The effects and acceptability of different exercise modes on glycemic control in type 2 diabetes mellitus: A protocol for systematic review and network meta-analysis

Introduction:Exercise has been believed to have positive effects on blood glucose control in patients with type 2 diabetes mellitus. However, few medical evidences have been found to ascertain which type of exercise has the best effect on blood glucose control in diabetes and which type of exercise is more acceptable. The purpose of this study is to compare the effects and acceptability of different exercise modes on glycemic control in type 2 diabetes patients by using systematic review and network meta-analysis.Methods and analysis:Relevant randomized controlled trial studies will be searched from PubMed, EMbase, CochraneCENTRAL, CNKI, VIP, and Chinese medical paper libraries. Primary outcome indicators: glycosylated hemoglobin and dropout rate of the research (number of dropouts/numbers of initially enrolled subjects). Secondary outcome measures: fasting blood glucose, body weight, total cholesterol (TC), low-density lipoprotein cholesterol (LDL), high-density lipoprotein cholesterol, triglycerides (TG), diastolic pressure, systolic pressure (SBP). Two reviewers are arranged to screen Title, Abstract, and then review full text to further extract data. Standard meta-analysis and network meta-analysis of the data are performed afterward. Methodological quality assessment is planned to be conducted using Cochrane risk of bias tool. The outcome will be analyzed statistically according to Bayesian analysis methods. After that, subgroup analysis is conducted on the duration of intervention, whether there is supervision of intervention, frequency of intervention per week, age, gender, and medication use.Trial registration number:PROSPERO CRD42020175181Discussion:The systematic review and network meta-analysis include evidence of the impact of different exercise modes on blood glucose control in type 2 diabetes mellitus. There are 2 innovative points in this study. One is to conduct a classified study on exercise in as much detail as possible, and the other is to study the acceptability of different exercise modes. The network meta-analysis will reduce the uncertainty of intervention and enable clinicians, sports practitioners, and patients to choose more effective and suitable exercise methods.Ethics and dissemination:The findings of the study will be disseminated through publications in peer-reviewed journals and scientific conferences and symposia. Further, no ethical approval is required in this study.     

Melatonin safeguards against fatty liver by antagonizing TRAFs‐mediated ASK1 deubiquitination and stabilization in a β‐arrestin‐1 dependent manner

Melatonin has been previously shown to prevent nonalcoholic fatty liver disease (NAFLD), yet the underlying mechanisms are poorly understood. Here, we identified a previously unknown regulatory action of melatonin on apoptosis signal‐regulating kinase 1 (ASK1) signaling pathway in the pathogenesis and development of NAFLD. Although melatonin administration did not alter food intake, it significantly alleviated fatty liver phenotypes, including the body weight gain, insulin resistance, hepatic lipid accumulation, steatohepatitis, and fibrosis in a high‐fat diet (HFD)‐induced NAFLD mouse model (in vivo). The protection of melatonin against NAFLD was not affected by inactivation of Kupffer cell in this model. In NAFLD mice liver, ASK1 signal cascade was substantially activated, evidence by the enhancement of total ASK1, phospho‐ASK1, phospho‐MKK3/6, phospho‐p38, phospho‐MKK4/7, and phospho‐JNK. Melatonin treatment significantly suppressed the ASK1 upregulation and the phosphorylation of ASK1, MKK3/6, MKK4/7, p38, and JNK. Mechanistically, we found that lipid stress triggered the interaction between ASK1 and TNF receptor‐associated factors (TRAFs), including TRAF1, TRAF2, and TRAF6, which resulted in ASK1 deubiquitination and thereby increased ASK1 protein stability. Melatonin did not alter ASK1 mRNA level; however, it activated a scaffold protein β‐arrestin‐1 and enabled it to bind to ASK1, which antagonized the TRAFs‐mediated ASK1 deubiquitination, and thus reduced ASK1 protein stability. Consistent with these findings, knockout of β‐arrestin‐1 in mice partly abolished the protection of melatonin against NAFLD. Taken together, our results for the first time demonstrate that melatonin safeguards against NAFLD by eliminating ASK1 activation via inhibiting TRAFs‐mediated ASK1 deubiquitination and stabilization in a β‐arrestin‐1 dependent manner.     

The effect of media reporting of a homicide committed by a patient with schizophrenia on the public stigma and knowledge of psychosis among the general population of Hong Kong

Social Psychiatry and Psychiatric Epidemiology - This study aimed to investigate the effects of media reporting of a homicide committed by a patient with schizophrenia on the knowledge about and...     

Genetic variants of DNA repair pathway genes on lung cancer risk

As is commonly perceived, polymorphisms in genes of deoxyribonucleic acid (DNA) repair pathway plays a fundamental role in defective DNA repair and mutagenesis prevention and serves to contribute to the individual susceptibility to the development of a variety of cancers. Recently, an increasing number of studies have been dedicated to the contentious and ambiguous links between polymorphisms in genes of DNA repair pathway and lung cancer (LC) risk. In response, a comprehensive updated meta-analysis has been proposed herein to assess the correlation between polymorphisms of DNA repair pathway genes and susceptibility to LC. This paper has identified and retrieved eligible articles from PubMed, Google Scholar, Web of Science, and CNKI databases till February 20, 2019. Finally, 295 case-control studies as to the fourteen polymorphisms of DNA repair pathway genes were enrolled. When the results have been pooled, we have brought to light the conclusion that ERCC2-rs13181 polymorphism has an elevated association with LC risk under allele, heterozygote, and dominant comparisons. In the subgroup analysis by ethnicity, we have found that the Caucasian individuals with “B” variant possess risk of LC which was more than twice as much as allele, homozygote, and recessive models. In comparison, Asian carriers of rs13181 polymorphism in ERCC2 gene are more susceptible to LC in heterozygote, dominant models. To sum up, ERCC2-rs13181 polymorphism could be a critical factor in stimulating LC evolvement. Future studies with a larger sample size and multivariate factors are needed to vindicate these findings.