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An infant mouse model of influenza-driven nontypeable Haemophilus influenzae colonization and acute otitis media suitable for preclinical testing of novel therapies

Nontypeable Haemophilus influenzae (NTHi) is a major otitis media (OM) pathogen, with colonization a prerequisite for disease development. Most acute OM is in children <5 years old, with recurrent and chronic OM impacting hearing and learning. Therapies to prevent NTHi colonization and/or disease are needed, especially for young children. Respiratory viruses are implicated in driving the development of bacterial OM in children.

Mucopolysaccharidosis (MPS IIIA) mice have increased lung compliance and airway resistance, decreased diaphragm strength, and no change in alveolar structure

Mucopolysaccharidosis type IIIA (MPS IIIA) is characterized by neurological and skeletal pathologies caused by reduced activity of the lysosomal hydrolase, sulfamidase, and the subsequent primary accumulation of undegraded heparan sulfate (HS). Respiratory pathology is considered secondary in MPS IIIA and the mechanisms are not well understood. 

Treatment with inhaled aerosolised ethanol reduces viral load and potentiates macrophage responses in an established influenza mouse model

Treatment options for viral lung infections are currently limited. We aimed to explore the safety and efficacy of inhaled ethanol in an influenza-infection mouse model.

Stiffness Mediated-Mechanosensation of Airway Smooth Muscle Cells on Linear Stiffness Gradient Hydrogels

In obstructive airway diseases such as asthma and chronic obstructive pulmonary disease (COPD), the extracellular matrix (ECM) protein amount and composition of the airway smooth muscle (ASM) is often remodelled, likely altering tissue stiffness. The underlying mechanism of how human ASM cell (hASMC) mechanosenses the aberrant microenvironment is not well understood.

Partial amelioration of a chronic cigarette-smoke-induced phenotype in mice by switching to electronic cigarettes

Electronic cigarettes ("e-cigarettes") are often marketed as smoking cessation tools and are used by smokers to reduce/quit cigarette smoking. The objective of this study was to assess the health effects of switching to e-cigarettes after long-term smoking in a mouse model and compare these effects with continued smoking, or quitting entirely. 

In utero and early-life nitrate in drinking water impacts lung function of weanling rats

Consumption of nitrate in drinking water has previously been associated with a range of adverse health effects, including methemoglobinemia and potentially cancer. In animal models, it has been shown to impact respiratory structure and function, however, there is a paucity of data of the effects of in utero exposure on the respiratory health of offspring.

The effects of e-cigarette use on asthma severity in adult BALB/c mice

Electronic cigarettes (e-cigarettes) are often perceived to be a less harmful alternative to tobacco cigarettes. Potentially due to this perception, they are used by people with pre-existing respiratory conditions, such as asthma, who otherwise would not smoke. Despite this, there are few studies exploring the health effects of e-cigarette use on pre-existing asthma.

Intrauterine growth restriction promotes hypothalamic circadian dysregulation in adult mouse offspring

Adverse prenatal conditions can induce intrauterine growth restriction and increase the risk of adulthood metabolic disease. Mechanisms underlying developmentally programmed metabolic disease remain unclear but may involve disrupted postnatal circadian rhythms and kisspeptin signalling. 

Hidden in plain sight: how vaping manufacturers exploit legislative loopholes

Alexander Larcombe BScEnv (Hons) PhD Honorary Research Fellow Honorary Research Fellow Associate Professor Alexander Larcombe began work at The Kids

Exposure to biodiesel exhaust is less harmful than exposure to mineral diesel exhaust on blood-brain barrier integrity in a murine model

Emerging data suggest that air pollution is a persistent source of neuroinflammation, reactive oxygen species, and neuropathology that contributes to central nervous system disorders. Previous research using animal models has shown that exposure to diesel exhaust causes considerable disruption of the blood-brain barrier, leading to marked neuroinflammation.