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- W1024478505 abstract "The inflammatory process has an essential impact on the development of atherosclerosis. Three mechanisms are mentioned: 1) possibility of direct development of Chlamydia infection in the vicinity of the blood vessel wall; 2) impact of persistent or recurrrent Chlamydia infection on the increased blood concentration of risk factors for atherosclerosis; 3) an autoimmunological reaction.Electron microscope examinations were performed on specimens from atherosclerotic lesions of the interior cervical arteries, collected from patients who had undergone endarterectomy. The material came from 8 patients (age from 58 to 72). The specimens were fixed for electron microscopy, and after dehydration were immersed in Spurr resin. Ultrathin slices were examined under a transmission electron microscope.In the successive tested layers nearest the lumen of the vessel we found erythrocytic elements, fibrin, and lipid membranes. In deeper layers there were lymphocytic cells, monocytes, and macrophages loaded with phagocyted lipid material. Under this layer we found in some specimens a coating which had undergone mineralization: calcium structures and cholesterol were overlaid on a proteoglycanate base. Smooth muscles cells had undergone the heaviest proliferation among the cells on artery wall. In the tested material we detected diversified morphological forms of Chlamydia sp. Particular attention should be drawn to the appearance of very young vessel forms, which suggests a process of angiogenesis in the atherosclerotic plaques.We found that one of the pathogens that may lead to atherosclerotic lesions is Chlamydia sp. The process of atherogenesis in cervical arteries is accompanied by angiogenetic processes." @default.
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- W1024478505 date "2002-01-01" @default.
- W1024478505 modified "2023-09-27" @default.
- W1024478505 title "Electron microscope investigation of the role of Chlamydia sp. in the process of rebuilding the arterial wall. Neoangiogenesis in atherosclerotic plaques in human cervical artery walls." @default.
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