Journal of the American College of Surgeons
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Gun violence remains a significant public health problem that is both understudied and underfunded, and plagued by inadequate or inaccessible data sources. Over the years, numerous trauma centers have attempted to use local registries to study single-institutional trends, however, this approach limits generalizability to our national epidemic. In fact, even easily accessible, health-centered data from the CDC lack national relevance because they are limited to those enrolled states only. We sought to examine how publicly available law enforcement data from all 50 states might complement our understanding of circumstances and demographics surrounding national firearm death and help forge the first step in partnering law enforcement with trauma centers. ⋯ Gun violence represents an ongoing public health concern, with the proportion of firearm homicide steadily and significantly increasing from 1980 to 2016. Homicide data from the Federal Bureau of Investigation can serve to supplement trauma registry data by helping to define gun violence patterns. However, stronger partnerships between local law enforcement agencies and trauma centers are necessary to better characterize firearm type and resultant injury patterns, direct prevention efforts and firearm policy, and reduce gun-related deaths.
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The presumptive overdiagnosis of papillary thyroid microcarcinoma (PTMC) has led to an emerging trend of less-extensive operation and an inclination toward active surveillance when possible. In this study, we aimed to examine the risk of advanced PTMC at presentation. ⋯ PTMC could exhibit advanced features in 19% of patients who underwent operation and some of those, such as LVI and microscopic ETE, are undetectable with preoperative workup. Clinicians need to be cognizant of this considerable risk in the era of less-aggressive management of PTMC.
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Mitochondrial oxidative stress plays a prominent role in the development of burn-induced cardiac dysfunction. AMP-activated kinase (AMPK), an energy sensor, has a central role in the pathogenesis of heart failure. However, its role in cardiac dysfunction after burn injury is unclear. Our hypothesis is that burn injury acts through the AMPK-sirtuin 1-PGC1α-nuclear factor erythroid 2-related factor 2 (NFE2L2)-ARE signaling pathway, leading to cardiac mitochondrial impairment, resulting in cardiac dysfunction. ⋯ Burn-induced cardiac dysfunction and cardiac mitochondrial damage occur via the AMPK-sirtuin 1-PGC1α-NFE2L2-ARE signaling pathway. AMPK and PGC1α agonists might be promising therapeutic agents to reverse cardiac dysfunction after burn injury.