Applications are invited for a post-doctoral research associate post in the Division of Cardiovascular Medicine (http://www.med.cam.ac.uk/divisions-and-research-groups/cardiovascular-medicine/). This post is funded by a BHF programme grant to Professor Martin Bennett . CLICK for details
Myocardial infarction is caused by rupture of the fibrous cap, with exposure of the lipid-rich core, or erosion, resulting in subsequent thrombosis and vessel occlusion. Plaques consist of a vascular smooth muscle cell (VSMC)-rich, fibrous cap, composed of collagen and extracellular matrix, which separates a lipid-rich core from the lumen. Our research studies the regulation of cell accumulation and interactions in vascular disease, using both human and mouse cells in vitro and models of atherosclerosis with genetic manipulation. We also have a major interest in vulnerable plaque imaging in patients using both invasive and non-invasive modalities. [Read More…]
Obaid, DR, Calvert,PA, Gopalan, D, Parker,RA, Hoole, SP, West, NEJ, Goddard,M, Rudd,JHF, Bennett, MR. Atherosclerotic plaque composition and classification identified by coronary CT: Assessment of CT- generated plaque maps compared with VH-IVUS and histology. Circulation Cardiovascular Imaging. 2013:6(5),655-664
Yu, E, Calvert, PA, Mercer, JR, Kumar, S, Harrison, J, Baker, L, Wang, J, Obaid, D, Figg, NL, Logan, A, West, N, Clarke, MCH, Vidal-Puig, A,Murphy, MP, Bennett, MR. Mitochondrial DNA damage can promote atherosclerosis independently of reactive oxygen species through effects on smooth muscle cells and monocytes, and correlates with higher risk plaques in humans. Circulation. 2013. In Press.
Zheng, Y, Humphry, M, Maguire, JJ, Bennett, MR, Clarke, MCH. Intracellular IL-1 receptor 2 binding prevents cleavage and activity of IL-1α, controlling necrosis-induced sterile inflammation. Immunity. 2013;38:285-295.