ObjectivesIn China, there have been an increasing number of migrant workers from rural to urban areas, and migrant workers have the highest incidence of occupational diseases. However, few studies have examined the impact of occupational stress on job burnout in these migrant workers. This study aimed to investigate the relationship between occupational stress and job burnout among migrant workers.DesignThis study used a cross-sectional survey.SettingThis investigation was conducted in Dongguan city, Guangdong Province, China.Participants3806 migrant workers, aged 18–60 years, were randomly selected using multistage sampling procedures.Primary and secondary outcome measuresMultistage sampling procedures were used to examine demographic characteristics, behaviour customs and job-related data. Hierarchical linear regression and logistic regression models were constructed to explore the relationship between occupational stress and burnout.ResultsDemographics, behaviour customs and job-related characteristics significantly affected on burnout. After adjusting for the control variable, a high level of emotional exhaustion was associated with high role overload, high role insufficiency, high role boundary, high physical environment, high psychological strain, high physical strain, low role ambiguity, low responsibility and low vocational strain. A high level of depersonalisation was associated with high role overload, high role ambiguity, high role boundary, high interpersonal strain, high recreation, low physical environment and low social support. A low level of personal accomplishment was associated with high role boundary, high role insufficiency, low responsibility, low social support, low physical environment, low self-care and low interpersonal strain. Compared to the personal resources, the job strain and personal strain were more likely to explain the burnout of rural-to-urban migrant workers in our study.ConclusionsThe migrant workers have increased job burnouts in relation to occupational stress. Relieving occupational stress and maintaining an appropriate quantity and quality of work could be important measures for preventing job burnout among these workers.

The function of Latexin (LXN) in inflammation has attracted attention. However, no data are available regarding its role in colitis. We report that LXN is a suppressor of colitis. LXN deficiency leads to the severity of colitis in DSS-induced mice, and LXN is required for the therapeutic effect of retinoic acid on colitis. Using a proteomics approach, we demonstrate that LXN interacts and forms a functional complex with HECTD1 (an E3 ubiquitin ligase) and ribosomal protein subunit3 (Rps3). IκBα is one of the substrates of HECTD1. Ectopic expression of LXN leads to IκBα accumulation in intestinal epithelial cells, however, LXN knockdown enhances the interaction of HECTD1 and Rps3, contributing to the ubiquitination degradation of IκBα, and subsequently enhances inflammatory response. Thus, our findings provided a novel mechanism underlying LXN modulates colitis via HECTD1/Rps3/NF-κB pathway and significant implications for the development of novel strategies for the treatment of colitis by targeting LXN.

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Background: The aim was to determine the prevalence of retinal lesions in patients infected by the human immunodeficiency virus (HIV) in China. Methods: The study included 105 consecutive patients with an HIV infection that underwent general and ophthalmologic examinations. In none of the patients was any systemic opportunistic infection found. The CD4+ T lymphocyte count determined in 89 patients revealed that 77 patients (87%) had a CD4+ lymphocyte count of >200 × 10⁶/l. Results: Retinal microvascular abnormalities were found in 12 subjects (11%) and local retinal nerve fiber layer defects in 13 patients (12%). Patients with fundus abnormalities compared to those with a normal fundus had a significantly (p = 0.013) lower CD4+ T cell count (166 ± 67) × 10⁶/l vs. 482 ± 33 × 10⁶/l) and did not vary significantly in visual acuity. Conclusions: In these HIV-positive Chinese patients attending a hospital for infectious diseases, retinal microvasculopathy and retinal nerve fiber layer defects were the most common fundus lesions, which were found in about 10% of the patients and which were inversely associated with the CD4+ T cell count, without marked effect on visual acuity.

Peroxisome proliferator-activated receptor α/δ (PPAR α/δ), regulating glucolipid metabolism and immune inflammation, has been identified as an effective therapeutic target in non-alcoholic steatohepatitis (NASH). Dual PPAR α/δ agonist, such as GFT505 (also known as elafibranor), demonstrated potential therapeutic effect for NASH in clinical trials. To profile the regulatory network of PPAR α/δ agonist in NASH, the choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD) induced NASH model was used to test the pharmacodynamics and transcriptome regulation of GFT505 in this study. The results showed that GFT505 ameliorated hepatic steatosis, inflammation and fibrosis in CDAHFD mice model. RNA-sequencing yielded 3995 up-regulated and 3576 down-regulated genes with GFT505 treatment. And the most significant differentialy expressed genes involved in glucolipid metabolism (Pparα, Acox1, Cpt1b, Fabp4, Ehhadh, Fabp3), inflammation (Ccl6, Ccl9, Cxcl14) and fibrosis (Timp1, Lamc3, Timp2, Col3a1, Col1a2, Col1a1, Hapln4, Timp3, Pik3r5, Pdgfα, Pdgfβ, Tgfβ1, Tgfβ2) were confirmed by RT-qPCR. The down-regulated genes were enriched in cytokine-cytokine receptor interaction pathway and ECM-receptor interaction pathway, while the up-regulated genes were enriched in PPAR signaling pathway and fatty acid degradation pathway. This study provides clues and basis for further understanding on the mechanism of PPAR α/δ agonist on NASH.