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[实验性支原体关节炎的发病机制概念]

[Pathogenetic concept of experimental mycoplasma arthritis].

作者信息

Klein G

出版信息

Fortschr Med. 1977 Feb 17;95(7):408-13.

PMID:849853
Abstract

Biochemical studies of rats with mycoplasma arthritis revealed new findings in pathogenesis and pathophysiology. Mycoplasma infection which resembles rheumatoid arthritis, leads to an inhibition of the DNA-repair. We were able to proof this enzyme--kinetically and autoradiographically. We also observed for the first time the occurrence of DNA-antibodies in this type of arthritis. It is possible that there is a relation between inhibition of DNA-repair and the occurrence of DNA-antibodies. Thus mycoplasma infection seems to influence DNA-metabolism. There are interesting parallels concerning DNA-antibodies and DNA-repair between experimental mycoplasma arthritis and human systemic lupus erythematosus and rheumatoid arthritis.

摘要

对患有支原体关节炎的大鼠进行的生化研究揭示了发病机制和病理生理学方面的新发现。类似于类风湿性关节炎的支原体感染会导致DNA修复受到抑制。我们能够从动力学和放射自显影方面证实这种酶的存在。我们还首次观察到在这类关节炎中出现了DNA抗体。DNA修复抑制与DNA抗体的出现之间可能存在关联。因此,支原体感染似乎会影响DNA代谢。在实验性支原体关节炎与人类系统性红斑狼疮和类风湿性关节炎之间,关于DNA抗体和DNA修复存在有趣的相似之处。

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