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.

[Q]: Context: Cilostazol, a potent type 3 phosphodiesterase inhibitor, is found to reduce neointimal formation by inhibiting vascular smooth muscle cell (VSMC) proliferation. The aim of this study is to investigate whether the inhibitory effect of cilostazol on VSMC proliferation is operated via heme oxygenase-1 (HO-1).', 'In rat carotid arteries, cilostazol up-regulated HO-1 in the neointima of balloon-injured arteries. Treatment of human VSMCs with cilostazol enhanced the expression of HO-1, which was mainly regulated at the transcriptional level. Small interfering RNA knock-down of HO-1 attenuated the inhibitory effect of cilostazol on VSMC proliferation, suggesting the critical role of HO-1 in cilostazol effect. The transcriptional responsiveness of HO-1 to cilostazol was inversely correlated with the length of GT-repeat in human HO-1 promoter. Deletion and mutational analysis of HO-1 promoter along with chromatin immunoprecipitation showed that cyclic AMP response element (CRE)-binding protein (CREB) participated in cilostazol-induced HO-1 transcription. Furthermore, cilostazol triggered a linkage between the CRE and GT-repeat regions in the HO-1 promoter. The promoting effect of cilostazol on HO-1 expression, proliferation inhibition, and chromatin conformation in the HO-1 promoter was greater in VSMCs from subjects with shorter GT-repeat alleles than those with longer alleles.
Answer: Cilostazol inhibits VSMC proliferation involving an association between CREB and HO-1. The length polymorphism of GT-repeat in human HO-1 promoter determines the effect of cilostazol.
[A]: Does gT-repeat length polymorphism in heme oxygenase-1 promoter determine the effect of cilostazol on vascular smooth muscle cells?


[Q]: Context: Rural primary health centers frequently treat patients with tick bites. This study compares everyday clinical practice at our primary healthcare center to practices recommended by current scientific evidence.', 'To describe the everyday management of tick bites by different healthcare professionals and to compare this management to evidence-based therapy guidelines.', 'Cross-sectional, descriptive observational study.', 'Data was collected through an anonymous self-completed questionnaire. The form was filled out by a consecutive sample of nurses, physicians and pediatricians of the clinical management unit of Medina-Sidonia (Cádiz).', 'Most nurses in the sample group use some type of product to facilitate the extraction of the tick (10 of the 11 surveyed nurses, 90.9%). The most frequently used products were chloroethyl and local anesthetic. In addition, nine nurses use gentle traction with tweezers (81.82%) to remove the tick. In the physician sample group, 3 out of 12 respondents (25%) prescribe antibiotics in all cases and nine stated that they knew which antibiotic should be used as first choice. In both cases, a high number of healthcare providers confirm giving post-extraction advice to patients: 11 in the medical community (91.66%) and nine nurses (81.82%).
Answer: We conclude that the performance of the healthcare providers that integrate this study does not closely follow general recommendations for extraction, treatment and follow-up care in patients with tick bites. Therefore, there is a need to improve the level of knowledge to ensure quality care in these instances.
[A]: Does [ Descriptive study of healthcare professionals ' management of tick bite ]?


[Q]: Context: A number of distinct stress signaling pathways in myocardium cause cardiac hypertrophy and heart failure. Class II histone deacetylases (HDACs) antagonize several stress-induced pathways and hypertrophy. However, cardiac hypertrophy induced by transgenic overexpression of the homeodomain only protein, HOP, can be prevented by the nonspecific HDAC inhibitors trichostatin A and valproic acid, suggesting that alternate targets that oppose class II HDAC function might exist in myocardium. We tested the effects of several HDAC inhibitors, including a class I HDAC-selective inhibitor, SK-7041, on cardiac hypertrophy induced by angiotensin II (Ang II) treatment or aortic banding (AB).', 'Cardiac hypertrophy was induced by chronic infusion of Ang II or by AB in mice or rats and evaluated by determining the ratio of heart weight to body weight or to tibia length, cross-sectional area, or echocardiogram. Cardiac hypertrophy induced by Ang II or AB for 2 weeks was significantly reduced by simultaneous administration of trichostatin A, valproic acid, or SK-7041. Echocardiogram revealed that exaggerated left ventricular systolic dimensions were relieved by HDAC inhibitors. HDAC inhibitors partially reversed preestablished cardiac hypertrophy and improved survival of AB mice. The expressions of atrial natriuretic factor, alpha-tubulin, beta-myosin heavy chain, and interstitial fibrosis were reduced by HDAC inhibition.
Answer: These results suggest that the predominant effect of HDAC inhibition, mainly mediated by class I HDACs, is to prevent cardiac hypertrophy in response to a broad range of agonist and stretch stimuli.
[A]:
Does inhibition of histone deacetylation block cardiac hypertrophy induced by angiotensin II infusion and aortic banding?