Objective:To explore the application of game-based teaching combined with Jeffries simulation teaching in training orthopedic trauma nursing interns.Methods:Totally 120 intern nurses who received orthopedic trauma nursing training from 2021 to 2023 were selected. They were divided into two groups according to their start dates, with 60 nurses in each group. The control group (started before December 2022) adopted routine teaching, whereas the observation group received game-based teaching combined with Jeffries simulation teaching. The assessment results, core competence [Competency Inventory for Registered Nurse (CIRN)], and learning enthusiasm [Active Learning Scale (ALS)] were compared both between the groups and within each group before and after the training. The course experience [Course Experience Questionnaire (CEQ)] of the trainees after training was recorded.Results:After the internship, the theoretical exam scores [(89.64±6.73) vs. (83.71±6.20)], practical operation scores [(80.82±5.94) vs. (75.61±5.73)], CIRN scores [(180.69±7.61) vs. (157.33±6.83)], and ALS scores [(89.48±6.83) vs. (73.22±6.25)] of two groups of nursing students increased compared to their scores before the internship, and the observation group showed significantly higher scores than the control group ( P<0.05). After the internship, the CEQ score was higher in the observation group than in the control group [(49.65±2.58) vs. (36.57±1.94)]. Conclusions:In the training of orthopedic trauma nursing interns, game-based teaching combined with Jeffries simulation teaching can not only improve course experience and learning enthusiasm, but also enhance the assessment results, core competence, and critical thinking.

Transforming growth factor-β (TGF-β) exerts apoptotic effects on various types of malignant cells, including liver cancer cells. However, the precise mechanisms by which TGF-β induces apoptosis remain poorly known. In the present study, we have showed that threonine 32 (Thr32) residue of FoxO3 is critical for TGF-β to induce apoptosis via Bim in hepatocarcinoma Hep3B cells. Our data demonstrated that TGF-β induced FoxO3 activation through specific de-phosphorylation at Thr32. TGF-β-activated FoxO3 cooperated with Smad2/3 to mediate Bim up-regulation and apoptosis. FoxO3 (de)phosphorylation at Thr32 was regulated by casein kinase I-ε (CKI-ε). CKI inhibition by small molecule D4476 could abrogate TGF-β-induced FoxO/Smad activation, reverse Bim up-regulation, and block the sequential apoptosis. More importantly, the deregulated levels of CKI-ε and p32FoxO3 were found in human malignant liver tissues. Taken together, our findings suggest that there might be a CKI-FoxO/Smad-Bim engine in which Thr32 of FoxO3 is pivotal for TGF-β-induced apoptosis, making it a potential therapeutic target for liver cancer treatment.
Apoptosis ; genetics ; Apoptosis Regulatory Proteins ; biosynthesis ; Bcl-2-Like Protein 11 ; Carcinoma, Hepatocellular ; genetics ; pathology ; Cell Line, Tumor ; Forkhead Box Protein O3 ; Forkhead Transcription Factors ; genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Liver Neoplasms ; genetics ; pathology ; Membrane Proteins ; biosynthesis ; Proto-Oncogene Proteins ; biosynthesis ; Threonine ; genetics ; Transforming Growth Factor beta ; genetics