38 research outputs found

    Nephrotic syndrome and collagenizing glomerulopathy in PVG/c rats treated with the α-mannosidase inhibitor "swainsonine"

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    Weanling PVG/c rats treated with the α-mannosidase inhibitor swainsonine developed increasing proteinuria which terminated as a severe nephrotic syndrome after 35 to 45 days. This was associated with a glomerulopathy characterized by the production of collagen fibrils adjacent to endothelial and mesangial cells, foot process expansion, subepithelial projections of the basement membrane, and splitting of the lamina densa. The swainsonine-induced glomerulopathy appeared to be an exacerbation of a spontaneous abnormality in this strain of rat

    Mannoside storage and axonal dystrophy in sensory neurones of swainsonine-treated rats: Morphogenesis of lesions

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    Young rats were treated with swainsonine for up to 200 days at a dose rate that restricted neuronal mannoside storage to neurones not protected by the blood/brain barrier. In lumbar dorsal root ganglion neurones, mannoside storage in the cell body developed in parallel to dystrophic changes at the extremities of peripherally and centrally directed axons. The dystrophic process involved the accumulation of autophagic structures. In the CNS, axonal dystrophy was confined to areas receiving long processes from affected neurones. The results suggest that axonal dystrophy is a direct consequence of the lysosomal storage process in parent cell bodies. The possible relationship of axonal dystrophy to neuronal lysosomal function is discussed

    Focal eosinophilic proctitis with associated rectal prolapse in a pony

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    Focal intramural nodules were palpated in the rectal wall of a 12-year-old pony mare presented for rectal prolapse. Eosinophilic proctitis was diagnosed by examination of fine needle aspirates and biopsy of the largest rectal nodule. After treatment with a course of corticosteroids, the rectal nodule and accompanying peripheral eosinophilia resolved. There was no recurrence of the condition during the follow-up period of 20 months. Focal eosinophilic proctitis appeared to be an unusual cause of tenesmus and rectal prolapse in this case

    Immunohistochemical demonstration of canine distemper virus antigen as an aid in the diagnosis of canine distemper encephalomyelitis

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    Brain tissue from 33 dogs with non-suppurative encephalitis was examined for evidence of canine distemper virus (CDV) encephalitis. Sections were examined for lesions, inclusion bodies, syncytial cells and CDV antigen using a double bridge unlabelled antibody enzyme technique. Histopathological lesions considered to be typical of granulomatous meningoencephalomyelitis were found in seven dogs. They all lacked inclusion bodies, syncytial cells and CDV antigen. The remaining 26 dogs all had histopathological lesions typical of CDV encephalitis. Inclusion bodies were found in 24 dogs, four of which also had syncytial cells and CDV antigen was detected immunocytochemically in 25. One dog had no inclusion bodies or syncytial cells and was immunohistochemically negative. Syncytial cells have been found to be of limited diagnostic value for the diagnosis of CDV encephalitis. While inclusion bodies proved to be a good diagnostic criterion for the confirmation of CDV infection, the immunohistochemical demonstration of CDV antigen proved to be superior. CDV antigen was more prevalent than inclusion bodies in tissue sections and much more easily detectable

    Stypandrone: A toxic naphthalene-14-quinone from Stypandra imbricata and Dianella revoluta

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    A compound, previously not isolated from dried, milled samples of Stypandra imbricata and Dianella revoluta, has now been obtained from fresh samples of these plants. The structure was shown, by spectroscopic techniques, to be identical to that of stypandrone. This quinone was found to be toxic to laboratory mice. However, it produces a different toxic effect to that observed when livestock ingest fresh Stypandra imbricata or when stypandrol is administered to laboratory mice

    Identification of galegine, an isoprenyl guanidine, as the toxic principle of Schoenus asperocarpus (poison sedge)

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    An Isoprenyl guanldine, galegine, was isolated from the Western Australian sedge Schoenus asperocarpus (Cyperaceae). Synthetic galegine was shown to reproduce the clinical and pathological features of poisoning by this plant. Preliminary results suggest that the massive thoracic effusion observed in sedge poisoning is the result of a direct effect on pulmonary vascular permeability
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