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Christopher Spry
2 May 2014

University of London, St. George's Hospital Medical School

The Chair of Cardiovascular Immunology

Held by: Prof. Christopher J.F. Spry MA DPhil FRCP FRCPath FESC

Annual lay report 1995

Our research group has had a very busy year in 1995. Not only have we finished a detailed study of two of the most important proteins from one of the blood cells that can cause a rare but fatal form of heart disease (eosinophilic endomyocardial fibrosis), but we have also started a new program of work to discover the basis of the most common form of heart muscle disease of unknown cause: dilated cardiomyopathy. We suspect that the development of dilated cardiomyopathy must be linked to the genetic makeup of the people who develop this serious disorder and the ways that their immune system reacts to infections. Two new Lecturers began work in the team with a technician (Mr. Robert Hollifield) in the Spring of 1995 . One Lecturer (Dr. Paul Nelson) is an Immunologist who is studying the immune responses in the heart and the other (Dr. Suzanne Ruddy) is a Molecular Biologist who is skilled in studying the genetic and molecular basis of disease. Together, we are beginning to set the ground work for the research that has to be done. We are also fortunate in being able to collaborate in our Medical School with Prof. Bill McKenna who is a leading authority on cardiomyopathies.

So far, after six months work, we have six projects under way and two are beginning to show useful results. We have discovered a protein on the surface of heart cells which may allow the persistence of some viruses there and we have shown that another protein is present in the hearts of fetuses but not adults, possibly accounting for a difference in the way that these proteins are involved in disease. It is too early to report on the other projects but they should take us close to the basis of dilated cardiomyopathy. These projects (a) deal with the genes that predispose to dilated cardiomyopathy, (b) examine antibodies to heart tissues, (c) measure the different ribonucleic acid molecules that form the proteins in cells to see if they are different in patients with dilated cardiomyopathy and ( d) provide a model of the disease. It looks as though 1996 will be even busier year than 1995 as we work to track down the elusive and complex processes that turn a normal healthy heart into one that begins to lose its capacity to pump properly so that the patient may die in heart failure. We acknowledge that it is a privilege to be allowed to work on such important topics and we take this opportunity to thank the British Heart Foundation, its loyal and generous supporters and our patients for enabling us to do this research in such an important area of cardiology.

Annual scientific report 1995

Last year we cloned, sequenced and defined the promoters of the principal granule proteins in eosinophils, the major basic protein (MBP) which is toxic to heart and other cells and the neurotoxin (EDN), which is particularly toxic to neurones and also damages heart cells. The work on ECP was published in the Biochemical Journal in February 1995 and Dr. Li’s Ph.D. thesis on this was accepted in September 1995. Dr. Sun’s work to clone and express EDN was also published in January 1996. Our clinical work to diagnose and treat patients with endomyocardial fibrosis has been less busy in 1995 as many of these patients can now be well looked after in their local hospitals, although we provide a tertiary referral service for the more complex clinical problems of patients with eosinophilia, with and without heart disease. Prof. Spry’s work in biomedical informatics has been noted in this rapidly developing field. Unfortunately the low band width and congestion on the UK cable and satellite data links to the States and pressure on Internet providers there has limited use of these systems. This will improve in 1996 as new resources are being installed both within the UK academic network, in the USA and on the Continent. Our facilities are among the best available today thanks to our considerable efforts in this field, and as a result of our collaboration with several of the principal commercial, academic and research teams implementing internet access and database provision internationally. The benefits of this will become more obvious as bandwidth and access times improve. In the Spring we began work on several important new area in cardiology research for our group. We recruited two Lecturer’s and a Technician to discover the nature of the molecular and immunological defects in patients with dilated cardiomyopathy. We have begun to characterize our many monoclonal antibodies to human heart antigens, the roles of Fas-ligand and adhesion molecules in this group of diseases, and define alterations in the mRNA profiles of myocytes in explanted hearts from patients undergoing heart transplantation. Two new projects are being done in close collaboration with Prof. Bill McKenna's group as outlined below, to map genetic defects leading to dilated cardiomyopathy and to learn more from an animal model of inflammatory heart disease leading to dilated cardiomyopathy.

Total annual support received in 1995:

 

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