R
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
James I. Griffin,Guankui Wang,Weston J. Smith,Vivian P. Vu,Robert I. Scheinman,Dominik Stitch,Radu Moldovan,Seyed Moein Moghimi,Dmitri Simberg +8 more
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
Nirmal K. Banda,Sumitra Acharya,Robert I. Scheinman,Gaurav Mehta,Minoru Takahashi,Yuichi Endo,Wuding Zhou,Conrad A. Farrar,Steven H. Sacks,Teizo Fujita,Hideharu Sekine,V. Michael Holers +11 more
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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Complement therapeutics meets nanomedicine: overcoming human complement activation and leukocyte uptake of nanomedicines with soluble domains of CD55.
Geoffrey Gifford,Vivian P. Vu,Nirmal K. Banda,V. Michael Holers,Guankui Wang,Ernest Groman,Donald S. Backos,Robert I. Scheinman,S. Moein Moghimi,Dmitri Simberg,Dmitri Simberg +10 more
TL;DR: Results suggest that soluble domains of membrane-bound complement inhibitors are potential candidates for preventing nanomedicine-mediated complement activation in human subjects.
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Loss of a gimap/ian gene leads to activation of NF-kappaB through a MAPK-dependent pathway.
Rene Kupfer,Julie Lang,Cheryll Williams-Skipp,Matt Nelson,Donald Bellgrau,Robert I. Scheinman +5 more
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.