![]() No other research group other than ours is able to produce such results to date. My current postdoctoral research project within Brad Launikonis’ lab utilizes my unique abilities to perform comprehensive physiological examinations (skinned muscle fibre technique coupled with confocal microscopy) on single segments of individual fresh muscle cells, obtained from animal models or muscle biopsies of human subjects. The aim of this project is to apply the latest techniques established in our lab to assess how calcium moves in muscle with these mutations to find targets to improve muscle strength in this disease. As the severity of the mutation increases, so does the weakness of the muscle. In the event of mutated RyRs the outcome for an individual can be no obvious effect on muscle strength, or mild, through to very severe and life-shortening myopathy. There are many known mutations in the RyR that can affect the function of this channel. Ryanodine receptors (RyR) are the Ca2+ release channels of skeletal muscle fibres that regulate muscle contraction. ![]() Ryanodine receptor mutations and skeletal muscle weakness.The identification in these populations of the precise molecular site and mechanisms involved in oxidative damage would be highly significant and make it realistic to design drugs to bind and protect this molecular site, and thereby aid muscle performance in disease states. ![]() Protecting muscle from exacerbated levels of oxidative stress represents a critical therapeutic approach to improve muscle function and quality of life of aged and inactive persons until a cure is developed. This is the first study to comprehensively investigate the effects of ageing and inactivity on the physiological and biochemical changes in human skeletal muscle at the single muscle cell level. The aims of this study is to identify the specific mechanism and target protein responsible for the loss of muscle force in these populations. ![]() This research interest is central to any understanding of the mechanism(s) underlying abnormalities in protein expression and oxidation-induced dysfunction responsible for marked muscle weakness and fatigability occurring during ageing or inactivity. Skeletal muscle weakness with ageing and inactivity.I’m now a world recognized expert of this technique which has immense potential for examining any number of physiological questions and even allows for biochemical analyses of any protein of interest in the same cell. This technical breakthrough has been recognized by editorials of different leading scientific journals in the field of Physiology. This is vitally important since most of our existing knowledge on muscle function comes from studies on muscles obtained from animal models. Importantly, I have developed this technique for the first time in human muscle which allows the exciting opportunity to investigate cellular mechanisms of muscle weakness in different clinical population. I am a physiologist first and foremost with a particular interest in understanding how skeletal muscle cell normally functions so as to try and elucidate what changes or factors contribute to various forms of muscle weakness with ageing, inactivity or various chronic diseases.ĭuring my previous postdoctoral appointment at La Trobe University (Melbourne, 2010-2017), I have gained considerable experience using the "mechanically skinned muscle fibre" technique in animal muscle. A life-long fascination in sciences provided me with the inspiration to graduate in exercise physiology (University of Sherbrooke, Canada, 2004), complete a PhD in physiology/biophysics (University of Sherbrooke, 2009) and continue in my current role as a postdoctoral researcher at the School of Biomedical Sciences (SBMS) of The University of Queensland.
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