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Dear Editor, Pityriasis lichenoides (PL) is an inflammatory skin disease of unknown etiology. The clinical spectrum of pityriasis lichenoides encompasses febrile ulcer-necrotic Mucha-Habermann disease (FUMHD), pityriasis lichenoides et varioliformis acuta (PLEVA), and pityriasis lichenoides chronica (PLC). Phototherapy is an effective and well-tolerated modality that is often successful for persistent PL or resistant to topical treatments. A retrospective observational study was conducted involving patients from the dermatology section of the University of Verona with a confirmed histological diagnosis of PLEVA and PLC accessed between January 2003 and June 2024. [...]

In the present study, continuous measurements of solar global (G) and ultraviolet-B (UVB) radiation are taken in Kuwait for 2014–2019 for all weather conditions. Hourly curves show a sinusoidal behavior for both G and UVB radiation. Statistical analysis indicates that there is a good agreement between hourly G and hourly UVB as the coefficients of determination (R2) for all years are larger than 0.91 and the root-mean-square error (RMSE) and mean bias error (MBE) are very small. The hourly percentage ratio (UVB/G) is found to decrease with G due to cloudy sky conditions. In addition, the ratio (UVB/G) tends to decrease with global clearness index (KT), indicating that a higher ratio of (UVB/G) can be obtained for a cloudier atmosphere. Another interesting finding is that KT and the UVB index (KTUVB) are directly proportional, and a third-order polynomial fit gives an acceptable formula (R2 = 0.859). Daily G and UVB values are very well correlated as R2 is very close to unity for all years. The values of RMSE and MBE obtained from daily analysis are greatly enhanced as the values of RMSE and MBE are almost zero. The maximum G and UVB radiation obtained is 27.94 MJ/m2 and 0.0044 MJ/m2, respectively, with both occurring in June 2015. Finally, there is an excellent linear fit between the monthly G and monthly UVB radiation as R2 is almost equal to unity and RMSE and MBE are negligible. Thus, the predicted daily or monthly empirical formula can be utilized with a very high accuracy to predict both daily and monthly UVB values at locations in Kuwait where G is measured.

Vitamin D is the sunshine vitamin that has been produced on this earth for more than 500 million years. During exposure to sunlight 7-dehydrocholesterol in the skin absorbs UV B radiation and is converted to previtamin D3 which in turn isomerizes into vitamin D3. Previtamin D3 and vitamin D3 also absorb UV B radiation and are converted into a variety of photoproducts some of which have unique biologic properties. Sun induced vitamin D synthesis is greatly influenced by season, time of day, latitude, altitude, air pollution, skin pigmentation, sunscreen use, passing through glass and plastic, and aging. Vitamin D is metabolized sequentially in the liver and kidneys into 25-hydroxyvitamin D which is a major circulating form and 1,25-dihydroxyvitamin D which is the biologically active form respectively. 1,25-dihydroxyvitamin D plays an important role in regulating calcium and phosphate metabolism for maintenance of metabolic functions and for skeletal health. Most cells and organs in the body have a vitamin D receptor and many cells and organs are able to produce 1,25-dihydroxyvitamin D. As a result 1,25-dihydroxyvitamin D influences a large number of biologic pathways which may help explain association studies relating vitamin D deficiency and living at higher latitudes with increased risk for many chronic diseases including autoimmune diseases, some cancers, cardiovascular disease, infectious disease, schizophrenia and type 2 diabetes. A three-part strategy of increasing food fortification programs with vitamin D, sensible sun exposure recommendations and encouraging ingestion of a vitamin D supplement when needed should be implemented to prevent global vitamin D deficiency and its negative health consequences.

BackgroundExcessive exposure of the skin to UV radiation (UVR) triggers a remodeling of the immune system and leads to the photoaging state which is reminiscent of chronological aging. Over 30 years ago, it was observed that UVR induced an immunosuppressive state which inhibited skin contact hypersensitivity.MethodsOriginal and review articles encompassing inflammation and immunosuppression in the photoaging and chronological aging processes were examined from major databases including PubMed, Scopus, and Google Scholar.ResultsCurrently it is known that UVR treatment can trigger a cellular senescence and inflammatory state in the skin. Chronic low-grade inflammation stimulates a counteracting immunosuppression involving an expansion of immunosuppressive cells, e.g., regulatory T cells (Treg), myeloid-derived suppressor cells (MDSC), and regulatory dendritic cells (DCreg). This increased immunosuppressive activity not only suppresses the function of effector immune cells, a state called immunosenescence, but it also induces bystander degeneration of neighboring cells. Interestingly, the chronological aging process also involves an accumulation of pro-inflammatory senescent cells and signs of chronic low-grade inflammation, called inflammaging. There is also clear evidence that inflammaging is associated with an increase in anti-inflammatory and immunosuppressive activities which promote immunosenescence.ConclusionIt seems that photoaging and normal aging evoke similar processes driven by the remodeling of the immune system. However, it is likely that there are different molecular mechanisms inducing inflammation and immunosuppression in the accelerated photoaging and the chronological aging processes.

Ultraviolet-B (UVB) radiation is an environmental factor that can cause crop plants to experience stress-related reactions that affect their growth, development, and productivity. For comprehending plant responses and the creation of effective mitigation plans, accurate measurements and evaluations of UVB sensitivity on crops are essential. Disparities in reported UVB sensitivity levels can result from differences in measurement methods and techniques. The methods used to measure UVB sensitivity in crops today are, however, still largely unknown. This review present current various measurement techniques for determining UVB sensitivity in crops. There is wide range of UVB sensitivity measurement methodologies, including by looking at cyclobutane pyrimidine dimer (CPD) photolyase activity, DNA damage repair, gene expression, and antioxidant capacity. These variations are brought on by experimental setups, including light sources, exposure times, and growth conditions. This study emphasizes the requirement for standardization and agreement on measurement protocols to guarantee an accurate evaluation of UVB stress in crop plants. This study will deepen our comprehension of the effects of UVB stress and offer practical solutions to reduce UVB sensitivity and protect crop productivity in climate change, which could increase crop yield and productivity.

UV radiation and H2O2 are the primary factors that cause skin aging. Both trigger oxidative stress and cellular aging. It has been reported that deacetylase silent information regulator 1 (SIRT1), a longevity gene, enhances activation of NF-E2-related factor-2 (Nrf2), as well as its downstream key antioxidant gene hemeoxygenase-1 (HO-1), to protect cells against oxidative damage by deacetylating the transcription coactivator PPARγ coactivator-1α (PGC-1α). Galangin, a flavonoid, possesses anti-oxidative and anti-inflammatory potential. In the present study, we applied Ultraviolet B/H2O2-induced human dermal fibroblast damage as an in vitro model and UVB-induced photoaging of C57BL/6J nude mice as an in vivo model to investigate the underlying dermo-protective mechanisms of galangin. Our results indicated that galangin treatment attenuates H2O2/UVB-induced cell viability reduction, dermal aging, and SIRT1/PGC-1α/Nrf2 signaling activation. Furthermore, galangin treatment enhanced Nrf2 activation and nuclear accumulation, in addition to inhibiting Nrf2 degradation. Interestingly, upregulation of antioxidant response element luciferase activity following galangin treatment indicated the transcriptional activation of Nrf2. However, knockdown of SIRT1, PGC-1α, or Nrf2 by siRNA reversed the antioxidant and anti-aging effects of galangin. In vivo evidence further showed that galangin treatment, at doses of 12 and 24 mg/kg on the dorsal skin cells of nude mice resulted in considerably reduced UVB-induced epidermal hyperplasia and skin senescence, and promoted SIRT1/PGC-1α/Nrf2 signaling. Furthermore, enhanced nuclear localization of Nrf2 was observed in galangin-treated mice following UVB irradiation. In conclusion, our data indicated that galangin exerts anti-photoaging and antioxidant effects by promoting SIRT1/PGC-1α/Nrf2 signaling. Therefore, galangin is a potentially promising agent for cosmetic skin care products against UV-induced skin aging.

[Display omitted] The association of sunrays with skin damage have been known since medieval times. The description of the electromagnetic spectrum facilitated the identification of the ultraviolet light spectrum as being responsible for skin damage resulting from prolonged skin exposure. Sunscreens have been used since ancient civilizations with various measures to limit exposure to sun exposure being employed. Awareness of the risks associated with sunrays has been increasing in the last century, and as a result, the science, technologies, and formulation have advanced significantly. The use of sunscreen products continues rising as government health agencies seek to contain increasing cases of UV induced melanomas. Recreational sunbathing and artificial tanning have increased the risk for these diseases significantly. This review article sought to expound the scientific basis of sunscreen use, the classification, formulation, quality control and regulation across the different countries around the world. The literature review was conducted on Google scholar, PubMed, SCOPUS, Cochrane, BMJ, SCIELO among others.

The world is in the grip of the COVID-19 pandemic. Public health measures that can reduce the risk of infection and death in addition to quarantines are desperately needed. This article reviews the roles of vitamin D in reducing the risk of respiratory tract infections, knowledge about the epidemiology of influenza and COVID-19, and how vitamin D supplementation might be a useful measure to reduce risk. Through several mechanisms, vitamin D can reduce risk of infections. Those mechanisms include inducing cathelicidins and defensins that can lower viral replication rates and reducing concentrations of pro-inflammatory cytokines that produce the inflammation that injures the lining of the lungs, leading to pneumonia, as well as increasing concentrations of anti-inflammatory cytokines. Several observational studies and clinical trials reported that vitamin D supplementation reduced the risk of influenza, whereas others did not. Evidence supporting the role of vitamin D in reducing risk of COVID-19 includes that the outbreak occurred in winter, a time when 25-hydroxyvitamin D (25(OH)D) concentrations are lowest; that the number of cases in the Southern Hemisphere near the end of summer are low; that vitamin D deficiency has been found to contribute to acute respiratory distress syndrome; and that case-fatality rates increase with age and with chronic disease comorbidity, both of which are associated with lower 25(OH)D concentration. To reduce the risk of infection, it is recommended that people at risk of influenza and/or COVID-19 consider taking 10,000 IU/d of vitamin D3 for a few weeks to rapidly raise 25(OH)D concentrations, followed by 5000 IU/d. The goal should be to raise 25(OH)D concentrations above 40–60 ng/mL (100–150 nmol/L). For treatment of people who become infected with COVID-19, higher vitamin D3 doses might be useful. Randomized controlled trials and large population studies should be conducted to evaluate these recommendations.

Skin aging is influenced by both intrinsic and extrinsic factors, particularly UV radiation, and is characterized by an accumulation of senescent cells. Remarkably, exposure to UV can trigger senescence in different skin cell types, including dermal fibroblasts. However, the molecular mechanisms underlying UV‐induced senescence and the impact of the related senescence‐associated secretory phenotype (SASP) on the homeostasis of the overlying epidermis remain poorly understood. Here, we identified that both chronological aging and photoaging induce the unfolded protein response (UPR) in human dermal samples. We demonstrated that silencing ATF6α disrupts the establishment of the UVB‐induced senescent phenotype by preventing the onset of several senescent biomarkers and alters the composition of the SASP, consequently affecting its impact on the increased proliferation of keratinocytes embedded in reconstructed human epidermis. Moreover, we found that ATF6α partially mediates IL8 expression involved in the hyperproliferation of cultured keratinocytes. Together, our findings highlight the importance of the ATF6α/IL8 axis in regulating the homeostasis of neighboring cells during skin photoaging, thus suggesting ATF6α as a potentially promising target for senotherapeutic interventions. UVB exposure can trigger senescence in dermal fibroblasts. We show that silencing ATF6α disrupts the establishment of the UVB‐induced senescent phenotype by preventing the onset of several senescent biomarkers and altering the composition of the SASP, consequently affecting its impact on the skin microenvironment.

This is a narrative review of the evidence supporting vitamin D’s anticancer actions. The first section reviews the findings from ecological studies of cancer with respect to indices of solar radiation, which found a reduced risk of incidence and mortality for approximately 23 types of cancer. Meta-analyses of observational studies reported the inverse correlations of serum 25-hydroxyvitamin D [25(OH)D] with the incidence of 12 types of cancer. Case-control studies with a 25(OH)D concentration measured near the time of cancer diagnosis are stronger than nested case-control and cohort studies as long follow-up times reduce the correlations due to changes in 25(OH)D with time. There is no evidence that undiagnosed cancer reduces 25(OH)D concentrations unless the cancer is at a very advanced stage. Meta-analyses of cancer incidence with respect to dietary intake have had limited success due to the low amount of vitamin D in most diets. An analysis of 25(OH)D-cancer incidence rates suggests that achieving 80 ng/mL vs. 10 ng/mL would reduce cancer incidence rates by 70 ± 10%. Clinical trials have provided limited support for the UVB-vitamin D-cancer hypothesis due to poor design and execution. In recent decades, many experimental studies in cultured cells and animal models have described a wide range of anticancer effects of vitamin D compounds. This paper will review studies showing the inhibition of tumor cell proliferation, dedifferentiation, and invasion together with the sensitization to proapoptotic agents. Moreover, 1,25-(OH)2D3 and other vitamin D receptor agonists modulate the biology of several types of stromal cells such as fibroblasts, endothelial and immune cells in a way that interferes the apparition of metastases. In sum, the available mechanistic data support the global protective action of vitamin D against several important types of cancer.