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  1. Article ; Online: Perturbation of a Cartilage Autocrine/Paracrine Basic Fibroblast Growth Factor Metabolic Regulatory Network by Osteoarthritic Synovial Tissue.

    Herman, Jerome H. / O'Connor, Michael P. / Lieberman, Michael A.

    American journal of therapeutics

    2002  Volume 3, Issue 1, Page(s) 52–62

    Abstract: Studies have focused on control of expression and the relative importance of basic fibroblast growth factor (bFGF) in a purported autocrine/paracrine regulatory network functioning in the modulation of cartilage metabolic and structural homeostasis. ... ...

    Abstract Studies have focused on control of expression and the relative importance of basic fibroblast growth factor (bFGF) in a purported autocrine/paracrine regulatory network functioning in the modulation of cartilage metabolic and structural homeostasis. Preformed and newly synthesized bFGF and concurrent antagonist activity could be identified by bioassay in cell/pericellular matrix extracts of normal bovine articular chondrocytes maintained in suspension culture. Specificity was determined using antibody neutralization. Prostanoids (PGE(1), PGE(2)) enhanced chondrocyte expression of the putative inhibitor. The antagonist, recognized in the presence of suboptimally triggered bFGF receptors, was active against both endogenously produced and recombinant bFGF. Chondrocyte expression of bFGF was significantly altered following exposure to conditioned medium obtained from explant cultures of osteoarthritic synovial tissue. Response pattern, that is, an upregulation or downregulation of growth factor expression, was dependent on medium concentration and the duration of chondrocyte exposure. Synovium-conditioned medium generated in the presence of PGE(1) appeared to attenuate suppressive responses seen with naive conditioned medium. Promotion of expression of bFGF inhibitory activity within the milieu of the diseased joint may negate potential detrimental pathophysiologic effects of this competence factor on cartilage, synovial tissue, and bone metabolism and repair.
    Language English
    Publishing date 2002-01-17
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1280786-2
    ISSN 1536-3686 ; 1075-2765
    ISSN (online) 1536-3686
    ISSN 1075-2765
    DOI 10.1097/00045391-199601000-00008
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Book: Rheumatoid arthritis: theoretical and clinical aspects

    Herman, Jerome H

    Papers by Jerome H. Herman [et al.]

    1973  

    MeSH term(s) Arthritis, Rheumatoid
    Language English
    Size 247 p., illus.
    Publisher MSS Information Corp
    Publishing place New York
    Document type Book
    Note Reprinted from various journals.
    ISBN 9780842271080 ; 0842271082
    Database Catalogue of the US National Library of Medicine (NLM)

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  3. Article: Hypertrophic pachymeningitis in rheumatoid arthritis after adalimumab administration.

    Ahmed, Mansoor / Luggen, Michael / Herman, Jerome H / Weiss, Kenneth L / Decourten-Myers, Gabrielle / Quinlan, John G / Khanna, Dinesh

    The Journal of rheumatology

    2006  Volume 33, Issue 11, Page(s) 2344–2346

    Abstract: Tumor necrosis factor-a (TNF-a) inhibition, used in the treatment of rheumatoid arthritis (RA), is associated with central nervous system (CNS) events including new onset and/or exacerbations of pre-existing demyelinating neurological diseases. We ... ...

    Abstract Tumor necrosis factor-a (TNF-a) inhibition, used in the treatment of rheumatoid arthritis (RA), is associated with central nervous system (CNS) events including new onset and/or exacerbations of pre-existing demyelinating neurological diseases. We describe a patient with refractory RA where adalimumab, a fully humanized IgG1 monoclonal antibody against TNF-a, may have contributed to the development of meningoencephalitis, with brain biopsy suggestive of hypertrophic pachymeningitis, a rare complication of this disease. The patient had recurrence of neurological symptoms upon repeated administration of adalimumab, and resolution of symptoms after withdrawal.
    MeSH term(s) Adalimumab ; Aged ; Anti-Inflammatory Agents/administration & dosage ; Antibodies, Monoclonal/adverse effects ; Antibodies, Monoclonal, Humanized ; Antirheumatic Agents/adverse effects ; Arthritis, Rheumatoid/drug therapy ; Histocytochemistry ; Humans ; Magnetic Resonance Imaging ; Male ; Meningitis/chemically induced ; Meningitis/diagnosis ; Meningitis/drug therapy ; Prednisone/administration & dosage
    Chemical Substances Anti-Inflammatory Agents ; Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Antirheumatic Agents ; Adalimumab (FYS6T7F842) ; Prednisone (VB0R961HZT)
    Language English
    Publishing date 2006-11
    Publishing country Canada
    Document type Case Reports ; Journal Article
    ZDB-ID 194928-7
    ISSN 1499-2752 ; 0315-162X
    ISSN (online) 1499-2752
    ISSN 0315-162X
    Database MEDical Literature Analysis and Retrieval System OnLINE

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