• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

小鼠实验性淀粉样变性中血管病变的超微结构研究

Ultrastructural studies of vascular lesions in experimental amyloidosis of mice.

作者信息

Schultz R T, Pitha J V, McDonald T, Debault L E

出版信息

Am J Pathol. 1985 Apr;119(1):138-50.

PMID:3985120
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1888088/
Abstract

Definite lesions of arteriolar capillaries have been demonstrated in early amyloid lesions of mice. Pathologic changes include multiple endothelial gaps, the loss of an identifiable basal lamina, variable degrees of endothelial alteration, and the presence of the developing amyloid lesions surrounding the affected vessels. Despite these changes, the vessels remain functional part of the local microcirculation as demonstrated by intravascular injection of electron dense markers. These structural changes of arteriolar capillaries explain the presence of circulating plasma as a constant and major component of the early amyloid lesions in these animals and on this basis may determine the time of onset and site of formation of the lesions. The vascular injury appears to be caused by immunologic reactions to injected foreign antigens which gain a close relation to the structures of these vessels.

摘要

在小鼠早期淀粉样病变中已证实存在小动脉毛细血管的明确病变。病理变化包括多个内皮间隙、可识别的基膜缺失、不同程度的内皮改变,以及受影响血管周围正在形成的淀粉样病变。尽管有这些变化,但通过血管内注射电子致密标记物表明,这些血管仍是局部微循环的功能组成部分。小动脉毛细血管的这些结构变化解释了循环血浆作为这些动物早期淀粉样病变的持续且主要成分的存在,并且在此基础上可能决定病变的起始时间和形成部位。血管损伤似乎是由对注射的外来抗原的免疫反应引起的,这些抗原与这些血管的结构密切相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d5/1888088/d83e736cfafa/amjpathol00169-0155-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d5/1888088/b20c99a29b8f/amjpathol00169-0145-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d5/1888088/0d4cbd89bb61/amjpathol00169-0146-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d5/1888088/b80dd2408e17/amjpathol00169-0147-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d5/1888088/617bf63c0d3b/amjpathol00169-0147-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d5/1888088/9e44ae1cd165/amjpathol00169-0148-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d5/1888088/b330dd7a5691/amjpathol00169-0150-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d5/1888088/fa92efed7f57/amjpathol00169-0151-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d5/1888088/ae5438018115/amjpathol00169-0152-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d5/1888088/6538f06cd233/amjpathol00169-0153-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d5/1888088/c8ee022f16aa/amjpathol00169-0154-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d5/1888088/d83e736cfafa/amjpathol00169-0155-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d5/1888088/b20c99a29b8f/amjpathol00169-0145-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d5/1888088/0d4cbd89bb61/amjpathol00169-0146-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d5/1888088/b80dd2408e17/amjpathol00169-0147-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d5/1888088/617bf63c0d3b/amjpathol00169-0147-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d5/1888088/9e44ae1cd165/amjpathol00169-0148-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d5/1888088/b330dd7a5691/amjpathol00169-0150-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d5/1888088/fa92efed7f57/amjpathol00169-0151-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d5/1888088/ae5438018115/amjpathol00169-0152-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d5/1888088/6538f06cd233/amjpathol00169-0153-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d5/1888088/c8ee022f16aa/amjpathol00169-0154-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27d5/1888088/d83e736cfafa/amjpathol00169-0155-a.jpg

相似文献

1
Ultrastructural studies of vascular lesions in experimental amyloidosis of mice.小鼠实验性淀粉样变性中血管病变的超微结构研究
Am J Pathol. 1985 Apr;119(1):138-50.
2
Relation of the hepatic and splenic microcirculations to the development of lesions in experimental amyloidosis.肝脏和脾脏微循环与实验性淀粉样变性中病变发展的关系。
Am J Pathol. 1985 Apr;119(1):127-37.
3
[Role of increased vascular permeability in the formation of dimorphic amyloid in mouse myocardium].[血管通透性增加在小鼠心肌中双态淀粉样蛋白形成中的作用]
Arkh Patol. 1977;39(2):58-64.
4
Cells of monocyte/microglial lineage are involved in both microvessel amyloidosis and fibrillar plaque formation in APPsw tg mice.在APPsw转基因小鼠中,单核细胞/小胶质细胞系的细胞参与了微血管淀粉样变性和纤维状斑块的形成。
Brain Res. 2004 Oct 1;1022(1-2):19-29. doi: 10.1016/j.brainres.2004.06.058.
5
Pathogenesis of African horse sickness: ultrastructural study of the capillaries in experimental infection.非洲马瘟的发病机制:实验性感染中毛细血管的超微结构研究
J Comp Pathol. 1999 Aug;121(2):101-16. doi: 10.1053/jcpa.1999.0305.
6
Secondary amyloidosis in normal and immunocompromised mice infected with Schistosoma japonicum.感染日本血吸虫的正常及免疫功能低下小鼠中的继发性淀粉样变性
Br J Exp Pathol. 1987 Dec;68(6):825-38.
7
Ultrastructural investigations on the cellular morphogenesis of experimental mouse amyloidosis.实验性小鼠淀粉样变性细胞形态发生的超微结构研究。
Acta Pathol Microbiol Scand. 1967;71(4):575-91. doi: 10.1111/j.1699-0463.1967.tb05178.x.
8
The SJL/J mouse: a new model for spontaneous age-associated amyloidosis. I. Morphologic and immunochemical aspects.SJL/J小鼠:自发性年龄相关性淀粉样变性的新模型。I. 形态学和免疫化学方面
Lab Invest. 1976 Jul;35(1):47-54.
9
Tunica propria in chronic allergic rhinitis. Electron-microscopic study. I. The nasal blood vessels.慢性变应性鼻炎的固有层。电子显微镜研究。I. 鼻血管
ORL J Otorhinolaryngol Relat Spec. 1976;38(2):86-92. doi: 10.1159/000275261.
10
Role of altered vascular permeability amyloid formation.血管通透性改变在淀粉样蛋白形成中的作用。
Am J Pathol. 1977 Feb;86(2):321-41.

本文引用的文献

1
Elastase-type proteases on the surface of human blood monocytes: possible role in amyloid formation.人血单核细胞表面的弹性蛋白酶型蛋白酶:在淀粉样蛋白形成中的可能作用。
J Immunol. 1980 Jul;125(1):175-80.
2
Amyloid deposits and amyloidosis. The beta-fibrilloses (first of two parts).淀粉样沉积物与淀粉样变性。β-纤维蛋白原(两部分中的第一部分)。
N Engl J Med. 1980 Jun 5;302(23):1283-92. doi: 10.1056/NEJM198006053022305.
3
The ultrastructural basis of capillary permeability studied with peroxidase as a tracer.以过氧化物酶为示踪剂研究毛细血管通透性的超微结构基础。
J Cell Biol. 1967 Oct;35(1):213-36. doi: 10.1083/jcb.35.1.213.
4
Occurrence of amyloid deposits in the skin in secondary systemic amyloidosis.继发性系统性淀粉样变中皮肤淀粉样沉积物的出现。
Acta Pathol Microbiol Scand A. 1972;80(6):718-20. doi: 10.1111/j.1699-0463.1972.tb00341.x.
5
Amyloidosis (concluded).
N Engl J Med. 1967 Sep 21;277(12):628-38. doi: 10.1056/NEJM196709212771205.
6
Role of altered vascular permeability amyloid formation.血管通透性改变在淀粉样蛋白形成中的作用。
Am J Pathol. 1977 Feb;86(2):321-41.