Due to the COVID-19 pandemic, planned medical and surgical activities are being postponed. For the dermatology community, this interruption to the healthcare system can lead to delays in the diagnosis and treatment of melanoma. Neglecting melanoma during this crisis can result in increased mortality, morbidity and healthcare costs. With the COVID-19 pandemic evolving and no clear solutions in sight, it is time for the prospective evaluation of teledermatology. However, dermatologists should be cautious and continue seeing patients with pigmented lesions in person due to the necessity of early surgical intervention.
ARTICLE HISTORY
Although the COVID-19 outbreak has decreased dermatology outpatient clinic visits, acne remains the most common condition among patients requesting an appointment. The widespread use of face masks may be a contributing factor to acne mechanica and folliculitis mechanica, where stopping the mechanical insult is essential to treatment. However, COVID-19 poses a unique challenge as mask wearing is crucial to limiting viral exposure. Although reported cases of mask-associated facial dermatoses are largely documented in healthcare workers, the general population is being affected by “maskne”. Pathogenesis and treatment options are discussed and the importance of counseling patients on proper skin hygiene is highlighted. As mask use increases, dermatologists should anticipate this trend in acne flare-ups.
Bisphenol A (BPA) leaches from plastics to contaminate foodstuffs. Analogs, such as bisphenol S (BPS), are now used increasingly in manufacturing. Greater BPA exposure has been correlated with exacerbation of cardiovascular disease, including myocardial infarction (MI). To test the hypothesis that bisphenol exposure impairs cardiac healing, we exposed C57bl/6n mice to water containing 25ng/ml BPA or BPS from conception and surgically induced an MI in adult male progeny. Increased early death and cardiac dilation, and reduced cardiac function were found post-MI in BPA- and BPS-exposed mice. Flow cytometry revealed increased monocyte and macrophage infiltration that correlated with increased chemokine C-C motif ligand-2 expression in the infarct. In vitro BPA and BPS addition increased matrix metalloproteinase-9 (MMP) protein and secreted activity in RAW264.7 macrophage cells suggesting that invivo increases in MMP2 and MMP9 in exposed infarcts were myeloid-derived. Bone marrow-derived monocytes isolated from exposed mice had greater expression of pro-inflammatory polarization markers when chemokine stimulated indicating an enhanced susceptibility to develop a pro-inflammatory monocyte population. Chronic BPA exposure of estrogen receptor beta (ERβ) deficient mice did not worsen early death, cardiac structure/function, or expression of myeloid markers after an MI. In contrast, BPS exposure of ERβ-deficient mice resulted in greater death and expression of myeloid markers. We conclude that lifelong exposure to BPA or BPS augmented the monocyte/macrophage inflammatory response and adverse remodeling from an MI thereby reducing the ability to survive and successfully recover, and that the adverse effect of BPA, but not BPS, is downstream of ERβ signaling.
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