In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

Ex Input:
Context: To evaluate the relationship between pro-atherogenic biomarkers and epicardial adipose tissue (EAT) thickness in patients with cardiovascular risk factors.', 'Plasma nitric oxide (NO), soluble intercellular adhesion molecule-1 and malondialdehyde (MDA) levels, EAT thickness, flow-mediated dilation (FMD) and carotid intima media thickness (CIMT) were determined in patients aged >18 years who were referred for echocardiography for heart ischemia or non-ischemic diseases. Cardiovascular risk factors (Framingham score [FS]\u2009≥\u200920) were weighted.', 'Hypertension, dyslipidaemia and type 2 diabetes mellitus were prevalent (≥55% of 40 patients). Patients with FS\u2009≥\u200920 (n\u2009=\u200921) showed significantly higher EAT and CIMT values. Globally, MDA, CIMT, age, waist circumference, high-density lipoprotein cholesterol (HDL-C) and FS were associated with EAT thickness. EAT was significantly associated with NO in patients with FS\u2009≥\u200920. Significant differences in EAT thickness were found between patients stratified by NO value, FMD, age, smoking status, dyslipidaemia, type 2 diabetes mellitus and FS. An EAT-associated atherogenic risk (CIMT\u2009≥\u20091\u2009mm) model was statistically significant when MDA and type 2 diabetes mellitus were included.\Question: Are pro-atherogenic mediators and subclinical atherogenesis related to epicardial adipose tissue thickness in patients with cardiovascular risk?

Ex Output:
EAT thickness was associated with MDA, CIMT, age, waist circumference, HDL-C and FS globally, but with NO only in patients with FS≥20. EAT may be used to identify vascular damage stage, possibly influenced by MDA and type 2 diabetes mellitus.


Ex Input:
Context: It has been shown that maternal mental health is associated with poorer skills development in the offspring. However, the evidence evaluating the association between social anxiety disorder (SAD) and cognitive or language development, is scarce.', 'To evaluate the association between maternal SAD and performance in cognitive and language tests in 30-month old children.', 'This was a cohort study involving young women evaluated since pregnancy.', 'We evaluated 520 mother-child dyads who received prenatal medical assistance through the National Public Health System in a southern Brazilian city, from October 2009 to March 2011.', 'We used the Mini Neuropsychiatric Interview Plus (MINI Plus) to assess SAD among young mothers. Cognitive and language performance in their offspring was analyzed using the Bayley Scales of Infant and Toddler Development - 3rd Edition.', 'We found an association between maternal SAD and performance in cognitive and language tests. Children of mothers with SAD had in average 4.5 less points in the Bayley scale, when compared to those with mothers without SAD: in the cognitive (β=-4.53 [95% CI -7.8; -1.1] p=0.008) and language subscales (β=-4.54 [95% CI -9.0; -0.5] p=0.047).\Question: Is cognitive and language performance in children associated with maternal social anxiety disorder : A study of young mothers in southern Brazil?

Ex Output:
Our findings suggest that children with mothers suffering from SAD have poorer cognitive abilities and language skills.


Ex Input:
Context: Clonidine prolongs the duration of sensory and motor block induced by bupivacaine, and this association, in constant infusion by the epidural route, is used for postoperative analgesia. After a near-fatal intravenous bolus of bupivacaine in dogs, clonidine improves ventricular electrophysiologic parameters, but probably worsens bupivacaine-induced bradycardia and depression of the myocardial contractility. The current study, using a rodent animal model, evaluated the influence of clonidine pretreatment on the systemic toxic effects of bupivacaine overdose induced by a constant intravenous infusion.', 'Twenty Wistar male rats were anesthetized with thiopental, and controlled ventilation was started with an equal mixture of O2 and N2O. Electrocardiogram (ECG), electroencephalogram (EEG), and invasive arterial blood pressure were continuously recorded. Clonidine (5 micrograms/kg) or saline was injected intravenously in a randomized fashion. After 15 min, an intravenous infusion of bupivacaine was started at 2 mg.kg-1 x min-1. The time of occurrence of the bupivacaine-induced toxic events was recorded and the doses were calculated. Ten (five in each group) additional rats, pretreated according to the same protocol, were killed at the time of the first dysrhythmia, for blood sampling and plasma bupivacaine concentration measurement.', 'Clonidine reduced heart rate and arterial blood pressure before bupivacaine infusion (P < 0.05). The threshold doses at the first QRS modification (11.3 +/- 5.6 vs. 2.1 +/- 0.9 mg/kg) and the first dysrhythmia (40.6 +/- 15.3 vs. 8.48 +/- 3.7 mg/kg), the increase in EEG total spectral power (33.3 +/- 21.9 vs. 8.2 +/- 5.1 mg/kg), the 25 and 50% reduction in baseline mean arterial pressure and heart rate, the isoelectric EEG (58.6 +/- 14 vs. 22 +/- 6.6 mg/kg), and the final systole (99 +/- 16 vs. 51.8 +/- 14.5 mg/kg) were significantly greater in the clonidine group than in the saline group (P < 0.01). The time between the first dysrhythmia and 50% reduction of baseline mean arterial blood pressure was not different between the groups. In the additional series, the first dysrhythmia occurred later (10.9 +/- 4.5 vs. 3.2 +/- 1.0 min, P < 0.01) and plasma bupivacaine levels were greater (18.7 +/- 8.0 vs. 7.8 +/- 3.2 micrograms/ml, P < 0.01) in the clonidine group than in the saline group.\Question: Does clonidine pretreatment reduce the systemic toxicity of intravenous bupivacaine in rats?

Ex Output:

In this model, clonidine given prophylactically delays the toxic manifestations of bupivacaine overdose and does not accentuate the subsequent hypotension.