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[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nIn previous work we (Fisher et al., 2011) examined the emergence of neurobehavioral disinhibition (ND) in adolescents with prenatal substance exposure. We computed ND factor scores at three age points (8/9, 11 and 13/14 years) and found that both prenatal substance exposure and early adversity predicted ND. The purpose of the current study was to determine the association between these ND scores and initiation of substance use between ages 8 and 16 in this cohort as early initiation of substance use has been related to later substance use disorders. Our hypothesis was that prenatal cocaine exposure predisposes the child to ND, which, in turn, is associated with initiation of substance use by age 16. We studied 386 cocaine exposed and 517 unexposed children followed since birth in a longitudinal study. Five dichotomous variables were computed based on the subject's report of substance use: alcohol only; tobacco only; marijuana only; illicit substances and any substance. Cox proportional hazard regression showed that the 8/9 year ND score was related to initiation of alcohol, tobacco, illicit and any substance use but not marijuana use. The trajectory of ND across the three age periods was related to substance use initiation in all five substance use categories. Prenatal cocaine exposure, although initially related to tobacco, marijuana and illicit substance initiation, was no longer significant with ND scores in the models.\n\nQuestion:\nDoes neurobehavioral disinhibition predict initiation of substance use in children with prenatal cocaine exposure?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nIn previous work we (Fisher et al., 2011) examined the emergence of neurobehavioral disinhibition (ND) in adolescents with prenatal substance exposure. We computed ND factor scores at three age points (8/9, 11 and 13/14 years) and found that both prenatal substance exposure and early adversity predicted ND. The purpose of the current study was to determine the association between these ND scores and initiation of substance use between ages 8 and 16 in this cohort as early initiation of substance use has been related to later substance use disorders. Our hypothesis was that prenatal cocaine exposure predisposes the child to ND, which, in turn, is associated with initiation of substance use by age 16. We studied 386 cocaine exposed and 517 unexposed children followed since birth in a longitudinal study. Five dichotomous variables were computed based on the subject's report of substance use: alcohol only; tobacco only; marijuana only; illicit substances and any substance. Cox proportional hazard regression showed that the 8/9 year ND score was related to initiation of alcohol, tobacco, illicit and any substance use but not marijuana use. The trajectory of ND across the three age periods was related to substance use initiation in all five substance use categories. Prenatal cocaine exposure, although initially related to tobacco, marijuana and illicit substance initiation, was no longer significant with ND scores in the models.\n\nQuestion:\nDoes neurobehavioral disinhibition predict initiation of substance use in children with prenatal cocaine exposure?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nIn previous work we (Fisher et al., 2011) examined the emergence of neurobehavioral disinhibition (ND) in adolescents with prenatal substance exposure. We computed ND factor scores at three age points (8/9, 11 and 13/14 years) and found that both prenatal substance exposure and early adversity predicted ND. The purpose of the current study was to determine the association between these ND scores and initiation of substance use between ages 8 and 16 in this cohort as early initiation of substance use has been related to later substance use disorders. Our hypothesis was that prenatal cocaine exposure predisposes the child to ND, which, in turn, is associated with initiation of substance use by age 16. We studied 386 cocaine exposed and 517 unexposed children followed since birth in a longitudinal study. Five dichotomous variables were computed based on the subject's report of substance use: alcohol only; tobacco only; marijuana only; illicit substances and any substance. Cox proportional hazard regression showed that the 8/9 year ND score was related to initiation of alcohol, tobacco, illicit and any substance use but not marijuana use. The trajectory of ND across the three age periods was related to substance use initiation in all five substance use categories. Prenatal cocaine exposure, although initially related to tobacco, marijuana and illicit substance initiation, was no longer significant with ND scores in the models.\n\nQuestion:\nDoes neurobehavioral disinhibition predict initiation of substance use in children with prenatal cocaine exposure?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nChronic inflammatory rheumatic diseases are associated with accelerated atherosclerosis, but data in ankylosing spondylitis (AS) are limited and the relative contribution of inflammation versus classical cardiovascular (CV) risk factors remains a matter of controversy. We addressed this in an original study and a metaanalysis of previous studies. Atheromatic plaques in carotid and femoral arteries, carotid hypertrophy [intima-media thickness (IMT), cross-sectional area], and carotid stiffness by ultrasound, as well as aortic stiffness by pulse wave velocity, were examined in consecutive nondiabetic, CV disease (CVD)-free patients with AS. Healthy individuals carefully matched 1:1 with patients for age, sex, smoking habits, hyperlipidemia, and hypertension served as controls. A metaanalysis of original studies that examined subclinical atherosclerosis in patients with AS versus controls with comparable CVD risk factors was also performed. Carotid and femoral atheromatic plaques were slightly less prevalent compared with controls in a contemporary cohort consisting of 67 patients with AS (82% men), aged 47.5 ± 12.5 years (mean ± SD), with a median disease duration of 12 years and a Bath AS Disease Activity Index (BASDAI) of 1.8 (interquartile range 0.4-3.6), of whom 66% were receiving anti-tumor necrosis factor (TNF) treatment. Carotid hypertrophy and stiffness, as well as aortic stiffness, were similar between patients and their matched controls. Metaanalysis of all published studies revealed a significantly increased carotid IMT, but not plaque burden, in AS versus controls. Notably, however, increased IMT was not evident in studies involving patients with low disease activity (mean BASDAI < 4) or in those studies that included > 50% of patients treated with anti-TNF.\n\nQuestion:\nIs subclinical Atherosclerosis Accelerated in Patients with Ankylosing Spondylitis with Low Disease Activity : New Data and Metaanalysis of Published Studies?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nChronic inflammatory rheumatic diseases are associated with accelerated atherosclerosis, but data in ankylosing spondylitis (AS) are limited and the relative contribution of inflammation versus classical cardiovascular (CV) risk factors remains a matter of controversy. We addressed this in an original study and a metaanalysis of previous studies. Atheromatic plaques in carotid and femoral arteries, carotid hypertrophy [intima-media thickness (IMT), cross-sectional area], and carotid stiffness by ultrasound, as well as aortic stiffness by pulse wave velocity, were examined in consecutive nondiabetic, CV disease (CVD)-free patients with AS. Healthy individuals carefully matched 1:1 with patients for age, sex, smoking habits, hyperlipidemia, and hypertension served as controls. A metaanalysis of original studies that examined subclinical atherosclerosis in patients with AS versus controls with comparable CVD risk factors was also performed. Carotid and femoral atheromatic plaques were slightly less prevalent compared with controls in a contemporary cohort consisting of 67 patients with AS (82% men), aged 47.5 ± 12.5 years (mean ± SD), with a median disease duration of 12 years and a Bath AS Disease Activity Index (BASDAI) of 1.8 (interquartile range 0.4-3.6), of whom 66% were receiving anti-tumor necrosis factor (TNF) treatment. Carotid hypertrophy and stiffness, as well as aortic stiffness, were similar between patients and their matched controls. Metaanalysis of all published studies revealed a significantly increased carotid IMT, but not plaque burden, in AS versus controls. Notably, however, increased IMT was not evident in studies involving patients with low disease activity (mean BASDAI < 4) or in those studies that included > 50% of patients treated with anti-TNF.\n\nQuestion:\nIs subclinical Atherosclerosis Accelerated in Patients with Ankylosing Spondylitis with Low Disease Activity : New Data and Metaanalysis of Published Studies?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nChronic inflammatory rheumatic diseases are associated with accelerated atherosclerosis, but data in ankylosing spondylitis (AS) are limited and the relative contribution of inflammation versus classical cardiovascular (CV) risk factors remains a matter of controversy. We addressed this in an original study and a metaanalysis of previous studies. Atheromatic plaques in carotid and femoral arteries, carotid hypertrophy [intima-media thickness (IMT), cross-sectional area], and carotid stiffness by ultrasound, as well as aortic stiffness by pulse wave velocity, were examined in consecutive nondiabetic, CV disease (CVD)-free patients with AS. Healthy individuals carefully matched 1:1 with patients for age, sex, smoking habits, hyperlipidemia, and hypertension served as controls. A metaanalysis of original studies that examined subclinical atherosclerosis in patients with AS versus controls with comparable CVD risk factors was also performed. Carotid and femoral atheromatic plaques were slightly less prevalent compared with controls in a contemporary cohort consisting of 67 patients with AS (82% men), aged 47.5 ± 12.5 years (mean ± SD), with a median disease duration of 12 years and a Bath AS Disease Activity Index (BASDAI) of 1.8 (interquartile range 0.4-3.6), of whom 66% were receiving anti-tumor necrosis factor (TNF) treatment. Carotid hypertrophy and stiffness, as well as aortic stiffness, were similar between patients and their matched controls. Metaanalysis of all published studies revealed a significantly increased carotid IMT, but not plaque burden, in AS versus controls. Notably, however, increased IMT was not evident in studies involving patients with low disease activity (mean BASDAI < 4) or in those studies that included > 50% of patients treated with anti-TNF.\n\nQuestion:\nIs subclinical Atherosclerosis Accelerated in Patients with Ankylosing Spondylitis with Low Disease Activity : New Data and Metaanalysis of Published Studies?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nWe sought to evaluate the role of exercise-related changes in left ventricular (LV) relaxation and of LV contractile function and vasculoventricular coupling (VVC) in the pathophysiology of heart failure with preserved ejection fraction (HFpEF) and to assess myocardial energetic status in these patients. To date, no studies have investigated exercise-related changes in LV relaxation and VVC as well as in vivo myocardial energetic status in patients with HFpEF. We studied 37 patients with HFpEF and 20 control subjects. The VVC and time to peak LV filling (nTTPF, a measure of LV active relaxation) were assessed while patients were at rest and during exercise by the use of radionuclide ventriculography. Cardiac energetic status (creatine phosphate/adenosine triphosphate ratio) was assessed by the use of (31)P magnetic resonance spectroscopy at 3-T. When patients were at rest, nTTPF and VVC were similar in patients with HFpEF and control subjects. The cardiac creatine phosphate/adenosine triphosphate ratio was reduced in patients with HFpEF versus control subjects (1.57 +/- 0.52 vs. 2.14 +/- 0.63; p = 0.003), indicating reduced energy reserves. Peak maximal oxygen uptake and the increase in heart rate during maximal exercise were lower in patients with HFpEF versus control subjects (19 +/- 4 ml/kg/min vs. 36 +/- 8 ml/kg/min, p < 0.001, and 52 +/- 16 beats/min vs. 81 +/- 14 beats/min, p < 0.001). The relative changes in stroke volume and cardiac output during submaximal exercise were lower in patients with HFpEF versus control subjects (ratio exercise/rest: 0.99 +/- 0.34 vs. 1.25 +/- 0.47, p = 0.04, and 1.36 +/- 0.45 vs. 2.13 +/- 0.72, p < 0.001). The nTTPF decreased during exercise in control subjects but increased in patients with HFpEF (-0.03 +/- 12 s vs. +0.07 +/- 0.11 s; p = 0.005). The VVC decreased on exercise in control subjects but was unchanged in patients with HFpEF (-0.01 +/- 0.15 vs. -0.25 +/- 0.19; p < 0.001).\n\nQuestion:\nIs heart failure with preserved ejection fraction characterized by dynamic impairment of active relaxation and contraction of the left ventricle on exercise and associated with myocardial energy deficiency?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nWe sought to evaluate the role of exercise-related changes in left ventricular (LV) relaxation and of LV contractile function and vasculoventricular coupling (VVC) in the pathophysiology of heart failure with preserved ejection fraction (HFpEF) and to assess myocardial energetic status in these patients. To date, no studies have investigated exercise-related changes in LV relaxation and VVC as well as in vivo myocardial energetic status in patients with HFpEF. We studied 37 patients with HFpEF and 20 control subjects. The VVC and time to peak LV filling (nTTPF, a measure of LV active relaxation) were assessed while patients were at rest and during exercise by the use of radionuclide ventriculography. Cardiac energetic status (creatine phosphate/adenosine triphosphate ratio) was assessed by the use of (31)P magnetic resonance spectroscopy at 3-T. When patients were at rest, nTTPF and VVC were similar in patients with HFpEF and control subjects. The cardiac creatine phosphate/adenosine triphosphate ratio was reduced in patients with HFpEF versus control subjects (1.57 +/- 0.52 vs. 2.14 +/- 0.63; p = 0.003), indicating reduced energy reserves. Peak maximal oxygen uptake and the increase in heart rate during maximal exercise were lower in patients with HFpEF versus control subjects (19 +/- 4 ml/kg/min vs. 36 +/- 8 ml/kg/min, p < 0.001, and 52 +/- 16 beats/min vs. 81 +/- 14 beats/min, p < 0.001). The relative changes in stroke volume and cardiac output during submaximal exercise were lower in patients with HFpEF versus control subjects (ratio exercise/rest: 0.99 +/- 0.34 vs. 1.25 +/- 0.47, p = 0.04, and 1.36 +/- 0.45 vs. 2.13 +/- 0.72, p < 0.001). The nTTPF decreased during exercise in control subjects but increased in patients with HFpEF (-0.03 +/- 12 s vs. +0.07 +/- 0.11 s; p = 0.005). The VVC decreased on exercise in control subjects but was unchanged in patients with HFpEF (-0.01 +/- 0.15 vs. -0.25 +/- 0.19; p < 0.001).\n\nQuestion:\nIs heart failure with preserved ejection fraction characterized by dynamic impairment of active relaxation and contraction of the left ventricle on exercise and associated with myocardial energy deficiency?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nWe sought to evaluate the role of exercise-related changes in left ventricular (LV) relaxation and of LV contractile function and vasculoventricular coupling (VVC) in the pathophysiology of heart failure with preserved ejection fraction (HFpEF) and to assess myocardial energetic status in these patients. To date, no studies have investigated exercise-related changes in LV relaxation and VVC as well as in vivo myocardial energetic status in patients with HFpEF. We studied 37 patients with HFpEF and 20 control subjects. The VVC and time to peak LV filling (nTTPF, a measure of LV active relaxation) were assessed while patients were at rest and during exercise by the use of radionuclide ventriculography. Cardiac energetic status (creatine phosphate/adenosine triphosphate ratio) was assessed by the use of (31)P magnetic resonance spectroscopy at 3-T. When patients were at rest, nTTPF and VVC were similar in patients with HFpEF and control subjects. The cardiac creatine phosphate/adenosine triphosphate ratio was reduced in patients with HFpEF versus control subjects (1.57 +/- 0.52 vs. 2.14 +/- 0.63; p = 0.003), indicating reduced energy reserves. Peak maximal oxygen uptake and the increase in heart rate during maximal exercise were lower in patients with HFpEF versus control subjects (19 +/- 4 ml/kg/min vs. 36 +/- 8 ml/kg/min, p < 0.001, and 52 +/- 16 beats/min vs. 81 +/- 14 beats/min, p < 0.001). The relative changes in stroke volume and cardiac output during submaximal exercise were lower in patients with HFpEF versus control subjects (ratio exercise/rest: 0.99 +/- 0.34 vs. 1.25 +/- 0.47, p = 0.04, and 1.36 +/- 0.45 vs. 2.13 +/- 0.72, p < 0.001). The nTTPF decreased during exercise in control subjects but increased in patients with HFpEF (-0.03 +/- 12 s vs. +0.07 +/- 0.11 s; p = 0.005). The VVC decreased on exercise in control subjects but was unchanged in patients with HFpEF (-0.01 +/- 0.15 vs. -0.25 +/- 0.19; p < 0.001).\n\nQuestion:\nIs heart failure with preserved ejection fraction characterized by dynamic impairment of active relaxation and contraction of the left ventricle on exercise and associated with myocardial energy deficiency?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nGestational diabetes mellitus (GDM) is a common endocrine complication in pregnancy. While it has been established that age, family history of diabetes, insulin resistance and several biomarkers are associated with GDM but significant gaps remain in understanding risk factors for GDM. Soluble pro-renin receptor (s [Pro] RR) as a biomarker reflects the activation of renin- angiotensin system in tissues which may be related to insulin resistance Objective: The aim of this study was to determine the role of (s [pro] RR) in predicting GDM. one hundred -eighty singleton pregnant women in first trimester were enrolled. We excluded women with previous history of GDM, hypertension and consumption of drugs affected renin-angiotensin system. A fasting blood glucose and s (pro) RR level were obtained during first trimester and OGTT was performed at 24-28 weeks of gestation. We used ROC curves to identify s (pro)RR cutoff points for detecting GDM and the difference in s (pro)RR level was assessed in GDM and non- GDM women. Among 180 women, 24 (13.33%) had GDM. There was no significant difference between age and body mass index in subjects with GDM compared to non- GDM. The concentration of s (pro) RR was significantly higher in GDM subjects rather than non- GDM [29.27(24.60-35.92) vs 22.89(19.46-24.27), P&lt;0.001]. Multiple logistic regression analysis revealed a significant association of s(pro)RR with GDM (odd ratio: 1.32, 95% CI: 1.17-1.48, P=0.04). A cut-off point 24.52 ng/ml of s(pro)RR had 75% sensitivity and 80% specificity for predicting GDM.\n\nQuestion:\nIs soluble ( Pro ) Renin Receptor a predictor of gestational diabetes mellitus?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nGestational diabetes mellitus (GDM) is a common endocrine complication in pregnancy. While it has been established that age, family history of diabetes, insulin resistance and several biomarkers are associated with GDM but significant gaps remain in understanding risk factors for GDM. Soluble pro-renin receptor (s [Pro] RR) as a biomarker reflects the activation of renin- angiotensin system in tissues which may be related to insulin resistance Objective: The aim of this study was to determine the role of (s [pro] RR) in predicting GDM. one hundred -eighty singleton pregnant women in first trimester were enrolled. We excluded women with previous history of GDM, hypertension and consumption of drugs affected renin-angiotensin system. A fasting blood glucose and s (pro) RR level were obtained during first trimester and OGTT was performed at 24-28 weeks of gestation. We used ROC curves to identify s (pro)RR cutoff points for detecting GDM and the difference in s (pro)RR level was assessed in GDM and non- GDM women. Among 180 women, 24 (13.33%) had GDM. There was no significant difference between age and body mass index in subjects with GDM compared to non- GDM. The concentration of s (pro) RR was significantly higher in GDM subjects rather than non- GDM [29.27(24.60-35.92) vs 22.89(19.46-24.27), P&lt;0.001]. Multiple logistic regression analysis revealed a significant association of s(pro)RR with GDM (odd ratio: 1.32, 95% CI: 1.17-1.48, P=0.04). A cut-off point 24.52 ng/ml of s(pro)RR had 75% sensitivity and 80% specificity for predicting GDM.\n\nQuestion:\nIs soluble ( Pro ) Renin Receptor a predictor of gestational diabetes mellitus?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nGestational diabetes mellitus (GDM) is a common endocrine complication in pregnancy. While it has been established that age, family history of diabetes, insulin resistance and several biomarkers are associated with GDM but significant gaps remain in understanding risk factors for GDM. Soluble pro-renin receptor (s [Pro] RR) as a biomarker reflects the activation of renin- angiotensin system in tissues which may be related to insulin resistance Objective: The aim of this study was to determine the role of (s [pro] RR) in predicting GDM. one hundred -eighty singleton pregnant women in first trimester were enrolled. We excluded women with previous history of GDM, hypertension and consumption of drugs affected renin-angiotensin system. A fasting blood glucose and s (pro) RR level were obtained during first trimester and OGTT was performed at 24-28 weeks of gestation. We used ROC curves to identify s (pro)RR cutoff points for detecting GDM and the difference in s (pro)RR level was assessed in GDM and non- GDM women. Among 180 women, 24 (13.33%) had GDM. There was no significant difference between age and body mass index in subjects with GDM compared to non- GDM. The concentration of s (pro) RR was significantly higher in GDM subjects rather than non- GDM [29.27(24.60-35.92) vs 22.89(19.46-24.27), P&lt;0.001]. Multiple logistic regression analysis revealed a significant association of s(pro)RR with GDM (odd ratio: 1.32, 95% CI: 1.17-1.48, P=0.04). A cut-off point 24.52 ng/ml of s(pro)RR had 75% sensitivity and 80% specificity for predicting GDM.\n\nQuestion:\nIs soluble ( Pro ) Renin Receptor a predictor of gestational diabetes mellitus?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nEmphysematous change on computed tomography (CT) during the stable phase of chronic obstructive pulmonary disease (COPD) is reported to correlate with COPD prognosis. Acute exacerbation of COPD (AECOPD) is associated with a high risk of mortality and a poor prognosis. This study aims to study the relationship between prognosis and emphysematous changes on CT during an AECOPD. Histories were recorded, and CT acquired for 106 patients who visited the emergency department for an AECOPD. Emphysematous change was quantified by measuring the percentage of low-attenuation areas (LAA%) in the entire lung on CT images with a threshold of -950 Hounsfield units. Other factors that could influence AECOPD prognosis were also recorded on admission and analysed. At follow ups conducted in 1 year, patient survival, the modified Medical Research Council (mMRC) Dyspnoea Scale, and performance status (PS) were evaluated, and a COPD Assessment Test (CAT) was completed. The 1-year follow up was completed by 103 of 106 patients. The median LAA% was significantly higher in non-survivors (11%, n = 16) than in survivors (5.69%, n = 87) (P = 0.006) at the 1-year follow up. LAA% was significantly correlated with mMRC grade (r = 0.285, P = 0.008), PS (r = 0.397, P < 0.001) and CAT score (r = 0.27, P = 0.017) at the 3-month follow up, and with mMRC grade (r = 0.405, P < 0.001) and PS (r = 0.377, P < 0.001) at the 1-year follow up. LAA% > 7.5% was a significant predictor of 1-year mortality, higher mMRC and PS at the 3-month and 1-year follow ups, after adjustment for other prognostic predictors.\n\nQuestion:\nDoes obvious emphysema on computed tomography during an acute exacerbation of chronic obstructive pulmonary disease predict a poor prognosis?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nEmphysematous change on computed tomography (CT) during the stable phase of chronic obstructive pulmonary disease (COPD) is reported to correlate with COPD prognosis. Acute exacerbation of COPD (AECOPD) is associated with a high risk of mortality and a poor prognosis. This study aims to study the relationship between prognosis and emphysematous changes on CT during an AECOPD. Histories were recorded, and CT acquired for 106 patients who visited the emergency department for an AECOPD. Emphysematous change was quantified by measuring the percentage of low-attenuation areas (LAA%) in the entire lung on CT images with a threshold of -950 Hounsfield units. Other factors that could influence AECOPD prognosis were also recorded on admission and analysed. At follow ups conducted in 1 year, patient survival, the modified Medical Research Council (mMRC) Dyspnoea Scale, and performance status (PS) were evaluated, and a COPD Assessment Test (CAT) was completed. The 1-year follow up was completed by 103 of 106 patients. The median LAA% was significantly higher in non-survivors (11%, n = 16) than in survivors (5.69%, n = 87) (P = 0.006) at the 1-year follow up. LAA% was significantly correlated with mMRC grade (r = 0.285, P = 0.008), PS (r = 0.397, P < 0.001) and CAT score (r = 0.27, P = 0.017) at the 3-month follow up, and with mMRC grade (r = 0.405, P < 0.001) and PS (r = 0.377, P < 0.001) at the 1-year follow up. LAA% > 7.5% was a significant predictor of 1-year mortality, higher mMRC and PS at the 3-month and 1-year follow ups, after adjustment for other prognostic predictors.\n\nQuestion:\nDoes obvious emphysema on computed tomography during an acute exacerbation of chronic obstructive pulmonary disease predict a poor prognosis?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nEmphysematous change on computed tomography (CT) during the stable phase of chronic obstructive pulmonary disease (COPD) is reported to correlate with COPD prognosis. Acute exacerbation of COPD (AECOPD) is associated with a high risk of mortality and a poor prognosis. This study aims to study the relationship between prognosis and emphysematous changes on CT during an AECOPD. Histories were recorded, and CT acquired for 106 patients who visited the emergency department for an AECOPD. Emphysematous change was quantified by measuring the percentage of low-attenuation areas (LAA%) in the entire lung on CT images with a threshold of -950 Hounsfield units. Other factors that could influence AECOPD prognosis were also recorded on admission and analysed. At follow ups conducted in 1 year, patient survival, the modified Medical Research Council (mMRC) Dyspnoea Scale, and performance status (PS) were evaluated, and a COPD Assessment Test (CAT) was completed. The 1-year follow up was completed by 103 of 106 patients. The median LAA% was significantly higher in non-survivors (11%, n = 16) than in survivors (5.69%, n = 87) (P = 0.006) at the 1-year follow up. LAA% was significantly correlated with mMRC grade (r = 0.285, P = 0.008), PS (r = 0.397, P < 0.001) and CAT score (r = 0.27, P = 0.017) at the 3-month follow up, and with mMRC grade (r = 0.405, P < 0.001) and PS (r = 0.377, P < 0.001) at the 1-year follow up. LAA% > 7.5% was a significant predictor of 1-year mortality, higher mMRC and PS at the 3-month and 1-year follow ups, after adjustment for other prognostic predictors.\n\nQuestion:\nDoes obvious emphysema on computed tomography during an acute exacerbation of chronic obstructive pulmonary disease predict a poor prognosis?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nUnderstanding the genital mucosal immunity and the factors involved in linking innate to adaptive immunity is crucial for the design of efficient preventive strategies against human immunodeficiency virus (HIV)-1. Levels of both genital mucosal and blood chemokines were compared between 58 HIV-1-uninfected and 50 HIV-1-infected female commercial sex workers (CSWs) as well as 53 HIV-1-uninfected non-CSW control women at low risk for exposure, recruited in Cotonou, Benin. HIV-1-infected CSWs had significantly higher blood and genital levels of monocyte chemotactic protein (MCP-3/CCL7) and monokine induced by gamma interferon (MIG/CXCL9) compared with those in both the HIV-1-uninfected CSW and non-CSW groups. In the HIV-1-infected group, levels of MCP-3 and MIG were significantly higher in the genital mucosa than in the blood. However, the blood levels of macrophage inflammatory protein (MIP-1a/CCL3) and MIP-1b/CCL4 were higher in HIV-1-uninfected CSWs compared with those in the other groups.\n\nQuestion:\nAre chemokine expression patterns in the systemic and genital tract compartments associated with HIV-1 infection in women from Benin?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nUnderstanding the genital mucosal immunity and the factors involved in linking innate to adaptive immunity is crucial for the design of efficient preventive strategies against human immunodeficiency virus (HIV)-1. Levels of both genital mucosal and blood chemokines were compared between 58 HIV-1-uninfected and 50 HIV-1-infected female commercial sex workers (CSWs) as well as 53 HIV-1-uninfected non-CSW control women at low risk for exposure, recruited in Cotonou, Benin. HIV-1-infected CSWs had significantly higher blood and genital levels of monocyte chemotactic protein (MCP-3/CCL7) and monokine induced by gamma interferon (MIG/CXCL9) compared with those in both the HIV-1-uninfected CSW and non-CSW groups. In the HIV-1-infected group, levels of MCP-3 and MIG were significantly higher in the genital mucosa than in the blood. However, the blood levels of macrophage inflammatory protein (MIP-1a/CCL3) and MIP-1b/CCL4 were higher in HIV-1-uninfected CSWs compared with those in the other groups.\n\nQuestion:\nAre chemokine expression patterns in the systemic and genital tract compartments associated with HIV-1 infection in women from Benin?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nUnderstanding the genital mucosal immunity and the factors involved in linking innate to adaptive immunity is crucial for the design of efficient preventive strategies against human immunodeficiency virus (HIV)-1. Levels of both genital mucosal and blood chemokines were compared between 58 HIV-1-uninfected and 50 HIV-1-infected female commercial sex workers (CSWs) as well as 53 HIV-1-uninfected non-CSW control women at low risk for exposure, recruited in Cotonou, Benin. HIV-1-infected CSWs had significantly higher blood and genital levels of monocyte chemotactic protein (MCP-3/CCL7) and monokine induced by gamma interferon (MIG/CXCL9) compared with those in both the HIV-1-uninfected CSW and non-CSW groups. In the HIV-1-infected group, levels of MCP-3 and MIG were significantly higher in the genital mucosa than in the blood. However, the blood levels of macrophage inflammatory protein (MIP-1a/CCL3) and MIP-1b/CCL4 were higher in HIV-1-uninfected CSWs compared with those in the other groups.\n\nQuestion:\nAre chemokine expression patterns in the systemic and genital tract compartments associated with HIV-1 infection in women from Benin?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nTo explore the characters of lung injury induced by tin dusts and to provide the diagnosis evidence of tin pneumoconiosis. Forty SD rats were randomly divided into four groups: the group exposed to tin dusts from smelting workshop, the group exposed to tin dusts from tin refining workshop, the positive control group exposed to standard quartz dusts and the negative control group exposed to saline. The pathological changes of rat lungs were observed dynamically. In rats exposed to tin dusts, on the 30th day after exposure to tin dusts, the scattered hoar tip size of the spots in surface and section of the lungs were observed, the scattered focal granulomatous inflammation around the small bronchi and dust particles in lung tissue were observed under microscope; on the 90th day after exposure to tin dusts, the granulomatous inflammation increase, the fibroblasts proliferation, collagen fibers formation and positive VG staining were found. There were significant differences, as compared with positive or negative controls (P < 0.05). These pathological changes were basically the characters of specific pathological changes in early tin pneumoconiosis.\n\nQuestion:\nDoes [ Pathological observation of lung injury in experimental animals induced by non-ferrous metal ( tin ) dust ]?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nTo explore the characters of lung injury induced by tin dusts and to provide the diagnosis evidence of tin pneumoconiosis. Forty SD rats were randomly divided into four groups: the group exposed to tin dusts from smelting workshop, the group exposed to tin dusts from tin refining workshop, the positive control group exposed to standard quartz dusts and the negative control group exposed to saline. The pathological changes of rat lungs were observed dynamically. In rats exposed to tin dusts, on the 30th day after exposure to tin dusts, the scattered hoar tip size of the spots in surface and section of the lungs were observed, the scattered focal granulomatous inflammation around the small bronchi and dust particles in lung tissue were observed under microscope; on the 90th day after exposure to tin dusts, the granulomatous inflammation increase, the fibroblasts proliferation, collagen fibers formation and positive VG staining were found. There were significant differences, as compared with positive or negative controls (P < 0.05). These pathological changes were basically the characters of specific pathological changes in early tin pneumoconiosis.\n\nQuestion:\nDoes [ Pathological observation of lung injury in experimental animals induced by non-ferrous metal ( tin ) dust ]?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nTo explore the characters of lung injury induced by tin dusts and to provide the diagnosis evidence of tin pneumoconiosis. Forty SD rats were randomly divided into four groups: the group exposed to tin dusts from smelting workshop, the group exposed to tin dusts from tin refining workshop, the positive control group exposed to standard quartz dusts and the negative control group exposed to saline. The pathological changes of rat lungs were observed dynamically. In rats exposed to tin dusts, on the 30th day after exposure to tin dusts, the scattered hoar tip size of the spots in surface and section of the lungs were observed, the scattered focal granulomatous inflammation around the small bronchi and dust particles in lung tissue were observed under microscope; on the 90th day after exposure to tin dusts, the granulomatous inflammation increase, the fibroblasts proliferation, collagen fibers formation and positive VG staining were found. There were significant differences, as compared with positive or negative controls (P < 0.05). These pathological changes were basically the characters of specific pathological changes in early tin pneumoconiosis.\n\nQuestion:\nDoes [ Pathological observation of lung injury in experimental animals induced by non-ferrous metal ( tin ) dust ]?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nHypermethylation of CpG islands has been associated with silencing of various tumor suppressor genes, and the retinoid acid receptor beta (RARbeta), cellular retinol-binding protein 1 (CRBP1), and tazarotene-induced gene 1 (TIG1) genes have been associated with retinoic acid signaling. To the authors' knowledge, little is known regarding the involvement of these three genes in gastric carcinoma (GC). In this study, the authors investigated the methylation status of these genes and analyzed the role of their DNA methylation in GC. DNA methylation of 3 retinoic acid-associated genes was analyzed in 42 samples of GC from 42 patients and in 8 GC cell lines by methylation-specific polymerase chain reaction (PCR) analysis. The mRNA expression levels for these three genes were measured by quantitative reverse transcription-PCR. In 7 of 8 GC cell lines, the CRBP1 gene was hypermethylated, and CRBP1 transcription was inactive. In 6 of 8 GC cell lines, the TIG1 gene was hypermethylated, and TIG1 transcription was inactive. Treatment with demethylating agent 5-aza-2'-deoxycytidine restored both CRBP1 and TIG1 transcription. DNA methylation of the RARbeta, CRBP1, and TIG1 genes was detected in 15 of 42 GC samples (36%), 14 of 42 GC samples (33%), and 4 of 42 GC samples (10%), respectively, and in 6 of 30 samples (20%), 0 of 30 samples (0%), and 1 of 30 samples (3%) of corresponding nonneoplastic mucosa. None of the 10 normal gastric mucosa samples from young, healthy individuals demonstrated hypermethylation of any of these genes. DNA methylation of each gene was associated significantly with low mRNA expression of the respective gene. Twenty-four of 42 GC samples (57%) demonstrated hypermethylation of at least 1 of the 3 genes. However, no significant, concordant hypermethylation of these genes was observed.\n\nQuestion:\nIs dNA methylation of genes linked with retinoid signaling in gastric carcinoma : expression of the retinoid acid receptor beta , cellular retinol-binding protein 1 , and tazarotene-induced gene 1 genes associated with DNA methylation?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nHypermethylation of CpG islands has been associated with silencing of various tumor suppressor genes, and the retinoid acid receptor beta (RARbeta), cellular retinol-binding protein 1 (CRBP1), and tazarotene-induced gene 1 (TIG1) genes have been associated with retinoic acid signaling. To the authors' knowledge, little is known regarding the involvement of these three genes in gastric carcinoma (GC). In this study, the authors investigated the methylation status of these genes and analyzed the role of their DNA methylation in GC. DNA methylation of 3 retinoic acid-associated genes was analyzed in 42 samples of GC from 42 patients and in 8 GC cell lines by methylation-specific polymerase chain reaction (PCR) analysis. The mRNA expression levels for these three genes were measured by quantitative reverse transcription-PCR. In 7 of 8 GC cell lines, the CRBP1 gene was hypermethylated, and CRBP1 transcription was inactive. In 6 of 8 GC cell lines, the TIG1 gene was hypermethylated, and TIG1 transcription was inactive. Treatment with demethylating agent 5-aza-2'-deoxycytidine restored both CRBP1 and TIG1 transcription. DNA methylation of the RARbeta, CRBP1, and TIG1 genes was detected in 15 of 42 GC samples (36%), 14 of 42 GC samples (33%), and 4 of 42 GC samples (10%), respectively, and in 6 of 30 samples (20%), 0 of 30 samples (0%), and 1 of 30 samples (3%) of corresponding nonneoplastic mucosa. None of the 10 normal gastric mucosa samples from young, healthy individuals demonstrated hypermethylation of any of these genes. DNA methylation of each gene was associated significantly with low mRNA expression of the respective gene. Twenty-four of 42 GC samples (57%) demonstrated hypermethylation of at least 1 of the 3 genes. However, no significant, concordant hypermethylation of these genes was observed.\n\nQuestion:\nIs dNA methylation of genes linked with retinoid signaling in gastric carcinoma : expression of the retinoid acid receptor beta , cellular retinol-binding protein 1 , and tazarotene-induced gene 1 genes associated with DNA methylation?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nHypermethylation of CpG islands has been associated with silencing of various tumor suppressor genes, and the retinoid acid receptor beta (RARbeta), cellular retinol-binding protein 1 (CRBP1), and tazarotene-induced gene 1 (TIG1) genes have been associated with retinoic acid signaling. To the authors' knowledge, little is known regarding the involvement of these three genes in gastric carcinoma (GC). In this study, the authors investigated the methylation status of these genes and analyzed the role of their DNA methylation in GC. DNA methylation of 3 retinoic acid-associated genes was analyzed in 42 samples of GC from 42 patients and in 8 GC cell lines by methylation-specific polymerase chain reaction (PCR) analysis. The mRNA expression levels for these three genes were measured by quantitative reverse transcription-PCR. In 7 of 8 GC cell lines, the CRBP1 gene was hypermethylated, and CRBP1 transcription was inactive. In 6 of 8 GC cell lines, the TIG1 gene was hypermethylated, and TIG1 transcription was inactive. Treatment with demethylating agent 5-aza-2'-deoxycytidine restored both CRBP1 and TIG1 transcription. DNA methylation of the RARbeta, CRBP1, and TIG1 genes was detected in 15 of 42 GC samples (36%), 14 of 42 GC samples (33%), and 4 of 42 GC samples (10%), respectively, and in 6 of 30 samples (20%), 0 of 30 samples (0%), and 1 of 30 samples (3%) of corresponding nonneoplastic mucosa. None of the 10 normal gastric mucosa samples from young, healthy individuals demonstrated hypermethylation of any of these genes. DNA methylation of each gene was associated significantly with low mRNA expression of the respective gene. Twenty-four of 42 GC samples (57%) demonstrated hypermethylation of at least 1 of the 3 genes. However, no significant, concordant hypermethylation of these genes was observed.\n\nQuestion:\nIs dNA methylation of genes linked with retinoid signaling in gastric carcinoma : expression of the retinoid acid receptor beta , cellular retinol-binding protein 1 , and tazarotene-induced gene 1 genes associated with DNA methylation?", "role": "user" } ]

[ { "content": "Please provide a concise response that does not exceed 200 words. First, using 'yes：', provide a clear 'yes' answer, followed by a brief explanation supporting your answer. Then, using 'no：', provide a clear 'no' answer, also followed by an explanation supporting that answer. Ensure your responses are based on the context and current scientific understanding.\n\nContext:\nIn the brain, tumors may grow without inducing angiogenesis, via co-option of the dense pre-existent capillary bed. The purpose of this study was to investigate how this phenomenon influences the outcome of antiangiogenic therapy. Mice carrying brain metastases of the human, highly angiogenic melanoma cell line Mel57-VEGF-A were either or not treated with different dosages of ZD6474, a vascular endothelial growth factor (VEGF) receptor 2 tyrosine kinase inhibitor with additional activity against epidermal growth factor receptor. Effect of treatment was evaluated using contrast-enhanced magnetic resonance imaging (CE- MRI) and (immuno)morphologic analysis. Placebo-treated Mel57-VEGF-A brain metastases evoked an angiogenic response and were highlighted in CE-MRI. After treatment with ZD6474 (100 mg/kg), CE-MRI failed to detect tumors in either prevention or therapeutic treatment regimens. However, (immuno)histologic analysis revealed the presence of numerous, small, nonangiogenic lesions. Treatment with 25 mg/kg ZD6474 also resulted in efficient blockade of vessel formation, but it did not fully inhibit vascular leakage, thereby still allowing visualization in CE-MRI scans.\n\nQuestion:\nDoes antiangiogenic therapy of cerebral melanoma metastases result in sustained tumor progression via vessel co-option?", "role": "user" } ]

[ { "content": "Please provide a balanced response that presents two distinct perspectives on the question. Your response should include both a 'yes' and a 'no' answer, each accompanied by a brief explanation based on the context and current scientific understanding. Ensure that your response does not exceed 200 words.\n\nYes: First, provide a clear 'yes' answer, explaining why the evidence supports this perspective.\nNo: Then, provide a clear 'no' answer, offering an explanation that presents a contrasting viewpoint, based on the same context.\n\nThis approach will ensure that you address the question from both angles, providing a comprehensive view of the topic.\n\nContext:\nIn the brain, tumors may grow without inducing angiogenesis, via co-option of the dense pre-existent capillary bed. The purpose of this study was to investigate how this phenomenon influences the outcome of antiangiogenic therapy. Mice carrying brain metastases of the human, highly angiogenic melanoma cell line Mel57-VEGF-A were either or not treated with different dosages of ZD6474, a vascular endothelial growth factor (VEGF) receptor 2 tyrosine kinase inhibitor with additional activity against epidermal growth factor receptor. Effect of treatment was evaluated using contrast-enhanced magnetic resonance imaging (CE- MRI) and (immuno)morphologic analysis. Placebo-treated Mel57-VEGF-A brain metastases evoked an angiogenic response and were highlighted in CE-MRI. After treatment with ZD6474 (100 mg/kg), CE-MRI failed to detect tumors in either prevention or therapeutic treatment regimens. However, (immuno)histologic analysis revealed the presence of numerous, small, nonangiogenic lesions. Treatment with 25 mg/kg ZD6474 also resulted in efficient blockade of vessel formation, but it did not fully inhibit vascular leakage, thereby still allowing visualization in CE-MRI scans.\n\nQuestion:\nDoes antiangiogenic therapy of cerebral melanoma metastases result in sustained tumor progression via vessel co-option?", "role": "user" } ]

[ { "content": "For a yes/no question, provide two answers: one that is factually correct and another that is intentionally incorrect, each with a brief explanation. Ensure that your response does not exceed 200 words.\n\nCorrect Answer: Choose 'yes' or 'no' based on the context and current scientific understanding, and provide a brief explanation that accurately supports this answer.\nIncorrect Answer: Then, provide the opposite answer ('no' if you chose 'yes' and vice versa) with an explanation that intentionally includes a common misconception, flawed reasoning, or misinterpretation of the context.\n\nContext:\nIn the brain, tumors may grow without inducing angiogenesis, via co-option of the dense pre-existent capillary bed. The purpose of this study was to investigate how this phenomenon influences the outcome of antiangiogenic therapy. Mice carrying brain metastases of the human, highly angiogenic melanoma cell line Mel57-VEGF-A were either or not treated with different dosages of ZD6474, a vascular endothelial growth factor (VEGF) receptor 2 tyrosine kinase inhibitor with additional activity against epidermal growth factor receptor. Effect of treatment was evaluated using contrast-enhanced magnetic resonance imaging (CE- MRI) and (immuno)morphologic analysis. Placebo-treated Mel57-VEGF-A brain metastases evoked an angiogenic response and were highlighted in CE-MRI. After treatment with ZD6474 (100 mg/kg), CE-MRI failed to detect tumors in either prevention or therapeutic treatment regimens. However, (immuno)histologic analysis revealed the presence of numerous, small, nonangiogenic lesions. Treatment with 25 mg/kg ZD6474 also resulted in efficient blockade of vessel formation, but it did not fully inhibit vascular leakage, thereby still allowing visualization in CE-MRI scans.\n\nQuestion:\nDoes antiangiogenic therapy of cerebral melanoma metastases result in sustained tumor progression via vessel co-option?", "role": "user" } ]

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