Cardiology

Project 1:Identification of mediators of fibrinolysis in plasminogen deficient mice.

Plasminogen is the major mediator of fibrinolysis, yet mice deficient in this protein survive to adulthood, suggesting the existence of physiologically important non-plasmin mediators of fibrinolysis. The purpose of this project is to characterize these non-plasmin mediators of fibrinolysis, using plasminogen deficient mice. In our current studies, we are using biochemical techniques to identify potential fibrinolytic proteins in the plasma of these animals. We are also analyzing their white cells, which appear to have enhanced lytic activity in the absence of plasminogen.

Techniques routinely employed include reverse transcriptase polymerase chain reaction (to confirm plasminogen deficiency in the mice), SDS-PAGE zymography and mass spectrometry (for peptide mass matching and sequence definition). The plasminogen deficient mouse model is available at the ANZAC Research Institute

Essential attributes include a background in biochemistry, molecular biology or a related subject.

Contact: Dr Paul Witting
Tel: +612 9767-9103
email:

A/Prof David Brieger
Tel: +612 9767-7358
email:

In vivo investigations of coronary disease

The Department of Cardiology has ongoing research studies in the detection of myocardial dysfunction using echocardiography, the detection of coronary disease and coronary bypass disease using CT scanning, and the cellular mechanisms of atherosclerosis. New projects being planned include the in vivo study of high density lipoprotein (HDL) metabolism in man, and, in collaboration with Dr Witting of the Vascular Biology laboratory of the Anzac Institute and colleagues from the Department of Cardiology, the detection of myocardial injury using biomarkers of oxidative damage.

Contact: A/Prof Len Kritharides
email: