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Cultural capital on the move: ethnic and class distinctions in Asian-Australian academic achievement
Get PDF“I Don't Really Wanna Go Back. I Know What I've Got in Front of Me.” Lived Experiences of Emergency Nurses 2 Years Into the Global COVID-19 Pandemic
Get PDFExamining emergency departments practices on advance care directives and medical treatment decision making using the victorian emergency minimum dataset
Get PDFAssociation of active mobilisation variables with adverse events and mortality in patients requiring mechanical ventilation in the intensive care unit: a systematic review and meta-analysis
No full textInvestigating the flood risk perception of residents in informal settlements around the floodplains of River Ravi in Lahore, Pakistan
No full textSingle-session measures of quadriceps neuromuscular function are reliable in healthy females and unaffected by age
Get PDFThis study aimed to determine the inter-session reliability of quadriceps neuromuscular function measurements in healthy young and older females
Loss of endogenous estrogen alters mitochondrial metabolism and muscle clock-related protein Rbm20 in female mdx mice
Get PDFFemale carriers of a Duchenne muscular dystrophy (DMD) gene mutation manifest exercise intolerance and metabolic anomalies that may be exacerbated following menopause due to the loss of estrogen, a known regulator of skeletal muscle function and metabolism. Here, we studied the impact of estrogen depletion (via ovariectomy) on exercise tolerance and muscle mitochondrial metabolism in female mdx mice and the potential of estrogen replacement therapy (using estradiol) to protect against functional and metabolic perturbations. We also investigated the effect of estrogen depletion, and replacement, on the skeletal muscle proteome through an untargeted proteomic approach with TMT-labelling. Our study confirms that loss of estrogen in female mdx mice reduces exercise capacity, tricarboxylic acid cycle intermediates, and citrate synthase activity but that these deficits are offset through estrogen replacement therapy. Furthermore, ovariectomy downregulated protein expression of RNA-binding motif factor 20 (Rbm20), a critical regulator of sarcomeric and muscle homeostasis gene splicing, which impacted pathways involving ribosomal and mitochondrial translation. Estrogen replacement modulated Rbm20 protein expression and promoted metabolic processes and the upregulation of proteins involved in mitochondrial dynamics and metabolism. Our data suggest that estrogen mitigates dystrophinopathic features in female mdx mice and that estrogen replacement may be a potential therapy for post-menopausal DMD carriers
