Recent views on cytohistological characteristics and pathogenic mechanisms of atherosclerotic lesions types I, II and III

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Histochemical and immunohistochemical analysis of ruptured atherosclerotic abdominal aortic aneurysm wall

Background/Aim. The main complication of the atherosclerotic abdominal aortic aneurism (AAA) is her rupture that begins with lesion in intima and rupture. The purpose of this work was to determine immunocytochemical and morphofunctional characteristics of the cells in aortic wall in ruptured atherosclerotic abdominal aortic aneurysm. Method. During the course of this study, 20 samples of atherosclerotic AAA were analyzed, all of them obtained during authopsy. The samples were fixed in 4% formalin and embedded in paraffin. Sections of 5 μm thickness were stained histochemically (of Heidenhain azan stain and Periodic acid Schiff - PAS stain) and immunocytochemically using a DAKO LSAB+/HRP technique to identify α-smooth muscle actin (α-SMA), vimentin, myosin heavy chains (MHC), desmin, S-100 protein, CD45 and CD68 (DAKO specification). Results. The results of our study showed that ruptured atherosclerotic AAA is characterized by a complete absence of endothelial cells, the disruption of basal membrane and internal elastic lamina, as well as a presence of the remains of hypocellular complicated atherosclerotic lesion in intima. On the plaque margins, as well as in the media, smooth muscle cells (SMCs) are present, which express a α-SMA and vimentin (but without MHC or desmin expression), as well as leukocyte infiltration, and a large number of foam cells. Some of the foam cells show a CD68-immunoreactivity, while the others show vimentin- and S-100 protein-immunoreactivity. Media is thinned out with a disorganized elastic lamellas, while adventitia is characterized by inflammatory inflitrate (infection). Conclusion. Rupture of aneurysm occurs from the primary intimal disruption, which spreads into thinned out media and adventitia. Rupture is caused by unstable atherom, hypocellularity, loss of contractile characteristics of smooth muscle cells in intima and media, neovascularization of the media, as well as by the activity of the macrophages in the lesion

DOI:10.2298/ABS1001039K MITOTIC ACTIVITY OF SMOOTH MUSCLE CELLS OF THE MYOMA: DOES HORMONAL STIMULATION HAVE AN EFFECT ON THE NUMBER OF MITOSES?

Abstract – Myomas develop as a result of increased mitotic (proliferating) activity of smooth muscle cells. In this study we examined the pathohistological samples of 176 myomas and their endometria that were obtained after hysterectomy from patients in the proliferative (follicular) and secretory (luteal) phase of the menstrual cycle. We examined the mitotic activity of the myoma cells in both phases and established that the average number of mitoses in the proliferative phase was significantly larger compared to the secretory phase, and that in the proliferative phase of the cycle there exists a statistically significant convergent association of the number of mitoses in the endometrium and in myomas. The number of endometrial mitoses is significantly larger than in myomas in both phases of the cycle

Mitotic activity of smooth muscle cells of the myoma: Does hormonal stimulation have an effect on the number of mitoses?

Myomas develop as a result of increased mitotic (proliferating) activity of smooth muscle cells. In this study we examined the pathohistological samples of 176 myomas and their endometria that were obtained after hysterectomy from patients in the proliferative (follicular) and secretory (luteal) phase of the menstrual cycle. We examined the mitotic activity of the myoma cells in both phases and established that the average number of mitoses in the proliferative phase was significantly larger compared to the secretory phase, and that in the proliferative phase of the cycle there exists a statistically significant convergent association of the number of mitoses in the endometrium and in myomas. The number of endometrial mitoses is significantly larger than in myomas in both phases of the cycle