Background Village clinic doctors (VCDs) are part of the health service force in rural China. VCDs’ job satisfaction (JS) is important to the stability of the three-tiered health service system. Since 2009, the Chinese government launched a new health care system reform (NHCSR) which affected VCDs significantly. This study aimed to analysing the effect of NHCSR on JS among VCDs. Methods All the data came from three surveys in Shandong Province conducted in 2012, 2015 and 2018. In 2012, an originally designed questionnaire was used to conduct a baseline survey of 405 VCDs from 27 townships in nine counties. In 2015 and 2018, 519 and 223 VCDs in the same counties were surveyed with the same questionnaire. Descriptive analysis and ANOVA were used to analyse the level and changes in VCDs’ JS. Results The mean scores of VCDs’ total JS were 2.664 ± 1.069, 3.121 ± 0.931 and 2.676 ± 1.044 in 2012, 2015 and 2018, respectively, with a significant difference (F = 28.732, P < 0.001). The mean scores of the medical practice environment and the job itself showed a continuous downward trend. The trends of the mean scores for job reward, internal work environment and organizational management were consistent with the trend for total JS. Conclusion The NHCSR had a partly negative impact on VCDs’ JS. Policy-makers should pay more attention to VCDs’ job reward and medical practice environment. With the implementation of new reform policies, VCDs’ JS should be the subject of more systematic and detailed research.

Background Family doctors in rural China are the main force for primary health care, but the workforce has not been well stabilized in recent years. Surface acting is an emotional labor strategy with a disparity between inner feelings and emotional displays, provoking negative effects such as emotional exhaustion, occupational commitment reduction, and, consequently, increasing turnover rate. With the Conservation of Resources theory, this study explores how the surface acting of rural family doctors affects turnover intention through emotional exhaustion and investigates what role occupational commitment plays in this relationship. Methods With a valid response rate of 93.89%, 953 valid data were collected by an anonymous self-administered questionnaire survey in December 2021 in Shandong Province, China. Cronbach’s Alpha and confirmatory factor analysis (CFA) were used to estimate reliability and construct validity, respectively. The PROCESS macro in SPSS was performed to analyze the mediating and moderated mediation effects of surface acting, emotional exhaustion, occupational commitment, and turnover intention. Results Reliability and validity indicated that the measurement instruments were acceptable. Surface acting had a direct positive effect on turnover intention (β = 0.481, 95% CI [0.420, 0.543]). Emotional exhaustion partially mediated the effect of surface acting on turnover intention (indirect effect: 0.214, 95% CI [0.175, 0.256]). Occupational commitment moderated the effect of emotional exhaustion on turnover intention (β = − 0.065, 95% CI [− 0.111, − 0.019]), and moderated the indirect effect of surface acting on turnover intention via emotional exhaustion (index of moderated mediation: − 0.035). Conclusions Emotional exhaustion partially mediates the relationship between surface acting and turnover intention among family doctors in rural China, and occupational commitment moderates the direct effect of emotional exhaustion on turnover intention and further moderates the mediating effect. Policymakers should pay more attention to the effects of emotional labor and emotional resource depletion on the stability of rural health human resources.

CdS/CdTiO3–TiO2 composites prepared under different conditions contain a mixture of crystal phases of CdS, CdTiO3 and TiO2. The conditions of synthesis have an impact on the photocatalytic performance for dye degradation and hydrogen production.

BackgroundOsteoarthritis (OA) is a degenerative joint disease frequently diagnosed in the elderly and middle-aged population. However, its specific pathogenesis has not been clarified. This study aimed to identify biomarkers for OA diagnosis and elucidate their potential mechanisms for restoring OA-dysregulated autophagy and inhibiting chondrocyte apoptosis in vitro.Material and methodsTwo publicly available transcriptomic mRNA OA-related datasets (GSE10575 and GSE51588) were explored for biomarker identification by least absolute shrinkage and selection operator (LASSO) regression, weighted gene co-expression network analysis (WGCNA), and support vector machine recursive feature elimination (SVM-RFE). We applied the GSE32317 and GSE55457 cohorts to validate the markers’ efficacy for diagnosis. The connections of markers to chondrocyte autophagy and apoptosis in OA were also comprehensively explored in vitro using molecular biology approaches, including qRT-PCR and Western blot.ResultsWe identified 286 differentially expressed genes (DEGs). These DEGs were enriched in the ECM-receptor interaction and PI3K/AKT signaling pathway. After external cohort validation and protein-protein interaction (PPI) network construction, PDK1 was finally identified as a diagnostic marker for OA. The pharmacological properties of BX795-downregulated PDK1 expression inhibited LPS-induced chondrocyte inflammation and apoptosis and rescued OA-dysregulated autophagy. Additionally, the phosphorylation of the mediators associated with the MAPK and PI3K/AKT pathways was significantly downregulated, indicating the regulatory function of PDK1 in apoptosis and autophagy via MAPK and PI3K/AKT-associated signaling pathways in chondrocytes. A significantly positive association between the PDK1 expression and Neutrophils, Eosinophils, Plasma cells, and activated CD4 memory T cells, as well as an evident negative correlation between T cells follicular helper and CD4 naive T cells, were detected in the immune cell infiltration analysis.ConclusionsPDK1 can be used as a diagnostic marker for OA. Inhibition of its expression can rescue OA-dysregulated autophagy and inhibit apoptosis by reducing the phosphorylation of PI3K/AKT and MAPK signaling pathways.