Suppr超能文献

炎症细胞在淀粉样变性发病机制中的作用。

The role of inflammatory cells in the pathogenesis of amyloidosis.

作者信息

Kisilevsky R, Axelrad M, Corbett W, Brunet S, Scott F

出版信息

Lab Invest. 1977 Dec;37(6):544-53.

PMID:599900
Abstract

In the presence of amyloid enhancing factor, a variety of inflammatory stimuli, many of them nonantigenic, trigger amyloid deposition in 48 hours. There is a striking correlation between the extent of splenic amyloid deposition and the severity of inflammation at the injection site of the various irritants. Sublethal irradiation results in a parallel effect on the local inflammatory response and the accompanying extent of amyloid deposition produced in the spleen. Evidence that a product of local acute inflammatory responses is related to the deposition of amyloid is also presented. It is proposed that this product is a protease derived from the infiltrating polymorphonuclear leukocytes.

摘要

在淀粉样蛋白增强因子存在的情况下,多种炎症刺激(其中许多是非抗原性的)可在48小时内引发淀粉样蛋白沉积。脾脏淀粉样蛋白沉积的程度与各种刺激物注射部位的炎症严重程度之间存在显著相关性。亚致死剂量照射对局部炎症反应以及脾脏中伴随产生的淀粉样蛋白沉积程度具有类似影响。本文还提供了证据表明局部急性炎症反应的一种产物与淀粉样蛋白的沉积有关。有人提出该产物是一种源自浸润的多形核白细胞的蛋白酶。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验