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人类动脉粥样硬化斑块。

The human atherosclerotic plaque.

作者信息

Pearson T A, Kramer E C, Solez K, Heptinstall R H

出版信息

Am J Pathol. 1977 Mar;86(3):657-64.

Abstract

The fibrous plaque is regarded as the vascular lesion most characteristic of atherosclerosis. The notion that these lesions develop from mural thrombi has received considerable support, and there is also much support for the idea that plaques form as a reaction to mechanical or chemical damage to the endothelium. As an alternative to these two hypotheses, Benditt and Benditt have suggested that plaques represent monoclonal proliferation of altered smooth muscle cells similar to leiomyomas. Evidence in favor of this suggestion has been obtained using tissues from human black females who are heterozygous for the X-linked enzyme glucose-6-phosphate dehydrogenase (G6PD). In such individuals, as a result of random inactivation of the X-chromosome during embryogenesis, all normal tissues contain both the A and B isoenzymes of G6PD, when assayed electrophoretically, whereas plaques and other lesions suspected of being of monoclonal origin contain predominantly one isoenzyme. A certain proportion of fatty streaks also show a single G6PD isoenzyme pattern, suggesting that some fatty streaks act as the foreunners of the fibrous plaque.

摘要

纤维斑块被认为是动脉粥样硬化最具特征性的血管病变。这些病变由壁血栓发展而来的观点得到了相当多的支持,并且斑块是对内皮机械性或化学性损伤的反应这一观点也有很多支持。作为这两种假说的替代,本迪特和本迪特提出斑块代表类似于平滑肌瘤的改变的平滑肌细胞的单克隆增殖。使用来自X连锁酶葡萄糖-6-磷酸脱氢酶(G6PD)杂合的人类黑人女性的组织获得了支持这一观点的证据。在这类个体中,由于胚胎发育过程中X染色体的随机失活,当进行电泳分析时,所有正常组织都同时含有G6PD的A和B同工酶,而斑块和其他疑似起源于单克隆的病变主要含有一种同工酶。一定比例的脂肪条纹也显示出单一的G6PD同工酶模式,这表明一些脂肪条纹是纤维斑块的前身。

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The origins of atherosclerosis.动脉粥样硬化的起源。
Postgrad Med J. 1978 Mar;54(629):156-62. doi: 10.1136/pgmj.54.629.156.

本文引用的文献

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ARTERIOSCLEROSIS IN MAN, OTHER MAMMALS AND BIRDS.人类、其他哺乳动物和鸟类的动脉粥样硬化
Biol Rev Camb Philos Soc. 1964 Aug;39:372-423. doi: 10.1111/j.1469-185x.1964.tb01163.x.
9
The ultrastructure of uncomplicated human atheroma in surgically resected aortas.
J Atheroscler Res. 1966 Mar-Apr;6(2):120-31. doi: 10.1016/s0368-1319(66)80017-0.

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