The Use of the Video, "Dear 16-Year-Old Me," as a Melanoma Education Tool in Ambulatory Dermatology.

BACKGROUND: Skin cancer continues to be the most common cancer in the United States. The rise of social media platforms and internet use offers an opportunity to present health information through video-based education. The video "Dear 16-Year-OldMe," addresses the risks associated with tanning and sun exposure, the importance of practicing sun protection, and shares stories from melanoma survivors. OBJECTIVE: To evaluate the video "Dear 16-Year-Old Me," as a patient education tool in dermatology clinics and to investigate whether viewing a short educational video can change knowledge about skin cancer risks and intention to improve skin cancer prevention behavior. PATIENTS AND METHODS/MATERIALS AND METHODS/METHODS: English-speaking clinic patients between the ages of 14 to 45 years old were recruited. Exclusion criteria include both a personal or family history of skin cancer, dysplastic nevi, or other medical comorbidities. Forty-five participants agreed to participate; 38 were eligible for analysis. RESULTS: Comparison of prevideo and postvideo responses demonstrated a statistically significant reduction in participants reporting they were likely to tan outdoors (p-value = .001). A significant increase was observed in the reported likelihood to have a professional skin examination (p-value < .001) or self-examination (p-value < .001) in the future. CONCLUSION: and Relevance: Viewing "Dear 16-Year-Old Me," resulted in reported participant changes in intention to tan outdoors and participate in skin surveillance. Although these are encouraging results, future studies with a comparison group are needed to elucidate whether these results correspond to changes in behavior. In the age of viral videos and readily accessible health information via the internet, continued investigation of video media on patient health behaviors should be pursued.

Cutaneous Granular Cell Tumors in Children: Case Series and Review of the Literature.

Granular cell tumors (GCTs) are uncommon benign neoplasms thought to originate from Schwann cells. They most commonly present in adults as papules or nodules on mucosal sites. The clinical spectrum of GCT in children is not well delineated, although mucosal and cutaneous presentations have been reported. We present three children with cutaneous GCTs and review the literature in an attempt to further characterize this rare pediatric neoplasm.

Evidence that meningeal mast cells can worsen stroke pathology in mice.

Stroke is the leading cause of adult disability and the fourth most common cause of death in the United States. Inflammation is thought to play an important role in stroke pathology, but the factors that promote inflammation in this setting remain to be fully defined. An understudied but important factor is the role of meningeal-located immune cells in modulating brain pathology. Although different immune cells traffic through meningeal vessels en route to the brain, mature mast cells do not circulate but are resident in the meninges. With the use of genetic and cell transfer approaches in mice, we identified evidence that meningeal mast cells can importantly contribute to the key features of stroke pathology, including infiltration of granulocytes and activated macrophages, brain swelling, and infarct size. We also obtained evidence that two mast cell-derived products, interleukin-6 and, to a lesser extent, chemokine (C-C motif) ligand 7, can contribute to stroke pathology. These findings indicate a novel role for mast cells in the meninges, the membranes that envelop the brain, as potential gatekeepers for modulating brain inflammation and pathology after stroke.

ALK5-dependent TGF-ß signaling is a major determinant of late-stage adult neurogenesis.

The transforming growth factor-ß (TGF-ß) signaling pathway serves critical functions in CNS development, but, apart from its proposed neuroprotective actions, its physiological role in the adult brain is unclear. We observed a prominent activation of TGF-ß signaling in the adult dentate gyrus and expression of downstream Smad proteins in this neurogenic zone. Consistent with a function of TGF-ß signaling in adult neurogenesis, genetic deletion of the TGF-ß receptor ALK5 reduced the number, migration and dendritic arborization of newborn neurons. Conversely, constitutive activation of neuronal ALK5 in forebrain caused a marked increase in these aspects of neurogenesis and was associated with higher expression of c-Fos in newborn neurons and with stronger memory function. Our findings describe an unexpected role for ALK5-dependent TGF-ß signaling as a regulator of the late stages of adult hippocampal neurogenesis, which may have implications for changes in neurogenesis during aging and disease.