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Research

Phage therapy is a promising approach against multidrug-resistant infections, yet systemic administration can lead to incomplete cures. We investigated the distribution, immune responses, and efficacy of the therapeutic phage KPP10 delivered via intranasal or intraperitoneal routes in murine Pseudomonas aeruginosa lung infection models.

Research

Mycobacteroides abscessus (MABS) is within the non-tuberculous mycobacteria family. It inhabits soil and water, exhibits multi-antibiotic resistance and causes opportunistic lung infections, which may progress to symptomatic MABS-pulmonary disease (MABS-PD) associated with substantial morbidity, increased healthcare utilisation, impaired quality of life and increased mortality. 

Research

Influenza vaccines are important for reducing the burden of influenza, particularly for populations at risk of more severe infections. Obesity is associated with increased influenza severity and therefore individuals with obesity are often specifically recommended for annual influenza vaccination. Obesity is also associated with an altered inflammatory profile, which may influence vaccine responses. This systematic review aimed to evaluate the evidence for any association between obesity and influenza vaccine immunogenicity.

Research

Gram-negative bacterial infections remain a major cause of morbidity and mortality in children and neonates globally, compounded by the rise of antimicrobial resistance. Barriers to paediatric antibiotic licencing lead to reduced availability of potentially effective agents for treatment. For children and neonates in the Oceania region, specific challenges remain including a paucity of surveillance data on local rates of antimicrobial resistance, and lack of availability of newer, more costly agents.

Research

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. 

Research

In 2022, the World Health Organization extended their guidelines for perennial malaria chemoprevention (PMC) from infants to children up to 24 months old. However, evidence for PMC's public health impact is primarily limited to children under 15 months. Further research is needed to assess the public health impact and cost-effectiveness of PMC, and the added benefit of further age-expansion. We integrated an individual-based model of malaria with pharmacological models of drug action to address these questions for PMC and a proposed age-expanded schedule (referred as PMC+, for children 03-36 months).

Research

Intellectual and developmental disabilities (IDD) are varied in their nature and presentation. Barriers to oral healthcare are reported in studies of general populations with IDD but these may not reflect the barriers experienced by individuals with rare disorders such as Rett syndrome.

Research

The abstract screening process of systematic reviews can take thousands of hours by two researchers. We aim to determine the reliability and validity of Research Screener, a semi-automated abstract screening tool within a systematic review on non-specific and broader effects of respiratory vaccines on acute lower respiratory infection hospitalisations and antimicrobial prescribing patterns in young children.

Research

The transport of sick newborn infants with respiratory distress leads to unwanted stress at time of physiological instability. There is dearth of studies to evaluate these stress levels. This pilot prospective observational before-after study aimed to evaluate the plasma cortisol levels (as surrogate marker of stress) in infants with respiratory distress during different phases of neonatal transport.

Research

During mitochondrial damage, information is relayed between the mitochondria and nucleus to coordinate precise responses to preserve cellular health. One such pathway is the mitochondrial integrated stress response (mtISR), which is known to be activated by mitochondrial DNA (mtDNA) damage. However, the causal molecular signals responsible for activation of the mtISR remain mostly unknown.