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There has been increasing concern regarding the cosmetic aspects of skin in recent years. Computational simulation can be useful in understanding the mechanism underlying skin formation. The bottom of the epidermis is called the basal layer and is very undulation. In this study, we focus on the basal layer formation. We created a particle model, which forms an undulation basal layer and regenerates the basal layer formation by numerical simulation. At first, two-dimensional basal layer formation without epidermal turnover was simulated. The results showed film shape changes and the stability, as a layer in the process of long-time with an increase and decrease of basal cells. Next, the model was applied to three-dimensional basal layer formation with epidermal turnover. As the structure of the basal layer was deformed, the upper structure of the epidermis comprising the cells divided from the basal layer also became irregular. The simulation results accurately represented and reproduced the three-dimensional basal layer formation and epidermis turnover process., 2nd Conference on Advances in Prevention and Treatment of Cancer (CAPTC 2016), March 18-20, 2016, Los Angeles, USA

Skin is the largest organ of the human body. In recent years, concern regarding the cosmetics area has increased, and research studies on anti-aging therapy or cosmetics have been rapidly conducted. Skin cells are not only changing its shape but also its physical properties during the epidermal skin turnover process. Computational simulation can be useful in further understanding the mechanisms of skin formation. We propose a particle model that can handle complex biological phenomena, including cell interactions and is a suitable method for simulating skin formation. The particle model was applied to simulate three-dimensional skin formation accompanied by proliferation and cornification of skin cells. The simulation results represented and reproduced the epidermal skin turnover phenomenon.

For the first time, glycosidase (EC 3.2.2.) activity was applied to characterize and identify vegetables. To measure glycosidase activity in vegetables, 4-methylumbelliferyl (4MU) glycoside (Gly) was employed as the fluorescence enzyme substrate. By using either a cuvette-type or a 96-well micro-plate-type fluorescence reader, 7 kinds of glycosidase, including α- d -glucosidase (α-Glc-ase), β- d -glucosidase (β-Glc-ase), β- d -galactosidase (Gal-ase), α- d -mannnosidase (Man-ase), N-acetyl-β- d -glucosaminidase (GlcNAc-ase), β- d -glucuronidase (GA-ase) and β- d -xylosidase (Xyl-ase) were measured by incubating extracts of vegetables in the presence of 4MU-Gly at pH 6.0 for 60 min at 38 °C. After optimizing, both methods were applied to food matrices that included 10 different vegetables. Results of the application to both domestic and imported garlic ( Allium sativum ) and broccoli ( Brassica oleracea var. italica ), revealed that the glycosidase activities of Man-ase and GlcNAc-ase showed significant differences ( p n = 10) between domestic and imported varieties for both vegetables. Furthermore, the glycosidase activities in 30 heads of cabbage ( B. oleracea L. var. capitata ) itemized into 6 different cultivars were measured, and each profile was analyzed by employing a multivariate analysis. The results of their chemometric analyses showed that 29 out of 30 heads of cabbage were simultaneously and correctly discriminated into 6 different cultivars.

Hyperpigmentation of the skin is characterized by increases in melanin synthesis and deposition. Although considered a significant psychosocial distress, little is known about the detailed mechanisms of hyperpigmentation. Recently, the tumor suppressor protein p53 has been demonstrated to promote ultraviolet B-induced skin pigmentation by stimulating the transcription of a melanogenic cytokine, POMC (pro-opiomelanocortin), in keratinocytes. Given that p53 can be activated by various kinds of diverse stresses, including sun exposure, inflammation, and aging, this finding led us to examine the involvement of p53 in cytokine receptor signaling, which might result in skin hyperpigmentation. Immunohistochemical and reverse transcription-PCR analyses revealed the increased expression and phosphorylation of p53 in the epidermis of hyperpigmented spots, accompanied by the higher expression of melanogenic cytokines, including stem cell factor, endothelin-1, and POMC. The involvement of p53 in hyperpigmentation was also indicated by the significantly higher expression of p53 transcriptional targets in the epidermis of hyperpigmented spots. Treatment of human keratinocytes and melanocytes with known p53 activators or inhibitors, including pifithrin-alpha (PFT), demonstrated significant increases or decreases, respectively, in the expression of melanogenic factors, including cytokines and their receptors. Additionally, PFT administration abolished stem cell factor-induced phosphorylation of mitogen-activated protein kinase in human melanocytes. Furthermore, when organ-cultured hyperpigmented spots, in vitro human skin substitutes, and mouse skin were treated with PFT or p53 small interfering RNA, the expression of melanogenic cytokines and their receptors was significantly decreased, as were levels of tyrosinase and melanogenesis. Taken together, these data reveal the essential role of p53 in hyperpigmentation of the skin via the regulation of paracrine-cytokine signaling, both in keratinocytes and in melanocytes.

Electrophysiological studies (1-4) have shown that chlorpromazine acts on the several subcortical structures such as the brainstem reticular formation, hypothalamus and limbic system but does not appear to have significant effects on the cerebral cortex and thalamic relay nuclei. A reduction of the spontaneous unit activity by the drug has been reported in the reticular formation by Bradley (5) and Adey et al. (6), in the globus pallidus by Adey and Dunlop (7) and in the lateral hypothalamus by Zukauskas and Machine (8). However, information about effects of chlorpromazine on single neurons in the nuclear structures of the brainstem is still insufficient. We have studied the effects of morphine, aminopyrine and metoclopramide on the unit activities of single neurons in the subcortical areas (9-12), and have investigated the possible sites of action of these centrally affecting agents. The present experiment is an attempt to elucidate the mode of action of chlorpromazine upon the unit discharges in the Nucleus tractus solitarii, Nucleus vestibularis lateralis and Nucleus sensorius superior n. trigemini on the encephale isole preparations of cats.

Since lowering effects of essential fatty acids and vegetable oil on the blood cholesterol level were reported by Tuttle (1), Kinsell et al. (2) and Vles et al. (3), the similar studies were further extended to unsaturated fatty acids of longer chains. The lowering effects of pure linoleate and arachidonate on the elevated blood cholesterol level were presented by Kinsell et al. (2) and Kingsbury (4). However, the recent study by Beveridge and Connell (5) has shown that the large doses of margarine which contained large amounts of unsaturated fatty acids produced a slight elevation of the blood cholesterol level in humans. The histologically atherosclerotic or atheromatous changes of the tissues in rabbits caused by feeding with the diet containing between 1 and 3% of cholesterol for about 60 days were confirmed by many investigators including the present authors (6). In the present experiments attempts were made to observe the effects of mixing of linoleic acid ethylester in the high cholesterol diet on the atheromatous changes and to compare the difference in the effects of the mixings between the saturated and unsaturated fatty acids.

It is well-known that antiphlogistics such as salicylates and pyrazolon derivatives have the multiple effects on tissue metabolism. These metabolic effects including inhibition of corticosteroid biotransformation, uncoupling of oxidative phosphorylation, glycogenolysis, alteration of electrolyte balance and inhibition of mucopolysaccharide biosynthesis seem to merit attention in relation to their antiphlogistic activities (1-3). Tanabe and his co-workers (4, 5) have shown that a death caused by larger doses of phenylbutazone and 5-n-butyl-l-cyclohexyl-2, 4, 6-trioxoperhydropyrimidine (BCP) is probably due to the decompensation of adrenocortical function, since repeated administrations of these agents produce the diffuse hemorrhage and proliferation of adrenal cortex in the rat. Korus et al. (6) have reported that in the inactivation process of cortisone phenylbutazone not only inhibits the transformation of the α, β-unsaturated ketonic group of ring A, but also the degradation of the α-ketolic side chain of ring D. However, Dirscherl and Lutzmann (7) have observed only the inhibitory effect of aminophenazone on the reduction of ring A. These studies imply that the retardation of cortisone biotransformation is a possible component of the antiphlogistic action of these drugs. Ban (8) has emphasized that the site of stimulating action of aminopyrine is located in the hypothalamus. The hyperglycemic effects of morphine (9, 10) and salicylates (11) have been shown to be dependent on the release of catecholamines from the adrenal medulla presumably through the activation of the sympathetic centers in the brain. Therefore, it is conceivable that antiphlogistics such as aminopyrine, phenylbutazone, BCP and indomethacin modify the carbohydrate metabolism through the adrenal functions. The present experiment is an attempt to discover the effects of single and repeated administration of these antiphlogistics on the level of blood glucose in the rat.