Nutritional assessment of resettled paediatric refugees in Western Australia.

AIM: Nutritional deprivation, inadequate diet and food insecurity are common refugee experiences. The growth and nutritional status of paediatric refugees following resettlement in developed countries and the related interplay with socio-economic factors remain less defined; this study aims to describe these features. METHODS: Standardised dietary, medical and socio-demographic health assessments of new refugee patients attending a multidisciplinary paediatric Refugee Health Service (RHS) in Western Australia between 2010 and 2015 were analysed. RESULTS: Demographic data from 1131 paediatric refugees are described (age 2 months to 17.8 years). The majority experienced socio-economic disadvantage, had limited parental education and required interpreters. Nutritional deficiencies were common but varied across ethnicities: iron deficiency (ID) (12.3%), anaemia (7.3%) and inadequate dairy intake (41.0%). A third of children (32.6%) did not consume meat. Infant breastfeeding was sustained (77.8%) in infants <12 months. Prolonged breastfeeding (44.9% aged 12-24 months) was associated with an increased risk of ID (odds ratio 4.0, 95% confidence interval 1.4-11.6). Median body mass index increased significantly for those >24 months between referral and RHS assessment (median period 1.8 months). Overall, 27.1% required additional formal dietetic follow-up, with higher nutritional concerns in refugee children <24 months compared to older patients. CONCLUSIONS: Identification of frequent post-settlement nutritional concerns has been captured through structured multidisciplinary paediatric health screening. Specific screening for socio-economic influencing factors, including education, poverty and food insecurity, during refugee clinical assessments is recommended. Development of targeted, culturally appropriate parental education resources and interventions may improve management following resettlement. Longitudinal research assessing resettlement growth trajectories is required.

Experimental long-term diabetes mellitus alters the transcriptome and biomechanical properties of the rat urinary bladder.

Diabetes mellitus (DM) is the leading cause of chronic kidney disease and diabetic nephropathy is widely studied. In contrast, the pathobiology of diabetic urinary bladder disease is less understood despite dysfunctional voiding being common in DM. We hypothesised that diabetic cystopathy has a characteristic molecular signature. We therefore studied bladders of hyperglycaemic and polyuric rats with streptozotocin (STZ)-induced DM. Sixteen weeks after induction of DM, as assessed by RNA arrays, wide-ranging changes of gene expression occurred in DM bladders over and above those induced in bladders of non-hyperglycaemic rats with sucrose-induced polyuria. The altered transcripts included those coding for extracellular matrix regulators and neural molecules. Changes in key genes deregulated in DM rat bladders were also detected in db/db mouse bladders. In DM rat bladders there was reduced birefringent collagen between detrusor muscle bundles, and atomic force microscopy showed a significant reduction in tissue stiffness; neither change was found in bladders of sucrose-treated rats. Thus, altered extracellular matrix with reduced tissue rigidity may contribute to voiding dysfunction in people with long-term DM. These results serve as an informative stepping stone towards understanding the complex pathobiology of diabetic cystopathy.