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Job strain is a major concern in view of its effects among civil servants associated with job burnout, mental fatigue and chronic diseases. The objective of this study was to assess the job strain level among civil servants and examine the effect of job strain on job burnout, mental fatigue and the resulting chronic diseases. A cross-sectional study with a representative sample consisting of 5000 civil servants was conducted from March to August 2014. Using a structured questionnaire, the job strain level, job burnout and mental fatigue were measured by using the Personal Strain Questionnaire (PSQ), Maslach Burnout Inventory (MBI) and Multidimensional Fatigue Inventory (MFI-20), respectively. Overall, 33.8% of the civil servants were found to be afflicted with high and moderate job strain. The characteristics of most of the civil servants with a higher-job strain level were as follows: female, Uygur, lower educational level and job title rank, shorter working experience, married marital status, and lower income level. Civil servants suffering from chronic disease mainly had hypertension and coronary heart disease, which accounted for 18.5% of the diseases. Civil servants with a high-job strain level exhibited higher rates of burnout, mental fatigue scores and incidence of chronic diseases. There was a multiple linear regression model composed of three predictor variables in job burnout, which accounted for 45.0% of its occurrence: female gender, lower-income level, higher-job strain in civil servants, the greater the rate of job burnout was. Four factors—male gender, lower-job title rank, higher-job strain, shorter-job tenure of civil servants—explained 25.0% of the mental fatigue model. Binary logistic regression showed that intermediate-rank employees (OR = 0.442, 95% CI: 0.028–0.634; p < 0.05), job tenure of 10–20 years (OR = 0.632, 95% CI: 0.359–0.989; p < 0.05), and low-job strain (OR = 0.657, 95% CI: 0.052–0.698; p < 0.05) were all associated with significantly lower odds of chronic disease. The risk of chronic disease was higher in civil servants with high-job burnout scores and mental fatigue scores compared with civil servants with lower scores (OR = 1.139, 95% CI: 1.012–3.198; OR = 1.697, 95% CI: 1.097–2.962). These data provide evidence for the effects of job strain on job burnout, mental fatigue and chronic diseases among civil servants.

BackgroundTET1 is a tumor suppressor gene (TSG) that codes for ten-eleven translocation methyl cytosine dioxygenase1 (TET1) catalyzing the conversion of 5-methylcytosine to 5-hydroxy methyl cytosine as a first step of TSG demethylation. Its hypermethylation has been associated with cancer pathogenesis. However, whether TET1 plays any role in nasopharyngeal carcinoma (NPC) remains unclear. This study investigated the expression and methylation of TET1 in NPC and confirmed its role and mechanism as a TSG.ResultsTET1 expression was downregulated in NPC tissues compared with nasal septum deviation tissues. Demethylation of TET1 in HONE1 and HNE1 cells restored its expression with downregulated methylation, implying that TET1 was silenced by promoter hypermethylation. Ectopic expression of TET1 suppressed the growth of NPC cells, induced apoptosis, arrested cell division in G0/G1 phase, and inhibited cell migration and invasion, confirming TET1 TSG activity. TET1 decreased the expression of nuclear β-catenin and downstream target genes. Furthermore, TET1 could cause Wnt antagonists (DACT2, SFRP2) promoter demethylation and restore its expression in NPC cells.ConclusionsCollectively, we conclude that TET1 exerts its anti-tumor functions in NPC cells by suppressing Wnt/β-catenin signaling via demethylation of Wnt antagonists (DACT2 and SFRP2).Electronic supplementary materialThe online version of this article (10.1186/s13148-018-0535-7) contains supplementary material, which is available to authorized users.

BackgroundPrevious studies have shown that preoperative anemia is correlated with the prognoses of various solid tumors. This study was performed to determine the effect of preoperative anemia on relapse and survival in patients with breast cancer.MethodsA total of 2960 patients with breast cancer who underwent surgery between 2002 and 2008 at the Sun Yat-sen University Cancer Center (Guangzhou, PR China) were evaluated in a retrospective analysis. A total of 2123 qualified patients were divided into an anemic group [hemoglobin (Hb) < 12.0 g/dL, N = 535)] and a nonanemic group (Hb ≥ 12.0 g/dL, N = 1588). The effects of anemia on local relapse-free survival (LRFS), lymph node metastasis-free survival (LNMFS), distant metastasis-free survival (DMFS), relapse-free survival (RFS), and overall survival (OS) were assessed using Kaplan–Meier analysis. Independent prognostic factors were identified in the final multivariate Cox proportional hazards regression model.ResultsAmong the 2123 women who qualified for the analysis, 535 (25.2%) had a Hb level < 12.0 g/dL. The Kaplan–Meier curves showed that anemic patients had worse LRFS, LNMFS, DMFS, RFS, and OS than nonanemic patients, even in the same clinical stage of breast cancer. Cox proportional hazards regression model indicated that preoperative anemia was an independent prognostic factor of LRFS, LNMFS, DMFS, RFS, and OS for patients with breast cancer.ConclusionsPreoperative anemia was independently associated with poor prognosis of patients with breast cancer.

This study was designed to investigate the protective effect of resveratrol (RES) on premature ovarian failure (POF) and the proliferation of female germline stem cells (FGSCs) at the tissue and cell levels. POF mice were lavaged with RES, and POF ovaries were co-cultured with RES and/or GANT61 in vitro. FGSCs were pretreated with Busulfan and RES and/or GANT61 and co-cultured with M1 macrophages, which were pretreated with RES. The weights of mice and their ovaries, as well as their follicle number, were measured. Ovarian function, antioxidative stress, inflammation, and FGSCs survival were evaluated. RES significantly increased the weights of POF mice and their ovaries as well as the number of follicles, while it decreased the atresia rate of follicles. Higher levels of Mvh, Oct4, SOD2, GPx, and CAT were detected after treatment with RES in vivo and in vitro. RES treatment resulted in significantly lower TNF-α and IL-6 concentrations and an obviously higher IL-10 concentration in the ovaries. In FGSCs, higher Mvh, Oct4, and SOD2 concentrations and lower TNF-α, IL-6, and MDA concentrations were measured in the RES group. Blockage of the Hh signaling pathway reversed the protective effect of RES on FGSCs. In conclusion, RES effectively improved the ovarian function of the POF model and the productive capacity of FGSCs via relieving oxidative stress and inflammation and a mechanism involving the Hh signaling pathway, suggesting that RES is a potential agent against POF and can aid in the survival of FGSCs.