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stringlengths 17
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| context
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stringlengths 1
3.34k
| final_decision
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listlengths 2
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|---|---|---|---|---|---|
24,745,719 | Is unprovoked proximal venous thrombosis associated with an increased risk of asymptomatic pulmonary embolism? | {
"contexts": [
"Pulmonary embolism (PE) is common in patients with deep venous thrombosis (DVT). The outcome of DVT with concomitant symptomatic PE is worse than the outcome of isolated DVT. The risk factors for DVT and simultaneous asymptomatic PE have not been systematically studied yet.",
"To evaluate the frequency and risk factors for asymptomatic PE in patients with DVT.",
"In 155 consecutive patients with a first episode of DVT and no PE symptoms, a ventilation-perfusion lung scan was performed. Body mass index (BMI) and waist-to-hip ratio (WHR) were calculated and concentrations of D-dimer, high-sensitivity CRP (hsCRP), tissue plasminogen activator (t-PA) and troponin were measured. Laboratory tests for thrombophilia were performed.",
"Asymptomatic PE was present in 36% of patients. No differences in gender, age, BMI and WHR were found between the patients with and without PE. PE was more common in patients with proximal DVT than in those with distal DVT (42% vs. 17%, p<0.01), and in patients with unprovoked DVT compared to patients with provoked DVT (51% vs. 28%, p<0.01). The risk of silent PE was the highest in patients with unprovoked proximal DVT (OR, 6.9; 95% CI, 2.3-21.0). Patients with asymptomatic PE had significantly higher values of D-dimer, hsCRP, t-PA and troponin than patients with isolated DVT."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Female",
"Humans",
"Male",
"Middle Aged",
"Pulmonary Embolism",
"Risk Factors",
"Treatment Outcome",
"Venous Thrombosis"
]
} | Asymptomatic PE affected more than one third of patients with a first DVT. Unprovoked proximal DVT is the most important risk factor for the occurrence of silent PE. | yes | [
{
"from": "human",
"value": "Question: Is unprovoked proximal venous thrombosis associated with an increased risk of asymptomatic pulmonary embolism?\nContext: {'contexts': ['Pulmonary embolism (PE) is common in patients with deep venous thrombosis (DVT). The outcome of DVT with concomitant symptomatic PE is worse than the outcome of isolated DVT. The risk factors for DVT and simultaneous asymptomatic PE have not been systematically studied yet.', 'To evaluate the frequency and risk factors for asymptomatic PE in patients with DVT.', 'In 155 consecutive patients with a first episode of DVT and no PE symptoms, a ventilation-perfusion lung scan was performed. Body mass index (BMI) and waist-to-hip ratio (WHR) were calculated and concentrations of D-dimer, high-sensitivity CRP (hsCRP), tissue plasminogen activator (t-PA) and troponin were measured. Laboratory tests for thrombophilia were performed.', 'Asymptomatic PE was present in 36% of patients. No differences in gender, age, BMI and WHR were found between the patients with and without PE. PE was more common in patients with proximal DVT than in those with distal DVT (42% vs. 17%, p<0.01), and in patients with unprovoked DVT compared to patients with provoked DVT (51% vs. 28%, p<0.01). The risk of silent PE was the highest in patients with unprovoked proximal DVT (OR, 6.9; 95% CI, 2.3-21.0). Patients with asymptomatic PE had significantly higher values of D-dimer, hsCRP, t-PA and troponin than patients with isolated DVT.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Female', 'Humans', 'Male', 'Middle Aged', 'Pulmonary Embolism', 'Risk Factors', 'Treatment Outcome', 'Venous Thrombosis']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,746,975 | Does a longer time of exposure to antiretroviral therapy improve selenium levels? | {
"contexts": [
"Selenium is an essential mineral for immunological function, performing crucial functions at the cellular level. This micronutrient has been determined to be frequently deficient in HIV infected patients, with correlations between reduced immunological function and greater susceptibility to opportunistic infections. Our aim was to evaluate the influence of time of exposure to antiretroviral therapy (ART) on the biochemical profile of selenium in HIV-infected patients.",
"We performed a cross-sectional study on 50 HIV-positive men with different quantitations of viral load and CD4+ T cells, who were either receiving or not receiving ART. Dual energy X-ray absorptiometry (DXA) to determine body composition, biochemical analysis of selenium and albumin, anthropometric measurements were performed. The subjects were divided into groups according to the use of ART or not: The Control Group (CG) was 10 treatment-naïve volunteers, Group G < 2 was 20 volunteers on ART for less than 2 years, and Group G > 2 was 20 volunteers on ART for >2 years.",
"The body mass index showed that all subjects were of normal weight. The group with a longer time of exposure to ART (G > 2) had undetectable viremia and a higher CD4+ T cell count: 593.1 ± 234.6 mm(3). Selenium values (μg/L) were 55.9 ± 11.9 for CG, 52.1 ± 10.5 for G < 2, and 66.9 ± 20.8 for G > 2, with a significant difference between groups G < 2 and G > 2 (p < 0.05), and only G > 2 showed normal selenium values."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Absorptiometry, Photon",
"Adult",
"Albumins",
"Anti-Retroviral Agents",
"Body Composition",
"CD4-Positive T-Lymphocytes",
"Cross-Sectional Studies",
"Female",
"HIV Infections",
"Humans",
"Male",
"Micronutrients",
"Middle Aged",
"Selenium",
"Time Factors",
"Treatment Outcome",
"Viral Load"
]
} | Most of the men studied showed selenium deficiency, except for the subjects with a longer exposure to antiretroviral treatment. Thus, an adequate selenium concentration is related to better control of virology and of immunologic function. | yes | [
{
"from": "human",
"value": "Question: Does a longer time of exposure to antiretroviral therapy improve selenium levels?\nContext: {'contexts': ['Selenium is an essential mineral for immunological function, performing crucial functions at the cellular level. This micronutrient has been determined to be frequently deficient in HIV infected patients, with correlations between reduced immunological function and greater susceptibility to opportunistic infections. Our aim was to evaluate the influence of time of exposure to antiretroviral therapy (ART) on the biochemical profile of selenium in HIV-infected patients.', 'We performed a cross-sectional study on 50 HIV-positive men with different quantitations of viral load and CD4+ T cells, who were either receiving or not receiving ART. Dual energy X-ray absorptiometry (DXA) to determine body composition, biochemical analysis of selenium and albumin, anthropometric measurements were performed. The subjects were divided into groups according to the use of ART or not: The Control Group (CG) was 10 treatment-naïve volunteers, Group G < 2 was 20 volunteers on ART for less than 2 years, and Group G > 2 was 20 volunteers on ART for >2 years.', 'The body mass index showed that all subjects were of normal weight. The group with a longer time of exposure to ART (G > 2) had undetectable viremia and a higher CD4+ T cell count: 593.1 ± 234.6 mm(3). Selenium values (μg/L) were 55.9 ± 11.9 for CG, 52.1 ± 10.5 for G < 2, and 66.9 ± 20.8 for G > 2, with a significant difference between groups G < 2 and G > 2 (p < 0.05), and only G > 2 showed normal selenium values.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Absorptiometry, Photon', 'Adult', 'Albumins', 'Anti-Retroviral Agents', 'Body Composition', 'CD4-Positive T-Lymphocytes', 'Cross-Sectional Studies', 'Female', 'HIV Infections', 'Humans', 'Male', 'Micronutrients', 'Middle Aged', 'Selenium', 'Time Factors', 'Treatment Outcome', 'Viral Load']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,747,628 | Does mesenchymal stem cell application improve tendon healing via anti-apoptotic effect ( Animal study )? | {
"contexts": [
"The aim of this study was to determine the effects of mesenchymal stem cell (MSC) application and the possible pathways of MSC's effects on tendon strength and healing after tendon repair.",
"The study included 40 Wistar albino rats. Mesenchymal stem cells were obtained from the femurs and tibias of 6 rats. Achilles tendons of the remaining 34 rats were cut and repaired with open surgical procedures. Rats were divided into 2 groups. Percutaneous MSCs were applied to the study group (n=17) and physiological serum only was applied to the control group (n=17) at the 4th week. Rats were sacrificed using the cervical dislocation method under ether anesthesia at the 12th week and samples were analyzed by histological and immunohistochemical methods. For biomechanical analysis, a traction force was applied at 10 mm/min and load to failure was recorded for each specimen in Newtons.",
"Histologically, there was no significant difference between groups (p>0.05). In the immunohistochemical studies, MSCs were located more intensively at the repair zone. Apoptosis was minimally present in the study group and was clearly increased in the control group. Increase in tendon strength was significantly higher in the study group than in the control group at the 12th week (p<0.05)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Achilles Tendon",
"Administration, Cutaneous",
"Animals",
"Apoptosis",
"Biomechanical Phenomena",
"Disease Models, Animal",
"Female",
"Histological Techniques",
"Immunohistochemistry",
"Mesenchymal Stem Cell Transplantation",
"Rats",
"Rats, Wistar",
"Tendon Injuries",
"Treatment Outcome",
"Wound Healing"
]
} | The application of MSCs to decrease re-ruptures has a positive effect on tendon strength, probably due to their anti-apoptotic effects. Mesenchymal stem cell application can be used percutaneously and is effective in clinical practice in the late stages of tendon healing. | yes | [
{
"from": "human",
"value": "Question: Does mesenchymal stem cell application improve tendon healing via anti-apoptotic effect ( Animal study )?\nContext: {'contexts': [\"The aim of this study was to determine the effects of mesenchymal stem cell (MSC) application and the possible pathways of MSC's effects on tendon strength and healing after tendon repair.\", 'The study included 40 Wistar albino rats. Mesenchymal stem cells were obtained from the femurs and tibias of 6 rats. Achilles tendons of the remaining 34 rats were cut and repaired with open surgical procedures. Rats were divided into 2 groups. Percutaneous MSCs were applied to the study group (n=17) and physiological serum only was applied to the control group (n=17) at the 4th week. Rats were sacrificed using the cervical dislocation method under ether anesthesia at the 12th week and samples were analyzed by histological and immunohistochemical methods. For biomechanical analysis, a traction force was applied at 10 mm/min and load to failure was recorded for each specimen in Newtons.', 'Histologically, there was no significant difference between groups (p>0.05). In the immunohistochemical studies, MSCs were located more intensively at the repair zone. Apoptosis was minimally present in the study group and was clearly increased in the control group. Increase in tendon strength was significantly higher in the study group than in the control group at the 12th week (p<0.05).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Achilles Tendon', 'Administration, Cutaneous', 'Animals', 'Apoptosis', 'Biomechanical Phenomena', 'Disease Models, Animal', 'Female', 'Histological Techniques', 'Immunohistochemistry', 'Mesenchymal Stem Cell Transplantation', 'Rats', 'Rats, Wistar', 'Tendon Injuries', 'Treatment Outcome', 'Wound Healing']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,764,725 | Is a Polymorphism in the IL-5 Gene Associated with Inhibitor Development in Severe Hemophilia A Patients? | {
"contexts": [
"A severe complication in the replacement therapy of hemophilia A (HA) patients is the development of alloantibodies (inhibitors) against factor VIII, which neutralizes the substituted factor. The primary genetic risk factors influencing the development of inhibitors are F8 gene mutations. Interleukins and cytokines that are involved in the regulation of B-lymphocyte development are other possible targets as genetic risk factors. This study assesses the possible involvement of 9 selected single nucleotide gene polymorphisms (SNPs) with interleukins (IL-4, IL-5, and IL-10), transforming growth factor beta 1 (TGF-β1), and interferon gamma (IFN-γ) in inhibitor development in severely affected HA patients carrying a null mutation in the F8 gene.",
"A total of 173 HA patients were screened for intron 22 inversion and null mutations (nonsense and deletions). Genotyping of a total of 9 SNPs in genes IL-4, IL-5, IL-10, TGF-β1, and IFN-γ in 103 patients and 100 healthy individuals was carried out.",
"An association analysis between 42 inhibitor (+) and 61 inhibitor (-) patients showed a significant association with the T allele of rs2069812 in the IL-5 gene promoter and patients with inhibitors (p=0.0251). The TT genotype was also significantly associated with this group with a p-value of 0.0082, odds ratio of about 7, and confidence interval of over 90%, suggesting that it is the recessive susceptibility allele and that the C allele is the dominant protective allele."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": []
} | The lack of other variants in the IL-5 gene of patients and controls suggests that rs2069812 may be a regulatory SNP and may have a role in B-lymphocyte development, constituting a genetic risk factor in antibody development. | yes | [
{
"from": "human",
"value": "Question: Is a Polymorphism in the IL-5 Gene Associated with Inhibitor Development in Severe Hemophilia A Patients?\nContext: {'contexts': ['A severe complication in the replacement therapy of hemophilia A (HA) patients is the development of alloantibodies (inhibitors) against factor VIII, which neutralizes the substituted factor. The primary genetic risk factors influencing the development of inhibitors are F8 gene mutations. Interleukins and cytokines that are involved in the regulation of B-lymphocyte development are other possible targets as genetic risk factors. This study assesses the possible involvement of 9 selected single nucleotide gene polymorphisms (SNPs) with interleukins (IL-4, IL-5, and IL-10), transforming growth factor beta 1 (TGF-β1), and interferon gamma (IFN-γ) in inhibitor development in severely affected HA patients carrying a null mutation in the F8 gene.', 'A total of 173 HA patients were screened for intron 22 inversion and null mutations (nonsense and deletions). Genotyping of a total of 9 SNPs in genes IL-4, IL-5, IL-10, TGF-β1, and IFN-γ in 103 patients and 100 healthy individuals was carried out.', 'An association analysis between 42 inhibitor (+) and 61 inhibitor (-) patients showed a significant association with the T allele of rs2069812 in the IL-5 gene promoter and patients with inhibitors (p=0.0251). The TT genotype was also significantly associated with this group with a p-value of 0.0082, odds ratio of about 7, and confidence interval of over 90%, suggesting that it is the recessive susceptibility allele and that the C allele is the dominant protective allele.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,762,066 | Do changes in aldehyde dehydrogenase-1 expression during neoadjuvant chemotherapy predict outcome in locally advanced breast cancer? | {
"contexts": [
"Although neoadjuvant chemotherapy (NAC) for locally advanced breast cancer can improve operability and local disease control, there is a lack of reliable biomarkers that predict response to chemotherapy or long-term survival. Since expression of aldehyde dehydrogenase-1 (ALDH1) is associated with the stem-like properties of self-renewal and innate chemoresistance in breast cancer, we asked whether expression in serial tumor samples treated with NAC could identify women more likely to benefit from this therapy.",
"Women with locally advanced breast cancer were randomly assigned to receive four cycles of anthracycline-based chemotherapy, followed by four cycles of taxane therapy (Arm A), or the same regimen in reverse order (Arm B). Tumor specimens were collected at baseline, after four cycles, and then at surgical resection. ALDH1 expression was determined by immunohistochemistry and correlated with tumor response using Fisher's exact test while Kaplan-Meier method was used to calculate survival.",
"A hundred and nineteen women were enrolled into the study. Fifty seven (48%) were randomized to Arm A and 62 (52%) to Arm B. Most of the women (90%) had ductal carcinoma and 10% had lobular carcinoma. Of these, 26 (22%) achieved a pathological complete response (pCR) after NAC. There was no correlation between baseline ALDH1 expression and tumor grade, stage, hormone receptor, human epidermal growth factor receptor 2 (HER2) status and Ki67 index. ALDH1 negativity at baseline was significantly associated with pCR (P = 0.004). The presence of ALDH1(+) cells in the residual tumor cells in non-responding women was strongly predictive of worse overall survival (P = 0.024). Moreover, serial analysis of specimens from non-responders showed a marked increase in tumor-specific ALDH1 expression (P = 0.028). Overall, there was no survival difference according to the chemotherapy sequence. However, poorly responding tumours from women receiving docetaxel chemotherapy showed an unexpected significant increase in ALDH1 expression."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Antineoplastic Combined Chemotherapy Protocols",
"Breast Neoplasms",
"Cyclophosphamide",
"Docetaxel",
"Drug Administration Schedule",
"Epirubicin",
"Female",
"Fluorouracil",
"Humans",
"Immunohistochemistry",
"Isoenzymes",
"Kaplan-Meier Estimate",
"Ki-67 Antigen",
"Middle Aged",
"Multivariate Analysis",
"Neoadjuvant Therapy",
"Neoplasm Staging",
"Prognosis",
"Receptor, ErbB-2",
"Retinal Dehydrogenase",
"Taxoids",
"Treatment Outcome"
]
} | ALDH1 expression is a useful predictor of chemoresistance. The up-regulation of ALDH1 after NAC predicts poor survival in locally advanced breast cancer. Although the chemotherapy sequence had no effect on overall prognosis, our results suggest that anthracycline-based chemotherapy may be more effective at targeting ALDH1(+) breast cancer cells. | yes | [
{
"from": "human",
"value": "Question: Do changes in aldehyde dehydrogenase-1 expression during neoadjuvant chemotherapy predict outcome in locally advanced breast cancer?\nContext: {'contexts': ['Although neoadjuvant chemotherapy (NAC) for locally advanced breast cancer can improve operability and local disease control, there is a lack of reliable biomarkers that predict response to chemotherapy or long-term survival. Since expression of aldehyde dehydrogenase-1 (ALDH1) is associated with the stem-like properties of self-renewal and innate chemoresistance in breast cancer, we asked whether expression in serial tumor samples treated with NAC could identify women more likely to benefit from this therapy.', \"Women with locally advanced breast cancer were randomly assigned to receive four cycles of anthracycline-based chemotherapy, followed by four cycles of taxane therapy (Arm A), or the same regimen in reverse order (Arm B). Tumor specimens were collected at baseline, after four cycles, and then at surgical resection. ALDH1 expression was determined by immunohistochemistry and correlated with tumor response using Fisher's exact test while Kaplan-Meier method was used to calculate survival.\", 'A hundred and nineteen women were enrolled into the study. Fifty seven (48%) were randomized to Arm A and 62 (52%) to Arm B. Most of the women (90%) had ductal carcinoma and 10% had lobular carcinoma. Of these, 26 (22%) achieved a pathological complete response (pCR) after NAC. There was no correlation between baseline ALDH1 expression and tumor grade, stage, hormone receptor, human epidermal growth factor receptor 2 (HER2) status and Ki67 index. ALDH1 negativity at baseline was significantly associated with pCR (P\\u2009=\\u20090.004). The presence of ALDH1(+) cells in the residual tumor cells in non-responding women was strongly predictive of worse overall survival (P\\u2009=\\u20090.024). Moreover, serial analysis of specimens from non-responders showed a marked increase in tumor-specific ALDH1 expression (P\\u2009=\\u20090.028). Overall, there was no survival difference according to the chemotherapy sequence. However, poorly responding tumours from women receiving docetaxel chemotherapy showed an unexpected significant increase in ALDH1 expression.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Antineoplastic Combined Chemotherapy Protocols', 'Breast Neoplasms', 'Cyclophosphamide', 'Docetaxel', 'Drug Administration Schedule', 'Epirubicin', 'Female', 'Fluorouracil', 'Humans', 'Immunohistochemistry', 'Isoenzymes', 'Kaplan-Meier Estimate', 'Ki-67 Antigen', 'Middle Aged', 'Multivariate Analysis', 'Neoadjuvant Therapy', 'Neoplasm Staging', 'Prognosis', 'Receptor, ErbB-2', 'Retinal Dehydrogenase', 'Taxoids', 'Treatment Outcome']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,766,345 | Is dual oxidase 2 in lung epithelia essential for hyperoxia-induced acute lung injury in mice? | {
"contexts": [
"Acute lung injury (ALI) induced by excessive hyperoxia has been employed as a model of oxidative stress imitating acute respiratory distress syndrome. Under hyperoxic conditions, overloading quantities of reactive oxygen species (ROS) are generated in both lung epithelial and endothelial cells, leading to ALI. Some NADPH oxidase (NOX) family enzymes are responsible for hyperoxia-induced ROS generation in lung epithelial and endothelial cells. However, the molecular mechanisms of ROS production in type II alveolar epithelial cells (AECs) and ALI induced by hyperoxia are poorly understood.",
"In this study, we show that dual oxidase 2 (DUOX2) is a key NOX enzyme that affects hyperoxia-induced ROS production, particularly in type II AECs, leading to lung injury. In DUOX2 mutant mice (DUOX2(thyd/thyd)) or mice in which DUOX2 expression is knocked down in the lungs, hyperoxia-induced ALI was significantly lower than in wild-type (WT) mice. DUOX2 was mainly expressed in type II AECs, but not endothelial cells, and hyperoxia-induced ROS production was markedly reduced in primary type II AECs isolated from DUOX2(thyd/thyd) mice. Furthermore, DUOX2-generated ROS are responsible for caspase-mediated cell death, inducing ERK and JNK phophorylation in type II AECs.",
"To date, no role for DUOX2 has been defined in hyperoxia-mediated ALI despite it being a NOX homologue and major ROS source in lung epithelium."
],
"labels": [
"OBJECTIVE",
"RESULTS",
"METHODS"
],
"meshes": [
"Acute Lung Injury",
"Animals",
"Caspases",
"Cell Death",
"Dual Oxidases",
"Endothelial Cells",
"Epithelial Cells",
"Hyperoxia",
"Lung",
"MAP Kinase Signaling System",
"Mice",
"NADPH Oxidases",
"Oxidative Stress",
"Phosphorylation",
"Reactive Oxygen Species"
]
} | Here, we present the novel finding that DUOX2-generated ROS induce AEC death, leading to hyperoxia-induced lung injury. | yes | [
{
"from": "human",
"value": "Question: Is dual oxidase 2 in lung epithelia essential for hyperoxia-induced acute lung injury in mice?\nContext: {'contexts': ['Acute lung injury (ALI) induced by excessive hyperoxia has been employed as a model of oxidative stress imitating acute respiratory distress syndrome. Under hyperoxic conditions, overloading quantities of reactive oxygen species (ROS) are generated in both lung epithelial and endothelial cells, leading to ALI. Some NADPH oxidase (NOX) family enzymes are responsible for hyperoxia-induced ROS generation in lung epithelial and endothelial cells. However, the molecular mechanisms of ROS production in type II alveolar epithelial cells (AECs) and ALI induced by hyperoxia are poorly understood.', 'In this study, we show that dual oxidase 2 (DUOX2) is a key NOX enzyme that affects hyperoxia-induced ROS production, particularly in type II AECs, leading to lung injury. In DUOX2 mutant mice (DUOX2(thyd/thyd)) or mice in which DUOX2 expression is knocked down in the lungs, hyperoxia-induced ALI was significantly lower than in wild-type (WT) mice. DUOX2 was mainly expressed in type II AECs, but not endothelial cells, and hyperoxia-induced ROS production was markedly reduced in primary type II AECs isolated from DUOX2(thyd/thyd) mice. Furthermore, DUOX2-generated ROS are responsible for caspase-mediated cell death, inducing ERK and JNK phophorylation in type II AECs.', 'To date, no role for DUOX2 has been defined in hyperoxia-mediated ALI despite it being a NOX homologue and major ROS source in lung epithelium.'], 'labels': ['OBJECTIVE', 'RESULTS', 'METHODS'], 'meshes': ['Acute Lung Injury', 'Animals', 'Caspases', 'Cell Death', 'Dual Oxidases', 'Endothelial Cells', 'Epithelial Cells', 'Hyperoxia', 'Lung', 'MAP Kinase Signaling System', 'Mice', 'NADPH Oxidases', 'Oxidative Stress', 'Phosphorylation', 'Reactive Oxygen Species']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,751,137 | Does global transcriptional analysis reveal surface remodeling of Anaplasma marginale in the tick vector? | {
"contexts": [
"Pathogens dependent upon vectors for transmission to new hosts undergo environment specific changes in gene transcription dependent on whether they are replicating in the vector or the mammalian host. Differential gene transcription, especially of potential vaccine candidates, is of interest in Anaplasma marginale, the tick-borne causative agent of bovine anaplasmosis.",
"RNA-seq technology allowed a comprehensive analysis of the transcriptional status of A. marginale genes in two conditions: bovine host blood and tick derived cell culture, a model for the tick vector. Quantitative PCR was used to assess transcription of a set of genes in A. marginale infected tick midguts and salivary glands at two time points during the transmission cycle.",
"Genes belonging to fourteen pathways or component groups were found to be differentially transcribed in A. marginale in the bovine host versus the tick vector. One of the most significantly altered groups was composed of surface proteins. Of the 56 genes included in the surface protein group, eight were up regulated and 26 were down regulated. The down regulated surface protein encoding genes include several that are well studied due to their immunogenicity and function. Quantitative PCR of a set of genes demonstrated that transcription in tick cell culture most closely approximates transcription in salivary glands of recently infected ticks."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Anaplasma marginale",
"Animals",
"Bacterial Proteins",
"Dermacentor",
"Gene Expression Regulation, Bacterial",
"Male",
"Membrane Proteins",
"Transcription, Genetic"
]
} | The ISE6 tick cell culture line is an acceptable model for early infection in tick salivary glands, and reveals disproportionate down regulation of surface protein genes in the tick. Transcriptional profiling in other cell lines may help us simulate additional microenvironments. Understanding vector-specific alteration of gene transcription, especially of surface protein encoding genes, may aid in the development of vaccines or transmission blocking therapies. | yes | [
{
"from": "human",
"value": "Question: Does global transcriptional analysis reveal surface remodeling of Anaplasma marginale in the tick vector?\nContext: {'contexts': ['Pathogens dependent upon vectors for transmission to new hosts undergo environment specific changes in gene transcription dependent on whether they are replicating in the vector or the mammalian host. Differential gene transcription, especially of potential vaccine candidates, is of interest in Anaplasma marginale, the tick-borne causative agent of bovine anaplasmosis.', 'RNA-seq technology allowed a comprehensive analysis of the transcriptional status of A. marginale genes in two conditions: bovine host blood and tick derived cell culture, a model for the tick vector. Quantitative PCR was used to assess transcription of a set of genes in A. marginale infected tick midguts and salivary glands at two time points during the transmission cycle.', 'Genes belonging to fourteen pathways or component groups were found to be differentially transcribed in A. marginale in the bovine host versus the tick vector. One of the most significantly altered groups was composed of surface proteins. Of the 56 genes included in the surface protein group, eight were up regulated and 26 were down regulated. The down regulated surface protein encoding genes include several that are well studied due to their immunogenicity and function. Quantitative PCR of a set of genes demonstrated that transcription in tick cell culture most closely approximates transcription in salivary glands of recently infected ticks.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Anaplasma marginale', 'Animals', 'Bacterial Proteins', 'Dermacentor', 'Gene Expression Regulation, Bacterial', 'Male', 'Membrane Proteins', 'Transcription, Genetic']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,761,908 | Does cleistocalyx nervosum extract ameliorate chemical-induced oxidative stress in early stages of rat hepatocarcinogenesis? | {
"contexts": [
"To study the effect of Cleistocalyx nervosum extract (CE) on diethylnitrosamine (DEN) and phenobarbital (PB) induced oxidative stress in early stages of rat hepatocarcinogenesis.",
"Male Wistar rats were divided into 4 groups, with Group 1 as a negative control and Group 2 was a positive control receiving DEN injections once a week and PB in drinking water for 6 weeks. Two weeks before DEN initiation and PB treatment, Groups 3 and 4, were fed with 500 and 1000 mg/kg of CEs, respectively, for 8 weeks.",
"A number of GST-P-positive foci, preneoplastic lesions, in the liver were markedly increased in carcinogen administered rats, but was comparatively decreased in rats treated with 1000 mg/kg of CE. The CE reduced malondialdehyde in serum and in the livers of rats treated with DEN and PB. Moreover, CE significantly increased the activities of glutathione peroxidase and catalase in rat liver."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Alkylating Agents",
"Animals",
"Anticonvulsants",
"Antioxidants",
"Diethylnitrosamine",
"Immunoenzyme Techniques",
"Lipid Peroxidation",
"Liver Neoplasms, Experimental",
"Male",
"Oxidative Stress",
"Phenobarbital",
"Plant Extracts",
"Precancerous Conditions",
"Rats",
"Rats, Wistar",
"Syzygium"
]
} | CE appeared to exert its chemopreventive effects by modulating antioxidant status during DEN and PB induced early stages of hepatocarcinogenesis in rats. | yes | [
{
"from": "human",
"value": "Question: Does cleistocalyx nervosum extract ameliorate chemical-induced oxidative stress in early stages of rat hepatocarcinogenesis?\nContext: {'contexts': ['To study the effect of Cleistocalyx nervosum extract (CE) on diethylnitrosamine (DEN) and phenobarbital (PB) induced oxidative stress in early stages of rat hepatocarcinogenesis.', 'Male Wistar rats were divided into 4 groups, with Group 1 as a negative control and Group 2 was a positive control receiving DEN injections once a week and PB in drinking water for 6 weeks. Two weeks before DEN initiation and PB treatment, Groups 3 and 4, were fed with 500 and 1000 mg/kg of CEs, respectively, for 8 weeks.', 'A number of GST-P-positive foci, preneoplastic lesions, in the liver were markedly increased in carcinogen administered rats, but was comparatively decreased in rats treated with 1000 mg/kg of CE. The CE reduced malondialdehyde in serum and in the livers of rats treated with DEN and PB. Moreover, CE significantly increased the activities of glutathione peroxidase and catalase in rat liver.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Alkylating Agents', 'Animals', 'Anticonvulsants', 'Antioxidants', 'Diethylnitrosamine', 'Immunoenzyme Techniques', 'Lipid Peroxidation', 'Liver Neoplasms, Experimental', 'Male', 'Oxidative Stress', 'Phenobarbital', 'Plant Extracts', 'Precancerous Conditions', 'Rats', 'Rats, Wistar', 'Syzygium']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,757,658 | Is the Refit model for end-stage liver disease-Na a better predictor of mortality than the Refit model for end-stage liver disease in patients with cirrhosis and ascites? | {
"contexts": [
"The modification of the Model for End-Stage Liver Disease (MELD) scoring system (Refit MELD) and the modification of MELD-Na (Refit MELDNa), which optimized the MELD coefficients, were published in 2011. We aimed to validate the superiority of the Refit MELDNa over the Refit MELD for the prediction of 3-month mortality in Korean patients with cirrhosis and ascites.",
"We reviewed the medical records of patients admitted with hepatic cirrhosis and ascites to the Konkuk University Hospital between January 2006 and December 2011. The Refit MELD and Refit MELDNa were compared using the predictive value of the 3-month mortality, as assessed by the Child-Pugh score.",
"In total, 530 patients were enrolled, 87 of whom died within 3 months. Alcohol was the most common etiology of their cirrhosis (n=271, 51.1%), and the most common cause of death was variceal bleeding (n=20, 23%). The areas under the receiver operating curve (AUROCs) for the Child-Pugh, Refit MELD, and Refit MELDNa scores were 0.754, 0.791, and 0.764 respectively; the corresponding values when the analysis was performed only in patients with persistent ascites (n=115) were 0.725, 0.804, and 0.796, respectively. The significant difference found among the Child-Pugh, Refit MELD, and Refit MELDNa scores was between the Child-Pugh score and Refit MELD in patients with persistent ascites (P=0.039)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Alcohol Drinking",
"Area Under Curve",
"Ascites",
"End Stage Liver Disease",
"Female",
"Gastrointestinal Hemorrhage",
"Humans",
"Liver Cirrhosis",
"Male",
"Middle Aged",
"Models, Theoretical",
"ROC Curve",
"Retrospective Studies",
"Severity of Illness Index",
"Survival Analysis"
]
} | Refit MELD and Refit MELDNa exhibited good predictability for 3-month mortality in patients with cirrhosis and ascites. However, Refit MELDNa was not found to be a better predictor than Refit MELD, despite the known relationship between hyponatremia and mortality in cirrhotic patients with ascites. | no | [
{
"from": "human",
"value": "Question: Is the Refit model for end-stage liver disease-Na a better predictor of mortality than the Refit model for end-stage liver disease in patients with cirrhosis and ascites?\nContext: {'contexts': ['The modification of the Model for End-Stage Liver Disease (MELD) scoring system (Refit MELD) and the modification of MELD-Na (Refit MELDNa), which optimized the MELD coefficients, were published in 2011. We aimed to validate the superiority of the Refit MELDNa over the Refit MELD for the prediction of 3-month mortality in Korean patients with cirrhosis and ascites.', 'We reviewed the medical records of patients admitted with hepatic cirrhosis and ascites to the Konkuk University Hospital between January 2006 and December 2011. The Refit MELD and Refit MELDNa were compared using the predictive value of the 3-month mortality, as assessed by the Child-Pugh score.', 'In total, 530 patients were enrolled, 87 of whom died within 3 months. Alcohol was the most common etiology of their cirrhosis (n=271, 51.1%), and the most common cause of death was variceal bleeding (n=20, 23%). The areas under the receiver operating curve (AUROCs) for the Child-Pugh, Refit MELD, and Refit MELDNa scores were 0.754, 0.791, and 0.764 respectively; the corresponding values when the analysis was performed only in patients with persistent ascites (n=115) were 0.725, 0.804, and 0.796, respectively. The significant difference found among the Child-Pugh, Refit MELD, and Refit MELDNa scores was between the Child-Pugh score and Refit MELD in patients with persistent ascites (P=0.039).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Alcohol Drinking', 'Area Under Curve', 'Ascites', 'End Stage Liver Disease', 'Female', 'Gastrointestinal Hemorrhage', 'Humans', 'Liver Cirrhosis', 'Male', 'Middle Aged', 'Models, Theoretical', 'ROC Curve', 'Retrospective Studies', 'Severity of Illness Index', 'Survival Analysis']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
24,776,625 | Is metformin-induced thyrotropin suppression associated with cardiac effects? | {
"contexts": [
"Metformin treatment may induce a decrease/suppression in serum TSH levels, mimicking sub-clinical hyperthyroidism (SHT). The aim of the present study was to retrospectively evaluate changes in several electrocardiographic indices in euthyroid subjects with diabetes who, after starting metformin treatment, developed a low serum TSH as compared to patients with SHT resulting from an underlying thyroid disease or TSH suppressive treatment with L-thyroxine.",
"Heart rate, P wave duration, P wave dispersion, QTmax, QTmin and QT-dispersion were assessed in 23 patients with diabetes treated with metformin before and after 6 months of TSH-suppression and in 31 control patients with SHT.",
"No significant changes in electrocardiographic parameters were observed from baseline to the TSH-suppression measurement. A significant difference in P wave duration (102.9 ± 7.4 vs. 92.1 ± 5.8 ms, p<0.001), P wave dispersion (13.1 ± 3.4 vs. 7.1 ± 3.5 ms, p<0.001), QTmax (399 ± 18 vs. 388 ± 16 ms, p=0.024), QTmin (341 ± 14 vs. 350 ± 17 ms, p=0.038) and QT dispersion (49.9 ± 9.6 vs. 30.9 ± 9.2 ms, p<0.001) were observed between the control group with SHT and the group of diabetic patients with low serum levels of TSH."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Biomarkers",
"Diabetes Mellitus, Type 2",
"Down-Regulation",
"Electrocardiography",
"Female",
"Heart Rate",
"Humans",
"Hypoglycemic Agents",
"Male",
"Metformin",
"Middle Aged",
"Retrospective Studies",
"Risk Assessment",
"Thyrotropin",
"Time Factors"
]
} | Our results show that the TSH-suppressive effect observed in patients taking metformin is not associated with peripheral markers of thyroid hormone excess, at least at the cardiac level. | no | [
{
"from": "human",
"value": "Question: Is metformin-induced thyrotropin suppression associated with cardiac effects?\nContext: {'contexts': ['Metformin treatment may induce a decrease/suppression in serum TSH levels, mimicking sub-clinical hyperthyroidism (SHT). The aim of the present study was to retrospectively evaluate changes in several electrocardiographic indices in euthyroid subjects with diabetes who, after starting metformin treatment, developed a low serum TSH as compared to patients with SHT resulting from an underlying thyroid disease or TSH suppressive treatment with L-thyroxine.', 'Heart rate, P wave duration, P wave dispersion, QTmax, QTmin and QT-dispersion were assessed in 23 patients with diabetes treated with metformin before and after 6 months of TSH-suppression and in 31 control patients with SHT.', 'No significant changes in electrocardiographic parameters were observed from baseline to the TSH-suppression measurement. A significant difference in P wave duration (102.9 ± 7.4 vs. 92.1 ± 5.8 ms, p<0.001), P wave dispersion (13.1 ± 3.4 vs. 7.1 ± 3.5 ms, p<0.001), QTmax (399 ± 18 vs. 388 ± 16 ms, p=0.024), QTmin (341 ± 14 vs. 350 ± 17 ms, p=0.038) and QT dispersion (49.9 ± 9.6 vs. 30.9 ± 9.2 ms, p<0.001) were observed between the control group with SHT and the group of diabetic patients with low serum levels of TSH.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Biomarkers', 'Diabetes Mellitus, Type 2', 'Down-Regulation', 'Electrocardiography', 'Female', 'Heart Rate', 'Humans', 'Hypoglycemic Agents', 'Male', 'Metformin', 'Middle Aged', 'Retrospective Studies', 'Risk Assessment', 'Thyrotropin', 'Time Factors']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
24,757,593 | Does intravitreal Injection of Normal Saline induce Retinal Degeneration in the C57BL/6J Mouse? | {
"contexts": [
"To investigate the adverse effect of intravitreal injection of normal saline (NS) and phosphate buffered saline (PBS) in mouse eyes.",
"NS or PBS was injected intravitreally into C57BL/6J mouse eyes. Retinal lesions were monitored by fundus imaging, spectral-domain optical coherence tomography (SD-OCT), and histological investigations. Retinal immune gene expression was determined by real-time polymerase chain reaction (PCR). The toxic effect of NS and PBS or retinal protein from NS- or PBS-injected eyes on retinal pigment epithelium (RPE) was tested in B6-RPE-07 mouse RPE cell cultures.",
"Intravitreal injection of NS dose-dependently induced localized retinal lesion in mice. Histological investigations revealed multiple vacuoles in photoreceptor outer segments and RPE cells. The lesions recovered over time and by 3 weeks post injection the majority of lesions vanished in eyes receiving 1 μl NS. Inflammatory genes, including "
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": []
} | NS is toxic to the C57BL/6J mouse retina and should not be used as a vehicle for intraocular injection. PBS is not toxic to the retina and is a preferred vehicle. | yes | [
{
"from": "human",
"value": "Question: Does intravitreal Injection of Normal Saline induce Retinal Degeneration in the C57BL/6J Mouse?\nContext: {'contexts': ['To investigate the adverse effect of intravitreal injection of normal saline (NS) and phosphate buffered saline (PBS) in mouse eyes.', 'NS or PBS was injected intravitreally into C57BL/6J mouse eyes. Retinal lesions were monitored by fundus imaging, spectral-domain optical coherence tomography (SD-OCT), and histological investigations. Retinal immune gene expression was determined by real-time polymerase chain reaction (PCR). The toxic effect of NS and PBS or retinal protein from NS- or PBS-injected eyes on retinal pigment epithelium (RPE) was tested in B6-RPE-07 mouse RPE cell cultures.', 'Intravitreal injection of NS dose-dependently induced localized retinal lesion in mice. Histological investigations revealed multiple vacuoles in photoreceptor outer segments and RPE cells. The lesions recovered over time and by 3 weeks post injection the majority of lesions vanished in eyes receiving 1 μl NS. Inflammatory genes, including '], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,747,164 | Does cyclovirobuxinum D suppress lipopolysaccharide-induced inflammatory responses in murine macrophages in vitro by blocking JAK-STAT signaling pathway? | {
"contexts": [
"Cyclovirobuxinum D (CVB-D), an alkaloid isolated from the Chinese medicinal plant Buxus microphylla, has been found to be effective to treat cardiac insufficiency, arrhythmias and coronary heart disease. In the present study, we investigated the effects of CVB-D on the inflammatory responses in lipopolysaccharide (LPS)-stimulated murine macrophages in vitro and the underlying mechanisms.",
"Murine macrophage cell line RAW264.7 cells were incubated in the presence of LPS (0.1 μg/mL) for 24 h. The cell viability was measured using MTT assay. The release of NO and cytokines were detected using the Griess test and ELISA, respectively. The mRNA and protein levels were determined using RT-PCR and Western blot, respectively. Reporter gene assays were used to analyze the transcriptional activity of NF-κB.",
"Treatment of RAW264.7 cells with CVB-D (25-300 μmol/L) did not affect the cell viability. Pretreatment with CVB-D (50, 100 and 200 μmol/L) concentration-dependently decreased NO release and iNOS expression in LPS-treated RAW264.7 cells (its IC50 value in inhibition of NO production was 144 μmol/L). CVB-D also concentration-dependently inhibited the secretion and mRNA expression of IL-1β and IL-6 in LPS-treated RAW264.7 cells. Furthermore, CVB-D remarkably inhibited the phosphorylation of STAT1 and STAT3, as well as JAK2 in LPS-treated RAW264.7 cells, but did not affect the activation of NF-κB and MAPKs pathways. Pretreatment with the JAK2 specific inhibitor AG490 (30 μmol/L) produced similar effects on NO release and iNOS expression in LPS-treated RAW264.7 cells."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Anti-Inflammatory Agents",
"Cell Line",
"Drugs, Chinese Herbal",
"Interleukin-1beta",
"Interleukin-6",
"Janus Kinase 2",
"Lipopolysaccharides",
"Macrophages",
"Mice",
"NF-kappa B",
"Nitric Oxide",
"STAT Transcription Factors",
"Signal Transduction"
]
} | CVB-D exerts anti-inflammatory effects in LPS-stimulated murine macrophages in vitro at least in part by blocking the JAK-STAT signaling pathway. The anti-inflammatory actions of CVB-D may contribute to its cardioprotection. | yes | [
{
"from": "human",
"value": "Question: Does cyclovirobuxinum D suppress lipopolysaccharide-induced inflammatory responses in murine macrophages in vitro by blocking JAK-STAT signaling pathway?\nContext: {'contexts': ['Cyclovirobuxinum D (CVB-D), an alkaloid isolated from the Chinese medicinal plant Buxus microphylla, has been found to be effective to treat cardiac insufficiency, arrhythmias and coronary heart disease. In the present study, we investigated the effects of CVB-D on the inflammatory responses in lipopolysaccharide (LPS)-stimulated murine macrophages in vitro and the underlying mechanisms.', 'Murine macrophage cell line RAW264.7 cells were incubated in the presence of LPS (0.1 μg/mL) for 24 h. The cell viability was measured using MTT assay. The release of NO and cytokines were detected using the Griess test and ELISA, respectively. The mRNA and protein levels were determined using RT-PCR and Western blot, respectively. Reporter gene assays were used to analyze the transcriptional activity of NF-κB.', 'Treatment of RAW264.7 cells with CVB-D (25-300 μmol/L) did not affect the cell viability. Pretreatment with CVB-D (50, 100 and 200 μmol/L) concentration-dependently decreased NO release and iNOS expression in LPS-treated RAW264.7 cells (its IC50 value in inhibition of NO production was 144 μmol/L). CVB-D also concentration-dependently inhibited the secretion and mRNA expression of IL-1β and IL-6 in LPS-treated RAW264.7 cells. Furthermore, CVB-D remarkably inhibited the phosphorylation of STAT1 and STAT3, as well as JAK2 in LPS-treated RAW264.7 cells, but did not affect the activation of NF-κB and MAPKs pathways. Pretreatment with the JAK2 specific inhibitor AG490 (30 μmol/L) produced similar effects on NO release and iNOS expression in LPS-treated RAW264.7 cells.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Anti-Inflammatory Agents', 'Cell Line', 'Drugs, Chinese Herbal', 'Interleukin-1beta', 'Interleukin-6', 'Janus Kinase 2', 'Lipopolysaccharides', 'Macrophages', 'Mice', 'NF-kappa B', 'Nitric Oxide', 'STAT Transcription Factors', 'Signal Transduction']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,770,633 | Is the expression of Wnt-inhibitor DKK1 ( Dickkopf 1 ) determined by intercellular crosstalk and hypoxia in human malignant gliomas? | {
"contexts": [
"Wnt signalling pathways regulate proliferation, motility and survival in a variety of human cell types. Dickkopf 1 (DKK1) gene codes for a secreted Wnt inhibitory factor. It functions as tumour suppressor gene in breast cancer and as a pro-apoptotic factor in glioma cells. In this study, we aimed to demonstrate whether the different expression of DKK1 in human glioma-derived cells is dependent on microenvironmental factors like hypoxia and regulated by the intercellular crosstalk with bone-marrow-derived mesenchymal stem cells (bmMSCs).",
"Glioma cell line U87-MG, three cell lines from human glioblastoma grade IV (glioma-derived mesenchymal stem cells) and three bmMSCs were selected for the experiment. The expression of DKK1 in cell lines under normoxic/hypoxic environment or co-culture condition was measured using real-time PCR and enzyme-linked immunoadsorbent assay. The effect of DKK1 on cell migration and proliferation was evaluated by in vitro wound healing assays and sulphorhodamine assays, respectively.",
"Glioma-derived cells U87-MG displayed lower DKK1 expression compared with bmMSCs. Hypoxia led to an overexpression of DKK1 in bmMSCs and U87-MG when compared to normoxic environment, whereas co-culture of U87-MG with bmMSCs induced the expression of DKK1 in both cell lines. Exogenous recombinant DKK1 inhibited cell migration on all cell lines, but did not have a significant effect on cell proliferation of bmMSCs and glioma cell lines."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Cell Communication",
"Cell Hypoxia",
"Cell Line, Tumor",
"Cell Movement",
"Cell Proliferation",
"Coculture Techniques",
"Gene Expression",
"Gene Expression Regulation, Neoplastic",
"Glioma",
"Humans",
"Intercellular Signaling Peptides and Proteins",
"Mesenchymal Stem Cells",
"Neoplastic Stem Cells",
"Wnt Signaling Pathway"
]
} | In this study, we showed for the first time that the expression of DKK1 was hypoxia dependent in human malignant glioma cell lines. The induction of DKK1 by intracellular crosstalk or hypoxia stimuli sheds light on the intense adaption of glial tumour cells to environmental alterations. | yes | [
{
"from": "human",
"value": "Question: Is the expression of Wnt-inhibitor DKK1 ( Dickkopf 1 ) determined by intercellular crosstalk and hypoxia in human malignant gliomas?\nContext: {'contexts': ['Wnt signalling pathways regulate proliferation, motility and survival in a variety of human cell types. Dickkopf 1 (DKK1) gene codes for a secreted Wnt inhibitory factor. It functions as tumour suppressor gene in breast cancer and as a pro-apoptotic factor in glioma cells. In this study, we aimed to demonstrate whether the different expression of DKK1 in human glioma-derived cells is dependent on microenvironmental factors like hypoxia and regulated by the intercellular crosstalk with bone-marrow-derived mesenchymal stem cells (bmMSCs).', 'Glioma cell line U87-MG, three cell lines from human glioblastoma grade IV (glioma-derived mesenchymal stem cells) and three bmMSCs were selected for the experiment. The expression of DKK1 in cell lines under normoxic/hypoxic environment or co-culture condition was measured using real-time PCR and enzyme-linked immunoadsorbent assay. The effect of DKK1 on cell migration and proliferation was evaluated by in vitro wound healing assays and sulphorhodamine assays, respectively.', 'Glioma-derived cells U87-MG displayed lower DKK1 expression compared with bmMSCs. Hypoxia led to an overexpression of DKK1 in bmMSCs and U87-MG when compared to normoxic environment, whereas co-culture of U87-MG with bmMSCs induced the expression of DKK1 in both cell lines. Exogenous recombinant DKK1 inhibited cell migration on all cell lines, but did not have a significant effect on cell proliferation of bmMSCs and glioma cell lines.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Cell Communication', 'Cell Hypoxia', 'Cell Line, Tumor', 'Cell Movement', 'Cell Proliferation', 'Coculture Techniques', 'Gene Expression', 'Gene Expression Regulation, Neoplastic', 'Glioma', 'Humans', 'Intercellular Signaling Peptides and Proteins', 'Mesenchymal Stem Cells', 'Neoplastic Stem Cells', 'Wnt Signaling Pathway']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,761,754 | Are owner-reported coughing and nasal discharge associated with clinical findings , arterial oxygen tension , mucus score and bronchoprovocation in horses with recurrent airway obstruction in a field setting? | {
"contexts": [
"In clinical practice, veterinarians often depend on owner-reported signs to assess the clinical course of horses with recurrent airway obstruction (RAO).",
"To test whether owner-reported information on frequency of coughing and observation of nasal discharge are associated with clinical, cytological and bronchoprovocation findings in RAO-affected horses in nonstandardised field conditions.",
"Cross-sectional study comparing healthy and RAO-affected horses.",
"Twenty-eight healthy and 34 RAO-affected Swiss Warmblood horses were grouped according to owner-reported 'coughing frequency' and 'nasal discharge'. Differences between these groups were examined using clinical examination, blood gas analyses, endoscopic mucus scores, cytology of tracheobronchial secretion and bronchoalveolar lavage fluid, and airway hyperresponsiveness determined by plethysmography with histamine bronchoprovocation.",
"Frequently coughing horses differed most markedly from healthy control animals. Histamine bronchoprovocation-derived parameters were significantly different between the healthy control group and all RAO groups. Mucus grades and tracheobronchial secretion and bronchoalveolar lavage fluid neutrophil percentages had particularly high variability, with overlap of findings between groups. Owner satisfaction with the clinical status of the horse was high, even in severely affected horses."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Bronchial Spasm",
"Bronchoalveolar Lavage Fluid",
"Cough",
"Cross-Sectional Studies",
"Histamine",
"Horse Diseases",
"Horses",
"Lung Diseases, Obstructive",
"Mucus",
"Oxygen",
"Respiratory Function Tests",
"Respiratory System"
]
} | Owner-reported coughing and nasal discharge are associated with specific clinical and diagnostic findings in RAO-affected horses in field settings. While airway hyperresponsiveness differentiates best between healthy horses and asymptomatic RAO-affected horses, the absence of coughing and nasal discharge does not rule out significant neutrophilic airway inflammation. Owner satisfaction with the clinical status of the horse was uninformative. | yes | [
{
"from": "human",
"value": "Question: Are owner-reported coughing and nasal discharge associated with clinical findings , arterial oxygen tension , mucus score and bronchoprovocation in horses with recurrent airway obstruction in a field setting?\nContext: {'contexts': ['In clinical practice, veterinarians often depend on owner-reported signs to assess the clinical course of horses with recurrent airway obstruction (RAO).', 'To test whether owner-reported information on frequency of coughing and observation of nasal discharge are associated with clinical, cytological and bronchoprovocation findings in RAO-affected horses in nonstandardised field conditions.', 'Cross-sectional study comparing healthy and RAO-affected horses.', \"Twenty-eight healthy and 34 RAO-affected Swiss Warmblood horses were grouped according to owner-reported 'coughing frequency' and 'nasal discharge'. Differences between these groups were examined using clinical examination, blood gas analyses, endoscopic mucus scores, cytology of tracheobronchial secretion and bronchoalveolar lavage fluid, and airway hyperresponsiveness determined by plethysmography with histamine bronchoprovocation.\", 'Frequently coughing horses differed most markedly from healthy control animals. Histamine bronchoprovocation-derived parameters were significantly different between the healthy control group and all RAO groups. Mucus grades and tracheobronchial secretion and bronchoalveolar lavage fluid neutrophil percentages had particularly high variability, with overlap of findings between groups. Owner satisfaction with the clinical status of the horse was high, even in severely affected horses.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Bronchial Spasm', 'Bronchoalveolar Lavage Fluid', 'Cough', 'Cross-Sectional Studies', 'Histamine', 'Horse Diseases', 'Horses', 'Lung Diseases, Obstructive', 'Mucus', 'Oxygen', 'Respiratory Function Tests', 'Respiratory System']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,750,178 | Are neuroprotective effects of enriched environment housing after transient global cerebral ischaemia associated with the upregulation of insulin-like growth factor-1 signalling? | {
"contexts": [
"Use of enriched environment (EE) housing has been shown to promote recovery from cerebral ischaemic injury but the underlying mechanisms of their beneficial effects remains unclear. Here we examined whether the beneficial effects of EE housing on ischaemia-induced neurodegeneration and cognitive impairment are associated with increased insulin-like growth factor-1 (IGF-1) signalling in the hippocampus.",
"Forty-two adult male Wistar rats were included in the study and received either ischaemia or sham surgery. Rats in each group were further randomized to either: EE or standard laboratory cage housing (control). Rats were placed in their assigned housing condition immediately after recovery from anaesthesia. Behavioural testing in the cued learning and discrimination learning tasks were conducted 2 weeks after ischaemia. Rats were euthanized after behavioural testing and the hippocampus was analysed for IGF-1 level, IGF-1 receptor (IGF-1R) activation, protein kinase B (Akt) pathway activation, neurone loss and caspase 3 expression.",
"Our data showed that EE housing: (1) mitigated ischaemia-induced neuronal loss; (2) attenuated ischaemia-induced increase in caspase 3 immunoreactivity in the hippocampus; (3) ameliorated ischaemia-induced cognitive impairments; and (4) increased IGF-1R activation and signalling through the Akt pathway after ischaemic injury."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Apoptosis",
"Environment",
"Hippocampus",
"Insulin-Like Growth Factor I",
"Ischemic Attack, Transient",
"Male",
"Maze Learning",
"Phosphorylation",
"Rats",
"Rats, Wistar",
"Recovery of Function",
"Signal Transduction",
"Up-Regulation"
]
} | Ultimately, these findings suggest the possibility that IGF-1 signalling may be one of the underlying mechanisms involved in the beneficial effects of EE in optimizing recovery following cerebral ischaemic injury. | yes | [
{
"from": "human",
"value": "Question: Are neuroprotective effects of enriched environment housing after transient global cerebral ischaemia associated with the upregulation of insulin-like growth factor-1 signalling?\nContext: {'contexts': ['Use of enriched environment (EE) housing has been shown to promote recovery from cerebral ischaemic injury but the underlying mechanisms of their beneficial effects remains unclear. Here we examined whether the beneficial effects of EE housing on ischaemia-induced neurodegeneration and cognitive impairment are associated with increased insulin-like growth factor-1 (IGF-1) signalling in the hippocampus.', 'Forty-two adult male Wistar rats were included in the study and received either ischaemia or sham surgery. Rats in each group were further randomized to either: EE or standard laboratory cage housing (control). Rats were placed in their assigned housing condition immediately after recovery from anaesthesia. Behavioural testing in the cued learning and discrimination learning tasks were conducted 2\\u2009weeks after ischaemia. Rats were euthanized after behavioural testing and the hippocampus was analysed for IGF-1 level, IGF-1 receptor (IGF-1R) activation, protein kinase B (Akt) pathway activation, neurone loss and caspase 3 expression.', 'Our data showed that EE housing: (1) mitigated ischaemia-induced neuronal loss; (2) attenuated ischaemia-induced increase in caspase 3 immunoreactivity in the hippocampus; (3) ameliorated ischaemia-induced cognitive impairments; and (4) increased IGF-1R activation and signalling through the Akt pathway after ischaemic injury.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Apoptosis', 'Environment', 'Hippocampus', 'Insulin-Like Growth Factor I', 'Ischemic Attack, Transient', 'Male', 'Maze Learning', 'Phosphorylation', 'Rats', 'Rats, Wistar', 'Recovery of Function', 'Signal Transduction', 'Up-Regulation']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,757,258 | Does pI3K and Bcl-2 inhibition prime glioblastoma cells to apoptosis through downregulation of Mcl-1 and Phospho-BAD? | {
"contexts": [
"Glioblastoma multiforme (GBM) is a highly malignant human brain neoplasm with limited therapeutic options. GBMs display a deregulated apoptotic pathway with high levels of the antiapoptotic Bcl-2 family of proteins and overt activity of the phosphatidylinositol 3-kinase (PI3K) signaling pathway. Therefore, combined interference of the PI3K pathway and the Bcl-2 family of proteins is a reasonable therapeutic strategy. ABT-263 (Navitoclax), an orally available small-molecule Bcl-2 inhibitor, and GDC-0941, a PI3K inhibitor, were used to treat established glioblastoma and glioblastoma neurosphere cells, alone or in combination. Although GDC-0941 alone had a modest effect on cell viability, treatment with ABT-263 displayed a marked reduction of cell viability and induction of apoptotic cell death. Moreover, combinatorial therapy using ABT-263 and GDC-0941 showed an enhanced effect, with a further decrease in cellular viability. Furthermore, combination treatment abrogated the ability of stem cell-like glioma cells to form neurospheres. ABT-263 and GDC-0941, in combination, resulted in a consistent and significant increase of Annexin V positive cells and loss of mitochondrial membrane potential compared with either monotherapy. The combination treatment led to enhanced cleavage of both initiator and effector caspases. Mechanistically, GDC-0941 depleted pAKT (Serine 473) levels and suppressed Mcl-1 protein levels, lowering the threshold for the cytotoxic actions of ABT-263. GDC-0941 decreased Mcl-1 in a posttranslational manner and significantly decreased the half-life of Mcl-1 protein. Ectopic expression of human Mcl-1 mitigated apoptotic cell death induced by the drug combination. Furthermore, GDC-0941 modulated the phosphorylation status of BAD, thereby further enhancing ABT-263-mediated cell death."
],
"labels": [
"UNLABELLED"
],
"meshes": [
"Aniline Compounds",
"Apoptosis",
"Cell Line, Tumor",
"Down-Regulation",
"Glioblastoma",
"Humans",
"Indazoles",
"Myeloid Cell Leukemia Sequence 1 Protein",
"Phosphatidylinositol 3-Kinases",
"Phosphorylation",
"Proto-Oncogene Proteins c-bcl-2",
"Signal Transduction",
"Sulfonamides",
"Transfection",
"bcl-Associated Death Protein"
]
} | Combination therapy with ABT-263 and GDC-0941 has novel therapeutic potential by specifically targeting aberrantly active, deregulated pathways in GBM, overcoming endogenous resistance to apoptosis. | yes | [
{
"from": "human",
"value": "Question: Does pI3K and Bcl-2 inhibition prime glioblastoma cells to apoptosis through downregulation of Mcl-1 and Phospho-BAD?\nContext: {'contexts': ['Glioblastoma multiforme (GBM) is a highly malignant human brain neoplasm with limited therapeutic options. GBMs display a deregulated apoptotic pathway with high levels of the antiapoptotic Bcl-2 family of proteins and overt activity of the phosphatidylinositol 3-kinase (PI3K) signaling pathway. Therefore, combined interference of the PI3K pathway and the Bcl-2 family of proteins is a reasonable therapeutic strategy. ABT-263 (Navitoclax), an orally available small-molecule Bcl-2 inhibitor, and GDC-0941, a PI3K inhibitor, were used to treat established glioblastoma and glioblastoma neurosphere cells, alone or in combination. Although GDC-0941 alone had a modest effect on cell viability, treatment with ABT-263 displayed a marked reduction of cell viability and induction of apoptotic cell death. Moreover, combinatorial therapy using ABT-263 and GDC-0941 showed an enhanced effect, with a further decrease in cellular viability. Furthermore, combination treatment abrogated the ability of stem cell-like glioma cells to form neurospheres. ABT-263 and GDC-0941, in combination, resulted in a consistent and significant increase of Annexin V positive cells and loss of mitochondrial membrane potential compared with either monotherapy. The combination treatment led to enhanced cleavage of both initiator and effector caspases. Mechanistically, GDC-0941 depleted pAKT (Serine 473) levels and suppressed Mcl-1 protein levels, lowering the threshold for the cytotoxic actions of ABT-263. GDC-0941 decreased Mcl-1 in a posttranslational manner and significantly decreased the half-life of Mcl-1 protein. Ectopic expression of human Mcl-1 mitigated apoptotic cell death induced by the drug combination. Furthermore, GDC-0941 modulated the phosphorylation status of BAD, thereby further enhancing ABT-263-mediated cell death.'], 'labels': ['UNLABELLED'], 'meshes': ['Aniline Compounds', 'Apoptosis', 'Cell Line, Tumor', 'Down-Regulation', 'Glioblastoma', 'Humans', 'Indazoles', 'Myeloid Cell Leukemia Sequence 1 Protein', 'Phosphatidylinositol 3-Kinases', 'Phosphorylation', 'Proto-Oncogene Proteins c-bcl-2', 'Signal Transduction', 'Sulfonamides', 'Transfection', 'bcl-Associated Death Protein']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,754,876 | Is harm avoidance associated with progression of parkinsonism in community-dwelling older adults : a prospective cohort study? | {
"contexts": [
"We tested the hypothesis that harm avoidance, a trait associated with behavioral inhibition, is associated with the rate of change in parkinsonism in older adults.",
"At baseline harm avoidance was assessed with a standard self-report instrument in 969 older people without dementia participating in the Rush Memory and Aging Project, a longitudinal community-based cohort study. Parkinsonism was assessed annually with a modified version of the motor section of the Unified Parkinson's Disease Rating Scale (mUPDRS).",
"Average follow-up was 5 years. A linear mixed-effects model controlling for age, sex and education showed that for an average participant (female, 80 years old at baseline, with 14 years of education and a harm avoidance score of 10), the overall severity of parkinsonism increased by about 0.05 unit/ year (Estimate, 0.054, S.E., 0.007, p <0.001) and that the level of harm avoidance was associated with the progression of parkinsonism (Estimate, 0.004, S.E., 0.001, p <0.001). Thus, for an average participant, every 6 point (~1 SD) increase in harm avoidance score at baseline, the rate of progression of parkinsonism increased about 50% compared to an individual with an average harm avoidance score. This amount of change in parkinsonism over the course of the study was associated with about a 5% increased risk of death. The association between harm avoidance and progression of parkinsonism persisted when controlling for cognitive function, depressive symptoms, loneliness, neuroticism, late-life cognitive, social and physical activities and chronic health conditions."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Aged, 80 and over",
"Cohort Studies",
"Disease Progression",
"Female",
"Follow-Up Studies",
"Harm Reduction",
"Humans",
"Longitudinal Studies",
"Male",
"Parkinsonian Disorders",
"Prospective Studies",
"Residence Characteristics"
]
} | A higher level of the harm avoidance trait is associated with a more rapid progression of parkinsonism in older adults. | yes | [
{
"from": "human",
"value": "Question: Is harm avoidance associated with progression of parkinsonism in community-dwelling older adults : a prospective cohort study?\nContext: {'contexts': ['We tested the hypothesis that harm avoidance, a trait associated with behavioral inhibition, is associated with the rate of change in parkinsonism in older adults.', \"At baseline harm avoidance was assessed with a standard self-report instrument in 969 older people without dementia participating in the Rush Memory and Aging Project, a longitudinal community-based cohort study. Parkinsonism was assessed annually with a modified version of the motor section of the Unified Parkinson's Disease Rating Scale (mUPDRS).\", 'Average follow-up was 5 years. A linear mixed-effects model controlling for age, sex and education showed that for an average participant (female, 80 years old at baseline, with 14 years of education and a harm avoidance score of 10), the overall severity of parkinsonism increased by about 0.05 unit/ year (Estimate, 0.054, S.E., 0.007, p <0.001) and that the level of harm avoidance was associated with the progression of parkinsonism (Estimate, 0.004, S.E., 0.001, p <0.001). Thus, for an average participant, every 6 point (~1 SD) increase in harm avoidance score at baseline, the rate of progression of parkinsonism increased about 50% compared to an individual with an average harm avoidance score. This amount of change in parkinsonism over the course of the study was associated with about a 5% increased risk of death. The association between harm avoidance and progression of parkinsonism persisted when controlling for cognitive function, depressive symptoms, loneliness, neuroticism, late-life cognitive, social and physical activities and chronic health conditions.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Aged, 80 and over', 'Cohort Studies', 'Disease Progression', 'Female', 'Follow-Up Studies', 'Harm Reduction', 'Humans', 'Longitudinal Studies', 'Male', 'Parkinsonian Disorders', 'Prospective Studies', 'Residence Characteristics']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,766,641 | Do mutations in the non-structural protein region contribute to intra-genotypic evolution of enterovirus 71? | {
"contexts": [
"Clinical manifestations of enterovirus 71 (EV71) range from herpangina, hand-foot-and-mouth disease (HFMD), to severe neurological complications. Unlike the situation of switching genotypes seen in EV71 outbreaks during 1998-2008 in Taiwan, genotype B5 was responsible for two large outbreaks in 2008 and 2012, respectively. In China, by contrast, EV71 often persists as a single genotype in the population and causes frequent outbreaks. To investigate genetic changes in viral evolution, complete EV71 genome sequences were used to analyze the intra-genotypic evolution pattern in Taiwan, China, and the Netherlands.",
"Genotype B5 was predominant in Taiwan's 2008 outbreak and was re-emergent in 2012. EV71 strains from both outbreaks were phylogenetically segregated into two lineages containing fourteen non-synonymous substitutions predominantly in the non-structural protein coding region. In China, genotype C4 was first seen in 1998 and caused the latest large outbreak in 2008. Unlike shifting genotypes in Taiwan, genotype C4 persisted with progressive drift through time. A majority of non-synonymous mutations occurred in residues located in the non-structural coding region, showing annual increases. Interestingly, genotype B1/B2 in the Netherlands showed another stepwise evolution with dramatic EV71 activity increase in 1986. Phylogeny of the VP1 coding region in 1971-1986 exhibited similar lineage turnover with genotype C4 in China; however, phylogeny of the 3D-encoding region indicated separate lineage appearing after 1983, suggesting that the 3D-encoding region of genotype B2 was derived from an unidentified ancestor that contributed to intra-genotypic evolution in the Netherlands."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Amino Acid Substitution",
"Animals",
"Capsid Proteins",
"Enterovirus A, Human",
"Enterovirus Infections",
"Evolution, Molecular",
"Foot-and-Mouth Disease",
"Genome, Viral",
"Humans",
"Mutation",
"Viral Nonstructural Proteins"
]
} | Unlike VP1 coding sequences long used for phylogenetic study of enteroviruses due to expected host immune escape, our study emphasizes a dominant role of non-synonymous mutations in non-structural protein regions that contribute to (re-)emergent genotypes in continuous stepwise evolution. Dozens of amino acid substitutions, especially in non-structural proteins, were identified via genetic changes driven through intra-genotypic evolution worldwide. These identified substitutions appeared to increase viral fitness in the population, affording valuable insights not only for viral evolution but also for prevention, control, and vaccine against EV71 infection. | yes | [
{
"from": "human",
"value": "Question: Do mutations in the non-structural protein region contribute to intra-genotypic evolution of enterovirus 71?\nContext: {'contexts': ['Clinical manifestations of enterovirus 71 (EV71) range from herpangina, hand-foot-and-mouth disease (HFMD), to severe neurological complications. Unlike the situation of switching genotypes seen in EV71 outbreaks during 1998-2008 in Taiwan, genotype B5 was responsible for two large outbreaks in 2008 and 2012, respectively. In China, by contrast, EV71 often persists as a single genotype in the population and causes frequent outbreaks. To investigate genetic changes in viral evolution, complete EV71 genome sequences were used to analyze the intra-genotypic evolution pattern in Taiwan, China, and the Netherlands.', \"Genotype B5 was predominant in Taiwan's 2008 outbreak and was re-emergent in 2012. EV71 strains from both outbreaks were phylogenetically segregated into two lineages containing fourteen non-synonymous substitutions predominantly in the non-structural protein coding region. In China, genotype C4 was first seen in 1998 and caused the latest large outbreak in 2008. Unlike shifting genotypes in Taiwan, genotype C4 persisted with progressive drift through time. A majority of non-synonymous mutations occurred in residues located in the non-structural coding region, showing annual increases. Interestingly, genotype B1/B2 in the Netherlands showed another stepwise evolution with dramatic EV71 activity increase in 1986. Phylogeny of the VP1 coding region in 1971-1986 exhibited similar lineage turnover with genotype C4 in China; however, phylogeny of the 3D-encoding region indicated separate lineage appearing after 1983, suggesting that the 3D-encoding region of genotype B2 was derived from an unidentified ancestor that contributed to intra-genotypic evolution in the Netherlands.\"], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Amino Acid Substitution', 'Animals', 'Capsid Proteins', 'Enterovirus A, Human', 'Enterovirus Infections', 'Evolution, Molecular', 'Foot-and-Mouth Disease', 'Genome, Viral', 'Humans', 'Mutation', 'Viral Nonstructural Proteins']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,774,100 | Does gastric Helicobacter pylori infection associate with an increased risk of colorectal polyps in African Americans? | {
"contexts": [
"Gastric Helicobacter pylori (H. pylori) infection and colorectal polyps are more prevalent in African Americans than in the general population. We aimed to investigate whether gastric H. pylori infection is associated with colorectal polyps in African Americans.",
"Medical records of African Americans, 40 years and older (n = 1256) who underwent bidirectional gastrointestinal endoscopy on the same day were reviewed. H. pylori status was assessed by immunohistochemistry on gastric specimens. Colorectal polyps were confirmed by histological examination of colorectal biopsies. A subset of serum samples from healthy and polyp-bearing patients (n = 163) were analyzed by ELISA for anti-H. pylori and anti-CagA antibodies. The crude and adjusted effect of H. pylori on the risk of colorectal adenoma and polyp were computed by logistic regression models.",
"The prevalence of colorectal polyps and adenomas were 456 (36%) and 300 (24%) respectively. Colorectal polyps were more prevalent in gastric H. pylori infected than non-infected subjects [43% vs. 34%; Odds Ratio (OR) (95% CI): 1.5 (1.2-1.9), P = 0.001]. Patients with H. pylori-associated chronic active gastritis were at high risk to have adenomas [Unadjusted OR (95% CI): 1.3 (1.0-1.8); P = 0.04]. There was no difference in histopathology, size, or location of polyps with respect to H. pylori status. Gastric H. pylori infection, age, male gender and high risk clinical presentations were independent risk factors for colorectal polyps. Serological testing also revealed a higher prevalence of H. pylori and its toxin Cag-A in polyp patients vs. non polyp patients' sera, although in a non-statistically significant manner."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"African Americans",
"Aged",
"Aged, 80 and over",
"Biopsy",
"Colonic Polyps",
"Colorectal Neoplasms",
"Endoscopy, Gastrointestinal",
"Female",
"Helicobacter Infections",
"Helicobacter pylori",
"Humans",
"Male",
"Middle Aged",
"Risk Factors"
]
} | This study showed that current gastric H. pylori infection is associated with an increased risk of colorectal polyps in African Americans. Patients with H. pylori induced gastritis may benefit from early screening colonoscopy as a preventative measure for colorectal cancer. | yes | [
{
"from": "human",
"value": "Question: Does gastric Helicobacter pylori infection associate with an increased risk of colorectal polyps in African Americans?\nContext: {'contexts': ['Gastric Helicobacter pylori (H. pylori) infection and colorectal polyps are more prevalent in African Americans than in the general population. We aimed to investigate whether gastric H. pylori infection is associated with colorectal polyps in African Americans.', 'Medical records of African Americans, 40 years and older (n = 1256) who underwent bidirectional gastrointestinal endoscopy on the same day were reviewed. H. pylori status was assessed by immunohistochemistry on gastric specimens. Colorectal polyps were confirmed by histological examination of colorectal biopsies. A subset of serum samples from healthy and polyp-bearing patients (n = 163) were analyzed by ELISA for anti-H. pylori and anti-CagA antibodies. The crude and adjusted effect of H. pylori on the risk of colorectal adenoma and polyp were computed by logistic regression models.', \"The prevalence of colorectal polyps and adenomas were 456 (36%) and 300 (24%) respectively. Colorectal polyps were more prevalent in gastric H. pylori infected than non-infected subjects [43% vs. 34%; Odds Ratio (OR) (95% CI): 1.5 (1.2-1.9), P = 0.001]. Patients with H. pylori-associated chronic active gastritis were at high risk to have adenomas [Unadjusted OR (95% CI): 1.3 (1.0-1.8); P = 0.04]. There was no difference in histopathology, size, or location of polyps with respect to H. pylori status. Gastric H. pylori infection, age, male gender and high risk clinical presentations were independent risk factors for colorectal polyps. Serological testing also revealed a higher prevalence of H. pylori and its toxin Cag-A in polyp patients vs. non polyp patients' sera, although in a non-statistically significant manner.\"], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['African Americans', 'Aged', 'Aged, 80 and over', 'Biopsy', 'Colonic Polyps', 'Colorectal Neoplasms', 'Endoscopy, Gastrointestinal', 'Female', 'Helicobacter Infections', 'Helicobacter pylori', 'Humans', 'Male', 'Middle Aged', 'Risk Factors']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,749,812 | Is itching a significant problem and a mediator between disease severity and quality of life for patients with psoriasis : results from a randomized controlled trial? | {
"contexts": [
"In patients with moderate-to-severe psoriasis, health-related quality of life (HRQOL) has been shown to improve in parallel with improvement in disease severity.",
"To evaluate the role of pruritus (itch) in mediating the relationship between improvements in disease severity and HRQOL.",
"Data from a phase 2 clinical trial, in which 142 patients with moderate-to-severe plaque psoriasis received ixekizumab or placebo, were used for this posthoc analysis. Relationships between improvement in Psoriasis Area and Severity Index (PASI), Itch Visual Analogue Scale (VAS) and Dermatology Life Quality Index (DLQI), as well as in individual DLQI domains (symptoms and feelings, treatment, work and school, daily activities, leisure, and personal relationships) from baseline to week 16 were determined. Multiple hierarchical linear regressions and Sobel tests were conducted to evaluate the results.",
"Improvement in PASI was highly correlated with pruritus improvement and improvements in DLQI total and domain scores at week 16 (P < 0·01). Multiple hierarchical linear regression analyses showed a statistically significant (P < 0·01) association between improvement in pruritus and improvement in DLQI total score and each of the six DLQI domain scores after adjusting for improvement in PASI. Sobel tests indicated that pruritus had a significant mediation effect (P < 0·05) on the association of PASI improvement with improvement in DLQI total score and all domains except the personal relationships score."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Antibodies, Monoclonal, Humanized",
"Dermatologic Agents",
"Double-Blind Method",
"Female",
"Humans",
"Male",
"Middle Aged",
"Pruritus",
"Psoriasis",
"Quality of Life",
"Severity of Illness Index"
]
} | Pruritus appears to be an important mediator of the association between improvements in disease severity and HRQOL in patients with moderate-to-severe psoriasis. | yes | [
{
"from": "human",
"value": "Question: Is itching a significant problem and a mediator between disease severity and quality of life for patients with psoriasis : results from a randomized controlled trial?\nContext: {'contexts': ['In patients with moderate-to-severe psoriasis, health-related quality of life (HRQOL) has been shown to improve in parallel with improvement in disease severity.', 'To evaluate the role of pruritus (itch) in mediating the relationship between improvements in disease severity and HRQOL.', 'Data from a phase 2 clinical trial, in which 142 patients with moderate-to-severe plaque psoriasis received ixekizumab or placebo, were used for this posthoc analysis. Relationships between improvement in Psoriasis Area and Severity Index (PASI), Itch Visual Analogue Scale (VAS) and Dermatology Life Quality Index (DLQI), as well as in individual DLQI domains (symptoms and feelings, treatment, work and school, daily activities, leisure, and personal relationships) from baseline to week 16 were determined. Multiple hierarchical linear regressions and Sobel tests were conducted to evaluate the results.', 'Improvement in PASI was highly correlated with pruritus improvement and improvements in DLQI total and domain scores at week 16 (P\\xa0<\\xa00·01). Multiple hierarchical linear regression analyses showed a statistically significant (P\\xa0<\\xa00·01) association between improvement in pruritus and improvement in DLQI total score and each of the six DLQI domain scores after adjusting for improvement in PASI. Sobel tests indicated that pruritus had a significant mediation effect (P\\xa0<\\xa00·05) on the association of PASI improvement with improvement in DLQI total score and all domains except the personal relationships score.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Antibodies, Monoclonal, Humanized', 'Dermatologic Agents', 'Double-Blind Method', 'Female', 'Humans', 'Male', 'Middle Aged', 'Pruritus', 'Psoriasis', 'Quality of Life', 'Severity of Illness Index']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,759,621 | Does epigenetic silencing of RASSF10 promote tumor growth in esophageal squamous cell carcinoma? | {
"contexts": [
"Esophageal squamous cell carcinoma (ESCC) is one of the most malignant diseases and the five year survival rate remains less than 10%. RASSF10 is a newly identified member of the Ras-association family, but the regulation and the function of RASSF10 in ESCC remain unclear. Research methodologies such as methylation specific PCR (MSP), semi-quantitative RT-PCR, immunohistochemistry, Sodium bisulfite sequencing, and colony formation assay were utilized in this investigation. Loss of RASSF10 expression was found in KYSE150 cells and reduced expression was found in KYSE70 and KYSE180 cells. Expression of RASSF10 was found in KYSE140, KYSE450, KYSE510, TE1, TE3, and TE8 cell lines. Complete methylation was found in KYSE30 and KYSE150 cells, partial methylation was found in KYSE70, KYSE180, KYSE510, and TE1, and unmethylation was found in KYSE140, KYSE450, TE3, and TE8. Re-expression or increased expression was induced by 5-Aza-dC treatment. RASSF10 was methylated in 44.3% primary esophageal squamous cell carcinoma. RASSF10 inhibits cell proliferation and induces G2/M phase arrest in esophageal cancer cells."
],
"labels": [
"UNLABELLED"
],
"meshes": [
"Base Sequence",
"Carcinoma, Squamous Cell",
"Cell Division",
"Cell Line, Tumor",
"DNA Primers",
"Epigenesis, Genetic",
"Esophageal Neoplasms",
"Gene Silencing",
"Humans",
"Polymerase Chain Reaction",
"Tumor Suppressor Proteins"
]
} | RASSF10 was frequently methylated in human esophageal squamous cell carcinoma and expression of RASSF10 was regulated by promoter region hypermethylation. RASSF10 may serve as a tumor suppressor of esophageal cancer. | yes | [
{
"from": "human",
"value": "Question: Does epigenetic silencing of RASSF10 promote tumor growth in esophageal squamous cell carcinoma?\nContext: {'contexts': ['Esophageal squamous cell carcinoma (ESCC) is one of the most malignant diseases and the five year survival rate remains less than 10%. RASSF10 is a newly identified member of the Ras-association family, but the regulation and the function of RASSF10 in ESCC remain unclear. Research methodologies such as methylation specific PCR (MSP), semi-quantitative RT-PCR, immunohistochemistry, Sodium bisulfite sequencing, and colony formation assay were utilized in this investigation. Loss of RASSF10 expression was found in KYSE150 cells and reduced expression was found in KYSE70 and KYSE180 cells. Expression of RASSF10 was found in KYSE140, KYSE450, KYSE510, TE1, TE3, and TE8 cell lines. Complete methylation was found in KYSE30 and KYSE150 cells, partial methylation was found in KYSE70, KYSE180, KYSE510, and TE1, and unmethylation was found in KYSE140, KYSE450, TE3, and TE8. Re-expression or increased expression was induced by 5-Aza-dC treatment. RASSF10 was methylated in 44.3% primary esophageal squamous cell carcinoma. RASSF10 inhibits cell proliferation and induces G2/M phase arrest in esophageal cancer cells.'], 'labels': ['UNLABELLED'], 'meshes': ['Base Sequence', 'Carcinoma, Squamous Cell', 'Cell Division', 'Cell Line, Tumor', 'DNA Primers', 'Epigenesis, Genetic', 'Esophageal Neoplasms', 'Gene Silencing', 'Humans', 'Polymerase Chain Reaction', 'Tumor Suppressor Proteins']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,758,177 | Is nuclear factor κB-dependent regulation of angiogenesis , and metastasis in an in vivo model of thyroid cancer associated with secreted interleukin-8? | {
"contexts": [
"Development of novel strategies in the treatment of advanced thyroid cancer are needed. Our laboratory has previously identified a role for nuclear factor κB (NF-κB) signaling in human thyroid cancer cell growth, survival, and invasion.",
"Our goal was to establish the role of NF-κB signaling on thyroid cancer growth and metastases in vivo and to begin to dissect mechanisms regulating this effect.",
"We examined tumor formation of five thyroid cancer cell lines in an in vivo model of thyroid cancer and observed tumor establishment in two of the cell lines (8505C and BCPAP).",
"Inhibition of NF-κB signaling by overexpression of a dominant-negative IκBα (mIκBα) significantly inhibited thyroid tumor growth in tumors derived from both cell lines. Further studies in an experimental metastasis model demonstrated that NF-κB inhibition impaired growth of tumor metastasis and prolonged mouse survival. Proliferation (mitotic index) was decreased in 8505C tumors, but not in BCPAP tumors, while in vitro angiogenesis and in vivo tumor vascularity were significantly inhibited by mIkBα only in the BCPAP cells. Cytokine antibody array analysis demonstrated that IL-8 secretion was blocked by mIκBα expression. Interestingly, basal NF-κB activity and IL-8 levels were significantly higher in the two tumorigenic cell lines compared with the nontumorigenic lines. Furthermore, IL-8 transcript levels were elevated in high-risk human tumors, suggesting that NF-κB and IL-8 are associated with more aggressive tumor behavior."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Cells, Cultured",
"Gene Expression Regulation, Neoplastic",
"Human Umbilical Vein Endothelial Cells",
"Humans",
"I-kappa B Proteins",
"Interleukin-8",
"Male",
"Mice",
"Mice, Nude",
"NF-KappaB Inhibitor alpha",
"NF-kappa B",
"Neoplasm Metastasis",
"Neoplasm Transplantation",
"Neovascularization, Pathologic",
"Thyroid Neoplasms"
]
} | These studies suggest that NF-κB signaling is a key regulator of angiogenesis and growth of primary and metastatic thyroid cancer, and that IL-8 may be an important downstream mediator of NF-κB signaling in advanced thyroid cancer growth and progression. | yes | [
{
"from": "human",
"value": "Question: Is nuclear factor κB-dependent regulation of angiogenesis , and metastasis in an in vivo model of thyroid cancer associated with secreted interleukin-8?\nContext: {'contexts': ['Development of novel strategies in the treatment of advanced thyroid cancer are needed. Our laboratory has previously identified a role for nuclear factor κB (NF-κB) signaling in human thyroid cancer cell growth, survival, and invasion.', 'Our goal was to establish the role of NF-κB signaling on thyroid cancer growth and metastases in vivo and to begin to dissect mechanisms regulating this effect.', 'We examined tumor formation of five thyroid cancer cell lines in an in vivo model of thyroid cancer and observed tumor establishment in two of the cell lines (8505C and BCPAP).', 'Inhibition of NF-κB signaling by overexpression of a dominant-negative IκBα (mIκBα) significantly inhibited thyroid tumor growth in tumors derived from both cell lines. Further studies in an experimental metastasis model demonstrated that NF-κB inhibition impaired growth of tumor metastasis and prolonged mouse survival. Proliferation (mitotic index) was decreased in 8505C tumors, but not in BCPAP tumors, while in vitro angiogenesis and in vivo tumor vascularity were significantly inhibited by mIkBα only in the BCPAP cells. Cytokine antibody array analysis demonstrated that IL-8 secretion was blocked by mIκBα expression. Interestingly, basal NF-κB activity and IL-8 levels were significantly higher in the two tumorigenic cell lines compared with the nontumorigenic lines. Furthermore, IL-8 transcript levels were elevated in high-risk human tumors, suggesting that NF-κB and IL-8 are associated with more aggressive tumor behavior.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Cells, Cultured', 'Gene Expression Regulation, Neoplastic', 'Human Umbilical Vein Endothelial Cells', 'Humans', 'I-kappa B Proteins', 'Interleukin-8', 'Male', 'Mice', 'Mice, Nude', 'NF-KappaB Inhibitor alpha', 'NF-kappa B', 'Neoplasm Metastasis', 'Neoplasm Transplantation', 'Neovascularization, Pathologic', 'Thyroid Neoplasms']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,758,170 | Does fear extinction require Arc/Arg3.1 expression in the basolateral amygdala? | {
"contexts": [
"Prolonged re-exposure to a fear-eliciting cue in the absence of an aversive event extinguishes the fear response to the cue, and has been clinically used as an exposure therapy. Arc (also known as Arg3.1) is implicated in synaptic and experience-dependent plasticity. Arc is regulated by the transcription factor cAMP response element binding protein, which is upregulated with and necessary for fear extinction. Because Arc expression is also activated with fear extinction, we hypothesized that Arc expression is required for fear extinction.",
"Extinction training increased the proportion of Arc-labeled cells in the basolateral amygdala (BLA). Arc was transcribed during latter part of extinction training, which is possibly associated with fear extinction, as well as former part of extinction training. Intra-BLA infusions of Arc antisense oligodeoxynucleotide (ODN) before extinction training impaired long-term but not short-term extinction memory. Intra-BLA infusions of Arc antisense ODN 3 h after extinction training had no effect on fear extinction."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Amygdala",
"Animals",
"Conditioning (Psychology)",
"Cytoskeletal Proteins",
"Early Growth Response Protein 1",
"Extinction, Psychological",
"Fear",
"Male",
"Mice",
"Mice, Inbred C57BL",
"Nerve Tissue Proteins",
"Oligonucleotides, Antisense",
"Protein Biosynthesis",
"Proto-Oncogene Proteins c-fos",
"Time Factors",
"Transcription, Genetic",
"Up-Regulation"
]
} | Our findings demonstrate that Arc is required for long-term extinction of conditioned fear and contribute to the understanding of extinction as a therapeutic manner. | yes | [
{
"from": "human",
"value": "Question: Does fear extinction require Arc/Arg3.1 expression in the basolateral amygdala?\nContext: {'contexts': ['Prolonged re-exposure to a fear-eliciting cue in the absence of an aversive event extinguishes the fear response to the cue, and has been clinically used as an exposure therapy. Arc (also known as Arg3.1) is implicated in synaptic and experience-dependent plasticity. Arc is regulated by the transcription factor cAMP response element binding protein, which is upregulated with and necessary for fear extinction. Because Arc expression is also activated with fear extinction, we hypothesized that Arc expression is required for fear extinction.', 'Extinction training increased the proportion of Arc-labeled cells in the basolateral amygdala (BLA). Arc was transcribed during latter part of extinction training, which is possibly associated with fear extinction, as well as former part of extinction training. Intra-BLA infusions of Arc antisense oligodeoxynucleotide (ODN) before extinction training impaired long-term but not short-term extinction memory. Intra-BLA infusions of Arc antisense ODN 3\\xa0h after extinction training had no effect on fear extinction.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Amygdala', 'Animals', 'Conditioning (Psychology)', 'Cytoskeletal Proteins', 'Early Growth Response Protein 1', 'Extinction, Psychological', 'Fear', 'Male', 'Mice', 'Mice, Inbred C57BL', 'Nerve Tissue Proteins', 'Oligonucleotides, Antisense', 'Protein Biosynthesis', 'Proto-Oncogene Proteins c-fos', 'Time Factors', 'Transcription, Genetic', 'Up-Regulation']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,758,171 | Do mKL1/2 and ELK4 co-regulate distinct serum response factor ( SRF ) transcription programs in macrophages? | {
"contexts": [
"Serum response factor (SRF) is a widely expressed transcription factor involved in multiple regulatory programs. It is believed that SRF can toggle between disparate programs of gene expression through association with different cofactors. However, the direct evidence as to how these factors function on a genome-wide level is still lacking.",
"In the present study, I explored the functions of SRF and its representative cofactors, megakaryoblastic leukemia 1/2 (MKL1/2) and ETS-domain protein 4 (ELK4), during fungal infection challenge in macrophages. The knockdown study, combined with gene expression array analysis, revealed that MKL1/2 regulated SRF-dependent genes were related to actin cytoskeleton organization, while ELK4 regulated SRF-dependent genes were related to external stimulus responses. Subsequent chromatin immunoprecipitation coupled with massively parallel sequencing (ChIP-seq) suggested that many of these regulations were mediated directly in cis."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Animals",
"Binding Sites",
"Cell Line",
"Gene Expression Regulation",
"Gene Knockdown Techniques",
"Macrophages",
"Male",
"Mice",
"Nucleotide Motifs",
"Position-Specific Scoring Matrices",
"Promoter Regions, Genetic",
"Protein Binding",
"Protein Transport",
"Reproducibility of Results",
"Serum Response Factor",
"Trans-Activators",
"Transcription Factors",
"Transcription, Genetic",
"Zymosan",
"ets-Domain Protein Elk-4"
]
} | I conclude that SRF utilizes MKL1/2 to fulfill steady state cellular functions, including cytoskeletal organization, and utilizes ELK4 to facilitate acute responses to external infection. Together, these findings indicate that SRF, along with its two cofactors, are important players in both cellular homeostasis and stress responses in macrophages. | yes | [
{
"from": "human",
"value": "Question: Do mKL1/2 and ELK4 co-regulate distinct serum response factor ( SRF ) transcription programs in macrophages?\nContext: {'contexts': ['Serum response factor (SRF) is a widely expressed transcription factor involved in multiple regulatory programs. It is believed that SRF can toggle between disparate programs of gene expression through association with different cofactors. However, the direct evidence as to how these factors function on a genome-wide level is still lacking.', 'In the present study, I explored the functions of SRF and its representative cofactors, megakaryoblastic leukemia 1/2 (MKL1/2) and ETS-domain protein 4 (ELK4), during fungal infection challenge in macrophages. The knockdown study, combined with gene expression array analysis, revealed that MKL1/2 regulated SRF-dependent genes were related to actin cytoskeleton organization, while ELK4 regulated SRF-dependent genes were related to external stimulus responses. Subsequent chromatin immunoprecipitation coupled with massively parallel sequencing (ChIP-seq) suggested that many of these regulations were mediated directly in cis.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Animals', 'Binding Sites', 'Cell Line', 'Gene Expression Regulation', 'Gene Knockdown Techniques', 'Macrophages', 'Male', 'Mice', 'Nucleotide Motifs', 'Position-Specific Scoring Matrices', 'Promoter Regions, Genetic', 'Protein Binding', 'Protein Transport', 'Reproducibility of Results', 'Serum Response Factor', 'Trans-Activators', 'Transcription Factors', 'Transcription, Genetic', 'Zymosan', 'ets-Domain Protein Elk-4']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,762,979 | Do leishmania aethiopica field isolates bearing an endosymbiontic dsRNA virus induce pro-inflammatory cytokine response? | {
"contexts": [
"Infection with Leishmania parasites causes mainly cutaneous lesions at the site of the sand fly bite. Inflammatory metastatic forms have been reported with Leishmania species such as L. braziliensis, guyanensis and aethiopica. Little is known about the factors underlying such exacerbated clinical presentations. Leishmania RNA virus (LRV) is mainly found within South American Leishmania braziliensis and guyanensis. In a mouse model of L. guyanensis infection, its presence is responsible for an hyper-inflammatory response driven by the recognition of the viral dsRNA genome by the host Toll-like Receptor 3 leading to an exacerbation of the disease. In one instance, LRV was reported outside of South America, namely in the L. major ASKH strain from Turkmenistan, suggesting that LRV appeared before the divergence of Leishmania subgenera. LRV presence inside Leishmania parasites could be one of the factors implicated in disease severity, providing rationale for LRV screening in L. aethiopica.",
"A new LRV member was identified in four L. aethiopica strains (LRV-Lae). Three LRV-Lae genomes were sequenced and compared to L. guyanensis LRV1 and L. major LRV2. LRV-Lae more closely resembled LRV2. Despite their similar genomic organization, a notable difference was observed in the region where the capsid protein and viral polymerase open reading frames overlap, with a unique -1 situation in LRV-Lae. In vitro infection of murine macrophages showed that LRV-Lae induced a TLR3-dependent inflammatory response as previously observed for LRV1."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Animals",
"Cytokines",
"Ethiopia",
"Humans",
"Leishmania",
"Leishmaniasis",
"Mice",
"Molecular Sequence Data",
"RNA Viruses",
"RNA, Viral",
"Sequence Analysis, DNA"
]
} | In this study, we report the presence of an immunogenic dsRNA virus in L. aethiopica human isolates. This is the first observation of LRV in Africa, and together with the unique description of LRV2 in Turkmenistan, it confirmed that LRV was present before the divergence of the L. (Leishmania) and (Viannia) subgenera. The potential implication of LRV-Lae on disease severity due to L. aethiopica infections is discussed. | yes | [
{
"from": "human",
"value": "Question: Do leishmania aethiopica field isolates bearing an endosymbiontic dsRNA virus induce pro-inflammatory cytokine response?\nContext: {'contexts': ['Infection with Leishmania parasites causes mainly cutaneous lesions at the site of the sand fly bite. Inflammatory metastatic forms have been reported with Leishmania species such as L. braziliensis, guyanensis and aethiopica. Little is known about the factors underlying such exacerbated clinical presentations. Leishmania RNA virus (LRV) is mainly found within South American Leishmania braziliensis and guyanensis. In a mouse model of L. guyanensis infection, its presence is responsible for an hyper-inflammatory response driven by the recognition of the viral dsRNA genome by the host Toll-like Receptor 3 leading to an exacerbation of the disease. In one instance, LRV was reported outside of South America, namely in the L. major ASKH strain from Turkmenistan, suggesting that LRV appeared before the divergence of Leishmania subgenera. LRV presence inside Leishmania parasites could be one of the factors implicated in disease severity, providing rationale for LRV screening in L. aethiopica.', 'A new LRV member was identified in four L. aethiopica strains (LRV-Lae). Three LRV-Lae genomes were sequenced and compared to L. guyanensis LRV1 and L. major LRV2. LRV-Lae more closely resembled LRV2. Despite their similar genomic organization, a notable difference was observed in the region where the capsid protein and viral polymerase open reading frames overlap, with a unique -1 situation in LRV-Lae. In vitro infection of murine macrophages showed that LRV-Lae induced a TLR3-dependent inflammatory response as previously observed for LRV1.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Animals', 'Cytokines', 'Ethiopia', 'Humans', 'Leishmania', 'Leishmaniasis', 'Mice', 'Molecular Sequence Data', 'RNA Viruses', 'RNA, Viral', 'Sequence Analysis, DNA']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,768,366 | Does cromolyn ameliorate acute and chronic injury in a rat lung transplant model? | {
"contexts": [
"Mast cells have been associated with obliterative bronchiolitis (OB) in human pulmonary allografts, although their role in the development of OB remains unknown.",
"In this study, we evaluated the role of mast cells in pulmonary allograft rejection using an orthotopic rat pulmonary allograft model that utilizes chronic aspiration of gastric fluid to reliably obtain OB. Pulmonary allograft recipients (n = 35) received chronic aspiration of gastric fluid with (n = 10) and without (n = 16) treatment with a mast cell membrane stabilizer, cromolyn sodium, or chronic aspiration with normal saline (n = 9) as a control.",
"The acute graft injury associated with long ischemic time in the model (6 hours total ischemic time; typical acute graft injury rate ~30%) was apparently blocked by cromolyn, because peri-operative mortality associated with the acute graft injury was not observed in any of the animals receiving cromolyn (p = 0.045). Further, the rats receiving cromolyn developed significantly fewer OB lesions than those treated with gastric fluid alone (p < 0.001), with a mean reduction of 46% of the airways affected."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Acute Lung Injury",
"Allografts",
"Animals",
"Anti-Asthmatic Agents",
"Bronchiolitis Obliterans",
"Chemokines",
"Cromolyn Sodium",
"Cytokines",
"Disease Models, Animal",
"Graft Rejection",
"Lung",
"Lung Injury",
"Lung Transplantation",
"Male",
"Mast Cells",
"Postoperative Complications",
"Rats",
"Rats, Inbred WKY"
]
} | These findings provide impetus for further studies aimed at elucidating the effects of cromolyn and the role of mast cells in pulmonary allotransplantation. | yes | [
{
"from": "human",
"value": "Question: Does cromolyn ameliorate acute and chronic injury in a rat lung transplant model?\nContext: {'contexts': ['Mast cells have been associated with obliterative bronchiolitis (OB) in human pulmonary allografts, although their role in the development of OB remains unknown.', 'In this study, we evaluated the role of mast cells in pulmonary allograft rejection using an orthotopic rat pulmonary allograft model that utilizes chronic aspiration of gastric fluid to reliably obtain OB. Pulmonary allograft recipients (n = 35) received chronic aspiration of gastric fluid with (n = 10) and without (n = 16) treatment with a mast cell membrane stabilizer, cromolyn sodium, or chronic aspiration with normal saline (n = 9) as a control.', 'The acute graft injury associated with long ischemic time in the model (6 hours total ischemic time; typical acute graft injury rate ~30%) was apparently blocked by cromolyn, because peri-operative mortality associated with the acute graft injury was not observed in any of the animals receiving cromolyn (p = 0.045). Further, the rats receiving cromolyn developed significantly fewer OB lesions than those treated with gastric fluid alone (p < 0.001), with a mean reduction of 46% of the airways affected.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Acute Lung Injury', 'Allografts', 'Animals', 'Anti-Asthmatic Agents', 'Bronchiolitis Obliterans', 'Chemokines', 'Cromolyn Sodium', 'Cytokines', 'Disease Models, Animal', 'Graft Rejection', 'Lung', 'Lung Injury', 'Lung Transplantation', 'Male', 'Mast Cells', 'Postoperative Complications', 'Rats', 'Rats, Inbred WKY']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,755,044 | Is the phenotypic predisposition of the parent in F1 hybrid correlated with transcriptome preference of the positive general combining ability parent? | {
"contexts": [
"Sprague and Tatum (1942) introduced the concepts of general combining ability (GCA) and specific combining ability (SCA) to evaluate the breeding parents and F1 hybrid performance, respectively. Since then, the GCA was widely used in cross breeding for elite parent selection. However, the molecular basis of GCA remains to unknown.",
"We studied the transcriptomes of three varieties and three F1 hybrids using RNA-Sequencing. Transcriptome sequence analysis revealed that the transcriptome profiles of the F1s were similar to the positive GCA-effect parent. Moreover, the expression levels of most differentially expressed genes (DEGs) were equal to the parent with a positive GCA effect. Analysis of the gene expression patterns of gibberellic acid (GA) and flowering time pathways that determine plant height and flowering time in rice validated the preferential transcriptome expression of the parents with positive GCA effect. Furthermore, H3K36me3 modification bias in the Pseudo-Response Regulators (PRR) gene family was observed in the positive GCA effect parents and demonstrated that the phenotype and transcriptome bias in the positive GCA effect parents have been epigenetically regulated by either global modification or specific signaling pathways in rice."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Epigenesis, Genetic",
"Flowers",
"Gene Expression Profiling",
"Gene Expression Regulation, Plant",
"Genotype",
"Histones",
"Hybridization, Genetic",
"Metabolic Networks and Pathways",
"Oryza",
"Phenotype",
"Quantitative Trait, Heritable",
"Signal Transduction",
"Transcriptome"
]
} | The results revealed that the transcriptome profiles and DEGs in the F1s were highly related to phenotype bias to the positive GCA-effect parent. The transcriptome bias toward high GCA parents in F1 hybrids attributed to H3K36me3 modification both on global modification level and specific signaling pathways. Our results indicated the transcriptome profile and epigenetic modification level bias to high GCA parents could be the molecular basis of GCA. | yes | [
{
"from": "human",
"value": "Question: Is the phenotypic predisposition of the parent in F1 hybrid correlated with transcriptome preference of the positive general combining ability parent?\nContext: {'contexts': ['Sprague and Tatum (1942) introduced the concepts of general combining ability (GCA) and specific combining ability (SCA) to evaluate the breeding parents and F1 hybrid performance, respectively. Since then, the GCA was widely used in cross breeding for elite parent selection. However, the molecular basis of GCA remains to unknown.', 'We studied the transcriptomes of three varieties and three\\xa0F1 hybrids using RNA-Sequencing. Transcriptome sequence analysis revealed that the transcriptome profiles of the F1s were similar to the positive GCA-effect parent. Moreover, the expression levels of most differentially expressed genes (DEGs) were equal to the parent with a positive GCA effect. Analysis of the gene expression patterns of gibberellic acid (GA) and flowering time pathways that determine plant height and flowering time in rice validated the preferential transcriptome expression of the parents with positive GCA effect. Furthermore, H3K36me3 modification bias in the Pseudo-Response Regulators (PRR) gene family was observed in the positive GCA effect parents and demonstrated that the phenotype and transcriptome bias in the positive GCA effect parents have been epigenetically regulated by either global modification or specific signaling pathways in rice.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Epigenesis, Genetic', 'Flowers', 'Gene Expression Profiling', 'Gene Expression Regulation, Plant', 'Genotype', 'Histones', 'Hybridization, Genetic', 'Metabolic Networks and Pathways', 'Oryza', 'Phenotype', 'Quantitative Trait, Heritable', 'Signal Transduction', 'Transcriptome']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,768,004 | Does after adjusting for bias in meta-analysis seasonal influenza vaccine remain effective in community-dwelling elderly? | {
"contexts": [
"To compare the performance of the bias-adjusted meta-analysis to the conventional meta-analysis assessing seasonal influenza vaccine effectiveness among community-dwelling elderly aged 60 years and older.",
"Systematic literature search revealed 14 cohort studies that met inclusion and exclusion criteria. Laboratory-confirmed influenza, influenza-like illness, hospitalization from influenza and/or pneumonia, and all-cause mortality were study outcomes. Potential biases were identified using bias checklists. The magnitude and uncertainty of biases were assessed by expert opinion. Pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated using random effects model.",
"After incorporating biases, overall effect estimates regressed slightly toward no effect, with the largest relative difference between conventional and bias-adjusted ORs for laboratory-confirmed influenza (OR, 0.18; 95% CI: 0.01, 3.00 vs. OR, 0.23; 95% CI: 0.03, 2.04). In most of the studies, CIs widened reflecting uncertainties about the biases. The between-study heterogeneity reduced considerably with the largest reduction for all-cause mortality (I(2) = 4%, P = 0.39 vs. I(2) = 91%, P < 0.01)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": []
} | This case study showed that after addressing potential biases influenza vaccine was still estimated effective in preventing hospitalization from influenza and/or pneumonia and all-cause mortality. Increasing the number of assessors and incorporating empirical evidence might improve the new bias-adjustment method. | yes | [
{
"from": "human",
"value": "Question: Does after adjusting for bias in meta-analysis seasonal influenza vaccine remain effective in community-dwelling elderly?\nContext: {'contexts': ['To compare the performance of the bias-adjusted meta-analysis to the conventional meta-analysis assessing seasonal influenza vaccine effectiveness among community-dwelling elderly aged 60 years and older.', 'Systematic literature search revealed 14 cohort studies that met inclusion and exclusion criteria. Laboratory-confirmed influenza, influenza-like illness, hospitalization from influenza and/or pneumonia, and all-cause mortality were study outcomes. Potential biases were identified using bias checklists. The magnitude and uncertainty of biases were assessed by expert opinion. Pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated using random effects model.', 'After incorporating biases, overall effect estimates regressed slightly toward no effect, with the largest relative difference between conventional and bias-adjusted ORs for laboratory-confirmed influenza (OR, 0.18; 95% CI: 0.01, 3.00 vs. OR, 0.23; 95% CI: 0.03, 2.04). In most of the studies, CIs widened reflecting uncertainties about the biases. The between-study heterogeneity reduced considerably with the largest reduction for all-cause mortality (I(2) = 4%, P = 0.39 vs. I(2) = 91%, P < 0.01).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,753,183 | Do neuropsychological function before and after subcallosal cingulate deep brain stimulation in patients with treatment-resistant depression? | {
"contexts": [
"Treatment-resistant depression (TRD) is a pervasive and difficult to treat condition for which deep brain stimulation (DBS) of the subcallosal cingulate white matter (SCCwm) is an emerging therapeutic option. However, neuropsychological safety data for this novel treatment have only been published for a small number of subjects. Moreover, little is known regarding the neuropsychological profile present in TRD patients at baseline, prior to initiation of DBS therapy. This report describes the neuropsychological effects of TRD and acute and chronic DBS of the SCCwm in patients with unipolar and bipolar TRD.",
"Patients with TRD (N = 17) were compared to a healthy control group (N = 15) on subtests from the Cambridge Neuropsychological Test Automated Battery and the Stroop Task. Patients were then tested again at subsequent time points of 1 and 6 months following the initiation of chronic DBS of the SCCwm.",
"Patients with TRD showed similar levels of performance to healthy controls on most neuropsychological measures, with the exception that the TRD group had slower processing speed. Patients with bipolar TRD, relative to those with unipolar TRD, obtained lower scores on measures of executive function and memory only at baseline. With acute and chronic SCCwm DBS, neuropsychological function improved in multiple domains including processing speed and executive function (planning, set shifting, response inhibition), and memory remained stable."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Corpus Callosum",
"Deep Brain Stimulation",
"Depressive Disorder, Treatment-Resistant",
"Executive Function",
"Female",
"Gyrus Cinguli",
"Humans",
"Male",
"Middle Aged",
"Neuropsychological Tests",
"Treatment Outcome"
]
} | Patients with TRD show slowed processing speed but otherwise largely preserved neuropsychological functioning. DBS of the SCCwm does not result in worsening of any aspect of neuropsychological function and may improve certain domains. Future research is warranted to better understand the effects of TRD and DBS on neuropsychological function. | yes | [
{
"from": "human",
"value": "Question: Do neuropsychological function before and after subcallosal cingulate deep brain stimulation in patients with treatment-resistant depression?\nContext: {'contexts': ['Treatment-resistant depression (TRD) is a pervasive and difficult to treat condition for which deep brain stimulation (DBS) of the subcallosal cingulate white matter (SCCwm) is an emerging therapeutic option. However, neuropsychological safety data for this novel treatment have only been published for a small number of subjects. Moreover, little is known regarding the neuropsychological profile present in TRD patients at baseline, prior to initiation of DBS therapy. This report describes the neuropsychological effects of TRD and acute and chronic DBS of the SCCwm in patients with unipolar and bipolar TRD.', 'Patients with TRD (N = 17) were compared to a healthy control group (N = 15) on subtests from the Cambridge Neuropsychological Test Automated Battery and the Stroop Task. Patients were then tested again at subsequent time points of 1 and 6 months following the initiation of chronic DBS of the SCCwm.', 'Patients with TRD showed similar levels of performance to healthy controls on most neuropsychological measures, with the exception that the TRD group had slower processing speed. Patients with bipolar TRD, relative to those with unipolar TRD, obtained lower scores on measures of executive function and memory only at baseline. With acute and chronic SCCwm DBS, neuropsychological function improved in multiple domains including processing speed and executive function (planning, set shifting, response inhibition), and memory remained stable.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Corpus Callosum', 'Deep Brain Stimulation', 'Depressive Disorder, Treatment-Resistant', 'Executive Function', 'Female', 'Gyrus Cinguli', 'Humans', 'Male', 'Middle Aged', 'Neuropsychological Tests', 'Treatment Outcome']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,755,282 | Does toll-like receptor 4 signaling contribute to Paclitaxel-induced peripheral neuropathy? | {
"contexts": [
"This paper tests the contribution of the toll-like receptors, TLR4 in particular, in the initiation and maintenance of paclitaxel-related chemotherapy-induced peripheral neuropathy. TLR4 and its immediate downstream signaling molecules-myeloid differentiation primary response gene 88 (MyD88) and toll/interleukin 1 receptor domain-containing adapter-inducing interferon-β (TRIF)-were found to be increased in the dorsal root ganglion (DRG) using Western blot by day 7 of paclitaxel treatment. The behavioral phenotype, the increase of both TLR4 and MyD88, was blocked by cotreatment with the TLR4 antagonist lipopolysaccharide-Rhodobacter sphaeroides during chemotherapy. A similar, but less robust, behavioral effect was observed using intrathecal treatment of MyD88 homodimerization inhibitory peptide. DRG levels of TLR4 and MyD88 reduced over the next 2 weeks, whereas these levels remained increased in spinal cord through day 21 following chemotherapy. Immunohistochemical analysis revealed TLR4 expression in both calcitonin gene-related peptide-positive and isolectin B4-positive small DRG neurons. MyD88 was only found in calcitonin gene-related peptide-positive neurons, and TRIF was found in both calcitonin gene-related peptide-positive and isolectin B4-positive small DRG neurons as well as in medium- and large-size DRG neurons. In the spinal cord, TLR4 was only found colocalized to astrocytes but not with either microglia or neurons. Intrathecal treatment with the TLR4 antagonist lipopolysaccharide-R. sphaeroides transiently reversed preestablished chemotherapy-induced peripheral neuropathy mechanical hypersensitivity. These results strongly implicate TLR4 signaling in the DRG and the spinal cord in the induction and maintenance of paclitaxel-related chemotherapy-induced peripheral neuropathy."
],
"labels": [
"UNLABELLED"
],
"meshes": [
"Animals",
"Antineoplastic Agents, Phytogenic",
"Astrocytes",
"Disease Models, Animal",
"Ganglia, Spinal",
"Gene Expression Regulation",
"Male",
"Myeloid Differentiation Factor 88",
"Nerve Tissue Proteins",
"Neurons",
"Paclitaxel",
"Pain Threshold",
"Peripheral Nervous System Diseases",
"Physical Stimulation",
"Polysaccharides",
"Rats",
"Rats, Sprague-Dawley",
"Signal Transduction",
"Time Factors",
"Toll-Like Receptor 4"
]
} | The toll-like receptor TLR4 and MyD88 signaling pathway could be a new potential therapeutic target in paclitaxel-induced painful neuropathy. | yes | [
{
"from": "human",
"value": "Question: Does toll-like receptor 4 signaling contribute to Paclitaxel-induced peripheral neuropathy?\nContext: {'contexts': ['This paper tests the contribution of the toll-like receptors, TLR4 in particular, in the initiation and maintenance of paclitaxel-related chemotherapy-induced peripheral neuropathy. TLR4 and its immediate downstream signaling molecules-myeloid differentiation primary response gene 88 (MyD88) and toll/interleukin 1 receptor domain-containing adapter-inducing interferon-β (TRIF)-were found to be increased in the dorsal root ganglion (DRG) using Western blot by day 7 of paclitaxel treatment. The behavioral phenotype, the increase of both TLR4 and MyD88, was blocked by cotreatment with the TLR4 antagonist lipopolysaccharide-Rhodobacter sphaeroides during chemotherapy. A similar, but less robust, behavioral effect was observed using intrathecal treatment of MyD88 homodimerization inhibitory peptide. DRG levels of TLR4 and MyD88 reduced over the next 2 weeks, whereas these levels remained increased in spinal cord through day 21 following chemotherapy. Immunohistochemical analysis revealed TLR4 expression in both calcitonin gene-related peptide-positive and isolectin B4-positive small DRG neurons. MyD88 was only found in calcitonin gene-related peptide-positive neurons, and TRIF was found in both calcitonin gene-related peptide-positive and isolectin B4-positive small DRG neurons as well as in medium- and large-size DRG neurons. In the spinal cord, TLR4 was only found colocalized to astrocytes but not with either microglia or neurons. Intrathecal treatment with the TLR4 antagonist lipopolysaccharide-R. sphaeroides transiently reversed preestablished chemotherapy-induced peripheral neuropathy mechanical hypersensitivity. These results strongly implicate TLR4 signaling in the DRG and the spinal cord in the induction and maintenance of paclitaxel-related chemotherapy-induced peripheral neuropathy.'], 'labels': ['UNLABELLED'], 'meshes': ['Animals', 'Antineoplastic Agents, Phytogenic', 'Astrocytes', 'Disease Models, Animal', 'Ganglia, Spinal', 'Gene Expression Regulation', 'Male', 'Myeloid Differentiation Factor 88', 'Nerve Tissue Proteins', 'Neurons', 'Paclitaxel', 'Pain Threshold', 'Peripheral Nervous System Diseases', 'Physical Stimulation', 'Polysaccharides', 'Rats', 'Rats, Sprague-Dawley', 'Signal Transduction', 'Time Factors', 'Toll-Like Receptor 4']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,750,552 | Does vSL # 3 probiotic treatment decrease bacterial translocation in rats with carbon tetrachloride-induced cirrhosis? | {
"contexts": [
"Probiotics can prevent pathological bacterial translocation in cirrhosis by modulating intestinal microbiota and improving gut barrier and immune disturbances. To evaluate the effect of probiotic VSL#3 on bacterial translocation, intestinal microbiota, gut barrier and inflammatory response in rats with experimental cirrhosis.",
"Forty-six Sprague-Dawley rats with CCl4 -induced cirrhosis were randomized into two groups: VSL#3 group (n = 22) that received VSL#3 in drinking water, and water group (n = 24) that received water only. Treatment began at week 6 of cirrhosis induction and continued until laparotomy, performed 1 week after development of ascites or at week 20. A control group included 11 healthy rats. At this study end, we evaluated bacterial translocation, intestinal flora, intestinal barrier (ileal claudin-2 and 4, β-defensin-1, occludin and malondialdehyde as index of oxidative damage) and serum cytokines.",
"Mortality during this study was similar in the VSL#3 group (10/22, 45%) and the water group (10/24, 42%) (P = 1). The incidence of bacterial translocation was 1/12 (8%) in the VSL#3 group, 7/14 (50%) in the water group (P = 0.03 vs. VSL#3 group) and 0/11 in the control group (P = 0.008 vs. water group). The concentration of ileal and caecal enterobacteria and enterococci was similar in the two groups of cirrhotic rats. The ileal occludin concentration was higher and ileal malondialdehyde and serum levels of TNF-α were lower in the VSL#3 group than in the water group (P < 0.05)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Ascites",
"Bacterial Translocation",
"Carbon Tetrachloride",
"Disease Models, Animal",
"Intestinal Mucosa",
"Laparotomy",
"Liver Cirrhosis, Experimental",
"Male",
"Malondialdehyde",
"Probiotics",
"Rats",
"Rats, Sprague-Dawley",
"Renin",
"Tumor Necrosis Factor-alpha"
]
} | VSL#3 decreases bacterial translocation, the pro-inflammatory state and ileal oxidative damage and increases ileal occludin expression in rats with experimental cirrhosis. | yes | [
{
"from": "human",
"value": "Question: Does vSL # 3 probiotic treatment decrease bacterial translocation in rats with carbon tetrachloride-induced cirrhosis?\nContext: {'contexts': ['Probiotics can prevent pathological bacterial translocation in cirrhosis by modulating intestinal microbiota and improving gut barrier and immune disturbances. To evaluate the effect of probiotic VSL#3 on bacterial translocation, intestinal microbiota, gut barrier and inflammatory response in rats with experimental cirrhosis.', 'Forty-six Sprague-Dawley rats with CCl4 -induced cirrhosis were randomized into two groups: VSL#3 group (n = 22) that received VSL#3 in drinking water, and water group (n = 24) that received water only. Treatment began at week 6 of cirrhosis induction and continued until laparotomy, performed 1 week after development of ascites or at week 20. A control group included 11 healthy rats. At this study end, we evaluated bacterial translocation, intestinal flora, intestinal barrier (ileal claudin-2 and 4, β-defensin-1, occludin and malondialdehyde as index of oxidative damage) and serum cytokines.', 'Mortality during this study was similar in the VSL#3 group (10/22, 45%) and the water group (10/24, 42%) (P = 1). The incidence of bacterial translocation was 1/12 (8%) in the VSL#3 group, 7/14 (50%) in the water group (P = 0.03 vs. VSL#3 group) and 0/11 in the control group (P = 0.008 vs. water group). The concentration of ileal and caecal enterobacteria and enterococci was similar in the two groups of cirrhotic rats. The ileal occludin concentration was higher and ileal malondialdehyde and serum levels of TNF-α were lower in the VSL#3 group than in the water group (P < 0.05).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Ascites', 'Bacterial Translocation', 'Carbon Tetrachloride', 'Disease Models, Animal', 'Intestinal Mucosa', 'Laparotomy', 'Liver Cirrhosis, Experimental', 'Male', 'Malondialdehyde', 'Probiotics', 'Rats', 'Rats, Sprague-Dawley', 'Renin', 'Tumor Necrosis Factor-alpha']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,748,417 | Does addition of aprepitant improve protection against cisplatin-induced emesis when a conventional anti-emetic regimen fails? | {
"contexts": [
"We investigated whether aprepitant, a neurokinin-1 antagonist, could decrease chemotherapy-induced nausea and vomiting (CINV) following cisplatin, when a conventional anti-emetic regimen had failed.",
"This was a prospective study (April 2011-April 2012) of patients with lung cancer, treated with cisplatin at the Beijing Cancer Hospital, and initially receiving granisetron, dexamethasone, and metoclopramide as anti-emetics. If patients experienced vomiting of grade ≥2 and required rescue anti-emetic medications during the first cycle, oral aprepitant was added in subsequent cycles (day 1: 125 mg; days 2-3: 80 mg once daily). Acute (day 1) and delayed (days 2-5) nausea and vomiting, use of rescue medications, and occurrence of adverse reactions were monitored after the start of chemotherapy.",
"Twenty-five of 132 patients (18.9 %) were administered aprepitant for secondary prophylaxis against emesis during the second cycle of chemotherapy. The incidences of acute and delayed nausea were 52 and 100 % in the first cycle, but 8 and 72 % in the second cycle. The incidences of acute and delayed vomiting were 20 and 100 % in the first cycle, but 0 and 36 % in the second cycle. No patients required rescue medications or intravenous rehydration during the second cycle. Aprepitant was not associated with additional adverse events."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Antiemetics",
"Antineoplastic Combined Chemotherapy Protocols",
"Aprepitant",
"Cisplatin",
"Female",
"Humans",
"Lung Neoplasms",
"Male",
"Middle Aged",
"Morpholines",
"Nausea",
"Prospective Studies",
"Treatment Outcome"
]
} | In patients with lung cancer receiving cisplatin-based chemotherapy, the addition of aprepitant to a 5-HT3 antagonist, dexamethasone, and metoclopramide improves protection against CINV when the conventional anti-emetic regimen fails. | yes | [
{
"from": "human",
"value": "Question: Does addition of aprepitant improve protection against cisplatin-induced emesis when a conventional anti-emetic regimen fails?\nContext: {'contexts': ['We investigated whether aprepitant, a neurokinin-1 antagonist, could decrease chemotherapy-induced nausea and vomiting (CINV) following cisplatin, when a conventional anti-emetic regimen had failed.', 'This was a prospective study (April 2011-April 2012) of patients with lung cancer, treated with cisplatin at the Beijing Cancer Hospital, and initially receiving granisetron, dexamethasone, and metoclopramide as anti-emetics. If patients experienced vomiting of grade ≥2 and required rescue anti-emetic medications during the first cycle, oral aprepitant was added in subsequent cycles (day 1: 125 mg; days 2-3: 80 mg once daily). Acute (day 1) and delayed (days 2-5) nausea and vomiting, use of rescue medications, and occurrence of adverse reactions were monitored after the start of chemotherapy.', 'Twenty-five of 132 patients (18.9 %) were administered aprepitant for secondary prophylaxis against emesis during the second cycle of chemotherapy. The incidences of acute and delayed nausea were 52 and 100 % in the first cycle, but 8 and 72 % in the second cycle. The incidences of acute and delayed vomiting were 20 and 100 % in the first cycle, but 0 and 36 % in the second cycle. No patients required rescue medications or intravenous rehydration during the second cycle. Aprepitant was not associated with additional adverse events.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Antiemetics', 'Antineoplastic Combined Chemotherapy Protocols', 'Aprepitant', 'Cisplatin', 'Female', 'Humans', 'Lung Neoplasms', 'Male', 'Middle Aged', 'Morpholines', 'Nausea', 'Prospective Studies', 'Treatment Outcome']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,755,675 | Does the secretome of endothelial progenitor cells promote brain endothelial cell activity through PI3-kinase and MAP-kinase? | {
"contexts": [
"Angiogenesis and vascular remodelling are crucial events in tissue repair mechanisms promoted by cell transplantation. Current evidence underscores the importance of the soluble factors secreted by stem cells in tissue regeneration. In the present study we investigated the effects of paracrine factors derived from cultured endothelial progenitor cells (EPC) on rat brain endothelial cell properties and addressed the signaling pathways involved.",
"Endothelial cells derived from rat brain (rBCEC4) were incubated with EPC-derived conditioned medium (EPC-CM). The angiogenic response of rBCEC4 to EPC-CM was assessed as effect on cell number, migration and tubular network formation. In addition, we have compared the outcome of the in vitro experiments with the effects on capillary sprouting from rat aortic rings. The specific PI3K/AKT inhibitor LY294002 and the MEK/ERK inhibitor PD98059 were used to study the involvement of these two signaling pathways in the transduction of the angiogenic effects of EPC-CM.",
"Viable cell number, migration and tubule network formation were significantly augmented upon incubation with EPC-CM. Similar findings were observed for aortic ring outgrowth with significantly longer sprouts. The EPC-CM-induced activities were significantly reduced by the blockage of the PI3K/AKT and MEK/ERK signaling pathways. Similarly to the outcome of the rBCEC4 experiments, inhibition of the PI3K/AKT and MEK/ERK pathways significantly interfered with capillary sprouting induced by EPC-CM."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Angiogenesis Inducing Agents",
"Animals",
"Brain",
"Cell Line",
"Cell Survival",
"Cells, Cultured",
"Culture Media, Conditioned",
"Cytokines",
"Endothelial Cells",
"Endothelial Progenitor Cells",
"Enzyme Activation",
"Microvessels",
"Mitogen-Activated Protein Kinases",
"Neovascularization, Physiologic",
"Phosphatidylinositol 3-Kinase",
"Proto-Oncogene Proteins c-akt",
"Rats",
"Signal Transduction",
"Wound Healing"
]
} | The present study demonstrates that EPC-derived paracrine factors substantially promote the angiogenic response of brain microvascular endothelial cells. In addition, our findings identified the PI3K/AKT and MEK/ERK pathways to play a central role in mediating these effects. | yes | [
{
"from": "human",
"value": "Question: Does the secretome of endothelial progenitor cells promote brain endothelial cell activity through PI3-kinase and MAP-kinase?\nContext: {'contexts': ['Angiogenesis and vascular remodelling are crucial events in tissue repair mechanisms promoted by cell transplantation. Current evidence underscores the importance of the soluble factors secreted by stem cells in tissue regeneration. In the present study we investigated the effects of paracrine factors derived from cultured endothelial progenitor cells (EPC) on rat brain endothelial cell properties and addressed the signaling pathways involved.', 'Endothelial cells derived from rat brain (rBCEC4) were incubated with EPC-derived conditioned medium (EPC-CM). The angiogenic response of rBCEC4 to EPC-CM was assessed as effect on cell number, migration and tubular network formation. In addition, we have compared the outcome of the in vitro experiments with the effects on capillary sprouting from rat aortic rings. The specific PI3K/AKT inhibitor LY294002 and the MEK/ERK inhibitor PD98059 were used to study the involvement of these two signaling pathways in the transduction of the angiogenic effects of EPC-CM.', 'Viable cell number, migration and tubule network formation were significantly augmented upon incubation with EPC-CM. Similar findings were observed for aortic ring outgrowth with significantly longer sprouts. The EPC-CM-induced activities were significantly reduced by the blockage of the PI3K/AKT and MEK/ERK signaling pathways. Similarly to the outcome of the rBCEC4 experiments, inhibition of the PI3K/AKT and MEK/ERK pathways significantly interfered with capillary sprouting induced by EPC-CM.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Angiogenesis Inducing Agents', 'Animals', 'Brain', 'Cell Line', 'Cell Survival', 'Cells, Cultured', 'Culture Media, Conditioned', 'Cytokines', 'Endothelial Cells', 'Endothelial Progenitor Cells', 'Enzyme Activation', 'Microvessels', 'Mitogen-Activated Protein Kinases', 'Neovascularization, Physiologic', 'Phosphatidylinositol 3-Kinase', 'Proto-Oncogene Proteins c-akt', 'Rats', 'Signal Transduction', 'Wound Healing']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,759,089 | Does autocrine VEGF/VEGFR1 signaling in a subpopulation of cells associate with aggressive osteosarcoma? | {
"contexts": [
"Osteosarcoma is the most common primary bone malignancy and accounts for more than half of primary skeletal malignancies in children and young adults. Although vascular endothelial growth factor (VEGF) expression in osteosarcoma has been associated with poor outcome, its role in the pathogenesis of osteosarcoma remains controversial. Here, VEGF and VEGFR1 expression in both human and murine osteosarcoma cells associated with increasing malignant potential. Autocrine VEGF/VEGFR1 signaling resulted in constitutive activation of VEGFR1 in highly aggressive osteosarcoma cells. In addition, survival and proliferation of highly aggressive osteosarcoma cells was dependent on autocrine VEGF/R1 signaling in vitro. The effect of VEGFR1 expression on in vivo tumor growth and angiogenesis was evaluated by immunoselecting subpopulations of osteosarcoma cells that express high or low levels of VEGFR1. Cell enriched for high VEGFR1 expression showed increased VEGF production, tumor growth, tumor angiogenesis, and osteolysis in vivo. In addition, it was demonstrated that VEGF and VEGFR1 are coexpressed by a subset of tumor cells in human osteosarcoma, similar to what was observed in the murine osteosarcoma cells. These results suggest that autocrine VEGF/VEGFR1 signaling in a subpopulation of tumor cells plays a pivotal role in osteosarcoma progression."
],
"labels": [
"UNLABELLED"
],
"meshes": [
"Animals",
"Autocrine Communication",
"Bone Neoplasms",
"Cell Line, Tumor",
"Cell Proliferation",
"Humans",
"Mice",
"Mice, Inbred BALB C",
"Neovascularization, Pathologic",
"Osteolysis",
"Osteosarcoma",
"Signal Transduction",
"Vascular Endothelial Growth Factor A",
"Vascular Endothelial Growth Factor Receptor-1"
]
} | Aggressive osteosarcoma phenotypes are mediated by autocrine VEGF/VEGFR1 signaling and improved stratification measures and novel anti-angiogenic strategies may benefit this specific tumor type. | yes | [
{
"from": "human",
"value": "Question: Does autocrine VEGF/VEGFR1 signaling in a subpopulation of cells associate with aggressive osteosarcoma?\nContext: {'contexts': ['Osteosarcoma is the most common primary bone malignancy and accounts for more than half of primary skeletal malignancies in children and young adults. Although vascular endothelial growth factor (VEGF) expression in osteosarcoma has been associated with poor outcome, its role in the pathogenesis of osteosarcoma remains controversial. Here, VEGF and VEGFR1 expression in both human and murine osteosarcoma cells associated with increasing malignant potential. Autocrine VEGF/VEGFR1 signaling resulted in constitutive activation of VEGFR1 in highly aggressive osteosarcoma cells. In addition, survival and proliferation of highly aggressive osteosarcoma cells was dependent on autocrine VEGF/R1 signaling in vitro. The effect of VEGFR1 expression on in vivo tumor growth and angiogenesis was evaluated by immunoselecting subpopulations of osteosarcoma cells that express high or low levels of VEGFR1. Cell enriched for high VEGFR1 expression showed increased VEGF production, tumor growth, tumor angiogenesis, and osteolysis in vivo. In addition, it was demonstrated that VEGF and VEGFR1 are coexpressed by a subset of tumor cells in human osteosarcoma, similar to what was observed in the murine osteosarcoma cells. These results suggest that autocrine VEGF/VEGFR1 signaling in a subpopulation of tumor cells plays a pivotal role in osteosarcoma progression.'], 'labels': ['UNLABELLED'], 'meshes': ['Animals', 'Autocrine Communication', 'Bone Neoplasms', 'Cell Line, Tumor', 'Cell Proliferation', 'Humans', 'Mice', 'Mice, Inbred BALB C', 'Neovascularization, Pathologic', 'Osteolysis', 'Osteosarcoma', 'Signal Transduction', 'Vascular Endothelial Growth Factor A', 'Vascular Endothelial Growth Factor Receptor-1']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,756,974 | Is increased urine semaphorin-3A associated with renal damage in hypertensive patients with chronic kidney disease : a nested case-control study? | {
"contexts": [
"Semaphorins are guidance proteins implicated in several processes such as angiogenesis, organogenesis, cell migration, and cytokine release. Experimental studies showed that semaphorin-3a (SEMA3A) administration induces transient massive proteinuria, podocyte foot process effacement and endothelial cell damage in healthy animals. While SEMA3A signaling has been demonstrated to be mechanistically involved in experimental diabetic glomerulopathy and in acute kidney injury, to date its role in human chronic kidney disease (CKD) has not been investigated.",
"To test the hypothesis that SEMA3A may play a role in human CKD, we performed a cross-sectional, nested, case-control study on 151 matched hypertensive patients with and without CKD. SEMA3A was quantified in the urine (USEMA) by ELISA. Glomerular filtration rate was estimated (eGFR) by the CKD-EPI formula and albuminuria was measured as albumin-to-creatinine ratio (ACR).",
"USEMA levels were positively correlated with urine ACR (p = 0.001) and serum creatinine (p < 0.001). USEMA was higher in patients with both components of renal damage as compared to those with only one and those with normal renal function (p < 0.007 and <0.001, respectively). The presence of increased USEMA levels (i.e. top quartile) entailed a fourfold higher risk of combined renal damage (p < 0.001) and an almost twofold higher risk of macroalbuminuria (p = 0.005) or of reduced eGFR, even adjusting for confounding factors (p = 0.002)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Albuminuria",
"Biomarkers",
"Case-Control Studies",
"Cross-Sectional Studies",
"Diabetic Nephropathies",
"Enzyme-Linked Immunosorbent Assay",
"Female",
"Glomerular Filtration Rate",
"Humans",
"Hypertension",
"Kidney",
"Male",
"Middle Aged",
"Predictive Value of Tests",
"Renal Insufficiency, Chronic",
"Risk Factors",
"Semaphorin-3A",
"Up-Regulation",
"Urinalysis"
]
} | USEMA is independently associated with CKD in both diabetic and non diabetic hypertensive patients. Further studies may help clarify the mechanisms underlying this association and possibly the pathogenic changes leading to the development of CKD. | yes | [
{
"from": "human",
"value": "Question: Is increased urine semaphorin-3A associated with renal damage in hypertensive patients with chronic kidney disease : a nested case-control study?\nContext: {'contexts': ['Semaphorins are guidance proteins implicated in several processes such as angiogenesis, organogenesis, cell migration, and cytokine release. Experimental studies showed that semaphorin-3a (SEMA3A) administration induces transient massive proteinuria, podocyte foot process effacement and endothelial cell damage in healthy animals. While SEMA3A signaling has been demonstrated to be mechanistically involved in experimental diabetic glomerulopathy and in acute kidney injury, to date its role in human chronic kidney disease (CKD) has not been investigated.', 'To test the hypothesis that SEMA3A may play a role in human CKD, we performed a cross-sectional, nested, case-control study on 151 matched hypertensive patients with and without CKD. SEMA3A was quantified in the urine (USEMA) by ELISA. Glomerular filtration rate was estimated (eGFR) by the CKD-EPI formula and albuminuria was measured as albumin-to-creatinine ratio (ACR).', 'USEMA levels were positively correlated with urine ACR (p = 0.001) and serum creatinine (p < 0.001). USEMA was higher in patients with both components of renal damage as compared to those with only one and those with normal renal function (p < 0.007 and <0.001, respectively). The presence of increased USEMA levels (i.e. top quartile) entailed a fourfold higher risk of combined renal damage (p < 0.001) and an almost twofold higher risk of macroalbuminuria (p = 0.005) or of reduced eGFR, even adjusting for confounding factors (p = 0.002).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Albuminuria', 'Biomarkers', 'Case-Control Studies', 'Cross-Sectional Studies', 'Diabetic Nephropathies', 'Enzyme-Linked Immunosorbent Assay', 'Female', 'Glomerular Filtration Rate', 'Humans', 'Hypertension', 'Kidney', 'Male', 'Middle Aged', 'Predictive Value of Tests', 'Renal Insufficiency, Chronic', 'Risk Factors', 'Semaphorin-3A', 'Up-Regulation', 'Urinalysis']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,763,279 | Do dietary flavanols modulate the transcription of genes associated with cardiovascular pathology without changes in their DNA methylation state? | {
"contexts": [
"In a recent intervention study, the daily supplementation with 200 mg monomeric and oligomeric flavanols (MOF) from grape seeds for 8 weeks revealed a vascular health benefit in male smokers. The objective of the present study was to determine the impact of MOF consumption on the gene expression profile of leukocytes and to assess changes in DNA methylation.",
"Gene expression profiles were determined using whole genome microarrays (Agilent) and DNA methylation was assessed using HumanMethylation450 BeadChips (Illumina). MOF significantly modulated the expression of 864 genes. The majority of the affected genes are involved in chemotaxis, cell adhesion, cell infiltration or cytoskeleton organisation, suggesting lower immune cell adhesion to endothelial cells. This was corroborated by in vitro experiments showing that MOF exposure of monocytes attenuates their adhesion to TNF-α-stimulated endothelial cells. Nuclear factor kappa B (NF-κB) reporter gene assays confirmed that MOF decrease the activity of NF-κB. Strong inter-individual variability in the leukocytes' DNA methylation was observed. As a consequence, on group level, changes due to MOF supplementation could not be found."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Adult",
"Cardiovascular Diseases",
"Cell Adhesion",
"Cells, Cultured",
"Coculture Techniques",
"CpG Islands",
"DNA Methylation",
"Flavonoids",
"Gene Expression Regulation",
"Grape Seed Extract",
"Human Umbilical Vein Endothelial Cells",
"Humans",
"Leukocytes",
"Male",
"Middle Aged",
"NF-kappa B",
"Oligonucleotide Array Sequence Analysis",
"Sequence Analysis, DNA",
"Transcription, Genetic",
"Transcriptome"
]
} | Our study revealed that an 8 week daily supplementation with 200 mg MOF modulates the expression of genes associated with cardiovascular disease pathways without major changes of their DNA methylation state. However, strong inter-individual variation in leukocyte DNA methylation may obscure the subtle epigenetic response to dietary flavanols. Despite the lack of significant changes in DNA methylation, the modulation of gene expression appears to contribute to the observed vascular health effect of MOF in humans. | yes | [
{
"from": "human",
"value": "Question: Do dietary flavanols modulate the transcription of genes associated with cardiovascular pathology without changes in their DNA methylation state?\nContext: {'contexts': ['In a recent intervention study, the daily supplementation with 200 mg monomeric and oligomeric flavanols (MOF) from grape seeds for 8 weeks revealed a vascular health benefit in male smokers. The objective of the present study was to determine the impact of MOF consumption on the gene expression profile of leukocytes and to assess changes in DNA methylation.', \"Gene expression profiles were determined using whole genome microarrays (Agilent) and DNA methylation was assessed using HumanMethylation450 BeadChips (Illumina). MOF significantly modulated the expression of 864 genes. The majority of the affected genes are involved in chemotaxis, cell adhesion, cell infiltration or cytoskeleton organisation, suggesting lower immune cell adhesion to endothelial cells. This was corroborated by in vitro experiments showing that MOF exposure of monocytes attenuates their adhesion to TNF-α-stimulated endothelial cells. Nuclear factor kappa B (NF-κB) reporter gene assays confirmed that MOF decrease the activity of NF-κB. Strong inter-individual variability in the leukocytes' DNA methylation was observed. As a consequence, on group level, changes due to MOF supplementation could not be found.\"], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Adult', 'Cardiovascular Diseases', 'Cell Adhesion', 'Cells, Cultured', 'Coculture Techniques', 'CpG Islands', 'DNA Methylation', 'Flavonoids', 'Gene Expression Regulation', 'Grape Seed Extract', 'Human Umbilical Vein Endothelial Cells', 'Humans', 'Leukocytes', 'Male', 'Middle Aged', 'NF-kappa B', 'Oligonucleotide Array Sequence Analysis', 'Sequence Analysis, DNA', 'Transcription, Genetic', 'Transcriptome']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,764,267 | Are high expression levels of the B cell chemoattractant CXCL13 in rheumatoid synovium a marker of severe disease? | {
"contexts": [
"The B cell chemoattractant chemokine ligand 13 (CXCL13) is emerging as a new biochemical marker in RA. This study was undertaken to dissect the relationship between CXCL13 expression levels in the synovium and clinico-pathological variables relevant to RA pathogenesis and outcome.",
"Synovial tissues from 71 RA patients were evaluated by immunohistochemistry. Thirty paired samples were used for comparative gene expression analysis by quantitative real-time PCR. CXCL13 levels were analysed in relation to cellular, molecular and clinical features of inflammation, lymphocyte activation and joint damage.",
"In patients with early disease (<12 months duration), CXCL13 expression correlated significantly with synovial markers of local disease activity and systemic inflammation. Such correlation was less evident in established RA. Notably, the association with lymphocyte infiltration and with expression of B/T cell-related activation and proliferation genes, such as activation-induced cytidine deaminase, IFN-γ and IL-2, remained highly significant independent of disease duration and local disease activity. Patients featuring the highest levels of CXCL13 were more frequently ACPA positive and IgG ACPA titres were increased in the high CXCL13 expression group. Furthermore, the frequency of erosive disease on radiographs was significantly higher in the upper tertile of CXCL13 expression (P = 0.01 with adjustment for disease duration and ACPA). Accordingly, synovial CXCL13 and the local receptor activator of nuclear factor κB ligand (RANKL)/osteoprotegerin (OPG) ratio significantly co-varied (ρ = 0.52, P < 0.01), independent of the level of local inflammation."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Arthritis, Rheumatoid",
"Biomarkers",
"Bone Remodeling",
"Chemokine CXCL13",
"Disease Progression",
"Female",
"Humans",
"Inflammation",
"Joints",
"Lymphocyte Activation",
"Male",
"Middle Aged",
"Severity of Illness Index",
"Synovial Membrane"
]
} | Synovial CXCL13 appears to be a marker of a more severe pattern of RA disease, characterized by increased lymphocyte activation and bone remodelling beyond the level of conventional markers of inflammation. | yes | [
{
"from": "human",
"value": "Question: Are high expression levels of the B cell chemoattractant CXCL13 in rheumatoid synovium a marker of severe disease?\nContext: {'contexts': ['The B cell chemoattractant chemokine ligand 13 (CXCL13) is emerging as a new biochemical marker in RA. This study was undertaken to dissect the relationship between CXCL13 expression levels in the synovium and clinico-pathological variables relevant to RA pathogenesis and outcome.', 'Synovial tissues from 71 RA patients were evaluated by immunohistochemistry. Thirty paired samples were used for comparative gene expression analysis by quantitative real-time PCR. CXCL13 levels were analysed in relation to cellular, molecular and clinical features of inflammation, lymphocyte activation and joint damage.', 'In patients with early disease (<12 months duration), CXCL13 expression correlated significantly with synovial markers of local disease activity and systemic inflammation. Such correlation was less evident in established RA. Notably, the association with lymphocyte infiltration and with expression of B/T cell-related activation and proliferation genes, such as activation-induced cytidine deaminase, IFN-γ and IL-2, remained highly significant independent of disease duration and local disease activity. Patients featuring the highest levels of CXCL13 were more frequently ACPA positive and IgG ACPA titres were increased in the high CXCL13 expression group. Furthermore, the frequency of erosive disease on radiographs was significantly higher in the upper tertile of CXCL13 expression (P = 0.01 with adjustment for disease duration and ACPA). Accordingly, synovial CXCL13 and the local receptor activator of nuclear factor κB ligand (RANKL)/osteoprotegerin (OPG) ratio significantly co-varied (ρ = 0.52, P < 0.01), independent of the level of local inflammation.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Arthritis, Rheumatoid', 'Biomarkers', 'Bone Remodeling', 'Chemokine CXCL13', 'Disease Progression', 'Female', 'Humans', 'Inflammation', 'Joints', 'Lymphocyte Activation', 'Male', 'Middle Aged', 'Severity of Illness Index', 'Synovial Membrane']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,753,296 | Does obesity independently influence gonadal function in very long-term adult male survivors of childhood cancer? | {
"contexts": [
"Although obesity is associated with gonadal dysfunction in the general population, gonadotoxic treatment might diminish the impact of obesity in childhood cancer survivors (CCS). The aim was to evaluate whether altered body composition is associated with gonadal dysfunction in male CCS, independent of gonadotoxic cancer treatment.",
"Three hundred fifty-one male CCS were included. Median age at diagnosis was 5.9 years (0-17.8) and median age at follow-up 25.6 years (18.0-45.8). Total and non-SHBG-bound testosterone, sex hormone-binding globulin, inhibin B, and follicle-stimulating hormone (FSH) were studied. Potential determinants were BMI, waist circumference, waist-hip ratio, and body composition measures (dual energy X-ray absorptiometry).",
"Non-SHBG-bound testosterone was significantly decreased in survivors with BMI ≥ 30 kg/m(2) (adjusted mean 9.1 nmol/L vs. 10.2 nmol/L, P = 0.015), high fat percentage (10.0 vs. 11.2, P = 0.004), and high waist circumference (>102 cm) (9.0 vs. 11.0, P = 0.020). Survivors with high fat percentage (≥25%) had significantly lower inhibin B/FSH ratios (inhibin B/FSH ratio: β -34%, P = 0.041)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Body Composition",
"Body Mass Index",
"Case-Control Studies",
"Child",
"Child, Preschool",
"Follicle Stimulating Hormone",
"Humans",
"Infant",
"Inhibins",
"Male",
"Middle Aged",
"Neoplasms",
"Obesity",
"Retrospective Studies",
"Sex Hormone-Binding Globulin",
"Survivors",
"Testis",
"Testosterone",
"Waist Circumference",
"Waist-Hip Ratio",
"Young Adult"
]
} | Obesity is associated with gonadal dysfunction in male CCS, independent of the irreversible effect of previous cancer treatment. Randomized controlled trials are required to evaluate whether weight normalization could improve gonadal function, especially in obese survivors with potential other mechanisms than lifestyle causing their obesity. | yes | [
{
"from": "human",
"value": "Question: Does obesity independently influence gonadal function in very long-term adult male survivors of childhood cancer?\nContext: {'contexts': ['Although obesity is associated with gonadal dysfunction in the general population, gonadotoxic treatment might diminish the impact of obesity in childhood cancer survivors (CCS). The aim was to evaluate whether altered body composition is associated with gonadal dysfunction in male CCS, independent of gonadotoxic cancer treatment.', 'Three hundred fifty-one male CCS were included. Median age at diagnosis was 5.9 years (0-17.8) and median age at follow-up 25.6 years (18.0-45.8). Total and non-SHBG-bound testosterone, sex hormone-binding globulin, inhibin B, and follicle-stimulating hormone (FSH) were studied. Potential determinants were BMI, waist circumference, waist-hip ratio, and body composition measures (dual energy X-ray absorptiometry).', 'Non-SHBG-bound testosterone was significantly decreased in survivors with BMI ≥ 30 kg/m(2) (adjusted mean 9.1 nmol/L vs. 10.2 nmol/L, P = 0.015), high fat percentage (10.0 vs. 11.2, P = 0.004), and high waist circumference (>102 cm) (9.0 vs. 11.0, P = 0.020). Survivors with high fat percentage (≥25%) had significantly lower inhibin B/FSH ratios (inhibin B/FSH ratio: β -34%, P = 0.041).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Body Composition', 'Body Mass Index', 'Case-Control Studies', 'Child', 'Child, Preschool', 'Follicle Stimulating Hormone', 'Humans', 'Infant', 'Inhibins', 'Male', 'Middle Aged', 'Neoplasms', 'Obesity', 'Retrospective Studies', 'Sex Hormone-Binding Globulin', 'Survivors', 'Testis', 'Testosterone', 'Waist Circumference', 'Waist-Hip Ratio', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,750,984 | Does ginsenoside Rg1 protect mouse liver against ischemia-reperfusion injury through anti-inflammatory and anti-apoptosis properties? | {
"contexts": [
"Ginsenoside Rg1, the major effective component of ginseng, possesses a variety of pharmacologic activities. The objective of this study was to investigate the effects of Rg1 on liver ischemia-reperfusion (IR) injury and explore its potential mechanisms.",
"Liver warm IR injury was achieved by occluding the portal vein and hepatic artery for 1 h followed by 6-h reperfusion. Eighteen mice were equally randomized into three groups: sham group, IR group, and IR plus Rg1 group (n = 6 mice per group). Mice received an intravenous dose of 20 mg/kg Rg1 or an equivalent volume of saline before ischemic insult. Liver samples and serum were collected for analyses. Serum aminotransferase, histopathology, and apoptosis were determined. Cytokines were measured by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). The phosphorylation of nuclear factor kappa B (NF-κB) p65 was assessed by Western blotting. In addition, the effect of Rg1 in a simulated IR model in vitro was also investigated. Rg1 (100 ug/mL and 500 ug/mL) was administered 1 h before hypoxia insult, and then apoptosis was measured after 12-h reperfusion.",
"Liver IR injury led to a dramatic increase in aminopherase activity, apoptosis and necrosis of hepatocytes, and production of proinflammatory cytokines. Pretreatment with Rg1 protected mice from IR-induced liver injury. Treatment with a high-dose Rg1 (500 ug/mL) significantly suppressed apoptosis compared with a lower dose or control (both P < 0.001). Phosphorylation of NF-κB p65 was increased significantly in IR group, and administration with Rg1 suppressed the level of phosphorylation."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Anti-Inflammatory Agents",
"Apoptosis",
"Cell Adhesion Molecules",
"Cytokines",
"Disease Models, Animal",
"Down-Regulation",
"Drugs, Chinese Herbal",
"Ginsenosides",
"Hepatitis",
"Macrophages, Peritoneal",
"Male",
"Mice, Inbred C57BL",
"Necrosis",
"Reperfusion Injury",
"Transplantation Immunology",
"Warm Ischemia"
]
} | Pretreatment of mice with Rg1 reduced hepatocellular apoptosis and inhibited inflammatory response, which was in part through the NF-κB signaling pathway. Rg1 may provide a novel therapeutic strategy for the treatment of IR-induced liver injury. | yes | [
{
"from": "human",
"value": "Question: Does ginsenoside Rg1 protect mouse liver against ischemia-reperfusion injury through anti-inflammatory and anti-apoptosis properties?\nContext: {'contexts': ['Ginsenoside Rg1, the major effective component of ginseng, possesses a variety of pharmacologic activities. The objective of this study was to investigate the effects of Rg1 on liver ischemia-reperfusion (IR) injury and explore its potential mechanisms.', 'Liver warm IR injury was achieved by occluding the portal vein and hepatic artery for 1 h followed by 6-h reperfusion. Eighteen mice were equally randomized into three groups: sham group, IR group, and IR plus Rg1 group (n = 6 mice per group). Mice received an intravenous dose of 20 mg/kg Rg1 or an equivalent volume of saline before ischemic insult. Liver samples and serum were collected for analyses. Serum aminotransferase, histopathology, and apoptosis were determined. Cytokines were measured by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). The phosphorylation of nuclear factor kappa B (NF-κB) p65 was assessed by Western blotting. In addition, the effect of Rg1 in a simulated IR model in vitro was also investigated. Rg1 (100 ug/mL and 500 ug/mL) was administered 1 h before hypoxia insult, and then apoptosis was measured after 12-h reperfusion.', 'Liver IR injury led to a dramatic increase in aminopherase activity, apoptosis and necrosis of hepatocytes, and production of proinflammatory cytokines. Pretreatment with Rg1 protected mice from IR-induced liver injury. Treatment with a high-dose Rg1 (500 ug/mL) significantly suppressed apoptosis compared with a lower dose or control (both P < 0.001). Phosphorylation of NF-κB p65 was increased significantly in IR group, and administration with Rg1 suppressed the level of phosphorylation.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Anti-Inflammatory Agents', 'Apoptosis', 'Cell Adhesion Molecules', 'Cytokines', 'Disease Models, Animal', 'Down-Regulation', 'Drugs, Chinese Herbal', 'Ginsenosides', 'Hepatitis', 'Macrophages, Peritoneal', 'Male', 'Mice, Inbred C57BL', 'Necrosis', 'Reperfusion Injury', 'Transplantation Immunology', 'Warm Ischemia']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,749,557 | Is congenital cytomegalovirus associated with severe forms of cerebral palsy and female sex in a retrospective population-based study? | {
"contexts": [
"Congenital cytomegalovirus (cCMV) infection can result in poor outcomes including cerebral palsy (CP). The aim of this study was to describe the incidence and comorbidities of CP reported to the Australian Cerebral Palsy Register (ACPR) as attributed to cCMV infection.",
"This was a retrospective population-based study. Cases were drawn from Australian state CP registers with population level ascertainment, 1993 to 2003 (n=2265; 56.4% males, Gross Motor Function Classification System [GMFCS] ratings available for Victorian cases only: 70% GMFCS levels I to III and 30% GMFCS levels IV to V). Clinical data were extracted and cases with cCMV reported as a known cause were compared with cases where cCMV was not reported.",
"Children with cCMV (n=34; 12 males, 22 females; mean [SD] gestational age, 36.4 wk [4.4], range 24-41 wk) accounted for 1.5% of CP cases; 2.9 per 100,000 live births, (95% confidence intervals 1.9-3.9). When compared with CP cases where cCMV was not reported, proportionally, more CP cases with cCMV were born to younger mothers (p<0.001), were female (64% vs 43%, p=0.014), had spastic quadriplegia (73% vs 21%, p<0.001), required wheeled mobility i.e. GMFCS IV or V (78% vs 28%, p<0.001), had epilepsy (70% vs 30%, p<0.001), deafness (40% vs 2%, p<0.001), functional blindness (20% vs 5%, p<0.001), and severe communication impairment (71% vs 25%, p<0.001)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Australia",
"Cerebral Palsy",
"Comorbidity",
"Cytomegalovirus Infections",
"Female",
"Gestational Age",
"Humans",
"Incidence",
"Infant, Newborn",
"Male",
"Maternal Age",
"Registries",
"Retrospective Studies",
"Severity of Illness Index",
"Sex Factors"
]
} | cCMV is an important potentially preventable cause of CP and is associated with severe disability and female sex in cases reported to the ACPR. Future studies utilising prospective sample collection for cCMV testing are needed to confirm these findings. | yes | [
{
"from": "human",
"value": "Question: Is congenital cytomegalovirus associated with severe forms of cerebral palsy and female sex in a retrospective population-based study?\nContext: {'contexts': ['Congenital cytomegalovirus (cCMV) infection can result in poor outcomes including cerebral palsy (CP). The aim of this study was to describe the incidence and comorbidities of CP reported to the Australian Cerebral Palsy Register (ACPR) as attributed to cCMV infection.', 'This was a retrospective population-based study. Cases were drawn from Australian state CP registers with population level ascertainment, 1993 to 2003 (n=2265; 56.4% males, Gross Motor Function Classification System [GMFCS] ratings available for Victorian cases only: 70% GMFCS levels I to III and 30% GMFCS levels IV to V). Clinical data were extracted and cases with cCMV reported as a known cause were compared with cases where cCMV was not reported.', 'Children with cCMV (n=34; 12 males, 22 females; mean [SD] gestational age, 36.4 wk [4.4], range 24-41 wk) accounted for 1.5% of CP cases; 2.9 per 100,000 live births, (95% confidence intervals 1.9-3.9). When compared with CP cases where cCMV was not reported, proportionally, more CP cases with cCMV were born to younger mothers (p<0.001), were female (64% vs 43%, p=0.014), had spastic quadriplegia (73% vs 21%, p<0.001), required wheeled mobility i.e. GMFCS IV or V (78% vs 28%, p<0.001), had epilepsy (70% vs 30%, p<0.001), deafness (40% vs 2%, p<0.001), functional blindness (20% vs 5%, p<0.001), and severe communication impairment (71% vs 25%, p<0.001).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Australia', 'Cerebral Palsy', 'Comorbidity', 'Cytomegalovirus Infections', 'Female', 'Gestational Age', 'Humans', 'Incidence', 'Infant, Newborn', 'Male', 'Maternal Age', 'Registries', 'Retrospective Studies', 'Severity of Illness Index', 'Sex Factors']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,753,151 | Is aP-2α required after lens vesicle formation to maintain lens integrity? | {
"contexts": [
"Transcription factors are critical in regulating lens development. The AP-2 family of transcription factors functions in differentiation, cell growth and apoptosis, and in lens and eye development. AP-2α, in particular, is important in early lens development, and when conditionally deleted at the placode stage defective separation of the lens vesicle from the surface ectoderm results. AP-2α's role during later stages of lens development is unknown. To address this, the MLR10-Cre transgene was used to delete AP-2α from the lens epithelium beginning at embryonic day (E) 10.5.",
"The loss of AP-2α after lens vesicle separation resulted in morphological defects beginning at E18.5. By P4, a small highly vacuolated lens with a multilayered epithelium was evident in the MLR10-AP-2α mutants. Epithelial cells appeared elongated and expressed fiber cell specific βB1 and γ-crystallins. Epithelial cell polarity and lens cell adhesion was disrupted and accompanied by the misexpression of ZO-1, N-Cadherin, and β-catenin. Cell death was observed in the mutant lens epithelium between postnatal day (P) 14 and P30, and correlated with altered arrangements of cells within the epithelium."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Animals",
"Cataract",
"Cell Adhesion",
"Cell Differentiation",
"Cell Polarity",
"Embryo, Mammalian",
"Epithelial Cells",
"Epithelium",
"Gene Expression Regulation, Developmental",
"Lens, Crystalline",
"Mice",
"Mice, Transgenic",
"Phenotype",
"Transcription Factor AP-2"
]
} | Our findings demonstrate that AP-2α continues to be required after lens vesicle separation to maintain a normal lens epithelial cell phenotype and overall lens integrity and to ensure correct fiber cell differentiation. | yes | [
{
"from": "human",
"value": "Question: Is aP-2α required after lens vesicle formation to maintain lens integrity?\nContext: {'contexts': [\"Transcription factors are critical in regulating lens development. The AP-2 family of transcription factors functions in differentiation, cell growth and apoptosis, and in lens and eye development. AP-2α, in particular, is important in early lens development, and when conditionally deleted at the placode stage defective separation of the lens vesicle from the surface ectoderm results. AP-2α's role during later stages of lens development is unknown. To address this, the MLR10-Cre transgene was used to delete AP-2α from the lens epithelium beginning at embryonic day (E) 10.5.\", 'The loss of AP-2α after lens vesicle separation resulted in morphological defects beginning at E18.5. By P4, a small highly vacuolated lens with a multilayered epithelium was evident in the MLR10-AP-2α mutants. Epithelial cells appeared elongated and expressed fiber cell specific βB1 and γ-crystallins. Epithelial cell polarity and lens cell adhesion was disrupted and accompanied by the misexpression of ZO-1, N-Cadherin, and β-catenin. Cell death was observed in the mutant lens epithelium between postnatal day (P) 14 and P30, and correlated with altered arrangements of cells within the epithelium.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Animals', 'Cataract', 'Cell Adhesion', 'Cell Differentiation', 'Cell Polarity', 'Embryo, Mammalian', 'Epithelial Cells', 'Epithelium', 'Gene Expression Regulation, Developmental', 'Lens, Crystalline', 'Mice', 'Mice, Transgenic', 'Phenotype', 'Transcription Factor AP-2']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,748,529 | Does high-intensity intermittent cycling increase purine loss compared with workload-matched continuous moderate intensity cycling? | {
"contexts": [
"Exercise at 50-60 % of peak oxygen consumption (VO2 peak) stimulates maximal fat oxidation rates. Despite a lower estimated work performed; high-intensity intermittent exercise (HIIE) training produces greater fat mass reductions when compared with workload-matched continuous (CON) steady state exercise. No metabolic basis has been documented nor mechanisms offered to explain this anomaly. This study investigated the physiological and metabolic responses of two different workload-matched exercise protocols.",
"On separate occasions and at least 1 week apart, eight apparently healthy males cycled for 30 min at either 50 % VO2 peak (CON) or performed repeated 20 s bouts of supramaximal exercise at 150 %VO2 peak separated by 40 s rest (HIIE).",
"The average heart rate, oxygen consumption, plasma glycerol and free fatty acid concentrations were not different during exercise and recovery between the trials. Plasma lactate and hypoxanthine (Hx) concentrations were elevated and urinary excretion rates of Hx and uric acid were greater following HIIE as compared to CON (P < 0.05)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adenosine Triphosphate",
"Adolescent",
"Adult",
"Bicycling",
"Biomarkers",
"Healthy Volunteers",
"Heart Rate",
"Humans",
"Hypoxanthine",
"Lactic Acid",
"Lipid Metabolism",
"Male",
"Muscle, Skeletal",
"Oxygen Consumption",
"Purines",
"Time Factors",
"Uric Acid",
"Victoria",
"Young Adult"
]
} | Exercise-induced plasma Hx accumulation and urinary purine excretion are greater following HIIE and indirectly represents a net loss of adenosine triphosphate (ATP) from the muscle. The subsequent restorative processes required for intramuscular de novo replacement of ATP may contribute to a negative energy balance and in part, account for the potential accelerated fat loss observed with HIIE when compared with CON training programs. | yes | [
{
"from": "human",
"value": "Question: Does high-intensity intermittent cycling increase purine loss compared with workload-matched continuous moderate intensity cycling?\nContext: {'contexts': ['Exercise at 50-60\\xa0% of peak oxygen consumption (VO2 peak) stimulates maximal fat oxidation rates. Despite a lower estimated work performed; high-intensity intermittent exercise (HIIE) training produces greater fat mass reductions when compared with workload-matched continuous (CON) steady state exercise. No metabolic basis has been documented nor mechanisms offered to explain this anomaly. This study investigated the physiological and metabolic responses of two different workload-matched exercise protocols.', 'On separate occasions and at least 1\\xa0week apart, eight apparently healthy males cycled for 30\\xa0min at either 50\\xa0% VO2 peak (CON) or performed repeated 20\\xa0s bouts of supramaximal exercise at 150\\xa0%VO2 peak separated by 40\\xa0s rest (HIIE).', 'The average heart rate, oxygen consumption, plasma glycerol and free fatty acid concentrations were not different during exercise and recovery between the trials. Plasma lactate and hypoxanthine (Hx) concentrations were elevated and urinary excretion rates of Hx and uric acid were greater following HIIE as compared to CON (P\\xa0<\\xa00.05).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adenosine Triphosphate', 'Adolescent', 'Adult', 'Bicycling', 'Biomarkers', 'Healthy Volunteers', 'Heart Rate', 'Humans', 'Hypoxanthine', 'Lactic Acid', 'Lipid Metabolism', 'Male', 'Muscle, Skeletal', 'Oxygen Consumption', 'Purines', 'Time Factors', 'Uric Acid', 'Victoria', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,777,277 | Does cognitive impairment in patients with multiple sclerosis predict worse caregiver 's health-related quality of life? | {
"contexts": [
"Little information exists about how cognitive impairment in multiple sclerosis (MS) patients impacts on their caregivers' health-related quality of life (HRQoL).",
"The objective of this paper is to examine the extent to which cognitive impairment in MS patients contributes to caregivers' HRQoL.",
"A total of 63 MS patients, 63 caregivers and 59 matched controls were recruited. Patients and controls underwent a neuropsychological assessment, including tests of working memory, speed of information processing, executive function, and verbal fluency. HRQoL of the caregivers was assessed by CAREQOL-MS. In logistic regression models, we adjusted for the effects of confounding variables. In these models, the dependent variable was the CAREQOL-MS (higher median of CAREQOL-MS (worse HRQoL) vs. lower median of CAREQOL-MS (better HRQoL) (reference)), and the independent variable was the impairment on each neuropsychological test vs. its integrity (reference).",
"Cognitive impairment in MS patients was significantly associated with worse caregiver HRQoL (adjusted odds ratio (OR) = 3.10, 95% confidence interval (CI) = 1.07-11.55, p = 0.04). In secondary analyses in which each neuropsychological test was entered in the analyses separately, only Symbol Digit Modalities Test (a measurement of information processing speed) impairment (OR = 4.22, 95%, CI = 1.16-14.53, p = 0.03) was significantly associated with worse caregiver HRQoL."
],
"labels": [
"BACKGROUND",
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Caregivers",
"Cognition Disorders",
"Female",
"Humans",
"Male",
"Middle Aged",
"Multiple Sclerosis",
"Neuropsychological Tests",
"Quality of Life"
]
} | MS patients' caregivers' HRQoL is significantly influenced by information processing speed impairment of MS patients. | yes | [
{
"from": "human",
"value": "Question: Does cognitive impairment in patients with multiple sclerosis predict worse caregiver 's health-related quality of life?\nContext: {'contexts': [\"Little information exists about how cognitive impairment in multiple sclerosis (MS) patients impacts on their caregivers' health-related quality of life (HRQoL).\", \"The objective of this paper is to examine the extent to which cognitive impairment in MS patients contributes to caregivers' HRQoL.\", 'A total of 63 MS patients, 63 caregivers and 59 matched controls were recruited. Patients and controls underwent a neuropsychological assessment, including tests of working memory, speed of information processing, executive function, and verbal fluency. HRQoL of the caregivers was assessed by CAREQOL-MS. In logistic regression models, we adjusted for the effects of confounding variables. In these models, the dependent variable was the CAREQOL-MS (higher median of CAREQOL-MS (worse HRQoL) vs. lower median of CAREQOL-MS (better HRQoL) (reference)), and the independent variable was the impairment on each neuropsychological test vs. its integrity (reference).', 'Cognitive impairment in MS patients was significantly associated with worse caregiver HRQoL (adjusted odds ratio (OR) = 3.10, 95% confidence interval (CI) = 1.07-11.55, p = 0.04). In secondary analyses in which each neuropsychological test was entered in the analyses separately, only Symbol Digit Modalities Test (a measurement of information processing speed) impairment (OR = 4.22, 95%, CI = 1.16-14.53, p = 0.03) was significantly associated with worse caregiver HRQoL.'], 'labels': ['BACKGROUND', 'BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Caregivers', 'Cognition Disorders', 'Female', 'Humans', 'Male', 'Middle Aged', 'Multiple Sclerosis', 'Neuropsychological Tests', 'Quality of Life']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,754,438 | Does berberine ameliorate renal interstitial fibrosis induced by unilateral ureteral obstruction in rats? | {
"contexts": [
"To investigate the potential effects of berberine on renal interstitial fibrosis (RIF) of obstructed kidneys in a unilateral ureteral obstruction (UUO) rat model.",
"Forty-eight rats were randomly divided into three groups: sham-operated, vehicle-treated UUO, and berberine-treated UUO. Rats were gavaged with berberine (200 mg/kg per day) or vehicle. Eight randomly chosen rats in each group were kiled and specimens were collected at day 14 after UUO. Physiological parameters and histological changes were assessed, RIF was evaluated using Masson's trichrome and Sirius red staining, oxidative stress and inflammation markers were determined, transforming growth factor β1 (TGF-β1), phosphorylated Smad3 (pSmad3) and α-smooth muscle actin (α-SMA) were measured using immunohistochemistry or western blotting analysis. The obstruction was relieved at day 14 by percutaneous nephrostomy in the remaining UUO rats. The resistive index of left kidneys was undertaken by coloured Doppler flow imaging at day 14 before nephrostomy and day 7 after the relief.",
"Berberine treatment significantly attenuated RIF induced by UUO. The UUO-induced reduction in kidney superoxide dismutase and catalase activities increased, whereas elevated kidney malondialdehyde level markedly decreased. Berberine treatment significantly ameliorated UUO-induced inflammation, and decreased TGF-β1, pSmad3 and α-SMA expression of UUO kidneys. Moreover, berberine treatment significantly suppressed the increase of resistive index compared with UUO group at day 14 after UUO as well as day 7 after the relief of obstruction."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Actins",
"Animals",
"Berberine",
"Biomarkers",
"Catalase",
"Cytoprotection",
"Disease Models, Animal",
"Fibrosis",
"Hemodynamics",
"Hydronephrosis",
"Inflammation Mediators",
"Kidney",
"Kidney Diseases",
"Male",
"Malondialdehyde",
"Oxidative Stress",
"Phosphorylation",
"Rats, Sprague-Dawley",
"Renal Circulation",
"Signal Transduction",
"Smad3 Protein",
"Superoxide Dismutase",
"Time Factors",
"Transforming Growth Factor beta1",
"Ureteral Obstruction",
"Urological Agents"
]
} | Berberine treatment ameliorates RIF in a UUO rat model by inhibition of oxidative stress, inflammatory responses, and TGF-β1/pSmad3 signalling. | yes | [
{
"from": "human",
"value": "Question: Does berberine ameliorate renal interstitial fibrosis induced by unilateral ureteral obstruction in rats?\nContext: {'contexts': ['To investigate the potential effects of berberine on renal interstitial fibrosis (RIF) of obstructed kidneys in a unilateral ureteral obstruction (UUO) rat model.', \"Forty-eight rats were randomly divided into three groups: sham-operated, vehicle-treated UUO, and berberine-treated UUO. Rats were gavaged with berberine (200\\u2009mg/kg per day) or vehicle. Eight randomly chosen rats in each group were kiled and specimens were collected at day 14 after UUO. Physiological parameters and histological changes were assessed, RIF was evaluated using Masson's trichrome and Sirius red staining, oxidative stress and inflammation markers were determined, transforming growth factor β1 (TGF-β1), phosphorylated Smad3 (pSmad3) and α-smooth muscle actin (α-SMA) were measured using immunohistochemistry or western blotting analysis. The obstruction was relieved at day 14 by percutaneous nephrostomy in the remaining UUO rats. The resistive index of left kidneys was undertaken by coloured Doppler flow imaging at day 14 before nephrostomy and day 7 after the relief.\", 'Berberine treatment significantly attenuated RIF induced by UUO. The UUO-induced reduction in kidney superoxide dismutase and catalase activities increased, whereas elevated kidney malondialdehyde level markedly decreased. Berberine treatment significantly ameliorated UUO-induced inflammation, and decreased TGF-β1, pSmad3 and α-SMA expression of UUO kidneys. Moreover, berberine treatment significantly suppressed the increase of resistive index compared with UUO group at day 14 after UUO as well as day 7 after the relief of obstruction.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Actins', 'Animals', 'Berberine', 'Biomarkers', 'Catalase', 'Cytoprotection', 'Disease Models, Animal', 'Fibrosis', 'Hemodynamics', 'Hydronephrosis', 'Inflammation Mediators', 'Kidney', 'Kidney Diseases', 'Male', 'Malondialdehyde', 'Oxidative Stress', 'Phosphorylation', 'Rats, Sprague-Dawley', 'Renal Circulation', 'Signal Transduction', 'Smad3 Protein', 'Superoxide Dismutase', 'Time Factors', 'Transforming Growth Factor beta1', 'Ureteral Obstruction', 'Urological Agents']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,756,886 | Does resveratrol reduce morphine tolerance by inhibiting microglial activation via AMPK signalling? | {
"contexts": [
"Evidence has accumulated indicating that microglia within the spinal cord play a critical role in morphine tolerance. The present study investigated the effects and possible mechanisms of 5' adenosine monophosphate-activated protein kinase (AMPK) activator resveratrol and AICAR to inhibit microglial activation and to limit the decrease in antinociceptive effects of morphine.",
"The microglial cell line BV-2 was used. Cytokine expression was measured using quantitative polymerase chain reaction. Cell signalling was assayed by Western blot and immunohistochemistry. The antinociception and morphine tolerance were assessed in CD-1 mice using the hot plate and tail-flick tests.",
"(1) Morphine induces robust BV-2 cell activation, as evidenced by increased p38 mitogen-activated protein kinase phosphorylation, nuclear factor-κB translocation and mRNA expression of pro-inflammatory cytokines [including interleukin-1β (IL-1β), IL-6 and tumour necrosis factor-α], inducible nitric oxide synthase and Toll-like receptor-4, and these changes are inhibited by resveratrol. (2) Resveratrol activates AMPK to suppress morphine-induced BV-2 cell activation. AICAR, another AMPK activator, can mimic the effects of resveratrol, whereas compound C, an AMPK inhibitor, reverses the inhibitory effects of resveratrol treatment. (3) Systemic or spinal administration of resveratrol with morphine significantly blocks microglial activation in the spinal cord and then attenuates the development of acute and chronic morphine tolerance in both male and female mice."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"AMP-Activated Protein Kinases",
"Aminoimidazole Carboxamide",
"Analgesics, Opioid",
"Animals",
"Anti-Inflammatory Agents, Non-Steroidal",
"Behavior, Animal",
"Cell Line",
"Drug Tolerance",
"Interleukin-1beta",
"Interleukin-6",
"Mice",
"Microglia",
"Morphine",
"NF-kappa B",
"Nitric Oxide Synthase Type II",
"Nociceptive Pain",
"Resveratrol",
"Ribonucleotides",
"Signal Transduction",
"Stilbenes",
"Toll-Like Receptor 4",
"Tumor Necrosis Factor-alpha",
"p38 Mitogen-Activated Protein Kinases"
]
} | Resveratrol directly suppresses morphine-induced microglial activation through activating AMPK, resulting in significant attenuation of morphine antinociceptive tolerance. | yes | [
{
"from": "human",
"value": "Question: Does resveratrol reduce morphine tolerance by inhibiting microglial activation via AMPK signalling?\nContext: {'contexts': [\"Evidence has accumulated indicating that microglia within the spinal cord play a critical role in morphine tolerance. The present study investigated the effects and possible mechanisms of 5' adenosine monophosphate-activated protein kinase (AMPK) activator resveratrol and AICAR to inhibit microglial activation and to limit the decrease in antinociceptive effects of morphine.\", 'The microglial cell line BV-2 was used. Cytokine expression was measured using quantitative polymerase chain reaction. Cell signalling was assayed by Western blot and immunohistochemistry. The antinociception and morphine tolerance were assessed in CD-1 mice using the hot plate and tail-flick tests.', '(1) Morphine induces robust BV-2 cell activation, as evidenced by increased p38 mitogen-activated protein kinase phosphorylation, nuclear factor-κB translocation and mRNA expression of pro-inflammatory cytokines [including interleukin-1β (IL-1β), IL-6 and tumour necrosis factor-α], inducible nitric oxide synthase and Toll-like receptor-4, and these changes are inhibited by resveratrol. (2) Resveratrol activates AMPK to suppress morphine-induced BV-2 cell activation. AICAR, another AMPK activator, can mimic the effects of resveratrol, whereas compound C, an AMPK inhibitor, reverses the inhibitory effects of resveratrol treatment. (3) Systemic or spinal administration of resveratrol with morphine significantly blocks microglial activation in the spinal cord and then attenuates the development of acute and chronic morphine tolerance in both male and female mice.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['AMP-Activated Protein Kinases', 'Aminoimidazole Carboxamide', 'Analgesics, Opioid', 'Animals', 'Anti-Inflammatory Agents, Non-Steroidal', 'Behavior, Animal', 'Cell Line', 'Drug Tolerance', 'Interleukin-1beta', 'Interleukin-6', 'Mice', 'Microglia', 'Morphine', 'NF-kappa B', 'Nitric Oxide Synthase Type II', 'Nociceptive Pain', 'Resveratrol', 'Ribonucleotides', 'Signal Transduction', 'Stilbenes', 'Toll-Like Receptor 4', 'Tumor Necrosis Factor-alpha', 'p38 Mitogen-Activated Protein Kinases']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,752,012 | Does hepatic HMOX1 expression positively correlate with Bach-1 and miR-122 in patients with HCV mono and HIV/HCV coinfection? | {
"contexts": [
"To analyze the expression of HMOX1 and miR-122 in liver biopsy samples obtained from HCV mono-and HIV/HCV co-infected patients in relation to selected clinical parameters, histological examination and IL-28B polymorphism as well as to determine whether HMOX1 expression is dependent on Bach-1.",
"The study group consisted of 90 patients with CHC: 69 with HCV mono and 21 with HIV/HCV co-infection. RT-PCR was used in the analysis of HMOX1, Bach-1 and miR-122 expression in liver biopsy samples and in the assessment of IL-28B single-nucleotide polymorphism C/T (rs12979860) in the blood. Moreover in liver biopsy samples an analysis of HO-1 and Bach-1 protein level by Western Blot was performed.",
"HCV mono-infected patients, with lower grading score (G<2) and higher HCV viral load (>600000 IU/mL) demonstrated higher expression of HMOX1. In patients with HIV/HCV co-infection, the expression of HMOX1 was lower in patients with lower lymphocyte CD4 count and higher HIV viral load. IL28B polymorphism did not affect the expression of either HMOX1 or miR-122. Higher HMOX1 expression correlated with higher expression of Bach-1 (Spearman's ρ = 0.586, p = 0.000001) and miR-122 (Spearman's ρ = 0.270, p = 0.014059)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Basic-Leucine Zipper Transcription Factors",
"CD4 Lymphocyte Count",
"Coinfection",
"Demography",
"Fanconi Anemia Complementation Group Proteins",
"Female",
"HIV Infections",
"Heme Oxygenase-1",
"Hepatitis C, Chronic",
"Humans",
"Liver",
"Male",
"MicroRNAs",
"Middle Aged",
"Viral Load"
]
} | HMOX1 and miR-122 play an important role in the pathogenesis of CHC in HCV mono-and HIV/HCV co-infected patients. Reduced expression of HMOX1 in patients with HIV/HCV co-infection may indicate a worse prognosis in this group. Our results do not support the importance of Bach-1 in repression of HMOX1 in patients with chronic hepatitis C. | yes | [
{
"from": "human",
"value": "Question: Does hepatic HMOX1 expression positively correlate with Bach-1 and miR-122 in patients with HCV mono and HIV/HCV coinfection?\nContext: {'contexts': ['To analyze the expression of HMOX1 and miR-122 in liver biopsy samples obtained from HCV mono-and HIV/HCV co-infected patients in relation to selected clinical parameters, histological examination and IL-28B polymorphism as well as to determine whether HMOX1 expression is dependent on Bach-1.', 'The study group consisted of 90 patients with CHC: 69 with HCV mono and 21 with HIV/HCV co-infection. RT-PCR was used in the analysis of HMOX1, Bach-1 and miR-122 expression in liver biopsy samples and in the assessment of IL-28B single-nucleotide polymorphism C/T (rs12979860) in the blood. Moreover in liver biopsy samples an analysis of HO-1 and Bach-1 protein level by Western Blot was performed.', \"HCV mono-infected patients, with lower grading score (G<2) and higher HCV viral load (>600000 IU/mL) demonstrated higher expression of HMOX1. In patients with HIV/HCV co-infection, the expression of HMOX1 was lower in patients with lower lymphocyte CD4 count and higher HIV viral load. IL28B polymorphism did not affect the expression of either HMOX1 or miR-122. Higher HMOX1 expression correlated with higher expression of Bach-1 (Spearman's ρ\\u200a=\\u200a0.586, p\\u200a=\\u200a0.000001) and miR-122 (Spearman's ρ\\u200a=\\u200a0.270, p\\u200a=\\u200a0.014059).\"], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Basic-Leucine Zipper Transcription Factors', 'CD4 Lymphocyte Count', 'Coinfection', 'Demography', 'Fanconi Anemia Complementation Group Proteins', 'Female', 'HIV Infections', 'Heme Oxygenase-1', 'Hepatitis C, Chronic', 'Humans', 'Liver', 'Male', 'MicroRNAs', 'Middle Aged', 'Viral Load']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,757,044 | Do dual echo vessel-encoded ASL for simultaneous BOLD and CBF reactivity assessment in patients with ischemic cerebrovascular disease? | {
"contexts": [
"Blood oxygenation level-dependent (BOLD)-weighted and vessel-encoded arterial spin labeling (VE-ASL) MRI provide complementary information and can be used in sequence to gauge hemodynamic contributions to cerebrovascular reactivity. Here, cerebrovascular reactivity is assessed using dual echo VE-ASL MRI to understand how VE labeling preparations influence BOLD and ASL contrast in flow-limited and healthy perfusion territories.",
"Patients (n = 12; age = 55 +/- 14 years; 6F/6M) presenting with ischemic steno-occlusive cerebrovascular disease underwent 3.0T angiographic imaging, T1 -weighted structural, and planning-free dual echo hypercarbic hyperoxic (i.e., carbogen) VE-ASL MRI. Vasculopathy extent, timecourses, and cerebrovascular reactivity (signal change and Z-statistic) for different VE-ASL images were contrasted across flow territories and Bonferroni-corrected P-values reported.",
"BOLD cerebrovascular reactivity (i.e., long-TE VE-ASL) Z-statistics were similarly sensitive to asymmetric disease (P ≤ 0.002) regardless of labeling scenario. Cerebral blood flow reactivity correlated significantly with BOLD reactivity (Z-statistic). However, BOLD signal changes did not differ significantly between labeling scenarios (P > 0.003) or across territories (P > 0.002), indicating BOLD signal changes in response to carbogen offer low sensitivity to lateralizing disease."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Algorithms",
"Blood Flow Velocity",
"Brain Ischemia",
"Cerebral Arteries",
"Cerebrovascular Circulation",
"Female",
"Humans",
"Image Interpretation, Computer-Assisted",
"Magnetic Resonance Angiography",
"Male",
"Middle Aged",
"Oxygen",
"Reproducibility of Results",
"Sensitivity and Specificity"
]
} | Dual echo VE-ASL can provide simultaneous cerebral blood flow and qualitative BOLD contrast consistent with lateralizing disease severity in patients with asymmetric steno-occlusive disease. The methodological strengths and limitations of composite BOLD and VE-ASL measurements in the clinic are discussed. | yes | [
{
"from": "human",
"value": "Question: Do dual echo vessel-encoded ASL for simultaneous BOLD and CBF reactivity assessment in patients with ischemic cerebrovascular disease?\nContext: {'contexts': ['Blood oxygenation level-dependent (BOLD)-weighted and vessel-encoded arterial spin labeling (VE-ASL) MRI provide complementary information and can be used in sequence to gauge hemodynamic contributions to cerebrovascular reactivity. Here, cerebrovascular reactivity is assessed using dual echo VE-ASL MRI to understand how VE labeling preparations influence BOLD and ASL contrast in flow-limited and healthy perfusion territories.', 'Patients (n\\u2009=\\u200912; age\\u2009=\\u200955 +/- 14 years; 6F/6M) presenting with ischemic steno-occlusive cerebrovascular disease underwent 3.0T angiographic imaging, T1 -weighted structural, and planning-free dual echo hypercarbic hyperoxic (i.e., carbogen) VE-ASL MRI. Vasculopathy extent, timecourses, and cerebrovascular reactivity (signal change and Z-statistic) for different VE-ASL images were contrasted across flow territories and Bonferroni-corrected P-values reported.', 'BOLD cerebrovascular reactivity (i.e., long-TE VE-ASL) Z-statistics were similarly sensitive to asymmetric disease (P\\u2009≤\\u20090.002) regardless of labeling scenario. Cerebral blood flow reactivity correlated significantly with BOLD reactivity (Z-statistic). However, BOLD signal changes did not differ significantly between labeling scenarios (P\\u2009>\\u20090.003) or across territories (P\\u2009>\\u20090.002), indicating BOLD signal changes in response to carbogen offer low sensitivity to lateralizing disease.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Algorithms', 'Blood Flow Velocity', 'Brain Ischemia', 'Cerebral Arteries', 'Cerebrovascular Circulation', 'Female', 'Humans', 'Image Interpretation, Computer-Assisted', 'Magnetic Resonance Angiography', 'Male', 'Middle Aged', 'Oxygen', 'Reproducibility of Results', 'Sensitivity and Specificity']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,754,289 | Is a sheathless retrograde approach via the popliteal artery useful and safe for treating chronic total occlusions in the superficial femoral artery? | {
"contexts": [
"To compare the safety and success of a retrograde approach using a microcatheter vs. a sheath in the treatment of superficial femoral artery (SFA) chronic total occlusions (CTOs).",
"From April 2007 to December 2012, 188 consecutive patients underwent EVT for 229 de novo SFA CTOs using the retrograde approach in 68 patients (35 men; mean age 72 years). This cohort was divided into cases performed with a 4-F or 6-F sheath (n=28, 36 limbs) and those with a 2.1-F microcatheter (n=35, 49 limbs). The primary outcomes were mean time to hemostasis and number of intra- and postoperative puncture site complications, as well as the success of popliteal artery puncture, lesion crossing, and reperfusion.",
"There were no significant differences between two groups in baseline characteristics. PA puncture was successful in all limbs, and the success in crossing the lesion with the wire was not significantly different (91.9% in the sheath group vs. 89.8% in the microcatheter group). Mean time to hemostasis was 8.9±8.8 minutes in the microcatheter group vs. 47.7±13 minutes in the sheath group (p<0.0001). There was a significant difference in intraoperative and postoperative complications (22.2% in the sheath group vs. 2.0% in the microcatheter group, p=0.002)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Arterial Occlusive Diseases",
"Catheterization, Peripheral",
"Chronic Disease",
"Constriction, Pathologic",
"Endovascular Procedures",
"Equipment Design",
"Female",
"Femoral Artery",
"Humans",
"Male",
"Miniaturization",
"Popliteal Artery",
"Punctures",
"Retrospective Studies",
"Time Factors",
"Treatment Outcome",
"Vascular Access Devices"
]
} | Based on this retrospective analysis, the use of a microcatheter for SFA CTO retrograde access appears to be superior to 4-F or 6-F sheaths in terms of shorter time to hemostasis and fewer complications. | yes | [
{
"from": "human",
"value": "Question: Is a sheathless retrograde approach via the popliteal artery useful and safe for treating chronic total occlusions in the superficial femoral artery?\nContext: {'contexts': ['To compare the safety and success of a retrograde approach using a microcatheter vs. a sheath in the treatment of superficial femoral artery (SFA) chronic total occlusions (CTOs).', 'From April 2007 to December 2012, 188 consecutive patients underwent EVT for 229 de novo SFA CTOs using the retrograde approach in 68 patients (35 men; mean age 72 years). This cohort was divided into cases performed with a 4-F or 6-F sheath (n=28, 36 limbs) and those with a 2.1-F microcatheter (n=35, 49 limbs). The primary outcomes were mean time to hemostasis and number of intra- and postoperative puncture site complications, as well as the success of popliteal artery puncture, lesion crossing, and reperfusion.', 'There were no significant differences between two groups in baseline characteristics. PA puncture was successful in all limbs, and the success in crossing the lesion with the wire was not significantly different (91.9% in the sheath group vs. 89.8% in the microcatheter group). Mean time to hemostasis was 8.9±8.8 minutes in the microcatheter group vs. 47.7±13 minutes in the sheath group (p<0.0001). There was a significant difference in intraoperative and postoperative complications (22.2% in the sheath group vs. 2.0% in the microcatheter group, p=0.002).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Arterial Occlusive Diseases', 'Catheterization, Peripheral', 'Chronic Disease', 'Constriction, Pathologic', 'Endovascular Procedures', 'Equipment Design', 'Female', 'Femoral Artery', 'Humans', 'Male', 'Miniaturization', 'Popliteal Artery', 'Punctures', 'Retrospective Studies', 'Time Factors', 'Treatment Outcome', 'Vascular Access Devices']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,753,878 | Do identification of neonatal near miss by systematic screening for metabolic acidosis at birth? | {
"contexts": [
"To evaluate the relevance of systematic screening for neonatal metabolic acidosis at birth as part of perinatal audit.",
"For every baby, born in Ziekenhuis Oost Limburg, Genk Belgium between 1/1/2010 and 31/12/2010, cord blood was analysed to diagnose metabolic acidosis, defined as arterial or venous pH ≤ 7.05 or 7.17 respectively, in association with base excess of ≤ -10 mmol/L. Three observers identified indicators for suboptimal peripartal care with likely contribution to metabolic acidosis. In a multidisciplinary consensus meeting, these indicators were classified into 5 categories : (a) fetal monitoring error (b) labour management error, (c) instrumental vaginal delivery for fetal distress within 2 h of second stage, (d) non-obstetric medical complications, (e) preterm births or accidental cases at term.",
"In a total of 2117 neonates, there were 11 intra-uterine, 1 intrapartum and 3 early neonatal deaths, bringing early perinatal mortality rate at 7.1‰. Metabolic acidosis was identified in 23 (1.1%) babies, of which 21 (91.3%) left hospital in good clinical condition. Two babies (0.9‰), born in category c, had chronic neurologic symptoms."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": []
} | Systematic screening for neonatal metabolic acidosis caused a 2.5-fold increase of case identifications eligible for perinatal audit and opened perspectives towards rationalised improvement of perinatal care, in addition to the information obtained from cases of perinatal mortality. Next to indicators of perinatal mortality, perinatal audit programs should include neonatal metabolic acidosis as an extra parameter for quality assessment of perinatal care. | yes | [
{
"from": "human",
"value": "Question: Do identification of neonatal near miss by systematic screening for metabolic acidosis at birth?\nContext: {'contexts': ['To evaluate the relevance of systematic screening for neonatal metabolic acidosis at birth as part of perinatal audit.', 'For every baby, born in Ziekenhuis Oost Limburg, Genk Belgium between 1/1/2010 and 31/12/2010, cord blood was analysed to diagnose metabolic acidosis, defined as arterial or venous pH ≤ 7.05 or 7.17 respectively, in association with base excess of ≤ -10\\u2008mmol/L. Three observers identified indicators for suboptimal peripartal care with likely contribution to metabolic acidosis. In a multidisciplinary consensus meeting, these indicators were classified into 5 categories : (a) fetal monitoring error (b) labour management error, (c) instrumental vaginal delivery for fetal distress within 2\\u2008h of second stage, (d) non-obstetric medical complications, (e) preterm births or accidental cases at term.', 'In a total of 2117 neonates, there were 11 intra-uterine, 1 intrapartum and 3 early neonatal deaths, bringing early perinatal mortality rate at 7.1‰. Metabolic acidosis was identified in 23 (1.1%) babies, of which 21 (91.3%) left hospital in good clinical condition. Two babies (0.9‰), born in category c, had chronic neurologic symptoms.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,767,784 | Is low caregiver health literacy associated with higher pediatric emergency department use and nonurgent visits? | {
"contexts": [
"We sought to determine the association between low caregiver health literacy and child emergency department (ED) use, both the number and urgency of ED visits.",
"This year long cross-sectional study utilized the Newest Vital Sign questionnaire to measure the health literacy of caregivers accompanying children to a pediatric ED. Prior ED visits were extracted from a regional database. ED visit urgency was classified by resources utilized during the index ED visit. Regression analyses were used to model 2 outcomes-prior ED visits and ED visit urgency-stratified by chronic illness. Analyses were weighted by triage level.",
"Overall, 503 caregivers completed the study; 55% demonstrated low health literacy. Children of caregivers with low health literacy had more prior ED visits (adjusted incidence rate ratio 1.5; 95% confidence interval 1.2, 1.8) and increased odds of a nonurgent index ED visit (adjusted odds ratio 2.4; 95% confidence interval 1.3, 4.4). Among children without chronic illness, low caregiver health literacy was associated with an increased proportion of nonurgent index ED visits (48% vs. 22%; adjusted odds ratio 3.2; 1.8, 5.7)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Age Factors",
"Aged",
"Caregivers",
"Child",
"Child Health Services",
"Child, Preschool",
"Cross-Sectional Studies",
"Educational Status",
"Emergency Service, Hospital",
"Female",
"Health Literacy",
"Health Services Misuse",
"Humans",
"Infant",
"Insurance, Health",
"Male",
"Middle Aged",
"Severity of Illness Index",
"Young Adult"
]
} | Over half of caregivers presenting with their children to the ED have low health literacy. Low caregiver health literacy is an independent predictor of higher ED use and use of the ED for nonurgent conditions. In children without a chronic illness, low health literate caregivers had more than 3 times greater odds of presenting for a nonurgent condition than those with adequate health literacy. | yes | [
{
"from": "human",
"value": "Question: Is low caregiver health literacy associated with higher pediatric emergency department use and nonurgent visits?\nContext: {'contexts': ['We sought to determine the association between low caregiver health literacy and child emergency department (ED) use, both the number and urgency of ED visits.', 'This year long cross-sectional study utilized the Newest Vital Sign questionnaire to measure the health literacy of caregivers accompanying children to a pediatric ED. Prior ED visits were extracted from a regional database. ED visit urgency was classified by resources utilized during the index ED visit. Regression analyses were used to model 2 outcomes-prior ED visits and ED visit urgency-stratified by chronic illness. Analyses were weighted by triage level.', 'Overall, 503 caregivers completed the study; 55% demonstrated low health literacy. Children of caregivers with low health literacy had more prior ED visits (adjusted incidence rate ratio 1.5; 95% confidence interval 1.2, 1.8) and increased odds of a nonurgent index ED visit (adjusted odds ratio 2.4; 95% confidence interval 1.3, 4.4). Among children without chronic illness, low caregiver health literacy was associated with an increased proportion of nonurgent index ED visits (48% vs. 22%; adjusted odds ratio 3.2; 1.8, 5.7).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Age Factors', 'Aged', 'Caregivers', 'Child', 'Child Health Services', 'Child, Preschool', 'Cross-Sectional Studies', 'Educational Status', 'Emergency Service, Hospital', 'Female', 'Health Literacy', 'Health Services Misuse', 'Humans', 'Infant', 'Insurance, Health', 'Male', 'Middle Aged', 'Severity of Illness Index', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,760,104 | Does inducible nitric oxide synthase inhibition reverse pulmonary arterial dysfunction in lung transplantation? | {
"contexts": [
"Ischemia-reperfusion injury (IRI) after lung transplantation remains a significant cause of morbidity and mortality. Lung IRI induces nitric oxide synthesis (iNOS) and reactive nitrogen species, decreasing nitric oxide bioavailability. We hypothesized that ischemia-induced iNOS intensifies with reperfusion and contributes to IRI-induced pulmonary arterial regulatory dysfunction, which may lead to early graft failure and cause pulmonary edema. The aim of this study was to determine whether ischemia-reperfusion alters inducible and endothelial nitric oxide synthase expression, potentially affecting pulmonary perfusion. We further evaluated the role of iNOS in post-transplantation pulmonary arterial disorder.",
"We randomized 32 Sprague-Dawley rats into two groups. The control group was given a sham operation whilst the experimental group received orthotropic lung transplants with a modified three-cuff technique. Changes in lung iNOS, and endothelial nitric oxide synthase expression were measured after lung transplantation by enzyme-linked immunosorbent assay (ELISA). Vasoconstriction in response to exogenous phenylephrine and vasodilation in response to exogenous acetylcholine of pulmonary arterial rings were measured in vitro as a measure of vascular dysfunction. To elucidate the roles of iNOS in regulating vascular function, an iNOS activity inhibitor (N6-(1-iminoethyl)-L-lysine, L-NIL) was used to treat isolated arterial rings. In order to test whether iNOS inhibition has a therapeutic effect, we further used L-NIL to pre-treat transplanted lungs and then measured post-transplantation arterial responses.",
"Lung transplantation caused upregulation of iNOS expression. This was also accompanied by suppression of both vasoconstriction and vasodilation of arterial rings from transplanted lungs. Removal of endothelium did not interfere with the contraction of pulmonary arterial rings from transplanted lungs. In contrast, iNOS inhibition rescued the vasoconstriction response to exogenous phenylephrine of pulmonary arterial rings from transplanted lungs. In addition, lung transplantation led to suppression of PaO2/FiO2 ratio, increased intrapulmonary shunt (Q s/Q t), and increase of lung wet to dry ratio (W/D), malondialdehyde and myeloperoxidase levels, all of which were reversed upon iNOS inhibition. Furthermore, inhibition of iNOS significantly rescued vascular function and alleviated edema and inflammatory cell infiltration in the transplanted lung."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"In Vitro Techniques",
"Lung",
"Lung Transplantation",
"Lysine",
"Male",
"Malondialdehyde",
"Nitric Oxide Synthase Type II",
"Nitric Oxide Synthase Type III",
"Peroxidase",
"Phenylephrine",
"Pulmonary Artery",
"Rats, Sprague-Dawley",
"Reperfusion Injury",
"Vasoconstriction",
"Vasodilation"
]
} | Our data suggest that lung transplantation causes upregulation of iNOS expression, and pulmonary vascular dysfunction. iNOS inhibition reverses the post-transplantational pulmonary vascular dysfunction. | yes | [
{
"from": "human",
"value": "Question: Does inducible nitric oxide synthase inhibition reverse pulmonary arterial dysfunction in lung transplantation?\nContext: {'contexts': ['Ischemia-reperfusion injury (IRI) after lung transplantation remains a significant cause of morbidity and mortality. Lung IRI induces nitric oxide synthesis (iNOS) and reactive nitrogen species, decreasing nitric oxide bioavailability. We hypothesized that ischemia-induced iNOS intensifies with reperfusion and contributes to IRI-induced pulmonary arterial regulatory dysfunction, which may lead to early graft failure and cause pulmonary edema. The aim of this study was to determine whether ischemia-reperfusion alters inducible and endothelial nitric oxide synthase expression, potentially affecting pulmonary perfusion. We further evaluated the role of iNOS in post-transplantation pulmonary arterial disorder.', 'We randomized 32 Sprague-Dawley rats into two groups. The control group was given a sham operation whilst the experimental group received orthotropic lung transplants with a modified three-cuff technique. Changes in lung iNOS, and endothelial nitric oxide synthase expression were measured after lung transplantation by enzyme-linked immunosorbent assay (ELISA). Vasoconstriction in response to exogenous phenylephrine and vasodilation in response to exogenous acetylcholine of pulmonary arterial rings were measured in vitro as a measure of vascular dysfunction. To elucidate the roles of iNOS in regulating vascular function, an iNOS activity inhibitor (N6-(1-iminoethyl)-L-lysine, L-NIL) was used to treat isolated arterial rings. In order to test whether iNOS inhibition has a therapeutic effect, we further used L-NIL to pre-treat transplanted lungs and then measured post-transplantation arterial responses.', 'Lung transplantation caused upregulation of iNOS expression. This was also accompanied by suppression of both vasoconstriction and vasodilation of arterial rings from transplanted lungs. Removal of endothelium did not interfere with the contraction of pulmonary arterial rings from transplanted lungs. In contrast, iNOS inhibition rescued the vasoconstriction response to exogenous phenylephrine of pulmonary arterial rings from transplanted lungs. In addition, lung transplantation led to suppression of PaO2/FiO2 ratio, increased intrapulmonary shunt (Q s/Q t), and increase of lung wet to dry ratio (W/D), malondialdehyde and myeloperoxidase levels, all of which were reversed upon iNOS inhibition. Furthermore, inhibition of iNOS significantly rescued vascular function and alleviated edema and inflammatory cell infiltration in the transplanted lung.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'In Vitro Techniques', 'Lung', 'Lung Transplantation', 'Lysine', 'Male', 'Malondialdehyde', 'Nitric Oxide Synthase Type II', 'Nitric Oxide Synthase Type III', 'Peroxidase', 'Phenylephrine', 'Pulmonary Artery', 'Rats, Sprague-Dawley', 'Reperfusion Injury', 'Vasoconstriction', 'Vasodilation']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,768,758 | Do iFNL3 polymorphisms predict response to therapy in chronic hepatitis C genotype 2/3 infection? | {
"contexts": [
"Single nucleotide polymorphisms (SNPs) near the interferon lambda 3 (IFNL3, previously known as IL28B) region are the strongest baseline predictors of sustained virologic response (SVR) to pegylated interferon and ribavirin therapy in hepatitis C virus (HCV) genotype 1 infection. Whether IFNL3 SNPs influence treatment response in genotype 2 and 3 (HCV-2/3) infection remains controversial. This study sought to clarify in a large cohort, whether SNPs in the IFNL3 region are associated with treatment response in HCV-2/3 patients.",
"The cohort comprised 1002 HCV-2/3 Caucasians patients treated with pegylated interferon-alpha and ribavirin who underwent genotyping for the SNPs rs12979860 and rs8099917.",
"Overall, 736 (73.5%) patients achieved SVR (81.9%, 67.9%, and 57.8% for rs12979860 CC, CT, and TT [p = 0.0001]; 78%, 68.7%, and 46.3% for rs8099917 TT, TG, and GG [p = 0.0001]). By logistic regression, both rs12979860 CC and rs8099917 TT were independent predictors of SVR with an odds ratio (OR) of 2.39 (1.19-3.81) p = 0.0001 and OR 1.85 (1.15-2.23) p = 0.0001, respectively. IFNL3 responder genotypes were more frequent in relapsers than null-responders (p = 0.0001 for both SNPs). On-treatment rapid virological response (RVR) was predictive of SVR only in those individuals with IFNL3 non-responder genotypes (rs12979860 CT/TT and rs8099917 TG/GG)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Female",
"Genotype",
"Hepacivirus",
"Hepatitis C, Chronic",
"Humans",
"Interleukins",
"Male",
"Middle Aged",
"Polymorphism, Single Nucleotide"
]
} | This adequately powered study in patients with HCV genotypes 2 or 3 infection clearly demonstrates that IFNL3 genotypes are the strongest baseline predictor of SVR, in keeping with the known association for genotype 1 infection. IFNL3 genotyping can aid in therapeutic decision making for these patients. | yes | [
{
"from": "human",
"value": "Question: Do iFNL3 polymorphisms predict response to therapy in chronic hepatitis C genotype 2/3 infection?\nContext: {'contexts': ['Single nucleotide polymorphisms (SNPs) near the interferon lambda 3 (IFNL3, previously known as IL28B) region are the strongest baseline predictors of sustained virologic response (SVR) to pegylated interferon and ribavirin therapy in hepatitis C virus (HCV) genotype 1 infection. Whether IFNL3 SNPs influence treatment response in genotype 2 and 3 (HCV-2/3) infection remains controversial. This study sought to clarify in a large cohort, whether SNPs in the IFNL3 region are associated with treatment response in HCV-2/3 patients.', 'The cohort comprised 1002 HCV-2/3 Caucasians patients treated with pegylated interferon-alpha and ribavirin who underwent genotyping for the SNPs rs12979860 and rs8099917.', 'Overall, 736 (73.5%) patients achieved SVR (81.9%, 67.9%, and 57.8% for rs12979860 CC, CT, and TT [p = 0.0001]; 78%, 68.7%, and 46.3% for rs8099917 TT, TG, and GG [p = 0.0001]). By logistic regression, both rs12979860 CC and rs8099917 TT were independent predictors of SVR with an odds ratio (OR) of 2.39 (1.19-3.81) p = 0.0001 and OR 1.85 (1.15-2.23) p = 0.0001, respectively. IFNL3 responder genotypes were more frequent in relapsers than null-responders (p = 0.0001 for both SNPs). On-treatment rapid virological response (RVR) was predictive of SVR only in those individuals with IFNL3 non-responder genotypes (rs12979860 CT/TT and rs8099917 TG/GG).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Female', 'Genotype', 'Hepacivirus', 'Hepatitis C, Chronic', 'Humans', 'Interleukins', 'Male', 'Middle Aged', 'Polymorphism, Single Nucleotide']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,756,473 | Does gSH protect against oxidative stress and toxicity in VL-17A cells exposed to high glucose? | {
"contexts": [
"The deficiency of glutathione (GSH) has been linked to several diseases. The study investigated the role of GSH as a protective factor against hyperglycemia-mediated injury in VL-17A cells treated with 50 mM glucose.",
"The cell viability and different oxidative stress parameters including glyoxalase I activity were measured.",
"GSH supplementation with 2 mM N-acetyl cysteine (NAC) or 0.1 mM ursodeoxycholic acid (UDCA) increased the viability, GSH level and the GSH-dependent glyoxalase I activity in 50 mM glucose-treated VL-17A cells. Further, pretreatment of 50 mM glucose-treated VL-17A cells with NAC or UDCA decreased oxidative stress (levels of reactive oxygen species and protein carbonylation), apoptosis (caspase 3 activity and annexin V-propidium iodide positive cells) and glutathionylated protein formation, a measure of oxidative stress. GSH depletion with 0.4 mM buthionine sulfoximine (BSO) or 1 mM diethyl maleate (DEM) potentiated the decrease in viability, glyoxalase I activity and increase in oxidative stress and apoptosis, with decreased GSH levels in 50 mM glucose-treated VL-17A cells."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Acetylcysteine",
"Alcohol Dehydrogenase",
"Antimetabolites",
"Antioxidants",
"Apoptosis",
"Buthionine Sulfoximine",
"Cell Survival",
"Clone Cells",
"Cytochrome P-450 CYP2E1",
"Glucose",
"Glutathione",
"Hep G2 Cells",
"Hepatocytes",
"Humans",
"Hyperglycemia",
"Lactoylglutathione Lyase",
"Maleates",
"Oxidative Stress",
"Reactive Oxygen Species",
"Recombinant Proteins",
"Ursodeoxycholic Acid"
]
} | Thus, changes in GSH levels with exogenous agents such as NAC, UDCA, BSO or DEM modulate hyperglycemia-mediated injury in a cell model of VL-17A liver cells. | yes | [
{
"from": "human",
"value": "Question: Does gSH protect against oxidative stress and toxicity in VL-17A cells exposed to high glucose?\nContext: {'contexts': ['The deficiency of glutathione (GSH) has been linked to several diseases. The study investigated the role of GSH as a protective factor against hyperglycemia-mediated injury in VL-17A cells treated with 50 mM glucose.', 'The cell viability and different oxidative stress parameters including glyoxalase I activity were measured.', 'GSH supplementation with 2 mM N-acetyl cysteine (NAC) or 0.1 mM ursodeoxycholic acid (UDCA) increased the viability, GSH level and the GSH-dependent glyoxalase I activity in 50 mM glucose-treated VL-17A cells. Further, pretreatment of 50 mM glucose-treated VL-17A cells with NAC or UDCA decreased oxidative stress (levels of reactive oxygen species and protein carbonylation), apoptosis (caspase 3 activity and annexin V-propidium iodide positive cells) and glutathionylated protein formation, a measure of oxidative stress. GSH depletion with 0.4 mM buthionine sulfoximine (BSO) or 1 mM diethyl maleate (DEM) potentiated the decrease in viability, glyoxalase I activity and increase in oxidative stress and apoptosis, with decreased GSH levels in 50 mM glucose-treated VL-17A cells.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Acetylcysteine', 'Alcohol Dehydrogenase', 'Antimetabolites', 'Antioxidants', 'Apoptosis', 'Buthionine Sulfoximine', 'Cell Survival', 'Clone Cells', 'Cytochrome P-450 CYP2E1', 'Glucose', 'Glutathione', 'Hep G2 Cells', 'Hepatocytes', 'Humans', 'Hyperglycemia', 'Lactoylglutathione Lyase', 'Maleates', 'Oxidative Stress', 'Reactive Oxygen Species', 'Recombinant Proteins', 'Ursodeoxycholic Acid']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,774,224 | Is down-regulation of sirtuin 3 associated with poor prognosis in hepatocellular carcinoma after resection? | {
"contexts": [
"Sirtuin 3 (Sirt3), one of the seven Sirtuins family members, plays critical roles in the progression of multiple cancer types. However, its role in the prognosis of hepatocellular carcinoma (HCC) has not yet been investigated systematically.",
"The correlation of Sirtuins expression with prognosis of HCC was determined by immunohistochemistry (IHC) in a large HCC patient cohort (n = 342). Expression of Sirt3 in tumoral and peritumoral tissues of HCC patients were further determined by western blotting (WB).",
"IHC and WB studies both showed a decreased expression of Sirt3 in tumoral tissues compared with peritumoral tissues (P = 0.003 for IHC, P = 0.0042 for WB). Decreased expression of Sirt3 in both tumoral and peritumoral tissues was associated with increased recurrence probability and decreased overall survival rate by univariate analyses (intratumoral Sirt3: P = 0.011 for TTR, P = 0.001 for OS; peritumoral Sirt3: P = 0.017 for TTR, P = 0.023 for OS), the prognostic value was strengthened by multivariate analyses (intratumoral Sirt3: P = 0.031 for TTR, P = 0.001 for OS; peritumoral Sirt3: P = 0.047 for TTR, P = 0.031 for OS). Intratumoral Sirt3 also showed a favorable prognostic value in patients with BCLC stage A (TTR, P = 0.011; OS, P < 0.001). In addition, we found that IHC studies of other sirtuin members showed a decreased expression of Sirt2, Sirt4 and Sirt5 and an increased expression of Sirt1, Sirt6 and Sirt7 in intratumoral tissues compared with peritumoral tissues. In contrast to Sirt3, other members did not showed a remarkable correlation with HCC prognosis."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Aged",
"Carcinoma, Hepatocellular",
"Child",
"Female",
"Gene Expression Regulation, Neoplastic",
"Humans",
"Liver Neoplasms",
"Male",
"Middle Aged",
"Neoplasm Recurrence, Local",
"Prognosis",
"Sirtuin 3",
"Survival Rate"
]
} | Down-regulation of intratumoral and peritumoral Sirt3 were both associated with poor outcome in HCC, moreover, intratumoral Sirt3 was a favorable prognostic predictor in early stage patients. | yes | [
{
"from": "human",
"value": "Question: Is down-regulation of sirtuin 3 associated with poor prognosis in hepatocellular carcinoma after resection?\nContext: {'contexts': ['Sirtuin 3 (Sirt3), one of the seven Sirtuins family members, plays critical roles in the progression of multiple cancer types. However, its role in the prognosis of hepatocellular carcinoma (HCC) has not yet been investigated systematically.', 'The correlation of Sirtuins expression with prognosis of HCC was determined by immunohistochemistry (IHC) in a large HCC patient cohort (n = 342). Expression of Sirt3 in tumoral and peritumoral tissues of HCC patients were further determined by western blotting (WB).', 'IHC and WB studies both showed a decreased expression of Sirt3 in tumoral tissues compared with peritumoral tissues (P = 0.003 for IHC, P = 0.0042 for WB). Decreased expression of Sirt3 in both tumoral and peritumoral tissues was associated with increased recurrence probability and decreased overall survival rate by univariate analyses (intratumoral Sirt3: P = 0.011 for TTR, P = 0.001 for OS; peritumoral Sirt3: P = 0.017 for TTR, P = 0.023 for OS), the prognostic value was strengthened by multivariate analyses (intratumoral Sirt3: P = 0.031 for TTR, P = 0.001 for OS; peritumoral Sirt3: P = 0.047 for TTR, P = 0.031 for OS). Intratumoral Sirt3 also showed a favorable prognostic value in patients with BCLC stage A (TTR, P = 0.011; OS, P < 0.001). In addition, we found that IHC studies of other sirtuin members showed a decreased expression of Sirt2, Sirt4 and Sirt5 and an increased expression of Sirt1, Sirt6 and Sirt7 in intratumoral tissues compared with peritumoral tissues. In contrast to Sirt3, other members did not showed a remarkable correlation with HCC prognosis.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Aged', 'Carcinoma, Hepatocellular', 'Child', 'Female', 'Gene Expression Regulation, Neoplastic', 'Humans', 'Liver Neoplasms', 'Male', 'Middle Aged', 'Neoplasm Recurrence, Local', 'Prognosis', 'Sirtuin 3', 'Survival Rate']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,771,846 | Does a melanoma cell state distinction influence sensitivity to MAPK pathway inhibitors? | {
"contexts": [
"Most melanomas harbor oncogenic BRAF(V600) mutations, which constitutively activate the MAPK pathway. Although MAPK pathway inhibitors show clinical benefit in BRAF(V600)-mutant melanoma, it remains incompletely understood why 10% to 20% of patients fail to respond. Here, we show that RAF inhibitor-sensitive and inhibitor-resistant BRAF(V600)-mutant melanomas display distinct transcriptional profiles. Whereas most drug-sensitive cell lines and patient biopsies showed high expression and activity of the melanocytic lineage transcription factor MITF, intrinsically resistant cell lines and biopsies displayed low MITF expression but higher levels of NF-κB signaling and the receptor tyrosine kinase AXL. In vitro, these MITF-low/NF-κB-high melanomas were resistant to inhibition of RAF and MEK, singly or in combination, and ERK. Moreover, in cell lines, NF-κB activation antagonized MITF expression and induced both resistance marker genes and drug resistance. Thus, distinct cell states characterized by MITF or NF-κB activity may influence intrinsic resistance to MAPK pathway inhibitors in BRAF(V600)-mutant melanoma."
],
"labels": [
"UNLABELLED"
],
"meshes": [
"Anilides",
"Benzimidazoles",
"Benzocycloheptenes",
"Cell Line, Tumor",
"Cells, Cultured",
"Drug Resistance, Neoplasm",
"Gene Expression Regulation, Neoplastic",
"Hepatocyte Growth Factor",
"Humans",
"Indoles",
"MAP Kinase Signaling System",
"Melanocytes",
"Melanoma",
"Microphthalmia-Associated Transcription Factor",
"NF-kappa B p50 Subunit",
"Protein Kinase Inhibitors",
"Proto-Oncogene Proteins B-raf",
"Proto-Oncogene Proteins c-met",
"Pyridines",
"Quinolines",
"Sulfonamides",
"Triazoles"
]
} | Although most BRAF(V600)-mutant melanomas are sensitive to RAF and/or MEK inhibitors, a subset fails to respond to such treatment. This study characterizes a transcriptional cell state distinction linked to MITF and NF-κB that may modulate intrinsic sensitivity of melanomas to MAPK pathway inhibitors. | yes | [
{
"from": "human",
"value": "Question: Does a melanoma cell state distinction influence sensitivity to MAPK pathway inhibitors?\nContext: {'contexts': ['Most melanomas harbor oncogenic BRAF(V600) mutations, which constitutively activate the MAPK pathway. Although MAPK pathway inhibitors show clinical benefit in BRAF(V600)-mutant melanoma, it remains incompletely understood why 10% to 20% of patients fail to respond. Here, we show that RAF inhibitor-sensitive and inhibitor-resistant BRAF(V600)-mutant melanomas display distinct transcriptional profiles. Whereas most drug-sensitive cell lines and patient biopsies showed high expression and activity of the melanocytic lineage transcription factor MITF, intrinsically resistant cell lines and biopsies displayed low MITF expression but higher levels of NF-κB signaling and the receptor tyrosine kinase AXL. In vitro, these MITF-low/NF-κB-high melanomas were resistant to inhibition of RAF and MEK, singly or in combination, and ERK. Moreover, in cell lines, NF-κB activation antagonized MITF expression and induced both resistance marker genes and drug resistance. Thus, distinct cell states characterized by MITF or NF-κB activity may influence intrinsic resistance to MAPK pathway inhibitors in BRAF(V600)-mutant melanoma.'], 'labels': ['UNLABELLED'], 'meshes': ['Anilides', 'Benzimidazoles', 'Benzocycloheptenes', 'Cell Line, Tumor', 'Cells, Cultured', 'Drug Resistance, Neoplasm', 'Gene Expression Regulation, Neoplastic', 'Hepatocyte Growth Factor', 'Humans', 'Indoles', 'MAP Kinase Signaling System', 'Melanocytes', 'Melanoma', 'Microphthalmia-Associated Transcription Factor', 'NF-kappa B p50 Subunit', 'Protein Kinase Inhibitors', 'Proto-Oncogene Proteins B-raf', 'Proto-Oncogene Proteins c-met', 'Pyridines', 'Quinolines', 'Sulfonamides', 'Triazoles']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,768,059 | Is application of a Scale for the Assessment and Rating of Ataxia ( SARA ) in Friedreich 's ataxia patients according to posturography limited? | {
"contexts": [
"A scale for the Assessment and Rating of Ataxia (SARA) was developed for evaluation of autosomal dominant cerebellar ataxias (ADCA) and was also recommended for clinical trials of Friedreich's ataxia patients (FRDA). FRDA, unlike ADCA, is characterized as being a sensory type of ataxia for which the disease-specific Friedreich ataxia rating scale (FARS) was developed. The objective of this study was to determine whether SARA and FARS scores are associated with posturographic parameters in FRDA patients.",
"Adult patients with genetically confirmed FRDA (n=11) and ADCA (n=13) were evaluated by SARA, FARS and posturography.",
"FRDA patients' postural stability parameters, in stance with visual control, correlated with balance impairment in FARS (r=0.622; p<0.05) and SARA (r=0.735; p<0.05). Without visual control, only FARS correlated with balance impairment (r=0.732; p<0.05)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Ataxins",
"Child",
"Female",
"Friedreich Ataxia",
"Humans",
"Male",
"Middle Aged",
"Nerve Tissue Proteins",
"Postural Balance",
"Posture",
"Severity of Illness Index",
"Statistics, Nonparametric",
"Young Adult"
]
} | The SARA, in FRDA patients, correlates with stance with visual control but not without visual control which emphasizes sensory ataxia. This suggests that application of the SARA in Friedreich's ataxia patients according to posturography is possible but presumably limited and FARS, although being a more time consuming scale, may have advantages over SARA in FRDA patients. | yes | [
{
"from": "human",
"value": "Question: Is application of a Scale for the Assessment and Rating of Ataxia ( SARA ) in Friedreich 's ataxia patients according to posturography limited?\nContext: {'contexts': [\"A scale for the Assessment and Rating of Ataxia (SARA) was developed for evaluation of autosomal dominant cerebellar ataxias (ADCA) and was also recommended for clinical trials of Friedreich's ataxia patients (FRDA). FRDA, unlike ADCA, is characterized as being a sensory type of ataxia for which the disease-specific Friedreich ataxia rating scale (FARS) was developed. The objective of this study was to determine whether SARA and FARS scores are associated with posturographic parameters in FRDA patients.\", 'Adult patients with genetically confirmed FRDA (n=11) and ADCA (n=13) were evaluated by SARA, FARS and posturography.', \"FRDA patients' postural stability parameters, in stance with visual control, correlated with balance impairment in FARS (r=0.622; p<0.05) and SARA (r=0.735; p<0.05). Without visual control, only FARS correlated with balance impairment (r=0.732; p<0.05).\"], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Ataxins', 'Child', 'Female', 'Friedreich Ataxia', 'Humans', 'Male', 'Middle Aged', 'Nerve Tissue Proteins', 'Postural Balance', 'Posture', 'Severity of Illness Index', 'Statistics, Nonparametric', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,775,920 | Does continuous theta-burst stimulation over primary somatosensory cortex modulate short-latency afferent inhibition? | {
"contexts": [
"The present study investigated the effects of continuous theta-burst stimulation (cTBS) over primary somatosensory (SI) and motor (M1) cortices on motor-evoked potentials (MEPs) and short-latency afferent inhibition (SAI).",
"MEPs and SAI were recorded from the first dorsal interosseous (FDI) muscle of the right hand following 30Hz cTBS over left-hemisphere SI and M1 delivered to the same participants in separate sessions. Measurements were taken before and up to 60min following cTBS.",
"CTBS over M1 suppressed MEPs and did not alter SAI. In contrast cTBS over SI facilitated MEPs and decreased median and digital nerve evoked SAI."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Electromyography",
"Evoked Potentials, Motor",
"Female",
"Hand",
"Humans",
"Learning",
"Male",
"Motor Cortex",
"Muscle, Skeletal",
"Somatosensory Cortex",
"Transcranial Magnetic Stimulation",
"Young Adult"
]
} | These findings indicate that SAI amplitude is influenced by cTBS over SI but not M1, suggesting an important role for SI in the modulation of this circuit. These data provide further evidence that cTBS over SI versus M1 has opposite effects on corticospinal excitability. | yes | [
{
"from": "human",
"value": "Question: Does continuous theta-burst stimulation over primary somatosensory cortex modulate short-latency afferent inhibition?\nContext: {'contexts': ['The present study investigated the effects of continuous theta-burst stimulation (cTBS) over primary somatosensory (SI) and motor (M1) cortices on motor-evoked potentials (MEPs) and short-latency afferent inhibition (SAI).', 'MEPs and SAI were recorded from the first dorsal interosseous (FDI) muscle of the right hand following 30Hz cTBS over left-hemisphere SI and M1 delivered to the same participants in separate sessions. Measurements were taken before and up to 60min following cTBS.', 'CTBS over M1 suppressed MEPs and did not alter SAI. In contrast cTBS over SI facilitated MEPs and decreased median and digital nerve evoked SAI.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Electromyography', 'Evoked Potentials, Motor', 'Female', 'Hand', 'Humans', 'Learning', 'Male', 'Motor Cortex', 'Muscle, Skeletal', 'Somatosensory Cortex', 'Transcranial Magnetic Stimulation', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,770,620 | Does reduced hepatic arterial perfusion impair the recovery from focal hepatic venous outflow obstruction in liver-resected rats? | {
"contexts": [
"Extended partial hepatectomy (PH) in patients is leading to portal hyperperfusion but reduced hepatic arterial perfusion (HAP), and is invariably causing focal hepatic venous outflow obstruction (FHVOO). We observed in a rat model that PH in combination with right median hepatic vein ligation (RMHV-L) caused confluent parenchymal necrosis interspersed with viable portal tracts in the obstructed territory and large sinusoidal vascular canals in the border zone. Lack of HAP impaired the spontaneous course of recovery in terms of enlarged parenchymal necrosis, delayed regeneration, and the absence of draining vascular canals. We aimed to investigate whether pharmacological intervention modulates the imbalance between portal venous and hepatic arterial inflow, aggravates the liver damage, and delays the recovery process after FHVOO in liver-resected rats.",
"Male Lewis rats were subjected to 70% PH and RMHV-L. Molsidomine or NG-nitro-L-arginine methyl ester (L-NAME) or saline were applied daily. Hepatic damage, microcirculation, regeneration, and vascular remodeling were evaluated at postoperative days 1, 2, and 7. Animals subjected to RMHV-L only were used as \"no HAP\" control.",
"Significant increase of portal venous inflow with a concomitant decrease in HAP was observed in all groups after PH. Molsidomine treatment did neither affect hepatic hemodynamics nor the spontaneous recovery. In contrast, L-NAME treatment further decreased HAP which impaired hepatic microcirculation, aggravated parenchymal damage, decelerated recovery, and impaired the formation of sinusoidal canals."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Budd-Chiari Syndrome",
"Disease Models, Animal",
"Hepatectomy",
"Hepatic Artery",
"Hepatic Veins",
"Liver",
"Liver Circulation",
"Liver Regeneration",
"Male",
"Necrosis",
"Perfusion",
"Rats",
"Rats, Inbred Lew",
"Regional Blood Flow"
]
} | Reduction of HAP through inhibition of nitric oxide production worsened the recovery from FHVOO. Drugs increasing HAP need to be evaluated to reverse the hyperperfusion-induced impairment of the spontaneous course after FHVOO. | yes | [
{
"from": "human",
"value": "Question: Does reduced hepatic arterial perfusion impair the recovery from focal hepatic venous outflow obstruction in liver-resected rats?\nContext: {'contexts': ['Extended partial hepatectomy (PH) in patients is leading to portal hyperperfusion but reduced hepatic arterial perfusion (HAP), and is invariably causing focal hepatic venous outflow obstruction (FHVOO). We observed in a rat model that PH in combination with right median hepatic vein ligation (RMHV-L) caused confluent parenchymal necrosis interspersed with viable portal tracts in the obstructed territory and large sinusoidal vascular canals in the border zone. Lack of HAP impaired the spontaneous course of recovery in terms of enlarged parenchymal necrosis, delayed regeneration, and the absence of draining vascular canals. We aimed to investigate whether pharmacological intervention modulates the imbalance between portal venous and hepatic arterial inflow, aggravates the liver damage, and delays the recovery process after FHVOO in liver-resected rats.', 'Male Lewis rats were subjected to 70% PH and RMHV-L. Molsidomine or NG-nitro-L-arginine methyl ester (L-NAME) or saline were applied daily. Hepatic damage, microcirculation, regeneration, and vascular remodeling were evaluated at postoperative days 1, 2, and 7. Animals subjected to RMHV-L only were used as \"no HAP\" control.', 'Significant increase of portal venous inflow with a concomitant decrease in HAP was observed in all groups after PH. Molsidomine treatment did neither affect hepatic hemodynamics nor the spontaneous recovery. In contrast, L-NAME treatment further decreased HAP which impaired hepatic microcirculation, aggravated parenchymal damage, decelerated recovery, and impaired the formation of sinusoidal canals.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Budd-Chiari Syndrome', 'Disease Models, Animal', 'Hepatectomy', 'Hepatic Artery', 'Hepatic Veins', 'Liver', 'Liver Circulation', 'Liver Regeneration', 'Male', 'Necrosis', 'Perfusion', 'Rats', 'Rats, Inbred Lew', 'Regional Blood Flow']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,770,628 | Does enriched environment prevent cognitive and motor deficits associated with postnatal MK-801 treatment? | {
"contexts": [
"Previous studies have shown the beneficial effects of enriched environment (EE) in rescuing behavioral deficits such as pre-pulse inhibition and locomotor hyperactivity associated with N-methyl-D-aspartate (NMDA) receptor blockade; however, cognitive deficits remain unresponsive.",
"We designed experiments to determine the consequences of raising rat pups in an EE on several behavioral aberrations, mainly cognitive deficits, observed in rats postnatally exposed to MK-801 (NMDA receptor antagonist).",
"Male Wistar rats were injected with MK-801 (1 mg/kg) from postnatal day (P) 6-10. Rat pups were housed in an EE from birth up to the time of behavioral experiments at P28-34. The effects of EE in correcting MK-801-associated behaviors were assessed by rotarod, wire grip, open filed, and Morris water maze tests.",
"We found that EE not only has beneficial effects on cognitive performance of normal rats but also prevents spatial learning and memory deficits in Morris water maze induced by MK-801. Postnatal MK-801 treatment also led to motor deficits both in wire grip and accelerating rotarod tests. These deficits were not observed in MK-801-treated rats raised in EE. In the open field test, EE prevented increase in \"frequency of grooming\" and decrease in \"time spent in the center\" associated with MK-801."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Behavior, Animal",
"Cognition Disorders",
"Dizocilpine Maleate",
"Environment",
"Excitatory Amino Acid Antagonists",
"Male",
"Motor Activity",
"Rats",
"Rats, Wistar",
"Receptors, N-Methyl-D-Aspartate"
]
} | Our results suggest that exposure to an EE would be strongly beneficial in correcting deficits, notably cognitive, associated with MK-801. Given that the postnatal MK-801 treatment represents an animal model of schizophrenia, we propose timely environmental interventions might be an effective strategy in the protection against schizophrenia. | yes | [
{
"from": "human",
"value": "Question: Does enriched environment prevent cognitive and motor deficits associated with postnatal MK-801 treatment?\nContext: {'contexts': ['Previous studies have shown the beneficial effects of enriched environment (EE) in rescuing behavioral deficits such as pre-pulse inhibition and locomotor hyperactivity associated with N-methyl-D-aspartate (NMDA) receptor blockade; however, cognitive deficits remain unresponsive.', 'We designed experiments to determine the consequences of raising rat pups in an EE on several behavioral aberrations, mainly cognitive deficits, observed in rats postnatally exposed to MK-801 (NMDA receptor antagonist).', 'Male Wistar rats were injected with MK-801 (1\\xa0mg/kg) from postnatal day (P) 6-10. Rat pups were housed in an EE from birth up to the time of behavioral experiments at P28-34. The effects of EE in correcting MK-801-associated behaviors were assessed by rotarod, wire grip, open filed, and Morris water maze tests.', 'We found that EE not only has beneficial effects on cognitive performance of normal rats but also prevents spatial learning and memory deficits in Morris water maze induced by MK-801. Postnatal MK-801 treatment also led to motor deficits both in wire grip and accelerating rotarod tests. These deficits were not observed in MK-801-treated rats raised in EE. In the open field test, EE prevented increase in \"frequency of grooming\" and decrease in \"time spent in the center\" associated with MK-801.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Behavior, Animal', 'Cognition Disorders', 'Dizocilpine Maleate', 'Environment', 'Excitatory Amino Acid Antagonists', 'Male', 'Motor Activity', 'Rats', 'Rats, Wistar', 'Receptors, N-Methyl-D-Aspartate']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,764,137 | Is nitric-oxide-mediated cell death triggered by chitosan in Fusarium eumartii spores? | {
"contexts": [
"The genus Fusarium comprises a heterogeneous group of fungi important for agriculture. Fusarium solani f. sp. eumartii (F. eumartii), historically considered to be a fungal pathogen of potato, has also been associated with tomato disease. Currently, chitosan and its derivatives have been receiving more attention as environmentally friendly antimicrobial compounds in sustainable practices. The aim of the present work was to characterize downstream events associated with the mode of action of chitosan, including nitrosative reactive species, in order to identify new biomarkers of its cytotoxic action.",
"Data indicated that chitosan-mediated nitric oxide (NO) production might lead to conidial death, concomitant with the strong reduction in fungal pathogenicity in tomato plants. Following chitosan applications, a notably dose-dependent reduction in conidial viability was demonstrated in F. eumartii. Thereafter, the infectivity of chitosan-treated spores was tested by a bioassay using tomato seedlings."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Cell Death",
"Chitosan",
"Fungicides, Industrial",
"Fusarium",
"Lycopersicon esculentum",
"Nitric Oxide",
"Plant Diseases",
"Spores, Fungal"
]
} | All these data highlight NO valuable properties as a quantitative and qualitative biomarker of cytotoxic action of chitosan in conidial cells. In addition, these findings place the chitosan assayed here as a fungicide with a high potential of application in sustainable horticultural practices. | yes | [
{
"from": "human",
"value": "Question: Is nitric-oxide-mediated cell death triggered by chitosan in Fusarium eumartii spores?\nContext: {'contexts': ['The genus Fusarium comprises a heterogeneous group of fungi important for agriculture. Fusarium solani f. sp. eumartii (F. eumartii), historically considered to be a fungal pathogen of potato, has also been associated with tomato disease. Currently, chitosan and its derivatives have been receiving more attention as environmentally friendly antimicrobial compounds in sustainable practices. The aim of the present work was to characterize downstream events associated with the mode of action of chitosan, including nitrosative reactive species, in order to identify new biomarkers of its cytotoxic action.', 'Data indicated that chitosan-mediated nitric oxide (NO) production might lead to conidial death, concomitant with the strong reduction in fungal pathogenicity in tomato plants. Following chitosan applications, a notably dose-dependent reduction in conidial viability was demonstrated in F. eumartii. Thereafter, the infectivity of chitosan-treated spores was tested by a bioassay using tomato seedlings.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Cell Death', 'Chitosan', 'Fungicides, Industrial', 'Fusarium', 'Lycopersicon esculentum', 'Nitric Oxide', 'Plant Diseases', 'Spores, Fungal']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,776,858 | Do surgery residency curriculum examination scores predict future American Board of Surgery in-training examination performance? | {
"contexts": [
"A protected block curriculum (PBC) with postcurriculum examinations for all surgical residents has been provided to assure coverage of core curricular topics. Biannual assessment of resident competency will soon be required by the Next Accreditation System.",
"To identify opportunities for early medical knowledge assessment and interventions, we examined whether performance in postcurriculum multiple-choice examinations (PCEs) is predictive of performance in the American Board of Surgery In-Training Examination (ABSITE) and clinical service competency assessments.",
"Retrospective single-institutional education research study.",
"Academic general surgery residency program.",
"A total of 49 surgical residents.",
"Data for PGY1 and PGY2 residents participating in the 2008 to 2012 PBC are included. Each resident completed 6 PCEs during each year.",
"The results of 6 examinations were correlated to percentage-correct ABSITE scores and clinical assessments based on the 6 Accreditation Council for Graduate Medical Education core competencies. Individual ABSITE performance was compared between PGY1 and PGY2. Statistical analysis included multivariate linear regression and bivariate Pearson correlations.",
"A total of 49 residents completed the PGY1 PBC and 36 completed the PGY2 curriculum. Linear regression analysis of percentage-correct ABSITE and PCE scores demonstrated a statistically significant correlation between the PGY1 PCE 1 score and the subsequent PGY1 ABSITE score (p = 0.037, β = 0.299). Similarly, the PGY2 PCE 1 score predicted performance in the PGY2 ABSITE (p = 0.015, β = 0.383). The ABSITE scores correlated between PGY1 and PGY2 with statistical significance, r = 0.675, p = 0.001. Performance on the 6 Accreditation Council for Graduate Medical Education core competencies correlated between PGY1 and PGY2, r = 0.729, p = 0.001, but did not correlate with PCE scores during either years."
],
"labels": [
"OBJECTIVE",
"OBJECTIVE",
"METHODS",
"METHODS",
"METHODS",
"METHODS",
"METHODS",
"RESULTS"
],
"meshes": [
"Clinical Competence",
"Curriculum",
"Forecasting",
"Internship and Residency",
"Retrospective Studies",
"Specialties, Surgical",
"Specialty Boards",
"United States"
]
} | Within a mature PBC, early performance in a PGY1 and PGY2 PCE is predictive of performance in the respective ABSITE. This information can be used for formative assessment and early remediation of residents who are predicted to be at risk for poor performance in the ABSITE. | yes | [
{
"from": "human",
"value": "Question: Do surgery residency curriculum examination scores predict future American Board of Surgery in-training examination performance?\nContext: {'contexts': ['A protected block curriculum (PBC) with postcurriculum examinations for all surgical residents has been provided to assure coverage of core curricular topics. Biannual assessment of resident competency will soon be required by the Next Accreditation System.', 'To identify opportunities for early medical knowledge assessment and interventions, we examined whether performance in postcurriculum multiple-choice examinations (PCEs) is predictive of performance in the American Board of Surgery In-Training Examination (ABSITE) and clinical service competency assessments.', 'Retrospective single-institutional education research study.', 'Academic general surgery residency program.', 'A total of 49 surgical residents.', 'Data for PGY1 and PGY2 residents participating in the 2008 to 2012 PBC are included. Each resident completed 6 PCEs during each year.', 'The results of 6 examinations were correlated to percentage-correct ABSITE scores and clinical assessments based on the 6 Accreditation Council for Graduate Medical Education core competencies. Individual ABSITE performance was compared between PGY1 and PGY2. Statistical analysis included multivariate linear regression and bivariate Pearson correlations.', 'A total of 49 residents completed the PGY1 PBC and 36 completed the PGY2 curriculum. Linear regression analysis of percentage-correct ABSITE and PCE scores demonstrated a statistically significant correlation between the PGY1 PCE 1 score and the subsequent PGY1 ABSITE score (p = 0.037, β = 0.299). Similarly, the PGY2 PCE 1 score predicted performance in the PGY2 ABSITE (p = 0.015, β = 0.383). The ABSITE scores correlated between PGY1 and PGY2 with statistical significance, r = 0.675, p = 0.001. Performance on the 6 Accreditation Council for Graduate Medical Education core competencies correlated between PGY1 and PGY2, r = 0.729, p = 0.001, but did not correlate with PCE scores during either years.'], 'labels': ['OBJECTIVE', 'OBJECTIVE', 'METHODS', 'METHODS', 'METHODS', 'METHODS', 'METHODS', 'RESULTS'], 'meshes': ['Clinical Competence', 'Curriculum', 'Forecasting', 'Internship and Residency', 'Retrospective Studies', 'Specialties, Surgical', 'Specialty Boards', 'United States']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,759,929 | Does eHD3-dependent endosome pathway regulate cardiac membrane excitability and physiology? | {
"contexts": [
"Cardiac function is dependent on the coordinate activities of membrane ion channels, transporters, pumps, and hormone receptors to tune the membrane electrochemical gradient dynamically in response to acute and chronic stress. Although our knowledge of membrane proteins has rapidly advanced during the past decade, our understanding of the subcellular pathways governing the trafficking and localization of integral membrane proteins is limited and essentially unstudied in vivo. In the heart, to our knowledge, there are no in vivo mechanistic studies that directly link endosome-based machinery with cardiac physiology.",
"To define the in vivo roles of endosome-based cellular machinery for cardiac membrane protein trafficking, myocyte excitability, and cardiac physiology.",
"We identify the endosome-based Eps15 homology domain 3 (EHD3) pathway as essential for cardiac physiology. EHD3-deficient hearts display structural and functional defects including bradycardia and rate variability, conduction block, and blunted response to adrenergic stimulation. Mechanistically, EHD3 is critical for membrane protein trafficking, because EHD3-deficient myocytes display reduced expression/localization of Na/Ca exchanger and L-type Ca channel type 1.2 with a parallel reduction in Na/Ca exchanger-mediated membrane current and Cav1.2-mediated membrane current. Functionally, EHD3-deficient myocytes show increased sarcoplasmic reticulum [Ca], increased spark frequency, and reduced expression/localization of ankyrin-B, a binding partner for EHD3 and Na/Ca exchanger. Finally, we show that in vivo EHD3-deficient defects are attributable to cardiac-specific roles of EHD3 because mice with cardiac-selective EHD3 deficiency demonstrate both structural and electric phenotypes."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Animals",
"Ankyrins",
"Calcium",
"Calcium Channels, L-Type",
"Carrier Proteins",
"Endosomes",
"Heart",
"Heart Rate",
"Mice",
"Myocytes, Cardiac",
"Stroke Volume"
]
} | These data provide new insight into the critical role of endosome-based pathways in membrane protein targeting and cardiac physiology. EHD3 is a critical component of protein trafficking in heart and is essential for the proper membrane targeting of select cellular proteins that maintain excitability. | yes | [
{
"from": "human",
"value": "Question: Does eHD3-dependent endosome pathway regulate cardiac membrane excitability and physiology?\nContext: {'contexts': ['Cardiac function is dependent on the coordinate activities of membrane ion channels, transporters, pumps, and hormone receptors to tune the membrane electrochemical gradient dynamically in response to acute and chronic stress. Although our knowledge of membrane proteins has rapidly advanced during the past decade, our understanding of the subcellular pathways governing the trafficking and localization of integral membrane proteins is limited and essentially unstudied in vivo. In the heart, to our knowledge, there are no in vivo mechanistic studies that directly link endosome-based machinery with cardiac physiology.', 'To define the in vivo roles of endosome-based cellular machinery for cardiac membrane protein trafficking, myocyte excitability, and cardiac physiology.', 'We identify the endosome-based Eps15 homology domain 3 (EHD3) pathway as essential for cardiac physiology. EHD3-deficient hearts display structural and functional defects including bradycardia and rate variability, conduction block, and blunted response to adrenergic stimulation. Mechanistically, EHD3 is critical for membrane protein trafficking, because EHD3-deficient myocytes display reduced expression/localization of Na/Ca exchanger and L-type Ca channel type 1.2 with a parallel reduction in Na/Ca exchanger-mediated membrane current and Cav1.2-mediated membrane current. Functionally, EHD3-deficient myocytes show increased sarcoplasmic reticulum [Ca], increased spark frequency, and reduced expression/localization of ankyrin-B, a binding partner for EHD3 and Na/Ca exchanger. Finally, we show that in vivo EHD3-deficient defects are attributable to cardiac-specific roles of EHD3 because mice with cardiac-selective EHD3 deficiency demonstrate both structural and electric phenotypes.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'RESULTS'], 'meshes': ['Animals', 'Ankyrins', 'Calcium', 'Calcium Channels, L-Type', 'Carrier Proteins', 'Endosomes', 'Heart', 'Heart Rate', 'Mice', 'Myocytes, Cardiac', 'Stroke Volume']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,745,346 | Does inhibition of autophagy enhance the cytotoxic effect of PA-MSHA in breast cancer? | {
"contexts": [
"PA-MSHA, a genetically engineered Pseudomonas aeruginosa (PA) strain, is currently under investigation as a new anti-cancer drug. It can induce cell cycle arrest and apoptosis in different human cancer cells, including hormone receptor negative breast cancer cells. However, the underlying mechanism of tumor lethality mediated by PA-MSHA remains to be fully investigated.",
"The effect of PA-MSHA on human hormone receptor negative breast cancer cells was analyzed by morphological measurement, western blot, cell proliferation assay and mouse xenograft model.",
"PA-MSHA was found to induce endoplasmic reticulum (ER) stress in breast cancer cell lines through the IRE1 signaling pathway. Inhibiting autophagy potentiated the cytotoxic effect of PA-MSHA while treating breast cancer cell lines. In mouse xenograft model, PA-MSHA produced more pronounced tumor suppression in mice inoculated with IRE1 gene knockdown. MDA-MB-231HM cells."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Apoptosis",
"Autophagy",
"Breast Neoplasms",
"Cell Line, Tumor",
"Cell Proliferation",
"Endoplasmic Reticulum Stress",
"Endoribonucleases",
"Female",
"Gene Knockdown Techniques",
"Hemagglutinins",
"Humans",
"Mice",
"Protein-Serine-Threonine Kinases",
"Pseudomonas aeruginosa",
"Signal Transduction",
"Xenograft Model Antitumor Assays"
]
} | These findings demonstrated inhibiting autophagy together with PA-MSHA might be a promising therapeutic strategy in treating hormone receptor negative breast cancer cells. | yes | [
{
"from": "human",
"value": "Question: Does inhibition of autophagy enhance the cytotoxic effect of PA-MSHA in breast cancer?\nContext: {'contexts': ['PA-MSHA, a genetically engineered Pseudomonas aeruginosa (PA) strain, is currently under investigation as a new anti-cancer drug. It can induce cell cycle arrest and apoptosis in different human cancer cells, including hormone receptor negative breast cancer cells. However, the underlying mechanism of tumor lethality mediated by PA-MSHA remains to be fully investigated.', 'The effect of PA-MSHA on human hormone receptor negative breast cancer cells was analyzed by morphological measurement, western blot, cell proliferation assay and mouse xenograft model.', 'PA-MSHA was found to induce endoplasmic reticulum (ER) stress in breast cancer cell lines through the IRE1 signaling pathway. Inhibiting autophagy potentiated the cytotoxic effect of PA-MSHA while treating breast cancer cell lines. In mouse xenograft model, PA-MSHA produced more pronounced tumor suppression in mice inoculated with IRE1 gene knockdown. MDA-MB-231HM cells.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Apoptosis', 'Autophagy', 'Breast Neoplasms', 'Cell Line, Tumor', 'Cell Proliferation', 'Endoplasmic Reticulum Stress', 'Endoribonucleases', 'Female', 'Gene Knockdown Techniques', 'Hemagglutinins', 'Humans', 'Mice', 'Protein-Serine-Threonine Kinases', 'Pseudomonas aeruginosa', 'Signal Transduction', 'Xenograft Model Antitumor Assays']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,775,184 | Do noradrenergic terminals regulate L-DOPA-derived dopamine extracellular levels in a region-dependent manner in Parkinsonian rats? | {
"contexts": [
"Serotonin (5-HT) neurons mediate the ectopic release of dopamine (DA) induced by L-DOPA in the Parkinsonian brain. We hypothesized that the participation of noradrenalin transporters (NET) in the clearance of DA may account for the lower effect of L-DOPA in extrastriatal regions compared with the striatum.",
"Using a multisite intracerebral microdialysis approach, we tested the influence of the pharmacological blockade of NET and/or the destruction of noradrenalin (NE) fibers on DA and 5-HT release in the striatum, hippocampus (HIPP), substantia nigra pars reticulata (SNr) and prefrontal cortex (PFC) of 6-hydroxydopamine-lesioned rats.",
"L-DOPA (12 mg/kg, i.p.) increased DA extracellular levels to a lesser extent in the SNr, PFC and HIPP compared with the striatum. The NET blockers desipramine (10 mg/kg, i.p.) and reboxetine (3 mg/kg, i.p.) potentiated L-DOPA effect in the PFC, SNr and HIPP but not in the striatum. The NE neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (50 mg/kg, i.p. 1 week before dialysis experiment) potentiated L-DOPA effect in the SNr and HIPP. 5-HT extracellular levels were enhanced only when L-DOPA was combined to NET blockers."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adrenergic Neurons",
"Animals",
"Cerebral Cortex",
"Corpus Striatum",
"Dopamine",
"Extracellular Fluid",
"Levodopa",
"Male",
"Parkinsonian Disorders",
"Rats",
"Rats, Sprague-Dawley"
]
} | Noradrenalin neurons are indirectly involved in the mechanism of action of L-DOPA in part through the heterologous reuptake of DA in extrastriatal regions. | yes | [
{
"from": "human",
"value": "Question: Do noradrenergic terminals regulate L-DOPA-derived dopamine extracellular levels in a region-dependent manner in Parkinsonian rats?\nContext: {'contexts': ['Serotonin (5-HT) neurons mediate the ectopic release of dopamine (DA) induced by L-DOPA in the Parkinsonian brain. We hypothesized that the participation of noradrenalin transporters (NET) in the clearance of DA may account for the lower effect of L-DOPA in extrastriatal regions compared with the striatum.', 'Using a multisite intracerebral microdialysis approach, we tested the influence of the pharmacological blockade of NET and/or the destruction of noradrenalin (NE) fibers on DA and 5-HT release in the striatum, hippocampus (HIPP), substantia nigra pars reticulata (SNr) and prefrontal cortex (PFC) of 6-hydroxydopamine-lesioned rats.', 'L-DOPA (12 mg/kg, i.p.) increased DA extracellular levels to a lesser extent in the SNr, PFC and HIPP compared with the striatum. The NET blockers desipramine (10 mg/kg, i.p.) and reboxetine (3 mg/kg, i.p.) potentiated L-DOPA effect in the PFC, SNr and HIPP but not in the striatum. The NE neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (50 mg/kg, i.p. 1 week before dialysis experiment) potentiated L-DOPA effect in the SNr and HIPP. 5-HT extracellular levels were enhanced only when L-DOPA was combined to NET blockers.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adrenergic Neurons', 'Animals', 'Cerebral Cortex', 'Corpus Striatum', 'Dopamine', 'Extracellular Fluid', 'Levodopa', 'Male', 'Parkinsonian Disorders', 'Rats', 'Rats, Sprague-Dawley']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,759,887 | Does a MAP3k1 SNP predict survival of gastric cancer in a Chinese population? | {
"contexts": [
"Genome-wide association studies (GWAS) have demonstrated that the single nucleotide polymorphism (SNP) MAP3K1 rs889312 is a genetic susceptibility marker significantly associated with a risk of hormone-related tumors such as breast cancer. Considering steroid hormone-mediated signaling pathways have an important role in the progression of gastric cancer, we hypothesized that MAP3K1 rs889312 may be associated with survival outcomes in gastric cancer. The purpose of this study was to test this hypothesis.",
"We genotyped MAP3K1 rs889312 using TaqMan in 884 gastric cancer patients who received subtotal or total gastrectomy. Kaplan-Meier survival analysis and Cox proportional hazard regression were used to analyze the association between MAP3K1 rs889312 genotypes and survival outcomes of gastric cancer.",
"Our findings reveal that the rs889312 heterozygous AC genotype was significantly associated with an increased rate of mortality among patients with diffuse-type gastric cancer (log-rank P = 0.028 for AC versus AA/CC, hazard ratio [HR] = 1.32, 95% confidence interval [CI] = 1.03-1.69), compared to those carrying the homozygous variant genotypes (AA/CC). Additionally, univariate and multivariate Cox regression analysis demonstrate that rs889312 polymorphism was an independent risk factor for poor survival in these patients."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Aged, 80 and over",
"Asian Continental Ancestry Group",
"China",
"Female",
"Gastrectomy",
"Genome-Wide Association Study",
"Humans",
"MAP Kinase Kinase Kinase 1",
"Male",
"Middle Aged",
"Polymorphism, Single Nucleotide",
"Prognosis",
"Risk Factors",
"Stomach Neoplasms",
"Survival Analysis"
]
} | In conclusion, we demonstrate that MAP3K1 rs889312 is closely correlated with outcome among diffuse-type gastric cancer. This raises the possibility for rs889312 polymorphisms to be used as an independent indicator for predicting the prognosis of diffuse-type gastric cancer within the Chinese population. | yes | [
{
"from": "human",
"value": "Question: Does a MAP3k1 SNP predict survival of gastric cancer in a Chinese population?\nContext: {'contexts': ['Genome-wide association studies (GWAS) have demonstrated that the single nucleotide polymorphism (SNP) MAP3K1 rs889312 is a genetic susceptibility marker significantly associated with a risk of hormone-related tumors such as breast cancer. Considering steroid hormone-mediated signaling pathways have an important role in the progression of gastric cancer, we hypothesized that MAP3K1 rs889312 may be associated with survival outcomes in gastric cancer. The purpose of this study was to test this hypothesis.', 'We genotyped MAP3K1 rs889312 using TaqMan in 884 gastric cancer patients who received subtotal or total gastrectomy. Kaplan-Meier survival analysis and Cox proportional hazard regression were used to analyze the association between MAP3K1 rs889312 genotypes and survival outcomes of gastric cancer.', 'Our findings reveal that the rs889312 heterozygous AC genotype was significantly associated with an increased rate of mortality among patients with diffuse-type gastric cancer (log-rank P\\u200a=\\u200a0.028 for AC versus AA/CC, hazard ratio [HR]\\u200a=\\u200a1.32, 95% confidence interval [CI]\\u200a=\\u200a1.03-1.69), compared to those carrying the homozygous variant genotypes (AA/CC). Additionally, univariate and multivariate Cox regression analysis demonstrate that rs889312 polymorphism was an independent risk factor for poor survival in these patients.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Aged, 80 and over', 'Asian Continental Ancestry Group', 'China', 'Female', 'Gastrectomy', 'Genome-Wide Association Study', 'Humans', 'MAP Kinase Kinase Kinase 1', 'Male', 'Middle Aged', 'Polymorphism, Single Nucleotide', 'Prognosis', 'Risk Factors', 'Stomach Neoplasms', 'Survival Analysis']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,766,657 | Is sARS-CoV envelope protein palmitoylation or nucleocapid association required for promoting virus-like particle production? | {
"contexts": [
"Coronavirus membrane (M) proteins are capable of interacting with nucleocapsid (N) and envelope (E) proteins. Severe acute respiratory syndrome coronavirus (SARS-CoV) M co-expression with either N or E is sufficient for producing virus-like particles (VLPs), although at a lower level compared to M, N and E co-expression. Whether E can release from cells or E/N interaction exists so as to contribute to enhanced VLP production is unknown. It also remains to be determined whether E palmitoylation or disulfide bond formation plays a role in SARS-CoV virus assembly.",
"SARS-CoV N is released from cells through an association with E protein-containing vesicles. Further analysis suggests that domains involved in E/N interaction are largely located in both carboxyl-terminal regions. Changing all three E cysteine residues to alanines did not exert negative effects on E release, E association with N, or E enhancement of VLP production, suggesting that E palmitoylation modification or disulfide bond formation is not required for SARS-CoV virus assembly. We found that removal of the last E carboxyl-terminal residue markedly affected E release, N association, and VLP incorporation, but did not significantly compromise the contribution of E to efficient VLP production."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Humans",
"Lipoylation",
"Nucleocapsid",
"SARS Virus",
"Viral Envelope Proteins",
"Virion",
"Virus Assembly"
]
} | The independence of the SARS-CoV E enhancement effect on VLP production from its viral packaging capacity suggests a distinct SARS-CoV E role in virus assembly. | no | [
{
"from": "human",
"value": "Question: Is sARS-CoV envelope protein palmitoylation or nucleocapid association required for promoting virus-like particle production?\nContext: {'contexts': ['Coronavirus membrane (M) proteins are capable of interacting with nucleocapsid (N) and envelope (E) proteins. Severe acute respiratory syndrome coronavirus (SARS-CoV) M co-expression with either N or E is sufficient for producing virus-like particles (VLPs), although at a lower level compared to M, N and E co-expression. Whether E can release from cells or E/N interaction exists so as to contribute to enhanced VLP production is unknown. It also remains to be determined whether E palmitoylation or disulfide bond formation plays a role in SARS-CoV virus assembly.', 'SARS-CoV N is released from cells through an association with E protein-containing vesicles. Further analysis suggests that domains involved in E/N interaction are largely located in both carboxyl-terminal regions. Changing all three E cysteine residues to alanines did not exert negative effects on E release, E association with N, or E enhancement of VLP production, suggesting that E palmitoylation modification or disulfide bond formation is not required for SARS-CoV virus assembly. We found that removal of the last E carboxyl-terminal residue markedly affected E release, N association, and VLP incorporation, but did not significantly compromise the contribution of E to efficient VLP production.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Humans', 'Lipoylation', 'Nucleocapsid', 'SARS Virus', 'Viral Envelope Proteins', 'Virion', 'Virus Assembly']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
24,766,284 | Does characteristic epithelium with low-grade atypia appear on the surface of gastric cancer after successful Helicobacter pylori eradication therapy? | {
"contexts": [
"The incidence of gastric cancer after successful Helicobacter pylori eradication has been increasing. We previously reported that epithelium with low-grade atypia (ELA) appeared on the surface of gastric cancer after H. pylori eradication. Here, we investigate the clinical and biological characteristics of such ELA.",
"We studied 27 cases of gastric cancer detected after successful H. pylori eradication therapy. We examined the prevalence of ELA among these cases and its significance for endoscopic discovery after H. pylori eradication. We additionally investigated the mucus, p53 and Ki67 expressions in ELA.",
"Epithelium with low-grade atypia that continuous with the gastric tumor was detected in 22 of 27 cases (81%), a significantly greater percentage than that for controls (p < 0.01). We found that gastric-type mucin was frequently expressed in this epithelium. Neither p53- nor Ki67-positive cells were found in ELA, irrespective of their expression in tumor tissue. The presence of ELA was positively correlated with the clinical interval between H. pylori eradication and gastric cancer detection."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Endoscopy, Gastrointestinal",
"Epithelium",
"Female",
"Gastric Mucosa",
"Helicobacter Infections",
"Humans",
"Ki-67 Antigen",
"Male",
"Middle Aged",
"Mucus",
"Stomach Neoplasms",
"Tumor Suppressor Protein p53"
]
} | Epithelium with low-grade atypia on gastric cancer tissue, which may develop from gastric cancer cells, is frequently present after successful eradication therapy. This phenomenon could influence the practice of endoscopic diagnosis of gastric cancers. | yes | [
{
"from": "human",
"value": "Question: Does characteristic epithelium with low-grade atypia appear on the surface of gastric cancer after successful Helicobacter pylori eradication therapy?\nContext: {'contexts': ['The incidence of gastric cancer after successful Helicobacter pylori eradication has been increasing. We previously reported that epithelium with low-grade atypia (ELA) appeared on the surface of gastric cancer after H. pylori eradication. Here, we investigate the clinical and biological characteristics of such ELA.', 'We studied 27 cases of gastric cancer detected after successful H. pylori eradication therapy. We examined the prevalence of ELA among these cases and its significance for endoscopic discovery after H. pylori eradication. We additionally investigated the mucus, p53 and Ki67 expressions in ELA.', 'Epithelium with low-grade atypia that continuous with the gastric tumor was detected in 22 of 27 cases (81%), a significantly greater percentage than that for controls (p < 0.01). We found that gastric-type mucin was frequently expressed in this epithelium. Neither p53- nor Ki67-positive cells were found in ELA, irrespective of their expression in tumor tissue. The presence of ELA was positively correlated with the clinical interval between H. pylori eradication and gastric cancer detection.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Endoscopy, Gastrointestinal', 'Epithelium', 'Female', 'Gastric Mucosa', 'Helicobacter Infections', 'Humans', 'Ki-67 Antigen', 'Male', 'Middle Aged', 'Mucus', 'Stomach Neoplasms', 'Tumor Suppressor Protein p53']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,760,094 | Are delayed latencies of auditory evoked potential P300 associated with the severity of Parkinson 's disease in older patients? | {
"contexts": [
"Electrophysiological methods could provide important information about the neurophysiological status in Parkinson's disease (PD).",
"To investigate the prolonged auditory P300 latency in PD and its association with the disease clinical stage.",
"Clinical profiles of 44 patients were evaluated and those in initial and advanced stages of PD were identified. The frequency of altered latencies, median of latencies in each stage, and correlation between latencies and motor and non-motor clinical features were analyzed. Latencies were considered altered when they were more than two standard deviations from the mean of controls, per age group.",
"It was verified 10% of alterations in initial stages and 31% in advanced. There was correlation between latencies and non-motor clinical features. Subjects older than 65, in advanced stages, presented a significant increase of latencies."
],
"labels": [
"UNLABELLED",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Age Factors",
"Aged",
"Aged, 80 and over",
"Aging",
"Case-Control Studies",
"Cognition",
"Cross-Sectional Studies",
"Event-Related Potentials, P300",
"Evoked Potentials, Auditory, Brain Stem",
"Female",
"Humans",
"Male",
"Middle Aged",
"Parkinson Disease",
"Reaction Time",
"Severity of Illness Index",
"Statistics, Nonparametric",
"Time Factors"
]
} | There was an association between PD severity and P300 prolonged latencies among subjects 65 years old or older. | yes | [
{
"from": "human",
"value": "Question: Are delayed latencies of auditory evoked potential P300 associated with the severity of Parkinson 's disease in older patients?\nContext: {'contexts': [\"Electrophysiological methods could provide important information about the neurophysiological status in Parkinson's disease (PD).\", 'To investigate the prolonged auditory P300 latency in PD and its association with the disease clinical stage.', 'Clinical profiles of 44 patients were evaluated and those in initial and advanced stages of PD were identified. The frequency of altered latencies, median of latencies in each stage, and correlation between latencies and motor and non-motor clinical features were analyzed. Latencies were considered altered when they were more than two standard deviations from the mean of controls, per age group.', 'It was verified 10% of alterations in initial stages and 31% in advanced. There was correlation between latencies and non-motor clinical features. Subjects older than 65, in advanced stages, presented a significant increase of latencies.'], 'labels': ['UNLABELLED', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Age Factors', 'Aged', 'Aged, 80 and over', 'Aging', 'Case-Control Studies', 'Cognition', 'Cross-Sectional Studies', 'Event-Related Potentials, P300', 'Evoked Potentials, Auditory, Brain Stem', 'Female', 'Humans', 'Male', 'Middle Aged', 'Parkinson Disease', 'Reaction Time', 'Severity of Illness Index', 'Statistics, Nonparametric', 'Time Factors']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,762,043 | Is the YXXΦ motif within the severe acute respiratory syndrome coronavirus ( SARS-CoV ) 3a protein crucial for its intracellular transport? | {
"contexts": [
"The SARS coronavirus (SARS-CoV) 3a protein functions as an ion channel, induces apoptosis and is important for viral pathogenesis. It is expressed on the cell surface and contains a tyrosine-based sorting motif and a di-acidic motif, which may be crucial for its intracellular trafficking. However the role of these motifs is not fully understood in the case of 3a protein.",
"The subcellular distribution of the 3a protein was studied by immunofluorescence staining of cells transfected with wild type and mutant constructs along with markers for different intracellular compartments. Semi-quantitative RT-PCR was performed to estimate the mRNA where as western blotting was carried out to detect protein levels of wild type and mutant 3a proteins. In vitro transcription- translation was performed to estimate cell free protein synthesis.",
"While the wild type 3a protein is efficiently transported to the plasma membrane, the protein with mutations in the tyrosine and valine residues within the YXXV motif (ΔYXXΦ) accumulated in the Golgi compartment. However the 3a protein with mutations within the EXD di-acidic motif (ΔEXD) showed an intracellular distribution similar to the wild type protein. Increased retention of the ΔYXXΦ protein in the Golgi compartment also increased its association with lipid droplets. The ΔYXXΦ protein also expressed at significantly lower levels compared to the wild type 3a protein, which was reversed with Brefeldin A and Aprotinin."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Amino Acid Motifs",
"Cytoplasm",
"DNA Mutational Analysis",
"Golgi Apparatus",
"Humans",
"Mutant Proteins",
"Protein Transport",
"SARS Virus",
"Viral Proteins",
"Virus Replication"
]
} | The data suggest that the YXXΦ motif of the SARS-CoV 3a protein is necessary for Golgi to plasma membrane transport, in the absence of which the protein is targeted to lysosomal degradation compartment via lipid droplets. | yes | [
{
"from": "human",
"value": "Question: Is the YXXΦ motif within the severe acute respiratory syndrome coronavirus ( SARS-CoV ) 3a protein crucial for its intracellular transport?\nContext: {'contexts': ['The SARS coronavirus (SARS-CoV) 3a protein functions as an ion channel, induces apoptosis and is important for viral pathogenesis. It is expressed on the cell surface and contains a tyrosine-based sorting motif and a di-acidic motif, which may be crucial for its intracellular trafficking. However the role of these motifs is not fully understood in the case of 3a protein.', 'The subcellular distribution of the 3a protein was studied by immunofluorescence staining of cells transfected with wild type and mutant constructs along with markers for different intracellular compartments. Semi-quantitative RT-PCR was performed to estimate the mRNA where as western blotting was carried out to detect protein levels of wild type and mutant 3a proteins. In vitro transcription- translation was performed to estimate cell free protein synthesis.', 'While the wild type 3a protein is efficiently transported to the plasma membrane, the protein with mutations in the tyrosine and valine residues within the YXXV motif (ΔYXXΦ) accumulated in the Golgi compartment. However the 3a protein with mutations within the EXD di-acidic motif (ΔEXD) showed an intracellular distribution similar to the wild type protein. Increased retention of the ΔYXXΦ protein in the Golgi compartment also increased its association with lipid droplets. The ΔYXXΦ protein also expressed at significantly lower levels compared to the wild type 3a protein, which was reversed with Brefeldin A and Aprotinin.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Amino Acid Motifs', 'Cytoplasm', 'DNA Mutational Analysis', 'Golgi Apparatus', 'Humans', 'Mutant Proteins', 'Protein Transport', 'SARS Virus', 'Viral Proteins', 'Virus Replication']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,759,636 | Do mRI biomarkers identify the differential response of glioblastoma multiforme to anti-angiogenic therapy? | {
"contexts": [
"Although anti-angiogenic therapy (AATx) holds great promise for treatment of malignant gliomas, its therapeutic efficacy is not well understood and can potentially increase the aggressive recurrence of gliomas. It is essential to establish sensitive, noninvasive biomarkers that can detect failure of AATx and tumor recurrence early so that timely adaptive therapy can be instituted. We investigated the efficacy of MRI biomarkers that can detect response to different classes of AATxs used alone or in combination with radiation.",
"Murine intracranial glioma xenografts (NOD/SCID) were treated with sunitinib, VEGF-trap or B20 (a bevacizumab equivalent) alone or in combination with radiation. MRI images were acquired longitudinally before and after treatment, and various MRI parameters (apparent diffusion coefficient, T1w + contrast, dynamic contrast-enhanced [DCE], initial area under the contrast enhancement curve, and cerebral blood flow) were correlated to tumor cell proliferation, overall tumor growth, and tumor vascularity.",
"Combinatorial therapies reduced tumor growth rate more efficiently than monotherapies. Apparent diffusion coefficient was an accurate measure of tumor cell density. Vascular endothelial growth factor (VEGF)-trap or B20, but not sunitinib, resulted in significant reduction or complete loss of contrast enhancement. This reduction was not due to a reduction in tumor growth or microvascular density, but rather was explained by a reduction in vessel permeability and perfusion. We established that contrast enhancement does not accurately reflect tumor volume or vascular density; however, DCE-derived parameters can be used as efficient noninvasive biomarkers of response to AATx."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Angiogenesis Inhibitors",
"Animals",
"Antibodies, Monoclonal, Humanized",
"Bevacizumab",
"Biomarkers",
"Brain Neoplasms",
"Cell Line, Tumor",
"Combined Modality Therapy",
"Glioblastoma",
"Humans",
"Image Processing, Computer-Assisted",
"Indoles",
"Magnetic Resonance Imaging",
"Mice",
"Pyrroles",
"Receptors, Vascular Endothelial Growth Factor",
"Recombinant Fusion Proteins",
"Sunitinib"
]
} | MRI parameters following therapy vary based on class of AATx. Validation of clinically relevant MRI parameters for individual AATx agents is necessary before incorporation into routine practice. | yes | [
{
"from": "human",
"value": "Question: Do mRI biomarkers identify the differential response of glioblastoma multiforme to anti-angiogenic therapy?\nContext: {'contexts': ['Although anti-angiogenic therapy (AATx) holds great promise for treatment of malignant gliomas, its therapeutic efficacy is not well understood and can potentially increase the aggressive recurrence of gliomas. It is essential to establish sensitive, noninvasive biomarkers that can detect failure of AATx and tumor recurrence early so that timely adaptive therapy can be instituted. We investigated the efficacy of MRI biomarkers that can detect response to different classes of AATxs used alone or in combination with radiation.', 'Murine intracranial glioma xenografts (NOD/SCID) were treated with sunitinib, VEGF-trap or B20 (a bevacizumab equivalent) alone or in combination with radiation. MRI images were acquired longitudinally before and after treatment, and various MRI parameters (apparent diffusion coefficient, T1w + contrast, dynamic contrast-enhanced [DCE], initial area under the contrast enhancement curve, and cerebral blood flow) were correlated to tumor cell proliferation, overall tumor growth, and tumor vascularity.', 'Combinatorial therapies reduced tumor growth rate more efficiently than monotherapies. Apparent diffusion coefficient was an accurate measure of tumor cell density. Vascular endothelial growth factor (VEGF)-trap or B20, but not sunitinib, resulted in significant reduction or complete loss of contrast enhancement. This reduction was not due to a reduction in tumor growth or microvascular density, but rather was explained by a reduction in vessel permeability and perfusion. We established that contrast enhancement does not accurately reflect tumor volume or vascular density; however, DCE-derived parameters can be used as efficient noninvasive biomarkers of response to AATx.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Angiogenesis Inhibitors', 'Animals', 'Antibodies, Monoclonal, Humanized', 'Bevacizumab', 'Biomarkers', 'Brain Neoplasms', 'Cell Line, Tumor', 'Combined Modality Therapy', 'Glioblastoma', 'Humans', 'Image Processing, Computer-Assisted', 'Indoles', 'Magnetic Resonance Imaging', 'Mice', 'Pyrroles', 'Receptors, Vascular Endothelial Growth Factor', 'Recombinant Fusion Proteins', 'Sunitinib']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,758,146 | Does chemerin suppress murine allergic asthma by inhibiting CCL2 production and subsequent airway recruitment of inflammatory dendritic cells? | {
"contexts": [
"Chemerin has been implicated to play opposing roles, either pro-inflammatory or anti-inflammatory, in various tissue inflammation processes primarily through the regulation of tissue recruitment of immune cells. However, the effect of chemerin in allergic asthma has not yet been explored. We sought to investigate the role of chemerin in the murine model of allergic asthma and explore the underlying mechanism.",
"We examined the effect of intranasal (i.n.) administration of chemerin during antigen challenge in murine models of asthma. Moreover, we examined whether administration of CCL2 or bone marrow-derived dendritic cells (BMDCs) transfer reversed the effects of chemerin on ovalbumin-induced asthma. We finally examined the effect of chemerin on CCL2 expression in activated lung epithelial cells in vitro.",
"The administration of chemerin attenuated allergic airway inflammation and airway hyperreactivity during antigen challenge. Chemerin treatment caused significant decreases in BALF CD4(+) T-cell accumulation and mRNA expression of Th2-attracting chemokines, CCL17 and CCL22, which was accompanied by significantly decreased BALF CD11c(+) CD11b(+) inflammatory DC accumulation and CCL2 production. Furthermore, airway administration of exogenous CCL2 or adoptive transfer of CD11c(+) CD11b(+) BMDCs abrogated the suppressive effects of chemerin on allergic asthma. Finally, in vitro study showed that chemerin inhibited CCL2 secretion by low-dose LPS-stimulated lung epithelial cells, which led to decreased chemotaxis of BMDCs."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adoptive Transfer",
"Alveolar Epithelial Cells",
"Animals",
"Asthma",
"Bronchoalveolar Lavage Fluid",
"CD11b Antigen",
"CD11c Antigen",
"CD4-Positive T-Lymphocytes",
"Chemokine CCL2",
"Chemokines",
"Chemotactic Factors",
"Dendritic Cells",
"Disease Models, Animal",
"Female",
"Immunophenotyping",
"Intercellular Signaling Peptides and Proteins",
"Mice",
"Ovalbumin",
"Respiratory Hypersensitivity"
]
} | Our study demonstrates that chemerin plays a protective role in allergic asthma by suppressing airway recruitment of inflammatory CD11c(+) CD11b(+) DCs through the inhibition of CCL2 secretion by active lung epithelial cells. | yes | [
{
"from": "human",
"value": "Question: Does chemerin suppress murine allergic asthma by inhibiting CCL2 production and subsequent airway recruitment of inflammatory dendritic cells?\nContext: {'contexts': ['Chemerin has been implicated to play opposing roles, either pro-inflammatory or anti-inflammatory, in various tissue inflammation processes primarily through the regulation of tissue recruitment of immune cells. However, the effect of chemerin in allergic asthma has not yet been explored. We sought to investigate the role of chemerin in the murine model of allergic asthma and explore the underlying mechanism.', 'We examined the effect of intranasal (i.n.) administration of chemerin during antigen challenge in murine models of asthma. Moreover, we examined whether administration of CCL2 or bone marrow-derived dendritic cells (BMDCs) transfer reversed the effects of chemerin on ovalbumin-induced asthma. We finally examined the effect of chemerin on CCL2 expression in activated lung epithelial cells in vitro.', 'The administration of chemerin attenuated allergic airway inflammation and airway hyperreactivity during antigen challenge. Chemerin treatment caused significant decreases in BALF CD4(+) T-cell accumulation and mRNA expression of Th2-attracting chemokines, CCL17 and CCL22, which was accompanied by significantly decreased BALF CD11c(+) CD11b(+) inflammatory DC accumulation and CCL2 production. Furthermore, airway administration of exogenous CCL2 or adoptive transfer of CD11c(+) CD11b(+) BMDCs abrogated the suppressive effects of chemerin on allergic asthma. Finally, in vitro study showed that chemerin inhibited CCL2 secretion by low-dose LPS-stimulated lung epithelial cells, which led to decreased chemotaxis of BMDCs.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adoptive Transfer', 'Alveolar Epithelial Cells', 'Animals', 'Asthma', 'Bronchoalveolar Lavage Fluid', 'CD11b Antigen', 'CD11c Antigen', 'CD4-Positive T-Lymphocytes', 'Chemokine CCL2', 'Chemokines', 'Chemotactic Factors', 'Dendritic Cells', 'Disease Models, Animal', 'Female', 'Immunophenotyping', 'Intercellular Signaling Peptides and Proteins', 'Mice', 'Ovalbumin', 'Respiratory Hypersensitivity']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,755,297 | Is mesoderm required for coordinated cell movements within zebrafish neural plate in vivo? | {
"contexts": [
"Morphogenesis of the zebrafish neural tube requires the coordinated movement of many cells in both time and space. A good example of this is the movement of the cells in the zebrafish neural plate as they converge towards the dorsal midline before internalizing to form a neural keel. How these cells are regulated to ensure that they move together as a coherent tissue is unknown. Previous work in other systems has suggested that the underlying mesoderm may play a role in this process but this has not been shown directly in vivo.",
"Here we analyze the roles of subjacent mesoderm in the coordination of neural cell movements during convergence of the zebrafish neural plate and neural keel formation. Live imaging demonstrates that the normal highly coordinated movements of neural plate cells are lost in the absence of underlying mesoderm and the movements of internalization and neural tube formation are severely disrupted. Despite this, neuroepithelial polarity develops in the abnormal neural primordium but the resulting tissue architecture is very disorganized."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Animals",
"Body Patterning",
"Cell Movement",
"Mesoderm",
"Neural Plate",
"Neural Tube",
"Nodal Signaling Ligands",
"Zebrafish"
]
} | We show that the movements of cells in the zebrafish neural plate are highly coordinated during the convergence and internalization movements of neurulation. Our results demonstrate that the underlying mesoderm is required for these coordinated cell movements in the zebrafish neural plate in vivo. | yes | [
{
"from": "human",
"value": "Question: Is mesoderm required for coordinated cell movements within zebrafish neural plate in vivo?\nContext: {'contexts': ['Morphogenesis of the zebrafish neural tube requires the coordinated movement of many cells in both time and space. A good example of this is the movement of the cells in the zebrafish neural plate as they converge towards the dorsal midline before internalizing to form a neural keel. How these cells are regulated to ensure that they move together as a coherent tissue is unknown. Previous work in other systems has suggested that the underlying mesoderm may play a role in this process but this has not been shown directly in vivo.', 'Here we analyze the roles of subjacent mesoderm in the coordination of neural cell movements during convergence of the zebrafish neural plate and neural keel formation. Live imaging demonstrates that the normal highly coordinated movements of neural plate cells are lost in the absence of underlying mesoderm and the movements of internalization and neural tube formation are severely disrupted. Despite this, neuroepithelial polarity develops in the abnormal neural primordium but the resulting tissue architecture is very disorganized.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Animals', 'Body Patterning', 'Cell Movement', 'Mesoderm', 'Neural Plate', 'Neural Tube', 'Nodal Signaling Ligands', 'Zebrafish']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,758,766 | Do adipose-derived stem cells stimulate reendothelialization in stented rat abdominal aorta? | {
"contexts": [
"Although drug-eluting stents (DES) have been widely used for the treatment of coronary artery disease, they potentially increase the risk of late thrombosis. It is, therefore, desirable to establish a strategy to stimulate reendothelialization. Endothelial injury models have been widely used to analyze the mechanisms of coronary restenosis. However, animal models deployed with coronary stents in the blood vessels are necessary to accurately analyze the mechanisms of coronary restenosis and late thrombosis because persistent inflammation occurs around the coronary stents.",
"Coronary stents were implanted into rat abdominal aorta and adipose tissue-derived stem cells (ASC) were administered from the adventitial side. Reendothelialization was then visualized by Evans blue staining, and neointimal formation was analyzed histologically. ASC significantly stimulated reendothelialization and inhibited neointimal formation in bare metal stents (BMS)-implanted aorta. In addition, ASC promoted reendothelialization in DES-implanted aorta; however, the effects were weaker than in BMS-implanted aorta. Among the cytokines that ASC produce, adrenomedullin (AM) significantly stimulated reendothelialization and inhibited neointimal formation in BMS-implanted aorta, when an adenovirus expressing AM was administered from the adventitial side."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Adipose Tissue",
"Adrenomedullin",
"Animals",
"Aorta, Abdominal",
"Cells, Cultured",
"Coronary Restenosis",
"Disease Models, Animal",
"Male",
"Neointima",
"Rats",
"Rats, Wistar",
"Stem Cell Transplantation",
"Stem Cells",
"Stents"
]
} | These results suggest that ASC produce several cytokines that stimulate reendothelialization and inhibit neointimal formation in stent-deployed vessels, and that AM could mediate these effects. | yes | [
{
"from": "human",
"value": "Question: Do adipose-derived stem cells stimulate reendothelialization in stented rat abdominal aorta?\nContext: {'contexts': ['Although drug-eluting stents (DES) have been widely used for the treatment of coronary artery disease, they potentially increase the risk of late thrombosis. It is, therefore, desirable to establish a strategy to stimulate reendothelialization. Endothelial injury models have been widely used to analyze the mechanisms of coronary restenosis. However, animal models deployed with coronary stents in the blood vessels are necessary to accurately analyze the mechanisms of coronary restenosis and late thrombosis because persistent inflammation occurs around the coronary stents.', 'Coronary stents were implanted into rat abdominal aorta and adipose tissue-derived stem cells (ASC) were administered from the adventitial side. Reendothelialization was then visualized by Evans blue staining, and neointimal formation was analyzed histologically. ASC significantly stimulated reendothelialization and inhibited neointimal formation in bare metal stents (BMS)-implanted aorta. In addition, ASC promoted reendothelialization in DES-implanted aorta; however, the effects were weaker than in BMS-implanted aorta. Among the cytokines that ASC produce, adrenomedullin (AM) significantly stimulated reendothelialization and inhibited neointimal formation in BMS-implanted aorta, when an adenovirus expressing AM was administered from the adventitial side.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Adipose Tissue', 'Adrenomedullin', 'Animals', 'Aorta, Abdominal', 'Cells, Cultured', 'Coronary Restenosis', 'Disease Models, Animal', 'Male', 'Neointima', 'Rats', 'Rats, Wistar', 'Stem Cell Transplantation', 'Stem Cells', 'Stents']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,764,681 | Is caspase-3 expression in metastatic lymph nodes of esophageal squamous cell carcinoma prognostic of survival? | {
"contexts": [
"To assess whether differential expression of caspase-3 in paired metastatic lymph nodes (LNs) is prognostic of survival in patients with resectable esophageal squamous cell carcinoma (ESCC).",
"Capases-3 expression was evaluated immunohistochemically in 122 pairs of primary ESCCs and regional metastatic LNs assembled on tissue microarrays. The impact of caspase-3 expression on survival outcomes was analyzed by the Kaplan-Meier method and Cox proportional hazards regression model.",
"The level of caspase-3 expression was significantly higher in LN metastases than in primary tumors (P < 0.001). Caspase-3 expression in the primary tumors was associated with longer median survival (23 mo vs 21 mo, P = 0.033), whereas higher expression in paired metastatic LNs was associated with shorter median survival (20 mo vs 22 mo, P = 0.043). Multivariate analysis showed that both were independent prognostic factors."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Biomarkers, Tumor",
"Carcinoma, Squamous Cell",
"Caspase 3",
"Esophageal Neoplasms",
"Esophageal Squamous Cell Carcinoma",
"Female",
"Gene Expression Regulation, Enzymologic",
"Gene Expression Regulation, Neoplastic",
"Humans",
"Immunohistochemistry",
"Kaplan-Meier Estimate",
"Lymph Nodes",
"Lymphatic Metastasis",
"Male",
"Middle Aged",
"Multivariate Analysis",
"Oligonucleotide Array Sequence Analysis",
"Prognosis",
"Proportional Hazards Models",
"Treatment Outcome"
]
} | Caspase-3 expression in metastatic LNs may be a potential independent predictor of poorer overall survival in patients with resected ESCC and LN metastasis. Protein expression in metastatic tumors may be a biomarker prognostic of survival. | yes | [
{
"from": "human",
"value": "Question: Is caspase-3 expression in metastatic lymph nodes of esophageal squamous cell carcinoma prognostic of survival?\nContext: {'contexts': ['To assess whether differential expression of caspase-3 in paired metastatic lymph nodes (LNs) is prognostic of survival in patients with resectable esophageal squamous cell carcinoma (ESCC).', 'Capases-3 expression was evaluated immunohistochemically in 122 pairs of primary ESCCs and regional metastatic LNs assembled on tissue microarrays. The impact of caspase-3 expression on survival outcomes was analyzed by the Kaplan-Meier method and Cox proportional hazards regression model.', 'The level of caspase-3 expression was significantly higher in LN metastases than in primary tumors (P < 0.001). Caspase-3 expression in the primary tumors was associated with longer median survival (23 mo vs 21 mo, P = 0.033), whereas higher expression in paired metastatic LNs was associated with shorter median survival (20 mo vs 22 mo, P = 0.043). Multivariate analysis showed that both were independent prognostic factors.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Biomarkers, Tumor', 'Carcinoma, Squamous Cell', 'Caspase 3', 'Esophageal Neoplasms', 'Esophageal Squamous Cell Carcinoma', 'Female', 'Gene Expression Regulation, Enzymologic', 'Gene Expression Regulation, Neoplastic', 'Humans', 'Immunohistochemistry', 'Kaplan-Meier Estimate', 'Lymph Nodes', 'Lymphatic Metastasis', 'Male', 'Middle Aged', 'Multivariate Analysis', 'Oligonucleotide Array Sequence Analysis', 'Prognosis', 'Proportional Hazards Models', 'Treatment Outcome']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,747,581 | Are elevated levels of pro-inflammatory oxylipins in older subjects normalized by flaxseed consumption? | {
"contexts": [
"Oxylipins, including eicosanoids, are highly bioactive molecules endogenously produced from polyunsaturated fatty acids. Oxylipins play a key role in chronic disease progression. It is possible, but unknown, if oxylipin concentrations change with the consumption of functional foods or differ with subject age.",
"Therefore, in a parallel comparator trial, 20 healthy individuals were recruited into a younger (19-28years) or older (45-64years) age group (n=10/group). Participants ingested one muffin/day containing 30g of milled flaxseed (6g alpha-linolenic acid) for 4weeks. Plasma oxylipins were isolated through solid phase extraction, analyzed with HPLC-MS/MS targeted lipidomics, and quantified with the stable isotope dilution method.",
"At baseline, the older group exhibited 13 oxylipins ≥2-fold the concentration of the younger group. Specifically, pro-inflammatory oxylipins 5-hydroxyeicosatetraenoic acid, 9,10,13-trihydroxyoctadecenoic acid, and 9,12,13-trihydroxyoctadecenoic acid were significantly greater in the older (1.1±0.23nM, 5.6±0.84nM, and 4.5±0.58nM, respectively) versus the younger group (0.34±0.12nM, 3.5±0.33nM, and 3.0±0.24nM, respectively) (p<0.05). After 4weeks of flaxseed consumption the number of oxylipins that were ≥2-fold higher in the older versus the younger group was reduced to 3. 5-Hydroxyeicosatetraenoic acid, 9,10,13-trihydroxyoctadecenoic acid, and 9,12,13-trihydroxyoctadecenoic acid decreased in the older group to concentrations equivalent to the younger group after flaxseed consumption."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Age Factors",
"Aging",
"Diet",
"Female",
"Flax",
"Humans",
"Inflammation Mediators",
"Male",
"Middle Aged",
"Oxylipins",
"Seeds",
"Sex Characteristics",
"Single-Blind Method",
"Young Adult"
]
} | These data suggest a potential role for oxylipins in the aging process and how nutritional interventions like flaxseed can beneficially disrupt these biological changes associated with inflammation and aging. | yes | [
{
"from": "human",
"value": "Question: Are elevated levels of pro-inflammatory oxylipins in older subjects normalized by flaxseed consumption?\nContext: {'contexts': ['Oxylipins, including eicosanoids, are highly bioactive molecules endogenously produced from polyunsaturated fatty acids. Oxylipins play a key role in chronic disease progression. It is possible, but unknown, if oxylipin concentrations change with the consumption of functional foods or differ with subject age.', 'Therefore, in a parallel comparator trial, 20 healthy individuals were recruited into a younger (19-28years) or older (45-64years) age group (n=10/group). Participants ingested one muffin/day containing 30g of milled flaxseed (6g alpha-linolenic acid) for 4weeks. Plasma oxylipins were isolated through solid phase extraction, analyzed with HPLC-MS/MS targeted lipidomics, and quantified with the stable isotope dilution method.', 'At baseline, the older group exhibited 13 oxylipins ≥2-fold the concentration of the younger group. Specifically, pro-inflammatory oxylipins 5-hydroxyeicosatetraenoic acid, 9,10,13-trihydroxyoctadecenoic acid, and 9,12,13-trihydroxyoctadecenoic acid were significantly greater in the older (1.1±0.23nM, 5.6±0.84nM, and 4.5±0.58nM, respectively) versus the younger group (0.34±0.12nM, 3.5±0.33nM, and 3.0±0.24nM, respectively) (p<0.05). After 4weeks of flaxseed consumption the number of oxylipins that were ≥2-fold higher in the older versus the younger group was reduced to 3. 5-Hydroxyeicosatetraenoic acid, 9,10,13-trihydroxyoctadecenoic acid, and 9,12,13-trihydroxyoctadecenoic acid decreased in the older group to concentrations equivalent to the younger group after flaxseed consumption.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Age Factors', 'Aging', 'Diet', 'Female', 'Flax', 'Humans', 'Inflammation Mediators', 'Male', 'Middle Aged', 'Oxylipins', 'Seeds', 'Sex Characteristics', 'Single-Blind Method', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,750,990 | Does use of statin during hospitalization improve the outcome after intracerebral hemorrhage? | {
"contexts": [
"To examine the relationship between statin use in Chinese patients with intracerebral hemorrhage (ICH) during their hospitalization and the outcomes.",
"Data were collected from the China National Stroke Registry. Good functional outcome was defined by a modified Rankin Scale score between 0-2. Functional outcome and rate of mortality at 3 months and 1 year were compared between ICH patients on statin and those without it during their hospitalization. Odds ratios (ORs) with 95% confidence intervals (CI) were calculated using the multivariable logistic regression model adjusted for baseline risk factors.",
"Among 3218 consecutive ICH patients from 2007 to 2008, 220 (6.8%) were on statin during their hospitalization. Compared with those without statin, patients on statin were younger, had more stroke risk factors but lower stroke severity. ICH patients on statin had better functional outcome at 3 months (OR 2.24, 95% CI 1.49-3.36) and at 1 year (OR 2.04, 95% CI 1.37-3.06). They also had lower rate of mortality at 3 months (OR 0.44, 95% CI 0.22-0.87) and 1 year (OR 0.49, 95% CI 0.27-0.86)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Cerebral Hemorrhage",
"China",
"Female",
"Follow-Up Studies",
"Hospitalization",
"Humans",
"Hydroxymethylglutaryl-CoA Reductase Inhibitors",
"Male",
"Middle Aged",
"Outcome Assessment (Health Care)",
"Registries",
"Retrospective Studies",
"Risk Factors",
"Severity of Illness Index",
"Statistics, Nonparametric",
"Treatment Outcome"
]
} | In-hospital statin use in ICH patients is associated with better functional outcome and lower mortality at 3 months and 1 year. | yes | [
{
"from": "human",
"value": "Question: Does use of statin during hospitalization improve the outcome after intracerebral hemorrhage?\nContext: {'contexts': ['To examine the relationship between statin use in Chinese patients with intracerebral hemorrhage (ICH) during their hospitalization and the outcomes.', 'Data were collected from the China National Stroke Registry. Good functional outcome was defined by a modified Rankin Scale score between 0-2. Functional outcome and rate of mortality at 3 months and 1 year were compared between ICH patients on statin and those without it during their hospitalization. Odds ratios (ORs) with 95% confidence intervals (CI) were calculated using the multivariable logistic regression model adjusted for baseline risk factors.', 'Among 3218 consecutive ICH patients from 2007 to 2008, 220 (6.8%) were on statin during their hospitalization. Compared with those without statin, patients on statin were younger, had more stroke risk factors but lower stroke severity. ICH patients on statin had better functional outcome at 3 months (OR 2.24, 95% CI 1.49-3.36) and at 1 year (OR 2.04, 95% CI 1.37-3.06). They also had lower rate of mortality at 3 months (OR 0.44, 95% CI 0.22-0.87) and 1 year (OR 0.49, 95% CI 0.27-0.86).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Cerebral Hemorrhage', 'China', 'Female', 'Follow-Up Studies', 'Hospitalization', 'Humans', 'Hydroxymethylglutaryl-CoA Reductase Inhibitors', 'Male', 'Middle Aged', 'Outcome Assessment (Health Care)', 'Registries', 'Retrospective Studies', 'Risk Factors', 'Severity of Illness Index', 'Statistics, Nonparametric', 'Treatment Outcome']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,760,722 | Do human blastocysts exhibit unique microrna profiles in relation to maternal age and chromosome constitution? | {
"contexts": [
"To determine microRNA (miRNA) expression in human blastocysts relative to advanced maternal age and chromosome constitution.",
"Cryopreserved human blastocysts were warmed and underwent a trophectoderm biopsy for comprehensive chromosomal screening. Select blastocysts were then lysed, reverse transcribed, and pre-amplified prior to running real-time PCR. Statistical analysis was performed using an internal constant housekeeping miRNA. Significant microRNA's of interest were then analyzed for their predicted genes and biological pathways. Additional cryopreserved blastocysts were warmed and stained for the SIRT1 protein for validation.",
"Human blastocysts exhibit unique miRNA expression profiles in relation to maternal age and chromosome constitution. miR-93 was exclusively expressed in blastocysts from women in their forties and further up-regulated with an abnormal chromosome complement. Up-regulated miR-93 resulted in an inverse down-regulation of targets like SIRT1, resulting in reduced oxidative defense."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aneuploidy",
"Blastocyst",
"Chromosomes",
"Female",
"Gene Expression Profiling",
"Humans",
"Maternal Age",
"MicroRNAs"
]
} | MiRNAs play an important role in aging as well as chromosome constitution and have downstream effects that regulate proteins which can compromise embryonic development. | yes | [
{
"from": "human",
"value": "Question: Do human blastocysts exhibit unique microrna profiles in relation to maternal age and chromosome constitution?\nContext: {'contexts': ['To determine microRNA (miRNA) expression in human blastocysts relative to advanced maternal age and chromosome constitution.', \"Cryopreserved human blastocysts were warmed and underwent a trophectoderm biopsy for comprehensive chromosomal screening. Select blastocysts were then lysed, reverse transcribed, and pre-amplified prior to running real-time PCR. Statistical analysis was performed using an internal constant housekeeping miRNA. Significant microRNA's of interest were then analyzed for their predicted genes and biological pathways. Additional cryopreserved blastocysts were warmed and stained for the SIRT1 protein for validation.\", 'Human blastocysts exhibit unique miRNA expression profiles in relation to maternal age and chromosome constitution. miR-93 was exclusively expressed in blastocysts from women in their forties and further up-regulated with an abnormal chromosome complement. Up-regulated miR-93 resulted in an inverse down-regulation of targets like SIRT1, resulting in reduced oxidative defense.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aneuploidy', 'Blastocyst', 'Chromosomes', 'Female', 'Gene Expression Profiling', 'Humans', 'Maternal Age', 'MicroRNAs']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,745,780 | Is the relation between hostility and concurrent levels of inflammation sex , age , and measure dependent? | {
"contexts": [
"Hostility may be associated with greater systemic inflammation. However, contradictory evidence exists. Certain individuals or dimensions of hostility may be more susceptible to these effects. Main and interactive effects of hostility with sex and/or age were evaluated on markers of inflammation, independently of traditional risk factors for coronary artery disease.",
"199 healthy men (81) and women (118), aged 20-64 years (M=41 ± 11 years) were recruited. Hostility was assessed using the Cook-Medley Hostility Inventory (CMHo) and ecological momentary assessments (EMA) of quarrelsome behavior and angry affect in daily living. Blood samples were drawn to measure inflammatory activity (Il-6, TNF-α, hsCRP, Il-8, Il-10, Il-18, MCP-1) and lipid oxidation (Myeloperoxidase; MPO). Correlations and hierarchical regression analyses were performed controlling for pertinent behavioral, psychological, medical, and socio-demographic factors.",
"Significant univariate associations emerged between CMHo and Il-6, TNF-α, MCP-1 (p<.05). Hierarchical regressions showed interactions of hostility with sex (Il-6, TNF-α; p<.05) and age (hsCRP, Il-6, TNF-α; p<.05). For example, in simple slope analyses, hostility was positively related to TNF-α in women (b=0.009, p=0.006) but not men. Greater hostility was also related to greater Il-6 levels among younger women (b=. 027, p=0.000)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Biomarkers",
"C-Reactive Protein",
"Coronary Artery Disease",
"Female",
"Hostility",
"Humans",
"Inflammation",
"Interleukin-6",
"Male",
"Middle Aged",
"Personality Inventory",
"Risk Assessment",
"Risk Factors",
"Tumor Necrosis Factor-alpha"
]
} | Hostility, particularly cynical hostility, may be detrimental to (younger) women. The TNF-α, Il-6, CRP triad appears vulnerable to psychological and behavioral factors, and may be one mechanism by which cynical hostility (CMHo) contributes to increased cardiovascular risk in women. Prospective research is needed to verify this. | yes | [
{
"from": "human",
"value": "Question: Is the relation between hostility and concurrent levels of inflammation sex , age , and measure dependent?\nContext: {'contexts': ['Hostility may be associated with greater systemic inflammation. However, contradictory evidence exists. Certain individuals or dimensions of hostility may be more susceptible to these effects. Main and interactive effects of hostility with sex and/or age were evaluated on markers of inflammation, independently of traditional risk factors for coronary artery disease.', '199 healthy men (81) and women (118), aged 20-64 years (M=41 ± 11 years) were recruited. Hostility was assessed using the Cook-Medley Hostility Inventory (CMHo) and ecological momentary assessments (EMA) of quarrelsome behavior and angry affect in daily living. Blood samples were drawn to measure inflammatory activity (Il-6, TNF-α, hsCRP, Il-8, Il-10, Il-18, MCP-1) and lipid oxidation (Myeloperoxidase; MPO). Correlations and hierarchical regression analyses were performed controlling for pertinent behavioral, psychological, medical, and socio-demographic factors.', 'Significant univariate associations emerged between CMHo and Il-6, TNF-α, MCP-1 (p<.05). Hierarchical regressions showed interactions of hostility with sex (Il-6, TNF-α; p<.05) and age (hsCRP, Il-6, TNF-α; p<.05). For example, in simple slope analyses, hostility was positively related to TNF-α in women (b=0.009, p=0.006) but not men. Greater hostility was also related to greater Il-6 levels among younger women (b=. 027, p=0.000).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Biomarkers', 'C-Reactive Protein', 'Coronary Artery Disease', 'Female', 'Hostility', 'Humans', 'Inflammation', 'Interleukin-6', 'Male', 'Middle Aged', 'Personality Inventory', 'Risk Assessment', 'Risk Factors', 'Tumor Necrosis Factor-alpha']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,762,259 | Is a decline in inflammation associated with less depressive symptoms after a dietary intervention in metabolic syndrome patients : a longitudinal study? | {
"contexts": [
"Metabolic syndrome (MetS) and depression have become two prevalent diseases worldwide, whose interaction needs further investigation. Dietary treatment for weight loss in patients with MetS may improve depressive manifestations, however, the precise interactive pathways remain uncertain. Therefore, the aim of this study was to examine the effects of a hypocaloric diet designed to reduce MetS features on self-perceived depression and the possible underlying factors.",
"Sixty subjects (Age: 50 ± 1 y; BMI: 36.1 ± 0.6 kg/m(2)) with MetS were selected from the RESMENA study (control and intervention) after they completed the 6-months hypocaloric treatment and rated for depressive symptoms using the Beck Depression Inventory (BDI). Anthropometric and biochemical measurements including leptin, C-reactive protein (CRP) and insulin levels were evaluated.",
"Depressive symptoms decreased during the weight loss intervention, with no differences between both dietary groups (control group -4.2 ± 0.8 vs RESMENA group -3.2 ± 0.6, P = 0.490). The number of criteria of the MetS was higher among subjects with more somatic-related depressive symptoms at baseline (B = 1.032, P-trend = 0.017). After six months of dietary treatment, body weight decreased in all subjects (-8.7%; confidence interval (95% CI) = 7.0-9.7) and also self-perceived depression (-37.9%; 95% CI = 2.7-4.9), as well as circulating leptin (-20.1%; 95% CI = 1.8-6.8), CRP (-42.8%; 95% CI = 0.6-3.0) and insulin (-37.7%; 95% CI = 4.1-7.2) concentrations. The decrease in BDI was significantly associated with declines in body fat mass (B = 0.34, 95% CI = 0.11-0.56) and also with the decrease in leptin (B = 0.16, 95% CI = 0.04-0.28) and CRP (B = 0.24, 95% CI = 0.01-0.46) concentrations."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"C-Reactive Protein",
"Depression",
"Diet, Reducing",
"Female",
"Humans",
"Inflammation",
"Longitudinal Studies",
"Male",
"Metabolic Syndrome",
"Middle Aged",
"Weight Loss"
]
} | The decrease in depressive manifestations after a weight loss intervention was related with adiposity, CRP and leptin in subjects with MetS. | yes | [
{
"from": "human",
"value": "Question: Is a decline in inflammation associated with less depressive symptoms after a dietary intervention in metabolic syndrome patients : a longitudinal study?\nContext: {'contexts': ['Metabolic syndrome (MetS) and depression have become two prevalent diseases worldwide, whose interaction needs further investigation. Dietary treatment for weight loss in patients with MetS may improve depressive manifestations, however, the precise interactive pathways remain uncertain. Therefore, the aim of this study was to examine the effects of a hypocaloric diet designed to reduce MetS features on self-perceived depression and the possible underlying factors.', 'Sixty subjects (Age: 50 ± 1 y; BMI: 36.1 ± 0.6 kg/m(2)) with MetS were selected from the RESMENA study (control and intervention) after they completed the 6-months hypocaloric treatment and rated for depressive symptoms using the Beck Depression Inventory (BDI). Anthropometric and biochemical measurements including leptin, C-reactive protein (CRP) and insulin levels were evaluated.', 'Depressive symptoms decreased during the weight loss intervention, with no differences between both dietary groups (control group -4.2 ± 0.8 vs RESMENA group -3.2 ± 0.6, P = 0.490). The number of criteria of the MetS was higher among subjects with more somatic-related depressive symptoms at baseline (B = 1.032, P-trend = 0.017). After six months of dietary treatment, body weight decreased in all subjects (-8.7%; confidence interval (95% CI)\\u2009= 7.0-9.7) and also self-perceived depression (-37.9%; 95% CI = 2.7-4.9), as well as circulating leptin (-20.1%; 95% CI = 1.8-6.8), CRP (-42.8%; 95% CI = 0.6-3.0) and insulin (-37.7%; 95% CI = 4.1-7.2) concentrations. The decrease in BDI was significantly associated with declines in body fat mass (B = 0.34, 95% CI = 0.11-0.56) and also with the decrease in leptin (B = 0.16, 95% CI = 0.04-0.28) and CRP (B = 0.24, 95% CI = 0.01-0.46) concentrations.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['C-Reactive Protein', 'Depression', 'Diet, Reducing', 'Female', 'Humans', 'Inflammation', 'Longitudinal Studies', 'Male', 'Metabolic Syndrome', 'Middle Aged', 'Weight Loss']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,776,841 | Is low serum allopregnanolone associated with symptoms of depression in late pregnancy? | {
"contexts": [
"Allopregnanolone (3α-hydroxy-5α-pregnan-20-one) is a neurosteroid which has an inhibitory function through interaction with the GABAA receptor. This progesterone metabolite has strong sedative and anxiolytic properties, and low endogenous levels have been associated with depressed mood. This study aimed to investigate whether the very high serum allopregnanolone levels in late pregnancy covary with concurrent self-rated symptoms of depression and anxiety.",
"Ninety-six women in pregnancy weeks 37-40 rated symptoms of depression and anxiety with the Montgomery-Åsberg Depression Rating Scale (MADRS-S) and Spielberger State-Trait Anxiety Inventory. Their serum allopregnanolone was analyzed by Celite chromatography and radioimmunoassay.",
"Ten women had elevated depression scores (MADRS-S ≥ 13), and this group had significantly lower allopregnanolone levels compared to women with MADRS-S scores in the normal range (39.0 ± 17.9 vs. 54.6 ± 18.7 nmol/l, p = 0.014). A significant negative correlation was found between self-rated depression scores and allopregnanolone concentrations (Pearson's correlation coefficient = -0.220, p = 0.031). The linear association between self-rated depression scores and allopregnanolone serum concentrations remained significant when adjusted for gestational length, progesterone levels, and parity. Self-rated anxiety, however, was not associated with allopregnanolone serum concentrations during pregnancy."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Anxiety",
"Depression",
"Depression, Postpartum",
"Female",
"Humans",
"Pregnancy",
"Pregnancy Complications",
"Pregnancy Trimester, Third",
"Pregnanolone",
"Self Report",
"Young Adult"
]
} | High allopregnanolone serum concentrations may protect against depressed mood during pregnancy. | yes | [
{
"from": "human",
"value": "Question: Is low serum allopregnanolone associated with symptoms of depression in late pregnancy?\nContext: {'contexts': ['Allopregnanolone (3α-hydroxy-5α-pregnan-20-one) is a neurosteroid which has an inhibitory function through interaction with the GABAA receptor. This progesterone metabolite has strong sedative and anxiolytic properties, and low endogenous levels have been associated with depressed mood. This study aimed to investigate whether the very high serum allopregnanolone levels in late pregnancy covary with concurrent self-rated symptoms of depression and anxiety.', 'Ninety-six women in pregnancy weeks 37-40 rated symptoms of depression and anxiety with the Montgomery-Åsberg Depression Rating Scale (MADRS-S) and Spielberger State-Trait Anxiety Inventory. Their serum allopregnanolone was analyzed by Celite chromatography and radioimmunoassay.', \"Ten women had elevated depression scores (MADRS-S ≥ 13), and this group had significantly lower allopregnanolone levels compared to women with MADRS-S scores in the normal range (39.0 ± 17.9 vs. 54.6 ± 18.7 nmol/l, p = 0.014). A significant negative correlation was found between self-rated depression scores and allopregnanolone concentrations (Pearson's correlation coefficient = -0.220, p = 0.031). The linear association between self-rated depression scores and allopregnanolone serum concentrations remained significant when adjusted for gestational length, progesterone levels, and parity. Self-rated anxiety, however, was not associated with allopregnanolone serum concentrations during pregnancy.\"], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Anxiety', 'Depression', 'Depression, Postpartum', 'Female', 'Humans', 'Pregnancy', 'Pregnancy Complications', 'Pregnancy Trimester, Third', 'Pregnanolone', 'Self Report', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,767,726 | Does chronic intermittent hypoxia cause endothelial dysfunction in a mouse model of diet-induced obesity? | {
"contexts": [
"Obstructive sleep apnea (OSA) is a common disorder characterized by chronic intermittent hypoxia (CIH). OSA is prevalent in obese subjects and is associated with endothelial dysfunction and cardiovascular disorders. We tested the hypothesis that the deleterious effects of IH could be further modulated by diet-induced obesity.",
"Thirty adult (8-10 weeks) male C57BL/6J mice were divided into four groups. Mice were subjected to CIH or intermittent air (IA) for 12h a day and fed either a high fat (HF) or a low fat control diet (CD) for 6weeks. We analyzed endothelial function using a wire myograph, and measured markers of oxidative stress (plasma malondialdehyde (MDA) and total antioxidant capacity (TAC)) using colorimetrical assays. We also measured C-reactive protein (CRP) using ELISA and endothelial nitric oxide (eNOS) gene expression using real time PCR.",
"Stimulated endothelial dependent dilation was significantly impaired only in the group fed high fat diet and subjected to CIH (Emax: HFIH 78±2%, p<0.0001) when compared to the other groups (Emax: HFIA 95±0.7%, CDIH 94±2%, CDIA 97±1%). Also basal endothelial dependant dilation was attenuated in the HFIH group compared to the HFIA group (Emax: HFIH: 179±10% vs. HFIA: 149±11% in the presence of L-NAME). Levels of MDA were elevated in the CDIH group when compared to CDIA (0.68±0.04 vs. 0.41±0.03 μM, p<0.05) but were greatest in the HFIH group (0.83±0.08 μM, p<0.05). However, there was no significant increase in MDA levels in the HFIA group (0.45±0.03 μM, p=NS) when compared to all other groups. Similar effects were observed with CRP levels; CRP levels were significantly higher in the CDIH group compared with intermittent air (10.39±0.38 vs. 8.70±0.21 μg/ml, p<0.05) but the HFIH had the greatest levels of CRP (11.87±0.31 μg/ml, p<0.05). In the HFIA group, CRP levels were not elevated (9.96±0.37 μg/ml, p=NS). Nevertheless, total antioxidant capacity and eNOS gene expression were not significantly different in the groups."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Aorta",
"C-Reactive Protein",
"Diet",
"Disease Models, Animal",
"Endothelium, Vascular",
"Hypoxia",
"Male",
"Malondialdehyde",
"Mice",
"Mice, Inbred C57BL",
"Myography",
"Nitric Oxide Synthase Type III",
"Obesity",
"Oxidative Stress",
"Real-Time Polymerase Chain Reaction",
"Sleep Apnea, Obstructive",
"Vasodilation"
]
} | CIH caused endothelial dysfunction in mice fed an obesogenic diet. Inflammation and oxidative stress were increased in CIH and an obesogenic diet exacerbated these effects. | yes | [
{
"from": "human",
"value": "Question: Does chronic intermittent hypoxia cause endothelial dysfunction in a mouse model of diet-induced obesity?\nContext: {'contexts': ['Obstructive sleep apnea (OSA) is a common disorder characterized by chronic intermittent hypoxia (CIH). OSA is prevalent in obese subjects and is associated with endothelial dysfunction and cardiovascular disorders. We tested the hypothesis that the deleterious effects of IH could be further modulated by diet-induced obesity.', 'Thirty adult (8-10 weeks) male C57BL/6J mice were divided into four groups. Mice were subjected to CIH or intermittent air (IA) for 12h a day and fed either a high fat (HF) or a low fat control diet (CD) for 6weeks. We analyzed endothelial function using a wire myograph, and measured markers of oxidative stress (plasma malondialdehyde (MDA) and total antioxidant capacity (TAC)) using colorimetrical assays. We also measured C-reactive protein (CRP) using ELISA and endothelial nitric oxide (eNOS) gene expression using real time PCR.', 'Stimulated endothelial dependent dilation was significantly impaired only in the group fed high fat diet and subjected to CIH (Emax: HFIH 78±2%, p<0.0001) when compared to the other groups (Emax: HFIA 95±0.7%, CDIH 94±2%, CDIA 97±1%). Also basal endothelial dependant dilation was attenuated in the HFIH group compared to the HFIA group (Emax: HFIH: 179±10% vs. HFIA: 149±11% in the presence of L-NAME). Levels of MDA were elevated in the CDIH group when compared to CDIA (0.68±0.04 vs. 0.41±0.03 μM, p<0.05) but were greatest in the HFIH group (0.83±0.08 μM, p<0.05). However, there was no significant increase in MDA levels in the HFIA group (0.45±0.03 μM, p=NS) when compared to all other groups. Similar effects were observed with CRP levels; CRP levels were significantly higher in the CDIH group compared with intermittent air (10.39±0.38 vs. 8.70±0.21 μg/ml, p<0.05) but the HFIH had the greatest levels of CRP (11.87±0.31 μg/ml, p<0.05). In the HFIA group, CRP levels were not elevated (9.96±0.37 μg/ml, p=NS). Nevertheless, total antioxidant capacity and eNOS gene expression were not significantly different in the groups.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Aorta', 'C-Reactive Protein', 'Diet', 'Disease Models, Animal', 'Endothelium, Vascular', 'Hypoxia', 'Male', 'Malondialdehyde', 'Mice', 'Mice, Inbred C57BL', 'Myography', 'Nitric Oxide Synthase Type III', 'Obesity', 'Oxidative Stress', 'Real-Time Polymerase Chain Reaction', 'Sleep Apnea, Obstructive', 'Vasodilation']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,748,552 | Is cXCR4 highly expressed at the tumor front but not in the center of prostate cancers? | {
"contexts": [
"To evaluate the expression of CXCR4, its ligand SDF-1, β-catenin and E-cadherin throughout the local tumor microenvironment of prostate cancer.",
"A total of 64 prostate cancer specimens, 24 frozen and 40 paraffin-embedded sections, were obtained from patients treated with radical prostatectomy for clinically localized cancer. Real-time RT-PCR was used for mRNA quantification of CXCR4 and SDF-1 in the tumor center (T), tumor front (F) and distant peritumoral tissue (D). Immunohistochemical analysis was used to investigate the expression patterns of CXCR4, E-cadherin and β-catenin. Clinical records of these patients were studied for follow-up data, and the prognostic value of these molecules' expression was statistically assessed.",
"CXCR4 mRNA and protein were significantly increased at the tumor front as compared to distant tissue or tumor center. In comparison, SDF-1 mRNA level gradually increased from the tumor center to the distant peritumoral tissue. High CXCR4 at the tumor front was associated with high Gleason score. Low SDF-1 at the tumor front was associated with locally advanced cancer and disease recurrence. Moreover, high CXCR4 staining at the tumor front and increased cytosolic E-cadherin expression in the same location was associated with locally advanced disease."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Biomarkers, Tumor",
"Cadherins",
"Cell Movement",
"Chemokine CXCL12",
"Humans",
"Male",
"Middle Aged",
"Prognosis",
"Prostatectomy",
"Prostatic Neoplasms",
"RNA, Messenger",
"Receptors, CXCR4",
"beta Catenin"
]
} | CXCR4 seems overexpressed at the tumor front of prostate tumors, where it potentially promotes cell migration toward the SDF-1 centrifugal attracting gradient, as well as epithelial-mesenchymal transition. High CXCR4 and low SDF-1 levels at tumor front were both associated with adverse histological features. | yes | [
{
"from": "human",
"value": "Question: Is cXCR4 highly expressed at the tumor front but not in the center of prostate cancers?\nContext: {'contexts': ['To evaluate the expression of CXCR4, its ligand SDF-1, β-catenin and E-cadherin throughout the local tumor microenvironment of prostate cancer.', \"A total of 64 prostate cancer specimens, 24 frozen and 40 paraffin-embedded sections, were obtained from patients treated with radical prostatectomy for clinically localized cancer. Real-time RT-PCR was used for mRNA quantification of CXCR4 and SDF-1 in the tumor center (T), tumor front (F) and distant peritumoral tissue (D). Immunohistochemical analysis was used to investigate the expression patterns of CXCR4, E-cadherin and β-catenin. Clinical records of these patients were studied for follow-up data, and the prognostic value of these molecules' expression was statistically assessed.\", 'CXCR4 mRNA and protein were significantly increased at the tumor front as compared to distant tissue or tumor center. In comparison, SDF-1 mRNA level gradually increased from the tumor center to the distant peritumoral tissue. High CXCR4 at the tumor front was associated with high Gleason score. Low SDF-1 at the tumor front was associated with locally advanced cancer and disease recurrence. Moreover, high CXCR4 staining at the tumor front and increased cytosolic E-cadherin expression in the same location was associated with locally advanced disease.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Biomarkers, Tumor', 'Cadherins', 'Cell Movement', 'Chemokine CXCL12', 'Humans', 'Male', 'Middle Aged', 'Prognosis', 'Prostatectomy', 'Prostatic Neoplasms', 'RNA, Messenger', 'Receptors, CXCR4', 'beta Catenin']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,757,684 | Do adipose-derived mesenchymal stem cells from ventral hernia repair patients demonstrate decreased vasculogenesis? | {
"contexts": [
"In adipose tissue healing, angiogenesis is stimulated by adipose-derived stromal stem cells (ASCs). Ventral hernia repair (VHR) patients are at high risk for wound infections. We hypothesize that ASCs from VHR patients are less vasculogenic than ASCs from healthy controls.",
"ASCs were harvested from the subcutaneous fat of patients undergoing VHR by the component separation technique and from matched abdominoplasty patients. RNA and protein were harvested on culture days 0 and 3. Both groups of ASCs were subjected to hypoxic conditions for 12 and 24 hours. RNA was analyzed using qRT-PCR, and protein was used for western blotting. ASCs were also grown in Matrigel under hypoxic conditions and assayed for tubule formation after 24 hours.",
"Hernia patient ASCs demonstrated decreased levels of VEGF-A protein and vasculogenic RNA at 3 days of growth in differentiation media. There were also decreases in VEGF-A protein and vasculogenic RNA after growth in hypoxic conditions compared to control ASCs. After 24 hours in hypoxia, VHR ASCs formed fewer tubules in Matrigel than in control patient ASCs."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Cells, Cultured",
"Female",
"Hernia, Ventral",
"Humans",
"Male",
"Mesenchymal Stem Cells",
"Middle Aged",
"Neovascularization, Physiologic",
"RNA",
"Vascular Endothelial Growth Factor A"
]
} | ASCs derived from VHR patients appear to express fewer vasculogenic markers and form fewer tubules in Matrigel than ASCs from abdominoplasty patients, suggesting decreased vasculogenic activity. | yes | [
{
"from": "human",
"value": "Question: Do adipose-derived mesenchymal stem cells from ventral hernia repair patients demonstrate decreased vasculogenesis?\nContext: {'contexts': ['In adipose tissue healing, angiogenesis is stimulated by adipose-derived stromal stem cells (ASCs). Ventral hernia repair (VHR) patients are at high risk for wound infections. We hypothesize that ASCs from VHR patients are less vasculogenic than ASCs from healthy controls.', 'ASCs were harvested from the subcutaneous fat of patients undergoing VHR by the component separation technique and from matched abdominoplasty patients. RNA and protein were harvested on culture days 0 and 3. Both groups of ASCs were subjected to hypoxic conditions for 12 and 24 hours. RNA was analyzed using qRT-PCR, and protein was used for western blotting. ASCs were also grown in Matrigel under hypoxic conditions and assayed for tubule formation after 24 hours.', 'Hernia patient ASCs demonstrated decreased levels of VEGF-A protein and vasculogenic RNA at 3 days of growth in differentiation media. There were also decreases in VEGF-A protein and vasculogenic RNA after growth in hypoxic conditions compared to control ASCs. After 24 hours in hypoxia, VHR ASCs formed fewer tubules in Matrigel than in control patient ASCs.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Cells, Cultured', 'Female', 'Hernia, Ventral', 'Humans', 'Male', 'Mesenchymal Stem Cells', 'Middle Aged', 'Neovascularization, Physiologic', 'RNA', 'Vascular Endothelial Growth Factor A']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,769,560 | Are blood cadmium levels associated with a decline in lung function in males? | {
"contexts": [
"Cadmium exposure was found to cause a decline in lung function among the general population, but these findings were limited to smokers and gender differences were not explored.",
"To examine the relationship between cadmium and chronic obstructive pulmonary disease (COPD) according to gender and smoking status in Korea.",
"Cross-sectional data from the Korean National Health and Nutrition Examination Survey from 2008 to 2011 were analyzed. COPD was defined by a pre-bronchodilator forced expiratory volume in 1s divided by forced vital capacity of <0.70. A logistic regression model was used to elucidate the association between blood cadmium levels and COPD according to gender and smoking status.",
"Among 3861 eligible participants, 3622 were included in the analysis. The prevalence of COPD demonstrated an increasing trend in males (P for trend<0.001), but not in females (P for trend=0.67). After adjusting for covariates, a higher blood cadmium level, but within the normal range, was associated with COPD in males, including those who had never-smoked (P for trend <0.001 and P for trend=0.008). However, a higher blood cadmium level was not significantly associated with COPD in females, including those who had never smoked (P for trend=0.39 and P for trend=0.43)."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Cadmium",
"Cross-Sectional Studies",
"Female",
"Humans",
"Lung",
"Male",
"Middle Aged",
"Pulmonary Disease, Chronic Obstructive",
"Respiratory Function Tests",
"Sex Characteristics"
]
} | A higher blood cadmium level, within the normal range, was associated with COPD in males, including those who had never smoked. However, there was no significant association between blood cadmium levels and COPD in females. | yes | [
{
"from": "human",
"value": "Question: Are blood cadmium levels associated with a decline in lung function in males?\nContext: {'contexts': ['Cadmium exposure was found to cause a decline in lung function among the general population, but these findings were limited to smokers and gender differences were not explored.', 'To examine the relationship between cadmium and chronic obstructive pulmonary disease (COPD) according to gender and smoking status in Korea.', 'Cross-sectional data from the Korean National Health and Nutrition Examination Survey from 2008 to 2011 were analyzed. COPD was defined by a pre-bronchodilator forced expiratory volume in 1s divided by forced vital capacity of <0.70. A logistic regression model was used to elucidate the association between blood cadmium levels and COPD according to gender and smoking status.', 'Among 3861 eligible participants, 3622 were included in the analysis. The prevalence of COPD demonstrated an increasing trend in males (P for trend<0.001), but not in females (P for trend=0.67). After adjusting for covariates, a higher blood cadmium level, but within the normal range, was associated with COPD in males, including those who had never-smoked (P for trend <0.001 and P for trend=0.008). However, a higher blood cadmium level was not significantly associated with COPD in females, including those who had never smoked (P for trend=0.39 and P for trend=0.43).'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Cadmium', 'Cross-Sectional Studies', 'Female', 'Humans', 'Lung', 'Male', 'Middle Aged', 'Pulmonary Disease, Chronic Obstructive', 'Respiratory Function Tests', 'Sex Characteristics']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,778,036 | Does genetics of lymphocytes influence the emergence of second cancer in chronic lymphocytic leukemia? | {
"contexts": [
"Patients affected by chronic lymphocytic leukemia (CLL) have an increased risk of developing a second cancer. There is not a definitive explanation for this phenomenon, although some hypotheses have been postulated. The aim of the present work was to assess the presence of second cancer in untreated patients with CLL who were cytogenetically characterized, and secondly to investigate if there is a correlation between the genetics of CLL and the emergence of second cancer.",
"We performed conventional cytogenetics and Fluorescent in situ hybridization analyses in a series of 106 patients.",
"We observed that nearly 8% of cases developed second cancer, mostly epithelial tumors. The majority of them presented two common features, del(13)(q14.3) and the presence of at least two genetic alterations."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Abnormal Karyotype",
"Aged",
"Aged, 80 and over",
"Chromosome Aberrations",
"Cytogenetics",
"Female",
"Humans",
"In Situ Hybridization, Fluorescence",
"Leukemia, Lymphocytic, Chronic, B-Cell",
"Male",
"Middle Aged",
"Neoplasms, Second Primary"
]
} | We suggest that the genetic background of CLL, particularly the presence of several genetic alterations, influences the emergence of second cancer in patients affected by CLL. | yes | [
{
"from": "human",
"value": "Question: Does genetics of lymphocytes influence the emergence of second cancer in chronic lymphocytic leukemia?\nContext: {'contexts': ['Patients affected by chronic lymphocytic leukemia (CLL) have an increased risk of developing a second cancer. There is not a definitive explanation for this phenomenon, although some hypotheses have been postulated. The aim of the present work was to assess the presence of second cancer in untreated patients with CLL who were cytogenetically characterized, and secondly to investigate if there is a correlation between the genetics of CLL and the emergence of second cancer.', 'We performed conventional cytogenetics and Fluorescent in situ hybridization analyses in a series of 106 patients.', 'We observed that nearly 8% of cases developed second cancer, mostly epithelial tumors. The majority of them presented two common features, del(13)(q14.3) and the presence of at least two genetic alterations.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Abnormal Karyotype', 'Aged', 'Aged, 80 and over', 'Chromosome Aberrations', 'Cytogenetics', 'Female', 'Humans', 'In Situ Hybridization, Fluorescence', 'Leukemia, Lymphocytic, Chronic, B-Cell', 'Male', 'Middle Aged', 'Neoplasms, Second Primary']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,778,030 | Does targeting aurora kinase A inhibit hypoxia-mediated neuroblastoma cell tumorigenesis? | {
"contexts": [
"It is unknown whether hypoxia regulates aurora kinase A (AURKA), a serine/threonine kinase, in neuroblastoma to stimulate cell growth or migration. We sought to determine whether AURKA mediates hypoxia-induced regulation of neuroblastoma tumorigenicity.",
"Human neuroblastoma BE(2)-C cells were treated with CoCl2, a chemical hypoxia mimetic, and MLN8237, a pharmalogical inhibitor of AURKA, to assess cell viability, colony formation and transwell migration. Focal adhesion kinase (FAK) expression was analyzed after silencing of AURKA under normoxic vs. hypoxic conditions.",
"Hypoxia up-regulated expression of AURKA mRNA and protein. CoCl2 stimulated cell proliferation and migration, while inhibiting colony formation. MLN8237 reduced colony formation and cell migration. Silencing of AURKA reduced expression of FAK and pFAK under normoxia and hypoxia."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aurora Kinase A",
"Carcinogenesis",
"Cell Hypoxia",
"Cell Line, Tumor",
"Cell Movement",
"Cell Proliferation",
"Humans",
"Immunoblotting",
"Neuroblastoma",
"RNA Interference",
"Real-Time Polymerase Chain Reaction",
"Reverse Transcriptase Polymerase Chain Reaction",
"Transfection"
]
} | Hypoxia positively regulates AURKA expression. Hypoxia-induced stimulation of colony formation and migration is, in part, mediated by AURKA. These findings establish that AURKA is a critical regulator of hypoxia-mediated tumor progression in neuroblastoma. | yes | [
{
"from": "human",
"value": "Question: Does targeting aurora kinase A inhibit hypoxia-mediated neuroblastoma cell tumorigenesis?\nContext: {'contexts': ['It is unknown whether hypoxia regulates aurora kinase A (AURKA), a serine/threonine kinase, in neuroblastoma to stimulate cell growth or migration. We sought to determine whether AURKA mediates hypoxia-induced regulation of neuroblastoma tumorigenicity.', 'Human neuroblastoma BE(2)-C cells were treated with CoCl2, a chemical hypoxia mimetic, and MLN8237, a pharmalogical inhibitor of AURKA, to assess cell viability, colony formation and transwell migration. Focal adhesion kinase (FAK) expression was analyzed after silencing of AURKA under normoxic vs. hypoxic conditions.', 'Hypoxia up-regulated expression of AURKA mRNA and protein. CoCl2 stimulated cell proliferation and migration, while inhibiting colony formation. MLN8237 reduced colony formation and cell migration. Silencing of AURKA reduced expression of FAK and pFAK under normoxia and hypoxia.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aurora Kinase A', 'Carcinogenesis', 'Cell Hypoxia', 'Cell Line, Tumor', 'Cell Movement', 'Cell Proliferation', 'Humans', 'Immunoblotting', 'Neuroblastoma', 'RNA Interference', 'Real-Time Polymerase Chain Reaction', 'Reverse Transcriptase Polymerase Chain Reaction', 'Transfection']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,766,647 | Does wNT5A induce release of exosomes containing pro-angiogenic and immunosuppressive factors from malignant melanoma cells? | {
"contexts": [
"Wnt proteins are important for developmental processes and certain diseases. WNT5A is a non-canonical Wnt protein that previously has been shown to play a role in the progression of malignant melanoma. High expression of WNT5A in melanoma tumors correlates to formation of distant metastasis and poor prognosis. This has partly been described by the findings that WNT5A expression in melanoma cell lines increases migration and invasion.",
"Malignant melanoma cell lines were treated with rWNT5A or WNT5A siRNA, and mRNA versus protein levels of soluble mediators were measured using RT-PCR, cytokine bead array and ELISA. The induced signaling pathways were analyzed using inhibitors, Rho-GTPase pull down assays and western blot. Ultracentrifugation and electron microscopy was used to analyze microvesicles. Gene expression microarray data obtained from primary malignant melanomas was used to verify our data.",
"We show that WNT5A signaling induces a Ca2+-dependent release of exosomes containing the immunomodulatory and pro-angiogenic proteins IL-6, VEGF and MMP2 in melanoma cells. The process was independent of the transcriptional machinery and depletion of WNT5A reduced the levels of the exosome-derived proteins. The WNT5A induced exosomal secretion was neither affected by Tetanus toxin nor Brefeldin A, but was blocked by the calcium chelator Bapta, inhibited by a dominant negative version of the small Rho-GTPase Cdc42 and was accompanied by cytoskeletal reorganization. Co-cultures of melanoma/endothelial cells showed that depletion of WNT5A in melanoma cells decreased endothelial cell branching, while stimulation of endothelial cells with isolated rWNT5A-induced melanoma exosomes increased endothelial cell branching in vitro. Finally, gene expression data analysis of primary malignant melanomas revealed a correlation between WNT5A expression and the angiogenesis marker ESAM."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Brefeldin A",
"Calcium",
"Cell Adhesion Molecules",
"Cell Line, Tumor",
"Cell Movement",
"Cell Proliferation",
"Coculture Techniques",
"Egtazic Acid",
"Endothelial Cells",
"Exosomes",
"Gene Expression Regulation, Neoplastic",
"Humans",
"Interleukin-6",
"Matrix Metalloproteinase 2",
"Melanoma",
"Neovascularization, Pathologic",
"Proto-Oncogene Proteins",
"Signal Transduction",
"Skin Neoplasms",
"Tetanus Toxin",
"Vascular Endothelial Growth Factor A",
"Wnt Proteins",
"Wnt-5a Protein",
"cdc42 GTP-Binding Protein"
]
} | These data indicate that WNT5A has a broader function on tumor progression and metastatic spread than previously known; by inducing exosome-release of immunomodulatory and pro-angiogenic factors that enhance the immunosuppressive and angiogenic capacity of the tumors thus rendering them more aggressive and more prone to metastasize. | yes | [
{
"from": "human",
"value": "Question: Does wNT5A induce release of exosomes containing pro-angiogenic and immunosuppressive factors from malignant melanoma cells?\nContext: {'contexts': ['Wnt proteins are important for developmental processes and certain diseases. WNT5A is a non-canonical Wnt protein that previously has been shown to play a role in the progression of malignant melanoma. High expression of WNT5A in melanoma tumors correlates to formation of distant metastasis and poor prognosis. This has partly been described by the findings that WNT5A expression in melanoma cell lines increases migration and invasion.', 'Malignant melanoma cell lines were treated with rWNT5A or WNT5A siRNA, and mRNA versus protein levels of soluble mediators were measured using RT-PCR, cytokine bead array and ELISA. The induced signaling pathways were analyzed using inhibitors, Rho-GTPase pull down assays and western blot. Ultracentrifugation and electron microscopy was used to analyze microvesicles. Gene expression microarray data obtained from primary malignant melanomas was used to verify our data.', 'We show that WNT5A signaling induces a Ca2+-dependent release of exosomes containing the immunomodulatory and pro-angiogenic proteins IL-6, VEGF and MMP2 in melanoma cells. The process was independent of the transcriptional machinery and depletion of WNT5A reduced the levels of the exosome-derived proteins. The WNT5A induced exosomal secretion was neither affected by Tetanus toxin nor Brefeldin A, but was blocked by the calcium chelator Bapta, inhibited by a dominant negative version of the small Rho-GTPase Cdc42 and was accompanied by cytoskeletal reorganization. Co-cultures of melanoma/endothelial cells showed that depletion of WNT5A in melanoma cells decreased endothelial cell branching, while stimulation of endothelial cells with isolated rWNT5A-induced melanoma exosomes increased endothelial cell branching in vitro. Finally, gene expression data analysis of primary malignant melanomas revealed a correlation between WNT5A expression and the angiogenesis marker ESAM.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Brefeldin A', 'Calcium', 'Cell Adhesion Molecules', 'Cell Line, Tumor', 'Cell Movement', 'Cell Proliferation', 'Coculture Techniques', 'Egtazic Acid', 'Endothelial Cells', 'Exosomes', 'Gene Expression Regulation, Neoplastic', 'Humans', 'Interleukin-6', 'Matrix Metalloproteinase 2', 'Melanoma', 'Neovascularization, Pathologic', 'Proto-Oncogene Proteins', 'Signal Transduction', 'Skin Neoplasms', 'Tetanus Toxin', 'Vascular Endothelial Growth Factor A', 'Wnt Proteins', 'Wnt-5a Protein', 'cdc42 GTP-Binding Protein']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,757,150 | Does cTLA-4Ig-induced T cell anergy promote Wnt-10b production and bone formation in a mouse model? | {
"contexts": [
"Rheumatoid arthritis (RA) is an inflammatory autoimmune disease characterized by severe joint erosion and systemic osteoporosis. Chronic T cell activation is a hallmark of RA, and agents that target the CD28 receptor on T cells, which is required for T cell activation, are being increasingly used as therapies for RA and other inflammatory diseases. Lymphocytes play complex roles in the regulation of the skeleton, and although activated T cells and B cells secrete cytokines that promote skeletal decline, under physiologic conditions lymphocytes also have key protective roles in the stabilization of skeletal mass. Consequently, disruption of T cell costimulation may have unforeseen consequences for physiologic bone turnover. This study was undertaken to investigate the impact of pharmacologic CD28 T cell costimulation blockade on physiologic bone turnover and structure.",
"C57BL6 mice were treated with CTLA-4Ig, a pharmacologic CD28 antagonist or with irrelevant control antibody (Ig), and serum biochemical markers of bone turnover were quantified by enzyme-linked immunosorbent assay. Bone mineral density and indices of bone structure were further measured by dual x-ray absorptiometry and micro-computed tomography, respectively, and static and dynamic indices of bone formation were quantified using bone histomorphometry.",
"Pharmacologic disruption of CD28 T cell costimulation in mice significantly increased bone mass and enhanced indices of bone structure, a consequence of enhanced bone formation, concurrent with enhanced secretion of the bone anabolic factor Wnt-10b by T cells."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Abatacept",
"Animals",
"Arthritis, Rheumatoid",
"Bone Density",
"Disease Models, Animal",
"Female",
"Immunoconjugates",
"Lymphocyte Activation",
"Mice",
"Osteogenesis",
"T-Lymphocytes",
"Wnt Proteins"
]
} | Inhibition of CD28 costimulation by CTLA-4Ig promotes T cell Wnt-10b production and bone formation and may represent a novel anabolic strategy for increasing bone mass in osteoporotic conditions. | yes | [
{
"from": "human",
"value": "Question: Does cTLA-4Ig-induced T cell anergy promote Wnt-10b production and bone formation in a mouse model?\nContext: {'contexts': ['Rheumatoid arthritis (RA) is an inflammatory autoimmune disease characterized by severe joint erosion and systemic osteoporosis. Chronic T cell activation is a hallmark of RA, and agents that target the CD28 receptor on T cells, which is required for T cell activation, are being increasingly used as therapies for RA and other inflammatory diseases. Lymphocytes play complex roles in the regulation of the skeleton, and although activated T cells and B cells secrete cytokines that promote skeletal decline, under physiologic conditions lymphocytes also have key protective roles in the stabilization of skeletal mass. Consequently, disruption of T cell costimulation may have unforeseen consequences for physiologic bone turnover. This study was undertaken to investigate the impact of pharmacologic CD28 T cell costimulation blockade on physiologic bone turnover and structure.', 'C57BL6 mice were treated with CTLA-4Ig, a pharmacologic CD28 antagonist or with irrelevant control antibody (Ig), and serum biochemical markers of bone turnover were quantified by enzyme-linked immunosorbent assay. Bone mineral density and indices of bone structure were further measured by dual x-ray absorptiometry and micro-computed tomography, respectively, and static and dynamic indices of bone formation were quantified using bone histomorphometry.', 'Pharmacologic disruption of CD28 T cell costimulation in mice significantly increased bone mass and enhanced indices of bone structure, a consequence of enhanced bone formation, concurrent with enhanced secretion of the bone anabolic factor Wnt-10b by T cells.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Abatacept', 'Animals', 'Arthritis, Rheumatoid', 'Bone Density', 'Disease Models, Animal', 'Female', 'Immunoconjugates', 'Lymphocyte Activation', 'Mice', 'Osteogenesis', 'T-Lymphocytes', 'Wnt Proteins']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,760,439 | Does biliopancreatic diversion with duodenal switch improve insulin sensitivity and secretion through caloric restriction? | {
"contexts": [
"To assess the rapid improvement of insulin sensitivity and β-cell function following biliopancreatic diversion with duodenal switch (BPD-DS) and determine the role played by caloric restriction in these changes.",
"Standard meals were administrated before and on day 3, 4, and 5 after BPD-DS to measure total caloric intake, glucose excursion, insulin sensitivity, and secretion in matched type 2 diabetes and normoglycemic (NG) subjects. In a second set of study, other subjects with type 2 diabetes had the same meal tests prior to and after a 3-day caloric restriction identical to that observed after BPD-DS and then 3 days after actually undergoing BPD-DS.",
"Improvement of HOMA-IR occurred at day 3 after BPD-DS in diabetes and after 3 days of caloric restriction. The disposition index (DI) improved rapidly in diabetes after BPD-DS and to a similar extent after caloric restriction. DI was higher and did not change after BPD-DS in NG. Changes in glucagon-like peptide-1, gastric inhibitory peptide, peptide tyrosine tyrosine, ghrelin, and pancreatic polypeptide levels were not associated with modulation of DI in the participants."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Biliopancreatic Diversion",
"Blood Glucose",
"Caloric Restriction",
"Diabetes Mellitus, Type 2",
"Duodenum",
"Female",
"Gastric Inhibitory Polypeptide",
"Ghrelin",
"Glucagon-Like Peptide 1",
"Glucose Tolerance Test",
"Humans",
"Insulin",
"Insulin Resistance",
"Insulin-Secreting Cells",
"Male",
"Middle Aged",
"Obesity, Morbid",
"Peptide YY",
"Pilot Projects"
]
} | Caloric restriction is the major mechanism underlying the early improvement of insulin sensitivity and β-cell function after BPD-DS in type 2 diabetes. | yes | [
{
"from": "human",
"value": "Question: Does biliopancreatic diversion with duodenal switch improve insulin sensitivity and secretion through caloric restriction?\nContext: {'contexts': ['To assess the rapid improvement of insulin sensitivity and β-cell function following biliopancreatic diversion with duodenal switch (BPD-DS) and determine the role played by caloric restriction in these changes.', 'Standard meals were administrated before and on day 3, 4, and 5 after BPD-DS to measure total caloric intake, glucose excursion, insulin sensitivity, and secretion in matched type 2 diabetes and normoglycemic (NG) subjects. In a second set of study, other subjects with type 2 diabetes had the same meal tests prior to and after a 3-day caloric restriction identical to that observed after BPD-DS and then 3 days after actually undergoing BPD-DS.', 'Improvement of HOMA-IR occurred at day 3 after BPD-DS in diabetes and after 3 days of caloric restriction. The disposition index (DI) improved rapidly in diabetes after BPD-DS and to a similar extent after caloric restriction. DI was higher and did not change after BPD-DS in NG. Changes in glucagon-like peptide-1, gastric inhibitory peptide, peptide tyrosine tyrosine, ghrelin, and pancreatic polypeptide levels were not associated with modulation of DI in the participants.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Biliopancreatic Diversion', 'Blood Glucose', 'Caloric Restriction', 'Diabetes Mellitus, Type 2', 'Duodenum', 'Female', 'Gastric Inhibitory Polypeptide', 'Ghrelin', 'Glucagon-Like Peptide 1', 'Glucose Tolerance Test', 'Humans', 'Insulin', 'Insulin Resistance', 'Insulin-Secreting Cells', 'Male', 'Middle Aged', 'Obesity, Morbid', 'Peptide YY', 'Pilot Projects']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,756,658 | Does prevalence and correlate of personality disorder in the Jamaican population? | {
"contexts": [
"To identify the prevalence and correlates of personality disorder in a representative sample of the Jamaican population using the Jamaica Personality Disorder Inventory (JPDI).",
"A four-stage stratified random sampling method was used to obtain a representative population sample consisting of 1506 Jamaicans, M:F = 727 (48.3%):779 (51.7%), ages 18-64 years. A demographic questionnaire and the JPDI were administered to all participants.",
"Two-fifths of the population (41.4%) scored above the scale's cut-point indicating a diagnosis of personality disorder with the level of severity ranging from mild to severe. Persons with personality disorder were significantly more likely to be single (63%), male (60%), between the ages 18 and 44 years (77%) and of a lower socio-economic status (65%) (p < 0.50 to p < 0.001)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Demography",
"Female",
"Humans",
"Jamaica",
"Male",
"Middle Aged",
"Personality Disorders",
"Personality Inventory",
"Prevalence",
"Surveys and Questionnaires"
]
} | This is the only population study of personality disorder recorded in the English-speaking Caribbean. This suggests a high risk of behavioural dysfunction in the Jamaican population, having significant implications in light of the country's high rate of crime and violence. The findings highlight the need to develop effective and targeted prevention and intervention measures. | yes | [
{
"from": "human",
"value": "Question: Does prevalence and correlate of personality disorder in the Jamaican population?\nContext: {'contexts': ['To identify the prevalence and correlates of personality disorder in a representative sample of the Jamaican population using the Jamaica Personality Disorder Inventory (JPDI).', 'A four-stage stratified random sampling method was used to obtain a representative population sample consisting of 1506 Jamaicans, M:F = 727 (48.3%):779 (51.7%), ages 18-64 years. A demographic questionnaire and the JPDI were administered to all participants.', \"Two-fifths of the population (41.4%) scored above the scale's cut-point indicating a diagnosis of personality disorder with the level of severity ranging from mild to severe. Persons with personality disorder were significantly more likely to be single (63%), male (60%), between the ages 18 and 44 years (77%) and of a lower socio-economic status (65%) (p < 0.50 to p < 0.001).\"], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Demography', 'Female', 'Humans', 'Jamaica', 'Male', 'Middle Aged', 'Personality Disorders', 'Personality Inventory', 'Prevalence', 'Surveys and Questionnaires']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,767,614 | Does brief mindfulness meditation training alter psychological and neuroendocrine responses to social evaluative stress? | {
"contexts": [
"To test whether a brief mindfulness meditation training intervention buffers self-reported psychological and neuroendocrine responses to the Trier Social Stress Test (TSST) in young adult volunteers. A second objective evaluates whether pre-existing levels of dispositional mindfulness moderate the effects of brief mindfulness meditation training on stress reactivity.",
"Sixty-six (N=66) participants were randomly assigned to either a brief 3-day (25-min per day) mindfulness meditation training or an analytic cognitive training control program. All participants completed a standardized laboratory social-evaluative stress challenge task (the TSST) following the third mindfulness meditation or cognitive training session. Measures of psychological (stress perceptions) and biological (salivary cortisol, blood pressure) stress reactivity were collected during the social evaluative stress-challenge session.",
"Brief mindfulness meditation training reduced self-reported psychological stress reactivity but increased salivary cortisol reactivity to the TSST, relative to the cognitive training comparison program. Participants who were low in pre-existing levels of dispositional mindfulness and then received mindfulness meditation training had the greatest cortisol reactivity to the TSST. No significant main or interactive effects were observed for systolic or diastolic blood pressure reactivity to the TSST."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adaptation, Psychological",
"Adolescent",
"Adult",
"Anxiety",
"Female",
"Heart Rate",
"Humans",
"Hydrocortisone",
"Interpersonal Relations",
"Male",
"Meditation",
"Mindfulness",
"Saliva",
"Stress, Psychological",
"Treatment Outcome",
"Young Adult"
]
} | The present study provides an initial indication that brief mindfulness meditation training buffers self-reported psychological stress reactivity, but also increases cortisol reactivity to social evaluative stress. This pattern may indicate that initially brief mindfulness meditation training fosters greater active coping efforts, resulting in reduced psychological stress appraisals and greater cortisol reactivity during social evaluative stressors. | yes | [
{
"from": "human",
"value": "Question: Does brief mindfulness meditation training alter psychological and neuroendocrine responses to social evaluative stress?\nContext: {'contexts': ['To test whether a brief mindfulness meditation training intervention buffers self-reported psychological and neuroendocrine responses to the Trier Social Stress Test (TSST) in young adult volunteers. A second objective evaluates whether pre-existing levels of dispositional mindfulness moderate the effects of brief mindfulness meditation training on stress reactivity.', 'Sixty-six (N=66) participants were randomly assigned to either a brief 3-day (25-min per day) mindfulness meditation training or an analytic cognitive training control program. All participants completed a standardized laboratory social-evaluative stress challenge task (the TSST) following the third mindfulness meditation or cognitive training session. Measures of psychological (stress perceptions) and biological (salivary cortisol, blood pressure) stress reactivity were collected during the social evaluative stress-challenge session.', 'Brief mindfulness meditation training reduced self-reported psychological stress reactivity but increased salivary cortisol reactivity to the TSST, relative to the cognitive training comparison program. Participants who were low in pre-existing levels of dispositional mindfulness and then received mindfulness meditation training had the greatest cortisol reactivity to the TSST. No significant main or interactive effects were observed for systolic or diastolic blood pressure reactivity to the TSST.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adaptation, Psychological', 'Adolescent', 'Adult', 'Anxiety', 'Female', 'Heart Rate', 'Humans', 'Hydrocortisone', 'Interpersonal Relations', 'Male', 'Meditation', 'Mindfulness', 'Saliva', 'Stress, Psychological', 'Treatment Outcome', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,745,779 | Is burnout associated with elevated prolactin levels in men but not in women? | {
"contexts": [
"Prolactin levels have been shown to be increased by different types of psychosocial stress. Since burnout is a consequence of long-term psychosocial stress, prolactin levels might also be affected in burnout. The aim of this study was to investigate whether there are differences in prolactin levels between individuals who report burnout and others.",
"Morning fasting serum prolactin levels were compared between individuals who reported burnout (24 men and 25 women) and individuals who reported no burnout (25 men and 13 women). Women were tested in the follicular phase of the menstrual cycle. Men and women were analysed separately.",
"Men who reported burnout exhibited significantly higher (34%) serum prolactin levels compared to men who reported no burnout. The prolactin levels in women who reported burnout were not different from the levels in the women who reported no burnout before or after adjusting for estradiol levels."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Biomarkers",
"Burnout, Professional",
"Fasting",
"Female",
"Humans",
"Male",
"Prolactin",
"Sex Factors",
"Stress, Psychological"
]
} | This study indicates that prolactin levels are higher in men with burnout than men without burnout but not affected in women with burnout. Why no association was seen in women needs to be further explored. | yes | [
{
"from": "human",
"value": "Question: Is burnout associated with elevated prolactin levels in men but not in women?\nContext: {'contexts': ['Prolactin levels have been shown to be increased by different types of psychosocial stress. Since burnout is a consequence of long-term psychosocial stress, prolactin levels might also be affected in burnout. The aim of this study was to investigate whether there are differences in prolactin levels between individuals who report burnout and others.', 'Morning fasting serum prolactin levels were compared between individuals who reported burnout (24 men and 25 women) and individuals who reported no burnout (25 men and 13 women). Women were tested in the follicular phase of the menstrual cycle. Men and women were analysed separately.', 'Men who reported burnout exhibited significantly higher (34%) serum prolactin levels compared to men who reported no burnout. The prolactin levels in women who reported burnout were not different from the levels in the women who reported no burnout before or after adjusting for estradiol levels.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Biomarkers', 'Burnout, Professional', 'Fasting', 'Female', 'Humans', 'Male', 'Prolactin', 'Sex Factors', 'Stress, Psychological']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,754,336 | Is cD10 useful to identify gastrointestinal contamination in endoscopic ultrasound-guided fine needle aspiration ( EUS-FNA ) cytology from pancreatic ductal adenocarcinoma? | {
"contexts": [
"Endoscopic ultrasound-guided fine needle aspiration (EUS-FNA) cytology is an effective tool to diagnose pancreatic ductal adenocarcinoma (PDA). Standard morphological criteria are usually reliable. When contaminating gastrointestinal (GI) epithelial cells are prevalent among neoplastic cells, these can be highlighted by carcinoembryonic antigen (CEA) staining. CD10 is a cell-surface metallopeptidase normally expressed by the GI epithelial apical border, whose expression is decreased or lost in PDA. We included CD10 in a panel, together with CEA, to discriminate the GI contaminant cells from PDA cells on cell blocks.",
"Eight cases of EUS-FNA of PDA, featuring both contaminating GI cells and neoplastic cells, whose corresponding cell blocks were available for immunostaining, were selected. CD10 and CEA were stained on cell blocks by standard methods.",
"CD10 strongly labelled only the GI cells, with a well-defined apical membrane signal; conversely, GI cells did not show CEA staining; benign duodenal cells were faintly labelled in only one case. Malignant cells were positive for CEA and negative for CD10, with the exception of one case with labelled neoplastic cells with weak diffuse cytoplasmic positivity. CD10 apical membrane staining was a feature only seen in benign GI cells."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Carcinoembryonic Antigen",
"Carcinoma, Pancreatic Ductal",
"Endoscopic Ultrasound-Guided Fine Needle Aspiration",
"Endosonography",
"Humans",
"Neprilysin",
"Pancreatic Neoplasms"
]
} | As a loss of CD10 is a consistent feature of PDA, this marker can be useful, together with CEA, to aid the cytopathologist to identify neoplastic cells in a background rich in GI contaminant cells. | yes | [
{
"from": "human",
"value": "Question: Is cD10 useful to identify gastrointestinal contamination in endoscopic ultrasound-guided fine needle aspiration ( EUS-FNA ) cytology from pancreatic ductal adenocarcinoma?\nContext: {'contexts': ['Endoscopic ultrasound-guided fine needle aspiration (EUS-FNA) cytology is an effective tool to diagnose pancreatic ductal adenocarcinoma (PDA). Standard morphological criteria are usually reliable. When contaminating gastrointestinal (GI) epithelial cells are prevalent among neoplastic cells, these can be highlighted by carcinoembryonic antigen (CEA) staining. CD10 is a cell-surface metallopeptidase normally expressed by the GI epithelial apical border, whose expression is decreased or lost in PDA. We included CD10 in a panel, together with CEA, to discriminate the GI contaminant cells from PDA cells on cell blocks.', 'Eight cases of EUS-FNA of PDA, featuring both contaminating GI cells and neoplastic cells, whose corresponding cell blocks were available for immunostaining, were selected. CD10 and CEA were stained on cell blocks by standard methods.', 'CD10 strongly labelled only the GI cells, with a well-defined apical membrane signal; conversely, GI cells did not show CEA staining; benign duodenal cells were faintly labelled in only one case. Malignant cells were positive for CEA and negative for CD10, with the exception of one case with labelled neoplastic cells with weak diffuse cytoplasmic positivity. CD10 apical membrane staining was a feature only seen in benign GI cells.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Carcinoembryonic Antigen', 'Carcinoma, Pancreatic Ductal', 'Endoscopic Ultrasound-Guided Fine Needle Aspiration', 'Endosonography', 'Humans', 'Neprilysin', 'Pancreatic Neoplasms']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,777,268 | Do on-Q pump for pain control after orbital implant surgery? | {
"contexts": [
"To introduce an elastomeric continuous infusion pump for pain control after outpatient orbital implant surgery.",
"Retrospective, noncomparative consecutive case series of all patients undergoing enucleation, evisceration, or secondary orbital implantation using the On-Q pain system between August 2004 and January 2006. Postoperative pain score, need for narcotics, and adverse events were recorded. The On-Q catheter is inserted intraoperatively through the lateral lower eyelid into the muscle cone under direct visualization, prior to the orbital implant placement. The On-Q system continually infuses anesthesia (bupivacaine) to the retrobulbar site for 5 days.",
"Among 20 patients, mean postoperative period pain score, with On-Q in place, was 1.3 (scale of 0 to 10). Nine patients (45%) did not need any adjunctive oral narcotics. Two patients experienced postoperative nausea. One catheter connector leaked, thereby decreasing delivery of retrobulbar anesthetic resulting a pain level of 6, the highest level in the study. There were no postoperative infections. No systemic toxic effects from bupivacaine were observed clinically."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Aged, 80 and over",
"Anesthetics",
"Bupivacaine",
"Eye Enucleation",
"Eye Evisceration",
"Eye Pain",
"Female",
"Humans",
"Infusion Pumps",
"Male",
"Middle Aged",
"Orbital Implants",
"Pain Measurement",
"Pain, Postoperative",
"Retrospective Studies"
]
} | The On-Q pain pump is widely available, low cost, and requires minimal patient manipulation for the use in orbital implant surgery. The device was safe and appeared to minimize postoperative pain in the authors' case series. | yes | [
{
"from": "human",
"value": "Question: Do on-Q pump for pain control after orbital implant surgery?\nContext: {'contexts': ['To introduce an elastomeric continuous infusion pump for pain control after outpatient orbital implant surgery.', 'Retrospective, noncomparative consecutive case series of all patients undergoing enucleation, evisceration, or secondary orbital implantation using the On-Q pain system between August 2004 and January 2006. Postoperative pain score, need for narcotics, and adverse events were recorded. The On-Q catheter is inserted intraoperatively through the lateral lower eyelid into the muscle cone under direct visualization, prior to the orbital implant placement. The On-Q system continually infuses anesthesia (bupivacaine) to the retrobulbar site for 5 days.', 'Among 20 patients, mean postoperative period pain score, with On-Q in place, was 1.3 (scale of 0 to 10). Nine patients (45%) did not need any adjunctive oral narcotics. Two patients experienced postoperative nausea. One catheter connector leaked, thereby decreasing delivery of retrobulbar anesthetic resulting a pain level of 6, the highest level in the study. There were no postoperative infections. No systemic toxic effects from bupivacaine were observed clinically.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Aged, 80 and over', 'Anesthetics', 'Bupivacaine', 'Eye Enucleation', 'Eye Evisceration', 'Eye Pain', 'Female', 'Humans', 'Infusion Pumps', 'Male', 'Middle Aged', 'Orbital Implants', 'Pain Measurement', 'Pain, Postoperative', 'Retrospective Studies']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,752,242 | Does non-muscle myosin II regulate neuronal actin dynamics by interacting with guanine nucleotide exchange factors? | {
"contexts": [
"Non-muscle myosin II (NM II) regulates a wide range of cellular functions, including neuronal differentiation, which requires precise spatio-temporal activation of Rho GTPases. The molecular mechanism underlying the NM II-mediated activation of Rho GTPases is poorly understood. The present study explored the possibility that NM II regulates neuronal differentiation, particularly morphological changes in growth cones and the distal axon, through guanine nucleotide exchange factors (GEFs) of the Dbl family.",
"NM II colocalized with GEFs, such as βPIX, kalirin and intersectin, in growth cones. Inactivation of NM II by blebbistatin (BBS) led to the increased formation of short and thick filopodial actin structures at the periphery of growth cones. In line with these observations, FRET analysis revealed enhanced Cdc42 activity in BBS-treated growth cones. BBS treatment also induced aberrant targeting of various GEFs to the distal axon where GEFs were seldom observed under physiological conditions. As a result, numerous protrusions and branches were generated on the shaft of the distal axon. The disruption of the NM II-GEF interactions by overexpression of the DH domains of βPIX or Tiam1, or by βPIX depletion with specific siRNAs inhibited growth cone formation and induced slender axons concomitant with multiple branches in cultured hippocampal neurons. Finally, stimulation with nerve growth factor induced transient dissociation of the NM II-GEF complex, which was closely correlated with the kinetics of Cdc42 and Rac1 activation."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Actins",
"Animals",
"Axons",
"Cells, Cultured",
"Female",
"Growth Cones",
"Heterocyclic Compounds, 4 or More Rings",
"Hippocampus",
"Models, Biological",
"Nerve Growth Factors",
"Neurites",
"Neurons",
"Nonmuscle Myosin Type IIB",
"Protein Binding",
"Protein Structure, Tertiary",
"Pseudopodia",
"Rats, Sprague-Dawley",
"Rho Guanine Nucleotide Exchange Factors",
"Signal Transduction",
"cdc42 GTP-Binding Protein",
"p21-Activated Kinases",
"rac1 GTP-Binding Protein"
]
} | Our results suggest that NM II maintains proper morphology of neuronal growth cones and the distal axon by regulating actin dynamics through the GEF-Rho GTPase signaling pathway. | yes | [
{
"from": "human",
"value": "Question: Does non-muscle myosin II regulate neuronal actin dynamics by interacting with guanine nucleotide exchange factors?\nContext: {'contexts': ['Non-muscle myosin II (NM II) regulates a wide range of cellular functions, including neuronal differentiation, which requires precise spatio-temporal activation of Rho GTPases. The molecular mechanism underlying the NM II-mediated activation of Rho GTPases is poorly understood. The present study explored the possibility that NM II regulates neuronal differentiation, particularly morphological changes in growth cones and the distal axon, through guanine nucleotide exchange factors (GEFs) of the Dbl family.', 'NM II colocalized with GEFs, such as βPIX, kalirin and intersectin, in growth cones. Inactivation of NM II by blebbistatin (BBS) led to the increased formation of short and thick filopodial actin structures at the periphery of growth cones. In line with these observations, FRET analysis revealed enhanced Cdc42 activity in BBS-treated growth cones. BBS treatment also induced aberrant targeting of various GEFs to the distal axon where GEFs were seldom observed under physiological conditions. As a result, numerous protrusions and branches were generated on the shaft of the distal axon. The disruption of the NM II-GEF interactions by overexpression of the DH domains of βPIX or Tiam1, or by βPIX depletion with specific siRNAs inhibited growth cone formation and induced slender axons concomitant with multiple branches in cultured hippocampal neurons. Finally, stimulation with nerve growth factor induced transient dissociation of the NM II-GEF complex, which was closely correlated with the kinetics of Cdc42 and Rac1 activation.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Actins', 'Animals', 'Axons', 'Cells, Cultured', 'Female', 'Growth Cones', 'Heterocyclic Compounds, 4 or More Rings', 'Hippocampus', 'Models, Biological', 'Nerve Growth Factors', 'Neurites', 'Neurons', 'Nonmuscle Myosin Type IIB', 'Protein Binding', 'Protein Structure, Tertiary', 'Pseudopodia', 'Rats, Sprague-Dawley', 'Rho Guanine Nucleotide Exchange Factors', 'Signal Transduction', 'cdc42 GTP-Binding Protein', 'p21-Activated Kinases', 'rac1 GTP-Binding Protein']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,761,880 | Does talin-1 correlate with reduced invasion and migration in human hepatocellular carcinoma cells? | {
"contexts": [
"Talin-1 is a cytoskeleton protein that participates in cell migration and plays a role in tumor formation, migration, and metastasis in different types of cancer. Chinese investigators have observed that the levels of Talin-1 protein and mRNA expression in HCC tissues are significantly lower than in the adjacent non-cancerous tissue. However, Japanese investigators have reported that Talin-1 is upregulated in HCC. Tln2 as homologous gene of Tln-1, which encodes a very similar protein, but the role of Talin-2 is very little known in primary liver cancer (PLC). We investigated whether the expression of Talin-1 in PLC may be associated with the histological subtype as well as the role of Talin-1 in tumor cell invasion and migration using human hepatocellular carcinoma cell lines.",
"We measured the mRNA expression levels of Talin-1 and Talin-2 in five human liver cancer cell lines and normal human liver cell (LO2 cell line) by real-time PCR and the protein expression levels of Talin-1 by Western blot. Migration and invasion of the cells were assessed using transwell assays and cell scratch experiments, respectively, and proliferation was assessed by soft AGAR colony formation.",
"Talin-1 and Talin-2 expression differed significantly between the five human liver cancer cell lines and LO2 cell line (p<0.05). Compared with the LO2 cell line, the invasion and migration capabilities of the five cancer cell lines differed significantly (p<0.05). Similarly, the colony-forming ability differed (p<0.05)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Blotting, Western",
"Carcinoma, Hepatocellular",
"Cell Movement",
"Humans",
"Liver Neoplasms",
"Neoplasm Invasiveness",
"RNA, Messenger",
"Real-Time Polymerase Chain Reaction",
"Reverse Transcriptase Polymerase Chain Reaction",
"Talin",
"Tumor Cells, Cultured",
"Tumor Stem Cell Assay"
]
} | High levels of Talin-1 expression are correlated with reduced invasion and migration as well as decreased malignancy in human liver cancer cell lines; the suppression of Talin-1 promotes invasion and migration. In addition, Talin-2 may be correlated with invasion and migration in human hepatocellular carcinoma. | yes | [
{
"from": "human",
"value": "Question: Does talin-1 correlate with reduced invasion and migration in human hepatocellular carcinoma cells?\nContext: {'contexts': ['Talin-1 is a cytoskeleton protein that participates in cell migration and plays a role in tumor formation, migration, and metastasis in different types of cancer. Chinese investigators have observed that the levels of Talin-1 protein and mRNA expression in HCC tissues are significantly lower than in the adjacent non-cancerous tissue. However, Japanese investigators have reported that Talin-1 is upregulated in HCC. Tln2 as homologous gene of Tln-1, which encodes a very similar protein, but the role of Talin-2 is very little known in primary liver cancer (PLC). We investigated whether the expression of Talin-1 in PLC may be associated with the histological subtype as well as the role of Talin-1 in tumor cell invasion and migration using human hepatocellular carcinoma cell lines.', 'We measured the mRNA expression levels of Talin-1 and Talin-2 in five human liver cancer cell lines and normal human liver cell (LO2 cell line) by real-time PCR and the protein expression levels of Talin-1 by Western blot. Migration and invasion of the cells were assessed using transwell assays and cell scratch experiments, respectively, and proliferation was assessed by soft AGAR colony formation.', 'Talin-1 and Talin-2 expression differed significantly between the five human liver cancer cell lines and LO2 cell line (p<0.05). Compared with the LO2 cell line, the invasion and migration capabilities of the five cancer cell lines differed significantly (p<0.05). Similarly, the colony-forming ability differed (p<0.05).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Blotting, Western', 'Carcinoma, Hepatocellular', 'Cell Movement', 'Humans', 'Liver Neoplasms', 'Neoplasm Invasiveness', 'RNA, Messenger', 'Real-Time Polymerase Chain Reaction', 'Reverse Transcriptase Polymerase Chain Reaction', 'Talin', 'Tumor Cells, Cultured', 'Tumor Stem Cell Assay']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,775,450 | Does distension of the ischemic region predict increased ventricular fibrillation inducibility following coronary occlusion in swine? | {
"contexts": [
"Distension of the ischemic region has been related to an increased incidence of spontaneous ventricular arrhythmias following coronary occlusion. This study analyzed whether regional ischemic distension predicts increased ventricular fibrillation inducibility after coronary occlusion in swine.",
"In 18 anesthetized, open-chest pigs, the left anterior descending coronary artery was ligated for 60 min. Myocardial segment length in the ischemic region was monitored by means of ultrasonic crystals. Programmed stimulation was applied at baseline and then continuously between 10 and 60 min after coronary occlusion.",
"Coronary occlusion induced a rapid increase in end-diastolic length in the ischemic region, which reached 109.4% (0.9%) of baseline values 10 min after occlusion (P<.001). On average, 6.6 (0.5) stimulation protocols were completed and 5.4 (0.6) ventricular fibrillation episodes induced between 10 and 60 min of coronary occlusion. Neither baseline serum potassium levels nor the size of the ischemic region were significantly related to ventricular fibrillation inducibility. In contrast, the increase in end-diastolic length 10 min after coronary occlusion was associated directly (r=0.67; P=.002) with the number of induced ventricular fibrillation episodes and inversely (r=-0.55; P=.018) with the number of extrastimuli needed for ventricular fibrillation induction."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Biomechanical Phenomena",
"Coronary Occlusion",
"Female",
"Male",
"Myocardial Ischemia",
"Prognosis",
"Swine",
"Ventricular Fibrillation"
]
} | Regional ischemic expansion predicts increased ventricular fibrillation inducibility following coronary occlusion. These results highlight the potential influence of mechanical factors, acting not only on the triggers but also on the substrate, in the genesis of malignant ventricular arrhythmias during acute ischemia. | yes | [
{
"from": "human",
"value": "Question: Does distension of the ischemic region predict increased ventricular fibrillation inducibility following coronary occlusion in swine?\nContext: {'contexts': ['Distension of the ischemic region has been related to an increased incidence of spontaneous ventricular arrhythmias following coronary occlusion. This study analyzed whether regional ischemic distension predicts increased ventricular fibrillation inducibility after coronary occlusion in swine.', 'In 18 anesthetized, open-chest pigs, the left anterior descending coronary artery was ligated for 60 min. Myocardial segment length in the ischemic region was monitored by means of ultrasonic crystals. Programmed stimulation was applied at baseline and then continuously between 10 and 60 min after coronary occlusion.', 'Coronary occlusion induced a rapid increase in end-diastolic length in the ischemic region, which reached 109.4% (0.9%) of baseline values 10 min after occlusion (P<.001). On average, 6.6 (0.5) stimulation protocols were completed and 5.4 (0.6) ventricular fibrillation episodes induced between 10 and 60 min of coronary occlusion. Neither baseline serum potassium levels nor the size of the ischemic region were significantly related to ventricular fibrillation inducibility. In contrast, the increase in end-diastolic length 10 min after coronary occlusion was associated directly (r=0.67; P=.002) with the number of induced ventricular fibrillation episodes and inversely (r=-0.55; P=.018) with the number of extrastimuli needed for ventricular fibrillation induction.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Biomechanical Phenomena', 'Coronary Occlusion', 'Female', 'Male', 'Myocardial Ischemia', 'Prognosis', 'Swine', 'Ventricular Fibrillation']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,772,152 | Do high fluoride and low pH level have been detected in popular flavoured beverages in Malaysia? | {
"contexts": [
"In children, excessive ingestion of fluoride from different sources including bottled drinking water and flavoured beverages or soft drinks can lead to the development of dental fluorosis. In addition, the pH level of beverages is important. Low pH can cause dental erosion. In this study we explore the fluoride content and pH level of certain popular beverages available in Malaysian supermarkets and hawkers' stalls.",
"Bottled drinking water and selected popular flavoured packet drinks were purchased from a supermarket and the corresponding flavoured hawkers' drinks, from a hawker's stall in Kuala Lumpur. Fluoride and pH of the beverages were determined using digital fluoride meter and digital pH meter respectively.",
"It was found that fluoride content and pH level vary among the beverages. The mean fluoride content in both packet and hawkers' drinks (7.64±1.88 mg/L, 7.51±1.60 mg/L, respectively) was approximately 7 times higher than the bottled drinking water (1.05±0.35 mg/L). Among the beverages, the tea packet drink was found to contain the highest amount of fluoride (13.02±0.23 mg/L). The mean pH of bottled-drinking water was near neutral (6.96±0.17), but acidic for both supermarket (4.78.00±0.49) and hawkers' drinks (5.73±0.24). The lychee packet drink had the lowest pH level (2.97±0.03)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": []
} | Due to the wide variation of the fluoride content and pH level of the drinks tested in this study, it is recommended that steps should be taken to control the fluoride concentration and pH level in beverages if dental fluorosis and erosion are to be prevented. | yes | [
{
"from": "human",
"value": "Question: Do high fluoride and low pH level have been detected in popular flavoured beverages in Malaysia?\nContext: {'contexts': [\"In children, excessive ingestion of fluoride from different sources including bottled drinking water and flavoured beverages or soft drinks can lead to the development of dental fluorosis. In addition, the pH level of beverages is important. Low pH can cause dental erosion. In this study we explore the fluoride content and pH level of certain popular beverages available in Malaysian supermarkets and hawkers' stalls.\", \"Bottled drinking water and selected popular flavoured packet drinks were purchased from a supermarket and the corresponding flavoured hawkers' drinks, from a hawker's stall in Kuala Lumpur. Fluoride and pH of the beverages were determined using digital fluoride meter and digital pH meter respectively.\", \"It was found that fluoride content and pH level vary among the beverages. The mean fluoride content in both packet and hawkers' drinks (7.64±1.88 mg/L, 7.51±1.60 mg/L, respectively) was approximately 7 times higher than the bottled drinking water (1.05±0.35 mg/L). Among the beverages, the tea packet drink was found to contain the highest amount of fluoride (13.02±0.23 mg/L). The mean pH of bottled-drinking water was near neutral (6.96±0.17), but acidic for both supermarket (4.78.00±0.49) and hawkers' drinks (5.73±0.24). The lychee packet drink had the lowest pH level (2.97±0.03).\"], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,771,157 | Does a new IOL with labeled accurate dioptric powers reduce the postoperative refractive error? | {
"contexts": [
"There is a need for improved predictability in cataract surgery. The aim of this study was to investigate whether implantation of intraocular lenses (IOLs) with accurately labeled dioptric power could improve the postoperative results and allow better predictability.",
"113 eyes were implanted with Crystal Evolution® (MTO) IOLs and 261 eyes with AF-1 iMics1® (Hoya) IOLs. The predictability of the postoperative spherical equivalence (SE) and the best-corrected visual acuity (BCVA) were compared between both groups. The predictability was also compared to 2 previous studies.",
"With Crystal Evolution®, the predictability was significantly better than with AF-1 iMics1® (p<0.0001). The results were also better than those described in the 2 studies. Although the BCVA obtained with Crystal Evolution® were better than with AF-1 iMics1®, the difference were not significant."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Cataract Extraction",
"Equipment Failure Analysis",
"Female",
"Humans",
"Lens Implantation, Intraocular",
"Lenses, Intraocular",
"Male",
"Prosthesis Design",
"Refractive Errors",
"Treatment Outcome",
"Visual Acuity"
]
} | Our data indicate that accurate dioptric labeling of IOLs may improve the postoperative refraction outcome. | yes | [
{
"from": "human",
"value": "Question: Does a new IOL with labeled accurate dioptric powers reduce the postoperative refractive error?\nContext: {'contexts': ['There is a need for improved predictability in cataract surgery. The aim of this study was to investigate whether implantation of intraocular lenses (IOLs) with accurately labeled dioptric power could improve the postoperative results and allow better predictability.', '113 eyes were implanted with Crystal Evolution® (MTO) IOLs and 261 eyes with AF-1 iMics1® (Hoya) IOLs. The predictability of the postoperative spherical equivalence (SE) and the best-corrected visual acuity (BCVA) were compared between both groups. The predictability was also compared to 2 previous studies.', 'With Crystal Evolution®, the predictability was significantly better than with AF-1 iMics1® (p<0.0001). The results were also better than those described in the 2 studies. Although the BCVA obtained with Crystal Evolution® were better than with AF-1 iMics1®, the difference were not significant.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Cataract Extraction', 'Equipment Failure Analysis', 'Female', 'Humans', 'Lens Implantation, Intraocular', 'Lenses, Intraocular', 'Male', 'Prosthesis Design', 'Refractive Errors', 'Treatment Outcome', 'Visual Acuity']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,759,419 | Do self-report symptoms differ between younger and older dizzy patients? | {
"contexts": [
"To determine whether the responses of elders compared with younger patients differed significantly on a structured dizziness case history.",
"Retrospective case reviews.",
"Outpatient balance function testing center.",
"Two-hundred thirty-three adults who underwent vestibular function testing and completed a structured case history. The mean age of the adult group (18-64 yr) was 46.4 years. The mean age of the old adult group (65 yr and older) was 76.2 years.",
"Patient's self-reported symptoms on a structured case history questionnaire.",
"Younger adults reported significantly more complaints of true vertigo and associated nausea and vomiting compared with older patients. Older patients tended to report symptoms of unsteadiness or falling. Despite the lack of vertiginous symptoms, BPPV was common in older adults."
],
"labels": [
"OBJECTIVE",
"METHODS",
"METHODS",
"METHODS",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Age Factors",
"Aged",
"Aged, 80 and over",
"Diagnostic Self Evaluation",
"Dizziness",
"Female",
"Humans",
"Male",
"Middle Aged",
"Retrospective Studies",
"Self Report",
"Severity of Illness Index",
"Surveys and Questionnaires",
"Vertigo",
"Vestibular Function Tests",
"Young Adult"
]
} | The clinician should be aware of differences in self-report dizziness symptoms in older patients. Older patients who do not have vertigo may be told that their symptoms are normal for their age, when, in fact, they may have an undiagnosed vestibular system impairment. | yes | [
{
"from": "human",
"value": "Question: Do self-report symptoms differ between younger and older dizzy patients?\nContext: {'contexts': ['To determine whether the responses of elders compared with younger patients differed significantly on a structured dizziness case history.', 'Retrospective case reviews.', 'Outpatient balance function testing center.', 'Two-hundred thirty-three adults who underwent vestibular function testing and completed a structured case history. The mean age of the adult group (18-64 yr) was 46.4 years. The mean age of the old adult group (65 yr and older) was 76.2 years.', \"Patient's self-reported symptoms on a structured case history questionnaire.\", 'Younger adults reported significantly more complaints of true vertigo and associated nausea and vomiting compared with older patients. Older patients tended to report symptoms of unsteadiness or falling. Despite the lack of vertiginous symptoms, BPPV was common in older adults.'], 'labels': ['OBJECTIVE', 'METHODS', 'METHODS', 'METHODS', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Age Factors', 'Aged', 'Aged, 80 and over', 'Diagnostic Self Evaluation', 'Dizziness', 'Female', 'Humans', 'Male', 'Middle Aged', 'Retrospective Studies', 'Self Report', 'Severity of Illness Index', 'Surveys and Questionnaires', 'Vertigo', 'Vestibular Function Tests', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
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