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  • Langerhans cell histiocytosis  (1)
  • experimenteller Schock  (1)
  • 1
    ISSN: 1432-2307
    Keywords: Langerhans cell histiocytosis ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The immunophenotypic properties of the abnormal cells in routine specimens from 16 cases of Langerhans cell histiocytosis (LCH) were examined. In five cases, cryostat sections were also available. The abnormal cells expressed a similar phenotype and were positive for HLA-DR, S-100 protein, peanut agglutinin (PNA), CD1a, CD4 and several macrophage-associated markers, including CD11c, CDw32 and CD68 (the latter detectable in routine sections with antibody KP1). Staining with CD14, CD35 (C3b receptor), and CD11b (C3bi receptor) was negative with the exception of one of the cases in which a proportion of the cells showed faint positivity with CD11b. Staining for pan-T-cell (CD2, CD3, CD5) and panB-cell (CD 19, CD22) antigens was negative in all lesions. It is concluded that LCH expresses a characteristic phenotype with some heterogeneity with regard to macrophage markers and that immunohistochemical methods in cryostat sections and routine specimens form a useful supplement to other techniques for the diagnosis of this condition.
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  • 2
    ISSN: 1591-9528
    Keywords: Shock ; Blood Cytology ; Circulatory failure ; Shock, experimental ; Bone marrow, Cytology ; Schock ; experimenteller Schock ; Blut-Cytologie ; Knochenmarks-Cytologie
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung 1. In Untersuchungen an Leukocytenkonzentraten des peripheren Blutes von 40 Patienten mit klinisch gesichertem Schock und von 20 Kontrollpersonen ohne Schockzeichen konnte gezeigt werden, daß Plasmoblasten, Proplasmazellen, Plasmazellen, Promyelocyten, Myelocyten und Erythroblasten bei den Schockpatienten statistisch signifikant häufiger vorkamen als in der Kontrollgruppe. 2. Weiterhin wurden Zellkonzentrate aus dem Blut und aus den Nierenperfusaten von 15 Kaninchen mit experimentellem Entblutungsschock und von 10 Kontrolltieren cytologisch untersucht. Folgende Zellformen wurden in der Schockgruppe statistisch signifikant häufiger angetroffen: in den Blutkonzentraten Myelocyten und Plasmoblasten; in den Nierenperfusaten Myelocyten, Proplasmazellen und Plasmazellen. 3. Die Gesamtzahl kernhaltiger Zellen (einschließlich Lymphocyten und segmentkerniger Granulocyten) war in den Ausstrichpräparaten der Konzentrate aus Blut und Nierenperfusat der Schocktiere statistisch signifikant höher als in den entsprechenden Präparaten der Kontrolltiere. 4. Die Ergebnisse zeigen, daß Schockzustände mit einer vermehrten Ausschwemmung der genannten Zellen in das periphere Blut einhergehen, und tragen somit dazu bei, das Auftreten intravasaler Zellansammlungen in menschlichen Schocknieren zu erklären.
    Notes: Summary 1. Leucocyte concentrates of peripheral blood from 40 patients with shock and 20 control persons without clinical symptoms of shock were investigated for the presence of immature blood and bone marrow cells. The number of cases containing plasmoblasts, proplasmocytes, plasmocytes, promyelocytes, myelocytes, and erythroblasts, was significantly higher in the shock group. 2. Leucocyte concentrates were also investigated from the blood and from the kidney perfusion fluid of 15 rabbits with experimental hemorrhagic shock and 10 control animals. The blood concentrates of the shock group contained significantly more myelocytes and plasmoblasts, the kidney perfusates significantly more myelocytes, proplasmocytes, and plasmocytes. 3. The number of nucleated cells including lymphocytes and polymorphonuclear leucocytes was significantly higher in the smears of the leucocyte concentrates from blood and kidney perfusates within the shock group compared to the control group. 4. It may be concluded from the present results that circulatory failure is accompanied by increased delivery of immature cells into the blood. The cell accumulations in the renal blood vessels following shock may be explained by this mechanism.
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