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Manipulation Of Intracellular Arginine Content In Endothelial Cells
Funder
National Health and Medical Research Council
Funding Amount
$476,264.00
Summary
The lining layer of blood vessels (termed the 'endothelium') plays a vital role in the control of blood vessel function. Recently it has been shown that risk factors for heart and vascular disease (smoking, high blood pressure, high cholesterol and diabetes), heart attack and heart failure are associated with an abnormally functioning endothelium. In particular, the endothelium maintains blood vessels in a relaxed state, prevents the formation of blood clots (which may cause heart attack and str ....The lining layer of blood vessels (termed the 'endothelium') plays a vital role in the control of blood vessel function. Recently it has been shown that risk factors for heart and vascular disease (smoking, high blood pressure, high cholesterol and diabetes), heart attack and heart failure are associated with an abnormally functioning endothelium. In particular, the endothelium maintains blood vessels in a relaxed state, prevents the formation of blood clots (which may cause heart attack and stroke) and prevents the thickening of blood vessels. These important actions of the endothelium are explained by the production of nitric oxide (NO) a small chemical messenger that is derived from an amino acid, L-arginine, which circulates in blood. The amount of NO produced by endothelial cells is very dependent on the amount of arginine available, and this is determined by a careful balance between the amount of arginine taken (transported) into cells and the amount that is destroyed (metabolized) by an enzyme called arginase. Research undertaken in our laboratory is directed at understanding the important balance between arginine transport and arginase activity, as a basis for identifying new ways to prevent and treat cardiovascular disease. The current proposal describes a series of studies which will critically examine the importance of arginine transport and arginase activity, using transgenic models of over-activity and under-activity of these systems. Once established we will test the possibility that manipulating these systems may prevent atherosclerosis.Read moreRead less
Platelet Receptor Shedding In Stroke And Thrombosis
Funder
National Health and Medical Research Council
Funding Amount
$552,503.00
Summary
In response to tissue injury and bleeding, blood platelets use receptors to form a thrombus (blood clot) and block further loss of blood and aid tissue repair. In inflammation or disease, abberant platelet activation can form a thrombus within cerebral (stroke) or coronary vessels (heart attack). We examine how a thrombus-limiting step (platelet receptor shedding) is triggered in thrombus-forming platelets, and if shed receptor can be used as a blood marker of abberant platelet activation.
Investigation Of The Role For GPVI In Platelet Function And Thrombosis
Funder
National Health and Medical Research Council
Funding Amount
$542,772.00
Summary
Blood cells play an important role in maintaining healthy blood vessels. We are studying the role of platelets in blood clots following vessel injury. However, while critical for normal blood vessel maintenance, these cells also contribute to diseases including thrombosis. We will examine how an important platelet receptor called GPVI promotes blood clot formation, and examine whether combining anticoagulant drugs with GPVI deficient platelets leads to a more effective anticlotting approach.
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.
Activation Of Persistent Na+ Current During Hypoxia: Oxygen Sensors, Na+ Channel Subunits And Drugs.
Funder
National Health and Medical Research Council
Funding Amount
$338,820.00
Summary
Cardiac arrhythmias (a variation in the normal rhythm of a heart beat) and stroke are a major causes of sudden death in industrialised countries. Stroke is the second greatest killer in Australia, claiming 12, 133 lives in 1997. It is also the leading cause of long term disability in adults, costing ~$630 million-year. Both stroke and arrhythmias are often caused by occlusion (closure or blockage) of arteries which deprives the brain or the heart of oxygen (hypoxia). Clinicians and pharmaceutica ....Cardiac arrhythmias (a variation in the normal rhythm of a heart beat) and stroke are a major causes of sudden death in industrialised countries. Stroke is the second greatest killer in Australia, claiming 12, 133 lives in 1997. It is also the leading cause of long term disability in adults, costing ~$630 million-year. Both stroke and arrhythmias are often caused by occlusion (closure or blockage) of arteries which deprives the brain or the heart of oxygen (hypoxia). Clinicians and pharmaceutical companies are very aware of the need for better treatments for these disorders. While we understand some of the cellular changes and events that take place when a cell is deprived of oxygen, we lack the precise knowledge of the critical timing and the sequence of events that eventually lead to cell damage and death. It can be appreciated that this knowledge would greatly aid the development of new drug treatments. The market for new drugs to prevent cell damage during heart attack and stroke has been estimated at ~$2 billion. This project has great clinical significance since we are looking at inhibiting the cascade set in motion by hypoxia at an early stage via a persistent sodium current. We believe this will give better and more effective treatments than are currently available.Read moreRead less
Role Of Tenascin-C And TLR-4 In Carotid Atherosclerosis Related Stroke
Funder
National Health and Medical Research Council
Funding Amount
$308,071.00
Summary
It is estimated that approximately 10,000 Australians per year suffer from strokes related to neck artery disease. Warning signs often go undiagnosed and unreported. Currently there are no blood tests available for early simple diagnosis and few specific drugs available to reduce the number of strokes. Based on preliminary studies we will investigate the role of a novel protein and its related pathway in stroke. We will also study the value of these proteins as a blood test for this problem.
VITATOPS Study - A Randomised, Double-blind, Placebo-controlled Trial Of Vitamins To Prevent Stroke.
Funder
National Health and Medical Research Council
Funding Amount
$1,477,963.00
Summary
Stroke is one of the most important causes of death and long-term disability in developed countries. Hardening of the arteries (atherosclerosis) is the major cause of stroke and heart attacks. High blood pressure, high blood concentrations of cholesterol, cigarette smoking and diabetes accelerate the formation of atherosclerosis, but they do not account for all strokes and heart attacks caused by atherosclerosis. There is now increasing evidence that high blood concentrations of homocysteine, a ....Stroke is one of the most important causes of death and long-term disability in developed countries. Hardening of the arteries (atherosclerosis) is the major cause of stroke and heart attacks. High blood pressure, high blood concentrations of cholesterol, cigarette smoking and diabetes accelerate the formation of atherosclerosis, but they do not account for all strokes and heart attacks caused by atherosclerosis. There is now increasing evidence that high blood concentrations of homocysteine, a normal protein in the blood, are another major causal risk factor for atherosclerosis (and stroke and heart attacks). Furthermore, blood concentrations of homocysteine can be lowered by about one quarter with simple, safe and inexpensive multivitamin therapy (folic acid, vitamin B12, and vitamin B6). However, despite the potentially massive public health benefits of such a strategy, it remains to be demonstrated in properly designed clinical trials that lowering homocysteine levels in the blood actually prevents stroke and heart attack. The VITATOPS trial is the only ongoing randomised, double-blind, placebo-controlled trial in the world which aims to determine whether multivitamin therapy (folic acid 2 mg, vitamin B12 0.5 mg, and vitamin B6 25 mg) prevents recurrent stroke and heart attacks in patients who have suffered a recent stroke.Read moreRead less
VITATOPS Study - A Randomised, Double-blind, Placebo-controlled Trial Of Vitamins To Prevent Stroke.
Funder
National Health and Medical Research Council
Funding Amount
$470,887.00
Summary
The VITAmins To Prevent Stroke (VITATOPS) trial is the only ongoing randomised, double-blind, placebo-controlled trial in the world which aims to determine whether multivitamin therapy (folic acid 2 mg, vitamin B12 0.5 mg, and vitamin B6 25 mg) prevents recurrent stroke and heart attacks in patients who have suffered a recent stroke. To date more than 7,500 patients have been randomised. Ongoing support is requested to complete the follow-up of 8,000 patients by middle of 2009.
Substance P Antagonists As A Novel Therapeutic Intervention In Stroke
Funder
National Health and Medical Research Council
Funding Amount
$318,267.00
Summary
Stroke is the major cause of disability in adults over 45 years of age in Australia. The economic and social cost of stroke is enormous with billions of dollars spent each year on the management and rehabilitation of stroke patients. Despite the enormity of this public health problem, no effective treatment currently exists. A number of studies have now demonstrated that much of the morbidity following stroke is associated with the breakdown of the blood brain barrier, development of oedema, and ....Stroke is the major cause of disability in adults over 45 years of age in Australia. The economic and social cost of stroke is enormous with billions of dollars spent each year on the management and rehabilitation of stroke patients. Despite the enormity of this public health problem, no effective treatment currently exists. A number of studies have now demonstrated that much of the morbidity following stroke is associated with the breakdown of the blood brain barrier, development of oedema, and subsequent brain damage in areas surrounding the central region of the stroke. These events develop over hours to days following the stroke and are known as secondary injury. This delayed progression of injury suggests that appropriate pharmacologic intervention can prevent, or at least attenuate, this secondary injury process with a resultant improvement in outcome. Nonetheless, few interventions are available that can limit this development. Our own recent studies have demonstrated that regions in brains which demonstrate the presence of stroke also exhibit signs of neurogenic inflammation, which has been associated with oedema formation, oxidative damage and cell death in other tissues. Although a number of neuropeptides have been implicated in this process, it is thought that substance P release is closely associated with these pathophysiological processes. Thus, inhibiting substance P binding may offer a novel therapeutic approach to attenuating oedema formation and the development of neurologic deficits following stroke. This proposal will utilise a combined biochemical, pharmacologic and behavioural approach to characterize the role of neurogenic inflammation in the development of oedema and neurologic deficits following stroke. Moreover, we will develop a novel pharmacotherapy that can potentially be used in the treatment of clinical stroke.Read moreRead less
Effects And Mechanisms Of Direct Cardiac Compression In Interruption Of Myocardial Remodelling In Chronic Heart Failure.
Funder
National Health and Medical Research Council
Funding Amount
$392,250.00
Summary
Heart failure (HF) is a disease where the heart pumping function is insufficient to provide adequate blood supply to the rest of the body. It is a highly debilitating disease affecting nearly 10 million people worldwide and has a <50% one-year survival in severe cases. Despite significant advances in pharmacotherapy, heart transplant is the only alternative for severe HF but is restricted by lack of donor organs to only ~ 5% of those requiring it. Research has shown that progression of HF is ....Heart failure (HF) is a disease where the heart pumping function is insufficient to provide adequate blood supply to the rest of the body. It is a highly debilitating disease affecting nearly 10 million people worldwide and has a <50% one-year survival in severe cases. Despite significant advances in pharmacotherapy, heart transplant is the only alternative for severe HF but is restricted by lack of donor organs to only ~ 5% of those requiring it. Research has shown that progression of HF is related to many subsequent changes after an initial insult. In addition to pumping failure, HF is associated with deranged compensatory responses such as neurohumoral over-activation, heart chamber enlargement, loss of functional cells, increase of inflammatory mediators and changes in cardiac skeleton (extracellular matrix). The changes in the heart are collectively known as remodelling. Mechanical heart assist is now considered a potential destination therapy for severe HF, superior to pharmacotherapy alone. Improvement of cardiac pumping function and even successful weaning from devices has been reported, along with observations of reverse remodelling. The success of this approach has been limited however, particularly with HF due to coronary disease, the most prevalent form. We developed a novel HeartPatch mechanical assist device to compress the heart from its outer surface. It gives support to both main chambers and avoids blood contact, a feature of currently available devices associated with complications such as blood clotting and infection. Our device has proved effective in animals with acute HF and even with cardiac arrest. We propose to study the effects of our device on the process of remodelling in HF with coronary disease in a controlled manner. The project will enhance understanding of the mechanisms involved in reverse remodelling and further the development of a device which may potentially benefit many severe HF patients.Read moreRead less