Publications by authors named "Linxia Cao"
Background: Bronchopulmonary dysplasia (BPD) is a chronic lung disorder predominantly affecting preterm infants. Oxygen therapy, a common treatment for BPD, often leads to hyperoxia-induced pulmonary damage, particularly targeting alveolar epithelial cells (AECs). Crucially, disrupted lung epithelium-fibroblast interactions significantly contribute to BPD's pathogenesis.
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- - The study investigates the role of N-methyladenosine (m6A) RNA methylation regulators in the development of bronchopulmonary dysplasia (BPD), a condition affecting premature infants, as its relationship with gene expression is not well understood.
- - Researchers identified and compared differentially expressed m6A regulators in BPD patients through transcriptome data analysis, revealing significant changes in molecules like IGF2BP1/2/3 and classifying BPD into two subsets based on severity.
- - Functional analysis indicated a disrupted immune-related signaling pathway in one subset of BPD, suggesting that understanding m6A regulation could offer new insights into diagnosing and treating this condition.
Background: Bronchopulmonary dysplasia (BPD) is the most common respiratory complication in preterm infants, and there is a lag in the diagnosis of BPD. Inflammation is a vital pathogenic factor for BPD; we aim to evaluate the predictive and diagnostic values of systemic inflammatory indices in BPD.
Methods: Between 1 January 2019 and 31 May 2023, the clinical data of 122 premature infants with a gestational age of <32 weeks in the Department of Neonatology, the Affiliated Huai'an No.
Article Synopsis
- The study aimed to create a juvenile mouse model of asthma using postnatal exposure to high oxygen levels (hyperoxia) along with early sensitization to ovalbumin (OVA).
- The researchers exposed newborn mice to 95% oxygen and administered OVA injections, followed by inhalation challenges, then measured various asthma-related symptoms and immune responses.
- Results showed that the combination of hyperoxia and OVA significantly increased asthma-like symptoms, airway sensitivity, and certain immune markers compared to either treatment alone, suggesting the model effectively mimics juvenile asthma.
Article Synopsis
- Bronchopulmonary dysplasia (BPD) is a chronic lung disease affecting preterm infants, and oxygen therapy used to treat BPD can inadvertently cause lung damage due to high oxygen levels.
- A study identified the PVT1/IL-33 axis's role in BPD; hyperoxia exposure increased RNA levels of IL-33 and PVT1, leading to lung cell apoptosis.
- Silencing PVT1 was found to reduce apoptosis and improve lung function, suggesting that targeting the PVT1/IL-33 pathway could be a potential treatment strategy for lung injuries in BPD.
Bronchopulmonary dysplasia (BPD) is a common complication of prematurity and has no specific treatment option. Moreover, inflammation and fibrosis play a vital role in the development of BPD. Thus, this study aimed to explore the role of the anti-inflammatory and anti-fibrotic drug cryptotanshinone (CTS) in the treatment of inflammation and fibrosis in BPD.
View Article and Find Full Text PDFObjective: The aim of this study is to explore the effects of early postnatal hyperoxia exposure combined with early ovalbumin (OVA) sensitization on lung inflammation and bacterial flora in neonatal mice on a juvenile mouse model of asthma.
Methods: Thirty-two newborn female C57BL/6 J mice were randomly divided into four groups, which including room air+phosphate-buffered saline (PBS) group, hyperoxia+PBS group, room air+OVA group, and hyperoxia+OVA group, according to the hyperoxia exposure and/or OVA induction. Mice were exposed to either 95% O or room air for 7 days after birth; after 7 days, they were exposed to air and received an intraperitoneal injection of OVA suspension or PBS solution on postnatal days 21 (P21) and 28 (P28).