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@# ObjectiveTo investigate the clinical effect of vitamin E in the treatment of nonalcoholic fatty liver disease (NAFLD) in children. MethodsPubMed, Web of Science, The Cochran Library, Embase, OVID/NEJM, CNKI, and Wanfang Data were searched for the articles on vitamin E in the treatment of NAFLD in children published up to December 2019. The data of 8 parameters were analyzed, i.e., body mass index (BMI), liver enzymes ［alanine aminotransferase (ALT) and aspartate aminotransferase (AST)］, blood lipid levels ［triglyceride (TG), total cholesterol (TC), low-density lipoprotein (LDL), and high-density lipoprotein (HDL)］, and remission rate of hepatic steatosis. RevMan 5.3 was used to perform a Meta-analysis. Continuous variables were analyzed by standardized mean difference (SMD) and 95% confidence interval (CI), and the changes after intervention were analyzed; categorical variables were analyzed by risk difference (RD) and 95%CI. A fixed effects model was used for homogeneous data, and a random effects model was used for heterogeneous data. Funnel plots were used to evaluate publication bias. ResultsA total of 599 articles were retrieved, among which 9 were included in the Meta-analysis, with 607 subjects in total. Vitamin E significantly improved the level of ALT (SMD = -0.27, 95%CI: -0.48 to -0.06, P=0.01), but it did not improve the levels of BMI (SMD=-0.09, 95%CI: -0.28 to 0.10, P=0.34), AST (SMD=-020, 95%CI: -0.42 to 0.02, P=0.07), TG (SMD=-0.19, 95%CI: -0.51 to 0.12, P=0.22), TCHO (SMD=-0.11, 95%CI: -0.31 to 0.08, P=0.24), HDL (SMD=-0.02, 95%CI: -0.27 to 0.23, P=0.88), LDL (SMD= -0.04, 95%CI: -0.27 to 019, P=072), and the remission rate of hepatic steatosis (RD=0.06, 95%CI: -0.05 to 0.17, P=0.29). ConclusionVitamin E can significantly improve the level of ALT in children with NAFLD and can be considered as an adjuvant drug for clinical treatment.
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With the abuse of antibiotics, pathogenic bacteria more resistant to infection, prevention and control of postoperative, we conducted a systematic analysis of the pathogenic bacteria and drug resistance in patients with infection after surgery. At the same time, we evaluate long-term outcomes between laparoscopy-assisted and open approaches to total gastrectomy for upper gastric cancer. Overall survival [OS] and disease-free survival [DFS] was evaluated using the Kaplan-Meier method. We matched all 246 laparoscopic cases 1:1 with open cases according to age, sex, body mass index and clinical TNM stage. The laparoscopy-assisted approach was associated with a significant decrease in surgical blood loss, number of analgesic injections, time to first flatus and length of hospital stay relative to the open approach. The postoperative morbidity did not differ between the two groups. There were no significant differences between the two groups in OS and DFS. The laparoscopy-assisted approach to total gastrectomy for upper gastric cancer results in comparable long-term survival compared with laparotomy
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Humans , Male , Female , Adult , Middle Aged , Aged , Gastrectomy , Laparoscopy , Drug Resistance , Infections , Drug Resistance, MicrobialABSTRACT
Objective To investigate the effect of astaxanthin on the peripheral blood endothelial progenitor cells (EPCs) apop-tosis induced by oxidative stress in vitro and to explore its underlying mechanism .Methods Human peripheral blood EPCs were in vitro cultured and divided into the control group ,model group with 100 μmol/L tert-butyl hydroperoxide(tBHP) and the astaxan-thin plus tBHP group(with 0 .10 ,1 .00 ,10 .00 nmol/L astaxanthin pretreatment for 24 h ,then adding the final concentration of 100μmol/L tBHP for 6 h continuous culture) .The cell viability was measured by the MTT method .The level of reactive oxygen spe-cies (ROS) was determined by the DCFH-DA method .The changes of mitochondrial membrane potential(MMP) and the apoptosis ratio were detected by the JC-1 method and the DAPI method ,respectively .Results Compared with control group ,100μmol/L tB-HP could obviously caused the apoptosis of EPCs(P<0 .05) ,while astaxanthin could decrease tBHP induced apoptosis ,which man-ifested by the decrease of the apoptosis ratio (P<0 .05) and MMP increase .Conclusion Astaxanthin has the protective effect on the apoptosis of EPCs ,its mechanism may be related with the protection of the mitochondrial function .