Defining The Molecular Effectors Of Gene/environment Interaction On Mouse Heart Development
Funder
National Health and Medical Research Council
Funding Amount
$749,271.00
Summary
One third of all birth defects involve the heart, and are the most common cause of infant death. Some defects are due to genetic factors, but others arise when the pregnant mother is exposed to environmental stress. We will examine how one stress (low oxygen levels) causes abnormal heart formation in the embryo, look at what causes this at a molecular level, and explore if such stress increases the risk of heart defects in families with a history of such abnormalities
Therapeutic Targeting Of A New Growth Factor In Mesothelioma
Funder
National Health and Medical Research Council
Funding Amount
$317,775.00
Summary
Malignant mesothelioma is an aggressive and incurable cancer. This study will build on our recent data showing a protein termed FGF-9, not previously linked with mesothelioma, could significantly stimulate mesothelioma growth. This project will examine the biologic activities of FGF-9 and its receptors in mesothelioma, and the therapeutic benefits of antagonizing FGF-9 in mesothelioma in vivo.
Identification Of Novel Biomarkers And Risk Factors For Cardiovascular Disease
Funder
National Health and Medical Research Council
Funding Amount
$425,048.00
Summary
Heart disease is the leading cause of death in Australia. In this fellowship, I will investigate different markers in the blood and risk factors that can help to identify people at an increased risk of developing heart disease. The ultimate aim of this project is to identify blood markers or factors that can be used to identify and treat people at the early stages of heart disease, thus reducing the death rate and associated economic burden of the disease.
Does Enhanced Vitamin D Activity In Bone Heal The Skeleton In Disorders Of FGF23 Excess?
Funder
National Health and Medical Research Council
Funding Amount
$855,925.00
Summary
X-linked hypophosphatemia (XLH) is a genetic disorder which results in phosphate wasting and rickets. This severe disorder has no effective treatment. We have compelling new evidence that the rickets in XLH is not primarily a disorder of low blood phosphate, but rather specific issue of low cellular levels and activity of vitamin D (1,25D) within bone. This proposal is designed to specifically demonstrate this new concept and outline a new paradigm for a new XLH treatment.