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  • 1
    ISSN: 1432-0533
    Keywords: Alkaline phosphatase ; Blood-brainbarrier ; Cytochemistry ; Endothelial cell ; Experimental allergic encephalomyelitis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To investigate the functions of endothelial cell (ECs) in chronic relapsing experimental allergic encephalomyelitis (EAE), we examined ECs ultracytochemically in various stages of EAE, in conjunction with the localization of alkaline phosphatase (AP) activity. We also studied the relation between the specific localization of AP activity and pathological features at each stage. Chronic relapsing EAE was induced in strain-13 guinea pigs by inoculation with homologous myelin. Controls were inoculated with complete Freund's adjuvant. The controls showed AP activity on the luminal and abluminal surfaces of the plasmalemma, and in pinocytic vesicles and vesicular pits. The localization of AP activity in the preclinical stage of EAE was similar to that in control animals. The initial inflammatory and actively demyelinating stage with perivascular cuffs of mononuclear cells showed AP-positive reactions on the abluminal surface of the plasmalemma, and in vesicles and pits, but not on the luminal surface in many ECs. In a later stage showing relatively old plaques with perivascular accumulation of debris-containing macrophages, AP activity continued to show localization similar to that seen in the initial stage, except for the presence of AP activity on some segments of the abluminal plasmalemma. Inactive lesions with marked perivascular fibrosis showed no AP reaction products. AP activity in unaffected areas showed the same localization as that in control animals throughout the various clinical stages of EAE. These findings suggest that AP activity decreased as the inflammatory demyelination in EAE progressed. The gradual disappearance of AP activity suggests development of functional impairment of ECs.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 75 (1988), S. 337-344 
    ISSN: 1432-0533
    Keywords: Experimental allergic encephalomyelitis ; Serum thymic factor ; Suppressor T cell ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Acute experimental allergic encephalomyelitis (EAE) was induced in Hartley guinea pigs and Lewis rats, which were then treated with synthetic serum thymic factor (FTS). When a dose of 30 μg/100 g body weight of FTS was subcutaneously administered to the animals on days — 1 (before inoculation), 4, 9 and 15 intermittently, clinical symptoms of acute EAE were suppressed. Histopathological evaluation showed that the severity of EAE in FTS-treated guinea pigs was less than in unteated guinea pigs. Immunohistochemical examination showed that the numbers of OX6+, W3/25+, W3/13+ and OX19+ cells in FTS-treated rats were less than in untreated rats and that the number of OX8+ cells in FTS-treated rats was greater than in untreated rats. These findings suggest that FTS induced OX8+ cells in inflammatory lesions and suppressed inflammation in acute EAE.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0533
    Keywords: Experimental allergic encephalomyelitis ; Blood-brain barrier ; Na+, K+-Adenosine triphosphatase ; Basal lamina ; Horseradish peroxidase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We induced chronic relapsing experimental allergic encephalomyelitis (EAE), and studied the ultrastructural and ultracytochemical changes of the blood-brain barrier (BBB) in the demyelinating lesions of various stages of EAE. In the chronic, inactive stage with gliosis and perivascular fibrosis, the basal lamina (BL) of the perivascular processes of astrocytes was formed only partially, and neural parenchyma was not fully separated from the perivascular mesenchymal tissues by the BL of astrocytic processes. Vascular permeability of the BBB was studied using exogenous horseradish peroxidase (HRP) as the tracer: HRP extravasation was marked during the stages of both active myelin breakdown and removal of debris, and was recognized even at the inactive stage, although the degree was reduced to a very low level. The functions of the endothelia, assessed by ouabain-sensitive, K+-dependentp-nitrophenylphosphatase activity, were impaired as EAE progressed. The decrease in HRP leakage at the inactive stage suggests the endothelial impairment of active transport of metabolites including HRP. Along with the development of infammatory demyelination in EAE, the BBB in affected areas became more and more altered, and gradual morphological and functional impairment of the BBB developed.
    Type of Medium: Electronic Resource
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