To identify itch-related mediators and receptors that are differentially expressed in pruritic skin, we used RNA sequencing to analyze the complete transcriptome in skin from paired itchy, lesional and nonitchy, nonlesional skin biopsies from 25 patients with atopic dermatitis and 25 patients with psoriasis and site-matched biopsies from 30 healthy controls. This analysis identified 18,000 differentially expressed genes common between itchy atopic and psoriatic skin compared with healthy skin. Of those, almost 2,000 genes were differentially expressed between itchy and nonitchy skin in atopic and psoriatic subjects. Overexpression of several genes, such as phospholipase A2 IVD, substance P, voltage-gated sodium channel 1.7, and transient receptor potential (TRP) vanilloid 1, in itchy skin was positively correlated with itch intensity ratings in both atopic dermatitis and psoriasis. Cytokines such as IL-17A, IL-23A, and IL-31 had elevated gene transcript levels in both itchy atopic and psoriatic skin. However, expression of genes for TRP vanilloid 2, TRP ankyrin 1, protease-activated receptor 2, protease-activated receptor 4, and IL-10 was found to be increased only in pruritic atopic skin, whereas expression of genes for TRP melastatin 8, TRP vanilloid 3, phospholipase C, and IL-36α/γ was elevated only in pruritic psoriatic skin. This "itchscriptome" analysis will lead to an increased understanding of the molecular mechanisms of chronic pruritus and provide targets for itch treatment irrespective of disease state.

Highlights d Ribosomal profiling of AD vulnerable/resistant neurons in 5-, 12-, 24-month old mice d Using human neuron-type functional networks and GWASs to model vulnerability d Identification of axon plasticity genes linking Aß, aging, tau in vulnerable neurons d PTB, regulator of tau exon 10 splicing, might contribute to selective vulnerability

BACKGROUND Medical spas have experienced a recent rise in popularity. However, rules and regulations vary nationwide. Given the number of complications attributable to medical spas, questions remain about currently regulatory practices and whether they are sufficient to protect patients from harm. OBJECTIVE Our study investigated the current state of medical spas and their associated patient complications in the aesthetic field as well as the experiences and attitudes of practitioners. MATERIALS AND METHODS A survey was distributed to current members of the American Society for Dermatologic Surgery. RESULTS Of all cosmetic complications encountered in the past 2 years, the majority reported that the percentage of complications seen in their practice attributable to medical spas ranged from 61% to 100%. The most commonly cited complications from medical spas were burn, discoloration, and misplacement of product, whereas the most commonly cited treatments resulting in complications were fillers, intense pulsed light, and laser hair removal. For safety and outcomes, medical spas were rated as inferior to physician-based practices. CONCLUSION Patient complications associated with medical spas are not uncommon. Overall, practitioners believe medical spas are endangering to patient safety, think that stricter rules and regulations are necessary, and request more support from the specialty medical societies.

We speculate that psychological stress increases spontaneous scratching in patients with AD, which may enhance the vicious cycle of itching and scratching, resulting in aggravation of the skin eczema. These results provide new insights on the mechanism of acute stress-related exacerbation of itch in patients with AD.

A major obstacle to treating Alzheimer's disease (AD) is our lack of understanding of the molecular mechanisms underlying selective neuronal vulnerability, which is a key characteristic of the disease. Here we present a framework to integrate highquality neuron-type specific molecular profiles across the lifetime of the healthy mouse, which we generated using bacTRAP, with postmortem human functional genomics and quantitative genetics data. We demonstrate human-mouse conservation of cellular taxonomy at the molecular level for AD vulnerable and resistant neurons, identify specific genes and pathways associated with AD pathology, and pinpoint a specific functional gene module underlying selective vulnerability, enriched in processes associated with axonal remodeling, and affected by both amyloid accumulation and aging. Overall, our study provides a molecular framework for understanding the complex interplay between Aβ, aging, and neurodegeneration within the most vulnerable neurons in AD.