Background: The public now imposes higher demands on the government than in the past, which has created the role overload faced by low-ranking government employees in China. This research investigates the relationship between role overload and health among low-ranking government employees and explores the mediating effects of burnout.
Methods: It draws on a survey of 2064 low-ranking government employees by probability proportionate to size sampling in China's Shandong Province. Structural equation modeling (SEM) methods are used to analyze the data.
Results: Both role overload and burnout were found to have negative effects on low-ranking government employees' health; however, the associations varied among the three age groups (less than 36, between 36 and 45, and over 45). Those over 45 reported the highest level of both physical and psychological health, while the youngest age group (less than 36) reported the lowest level of health. Role overload has a direct influence on health among government employees over 45 but not among those below 45. Burnout's mediating effects between role overload and health are significant among all age groups, but most significant among the youngest civil servants below 36.
Conclusions: The findings evidenced that both role overload and burnout affect low-ranking government employees' self-reported physical and psychological health. In addition, the effect of age differences in coping with role stressors and burnout should be considered.
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http://dx.doi.org/10.1016/j.shaw.2022.02.002 | DOI Listing |
Am J Physiol Heart Circ Physiol
January 2025
Department of Medicine, Division of Cardiovascular Disease, The University of Alabama at Birmingham, Birmingham, AL-35233.
Heart failure (HF) is a leading cause of death worldwide. We have shown that pressure overload (PO)-induced inflammatory cell recruitment leads to heart failure in IL-10 knockout (KO) mice. However, it's unclear if PO-induced inflammatory cells also target the gut mucosa, causing gut dysbiosis and leakage.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
January 2025
Inner Mongolia Key Laboratory of Disease-Related Biomarkers, The Second Affiliated Hospital, Baotou Medical College, Baotou, China.
Cardiac hypertrophy is an adaptive response to pressure or volume overload such as hypertension and ischemic heart diseases. Sustained cardiac hypertrophy eventually leads to heart failure. The pathophysiological alterations of hypertrophy are complex, involving both cellular and molecular systems.
View Article and Find Full Text PDFCirc Res
January 2025
Key Laboratory of Drug Targets and Translational Medicine for Cardio-cerebrovascular Diseases, Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Jiangsu, China (X.T., X.L., X.S., Y. Zhang, Y. Zu, Q.F., L.H., S.S., F.C., L.X., Y.J.).
Background: The decrease in S-nitrosoglutathione reductase (GSNOR) leads to an elevation of S-nitrosylation, thereby exacerbating the progression of cardiomyopathy in response to hemodynamic stress. However, the mechanisms under GSNOR decrease remain unclear. Here, we identify NEDD4 (neuronal precursor cell expressed developmentally downregulated 4) as a novel molecule that plays a crucial role in the pathogenesis of pressure overload-induced cardiac hypertrophy, by modulating GSNOR levels, thereby demonstrating significant therapeutic potential.
View Article and Find Full Text PDFFront Pharmacol
January 2025
Department of Emergency Intensive Care Unit, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Introduction: In patients with acute respiratory distress syndrome, mechanical ventilation often leads to ventilation-induced lung injury (VILI), which is attributed to unphysiological lung strain (UPLS) in respiratory dynamics. Platelet endothelial cell adhesion molecule-1 (PECAM-1), a transmembrane receptor, senses mechanical signals. The Src/STAT3 pathway plays a crucial role in the mechanotransduction network, concurrently triggering pyroptosis related inflammatory responses.
View Article and Find Full Text PDFFront Cardiovasc Med
January 2025
School of Cardiovascular Medicine & Sciences, Faculty of Life Sciences & Medicine, King's College London, London, United Kingdom.
Aortic stenosis (AS) was historically considered a disease of the left side of the heart, with the main pathophysiological impact being predominantly on the left ventricle (LV). However, progressive pressure overload in AS can initiate a cascade of extra-valvular myocardial remodeling that could also precipitate maladaptive alterations in the structure and function of the right ventricle (RV). The haemodynamic and clinical importance of these changes in patients with AS have been largely underappreciated in the past.
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