Medically, ultraviolet light treatment is often used with topical coal tar or retinoid as their may be a synergy in their combinations. Psoriasis phototherapy in simple non scientific terms is the treatment of psoriasis using light. Although phototherapy is said to be good at greatly reducing the effects of psoriasis on the skin, there are serious consequences of using this method of treatment as you can get your skin burnt by the sun and also encounter other complications.
There is a new cream out now that works perfectly well for the complete treatment of psoriasis, so you don’t have to used harsh treatment methods like phototherapy any more. Steriod creams have been produced by medical experts to help soothe the itching, redness and scaling of psoriasis in just days. You’ll see visible signs of improvements in the 1st week of usage but unfortunately the free samples are available only to people in the US and in Canada. I personally recommend Dermasis Psoriasis Cream as the best treatment option for all psoriasis types. Psoriasis Wisdom is a compendium of information providing tips, techniques, and other information to help treat, relieve, and heal Psoriasis. The scientists believe that a new type of 'evening after' sunscreen containing vitamin E could be developed to block this transfer of energy. Professor Douglas Brash, a dermatologist at Yale University, said: 'So our understanding has been that you put on sunscreen before you go out into the sun and that protects your skin. In tests using mouse and human melanocytes, experts found UV radiation from sunlight causes enzymes in the cells to create two chemicals that react together. However, in the dark the melanin transfers this energy to the DNA to cause the same damage that can occur in sunlight. The diagram above shows the effects of ultraviolet radiation (yellow arrows) on the upper layers of the skin. This item has been provided for private study purposes (such as school projects, family and local history research) and any published reproduction (print or electronic) may infringe copyright law. All text licensed under the Creative Commons Attribution-NonCommercial 3.0 New Zealand Licence unless otherwise stated. Science, Technology and Medicine open access publisher.Publish, read and share novel research.
Ultraviolet Light as a Modulator of Melanoma DevelopmentGraeme Walker1 and Elke Hacker2[1] Skin Carcinogenesis Laboratory, Queensland Institute of Medical Research, Herston, Qld, Australia[2] AusSun Laboratory, Queensland University of Technology, Kelvin Grove, Qld, Australia1. MC1R, the receptor for ??melanocyte stimulating hormone, is the most thoroughly studied melanoma risk gene.
An exceptionally close exploding star, discovered on 21 January, is the focus of observatories on Earth and in orbit, including the Swift satellite and several other NASA spacecraft. The blast, named SN 2014J, occurred in the galaxy M82 and lies only about 12 million light-years away.
Astronomers expect SN 2014J to continue brightening into the first week of February, by which time it may be visible from Earth with binoculars. Michael Siegel, a senior research scientist on the Swift team at Penn State, said "Swift is especially well-suited to studying supernovae, since we can study them in the optical, ultraviolet and X-ray wavelengths at the earliest stages, when you can learn the most about the physics. Although the explosion is unusually close, the supernova's light is diluted by thick dust clouds in its galaxy, which may slightly reduce its apparent peak brightness.
Brown notes that X-rays have never been conclusively observed from a type Ia supernova, so a detection by Swift's X-ray Telescope, Chandra, or NuSTAR would be significant, as would a Fermi detection of high-energy gamma rays. The total destruction of a white dwarf star by one of two possible scenarios results in a type Ia supernova. Either way, the explosion produces a superheated shell of plasma that expands outward into space at tens of millions of miles an hour.
This super-close supernova provides astronomers with an important opportunity to study how interstellar dust affects its light. Sunlight that will not burn your skin helps to improve psoriasis in a person suffering from the disorder. In the early part of the twentieth centuries, it was discovered that the sunlight therapeutic properties for treatment of psoriasis was due to the wave length also classified as ultraviolet light.
These creams have proven to work effectively for many Psoriasis sufferers for quite some time now. The last time I checked the trial offer is for a limited time only, so you’ve got to hurry to grab one. It is the responsibility of the user of any material to obtain clearance from the copyright holder.
Pathways regulating melanocyte function.Keratinocytes expresses various growth factors that bind to melanocyte receptors that regulate critical intracellular pathways.
IntroductionEpidemiological evidence is overwhelming that exposure of the skin to ultraviolet radiation (UVR) can increase one’s risk of developing malignant melanoma. The science and flight operations of the Swift observatory are controlled by Penn State from the Mission Operations Center on the University Park campus.
M82, also known as the Cigar Galaxy, is located in the constellation Ursa Major and is a popular target for small telescopes. Remarkably, SN 2014J can be seen on images taken up to a week before anyone noticed its presence. In one, the white dwarf orbits a normal star, pulls a stream of matter from it, and gains mass until it reaches a critical threshold and explodes.
As a class, type Ia supernovae explode with remarkably similar intrinsic brightness, a property that makes them useful "standard candles" -- some say "standard bombs" -- for exploring the distant universe.
Either ways experiment has shown that sunlight or medical therapeutic light helps in the treatment of psoriasis. The good news is that you can get a free trial sample jar before even buying to see results.

Expression of these factors is increased after damage to the skin such as after UVR exposure. However the situation is complex, as melanoma development is associated with “intermittent” sun exposure, whereas epidermal keratinocyte-based skin cancers like squamous cell carcinoma (SCC) are associated with chronic UVR exposure.
It also is potentially the closest type Ia supernova that will have occurred during the life of the currently operating space missions.
M82 is undergoing a powerful episode of star formation that makes it many times brighter than our own Milky Way galaxy and accounts for its unusual and photogenic appearance. Each one is amazing, but this one is particularly fascinating because it is behind a thick wall of dust and because it is so close to us." Links to images of the M82 supernova and five other supernovae, plus an app, are online here.
It was only when Steve Fossey and his students at the University of London Observatory imaged the galaxy during a brief workshop that the supernova came to light. In the other, the blast begins when two white dwarfs in a binary system eventually spiral inward and collide. The interplay between the shell's size, transparency and radioactive heating determines when the supernova reaches peak brightness. Who studied the therapeutic effect of the sun on the skin scientifically by experimenting with a portion of the solar spectrum in laboratory practice. Tagged harsh method, natural sunlight, phototherapy, psoriasis, steroid creams, therapeutic effect, topical coal tar, ultraviolet light, wavelength.
Germline mutations in p16INK4A and CDK4 (light blue) confer susceptibility to familial melanoma.
Thus it is difficult to talk in terms of a classical UVR carcinogenic mechanism for melanoma in general.
Variants have been classed into two groups based on the strength of their association with red hair (Sturm et al., 2003). Genome wide association studies identify variants in genes involved in pigmentation as risk factors, generally the strongest signal being for the melanocortin receptor 1 gene (MC1R). One reason postulated to explain the odd relationship between UVR exposure and tumorigenesis is that there may be a unique carcinogenic mechanisms at play involving UVA, that is a weak carcinogen for skin cancer in general. MC1R variants are not the sole determinant of hair colour, twin studies have observed discordant hair colour but identical MC1R haplotypes (Box et al., 1997).
Conflicting data has continued to appear, with results from a German sample of 173 melanoma patients showing the opposite effect, with individuals carrying MC1R variants less likely to acquire somatic BRAF mutations in tumours (Scherer et al., 2010). Evidence for UVA causality in melanoma comes from some epidemiological studies, and to some extent from work with animal models. The molecular consequences of UVR upon melanocytes with variant melanocortin-1 receptors are variable.
On the other hand, one can argue that there may not be a unique carcinogenic mechanism for melanoma, and that there are several factors that may help explain the apparent difference from typical mechanism of UVR mutagenesis involving classical UVR mutations.
This has lead to debate over MC1R classification and which variants to include in assessing the impact of impaired MC1R function in melanoma (Hacker & Hayward, 2008). Firstly, in terms of normal cellular function, melanocytes principal function is to produce melanin pigment while epidermal keratinocytes are programmed to proliferate and then die as they generate and maintain the epidermis, a barrier for internal tissues and organs. It is possible that the discordant study findings reflect that fact that MC1R is extremely polymorphic within and between ethnic populations, and that the small sample sizes for each study means that chance association with the non-CSD melanoma pathway cannot be excluded. Thus particularly relates to susceptibility to naevus development, a critical factor associated melanoma development on the trunk, a site presumably receiving mainly “intermittent” sun exposure.
Normal receptor expression was found for R142H and D294H variants, but reduced functional responses were observed, indicating that altered G-protein coupling may be responsible for this loss of function. Genes controlling the development of naeviGiven that the “intermittent” exposure arm of the divergent pathway is associated with the presence of naevi, we should be able to obtain clues about how to differentiate the pathways based on genes that confer naevus risk.
The V92M isoform shows similar activity to the wild-type receptor, and along with V60L, is not associated with melanoma (Raimondi et al., 2008). Interestingly, melanoma risk due to the carriage of MC1R variants is stronger in individuals with dark hair and eyes, who do not have freckles, and tan well (Kanetsky et al., 2010). Sunlight is the only environmental factor that has been consistently implicated as a cause of melanoma, leading to a melanoma incidence 10- to 20- fold higher among fair-skinned than dark-skinned peoples (Armstrong & Kricker, 1993). Thus the risk due to MC1R variation is certainly not limited to red heads.The mechanism by which the carriage of MC1R variants increases melanoma risk is an area of intense investigation. Among fair-skinned people, melanoma incidence increases with proximity to the equator and several studies have shown that fair-skinned migrants moving from high (e.g.
Notably, MC1R variants are also associated with increased risk of non-melanoma skin cancer (table 1). Functional MC1R appears to be necessary to prevent UV-induced genomic instability within melanocytes.
Genes involved in familial melanoma susceptibilityAlthough many different genes can be somatically mutated in melanoma, as yet there are only two confirmed familial melanoma susceptibility loci, CDKN2A and CDK4. The epidemiological association between sunlight and melanoma is complexDespite the persuasive descriptive evidence linking sunlight with melanoma, several observations make clear that the association is complex and does not accord with a simple model in which the risk of melanoma increases directly with increasing levels of exposure to the sun. Melanoma occurs more commonly among indoor than outdoor workers (Beral & Robinson, 1981). The overwhelming majority of CDKN2A mutations in melanoma-prone kindreds affect only the INK4A transcript, or both transcripts, but ARF-specific mutations also predispose to melanoma (e.g. Even in sunny countries most melanomas develop on sites that are habitually covered by clothing (such as the back), as opposed to sites more frequently exposed to the sun such as the face (Green et al., 1993). Many case-control studies of melanoma incidence report stronger associations with intermittent (short periods of intense sun exposure to untanned skin) rather than chronic patterns of sun exposure (Elwood & Jopson, 1997).
Recreational sun exposure is a risk factor for melanoma on the trunk and limbs but not on the head and neck (Chang et al., 2009). Families carrying CDKN2A mutations usually, although not always, exhibit a naevus-prone phenotype (Goldstein et al., 2000) indicating that relaxation of melanocyte proliferation control induced by INK4A (or ARF) loss may be important in naevogenesis.

Chronic sun exposure and a “classical” UVR carcinogenic mechanism involving UVB-induced DNA damage is accepted to be responsible for the development of SCC. However a recent study comparing the influence of sun exposure on melanoma risk in CDKN2A mutations carriers in Australia and the United Kingdom (Cust et al., 2011) suggests that they have to have the same cumulative risk of melanoma irrespective of the ambient UV irradiance in the region in which they live.
One reason frequently proposed for the lack of association of melanoma with chronic sun exposure is that there may be a different carcinogenic mechanism for melanoma, possibly involving UVA exposure.
Genes associated with melanoma in genome wide association studiesGenome wide association (GWA) studies have been used to discover genes that confer risk for skin cancer development (Table 1). Some genes are associated both melanoma and non-melanoma skin cancer, especially basal cell carcinoma (BCC). Five genes associated with melanoma, SLC45A2, TYRP1, TYR, MC1R, and ASIP, encode proteins that are involved in various ways in regulating pigmentation. Little is known about how most of these may effect melanoma genesis and we are left to assume that the risk alleles may encode variants in these genes that simply result in lower levels of protective pigmentation. Notably, in respect to MC1R and ASIP (agouti signaling protein, an MC1R antagonist), there may be other explanations, which will be discussed below. Other ideas revolve around the notion that office workers are at higher relative risk possibly due excessive UVA that can penetrate glass (Godar et al., 2009). Further, recreational exposure, generally agreed to increase melanoma risk, can include solarium use. Thus epidemiological evidence suggests that sunbeds are health hazards in terms of melanoma risk and that UVA has a plausible role in the development of this neoplasm. Hence epidemiological data is somewhat supportive of the view that the full UVR spectrum may be carcinogenic in melanoma.
Naevus and melanoma subtypesFrom the point of view of basic biology differences between melanoma and non-melanoma skin cancer in terms of their relationship with UVR exposure is not surprising.
Melanocytes are long living cells, resistant to apoptosis, whose principal function is to produce melanin. In contrast, the primary function of keratinocytes is to provide a protective barrier, the epidermis, which is in a continual state of regeneration, supplied by proliferation of epidermal basal layer keratinocytes that initiates a programmed process of differentiation and apoptosis as needed. Melanocytes can undergo a form of proliferation, where they form senescent groups, or nests, which are termed naevi. Such lesions are negative for proliferation markers, but can progress to malignancy, albeit at an extremely low frequency (Grichnik, 2008).
These include dermal (blue naevi), compound (common acquired, spitz and congenital naevi) and epidermal (e.g. These subtypes may be influenced differently by UVR exposure, and there may be differences in their propensities for transformation (e.g. Hence the subtype of naevus can be a confounding factor when studying environmental and genetic factors influencing naevo genesis. For instance the positive association between naevus count and IRF4 gene variation (Duffy et al., 2010) varies greatly for different subtypes (dermal versus compound naevi). Likewise there are several major melanoma subtypes, and then subtle forms within each group. Superficial spreading melanoma (SSM) is the most common form in Caucasians (around 70% of all melanomas). It follows a radial growth phase with atypical melanocytes, either as single cells or nests at all levels of the epidermis (Smoller, 2006), followed by an invasive vertical growth phase. Nodular melanoma (NM) are primary dermal lesions characterized by growth through the dermis, generally lack epidermal involvement, and a very sharply circumscribed with virtual lack of radial spread (Smoller, 2006). Lentigo maligna melanoma (LMM) is the only subtype unequivocally associated with chronic sun exposure. Lesions display confluent spread of melanocytes along the epidermal basal layer and in the upper portion of the hair follicle and are invariably associated with solar elastosis in adjacent skin (Smoller, 2006). Acral lentiginous and mucosal melanomas are epidermal lesions that occur on palmoplantar and mucosal surfaces respectively, and are assumed not to be influenced by UVR exposure.
Clearly, any discussion of the effects of chronic versus intermittent sun exposure has to consider melanoma subtype. The divergent pathway model of melanomaTo assess the effects of chronic versus intermittent sun exposure melanomas have been stratified into chronic sun damage (CSD) or non-chronic sun damage (non-CSD) melanomas, either histologically by assessing solar elastosis, a measure of chronic exposure (e.g. Curtin et al., 2005), or by comparing melanomas developing on the head and neck (an anatomical region of high cumulative sun exposure), and the trunk (a region of intermittent exposure).
While these two methods of classification may create some confounding differences, overall the use of either system supports the conclusion of a complex relationship between melanoma and sun exposure that has lead to the proposal of a “divergent pathway” model (Whiteman et al., 2003).
According to this model (Figure 1) the pathways diverge after an initial insult that stabilizes the melanocyte. This may be early life exposure to UVR given that childhood sunburns are a risk factor for melanoma (Whiteman et al., 2001). What happens thereafter depends upon a combination of host characteristics and subsequent patterns and doses of UVR exposure.
Melanomas that develop on the head and neck are associated with solar elastosis (a marker of CSD), low naevus count, and relatively late age of onset. In contrast, melanomas developing on the trunk via the intermittent UVR (non-CSD) pathway tend to have relatively earlier age of onset and are associated with higher naevus count.

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