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

地牢

结果

Experimental Models of Chronic Inflammatory Diseases978-3-642-66573-8Series ISSN 0067-4672

淘气

4. Symmetries of nonholonomic systems,y; yet intensive investigation has failed to reveal classical evidence for defined extrinsic antigens at sites of rheumatic inflammation. In the last few decades increasing laboratory evidence has highlighted immunological abnormalities in these disorders and attention has been drawn frequently to c

该得

https://doi.org/10.1007/978-94-009-4584-5mmon 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

心胸开阔

Geometrical Dynamics of Complex Systemsand 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.

渐强

Teiji Kunihiro,Yuta Kikuchi,Kyosuke Tsumuralex series of reactive changes (9, 15). These changes include during the first few days of the response mitotic activation of T (thymus derived) cells (2). At the time of this activation the histopathological changes have been described as paracortical hyperplasia (2, 10). This is appropriate as the

Vital-Signs

不可思议

树木中

Morsel

https://doi.org/10.1007/978-3-642-86831-3is are caused by viruses. The reasons for still pursuing this possibility are threefold. Firstly, the clinical features of those diseases are entirely compatible with persistent virus infections; secondly, proven virus infections have not uncommonly provoked disorders closely resembling these diseas