Tuesday, 4 February 2014

ICM students' seminar, Wednesday 5 February 2014, 1.00pm, Room L2.5, 2nd floor, Leech Bldg, Medical School

 

 

Institute Research Student Seminars

Speakers:  Dr Amy Anderson, Research Associate (Musculoskeletal), Alison Heggie, PhD student (Diabetes) and Emily Mavin, PhD student (Haematology)

 

Venue: Seminar room L2.5, 2nd floor, Leech Building, Medical School

Date and time:  Wednesday 5 February 2014 at 1.00pm

 

Dr Amy Anderson will present:

 

“A Diagnostic Gene Signature for Patients with Rheumatoid Arthritis”.

 

We have recently identified a transcriptional signature in circulating CD4+ T-cells which predicted rheumatoid arthritis progression amongst patients attending an early arthritis clinic. The signature contained an over-representation of Stat3 regulated genes, whose expression in turn correlated with serum IL-6. The aim of this project was to investigate Stat3 signalling amongst immune cell subsets of an independent early arthritis patient cohort.

 

Key words: CD4+ T cells, rheumatoid arthritis, Stat3, IL-6

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Alison Heggie will discuss:

 

“DIRECT T2DM Progression: Identifying biomarkers of glycaemic deterioration and loss of beta-cell function in newly diagnosed patients with type 2 diabetes".

 

Type 2 diabetes is an increasingly prevalent disease, with variable rates of deterioration in beta cell function and glycaemic control over time.  At present we do not have any method of predicting how quickly individual patients will progress, and national protocols are used to guide treatment.  This European multicentre trial is the major part of my PhD, and aims to identify biomarkers for predicting rates of glycaemic deterioration, with the eventual aim of better stratification of treatment.

 

Key words: Type 2 diabetes, beta cell dysfunction, patient stratification

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Emily Mavin will speak on:

 

"Regulatory T cells in Haematopoietic Stem Cell Transplantation”

 

Regulatory T cells (Treg) are known to prevent GVHD in experimental models of HSCT, and clinical trials using Treg have shown promising results. This work demonstrates one possible mechanism of Treg action is modulation of moDC function, resulting in a less severe GVH response in our unique in vitro model of GVHD.

 

Keywords:  Treg, moDC, GvHD

 

Chair:  Rachel Williams, PhD student (Oral & Dental Sciences)

 

 

 

 

 

 

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