Preventing Stroke From Arteriovenous Malformations Using Precision Thrombosis
Funder
National Health and Medical Research Council
Funding Amount
$993,866.00
Summary
Brain arteriovenous malformations are rupture-prone blood vessels that cause stroke in children and young adults. One third of patients have no current treatment options. We aim to develop new medicines that cause blockage of the abnormal vessels, thus preventing them from bleeding and causing stroke. Focused radiation is used to produce molecular changes in the abnormal vessels; these molecules are then the target for the new medicines. We will develop several new drugs for clinical testing.
Bivalent Analgesics: Rational Design Of Selective Ion Channel Inhibitors With Optimised Mechanism Of Action
Funder
National Health and Medical Research Council
Funding Amount
$904,890.00
Summary
The so-called 'opioid crisis' leading to the death of millions of people worldwide has highlighted the urgent need for development of novel safe and efficacious pain killers without addictive potential. This proposal aims to rationally design novel analgesic compounds by linking different classes of ion channel modulators with desirable properties.
A Wireless Electric Nerve-guide For Peripheral Nerve Repair
Funder
National Health and Medical Research Council
Funding Amount
$805,064.00
Summary
We aim to deliver a radical new precision intervention for peripheral nerve repair to improve the lives of people with peripheral nerve damage. Drawing from our recently awarded work on 'electric neural tissue engineering', we will pre-clinically test our invention of a unique clinically-amenable electric nerve-guide (e-nerve-guide), designed to act as a protective nerve conduit and wirelessly electrically-stimulate damaged nerves for their regeneration and restoration of function.
Targeting Neurovascular Communication As A Novel Way Of Reducing Vision Loss In Diabetes
Funder
National Health and Medical Research Council
Funding Amount
$986,663.00
Summary
Diabetes is a leading cause of blindness. Here, we evaluate whether diabetes causes changes in the way neurons signal to blood vessels, and whether blocking some of the signals from neurons reduces blood vessel abormalities. Overall, this information is critical to our understanding of the early changes that occur during diabetes and whether novel treatments used early in diabetes can prevent long term changes and vision loss.
Epigenetic Reprogramming Of Calcified Vascular Smooth Muscle Cells As A Treatment For Vascular Calcification
Funder
National Health and Medical Research Council
Funding Amount
$1,285,195.00
Summary
Pathological hardening of blood vessels, or vascular calcification, is a frequent and deadly complication of many cardiovascular disorders. It is caused by the irreversible change in mature vascular smooth muscle cells (the main cell type in the blood vessel walls) to a bone-forming cell type. We have now identified a new gene that can potentially revert calcified vascular cells back to their physiological state. This represents a promising new approach for treatment of vascular calcification.
Influenza A Viral Infection And Pregnancy Complications
Funder
National Health and Medical Research Council
Funding Amount
$1,346,858.00
Summary
Pregnant women who contract influenza are 5 times more likely to be hospitalised than the general population. Babies of mothers with influenza are also associated with increased perinatal mortality rates. We hypothesise that influenza infection in pregnancy significantly impairs the maternal vascular system resulting in maternal and foetal morbidity. Outcomes from this research may change current treatment modalities to improve maternal and foetal outcomes complicated by influenza infection.
An Integrative Approach To Define And Attenuate Genomic Risk Of Coronary Artery Disease
Funder
National Health and Medical Research Council
Funding Amount
$988,454.00
Summary
One in four individuals that have a heart attack do not have traditional risk factors such as high blood cholesterol levels. This highlights the importance of 'family history', which we can now quantify as 'genetic risk'. These studies will determine (i) which genes are important in contributing to this genetic risk (ii) how these genes change biological pathways to increase risk and (iii) the effectiveness of modulating these biological pathways to reduce the risk of heart disease.
HTLV-1 is a lifelong infection of immune cells that sustains high infection rates up to 45% in key Australian communities. Despite HTLV-1 causing serious malignancy and inflammatory co-morbidities that shorten lifespan, few biomedical interventions are available. We will examine how the virus grows and alters immune responses to cause disease. With this, we can develop antiviral treatments to reduce virus infected cells, and make new diagnostic biomarker assays suitable for remote settings.
Structure And Biophysical Analysis Aided Design Of Novel Toxoid Vaccines For A Major Class Of Bacterial Toxins.
Funder
National Health and Medical Research Council
Funding Amount
$608,425.00
Summary
Inactivated bacterial toxins (toxoids), such as the tetanus vaccine, are safe and effective vaccines. Cholesterol dependent cytolysins (CDCs) are bacterial toxins produced by many important human pathogens including Group A Streptococcus (GAS) and Pneumococcus. GAS has no available vaccine and Pneumococcus does not have a universal vaccine. We have developed a new way of inactivating CDCs based on new knowledge of how they target human cells and will use this knowledge to make new vaccines.
Targeting The Crosstalk Between Metabolism And Epigenetics To Treat Liver Fibrosis
Funder
National Health and Medical Research Council
Funding Amount
$1,032,259.00
Summary
Virtually all liver disease related morbidity and mortality is a consequence of fibrosis that culminates in liver failure or liver cancer. Since anti-fibrotic drugs are not available, new approaches to drug development are required. We have discovered a novel strategy for such drug development by modifying the expression of a specific gene (RARRES1) in a highly targeted manner and thereby interrupting the energy production that is needed by cells to drive fibrosis.