Articles: cations.
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Our investigation on in-hospital mortality after 4474 pancreatoduodenectomies aimed to identify time-dependent risks as well as windows of opportunity to rescue patients from complications. ⋯ Postpancreatectomy-specific complications prompt almost half of in-hospital mortalities after pancreatoduodenectomy, with rather long intervals for interventions to prevent failure to rescue. In contrast, visceral vasculature-related events and cardiopulmonary complications dominate early in-hospital mortalities with short intervals until mortality, demanding rigorous management of such events or preoperative conditioning. These data externally validate a previous high-volume initiative and highlight distinct windows of opportunity to optimize perioperative safety.
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Proinflammatory hyperactivation of Kupffer cells (KCs) is foremost involved in the pathogenesis of sepsis-induced liver injury. Our previous study found that stimulator of interferon genes (STING) signaling was activated in KCs in response of lipopolysaccharide (LPS) and knocking down dynamin-related protein 1 (DRP1) in KCs effectively inhibited the activation of STING signaling and the subsequent production of proinflammatory cytokines. In this study, we demonstrated that in vivo treatment with mitochondrial division inhibitor 1 (Mdivi-1), a selective inhibitor of DRP1, alleviated cecal ligation and puncture (CLP)-induced liver injury with the improvement of liver pathology and function. ⋯ The further study showed that Mdivi-1 markedly attenuated STING signaling activation in KCs and inhibited systemic inflammatory response. Importantly, DMXAA application in CLP mice blunted Mdivi-1's liver protection effect. Taken together, our study confirmed Mdivi-1 effectively alleviated CLP-induced liver injury partially through inhibiting STING signaling activation in KCs, which provides new insights and a novel potential pharmacological therapeutic target for treating septic liver injury.
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Anesthesia and analgesia · Jul 2024
ReviewPositive Airway Pressure in Surgical Patients with Sleep Apnea: What is the Supporting Evidence?
Obstructive sleep apnea (OSA) is prevalent amongst surgical patients and associated with an increased incidence of perioperative complications. The gold standard treatment for moderate-to-severe OSA is positive airway pressure (PAP) therapy. Practice guidelines by the American Society of Anesthesiologists and the Society of Anesthesia and Sleep Medicine have recommended preoperative screening for OSA and consideration of initiation of PAP therapy for patients with severe OSA. ⋯ Our review provides an update on the existing literature on the efficacy of PAP therapy in surgical patients with OSA. We focus on the postoperative complications associated with OSA, potential mechanisms leading to the increased risk of postoperative adverse events, and summarize the perioperative guidelines for the management of patients with OSA, evidence supporting perioperative PAP therapy, as well as limitations to PAP therapy and alternatives. An update on the existing literature of the efficacy of PAP therapy in surgical patients with OSA is critical to assess the impact of prior guidelines, determine when and how to effectively implement PAP therapy, and target barriers to PAP adherence in the perioperative setting.
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Introduction: Intestinal flora and the translocation of its products, such as muramyl dipeptide (MDP), are common causes of sepsis. MDP is a common activator of the intracellular pattern recognition receptor NOD2, and MDP translocation can cause inflammatory damage to the small intestine and systemic inflammatory responses in rats. Therefore, this study investigated the effects of MDP on the intestinal mucosa and distant organs during sepsis and the role of the NOD2/AMPK/LC3 pathway in MDP-induced mitochondrial dysfunction in the intestinal epithelium. ⋯ Compared to the MDP+LPS groups, the MDP+SPEN+LPS groups had decreased IL-6 and MDP production, increased AMPK and LC3 protein expression, and protected mitochondrial and organ functions. Conclusions: MDP translocation reduced mitochondrial autophagy by regulating the NOD2/AMPK/LC3 pathway, causing mitochondrial dysfunction. SPEN protected against MDP-induced impairment of intestinal epithelial mitochondrial function during sepsis.