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  • Electronic Resource  (3)
  • Endothelial cells  (2)
  • B and T lymphocytes  (1)
  • 1
    ISSN: 1437-160X
    Keywords: Rheumatoid arthritis ; Ki 67 ; Synovial lining cells ; B and T lymphocytes ; Dysmorphic follicle ; Antigen-presenting cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We analysed the proliferative activity of synovial lining cells (SLCs), the distribution of proliferating B and T lymphocytes and the relationship of proliferating B and T lymphocytes to the pattern of antigen-presenting cells (APCs) within the rheumatoid synovial tissue (n=21). The immunohistochemical detection of the proliferation-associated antigen Ki 67 revealed low proliferative activity of SCL with and without expression of the Kim 8 (CD 68) antigen. Ki 67-positive B lymphocytes could be observed within secondary follicles (2/21), in small follicular dendritic reticulum cell (FDC)-containing follicle-like aggregates (7/21) and near the enlarged synovial intima (6/21). Ki 67-positive T lymphocytes could be detected in T-lymphocyte aaggregates (8/21), in the vicinity of blood vessels (18/21) and within the enlarged synovial intima (15/21). Semiquantitative analysis showed a strong correlation between the numbers of Ki 67-positive B lymphocytes and FDCs and between the numbers of Ki 67-positive T lymphocytes and interdigitating dendritic reticulum cells (IDC). There were significant differences in the number of Ki 67-positive B and T lymphocytes, IDCs and FDCs between the two groups of rheumatoid arthritis (RA) patients with different local clinical activity. These findings demonstrate a low proliferation of SLCs with and without expression of the monocyte-specific antigen Kim 8 and imply that B and T lymphocyte proliferation occurs in the presence of FDCs and IDCs. These results indicate that the RA synovial tissue is a site for antigen-dependent proliferation and maturation of B and T lymphocytes. The atypical pattern of FDC distribution within the rheumatoid synovial tissue “dysmorphic follicle” may be regarded as morphological substrate for a dysmaturation compartment of B lymphocytes leading to pathogenetic autoimmune phenomena in RA patients.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1437-160X
    Keywords: Key words Rheumatoid arthritis ; sICAM-1 ; Endothelial cells ; Synovial tissue
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The objective of this research was to investigate the cellular source of soluble ICAM-1 (siCAM-1) from rheumatoid synovial tissue (RS) and its relation to sICAM-1 in synovial fluid (SF) and serum, and to study the expression of ICAM-1 in isolated cells of RS. sICAM-1 was determined by using the enzyme-linked immunosorbent assay (ELISA) and Western blot analysis in supernatants from RS cultured for short periods (n = 19), in SF (n = 7) and in serum (n = 19). ICAM-1 expression, vascularization and inflammatory infiltration (CD3, CD68, CD22) were characterized immunohistochemically in cytospin preparations (n = 18), cryosections (n = 18) and in conventionally stained paraffin sections (n = 19) of RS. The degree of RS vascularization was analysed morphometrically in immunohistochemically stained cryosections (factor VIII related antigen). We found 90-kD sICAM-1 in supernatants of cultured cells, in SF and in sera. sICAM-1 in cellular supernatant correlated significantly (P 〈 0.01) with SF sICAM-1. The amount of sICAM in cellular supernatants showed no correlation to the score of inflammatory infiltration, but correlated significantly (P 〈 0.001) with the vascularization index of RS. The percentage of ICAM-1-expressing cells correlated significantly (P 〈 0.001) with the percentage of CD68-positive macrophages, but not with CD3- and CD22-positive lymphocytes. Macrophages, multinucleated giant cells and endothelial cells exhibited a higher expression of ICAM-1 as compared to lymphocytes and fibroblasts. The differential expression of ICAM-1 on infiltrating leucocytes and resident cells of RS indicates a functional role of ICAM-1 in the local inflammatory process. SF sICAM-1 originated in RS, but serum sICAM-1 did not. Shedding of sICAM-1 by RS was independent of inflammatory infiltration, but depended on the degree of vascularization, indicating that endothelial cells are the major source of sICAM-1 in RS.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Langenbeck's archives of surgery 366 (1985), S. 700-700 
    ISSN: 1435-2451
    Keywords: Transplantation ; Aortic allograft ; Endothelial cells ; Histoincompatibility ; Transplantation ; Allogene Aortenklappe ; Endothelzellen ; Histoinkompatibilitat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Durch die gegenwärtige Operationstechnik bei Transplantation allogener Aortenklappen in subkoronare Position (n=35) wird die normale Anatomie and Hamodynamik der Aortenwurzel und der Taschenklappen gewährleistet. Die allogene Aortenklappe ist nicht thrombogen. Die postoperative Anticoagulantientherapie ist daher nicht notwendig. Bei 25 invasiv Nachuntersuchten bestand praktisch kein Druckgradient fiber dem Transplantat noch ein Reflux in die linke Kammer. Wie bei Versuchen mit Ratteninzuchtstämmen könnte bei den allogenen Transplantaten in Abhän-gigkeit der immunogenetischen Histoinkompatibilität der Endothelerhaltungsgrad abnehmen während die Degeneration des Transplantates zunimmt.
    Notes: Summary The present technique of transplantation of the aortic valve allograft in the subcoronary position (n = 35) provides normal anatomy and hemodynamics of the aortic root and valves. The aortic valve allograft is not thrombogenic and therefore requires no postoperative anticoagulant therapy. Postoperative invasive studies in 25 patients indicate that there was practically no gradient across the valve or regurgitation into the left ventricle. Animal experiments with inbred rat strains have demonstrated that the degree of maintenance of endothelial cells and increased degeneration are dependent on immunogenetic histoincompatibility.
    Type of Medium: Electronic Resource
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