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[阿留申水貂病的发病机制。VII. 伴有胆管增生的慢性肝炎]

[Pathogenesis of aleutian mink disease. VII. Chronic hepatitis with bile duct proliferation].

作者信息

Drommer W, Trautwein G

出版信息

Vet Pathol. 1975;12(2):77-93. doi: 10.1177/030098587501200201.

DOI:10.1177/030098587501200201
PMID:242113
Abstract

Aleutian disease is a chronic persistent viral infection of mink characterized by hypergammaglobulinema, generalized plasmacytosis, sclerosing glomerulonephritis, polyarteritis, and plasma cell hepatitis with bile duct proliferation. The development of hepatic lesions was studied both light- and electron-microscopically in mink experimentally infected with Aleutian disease virus. Fifteen normal and 99 mink experimentally infected with Aleutian disease virus were used. Experimental mink were killed in intervals from 3 weeks to 23 months after infection, and liver sections were processed for both light- and electron-microscopic studies. Experimentally infected mink developed portal and intralobular lymphocytic and plasmacytic infiltrates in the liver 3 weeks after infection. Four to five weeks after infection there was evidence of early bile duct proliferation that began as an outgrowth of the portal bile ducts. Three to five months after infection a marked bile duct proliferation was present in some of the portal triads and adjacent liver lobules; but there was no tendency of these lesions to progress into biliary cirrhosis. Ultrastructural characteristics of proliferating bile duct cells were marked deformation, formation of multiple cell layers, reduction in the number of microvilli and desmosomes, and infiltration of the epithelial cells by lymphoid cells and plasmacytes. The hepatic lesions either develop by direct virus stimulation or by the deposition of virus-antibody complexes.

摘要

阿留申病是水貂的一种慢性持续性病毒感染,其特征为高球蛋白血症、全身性浆细胞增多、硬化性肾小球肾炎、多动脉炎以及伴有胆管增生的浆细胞性肝炎。利用光镜和电镜研究了感染阿留申病病毒的实验性水貂肝脏病变的发展情况。使用了15只正常水貂和99只感染阿留申病病毒的实验性水貂。实验性水貂在感染后3周-23个月期间分批处死,肝脏切片用于光镜和电镜研究。实验性感染的水貂在感染后3周肝脏出现门管区和小叶内淋巴细胞及浆细胞浸润。感染后4-5周有早期胆管增生的迹象,表现为门管区胆管的增生。感染后3-5个月,一些门管区三联体和相邻肝小叶出现明显的胆管增生;但这些病变无发展为胆汁性肝硬化的趋势。增生胆管细胞的超微结构特征为明显变形、形成多层细胞、微绒毛和桥粒数量减少以及上皮细胞被淋巴细胞和浆细胞浸润。肝脏病变要么是由病毒直接刺激引起,要么是由病毒-抗体复合物的沉积所致。

相似文献

1
[Pathogenesis of aleutian mink disease. VII. Chronic hepatitis with bile duct proliferation].[阿留申水貂病的发病机制。VII. 伴有胆管增生的慢性肝炎]
Vet Pathol. 1975;12(2):77-93. doi: 10.1177/030098587501200201.
2
Comparison of the lesions of Aleutian disease in mink and hypergammaglobulinemia in ferrets.水貂阿留申病病变与雪貂高球蛋白血症的比较。
Am J Vet Res. 1978 Apr;39(4):653-7.
3
Aleutian disease in mink: virology, immunology and pathogenesis.水貂阿留申病:病毒学、免疫学与发病机制
J Rheumatol. 1984 Oct;11(5):576-7.
4
Reduced severity of lesions in mink infected transplacentally with Aleutian disease virus.经胎盘感染阿留申病病毒的水貂病变严重程度降低。
J Immunol. 1977 Sep;119(3):872-6.
5
Aleutian disease of mink. Prevention of lesions by immunosuppression.水貂阿留申病。通过免疫抑制预防病变。
Am J Pathol. 1972 Mar;66(3):543-56.
6
Studies on the pathogenesis of Aleutian disease of mink. XII. Immunopathological determinants of immune complex glomerulonephritis.水貂阿留申病发病机制的研究。十二、免疫复合物性肾小球肾炎的免疫病理决定因素。
Zentralbl Veterinarmed B. 1983 Aug;30(7):487-501.
7
Much of the increased IgG in Aleutian disease of mink is viral antibody.水貂阿留申病中增加的大部分免疫球蛋白G是病毒抗体。
J Exp Pathol. 1984;1(2):79-88.
8
Transmission of Aleutian disease from mink with inapparent infections.隐性感染水貂传播阿留申病
Am J Vet Res. 1978 Feb;39(2):309-13.
9
Pathogenesis of aleutian disease of mink: identification of nonpersistent infections.水貂阿留申病的发病机制:非持续性感染的鉴定
Infect Immun. 1975 Jan;11(1):92-4. doi: 10.1128/iai.11.1.92-94.1975.
10
The immunoglobulins in Aleutian disease (viral plasmacytosis) of mink. Different types of hypergammaglobulinemias.水貂阿留申病(病毒性浆细胞增多症)中的免疫球蛋白。不同类型的高球蛋白血症。
Can J Comp Med. 1970 Oct;34(4):329-32.

引用本文的文献

1
Interferon response in normal and Aleutian disease virus-infected mink.正常及感染阿留申病病毒的水貂的干扰素反应
J Virol. 1986 Aug;59(2):514-7. doi: 10.1128/JVI.59.2.514-517.1986.