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  • 1970-1974  (5)
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  • 1
    Publication Date: 1972-01-01
    Description: Alterations in the vascular sinus and hematopoietic compartment of rat bone marrow were observed with electron microscopy during the pathogenesis of an acute myelogenous leukemia. As the disease progresses, the sinus wall becomes damaged and disintegrates; normal hemic elements disappear, and the marrow compartment becomes packed with leukemic myeloblasts. Viruslike particles are present in intercellular spaces and appear to bud from leukemic cells.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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  • 2
    Publication Date: 1973-08-01
    Description: The ultrastructure of the spleen was studied in four patients with myelofibrosis with myeloid metaplasia (MMM) who underwent splenectomy. The basic structure of the spleen is not altered. Degenerative changes are seen in the white pulp, which appears atrophic. Hemopoietic tissue (erythropoietic and granulopoietic cells, as well as megakaryocytes) is seen in the sinuses, as well as in the cords of the red pulp, but is not seen in the white pulp. Nuclear and cytoplasmic abnormalities are seen in hemopoietic cells. Nuclear changes consist of the nuclear membrane projecting into the cytoplasm and forming nuclear blebs or loops. The nuclear blebs are sometimes connected to the main nuclear body by a stalk containing fibrillar structures. The nuclear loops may be so large as to engulf almost all the cytoplasm. Cytoplasmic changes are degenerative in nature and result in premature destruction followed by phagocytosis. Macrophages are ubiquitous in the red pulp, particularly in association with extracellular reticulum and the basement membranes. They often contain debris of developing hemopoietic cells. These findings support previous studies that indicate that a portion of splenic hemopoiesis in MMM is ineffective.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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  • 3
    Publication Date: 1974-05-01
    Description: The reticulum and vascular sinuses of the normal rat spleen were studied by scanning electron microscopy. Observations were also made of erythrocytes, macrophages, platelets, and other migratory elements. Reticular cells of the periarterial lymphatic sheath, the marginal zone, and cordal spaces were large, bulky, irregular cells with broad processes that formed a spongework. When marked retraction of these cells was induced in the drying phase of tissue preparation, they showed the slender multiple fingerlike processes characteristic of the argyrophilic reticulum. The reticular cells at the periphery of the periarterial lymphatic sheath were flattened and formed cylinders about the central artery. They were, moreover, associated with unusually heavy extracellular fibers. Vascular sinuses were suspended in the reticulum by attachments of cordal reticular cells and of fibrillar reticulum to the adventitial surface. Adventitial cells of the sinus, moreover, branched into the cords. Endothelial cells typically lay side by side without gaps, except as migratory cells passed through the wall. Erythrocytes were commonly observed in passage across the sinus wall. In sinuses and cords, they were often swollen, irregular, and bore blebs and crenulations. Macrophages displayed rich surface folds and processes. Platelets were abundant and were adherent to the surface of reticular cells and the endothelium of sinuses. Such adherence appeared to be the manner in which the platelets were sequestered in the spleen.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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  • 4
    Publication Date: 1970-08-01
    Description: The structure of vascular sinuses in rat bone marrow is modified as cells cross their wall. Endotoxin, by causing withdrawal of granulocytes from the circulation, induces a compensatory discharge of fresh granulocytes through the wall of sinuses. As a result the sinus wall becomes infiltrated by clusters of late-stage hematopoietic cells which appear in transmural passage. Two correlates of such infiltration are elevation of adventitial cells from the wall and the creation of adventitial spurs extending into perisinusal hematopoietic spaces. In untreated rats adventitial cells cover, on the average, about 65 per cent of the sinus wall. After 0.04 µg. endotoxin the cover is reduced, fitting a slope regressing at the rate of 0.22 per cent/min. (t = 3.1038, p = 〈 0.003), the last determinations made at 120 minutes. Values for the percentage of adventitial cover calculated from observations after endotoxin are 52.5 per cent in 90 minutes and 32 per cent in 120 minutes. Even after endotoxin, a number of sinuses retain full cover while a number of control sinuses, likely reflecting normal cell passages, have little adventitial cover. Endothelial cells form a continuous layer. Apertures occur in the wall normally and increase in number after endotoxin. These apertures may contain cells, apparently in passage, or may be free of cells. Lysosomal disruption occurs in mural cells, particularly in segments of wall associated with cellular passage and with gelatinous change.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
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  • 5
    Publication Date: 1973-04-01
    Description: The passage of erythrocytes through the walls of splenic sinuses was studied in rats treated with phenylhydrazine. The sinus wall contained no preformed apertures. Instead, erythrocytes and other cells passing through the spleen entered interendothelial slits and squeezed through. The presence of phenylhydrazine-induced Heinz bodies within erythrocytes impeded their transmural passage. Normally, few erythrocytes were found in transit across the walls of sinuses. However, after phenylhydrazine, many of the interendothelial slits in sinuses were occupied by damaged erythrocytes. Virtually all of the interendothelial slits in sinuses appeared capable of passing erythrocytes. The slits seldom exceeded 0.2-0.5 µ in width, even with an erythrocyte in passage. Bands of intraendothelial microfilaments running alongside the interendothelial slits appeared to have a major role in causing the slits to remain narrow. Thus, the sinus wall, reinforced by microfilamentous bands, significantly controlled the circulation of erythrocytes through the spleen. Normal red cells were pliant enough to squeeze through, but cells containing large rigid inclusions were held in the slits or delayed in their passage. When many of the slits were occupied by cells slow in passage, the outflow track became blocked, and circulation through the spleen was impeded. Therefore, cells pooled in the cords, macrophages increased in number, and the sequences initiated that resulted in splenomegaly.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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