Given a passage, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

Example Input: To investigate whether leukocyte count, fibrinogen, von Willebrand factor (vWF) and plasminogen activator inhibitor-1 activity (PAI-1) are increased in subjects with the metabolic syndrome as defined by the National Cholesterol Education Program-Adult Treatment Panel III (NCEP-ATPIII) and the World Health Organisation (WHO).', 'Cross-sectional study.', 'A total of 520 overweight and obese subjects: 379 women and 141 men, visiting the weight management clinic of a University Hospital.', 'Waist circumference, triglycerides, HDL cholesterol, blood pressure and fasting glucose were determined, and the presence or absence of the metabolic syndrome according to the NCEP-ATPIII criteria was assessed. In 349 subjects, data on the waist-to-hip ratio (WHR) and albumin excretion rate were available and the WHO criteria were applied. Insulin resistance was defined using the HOMA-IR index.', 'Subjects with the metabolic syndrome according to the NCEP-ATPIII criteria had significantly higher levels of leukocyte count (P < 0.001) and PAI-1 (P < 0.001), while no significant differences were found for fibrinogen or vWF (P > 0.05). Using the WHO criteria, similar results were found except for vWF, where higher levels were found in subjects with the metabolic syndrome. When subjects were classified according to the number of components of the metabolic syndrome, levels of leukocyte count, vWF and PAI-1 activity were significantly different (P < 0.05). In logistic regression analysis PAI-1, gender and leukocyte count were independent determinants of the metabolic syndrome (P < 0.001).
Example Output: Is among inflammation and coagulation markers , PAI-1 a true component of the metabolic syndrome?

Example Input: Sigma-1 receptors are involved in the pathophysiological process of several neuropsychiatric diseases such as epilepsy, depression. Allosteric modulation represents an important mechanism for receptor functional regulation. In this study, we examined antidepressant activity of the latest identified novel and selective allosteric modulator of sigma-1 receptor 3-methyl-phenyl-2, 3, 4, 5-tetrahydro-1H-benzo[d]azepin-7-ol (SOMCL-668).', 'A single administration of SOMCL-668 decreased the immobility time in the forced swimming test (FST) and tailing suspended test in mice, which were abolished by pretreatment of sigma-1 receptor antagonist BD1047. In the chronic unpredicted mild stress (CUMS) model, chronic application of SOMCL-668 rapidly ameliorated anhedonia-like behavior (within a week), accompanying with the enhanced expression of brain-derived neurotrophic factor (BDNF) and phosphorylation of glycogen synthase kinase 3β (GSK3β) (Ser-9) in the hippocampus. SOMCL-668 also rapidly promoted the phosphorylation of GSK3β (Ser-9) in an allosteric manner in vitro. In the cultured primary neurons, SOMCL-668 enhanced the sigma-1 receptor agonist-induced neurite outgrowth and the secretion of BDNF.
Example Output: Does allosteric Modulation of Sigma-1 Receptors elicit Rapid Antidepressant Activity?

Example Input: Non-alcoholic fatty liver disease (NAFLD) and dyslipidemia are closely related. Diet plays an important role in the progression of these diseases, but the role of specific dietary components is not completely understood. Therefore, we investigated the role of dietary sucrose and fat/cholesterol on the development of dyslipidemia and NAFLD.', 'Seventy female guinea pigs were block-randomized (based on weight) into five groups and fed a normal chow diet (control: 4\xa0% fat), a very high-sucrose diet (vHS: 4\xa0% fat, 25\xa0% sucrose), a high-fat diet (HF: 20\xa0% fat, 0.35\xa0% cholesterol), a high-fat/high-sucrose diet (HFHS: 20\xa0% fat, 15\xa0% sucrose, 0.35\xa0% cholesterol) or a high-fat/very high-sucrose diet (HFvHS: 20\xa0% fat, 25\xa0% sucrose, 0.35\xa0% cholesterol) for 16 and 25\xa0weeks.', 'All three high-fat diets induced dyslipidemia with increased concentrations of plasma cholesterol (p\u2009<\u20090.0001), LDL-C (p\u2009<\u20090.0001) and VLDL-C (p\u2009<\u20090.05) compared to control and vHS. Contrary to this, plasma triglycerides were increased in control and vHS compared to high-fat fed animals (p\u2009<\u20090.01), while circulating levels of free fatty acids were even between groups. Histological evaluation of liver sections revealed non-alcoholic steatohepatitis (NASH) with progressive inflammation and bridging fibrosis in high-fat fed animals. Accordingly, hepatic triglycerides (p\u2009<\u20090.05) and cholesterol (p\u2009<\u20090.0001) was increased alongside elevated levels of alanine and aspartate aminotransferase (p\u2009<\u20090.01) compared to control and vHS.
Example Output:
Is high-fat but not sucrose intake essential for induction of dyslipidemia and non-alcoholic steatohepatitis in guinea pigs?