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Judy Turner


Warden, Battersea, Surrey, Cathedral, Twyford, International & Guildford Courts
+44 (0)1483 683091

Biography

Biography

What's your day job?I am a Senior Administrative Officer within the Exams and Graduation Team. My responsibility revolves around the co-ordination and delivery of in-semester tests, final examinations and graduation ceremonies. I also support the Awards team with processing awards and creating degree certificates.

What did you do before you came to Surrey?I worked for a number of seasons at Legoland Windsor. I then came to Surrey as a student and have not left. Whist at University I completed placement year working in HR for Monsoon / Accessorize. I was part of Team Surrey Ultimate and the Trampolining Club.

What do you do when you're not at work?I have a beautiful family with 3 young children so when I am not at work I spend most of my time tidying up toys! My children have very active social lives so I am forever taking them to birthday parties, swimming training, gymnastics, rugby, ballet or cub scouts. We love going to theme parks and spend lots of time visiting National Trust properties and exploring the Surrey Hills.

My publications

Publications

C Brenner, RE Simmonds, S Wood, V Rose, M Feldmann, J Turner (2012)TLR signalling and adapter utilization in primary human in vitro differentiated adipocytes., In: Scand J Immunol76(4)pp. 359-370 John Wiley & Sons

Toll-like receptors (TLRs) are central to innate immunity and yet their expression is widespread and not restricted to professional inflammatory cells. TLRs have been reported on adipocytes and have been implicated in obesity-associated pathologies such as diabetes. Why TLRs are found on adipocytes is not clear although one hypothesis is that they may coordinate energy utilization for the energy intensive process of an immune response. We have explored TLR signalling in primary human in vitro differentiated adipocytes and investigated the specific adapter molecules that are involved. Only lipopolysaccharide (LPS), poly(I:C), Pam3CSK4 and MALP-2 could induce the production of IL-6, IL-8 and MCP-1 by adipocytes. Poly(I:C) alone caused a strong induction of type I interferons, as assessed by IP-10 production. Using siRNA, it was confirmed that LPS-dependent signalling in adipocytes occurs via TLR4 utilizing the adapter molecules MyD88, Mal and TRIF and caused rapid degradation of IκBα. Pam3CSK4 signalling utilized TLR2, MyD88 and Mal (but not TRIF). However, the response to poly(I:C) observed in these cells appeared not to require TRIF, but MyD88 was required for induction of NFκB-dependent cytokines by Poly(I:C). Despite this, IκBα degradation could not be detected in poly(I:C) stimulated adipocytes at any time-point up to 4 h. Indeed, IL-6 transcription was not induced until 8-16 h after exposure. These data suggest that Pam3CSK4 and LPS signal via the expected routes in human adipocytes, whereas poly(I:C)/TLR3 signalling may act via a TRIF-independent, MyD88-dependent route.