TASK DEFINITION: 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.
PROBLEM: The antidepressant drug fluoxetine (FLU) is considered in the group of selective serotonine re-uptake inhibitors. Its distribution in brain and binding to human brain glutathione S-transferase-π (GST-π) have been shown. FLU can cross blood brain barrier and placenta, accumulate in fetus and may cause congenital malformations.', 'To elucidate the interaction of placental GST-π with FLU.', 'First, concentration-dependent inhibition of human placental GST-π was evaluated by using different FLU concentrations and then 0.3125, 0.625, 1.25, 2.5 and 5\u2009mM FLU concentrations were chosen and tested while keeping GSH concentration constant and 1-chloro-2,4-dinitrobenzene (CDNB) concentration varied and vice versa. The data were evaluated with different kinetic models and Statistica 9.00 for Windows.', 'The Vm, at variable [CDNB] (142\u2009±\u200916\u2009U/mg protein) was 3 times higher than the Vm obtained at variable [GSH] (49\u2009±\u20094\u2009U/mg protein). On the other hand, the Km for CDNB was ∼10 times higher than the Km for GSH (1.99\u2009±\u20090.36\u2009mM versus 0.21\u2009±\u20090.06\u2009mM). The IC50 value for FLU was 8.6\u2009mM. Both at constant [CDNB] and variable [GSH] and at constant [GSH] and variable [CDNB] the inhibition types were competitive with the Ki values of 5.62\u2009±\u20094.37 and 8.09\u2009±\u20091.27\u2009mM, respectively.

SOLUTION: Does fluoxetine-induced toxicity result in human placental glutathione S-transferase-π ( GST-π ) dysfunction?

PROBLEM: High mobility group box 1 (HMGB1) protein has been identified as a novel pro-inflammatory cytokine in coronary artery disease (CAD). We investigated the relationship between serum HMGB1 level and the severity of coronary artery stenosis.', 'Serum HMGB1 concentration in patients was measured by ELISA. All patients underwent coronary angiography and were assigned into groups according to the quartile of HMGB1 level.', 'HMGB1 level in USAP group was higher than that in control and SAP group. HMGB1 level in SAP group was higher than that in control group (p<0.05). Gensini scores in the highest quartile group (group IV), group III and group II were all significantly higher than that in the lowest quartile group (group I). There was significant correlation between angiographic Gensini score and serum level of HMGB1 (r=0.710, p<0.05). However, in subgroup analysis, we found that serum HMGB1 level was only correlated with angiographic Gensini score in SAP patients (r=0.786, p<0.05), but not USAP patients.

SOLUTION: Is increased serum HMGB1 related to the severity of coronary artery stenosis?

PROBLEM: Diets rich in n-3 polyunsaturated fatty acids, namely eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), protect against insulin resistance and obesity in rodents and increase insulin sensitivity in healthy humans. We tested whether the anti-diabetic effects of EPA and DHA involve enhanced production of the endogenous insulin sensitiser, adiponectin.', 'We studied the effects, in an obesity-promoting high-fat diet, of partial replacement of vegetable oils by EPA/DHA concentrate (6% EPA, 51% DHA) over a 5-week period in adult male C57BL/6J mice that either had free access to food or had their food intake restricted by 30%. At the end of the treatment, systemic markers of lipid and glucose metabolism and full-length adiponectin and leptin were measured. Adiponectin (Adipoq) and leptin (Lep) gene expression in dorsolumbar and epididymal white adipose tissue (WAT) and isolated adipocytes was quantified and adipokine production from WAT explants evaluated.', 'In mice with free access to food, plasma triacylglycerols, NEFA, and insulin levels were lower in the presence of EPA/DHA, while glucose and leptin levels were not significantly altered. Food restriction decreased plasma triacylglycerols, glucose, insulin and leptin, but not adiponectin. EPA/DHA increased plasma adiponectin levels, independent of food intake, reflecting the stimulation of Adipoq expression in adipocytes and the release of adiponectin from WAT, particularly from epididymal fat. Expression of Lep and the release of leptin from WAT, while being extremely sensitive to caloric restriction, was unaltered by EPA/DHA.

SOLUTION:
Do polyunsaturated fatty acids of marine origin induce adiponectin in mice fed a high-fat diet?