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由泰勒氏鼠脑脊髓炎病毒引起的慢性中枢神经系统感染中的复发性脱髓鞘病变。

Recurrent demyelination in chronic central nervous system infection produced by Theiler's murine encephalomyelitis virus.

作者信息

Dal Canto M C, Lipton H L

出版信息

J Neurol Sci. 1979 Aug;42(3):391-405. doi: 10.1016/0022-510x(79)90172-2.

Abstract

A morphologic study of demyelination produced by Theiler's encephalomyelitis virus (TMEV) infection in C3H/He mice was performed. Demyelination in this strain of mouse was less intense and had a milder gliomesodermal response than that observed in SJL mice. As early as 80 days after infection numerous remyelinated axons were present in C3H/He mice, and later, extensive remyelination was observed and was mainly by Schwann cells. About one-third of remyelinated plaques showed recurrent demyelinating activity at 200 days. The best evidence of recurrent demyelination was the loss of myelin by abons which had been previously remyelinated by Schwann cells. In addition, acute areas of demyelination were also seen in spinal cords which contained chronic or quiescent plaques. The demonstration of recurrent demyelination in TMEV infection is important for it increases the relevance of this model to multiple sclerosis (MS). In addition TMEV infection of C3H/He mice appears to be an excellent model for further studies of Schwann cell remyelination and recurrent demyelination in the central nervous system (CNS).

摘要

对感染泰勒氏脑脊髓炎病毒(TMEV)的C3H/He小鼠所产生的脱髓鞘进行了形态学研究。该品系小鼠的脱髓鞘程度较轻,与SJL小鼠相比,其胶质中胚层反应也较温和。早在感染后80天,C3H/He小鼠体内就出现了大量再髓鞘化的轴突,随后观察到广泛的再髓鞘化,主要由雪旺细胞完成。在200天时,约三分之一的再髓鞘化斑块显示出复发性脱髓鞘活动。复发性脱髓鞘的最佳证据是先前由雪旺细胞再髓鞘化的轴突失去髓鞘。此外,在含有慢性或静止斑块的脊髓中也可见急性脱髓鞘区域。TMEV感染中复发性脱髓鞘的证实很重要,因为这增加了该模型与多发性硬化症(MS)的相关性。此外,C3H/He小鼠的TMEV感染似乎是进一步研究中枢神经系统(CNS)中雪旺细胞再髓鞘化和复发性脱髓鞘的极佳模型。

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