instruction:
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.
question:
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.\Question: Does mST1 coordinately regulate autophagy and apoptosis in diabetic cardiomyopathy in mice?
answer:
Mst1 knockout restores autophagy and protects against apoptosis in cardiomyocytes, en route to the rescue against DCM.


question:
Context: Total shoulder arthroplasty (TSA) results in superior clinical outcomes to hemiarthroplasty (HA); however, TSA is a more technical and invasive procedure. This study retrospectively compares perioperative complications after HA and TSA using the National Surgical Quality Improvement Program (NSQIP) database.', 'The NSQIP user file was queried for HA and TSA cases from the years 2005 through 2010. Major complications were defined as life-threatening or debilitating. All complications occurred within 30 days of the initial procedure. We performed multivariate analysis to compare complication rates between the two procedures, controlling for patient comorbidities.', 'The database returned 1,718 patients (HA in 30.4% [n = 523] and TSA in 69.6% [n = 1,195]). The major complication rates in the HA group (5.2%, n = 29) and TSA group (5.1%, n = 61) were similar (P = .706). Rates of blood transfusions for postoperative bleeding in patients undergoing HA (2.3%, n = 12) and TSA (2.9%, n = 35) were indistinguishable (P = .458). Venous thromboembolism was a rare complication, occurring in 0.4% of patients in each group (2 HA patients and 5 TSA patients, P > .999). On multivariate analysis, the operative procedure was not associated with major complications (P = .349); however, emergency case, pulmonary comorbidity, anemia with a hematocrit level lower than 36%, and wound class of III or IV increased the risk of a major complication (P < .05 for all).\Question: Are perioperative complications after hemiarthroplasty and total shoulder arthroplasty equivalent?
answer:
Multivariate analysis of patients undergoing TSA or HA in the NSQIP database suggests that patient factors-not the procedure being performed-are significant predictors of major complications. Controlling for patient comorbidities, we found no increased risk of perioperative major complications in patients undergoing TSA compared with HA.


question:
Context: General anesthesia induces long-lasting cognitive and learning deficits. However, the underlying mechanism remains unknown. The GluA1 subunit of AMPAR is a key molecule for learning and synaptic plasticity, which requires trafficking of GluA1-containing AMPARs into the synapse.', 'Adult male rats were exposed to 1.8% isoflurane for 2 h and subjected to an inhibitory avoidance task, which is a hippocampus-dependent contextual fear learning paradigm (n = 16 to 39). The in vitro extracellular field potential of hippocampal synapses between the Schaffer collateral and the CA1 was evaluated using a multielectrode recorder (n = 6 per group). GluA1 expression in the synaptoneurosome was assessed using Western blotting (n = 5 to 8). The ubiquitination level of GluA1 was evaluated using immunoprecipitation and Western blotting (n = 7 per group).', 'Seven days after exposure to 1.8% isoflurane for 2 h (Iso1.8), the inhibitory avoidance learning (control vs. Iso1.8; 294 ± 34 vs. 138 ± 28, the mean ± SEM [%]; P = 0.002) and long-term potentiation (125.7 ± 6.1 vs. 105.7 ± 3.3; P < 0.001) were impaired. Iso1.8 also temporarily increased GluA1 in the synaptoneurosomes (100 ± 9.7 vs. 138.9 ± 8.9; P = 0.012) and reduced the GluA1 ubiquitination, a main degradation pathway of GluA1 (100 ± 8.7 vs. 71.1 ± 6.1; P = 0.014).\Question: Does isoflurane impair learning and hippocampal long-term potentiation via the saturation of synaptic plasticity?
answer:

Isoflurane impairs hippocampal learning and modulates synaptic plasticity in the postanesthetic period. Increased GluA1 may reduce synaptic capacity for additional GluA1-containing AMPARs trafficking.