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Development Of A Preventive Strategy For Rheumatic Heart Disease Using An Experimental Model
Funder
National Health and Medical Research Council
Funding Amount
$370,846.00
Summary
Based on animal studies, we aim to demonstrate that the worsening of heart damage seen in patients with rheumatic heart disease (RHD) is due to repeated infections with bacteria (group A streptococci: GAS). The heart damage is caused by continual immune damage to the heart and valves and this has adverse effects on heart function. We will also investigate a novel way to prevent the development of RHD.
Duty Ratio: A Simple Method For Quantifying Loop Gain During Breathing Instability
Funder
National Health and Medical Research Council
Funding Amount
$343,514.00
Summary
This proposal presents a new method for calculating the severity of sleep disordered breathing in patients. The proposal also tests the effectiveness of our method in experiments in animals and humans. The method, which requires no intervention in the patient, offers promise as a means for testing the efficacy of treatments for the unstable breathing pattern found in patients with heart failure in whom the presence of unstable breathing is associated with poor outcome.
Guidance Of Heart Failure Management Programs By Risk Assessment
Funder
National Health and Medical Research Council
Funding Amount
$991,654.00
Summary
After admission with acute heart failure (HF), readmissions to hospital are frequent. This Partnership project aims to reduce HF readmissions by using data linkage to target community services, developing a HF readmission prediction score, and applying this to a novel, variable intensity HF management program, so resources are directed towards the highest risk patients. The study will evaluate the cost-effectiveness of this approach and provide educate community-based providers on the process.
Role Of Calcium Stores And Phosphate Channels In Muscle Fatigue
Funder
National Health and Medical Research Council
Funding Amount
$221,640.00
Summary
Muscles become weaker when ever they are used intensively; this is the familiar muscle fatigue. We are studying the mechanism of muscle fatigue and believe it is caused by depletion of a store of calcium inside the muscle. We suspect the store of calcium declines because phosphate, which is a product of muscle metabolism, enters the calcium store and precipitates as calcium phosphate. Currently we are trying to prove this hypothesis and extend it by studying the channels through which phosphate ....Muscles become weaker when ever they are used intensively; this is the familiar muscle fatigue. We are studying the mechanism of muscle fatigue and believe it is caused by depletion of a store of calcium inside the muscle. We suspect the store of calcium declines because phosphate, which is a product of muscle metabolism, enters the calcium store and precipitates as calcium phosphate. Currently we are trying to prove this hypothesis and extend it by studying the channels through which phosphate passes from the muscle cell into the calcium store. It may be possible to find or design drugs which minimise the movement of phosphate through this channel and such a drug might reduce the component of fatigue caused by this mechanism. Such a drug might benefit patients whose normal activities are limited by muscle fatigue; this includes patients with any disabling muscle disease, such as muscular dystrophy or stroke, and patients with heart failure. In addition elderly people suffer a loss of muscle bulk and the remaining muscle is easily fatigued causing loss of mobility and independence; so the elderly might also benefit from such a drug.Read moreRead less
The Structural Basis For Amyloid Formation By Human Apolipoproteins
Funder
National Health and Medical Research Council
Funding Amount
$210,990.00
Summary
Amyloid formation is considered an abnormal state of protein aggregation that accompanies numerous medical conditions, notably Alzheimer disease, Parkinson's disease, the transmissible spongiform encephalopathies (e.g. scrapie, Creutzfeldt-Jakob disease) and metabolic diseases such as diabetes. These diseases involve a variety of normally non-fibrillar proteins with at least 20 human proteins identified as components of different types of amyloid. The current wide publicity given to bovine spong ....Amyloid formation is considered an abnormal state of protein aggregation that accompanies numerous medical conditions, notably Alzheimer disease, Parkinson's disease, the transmissible spongiform encephalopathies (e.g. scrapie, Creutzfeldt-Jakob disease) and metabolic diseases such as diabetes. These diseases involve a variety of normally non-fibrillar proteins with at least 20 human proteins identified as components of different types of amyloid. The current wide publicity given to bovine spongiform encephalopathy (BSE) disease and the potential impact on human health highlights the importance of developing strategies for treating these conditions. The prevalence of apolipoproteins in atherosclerotic amyloid deposits and senile plaques suggests a general propensity for human apolipoproteins to form pathogenic amyloid fibrils. Our recent observations that lipid-free human apolipoprotein C-II (apoC-II) forms ribbon-like fibrils in vitro provides an experimental system to explore this phenomenon. We propose to determine the structural requirements for the formation of amyloid fibrils human apoC-II and whether lipid-free human apolipoproteins form mixed-amyloid fibrils. Future strategies for treatment require better information on amyloid structure, the potential for mixed amyloid formation and the role of in vivo factors such as lipids and macromolecular crowding in regulating amyloid growth.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
Beta-Adrenergic Activation: A Double-edged Sword On Cardiac Angiogenesis
Funder
National Health and Medical Research Council
Funding Amount
$365,126.00
Summary
We will test our hypothesis that activation of beta-adrenergic receptors (b-AR) regulates significantly on growth of blood vessels in the heart. While initialy promoting vessel growth, prolonged stimulation of b-AR, a situation seen with diseased hearts, suppresses vessel growth thereby promoting disease progression. This hypothesis is strongly supported by our recent experimental findings and would have important clinical implication on the treatment of patients with heart disease.