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.

[Q]: The aim of the study was to determine whether medial meniscal substitution with a polyurethane scaffold (Actifit(®)) improves the outcome of medial meniscal-deficient varus knees undergoing open-wedge high tibial osteotomy.', 'Sixty patients with symptomatic varus knees those who underwent open-wedge high tibial osteotomies were prospectively studied. In 30 patients, the medial meniscus was left with a defect larger than 25 mm (Group M). An Actifit(®) device was implanted (Group A) in the remaining 30 patients. Patients were functionally evaluated with WOMET, IKDC and VAS. Patient satisfaction was graded from 0 (not satisfied) to 4 (very satisfied).', 'Both groups were comparable preoperatively. They had similar follow-up periods (31.2 months; range 24-47.5; n.s.). WOMET improved a mean of 53.4 ± 8.4 and 42.4 ± 17.2 points in Groups M and A, respectively (p = 0.002). IKDC improved a mean of 56.7 ± 12 and 50.3 ± 15.6 points in Groups M and A, respectively (n.s.). VAS dropped 5.9 ± 2.1 and 4.7 ± 2.8 points in Groups M and A, respectively (p = 0.006). Patient satisfaction averaged 3.3 ± 0.8 and 3.3 ± 1 in Groups M and A, respectively (n.s.).
[A]: Does partial meniscus substitution with a polyurethane scaffold improve outcome after an open-wedge high tibial osteotomy?


[Q]: Physiological roles of apelin and its specific receptor APJ signaling were investigated in vascular smooth muscle cells (VSMCs). The present study determined whether apelin activates myosin light chain (MLC), a major regulatory event in initiating smooth muscle contraction.', 'To assess MLC activation, we performed Western blot and immunohistochemical studies using an antibody against the phospho-MLC. In VSMCs, apelin induces the phosphorylation of MLC in a concentration-dependent manner with a peak at 2 minutes. Pretreatment of VSMCs with pertussis toxin abolishes the apelin-induced phosphorylation of MLC. Inhibition of protein kinase C (PKC) with GF-109203X markedly attenuated the apelin-induced MLC phosphorylation. In addition, methylisobutyl amiloride, a specific inhibitor of the Na+/H+ exchanger (NHE), and KB-R7943, a potent inhibitor for the reverse mode of the Na+/Ca2+ exchanger (NCX), significantly suppressed the action of apelin. In wild-type mice, apelin phosphorylates MLC in vascular tissue, whereas it had no response in APJ-deficient mice by Western blot and immunohistochemistry. Apelin-induced phosphorylation of MLC was accompanied with myosin phosphatase target subunit phosphorylation.
[A]: Does apelin stimulate myosin light chain phosphorylation in vascular smooth muscle cells?


[Q]: Arginine vasopressin is a vasoactive drug commonly used in distributive shock states including mixed shock with a cardiac component. However, the direct effect of arginine vasopressin on the function of the ischemia/reperfusion injured heart has not been clearly elucidated.', 'We measured left ventricular ejection fraction using trans-thoracic echocardiography in C57B6 mice, both in normal controls and following ischemia/reperfusion injury induced by a one hour ligation of the left anterior descending coronary artery. Mice were treated with one of normal saline, dobutamine (8.33 microg/kg/min), or arginine vasopressin (0.00057 Units/kg/min, equivalent to 0.04 Units/min in a 70 kg human) delivered by an intraperitoneal micro-osmotic pump. Arterial blood pressure was measured using a micromanometer catheter. In addition, mortality was recorded and cardiac tissues processed for RNA and protein.', 'Baseline left ventricular ejection fraction was 65.6% (60 to 72). In normal control mice, there was no difference in left ventricular ejection fraction according to infusion group. Following ischemia/reperfusion injury, AVP treatment significantly reduced day 1 left ventricular ejection fraction 46.2% (34.4 to 52.0), both in comparison with baseline and day 1 saline treated controls 56.9% (42.4 to 60.2). There were no significant differences in preload (left ventricular end diastolic volume), afterload (blood pressure) or heart rate to account for the effect of AVP on left ventricular ejection fraction. The seven-day mortality rate was highest in the arginine vasopressin group. Following ischemia/reperfusion injury, we found no change in cardiac V1 Receptor expression but a 40% decrease in Oxytocin Receptor expression.
[A]:
Does low-dose vasopressin infusion result in increased mortality and cardiac dysfunction following ischemia-reperfusion injury in mice?