Objective:To explore the effect of communication competence and psychological resilience on job burnout among Operating Room nurses.Methods:From March to June 2023, randomized clustering sampling was used to select 138 registered Operating Room nurses from four ClassⅢ Grade A hospitals in Taizhou for investigation. The survey was conducted using the general information questionnaire, Operating Room Nurses' Job Stressor Scale, Chinese version of the Connor-Davidson Resilience Scale, Nurses' Clinic Communication Competence Scale, and Maslach Burnout Inventory-General Survey. Hierarchical linear regression analysis was used to explore the effects of communication competence and psychological resilience on job burnout among Operating Room nurses.Results:A total of 138 questionnaires were sent out, and 133 valid questionnaires were collected, with a valid response rate of 96.38% (133/138). Among 133 Operating Room nurses, the job burnout score was (56.35±9.28), and the communication competence, psychological resilience, and work stress scale scores were (196.71±18.92), (78.09±18.31), and (96.37±22.47), respectively. Pearson correlation showed that job burnout among Operating Room nurses was negatively correlated with psychological resilience ( r=-0.475, P<0.01) and communication competence ( r=-0.241, P<0.01), and positively correlated with work stress ( r=0.360, P<0.01). Hierarchical linear regression analysis showed that, after controlling for other variables, psychological resilience and communication competence were the influencing factors of job burnout among Operating Room nurses ( P<0.01), which could explain 17.70% of the variation. Conclusions:The level of job burnout among Operating Room nurses is relatively high, and psychological resilience and communication competence are independent influencing factors. Managers can provide psychological counseling and support services for Operating Room nurses, offer communication competence training programs, and prevent and reduce job burnout among Operating Room nurses.

Objective To investigate the ability and underlying mechanism of hepatitis B virus X protein (HBx)regulationofPolo-likekinase 1 (Plk1)expression.Methods The human HCC cell line HepG2 was transfected (transiently and stably) with an HBx plasmid expression vector (pCMV-HA-HBx) or empty plasmid vector (control),with and without expression plasmids with the Plk1 promoter.Effects on Plk1 expression were assessed by western blotting.Functional effects on the Plk1 promoter were assessed by luciferase reporter assay.Effects on the mRNA level of Plk1 in S phase HepG2 cells were assessed by quantitative real-time reverse transcriptase polymerase chain reaction.After blocking protein synthesis by treatment with cycloheximide (CHX),the turnover rate of Plk1 was assessed by western blotting.Lastly,the effect of HBx on cell cycle was assessed by flow cytometry.Results HBx did not increase the protein expression of Plk1 in non-synchronized HepG2 cells,but did significantly up-regulate the Plkt protein level in the synchronized S phase cells (P =0.026 and P =0.003,respectively).Ectopic expression of HBx did not increase the mRNA level of Plk1 in HepG2 cells,but did inhibit the degradation of Plk1,as evidenced by an increased half-life of Plk1 protein (from 30 to 90 minutes).The HBx-expressing HepG2 cells showed more trequent entry into the S or G2/M phase than the control cells (31.65％ vs.24.56％ or 9.43％ vs.4.47％,respectively) and less in the G0/G1 phase (decrease from 70.97％ to 58.92％ for the HBx-expressing HepG2 cells).Conclusion HBx is able to up-regulate the expression of Plk1 in HepG2 cells by a mechanism involving stabilization of the Plkl protein primarily in the S phase of the cell cycl.