The present study examined theoretical mediators of a parent-based intervention on sunbathing tendencies and sunburn frequencies based on the work of Turrisi et al. [Turrisi, R., Hillhouse, J., Heavin, S., Robinson, J., Adams, M., & Berry, J. (2004). Journal of Behavioral Medicine, 27, 393-412.]. Three hundred and forty parents in two regions of the United States were educated about the dangers of risky sun behavior and how to convey information about skin cancer prevention to their children. Attitudes toward sunbathing, health beliefs, appearance beliefs, and social normative beliefs were examined and found to be significant mediators of program effects on sunbathing tendencies and sunburn frequencies. The findings are discussed with respect to maximizing the effectiveness of future skin cancer interventions with children.

Indoor tanning remains a popular activity in Western cultures despite a growing body of literature suggesting its link to skin cancer and melanoma. Advances in indoor tanning research have illuminated problematic patterns of its use. With problems such as difficulty quitting, devoting resources toward its use at the expense of healthy activities, and excessive motivation and urges to tan, symptoms of excessive indoor tanning appear consistent with behavioral addiction. The present study bridges the gap between clinical approaches to understanding indoor tanning problems and behavioral economic considerations of unhealthy habits and addiction. Eighty undergraduate females completed both the Behavioral Addiction Indoor Tanning Screener and the Tanning Purchase Task. Results suggest that behavioral economic demand for tanning significantly differs between risk classification groups, providing divergent validity to the Behavioral Addiction Indoor Tanning Screener and offering additional evidence of the sensitivity of the Tanning Purchase Task to differentiating groups according to tanning profiles.

Given the prevalence and risk associated with indoor tanning among college students, university campuses constitute a prime target for skin cancer prevention. This report identifies the successes and challenges faced in promoting a campus-wide tan-free policy through the National Council on Skin Cancer Prevention (NCSCP) Indoor Tan-Free Skin Smart Campus Initiative. Beginning in February 2016, we communicated with university faculty or staff members who have participated in skin cancer prevention via education, clinical care, or research at 20 universities regarding the steps to adopt the tan-free policy. One campus, East Tennessee State University (ETSU), successfully fulfilled all criteria and implemented the policy change to become the first US Indoor Tan-Free Skin Smart Campus. The greatest challenge faced in recruiting campuses was gaining administrative support. Reported reasons for not adopting the policy change included wanting to wait for other schools to join first and not seeing it as a top priority. Despite the importance of improving skin cancer awareness and decreasing tanning among university students, we faced several challenges in promoting campus-wide policy change. We identify a need for research on effective ways to disseminate university health policies and increased involvement of healthcare providers in policy-related work.

Millions of Americans engage in tanning each year, defined as intentional ultraviolet radiation (UVR) exposure in the form of sunbathing or the use of indoor tanning beds. An emerging body of research suggests that UVR has addictive properties and some tanners engage in excessive tanning. This article provides an overview of the evidence of tanning addiction and a systematic review of existing tanning interventions with the goal of evaluating their potential to impact addicted tanners. Our search identified 24 intervention studies that were summarized and discussed according to 3 primary themes. First, there is a dearth of tanning interventions that target excessive tanning or are designed as treatments for tanning addiction. Second, tanning interventions are primarily educational interventions designed to increase knowledge of the risks of tanning. Third, there are notable aspects of existing tanning interventions that are relevant to addiction science, including the use of brief motivational and cognitive-behavioral-based interventions. Future directions are considered including recommendations for utilizing the existing evidence base to formulate interventions targeting excessive tanners.

No description available.

Skin cancer is the most common type of cancer in the US. The American Academy of Dermatology estimated that more than 3.5 million new cases of skin cancer are diagnosed in the US each year and 1 in 5 Americans will likely to develop skin cancer in their life time. Most cases of skin cancer are caused by exposure to ultraviolet (UV) radiation from the sun. Some of the most common sunscreen ingredients are unstable and can form harmful radicals upon exposure to UV radiation. There is a strong clinical need for a more stable and effective sunscreen ingredient such as bovine milk phospholipids (MP). Phospholipids were shown to have beneficial health effects such as regulation of the inflammatory reactions, protective effects against colon cancer, and reducing cardiovascular risk factors. Previous histology and MTT tissue viability research studies suggested that MP act upon skin cells in a protective manner against UV radiation. This thesis aims to further investigate the protective effects of bovine milk phospholipids by evaluating the expression of a UV-induced DNA damage marker, cyclin-dependent kinase inhibitor, p21WAF1/CIP1. Western blots were used to quantify p21 expression in human keratinocytes in four categories of samples: No-UV, UV, UV+MP, MP and in HeLa (p21 positive control). In the No-UV samples, cells were not irradiated by UV light. However, in the UV samples, keratinocytes were exposed to a UV dosage of 10 mJ/cm2. In the UV+MP samples, keratinocytes were first treated with 1% MP solution (w/v) in their culture media for 24 hours then exposed to a UV dosage of 10 mJ/cm2. In MP, keratinocytes were treated with 1% MP solution in their culture media for 24 hours. Total cell proteins were extracted 24 hours post-UV irradiation. The same amount of protein from each sample (determined by BCA assay) was loaded into a 4-12% Bis-Tris SDS-PAGE gel, run under denaturing, non-reducing conditions then blotted and treated with antibodies for the quantitative detection of p21 proteins. Finally, intensities of p21 protein bands were analyzed by using ImageJ software. Under non-reducing conditions, three p21 proteins covalently bonded with each other showed up as 63 KDa molecules on the PVDF membrane. The UV, and HeLa samples showed a 2.28 fold, and 1.23 fold increase in p21 expression, respectively, compared with the No-UV samples control. The MP samples showed a 0.948 fold decrease in p21 compared with the No-UV samples, and the UV+MP samples showed only a 1.13 fold increase in p21. When comparing with the UV sample, the UV+MP sample has 50.4% less p21 expression. Less p21 expression in the UV+MP sample compare with the UV sample suggested that less DNA damage occurred in the sample that was treated with milk phospholipids. This result strongly suggests that 1% bovine milk phospholipids can protect skin cells from UV induced DNA damage.

Ultraviolet (UV) radiation has been demonstrated in numerous studies to be a major risk factor for non-melanoma skin cancer development. Despite the emergence of current UV-preventative strategies, such as sunscreens and skin-protective clothing, the incidence of non-melanoma skin cancer has continued to rise. This has encouraged investigations on alternative methods for UV prevention. In particular, bovine milk sphingomyelin has been studied for its potential in protecting human skin against UV photodamage. While the previous studies have suggested that sphingomyelin exhibits UV-protective properties in a human skin equivalent model, the exact mechanisms behind sphingomyelin’s photoprotective effects are yet unknown. This thesis aims to further investigate the UV-protective effects of sphingomyelin in normal human epidermal keratinocytes, using nuclear p21 expression as a marker for UV photodamage. Keratinocytes were incubated for 24 hours in a 0.1% sphingomyelin solution and then exposed to 40mJ/cm2 of 302nm UV radiation. After 24 hours of post-UV incubation, nuclear p21 expression was evaluated using immunofluorescence. Confocal images were analyzed for their mean nuclear p21 fluorescence intensity measured in grayscale (0-255). Keratinocytes treated with sphingomyelin showed approximately a 50% decrease in UV-induced mean nuclear p21 intensity compared to keratinocytes with no sphingomyelin treatment (via Tukey’s test; p

No description available.

Malignant melanoma is an invasive type of skin cancer with high mortality rates, if not detected promptly. The mortality trends are generally linked to multiple dysplastic nevi, positive family history, genetic susceptibility and phenotypic features including fair skin, freckles, numerous atypical nevi, light coloured hair and eyes, inability to tan and prolonged exposure to ultraviolet radiation B (UVB). To date, the major anti-cancer therapeutics for melanoma include surgery, chemotherapy, radiotherapy, and immunotherapy. Recently, extracellular vesicles, especially exosomes, have been highlighted for their therapeutic benefits in numerous chronic diseases such as cancer. Exosomes display multifunctional properties, including inhibition of cancer cell proliferation and initiation of apoptosis. Hence, this study aimed to evaluate the genotoxicity and cytotoxicity of cord blood stem cell-derived (CBSC) exosomes on 6 samples of peripheral blood lymphocytes taken from healthy individuals and melanoma patients and on 3 samples of melanoma (CHL-1) cells. The limited number of samples was due to the time limitations and restrictions that were in place due to the COVID-19 pandemic. In this in vitro study, the optimal concentration of CBSC-derived exosomes (0, 100, 200, 300, 400 μg/ml protein at 24, 48 and 72h treatments) was confirmed by the CCK-8 assay. CBSC exosomes (300 μg/ml) were used to treat lymphocytes and CHL-1 cells in the Comet assay and evaluated using the real-time polymerase chain reaction (qPCR) and Western blotting (WB). The data of the CCK-8 and Comet assays illustrated that exosomes exerted genotoxic effects on CHL-1 cells (CCK-8 assay, ****p < 0.0001), (Comet assay, *p <0.05, **p < 0.01). However, the data portraying a reduction in the viability of lymphocytes needs further investigation as the number of samples was limited, therefore, further clarification is required. Importantly, no significant adverse effect was observed in healthy lymphocytes when treated with the same exosomes (p = ns). When further challenged with UVA+B radiation, the exosomes did not induce any genoprotective effect on ROS-induced CHL-1 cells, compared to the positive control (p = ns). Our data insinuates that the damage might be caused by inducing apoptosis. The anti-tumourigenic potential of exosomes was observed by activating the p53-mediated apoptotic pathway in CHL-1 cells, up-regulating p53, p21 and caspase 3 and down-regulating BCL-2 at mRNA (**p < 0.01, ***p <0.001, ****p <0.0001) and protein levels (*p < 0.05, **p <0.01). The potency of CBSC exosomes in inhibiting cancer progression in CHL-1 cells whilst causing no harm to the healthy lymphocytes makes it an ideal potential candidate for anti-cancer therapy. More samples are required to evaluate the therapeutic effect of exosomes on lymphocytes from cancer patients to fully understand their mechanism of action.

No description available.