Introduction: Seborrheic dermatitis (SD) is a chronic, relapsing, inflammatory disorder of the head and trunk.
Objectives: To explore the potential of a 1% Selenium disulphide (SeS2)-based shampoo to prevent relapses of scalp SD (SSD) following corticosteroid/salicylic acid (TCS/SA) treatment.
Materials & Methods: After a 2-week treatment with TCS/SA, adult patients with moderate-to-severe SSD received either the SeS2-based shampoo or its vehicle for eight weeks in a randomized, double-blinded fashion.
To study cutaneous pigmentation in a physiological context, we have previously developed a functional pigmented reconstructed skin model composed of a melanocyte-containing epidermis grown on a dermal equivalent comprising living fibroblasts. The present studies, using the same model, aimed to demonstrate that dermal fibroblasts influence skin pigmentation up to the macroscopic level. The proof of principle was performed with pigmented skins differing only in the fibroblast component.
View Article and Find Full Text PDFTo study human skin pigmentation in a physiological in vitro model, we developed a pigmented reconstructed skin reproducing the three-dimensional architecture of the melanocyte environment and the interactions of melanocyte with its cellular partners, keratinocytes, and fibroblasts. Co-seeding melanocytes and keratinocytes onto a fibroblast-populated collagen matrix led to a correct integration of melanocytes within the epidermal basal layer, but melanocytes remained amelanotic even after supplementation with promelanogenic factors. Interestingly, normalization of keratinocyte differentiation using keratinocyte growth factor instead of epidermal growth factor finally allowed an active pigmentary system to develop, as shown by the expression of key melanogenic markers, the production, and transfer of melanosome-containing melanin into keratinocytes.
View Article and Find Full Text PDFXeroderma pigmentosum (XP) is a devastating disease associated with dramatic skin cancer proneness. XP cells are deficient in nucleotide excision repair (NER) of bulky DNA adducts including ultraviolet (UV)-induced mutagenic lesions. Approaches of corrective gene transfer in NER-deficient keratinocyte stem cells hold great hope for the long-term treatment of XP patients.
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