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Results for “ULTRAVIOLET RAYS”

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At least 55 records · Page 3Linked to original sources
PubMed1984

[Effect of ultraviolet rays on alpha-MSH plasma concentration].

Influence of Ultraviolet Rays on alpha-MSH Plasmaconcentration. Ultraviolet total-body irradiation induces changes of alpha-MSH plasmaconcentration dependent on wave-length of the source of radiation as well as skin type of the volunteers. Following UV-A total-body irradiation, we observed a significant increase of the proteohormone alpha-MSH, whereas UV-B rays did not change the plasma concentration. With regard to persons showing skin type I or II, we found low alpha-MSH basic values which were significantly increased 1 hour after UV-A irradiation; in contrast, more pigmented volunteers (skin type III or VI) showed far higher basic values but only little increase after UV-A irradiation.

Adult↗
PubMed1991

Insusceptibility of Cockayne syndrome-derived lymphocytes to plasminogen activator-like protease induction by ultraviolet rays and its abolition by interferon.

Protease induced by ultraviolet rays (UV) has been extensively investigated in human cells. Plasminogen activator-like protease (PA) activity was induced soon after UV irradiation in peripheral lymphocytes derived from healthy donors. In contrast, UV-irradiated lymphocytes derived from Cockayne syndrome (CS) cases did not show marked protease inducibility. Epstein-Barr (EB) virus-transformed CS lymphoblastoid cells were also characterized by insusceptibility to UV-induction of PA. However, when CS-derived cells were treated with a human interferon (HuIFN) preparation prior to irradiation, induction of PA activity was detected, irrespective of the kind of HuIFN (alpha or gamma). The results indicate the possibility of abnormal PA metabolism in CS-derived cells.

Cell Survival↗
PubMed1995

Rat ultraviolet ray B photodermatitis: an experimental model of psoriasis vulgaris.

Ultraviolet ray B (UV-B) induced dermatitis in the rat may be a model for human psoriasis vulgaris. Detailed studies of this model are reported. Rat skin responded to UV-B irradiation quite differently from human, guinea-pig, or mouse skin. Rat UV-B dermatitis was characterized by a sharply demarcated brownish-red lesion with scale formation lasting for 10 days. Histologically, microvascular dilatation, intraepidermal accumulation of polymorphonuclear leucocytes with microabscess, mononuclear cell infiltration at the papillary dermis and hyperproliferation of epidermal cells were observed. These features were similar to those of clinical psoriasis vulgaris in man. Leucocyte suppression, induced by systemic ferritin administration to the irradiated rats, resulted in loss of the epidermal hyperproliferation and inhibition of the tissue leucocytosis. This leucocyte suppression remodelled the picture of the rat UV-B dermatitis into that seen in other mammalian species, where microvascular dilatation and degeneration of keratinocytes (so-called sunburn cells) are characteristic. The irradiated epidermis of the rats treated with ferritin possessed an in vitro PMN chemotactic property. Rat UV-B dermatitis seems to be a useful model to investigate aetiopathogenic mechanisms in psoriasis vulgaris. However, the former heals after injury and does not relapse as does psoriasis.

Animals↗
PubMed1992

Differences in effects of oncogenes on resistance of gamma rays, ultraviolet light, and heat shock.

The effects of viral or activated cellular oncogenes on sensitivity to gamma rays, ultraviolet light, and heat shock were examined in SHOK (Syrian hamster Osaka-Kanazawa) cells and their transfectants. Resistance to gamma rays was conferred by the introduction of v-mos or c-cot genes, which coded serine/threonine kinase. Cells transfected with v-mos and c-cot genes increased their resistance to ultraviolet light and heat shock compared to their parent cells (SHOK cells). Of the activated ras genes, the N-ras gene developed a SHOK cell phenotype resistant to gamma rays and ultraviolet light. The Ha-ras gene produced SHOK cells resistant to ultraviolet light and heat shock, while introduction of the Ki-ras gene did not affect sensitivity. The v-erbB gene was found to be involved in the development of resistance to heat shock. Transfection with neo, c-myc, and v-fgr genes had little or no effect on cell survival. The karyotypes of SHOK cells and oncogene-containing cells were compared. No alterations were seen after the introduction of a foreign gene. Using cell cycle analysis, we found no apparent difference between SHOK cells and their transfectants. These results suggest that activation of serine/threonine kinase may be involved in common processes occurring after gamma-ray, ultraviolet-light, and heat-shock treatment, and that each oncogene may have a different effect on the development of a resistant phenotype.

Animals↗