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n hexadecane/hyperplasia

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StraipsniaiKlinikiniai tyrimaiPatentai
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Inhibition of n-hexadecane-induced epidermal hyperplasia due to systemically administered ciclosporin.

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Epidermal hyperplasia was induced in hairless mice (hr/hr) by topical n-hexadecane treatment of tail and back skin. Following this skin irritation, a granular layer developed in interfollicular regions of the tail epidermis. An increase of ornithine decarboxylase activity, of thymidine triphosphate

Changes in sodium-potassium ratio in guinea pig epidermis in n-hexadecane-induced hyperplasia.

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A transient epidermal hyperplasia was induced in guinea pig epidermis by a single application of n-hexadecane. The epidermal response was analysed by light microscopy and by energy dispersive X-ray microanalysis (EDX). The epidermal hyperplasia reached a maximum between 96 and 192 h after the

Cytofluorometric study of nuclear DNA in experimentally induced epidermal hyperplasia.

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The rate of cell proliferation in the basal cell layer by epidermal hyperplasia of guinea pig ear was investigated with cytofluorometric method. Epidermal hyperplasia was caused by tape stripping or the application of n-hexadecane or retinoic acid. In non-treated epidermis, the mean of the relative
Sequential changes in skin metabolism have been studied in a model system of epidermal hyperplasia and hyperkeratinization induced by the application of n-hexadecane to shaved rat skin. The epidermal accumulation of glycogen typical of the hyperplastic response has been correlated with an increase
Several biochemical parameters including ornithine decarboxylase activity (ODC) and tissue polyamine levels were measured during the hexadecane-induced epidermal hyperplasia of hairless rat skin. Animals received three applications of 200 microliters pure n-hexadecane on day 1. ODC activity and
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