The Branches Scholarship is for the amount of $25,000 each year to aid research into the causes and cures for arthritis.

This amount of money is raised entirely by the Arthritis NSW Branches holding fund raising activities throughout the year making it possible for a researcher to continue their work.

The 2007 Branches Scholarship for Research has been awarded to Dr Tanya Covic.
Dr Covic is from the School of Psychology at the University of Western Sydney, Westmead NSW. She will be doing research into the development of a precise and brief measurement of depression in Rheumatoid Arthritis to be used in rheumatology clinical settings.

In 2006 Elliott Taranto was the successful applicant for the Branches Scholarship for research into RA.
He is a researcher based in the Centre for Inflammatory Diseases at the Monash Institute of Medical Research, a part of Monash University in Melbourne. The information below was published by Elliott in spring 2006 in Arthritis News:

Rheumatoid Arthritis (RA) is a destructive joint disease affecting 1-3% of Australians causing significant disability and reduction in quality of life. The disease is characterised by abnormal growth of the usually thin membrane that lines the joints called the synovium. In RA the synovium grows into a thick cellular mass
resulting in a joint that is swollen and inflamed. As RA progresses, the cells of the synovium, called synoviocytes, invade and mediate the destruction of cartilage and bone resulting in severe pain and joint deformity.

Research has revealed that RA synoviocytes found at the site of cartilage invasion display distinct biological properties from normal synoviocytes, distinguishing them as key players in the development of RA. Experimentally, these abnormal synoviocytes have been shown to escape the constraints of normal cell growth and independently invade cartilage. Recent studies suggest that the pro-inflammatory protein MIF,
(macrophage migration inhibitory factor), plays a pivotal role in RA. It has been shown that MIF is over-expressed in RA patient synovial fluid, blood serum and tissue. Moreover, MIF is also increased in animal models of RA. MIF has been shown activate synoviocytes to stimulate the release of cartilage and bone
degrading enzymes and other inflammatory substances in the joint. Blocking MIF in models of arthritis results in a dramatic decrease in joint inflammation and disease severity. In addition to promoting inflammation in
RA, we believe MIF is also able to stimulate the over-growth of synoviocytes. We have demonstrated MIF can increase cell growth and even stop cells from dying off.

By contributing to the overgrowth of synovial tissue, factors such as increased cell growth and reduced cell death are able to directly influence the pathological outcome of RA. The mammalian cell cycle is a tightly regulated process which governs the potential of a cell to undergo growth or death. My research is concerned with examining the dysregulation of specific genes involved in maintaining normal control of the cell cycle which may be responsible for the altered growth observed in RA. Recently, we have shown MIF can change
the distribution of specific growth proteins within the cell. One such protein is p21, which functions as both a positive and negative regulator of cell growth. We have shown that in the presence of MIF, p21 moves to the nucleus of a cell. This was correlated with an increase in cell growth and a reduction in cell death.

These observations suggest that the change in the position of p21, which is caused by MIF, contributes to synovial growth in RA by enhancing cell survival and promoting cell division. We can now take advantage of
new technology to target these proteins, temporarily switching off the function of specific cell cycle genes in human donor RA synoviocytes. We aim to use these and other techniques to determine the precise functional
consequences of nuclear localised p21 protein in RA and additionally determine the molecular mechanism through which MIF is capable of modulating p21. These observations have important implications in terms of potential to modulate the excessive growth and invasion displayed in RA synoviocytes and could alter our
understanding of RA.