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.

Input: Consider Input: Cardiac rupture is a catastrophic complication that occurs after acute myocardial infarction (MI) and, at present, there are no effective pharmacological strategies for preventing this condition. Here we investigated the effect of the angiotensin II receptor blocker olmesartan (Olm) on post-infarct cardiac rupture and its underlying mechanisms of action.', 'C57Bl/6 mice with MI were treated with Olm, aldosterone (Aldo) or vehicle. Cultured neonatal cardiomyocytes and fibroblasts were exposed to normoxia or anoxia and treated with angiotensin II (Ang II), RNH6270 (active ingredient of Olm) or Aldo.', 'The mortality rate and incidence of cardiac rupture in MI mice during the first week in the Olm-treated group were significantly lower than in the vehicle-treated group. Olm or RNH6270 reduced myeloperoxidase staining in the infarcted myocardium, decreased apoptosis in cultured cardiomyocytes and fibroblasts, as assessed by Hoechst staining and TUNEL assay, attenuated the accumulation of p53 and phosphorylated p53 and cleaved caspase 3 induced by MI or Ang II, as assessed by Western blotting, and up-regulated growth differentiation factor-15 (GDF-15). In cultured cardiomyocytes and fibroblasts, treatment with Ang II, Aldo or anoxia significantly down-regulated the expression of GDF-15.

Output: Does olmesartan prevent cardiac rupture in mice with myocardial infarction by modulating growth differentiation factor 15 and p53?


Input: Consider Input: Our objective was to study the direct effects of meconium on isolated umbilical artery and vein in vitro.', "Intact umbilical artery and vein rings were suspended in 5 ml organ baths containing kreb's solution (pH 7.2, 37 degrees C; bubbled with 2.5% oxygen and 8.07% carbon dioxide, balance nitrogen) for isometric tension recording. Meconium alone (final bath concentration 1%), centrifuged and filtered meconium, and meconium with the lipid fraction removed (separated into < 30,000 kd and > 30,000 kd) were added to the baths. Some vessels were also incubated in 1% meconium for 30 minutes, after which the meconium was washed out. Concentration-response curves to U46619 were obtained. The negative log of the concentration that evokes 50% of the maximal contraction was determined.", 'Umbilical artery and vein had no sustained response to meconium. Tension that developed by rings exposed to meconium was significantly less than control at all concentrations of U46619. There was some loss of the efficacy of meconium after centrifugation-filtration and washing out. Meconium without the lipid fraction had less inhibitory effect than did native meconium.

Output: Does meconium inhibit the contraction of umbilical vessels induced by the thromboxane A2 analog U46619?


Input: Consider Input: Intracerebral hemorrhage (ICH) induces microglial activation and the release of inflammatory cytokines, leading to inflammation in the brain. IRAK4, an essential component of the MyD88-dependent pathway, activates subsets of divergent signaling pathways in inflammation.', 'In the experiment, microglia were stimulated with erythrocyte lysates, and then miR-367, IRAK4, NF-ĸB activation and downstream proinflammatory mediator production were analyzed. In addition, inflammation, brain edema, and neurological functions in ICH mice were also assessed.', "Here, we report that ICH downregulated miR-367 expression but upregulated IRAK4 expression in primary microglia. We also demonstrate that miR-367 suppressed IRAK4 expression by directly binding its 3'-untranslated region. MiR-367 inhibited NF-ĸB activation and downstream proinflammatory mediator production. Knocking down IRAK4 in microglia significantly decreased the IRAK4 expression and inhibited the NF-ĸB activation and the downstream production of proinflammatory mediators. In addition, our results indicate that miR-367 could inhibit expression of proinflammatory cytokines, reduce brain edema, and improve neurological functions in ICH mice.


Output: Does microRNA367 negatively regulate the inflammatory response of microglia by targeting IRAK4 in intracerebral hemorrhage?