Thrombosis

Rodman, Nathaniel

doi:10.1016/b978-0-12-783402-3.50018-4

Cited by 3 publications

(1 citation statement)

References 91 publications

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“…Recent evidence has suggested that tissue factor is present in cell membranes in an inactive form which is "activated" by an unknown mechanism as a result of the interaction of the cell with various agents (3,6). The location of tissue factor in the surface coat of endothelial cells and fibroblasts provides a ready source of procoagulant material for intravascular thrombus formation, while its presence in mononuclear cells (monocytes and lymphocytes) may explain the prominence of fibrin in many inflammatory disorders (22,47,48). We have suggested that antigens or antigen-antibody complexes, such as those elaborated during the renal allograft rejection reaction, can activate mononuclear cell tissue factor (7).…”

Section: Discussionmentioning

confidence: 99%

Structural features of Salmonella typhimurium lipopolysaccharide required for activation of tissue factor in human mononuclear cells.

Rickles¹,

Rick²

1977

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 99%

Structural features of Salmonella typhimurium lipopolysaccharide required for activation of tissue factor in human mononuclear cells.

Rickles¹,

Rick²

1977

J. Clin. Invest.

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Platelet Aggregation Mechanisms and Their Implications in Haemostasis and Inflammatory Disease

Willis¹

1978

Inflammation

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Morphology of the fibrinogen exudate during evolution of a mycobacterial-induced murine eye granuloma

O’Rourke

Wang

et al. 1988

Current Eye Research

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The intent of this study was to visualize changes in the density and location of fibrinogen-related antigen (FRA) depositions within the murine vitreous space during the formation of a chronic mycobacterial-induced uveitis (CMIU) granuloma. Concurrent changes in cellular morphology of the granuloma were also examined. Fibrinogen derivatives within the exudates of granulomatous cell-mediated inflammations may induce physical induration and numerous other phlogistic effects. However, technical limitations of conventional FRA staining methods have tended to underestimate the extent of their presence within this category of inflammatory lesions. Conventional H and E sections of the CMIU granuloma confirmed the classic progression-early PMN influx, monocyte maturation and final macrophage and epithelioid cell dominance-described for such lesions. Avidin-biotin-complex staining utilizing a polyclonal mouse antifibrinogen then revealed a progressive increase in amorphous extracellular fibrinogen-FRA-positive staining material as the granuloma evolved. Thus, on day one the PMN influx showed no evidence of fibrinogen-FRA staining; at one week heavy staining was evident in the anterior chamber and in consolidated (i.e. macrophage) regions of the granuloma; at one month a heavy uniform staining appeared throughout the indurated granuloma where macrophages and epithelioid cells predominated. Patterns of heavy deposition on macrophage surfaces were suggested. The likelihood that bulky accumulations of FRA in mature granulomas are not solely fibrin, and may account for granulomatous induration and persistence, is discussed.

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Thrombosis

Cited by 3 publications

References 91 publications

Structural features of Salmonella typhimurium lipopolysaccharide required for activation of tissue factor in human mononuclear cells.

Structural features of Salmonella typhimurium lipopolysaccharide required for activation of tissue factor in human mononuclear cells.

Platelet Aggregation Mechanisms and Their Implications in Haemostasis and Inflammatory Disease

Morphology of the fibrinogen exudate during evolution of a mycobacterial-induced murine eye granuloma

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