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Titlebook: Experimental Models of Chronic Inflammatory Diseases; Leonard Eleazar Glynn,Horst Dieter Schlumberger Conference proceedings 1977 Springer

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書目名稱Experimental Models of Chronic Inflammatory Diseases
編輯Leonard Eleazar Glynn,Horst Dieter Schlumberger
視頻videohttp://file.papertrans.cn/319/318882/318882.mp4
叢書名稱Bayer-Symposium
圖書封面Titlebook: Experimental Models of Chronic Inflammatory Diseases;  Leonard Eleazar Glynn,Horst Dieter Schlumberger Conference proceedings 1977 Springer
描述With the introduction of antibiotics acute inflammatory disease has ceased to be the dominant problem in general medical practice and its place is now increasingly occupied by chronic inflamma- tory disease of which the rheumatic diseases constitute the most important group. lwo aspects of these diseases need to be consid- ered, their aetiology and their pathogenesis. In some respects the latter is more important since even when the aetiology is known, as for example the haemolytic streptococcus in rheumatic fever, the mechanism by which the infecting agent accomplishes the development of the lesions that characterise the disease are still largely unknown. Still more so is this the case in rheuma- toid arthritis and other chronic inflammations where the aetio- logical agents are unknown. In an attempt to clarify the pathogenic mechanisms involved, sev- eral attempts have been made to induce comparable lesions in ex- perimental animals, partly to test underlying hypotheses, and partly to provide test situations for the trial of new therapeu- tic agents. In view of the deficiencies in the current drug treat- ment of chronic inflammatory disease there are many who feel that this is la
出版日期Conference proceedings 1977
關(guān)鍵詞Arthritis; antibiotics; diseases; inflammation; pathogenesis; rheumatic diseases; rheumatism
版次1
doihttps://doi.org/10.1007/978-3-642-66573-8
isbn_softcover978-3-642-66575-2
isbn_ebook978-3-642-66573-8Series ISSN 0067-4672
issn_series 0067-4672
copyrightSpringer-Verlag Berlin Heidelberg 1977
The information of publication is updating

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Persistence of Antigen in Experimental Allergic Monoarthritismmon with rheumatoid arthritis: it is chronic, it is immunologically induced and the histological picture of the synovitis is similar to that seen in rheumatoid arthritis (1, 2). In this experimental model it has been previously shown in our laboratory that antigen and antibody, in the form of immun
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Experimental Subcutaneous Granulomata Simulating R. A. Nodulesand histiocytes. The necrotic area contains collagen fibres in various stages of fragmentation and dissolution, intimately associated with fibrin and other serum proteins. The cells bordering the necrotic zone are characteristically elongated at right angles to its surface in the form of a palisade.
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Rheumatoid-Type Lymph Node Changes in Animals Exhibiting Immunoregulatory Defectslogic studies have revealed marked hypertrophy of the B-cell microenvironments (6) with excessive germinal centre formation and plasma cell cytodifferentiation, both in organised lymphoid tissue (7, 19, 22) and at ectopic foci (12, 21, 27). The hyperplastic changes in lymph nodes may, at times, be s
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Antibody Affinity, Macrophage Function and Immunoregulation in Murine Immune Complex Diseasetigens has shown that both quantitative and qualitative variations in antibody response underlie differences in susceptibility to this disease (3, 25). Furthermore, the observations that there are clear inter-strain differences in susceptibility to chronic ICD following neonatal infection of inbred
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