[Effect of workplace bullying on posttraumatic stress disorder in nursing staff].

Objective: To investigate the relationship between workplace bullying and posttraumatic stress disorder (PTSD) in nursing staff, and to analyze the role of psychological capital between workplace bullying and PTSD. Methods: From December 2014 to June 2015, convenience sampling was used to collect 496 nurses from 5 grade A tertiary hospitals in a province of China. Their workplace bullying, psychological capital, and PTSD status were assessed using the Negative Acts Questionnaire, Psychological Capital Questionnaire, and Posttraumatic Stress Disorder Self-Rating Scale, respectively. The correlation between variables was analyzed using a structural equation model. Results: Among these nurses, the scores of negative acts, psychological capital, and PTSD were 37.15±12.83, 78.81±16.54, and 34.56±12.52, respectively. The score on each dimension of negative acts was positively correlated with that on each dimension of PTSD (P<0.01) ; the score on each dimension of psychological capital was negatively correlated with that on each dimension of PTSD and negative acts (P<0.01). Negative acts had a positive predictive effect on PTSD (ß=0.539, P<0.01) , which was reduced after inclusion of psychological capital (ß=0.513, P<0.01). The path coefficient was 0.62 for the effect of negative acts on PTSD, -0.18 for the effect of negative acts on psychological capital, and -0.11 for the effect of psychological capital on PTSD (P<0.05) . Conclusion: Workplace bullying is a predictive factor for PTSD, and psychological capital plays a mediating role between workplace bullying and PTSD. The manager should reduce workplace bullying to improve the psychological capital in nursing staff and to prevent and reduce PTSD.

Patterns in default-mode network connectivity for determining outcomes in cognitive function in acute stroke patients.

OBJECT: To investigate whether resting-state functional connectivity (FC) differed in the default mode network (DMN) in stroke patients with and without post-stroke cognitive impairment (PSCI vs. Non-PSCI) and to explore the relationship between DMN connectivity and the cognitive performance in stroke patients. METHODS: We totally enrolled twenty healthy controls and 18 stroke patients. The stroke patients were divided into two subgroups on the basis of the cognitive assays. Montreal Cognitive Assessment (MoCA) and Mini-Mental State Examination (MMSE) scores were recorded 10 days and 3 months after the stroke. Independent component analysis was used to isolate the DMN. One-way analysis of variance was performed to detect different FC among groups. Pearson correlation analyses were conducted to determine the relationships between FC strength and the MoCA and MMSE scores. RESULTS: Compared to healthy controls, both Non-PSCI patients and PSCI patients showed significantly decreased FC in the posterior cingulate cortex/precuneus (PCC/PCu), as well as increased FC in the medial prefrontal cortex (MPFC) and left hippocampus. However, Non-PSCI patients showed more significantly increased FC in the MPFC and hippocampus than PSCI patients did. The FC in the PCC/PCu was related to the MoCA score measured at a 10-day follow-up, and the FC in the left hippocampus predicted the MoCA score measured at 3 months follow-up. CONCLUSIONS: Our findings may be helpful for facilitating further understanding of the potential mechanism underlying PSCI, and suggests that resting-state DMN connectivity could serve as neuroimaging biomarkers for future interventional studies.