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猴子实验性维生素B12缺乏的神经病理学

Neuropathology of experimental vitamin B12 deficiency in monkeys.

作者信息

Agamanolis D P, Chester E M, Victor M, Kark J A, Hines J D, Harris J W

出版信息

Neurology. 1976 Oct;26(10):905-14. doi: 10.1212/wnl.26.10.905.

Abstract

We have produced severe vitamin B12 deficiency in rhesus monkeys by feeding them a defined experimental diet under controlled conditions. Five years after institution of the deficient diet, the morphology and counts of peripheral blood and bone marrow are normal. Gross visual impairment appeared in five of the monkeys between 33 and 45 months after the institution of the vitamin B12 deficient diet. Subsequently, in three of the visually impaired animals, a gradually progressive spastic paralysis of their hind limbs developed. Autopsies of six deficient animals showed degeneration of the peripheral visual pathway in all and of white matter in the spinal cord in four. Degeneration of several cranial nerve roots was found in four monkeys and a mild diffuse degeneration of cerebral white matter in four. The lesions in all affected parts of the central nervous system were bilaterally symmetrical and were indistinguishable from those due to B12 deficiency in the human. No abnormalities were found in one B12 supplemented control animal.

摘要

我们通过在可控条件下给恒河猴喂食特定的实验性饮食,使其产生了严重的维生素B12缺乏症。在开始缺乏维生素B12的饮食五年后,外周血和骨髓的形态及计数均正常。在开始维生素B12缺乏饮食后的33至45个月之间,五只猴子出现了明显的视力损害。随后,在三只视力受损的动物中,其出现了后肢逐渐进展性的痉挛性麻痹。对六只缺乏维生素B12的动物进行尸检发现,所有动物的外周视觉通路均发生退化,四只动物的脊髓白质也出现退化。在四只猴子中发现了几条颅神经根的退化,四只猴子出现了轻度弥漫性脑白质退化。中枢神经系统所有受影响部位的病变均为双侧对称,与人类维生素B12缺乏所致病变无法区分。在一只补充了维生素B12的对照动物中未发现异常。

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