PubMed · 13892919
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
G H FINDLAY. 1962. Epidermal phosphate.. https://doi.org/10.1111/j.1365-2133.1962.tb13503.x
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Our understanding of the formation, structure, composition, and maturation of the stratum corneum (SC) has progressed enormously over the past 30 years. Today, there is a growing realization that this structure, while faithfully providing a truly magnificent barrier to water loss, is a unique, intricate biosensor that responds to environmental challenges and surface trauma by initiating a series of biologic processes which rapidly seek to repair the damage and restore barrier homeostasis. The detailed ultrastructural, biochemical, and molecular dissection of the classic "bricks and mortar" model of the SC has provided insights into the basis of dry, scaly skin disorders that range from the cosmetic problems of winter xerosis to severe conditions such as psoriasis. With this knowledge comes the promise of increasingly functional topical therapies.
Over the past decade, great progress has been made toward elucidating the structure and function of the stratum corneum (SC), the outermost layer of the epidermis. SC cells (corneocytes) protect against desiccation and environmental challenge by regulating water flux and retention. Maintenance of an optimal level of hydration by the SC is largely dependent on several factors. First, intercellular lamellar lipids, organized predominantly in an orthorhombic gel phase, provide an effective barrier to the passage of water through the tissue. Secondly, the diffusion path length also retards water loss, since water must traverse the tortuous path created by the SC layers and corneocyte envelopes. Thirdly, and equally important, is natural moisturizing factor (NMF), a complex mixture of low-molecular-weight, water-soluble compounds first formed within the corneocytes by degradation of the histidine-rich protein known as filaggrin. Each maturation step leading to the formation of an effective moisture barrier--including corneocyte strengthening, lipid processing, and NMF generation--is influenced by the level of SC hydration. These processes, as well as the final step of corneodesmolysis that mediates exfoliation, are often disturbed upon environmental challenge, resulting in dry, flaky skin conditions. The present paper reviews our current understanding of the biology of the SC, particularly its homeostatic mechanisms of hydration.
Generalized pustular psoriasis (GPP) is a serious dermatological disease characterized by fever, chills, rigors, and generalized pustule formation on the skin. Previous analyses in Japan have led to the proposal to divide GPP into two groups, one with a history of ordinary psoriasis (pso(+) GPP) and the other without a history of psoriasis (pso(-) GPP). Clinically the onset of the pustular outbreak is earlier in pso(-) GPP, which occurs more frequently after infections, whereas pso(+) GPP occurs more frequently following corticosteroid therapy. Substantial differences are also noted in HLA analyses. Activation of neutrophils is a basic mechanism in both types of GPP. Although the epidermal structural changes in GPP are usually not so prominent as those in psoriasis vulgaris, pso(+) GPP shows a more psoriasiform architecture than pso(-) GPP. Analysis of epidermal cell proliferation in GPP indicates that it is not less than that seen in psoriasis vulgaris. The occasional psoriasiform epidermal architecture especially seen in pso(+) GPP may be considered to be a steady-state condition achieved after epidermal cell proliferation has continued for a sustained period. Various inflammatory cytokines appear to be involved in the neutrophilic infiltrate seen in GPP.