Impact of ultraviolet radiation-induced damage to hair fiber integrity: A multi-technique physicochemical characterization of surface and cortex properties.

Dermatomyositis (DM) is an autoimmune disease, which is often accompanied by the development of disease-specific autoantibodies directed against the SNF2-superfamily helicase, Mi-2. Recent evidence suggests that ultraviolet radiation exposure may be an important risk factor for the development of not only the disease but also specific autoimmunity against Mi-2. Consequently, we investigated the effects of ultraviolet radiation on Mi-2 protein expression. We observed an increase in protein levels upon ultraviolet radiation exposure in cell culture systems. These changes in expression occur quite rapidly, are maximized just 1 h following exposure, and are unique to Mi-2 when compared with other members of the NuRD complex. Changes in protein levels are not mediated through transcriptional mechanisms. Treatment results in a more efficiently translated message through regulatory elements in the 5'-UTR region of the transcript. Investigation into protein half-life further demonstrated increased stability of Mi-2 following UV exposure. Taken together, we describe a system by which Mi-2 protein expression can be quickly increased following UV exposure and then maintained up to 16 h later. These data provide a novel regulation of an important transcriptional regulator and provide insight into the possible mechanisms of the development of DM and associated autoantibodies.

Protection against ultraviolet (UV) radiation is the major function of sunscreen lotions and UV-protective coatings for vehicles, homes, equipment and clothing. Sunscreen formulations have been optimized to become protective over a broader spectrum of UV radiation and maintain greater photostability. They are comprised of organic and inorganic components that act as chemical and physical UV protectors, respectively. Some of the organic components are limited by their spectrum of protection and photostability. Studies using solid lipid nanoparticles, recently explored organic molecules, inorganic components and antioxidants attempt to further optimize UV protection. In this review, we examine traditional and emerging nanoparticle components and highlight novel ideas in UV protection which may provide pathways for future studies.

Ultraviolet (UV) radiation is one of the most important environmental factors. Besides its well-known advantages and its indispensable effects on human life, UV light, particularly the middle wavelength range (290–320 nm [UVB]), can harm human health by inducing skin cancer, premature skin aging, inflammation, and cell death ( 1-4). Over the last 25 years, it has become apparent that exposure to UVB radiation may also suppress immune reactions. Review of the numerous studies on the immunosuppressive properties of UV radiation led to two quite surprising observations: that UV exposure can have systemic immunologic consequences that UV radiation can induce antigen-specific tolerance. This paper briefly reviews the phenomenon of UV-induced tolerance. Photoimmunology was born in the mid-1970s in the recognition of an association between UV radiation and immune suppression during photocarcinogenesis. Kripke and coworkers induced skin tumors in mice by chronic UVB exposure. These tumors appeared to be highly antigenic since they were rejected when transplanted onto syngeneic healthy recipients ( 5-7). When the recipients were treated with immunosuppressive drugs, the transplanted tumors were not rejected, indicating that this type of rejection was immunologic in nature. Rejection also failed to occur when recipients were exposed to rather low doses of UVB ( 8-10). This was the first indication that UVB radiation can exert immunosuppressive properties. Since the tumors grew even when transplanted into sites not directly exposed to UV radiation, it was concluded that UV radiation exerts also a systemic immunosuppressive effect ( 9, 10). Suppression of tumor rejection could be transferred by injecting T cells from UV-irradiated mice into normal recipients, which subsequently became unable to reject UV-induced tumors ( 11, 12). In contrast, rejection of non-UV-induced neoplasms (e.g., chemically induced tumors) was not affected ( 13-16). These findings suggested that UV exposure induced T cells which inhibit the immune response specifically to UV-induced tumors (T suppressor cells). The phenotype of these T suppressor cells is generally Thy-1+, Lyt-1+ (CD5), Lyt-2− (CD8), L3T4+ (CD4), and I-A−, but varies among the different tumor systems and wavelengths used for irradiation ( 11, 12, 17-19). Although the initial photoimmunologic studies investigated the effect of UV radiation on the immune response to UV-induced tumors, most of the subsequent studies used the model of allergic contact hypersensitivity (CHS). CHS is a special form of the delayed-type hypersensitivity response which is induced by epicutaneous application of low-molecular-weight reactive chemical compounds (e.g., dinitrofluorobenzene or oxazolone). Since these molecules bind to a host protein presumably in the skin to form the antigen, they are called haptens. Application of haptens to skin which has been exposed to rather low doses of UVB radiation (around 1 kJ/m2) failed to induce CHS, whereas application of the hapten at an unirradiated site produced a normal CHS response ( 20). The induction of this immunologic alteration by UV radiation correlated with a reduction in the number of Langerhans cells at the site of exposure and with changes in their structure ( 20). The UV-mediated alterations of Langerhans cells, which are the crucial cells in the epidermis for sensitization, were confirmed shortly thereafter by Aberer et al. ( 21). The ability of low-dose UVB to impair the induction of CHS appears to be genetically determined, since inhibition of CHS was observed only in some particular strains (e.g., C3H/HeN, C57BL/6), called UV susceptible, while other strains (C3H/HeJ, Balb/c), called UV resistant, responded with normal sensitization despite UV exposure ( 22). The phenotypic traits of UVB-resistant and -susceptible mice are polygenically inherited. The relevant loci at which polymorphic alleles reside are LPS and TNF-α ( 23). Accordingly, tumor necrosis factor (TNF)-α seems to be relevant to the inhibition of CHS by low-dose UV exposure, since UV-susceptible mice can be sensitized upon receiving neutralizing anti-TNF-α antibodies when the hapten is applied on UVB-exposed skin ( 24). In addition, the CHS response was significantly impaired when the hapten was painted on murine skin shortly after the site had received an injection of a subinflammatory dose of recombinant TNF-α ( 24). On the other hand, whether mice are UV-resistant or-susceptible may also depend on the time lag between UV exposure and sensitization ( 25) and on the concentration of the hapten ( 26). However, UV exposure not only inhibits the induction of CHS, but even induces hapten-specific tolerance, since the affected animals cannot be resensitized with the same hapten at a later time ( 20). This long-term suppression is hapten specific, since the same mice can be perfectly sensitized to another unrelated hapten, indicating that the initial low-dose UV exposure immunosuppressed the animals in a specific rather than general way. The use of higher UVB doses (around 20 kJ/m2) can also affect immune reactions initiated at distant, non-UV-exposed sites (“systemic immunosuppression”). Accordingly, CHS cannot be induced in mice which are exposed to high doses of UVB even if the hapten is applied at unirradiated sites ( 27). Furthermore, as observed with local immunosuppression, hapten-specific tolerance develops, since the mice cannot be resensitized to the very same hapten at a later time point. There were two investigations of whether UVB induces hapten-specific tolerance also in man. In one study, only 10% of the subejcts failed to develop specific CHS when subsequently reimmunized with the same hapten ( 28). Tolerance demonstrated in these human subjects was hapten specific, since they revealed pronounced CHS responses upon subsequent immunization with another, unrelated hapten ( 28). Cooper et al. reported that a higher proportion of subjects developed tolerance when the hapten was applied onto skin areas exposed to erythemogenic UV doses ( 29). Despite these differences, which may be due to different protocols, both studies show that a human subset who fail to develop CHS when the hapten is first applied to UVB-exposed skin also develop tolerance. The study by Cooper et al. ( 29) also demonstrated that the application of erythemogenic UVB doses depleted Langerhans cells (CD1a+, HLA-DR+) and induced the infiltration of CD1a− HLA-DR+ macrophages, thereby confirming previous observations. In earlier studies, Cooper et al. showed in vivo that UV-exposed human epidermis contains a population of CD1a− HLA-DR+ CD36+ infiltrating macrophages with antigen-presenting capabilities ( 30). These macrophages were observed only after UV exposure conditions which induce tolerance of contact allergens, but not after regimens unassociated with tolerance induction. Accordingly, these infiltrating macrophages were found to activate autoreactive T cells ( 31), specifically CD4+ suppressor-inducer cells ( 32), which in turn induce the maturation of suppressor T cells ( 33). These CD11b+ macrophages infiltrating the epidermis after in vivo UV exposure were found to produce interleukin (IL)-10 potently and to represent the major secretory source of epidermal IL-10 protein in the human system ( 34). This observation might be important, since IL-10 can act in an immunosuppressive way and appears to be involved in UV-induced immunosuppression (see section VI). In addition, UV-induced epidermal macrophages were found to induce in vitro CD4+ T cells, which are characterized by deficient expression of the IL-2 receptor alpha chain ( 35). Inhibition of the IL-2 receptor alpha chain apparently depends on transforming growth factor-beta. In the murine system, the same group recently demonstrated convincingly that these UV-induced macrophages might indeed play an important role in tolerance induction in vivo (see section V). As observed in the tumor model (see section I), UV-mediated suppression can be transferred by injecting T cells obtained from the lymph nodes and spleens of UV-exposed and hapten-treated animals into naive recipients. Thus, transferred suppression is hapten specific, since the recipients do not respond to the specific hapten, whereas a normal CHS response can be obtained to non-cross-reacting haptens ( 36, 37). Taken together, these findings suggest that tolerance is mediated via induction of hapten-specific T suppressor cells. Although transfer of tolerance could be observed in both the high- ( 37) and the low-dose models ( 36), different types of T cells appear to be responsible for transfer of suppression. In the systemic form of UV-induced suppression (high-dose model), transfer of tolerance is mediated by the induction of antigen-specific, CD3+, CD4+, and CD8− suppressor cells ( 38). In the local form of UV-induced immunosuppression (low-dose model), Elmets et al. ( 36) showed that treatment of cells from UV-irradiated animals with antibodies against Lyt-1 (CD5) completely abrogated their ability to transfer suppression, while treatment of cells with antibodies against Lyt-2 (CD8) inhibited suppression partially ( 36). Accordingly, Schwarz et al. recently reported that transfer of suppression was lost in the low-dose model when T cells were depleted of CD8+ cells ( 39). When UV-induced T suppressor cells are transferred into sensitized but not naive mice, the CHS response in the recipients is not affected ( 40). This indicates that T suppressor cells can affect the induction of CHS but cannot interfere with the elicitation of CHS. Although the adoptive transfer experiments in both the low- and high-dose UV models were quite convincing, implying that sensitization in combination with UV light induces T suppressor cells, attempts to purify and clone these cells were unsuccessful for many years. Hence, the term “T suppressor cells” was virtually banned and the entire concept of UV-induced tolerance brought into question. On the other hand, the transfer experiments failed to detect whether T suppressor cells originate in the donor, as usually claimed, or in the recipient. The latter possibility could be due to the transfer of cells which induce the development of cells with negative regulatory function in the recipient. Although it was recently shown that transferable suppression was mediated by a small number of donor-derived CD4+ T cells which copurify with donor hapten-bearing, antigen-presenting cells ( 41), this did not clarify whether the donor T cells were T suppressor precursors or whether they induced T suppressor cells in the recipients. By using Thy-1.1+ and Thy-1.2+ congenic mice, Shreedar et al. very recently showed that the T suppressor cells in the recipients (Thy-1.2) were derived from T cells in the draining lymph nodes of the UV-exposed donors (Thy-1.1) ( 42). In addition, these authors werethe first to clone T cells from UVB-exposed mice which were sensitized with fluorescein isothiocyanate (FITC). Cells cloned from UV-exposed mice were CD4+, CD8−, TCR-α/β+, MHC restricted, and specific for FITC. They produced IL-10, but not IL-4 or interferon-γ, whereas cells from unirradiated animals produced high amounts of interferon-γ and little IL-4 and IL-10. T cells from UV-exposed mice blocked antigen-presenting cell functions and IL-12 production. Even more importantly, injection of 5×104 cloned T cells into untreated recipients suppressed the induction of CHS against FITC. Since impairment of CHS and induction of tolerance are the consequence of the same event, i.e., low- or high-dose UV exposure followed by hapten application, it was thought for years that the same mechanisms are involved. Irradiation of skin with either low- or high-dose UVB results in depletion of epidermal Langerhans cells ( 21), which are crucial for the induction of CHS ( 43). Under normal conditions, Langerhans cells take up the hapten and migrate with it to the regional lymph nodes, where the Langerhans cells, which have developed during their journey into potent immunostimulatory dendritic cells, present the antigen to T cells ( 44). Thus, impairment of the induction of CHS upon application of the hapten onto UVB-exposed skin can be easily explained by the depletion of Langerhans cells. However, this does not apply to systemic UV-mediated immunosuppression, since even after multiple UVB exposures, Langerhans cells are not affected in skin areas which are not directly exposed to UV radiation ( 45). In this case, secretion of soluble mediators by keratinocytes appears to be important (see section VI). Since application of haptens onto UVB-exposed mice results in both the impairment of CHS and the induction of hapten-specific tolerance, it was long postulated that the same mechanisms are involved and that induction of tolerance is the consequence of the inhibition of CHS induction. However, there is growing evidence that the molecular basis of UVB-induced tolerance is different from the mechanism responsible for UVB-impaired induction of CHS. Although TNF-α induces alterations in epidermal Langerhans cells like those of UVB ( 46) and although injection of anti-TNF-α antibodies inhibits UV-mediated impairment of CHS, development of tolerance cannot be prevented by injection of neutralizing TNF-α antibodies ( 47, 48). Hammerberg et al. observed that application of a hapten immediately after a single low-dose UVB exposure resulted in inhibition of the induction of CHS but failed to induce tolerance ( 49). A state of tolerance could be achieved only if a delay of 72 h was allowed between the UV exposure and the initial sensitization. By 72 h after in vivo UV exposure, Langerhans cells were depleted, and Ia+ CD11bbright macrophages had appeared in the epidermis. The appearance of this macrophage cell type was initially observed by the same group in the human system (see section III). Intracutaneous injection of haptenated epidermal cell suspensions obtained from in vivo UV-exposed skin induced hapten-specific tolerance. Induction of tolerance was lost when CD11bbright cells were removed from the epidermal cell suspensions before injection. In addition, induction of UV-mediated tolerance was blocked when mice were treated with an antibody blocking CD11b ( 50). CD11b can serve as a receptor for the fragment of the complement component 3, iC3b. Mice with a genetic disruption of the C3 gene were used to test whether C3 activation is essential for UV-induced immunosuppression. Indeed, C3-deficient mice did not develop tolerance after hapten application through a skin area which received a single low-dose UVB exposure ( 51). Inhibition of C3 activation partially blocked UV-induced infiltration of CD11bbright macrophages but did not prevent UV-induced depletion of Ia+ CD11blow Langerhans cells. Taken together, these findings indicate that the ability of UV-exposed skin to induce tolerance critically depends on inflammatory Ia+ CD11bbright monocytic/macrophagic cells, which infiltrate UV-exposed skin, and not on the depletion of Langerhans cells. The observation that mice which are exposed to higher doses of UV radiation cannot be sensitized even when the antigen is applied on a skin area which was not exposed to UV radiation ( 27, 37) was the first indication that this radiation can suppress the immune system in a systemic fashion. How the events occurring at the irradiated site led to an abnormal response to an antigen applied at a distant, non-UV-exposed skin area remained unclear for quite a long time, since Langerhans cells, which were found to be critically involved in local immunosuppression ( 20), were unaffected in non-UV-exposed skin ( 45). UV radiation has turned out to be an effective inducer of cytokine release. Since keratinocytes were identified as a potent source of cytokines ( 52), and by virtue of their anatomic location are the natural target for UV radiation, Schwarz et al. postulated that UV-exposed keratinocytes could be the source of an immunosuppressive soluble mediator which enters the circulation and thereby mediates systemic immunosuppressive effects ( 53). Accordingly, it was shown that intravenous injection of supernatants obtained from UV-exposed murine keratinocytes into naive mice 5 days before hapten application results in suppression of the induction of CHS ( 53). Meanwhile, the concept of UV-exposed keratinocytes as a source of immunosuppressive factors was supported by various other studies. For example, injection of supernatants from UV-exposed murine keratinocytes suppressed the induction of delayed-type hypersensitivity to alloantigen and trinitrophenyl-modified self-antigens in syngeneic and allogeneic mice ( 54). There is also evidence of in vivo release of suppressor factors. Injection of plasma obtained from UV-exposed mice into normal animals suppressed the ability of the recipient mice to generate CHS reactions ( 55). Moreover, a UV-inducible serum factor that suppresses allergic contact dermatitis has also been described in guinea pigs ( 56). With regard to immunosuppression, two cytokines appear to be of particular interest: TNF-α and IL-10. Injection of anti-TNF-α antibodies was found to block the induction of UV-induced immune suppression, suggesting that TNF-α is a critical mediator in this type of compromise of the immune system ( 57). This is also supported by the finding that injection of TNF-α mimics the effects of UVB radiation ( 46). However, as already mentioned above (see section V), neutralization of TNF-α does not prevent the induction of tolerance ( 47, 48), confirming that different pathways are responsible for the impairment of CHS on the one hand, and for the induction of tolerance on the other hand. IL-10 was found to be able to interfere with the antigen-presenting capacity of Langerhans cells. In an in vitro system, it was observed that incubation of Langerhans cells with IL-10 abrogates the ability of these cells to present antigen to Th1 clones and even tolerizes them ( 58). In addition to macrophages, B cells, and T cells, keratinocytes can function as a source of IL-10 ( 59, 60). IL-10 production in the skin is enhanced upon application of contact allergens, whereas tolerogens or irritants have no effect ( 61). In addition, injection of IL-10 in the skin area of hapten application prevents the induction of CHS and induces hapten-specific tolerance ( 62). Furthermore, it was demonstrated that UV radiation upregulates IL-10 in both murine and human keratinocytes ( 60). Due to its ability to downregulate inflammatory and immune reactions, keratinocyte-derived IL-10 may play an important role in UV-induced immunosuppression ( 60). Accordingly, injection of an anti-IL-10 antibody into UV-irradiated mice prevented systemic UV-induced suppression of the induction of delayed-type hypersensitivity ( 60). Moreover, it was observed that spleen cells from UV-exposed animals did not present antigen to Th1 cells, while presentation to Th2 cells was even enhanced ( 63). Both of these effects could be prevented by injection of an anti-IL-10 antibody, suggesting a crucial role of IL-10 in UV-induced systemic immunosuppression. On the other hand, IL-10 was also found to influence not only the induction, but also the elicitation phase of both contact and delayed-type hypersensitivity ( 64). As a whole, these data suggest that UV radiation with the help of IL-10 tolerizes Th1 cells and activates Th2 cells. The Th2 shift in systemic immunosuppression is further supported by the observation that immune suppression is blocked in mice treated with an anti-IL-4 antiserum ( 65). However, UV light does not directly induce IL-4 release. This might be mediated indirectly via UV-induced release of prostaglandin E2 by keratinocytes. Accordingly, cylcooxygenase-2 inhibitors blocked IL-4 production. This suggests that UV exposure activates a cytokine cascade (prostaglandin E2→ IL-4 → IL-10) that finally results in systemic immunosuppression ( 65). Hence, there is extensive evidence that in vivo exposure to UV radiation induces a shift toward a Th2 immune response in vivo, and this explains why mostly Th1-mediated cellular immune reactions are impaired by UV radiation. However, IL-10 appears to be involved not only in mediating tolerance induced by high-dose UV, but also in tolerance induced by low-dose UV. Niizeki & Streilein observed that tolerance develops when haptens are applied onto skin areas in which IL-10 was injected intraperitoneal injection of an anti-IL-10 antibody prevented tolerance induced by low-dose UV ( 66). In contrast, tolerance induced by intracutaneous injection of cis-urocanic acid (UCA) was only partially inhibited by anti-IL-10 antibodies ( 66). cis-UCA is the photoisomer of trans-UCA, a natural component of the stratum corneum ( 67). Since removal of the stratum corneum by tape stripping prevented the particular immunosuppressive effects of UVB radiation ( 68), it was supposed that cis-UCA is involved in UV-induced immunosuppression. Indeed, cis-UCA has immunosuppressive properties, since hapten application onto skin in which cis-UCA was injected results in the induction of hapten-specific tolerance which can even be adoptively transferred ( 48). Although these findings clearly show the immunosuppressive properties of cis-UCA, the relative contribution of cis-UCA to UV-induced tolerance is not yet completely clarified. As already mentioned, anti-IL-10 antibodies block the induction of UV-induced tolerance completely, while cis-UCA induced tolerance only partially ( 66). Moreover, complete inhibition of UV-induced tolerance by application of antibodies against cis-UCA ( 69) has not yet been demonstrated. The cytokine IL-12 plays an important role in the development of Th1 cells ( 70), which are crucial effector cells in contact and delayed-type hypersensitivity reactions ( 71). The critical functional role of IL-12 during cutaneous sensitization was proven by the finding that intraperitoneal injection of an anti-IL-12 antibody into naive mice before epicutaneous hapten application resulted in the failure to induce sensitization in these animals ( 72). Similar findings were obtained by Müller et al. ( 73). In addition, in vivo blocking of IL-12 before sensitization appears to induce tolerance; when mice which were initially anti-IL-12 treated and sensitized were resensitized with the same hapten after a resting period of 14 days, sensitization again was not inducible, suggesting that these animals had become tolerant to this hapten ( 72). Tolerance was hapten specific, since the animals could be successfully sensitized to another unrelated hapten. Since IL-12 and IL-10 counteract in some sense ( 74, 75), it was investigated whether IL-12 could overcome the systemic immunosuppression induced by UV radiation. Administration of IL-12 blocked systemic suppression of contact and delayed-type hypersensitivity in animals exposed to a single exposure ( IL-12 was supposed to prevent the of UV-induced T suppressor cells, since adoptive transfer of spleen cells from UV-exposed animals treated with IL-12 had no effect on the CHS response of the recipient mice, while transfer of cells from but not mice inhibited sensitization ( IL-12 is able to overcome UV-induced local immunosuppression as Schwarz et al. ( reported that a single intraperitoneal injection of IL-12 after the last of low-dose UV before hapten application to the irradiated skin area completely the CHS Moreover, it was observed that IL-12 a immune response when injected into animals that were initially sensitized through UV-exposed skin, before This clearly that IL-12 not only prevents UV-induced immunosuppression upon but also UV-induced tolerance when injected into animals that were initially by application of haptens through UV-exposed skin ( transfer of cells from UV-irradiated and no immunosuppression was in the recipient mice, suggesting that injection of IL-12 abrogates the induction of suppressor cells. The observation that the effect of IL-12 in the transfer experiments was not lost when CD4+ T cells were depleted that IL-12 does not the immune response by inducing Th1 this observation suggests that IL-12 on CD8+ cells, which to tolerance in the low-dose UV model ( 39). Although the transfer of UV-induced tolerance by injecting T cells from UV-exposed mice into naive recipients was described more than years ( 36), the mechanisms by which T suppressor cells tolerance to be There is evidence that plays an important role in immune reactions ( also called or is a ( which induces cell death after with its natural also called ( cells or with high expression of can T cells which thereby the immune response and an immune ( Tolerance can be a form of immune and Schwarz et al. were the first to whether the system is important for UV-induced tolerance ( do they mice, which and mice, which ( of both strains to low doses of UV radiation inhibited the induction of CHS after hapten application to UV-irradiated skin, indicating that both strains are UV However, in to UV-exposed mice, UV-exposed and mice did not develop tolerance. This clearly suggested that the system is crucial for the development of tolerance ( suppression was observed when cells from UV-exposed and hapten-treated donors were injected into naive mice, but also when cells from UV-exposed and hapten-treated mice were transferred into naive recipients. In contrast, both naive and naive recipients of T suppressor cells from UV-exposed and hapten-treated mice could be Thus, these findings suggested that the transfer of tolerance does not or expression on the suppressor cells but does both molecules on cells in the recipient ( These findings were with the that T suppressor cells do not their via expression of but rather into cells in the recipient that are essential during sensitization, and that this may be mediated via the When dendritic cells used as antigen-presenting cells were with T cells from mice in the of the specific hapten, enhanced of dendritic cells was This that T suppressor cells may their by inducing of antigen-presenting cells. of IL-12 to of T suppressor cells and dendritic cells significantly the number of dendritic cells ( This is a very observation as mentioned above (see section IL-12 is the first the only cytokine to be able to UV-mediated tolerance ( By antigen-presenting cells from cell death induced by T suppressor cells, IL-12 might be able to and thereby tolerance. The critical role of the system in UV-induced immunosuppression was recently confirmed by another the high-dose UV et al. showed that but not expression is essential for the function of UV-induced suppressor cells ( These findings from those of Schwarz et al. ( a which may in local or systemic UV-induced immunosuppression. appear to be essential for both types of suppression. UV-induced tolerance is one of the most and in and it is one of the most growing areas in Although the induction of tolerance by UV radiation was first described more than 25 years are from the mechanisms involved. This may be due to the that different models of UV-induced tolerance as high- and dose tolerance, and systemic and local tolerance. Accordingly, in have that the UV dose the concentration of the hapten, and also the type of the hapten can ( Thus, one has to be when studies using different models of UV-induced tolerance. in years, numerous studies have major to this These the recognition that impairment of CHS and induction of tolerance are mediated by different the first attempts to UV-induced T suppressor cells, and the of the between and tolerance, to a These findings have influence on on other tolerance models as tolerance ( or high- ( and low-dose tolerance ( is supported by from the and the

Solar radiation, especially ultraviolet A (UVA) and ultraviolet B (UVB), can cause damage to the human body, and exposure to the radiation may vary according to the geographical location, time of year and other factors. The effects of UVA and UVB radiation on organisms range from erythema formation, through tanning and reduced synthesis of macromolecules such as collagen and elastin, to carcinogenic DNA mutations. Some studies suggest that, in addition to the radiation emitted by the sun, artificial sources of radiation, such as commercial lamps, can also generate small amounts of UVA and UVB radiation. Depending on the source intensity and on the distance from the source, this radiation can be harmful to photosensitive individuals. In healthy subjects, the evidence on the danger of this radiation is still far from conclusive.

20 years after--milestones in molecular photobiology.

Every year, millions of people climb in various states of undress into warm, glowing tanning beds, where during a typical 2- to 15-minute session they’ll absorb a controlled dose of ultraviolet (UV) radiation at an intensity up to two to three times stronger than the sunlight striking the equator at noon. The tanning industry has grown rapidly since the 1980s,1 rising to an estimated 28 million users in the United States.2 This rise has been accompanied by an increase in diagnoses of skin cancer. The reasons behind the rising skin cancer diagnoses remain open to debate. Some experts attribute the rise to more frequent skin cancer screening, whereas others blame environmental and behavioral risk factors, particularly changes in UV exposure. In this latter context, UV-emitting tanning beds—classified as carcinogenic to humans by the International Agency for Research on Cancer (IARC)3—have come under growing scrutiny. People tan to look healthy, but looks can be deceiving; UV radiation causes all three types of skin cancer. Melanoma, a tumor of the cells that produce the skin pigment melanin, is the rarest but deadliest type, accounting for 75% of skin cancer deaths worldwide.4 According to the National Cancer Institute’s Surveillance, Epidemiology and End Results (SEER) program, melanoma incidence among U.S. whites (who develop the disease more often than other races) rose from 8.7 cases per 100,000 people in 1975 to 28 cases per 100,000 in 2009.5 Most of that increase occurred in older men, who rarely tan indoors. But a closer look at the age-stratified SEER data reveals that melanoma rates among white girls and women aged 15–39 rose by 3.6% per year between 1992 and 2006, compared with a 2% increase per year among boys and men of the same ages.6 Although they’re not tracked by SEER, squamous cell carcinoma (SCC) and basal cell carcinoma (BCC)—the other two types of skin cancer—also appear to be on the rise, according to regional studies from the United States and Europe. A recent study by Anne Marie Skellett, a consulting dermatologist at Norfolk and Norwich University Hospital, reveals that BCC diagnoses among people under age 30 in the United Kingdom jumped 145% between 1981 and 2006.7 Statistics such as these have prompted 33 U.S. states and some municipalities to ban or restrict indoor tanning among children under age 18.8 California’s ban, signed into law in October 2011, was the first,9 followed by Vermont in April 201210 and the city of Chicago the following June.11 Other states have introduced legislation to limit indoor tanning among minors.8 Melanoma in the United States Scanning electron micrograph of a melanoma cell magnified 8,000 times Mary Brady, an associate professor of surgery at Weill Medical College in New York and the author of an editorial on indoor tanning that appeared in the May 2012 issue of the Journal of Clinical Oncology,12 says the bans make sense. “We legislate against smoking in kids less than 18, and that sends a strong message that there’s something wrong with it,” she says. “We need to send the same message on indoor tanning.” But the bans have drawn a backlash from the tanning bed industry, whose representatives say they’ve been unfairly and incorrectly singled out. John Overstreet, executive director at the Indoor Tanning Association in Washington, DC, describes the evidence linking indoor tanning to skin cancer as speculation and advocacy science reported by the media as fact. He points out that UV light triggers skin cells to produce vitamin D, which may have cancer-protective effects. “It’s frustrating,” he says. “There’s no doubt that repeated overexposure to UV or burning can cause skin problems, but you also have to look at the health benefits, and that issue always gets lost.”

Central centrifugal cicatricial alopecia: possible familial aetiology in two African families from South Africa

Chapter 9 Photodegradation of human hair: a microscopy study

Background: Overexposure to ultraviolet (UV) radiation is linked to serious adverse health effects that are cumulative in nature and affect children more than adults. UV radiation has also been reported to have serious complications for the eye, particularly in areas with a high UV radiation index. Increasing public awareness about the harmful effects of UV radiation on the eye and promoting awareness about protection against UV radiation may prevent eye disease related to UV radiation damage and help in the improvement of public health in general. This study aims to assess public awareness and knowledge of UV radiation and practices toward UV protection in Jordan, which is a country recognized as having a relatively high UV index throughout the year. Methods: A cross-sectional study was performed using an online questionnaire using Google Forms® to assess people's awareness, knowledge, practices toward eye protection from UV radiation, and the reasons for not wearing UV-protective eyeglasses in Jordan. Sociodemographic information of participants including age, gender, education level, and employment status was also acquired. People's knowledge on UV protection and harmfulness was measured via rewarding their correctly answered knowledge questions with one mark and zero for incorrectly answered questions based on key answers defined from the literature. Results: A total of 1331 participants (77% females and 23% males) with an average age of 26(±10) years completed the online questionnaire. Participants showed generally high levels of knowledge and awareness about UV radiation and its harmful effects. Nevertheless, participants showed a low level of knowledge about the link between UV radiation and some of the ocular diseases in the questionnaire. Practices toward UV radiation protection where inadequate, with 59% of the respondents reporting that they do not use any protective eyewear from natural UV radiation. The main reported reason for not wearing UV-protective sunglasses was uncertainty in the efficiency of UV protection in sunglasses, as reported by 47% of the participants who do not wear UV-protective sunglasses. Conclusions: The awareness of UV radiation and its harmful effects is high in the studied population. Participant knowledge is also relatively high in relation to nature of solar UV radiation, other synthetic sources of UV radiation, and the most dangerous UV exposure time. However, low participant knowledge was measured on the association between UV radiation with ocular disease and the role of UV-protective eyeglasses. Participant practice toward UV radiation protection was found to be insufficient. Thus, it is important to further increase the knowledge of damaging effects of solar and synthetic UV radiation and emphasize the benefits of eye protection from UV radiation. Eye care practitioners should target youth by different strategies including health campaigns, media, and clinics.

A review on the ability of smartphones to detect ultraviolet (UV) radiation and their potential to be used in UV research and for public education purposes

Levels of ultraviolet (UV) radiation have increased in many parts of the world due to the anthropogenic destruction of the ozone layer. UV radiation is a potent immunosuppressant and can increase the susceptibility of animal hosts to pathogens. UV radiation can directly alter immune function via immunosuppression and photoimmunotolerance; however, UV may also influence pathogen defences by affecting the distribution of energy resources among competing physiological processes. Both defence against UV damage and repair of incurred damage, as well as the maintenance of immune defences and responding to an immune challenge, are energetically expensive. These competing demands for finite energy resources could trade off against one another, resulting in sub-optimal performance in one or both processes. We examined the potential for a disease-related energy trade-off in green tree frog (Litoria caerulea) larvae. Larvae were reared under high- or low-UV conditions for 12weeks during which time we measured growth rates, metabolic rate and susceptibility to the amphibian fungal pathogen, Batrachochytrium dendrobatidis (Bd). We found that larvae exposed to high levels of UV radiation had higher rates of energy expenditure than those exposed to low UV levels; however, UV exposure did not affect growth rates or developmental timings. Larvae exposed to high UV radiation also experienced greater Bd infection rates and carried a higher infection burden than those not exposed to elevated UV radiation. We propose that the increased energetic costs of responding to UV radiation were traded off against immune defences to protect larval growth rates. These findings have important implications for the aetiology of some Bd-associated amphibian declines, particularly in montane environments where Bd infections are most severe and where UV levels are highest.

Extended survival times of Mycoplasma gallisepticum and Mycoplasma synoviae on kanekalon synthetic hair fibres

The effect of ultraviolet (UV) radiation exposure on the room-temperature hydrogen (H2) sensitivity of nanocrystalline indium oxide (In2O3)-doped tin oxide (SnO2) thin-film gas sensor is investigated in this article. The present sensor is incorporated into microelectromechanical systems device using sol-gel dip-coating technique. The present sensor exhibits a very high sensitivity, as high as 65 000–110 000, at room temperature, for 900ppm of H2 under the dynamic test condition without UV exposure. The H2 sensitivity is, however, observed to reduce to 200 under UV radiation, which is contrary to the literature data, where an enhanced room-temperature gas sensitivity has been reported under UV radiation. The observed phenomenon is attributed to the reduced surface coverage by the chemisorbed oxygen ions under UV radiation, which is in consonance with the prediction of the constitutive equation, proposed recently by the authors, for the gas sensitivity of nanocrystalline semiconductor oxide thin-film sensors.

To investigate ultraviolet (UV) radiation effects on tribological properties of Mo/MoS2-Pb-PbS film, ultraviolet (UV) radiation exposure tests were carried out for 20 h, 40 h, 60 h and 80 h by space UV radiation simulation device developed by our team, which can reach 3 UV radiation intensity. The exposure time in test was equivalent to the radiation of 100 h, 200 h, 300 h and 400 h in the space. Then, the vacuum friction test of Mo/MoS2-Pb-PbS thin film was performed under the 6 N load and 100 r/min, and friction test time of each sample was 20 min. By SEM, TEM, XPS the composition and morphology of Mo/MoS2-Pb-PbS film surface after UV radiation were analyzed. UV radiation could change the microstructure significantly and relative content of S element and MoS2 on the surface of the films decreased, and light mass loss of the films occurred. The tribological properties will also recover with the increase of sliding time, although the friction coefficient fluctuation of the film increased at the starting stage of the friction test. The damage of Mo/MoS2-Pb-PbS under UV irradiation was mainly caused by the volatilization of the enriched S element in the surface layer due to the high temperature heating of UV irradiation.

Elevated ultraviolet (UV) radiation has been demonstrated to stimulate litter decomposition. Despite years of research, it is still not fully understood whether the acceleration in litter degradation is primarily attributed to abiotic photodegradation or the combined effects of abiotic photodegradation and microbial decomposition. In this study, we used meta-analysis to synthesize photodegradation studies and compared the effects of UV radiation on litter decomposition between abiotic and biotic conditions. We also conducted a microcosm experiment to assess the effects of UV radiation on litter biodegradability and microbial activity. Overall, our meta-analysis found that under abiotic photodegradation, UV radiation reduced the remaining litter mass by 1.44% (95% CI: 0.85% to 2.08%), did not affect the remaining lignin and increased the dissolved organic carbon (DOC) concentration by 14.01% (1.49-23.67%). Under combined abiotic photodegradation and microbial decomposition, UV radiation reduced the remaining litter mass and lignin by 1.60% (0.04-3.58%) and 16.07% (9.27-24.23%), respectively, but did not alter DOC concentration. UV radiation had no significant impact on soil microbial biomass carbon (MBC), but it reduced microbial respiration by 44.91% (2.26-78.62%) and altered the composition of the microbial community. In addition, UV radiation reduced nitrogen (N) immobilization by 19.44% (4.77-37.92%). Our microcosm experiment further indicated that DOC concentration and the amount of respired C in UV-treated litter increased with UV exposure time, suggesting that longer UV exposure resulted in greater biodegradability. Overall, our study suggested that UV exposure could increase litter biodegradability by increasing the microbial accessibility of lignin, as well as the labile carbon supply to microbes. However, the remaining litter mass was not different between the abiotic and biotic conditions, most likely because the positive effect of UV radiation on litter biodegradability was offset by its negative effect on microbial activity. Our results also suggested that UV radiation could alter the N cycle during decomposition, primarily by inhibiting N immobilization.