Integrative virtual nursing simulation in teaching cardiopulmonary resuscitation: A blended learning approach.

BACKGROUND: Online learning resources facilitated educational development during the COVID-19 pandemic. This study focuses on the integration of online virtual simulation with interactive exercises and offline low-fidelity simulation for the first time to explore the impact on CPR skills. METHODS: First year nursing students from a medical college participated as volunteers in this study. They were divided randomly into two groups with both having a cardiopulmonary resuscitation (CPR) lesson with the same timings and objectives. The experimental group (n = 36) adopted a blended learning method, with virtual simulation and low-fidelity simulation as resources; the control group (n = 36) used the same method without virtual simulation. The same lecturers taught both classes. Students' self-directed learning (SDL) and critical thinking skills were assessed before and after the intervention and their CPR skills were examined afterward. RESULTS: The experimental group exhibited significantly greater improvement in their SDL abilities and CPR skills. By contrast, we found no statistical differences in their critical thinking abilities. CONCLUSIONS: During CPR training, blended learning method was used to integrate virtual nursing simulation in teaching, which effectively improved students' SDL and CPR skills.

Maackiain Prevents Amyloid-Beta-Induced Cellular Injury via Priming PKC-Nrf2 Pathway.

Amyloid-beta (Aß) peptide induces neurotoxicity through oxidative stress and inflammatory response. Brain deposition of a large amount of amyloid-beta (Aß), in particular Aß 42, promotes the development of Alzheimer's disease (AD). Maackiain is extracted from traditional Chinese medicine peony root and possesses antioxidative, antiosteoporosis, antitumor, and immunoregulatory effects. Whether Maackiain can reduce neurotoxicity caused by Aß accumulation remains elusive. Herein, we found that Maackiain downregulated Aß 42-induced cell injury and apoptosis in PC12 cells. Moreover, Maackiain prevented Aß 42 stimulation-induced generation of oxidative stress and reduced Aß 42-caused impairment of mitochondrial membrane potential in PC12 cells. Maackiain increased the superoxide dismutase activity and decreased malondialdehyde content that was induced by Aß 42. Mechanistic studies showed that Maackiain increased intranuclear Nrf2 expression. Consistently, Nrf2 silencing by RNA interference weakened the protective role of Maackiain against Aß exposure. In addition, calphostin C, a specific antagonist of protein kinase C, attenuated the promoting effects of Maackiain on Nrf2 nuclear translocation. Moreover, calphostin C attenuated the antioxidant and anti-inflammatory capabilities of Maackiain in PC12 cells. Collectively, Maackiain promoted Nrf2 activation through the PKC signaling pathway, thus preventing PC12 cells from Aß-induced oxidative stress and cell injury, suggesting that Maackiain is a potential drug for AD treatment.