Improving the Health of the Nation
Medical Research Scotland aims to support medical research of the highest quality in Scotland. Its scope is unrestricted. Medical Research Scotland therefore supports research into any disease. It awards grants for scientific research aimed at understanding the mechanisms and causes of all or any diseases and improving methods of their detection, prevention and treatment.
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about Medical Research Scotland.
Medical Research Scotland supports research in universities and hospital-based research centres throughout Scotland. You can see lists of the projects currently receiving support in all the institutions associated with these geographic, not institutional, links below or those in the navigation panel on the left. Information about the grants awarded at the most recent meeting are shown further below:
Aberdeen : Dundee : Edinburgh : Glasgow : St Andrews : Stirling
A full list of current and recent grantholders is also available, while the Archive pages in the News & Publications section provide information about previously-supported research.
Grants Awarded - August 2009
£135,287 over two years to Dr Christine M. Dufes (Strathclyde Institute of Pharmacy & Biomedical Sciences) & Professor Kevin Ryan (Beatson Institute for Cancer Research, Glasgow), for the evaluation of systemic p73 gene therapy of cancer, using a novel transferrin-targeted dendrimer.
The potential for using gene therapy in cancer treatment is currently limited by the inability to get the modified genes to deep-seated tumours efficiently and without healthy tissues being damaged in the process. This project aims to improve the efficiency of these 'seek and destroy' therapies by using an iron-targeted delivery system to carry the tumour-suppressor gene, p73 directly to the tumour. Iron is essential for tumour cell growth and the tumour cells have many iron-carrier receptors on their surface. The hope is that intravenously-administered iron-targeted carriers will prove to be a highly effective and specific means of anti-cancer treatment.
£149,947 over two years to Dr Nancy Sabatier (Centre for Integrative Physiology, University of Edinburgh) for an investigation of hypothalamic mechanisms in obesity.
One in four UK adults is obese and, as obesity can lead to diabetes, heart disease and stroke, NHS costs are escalating, so tackling it is a policy priority. Before we can develop drugs to combat obesity however, we first need to find viable drug targets. How much we eat is largely controlled by a balance between brain signals of hunger and satiety ('fullness') and obesity often develops because of a defect in the 'fullness' signalling. Many nerve cells in one part of the hypothalamus express the SF1 gene. They are the only brain neurones to do so and mutations in the gene are associated with obesity. By learning exactly what part these neurones play in appetite, studying how they respond to two hormones involved in meal termination and how their responses change when an animal becomes obese, this project will assess whether they are likely to be a good target for therapeutic intervention.
£142,239 over two years to Dr John A. Marwick (moving to Edinburgh from the National Heart & Lung Institute, London) & Professor Adriano G. Rossi (MRC Centre for Inflammation Research, University of Edinburgh) to study the impact of oxidative stress and glucocorticoids on neutrophil function and macrophage clearance.
Neutrophils and macrophages are white blood cells which play a major part in inflammation and both are important in controlling the duration of this natural, but potentially damaging defence response. Neutrophils release toxic agents designed to kill foreign invaders such as bacteria, but also die shortly thereafter, limiting levels of damaging agents released. One of the macrophages' functions is to ingest and remove dying cells, including neutrophils. Failure of removal by macrophages can fuel inflammation; commonly prescribed anti-inflammatory drugs (steroids) reduce the rate of neutrophil death, which may prolong an inflammatory response; and there are suggestions that oxidative stress, which occurs in severe asthma and chronic obstructive pulmonary disease, may impair removal of dead neutrophils by macrophages. A better understanding of how steroids and oxidative stress affect neutrophils may help to identify potential therapies that restore steroid efficacy or provide targets for new alternative anti-inflammatory agents. In turn, this would result in improved disease control, reduced side-effects and decreased patient hospitalisation.