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National E-cigarette Monitoring and Evidence Consortium: Supporting informed research, policy and practice in Australia

Alexander Larcombe BScEnv (Hons) PhD Honorary Research Fellow Honorary Research Fellow Associate Professor Alexander Larcombe began work at The Kids in 2005 and is now an Honorary Research Fellow. During his time at the Institute Associate Professor

Clinical Predictors of Longitudinal Respiratory Exacerbation Outcomes in Young Hospitalised Children

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.

Innate epithelial and functional differences in airway epithelium of children with acute wheeze

Early childhood wheeze is a major risk factor for asthma. However, not all children who wheeze will develop the disease. The airway epithelium has been shown to be involved in asthma pathogenesis. Despite this, the airway epithelium of children with acute wheeze remains poorly characterized.

Guiding practice principles for clinicians who work with Indigenous people

Culturally safe healthcare approaches are important to improve outcomes of Indigenous people. Non-Indigenous clinicians are often ill-prepared to provide such healthcare. The NHMRC Centre for Research Excellence (CRE) especially for First Nations Children has been studying for several years how to improve clinical care for Indigenous children with respiratory disease in hospital, clinic, urban, rural and remote settings. 

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.