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For 20 years, the hygiene hypothesis has dominated attempts to explain the increasing prevalence of allergic disease. A causal link between maternal innate immu
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.
Alexander Larcombe BScEnv (Hons) PhD Honorary Research Fellow Honorary Research Fellow Associate Professor Alexander Larcombe began work at The Kids
Alexander Larcombe BScEnv (Hons) PhD Honorary Research Fellow Honorary Research Fellow Associate Professor Alexander Larcombe began work at The Kids
A wet cough in a child for more than four weeks could indicate infection in the lungs. The wet cough is caused by mucus in the airway. The mucus becomes infected with bacteria and causes airway inflammation that can progress to permanent lung damage known as bronchiectasis.
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.
The purpose of this paper is to highlight a perspective for decolonizing research with Australian First Nations and provide a framework for successful and sustained knowledge translation by drawing on the recent work conducted by a research group, in five remote communities in North-Western Australia.
Amoxicillin-clavulanate treatment is beneficial in terms of resolution of non-severe exacerbations of bronchiectasis in children
ATP Binding Cassette Subfamily A Member 3 (ABCA-3) is a lipid transporter protein highly expressed in type-II alveolar (AT-II) cells. Mutations in ABCA3 can result in severe respiratory disease in infants and children. To study ABCA-3 deficiency in vitro, primary AT-II cells would be the cell culture of choice although sample accessibility is limited. Our aim was to investigate the suitability of primary nasal epithelial cells, as a surrogate culture model for AT-II cells, to study ABCA-3 deficiency.