Exploratory analysis of the key role of immune function changes in BPD.

Bronchopulmonary dysplasia (BPD) is one of the most prevalent and severe chronic lung diseases in premature infants. The objective of the current study was to screen for key BPD-associated genes and pathways by transcriptomic analysis from clinical patients and animal models. In our study, the differentially expressed genes were screened from 58 children with 14-day BPD and 40 normal children in the GSE32472 dataset of the Gene Expression Omnibus database.

[Prognosis of bronchopulmonary dysplasia].

Children with bronchopulmonary dysplasia (BPD) often exhibit severe respiratory problems and significant pulmonary dysfunction during school age and adulthood. Exercise tests show a decline in cardiopulmonary function and physical performance in children with BPD, who also have a higher incidence of pulmonary hypertension. These children generally perform poorly in terms of intelligence, language, and motor development.

Idbview: a database and interactive platform for respiratory-associated disease.

Public databases have become invaluable resources for disease research, particularly in the realm of identifying and validating biomarkers, thus playing a significant role in enhancing our understanding of respiratory diseases. To facilitate this understanding, the development of user-friendly analytical tools and advanced systematic models that leverage the growing omics data and clinical information datasets is essential. Despite the importance of such resources, the research progress related to respiratory diseases is hindered by the absence of a centralized platform housing easily accessible datasets and accompanying visualization tools.

Effect and mechanism of transient receptor potential canonical channel 3 on hyperoxic lung injury in neonatal rats.

The aim of this study is to research the expression of the transient receptor potential canonical channel 3 (TRPC3) in a neonatal hyperoxic lung injury model of bronchopulmonary dysplasia (BPD), and to further investigate the role of the TRPC3/nuclear factor-κB (NF-κB) signaling pathway in hyperoxia-induced BPD by a TRPC3 agonist (GSK1702934A). The hyperoxic lung injury model of BPD was established in Sprague-Dawley neonatal rats. Hematoxylin and eosin (HE) staining and radial alveolar count (RAC) values showed that the hyperoxic lung injury model of BPD was successfully established in the neonatal rats, and pulmonary edema was found in the neonatal rats with BPD.