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Robert I. Scheinman

Researcher at Anschutz Medical Campus

Publications -  58
Citations -  6050

Robert I. Scheinman is an academic researcher from Anschutz Medical Campus. The author has contributed to research in topics: Complement system & Arthritis. The author has an hindex of 26, co-authored 56 publications receiving 5784 citations. Previous affiliations of Robert I. Scheinman include University of Washington & University of Montana.

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Feraheme (Ferumoxytol) Is Recognized by Proinflammatory and Anti-inflammatory Macrophages via Scavenger Receptor Type AI/II

TL;DR: Feraheme is efficiently recognized via SR-AI/II but not via complement by different macrophage types, and the recognition by the common phagocytic receptor has implications for specificity of imaging of macrophages subtypes.
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Revealing Dynamics of Accumulation of Systemically Injected Liposomes in the Skin by Intravital Microscopy

TL;DR: A regulatory approved PEGylated liposomal doxorubicin and empty liposomes of the same composition as LipoDox showed similar skin distribution as P EGylated egg PCliposomes, suggesting that this phenomenon is relevant to liposome of different lipid composition.
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Deconstructing the Lectin Pathway in the Pathogenesis of Experimental Inflammatory Arthritis: Essential Role of the Lectin Ficolin B and Mannose-Binding Protein-Associated Serine Protease 2

TL;DR: It is shown that FCN A and CL-11−/− mice are fully susceptible to collagen Ab–induced arthritis (CAIA), and FCN B and MASP-2 are substantially protected, with clinical disease activity decreased significantly and it is speculated that the residual disease seen in these studies is driven by the AP and/or the C2/C4 bypass pathway via the direct cleavage of C3 through an LP-dependent mechanism.
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Loss of a gimap/ian gene leads to activation of NF-kappaB through a MAPK-dependent pathway.

TL;DR: Data is interpreted as demonstrating that the activation caused by loss of Gimap5 is a cell intrinsic phenomenon caused, in part, by a MEK-dependent activation of IKK, which would suggest that Gimap 5 functions to promote both T cell survival and quiescence and that these pathways are biochemically linked.