A neutrophil elastase inhibitor, sivelestat, attenuates sepsis-induced acute kidney injury by inhibiting oxidative stress.

Background: Sivelestat, a selective inhibitor of neutrophil elastase (NE), can mitigate sepsis-related acute lung injury. However, the role of sivelestat in inhibiting oxidative stress and attenuating sepsis-related acute kidney injury (AKI) remains unclear. Here, we reported the effects of sivelestat against oxidative stress-induced AKI by suppressing the production of oxidative stress indicators.

Epidemiology and Risk Factors of Community-Associated Bloodstream Infections in Zhejiang Province, China, 2017-2020.

Purpose: Community-associated bloodstream infection (CA-BSI) is increasing in many community settings. However, the clinical significance and epidemiology of CA-BSI present in hospital admissions in China are not well established. In this work, we identified the risk factors in outpatients presenting with CA-BSI, and investigate the role of procalcitonin (PCT) and hypersensitive C-reactive protein (CRP) in diagnosing different types of the pathogen in patients with acute CA-BSI.

Oxidative stress-related circulating miRNA-27a is a potential biomarker for diagnosis and prognosis in patients with sepsis.

Background: Oxidative stress plays a critical role on the processes of sepsis, and several microRNAs have been identified that may regulate the occurrence of oxidative stress. However, the relation between oxidative stress-related microRNA 27a (miR-27a) and sepsis is unknown. The present study aimed to determine the value of circulating miR-27a for the diagnosis and prognosis of sepsis.

Bone marrow-derived mesenchymal stem cells attenuate myocardial ischemia-reperfusion injury via upregulation of splenic regulatory T cells.

Background: Myocardial ischemia-reperfusion injury (MIRI) is the main pathological manifestation of cardiovascular diseases such as myocardial infarction. The potential therapeutic effects of bone marrow-derived mesenchymal stem cells (BM-MSCs) and the participation of regulatory T cells (Tregs) in MIRI remains to be defined.

Methods: We used the experimental acute MIRI that was induced in mice by left ascending coronary ischemia, which were subsequently randomized to receive immunoglobulin G (IgG) or anti-CD25 antibody PC61 with or without intravenously injected BM-MSCs.