Use of the multi-theory model (MTM) in explaining initiation and sustenance of indoor tanning cessation among college students.

Skin cancer, including melanoma, is the most common cancer worldwide and a significant public health concern. A significant risk factor for melanoma is through increased exposure to ultraviolet (UV) radiation through the use of indoor tanning beds. Although rates of indoor tanning bed use have decreased in recent years, young adults, particularly White, college-age women, comprise the majority of indoor tanning bed users in the United States. The purpose of this cross-sectional study was to explore and explain the initiation and sustenance of indoor tanning cessation among college students using the multi-theory model (MTM) of health behavior change. Data were collected from 254 college students who reported current indoor tanning use using a validated 46-item survey to assess demographics and the MTM constructs. Data were analyzed using multiple linear regression to determine the ability of the MTM constructs to predict the initiation and sustenance of indoor tanning cessation. For initiation of indoor tanning cessation, participatory dialogue: advantages (B = 0.038, p = 0.001), behavioral confidence (B = 0.129, p < 0.001) and changes in the physical environment (B = 0.088, p < 0.001) were significantly associated with indoor tanning cessation following covariate adjustment. For sustenance, only emotional transformation (B = 0.140, p < 0.001) demonstrated a significant relationship with indoor tanning cessation, following adjustment. Findings from this study demonstrate the utility of the MTM in explaining indoor tanning cessation and designing intervention strategies and clinical recommendations to encourage indoor tanning cessation among college students.

Deletion of the Stress Response Gene DDR48 from Histoplasma capsulatum Increases Sensitivity to Oxidative Stress, Increases Susceptibility to Antifungals, and Decreases Fitness in Macrophages.

The stress response gene DDR48 has been characterized in Saccharomyces cerevisiae and Candida albicans to be involved in combating various cellular stressors, from oxidative agents to antifungal compounds. Surprisingly, the biological function of DDR48 has yet to be identified, though it is likely an important part of the stress response. To gain insight into its function, we characterized DDR48 in the dimorphic fungal pathogen Histoplasma capsulatum. Transcriptional analyses showed preferential expression of DDR48 in the mycelial phase. Induction of DDR48 in Histoplasma yeasts developed after treatment with various cellular stress compounds. We generated a ddr48∆ deletion mutant to further characterize DDR48 function. Loss of DDR48 alters the transcriptional profile of the oxidative stress response and membrane synthesis pathways. Treatment with ROS or antifungal compounds reduced survival of ddr48∆ yeasts compared to controls, consistent with an aberrant cellular stress response. In addition, we infected RAW 264.7 macrophages with DDR48-expressing and ddr48∆ yeasts and observed a 50% decrease in recovery of ddr48∆ yeasts compared to wild-type yeasts. Loss of DDR48 function results in numerous negative effects in Histoplasma yeasts, highlighting its role as a key player in the global sensing and response to cellular stress by fungi.

The Impact of Diabetic Conditions and AGE/RAGE Signaling on Cardiac Fibroblast Migration.

Diabetic individuals have an increased risk for developing cardiovascular disease due to stiffening of the left ventricle (LV), which is thought to occur, in part, by increased AGE/RAGE signaling inducing fibroblast differentiation. Advanced glycated end-products (AGEs) accumulate within the body over time, and under hyperglycemic conditions, the formation and accumulation of AGEs is accelerated. AGEs exert their effect by binding to their receptor (RAGE) and can induce myofibroblast differentiation, leading to increased cell migration. Previous studies have focused on fibroblast migration during wound healing, in which diabetics have impaired fibroblast migration compared to healthy individuals. However, the impact of diabetic conditions as well as AGE/RAGE signaling has not been extensively studied in cardiac fibroblasts. Therefore, the goal of this study was to determine how the AGE/RAGE signaling pathway impacts cell migration in non-diabetic and diabetic cardiac fibroblasts. Cardiac fibroblasts were isolated from non-diabetic and diabetic mice with and without functional RAGE and used to perform a migration assay. Cardiac fibroblasts were plated on plastic, non-diabetic, or diabetic collagen, and when confluency was reached, a line of migration was generated by scratching the plate and followed by treatment with pharmacological agents that modify AGE/RAGE signaling. Modification of the AGE/RAGE signaling cascade was done with ERK1/2 and PKC-ζ inhibitors as well as treatment with exogenous AGEs. Diabetic fibroblasts displayed an increase in migration compared to non-diabetic fibroblasts whereas inhibiting the AGE/RAGE signaling pathway resulted in a significant increase in migration. The results indicate that the AGE/RAGE signaling cascade causes a decrease in cardiac fibroblast migration and altering the pathway will produce alterations in cardiac fibroblast migration.