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• W4243662040 abstract "UVB is the proximal excitor of the epidermal hyperpigmentation of the common solar lentigo (aka senile lentigo). Now stem cell factor and the c-kit receptor, the same pathway responsible for the hyperpigmentation in urticaria pigmentosa, are implicated in the lentigo-like pigmentation of the age spot, as is the endothelian B receptor as reported by Imokawa and colleagues. Understanding the intimate details of signaling in these common lesions could lead to novel therapeutic approaches for their reversal or prevention. J Invest Dermatol 122:1256–1265, 2004. Epidermal lamellar granules act as cargo containers filled with a variety of natural products destined for export to the intercellular space of the stratum corneum. Enzymes, lipids, and structural proteins are some of these natural products. Cathepsin D and kallikrein are two of the latest examples of material being exported, as reported by Ishida-Yamamoto and coworkers. Will it be long before this carrier system is hijacked and used for the delivery of synthetic antimicrobial agents, replacement lipids for the stratum corneum, and similar agents to repair or alter epidermal function? J Invest Dermatol 122: 1137–1144, 2004. Defects in connexins, the membrane protein of gap junctions, are associated with similar but distinct diseases including erythrokeratoderma variabilis, keratosis palmaris/plantaris, Vohwinkel disease, and KID syndrome. KID syndrome is usually due to mutations in the Cx26 gene, GJB2; and Cx30, the GJD6 gene, is associated with hidrotic ectodermal dysplasia. Now a mutation in Cx30 is associated with KID syndrome. Heterogeneity is an underlying feature in many genetic diseases; patients like the one described by Jan and colleagues will be valuable in constructing the detailed pathophysiology of the associated disorders. J Invest Dermatol 122:1108–1113, 2004. Living in the cytoplasm is the predominantly maternally-derived mitochondrial genome that is often spoken of as being derived from Eve. Genetic disorders of energy and muscle metabolism are carried in the mitochondrial genome. UVA exposure of human skin causes a large deletion (the “common deletion”), as reported by Burneberg and coworkers. This distinctive deletion may be a useful biomarker for UVA exposure since it would persist in daughter cells after epidermal division and would be important in epidemiological studies to determine the amount of sunlight exposure. J Invest Dermatol 122:1277–1283, 2004. Removal of the stratum corneum by stripping with cellophane tape is a classic method of altering keratinocyte division and differentiation. With stripping there may be inflammation, and in a mouse model the Langerhans cells (LC) begin to migrate and immigrate into the epidermis. The authors studied changes in LC during migration and found 500 times more LC in the stripped epidermis. The integration of epidermal cells and probably their interactions with other cells living in the tissue is suggested by the results of Holzmann et al. Treatments that seem to be “specific” for one cell type must be carefully evaluated to avoid false interpretations, since the cells live in a rich soup of cytokines and growth factors. J Invest Dermatol 122:1165–1174, 2004. Persistent hyperpigmentation complicates many skin disorders, especially in individuals with Fitzpatrick type V and VI skin. Scott and colleagues report that prostaglandins increase melanosome uptake by the keratinocyte and increase melanocyte dendricity, indicating prostaglandins in the process of hyperpigmentation. Drugs for altering prostaglandins are under intensive study in many physiological systems and may lead to agents to prevent or decrease hyperpigmentation. J Invest Dermatol 122:1214–1224, 2004." @default.
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• W4243662040 date "2004-05-01" @default.
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• W4243662040 title "Clinical Snippets" @default.
• W4243662040 doi "https://doi.org/10.1111/j.1523-1747.2004.22536.x" @default.
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