The effect of eight vitamin E analogues (d-a-, dl-a-, d-b-, d-c-, and d-d-tocopherols, d-a-and dl-a-tocopheryl acetates) and 2,2,5,7,8-pentamethyl-6-hydroxychroman (PMC) on melanogenesis were compared in mouse B16 melanoma cells. D-btocopherol at 250 lg ml -1 inhibited not only 28% of melanin synthesis in B16 cells, but also 34% of the tyrosinase activity, a very important cascade enzyme involved in the synthesis of melanin in melanoma cells. D-c-tocopherol also strongly inhibited up to 39% of melanin synthesis and 45% of the tyrosinase enzyme activity at the same concentration. The inhibitory activity of both d-b-and d-c-tocopherols was observed without cytotoxicity up to a concentration of 250 lg ml -1 . Weak activity was also observed with d-d-tocopherol at 8 lg ml -1 and with PMC at 16 lg ml -1 , with 19% and 25% inhibition of melanin synthesis, respectively. However, PMC did not directly inhibit tyrosinase, as was observed with d-b-, d-c-, and d-d-tocopherols. Analysis by reverse transcription-polymerase chain reaction showed that the mechanism of melanogenesis inhibition by d-band d-c-tocopherols in cells might be attributed to reduced expression of tyrosinase and tyrosinase related protein-2 mRNA in addition to direct inhibition of the tyrosinase. These findings suggest that both d-b-tocopherol and d-c-tocopherol might be useful as effective ingredients in whitening cosmetics with lower skin toxicity to prevent or improve skin pigmentation such as skin spots and freckles caused by UV exposure.

Insulin signaling is mediated via a network of protein phosphorylation. Dysregulation of this network is central to obesity, type 2 diabetes and metabolic syndrome. Here we investigate the role of phosphatase binding protein Alpha4 (α4) that is essential for the serine/threonine protein phosphatase 2A (PP2A) in insulin action/resistance in adipocytes. Unexpectedly, adipocyte-specific inactivation of α4 impairs insulin-induced Akt-mediated serine/threonine phosphorylation despite a decrease in the protein phosphatase 2A (PP2A) levels. Interestingly, loss of α4 also reduces insulin-induced insulin receptor tyrosine phosphorylation. This occurs through decreased association of α4 with Y-box protein 1, resulting in the enhancement of the tyrosine phosphatase protein tyrosine phosphatase 1B (PTP1B) expression. Moreover, adipocyte-specific knockout of α4 in male mice results in impaired adipogenesis and altered mitochondrial oxidation leading to increased inflammation, systemic insulin resistance, hepatosteatosis, islet hyperplasia, and impaired thermogenesis. Thus, the α4 /Y-box protein 1(YBX1)-mediated pathway of insulin receptor signaling is involved in maintaining insulin sensitivity, normal adipose tissue homeostasis and systemic metabolism.

This paper theoretically induces the response reduction factor of the elastic single-mass system based on the equilibrium of the absorbed energy and the input energy during one cycle just before the maximum response. The fundamental relation adopted in the theory is that the response waveform with random damping factor is expressed as α times that of the basic damping factor. This value of α corresponds to the response reduction factor and is greatly affected by a projecting ratio of the maximum response to the peak response just before it.Finally, the paper presents the equation to calculate the response reduction factor as the function of projecting ratio. The theoretical values given by the proposed equation show excellent agreement with those of the time history analyses.

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