Sunburn
Mostrando 13-22 de 22 artigos, teses e dissertações.
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13. A role for NF-κB–dependent gene transactivation in sunburn
Exposure of skin to ultraviolet (UV) radiation is known to induce NF-κB activation, but the functional role for this pathway in UV-induced cutaneous inflammation remains uncertain. In this study, we examined whether experimentally induced sunburn reactions in mice could be prevented by blocking UV-induced, NF-κB–dependent gene transactivation with oligod
American Society for Clinical Investigation.
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14. Can an hour or two of sun protection education keep the sunburn away? Evaluation of the Environmental Protection Agency's Sunwise School Program
BioMed Central.
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15. Galectin-7 overexpression is associated with the apoptotic process in UVB-induced sunburn keratinocytes
Galectin-7 is a β-galactoside binding protein specifically expressed in stratified epithelia and notably in epidermis, but barely detectable in epidermal tumors and absent from squamous carcinoma cell lines. Galectin-7 gene is an early transcriptional target of the tumor suppressor protein P53 [Polyak, K., Xia, Y., Zweier, J., Kinzler, K. & Vogelstein, B. (
The National Academy of Sciences.
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16. Melanin acts as a potent UVB photosensitizer to cause an atypical mode of cell death in murine skin
Melanin protects the skin against DNA damage induced by direct absorption of sunlight's UV radiation. Yet, irradiating melanin in vitro or in cultured cells also generates active oxygen species such as superoxide, which can indirectly induce oxidative base lesions and DNA strand breaks. This photosensitization is greater for pheomelanin (yellow and red melan
National Academy of Sciences.
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17. UV exposure reduces immunization rates and promotes tolerance to epicutaneous antigens in humans: relationship to dose, CD1a-DR+ epidermal macrophage induction, and Langerhans cell depletion.
Increasing UVB radiation at the earth's surface might have adverse effects on in vivo immunologic responses in humans. We prospectively randomized subjects to test whether epicutaneous immunization is altered by prior administration of biologically equalized doses of UV radiation. Multiple doses of antigens on upper inner arm skin (UV protected) were used to
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18. Enhanced repair of cyclobutane pyrimidine dimers and improved UV resistance in photolyase transgenic mice
During evolution, placental mammals appear to have lost cyclobutane pyrimidine dimer (CPD) photolyase, an enzyme that efficiently removes UV-induced CPDs from DNA in a light-dependent manner. As a consequence, they have to rely solely on the more complex, and for this lesion less efficient, nucleotide excision repair pathway. To assess the contribution of po
Oxford University Press.
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19. Transgenic expression of survivin in keratinocytes counteracts UVB-induced apoptosis and cooperates with loss of p53
The inhibitor of apoptosis protein survivin has been implicated in both cell cycle control and apoptosis resistance. To discriminate between these different roles, we used transgenic expression of survivin in the skin as a model for cell proliferation, differentiation, and apoptosis. Transgenic mice expressing survivin under the control of a keratin-14 promo
American Society for Clinical Investigation.
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20. MDM2 induces hyperplasia and premalignant lesions when expressed in the basal layer of the epidermis
The MDM2 oncogene is overexpressed in 5–10% of human tumours. Its major physiological role is to inhibit the tumour suppressor p53. However, MDM2 has p53-independent effects on differentiation and does not predispose to tumorigenesis when it is expressed in the granular layer of the epidermis. These unexpected properties of MDM2 could be tissue specific or
Oxford University Press.
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21. Public awareness of malignant melanoma risk factors in Germany.
STUDY OBJECTIVE: To evaluate the effects of a German public education campaign which aimed to improve knowledge on risk factors for malignant melanoma. DESIGN: Comparison of data from two successive cross sectional surveys conducted before (spring 1993) and after (autumn 1994) the campaign. SETTING: All 56 nursery schools in Göttingen, the capital of southe
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22. Enzyme plus light therapy to repair DNA damage in ultraviolet-B-irradiated human skin
Ultraviolet-B (UVB) (290–320 nm) radiation-induced cyclobutane pyrimidine dimers within the DNA of epidermal cells are detrimental to human health by causing mutations and immunosuppressive effects that presumably contribute to photocarcinogenesis. Conventional photoprotection by sunscreens is exclusively prophylactic in nature and of no value once DNA dam
The National Academy of Sciences.