Cardioprotection from heart attacks

Co-supervisor: A/Prof. Clive May

After a heart attack the primary aim is to unblock the coronary artery and reperfuse the ischaemic area of the heart, but this causes further cardiomyocyte death. We have developed a pro-drug that when injected into the bloodstream releases a novel flavonol compound, which significantly reduces this reperfusion injury. This project will investigate the cardioprotective mechanisms of this drug, in particular the interaction with the cell signalling pathways that are activated after reperfusion.

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Cell transplantation for forebrain striatal injuries

Co-supervisor: Dr Clare Parish

The striatum is a structure in the forebrain that plays an important role in many aspects of motor function and emotion. Damage to neurons within the striatum occurs in a number of human conditions including Huntington’s disease (HD), stroke, and traumatic injury. The aim of the project is to assess the feasibility of repairing the damaged striatum in the adult brain by replacing the striatal neurons through transplantation of foetal tissue.

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Central mechanisms causing increased sympathetic nerve activity in heart failure

Supervisors: Dr. Rohit Ramchandra, A/Prof Clive N May

In heart failure cardiac output is reduced causing inadequate organ perfusion. In response the brain stimulates sympathetic nerve activity to try to maintain cardiac output and blood pressure. As the disease progresses the increase in sympathetic nerve activity, in particular to the heart, is detrimental, but the mechanisms causing this increase are poorly understood. The aim of this project is to determine what signals to the brain stimulate sympathetic nerve activity in heart failure and the pathways in the brain that initiate and maintain this increase.

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Central mechanisms subserving the thirst response to bacterial endotoxin

Fever can be induced in experimental animals by injection with bacterial endotoxin.

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Cerebral blood flow changes with body position after stroke

Co-supervisor: Prof Brian Chambers

A stroke is most commonly due to a clot lodged in blood vessels in the brain. For a time, vulnerable, but potentially salvageable brain tissue (the penumbra) is present. Determining how changes in body position within the first 24 hours after a stroke affects cerebral circulation, has the potential to inform clinical practice.

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