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      Sunlight, Immunosuppression And Skin Cancer: Role Of Histamine And Mast Cells

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      Clinical and Experimental Pharmacology and Physiology

      Wiley

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          Most cited references 52

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          Human keratinocytes are a source for tumor necrosis factor alpha: evidence for synthesis and release upon stimulation with endotoxin or ultraviolet light

          Tumor necrosis factor alpha (TNF-alpha), in addition to being cytotoxic for certain tumor cells, has turned out as a multifunctional cytokine that is involved in the regulation of immunity and inflammation. Since human keratinocytes have been demonstrated to be a potent source of various cytokines, it was investigated whether epidermal cells synthesize and release TNF-alpha. Supernatants derived from normal human keratinocytes (HNK) and human epidermoid carcinoma cell lines (KB, A431) were tested both in a TNF-alpha-specific ELISA and a bioassay. In supernatants of untreated epidermal cells, no or minimal TNF-alpha activity was found, while after stimulation with lipopolysaccharide (LPS) or ultraviolet (UV) light, significant amounts were detected. Western blot analysis using an antibody directed against human TNF-alpha revealed a molecular mass of 17 kD for keratinocyte- derived TNF-alpha. These biological and biochemical data were also confirmed by Northern blot analysis revealing mRNA specific for TNF- alpha in LPS- or ultraviolet B (UVB)-treated HNK and KB cells. In addition, increased TNF-alpha levels were detected in the serum obtained from human volunteers 12 and 24 h after a single total body UVB exposure, which caused a severe sunburn reaction. These findings indicate that keratinocytes upon stimulation are able to synthesize and release TNF-alpha, which may gain access to the circulation. Thus, TNF- alpha in concert with other epidermal cell-derived cytokines may mediate local and systemic inflammatory reactions during host defense against injurious events caused by microbial agents or UV irradiation.
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            Does intermittent sun exposure cause basal cell carcinoma? a case-control study in Western Australia.

            Our report deals with the relationship of pattern and timing of sun exposure to basal cell carcinoma (BCC) in a population-based case-control study conducted in Western Australia in 1988. The main measure of intermittent exposure was based on the amount of exposure on non-working days relative to that over the whole week. Outdoor recreational activities, holidays and sunburn were also considered to be markers of intermittent exposure. We observed a statistically significant increase in risk of BCC with increasing proportion of weekly sun exposure obtained at the weekend, especially in late teenage (OR = 3.9, 95% CI 1.9-7.8 for maximum intermittency of exposure), exposure of the site of skin cancer during holidays (OR = 1.9, 95% CI 1.1-3.1 for the highest exposure quarter) and sunburn to the site (ORs of 1.8 for 3-10 and 1.5 for 11+ sunburns in a lifetime). Risk of BCC increased substantially with increasing intermittency in poor tanners but not at all in good tanners. Our data suggest that a particular amount of sun exposure delivered in infrequent, probably intense increments will increase risk of BCC more than a similar dose delivered more continuously over the same total period of time.
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              Increased summertime UV radiation in New Zealand in response to ozone loss.

              Long-term decreases in summertime ozone over Lauder, New Zealand (45 degrees S), are shown to have led to substantial increases in peak ultraviolet (UV) radiation intensities. In the summer of 1998-99, the peak sunburning UV radiation was about 12 percent more than in the first years of the decade. Larger increases were seen for DNA-damaging UV radiation and plant-damaging UV radiation, whereas UV-A (315 to 400 nanometers) radiation, which is insensitive to ozone, showed no increase, in agreement with model calculations. These results provide strong evidence of human-induced increases in UV radiation, in a region where baseline levels of UV radiation were already relatively high.
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                Author and article information

                Journal
                Clinical and Experimental Pharmacology and Physiology
                Clin Exp Pharmacol Physiol
                Wiley
                0305-1870
                1440-1681
                January 2001
                January 2001
                : 28
                : 1-2
                : 1-8
                Article
                10.1046/j.1440-1681.2001.03392.x
                © 2001

                http://doi.wiley.com/10.1002/tdm_license_1.1

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