Background: The association between theVitamin D Receptor(VDR) gene polymorphism and the risk of Multiple sclerosis (MS) has been evaluated in several researches. However, the findings were inconsistent and inconclusive. Therefore, we set out a meta-analysis of all eligible published case-control studies to obtain an exact evaluation of the association betweenVDRgene polymorphisms and MS.Method: All relevant studies reporting the association between theVDRgene FokI (rs2228570), or/and TaqI (rs731236) or/and BsmI (rs1544410) or/and ApaI (rs7975232) polymorphisms and susceptibility to MS published up to May, 2019 were identified by comprehensive systematic search in the electronic database of web of science, Scopus, and PubMed. After that, the strength of association betweenVDRgene polymorphisms and susceptibility to MS was evaluated by odds ratio (OR) and 95% confidence interval (CI).Results: A total of 30 case–control studies were included in the meta-analysis. The overall results suggested a significant association between TaqI polymorphism and MS risk under heterozygote genetic model (OR = 1.27, 95%CI = 1.01–1.59, random effect). Moreover, the pooled results of subgroup analysis declined presence of significant association under all defined genetic model. In subgroup analysis, BsmI polymorphisms was associated with increased risk of MS under recessive model in Asian populations. On the other hand, ApaI polymorphism was associated with decreased risk of MS under recessive and aa vs. AA model in Asian populations.Conclusion: This meta-analysis suggested a significant association between TaqI polymorphism and MS susceptibility. Furthermore, BsmI polymorphism was associated with increased risk of MS in Asian populations. In contrast, ApaI polymorphism was associated with decreased risk of MS in Asian populations. Future large-scale studies on gene–environment and gene–gene interactions are required to estimate risk factors and assist early diagnosis of patients at high risk for MS.

Background: Ischemia-reperfusion (I/R) of the liver is a multifactorial condition that happens during transplantation and surgery. The deleterious effects of I/R result from the acute production of reactive oxygen species (ROS), which can trigger immediate tissue damage and induce a series of destructive cellular responses, including apoptosis organ failure and inflammation. The production of ROS in the I/R process can damage the antioxidant system and cause liver damage. Resveratrol has been shown to have antioxidant properties in several investigations. Here, we address the therapeutic effect of resveratrol on I/R-induced liver injury by focusing on unfolded protein response (UPR) signaling pathway. Methods: Five minutes before reperfusion, resveratrol was injected into the tail vein of mice. They were ischemic for 1 h and then re-perfused for 3 h before being slaughtered (I/R). The activity of liver enzymes and the expression levels of genes involved in the unfolded protein response pathway were used to measure the hepatic damage. Results: Our results revealed that the low dose of resveratrol (0.02 and 0.2 mg/kg) post-ischemic treatment significantly reduced the ALT and AST levels. In addition, compared with the control group, the expression of UPR pathway genes GRP78, PERK, IRE1α, CHOP, and XBP1 was significantly reduced in the resveratrol group. In the mice that received lower doses of resveratrol (0.02 and 0.2 mg/kg), the histopathological changes induced by I/R were significantly improved; however, the highest dose (2 mg/kg) of resveratrol could not significantly protect and solve the I/R damage. Conclusion: The findings of this study suggest that hepatic ischemia occurs after liver transplantation and that receiving low-dose resveratrol treatment before reperfusion may promote graft survival through inhibition of UPR arms, especially PERK and IRE1α.

Background: Vitamin D has mainly been described in the literature beyond its skeletal functions, including an influence on the immune responses against infections. Observational and interventional studies have represented evidence that Vitamin D deficiency may cause increased risk of seasonal influenza and pulmonary tract infection. Methods: A structured search of EMBASE, Medline, and Web of Science databases was fulfilled to extract all eligible articles published prior to September 2017. Results: In this review, our goal is to define the possible mechanisms that link influenza-mediated immune responses to Vitamin D. Herein, we first briefly describe the role of Vitamin D in the immune responses and then elucidate three immunological processes that connect Vitamin D to influenza infection. Finally, we describe randomized controlled trials and observational studies exploring the effect of Vitamin D supplementation on seasonal influenza infections and vaccinations. Conclusion: Our literature review suggests that treatment of influenza-infected individuals with Vitamin D supplements or cathelicidin-derived agents may provide appreciable protection against natural influenza infection. Moreover, Vitamin D given at appropriate doses may facilitate protection against seasonal flu.