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Anthropogenic activities are increasing the amount of carbon dioxide (CO2) in the atmosphere. There is mounting experimental evidence that lifetime exposure to these increasing atmospheric CO2 levels can negatively impact the normal physiology of organisms. However, directly assessing this in humans is very difficult.
Asthma affects more than 300 million people worldwide and is frequently associated with other medical conditions in adults, including chronic obstructive pulmonary disease, ischaemic heart disease, and stroke. Despite the huge burden, there has been little progress toward prevention and cure, possibly related to a one-size-fits-all approach.
Respiratory infection and wheezing illness are leading causes of hospitalisation in childhood, placing a significant burden on families and healthcare systems. However, reliably distinguishing children at risk of developing persistent disease from those likely to outgrow their symptoms remains a clinical challenge. Earlier identification would allow clinicians to focus care and resources on those most likely to benefit from long-term management, while reducing anxiety and uncertainty about the future for families.
Preterm birth is associated with increased mortality and morbidity, particularly due to lung disease. Low- and middle-income countries (LMIC) have the highest rates of preterm birth. Infants born extremely preterm rarely survive, so the largest burden is amongst moderate-to-late preterm (MLP) infants. The long-term health impact on MLP children in LMIC is poorly understood. The aim of this study was to assess the effect of MLP birth on lung function trajectories from birth to 5 years in the Drakenstein Child Health Study.
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.