Objective:To characterize autophagy dysregulation and immune cell infiltration in bronchopulmonary dysplasia (BPD) and identify potential therapeutic targets for clinical intervention.Methods:Gene expression profiles of BPD and an autophagy-related gene list were obtained from the Gene Expression Omnibus and Human Autophagy Database. Raw data were processed using bioinformatics approaches to identify differentially expressed genes (DEGs), followed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses. A protein-protein interaction (PPI) network was constructed to screen hub autophagy genes and the expression levels were validated in a BPD animal model through animal experiments. Drug-target prediction of autophagy-related genes was performed using network analysis, and immune infiltration features in BPD were analyzed by ssGSEA and CIBERSORT algorithms. Statistical significance was assessed via two-sample t-tests. Results:We identified 4 866 DEGs in BPD, including 61 autophagy-related genes enriched in macroautophagy and autophagy regulation pathways. PPI analysis revealed ten hub genes, including PARP1, HSP90AB1, and PTEN, with downregulated expression in BPD animal model. The expression levels of PARP1, HSP90AB1, and PTEN in the BPD mice were all lower than those in the control group (0.33±0.07 vs. 0.66±0.15, t=3.54; 0.46±0.41 vs. 1.45±0.33, t=3.39; 0.72±0.19 vs. 1.25±0.25; t=2.91; all P<0.05). Drug-target prediction highlighted N-acetyl-L-cysteine, vorinostat, and sorafenib as potential therapies. Immune profiling demonstrated significant shifts in naive B cells, memory B cells, CD8 +T cells, and neutrophils, indicating a pro-inflammatory and immunosuppressive microenvironment. Conclusions:Autophagy-immune axis dysregulation may contribute to BPD pathogenesis. The aberrant expression of PARP1, HSP90AB1, and PTEN provides novel mechanistic insights into BPD, while identified drug candidates targeting autophagy genes offer translational potential for BPD treatment.

Objective:To characterize autophagy dysregulation and immune cell infiltration in bronchopulmonary dysplasia (BPD) and identify potential therapeutic targets for clinical intervention.Methods:Gene expression profiles of BPD and an autophagy-related gene list were obtained from the Gene Expression Omnibus and Human Autophagy Database. Raw data were processed using bioinformatics approaches to identify differentially expressed genes (DEGs), followed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses. A protein-protein interaction (PPI) network was constructed to screen hub autophagy genes and the expression levels were validated in a BPD animal model through animal experiments. Drug-target prediction of autophagy-related genes was performed using network analysis, and immune infiltration features in BPD were analyzed by ssGSEA and CIBERSORT algorithms. Statistical significance was assessed via two-sample t-tests. Results:We identified 4 866 DEGs in BPD, including 61 autophagy-related genes enriched in macroautophagy and autophagy regulation pathways. PPI analysis revealed ten hub genes, including PARP1, HSP90AB1, and PTEN, with downregulated expression in BPD animal model. The expression levels of PARP1, HSP90AB1, and PTEN in the BPD mice were all lower than those in the control group (0.33±0.07 vs. 0.66±0.15, t=3.54; 0.46±0.41 vs. 1.45±0.33, t=3.39; 0.72±0.19 vs. 1.25±0.25; t=2.91; all P<0.05). Drug-target prediction highlighted N-acetyl-L-cysteine, vorinostat, and sorafenib as potential therapies. Immune profiling demonstrated significant shifts in naive B cells, memory B cells, CD8 +T cells, and neutrophils, indicating a pro-inflammatory and immunosuppressive microenvironment. Conclusions:Autophagy-immune axis dysregulation may contribute to BPD pathogenesis. The aberrant expression of PARP1, HSP90AB1, and PTEN provides novel mechanistic insights into BPD, while identified drug candidates targeting autophagy genes offer translational potential for BPD treatment.

Visual endotracheal intubation technique was applied in the endotracheal intubation teaching for standardized resident training as a routine teaching appliance.The residents were divided into two groups,the anesthetic speciality group and the non-anesthetic speciality group.According to the different teaching targets,teaching periods and basic abilities,the differentiated teaching Settings were built and the different teaching schemes,evaluation index and teachers were applied for the two groups respectively for fulfilling the advantages of visual laryngoscope.Until now,more than a hundred residents were educated with the endotracheal intubation,and the teaching efficiency and quality were significantly improved,which also reduced the incidence of the complications related to endotracheal intubation.

Objective To explore the effects of penehyclidine hydrochloride (PHC) on lung epithelial type Ⅱcells against oxidative stress damage. Methods A549 cells treated with H2O2 were used as oxidative stress damage cell model. A549 cells were divided into 3 groups: control group (C group), H2O2 treated group (H group) and PHC treated group (P group). The viability of A549 cells was measured by MTT assay. The apoptotic rate was measured by TUNEL assay. The lev?els of malonicdialed (MDA), reactive oxygen species (SOD), reduced glutathione hormone (GSH) and nicotinamide adenine dinucleotide phosphate (NADPH) of cells were detected by biochemistry colorimetry. Results Compared with group C, the viability of A549 and the contents of SOD, GSH and NADPH were significantly decreased in group H, while MDA content and apoptotic rate were increased (P<0.05). Compared with group H, the viability of A549, the contents of SOD, GSH and NADPH were significantly increased in group P, while MDA content and apoptotic rate were reduced (P<0.05). Conclu?sion Penehyclidine hydrochloride shows protective effects on A549 cells through reducing the oxidative damage induced by H2O2.