These data represent the first reported evidence of increased plasma levels of NGF and SP in an allergic human skin disease. They suggest that these neurogenic factors systemically modulate the allergic response in AD, probably through interactions with cells of the immune-inflammatory component. In addition, NGF and SP may be useful markers of disease activity in patients with AD.

Acne is a complex, chronic and common skin disorder of pilosebaceous units. Although it is known that exacerbation of acne results from emotional stress, the nature of the association between stress and acne remains unclear. This is due in part to the lack of substantial evidence regarding the participation of cutaneous neurogenic factors in the pathogenesis of acne. To examine the possible involvement of neurogenic factors in the etiology of acne, we used immunohistochemistry to compare the distribution of SP-containing nerve fibers around sebaceous glands and the expression of neutral endopeptidase in sebaceous acini of the facial skin of acne patients and of healthy subjects. More numerous substance P immunoreactive nerve fibers in close apposition to the sebaceous glands and an increase in expression of neutral endopeptidase in sebaceous acini were observed in acne patients compared with the controls. Immunoelectron microscopy revealed that the subcellular localization of neutral endopeptidase was restricted to the Golgi apparatus and the endoplasmic reticulum within sebaceous germinative cells. In addition, in vitro experiments using an organ culture system demonstrated that substance P induced expression of neutral endopeptidase in sebaceous glands in a dose dependent manner. This study reveals that substance P and its degrading enzymes are involved in the pathogenesis of acne, which in turn might partially explain the pathologic significance of neurogenic and psychogenic aspects in the disease process.

These results indicate that the intensity of COX-2 staining and its heterogeneous distribution are related to the degree of cellular differentiation and the various phenotypes of tumor cells, but the extent of COX-2 staining did not correlate with the degree of malignancy.

These findings suggest that SP is endogenously released by dermal nerve fibres around hair follicles and that it may play an important part in epithelial-mesenchymal-neuroectodermal interactions in AA. This study reveals that SP and its degrading enzymes are involved in the pathogenesis of AA, which in turn might explain the pathological significance of neurogenic and psychogenic aspects in the disease process.

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We examined the possible correlation between biotypes of Propionibacterium acnes, lipase activity, and rash degree in acne patients. Among 5 P. acnes biotypes, P. acnes biotype 3 (B3) was the most common, followed by P. acnes biotypes 1, 2 and 4; P. acnes biotype 5 was not found. P. acnes B3 was isolated from more severe skin rashes than those of the other biotypes. Production of propionic acid (PA) and butyric acid (BA) by P. acnes B3 was higher than those by the other P. acnes biotypes. As the rash degree in acne patients was more severe, the production of PA and BA elevated. Although only a few P. acnes strains were examined in the present study, P. acnes B3 had the highest lipase activity and might have the greatest influence on skin rash in acne patients.

The increase in total number of hairs in a designated scalp area of the procyanidin group subjects after the 6-month trial was significantly greater than that of the placebo control group subjects (procyanidin, 3.3 +/- 13.0 (mean +/- SD)/0.50 cm(2); placebo, -3.6 +/- 8.1/0.50 cm(2); P < 0.001, two-sample t-test). Time course-dependent improvement in hair density was observed in the procyanidin subjects. No adverse side effects were observed in any of the subjects. Procyanidin therapy thus shows potential hair-growing activity.

Phytol is a branched, long-chain aliphatic alcohol which has various biological effects. In this study, we examined phytol as a tumor promoter in a mouse skin initiation-promotion model, and compared its promotion activity with that of 12-O-tetradecanoyl phorbol-13-acetate (TPA). Female ICR mice, 7 weeks of age, were initiated with 100 µ µ µ µg of 7,12-dimethylbenz(a)anthracene, and were then topically promoted twice a week for 16 weeks with 100 mg of phytol or with 2.5 µ µ µ µg of TPA.In this model 95% of animals treated with phytol developed skin tumors within 16 weeks. The average number of lesions per mouse treated with phytol was significantly lower than that in mice treated with TPA, and this significant difference continued up to 16 weeks after the end of promotion treatment. Characterization of hyperplasia 48 h after topical application of agents showed that epidermal thickness and vertical thickness following topical application of phytol were significantly increased compared with vehicle controls, but were significantly smaller than in animals treated with TPA. Ornithine decarboxylase (ODC) activity following topical application of phytol was increased in a dose-dependent manner and showed a weak, delayed induction (which was maximal 11-12 h after treatment) as compared with the case of TPA. The specific binding of [ 3 H]phorbol-12,13-dibutyrate (PDBU) by JB6 cells was not inhibited by phytol at concentrations up to 1 mM. These results indicate that phytol has a weak tumor promoter activity compared to TPA and is a non-TPA-type tumor promoter in this model of mouse skin carcinogenesis. Key words:Phytol -Non-TPA-type tumor promoter -Two-stage mouse skin carcinogenesisOrnithine decarboxylase -Radioligand assay Mouse skin tumorigenesis can be divided into distinct stages of tumor initiation and promotion. According to carcinogenesis experiments, tumor development on mouse skin can be provoked by topical application of an initiator, such as the polycyclic aromatic hydrocarbon 7,12-dimethylbenz(a)anthracene (DMBA), followed by repeated treatment with a tumor promoter.1, 2) Our current understanding of responses to skin tumor promoters has been derived primarily from studies with 12-O-tetradecanoylphorbol-13-acetate (TPA), which affects basal cells but not differentiating cells in mouse epidermis.3) While TPA is the strongest and most widely studied skin tumor promoter, other chemical compounds are known to possess tumorpromoting properties in mouse skin. There have been many reports which have described TPA-type promoters, such as Roussin red methyl ester, 4) and teleocidin, 5) and non-TPA-type promoters, such as okadaic acid, 6) thapsigargin, 7,8) and mirex. 9)Phytol (3,7,11,15-tetramethyl-2-hexadecen-1-ol), the fatty acid side chain of tocopherol, is a branched, longchain aliphatic alcohol contained in large quantities in plants and is a component of chlorophyll. In recent extensive studies, various cellular and biological effects of phytol have been demonstrated, such as its action as an agonist in hypox...