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.
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Question: Context: To test the hypothesis that pharmacological plasminogen activator inhibitor (PAI)-1 inhibition protects against renin-angiotensin-aldosterone system-induced cardiovascular injury, the effect of a novel orally active small-molecule PAI-1 inhibitor, PAI-039, was examined in a mouse model of angiotensin (Ang) II-induced vascular remodeling and cardiac fibrosis.', 'Uninephrectomized male C57BL/6J mice were randomized to vehicle subcutaneus, Ang II (1 mug/h) subcutaneous, vehicle+PAI-039 (1 mg/g chow), or Ang II+PAI-039 during high-salt intake for 8 weeks. Ang II caused significant medial, adventitial, and aortic wall thickening compared with vehicle. PAI-039 attenuated Ang II-induced aortic remodeling without altering the pressor response to Ang II. Ang II increased heart/body weight ratio and cardiac fibrosis. PAI-039 did not attenuate the effect of Ang II on cardiac hypertrophy and increased fibrosis. The effect of PAI-039 on Ang II/salt-induced aortic remodeling and cardiac fibrosis was comparable to the effect of genetic PAI-1 deficiency. Ang II increased aortic mRNA expression of PAI-1, collagen I, collagen III, fibronectin, osteopontin, monocyte chemoattractant protein-1, and F4/80; PAI-039 significantly decreased the Ang II-induced increase in aortic osteopontin expression at 8 weeks.
Answer: This study demonstrates that pharmacological inhibition of PAI-1 protects against Ang II-induced aortic remodeling. Future studies are needed to determine whether the interactive effect of Ang II/salt and reduced PAI-1 activity on cardiac fibrosis is species-specific. In this study, the effect of pharmacological PAI-1 inhibition in a mouse model of Ang II-induced vascular remodeling and cardiac fibrosis was examined. PAI-1 inhibition significantly attenuated Ang II-induced aortic medial and wall thickening, but not cardiac hypertrophy, and enhanced Ang II/salt-induced cardiac fibrosis.

Answer: Does pharmacological inhibition and genetic deficiency of plasminogen activator inhibitor-1 attenuate angiotensin II/salt-induced aortic remodeling?

Question: Context: Impaired endothelial function, as assessed by brachial artery flow-mediated dilation (FMD), is an established risk factor for cardiovascular events. FMD is impaired in heart failure (HF) patients, but less is known about hyperemic brachial artery flow. We investigated the relationship between FMD and hyperemic flow with adverse clinical outcomes in HF patients.', 'Brachial artery FMD and hyperemic flow were assessed in 156 patients (70.5 % Male; 45.5% Caucasian; mean age ( SD) = 56.2 (12.4) years) with HF and reduced left ventricular ejection fraction (LVEF). Cox proportional hazard models were used to assess the potential explanatory association of FMD and hyperemic flow with the composite outcome of death or cardiovascular hospitalization over a median 5-year follow-up period.', 'Both FMD and hyperemic flow were negatively correlated with age, but unrelated to sex, race, body mass index, LVEF or N-terminal pro-B-Type natriuretic peptide (NT-ProBNP). Reduced hyperemic flow, but not FMD, was associated with an increased risk of death or cardiac hospitalization after controlling for traditional risk factors.
Answer: The association of reduced hyperemic flow with increased risk of adverse clinical outcomes suggests that micro-vascular function may be an important prognostic marker in patients with HF.

Answer: Is reactive hyperemia associated with adverse clinical outcomes in heart failure?

Question: Context: Cam impingement as a known sequelae of slipped capital femoral epiphysis (SCFE) has led to speculation that subclinical SCFEs may be the causative factor in idiopathic cam morphology; alternatively, others have implicated an abnormal extension of the growth plate as a causative factor.', 'To investigate the growth plate tilt angle in 4 patient cohorts: normal patients, patients with idiopathic cam morphology (CamIP), patients with cam morphology secondary to known SCFE (CamSCFE), and patients with incidental findings of an asymptomatic cam (Camasymp).', 'Case-control study; Level of evidence, 3.', 'A database of 192 computed tomography scans of abdomens/pelvises of patients (ages, 5-19 years) with no known orthopaedic issues, reformatted to neutral tilt, inclination, and rotation, were utilized for the normal cohort, the Camasymp cohort, and to create an age- and sex-matched control cohort. In addition, a retrospective review of all patients treated for femoroacetabular impingement (FAI) with preoperative advance imaging was conducted, and patients were separated to CamIP and CamSCFE cohorts. The alpha angle and tilt angle were measured on each hip. Statistical analysis was performed.', 'The mean tilt angle among the normal patients was 12.1, with 1.9% of the variation in tilt angle being explained by age; each additional year of age decreased the tilt angle by 0.27 (P = .008). The tilt angle for the CamSCFE cohort (mean, 44.5) was found to be significantly greater than both the CamIP cohort (mean, 5.9; P < .001) and the control cohort (mean, 12.8; P < .001). The tilt angle for the CamIP cohort was found to be significantly less than the control cohort (P = .003). The alpha angle and tilt angle were positively correlated in the CamIP cohort, but no correlation was found in the other cohorts. The mean tilt angle of the 18 hips in the Camasymp cohort was 13.9 11.5 (range, -12 to 37), with 12 hips (67%) in the tilt angle range of CamIP cohort and 6 in the tilt angle range of CamSCFE.
Answer: The proximal femoral growth plate normally has a posterior tilt that becomes more anterior through maturation. Idiopathic cam morphology has a drastically different growth plate tilt angle than cam morphology secondary to SCFE, suggesting that a majority of idiopathic cam morphology is not the result of subclinical SCFEs.

Answer:
Is idiopathic Cam Morphology Caused by Subclinical Slipped Capital Femoral Epiphysis : An MRI and CT Study?