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BEGIN:VEVENT
DTSTAMP:20260627T015218Z
DTSTART;VALUE=DATE-TIME:20180222T123000
DTEND;VALUE=DATE-TIME:20180222T133000
SUMMARY:Seminar: Osteoarthritis: predicting the unpredictable\, Dr Fiona 
 Watt\, Kennedy Institute of Rheumatology\, NDORMS\, University of Oxford
 
TZID:Europe/London
UID:20180222-8a17841a617a58ad016189db476f3692@warwick.ac.uk
CREATED:20180212T115144Z
DESCRIPTION:Abstract: Osteoarthritis (OA) is the commonest form of arthri
 tis\, and presents us with an enormous healthcare burden. Identifying ne
 w ways of intervening non-surgically in this disease would seem essentia
 l. An overview of our work in clinical translation of laboratory finding
 s in the Arthritis Research UK Centre for OA Pathogenesis will be given\
 , which aims to identify new tests and treatments for OA. Joint injury i
 s the greatest risk factor for development of OA. Our translational stud
 ies investigate how tissues respond to injury with the aim of increasing
  our understanding of the initiating processes in this disease. In labor
 atory studies\, we have shown that articular cartilage\, but also other 
 connective tissues\, respond within seconds to injury. A range of inflam
 matory signalling pathways are activated\, inducing a discrete set of in
 flammatory response genes implicated in inflammation but also cartilage 
 repair. The release of FGF-2 from articular cartilage appears important 
 in activation of many pathways on damage of connective tissues. Elements
  of this response\, regulated by mechanical load\, appear necessary for 
 development of later disease. To investigate whether this response trans
 lates to humans\, the Knee Injury Cohort at the Kennedy (KICK) study is 
 following 150 individuals with acute knee injury\, with clinical\, biolo
 gical sampling and imaging over 5 years. The majority of candidate bioma
 rkers from our pre-clinical studies were also found to be highly up-regu
 lated in the synovial fluid of those with acute joint injury. This bioma
 rker response\, best characterised by synovial fluid IL-6\, was signific
 antly associated with symptoms and function at the time of the injury\, 
 but also over the following 3 months. Studying the development of sympto
 matic OA in this setting may lead to better understanding of underlying 
 mechanisms of disease initiation\, but also resolution\, and we hope wil
 l help to develop much-needed prognostic tests and novel therapies for O
 A.
LOCATION:CSRL Seminar Room\, Clinical Sciences Buildingm UHCW
CATEGORIES:BiomedicalSciences,BMS_TEM
LAST-MODIFIED:20180212T115331Z
ORGANIZER;CN=Jas Bains:
END:VEVENT
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