EI and MI images are reliable and useful for quantifying erythema and pigmentation, if obtained under constant and consistent conditions. Apart from financial benefits, this method has many advantages and greater clinical utility in comparison with reflectance instruments.
Although R parameters have been used to evaluate skin elasticity, our study showed that F3 parameters derived from multiple suctions appear to be suitable for evaluating the elasticity of cheek skin, since this parameter is less influenced by environmental factors compared with R parameters.
Two types of portable reflectance instruments, tristimulus colorimeters (Chroma Meter CR-200®) and narrow-band spectro-photometers (Dermaspectrometer®), have recently become available for the quantification of skin color. In order to know the difference and the relationship between the different color systems, the CIE L*a*b* system and the erythema melanin (E/M) indices, respectively, adopted by the two, the variations in skin color were measured at 23 different anatomical sites of 10 healthy Caucasian male subjects. The reddish tint of the skin color of the face, palm and sole was readily detected by either of them in the increase in the a* value or in the E index, and a strong linear correlation (r = 0.92, p < 0.001) was noted between the two values. The fair color appearance of the trunk was detected in the high L* value and in the low M index, but the correlation between the two was much less significant (r = -0.56, p < 0.001). Although the mean b* values were highest in the trunk, they are significantly lower on the non-light-exposed side than those on the light-exposed side of the arm. The correlation between the b* value and the M index was weak.
Skin thickness and acoustic density reflecting intradermal structure exhibit systematic regional variation with thin and dense skin on extremities in comparison with the trunk and special ultrasound profiles in selected sites such as the face, the palp and sole. Female skin is thinner and more dense in comparison with male skin.
Skin pigmentation results in part from the transfer of melanized melanosomes synthesized by melanocytes to neighboring keratinocytes. Plasma membrane lectins and their glycoconjugates expressed by these epidermal cells are critical molecules involved in this transfer process. In addition, the derivative of vitamin B(3), niacinamide, can inhibit melanosome transfer and induce skin lightening. We investigated the effects of these molecules on the viability of melanocytes and keratinocytes and on the reversibility of melanosome-transfer inhibition induced by these agents using an in vitro melanocyte-keratinocyte coculture model system. While lectins and neoglycoproteins could induce apoptosis in a dose-dependent manner to melanocytes or keratinocytes in monoculture, similar dosages of the lectins, as opposed to neoglycoproteins, did not induce apoptosis to either cell type when treated in coculture. The dosages of lectins and niacinamide not affecting cell viability produced an inhibitory effect on melanosome transfer, when used either alone or together in cocultures of melanocytes-keratinocytes. Cocultures treated with lectins or niacinamide resumed normal melanosome transfer in 3 days after removal of the inhibitor, while cocultures treated with a combination of lectins and niacinamide demonstrated a lag in this recovery. Subsequently, we assessed the effect of niacinamide on facial hyperpigmented spots using a vehicle-controlled, split-faced design human clinical trial. Topical application of niacinamide resulted in a dose-dependent and reversible reduction in hyperpigmented lesions. These results suggest that lectins and niacinamide at concentrations that do not affect cell viability are reversible inhibitors of melanosome transfer.
Hermansky-Pudlak syndrome (HPS) is an autosomal recessive disorder characterized by oculocutaneous albinism (OCA), bleeding tendency, and lysosomal accumulation of ceroid-like material. Seven genetically distinct subtypes of HPS are known in humans; most are rare outside of Puerto Rico. Here, we describe the analysis of the HPS1 gene in 24 Japanese OCA patients who lacked mutations in the four genes known to cause OCA (TYR/OCA1, P/OCA2, TYRP1/OCA3, and MATP/OCA4), and the identification of eight different HPS1 mutations in ten of these patients, four of which were novel (W583X, L668P, 532insC, 1691delA). An IVS5+5G --> A splice consensus mutation was particularly frequent, the result of a founder effect for this allele in Japanese patients. Functional analysis by transfection of the L668P variant into Hps1-mutant melan-ep mouse melanocytes showed that this missense substitution is pathologic, resulting in an Hps-1 protein that is unable to assemble into the biogenesis of lysosome-related organelles complex-3.
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