Publications by authors named "Brian Coppin"

Aim: Australian and New Zealand (NZ) paediatric endocrinologists' and NZ general paediatricians' insulin initiation strategies for children with type 1 diabetes (T1D) was recently described. The aim of this study was to document the insulin initiation practices of Australian general paediatricians in newly diagnosed children with T1D.

Methods: An online survey was sent to Australian general paediatricians identified through the Australian Paediatric Society diabetes database.

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Context: Children with type 1 diabetes have vascular dysfunction preceding atherosclerosis. Early interventions are needed to reduce cardiovascular disease.

Objective: To evaluate the effect of metformin on vascular function in children with type 1 diabetes.

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Background And Objective: Children with type 1 diabetes (T1D) have vascular dysfunction and frequently struggle to adhere to dietary recommendations. Limited data exist for the vascular consequences of poor diet quality in children. We aimed to evaluate the association between dietary components and vascular function in children with T1D.

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Background: Cardiovascular disease is the leading cause of mortality in Type 1 diabetes (T1D). Vascular dysfunction is an early and critical event in the development of cardiovascular disease. Children with T1D have vascular dysfunction therefore early interventions to improve vascular health are essential to reduce cardiovascular mortality in T1D.

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Mutations conferring loss of function at the FLNA (encoding filamin A) locus lead to X-linked periventricular nodular heterotopia (XL-PH), with seizures constituting the most common clinical manifestation of this disorder in female heterozygotes. Vascular dilatation (mainly the aorta), joint hypermobility and variable skin findings are also associated anomalies, with some reports suggesting that this might represents a separate syndrome allelic to XL-PH, termed as Ehlers-Danlos syndrome-periventricular heterotopia variant (EDS-PH). Here, we report a cohort of 11 males and females with both hypomorphic and null mutations in FLNA that manifest a wide spectrum of connective tissue and vascular anomalies.

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