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.

[EX 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.
[EX A]: Does gT-repeat length polymorphism in heme oxygenase-1 promoter determine the effect of cilostazol on vascular smooth muscle cells?

[EX Q]: Context: To establish leukocyte count and leukocyte differential percentiles in normal uncomplicated pregnancy.', 'This retrospective longitudinal study was performed in an outpatient facility for routine antenatal care. The study population comprised of 726 healthy women from the 5th to the 41st week of pregnancy. Altogether, there were 1749 complete blood count evaluations, of which 481 were in the 1st trimester, 687 in the 2nd trimester and 581 in the 3rd trimester. The total and differential leukocyte counts were determined by an automated cell counter.', 'The leukocyte and neutrophil counts gradually and significantly increased form the 1st to the 3rd trimester. The monocyte count increase became significant only during the 3rd trimester. The eosinophil count did not significantly change throughout pregnancy. The basophil count significantly decreased during the 2nd trimester and returned to 1st trimester values during the 3rd trimester.
Answer: In this study, we provide total and differential leukocyte counts' mean+/-S.D., minimal and maximal values, and the 3rd, 5th, 10th, 50th, 90th, 95th, and 99th percentiles for entire pregnancy and for each trimester separately. These reference values should prove useful for diagnostic and research purposes.
[EX A]: Does total and differential leukocyte count percentiles in normal pregnancy?

[EX Q]: Context: Little is known about causes of intimal hyperplasia (IH) after sirolimus-eluting stent (SES) implantation.', 'Intravascular ultrasound was performed in 24 lesions with intra-SES restenosis and a comparison group of 25 nonrestenotic SESs. To assess stent strut distribution, the maximum interstrut angle was measured with a protractor centered on the stent, and the visible struts were counted and normalized for the number of stent cells. In SES restenosis patients, minimum lumen site was compared with image slices 2.5, 5.0, 7.5, and 10.0 mm proximal and distal to this site. The minimum lumen site had a smaller IVUS lumen area at follow-up (2.7+/-0.9 versus 6.2+/-1.9 mm2; P<0.01), larger maximum interstrut angle (135+/-39 degrees versus 72+/-23 degrees; P<0.01), larger IH area (3.4+/-1.5 versus 0.6+/-1.1 mm2; P<0.01) and thickness (0.7+/-0.3 versus 0.1+/-0.2 mm; P<0.01) at maximum interstrut angle, and fewer stent struts (4.9+/-1.0 versus 6.0+/-0.5; P<0.01) even when normalized for the number of stent cells (0.78+/-0.15 versus 0.97+/-0.07; P<0.01). Compared with nonrestenotic SES, the restenosis lesions also had a smaller minimal lumen area, larger IH area, thicker IH at maximum interstrut angle, fewer stent struts, and larger maximum interstrut angle. Multivariate analysis identified the number of visualized stent struts normalized for the number of stent cells and maximum interstrut angle as the only independent IVUS predictor of IH cross-sectional area (P<0.01 and P<0.01), minimum lumen area (P<0.01 and P<0.01), and IH thickness (P<0.01 and P<0.01).
Answer: The number and distribution of stent struts affect the amount of neointima after SES implantation.
[EX A]:
Does nonuniform strut distribution correlate with more neointimal hyperplasia after sirolimus-eluting stent implantation?