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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Background: Thrombocytopenia (TP), a common occurrence among patients admitted to the intensive care unit (ICU), is significantly associated with prolonged ventilator use, prolonged ICU stay, and increased mortality. The duration of TP serves as an indicator of patient outcome, although the exact duration of TP associated with poor patient outcome remains unclear. In this study, the data of 3,291 patients on their first admission to the ICU between January 2010 and December 2020 were retrospectively analyzed. ⋯ Conclusions: The duration of TP in critically ill patients is positively correlated with poor patient outcome. We classified TP as either transient TP or persistent TP based on a cutoff duration of 2 days. Monitoring the duration of TP may aid in the prediction of patients' outcome in the ICU.
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Background: This study aims to assess the prognostic value of red blood cell distribution width-to-platelet ratio (RPR) in acute respiratory distress syndrome (ARDS) patients. Methods: The data collected from 540 ARDS patients from 2001 to 2012 were obtained from the Medical Information Mart for Intensive Care III Database. The 28-day all-cause mortality risk was considered as the primary outcome parameter, and the secondary outcomes were 60- and 90-day all-cause mortality. ⋯ There was no nonlinear relationship between RPR and the risk of 28-day all-cause mortality ( P for overall association <0.001, P for nonlinear = 0.635). Similar results were observed for both the pneumonia and nonpneumonia subgroups and sensitivity analyses. Conclusions: The data promote the use of RPR as a valuable prognostic indicator for ARDS patients.
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Our previous study confirmed that cardiopulmonary bypass (CPB) leads to acute lung injury (ALI) via inducing high-mobility group box 1 (HMGB1) release. Recent research showed that HMGB1 promotes pulmonary injury mainly via exosomes transport. Currently, alveolar epithelial cell (AEC) necroptosis has been demonstrated to be involved in ALI. ⋯ Twenty-four-hour treatment of CPB-derived exosomes at 150 μg/mL for 24 h could induce necroptosis by promoting mitochondrial fission and further elevating cytoplasm mtDNA levels in A549 cells, which was successfully blocked by Box A or EtBr. Most importantly, EtBr significantly inhibited cytoplasm mtDNA downstream guanosine monophosphate (GMP)-AMP synthase (cGAS)/stimulator of interferon gene (STING) signal pathway. Collectively, these data demonstrate that CPB-derived plasma exosomal HMGB1 contributes to AEC necroptosis through the mtDNA/cGAS/STING pathway.
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Trauma hemorrhagic shock (THS) is a major cause of death and disability worldwide. It is the leading cause of death with or without sepsis in approximately 50% of patients. In THS, there is an incidence of cellular apoptosis, which contributes majorly to cellular dysfunction, organ failure, and mortality. ⋯ For the first time, this study shows that a dysregulated pAkt1-GSK3β pathway causes contrasting cell fates in THS, leading to trauma pathology. Hence, the delineation and the implications of this signaling system may provide a new important target for the treatment of THS. In addition, Akt activation may become a potential strategy for increasing the survival rate following THS.
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Introduction: The optimal management strategies for patients with polytraumatic injuries that include traumatic brain injury (TBI) are not well defined. Specific interventions including tranexamic acid (TXA), propranolol, and hypertonic saline (HTS) have each demonstrated benefits in patient mortality after TBI, but have not been applied to TBI patients with concomitant hemorrhage. The goals of our study were to determine the inflammatory effects of resuscitation strategy using HTS or shed whole blood (WB) and evaluate the cerebral and systemic inflammatory effects of adjunct treatment with TXA and propranolol after combined TBI + hemorrhagic shock. ⋯ Conclusions: Whole blood resuscitation can reduce the acute postinjury neuroinflammatory response after combined TBI/shock compared with HTS. The addition of either propranolol or TXA may modulate the postinjury systemic and cerebral inflammatory response with more improvements noted after propranolol administration. Multimodal treatment with resuscitation and pharmacologic therapy after TBI and hemorrhagic shock may mitigate the inflammatory response to these injuries to improve recovery.