Development of a multivariate physiologic state space analysis framework for characterising functional properties of the cardiovascular system. Pathologies of the cardiovascular system arising from heart diseases make a major contribution to morbidity and mortality in the Australian community. This project will provide new diagnostic modalities based on advanced noninvasive bioinstrumentation, signal processing and model-based analytical methods to identify early signs of developing disease or t ....Development of a multivariate physiologic state space analysis framework for characterising functional properties of the cardiovascular system. Pathologies of the cardiovascular system arising from heart diseases make a major contribution to morbidity and mortality in the Australian community. This project will provide new diagnostic modalities based on advanced noninvasive bioinstrumentation, signal processing and model-based analytical methods to identify early signs of developing disease or the acute exacerbation of existing disease. The impact of these new technologies on the early diagnosis and improved triaging of patients in emergency departments is potentially profound and could result in improved healthcare outcomes for the patients and reduced admissions to hospital as well as the development of a substantial international market.Read moreRead less
Statistical Methods for Discovering Ribonucleic acids (RNAs) contributing to human diseases and phenotypes. Identifying the causative genetic factors involved in quantitative phenotypes and diseases is a major goal of biology in the 21st century and beyond. A crucial step towards this goal is identifying and classifying the functional non-protein-coding Ribonucleic acids (RNAs) encoded in the human genome. This project will make major contributions to international efforts in this area by identi ....Statistical Methods for Discovering Ribonucleic acids (RNAs) contributing to human diseases and phenotypes. Identifying the causative genetic factors involved in quantitative phenotypes and diseases is a major goal of biology in the 21st century and beyond. A crucial step towards this goal is identifying and classifying the functional non-protein-coding Ribonucleic acids (RNAs) encoded in the human genome. This project will make major contributions to international efforts in this area by identifying RNA molecules that contribute to quantitative phenotypes including susceptibility to disease. As such, it will directly benefit fundamental science via the discovery and classification of new molecules. Indirectly, it will lead to breakthroughs in biology, and consequently to major medical and pharmaceutical advances in the diagnosis and treatment of genetic disease.Read moreRead less
Mathematical Modelling of the Mechanobiology of Arterial Plaque Growth. Plaque growth is a chronic inflammatory response induced by the interactions between endothelial cells, lipids, monocytes/macrophages, smooth muscle cells and platelets in the arteries. It involves many different biological processes, such as lipid deposition, inflammation and angiogenesis, and their interactions with the microcirculation. To understand the underlying mechanobiology, we propose to develop a mathematical mode ....Mathematical Modelling of the Mechanobiology of Arterial Plaque Growth. Plaque growth is a chronic inflammatory response induced by the interactions between endothelial cells, lipids, monocytes/macrophages, smooth muscle cells and platelets in the arteries. It involves many different biological processes, such as lipid deposition, inflammation and angiogenesis, and their interactions with the microcirculation. To understand the underlying mechanobiology, we propose to develop a mathematical model to interpret plaque growth by integrating these dynamic biological processes. It will offer a systematic rational understanding of plaque growth. New models will be provided to better interpret biological data and contribute to our knowledge in quantifying complex biological mechanisms during growth and development.Read moreRead less