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Job satisfaction has been linked to many positive outcomes, such as greater work performance, increased organizational commitment, reduced job burnout, decreased absenteeism, and lower turnover intent/turnover. A substantial body of research has examined how work environment variables are linked to job satisfaction among U.S. correctional staff; far less research has examined prison staff in non-Western nations, especially China. Using survey data collected from two prisons in Guangzhou, China, this study investigated the level of job satisfaction among prison staff and how personal characteristics (i.e., gender, tenure, age, and educational level) and work environment variables (i.e., perceived dangerousness of the job, job variety, supervision, instrumental communication, and input into decision making) affect job satisfaction. The findings from ordinary least squares regression equations indicated that the work environment variables explained a greater proportion of the variance in the job satisfaction measure than the personal characteristics. In the full multivariate regression model, gender was the only personal characteristic to have a significant association with job satisfaction, with female staff reporting higher satisfaction. Input into decision making and job variety had significant positive associations, whereas dangerousness had a significant negative relationship with job satisfaction.

Working in prisons is a demanding career. While a growing number of studies have explored the predictors of job stress, job involvement, and job satisfaction, very few studies have examined how job stress, job involvement, and job satisfaction effect prison staff life satisfaction. Moreover, past studies on prison staff life satisfaction have all been conducted among those working in the United States. The current study examined how job stress, job involvement and job satisfaction were associated with satisfaction with life among surveyed staff at two Chinese prisons. Job involvement and job satisfaction had positive effects on life satisfaction, while job stress had a negative effect.

Background Long noncoding RNA urothelial carcinoma‐associated 1 (lncRNA‐UCA1) is generally recognized as an oncogenic molecule in several human malignant tumors. However, the available evidence does not necessarily imply an unequivocal causal function of UCA1 in glioblastoma. The current study was aimed to probe the biological function of lncRNA‐UCA1 in human glioblastoma cell lines. Besides, we further investigated the potential mechanisms. Methods Cell viability, apoptosis, as well as migration and invasion were measured using a commercial cell counting kit‐8, flow cytometry, and 24‐Transwell assay, respectively. LncRNA‐UCA1, microRNA‐193a (miR‐193a), and CDK6 at messenger RNA levels were evaluated by quantitative real‐time polymerase chain reaction method. Protein level was examined by Western blot analysis. RNA immunoprecipitation was utilized to validate lncRNA‐UCA1 associated with miR‐193a. Luciferase activity assay was used to identify the miR‐193a‐targeted CDK6 3′‐untranslated region. Results lncRNA‐UCA1 knockdown weakened cell viability, augmented apoptosis progression, as well as suppressed migration and invasion behaviors in glioblastoma cells, whereas lncRNA‐UCA1 silence exhibited the opposite functions. lncRNA‐UCA1 functioned as an endogenous sponge of miR‐193a. miR‐193a silence reversed the biological function of lncRNA‐UCA1 knockdown on U‐118 MG cells. miR‐193a negatively regulated the expression of CDK6, and it affected the U‐118 MG cells through regulating CDK6 expression. CDK6 overexpression abrogated the blockage of PI3K/AKT, mitogen‐activated protein kinase (MAPK), and Notch signaling pathways. Furthermore, lncRNA‐UCA1 and miR‐193a could affect these signaling cascades through regulating CDK6 expression. The regulatory mechanisms of lncRNA‐UCA1 were further consolidated in clinical specimens. Conclusion lncRNA‐UCA1 silence reduced cell viability, promoted apoptosis progression, while impeding the migration and invasion of glioblastoma cells by miR‐193a‐mediated silence of CDK6, with blockage of PI3K/AKT, MAPK, and Notch pathways.