Thursday, 17 March 2016

MRG lab meeting Friday 18th March 2016

Friday 18th March 2016 at 9.00am in the Baddiley Clark Seminar Room.

Chair

Dr Carole Proctor

Speakers

Nicola Maney. Title of talk "Refining a flow cytometric biomarker as an in vitro assay for clinical application in RA". (Post Doc, Supervisor Arthur Pratt)

Nishanthi Thalayasingam. Title of talk "Microarray analysis of the gene expression profile of peripheral blood B cells in early arthritis patients". (Clinical Fellow/PhD studentship. Supervisors John Isaacs, Amy Anderson and Arthur Pratt)

SilvIa Lecci. Title of talk "Identifying disease mechanisms to discover therapeutic targets for chondrodysplasias". ( PhD student, supervisors Drew Rowan and David Young)

Monday, 14 March 2016

An Osteoarthritis Special - Scaffolding, Mesenchymal Stem Cells and Gene Editing

 

 

 

 

 

 

 

 


ICM Research Seminar

 

Speakers: Dr David Almarza Gomez, (Prof J Loughlin)

Sylvia Muller (Dr Xiao Wang, Prof A Dickinson)

 

Venue: Dental Lecture Theatre F, Dental School

Date and Time:  Wednesday 16th March 2016, 13.00 pm – 14.00 pm

 

David Almarza Gomez will discuss

 

“Genome editing using CRISPR/Cas9 system to target OA risk loci”

 

Genome editing is a powerful tool to establish the functional and mechanistic roles of disease-associated single nucleotide polymorphisms (SNPs) mapped by genome wide association studies (GWASs). This project is intended to address causality of osteoarthritis (OA)-associated SNPs by generation of isogenic cell lines using CRISPR-Cas9 technology followed by phenotypic characterization. I will talk about my current work focussed on targeting OA risk loci with CRISPR-Cas9 system, as well as the establishment of a delivery system for genome editing substrates based on Integrase-defective lentiviral vectors.”

 

Sylvia Muller will discuss

 

'The effect of apatite-wollastonite glass ceramics on MSC growth, osteogenic differentiation and migration'

 

Apatite wollastonite (AW) is a bioactive glass ceramic used to produce osteoconductive scaffolds for bone repair. To produce high levels of integration and tissue regeneration scaffolds can be seeded with osteogenic precursors prior to implantation or be designed to recruit cells in from the surrounding tissues. In this study we investigate the osteogenic potency of CD271-enriched mesenchymal stromal cells (MSCs) and assess is AW scaffolds provide MSCs with any migratory stimulation

 

Chair: Nina Jordan

 

 

 

 

 

 

Toni Bell

 

Clerical Assistant

Institute of Cellular Medicine

4th Floor, William Leech Building | Newcastle University | Framlington Place | NE2 4HH

 

0191 208 5851

toni.bell@ncl.ac.uk

http://www.ncl.ac.uk/

 

 

 

Thursday, 10 March 2016

Dendritic Cells in RA

Our very own, Gary Reynolds...

 

 

VIVA SEMINAR

 

Speaker:  Gary Reynolds

 

Supervisors: Prof J Isaacs, Dr C Hilkens

 

 

Title : The origin and function of CD1c+ dendritic cells in rheumatoid arthritis

 

Abstract: Rheumatoid arthritis (RA) is a common autoimmune disease in which CD4+ T cells play a central role. The major subset of human myeloid dendritic cells identified by expression of CD1c+ specialises in modulating CD4+ T cell adaptive immune responses. As such they may represent a therapeutic target. In this work the origin and function of this DC subset in RA is explored.

 

 

Venue: Seminar Room 1.52, Ridley Building 2,

 

Date & time: Tuesday 15th March 2016, 11.30 am

 

 


 

 

Monday, 7 March 2016

ICM Seminar Wendesday 9th March 2016, Dental Lecture Theatre F, Dental School, 13.00 pm

Varied fare this Wednesday including osteoarthritis and physical exercise...


 

 

 

ICM Research Seminar

 

Speakers: Kile Green, (Prof M Collin, Dr V Bigley, Dr G Smith)

Rebecca Brown,  (Prof J Mathers, Dr L Avery, Dr N O’Brien, Dr D Cuthbertson)

Dr Pawel Palmowski, (Prof M Taggrt, Prof N Europe-Finner, Dr A Treumann

 

Venue: Dental Lecture Theatre F, Dental School

Date and Time:  Wednesday 9th March 2016, 13.00 pm – 14.00 pm

 

Kile Green will discuss

‘Array-based gene signature generation and gene set reduction in human blood monocyte and dendritic cell subsets’

 

Gene expression microarray data is typically composed of far more variables than samples. A major issue with this data format is revealed when using the data for the classification of samples or in the prediction of a clinical outcome. The problem of 'small n, large p' may be addressed through gene selection and dimension reduction under the presumption that while there are a large number of genes in the dataset, only a small number of these may actually account for the majority of the sample variation.

 

Rebecca Brown will discuss

'The Impact of Vitamin D and Physical Activity on Older Obese people with Knee Osteoarthritis - a cross sectional study'

 

Dr Pawel Palmowski will discuss

‘Protein expression changes in heart development. Mass spectrometry based proteomics analysis of fetal and adult guinea pig ventricular muscle’

 

Over the past 10 years we can observe a rapid expansion of proteomics technologies into all branches of biological science. They have a potential to provide an in depth qualitative and quantitative characterisation of a biological system in terms of protein expression, post translational modifications and interactions. In our study we utilise proteomics tools to identify processes and pathways involved in the process of heart development/maturation

 

Chair: Dara O’Hogain

 

 


Friday, 4 March 2016

Fibroblast Phenotypes

 

 

 

 

 

PI Seminar Series

 

Speaker:  Dr Lee Borthwick

Newcastle University Research Fellow

 

Venue:      Dental Lecture Theatre C

Date:          7th March 2016

Time:               13.00-14.00

 

Dr Lee Borthwick will present:

 

Investigating the regulation of fibroblast phenotype during fibrosis’

 

Abstract

Fibrosis causes excessive extra-cellular matrix deposition in an organ as part of an attempted reparative process following injury. It may represent an aberrant response to a single major injury or a response to persistent or repetitive injury.  The association of fibrosis with many chronic inflammatory conditions suggests that beneficial reparative processes that restore tissue homeostasis in physiological healing continue unchecked and result in pathological damage and loss of organ function.  Improving our understanding of the critical processes that fail to orchestrate physiological repair in an injured organ and instead cause pathological repair as fibrosis is critical to finding new therapeutic approaches.  

 

Fibroblasts constitute ~30% of cells in normal tissue and >50% of cells in diseased tissue.  The role of fibroblasts as the major fibrogenic cell is well characterized, however less is known about the potential of fibroblasts to contribute to innate immune and inflammatory responses.  Recent work from our laboratory has shown that human lung fibroblasts adopt a highly pro-inflammatory phenotype in response to epithelial damage and that this phenotypic switch is controlled by IL-1α/IL-1R1.  Conversely, the same fibroblasts are induced to adopt a highly fibrotic phenotype in response to treatment with the pro-fibrotic growth factor TGF-β1.  My research aims to investigate the mechanisms regulating fibroblast phenotypes and determine whether modulating fibroblast phenotypes in vivo provides a potential novel therapeutic strategy for patients with chronic inflammatory and fibrotic disease. 

 

Chair: Dr Ana Moles

 

 

 

Wednesday, 2 March 2016

ICM Research Seminar Wednesday 2nd March 2016, 13.00 pm, Dental Lecture Theatre F.

Good talks today

 

 

 

ICM Research Seminar

 

Speakers: Anna Lena Dittrich (Dr A Tyson-Capper, Dr H Gautrey)

Audrey Brown (Prof M Walker)

Matthew John Wood (Dr C Hilkens, Dr M Haniffa, Prof J Isaacs)

 

Venue: Dental Lecture Theatre F, Dental School

Date and Time:  Wednesday 2nd March 2016, 13.00 pm – 14.00 pm

 

Anna Lena Dittrich

Tumour promoting HER2 Splice Variant Δ16HER2: Regulation and Implication in Breast Cancer

Breast cancer is one of the major types of cancer for women. The human epidermal growth factor receptor 2 (HER2) is a well-known oncogene and therapy target in 20-30% of breast tumours. Although these therapies have proven efficient, therapy resistance has been observed. The underlying mechanisms are not well understood. One possible cause are HER2 protein variants generated by alternative splicing. The aim of this project is to uncover the processes regulating the production of the highly oncogenic HER2 splice variant Δ16HER2

 

Audrey Brown

Decreased TCF7L2 expression enhances insulin action in primary human skeletal muscle cell cultures

Variants within transcription factor 7-like 2 (TCF7L2) are the strongest genetic predictor of type 2 diabetes risk. Expression of TCF7L2 is ubiquitous but while many studies have examined the role of TCF7L2 in beta cells, few have examined TCF7L2 function in relation to glucose metabolism in peripheral tissues. The aim of the current study is to explore if TCF7L2 has a role in glucose metabolism in primary human skeletal muscle cells.

 

Matthew Wood

Do Synovial Dendritic Cells Contribute to the Pathogenesis of Rheumatoid Arthritis?

Dendritic cells (DCs) are thought to play an important role in rheumatoid arthritis (RA). Found clustered with T-cells in the synovium, they may activate auto-reactive lymphocytes locally. However, the precise role they play in RA pathogenesis remains unclear. We aim to identify and compare DC subsets by phenotyping, transcriptomics and functional capacity.  These subsets will be derived from the synovial tissue, fluid and peripheral blood of rheumatoid and osteoarthritis patients as well as healthy controls. These findings will be instrumental to delineating the mechanisms by which DCs contribute to the pathogenesis of RA.

 

 

 

Chair: Matt Barter