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Howard J. Meyerson

Researcher at University Hospitals of Cleveland

Publications -  127
Citations -  3396

Howard J. Meyerson is an academic researcher from University Hospitals of Cleveland. The author has contributed to research in topics: Bone marrow & Leukemia. The author has an hindex of 30, co-authored 121 publications receiving 2986 citations. Previous affiliations of Howard J. Meyerson include Case Western Reserve University.

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Proteomic analysis and quantification of cytokines and chemokines from biomaterial surface-adherent macrophages and foreign body giant cells

TL;DR: Evidence that material surface chemistry can differentially affect monocyte/macrophage/FB GC adhesion and cytokine/chemokine profiles derived from activated macrophages/FBGCs adherent to biomaterial surfaces is presented.
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Type I IFN Drives a Distinctive Dendritic Cell Maturation Phenotype That Allows Continued Class II MHC Synthesis and Antigen Processing

TL;DR: It is suggested that IFN-I drives a distinctive DC maturation program that enhances Ag presentation to T cells without a shutdown of Ag processing, allowing continued sampling of Ags for presentation.
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Lymphocytes and the foreign body response: lymphocyte enhancement of macrophage adhesion and fusion.

TL;DR: These studies begin to detail the interactions between lymphocytes and macrophages in the absence of known antigen that appropriately relates to the scenarios experienced upon implantation of biomedical devices and the initiation of the foreign body response.
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Matrix metalloproteinases and their inhibitors in the foreign body reaction on biomaterials.

TL;DR: Analysis of the MMP/TIMP quantities produced per cell revealed that the hydrophilic/neutral surfaces, which inhibited macrophage adhesion, activated the adherent macrophages/FBGCs to produce a greater quantity of MMP-9, TIMP, and TIMP-2 per cell.
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Non–lineage/stage-restricted effects of a gain-of-function mutation in tyrosine phosphatase Ptpn11 (Shp2) on malignant transformation of hematopoietic cells

TL;DR: A common Shp2 mutation leads to myeloproliferative disease and malignant acute leukemia in stem cells and committed progenitors, associated with Sh p2 maintaining chromosomal stability.