Simon Cuhlmann
Imperial College London
12 Papers
73 Citations
Simon Cuhlmann is an academic researcher from Imperial College London. The author has contributed to research in topics: Inflammation & Endothelium. The author has an hindex of 10, co-authored 12 publications. Previous affiliations of Simon Cuhlmann include British Heart Foundation & National Institutes of Health.
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Papers
Shear stress modulates the expression of the atheroprotective protein Cx37 in endothelial cells
Anna Pfenniger,Cindy W Wong,Esther Sutter,Simon Cuhlmann,Sylvie Dunoyer-Geindre,François Mach,Anton J.G. Horrevoets,Paul C. Evans,Rob Krams,Brenda R. Kwak +9 more
TL;DR: The effect of shear stress on Cx37 expression may contribute to the synchronization of ECs and participate in the protective effect of HLSS.
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In vivo mapping of vascular inflammation using the translocator protein tracer 18F-FEDAA1106
Simon Cuhlmann,Willy Gsell,Kim Van der Heiden,Josef Habib,Jordi L. Tremoleda,Magdy T. Khalil,Federico Turkheimer,Merlijn J. Meens,Brenda R. Kwak,Joseph L E Bird,Anthony P. Davenport,John W. Clark,Dorian O. Haskard,Rob Krams,Hazel A. Jones,Paul C. Evans +15 more
TL;DR: 18F-FEDAA1106 can be used in vivo for detection of vascular inflammation more specifically than FDG uptake, and the signal pattern of 18F- FEDAA 1106 corresponded with vascular inflammationMore specifically thanFDG uptake.
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Control of tissue morphology by Fasciclin III-mediated intercellular adhesion.
Richard E. Wells,Joseph Barry,Samantha J. Warrington,Simon Cuhlmann,Paul C. Evans,Wolfgang Huber,David Strutt,Martin P. Zeidler +7 more
TL;DR: A mathematical model of the developing hindgut, based on the differential interfacial tension hypothesis (DITH), suggests that increased intercellular adhesion provided by FasIII can be sufficient to drive the tightening of tube curvature observed, and identifies a conserved molecular mechanism that directly links JAK/STAT pathway signalling to intercellULAR adhesion.
Shear stress, inflammation and Atherosclerosis
TL;DR: The new hypothesis is discussed that blood flow and lipid driven inflammation are intimately related to each other and that shear stress induced expression of chemokines and the resulting coordinated homing of inflammatory cells influence plaque composition in such a way that vulnerable plaque may be induced.
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