In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

Input: Consider Input: Context: Acute kidney injury (AKI) is an established indicator of all-cause mortality in a coronary care unit (CCU), and evaluating the risks of renal dysfunction can guide treatment decisions. In this study we used the Society of Thoracic Surgeons (STS) score to predict the incidence of AKI in CCU patients who had not undergone coronary artery bypass surgery (CABG) after a cardiac angiogram.', 'The study cohort comprised 126 patients diagnosed with 2 or 3 coronary vessels disease who did not receive CABG during their hospital course. This study was performed in the CCU of a tertiary referral university hospital between September 2012 and August 2013. The STS score was evaluated with adjustment in all patients and the outcomes of the risk of mortality, morbidity, or mortality and renal failure were selected for predicting assessment. Furthermore, the performance of the STS scores was compared with that of other scoring systems.', 'A total of 28.5% (36 of 126) of the patients had AKI of varying severity. For predicting AKI, the STS renal failure score was excellent, with areas under the receiver operating characteristic curve of 0.851 0.039, p < 0.001. When compared with other scoring systems, the STS renal failure score demonstrated the highest discriminatory power, the most favorable Youden index, and the highest overall correctness of prediction.\Question: Do society of Thoracic Surgeons score predicts kidney injury in patients not undergoing bypass surgery?

Output: The STS score is an effective tool for predicting AKI in patients with coronary artery disease who have not undergone CABG. Frequent monitoring of serum creatinine level or early application of AKI biomarkers are warranted for STS renal failure 5.7% or greater.

Input: Consider Input: Context: Vasopeptidase inhibitors are drugs that inhibit angiotensin-converting enzyme and neutral endopeptidase (NEP). The latter is a protease that degrades vasoactive peptides and is increased in diabetes. We have previously shown that treating streptozotocin-induced diabetic rats, an animal model of type 1 diabetes, with AVE7688, a vasopeptidase inhibitor, improves neurovascular and neural function. In this study, we determined the effect of treating Zucker diabetic fatty (ZDF) rats, an animal model of type 2 diabetes, with AVE7688 on vascular and neural function.', 'ZDF rats at 12 weeks of age were treated for 12 weeks with AVE7688 (500 mg/kg diet). Afterwards, vascular reactivity of epineurial arterioles of the sciatic nerve and nerve conduction velocity and blood flow was determined.', 'Vascular and neural function was significantly impaired in ZDF rats compared with age-matched lean (control) rats. Treating ZDF rats with AVE7688 improved vascular relaxation to acetylcholine and calcitonin gene-related peptide in epineurial arterioles. Motor and sensory nerve conduction velocity, endoneurial blood flow and thermal nociception end-points were also improved by treatment compared with untreated ZDF rats. Superoxide and expression of NEP were increased in epineurial arterioles from ZDF rats and attenuated by treatment with AVE7688.\Question: Does treatment of Zucker diabetic fatty rats with AVE7688 improve vascular and neural dysfunction?

Output: AVE7688 is an effective treatment for microvascular and neural disease in ZDF rats. Thus, vasopeptidase inhibitors may be an effective treatment for diabetic microvascular and neural complication in type 2 diabetes.

Input: Consider Input: Context: This study was designed to examine the effects of verapamil and aspirin, which decrease thromboxane A2 and serotonin release, on the modulation of vascular tone by platelets.', 'Aggregating platelets cause constriction of de-endothelialized arterial segments through thromboxane A2 and serotonin release. These cells cause relaxation of arterial segments with intact endothelium through release of the endothelium-derived relaxing factor.', 'Healthy subjects were given either no drug, verapamil or aspirin for > or = 5 days before their platelets were obtained. The effects of platelets obtained from subjects before and after treatment with aspirin or verapamil on the tone of rat aortic rings were determined.', 'As expected, control platelets (before verapamil or aspirin treatment) induced concentration-dependent relaxation of rat aortic rings with intact endothelium and a concentration-dependent contraction of de-endothelialized rings. Verapamil treatment enhanced (p < 0.02) the platelet-mediated relaxation in rings with intact endothelium and abolished platelet-mediated constriction (p < 0.01) in the de-endothelialized rings. Aspirin treatment also abolished (p < 0.05) platelet-mediated constriction of the de-endothelialized rings. The de-endothelialized rings contracted normally in response to the synthetic thromboxane A2 analogue U46,619, as well as to serotonin, indicating that the vascular smooth muscle response to thromboxane A2 and serotonin was intact.\Question: Do verapamil and aspirin modulate platelet-mediated vasomotion in arterial segments with intact or disrupted endothelium?
Output: This study provides evidence for the modulation of platelet-mediated vasoconstriction of de-endothelialized arterial segments by prior treatment of subjects with verapamil or aspirin. In clinical syndromes characterized by endothelial dysfunction or disruption, treatment with verapamil or aspirin may modify platelet-vessel wall interactions.