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1.  Genetics of osteoarticular disorders, Florence, Italy, 22–23 February 2002 
Arthritis Research  2002;4(5):326-331.
Osteoporosis (OP) and osteoarthritis (OA), the two most common age-related chronic disorders of articular joints and skeleton, represent a major public health problem in most developed countries. They are influenced by environmental factors and exhibit a strong genetic component. Large population studies clearly show their inverse relationship; therefore, an accurate analysis of the genetic bases of one of these two diseases may provide data of interest for the other disorder. The discovery of risk and protective genes for OP and OA promises to revolutionize strategies for diagnosing and treating these disorders. The primary goal of this symposium was to bring together scientists and clinicians working on OP and OA in order to identify the most promising and collaborative approaches for the coming decade. This meeting put into focus the importance of an adequate genetic approach to several areas of research: the search for the genetic determinants underlying new susceptibilities, the optimization of previously acquired data; the establishment of correlations between genetic polymorphism and functional variants, and gene–gene and gene–environment interactions (particularly those between genes and nutrients). An adequate genetic approach is also essential with regard to determining more selective criteria for phenotypic definition of familial OP, in order to obtain more homogeneous and statistically powerful family-based studies. The symposium concluded with an interesting overview of the future perspectives offered by DNA microarray technologies for identifying novel candidate genes, for developing proteomics and bioinformatics analyses and for designing low-cost clinical trials.
PMCID: PMC128940  PMID: 12223106
estrogen; genetics; osteoarthritis; osteochondrodysplasia; osteoporosis
2.  22nd European Workshop for Rheumatology Research, Leiden, The Netherlands, 28 February–3 March 2002 
Arthritis Research  2002;4(4):276-279.
The European Workshop for Rheumatology Research met this year in Leiden, The Netherlands. The Workshop provided a platform to feast on new technologies and how they have taken research programmes forward. While there will be the inevitable delay during which mechanisms are devised for analysing the huge amount of information generated by these technologies, there is a lot already to look forward to. Highlights included genomic, reverse genomic and proteomic approaches to understanding disease pathogenesis and to identifying new therapeutic targets. Opportunities for exploring whether pharmacogenomics has a place in the clinic are now a reality, and phage display technology has been applied to in vivo arthritis models to identify human synovial microvascular 'post codes'.
doi:10.1186/ar418
PMCID: PMC128934  PMID: 12106499
diagnostics; inflammation; prognostics; research; workshop
3.  Advances in Targeted Therapies III, Nassau, Bahamas, 27 April-1 May 2001 
Arthritis Research  2001;3(5):E005.
This conference was the third in a series focusing on developments in the therapy of rheumatoid arthritis (RA) and other rheumatic conditions with biologicals; in many ways, it was perhaps the best one so far. One strength of the meeting was the mix of scientists from academia and from industry, and of workers in basic science as well as clinical investigators. The risks of inhibition of tumor necrosis factor (TNF) were covered in depth for the first time. A number of putative and actual new targets were presented. An updated consensus document on the use of TNF inhibitors will appear in the near future in the Annals of Rheumatic Diseases, authored by Dan Furst et al.
doi:10.1186/ar323
PMCID: PMC128906
cytokine biology; cytokine blockade; joint damage; regulatory agents; rheumatic diseases
4.  Gene therapy moves forward - The Second International Meeting on Gene and Cell Therapies of Arthritis and Related Disorders, 17-18 May 2001, Montpellier, France 
Arthritis Research  2001;3(5):289-292.
The field of gene therapy for bone and joint disorders has grown considerably over the last two and a half years. Investigators have shown that ex vivo or in vivo gene transfer is highly effective in blocking arthritis or facilitating repair of damaged cartilage or bone. The feasibility of applying gene therapy for the treatment of arthritis in humans has also been demonstrated. Thus, gene therapy appears poised to make significant contributions to the clinical treatment of joint and bone diseases in the near future.
doi:10.1186/ar317
PMCID: PMC128905
arthritis; bone; cartilage; clinical trial; gene therapy; vector
5.  21st European Workshop for Rheumatology Research, Vienna, Austria, 1–4 March 2001 
Arthritis Research  2001;3(4):237-240.
Major advances in technology now drive how we approach questions in immunology, particularly in analyzing complex data sets commonly encountered in genomics and proteomics studies. Active areas of investigation include development of novel technologies, identification of elusive target antigens for RA and other diseases, dissection of signaling pathways connecting the lymphocyte cell surface with the nucleus, and exploration of new avenues for therapeutic interventions. The European Workshop for Rheumatology Research (EWRR) is a forum for many European and non-European scientists to present research findings of high quality. Arthritis researchers from around the globe should be strongly encouraged to attend future meetings, the next of which is the 22nd EWRR meeting in Leiden, the Netherlands, in 2002.
doi:10.1186/ar306
PMCID: PMC128901  PMID: 11438041
apoptosis; autoimmunity; autoantibodies; cytokine; signaling
6.  Sixth International Workshop on Scleroderma Research, Oxford, UK, 30 July–2 August 2000 
Arthritis Research  2000;3(1):34-40.
We discuss major topics presented at this recent international workshop, illustrating how recent progress in areas as diverse as free radical biochemistry, developmental biology, molecular genetics and vascular biology is facilitating greater understanding of the multisystem connective tissue disease scleroderma. Some of the opportunities for translating this into novel and improved therapy are considered.
doi:10.1186/ar137
PMCID: PMC128881  PMID: 11269238
experimental; human; organ manifestations; pathogenesis; scleroderma; therapy
7.  Cell contact interactions in rheumatology, The Kennedy Institute for Rheumatology, London, UK, 1-2 June 2000 
Arthritis Research  2000;2(6):472-476.
The intricate interactions that regulate relationships between endogenous tissue cells and infiltrating immune cells in the rheumatic joint, particularly in rheumatoid arthritis (RA), were the subject of the meeting. A better understanding of these interactions might help to define intervention points that could be used to develop specific therapies. The presentations and discussions highlighted the fact that, once chronic inflammation is established, several pro-inflammatory loops involving tumour necrosis factor (TNF)-α and interleukin (IL)-1β can be defined. Direct cellular contact with stimulated T lymphocytes induces TNF-α and IL-1β in monocytes which in turn induce functions in fibroblast-like synoviocytes. The latter include the production of stromal cell-derived factor-1α (SDF-1α) which enhances the expression of CD40L in T cells, which stimulates SDF-1α production in synoviocytes, which in turn protects T and B cells from apoptosis and enhances cell recruitment thus favoring inflammatory processes. IL-1β and TNF-α also induce IL-15 in fibroblast-like synoviocytes, which induces the production of IL-17 which in turn potentiates IL-1β and TNF-α production in monocyte-macrophages. This underlines the importance of TNF-α and IL-1β in RA pathogenesis, and helps explain the efficiency of agents blocking the activity of these cytokines in RA. Factors able to block the induction of cytokine production (such as apolipoprotein A-I [apo A-I] and interferon [IFN]-β) might interfere more distally in the inflammatory process. Furthermore, stimulated T lymphocytes produce osteoclast differentiation factor (ODF), which triggers erosive functions of osteoclasts. Therefore, factors capable of affecting the level of T lymphocyte activation, such as IFN-β, IL-15 antagonist, or SDF-1α antagonist, might be of interest in RA therapy.
doi:10.1186/ar129
PMCID: PMC128876  PMID: 11219394
cell–cell interactions; cytokines; inflammation; rheumatoid arthritis
8.  Ninth Asia Pacific League Of Associations For Rheumatology (APLAR) Congress, Beijing, China, 21-26 May, 2000 
Arthritis Research  2000;2(5):395-398.
The Congress covered the broad field of rheumatology, with participants from China, the Asia Pacific League of Associations for Rheumatology (APLAR) region and the rest of the world. The programme consisted of a mix of plenary lectures, concurrent symposia, workshops, free paper sessions and poster presentations. Basic sciences were well represented, with the general theme of inflammatory cytokines being of particular interest. One plenary lecture and a number of other presentations addressed the problem of atherosclerosis and rheumatic diseases. Diseases prominent in the region, such as Behcet's disease and Takayasu's disease, were represented with large series. Other areas of interest were musculoskeletal infections in HIV-positive patients and the management of spondyloarthritis. Although the use of the most recently developed drugs is restricted in the APLAR region because of cost factors, there were symposia on the latest pharmacological advances such as COX-2 technology, leflunomide and anti-tumour necrosis factor (TNF) therapy.
doi:10.1186/ar117
PMCID: PMC130141  PMID: 11219393
atherosclerosis; Behcets; congress; cytokines; summary

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