Defining The Function Of The Thrombin Receptor, PAR4, On Human Platelets
Funder
National Health and Medical Research Council
Funding Amount
$541,402.00
Summary
Inappropriate blood clot formation is the cause of most heart attacks and strokes, and platelets are the cells in the blood which form these clots. Drugs that block platelet function, such as aspirin, are used to prevent heart attack and stroke but are frequently ineffective. We will study the signals which control platelet incorporation into clots in order to discover improved therapeutic strategies for heart attack and stroke prevention.
Proof-of-concept Studies For A Novel Anti-thrombotic Agent
Funder
National Health and Medical Research Council
Funding Amount
$632,352.00
Summary
Blood clots cause most heart attacks and strokes, and platelets are the blood cells that form these clots. Drugs that block platelet function, such as aspirin, are used to prevent heart attack and stroke but are frequently ineffective. Here, we will develop a new drug that prevents platelet incorporation into blood clots, that will be suitable for the prevention of heart attack and stroke in humans, and that may improve on existing therapies.
Novel Single-chain Antibody-targeted Nanoparticles For Diagnosis Of Vascular Diseases In Magnetic Resonance Imaging
Funder
National Health and Medical Research Council
Funding Amount
$460,797.00
Summary
The aim of this project is to develop targeted imaging agents that seek out specific markers for various states of cardiovascular disease. These agents would provide a method for detecting the presence and level of atherosclerosis and thrombotic events. The targeted nanoparticles may provide a unique opportunity to detect very early plaques, the vulnerability of existing plaques and difficult to diagnose vessel blockages such as pulmonary embolism.
Defining The Roles Of Platelet Protease-activated Receptors In Thrombosis
Funder
National Health and Medical Research Council
Funding Amount
$330,690.00
Summary
Inappropriate blood clot formation is the cause of most heart attacks and some strokes. Platelets are the blood cells responsible for such clots. We are interested in the signals which control platelet incorporation into clots because drugs that interfere with this may be effective at inhibiting unwanted clot formation. Our studies determining the importance of platelet signals will provide strong clues to the likely effectiveness of blocking such signals as anti-clotting agents.
I am a cardiovascular scientist and interventional cardiologist using biotechnological, molecular and cell biological methods as well as in vivo and ex vivo models to address translational research questions in the fields of inflammation, thrombosis and atherosclerosis. The aim of my research is to better understand the pathogenesis of cardiovascular disease and to develop new diagnostic and therapeutic strategies that ultimately provide direct benefits to patients.
Coronary Atherosclerosis And Its Relationship With Platelet Activation
Funder
National Health and Medical Research Council
Funding Amount
$101,039.00
Summary
Blood clots are critical to the development of heart attacks, which kill many thousands of Australians annually. Platelets are cells in the blood that play an essential role in formation of blood clots, and coronary disease is associated with platelet activation. This research study will investigate the nature of platelet activation in the arteries of the human heart, its relationship to activation of inflammatory cells, and to the severity of narrowings in the arteries of the human heart.
Activated Protein C As A Promoter Of Wound Healing
Funder
National Health and Medical Research Council
Funding Amount
$391,650.00
Summary
The healing of wounds is a complex process involving a number of stages, including coagulation, inflammation, remodelling and finally development of full strength skin. Impaired wound healing and-or skin ulcers occur in patients with peripheral arterial occlusive disease, deep vein thrombosis, diabetes, pressure sores and burns. Despite intense investigation, the precise mechanisms associated with impaired healing are poorly understood. APC is a serine protease that plays a central role in physi ....The healing of wounds is a complex process involving a number of stages, including coagulation, inflammation, remodelling and finally development of full strength skin. Impaired wound healing and-or skin ulcers occur in patients with peripheral arterial occlusive disease, deep vein thrombosis, diabetes, pressure sores and burns. Despite intense investigation, the precise mechanisms associated with impaired healing are poorly understood. APC is a serine protease that plays a central role in physiological anticoagulation. APC potently activates gelatinase A, an enzyme that plays a prominent role during the remodelling phase of wound healing and angiogenesis. Our preliminary experiments provide very strong evidence that APC accelerates wound healing using both cultured cells and a rat skin wounding model. There are three aims to this study. The first will use cell culture techniques to investigate the mechanisms of action of APC during wound healing. Secondly, we will expand our pilot studies on the effect of APC as a promoter of wound healing in vivo. These studies will examine the exact dosing and timing regime for APC, using a rat wound healing model. In addition, we will test the effect of APC on slow healing wounds, present in diabetic rats. Thirdly, we will determine whether APC is quantitatively or functionally deficient in human wound fluid derived from slow-healing wounds compared to wounds that heal normally. This is the first time that APC has been implicated in wound healing. It is envisaged that this work will ultimately lead to a novel topical treatment of APC to accelerate slow-healing wounds.Read moreRead less
Identification Of A New Thrombosis Mechanism Triggered By Dying Platelets
Funder
National Health and Medical Research Council
Funding Amount
$608,742.00
Summary
A severe reduction in blood flow (ischemia) to the intestines can trigger blood clot formation (thrombosis) in multiple organs, including the lungs. We have identified a new thrombosis mechanism that is triggered by the clumping of white blood cells in the intestines, leading to widespread thrombosis in the lung. Here we will investigate the mechanisms triggering this thrombosis mechanism with the ultimate aim of identifying more effective antithrombotic approaches.