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In this study, we compared the physiological consequences of short-term exposure to diesel exhaust via inhalation to those due to exposure to the same diesel...
In this study, we combined human-rhinovirus infection with a clinically relevant mouse model of aero-allergen exposure using house-dust-mite in an attempt to...
Mineral dusts in the occupational setting are associated with poor lung health, however very little is known about the impact of heterogeneous community...
This work initially examines particle deposition in a Weibull-type geometry, comparing traditional computational fluid dynamics approaches with a novel...
All alterations to lung mechanics following in utero arsenic exposure were recovered by adulthood.
Obesity is a contributing factor to asthma severity; while it has long been understood that obesity is related to greater asthma burden, the mechanisms though which this occurs have not been fully elucidated. One common explanation is that obesity mechanically reduces lung volume through accumulation of adipose tissue external to the thoracic cavity.
Once upon a time it was infectious diseases like polio, measles or tuberculosis that most worried parents. With these threats now largely under control, parents face a new challenge – sky-rocketing rates of non-infectious diseases such as asthma, allergies and autism.
Treatment strategies for juvenile idiopathic arthritis (JIA) have shifted significantly over the last 20 years. We examined the effect of the introduction of government-subsidised TNF inhibitor (TNFi) treatment on incident hospitalisation for JIA.
Despite their increasing popularity, and Australia's unique regulatory environment, how and why Australian adults use e-cigarettes and their perceptions of their safety, efficacy and regulation have not been extensively reported before. In this study, we screened 2217 adult Australians with the aim of assessing these questions in a sample of current or former e-cigarette users.
Patients with comorbid asthma-obesity experience greater disease severity and are less responsive to therapy. We have previously reported adipose tissue within the airway wall that positively correlated with body mass index. Accumulation of biologically active adipose tissue may result in the local release of adipokines and disrupt large and small airway function depending on its anatomical distribution. This study therefore characterized airway-associated adipose tissue distribution, lipid composition, and adipokine activity in a porcine model.