Objective: The aim of this study was to evaluate the impact of peer role-playing on the clinical skills performance of pediatric trainees.Methods: Seventy-eight clinical medicine trainees were randomly divided into a role-playing group and a traditional teaching group, with 39 students in each group. The role-playing group alternated between the roles of clinicians and patients, while the traditional teaching group received the bedside teaching mode of verbal instruction. After two weeks traineeship, mini-Clinical Evaluation Exercise(Mini-CEX) was used to evaluate the trainees’ competence in physician-patient communication and clinical practice. A questionnaire was given to the role-playing group to assess their satisfaction with the method.Results: The Mini-CEX scores showed that the role-playing group had superior clinical skills (p < 0.05), including communication, history taking, professionalism, organization, clinical skills, and physical examination, compared to the traditional teaching group. Furthermore, trainee satisfaction was high with the role-playing method,and the satisfaction were more than 95%.Conclusion: The role-playing method effectively improved the clinical skills of pediatric trainees, developed clinical communication skills, and enhanced the application of medical knowledge in a simulated medical environment.

Background: Bronchopulmonary dysplasia (BPD) is a severe respiratory disease that primarily affects premature infants, characterized by persistent inflammation and abnormal immune activation. This study aimed to elucidate the immunological mechanisms underlying BPD by integrating single‐cell RNA sequencing with T/B cell receptor profiling of peripheral blood mononuclear cells (PBMCs) from preterm infants with BPD, complemented by validation in a murine BPD model.Methods: We profiled PBMCs from preterm infants diagnosed with BPD and healthy controls, identifying 22 distinct cell clusters corresponding to major immune cell types.Results: Significant alterations were observed in myeloid and lymphoid subsets, with neutrophils undergoing metabolic reprogramming toward oxidative phosphorylation. T and B cell subsets exhibited phenotypic and functional changes, with B cells serving as crucial interaction hubs in cell communication networks. Progenitor cell analysis in BPD mouse models revealed specific alterations in hematopoietic stem cells. Analysis of cell–cell communication networks highlighted intricate intercellular interactions in BPD, emphasizing a pivotal role for the BTLA‐TNFRSF14 signaling axis in disease pathogenesis. Additionally, pharmacological blockade of BTLA in mouse models alleviated disease severity, suggesting its potential therapeutic effects through modulation of the BTLA‐TNFRSF14 pathway.Conclusion: These findings enhance the understanding of the BPD immune microenvironment and lay the foundation for developing targeted immunomodulatory therapies.Highlights: Single‐cell sequencing revealed immune cell profiles in bronchopulmonary dysplasia (BPD). Neutrophils underwent metabolic changes, and B cells were key in immune communication. Targeting B and T lymphocyte attenuator (BTLA)‐TNFRSF14 signalling reduced BPD severity in mouse models, suggesting a potential therapy.

Background. Bronchopulmonary dysplasia (BPD) is one of the most serious complications in premature infants. Myeloid‐derived suppressor cells (MDSCs) have been indicated to promote immune tolerance and induce anti‐inflammatory responses during the neonatal stage. However, the role of MDSCs in BPD has not been completely expounded. Methods. 130 cases of newborns were collected from six tertiary hospitals in Guangzhou from August 2019 to June 2022. They were divided into BPD group, non‐BPD preterm infants group, and term infants group according to gestational age and presence of BPD. The peripheral blood was collected and used to analyze the proportion, phenotypic, and function of MDSCs at 3 to 7 days and 8 to 14 days after birth, respectively. Results. We indicated that the number of both MDSCs in premature infants is reduced, and the number of polymorphonuclear myeloid‐derived suppressor cells (PMN‐MDSCs) in peripheral blood of BPD infants was significantly lower than that of non‐BPD infants under 34 weeks of gestational age (P < 0.05). Furthermore, PMN‐MDSCs from peripheral blood of patients presented inhibitory effect on proliferation of CD4⁺T and CD8⁺T cells in each group. However, PMN‐MDSCs from BPD group had obviously weaker inhibitory effect on proliferation of CD4⁺T and CD8⁺T cells than that from non‐BPD preterm infants group. In addition, we demonstrated that the expression of NADPH oxidase (Nox2) and reactive oxygen species (ROS) in PMN‐MDSCs of BPD children was significantly lower than that in non‐BPD preterm infants, suggesting that ROS pathway was affected in BPD in premature infants. Conclusion. This study preliminarily revealed the role of PMN‐MDSCs in the pathogenesis of BPD in premature infants. The specific immune regulation mechanism of PMN‐MDSCs in BPD will provide new ideas and strategies for clinical prevention and treatment of BPD in premature infants.