human
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.
INPUT: ['Diabetes is associated with increased sympathetic activity, elevated norepinephrine, impaired heart rate variability, and the added risk of cardiovascular mortality. The temporal development of sympathetic neuronal dysfunction, response to therapy, and relation to ventricular function is not well characterized.', 'Sympathetic neuronal integrity was serially investigated in high fat diet-fed streptozotocin diabetic rats using [(11)C]meta-hydroxyephedrine (HED) positron emission tomography at baseline, 8\xa0weeks of diabetes, and after a further 8\xa0weeks of insulin or insulin-sensitizing metformin therapy. Myocardial HED retention was reduced in diabetic rats (n\xa0=\xa016) compared to non-diabetics (n\xa0=\xa06) at 8\xa0weeks by 52-57% (P\xa0=\xa0.01) with elevated plasma and myocardial norepinephrine levels. Echocardiography pulse-wave Doppler measurements demonstrated prolonged mitral valve deceleration and increased early-to-atrial filling velocity, consistent with diastolic dysfunction. Insulin but not metformin evoked recovery of HED retention and plasma norepinephrine (P\xa0<\xa0.05), whereas echocardiography measurements of diastolic function were not improved by either treatment. Relative expressions of norepinephrine reuptake transporter and β-adrenoceptors were lower in metformin-treated as compared to insulin-treated diabetic and non-diabetic rats. Diabetic rats exhibited depressed heart rate variability and impaired diastolic function which persisted despite insulin treatment.'] Does insulin restore myocardial presynaptic sympathetic neuronal integrity in insulin-resistant diabetic rats?
OUTPUT:

agent
yes
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.
INPUT: ['Diabetes is associated with increased sympathetic activity, elevated norepinephrine, impaired heart rate variability, and the added risk of cardiovascular mortality. The temporal development of sympathetic neuronal dysfunction, response to therapy, and relation to ventricular function is not well characterized.', 'Sympathetic neuronal integrity was serially investigated in high fat diet-fed streptozotocin diabetic rats using [(11)C]meta-hydroxyephedrine (HED) positron emission tomography at baseline, 8\xa0weeks of diabetes, and after a further 8\xa0weeks of insulin or insulin-sensitizing metformin therapy. Myocardial HED retention was reduced in diabetic rats (n\xa0=\xa016) compared to non-diabetics (n\xa0=\xa06) at 8\xa0weeks by 52-57% (P\xa0=\xa0.01) with elevated plasma and myocardial norepinephrine levels. Echocardiography pulse-wave Doppler measurements demonstrated prolonged mitral valve deceleration and increased early-to-atrial filling velocity, consistent with diastolic dysfunction. Insulin but not metformin evoked recovery of HED retention and plasma norepinephrine (P\xa0<\xa0.05), whereas echocardiography measurements of diastolic function were not improved by either treatment. Relative expressions of norepinephrine reuptake transporter and β-adrenoceptors were lower in metformin-treated as compared to insulin-treated diabetic and non-diabetic rats. Diabetic rats exhibited depressed heart rate variability and impaired diastolic function which persisted despite insulin treatment.'] Does insulin restore myocardial presynaptic sympathetic neuronal integrity in insulin-resistant diabetic rats?
OUTPUT:
