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.

[EX Q]: Patients with diabetes are at greater risk of cardiovascular events. Insulin resistance (IR) and hyperinsulinaemia are both related to an increased cardiovascular risk, but whether IR predicts coronary heart disease (CHD) independently of other risk factors in patients with type 2 diabetes (T2D) is a topic of considerable controversy. The aim of the present study was to evaluate the prospective relationship of fasting insulin, HOMA-IR, fasting plasma glucose (FPG) and 2-h post-load glucose (2hPG) load with CHD incidence among such patients.', 'A total of 2607 patients with T2D were enrolled in a community-dwelling cohort and followed for an average of 7.2 years. Conventional CHD risk factors, FPG, 2hPG, fasting insulin levels and HOMA-IR index were measured at baseline. Cox regression hazard ratios (HRs) were used to assess CHD risk.', "A total of 299 'hard' CHD events were registered (in 114 women and 185 men). Increasing levels of fasting insulinaemia were positively associated with CHD incidence. This correlation persisted after controlling for gender, body mass index, blood pressure, lipid profile, medication use and HbA1c [HR for each increase in quartile (fully adjusted model): 1.18 (95% CI: 1.06-1.32); P<0.01]. 2hPG showed a non-linear association with incident CHD [HR of highest vs lowest quartile: 1.64 (95% CI: 1.03-2.61)]. Fasting glycaemia was not associated with CHD risk, whereas HOMA-IR had a direct and independent correlation with CHD risk [HR for each one-quartile increase: 1.19 (95% CI: 1.07-1.34); P<0.01].
[EX A]: Do fasting hyperinsulinaemia and 2-h glycaemia predict coronary heart disease in patients with type 2 diabetes?

[EX Q]: Airway remodeling in asthma is the result of increased expression of connective tissue proteins, airway smooth muscle cell (ASMC) hyperplasia and hypertrophy. TGF-beta1 has been found to increase ASMC proliferation. The activation of mitogen-activated protein kinases (MAPKs), p38, ERK, and JNK, is critical to the signal transduction associated with cell proliferation. In the present study, we determined the role of phosphorylated MAPKs in TGF-beta1 induced ASMC proliferation.', 'Confluent and growth-arrested bovine ASMCs were treated with TGF-beta1. Proliferation was measured by [3H]-thymidine incorporation and cell counting. Expressions of phosphorylated p38, ERK1/2, and JNK were determined by Western analysis.', 'In a concentration-dependent manner, TGF-beta1 increased [3H]-thymidine incorporation and cell number of ASMCs. TGF-beta1 also enhanced serum-induced ASMC proliferation. Although ASMCs cultured with TGF-beta1 had a significant increase in phosphorylated p38, ERK1/2, and JNK, the maximal phosphorylation of each MAPK had a varied onset after incubation with TGF-beta1. TGF-beta1 induced DNA synthesis was inhibited by SB 203580 or PD 98059, selective inhibitors of p38 and MAP kinase kinase (MEK), respectively. Antibodies against EGF, FGF-2, IGF-I, and PDGF did not inhibit the TGF-beta1 induced DNA synthesis.
[EX A]: Does tGF-beta1 increase proliferation of airway smooth muscle cells by phosphorylation of map kinases?

[EX Q]: It has been speculated that invasive revascularization prevents development of cardiogenic shock. Data from randomised trials comparing angioplasty with fibrinolysis on the development of cardiogenic shock are lacking.', 'To elucidate the effect of angioplasty on in-hospital development of cardiogenic shock compared to fibrinolysis. To evaluate whether mortality in patients who develop cardiogenic shock after treatment is dependent on revascularization strategy.', 'DANAMI-2 randomly assigned 1572 STEMI patients to fibrinolysis (782 patients) or angioplasty (790 patients). Data on patients with in-hospital development of cardiogenic shock after randomisation were included. Of the 103 patients (6.6%) patients developing cardiogenic shock 57% were randomised to angioplasty with an unadjusted odds ratio of 1.39 (0.92-2.11, p=0.14). During the three year follow-up 58% of the total mortality was due to cardiogenic shock, and treatment strategy did not influence the risk associated with shock (hazard ratio of 1.05 (0.67-1.64) for angioplasty vs. fibrinolysis).
[EX A]:
Does percutaneous coronary intervention for acute MI prevent in-hospital development of cardiogenic shock compared to fibrinolysis?