High‐Productivity Nursing: Occupational Calling as a Moderator in the Post‐Pandemic Hospital Environment

ABSTRACT

Aims

This study investigates the impact of the hospital environment on nurse job productivity in the post-pandemic era, with a focus on the moderating role of occupational calling, based on the person-environment-occupation-productivity (PEOP) theory.

Design

A mixed-methods approach was employed, combining two-stage quantitative surveys and qualitative interviews.

Methods

In April 2022, 230 nurses from 11 Chinese public hospitals participated in a two-stage quantitative survey. Additionally, qualitative interviews were conducted with 10 nurses and 2 physicians. Quantitative data were analysed using partial least squares structural equation modelling (PLS-SEM), while qualitative data were analysed through Colaizzi's method to identify themes. To ensure the validity and reliability of the mixed-methods design, the study adhered to the Mixed Methods Appraisal Tool (MMAT) guidelines. Both sets of data were used to evaluate the relationships between hospital environments, job productivity, and occupational calling.

Results

The study found significant correlations between the hospital's indoor, spatial and sanitary environments and nurses' job productivity. Additionally, the research revealed that occupational calling moderates the relationship between indoor and spatial environments and job productivity to varying extents. However, occupational calling does not significantly moderate the impact of the sanitary environment on job productivity.

Conclusion

This study provides insights into the transformative effects on hospital environments in the post-pandemic era, emphasising the importance of combining personal intrinsic and environmental extrinsic factors to boost nursing productivity. It proposes strategies for optimising hospital indoor, spatial, sanitary environments and enhancing nurses' occupational calling, providing practical, theoretical and educational insights to healthcare policymakers and practitioners.

Patient or Public Contribution

There was no patient or public contribution in this study, as the focus was on nurses.

Multi-omics analysis reveals diagnostic and therapeutic biomarkers for aging phenotypes in ulcerative colitis

by Lei Guo, Jun Ge, Li Cheng, Xinyi Zhang, Zhengzheng Wu, Meili Liu, Hanmei Jiang, Wei Gong, Yi Liu

The incidence of ulcerative colitis (UC) remains high, with an increasing prevalence among elderly patients. Cellular senescence has been widely recognized as a contributor to UC susceptibility; however, the underlying molecular mechanisms remain incompletely understood. This study aimed to identify senescence-associated biomarkers in UC to provide new insight for diagnosis and treatment.

By integrating transcriptomic data from UC patients with established aging-related databases, we identified aging-associated differentially expressed genes (DEGs). Using weighted gene co-expression network analysis (WGCNA) and Cytoscape, we pinpointed the core genes involved. A diagnostic model for UC was then developed based on these core genes, and their expression patterns were characterized at single-cell resolution. The roles of these genes were ultimately validated through in vitro and animal experiments.

We identified 24 aging-related DEGs in UC, which were primarily implicated in inflammatory responses and cytokine-receptor interactions. Further analyses pinpointed three core genes (CXCL1, MMP9, and STAT1) that were predominantly expressed in macrophages. A diagnostic model constructed using these genes exhibited robust predictive performance. Experimental validation confirmed that the expression levels of all three core genes were significantly upregulated in both a UC mouse model and in macrophages compared to controls. Additionally, pathway analyses revealed elevated levels of CXCL12 and VEGFA in the enriched pathways.

Our findings underscore the pivotal roles of CXCL1, MMP9, and STAT1 in UC-associated cellular senescence. The analysis positions these molecules as promising macrophage-mediated diagnostic biomarkers and therapeutic targets. Collectively, this work provides novel insights into UC pathogenesis and lays a foundation for developing precision medicine strategies that target senescence pathways.