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 Input:
Context: Evidence suggests that induction of heme oxygenase-1 (HO-1) inhibits proliferation of vascular smooth muscle cells and intimal thickening after arterial injury, and therapeutic molecules induce HO-1. Probucol is the only oral drug that inhibits restenosis in humans and intimal thickening in animals, although its underlying mechanism remains unclear.', 'Aortas were harvested from New Zealand White rabbits fed normal or 0.75% (wt/wt) probucol-fortified chow, with or without endothelial denudation of the abdominal aorta on day 21, and analyzed for heme oxygenase and apoptosis. Uninjured aortas were harvested on day 21 and balloon-injured aortas on days 22 and 25. Probucol significantly increased mRNA of HO-1 assessed by real-time PCR and HO activity in aortas at all time points. Probucol also enhanced apoptosis of medial cells in the injured aorta, as evidenced by the TUNEL assay. Furthermore, probucol (100 micromol/L) increased HO-1 mRNA and HO activity when added to rabbit aortic smooth muscle cells (RASMCs) cultured in serum-free medium for 24 hours. Induction of HO-1 mRNA was inhibited by actinomycin D and was associated with inhibition of RASMC proliferation. This probucol-induced increase in HO-1 mRNA and inhibition of RASMC proliferation was prevented by the HO inhibitor Sn(IV) protoporphyrin or transfection with small interference RNA (siRNA) to knockdown HO-1, but not by inactive Cu(II) protoporphyrin or scrambled siRNA.
Answer: Probucol induces HO-1, and this contributes to the inhibition of vascular SMC proliferation. This novel finding may explain how probucol inhibits restenosis and highlights HO-1 as a target for therapeutic intervention against occlusive vascular disease.

Ex Output:
Does probucol protect against smooth muscle cell proliferation by upregulating heme oxygenase-1?


Ex Input:
Context: Noninvasive pacemaker stress echocardiography is a newly introduced method for the diagnosis of coronary artery disease in patients with a permanent pacemaker. The prognostic value of pacemaker stress echocardiography has not been studied.', 'We studied 136 patients (mean age 64+/-12 years) with a permanent pacemaker who underwent pacemaker stress echocardiography for evaluation of coronary artery disease. All patients underwent pacemaker stress echocardiography by external programming (pacing heart rate up to ischemia or target heart rate).', 'Thirty-one patients (23%) had normal study results. Ischemia was detected in 75 patients (55%). During a mean follow-up of 3.5+/-2.4 years, 35 deaths (26%) (20 the result of cardiac causes) and 2 nonfatal myocardial infarctions (1%) occurred. The annual cardiac death rate was 1.3% in patients without ischemia and 4.6% in patients with ischemia (P=.01). The annual all-cause mortality rate was 3.1% in patients without ischemia and 7% in patients with ischemia (P=.004). The presence of ischemia during pacemaker stress echocardiography was the strongest independent predictor of cardiac death (hazard ratio 4.1, confidence interval 1.2-14.5) and all-cause mortality (hazard ratio 2.7, confidence interval 1.2-6.0) in a multivariable model.
Answer: Myocardial ischemia during pacemaker stress echocardiography is an independent predictor of cardiac death and all-cause mortality in patients with a permanent pacemaker.

Ex Output:
Does pacemaker stress echocardiography predict cardiac events in patients with permanent pacemaker?


Ex Input:
Context: To determine whether a paper-based antibiotic ordering system is an effective antibiotic stewardship measure.', 'An antibiotic order form (AOF) was introduced in July 2001 at a pediatric tertiary care hospital. Vancomycin courses prescribed before and after the AOF introduction were retrospectively reviewed based on Hospital Infection Control Practices Advisory Committee guidelines. The impact of the AOF on the appropriateness of vancomycin prescribing was evaluated in univariate and multivariable analyses that adjusted for other factors associated with appropriateness of vancomycin use. The density of vancomycin use after introduction of the AOF was also assessed.', 'Compliance with the AOF was poor (<50%) during the planned study period; therefore an additional 2 months of improved compliance (70-80%) were included. Rates of inappropriate vancomycin use increased during the study periods: 35% before AOF; 39% post-AOF; and 51% during the improved compliance period. On adjusted analysis, vancomycin utilization was significantly more inappropriate after introduction of the AOF. Vancomycin doses per 1000 patient days increased after introduction of the AOF.
Answer: Inappropriate vancomycin use and vancomycin use overall increased after the introduction of an AOF. An AOF intervention did not have its intended effect of improving and reducing vancomycin use.

Ex Output:

Does an antibiotic order form intervention improve or reduce vancomycin use?