Prevention Of Pleural Adhesion Formation By Treatment With Growth Factors
Funder
National Health and Medical Research Council
Funding Amount
$268,000.00
Summary
Damage to the lining of the chest and abdominal cavities and to cells covering the lungs and other internal organs by infection or surgery almost always results in the formation of adhesions. Adhesions are bridges of fibrous material between organs and the body wall. In the chest cavity they can prevent the effective drainage of fluids that build up during infection or after injury leading to deterioration of health and even death. In the abdominal cavity they are a major cause of intestinal obs ....Damage to the lining of the chest and abdominal cavities and to cells covering the lungs and other internal organs by infection or surgery almost always results in the formation of adhesions. Adhesions are bridges of fibrous material between organs and the body wall. In the chest cavity they can prevent the effective drainage of fluids that build up during infection or after injury leading to deterioration of health and even death. In the abdominal cavity they are a major cause of intestinal obstruction and female infertility. In Australia, adhesions affect 9,500 patients annually, accounting for 6% of all hospital readmissions at a cost of over $100 million. This project will use animal models to investigate the specific role of a growth factor called hepatocyte growth factor (HGF) on the healing of the cells lining the internal body cavity and its effect on inhibiting adhesion formation. Using genetically manipulated mice, drug delivery and gene therapy approaches, the effect of changing the levels of HGF in tissues lining the internal body cavities on repair and adhesion formation will be assessed and mechanisms of action elucidated . A better understanding of the way cells lining these cavities heal and the factors that can improve the healing process, may lead to the development of novel therapies to prevent adhesion formation, which will benefit all future patients with chest cavity infections and those who undergo thoracic and abdominal surgery.Read moreRead less
Role Of Plzf – Sall4 Interactions In Germline Progenitor Function And Development
Funder
National Health and Medical Research Council
Funding Amount
$565,079.00
Summary
PLZF and SALL4 are critical stem cell factors and mutations in these genes are associated with developmental defects and cancer. SALL4 mutations are responsible for the malformation disease Duane-radial ray syndrome, while PLZF mutations lead to severe defects in the skeleton and gonads. We surprisingly found that PLZF and SALL4 interact and oppose each other’s functions. Our study of PLZF–SALL4 crosstalk will provide important insight into infertility, developmental disorders and cancer.
Blood clotting in the wrong place at the wrong time is responsible for up to 50% of the morbidity and mortality of the population through diseases such as heart attack, stroke, venous thrombosis. It also contributes to cancer progression and cancer related death. Blood clotting is initiated when a protein on the cell surface known as tissue factor becomes active. We will determine how activation of tissue factor participates in the blood clotting process. This will help in disease prevention.
Deadly Commute - Targeting The Trafficking Mechanisms That Licence Inflammatory Cell Death
Funder
National Health and Medical Research Council
Funding Amount
$774,544.00
Summary
MLKL is a protein naturally found inside cells. MLKL is activated by inflammation. Once activated, MLKL relocates to the outer periphery of cells and kills them. Gut cells are especially vulnerable to death-by-MLKL and this problem causes Inflammatory Bowel Disease. Using cutting edge microscopy, we have discovered how MLKL moves to the periphery of cells prior to killing them. We will test if blocking this movement of MLKL to the cell periphery stops gut death and Inflammatory Bowel Disease.
Tissue factor is a central and major player in the clotting process. It exists in both active and inactive forms. The active form initiates clot formation. How it gets activated is one of the most important unanswered questions in this area of research. Our aim is to discover tissue factorÍs mechanism of activation. The outcome will provide more specific targets for therapeutic drug development for cardiovascular disease, strokes and deep venous thrombosis.