54 results match your criteria: "E.N.Meshalkin National Medical Research Center[Affiliation]"

We performed a complex morphological analysis of atherosclerotic plaques obtained from 68 men with coronary atherosclerosis during coronary bypass surgery with endarterectomy. The expression of MMP-2 and MMP-9, collagen IV, CD31, CD34, factor VIII, and of smooth muscle cell actin was measured in the samples by morphometric and immunohistochemical methods. The expression of MMP-2 and MMP-9 as well as the intensity of neoangiogenesis estimated by the expression of CD31, CD34, and factor VIII in unstable plaques was significantly higher than in stable ones.

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Background: This paper describes and analyzes the cellular and molecular mechanisms underlying atherosclerosis development. In particular, the roles of monocytes/macrophages, smooth muscle cells, and vascular endothelium in the formation of stable/unstable atheromatous plaques, and the contributions of some processes to atheroma formation.

Methods And Results: In this study we analyzed endothelium: function, dysfunction, and involvement into atherogenesis; cell proteins mediating mechanotransduction; proatherogenic role of monocytes; the role of macrophages in the development of unstable atheromatous plaques and smooth muscle cell origin in atherosclerosis.

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Objective: We performed prospective randomized comparison of clinical and surgical outcomes of flow diversion versus PVO and bypass in patients with complex anterior circulation aneurysms.

Patients And Methods: Open, prospective, randomized, parallel group, multicenter study of complex intracranial aneurysms treatment was conducted. Patients with complex intracranial aneurysms of anterior circulation with neck is more than 4 mm wide, dome/neck ratio is equal or less than 2:1, which is suitable for flow diversion and occlusion with bypass were included in the study.

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Background: The objective of this article is to review cellular mechanism of atherosclerosis (AS) development. The pathogenesis of AS comprises a sequence of biological events leading to build up of a dense or loose atheromatous plaque (AP).

Methods: In this review, we tried to attempt to analyze the cellular mechanisms underlying AS development, including the roles of monocytes/macrophages and smooth muscle cells in the formation of stable/unstable APs.

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