It's big – and it's getting bigger
Reproduced from Issue 106 of Arthritis Today
Left to right: Dr Clare Isacke, Professor Roger Mason and Dr Andrew Amis.
Not only does it make up London's biggest medical school; it also boasts the largest research income and occupies seven major sites north of the Thames. The Arthritis Research Campaign is playing its part in the college's growing success story by providing a major investment of almost £2.5m of funding.
Last year when the Queen opened the new Alexander Fleming Building at Imperial College of Science, Technology and Medicine, it marked another stage in the history of an institution which is expanding inexorably year by year.
A series of mergers between hospitals and medical schools over the past decade has resulted in the college boasting a turnover of £300m, and research income of £180m. Sites at Queen Charlotte's, Hammersmith and Charing Cross Hospital in west London, St Mary's in Paddington, Chelsea and Westminster Hospital, the Royal Brompton and South Kensington campus in the south west of the capital cover an enormous geographical area, and a catchment of five million patients.
It also means more collaborative research projects between the numerous departments, and closer links between the scientists, engineers and clinicians who work there. And that's good news for the dozens of researchers employed on around 20 arc research grants.
Much
of the arc-funded work is now based at the new Alexander Fleming Building
in South Kensington, which houses biology and biomedical sciences.
Professor Roger Mason, leading arc scientist, and chairman of arc's research committee, moved to the new building from Charing Cross Hospital last year. Professor Mason, biologist Dr Clare Isacke and engineer Dr Andrew Amis are all pursuing different lines of arthritis research on the site, while a fourth, lupus expert Professor Mark Walport, remains at Hammersmith.
"Rheumatology research is much more concentrated than it was, the fact that so many of us are now on the same site increases the amount of interaction," explained Professor Mason. "In the medical school there is a good interface between the clinical and academic sides of research, and we have research groups of clinical scientists, clinicians, and basic scientists who have shared interests in particular areas, who get together for regular meetings." The aim is to translate basic science to patient care, more or less under one roof.
arc funding remains a highly significant factor in Imperial's arthritis research programme.
"Obviously those of us who have been involved long-term get funding from other sources, such as industry and the Wellcome Trust, but for all of us arc is our core funding that we rely on to form the spine of our research activities in rheumatology," added Professor Mason.
Some major areas of researchOsteoarthritis"Osteoarthritis (OA) affects articular cartilage, which is able to absorb the load imposed on the bones when we move our joints. In OA, the smooth surfaced cartilage becomes roughened, then eroded, and finally splits, with whole areas of the cushion being lost from the end of the bone. We still do not understand whey people develop OA or what changes occur in cartilage cells and the material surrounding them. But if we are to develop more effective therapies we need to define the biochemical abnormalities which occur in the tissue in the early stages of the disease, and currently this knowledge can only be obtained by studying animals which develop OA. Our recent work has addressed the question of which proteinase enzymes are produced by the cartilage cells in a strain of mouse which develops OA, and whether they degrade the major components of the cartilage matrix – proteoglycan and collagen. The proteoglycan has a major role in determining the properties of articular cartilage as a shock-absorbing cushion over the ends of the long bones, and inhibiting its breakdown by proteinases in OA may help to prolong the function of the tissue. As a first step to testing this we, together with Professor Mike Bayliss at the Royal Veterinary College, are working with a major pharmaceutical company to establish whether a proteinase inhibitor drug made by the company can retard the progressive development of OA in the mouse. Similar arc-funded studies to identify collagen-degrading enzymes in the cartilage are also under way. I would say that within the next five years there are going to be drugs on the market which block the disease activity, and offer a much more specific remedy than NSAIDs. We discovered recently that mouse cartilage cells close to developing arthritis lesions undergo apoptosis (cell death). In this process, cells receive a signal which tells them to go through a series of changes, ending in their death. Apoptosis also appears to be a feature of human OA. So the mouse provides us with an opportunity to investigate the nature of the signal which initiates apoptosis in OA. Once identified, it may be feasible to design drugs which prevent apoptosis in OA, slowing down the progression of the disease." Professor Roger Mason, Division of Biomedical Sciences. Bioengineering"Our current research project should help surgeons improve operating techniques on patients with knee problems, which are common in young people as well as the elderly. Many problems arise from the kneecap not moving smoothly, and in severe cases, it can jump sideways out of place. We are using a magnetic tracking system to study the motion of the kneecap in patients having surgery to correct the problem; this is then repeated after surgery to assess the changes resulting from the operation. This work is providing data that can be used to develop a computer system that will help surgeons plan their operations, leading to more reliable results. In another recently completed project we studied the changes in bone density that take place after hip replacement surgery. The aim is to evaluate new hip designs before they are tried in patients, to try to minimise bone loss." Dr Andrew Amis, Biomechanics Section, Mechanical Engineering Department. Inflammatory arthritis and cell adhesion"Much of the swelling in arthritis joints is due to an excess of a jelly-like substance called hyaluronan. It is also known that abnormal numbers of cells migrate into the arthritic joint from the blood, and it is these cells that release many of the chemical signals responsible for joint damage and inflammation. Our lab has found that the unwanted cells infiltrating the arthritic joint have acquired the ability to crawl through the hyaluronan, and have discovered two main control mechanisms which normally prevent this cell migration. "We are currently investigating why control mechanisms have gone wrong in rheumatoid arthritis so that we can identify targets for specific therapies to reduce joint swelling, and the invasion of harmful cells." Dr Clare Isacke, Department of Biology. |
