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World-first study shows increased atmospheric CO2 levels damage young lungs

Australian researchers who have conducted the first study looking at the direct health impacts of predicted carbon dioxide levels say the results are worrying and highlight the urgent need for more research into the issue.

Does lung function in preschoolers help to predict asthma in later life?

The earliest respiratory function assessments, within or close to the neonatal period, consistently show correlations with lung function and with the development of asthma into adulthood. Measurements of lung function in infancy reflect the in utero period of lung development, and if early enough, show little influence of postnatal environmental exposures. 

Phage therapy could be key to conquering persistent bacterial lung infections in children

Persistent bacterial lung infections in children lead to significant morbidity and mortality due to antibiotic resistance. In this paper, we describe how phage therapy has shown remarkable efficacy in preclinical and clinical studies, demonstrating significant therapeutic benefits through various administration routes. 

Global change, climate change, and asthma in children: Direct and indirect effects - A WAO Pediatric Asthma Committee Report

The twenty-first century has seen a fundamental shift in disease epidemiology with anthropogenic environmental change emerging as the likely dominant factor affecting the distribution and severity of current and future human disease. This is especially true of allergic diseases and asthma with their intimate relationship with the natural environment.

Early moderate prenatal alcohol exposure and maternal diet impact offspring DNA methylation across species

Alcohol consumption in pregnancy can affect genome regulation in the developing offspring but results have been contradictory. We employed a physiologically relevant murine model of short-term moderate prenatal alcohol exposure resembling common patterns of alcohol consumption in pregnancy in humans. 

DNA Methylation signatures underpinning blood neutrophil to lymphocyte ratio during first week of human life

Understanding of newborn immune ontogeny in the first week of life will enable age-appropriate strategies for safeguarding vulnerable newborns against infectious diseases. Here we conducted an observational study exploring the immunological profile of infants longitudinally throughout their first week of life. 

Can lung disease be averted by focusing on early-life inequities?

Shannon Simpson BMedSci (hons), PhD Head, Strong Beginnings Research, Co-head Foundations of Lung Disease 08 6319 1631 Shannon.simpson@thekids.org.au

Interactions between bacteria in the human nasopharynx: a scoping review

Emerging evidence indicates that interactions between bacteria shape the nasopharyngeal microbiome and influence respiratory health. This Review uses the systematic scoping methodology to summarise 88 studies including observational and experimental studies, identifying key interactions between bacteria that colonise the human nasopharynx. 

What goes up must come down: dynamics of type 1 interferon signaling across the lifespan

Type 1 interferons (T1IFNs) are typically expressed in low concentrations under homeostatic conditions, but upon pathogenic insult or perturbation of the pathway, these critical immune signaling molecules can become either protectors from or drivers of pathology. While essential for initiating antiviral defense and modulating inflammation, dysregulation of T1IFN signaling can contribute to immunopathology, making it and its associated pathways prime targets for immune evasion and disruption by pathogens. 

Suppression of TGF-β/SMAD signaling by an inner nuclear membrane phosphatase complex

Cytokines of the TGF-β superfamily control essential cell fate decisions via receptor regulated SMAD (R-SMAD) transcription factors. Ligand-induced R-SMAD phosphorylation in the cytosol triggers their activation and nuclear accumulation. We determine how R-SMADs are inactivated by dephosphorylation in the cell nucleus to counteract signaling by TGF-β superfamily ligands.