Background: Surgical Nursing is a core subject for nursing undergraduates that requires active and effective learning strategies to cultivate students’ autonomous learning competencies and critical thinking. The effects of BOPPPS (Bridge-in, Objectives, Pretest, Participatory Learning, Post-test and Summary) model combined with team-based learning (TBL) have rarely been explored in Surgical Nursing courses. Objective: To explore the effects of BOPPPS combined with TBL in Surgical Nursing for nursing undergraduates. Methods: A mixed research method of quasi-experimental study design and descriptive qualitative research was used. The control group included 27 nursing undergraduates who had finished the Surgical Nursing course using traditional learning. The experimental group included 36 nursing undergraduates were enrolled in to receive the Surgical Nursing course in the teaching mode of BOPPPS combined with TBL. The quantitative data of students’ Surgical Nursing final scores, autonomous learning competencies and critical thinking ability of the two groups were collected and compared by t-test. Qualitative results were obtained through semi-structured interviews and data were analyzed by thematic analysis method. Results: Compared with the traditional learning mode, BOPPPS combined with TBL significantly improved nursing students’ final examination scores, autonomous learning competencies and critical thinking ability (p < 0.05). Qualitative results from 14 undergraduate nursing students’ interviews were summarized into five themes: (1) stimulating learning interest; (2) improving autonomous learning ability; (3) improving the sense of teamwork; (4) exercising critical thinking; and (5) suggestions for improvement. Conclusions: The combination of BOPPPS and TBL positively impacted nursing students by improving their autonomous learning competencies and critical thinking ability. The study suggests BOPPPS combined with TBL learning as an effective, alternative learning mode.

Dietary restriction (DR), which is defined as a reduction of particular or total nutrient intake without causing malnutrition, has been proved to be a robust way to extend both lifespan and health-span in various species from yeast to mammal. However, the molecular mechanisms by which DR confers benefits on longevity were not yet fully elucidated. The forkhead box O transcription factors (FOXOs), identified as downstream regulators of the insulin/IGF-1 signaling pathway, control the expression of many genes regulating crucial biological processes such as metabolic homeostasis, redox balance, stress response and cell viability and proliferation. The activity of FOXOs is also mediated by AMP-activated protein kinase (AMPK), sirtuins and the mammalian target of rapamycin (mTOR). Therefore, the FOXO-related pathways form a complex network critical for coordinating a response to environmental fluctuations in order to maintain cellular homeostasis and to support physiological aging. In this review, we will focus on the role of FOXOs in different DR interventions. As different DR regimens or calorie (energy) restriction mimetics (CRMs) can elicit both distinct and overlapped DR-related signaling pathways, the benefits of DR may be maximized by combining diverse forms of interventions. In addition, a better understanding of the precise role of FOXOs in different mechanistic aspects of DR response would provide clear cellular and molecular insights on DR-induced increase of lifespan and health-span.

The damage of vascular endothelial cells induced by oxidative stress plays an important role in the pathogenesis of atherosclerosis. Dihydromyricetin (DMY) is considered as a natural antioxidant. However, the mechanism of DMY on endothelial cell injury induced by oxidative stress remains unclear. In this study, we found that DMY could reduce the oxidative damage of HUVECs induced by sodium nitroprusside (SNP), HUVECs pre‐treated with DMY suppressed SNP‐induced apoptosis by reduced ROS overproduction of intracellular, decreased MDA level and elevated the superoxide dismutase activity. Meanwhile, we found that DMY could promote the expression of phosphorylated FoxO3a and Akt, and affect the nuclear localization of FoxO3a, when treated with the PI3K inhibitor LY294002, the effect of DMY was blocked. These data suggest that DMY protects HUVECs from oxidative stress by activating PI3K/Akt/FoxO3a signalling pathway. Therefore, DMY may have great therapeutic potential as a new drug for atherosclerosis.

Uveal melanoma (UM) is a highly invasive intraocular malignancy with high mortality. Presently, there is no FDA‐approved standard for the treatment of metastatic UM. Pristimerin is a natural quinine methide triterpenoid compound with anti‐angiogenic, anti‐cancer and anti‐inflammatory activities. However, Pristimerin potential cytotoxic effect on UM was poorly investigated. In the present study, we found the migration and invasion of UM‐1 cells were inhibited by Pristimerin which also caused a rapid increase of ROS, decreased mitochondrial membrane potential, induced the accumulation of cells in G0/G1 phase, ending with apoptotic cell death. Pristimerin inhibited Akt and FoxO3a phosphorylation and induced nuclear accumulation of FoxO3a in UM‐1 cells, increased the expression of pro‐apoptotic proteins Bim、p27^Kip1, cleaved caspase‐3, PARP and Bax, and decreased the expression of Cyclin D1 and Bcl‐2. LY294002 or Akt‐siRNA inhibited the PI3K/Akt/FoxO3a pathway and promoted the Pristimerin‐induced apoptosis, while Pristimerin effects were partially abolished in FoxO3a knockdown UM‐1 cell cultures. Taken together, present results showed that Pristimerin induced apoptotic cell death through inhibition of PI3K/Akt/FoxO3a pathway in UM‐1 cells. These findings indicate that Pristimerin may be considered as a potential chemotherapeutic agent for patients with UM.