Efficacy of intraoperative subanesthetic dose of ketamine/esketamine in preventing postoperative cognitive dysfunction: a systematic review and meta-analysis.

Background: Postoperative cognitive dysfunction (POCD) is a common complication after anesthesia surgery, especially in older people, that can persist weeks or months after surgery as a short-term impairment of cognitive abilities, or even for a prolonged duration over years, potentially progressing into permanent cognitive dysfunction. However, the pathogenesis of POCD is not fully understood, and therefore an optimal solution for preventing POCD has yet to be established. Some studies have shown that intraoperative ketamine/esketamine reduces the incidence of POCD, but this remains controversial. Objectives: We evaluated the effect of intraoperative subanesthetic doses of ketamine/esketamine versus no intervention in adults undergoing general anesthesia surgery on the incidence of POCD. Data Sources: We followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines and searched the PubMed, Embase, Ovid, Cochrane, Scopus, and Web of Science databases for the MeSH terms 'ketamine', 'esketamine', and 'Postoperative Cognitive Complications' from database inception to 25 June 2023. Results: We found no statistically significant difference in the incidence of POCD within 7 days for intraoperative subanesthetic dose of ketamine/esketamine compared with the control group [relative risk (RR) = 0.57, 95% confidence interval (CI): 0.32, 1.01], and the results from the subgroup analysis based on age (>60 years) also revealed that the difference was not statistically significant (RR = 0.49, 95% CI: 0.23, 1.04). Conclusion: Compared with controls, intraoperative subanesthetic dose of ketamine/esketamine has no advantage in preventing POCD in patients, or in elderly patients. This study provides reference data for POCD research and clinical drug intervention strategies. Registration: Prospective Register of Systematic Reviews (PROSPERO; registration number CRD42023401159).

Constructing an emergency preparedness evaluation index system for public use during major emerging infectious disease outbreaks: a Delphi study.

BACKGROUND: The major emerging infectious diseases (MEIDs) have occurred frequently and become increasingly serious in the world. Sufficient personal emergency preparedness is critical for the general people in efficiently responding to and recovering from MEIDs. Nevertheless, few specific indicators are available for assessing the individual emergency preparedness of the general public during these periods. Therefore, the aim of this study was to construct an index system for comprehensively evaluating the personal emergency preparedness of the public regarding MEIDs. METHODS: Based on the global national-level emergency preparedness index framework and a literature review, a preliminary index system was constructed. From June 2022 to September 2022, a panel of 20 experts from nine provinces and municipalities across multiple research areas participated in this Delphi study. They rated the importance of pre-defined indicators using a five-point Likert scale and provided their qualitative comments. According to the feedback of each round of experts, the indicators of the evaluation index system were revised. RESULTS: After two rounds of expert consultation the evaluation index system reached a consensus, containing five first-level indicators, cooperating with prevention and control work, improving emergency response capacity, securing supplies and equipment, preparing economic resources, maintaining physical and mental health with affiliated 20 s-level indicators and 53 third-level indicators. The expert authority coefficient of consultation was 0.88 and 0.90. The Kendall's coefficient of concordance of expert consultations was 0.294 and 0.322, respectively. The differences were statistically significant (P < 0.05). CONCLUSION: A valid, reliable and scientific evaluation index system was established. This personal emergency preparedness index system, as a precursor form, will further lay the foundation for the formation of an assessment instrument. At the same time, it could provide a reference for future education and training of emergency preparedness for the general public.

Geniposide suppresses liver injury in a mouse model of DDC-induced sclerosing cholangitis.

Sclerosing cholangitis, characterized by biliary inflammation, fibrosis, and stricturing, remains one of the most challenging conditions of clinical hepatology. Geniposide (GE) has anti-inflammatory, hepatoprotective, and cholagogic effects. Whether GE provides inhibition on the development of sclerosing cholangitis is unknown. Here, we investigated the role of GE in a mouse model in which mice were fed with 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) for 4 weeks to induce sclerosing cholangitis. The results demonstrated that the increased hepatic gene expressions of pro-inflammatory (IL-6, VCAM-1, MCP-1, and F4/80) and profibrogenic markers (Col1α1, Col1α2, TGF-ß, and α-SMA) in DDC feeding mice were reversed after treatment with GE. GE also suppressed expressions of CK19 and Ki67 in DDC-fed mice, suggesting that GE could ameliorate DDC-induced hepatocytes and cholangiocytes proliferation. In addition, GE significantly increased bile acids (BAs) secretion in bile, which correlated with induced expressions of hepatic FXR, BAs secretion transporters (BSEP, MRP2, MDR1, and MDR2), and reduced CYP7A1 mRNA expression. Furthermore, higher expressions of ileal FXR-FGF15 signaling and reduced ASBT were also observed after GE treatment. Taken together, these data showed that GE could modulate inflammation, fibrosis, and BAs homeostasis in DDC-fed mice, which lead to efficiently delay the progression of sclerosing cholangitis.

Synergistic degradation of sulfamethoxazole in an oxalate-enhanced Fered-Fenton system: The critical heterogeneous solid-liquid interfacial mechanism and an insight in practical application.

It was demonstrated in this study that appropriate concentrations of oxalate (Ox) would lead to greatly accelerated electro-generation of Fe2+ but obviously lower power consumption in the Fered-Fenton system. Depending on the Ti electrode with pristine TiO2 layer, effects of important parameters on the SMX degradation were investigated in the Fered-Fenton-Ox system. It was found that the heterogeneous interfacial electrochemically reduction of FeIII was critical in the Fered-Fenton-Ox system relying on the surface hydroxyl bonding FeIII-Ox and formation of FeOTi bonds. A heterogeneous-homogeneous reaction mechanism was therefore proposed. It included the heterogeneous interfacial electrochemical generation of FeII-Ox and the heterogeneous-homogenous Fenton oxidation of pollutants. The promotional role of Ox would be also homogenous and heterogeneous, i.e. maintaining ferric at higher pH and forming specific FeIII-Ox complex as well as accelerating the solid-liquid interfacial heterogeneous iron cycle. Furthermore, a continuous-flow pilot study was conducted in treating a printing and dyeing industrial wastewater. As compared to conventional Fenton and Fered-Fenton systems, the Fered-Fenton-Ox system could achieve more efficient COD removal with a relative low cost/△COD, suggesting great advantages in its practical applications for treating real industrial complex wastewaters.

Mechanistic insights into geniposide regulation of bile salt export pump (BSEP) expression.

Geniposide (GE) is a major component isolated from Gardenia jasminoides Ellis, which has been used to treat cholestasis liver diseases. Our previous study has shown that GE could notably increase mRNA and protein expressions of BSEP in cholestatic rats. BSEP plays a critical role in maintenance of the enterohepatic circulation of bile acids. BSEP could be regulated by the transactivation pathway of farnesoid X receptor (FXR) and nuclear factor erythroid 2-related factor (Nrf2). Here the mechanisms for BSEP regulation by GE were investigated. GE induced the mRNA levels of BSEP in HepG2 cells and cholestatic mice, and knockdown of FXR and Nrf2 reduced the mRNA expression of BSEP at varying degrees after treatment of GE. FXR acts as the major regulator of BSEP transcription. The involvement of FXR regulated BSEP expression by GE was further investigated. An enhancement was observed in FXR-dependent BSEP promoter activation using luciferase assay. ChIP assay further confirmed the interaction between FXR and BSEP after GE treatment. Using siRNA and ChIP assays, we demonstrated that peroxisome-proliferator-activated receptor γ co-activator-1α (PGC-1α) and co-activator-associated arginine methyltransferase 1 (CARM1) were predominantly recruited to the BSEP promoter upon FXR activation by GE. In conclusion, GE regulated the expression of BSEP through FXR and Nrf2 signaling pathway. The FXR transactivation pathway was enhanced by increasing recruitment of coactivators PGC-1α and CARM1 upon GE treatment, coupled with an increased binding of FXR to the BSEP promoter.