The role of effort-reward imbalance and depressive symptoms in the relationship between long working hours and presenteeism among Chinese village doctors: a moderated mediation model.

BACKGROUND: Long working hours and effort-reward imbalance (ERI) among medical workers may contribute to poor mental health and reduced productivity. However, the potential mechanisms among them are not well understood. This study aimed to explore the role of depressive symptoms and ERI in the relationship between long working hours and presenteeism among village doctors. METHODS: We conducted a cross-sectional study in Jiangsu Province, eastern China. 705 village doctors were assessed for working hours, ERI (the Effort-Reward Imbalance Questionnaire, ERI questionnaire), presenteeism (6-item Stanford Presenteeism Scale, SPS-6 Scale), and depressive symptoms (12-item General Health Questionnaire, GHQ-12). A moderated mediation model was used to test the role of depressive symptoms (M), and ERI (W) in the relationship between long working hours (X) and presenteeism (Y). RESULTS: 45.11% of the village doctors worked more than 55 h per week, and 55.89% were exposed to ERI. The prevalence of depressive symptoms among Chinese village doctors was 40.85%. Long working hours (≥ 55 h per week) were significantly associated with presenteeism behaviors (ß = 2.17, P < 0.001). Mediation analysis demonstrated that depressive symptoms (GHQ score > 3) could partly mediate the relationship between long working hours and presenteeism (indirect effect ß = 0.64, P < 0.001). Moderated mediation further indicated that the interaction of long working hours and ERI was significantly and positively associated with depressive symptoms, which in turn predicted elevated presenteeism behaviors. CONCLUSIONS: Depressive symptoms had a mediating role in the association of long working hours with presenteeism behaviors among Chinese village doctors and ERI augment their negative effects.

Self-efficacy mediates the associations of diabetes distress and depressive symptoms with type 2 diabetes management and glycemic control.

BACKGROUND: Adults with type 2 diabetes (T2D) often experience two common diabetes-related psychological distress: diabetes distress and depressive symptoms. Both are associated with adverse diabetes outcomes including poor self-management and glycemic control. However, diabetes distress and depressive symptoms differ in their associations with diabetes outcomes in T2D patients. OBJECTIVE: This study proposes a hypothetical model to examine whether self-efficacy mediates the adverse effects of depressive symptoms and/or diabetes distress on self-care behaviors and glycemic control. Additionally, we examined the bi-directional relationships between diabetes distress and depressive symptoms to identify potential underlying mechanisms. METHODS: This study conducted in 15 rural health clinics in Jiangsu province China. 900 adults with T2D participated in the prospective cohort study. The data Diabetes distress (the 17-item Diabetes Distress Scale, DDS17), depressive symptoms(the 10-item Center for Epidemiologic Studies Depression Scale, CESD-10), self-efficacy, self-care behaviors (diet and physical activity), metabolic variables (fasting plasma glucose, FPG) and demographic characteristics were assessed at baseline. Subsequent 12-month Hemoglobin A1C (HbA1c) were measured after baseline. Hierarchical multiple regression and bootstrap mediation analysis were used to test the effects and pathways among these associations. RESULTS: Of 843 participants (93.67%) of total cohort with available subsequent 12-month HbA1c levels, mean age was 66.08 years and 66.55% were women, 25.15% of them had depressive symptoms (CES-D ≥ 10), 12.20% had moderate diabetes distress (mean DDS ≥2) and 4.98% had the both two psychological distress. Hierarchical multiple regression showed higher DDS score significantly predicted unhealthy diet(ß = -1.10, P < 0.001) but not physical activities, while CESD score was negatively associated with physical activity (ß = -0.06, P < 0.001) but not diet. No independent effects of the two psychological distress variables on subsequent 12-month HbA1c were observed. Mediation analysis supported that elevated self-efficacy solely mediated the negative effect of both diabetes distress and depressive symptoms on diet (DDS score: ß = -0.238, 95 BCE% CI [-0.350, -0.141]; CESD score: ß = -0.010, 95 BCE% CI [-0.016, -0.005]), physical activities (DDS score: ß = -0.446, 95 BCE% CI [-0.630, -0.283]; CESD score: ß = -0.019, 95 BCE% CI [-0.030, -0.010]) and subsequent 12-month HbA1c (DDS score: ß = 0.105, 95 BCE% CI [0.030,0.189]; CESD score: ß = 0.004, 95 BCE% CI [0.001,0.009]). Additionally, the interplay of diabetes distress and depressive symptoms exerts their effects on diabetes outcomes directly and indirectly via self-efficacy. CONCLUSIONS: Self-efficacy may contribute to better diabetes outcomes and ameliorate negative effects of diabetes distress and depressive symptoms.

Resveratrol improves mitochondrial function in the remnant kidney from 5/6 nephrectomized rats.

Mitochondrial dysfunction is involved in the pathogenesis of chronic kidney disease (CKD). Resveratrol has been demonstrated to be beneficial for the recovery of kidney diseases. In this study, the 5/6 nephrectomized rat was used as a CKD model and the TGF-ß1-exposed mouse mesangial cells were used as an in vitro model. Pathological examination showed that resveratrol treatment attenuated glomerular injury in the remnant kidney of 5/6 nephrectomized rat. Additionally, resveratrol improved mitochondrial function in vivo and in vitro, as evidenced by increasing mitochondrial membrane potential, increasing ATP, decreasing reactive oxygen species production and enhancing activities of complex I and III. Furthermore, the dysregulated expressions of electron transport chain proteins and fission/fusion proteins in the kidney of 5/6 nephrectomize rats and TGF-ß1-exposed mesangial cells were restored by resveratrol. Finally, upregulated sirt1 and PGC-1α deacetylation were found after treatment with resveratrol in vivo and in vitro, which may contribute to the mitochondrial protective effects of resveratrol. The results demonstrate that resveratrol protects the mitochondria of kidney in 5/6 nephrectomized rats and TGF-ß1 induced mesangial cells. The study provides new insights into the renoprotective mechanisms of resveratrol.

Probucol inhibits JAK2-STAT pathway activation and protects human glomerular mesangial cells from tert-butyl hydroperoxide induced premature senescence.

Human mesangial cells (HMCs) have a finite lifespan and eventually enter irreversible growth arrest known as cellular senescence, which is thought to contribute to kidney ageing and age-related kidney disorders such as chronic kidney disease. The JAK2-STAT pathway plays a pivotal role in transmitting cytokine signals, including cell proliferation, apoptosis, and differentiation, but whether it could regulate HMC senescence still remains to be explored. In our study, tert-butyl hydroperoxide (tBHP)-induced cells accelerated HMC senescence, as judged by increased senescence-associated ß-galactosidase stained positive cells, morphological changes, and G0-G1 cell cycle arrest. STAT1 and STAT3 activity were increased in tBHP-induced cells. After tBHP treatment, Bcl-2 protein expression decreased and Bax protein expression increased. Blocking the JAK2-STAT pathway with AG490 and using probucol significantly inhibited the progression of HMC senescence. Bax protein expression decreased, but Bcl-2 protein expression increased after AG490 and probucol treatment. Our results indicated that the JAK2-STAT pathway might mediate tBHP-induced HMC senescence through the Bcl-2-Bax pathway, and that probucol could attenuate HMC senescence by regulating STATs.