The role and safety of UVA and UVB in UV-induced skin erythema.

Background: Different wavelengths of ultraviolet (UV) light cause skin damage through different mechanisms. Minimal erythema dose (MED) is usually used to clinically evaluate skin sensitivity to ultraviolet radiation by inducing skin erythema using ultraviolet B (UVB) or ultraviolet A (UVA) + UVB. Aims: In this study, we detected changes in the blood flow at the MED erythema caused by UVB and UVA + UVB radiation through optical coherence tomography (OCT) to explain the role of different bands of ultraviolet rays in erythema induction. Methods: Two MED irradiation areas on the subjects' back were irradiated with UVB alone or UVA + UVB (UVA: UVB = 8:1). The absolute energy of UVB remained the same in UVB and UVA+UVB. At 24 h after the irradiation, the changes in the blood flow in the MED area were detected using OCT. Results: Compared with the blank control, the maximum blood flow depth, blood flow peak, and total blood flow of UVB-MED and UVA+UVB-MED were significantly increased. Notably, the maximum blood flow depth and blood flow peak of UVB-MED were higher than UVA+UVB-MED. There was no significant difference in total blood perfusion between UVA+UVB-MED and UVB-MED. Under the same UVB energy, the skin erythema caused by UVA + UVB was weaker than UVB alone. Conclusions: The analysis of local blood flow by OCT showed that the peak and maximum depth of local blood flow caused by UVB alone were significantly higher than UVA + UVB.

Evaluation and detection of early nail damage caused by nail enamel.

BACKGROUND: Many nail cosmetics have components that are considered irritants or allergens. Due to the current clinical assessment limitations, it is often too late to identify nail enamel hazards until they cause disease. Thus, it is essential to investigate effective methods of detecting minor changes and early lesions in nails before they worsen. OBJECTIVES: To provide a reliable method to investigate and evaluate nail enamel hazards on nails earlier using ultrasonic equipment. METHODS: Eighty-three volunteers with smooth, lustrous nails were enrolled after being clinically examined. The thumbnails and middle nails were evaluated before and after using nail enamel for 2 weeks. Nail health was then assessed using three methods: clinical evaluation, nail surface image analysis, and an ultrasonic device. RESULTS: Using clinical diagnostic and imaging methods for analyzing the nail surface showed no visible differences before and after using nail enamel for 2 weeks. However, there was a significant difference in the nails' depth and density (p < 0.001). The depth had increased 10% for thumbnails (about 20 µm), and the density had decreased by 3.0%. As for middle nails, the depth had increased by 9.4% (about 19 µm), and the density had decreased by 3.0%. CONCLUSION: The present study provided evidence that nail enamel can significantly irritate hyperplasia and decrease the density of the nails, but detecting that slow process of pathological changes cannot currently be assessed by conventional clinical evaluation and image analysis. Thus, our study provided a practical novel approach for evaluating these visually imperceptible nail changes.

RTL1 promotes melanoma proliferation by regulating Wnt/ß-catenin signalling.

Cutaneous melanoma is a highly malignant and metastatic skin cancer with high mortality. However, its underlying mechanisms remain largely unclear. Here, we found that retrotransposon-like 1 (RTL1) is highly enriched in melanoma tissue, especially in early and horizontal growth tissues. Knockdown of RTL1 in melanoma cells resulted in cell proliferation suppression; cell cycle arrest at G1 phase; and down-regulation of E2F1, CYCLIN D1, cyclin-dependent kinase 6 (CDK6) and c-MYC. Moreover, overexpression of RTL1 in melanoma cells accelerated cell proliferation, promoted passage of the cell cycle beyond G1 phase, and increased the expression of cell cycle related genes. Mechanistically, we found that knockdown of RTL1 inhibited the Wnt/ß-Catenin pathway by regulating the expression of genes specifically involved in ß-CATENIN stabilization. Furthermore, the overexpression and knockdown of ß-CATENIN rescued the effects of RTL1 on melanoma cell proliferation and the cell cycle. These findings were also confirmed via tumour xenografts in nude mice. Together, our results demonstrated that RTL1 promotes melanoma cell proliferation by regulating the Wnt/ß-Catenin signalling pathway.

Pre-clinical assessment of A-674563 as an anti-melanoma agent.

The present study aims to investigate the anti-melanoma activity by an Akt1 specific inhibitor A-674563. We showed that A-674563 was anti-proliferative and cytotoxic when added to human melanoma cells (A375, WM-115 and SK-Mel-2 lines). A-674563 induced caspase-dependent apoptotic death of human melanoma cells, and its cytotoxicity was inhibited with pre-treatment of caspase inhibitors. Further, A-674563 treatment blocked Akt and its downstream S6 Kinase 1 (S6K1) activation in A375 melanoma cells. Significantly, restoring Akt-S6K1 activation via introduction of constitutively-active Akt1 (ca-Akt1) only partially attenuated A-674563's cytotoxicity against A375 cells. Further, A-674563 induced pro-apoptotic ceramide production in A375 cells. Significantly, sphingosine-1-phosphate (S1P) inhibited A-674563-induced ceramide production and subsequent A375 cell apoptosis. On the other hand, co-treatment with the glucosylceramide synthase (GCS) inhibitor PDMP or the cell permeable short-chain ceramide (C6) potentiated A-674563's cytotoxicity against A375 cells. In vivo, A-674563 oral gavage inhibited A375 xenograft growth in severe combined immunodeficiency (scid) mice. Akt inactivation, caspase-3 activation and ceramide production were also observed in A-674563-treated A375 xenografts. Together, these results suggest that A-674563 exerts potent anti-melanoma activity, involving Akt-dependent and Akt-independent mechanisms.

Relationship between skin parameters (darkness or thickness) and photoreaction of Chinese Han skin.

BACKGROUND: Skin pigmentation and the stratum corneum are the two primary natural factors that protect against UV damage. Although several classification systems exist to quantify the ability of the skin to protect itself from damaging UV radiation, few reports have assessed skin parameters and photoreaction in persons of Han Chinese descent. AIMS: To understand the relationship between skin darkness, skin thickness, and photoreaction in Chinese Han subjects. METHODS: Thirty-one subjects were exposed to UVA and UVB. Minimal persistent pigment darkening dose (MPPD) and minimal erythema dose (MED) were obtained. Before the UV irradiation, the test sites were measured by the Mexameter MX 16, Chromameter CR400, and Skin B-ultrasonic to determine skin color and thickness>. Using the ratio of J(MPPD)/J(MED), we classified the subjects into four energy skin phototypes (ESPTs) and the skin parameters for each of these groups were analyzed. RESULTS: Skin color and skin thickness were significantly different among the ESPTs. There was also a significant positive correlation between skin group and the skin color and thickness parameters (b*, melanin index [MI], thickness). As the ESPTs increased from ESPT A to ESPT D, the mean dose to achieve MED increased, while the MPPD decreased. CONCLUSION: As the ESPTs increased from type A to type D, there was a proclivity to tan rather than burn. Similarly, the skin became darker and thicker as the phototype increased from A to D.

Changes of oxygen content in facial skin before and after cigarette smoking.

BACKGROUND/PURPOSE: Cigarette smoking not only causes systemic health problems, but may also be an underlying cause of premature skin aging. Cigarette smokers frequently have morphological changes in facial skin that may be attributed to reduced oxygen in this region. The purpose of this study was to measure the oxygen content in facial skin before and after smoking. METHODS: Twenty-five volunteers participated in this study. Changes in oxygen content of the facial skin were measured before and after 30 min of cigarette smoking. Skin temperature and oxygen content were evaluated in the periorbital and periolar regions. RESULTS: There was a significant increase in temperature after smoking. The oxy hemoglobin and partial pressure of oxygen decreased in both the periocular and perioral areas after smoking. There were no changes in deoxy hemoglobin and partial pressure of carbon dioxide at these areas. CONCLUSION: Significant changes were seen in temperature and oxygen content after only 30 min of smoking. The results from this study suggest that alterations in the skin temperature and oxygen content in facial skin after smoking may be an underlying cause of premature skin aging.