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Inhaled Mannitol For The Treatment Of Mucociliary Dysfunction- Its Effect And Mechanisms On The Clearance Of Mucus
Funder
National Health and Medical Research Council
Funding Amount
$324,100.00
Summary
Excessive secretion of mucus is a problem in asthma and bronchiectasis. Mucus is secreted from submucosal glands and goblet cells as a result of inflammation present in the airways. Excessive mucus is not easily transported by the cilia (hair like structures) in the airways and accumulation leads to productive cough and to recurrent infections. Cough is a secondary mechanism to clear mucus when the mucociliary system fails. Cough generates high airflow rates that can move mucus. However, patient ....Excessive secretion of mucus is a problem in asthma and bronchiectasis. Mucus is secreted from submucosal glands and goblet cells as a result of inflammation present in the airways. Excessive mucus is not easily transported by the cilia (hair like structures) in the airways and accumulation leads to productive cough and to recurrent infections. Cough is a secondary mechanism to clear mucus when the mucociliary system fails. Cough generates high airflow rates that can move mucus. However, patients with moderately to severely obstructed airways cannot generate high airflow rates. In addition, cough becomes very inefficient in moving mucus if it is sticky and viscous. As the cilia cannot transport large quantities of mucus the best approach is to alter the properties of mucus that would facilitate cough clearance. Increased hydration of mucus could change its surface and rheological properties. Increased hydration can be achieved by the osmotic movement of water into the airway lumen in response to inhaling an aerosol of salt or sugar. We have evidence using radioactive aerosols, that mannitol, a sugar, increases clearance of mucus acutely in patients with excessive secretions. We also have new evidence that mannitol taken daily over two weeks increases the health status in patients with bronchiectasis. Further we now have preliminary data demonstrating that mannitol changes the surface properties of mucus. We aim to study the properties of mucus in relation to its clearance in vivo in humans. This has not been done before. If we can demonstrate that changes in clearance in response to mannitol relate to the changes in mucus then we will be able to easily evaluate current treatments and doses for patients with excessive secretions and to identify new treatments. Mannitol is a potential treatment for diseases with excessive secretions and understanding of how it works will hopefully lead to better outcomes for patients.Read moreRead less
Activated Protein C Utilises Protease Activated Receptors And Epidermal Growth Factor Receptor To Heal Wounds
Funder
National Health and Medical Research Council
Funding Amount
$436,882.00
Summary
Chronic leg ulcers are a major burden to the individual sufferer and to the health system. We have discovered that activated protein C (APC) potently stimulates wound healing in the laboratory and now have exciting positive results from a small pilot clinical trial showing that applying APC solution to leg ulcers also helps healing in patients. This study plans to discover how APC works at the molecular level.
Epigenetic Control Of Antigenic Variation In Plasmodium Falciparum
Funder
National Health and Medical Research Council
Funding Amount
$505,563.00
Summary
Malaria is an enormous global health problem that kills millions of people each year. Humans develop only partial immunity to malaria only if they survive many years of repeated infection. Much of the difficulty in developing immunity to malaria lies in the ability of the causative agent, Plasmodium falciparum, to continually change the properties of its surface coat. The parasite achieves this immune evasion through a process called antigenic variation. Genetically identical parasites can expre ....Malaria is an enormous global health problem that kills millions of people each year. Humans develop only partial immunity to malaria only if they survive many years of repeated infection. Much of the difficulty in developing immunity to malaria lies in the ability of the causative agent, Plasmodium falciparum, to continually change the properties of its surface coat. The parasite achieves this immune evasion through a process called antigenic variation. Genetically identical parasites can express different surface coats, and the control of this process is superimposed above the level of genetic control. This system is referred to as epigenetic control. Epigenetic control includes regulatory mechanisms such as the way that genes are packed inside the parasite, and chemical modifications to the proteins (called histones) around which genes are wrapped. We wish to understand the epigenetic control system that the parasite uses to orchestrate the phenomenon of antigenic variation. We will use two methods to gain this understanding; the first is a genetic screen that will create mutations in the parasite using jumping DNA (called transposons) that will break down the control mechanism behind antigenic variation. Identifying the mutated genes will show us which genes organize antigenic variation in normal parasites. Our second approach is to genetically knockout parasite genes that are related to the genes that govern epigenetic mechanisms in other, better understood organisms like humans and yeast. We will test the effect of these targeted gene deletions to discover which of these genes are involved in regulating antigenic variation. The insights gained from these discoveries will improve our understanding of how the malaria parasite evades our immune system. A better understanding of this immune evasion may help us to understand how to build better vaccines against malaria.Read moreRead less
Deciphering Posttranslational Codes Of The Dioxin Receptor
Funder
National Health and Medical Research Council
Funding Amount
$540,083.00
Summary
The dioxin receptor (DR) is a protein which protects human cells by binding xenobiotics, ie foreign or anti-nutritional chemicals found in food sources and the general environment. When these chemicals bind the DR, it becomes an active gene regulatory protein, turning on genes that are involved in breakdown and excretion of the xenobiotics. Recently it has been found that the DR performs other important functions which are unrelated to xenobiotic breakdown. These include blood vessel development ....The dioxin receptor (DR) is a protein which protects human cells by binding xenobiotics, ie foreign or anti-nutritional chemicals found in food sources and the general environment. When these chemicals bind the DR, it becomes an active gene regulatory protein, turning on genes that are involved in breakdown and excretion of the xenobiotics. Recently it has been found that the DR performs other important functions which are unrelated to xenobiotic breakdown. These include blood vessel development in the embryonic liver and hormone production during the estrous cycle. These observations imply that natural physiological mechanisms also exist for activating the DR, providing it with a separate code to perform these innate functions. A number of man-made chemicals, such as dioxins and PCBs, are especially good at activating the DR. However, they have chlorinated chemical structures, which are not broken down by the protective system. This creates a wide range of severe toxic responses. It has been established that toxicities result from persistent hyperactivation of the DR, but how this hyperactivation induces the toxic outcomes is not known. As the DR has roles in early development and estrogen production, this project will investigate how the DR becomes activated to perform these functions. Our initial experiments have shown that the DR can be activated by normal cell signalling systems, which induce distinct modifications (a distinct code) to the protein. We are comparing this code of modifications to those induced by xenobiotics which are able to be broken down, and dioxins which are resistant to breakdown. We hypothesise that dioxins will give an excessive code of activating modifications, resulting in uncontrolled regulation of genes used in both the developmental and xenobiotic breakdown pathways. We will explore the hypothesis that this gross loss of gene regulatory control underpins the multifarious toxicities of dioxin poisoning.Read moreRead less
Resolvin E1 Is A Novel Anti-inflammatory And Anti-fibrotic Lipid Mediator For The Treatment Of Chronic Kidney Disease.
Funder
National Health and Medical Research Council
Funding Amount
$519,246.00
Summary
This project will ascertain whether a naturally occurring compound, Resolvin E1 with potent anti-inflammatory properties, can effectively halt the progression of experimental kidney disease. We will also test whether Resolvin E1 can exert other potential benefits in suppressing progressive fibrosis of the kidney. The outcome of this study will allow us to evaluate the therapeutical potential of Resolvin E1 for the treatment of acute and chronic kidney diseases.