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.
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Question: To examine the effect of TRIB3 on endoplasmic reticulum stress induced -cell apoptosis and to investigate the mechanism with a specific emphasis on the role of NF-B pathway.', 'We investigated the effect of TRIB3 on ER stress-induced -cell apoptosis in INS-1 cells and primary rodent islets. The potential role of TRIB3 in ER stress inducer thapsigargin (Tg)-induced -cell apoptosis was assessed using overexpression and siRNA knockdown approaches. Inducible TRIB3 -cells, regulated by the tet-on system, were used for sub-renal capsule transplantation in streptozotocin (STZ)-diabetic mice, to study the effect of TRIB3 on ER stress-induced -cell apoptosis in vivo. Apoptosis was determined by TUNEL staining both in vivo and in vitro, while the molecular mechanisms of NF-B activation were investigated.', 'TRIB3 was induced in ER-stressed INS-1 cells and rodent islets, and its overexpression was accompanied by increased -cell apoptosis. Specifically, TRIB3 overexpression enhanced Tg-induced INS-1 derived -cell apoptosis both in vitro and in sub-renal capsular transplantation animal model. Additionally, knockdown of Trib3 blocked Tg-induced apoptosis. Mechanistically, the induction of TRIB3 during ER stress resulted in the activation of NF-B and aggravated INS-1 derived -cell apoptosis, while inhibiting the NF-B pathway significantly abrogated this response and prevented -cell apoptosis, both in vitro and in sub-renal capsular transplantation animal model.

Answer: Does tRIB3 alter endoplasmic reticulum stress-induced -cell apoptosis via the NF-B pathway?

Question: Pulmonary hypertension (PH) is associated with a poor prognosis in diffuse lung disease (DLD). A study was undertaken to compare the prognostic significance of invasive and non-invasive parameters in patients with DLD and suspected PH.', 'Hospital records of consecutive patients with DLD undergoing right heart catheterisation (RHC) were reviewed (n = 66). Mean pulmonary artery pressure (mPAP), pulmonary vascular resistance (PVR) and non-invasive variables were examined against early (within 12 months) and overall mortality. A priori thresholds were examined against early mortality. Relationships between mPAP, PVR and non-invasive markers were assessed.', 'Fifty patients had PH on RHC (mean (SD) mPAP 33.5 (11.8) mm Hg, PVR 5.9 (4.3) Wood units (WU)). Raised PVR was strongly associated with early mortality (odds ratio (OR) 1.30; 95% confidence interval (CI) 1.11 to 1.52; p = 0.001), with PVR > or = 6.23 WU being the optimal threshold after adjustment for age, gender, composite physiological index (CPI) and diagnosis of idiopathic pulmonary fibrosis (OR 11.09; 95% CI 2.54 to 48.36; p = 0.001). Early mortality was linked, albeit less strongly, to right ventricular dilation at echocardiography, but not to other non-invasive variables or mPAP. Overall mortality was most strongly associated with increasing CPI levels. Correlations between PVR and non-invasive variables were moderate (R(2) <0.32), improving little following construction of a multivariate index which did not itself predict mortality.

Answer: Does pulmonary vascular resistance predict early mortality in patients with diffuse fibrotic lung disease and suspected pulmonary hypertension?

Question: Gastric mucosal injury by Helicobacter pylori has been suggested to be mediated by various cytokines induced by this organism. Nitric oxide (NO) is an important effector molecule involved in immune regulation and defence. To clarify the mechanisms by which H. pylori induces gastric mucosal cell injury, we examined whether H. pylori induces gastric epithelial death via NO production.', 'Cytotoxic and non-cytotoxic strains of H. pylori were used. The death of MKN45 cells caused by H. pylori was examined by the 3-(4,5-dimethyl-thiazole-2yl)-2,5-diphenyl tetrazolium bromide (MTT) assays. Aminoguanidine was used to inhibit inducible nitric oxide synthase (iNOS) activity. Expression of iNOS mRNA was determined by the reverse transcriptase-polymerase chain reaction and the DNA fragmentation analysis was performed by using agarose gel electrophoresis.', 'The MTT assay revealed that neither viable H. pylori nor other components of the microorganism induced cell death. Both preincubation of MKN45 cells with interferon-gamma for 6 h and coculture with TNF-alpha significantly increased the cytotoxicity of H. pylori. Both cytotoxic and non-cytotoxic strains of H. pylori induced cell death. Expression of iNOS mRNA was observed in MKN45 cells at 6, 8 and 12 h after H. pylori inoculation. The cytotoxicity of H. pylori was inhibited by aminoguanidine and DNA fragmentation analysis showed that H. pylori induced apoptosis.

Answer:
Does helicobacter pylori induce apoptosis in gastric epithelial cells through inducible nitric oxide?