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: Peritoneal dialysis is complicated by mesothelial cell injury due to low biocompatibility of peritoneal dialysis fluid (PDF). We have previously demonstrated that heat shock protein (HSP)-72 is potently up-regulated in response to PDF exposure of mesothelial cells in in vitro and in vivo models of peritoneal dialysis. The aim of this study was to evaluate potential cytoprotective effects of overexpression of HSP-72.', 'Cytoprotection was assessed by comparing cellular viability between pretreated versus nonpretreated human mesothelial cells (Met 5a; ATCC, Manassas, VA, USA, and primary cell cultures) subjected to extended, usually lethal PDF exposure times (120 min, CAPD2; Fresenius, Bad Homburg, Germany). Pretreatment was performed with exposure to PDF (60 min, CAPD2; Fresenius) or heat (15 min, 41.5 degrees C), and by transient transfection with HSP-72.', 'When mesothelial cells were pretreated by nonlethal exposure to PDF or heat, HSP-72 was markedly up-regulated (>5-fold, P < 0.01). Pretreated human mesothelial cells were significantly protected against subsequent "lethal" exposures to PDF, as assessed by dye exclusion (>50% reduction, P < 0.05) and lactate dehydrogenase (LDH) release (>30% reduction, P < 0.05). Comparable cytoprotection (50% reduction by dye exclusion) was indicated by overexpression of HSP-72 in cultered human mesothelial cells (>5-fold) after transient transfection with HSP-72. This cytoprotection was confirmed at a cellular basis by double staining techniques with HSP-72 and ApopTag (apoptosis detection kit).\Question: Does overexpression of HSP-72 confer cytoprotection in experimental peritoneal dialysis?
[EX A]: Our study therefore shows that the mesothelial stress response confers cytoprotection in experimental peritoneal dialysis, mediated by the induction of HSP-72, and that the stimulus of the pretreatment does not have to be identical to the subsequent injury. These data offer the basis for an attractive novel therapeutic approach against PDF toxicity.

[EX Q]: Context: Talin-1 is a cytoskeleton protein that participates in cell migration and plays a role in tumor formation, migration, and metastasis in different types of cancer. Chinese investigators have observed that the levels of Talin-1 protein and mRNA expression in HCC tissues are significantly lower than in the adjacent non-cancerous tissue. However, Japanese investigators have reported that Talin-1 is upregulated in HCC. Tln2 as homologous gene of Tln-1, which encodes a very similar protein, but the role of Talin-2 is very little known in primary liver cancer (PLC). We investigated whether the expression of Talin-1 in PLC may be associated with the histological subtype as well as the role of Talin-1 in tumor cell invasion and migration using human hepatocellular carcinoma cell lines.', 'We measured the mRNA expression levels of Talin-1 and Talin-2 in five human liver cancer cell lines and normal human liver cell (LO2 cell line) by real-time PCR and the protein expression levels of Talin-1 by Western blot. Migration and invasion of the cells were assessed using transwell assays and cell scratch experiments, respectively, and proliferation was assessed by soft AGAR colony formation.', 'Talin-1 and Talin-2 expression differed significantly between the five human liver cancer cell lines and LO2 cell line (p<0.05). Compared with the LO2 cell line, the invasion and migration capabilities of the five cancer cell lines differed significantly (p<0.05). Similarly, the colony-forming ability differed (p<0.05).\Question: Does talin-1 correlate with reduced invasion and migration in human hepatocellular carcinoma cells?
[EX A]: High levels of Talin-1 expression are correlated with reduced invasion and migration as well as decreased malignancy in human liver cancer cell lines; the suppression of Talin-1 promotes invasion and migration. In addition, Talin-2 may be correlated with invasion and migration in human hepatocellular carcinoma.

[EX Q]: Context: The goal of the present study was to identify predictors of event-free survival in nonischemic dilated cardiomyopathy (NIDCM) patients after administration of angiotensin-converting enzyme inhibitors (ACEI)/angiotensin receptor blockers (ARB) and beta-blockers.', "The study group comprised 78 consecutive patients with NIDCM between 1997 and 2002. NIDCM was defined as ejection fraction (EF) <0.40 and left ventricular end-diastolic diameter (LVEDD) >55 mm on echocardiography and normal coronary angiography. The mean EF and LVEDD was 26.3 +/- 10.5%, and 62.9 +/- 7.1 mm, respectively. Patients were treated with optimal medical therapy including ACEI/ARBs and/or beta-blockers and followed up for 35.6 +/- 27.8 months. The primary endpoint was either cardiac death or hospitalization because of deterioration of heart failure. Cox's regression analysis was used to establish the association of age, sex, EF, LVEDD, left atrial diameter, cardiac index, pulmonary capillary wedge pressure, QRS duration, severity of mitral regurgitation, body mass index, New York Heart Association class and the presence of atrial fibrillation with these events. During follow-up, 23 patients reached the primary endpoint. In a multivariate analysis, EF (chi-square 5.74, p=0.0166), severity of mitral regurgitation (chi-square 12.31, p=0.0004), and QRS duration (chi-square 11.20, p=0.0008) remained significant predictors.\Question: Are prolonged QRS duration and severity of mitral regurgitation unfavorable prognostic markers of heart failure in patients with nonischemic dilated cardiomyopathy?
[EX A]:
In NIDCM patients, prolonged QRS duration is a high risk factor for remodeling and unfavorable events. The severity of mitral regurgitation was also a strong risk predictor.