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 Q]: 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 A]: 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 Q]: Context: Progress in the management of patients with medically intractable epilepsy is impeded because we do not fully understand why pharmacoresistance happens and how it can be predicted. The presence of multiple seizures prior to medical treatment has been suggested as a potential predictor of poor outcome. In the present study, we used an animal model of temporal lobe epilepsy to investigate whether pharmacoresistant rats differ in seizure frequency from pharmacoresponsive animals.', 'Epilepsy with spontaneous recurrent seizures (SRS) was induced by status epilepticus. Frequency of SRS was determined by video/EEG (electroencephalography) monitoring in a total of 33 epileptic rats before onset of treatment with phenobarbital (PB).', 'Thirteen (39%) rats did not respond to treatment with PB. Before treatment with PB, average seizure frequency in PB nonresponders was significantly higher than seizure frequency in responders, which, however, was due to six nonresponders that exhibited > 3 seizures per day. Such high seizure frequency was not observed in responders, demonstrating that high seizure frequency predicts pharmacoresistance in this model, but does not occur in all nonresponders.\Question: Is high seizure frequency prior to antiepileptic treatment a predictor of pharmacoresistant epilepsy in a rat model of temporal lobe epilepsy?
[EX A]: The data from this study are in line with clinical experience that the frequency of seizures in the early phase of epilepsy is a dominant risk factor that predicts refractoriness. However, resistance to treatment also occurred in rats that did not differ in seizure frequency from responders, indicating that disease severity alone is not sufficient to explain antiepileptic drug (AED) resistance. These data provide further evidence that epilepsy models are useful in the search for predictors and mechanisms of pharmacoresistance.

[EX Q]: Context: To examine the association between insomnia with short sleep duration and hypercholesterolemia in Taiwanese adults.', 'Previous studies mostly focused on the association between sleep duration and hyperlipidemia, but the results were not consistent. Besides, very few studies extensively examined the association between insomnia and hypercholesterolemia. This study hypothesized that insomnia with short sleep duration is associated with hypercholesterolemia.', 'Secondary data analysis. This study analysed the latest database of the cross-sectional Nutrition and Health Survey in Taiwan which was released on 2011 (data collected between 2005-2008) and collected data using stratified three-staged probability sampling design.', 'This study analysed 1533 participants aged between 19-64 (733 males and 800 females) and used logistic regression model to calculate the odds ratio and the 95% confidence interval of insomnia with short sleep duration to hypercholesterolemia. Controlled confounders included age, gender, sample weight, body mass index, waist circumference, fasting plasma glucose, hypertension and diabetes.', 'Insomnia with 5-6\xa0hours of sleep duration was significantly associated with hypercholesterolemia. The odds ratio of mild insomnia or moderate/severe insomnia with 5-6\xa0hours of sleep duration to hypercholesterolemia was higher, compared with the reference group (without insomnia and >6\xa0hours of sleep duration).\Question: Is the relationship between insomnia with short sleep duration associated with hypercholesterolemia : a cross-sectional study?
[EX A]:
Insomnia with short sleep duration was associated with increased odds of hypercholesterolemia. Caregivers in clinical practice should watch out for the effect brought by this novel factor.