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Understanding the role of the circadian molecular clock in the development of dilated cardiac myopathy and atrial fibrillation.

Description 
Virtually all cardiac functions, including the incidence of atrial fibrillation (AF) follow a circadian rhythm. Loss of appropriate timing keeping can lead to increased cardiovascular disease (CVD). Cardiac events often follow a circadian pattern, i.e. a heart attack or arrhythmia is more likely to occur in the morning. Atrial fibrillation (AF) or ‘arrhythmia’ in which your heart beats irregularly, reducing the heart’s ability to pump blood properly and increases the chance of a blood clots forming. This project will investigate whether the circadian molecular clock that underlies the circadian function of the heart, is dysregulated in a variety of cardiac disease models with and without AF. Models to be assessed include a transgenic mouse model with dilated cardiomyopathy (DCM) due to overexpression of mammalian sterile 20-like kinase 1 (Mst1), a model with DCM and AF due to overexpression of Mst1 together with reduced protective signalling due to reduced PI3K (Mst1-dnPI3K), and another transgenic model with DCM and AF due to overexpression of MURC (muscle-restricted coiled-coil; activates the RhoA/ROCK pathway). Techniques: RNA isolation, RT and PCR, Immunostaining, Histology, western block, immunostaining/histology, cell culture.
Essential criteria: 
Minimum entry requirements can be found here: https://www.monash.edu/admissions/entry-requirements/minimum
Keywords 
cardiomyocyte, PI3K, cardiac hypertrophy, mineralocorticoid receptor, hormone, cardiac fibrosis, circadian clock, atrial fibrillation
Available options 
PhD/Doctorate
Masters by research
Masters by coursework
Honours
Time commitment 
Full-time
Part-time
Physical location 
Baker Heart & Diabetes Instititute, Prahran (Next to Alfred Hospital)
Co-supervisors 
Assoc Prof 
Julie McMullen

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