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Showing results for "lung disease preterm"
Between 1989 and 1991, almost 3,000 WA babies were recruited to the Raine Study - an ambitious research project which would yield a series of paradigm-shifting findings that changed scientific thinking. Three decades on, it has also changed the lives of those taking part.
This genome-wide association study (GWAS) utilises data from the Western Australian Pregnancy Cohort (Raine) Study for 25-hydroxyvitamin D (25(OH)D) levels...
An ambitious project that could stop children developing asthma is the centrepiece of a new world-class respiratory research centre launched in Perth.
The aim of this study was to validate a model for optimal birth weight derived from neonatal records, and to test the assumption that preterm births may be...
Professor Jonathan Carapetis has made eliminating rheumatic heart disease his life’s work.
Human perinatal life is characterized by a period of extraordinary change during which newborns encounter abundant environmental stimuli and exposure to potential pathogens. To meet such challenges, the neonatal immune system is equipped with unique functional characteristics that adapt to changing conditions as development progresses across the early years of life, but the molecular characteristics of such adaptations remain poorly understood.
We recently reported that offspring of mice treated during pregnancy with the microbial-derived immunomodulator OM-85 manifest striking resistance to allergic airways inflammation, and localized the potential treatment target to fetal conventional dendritic cell (cDC) progenitors. Here, we profile maternal OM-85 treatment-associated transcriptomic signatures in fetal bone marrow, and identify a series of immunometabolic pathways which provide essential metabolites for accelerated myelopoiesis.
Neonatal dendritic cells generated form CD34+ cord blood progenitors have a higher inflammatory potential when exposed to viral than bacterial related stimuli
Information is accumulating which implicates airway inflammation resulting from respiratory viral infections, acting against a background of atopy.
To show underlying mechanisms, we examined differences in T-cell gene expression in samples at birth and at 1 year in children with and without IgE allergy.