[Possibility of thermography to differentiate pigmental skin tumors (author's transl)].
Problems and criteria to evaluate thermographic profiles and the differentiation of pigmental skin tumors are discussed.
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Problems and criteria to evaluate thermographic profiles and the differentiation of pigmental skin tumors are discussed.
A 76-year-old man with pigmentation and Cushing's disease is described, who was found to have a large chromophobe adenoma of the pituitary. Despite normal skull X-rays the presence of bitemporal hemianopia led to the diagnosis which was later confirmed at post-mortem. Adrenalectomy performed in the treatment of Cushing's disease may be followed by skin pigmentation and an enlarging pituitary tumour (Nelson's syndrome), changes which are commonly attributed to the removal of the negative feed-back mechanism. The spontaneous occurrence of these changes in this patient who did not undergo adrenalectomy supports the view that a pituitary tumour pre-exists in cases of Nelson's syndrome and emphasizes the importance of directing initial treatment to the pituitary.
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The authors present a pathological study of the skin in a 62 year-old man with facial pigmentation due to amiodarone. They found under the light microscope, cells resembling histiocytes filled with pigment. They were less numerous than usually reported, but were found associated with a pericapillary and periglandular lymphocytic infiltration, which raises the problem of iatrogenic lupus or Jessner-Kanoff's disease. Examination under the electron microscope, permitted identification of 5 groups of granulations, three of which had already been observed by Mrs. Fagola. These pigments correspond to lipofuscins, melanin, but also yet unidentified substances, may be metabolites of amiodarone.
The various colours of the red-bellied toad Bombina bombina are caused by 3 types of chromatophores, the red xanthophores, the white iridophores and the black melanophores. In the brownish skin and in the black spots of the dorsal region all types of chromatophores are found. But in the epidermis of the black spots there are more grana of melanin than in the other region of the back. The 3 types of chromatophores are not present in the skin of all parts of the body. The dark blue colour of the belly is caused only by melanophores, whereas in the ventral parts with light blue colour there occur melanophores and iridophores. The white spots of the belly contain only iridophores, the red spots have iridophores and xanthophores.
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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.
Three findings from a study of one hundred black newborn infants examined for pigmented lesions are presented herein: significantly higher incidence than in prior neonatal examinations, a frequent clinical pattern of grouped macules, and an unusual histologic distribution of nevus cell theques. Fifty-one percent of the infants had congenital pigmented lesions. Biopsy specimens of thirty-two lesions were obtained, twenty-six showing histologic changes of lentigo, four melanocytic nevi (nevus-cell nevi), and two ephelides. Three of the four nevi were less than 1.5 cm in diameter and all were of the predominantly junctional type. Clinical appearance was not a consistent guide for classification in the newborn.
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A method of repigmenting some leukodermas by transplantation of minigrafts of normally pigmented, autologous skin into them is described. Such grafts in addition to retaining their pigment stimulate repigmentation around them by migration of melanocytes and spread of pigment from the grafts. Three patients, one with piebaldism, another with leukoderma from monobenzyl ether of hydroguinone, and a third with depigmentation following healing of a burn enjoyed successful and cosmetically acceptable repigmentation from practice of the method.
A case characterized by a dark pigmentation of the skin with an initial hypotension and a lung tuberculosis in the remote anamnesis is described. The skin pigment was formed by lipofuscin and emosiderin, but only the former was found in the liver biopsy. Anyway, the pigment was not melanine and the surrenalic function of the patient was completely normal; therefore, an Addisonism syndrome is excluded. The patient was treated for a very long time with DOCA: this caused hypertension, probably supported by the hypervolemia triggered by the DOCA depending retenction of sodium and water. A sure diagnosis of the case was not made, but an Addisonism syndrome was certainly excluded.
Pathological features of twenty-one cases of malignant melanoma studied in the University of Nigeria Teaching Hospital, Enugu during the period January, 1974 to December, 1975 are presented. Malignant melanoma accounted for 2.4% of all tumours and 4.5% of all malignant tumours, greatest age incidence being in the fifth to seventh decades. The male to female sex ratio was 2:1. 73.2% of cases were of the nodular variety. 81% melanomas occurred on the sole of feet validating the hypothesis that the pigmented skin in Africans is resistant to malignant melanoma. Melanoma in Nigerians would appear essentially to be arising from epidermal melanocytes and not from preexisting naevus cells. Hence we do not feel prophylactic removal of plantar moles as suggested by Onuigbo (1975) is desirable. Histologically, there was no clear association between the cell types and the kind of melanoma or invasion of the tumour. The difference in behaviour and natural history of malignant melanoma would appear to have a bearing on the local tissue and also general immune mechanisms of the host.
We carried out ultrastructural studies on the epidermal melanocytes in human skin autografts, before and after transplantation. On comparing the results with those described in our previous paper, the present findings are in accord with those light microscope findings. As we suggested earlier, the degree of pigmentation in a skin graft is probably due not only to quantitative changes in the transfer and formation of melanosomes, but also to the distribution, the degradation pattern, and the size of the melanosomes within the keratinocytes. Rupture of lysosomes, as a consequence of transplantation, may also contribute to the pigmentation of the skin graft.
The case history is presented of a woman with acquired lesions in the axillary, submammary, intermammary, inguinal, genitocrural and perianal skin folds. These lesions were confluent pigmented macules, giving rise to extensive (en nappe) reticulate patches. History revealed changes typical of seborrhoeic wart. The name patchy (en nappe) seborrhoeic wart is suggested for this condition.