question: Does tCF7L2 rs7903146 impair islet function and morphology in non-diabetic individuals? Output:
PubmedQA65809	[ { "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: Oxidative stress plays a critical role in the development of cataracts, and glutaredoxins (Grxs) play a major protective role against oxidative stress in the lens. This study aimed to reveal the global regulatory network of Grx1. Stable isotope labeling by amino acids in cell culture (SILAC) was used in a proteome-wide quantitative approach to identify the Grx1 regulatory signaling cascades at a subcellular resolution in response to oxidative stress. A total of 1,291 proteins were identified to be differentially expressed, which were further categorized into a variety of signaling cascades including redox regulation, apoptosis, cell cycle control, glucose metabolism, protein synthesis, DNA damage response, protein folding, proteasome and others. Thirteen key signaling node molecules representing each pathway were verified. Notably, the subunits of proteasome complexes, which play a pivotal role in preventing cytotoxicity via the degradation of oxidized proteins, were highly enriched by Grx1. By data-dependent network analysis, we found global functional links among these signaling pathways which elucidate how Grx1 integrates the operation of these regulatory networks in an interconnected way for H2O2-induced response.\n Question: Does glutaredoxin desensitize Lens to Oxidative Stress by Connecting and Integrating Specific Signaling and Transcriptional Regulation for Antioxidant 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: Oxidative stress plays a critical role in the development of cataracts, and glutaredoxins (Grxs) play a major protective role against oxidative stress in the lens. This study aimed to reveal the global regulatory network of Grx1. Stable isotope labeling by amino acids in cell culture (SILAC) was used in a proteome-wide quantitative approach to identify the Grx1 regulatory signaling cascades at a subcellular resolution in response to oxidative stress. A total of 1,291 proteins were identified to be differentially expressed, which were further categorized into a variety of signaling cascades including redox regulation, apoptosis, cell cycle control, glucose metabolism, protein synthesis, DNA damage response, protein folding, proteasome and others. Thirteen key signaling node molecules representing each pathway were verified. Notably, the subunits of proteasome complexes, which play a pivotal role in preventing cytotoxicity via the degradation of oxidized proteins, were highly enriched by Grx1. By data-dependent network analysis, we found global functional links among these signaling pathways which elucidate how Grx1 integrates the operation of these regulatory networks in an interconnected way for H2O2-induced response. Question: Does glutaredoxin desensitize Lens to Oxidative Stress by Connecting and Integrating Specific Signaling and Transcriptional Regulation for Antioxidant Response? Output:
PubmedQA88	[ { "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: Guillotine below-knee amputation (BKA) for wet gangrene is an unfortunate complication of poorly controlled diabetes. We examined risk factors associated with wound complications after amputation formalization in this patient population. Retrospective data over a 4-year period were collected for patients undergoing guillotine BKA for wet gangrene followed by staged formalization. Patients with abnormal distal pulses underwent evaluation before formalization to stratify for peripheral arterial disease (PAD). Those patients with palpable pulses and no known PAD went to formalization without further investigation. Poor operative candidates underwent delayed formalization to allow for preoperative optimization. Patient history, interval between surgeries, pathology, and preformalization laboratories were tested for significance. Primary outcome was postformalization wound complication. Fifty-six amputations in 55 patients met inclusion criteria. Wound complications after formalization occurred in 18 cases, all BKAs (32%). A history of PAD was present in 19 patients (34.5%). On pathology, 23 patients (41%) had small-vessel atherosclerosis or arteriosclerosis. There was no association between wound complications and history of PAD (P = 0.4), preformalization albumin (P = 0.09), glucose (P = 0.9), white blood cell count (P = 0.4), or delayed versus expedited formalization (P = 0.8). Only the presence of microvascular disease on formal pathology was predictive of wound complications (P = 0.03). There was no association between microvascular disease on pathology and a history of PAD (P = 0.07).\n Question: Is unrecognized arteriosclerosis associated with wound complications after below-knee amputation?\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: Guillotine below-knee amputation (BKA) for wet gangrene is an unfortunate complication of poorly controlled diabetes. We examined risk factors associated with wound complications after amputation formalization in this patient population. Retrospective data over a 4-year period were collected for patients undergoing guillotine BKA for wet gangrene followed by staged formalization. Patients with abnormal distal pulses underwent evaluation before formalization to stratify for peripheral arterial disease (PAD). Those patients with palpable pulses and no known PAD went to formalization without further investigation. Poor operative candidates underwent delayed formalization to allow for preoperative optimization. Patient history, interval between surgeries, pathology, and preformalization laboratories were tested for significance. Primary outcome was postformalization wound complication. Fifty-six amputations in 55 patients met inclusion criteria. Wound complications after formalization occurred in 18 cases, all BKAs (32%). A history of PAD was present in 19 patients (34.5%). On pathology, 23 patients (41%) had small-vessel atherosclerosis or arteriosclerosis. There was no association between wound complications and history of PAD (P = 0.4), preformalization albumin (P = 0.09), glucose (P = 0.9), white blood cell count (P = 0.4), or delayed versus expedited formalization (P = 0.8). Only the presence of microvascular disease on formal pathology was predictive of wound complications (P = 0.03). There was no association between microvascular disease on pathology and a history of PAD (P = 0.07). Question: Is unrecognized arteriosclerosis associated with wound complications after below-knee amputation? Output:
PubmedQA106087	[ { "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: Septic shock is a major healthcare problem with a high mortality rate that might be caused by immunosuppression. Programmed cell death receptor-1 (PD-1) and programmed cell death receptor ligand-1 (PD-L1), which are co-inhibitory receptor molecules, participate in sepsis-induced immunosuppression. In this study, we investigated which PD-1-related molecules can be used to evaluate the risk stratification and prognosis of septic patients. Furthermore, we explored the prognostic significance of a combination of ideal predictors and conventional clinical risk parameters in septic shock patients. In total, 29 healthy controls, 59 septic patients, and 76 septic shock patients were enrolled in this study. Considering that the focus of the research was on the second phase of sepsis, blood samples were obtained at days 3-4 after the onset of systemic inflammatory response syndrome (SIRS). PD-1 and PD-L1 expression were measured on circulating CD4(+) T cells, CD8(+) T cells, and monocytes (PD-L1 only) by flow cytometry. Our results showed that only monocyte PD-L1 expression gradually increased, based on the increasing severity of disease (P < 0.001). Similarly, multivariate logistic regression analysis showed that only monocyte PD-L1 expression was an independent predictor of 28-day mortality in septic shock patients. Area under the receiver operating characteristic curve analysis of the combination of monocyte PD-L1 expression and conventional clinical risk parameters indicated a more significant prognostic ability than analysis of each parameter alone.\n Question: Is monocyte programmed death ligand-1 expression after 3-4 days of sepsis associated with risk stratification and mortality in septic patients : a prospective cohort study?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Septic shock is a major healthcare problem with a high mortality rate that might be caused by immunosuppression. Programmed cell death receptor-1 (PD-1) and programmed cell death receptor ligand-1 (PD-L1), which are co-inhibitory receptor molecules, participate in sepsis-induced immunosuppression. In this study, we investigated which PD-1-related molecules can be used to evaluate the risk stratification and prognosis of septic patients. Furthermore, we explored the prognostic significance of a combination of ideal predictors and conventional clinical risk parameters in septic shock patients. In total, 29 healthy controls, 59 septic patients, and 76 septic shock patients were enrolled in this study. Considering that the focus of the research was on the second phase of sepsis, blood samples were obtained at days 3-4 after the onset of systemic inflammatory response syndrome (SIRS). PD-1 and PD-L1 expression were measured on circulating CD4(+) T cells, CD8(+) T cells, and monocytes (PD-L1 only) by flow cytometry. Our results showed that only monocyte PD-L1 expression gradually increased, based on the increasing severity of disease (P < 0.001). Similarly, multivariate logistic regression analysis showed that only monocyte PD-L1 expression was an independent predictor of 28-day mortality in septic shock patients. Area under the receiver operating characteristic curve analysis of the combination of monocyte PD-L1 expression and conventional clinical risk parameters indicated a more significant prognostic ability than analysis of each parameter alone. Question: Is monocyte programmed death ligand-1 expression after 3-4 days of sepsis associated with risk stratification and mortality in septic patients : a prospective cohort study? Output:
PubmedQA94058	[ { "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 adults, the treatment of Helicobacter pylori infection is only recommended for patients with active gastric or duodenal ulcers. It is not known whether similar guidelines can be applied to children because the prevalence of peptic ulcer disease in childhood is estimated to be much lower than in adults. The purpose of this study was to determine whether treatment of H. pylori gastritis would improve symptoms of dyspepsia in children. Sixteen patients (5 boys, 11 girls) aged 14 +/- 1.2 years who had symptoms of dyspepsia were evaluated using upper gastrointestinal endoscopy with biopsies to establish the diagnosis of H. pylori gastritis. They were treated for 2 weeks with clarithromycin, amoxicillin, and a proton pump inhibitor. Dyspepsia symptoms were evaluated by a questionnaire before and after treatment of the infection. The effect of H. pylori treatment on the total symptom score was analyzed with use of the Student t test. Values are presented as mean +/- SEM. All patients had antral nodularity and chronic active gastritis with spiral-shaped organisms but no evidence of peptic ulcer disease. Mean total symptom score decreased significantly at 2 to 4 weeks after treatment (12.6 +/- 0.9 vs. 2.1 +/- 0.5 P < 0.001), and it remained low (2.9 +/- 0.7) at follow-up 9.7 +/- 1.4 months (range, 2-24 months later).\n Question: Does treatment of Helicobacter pylori gastritis improve dyspeptic symptoms in children?\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 adults, the treatment of Helicobacter pylori infection is only recommended for patients with active gastric or duodenal ulcers. It is not known whether similar guidelines can be applied to children because the prevalence of peptic ulcer disease in childhood is estimated to be much lower than in adults. The purpose of this study was to determine whether treatment of H. pylori gastritis would improve symptoms of dyspepsia in children. Sixteen patients (5 boys, 11 girls) aged 14 +/- 1.2 years who had symptoms of dyspepsia were evaluated using upper gastrointestinal endoscopy with biopsies to establish the diagnosis of H. pylori gastritis. They were treated for 2 weeks with clarithromycin, amoxicillin, and a proton pump inhibitor. Dyspepsia symptoms were evaluated by a questionnaire before and after treatment of the infection. The effect of H. pylori treatment on the total symptom score was analyzed with use of the Student t test. Values are presented as mean +/- SEM. All patients had antral nodularity and chronic active gastritis with spiral-shaped organisms but no evidence of peptic ulcer disease. Mean total symptom score decreased significantly at 2 to 4 weeks after treatment (12.6 +/- 0.9 vs. 2.1 +/- 0.5 P < 0.001), and it remained low (2.9 +/- 0.7) at follow-up 9.7 +/- 1.4 months (range, 2-24 months later). Question: Does treatment of Helicobacter pylori gastritis improve dyspeptic symptoms in children? Output:
PubmedQA90438	[ { "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: Drozitumab is a fully human agonistic monoclonal antibody that binds to death receptor DR5 and induces apoptosis. However, drozitumab resistance is a major obstacle limiting anticancer efficacy. We examined the potential for the chemotherapeutic agent doxorubicin to overcome resistance against drozitumab-resistant breast cancer cells both in vitro and in vivo. Treatment with doxorubicin increased cell surface expression of DR5, reduced levels of Inhibitors of Apoptosis Proteins (cIAPs) and re-sensitised cells to drozitumab-induced apoptosis. Animals implanted with resistant breast cancer cells into the mammary fat pad and treated with a combination of drozitumab and doxorubicin showed inhibition of tumor growth and a substantial delay in tumor progression compared to untreated controls and mice treated with each agent alone.\n Question: Does doxorubicin overcome resistance to drozitumab by antagonizing Inhibitor of Apoptosis Proteins ( IAPs )?\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: Drozitumab is a fully human agonistic monoclonal antibody that binds to death receptor DR5 and induces apoptosis. However, drozitumab resistance is a major obstacle limiting anticancer efficacy. We examined the potential for the chemotherapeutic agent doxorubicin to overcome resistance against drozitumab-resistant breast cancer cells both in vitro and in vivo. Treatment with doxorubicin increased cell surface expression of DR5, reduced levels of Inhibitors of Apoptosis Proteins (cIAPs) and re-sensitised cells to drozitumab-induced apoptosis. Animals implanted with resistant breast cancer cells into the mammary fat pad and treated with a combination of drozitumab and doxorubicin showed inhibition of tumor growth and a substantial delay in tumor progression compared to untreated controls and mice treated with each agent alone. Question: Does doxorubicin overcome resistance to drozitumab by antagonizing Inhibitor of Apoptosis Proteins ( IAPs )? Output:
PubmedQA64822	[ { "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 ketogenic diet has long been used to treat epilepsy, but its mechanism is not yet clearly understood. To explore the potential mechanism, we analyzed the changes in gene expression induced by the ketogenic diet in the rat kainic acid (KA) epilepsy model. KA-administered rats were fed the ketogenic diet or a normal diet for 4 weeks, and microarray analysis was performed with their brain tissues. The effects of the ketogenic diet on cathepsin E messenger ribonucleic acid (mRNA) expression were analyzed in KA-administered and normal saline-administered groups with semi-quantitative and real-time reverse transcription polymerase chain reaction (RT-PCR). Brain tissues were dissected into 8 regions to compare differential effects of the ketogenic diet on cathepsin E mRNA expression. Immunohistochemistry with an anti-cathepsin E antibody was performed on slides of hippocampus obtained from whole brain paraffin blocks. The microarray data and subsequent RT-PCR experiments showed that KA increased the mRNA expression of cathepsin E, known to be related to neuronal cell death, in most brain areas except the brain stem, and these increases of cathepsin E mRNA expression were suppressed by the ketogenic diet. The expression of cathepsin E mRNA in the control group, however, was not significantly affected by the ketogenic diet. The change in cathepsin E mRNA expression was greatest in the hippocampus. The protein level of cathepsin E in the hippocampus of KA-administered rat was elevated in immunohistochemistry and the ketogenic diet suppressed this increase.\n Question: Does the ketogenic diet suppress the cathepsin E expression induced by kainic acid in the 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 ketogenic diet has long been used to treat epilepsy, but its mechanism is not yet clearly understood. To explore the potential mechanism, we analyzed the changes in gene expression induced by the ketogenic diet in the rat kainic acid (KA) epilepsy model. KA-administered rats were fed the ketogenic diet or a normal diet for 4 weeks, and microarray analysis was performed with their brain tissues. The effects of the ketogenic diet on cathepsin E messenger ribonucleic acid (mRNA) expression were analyzed in KA-administered and normal saline-administered groups with semi-quantitative and real-time reverse transcription polymerase chain reaction (RT-PCR). Brain tissues were dissected into 8 regions to compare differential effects of the ketogenic diet on cathepsin E mRNA expression. Immunohistochemistry with an anti-cathepsin E antibody was performed on slides of hippocampus obtained from whole brain paraffin blocks. The microarray data and subsequent RT-PCR experiments showed that KA increased the mRNA expression of cathepsin E, known to be related to neuronal cell death, in most brain areas except the brain stem, and these increases of cathepsin E mRNA expression were suppressed by the ketogenic diet. The expression of cathepsin E mRNA in the control group, however, was not significantly affected by the ketogenic diet. The change in cathepsin E mRNA expression was greatest in the hippocampus. The protein level of cathepsin E in the hippocampus of KA-administered rat was elevated in immunohistochemistry and the ketogenic diet suppressed this increase. Question: Does the ketogenic diet suppress the cathepsin E expression induced by kainic acid in the rat brain? Output:
PubmedQA7426	[ { "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: Liver cirrhosis has been shown to be associated with impaired outcome in patients who underwent elective surgery. We therefore investigated the impact of alcohol abuse and subsequent liver cirrhosis on outcome in multiple trauma patients. Using the multi-centre population-based Trauma Registry of the German Society for Trauma Surgery, we retrospectively compared outcome in patients (ISS ≥ 9, ≥ 18) with pre-existing alcohol abuse and liver cirrhosis with healthy trauma victims in univariate and matched-pair analysis. Means were compared using Student's t-test and analysis of variance (ANOVA) and categorical variables using χ(2) (p<0.05=significant). Overall 13,527 patients met the inclusion criteria and were, thus, analyzed. 713 (5.3%) patients had a documented alcohol abuse and 91 (0.7%) suffered from liver cirrhosis. Patients abusing alcohol and suffering from cirrhosis differed from controls regarding injury pattern, age and outcome. More specific, liver cirrhotic patients showed significantly higher in-hospital mortality than predicted (35% vs. predicted 19%) and increased single- and multi-organ failure rates. While alcohol abuse increased organ failure rates as well this did not affect in-hospital mortality.\n Question: Is liver cirrhosis but not alcohol abuse associated with impaired outcome in trauma patients - a retrospective , multicentre 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: Liver cirrhosis has been shown to be associated with impaired outcome in patients who underwent elective surgery. We therefore investigated the impact of alcohol abuse and subsequent liver cirrhosis on outcome in multiple trauma patients. Using the multi-centre population-based Trauma Registry of the German Society for Trauma Surgery, we retrospectively compared outcome in patients (ISS ≥ 9, ≥ 18) with pre-existing alcohol abuse and liver cirrhosis with healthy trauma victims in univariate and matched-pair analysis. Means were compared using Student's t-test and analysis of variance (ANOVA) and categorical variables using χ(2) (p<0.05=significant). Overall 13,527 patients met the inclusion criteria and were, thus, analyzed. 713 (5.3%) patients had a documented alcohol abuse and 91 (0.7%) suffered from liver cirrhosis. Patients abusing alcohol and suffering from cirrhosis differed from controls regarding injury pattern, age and outcome. More specific, liver cirrhotic patients showed significantly higher in-hospital mortality than predicted (35% vs. predicted 19%) and increased single- and multi-organ failure rates. While alcohol abuse increased organ failure rates as well this did not affect in-hospital mortality. Question: Is liver cirrhosis but not alcohol abuse associated with impaired outcome in trauma patients - a retrospective , multicentre study? Output:
PubmedQA168505	[ { "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 hypothesized that the genetic makeup has an impact on the functional behavior of the uterine cervix. Therefore, we compared the biomechanical properties of uterine cervix in postpartum in 2 strains of mice that differ in their underlying regenerative collagen remodeling characteristics: MRL/MpJ+/+ (MRL: high regenerative repair) and C57BL/6 (C57: low regenerative high fibrotic repair). Cervical tensile proprieties were assessed on day 3, 15, and 60 postpartum in MRL (n = 14) and C57 (n = 13) mice (4-5 animals at each time point). Stress-strain curves were generated using Shimadzu EZ-test instrumentation. Cervical tissue was stretched by 0.42 mm/min until rupture. Parameters of viscoelasticity including slope (a measure of stiffness), yield point (YP; moment when tissue changes its proprieties from elastic to plastic), and break point (BP; measure of tissue strength) were recorded and analyzed blindly between strains. Data were normalized to the weight of the tissue and analyzed by 2-way analysis of variance. Histological and collagen birefringence evaluation of the uterine cervix (MRL: n = 4; C57: n = 4) was performed 5 days after delivery. At 3 and 15 days postpartum, cervices of MRL mice were significantly more compliant than those of C57 (P < .001). MRL mice displayed a significant increase in stiffness from day 3 to day 60 (slope, median +/- SEM: day 3: 3.1 +/- 0.5 vs day 15: 20.3 +/- 4.9 vs day 60: 33.1 +/- 3.5 N/mm per gram; P < .001). In contrast, the stiffness of C57 cervices reached maximum on day 15 (slope day 3: 14.1 +/- 4.3 vs day 15: 40.0 +/- 6.5 N/mm per gram; P = .02) and rested at a similar level on day 60 (day 60: 26.1 +/- 7.0 N/mm per gram; day 60 vs day 15: P = .937). More force was required to reach YP in C57 on day 3 (C57: 72.5 +/- 14.7 vs MRL: 19.9 +/- 1.6 N/g; P < .001) but not on either day 15 (C57: 156.1 +/- 27.5 vs MRL: 109.2 +/- 26.0 N/g; P = .120) or on day 60 (C57: 143.4 +/- 26.5 vs MRL: 164.5 +/- 18.7 N/g; P = .412). There was a significant decrease in BP in both strains on both day 15 and day 60 compared with day 3 postpartum (P = .856 for strain, P = .008 for day). MRL mice displayed significantly less cervical collagen birefringence compared with C57 control (P < .001) but increased proteoglycan staining and increased water content.\n Question: Does genetic background affect the biomechanical behavior of the postpartum mouse cervix?\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 hypothesized that the genetic makeup has an impact on the functional behavior of the uterine cervix. Therefore, we compared the biomechanical properties of uterine cervix in postpartum in 2 strains of mice that differ in their underlying regenerative collagen remodeling characteristics: MRL/MpJ+/+ (MRL: high regenerative repair) and C57BL/6 (C57: low regenerative high fibrotic repair). Cervical tensile proprieties were assessed on day 3, 15, and 60 postpartum in MRL (n = 14) and C57 (n = 13) mice (4-5 animals at each time point). Stress-strain curves were generated using Shimadzu EZ-test instrumentation. Cervical tissue was stretched by 0.42 mm/min until rupture. Parameters of viscoelasticity including slope (a measure of stiffness), yield point (YP; moment when tissue changes its proprieties from elastic to plastic), and break point (BP; measure of tissue strength) were recorded and analyzed blindly between strains. Data were normalized to the weight of the tissue and analyzed by 2-way analysis of variance. Histological and collagen birefringence evaluation of the uterine cervix (MRL: n = 4; C57: n = 4) was performed 5 days after delivery. At 3 and 15 days postpartum, cervices of MRL mice were significantly more compliant than those of C57 (P < .001). MRL mice displayed a significant increase in stiffness from day 3 to day 60 (slope, median +/- SEM: day 3: 3.1 +/- 0.5 vs day 15: 20.3 +/- 4.9 vs day 60: 33.1 +/- 3.5 N/mm per gram; P < .001). In contrast, the stiffness of C57 cervices reached maximum on day 15 (slope day 3: 14.1 +/- 4.3 vs day 15: 40.0 +/- 6.5 N/mm per gram; P = .02) and rested at a similar level on day 60 (day 60: 26.1 +/- 7.0 N/mm per gram; day 60 vs day 15: P = .937). More force was required to reach YP in C57 on day 3 (C57: 72.5 +/- 14.7 vs MRL: 19.9 +/- 1.6 N/g; P < .001) but not on either day 15 (C57: 156.1 +/- 27.5 vs MRL: 109.2 +/- 26.0 N/g; P = .120) or on day 60 (C57: 143.4 +/- 26.5 vs MRL: 164.5 +/- 18.7 N/g; P = .412). There was a significant decrease in BP in both strains on both day 15 and day 60 compared with day 3 postpartum (P = .856 for strain, P = .008 for day). MRL mice displayed significantly less cervical collagen birefringence compared with C57 control (P < .001) but increased proteoglycan staining and increased water content. Question: Does genetic background affect the biomechanical behavior of the postpartum mouse cervix? Output:
PubmedQA28257	[ { "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: Serum periostin is increased in asthma and serves as a surrogate marker for IL-13 activity in the lung. Serum levels of periostin are the most robust biomarker predicting a favourable response to the anti-IL-13 drug, lebrikizumab. We investigated the mechanisms of IL-13 stimulation of periostin, the polarized secretion of periostin and whether periostin would have a direct effect on mucin secretion by airway cells. Normal human bronchial epithelial (NHBE) cells were cultured at air-liquid interface (ALI) in the presence of IL-13, and we evaluated the effect of the specific inhibitors, leflunomide (Janus kinase (JAK)/signal transducer and activator of transcription factor 6 (STAT6) inhibitor) or PD98059 (MEK/extracellular regulated protein kinase (ERK) inhibitor), on periostin production. We examined MUC5AC secretion from NHBE cells exposed to recombinant human (rh) periostin or IL-13 in the presence and absence of OC-20, a periostin-neutralizing antibody. IL-13 induced periostin protein which was predominantly secreted towards the basal surface of the cells. Periostin production was much greater from goblet cells than ciliated cells (P < 0.001). Periostin production after exposure to IL-13 was attenuated by both leflunomide (P < 0.001) and PD98059 (P < 0.001). The addition of exogenous periostin modestly increased MUC5AC secretion (P < 0.01), but did not visibly change cell morphology. IL-13-induced MUC5AC secretion was attenuated by OC-20 (P < 0.01).\n Question: Does inhibition of IL-13-induced periostin in airway epithelium attenuate cellular protein expression of MUC5AC?\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: Serum periostin is increased in asthma and serves as a surrogate marker for IL-13 activity in the lung. Serum levels of periostin are the most robust biomarker predicting a favourable response to the anti-IL-13 drug, lebrikizumab. We investigated the mechanisms of IL-13 stimulation of periostin, the polarized secretion of periostin and whether periostin would have a direct effect on mucin secretion by airway cells. Normal human bronchial epithelial (NHBE) cells were cultured at air-liquid interface (ALI) in the presence of IL-13, and we evaluated the effect of the specific inhibitors, leflunomide (Janus kinase (JAK)/signal transducer and activator of transcription factor 6 (STAT6) inhibitor) or PD98059 (MEK/extracellular regulated protein kinase (ERK) inhibitor), on periostin production. We examined MUC5AC secretion from NHBE cells exposed to recombinant human (rh) periostin or IL-13 in the presence and absence of OC-20, a periostin-neutralizing antibody. IL-13 induced periostin protein which was predominantly secreted towards the basal surface of the cells. Periostin production was much greater from goblet cells than ciliated cells (P < 0.001). Periostin production after exposure to IL-13 was attenuated by both leflunomide (P < 0.001) and PD98059 (P < 0.001). The addition of exogenous periostin modestly increased MUC5AC secretion (P < 0.01), but did not visibly change cell morphology. IL-13-induced MUC5AC secretion was attenuated by OC-20 (P < 0.01). Question: Does inhibition of IL-13-induced periostin in airway epithelium attenuate cellular protein expression of MUC5AC? Output:
PubmedQA158040	[ { "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 variability in speech perception between cochlear implant users is thought to result from the degeneration of the auditory nerve. Degeneration of the auditory nerve, histologically assessed, correlates with electrophysiologically acquired measures, such as electrically evoked compound action potentials (eCAPs) in experimental animals. To predict degeneration of the auditory nerve in humans, where histology is impossible, this paper reviews the correlation between speech perception and eCAP recordings in cochlear implant patients. PubMed and Embase. We performed a systematic search for articles containing the following major themes: cochlear implants, evoked potentials, and speech perception. Two investigators independently conducted title-abstract screening, full-text screening, and critical appraisal. Data were extracted from the remaining articles. Twenty-five of 1,429 identified articles described a correlation between speech perception and eCAP attributes. Due to study heterogeneity, a meta-analysis was not feasible, and studies were descriptively analyzed. Several studies investigating presence of the eCAP, recovery time constant, slope of the amplitude growth function, and spatial selectivity showed significant correlations with speech perception. In contrast, neural adaptation, eCAP threshold, and change with varying interphase gap did not significantly correlate with speech perception in any of the identified studies.\n Question: Do systematic review of compound action potentials as predictors for cochlear implant performance?\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 variability in speech perception between cochlear implant users is thought to result from the degeneration of the auditory nerve. Degeneration of the auditory nerve, histologically assessed, correlates with electrophysiologically acquired measures, such as electrically evoked compound action potentials (eCAPs) in experimental animals. To predict degeneration of the auditory nerve in humans, where histology is impossible, this paper reviews the correlation between speech perception and eCAP recordings in cochlear implant patients. PubMed and Embase. We performed a systematic search for articles containing the following major themes: cochlear implants, evoked potentials, and speech perception. Two investigators independently conducted title-abstract screening, full-text screening, and critical appraisal. Data were extracted from the remaining articles. Twenty-five of 1,429 identified articles described a correlation between speech perception and eCAP attributes. Due to study heterogeneity, a meta-analysis was not feasible, and studies were descriptively analyzed. Several studies investigating presence of the eCAP, recovery time constant, slope of the amplitude growth function, and spatial selectivity showed significant correlations with speech perception. In contrast, neural adaptation, eCAP threshold, and change with varying interphase gap did not significantly correlate with speech perception in any of the identified studies. Question: Do systematic review of compound action potentials as predictors for cochlear implant performance? Output:
PubmedQA98446	[ { "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: Systemic inflammation may inhibit neutrophil (PMN) apoptosis and promote multiple organ dysfunction syndrome. We hypothesize that severe trauma causes dysregulation of PMN apoptosis. Neutrophils were isolated from trauma patients (24-72 hours after injury; n = 16) and controls (healthy volunteers) and incubated for 18 hours. In separate experiments, control cells were treated +/- the nuclear factor kappa beta (NFkappabeta) inhibitor pyrrolidinithiocarbamate then incubated with 25% patient or control plasma. Apoptosis was quantified by enzyme-linked immunosorbent assay for histone-associated DNA and annexin V fluorescence-activated cell sorter. NFkappabeta activation was determined by Western blot for phosphorylated I kappabeta. Apoptosis was inhibited in trauma patient PMN. Neutrophil apoptosis correlated with multiple organ dysfunction syndrome score, Acute Physiology and Chronic Health Evaluation II, and platelet count. Patient plasma inhibited apoptosis and induced phosphorylation of I kappabeta in control cells. Inhibition of PMN apoptosis by patient plasma was blocked by pretreatment with pyrrolidinithiocarbamate.\n Question: Is inhibition of neutrophil apoptosis after severe trauma NFkappabeta dependent?\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: Systemic inflammation may inhibit neutrophil (PMN) apoptosis and promote multiple organ dysfunction syndrome. We hypothesize that severe trauma causes dysregulation of PMN apoptosis. Neutrophils were isolated from trauma patients (24-72 hours after injury; n = 16) and controls (healthy volunteers) and incubated for 18 hours. In separate experiments, control cells were treated +/- the nuclear factor kappa beta (NFkappabeta) inhibitor pyrrolidinithiocarbamate then incubated with 25% patient or control plasma. Apoptosis was quantified by enzyme-linked immunosorbent assay for histone-associated DNA and annexin V fluorescence-activated cell sorter. NFkappabeta activation was determined by Western blot for phosphorylated I kappabeta. Apoptosis was inhibited in trauma patient PMN. Neutrophil apoptosis correlated with multiple organ dysfunction syndrome score, Acute Physiology and Chronic Health Evaluation II, and platelet count. Patient plasma inhibited apoptosis and induced phosphorylation of I kappabeta in control cells. Inhibition of PMN apoptosis by patient plasma was blocked by pretreatment with pyrrolidinithiocarbamate. Question: Is inhibition of neutrophil apoptosis after severe trauma NFkappabeta dependent? Output:
PubmedQA160531	[ { "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: Hepatitis C (HCV) treatment options have changed with the development of direct activity antivirals (DAAs) and the availability of triple therapies have improved HCV cure rates. A common neuropsychiatric side effect of pegylated-interferon and ribavirin treatment is major depressive disorder (MDD), however little is known about such adverse events with protease inhibitor-based triple therapy. The aim of this study was to assess the rate of MDD in co-infected HIV HCV patients undergoing different HCV treatments. All participants were co-infected HIV HCV attending the Royal Sussex County Hospital Brighton hepatology outpatient clinic between 2010 and 2014. Participants were assessed for DSM-IV MDD and depression severity (using the Hamilton depression scale (HAMD)) at baseline and monthly after treatment initiation. HIV and HCV stages, genotype, reinfection and standard demographic variables were recorded. Influence of HCV stage (acute vs. chronic) and type of treatment (classic vs triple), emergence of MDD and clearance outcomes were analyzed using repeated measures and logistic regression models. Fifty participants with a mean age of 42.65 years (SD=10.32) were included; most were male (98%). The majority had contracted HCV genotype 1 (64%) or 4 (26%). The HCV stage and treatment groups were matched for age and depression at baseline. No significant differences were found on virological outcomes considering HCV stage and treatment. From baseline to SVR, there was a significant increase in HAMD scores, F(4,36)=10.09, p<.001; this was not significantly influenced by HCV stage, F(4,35)=0.54, p=.708 or HCV treatment group, F(4,35)=0.60, p=.664. Those with chronic HCV were more likely to transition to MDD than acute infection (OR 7.77, 95% CI 2.04-29.54, p=.003). No differences were found for depression emergence by HCV treatment group (OR 0.83, 95% CI 0.22-3.13, p=.787).\n Question: Is hCV triple therapy in co-infection HIV/HCV associated with a different risk of developing major depressive disorder?\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: Hepatitis C (HCV) treatment options have changed with the development of direct activity antivirals (DAAs) and the availability of triple therapies have improved HCV cure rates. A common neuropsychiatric side effect of pegylated-interferon and ribavirin treatment is major depressive disorder (MDD), however little is known about such adverse events with protease inhibitor-based triple therapy. The aim of this study was to assess the rate of MDD in co-infected HIV HCV patients undergoing different HCV treatments. All participants were co-infected HIV HCV attending the Royal Sussex County Hospital Brighton hepatology outpatient clinic between 2010 and 2014. Participants were assessed for DSM-IV MDD and depression severity (using the Hamilton depression scale (HAMD)) at baseline and monthly after treatment initiation. HIV and HCV stages, genotype, reinfection and standard demographic variables were recorded. Influence of HCV stage (acute vs. chronic) and type of treatment (classic vs triple), emergence of MDD and clearance outcomes were analyzed using repeated measures and logistic regression models. Fifty participants with a mean age of 42.65 years (SD=10.32) were included; most were male (98%). The majority had contracted HCV genotype 1 (64%) or 4 (26%). The HCV stage and treatment groups were matched for age and depression at baseline. No significant differences were found on virological outcomes considering HCV stage and treatment. From baseline to SVR, there was a significant increase in HAMD scores, F(4,36)=10.09, p<.001; this was not significantly influenced by HCV stage, F(4,35)=0.54, p=.708 or HCV treatment group, F(4,35)=0.60, p=.664. Those with chronic HCV were more likely to transition to MDD than acute infection (OR 7.77, 95% CI 2.04-29.54, p=.003). No differences were found for depression emergence by HCV treatment group (OR 0.83, 95% CI 0.22-3.13, p=.787). Question: Is hCV triple therapy in co-infection HIV/HCV associated with a different risk of developing major depressive disorder? Output:
PubmedQA208556	[ { "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 investigations have suggested an important role of statins in the prevention of stroke and dementia independent of their lipid-lowering properties. Using transcranial Doppler sonography (TCD), we examined acetazolamide reactivity as a marker of cerebral vasoreactivity in patients with subcortical small-vessel disease before and after pravastatin treatment. In 16 patients (mean age 68+/-10 years) with subcortical small-vessel disease, cerebral vasomotor reactivity was tested using TCD insonating the middle cerebral artery. Cerebral blood flow velocity (CBFV) increase after bolus injection of 1 g acetazolamide was determined before and after 2-month treatment with pravastatin sodium 20 mg daily. Relative CBFV increase was significantly greater after pravastatin treatment (41.9+/-23.7% versus 55.7+/-18.3%, P=0.004). Comparison of CBFV at rest before and after treatment with pravastatin did not show significant differences. There was a strong negative correlation between the pravastatin-induced enhancement of vasomotor reactivity and the pretreatment CBFV increase (beta=-0.64, P=0.019). No associations were found between the effect of pravastatin on vasomotor reactivity and pretreatment levels or changes of LDL cholesterol.\n Question: Does pravastatin improve cerebral vasomotor reactivity in patients with subcortical small-vessel 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: Recent investigations have suggested an important role of statins in the prevention of stroke and dementia independent of their lipid-lowering properties. Using transcranial Doppler sonography (TCD), we examined acetazolamide reactivity as a marker of cerebral vasoreactivity in patients with subcortical small-vessel disease before and after pravastatin treatment. In 16 patients (mean age 68+/-10 years) with subcortical small-vessel disease, cerebral vasomotor reactivity was tested using TCD insonating the middle cerebral artery. Cerebral blood flow velocity (CBFV) increase after bolus injection of 1 g acetazolamide was determined before and after 2-month treatment with pravastatin sodium 20 mg daily. Relative CBFV increase was significantly greater after pravastatin treatment (41.9+/-23.7% versus 55.7+/-18.3%, P=0.004). Comparison of CBFV at rest before and after treatment with pravastatin did not show significant differences. There was a strong negative correlation between the pravastatin-induced enhancement of vasomotor reactivity and the pretreatment CBFV increase (beta=-0.64, P=0.019). No associations were found between the effect of pravastatin on vasomotor reactivity and pretreatment levels or changes of LDL cholesterol. Question: Does pravastatin improve cerebral vasomotor reactivity in patients with subcortical small-vessel disease? Output:
PubmedQA93586	[ { "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 explore whether pre-treatment swallowing measures predict swallowing recovery at 6 weeks after transoral robotic surgery (TORS). Prospective cohort study. Tertiary care cancer centre in the United Kingdom. Fifty-one consecutive patients undergoing TORS for head and neck cancer, between April 2013 and February 2015. Swallowing function assessed by Performance Status Scale (PSS) Normalcy of Diet, timed water swallow test capacity scores (WST) and duration of tube feeding. The primary site distribution was as follows: 21 oropharynx, 8 larynx, 6 mucosectomy and 6 hypopharynx. T stages included 7 staged Tx, 21 T1-T2 tumours and 1 T3 tumour. Moderate-to-severe comorbidity was found in 45/51 patients. Mean PSS score was 83 (sd 27.54); mean WST score was 11.14 (sd 7.97). Most patients (73%) required tube feeding post-operatively, with mean tube feed duration of 18.08 days (sd 17.91); 76% resumed oral intake by 6 weeks. Pre-treatment swallow tests showed moderate negative correlation with tube feeding duration: PSS (rho 0-.430, P = .003); WST (rho 0-.503, P = 0.002).\n Question: Do baseline swallowing measures predict recovery at 6 weeks after transoral robotic surgery for head and neck cancer?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To explore whether pre-treatment swallowing measures predict swallowing recovery at 6 weeks after transoral robotic surgery (TORS). Prospective cohort study. Tertiary care cancer centre in the United Kingdom. Fifty-one consecutive patients undergoing TORS for head and neck cancer, between April 2013 and February 2015. Swallowing function assessed by Performance Status Scale (PSS) Normalcy of Diet, timed water swallow test capacity scores (WST) and duration of tube feeding. The primary site distribution was as follows: 21 oropharynx, 8 larynx, 6 mucosectomy and 6 hypopharynx. T stages included 7 staged Tx, 21 T1-T2 tumours and 1 T3 tumour. Moderate-to-severe comorbidity was found in 45/51 patients. Mean PSS score was 83 (sd 27.54); mean WST score was 11.14 (sd 7.97). Most patients (73%) required tube feeding post-operatively, with mean tube feed duration of 18.08 days (sd 17.91); 76% resumed oral intake by 6 weeks. Pre-treatment swallow tests showed moderate negative correlation with tube feeding duration: PSS (rho 0-.430, P = .003); WST (rho 0-.503, P = 0.002). Question: Do baseline swallowing measures predict recovery at 6 weeks after transoral robotic surgery for head and neck cancer? Output:
PubmedQA200757	[ { "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: Thallium 201 reinjection has been shown to enhance the detection of myocardial ischemia in patients with chronic coronary artery disease. However, limited data are available regarding its value in patients after acute myocardial infarction. We performed adenosine Tl-201 tomography in 126 patients in stable condition at a mean of 5 +/- 3 days after acute myocardial infarction (MI). After acquisition of redistribution images, patients were reinjected with 1 mCi of Tl-201 and reinjection images were then obtained. The stress, redistribution, and reinjection images were quantified to determine the total perfusion defect size and percent ischemia and scar. The mean age of patients was 54 +/- 10 years. Of the patients, 64% were male, 56% had Q-wave MI, 46% had anterior MI, and 34% received thrombolysis. The percent total defect size was the same on the stress-redistribution and stress-reinjection images (28.3% +/- 19.0%). The reinjection images showed an increase in ischemic defect size (14.7% +/- 13.5% vs 12.8% +/- 12.0%, P =.001) and a decrease in scar defect size (13.6% +/- 13.1% vs 15.5% +/- 13.9%, P =.001) compared with the redistribution images. The enhancement in the detection of myocardial ischemia was seen in both the infarct (P =.001) and noninfarct (P =.01) zones.\n Question: Does tl-201 reinjection enhance the detection of myocardial ischemia after acute myocardial infarction?\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: Thallium 201 reinjection has been shown to enhance the detection of myocardial ischemia in patients with chronic coronary artery disease. However, limited data are available regarding its value in patients after acute myocardial infarction. We performed adenosine Tl-201 tomography in 126 patients in stable condition at a mean of 5 +/- 3 days after acute myocardial infarction (MI). After acquisition of redistribution images, patients were reinjected with 1 mCi of Tl-201 and reinjection images were then obtained. The stress, redistribution, and reinjection images were quantified to determine the total perfusion defect size and percent ischemia and scar. The mean age of patients was 54 +/- 10 years. Of the patients, 64% were male, 56% had Q-wave MI, 46% had anterior MI, and 34% received thrombolysis. The percent total defect size was the same on the stress-redistribution and stress-reinjection images (28.3% +/- 19.0%). The reinjection images showed an increase in ischemic defect size (14.7% +/- 13.5% vs 12.8% +/- 12.0%, P =.001) and a decrease in scar defect size (13.6% +/- 13.1% vs 15.5% +/- 13.9%, P =.001) compared with the redistribution images. The enhancement in the detection of myocardial ischemia was seen in both the infarct (P =.001) and noninfarct (P =.01) zones. Question: Does tl-201 reinjection enhance the detection of myocardial ischemia after acute myocardial infarction? Output:
PubmedQA70051	[ { "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 whether mangiferin can increase the viability of retinal ganglion cells (RGCs) in ischemic mouse retina, and to determine the possible mechanism of neuroprotection. C57BL/6J mice underwent constant elevation of intraocular pressure for 60 min and received saline or mangiferin (30 mg/kg) intraperitoneally once daily until sacrifice. HIF-1α, GFAP and SIRT1 expression was assessed at 1, 4, and 7 days after retinal ischemia. Bax and Bcl-2 expression was also analyzed at 1 and 4 days. RGC survival was assessed by labeling flat-mounted retinas with Brn3a at 2 weeks after retinal ischemia. The effect of co-treatment with mangiferin and sirtinol (SIRT1 inhibitor) was also evaluated. The expression of HIF-1α and GFAP was upregulated in saline-treated retinas within 7 days after ischemia. Mangiferin treatment suppressed this upregulation. The expression of SIRT1 was downregulated in saline-treated ischemic retinas. This downregulation was reversed by mangiferin treatment, resulting in a significant difference from saline-treated ischemic retinas. In mangiferin-treated ischemic retinas, Bax expression was downregulated, whereas Bcl-2 expression was upregulated in comparison with saline-treated ischemic retinas. Mangiferin treatment protected ischemic retinas against RGC loss. Treatment of sirtinol decreased the neuroprotective effect of mangiferin.\n Question: Does mangiferin protect Retinal Ganglion Cells in Ischemic Mouse Retina via SIRT1?\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 whether mangiferin can increase the viability of retinal ganglion cells (RGCs) in ischemic mouse retina, and to determine the possible mechanism of neuroprotection. C57BL/6J mice underwent constant elevation of intraocular pressure for 60 min and received saline or mangiferin (30 mg/kg) intraperitoneally once daily until sacrifice. HIF-1α, GFAP and SIRT1 expression was assessed at 1, 4, and 7 days after retinal ischemia. Bax and Bcl-2 expression was also analyzed at 1 and 4 days. RGC survival was assessed by labeling flat-mounted retinas with Brn3a at 2 weeks after retinal ischemia. The effect of co-treatment with mangiferin and sirtinol (SIRT1 inhibitor) was also evaluated. The expression of HIF-1α and GFAP was upregulated in saline-treated retinas within 7 days after ischemia. Mangiferin treatment suppressed this upregulation. The expression of SIRT1 was downregulated in saline-treated ischemic retinas. This downregulation was reversed by mangiferin treatment, resulting in a significant difference from saline-treated ischemic retinas. In mangiferin-treated ischemic retinas, Bax expression was downregulated, whereas Bcl-2 expression was upregulated in comparison with saline-treated ischemic retinas. Mangiferin treatment protected ischemic retinas against RGC loss. Treatment of sirtinol decreased the neuroprotective effect of mangiferin. Question: Does mangiferin protect Retinal Ganglion Cells in Ischemic Mouse Retina via SIRT1? Output:
PubmedQA167092	[ { "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 investigates the effect of amlodipine on arterial compliance (AC), and the effect of atorvastatin on AC when given in combination with amlodipine. Twenty-one consecutive hypertensive hyperlipidemic patients were included in this study. Patients were followed every month for 6 months (3 months of amlodipine therapy and 3 months of amlodipine and atorvastatin combination). During the 3 months of amlodipine monotherapy, large and small AC were improved by 26% and 38%, respectively, and the systemic vascular resistance was reduced by 10%. The addition of atorvastatin during the next 3 months improved small AC by an additional 42% and decreased the systemic vascular resistance by another 5%, but large AC and blood pressure did not change.\n Question: Do treatment with amlodipine and atorvastatin have additive effect in improvement of arterial compliance in hypertensive hyperlipidemic patients?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: This study investigates the effect of amlodipine on arterial compliance (AC), and the effect of atorvastatin on AC when given in combination with amlodipine. Twenty-one consecutive hypertensive hyperlipidemic patients were included in this study. Patients were followed every month for 6 months (3 months of amlodipine therapy and 3 months of amlodipine and atorvastatin combination). During the 3 months of amlodipine monotherapy, large and small AC were improved by 26% and 38%, respectively, and the systemic vascular resistance was reduced by 10%. The addition of atorvastatin during the next 3 months improved small AC by an additional 42% and decreased the systemic vascular resistance by another 5%, but large AC and blood pressure did not change. Question: Do treatment with amlodipine and atorvastatin have additive effect in improvement of arterial compliance in hypertensive hyperlipidemic patients? Output:
PubmedQA119414	[ { "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: Biomarkers caused by blunt chest trauma might leak into the vascular compartment and therefore reflect the severity of parenchymal lung injury (PLI). Five promising proteins were preselected after a literature scan. The objective of our study was to identify a biomarker that is released abundantly into the serum shortly after trauma and reliably quantifies the loss of functional lung tissue. Polytraumatized patients (aged ≥18 years, Injury Severity Score [ISS] ≥16) were included in our prospective observational study if they were admitted directly to our level I trauma center during the first hour after trauma occurred. Immediately after stabilizing the patient's condition, blood samples were taken and a whole-body computed tomographic (CT) scan was obtained. Biomarker levels were measured directly after admission and on day 2. PLI volume was calculated using volumetric analysis. One hundred thirty patients met the inclusion criteria. Compared with a matched healthy control population, median levels of the soluble receptor for advanced glycation end products (sRAGE) was almost 3 times higher and decreased by 41% on day 2. Higher initial median sRAGE levels were detected in patients with PLI compared with patients without PLI and in individuals with severe PLI compared with those with mild PLI. Spearman correlation analysis and a univariate linear log regression model revealed a significant correlation/equation between initial sRAGE levels and relative PLI volume. Receiver operating characteristic (ROC) statistics identified the initial sRAGE level as an indicator of severe PLI.\n Question: Does soluble Receptor for Advanced Glycation End Products quantify Lung Injury in Polytraumatized Patients?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Biomarkers caused by blunt chest trauma might leak into the vascular compartment and therefore reflect the severity of parenchymal lung injury (PLI). Five promising proteins were preselected after a literature scan. The objective of our study was to identify a biomarker that is released abundantly into the serum shortly after trauma and reliably quantifies the loss of functional lung tissue. Polytraumatized patients (aged ≥18 years, Injury Severity Score [ISS] ≥16) were included in our prospective observational study if they were admitted directly to our level I trauma center during the first hour after trauma occurred. Immediately after stabilizing the patient's condition, blood samples were taken and a whole-body computed tomographic (CT) scan was obtained. Biomarker levels were measured directly after admission and on day 2. PLI volume was calculated using volumetric analysis. One hundred thirty patients met the inclusion criteria. Compared with a matched healthy control population, median levels of the soluble receptor for advanced glycation end products (sRAGE) was almost 3 times higher and decreased by 41% on day 2. Higher initial median sRAGE levels were detected in patients with PLI compared with patients without PLI and in individuals with severe PLI compared with those with mild PLI. Spearman correlation analysis and a univariate linear log regression model revealed a significant correlation/equation between initial sRAGE levels and relative PLI volume. Receiver operating characteristic (ROC) statistics identified the initial sRAGE level as an indicator of severe PLI. Question: Does soluble Receptor for Advanced Glycation End Products quantify Lung Injury in Polytraumatized Patients? Output:
PubmedQA8968	[ { "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: Active immunization against Aβ was reported to have a therapeutic effect in murine models of Alzheimer's disease. Clinical Aβ vaccination trial AN1792 was interrupted due to the development in 6 % of the patients of meningoencephalitis likely involving pro-inflammatory CD4(+) T cells. However, the potential implication of auto-aggressive anti-Aβ CD8(+) T cells has been poorly investigated. Potential MHC-I-restricted Aβ-derived epitopes were first analyzed for their capacity to recruit functional CD8(+) T cell responses in mouse models. Their impact on migration of CD8(+) T cells into the brain parenchyma and potential induction of meningoencephalitis and/or neuronal damage was investigated upon vaccination in the APPPS1 mouse model of AD. We identified one nonamer peptide, Aβ33-41, which was naturally processed and presented in association with H-2-D(b) molecule on neurons and CD11b(+) microglia. Upon optimization of anchor residues for enhanced binding to H-2-D(b), immunization with the modified Aβ33-41NP peptide elicited Aβ-specific IFNγ-secreting CD8(+) T cells, which are cytotoxic towards Aβ-expressing targets. Whereas T cell infiltration in the brain of APPPS1 mice is dominated by CD3(+)CD8(-) T cells and increases with disease evolution between 4 and 7 months of age, a predominance of CD3(+)CD8(+) over CD3(+)CD8(-) cells was observed in 6- to 7-month-old APPPS1 but not in WT animals, only after vaccination with Aβ33-41NP. The number of CD11b(+) mononuclear phagocytes, which significantly increases with age in the brain of APPPS1 mice, was reduced following immunization with Aβ33-41NP. Despite peripheral activation of Aβ-specific CD8(+) cytotoxic effectors and enhanced infiltration of CD8(+) T cells in the brain of Aβ33-41NP-immunized APPPS1 mice, no clinical signs of severe autoimmune neuroinflammation were observed.\n Question: Do vaccine-induced Aβ-specific CD8+ T cells do not trigger autoimmune neuroinflammation in a murine model of Alzheimer 's disease?\n Output: " }, { "role": "assistant", "content": "yes" } ]	TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Active immunization against Aβ was reported to have a therapeutic effect in murine models of Alzheimer's disease. Clinical Aβ vaccination trial AN1792 was interrupted due to the development in 6 % of the patients of meningoencephalitis likely involving pro-inflammatory CD4(+) T cells. However, the potential implication of auto-aggressive anti-Aβ CD8(+) T cells has been poorly investigated. Potential MHC-I-restricted Aβ-derived epitopes were first analyzed for their capacity to recruit functional CD8(+) T cell responses in mouse models. Their impact on migration of CD8(+) T cells into the brain parenchyma and potential induction of meningoencephalitis and/or neuronal damage was investigated upon vaccination in the APPPS1 mouse model of AD. We identified one nonamer peptide, Aβ33-41, which was naturally processed and presented in association with H-2-D(b) molecule on neurons and CD11b(+) microglia. Upon optimization of anchor residues for enhanced binding to H-2-D(b), immunization with the modified Aβ33-41NP peptide elicited Aβ-specific IFNγ-secreting CD8(+) T cells, which are cytotoxic towards Aβ-expressing targets. Whereas T cell infiltration in the brain of APPPS1 mice is dominated by CD3(+)CD8(-) T cells and increases with disease evolution between 4 and 7 months of age, a predominance of CD3(+)CD8(+) over CD3(+)CD8(-) cells was observed in 6- to 7-month-old APPPS1 but not in WT animals, only after vaccination with Aβ33-41NP. The number of CD11b(+) mononuclear phagocytes, which significantly increases with age in the brain of APPPS1 mice, was reduced following immunization with Aβ33-41NP. Despite peripheral activation of Aβ-specific CD8(+) cytotoxic effectors and enhanced infiltration of CD8(+) T cells in the brain of Aβ33-41NP-immunized APPPS1 mice, no clinical signs of severe autoimmune neuroinflammation were observed. Question: Do vaccine-induced Aβ-specific CD8+ T cells do not trigger autoimmune neuroinflammation in a murine model of Alzheimer 's disease? Output:
PubmedQA144401	[ { "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 study the incidence of ulcerative colitis and to analyse the pattern of the disease in the prefecture of Heraklion, Crete. The population at risk comprised 263,670 inhabitants in the prefecture of Heraklion (2641 km2). The two regional hospitals, five health centres, 109 private family doctors and 145 specialists participated in the study. A prospective and population-based epidemiological study of ulcerative colitis over five years from 1990 to the end of 1994. Overall, 117 patients with ulcerative colitis (75 males and 42 females) were newly diagnosed during the study period. The mean annual incidence of the disease for the years 1990-1994 was 8.9 per 10(5) inhabitants (95% CI 7.2-10.4). The male to female ratio was 1.8:1. There were no significant difference between the age-specific incidences of the age groups. The majority (51.3%) of the patients were exsmokers and one-third had never smoked. A family history of first-degree relatives positive for inflammatory bowel disease was obtained in 9.6% of our patients.\n Question: Is ulcerative colitis as common in Crete as in northern Europe : a 5-year prospective 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: To study the incidence of ulcerative colitis and to analyse the pattern of the disease in the prefecture of Heraklion, Crete. The population at risk comprised 263,670 inhabitants in the prefecture of Heraklion (2641 km2). The two regional hospitals, five health centres, 109 private family doctors and 145 specialists participated in the study. A prospective and population-based epidemiological study of ulcerative colitis over five years from 1990 to the end of 1994. Overall, 117 patients with ulcerative colitis (75 males and 42 females) were newly diagnosed during the study period. The mean annual incidence of the disease for the years 1990-1994 was 8.9 per 10(5) inhabitants (95% CI 7.2-10.4). The male to female ratio was 1.8:1. There were no significant difference between the age-specific incidences of the age groups. The majority (51.3%) of the patients were exsmokers and one-third had never smoked. A family history of first-degree relatives positive for inflammatory bowel disease was obtained in 9.6% of our patients. Question: Is ulcerative colitis as common in Crete as in northern Europe : a 5-year prospective study? Output:
PubmedQA194743	[ { "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 aimed to evaluate the in vitro effects of genistein, both pure genistein and a commercially available form of genistein called Genistein Combined Polysacharride (GCP), against two canine B-cell lymphoid cell lines and determine the oral bioavailability of GCP when fed to normal dogs. The in vitro effect of genistein and GCP was evaluated using cell proliferation and apoptotic assays. The IC50 of both compounds was determined using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) cell proliferation assay and propidium idodide staining. Apoptosis was evaluated using Annexin V staining, caspase 3 and 9 staining, and DNA laddering. Cell cycle analysis and Bcl-2/Bax ratios were also examined. An initial dose escalating pharmacokinetic study was used to determine if therapeutic serum levels of genistein could be reached with oral dosing of GCP in normal dogs. The 72-hour in vitro IC50 of genistein and GCP against the GL-1 and 17-71 cells were both 10 microg/mL and 20 microg/mL, respectively. GCP led to cell death in both cell lines via apoptosis and treated cells exhibited increased Bax:Bcl-2 ratios. The serum concentrations of genistein in normal dogs given increasing oral doses of GCP did not reach the 72-hour in vitro IC50 in a dose escalation study.\n Question: Do soy-derived isoflavones inhibit the growth of canine lymphoid cell lines?\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 aimed to evaluate the in vitro effects of genistein, both pure genistein and a commercially available form of genistein called Genistein Combined Polysacharride (GCP), against two canine B-cell lymphoid cell lines and determine the oral bioavailability of GCP when fed to normal dogs. The in vitro effect of genistein and GCP was evaluated using cell proliferation and apoptotic assays. The IC50 of both compounds was determined using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) cell proliferation assay and propidium idodide staining. Apoptosis was evaluated using Annexin V staining, caspase 3 and 9 staining, and DNA laddering. Cell cycle analysis and Bcl-2/Bax ratios were also examined. An initial dose escalating pharmacokinetic study was used to determine if therapeutic serum levels of genistein could be reached with oral dosing of GCP in normal dogs. The 72-hour in vitro IC50 of genistein and GCP against the GL-1 and 17-71 cells were both 10 microg/mL and 20 microg/mL, respectively. GCP led to cell death in both cell lines via apoptosis and treated cells exhibited increased Bax:Bcl-2 ratios. The serum concentrations of genistein in normal dogs given increasing oral doses of GCP did not reach the 72-hour in vitro IC50 in a dose escalation study. Question: Do soy-derived isoflavones inhibit the growth of canine lymphoid cell lines? Output:
PubmedQA153077	[ { "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: Ethanol causes both tolerance and sensitization of Kupffer cells. Accordingly, this study examines the effect of acute ethanol consumption on nitric oxide (NO) production from Kupffer cells with or without lipopolysaccharide (LPS) treatment. Rats were given ethanol (4 g/kg body weight) intragastrically, and Kupffer cells were isolated 2 and 24 hr later. Some rats were treated for 4 days with 150 mg/kg/day of polymyxin B and 450 mg/kg/day of neomycin to prevent growth of intestinal bacteria, the primary source of endotoxin in the gastrointestinal tract. After addition of LPS, NO was measured by the Griess reaction. Two hours after ethanol administration, LPS-induced NO production by Kupffer cells was diminished by 50% but was enhanced 2-fold at 24 hr. Sterilization of the gut with antibiotics blocked this enhancement.\n Question: Does alcohol enhance lipopolysaccharide-induced increases in nitric oxide production by Kupffer cells via mechanisms dependent on endotoxin?\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: Ethanol causes both tolerance and sensitization of Kupffer cells. Accordingly, this study examines the effect of acute ethanol consumption on nitric oxide (NO) production from Kupffer cells with or without lipopolysaccharide (LPS) treatment. Rats were given ethanol (4 g/kg body weight) intragastrically, and Kupffer cells were isolated 2 and 24 hr later. Some rats were treated for 4 days with 150 mg/kg/day of polymyxin B and 450 mg/kg/day of neomycin to prevent growth of intestinal bacteria, the primary source of endotoxin in the gastrointestinal tract. After addition of LPS, NO was measured by the Griess reaction. Two hours after ethanol administration, LPS-induced NO production by Kupffer cells was diminished by 50% but was enhanced 2-fold at 24 hr. Sterilization of the gut with antibiotics blocked this enhancement. Question: Does alcohol enhance lipopolysaccharide-induced increases in nitric oxide production by Kupffer cells via mechanisms dependent on endotoxin? Output:
PubmedQA26522	[ { "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: Controversies surrounding the physiological effects of hormone replacement therapy (HRT) currently lie at the forefront of medicine. Important interindividual factors that affect blood pressure, such as smoking, body mass and sodium intake, may account for the conflicting findings seen in studies examining the effects of HRT on blood pressure. The study was a randomized, double-blind, placebo-controlled trial. The effect of combination HRT and estrogen-only replacement therapy (ERT) on ambulatory blood pressure was examined in a sample of 46 healthy, normotensive, non-smoking, non-obese postmenopausal women between 45 and 65 years of age. Twenty-four hour urinary sodium excretion was examined prior to and following treatment. The women were randomized to 3 months' treatment with HRT, ERT or placebo. After treatment, there were no significant effects of either HRT or ERT on daytime or night-time systolic or diastolic blood pressure. Sodium excretion was similar across the groups. There were no effects of treatment on night-time blood pressure dipping.\n Question: Does hormone replacement therapy affect 24-h ambulatory blood pressure in healthy non-smoking postmenopausal women?\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: Controversies surrounding the physiological effects of hormone replacement therapy (HRT) currently lie at the forefront of medicine. Important interindividual factors that affect blood pressure, such as smoking, body mass and sodium intake, may account for the conflicting findings seen in studies examining the effects of HRT on blood pressure. The study was a randomized, double-blind, placebo-controlled trial. The effect of combination HRT and estrogen-only replacement therapy (ERT) on ambulatory blood pressure was examined in a sample of 46 healthy, normotensive, non-smoking, non-obese postmenopausal women between 45 and 65 years of age. Twenty-four hour urinary sodium excretion was examined prior to and following treatment. The women were randomized to 3 months' treatment with HRT, ERT or placebo. After treatment, there were no significant effects of either HRT or ERT on daytime or night-time systolic or diastolic blood pressure. Sodium excretion was similar across the groups. There were no effects of treatment on night-time blood pressure dipping. Question: Does hormone replacement therapy affect 24-h ambulatory blood pressure in healthy non-smoking postmenopausal women? Output:
PubmedQA128435	[ { "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: Androgens are assumed to play a central role in the pathophysiology of both prostate cancer (PC) and androgenic alopecia (AA). A correlation between the two phenotypes may be relevant for identification of men at high risk of PC. We evaluated the association between AA at different ages and PC in a large case-control study. The case group comprised 938 PC patients recruited from a population-based cancer registry. The controls (n = 2160) were a random sample of the male general population. All subjects completed a questionnaire on risk factors for cancer, including questions on hair pattern at different ages using an adapted version of the Hamilton-Norwood scale, race and family history of PC. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using multivariable logistic regression. Baldness at early age appeared to be associated with a lower risk of PC (baldness at age 20: OR = 0.86; 95% CI 0.69-1.07 and baldness at age 40: OR = 0.81; 95% CI 0.70-0.96). Baldness at completion of the questionnaire was not associated with PC: OR = 1.10; 95% CI 0.89-1.34. An isolated 'frontal baldness' or 'vertex baldness' pattern was not significantly associated with PC at any age. Presence of a combined 'frontal and vertex' baldness pattern at age 40 was associated with a decreased risk of PC (OR = 0.62; 95% CI 0.45-0.86). There were no significant associations between AA and aggressive PC.\n Question: Is androgenic alopecia useful as an indicator of men at high risk of prostate cancer?\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: Androgens are assumed to play a central role in the pathophysiology of both prostate cancer (PC) and androgenic alopecia (AA). A correlation between the two phenotypes may be relevant for identification of men at high risk of PC. We evaluated the association between AA at different ages and PC in a large case-control study. The case group comprised 938 PC patients recruited from a population-based cancer registry. The controls (n = 2160) were a random sample of the male general population. All subjects completed a questionnaire on risk factors for cancer, including questions on hair pattern at different ages using an adapted version of the Hamilton-Norwood scale, race and family history of PC. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using multivariable logistic regression. Baldness at early age appeared to be associated with a lower risk of PC (baldness at age 20: OR = 0.86; 95% CI 0.69-1.07 and baldness at age 40: OR = 0.81; 95% CI 0.70-0.96). Baldness at completion of the questionnaire was not associated with PC: OR = 1.10; 95% CI 0.89-1.34. An isolated 'frontal baldness' or 'vertex baldness' pattern was not significantly associated with PC at any age. Presence of a combined 'frontal and vertex' baldness pattern at age 40 was associated with a decreased risk of PC (OR = 0.62; 95% CI 0.45-0.86). There were no significant associations between AA and aggressive PC. Question: Is androgenic alopecia useful as an indicator of men at high risk of prostate cancer? Output:
PubmedQA209464	[ { "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 a prospective study we evaluated whether late recanalization of the left anterior descending coronary artery (LAD) affects ventricular volume and function after anterior myocardial infarction. Persistent coronary occlusion after anterior myocardial infarction leads to ventricular dilation and heart failure. We studied 73 consecutive patients with acute anterior myocardial infarction as a first cardiac event; all had an isolated lesion or occlusion of the proximal LAD. Six patients died before hospital discharge. The 67 survivors were classified into two groups: group I (patent LAD and good distal flow, n = 40) and group II (LAD occlusion or subocclusion, n = 27). The 20 patients in group I who had significant residual stenosis and all patients in group II underwent elective percutaneous transluminal coronary angioplasty (PTCA) within 18 days of myocardial infarction. The procedure was successful in 17 patients in group I (group IB) and in 16 patients in group II (group IIA): in the remaining 11 patients of group II, patency could not be reestablished (group IIB). Left ventricular volumes, ejection fraction and a dysfunction score were measured by echocardiography on admission, before PTCA, at discharge and after 3 and 6 months. Although cumulative ST segment elevation was similar in groups I and II, ejection fraction and dysfunction score were significantly worse in group II. However, ventricular function and volumes progressively improved in group IIA, whereas group IIB exhibited progressive deterioration of function (dysfunction score [mean +/- SD] increased from 21 +/- 6 to 25 +/- 8, p < 0.05; ejection fraction decreased from 43 +/- 10% to 37 +/- 11%, p < 0.05); and end-systolic volume increased from 34 +/- 10 to 72 +/- 28 ml/m2, p < 0.05). Patients in group IIB also had worse effort tolerance, higher heart rate at rest, lower blood pressure and significantly greater prevalence of chronic heart failure.\n Question: Does coronary recanalization by elective angioplasty prevent ventricular dilation after anterior myocardial infarction?\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 a prospective study we evaluated whether late recanalization of the left anterior descending coronary artery (LAD) affects ventricular volume and function after anterior myocardial infarction. Persistent coronary occlusion after anterior myocardial infarction leads to ventricular dilation and heart failure. We studied 73 consecutive patients with acute anterior myocardial infarction as a first cardiac event; all had an isolated lesion or occlusion of the proximal LAD. Six patients died before hospital discharge. The 67 survivors were classified into two groups: group I (patent LAD and good distal flow, n = 40) and group II (LAD occlusion or subocclusion, n = 27). The 20 patients in group I who had significant residual stenosis and all patients in group II underwent elective percutaneous transluminal coronary angioplasty (PTCA) within 18 days of myocardial infarction. The procedure was successful in 17 patients in group I (group IB) and in 16 patients in group II (group IIA): in the remaining 11 patients of group II, patency could not be reestablished (group IIB). Left ventricular volumes, ejection fraction and a dysfunction score were measured by echocardiography on admission, before PTCA, at discharge and after 3 and 6 months. Although cumulative ST segment elevation was similar in groups I and II, ejection fraction and dysfunction score were significantly worse in group II. However, ventricular function and volumes progressively improved in group IIA, whereas group IIB exhibited progressive deterioration of function (dysfunction score [mean +/- SD] increased from 21 +/- 6 to 25 +/- 8, p < 0.05; ejection fraction decreased from 43 +/- 10% to 37 +/- 11%, p < 0.05); and end-systolic volume increased from 34 +/- 10 to 72 +/- 28 ml/m2, p < 0.05). Patients in group IIB also had worse effort tolerance, higher heart rate at rest, lower blood pressure and significantly greater prevalence of chronic heart failure. Question: Does coronary recanalization by elective angioplasty prevent ventricular dilation after anterior myocardial infarction? Output:
PubmedQA21313	[ { "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 intraparenchymal hyperattenuations (IPH) on flat-panel computed tomography (FP-CT) after endovascular recanalization in stroke patients is a common phenomenon. They are thought to occur in ischemic areas with breakdown of the blood-brain barrier but previous studies that investigated a mutual interaction are scarce. We aimed to assess the relationship of IPH localization with prethrombectomy diffusion-weighted imaging (DWI) lesions. This retrospective multicenter study included 27 acute stroke patients who underwent DWI prior to FP-CT following mechanical thrombectomy. After software-based coregistration of DWI and FP-CT, lesion volumetry was conducted and overlapping was analyzed. Two different patterns were observed: IPH corresponding to the DWI lesion and IPH exceeding the DWI lesion. The latter showed demarcated infarction of DWI exceeding IPH at 24 h. No major hemorrhage following IPH was observed. Most IPH were manifested within the basal ganglia and insular cortex.\n Question: Are intraparenchymal Hyperattenuations on Flat-Panel CT Directly After Mechanical Thrombectomy Restricted to the Initial Infarct Core on Diffusion-Weighted Imaging?\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 intraparenchymal hyperattenuations (IPH) on flat-panel computed tomography (FP-CT) after endovascular recanalization in stroke patients is a common phenomenon. They are thought to occur in ischemic areas with breakdown of the blood-brain barrier but previous studies that investigated a mutual interaction are scarce. We aimed to assess the relationship of IPH localization with prethrombectomy diffusion-weighted imaging (DWI) lesions. This retrospective multicenter study included 27 acute stroke patients who underwent DWI prior to FP-CT following mechanical thrombectomy. After software-based coregistration of DWI and FP-CT, lesion volumetry was conducted and overlapping was analyzed. Two different patterns were observed: IPH corresponding to the DWI lesion and IPH exceeding the DWI lesion. The latter showed demarcated infarction of DWI exceeding IPH at 24 h. No major hemorrhage following IPH was observed. Most IPH were manifested within the basal ganglia and insular cortex. Question: Are intraparenchymal Hyperattenuations on Flat-Panel CT Directly After Mechanical Thrombectomy Restricted to the Initial Infarct Core on Diffusion-Weighted Imaging? Output:
PubmedQA111439	[ { "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: Anal incontinence is a common disorder but current treatment modalities are not ideal and the development of new treatments is needed. The aim of this review was to identify the existing knowledge of regenerative medicine strategies in the form of cellular therapies or bioengineering as a treatment for anal incontinence caused by anal sphincter defects. PubMed was searched for preclinical and clinical studies in English published from January 2005 to January 2016. Animal studies have demonstrated that cellular therapy in the form of local injections of culture-expanded skeletal myogenic cells stimulates repair of both acute and 2 - 4-week-old anal sphincter injuries. The results from a small clinical trial with ten patients and a case report support the preclinical findings. Animal studies have also demonstrated that local injections of mesenchymal stem cells stimulate repair of sphincter injuries, and a complex bioengineering strategy for creation and implantation of an intrinsically innervated internal anal sphincter construct has been successfully developed in a series of animal studies.\n Question: Does regenerative medicine provide alternative strategies for the treatment of anal incontinence?\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: Anal incontinence is a common disorder but current treatment modalities are not ideal and the development of new treatments is needed. The aim of this review was to identify the existing knowledge of regenerative medicine strategies in the form of cellular therapies or bioengineering as a treatment for anal incontinence caused by anal sphincter defects. PubMed was searched for preclinical and clinical studies in English published from January 2005 to January 2016. Animal studies have demonstrated that cellular therapy in the form of local injections of culture-expanded skeletal myogenic cells stimulates repair of both acute and 2 - 4-week-old anal sphincter injuries. The results from a small clinical trial with ten patients and a case report support the preclinical findings. Animal studies have also demonstrated that local injections of mesenchymal stem cells stimulate repair of sphincter injuries, and a complex bioengineering strategy for creation and implantation of an intrinsically innervated internal anal sphincter construct has been successfully developed in a series of animal studies. Question: Does regenerative medicine provide alternative strategies for the treatment of anal incontinence? Output: