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.

[Q]: Obesity and its related co-morbidities such as non-alcoholic fatty liver disease (NAFLD) are increasing dramatically worldwide. The genetic variation in Patatin-like phospholipase domain-containing protein 3 (PNPLA3), which is also called adiponutrin (ADPN), in residue 148 (I148M, rs738409) has been associated with NAFLD. However, the regulation and function of PNPLA3 in metabolic diseases remains unclear. Laparoscopic gastric banding (LAGB) of severely obese patients reduces body weight, liver and adipose tissue inflammation. In this study, we investigated whether weight loss induced by LAGB affected PNPLA3 expression in hepatic and adipose tissue.', 'Liver and subcutaneous adipose tissue samples were collected from 28 severely obese patients before and 6\xa0months after LAGB. PNPLA3 expression was assessed by quantitative real-time PCR. To understand whether inflammatory stimuli regulated PNPLA3 expression, we studied the effect of tumour necrosis factor alpha (TNFα) and lipopolysaccharide (LPS) on PNPLA3 expression in human adipocytes and hepatocytes.', 'PNPLA3 was strongly expressed in the liver and clearly detectable in subcutaneous adipose tissue of obese patients. Weight loss induced by LAGB of severely obese patients led to significantly increased adipose, but not hepatic, tissue expression of PNPLA3. Subcutaneous PNPLA3 expression negatively correlated with body-mass-index, fasting glucose and fasting insulin. TNFα potently suppressed PNPLA3 expression in adipocytes but not hepatocytes.
[A]: Does weight loss induced by bariatric surgery restore adipose tissue PNPLA3 expression?


[Q]: Clinical predictors associated with acute paraquat (PQ) poisoning have not been systematically studied.', 'To identify independent predictors of death in patients with acute PQ poisoning.', 'This is a retrospective study executed in the emergency department of a university hospital. One hundred three consecutive patients poisoned with PQ between January 1999 and December 2004 were enrolled. Urine PQ concentration, electrolyte and renal function, detailed history, and Acute Physiology and Chronic Health Evaluation II were extracted from medical records. The outcome measure was 30-day mortality. Multivariate analysis was done by Cox-proportional hazard regression model. Receiver operating characteristics area under the curve was calculated for selected predictors.', 'The crude 30-day mortality was 67.9% (70 of 103). Independent predictors of death were acute renal failure (hazard ratio, 3.53; 95% confidence interval, 1.97-6.32), hypokalemia (2.07, 1.21-3.51), hypothermia (2.91, 1.67-5.07), suicide (2.11, 1.04-4.29), and self-reported ingested dose (2.06, 1.38-3.06). The receiver operating characteristics area under the curve of serum potassium concentrations, maximal urine PQ concentrations, and Acute Physiology and Chronic Health Evaluation II scores were 0.75 (95% confidence interval, 0.60-0.81), 0.71 (0.66-0.84), and 0.80 (0.71-0.88), respectively. Under the cutoff value of 3.6 mEq/L, hypokalemia had a sensitivity of 75% and specificity of 54% in predicting mortality.
[A]: Are hypokalemia and hypothermia associated with 30-day mortality in patients with acute paraquat poisoning?


[Q]: This study was performed to evaluate the effects of acute systemic inflammation on peritoneal solute transport rate (PSTR) in chronic peritoneal dialysis (CPD) patients.', 'A baseline standard peritoneal equilibration test (PET) was performed on each patient every 6 months, and blood concentration of high-sensitivity C-reactive protein (hs-CRP) was assayed every 2 months in our peritoneal dialysis clinic. Acute systemic inflammation was defined as a greater than 10-fold increase in hs-CRP concentration compared with baseline value, in the absence of peritonitis, and returning to baseline level in 2 months. In patients with acute systemic inflammation, PET and hs-CRP concentration assays were performed during inflammation and after recovery. Ten patients with acute systemic inflammation were enrolled in the inflammation group and 42 other patients served as controls.', 'There were no significant changes in hs-CRP and dialysate-to-plasma ratio of creatinine (D/Pcreat) in the control group during the study period. In the inflammation group, median hs-CRP levels at baseline, during acute inflammation, and at recovery were 2.3 mg/L (range 0.3 - 4.5 mg/L), 39.2 mg/L (range 15.1 - 117.4 mg/L), and 3.7 mg/L (range 0.9 - 8.9 mg/L), respectively. Median D/Pcreat increased significantly from baseline (0.64; range 0.55 - 0.98) to time of acute inflammation (0.72; range 0.60 - 0.96) (p < 0.05). The D/Pcreat at recovery was 0.67 (range 0.52 - 0.94), which decreased significantly from time of acute inflammation (p < 0.05). There was no correlation between changes in log (hs-CRP) and changes in D/Pcreat.
[A]:
Is acute systemic inflammation associated with an increase in peritoneal solute transport rate in chronic peritoneal dialysis patients?