Effect of applied muscle tension on improving vasovagal reactions among blood donors: a meta-analysis / 中国输血杂志

【Objective】 To systematically evaluate the effect of applied muscle tension (AMT) exercises on reducing vasovagal reactions(VVRs) among blood donors by meta-analysis. 【Methods】 Nine related databases including MEDLINE, Web of Science and CINAHL were searched using "applied muscle tension" and "vasovagal reactions" as keywords to collect clinical studies on the effects of AMT exercise on VVRs during blood donation. Two researchers independently screened, evaluated the quality and extracted data from the retrieved literature according to the inclusion and exclusion criteria. RevMan 5.4 was used to conduct meta-analysis on the extracted data. 【Results】 A total of 7 articles were finally included, 5 in English and 2 in Chinese, covering 6 808 blood donors. The experimental group performed AMT during blood donation, while the control group did not. Compared with the control group, the difference in reducing the incidence of VVRs [ RR = 0.60, 95%CI (0.42, 0.87), P<0.01] was statistically significant in the AMT group. 【Conclusion】 AMT can effectively reduce the incidence of VVRs during blood donation. However, due to the limitation in the included studies, high-quality studies with perspectiveness, multicenter, large-sample size are further needed for validation in the future.

The zinc transporter Slc39a5 controls glucose sensing and insulin secretion in pancreatic β-cells via Sirt1- and Pgc-1α-mediated regulation of Glut2

Zinc levels are high in pancreatic β-cells, and zinc is involved in the synthesis, processing and secretion of insulin in these cells. However, precisely how cellular zinc homeostasis is regulated in pancreatic β-cells is poorly understood. By screening the expression of 14 Slc39a metal importer family member genes, we found that the zinc transporter Slc39a5 is significantly down-regulated in pancreatic β-cells in diabetic db/db mice, obese ob/ob mice and high-fat diet-fed mice. Moreover, β-cell-specific Slc39a5 knockout mice have impaired insulin secretion. In addition, Slc39a5-deficient pancreatic islets have reduced glucose tolerance accompanied by reduced expression of Pgc-1α and its downstream target gene Glut2. The down-regulation of Glut2 in Slc39a5-deficient islets was rescued using agonists of Sirt1, Pgc-1α and Ppar-γ. At the mechanistic level, we found that Slc39a5-mediated zinc influx induces Glut2 expression via Sirt1-mediated Pgc-1α activation. These findings suggest that Slc39a5 may serve as a possible therapeutic target for diabetes-related conditions.