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B Light (b + light)

Distribution by Scientific Domains
Medical Sciences80%

Kinds of B Light

  • ultraviolet b light
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    Selected Abstracts

    Protective effect of vitamin E on ultraviolet B light,induced damage in keratinocytes

    MOLECULAR CARCINOGENESIS, Issue 3 2002
    Samar Maalouf
    Abstract Ultraviolet (UV) B radiation is the most common environmental factor in the pathogenesis of skin cancer. Exposure of human skin to UVB radiation leads to the depletion of cutaneous antioxidants, the activation of nuclear factor kappa B (NF-,B), and programmed cell death (apoptosis). Although antioxidant supplementation has been shown to prevent UVB-induced photooxidative damage, its effect on components of cell signaling pathways leading to gene expression has not been clearly established. In the present study, the effect of the antioxidant vitamin, ,-tocopherol (,-T), and its acetate analog, ,-tocopherol acetate (,-TAc), on UVB-induced damage in primary and neoplastic mouse keratinocytes was investigated. The ability of both vitamins to modulate UVB-induced apoptosis and activation of the transcription factor NF-,B were studied. Treatment of normal and neoplastic mouse epidermal keratinocytes (308 cells) with 30,60 mJ/cm2 UVB markedly decreased viable cell number and was accompanied by DNA fragmentation. When both vitamins were applied to cells at times before and after UVB radiation, a significant increase in the percentage of viable cells and concomitant decrease in the number of apoptotic cells was noted, with vitamin pretreatment providing a better protection than posttreatment. Simultaneous posttreatment of irradiated cells with ,-TAc abolished the cytotoxic effects of UVB and restored cell viability to control levels. In addition, simultaneous posttreatment of irradiated cells with ,-T reduced the number of apoptotic cells by half, indicating a synergistic effect of two such treatments compared with any single one. Flow cytometry analysis indicated that vitamin treatment suppressed both an increase in pre-G0 cells and a decrease in cycling cells by UVB exposure. In addition, NF-,B activation was detected 2 h after UV exposure and was maintained for up to 8 h. Pretreatment with vitamins significantly inhibited NF-,B activation at 4 and 8 h. These results indicate that vitamin E and its acetate analog can modulate the cellular response to UVB partly through their action on NF-,B activation. Thus, these antioxidant vitamins are potential drugs for the protection from or the reduction of UVB-associated epidermal damage. © 2002 Wiley-Liss, Inc. [source]

    Effects of repeated low-dose UVB irradiation on the hyphal growth of Candida albicans

    MYCOSES, Issue 1 2006
    J. Brasch
    Summary Ultraviolet B light (UVB) can have negative phototropic effects on fungi. Candida albicans is often found on human skin exposed to UVB. Therefore, it is of medical interest to know whether a negative phototropic response to UVB irradiation can support an invasive growth of this potentially dangerous agent. In our study we investigated how repeated irradiation with low doses of UVB can influence the hyphal growth of C. albicans. Six randomly chosen strains of C. albicans were tested. Formation of hyphae was induced and maintained within transparent agar plates. The fungi were exposed to UVB three times daily for 7 days from either the obverse or the reverse side during incubation. The wavelength spectrum was in the range of 310,315 nm, single doses were between 0.0018 and 0.432 J cm,2. After 7 days the morphology and growth direction of C. albicans cells were determined microscopically. All six strains showed a common and dose-dependent response to UVB irradiation: the progression of hyphal growth was inhibited, no phototropic effects were seen and as a new finding an increased formation of blastospores was observed. We conclude that an irradiation of human skin colonized by C. albicans with doses of UVB that can occur under natural or artificial conditions is unlikely to trigger skin invasion by C. albicans. [source]

    Ultraviolet B Light-induced Nitric Oxide/Peroxynitrite Imbalance in Keratinocytes,Implications for Apoptosis and Necrosis

    PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 2 2010
    Shiyong Wu
    Elevation of nitric oxide (NO,) can either promote or inhibit ultraviolet B light (UVB)-induced apoptosis. In this study, we determined real-time concentration of NO, and peroxynitrite (ONOO,) and their role in regulation of membrane integrity and apoptosis. Nanosensors (diameter 300,500 nm) were used for direct in situ simultaneous measurements of NO, and ONOO, generated by UVB in cultured keratinocytes and mice epidermis. An exposure of keratinocytes to UVB immediately generated ONOO, at maximal concentration of 190 nm followed by NO, release with a maximal concentration of 91 nm. The kinetics of UVB-induced NO,/ONOO, was in contrast to cNOS agonist stimulated NO,/ONOO, from keratinocytes. After stimulating cNOS by calcium ionophore (CaI), NO, release from keratinocytes was followed by ONOO, production. The [NO,] to [ONOO,] ratio generated by UVB decreased below 0.5 indicating a serious imbalance between cytoprotective NO, and cytotoxic ONOO,,a main component of nitroxidative stress. The NO,/ONOO, imbalance increased membrane damage and cell apoptosis was partially reversed in the presence of free radical scavenger. The results suggest that UVB-induced and cNOS-produced NO, is rapidly scavenged by photolytically and enzymatically generated superoxide (O2,,) to produce high levels of ONOO,, which enhances oxidative injury and apoptosis of the irradiated cells. [source]

    Decreased incidence of nonmelanoma skin cancer in patients with type 2 diabetes mellitus using insulin: a pilot study

    BRITISH JOURNAL OF DERMATOLOGY, Issue 3 2005
    T-Y. Chuang
    Summary Background, In order to prevent the propagation of genetic mutations, human keratinocytes irradiated with ultraviolet (UV) B light in vitro undergo premature stress-induced senescence or apoptosis. This response to UVB irradiation is dependent on the functional activation of the insulin-like growth factor-1 receptor (IGF-1R). Based on this in vitro functional data, we hypothesized that the increased serum levels of insulin in patients with type 2 diabetes may activate the IGF-1R in skin and lead to a decreased frequency of skin cancer in these patients. Objectives, To determine whether the use of insulin by patients with type 2 diabetes correlated with a change in the incidence in nonmelanoma skin cancer (NMSC). Methods, A historical cohort study identifying the incidence of NMSC following the use of two different pharmacological therapies. The patient population was restricted to caucasians who were at least 50 years old when they began the indicated pharmacological therapy. The first group consisted of 1440 patients who used insulin therapy to treat type 2 diabetes and the second group comprised 4135 patients who used cimetidine to treat their gastrointestinal ailments. An additional group of 6131 patients with diabetes who used noninsulin antidiabetics was added to examine the effect of noninsulin therapies. All patients had regular follow-up visits at the Regenstrief Clinics during the study period between 1980 and 1999. The Regenstrief Clinics is an outpatient facility which serves the general population in Metro-Indianapolis, Indiana, U.S.A. Results, The incidence of NMSC in patients using insulin was significantly lower than in patients using cimetidine (1·25% vs. 2·35%, P < 0·02). The decrease in NMSC in patients with type 2 diabetes correlated specifically with the use of insulin (NMSC incidence insulin-only patients with diabetes: 1·40% vs. those with diabetes using noninsulin therapies: 2·35%, P = 0·11). Conclusions, Patients using exogenous insulin had a lower risk of developing NMSC and the protective effect of insulin use becomes more distinct with increasing age. [source]

    Sensitivity to ultraviolet B is a risk factor for cutaneous melanoma in a Mediterranean population: results from an Italian case,control study

    CLINICAL & EXPERIMENTAL DERMATOLOGY, Issue 1 2009
    A. Chiarugi
    Summary Background., Sun sensitivity is one of the predictors of melanoma risk, together with other individual characteristics such as skin and eye colour and number of naevi. However, it is unclear how best to measure sun sensitivity in order to quantify the individual risk of melanoma. Objectives., In this case,control study, the relationship between minimal erythema dose (MED) and skin colour (both instrumentally assessed) was investigated, and their possible role as independent risk factors for melanoma in a Mediterranean population evaluated. Methods., In total, 143 patients with cutaneous melanoma and 102 controls were enrolled in the study. Skin colour was assessed using a Minolta CR-200 chromameter. For MED calculation, a fluorescent lamp (Philips TL 4W/12) was used as a source of ultraviolet B light. MED was defined as the lowest dose that produced an increase of 2.5 in the redness value, expressed by the parameter a* of the Commission Internationale d'Eclairage (CIE) L*a*b* colour space (,a* = 2.5). Results., A significant excess of risk was associated with increasing L* values of skin colour (P < 0.05; OR = 1.12; 95% CI 1.01,1.24) for each unit of change. Low MED values were also associated with an increasing risk of melanoma, with an excess of risk of 18% (OR = 1.18, 95% CI 1.04,1.35) for every 10 mJ/cm2 of MED reduction. Compared with the highest MED values (> 97.7 mJ/cm2), subjects with MED values , ,50 mJ/cm2 or lower had a > 2-fold increased risk of melanoma (OR = 2.37, 95% CI 1.05,5.38). The effect of decreasing MED value as a melanoma risk factor persisted after adjustment for skin colour and atypical naevi in a multivariate model. Conclusions., In conclusion, both instrumentally assessed skin colour and MED are significant risk factors for malignant melanoma in a Mediterranean population. MED seems be an independent variable in establishing the subject's risk profile. [source]