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  • Membranocystic lesion  (1)
  • Tumor necrosis factor-α  (1)
  • 1
    ISSN: 1432-2307
    Keywords: Membranous lipodystrophy (Nasu-Hakola disease) ; Membranocystic lesion ; Lectin histochemistry ; α-D-galactose ; MPA-HPR colloidal gold
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary This paper reports three cases of membranous lipodystrophy (Nasu-Hakola disease) in two families and studies the carbohydrate components of membranocystic lesions in all three cases, using twelve kinds of lectins labelled by horseradish peroxidase (HRP).Maclura pomifera agglutinin (MPA), which specifically binds α-D-galactose residues, strongly stained typical membranocystic lesions, whereas the other lectins did not. However,Helix pomatia agglutinin (HPA), which specifically binds to N-acetyl-D-galactosamine (GalNAc), stained the membranes of degenerated adipose cells. These were thought to appear during the initial or early stage of the membranocystic lesions. This suggests that a change of carbohydrate residues occurs during the formation of the membranocystic lesions. We also investigated the lectin binding sites at the ultrastructural level using MPA-HRP colloidal gold (CG) conjugate. In the well developed membrane, CG particles were arranged regularly along the minute tubular structures. On the other hand, there were a few irregularly spaced CG particles on the thinner membranes and also on the membranes of the degenerating adipose cells. No CG particles labelled the cell membranes of normal adipose cells. The presence of α-D-galactose residues in the membranocystic lesions is demonstrated for the first time at the electron microscopic level.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1831
    Keywords: Key words HIV-1 ; Myelomonocyte ; Apoptosis ; Tumor necrosis factor-α ; Fas
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To get insight into the involvement of tumor necrosis factor-α (TNF-α) and Fas (CD95) ligand in apoptosis (programmed cell death) of monocyte/macrophages in HIV-1-infected individuals, various T cell and myelomonocytic cell lines, including the HIV-1-infected clones OM-10.1 and U1 cells, were cultured in the presence of either TNF-α alone, anti-Fas agonist monoclonal antibody (Fas-mAb) alone, or their combinations. TNF-α moderately decreased the viability of myelomonocytic cell lines in a dose-dependent fashion (1–100 ng/ml). Unlike HIV-1-infected T cell lines, the viability of OM-10.1 and U1 cells was not affected by the treatment with Fas-mAb alone at concentrations up to 1,000 ng/ml. However, the viability of OM-10.1 cells further decreased with increasing concentrations of Fas-mAb when exposed simultaneously to TNF-α, suggesting that TNF-α sensitizes the cells to Fas-mAb-induced cell death. FACScan analysis and DNA gel electrophoresis revealed that the cell death was due to apoptosis. Such an effect of Fas-mAb was not identified in U1 cells. TNF-α but not Fas-mAb activated latent HIV-1 in OM-10.1 and U1 cells. Although all myelo-monocytic cell lines expressed Fas on their cell surface, TNF-α significantly up-regulated the expression of Fas in only OM-10.1 cells. These results indicate that, unlike T cells, HIV-1-infected myelomonocytic cells are generally resistant to the Fas-mediated apoptosis. However, they would become sensitive to the apoptosis if the expression of Fas could be up-regulated by TNF-α or other factors.
    Type of Medium: Electronic Resource
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