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Research Topic : broncho-alveolar
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  • Funded Activity

    Causes And Prevention Of Dust-related Diseases

    Funder
    National Health and Medical Research Council
    Funding Amount
    $308,641.00
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    Funded Activity

    Role Of Physical Forces In The Determination Of Pulmonary Epithelial Cell Phenotypes

    Funder
    National Health and Medical Research Council
    Funding Amount
    $183,408.00
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    Funded Activity

    How The Amount Of Liquid In The Lung Is Controlled

    Funder
    National Health and Medical Research Council
    Funding Amount
    $130,625.00
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    Funded Activity

    Effect Of Prostaglandin E2 On The Periodontium And Alveolar Bone Formation

    Funder
    National Health and Medical Research Council
    Funding Amount
    $211,527.00
    Summary
    Dental disease affecting the supporting structures of teeth (the periodontium), is prevalent in our society. Periodontal disease results in destruction of bone around teeth, loosening of teeth, compromised chewing function, and tooth loss. Over the last twenty years reports into the effects of prostaglandin E2 (PGE2) on the skeleton have been divided and controversial. While historically PGE2 has been reported to promote bone resorption, more recently it has been demonstrated that when PGE is pl .... Dental disease affecting the supporting structures of teeth (the periodontium), is prevalent in our society. Periodontal disease results in destruction of bone around teeth, loosening of teeth, compromised chewing function, and tooth loss. Over the last twenty years reports into the effects of prostaglandin E2 (PGE2) on the skeleton have been divided and controversial. While historically PGE2 has been reported to promote bone resorption, more recently it has been demonstrated that when PGE is placed in contact with mandibular bone, adjacent to erupted teeth, new bone and cementum formation occurs. The ability of PGE2 to induce new bone formation indicates a potential use for PGE2 in the management of bone loss associated with periodontal diseases, and the formation of new bone around dental implants, and around teeth following orthodontic movement. Growth factors are active in healing and have valuable applications in augmenting wound repair. Osseous and dental tissues are rich in growth factors, and these factors are involved with the regulation of bone metabolism as well as tissue repair, thus the action of PGE2 on the periodontium is most likely regulated via these factors. Since regeneration of the periodontium is a fundamental goal of dentistry, any treatment which leads to predictable formation of new connective tissues and their long term stability would be a major clinical advance.
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    Funded Activity

    Targeting Macrophage Subtypes As A Strategy For Chronic Inflammatory Lung Disease Therapy

    Funder
    National Health and Medical Research Council
    Funding Amount
    $660,471.00
    Summary
    Researchers in Melbourne have discovered a possible cause of severe emphysema. Using disease models, patients’ samples and advanced genetic techniques they are now searching for ways to turn this discovery into effective treatments for this disease which is currently fatal and incurable.
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    Funded Activity

    Surfactant Protein A: Role In Surfactant Homeostasis An D Host Defence

    Funder
    National Health and Medical Research Council
    Funding Amount
    $125,156.00
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    Funded Activity

    The Role Of Pulmonary Macrophages In The Pathogenesis Of An Acute Exacerbation Of Chronic Asthma

    Funder
    National Health and Medical Research Council
    Funding Amount
    $495,710.00
    Summary
    We will examine the role of lung defence cells, known as macrophages, in triggering the inflammation of acute severe asthma. The experimental work will use unique mouse models of mild chronic asthma and of an acute exacerbation of the illness, which have been developed in our laboratories. We will study the mechanisms of activation of the asthmatic response and assess whether treatment with drugs that suppress the function of macrophages can help to control steroid-resistant exacerbations.
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    Funded Activity

    Uncoupled Research Fellowship

    Funder
    National Health and Medical Research Council
    Funding Amount
    $558,000.00
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    Funded Activity

    Cytokine And Macrophage Determinants Of Pulmonary Inflammation During Tuberculosis

    Funder
    National Health and Medical Research Council
    Funding Amount
    $455,899.00
    Summary
    Tuberculosis (TB) infects 33% of the world, causing over 2 million deaths per year. TB disease causes damaging lung pathology and new therapies to treat the infection and moderate inflammation are urgently required. TNF is essential for immunity to TB, acting to modulate inflammation. This grant will determine how soluble and membrane- bound TNF regulate the cellular and cytokine control of TB pathology and may lead to new therapies to limit inflammation in TB and other inflammatory diseases.
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    Funded Activity

    Novel Strategies For Improving Respiratory Support And Outcomes For Very Preterm Babies

    Funder
    National Health and Medical Research Council
    Funding Amount
    $8,381,820.00
    Summary
    Very premature birth is the commonest cause of illness and death in newborn babies, making it one of the most serious and costly issues in perinatal medicine. The major problem suffered by very premature babies is lung immaturity and its associated harmful effects on brain development. Most very premature babies require resuscitation followed by ventilatory support,often for several weeks. This is extremely expensive and places an enormous financial burden on health care systems. Furthermore, it .... Very premature birth is the commonest cause of illness and death in newborn babies, making it one of the most serious and costly issues in perinatal medicine. The major problem suffered by very premature babies is lung immaturity and its associated harmful effects on brain development. Most very premature babies require resuscitation followed by ventilatory support,often for several weeks. This is extremely expensive and places an enormous financial burden on health care systems. Furthermore, it increases the risks of respiratory illnesses, including bronchopulmonary dysplasia and chronic lung disease which can impair breathing and increase susceptibility to respiratory disease such as asthma later in life. The overall aim of this program is to improve outcomes for very premature babies, including less lung injury, better respiratory health and shorter stays in hospitals. In order to reduce the health burden caused by very premature birth on the community we need to know more about how it alters the normal development of the lungs in the newborn period and into later life. In particular, we need to understand the cellular and molecular processes involved in lung development so that we can identify gene networks and developmental processes that are disrupted by severe premature birth. Such knowledge is necessary to provide a more rational, scientific basis for managing and treating the alterations in lung structure and function caused by premature birth. We also need to develop better ways of resuscitating and ventilating these infants so that lung injury is minimized.The research team is led by two neonatologists and three biomedical research scientists with a proven record of effective collaboration. This team is internationally unique in that it includes practicing neonatologists, respiratory physiologists and molecular biologists who have collaborated together productively and are regarded as world leaders in their respective fields. New talents have been brought into the team to provide expertise in pulmonary stem cell biology, the design of novel steroid drugs, and clinical follow-up. Together, this team has the potential (a) to greatly enhance the understanding of the impact of very premature birth on the developing lung, (b) to improve resuscitation and ventilation techniques, and (c) to translate the new knowledge into clinical practice to improve the outcome for prematurely born babies. Using well characterized animal models we will determine gene networks involved in fetal lung development and how these are altered by premature birth. The successful transition from fetal to postnatal life is critical for survival at birth but more information is needed. Using newborn lambs and rabbits, we will trial novel strategies for enhancing the transformation of the immaturelung into an effective gas exchange organ at birth. New data on lung aeratio
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