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Neurogenic Mechanisms Of Cardiovascular Risk In The Metabolic Syndrome: Benefits Of Lifestyle Interventions
Funder
National Health and Medical Research Council
Funding Amount
$328,194.00
Summary
One in four adult Australians has the 'metabolic syndrome' (MetS), a clustering of metabolic and heart disease risk factors associated with abdominal obesity. Sympathetic nervous system (SNS) activity is increased in the MetS resulting in enhanced release of the stress hormone 'noradrenaline' . This project will examine the biological and genetic determinants of enhanced SNS activity and the benefits of lifestyle interventions (weight loss, weight loss maintenance and aerobic exercise).
TNF Receptor 2 And INOS Genes In Basis Of Cardiovascular Disease
Funder
National Health and Medical Research Council
Funding Amount
$242,545.00
Summary
Cardiovascular diseases account for almost half of total deaths in Australia and other industrialized countries. Hypertesnion, coronary artery disease and diabetes are major contributing factors to mortality and morbidity. It is well known that each of these have a genetic basis, as well as having environmental influences. A key focus of reseach internationally is discovery of the molecular mechanisms involved. Our recent findings point to a role for the inducible nitric oxide synthase gene (whi ....Cardiovascular diseases account for almost half of total deaths in Australia and other industrialized countries. Hypertesnion, coronary artery disease and diabetes are major contributing factors to mortality and morbidity. It is well known that each of these have a genetic basis, as well as having environmental influences. A key focus of reseach internationally is discovery of the molecular mechanisms involved. Our recent findings point to a role for the inducible nitric oxide synthase gene (which generates nitric oxide, a potent blood vessel dilator) and tumor necrosis factor receptor 2 gene (whose product sends signals to the former gene) in heart, kidney and blood vessel diseases. We now propose to find the actual gene changes responsible and the molecules and mechanisms involved. By elucidating roles in cardiovascular physiology and pathology the importance of these for cardiovascular function will be ascertained, and may open up new avenues for treatment.Read moreRead less
Defective Tracfficking Of HERG K+ Channels: Risk Stratification In Patients With Long QT Syndrome Type 2.
Funder
National Health and Medical Research Council
Funding Amount
$483,406.00
Summary
Disturbances of the rhythm of the heartbeat are a major cause of death and disability. Due to the sudden onset and rapidity of death with cardiac arrhythmias it is important to be able to predict in advance who is most at risk. In this study we will investigate whether it is possible to develop in vitro assays to stratify risk in patients with congenital long QT syndrome type 2, an inherited arrhythmia syndrome.
The Role Of Calcium And TRPC Channels In Sinoatrial Node Ageing
Funder
National Health and Medical Research Council
Funding Amount
$385,301.00
Summary
The failure of pacemaker function is a common clinical problem in the elderly who become more susceptible to cardiac arrhythmias. We recently discovered a new calcium channel called the transient receptor potential canonical channel (TRPC) in the pacemaker cells. The aim of this research is to study the role of TRPC channels in pacemaker ageing. Improved understanding of the mechanisms of the pacemaker ageing may provide new therapeutic strategies for reducing the risk of cardiac arrhythmias.
The Role Of The Calcineurin Negative Regulator, DSCR1, In Heart Development And Hypertrophy.
Funder
National Health and Medical Research Council
Funding Amount
$431,310.00
Summary
Congenital heart defects in the young and heart disease later in life place a heavy burden on our society in terms of illness, disability and death and are very costly in terms of the health care budget. Failure of heart valve development and holes in the heart, are very common abnormalities occurring in nearly 1 % of all live births. This type of anomaly is also observed in about 44 % of individuals with Down syndrome, which results when individuals carry an extra copy of chromosome 21. Thus, i ....Congenital heart defects in the young and heart disease later in life place a heavy burden on our society in terms of illness, disability and death and are very costly in terms of the health care budget. Failure of heart valve development and holes in the heart, are very common abnormalities occurring in nearly 1 % of all live births. This type of anomaly is also observed in about 44 % of individuals with Down syndrome, which results when individuals carry an extra copy of chromosome 21. Thus, it is likely that a gene located on human chromosome 21 contributes to this pathology and indeed our work on the identification of genes with the potential to cause the heart defect observed in Down syndrome, has led to the discovery of a gene called DSCR1. DSCR1 is a negative regulator of a biological pathway which when disturbed in the heart can lead to developmental heart malformations, similar to the type seen in Down syndrome, and when over stimulated can result in the abnormal growth of the heart seen in humans with hypertension and heart disease. If we are to make rational decisions about the design of potential treatments for heart defects and disease, we firstly need to understand how these biological pathways work and how molecules such as DSCR1 regulate them. We aim to investigate how DSCR1 functions by generating mice that lack the gene, to see what happens when it is missing and mice over expressing the gene to investigate the consequences of elevated levels of DSCR1 analogous to the situation in Down syndrome.Read moreRead less
State-dependence Of Drug Binding To HERG K+ Channels.
Funder
National Health and Medical Research Council
Funding Amount
$397,224.00
Summary
In recent years, it has become apparent that a wide range of prescription drugs can cause inadvertent inhibition of a potassium channel in the heart known as hERG, resulting in an increased risk of cardiac arrhythmias and death. This has prompted the withdrawal from the market of 9 drugs and the introduction of mandatory testing of all drugs for inhibition of hERG channels. In this proposal we seek a molecular explanation for the promiscuity of drug binding to hERG channels
State Dependent Drug Binding To The Human Ether-à-go-go Related Gene Channel
Funder
National Health and Medical Research Council
Funding Amount
$33,193.00
Summary
Heart rhythm disturbance is a common cause of death in our community. In a subset of patients the heart rhythm disturbance is caused by mutations in genes that encode for special proteins called ion channels. However, even in patients without a mutation certain drugs can cause the same problem. Such drugs need to be identified early in their development but current methods to do this are inaccurate. An understanding of how these drugs disturb the heart rhythm will allow more accurate testing.