Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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Early warning prediction of traumatic hemorrhagic shock (THS) can greatly reduce patient mortality and morbidity. We aimed to develop and validate models with different stepped feature sets to predict THS in advance. From the PLA General Hospital Emergency Rescue Database and Medical Information Mart for Intensive Care III, we identified 604 and 1,614 patients, respectively. ⋯ The model using vital signs alone achieved good performance at the half-hour time window (AUROC = 0.935), and the performance was increased when laboratory results were added, especially when the time window was 1 h (AUROC = 0.950 and 0.968, respectively). These good-performing interpretable models demonstrated acceptable generalization ability in external validation, which could flexibly and rollingly predict THS T hours (where T = 0.5, 1) prior to clinical recognition. A prospective study is necessary to determine the clinical utility of the proposed THS prediction models.
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Microglial activation is a vital process in the neuroinflammatory response induced by I/R injury. It has been reported that myocyte enhancer factor (MEF)2D expression in activated microglia is associated with microglia-induced inflammatory responses and plays an important role in neuronal survival. This research aimed to investigate the role and mechanism of MEF2D in microglial activation and neuroinflammation in cerebral I/R in vitro and in vivo. ⋯ These results indicate that MEF2D is a necessary molecule for neuroinflammation regulation and neuronal injury in cerebral ischemia.
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Mechanical stretch-induced alveolar epithelial cell (AEC) apoptosis participates in the onset of ventilator-induced lung injury (VILI). In this study, we explored whether death-associated protein kinase 1 (DAPK1) mediated cyclic stretch (CS)-induced AEC apoptosis and VILI though P53 pathway. ⋯ DAPK1 contributes to AEC apoptosis and the onset of VILI though P53 and its intrinsic pro-apoptotic pathway. Inhibition of DAPK1 or P53 alleviates high tidal volume ventilation-induced lung injury and AEC apoptosis.
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Despite the known deleterious effects of obesity, clinical data indicate that overweight or obese patients experience higher rates of sepsis survival compared to normal and underweight patients; a phenomenon called the obesity paradox. Results from preclinical sepsis studies have not been able to replicate these findings. The objective of this study was to test the existence of the obesity paradox in a murine model of cecal slurry (CS)-induced sepsis with insulin-resistant diet-induced obese mice. ⋯ This murine study corroborates clinical data that obesity confers a survival benefit in sepsis, albeit at the expense of more significant organ injury. The mechanisms promoting survival in the obese remain unknown; however, this model appears to be well-poised to begin answering this question. Differences in glucose utilization are a novel target to investigate this paradox.