instruction:
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.
question:
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.).
answer:
Does partial meniscus substitution with a polyurethane scaffold improve outcome after an open-wedge high tibial osteotomy?


question:
Regular physical activity is an effective non-pharmacological therapy for prevention and control of hypertension. However, the underlying mechanisms are not fully understood. Accumulating evidence shows that the elevated vascular tone in hypertension is a consequence of the 'ion channel remodelling' that occurs during sustained high BP. The present study investigated the effects of aerobic exercise on the electrical remodelling of L-type Ca(2+) (Cav 1.2) and large-conductance Ca(2+) -activated K(+) (KCa 1.1) channels in mesenteric arteries (MAs) from spontaneously hypertensive rats (SHRs).", 'SHRs and normotensive (Wistar-Kyoto) rats were subjected to aerobic training or kept sedentary, and vascular mechanical and functional properties were evaluated.', 'Exercise did not affect the heart weight, but reduced the heart rate and body weight in SHR. In mesenteric arterial myocytes, exercise normalized the increased Cav 1.2 and KCa 1.1 current density in SHRs. Exercise also ameliorated the increased open probability and mean open time of the single KCa 1.1 channel in hypertension. The isometric contraction study revealed that both nifedipine (Cav 1.2 channel blocker) and NS11021 (KCa 1.1 channel activator) induced concentration-dependent vasorelaxation in MAs precontracted with noradrenaline. Exercise normalized the increased sensitivity of tissues to nifedipine and NS11021 in SHR. Furthermore, protein expression of the Cav 1.2 α1C -subunit together with the KCa 1.1 α- and β1-subunit was significantly increased in SHRs; and exercise ameliorated these molecular alterations in hypertension.
answer:
Does chronic exercise normalize changes in Cav 1.2 and KCa 1.1 channels in mesenteric arteries from spontaneously hypertensive rats?


question:
The mitotic kinases, Cdk1, Aurora A/B, and Polo-like kinase 1 (Plk1) have been characterized extensively to further understanding of mitotic mechanisms and as potential targets for cancer therapy. Cdk1 and Aurora kinase studies have been facilitated by small-molecule inhibitors, but few if any potent Plk1 inhibitors have been identified.', "We describe the cellular effects of a novel compound, BI 2536, a potent and selective inhibitor of Plk1. The fact that BI 2536 blocks Plk1 activity fully and instantaneously enabled us to study controversial and unknown functions of Plk1. Cells treated with BI 2536 are delayed in prophase but eventually import Cdk1-cyclin B into the nucleus, enter prometaphase, and degrade cyclin A, although BI 2536 prevents degradation of the APC/C inhibitor Emi1. BI 2536-treated cells lack prophase microtubule asters and thus polymerize mitotic microtubules only after nuclear-envelope breakdown and form monopolar spindles that do not stably attach to kinetochores. Mad2 accumulates at kinetochores, and cells arrest with an activated spindle-assembly checkpoint. BI 2536 prevents Plk1's enrichment at kinetochores and centrosomes, and when added to metaphase cells, it induces detachment of microtubules from kinetochores and leads to spindle collapse.
answer:

Does the small-molecule inhibitor BI 2536 reveal novel insights into mitotic roles of polo-like kinase 1?