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Elucidating The Mechanism And Function Of Extracellular Vesicle Formation During Cell Death
Funder
National Health and Medical Research Council
Funding Amount
$318,768.00
Summary
In humans, billions of cells will die daily as part of normal turnover in various organs. It is vital that dying cells are rapidly removed as their accumulation has been linked to autoimmunity and inflammation. To aid efficient removal of dead cells, dying cells can disassemble into smaller fragments for neighbouring cells to engulf. We aim to understand the machinery that control how dying cells can disassemble into smaller pieces and their function in efficient cell clearance and autoimmunity.
Renal Sympathetic Denervation As An Adjunct To Catheter-based Ventricular Tachycardia Abaltion
Funder
National Health and Medical Research Council
Funding Amount
$188,226.00
Summary
The most common cause of sudden death is lethal heart rhythms. Despite medications and medical procedures, many patients still suffer from these life-threatening rhythms. Treatment of the nerves around the kidneys may alter the production of hormones that contribute to these rhythms which could have a significant impact on these patients.
Regulation Of Autoimmunity By Non-apoptotic Caspases
Funder
National Health and Medical Research Council
Funding Amount
$318,768.00
Summary
Excessive cell death can lead to chronic inflammation and autoimmunity. Cells can die by different mechanisms including necroptosis which causes inflammation, and apoptosis which does not. Recent studies show that caspases, a component of the apoptosis pathway which accelerate cell death, also prevent immune activation by dying cells. I will investigate whether caspases contribute to autoimmune disease and whether caspases can dampen the inflammation that occurs during necroptotic cell death.
Pre-clinical Evaluation Of The LSD1 Inhibitor HCI-2509: Defining The Biomarkers Of Sensitivity And The Mechanisms Of Resistance
Funder
National Health and Medical Research Council
Funding Amount
$340,068.00
Summary
Despite aggressive multi-modal treatment strategies, limited progress in the treatment of Ewing sarcoma (paediatric bone malignancy), has been achieved over the past 30 years. As such, the advent of novel and targeted therapeutics with favourable efficacy/toxicity profiles are eagerly awaited. This proposal will investigate the therapeutic utility of LSD1 inhibition as a treatment for Ewing sarcoma and the underlying mechanisms of sensitivity/resistance to this unique agent.
Electrophysiologic Properties Of The Ventricular Myocardium Promoting Reentry
Funder
National Health and Medical Research Council
Funding Amount
$272,871.00
Summary
Ventricular tachycardia is a dangerous heart rhythm that usually occurs in people with prior heart attacks. These people often have scarring on their heart and the tachycardia occurs due to electrical activity forming a circuit around the scar. This study will examine the factors that cause ventricular tachycardia to begin by looking at the characteristics of the scarring.
Positive Allosteric Modulation Of Metabotropic Glutamate Receptor 5; A Novel Approach For The Treatment Of Schizophrenia And Cognitive Disorders
Funder
National Health and Medical Research Council
Funding Amount
$348,428.00
Summary
The metabotropic glutamate receptor subtype 5 (mGluR5) has emerged as an exciting new target for the treatment of schizophrenia and cognitive disorders. We will investigate novel drug-binding sites on these receptors with the aim to discover new therapeutics. These studies also aim to definitively characterize mGluR5 activity following treatment with novel compounds to improve our understanding of the normal function of these important receptors.
Innate lymphoid cells (ILCs) are found in the lining of the intestine and are part of the intricate crosstalk between the food we eat, good bacteria, epithelial cells and other immune cells. Without ILCs, the body is susceptible to infections through the intestinal tract. I will investigate the signals from nerve cells that control that activity of ILCs during infection to give us insights into pathways that activate ILCs in situations where they are reduced or inactive.