TASK DEFINITION: Given a passage with a context and an answer, 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: Context: Severe mitral regurgitation (MR) reduces left atrial thrombus formation in patients with mitral stenosis (MS) and atrial fibrillation (AF). Plasma D-dimer levels represent a biochemical marker for fibrinolytic activity in prothrombotic states. The prothrombotic burden in patients with mitral valve disease and/or AF was assessed using plasma D-dimer levels.', 'The study population included 89 patients with mitral valve disease, 21 with AF but normal valves, and 15 healthy controls. The mitral valve group was subdivided into patients with MS (n = 27), severe MR (n = 26), and MS with concomitant with severe MR (MS/MR; n = 36). These subgroups were further subdivided according to the atrial rhythm (sinus rhythm (SR)+AF).', 'The mean left atrial size was increased in all groups with cardiac disease. D-dimer levels were highest in the MS+AF subgroup (527 +/- 134 microg/l). Patients with MS+AF, MS+SR, and nonvalvular AF had significantly higher D-dimer levels than controls (p < 0.01, by ANOVA). Patients with MR had normal levels of D-dimer. The atrial rhythm did not influence D-dimer levels in the MS/MR subgroup, or in the pure MR subgroup (p = NS).
Answer: Plasma D-dimer levels correlated with the embolic risk in mitral valve disease and non-valvular AF. The highest levels were found in patients with MS+AF and non-valvular AF. Severe MR decreased the D-dimer levels in MS and/or AF to control levels.

SOLUTION: Does mitral regurgitation reduce systemic coagulation activity in patients with rheumatic heart disease?

PROBLEM: Context: The orphan G protein-coupled receptor (GPR) 39 was originally identified as the receptor of obestatin. In this study, the effects and mechanisms of GPR39 on cell proliferation and differentiation were investigated in cultured porcine intramuscular preadipocytes.', 'Morphology of preadipocytes and accumulated lipid droplets within cells were identified by an inverted microscope. After transfected with constructed pCMV-GPR39 plasmid, cell proliferation was measured by using methyl thiazolyl tetrazolium method, mRNA expression of GPR39, CCAAT/enhancer binding protein-α (C/EBPα), peroxisome proliferator-activated receptor-γ (PPARγ), Caspase-9 and adipocyte determination and differentiation factor-1 (ADD1) was determined by RNA preparation and reverse transcription polymerase chain reaction, protein expression of phosphoinositide-3 kinase (PI3K), 3-phosphoinositide-dependent protein kinase 1, phosphorylated glycogen synthase kinase 3 (pGSK3), total Akt and phosphorylated Akt (pAkt) was analyzed by Western blot.', 'It found that GPR39 mRNA and protein were expressed in porcine intramuscular preadipocytes and its expression was significantly up-regulated after treatment with Zn(2+) whose function is found to be mediated by GPR39. Furthermore, over-expression of GPR39 further promoted the optical density value of cells, enhanced mRNA expression of PPARγ, C/EBPα and ADD1, and inhibited mRNA expression of Caspase-9. Protein expression of pGSK3 and pAkt was also increased by GPR39 stimulation. In addition, GPR39-induced proliferation and differentiation of porcine intramuscular preadipocytes was partially blocked by the Akt inhibitor (PDTC) and the PI3K inhibitor (LY294002).
Answer: It indicated that GPR39 was a transducer of Zn(2+), and enhanced proliferation and differentiation of porcine intramuscular preadipocytes through activation of the PI3K/Akt signaling pathway.

SOLUTION: Does gPR39 activate proliferation and differentiation of porcine intramuscular preadipocytes through targeting the PI3K/AKT cell signaling pathway?

PROBLEM: Context: In diabetics with end-stage renal disease (ESRD), risk of death has been reported to be non-constant after the first dialysis, and different outcomes have been observed between genders. We assessed the impact of type 2 diabetes (T2DM) on mortality in dialysis regarding its differential effect by gender using time-dependent analyses.', 'All T2DM and non-diabetic (no-DM) patients who started dialysis in two renal units in Lyon, France, between January 1, 1995, and December 31, 2007, were included. In multivariate analyses, the Cox model and Shoenfeld residual approach were used to assess the effect of T2DM on dialysis mortality by gender.', 'We included 235 T2DM (males: 57.9%) and 480 no-DM (males: 65.6%) patients. In males, the adjusted hazard ratio (aHR) for death in T2DM versus no-DM was 0.83 (p = 0.20) and was constant over time after the first renal replacement therapy (RRT) (p = 0.88). In females, aHR for death in T2DM versus no-DM patients was not constant over time (p = 0.002). It was 0.64 (p = 0.13) within the first year after the first RRT and 2.10 (p = 0.002) after the first year. Evolutions with time of these aHR by gender were significantly different (p = 0.009).
Answer: T2DM was associated with death only in females. This association was not constant over time after the first dialysis.

SOLUTION:
Does the Impact of type 2 diabetes on mortality in end-stage renal disease patients differ between genders?