Search

Background Although the standard of care for anterior abdominal gunshot wounds (AAGSWs) is immediate laparotomy, these operations are associated with a high rate of negativity and potentially serious complications. Recent data suggest the possibility of selective non-operative management (SNOM) of AAGSWs, but none implicate body mass index (BMI) as a factor in patient selection. Anecdotal experience at our trauma center suggested a protective effect of obesity among patients with AAGSWs, and given the exceptionally high rate of obesity in the Bronx, we sought to analyze the associations of AAGSWs and BMI to inform future trauma research and management. In this study, we aimed to evaluate whether BMI is associated with injury severity, resource utilization, and clinical outcomes of AAGSWs. Methodology From our prospectively accrued trauma registry, we retrospectively abstracted all patients greater than 16 years old with Current Procedural Terminology codes associated with gunshot wounds from 2008 to 2016. The electronic medical record was reviewed to define a cohort of patients with at least one AAGSW. Patients were divided into the following cohorts based on BMI: underweight (UW, BMI

Heart disease and diabetes are among the leading causes of morbidity and mortality. Diabetes can result in diabetic cardiomyopathy, which further increases the risk of heart failure and mortality in diabetic patients. Diabetic cardiac injury has been associated with altered mitochondrial quality control mechanisms including mitophagy, a selective autophagy in which dysfunctional mitochondria are degraded through the lysosome. Lysophagy is the elimination of injured lysosomes by healthy lysosomes which is extremely important for all forms of autophagy. In the present study, we examined the functional status of mitophagy-lysosome system in the diabetic mouse heart. Cardiac mitophagy and lysophagy were determined by using novel dual fluorescent reporter mice, namely, mt-rosella that express mitochondria-targeted RFP-GFP fusion protein and tfgal3 that express RFP-GFP-galectin3, a galactoside-binding lectin. Mice were fed a high fat diet (60%calories by fat) for 1 month and then injected i.p. with streptozotocin (30 mg/kg/d for 3 days). Mice continued on HFD for additional 3 months. Echocardiographic data showed impaired cardiac function in the diabetic mice. Merged confocal images demonstrated that diabetes increased mitophagy flux in the heart as indicated by the red puncta from mt-Rosella and the mitochondrial LC3-II levels with and without lysosomal protease inhibitors pepstatin A and E64d. In addition, diabetes triggered lysosomal injury in the heart as shown by the increased total number of puncta (yellow plus red) from tfgal3 reporter on the merged confocal images. This was associated with accelerated lysophagy flux as shown by the red puncta, suggesting that the injured lysosomes were being actively degraded in the diabetic heart. The increased lysophagy may have contributed to the increased mitophagy flux since the enhanced elimination of injured lysosomes would be expected to help maintain a pool of healthy lysosomes which is essential for the efficient execution of all forms of autophagy. In summary, our results showed an enhanced mitophagy-lysosome system in the diabetic heart which may be an adaptive response that serves to limit diabetic cardiac injury.