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]: Erectile dysfunction (ED) and atherosclerotic cardiovascular disease (ASCVD) share many common risk factors, and vascular ED is a marker for increased ASCVD risk. Low 25-hydroxyvitamin D [25(OH)D] concentrations have been associated with increased ASCVD risk, but less is known regarding the relationship of low 25(OH)D with ED. We determined whether 25(OH)D deficiency is associated with ED independent of ASCVD risk factors.', 'We performed cross-sectional analyses of 3390 men aged ≥20 years free of ASCVD who participated in NHANES 2001-2004. Serum 25(OH)D was measured by the DiaSorin radioimmunoassay; deficiency was defined as levels <20\xa0ng/ml (<50\xa0nmol/L). Self-reported ED, assessed by a single validated question, was defined as men who reported being "never" or "sometimes able" to maintain an erection. We assessed the relationship between 25(OH)D deficiency and ED prevalence using adjusted Poisson regression methods.', 'After accounting for NHANES sampling, the weighted prevalence of 25(OH)D deficiency and of ED were 30% and 15.2%, respectively. 25(OH)D levels were lower in men with vs. those without ED (mean 22.8 vs 24.3\xa0ng/mL, respectively; p\xa0=\xa00.0005). After adjusting for lifestyle variables, comorbidities, and medication use, men with 25(OH)D deficiency had a higher prevalence of ED compared to those with levels ≥30\xa0ng/ml (Prevalence Ratio 1.30, 95% CI 1.08-1.57).
[A]: Is vitamin D deficiency independently associated with greater prevalence of erectile dysfunction : The National Health and Nutrition Examination Survey ( NHANES ) 2001-2004?


[Q]: 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.
[A]: Does microRNA367 negatively regulate the inflammatory response of microglia by targeting IRAK4 in intracerebral hemorrhage?


[Q]: Intravascular volume loss from ischemia-reperfusion (IR) injury is a major clinical concern. We hypothesize that angiotensin II decreases IR-mediated microvascular fluid leak via the angiotensin II type 2 receptor in a cAMP dependent manner. We therefore sought to determine hydraulic permeability after IR of venules treated with 1) angiotensin II, 2) angiotensin II and cAMP synthesis inhibitor, and 3) angiotensin II and an angiotensin II type 2 receptor antagonist.', 'Rat mesenteric post-capillary venules were micro-cannulated to measure hydraulic permeability (L(p)). IR was achieved by placing animals in a 5% oxygen environment and preventing venular flow, after which blood flow was allowed to resume. L(p) was measured after IR and treatment with 1) angiotensin II (20 nm), 2) angiotensin II (20 nm) + cAMP synthesis inhibitor (DDA,10uM), and 3) angiotensin II (20 nm) + type 2 receptor antagonist (PD-123319, 300 mum) (n=6 in each group).', 'Compared with the seven-fold increase in L(p) because of IR alone: 1) angiotensin II attenuated the seven-fold increase by 50% (P<0.005), 2) cAMP inhibition did not change the effect of angiotensin II on leak, and the type 2 receptor antagonist completely blocked the effects of angiotensin II on IR mediated leak.
[A]:
Does angiotensin II type 2 receptor decrease ischemia reperfusion induced fluid leak?