Infrared spectroscopic studies of pigmented skin tumors.
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Reflectance spectrophotometry from 400 to 800 nm on different cutaneous pigmented lesions, including primary and metastatic malignant melanoma, pigmented nevi, lentigo and seborrhoeic keratosis, has been performed by using an external integrating sphere coupled to a spectrophotometer. Measurements show that reflectance spectra of the different lesions manifest dissimilar patterns, particularly in the near IR region. Comparison of reflectance of nevi with that of malignant melanomas results in a highly significant difference (P less than 10(-6)) between the two samples. Though interpretation of the spectra remains difficult as a result of the complexity of the optical processes of scattering and absorption, our results suggest that a detailed analysis of the reflectance spectrum may give clinically useful information, and could be utilized as an aid in clinical diagnosis of cutaneous pigmented lesions, especially where malignant melanoma is concerned.
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Analysis of the topography peculiarities and distribution of oxidized melanine and its precursors (DOPA-oxide activity and catecholamine) in pigment nevuses and malignant melanomas of skin shows that the studied peculiarities are a complex of intersupplementary markers of melanine formation, correlate with the quality and the degree of proliferative process expression in tumours of this genesis and may be used for their malignancy rating.
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BACKGROUND: Little has been known about the effects of visible light in mammalian cells. We recently found that blue light not only suppressed the growth of B16 melanoma cells in a time-dependent manner but also inhibited metastasis of the B16 melanoma cells to the lung. These findings suggest that exposure to blue light modifies the functions of B16 melanoma cells. The present study investigated the effects of blue light on B16 melanoma 4A5 cells and Weiser-Maple guinea-pigs to confirm the biological effect of blue light on melanin formation. METHODS: The effect of red, green, and blue light on melanin synthesis in B16 melanoma 4A5 cells was measured. The back skin of brown Weiser-Maple guinea-pigs was exposed to ultraviolet B (UVB; 588 mJ/cm(2) (0.7 mW/cm(2)x 14 min) three times a week for 2 weeks to induce melanin deposition. Thirty minutes after each UVB exposure, blue light was applied for 30 min. Pigmentation of the exposed areas of skin was checked once a week, and photographs of the skin were taken by digital camera. Observation was continued for 18 days after the final UVB exposure. RESULTS: Melanin synthesis in B16 melanoma 4A5 cells was selectively suppressed by blue light, but blue light did not induce decolorization of previously produced melanin. In the back skin of brown guinea-pigs, the brightness of the sites exposed to UVB began to decrease on the fifth day of the experiment, decreasing further from the 12th day to the 18th day after UVB exposure. The brightness of the sites exposed to UVB and blue light decreased in a manner similar during the UVB exposure, but remained relatively unchanged from the 12th day to the 30th day. CONCLUSIONS: These results suggest that blue light suppresses melanin formation following repeated UVB exposure. Further investigation with various light such as blue light may lead to a new approach to the care of ultraviolet-affected skin such as hyperpigmentation.
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The Q-switched ruby laser (694 nm, 25-40 nsec) is an effective and safe therapeutic device for the treatment of tattoos and well-defined, benign, pigmented epidermal and dermal lesions. Because of its selective mode of action, dermal pigments of natural and artificial origin are destroyed photothermically and removed without scar. This method is exceptionally suited for the elimination of lay and professional tattoos, traumatic tattoos, and permanent makeup. Other frequent indications include benign pigmented lesions such as lentigines, freckles, café-au-lait spots, seborrheic keratosis, and Becker nevi. As a dermal pigmented lesion, the nevus of Ota is perfectly treatable. However, chloasma can no longer be considered an indication for ruby laser treatment due to unsatisfactory results. Melanocytic nevi and congenital nevi should be treated only in clinical studies. The effectiveness of the long-term epilation of dark hair with this laser device has to be verified in future investigations. Particularly attractive is the nonproblematic and straightforward removal of pigmented lesions in precarious anatomic regions like the lips, eyelids, and genitals (e.g., benign melanosis of the lips or of the penis, seborrheic keratosis of the lid angle).
This study evaluated two changes in fluorometric assessment of fluorescein dye delivery: (1) monitoring the proportional, rather than the absolute, increase above the preinjection background reading at each site to obviate the effect of skin color and (2) employing gradual means of dye administration to facilitate monitoring uptake kinetics and to lessen the likelihood and severity of histamine-mediated reactions. In 15 beagles, background and postdye readings were obtained with the fiberoptic fluorometer at 27 pairs of matched light- and dark-skin sites of intact perfusion. After dye administration, the absolute increase in fluorescence at light sites averaged more than twice (approximately 225%) that at dark sites. However, the newly introduced proportional increase (PI) was independent of pigmentation. The PI of comparably perfused light and dark sites differed by an average of 3.9% (p greater than 0.05 for difference between PIdark and PIlight). This consistency was maintained after each of three methods of fluorescein administration. After the color independence of the PI was established, its relation to perfusion was assessed in nine 3 X 12 cm pedicle flaps of varied pigmentation. Background fluorometric readings were obtained at eight sites along the longitudinal axis of each flap. Dye was administered as a 20-minute 0.25 mg/kg/min infusion. The PI clearly delineated gradations in perfusion, correlating highly with more time-consuming kinetic indexes and accurately predicting viability. The pedicle row, last viable row (V1), and first nonviable row (N1) had mean PI values of 10.5 +/- 4.5, 4.2 +/- 2.6, and 0.1 +/- 0.1, respectively, at 25 minutes after the start of infusion (p less than 0.05 for pedicle vs V1, pedicle vs N1, and V1 vs N1).
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The yellow body coloration of large yellow croaker (Larimichthys crocea) constitutes a crucial economic trait, yet its underlying genetic regulatory mechanisms remain poorly understood. This study systematically elucidated the molecular basis of body color variation by integrating genome resequencing and skin transcriptome analyses, combined with the contextual analysis of key pigmentation-related genes and phenotypic histological validation. 200 phenotyped individuals (including yellow-selected lines, F1 progeny, and normal control groups, all derived from a well-characterized aquaculture stock) identified 39 significantly associated SNPs (-log₁₀(P) ≥ 6), mapping to multiple candidate genes. These genes were significantly enriched in pathways related to pigment deposition (GO:0033059), melanosome organization (GO:0032438), melanogenesis, and tyrosine metabolism. Cross-developmental stage transcriptome analysis revealed 2395 differentially expressed genes (DEGs). Multi-omics integration identified eight overlapping candidate genes, including tyrp1, slc45a2, oca2, and dgat2, among which tyrp1 was prioritized for in-depth validation based on its core regulatory role in eumelanin synthesis, significant SNP association signal, and consistent downregulation in transcriptomic data. Experimental validation demonstrated that the g.895C > T mutation in exon 2 of tyrp1b was strongly significantly associated with the yellow phenotype: the frequency of mutant genotypes (TT/CT) reached 92.86%in the yellow-selected group, whereas the control group exclusively exhibited the wild-type genotype (CC). qPCR confirmed significantly downregulated tyrp1b expression in the skin of yellow individuals, consistent with the transcriptome trend. Histological and stereomicroscopic observations of skin tissues further validated the physiological basis of the yellow phenotype, revealing a significant reduction in melanophore number and abnormal melanosome morphology in yellow-phenotype individuals, accompanied by increased xanthophore density. These results suggest that tyrp1b mutation is strongly associated with the yellow phenotype. However, the presence of a wild-type CC individual in the yellow group indicates that this mutation is not strictly required for yellow coloration, suggesting that other genetic or environmental factors may also contribute to the phenotype, Additionally, downregulation of the carotenoid metabolism gene bco2 coupled with upregulation of xdh, together with the functional changes of slc45a2 and oca2, may synergistically promote xanthophore pigment deposition, contributing to the yellow phenotype. As melanin synthesis in large yellow croaker relies on the conserved tyrosinase pathway and transporter proteins, mutations in associated genes (tyrp1b, slc45a2, oca2) represent a primary underlying cause for the loss of melanin-based coloration and transition to a yellow phenotype in L. crocea. These findings provide key molecular targets and a theoretical foundation for molecular breeding of body color in this species, and also enrich the understanding of xanthism regulatory mechanisms in teleosts.
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