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Small airway and lung parenchymal abnormalities frequently occur following preterm birth but are commonly missed by spirometry. Static lung volumes, diffusing capacity of the lung for carbon monoxide (D LCO) and oscillometry provide a more precise characterisation of these conditions. We hypothesised that differences in these measures exist between individuals born preterm and at term and we aimed to systematically review the literature to identify and quantify these differences in lung function.
Electronic cigarettes (e-cigarettes) are often perceived to be a less harmful alternative to tobacco cigarettes. Potentially due to this perception, they are used by people with pre-existing respiratory conditions, such as asthma, who otherwise would not smoke. Despite this, there are few studies exploring the health effects of e-cigarette use on pre-existing asthma.
Adverse prenatal conditions can induce intrauterine growth restriction and increase the risk of adulthood metabolic disease. Mechanisms underlying developmentally programmed metabolic disease remain unclear but may involve disrupted postnatal circadian rhythms and kisspeptin signalling.
Many survivors of preterm birth (<37 weeks gestation) have lifelong respiratory deficits, the drivers of which remain unknown. Influencers of pathophysiological outcomes are often detectable at the gene level and pinpointing these differences can help guide targeted research and interventions. This study provides the first transcriptomic analysis of primary nasal airway epithelial cells in survivors of preterm birth at approximately 1 year of age.
Mucopolysaccharidosis type IIIA (MPS IIIA) is characterized by neurological and skeletal pathologies caused by reduced activity of the lysosomal hydrolase, sulfamidase, and the subsequent primary accumulation of undegraded heparan sulfate (HS). Respiratory pathology is considered secondary in MPS IIIA and the mechanisms are not well understood.