Coronavirus disease 2019 (COVID-19) has led dermatology practices to severely limit in-person appointments due to social distancing and shelter-in-place measures.1 Even as infection rates fall and practices reopen, epidemiologic modeling predicts future resurgences of COVID-19, likely compelling practices to intermittently restrict in-person appointments again.2 Principles of scarce health care resource distribution have been applied during the COVID-19 pandemic, commonly for critical care resources.3 , 4 However, these principles have not been modified for or applied to limited in-person dermatology appointments during the pandemic. Guiding principles can inform dermatologists about how to prioritize patients and skin diseases in this context.

Lesions with driver mutations, including atypical nevi and seborrheic keratoses, are very common in dermatology, and are prone to senescence. The molecular events that prevent senescent lesions from becoming malignant are not well understood. We have developed a model of vascular proliferation using a temperature-sensitive, large T antigen and oncogenic HRas. By elevating the temperature to 39 °C, we can turn off large T antigen and study the molecular events in cells with the Ras driver mutation. To assess the signaling events associated with the switch from a proliferative to a nonproliferative state in the constant presence of a driver oncogene, SVR cells were cultivated for 24 and 48 hours and compared with SVR cells at 37 °C. Cells were evaluated by Western Blot (WB) gene chip microarray (GC) and quantitative reverse transcription polymerase chain reaction (RT-qPCR). Upon evaluation, a novel phenotype was observed in endothelial cells after switching off the large T antigen. This phenotype was characterized by Notch activation, downregulation of p38 phosphorylation, downregulation of the master immune switch IRF7, and downregulation of hnRNP A0. Switching off proliferative signaling may result in immune privilege and Notch activation, which may account, in part, for the survival of common skin lesions.

Exposing wet hair to high temperatures can create gas bubbles within the hair shaft, leading to brittle, dry hairs in a disorder known as bubble hair abnormality. We present a case of a 61-year-old woman who presented for hair breakage over her crown. She regularly dried her damp hair with a blow dryer. Dermoscopy revealed multiple bubbles within the hair shaft, and diagnosis of bubble hair abnormality was confirmed by light microscopy. Our unusual case highlights the ease of acquisition of this abnormality by means of a common hair dryer, and the utility of dermoscopy to make a fast and accurate diagnosis within the office.

Hemangiomas are the most common type of tumor in infants. As they are endothelial cell–derived neoplasias, their growth can be regulated by the autocrine-acting Tie2 ligand angiopoietin 2 (Ang2). Using an experimental model of human hemangiomas, in which polyoma middle T–transformed brain endothelial (bEnd) cells are grafted subcutaneously into nude mice, we compared hemangioma growth originating from bEnd cells derived from wild-type, Ang2+/–, and Ang2–/– mice. Surprisingly, Ang2-deficient bEnd cells formed endothelial tumors that grew rapidly and were devoid of the typical cavernous architecture of slow-growing Ang2-expressing hemangiomas, while Ang2+/– cells were greatly impaired in their in vivo growth. Gene array analysis identified a strong downregulation of NADPH oxidase 4 (Nox4) in Ang2+/– cells. Correspondingly, lentiviral silencing of Nox4 in an Ang2-sufficient bEnd cell line decreased Ang2 mRNA levels and greatly impaired hemangioma growth in vivo. Using a structure-based approach, we identified fulvenes as what we believe to be a novel class of Nox inhibitors. We therefore produced and began the initial characterization of fulvenes as potential Nox inhibitors, finding that fulvene-5 efficiently inhibited Nox activity in vitro and potently inhibited hemangioma growth in vivo. In conclusion, the present study establishes Nox4 as a critical regulator of hemangioma growth and identifies fulvenes as a potential class of candidate inhibitor to therapeutically interfere with Nox function.

The authors wish to make the following corrections to this paper [1]: The following words in bold face are to be added: In Section 2.1 "Cells", lines 3 and 4: 1% complex of antibiotics/L-glutamine (stock = 10,000 IU/mL penicillin, 10,000 µg/mL streptomycin, and 29.2 mg/mL L-glutamine; Mediatech Inc., Manassas, VA, USA); in Section 2.4 "Western Blot (WB)", lines 5 and 7: "tri-buffered saline" should be changed to "Tris-buffered saline" on both lines.

The ongoing COVID-19 pandemic has necessitated mask wearing in public settings. Ubiquitous mask wearing has been associated with an increase in the incidences of multiple dermatologic conditions, such as frictional or irritant dermatitis, contact dermatitis, and “maskne.”1 In addition to these associated pathologies, mask wearing may produce significant mechanical or frictional stress on facial hair shafts. Physical trauma to the hair shaft is associated with trichorrhexis nodosa (TN)—a condition characterized by focal hair splaying and breakage at weakened points in the hair shaft. The following case report describes acquired TN of the beard associated with mask wearing.