Post-traumatic stress disorder (PTSD), a complex and chronic disorder caused by exposure to a traumatic event, is a common psychological result of current military operations. It causes substantial distress and interferes with personal and social functioning. Consequently, identifying the risk factors that make military personnel and veterans more likely to experience PTSD is of academic, clinical, and social importance. Four electronic databases (PubMed, Embase, Web of Science, and PsycINFO) were used to search for observational studies (cross-sectional, retrospective, and cohort studies) about PTSD after deployment to combat areas. The literature search, study selection, and data extraction were conducted by two of the authors independently. Thirty-two articles were included in this study. Summary estimates were obtained using random-effects models. Subgroup analyses, sensitivity analyses, and publication bias tests were performed. The prevalence of combat-related PTSD ranged from 1.09% to 34.84%. A total of 18 significant predictors of PTSD among military personnel and veterans were found. Risk factors stemming from before the trauma include female gender, ethnic minority status, low education, non-officer ranks, army service, combat specialization, high numbers of deployments, longer cumulative length of deployments, more adverse life events, prior trauma exposure, and prior psychological problems. Various aspects of the trauma period also constituted risk factors. These include increased combat exposure, discharging a weapon, witnessing someone being wounded or killed, severe trauma, and deployment-related stressors. Lastly, lack of post-deployment support during the post-trauma period also increased the risk of PTSD. The current analysis provides evidence of risk factors for combat-related PTSD in military personnel and veterans. More research is needed to determine how these variables interact and how to best protect against susceptibility to PTSD.

Background The long non-coding RNA PVT1 (lncRNA PVT1) has been reported to act as an oncogenic regulator of several cancers. However, its expression and function in gallbladder cancer (GBC) remain largely unknown. Methods In situ hybridization (ISH) and quantitative real-time PCR (qPCR) were performed to detect the expression of PVT1 and miR-143 in GBC tissues and cell lines. Immunohistochemistry (IHC) assays were performed to assess the expression of the hexokinase 2 (HK2) protein. The relationships among PVT1, miR-143 and HK2 were evaluated using dual-luciferase reporter, RNA immunoprecipitation (RIP) and biotin pull-down assays. The biological functions of PVT1, miR-143 and HK2 in GBC cells were explored with cell counting kit 8 (CCK-8), 5-ethynyl-20-deoxyuridine (EdU), colony formation, transwell, wound healing and glucose metabolism assays in vitro. For in vivo experiments, a xenograft model was used to investigate the effects of PVT1 and HK2 on GBC. Results PVT1 was upregulated in GBC tissues and cells and was positively associated with malignancies and worse overall survival. PVT1 knockdown inhibited cell proliferation, migration, and invasion in vitro and restrained tumor growth in vivo. Further studies demonstrated that PVT1 positively regulated HK2 expression via its competing endogenous RNA (ceRNA) activity on miR-143. Additionally, HK2 expression and function were positively correlated with PVT1. Furthermore, we observed that the PVT1/miR-143/HK2 axis promoted cell proliferation and metastasis by regulating aerobic glucose metabolism in GBC cells. Conclusions The results of our study reveal a potential ceRNA regulatory pathway in which PVT1 modulates HK2 expression by competitively binding to endogenous miR-143 in GBC cells, which may provide new insights into novel molecular therapeutic targets for GBC. Electronic supplementary material The online version of this article (10.1186/s12943-019-0947-9) contains supplementary material, which is available to authorized users.

We previously showed that the content of advanced glycation end products (AGEs) in the diet correlates with serum AGE levels, oxidant stress (OS), organ dysfunction, and lifespan. We now show that the addition of a chemically defined AGE (methyl-glyoxal-BSA) to low-AGE mouse chow increased serum levels of AGEs and OS, demonstrating that dietary AGEs are oxidants that can induce systemic OS. OS predisposes to the development of cardiovascular and chronic kidney diseases; calorie restriction (CR) is the most studied means to decrease OS, increase longevity, and reduce OS-related organ damage in mammals. Because reduction of food intake also decreases oxidant AGE s intake , we asked whether the beneficial effects of CR in mammals are related to the restriction of oxidants or energy. Pair-fed mice were provided either a CR diet or a high-AGE CR diet in which AGEs were elevated by brief heat treatment (CR-high). Old CR-high mice developed high levels of 8-isoprostanes , AGEs , RAGE , and p66shc , coupled with low AGER1 and GSH/GSSG levels , insulin resistance , marked myocardial and renal fibrosis , and shortened lifespan. In contrast , old CR mice had low OS , p66shc , RAGE , and AGE levels , but high AGER1 levels , coupled with longer lifespan. Therefore , the beneficial effects of a CR diet may be partly related to reduced oxidant intake, a principal determinant of oxidant status in aging mice, rather than decreased energy intake.

BackgroundA number of studies have shown a range of negative psychological symptoms (e.g. depression) after exposure to natural disasters. The aim of this study was to determine risk factors for depression in both children and adults who have survived natural disasters.MethodsFour electronic databases (PubMed, Embase, Web of Science, and PsychInfo) were used to search for observational studies (case–control, cross-sectional, and cohort studies) about depression following natural disasters. The literature search, study selection, and data extraction were conducted independently by two authors. Thirty-one articles were included in the study, of which twenty included adult participants and eleven included child participants. Summary estimates were obtained using random-effects models. Subgroup analysis, sensitivity analysis, and publication bias tests were performed on the data.ResultsThe prevalence of depression after natural disasters ranged from 5.8% to 54.0% in adults and from 7.5% to 44.8% in children. We found a number of risk factors for depression after exposure to natural disasters. For adults, the significant predictors were being female ;not married;holding religious beliefs; having poor education; prior trauma; experiencing fear, injury, or bereavement during the disaster; or losing employment or property, suffering house damage as a result of the disaster. For children, the significant predictors were prior trauma; being trapped during the disaster; experiencing injury, fear, or bereavement during the disaster; witnessing injury/death during the disaster; or having poor social support.ConclusionsThe current analysis provides evidence of risk factors for depression in survivors of natural disasters. Further research is necessary to design interventions to improve the mental health of survivors of natural disasters.

Aging is accompanied by increased oxidative stress (OS) and accumulation of advanced glycation end products (AGEs). AGE formation in food is temperature-regulated , and ingestion of nutrients prepared with excess heat promotes AGE formation , OS , and cardiovascular disease in mice. We hypothesized that sustained exposure to the high levels of pro-oxidant AGEs in normal diets (Reg AGE ) contributes to aging via an increased AGE load , which causes AGER1 dysregulation and depletion of antioxidant capacity , and that an isocaloric , but AGErestricted (by 50%) diet (Low AGE ) , would decrease these abnormalities. C57BL6 male mice with a lifelong exposure to a Low AGE diet had higher than baseline levels of tissue AGER1 and glutathione/ oxidized glutathione and reduced plasma 8-isoprostanes and tissue RAGE and p66 shc levels compared with mice pair-fed the regular (Reg AGE ) diet. This was associated with a reduction in systemic AGE accumulation and amelioration of insulin resistance , albuminuria , and glomerulosclerosis. Moreover , lifespan was extended in Low AGE mice , compared with Reg AGE mice. Thus , OS-dependent metabolic and end organ dysfunction of aging may result from life-long exposure to high levels of glycoxidants that exceed AGER1 and anti-oxidant reserve capacity. A reduced AGE diet preserved these innate defenses , resulting in decreased tissue damage and a longer lifespan in mice. Environmental and genetic factors including elevated oxidant stress (OS), cumulative DNA damage, altered gene expression, telomere shortening, and energy utilization are among the postulated mechanisms of senescence and aging in organisms from yeast to mammals.