C
Carl Soderland
Researcher at University of Washington
Publications - 32
Citations - 2137
Carl Soderland is an academic researcher from University of Washington. The author has contributed to research in topics: Endothelial stem cell & Apoptosis. The author has an hindex of 21, co-authored 32 publications receiving 2064 citations. Previous affiliations of Carl Soderland include Lahey Hospital & Medical Center & Cornell University.
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Journal ArticleDOI
Endothelial cells release phenotypically and quantitatively distinct microparticles in activation and apoptosis.
TL;DR: EC release qualitatively and quantitatively distinct EMP during activation compared to apoptosis, and analysis of EMP phenotypic signatures may provide clinically useful information on the status of the endothelium.
Journal Article
Mechanisms for the transendothelial migration of HIV-1-infected monocytes into brain.
Hans S. L. M. Nottet,Y. Persidsky,Vito G. Sasseville,Adeline Nukuna,Paul J. Bock,Qi hui Zhai,Leroy R. Sharer,Rodney D. McComb,Susan Swindells,Carl Soderland,Howard E. Gendelman +10 more
TL;DR: HIV entry into brain is a consequence of the ability of virus-infected and immune-activated monocytes to induce adhesion molecules on brain endothelium, and an association between macrophage infiltration and increased endothelial cell adhesion molecule was observed in encephalitic brains.
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Thrombotic Thrombocytopenic Purpura and Sporadic Hemolytic-Uremic Syndrome Plasmas Induce Apoptosis in Restricted Lineages of Human Microvascular Endothelial Cells
Debashis Mitra,Eric A. Jaffe,Babette B. Weksler,Katherine A. Hajjar,Carl Soderland,Jeffrey Laurence +5 more
TL;DR: These phenomena support the pathophysiologic significance of microvascular EC apoptosis in TTP, extend it to a related disorder (sporadic HUS), and suggest consideration of apoptosis inhibitors in the experimental therapeutics of these syndromes.
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Endothelial microparticles released in thrombotic thrombocytopenic purpura express von Willebrand factor and markers of endothelial activation.
TL;DR: Studies indicate endothelial activation in TTP, and EMP that co‐express VWF and CD62E could play a role in the pathogenesis of TTP.
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Group B streptococci invade endothelial cells: type III capsular polysaccharide attenuates invasion.
TL;DR: It is concluded that endothelial cell invasion and injury are potential mechanisms in the pathogenesis of GBS disease.