Burns : journal of the International Society for Burn Injuries
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Literature examining the impact of obesity on burn injury remains mixed. Previous examination of the National Burn Repository, now the BCQP, in obesity-related burn research is limited. The aim of this work was to provide an assessment of the BCQP dataset to examine the effect of obesity on burn-related outcomes. ⋯ The presence of obesity in this dataset was not found to be a predictor of mortality for any burn size, but was a predictor of overall LOS, ICU LOS, and total hospital costs. Including obesity-related variables in databases may improve analysis in obesity-related burn research.
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The aim of this study was to explore the effect and mechanism of formononetin (FMNT) in thermal-injured fibroblast proliferation, apoptosis, and oxidative stress. After thermal injury, human skin fibroblast (HSF) cells showed inhibited proliferation, migration, extracellular matrix (ECM) synthesis; and increased apoptosis, reactive oxygen species (ROS) production, and inflammation. Specifically, after thermal injury, cell viability, migration distance, and protein levels of collagen I, collagen III, α-SMA, MMP1, and MMP3 were reduced; cell apoptosis rate and TUNEL-positive cell numbers were increased; the levels of Bax and cleaved caspase-3 were elevated, while Bcl-2 level was reduced. ⋯ Additionally, the levels of the P13K/AKT/mTOR signaling-related proteins (p-P13K, p-AKT, and p-mTOR) were reduced in thermally injured HSF cells, whereas FMNT could promote p-P13K, p-AKT, and p-mTOR levels. FMNT can partially alleviate the thermal injury-induced inhibition of fibroblast proliferation and migration; FMNT also inhibited the apoptosis, ROS level, and inflammation in thermal-injured cells. The effects of FMNT may be mediated by regulating the P13K/AKT/mTOR pathway.