Effects of virtual reality simulation on medical students’ learning and motivation in human parasitology instruction: a quasi-experimental study

Abstract Background Despite the proven effectiveness of simulation-based learning activities, its adoption in medical education remains limited, and the influence of simulation on student motivation, particularly subjective task values, is seldom explored. This study aimed to investigate the impact of a simulation-based learning activity on student learning and subjective task values in a medical morphology-related course of Human Parasitology. Methods A quasi-experimental study was conducted with 113 Chinese undergraduate medical students who participated in a Human Parasitology course during April to May 2022. Students were divided into two groups: Simulation Group (n = 55), where students used the simulation, and Lecture Group (n = 58), where students attended an online lecture. Students’ learning was measured prior to the intervention, immediately after the intervention, and three weeks later to assess knowledge retention. The subjective task values questionnaire was administered before and after the interventions. Data were analyzed using one-way ANCOVA and MANOVA. Results Students in the Simulation Group exhibited significantly higher knowledge gain compared to the Lecture Group [F (1,110) = 23.69, p < 0.01]. Additionally, the Simulation Group retained knowledge significantly better than the Lecture Group [F (1,101) = 10.05, p < 0.005]. Furthermore, students in the Simulation Group experienced a significant increase in subjective task values after the intervention [F (3, 52) = 3.57, p < 0.05, η p 2  = 0.17], while students in the Lecture Group reported a significant decrease in subjective task values [F (3, 55) = 2.96, p < 0.05, η p 2  = 0.14]. Conclusions Simulation-based learning not only leads to superior learning but also enhances students’ subjective task values. These findings offer valuable insights into designing effective simulation-based learning experiences in medical education and have significant practical implications for educators and medical professionals

Terpinen-4-ol Improves Lipopolysaccharide-Induced Macrophage Inflammation by Regulating Glutamine Metabolism

Terpinen-4-ol (T-4-O) is an important component of tea tree oil and has anti-inflammatory effects. Currently, there are very few studies on the mechanisms by which T-4-O improves lipopolysaccharide (LPS)-induced macrophage inflammation. In this study, LPS-stimulated mouse RAW264.7 macrophages were used as a model to analyze the effects of T-4-O on macrophage inflammatory factors and related metabolic pathways in an inflammatory environment. The results showed that T-4-O significantly decreased the expression levels of inflammatory cytokines induced by LPS. Cellular metabolism results showed that T-4-O significantly decreased the ratio of the extracellular acidification rate and oxygen consumption rate. Non-targeted metabolomics results showed that T-4-O mainly affected glutamine and glutamate metabolism and glycine, serine, and threonine metabolic pathways. qPCR results showed that T-4-O increased the transcript levels of GLS and GDH and promoted glutamine catabolism. Western blotting results showed that T-4-O inhibited the mTOR and IκB, thereby decreasing NF-κB activity. The overall results showed that T-4-O inhibited mTOR phosphorylation to promote glutamine metabolism and increased cell oxidative phosphorylation levels, thereby inhibiting the expression of LPS-induced inflammatory cytokines

Estradiol Attenuates the Severity of Primary Toxoplasma gondii Infection-Induced Adverse Pregnancy Outcomes Through the Regulation of Tregs in a Dose-Dependent Manner

Estradiol (E2) plays a crucial and intricate role during pregnancy to mediate several aspects of the pregnancy process. A perplexing phenomenon in congenital toxoplasmosis is that the severity of Toxoplasma gondii (T. gondii)-mediated adverse pregnancy outcome is closely related with time of primary maternal infection during pregnancy. In this study, the results showed that T. gondii infection in early pregnancy was more likely to induce miscarriage in mice than in late pregnancy, which may be related to inflammation of the maternal–fetal interface. Meanwhile, the T. gondii infection-induced-apoptotic rate of Tregs was higher and the expression of programmed death-1 (PD-1) on Tregs was lower in early pregnancy than in late pregnancy. As the level of E2 in mouse serum gradually increased with the development of pregnancy, we proposed that E2 may contribute to the discrepancy of Tregs at different stages of pregnancy. Thus, we investigated in vitro and in vivo effects of E2 in regulating Tregs. We found that E2 in vitro could protect Tregs against apoptosis and upregulate the expression of PD-1 on Tregs in a dose-dependent manner through ERα. Likewise, the simulated mid-pregnancy level of E2 in nonpregnant mice also alleviated the T. gondii infection-induced apoptosis of Tregs and potentiated the PD-1 expression on Tregs. Therefore, in the pathogenesis of T. gondii-induced abnormal pregnancy, E2 helped maintain the immune balance and improve the pregnancy outcome through regulating Tregs. This finding illustrates the intricate working of hormone–immune system interaction in infection-induced abnormal pregnancy

Data_Sheet_1_Estradiol Attenuates the Severity of Primary Toxoplasma gondii Infection-Induced Adverse Pregnancy Outcomes Through the Regulation of Tregs in a Dose-Dependent Manner.PDF

<p>Estradiol (E2) plays a crucial and intricate role during pregnancy to mediate several aspects of the pregnancy process. A perplexing phenomenon in congenital toxoplasmosis is that the severity of Toxoplasma gondii (T. gondii)-mediated adverse pregnancy outcome is closely related with time of primary maternal infection during pregnancy. In this study, the results showed that T. gondii infection in early pregnancy was more likely to induce miscarriage in mice than in late pregnancy, which may be related to inflammation of the maternal–fetal interface. Meanwhile, the T. gondii infection-induced-apoptotic rate of Tregs was higher and the expression of programmed death-1 (PD-1) on Tregs was lower in early pregnancy than in late pregnancy. As the level of E2 in mouse serum gradually increased with the development of pregnancy, we proposed that E2 may contribute to the discrepancy of Tregs at different stages of pregnancy. Thus, we investigated in vitro and in vivo effects of E2 in regulating Tregs. We found that E2 in vitro could protect Tregs against apoptosis and upregulate the expression of PD-1 on Tregs in a dose-dependent manner through ERα. Likewise, the simulated mid-pregnancy level of E2 in nonpregnant mice also alleviated the T. gondii infection-induced apoptosis of Tregs and potentiated the PD-1 expression on Tregs. Therefore, in the pathogenesis of T. gondii-induced abnormal pregnancy, E2 helped maintain the immune balance and improve the pregnancy outcome through regulating Tregs. This finding illustrates the intricate working of hormone–immune system interaction in infection-induced abnormal pregnancy.</p