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PubmedQA154551
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Increased renal vascular resistance contributes to the pathogenesis of hypertension. The new Rho kinase (ROCK) inhibitor SAR407899 more potently lowers arterial pressure than the commercially available ROCK inhibitor Y27623. We tested whether ROCK inhibition more effectively reduced agonist-induced vasoconstriction in renal than in nonrenal resistance arteries and if SAR407899 more potently inhibits agonist-induced vasoconstriction than Y27632. The effects of the ROCK inhibitors on endothelin-1 (ET-1) induced vasoconstriction were investigated in isolated renal and coronary arteries from lean, normotensive Dark Agouti and obese, type 2 diabetic Zucker diabetic fatty (ZDF) rats as well as in isolated human resistance arteries from the kidney and thymus. Vascular ROCK mRNA abundance was studied by real-time PCR (RT-PCR). ET-1-induced constriction depended more on ROCK in rat and human renal resistance arteries than in rat coronary or human thymic arteries, respectively. SAR407899 was more effective than Y27632 in reducing ET-1-induced vasoconstriction in ZDF rat renal resistance arteries. Maximum ET-1-induced vasoconstriction in SAR407899-treated and Y27632-treated human renal resistance arteries was 23 ± 5 and 48 ± 6% of control values, respectively. Transcripts of both ROCK isoforms were detected in rat and human renal resistance arteries. In human thymic arteries, only the ROCK2 transcript was found.\n Question: Does the Rho kinase inhibitor SAR407899 potently inhibit endothelin-1-induced constriction of renal resistance arteries?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Increased renal vascular resistance contributes to the pathogenesis of hypertension. The new Rho kinase (ROCK) inhibitor SAR407899 more potently lowers arterial pressure than the commercially available ROCK inhibitor Y27623. We tested whether ROCK inhibition more effectively reduced agonist-induced vasoconstriction in renal than in nonrenal resistance arteries and if SAR407899 more potently inhibits agonist-induced vasoconstriction than Y27632. The effects of the ROCK inhibitors on endothelin-1 (ET-1) induced vasoconstriction were investigated in isolated renal and coronary arteries from lean, normotensive Dark Agouti and obese, type 2 diabetic Zucker diabetic fatty (ZDF) rats as well as in isolated human resistance arteries from the kidney and thymus. Vascular ROCK mRNA abundance was studied by real-time PCR (RT-PCR). ET-1-induced constriction depended more on ROCK in rat and human renal resistance arteries than in rat coronary or human thymic arteries, respectively. SAR407899 was more effective than Y27632 in reducing ET-1-induced vasoconstriction in ZDF rat renal resistance arteries. Maximum ET-1-induced vasoconstriction in SAR407899-treated and Y27632-treated human renal resistance arteries was 23 ± 5 and 48 ± 6% of control values, respectively. Transcripts of both ROCK isoforms were detected in rat and human renal resistance arteries. In human thymic arteries, only the ROCK2 transcript was found.
Question: Does the Rho kinase inhibitor SAR407899 potently inhibit endothelin-1-induced constriction of renal resistance arteries?
Output:
|
PubmedQA66966
|
[
{
"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: Invasive predators may change the structure of invaded communities through predation and competition with native species. In Europe, the invasive signal crayfish Pacifastacus leniusculus is excluding the native white clawed crayfish Austropotamobius pallipes. This study compared the predatory functional responses and prey choice of native and invasive crayfish and measured impacts of parasitism on the predatory strength of the native species. Invasive crayfish showed a higher (>10%) prey (Gammarus pulex) intake rate than (size matched) natives, reflecting a shorter (16%) prey handling time. The native crayfish also showed greater selection for crustacean prey over molluscs and bloodworm, whereas the invasive species was a more generalist predator. A. pallipes parasitised by the microsporidian parasite Thelohania contejeani showed a 30% reduction in prey intake. We suggest that this results from parasite-induced muscle damage, and this is supported by a reduced (38%) attack rate and increased (30%) prey handling time.\n Question: Do predatory functional response and prey choice identify predation differences between native/invasive and parasitised/unparasitised crayfish?\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: Invasive predators may change the structure of invaded communities through predation and competition with native species. In Europe, the invasive signal crayfish Pacifastacus leniusculus is excluding the native white clawed crayfish Austropotamobius pallipes. This study compared the predatory functional responses and prey choice of native and invasive crayfish and measured impacts of parasitism on the predatory strength of the native species. Invasive crayfish showed a higher (>10%) prey (Gammarus pulex) intake rate than (size matched) natives, reflecting a shorter (16%) prey handling time. The native crayfish also showed greater selection for crustacean prey over molluscs and bloodworm, whereas the invasive species was a more generalist predator. A. pallipes parasitised by the microsporidian parasite Thelohania contejeani showed a 30% reduction in prey intake. We suggest that this results from parasite-induced muscle damage, and this is supported by a reduced (38%) attack rate and increased (30%) prey handling time.
Question: Do predatory functional response and prey choice identify predation differences between native/invasive and parasitised/unparasitised crayfish?
Output:
|
PubmedQA51915
|
[
{
"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: Appendicitis continues to present a diagnostic dilemma in children of all ages leading to increased utilization of radiographic studies. Focused computed tomography (CT) scanning has become the diagnostic test of choice in many hospitals. The purpose of this study was to critically evaluate the use of radiographic studies for the evaluation of acute appendicitis in children and to determine if diagnostic accuracy has improved. Children undergoing appendectomy for acute appendicitis were reviewed from 1997 to 2001. Diagnostic workup (CT scan, ultrasound [US], or no radiographic study) was recorded as were the final pathology results. Six hundred sixteen appendectomies were performed. Mean age was 10.4 +/- 4.1 years, and 60% were boys. Overall, 184 children (30%) underwent CT scanning, 104 (17%) had US performed, and 310 (50%) had no radiographic study (18 patients had both CT and US performed). A pathologically normal appendix was removed in 7% (14 of 202) of CT patients, 11% (14 of 122) of US patients, and 8% (26 of 310) of patients without a study. The frequency of CT scanning increased from 1.3% of all children in 1997 to 58% in 2001, whereas utilization of US decreased from 40% to 7%. Over the same period, the overall negative appendectomy rate did not change significantly from 8% to 7%.\n Question: Does increased CT scan utilization improve the diagnostic accuracy of appendicitis in children?\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: Appendicitis continues to present a diagnostic dilemma in children of all ages leading to increased utilization of radiographic studies. Focused computed tomography (CT) scanning has become the diagnostic test of choice in many hospitals. The purpose of this study was to critically evaluate the use of radiographic studies for the evaluation of acute appendicitis in children and to determine if diagnostic accuracy has improved. Children undergoing appendectomy for acute appendicitis were reviewed from 1997 to 2001. Diagnostic workup (CT scan, ultrasound [US], or no radiographic study) was recorded as were the final pathology results. Six hundred sixteen appendectomies were performed. Mean age was 10.4 +/- 4.1 years, and 60% were boys. Overall, 184 children (30%) underwent CT scanning, 104 (17%) had US performed, and 310 (50%) had no radiographic study (18 patients had both CT and US performed). A pathologically normal appendix was removed in 7% (14 of 202) of CT patients, 11% (14 of 122) of US patients, and 8% (26 of 310) of patients without a study. The frequency of CT scanning increased from 1.3% of all children in 1997 to 58% in 2001, whereas utilization of US decreased from 40% to 7%. Over the same period, the overall negative appendectomy rate did not change significantly from 8% to 7%.
Question: Does increased CT scan utilization improve the diagnostic accuracy of appendicitis in children?
Output:
|
PubmedQA159234
|
[
{
"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: Based on current knowledge, it is possible to have an initial diagnosis of intrinsic or extrinsic ureteropelvic junction obstruction (UPJO) based solely on clinical and imaging findings. However, it may not be possible to strictly discriminate an intrinsic case with an additional extrinsic component from a primarily intrinsic stenosis because of lower pole aberrant vessels. These two disorders may coexist or trigger each other. Herein, we aimed to compare the histological changes observed in intrinsic and extrinsic types of UPJO. Our hypothesis is that inspecting the UPJ during pyeloplasty may not be a sufficient way to delineate the underlying cause of obstruction in every individual. We retrospectively reviewed the data of 56 patients who had dismembered pyeloplasty. The intrinsic and extrinsic groups consisted of 38 and 18 patients, respectively. Masson's trichrome stain, CD117, and connexin 43 (Cx43) antibody were used in histopathology and immunochemistry. Statistical calculations were done with chi-square and Mann-Whitney U tests.\n Question: Is intraoperative inspection of the ureteropelvic junction during pyeloplasty sufficient to distinguish between extrinsic and intrinsic causes of obstruction : Correlation with histological analysis?\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: Based on current knowledge, it is possible to have an initial diagnosis of intrinsic or extrinsic ureteropelvic junction obstruction (UPJO) based solely on clinical and imaging findings. However, it may not be possible to strictly discriminate an intrinsic case with an additional extrinsic component from a primarily intrinsic stenosis because of lower pole aberrant vessels. These two disorders may coexist or trigger each other. Herein, we aimed to compare the histological changes observed in intrinsic and extrinsic types of UPJO. Our hypothesis is that inspecting the UPJ during pyeloplasty may not be a sufficient way to delineate the underlying cause of obstruction in every individual. We retrospectively reviewed the data of 56 patients who had dismembered pyeloplasty. The intrinsic and extrinsic groups consisted of 38 and 18 patients, respectively. Masson's trichrome stain, CD117, and connexin 43 (Cx43) antibody were used in histopathology and immunochemistry. Statistical calculations were done with chi-square and Mann-Whitney U tests.
Question: Is intraoperative inspection of the ureteropelvic junction during pyeloplasty sufficient to distinguish between extrinsic and intrinsic causes of obstruction : Correlation with histological analysis?
Output:
|
PubmedQA143799
|
[
{
"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: Two randomized, six-week, double-blind, parallel group, clinical trials were independently conducted to compare the extrinsic stain removal efficacy of a novel whitening therapeutic dentifrice containing 0.454% stannous fluoride and sodium hexametaphosphate in a formulation with high cleaning silica, relative to a positive control whitening dentifrice. Generally healthy adults, 56 for study 1 and 60 for study 2, with visible extrinsic tooth stain were enrolled in the studies. At the baseline visit, stain was assessed on the facial surfaces of the eight central and lateral incisors using the modified Lobene Stain Index. Oral soft and hard tissue examinations were also conducted. In each study, subjects were randomized to either the stannous fluoride + sodium hexametaphosphate toothpaste (Crest Pro-Health) or the positive control toothpaste (Colgate Total Plus Whitening) to use twice per day for six weeks. Stain and safety were reassessed at weeks three and six. Fifty-two and 58 subjects completed studies 1 and 2, respectively. In each study, there were no statistically significant differences in Lobene composite stain scores between the two treatment groups across all three visits. Both groups showed statistically significant reductions in Lobene composite stain scores at week three (p < 0.0001) and week six (p < 0.0001) relative to baseline. The percent of Lobene composite scores with a greater than 0.5 unit reduction from baseline at week six was 86% for study 1 and 97% for study 2 for the stannous fluoride + sodium hexametaphosphate dentifrice group.\n Question: Do extrinsic stain removal efficacy of a stannous fluoride dentifrice with sodium hexametaphosphate?\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: Two randomized, six-week, double-blind, parallel group, clinical trials were independently conducted to compare the extrinsic stain removal efficacy of a novel whitening therapeutic dentifrice containing 0.454% stannous fluoride and sodium hexametaphosphate in a formulation with high cleaning silica, relative to a positive control whitening dentifrice. Generally healthy adults, 56 for study 1 and 60 for study 2, with visible extrinsic tooth stain were enrolled in the studies. At the baseline visit, stain was assessed on the facial surfaces of the eight central and lateral incisors using the modified Lobene Stain Index. Oral soft and hard tissue examinations were also conducted. In each study, subjects were randomized to either the stannous fluoride + sodium hexametaphosphate toothpaste (Crest Pro-Health) or the positive control toothpaste (Colgate Total Plus Whitening) to use twice per day for six weeks. Stain and safety were reassessed at weeks three and six. Fifty-two and 58 subjects completed studies 1 and 2, respectively. In each study, there were no statistically significant differences in Lobene composite stain scores between the two treatment groups across all three visits. Both groups showed statistically significant reductions in Lobene composite stain scores at week three (p < 0.0001) and week six (p < 0.0001) relative to baseline. The percent of Lobene composite scores with a greater than 0.5 unit reduction from baseline at week six was 86% for study 1 and 97% for study 2 for the stannous fluoride + sodium hexametaphosphate dentifrice group.
Question: Do extrinsic stain removal efficacy of a stannous fluoride dentifrice with sodium hexametaphosphate?
Output:
|
PubmedQA130095
|
[
{
"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 QT interval, an index of ventricular repolarization, is rate dependent. Exaggerated rate dependence of repolarization is arrhythmogenic. Whether there are differences in rate-dependent repolarization among different heart chambers is unknown. The purpose of this study was to test our hypothesis that heterogeneous distribution in late sodium current (INa-L) is responsible for interregional differences in rate adaptation of repolarization. Action potential duration (APD), QT intervals, and their rate adaptation were studied in isolated arterially perfused ventricular and atrial wedge preparations. APD and INa-L were recorded in isolated rabbit myocytes using the microelectrode and the whole-cell patch clamp technique, respectively. There were distinct interregional differences in repolarization and its rate adaptations among different cardiac chambers: the left ventricle exhibited the longest QT and APD with the greatest rate dependence, followed by the right ventricle, whereas the atria had the shortest APD without significant rate dependence. Interestingly, INa-L densities distributed heterogeneously and matched to interregional APDs and rate dependences as follows: left ventricle > right ventricle > left/right atria. Both dofetilide (an IKr blocker) and anemone toxin (a specific INa-L enhancer) amplified QT/APD rate adaptation preferentially in the left ventricle and therefore exacerbated interregional dispersion of repolarization. On the other hand, the atria exhibited blunted responses to both QT-prolonging agents. Mexiletine with an INa-L blockade effect blunted QT/APD rate adaptation preferentially in the ventricles and significantly reduced bradycardia-dependent interregional dispersion of repolarization.\n Question: Does heterogeneous distribution of INa-L determine interregional differences in rate adaptation of repolarization?\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 QT interval, an index of ventricular repolarization, is rate dependent. Exaggerated rate dependence of repolarization is arrhythmogenic. Whether there are differences in rate-dependent repolarization among different heart chambers is unknown. The purpose of this study was to test our hypothesis that heterogeneous distribution in late sodium current (INa-L) is responsible for interregional differences in rate adaptation of repolarization. Action potential duration (APD), QT intervals, and their rate adaptation were studied in isolated arterially perfused ventricular and atrial wedge preparations. APD and INa-L were recorded in isolated rabbit myocytes using the microelectrode and the whole-cell patch clamp technique, respectively. There were distinct interregional differences in repolarization and its rate adaptations among different cardiac chambers: the left ventricle exhibited the longest QT and APD with the greatest rate dependence, followed by the right ventricle, whereas the atria had the shortest APD without significant rate dependence. Interestingly, INa-L densities distributed heterogeneously and matched to interregional APDs and rate dependences as follows: left ventricle > right ventricle > left/right atria. Both dofetilide (an IKr blocker) and anemone toxin (a specific INa-L enhancer) amplified QT/APD rate adaptation preferentially in the left ventricle and therefore exacerbated interregional dispersion of repolarization. On the other hand, the atria exhibited blunted responses to both QT-prolonging agents. Mexiletine with an INa-L blockade effect blunted QT/APD rate adaptation preferentially in the ventricles and significantly reduced bradycardia-dependent interregional dispersion of repolarization.
Question: Does heterogeneous distribution of INa-L determine interregional differences in rate adaptation of repolarization?
Output:
|
PubmedQA208874
|
[
{
"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: Lipopolysaccharide (LPS) injection in mammals orchestrates the release of many proinflammatory and anti-inflammatory cytokines. Intravenous administration of 0.2 mg/kg of LPS into unanesthetized rats with indwelling jugular catheters provoked a rapid, 50-fold increase in plasma tumor necrosis factor (TNF)-alpha within 30 min, which declined by 60% by 120 min. To test our hypothesis that such a rapid increase of TNF-alpha would be either neurally or hormonally controlled, the effect on TNF-alpha release of anesthesia (ketamine/acepromazine/xylazine) and catecholaminergic agonists and antagonists, either alone or in the presence of LPS, was determined. Rats bearing indwelling external jugular catheters were injected with the test drug or saline after removal of 0.6 ml of blood (-10 min). At time zero, LPS or saline was administered. Thereafter, blood samples were drawn at 15, 30, 120, 240 and 360 min. TNF-alpha was measured by immunoassay. Among all the drugs tested, only propranolol increased plasma TNF-alpha. Anesthesia significantly blunted the LPS-induced TNF-alpha peak by 50%. Isoproterenol, a beta-adrenergic agonist, also blocked LPS-induced TNF-alpha release by 70% at 30 min and 90% at 120 min. On the contrary, propranolol, a beta-receptor blocker, induced a highly significant 3-fold increase in plasma TNF-alpha concentrations at 30 min and augmented the response to LPS 2-fold after endotoxin injection. Phentolamine, an alpha-receptor blocker, decreased the LPS-induced TNF-alpha release by 57% at 30 min. Similarly, alpha-bromoergocryptine, a dopamine D2 receptor agonist, decreased the LPS-induced TNF-alpha peak by 70% at 30 min and 50% at 120 min.\n Question: Is lipopolysaccharide-induced tumor necrosis factor-alpha release controlled by the central nervous system?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Lipopolysaccharide (LPS) injection in mammals orchestrates the release of many proinflammatory and anti-inflammatory cytokines. Intravenous administration of 0.2 mg/kg of LPS into unanesthetized rats with indwelling jugular catheters provoked a rapid, 50-fold increase in plasma tumor necrosis factor (TNF)-alpha within 30 min, which declined by 60% by 120 min. To test our hypothesis that such a rapid increase of TNF-alpha would be either neurally or hormonally controlled, the effect on TNF-alpha release of anesthesia (ketamine/acepromazine/xylazine) and catecholaminergic agonists and antagonists, either alone or in the presence of LPS, was determined. Rats bearing indwelling external jugular catheters were injected with the test drug or saline after removal of 0.6 ml of blood (-10 min). At time zero, LPS or saline was administered. Thereafter, blood samples were drawn at 15, 30, 120, 240 and 360 min. TNF-alpha was measured by immunoassay. Among all the drugs tested, only propranolol increased plasma TNF-alpha. Anesthesia significantly blunted the LPS-induced TNF-alpha peak by 50%. Isoproterenol, a beta-adrenergic agonist, also blocked LPS-induced TNF-alpha release by 70% at 30 min and 90% at 120 min. On the contrary, propranolol, a beta-receptor blocker, induced a highly significant 3-fold increase in plasma TNF-alpha concentrations at 30 min and augmented the response to LPS 2-fold after endotoxin injection. Phentolamine, an alpha-receptor blocker, decreased the LPS-induced TNF-alpha release by 57% at 30 min. Similarly, alpha-bromoergocryptine, a dopamine D2 receptor agonist, decreased the LPS-induced TNF-alpha peak by 70% at 30 min and 50% at 120 min.
Question: Is lipopolysaccharide-induced tumor necrosis factor-alpha release controlled by the central nervous system?
Output:
|
PubmedQA123281
|
[
{
"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 assess the association of user interest in various activities with personality traits for the provision of activity programs at adult day centers. A self-reported questionnaire survey of service users was conducted at 25 day centers in Tokyo; 133 men and 344 women, with a mean age of 81.6 +/- 7.9 years, responded. The questionnaire examined their demographics, lifestyles, requested activities, purpose of activity participation, attitudes toward participation, and personality traits by using the BASIC-3 Personality Inventory (PI)-short version. The participants with higher sociability and novelty-seeking scores on the BASIC-3 PI-short version requested significantly more activities than those with lower scores. Music appreciation and singing were significantly associated with both sociability and novelty-seeking facets. The sociability facets were significantly associated with activities, such as walking and interaction with children, while the novelty-seeking facets were significantly associated with contact with animals and the Internet. There was no significant relationship between the neuroticism facets and any specific activity. Flower arrangement, handicrafts, fashion or make up, cooking, and singing were significantly more frequently requested by the women than by the men, while shogi or mahjong was requested significantly more frequently by the men than by the women.\n Question: Do personality traits affect individual interests in day service activities?\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 assess the association of user interest in various activities with personality traits for the provision of activity programs at adult day centers. A self-reported questionnaire survey of service users was conducted at 25 day centers in Tokyo; 133 men and 344 women, with a mean age of 81.6 +/- 7.9 years, responded. The questionnaire examined their demographics, lifestyles, requested activities, purpose of activity participation, attitudes toward participation, and personality traits by using the BASIC-3 Personality Inventory (PI)-short version. The participants with higher sociability and novelty-seeking scores on the BASIC-3 PI-short version requested significantly more activities than those with lower scores. Music appreciation and singing were significantly associated with both sociability and novelty-seeking facets. The sociability facets were significantly associated with activities, such as walking and interaction with children, while the novelty-seeking facets were significantly associated with contact with animals and the Internet. There was no significant relationship between the neuroticism facets and any specific activity. Flower arrangement, handicrafts, fashion or make up, cooking, and singing were significantly more frequently requested by the women than by the men, while shogi or mahjong was requested significantly more frequently by the men than by the women.
Question: Do personality traits affect individual interests in day service activities?
Output:
|
PubmedQA105907
|
[
{
"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: Fibroblast growth factor 1 (FGF1) binds and activates FGF receptors, thereby regulating cell proliferation and neurogenesis. Human FGF1 gene 1B promoter (-540 to +31)-driven SV40 T antigen has been shown to result in tumorigenesis in the brains of transgenic mice. FGF1B promoter (-540 to +31)-driven green fluorescent protein (F1BGFP) has also been used in isolating neural stem cells (NSCs) with self-renewal and multipotency from developing and adult mouse brains. In this study, we provide six lines of evidence to demonstrate that FGF1/FGFR signaling is implicated in the expression of Aurora A (AurA) and the activation of its kinase domain (Thr288 phosphorylation) in the maintenance of glioblastoma (GBM) cells and NSCs. First, treatment of FGF1 increases AurA expression in human GBM cell lines. Second, using fluorescence-activated cell sorting, we observed that F1BGFP reporter facilitates the isolation of F1BGFP(+) GBM cells with higher expression levels of FGFR and AurA. Third, both FGFR inhibitor (SU5402) and AurA inhibitor (VX680) could down-regulate F1BGFP-dependent AurA activity. Fourth, inhibition of AurA activity by two different AurA inhibitors (VX680 and valproic acid) not only reduced neurosphere formation but also induced neuronal differentiation of F1BGFP(+) GBM cells. Fifth, flow cytometric analyses demonstrated that F1BGFP(+) GBM cells possessed different NSC cell surface markers. Finally, inhibition of AurA by VX680 reduced the neurosphere formation of different types of NSCs. Our results show that activation of AurA kinase through FGF1/FGFR signaling axis sustains the stem cell characteristics of GBM cells.\n Question: Does activation of Aurora A kinase through the FGF1/FGFR signaling axis sustain the stem cell characteristics of glioblastoma cells?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Fibroblast growth factor 1 (FGF1) binds and activates FGF receptors, thereby regulating cell proliferation and neurogenesis. Human FGF1 gene 1B promoter (-540 to +31)-driven SV40 T antigen has been shown to result in tumorigenesis in the brains of transgenic mice. FGF1B promoter (-540 to +31)-driven green fluorescent protein (F1BGFP) has also been used in isolating neural stem cells (NSCs) with self-renewal and multipotency from developing and adult mouse brains. In this study, we provide six lines of evidence to demonstrate that FGF1/FGFR signaling is implicated in the expression of Aurora A (AurA) and the activation of its kinase domain (Thr288 phosphorylation) in the maintenance of glioblastoma (GBM) cells and NSCs. First, treatment of FGF1 increases AurA expression in human GBM cell lines. Second, using fluorescence-activated cell sorting, we observed that F1BGFP reporter facilitates the isolation of F1BGFP(+) GBM cells with higher expression levels of FGFR and AurA. Third, both FGFR inhibitor (SU5402) and AurA inhibitor (VX680) could down-regulate F1BGFP-dependent AurA activity. Fourth, inhibition of AurA activity by two different AurA inhibitors (VX680 and valproic acid) not only reduced neurosphere formation but also induced neuronal differentiation of F1BGFP(+) GBM cells. Fifth, flow cytometric analyses demonstrated that F1BGFP(+) GBM cells possessed different NSC cell surface markers. Finally, inhibition of AurA by VX680 reduced the neurosphere formation of different types of NSCs. Our results show that activation of AurA kinase through FGF1/FGFR signaling axis sustains the stem cell characteristics of GBM cells.
Question: Does activation of Aurora A kinase through the FGF1/FGFR signaling axis sustain the stem cell characteristics of glioblastoma cells?
Output:
|
PubmedQA202156
|
[
{
"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: An increase in intrapulpal pressure occurs during inflammation and restorative procedures; however, the role of the pressure on human dental pulp cell (HDPC) is not yet clarified. In this study, the effect of pressure on interleukin-6 (IL-6) expression of HDPCs was examined. HDPCs were applied with pressure (0.7-1.4 g/cm(2)). The level of IL-6 mRNA and protein release was determined by RT-PCR and ELISA, respectively. The signalling pathways were investigated using inhibitors, antagonists, and small interfering RNA. The results showed that pressure up-regulated IL-6 mRNA expression and protein release in a time- and dose-dependent manner. The implication of P2Y receptor was exhibited by a significant inhibition of pressure-induced IL-6 expression by suramin, an antagonist for the non-specific purinergic receptor family. Using loss of function experiments, we showed MRS2578 (a specific P2Y6 antagonist), as well as P2Y6 small interfering RNA, abolished pressure-induced IL-6, whilst MRS2179 (a specific P2Y1 antagonist) and NF449 (a P2X1, P2X3, P2Y1, and P2Y2 antagonist) had no effect. Finally, we demonstrated that either the conditioned medium collected from pressurised dental pulp cells or addition of UDP, a selective agonist of P2Y6, up-regulated IL-6 expression in HDPCs.\n Question: Does pressure induce interleukin-6 expression via the P2Y6 receptor in human dental pulp cells?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: An increase in intrapulpal pressure occurs during inflammation and restorative procedures; however, the role of the pressure on human dental pulp cell (HDPC) is not yet clarified. In this study, the effect of pressure on interleukin-6 (IL-6) expression of HDPCs was examined. HDPCs were applied with pressure (0.7-1.4 g/cm(2)). The level of IL-6 mRNA and protein release was determined by RT-PCR and ELISA, respectively. The signalling pathways were investigated using inhibitors, antagonists, and small interfering RNA. The results showed that pressure up-regulated IL-6 mRNA expression and protein release in a time- and dose-dependent manner. The implication of P2Y receptor was exhibited by a significant inhibition of pressure-induced IL-6 expression by suramin, an antagonist for the non-specific purinergic receptor family. Using loss of function experiments, we showed MRS2578 (a specific P2Y6 antagonist), as well as P2Y6 small interfering RNA, abolished pressure-induced IL-6, whilst MRS2179 (a specific P2Y1 antagonist) and NF449 (a P2X1, P2X3, P2Y1, and P2Y2 antagonist) had no effect. Finally, we demonstrated that either the conditioned medium collected from pressurised dental pulp cells or addition of UDP, a selective agonist of P2Y6, up-regulated IL-6 expression in HDPCs.
Question: Does pressure induce interleukin-6 expression via the P2Y6 receptor in human dental pulp cells?
Output:
|
PubmedQA79688
|
[
{
"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: Immature B lymphocytes and certain B cell lymphomas undergo apoptotic cell death following activation of the B cell antigen receptor (BCR) signal transduction pathway. Several biochemical changes occur in response to BCR engagement, including activation of the Syk tyrosine kinase. Although Syk activation appears to be necessary for some downstream biochemical and cellular responses, the signaling events that precede Syk activation remain ill defined. In addition, the requirements for complete activation of the Syk-dependent signaling step remain to be elucidated. A mutant form of Syk carrying a combination of a K395A substitution in the kinase domain and substitutions of three phenylalanines (3F) for the three C-terminal tyrosines was expressed in a murine B cell lymphoma cell line, BCL1.3B3 to interfere with normal Syk regulation as a means to examine the Syk activation step in BCR signaling. Introduction of this kinase-inactive mutant led to the constitutive activation of the endogenous wildtype Syk enzyme in the absence of receptor engagement through a 'dominant-positive' effect. Under these conditions, Syk kinase activation occurred in the absence of phosphorylation on Syk tyrosine residues. Although Syk appears to be required for BCR-induced apoptosis in several systems, no increase in spontaneous cell death was observed in these cells. Surprisingly, although the endogenous Syk kinase was enzymatically active, no enhancement in the phosphorylation of cytoplasmic proteins, including phospholipase Cgamma2 (PLCgamma2), a direct Syk target, was observed.\n Question: Is activation of the Syk tyrosine kinase insufficient for downstream signal transduction in B lymphocytes?\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: Immature B lymphocytes and certain B cell lymphomas undergo apoptotic cell death following activation of the B cell antigen receptor (BCR) signal transduction pathway. Several biochemical changes occur in response to BCR engagement, including activation of the Syk tyrosine kinase. Although Syk activation appears to be necessary for some downstream biochemical and cellular responses, the signaling events that precede Syk activation remain ill defined. In addition, the requirements for complete activation of the Syk-dependent signaling step remain to be elucidated. A mutant form of Syk carrying a combination of a K395A substitution in the kinase domain and substitutions of three phenylalanines (3F) for the three C-terminal tyrosines was expressed in a murine B cell lymphoma cell line, BCL1.3B3 to interfere with normal Syk regulation as a means to examine the Syk activation step in BCR signaling. Introduction of this kinase-inactive mutant led to the constitutive activation of the endogenous wildtype Syk enzyme in the absence of receptor engagement through a 'dominant-positive' effect. Under these conditions, Syk kinase activation occurred in the absence of phosphorylation on Syk tyrosine residues. Although Syk appears to be required for BCR-induced apoptosis in several systems, no increase in spontaneous cell death was observed in these cells. Surprisingly, although the endogenous Syk kinase was enzymatically active, no enhancement in the phosphorylation of cytoplasmic proteins, including phospholipase Cgamma2 (PLCgamma2), a direct Syk target, was observed.
Question: Is activation of the Syk tyrosine kinase insufficient for downstream signal transduction in B lymphocytes?
Output:
|
PubmedQA102585
|
[
{
"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 measure the effect of exposure to a specific spatial-temporal, hysiologically-patterned electromagnetic field presented using different geometric configurations on the growth of experimental tumours in mice. C57b male mice were inoculated subcutaneously with B16-BL6 melanoma cells in two blocks of experiments separated by six months (to control for the effects of geomagnetic field). The mice were exposed to the same time-varying electromagnetic field nightly for 3 h in one of six spatial configurations or two control conditions and tumour growth assessed. Mice exposed to the field that was rotated through the three spatial dimensions and through all three planes every 2 sec did not grow tumours after 38 days. However, the mice in the sham-field and reference controls showed massive tumours after 38 days. Tumour growth was also affected by the intensity of the field, with mice exposed to a weak intensity field (1-5 nT) forming smaller tumours than mice exposed to sham or stronger, high intensity (2-5 microT) fields. Immunochemistry of tumours from those mice exposed to the different intensity fields suggested that alterations in leukocyte infiltration or vascularisation could contribute to the differences in tumour growth.\n Question: Is growth of injected melanoma cells suppressed by whole body exposure to specific spatial-temporal configurations of weak intensity magnetic fields?\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 measure the effect of exposure to a specific spatial-temporal, hysiologically-patterned electromagnetic field presented using different geometric configurations on the growth of experimental tumours in mice. C57b male mice were inoculated subcutaneously with B16-BL6 melanoma cells in two blocks of experiments separated by six months (to control for the effects of geomagnetic field). The mice were exposed to the same time-varying electromagnetic field nightly for 3 h in one of six spatial configurations or two control conditions and tumour growth assessed. Mice exposed to the field that was rotated through the three spatial dimensions and through all three planes every 2 sec did not grow tumours after 38 days. However, the mice in the sham-field and reference controls showed massive tumours after 38 days. Tumour growth was also affected by the intensity of the field, with mice exposed to a weak intensity field (1-5 nT) forming smaller tumours than mice exposed to sham or stronger, high intensity (2-5 microT) fields. Immunochemistry of tumours from those mice exposed to the different intensity fields suggested that alterations in leukocyte infiltration or vascularisation could contribute to the differences in tumour growth.
Question: Is growth of injected melanoma cells suppressed by whole body exposure to specific spatial-temporal configurations of weak intensity magnetic fields?
Output:
|
PubmedQA157540
|
[
{
"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: Anaemia is a common complication of diabetes mellitus (DM), usually related to renal failure. There is scarce information as to the levels of haemoglobin (Hb) and the rate of anaemia in diabetic patients with normal renal function. We, therefore, evaluated haemoglobin levels and the rate of anaemia in diabetic subjects with normal renal functions [estimated glomerular filtration rate (eGFR) > 60 mL/min]. The charts of 9250 subjects who attended the Institute of Periodic Medical Examinations at the Chaim Sheba Medical Center for a routine yearly check-up were reviewed. Four hundred and forty-five subjects with type 2 DM and normal renal function were indentified and compared with those without DM who were routinely examined at the same time. Subjects' electronic records were used to build a biochemical and clinical database. Mean haemoglobin levels were lower in subjects with DM than in those without (14.2 vs. 14.7 g/dL, respectively; p < 0.001). Anaemia was observed in 48 (10.8%) subjects in the diabetic group and in only 12 (2.7%) in the nondiabetic group (p < 0.001). Multivariate analysis revealed that age, gender, history of gastrointestinal disease, use of beta blockers, renal function and DM were independent determinants of haemoglobin levels. After adjustment for age, gender, history of gastrointestinal tract diseases and renal function, DM remained a significant determinant of anaemia with an odds ratio of 2.15 (confidence interval: 1.07-4.31).\n Question: Is diabetes mellitus with normal renal function associated with anaemia?\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: Anaemia is a common complication of diabetes mellitus (DM), usually related to renal failure. There is scarce information as to the levels of haemoglobin (Hb) and the rate of anaemia in diabetic patients with normal renal function. We, therefore, evaluated haemoglobin levels and the rate of anaemia in diabetic subjects with normal renal functions [estimated glomerular filtration rate (eGFR) > 60 mL/min]. The charts of 9250 subjects who attended the Institute of Periodic Medical Examinations at the Chaim Sheba Medical Center for a routine yearly check-up were reviewed. Four hundred and forty-five subjects with type 2 DM and normal renal function were indentified and compared with those without DM who were routinely examined at the same time. Subjects' electronic records were used to build a biochemical and clinical database. Mean haemoglobin levels were lower in subjects with DM than in those without (14.2 vs. 14.7 g/dL, respectively; p < 0.001). Anaemia was observed in 48 (10.8%) subjects in the diabetic group and in only 12 (2.7%) in the nondiabetic group (p < 0.001). Multivariate analysis revealed that age, gender, history of gastrointestinal disease, use of beta blockers, renal function and DM were independent determinants of haemoglobin levels. After adjustment for age, gender, history of gastrointestinal tract diseases and renal function, DM remained a significant determinant of anaemia with an odds ratio of 2.15 (confidence interval: 1.07-4.31).
Question: Is diabetes mellitus with normal renal function associated with anaemia?
Output:
|
PubmedQA82881
|
[
{
"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 extrapulmonary sarcomatous metastases has traditionally been a contraindication for the resection of pulmonary metastases. We, therefore, reviewed our experience with resection of pulmonary metastases in patients who had documented extrapulmonary metastases to determine long-term outcome. From 1998 to 2006, 234 patients underwent pulmonary metastasectomy. They were grouped as follows: group A (lung metastasectomy only); group B1 (with either synchronous or prior extrapulmonary metastasectomy); group B2 (with nonsurgical treatment of synchronous or prior extrapulmonary metastases); group C1 (with later extrapulmonary metastasectomy); group C2 (with later extrapulmonary metastasis which was not resected). Groups A, B1, and B2 consisted of 147 (62.8%), 26 (11.1%), and 13 (5.6%) patients, respectively. The median survival from lung metastasectomy date was 35.5, 37.8, and 13.5 months in groups A, B1, and B2, respectively. Comparison among the three groups showed no significant survival difference in groups A versus B1 (p = 0.96), but a survival difference was found comparing groups A versus B2 (p < 0.001) and B1 versus B2 (p < 0.001). Prognostic factors for increased survival included 3 or greater redo pulmonary operations, greater than 12 month mean time between pulmonary recurrences, greater than 24 month mean time between extrathoracic recurrences, and a prolonged disease-free interval. Prognostic factors for decreased survival included 3 or greater pulmonary metastases and group B2 patients.\n Question: Is resection of pulmonary and extrapulmonary sarcomatous metastases associated with long-term survival?\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 extrapulmonary sarcomatous metastases has traditionally been a contraindication for the resection of pulmonary metastases. We, therefore, reviewed our experience with resection of pulmonary metastases in patients who had documented extrapulmonary metastases to determine long-term outcome. From 1998 to 2006, 234 patients underwent pulmonary metastasectomy. They were grouped as follows: group A (lung metastasectomy only); group B1 (with either synchronous or prior extrapulmonary metastasectomy); group B2 (with nonsurgical treatment of synchronous or prior extrapulmonary metastases); group C1 (with later extrapulmonary metastasectomy); group C2 (with later extrapulmonary metastasis which was not resected). Groups A, B1, and B2 consisted of 147 (62.8%), 26 (11.1%), and 13 (5.6%) patients, respectively. The median survival from lung metastasectomy date was 35.5, 37.8, and 13.5 months in groups A, B1, and B2, respectively. Comparison among the three groups showed no significant survival difference in groups A versus B1 (p = 0.96), but a survival difference was found comparing groups A versus B2 (p < 0.001) and B1 versus B2 (p < 0.001). Prognostic factors for increased survival included 3 or greater redo pulmonary operations, greater than 12 month mean time between pulmonary recurrences, greater than 24 month mean time between extrathoracic recurrences, and a prolonged disease-free interval. Prognostic factors for decreased survival included 3 or greater pulmonary metastases and group B2 patients.
Question: Is resection of pulmonary and extrapulmonary sarcomatous metastases associated with long-term survival?
Output:
|
PubmedQA109235
|
[
{
"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: Ankaferd blood stopper (ABS) is a standardized herbal extract obtained from 5 different plants. In Turkey, it has been approved for local topical applications in external postsurgical and postdental surgery bleedings. Ankaferd blood stopper, besides its hemostatic activity, has in vitro anti-infectious and antineoplastic actions. The aim of this study was to assess short-term hematological and biochemical safety following the oral systemic administration of ABS to rabbits. Twelve rabbits (aged 6-12 months) were included to test the safety of oral ABS. Animals were divided into 4 groups, which had ABS administered orally at doses of 1, 3, 6, and 9 mL, irrespective of their weight. The general well-being and feeding patterns of the animals were observed for a period of 7 days. Blood samples (5.5 mL) were obtained just before oral administration, on days 1 and 4. During the observation period of 7 days, none of the animals showed any abnormal behavior or deviation from the normal. Acute mucosal toxicity, hematotoxicity, hepatotoxicity, nephrotoxicity, and biochemical toxicity were not observed during the short-term follow-up of the animals.\n Question: Does oral systemic administration of Ankaferd blood stopper have no short-term toxicity in an in vivo rabbit experimental model?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Ankaferd blood stopper (ABS) is a standardized herbal extract obtained from 5 different plants. In Turkey, it has been approved for local topical applications in external postsurgical and postdental surgery bleedings. Ankaferd blood stopper, besides its hemostatic activity, has in vitro anti-infectious and antineoplastic actions. The aim of this study was to assess short-term hematological and biochemical safety following the oral systemic administration of ABS to rabbits. Twelve rabbits (aged 6-12 months) were included to test the safety of oral ABS. Animals were divided into 4 groups, which had ABS administered orally at doses of 1, 3, 6, and 9 mL, irrespective of their weight. The general well-being and feeding patterns of the animals were observed for a period of 7 days. Blood samples (5.5 mL) were obtained just before oral administration, on days 1 and 4. During the observation period of 7 days, none of the animals showed any abnormal behavior or deviation from the normal. Acute mucosal toxicity, hematotoxicity, hepatotoxicity, nephrotoxicity, and biochemical toxicity were not observed during the short-term follow-up of the animals.
Question: Does oral systemic administration of Ankaferd blood stopper have no short-term toxicity in an in vivo rabbit experimental model?
Output:
|
PubmedQA101326
|
[
{
"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 characterize a 33-kDa protein (p33) isolated from bovine liver and to determine the subcellular localization of the protein in rat cardiocytes as well as in non-cardiac tissues. Cycles of calcium-induced precipitation coupled with EGTA-resolubilization were used to isolate crude annexins from bovine and rat tissues. Column chromatography was performed to purify the p33 from the crude annexins. The protein was identified as annexin V by partial amino acid sequence determination. Specificity of anti-annexin V antibody was examined by using Western blotting after one- or two-dimensional electrophoresis. For characterization of the protein, immunofluorescence microscopy and actin-binding assays were carried out. Immunofluorescence microscopy showed that annexin V was stained as a striated pattern along myofibrils on frozen sections of both atria and ventricles of adult rats. The striations were seen more clearly in cultured rat atrial myocytes. Examination of doubly stained cardiocytes with anti-annexin V and anti-alpha-actinin by a confocal laser scanning microscope suggests that annexin V is localized in association with the Z-line of rat cardiac myocytes. We also found that annexin V was stained intensely in actin-rich regions of non-cardiac tissues such as bile canaliculi of rat liver and brush border-terminal web region in the epithelial cells of both small intestine and kidney proximal tubular cells. F-actin binding experiments revealed that annexin V failed to bind to F-actin directly in vitro.\n Question: Is annexin V localized in association with Z-line of rat cardiac myocytes?\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 characterize a 33-kDa protein (p33) isolated from bovine liver and to determine the subcellular localization of the protein in rat cardiocytes as well as in non-cardiac tissues. Cycles of calcium-induced precipitation coupled with EGTA-resolubilization were used to isolate crude annexins from bovine and rat tissues. Column chromatography was performed to purify the p33 from the crude annexins. The protein was identified as annexin V by partial amino acid sequence determination. Specificity of anti-annexin V antibody was examined by using Western blotting after one- or two-dimensional electrophoresis. For characterization of the protein, immunofluorescence microscopy and actin-binding assays were carried out. Immunofluorescence microscopy showed that annexin V was stained as a striated pattern along myofibrils on frozen sections of both atria and ventricles of adult rats. The striations were seen more clearly in cultured rat atrial myocytes. Examination of doubly stained cardiocytes with anti-annexin V and anti-alpha-actinin by a confocal laser scanning microscope suggests that annexin V is localized in association with the Z-line of rat cardiac myocytes. We also found that annexin V was stained intensely in actin-rich regions of non-cardiac tissues such as bile canaliculi of rat liver and brush border-terminal web region in the epithelial cells of both small intestine and kidney proximal tubular cells. F-actin binding experiments revealed that annexin V failed to bind to F-actin directly in vitro.
Question: Is annexin V localized in association with Z-line of rat cardiac myocytes?
Output:
|
PubmedQA71846
|
[
{
"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 association between hypertension and obesity and also their prevalence in the adult population from Ilha do Governador-Rio de Janeiro. It is a domiciliar inquiry, with a probalistic cluster sample in two stages. We interviewed 1272 adult residents in the selected households. Social-demographic information, anthropometric measures, habits related to smoking, physical activities and blood pressure were registered. The prevalence of hypertension-systolic pressure > or = 160mmHg or diastolic pressure > or = 95mmHg or anti-hypertensive treatment at the moment of the interview, was 24.9% whereas the prevalence of obesity-body mass index (BMI) > or = 27kg/m2 was 28.4%. The prevalence of hypertension increased 2.4 fold from the lowest (< 25kg/m2) to the highest (> or = 30kg/m2) band of BMI. It was observed an association between hypertension and obesity that persisted after adjusting for sex, age, skin color, smoking, physical activity and level of education. Interaction of obesity with sex, age and skin color was found. The association between hypertension and obesity was stronger for men, for the youngest and also for the white people.\n Question: Do [ Arterial hypertension and obesity in Ilha do Governador-Rio de Janeiro ]?\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 association between hypertension and obesity and also their prevalence in the adult population from Ilha do Governador-Rio de Janeiro. It is a domiciliar inquiry, with a probalistic cluster sample in two stages. We interviewed 1272 adult residents in the selected households. Social-demographic information, anthropometric measures, habits related to smoking, physical activities and blood pressure were registered. The prevalence of hypertension-systolic pressure > or = 160mmHg or diastolic pressure > or = 95mmHg or anti-hypertensive treatment at the moment of the interview, was 24.9% whereas the prevalence of obesity-body mass index (BMI) > or = 27kg/m2 was 28.4%. The prevalence of hypertension increased 2.4 fold from the lowest (< 25kg/m2) to the highest (> or = 30kg/m2) band of BMI. It was observed an association between hypertension and obesity that persisted after adjusting for sex, age, skin color, smoking, physical activity and level of education. Interaction of obesity with sex, age and skin color was found. The association between hypertension and obesity was stronger for men, for the youngest and also for the white people.
Question: Do [ Arterial hypertension and obesity in Ilha do Governador-Rio de Janeiro ]?
Output:
|
PubmedQA203420
|
[
{
"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 circadian clock represents the body's molecular time-keeping system. Recent findings revealed strong changes of clock gene expression in various types of human cancers. Due to emerging evidence on the connection between the circadian oscillator, cell cycle, and oncogenic transformation, we aimed to characterize the circadian clockwork in human benign and malignant thyroid nodules. Clock transcript levels were assessed by quantitative RT-PCR in thyroid tissues. To provide molecular characteristics of human thyroid clockwork, primary thyrocytes established from normal or nodular thyroid tissue biopsies were subjected to in vitro synchronization with subsequent clock gene expression analysis by circadian bioluminescence reporter assay and by quantitative RT-PCR. The expression levels of the Bmal1 were up-regulated in tissue samples of follicular thyroid carcinoma (FTC), and in papillary thyroid carcinoma (PTC), as compared with normal thyroid and benign nodules, whereas Cry2 was down-regulated in FTC and PTC. Human thyrocytes derived from normal thyroid tissue exhibited high-amplitude circadian oscillations of Bmal1-luciferase reporter expression and endogenous clock transcripts. Thyrocytes established from FTC and PTC exhibited clock transcript oscillations similar to those of normal thyroid tissue and benign nodules (except for Per2 altered in PTC), whereas cells derived from poorly differentiated thyroid carcinoma exhibited altered circadian oscillations.\n Question: Are circadian clock characteristics altered in human thyroid malignant nodules?\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 circadian clock represents the body's molecular time-keeping system. Recent findings revealed strong changes of clock gene expression in various types of human cancers. Due to emerging evidence on the connection between the circadian oscillator, cell cycle, and oncogenic transformation, we aimed to characterize the circadian clockwork in human benign and malignant thyroid nodules. Clock transcript levels were assessed by quantitative RT-PCR in thyroid tissues. To provide molecular characteristics of human thyroid clockwork, primary thyrocytes established from normal or nodular thyroid tissue biopsies were subjected to in vitro synchronization with subsequent clock gene expression analysis by circadian bioluminescence reporter assay and by quantitative RT-PCR. The expression levels of the Bmal1 were up-regulated in tissue samples of follicular thyroid carcinoma (FTC), and in papillary thyroid carcinoma (PTC), as compared with normal thyroid and benign nodules, whereas Cry2 was down-regulated in FTC and PTC. Human thyrocytes derived from normal thyroid tissue exhibited high-amplitude circadian oscillations of Bmal1-luciferase reporter expression and endogenous clock transcripts. Thyrocytes established from FTC and PTC exhibited clock transcript oscillations similar to those of normal thyroid tissue and benign nodules (except for Per2 altered in PTC), whereas cells derived from poorly differentiated thyroid carcinoma exhibited altered circadian oscillations.
Question: Are circadian clock characteristics altered in human thyroid malignant nodules?
Output:
|
PubmedQA63040
|
[
{
"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: Cysteinyl leukotrienes contribute to Th2-type inflammatory immune responses. Their levels in oesophageal tissue, however, do not distinguish patients with eosinophilic oesophagitis (EoE) from controls. We asked whether mRNA levels of leukotriene C4 synthase (LTC4 S), a key regulator of leukotriene production, could serve as a marker for EoE. Digital mRNA expression profiling (nCounter(®) Technology) was performed on proximal and distal oesophageal biopsies of 30 paediatric EoE patients and 40 non-EoE controls. Expression data were confirmed with RT-qPCR. LTC4 S mRNA levels were quantified in whole blood samples. Leukotriene E4 was measured in urine. LTC4 S mRNA levels were elevated in proximal (2.6-fold, P < 0.001) and distal (2.9-fold, P < 0.001) oesophageal biopsies from EoE patients. Importantly, increased LTC4 S mRNA transcripts identified a subpopulation of EoE patients (28%). This patient subgroup had higher serum IgE levels (669 U/mL vs. 106 U/mL, P = 0.01), higher mRNA transcript numbers of thymic stromal lymphopoietin (TSLP) (1.6-fold, P = 0.009) and CD4 (1.4-fold, P = 0.04) but lower IL-23 mRNA levels (0.5-fold, P = 0.04). In contrast, elevated levels of IL-23 mRNA were found in oesophageal biopsies of patients with reflux oesophagitis. LTC4 S mRNA transcripts in whole blood and urinary excretion of leukotriene E4 were similar in EoE patient subgroups and non-EoE patients.\n Question: Do elevated levels of leukotriene C4 synthase mRNA distinguish a subpopulation of eosinophilic oesophagitis 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: Cysteinyl leukotrienes contribute to Th2-type inflammatory immune responses. Their levels in oesophageal tissue, however, do not distinguish patients with eosinophilic oesophagitis (EoE) from controls. We asked whether mRNA levels of leukotriene C4 synthase (LTC4 S), a key regulator of leukotriene production, could serve as a marker for EoE. Digital mRNA expression profiling (nCounter(®) Technology) was performed on proximal and distal oesophageal biopsies of 30 paediatric EoE patients and 40 non-EoE controls. Expression data were confirmed with RT-qPCR. LTC4 S mRNA levels were quantified in whole blood samples. Leukotriene E4 was measured in urine. LTC4 S mRNA levels were elevated in proximal (2.6-fold, P < 0.001) and distal (2.9-fold, P < 0.001) oesophageal biopsies from EoE patients. Importantly, increased LTC4 S mRNA transcripts identified a subpopulation of EoE patients (28%). This patient subgroup had higher serum IgE levels (669 U/mL vs. 106 U/mL, P = 0.01), higher mRNA transcript numbers of thymic stromal lymphopoietin (TSLP) (1.6-fold, P = 0.009) and CD4 (1.4-fold, P = 0.04) but lower IL-23 mRNA levels (0.5-fold, P = 0.04). In contrast, elevated levels of IL-23 mRNA were found in oesophageal biopsies of patients with reflux oesophagitis. LTC4 S mRNA transcripts in whole blood and urinary excretion of leukotriene E4 were similar in EoE patient subgroups and non-EoE patients.
Question: Do elevated levels of leukotriene C4 synthase mRNA distinguish a subpopulation of eosinophilic oesophagitis patients?
Output:
|
PubmedQA206232
|
[
{
"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: Respiratory syncytial virus (RSV) is the most common cause of bronchiolitis in infants. Following RSV bronchiolitis, 50% of children develop post-bronchiolitis wheeze (PBW). Animal studies have suggested that interleukin (IL)-10 plays a critical role in the pathogenesis of RSV bronchiolitis and subsequent airway hyperresponsiveness. Previously, we showed that ex vivo monocyte IL-10 production is a predictor of PBW. Additionally, heterozygosity of the single-nucleotide polymorphism (SNP) rs1800872 in the IL10 promoter region was associated with protection against RSV bronchiolitis. This study aimed to determine the in vivo role of IL-10 in RSV pathogenesis and recurrent wheeze in a new cohort of 235 infants hospitalized for RSV bronchiolitis. IL-10 levels in nasopharyngeal aspirates (NPAs) were measured at the time of hospitalization and the IL10 SNP rs1800872 genotype was determined. Follow-up data were available for 185 children (79%). Local IL-10 levels during RSV infection turned out to be higher in infants that later developed physician diagnosed PBW as compared to infants without PBW in the first year after RSV infection (958 vs 692 pg/ml, p = 0.02). The IL10 promoter SNP rs1800872 was not associated with IL-10 concentration in NPAs.\n Question: Is local interleukin-10 production during respiratory syncytial virus bronchiolitis associated with post-bronchiolitis wheeze?\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: Respiratory syncytial virus (RSV) is the most common cause of bronchiolitis in infants. Following RSV bronchiolitis, 50% of children develop post-bronchiolitis wheeze (PBW). Animal studies have suggested that interleukin (IL)-10 plays a critical role in the pathogenesis of RSV bronchiolitis and subsequent airway hyperresponsiveness. Previously, we showed that ex vivo monocyte IL-10 production is a predictor of PBW. Additionally, heterozygosity of the single-nucleotide polymorphism (SNP) rs1800872 in the IL10 promoter region was associated with protection against RSV bronchiolitis. This study aimed to determine the in vivo role of IL-10 in RSV pathogenesis and recurrent wheeze in a new cohort of 235 infants hospitalized for RSV bronchiolitis. IL-10 levels in nasopharyngeal aspirates (NPAs) were measured at the time of hospitalization and the IL10 SNP rs1800872 genotype was determined. Follow-up data were available for 185 children (79%). Local IL-10 levels during RSV infection turned out to be higher in infants that later developed physician diagnosed PBW as compared to infants without PBW in the first year after RSV infection (958 vs 692 pg/ml, p = 0.02). The IL10 promoter SNP rs1800872 was not associated with IL-10 concentration in NPAs.
Question: Is local interleukin-10 production during respiratory syncytial virus bronchiolitis associated with post-bronchiolitis wheeze?
Output:
|
PubmedQA130444
|
[
{
"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: Sitting is one of milestones in motor development. However, reaching of the sitting position must precede achieving the ability of independent sitting. Qualitative assessment of motor performance at 3 months of age, with the prospective quantitative assessment of the function of independent reaching of the sitting position at the age of 8 months. 125 children, 51 girls and 74 boys (born at term n = 78; born prematurely n = 47) were subject to prospective assessment of motor development with qualitative characteristics at the age of 3 months and quantitative characteristics at the age of 8 months. In parallel, the children were subjected to neurological assessment. Risk factors that could potentially affect motor development were analyzed. Children who at the age of 3 months performed at least 13 /15 qualitative elements in the prone position and at least 13/15 qualitative elements in the supine position, at the age of 8 months reached independently the sitting position. Poor qualitative assessment at the age of 3 months and a higher prevalence of risk factors increased the risk of non-reaching the sitting position. In the prone position, the pelvis, lower limbs, the arms and shoulders showed the most expressed differences between the children who reached or did not reached the independent sitting. For the supine position, the pelvis and lower limbs, as well as the extension of the spine and correct alignment of the shoulders showed the most expressed differences.\n Question: Does independent reaching of the sitting position depend on the motor performance in the 3rd month of life?\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: Sitting is one of milestones in motor development. However, reaching of the sitting position must precede achieving the ability of independent sitting. Qualitative assessment of motor performance at 3 months of age, with the prospective quantitative assessment of the function of independent reaching of the sitting position at the age of 8 months. 125 children, 51 girls and 74 boys (born at term n = 78; born prematurely n = 47) were subject to prospective assessment of motor development with qualitative characteristics at the age of 3 months and quantitative characteristics at the age of 8 months. In parallel, the children were subjected to neurological assessment. Risk factors that could potentially affect motor development were analyzed. Children who at the age of 3 months performed at least 13 /15 qualitative elements in the prone position and at least 13/15 qualitative elements in the supine position, at the age of 8 months reached independently the sitting position. Poor qualitative assessment at the age of 3 months and a higher prevalence of risk factors increased the risk of non-reaching the sitting position. In the prone position, the pelvis, lower limbs, the arms and shoulders showed the most expressed differences between the children who reached or did not reached the independent sitting. For the supine position, the pelvis and lower limbs, as well as the extension of the spine and correct alignment of the shoulders showed the most expressed differences.
Question: Does independent reaching of the sitting position depend on the motor performance in the 3rd month of life?
Output:
|
PubmedQA197162
|
[
{
"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 if previous intravitreal therapy is a predictor of posterior capsule rupture (PCR) during cataract surgery. Multicenter, national electronic medical record (EMR) database study with univariate and multivariate regression modeling. A total of 65 836 eyes of 44 635 patients undergoing cataract surgery. Anonymized data were extracted for eyes undergoing cataract surgery from 20 hospitals using the same EMR for cases performed between 2004 and 2014. Variables included as possible risk indicators for PCR were age, sex, number of previous intravitreal injections, indication for intravitreal therapy, grade of healthcare professional administering intravitreal therapy, advanced cataract, and cataract surgeon grade. Presence or absence of posterior capsular rupture during cataract surgery. Data were available on 65 836 cataract operations, of which 1935 had undergone previous intravitreal therapy (2.9%). In univariate regression analyses, patient age, advanced cataract, junior cataract surgeon grade, and number of previous intravitreal injections were significant predictors of PCR. By considering the number of previous intravitreal injections as a continuous variable, the odds ratio for PCR per intravitreal injection was 1.04 (P = 0.016) after adjusting for age, advanced cataract, and cataract surgeon grade. Repeat analysis considering intravitreal injections as a categoric variable showed 10 or more previous injections were associated with a 2.59 times higher likelihood of PCR (P = 0.003) after again adjusting for other significant independent predictors.\n Question: Does previous Intravitreal Therapy be Associated with Increased Risk of Posterior Capsule Rupture during Cataract Surgery?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To investigate if previous intravitreal therapy is a predictor of posterior capsule rupture (PCR) during cataract surgery. Multicenter, national electronic medical record (EMR) database study with univariate and multivariate regression modeling. A total of 65 836 eyes of 44 635 patients undergoing cataract surgery. Anonymized data were extracted for eyes undergoing cataract surgery from 20 hospitals using the same EMR for cases performed between 2004 and 2014. Variables included as possible risk indicators for PCR were age, sex, number of previous intravitreal injections, indication for intravitreal therapy, grade of healthcare professional administering intravitreal therapy, advanced cataract, and cataract surgeon grade. Presence or absence of posterior capsular rupture during cataract surgery. Data were available on 65 836 cataract operations, of which 1935 had undergone previous intravitreal therapy (2.9%). In univariate regression analyses, patient age, advanced cataract, junior cataract surgeon grade, and number of previous intravitreal injections were significant predictors of PCR. By considering the number of previous intravitreal injections as a continuous variable, the odds ratio for PCR per intravitreal injection was 1.04 (P = 0.016) after adjusting for age, advanced cataract, and cataract surgeon grade. Repeat analysis considering intravitreal injections as a categoric variable showed 10 or more previous injections were associated with a 2.59 times higher likelihood of PCR (P = 0.003) after again adjusting for other significant independent predictors.
Question: Does previous Intravitreal Therapy be Associated with Increased Risk of Posterior Capsule Rupture during Cataract Surgery?
Output:
|
PubmedQA154014
|
[
{
"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: Optimal resuscitation of hypotensive trauma patients has not been defined. This trial was performed to assess the feasibility and safety of controlled resuscitation (CR) versus standard resuscitation (SR) in hypotensive trauma patients. Patients were enrolled and randomized in the out-of-hospital setting. Nineteen emergency medical services (EMS) systems in the Resuscitation Outcome Consortium participated. Eligible patients had an out-of-hospital systolic blood pressure (SBP) of 90 mm Hg or lower. CR patients received 250 mL of fluid if they had no radial pulse or an SBP lower than 70 mm Hg and additional 250-mL boluses to maintain a radial pulse or an SBP of 70 mm Hg or greater. The SR group patients received 2 L initially and additional fluid as needed to maintain an SBP of 110 mm Hg or greater. The crystalloid protocol was maintained until hemorrhage control or 2 hours after hospital arrival. A total of 192 patients were randomized (97 CR and 95 SR). The CR and SR groups were similar at baseline. The mean (SD) crystalloid volume administered during the study period was 1.0 L (1.5) in the CR group and 2.0 L (1.4) in the SR group, a difference of 1.0 L (95% confidence interval [CI], 0.6-1.4). Intensive care unit-free days, ventilator-free days, renal injury, and renal failure did not differ between the groups. At 24 hours after admission, there were 5 deaths (5%) in the CR group and 14 (15%) in the SR group (adjusted odds ratio, 0.39; 95% CI, 0.12-1.26). Among patients with blunt trauma, 24-hour mortality was 3% (CR) and 18% (SR) with an adjusted odds ratio of 0.17 (0.03-0.92). There was no difference among patients with penetrating trauma (9% vs. 9%; adjusted odds ratio, 1.93; 95% CI, 0.19-19.17).\n Question: Is a controlled resuscitation strategy feasible and safe in hypotensive trauma patients : results of a prospective randomized pilot trial?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Optimal resuscitation of hypotensive trauma patients has not been defined. This trial was performed to assess the feasibility and safety of controlled resuscitation (CR) versus standard resuscitation (SR) in hypotensive trauma patients. Patients were enrolled and randomized in the out-of-hospital setting. Nineteen emergency medical services (EMS) systems in the Resuscitation Outcome Consortium participated. Eligible patients had an out-of-hospital systolic blood pressure (SBP) of 90 mm Hg or lower. CR patients received 250 mL of fluid if they had no radial pulse or an SBP lower than 70 mm Hg and additional 250-mL boluses to maintain a radial pulse or an SBP of 70 mm Hg or greater. The SR group patients received 2 L initially and additional fluid as needed to maintain an SBP of 110 mm Hg or greater. The crystalloid protocol was maintained until hemorrhage control or 2 hours after hospital arrival. A total of 192 patients were randomized (97 CR and 95 SR). The CR and SR groups were similar at baseline. The mean (SD) crystalloid volume administered during the study period was 1.0 L (1.5) in the CR group and 2.0 L (1.4) in the SR group, a difference of 1.0 L (95% confidence interval [CI], 0.6-1.4). Intensive care unit-free days, ventilator-free days, renal injury, and renal failure did not differ between the groups. At 24 hours after admission, there were 5 deaths (5%) in the CR group and 14 (15%) in the SR group (adjusted odds ratio, 0.39; 95% CI, 0.12-1.26). Among patients with blunt trauma, 24-hour mortality was 3% (CR) and 18% (SR) with an adjusted odds ratio of 0.17 (0.03-0.92). There was no difference among patients with penetrating trauma (9% vs. 9%; adjusted odds ratio, 1.93; 95% CI, 0.19-19.17).
Question: Is a controlled resuscitation strategy feasible and safe in hypotensive trauma patients : results of a prospective randomized pilot trial?
Output:
|
PubmedQA53008
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Some investigators have analyzed the rate of growth of prostate cancer that has recurred after definitive radiotherapy or radical prostatectomy using serum prostate-specific antigen (PSA) doubling times (DT). We examined all PSA values in recurrent patients to determine the pattern and rate of increase in PSA after radiation therapy and radical prostatectomy. Charts of 96 recurrent radical prostatectomy patients (mean age, 62.8 years; range, 47 to 76) and 42 recurrent radiation therapy patients (mean age, 67.2 years; range, 52 to 83) were reviewed. All available PSA values between the date of operation/radiation treatment and last follow-up evaluation or the initiation of second-line therapy are included. Rate of PSA DT was not assumed to be constant over time; it was instead allowed to vary. We use a piecewise linear random-coefficients model in time for log (PSA), which allowed different mean models for both treatments. The PSA DT in the first year after radiation therapy was--1.17 years, which reflects the continuous decline in PSA in the average patients during the first year after radiotherapy despite eventual biochemical progression. In contrast, the PSA DT in the radical prostatectomy group was 0.66 in the first year. In year 2, after radiation therapy, the PSA DT was lengthy at 1.82 years, significantly longer (P = .0025) than in the radical prostatectomy group (0.76 years). After year 2, there were no significant differences between the two groups (P > .05).\n Question: Are prostate-specific antigen doubling times similar in patients with recurrence after radical prostatectomy or radiotherapy : a novel analysis?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Some investigators have analyzed the rate of growth of prostate cancer that has recurred after definitive radiotherapy or radical prostatectomy using serum prostate-specific antigen (PSA) doubling times (DT). We examined all PSA values in recurrent patients to determine the pattern and rate of increase in PSA after radiation therapy and radical prostatectomy. Charts of 96 recurrent radical prostatectomy patients (mean age, 62.8 years; range, 47 to 76) and 42 recurrent radiation therapy patients (mean age, 67.2 years; range, 52 to 83) were reviewed. All available PSA values between the date of operation/radiation treatment and last follow-up evaluation or the initiation of second-line therapy are included. Rate of PSA DT was not assumed to be constant over time; it was instead allowed to vary. We use a piecewise linear random-coefficients model in time for log (PSA), which allowed different mean models for both treatments. The PSA DT in the first year after radiation therapy was--1.17 years, which reflects the continuous decline in PSA in the average patients during the first year after radiotherapy despite eventual biochemical progression. In contrast, the PSA DT in the radical prostatectomy group was 0.66 in the first year. In year 2, after radiation therapy, the PSA DT was lengthy at 1.82 years, significantly longer (P = .0025) than in the radical prostatectomy group (0.76 years). After year 2, there were no significant differences between the two groups (P > .05).
Question: Are prostate-specific antigen doubling times similar in patients with recurrence after radical prostatectomy or radiotherapy : a novel analysis?
Output:
|
PubmedQA148303
|
[
{
"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 describe patients' generic health status and health-related quality of life (HRQoL) 12-months following admission to a state-wide burns service. A total of 114 injured adults with >10% total body surface area burned (TBSA) or burns less than 10% TBSA to smaller anatomical areas such as the hands and feet participated in this study. Retrospective assessment of pre-burn injury status and prospective assessment of generic health and HRQoL were followed up at 3, 6 and 12-months after injury using the 36-item Short Form Health Survey (SF-36 v.2) and Burns Specific Health Scale-Brief (BSHS-B). The SF-36 v.2 was administered retrospectively during the initial hospital stay to assess pre-injury HRQoL. Changes in instruments scores were assessed using multilevel mixed effects regression models. Mean scores were compared over time and between severity groups as defined by <10%, 10-30% and >30% TBSA. For the overall sample, the SF-36 v.2 physical component scale (PCS) score between 3 and 12-months post-burn injury were significantly lower than pre-injury scores (p<0.01), with no significant change over time for the mental component scale (MCS) (p=0.36). Significant %TBSA-burden by time interactions highlighted changes from pre-burn injury in overall PCS (p=0.02), physical functioning (p<0.001) and role-physical (p=0.03), with subscales worse for the TBSA >30% group. With respect to the BSHS-B, significant improvement from 3 to 12-months post-burn injury was seen for the entire sample in simple abilities (p<0.001), hand function (p=0.001), work (p=0.01), and treatment regime (p=0.004) subscales. The TBSA >30% group showed a greater rate of improvement in simple abilities (p=0.01) and hand function (p=0.005) between 3 and 12 months post-burn injury.\n Question: Do patterns of recovery over 12 months following a burn injury in Australia?\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 describe patients' generic health status and health-related quality of life (HRQoL) 12-months following admission to a state-wide burns service. A total of 114 injured adults with >10% total body surface area burned (TBSA) or burns less than 10% TBSA to smaller anatomical areas such as the hands and feet participated in this study. Retrospective assessment of pre-burn injury status and prospective assessment of generic health and HRQoL were followed up at 3, 6 and 12-months after injury using the 36-item Short Form Health Survey (SF-36 v.2) and Burns Specific Health Scale-Brief (BSHS-B). The SF-36 v.2 was administered retrospectively during the initial hospital stay to assess pre-injury HRQoL. Changes in instruments scores were assessed using multilevel mixed effects regression models. Mean scores were compared over time and between severity groups as defined by <10%, 10-30% and >30% TBSA. For the overall sample, the SF-36 v.2 physical component scale (PCS) score between 3 and 12-months post-burn injury were significantly lower than pre-injury scores (p<0.01), with no significant change over time for the mental component scale (MCS) (p=0.36). Significant %TBSA-burden by time interactions highlighted changes from pre-burn injury in overall PCS (p=0.02), physical functioning (p<0.001) and role-physical (p=0.03), with subscales worse for the TBSA >30% group. With respect to the BSHS-B, significant improvement from 3 to 12-months post-burn injury was seen for the entire sample in simple abilities (p<0.001), hand function (p=0.001), work (p=0.01), and treatment regime (p=0.004) subscales. The TBSA >30% group showed a greater rate of improvement in simple abilities (p=0.01) and hand function (p=0.005) between 3 and 12 months post-burn injury.
Question: Do patterns of recovery over 12 months following a burn injury in Australia?
Output:
|
PubmedQA12487
|
[
{
"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 incidence of breast cancer (BC)-related lymphedema (LE) ranges from 7% to 47%. Successful management of LE relies on early diagnosis using sensitive measurement techniques. In the current study, the authors demonstrated the effectiveness of a surveillance program that included preoperative limb volume measurement and interval postoperative follow-up to detect and treat subclinical LE. LE was identified in 43 of 196 women who participated in a prospective BC morbidity trial. Limb volume was measured preoperatively and at 3-month intervals after surgery. If an increase>3% in upper limb (UL) volume developed compared with the preoperative volume, then a diagnosis of LE was made, and a compression garment intervention was prescribed for 4 weeks. Upon reduction of LE, garment wear was continued only during strenuous activity, with symptoms of heaviness, or with visible swelling. Women returned to the 3-month interval surveillance pathway. Statistical analysis was a repeated-measures analysis of variance by time and limb (P<or=.001) comparing the LE cohort with an age-matched control group. The time to onset of LE averaged 6.9 months postoperatively. The mean (+/-standard deviation) affected limb volume increase was 83 mL (+/-119 mL; 6.5%+/-9.9%) at LE onset (P=.005) compared with baseline. After the intervention, a statistically significant mean 48 mL (+/-103 mL; 4.1%+/-8.8%) volume decrease was realized (P<.0001). The mean duration of the intervention was 4.4 weeks (+/-2.9 weeks). Volume reduction was maintained at an average follow-up of 4.8 months (+/-4.1 months) after the intervention.\n Question: Does preoperative assessment enable the early diagnosis and successful treatment of lymphedema?\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 incidence of breast cancer (BC)-related lymphedema (LE) ranges from 7% to 47%. Successful management of LE relies on early diagnosis using sensitive measurement techniques. In the current study, the authors demonstrated the effectiveness of a surveillance program that included preoperative limb volume measurement and interval postoperative follow-up to detect and treat subclinical LE. LE was identified in 43 of 196 women who participated in a prospective BC morbidity trial. Limb volume was measured preoperatively and at 3-month intervals after surgery. If an increase>3% in upper limb (UL) volume developed compared with the preoperative volume, then a diagnosis of LE was made, and a compression garment intervention was prescribed for 4 weeks. Upon reduction of LE, garment wear was continued only during strenuous activity, with symptoms of heaviness, or with visible swelling. Women returned to the 3-month interval surveillance pathway. Statistical analysis was a repeated-measures analysis of variance by time and limb (P<or=.001) comparing the LE cohort with an age-matched control group. The time to onset of LE averaged 6.9 months postoperatively. The mean (+/-standard deviation) affected limb volume increase was 83 mL (+/-119 mL; 6.5%+/-9.9%) at LE onset (P=.005) compared with baseline. After the intervention, a statistically significant mean 48 mL (+/-103 mL; 4.1%+/-8.8%) volume decrease was realized (P<.0001). The mean duration of the intervention was 4.4 weeks (+/-2.9 weeks). Volume reduction was maintained at an average follow-up of 4.8 months (+/-4.1 months) after the intervention.
Question: Does preoperative assessment enable the early diagnosis and successful treatment of lymphedema?
Output:
|
PubmedQA156622
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To examine the association between familial high lipoprotein(a), or Lp(a), concentrations and endothelial function in children participating in the Special Turku Coronary Risk Factor Intervention Project study. Seven-month-old children (n = 1062) with their families were randomized to a risk intervention group or to a control group. The intervention group received individualized dietary counseling to reduce the total cholesterol concentration. Children's Lp(a) and lipid values were measured repeatedly. At age 11 years, children were recruited to an ultrasound study of the flow-mediated dilation (FMD) of the brachial artery. The association between relative peak FMD and Lp(a) concentration was examined in 198 control and 193 intervention group children by linear regression analyses adjusted for sex, total cholesterol concentration, and basal artery diameter. The analyses were made in both the control and intervention groups and in the familial risk children who had a parent with Lp(a) concentration greater than 250 mg/l. Lp(a) concentrations were similar at age 11 years in the intervention and control groups. In all control children, FMD (%) associated inversely with Lp(a) concentration: (β [%/1000 mg/L] = -3.74, 95% CI [-6.43, -1.45]; P = .007) and in 68 familial risk children (β = -4.92, 95% CI [-8.18, -1.66]; P = .0037). In the intervention group the associations were lacking (P > .5), and FMD in the children with high Lp(a) concentrations (>500 mg/L, n = 12) had no attenuation (P = .027).\n Question: Are high lipoprotein ( a ) concentrations associated with impaired endothelial function 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: To examine the association between familial high lipoprotein(a), or Lp(a), concentrations and endothelial function in children participating in the Special Turku Coronary Risk Factor Intervention Project study. Seven-month-old children (n = 1062) with their families were randomized to a risk intervention group or to a control group. The intervention group received individualized dietary counseling to reduce the total cholesterol concentration. Children's Lp(a) and lipid values were measured repeatedly. At age 11 years, children were recruited to an ultrasound study of the flow-mediated dilation (FMD) of the brachial artery. The association between relative peak FMD and Lp(a) concentration was examined in 198 control and 193 intervention group children by linear regression analyses adjusted for sex, total cholesterol concentration, and basal artery diameter. The analyses were made in both the control and intervention groups and in the familial risk children who had a parent with Lp(a) concentration greater than 250 mg/l. Lp(a) concentrations were similar at age 11 years in the intervention and control groups. In all control children, FMD (%) associated inversely with Lp(a) concentration: (β [%/1000 mg/L] = -3.74, 95% CI [-6.43, -1.45]; P = .007) and in 68 familial risk children (β = -4.92, 95% CI [-8.18, -1.66]; P = .0037). In the intervention group the associations were lacking (P > .5), and FMD in the children with high Lp(a) concentrations (>500 mg/L, n = 12) had no attenuation (P = .027).
Question: Are high lipoprotein ( a ) concentrations associated with impaired endothelial function in children?
Output:
|
PubmedQA24958
|
[
{
"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: Polymorphisms in more than 100 genes have been associated with asthma susceptibility, yet much of the heritability remains to be explained. Asthma disproportionately affects different racial and ethnic groups in the United States, suggesting that admixture mapping is a useful strategy to identify novel asthma-associated loci. We sought to identify novel asthma-associated loci in Latino populations using case-control admixture mapping. We performed genome-wide admixture mapping by comparing levels of local Native American, European, and African ancestry between children with asthma and nonasthmatic control subjects in Puerto Rican and Mexican populations. Within candidate peaks, we performed allelic tests of association, controlling for differences in local ancestry. Between the 2 populations, we identified a total of 62 admixture mapping peaks at a P value of less than 10(-3) that were significantly enriched for previously identified asthma-associated genes (P= .0051). One of the peaks was statistically significant based on 100 permutations in the Mexican sample (6q15); however, it was not significant in Puerto Rican subjects. Another peak was identified at nominal significance in both populations (8q12); however, the association was observed with different ancestries.\n Question: Does case-control admixture mapping in Latino populations enrich for known asthma-associated genes?\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: Polymorphisms in more than 100 genes have been associated with asthma susceptibility, yet much of the heritability remains to be explained. Asthma disproportionately affects different racial and ethnic groups in the United States, suggesting that admixture mapping is a useful strategy to identify novel asthma-associated loci. We sought to identify novel asthma-associated loci in Latino populations using case-control admixture mapping. We performed genome-wide admixture mapping by comparing levels of local Native American, European, and African ancestry between children with asthma and nonasthmatic control subjects in Puerto Rican and Mexican populations. Within candidate peaks, we performed allelic tests of association, controlling for differences in local ancestry. Between the 2 populations, we identified a total of 62 admixture mapping peaks at a P value of less than 10(-3) that were significantly enriched for previously identified asthma-associated genes (P= .0051). One of the peaks was statistically significant based on 100 permutations in the Mexican sample (6q15); however, it was not significant in Puerto Rican subjects. Another peak was identified at nominal significance in both populations (8q12); however, the association was observed with different ancestries.
Question: Does case-control admixture mapping in Latino populations enrich for known asthma-associated genes?
Output:
|
PubmedQA19497
|
[
{
"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: Previous studies have documented abnormalities of arterial baroreflexes in animals and patients with congestive heart failure. This study determined whether cardiopulmonary reflex control of sympathetic nerve activity was abnormal in a canine model of low-output heart failure induced by rapid ventricular pacing. We stimulated mechanoreceptors throughout the cardiopulmonary region by volume expansion and left atrial mechanoreceptors selectively by inflating small balloons at the junctions of the pulmonary veins and left atrium. Responses of renal sympathetic nerve activity and left atrial and systemic arterial pressures were recorded. In the control group, 15% volume expansion raised left atrial pressure 3.5 +/- 0.8 mm Hg and resulted in a 70 +/- 8% reduction in renal nerve activity. In the heart failure group, 15% volume expansion resulted in a 6.8 +/- 3.0 mm Hg rise in left atrial pressure with only a 16 +/- 20% reduction in renal nerve activity (p < 0.01). When volume expansion was performed after pretreatment with hemorrhage to lower left atrial pressure to the normal range in the heart failure group, the markedly attenuated response in the heart failure group persisted. After vagotomy, volume expansion elicited no change in renal nerve activity. Inflation of the atrial balloons caused a 28 +/- 9% reduction in renal sympathetic nerve activity and a 13 +/- 4 mm Hg decrease in arterial pressure in the control group. Renal nerve activity (-5 +/- 3%) and mean arterial pressure (-1 +/- 1 mm Hg) did not change with balloon inflation in the heart failure group.\n Question: Is control of sympathetic nerve activity by vagal mechanoreflexes blunted in heart failure?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Previous studies have documented abnormalities of arterial baroreflexes in animals and patients with congestive heart failure. This study determined whether cardiopulmonary reflex control of sympathetic nerve activity was abnormal in a canine model of low-output heart failure induced by rapid ventricular pacing. We stimulated mechanoreceptors throughout the cardiopulmonary region by volume expansion and left atrial mechanoreceptors selectively by inflating small balloons at the junctions of the pulmonary veins and left atrium. Responses of renal sympathetic nerve activity and left atrial and systemic arterial pressures were recorded. In the control group, 15% volume expansion raised left atrial pressure 3.5 +/- 0.8 mm Hg and resulted in a 70 +/- 8% reduction in renal nerve activity. In the heart failure group, 15% volume expansion resulted in a 6.8 +/- 3.0 mm Hg rise in left atrial pressure with only a 16 +/- 20% reduction in renal nerve activity (p < 0.01). When volume expansion was performed after pretreatment with hemorrhage to lower left atrial pressure to the normal range in the heart failure group, the markedly attenuated response in the heart failure group persisted. After vagotomy, volume expansion elicited no change in renal nerve activity. Inflation of the atrial balloons caused a 28 +/- 9% reduction in renal sympathetic nerve activity and a 13 +/- 4 mm Hg decrease in arterial pressure in the control group. Renal nerve activity (-5 +/- 3%) and mean arterial pressure (-1 +/- 1 mm Hg) did not change with balloon inflation in the heart failure group.
Question: Is control of sympathetic nerve activity by vagal mechanoreflexes blunted in heart failure?
Output:
|
PubmedQA56365
|
[
{
"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: HDL-cholesterol (HDL-C) is a recognized athero-protective factor and low levels of HDL-C occur frequently in patients with coronary artery disease. Regulation of HDL-C level most probably results from the interaction of genes involved in lipoprotein metabolism and also from non-genetic factors. We studied associations and interactions among HindIII polymorphisms of the lipoprotein lipase gene LPL and selected non-genetic factors with respect to HDL-C levels in patients with coronary artery disease. 288 Slovak patients (35% women) with documented coronary artery disease, age (mean +/- SEM) 60 +/- 1 years and BMI 29 +/- 0.3 kg/m(2), were examined and genotyped for LPL HindIII (rs320) using a PCR/RFLP method. HDL-C levels were determined in a direct enzymatic assay. In the sample overall there were no significant differences across the LPL genotypes in adjusted HDL-C levels or in other lipids, although a trend toward higher HDL-C and lower triglycerides in H-H- homozygotes was observed. Multiple linear regression identified a significant interaction between LPL HindIII and statin treatment, which together with sex and diabetes explained 12.1% of HDL-C variance. Accordingly, in statin-treated patients we observed significant stepwise increments of the HDL-C level related to the increasing number of H- alleles (P = 0.04 for linear trend), whereas no such association was observed in patients without hypolipidemic treatment. H-H- homozygotes had a 16% (0.19 mmol/l) higher level of HDL-C than the H+H+ homozygotes (P = 0.06).\n Question: Does lipoprotein lipase HindIII polymorphism influence HDL-cholesterol levels in statin-treated patients with coronary artery disease?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: HDL-cholesterol (HDL-C) is a recognized athero-protective factor and low levels of HDL-C occur frequently in patients with coronary artery disease. Regulation of HDL-C level most probably results from the interaction of genes involved in lipoprotein metabolism and also from non-genetic factors. We studied associations and interactions among HindIII polymorphisms of the lipoprotein lipase gene LPL and selected non-genetic factors with respect to HDL-C levels in patients with coronary artery disease. 288 Slovak patients (35% women) with documented coronary artery disease, age (mean +/- SEM) 60 +/- 1 years and BMI 29 +/- 0.3 kg/m(2), were examined and genotyped for LPL HindIII (rs320) using a PCR/RFLP method. HDL-C levels were determined in a direct enzymatic assay. In the sample overall there were no significant differences across the LPL genotypes in adjusted HDL-C levels or in other lipids, although a trend toward higher HDL-C and lower triglycerides in H-H- homozygotes was observed. Multiple linear regression identified a significant interaction between LPL HindIII and statin treatment, which together with sex and diabetes explained 12.1% of HDL-C variance. Accordingly, in statin-treated patients we observed significant stepwise increments of the HDL-C level related to the increasing number of H- alleles (P = 0.04 for linear trend), whereas no such association was observed in patients without hypolipidemic treatment. H-H- homozygotes had a 16% (0.19 mmol/l) higher level of HDL-C than the H+H+ homozygotes (P = 0.06).
Question: Does lipoprotein lipase HindIII polymorphism influence HDL-cholesterol levels in statin-treated patients with coronary artery disease?
Output:
|
PubmedQA150753
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To determine the prevalence of food-safety education in didactic programs in dietetics (DPDs) across the United States and factors associated with the provision of this education and to explore DPD directors' attitudes toward food safety. The population consisted of 230 DPD directors listed in The American Dietetic Association's 1998-1999 Directory of Dietetics Programs. Overall, 146 directors participated in the study, yielding a 64% response rate. The nature and prevalence of food-safety education and certification, as well as DPD directors' attitudes toward food safety, were assessed by means of a survey instrument. Statistical analyses Descriptive statistics were calculated. Analysis of variance, t test, and chi2 were used to assess differences in DPD directors' attitudes toward food-safety education and certification on the basis of demographic variables. Among dietetics programs, 40% had dietetics majors receive 16 or more hours of food-safety education; 38% (n=54) of DPDs had dietetics majors complete a food-safety certification examination. DPD directors agreed that food safety is an important concept within dietetics education; however, they held differing views regarding certification.\n Question: Are dPD directors ' attitudes more favorable toward food-safety education than certification?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To determine the prevalence of food-safety education in didactic programs in dietetics (DPDs) across the United States and factors associated with the provision of this education and to explore DPD directors' attitudes toward food safety. The population consisted of 230 DPD directors listed in The American Dietetic Association's 1998-1999 Directory of Dietetics Programs. Overall, 146 directors participated in the study, yielding a 64% response rate. The nature and prevalence of food-safety education and certification, as well as DPD directors' attitudes toward food safety, were assessed by means of a survey instrument. Statistical analyses Descriptive statistics were calculated. Analysis of variance, t test, and chi2 were used to assess differences in DPD directors' attitudes toward food-safety education and certification on the basis of demographic variables. Among dietetics programs, 40% had dietetics majors receive 16 or more hours of food-safety education; 38% (n=54) of DPDs had dietetics majors complete a food-safety certification examination. DPD directors agreed that food safety is an important concept within dietetics education; however, they held differing views regarding certification.
Question: Are dPD directors ' attitudes more favorable toward food-safety education than certification?
Output:
|
PubmedQA157091
|
[
{
"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: Aggressive behavior in animals is important for survival and reproduction. Identifying the underlying genes and environmental contexts that affect aggressive behavior is important for understanding the evolutionary forces that maintain variation for aggressive behavior in natural populations, and to develop therapeutic interventions to modulate extreme levels of aggressive behavior in humans. While the role of neurotransmitters and a few other molecules in mediating and modulating levels of aggression is well established, it is likely that many additional genetic pathways remain undiscovered. Drosophila melanogaster has recently been established as an excellent model organism for studying the genetic basis of aggressive behavior. Here, we present the results of a screen of 170 Drosophila P-element insertional mutations for quantitative differences in aggressive behavior from their co-isogenic control line. We identified 59 mutations in 57 genes that affect aggressive behavior, none of which had been previously implicated to affect aggression. Thirty-two of these mutants exhibited increased aggression, while 27 lines were less aggressive than the control. Many of the genes affect the development and function of the nervous system, and are thus plausibly relevant to the execution of complex behaviors. Others affect basic cellular and metabolic processes, or are mutations in computationally predicted genes for which aggressive behavior is the first biological annotation. Most of the mutations had pleiotropic effects on other complex traits. We characterized nine of these mutations in greater detail by assessing transcript levels throughout development, morphological changes in the mushroom bodies, and restoration of control levels of aggression in revertant alleles. All of the P-element insertions affected the tagged genes, and had pleiotropic effects on brain morphology.\n Question: Do mutations in many genes affect aggressive behavior in Drosophila melanogaster?\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: Aggressive behavior in animals is important for survival and reproduction. Identifying the underlying genes and environmental contexts that affect aggressive behavior is important for understanding the evolutionary forces that maintain variation for aggressive behavior in natural populations, and to develop therapeutic interventions to modulate extreme levels of aggressive behavior in humans. While the role of neurotransmitters and a few other molecules in mediating and modulating levels of aggression is well established, it is likely that many additional genetic pathways remain undiscovered. Drosophila melanogaster has recently been established as an excellent model organism for studying the genetic basis of aggressive behavior. Here, we present the results of a screen of 170 Drosophila P-element insertional mutations for quantitative differences in aggressive behavior from their co-isogenic control line. We identified 59 mutations in 57 genes that affect aggressive behavior, none of which had been previously implicated to affect aggression. Thirty-two of these mutants exhibited increased aggression, while 27 lines were less aggressive than the control. Many of the genes affect the development and function of the nervous system, and are thus plausibly relevant to the execution of complex behaviors. Others affect basic cellular and metabolic processes, or are mutations in computationally predicted genes for which aggressive behavior is the first biological annotation. Most of the mutations had pleiotropic effects on other complex traits. We characterized nine of these mutations in greater detail by assessing transcript levels throughout development, morphological changes in the mushroom bodies, and restoration of control levels of aggression in revertant alleles. All of the P-element insertions affected the tagged genes, and had pleiotropic effects on brain morphology.
Question: Do mutations in many genes affect aggressive behavior in Drosophila melanogaster?
Output:
|
PubmedQA210885
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The objective of this study was to determine the relationship between the growth of three foodborne fungi and high-oxygen modified atmosphere. Petri dishes were incubated in a series of connected flasks, which were placed in a climatized room and flushed continuously with the desired gas atmosphere. A combination of 80% oxygen and 20% carbon dioxide resulted in reduced growth of Rhizopus stolonifer, Botrytis cinerea and Penicillium discolor compared with ambient atmosphere conditions. Combining 80% oxygen and 20% carbon dioxide at 10 degrees C arrested growth of B. cinerea for 17 d while an elevated carbon dioxide concentration only inhibited growth up to 11 d. In addition, the peroxidase activity was doubled at 80% oxygen and decreased when 10% carbon dioxide was present.\n Question: Do high-oxygen and high-carbon dioxide containing atmospheres inhibit growth of food associated moulds?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: The objective of this study was to determine the relationship between the growth of three foodborne fungi and high-oxygen modified atmosphere. Petri dishes were incubated in a series of connected flasks, which were placed in a climatized room and flushed continuously with the desired gas atmosphere. A combination of 80% oxygen and 20% carbon dioxide resulted in reduced growth of Rhizopus stolonifer, Botrytis cinerea and Penicillium discolor compared with ambient atmosphere conditions. Combining 80% oxygen and 20% carbon dioxide at 10 degrees C arrested growth of B. cinerea for 17 d while an elevated carbon dioxide concentration only inhibited growth up to 11 d. In addition, the peroxidase activity was doubled at 80% oxygen and decreased when 10% carbon dioxide was present.
Question: Do high-oxygen and high-carbon dioxide containing atmospheres inhibit growth of food associated moulds?
Output:
|
PubmedQA202764
|
[
{
"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: Human cytomegalovirus (HCMV) can be reactivated under immunosuppressive conditions causing several fatal pneumonitis, hepatitis, retinitis, and gastrointestinal diseases. HCMV also causes deafness and mental retardation in neonates when primary infection has occurred during pregnancy. In the genome of HCMV at least 194 known open reading frames (ORFs) have been predicted, and approximately one-quarter, or 41 ORFs, are required for viral replication in cell culture. In contrast, the majority of the predicted ORFs are nonessential for viral replication in cell culture. However, it is also possible that these ORFs are required for the efficient viral replication in the host. The UL77 gene of HCMV is essential for viral replication and has a role in viral DNA packaging. The function of the upstream UL76 gene in the HCMV-infected cells is not understood. UL76 and UL77 are cistons on the same viral mRNA and a conventional 5' mRNA for UL77 has not been detected. The vast majority of eukaryotic mRNAs are monocistronic, i.e., they encode only a single protein. To determine whether the UL76 ORF affects UL77 gene expression, we mutated UL76 by ORF frame-shifts, stop codons or deletion of the viral gene. The effect on UL77 protein expression was determined by either transfection of expression plasmids or infection with recombinant viruses. Mutation of UL76 ORF significantly increased the level of UL77 protein expression. However, deletion of UL76 upstream of the UL77 ORF had only marginal effects on viral growth.\n Question: Does the human cytomegalovirus UL76 gene regulate the level of expression of the UL77 gene?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Human cytomegalovirus (HCMV) can be reactivated under immunosuppressive conditions causing several fatal pneumonitis, hepatitis, retinitis, and gastrointestinal diseases. HCMV also causes deafness and mental retardation in neonates when primary infection has occurred during pregnancy. In the genome of HCMV at least 194 known open reading frames (ORFs) have been predicted, and approximately one-quarter, or 41 ORFs, are required for viral replication in cell culture. In contrast, the majority of the predicted ORFs are nonessential for viral replication in cell culture. However, it is also possible that these ORFs are required for the efficient viral replication in the host. The UL77 gene of HCMV is essential for viral replication and has a role in viral DNA packaging. The function of the upstream UL76 gene in the HCMV-infected cells is not understood. UL76 and UL77 are cistons on the same viral mRNA and a conventional 5' mRNA for UL77 has not been detected. The vast majority of eukaryotic mRNAs are monocistronic, i.e., they encode only a single protein. To determine whether the UL76 ORF affects UL77 gene expression, we mutated UL76 by ORF frame-shifts, stop codons or deletion of the viral gene. The effect on UL77 protein expression was determined by either transfection of expression plasmids or infection with recombinant viruses. Mutation of UL76 ORF significantly increased the level of UL77 protein expression. However, deletion of UL76 upstream of the UL77 ORF had only marginal effects on viral growth.
Question: Does the human cytomegalovirus UL76 gene regulate the level of expression of the UL77 gene?
Output:
|
PubmedQA178844
|
[
{
"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 assess the health needs of prisoners in a male category B prison in Bristol, England, to identify areas for improving health in the prison. Cross-sectional and qualitative. Analysis of prisoners' self-reported health needs at reception and at a secondary health screen; prisoners' access to primary care, inpatients, mental health, sexual health and substance misuse services; and prescribed medications. Random selection of prisoners for interviews. Focus groups and interviews with staff and stakeholders. 18 prisoners were interviewed (29% of those randomly selected), five focus groups were held with staff and stakeholders involved in health care provision in the prison and four interviews were held with staff and stakeholders. The areas of greatest health needs were identified as dental care, mental health and substance misuse. Prisoners and staff generally reported good access to most health care staff, provision of prescribed medication, bloodborne virus vaccination and treatment of substance misuse. Twenty nine recommendations were identified with five high-priority areas for improvement including an urgent review of dental services; stronger joint commissioning arrangements for health and social care; installing an integrated IT system; prevention of disease and health promotion; better use of the voluntary sector. A detailed action plan was developed to address all the recommendations and this has formed the basis of a programme of ongoing quality improvement work which is monitored by the Prison Partnership Board. Progress has been made against all key areas.\n Question: Does health need assessment in a male prison in England?\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 assess the health needs of prisoners in a male category B prison in Bristol, England, to identify areas for improving health in the prison. Cross-sectional and qualitative. Analysis of prisoners' self-reported health needs at reception and at a secondary health screen; prisoners' access to primary care, inpatients, mental health, sexual health and substance misuse services; and prescribed medications. Random selection of prisoners for interviews. Focus groups and interviews with staff and stakeholders. 18 prisoners were interviewed (29% of those randomly selected), five focus groups were held with staff and stakeholders involved in health care provision in the prison and four interviews were held with staff and stakeholders. The areas of greatest health needs were identified as dental care, mental health and substance misuse. Prisoners and staff generally reported good access to most health care staff, provision of prescribed medication, bloodborne virus vaccination and treatment of substance misuse. Twenty nine recommendations were identified with five high-priority areas for improvement including an urgent review of dental services; stronger joint commissioning arrangements for health and social care; installing an integrated IT system; prevention of disease and health promotion; better use of the voluntary sector. A detailed action plan was developed to address all the recommendations and this has formed the basis of a programme of ongoing quality improvement work which is monitored by the Prison Partnership Board. Progress has been made against all key areas.
Question: Does health need assessment in a male prison in England?
Output:
|
PubmedQA111396
|
[
{
"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: Subarachnoid hemorrhage (SAH) is a severe cerebrovascular disease frequently caused by ruptured aneurysms. Early brain injury (EBI) is the primary cause of morbidity and mortality in patients diagnosed with SAH and is associated with increased intracranial pressure, decreased cerebral blood flow and cerebral ischemia. Pentoxifylline (PTX) is a methylxanthine derivative clinically proven to improve perfusion in the peripheral microcirculation and has been shown to have neuroprotective effects in brain trauma and global cerebral ischemia in experimental animal models. This study aimed to determine the effect of PTX in experimental SAH, which has not been investigated yet. An experimental SAH model was induced in male Wistar rats by autologous blood injection into the prechiasmatic cistern, and PTX was injected intraperitoneally immediately after SAH. The effects of PTX were evaluated 24 h after SAH via assessing the cerebral ultrastructure via transmission electron microscopy (TEM). Brain edema, blood-brain barrier (BBB) permeability, red blood cell deformability, tumor necrosis factor-alpha (TNF-alpha), nitrite-nitrate levels and apoptotic neuron death were also determined 24 h after SAH. The BBB permeability was measured by Evans blue (EB) extravasation, erythrocyte deformability was determined by filtration technique, and TNF-alpha and reactive nitrogen metobolites were analyzed in brain tissue by ELISA and spectral analysis, respectively. Apoptotic neurons were determined in brain sections by cleaved caspase-3 immunohistochemical analysis, and expression intensity was quantified using image J software. Cerebral ultrastructure in SAH group animals revealed intense perivascular edema and distortion in the astrocyte foot processes. PTX treatment attenuated structural deterioration due to SAH. Brain water content, BBB permeability, TNF-alpha, nitrite-nitrate levels and apoptotic neuronal death were significantly increased 24 h after SAH and were significantly alleviated by PTX treatment. There was no significant change in red cell deformability after SAH.\n Question: Does pentoxifylline alleviate Early Brain Injury in a Rat Model of Subarachnoid Hemorrhage?\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: Subarachnoid hemorrhage (SAH) is a severe cerebrovascular disease frequently caused by ruptured aneurysms. Early brain injury (EBI) is the primary cause of morbidity and mortality in patients diagnosed with SAH and is associated with increased intracranial pressure, decreased cerebral blood flow and cerebral ischemia. Pentoxifylline (PTX) is a methylxanthine derivative clinically proven to improve perfusion in the peripheral microcirculation and has been shown to have neuroprotective effects in brain trauma and global cerebral ischemia in experimental animal models. This study aimed to determine the effect of PTX in experimental SAH, which has not been investigated yet. An experimental SAH model was induced in male Wistar rats by autologous blood injection into the prechiasmatic cistern, and PTX was injected intraperitoneally immediately after SAH. The effects of PTX were evaluated 24 h after SAH via assessing the cerebral ultrastructure via transmission electron microscopy (TEM). Brain edema, blood-brain barrier (BBB) permeability, red blood cell deformability, tumor necrosis factor-alpha (TNF-alpha), nitrite-nitrate levels and apoptotic neuron death were also determined 24 h after SAH. The BBB permeability was measured by Evans blue (EB) extravasation, erythrocyte deformability was determined by filtration technique, and TNF-alpha and reactive nitrogen metobolites were analyzed in brain tissue by ELISA and spectral analysis, respectively. Apoptotic neurons were determined in brain sections by cleaved caspase-3 immunohistochemical analysis, and expression intensity was quantified using image J software. Cerebral ultrastructure in SAH group animals revealed intense perivascular edema and distortion in the astrocyte foot processes. PTX treatment attenuated structural deterioration due to SAH. Brain water content, BBB permeability, TNF-alpha, nitrite-nitrate levels and apoptotic neuronal death were significantly increased 24 h after SAH and were significantly alleviated by PTX treatment. There was no significant change in red cell deformability after SAH.
Question: Does pentoxifylline alleviate Early Brain Injury in a Rat Model of Subarachnoid Hemorrhage?
Output:
|
PubmedQA146068
|
[
{
"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 aims to examine the relationship between middle-aged and older adults' depressive symptomology and anti-depressant use and the frequency of falls within the previous 12 months, controlling for sociodemographic variables, health indicators, and health behaviors. From the 2010 National Social Life, Health, and Aging Project, 2338 cases were examined. Falls were categorized into a binary variable, comparing zero falls with one or more falls. An unadjusted model was run to examine the relationship between independent and dependent variables. Potential covariates were added into the model, and backward elimination was used among independent variables with a univariate P < 0.05 to identify the covariates with the strongest association with falls. This final adjusted binary logistic regression model was then used to examine the relationship between falls and the independent variables. In the adjusted model, anti-depressant use was positively associated with falls (P = 0.001), as was being female (P < 0.001), having diabetes (P = 0.018), and having increased limitations in daily activities (P < 0.001). The relationship between depressive symptomology and anti-depressant prescription was also significantly associated with falls (P = 0.006).\n Question: Does depressive symptomology management and fall among middle aged and older adults?\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 aims to examine the relationship between middle-aged and older adults' depressive symptomology and anti-depressant use and the frequency of falls within the previous 12 months, controlling for sociodemographic variables, health indicators, and health behaviors. From the 2010 National Social Life, Health, and Aging Project, 2338 cases were examined. Falls were categorized into a binary variable, comparing zero falls with one or more falls. An unadjusted model was run to examine the relationship between independent and dependent variables. Potential covariates were added into the model, and backward elimination was used among independent variables with a univariate P < 0.05 to identify the covariates with the strongest association with falls. This final adjusted binary logistic regression model was then used to examine the relationship between falls and the independent variables. In the adjusted model, anti-depressant use was positively associated with falls (P = 0.001), as was being female (P < 0.001), having diabetes (P = 0.018), and having increased limitations in daily activities (P < 0.001). The relationship between depressive symptomology and anti-depressant prescription was also significantly associated with falls (P = 0.006).
Question: Does depressive symptomology management and fall among middle aged and older adults?
Output:
|
PubmedQA96664
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: A microRNA (miRNA) study. The purpose of this study was to identify intervertebral disc degeneration (IDD)-specific miRNAs, followed by functional validation of results. IDD is the major contributor to back radicular pain, and the molecular mechanisms underlying this disease are not completely understood. Accumulating evidence suggests that miRNAs play an important role in IDD, but the role of specific miRNAs involved in this disease remains elusive. An initial screening of nucleus pulposus (NP) tissues, miRNA expression by miRNA microarray, was performed using samples from 10 patients with degenerative disc disease and 10 patients with lumbar fracture (as controls). Subsequently, differential expression was validated using quantitative reverse transcriptase PCR (qRT-PCR). The level of differentially expressed miRNAs in degenerative NP tissues was investigated, and then functional analysis of the miRNAs in regulating collagen II expression was carried out. Western blotting and luciferase reporter assays were also used to detect the target gene. We identified 23 miRNAs that were differentially expressed (16 upregulated and 7 downregulated) in patients compared with controls. After qRT-PCR confirmation, miR-27b was significantly downregulated in degenerative NP tissues when compared with controls. Moreover, its level was correlated with grade of disc degeneration. Overexpression of miR-27b promoted type II collagen expression in NP cells. Bioinformatics target prediction identified matrix metalloproteinase 13 (MMP13) as a putative target of miR-27b. Futhermore, luciferase reporter assays demonstrated that miR-27b directly targets MMP13 and affects the protein expression of MMP13 in NP cells. Expression of MMP13 negatively correlated with miR-27b expression in degenerative NP tissues.\n Question: Is downregulation of miR-27b Involved in Loss of Type II Collagen by Directly Targeting Matrix Metalloproteinase 13 ( MMP13 ) in Human Intervertebral Disc Degeneration?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: A microRNA (miRNA) study. The purpose of this study was to identify intervertebral disc degeneration (IDD)-specific miRNAs, followed by functional validation of results. IDD is the major contributor to back radicular pain, and the molecular mechanisms underlying this disease are not completely understood. Accumulating evidence suggests that miRNAs play an important role in IDD, but the role of specific miRNAs involved in this disease remains elusive. An initial screening of nucleus pulposus (NP) tissues, miRNA expression by miRNA microarray, was performed using samples from 10 patients with degenerative disc disease and 10 patients with lumbar fracture (as controls). Subsequently, differential expression was validated using quantitative reverse transcriptase PCR (qRT-PCR). The level of differentially expressed miRNAs in degenerative NP tissues was investigated, and then functional analysis of the miRNAs in regulating collagen II expression was carried out. Western blotting and luciferase reporter assays were also used to detect the target gene. We identified 23 miRNAs that were differentially expressed (16 upregulated and 7 downregulated) in patients compared with controls. After qRT-PCR confirmation, miR-27b was significantly downregulated in degenerative NP tissues when compared with controls. Moreover, its level was correlated with grade of disc degeneration. Overexpression of miR-27b promoted type II collagen expression in NP cells. Bioinformatics target prediction identified matrix metalloproteinase 13 (MMP13) as a putative target of miR-27b. Futhermore, luciferase reporter assays demonstrated that miR-27b directly targets MMP13 and affects the protein expression of MMP13 in NP cells. Expression of MMP13 negatively correlated with miR-27b expression in degenerative NP tissues.
Question: Is downregulation of miR-27b Involved in Loss of Type II Collagen by Directly Targeting Matrix Metalloproteinase 13 ( MMP13 ) in Human Intervertebral Disc Degeneration?
Output:
|
PubmedQA170359
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Endoscopic treatment has been increasingly used for T1 esophageal squamous cell carcinoma (ESCC). However, this therapy is sometimes incomplete if the depth of the T1 primary tumor reaches the muscularis mucosae or submucosal layer because these tumors have a relatively high incidence of lymph node metastasis. However, to our knowledge, no previous reports on the prediction of nodal metastasis determined by evaluating primary tumor specimens of patients with ESCC are available. A total of 55 patients with T1 ESCC invading as deep as the submucosal layer who underwent curative esophagectomy were examined. We investigated the significance of the immunohistochemical staining of Vascular endothelial growth factor-C (VEGF-C) and E-cadherin in the primary tumor and Tumor budding for prediction of nodal metastasis. Metastasis to the regional lymph nodes was observed in 26 cases (47.3%) in this setting. VEGF-C expression and reduced E-Cadherin expression in the primary tumor was observed in 32 (58.1%) and 38 cases (69.1%), respectively. High-grade tumor budding was observed in 29 cases (52.7%). E-cadherin expression and tumor budding were closely correlated with nodal metastasis (p=0.04 and <0.01 respectively), whereas VEGF-C expression tended to correlate with lymph node metastasis (p=0.06). In addition, high-grade tumor budding was significantly correlated (p<0.01) with reduced E-cadherin expression. The accuracy of tumor budding and E-cadherin expression for nodal metastasis were 67.3% and 65.4% respectively, comparable with the one of lymphatic involvement (63%). Tumor budding (p<0.01), but not E-cadherin and VEGF-C expression, was significantly correlated with poor survival.\n Question: Are tumor budding and E-cadherin expression useful predictors of nodal involvement in T1 esophageal squamous cell carcinoma?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Endoscopic treatment has been increasingly used for T1 esophageal squamous cell carcinoma (ESCC). However, this therapy is sometimes incomplete if the depth of the T1 primary tumor reaches the muscularis mucosae or submucosal layer because these tumors have a relatively high incidence of lymph node metastasis. However, to our knowledge, no previous reports on the prediction of nodal metastasis determined by evaluating primary tumor specimens of patients with ESCC are available. A total of 55 patients with T1 ESCC invading as deep as the submucosal layer who underwent curative esophagectomy were examined. We investigated the significance of the immunohistochemical staining of Vascular endothelial growth factor-C (VEGF-C) and E-cadherin in the primary tumor and Tumor budding for prediction of nodal metastasis. Metastasis to the regional lymph nodes was observed in 26 cases (47.3%) in this setting. VEGF-C expression and reduced E-Cadherin expression in the primary tumor was observed in 32 (58.1%) and 38 cases (69.1%), respectively. High-grade tumor budding was observed in 29 cases (52.7%). E-cadherin expression and tumor budding were closely correlated with nodal metastasis (p=0.04 and <0.01 respectively), whereas VEGF-C expression tended to correlate with lymph node metastasis (p=0.06). In addition, high-grade tumor budding was significantly correlated (p<0.01) with reduced E-cadherin expression. The accuracy of tumor budding and E-cadherin expression for nodal metastasis were 67.3% and 65.4% respectively, comparable with the one of lymphatic involvement (63%). Tumor budding (p<0.01), but not E-cadherin and VEGF-C expression, was significantly correlated with poor survival.
Question: Are tumor budding and E-cadherin expression useful predictors of nodal involvement in T1 esophageal squamous cell carcinoma?
Output:
|
PubmedQA2337
|
[
{
"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: Radiography is an unreliable and insensitive tool for the assessment of structural lesions in the sacroiliac joints (SIJ). Magnetic resonance imaging (MRI) detects a wider spectrum of structural lesions but has undergone minimal validation in prospective studies. The Spondyloarthritis Research Consortium of Canada (SPARCC) MRI Sacroiliac Joint (SIJ) Structural Score (SSS) assesses a spectrum of structural lesions (erosion, fat metaplasia, backfill, ankylosis) and its potential to discriminate between therapies requires evaluation. The SSS score assesses five consecutive coronal slices through the cartilaginous portion of the joint on T1-weighted sequences starting from the transitional slice between cartilaginous and ligamentous portions of the joint. Lesions are scored dichotomously (present/absent) in SIJ quadrants (fat metaplasia, erosion) or halves (backfill, ankylosis). Two readers independently scored 147 pairs (baseline, 2 years) of scans from a prospective cohort of patients with SpA who received either standard (n = 69) or tumor necrosis factor alpha (TNFα) inhibitor (n = 78) therapy. Smallest detectable change (SDC) was calculated using analysis of variance (ANOVA), discrimination was assessed using Guyatt's effect size, and treatment group differences were assessed using t-tests and the Mann-Whitney test. We identified baseline demographic and structural damage variables associated with change in SSS score by univariate analysis and analyzed the effect of treatment by multivariate stepwise regression adjusted for severity of baseline structural damage and demographic variables. A significant increase in mean SSS score for fat metaplasia (P = 0.017) and decrease in mean SSS score for erosion (P = 0.017) was noted in anti-TNFα treated patients compared to those on standard therapy. Effect size for this change in SSS fat metaplasia and erosion score was moderate (0.5 and 0.6, respectively). Treatment and baseline SSS score for erosion were independently associated with change in SSS erosion score (β = 1.75, P = 0.003 and β = 0.40, P < 0.0001, respectively). Change in ASDAS (β = -0.46, P = 0.006), SPARCC MRI SIJ inflammation (β = -0.077, P = 0.019), and baseline SSS score for fat metaplasia (β = 0.085, P = 0.034) were independently associated with new fat metaplasia.\n Question: Is tumor necrosis factor inhibitor therapy but not standard therapy associated with resolution of erosion in the sacroiliac joints of patients with axial spondyloarthritis?\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: Radiography is an unreliable and insensitive tool for the assessment of structural lesions in the sacroiliac joints (SIJ). Magnetic resonance imaging (MRI) detects a wider spectrum of structural lesions but has undergone minimal validation in prospective studies. The Spondyloarthritis Research Consortium of Canada (SPARCC) MRI Sacroiliac Joint (SIJ) Structural Score (SSS) assesses a spectrum of structural lesions (erosion, fat metaplasia, backfill, ankylosis) and its potential to discriminate between therapies requires evaluation. The SSS score assesses five consecutive coronal slices through the cartilaginous portion of the joint on T1-weighted sequences starting from the transitional slice between cartilaginous and ligamentous portions of the joint. Lesions are scored dichotomously (present/absent) in SIJ quadrants (fat metaplasia, erosion) or halves (backfill, ankylosis). Two readers independently scored 147 pairs (baseline, 2 years) of scans from a prospective cohort of patients with SpA who received either standard (n = 69) or tumor necrosis factor alpha (TNFα) inhibitor (n = 78) therapy. Smallest detectable change (SDC) was calculated using analysis of variance (ANOVA), discrimination was assessed using Guyatt's effect size, and treatment group differences were assessed using t-tests and the Mann-Whitney test. We identified baseline demographic and structural damage variables associated with change in SSS score by univariate analysis and analyzed the effect of treatment by multivariate stepwise regression adjusted for severity of baseline structural damage and demographic variables. A significant increase in mean SSS score for fat metaplasia (P = 0.017) and decrease in mean SSS score for erosion (P = 0.017) was noted in anti-TNFα treated patients compared to those on standard therapy. Effect size for this change in SSS fat metaplasia and erosion score was moderate (0.5 and 0.6, respectively). Treatment and baseline SSS score for erosion were independently associated with change in SSS erosion score (β = 1.75, P = 0.003 and β = 0.40, P < 0.0001, respectively). Change in ASDAS (β = -0.46, P = 0.006), SPARCC MRI SIJ inflammation (β = -0.077, P = 0.019), and baseline SSS score for fat metaplasia (β = 0.085, P = 0.034) were independently associated with new fat metaplasia.
Question: Is tumor necrosis factor inhibitor therapy but not standard therapy associated with resolution of erosion in the sacroiliac joints of patients with axial spondyloarthritis?
Output:
|
PubmedQA98896
|
[
{
"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: Somatostatin (SST) is a regulatory peptide with a wide variety of activities in different tissues. SST activates G(alpha i)-protein-coupled receptors of a family comprising five members (SSTR1-5). Despite the broad use of SST and its analogs in clinical practice, the spectrum of activities of SST is incompletely defined. Here, we examined the role of SST and its receptors in hematopoiesis. SSTR expression on human and mouse hematopoietic cells was analyzed by flow cytometry and reverse transcriptase polymerase chain reaction. The effects of SST on cell migration were measured in transwell assays. Using selective inhibitors, signaling mechanisms involved in SSTR2-mediated migration were studied in 32D cell transfectants expressing SSTR2. Human hematopoietic cells exclusively expressed SSTR2, whereas mouse bone marrow cells expressed SSTR2 and SSTR4. SSTR levels were high on primitive (CD34(+), Lin(-)) but low or absent on more mature (CD34(-), Lin(+)) cell types. Both SST and its analog octreotide acted as chemoattractants for primitive hematopoietic cells. Despite the presence of SSTR4, bone marrow cells from SSTR2-deficient mice failed to migrate toward SST gradients, suggesting that SSTR2 and SSTR4 are functionally different in this respect. SST activated phosphatidylinositol 3-kinase and the MAP kinases Erk1/2 and p38 in 32D[SSTR2] cells. While chemical inhibitors of these kinases had some effect, SST-induced migration was most strongly affected by blocking G(alpha i) activity or by elevating intracellular cAMP levels.\n Question: Is somatostatin a selective chemoattractant for primitive ( CD34 ( + ) ) hematopoietic progenitor cells?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Somatostatin (SST) is a regulatory peptide with a wide variety of activities in different tissues. SST activates G(alpha i)-protein-coupled receptors of a family comprising five members (SSTR1-5). Despite the broad use of SST and its analogs in clinical practice, the spectrum of activities of SST is incompletely defined. Here, we examined the role of SST and its receptors in hematopoiesis. SSTR expression on human and mouse hematopoietic cells was analyzed by flow cytometry and reverse transcriptase polymerase chain reaction. The effects of SST on cell migration were measured in transwell assays. Using selective inhibitors, signaling mechanisms involved in SSTR2-mediated migration were studied in 32D cell transfectants expressing SSTR2. Human hematopoietic cells exclusively expressed SSTR2, whereas mouse bone marrow cells expressed SSTR2 and SSTR4. SSTR levels were high on primitive (CD34(+), Lin(-)) but low or absent on more mature (CD34(-), Lin(+)) cell types. Both SST and its analog octreotide acted as chemoattractants for primitive hematopoietic cells. Despite the presence of SSTR4, bone marrow cells from SSTR2-deficient mice failed to migrate toward SST gradients, suggesting that SSTR2 and SSTR4 are functionally different in this respect. SST activated phosphatidylinositol 3-kinase and the MAP kinases Erk1/2 and p38 in 32D[SSTR2] cells. While chemical inhibitors of these kinases had some effect, SST-induced migration was most strongly affected by blocking G(alpha i) activity or by elevating intracellular cAMP levels.
Question: Is somatostatin a selective chemoattractant for primitive ( CD34 ( + ) ) hematopoietic progenitor cells?
Output:
|
PubmedQA105483
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To investigate the effect of HGF on proliferation, apoptosis and migratory ability of human vascular endothelial cells against gamma ray irradiation. ECV304 cells derived from adult human umbilical vein endothelial cells (HUVEC) were irradiated with a single gamma ray dose of 20 Gy. Immunocytochemistry and Western blot analysis were used to detect c-Met protein expression and HGF/c-Met signal pathway. In the HGF-treated groups, ECV304 cells were incubated with HGF (20 or 40 ng/mL) 3 h prior to irradiation. At 48 h post-irradiation, the proliferation of ECV304 cells was measured by MTT assay, the apoptosis was assessed by flow cytometry, and the migratory ability of ECV304 cells was measured by transwell chamber assay. c-Met protein is expressed in ECV304 cells and can be activated by HGF. Gamma ray irradiation inhibits proliferation and migration of ECV304 cells in a dose-dependent manner. HGF significantly promoted the proliferation of ECV304 cells, and flow cytometry revealed that HGF can inhibit apoptosis of ECV304 cells. Transwell chamber assay also showed that HGF increases migration activity of endothelial cells.\n Question: Does hepatocyte growth factor protect endothelial cells against gamma ray irradiation-induced damage?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To investigate the effect of HGF on proliferation, apoptosis and migratory ability of human vascular endothelial cells against gamma ray irradiation. ECV304 cells derived from adult human umbilical vein endothelial cells (HUVEC) were irradiated with a single gamma ray dose of 20 Gy. Immunocytochemistry and Western blot analysis were used to detect c-Met protein expression and HGF/c-Met signal pathway. In the HGF-treated groups, ECV304 cells were incubated with HGF (20 or 40 ng/mL) 3 h prior to irradiation. At 48 h post-irradiation, the proliferation of ECV304 cells was measured by MTT assay, the apoptosis was assessed by flow cytometry, and the migratory ability of ECV304 cells was measured by transwell chamber assay. c-Met protein is expressed in ECV304 cells and can be activated by HGF. Gamma ray irradiation inhibits proliferation and migration of ECV304 cells in a dose-dependent manner. HGF significantly promoted the proliferation of ECV304 cells, and flow cytometry revealed that HGF can inhibit apoptosis of ECV304 cells. Transwell chamber assay also showed that HGF increases migration activity of endothelial cells.
Question: Does hepatocyte growth factor protect endothelial cells against gamma ray irradiation-induced damage?
Output:
|
PubmedQA54980
|
[
{
"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: During development neural crest derived Schwann Cell (SC) precursors migrate to nerve trunks and populate nascent nerves. Axonal ensheathment by SC is a prerequisite for normal nerve function and the integrity of myelinated as well as nonmyelinated axons. To provide adequate support functions, SC colonize entire nerves. One important prerequisite for this is their migration into distal axonal regions. Here, we studied the role of Glial cell line derived neurotrophic factor (GDNF), a TGF-beta related growth factor, for SC migration. To this end we used a superior cervical ganglion (SCG) explant-SC migration assay, GDNF null mutant mouse embryos and a chemical inhibitor for GDNF signaling in combination with time-lapse imaging. We found that GDNF signaling is dispensable for SC migration along murine embryonic sympathetic axons. Furthermore, in vivo analyzes revealed that SC migration along the sciatic nerve is also not dependent on GDNF.\n Question: Do schwann cells migrate along axons in the absence of GDNF signaling?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: During development neural crest derived Schwann Cell (SC) precursors migrate to nerve trunks and populate nascent nerves. Axonal ensheathment by SC is a prerequisite for normal nerve function and the integrity of myelinated as well as nonmyelinated axons. To provide adequate support functions, SC colonize entire nerves. One important prerequisite for this is their migration into distal axonal regions. Here, we studied the role of Glial cell line derived neurotrophic factor (GDNF), a TGF-beta related growth factor, for SC migration. To this end we used a superior cervical ganglion (SCG) explant-SC migration assay, GDNF null mutant mouse embryos and a chemical inhibitor for GDNF signaling in combination with time-lapse imaging. We found that GDNF signaling is dispensable for SC migration along murine embryonic sympathetic axons. Furthermore, in vivo analyzes revealed that SC migration along the sciatic nerve is also not dependent on GDNF.
Question: Do schwann cells migrate along axons in the absence of GDNF signaling?
Output:
|
PubmedQA130847
|
[
{
"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: Minimally invasive esophagectomy (MIE) has the potential to reduce the morbidity and mortality of esophageal cancer surgery. Esophageal squamous cell carcinoma (ESCC) has a high incidence of earlier lymphatic spread and is usually located more proximal to the incisor than esophageal adenocarcinoma; consequently, the anastomosis should be made more proximal in the thorax or in the neck. We adopted the proximal intrathoracic anastomotic technique using thoracoscopy for mid-to-lower ESCC. From October 2010 to August 2014, fifty-eight consecutive patients underwent MIE for ESCC. After laparoscopic gastric tubing, thoracoscopic esophageal resection and reconstruction were performed using a 28-mm circular stapler following radical mediastinal lymph node dissection. We tried to make an anastomosis at the apex of the chest. Postoperative outcomes, including overall survival and recurrence, were assessed. The mean patient age was 64.3±9 years. The mean operative time was 371.8±51.6 minutes, and the duration of the thorax procedure was 254.8±38.3 minutes. The mean number of lymph nodes dissected was 31±11.7. The mean intensive care unit (ICU) stay and hospital stay were 3.5±8.2 hours and 13.6±7.4 days, respectively. The level of anastomosis was 22.3±1.8cm from the incisor. One patient died of uncontrolled sepsis due to necrosis of the gastric graft. Two patients developed small contained leakage. Nine patients exhibited distant metastasis during the follow-up period.\n Question: Does high Intrathoracic Anastomosis with Thoracoscopy be Safe and Feasible for Treatment of Esophageal Squamous Cell Carcinoma?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Minimally invasive esophagectomy (MIE) has the potential to reduce the morbidity and mortality of esophageal cancer surgery. Esophageal squamous cell carcinoma (ESCC) has a high incidence of earlier lymphatic spread and is usually located more proximal to the incisor than esophageal adenocarcinoma; consequently, the anastomosis should be made more proximal in the thorax or in the neck. We adopted the proximal intrathoracic anastomotic technique using thoracoscopy for mid-to-lower ESCC. From October 2010 to August 2014, fifty-eight consecutive patients underwent MIE for ESCC. After laparoscopic gastric tubing, thoracoscopic esophageal resection and reconstruction were performed using a 28-mm circular stapler following radical mediastinal lymph node dissection. We tried to make an anastomosis at the apex of the chest. Postoperative outcomes, including overall survival and recurrence, were assessed. The mean patient age was 64.3±9 years. The mean operative time was 371.8±51.6 minutes, and the duration of the thorax procedure was 254.8±38.3 minutes. The mean number of lymph nodes dissected was 31±11.7. The mean intensive care unit (ICU) stay and hospital stay were 3.5±8.2 hours and 13.6±7.4 days, respectively. The level of anastomosis was 22.3±1.8cm from the incisor. One patient died of uncontrolled sepsis due to necrosis of the gastric graft. Two patients developed small contained leakage. Nine patients exhibited distant metastasis during the follow-up period.
Question: Does high Intrathoracic Anastomosis with Thoracoscopy be Safe and Feasible for Treatment of Esophageal Squamous Cell Carcinoma?
Output:
|
PubmedQA148910
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: In this study, we evaluated the effect of capsaicin on the interaction of redox-sensitive thioredoxin (Trx)/apoptosis signal-regulating kinase 1 (ASK1) in pancreatic cancer cells. Capsaicin treatment downregulated Trx and increased the phosphorylation (activation) of ASK1 at Thr845 and kinase activity in AsPC-1 and BxPC-3 cells. Capsaicin treatment also activated downstream effector molecules MKK4/7, caspase-9, and caspase-3. Antioxidants tiron or PEG-catalase blocked the activation of ASK1 cascade by capsaicin and protected the cells from apoptosis, indicating the involvement of reactive oxygen species in the activation of ASK1. Our results further revealed that Trx overexpression suppressed the effects of capsaicin, whereas ASK1 overexpression enhanced the apoptosis-inducing effects of capsaicin. β-mercaptoethanol, a reducing agent, blocked capsaicin-mediated activation of ASK1, indicating that Trx-ASK1 complex exists and requires reducing conditions in the cell. On the other hand, the Trx inhibitor (1-chloro-2-4-dinitrobenzene) increased capsaicin-induced ASK1 kinase activity, suggesting that Trx inhibition by capsaicin is essential for ASK1 activation. Oral administration of 5 mg capsaicin/kg body weight substantially suppressed the growth of tumors in xenograft and orthotopic mouse model. Tumors from capsaicin-treated mice showed reduced levels of Trx, increased phosphorylation of ASK1 at Thr845, and cleavage of caspase-3 and poly (ADP-ribose) polymerase. Our results for the first time demonstrated a new perspective that Trx-ASK1 complex can be targeted by capsaicin in pancreatic cancer.\n Question: Does apoptosis signal-regulating kinase 1-thioredoxin complex dissociation by capsaicin cause pancreatic tumor growth suppression by inducing apoptosis?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: In this study, we evaluated the effect of capsaicin on the interaction of redox-sensitive thioredoxin (Trx)/apoptosis signal-regulating kinase 1 (ASK1) in pancreatic cancer cells. Capsaicin treatment downregulated Trx and increased the phosphorylation (activation) of ASK1 at Thr845 and kinase activity in AsPC-1 and BxPC-3 cells. Capsaicin treatment also activated downstream effector molecules MKK4/7, caspase-9, and caspase-3. Antioxidants tiron or PEG-catalase blocked the activation of ASK1 cascade by capsaicin and protected the cells from apoptosis, indicating the involvement of reactive oxygen species in the activation of ASK1. Our results further revealed that Trx overexpression suppressed the effects of capsaicin, whereas ASK1 overexpression enhanced the apoptosis-inducing effects of capsaicin. β-mercaptoethanol, a reducing agent, blocked capsaicin-mediated activation of ASK1, indicating that Trx-ASK1 complex exists and requires reducing conditions in the cell. On the other hand, the Trx inhibitor (1-chloro-2-4-dinitrobenzene) increased capsaicin-induced ASK1 kinase activity, suggesting that Trx inhibition by capsaicin is essential for ASK1 activation. Oral administration of 5 mg capsaicin/kg body weight substantially suppressed the growth of tumors in xenograft and orthotopic mouse model. Tumors from capsaicin-treated mice showed reduced levels of Trx, increased phosphorylation of ASK1 at Thr845, and cleavage of caspase-3 and poly (ADP-ribose) polymerase. Our results for the first time demonstrated a new perspective that Trx-ASK1 complex can be targeted by capsaicin in pancreatic cancer.
Question: Does apoptosis signal-regulating kinase 1-thioredoxin complex dissociation by capsaicin cause pancreatic tumor growth suppression by inducing apoptosis?
Output:
|
PubmedQA157818
|
[
{
"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 demonstrate the feasibility and benefits of custom designed perfusion bioreactor in conjunction with well-defined three-dimensional (3D) environment for enhanced proliferation and homogeneous distribution of human fetal osteoblasts in large scaffold in vitro. Large-scale β-tricalcium phosphate (β-TCP) scaffolds with tightly controlled architectures were fabricated. And a custom designed perfusion bioreactor was developed. Human fetal osteoblasts were seeded onto the scaffolds, cultured for up to 16 days in static or flow perfusion conditions. At Days 4, 8 & 16 post-incubation, the proliferation and distribution of osteoblasts were determined by daily D-glucose consumption, cell viability (methyl thiazolyl tetrazolium (MTT) assay), histological evaluation and scanning electron microcopy (SEM). Sphere like structures observed in the SEM images were assessed by energy dispersive X-ray (EDX) analysis. In both static and perfusion cultures, the daily D-glucose consumption increased with prolonged time. The daily D-glucose consumption was significantly higher in the perfusion culture than that in static culture (P < 0.05). The increased cell viability with time during the culture was similar to the daily D-glucose consumption under both conditions. There was much greater cell viability under flow perfusion culture compared to static culture (P < 0.05). Flow perfused constructs demonstrated improved cell proliferation and a homogeneous layer composed of cells and extracellular matrix in channels throughout the whole scaffold. However, the cells were biased to periphery in scaffolds culture statically. Sphere like structures present in the matrix were identified as calcium phosphate nodules via EDX analysis.\n Question: Does [ Three-dimensional flow perfusion culture enhance proliferation of human fetal osteoblasts in large scaffold with controlled architecture ]?\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 demonstrate the feasibility and benefits of custom designed perfusion bioreactor in conjunction with well-defined three-dimensional (3D) environment for enhanced proliferation and homogeneous distribution of human fetal osteoblasts in large scaffold in vitro. Large-scale β-tricalcium phosphate (β-TCP) scaffolds with tightly controlled architectures were fabricated. And a custom designed perfusion bioreactor was developed. Human fetal osteoblasts were seeded onto the scaffolds, cultured for up to 16 days in static or flow perfusion conditions. At Days 4, 8 & 16 post-incubation, the proliferation and distribution of osteoblasts were determined by daily D-glucose consumption, cell viability (methyl thiazolyl tetrazolium (MTT) assay), histological evaluation and scanning electron microcopy (SEM). Sphere like structures observed in the SEM images were assessed by energy dispersive X-ray (EDX) analysis. In both static and perfusion cultures, the daily D-glucose consumption increased with prolonged time. The daily D-glucose consumption was significantly higher in the perfusion culture than that in static culture (P < 0.05). The increased cell viability with time during the culture was similar to the daily D-glucose consumption under both conditions. There was much greater cell viability under flow perfusion culture compared to static culture (P < 0.05). Flow perfused constructs demonstrated improved cell proliferation and a homogeneous layer composed of cells and extracellular matrix in channels throughout the whole scaffold. However, the cells were biased to periphery in scaffolds culture statically. Sphere like structures present in the matrix were identified as calcium phosphate nodules via EDX analysis.
Question: Does [ Three-dimensional flow perfusion culture enhance proliferation of human fetal osteoblasts in large scaffold with controlled architecture ]?
Output:
|
PubmedQA185845
|
[
{
"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 distribution of cardiovascular risk factors in patients with chronic gastrointestinal ischemia due to atherosclerosis of the splanchnic vessels (chronic splanchnic syndrome) is not well studied. The aim of this study was to determine the cardiovascular risk factor pattern in patients with chronic splanchnic syndrome. From April 2003 to September 2007, atherosclerotic risk factors in consecutive patients with chronic splanchnic syndrome were compared prospectively with the general atherosclerotic risk profile in Western Europe and worldwide risk profile of coronary heart disease, peripheral artery disease, and cerebral vascular disease. Of 376 analyzed patients, 97 were diagnosed with chronic splanchnic syndrome. Data from 90 patients were available for analysis (7 were excluded because of incomplete data). Mean age was 63 years (range 28-86 years), and 74% were female. Fifty-nine percent of the patients had atherosclerotic disease in other vascular beds. Smoking was reported in 57%, and increased bodyweight in 21%. Hypercholesterolemia was present in 53%, hypertension in 62%, and diabetes in 21%.\n Question: Is the cardiovascular risk profile of atherosclerotic gastrointestinal ischemia different from other vascular beds?\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 distribution of cardiovascular risk factors in patients with chronic gastrointestinal ischemia due to atherosclerosis of the splanchnic vessels (chronic splanchnic syndrome) is not well studied. The aim of this study was to determine the cardiovascular risk factor pattern in patients with chronic splanchnic syndrome. From April 2003 to September 2007, atherosclerotic risk factors in consecutive patients with chronic splanchnic syndrome were compared prospectively with the general atherosclerotic risk profile in Western Europe and worldwide risk profile of coronary heart disease, peripheral artery disease, and cerebral vascular disease. Of 376 analyzed patients, 97 were diagnosed with chronic splanchnic syndrome. Data from 90 patients were available for analysis (7 were excluded because of incomplete data). Mean age was 63 years (range 28-86 years), and 74% were female. Fifty-nine percent of the patients had atherosclerotic disease in other vascular beds. Smoking was reported in 57%, and increased bodyweight in 21%. Hypercholesterolemia was present in 53%, hypertension in 62%, and diabetes in 21%.
Question: Is the cardiovascular risk profile of atherosclerotic gastrointestinal ischemia different from other vascular beds?
Output:
|
PubmedQA118216
|
[
{
"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 WNT signaling pathway effector gene TCF7L2 has been associated with an increased risk of type 2 diabetes. However, it remains unclear how this gene affects diabetic pathogenesis. The goal of this study was to investigate the effects of Tcf7l2 haploinsufficiency on metabolic phenotypes in mice. Tcf7l2 knockout (Tcf7l⁻/⁻) mice were generated. Because of the early mortality of Tcf7l2⁻/⁻ mice, we characterized the metabolic phenotypes of heterozygous Tcf7l2⁺/⁻ mice in comparison to the wild-type controls. The mice were fed a normal chow diet or a high fat diet (HFD) for 9 weeks. The Tcf7l2⁺/⁻ mice showed significant differences from the wild-type mice with regards to body weight, fasting glucose and insulin levels. Tcf7l2⁺/⁻ mice displayed improved glucose tolerance. In the liver of Tcf7l2⁺/⁻ mice fed on the HFD, reduced lipogenesis and hepatic triglyceride levels were observed when compared with those of wild-type mice. Furthermore, the Tcf7l2⁺/⁻ mice fed on the HFD exhibited decreased peripheral fat deposition. Immunohistochemistry in mouse pancreatic islets showed that endogenous expression of Tcf7l2 was upregulated in the wild-type mice, but not in the Tcf7l2⁺/⁻ mice, after feeding with the HFD. However, the haploinsufficiency of Tcf7l2 in mouse pancreatic islets resulted in little changes in glucose-stimulated insulin secretion.\n Question: Does reduction in Tcf7l2 expression decrease diabetic susceptibility in mice?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: The WNT signaling pathway effector gene TCF7L2 has been associated with an increased risk of type 2 diabetes. However, it remains unclear how this gene affects diabetic pathogenesis. The goal of this study was to investigate the effects of Tcf7l2 haploinsufficiency on metabolic phenotypes in mice. Tcf7l2 knockout (Tcf7l⁻/⁻) mice were generated. Because of the early mortality of Tcf7l2⁻/⁻ mice, we characterized the metabolic phenotypes of heterozygous Tcf7l2⁺/⁻ mice in comparison to the wild-type controls. The mice were fed a normal chow diet or a high fat diet (HFD) for 9 weeks. The Tcf7l2⁺/⁻ mice showed significant differences from the wild-type mice with regards to body weight, fasting glucose and insulin levels. Tcf7l2⁺/⁻ mice displayed improved glucose tolerance. In the liver of Tcf7l2⁺/⁻ mice fed on the HFD, reduced lipogenesis and hepatic triglyceride levels were observed when compared with those of wild-type mice. Furthermore, the Tcf7l2⁺/⁻ mice fed on the HFD exhibited decreased peripheral fat deposition. Immunohistochemistry in mouse pancreatic islets showed that endogenous expression of Tcf7l2 was upregulated in the wild-type mice, but not in the Tcf7l2⁺/⁻ mice, after feeding with the HFD. However, the haploinsufficiency of Tcf7l2 in mouse pancreatic islets resulted in little changes in glucose-stimulated insulin secretion.
Question: Does reduction in Tcf7l2 expression decrease diabetic susceptibility in mice?
Output:
|
PubmedQA99435
|
[
{
"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 if hyperinsulinemia or insulin resistance could predict the elevation of blood pressure in non-diabetic adults. One hundred and seventy non-diabetic adults (NGT 107, IGT 63) were included based on the screen by OGTT in 1986. Height, weight, blood pressure were measured. Plasma glucose and insulin concentration at 0.60 and 120 min during OGTT were determined at baseline. All the subjects were followed for six years with blood pressure and plasma glucose examined at the end of the study. Subjects worsening to diabetes were excluded. Insulin area under-curve (INSAUC) and insulin sensitivity index [IAI = (1/FINS x FPG)] were calculated. Stepwise regression analysis was performed to evaluate the effects of INSAUC and insulin sensitivity to the elevation of blood pressure. Both SBP and DBP levels at the end of the study were increased with increased INSAUC baseline. The SBP were (119.5 +/- 2.3), (122.1 +/- 2.5), (129.4 +/- 2.4) and (128.3 +/- 2.6) mmHg, and the DBP were (78.6 +/- 1.6), (79.7 +/- 1.7), (85.2 +/- 1.4) and (84.0 +/- 1.0) mmHg from the lowest to the highest quartiles of INSAUC respectively. Pearson correlation analysis showed Age, SBP, DBP, BMI, FINS, INS1h, INSAUC at baseline were positively correlated to blood pressure levels at the end of the study. After the adjustment of Age, sex, BMI, smoking, PG2 h and blood pressure at baseline, the INSAUC was significantly correlated to blood pressure six years later, while the insulin sensitivity index was not.\n Question: Does [ Compensated hyperinsulinemia based on selective insulin resistance predict elevation of blood pressure in non-diabetic adults ]?\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 if hyperinsulinemia or insulin resistance could predict the elevation of blood pressure in non-diabetic adults. One hundred and seventy non-diabetic adults (NGT 107, IGT 63) were included based on the screen by OGTT in 1986. Height, weight, blood pressure were measured. Plasma glucose and insulin concentration at 0.60 and 120 min during OGTT were determined at baseline. All the subjects were followed for six years with blood pressure and plasma glucose examined at the end of the study. Subjects worsening to diabetes were excluded. Insulin area under-curve (INSAUC) and insulin sensitivity index [IAI = (1/FINS x FPG)] were calculated. Stepwise regression analysis was performed to evaluate the effects of INSAUC and insulin sensitivity to the elevation of blood pressure. Both SBP and DBP levels at the end of the study were increased with increased INSAUC baseline. The SBP were (119.5 +/- 2.3), (122.1 +/- 2.5), (129.4 +/- 2.4) and (128.3 +/- 2.6) mmHg, and the DBP were (78.6 +/- 1.6), (79.7 +/- 1.7), (85.2 +/- 1.4) and (84.0 +/- 1.0) mmHg from the lowest to the highest quartiles of INSAUC respectively. Pearson correlation analysis showed Age, SBP, DBP, BMI, FINS, INS1h, INSAUC at baseline were positively correlated to blood pressure levels at the end of the study. After the adjustment of Age, sex, BMI, smoking, PG2 h and blood pressure at baseline, the INSAUC was significantly correlated to blood pressure six years later, while the insulin sensitivity index was not.
Question: Does [ Compensated hyperinsulinemia based on selective insulin resistance predict elevation of blood pressure in non-diabetic adults ]?
Output:
|
PubmedQA160749
|
[
{
"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 the relationship between birth weight and fat mass- and obesity-associated (FTO) gene expression and promoter methylation status in the Chinese population. Seventy-five neonates and their mothers were recruited from Yuying Children's Hospital of Wenzhou Medical University. Subjects were divided into three groups by birth weight: low (< 3,500 g, n = 20), medium (3,500-3,999 g, n = 30) and high (≥ 4,000 g, n = 25). Placental FTO transcript levels and promoter methylation were determined by quantitative PCR and Sequenom MassARRAY®. Placental FTO mRNA expression was significantly increased in the high- and medium-weight groups compared to the low-weight group (p = 0.023). Methylation rates of CpG11 sites were significantly decreased in high-birth weight newborns (p = 0.018). Multiple linear regressions showed placental FTO mRNA, maternal pre-pregnancy body mass index (BMI) and CpG11 methylation rate were independently associated with increased fetal birth weight. Additionally, FTO mRNA expression was negatively associated with CpG6.7.8.9 methylation in mothers that underwent C-section.\n Question: Is birth weight associated with placental fat mass- and obesity-associated gene expression and promoter methylation in a Chinese population?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To explore the relationship between birth weight and fat mass- and obesity-associated (FTO) gene expression and promoter methylation status in the Chinese population. Seventy-five neonates and their mothers were recruited from Yuying Children's Hospital of Wenzhou Medical University. Subjects were divided into three groups by birth weight: low (< 3,500 g, n = 20), medium (3,500-3,999 g, n = 30) and high (≥ 4,000 g, n = 25). Placental FTO transcript levels and promoter methylation were determined by quantitative PCR and Sequenom MassARRAY®. Placental FTO mRNA expression was significantly increased in the high- and medium-weight groups compared to the low-weight group (p = 0.023). Methylation rates of CpG11 sites were significantly decreased in high-birth weight newborns (p = 0.018). Multiple linear regressions showed placental FTO mRNA, maternal pre-pregnancy body mass index (BMI) and CpG11 methylation rate were independently associated with increased fetal birth weight. Additionally, FTO mRNA expression was negatively associated with CpG6.7.8.9 methylation in mothers that underwent C-section.
Question: Is birth weight associated with placental fat mass- and obesity-associated gene expression and promoter methylation in a Chinese population?
Output:
|
PubmedQA55960
|
[
{
"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: Previous studies have shown that blockade of LIGHT, a T-cell costimulatory molecule belonging to the tumor necrosis factor (TNF) superfamily, by soluble lymphotoxin beta receptor-Ig (LTbetaR-Ig) inhibited the development of graft-versus-host disease. The cardiac allografts were significantly prolonged in LIGHT deficient mice. No data are yet available regarding the role of the LIGHT/HVEM pathway in more stringent fully allogeneic models such as skin and islet transplantation models. Streptozotocin-induced chemical diabetic BALB/C mice underwent transplantation with allogeneic C57BL/6 islets and were treated with LTbetaR-Ig, CTLA4-Ig or a combination of both in the early peritransplant period. Administration of CTLA4-Ig or LTbeta R-Ig alone only increased graft survival to 55 days and 27 days respectively, whereas simultaneous blockade of both pathways significantly prolonged the islet allograft survival for more than 100 days. Long-term survivors were retransplanted with donor-specific (C57BL/6) islets and the grafted islets remained functional for more than 100 days. All of islet allografts were protected against rejection when the mixtures of 1x10(6) CD4+ T cells from tolerant mice and islet allografts were cotransplanted under the renal capsule of the naïve BALB/c recipients.\n Question: Does blockade of LIGHT/HVEM and B7/CD28 signaling facilitate long-term islet graft survival with development of allospecific tolerance?\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: Previous studies have shown that blockade of LIGHT, a T-cell costimulatory molecule belonging to the tumor necrosis factor (TNF) superfamily, by soluble lymphotoxin beta receptor-Ig (LTbetaR-Ig) inhibited the development of graft-versus-host disease. The cardiac allografts were significantly prolonged in LIGHT deficient mice. No data are yet available regarding the role of the LIGHT/HVEM pathway in more stringent fully allogeneic models such as skin and islet transplantation models. Streptozotocin-induced chemical diabetic BALB/C mice underwent transplantation with allogeneic C57BL/6 islets and were treated with LTbetaR-Ig, CTLA4-Ig or a combination of both in the early peritransplant period. Administration of CTLA4-Ig or LTbeta R-Ig alone only increased graft survival to 55 days and 27 days respectively, whereas simultaneous blockade of both pathways significantly prolonged the islet allograft survival for more than 100 days. Long-term survivors were retransplanted with donor-specific (C57BL/6) islets and the grafted islets remained functional for more than 100 days. All of islet allografts were protected against rejection when the mixtures of 1x10(6) CD4+ T cells from tolerant mice and islet allografts were cotransplanted under the renal capsule of the naïve BALB/c recipients.
Question: Does blockade of LIGHT/HVEM and B7/CD28 signaling facilitate long-term islet graft survival with development of allospecific tolerance?
Output:
|
PubmedQA20447
|
[
{
"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 relationship between abnormalities found by magnetic resonance imaging (MRI) and proton spectroscopy (MRS) and the clinical signs of hepatic encephalopathy is not well characterized. Motor disturbances have been described, suggesting that basal ganglia (BG) are altered. We evaluated 19 unselected consecutive patients with biopsy-proven cirrhosis evaluated for liver transplantation for the presence of parkinsonian signs using the Unified Parkinson's Disease Rating Scale (UPDRS) and Purdue Pegboard test, and correlated these neurologic abnormalities with MRI and MRS studies. Brain MRI intensities were expressed as signal-to-noise ratios. MRS findings obtained from one voxel in the BG and one in the occipital white matter (WM) were expressed as metabolite ratios. Six healthy subjects had normal values. Compared with healthy subjects, patients with subclinical or grade 1 hepatic encephalopathy had hyperintensity in occipital WM and all BG tissues except thalamus and reduced Ino/Cr and Cho/Cr ratios in both voxels. In the BG, MRI intensity was correlated with the UPDRS (P < 0.05, r = 0.56). The Cho/Cr ratio also correlated with both UPDRS (P < 0.02, r = -0.59) and Pegboard scores (P < 0.02, r = 0.61).\n Question: Do magnetic resonance imaging and proton spectroscopic alterations correlate with parkinsonian signs in patients with cirrhosis?\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 relationship between abnormalities found by magnetic resonance imaging (MRI) and proton spectroscopy (MRS) and the clinical signs of hepatic encephalopathy is not well characterized. Motor disturbances have been described, suggesting that basal ganglia (BG) are altered. We evaluated 19 unselected consecutive patients with biopsy-proven cirrhosis evaluated for liver transplantation for the presence of parkinsonian signs using the Unified Parkinson's Disease Rating Scale (UPDRS) and Purdue Pegboard test, and correlated these neurologic abnormalities with MRI and MRS studies. Brain MRI intensities were expressed as signal-to-noise ratios. MRS findings obtained from one voxel in the BG and one in the occipital white matter (WM) were expressed as metabolite ratios. Six healthy subjects had normal values. Compared with healthy subjects, patients with subclinical or grade 1 hepatic encephalopathy had hyperintensity in occipital WM and all BG tissues except thalamus and reduced Ino/Cr and Cho/Cr ratios in both voxels. In the BG, MRI intensity was correlated with the UPDRS (P < 0.05, r = 0.56). The Cho/Cr ratio also correlated with both UPDRS (P < 0.02, r = -0.59) and Pegboard scores (P < 0.02, r = 0.61).
Question: Do magnetic resonance imaging and proton spectroscopic alterations correlate with parkinsonian signs in patients with cirrhosis?
Output:
|
PubmedQA14326
|
[
{
"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 response to interferon therapy for chronic hepatitis is known to decrease with progression of the hepatic fibrosis. On the other hand, serum hyaluronate reflects hepatic sinusoidal capillarization or liver cirrhosis, and also serum type IV collagen, which is one of the main components of the basement membrane, rises with the progression of hepatic fibrosis. In this study, the relationship between the degree of hepatic fibrosis and the response to interferon-alpha was determined retrospectively in patients with chronic hepatitis C. In addition, whether the measurement of serum hyaluronate and type IV collagen before interferon-alpha therapy was useful for predicting the response to interferon-alpha therapy in chronic hepatitis C was determined. Thirty-seven patients with elevated serum ALT levels for at least 6 months and histologically determined chronic hepatitis were studied. All patients were positive for anti-HCV and negative for hepatitis B surface antigen. Twenty-eight healthy adults with normal blood biochemical data, who were negative for hepatitis B antigen and HCV antibody tests, had limited alcohol intake were used as controls. The test group was given IFN-alpha by intramuscular injection for 14 days, and then were treated 3 times per week for 24 weeks. The extent of hepatic fibrosis, particularly, perisinusoidal fibrosis (P < 0.01) was significantly greater in nonresponders than in responders. The mean serum hyaluronate and type IV collagen levels were more elevated in nonresponders than in responders, especially, the serum hyaluronate level showed a significant difference (P < 0.01). Most of the patients having a serum hyaluronate level of more than 100 ng/ml were nonresponders who had chronic active hepatitis with bridging necrosis on liver biopsy. Serum hyaluronate and type IV collagen levels showed significant positive correlation with degree of the portal fibrosis (P < 0.01), perisinusoidal fibrosis (P < 0.001) and focal necrosis (P < 0.01) in histological findings of liver biopsy specimens.\n Question: Does serum hyaluronate predict response to interferon-alpha therapy in patients with chronic hepatitis C?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: The response to interferon therapy for chronic hepatitis is known to decrease with progression of the hepatic fibrosis. On the other hand, serum hyaluronate reflects hepatic sinusoidal capillarization or liver cirrhosis, and also serum type IV collagen, which is one of the main components of the basement membrane, rises with the progression of hepatic fibrosis. In this study, the relationship between the degree of hepatic fibrosis and the response to interferon-alpha was determined retrospectively in patients with chronic hepatitis C. In addition, whether the measurement of serum hyaluronate and type IV collagen before interferon-alpha therapy was useful for predicting the response to interferon-alpha therapy in chronic hepatitis C was determined. Thirty-seven patients with elevated serum ALT levels for at least 6 months and histologically determined chronic hepatitis were studied. All patients were positive for anti-HCV and negative for hepatitis B surface antigen. Twenty-eight healthy adults with normal blood biochemical data, who were negative for hepatitis B antigen and HCV antibody tests, had limited alcohol intake were used as controls. The test group was given IFN-alpha by intramuscular injection for 14 days, and then were treated 3 times per week for 24 weeks. The extent of hepatic fibrosis, particularly, perisinusoidal fibrosis (P < 0.01) was significantly greater in nonresponders than in responders. The mean serum hyaluronate and type IV collagen levels were more elevated in nonresponders than in responders, especially, the serum hyaluronate level showed a significant difference (P < 0.01). Most of the patients having a serum hyaluronate level of more than 100 ng/ml were nonresponders who had chronic active hepatitis with bridging necrosis on liver biopsy. Serum hyaluronate and type IV collagen levels showed significant positive correlation with degree of the portal fibrosis (P < 0.01), perisinusoidal fibrosis (P < 0.001) and focal necrosis (P < 0.01) in histological findings of liver biopsy specimens.
Question: Does serum hyaluronate predict response to interferon-alpha therapy in patients with chronic hepatitis C?
Output:
|
PubmedQA206479
|
[
{
"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: Hypothetical correlation between chronic cerebrospinal venous insufficiency and MS has gained the attention of patients and the scientific community. Studies performed by echo-color Doppler ultrasonography have shown different results, and it is necessary to use more objective diagnostic techniques. The aim of our study was to evaluate the presence of stenoses affecting azygos veins and internal jugular veins by use of venography in patients with MS. We recruited 2 groups of subjects who underwent venography: the study group included 29 patients with MS and the control group included 15 healthy volunteers. The ileo-lumbar plexus, the azygos, and the internal jugular veins were selectively catheterized. We considered any cross-sectional area reduction of the venous lumen >50% to be a significant stenosis. Furthermore, blood pressure was measured in the studied vessels at the stenotic internal jugular veins. Selective venography showed at least 1 significant venous stenosis in 84% of subjects examined, without significant difference between the study group and the control group. Positive venography chronic cerebrospinal venous insufficiency patterns were found in 50% of all subjects examined, without any significant difference between the 2 groups. The multivariate logistic regression analysis failed to assess any significant association between the presence of a positive venography and MS condition. The difference between the median blood pressure of stenotic and nonstenotic internal jugular veins was not statistically significant (P = .46).\n Question: Does phlebographic study show differences between patients with MS and control subjects?\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: Hypothetical correlation between chronic cerebrospinal venous insufficiency and MS has gained the attention of patients and the scientific community. Studies performed by echo-color Doppler ultrasonography have shown different results, and it is necessary to use more objective diagnostic techniques. The aim of our study was to evaluate the presence of stenoses affecting azygos veins and internal jugular veins by use of venography in patients with MS. We recruited 2 groups of subjects who underwent venography: the study group included 29 patients with MS and the control group included 15 healthy volunteers. The ileo-lumbar plexus, the azygos, and the internal jugular veins were selectively catheterized. We considered any cross-sectional area reduction of the venous lumen >50% to be a significant stenosis. Furthermore, blood pressure was measured in the studied vessels at the stenotic internal jugular veins. Selective venography showed at least 1 significant venous stenosis in 84% of subjects examined, without significant difference between the study group and the control group. Positive venography chronic cerebrospinal venous insufficiency patterns were found in 50% of all subjects examined, without any significant difference between the 2 groups. The multivariate logistic regression analysis failed to assess any significant association between the presence of a positive venography and MS condition. The difference between the median blood pressure of stenotic and nonstenotic internal jugular veins was not statistically significant (P = .46).
Question: Does phlebographic study show differences between patients with MS and control subjects?
Output:
|
PubmedQA42695
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The purpose of the ventilatory management of acute respiratory distress syndrome (ARDS) is to avoid any barotrauma to the lungs by decreasing the tidal volume at the expense of permissive hypercapnia. This hypercapnia is extremely dangerous for severe head trauma patients because it increases intracranial pressure. The solution could be the use of tracheal gas which insufflation (TGI) allows the reduction of arterial carbon dioxide tension (PaCO(2)) while controlling airway pressures. We report the cases of two patients with ARDS and severe head trauma. The decrease of tidal volume ( by 60 and 25% respectively) in association with tracheal gas insufflation allowed to reduce plateau airway pressure (<35 cm d'H(2)O) and PaCO(2) (in the first case by 23% and in the second case, by 11% for the second hour then by 24%), while intracranial pressure remained constant or was lowered (in the second case by 39% for the second hour). TGI consisted in insufflating fresh gas via a small catheter placed in the trachea (0(2) at 6 L*min(-1) in the first patient and 4 L*min(-1) in the second case).\n Question: Does [ Tracheal gas insufflation avoid hypercapnia in patients with severe head trauma and acute lung 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 purpose of the ventilatory management of acute respiratory distress syndrome (ARDS) is to avoid any barotrauma to the lungs by decreasing the tidal volume at the expense of permissive hypercapnia. This hypercapnia is extremely dangerous for severe head trauma patients because it increases intracranial pressure. The solution could be the use of tracheal gas which insufflation (TGI) allows the reduction of arterial carbon dioxide tension (PaCO(2)) while controlling airway pressures. We report the cases of two patients with ARDS and severe head trauma. The decrease of tidal volume ( by 60 and 25% respectively) in association with tracheal gas insufflation allowed to reduce plateau airway pressure (<35 cm d'H(2)O) and PaCO(2) (in the first case by 23% and in the second case, by 11% for the second hour then by 24%), while intracranial pressure remained constant or was lowered (in the second case by 39% for the second hour). TGI consisted in insufflating fresh gas via a small catheter placed in the trachea (0(2) at 6 L*min(-1) in the first patient and 4 L*min(-1) in the second case).
Question: Does [ Tracheal gas insufflation avoid hypercapnia in patients with severe head trauma and acute lung injury ]?
Output:
|
PubmedQA21170
|
[
{
"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: Skeletal muscle regeneration is a complex process involving the coordinated input from multiple stimuli. Of these processes, actions of the insulin-like growth factor-I (IGF-I) and phosphoinositide 3-kinase (PI3K) pathways are vital; however, whether IGF-I or PI3K expression is modified during regeneration relative to initial damage intensity is unknown. The objective of this study was to determine whether mRNA expression of IGF-I/PI3K pathway components was differentially regulated during muscle regeneration in mice in response to traumatic injury induced by freezing of two different durations. Traumatic injury was imposed by applying a 6-mm diameter cylindrical steel probe, cooled to the temperature of dry ice (-79°C), to the belly of the left tibialis anterior muscle of 12-week-old C57BL/6J mice for either 5s (5s) or 10s (10s). The right leg served as the uninjured control. RNA was obtained from injured and control muscles following 3, 7, and 21days recovery and examined by real-time PCR. Expression of transcripts within the IGF, PI3K, and Akt families, as well as for myogenic regulatory factors and micro-RNAs were studied. Three days following injury, there was significantly increased expression of Igf1, Igf2, Igf1r, Igf2r, Pik3cb, Pik3cd, Pik3cg, Pik3r1, Pik3r5, Akt1, and Akt3 in response to either 5s or 10s injury compared to uninjured control muscle. There was a significantly greater expression of Pik3cb, Pik3cd, Pik3cg, Pik3r5, Akt1, and Akt3 in 10s injured muscle compared to 5s injured muscle. Seven days following injury, we observed significantly increased expression of Igf1, Igf2, Pik3cd, and Pik3cg in injured muscle compared to control muscle in response to 10s freeze injury. We also observed significantly reduced expression of Igf1r and miR-133a in response to 5s freeze injury compared to control muscle, and significantly reduced expression of Ckm, miR-1 and miR-133a in response to 10s freeze injury as compared to control. Twenty-one days following injury, 5s freeze-injured muscle exhibited significantly increased expression of Igf2, Igf2r, Pik3cg, Akt3, Myod1, Myog, Myf5, and miR-206 compared to control muscle, while 10s freeze-injured muscles showed significantly increased expression of Igf2, Igf2r, Pik3cb, Pik3cd, Pik3r5, Akt1, Akt3, and Myog compared to control. Expression of miR-1 was significantly reduced in 10s freeze-injured muscle compared to control muscle at this time. There were no significant differences in RNA expression between 5s and 10s injury at either 7d or 21d recovery in any transcript examined.\n Question: Is rNA transcript expression of IGF-I/PI3K pathway components in regenerating skeletal muscle sensitive to initial injury intensity?\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: Skeletal muscle regeneration is a complex process involving the coordinated input from multiple stimuli. Of these processes, actions of the insulin-like growth factor-I (IGF-I) and phosphoinositide 3-kinase (PI3K) pathways are vital; however, whether IGF-I or PI3K expression is modified during regeneration relative to initial damage intensity is unknown. The objective of this study was to determine whether mRNA expression of IGF-I/PI3K pathway components was differentially regulated during muscle regeneration in mice in response to traumatic injury induced by freezing of two different durations. Traumatic injury was imposed by applying a 6-mm diameter cylindrical steel probe, cooled to the temperature of dry ice (-79°C), to the belly of the left tibialis anterior muscle of 12-week-old C57BL/6J mice for either 5s (5s) or 10s (10s). The right leg served as the uninjured control. RNA was obtained from injured and control muscles following 3, 7, and 21days recovery and examined by real-time PCR. Expression of transcripts within the IGF, PI3K, and Akt families, as well as for myogenic regulatory factors and micro-RNAs were studied. Three days following injury, there was significantly increased expression of Igf1, Igf2, Igf1r, Igf2r, Pik3cb, Pik3cd, Pik3cg, Pik3r1, Pik3r5, Akt1, and Akt3 in response to either 5s or 10s injury compared to uninjured control muscle. There was a significantly greater expression of Pik3cb, Pik3cd, Pik3cg, Pik3r5, Akt1, and Akt3 in 10s injured muscle compared to 5s injured muscle. Seven days following injury, we observed significantly increased expression of Igf1, Igf2, Pik3cd, and Pik3cg in injured muscle compared to control muscle in response to 10s freeze injury. We also observed significantly reduced expression of Igf1r and miR-133a in response to 5s freeze injury compared to control muscle, and significantly reduced expression of Ckm, miR-1 and miR-133a in response to 10s freeze injury as compared to control. Twenty-one days following injury, 5s freeze-injured muscle exhibited significantly increased expression of Igf2, Igf2r, Pik3cg, Akt3, Myod1, Myog, Myf5, and miR-206 compared to control muscle, while 10s freeze-injured muscles showed significantly increased expression of Igf2, Igf2r, Pik3cb, Pik3cd, Pik3r5, Akt1, Akt3, and Myog compared to control. Expression of miR-1 was significantly reduced in 10s freeze-injured muscle compared to control muscle at this time. There were no significant differences in RNA expression between 5s and 10s injury at either 7d or 21d recovery in any transcript examined.
Question: Is rNA transcript expression of IGF-I/PI3K pathway components in regenerating skeletal muscle sensitive to initial injury intensity?
Output:
|
PubmedQA124953
|
[
{
"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: Experimental evidence correlates anesthetic exposure during early development with neuronal and glial injury and death, as well as behavioral and cognitive impairments, in young animals. Several, although not all, retrospective human studies of neurocognitive and behavioral disorders after childhood exposure to anesthesia suggest a similar association. Few studies have specifically investigated the effects of infant anesthesia exposure on subsequent neurobehavioral development. Using a highly translational nonhuman primate model, the authors investigated the potential dose-dependent effects of anesthesia across the first year of development. The authors examined the effects of single or multiple early postnatal isoflurane exposures on subsequent behavioral development in 24 socially reared rhesus macaques. Infants were exposed to 5 h of isoflurane anesthesia once, three times (ISO-3), or not at all (control). The authors assessed reflex development and anxiety using standardized tests. At approximately 1 yr, infants (n = 23) were weaned and housed indoors with 5 to 6 other subjects. The authors recorded their response to this move and reassessed anxiety. Compared to controls, animals exposed to repeated isoflurane (ISO-3) presented with motor reflex deficits at 1 month (median [range]: ISO-3 = 2 [1 to 5] vs. control = 5 [3 to 7]; P < 0.005) and responded to their new social environment with increased anxiety (median [range]: ISO-3 = 0.4 bouts/min [0.2 to 0.6]; control = 0.25 bouts/min [0.1 to 0.3]; P = 0.05) and affiliative/appeasement behavior (median [range]: ISO-3 = 0.1 [0 to 0.2]; control = 0 bouts/min [0 to 0.1]; P < 0.01) at 12 months. There were no statistically significant behavioral alterations after single isoflurane exposure.\n Question: Does isoflurane Anesthesia have Long-term Consequences on Motor and Behavioral Development in Infant Rhesus Macaques?\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: Experimental evidence correlates anesthetic exposure during early development with neuronal and glial injury and death, as well as behavioral and cognitive impairments, in young animals. Several, although not all, retrospective human studies of neurocognitive and behavioral disorders after childhood exposure to anesthesia suggest a similar association. Few studies have specifically investigated the effects of infant anesthesia exposure on subsequent neurobehavioral development. Using a highly translational nonhuman primate model, the authors investigated the potential dose-dependent effects of anesthesia across the first year of development. The authors examined the effects of single or multiple early postnatal isoflurane exposures on subsequent behavioral development in 24 socially reared rhesus macaques. Infants were exposed to 5 h of isoflurane anesthesia once, three times (ISO-3), or not at all (control). The authors assessed reflex development and anxiety using standardized tests. At approximately 1 yr, infants (n = 23) were weaned and housed indoors with 5 to 6 other subjects. The authors recorded their response to this move and reassessed anxiety. Compared to controls, animals exposed to repeated isoflurane (ISO-3) presented with motor reflex deficits at 1 month (median [range]: ISO-3 = 2 [1 to 5] vs. control = 5 [3 to 7]; P < 0.005) and responded to their new social environment with increased anxiety (median [range]: ISO-3 = 0.4 bouts/min [0.2 to 0.6]; control = 0.25 bouts/min [0.1 to 0.3]; P = 0.05) and affiliative/appeasement behavior (median [range]: ISO-3 = 0.1 [0 to 0.2]; control = 0 bouts/min [0 to 0.1]; P < 0.01) at 12 months. There were no statistically significant behavioral alterations after single isoflurane exposure.
Question: Does isoflurane Anesthesia have Long-term Consequences on Motor and Behavioral Development in Infant Rhesus Macaques?
Output:
|
PubmedQA98110
|
[
{
"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: Recently, variants in the TCF7L2 gene have been reported to be associated with type 2 diabetes across multiple Europid populations, but only one small sample of African-American type 2 diabetic patients has been examined. Our objective was to investigate the importance of TCF7L2 in a larger African-American case-control population. We investigated single nucleotide polymorphisms (SNPs) in six known type 2 diabetes genes in 577 African-American case subjects with type 2 diabetes enriched for nephropathy and 596 African-American control subjects. Additionally, we genotyped 70 ancestry-informative markers (AIMs) to apply adjustments for differences in ancestral proportions. The most significant associations were observed with TCF7L2 intron 3 SNPs rs7903146 (additive P = 4.10 x 10(-6), odds ratio [OR] 1.51; admixture-adjusted P(a) = 3.77 x 10(-6)) and rs7901695 (P = 0.001, OR 1.30; P(a) = 0.003). The 2-SNP haplotype containing these SNPs was also associated with type 2 diabetes (P = 3 x 10(-5)). Modest associations were also seen with TCF7L2 intron 4 SNPs rs7895340, rs11196205, and rs12255372 (0.01 < P < 0.05; 0.03 < P(a) < 0.08), as well as with ATP-sensitive inwardly rectifying potassium channel subunit Kir6.2 (KCNJ11) and hepatocyte nuclear factor 4-alpha (HNF4A) SNPs (0.01 < P < 0.05; 0.01 < P(a) < 0.41). No significant associations were detected with genotyped calpain 10 (CAPN10), peroxisome proliferator-activated receptor gamma (PPARG), and transcription factor 1 (TCF1) SNPs.\n Question: Are variants of the transcription factor 7-like 2 ( TCF7L2 ) gene associated with type 2 diabetes in an African-American population enriched for nephropathy?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Recently, variants in the TCF7L2 gene have been reported to be associated with type 2 diabetes across multiple Europid populations, but only one small sample of African-American type 2 diabetic patients has been examined. Our objective was to investigate the importance of TCF7L2 in a larger African-American case-control population. We investigated single nucleotide polymorphisms (SNPs) in six known type 2 diabetes genes in 577 African-American case subjects with type 2 diabetes enriched for nephropathy and 596 African-American control subjects. Additionally, we genotyped 70 ancestry-informative markers (AIMs) to apply adjustments for differences in ancestral proportions. The most significant associations were observed with TCF7L2 intron 3 SNPs rs7903146 (additive P = 4.10 x 10(-6), odds ratio [OR] 1.51; admixture-adjusted P(a) = 3.77 x 10(-6)) and rs7901695 (P = 0.001, OR 1.30; P(a) = 0.003). The 2-SNP haplotype containing these SNPs was also associated with type 2 diabetes (P = 3 x 10(-5)). Modest associations were also seen with TCF7L2 intron 4 SNPs rs7895340, rs11196205, and rs12255372 (0.01 < P < 0.05; 0.03 < P(a) < 0.08), as well as with ATP-sensitive inwardly rectifying potassium channel subunit Kir6.2 (KCNJ11) and hepatocyte nuclear factor 4-alpha (HNF4A) SNPs (0.01 < P < 0.05; 0.01 < P(a) < 0.41). No significant associations were detected with genotyped calpain 10 (CAPN10), peroxisome proliferator-activated receptor gamma (PPARG), and transcription factor 1 (TCF1) SNPs.
Question: Are variants of the transcription factor 7-like 2 ( TCF7L2 ) gene associated with type 2 diabetes in an African-American population enriched for nephropathy?
Output:
|
PubmedQA99881
|
[
{
"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: Poor oral health, chronic diseases, functional decline, and low cognitive ability can increase the risk of falls in the elderly. The current study aimed to show the effects of oral health, diabetes mellitus (DM), hypertension (HT), heart disease, functional status, and sociodemographic factors on the risk of falls in elderly with dementia. The sample comprised 1,210 Malaysian elderly who were demented and noninstitutionalized. This study was a national cross-sectional survey entitled \"Determinants of Health Status among Older Malaysians\". The effects of age, ethnicity, sex differences, marital status, educational level, oral health, DM, HT, heart disease, and functional status on the risk of falls were evaluated. The multiple logistic regression model was used to estimate the effects of contributing variables on the risk of falls in samples. The prevalence of falls was approximately 17% in subjects. It was found that age (odds ratio [OR] 1.02), non-Malay ethnicity (OR 1.66), heart disease (OR 1.92), and functional decline (OR 1.58) significantly increased the risk of falls in respondents (P<0.05). Furthermore, having teeth (OR 0.59) and dentures (OR 0.66) significantly decreased the rate of falls (P<0.05).\n Question: Does association between dentures and the rate of fall in dementia?\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: Poor oral health, chronic diseases, functional decline, and low cognitive ability can increase the risk of falls in the elderly. The current study aimed to show the effects of oral health, diabetes mellitus (DM), hypertension (HT), heart disease, functional status, and sociodemographic factors on the risk of falls in elderly with dementia. The sample comprised 1,210 Malaysian elderly who were demented and noninstitutionalized. This study was a national cross-sectional survey entitled "Determinants of Health Status among Older Malaysians". The effects of age, ethnicity, sex differences, marital status, educational level, oral health, DM, HT, heart disease, and functional status on the risk of falls were evaluated. The multiple logistic regression model was used to estimate the effects of contributing variables on the risk of falls in samples. The prevalence of falls was approximately 17% in subjects. It was found that age (odds ratio [OR] 1.02), non-Malay ethnicity (OR 1.66), heart disease (OR 1.92), and functional decline (OR 1.58) significantly increased the risk of falls in respondents (P<0.05). Furthermore, having teeth (OR 0.59) and dentures (OR 0.66) significantly decreased the rate of falls (P<0.05).
Question: Does association between dentures and the rate of fall in dementia?
Output:
|
PubmedQA117445
|
[
{
"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: Postprandial hyperglycemia has emerged as a new glycometabolic condition associated with an excessive risk for coronary artery disease. We therefore attempted to evaluate the frequency of postchallenge hyperglycemia in patients with acute coronary syndrome (ACS) who were not previously diagnosed to have diabetes and did not have a fasting glucose concentration of > or =7 mmol/l or an HbA(1c) level >6.0%. We further correlated the presence of postchallenge hyperglycemia with the extent of coronary atherosclerosis. In all, 134 consecutive ACS patients who met the above inclusion criteria were studied. An oral glucose tolerance test was performed before discharge. The mean age, fasting glucose, and HbA(1c) were 60 years, 5.15 mmol/l, and 5.4%, respectively. Among ACS patients, impaired glucose tolerance (IGT) and diabetes were found in 50 (37%) and 13 patients (10%), respectively. The homeostasis model assessment for insulin resistance did not differ substantially among the normal glucose tolerance (NGT), IGT, and diabetic groups. Insulinogenic index, however, was lower and the number of stenosed vessels higher in diabetic patients compared with NGT patients.\n Question: Is glucose intolerance common in Japanese patients with acute coronary syndrome who were not previously diagnosed with diabetes?\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: Postprandial hyperglycemia has emerged as a new glycometabolic condition associated with an excessive risk for coronary artery disease. We therefore attempted to evaluate the frequency of postchallenge hyperglycemia in patients with acute coronary syndrome (ACS) who were not previously diagnosed to have diabetes and did not have a fasting glucose concentration of > or =7 mmol/l or an HbA(1c) level >6.0%. We further correlated the presence of postchallenge hyperglycemia with the extent of coronary atherosclerosis. In all, 134 consecutive ACS patients who met the above inclusion criteria were studied. An oral glucose tolerance test was performed before discharge. The mean age, fasting glucose, and HbA(1c) were 60 years, 5.15 mmol/l, and 5.4%, respectively. Among ACS patients, impaired glucose tolerance (IGT) and diabetes were found in 50 (37%) and 13 patients (10%), respectively. The homeostasis model assessment for insulin resistance did not differ substantially among the normal glucose tolerance (NGT), IGT, and diabetic groups. Insulinogenic index, however, was lower and the number of stenosed vessels higher in diabetic patients compared with NGT patients.
Question: Is glucose intolerance common in Japanese patients with acute coronary syndrome who were not previously diagnosed with diabetes?
Output:
|
PubmedQA142197
|
[
{
"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: β-lapachone (β-lap), has been known to cause NQO1-dependnet death in cancer cells and sensitize cancer cells to ionizing radiation (IR). We investigated the mechanisms underlying the radiosensitization caused by β-lap. β-lap enhanced the effect of IR to cause clonogenic cells in NQO1(+)-MDA-MB-231 cells but not in NQO1(-)-MDA-MB-231 cells. β-lap caused apoptosis only in NQO1(+) cells and not in NQO1(-) cells and it markedly increased IR-induced apoptosis only in NQO1(+) cells. Combined treatment of NQO1(+) cells induced ROS generation, triggered ER stress and stimulated activation of ERK and JNK. Inhibition of ROS generation by NAC effectively attenuated the activation of ERK and JNK, induction of ER stress, and subsequent apoptosis. Importantly, inhibition of ERK abolished ROS generation and ER stress, whereas inhibition of JNK did not, indicating that positive feedback regulation between ERK activation and ROS generation triggers ER stress in response to combined treatment. Furthermore, prevention of ER stress completely blocked combination treatment-induced JNK activation and subsequent apoptotic cell death. In addition, combined treatment efficiently induced the mitochondrial translocation of cleaved Bax, disrupted mitochondrial membrane potential, and the nuclear translocation of AIF, all of which were efficiently blocked by a JNK inhibitor. Caspases 3, 8 and 9 were activated by combined treatment but inhibition of these caspases did not abolish apoptosis indicating caspase activation played a minor role in the induction of apoptosis.\n Question: Does β-lapachone significantly increase the effect of ionizing radiation to cause mitochondrial apoptosis via JNK activation in cancer cells?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: β-lapachone (β-lap), has been known to cause NQO1-dependnet death in cancer cells and sensitize cancer cells to ionizing radiation (IR). We investigated the mechanisms underlying the radiosensitization caused by β-lap. β-lap enhanced the effect of IR to cause clonogenic cells in NQO1(+)-MDA-MB-231 cells but not in NQO1(-)-MDA-MB-231 cells. β-lap caused apoptosis only in NQO1(+) cells and not in NQO1(-) cells and it markedly increased IR-induced apoptosis only in NQO1(+) cells. Combined treatment of NQO1(+) cells induced ROS generation, triggered ER stress and stimulated activation of ERK and JNK. Inhibition of ROS generation by NAC effectively attenuated the activation of ERK and JNK, induction of ER stress, and subsequent apoptosis. Importantly, inhibition of ERK abolished ROS generation and ER stress, whereas inhibition of JNK did not, indicating that positive feedback regulation between ERK activation and ROS generation triggers ER stress in response to combined treatment. Furthermore, prevention of ER stress completely blocked combination treatment-induced JNK activation and subsequent apoptotic cell death. In addition, combined treatment efficiently induced the mitochondrial translocation of cleaved Bax, disrupted mitochondrial membrane potential, and the nuclear translocation of AIF, all of which were efficiently blocked by a JNK inhibitor. Caspases 3, 8 and 9 were activated by combined treatment but inhibition of these caspases did not abolish apoptosis indicating caspase activation played a minor role in the induction of apoptosis.
Question: Does β-lapachone significantly increase the effect of ionizing radiation to cause mitochondrial apoptosis via JNK activation in cancer cells?
Output:
|
PubmedQA164481
|
[
{
"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 measure the association between smoking and serum adiponectin, taking into consideration insulin resistance and obesity. The cross-sectional study was carried out in Seoul, Korea in 2006. Waist circumference (WC), body mass index (BMI), and serum adiponectin were measured in 2,500 healthy Korean men. Multiple linear regression models were used to assess the association of smoking status with serum adiponectin level. WC, BMI, and homeostasis model assessment (HOMA) were classified into two groups according to median values. The mean adiponectin concentrations were 6.6 microg/ml and 7.3 microg/ml in current smokers and non-smokers. After adjusting for age, BMI, and alcohol consumption, mean log adiponectin levels decreased by 0.064 microg/ml in current smokers compared with non-smokers (P = 0.0190). Mean log adiponectin levels also decreased by 0.030 and 0.095 microg/ml in moderate and heavy smokers compared to non-smokers. The relationship between adiponectin and smoking was similar between the high and low insulin resistance, BMI, and WC groups.\n Question: Is serum adiponectin associated with smoking status in healthy Korean 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 measure the association between smoking and serum adiponectin, taking into consideration insulin resistance and obesity. The cross-sectional study was carried out in Seoul, Korea in 2006. Waist circumference (WC), body mass index (BMI), and serum adiponectin were measured in 2,500 healthy Korean men. Multiple linear regression models were used to assess the association of smoking status with serum adiponectin level. WC, BMI, and homeostasis model assessment (HOMA) were classified into two groups according to median values. The mean adiponectin concentrations were 6.6 microg/ml and 7.3 microg/ml in current smokers and non-smokers. After adjusting for age, BMI, and alcohol consumption, mean log adiponectin levels decreased by 0.064 microg/ml in current smokers compared with non-smokers (P = 0.0190). Mean log adiponectin levels also decreased by 0.030 and 0.095 microg/ml in moderate and heavy smokers compared to non-smokers. The relationship between adiponectin and smoking was similar between the high and low insulin resistance, BMI, and WC groups.
Question: Is serum adiponectin associated with smoking status in healthy Korean men?
Output:
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PubmedQA140085
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: There is currently no standard for the assessment of contractile function in animals. We aimed to determine whether transthoracic echocardiography in rats with chronic pressure overload allows determining the stage of hypertrophy and heart failure (HF). Pressure overload was created by placement of a metal clip around the thoracic aorta at a weight of 40 to 50 g. After 1, 2, 6, 10, and 20 weeks, we performed echocardiography according to the American Heart Association guidelines (n = 26, four to six rats for each time point). We also obtained heart, lung, and body weights and regularly evaluated clinical signs of HF. : Pressure overload caused significant hypertrophy within 1 week. Contractile function was normal until 6 weeks when diastolic dysfunction appeared. After 10 weeks of pressure overload, systolic function decreased. At 20 weeks, hearts were dilated and cardiac index was decreased. These findings correlated with increased lung-to-body weight ratio after 6 weeks and clinical signs of HF after 20 weeks.\n Question: Does echocardiography alone allow the determination of heart failure stages in rats with pressure overload?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: There is currently no standard for the assessment of contractile function in animals. We aimed to determine whether transthoracic echocardiography in rats with chronic pressure overload allows determining the stage of hypertrophy and heart failure (HF). Pressure overload was created by placement of a metal clip around the thoracic aorta at a weight of 40 to 50 g. After 1, 2, 6, 10, and 20 weeks, we performed echocardiography according to the American Heart Association guidelines (n = 26, four to six rats for each time point). We also obtained heart, lung, and body weights and regularly evaluated clinical signs of HF. : Pressure overload caused significant hypertrophy within 1 week. Contractile function was normal until 6 weeks when diastolic dysfunction appeared. After 10 weeks of pressure overload, systolic function decreased. At 20 weeks, hearts were dilated and cardiac index was decreased. These findings correlated with increased lung-to-body weight ratio after 6 weeks and clinical signs of HF after 20 weeks.
Question: Does echocardiography alone allow the determination of heart failure stages in rats with pressure overload?
Output:
|
PubmedQA104959
|
[
{
"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: Biliary cystadenoma (BCA) and cystadenocarcinoma (BCCA) are rare cystic hepatic neoplasms. Prior reports concerning the proper surgical treatment and long-term survival are scarce. We report our experience and survival outcome of 30 patients over the last 25 years. We retrospectively reviewed the clinicopathologic data of the pathologically confirmed 18 BCA and 12 BCCA patients, who underwent operations from 1983 to 2006, at the Seoul National University Hospital. The patients consisted of 8 men and 22 women with a mean age of 51 years. With abdominal computed tomography scans, 73.3% (n=22) were preoperatively diagnosed as BCA or BCCA, and differentiating BCCA from BCA was accurate in 58.3% patients. R0 resection was achieved in 90% (n=27). The differentiating factors included the presence of mural nodule (4/18 vs. 8/12; p=0.009) and mucinous content (2/9 vs. 8/1; p=0.005), and tumor size tending to be larger in BCCA (11.7 cm vs. 7.9 cm; p=0.067). Overall 5-year and 10-year survival rates of BCCA were 72.9% and 60.9%, respectively. Of patients with BCCA, 4 experienced recurrence. In case of recurrence, patients tended to be younger than 50 years (p=0.061) and the lesions tended to be larger than those without recurrence (p=0.088).\n Question: Does clinical outcome and long term result after surgical treatment of biliary cystadenoma and cystadenocarcinoma?\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: Biliary cystadenoma (BCA) and cystadenocarcinoma (BCCA) are rare cystic hepatic neoplasms. Prior reports concerning the proper surgical treatment and long-term survival are scarce. We report our experience and survival outcome of 30 patients over the last 25 years. We retrospectively reviewed the clinicopathologic data of the pathologically confirmed 18 BCA and 12 BCCA patients, who underwent operations from 1983 to 2006, at the Seoul National University Hospital. The patients consisted of 8 men and 22 women with a mean age of 51 years. With abdominal computed tomography scans, 73.3% (n=22) were preoperatively diagnosed as BCA or BCCA, and differentiating BCCA from BCA was accurate in 58.3% patients. R0 resection was achieved in 90% (n=27). The differentiating factors included the presence of mural nodule (4/18 vs. 8/12; p=0.009) and mucinous content (2/9 vs. 8/1; p=0.005), and tumor size tending to be larger in BCCA (11.7 cm vs. 7.9 cm; p=0.067). Overall 5-year and 10-year survival rates of BCCA were 72.9% and 60.9%, respectively. Of patients with BCCA, 4 experienced recurrence. In case of recurrence, patients tended to be younger than 50 years (p=0.061) and the lesions tended to be larger than those without recurrence (p=0.088).
Question: Does clinical outcome and long term result after surgical treatment of biliary cystadenoma and cystadenocarcinoma?
Output:
|
PubmedQA182553
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Although excellent outcomes are routinely reported following total knee replacement, up to 20 % of patients remain dissatisfied. The aim of this study was to determine whether pre-operative radiographic classification was associated with functional outcomes following surgery. A retrospective review of a prospective arthroplasty database identified 256 patients that fulfilled the inclusion criteria over an 18-month period. Baseline demographic data on all patients were collected prospectively. All pre-operative radiographs were assessed using the Kellgren and Lawrence (K&L) classification system. Patients were prospectively assessed using the American Knee Society Score pre-operatively and at 1, 3 and 5 years post-surgery. An association was found between the pre-operative radiographic severity of arthritis and the pre-operative American Knee Society Knee (AKSK) scores, with worsening radiographic grade corresponding to worsening AKSK scores (p = 0.020). There was an association between K&L classification and improvement in AKSK scores from pre-operative to 1 year (p = 0.003) and 3 years (p = 0.04), with K&L grades 3 and 4 demonstrating the most significant improvements. On multivariate regression analysis, K&L classification was the only significant predictor of improvement in AKSK at 1 year (p = 0.009). No correlation was found between K&L grade and the American Knee Society Functional Scores at any stage.\n Question: Does severe arthritis predict greater improvements in function following total knee arthroplasty?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Although excellent outcomes are routinely reported following total knee replacement, up to 20 % of patients remain dissatisfied. The aim of this study was to determine whether pre-operative radiographic classification was associated with functional outcomes following surgery. A retrospective review of a prospective arthroplasty database identified 256 patients that fulfilled the inclusion criteria over an 18-month period. Baseline demographic data on all patients were collected prospectively. All pre-operative radiographs were assessed using the Kellgren and Lawrence (K&L) classification system. Patients were prospectively assessed using the American Knee Society Score pre-operatively and at 1, 3 and 5 years post-surgery. An association was found between the pre-operative radiographic severity of arthritis and the pre-operative American Knee Society Knee (AKSK) scores, with worsening radiographic grade corresponding to worsening AKSK scores (p = 0.020). There was an association between K&L classification and improvement in AKSK scores from pre-operative to 1 year (p = 0.003) and 3 years (p = 0.04), with K&L grades 3 and 4 demonstrating the most significant improvements. On multivariate regression analysis, K&L classification was the only significant predictor of improvement in AKSK at 1 year (p = 0.009). No correlation was found between K&L grade and the American Knee Society Functional Scores at any stage.
Question: Does severe arthritis predict greater improvements in function following total knee arthroplasty?
Output:
|
PubmedQA167107
|
[
{
"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 xanthine oxidase (XO) polymorphism in Ethiopians and influence of environmental factors, smoking habit and gender-related differences on enzyme activity among Ethiopians living in Ethiopia or Sweden. One hundred healthy unrelated Ethiopians living in Ethiopia and 73 living in Sweden participated in the study. Subjects received a 100-mg oral dose of caffeine before bedtime. All urine voided in the following 8 h was collected and the concentrations of 1-methyluracil (1U) and 1-methylxanthine (1X) micromol/l) were analyzed by means of high-performance liquid chromatography. The 1U/(1X+1U) metabolic ratio (MR) was calculated and used as an index of XO activity. XO activity was not normally distributed ( P<0.0001; Shapiro-Wilk's test). The incidence of putative XO poor metabolizers in Ethiopians was 4%. The effect of differences in country of residence, gender and smoking habit was analyzed using three-way ANOVA/MANOVA. The post-hoc test ( P<0.05) and Kruskal-Wallis ANOVA ( P<0.004), median test showed a significant difference in XO activity among Ethiopians living in Ethiopia compared with those living in Sweden, the activity being higher in Ethiopians living in Ethiopia. The 95% CI for differences between the two means was (0.012; 0.044). No significant difference was observed in XO MR between men and women or between smokers and non-smokers, the 95% CI for the differences being (-0.059; 0.037) and (-0.010; 0.016) respectively.\n Question: Is xanthine oxidase activity influenced by environmental factors in Ethiopians?\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 xanthine oxidase (XO) polymorphism in Ethiopians and influence of environmental factors, smoking habit and gender-related differences on enzyme activity among Ethiopians living in Ethiopia or Sweden. One hundred healthy unrelated Ethiopians living in Ethiopia and 73 living in Sweden participated in the study. Subjects received a 100-mg oral dose of caffeine before bedtime. All urine voided in the following 8 h was collected and the concentrations of 1-methyluracil (1U) and 1-methylxanthine (1X) micromol/l) were analyzed by means of high-performance liquid chromatography. The 1U/(1X+1U) metabolic ratio (MR) was calculated and used as an index of XO activity. XO activity was not normally distributed ( P<0.0001; Shapiro-Wilk's test). The incidence of putative XO poor metabolizers in Ethiopians was 4%. The effect of differences in country of residence, gender and smoking habit was analyzed using three-way ANOVA/MANOVA. The post-hoc test ( P<0.05) and Kruskal-Wallis ANOVA ( P<0.004), median test showed a significant difference in XO activity among Ethiopians living in Ethiopia compared with those living in Sweden, the activity being higher in Ethiopians living in Ethiopia. The 95% CI for differences between the two means was (0.012; 0.044). No significant difference was observed in XO MR between men and women or between smokers and non-smokers, the 95% CI for the differences being (-0.059; 0.037) and (-0.010; 0.016) respectively.
Question: Is xanthine oxidase activity influenced by environmental factors in Ethiopians?
Output:
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PubmedQA47789
|
[
{
"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: Proliferation in transformed β-cell lines is high compared to primary islet cells and is accompanied by reduced insulin content and release. Our aim was to determine whether experimental reduction of proliferation restores the cells to a more authentic β-cell phenotype in terms of secretory function and to investigate the potential beneficial effect of their configuration as islet-like structures. Mitosis inhibitor mitomycin c treatment neither altered the rate of proliferation nor improved the secretory responses of MIN6 monolayer cells. The proliferative rate of MIN6 cells was not affected by pseudoislet formation, but in contrast to monolayer cells, pseudoislets responded to 20 mM glucose with a 2.6-fold increase in insulin secretion. MMC reduced proliferation in MIN6 pseudoislets, but did not further improve their secretory responsiveness. Withdrawal of doxycycline resulted in complete growth-arrest in R7T1 cells, but monolayer and pseudoislet R7T1 cells were unresponsive to glucose and remained so upon growth-arrest although insulin content was increased in growth-arrested pseudoislets. MIN6 monolayer and pseudoislet cells were treated with MMC whereas growth-arrest was induced in R7T1 monolayer and pseudoislet cells by withdrawal of doxycycline. Proliferation rates were determined by immunocytochemical measurements of BrdU incorporation and insulin secretion was assessed by radioimmunoassay.\n Question: Does down-regulation of proliferation affect the secretory function of transformed β-cell lines regardless of their anatomical configuration?\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: Proliferation in transformed β-cell lines is high compared to primary islet cells and is accompanied by reduced insulin content and release. Our aim was to determine whether experimental reduction of proliferation restores the cells to a more authentic β-cell phenotype in terms of secretory function and to investigate the potential beneficial effect of their configuration as islet-like structures. Mitosis inhibitor mitomycin c treatment neither altered the rate of proliferation nor improved the secretory responses of MIN6 monolayer cells. The proliferative rate of MIN6 cells was not affected by pseudoislet formation, but in contrast to monolayer cells, pseudoislets responded to 20 mM glucose with a 2.6-fold increase in insulin secretion. MMC reduced proliferation in MIN6 pseudoislets, but did not further improve their secretory responsiveness. Withdrawal of doxycycline resulted in complete growth-arrest in R7T1 cells, but monolayer and pseudoislet R7T1 cells were unresponsive to glucose and remained so upon growth-arrest although insulin content was increased in growth-arrested pseudoislets. MIN6 monolayer and pseudoislet cells were treated with MMC whereas growth-arrest was induced in R7T1 monolayer and pseudoislet cells by withdrawal of doxycycline. Proliferation rates were determined by immunocytochemical measurements of BrdU incorporation and insulin secretion was assessed by radioimmunoassay.
Question: Does down-regulation of proliferation affect the secretory function of transformed β-cell lines regardless of their anatomical configuration?
Output:
|
PubmedQA31558
|
[
{
"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 role of Rho-associated protein kinase (ROCK) inhibitor, Y27632, in mediating the production of extracellular matrix (ECM) components including fibronectin, matrix metallo-proteinase-2 (MMP-2) and type I collagen as induced by connective tissue growth factor (CTGF) or transforming growth factor-β (TGF-β) in a human retinal pigment epithelial cell line, ARPE-19. The effect of Y27632 on the CTGF or TGF-β induced phenotype in ARPE-19 cells was measured with immunocytochemistry as the change in F-actin. ARPE-19 cells were treated with CTGF (1, 10, 100ng/mL) and TGF-β (10ng/mL) in serum free media, and analyzed for fibronectin, laminin, and MMP-2 and type I collagen by RT-qPCR and immunocytochemistry. Cells were also pretreated with an ROCK inhibitor, Y27632, to analyze the signaling contributing to ECM production. Treatment of ARPE-19 cells in culture with TGF-β or CTGF induced an ECM change from a cobblestone morphology to a more elongated swirl pattern indicating a mesenchymal phenotype. RT-qPCR analysis and different gene expression analysis demonstrated an upregulation in expression of genes associated with cytoskeletal structure and motility. CTGF or TGF-β significantly increased expression of fibronectin mRNA (P=0.006, P=0.003 respectively), laminin mRNA (P=0.006, P=0.005), MMP-2 mRNA (P= 0.006, P= 0.001), COL1A1 mRNA (P=0.001, P=0.001), COL1A2 mRNA (P=0.001, P=0.001). Preincubation of ARPE-19 with Y27632 (10mmol/L) significantly prevented CTGF or TGF- β induced fibronectin (P=0.005, P=0.003 respectively), MMP-2 (P= 0.003, P=0.002), COL1A1 (P=0.006, P=0.003), and COL1A2 (P=0.006, P=0.004) gene expression, but not laminin (P=0.375, P=0.516).\n Question: Does inhibition of RhoA/Rho-kinase pathway suppress the expression of extracellular matrix induced by CTGF or TGF-β in ARPE-19?\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 role of Rho-associated protein kinase (ROCK) inhibitor, Y27632, in mediating the production of extracellular matrix (ECM) components including fibronectin, matrix metallo-proteinase-2 (MMP-2) and type I collagen as induced by connective tissue growth factor (CTGF) or transforming growth factor-β (TGF-β) in a human retinal pigment epithelial cell line, ARPE-19. The effect of Y27632 on the CTGF or TGF-β induced phenotype in ARPE-19 cells was measured with immunocytochemistry as the change in F-actin. ARPE-19 cells were treated with CTGF (1, 10, 100ng/mL) and TGF-β (10ng/mL) in serum free media, and analyzed for fibronectin, laminin, and MMP-2 and type I collagen by RT-qPCR and immunocytochemistry. Cells were also pretreated with an ROCK inhibitor, Y27632, to analyze the signaling contributing to ECM production. Treatment of ARPE-19 cells in culture with TGF-β or CTGF induced an ECM change from a cobblestone morphology to a more elongated swirl pattern indicating a mesenchymal phenotype. RT-qPCR analysis and different gene expression analysis demonstrated an upregulation in expression of genes associated with cytoskeletal structure and motility. CTGF or TGF-β significantly increased expression of fibronectin mRNA (P=0.006, P=0.003 respectively), laminin mRNA (P=0.006, P=0.005), MMP-2 mRNA (P= 0.006, P= 0.001), COL1A1 mRNA (P=0.001, P=0.001), COL1A2 mRNA (P=0.001, P=0.001). Preincubation of ARPE-19 with Y27632 (10mmol/L) significantly prevented CTGF or TGF- β induced fibronectin (P=0.005, P=0.003 respectively), MMP-2 (P= 0.003, P=0.002), COL1A1 (P=0.006, P=0.003), and COL1A2 (P=0.006, P=0.004) gene expression, but not laminin (P=0.375, P=0.516).
Question: Does inhibition of RhoA/Rho-kinase pathway suppress the expression of extracellular matrix induced by CTGF or TGF-β in ARPE-19?
Output:
|
PubmedQA127291
|
[
{
"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 intestinal epithelium generates a barrier that protects mammals from potentially harmful intestinal contents, such as pathogenic bacteria. Dysregulation of epithelial cell death has been implicated in barrier dysfunction and in the pathogenesis of intestinal inflammation. We investigated mechanisms of cell-death regulation in the intestinal epithelium of mice. Conditional knockout mice (either inducible or permanent) with deletion of cellular FLICE-inhibitory protein (cFlip) or caspase-8 in the intestinal epithelium were analyzed by histology and high-resolution endoscopy. We assessed the effects of cFlip or caspase-8 deficiency on intestinal homeostasis. Expression of cFlip in the intestinal epithelium was required for constitutive activation of caspase-8 under steady-state conditions. Intestinal expression of cFlip was required for development; disruption of the gene encoding cFlip from the intestinal epithelium (cFlip(fl/fl) VillinCre(+) mice) resulted in embryonic lethality. When cFlip was deleted from the intestinal epithelium of adult mice (cFlip(iΔIEC) mice), the animals died within a few days from severe tissue destruction, epithelial cell death, and intestinal inflammation. Death of cFlip-depleted intestinal epithelial cells was regulated extrinsically and required the presence of death receptor ligands, such as tumor necrosis factor-α and CD95 ligand, but was independent of receptor-interacting protein 3. cFlip deficiency was associated with strong up-regulation of caspase-8 and caspase-3 activity and excessive apoptosis in intestinal crypts.\n Question: Does cellular FLICE-like inhibitory protein secure intestinal epithelial cell survival and immune homeostasis by regulating caspase-8?\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 intestinal epithelium generates a barrier that protects mammals from potentially harmful intestinal contents, such as pathogenic bacteria. Dysregulation of epithelial cell death has been implicated in barrier dysfunction and in the pathogenesis of intestinal inflammation. We investigated mechanisms of cell-death regulation in the intestinal epithelium of mice. Conditional knockout mice (either inducible or permanent) with deletion of cellular FLICE-inhibitory protein (cFlip) or caspase-8 in the intestinal epithelium were analyzed by histology and high-resolution endoscopy. We assessed the effects of cFlip or caspase-8 deficiency on intestinal homeostasis. Expression of cFlip in the intestinal epithelium was required for constitutive activation of caspase-8 under steady-state conditions. Intestinal expression of cFlip was required for development; disruption of the gene encoding cFlip from the intestinal epithelium (cFlip(fl/fl) VillinCre(+) mice) resulted in embryonic lethality. When cFlip was deleted from the intestinal epithelium of adult mice (cFlip(iΔIEC) mice), the animals died within a few days from severe tissue destruction, epithelial cell death, and intestinal inflammation. Death of cFlip-depleted intestinal epithelial cells was regulated extrinsically and required the presence of death receptor ligands, such as tumor necrosis factor-α and CD95 ligand, but was independent of receptor-interacting protein 3. cFlip deficiency was associated with strong up-regulation of caspase-8 and caspase-3 activity and excessive apoptosis in intestinal crypts.
Question: Does cellular FLICE-like inhibitory protein secure intestinal epithelial cell survival and immune homeostasis by regulating caspase-8?
Output:
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PubmedQA95874
|
[
{
"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: Overexpression of matrix metalloproteinase (MMP) has been implicated in the incidence of restenosis after vascular angioplasty. Reversion-inducing cysteine-rich protein with kazal motifs (RECK) is a membrane-anchored glycoprotein that negatively regulates the activity of MMPs, such as MMP-9 and MMP-2, which play a key role in the angiogenesis during tumor growth. This study was designed to investigate the potential association between RECK and restenosis after vascular angioplasty. Balloon-injured rabbit carotid arterial models were established. Arterial morphology was assessed by hematoxylin-eosin staining. The area of intimal hyperplasia was measured using image microscopy and image analyzer. The messenger RNA (mRNA) expression levels of RECK, MMP-9, and MMP-2 were detected using reverse transcription-polymerase chain reaction (RT-PCR) at 7, 14, and 21 days. Vascular smooth muscle cells (VSMCs) were transfected with RECK small interfering RNA (siRNA). VSMC proliferation rate was detected by MTT assay at 24, 48 and 72 hr. The protein expression of RECK, MMP-9, and MMP-2 was determined by Western blot. MMP-2 and MMP-9 in carotid artery of rats were significantly overexpressed in the injured-artery group, compared with unmanipulated control and contralateral uninjured groups (P < 0.05). With the time of the injury extended, MMP-2 and MMP-9 mRNA levels gradually increased. RECK showed a marked peak of mRNA level at 7 days after injury, compared with unmanipulated control and contralateral uninjured groups (P < 0.001). However, the increasing trend gradually decreased at 14 days after the balloon surgery. RECK mRNA was still detectable at 21 days postoperatively, but the expression level of RECK mRNA in injured and contralateral uninjured groups was significantly lower than that in unmanipulated control group (P < 0.001). The expression level of RECK protein in VSMCs in transfected group was significantly lower compared with that in untransfected group, whereas the expression of MMP-2 and MMP-9 proteins in transfected group was significantly higher compared with that in untransfected group. Over the extension of transfection time, the proliferation of VSMCs in transfected group was increased gradually, compared with negative and blank plasmid controls (P < 0.05).\n Question: Is reversion-inducing-cysteine-rich protein with Kazal motif involved in intimal hyperplasia in carotid arteries : a new insight in the prevention of restenosis after vascular angioplasty?\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: Overexpression of matrix metalloproteinase (MMP) has been implicated in the incidence of restenosis after vascular angioplasty. Reversion-inducing cysteine-rich protein with kazal motifs (RECK) is a membrane-anchored glycoprotein that negatively regulates the activity of MMPs, such as MMP-9 and MMP-2, which play a key role in the angiogenesis during tumor growth. This study was designed to investigate the potential association between RECK and restenosis after vascular angioplasty. Balloon-injured rabbit carotid arterial models were established. Arterial morphology was assessed by hematoxylin-eosin staining. The area of intimal hyperplasia was measured using image microscopy and image analyzer. The messenger RNA (mRNA) expression levels of RECK, MMP-9, and MMP-2 were detected using reverse transcription-polymerase chain reaction (RT-PCR) at 7, 14, and 21 days. Vascular smooth muscle cells (VSMCs) were transfected with RECK small interfering RNA (siRNA). VSMC proliferation rate was detected by MTT assay at 24, 48 and 72 hr. The protein expression of RECK, MMP-9, and MMP-2 was determined by Western blot. MMP-2 and MMP-9 in carotid artery of rats were significantly overexpressed in the injured-artery group, compared with unmanipulated control and contralateral uninjured groups (P < 0.05). With the time of the injury extended, MMP-2 and MMP-9 mRNA levels gradually increased. RECK showed a marked peak of mRNA level at 7 days after injury, compared with unmanipulated control and contralateral uninjured groups (P < 0.001). However, the increasing trend gradually decreased at 14 days after the balloon surgery. RECK mRNA was still detectable at 21 days postoperatively, but the expression level of RECK mRNA in injured and contralateral uninjured groups was significantly lower than that in unmanipulated control group (P < 0.001). The expression level of RECK protein in VSMCs in transfected group was significantly lower compared with that in untransfected group, whereas the expression of MMP-2 and MMP-9 proteins in transfected group was significantly higher compared with that in untransfected group. Over the extension of transfection time, the proliferation of VSMCs in transfected group was increased gradually, compared with negative and blank plasmid controls (P < 0.05).
Question: Is reversion-inducing-cysteine-rich protein with Kazal motif involved in intimal hyperplasia in carotid arteries : a new insight in the prevention of restenosis after vascular angioplasty?
Output:
|
PubmedQA7581
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: A laboratory study was conducted to evaluate the influence of cocultivation of toxigenic Fusarium (F.) and Alternaria (A.) fungi with respect to growth and mycotoxin production. Fusarium culmorum Fc13, Fusarium graminearum Fg23 and two Alternaria tenuissima isolates (At18 and At220) were simultaneously or consecutively co-incubated on wheat kernels in an in vitro test system. Fungal biomass was quantified by determining ergosterol content. Three Fusarium toxins (DON, NIV and ZON) and three Alternaria toxins (AOH, AME and ALT) were analysed by a newly developed HPLC/MS/MS method. In simultaneous cocultures, the fungal biomass was enhanced up to 460% compared with individual cultures; Alternaria toxins were considerably depressed down to <5%. Combining At18 and At220 with Fg23 inhibited the toxin production of both fungal partners. In contrast, Fc13 increased its DON and ZON production in competitive interaction with both A. strains.\n Question: Does cocultivation of phytopathogenic Fusarium and Alternaria strains affect fungal growth and mycotoxin production?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: A laboratory study was conducted to evaluate the influence of cocultivation of toxigenic Fusarium (F.) and Alternaria (A.) fungi with respect to growth and mycotoxin production. Fusarium culmorum Fc13, Fusarium graminearum Fg23 and two Alternaria tenuissima isolates (At18 and At220) were simultaneously or consecutively co-incubated on wheat kernels in an in vitro test system. Fungal biomass was quantified by determining ergosterol content. Three Fusarium toxins (DON, NIV and ZON) and three Alternaria toxins (AOH, AME and ALT) were analysed by a newly developed HPLC/MS/MS method. In simultaneous cocultures, the fungal biomass was enhanced up to 460% compared with individual cultures; Alternaria toxins were considerably depressed down to <5%. Combining At18 and At220 with Fg23 inhibited the toxin production of both fungal partners. In contrast, Fc13 increased its DON and ZON production in competitive interaction with both A. strains.
Question: Does cocultivation of phytopathogenic Fusarium and Alternaria strains affect fungal growth and mycotoxin production?
Output:
|
PubmedQA136822
|
[
{
"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: Diabetic retinopathy (DR) is a leading cause of blindness in working age adults. Approximately 95% of patients with Type 1 diabetes develop some degree of retinopathy within 25 years of diagnosis despite normalization of blood glucose by insulin therapy. The goal of this study was to identify molecular changes in the rodent retina induced by diabetes that are not normalized by insulin replacement and restoration of euglycemia. The retina transcriptome (22,523 genes and transcript variants) was examined after three months of streptozotocin-induced diabetes in male Sprague Dawley rats with and without insulin replacement for the later one and a half months of diabetes. Selected gene expression changes were confirmed by qPCR, and also examined in independent control and diabetic rats at a one month time-point. Transcriptomic alterations in response to diabetes (1376 probes) were clustered according to insulin responsiveness. More than half (57%) of diabetes-induced mRNA changes (789 probes) observed at three months were fully normalized to control levels with insulin therapy, while 37% of probes (514) were only partially normalized. A small set of genes (5%, 65 probes) was significantly dysregulated in the insulin-treated diabetic rats. qPCR confirmation of findings and examination of a one month time point allowed genes to be further categorized as prevented or rescued with insulin therapy. A subset of genes (Ccr5, Jak3, Litaf) was confirmed at the level of protein expression, with protein levels recapitulating changes in mRNA expression.\n Question: Does chronic insulin treatment of diabetes fully normalize alterations in the retinal transcriptome?\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: Diabetic retinopathy (DR) is a leading cause of blindness in working age adults. Approximately 95% of patients with Type 1 diabetes develop some degree of retinopathy within 25 years of diagnosis despite normalization of blood glucose by insulin therapy. The goal of this study was to identify molecular changes in the rodent retina induced by diabetes that are not normalized by insulin replacement and restoration of euglycemia. The retina transcriptome (22,523 genes and transcript variants) was examined after three months of streptozotocin-induced diabetes in male Sprague Dawley rats with and without insulin replacement for the later one and a half months of diabetes. Selected gene expression changes were confirmed by qPCR, and also examined in independent control and diabetic rats at a one month time-point. Transcriptomic alterations in response to diabetes (1376 probes) were clustered according to insulin responsiveness. More than half (57%) of diabetes-induced mRNA changes (789 probes) observed at three months were fully normalized to control levels with insulin therapy, while 37% of probes (514) were only partially normalized. A small set of genes (5%, 65 probes) was significantly dysregulated in the insulin-treated diabetic rats. qPCR confirmation of findings and examination of a one month time point allowed genes to be further categorized as prevented or rescued with insulin therapy. A subset of genes (Ccr5, Jak3, Litaf) was confirmed at the level of protein expression, with protein levels recapitulating changes in mRNA expression.
Question: Does chronic insulin treatment of diabetes fully normalize alterations in the retinal transcriptome?
Output:
|
PubmedQA161744
|
[
{
"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 association between -336 A/G polymorphism of CD209 and susceptibility to/protection from tuberculosis is inconsistent. The present study aimed at evaluating the possible association between CD209 rs4804803 (-336 A/G) gene polymorphism and pulmonary tuberculosis (PTB) in a sample of Iranian population. This case-control study was performed on 156 PTB patients and 154 healthy individuals. Tetra-amplification refractory mutation system-polymerase chain reaction was used to detect the polymorphisms. Our findings revealed that the CD209 rs4804803 increased the risk of PTB in codominant [odds ratio (OR) = 5.16, 95% confidence interval (CI) = 1.60-16.59, p = 0.006, GG vs. AA], dominant (OR = 1.69, 95% CI = 1.07-2.66, p = 0.024, AG + GG vs. AA), and recessive (OR = 4.20, 95% CI = 1.34-13.16, p = 0.014, GG vs. AA + AG) tested inheritance models. Furthermore, the rs4804803 G allele increased the risk of PTB (OR = 1.58, 95% CI = 1.12-2.23, p = 0.011) as compared to the A allele.\n Question: Is cD209 promoter -336 A/G ( rs4804803 ) polymorphism associated with susceptibility to pulmonary tuberculosis in Zahedan , southeast Iran?\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 association between -336 A/G polymorphism of CD209 and susceptibility to/protection from tuberculosis is inconsistent. The present study aimed at evaluating the possible association between CD209 rs4804803 (-336 A/G) gene polymorphism and pulmonary tuberculosis (PTB) in a sample of Iranian population. This case-control study was performed on 156 PTB patients and 154 healthy individuals. Tetra-amplification refractory mutation system-polymerase chain reaction was used to detect the polymorphisms. Our findings revealed that the CD209 rs4804803 increased the risk of PTB in codominant [odds ratio (OR) = 5.16, 95% confidence interval (CI) = 1.60-16.59, p = 0.006, GG vs. AA], dominant (OR = 1.69, 95% CI = 1.07-2.66, p = 0.024, AG + GG vs. AA), and recessive (OR = 4.20, 95% CI = 1.34-13.16, p = 0.014, GG vs. AA + AG) tested inheritance models. Furthermore, the rs4804803 G allele increased the risk of PTB (OR = 1.58, 95% CI = 1.12-2.23, p = 0.011) as compared to the A allele.
Question: Is cD209 promoter -336 A/G ( rs4804803 ) polymorphism associated with susceptibility to pulmonary tuberculosis in Zahedan , southeast Iran?
Output:
|
PubmedQA151307
|
[
{
"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 diverse microbial populations that inhabit pristine aquifers are known to catalyze critical in situ biogeochemical reactions, yet little is known about how the structure and diversity of this subsurface community correlates with and impacts upon groundwater chemistry. Herein we examine 8,786 bacterial and 8,166 archaeal 16S rRNA gene sequences from an array of monitoring wells in the Mahomet aquifer of east-central Illinois. Using multivariate statistical analyses we provide a comparative analysis of the relationship between groundwater chemistry and the microbial communities attached to aquifer sediment along with those suspended in groundwater. Statistical analyses of 16S rRNA gene sequences showed a clear distinction between attached and suspended communities; with iron-reducing bacteria far more abundant in attached samples than suspended, while archaeal clones related to groups associated with anaerobic methane oxidation and deep subsurface gold mines (ANME-2D and SAGMEG-1, respectively) distinguished the suspended community from the attached. Within the attached bacterial community, cloned sequences most closely related to the sulfate-reducing Desulfobacter and Desulfobulbus genera represented 20% of the bacterial community in wells where the concentration of sulfate in groundwater was high (> 0.2 mM), compared to only 3% in wells with less sulfate. Sequences related to the genus Geobacter, a genus containing ferric-iron reducers, were of nearly equal abundance (15%) to the sulfate reducers under high sulfate conditions, however their relative abundance increased to 34% when sulfate concentrations were < 0.03 mM. Also, in areas where sulfate concentrations were <0.03 mM, archaeal 16S rRNA gene sequences similar to those found in methanogens such as Methanosarcina and Methanosaeta comprised 73-80% of the community, and dissolved CH4 ranged between 220 and 1240 μM in these groundwaters. In contrast, methanogens (and their product, CH4) were nearly absent in samples collected from groundwater samples with > 0.2 mM sulfate. In the suspended fraction of wells where the concentration of sulfate was between 0.03 and 0.2 mM, the archaeal community was dominated by sequences most closely related to the ANME-2D, a group of archaea known for anaerobically oxidizing methane. Based on available energy (∆GA) estimations, results varied little for both sulfate reduction and methanogenesis throughout all wells studied, but could favor anaerobic oxidation of methane (AOM) in wells containing minimal sulfate and dihydrogen, suggesting AOM coupled with H2-oxidizing organisms such as sulfate or iron reducers could be an important pathway occurring in the Mahomet aquifer.\n Question: Does functional microbial diversity explain groundwater chemistry in a pristine aquifer?\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 diverse microbial populations that inhabit pristine aquifers are known to catalyze critical in situ biogeochemical reactions, yet little is known about how the structure and diversity of this subsurface community correlates with and impacts upon groundwater chemistry. Herein we examine 8,786 bacterial and 8,166 archaeal 16S rRNA gene sequences from an array of monitoring wells in the Mahomet aquifer of east-central Illinois. Using multivariate statistical analyses we provide a comparative analysis of the relationship between groundwater chemistry and the microbial communities attached to aquifer sediment along with those suspended in groundwater. Statistical analyses of 16S rRNA gene sequences showed a clear distinction between attached and suspended communities; with iron-reducing bacteria far more abundant in attached samples than suspended, while archaeal clones related to groups associated with anaerobic methane oxidation and deep subsurface gold mines (ANME-2D and SAGMEG-1, respectively) distinguished the suspended community from the attached. Within the attached bacterial community, cloned sequences most closely related to the sulfate-reducing Desulfobacter and Desulfobulbus genera represented 20% of the bacterial community in wells where the concentration of sulfate in groundwater was high (> 0.2 mM), compared to only 3% in wells with less sulfate. Sequences related to the genus Geobacter, a genus containing ferric-iron reducers, were of nearly equal abundance (15%) to the sulfate reducers under high sulfate conditions, however their relative abundance increased to 34% when sulfate concentrations were < 0.03 mM. Also, in areas where sulfate concentrations were <0.03 mM, archaeal 16S rRNA gene sequences similar to those found in methanogens such as Methanosarcina and Methanosaeta comprised 73-80% of the community, and dissolved CH4 ranged between 220 and 1240 μM in these groundwaters. In contrast, methanogens (and their product, CH4) were nearly absent in samples collected from groundwater samples with > 0.2 mM sulfate. In the suspended fraction of wells where the concentration of sulfate was between 0.03 and 0.2 mM, the archaeal community was dominated by sequences most closely related to the ANME-2D, a group of archaea known for anaerobically oxidizing methane. Based on available energy (∆GA) estimations, results varied little for both sulfate reduction and methanogenesis throughout all wells studied, but could favor anaerobic oxidation of methane (AOM) in wells containing minimal sulfate and dihydrogen, suggesting AOM coupled with H2-oxidizing organisms such as sulfate or iron reducers could be an important pathway occurring in the Mahomet aquifer.
Question: Does functional microbial diversity explain groundwater chemistry in a pristine aquifer?
Output:
|
PubmedQA67123
|
[
{
"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: Hepatic stellate cells (HSC) play a major role in the progression of liver fibrosis. The aim of our study was to investigate whether rat HSC cultured on a nanofiber membrane (NM) retain their quiescent phenotype during both short- and long-term culture and whether activated HSC revert to a quiescent form when re-cultured on NM. Rat HSC cultured for 1 day on plastic plates (PP) were used as quiescent HSC, while cells cultured for 1 week on PP were considered to be activated HSC. Quiescent or activated HSC were subsequently plated on PP or NM and cultured for an additional 4 days at which time their gene expression, stress fiber development, and growth factor production were determined. For long-term culture, HSC were grown on NM for 20 days and the cells then replated on PP and cultured for another 10 days. Expression of marker genes for HSC activation, stress fiber development, and growth factor production were significantly lower in both quiescent and activated HSC cultured on NM than in those cultured on PP. After long-term culture on NM, activation marker gene expression and stress fiber development were still significantly lower in HSC than in PP, and HSC still retained the ability to activate when replated onto PP.\n Question: Does a nanofiber membrane maintain the quiescent phenotype of hepatic stellate cells?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Hepatic stellate cells (HSC) play a major role in the progression of liver fibrosis. The aim of our study was to investigate whether rat HSC cultured on a nanofiber membrane (NM) retain their quiescent phenotype during both short- and long-term culture and whether activated HSC revert to a quiescent form when re-cultured on NM. Rat HSC cultured for 1 day on plastic plates (PP) were used as quiescent HSC, while cells cultured for 1 week on PP were considered to be activated HSC. Quiescent or activated HSC were subsequently plated on PP or NM and cultured for an additional 4 days at which time their gene expression, stress fiber development, and growth factor production were determined. For long-term culture, HSC were grown on NM for 20 days and the cells then replated on PP and cultured for another 10 days. Expression of marker genes for HSC activation, stress fiber development, and growth factor production were significantly lower in both quiescent and activated HSC cultured on NM than in those cultured on PP. After long-term culture on NM, activation marker gene expression and stress fiber development were still significantly lower in HSC than in PP, and HSC still retained the ability to activate when replated onto PP.
Question: Does a nanofiber membrane maintain the quiescent phenotype of hepatic stellate cells?
Output:
|
PubmedQA31846
|
[
{
"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 xanthine oxidase system produces reactive oxidative species and its inhibition by allopurinol has been shown to have beneficial effects on cardiovascular function. Oxidative stress has also been implicated in the development of sarcopenia. Allopurinol, a xanthine oxidase inhibitor, both reduces oxidative stress and acts as a potential oxygen-sparing agent. We examined the association between allopurinol use and functional outcomes after rehabilitation in a cohort of older people. analysis of routinely collected clinical data from a single rehabilitation unit. Data were prospectively collected on all admissions to the Dundee Medicine for the Elderly rehabilitation unit between 1 January 1999 and 31 December 2008. Multivariate analyses were performed to examine the difference between the 20-point Barthel score on admission and discharge, adjusting for age, sex, admission Barthel score, anti-platelet use and comorbid disease. a total of 3,593 patients were included in the analysis and 3% of patients were taking allopurinol on discharge (n = 102). Improvement in Barthel scores was greater in the allopurinol group than the non-allopurinol group (4.7 versus 3.6 points, mean difference 1.1, 95% CI: 0.4-1.8, P = 0.002). When adjusted for age, sex, admission Barthel, presenting disease and number of drugs on discharge, improvement in the Barthel score was still greater in the allopurinol group (4.8 versus 3.8 points, mean difference 0.94, 95% CI: 0.3 to 1.6, P = 0.006).\n Question: Is allopurinol use associated with greater functional gains in older rehabilitation 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: the xanthine oxidase system produces reactive oxidative species and its inhibition by allopurinol has been shown to have beneficial effects on cardiovascular function. Oxidative stress has also been implicated in the development of sarcopenia. Allopurinol, a xanthine oxidase inhibitor, both reduces oxidative stress and acts as a potential oxygen-sparing agent. We examined the association between allopurinol use and functional outcomes after rehabilitation in a cohort of older people. analysis of routinely collected clinical data from a single rehabilitation unit. Data were prospectively collected on all admissions to the Dundee Medicine for the Elderly rehabilitation unit between 1 January 1999 and 31 December 2008. Multivariate analyses were performed to examine the difference between the 20-point Barthel score on admission and discharge, adjusting for age, sex, admission Barthel score, anti-platelet use and comorbid disease. a total of 3,593 patients were included in the analysis and 3% of patients were taking allopurinol on discharge (n = 102). Improvement in Barthel scores was greater in the allopurinol group than the non-allopurinol group (4.7 versus 3.6 points, mean difference 1.1, 95% CI: 0.4-1.8, P = 0.002). When adjusted for age, sex, admission Barthel, presenting disease and number of drugs on discharge, improvement in the Barthel score was still greater in the allopurinol group (4.8 versus 3.8 points, mean difference 0.94, 95% CI: 0.3 to 1.6, P = 0.006).
Question: Is allopurinol use associated with greater functional gains in older rehabilitation patients?
Output:
|
PubmedQA17262
|
[
{
"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: Infection with the Epstein-Barr virus (EBV) is associated with an increased risk of multiple sclerosis (MS). We sought genetic loci influencing EBV nuclear antigen-1 (EBNA-1) IgG titers and hypothesized that they may play a role in MS risk. We performed a genome-wide association study (GWAS) of anti-EBNA-1 IgG titers in 3599 individuals from an unselected twin family cohort, followed by a meta-analysis with data from an independent EBNA-1 GWAS. We then examined the shared polygenic risk between the EBNA-1 GWAS (effective sample size (N We identified one locus of strong association within the human leukocyte antigen (HLA) region, of which the most significantly associated genotyped single nucleotide polymorphism (SNP) was rs2516049 (p = 4.11 × 10\n Question: Are genetic loci for Epstein-Barr virus nuclear antigen-1 associated with risk of multiple sclerosis?\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: Infection with the Epstein-Barr virus (EBV) is associated with an increased risk of multiple sclerosis (MS). We sought genetic loci influencing EBV nuclear antigen-1 (EBNA-1) IgG titers and hypothesized that they may play a role in MS risk. We performed a genome-wide association study (GWAS) of anti-EBNA-1 IgG titers in 3599 individuals from an unselected twin family cohort, followed by a meta-analysis with data from an independent EBNA-1 GWAS. We then examined the shared polygenic risk between the EBNA-1 GWAS (effective sample size (N We identified one locus of strong association within the human leukocyte antigen (HLA) region, of which the most significantly associated genotyped single nucleotide polymorphism (SNP) was rs2516049 (p = 4.11 × 10
Question: Are genetic loci for Epstein-Barr virus nuclear antigen-1 associated with risk of multiple sclerosis?
Output:
|
PubmedQA198353
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Although calcitriol (1,25(OH)2D) is considered the biologically active vitamin D metabolite, several studies have shown that calcidiol (25OHD) is the vitamin D metabolite that is most closely linked to parathyroid function and indices of calcium homeostasis. Moreover, low levels of 25OHD have been associated with increased risk of different diseases including cancer, diabetes, and myopathy. Cross-sectional study. We studied relations between plasma concentrations of 25OHD, 1,25(OH)2D, and parathyroid hormone (PTH) in fasting plasma samples from 315 healthy postmenopausal women randomly selected from the local background population. P-1,25(OH)2D levels varied in a concentration-dependent manner with P-25OHD levels (P<0.001). Thus, P-1,25(OH)2D levels were the lowest in women with vitamin D insufficiency, i.e., P-1,25(OH)2D levels were reduced by approximately one-third in subjects with P-25OHD levels below 25 nmol/l compared with levels above 80 nmol/l (P<0.01). The association was most pronounced at P-25OHD concentrations below 80 nmol/l, whereas no major increase in P-1,25(OH)2D was observed at P-25OHD concentrations above 80 nmol/l. In multiple regression analysis, PTH was a minor although significant predictor of P-1,25(OH)2D levels.\n Question: Do plasma 1,25 ( OH ) 2D levels decrease in postmenopausal women with hypovitaminosis D?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Although calcitriol (1,25(OH)2D) is considered the biologically active vitamin D metabolite, several studies have shown that calcidiol (25OHD) is the vitamin D metabolite that is most closely linked to parathyroid function and indices of calcium homeostasis. Moreover, low levels of 25OHD have been associated with increased risk of different diseases including cancer, diabetes, and myopathy. Cross-sectional study. We studied relations between plasma concentrations of 25OHD, 1,25(OH)2D, and parathyroid hormone (PTH) in fasting plasma samples from 315 healthy postmenopausal women randomly selected from the local background population. P-1,25(OH)2D levels varied in a concentration-dependent manner with P-25OHD levels (P<0.001). Thus, P-1,25(OH)2D levels were the lowest in women with vitamin D insufficiency, i.e., P-1,25(OH)2D levels were reduced by approximately one-third in subjects with P-25OHD levels below 25 nmol/l compared with levels above 80 nmol/l (P<0.01). The association was most pronounced at P-25OHD concentrations below 80 nmol/l, whereas no major increase in P-1,25(OH)2D was observed at P-25OHD concentrations above 80 nmol/l. In multiple regression analysis, PTH was a minor although significant predictor of P-1,25(OH)2D levels.
Question: Do plasma 1,25 ( OH ) 2D levels decrease in postmenopausal women with hypovitaminosis D?
Output:
|
PubmedQA21052
|
[
{
"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 prospective association between parental pre-pregnancy BMI and adult male and female offspring BMI and waist circumference (WC). Sub-sample of 2,229 parent-offspring pairs with parental pre-pregnancy BMI and offspring BMI and WC at 21 years were used from the MUSP (Mater-University of Queensland Study of Pregnancy cohort). Multivariable results were adjusted for maternal factors around pregnancy (e.g. gestational weight and smoking during pregnancy) and offspring factors in early life (e.g. birth weight) and at 14 years (e.g. sports participation and mealtime with family). After adjustments for confounders, each unit increase in paternal and maternal BMI, the BMI of young adult offspring increased by 0.33kg/m\n Question: Does parental pre-pregnancy BMI influence on offspring BMI and waist circumference at 21 years?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To investigate the prospective association between parental pre-pregnancy BMI and adult male and female offspring BMI and waist circumference (WC). Sub-sample of 2,229 parent-offspring pairs with parental pre-pregnancy BMI and offspring BMI and WC at 21 years were used from the MUSP (Mater-University of Queensland Study of Pregnancy cohort). Multivariable results were adjusted for maternal factors around pregnancy (e.g. gestational weight and smoking during pregnancy) and offspring factors in early life (e.g. birth weight) and at 14 years (e.g. sports participation and mealtime with family). After adjustments for confounders, each unit increase in paternal and maternal BMI, the BMI of young adult offspring increased by 0.33kg/m
Question: Does parental pre-pregnancy BMI influence on offspring BMI and waist circumference at 21 years?
Output:
|
PubmedQA13315
|
[
{
"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: Approximately one-third of the Drosophila kinome has been ascribed some cell-cycle function. However, little is known about which of its 117 protein phosphatases (PPs) or subunits have counteracting roles. We investigated mitotic roles of PPs through systematic RNAi. We found that G(2)-M progression requires Puckered, the JNK MAP-kinase inhibitory phosphatase and PP2C in addition to string (Cdc25). Strong mitotic arrest and chromosome congression failure occurred after Pp1-87B downregulation. Chromosome alignment and segregation defects also occurred after knockdown of PP1-Flapwing, not previously thought to have a mitotic role. Reduction of several nonreceptor tyrosine phosphatases produced spindle and chromosome behavior defects, and for corkscrew, premature chromatid separation. RNAi of the dual-specificity phosphatase, Myotubularin, or the related Sbf \"antiphosphatase\" resulted in aberrant mitotic chromosome behavior. Finally, for PP2A, knockdown of the catalytic or A subunits led to bipolar monoastral spindles, knockdown of the Twins B subunit led to bridged and lagging chromosomes, and knockdown of the B' Widerborst subunit led to scattering of all mitotic chromosomes. Widerborst was associated with MEI-S332 (Shugoshin) and required for its kinetochore localization.\n Question: Are multiple protein phosphatases required for mitosis in Drosophila?\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: Approximately one-third of the Drosophila kinome has been ascribed some cell-cycle function. However, little is known about which of its 117 protein phosphatases (PPs) or subunits have counteracting roles. We investigated mitotic roles of PPs through systematic RNAi. We found that G(2)-M progression requires Puckered, the JNK MAP-kinase inhibitory phosphatase and PP2C in addition to string (Cdc25). Strong mitotic arrest and chromosome congression failure occurred after Pp1-87B downregulation. Chromosome alignment and segregation defects also occurred after knockdown of PP1-Flapwing, not previously thought to have a mitotic role. Reduction of several nonreceptor tyrosine phosphatases produced spindle and chromosome behavior defects, and for corkscrew, premature chromatid separation. RNAi of the dual-specificity phosphatase, Myotubularin, or the related Sbf "antiphosphatase" resulted in aberrant mitotic chromosome behavior. Finally, for PP2A, knockdown of the catalytic or A subunits led to bipolar monoastral spindles, knockdown of the Twins B subunit led to bridged and lagging chromosomes, and knockdown of the B' Widerborst subunit led to scattering of all mitotic chromosomes. Widerborst was associated with MEI-S332 (Shugoshin) and required for its kinetochore localization.
Question: Are multiple protein phosphatases required for mitosis in Drosophila?
Output:
|
PubmedQA64319
|
[
{
"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: Central obesity, based on waist circumference (WC), has more adverse effects on health than general obesity, determined by body mass index. To date, eating quickly has been reported to be risk factors for overweight/obesity among children, adolescents, and adults. In contrast, there are few studies on the relationship between fast eating and central obesity among adolescents, particularly in Japan, where WC is not commonly measured in junior high schools. The aim of the present study was to investigate the relationship between eating quickly and waist-to-height ratio (WHtR), an index of central obesity, among adolescents in Japan. Study subjects were 2136 seventh-grade school children (12 or 13 years of age) from Ina town junior high schools in Japan, between 2004 and 2009. Measurements of height, weight, and WC were performed, and information about eating habits was collected using a self-administered questionnaire. A logistic regression model was used to calculate the odds ratio (OR) and 95 % confidence interval (95 % CI) for WHtR ≥ 0.5. Eating quickly significantly increased the OR for WHtR ≥ 0.5 in boys (OR: 2.05, 95 % CI: 1.31-3.23) and girls (2.09, 1.15-3.81). When compared with the \"not eating quickly and not eating until full\" group, the OR for WHtR ≥ 0.5 in the \"eating quickly and eating until full\" group was 2.67 (95 % CI: 1.50-4.73) in boys and 2.59 (1.17-5.73) in girls, whereas that in the \"eating quickly and not eating until full\" group or the \"not eating quickly and eating until full\" group was not statistically significant regardless of sex.\n Question: Is eating quickly associated with waist-to-height ratio among Japanese adolescents : a cross-sectional survey?\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: Central obesity, based on waist circumference (WC), has more adverse effects on health than general obesity, determined by body mass index. To date, eating quickly has been reported to be risk factors for overweight/obesity among children, adolescents, and adults. In contrast, there are few studies on the relationship between fast eating and central obesity among adolescents, particularly in Japan, where WC is not commonly measured in junior high schools. The aim of the present study was to investigate the relationship between eating quickly and waist-to-height ratio (WHtR), an index of central obesity, among adolescents in Japan. Study subjects were 2136 seventh-grade school children (12 or 13 years of age) from Ina town junior high schools in Japan, between 2004 and 2009. Measurements of height, weight, and WC were performed, and information about eating habits was collected using a self-administered questionnaire. A logistic regression model was used to calculate the odds ratio (OR) and 95 % confidence interval (95 % CI) for WHtR ≥ 0.5. Eating quickly significantly increased the OR for WHtR ≥ 0.5 in boys (OR: 2.05, 95 % CI: 1.31-3.23) and girls (2.09, 1.15-3.81). When compared with the "not eating quickly and not eating until full" group, the OR for WHtR ≥ 0.5 in the "eating quickly and eating until full" group was 2.67 (95 % CI: 1.50-4.73) in boys and 2.59 (1.17-5.73) in girls, whereas that in the "eating quickly and not eating until full" group or the "not eating quickly and eating until full" group was not statistically significant regardless of sex.
Question: Is eating quickly associated with waist-to-height ratio among Japanese adolescents : a cross-sectional survey?
Output:
|
PubmedQA116440
|
[
{
"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: Pluripotent embryonic stem cells (ESCs) have the unique ability to differentiate into every cell type and to self-renew. These characteristics correlate with a distinct nuclear architecture, epigenetic signatures enriched for active chromatin marks and hyperdynamic binding of structural chromatin proteins. Recently, several chromatin-related proteins have been shown to regulate ESC pluripotency and/or differentiation, yet the role of the major heterochromatin proteins in pluripotency is unknown. Here we identify Heterochromatin Protein 1β (HP1β) as an essential protein for proper differentiation, and, unexpectedly, for the maintenance of pluripotency in ESCs. In pluripotent and differentiated cells HP1β is differentially localized and differentially associated with chromatin. Deletion of HP1β, but not HP1α, in ESCs provokes a loss of the morphological and proliferative characteristics of embryonic pluripotent cells, reduces expression of pluripotency factors and causes aberrant differentiation. However, in differentiated cells, loss of HP1β has the opposite effect, perturbing maintenance of the differentiation state and facilitating reprogramming to an induced pluripotent state. Microscopy, biochemical fractionation and chromatin immunoprecipitation reveal a diffuse nucleoplasmic distribution, weak association with chromatin and high expression levels for HP1β in ESCs. The minor fraction of HP1β that is chromatin-bound in ESCs is enriched within exons, unlike the situation in differentiated cells, where it binds heterochromatic satellite repeats and chromocenters.\n Question: Does heterochromatin Protein 1β ( HP1β ) have distinct functions and distinct nuclear distribution in pluripotent versus differentiated cells?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Pluripotent embryonic stem cells (ESCs) have the unique ability to differentiate into every cell type and to self-renew. These characteristics correlate with a distinct nuclear architecture, epigenetic signatures enriched for active chromatin marks and hyperdynamic binding of structural chromatin proteins. Recently, several chromatin-related proteins have been shown to regulate ESC pluripotency and/or differentiation, yet the role of the major heterochromatin proteins in pluripotency is unknown. Here we identify Heterochromatin Protein 1β (HP1β) as an essential protein for proper differentiation, and, unexpectedly, for the maintenance of pluripotency in ESCs. In pluripotent and differentiated cells HP1β is differentially localized and differentially associated with chromatin. Deletion of HP1β, but not HP1α, in ESCs provokes a loss of the morphological and proliferative characteristics of embryonic pluripotent cells, reduces expression of pluripotency factors and causes aberrant differentiation. However, in differentiated cells, loss of HP1β has the opposite effect, perturbing maintenance of the differentiation state and facilitating reprogramming to an induced pluripotent state. Microscopy, biochemical fractionation and chromatin immunoprecipitation reveal a diffuse nucleoplasmic distribution, weak association with chromatin and high expression levels for HP1β in ESCs. The minor fraction of HP1β that is chromatin-bound in ESCs is enriched within exons, unlike the situation in differentiated cells, where it binds heterochromatic satellite repeats and chromocenters.
Question: Does heterochromatin Protein 1β ( HP1β ) have distinct functions and distinct nuclear distribution in pluripotent versus differentiated cells?
Output:
|
PubmedQA125638
|
[
{
"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 mandatory 5-day of shelf-life platelet concentrates (PCs) creates outdating and inventory control problems in blood banking. Moreover, storage of PCs at 22-24 degrees C has been associated with a time-dependent accumulation of pyrogenic cytokines, potentially harmful for recipients. Previous studies have shown that supplementation of PCs with ThromboSol, a mixture of second-messengers effectors, might allow storage of functionally active platelets at refrigerated temperature to be extended. This study further investigates this storage approach by comparing the accumulation of bioactive compounds in standard and refrigerated PCs. The PCs were supplemented with ThromboSol or a control solution and stored in parallel at 24 degrees C with continuous agitation or undisturbed at 4 degrees C. Samples were removed on days 1, 5, 9 of storage, and assayed for their content of interleukin (IL)-6, IL-8, tumour necrosis factor (TNF)-alpha, transforming growth factor (TGF)-beta1, and anaphylatoxins C3a and C4a. Throughout storage, refrigerated PCs, both ThromboSol-treated and untreated units, displayed a slightly lower level of IL-6 and significantly lower concentration of IL-8 than conventionally stored PCs. ThromboSol slightly reduced the level of these cytokines in PCs. Throughout storage at 22 degrees C, an accumulation of anaphylatoxins C3a and C4a was seen both in both control and ThromboSol-treated PCs. This accumulation was significantly reduced in control PCs stored at 4 degrees C, but not in refrigerated PCs supplemented with ThromboSol. Cold-storage, with or without ThromboSol, had a minor effect on the accumulation of TGF-beta1 in PCs.\n Question: Does effect of cold-storage in the accumulation of bioreactive substances in platelet concentrate treated with second messenger effects?\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 mandatory 5-day of shelf-life platelet concentrates (PCs) creates outdating and inventory control problems in blood banking. Moreover, storage of PCs at 22-24 degrees C has been associated with a time-dependent accumulation of pyrogenic cytokines, potentially harmful for recipients. Previous studies have shown that supplementation of PCs with ThromboSol, a mixture of second-messengers effectors, might allow storage of functionally active platelets at refrigerated temperature to be extended. This study further investigates this storage approach by comparing the accumulation of bioactive compounds in standard and refrigerated PCs. The PCs were supplemented with ThromboSol or a control solution and stored in parallel at 24 degrees C with continuous agitation or undisturbed at 4 degrees C. Samples were removed on days 1, 5, 9 of storage, and assayed for their content of interleukin (IL)-6, IL-8, tumour necrosis factor (TNF)-alpha, transforming growth factor (TGF)-beta1, and anaphylatoxins C3a and C4a. Throughout storage, refrigerated PCs, both ThromboSol-treated and untreated units, displayed a slightly lower level of IL-6 and significantly lower concentration of IL-8 than conventionally stored PCs. ThromboSol slightly reduced the level of these cytokines in PCs. Throughout storage at 22 degrees C, an accumulation of anaphylatoxins C3a and C4a was seen both in both control and ThromboSol-treated PCs. This accumulation was significantly reduced in control PCs stored at 4 degrees C, but not in refrigerated PCs supplemented with ThromboSol. Cold-storage, with or without ThromboSol, had a minor effect on the accumulation of TGF-beta1 in PCs.
Question: Does effect of cold-storage in the accumulation of bioreactive substances in platelet concentrate treated with second messenger effects?
Output:
|
PubmedQA38825
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To examine the prognostic value of lymphovascular invasion (LVI) in different tumor locations (i.e., renal pelvis and ureter) of upper urinary tract urothelial carcinoma (UTUC). Data from a total of 250 patients with nonmetastatic UTUC who received radical nephroureterectomy between 2004 and 2010 at our institution were analyzed retrospectively. The significance of LVI and other relevant factors on cancer-specific survival (CSS), metastasis-free survival (MFS), and intraluminal recurrence-free survival (IRFS) were evaluated. Lymphovascular invasion was present in 60 patients (24 %) and was related to advanced pathological T stage (P < 0.001), higher tumor grade (P < 0.001), lymph node metastasis (P = 0.005), and pyelocaliceal tumor location (P = 0.002). By Kaplan-Meier analysis, LVI was found to be significantly correlated with worse CSS and MFS but not with IRFS. Multivariate analysis showed that high pathological T stage and regional lymph node involvement were significant prognostic factors for CSS and MFS, and LVI was an independent predictor for MFS (hazard ratio 1.71, 95 % confidence interval 1.00-2.93, P = 0.049). In patients with ureteral tumors, LVI represented the only significant prognosticator for both CSS and MFS in multivariate analysis. The prognostic value of LVI was not observed in pyelocaliceal tumors.\n Question: Is prognostic significance of lymphovascular invasion in upper urinary tract urothelial carcinoma influenced by tumor location?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To examine the prognostic value of lymphovascular invasion (LVI) in different tumor locations (i.e., renal pelvis and ureter) of upper urinary tract urothelial carcinoma (UTUC). Data from a total of 250 patients with nonmetastatic UTUC who received radical nephroureterectomy between 2004 and 2010 at our institution were analyzed retrospectively. The significance of LVI and other relevant factors on cancer-specific survival (CSS), metastasis-free survival (MFS), and intraluminal recurrence-free survival (IRFS) were evaluated. Lymphovascular invasion was present in 60 patients (24 %) and was related to advanced pathological T stage (P < 0.001), higher tumor grade (P < 0.001), lymph node metastasis (P = 0.005), and pyelocaliceal tumor location (P = 0.002). By Kaplan-Meier analysis, LVI was found to be significantly correlated with worse CSS and MFS but not with IRFS. Multivariate analysis showed that high pathological T stage and regional lymph node involvement were significant prognostic factors for CSS and MFS, and LVI was an independent predictor for MFS (hazard ratio 1.71, 95 % confidence interval 1.00-2.93, P = 0.049). In patients with ureteral tumors, LVI represented the only significant prognosticator for both CSS and MFS in multivariate analysis. The prognostic value of LVI was not observed in pyelocaliceal tumors.
Question: Is prognostic significance of lymphovascular invasion in upper urinary tract urothelial carcinoma influenced by tumor location?
Output:
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PubmedQA196788
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To investigate the effect of transforming growth factor-β1 (TGF-β1) on the differentiation of bone marrow-derived mesenchymal stem cells (MSCs) into cancer-associated fibroblasts(CAFs). MSCs were cultured in α-MEM with recombinant human TGF-β1 or in tumor-conditioned medium.The expression of CAFs markers were detected by immunofluorescence and quantitative RT-PCR. The qRT-PCR assay showed that the expression of CAFs markers FAP, ACTA, CAV, CCL5, CXCR4, FSP1, SDF-1 and vimentin were 9.92±2.16, 7.76±1.28, 3.04±0.95, 3.28±2.16, 2.13±0.71, 1.41±0.66, 2.25±0.86 and 1.38±0.56, respectively, significantly upregulated in the MSCs co-cultured with TGF-β1 or TCM. The relative levels of FAP, ACTA, CAV, CCL5, CXCR4, FSP1, SDF-1 and vimentin mRNA in the TCM group were 7.52±1.76, 5.02±1.18, 1.98±1.19, 1.82±1.19, 2.95±0.86, 1.44±0.67, 2.08±0.74 and 1.47±0.55, respectively, indicating that MSCs can express CAFs phenotype.TGF beta signaling pathway inhibitor SB-431542 could inhibit the differentiation. Both immunofluorescence and Western blot confirmed the above results.\n Question: Does [ Transforming growth factor-β1 induce bone marrow-derived mesenchymal stem cells to differentiate into cancer-associated fibroblasts ]?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To investigate the effect of transforming growth factor-β1 (TGF-β1) on the differentiation of bone marrow-derived mesenchymal stem cells (MSCs) into cancer-associated fibroblasts(CAFs). MSCs were cultured in α-MEM with recombinant human TGF-β1 or in tumor-conditioned medium.The expression of CAFs markers were detected by immunofluorescence and quantitative RT-PCR. The qRT-PCR assay showed that the expression of CAFs markers FAP, ACTA, CAV, CCL5, CXCR4, FSP1, SDF-1 and vimentin were 9.92±2.16, 7.76±1.28, 3.04±0.95, 3.28±2.16, 2.13±0.71, 1.41±0.66, 2.25±0.86 and 1.38±0.56, respectively, significantly upregulated in the MSCs co-cultured with TGF-β1 or TCM. The relative levels of FAP, ACTA, CAV, CCL5, CXCR4, FSP1, SDF-1 and vimentin mRNA in the TCM group were 7.52±1.76, 5.02±1.18, 1.98±1.19, 1.82±1.19, 2.95±0.86, 1.44±0.67, 2.08±0.74 and 1.47±0.55, respectively, indicating that MSCs can express CAFs phenotype.TGF beta signaling pathway inhibitor SB-431542 could inhibit the differentiation. Both immunofluorescence and Western blot confirmed the above results.
Question: Does [ Transforming growth factor-β1 induce bone marrow-derived mesenchymal stem cells to differentiate into cancer-associated fibroblasts ]?
Output:
|
PubmedQA119056
|
[
{
"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 obstructive pulmonary disease (COPD) exacerbations are associated with virus (mostly rhinovirus) and bacterial infections, but it is not known whether rhinovirus infections precipitate secondary bacterial infections. To investigate relationships between rhinovirus infection and bacterial infection and the role of antimicrobial peptides in COPD exacerbations. We infected subjects with moderate COPD and smokers and nonsmokers with normal lung function with rhinovirus. Induced sputum was collected before and repeatedly after rhinovirus infection and virus and bacterial loads measured with quantitative polymerase chain reaction and culture. The antimicrobial peptides secretory leukoprotease inhibitor (SLPI), elafin, pentraxin, LL-37, α-defensins and β-defensin-2, and the protease neutrophil elastase were measured in sputum supernatants. After rhinovirus infection, secondary bacterial infection was detected in 60% of subjects with COPD, 9.5% of smokers, and 10% of nonsmokers (P < 0.001). Sputum virus load peaked on Days 5-9 and bacterial load on Day 15. Sputum neutrophil elastase was significantly increased and SLPI and elafin significantly reduced after rhinovirus infection exclusively in subjects with COPD with secondary bacterial infections, and SLPI and elafin levels correlated inversely with bacterial load.\n Question: Does rhinovirus infection induce degradation of antimicrobial peptides and secondary bacterial infection in chronic obstructive pulmonary 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 obstructive pulmonary disease (COPD) exacerbations are associated with virus (mostly rhinovirus) and bacterial infections, but it is not known whether rhinovirus infections precipitate secondary bacterial infections. To investigate relationships between rhinovirus infection and bacterial infection and the role of antimicrobial peptides in COPD exacerbations. We infected subjects with moderate COPD and smokers and nonsmokers with normal lung function with rhinovirus. Induced sputum was collected before and repeatedly after rhinovirus infection and virus and bacterial loads measured with quantitative polymerase chain reaction and culture. The antimicrobial peptides secretory leukoprotease inhibitor (SLPI), elafin, pentraxin, LL-37, α-defensins and β-defensin-2, and the protease neutrophil elastase were measured in sputum supernatants. After rhinovirus infection, secondary bacterial infection was detected in 60% of subjects with COPD, 9.5% of smokers, and 10% of nonsmokers (P < 0.001). Sputum virus load peaked on Days 5-9 and bacterial load on Day 15. Sputum neutrophil elastase was significantly increased and SLPI and elafin significantly reduced after rhinovirus infection exclusively in subjects with COPD with secondary bacterial infections, and SLPI and elafin levels correlated inversely with bacterial load.
Question: Does rhinovirus infection induce degradation of antimicrobial peptides and secondary bacterial infection in chronic obstructive pulmonary disease?
Output:
|
PubmedQA2121
|
[
{
"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: Human cytomegalovirus (HCMV) can cause congenital infection with risk of neurological disability. Maternal-fetal transmission is associated with placental inflammation. 5-lipoxygenase (5-LO) is the key enzyme in the biosynthesis of Leukotrienes (LTs), which are proinflammatory mediators. This study investigated the effect of HCMV infection on 5-LO expression and Leukotriene-B4 (LTB4) induction in human placentae and umbilical vein endothelial cells (HUVEC). Seven placentae from fetuses with congenital HCMV infection and brain damage and six controls were stained with HCMV-immediate-early-antigen (HCMV-IEA) and 5-LO by immunohistochemistry. 5-hydroxyeicosatetraenoic acid (5-HETE) and LTB4 were measured in culture supernatant from ex vivo HCMV-infected placental histocultures by liquid chromatography. In vitro, HCMV infected HUVEC cells were analyzed for 5-LO mRNA and protein expression by real time PCR and immunofluorescence staining. HCMV-IEA was abundant in all HCMV infected placentae but absent in control placentae. 5-LO expression was higher in endothelial and smooth muscle cells of HCMV-infected placentae, compared to control placentae. HCMV infection induced an up-regulation of LTB4 in ex vivo placental explants with higher levels of LTB4 at 72 h compared to controls (p = 0.002). In vitro, 5-LO transcript and protein expression were significantly induced in HCMV-infected HUVEC, compared to the control cultures (p = 0.036).\n Question: Does human cytomegalovirus infection induce leukotriene B4 and 5-lipoxygenase expression in human placentae and umbilical vein endothelial cells?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Human cytomegalovirus (HCMV) can cause congenital infection with risk of neurological disability. Maternal-fetal transmission is associated with placental inflammation. 5-lipoxygenase (5-LO) is the key enzyme in the biosynthesis of Leukotrienes (LTs), which are proinflammatory mediators. This study investigated the effect of HCMV infection on 5-LO expression and Leukotriene-B4 (LTB4) induction in human placentae and umbilical vein endothelial cells (HUVEC). Seven placentae from fetuses with congenital HCMV infection and brain damage and six controls were stained with HCMV-immediate-early-antigen (HCMV-IEA) and 5-LO by immunohistochemistry. 5-hydroxyeicosatetraenoic acid (5-HETE) and LTB4 were measured in culture supernatant from ex vivo HCMV-infected placental histocultures by liquid chromatography. In vitro, HCMV infected HUVEC cells were analyzed for 5-LO mRNA and protein expression by real time PCR and immunofluorescence staining. HCMV-IEA was abundant in all HCMV infected placentae but absent in control placentae. 5-LO expression was higher in endothelial and smooth muscle cells of HCMV-infected placentae, compared to control placentae. HCMV infection induced an up-regulation of LTB4 in ex vivo placental explants with higher levels of LTB4 at 72 h compared to controls (p = 0.002). In vitro, 5-LO transcript and protein expression were significantly induced in HCMV-infected HUVEC, compared to the control cultures (p = 0.036).
Question: Does human cytomegalovirus infection induce leukotriene B4 and 5-lipoxygenase expression in human placentae and umbilical vein endothelial cells?
Output:
|
PubmedQA65043
|
[
{
"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 objectives of this study were to determine the benefit of pretreatment magnetic resonance imaging (MRI)-based tumor volume (Tv) measurements in patients presenting with squamous cell carcinomas (SCCs) involving the oral cavity subsites most frequently associated with mandibular bone invasion. A 10-year retrospective study of all patients undergoing surgical resection for primary SCC of the retromolar trigone, mandible, or floor of mouth (with bone involvement) was completed. In total, 62 patients met the inclusion criteria, and Tv measurements completed on their pretreatment MRI. Tumor volume was significant at predicting all-cause survival and disease-free survival at 5 years. Tv stratification to correlate with the TNM staging system resulted in down-staging in 40 of the 62 cases.\n Question: Do magnetic resonance imaging-based tumor volume measurements predict outcome in patients with squamous cell carcinoma of the mandible?\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 objectives of this study were to determine the benefit of pretreatment magnetic resonance imaging (MRI)-based tumor volume (Tv) measurements in patients presenting with squamous cell carcinomas (SCCs) involving the oral cavity subsites most frequently associated with mandibular bone invasion. A 10-year retrospective study of all patients undergoing surgical resection for primary SCC of the retromolar trigone, mandible, or floor of mouth (with bone involvement) was completed. In total, 62 patients met the inclusion criteria, and Tv measurements completed on their pretreatment MRI. Tumor volume was significant at predicting all-cause survival and disease-free survival at 5 years. Tv stratification to correlate with the TNM staging system resulted in down-staging in 40 of the 62 cases.
Question: Do magnetic resonance imaging-based tumor volume measurements predict outcome in patients with squamous cell carcinoma of the mandible?
Output:
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PubmedQA1920
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: It remains controversial whether the cure of H. pylori infection improves NUD symptoms. To conduct a double-blind placebo-controlled single centre study with concealed allocation to investigate this question. Ninety NUD patients with H. pylori infection were randomly assigned to either the treatment group (50 patients) or placebo group (40 patients). The treatment group received omeprazole, amoxycillin, clarithromycin and the placebo group received omeprazole and placebos for 7 days. Symptoms were assessed every week for up to 12 weeks after completion of medication by a symptom questionnaire. Alteration of histological parameters for gastritis was also evaluated. The infection was cured in 41 out of 48 patients in the treatment group and none in the placebo group. There was no significant difference in the mean symptom scores at any assessment point up to 12 weeks between the treatment and placebo groups. Regarding histological parameters, activity and inflammation, not atrophy or intestinal metaplasia, were significantly improved in the treatment group.\n Question: Does cure of Helicobacter pylori infection improve symptoms in non-ulcer dyspepsia patients-a double-blind placebo-controlled study?\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: It remains controversial whether the cure of H. pylori infection improves NUD symptoms. To conduct a double-blind placebo-controlled single centre study with concealed allocation to investigate this question. Ninety NUD patients with H. pylori infection were randomly assigned to either the treatment group (50 patients) or placebo group (40 patients). The treatment group received omeprazole, amoxycillin, clarithromycin and the placebo group received omeprazole and placebos for 7 days. Symptoms were assessed every week for up to 12 weeks after completion of medication by a symptom questionnaire. Alteration of histological parameters for gastritis was also evaluated. The infection was cured in 41 out of 48 patients in the treatment group and none in the placebo group. There was no significant difference in the mean symptom scores at any assessment point up to 12 weeks between the treatment and placebo groups. Regarding histological parameters, activity and inflammation, not atrophy or intestinal metaplasia, were significantly improved in the treatment group.
Question: Does cure of Helicobacter pylori infection improve symptoms in non-ulcer dyspepsia patients-a double-blind placebo-controlled study?
Output:
|
PubmedQA117741
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Although the role of miRNA in cancer development and progression has been well established, the association between genetic variants in miRNA biogenesis pathway genes and breast cancer risk has been yet unclear. We analyzed data from two genome-wide association studies conducted in East Asian women including 5,066 cases and 4,337 controls. Among the single-nucleotide polymorphisms (SNP), which were directly genotyped or imputed, we selected 237 SNPs in 32 genes involved in miRNA biogenesis pathway and its regulation. Although eight SNPs were nominally associated with breast cancer risk in combined samples (P < 0.05), none of them were significant after adjustment for multiple comparisons.\n Question: Are common genetic variants in the microRNA biogenesis pathway associated with breast cancer risk in Asian 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: Although the role of miRNA in cancer development and progression has been well established, the association between genetic variants in miRNA biogenesis pathway genes and breast cancer risk has been yet unclear. We analyzed data from two genome-wide association studies conducted in East Asian women including 5,066 cases and 4,337 controls. Among the single-nucleotide polymorphisms (SNP), which were directly genotyped or imputed, we selected 237 SNPs in 32 genes involved in miRNA biogenesis pathway and its regulation. Although eight SNPs were nominally associated with breast cancer risk in combined samples (P < 0.05), none of them were significant after adjustment for multiple comparisons.
Question: Are common genetic variants in the microRNA biogenesis pathway associated with breast cancer risk in Asian women?
Output:
|
PubmedQA101519
|
[
{
"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 examined the effects of skin temperature (Ts) and skin blood flow (SKBF) on bioelectrical impedance (BIA) measurements of body composition in healthy young females. The Lukaski (FFM(LUK)) and Guo (FFM(GUO)) BIA equations for measuring female fat-free mass (FFM) were used. All subjects (N = 20, age = 18-22 yr) underwent the following measurements under three ambient temperatures (T(amb)): Ts and SKBF for the calf, thigh, biceps, and chest; oral temperature (T(OR)); and the BIA measures of resistance (R) and reactance (Xc). The three T(amb) were 17, 25, and 35 degrees C which were considered as cold (CT), neutral (NT), and hot (HT) conditions, respectively. Their underwater weighing (UWW), lung residual volume, and skinfold thickness were measured in the NT. Data were analyzed using repeated measures of ANOVA and Tukey post-hoc test. We observed that in the CT mean SKBF and Ts decreased (P < 0.05) and R and Xc increased (P < 0.05), compared with those in both NT and HT. However, in the HT both SKBF and Ts increased and R deceased, but Xc remained unchanged relative to the NT. In these subjects, a net change in Ts of 17 degrees C resulted in a net change in the BIA measure of R of 46 ohms or 2.5 ohms per degree C. These changes affected the estimate of FFM(LUK) between CT, NT, and HT, but not the estimate of FFM(GUO) Regarding the two BIA equations for estimating FFM, the Guo equation underestimated FFM(UWW) (P < 0.05) in the CT, NT, and HT, and the Lukaski equation underestimated FFM(UWW) (P < 0.05) only in the CT, compared with that in the UWW technique.\n Question: Do skin temperature and skin blood flow affect bioelectric impedance study of female fat-free mass?\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 examined the effects of skin temperature (Ts) and skin blood flow (SKBF) on bioelectrical impedance (BIA) measurements of body composition in healthy young females. The Lukaski (FFM(LUK)) and Guo (FFM(GUO)) BIA equations for measuring female fat-free mass (FFM) were used. All subjects (N = 20, age = 18-22 yr) underwent the following measurements under three ambient temperatures (T(amb)): Ts and SKBF for the calf, thigh, biceps, and chest; oral temperature (T(OR)); and the BIA measures of resistance (R) and reactance (Xc). The three T(amb) were 17, 25, and 35 degrees C which were considered as cold (CT), neutral (NT), and hot (HT) conditions, respectively. Their underwater weighing (UWW), lung residual volume, and skinfold thickness were measured in the NT. Data were analyzed using repeated measures of ANOVA and Tukey post-hoc test. We observed that in the CT mean SKBF and Ts decreased (P < 0.05) and R and Xc increased (P < 0.05), compared with those in both NT and HT. However, in the HT both SKBF and Ts increased and R deceased, but Xc remained unchanged relative to the NT. In these subjects, a net change in Ts of 17 degrees C resulted in a net change in the BIA measure of R of 46 ohms or 2.5 ohms per degree C. These changes affected the estimate of FFM(LUK) between CT, NT, and HT, but not the estimate of FFM(GUO) Regarding the two BIA equations for estimating FFM, the Guo equation underestimated FFM(UWW) (P < 0.05) in the CT, NT, and HT, and the Lukaski equation underestimated FFM(UWW) (P < 0.05) only in the CT, compared with that in the UWW technique.
Question: Do skin temperature and skin blood flow affect bioelectric impedance study of female fat-free mass?
Output:
|
PubmedQA63700
|
[
{
"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: Essential hypertension is frequently associated with hyperuricemia in both adult and pediatric patients. Lowering serum uric acid level may provide greater benefit than simply treating hypertension. Forty-four adolescents, aged 12-19 years, newly diagnosed as essential hypertension (secondary hypertension was excluded) and previously untreated were randomized (open label trial) to receive either enalapril or enalapril plus allopurinol in combination. All participants had baseline serum uric acid level ≥5.5 mg/dl. Baseline mean blood pressure (BP), age and body mass index were similar between the two groups. After 8 weeks' treatment, BP reduction was greater, percent of treatment group achieving target BP level was greater, and serum uric acid level was lower in the combination treatment group. There were no adverse effects during the course of therapy.\n Question: Does allopurinol enhance the blood pressure lowering effect of enalapril in children with hyperuricemic essential hypertension?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Essential hypertension is frequently associated with hyperuricemia in both adult and pediatric patients. Lowering serum uric acid level may provide greater benefit than simply treating hypertension. Forty-four adolescents, aged 12-19 years, newly diagnosed as essential hypertension (secondary hypertension was excluded) and previously untreated were randomized (open label trial) to receive either enalapril or enalapril plus allopurinol in combination. All participants had baseline serum uric acid level ≥5.5 mg/dl. Baseline mean blood pressure (BP), age and body mass index were similar between the two groups. After 8 weeks' treatment, BP reduction was greater, percent of treatment group achieving target BP level was greater, and serum uric acid level was lower in the combination treatment group. There were no adverse effects during the course of therapy.
Question: Does allopurinol enhance the blood pressure lowering effect of enalapril in children with hyperuricemic essential hypertension?
Output:
|
PubmedQA23568
|
[
{
"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: Rapid eye movement (REM) sleep has a suppressing effect on epileptic activity. This effect might be directly related to neuronal desynchronization mediated by cholinergic neurotransmission. We investigated whether interictal epileptiform discharges (IEDs) and high frequency oscillations-a biomarker of the epileptogenic zone-are evenly distributed across phasic and tonic REM sleep. We hypothesized that IEDs are more suppressed during phasic REM sleep because of additional cholinergic drive. Twelve patients underwent polysomnography during long-term combined scalp-intracerebral electroencephalography (EEG) recording. After sleep staging in the scalp EEG, we identified segments of REM sleep with rapid eye movements (phasic REM) and segments of REM sleep without rapid eye movements (tonic REM). In the intracerebral EEG, we computed the power in frequencies <30 Hz and from 30 to 500 Hz, and marked IEDs, ripples (>80 Hz) and fast ripples (>250 Hz). We grouped the intracerebral channels into channels in the seizure-onset zone (SOZ), the exclusively irritative zone (EIZ), and the normal zone (NoZ). Power in frequencies <30 Hz was lower during phasic than tonic REM sleep (p < 0.001), most likely reflecting increased desynchronization. IEDs, ripples and fast ripples, were less frequent during phasic than tonic REM sleep (phasic REM sleep: 39% of spikes, 35% of ripples, 18% of fast ripples, tonic REM sleep: 61% of spikes, 65% of ripples, 82% of fast ripples; p < 0.001). In contrast to ripples in the epileptogenic zone, physiologic ripples were more abundant during phasic REM sleep (phasic REM sleep: 73% in NoZ, 30% in EIZ, 28% in SOZ, tonic REM sleep: 27% in NoZ, 70% in EIZ, 72% in SOZ; p < 0.001).\n Question: Does eEG desynchronization during phasic REM sleep suppress interictal epileptic activity in humans?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Rapid eye movement (REM) sleep has a suppressing effect on epileptic activity. This effect might be directly related to neuronal desynchronization mediated by cholinergic neurotransmission. We investigated whether interictal epileptiform discharges (IEDs) and high frequency oscillations-a biomarker of the epileptogenic zone-are evenly distributed across phasic and tonic REM sleep. We hypothesized that IEDs are more suppressed during phasic REM sleep because of additional cholinergic drive. Twelve patients underwent polysomnography during long-term combined scalp-intracerebral electroencephalography (EEG) recording. After sleep staging in the scalp EEG, we identified segments of REM sleep with rapid eye movements (phasic REM) and segments of REM sleep without rapid eye movements (tonic REM). In the intracerebral EEG, we computed the power in frequencies <30 Hz and from 30 to 500 Hz, and marked IEDs, ripples (>80 Hz) and fast ripples (>250 Hz). We grouped the intracerebral channels into channels in the seizure-onset zone (SOZ), the exclusively irritative zone (EIZ), and the normal zone (NoZ). Power in frequencies <30 Hz was lower during phasic than tonic REM sleep (p < 0.001), most likely reflecting increased desynchronization. IEDs, ripples and fast ripples, were less frequent during phasic than tonic REM sleep (phasic REM sleep: 39% of spikes, 35% of ripples, 18% of fast ripples, tonic REM sleep: 61% of spikes, 65% of ripples, 82% of fast ripples; p < 0.001). In contrast to ripples in the epileptogenic zone, physiologic ripples were more abundant during phasic REM sleep (phasic REM sleep: 73% in NoZ, 30% in EIZ, 28% in SOZ, tonic REM sleep: 27% in NoZ, 70% in EIZ, 72% in SOZ; p < 0.001).
Question: Does eEG desynchronization during phasic REM sleep suppress interictal epileptic activity in humans?
Output:
|
PubmedQA18233
|
[
{
"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: Pleural malignant mesothelioma (PMM) is a rare and highly aggressive tumor, whose development is strictly related to occupational exposure to asbestos. The prognosis of PMM is generally poor (median survival, 4-12 months), but a few have a relatively long survival. The objective of this study was to evaluate the use of the cell cycle-related proteins p27(kip1) and MIB-1 as prognostic indicators of survival in PMMs. Of 621 PMMs, the authors selected 27 cases with a relatively long-term survival (> 24 months) and a control group of 36 PMMs having a shorter (usual) survival (< 24 months). The expression of the p27(kip1) was significantly higher in the long-term survival group compared with the control (short survival) group (81.41% vs. 31.94%; P < 0.0001). The PMMs of epithelioid histotype had a significantly higher p27(kip1) immunoreactivity compared with those of biphasic type (59.24% vs. 38.94%; P = 0.02). In agreement with the data in the literature, the proliferative activity (as detected by MIB-1 immunoreactivity) was significantly higher in short than long survival PMMs (43.53% vs. 14.11%; P < 0.0001) and in the biphasic histotype than in the epithelioid type (43.19% vs. 26.02%; P = 0.006).\n Question: Does p27 ( kip1 ) immunoreactivity correlate with long-term survival in pleural malignant mesothelioma?\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: Pleural malignant mesothelioma (PMM) is a rare and highly aggressive tumor, whose development is strictly related to occupational exposure to asbestos. The prognosis of PMM is generally poor (median survival, 4-12 months), but a few have a relatively long survival. The objective of this study was to evaluate the use of the cell cycle-related proteins p27(kip1) and MIB-1 as prognostic indicators of survival in PMMs. Of 621 PMMs, the authors selected 27 cases with a relatively long-term survival (> 24 months) and a control group of 36 PMMs having a shorter (usual) survival (< 24 months). The expression of the p27(kip1) was significantly higher in the long-term survival group compared with the control (short survival) group (81.41% vs. 31.94%; P < 0.0001). The PMMs of epithelioid histotype had a significantly higher p27(kip1) immunoreactivity compared with those of biphasic type (59.24% vs. 38.94%; P = 0.02). In agreement with the data in the literature, the proliferative activity (as detected by MIB-1 immunoreactivity) was significantly higher in short than long survival PMMs (43.53% vs. 14.11%; P < 0.0001) and in the biphasic histotype than in the epithelioid type (43.19% vs. 26.02%; P = 0.006).
Question: Does p27 ( kip1 ) immunoreactivity correlate with long-term survival in pleural malignant mesothelioma?
Output:
|
PubmedQA54188
|
[
{
"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: Onset of myocardial relaxation is highly energy dependent. Perfusion and therefore energy substrate delivery are predominantly reduced in the subendocardial myocardium in the early stages of progressive ischemia. We hypothesized that delayed onset of subendocardial diastolic thinning will functionally identify regionally hypoperfused resting myocardium. Progressive left anterior descending coronary artery stenosis was induced by an ameroid occluder and maintained for 1 or 2 weeks (end point) in 12 dogs. M-mode tissue Doppler images of the anterior apical and middle segments (testing region) and middle inferior segment (control region) were acquired selectively in the subendocardium and subepicardium. The time to the onset of thinning was measured with the use of tissue Doppler velocity (TOTv) and a thickness function (TOTt). At the end point in the testing region, myocardial flow was significantly lower in the subendocardial layer (P<0.05) in all animals, whereas viability staining showed preserved transmural viability in 10 dogs and thin subendocardial necrosis in 2 dogs. Both TOTv and TOTt were significantly (P<0.01) prolonged in the testing region. The mean difference between subendocardial and subepicardial TOTv values versus that in the control region identified the ischemic region, even when only dogs with hypoperfused but transmurally viable myocardium were considered (P<0.05). Systolic and diastolic myocardial velocities did not identify subendocardial hypoperfusion.\n Question: Does delayed onset of subendocardial diastolic thinning at rest identify hypoperfused myocardium?\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: Onset of myocardial relaxation is highly energy dependent. Perfusion and therefore energy substrate delivery are predominantly reduced in the subendocardial myocardium in the early stages of progressive ischemia. We hypothesized that delayed onset of subendocardial diastolic thinning will functionally identify regionally hypoperfused resting myocardium. Progressive left anterior descending coronary artery stenosis was induced by an ameroid occluder and maintained for 1 or 2 weeks (end point) in 12 dogs. M-mode tissue Doppler images of the anterior apical and middle segments (testing region) and middle inferior segment (control region) were acquired selectively in the subendocardium and subepicardium. The time to the onset of thinning was measured with the use of tissue Doppler velocity (TOTv) and a thickness function (TOTt). At the end point in the testing region, myocardial flow was significantly lower in the subendocardial layer (P<0.05) in all animals, whereas viability staining showed preserved transmural viability in 10 dogs and thin subendocardial necrosis in 2 dogs. Both TOTv and TOTt were significantly (P<0.01) prolonged in the testing region. The mean difference between subendocardial and subepicardial TOTv values versus that in the control region identified the ischemic region, even when only dogs with hypoperfused but transmurally viable myocardium were considered (P<0.05). Systolic and diastolic myocardial velocities did not identify subendocardial hypoperfusion.
Question: Does delayed onset of subendocardial diastolic thinning at rest identify hypoperfused myocardium?
Output:
|
PubmedQA207773
|
[
{
"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 effect(s) of interferon gamma (IFN-gamma) on the activity of human growth hormone (hGH) gene promoter in rat pituitary GH3 cells and the molecular mechanism underlying the effect(s). Cell transfection and luciferase reporter gene were used. IFN-gamma (10(2) and 10(3) U/ml) increased the activity of hGH in GH3 cells. The addition of the mitogen-activated protein kinase inhibitor PD98059 (40 micromol/l) to the cells blocked the stimulatory effect of IFN-gamma. Neither overexpression of Pit-1 nor inhibiting Pit-1 expression affected IFN-gamma induction of hGH promoter activity. To identify the DNA sequence that mediated the effect of IFN-gamma, four deletion constructs of hGH gene promoter were created. The stimulatory effect of IFN-gamma was abolished following deletion of the -250 to -132 fragment.\n Question: Does iFN-gamma increase the hGH gene promoter activity in rat GH3 cells?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To study the effect(s) of interferon gamma (IFN-gamma) on the activity of human growth hormone (hGH) gene promoter in rat pituitary GH3 cells and the molecular mechanism underlying the effect(s). Cell transfection and luciferase reporter gene were used. IFN-gamma (10(2) and 10(3) U/ml) increased the activity of hGH in GH3 cells. The addition of the mitogen-activated protein kinase inhibitor PD98059 (40 micromol/l) to the cells blocked the stimulatory effect of IFN-gamma. Neither overexpression of Pit-1 nor inhibiting Pit-1 expression affected IFN-gamma induction of hGH promoter activity. To identify the DNA sequence that mediated the effect of IFN-gamma, four deletion constructs of hGH gene promoter were created. The stimulatory effect of IFN-gamma was abolished following deletion of the -250 to -132 fragment.
Question: Does iFN-gamma increase the hGH gene promoter activity in rat GH3 cells?
Output:
|
PubmedQA20659
|
[
{
"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: Factor analysis of medical image sequences (FAMIS) applied to gadolinium chelate-enhanced subsecond magnetic resonance (MR) imaging was evaluated as a postprocessing method for assessing myocardial perfusion in coronary artery disease (CAD). To assess the accuracy of motion correction, five normal volunteers underwent MR imaging at rest. Thirteen patients with well-documented CAD and no myocardial infarction underwent MR imaging at rest and after dipyridamole administration. After motion correction, a single myocardial tissue factor (FAMISt) image was obtained with FAMIS for each raw MR imaging series acquisition. To evaluate how FAMIS could improve the analysis of these acquisitions, five readers visually assessed myocardial perfusion with FAMISt and raw MR images, and a multicase, multireader receiver operating characteristic analysis was performed. FAMISt images significantly improved detection of the perfusion defects when compared with raw MR images (P = .002). Areas under the receiver operating characteristic curves ranged from 0.84 to 0.93 with FAMISt images and from 0.48 to 0.85 with raw MR images.\n Question: Does factor analysis of medical image sequences improve evaluation of first-pass MR imaging acquisitions for myocardial perfusion?\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: Factor analysis of medical image sequences (FAMIS) applied to gadolinium chelate-enhanced subsecond magnetic resonance (MR) imaging was evaluated as a postprocessing method for assessing myocardial perfusion in coronary artery disease (CAD). To assess the accuracy of motion correction, five normal volunteers underwent MR imaging at rest. Thirteen patients with well-documented CAD and no myocardial infarction underwent MR imaging at rest and after dipyridamole administration. After motion correction, a single myocardial tissue factor (FAMISt) image was obtained with FAMIS for each raw MR imaging series acquisition. To evaluate how FAMIS could improve the analysis of these acquisitions, five readers visually assessed myocardial perfusion with FAMISt and raw MR images, and a multicase, multireader receiver operating characteristic analysis was performed. FAMISt images significantly improved detection of the perfusion defects when compared with raw MR images (P = .002). Areas under the receiver operating characteristic curves ranged from 0.84 to 0.93 with FAMISt images and from 0.48 to 0.85 with raw MR images.
Question: Does factor analysis of medical image sequences improve evaluation of first-pass MR imaging acquisitions for myocardial perfusion?
Output:
|
PubmedQA132410
|
[
{
"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: Patellofemoral pain is a common condition without a clear mechanism for its presentation. Recently significant focus has been placed on the hip and its potential role in patellofemoral pain (PFP). The majority of the research has examined hip strength and neuromuscular control. Less attention has been given to hip mobility and its potential role in subjects with PFP. The purpose of this study was to compare passive hip range of motion (ROM) of hip extension and hip internal and external rotation in subjects with PFP and healthy control subjects. The hypothesis was that subjects with PFP would present with less total hip ROM and greater asymmetry than controls. Two groups, case controlled. Clinical research laboratory. 30 healthy subjects without pain, radicular symptoms or history of surgery in the low back or lower extremity joints and 30 subjects with a diagnosis of PFP. Passive hip extension, hip internal rotation (IR) and hip external rotation (ER). A digital inclinometer was used for measurements. There was a statistically significant difference (p<0.001) in hip passive extension between the control group and the PFP group bilaterally. Mean hip extension for the control group was 6.8° bilaterally. For the PFP group, the mean hip extension was -4.0° on the left and -4.3° on the right. This corresponds to a difference of means between groups of 10.8° on the left and 11.1° on the right with a standard error of 2.1°. There was no statistically significant difference (p>0.05) in either hip IR or ER ROM or total rotation between or within groups.\n Question: Do patellofemoral pain subjects exhibit decreased passive hip range of motion compared to controls?\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: Patellofemoral pain is a common condition without a clear mechanism for its presentation. Recently significant focus has been placed on the hip and its potential role in patellofemoral pain (PFP). The majority of the research has examined hip strength and neuromuscular control. Less attention has been given to hip mobility and its potential role in subjects with PFP. The purpose of this study was to compare passive hip range of motion (ROM) of hip extension and hip internal and external rotation in subjects with PFP and healthy control subjects. The hypothesis was that subjects with PFP would present with less total hip ROM and greater asymmetry than controls. Two groups, case controlled. Clinical research laboratory. 30 healthy subjects without pain, radicular symptoms or history of surgery in the low back or lower extremity joints and 30 subjects with a diagnosis of PFP. Passive hip extension, hip internal rotation (IR) and hip external rotation (ER). A digital inclinometer was used for measurements. There was a statistically significant difference (p<0.001) in hip passive extension between the control group and the PFP group bilaterally. Mean hip extension for the control group was 6.8° bilaterally. For the PFP group, the mean hip extension was -4.0° on the left and -4.3° on the right. This corresponds to a difference of means between groups of 10.8° on the left and 11.1° on the right with a standard error of 2.1°. There was no statistically significant difference (p>0.05) in either hip IR or ER ROM or total rotation between or within groups.
Question: Do patellofemoral pain subjects exhibit decreased passive hip range of motion compared to controls?
Output:
|
PubmedQA197215
|
[
{
"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 investigate whether the single-nucleotide polymorphism (SNP) rs2910164 residing within microRNA-146a (miR-146a) is associated with diabetic microvascular complications diabetic nephropathy (DN), proliferative diabetic retinopathy (PDR) or diabetic macular oedema (DME) in either Caucasian patients with type 1 (T1DM) or type 2 (T2DM) diabetes mellitus. Caucasian patients with T1DM (n = 733) or T2DM (n = 2215) were recruited from ophthalmology, renal and endocrine clinics in Australia and the UK. Patients with T2DM were required to have diabetes mellitus (DM) for at least 5 years and be on treatment with oral hypoglycaemic drugs or insulin. In total, 890 participants had DN (168 with T1DM and 722 with T2DM), 731 had PDR (251 with T1DM and 480 with T2DM) and 1026 had DME (170 with T1DM and 856 with T2DM). Participants were genotyped for SNP rs2910164 in miR-146a. Analyses investigating association were adjusted for relevant clinical covariates including age, sex, DM duration, HbA1c and hypertension. A significant association was found between the C allele of rs2910164 and DN in the T1DM group (OR 1.93; CI 1.23-3.03; P = 0.004), but no association found in the T2DM group (OR 1.05; CI 0.83-1.32; P = 0.691). In the subset of T2DM patients, the C allele was specifically associated with DME (OR 1.25; CI 1.03-1.53; P = 0.025). No association with DME was found in the T1DM group (OR 0.87; CI 0.54-1.42); P = 0.583), or with PDR for either type of DM.\n Question: Is a single-nucleotide polymorphism in the MicroRNA-146a gene associated with diabetic nephropathy and sight-threatening diabetic retinopathy in Caucasian 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 aimed to investigate whether the single-nucleotide polymorphism (SNP) rs2910164 residing within microRNA-146a (miR-146a) is associated with diabetic microvascular complications diabetic nephropathy (DN), proliferative diabetic retinopathy (PDR) or diabetic macular oedema (DME) in either Caucasian patients with type 1 (T1DM) or type 2 (T2DM) diabetes mellitus. Caucasian patients with T1DM (n = 733) or T2DM (n = 2215) were recruited from ophthalmology, renal and endocrine clinics in Australia and the UK. Patients with T2DM were required to have diabetes mellitus (DM) for at least 5 years and be on treatment with oral hypoglycaemic drugs or insulin. In total, 890 participants had DN (168 with T1DM and 722 with T2DM), 731 had PDR (251 with T1DM and 480 with T2DM) and 1026 had DME (170 with T1DM and 856 with T2DM). Participants were genotyped for SNP rs2910164 in miR-146a. Analyses investigating association were adjusted for relevant clinical covariates including age, sex, DM duration, HbA1c and hypertension. A significant association was found between the C allele of rs2910164 and DN in the T1DM group (OR 1.93; CI 1.23-3.03; P = 0.004), but no association found in the T2DM group (OR 1.05; CI 0.83-1.32; P = 0.691). In the subset of T2DM patients, the C allele was specifically associated with DME (OR 1.25; CI 1.03-1.53; P = 0.025). No association with DME was found in the T1DM group (OR 0.87; CI 0.54-1.42); P = 0.583), or with PDR for either type of DM.
Question: Is a single-nucleotide polymorphism in the MicroRNA-146a gene associated with diabetic nephropathy and sight-threatening diabetic retinopathy in Caucasian patients?
Output:
|
PubmedQA72319
|
[
{
"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 intestinal microbiota is associated with human health and diseases. The luminal microbiota (LM) and the mucosal-associated microbiota (MAM) are 2 distinct ecosystems with different metabolic and immunological functions. To characterize the intestinal LM and MAM in humans using high throughput sequencing of the 16S rRNA gene. Fresh fecal samples and distal colonic mucosal biopsies collected from 24 healthy subjects before (fecal) and during (mucosa) a flexible sigmoidoscopy of an un-prepared bowel. High throughput sequencing of the 16S rRNA gene was used to characterize bacterial communities. Sequences were processed using the QIIME pipeline. LM and MAM populations were significantly different (ANOSIM: R = 0.49, P = 0.001). The LM displayed tighter clustering compared to the MAM (average weighted UniFrac distances 0.27 ± 0.05 vs. 0.43 ± 0.09, P < 0.001, respectively), and showed higher diversity (Shannon diversity index: 4.96 ± 0.37 vs 4.14 ± 0.56, respectively, P < 0.001). The dominant phyla in the LM and MAM were significantly different: Firmicutes (41.4% vs. 29.1%, FDR < 0.0001, respectively), Bacteroidetes (20.2% vs. 26.3%, FDR < 0.05, respectively), Actinobacteria (22% vs. 12.6%, FDR < 0.0001, respectively) and Proteobacteria (9.3% vs. 19.3%, FDR < 0.0001, respectively). The abundance of 56 genera differed significantly (FDR < 0.1) between the 2 niches. All of the genera in the fecal microbiota were present in the MAM while 10 genera were found to be unique to the MAM.\n Question: Does high throughput sequencing reveal distinct microbial populations within the mucosal and luminal niches in healthy 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: The intestinal microbiota is associated with human health and diseases. The luminal microbiota (LM) and the mucosal-associated microbiota (MAM) are 2 distinct ecosystems with different metabolic and immunological functions. To characterize the intestinal LM and MAM in humans using high throughput sequencing of the 16S rRNA gene. Fresh fecal samples and distal colonic mucosal biopsies collected from 24 healthy subjects before (fecal) and during (mucosa) a flexible sigmoidoscopy of an un-prepared bowel. High throughput sequencing of the 16S rRNA gene was used to characterize bacterial communities. Sequences were processed using the QIIME pipeline. LM and MAM populations were significantly different (ANOSIM: R = 0.49, P = 0.001). The LM displayed tighter clustering compared to the MAM (average weighted UniFrac distances 0.27 ± 0.05 vs. 0.43 ± 0.09, P < 0.001, respectively), and showed higher diversity (Shannon diversity index: 4.96 ± 0.37 vs 4.14 ± 0.56, respectively, P < 0.001). The dominant phyla in the LM and MAM were significantly different: Firmicutes (41.4% vs. 29.1%, FDR < 0.0001, respectively), Bacteroidetes (20.2% vs. 26.3%, FDR < 0.05, respectively), Actinobacteria (22% vs. 12.6%, FDR < 0.0001, respectively) and Proteobacteria (9.3% vs. 19.3%, FDR < 0.0001, respectively). The abundance of 56 genera differed significantly (FDR < 0.1) between the 2 niches. All of the genera in the fecal microbiota were present in the MAM while 10 genera were found to be unique to the MAM.
Question: Does high throughput sequencing reveal distinct microbial populations within the mucosal and luminal niches in healthy individuals?
Output:
|
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