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  • 1
    Electronic Resource
    Electronic Resource
    Increased hydroxyl radical generation by normal polymorphonuclear leukocytes incubated in sera from patients with leukocytoclastic vasculitis (1982)
    Springer
    Archives of dermatological research 274 (1982), S. 65-71 
    Details
    ISSN: 1432-069X
    Keywords: Leukocytoclastic vasculitis ; Oxygen intermediates ; Polymorphonuclear leukocyte ; Vascular injury ; Immune complexes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of sera from patients with untreated leukocytoclastic vasculitis was investigated on the generation of oxygen intermediates by normal polymorphonuclear leukocytes. Sera from untreated patients induced increased hydroxyl radical generation, which is one of the most potent oxidants capable of causing tissue damage. It is suggested that vascular injury may be mediated in part by enhanced production of hydroxyl radical by polymorphonuclear leukocytes. Circulating immune complexes in the sera of the patients are considered to be one of the factors responsible for enhanced generation of hydroxyl radical.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00510359
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Ultraviolet B radiation downregulates inducible nitric oxide synthase expression induced by interferon-γ or tumor necrosis factor-α in murine keratinocyte Pam 212 cells (2000)
    Springer
    Archives of dermatological research 292 (2000), S. 312-319 
    Details
    ISSN: 1432-069X
    Keywords: Key words Ultraviolet B radiation ; Nitric oxide ; Nitric oxide synthase ; Murine keratinocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Ultraviolet radiation causes inflammation characterized by erythema and swelling, but also exhibits antiinflammatory effects which have led to the use of ultraviolet B radiation (UVBR) and psoralen plus ultraviolet A (PUVA) in the treatment of psoriasis, chronic severe atopic dermatitis and uremic pruritus. In inflammatory dermatoses, a pathogenic role of nitric oxide (NO) derived from inducible nitric oxide synthase (iNOS) has been suggested. To elucidate how UVBR regulates iNOS expression in skin under inflammatory conditions, we investigated the effect of UVBR on NO production and iNOS expression in cultured murine keratinocyte Pam 212 cells stimulated with interferon-Á (IFN-Á) or tumor necrosis factor-· (TNF-·). Low doses of UVBR significantly suppressed IFN-Á- or TNF-·-induced NO production. UVBR also downregulated IFN-Á- or TNF-·-induced iNOS expression at both the mRNA level and the protein level. These findings suggest the possibility that the downregulatory effect of UVBR on IFN-Á- or TNF-·-induced iNOS expression may, in part, explain the antiinflammatory and therapeutic properties of UVBR in inflammatory dermatoses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004030000124
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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