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Characterisation Of The Molecular Pathogenesis Of Cancer Cachexia Syndrome In Colorectal Cancer.
Funder
National Health and Medical Research Council
Funding Amount
$100,381.00
Summary
Cachexia is a hypermetabolic wasting syndrome involving depletion of both fat and muscle which affects 80% of cancer patients. The exact mechanisms of this syndrome are unknown at the molecular level and this affects our ability to predict, prevent or treat this problem. This study aims to elucidate the molecular mechanisms of cancer cachexia syndrome with a view to implementing nutritional, exercise and pharmacological interventions to prevent its onset.
The Bioactivity And Binding Partners Of Irukandji And Box Jellyfish Venom
Funder
National Health and Medical Research Council
Funding Amount
$596,950.00
Summary
Venom from the Box Jellyfish and Irukandji jellyfish are considered the most leathal known to science yet precious little is known on the nature of these secretions or how they harm humans. This study aims to fully characterise bioactive proteins in jellyfish venom and attempt to block their activity using regulatory-approved and experimental drugs.
The Dengue Virus Glycoprotein NS1 Binds Cholesterol And Mediates Cellular Activation
Funder
National Health and Medical Research Council
Funding Amount
$632,029.00
Summary
Cholesterol has been shown to play a vital role in the life cycle of many viruses. This project will investigate the basis of dengue virus interaction with this important host molecule and along with investigations of how dengue is able to stimulate host cells, will provide new insights into the way these viruses cause severe disease. Findings from this study will also aid in the development of new drug strategies for dengue and related viruses such as West Nile virus.
Protein Prenylation And Inflammation: New Insights Into The Pathophysiology And Treatment Of Mevalonate Kinase Deficiency
Funder
National Health and Medical Research Council
Funding Amount
$715,755.00
Summary
This project is focused on a genetic, potentially fatal, inflammatory disease that appears in infancy. We have developed a new way of detecting the underlying defect as well as the first animal models that have the same genetic mutations and mimic the disease. With these revolutionary new approaches, we will discover the exact cause of the inflammation, test a new way of diagnosing the disease, and identify new and better therapies that treat the underlying cause rather than just the symptoms.
Targeting Autophagy As A Means Of Control Of Cytokine Production In SLE
Funder
National Health and Medical Research Council
Funding Amount
$616,518.00
Summary
Systemic lupus erythematosus (SLE, or lupus) is a common immune disease that causes organ damage and loss of life, chiefly affecting young women. There is no cure for SLE. We have discovered that a natural process called 'autophagy' could be a way to limit inflammation during SLE. In this project we will discover whether this could lead to a new way to treat this disease.
RP105 Is A New Innate Immune Receptor For Mycobacterium Tuberculosis
Funder
National Health and Medical Research Council
Funding Amount
$525,583.00
Summary
Tuberculosis (TB) is a major global health threat that causes 1.7 million deaths every year. This study will characterise the interactions between the bacteria that cause TB and a new immune sensor. We found that this sensor is involved in controlling TB and this project will determine how it contributes to the immune defence against the infection. Such knowledge will help improve patient management and develop an effective vaccine and better treatments for this devastating disease.
Dengue Virus NS1 Protein As A Mediator Of Pathology
Funder
National Health and Medical Research Council
Funding Amount
$621,979.00
Summary
Dengue virus is an increasing problem in the tropical world, with estimated infection of more than 300 million people annually. Severe dengue disease can cause life-threatening bleeding and shock. Our project investigates the basis for the pathology of the disease. We have found that a viral protein termed NS1 binds to a receptor on immune cells and leads to production of inflammatory proteins which can promote vessel leakage. We will investigate drugs blocking this, in a disease model.
Engineering The Second Generation Of Growth Factors And Cytokines For Regenerative Medicine Applications
Funder
National Health and Medical Research Council
Funding Amount
$538,848.00
Summary
Growth factors and cytokines have a great potential for regenerative medicine applications. Yet, most of these molecules have failed to show efficacy in humans or raised major safety concerns, due to high dosing and inappropriate delivery systems. In this project, we seek to engineer the next generation of growth factors and cytokines to display much better effectiveness at low doses. We will directly impact applications for chronic wounds, skin scar prevention, and bone regeneration.
Asthma is a significant burden to the health care system and to individual sufferers. Currently we can treat asthma with corticosteroids to reduce inflammation in the lung but the side effects of these medications, particularly in children, make them less than ideal treatments. In order to design a more specific treatment for asthma, which would only target the inflammatory cells which are involved in the lung, we need to understand how these cells behave and what initiates the cascade of events ....Asthma is a significant burden to the health care system and to individual sufferers. Currently we can treat asthma with corticosteroids to reduce inflammation in the lung but the side effects of these medications, particularly in children, make them less than ideal treatments. In order to design a more specific treatment for asthma, which would only target the inflammatory cells which are involved in the lung, we need to understand how these cells behave and what initiates the cascade of events in the lung. This project is designed to investigate how chemical mediators, cytokines, are produced by various cells in the lung and how they induce lung cells to make structural changes to the lung tissue and increase the inflammation. The source and specific types of cytokines released are being investigated to provide important information regarding the disease process of asthma. From this new knowledge, design of specific new treatments, with fewer unwanted side-effects, should be possible.Read moreRead less
Role Of The Natural Killer Complex In The Control Of Murine Malarial Pathogenesis
Funder
National Health and Medical Research Council
Funding Amount
$487,500.00
Summary
Natural Killer (NK )cells are an essential arm of the innate immune system. NK cell function is controlled by a series of cell surface receptors encoded within a defined genetic region named the Natural Killer Complex (NKC). This region appears to be highly polymorphic both in mice and humans. It is known that different mouse strains, which differ in the expression of NKC molecules have distinct ability to mount inflammatory responses during infection. In fact, we have previously shown that the ....Natural Killer (NK )cells are an essential arm of the innate immune system. NK cell function is controlled by a series of cell surface receptors encoded within a defined genetic region named the Natural Killer Complex (NKC). This region appears to be highly polymorphic both in mice and humans. It is known that different mouse strains, which differ in the expression of NKC molecules have distinct ability to mount inflammatory responses during infection. In fact, we have previously shown that the differential expression of NKC molecules in mice accounts for the degree of susceptibility to Plasmodium berghei-mediated cerebral malaria, a syndrome that accurately reproduces malarial disease induced by Plasmodium falciparum in humans and that results from an exacerbated pro-inflammatory response to infection. Since the NKC comprises several genes and multi-gene families, the main objective of this proposal is to identify which molecule-s within this genetic region are responsible for the induction of cerebral malaria pathogenesis. Our preliminary results indicate that an activation receptor named Ly49D, which is only expressed on the surface of NK cells from cerebral malaria-susceptible mice, plays a key role in disease-induction. Activation of Ly49D induces NK cells to secrete large amounts of IFN-gamma, a pro-inflammatory cytokine known to mediate cerebral-malaria pathogenesis. We will characterize the immunological function of Ly49D+ NK cells during P. berghei infection and determine whether these cells are the main source of IFN-gamma production. We will also identify the ligand (from parasite or host origin) responsible for the stimulation of this NKC activation receptor during malaria infection. The identification and characterization of these NKC receptors will provide new insights to explain the immunological basis of malarial pathogenesis and could lead to the development of therapeutical approaches designed to prevent severe malarial disease.Read moreRead less