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Biomedical subjects

E D Harris

Publications and source records attributed to E D Harris.

193 records · Page 11Linked to original sources
PubMedDate not supplied

Proliferative synovitis in hemophilia: biochemical and morphologic observations.

The synovium removed from the knee of a 10-year-old with hemophilia A was characterized morphologically and biochemically. The specimen showed villous hypertrophy with hyperplasia of synovial lining cells which contained abundant intracytoplasmic granules of hemosiderin. Monolayer cultures prepared from enzymatically dispersed tissue were characterized by pigment-laden fibroblast-like cells and round cells. Both explants of synovium and adherent cells secreted a large amount of latent collagenase and neutral proteinase into the culture medium. The secretion of these enzymes dropped sharply and intracellular pigment decreased with passage of these cultures. Lysozyme was secreted by the explants but was not detected in the monolayer culture medium. These data establish the degradative potential of the synovitis found in hemophilia and support the concept that recurrent hemarthrosis without inflammation is sufficient in and of itself to produce proliferative synovitis.

Cells, Cultured↗
PubMedDate not supplied

Collagen production by cultures containing multinucleated cells derived from synovial fibroblasts.

Multinucleate cells are found frequently in rheumatoid synovium. In this study, polyethylene glycol was used to fuse rabbit synovial fibroblasts. Approximately 40% of the cells developed more than one nucleus in a 24 hour period, during which time cell membranes had increased permeability. In cultures containing multinucleate cells, 3H-thymidine incorporation was depressed for 24 hours although 3H-leucine incorporation into TCA precipitable material was unaffected; autoradiography showed that depression of 3H-thymidine continued for at least 4 days. Collagenase production by cultures containing fused cells was increased more than 10-fold over control cultures during a 28 day period.

Animals↗
PubMedDate not supplied

Lead transport in IEC-6 intestinal epithelial cells.

This study evaluated the use of IEC-6 cells as a model for studying lead (Pb) transport by intestinal epithelial cells (IECs) and examined potential transport mechanisms for Pb uptake and extrusion. Pb accumulation in IEC-6 cells exposed to 5 and 10 microM Pb for up to 60 min was time- and dose-dependent. Reduction of incubation temperature significantly reduced the total cellular Pb content of IEC-6 cells. Simultaneous exposed of cells to zinc (Zn) and Pb resulted in decreased total cellular Pb contents compared to total cellular Pb contents of cells exposed to Pb only. IEC-6 cells treated with ouabain (1 mM) or sodium azide (1 mM) and 5 microM Pb accumulated more Pb than cells exposed to Pb only. Cells treated with p-chloromercuribenzensulfonic acid (50 microM), p-chloromercuribenzoic acid (50 microM), or iodoacetimide (50 microM) accumulated less Pb than cells treated with Pb only. We conclude that Pb uptake by IEC-6 cells depends on the extracellular Pb concentration. Our data suggest that the mechanism of Pb uptake by IECs is complex, and that Pb transport in IEC-6 cells is time- and temperature-dependent, involves sulfhydryl groups, and is decreased by the presence of Zn. Extrusion of Pb is at least partially dependent on metabolic energy.

Animals↗
PubMedDate not supplied

Collagenolytic systems in rheumatoid arthritis.

As the proliferative lesion of rheumatoid arthritis becomes polarized and invasion of articular cartilage and subchondral bone begins, it is likely that many mesenchymal cells, including periosteal and perichondral cells, and perhaps even the chondrocytes and osteoblasts themselves can be activated to produce destructive enzymes. Early in the course of RA cartilage proteoglycans are depleted, leaving the remaining collagen more susceptible to mechanical breakdown as well as to enzymatic breakdown. Specific collagenases are released by synovial cells and, in addition, by polymorphonuclear leukocytes. The latter enzyme may account for free collagenase found in synovial fluid, a finding possibly related to saturation of inhibitory proteins by proteases with greater affinity for them, leaving collagenase active. At this time in the course of rheumatoid arthritis, a joint would be under double jeopardy from enzymes released by the invading pannus as well as by collagenase free and active in the synovial fluid. Rapid destruction could occur. Although cartilage collagen has an intrinsic resistance to collagenase conferred by its primary structure and by higher order structure (e.g. intermolecular cross-links), it seems wise to cool down hot joints because increased temperature may increase the rate of collagen degradation and, therefore, cartilage destruction. In addition, superimposed sepsis or acute flares of rheumatoid disease result in enough influx of polymorphonuclear leukocytes into the joints to result in free collagenolytic activity being present. This provides a rationale for frequent aspiration of any joint fluid, septic or otherwise, containing high polymorphonuclear leukocyte counts.

Adult↗
PubMedDate not supplied

Pathogenesis of rheumatoid arthritis.

Rheumatoid arthritis (RA) is initiated by an unknown antigen(s) in the genetically programmed host. HLA-DR4 is associated with RA. The antigen could be exogenous (e.g., Epstein-Barr virus, bacterial cell wall products) or endogenous (e.g., collagen or immunoglobulin). Within the synovium, where the immune response begins, monocytes and lymphocytes are activated. Polyclonal B-cell proliferation results, as well as production of monokines and lymphokines. The antibodies form immune complexes with other antibody molecules or antigens. Phagocytosis of immune complexes results in production of many autacoids and activation of other soluble mediator systems, e.g., the coagulation, kinin, complement, and fibrinolytic systems in synovial fluid. Chemotactic factors draw polymorphonuclear leukocytes into the joint space. Monokines stimulate synovial cell proliferation; these cells, in turn, synthesize proteinases and products of arachidonate metabolism capable of destroying normal articular structures.

Antibodies, Antinuclear↗
PubMedDate not supplied

Interactions of murine macrophages with monosodium urate crystals: stimulation of lysosomal enzyme release and prostaglandin synthesis.

Exposure of murine peritoneal macrophages to crystals of monosodium urate monohydrate (MSUM) stimulated release of inflammatory mediators from the cells. There was an early, rapid burst of prostaglandin E2 (PGE2) synthesis which was complete by 2 h. Release of N-acetyl glucosaminidase (NAG), a lysosomal enzyme, was evident within 1 h and was maximal by 8 h. Early release of lysosomal enzymes (1-2 h) was not accompanied by leakage of cytoplasmic enzymes; however, treatment with high concentrations of MSUM, or prolonged exposure to crystals, provoked release of the cytoplasmic enzyme lactate dehydrogenase, presumably as a result os cell lysis. Responses of macrophages to MSUM occurred in the absence of serum but were modified by serum proteins. Prior exposure of crystals to IgG potentiated release of NAG and PGE2. Exposure to albumin slightly enhanced release of PGE2 induced by MSUM but did not affect NAG release. However, albumin prevented enhancement of NAG release by IgG. The interaction of MSUM with macrophages, and subsequent release of inflammatory mediators, may contribute to the inflammation association with both acute and chronic gouty arthritis.

Acetylglucosaminidase↗