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  • Slipped capital femoral epiphysis  (1)
  • Tumor necrosis factor-α  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of bone and mineral metabolism 7 (1989), S. 42-48 
    ISSN: 1435-5604
    Keywords: Male hypogonadal osteoporosis ; Slipped capital femoral epiphysis ; Testosterone ; GH ; Somatomedin C
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Two males with bone abnormalities associated with hypogonadotropic hypogonadism are reported. Case 1, 28 years old male, developed growth disturbance at the age of eight years, after suffering from tuberculous meningitis. No secondary sex characteristics appeared and fractures occurred at five times. Case 2, 29 years old male, also suffered from growth disturbance from around the age of 6 years, without appearance of secondary sex characteristics even after puberty. Bone X-ray studies and bone biopsy revealed marked osteoporosis in Case 1, while in Case 2, slipped capital femoral epiphysis was also noted with mild osteoporosis. In these two cases, osteoporosis is associated with eunuchoidism, in agreement of the concept of so-called “male hypogonadal osteoporosis”. Both patients showed insufficient secretion of somatomedin C, testosterone and growth hormone (GH) with insulin tolerance test and arginine tolerance test. The insufficient secretion of LH and FSH with LH-RH tolerance test was also revealed in both cases. The decrease of GH and somatomedin C was quite pronounced in Case 1, whereas the fall of testosterone was more conspicuous in Case 2. The imbalance between these hormone deficiencies might lead to different expression of bone abnormalities.
    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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