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Research Assistant, Children's Lung Health

An exciting opportunity to work in the Children's Lung Health research team to improve lung health in children and young people.

New risk factor identified to help predict the long-term lung health of young adults born very preterm

A study which set out to determine ways to predict the long-term lung health of young adults born very preterm has shown that a childhood history of respiratory hospital admission should be a key consideration in the management of preterm children and adults.

Preventing urinary tract infections in early childhood

Urinary tract infection (UTI) is common in children, causes them considerable discomfort, as well as distress to parents and has a tendency to recur.

Predicting long term lung health outcomes in young adults born very preterm (WALHIP 19 year old follow-up)

This study will conduct a detailed lung health assessment in a follow-up of a group of preterm individuals at 19 years of age.

Vitamin D supplementation of initially vitamin D-deficient mice diminishes lung inflammation with limited effects on pulmonary epithelial integrity

In disease settings, vitamin D may be important for maintaining optimal lung epithelial integrity and suppressing inflammation, but less is known of its effects prior to disease onset.

Vitamin D deficiency causes deficits in lung function and alters lung structure

The prevalence of vitamin D deficiency is increasing and has been linked to obstructive lung diseases including asthma and chronic obstructive pulmonary disease

Genetic susceptibility to otitis media in childhood

Reviewed in this article these studies have identified positive association at 21 genes with association at five of these replicated in independent populations.

Lung function in African infants in the Drakenstein child health study impact of lower respiratory tract illness

Early life lower respiratory tract illness impairs lung function at 1 year, independent of baseline lung function

Reduced socs1 expression in lung fibroblasts from patients with ipf is not mediated by promoter methylation or mir155

The interleukin (IL)-6 family of cytokines and exaggerated signal transducer and activator of transcription (STAT)3 signaling is implicated in idiopathic pulmonary fibrosis (IPF) pathogenesis, but the mechanisms regulating STAT3 expression and function are unknown. Suppressor of cytokine signaling (SOCS)1 and SOCS3 block STAT3, and low SOCS1 levels have been reported in IPF fibroblasts and shown to facilitate collagen production. Fibroblasts and lung tissue from IPF patients and controls were used to examine the mechanisms underlying SOCS1 down-regulation in IPF.

Defective respiratory tract immune surveillance in asthma : A primary causal factor in disease onset and progression

The relative importance of respiratory viral infections vs inhalant allergy in asthma pathogenesis is the subject of ongoing debate.