Objective:To search for evidence of capacity management in patients undergoing extracorporeal membrane oxygenation support therapy, and summarize the evidence to provide evidence-based basis for medical staff to evaluate and manage the capacity of such patients.Methods:This study was an evidence-based nursing study. Based on the 6S evidence model, relevant evidence on patient volume management in extracorporeal membrane oxygenation support therapy was systematically searched for relevant evidence on patient volume management in extracorporeal membrane oxygenation support therapy from top to bottom, including UpToDate, the National Guidelines Library of the United States, the Scottish Interhospital Guidelines Network, the Medical Guidelines Network, the Extracorporeal Life Support Organization website, Cochrane Library, PubMed, CINAHL, Wanfang, China National Knowledge Infrastructure, and the Chinese Biomedical Literature Database. Based on the inclusion criteria, clinical guidelines, expert consensus, clinical decision-making, evidence summary, and systematic evaluation were selected for literature quality evaluation to extract the best evidence. The search period was from April 10, 2017 to April 10, 2022.Results:A total of 11 articles were included and 20 pieces of evidence were extracted, which were categorized into four categories: extracorporeal membrane oxygenation team composition and personnel qualifications, evaluation and monitoring, capacity management objectives, and capacity management measures.Conclusions:Based on a large amount of evidence of extracorporeal membrane oxygenation support for patient capacity management, this study can provide a reference basis for clinical workers to develop extracorporeal membrane oxygenation support treatment capacity management plans.

Objective:To explore the effects of the fat mass and obesity-associated gene(FTO)on apoptosis and the inflammatory response of chondrocytes in osteoarthritis(OA).Methods:Differences in FTO expression between normal human cartilage tissue samples and OA cartilage tissue samples were examined.Primary OA chondrocytes were isolated and cultured, and a rat OA model was constructed.The expression of FTO was detected in clinical, animal and cellular samples.Cells were treated with an FTO knockdown lentivirus vector(sh-FTO)and an m 6A methylation inhibitor(cycloleucine). The amount of m 6A and the expression levels of inflammatory cytokines, interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α), were detected.Flow cytometry was used to detect apoptosis in OA chondrocytes, and Western blot was used to detect the expression levels of B-cell lymphoma 2(Bcl-2)and Bcl-2-associated X protein(Bax). Results:Compared with the normal control group, FTO mRNA and protein expression in human OA cartilage tissue, rat OA cartilage tissue and OA chondrocytes was significantly increased(all P<0.05). After FTO knockdown, the level of m 6A increased, the levels of IL-6 and TNF-α decreased considerably, the apoptosis rate decreased, the expression of the proapoptotic protein Bax decreased considerably, and the expression of Bcl-2 increased considerably in primary OA chondrocytes.However, cycloleucine intervention clearly reduced the level of m6A, increased the levels of IL-6 and TNF-α, promoted cell apoptosis and the expression of apoptosis-related proteins, and reversed the effect induced by the FTO knockdown lentivirus in OA chondrocytes(all P<0.05). Conclusions:FTO may be involved in mechanisms related to the action of m 6A to promote OA chondrocyte apoptosis and the inflammatory response, thus accelerating the progression of OA.

Chlorfenapyr,an emerging synthetic pesticide,has been linked to a growing number of poisoning incidents,attributed to heightened human exposure as its application becomes more widespread.However,the toxicokinetics and toxicology of chlorfenapyr remain incompletely understood.Research since the 1990s,including animal experiments,has illuminated the absorption,distribution,excretion,and metabolism of chlorfenapyr.Toxicological investigations have revealed that the primary toxicity of chlorfenapyr is the uncoupling of oxidative phosphorylation.Chlorfenapyr exposure in humans and other animals can lead to various toxic effects,including neurotoxicity,cardiotoxicity,skeletal muscle toxicity,genotoxicity,reproductive and developmental toxicity,renal toxicity,splenic toxicity,and hematotoxicity.This article presents a comprehensive review of the toxicokinetics and toxicology of chlorfenapyr,integrating data from animal experiments,human cell line studies,clinical reports,and human autopsy.Its objective is to raise clinical awareness regarding chlorfenapyr poisoning and offer valuable references for its treatment and management.