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14 results on '"Caterson B"'

1. ADAMTS-4 activity in synovial fluid as a biomarker of inflammation and effusion

Author

Roberts, S., Evans, H., Wright, K., van Niekerk, L., Caterson, B., Richardson, J.B., Kumar, K.H.S., and Kuiper, J.H.

Subjects
Inflammation, Rheumatology, Biomedical Engineering, Synovial fluid, Orthopedics and Sports Medicine, Knee osteoarthritis, ADAMTS-4 activity, Effusion, QR
Abstract

Objective To evaluate the potential of ADAMTS-4 (aggrecanase -1) activity in synovial fluid (SF) as a biomarker of knee injury and joint disease. Design We have measured ADAMTS-4 activity in the synovial fluid of 170 orthopaedic patients with different degrees of joint pathology, using a commercial ADAMTS-4 fluorescence resonance energy transfer (FRET) substrate assay. Patients were classified at arthroscopy as (i) macroscopically normal, (ii) with an injury of the meniscus, anterior cruciate ligament or chondral/osteochondral defects or (iii) with osteoarthritis, and the influence of independent factors (age, patient group, effusion and synovial inflammation) on ADAMTS-4 activity levels was assessed. Results In most patients (106/170) ADAMTS-4 activity was undetectable; ADAMTS-4 ranged from 0 to 2.8 ng/mL in synovial fluid from patients with an injury, 0–4.1 ng/mL in osteoarthritic patients and 4.0–12.3 ng/mL in patients with large effusions. Four independent variables each significantly influenced ADAMTS-4 activity in synovial fluid (all P < 0.001): age (concordance = 0.69), presence of osteoarthritis (OA) (concordance = 0.66), level of effusion (concordance = 0.78) and inflammation (concordance = 0.68). Not only did effusion influence the amount of ADAMTS-4 activity most strongly, but it also did this in an ordered manner (P < 0.001). Conclusions The main finding of this study is that ADAMTS-4 levels in synovial fluid are most strongly correlated with inflammation and severity of effusion in the knee. Further study is required to determine if it could provide a useful tool to aid clinical diagnoses, indicate treatment, to monitor progression of joint degeneration or OA or alternatively the success of treatment.

Published
2015
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2. Advances in the understanding of tendinopathies: a report on the Second Havemeyer Workshop on equine tendon disease

Author

Smith, R, McIlwraith, W, Schweitzer, R, Kadler, K, Cook, J, Caterson, B, Dakin, S, Heinegård, D, Screen, H, Stover, S, Crevier-Denoix, N, Clegg, P, Collins, M, Little, C, Frisbie, D, Kjaer, M, van Weeren, R, Werpy, N, Denoix, J-M, Carr, A, Goldberg, A, Bramlage, L, Smith, M, Nixon, A, Dep Gezondheidszorg Paard, LS Equine Muscoskeletal Biology, ES TR, Biomécanique et Pathologie Locomotrice du Cheval (BPLC), and École nationale vétérinaire d'Alfort (ENVA)-Institut National de la Recherche Agronomique (INRA)

Subjects
Tendons, [SDV]Life Sciences [q-bio], Tendinopathy, Animals, Horse Diseases, Horses, Models, Biological, Biomechanical Phenomena
Published
2013
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3. British society for matrix biology autumn meeting

Author

Sudre, L, Cheung, F, Kevorkian, L, Young, DA, Darrah, C, Donell, ST, Shepstone, L, Porter, S, Brockbank, S, Edwards, DR, Parker, AE, Clark, IM, Boubriak, OA, Urban, JPG, Cui, Z, Tew, SR, Li, Y, Tweats, LM, Hawkins, RE, Hardingham, TE, Green, D, Partridge, KA, Leveque, I, Mann, S, Oreffo, ROC, Ball, SG, Kielty, CM, Qin, M, Tai, G, Polak, JM, Bishop, AE, Stolzing, A, Scutt, A, Screen, HRC, Shelton, JC, Bader, DL, Lee, DA, Hall, A, Hayes, A, Brown, L, Tubo, R, Caterson, B, Blain, EJ, Gilbert, SJ, Duance, VC, Davies, L, Blain, E, Duance, V, Shengda, Z, Wu, M-H, Xu, X, Heywood, HK, Sims, T, Miot, S, Martin, I, Roughley, PJ, Soranzo, C, Pavesio, A, Hollander, AP, Yang, X, Webb, D, Blaker, J, Maquet, V, Boccaccini, AR, Cooper, C, Eves, P, Beck, AJ, Shard, AG, Gawkrodger, DJ, Mac Neil, S, Rajpar, MH, Kadler, KE, Thornton, DJ, Briggs, MD, Boot-Handford, RP, Ellis, MJ, Tai, C-C, Perera, S, Chaudhuri, JB, Callender, P, Mason, DJ, Colley, H, Mc Arthur, S, Mirmalek-Sani, SH, Roach, HI, Hanley, NA, Wilson, DI, MacIntosh, AC, Crawford, A, Hatton, PV, Wallis, G, Shah, R, Knowles, JC, Hunt, NP, Lewis, MP, Rippon, HJ, Ali, BE, De Bank, PA, Kellam, B, Shakesheff, KM, Comerford, EJ, Tarlton, JF, Wales, A, Bailey, AJ, Innes, JF, Olivier, V, Xie, Y, Descamps, M, Hivart, P, Lu, J, Hardouin, P, Anderson, V, Spiller, DG, Vaughan-Thomas, A, Eissa, SZS, Faram, T, Birch, HL, Zeugolis, D, Paul, G, Attenburrow, G, Bhadal, N, Whawell, SA, Worrall, LK, Rose, FRAJ, Bradshaw, TD, Stevens, MFG, Chuo, CB, Wiseman, MA, Phillips, JB, Brown, RA, Harrison, CA, Gossiel, F, Bullock, AJ, Blumsohn, A, Li, Z, Derham, B, Gaissmaier, C, Fritz, J, Krackhardt, T, Flesch, I, Aicher, WK, Ashammakhi, N, Liu, K-K, Yang, Y, Ahearne, M, Then, K, El Haj, A, Cheung, I, Wright, TC, Kostyuk, O, Baria, KE, Chowdhury, TT, Sharma, AM, Bomzon, Z, Kimmel, E, Knight, MM, Dickinson, S, Pittarello, L, Fish, RS, Ralphs, JR, Farjanel, J, Sève, S, Borel, A, Sommer, P, Hulmes, DJS, Whiting, CV, Dalton, SJ, Mitchell, DC, Kafienah, W, Mistry, S, Hollander, A, Cartmell, S, Magnay, J, Dobson, J, Appleby, RN, Salter, DM, Scutt, N, Rolf, CG, Barry, JJA, Nazhat, SN, Scotchford, CA, Howdle, SM, Roberts, S, Gargiulo, B, Evans, EH, Menage, J, Johnson, WEB, Eisenstein, S, Richardson, JB, Stenfeldt, C, Avery, NC, Tidswell, H, Crabtree, J, Frazer, A, Fraser, S, Wong, M, Beckett, K, Grobbelaar, A, Mudera, V, Bax, DV, Cain, SA, Humphries, MJ, Lomas, A, Oldershaw, R, Murdoch, A, Brennan, K, Redman, S, Haughton, L, Dowthwaite, G, Williams, A, Archer, CW, Esfandiari, E, Stokes, CR, Cox, TM, Evans, MJ, Bailey, M, Hayman, AR, Day, MJ, Williams, R, Evans, D, Adesida, A, Millwards-Sadler, J, Salter, D, Smith, R, Korda, M, Porter, R, Kalia, P, Wiseman, M, Blunn, G, Goodship, A, McClumpha, A, Horrocks, M, Pabbruwe, MB, Du, X, Stewart, K, Suciati, T, Lakey, RL, Pennington, CJ, Cawston, TE, Palmer, L, Tasman, C, Clare, M, Gidley, J, Sandy, J, Mansell, J, Ellis, T, Burger, F, Lauder, R, Khan, I, and Smith, M

Published
2005

14. The regulation of the ADAMTS4 and ADAMTS5 aggrecanases in osteoarthritis: a review

Author

Bondeson, J., Wainwright, S., Clare Hughes, and Caterson, B.

Subjects
ADAM Proteins, Drug Delivery Systems, Osteoarthritis, Synovial Membrane, ADAMTS4 Protein, Cytokines, Gene Expression, Humans, ADAMTS5 Protein, Procollagen N-Endopeptidase
Abstract

Destruction of articular cartilage is a key feature of a number of arthritides, osteoarthritis prominent among them. Aggrecan degradation, caused by increased activity of proteolytic enzymes that degrade macromolecules in the cartilage extracellular matrix, is followed by irreversible collagen degradation. The degradation of aggrecan is mediated by various matrix proteinases, mainly the aggrecanases, multidomain metalloproteinases belonging to the ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) family. There has been much interest in the possible role of these aggrecanases, mainly ADAMTS4 and ADAMTS5, as therapeutic targets in osteoarthritis. There is still debate which of them is the major aggrecanase in osteoarthritis, however, as well as major issues concerning how they are regulated, with possible discrepancies between murine models and results obtained using human osteoarthritis tissue. This review discusses some recent data regarding the regulation of ADAMTS4 and ADAMTS5 gene expression in osteoarthritis, with emphasis on the role of proinflammatory cytokines in driving these enzymes, and of the transcription factor NFkappaB in mediating their expression.

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