Biopsied skin specimens from 10 males with cutis rhomboidalis nuchae, 50-83 years in age, as well as age-matched non-sun-exposed skin and young normal skin specimens were subjected to a light and electron microscopic immunohistochemical study using anti-elastin polyclonal antibody and anti-microfibril HB-8 monoclonal antibody. Conventional histochemical and electron microscopic techniques were also used.The most severely degenerated elastotic materials had developed in the upper dermis of the cutis rhomboidalis nuchae cases. Light microscopic histochemistry with Elastica van Gieson and Azan staining revealed elastotic materials with elastic fiber characteristics. Electron microscopic observation showed that the elastotic materials consisted of disintegrated and dispersed tannicacid staining elastin, fine granular materials, and filamentous substances. Light microscopic immunohistochemistry showed that the upper dermis from cutis rhomboidalis nuchae samples was reactive to anti-elastin but not to anti-microfibril HB-8 antibody. Electron microscopic immunohistochemistry further revealed that reticularly disintegrated substances in the elastotic materials retained their reactivity to anti-elastin, but did not show any reactivity to anti-microfibril HB-8 monoclonal antibody. These findings show that these elastotic materials were derived from elastic fibers and partially retained their antigenicity for elastin, but not for microfibrils.
, in 1896, first described a case of angiokeratoma of the scrotum, many authors have reported and discussed about this dermatosis. However the classification and the nomenclature of this skin disease still remain in a state of confusion. Recently I had a chance to see the report of Robinson and Tasker (1946)(14), discussing the nomenclature of this condition, which held my attention considerably.
Enzymatic activities in a saline-extractable fraction from two polar types of murine lepromas were investigated using pyroglutamyl-glycyl-arginine-p-nitroanilide and plasminogen-rich, as well as plasminogen-free, fibrin plates. An inhibitor activity for urokinase was also measured. C57BL/6NJcl (immunologically high responder strain) mice inoculated with 2 X 10(8) Mycobacterium lepraemurium developed a localized lepromatous lesion after 4 weeks. The tissue extracts obtained after 4-6 weeks exhibited inhibition for urokinase (8.8 IU/mg protein), but no enzymatic activity. After 8-11 weeks, when the lepromas showed an ulcerative change, prominent peptide hydrolytic activity (84.8 nmol/mg/protein/ min) was demonstrated. The fibrin plate assay confirmed that plasminogen activator is predominantly involved (26.4 IU/mg protein). The proteolytic activation was apparently correlated with discharge of purulent materials containing the bacilli and subsequent limitation of leproma development. However, similar modulation of the fibrinolytic enzyme-inhibitor system was not shown in CBA/N mice (immunologically low responders). The tissue extracts showed a low level of urokinase inhibitor activity (1.9 IU/mg protein), but no peptidolytic or plasminogen activator activity. Consequently, lepromas were developed progressively until 25 weeks after infection and dissemination from the lepromatous lesion took place thereafter. In comparison with histologic findings, which revealed accumulation of lymphocytes and mononuclear cells in the peripheral zone of lepromatous lesions in the C57BL/ 6NJcl, but not in the CBA/N mice, a controlling mechanism of plasminogen activator in tissue is assumed to be involved in the development of the granulomatous tissue reaction.
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