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PubmedQA53280
|
[
{
"role": "user",
"content": "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 atrial ventricular (AV) intervals are often optimized at rest in patients receiving cardiac resynchronization therapy (CRT), there are limited data on the impact of exercise on optimal AV interval. In 15 patients with CRT, AV intervals were serially programmed while patients were supine and at rest, and during exercise with heart rates that averaged 20 and 40 beats per minute above their resting rates. Echocardiographic Doppler images were acquired at each programmed AV interval and each rate. Three independent echocardiographic criteria were retrospectively used to determine each patient's optimal AV interval as a function of exercise-induced increased heart rates: the duration of left ventricular filling, stroke volume, and a clinical assessment of left ventricular function. A negative correlation between the optimal AV interval and heart rate was observed across all patients using all three independent criterion: the maximum left ventricular filling time (slope =-0.77, intercept = 151.9, r = 0.55, P < 0.001), maximum stroke volume (slope =-0.93, intercept = 183.3, r = 0.50, P = 0.002), or the subjective clinical assessment (slope =-1.06, intercept = 182.0, r = 0.72, P < 0.001). Consistent trends were observed between all three parameters for 12 out of the 15 patients.\n Question: Do shorter AV delays provide improved echocardiographic hemodynamics during exercise in patients receiving cardiac resynchronization therapy?\n Output: "
},
{
"role": "assistant",
"content": "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 atrial ventricular (AV) intervals are often optimized at rest in patients receiving cardiac resynchronization therapy (CRT), there are limited data on the impact of exercise on optimal AV interval. In 15 patients with CRT, AV intervals were serially programmed while patients were supine and at rest, and during exercise with heart rates that averaged 20 and 40 beats per minute above their resting rates. Echocardiographic Doppler images were acquired at each programmed AV interval and each rate. Three independent echocardiographic criteria were retrospectively used to determine each patient's optimal AV interval as a function of exercise-induced increased heart rates: the duration of left ventricular filling, stroke volume, and a clinical assessment of left ventricular function. A negative correlation between the optimal AV interval and heart rate was observed across all patients using all three independent criterion: the maximum left ventricular filling time (slope =-0.77, intercept = 151.9, r = 0.55, P < 0.001), maximum stroke volume (slope =-0.93, intercept = 183.3, r = 0.50, P = 0.002), or the subjective clinical assessment (slope =-1.06, intercept = 182.0, r = 0.72, P < 0.001). Consistent trends were observed between all three parameters for 12 out of the 15 patients.
Question: Do shorter AV delays provide improved echocardiographic hemodynamics during exercise in patients receiving cardiac resynchronization therapy?
Output:
|
PubmedQA127038
|
[
{
"role": "user",
"content": "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 pathogenesis of primary sclerosing cholangitis (PSC) remains poorly understood. Since PSC predominantly occurs in patients with inflammatory bowel disease, autoimmunity triggered by activated T cells migrating from the gut to the liver is a possible mechanism. We hypothesized that T cells primed in the gut-associated lymphoid tissue (GALT) by a specific antigen migrate to the liver and cause cholangitis when they recognize the same antigen on cholangiocytes. We induced ovalbumin-dependent colitis in mice that express ovalbumin in biliary epithelia (ASBT-OVA mice) and crossed ASBT-OVA mice with mice that express ovalbumin in enterocytes (iFABP-OVA mice). We analyzed T-cell activation in the GALT and crossreactivity to the same antigen in the liver as well as the effects of colitis per se on antigen-presentation and T-cell activation in the liver. Intrarectal application of ovalbumin followed by transfer of CD8 OT-I T cells led to antigen-dependent colitis. CD8 T cells primed in the GALT acquired effector function and the capability to migrate to the liver, where they caused cholangitis in a strictly antigen-dependent manner. Likewise, cholangitis developed in mice expressing ovalbumin simultaneously in biliary epithelia and enterocytes after transfer of OT-I T cells. Dextran sodium sulfate colitis led to increased levels of inflammatory cytokines in the portal venous blood, induced activation of resident liver dendritic cells, and promoted the induction of T-cell-dependent cholangitis.\n Question: Do cD8 T cells primed in the gut-associated lymphoid tissue induce immune-mediated cholangitis 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 pathogenesis of primary sclerosing cholangitis (PSC) remains poorly understood. Since PSC predominantly occurs in patients with inflammatory bowel disease, autoimmunity triggered by activated T cells migrating from the gut to the liver is a possible mechanism. We hypothesized that T cells primed in the gut-associated lymphoid tissue (GALT) by a specific antigen migrate to the liver and cause cholangitis when they recognize the same antigen on cholangiocytes. We induced ovalbumin-dependent colitis in mice that express ovalbumin in biliary epithelia (ASBT-OVA mice) and crossed ASBT-OVA mice with mice that express ovalbumin in enterocytes (iFABP-OVA mice). We analyzed T-cell activation in the GALT and crossreactivity to the same antigen in the liver as well as the effects of colitis per se on antigen-presentation and T-cell activation in the liver. Intrarectal application of ovalbumin followed by transfer of CD8 OT-I T cells led to antigen-dependent colitis. CD8 T cells primed in the GALT acquired effector function and the capability to migrate to the liver, where they caused cholangitis in a strictly antigen-dependent manner. Likewise, cholangitis developed in mice expressing ovalbumin simultaneously in biliary epithelia and enterocytes after transfer of OT-I T cells. Dextran sodium sulfate colitis led to increased levels of inflammatory cytokines in the portal venous blood, induced activation of resident liver dendritic cells, and promoted the induction of T-cell-dependent cholangitis.
Question: Do cD8 T cells primed in the gut-associated lymphoid tissue induce immune-mediated cholangitis in mice?
Output:
|
PubmedQA47007
|
[
{
"role": "user",
"content": "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 biological pathways and functional properties by which misexpressed microRNAs (miRNAs) contribute to liver carcinogenesis have been intensively investigated. However, little is known about the upstream mechanisms that deregulate miRNA expressions in this process. In hepatocellular carcinoma (HCC), hepatitis B virus (HBV) X protein (HBx), a transcriptional trans-activator, is frequently expressed in truncated form without carboxyl-terminus but its role in miRNA expression and HCC development is unclear. Human non-tumorigenic hepatocytes were infected with lentivirus-expressing full-length and carboxyl-terminal truncated HBx (Ct-HBx) for cell growth assay and miRNA profiling. Chromatin immunoprecipitation microarray was performed to identify the miRNA promoters directly associated with HBx. Direct transcriptional control was verified by luciferase reporter assay. The differential miRNA expressions were further validated in a cohort of HBV-associated HCC tissues using real-time PCR. Hepatocytes expressing Ct-HBx grew significantly faster than the full-length HBx counterparts. Ct-HBx decreased while full-length HBx increased the expression of a set of miRNAs with growth-suppressive functions. Interestingly, Ct-HBx bound to and inhibited the transcriptional activity of some of these miRNA promoters. Notably, some of the examined repressed-miRNAs (miR-26a, -29c, -146a and -190) were also significantly down-regulated in a subset of HCC tissues with carboxyl-terminal HBx truncation compared to their matching non-tumor tissues, highlighting the clinical relevance of our data.\n Question: Does carboxyl-terminal truncated HBx regulate a distinct microRNA transcription program in hepatocellular carcinoma development?\n Output: "
},
{
"role": "assistant",
"content": "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 biological pathways and functional properties by which misexpressed microRNAs (miRNAs) contribute to liver carcinogenesis have been intensively investigated. However, little is known about the upstream mechanisms that deregulate miRNA expressions in this process. In hepatocellular carcinoma (HCC), hepatitis B virus (HBV) X protein (HBx), a transcriptional trans-activator, is frequently expressed in truncated form without carboxyl-terminus but its role in miRNA expression and HCC development is unclear. Human non-tumorigenic hepatocytes were infected with lentivirus-expressing full-length and carboxyl-terminal truncated HBx (Ct-HBx) for cell growth assay and miRNA profiling. Chromatin immunoprecipitation microarray was performed to identify the miRNA promoters directly associated with HBx. Direct transcriptional control was verified by luciferase reporter assay. The differential miRNA expressions were further validated in a cohort of HBV-associated HCC tissues using real-time PCR. Hepatocytes expressing Ct-HBx grew significantly faster than the full-length HBx counterparts. Ct-HBx decreased while full-length HBx increased the expression of a set of miRNAs with growth-suppressive functions. Interestingly, Ct-HBx bound to and inhibited the transcriptional activity of some of these miRNA promoters. Notably, some of the examined repressed-miRNAs (miR-26a, -29c, -146a and -190) were also significantly down-regulated in a subset of HCC tissues with carboxyl-terminal HBx truncation compared to their matching non-tumor tissues, highlighting the clinical relevance of our data.
Question: Does carboxyl-terminal truncated HBx regulate a distinct microRNA transcription program in hepatocellular carcinoma development?
Output:
|
PubmedQA196748
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Porcine parvovirus (PPV) infection primarily causes reproductive failure of pregnant swine and results in host cell death. Boars, as an important disseminator, shed PPV to sows via semen. PPV infects and numerously replicates in boar testicle, which results in damage of swine testicle in vivo. Reactive oxygen species (ROS), a mediator of cell apoptosis, play a crucial role in the mitochondria apoptotic pathway. However, whether PPV infection induces ST cells apoptosis and ROS accumulation is still unclear. To determine the effects of PPV infection on the apoptosis, we detected morphological changes, DNA ladder, activities of caspases, and expression of PARP in PPV-infected ST cells. Moreover, aiming to investigate the effect of PPV infection on the mitochondrial apoptotic pathway and ROS accumulation, we detected the Δψm, apoptosis-related genes, and ROS. To investigate the role of ROS in the process of PPV-induced apoptosis, the ST cells were infected with PPV and treated with the ROS antioxidants. The ROS level was measured using Reactive Oxygen Species Assay Kit and the Δψm, expression level of Bcl-2, translocation of Bax, and redistribution of mitochondria cytochrome c were tested. In this study, we demonstrated that PPV infection could induce apoptosis that was characterized by morphological changes, DNA fragmentation and activation of caspases. Moreover, PPV infection suppressed Bcl-2 expression, enhanced Bax expression and translocation to mitochondria, decreased the mitochondrial transmembrane potential, and triggered the release of cytochrome c, which caused the subsequent activation of caspase-9 and caspase-3 and initiation of apoptosis. However, during the process of PPV-induced apoptosis, the protein levels of Fas and FasL were not affected. Further studies showed that PPV infection caused ROS accumulation. Inhibition of ROS could reduce mitochondrial transmembrane potential and could significantly block ST cells apoptosis via suppressing Bax translocation, cytochrome c and caspase-3 activation.\n Question: Does porcine parvovirus infection activate mitochondria-mediated apoptotic signaling pathway by inducing ROS accumulation?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Porcine parvovirus (PPV) infection primarily causes reproductive failure of pregnant swine and results in host cell death. Boars, as an important disseminator, shed PPV to sows via semen. PPV infects and numerously replicates in boar testicle, which results in damage of swine testicle in vivo. Reactive oxygen species (ROS), a mediator of cell apoptosis, play a crucial role in the mitochondria apoptotic pathway. However, whether PPV infection induces ST cells apoptosis and ROS accumulation is still unclear. To determine the effects of PPV infection on the apoptosis, we detected morphological changes, DNA ladder, activities of caspases, and expression of PARP in PPV-infected ST cells. Moreover, aiming to investigate the effect of PPV infection on the mitochondrial apoptotic pathway and ROS accumulation, we detected the Δψm, apoptosis-related genes, and ROS. To investigate the role of ROS in the process of PPV-induced apoptosis, the ST cells were infected with PPV and treated with the ROS antioxidants. The ROS level was measured using Reactive Oxygen Species Assay Kit and the Δψm, expression level of Bcl-2, translocation of Bax, and redistribution of mitochondria cytochrome c were tested. In this study, we demonstrated that PPV infection could induce apoptosis that was characterized by morphological changes, DNA fragmentation and activation of caspases. Moreover, PPV infection suppressed Bcl-2 expression, enhanced Bax expression and translocation to mitochondria, decreased the mitochondrial transmembrane potential, and triggered the release of cytochrome c, which caused the subsequent activation of caspase-9 and caspase-3 and initiation of apoptosis. However, during the process of PPV-induced apoptosis, the protein levels of Fas and FasL were not affected. Further studies showed that PPV infection caused ROS accumulation. Inhibition of ROS could reduce mitochondrial transmembrane potential and could significantly block ST cells apoptosis via suppressing Bax translocation, cytochrome c and caspase-3 activation.
Question: Does porcine parvovirus infection activate mitochondria-mediated apoptotic signaling pathway by inducing ROS accumulation?
Output:
|
PubmedQA58513
|
[
{
"role": "user",
"content": "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 antibodies to CTLA-4, a negative regulator of T-cell activation, was investigated in multiply transfused patients with malignant and non- malignant hematologic diseases. A previous study showed that, in multiply transfused patients, an immune response against nuclear matrix proteins can be induced by WBCs undergoing apoptosis during RBC unit storage. This study evaluated whether the same phenomenon could be involved in the induction of CTLA-4 antibodies in the patients analyzed. Patient sera were tested for binding to the recombinant full-length CTLA-4 beta-galactosidase fusion protein by an ELISA. Immuno-fluorescence stainings were performed to analyze the CTLA-4 epitopes recognized by the antibodies and to detect such epitopes in the apoptotic cells present in the RBC units. CTLA-4 antibodies were found in multiply transfused patients with beta-thalassemia (40%) and with other hemolytic diseases (33%) including leukemias (42%). A higher incidence of CTLA-4 antibodies was found in patients receiving non-WBC-reduced blood (88%) than in those receiving WBC-reduced blood (26%). Immunofluorescence staining showed that WBCs undergoing apoptosis in the RBC unit expressed CTLA-4 epitopes.\n Question: Do patients with neoplastic and nonneoplastic hematologic diseases acquire CTLA-4 antibodies after blood transfusion?\n Output: "
},
{
"role": "assistant",
"content": "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 antibodies to CTLA-4, a negative regulator of T-cell activation, was investigated in multiply transfused patients with malignant and non- malignant hematologic diseases. A previous study showed that, in multiply transfused patients, an immune response against nuclear matrix proteins can be induced by WBCs undergoing apoptosis during RBC unit storage. This study evaluated whether the same phenomenon could be involved in the induction of CTLA-4 antibodies in the patients analyzed. Patient sera were tested for binding to the recombinant full-length CTLA-4 beta-galactosidase fusion protein by an ELISA. Immuno-fluorescence stainings were performed to analyze the CTLA-4 epitopes recognized by the antibodies and to detect such epitopes in the apoptotic cells present in the RBC units. CTLA-4 antibodies were found in multiply transfused patients with beta-thalassemia (40%) and with other hemolytic diseases (33%) including leukemias (42%). A higher incidence of CTLA-4 antibodies was found in patients receiving non-WBC-reduced blood (88%) than in those receiving WBC-reduced blood (26%). Immunofluorescence staining showed that WBCs undergoing apoptosis in the RBC unit expressed CTLA-4 epitopes.
Question: Do patients with neoplastic and nonneoplastic hematologic diseases acquire CTLA-4 antibodies after blood transfusion?
Output:
|
PubmedQA73595
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Our study is aimed to 1) clarify the vitamin D status in Uygur and Kazak ethnic populations and 2) elucidate the relationship between 14 SNPs (in 5 vitamin D-related genes) and vitamin D deficiency in these 2 ethnic populations. A multistage-cluster sampling survey was carried out for residents with Uygur or Kazak ethnicity in Xinjiang, China. Anthropometric measurements were taken and the concentrations of 25OHD were measured. Fourteen common variants in VDR, GC, CYP2R1, CYP27B1, and DHCR7/NADSYN1 were genotyped by using multiple SNaPshot assay. Logistic regression analysis was performed to identify the possible risk factors for vitamin D deficiency, after adjusting for several environmental and biological factors. The pattern of SNP associations was distinct between Uygurs and Kazaks. Anthropometric measurements and the concentrations of 25OHD were obtained from 1873 participants (945 Uygur ethnic and 928 Kazak ethnic). The genotypes of 14 SNPs were measured for 300 Uygurs and 300 Kazaks. The median 25OHD concentration was as low as 10.4 ng/ml in Uygurs and 16.2 ng/ml in Kazaks. In Uygurs, the prevalence of vitamin D deficiency, in-sufficiency, and sufficiency was 91.2%, 5.8%, and 3.0%, respectively. CYP2R1-rs10766197 was significantly associated with the presence of vitamin D deficiency in the Uygur ethnic population (P=0.019, OR=6.533, 95%C.I.: 361-31.357), while DHCR7/NADSYN1-rs12785878 was significantly associated with the presence of vitamin D deficiency in the Kazak ethnic population (P=0.011, OR=2.442, 95%C.I.: 1.224-4.873). Of 10 SNPs in VDR and GC genes, none was associated with vitamin D status in these 2 ethnic populations.\n Question: Does vitamin D Deficiency in Uygurs and Kazaks be Associated with Polymorphisms in CYP2R1 and DHCR7/NADSYN1 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: Our study is aimed to 1) clarify the vitamin D status in Uygur and Kazak ethnic populations and 2) elucidate the relationship between 14 SNPs (in 5 vitamin D-related genes) and vitamin D deficiency in these 2 ethnic populations. A multistage-cluster sampling survey was carried out for residents with Uygur or Kazak ethnicity in Xinjiang, China. Anthropometric measurements were taken and the concentrations of 25OHD were measured. Fourteen common variants in VDR, GC, CYP2R1, CYP27B1, and DHCR7/NADSYN1 were genotyped by using multiple SNaPshot assay. Logistic regression analysis was performed to identify the possible risk factors for vitamin D deficiency, after adjusting for several environmental and biological factors. The pattern of SNP associations was distinct between Uygurs and Kazaks. Anthropometric measurements and the concentrations of 25OHD were obtained from 1873 participants (945 Uygur ethnic and 928 Kazak ethnic). The genotypes of 14 SNPs were measured for 300 Uygurs and 300 Kazaks. The median 25OHD concentration was as low as 10.4 ng/ml in Uygurs and 16.2 ng/ml in Kazaks. In Uygurs, the prevalence of vitamin D deficiency, in-sufficiency, and sufficiency was 91.2%, 5.8%, and 3.0%, respectively. CYP2R1-rs10766197 was significantly associated with the presence of vitamin D deficiency in the Uygur ethnic population (P=0.019, OR=6.533, 95%C.I.: 361-31.357), while DHCR7/NADSYN1-rs12785878 was significantly associated with the presence of vitamin D deficiency in the Kazak ethnic population (P=0.011, OR=2.442, 95%C.I.: 1.224-4.873). Of 10 SNPs in VDR and GC genes, none was associated with vitamin D status in these 2 ethnic populations.
Question: Does vitamin D Deficiency in Uygurs and Kazaks be Associated with Polymorphisms in CYP2R1 and DHCR7/NADSYN1 Genes?
Output:
|
PubmedQA201264
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Glucose transport and metabolism are highly specialized in hepatocytes. Actin cytoskeleton is fundamental to the maintenance of their morphology as well as to ensure their functionality. Here we study the effect of the actin disrupting natural compounds cytochalasin B and latrunculin A on the glucose metabolism of the Clone 9 rat hepatocytes once the glucose molecule is inside them and the effects of two hormones which main function is regulating the glucose metabolism on the actin cytoskeleton of Clone 9 cells. F-actin was labeled by using Oregon Green 514 ® phalloidin and glucose inside cells was monitored with the fluorescent D-glucose derivative; 2-NBDG. Observations and measurements were carried out by using a confocal microscope. Nor insulin neither glucagon was able to induce any significant effect in the quantity of F-actin present on Clone 9 cells. But insulin triggers a strong reorganization on the pattern of distribution of F-actin. However, the actin cytoskeleton disruption induced by CB and more efficiently by Lat A caused accumulation of 2-NBDG in cells.\n Question: Does disruption of the actin cytoskeleton induce fluorescent glucose accumulation on the rat hepatocytes Clone 9?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Glucose transport and metabolism are highly specialized in hepatocytes. Actin cytoskeleton is fundamental to the maintenance of their morphology as well as to ensure their functionality. Here we study the effect of the actin disrupting natural compounds cytochalasin B and latrunculin A on the glucose metabolism of the Clone 9 rat hepatocytes once the glucose molecule is inside them and the effects of two hormones which main function is regulating the glucose metabolism on the actin cytoskeleton of Clone 9 cells. F-actin was labeled by using Oregon Green 514 ® phalloidin and glucose inside cells was monitored with the fluorescent D-glucose derivative; 2-NBDG. Observations and measurements were carried out by using a confocal microscope. Nor insulin neither glucagon was able to induce any significant effect in the quantity of F-actin present on Clone 9 cells. But insulin triggers a strong reorganization on the pattern of distribution of F-actin. However, the actin cytoskeleton disruption induced by CB and more efficiently by Lat A caused accumulation of 2-NBDG in cells.
Question: Does disruption of the actin cytoskeleton induce fluorescent glucose accumulation on the rat hepatocytes Clone 9?
Output:
|
PubmedQA181082
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Dedicated cardiac cameras offer improved sensitivity over conventional SPECT cameras. Sensitivity gains are obtained by large numbers of detectors and novel collimator arrangements such as an array of multiple pinholes that focus on the heart. Pinholes lead to variable amounts of attenuation as a source is moved within the camera field of view. This study evaluated the effects of this variable attenuation on myocardial SPECT images. Computer simulations were performed for a set of nine point sources distributed in the left ventricular wall (LV). Sources were placed at the location of the heart in both an anthropomorphic and a water-cylinder computer phantom. Sources were translated in x, y, and z by up to 5 cm from the center. Projections were simulated with and without attenuation and the changes in attenuation were compared. A LV with an inferior wall defect was also simulated in both phantoms over the same range of positions. Real camera data were acquired on a Discovery NM530c camera (GE Healthcare, Haifa, Israel) for five min in list-mode using an anthropomorphic phantom (DataSpectrum, Durham, NC) with 100 MBq of Tc-99m in the LV. Images were taken over the same range of positions as the simulations and were compared based on the summed perfusion score (SPS), defect width, and apparent defect uptake for each position. Point sources in the water phantom showed absolute changes in attenuation of ≤8% over the range of positions and relative changes of ≤5% compared to the apex. In the anthropomorphic computer simulations, absolute change increased to 20%. The changes in relative attenuation caused a change in SPS of <1.5 for the water phantom but up to 4.2 in the anthropomorphic phantom. Changes were larger for axial than for transverse translations. These results were supported by SPS changes of up to six seen in the physical anthropomorphic phantom for axial translations. Defect width was also seen to significantly increase. The position-dependent changes were removed with attenuation correction.\n Question: Does patient position alter attenuation effects in multipinhole cardiac SPECT?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Dedicated cardiac cameras offer improved sensitivity over conventional SPECT cameras. Sensitivity gains are obtained by large numbers of detectors and novel collimator arrangements such as an array of multiple pinholes that focus on the heart. Pinholes lead to variable amounts of attenuation as a source is moved within the camera field of view. This study evaluated the effects of this variable attenuation on myocardial SPECT images. Computer simulations were performed for a set of nine point sources distributed in the left ventricular wall (LV). Sources were placed at the location of the heart in both an anthropomorphic and a water-cylinder computer phantom. Sources were translated in x, y, and z by up to 5 cm from the center. Projections were simulated with and without attenuation and the changes in attenuation were compared. A LV with an inferior wall defect was also simulated in both phantoms over the same range of positions. Real camera data were acquired on a Discovery NM530c camera (GE Healthcare, Haifa, Israel) for five min in list-mode using an anthropomorphic phantom (DataSpectrum, Durham, NC) with 100 MBq of Tc-99m in the LV. Images were taken over the same range of positions as the simulations and were compared based on the summed perfusion score (SPS), defect width, and apparent defect uptake for each position. Point sources in the water phantom showed absolute changes in attenuation of ≤8% over the range of positions and relative changes of ≤5% compared to the apex. In the anthropomorphic computer simulations, absolute change increased to 20%. The changes in relative attenuation caused a change in SPS of <1.5 for the water phantom but up to 4.2 in the anthropomorphic phantom. Changes were larger for axial than for transverse translations. These results were supported by SPS changes of up to six seen in the physical anthropomorphic phantom for axial translations. Defect width was also seen to significantly increase. The position-dependent changes were removed with attenuation correction.
Question: Does patient position alter attenuation effects in multipinhole cardiac SPECT?
Output:
|
PubmedQA66410
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Inactivating heterozygous mutations in the GCK gene are a common cause of MODY and result in mild fasting hyperglycaemia, which does not require treatment. We aimed to identify the frequency, clinical and molecular features of GCK mutations in a Turkish paediatric cohort. Fifty-four unrelated probands were selected based on the following criteria: age of diagnosis ≤17 years, family history of diabetes in at least two generations, anti-GAD/ICA negative, BMI<95.p and follow-up with diet, oral antidiabetic drug or low-dose insulin treatment (≤0·5U/kg/d). A MODY probability score (www.diabetesgenes.org) was calculated and 21 patients with a score ≥75%, HbA1c levels ≤7·5% (58·5 mmol/mol) and fasting blood glucose (FBG) levels 99-145 mg/dl (5·5-8·0 mmol/l) were selected for Sanger sequencing of the GCK gene. Targeted next-generation sequencing for all known monogenic diabetes genes was undertaken for any patient without a GCK gene mutation. GCK gene mutations (pathogenic or likely pathogenic variants) and a novel intronic variant of uncertain significance (c.208 + 3A>T) were identified in 13/54 probands (24%). Twelve of these patients had a MODY probability score ≥75%. FBG level and 2-h glucose level in OGTT were 123 ± 14 mg/dl (6·8 ± 0·7 mmol/l) (107-157 mg/dl) and 181 ± 30 mg/dl (10·1 ± 1·6 mmol/l) (136-247 mg/dl), respectively. Average of glucose increment in OGTT was 58 ± 27 mg/dl (3·2 ± 1·5 mmol/l) (19-120 mg/dl), and mean HbA1c level was 6·5 ± 0·5% (47·5 ± 5·5 mmol/mol) (5·9-7·6%). Five novel missense mutations were identified (p.F123S, p.L58P, p.G246A, p.F419C, and p.S151C). Two patients treated with low-dose insulin before the molecular analysis were able to stop treatment.\n Question: Are gCK gene mutations a common cause of childhood-onset MODY ( maturity-onset diabetes of the young ) in Turkey?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Inactivating heterozygous mutations in the GCK gene are a common cause of MODY and result in mild fasting hyperglycaemia, which does not require treatment. We aimed to identify the frequency, clinical and molecular features of GCK mutations in a Turkish paediatric cohort. Fifty-four unrelated probands were selected based on the following criteria: age of diagnosis ≤17 years, family history of diabetes in at least two generations, anti-GAD/ICA negative, BMI<95.p and follow-up with diet, oral antidiabetic drug or low-dose insulin treatment (≤0·5U/kg/d). A MODY probability score (www.diabetesgenes.org) was calculated and 21 patients with a score ≥75%, HbA1c levels ≤7·5% (58·5 mmol/mol) and fasting blood glucose (FBG) levels 99-145 mg/dl (5·5-8·0 mmol/l) were selected for Sanger sequencing of the GCK gene. Targeted next-generation sequencing for all known monogenic diabetes genes was undertaken for any patient without a GCK gene mutation. GCK gene mutations (pathogenic or likely pathogenic variants) and a novel intronic variant of uncertain significance (c.208 + 3A>T) were identified in 13/54 probands (24%). Twelve of these patients had a MODY probability score ≥75%. FBG level and 2-h glucose level in OGTT were 123 ± 14 mg/dl (6·8 ± 0·7 mmol/l) (107-157 mg/dl) and 181 ± 30 mg/dl (10·1 ± 1·6 mmol/l) (136-247 mg/dl), respectively. Average of glucose increment in OGTT was 58 ± 27 mg/dl (3·2 ± 1·5 mmol/l) (19-120 mg/dl), and mean HbA1c level was 6·5 ± 0·5% (47·5 ± 5·5 mmol/mol) (5·9-7·6%). Five novel missense mutations were identified (p.F123S, p.L58P, p.G246A, p.F419C, and p.S151C). Two patients treated with low-dose insulin before the molecular analysis were able to stop treatment.
Question: Are gCK gene mutations a common cause of childhood-onset MODY ( maturity-onset diabetes of the young ) in Turkey?
Output:
|
PubmedQA3089
|
[
{
"role": "user",
"content": "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 DNA-methylation levels in the newly described MEG8 differentially methylated region (DMR) in the imprinted cluster in 14q32 in patients with Temple syndrome. We included three patients with Temple syndrome which were studied by Infinium HumanMethylation450 BeadChips, locus-specific bisulfite-pyrosequencing, methylation-specific-MLPA and microsatellite analyses. The tag-CpG of the MEG8-DMR was investigated using the Infinium HumanMethylation450 BeadChip. In all three patients, the identical pattern of DNA-hypermethylation of the MEG8-DMR was observed along with DNA-hypomethylation of the IG-DMR and MEG3-DMR.\n Question: Is the differentially methylated region of MEG8 hypermethylated in patients with Temple syndrome?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To investigate the DNA-methylation levels in the newly described MEG8 differentially methylated region (DMR) in the imprinted cluster in 14q32 in patients with Temple syndrome. We included three patients with Temple syndrome which were studied by Infinium HumanMethylation450 BeadChips, locus-specific bisulfite-pyrosequencing, methylation-specific-MLPA and microsatellite analyses. The tag-CpG of the MEG8-DMR was investigated using the Infinium HumanMethylation450 BeadChip. In all three patients, the identical pattern of DNA-hypermethylation of the MEG8-DMR was observed along with DNA-hypomethylation of the IG-DMR and MEG3-DMR.
Question: Is the differentially methylated region of MEG8 hypermethylated in patients with Temple syndrome?
Output:
|
PubmedQA60741
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Gluten (GLU)-specific T-cell responses in HLA-DQ2 positive adult celiac disease (CD) patients are directed to an immunodominant alpha-gliadin (GLIA) peptide that requires deamidation for T-cell recognition. The aim of the current study was to determine which GLU peptide(s) are involved early in disease. We have characterized the GLU-specific T-cell response in HLA-DQ2 positive children with recent onset CD. We found that 50% of these patients do not respond to the alpha-GLIA peptide but to a diverse set of GLIA and glutenin (GLT) peptides, including 6 novel epitopes. Moreover, individual patients respond to distinct (combinations of) GLU peptides. T-cell cross-reactivity toward homologous GLIA and GLT peptides was observed, which might play a role in the initial spreading of the GLU-specific T-cell response. Although all pediatric patients displayed deamidation-dependent responses, deamidation-independent responses were found in the majority of patients as well. Finally, T-cell responses to 3 of these novel GLU peptides were found in adult CD patients.\n Question: Is the gluten response in children with celiac disease directed toward multiple gliadin and glutenin peptides?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Gluten (GLU)-specific T-cell responses in HLA-DQ2 positive adult celiac disease (CD) patients are directed to an immunodominant alpha-gliadin (GLIA) peptide that requires deamidation for T-cell recognition. The aim of the current study was to determine which GLU peptide(s) are involved early in disease. We have characterized the GLU-specific T-cell response in HLA-DQ2 positive children with recent onset CD. We found that 50% of these patients do not respond to the alpha-GLIA peptide but to a diverse set of GLIA and glutenin (GLT) peptides, including 6 novel epitopes. Moreover, individual patients respond to distinct (combinations of) GLU peptides. T-cell cross-reactivity toward homologous GLIA and GLT peptides was observed, which might play a role in the initial spreading of the GLU-specific T-cell response. Although all pediatric patients displayed deamidation-dependent responses, deamidation-independent responses were found in the majority of patients as well. Finally, T-cell responses to 3 of these novel GLU peptides were found in adult CD patients.
Question: Is the gluten response in children with celiac disease directed toward multiple gliadin and glutenin peptides?
Output:
|
PubmedQA168334
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Pigmented villonodular synovitis (PVNS) is a rare proliferative disorder of the synovium with locally aggressive behavior. We reviewed our experience using radiation therapy in the treatment of PVNS. Seventeen patients with 18 sites of PVNS were treated with radiation between 1993 and 2007. Cases were retrospectively reviewed for patient information, treatment parameters, complications, and outcome. Seven sites were primary presentations and 11 were recurrent with an average of 2.5 prior surgical interventions. The most common location was the knee joint (67%). Cytoreductive surgery was performed before radiation therapy in 16/18 sites with all having proven or suspected residual disease. Radiation was delivered using 4-15 MV photons with an average total dose 34 Gy (range, 20-36 Gy). Seventeen of 18 sites (94%) had postradiotherapy imaging. With average follow-up of 46 months (range, 8-181 months), initial local control was achieved in 75% (12/16) of the sites with prior cytoreductive surgery (mean time to recurrence, 38 months). Ultimate local control was 100% after repeat resection (mean follow-up, 61 months). Two additional sites without prior cytoreductive surgery showed growth after radiotherapy (mean time to documented growth, 10.5 months). Seventeen of the 18 involved joints (94%) were scored as excellent or good PVNS-related function, one site (5%) as fair function, and no site with poor function. No patient required amputation; and there were no Grade 3/4 treatment-related complications.\n Question: Does external beam radiation therapy enhance local control in pigmented villonodular synovitis?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Pigmented villonodular synovitis (PVNS) is a rare proliferative disorder of the synovium with locally aggressive behavior. We reviewed our experience using radiation therapy in the treatment of PVNS. Seventeen patients with 18 sites of PVNS were treated with radiation between 1993 and 2007. Cases were retrospectively reviewed for patient information, treatment parameters, complications, and outcome. Seven sites were primary presentations and 11 were recurrent with an average of 2.5 prior surgical interventions. The most common location was the knee joint (67%). Cytoreductive surgery was performed before radiation therapy in 16/18 sites with all having proven or suspected residual disease. Radiation was delivered using 4-15 MV photons with an average total dose 34 Gy (range, 20-36 Gy). Seventeen of 18 sites (94%) had postradiotherapy imaging. With average follow-up of 46 months (range, 8-181 months), initial local control was achieved in 75% (12/16) of the sites with prior cytoreductive surgery (mean time to recurrence, 38 months). Ultimate local control was 100% after repeat resection (mean follow-up, 61 months). Two additional sites without prior cytoreductive surgery showed growth after radiotherapy (mean time to documented growth, 10.5 months). Seventeen of the 18 involved joints (94%) were scored as excellent or good PVNS-related function, one site (5%) as fair function, and no site with poor function. No patient required amputation; and there were no Grade 3/4 treatment-related complications.
Question: Does external beam radiation therapy enhance local control in pigmented villonodular synovitis?
Output:
|
PubmedQA194314
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: More superficially located tumors may be more likely than deeper tumors to metastasize to the axillary nodes via the lymphatics. The aim of this study was to determine whether breast cancer distance from the skin affects axillary node metastasis, ipsilateral breast cancer recurrence, or recurrence-free survival. A total of 1,005 consecutive patients with breast cancer who underwent surgery between January 2003 and December 2009 were selected. The distance of the tumor from the skin was measured from the skin to the most anterior hypoechoic leading edge of the lesion. In total, 603 (68%) patients had no axillary nodal metastasis, and 288 (32%) had axillary nodal metastasis. A breast cancer distance from the skin <3 mm induced more axillary nodal metastasis (P = 0.039). However, no significant correlation was observed between breast cancer distance from the skin <3 mm and ipsilateral breast cancer recurrence (P = 0.788) or recurrence-free survival (P = 0.353).\n Question: Is the distance between breast cancer and the skin associated with axillary nodal metastasis?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: More superficially located tumors may be more likely than deeper tumors to metastasize to the axillary nodes via the lymphatics. The aim of this study was to determine whether breast cancer distance from the skin affects axillary node metastasis, ipsilateral breast cancer recurrence, or recurrence-free survival. A total of 1,005 consecutive patients with breast cancer who underwent surgery between January 2003 and December 2009 were selected. The distance of the tumor from the skin was measured from the skin to the most anterior hypoechoic leading edge of the lesion. In total, 603 (68%) patients had no axillary nodal metastasis, and 288 (32%) had axillary nodal metastasis. A breast cancer distance from the skin <3 mm induced more axillary nodal metastasis (P = 0.039). However, no significant correlation was observed between breast cancer distance from the skin <3 mm and ipsilateral breast cancer recurrence (P = 0.788) or recurrence-free survival (P = 0.353).
Question: Is the distance between breast cancer and the skin associated with axillary nodal metastasis?
Output:
|
PubmedQA115080
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Enhanced secretion of type-2 T-helper (Th2) cytokine is a characteristic feature in normal physiological pregnancy. A study has demonstrated defective production of interleukine-4 (IL-4) and other Th2 cytokine in women with recurrent pregnancy loss (RPL). Several studies have suggested that IL-4 variable number of tandem repeat (VNTR) gene polymorphism is probably associated with different IL-4 production. The IL-4 VNTR genotypes were assessed in 109 Japanese women with RPL and 210 ethnically matched women experiencing at least one live birth and no spontaneous abortion. No significant differences in IL-4 VNTR genotype frequencies were found between the RPL and the control [B1B1 genotype (reference); B1/B2 and B2/B2 genotypes, odds ratio, 0.91; 95% confidence interval, 0.58-1.45].\n Question: Is interleukin-4 gene polymorphism involved in the risk of recurrent pregnancy loss?\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: Enhanced secretion of type-2 T-helper (Th2) cytokine is a characteristic feature in normal physiological pregnancy. A study has demonstrated defective production of interleukine-4 (IL-4) and other Th2 cytokine in women with recurrent pregnancy loss (RPL). Several studies have suggested that IL-4 variable number of tandem repeat (VNTR) gene polymorphism is probably associated with different IL-4 production. The IL-4 VNTR genotypes were assessed in 109 Japanese women with RPL and 210 ethnically matched women experiencing at least one live birth and no spontaneous abortion. No significant differences in IL-4 VNTR genotype frequencies were found between the RPL and the control [B1B1 genotype (reference); B1/B2 and B2/B2 genotypes, odds ratio, 0.91; 95% confidence interval, 0.58-1.45].
Question: Is interleukin-4 gene polymorphism involved in the risk of recurrent pregnancy loss?
Output:
|
PubmedQA76133
|
[
{
"role": "user",
"content": "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 combination of radiotherapy and good quality surgery reduces local recurrence rate for rectal cancer patients. This study assesses the prognostic value of both intrinsic and radiotherapy-induced apoptosis and evaluates the relevance of radiotherapy for outcome of rectal cancer patients. Tumor samples (1,198) were available from the Dutch Total Mesorectal Excision trial, in which rectal cancer patients were treated with standardized surgery and randomized for preoperative short-term radiotherapy or not. Tumor samples were obtained at time of surgery. Tissue microarrays were constructed and stained with the active caspase-specific M30 antibody to determine the amount of apoptotic epithelial tumor cells. Nonirradiated patients with a negative circumferential margin displaying lower than median levels of apoptosis developed more local recurrences (10.5% versus 6.1%; P=0.06) and more rapidly after surgery than patients with high intrinsic apoptosis in their tumors (median time to recurrence, 13.0 versus 21.3 months; P=0.04). In multivariate analysis, intrinsic apoptosis was an independent predictor for the development of local recurrences (hazard ratio, 2.0; P=0.05). Radiotherapy increased apoptosis level (11 versus 23 apoptotic cells/mm2 tumor epithelium; P<0.001), but this apoptosis did not influence patients' prognosis.\n Question: Is prognostic value of apoptosis in rectal cancer patients of the dutch total mesorectal excision trial : radiotherapy redundant in intrinsically high-apoptotic tumors?\n Output: "
},
{
"role": "assistant",
"content": "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 combination of radiotherapy and good quality surgery reduces local recurrence rate for rectal cancer patients. This study assesses the prognostic value of both intrinsic and radiotherapy-induced apoptosis and evaluates the relevance of radiotherapy for outcome of rectal cancer patients. Tumor samples (1,198) were available from the Dutch Total Mesorectal Excision trial, in which rectal cancer patients were treated with standardized surgery and randomized for preoperative short-term radiotherapy or not. Tumor samples were obtained at time of surgery. Tissue microarrays were constructed and stained with the active caspase-specific M30 antibody to determine the amount of apoptotic epithelial tumor cells. Nonirradiated patients with a negative circumferential margin displaying lower than median levels of apoptosis developed more local recurrences (10.5% versus 6.1%; P=0.06) and more rapidly after surgery than patients with high intrinsic apoptosis in their tumors (median time to recurrence, 13.0 versus 21.3 months; P=0.04). In multivariate analysis, intrinsic apoptosis was an independent predictor for the development of local recurrences (hazard ratio, 2.0; P=0.05). Radiotherapy increased apoptosis level (11 versus 23 apoptotic cells/mm2 tumor epithelium; P<0.001), but this apoptosis did not influence patients' prognosis.
Question: Is prognostic value of apoptosis in rectal cancer patients of the dutch total mesorectal excision trial : radiotherapy redundant in intrinsically high-apoptotic tumors?
Output:
|
PubmedQA148400
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Glucokinase encoded by GCK is a key enzyme that facilitates phosphorylation of glucose to glucose-6-phosphate. Variants of GCK gene were shown to be associated with type 2 diabetes (T2D) and coronary heart disease (CHD). The goal of this study was to investigate the contribution of GCK gene-body methylation to the risk of CHD. 36 patients (18 males and 18 females) and 36 age- and sex-matched controls were collected for the current methylation research. DNA methylation level of the CpG island (CGI) region on the GCK gene-body was measured through the sodium bisulfite DNA conversion and pyrosequencing technology. Our results indicated that CHD cases have a much lower methylation level (49.77 ± 6.43%) compared with controls (54.47 ± 7.65%, P = 0.018). In addition, GCK gene-body methylation was found to be positively associated with aging in controls (r = 0.443, P = 0.010).\n Question: Is gCK gene-body hypomethylation associated with the risk of coronary heart 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: Glucokinase encoded by GCK is a key enzyme that facilitates phosphorylation of glucose to glucose-6-phosphate. Variants of GCK gene were shown to be associated with type 2 diabetes (T2D) and coronary heart disease (CHD). The goal of this study was to investigate the contribution of GCK gene-body methylation to the risk of CHD. 36 patients (18 males and 18 females) and 36 age- and sex-matched controls were collected for the current methylation research. DNA methylation level of the CpG island (CGI) region on the GCK gene-body was measured through the sodium bisulfite DNA conversion and pyrosequencing technology. Our results indicated that CHD cases have a much lower methylation level (49.77 ± 6.43%) compared with controls (54.47 ± 7.65%, P = 0.018). In addition, GCK gene-body methylation was found to be positively associated with aging in controls (r = 0.443, P = 0.010).
Question: Is gCK gene-body hypomethylation associated with the risk of coronary heart disease?
Output:
|
PubmedQA170236
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Multi-marker approaches for risk prediction in coronary artery disease (CAD) have been inconsistent due to biased selection of specific know biomarkers. We have assessed the global proteome of CAD-affected and unaffected subjects, and developed a pathway network model for elucidating the mechanism and risk prediction for CAD. A total of 252 samples (112 CAD-affected without family history and 140 true controls) were analyzed by Surface-Enhanced Laser Desorption/Ionization Time of Flight Mass Spectrometry (SELDI-TOF-MS) by using CM10 cationic chips and bioinformatics tools. Out of 36 significant peaks in SELDI-TOF MS, nine peaks could do better discrimination of CAD subjects and controls (area under the curve (AUC) of 0.963) based on the Support Vector Machine (SVM) feature selection method. Of the nine peaks used in the model for discrimination of CAD-affected and unaffected, the m/z corresponding to 22,859 was identified as stress-related protein HSP27 and was shown to be highly associated with CAD (odds ratio of 3.47). The 36 biomarker peaks were identified and a network profile was constructed showing the functional association between different pathways in CAD.\n Question: Do novel network biomarkers profile based coronary artery disease risk stratification in Asian Indians?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Multi-marker approaches for risk prediction in coronary artery disease (CAD) have been inconsistent due to biased selection of specific know biomarkers. We have assessed the global proteome of CAD-affected and unaffected subjects, and developed a pathway network model for elucidating the mechanism and risk prediction for CAD. A total of 252 samples (112 CAD-affected without family history and 140 true controls) were analyzed by Surface-Enhanced Laser Desorption/Ionization Time of Flight Mass Spectrometry (SELDI-TOF-MS) by using CM10 cationic chips and bioinformatics tools. Out of 36 significant peaks in SELDI-TOF MS, nine peaks could do better discrimination of CAD subjects and controls (area under the curve (AUC) of 0.963) based on the Support Vector Machine (SVM) feature selection method. Of the nine peaks used in the model for discrimination of CAD-affected and unaffected, the m/z corresponding to 22,859 was identified as stress-related protein HSP27 and was shown to be highly associated with CAD (odds ratio of 3.47). The 36 biomarker peaks were identified and a network profile was constructed showing the functional association between different pathways in CAD.
Question: Do novel network biomarkers profile based coronary artery disease risk stratification in Asian Indians?
Output:
|
PubmedQA187377
|
[
{
"role": "user",
"content": "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 compare two different microelectrode materials--the conductive polymer composite poly-3,4-ethylenedioxythiophene (PEDOT)-carbon nanotube(CNT) and titanium nitride (TiN)--at activating spikes in retinal ganglion cells in whole mount rat retina through stimulation of the local retinal network. Stimulation efficacy of the microelectrodes was analyzed by comparing voltage, current and transferred charge at stimulation threshold. Retinal ganglion cell spikes were recorded by a central electrode (30 μm diameter) in the planar grid of an electrode array. Extracellular stimulation (monophasic, cathodic, 0.1-1.0 ms) of the retinal network was performed using constant voltage pulses applied to the eight surrounding electrodes. The stimulation electrodes were equally spaced on the four sides of a square (400 × 400 μm). Threshold voltage was determined as the pulse amplitude required to evoke network-mediated ganglion cell spiking in a defined post stimulus time window in 50% of identical stimulus repetitions. For the two electrode materials threshold voltage, transferred charge at threshold, maximum current and the residual current at the end of the pulse were compared. Stimulation of retinal interneurons using PEDOT-CNT electrodes is achieved with lower stimulation voltage and requires lower charge transfer as compared to TiN. The key parameter for effective stimulation is a constant current over at least 0.5 ms, which is obtained by PEDOT-CNT electrodes at lower stimulation voltage due to its faradaic charge transfer mechanism.\n Question: Do pEDOT-CNT coated electrodes stimulate retinal neurons at low voltage amplitudes and low charge densities?\n Output: "
},
{
"role": "assistant",
"content": "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 compare two different microelectrode materials--the conductive polymer composite poly-3,4-ethylenedioxythiophene (PEDOT)-carbon nanotube(CNT) and titanium nitride (TiN)--at activating spikes in retinal ganglion cells in whole mount rat retina through stimulation of the local retinal network. Stimulation efficacy of the microelectrodes was analyzed by comparing voltage, current and transferred charge at stimulation threshold. Retinal ganglion cell spikes were recorded by a central electrode (30 μm diameter) in the planar grid of an electrode array. Extracellular stimulation (monophasic, cathodic, 0.1-1.0 ms) of the retinal network was performed using constant voltage pulses applied to the eight surrounding electrodes. The stimulation electrodes were equally spaced on the four sides of a square (400 × 400 μm). Threshold voltage was determined as the pulse amplitude required to evoke network-mediated ganglion cell spiking in a defined post stimulus time window in 50% of identical stimulus repetitions. For the two electrode materials threshold voltage, transferred charge at threshold, maximum current and the residual current at the end of the pulse were compared. Stimulation of retinal interneurons using PEDOT-CNT electrodes is achieved with lower stimulation voltage and requires lower charge transfer as compared to TiN. The key parameter for effective stimulation is a constant current over at least 0.5 ms, which is obtained by PEDOT-CNT electrodes at lower stimulation voltage due to its faradaic charge transfer mechanism.
Question: Do pEDOT-CNT coated electrodes stimulate retinal neurons at low voltage amplitudes and low charge densities?
Output:
|
PubmedQA38174
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Ulceration is a common feature of inflammatory bowel diseases, where subepithelial cell growth is frequently necessary for resolution. In order to further understand the role of colonic fibroblasts in this process, we have used an in vitro model of wound repair to study the response of human colonic fibroblasts to several growth factors expressed in colonic tissues. Proliferation was determined by [(3)H]thymidine incorporation into DNA in subconfluent fibroblast cultures. In vitro wound repair was determined in confluent fibroblast monolayers after mechanical denudation. The presence of growth factors secreted by fibroblasts was studied in conditioned medium by heparin affinity chromatography and immunodetection with specific antibodies. Serum and platelet-derived growth factor (PDGF-BB) induced a dramatic increase in both colonic fibroblast proliferation and closure of wounded cell monolayers. Epidermal growth factor (EGF) stimulated both fibroblast activities, but the effect was less potent. However, colonic fibroblasts did not respond to transforming growth factor-beta(1). Conditioned medium stimulated fibroblast proliferation and wound repair activity, which was reverted by the addition of suramin. Furthermore, a PDGF-like factor was isolated from colonic fibroblast-conditioned medium.\n Question: Do platelet-derived growth factor and epidermal growth factor play a major role in human colonic fibroblast repair 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: Ulceration is a common feature of inflammatory bowel diseases, where subepithelial cell growth is frequently necessary for resolution. In order to further understand the role of colonic fibroblasts in this process, we have used an in vitro model of wound repair to study the response of human colonic fibroblasts to several growth factors expressed in colonic tissues. Proliferation was determined by [(3)H]thymidine incorporation into DNA in subconfluent fibroblast cultures. In vitro wound repair was determined in confluent fibroblast monolayers after mechanical denudation. The presence of growth factors secreted by fibroblasts was studied in conditioned medium by heparin affinity chromatography and immunodetection with specific antibodies. Serum and platelet-derived growth factor (PDGF-BB) induced a dramatic increase in both colonic fibroblast proliferation and closure of wounded cell monolayers. Epidermal growth factor (EGF) stimulated both fibroblast activities, but the effect was less potent. However, colonic fibroblasts did not respond to transforming growth factor-beta(1). Conditioned medium stimulated fibroblast proliferation and wound repair activity, which was reverted by the addition of suramin. Furthermore, a PDGF-like factor was isolated from colonic fibroblast-conditioned medium.
Question: Do platelet-derived growth factor and epidermal growth factor play a major role in human colonic fibroblast repair activities?
Output:
|
PubmedQA173556
|
[
{
"role": "user",
"content": "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 healthy subjects, observation of actions activates a motor network similar to that involved in the performance of the observed actions. Movement observation could perhaps be applied to functionally sustain brain motor functions when efferent motor commands and proprioceptive feedbacks are disconnected. The authors examined whether observation-induced brain activation is preserved in people with chronic complete spinal cord injury (SCI). Nine patients and 12 healthy subjects underwent behavioral assessment and functional magnetic resonance imaging. The SCI patients attempted to perform dorsal and plantar flexions of the right foot, and the controls also executed the same movement. Both groups observed subsequent video clips showing the same movement. In the SCI group, attempted and observed foot movements activated a common observation-execution network including ventral premotor, parietal cortex, and cerebellum as in healthy subjects.\n Question: Does movement observation activate lower limb motor networks in chronic complete paraplegia?\n Output: "
},
{
"role": "assistant",
"content": "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 healthy subjects, observation of actions activates a motor network similar to that involved in the performance of the observed actions. Movement observation could perhaps be applied to functionally sustain brain motor functions when efferent motor commands and proprioceptive feedbacks are disconnected. The authors examined whether observation-induced brain activation is preserved in people with chronic complete spinal cord injury (SCI). Nine patients and 12 healthy subjects underwent behavioral assessment and functional magnetic resonance imaging. The SCI patients attempted to perform dorsal and plantar flexions of the right foot, and the controls also executed the same movement. Both groups observed subsequent video clips showing the same movement. In the SCI group, attempted and observed foot movements activated a common observation-execution network including ventral premotor, parietal cortex, and cerebellum as in healthy subjects.
Question: Does movement observation activate lower limb motor networks in chronic complete paraplegia?
Output:
|
PubmedQA78956
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The present study was carried out to evaluate antimicrobial and antioxidant activities from Eriobotrya japonica stems as well investigation of its chemical composition. Methanol 80% extract of Eriobotrya japonica stems was tested for antimicrobial activity against bacterial and fungal strains and for antioxidant activity using oxygen radical absorbance capacity (ORAC) and the trolox equivalent antioxidant capacity (TEAC) assays and also total content of polyphenols with phytochemical analysis of the extract were determined. The results showed that the extract has a significant antimicrobial activity, it inhibited significantly the growth of Candida albicans suggesting that it can be used in the treatment of fungal infections, and it showed no effect on the other bacterial and fungal strains, the extract has a good antioxidant activity, it has shown high values of oxygen radical absorbance capacity and trolox equivalent antioxidant capacity, while it showed a low value of polyphenol content. Phytochemical analysis of the extract showed the presence of carbohydrates, terpenes, tannins and flavonoids, further phytochemical analysis resulted in the isolation and identification of three triterpenic acids, oleanolic, ursolic and corosolic acids and four flavonoids, naringenin, quercetin, kaempferol 3-O-β-glucoside and quercetin 3-O-α-rhamnoside.\n Question: Does isolation and antimicrobial and antioxidant evaluation of bio-active compounds from eriobotrya japonica stem?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: The present study was carried out to evaluate antimicrobial and antioxidant activities from Eriobotrya japonica stems as well investigation of its chemical composition. Methanol 80% extract of Eriobotrya japonica stems was tested for antimicrobial activity against bacterial and fungal strains and for antioxidant activity using oxygen radical absorbance capacity (ORAC) and the trolox equivalent antioxidant capacity (TEAC) assays and also total content of polyphenols with phytochemical analysis of the extract were determined. The results showed that the extract has a significant antimicrobial activity, it inhibited significantly the growth of Candida albicans suggesting that it can be used in the treatment of fungal infections, and it showed no effect on the other bacterial and fungal strains, the extract has a good antioxidant activity, it has shown high values of oxygen radical absorbance capacity and trolox equivalent antioxidant capacity, while it showed a low value of polyphenol content. Phytochemical analysis of the extract showed the presence of carbohydrates, terpenes, tannins and flavonoids, further phytochemical analysis resulted in the isolation and identification of three triterpenic acids, oleanolic, ursolic and corosolic acids and four flavonoids, naringenin, quercetin, kaempferol 3-O-β-glucoside and quercetin 3-O-α-rhamnoside.
Question: Does isolation and antimicrobial and antioxidant evaluation of bio-active compounds from eriobotrya japonica stem?
Output:
|
PubmedQA145956
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Evidence varies on the relation between parity and urgency or urge incontinence (UUI). We used data from the General Longitudinal Overactive Bladder Evaluation to determine whether differences in case definitions could account for variation in findings. We simulated case criteria to correspond to studies of urgency, UUI, and parity using data from 1,880 patients. Logistic models were run for each case-control scenario corresponding to previously used case definitions. Parity was significantly associated with urgency (odds ratios (OR) 1.70; CI: 1.30-2.22) and UUI (odds ratios (OR) 1.87; CI: 1.34-2.60) only when the case criteria included individuals with stress incontinence (SUI). Parity was not associated with UUI when individuals with SUI were excluded or with urgency when individuals with incontinence were excluded.\n Question: Is parity associated with urgency with or without urinary incontinence?\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: Evidence varies on the relation between parity and urgency or urge incontinence (UUI). We used data from the General Longitudinal Overactive Bladder Evaluation to determine whether differences in case definitions could account for variation in findings. We simulated case criteria to correspond to studies of urgency, UUI, and parity using data from 1,880 patients. Logistic models were run for each case-control scenario corresponding to previously used case definitions. Parity was significantly associated with urgency (odds ratios (OR) 1.70; CI: 1.30-2.22) and UUI (odds ratios (OR) 1.87; CI: 1.34-2.60) only when the case criteria included individuals with stress incontinence (SUI). Parity was not associated with UUI when individuals with SUI were excluded or with urgency when individuals with incontinence were excluded.
Question: Is parity associated with urgency with or without urinary incontinence?
Output:
|
PubmedQA26642
|
[
{
"role": "user",
"content": "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 was discovered that Skin Cap (Cheminova Internacional S.A., Madrid, Spain), an over-the-counter psoriasis therapy with zinc pyrithione, contained clobetasol propionate and it was withdrawn from the market by the US Food and Drug Administration review. Some suggested that there might be a synergistic effect of zinc pyrithione with clobetasol propionate. We sought to evaluate the efficacy of clobetasol propionate 0.05% foam with and without the coadministration of a topical 0.25% zinc pyrithione spray in treating psoriasis involving sites other than the scalp. We conducted a randomized, double-blind, right/left study of patients with mild to moderate, generally symmetric, plaque-type psoriasis. Patients were assigned to treatment with clobetasol propionate foam on all psoriatic lesions and then randomly assigned to use zinc pyrithione spray to either the right or left side of their body (vehicle spray to be applied to the opposite side). There was a 2-week treatment phase (visits at baseline, week 1, and week 2) and a follow-up phase (visit at week 4), and all treatments were administered twice daily for 2 weeks. The primary outcome measure was the change from baseline to week 2 in the composite score of the signs of psoriasis (erythema, scaling, plaque thickness) for symmetric target lesions. A total of 25 patients were enrolled; 24 completed the trial and 1 was lost to follow up. Of those who completed the study, 63% (15 of 24) were men, and the mean age (+/-SD) was 50 years (+/-12.2). After 2 weeks of therapy, the average decline in the composite score was 3.5 (+/-1.8) for monotherapy (clobetasol propionate foam and vehicle) and, similarly, 3.3 (+/-1.8) for clobetasol propionate foam plus zinc pyrithione spray (P =.5).\n Question: Does the use of 0.25 % zinc pyrithione spray enhance the efficacy of clobetasol propionate 0.05 % foam in the treatment of psoriasis?\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 was discovered that Skin Cap (Cheminova Internacional S.A., Madrid, Spain), an over-the-counter psoriasis therapy with zinc pyrithione, contained clobetasol propionate and it was withdrawn from the market by the US Food and Drug Administration review. Some suggested that there might be a synergistic effect of zinc pyrithione with clobetasol propionate. We sought to evaluate the efficacy of clobetasol propionate 0.05% foam with and without the coadministration of a topical 0.25% zinc pyrithione spray in treating psoriasis involving sites other than the scalp. We conducted a randomized, double-blind, right/left study of patients with mild to moderate, generally symmetric, plaque-type psoriasis. Patients were assigned to treatment with clobetasol propionate foam on all psoriatic lesions and then randomly assigned to use zinc pyrithione spray to either the right or left side of their body (vehicle spray to be applied to the opposite side). There was a 2-week treatment phase (visits at baseline, week 1, and week 2) and a follow-up phase (visit at week 4), and all treatments were administered twice daily for 2 weeks. The primary outcome measure was the change from baseline to week 2 in the composite score of the signs of psoriasis (erythema, scaling, plaque thickness) for symmetric target lesions. A total of 25 patients were enrolled; 24 completed the trial and 1 was lost to follow up. Of those who completed the study, 63% (15 of 24) were men, and the mean age (+/-SD) was 50 years (+/-12.2). After 2 weeks of therapy, the average decline in the composite score was 3.5 (+/-1.8) for monotherapy (clobetasol propionate foam and vehicle) and, similarly, 3.3 (+/-1.8) for clobetasol propionate foam plus zinc pyrithione spray (P =.5).
Question: Does the use of 0.25 % zinc pyrithione spray enhance the efficacy of clobetasol propionate 0.05 % foam in the treatment of psoriasis?
Output:
|
PubmedQA86800
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Clinical use of cyclosporine (CsA) is limited by its known nephrotoxicity. Parathyroid hormone (PTH)-related protein (PTHrP) increases after acute renal ischemia and stimulates proliferation of renal cells in culture. Herein, we have examined whether the renal expression of PTHrP and its PTH/PTHrP receptor is affected by chronic CsA nephrotoxicity. Rats were randomly assigned to receive daily intramuscular injections of either CsA (25 mg/kg) or the same volume of the vehicle olive oil (control) for 3 weeks. At this time interval, under ether anesthesia, rat blood and kidneys were obtained for analytical determinations, and total RNA isolation or immunohistochemistry, respectively. Serum urea was 11+/-2 and 6+/-1 mmol/L (P < 0.01) in CsA-treated and control rats, respectively. We found that PTH/PTHrP receptor mRNA was unchanged, but PTHrP mRNA, and also transforming growth factor-beta1 mRNA expression as positive control, was about twofold increased in the kidney of CsA-treated rats. This was accompanied by increased PTHrP immunostaining in renal cortical tubules, associated with tubule vacuolation.\n Question: Does cyclosporine increase renal parathyroid hormone-related protein expression in vivo in the rat?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Clinical use of cyclosporine (CsA) is limited by its known nephrotoxicity. Parathyroid hormone (PTH)-related protein (PTHrP) increases after acute renal ischemia and stimulates proliferation of renal cells in culture. Herein, we have examined whether the renal expression of PTHrP and its PTH/PTHrP receptor is affected by chronic CsA nephrotoxicity. Rats were randomly assigned to receive daily intramuscular injections of either CsA (25 mg/kg) or the same volume of the vehicle olive oil (control) for 3 weeks. At this time interval, under ether anesthesia, rat blood and kidneys were obtained for analytical determinations, and total RNA isolation or immunohistochemistry, respectively. Serum urea was 11+/-2 and 6+/-1 mmol/L (P < 0.01) in CsA-treated and control rats, respectively. We found that PTH/PTHrP receptor mRNA was unchanged, but PTHrP mRNA, and also transforming growth factor-beta1 mRNA expression as positive control, was about twofold increased in the kidney of CsA-treated rats. This was accompanied by increased PTHrP immunostaining in renal cortical tubules, associated with tubule vacuolation.
Question: Does cyclosporine increase renal parathyroid hormone-related protein expression in vivo in the rat?
Output:
|
PubmedQA15720
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: HIV-infected subjects are at increased risk for myocardial infarction. The mechanism of this increased risk remains unclear. Since cytomegalovirus (CMV) infection has been associated with accelerated atherosclerosis in the transplant population and immune responses against CMV may be altered by HIV disease, we hypothesized that enhanced T-cell responses against CMV would be associated with increased atherosclerosis in subjects with HIV. We measured high-sensitivity C-reactive protein (hs-CRP), T-cell activation, CMV-specific T-cell responses, and carotid artery intima-media thickness (IMT) in 93 HIV-infected subjects and in 37 uninfected controls. The mean age of the HIV-infected subjects was 48 years and 85 (91%) were male. The median carotid IMT was higher in the HIV-infected group compared to the uninfected group (0.95 mm versus 0.68 mm, P < 0.001). This difference remained significant after controlling for all traditional risk factors. Compared to HIV-negative controls, HIV-infected subjects had higher median levels of hs-CRP (P = 0.05), higher levels of CD4 and CD8 T-cell activation (P < 0.0001) and higher CMV-specific interferon-gamma CD8 T-cell responses (P < 0.0001). CMV-specific T-cell responses, but not hs-CRP and T-cell activation, were independently associated with higher carotid IMT (P = 0.001).\n Question: Is increased carotid intima-media thickness in HIV patients associated with increased cytomegalovirus-specific T-cell responses?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: HIV-infected subjects are at increased risk for myocardial infarction. The mechanism of this increased risk remains unclear. Since cytomegalovirus (CMV) infection has been associated with accelerated atherosclerosis in the transplant population and immune responses against CMV may be altered by HIV disease, we hypothesized that enhanced T-cell responses against CMV would be associated with increased atherosclerosis in subjects with HIV. We measured high-sensitivity C-reactive protein (hs-CRP), T-cell activation, CMV-specific T-cell responses, and carotid artery intima-media thickness (IMT) in 93 HIV-infected subjects and in 37 uninfected controls. The mean age of the HIV-infected subjects was 48 years and 85 (91%) were male. The median carotid IMT was higher in the HIV-infected group compared to the uninfected group (0.95 mm versus 0.68 mm, P < 0.001). This difference remained significant after controlling for all traditional risk factors. Compared to HIV-negative controls, HIV-infected subjects had higher median levels of hs-CRP (P = 0.05), higher levels of CD4 and CD8 T-cell activation (P < 0.0001) and higher CMV-specific interferon-gamma CD8 T-cell responses (P < 0.0001). CMV-specific T-cell responses, but not hs-CRP and T-cell activation, were independently associated with higher carotid IMT (P = 0.001).
Question: Is increased carotid intima-media thickness in HIV patients associated with increased cytomegalovirus-specific T-cell responses?
Output:
|
PubmedQA26418
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Nephrotoxicity of calcineurin inhibitors (CNIs) is partially responsible for the development of chronic allograft nephropathy (CAN). Sirolimus has demonstrated its potential to substitute for CNIs because it lacks significant nephrotoxicity and shows a short-term immunosuppressive capacity comparable with that of cyclosporine. This results in the maintenance of better renal function when cyclosporine is eliminated, but it has not been demonstrated whether this benefit is associated with an improvement in the pathologic substrate and a reduction in CAN. We analyzed pretransplant and 1-year renal-allograft biopsies from 64 patients enrolled in a multicenter trial. Patients received cyclosporine and sirolimus during the first 3 months after transplant and were then randomly assigned to continue with cyclosporine or have it withdrawn. Histologic chronic allograft lesions were compared between groups. The percentage of patients in whom chronic pathologic lesions progressed was lower in the group of cyclosporine elimination. Significant differences were observed in chronic interstitial and tubular lesions (70% vs. 40.9% [P<0.05] and 70% vs. 47.8% [P<0.05], respectively), whereas no differences were observed in acute lesions (subclinical rejection). Prevalence of CAN at 1 year was lower in this group, as was the severity and incidence of new cases (P<0.05).\n Question: Does early cyclosporine a withdrawal in kidney-transplant recipients receiving sirolimus prevent progression of chronic pathologic allograft lesions?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Nephrotoxicity of calcineurin inhibitors (CNIs) is partially responsible for the development of chronic allograft nephropathy (CAN). Sirolimus has demonstrated its potential to substitute for CNIs because it lacks significant nephrotoxicity and shows a short-term immunosuppressive capacity comparable with that of cyclosporine. This results in the maintenance of better renal function when cyclosporine is eliminated, but it has not been demonstrated whether this benefit is associated with an improvement in the pathologic substrate and a reduction in CAN. We analyzed pretransplant and 1-year renal-allograft biopsies from 64 patients enrolled in a multicenter trial. Patients received cyclosporine and sirolimus during the first 3 months after transplant and were then randomly assigned to continue with cyclosporine or have it withdrawn. Histologic chronic allograft lesions were compared between groups. The percentage of patients in whom chronic pathologic lesions progressed was lower in the group of cyclosporine elimination. Significant differences were observed in chronic interstitial and tubular lesions (70% vs. 40.9% [P<0.05] and 70% vs. 47.8% [P<0.05], respectively), whereas no differences were observed in acute lesions (subclinical rejection). Prevalence of CAN at 1 year was lower in this group, as was the severity and incidence of new cases (P<0.05).
Question: Does early cyclosporine a withdrawal in kidney-transplant recipients receiving sirolimus prevent progression of chronic pathologic allograft lesions?
Output:
|
PubmedQA195987
|
[
{
"role": "user",
"content": "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 reported an association between vitamin D deficiency and asthma. Hereditary 1,25-dihydroxyvitamin D-resistant rickets (HVDRR) patients provide a natural model to assess the role of the vitamin D receptor (VDR) in regulating human lung immune responses and airway hyperreactivity. The aim of the study was to determine the role of the VDR on lung functions, airways, and systemic markers of inflammation and allergy in HVDRR patients. Thirteen HVDRR patients (aged 6-37 y) and 17 normal controls (aged 6-38 y) underwent spirometry, a methacholine challenge test (MCT), blood tests, allergy skin tests, determination of fractional exhaled nitric oxide, and measurement of serum and exhaled breath condensate cytokines, including IL-4, IL-5, IL-10, IL-17, and interferon-γ levels. All HVDRR patients had negative MCT results, whereas six controls (35.3%) had positive MCT results (P < .014). Serum IgE levels, eosinophil counts, and fractional exhaled nitric oxide and allergy skin test results were similar for the HVDRR patients and controls, as were the serum cytokine concentrations. The HVDRR patients had different cytokine levels in their exhaled breath condensate (increased IL-4 and IL-17 and decreased IL-5, IL-10, and interferon-γ levels) compared to the controls (P < .005).\n Question: Does a mutated vitamin D receptor in hereditary vitamin D-resistant rickets prevent induction of bronchial hyperreactivity and inflammation?\n Output: "
},
{
"role": "assistant",
"content": "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 reported an association between vitamin D deficiency and asthma. Hereditary 1,25-dihydroxyvitamin D-resistant rickets (HVDRR) patients provide a natural model to assess the role of the vitamin D receptor (VDR) in regulating human lung immune responses and airway hyperreactivity. The aim of the study was to determine the role of the VDR on lung functions, airways, and systemic markers of inflammation and allergy in HVDRR patients. Thirteen HVDRR patients (aged 6-37 y) and 17 normal controls (aged 6-38 y) underwent spirometry, a methacholine challenge test (MCT), blood tests, allergy skin tests, determination of fractional exhaled nitric oxide, and measurement of serum and exhaled breath condensate cytokines, including IL-4, IL-5, IL-10, IL-17, and interferon-γ levels. All HVDRR patients had negative MCT results, whereas six controls (35.3%) had positive MCT results (P < .014). Serum IgE levels, eosinophil counts, and fractional exhaled nitric oxide and allergy skin test results were similar for the HVDRR patients and controls, as were the serum cytokine concentrations. The HVDRR patients had different cytokine levels in their exhaled breath condensate (increased IL-4 and IL-17 and decreased IL-5, IL-10, and interferon-γ levels) compared to the controls (P < .005).
Question: Does a mutated vitamin D receptor in hereditary vitamin D-resistant rickets prevent induction of bronchial hyperreactivity and inflammation?
Output:
|
PubmedQA18639
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: HCC is a common cause of morbidity and mortality. For patients who are not candidates for curative surgery, systemic chemotherapy is one of the standard treatments. In parts of China and the Far East, over 80% of HCC patients have chronic HBV infection. In this study, we aimed to assess the relationship between pre-chemotherapy HBV viral load and the survival of HCC patients. HBV infection status was determined prior to chemotherapy in 188 patients, 170 of whom had evidence of HBV chronic infection/exposure (160 hepatitis B surface antigen [HBsAg]-positive, 10 HBsAg-negative/hepatitis B core antibody-positive). Of these, 125 had pretreatment HBV DNA levels determined via real-time PCR. Virological data were analyzed using conventional clinical variables to identify factors that influenced survival. Multivariate analysis revealed that high total bilirubin (P = 0.0016; hazard ratio = 1.040 per 1 muM increase; 95% CI 1.015-1.065), HCV infection (P = 0.0095; hazard ratio = 6.955; 95% CI 1.606-30.129), and high HBV DNA level (P = 0.0217; hazard ratio = 1.650; 95% CI 1.076-2.531) affected survival significantly. Exploratory analysis revealed that high levels of pretreatment HBV DNA had a significantly higher incidence of severe hepatitis during chemotherapy.\n Question: Does hepatitis B viral load predict survival of HCC patients undergoing systemic chemotherapy?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: HCC is a common cause of morbidity and mortality. For patients who are not candidates for curative surgery, systemic chemotherapy is one of the standard treatments. In parts of China and the Far East, over 80% of HCC patients have chronic HBV infection. In this study, we aimed to assess the relationship between pre-chemotherapy HBV viral load and the survival of HCC patients. HBV infection status was determined prior to chemotherapy in 188 patients, 170 of whom had evidence of HBV chronic infection/exposure (160 hepatitis B surface antigen [HBsAg]-positive, 10 HBsAg-negative/hepatitis B core antibody-positive). Of these, 125 had pretreatment HBV DNA levels determined via real-time PCR. Virological data were analyzed using conventional clinical variables to identify factors that influenced survival. Multivariate analysis revealed that high total bilirubin (P = 0.0016; hazard ratio = 1.040 per 1 muM increase; 95% CI 1.015-1.065), HCV infection (P = 0.0095; hazard ratio = 6.955; 95% CI 1.606-30.129), and high HBV DNA level (P = 0.0217; hazard ratio = 1.650; 95% CI 1.076-2.531) affected survival significantly. Exploratory analysis revealed that high levels of pretreatment HBV DNA had a significantly higher incidence of severe hepatitis during chemotherapy.
Question: Does hepatitis B viral load predict survival of HCC patients undergoing systemic chemotherapy?
Output:
|
PubmedQA132289
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Thrombopoietin (TPO) is a liver-produced protein that drives megakaryocyte maturation. TPO regulates platelet production and can increase platelet and endothelial reactivity. We investigated the relationship between TPO and the occurrence of thrombocytopenia and thrombosis in patients with systemic lupus erythematosus (SLE). We undertook a cohort study of SLE patients (n = 98) with clinical data collected simultaneously with sampling for TPO, inflammatory cytokines and autoantibody detection. TPO levels were measured by sandwich ELISA with patients with rheumatoid arthritis (RA) (n = 100) and controls (n = 79) as comparators. Disease associations were evaluated using non-parametric methods. TPO levels in SLE (median 8 pg/ml, mean 326, range 8992) were moderately increased compared with RA (median 8 pg/ml, mean 100, range 1659, p = 0.07) and controls (median 8, mean 94, range 2088, p = 0.1). Among SLE patients, TPO levels did not correlate with platelet count or levels of antiphospholipid antibodies. The prevalence of thrombocytopenic episodes, thrombotic events or active disease was not increased in patients with high TPO levels. TPO levels correlated with MIP-1α (Rs 0.56, p < 0.001), IL6 (Rs 0.26, p = 0.02) and IL4 (Rs 0.29, p = 0.01), and inversely correlated to C4 (Rs -0.23, p = 0.04). MIP-1α was the strongest independent predictor of increased TPO levels.\n Question: Are thrombopoietin levels in systemic lupus erythematosus linked to inflammatory cytokines , but unrelated to thrombocytopenia or thrombosis?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Thrombopoietin (TPO) is a liver-produced protein that drives megakaryocyte maturation. TPO regulates platelet production and can increase platelet and endothelial reactivity. We investigated the relationship between TPO and the occurrence of thrombocytopenia and thrombosis in patients with systemic lupus erythematosus (SLE). We undertook a cohort study of SLE patients (n = 98) with clinical data collected simultaneously with sampling for TPO, inflammatory cytokines and autoantibody detection. TPO levels were measured by sandwich ELISA with patients with rheumatoid arthritis (RA) (n = 100) and controls (n = 79) as comparators. Disease associations were evaluated using non-parametric methods. TPO levels in SLE (median 8 pg/ml, mean 326, range 8992) were moderately increased compared with RA (median 8 pg/ml, mean 100, range 1659, p = 0.07) and controls (median 8, mean 94, range 2088, p = 0.1). Among SLE patients, TPO levels did not correlate with platelet count or levels of antiphospholipid antibodies. The prevalence of thrombocytopenic episodes, thrombotic events or active disease was not increased in patients with high TPO levels. TPO levels correlated with MIP-1α (Rs 0.56, p < 0.001), IL6 (Rs 0.26, p = 0.02) and IL4 (Rs 0.29, p = 0.01), and inversely correlated to C4 (Rs -0.23, p = 0.04). MIP-1α was the strongest independent predictor of increased TPO levels.
Question: Are thrombopoietin levels in systemic lupus erythematosus linked to inflammatory cytokines , but unrelated to thrombocytopenia or thrombosis?
Output:
|
PubmedQA199110
|
[
{
"role": "user",
"content": "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 analyze factors that may contribute to local relapse after laparoscopic cryoablation (LCA) of renal tumors. LCA has gained popularity in the treatment of small renal tumors, but local tumor control remains a concern. We analyzed 163 patients who underwent LCA between 2001 and 2008 either at Allegheny General Hospital or Duke University Medical Center, with at least 6 months of follow-up. Demographics, perioperative variables, tumor characteristics (size, pattern of growth, and biopsy results), and follow-up were recorded. Growth pattern was categorized as exophytic, mesophytic, or endophytic. Regression analyses were performed to evaluate risk factors for local relapse after LCA. Median patient age was 66 (range, 33-90) years, with men comprising 60.1% of the cohort. Median tumor size was 2.4 cm (range, 0.5-5.0). Pathology was as follows: renal cell carcinoma in 118 (72.4%), other malignancies in 2 (1.2%), and no malignancy in 43 (26.4%) patients. A single lesion was treated in 95.1% patients and multiple tumors in 4.9%. Endophytic growth pattern was present in 22.8% patients. We observed 7 (4.3%) local recurrences over a median follow-up of 20 months (range, 6-79). Median time to recurrence was 15 months (range, 6-48). On proportional hazards regression, tumor size and endophytic growth pattern were significantly associated with local recurrence (P = .003 and .028; odds ratios [OR] = 4.1 and 11.4, respectively).\n Question: Do tumor size and endophytic growth pattern affect recurrence rates after laparoscopic renal cryoablation?\n Output: "
},
{
"role": "assistant",
"content": "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 analyze factors that may contribute to local relapse after laparoscopic cryoablation (LCA) of renal tumors. LCA has gained popularity in the treatment of small renal tumors, but local tumor control remains a concern. We analyzed 163 patients who underwent LCA between 2001 and 2008 either at Allegheny General Hospital or Duke University Medical Center, with at least 6 months of follow-up. Demographics, perioperative variables, tumor characteristics (size, pattern of growth, and biopsy results), and follow-up were recorded. Growth pattern was categorized as exophytic, mesophytic, or endophytic. Regression analyses were performed to evaluate risk factors for local relapse after LCA. Median patient age was 66 (range, 33-90) years, with men comprising 60.1% of the cohort. Median tumor size was 2.4 cm (range, 0.5-5.0). Pathology was as follows: renal cell carcinoma in 118 (72.4%), other malignancies in 2 (1.2%), and no malignancy in 43 (26.4%) patients. A single lesion was treated in 95.1% patients and multiple tumors in 4.9%. Endophytic growth pattern was present in 22.8% patients. We observed 7 (4.3%) local recurrences over a median follow-up of 20 months (range, 6-79). Median time to recurrence was 15 months (range, 6-48). On proportional hazards regression, tumor size and endophytic growth pattern were significantly associated with local recurrence (P = .003 and .028; odds ratios [OR] = 4.1 and 11.4, respectively).
Question: Do tumor size and endophytic growth pattern affect recurrence rates after laparoscopic renal cryoablation?
Output:
|
PubmedQA106771
|
[
{
"role": "user",
"content": "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 use of early tangential excision or excision to fascia of burn wounds has led to the application of split-thickness skin grafts (STSGs) to a variety of graft beds, including dermis, granulation tissue, fat, and fascia. Because insufficient objective data are available on the effect of the graft bed on survival of an STSG, a 2-year review of success rates of STSGs on a variety of graft beds was completed. The success rates of all 599 STSGs applied to dermis, granulation tissue, fat, and fascia in 233 consecutive burn patients (mean total body surface area [TBSA] burned, 14.5%) by one surgeon at a regional burn center over a 2-year period were reviewed. Data were analyzed to compare outcomes of STSGs on the graft beds listed and in low-risk versus high-risk groups of patients (TBSA burned < or = 35% and > 35%; age < or = 18 years and > 18 years; age < or = 55 years and > 55 years; and diabetes mellitus). One-way analysis of variance was used to compare results of STSGs on different graft beds, and tests were used to analyze differences in results of STSGs in low-risk versus high-risk groups (p < 0.05, significant). The mean success rate at 14 days for all 599 STSGs applied in the 233 patients was 90 +/- 22%. The success rate of STSG on the various surfaces ranged from 85% (fascia) to 93% (dermis; granulation), but the differences among the four graft beds were not significant. Total body surface area burned (> 35%), older age (> 55 years), and the presence of diabetes mellitus each had a significant impact on the percentage take of STSGs at 14 days after application.\n Question: Do factors affecting success of split-thickness skin grafts in the modern burn unit?\n Output: "
},
{
"role": "assistant",
"content": "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 use of early tangential excision or excision to fascia of burn wounds has led to the application of split-thickness skin grafts (STSGs) to a variety of graft beds, including dermis, granulation tissue, fat, and fascia. Because insufficient objective data are available on the effect of the graft bed on survival of an STSG, a 2-year review of success rates of STSGs on a variety of graft beds was completed. The success rates of all 599 STSGs applied to dermis, granulation tissue, fat, and fascia in 233 consecutive burn patients (mean total body surface area [TBSA] burned, 14.5%) by one surgeon at a regional burn center over a 2-year period were reviewed. Data were analyzed to compare outcomes of STSGs on the graft beds listed and in low-risk versus high-risk groups of patients (TBSA burned < or = 35% and > 35%; age < or = 18 years and > 18 years; age < or = 55 years and > 55 years; and diabetes mellitus). One-way analysis of variance was used to compare results of STSGs on different graft beds, and tests were used to analyze differences in results of STSGs in low-risk versus high-risk groups (p < 0.05, significant). The mean success rate at 14 days for all 599 STSGs applied in the 233 patients was 90 +/- 22%. The success rate of STSG on the various surfaces ranged from 85% (fascia) to 93% (dermis; granulation), but the differences among the four graft beds were not significant. Total body surface area burned (> 35%), older age (> 55 years), and the presence of diabetes mellitus each had a significant impact on the percentage take of STSGs at 14 days after application.
Question: Do factors affecting success of split-thickness skin grafts in the modern burn unit?
Output:
|
PubmedQA41877
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Polycomb group (PcG) proteins play a crucial role in cellular senescence as key transcriptional regulators of the Ink4a/Arf tumor suppressor gene locus. However, how PcG complexes target and contribute to stable gene silencing of the Ink4a/Arf locus remains little understood. We examined the function of Zinc finger domain-containing protein 277 (Zfp277), a novel zinc finger protein that interacts with the PcG protein Bmi1. Zfp277 binds to the Ink4a/Arf locus in a Bmi1-independent manner and interacts with polycomb repressor complex (PRC) 1 through direct interaction with Bmi1. Loss of Zfp277 in mouse embryonic fibroblasts (MEFs) caused dissociation of PcG proteins from the Ink4a/Arf locus, resulting in premature senescence associated with derepressed p16(Ink4a) and p19(Arf) expression. Levels of both Zfp277 and PcG proteins inversely correlated with those of reactive oxygen species (ROS) in senescing MEFs, but the treatment of Zfp277(-/-) MEFs with an antioxidant restored the binding of PRC2 but not PRC1 to the Ink4a/Arf locus. Notably, forced expression of Bmi1 in Zfp277(-/-) MEFs did not restore the binding of Bmi1 to the Ink4a/Arf locus and failed to bypass cellular senescence. A Zfp277 mutant that could not bind Bmi1 did not rescue Zfp277(-/-) MEFs from premature senescence.\n Question: Does a novel zinc finger protein Zfp277 mediate transcriptional repression of the Ink4a/arf locus through polycomb repressive complex 1?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Polycomb group (PcG) proteins play a crucial role in cellular senescence as key transcriptional regulators of the Ink4a/Arf tumor suppressor gene locus. However, how PcG complexes target and contribute to stable gene silencing of the Ink4a/Arf locus remains little understood. We examined the function of Zinc finger domain-containing protein 277 (Zfp277), a novel zinc finger protein that interacts with the PcG protein Bmi1. Zfp277 binds to the Ink4a/Arf locus in a Bmi1-independent manner and interacts with polycomb repressor complex (PRC) 1 through direct interaction with Bmi1. Loss of Zfp277 in mouse embryonic fibroblasts (MEFs) caused dissociation of PcG proteins from the Ink4a/Arf locus, resulting in premature senescence associated with derepressed p16(Ink4a) and p19(Arf) expression. Levels of both Zfp277 and PcG proteins inversely correlated with those of reactive oxygen species (ROS) in senescing MEFs, but the treatment of Zfp277(-/-) MEFs with an antioxidant restored the binding of PRC2 but not PRC1 to the Ink4a/Arf locus. Notably, forced expression of Bmi1 in Zfp277(-/-) MEFs did not restore the binding of Bmi1 to the Ink4a/Arf locus and failed to bypass cellular senescence. A Zfp277 mutant that could not bind Bmi1 did not rescue Zfp277(-/-) MEFs from premature senescence.
Question: Does a novel zinc finger protein Zfp277 mediate transcriptional repression of the Ink4a/arf locus through polycomb repressive complex 1?
Output:
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PubmedQA130153
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Large-scale genome-wide association studies (GWAS) have so far identified 45 loci that are robustly associated with coronary heart disease (CHD) in data from adult men and women of European descent. To examine whether the CHD-associated loci are associated with measures of atherosclerosis in data from up to 9582 individuals of European ancestry. Forty-five SNPs representing the CHD-associated loci were genotyped in middle-aged to elderly individuals of European descent from four independent population-based studies (IMPROVE, MDC-CC, ULSAM and PIVUS). Intima-media thickness (IMT) was measured by external B-mode ultrasonography at the far wall of the bulb (sinus) and common carotid artery. Plaque presence was defined as a maximal IMT of the bulb >1.5 mm. We meta-analysed single-SNP associations across the four studies, and combined them in a genetic predisposition score. We subsequently examined the association of the genetic predisposition score with prevalent CHD and the three indices of atherosclerosis, adjusting for sex, age and Framingham risk factors. As anticipated, the genetic predisposition score was associated with prevalent CHD, with each additional risk allele increasing the odds of disease by 5.5% (p = 4.1 × 10(-6)). Moreover, each additional CHD-risk allele across the 45 loci was associated with a 0.24% increase in IMT (p = 4.0 × 10(-3)), and with a 2.8% increased odds of plaque presence (p = 7.4 × 10(-6)) at the far wall of the bulb. The genetic predisposition score was not associated with IMT of the common carotid artery (p = 0.47).\n Question: Are gWAS-identified loci for coronary heart disease associated with intima-media thickness and plaque presence at the carotid artery bulb?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Large-scale genome-wide association studies (GWAS) have so far identified 45 loci that are robustly associated with coronary heart disease (CHD) in data from adult men and women of European descent. To examine whether the CHD-associated loci are associated with measures of atherosclerosis in data from up to 9582 individuals of European ancestry. Forty-five SNPs representing the CHD-associated loci were genotyped in middle-aged to elderly individuals of European descent from four independent population-based studies (IMPROVE, MDC-CC, ULSAM and PIVUS). Intima-media thickness (IMT) was measured by external B-mode ultrasonography at the far wall of the bulb (sinus) and common carotid artery. Plaque presence was defined as a maximal IMT of the bulb >1.5 mm. We meta-analysed single-SNP associations across the four studies, and combined them in a genetic predisposition score. We subsequently examined the association of the genetic predisposition score with prevalent CHD and the three indices of atherosclerosis, adjusting for sex, age and Framingham risk factors. As anticipated, the genetic predisposition score was associated with prevalent CHD, with each additional risk allele increasing the odds of disease by 5.5% (p = 4.1 × 10(-6)). Moreover, each additional CHD-risk allele across the 45 loci was associated with a 0.24% increase in IMT (p = 4.0 × 10(-3)), and with a 2.8% increased odds of plaque presence (p = 7.4 × 10(-6)) at the far wall of the bulb. The genetic predisposition score was not associated with IMT of the common carotid artery (p = 0.47).
Question: Are gWAS-identified loci for coronary heart disease associated with intima-media thickness and plaque presence at the carotid artery bulb?
Output:
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PubmedQA57535
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: On dialysis, survival among patients with diabetes mellitus is inferior to survival of non-diabetic patients. We hypothesized that patients with diabetes as primary renal disease have worse survival compared to patients with diabetes as a co-morbid condition and aimed to compare all-cause mortality between these patient groups. Data were collected from the Netherlands Cooperative Study on the Adequacy of Dialysis (NECOSAD), a multicenter, prospective cohort study in which new patients with end stage renal disease (ESRD) were monitored until transplantation or death. Patients with diabetes as primary cause of ESRD were compared with patients with diabetes as co-morbid condition and both of these patient groups were compared to patients without diabetes. Analysis was performed using Kaplan-Meier and Cox regression. Fifteen % of the patients had diabetic nephropathy as primary renal disease (N = 281); 6% had diabetes as co-morbid condition (N = 107) and 79% had no diabetes (N = 1465). During follow-up 42% of patients (N = 787) died. Compared to non-diabetic patients, mortality risk was increased for both patients with diabetes as primary renal disease HR: 1.9 (95% CI 1.6, 2.3) and for patients with diabetes as co-morbid condition HR: 1.7 (95% CI 1.3, 2.2). Mortality was not significantly higher in patients with diabetes as primary renal disease compared to patients with diabetes as co-morbid condition (HR 1.06; 95% CI 0.79, 1.43).\n Question: Is survival in dialysis patients different between patients with diabetes as primary renal disease and patients with diabetes as a co-morbid condition?\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: On dialysis, survival among patients with diabetes mellitus is inferior to survival of non-diabetic patients. We hypothesized that patients with diabetes as primary renal disease have worse survival compared to patients with diabetes as a co-morbid condition and aimed to compare all-cause mortality between these patient groups. Data were collected from the Netherlands Cooperative Study on the Adequacy of Dialysis (NECOSAD), a multicenter, prospective cohort study in which new patients with end stage renal disease (ESRD) were monitored until transplantation or death. Patients with diabetes as primary cause of ESRD were compared with patients with diabetes as co-morbid condition and both of these patient groups were compared to patients without diabetes. Analysis was performed using Kaplan-Meier and Cox regression. Fifteen % of the patients had diabetic nephropathy as primary renal disease (N = 281); 6% had diabetes as co-morbid condition (N = 107) and 79% had no diabetes (N = 1465). During follow-up 42% of patients (N = 787) died. Compared to non-diabetic patients, mortality risk was increased for both patients with diabetes as primary renal disease HR: 1.9 (95% CI 1.6, 2.3) and for patients with diabetes as co-morbid condition HR: 1.7 (95% CI 1.3, 2.2). Mortality was not significantly higher in patients with diabetes as primary renal disease compared to patients with diabetes as co-morbid condition (HR 1.06; 95% CI 0.79, 1.43).
Question: Is survival in dialysis patients different between patients with diabetes as primary renal disease and patients with diabetes as a co-morbid condition?
Output:
|
PubmedQA24365
|
[
{
"role": "user",
"content": "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 neonates are highly susceptible to a wide range of infections, which has been attributed to deficiencies in their innate and adaptive immunity. In contrast to the well-documented immaturity in neonatal adaptive immunity, deficiencies in their innate immunity are less defined. This study examined the inflammatory response of neonatal monocytes to bacterial lipopolysaccharide (LPS) and peptidoglycan (PGN) stimulation and discriminated the underlying Toll-like receptor (TLR)-mediated signal transduction pathways. Cord blood from 30 healthy newborns of full-term elective cesarean sections and peripheral blood from 25 healthy adult volunteers were collected. Ex vivo production of inflammatory cytokines was assessed by cytometric bead array, and expression of CD14, TLR4, TLR2, phosphorylated NF-κB p65 and p38 on monocytes were detected by FACScan analysis. Neonatal whole blood showed significantly decreased ex vivo TNF-α and IL-1β production in response to stimulation with the TLR4 agonist LPS, but not the TLR2 agonist PGN, when compared with adult whole blood. Consistent with the diminished inflammatory cytokine response to LPS stimulation, neonatal monocytes exhibited substantially impaired TLR-mediated signal transduction pathways characterized by down-regulated expression of CD14 and TLR4, and suppressed phosphorylation of NF-κB p65 at Ser536 and p38 following LPS stimulation. In addition, neonates had a significantly lower percentage of TLR4(+)/CD14(+) monocytes than adults.\n Question: Is an impaired inflammatory cytokine response to gram-negative LPS in human neonates associated with the defective TLR-mediated signaling pathway?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Human neonates are highly susceptible to a wide range of infections, which has been attributed to deficiencies in their innate and adaptive immunity. In contrast to the well-documented immaturity in neonatal adaptive immunity, deficiencies in their innate immunity are less defined. This study examined the inflammatory response of neonatal monocytes to bacterial lipopolysaccharide (LPS) and peptidoglycan (PGN) stimulation and discriminated the underlying Toll-like receptor (TLR)-mediated signal transduction pathways. Cord blood from 30 healthy newborns of full-term elective cesarean sections and peripheral blood from 25 healthy adult volunteers were collected. Ex vivo production of inflammatory cytokines was assessed by cytometric bead array, and expression of CD14, TLR4, TLR2, phosphorylated NF-κB p65 and p38 on monocytes were detected by FACScan analysis. Neonatal whole blood showed significantly decreased ex vivo TNF-α and IL-1β production in response to stimulation with the TLR4 agonist LPS, but not the TLR2 agonist PGN, when compared with adult whole blood. Consistent with the diminished inflammatory cytokine response to LPS stimulation, neonatal monocytes exhibited substantially impaired TLR-mediated signal transduction pathways characterized by down-regulated expression of CD14 and TLR4, and suppressed phosphorylation of NF-κB p65 at Ser536 and p38 following LPS stimulation. In addition, neonates had a significantly lower percentage of TLR4(+)/CD14(+) monocytes than adults.
Question: Is an impaired inflammatory cytokine response to gram-negative LPS in human neonates associated with the defective TLR-mediated signaling pathway?
Output:
|
PubmedQA194028
|
[
{
"role": "user",
"content": "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 endothelial nitric oxide synthase (eNOS) contributes to cardiac remodelling. We studied the role of eNOS in the development of myocardial fibrosis during cardiac overload. Ten-week-old male C57/Bl6 wildtype (WT) and eNOS mice (eNOS(-/-)) were subjected to transverse aortic constriction (TAC, 360 μm) and WT were treated with L-N(G)-nitroarginine methyl ester (L-NAME, 100 mg/kg/day) for 35 days. Inhibition of eNOS by L-NAME induced interstitial fibrosis, augmented replacement fibrosis, and induced apoptosis of cardiac fibroblasts and cardiomyocytes. L-NAME and eNOS(-/-) markedly increased the fibrosis induced by TAC and enhanced the myocardial prevalence of CXCR4(pos) fibroblasts. Myocardial stromal-derived factor-1 (SDF-1) expression was up-regulated by l-NAME and down-regulated after TAC. Blood pressure lowering by co-treatment with hydralazine (250 mg/L/day) did not reverse the L-NAME effects. In mice transplanted with green fluorescent protein (GFP)(pos) bone marrow, L-NAME increased the percentage of GFP(pos) fibroblasts in the myocardium to 45-70%. Strain-mismatched BMT of eNOS(-/-)-BM increased and of WT-BM decreased the percentage of CXCR4(pos) fibroblasts in all groups. The number of fibrocytes (CD45(pos) collagen I(pos) cells) in the peripheral blood and in the bone marrow was increased both by TAC and L-NAME. L-NAME but not the inhibitor of inducible NOS 1400 W and of neuronal NOS 7-nitroindazole increased hydroxyproline and collagen Iα1. L-NAME up-regulated SDF-1 mRNA in cultured neonatal rat cardiac fibroblasts as well as their migratory capacity.\n Question: Does inhibition of endothelial nitric oxide synthase induce and enhances myocardial fibrosis?\n Output: "
},
{
"role": "assistant",
"content": "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 endothelial nitric oxide synthase (eNOS) contributes to cardiac remodelling. We studied the role of eNOS in the development of myocardial fibrosis during cardiac overload. Ten-week-old male C57/Bl6 wildtype (WT) and eNOS mice (eNOS(-/-)) were subjected to transverse aortic constriction (TAC, 360 μm) and WT were treated with L-N(G)-nitroarginine methyl ester (L-NAME, 100 mg/kg/day) for 35 days. Inhibition of eNOS by L-NAME induced interstitial fibrosis, augmented replacement fibrosis, and induced apoptosis of cardiac fibroblasts and cardiomyocytes. L-NAME and eNOS(-/-) markedly increased the fibrosis induced by TAC and enhanced the myocardial prevalence of CXCR4(pos) fibroblasts. Myocardial stromal-derived factor-1 (SDF-1) expression was up-regulated by l-NAME and down-regulated after TAC. Blood pressure lowering by co-treatment with hydralazine (250 mg/L/day) did not reverse the L-NAME effects. In mice transplanted with green fluorescent protein (GFP)(pos) bone marrow, L-NAME increased the percentage of GFP(pos) fibroblasts in the myocardium to 45-70%. Strain-mismatched BMT of eNOS(-/-)-BM increased and of WT-BM decreased the percentage of CXCR4(pos) fibroblasts in all groups. The number of fibrocytes (CD45(pos) collagen I(pos) cells) in the peripheral blood and in the bone marrow was increased both by TAC and L-NAME. L-NAME but not the inhibitor of inducible NOS 1400 W and of neuronal NOS 7-nitroindazole increased hydroxyproline and collagen Iα1. L-NAME up-regulated SDF-1 mRNA in cultured neonatal rat cardiac fibroblasts as well as their migratory capacity.
Question: Does inhibition of endothelial nitric oxide synthase induce and enhances myocardial fibrosis?
Output:
|
PubmedQA67968
|
[
{
"role": "user",
"content": "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 pathological proliferation of cardiac fibroblasts (CFs) in response to heart injury results in fibrosis, which correlates with arrhythmia generation and heart failure. Here we systematically examined the effect of fibroblast-derived paracrine factors on electrical propagation in cardiomyocytes. Neonatal rat cardiac monolayers were exposed for 24 h to media conditioned by CFs. Optical mapping, sharp microelectrode recordings, quantitative RT-PCR, and immunostaining were used to assess the changes in the propagation and shape of the action potential and underlying changes in gene and protein expression. The fibroblast paracrine factors produced a 52% reduction in cardiac conduction velocity, a 217% prolongation of action potential duration, a 64% decrease of maximum capture rate, a 21% increase in membrane resting potential, and an 80% decrease of action potential upstroke velocity. These effects were dose dependent and partially reversible with removal of the conditioned media. No fibroblast proliferation, cardiomyocyte apoptosis, or decreased connexin-43 expression, phosphorylation, and function were found in conditioned cardiac cultures. In contrast, the expression of the fast sodium, inward rectifying potassium, and transient outward potassium channels were, respectively, reduced 3.8-, 6.6-fold, and to undetectable levels. The expression of beta-myosin heavy chain increased 17.4-fold. No electrophysiological changes were observed from media conditioned by CFs in the presence of cardiomyocytes.\n Question: Do cardiac fibroblast paracrine factors alter impulse conduction and ion channel expression of neonatal rat cardiomyocytes?\n Output: "
},
{
"role": "assistant",
"content": "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 pathological proliferation of cardiac fibroblasts (CFs) in response to heart injury results in fibrosis, which correlates with arrhythmia generation and heart failure. Here we systematically examined the effect of fibroblast-derived paracrine factors on electrical propagation in cardiomyocytes. Neonatal rat cardiac monolayers were exposed for 24 h to media conditioned by CFs. Optical mapping, sharp microelectrode recordings, quantitative RT-PCR, and immunostaining were used to assess the changes in the propagation and shape of the action potential and underlying changes in gene and protein expression. The fibroblast paracrine factors produced a 52% reduction in cardiac conduction velocity, a 217% prolongation of action potential duration, a 64% decrease of maximum capture rate, a 21% increase in membrane resting potential, and an 80% decrease of action potential upstroke velocity. These effects were dose dependent and partially reversible with removal of the conditioned media. No fibroblast proliferation, cardiomyocyte apoptosis, or decreased connexin-43 expression, phosphorylation, and function were found in conditioned cardiac cultures. In contrast, the expression of the fast sodium, inward rectifying potassium, and transient outward potassium channels were, respectively, reduced 3.8-, 6.6-fold, and to undetectable levels. The expression of beta-myosin heavy chain increased 17.4-fold. No electrophysiological changes were observed from media conditioned by CFs in the presence of cardiomyocytes.
Question: Do cardiac fibroblast paracrine factors alter impulse conduction and ion channel expression of neonatal rat cardiomyocytes?
Output:
|
PubmedQA21528
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Alcohol may have a cardioprotective effect. One possible mechanism is by modifying insulin resistance/secretion. The aims of this study were: (i) to examine the effect of short-term alcohol consumption on the metabolic control of glucose tolerance; (ii) to study the influence of short-term alcohol consumption on cardiac autonomic activity using spectral analysis of heart rate variability. Twenty-one healthy subjects, in a randomized crossover design, either received three units of ethanol daily for 1 week or abstained from ethanol. The control of glucose tolerance was assessed using the intravenous glucose tolerance test with minimal modelling. There was no difference in fasting glucose, fasting insulin or insulin sensitivity between the two groups. Alcohol showed a lower insulin first phase insulin response (no alcohol 659.0 +/- 394.1 SD, alcohol 535.2 +/- 309.1) pmol L-1 min-1, P = 0.027). There was no difference in heart rate or blood pressure but a significant difference in the ratio of high to low frequency spectral power of heart rate variability; (no alcohol 4.55 +/- 3.78, alcohol 8.16 +/- 6.77, P = 0.033). This suggests decreased sympathetic and/or increased vagal modulation of heart rate in the alcohol group.\n Question: Does alcohol consumption alter insulin secretion and cardiac autonomic activity?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Alcohol may have a cardioprotective effect. One possible mechanism is by modifying insulin resistance/secretion. The aims of this study were: (i) to examine the effect of short-term alcohol consumption on the metabolic control of glucose tolerance; (ii) to study the influence of short-term alcohol consumption on cardiac autonomic activity using spectral analysis of heart rate variability. Twenty-one healthy subjects, in a randomized crossover design, either received three units of ethanol daily for 1 week or abstained from ethanol. The control of glucose tolerance was assessed using the intravenous glucose tolerance test with minimal modelling. There was no difference in fasting glucose, fasting insulin or insulin sensitivity between the two groups. Alcohol showed a lower insulin first phase insulin response (no alcohol 659.0 +/- 394.1 SD, alcohol 535.2 +/- 309.1) pmol L-1 min-1, P = 0.027). There was no difference in heart rate or blood pressure but a significant difference in the ratio of high to low frequency spectral power of heart rate variability; (no alcohol 4.55 +/- 3.78, alcohol 8.16 +/- 6.77, P = 0.033). This suggests decreased sympathetic and/or increased vagal modulation of heart rate in the alcohol group.
Question: Does alcohol consumption alter insulin secretion and cardiac autonomic activity?
Output:
|
PubmedQA30341
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Cardiac autonomic nervous system (ANS) dysfunction in Huntington's disease (HD) might affect both the sympathetic and parasympathetic branch of the ANS.\n Question: Is cardiovagal modulation upon postural change altered in Huntington 's disease?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Cardiac autonomic nervous system (ANS) dysfunction in Huntington's disease (HD) might affect both the sympathetic and parasympathetic branch of the ANS.
Question: Is cardiovagal modulation upon postural change altered in Huntington 's disease?
Output:
|
PubmedQA28694
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Dysregulated host/microbial interactions appear to play a central role in the development of inflammatory bowel disease (IBD). However, molecular events leading to the dysregulation have not yet been defined fully. Studies were designed to characterize a key molecule that is involved in the dysregulation. Colonic mucosal RNA from C57BL/6 mice on days 4 and 8 with administration of 4% dextran sulfate sodium for 5 days were subjected to DNA microarray analysis. Chitinase 3-like-1 (CHI3L1) messenger RNA and protein expressions were examined by reverse-transcription polymerase chain reaction and immunohistochemistry. A gentamicin protection assay of Salmonella typhimurium was performed using epithelial cell lines that are engineered genetically to overexpress or lack mouse CHI3L1. To examine the functional role of CHI3L1 in vivo, anti-CHI3L1 antibody was administered into the dextran sulfate sodium colitis model. Microarray analysis identified that CHI3L1 is up-regulated specifically in inflamed mucosa. The expression of CHI3L1 protein clearly was detectable in lamina propria and colonic epithelial cells (CECs) in several murine colitis models and ulcerative colitis and Crohn's disease patients but absent in normal controls. The gentamicin protection assays using intracellular bacteria showed that CHI3L1 is required for the enhancement of adhesion and internalization of these bacteria in CEC. In vivo neutralization experiments showed that CHI3L1 contributes to the facilitation of bacterial invasion into the intestinal mucosa and the development of acute colitis.\n Question: Does chitinase 3-like-1 exacerbate intestinal inflammation by enhancing bacterial adhesion and invasion in colonic epithelial 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: Dysregulated host/microbial interactions appear to play a central role in the development of inflammatory bowel disease (IBD). However, molecular events leading to the dysregulation have not yet been defined fully. Studies were designed to characterize a key molecule that is involved in the dysregulation. Colonic mucosal RNA from C57BL/6 mice on days 4 and 8 with administration of 4% dextran sulfate sodium for 5 days were subjected to DNA microarray analysis. Chitinase 3-like-1 (CHI3L1) messenger RNA and protein expressions were examined by reverse-transcription polymerase chain reaction and immunohistochemistry. A gentamicin protection assay of Salmonella typhimurium was performed using epithelial cell lines that are engineered genetically to overexpress or lack mouse CHI3L1. To examine the functional role of CHI3L1 in vivo, anti-CHI3L1 antibody was administered into the dextran sulfate sodium colitis model. Microarray analysis identified that CHI3L1 is up-regulated specifically in inflamed mucosa. The expression of CHI3L1 protein clearly was detectable in lamina propria and colonic epithelial cells (CECs) in several murine colitis models and ulcerative colitis and Crohn's disease patients but absent in normal controls. The gentamicin protection assays using intracellular bacteria showed that CHI3L1 is required for the enhancement of adhesion and internalization of these bacteria in CEC. In vivo neutralization experiments showed that CHI3L1 contributes to the facilitation of bacterial invasion into the intestinal mucosa and the development of acute colitis.
Question: Does chitinase 3-like-1 exacerbate intestinal inflammation by enhancing bacterial adhesion and invasion in colonic epithelial cells?
Output:
|
PubmedQA171713
|
[
{
"role": "user",
"content": "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 relation between low thyroid activity and prolonged life span in humans has been observed. Several studies have demonstrated hereditary and genetic influences on thyroid function. The objective of the study was to test whether low thyroid activity associated with extreme longevity constitutes a heritable phenotype, which could contribute to the familial longevity observed in the Leiden Longevity Study. This was a cross-sectional study. The study was conducted at a university hospital in the city of Leiden, The Netherlands. Eight hundred fifty-nine nonagenarian siblings (median age 92.9 yr) from 421 long-lived families participated in the study. Families were recruited from the entire Dutch population if at least two long-lived siblings were alive and fulfilled the age criterion of age of 89 yr or older for males and 91 yr or older for females. There were no selection criteria on health or demographic characteristics. Blood samples were taken for determination of serum parameters of thyroid function. We calculated the family mortality history score of the parents of the nonagenarian siblings and related this to thyroid function parameters in the nonagenarian siblings. We found that a lower family mortality history score (less mortality) of the parents of nonagenarian siblings was associated with higher serum TSH levels (P = 0.005) and lower free T(4) levels (P = 0.002) as well as lower free T(3) levels (P = 0.034) in the nonagenarian siblings.\n Question: Is familial longevity associated with decreased thyroid function?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: A relation between low thyroid activity and prolonged life span in humans has been observed. Several studies have demonstrated hereditary and genetic influences on thyroid function. The objective of the study was to test whether low thyroid activity associated with extreme longevity constitutes a heritable phenotype, which could contribute to the familial longevity observed in the Leiden Longevity Study. This was a cross-sectional study. The study was conducted at a university hospital in the city of Leiden, The Netherlands. Eight hundred fifty-nine nonagenarian siblings (median age 92.9 yr) from 421 long-lived families participated in the study. Families were recruited from the entire Dutch population if at least two long-lived siblings were alive and fulfilled the age criterion of age of 89 yr or older for males and 91 yr or older for females. There were no selection criteria on health or demographic characteristics. Blood samples were taken for determination of serum parameters of thyroid function. We calculated the family mortality history score of the parents of the nonagenarian siblings and related this to thyroid function parameters in the nonagenarian siblings. We found that a lower family mortality history score (less mortality) of the parents of nonagenarian siblings was associated with higher serum TSH levels (P = 0.005) and lower free T(4) levels (P = 0.002) as well as lower free T(3) levels (P = 0.034) in the nonagenarian siblings.
Question: Is familial longevity associated with decreased thyroid function?
Output:
|
PubmedQA41999
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Hypoperfusion of the bowel is a risk factor for anastomotic failure. Electrical field stimulation has been shown to improve repair in ischemic tissue, but its influence in hypoperfused colon has not been investigated. The hypothesis of this experimental animal study was that electrical field stimulation improves anastomotic healing in ischemic bowel. Thirty rats were divided evenly into three groups: control, ischemia/placebo, and ischemia/test group. Ischemia was induced by ligation of the arterial supply to the proximal colon. The watershed area was identified and transected. Field stimulation was achieved by application of negatively charged diethylaminoethyl Sephadex beads in methylcellulose gel to the colonic epithelium prior to anastomosis. The placebo group had methylcellulose gel only applied and control animals had anastomosis only. Anastomotic strength was measured using anastomotic bursting pressure and hydroxyproline content. Systemic effect was investigated via interleukin-6 and vascular endothelial growth factor assay. The ischemia/electrical field stimulation (EFS) group had significantly increased bursting pressure and hydroxyproline content in comparison with the placebo group (P < 0.001). Serum cytokine levels were unaffected.\n Question: Does electrical field stimulation promote anastomotic healing in poorly perfused rat colon?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Hypoperfusion of the bowel is a risk factor for anastomotic failure. Electrical field stimulation has been shown to improve repair in ischemic tissue, but its influence in hypoperfused colon has not been investigated. The hypothesis of this experimental animal study was that electrical field stimulation improves anastomotic healing in ischemic bowel. Thirty rats were divided evenly into three groups: control, ischemia/placebo, and ischemia/test group. Ischemia was induced by ligation of the arterial supply to the proximal colon. The watershed area was identified and transected. Field stimulation was achieved by application of negatively charged diethylaminoethyl Sephadex beads in methylcellulose gel to the colonic epithelium prior to anastomosis. The placebo group had methylcellulose gel only applied and control animals had anastomosis only. Anastomotic strength was measured using anastomotic bursting pressure and hydroxyproline content. Systemic effect was investigated via interleukin-6 and vascular endothelial growth factor assay. The ischemia/electrical field stimulation (EFS) group had significantly increased bursting pressure and hydroxyproline content in comparison with the placebo group (P < 0.001). Serum cytokine levels were unaffected.
Question: Does electrical field stimulation promote anastomotic healing in poorly perfused rat colon?
Output:
|
PubmedQA80450
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Little is known regarding the prenatal determinants of innate immune responses in relation to infant allergic risk. Environmental exposures, including microbial stimuli, might predispose susceptible subjects to atopy and asthma in early infancy or even in utero. Because Toll-like receptors (TLRs) recognize microbial products and because cord blood (CB) progenitor alterations have been observed in neonates at risk for atopy, we investigated the expression and function of TLRs on CB hematopoietic progenitors in relation to atopic risk, as defined by maternal allergic sensitization. Thirty-two (15 with low and 17 with high atopic risk) infant CB samples were assessed for phenotypic and functional alterations in CD34(+) cells by means of flow cytometry and methylcellulose culture, respectively. CD34(+) hematopoietic progenitors were stained for TLR-2, TLR-4, TLR-9, GM-CSF receptor α, IL-5 receptor α, and IL-3 receptor α or cultured in methylcellulose assays for hematopoietic cytokine-stimulated eosinophil-basophil (Eo/B) colony-forming units (CFUs) with or without LPS. High-atopic-risk infants had significantly lower CB CD34(+) cell TLR-2, TLR-4, and TLR-9 expression (P = .009). High-risk infant progenitors gave rise to significantly more Eo/B CFUs (P = .002) with hematopoietic cytokine (IL-3, IL-5, or GM-CSF) stimulation ex vivo. Although LPS costimulation induced Eo/B CFUs from both low- and high-risk infant CB CD34(+) cells, this response was significantly (P = .020) muted in the high-risk CB progenitors.\n Question: Does maternal allergy modulate cord blood hematopoietic progenitor Toll-like receptor expression and function?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Little is known regarding the prenatal determinants of innate immune responses in relation to infant allergic risk. Environmental exposures, including microbial stimuli, might predispose susceptible subjects to atopy and asthma in early infancy or even in utero. Because Toll-like receptors (TLRs) recognize microbial products and because cord blood (CB) progenitor alterations have been observed in neonates at risk for atopy, we investigated the expression and function of TLRs on CB hematopoietic progenitors in relation to atopic risk, as defined by maternal allergic sensitization. Thirty-two (15 with low and 17 with high atopic risk) infant CB samples were assessed for phenotypic and functional alterations in CD34(+) cells by means of flow cytometry and methylcellulose culture, respectively. CD34(+) hematopoietic progenitors were stained for TLR-2, TLR-4, TLR-9, GM-CSF receptor α, IL-5 receptor α, and IL-3 receptor α or cultured in methylcellulose assays for hematopoietic cytokine-stimulated eosinophil-basophil (Eo/B) colony-forming units (CFUs) with or without LPS. High-atopic-risk infants had significantly lower CB CD34(+) cell TLR-2, TLR-4, and TLR-9 expression (P = .009). High-risk infant progenitors gave rise to significantly more Eo/B CFUs (P = .002) with hematopoietic cytokine (IL-3, IL-5, or GM-CSF) stimulation ex vivo. Although LPS costimulation induced Eo/B CFUs from both low- and high-risk infant CB CD34(+) cells, this response was significantly (P = .020) muted in the high-risk CB progenitors.
Question: Does maternal allergy modulate cord blood hematopoietic progenitor Toll-like receptor expression and function?
Output:
|
PubmedQA30279
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To evaluate the effect of circumcision on the glans penis sensitivity by comparing the changes of the glans penis vibrotactile threshold between normal men and patients with simple redundant prepuce and among the patients before and after the operation. The vibrotactile thresholds were measured at the forefinger and glans penis in 73 normal volunteer controls and 96 patients with simple redundant prepuce before and after circumcision by biological vibration measurement instrument, and the changes in the perception sensitivity of the body surface were analyzed. The G/F (glans/finger) indexes in the control and the test group were respectively 2.39 +/- 1.72 and 1.97 +/- 0.71, with no significant difference in between (P > 0.05). And those of the test group were 1.97 +/- 0.71, 2.64 +/- 1.38, 3.09 +/-1.46 and 2.97 +/- 1.20 respectively before and 1, 2 and 3 months after circumcision, with significant difference between pre- and post-operation (P < 0.05).\n Question: Does [ Circumcision affect glans penis vibration perception threshold ]?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To evaluate the effect of circumcision on the glans penis sensitivity by comparing the changes of the glans penis vibrotactile threshold between normal men and patients with simple redundant prepuce and among the patients before and after the operation. The vibrotactile thresholds were measured at the forefinger and glans penis in 73 normal volunteer controls and 96 patients with simple redundant prepuce before and after circumcision by biological vibration measurement instrument, and the changes in the perception sensitivity of the body surface were analyzed. The G/F (glans/finger) indexes in the control and the test group were respectively 2.39 +/- 1.72 and 1.97 +/- 0.71, with no significant difference in between (P > 0.05). And those of the test group were 1.97 +/- 0.71, 2.64 +/- 1.38, 3.09 +/-1.46 and 2.97 +/- 1.20 respectively before and 1, 2 and 3 months after circumcision, with significant difference between pre- and post-operation (P < 0.05).
Question: Does [ Circumcision affect glans penis vibration perception threshold ]?
Output:
|
PubmedQA98180
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: We test the hypothesis that the frequency of postoperative nausea and vomiting is similar for the ProSeal laryngeal mask airway (LMA) and the tracheal tube. Two hundred consecutive female patients (ASA I-II, 18-75 yr) undergoing routine breast and gynaecological surgery were divided into two equal-sized groups for airway management with the ProSeal LMA or tracheal tube. Ventilation was better and airway trauma less frequent for the ProSeal LMA. For the ProSeal group, the time spent in the post-anaesthesia care unit was shorter (69 vs 88 min, P < 0.0001); fewer doses of tropisetron were required in the post-anaesthesia care unit (P < or = 0.001) and ward (P = 0.004); morphine requirements were lower in the post-anaesthesia care unit (6.0 vs 8.1 mg, P = 0.005) and ward (6.1 vs 8.9, P = 0.004); nausea was less frequent at all times (overall: 13% vs 53%, P < 0.0001); vomiting was less frequent at 2 h (4% vs 18%, P = 0.003) and 24 h (5% vs 19%, P = 0.004); and sore throat was less frequent at all times (overall: 12% vs 38%, P < 0.0001).\n Question: Are postoperative nausea , vomiting , airway morbidity , and analgesic requirements lower for the ProSeal laryngeal mask airway than the tracheal tube in females undergoing breast and gynaecological 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: We test the hypothesis that the frequency of postoperative nausea and vomiting is similar for the ProSeal laryngeal mask airway (LMA) and the tracheal tube. Two hundred consecutive female patients (ASA I-II, 18-75 yr) undergoing routine breast and gynaecological surgery were divided into two equal-sized groups for airway management with the ProSeal LMA or tracheal tube. Ventilation was better and airway trauma less frequent for the ProSeal LMA. For the ProSeal group, the time spent in the post-anaesthesia care unit was shorter (69 vs 88 min, P < 0.0001); fewer doses of tropisetron were required in the post-anaesthesia care unit (P < or = 0.001) and ward (P = 0.004); morphine requirements were lower in the post-anaesthesia care unit (6.0 vs 8.1 mg, P = 0.005) and ward (6.1 vs 8.9, P = 0.004); nausea was less frequent at all times (overall: 13% vs 53%, P < 0.0001); vomiting was less frequent at 2 h (4% vs 18%, P = 0.003) and 24 h (5% vs 19%, P = 0.004); and sore throat was less frequent at all times (overall: 12% vs 38%, P < 0.0001).
Question: Are postoperative nausea , vomiting , airway morbidity , and analgesic requirements lower for the ProSeal laryngeal mask airway than the tracheal tube in females undergoing breast and gynaecological surgery?
Output:
|
PubmedQA60128
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Hypoxia regulates key biological processes including angiogenesis via the transcription factor, hypoxia-inducible factor (HIF). In prostate cancer, angiogenesis is also influenced by androgens, and recent cell line studies suggest that this effect is partly mediated by HIF. The study aimed to assess whether a relationship exists in human prostate cancer between expression of the androgen receptor, HIFs, and the key angiogenesis factor, vascular endothelial growth factor (VEGF). A tissue microarray comprised of 149 radical prostatectomy specimens was constructed. Semiquantitative immunohistochemical analysis was used to assess the expression of the androgen receptor, VEGF and HIF-1a and 2a, and their regulatory prolyl hydroxylase enzymes (PHD1, PHD2, and PHD3). Statistical analysis compared these factors with each other and with prostate-specific antigen relapse. There was a significant correlation between HIF-1a and HIF-2a expression (P = 0.02), and with androgen receptor (P = 0.04 and P < 0.001, respectively) and VEGF expression (P = 0.05 and P < 0.001, respectively). VEGF was also significantly related to the androgen receptor (P = 0.05), whereas PHD2 was inversely related to HIF-2a expression. No significant association was shown between HIF-1a or HIF-2a and time to prostate-specific antigen recurrence (P = 0.20 and P = 0.94, respectively).\n Question: Is the androgen receptor significantly associated with vascular endothelial growth factor and hypoxia sensing via hypoxia-inducible factors HIF-1a , HIF-2a , and the prolyl hydroxylases in human prostate cancer?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Hypoxia regulates key biological processes including angiogenesis via the transcription factor, hypoxia-inducible factor (HIF). In prostate cancer, angiogenesis is also influenced by androgens, and recent cell line studies suggest that this effect is partly mediated by HIF. The study aimed to assess whether a relationship exists in human prostate cancer between expression of the androgen receptor, HIFs, and the key angiogenesis factor, vascular endothelial growth factor (VEGF). A tissue microarray comprised of 149 radical prostatectomy specimens was constructed. Semiquantitative immunohistochemical analysis was used to assess the expression of the androgen receptor, VEGF and HIF-1a and 2a, and their regulatory prolyl hydroxylase enzymes (PHD1, PHD2, and PHD3). Statistical analysis compared these factors with each other and with prostate-specific antigen relapse. There was a significant correlation between HIF-1a and HIF-2a expression (P = 0.02), and with androgen receptor (P = 0.04 and P < 0.001, respectively) and VEGF expression (P = 0.05 and P < 0.001, respectively). VEGF was also significantly related to the androgen receptor (P = 0.05), whereas PHD2 was inversely related to HIF-2a expression. No significant association was shown between HIF-1a or HIF-2a and time to prostate-specific antigen recurrence (P = 0.20 and P = 0.94, respectively).
Question: Is the androgen receptor significantly associated with vascular endothelial growth factor and hypoxia sensing via hypoxia-inducible factors HIF-1a , HIF-2a , and the prolyl hydroxylases in human prostate cancer?
Output:
|
PubmedQA54313
|
[
{
"role": "user",
"content": "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 is to determine the effect of the natural product parthenolide, a sesquiterpene lactone isolated from extracts of the herb Tanacetum parthenium, on the proliferation of vascular smooth muscle cells (VSMCs). Rat aortic VSMCs were isolated and cultured in vitro, and treated with different concentrations of parthenolide (10, 20 and 30 mumol/L). [(3)H]thymidine incorporation was used as an index of cell proliferation. Cell cycle progression and distribution were determined by flow cytometric analysis. Furthermore, the expression of several regulatory proteins relevant to VSMC proliferation including IkappaBalpha, cyclooxygenase-2 (Cox-2), p21, and p27 was examined to investigate the potential molecular mechanism. Treatment with parthenolide significantly decreased the [(3)H]thymidine incorporation into DNA by 30%~56% relative to control values in a dose-dependent manner (P<0.05). Addition of parthenolide also increased cell population at G(0)/G(1) phase by 19.2%~65.7% (P<0.05) and decreased cell population at S phase by 50.7%~84.8% (P<0.05), which is consistent with its stimulatory effects on p21 and p27. In addition, parthenolide also increased IkappaBalpha expression and reduced Cox-2 expression in a time-dependent manner.\n Question: Does parthenolide inhibit proliferation of vascular smooth muscle cells through induction of G0/G1 phase cell cycle arrest?\n Output: "
},
{
"role": "assistant",
"content": "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 is to determine the effect of the natural product parthenolide, a sesquiterpene lactone isolated from extracts of the herb Tanacetum parthenium, on the proliferation of vascular smooth muscle cells (VSMCs). Rat aortic VSMCs were isolated and cultured in vitro, and treated with different concentrations of parthenolide (10, 20 and 30 mumol/L). [(3)H]thymidine incorporation was used as an index of cell proliferation. Cell cycle progression and distribution were determined by flow cytometric analysis. Furthermore, the expression of several regulatory proteins relevant to VSMC proliferation including IkappaBalpha, cyclooxygenase-2 (Cox-2), p21, and p27 was examined to investigate the potential molecular mechanism. Treatment with parthenolide significantly decreased the [(3)H]thymidine incorporation into DNA by 30%~56% relative to control values in a dose-dependent manner (P<0.05). Addition of parthenolide also increased cell population at G(0)/G(1) phase by 19.2%~65.7% (P<0.05) and decreased cell population at S phase by 50.7%~84.8% (P<0.05), which is consistent with its stimulatory effects on p21 and p27. In addition, parthenolide also increased IkappaBalpha expression and reduced Cox-2 expression in a time-dependent manner.
Question: Does parthenolide inhibit proliferation of vascular smooth muscle cells through induction of G0/G1 phase cell cycle arrest?
Output:
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PubmedQA102723
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Cilostazol is a specific inhibitor of 3'-5'-cyclic adenosine monophosphate (cAMP) phosphodiesterase, which is widely used to treat ischemic symptoms of peripheral vascular disease. Although cilostazol has been shown to exhibit vasodilator properties as well as antiplatelet and anti-inflammatory effects, its cellular mechanism in microglia is unknown. In the present study, we assessed the anti-inflammatory effect of cilostazol on the production of pro-inflammatory mediators in lipopolysaccharide (LPS)-stimulated murine BV2 microglia. We examined the effects of cilostazol on LPS-induced nuclear factor-kappaB (NF-kappaB) activation and phosphorylation of mitogen-activated protein kinases (MAPKs). Cilostazol suppressed production of nitric oxide (NO), prostaglandin E(2) (PGE(2)) and the proinflammatory cytokines, interleukin-1 (IL-1), tumour necrosis factor-alpha, and monocyte chemoattractant protein-1 (MCP-1), in a concentration-dependent manner. Inhibitory effects of cilostazol were not affected by treatment with an adenylate cyclase inhibitor, SQ 22536, indicating that these actions of cilostazol were cAMP-independent. Cilostazol significantly inhibited the DNA binding and transcriptional activity of NF-kappaB. Moreover, cilostazol blocked signalling upstream of NF-kappaB activation by inhibiting extracellular signal-regulated kinases 1 and 2 (ERK1/2) and c-Jun N-terminal kinase (JNK), but without affecting the activity of p38 MAPK.\n Question: Is cilostazol anti-inflammatory in BV2 microglial cells by inactivating nuclear factor-kappaB and inhibiting mitogen-activated protein kinases?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Cilostazol is a specific inhibitor of 3'-5'-cyclic adenosine monophosphate (cAMP) phosphodiesterase, which is widely used to treat ischemic symptoms of peripheral vascular disease. Although cilostazol has been shown to exhibit vasodilator properties as well as antiplatelet and anti-inflammatory effects, its cellular mechanism in microglia is unknown. In the present study, we assessed the anti-inflammatory effect of cilostazol on the production of pro-inflammatory mediators in lipopolysaccharide (LPS)-stimulated murine BV2 microglia. We examined the effects of cilostazol on LPS-induced nuclear factor-kappaB (NF-kappaB) activation and phosphorylation of mitogen-activated protein kinases (MAPKs). Cilostazol suppressed production of nitric oxide (NO), prostaglandin E(2) (PGE(2)) and the proinflammatory cytokines, interleukin-1 (IL-1), tumour necrosis factor-alpha, and monocyte chemoattractant protein-1 (MCP-1), in a concentration-dependent manner. Inhibitory effects of cilostazol were not affected by treatment with an adenylate cyclase inhibitor, SQ 22536, indicating that these actions of cilostazol were cAMP-independent. Cilostazol significantly inhibited the DNA binding and transcriptional activity of NF-kappaB. Moreover, cilostazol blocked signalling upstream of NF-kappaB activation by inhibiting extracellular signal-regulated kinases 1 and 2 (ERK1/2) and c-Jun N-terminal kinase (JNK), but without affecting the activity of p38 MAPK.
Question: Is cilostazol anti-inflammatory in BV2 microglial cells by inactivating nuclear factor-kappaB and inhibiting mitogen-activated protein kinases?
Output:
|
PubmedQA140676
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Patients with severe left ventricular systolic dysfunction (LVSD) undergoing coronary artery bypass grafting (CABG) have an increased risk for morbidity and mortality. The purpose of this study was to assess the association of pre-CABG right ventricular (RV) function with outcome for patients with severe LVSD. We performed a retrospective evaluation of 41 patients with severe LVSD (left ventricular ejection fraction [LVEF] < or =25%) scheduled for nonemergent CABG. Data were obtained from review of medical records, transesophageal echocardiography tapes, and phone interview. The pre- and post-cardiopulmonary bypass (CPB) LVEF and the RV fractional area of contraction (RVFAC) were calculated by using intraoperative transesophageal echocardiography. Group 1 patients had an RVFAC < or =35% (n = 7), whereas Group 2 patients had RVFAC >35% (n = 34). The durations of mechanical ventilation and of intensive care unit and hospital stays are presented as the median. Pre-CABG LVEF was similar between Groups 1 and 2 (15.8% +/- 3.3% versus 17.8% +/- 3.9%). Compared with Group 2, Group 1 patients required greater duration of mechanical ventilation (12 days versus 1 day; P < 0.01), longer intensive care unit (14 versus 2 days; P < 0.01) and hospital (14 versus 7 days; P = 0.02) stays, had a more frequent incidence and severity of LV diastolic dysfunction, and had a smaller change in LVEF immediately after CPB (4.1% +/- 8.3% versus 12.5% +/- 9.2%; P = 0.03). All Group 1 patients died of cardiac causes within 2 yr of surgery; five died during the same hospital admission. Three Group 2 patients died: one of colon cancer at 18 mo after CABG and two of cardiac causes 24 and 48 mo after surgery. A fourth patient was awaiting cardiac transplantation 4 yr after surgery. The remaining Group 2 patients were New York Heart Association Classification I or II. For patients with severe LVSD undergoing CABG, pre-CPB RV dysfunction was associated with poor outcome. Patients with RVFAC >35% had a relatively uneventful perioperative course and good long-term survival, whereas patients with RVFAC < or =35% had a poor early and late outcome. Assessment of RV function is useful to further assess the risk of CABG.\n Question: Is precardiopulmonary bypass right ventricular function associated with poor outcome after coronary artery bypass grafting in patients with severe left ventricular systolic dysfunction?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Patients with severe left ventricular systolic dysfunction (LVSD) undergoing coronary artery bypass grafting (CABG) have an increased risk for morbidity and mortality. The purpose of this study was to assess the association of pre-CABG right ventricular (RV) function with outcome for patients with severe LVSD. We performed a retrospective evaluation of 41 patients with severe LVSD (left ventricular ejection fraction [LVEF] < or =25%) scheduled for nonemergent CABG. Data were obtained from review of medical records, transesophageal echocardiography tapes, and phone interview. The pre- and post-cardiopulmonary bypass (CPB) LVEF and the RV fractional area of contraction (RVFAC) were calculated by using intraoperative transesophageal echocardiography. Group 1 patients had an RVFAC < or =35% (n = 7), whereas Group 2 patients had RVFAC >35% (n = 34). The durations of mechanical ventilation and of intensive care unit and hospital stays are presented as the median. Pre-CABG LVEF was similar between Groups 1 and 2 (15.8% +/- 3.3% versus 17.8% +/- 3.9%). Compared with Group 2, Group 1 patients required greater duration of mechanical ventilation (12 days versus 1 day; P < 0.01), longer intensive care unit (14 versus 2 days; P < 0.01) and hospital (14 versus 7 days; P = 0.02) stays, had a more frequent incidence and severity of LV diastolic dysfunction, and had a smaller change in LVEF immediately after CPB (4.1% +/- 8.3% versus 12.5% +/- 9.2%; P = 0.03). All Group 1 patients died of cardiac causes within 2 yr of surgery; five died during the same hospital admission. Three Group 2 patients died: one of colon cancer at 18 mo after CABG and two of cardiac causes 24 and 48 mo after surgery. A fourth patient was awaiting cardiac transplantation 4 yr after surgery. The remaining Group 2 patients were New York Heart Association Classification I or II. For patients with severe LVSD undergoing CABG, pre-CPB RV dysfunction was associated with poor outcome. Patients with RVFAC >35% had a relatively uneventful perioperative course and good long-term survival, whereas patients with RVFAC < or =35% had a poor early and late outcome. Assessment of RV function is useful to further assess the risk of CABG.
Question: Is precardiopulmonary bypass right ventricular function associated with poor outcome after coronary artery bypass grafting in patients with severe left ventricular systolic dysfunction?
Output:
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PubmedQA155315
|
[
{
"role": "user",
"content": "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 the study was to assess the localization of Polysialic acid (polySia) and Neural cell adhesion molecule (NCAM) in grade I-IV astrocytomas by confocal microscopy, and also to clarify and compare their relationship to conventional clinicopathological features in these tumors. Study material was stained immunohistochemically for polySia, NCAM and IDH1-R132H point mutation. Confocal microscopy of polySia and NCAM staining was performed on tissue micro-array samples (TMA) of 242 diffusely infiltrating astrocytomas (grade II: 28; grade III: 33; grade IV: 181) and 82 pilocytic astrocytomas. The results were statistically correlated to clinicopathological factors and survival data. PolySia was observed in 45 cases (19%) and NCAM positivity in 92 cases (38%). All 45 tumors with polySia positivity were also positive for NCAM whereas there were 47 tumors which contained positive staining for NCAM but not for polySia. The simultaneous expression was concomitant and colocalized suggesting polysialyated NCAM (polySia-NCAM). PolySia expression was significantly stronger in IDH1 mutated tumors than in IDH1 non-mutated (p = 0.001, chi-square test). There were no significant differences in polySia-NCAM between primary tumors or recurrences (p = n.s., chi-square test). PolySia positivity was associated with longer patient survival in relation to total tumor material (p = 0.020, log-rank test). Furthermore, when only glioblastomas were assessed, patients with positive polySia had significantly better prognosis (p = 0.006, log-rank test). In multivariate survival analysis, polySia was found to be an independent prognostic factor. PolySia was nearly absent in grade I pilocytic astrocytomas (1 immunopositive tumor of 82).\n Question: Is polysialic acid associated with better prognosis and IDH1-mutation in diffusely infiltrating astrocytomas?\n Output: "
},
{
"role": "assistant",
"content": "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 the study was to assess the localization of Polysialic acid (polySia) and Neural cell adhesion molecule (NCAM) in grade I-IV astrocytomas by confocal microscopy, and also to clarify and compare their relationship to conventional clinicopathological features in these tumors. Study material was stained immunohistochemically for polySia, NCAM and IDH1-R132H point mutation. Confocal microscopy of polySia and NCAM staining was performed on tissue micro-array samples (TMA) of 242 diffusely infiltrating astrocytomas (grade II: 28; grade III: 33; grade IV: 181) and 82 pilocytic astrocytomas. The results were statistically correlated to clinicopathological factors and survival data. PolySia was observed in 45 cases (19%) and NCAM positivity in 92 cases (38%). All 45 tumors with polySia positivity were also positive for NCAM whereas there were 47 tumors which contained positive staining for NCAM but not for polySia. The simultaneous expression was concomitant and colocalized suggesting polysialyated NCAM (polySia-NCAM). PolySia expression was significantly stronger in IDH1 mutated tumors than in IDH1 non-mutated (p = 0.001, chi-square test). There were no significant differences in polySia-NCAM between primary tumors or recurrences (p = n.s., chi-square test). PolySia positivity was associated with longer patient survival in relation to total tumor material (p = 0.020, log-rank test). Furthermore, when only glioblastomas were assessed, patients with positive polySia had significantly better prognosis (p = 0.006, log-rank test). In multivariate survival analysis, polySia was found to be an independent prognostic factor. PolySia was nearly absent in grade I pilocytic astrocytomas (1 immunopositive tumor of 82).
Question: Is polysialic acid associated with better prognosis and IDH1-mutation in diffusely infiltrating astrocytomas?
Output:
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PubmedQA151600
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Psoriasis is one of the most frequent skin diseases world-wide. The disease impacts enormously on affected patients and poses a huge financial burden on health care providers. Several lines of evidence suggest that the nuclear hormone receptor peroxisome proliferator activator (PPAR) beta/delta, known to regulate epithelial differentiation and wound healing, contributes to psoriasis pathogenesis. It is unclear, however, whether activation of PPARbeta/delta is sufficient to trigger psoriasis-like changes in vivo. Using immunohistochemistry, we define the distribution of PPARbeta/delta in the skin lesions of psoriasis. By expression profiling, we confirm that PPARbeta/delta is overexpressed in the vast majority of psoriasis patients. We further establish a transgenic model allowing inducible activation of PPARbeta/delta in murine epidermis mimicking its distribution in psoriasis lesions. Upon activation of PPARbeta/delta, transgenic mice sustain an inflammatory skin disease strikingly similar to psoriasis, featuring hyperproliferation of keratinocytes, dendritic cell accumulation, and endothelial activation. Development of this phenotype requires the activation of the Th17 subset of T cells, shown previously to be central to psoriasis. Moreover, gene dysregulation in the transgenic mice is highly similar to that in psoriasis. Key transcriptional programs activated in psoriasis, including IL1-related signalling and cholesterol biosynthesis, are replicated in the mouse model, suggesting that PPARbeta/delta regulates these transcriptional changes in psoriasis. Finally, we identify phosphorylation of STAT3 as a novel pathway activated by PPARbeta/delta and show that inhibition of STAT3 phosphorylation blocks disease development.\n Question: Does activation of PPARbeta/delta cause a psoriasis-like skin disease in vivo?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Psoriasis is one of the most frequent skin diseases world-wide. The disease impacts enormously on affected patients and poses a huge financial burden on health care providers. Several lines of evidence suggest that the nuclear hormone receptor peroxisome proliferator activator (PPAR) beta/delta, known to regulate epithelial differentiation and wound healing, contributes to psoriasis pathogenesis. It is unclear, however, whether activation of PPARbeta/delta is sufficient to trigger psoriasis-like changes in vivo. Using immunohistochemistry, we define the distribution of PPARbeta/delta in the skin lesions of psoriasis. By expression profiling, we confirm that PPARbeta/delta is overexpressed in the vast majority of psoriasis patients. We further establish a transgenic model allowing inducible activation of PPARbeta/delta in murine epidermis mimicking its distribution in psoriasis lesions. Upon activation of PPARbeta/delta, transgenic mice sustain an inflammatory skin disease strikingly similar to psoriasis, featuring hyperproliferation of keratinocytes, dendritic cell accumulation, and endothelial activation. Development of this phenotype requires the activation of the Th17 subset of T cells, shown previously to be central to psoriasis. Moreover, gene dysregulation in the transgenic mice is highly similar to that in psoriasis. Key transcriptional programs activated in psoriasis, including IL1-related signalling and cholesterol biosynthesis, are replicated in the mouse model, suggesting that PPARbeta/delta regulates these transcriptional changes in psoriasis. Finally, we identify phosphorylation of STAT3 as a novel pathway activated by PPARbeta/delta and show that inhibition of STAT3 phosphorylation blocks disease development.
Question: Does activation of PPARbeta/delta cause a psoriasis-like skin disease in vivo?
Output:
|
PubmedQA125840
|
[
{
"role": "user",
"content": "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 articular-epiphyseal cartilage complex (AECC) is responsible for the expansion of the bone ends and serves the function of the articular cartilage in juvenile mammals. Bundles of collagen fibrils surrounding cells were in the literature observed more frequently near the articular surface of the AECC. The articular surface, the perichondrium, and cartilage canals are interfaces where appositional growth of the AECC has been demonstrated. The current study aimed to evaluate the potential of second harmonic generation (SHG) to locate the collagen fibril bundles near the articular surface and to examine whether a comparable collagen fibril organization could be observed near the other interfaces of the AECC. The study included the femoral condyle of four piglets aged 82-141 days. The forward and backward scattered SHG, and their ratio, was analyzed across the AECC using objectives with different numerical aperture. Two-photon-excited fluorescence was used to visualize cells. A similar pattern of collagen fibril organization was observed near the articular surface, around cartilage canals, and adjacent to the perichondrium. The pattern consisted of a higher ratio of forward to backward scattered SHG that increased relative to the surrounding matrix at lower numerical aperture. This was interpreted to reflect collagen fibril bundles in the territorial matrix of cells in these areas.\n Question: Does second harmonic generation imaging reveal a distinct organization of collagen fibrils in locations associated with cartilage growth?\n Output: "
},
{
"role": "assistant",
"content": "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 articular-epiphyseal cartilage complex (AECC) is responsible for the expansion of the bone ends and serves the function of the articular cartilage in juvenile mammals. Bundles of collagen fibrils surrounding cells were in the literature observed more frequently near the articular surface of the AECC. The articular surface, the perichondrium, and cartilage canals are interfaces where appositional growth of the AECC has been demonstrated. The current study aimed to evaluate the potential of second harmonic generation (SHG) to locate the collagen fibril bundles near the articular surface and to examine whether a comparable collagen fibril organization could be observed near the other interfaces of the AECC. The study included the femoral condyle of four piglets aged 82-141 days. The forward and backward scattered SHG, and their ratio, was analyzed across the AECC using objectives with different numerical aperture. Two-photon-excited fluorescence was used to visualize cells. A similar pattern of collagen fibril organization was observed near the articular surface, around cartilage canals, and adjacent to the perichondrium. The pattern consisted of a higher ratio of forward to backward scattered SHG that increased relative to the surrounding matrix at lower numerical aperture. This was interpreted to reflect collagen fibril bundles in the territorial matrix of cells in these areas.
Question: Does second harmonic generation imaging reveal a distinct organization of collagen fibrils in locations associated with cartilage growth?
Output:
|
PubmedQA157952
|
[
{
"role": "user",
"content": "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 breast cancer patients treated in the 1970s and 1980s, radiation therapy (RT) for left-sided tumors has been associated with an elevated risk of cardiac mortality. In recent years, improved RT techniques have reduced radiation exposure of the heart and major coronary vessels, but some exposure remains unavoidable. In a retrospective cohort study, we investigated the long-term cardiac mortality risk of breast cancer survivors treated with modern RT in Germany. A total of 11,982 women were included who were treated for breast cancer between 1998 and 2008. A systematic mortality follow-up was conducted until December 2012. The effect of breast cancer laterality on cardiac mortality and on overall mortality was investigated as a surrogate measure of exposure. Using Cox regression, we analyzed survival time as the primary outcome measure, taking potential confounding factors into account. We found no evidence for an effect of tumor laterality on mortality in irradiated patients (N = 9058). For cardiac mortality, the hazard ratio was 0.94 (95% CI 0.64-1.38) for left-sided versus right-sided tumors. For all causes of death, the hazard ratio was 0.95 (95% CI 0.85-1.05). A diagnosis of cardiac illness prior to breast cancer treatment increased both cardiac mortality risk and overall mortality risk.\n Question: Is 3D conformal radiotherapy associated with the long-term cardiac mortality in breast cancer patients : a retrospective cohort study in Germany ( PASSOS-Heart 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: In breast cancer patients treated in the 1970s and 1980s, radiation therapy (RT) for left-sided tumors has been associated with an elevated risk of cardiac mortality. In recent years, improved RT techniques have reduced radiation exposure of the heart and major coronary vessels, but some exposure remains unavoidable. In a retrospective cohort study, we investigated the long-term cardiac mortality risk of breast cancer survivors treated with modern RT in Germany. A total of 11,982 women were included who were treated for breast cancer between 1998 and 2008. A systematic mortality follow-up was conducted until December 2012. The effect of breast cancer laterality on cardiac mortality and on overall mortality was investigated as a surrogate measure of exposure. Using Cox regression, we analyzed survival time as the primary outcome measure, taking potential confounding factors into account. We found no evidence for an effect of tumor laterality on mortality in irradiated patients (N = 9058). For cardiac mortality, the hazard ratio was 0.94 (95% CI 0.64-1.38) for left-sided versus right-sided tumors. For all causes of death, the hazard ratio was 0.95 (95% CI 0.85-1.05). A diagnosis of cardiac illness prior to breast cancer treatment increased both cardiac mortality risk and overall mortality risk.
Question: Is 3D conformal radiotherapy associated with the long-term cardiac mortality in breast cancer patients : a retrospective cohort study in Germany ( PASSOS-Heart Study )?
Output:
|
PubmedQA167218
|
[
{
"role": "user",
"content": "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 mean platelet volume (MPV) is the most commonly used measure of platelet size and is a potential marker of platelet reactivity. In this study, we aimed to explore the relationship between hepatic histopathology in viral hepatitis and MPV levels, which are associated with platelet count and activity. We performed a retrospective case-control study of baseline histological and clinical parameters in chronic hepatitis B and C patients in our tertiary reference center between January 2005 and January 2011. Two hundred and five chronic hepatitis B patients and 133 chronic hepatitis C patients who underwent liver biopsy were included in the study. The patients were divided into two groups: Chronic hepatitis B and chronic hepatitis C and were additionally divided into groups of two according to histological activity index (HAI) and fibrosis scores obtained by liver biopsy results (according to the Ishak scoring system). The clinical characteristics of chronic viral hepatitis patients, including demographics, laboratory (especially MPV), and liver biopsy findings, were reviewed. One hundred and forty-three patients were male (69.1%), and the mean age was 41.9 ± 12.75 with an age range of 18-71 years in hepatitis B patients. In the classification made according to HAI, 181 patients were in the low activity group (88.3%) and 24 in the high activity group (11.7%). In the evaluation made according to fibrosis score, 169 patients were found to have early fibrosis (82.4%) and 36 were found to have advanced fibrosis (17.6%). In patients with hepatitis B, there was no statistically significant difference in terms of their MPV values between the two groups, separated according to their degree of activity and fibrosis. Sixty-three patients were male (47.3%), and the mean age was 50.03 ± 12.75 with an age range of 19-75 years. In the classification made according to HAI, 109 patients were in low activity group (81.9%) and 24 in high activity group (18.1%). In the evaluation made according to fibrosis score, 101 patients were found to have early fibrosis (75.9%) and 32 have advanced fibrosis (24.1%). There was a statistically significant difference between the activity and fibrosis groups of the hepatitis C patients (P = 0.04 and P = 0.02, respectively).\n Question: Is mean platelet volume an important predictor of hepatitis C but not hepatitis B liver 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: The mean platelet volume (MPV) is the most commonly used measure of platelet size and is a potential marker of platelet reactivity. In this study, we aimed to explore the relationship between hepatic histopathology in viral hepatitis and MPV levels, which are associated with platelet count and activity. We performed a retrospective case-control study of baseline histological and clinical parameters in chronic hepatitis B and C patients in our tertiary reference center between January 2005 and January 2011. Two hundred and five chronic hepatitis B patients and 133 chronic hepatitis C patients who underwent liver biopsy were included in the study. The patients were divided into two groups: Chronic hepatitis B and chronic hepatitis C and were additionally divided into groups of two according to histological activity index (HAI) and fibrosis scores obtained by liver biopsy results (according to the Ishak scoring system). The clinical characteristics of chronic viral hepatitis patients, including demographics, laboratory (especially MPV), and liver biopsy findings, were reviewed. One hundred and forty-three patients were male (69.1%), and the mean age was 41.9 ± 12.75 with an age range of 18-71 years in hepatitis B patients. In the classification made according to HAI, 181 patients were in the low activity group (88.3%) and 24 in the high activity group (11.7%). In the evaluation made according to fibrosis score, 169 patients were found to have early fibrosis (82.4%) and 36 were found to have advanced fibrosis (17.6%). In patients with hepatitis B, there was no statistically significant difference in terms of their MPV values between the two groups, separated according to their degree of activity and fibrosis. Sixty-three patients were male (47.3%), and the mean age was 50.03 ± 12.75 with an age range of 19-75 years. In the classification made according to HAI, 109 patients were in low activity group (81.9%) and 24 in high activity group (18.1%). In the evaluation made according to fibrosis score, 101 patients were found to have early fibrosis (75.9%) and 32 have advanced fibrosis (24.1%). There was a statistically significant difference between the activity and fibrosis groups of the hepatitis C patients (P = 0.04 and P = 0.02, respectively).
Question: Is mean platelet volume an important predictor of hepatitis C but not hepatitis B liver damage?
Output:
|
PubmedQA206538
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Ultraviolet (UV) absorbance of spent dialysate has been proposed as a method for monitoring hemodialysis efficiency. The contribution of the various uremic toxins to UV absorption, however, needs clarifying. Urea, creatinine and uric acid were measured in blood and dialysate before and during dialysis in 22 maintenance hemodialysis patients. Absorbance was measured in dialysate. High-performance liquid chromatography (HPLC) analyses of dialysate revealed uric acid as the predominant peak. Spent dialysate absorbance decreased, during dialysis, similarly to serum and dialysate urea, creatinine and uric acid. Dialysate urea correlated closely with absorbance, though urea did not contribute to absorbance, which was determined mostly by uric acid. Uric acid and urea removals were very similar. The spectrophotometric Kt/V correlated with spKt/V urea, with slight but significant differences between the two measurements.\n Question: Is uric acid the major determinant of absorbance in spent dialysate allowing spectrophotometric evaluation of dialysis dose?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Ultraviolet (UV) absorbance of spent dialysate has been proposed as a method for monitoring hemodialysis efficiency. The contribution of the various uremic toxins to UV absorption, however, needs clarifying. Urea, creatinine and uric acid were measured in blood and dialysate before and during dialysis in 22 maintenance hemodialysis patients. Absorbance was measured in dialysate. High-performance liquid chromatography (HPLC) analyses of dialysate revealed uric acid as the predominant peak. Spent dialysate absorbance decreased, during dialysis, similarly to serum and dialysate urea, creatinine and uric acid. Dialysate urea correlated closely with absorbance, though urea did not contribute to absorbance, which was determined mostly by uric acid. Uric acid and urea removals were very similar. The spectrophotometric Kt/V correlated with spKt/V urea, with slight but significant differences between the two measurements.
Question: Is uric acid the major determinant of absorbance in spent dialysate allowing spectrophotometric evaluation of dialysis dose?
Output:
|
PubmedQA102487
|
[
{
"role": "user",
"content": "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 synergistic action of L-carnitine (LC) and taurine (TAU) on the proliferation and osteoblastic differentiation of vascular smooth muscle cells (VSMCs). DNA and protein synthesis of VSMCs were assessed using scintillation counting. Alkaline phosphatase (ALP) activity and calcium content were determined to investigate the effects of LC and TAU on the osteoblastic differentiation and mineralization of VSMCs. TAU uptake by VSMCs was assayed. RNA interference was used to down-regulate the expression of the TAU transporter (TAUT) in rat VSMCs. LC and TAU synergistically inhibited the proliferation and beta-glycerophosphate (beta-GP)-induced osteoblastic differentiation of VSMCs as evidenced by the decreased [(3)H]thymidine incorporation, ALP activity and calcium deposition. Furthermore, LC stimulated the TAU uptake and TAUT expression in VSMCs. Suppression of TAUT with short hairpin RNA (shRNA) abolished the synergistic action of LC and TAU in VSMCs.\n Question: Do l-carnitine and taurine synergistically inhibit the proliferation and osteoblastic differentiation of vascular smooth muscle 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 investigate the synergistic action of L-carnitine (LC) and taurine (TAU) on the proliferation and osteoblastic differentiation of vascular smooth muscle cells (VSMCs). DNA and protein synthesis of VSMCs were assessed using scintillation counting. Alkaline phosphatase (ALP) activity and calcium content were determined to investigate the effects of LC and TAU on the osteoblastic differentiation and mineralization of VSMCs. TAU uptake by VSMCs was assayed. RNA interference was used to down-regulate the expression of the TAU transporter (TAUT) in rat VSMCs. LC and TAU synergistically inhibited the proliferation and beta-glycerophosphate (beta-GP)-induced osteoblastic differentiation of VSMCs as evidenced by the decreased [(3)H]thymidine incorporation, ALP activity and calcium deposition. Furthermore, LC stimulated the TAU uptake and TAUT expression in VSMCs. Suppression of TAUT with short hairpin RNA (shRNA) abolished the synergistic action of LC and TAU in VSMCs.
Question: Do l-carnitine and taurine synergistically inhibit the proliferation and osteoblastic differentiation of vascular smooth muscle cells?
Output:
|
PubmedQA184263
|
[
{
"role": "user",
"content": "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 demonstrated that induction of heme oxygenase-1 results in weight loss in several rodent models of obesity. However, the specific role of the heme oxygenase-1 metabolite, carbon monoxide (CO), in this response has yet to be established. We recently reported that chronic treatment with CO releasing molecules results in prevention of weight gain in mice fed a high fat diet. In the present study, we sought to determine the effect of chronic CO inhalation on the development and reversal of high fat diet induced obesity. CO inhalation at both levels initially resulted in a prevention and reversal of body weight and fat mass over the first 10 weeks of treatment, however, this effect was not sustained. CO inhalation in the prevention groups also had an early effect to lower fasting blood glucose but this effect also was not sustained.\n Question: Is inhalation of carbon monoxide ineffective as a long-term therapy to reduce obesity in mice fed a high fat diet?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Previous studies have demonstrated that induction of heme oxygenase-1 results in weight loss in several rodent models of obesity. However, the specific role of the heme oxygenase-1 metabolite, carbon monoxide (CO), in this response has yet to be established. We recently reported that chronic treatment with CO releasing molecules results in prevention of weight gain in mice fed a high fat diet. In the present study, we sought to determine the effect of chronic CO inhalation on the development and reversal of high fat diet induced obesity. CO inhalation at both levels initially resulted in a prevention and reversal of body weight and fat mass over the first 10 weeks of treatment, however, this effect was not sustained. CO inhalation in the prevention groups also had an early effect to lower fasting blood glucose but this effect also was not sustained.
Question: Is inhalation of carbon monoxide ineffective as a long-term therapy to reduce obesity in mice fed a high fat diet?
Output:
|
PubmedQA203132
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Although many patients with allergic rhinoconjunctivitis have symptoms due to sensitization with more than one pollen allergen, and mixed pollen extracts are widely used for allergen immunotherapy in practice, there are few published trials. We performed a 2-year multicentre, double-blind, placebo-controlled trial of subcutaneous immunotherapy with mixed depigmented-polymerized birch and grass pollen extract in 285 patients with allergic rhinoconjunctivitis symptomatic during both birch and grass pollen seasons. Primary outcome was combined symptom and medication score (SMS) assessed by daily visual analogue scales (VAS). Analysis included a placebo-based analysis examining the effect of treatment only on days when placebo patients were symptomatic. There was a significant reduction in median SMS for actively treated patients (median 5.70 (interquartile range 2.62-10.02) compared with 7.07 (3.47-10.71) for placebo, P = 0.0385). Rhinitis quality-of-life scores were significantly better for active compared with placebo, and other secondary endpoints were not significantly different. Placebo-based analysis showed a 33.7% reduced SMS at year 2 for active treatment compared with placebo on days when placebo patients were symptomatic. Both birch pollen- and grass pollen-specific IgG4 increased with active treatment.\n Question: Is depigmented-polymerized mixed grass/birch pollen extract immunotherapy effective in polysensitized 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: Although many patients with allergic rhinoconjunctivitis have symptoms due to sensitization with more than one pollen allergen, and mixed pollen extracts are widely used for allergen immunotherapy in practice, there are few published trials. We performed a 2-year multicentre, double-blind, placebo-controlled trial of subcutaneous immunotherapy with mixed depigmented-polymerized birch and grass pollen extract in 285 patients with allergic rhinoconjunctivitis symptomatic during both birch and grass pollen seasons. Primary outcome was combined symptom and medication score (SMS) assessed by daily visual analogue scales (VAS). Analysis included a placebo-based analysis examining the effect of treatment only on days when placebo patients were symptomatic. There was a significant reduction in median SMS for actively treated patients (median 5.70 (interquartile range 2.62-10.02) compared with 7.07 (3.47-10.71) for placebo, P = 0.0385). Rhinitis quality-of-life scores were significantly better for active compared with placebo, and other secondary endpoints were not significantly different. Placebo-based analysis showed a 33.7% reduced SMS at year 2 for active treatment compared with placebo on days when placebo patients were symptomatic. Both birch pollen- and grass pollen-specific IgG4 increased with active treatment.
Question: Is depigmented-polymerized mixed grass/birch pollen extract immunotherapy effective in polysensitized patients?
Output:
|
PubmedQA64382
|
[
{
"role": "user",
"content": "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 cytoplasmic oocyte maturation, Ca(2+) currents are vital for regulating a broad range of physiological processes. Recent studies have demonstrated that DMSO and EG cause large transient increases in intracellular Ca(2+) in mouse oocytes. The CP used in vitrifying protocols also increases the intracellular calcium transient. The aim of this study is to evaluate the effects of vitrifying time (before and after IVM) and exposure to the vitrification solutions and ionomycin on oocyte quality and embryonic development. 221 GV-oocytes unsuitable for IVF-ICSI cycles were randomly distributed into one of the following three groups. G1 (control group): 41 GV-oocytes IVM until MII; G2: 43 oocytes vitrified at GV stage and IVM until MII stage; and G3: 53 GV-oocytes IVM until MII and then vitrified. In order to clarify the effect of vitrification solutions (VS) on human oocyte IVM through the intracellular Ca(2+) oscillation, the following two groups were also included. G4: 43 GV-oocytes exposed to VS and IVM until MII; and G5: 41 GV-oocytes exposed to ionomycin and IVM until MII. All GV-oocytes that reached MII-stage were parthenogenetically activated to assess oocyte viability. IVM was performed in IVF-medium (24-48 h). Chemical treatment (ionomycin) and osmotic treatment (vitrification solutions) were performed without liquid-N2 immersion. The following rates were evaluated: survival (SR), in-vitro maturation (IVMR), activation (AR), development to 2-cell (DRC), development to morula (DRCM) and development to blastocyst (DRB). Ratios between the different treatment groups were compared using contingency tables analysis (chi-square test). A high survival rate was obtained in G2 (95.5 %) and G4 (96.6 %). In-vitro maturation rate was significantly higher for G4 (86 %) and G2 (83.7 %) compared to G1 (63.4 %), G3 (56.6 %) and G5 (48.8 %). DRCM was significantly higher for G1 and G2 compared to G3 (G1: 15.8 %, G2: 20.7 % and G3: 0 %). DRB was only obtained for the oocytes vitrified before IVM (G2: 3.4 %). AR was also significantly higher for G2 and G4 compared to G5 (G2: 80.5 %, G4: 86.5 % and G5: 55 %). DRCM and DRB were only obtained in G2 and G4. DRCM was significantly higher for oocytes vitrified at GV stage (G2) and for oocytes exposed to the VS in G4 compared to the oocytes exposed to the ionomycin in G5 (G2: 20.7 %; G4: 37.5 % and G5: 0 %).\n Question: Does osmotic-shock produced by vitrification solutions improve immature human oocytes in vitro maturation?\n Output: "
},
{
"role": "assistant",
"content": "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 cytoplasmic oocyte maturation, Ca(2+) currents are vital for regulating a broad range of physiological processes. Recent studies have demonstrated that DMSO and EG cause large transient increases in intracellular Ca(2+) in mouse oocytes. The CP used in vitrifying protocols also increases the intracellular calcium transient. The aim of this study is to evaluate the effects of vitrifying time (before and after IVM) and exposure to the vitrification solutions and ionomycin on oocyte quality and embryonic development. 221 GV-oocytes unsuitable for IVF-ICSI cycles were randomly distributed into one of the following three groups. G1 (control group): 41 GV-oocytes IVM until MII; G2: 43 oocytes vitrified at GV stage and IVM until MII stage; and G3: 53 GV-oocytes IVM until MII and then vitrified. In order to clarify the effect of vitrification solutions (VS) on human oocyte IVM through the intracellular Ca(2+) oscillation, the following two groups were also included. G4: 43 GV-oocytes exposed to VS and IVM until MII; and G5: 41 GV-oocytes exposed to ionomycin and IVM until MII. All GV-oocytes that reached MII-stage were parthenogenetically activated to assess oocyte viability. IVM was performed in IVF-medium (24-48 h). Chemical treatment (ionomycin) and osmotic treatment (vitrification solutions) were performed without liquid-N2 immersion. The following rates were evaluated: survival (SR), in-vitro maturation (IVMR), activation (AR), development to 2-cell (DRC), development to morula (DRCM) and development to blastocyst (DRB). Ratios between the different treatment groups were compared using contingency tables analysis (chi-square test). A high survival rate was obtained in G2 (95.5 %) and G4 (96.6 %). In-vitro maturation rate was significantly higher for G4 (86 %) and G2 (83.7 %) compared to G1 (63.4 %), G3 (56.6 %) and G5 (48.8 %). DRCM was significantly higher for G1 and G2 compared to G3 (G1: 15.8 %, G2: 20.7 % and G3: 0 %). DRB was only obtained for the oocytes vitrified before IVM (G2: 3.4 %). AR was also significantly higher for G2 and G4 compared to G5 (G2: 80.5 %, G4: 86.5 % and G5: 55 %). DRCM and DRB were only obtained in G2 and G4. DRCM was significantly higher for oocytes vitrified at GV stage (G2) and for oocytes exposed to the VS in G4 compared to the oocytes exposed to the ionomycin in G5 (G2: 20.7 %; G4: 37.5 % and G5: 0 %).
Question: Does osmotic-shock produced by vitrification solutions improve immature human oocytes in vitro maturation?
Output:
|
PubmedQA173408
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: P-selectin is released by activated platelets and endothelium contributing to inflammation and thrombosis. We evaluated the association between soluble P-selectin and atherosclerotic cardiovascular disease (ASCVD) in dialysis patients. We measured soluble P-selectin in serum from 824 incident dialysis patients. Using Cox proportional hazards models, we modeled the association of P-selectin levels with ASCVD events, cardiovascular mortality and sudden cardiac death. After adjustment for demographics, comorbidity and traditional cardiovascular risk factors, higher P-selectin levels were associated with increased risk of ASCVD and cardiovascular mortality among males (p = 0.02 and p = 0.01, respectively), but not females (p = 0.52 and p = 0.31, respectively; p interaction = 0.003), over a median of 38.2 months. Higher P-selectin was associated with a greater risk of sudden cardiac death among males (p = 0.05). The associations between increasing P-selectin and cardiovascular mortality as well as sudden cardiac death in males persisted after adjustment for C-reactive protein, interleukin-6, serum albumin and platelet count (p = 0.01 and p = 0.03, respectively). The risk for sudden cardiac death was more than 3 times greater for males in the highest tertile of soluble P-selectin compared with the lowest tertile after adjustment (HR: 3.19; 95% CI: 1.18 - 8.62; p = 0.02).\n Question: Are soluble P-selectin levels associated with cardiovascular mortality and sudden cardiac death in male dialysis 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: P-selectin is released by activated platelets and endothelium contributing to inflammation and thrombosis. We evaluated the association between soluble P-selectin and atherosclerotic cardiovascular disease (ASCVD) in dialysis patients. We measured soluble P-selectin in serum from 824 incident dialysis patients. Using Cox proportional hazards models, we modeled the association of P-selectin levels with ASCVD events, cardiovascular mortality and sudden cardiac death. After adjustment for demographics, comorbidity and traditional cardiovascular risk factors, higher P-selectin levels were associated with increased risk of ASCVD and cardiovascular mortality among males (p = 0.02 and p = 0.01, respectively), but not females (p = 0.52 and p = 0.31, respectively; p interaction = 0.003), over a median of 38.2 months. Higher P-selectin was associated with a greater risk of sudden cardiac death among males (p = 0.05). The associations between increasing P-selectin and cardiovascular mortality as well as sudden cardiac death in males persisted after adjustment for C-reactive protein, interleukin-6, serum albumin and platelet count (p = 0.01 and p = 0.03, respectively). The risk for sudden cardiac death was more than 3 times greater for males in the highest tertile of soluble P-selectin compared with the lowest tertile after adjustment (HR: 3.19; 95% CI: 1.18 - 8.62; p = 0.02).
Question: Are soluble P-selectin levels associated with cardiovascular mortality and sudden cardiac death in male dialysis patients?
Output:
|
PubmedQA175476
|
[
{
"role": "user",
"content": "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 validity of self-reported primary hip replacement, primary knee replacement, and cholecystectomy. The data from 28,524 participants in the Million Women Study who were recruited from Scotland were linked with routinely collected Scottish hospital admission data. We compared the reporting of three operations by the study participants on a postal questionnaire with that recorded in the hospital admission database. Annual incidence rates for the three operations were similar using hospital admission and self-reported data at: 2.1 (n=220) and 2.3 (n=247) per 1,000 women, respectively, for hip replacement; 1.1 per 1,000 women from both sources for knee replacement (n=118 and n=116, respectively); and 3.4 (n=357) and 3.2 (n=344) per 1,000 women, respectively, for cholecystectomy. Agreement between self-report and the hospital admission records was good for all three operations with agreements of 99.8%, 99.9%, and 99.6% for hip replacement, knee replacement, and cholecystectomy, respectively.\n Question: Does self-reported information on joint replacement and cholecystectomy agree well with that in medical records?\n Output: "
},
{
"role": "assistant",
"content": "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 validity of self-reported primary hip replacement, primary knee replacement, and cholecystectomy. The data from 28,524 participants in the Million Women Study who were recruited from Scotland were linked with routinely collected Scottish hospital admission data. We compared the reporting of three operations by the study participants on a postal questionnaire with that recorded in the hospital admission database. Annual incidence rates for the three operations were similar using hospital admission and self-reported data at: 2.1 (n=220) and 2.3 (n=247) per 1,000 women, respectively, for hip replacement; 1.1 per 1,000 women from both sources for knee replacement (n=118 and n=116, respectively); and 3.4 (n=357) and 3.2 (n=344) per 1,000 women, respectively, for cholecystectomy. Agreement between self-report and the hospital admission records was good for all three operations with agreements of 99.8%, 99.9%, and 99.6% for hip replacement, knee replacement, and cholecystectomy, respectively.
Question: Does self-reported information on joint replacement and cholecystectomy agree well with that in medical records?
Output:
|
PubmedQA75335
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Patients with inflammatory bowel disease, which includes ulcerative colitis and Crohn's disease, are at a significantly increased risk of developing colorectal cancer, and aberrant interleukin (IL)-6/STAT3 signaling pathway exists in both inflammatory bowel disease and inflammation-related gastrointestinal cancers. We have previously found that oroxylin A inhibited the NF-κB signaling in human colon tumor HCT-116 cells. However, whether oroxylin A could inhibit the colitis-associated carcinogenesis remains to be determined. HCT-116 cells were treated with various concentrations of oroxylin A. Expression of relative proteins of IL-6/STAT3 signaling pathway was assayed by Western blot and immunofluorescence analysis. Mouse model for colitis-associated colorectal cancer was induced by a combined treatment with 10 mg/kg azoxymethane (AOM) followed by 3 cycles of 2.5% dextran sodium sulfate in C57BL/6 mice. IL-6 and IL-1β gene expression were analyzed by quantitative real-time PCR. Expression of relative proteins was examined by immunohistochemistry and Western blot. Oroxylin A effectively inhibited IL-6/STAT3 pathway in human HCT-116 cells, and the effect of oroxylin A was reversible. Dietary administration of oroxylin A throughout the experimental period significantly reduced the tumor burden, inhibited cell proliferation, and induced apoptosis in colon carcinomas. The expression of inflammatory cytokines IL-6 and IL-1β decreased in tumors in oroxylin A-treated mice. The IL-6/STAT3 signaling pathway was attenuated in oroxylin A-treated mice.\n Question: Does oroxylin A inhibit colitis-associated carcinogenesis through modulating the IL-6/STAT3 signaling pathway?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Patients with inflammatory bowel disease, which includes ulcerative colitis and Crohn's disease, are at a significantly increased risk of developing colorectal cancer, and aberrant interleukin (IL)-6/STAT3 signaling pathway exists in both inflammatory bowel disease and inflammation-related gastrointestinal cancers. We have previously found that oroxylin A inhibited the NF-κB signaling in human colon tumor HCT-116 cells. However, whether oroxylin A could inhibit the colitis-associated carcinogenesis remains to be determined. HCT-116 cells were treated with various concentrations of oroxylin A. Expression of relative proteins of IL-6/STAT3 signaling pathway was assayed by Western blot and immunofluorescence analysis. Mouse model for colitis-associated colorectal cancer was induced by a combined treatment with 10 mg/kg azoxymethane (AOM) followed by 3 cycles of 2.5% dextran sodium sulfate in C57BL/6 mice. IL-6 and IL-1β gene expression were analyzed by quantitative real-time PCR. Expression of relative proteins was examined by immunohistochemistry and Western blot. Oroxylin A effectively inhibited IL-6/STAT3 pathway in human HCT-116 cells, and the effect of oroxylin A was reversible. Dietary administration of oroxylin A throughout the experimental period significantly reduced the tumor burden, inhibited cell proliferation, and induced apoptosis in colon carcinomas. The expression of inflammatory cytokines IL-6 and IL-1β decreased in tumors in oroxylin A-treated mice. The IL-6/STAT3 signaling pathway was attenuated in oroxylin A-treated mice.
Question: Does oroxylin A inhibit colitis-associated carcinogenesis through modulating the IL-6/STAT3 signaling pathway?
Output:
|
PubmedQA122697
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To evaluate the effectiveness of conducting medication management reviews (MMRs) and home medication reviews (HMRs) on improving undergraduate pharmacy students' pharmaceutical care skills and clinical knowledge. Fifth-year bachelor of science in pharmacy students were enrolled in a structured course in which MMR cases based on real patient scenarios were completed, findings were discussed in groups, and comprehensive feedback was provided by course instructors. Each student was then asked to recruit a real patient through a community pharmacy and conduct an HMR. Students' pre- and post-course scores on the same MMR case improved significantly, with 84.6% of students passing the post-course assessment. Students also completed a new post-course MMR case and 74.8% received a passing score. Students' answers on a post-course self-assessment showed a significant improvement in their scores regarding knowledge and skills in conducting MMRs and HMRs.\n Question: Does home medication review in a patient care experience for undergraduate pharmacy students?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To evaluate the effectiveness of conducting medication management reviews (MMRs) and home medication reviews (HMRs) on improving undergraduate pharmacy students' pharmaceutical care skills and clinical knowledge. Fifth-year bachelor of science in pharmacy students were enrolled in a structured course in which MMR cases based on real patient scenarios were completed, findings were discussed in groups, and comprehensive feedback was provided by course instructors. Each student was then asked to recruit a real patient through a community pharmacy and conduct an HMR. Students' pre- and post-course scores on the same MMR case improved significantly, with 84.6% of students passing the post-course assessment. Students also completed a new post-course MMR case and 74.8% received a passing score. Students' answers on a post-course self-assessment showed a significant improvement in their scores regarding knowledge and skills in conducting MMRs and HMRs.
Question: Does home medication review in a patient care experience for undergraduate pharmacy students?
Output:
|
PubmedQA108751
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: This study evaluated peripheral vasoconstriction in extremely low birth weight (ELBW) infants when body temperature decreased during the first 12 h of life. An exploratory, within-subjects design with 10 ELBW infants. Abdominal and foot temperatures were measured every minute. Peripheral vasoconstriction (abdominal>peripheral temperature by 2 degrees C) and abdominal-peripheral temperature difference were also evaluated. Abdominal and peripheral temperatures were significantly correlated within each infant. One 880 g infant exhibited isolated peripheral vasoconstriction; a 960-g infant had abdominal temperatures >1 degrees C higher than peripheral temperatures. Eight smaller infants exhibited no peripheral vasoconstriction and spent most of their observations with peripheral greater than abdominal temperatures. In eight infants, mean temperature difference was significantly higher when abdominal temperature was <36.5 degrees C.\n Question: Do extremely low birth weight preterm infants lack vasomotor response in relationship to cold body temperatures at birth?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: This study evaluated peripheral vasoconstriction in extremely low birth weight (ELBW) infants when body temperature decreased during the first 12 h of life. An exploratory, within-subjects design with 10 ELBW infants. Abdominal and foot temperatures were measured every minute. Peripheral vasoconstriction (abdominal>peripheral temperature by 2 degrees C) and abdominal-peripheral temperature difference were also evaluated. Abdominal and peripheral temperatures were significantly correlated within each infant. One 880 g infant exhibited isolated peripheral vasoconstriction; a 960-g infant had abdominal temperatures >1 degrees C higher than peripheral temperatures. Eight smaller infants exhibited no peripheral vasoconstriction and spent most of their observations with peripheral greater than abdominal temperatures. In eight infants, mean temperature difference was significantly higher when abdominal temperature was <36.5 degrees C.
Question: Do extremely low birth weight preterm infants lack vasomotor response in relationship to cold body temperatures at birth?
Output:
|
PubmedQA14813
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Olfactory dysfunction has been reported in multiple sclerosis (MS). However, to date no data are available on different qualities of olfactory function, namely odour identification, odour discrimination and odour perception threshold. To assess different qualities of olfactory function in patients with MS and correlate these with demographic data, clinical data, depression, quality of life and cognitive functions. In this cross-sectional study, 50 patients with MS or clinically isolated syndrome and 30 healthy controls were included. Olfactory function was measured using the Sniffin' Sticks test. The scores for odour identification (p = 0.001), odour perception threshold (p = 0.037) and the combined score of odour identification, discrimination and perception threshold (TDI, p = 0.002) were significantly lower in MS. Hyposmia for identification (p = 0.0017), threshold (p = 0.017) and TDI score (p = 0.0014) was more frequent in MS. Olfactory threshold was impaired in patients who were clinically active in the previous year (p = 0.026) and in patients with a disease duration less than 2 years (p = 0.0093). Identification score was negatively correlated with disease duration (p = 0.0017). Olfactory function was not associated with disability, depression or quality of life.\n Question: Is olfactory threshold impaired in early , active 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: Olfactory dysfunction has been reported in multiple sclerosis (MS). However, to date no data are available on different qualities of olfactory function, namely odour identification, odour discrimination and odour perception threshold. To assess different qualities of olfactory function in patients with MS and correlate these with demographic data, clinical data, depression, quality of life and cognitive functions. In this cross-sectional study, 50 patients with MS or clinically isolated syndrome and 30 healthy controls were included. Olfactory function was measured using the Sniffin' Sticks test. The scores for odour identification (p = 0.001), odour perception threshold (p = 0.037) and the combined score of odour identification, discrimination and perception threshold (TDI, p = 0.002) were significantly lower in MS. Hyposmia for identification (p = 0.0017), threshold (p = 0.017) and TDI score (p = 0.0014) was more frequent in MS. Olfactory threshold was impaired in patients who were clinically active in the previous year (p = 0.026) and in patients with a disease duration less than 2 years (p = 0.0093). Identification score was negatively correlated with disease duration (p = 0.0017). Olfactory function was not associated with disability, depression or quality of life.
Question: Is olfactory threshold impaired in early , active multiple sclerosis?
Output:
|
PubmedQA59765
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: We previously reported that dietary lipid quality during early life can have long-lasting effects on metabolic health and adiposity. Exposure to a postnatal diet with low dietary omega-6 (n-6) or high omega-3 (n-3) fatty acid (FA) content resulted in reduced body fat accumulation when challenged with a moderate Western-style diet (WSD) beginning in adolescence. We determined whether this programming effect is accompanied by changes in hypothalamic neural projections or modifications in the postnatal leptin surge, which would indicate the altered development of hypothalamic circuits that control energy balance. Neonatal mice were subjected to a control diet (CTR) or experimental diet with altered relative n-6 and n-3 FA contents [ie, a diet with a relative reduction in n-6 fatty acid (LOW n-6) or a diet with a relative increase in n-3 fatty acid (HIGH n-3) compared with the CTR from postnatal day (PN) 2 to 42]. Compared with CTR mice, mice fed a LOW n-6 or HIGH n-3 during postnatal life showed significant reductions in the density of both orexigenic and anorexigenic neural projections to the paraventricular nucleus of the hypothalamus at PN 28. These impairments persisted into adulthood and were still apparent after the WSD challenge between PNs 42 and 98. However, the neuroanatomical changes were not associated with changes in the postnatal leptin surge.\n Question: Does postnatal dietary fatty acid composition permanently affect the structure of hypothalamic pathways controlling energy balance in mice?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: We previously reported that dietary lipid quality during early life can have long-lasting effects on metabolic health and adiposity. Exposure to a postnatal diet with low dietary omega-6 (n-6) or high omega-3 (n-3) fatty acid (FA) content resulted in reduced body fat accumulation when challenged with a moderate Western-style diet (WSD) beginning in adolescence. We determined whether this programming effect is accompanied by changes in hypothalamic neural projections or modifications in the postnatal leptin surge, which would indicate the altered development of hypothalamic circuits that control energy balance. Neonatal mice were subjected to a control diet (CTR) or experimental diet with altered relative n-6 and n-3 FA contents [ie, a diet with a relative reduction in n-6 fatty acid (LOW n-6) or a diet with a relative increase in n-3 fatty acid (HIGH n-3) compared with the CTR from postnatal day (PN) 2 to 42]. Compared with CTR mice, mice fed a LOW n-6 or HIGH n-3 during postnatal life showed significant reductions in the density of both orexigenic and anorexigenic neural projections to the paraventricular nucleus of the hypothalamus at PN 28. These impairments persisted into adulthood and were still apparent after the WSD challenge between PNs 42 and 98. However, the neuroanatomical changes were not associated with changes in the postnatal leptin surge.
Question: Does postnatal dietary fatty acid composition permanently affect the structure of hypothalamic pathways controlling energy balance in mice?
Output:
|
PubmedQA8247
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Selenium (Se) is an essential trace element needed for the biosynthesis of selenoproteins. Selenocysteine incorporation sequence binding protein 2 (SBP2) represents a key trans-acting factor for the co-translational insertion of selenocysteine into selenoproteins. We recently described children with mutations in the SBP2 gene who displayed abnormal thyroid function tests and reduced selenoprotein concentrations. We have tried to improve selenoprotein biosynthesis and thyroid hormone metabolism in SBP2 deficient subjects by supplementing an organic and an inorganic Se form. Three affected and two unaffected siblings received daily doses of 100, 200, or 400 microg selenomethionine-rich yeast and 400 microg sodium selenite for one month each. Serum was drawn at baseline and after supplementations. Thyroid function tests, extracellular glutathione peroxidase activity, Se, and selenoprotein P concentrations were determined. Selenomethionine-rich yeast increased serum Se concentrations in all subjects irrespective of genotype. Sodium selenite was effective in increasing the selenoprotein P concentration in normal and to a lesser degree in affected subjects. Both forms failed to increase the glutathione peroxidase activity or to correct the thyroid function abnormalities in the SBP2 deficient individuals indicating that impaired deiodinase expression was not positively affected. No adverse side effects were observed.\n Question: Does selenium supplementation fail to correct the selenoprotein synthesis defect in subjects with SBP2 gene mutations?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Selenium (Se) is an essential trace element needed for the biosynthesis of selenoproteins. Selenocysteine incorporation sequence binding protein 2 (SBP2) represents a key trans-acting factor for the co-translational insertion of selenocysteine into selenoproteins. We recently described children with mutations in the SBP2 gene who displayed abnormal thyroid function tests and reduced selenoprotein concentrations. We have tried to improve selenoprotein biosynthesis and thyroid hormone metabolism in SBP2 deficient subjects by supplementing an organic and an inorganic Se form. Three affected and two unaffected siblings received daily doses of 100, 200, or 400 microg selenomethionine-rich yeast and 400 microg sodium selenite for one month each. Serum was drawn at baseline and after supplementations. Thyroid function tests, extracellular glutathione peroxidase activity, Se, and selenoprotein P concentrations were determined. Selenomethionine-rich yeast increased serum Se concentrations in all subjects irrespective of genotype. Sodium selenite was effective in increasing the selenoprotein P concentration in normal and to a lesser degree in affected subjects. Both forms failed to increase the glutathione peroxidase activity or to correct the thyroid function abnormalities in the SBP2 deficient individuals indicating that impaired deiodinase expression was not positively affected. No adverse side effects were observed.
Question: Does selenium supplementation fail to correct the selenoprotein synthesis defect in subjects with SBP2 gene mutations?
Output:
|
PubmedQA66079
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: This study aimed to evaluate the prognostic implications of insulin-like growth factor-II mRNA binding protein-3 (IMP3) and podoplanin (PDPN) as therapeutic targets against oral squamous cell carcinoma (OSCC) with bone invasion. We elucidated the correlation of IMP3 and PDPN expression with bone invasion in 160 OSCC tissue specimens, and assessed a mouse calvarium xenograft model using an IMP3- and PDPN-depleted OSCC cell line. The retrospective analysis revealed that the expression of IMP3 and PDPN is significantly correlated with T stage, lymph node metastasis, and the overall survival of OSCC patients. In addition, the dual expression of IMP3 and PDPN but not the single expression of either IMP3 or PDPN was associated with bone invasion and the number of osteoclasts in patients with OSCC. In support of these findings, IMP3 or PDPN depletion inhibited the invasive capacity of OSCC cells in a three-dimensional culture system, tumorigenesis, and regional bone destruction in a xenograft mouse model. In addition, IMP3 or PDPN depletion inhibited the expression of interleukin (IL)-6 and IL-8 in OSCC cells, and decreased the expression of receptor activator of NF-κB ligand (RANKL) in xenograft tumor tissues of OSCC.\n Question: Are insulin-like growth factor-II mRNA binding protein-3 and podoplanin expression associated with bone invasion and prognosis in oral 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: This study aimed to evaluate the prognostic implications of insulin-like growth factor-II mRNA binding protein-3 (IMP3) and podoplanin (PDPN) as therapeutic targets against oral squamous cell carcinoma (OSCC) with bone invasion. We elucidated the correlation of IMP3 and PDPN expression with bone invasion in 160 OSCC tissue specimens, and assessed a mouse calvarium xenograft model using an IMP3- and PDPN-depleted OSCC cell line. The retrospective analysis revealed that the expression of IMP3 and PDPN is significantly correlated with T stage, lymph node metastasis, and the overall survival of OSCC patients. In addition, the dual expression of IMP3 and PDPN but not the single expression of either IMP3 or PDPN was associated with bone invasion and the number of osteoclasts in patients with OSCC. In support of these findings, IMP3 or PDPN depletion inhibited the invasive capacity of OSCC cells in a three-dimensional culture system, tumorigenesis, and regional bone destruction in a xenograft mouse model. In addition, IMP3 or PDPN depletion inhibited the expression of interleukin (IL)-6 and IL-8 in OSCC cells, and decreased the expression of receptor activator of NF-κB ligand (RANKL) in xenograft tumor tissues of OSCC.
Question: Are insulin-like growth factor-II mRNA binding protein-3 and podoplanin expression associated with bone invasion and prognosis in oral squamous cell carcinoma?
Output:
|
PubmedQA42344
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Mammalian heparanase degrades heparan sulfate, the main polysaccharide of the basement membrane. Heparanase is an important determinant in cancer progression, acting via the breakdown of extracellular barriers for invasion, as well as release of heparan sulfate-bound angiogenic and growth-promoting factors. The present study was undertaken to elucidate molecular mechanisms responsible for heparanase overexpression in breast cancer. To characterize heparanase regulation by estrogen and tamoxifen and its clinical relevance for breast tumorigenesis, we applied immunohistochemical analysis of tissue microarray combined with chromatin immunoprecipitation assay, reverse transcription-PCR, and Western blot analysis. A highly significant correlation (P<0.0001) between estrogen receptor (ER) positivity and heparanase overexpression was found in breast cancer. Binding of ER to heparanase promoter accompanied estrogen-induced increase in heparanase expression by breast carcinoma cells. Surprisingly, heparanase transcription was also stimulated by tamoxifen, conferring a proliferation advantage to breast carcinoma cells grown on a naturally produced extracellular matrix. Heparanase overexpression was invariably detected in ER-positive second primary breast tumors, developed in patients receiving tamoxifen for the initial breast carcinoma. The molecular mechanism of the estrogenlike effect of tamoxifen on heparanase expression involves recruitment of transcription coactivator AIB1 to the heparanase promoter.\n Question: Does tamoxifen induce heparanase expression in estrogen receptor-positive breast cancer?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Mammalian heparanase degrades heparan sulfate, the main polysaccharide of the basement membrane. Heparanase is an important determinant in cancer progression, acting via the breakdown of extracellular barriers for invasion, as well as release of heparan sulfate-bound angiogenic and growth-promoting factors. The present study was undertaken to elucidate molecular mechanisms responsible for heparanase overexpression in breast cancer. To characterize heparanase regulation by estrogen and tamoxifen and its clinical relevance for breast tumorigenesis, we applied immunohistochemical analysis of tissue microarray combined with chromatin immunoprecipitation assay, reverse transcription-PCR, and Western blot analysis. A highly significant correlation (P<0.0001) between estrogen receptor (ER) positivity and heparanase overexpression was found in breast cancer. Binding of ER to heparanase promoter accompanied estrogen-induced increase in heparanase expression by breast carcinoma cells. Surprisingly, heparanase transcription was also stimulated by tamoxifen, conferring a proliferation advantage to breast carcinoma cells grown on a naturally produced extracellular matrix. Heparanase overexpression was invariably detected in ER-positive second primary breast tumors, developed in patients receiving tamoxifen for the initial breast carcinoma. The molecular mechanism of the estrogenlike effect of tamoxifen on heparanase expression involves recruitment of transcription coactivator AIB1 to the heparanase promoter.
Question: Does tamoxifen induce heparanase expression in estrogen receptor-positive breast cancer?
Output:
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PubmedQA6776
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Monoamine oxidase A (MAOA), a catecholamine neurotransmitter degrading enzyme, is closely associated with neurological and psychiatric disorders. However, its role in cancer progression remains unknown. Hepatocellular carcinoma (HCC) tissue arrays (n=254) were used to investigate the correlation between MAOA expression and clinicopathological findings. In vitro invasion and anoikis assays, and in vivo intrahepatic and lung metastasis models were used to determine the role of MAOA in HCC metastasis. Quantitative real-time PCR, western blotting, immunohistochemical staining and HPLC analysis were performed to uncover the mechanism of MAOA in HCC. We found that MAOA expression was significantly downregulated in 254 clinical HCC samples and was closely correlated with cancer vasoinvasion, metastasis, and poor prognoses. We then demonstrated that MAOA suppressed norepinephrine/epinephrine (NE/E)-induced HCC invasion and anoikis inhibition, and uncovered that the effects of NE/E on HCC behaviors were primarily mediated through alpha 1A (ADRA1A) and beta 2 adrenergic receptors (ADRB2). In addition to the canonical signaling pathway, which is mediated via adrenergic receptors (ADRs), we found that ADR-mediated EGFR transactivation was also involved in NE-induced HCC invasion and anoikis inhibition. Notably, we found that MAOA could synergize with EGFR inhibitors or ADR antagonists to abrogate NE-induced HCC behaviors.\n Question: Does monoamine oxidase A suppress hepatocellular carcinoma metastasis by inhibiting the adrenergic system and its transactivation of EGFR 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: Monoamine oxidase A (MAOA), a catecholamine neurotransmitter degrading enzyme, is closely associated with neurological and psychiatric disorders. However, its role in cancer progression remains unknown. Hepatocellular carcinoma (HCC) tissue arrays (n=254) were used to investigate the correlation between MAOA expression and clinicopathological findings. In vitro invasion and anoikis assays, and in vivo intrahepatic and lung metastasis models were used to determine the role of MAOA in HCC metastasis. Quantitative real-time PCR, western blotting, immunohistochemical staining and HPLC analysis were performed to uncover the mechanism of MAOA in HCC. We found that MAOA expression was significantly downregulated in 254 clinical HCC samples and was closely correlated with cancer vasoinvasion, metastasis, and poor prognoses. We then demonstrated that MAOA suppressed norepinephrine/epinephrine (NE/E)-induced HCC invasion and anoikis inhibition, and uncovered that the effects of NE/E on HCC behaviors were primarily mediated through alpha 1A (ADRA1A) and beta 2 adrenergic receptors (ADRB2). In addition to the canonical signaling pathway, which is mediated via adrenergic receptors (ADRs), we found that ADR-mediated EGFR transactivation was also involved in NE-induced HCC invasion and anoikis inhibition. Notably, we found that MAOA could synergize with EGFR inhibitors or ADR antagonists to abrogate NE-induced HCC behaviors.
Question: Does monoamine oxidase A suppress hepatocellular carcinoma metastasis by inhibiting the adrenergic system and its transactivation of EGFR signaling?
Output:
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PubmedQA206312
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Treatment for patients with N2-positive stage IIIA non-small cell lung cancer has been a controversial issue. The current study evaluated the outcomes in patients treated with trimodality therapy, which consisted of neoadjuvant radiation therapy concurrent with chemotherapy followed by surgical resection, with emphasis on clinical and pathologic nodal status. We reviewed the records of 355 patients who were treated with trimodality therapy between 1997 and 2011. After completion of neoadjuvant chemoradiation, overall down-staging and complete response rates were 50.4 % (179 patients), and 13.2 % (47 patients), respectively. With median follow-up of 35.3 months, median times of progression-free survival (PFS) and overall survival (OS) were 16.3 months and 45.5 months, respectively. Seventeen patients (4.8 %) died of postoperative complications, and the remaining 338 patients were analyzed on prognostic factors. Old age (p = 0.032), pneumonectomy (p < 0.001), and ypN+ (p < 0.001) were found to be the significant prognosticators for worse PFS, and old age (p = 0.013), pneumonectomy (p < 0.001), and ypN+ (p < 0.001) were related to worse OS. Clinical N2 status did not influence either OS or PFS: the number of involved stations (single station vs. multi-station; p = 0.187 for PFS; p = 0.492 for OS), and bulk (clinically evident vs. microscopic; p = 0.902 for PFS; p = 0.915 for OS).\n Question: Do pretreatment clinical mediastinal nodal bulk and extent influence survival in N2-positive stage IIIA non-small cell lung cancer patients treated with trimodality therapy?\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: Treatment for patients with N2-positive stage IIIA non-small cell lung cancer has been a controversial issue. The current study evaluated the outcomes in patients treated with trimodality therapy, which consisted of neoadjuvant radiation therapy concurrent with chemotherapy followed by surgical resection, with emphasis on clinical and pathologic nodal status. We reviewed the records of 355 patients who were treated with trimodality therapy between 1997 and 2011. After completion of neoadjuvant chemoradiation, overall down-staging and complete response rates were 50.4 % (179 patients), and 13.2 % (47 patients), respectively. With median follow-up of 35.3 months, median times of progression-free survival (PFS) and overall survival (OS) were 16.3 months and 45.5 months, respectively. Seventeen patients (4.8 %) died of postoperative complications, and the remaining 338 patients were analyzed on prognostic factors. Old age (p = 0.032), pneumonectomy (p < 0.001), and ypN+ (p < 0.001) were found to be the significant prognosticators for worse PFS, and old age (p = 0.013), pneumonectomy (p < 0.001), and ypN+ (p < 0.001) were related to worse OS. Clinical N2 status did not influence either OS or PFS: the number of involved stations (single station vs. multi-station; p = 0.187 for PFS; p = 0.492 for OS), and bulk (clinically evident vs. microscopic; p = 0.902 for PFS; p = 0.915 for OS).
Question: Do pretreatment clinical mediastinal nodal bulk and extent influence survival in N2-positive stage IIIA non-small cell lung cancer patients treated with trimodality therapy?
Output:
|
PubmedQA181295
|
[
{
"role": "user",
"content": "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 at investigating the association of socioeconomic status and health outcomes in populations of the two remote Croatian islands and one coastal city. Medical history and survey information were used to create 33 variables that were analysed using logistic regression. The population from the island of Vis was followed up and mortality data were used to calculate hazard ratios using Cox regression. Socioeconomic inequalities were poorly associated with health and disease indices. In the matrix of 33 outcome variables and 13 socioeconomic predictor classes, only 10 associations were significant at the level of P < 0.001. None of the associations was replicated across samples. We did not detect the association of any socioeconomic estimate with mortality data for the island of Vis.\n Question: Do socioeconomic inequalities show remarkably poor association with health and disease in Southern Croatia?\n Output: "
},
{
"role": "assistant",
"content": "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 at investigating the association of socioeconomic status and health outcomes in populations of the two remote Croatian islands and one coastal city. Medical history and survey information were used to create 33 variables that were analysed using logistic regression. The population from the island of Vis was followed up and mortality data were used to calculate hazard ratios using Cox regression. Socioeconomic inequalities were poorly associated with health and disease indices. In the matrix of 33 outcome variables and 13 socioeconomic predictor classes, only 10 associations were significant at the level of P < 0.001. None of the associations was replicated across samples. We did not detect the association of any socioeconomic estimate with mortality data for the island of Vis.
Question: Do socioeconomic inequalities show remarkably poor association with health and disease in Southern Croatia?
Output:
|
PubmedQA92104
|
[
{
"role": "user",
"content": "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 effect of N-desulfated heparin on Concanavalin A (Con A)-induced liver injury and its mechanisms of action. Liver injury was induced in mice by Con A. The in vitro assays for examining the adhesions of spleen T lymphocytes and Jurkat cells to extracellular matrix (ECM) were also performed. N-desulfated heparin significantly inhibited the elevation in alanine transaminase, aspartate transaminase and lactic dehydrogenase activities in serum, and recovered the superoxide dismutase activity in the liver tissue of mice with liver injury. In liver histological examination, the inflammatory infiltration, hepatocyte degeneration and Kupffer cell hyperplasia were remarkably improved by N-desulfated heparin. Multiple administrations of the heparin derivative for one day showed a more potent prevention of the liver injury than did single dosing for three days. N-desulfated heparin significantly inhibited the adhesion of spleen cells and purified T lymphocytes isolated from the liver injured mice to either type I collagen or fibronectin but not to laminin. The heparin derivative also showed a similar inhibition of the adhesion of spleen cells from normal mice, stimulated in vitro with Con A, whereas it did not affect their proliferation. Moreover, the adhesion of human leukemia Jurkat cells to collagen I was inhibited by N-desulfated heparin.\n Question: Does n-desulfated heparin improve concanavalin A-induced liver injury partly through inhibiting T lymphocyte adhesion?\n Output: "
},
{
"role": "assistant",
"content": "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 effect of N-desulfated heparin on Concanavalin A (Con A)-induced liver injury and its mechanisms of action. Liver injury was induced in mice by Con A. The in vitro assays for examining the adhesions of spleen T lymphocytes and Jurkat cells to extracellular matrix (ECM) were also performed. N-desulfated heparin significantly inhibited the elevation in alanine transaminase, aspartate transaminase and lactic dehydrogenase activities in serum, and recovered the superoxide dismutase activity in the liver tissue of mice with liver injury. In liver histological examination, the inflammatory infiltration, hepatocyte degeneration and Kupffer cell hyperplasia were remarkably improved by N-desulfated heparin. Multiple administrations of the heparin derivative for one day showed a more potent prevention of the liver injury than did single dosing for three days. N-desulfated heparin significantly inhibited the adhesion of spleen cells and purified T lymphocytes isolated from the liver injured mice to either type I collagen or fibronectin but not to laminin. The heparin derivative also showed a similar inhibition of the adhesion of spleen cells from normal mice, stimulated in vitro with Con A, whereas it did not affect their proliferation. Moreover, the adhesion of human leukemia Jurkat cells to collagen I was inhibited by N-desulfated heparin.
Question: Does n-desulfated heparin improve concanavalin A-induced liver injury partly through inhibiting T lymphocyte adhesion?
Output:
|
PubmedQA75150
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Growing evidence shows that non-high-density lipoprotein cholesterol (Non-HDL-C) is a strong and independent predictor of cardiovascular disease (CVD). Few studies have assessed the association between traditional lipid measures and subclinical end points. In this study we analyzed the association of Non-HDL-C, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG) with coronary artery calcium (CAC), a marker of subclinical atherosclerosis. The study population consisted of 1611 consecutive asymptomatic individuals (67% men, mean age: 53+/-10 years) referred to a single electron beam tomography (EBT) facility for CAC screening. Multivariate logistic regression was used to test the association between increasing quartiles of lipid levels and presence of CAC score (CACS)>0 and CACS>or=100, with the lowest levels (first quartile) of lipid values as reference. Overall CACS of 0, 1-99, 100-399 and >or=400, were observed in 35%, 44%, 12% and 9% of the study subjects, respectively. The prevalence of CAC increased significantly across increasing quartiles of LDL-C, TG and Non-HDL-C (all p<0.0001), whereas CACS was significantly lower across increasing quartiles of HDL-C (p<0.001). In a multivariate model controlling for age, gender, race, cigarette smoking, hypertension, family history of coronary artery disease and obesity, there was a significant increase in the prevalence of CAC with increasing values of each lipid variable. In a multivariate model simultaneously controlling for increasing quartiles of the remaining lipid variables, only the association of Non-HDL-C with CACS>0 remained statistically significant (p=0.002). Similar results were observed with CACS>or=100 (p=0.038).\n Question: Is non-HDL cholesterol strongly associated with coronary artery calcification in asymptomatic 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: Growing evidence shows that non-high-density lipoprotein cholesterol (Non-HDL-C) is a strong and independent predictor of cardiovascular disease (CVD). Few studies have assessed the association between traditional lipid measures and subclinical end points. In this study we analyzed the association of Non-HDL-C, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG) with coronary artery calcium (CAC), a marker of subclinical atherosclerosis. The study population consisted of 1611 consecutive asymptomatic individuals (67% men, mean age: 53+/-10 years) referred to a single electron beam tomography (EBT) facility for CAC screening. Multivariate logistic regression was used to test the association between increasing quartiles of lipid levels and presence of CAC score (CACS)>0 and CACS>or=100, with the lowest levels (first quartile) of lipid values as reference. Overall CACS of 0, 1-99, 100-399 and >or=400, were observed in 35%, 44%, 12% and 9% of the study subjects, respectively. The prevalence of CAC increased significantly across increasing quartiles of LDL-C, TG and Non-HDL-C (all p<0.0001), whereas CACS was significantly lower across increasing quartiles of HDL-C (p<0.001). In a multivariate model controlling for age, gender, race, cigarette smoking, hypertension, family history of coronary artery disease and obesity, there was a significant increase in the prevalence of CAC with increasing values of each lipid variable. In a multivariate model simultaneously controlling for increasing quartiles of the remaining lipid variables, only the association of Non-HDL-C with CACS>0 remained statistically significant (p=0.002). Similar results were observed with CACS>or=100 (p=0.038).
Question: Is non-HDL cholesterol strongly associated with coronary artery calcification in asymptomatic individuals?
Output:
|
PubmedQA211166
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Animal products contribute significantly to the saturated fat and cholesterol content of the American diet. Contrary to dietary advice, consumers have not limited their consumption of animal products. Thus, an alternative approach might be to modify the fatty acid composition of animal products. We tested the hypothesis that modified pork with a high content of polyunsaturated fatty acids (PUFAs) and a low content of saturated fatty acids (SFAs) would lower plasma LDL-cholesterol concentrations in women. Twenty women aged 19-24 y completed a crossover study with 2 diets. Nutritionally complete diets containing 42% of energy from fat differed only in the inclusion of either standard or modified pork. Venous blood samples were collected at weeks 0, 4, and 8. The diet containing modified pork significantly lowered total plasma (P < 0.0076) and LDL (P < 0.0382) cholesterol. The modified diet also resulted in an increase in the PUFA and a decrease in the SFA and monounsaturated fatty acid contents of the cholesteryl ester, free fatty acid, phospholipid, and triacylglycerol lipid classes in both plasma and erythrocytes. Plasma concentrations of glucose, insulin, triacylglycerol, and free fatty acids did not change significantly.\n Question: Does pork with a high content of polyunsaturated fatty acids lower LDL cholesterol in women?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Animal products contribute significantly to the saturated fat and cholesterol content of the American diet. Contrary to dietary advice, consumers have not limited their consumption of animal products. Thus, an alternative approach might be to modify the fatty acid composition of animal products. We tested the hypothesis that modified pork with a high content of polyunsaturated fatty acids (PUFAs) and a low content of saturated fatty acids (SFAs) would lower plasma LDL-cholesterol concentrations in women. Twenty women aged 19-24 y completed a crossover study with 2 diets. Nutritionally complete diets containing 42% of energy from fat differed only in the inclusion of either standard or modified pork. Venous blood samples were collected at weeks 0, 4, and 8. The diet containing modified pork significantly lowered total plasma (P < 0.0076) and LDL (P < 0.0382) cholesterol. The modified diet also resulted in an increase in the PUFA and a decrease in the SFA and monounsaturated fatty acid contents of the cholesteryl ester, free fatty acid, phospholipid, and triacylglycerol lipid classes in both plasma and erythrocytes. Plasma concentrations of glucose, insulin, triacylglycerol, and free fatty acids did not change significantly.
Question: Does pork with a high content of polyunsaturated fatty acids lower LDL cholesterol in women?
Output:
|
PubmedQA175048
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Supplementation with long-chain n-3 polyunsaturated fatty acids (LCPUFAs) has been found to reduce the development of allergic disease. The aim of this study was to compare the effectiveness of fish oil diets rich in eicosapentaenoic acid (20:5n-3; EPA) or docosahexaenoic acid (22:6n-3; DHA) in suppressing food allergic symptoms. Mice were fed a control diet (10% soybean oil) or fish oil diet rich in EPA (4% soybean oil + 6% EPA oil containing 28.8% EPA and 13.7% DHA) or DHA (4% soybean oil + 6% DHA oil containing 7% EPA and 27.8% DHA), starting 14 d before and for 5 wk during oral sensitization with peanut extract (PE) or whey. Acute allergic skin responses, serum immunoglobulins (Igs), and mucosal mast cell protease-1 (mmcp-1) were assessed. Hyperimmune serum was transferred to naive recipient mice fed the different diets. The DHA diet effectively reduced the acute allergic skin response compared with the control or EPA diet in PE-allergic mice (control, 159 ± 15, or EPA, 129 ± 8, vs. DHA, 78 ± 7 μm; P < 0.0001 or P < 0.05, respectively). In contrast, both the DHA and EPA diets reduced the allergic skin response in whey allergic mice (control, 169 ± 9, vs. DHA, 91 ± 13, or EPA, 106 ± 14 μm; P < 0.001 or P < 0.01, respectively); however, only the DHA diet reduced mmcp-1 and whey-specific IgE and IgG1. The DHA and EPA diets also reduced the acute skin response in passively immunized mice.\n Question: Does dHA-rich tuna oil effectively suppress allergic symptoms in mice allergic to whey or peanut?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Supplementation with long-chain n-3 polyunsaturated fatty acids (LCPUFAs) has been found to reduce the development of allergic disease. The aim of this study was to compare the effectiveness of fish oil diets rich in eicosapentaenoic acid (20:5n-3; EPA) or docosahexaenoic acid (22:6n-3; DHA) in suppressing food allergic symptoms. Mice were fed a control diet (10% soybean oil) or fish oil diet rich in EPA (4% soybean oil + 6% EPA oil containing 28.8% EPA and 13.7% DHA) or DHA (4% soybean oil + 6% DHA oil containing 7% EPA and 27.8% DHA), starting 14 d before and for 5 wk during oral sensitization with peanut extract (PE) or whey. Acute allergic skin responses, serum immunoglobulins (Igs), and mucosal mast cell protease-1 (mmcp-1) were assessed. Hyperimmune serum was transferred to naive recipient mice fed the different diets. The DHA diet effectively reduced the acute allergic skin response compared with the control or EPA diet in PE-allergic mice (control, 159 ± 15, or EPA, 129 ± 8, vs. DHA, 78 ± 7 μm; P < 0.0001 or P < 0.05, respectively). In contrast, both the DHA and EPA diets reduced the allergic skin response in whey allergic mice (control, 169 ± 9, vs. DHA, 91 ± 13, or EPA, 106 ± 14 μm; P < 0.001 or P < 0.01, respectively); however, only the DHA diet reduced mmcp-1 and whey-specific IgE and IgG1. The DHA and EPA diets also reduced the acute skin response in passively immunized mice.
Question: Does dHA-rich tuna oil effectively suppress allergic symptoms in mice allergic to whey or peanut?
Output:
|
PubmedQA82380
|
[
{
"role": "user",
"content": "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 seeks to explore whether antenatal supplement of taurine may improve the brain development of fetal rats with intrauterine growth restriction (IUGR) via the protein kinase A-cyclic adenosine monophosphate (cAMP) response element protein (PKA-CREB) pathway. Fifteen pregnant rats were randomly divided into control group, IUGR model, and IUGR with antenatal taurine supplement group. Brain tissues were obtained immediately after rats were born. PKA-CREB signal pathway activity and glial cell line-derived neurotrophic factor (GDNF) mRNA and protein levels were measured by reverse transcription polymerase chain reaction and immunohistochemistry stains, whereas immunoreactive cells of neuron-specific enolase (NSE) and proliferating cell nuclear antigen (PCNA) were detected by immunohistochemistry stains. The results showed that: (1) In the IUGR group, a greater number of PCNA and NSE immunoreactive cells were found in brain tissues compared with controls, and prenatal taurine supplementation led to a further increase. (2) Expression of PKA, CREB, and GDNF were increased in mRNA and protein levels due to taurine supplementation.\n Question: Does antenatal taurine supplementation improve cerebral neurogenesis in fetal rats with intrauterine growth restriction through the PKA-CREB signal pathway?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: This study seeks to explore whether antenatal supplement of taurine may improve the brain development of fetal rats with intrauterine growth restriction (IUGR) via the protein kinase A-cyclic adenosine monophosphate (cAMP) response element protein (PKA-CREB) pathway. Fifteen pregnant rats were randomly divided into control group, IUGR model, and IUGR with antenatal taurine supplement group. Brain tissues were obtained immediately after rats were born. PKA-CREB signal pathway activity and glial cell line-derived neurotrophic factor (GDNF) mRNA and protein levels were measured by reverse transcription polymerase chain reaction and immunohistochemistry stains, whereas immunoreactive cells of neuron-specific enolase (NSE) and proliferating cell nuclear antigen (PCNA) were detected by immunohistochemistry stains. The results showed that: (1) In the IUGR group, a greater number of PCNA and NSE immunoreactive cells were found in brain tissues compared with controls, and prenatal taurine supplementation led to a further increase. (2) Expression of PKA, CREB, and GDNF were increased in mRNA and protein levels due to taurine supplementation.
Question: Does antenatal taurine supplementation improve cerebral neurogenesis in fetal rats with intrauterine growth restriction through the PKA-CREB signal pathway?
Output:
|
PubmedQA117075
|
[
{
"role": "user",
"content": "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 observe the effect of the aqueous extract of hypocotyls of the plant Lepidium meyenii (Maca) on spermatogenic damage induced by the organophosphate insecticide malathion in mice. Mice were treated with 80 mg/kg of malathion in the presence or absence of an aqueous extract of Maca, which was orally administered 7, 14 or 21 days after injection of the malathion. Stages of the seminiferous epithelium were assessed by transillumination on days 0, 7, 14 and 21. The administration of Maca increased significantly the length of stage VIII on days 7, 14 and 21 of treatment compared with the controls. An increase in the length of stage IX occurred on day 14 of treatment. Malathion affected spermatogenesis by reducing the lengths of stage IX on day 7, stages VII and IX-XI on day 14 and a recovery of stages IX-XII on day 21. The magnitude of alteration in the length of stage IX produced by malathion was significantly reduced by Maca on days 7 and 14. The length of stage VIII was increased when Maca was administered to mice treated with malathion. Assessment of the relative length of stages of the seminiferous epithelium showed that Maca treatment resulted in rapid recovery of the effect of malathion.\n Question: Does lepidium meyenii ( Maca ) reduce spermatogenic damage induced by a single dose of malathion 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: To observe the effect of the aqueous extract of hypocotyls of the plant Lepidium meyenii (Maca) on spermatogenic damage induced by the organophosphate insecticide malathion in mice. Mice were treated with 80 mg/kg of malathion in the presence or absence of an aqueous extract of Maca, which was orally administered 7, 14 or 21 days after injection of the malathion. Stages of the seminiferous epithelium were assessed by transillumination on days 0, 7, 14 and 21. The administration of Maca increased significantly the length of stage VIII on days 7, 14 and 21 of treatment compared with the controls. An increase in the length of stage IX occurred on day 14 of treatment. Malathion affected spermatogenesis by reducing the lengths of stage IX on day 7, stages VII and IX-XI on day 14 and a recovery of stages IX-XII on day 21. The magnitude of alteration in the length of stage IX produced by malathion was significantly reduced by Maca on days 7 and 14. The length of stage VIII was increased when Maca was administered to mice treated with malathion. Assessment of the relative length of stages of the seminiferous epithelium showed that Maca treatment resulted in rapid recovery of the effect of malathion.
Question: Does lepidium meyenii ( Maca ) reduce spermatogenic damage induced by a single dose of malathion in mice?
Output:
|
PubmedQA47302
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: We aimed to evaluate the safety and long-term efficacy of the magnetic navigation system (MNS) in a large number of patients. The MNS has the potential for improving safety and efficacy based on atraumatic catheter design and superior navigation capabilities. In this study, 610 consecutive patients underwent ablation. Patients were divided into two age- and sex-matched groups. Ablations were performed either using MNS (group MNS, 292) or conventional manual ablation [group manual navigation (MAN), 318]. The following parameters were analysed: acute success rate, fluoroscopy time, procedure time, complications [major: pericardial tamponade, permanent atrioventricular (AV) block, major bleeding, and death; minor: minor bleeding and temporary AV block]. Recurrence rate was assessed during follow-up (15±9.5 months). Subgroup analysis was performed for the following groups: atrial fibrillation, isthmus dependent and atypical atrial flutter, atrial tachycardia, AV nodal re-entrant tachycardia, circus movement tachycardia, and ventricular tachycardia (VT). Magnetic navigation system was associated with less major complications (0.34 vs. 3.2%, P=0.01). The total numbers of complications were lower in group MNS (4.5 vs. 10%, P=0.005). Magnetic navigation system was equally effective as MAN in acute success rate for overall groups (92 vs. 94%, P=ns). Magnetic navigation system was more successful for VTs (93 vs. 72%, P<0.05). Less fluoroscopy was used in group MNS (30±20 vs. 35±25 min, P<0.01). There were no differences in procedure times and recurrence rates for the overall groups (168±67 vs. 159±75 min, P=ns; 14 vs. 11%, P=ns; respectively).\n Question: Does the magnetic navigation system allow safety and high efficacy for ablation of arrhythmias?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: We aimed to evaluate the safety and long-term efficacy of the magnetic navigation system (MNS) in a large number of patients. The MNS has the potential for improving safety and efficacy based on atraumatic catheter design and superior navigation capabilities. In this study, 610 consecutive patients underwent ablation. Patients were divided into two age- and sex-matched groups. Ablations were performed either using MNS (group MNS, 292) or conventional manual ablation [group manual navigation (MAN), 318]. The following parameters were analysed: acute success rate, fluoroscopy time, procedure time, complications [major: pericardial tamponade, permanent atrioventricular (AV) block, major bleeding, and death; minor: minor bleeding and temporary AV block]. Recurrence rate was assessed during follow-up (15±9.5 months). Subgroup analysis was performed for the following groups: atrial fibrillation, isthmus dependent and atypical atrial flutter, atrial tachycardia, AV nodal re-entrant tachycardia, circus movement tachycardia, and ventricular tachycardia (VT). Magnetic navigation system was associated with less major complications (0.34 vs. 3.2%, P=0.01). The total numbers of complications were lower in group MNS (4.5 vs. 10%, P=0.005). Magnetic navigation system was equally effective as MAN in acute success rate for overall groups (92 vs. 94%, P=ns). Magnetic navigation system was more successful for VTs (93 vs. 72%, P<0.05). Less fluoroscopy was used in group MNS (30±20 vs. 35±25 min, P<0.01). There were no differences in procedure times and recurrence rates for the overall groups (168±67 vs. 159±75 min, P=ns; 14 vs. 11%, P=ns; respectively).
Question: Does the magnetic navigation system allow safety and high efficacy for ablation of arrhythmias?
Output:
|
PubmedQA96740
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Opioids are widely used as effective analgesics, but opioid sensitivity is well known to vary widely among individuals and the underlying genetic factors are not fully understood, thus hampering efficient pain treatment. We explored the genetic factors that contribute to individual differences in opioid sensitivity by performing a genome-wide association study. We conducted a multistage genome-wide association study in subjects who underwent laparoscopic-assisted colectomy (LAC). A nonsynonymous SNP in the LAMB3 gene region, rs2076222, was strongly associated with postoperative opioid requirements. The C allele of this best-candidate SNP was associated with lower opioid sensitivity and/or higher pain sensitivity in the patient subjects.\n Question: Does genome-wide association study identify candidate loci associated with postoperative fentanyl requirements after laparoscopic-assisted colectomy?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Opioids are widely used as effective analgesics, but opioid sensitivity is well known to vary widely among individuals and the underlying genetic factors are not fully understood, thus hampering efficient pain treatment. We explored the genetic factors that contribute to individual differences in opioid sensitivity by performing a genome-wide association study. We conducted a multistage genome-wide association study in subjects who underwent laparoscopic-assisted colectomy (LAC). A nonsynonymous SNP in the LAMB3 gene region, rs2076222, was strongly associated with postoperative opioid requirements. The C allele of this best-candidate SNP was associated with lower opioid sensitivity and/or higher pain sensitivity in the patient subjects.
Question: Does genome-wide association study identify candidate loci associated with postoperative fentanyl requirements after laparoscopic-assisted colectomy?
Output:
|
PubmedQA180860
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Food insecurity is associated with deficits in child development and health, but little is known about how children's specific food-insecurity experiences play out through nutritional and non-nutritional pathways that may compromise well-being. This study used child self-reports of food insecurity to examine the types of food-insecurity experiences that were most prevalent and the relations between child food insecurity (CFI), child diet, and child physical activity (PA). A total of 3605 fourth- and fifth-grade children whose schools participated in the Network for a Healthy California-Children's PowerPlay! campaign completed 24-h diary-assisted recalls and surveys including items from the Child Food Security Assessment and questions about PA. Data were analyzed by using regression and logistic regression models. CFI was present in 60% of the children and included experiences of cognitive, emotional, and physical awareness of food insecurity. Greater levels of CFI were associated with higher consumption of energy, fat, sugar, and fiber and a diet lower in vegetables. For instance, a child at the highest level of CFI, on average, consumed ∼494 kJ/d (118 kcal), 8 g/d of sugar, and 4 g/d of fat more than a food-secure child. Higher CFI was associated with a marginally significant difference (P = 0.06) in minutes of PA (17 min/d less for children at the highest level of CFI vs. those who were food secure) and with significantly greater perceived barriers to PA.\n Question: Is child experience of food insecurity associated with child diet and physical activity?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Food insecurity is associated with deficits in child development and health, but little is known about how children's specific food-insecurity experiences play out through nutritional and non-nutritional pathways that may compromise well-being. This study used child self-reports of food insecurity to examine the types of food-insecurity experiences that were most prevalent and the relations between child food insecurity (CFI), child diet, and child physical activity (PA). A total of 3605 fourth- and fifth-grade children whose schools participated in the Network for a Healthy California-Children's PowerPlay! campaign completed 24-h diary-assisted recalls and surveys including items from the Child Food Security Assessment and questions about PA. Data were analyzed by using regression and logistic regression models. CFI was present in 60% of the children and included experiences of cognitive, emotional, and physical awareness of food insecurity. Greater levels of CFI were associated with higher consumption of energy, fat, sugar, and fiber and a diet lower in vegetables. For instance, a child at the highest level of CFI, on average, consumed ∼494 kJ/d (118 kcal), 8 g/d of sugar, and 4 g/d of fat more than a food-secure child. Higher CFI was associated with a marginally significant difference (P = 0.06) in minutes of PA (17 min/d less for children at the highest level of CFI vs. those who were food secure) and with significantly greater perceived barriers to PA.
Question: Is child experience of food insecurity associated with child diet and physical activity?
Output:
|
PubmedQA191072
|
[
{
"role": "user",
"content": "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 transfected survivin antisense oligonucleotide (ASODN) on proliferation and apoptosis of gastric cancer cells. The authors designed ASODNs targeting different regions of survivin mRNA, including surviving ASODN1, ASODN2 and ASODN3. ASODNs were transfected into gastric cancer cell line SGC 7901, cell growth was detected by MTT assay. Cells exposed to the potent oligonucleotide were also examined for apoptosis induction by FCM and fluorescence microscopy. Semiquantitive RT-PCR and Western blot examinations were carried for expression of survivin mRNA and protein. ASODN3 caused a statistically significant reduction of cell viability to 60.6% (+/-2.9%) (P<0.01), while ASODN1 and ASODN2 had no such changes (P>0.05). The cell growth was also significantly inhibited by ASODN3, compared with reversal and scrambled sequence. A significant loss of survivin mRNA was presented in ASODN3 treated cells and this was not seen in treatment with sense ODN or scramble ODN. Protein level was significantly decreased 48 h after survivin ASODN trasfected by approximately 2-fold decrease compared with untreated controls. However, ASODN3 did not induce significant apoptosis response until 48 h after transfection (P>0.05).\n Question: Does survivin antisense oligodeoxynucleotide inhibit growth of gastric 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: To investigate the effect of transfected survivin antisense oligonucleotide (ASODN) on proliferation and apoptosis of gastric cancer cells. The authors designed ASODNs targeting different regions of survivin mRNA, including surviving ASODN1, ASODN2 and ASODN3. ASODNs were transfected into gastric cancer cell line SGC 7901, cell growth was detected by MTT assay. Cells exposed to the potent oligonucleotide were also examined for apoptosis induction by FCM and fluorescence microscopy. Semiquantitive RT-PCR and Western blot examinations were carried for expression of survivin mRNA and protein. ASODN3 caused a statistically significant reduction of cell viability to 60.6% (+/-2.9%) (P<0.01), while ASODN1 and ASODN2 had no such changes (P>0.05). The cell growth was also significantly inhibited by ASODN3, compared with reversal and scrambled sequence. A significant loss of survivin mRNA was presented in ASODN3 treated cells and this was not seen in treatment with sense ODN or scramble ODN. Protein level was significantly decreased 48 h after survivin ASODN trasfected by approximately 2-fold decrease compared with untreated controls. However, ASODN3 did not induce significant apoptosis response until 48 h after transfection (P>0.05).
Question: Does survivin antisense oligodeoxynucleotide inhibit growth of gastric cancer cells?
Output:
|
PubmedQA193202
|
[
{
"role": "user",
"content": "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 if individuals who carry mitochondrial markers which have been previously shown to affect longevity also have differential lifetime reproductive success (LRS). We extracted the mtDNA from living subjects residing in Atenas, Costa Rica. Since mtDNA does not recombine, and its probability of mutation is low, we assume that all maternal ancestors of the living subjects have the same mtDNA. We reconstructed the maternal genealogy of the living subjects, so that we have information on the LRS and longevity of the maternal ancestors of the living subjects. We compared the LRS of women who carried the 5178A marker in haplogroup D (associated with decreased longevity) and who carried the 150T polymorphism (associated with increased longevity) with the LRS of controls born in the same half century time period from 1750 to 1939. We found that the LRS of neither group of women with a longevity-associated polymorphism (LAP) differed from the LRS of controls, even if these women differed significantly from the controls in their longevity.\n Question: Do mitochondrial polymorphisms associated with differential longevity impact lifetime-reproductive success?\n Output: "
},
{
"role": "assistant",
"content": "no"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To determine if individuals who carry mitochondrial markers which have been previously shown to affect longevity also have differential lifetime reproductive success (LRS). We extracted the mtDNA from living subjects residing in Atenas, Costa Rica. Since mtDNA does not recombine, and its probability of mutation is low, we assume that all maternal ancestors of the living subjects have the same mtDNA. We reconstructed the maternal genealogy of the living subjects, so that we have information on the LRS and longevity of the maternal ancestors of the living subjects. We compared the LRS of women who carried the 5178A marker in haplogroup D (associated with decreased longevity) and who carried the 150T polymorphism (associated with increased longevity) with the LRS of controls born in the same half century time period from 1750 to 1939. We found that the LRS of neither group of women with a longevity-associated polymorphism (LAP) differed from the LRS of controls, even if these women differed significantly from the controls in their longevity.
Question: Do mitochondrial polymorphisms associated with differential longevity impact lifetime-reproductive success?
Output:
|
PubmedQA205585
|
[
{
"role": "user",
"content": "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 \"triple test\" for palpable breast lesions consists of physical examination, mammography, and fine-needle aspiration. Forty-six lesions in 43 patients were subjected to all three components of the triple test, followed by confirmatory open biopsy. In all 21 cases where the triple test was concordant (elements had either all malignant or all benign results), pathologic analysis of open biopsy samples was confirmatory (predictive value and sensitivity 100%). Fine-needle aspiration was the most reliable element of the triple test in cases where the elements of the test were nonconcordant (negative predictive value and sensitivity of 95% and 96%, respectively).\n Question: Does use of the `` triple test '' for palpable breast lesions yield high diagnostic accuracy and cost savings?\n Output: "
},
{
"role": "assistant",
"content": "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 "triple test" for palpable breast lesions consists of physical examination, mammography, and fine-needle aspiration. Forty-six lesions in 43 patients were subjected to all three components of the triple test, followed by confirmatory open biopsy. In all 21 cases where the triple test was concordant (elements had either all malignant or all benign results), pathologic analysis of open biopsy samples was confirmatory (predictive value and sensitivity 100%). Fine-needle aspiration was the most reliable element of the triple test in cases where the elements of the test were nonconcordant (negative predictive value and sensitivity of 95% and 96%, respectively).
Question: Does use of the `` triple test '' for palpable breast lesions yield high diagnostic accuracy and cost savings?
Output:
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PubmedQA204094
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Hyperhomocysteinemia (HHcy) is associated with liver diseases such as fatty liver and hepatic fibrosis; however, the underlying mechanism is still largely unknown. The current study aimed to explore the signaling pathway involved in HHcy-induced hepatic steatosis (HS). C57BL/6 mice were fed a high-methionine diet (HMD) for 4 and 8 weeks to establish the HHcy mouse model. Compared to a chow diet, the HMD induced hepatic steatosis and elevated hepatic expression of CD36, a fatty acid transport protein. The increased CD36 expression was associated with activation of the aryl hydrocarbon receptor (AHR). In primary cultured hepatocytes, high levels of homocysteine (Hcy) treatment up-regulated CD36 and increased subsequent lipid uptake; both were significantly attenuated by small interfering RNA (siRNA) knockdown of CD36 and AHR. Chromatin immunoprecipitation assay revealed that Hcy promoted binding of AHR to the CD36 promoter, and transient transfection assay demonstrated markedly increased activity of the AHR response element by Hcy, which was ligand dependent. Mass spectrometry revealed significantly increased hepatic content of lipoxin A4 (LXA4 ), a metabolite of arachidonic acid, in HMD-fed mice. Furthermore, overexpression of 15-oxoprostaglandin 13-reductase 1, a LXA4 inactivation enzyme, inhibited Hcy-induced AHR activation, lipid uptake, and lipid accumulation. Moreover, LXA4 -induced up-regulation of CD36 and lipid uptake was inhibited by AHR siRNA in vitro in hepatocytes. Finally, treatment with an AHR antagonist reversed HHcy-induced lipid accumulation by inhibiting the AHR-CD36 pathway in mice.\n Question: Does hyperhomocysteinemia activate the aryl hydrocarbon receptor/CD36 pathway to promote hepatic steatosis 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: Hyperhomocysteinemia (HHcy) is associated with liver diseases such as fatty liver and hepatic fibrosis; however, the underlying mechanism is still largely unknown. The current study aimed to explore the signaling pathway involved in HHcy-induced hepatic steatosis (HS). C57BL/6 mice were fed a high-methionine diet (HMD) for 4 and 8 weeks to establish the HHcy mouse model. Compared to a chow diet, the HMD induced hepatic steatosis and elevated hepatic expression of CD36, a fatty acid transport protein. The increased CD36 expression was associated with activation of the aryl hydrocarbon receptor (AHR). In primary cultured hepatocytes, high levels of homocysteine (Hcy) treatment up-regulated CD36 and increased subsequent lipid uptake; both were significantly attenuated by small interfering RNA (siRNA) knockdown of CD36 and AHR. Chromatin immunoprecipitation assay revealed that Hcy promoted binding of AHR to the CD36 promoter, and transient transfection assay demonstrated markedly increased activity of the AHR response element by Hcy, which was ligand dependent. Mass spectrometry revealed significantly increased hepatic content of lipoxin A4 (LXA4 ), a metabolite of arachidonic acid, in HMD-fed mice. Furthermore, overexpression of 15-oxoprostaglandin 13-reductase 1, a LXA4 inactivation enzyme, inhibited Hcy-induced AHR activation, lipid uptake, and lipid accumulation. Moreover, LXA4 -induced up-regulation of CD36 and lipid uptake was inhibited by AHR siRNA in vitro in hepatocytes. Finally, treatment with an AHR antagonist reversed HHcy-induced lipid accumulation by inhibiting the AHR-CD36 pathway in mice.
Question: Does hyperhomocysteinemia activate the aryl hydrocarbon receptor/CD36 pathway to promote hepatic steatosis in mice?
Output:
|
PubmedQA172277
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Troponin elevations are common in critically ill patients. Whether they are predictors of mortality independent of the severity of the underlying disease is unclear. To determine whether troponin elevations predict in-hospital, short-term, and long-term mortality in medical intensive care unit patients independent of the severity of the underlying disease as measured by Acute Physiology and Chronic Health Evaluation III prognostic system. Retrospective study. We examined the Acute Physiology and Chronic Health Evaluation III database and cardiac troponin T levels of medical intensive care unit patients at Mayo Clinic, Rochester, MN. In all, 1,657 patients consecutively admitted to medical intensive care units between August 2000 and December 2001. In-hospital, short-term (30-day), and long-term all-cause mortality. During hospitalization, 12.5% of patients with a cardiac troponin T < 0.01 microg/L suffered deaths compared with 29.5% among those with cardiac troponin T > or = 0.01 microg/L (p < .001). At 30 days, mortality was 13.7% without and 34.6% with elevations (p < .001). The expected probability of survival at 1-, 2-, and 3-yr follow-up was 43.7%, 33.8%, and 25.7% among patients with cardiac troponin T > or = 0.01 microg/L and 75.3%, 67.6%, and 62.9% in those with cardiac troponin T < 0.01 microg/L, respectively (p < .001). After adjustment for the severity of disease and baseline characteristics, cardiac troponin levels were still associated with in-hospital, short-term, and long-term mortality (p = .006, p = .007, and p = .001, respectively).\n Question: Is elevated cardiac troponin an independent risk factor for short- and long-term mortality in medical intensive care unit 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: Troponin elevations are common in critically ill patients. Whether they are predictors of mortality independent of the severity of the underlying disease is unclear. To determine whether troponin elevations predict in-hospital, short-term, and long-term mortality in medical intensive care unit patients independent of the severity of the underlying disease as measured by Acute Physiology and Chronic Health Evaluation III prognostic system. Retrospective study. We examined the Acute Physiology and Chronic Health Evaluation III database and cardiac troponin T levels of medical intensive care unit patients at Mayo Clinic, Rochester, MN. In all, 1,657 patients consecutively admitted to medical intensive care units between August 2000 and December 2001. In-hospital, short-term (30-day), and long-term all-cause mortality. During hospitalization, 12.5% of patients with a cardiac troponin T < 0.01 microg/L suffered deaths compared with 29.5% among those with cardiac troponin T > or = 0.01 microg/L (p < .001). At 30 days, mortality was 13.7% without and 34.6% with elevations (p < .001). The expected probability of survival at 1-, 2-, and 3-yr follow-up was 43.7%, 33.8%, and 25.7% among patients with cardiac troponin T > or = 0.01 microg/L and 75.3%, 67.6%, and 62.9% in those with cardiac troponin T < 0.01 microg/L, respectively (p < .001). After adjustment for the severity of disease and baseline characteristics, cardiac troponin levels were still associated with in-hospital, short-term, and long-term mortality (p = .006, p = .007, and p = .001, respectively).
Question: Is elevated cardiac troponin an independent risk factor for short- and long-term mortality in medical intensive care unit patients?
Output:
|
PubmedQA14204
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Hyperproliferation of the colorectal mucosa is regarded as an early step in colorectal carcinogenesis. Deoxycholic acid, a secondary bile acid, stimulates colorectal epithelial proliferation in animals and is considered a tumor promoter in human colorectal carcinogenesis. The aim of this study was to investigate the correlation between colorectal mucosal proliferation and the serum deoxycholic acid level. From each of 19 patients (10 men and 9 women) with (n = 3) or without (n = 16) colorectal adenoma, 18 biopsy specimens were obtained by colonoscopy, 3 from each of the 6 colonic segments. A crude nuclei fraction was prepared, and DNA was stained by propidium iodide to determine the proliferative index (the percentage of cells in the S and G2/M phases of the cell cycle) by flow cytometry. Serum levels of deoxycholic acid were determined by gas-liquid chromatography. The colonic proliferation rates (median of the values obtained in all segments, 14.1%; range, 10.0-18.7%) and the fasting serum deoxycholic acid levels (median, 0.86 micromol/L; range, 0.28-1.58 micromol/L) showed a significant correlation (r = 0.51, P = 0.03). Serum lithocholic, cholic, chenodeoxycholic, and ursodeoxycholic acid levels were not correlated with the proliferation rates.\n Question: Is colonic mucosal proliferation related to serum deoxycholic acid levels?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Hyperproliferation of the colorectal mucosa is regarded as an early step in colorectal carcinogenesis. Deoxycholic acid, a secondary bile acid, stimulates colorectal epithelial proliferation in animals and is considered a tumor promoter in human colorectal carcinogenesis. The aim of this study was to investigate the correlation between colorectal mucosal proliferation and the serum deoxycholic acid level. From each of 19 patients (10 men and 9 women) with (n = 3) or without (n = 16) colorectal adenoma, 18 biopsy specimens were obtained by colonoscopy, 3 from each of the 6 colonic segments. A crude nuclei fraction was prepared, and DNA was stained by propidium iodide to determine the proliferative index (the percentage of cells in the S and G2/M phases of the cell cycle) by flow cytometry. Serum levels of deoxycholic acid were determined by gas-liquid chromatography. The colonic proliferation rates (median of the values obtained in all segments, 14.1%; range, 10.0-18.7%) and the fasting serum deoxycholic acid levels (median, 0.86 micromol/L; range, 0.28-1.58 micromol/L) showed a significant correlation (r = 0.51, P = 0.03). Serum lithocholic, cholic, chenodeoxycholic, and ursodeoxycholic acid levels were not correlated with the proliferation rates.
Question: Is colonic mucosal proliferation related to serum deoxycholic acid levels?
Output:
|
PubmedQA113356
|
[
{
"role": "user",
"content": "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 if young adults with a history of typical absence epilepsy (AE) in childhood have a greater risk of accidental injury than controls with juvenile rheumatoid arthritis (JRA). To assess the nature and severity of these injuries. All patients with AE or JRA diagnosed between 1977 and 1985, who were 18 years or older at the onset of the study, were identified from review of pediatric electroencephalographic records for the province of Nova Scotia (AE) or review of the medical records database at the only tertiary care pediatric center for the province (JRA). Fifty-nine (86%) of 69 patients with AE and 61 (80%) of 76 patients with JRA participated in an interview in 1994 or 1995, assessing nature, severity, and treatment of prior accidental injuries. Patients with AE were further questioned about injuries sustained during an absence seizure. Sixteen (27%) of 59 patients with AE reported accidental injury during an absence seizure, with risk of injury being 9% per person-year of AE. Most injuries (81%) occurred during anti-epileptic drug therapy. Although the majority of injuries did not require treatment, 2 (13%) of 16 patients required minor treatment and 2 (13%) of 16 were admitted to hospital. The risk of accidental injury resulting from an absence seizure in person-years at risk was highest in juvenile myoclonic epilepsy (45%), moderate in juvenile AE (14%), and lowest in childhood AE (3%). Patients with AE had a greater number of overall accidental injuries than those with JRA (P<.04), but these differences were particularly marked for bicycle (P<.003) and car accidents (P<.05) and for mild head injuries (P=.05).\n Question: Is accidental injury a serious risk in children with typical absence epilepsy?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: To determine if young adults with a history of typical absence epilepsy (AE) in childhood have a greater risk of accidental injury than controls with juvenile rheumatoid arthritis (JRA). To assess the nature and severity of these injuries. All patients with AE or JRA diagnosed between 1977 and 1985, who were 18 years or older at the onset of the study, were identified from review of pediatric electroencephalographic records for the province of Nova Scotia (AE) or review of the medical records database at the only tertiary care pediatric center for the province (JRA). Fifty-nine (86%) of 69 patients with AE and 61 (80%) of 76 patients with JRA participated in an interview in 1994 or 1995, assessing nature, severity, and treatment of prior accidental injuries. Patients with AE were further questioned about injuries sustained during an absence seizure. Sixteen (27%) of 59 patients with AE reported accidental injury during an absence seizure, with risk of injury being 9% per person-year of AE. Most injuries (81%) occurred during anti-epileptic drug therapy. Although the majority of injuries did not require treatment, 2 (13%) of 16 patients required minor treatment and 2 (13%) of 16 were admitted to hospital. The risk of accidental injury resulting from an absence seizure in person-years at risk was highest in juvenile myoclonic epilepsy (45%), moderate in juvenile AE (14%), and lowest in childhood AE (3%). Patients with AE had a greater number of overall accidental injuries than those with JRA (P<.04), but these differences were particularly marked for bicycle (P<.003) and car accidents (P<.05) and for mild head injuries (P=.05).
Question: Is accidental injury a serious risk in children with typical absence epilepsy?
Output:
|
PubmedQA163125
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Positive skin prick test (SPT) reactions to carmine red (E120) have been reported to occur concurrently with reactions to mites. The relationships between positive SPT reactions to carmine, carmine allergy and concurrent mite reactions are unknown. The aim of this study was to analyse the prevalence of carmine sensitization and its clinical importance among patients with suspected allergy to food additives. The occurrence of positive SPT reactions to mites was studied in 6,464 patients: 3,164 were tested with carmine and 2,837 with shrimp. Carmine ingestion-associated symptoms were registered at the time of testing. Patients with positive SPT to carmine received a follow-up questionnaire on their symptoms 1-5 years later. Positive SPT reactions to carmine were seen in 94 patients (3.0%) of whom 74% also had positive SPT reactions to mites and 22% to shrimp. Carmine ingestion-associated symptoms were not dependent on concurrent mite reactivity in 39/94 (42%) patients.\n Question: Is allergy to carmine red ( E120 ) dependent on concurrent mite allergy?\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: Positive skin prick test (SPT) reactions to carmine red (E120) have been reported to occur concurrently with reactions to mites. The relationships between positive SPT reactions to carmine, carmine allergy and concurrent mite reactions are unknown. The aim of this study was to analyse the prevalence of carmine sensitization and its clinical importance among patients with suspected allergy to food additives. The occurrence of positive SPT reactions to mites was studied in 6,464 patients: 3,164 were tested with carmine and 2,837 with shrimp. Carmine ingestion-associated symptoms were registered at the time of testing. Patients with positive SPT to carmine received a follow-up questionnaire on their symptoms 1-5 years later. Positive SPT reactions to carmine were seen in 94 patients (3.0%) of whom 74% also had positive SPT reactions to mites and 22% to shrimp. Carmine ingestion-associated symptoms were not dependent on concurrent mite reactivity in 39/94 (42%) patients.
Question: Is allergy to carmine red ( E120 ) dependent on concurrent mite allergy?
Output:
|
PubmedQA69768
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Iron plays a pivotal role in the pathogenesis of Trichomonas vaginalis, the causative agent of highly prevalent human trichomoniasis. T. vaginalis resides in the vaginal region, where the iron concentration is constantly changing. Hence, T. vaginalis must adapt to variations in iron availability to establish and maintain an infection. The free radical signaling molecules reactive oxygen species (ROS) and reactive nitrogen species (RNS) have been proven to participate in iron deficiency in eukaryotes. However, little is known about the roles of these molecules in iron-deficient T. vaginalis. T. vaginalis cultured in iron-rich and -deficient conditions were collected for all experiments in this study. Next generation RNA sequencing was conducted to investigate the impact of iron on transcriptome of T. vaginalis. The cell viabilities were monitored after the trophozoites treated with the inhibitors of nitric oxide (NO) synthase (L-NG-monomethyl arginine, L-NMMA) and proteasome (MG132). Hydrogenosomal membrane potential was measured using JC-1 staining. We demonstrated that NO rather than ROS accumulates in iron-deficient T. vaginalis. The level of NO was blocked by MG132 and L-NMMA, indicating that NO production is through a proteasome and arginine dependent pathway. We found that the inhibition of proteasome activity shortened the survival of iron-deficient cells compared with untreated iron-deficient cells. Surprisingly, the addition of arginine restored both NO level and the survival of proteasome-inhibited cells, suggesting that proteasome-derived NO is crucial for cell survival under iron-limited conditions. Additionally, NO maintains the hydrogenosomal membrane potential, a determinant for cell survival, emphasizing the cytoprotective effect of NO on iron-deficient T. vaginalis. Collectively, we determined that NO produced by the proteasome prolonged the survival of iron-deficient T. vaginalis via maintenance of the hydrogenosomal functions.\n Question: Does nitric oxide maintain cell survival of Trichomonas vaginalis upon iron depletion?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Iron plays a pivotal role in the pathogenesis of Trichomonas vaginalis, the causative agent of highly prevalent human trichomoniasis. T. vaginalis resides in the vaginal region, where the iron concentration is constantly changing. Hence, T. vaginalis must adapt to variations in iron availability to establish and maintain an infection. The free radical signaling molecules reactive oxygen species (ROS) and reactive nitrogen species (RNS) have been proven to participate in iron deficiency in eukaryotes. However, little is known about the roles of these molecules in iron-deficient T. vaginalis. T. vaginalis cultured in iron-rich and -deficient conditions were collected for all experiments in this study. Next generation RNA sequencing was conducted to investigate the impact of iron on transcriptome of T. vaginalis. The cell viabilities were monitored after the trophozoites treated with the inhibitors of nitric oxide (NO) synthase (L-NG-monomethyl arginine, L-NMMA) and proteasome (MG132). Hydrogenosomal membrane potential was measured using JC-1 staining. We demonstrated that NO rather than ROS accumulates in iron-deficient T. vaginalis. The level of NO was blocked by MG132 and L-NMMA, indicating that NO production is through a proteasome and arginine dependent pathway. We found that the inhibition of proteasome activity shortened the survival of iron-deficient cells compared with untreated iron-deficient cells. Surprisingly, the addition of arginine restored both NO level and the survival of proteasome-inhibited cells, suggesting that proteasome-derived NO is crucial for cell survival under iron-limited conditions. Additionally, NO maintains the hydrogenosomal membrane potential, a determinant for cell survival, emphasizing the cytoprotective effect of NO on iron-deficient T. vaginalis. Collectively, we determined that NO produced by the proteasome prolonged the survival of iron-deficient T. vaginalis via maintenance of the hydrogenosomal functions.
Question: Does nitric oxide maintain cell survival of Trichomonas vaginalis upon iron depletion?
Output:
|
PubmedQA68673
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Collateral artery growth (arteriogenesis) is an important adaptive response to hampered arterial perfusion. It is unknown whether preventive physical exercise before limb ischemia can improve arteriogenesis and modulate mononuclear cell function. This study aimed at investigating the effects of endurance exercise before arterial occlusion on MNC function and collateral artery growth. After 3 weeks of voluntary treadmill exercise, ligation of the right femoral artery was performed in mice. Hindlimb perfusion immediately after surgery did not differ from sedentary mice. However, previous exercise improved perfusion restoration ≤7 days after femoral artery ligation, also when exercise was stopped at ligation. This was accompanied by an accumulation of peri-collateral macrophages and increased expression of endothelial nitric oxide synthase and inducible nitric oxide synthase (iNOS) in hindlimb collateral and in MNC of blood and spleen. Systemic monocyte and macrophage depletion by liposomal clodronate but not splenectomy attenuated exercise-induced perfusion restoration, collateral artery growth, peri-collateral macrophage accumulation, and upregulation of iNOS. iNOS-deficient mice did not show exercise-induced perfusion restoration. Transplantation of bone marrow-derived MNC from iNOS-deficient mice into wild-type animals inhibited exercise-induced collateral artery growth. In contrast to sedentary controls, thrice weekly aerobic exercise training for 6 months in humans increased peripheral blood MNC iNOS expression.\n Question: Does exercise promote collateral artery growth mediated by monocytic nitric oxide?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Collateral artery growth (arteriogenesis) is an important adaptive response to hampered arterial perfusion. It is unknown whether preventive physical exercise before limb ischemia can improve arteriogenesis and modulate mononuclear cell function. This study aimed at investigating the effects of endurance exercise before arterial occlusion on MNC function and collateral artery growth. After 3 weeks of voluntary treadmill exercise, ligation of the right femoral artery was performed in mice. Hindlimb perfusion immediately after surgery did not differ from sedentary mice. However, previous exercise improved perfusion restoration ≤7 days after femoral artery ligation, also when exercise was stopped at ligation. This was accompanied by an accumulation of peri-collateral macrophages and increased expression of endothelial nitric oxide synthase and inducible nitric oxide synthase (iNOS) in hindlimb collateral and in MNC of blood and spleen. Systemic monocyte and macrophage depletion by liposomal clodronate but not splenectomy attenuated exercise-induced perfusion restoration, collateral artery growth, peri-collateral macrophage accumulation, and upregulation of iNOS. iNOS-deficient mice did not show exercise-induced perfusion restoration. Transplantation of bone marrow-derived MNC from iNOS-deficient mice into wild-type animals inhibited exercise-induced collateral artery growth. In contrast to sedentary controls, thrice weekly aerobic exercise training for 6 months in humans increased peripheral blood MNC iNOS expression.
Question: Does exercise promote collateral artery growth mediated by monocytic nitric oxide?
Output:
|
PubmedQA57533
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Liver stiffness (LS) correlates with portal pressure (hepatic venous pressure gradient, HVPG). However, the dynamic components of portal hypertension (PHT) in advanced cirrhosis may not be adequately assessed by TE. The influence of treatment with non-selective β-blockers (NSBB) on the correlation of HVPG and LS has not been investigated. One hundred and twenty-two patients with esophageal varices were included. LS, hemodynamic parameters, and HVPG were recorded at baseline (BL) and after 6 weeks of treatment with NSBB (FU). The correlation of LS and HVPG was compared to control patients with HVPG ≤ 12 mmHg. Patients with higher Child-Pugh stages (A:88/B:25/C:9) had higher levels of liver stiffness (47.4 ± 16.5 vs. 70.3 ± 7.9 vs. 73.7 ± 2.1 kPa) and HVPG (21 ± 5 vs. 26 ± 5 vs. 26 ± 4 mmHg). The correlation of LS and HVPG was stronger in controls with HVPG ≤ 12 mmHg (R = 0.951; P < 0.0001) than in patients with HVPG > 12 mmHg (R = 0.538; P = 0.0004). The association of HVPG with LS became stronger under treatment with NSBB, which finally restored the linear correlation of HVPG and LS (R = 0.930; P < 0.0001). Forty-three percent (53/122) of patients were hemodynamic responders to NSBB. The improvement in the correlation of LS and HVPG under NSBB was mainly noted in hemodynamic responders (R = 0.864), but not in nonresponders (R = 0.535), whereas changes in LS, heart rate, and MAP were similar in responders and nonresponders.\n Question: Do non-selective β-blockers improve the correlation of liver stiffness and portal pressure in advanced 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: Liver stiffness (LS) correlates with portal pressure (hepatic venous pressure gradient, HVPG). However, the dynamic components of portal hypertension (PHT) in advanced cirrhosis may not be adequately assessed by TE. The influence of treatment with non-selective β-blockers (NSBB) on the correlation of HVPG and LS has not been investigated. One hundred and twenty-two patients with esophageal varices were included. LS, hemodynamic parameters, and HVPG were recorded at baseline (BL) and after 6 weeks of treatment with NSBB (FU). The correlation of LS and HVPG was compared to control patients with HVPG ≤ 12 mmHg. Patients with higher Child-Pugh stages (A:88/B:25/C:9) had higher levels of liver stiffness (47.4 ± 16.5 vs. 70.3 ± 7.9 vs. 73.7 ± 2.1 kPa) and HVPG (21 ± 5 vs. 26 ± 5 vs. 26 ± 4 mmHg). The correlation of LS and HVPG was stronger in controls with HVPG ≤ 12 mmHg (R = 0.951; P < 0.0001) than in patients with HVPG > 12 mmHg (R = 0.538; P = 0.0004). The association of HVPG with LS became stronger under treatment with NSBB, which finally restored the linear correlation of HVPG and LS (R = 0.930; P < 0.0001). Forty-three percent (53/122) of patients were hemodynamic responders to NSBB. The improvement in the correlation of LS and HVPG under NSBB was mainly noted in hemodynamic responders (R = 0.864), but not in nonresponders (R = 0.535), whereas changes in LS, heart rate, and MAP were similar in responders and nonresponders.
Question: Do non-selective β-blockers improve the correlation of liver stiffness and portal pressure in advanced cirrhosis?
Output:
|
PubmedQA95377
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: If we initiate a sound by our own motor behavior, the N1 component of the auditory event-related brain potential (ERP) that the sound elicits is attenuated compared to the N1 elicited by the same sound when it is initiated externally. It has been suggested that this N1 suppression results from an internal predictive mechanism that is in the service of discriminating the sensory consequences of one's own actions from other sensory input. As the N1-suppression effect is becoming a popular approach to investigate predictive processing in cognitive and social neuroscience, it is important to exclude an alternative interpretation not related to prediction. According to the attentional account, the N1 suppression is due to a difference in the allocation of attention between self- and externally-initiated sounds. To test this hypothesis, we manipulated the allocation of attention to the sounds in different blocks: Attention was directed either to the sounds, to the own motor acts or to visual stimuli. If attention causes the N1-suppression effect, then manipulating attention should affect the effect for self-initiated sounds. We found N1 suppression in all conditions. The N1 per se was affected by attention, but there was no interaction between attention and self-initiation effects. This implies that self-initiation N1 effects are not caused by attention.\n Question: Is the N1-suppression effect for self-initiated sounds independent of attention?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: If we initiate a sound by our own motor behavior, the N1 component of the auditory event-related brain potential (ERP) that the sound elicits is attenuated compared to the N1 elicited by the same sound when it is initiated externally. It has been suggested that this N1 suppression results from an internal predictive mechanism that is in the service of discriminating the sensory consequences of one's own actions from other sensory input. As the N1-suppression effect is becoming a popular approach to investigate predictive processing in cognitive and social neuroscience, it is important to exclude an alternative interpretation not related to prediction. According to the attentional account, the N1 suppression is due to a difference in the allocation of attention between self- and externally-initiated sounds. To test this hypothesis, we manipulated the allocation of attention to the sounds in different blocks: Attention was directed either to the sounds, to the own motor acts or to visual stimuli. If attention causes the N1-suppression effect, then manipulating attention should affect the effect for self-initiated sounds. We found N1 suppression in all conditions. The N1 per se was affected by attention, but there was no interaction between attention and self-initiation effects. This implies that self-initiation N1 effects are not caused by attention.
Question: Is the N1-suppression effect for self-initiated sounds independent of attention?
Output:
|
PubmedQA162796
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Transmual endoscopic drainage of peripancreatic fluid collections under endoscopic ultrasound (EUS) control has been reported. We evaluated a facilitated technique of one-step puncture and drainage using a new stenting device and a large-channel echo endoscope. EUS-guided transumural drainage of cystic lesions was attempted in six male patients. The drainage sites were duodenal in two instances and gastric in four. The lesions were pseudocysts, arising from chronic pancreatitis (n=2), and following acute pancreatitis (n=3), and one abscess. The median size of the pseudocysts was 50mm (range, 25 to 90). The punctures were carried out under direct EUS guidance, using a new echo endoscope with a 3.2-mm working channel. Transmural drainage was done using modified 7-F stents. Stents were inserted directly over a 1-mm puncture needle and their position was optimized using a 7-F pusher connected to the stent by a special construction. The stents were released by withdrawing the needle. EUS-guided one-step drainage was technically successful in all 6 patients. It was possible to position the stents as desired, regardless of the location, size or pathogenesis of the target lesions. There were no complications associated with the endoscopic interventions. All the lesions, including two with putrid contents, had collapsed by the day following drainage. The stents were removed after a median period of 2 weeks (range 2-12). The cysts had completely resolved in four patients at follow-ups of 3-13 months (range). The patient with the gastric abscess underwent gastrectomy 2 weeks after stent extraction, because of a coincidental adenocarcinoma at the cardia, the abscess being resolved. One patient with necrotizing pancreatitis, who refused surgical treatment, died because of septic complications.\n Question: Do endoscopic ultrasound-guided one-step transmural drainage of cystic abdominal lesions with a large-channel echo endoscope?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Transmual endoscopic drainage of peripancreatic fluid collections under endoscopic ultrasound (EUS) control has been reported. We evaluated a facilitated technique of one-step puncture and drainage using a new stenting device and a large-channel echo endoscope. EUS-guided transumural drainage of cystic lesions was attempted in six male patients. The drainage sites were duodenal in two instances and gastric in four. The lesions were pseudocysts, arising from chronic pancreatitis (n=2), and following acute pancreatitis (n=3), and one abscess. The median size of the pseudocysts was 50mm (range, 25 to 90). The punctures were carried out under direct EUS guidance, using a new echo endoscope with a 3.2-mm working channel. Transmural drainage was done using modified 7-F stents. Stents were inserted directly over a 1-mm puncture needle and their position was optimized using a 7-F pusher connected to the stent by a special construction. The stents were released by withdrawing the needle. EUS-guided one-step drainage was technically successful in all 6 patients. It was possible to position the stents as desired, regardless of the location, size or pathogenesis of the target lesions. There were no complications associated with the endoscopic interventions. All the lesions, including two with putrid contents, had collapsed by the day following drainage. The stents were removed after a median period of 2 weeks (range 2-12). The cysts had completely resolved in four patients at follow-ups of 3-13 months (range). The patient with the gastric abscess underwent gastrectomy 2 weeks after stent extraction, because of a coincidental adenocarcinoma at the cardia, the abscess being resolved. One patient with necrotizing pancreatitis, who refused surgical treatment, died because of septic complications.
Question: Do endoscopic ultrasound-guided one-step transmural drainage of cystic abdominal lesions with a large-channel echo endoscope?
Output:
|
PubmedQA199876
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Oral glucocorticoids are administered in moderate and severe cases of subacute thyroiditis (SAT), providing dramatic relief from pain and fever. However, there have been no reports regarding the optimal dose of prednisolone (PSL) for treatment of SAT. In this study, we used 15 mg/day of PSL as the initial dosage and tapered it by 5 mg every 2 weeks. We assessed the effectiveness of this treatment protocol. We examined 384 consecutive and untreated patients with SAT who visited our thyroid clinic between February 2005 and December 2008. We excluded patients who did not fit our protocol, and the final number of subjects was 219. When patients complained of pain in their neck or C-reactive protein (CRP) was still high, physicians were able to extend the tapering of the dose of PSL or increase it at 2-week intervals. The endpoint of the study was the duration of the PSL medication. We also compared the severity of thyrotoxicosis and rate of hypothyroidism after SAT between the short medication group (patients who recovered within 6 weeks) and long medication group (patients who recovered in 12 weeks or more). The number of patients whose thyroiditis improved within 6 weeks and did not recur was 113 (51.6%), and 61 (27.9%) improved within 7 to 8 weeks and did not have a recurrence. The longest duration was 40 weeks. Seven patients (3.2%) needed increases in the dosage of PSL. Thyroid hormone (free thyroxine and free triiodothyronine) levels measured at the initial visit in the short medication group were significantly higher than those in the long medication group (p<0.05). Serum CRP, male-to-female ratio, body weight, and age showed no differences between the two groups. There were no differences in the rate of hypothyroidism after SAT between the two groups (p=0.0632).\n Question: Is initial treatment with 15 mg of prednisolone daily sufficient for most patients with subacute thyroiditis in Japan?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Oral glucocorticoids are administered in moderate and severe cases of subacute thyroiditis (SAT), providing dramatic relief from pain and fever. However, there have been no reports regarding the optimal dose of prednisolone (PSL) for treatment of SAT. In this study, we used 15 mg/day of PSL as the initial dosage and tapered it by 5 mg every 2 weeks. We assessed the effectiveness of this treatment protocol. We examined 384 consecutive and untreated patients with SAT who visited our thyroid clinic between February 2005 and December 2008. We excluded patients who did not fit our protocol, and the final number of subjects was 219. When patients complained of pain in their neck or C-reactive protein (CRP) was still high, physicians were able to extend the tapering of the dose of PSL or increase it at 2-week intervals. The endpoint of the study was the duration of the PSL medication. We also compared the severity of thyrotoxicosis and rate of hypothyroidism after SAT between the short medication group (patients who recovered within 6 weeks) and long medication group (patients who recovered in 12 weeks or more). The number of patients whose thyroiditis improved within 6 weeks and did not recur was 113 (51.6%), and 61 (27.9%) improved within 7 to 8 weeks and did not have a recurrence. The longest duration was 40 weeks. Seven patients (3.2%) needed increases in the dosage of PSL. Thyroid hormone (free thyroxine and free triiodothyronine) levels measured at the initial visit in the short medication group were significantly higher than those in the long medication group (p<0.05). Serum CRP, male-to-female ratio, body weight, and age showed no differences between the two groups. There were no differences in the rate of hypothyroidism after SAT between the two groups (p=0.0632).
Question: Is initial treatment with 15 mg of prednisolone daily sufficient for most patients with subacute thyroiditis in Japan?
Output:
|
PubmedQA12804
|
[
{
"role": "user",
"content": "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 establish monoclonal antibodies (mAb) against megakaryocyte potentiation factor (MPF) and detect MPF in the blood of patients with mesothelioma. Mice were immunized with a purified recombinant human MPF-rabbit-Fc fusion protein and with MPF. Several hybridomas producing mAbs to MPF were established. A double-determinant (sandwich) ELISA was constructed using mAbs to two different epitopes and used to determine if MPF is present in the serum of patients with mesothelioma. We established seven anti-MPF mAbs whose topographical epitopes were classified into three nonoverlapping groups. All the mAbs reacted with recombinant MPF protein by ELISA. One of the mAbs detected MPF and the mesothelin precursor protein containing MPF in cell lysates on Western blotting. A sandwich ELISA using mAbs to two different epitopes was constructed and used to measure the presence of MPF in the media of various mesothelin-expressing cancer cell lines and in human serum. The ELISA showed that MPF levels were elevated in 91% (51 of 56) of patients with mesothelioma compared with healthy controls. Furthermore, serum MPF fell to normal levels in two patients after surgery for their peritoneal mesothelioma.\n Question: Is megakaryocyte potentiation factor cleaved from mesothelin precursor a useful tumor marker in the serum of patients with 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: To establish monoclonal antibodies (mAb) against megakaryocyte potentiation factor (MPF) and detect MPF in the blood of patients with mesothelioma. Mice were immunized with a purified recombinant human MPF-rabbit-Fc fusion protein and with MPF. Several hybridomas producing mAbs to MPF were established. A double-determinant (sandwich) ELISA was constructed using mAbs to two different epitopes and used to determine if MPF is present in the serum of patients with mesothelioma. We established seven anti-MPF mAbs whose topographical epitopes were classified into three nonoverlapping groups. All the mAbs reacted with recombinant MPF protein by ELISA. One of the mAbs detected MPF and the mesothelin precursor protein containing MPF in cell lysates on Western blotting. A sandwich ELISA using mAbs to two different epitopes was constructed and used to measure the presence of MPF in the media of various mesothelin-expressing cancer cell lines and in human serum. The ELISA showed that MPF levels were elevated in 91% (51 of 56) of patients with mesothelioma compared with healthy controls. Furthermore, serum MPF fell to normal levels in two patients after surgery for their peritoneal mesothelioma.
Question: Is megakaryocyte potentiation factor cleaved from mesothelin precursor a useful tumor marker in the serum of patients with mesothelioma?
Output:
|
PubmedQA182245
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Open-heart surgery with cardiopulmonary bypass (CPB) is associated with a generalized immune response and postoperative lung dysfunction. Chemokines are involved in the pathogenesis of postoperative lung dysfunction. We investigated whether continued mechanical ventilation during CPB has an impact on chemokine serum concentrations. A total of 30 patients undergoing coronary artery bypass graft operation were randomized to either continuous ventilated group (n=15) or nonventilated group (n=15). Blood samples were drawn at the beginning and at the end of surgery and on the 5 consecutive days. Serum CCL2, CCL4, and CCL20 concentrations were measured and given as mean ± standard deviation. Chemokine concentrations were elevated at the end of surgery in both groups. CCL2 and CCL4 levels returned to baseline on postoperative day (POD)-1 in the ventilation group and stayed elevated in the nonventilation group. CCL4 serum levels were significantly lower in ventilated-group patients on POD-1 (10.9 [39.0] vs. 153.2 [168.1]; p=0.005), POD-2 (16.8 [36.8] vs. 147.9 [165.4]; p=0.019), POD-3 (14.2 [24.0] vs. 97.9 [87.1]; p=0.005), and POD-5 (6.5 [25.0] vs. 33.6 [38.4]; p=0.045).\n Question: Does low tidal volume ventilation during cardiopulmonary bypass reduce postoperative chemokine serum concentrations?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Open-heart surgery with cardiopulmonary bypass (CPB) is associated with a generalized immune response and postoperative lung dysfunction. Chemokines are involved in the pathogenesis of postoperative lung dysfunction. We investigated whether continued mechanical ventilation during CPB has an impact on chemokine serum concentrations. A total of 30 patients undergoing coronary artery bypass graft operation were randomized to either continuous ventilated group (n=15) or nonventilated group (n=15). Blood samples were drawn at the beginning and at the end of surgery and on the 5 consecutive days. Serum CCL2, CCL4, and CCL20 concentrations were measured and given as mean ± standard deviation. Chemokine concentrations were elevated at the end of surgery in both groups. CCL2 and CCL4 levels returned to baseline on postoperative day (POD)-1 in the ventilation group and stayed elevated in the nonventilation group. CCL4 serum levels were significantly lower in ventilated-group patients on POD-1 (10.9 [39.0] vs. 153.2 [168.1]; p=0.005), POD-2 (16.8 [36.8] vs. 147.9 [165.4]; p=0.019), POD-3 (14.2 [24.0] vs. 97.9 [87.1]; p=0.005), and POD-5 (6.5 [25.0] vs. 33.6 [38.4]; p=0.045).
Question: Does low tidal volume ventilation during cardiopulmonary bypass reduce postoperative chemokine serum concentrations?
Output:
|
PubmedQA62959
|
[
{
"role": "user",
"content": "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 investigate the using of bone marrow mesenchymal stem cells (BMSCs) genetically engineered to produce interferon-β (IFN-β) as a gene delivery system to treat hepatocellular carcinoma (HCC) in vitro and in vivo. To measure the effects on tumour cell growth in vitro, IFN-β-producing BMSCs (BMSC/IFN-β) were co-cultured with the HCC cell line HepG2 and Huh7. Enzyme-linked immunosorbent assay (ELISA) was used to detect the IFN-β secretion in the BMSC culture condition medium (CM). The effect of BMSC/IFN-β on HCC cells proliferation was examined both in vitro and in vivo by using MTT, colony formation assay, BrdU staining, cell cycle analysis, and xenografted NOD/SCID mouse tumour model. To examine the impact of BMSC/IFN-β on the AKT/FOXO3a signalling, RT-PCR and western blotting were performed. The BMSC/IFN-β cells can stably secrete high levels of IFN-β. Both MTT and colony forming assay showed that HCC cells had a lower growth rate when cultured in BMSC/IFN-β-CM as compared with that in BMSC/vector-CM or DMEM culture group. Co-culture with BMSC/IFN-β-CM dramatically decreased the percentages of cells with incorporated BrdUrd. In BMSC/IFN-β-CM-treated HCC cells, the proportion of G1-phase cells increased but it decreased in the S phase of the cell. The BMSC/IFN-β inhibited HCC growth in NOD/SCID mice and proved the survival period of these mice. Compared with the control group, p21 and p27 expression of hepatoma cells increased, whereas cyclin D1 and phosphorylation of Rb expression decreased when co-cultured with BMSC/IFN-β-CM. It was associated with suppression of Akt activity and enhanced transcriptional activity of FOXO3a.\n Question: Do interferon-β gene-modified human bone marrow mesenchymal stem cells attenuate hepatocellular carcinoma through inhibiting AKT/FOXO3a pathway?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: This study aims to investigate the using of bone marrow mesenchymal stem cells (BMSCs) genetically engineered to produce interferon-β (IFN-β) as a gene delivery system to treat hepatocellular carcinoma (HCC) in vitro and in vivo. To measure the effects on tumour cell growth in vitro, IFN-β-producing BMSCs (BMSC/IFN-β) were co-cultured with the HCC cell line HepG2 and Huh7. Enzyme-linked immunosorbent assay (ELISA) was used to detect the IFN-β secretion in the BMSC culture condition medium (CM). The effect of BMSC/IFN-β on HCC cells proliferation was examined both in vitro and in vivo by using MTT, colony formation assay, BrdU staining, cell cycle analysis, and xenografted NOD/SCID mouse tumour model. To examine the impact of BMSC/IFN-β on the AKT/FOXO3a signalling, RT-PCR and western blotting were performed. The BMSC/IFN-β cells can stably secrete high levels of IFN-β. Both MTT and colony forming assay showed that HCC cells had a lower growth rate when cultured in BMSC/IFN-β-CM as compared with that in BMSC/vector-CM or DMEM culture group. Co-culture with BMSC/IFN-β-CM dramatically decreased the percentages of cells with incorporated BrdUrd. In BMSC/IFN-β-CM-treated HCC cells, the proportion of G1-phase cells increased but it decreased in the S phase of the cell. The BMSC/IFN-β inhibited HCC growth in NOD/SCID mice and proved the survival period of these mice. Compared with the control group, p21 and p27 expression of hepatoma cells increased, whereas cyclin D1 and phosphorylation of Rb expression decreased when co-cultured with BMSC/IFN-β-CM. It was associated with suppression of Akt activity and enhanced transcriptional activity of FOXO3a.
Question: Do interferon-β gene-modified human bone marrow mesenchymal stem cells attenuate hepatocellular carcinoma through inhibiting AKT/FOXO3a pathway?
Output:
|
PubmedQA21135
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Rituximab has broad and increasing application in rheumatic diseases. It is known from lymphoma studies that natural killer (NK) cells can lyse rituximab-coated transformed B cells. However, the role of NK cells in mediating rituximab-induced depletion of non-malignant B cells is unknown. The purpose of this study was to provide fundamental data on rituximab-mediated effects on NK cells in PBMCs without tumor cells, in order to simulate effects that could be relevant in patients with rheumatic disease. Freshly isolated peripheral blood mononuclear cells (PBMCs) from healthy donors were cultured overnight with therapeutic antibodies. NK cells were isolated using a commercial kit or depleted from PBMCs using anti-CD56 and anti-CD16 monoclonal antibodies and magnetic beads. Cells were analyzed by multicolor flow cytometry. Cytotoxicity assays were performed using (51)Cr-labeled K562 target cells. Addition of rituximab to PBMCs resulted in depletion of B cells, which was dependent on NK cells and serum factors. The extent of B cell depletion correlated with the percentage of NK cells. Following incubation with rituximab, NK cells within PBMCs were activated, degranulated and downregulated the low affinitiy Fc-γ-receptor CD16 (FcγRIIIA). The co-activating receptor CD137 (41BB) was upregulated on a fraction of NK cells. NK cell function was altered in some donors in whom we observed rituximab-dependent reduction in NK cell cytotoxicity towards K562 tumor cells.\n Question: Does rituximab induce phenotypical and functional changes of NK cells in a non-malignant experimental setting?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Rituximab has broad and increasing application in rheumatic diseases. It is known from lymphoma studies that natural killer (NK) cells can lyse rituximab-coated transformed B cells. However, the role of NK cells in mediating rituximab-induced depletion of non-malignant B cells is unknown. The purpose of this study was to provide fundamental data on rituximab-mediated effects on NK cells in PBMCs without tumor cells, in order to simulate effects that could be relevant in patients with rheumatic disease. Freshly isolated peripheral blood mononuclear cells (PBMCs) from healthy donors were cultured overnight with therapeutic antibodies. NK cells were isolated using a commercial kit or depleted from PBMCs using anti-CD56 and anti-CD16 monoclonal antibodies and magnetic beads. Cells were analyzed by multicolor flow cytometry. Cytotoxicity assays were performed using (51)Cr-labeled K562 target cells. Addition of rituximab to PBMCs resulted in depletion of B cells, which was dependent on NK cells and serum factors. The extent of B cell depletion correlated with the percentage of NK cells. Following incubation with rituximab, NK cells within PBMCs were activated, degranulated and downregulated the low affinitiy Fc-γ-receptor CD16 (FcγRIIIA). The co-activating receptor CD137 (41BB) was upregulated on a fraction of NK cells. NK cell function was altered in some donors in whom we observed rituximab-dependent reduction in NK cell cytotoxicity towards K562 tumor cells.
Question: Does rituximab induce phenotypical and functional changes of NK cells in a non-malignant experimental setting?
Output:
|
PubmedQA162468
|
[
{
"role": "user",
"content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Several therapeutic strategies that target nucleic acids exist; however, most approaches target messenger RNA, rather than genomic DNA. We describe a novel oligonucleotide-based strategy, called anti-gene padlocks (AGPs), which eliminate Escherichia coli based on their genotype. The strategy employs an oligonucleotide with a double hairpin structure where both strands of the AGP are complementary to both strands of a target gene. We tested AGPs for in vitro binding and inhibition of DNA polymerization. AGPs were electroporated into bacterial cells with and without gene targets along with an ampicillin resistance plasmid, and cell survival was measured. In vitro, AGPs bound the DNA target in a sequence-dependent fashion and inhibited DNA synthesis. When transformed into bacterial cells containing 10, 20 or 30 bp lacZ or 20 bp proA DNA targets in their genomes, AGPs selectively killed or otherwise inhibited growth of these cells, while those lacking the target demonstrated little, if any, toxicity. A single transformation resulted in approximately 30% to 40% loss of target-bearing cells. Structure-function experiments were performed to define essential AGP requirements.\n Question: Do anti-gene padlocks eliminate Escherichia coli based on their genotype?\n Output: "
},
{
"role": "assistant",
"content": "yes"
}
] |
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.
INPUT: Several therapeutic strategies that target nucleic acids exist; however, most approaches target messenger RNA, rather than genomic DNA. We describe a novel oligonucleotide-based strategy, called anti-gene padlocks (AGPs), which eliminate Escherichia coli based on their genotype. The strategy employs an oligonucleotide with a double hairpin structure where both strands of the AGP are complementary to both strands of a target gene. We tested AGPs for in vitro binding and inhibition of DNA polymerization. AGPs were electroporated into bacterial cells with and without gene targets along with an ampicillin resistance plasmid, and cell survival was measured. In vitro, AGPs bound the DNA target in a sequence-dependent fashion and inhibited DNA synthesis. When transformed into bacterial cells containing 10, 20 or 30 bp lacZ or 20 bp proA DNA targets in their genomes, AGPs selectively killed or otherwise inhibited growth of these cells, while those lacking the target demonstrated little, if any, toxicity. A single transformation resulted in approximately 30% to 40% loss of target-bearing cells. Structure-function experiments were performed to define essential AGP requirements.
Question: Do anti-gene padlocks eliminate Escherichia coli based on their genotype?
Output:
|
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