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Showing results for "Childhood interstitial lung disease "
Seven innovative lung health research projects have received funding support as the 2023 Wal-yan Respiratory Research Centre Strategic Inspiration Projects.
Reviewed in this article these studies have identified positive association at 21 genes with association at five of these replicated in independent populations.
Here, we show that conditionally reprogrammed airway epithelial cells (CRAECs) can be established from both healthy and diseased phenotypes.
This review attempts to highlight migration-specific and cell-extracellular matrix (ECM) aspects of repair used by epithelial cells
A global network of researchers and clinicians, co-led by The Kids’ Professor Graham Hall, has transformed international best practice in identifying low lung function and diagnosing and treating lung disease.
The interleukin (IL)-6 family of cytokines and exaggerated signal transducer and activator of transcription (STAT)3 signaling is implicated in idiopathic pulmonary fibrosis (IPF) pathogenesis, but the mechanisms regulating STAT3 expression and function are unknown. Suppressor of cytokine signaling (SOCS)1 and SOCS3 block STAT3, and low SOCS1 levels have been reported in IPF fibroblasts and shown to facilitate collagen production. Fibroblasts and lung tissue from IPF patients and controls were used to examine the mechanisms underlying SOCS1 down-regulation in IPF.
We characterized the lower airways microbiome using BAL samples obtained from clinically stable CF young children who underwent bronchoscopy and chest CT.
Jonathan Carapetis AM AM MBBS FRACP FAFPHM PhD FAHMS Executive Director; Co-Head, Strep A Translation; Co-Founder of REACH 08 6319 1000 contact@
Although entirely preventable, rheumatic heart disease, a disease of poverty and social disadvantage resulting in high morbidity and mortality, remains an ever-present burden in low-income and middle-income countries and rural, remote, marginalised and disenfranchised populations within high-income countries.
Myeloperoxidase is released by neutrophils in inflamed tissues. MPO oxidizes chloride, bromide, and thiocyanate to produce hypochlorous acid, hypobromous acid, and hypothiocyanous acid, respectively. These oxidants are toxic to pathogens, but may also react with host cells to elicit biological activity and potential toxicity. In cystic fibrosis and related diseases, increased neutrophil inflammation leads to increased airway MPO and airway epithelial cell exposure to its oxidants.