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Solar Ultraviolet (solar + ultraviolet)
Terms modified by Solar Ultraviolet Selected AbstractsSunlight ultraviolet irradiation and BRAF V600 mutagenesis in human melanoma,HUMAN MUTATION, Issue 8 2008Ahmad Besaratinia Abstract The incidence of melanoma, the most lethal form of skin cancer, continues to increase in the Western world. In addition to genetic alterations in high- and low-susceptibility genes identified for melanoma, somatic mutations in BRAF gene occur frequently in human melanoma and are distinctively linked to sun exposure. Of significance is a single hotspot codon, i.e., BRAF V600, wherein up to 92% of all mutations arise. Recent work in our laboratory has demonstrated that solar ultraviolet (UV) irradiation triggers mutagenesis through induction of various DNA lesions, many of which capable of producing similar types of mutations, as those seen in BRAF V600 variants in human melanoma. In this review article, we have discussed application of "DNA damage-targeted mutagenicity" of solar UV-irradiation for determining the mechanistic involvement of sunlight UV in BRAF V600 mutagenesis in human melanoma. We envision that establishing "DNA-damage derived mutagenesis" in this exceptionally unique target gene may resolve the underlying mechanism(s) of melanoma-genesis, thus helping define preventive and therapeutic measures against this malignant disease. Hum Mutat 0, 1,9, 2008. © 2008, Wiley-Liss, Inc. [source] The association of use of sunbeds with cutaneous malignant melanoma and other skin cancers: A systematic reviewINTERNATIONAL JOURNAL OF CANCER, Issue 5 2007Article first published online: 27 NOV 200 Abstract Exposure to solar ultraviolet (UV) radiation is a known cause of skin cancer. Sunbed use represents an increasingly frequent source of artificial UV exposure in light-skinned populations. To assess the available evidence of the association between sunbed use and cutaneous malignant melanoma (melanoma) and other skin cancers, a systematic review of the literature till March 2006 on epidemiological and biological studies on sunbed use was performed in Pubmed, ISI Web of Science, Embase, Pascal, Cochrane library, Lilacs and Medcarib. Search for keywords in the title and in the abstract was done systematically and supplemented by manual searches. Only case,control, cohort or cross-sectional studies were selected. Data were abstracted by means of a standardized data-collection protocol. Based on 19 informative studies, ever-use of sunbeds was positively associated with melanoma (summary relative risk, 1.15; 95% CI, 1.00,1.31), although there was no consistent evidence of a dose,response relationship. First exposure to sunbeds before 35 years of age significantly increased the risk of melanoma, based on 7 informative studies (summary relative risk, 1.75; 95% CI, 1.35,2.26). The summary relative risk of 3 studies of squamous cell carcinoma showed an increased risk. For basal cell carcinoma, the studies did not support an association. The evidence does not support a protective effect of the use of sunbeds against damage to the skin from subsequent sun exposure. Young adults should be discouraged from using indoor tanning equipment and restricted access to sunbeds by minors should be strongly considered. © 2006 Wiley-Liss, Inc. [source] Review Article: A new wrinkle on old skin: the role of elastic fibres in skin ageingINTERNATIONAL JOURNAL OF COSMETIC SCIENCE, Issue 5 2010A. K. Langton Synopsis Cutaneous ageing is the result of two distinct, biological processes which may occur concurrently: (i) the passage of time, termed intrinsic ageing and (ii) environmental influences, termed extrinsic ageing. Intrinsic ageing of the skin is a slow process which causes changes in tissue structure and impairs function in the absence of additional biological, chemical and physical factors. The clinical features of intrinsically aged skin are not usually evident until old age when, although smooth and unblemished, the skin surface appears pale and is characterized by fine wrinkles with occasional exaggerated expression lines. Functionally, intrinsically aged skin is dry and less elastic than more youthful skin. In contrast, extrinsically aged skin is exemplified by deep, coarse wrinkles, mottled hyperpigmentation and a marked loss of elasticity and recoil. The two major environmental influences which induce extrinsic ageing are: (i) chronic exposure to solar ultraviolet (UV) irradiation (termed photoageing) and (ii) smoking. This review discusses the changes associated with the ageing process in the skin, with particular emphasis on the role played by the elastic fibre network in maintaining dermal function. The review concludes with a discussion of a short-term assay for independent assessment of the efficacy of anti-ageing cosmetic products using the elastic fibre component fibrillin-1 as a biomarker of extracellular matrix repair. Résumé Le vieillissement Cutané est le résultat de deux processus biologiques distincts, qui peuvent se produire concurremment : i) le passage de temps, désigné comme vieillissement intrinsèque et ii) les influences environnementales, désignées comme vieillissement extrinsèque. Le vieillissement intrinsèque de la peau est un processus lent provoquant des changements de la structure et détériorant la fonction tissulaire sans facteurs biologiques, chimiques ou physiques supplémentaires. Les caractéristiques cliniques de la peau intrinsèquement âgée sont peu visibles avant la vieillesse où, bien que lisse et impeccable, la surface de la peau apparaît pâle et marquée par des rides notables et des lignes d'expression exagérées. Au niveau fonctionnel, la peau intrinsèquement âgée est sèche et moins d'élastique que la peau plus jeune. Au contraire, la peau extrinsèquement âgée est caractérisée par des rides profondes, grossières, une hyperpigmentation en taches et une perte marquée d'élasticité. Les deux influences environnementales majeures à l'origine du vieillissement extrinsèque sont : i) l'exposition chronique aux ultra-violets (UV) et ii) l'exposition tabagique. Cette revue envisage les changements associés au processus de vieillissement cutané, avec une attention particulière sur le rôle joué par le réseau élastique dans le maintien de la fonction dermique. Cette analyse se termine par une discussion à propos d'un essai d'évaluation de l'efficacité de produits cosmétiques anti-âges utilisant un composant de fibre élastique la fibrillin-1 comme bio marqueur de la réparation de la matrice extracellulaire. [source] Protective Effect of Sanguinarine on Ultraviolet B-mediated Damages in SKH-1 Hairless Mouse Skin: Implications for Prevention of Skin CancerPHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 4 2007Haseeb Ahsan Excessive exposure of solar ultraviolet (UV) radiation, particularly its UVB component (280,320 nm), to human skin is the major cause of skin cancers. UV exposure also leads to the development of precancerous conditions such as actinic keratosis and elicits a variety of other adverse effects such as sunburn, inflammation, hyperplasia, immunosuppression and skin aging. Therefore, there is a need to intensify our efforts towards the development of novel mechanism-based approaches/agents for the protection of UVB-mediated damages. Chemoprevention is being investigated as a potential approach for the management of UV damages including skin cancer. We have earlier shown that sanguinarine, a benzophenanthridine alkaloid, inhibits UVB exposure-mediated damages in HaCaT keratinocytes. In this study, to determine the relevance of our in vitro findings to in vivo situations, we assessed the effects of sanguinarine on UVB-mediated damages in SKH-1 hairless mice. Our data demonstrated that a topical application of sanguinarine (5 ,mol 0.3 mL,1 ethanol per mouse), either as a pretreatment (30 min prior to UVB) or posttreatment (5 min after UVB), resulted in a significant decrease in UVB-mediated increases in skin edema, skin hyperplasia and infiltration of leukocytes. Further, sanguinarine treatments (pre and post) also resulted in a significant decrease in UVB mediated (1) generation of H2O2 and (2) increases in the protein levels of markers of tumor promotion/proliferation viz. ornithine decarboxylase (ODC), proliferating cell nuclear antigen (PCNA) and Kiel antigen-67. Based on this data, we suggest that sanguinarine could be developed as an agent for the management of conditions elicited by UV exposure including skin cancer. However, further detailed studies are needed to support this suggestion. [source] Gene expression profiles of TNF-,, TACE, furin, IL-1, and matrilysin in UVA- and UVB-irradiated HaCat cellsPHOTODERMATOLOGY, PHOTOIMMUNOLOGY & PHOTOMEDICINE, Issue 4 2005Beata Skiba Background/Purpose: It is known that solar ultraviolet (UV) irradiation exerts multiple effects on mammalian skin tissues, one of which is the induction of local and systemic immunosuppression as well as inflammation. Tumor necrosis factor-, (TNF-,) and other cytokines are suggested to play a role in these responses. Quantitative real-time polymerase chain reaction (TaqMan RTPCR) was used to elucidate the effect of UVA and UVB irradiation on the expression of genes coding for TNF-,, IL-1,, IL-10, FasL, matrilysin, TACE and furin in HaCaT cells over a 48 h period (IL-1,, interleukin-1,; FasL, Fas ligand). Methods: Cultured HaCaT cells were either sham irradiated (control) or exposed to UVA (2000 and 8000 J/m2) or UVB (200 and 2000 J/m2) radiation. RNA was extracted from cells at 0, 4, 8, 12, 16, 24, 48 h post-irradiation and reverse transcribed to generate cDNA for subsequent real-time PCR amplification. Results: Significant increases in the mRNA levels for all genes tested were detected in both UVA- and UVB-irradiated HaCaT cells compared with control (sham-irradiated) cells. TNF-, mRNA levels were immediately up-regulated (0 h) after irradiation, with maximal induction at 8 h post 2000 J/m2 UVA and 200 J/m2 UVB irradiation, at 4 h post 8000 J UVA irradiation and at 48 h post 2000 J/m2 UVB irradiation. No correlation was observed between TNF-,, TACE and furin mRNA induction in the different irradiated cohorts. Conclusion: Results suggest that time-distinct gene induction of TNF-,, furin, IL-1, and matrilysin may be involved in UV-induced cellular responses, but not for TACE. In general, mRNA induction was dose dependent at some time points post-irradiation, but not throughout the whole time course tested. Our results show that quantitative real-time PCR is a useful tool in the analysis of quantitative changes of mRNA levels in cultured HaCaT cells after UV exposure. [source] ,-MSH tripeptide analogs activate the melanocortin 1 receptor and reduce UV-induced DNA damage in human melanocytesPIGMENT CELL & MELANOMA RESEARCH, Issue 5 2009Zalfa A. Abdel-Malek Summary One skin cancer prevention strategy that we are developing is based on synthesizing and testing melanocortin analogs that reduce and repair DNA damage resulting from exposure to solar ultraviolet (UV) radiation, in addition to stimulating pigmentation. Previously, we reported the effects of tetrapeptide analogs of ,-melanocortin (,-MSH) that were more potent and stable than the physiological ,-MSH, and mimicked its photoprotective effects against UV-induced DNA damage in human melanocytes. Here, we report on a panel of tripeptide analogs consisting of a modified ,-MSH core His6 - d -Phe7 -Arg8, which contained different N -capping groups, C-terminal modifications, or arginine mimics. The most potent tripeptides in activating cAMP formation and tyrosinase of human melanocytes were three analogs with C-terminal modifications. The most effective C-terminal tripeptide mimicked ,-MSH in reducing hydrogen peroxide generation and enhancing nucleotide excision repair following UV irradiation. The effects of these three analogs required functional MC1R, as they were absent in human melanocytes that expressed non-functional receptor. These results demonstrate activation of the MC1R by tripeptide melanocortin analogs. Designing small analogs for topical delivery should prove practical and efficacious for skin cancer prevention. [source] Angiogenesis in skin aging and photoagingTHE JOURNAL OF DERMATOLOGY, Issue 9 2007Jin Ho CHUNG ABSTRACT Angiogenesis, the process of generating new blood vessels, is affected by various physiological and pathological conditions of skin. The skin aging process can be divided into intrinsic aging and photoaging. With aging, cutaneous blood vessels undergo pronounced alterations. A reduction of the cutaneous microvasculature has been observed in the skin of elderly individuals. Human skin is exposed daily to solar ultraviolet (UV) radiation, infrared rays and heat, and these stimuli are known to induce skin angiogenesis. Interestingly, although acute UV irradiation stimulates skin angiogenesis, cutaneous blood vessels are decreased in chronically photodamaged skin. The reason for the differential effects of acute and chronic UV exposure on skin angiogenesis remains to be elucidated. This review discusses the vascularization changes in intrinsically aged and photoaged human skin, the effects of UV irradiation, infrared rays and heat on skin angiogenesis, and the effects of topical retinoic acid treatment on UV-induced angiogenesis and cutaneous vascularity in aged and photoaged human skin. An understanding of the molecular mechanisms of aging- and photoaging-dependent changes of skin angiogenesis may provide us with new insights to prevent and treat the skin aging process. [source] | |||||||||||||