Articles: sepsis.
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Chinese medical journal · Dec 2024
ReviewEffect of endothelial responses on sepsis-associated organ dysfunction.
Sepsis-related organ dysfunction is associated with increased morbidity and mortality. Previous studies have found that the endothelium plays crucial roles in maintaining the vascular permeability during sepsis, as well as in regulating inflammation and thrombosis. During sepsis, endothelial cells may release cytokines, chemokines, and pro-coagulant factors, as well as express adhesion molecules. ⋯ However, excessive or prolonged endothelial activation can lead to impaired microcirculation, tissue hypoperfusion, and organ dysfunction. Given the structural and functional heterogeneity of endothelial cells in different organs, there are potential differences in endothelial responses by organ type, and the risk of organ damage may vary accordingly. This article reviews the endothelial response observed in sepsis and its effects on organ function, summarizes current progress in the development of therapeutic interventions targeting the endothelial response, and discusses future research directions to serve as a reference for researchers in the field.
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Background: Sepsis continues to pose a significant threat to human life and represents a substantial financial burden. In addition to replicative stress resulting from telomeric loss, recent studies have identified multiple factors contributing to cell cycle arrest. Furthermore, our understanding of pathways associated with cellular senescence, such as CD47-mediated suppression of efferocytosis, has expanded. ⋯ Later, at 7 d after CLP, pulmonary expression of CD47 and QPCTL-1 was decreased, whereas SHP-1 was significantly enhanced. Conclusion: Our findings suggest an activation of senescent-associated pathways during experimental sepsis. However, expanding the experiments to other organ systems and in vivo long-term models are necessary to further evaluate the sustained mechanisms and immunopathophysiological consequences of cellular senescence triggered by septic organ injury.
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Purpose: This study aims to establish and validate machine learning-based models to predict death in hospital among critical orthopaedic trauma patients with sepsis or respiratory failure. Methods: This study collected 523 patients from the Medical Information Mart for Intensive Care database. All patients were randomly classified into a training cohort and a validation cohort. ⋯ However, the eXGBM model consistently outperformed the RF model across multiple evaluation metrics, establishing itself as the superior option for predictive modeling in this scenario, with the RF model as a strong secondary choice. The SHAP analysis revealed that SAPS II, age, respiratory rate, OASIS, and temperature were the most important five features contributing to the outcome. Conclusions: This study develops an artificial intelligence application to predict in-hospital mortality among critical orthopaedic trauma patients with sepsis or respiratory failure.
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Sepsis induces intestinal hyperpermeability, which is associated with higher mortality. Occludin is a tight junction protein that plays a critical role in regulating disease-associated intestinal barrier loss. This study examined the role of intestinal occludin on gut barrier function and survival in a pre-clinical model of sepsis. ⋯ Notably, 7-day mortality was significantly higher in occludin KOIEC mice following sepsis. Occludin thus plays a critical role in preserving gut barrier function and mediating survival during sepsis, associated with alterations in inflammation and bacteremia. Agents that preserve occludin function may represent a new therapeutic strategy in the treatment of sepsis.