中國醫藥大學機構典藏 China Medical University Repository, Taiwan:Item 310903500/29424
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    jsp.display-item.identifier=請使用永久網址來引用或連結此文件: http://ir.cmu.edu.tw/ir/handle/310903500/29424


    题名: Regional cerebral blood flow in patients with systemic lupus erythematosus
    作者: Shen, YY;Kao, CH;Ho, YJ;Lee, JK
    贡献者: 附設醫院核子醫學部;Taichung Vet Gen Hosp, Dept Nucl Med, Taichung 40705, Taiwan;Shin Kong Wu Ho Su Mem Hosp, Dept Nucl Med, Taipei, Taiwan;Jen Ai Hosp, Dept Radiol, Taichung, Taiwan;China Med Coll Hosp, Dept Nucl Med, Taichung, Taiwan
    日期: 1999
    上传时间: 2010-09-24 14:34:16 (UTC+8)
    出版者: LIPPINCOTT WILLIAMS & WILKINS
    摘要: Acrylamide intoxication produces peripheral neuropathy characterized by weakness and ataxia in both humans and experimental animals. Previous studies on animals of different ages and species indicate that the longest and largest nerves are affected earlier with the major pathology in the terminal parts of axons, i.e., distal axonopathy However, several issues have remained elusive; for example, what are the earliest pathological changes? An equally intriguing question is whether younger animals are more susceptible to acrylamide than older animals. To address these issues, we compared the vulnerability to acrylamide of 3- and 8-week-old mice. These mice were intoxicated with acrylamide in drinking water (400 ppm). The sequence of intoxication could be categorized into three stages. In the initial stage, there was no visible weakness or ataxia. The only noticeable changes were poor performance on the rota-rod test and swelling of motor nerve terminals. Obvious weakness and ataxia of hindlimbs developed gradually (here designated as the early stage). The weakness and ataxia progressed at variable speeds in mice of different ages, and eventually the forelimbs (quadriparesis) were affected in the late stage. Each stage appeared earlier in 3-week-old mice than in 8-week-old mice (7.1 +/- 1.1 vs 15.6 +/- 4.0 days, P < 0.01 for the early stage; and 15.3 +/- 2.1 vs 31.7 +/- 6.0 days,P < 0.01 for the late stage). The progression of neurological deficits was also faster in the younger mice (7.2 +/- 1.8 vs 16.3 +/- 4.2 days, P < 0.01). Pathological changes in the distal parts of motor nerves innervating hindfoot muscles were evaluated by combined cholinesterase histochemistry and immunocytochemistry for neuronal markers to demonstrate motor nerve terminals and neuromuscular junctions simultaneously. In the initial stage, there was axonal swelling in motor nerve terminals. As acrylamide intoxication continued, axonal swelling extended into junctional folds and into the intramuscular nerves, which resulted in Wallerian-like degeneration. Our results indicate that younger mice show a much higher susceptibility to acrylamide intoxication, and pathological changes precede neurological symptoms. (C) 1999 Academic Press.
    關聯: JOURNAL OF NEUROIMAGING 9(3):160-164
    显示于类别:[台中附設醫院] 期刊論文

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