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Research

Differential cell counts using center-point networks achieves human-level accuracy and efficiency over segmentation

Differential cell counts is a challenging task when applying computer vision algorithms to pathology. Existing approaches to train cell recognition require high availability of multi-class segmentation and/or bounding box annotations and suffer in performance when objects are tightly clustered.

Research

Lung volumes, gas transfer and oscillometry after preterm birth: systematic review and meta-analysis

Small airway and lung parenchymal abnormalities frequently occur following preterm birth but are commonly missed by spirometry. Static lung volumes, diffusing capacity of the lung for carbon monoxide (D LCO) and oscillometry provide a more precise characterisation of these conditions. We hypothesised that differences in these measures exist between individuals born preterm and at term and we aimed to systematically review the literature to identify and quantify these differences in lung function.

Research

Global participatory wastewater surveillance to understand mpox clade diversity in war and conflict-affected countries

War and conflict severely disrupt public health systems, compromising infectious disease surveillance in many affected regions. Mpox, a re-emerging zoonotic disease, poses a growing global threat, especially in areas where traditional monitoring is inaccessible.The mpox virus has distinct clades with varying transmission and severity.

Research

Considerations for Causal Inference Studies

Rachel Foong BSc (hons), PhD, MBiostat Honorary Research Associate 08 6319 1626 Rachel.Foong@thekids.org.au Senior Research Fellow Dr Foong is an Honorary Research Associate at The Kids Research Institute Australia and Curtin University. She

Research

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.