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.

Q: Context: Diabetic cardiomyopathy (DCM) is associated with suppressed autophagy and augmented apoptosis in the heart although the interplay between the two remains elusive. The ability of mammalian sterile 20-like kinase 1 to regulate both autophagy and apoptosis prompted us to investigate it as a possible candidate in the progression of DCM.', 'Wild-type, Mst1 (also known as Stk4) transgenic and Mst1-knockout mice were challenged with streptozotocin to induce experimental diabetes. In addition, cultured neonatal mouse cardiomyocytes were subjected to simulated diabetes to probe mechanisms.', 'Mst1 knockout alleviated while Mst1 overexpression aggravated cardiac dysfunction in diabetes. Diabetic Mst1 transgenic mice exhibited decreased LC3 expression and enhanced protein aggregation. In contrast, typical autophagosomes were observed in diabetic Mst1-knockout mice with increased LC3 expression and reduced protein aggregation. Mst1 downregulation promoted autophagic flux as demonstrated by increased LC3-II and decreased p62 expression in the presence of bafilomycin A1. Furthermore, Mst1 overexpression increased, while Mst1 knockout decreased, cardiomyocyte apoptosis both in vivo and in vitro. Co-immunoprecipitation assays showed that Mst1 overexpression promoted Beclin1 binding to B cell lymphoma 2 (Bcl-2) and induced dissociation of Bcl-2 from Bax in diabetic mice. Conversely, Mst1 knockout disrupted the Beclin1-Bcl-2 complex and enhanced the interaction between Bcl-2 and Bax.
Answer: Mst1 knockout restores autophagy and protects against apoptosis in cardiomyocytes, en route to the rescue against DCM.

A: Does mST1 coordinately regulate autophagy and apoptosis in diabetic cardiomyopathy in mice?
****
Q: Context: The specific aim of the study was to investigate and compare epiphyseal length and extension in the proximal humerus, closure in the growth plate and bone marrow signal intensity related to the proximal humeral physis in the dominant arm and the non-dominant arm of the asymptomatic adolescent elite tennis player.', 'The study sample included 35 asymptomatic elite young tennis players (15 males and 20 females, mean age 17.4\xa0years\xa0±\xa02.7). Each player contributed with two shoulders to the MRI measurement. The non-dominant arm was used as a control.', 'Relative reliability between the radiologists was excellent (ICC 0.78-0.96). Statistically significant differences between dominant arm and non-dominant arm in epiphyseal length (mm) laterally (DA 27.3 vs NDA 26.7) were shown. Statistically significant differences were also found in epiphyseal extension (mm) laterally (DA 36.1 vs NDA 35.1) and ventrally (DA 36.2 vs NDA 34.8). No statistically significant differences were found between dominant arm and non-dominant arm in epiphyseal extension (mm) medially (DA 31.7 vs NDA 31.7) and dorsally (DA 22.6 vs NDA 22.1).
Answer: Significant findings assessing MRI measurements of the epiphyseal plate in the asymptomatic adolescent elite tennis player might reflect a development of consecutive alterations in the epiphyseal plate in the dominant arm.

A: Do asymptomatic elite young tennis players show lateral and ventral growth plate alterations of proximal humerus on MRI?
****
Q: Context: The purpose of our study was to evaluate the relationship between graft placement and in situ graft force after anterior cruciate ligament (ACL) reconstruction.', 'Magnetic resonance imaging (MRI) was obtained for twelve human cadaveric knees. The knees, in intact and deficient-ACL states, were subjected to external loading conditions as follows: an anterior tibial load of 89 N at 0°, 15°, 30°, 45°, 60°, and 90° of flexion and a combined rotatory (simulated pivot-shift) load of 5 Nm of internal tibial torque and 7 Nm of valgus torque at 0°, 15°, and 30° of flexion. Three ACL reconstructions were performed in a randomized order: from the center of the tibial insertion site to the center of the femoral insertion site (Mid), the center of the tibial insertion site to a more vertical femoral position (S1), and the center of the tibial insertion site to an even more vertical femoral position (S2). The reconstructions were tested following the same protocol used for the intact state, and graft in situ force was calculated for the two loadings at each flexion angle. MRI was used to measure the graft inclination angle after each ACL reconstruction.', 'The mean inclination angle (and standard deviation) was 51.7° ± 5.0° for the native ACL, 51.6° ± 4.1° for the Mid reconstruction (p = 0.85), 58.7° ± 5.4° for S1 (p < 0.001), and 64.7° ± 6.5° for S2 (p < 0.001). At 0°, 15°, and 30° of knee flexion, the Mid reconstruction showed in situ graft force that was closer to that of the native ACL during both anterior tibial loading and simulated pivot-shift loading than was the case for S1 and S2 reconstructions. At greater flexion angles, S1 and S2 had in situ graft force that was closer to that of the native ACL than was the case for the Mid reconstruction.
Answer: Anatomic ACL reconstruction exposes grafts to higher loads at lower angles of knee flexion.

A:
Does aCL Graft Position affect in Situ Graft Force Following ACL Reconstruction?
****