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CDB Seminars
All welcome

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All Seminars are held in the Gavin De Beer Lecture Theatre, Anatomy Building, Thursday 1-2pm (unless otherwise stated)

Thursday 9 July: midday-2.40pm

Host: Yoshiyuki Yamamoto

Room 249, 2nd Floor, Medical Sciences Building, Gower Street

12.00pm  Heather Steele-Stallard: “Human iPS cell-based platforms for disease modelling and therapy screening for laminopathies”
12.15pm  Terry Felton: “Regulation of asymmetric neurogenesis in C. elegans
12.30pm  Marcus Ghosh: “Assigning Behavioural and Neurodevelopmental Functions to Autism-associated Genes”
12.45pm  Giulia Ferrari: “Towards a genomic integration-free, iPS cell and human artificial chromosome-based therapy for Duchenne muscular dystrophy”
1.00pm  Michele Sammut: “Mystery cells in C.elegans: Sex, Glia transdifferation and Learning”
1.15pm  Johanna Buchler: "The Wnt co-receptor LRP6 and synapse regulation".
1.30pm  

Interval
1.40pm  Renato Martinho: “The Asymmetric Habenula of Zebrafish: from Transcriptome to Behaviour”
1.55pm  Alex Fedorec: “Plasmid persistence: balancing plasmid stability and host competitiveness”
2.10pm  Maryam Khosravi: "Investigating novel genetic associations with ciliopathy in the zebrafish"
2.25pm  Marc Williams: “Identification of neutral tumour evolution across cancer types”

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Dr Sean M Davidson

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Dr Sean M Davidson

Contact

Dr Sean M Davidson
Hatter Cardiovascular Institute
University College London
67 Chenies Mews
London, WC1E 6HX

Tel: 0203 447 5732
Email: s.davidson@ucl.ac.uk

Research

I am a senior research associate at the Hatter Cardiovascular Inst, and collaborate closely with Prof. Duchen on imaging the heart using both confocal and multiphoton microscopy.

These powerful techniques allow us to visualize real-time, physiological changes in the isolated, perfused heart. I am interested in the mechanism of ischaemia and reperfusion injury such as that caused by a heart attack. Using fluorescent dyes such as TMRM it is possible to detect changes in mitochondrial membrane potential that correspond to mitochondrial damage.

Alternatively, by using transgenic mice expressing a fluorescent reporter such as GCaMP2 it is possible to measure changes in cytosolic calcium during ischaemia and reperfusion and see how they correspond to regions of damage. Although cardiac muscle cells (cardiomyocytes) make up the bulk of the heart, they are actually outnumbered by the endothelial cells which line the vasculature.

Multiphoton microscopy allows visualization of both the cardiomyocytes and endothelial cells in the native arrangement, to see how they interact. Using these and other techniques I am exploring the possibility that damage to the mitochondria in endothelial cells contributes to ischaemia and reperfusion injury.

In addition to mitochondria, I am also interested in the role of lysosomes in cardiomyocytes and their possible contribution to cell damage.

Figures

Page last modified on 11 jul 12 11:52 by Edward D Whitfield