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Trichochromes in red human hair.
The presence of trichochromes B and C in red human hair was confirmed with an analytical procedure which does not give rise to the formation of these compounds as artifacts. The trichochrome precursor 5-S-cysteinyldopa previously demonstrated in red guinea-pig hair was not detected in red human hair.
Trichochromes in human malignant melanoma.
Decarboxytrichochromes B and C were isolated from a melanoma metastasis in a red-haired man, indicating the presence of trichochromes B and C in the tissue. Trichochromes E and F were not detected.
[Evaluation of the genetic quality of mice used in biomedical research].
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Influence of sex and phenotype of parents on the incidence of diabetes in BB/OK rat litters.
Because diabetes incidence (in the context of animal diabetes defined as percentage of animals developing diabetes until the age of 200 days) in BB rats is largely the same in males and females, a sex-influenced or sex-linked inheritance of diabetes has been excluded. However, in crossing studies using diabetic rats of the BB/OK rat subline and different diabetes-resistant rat strains, an excess of females was frequently observed, generally connected with an excess of diabetic males. Therefore the incidence of diabetes in 12 litters of [(dBB x DA)F1 x dBB] first backcross hybrids (BC1) and in 331 litters of BB/OK rats was analyzed according to sex ratio of litters and phenotype of parents (d-diabetic, nd-nondiabetic). In BC1 hybrids and BB/OK rats, about 50% of litters with an excess of females were observed, but an excess of diabetic males was established only in BC1 hybrids. However, in BB/OK rats correlations were found between diabetes incidence and litters with 1:1 proportion of diabetic males to females (r = -0.42 p < 0.05), phenotype of parents d x d (r = 0.73 p < 0.01) and nd x nd (r = -0.69 p < 0.01). Furthermore, an indirect influence is observable from correlations between the phenotype of parents d x d and litters with an excess of males (r = -0.40 p < 0.05) and diabetic females (r = -0.42 p < 0.05) as well as litters with a 1:1 proportion of diabetic males and females (r = -0.42 p < 0.05). It is concluded that diabetes in BB/OK rats is most probably incompatible with a "biologically normal" sex proportion in litters and that a sex-related inheritance appears to exist.
[The spectral characteristics of the fur as genotypic indices of the diversity of animals].
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[Turning white overnight, is it possible?].
A female aged 64 reported sudden whitening of the hair. Analysis proved it to be alopecia areata. Rarely, alopecia areata is of diffuse onset. If in such a case it is mostly the pigmented hairs that are lost the impression can be made of a person with grey hair turning white overnight. A review is given of some historical cases which may have been caused by this phenomenon.
[The effects of the white gene on coat pigmentation in mouse aggregation chimeras].
We obtained eight Mi(wh)/+<==>Mi(wh)/Mi(wh) chimeras using embryos of two mutant substrains of Mi(wh)/Mi(wh) mice with different isozymes Gpi-1(aa) and Gpi-1(bb). Chimerism was determined by the mosaicism of retinal pigment epithelium and electrophoretically different variants of glucose phosphate isomerase. The patterns of coat pigmentation in all chimeras were similar to those in Mi(wh)/+ heterozygotes. Despite the high proportion of the parental Mi(wh)/Mi(wh) component in three chimeras, the phenotype of their coat pigmentation was also similar with that of Mi(wh)/+ mice. The chimeras lacked mosaic-pigmented hairs. These data suggest presence only one cell population of Mi(wh)/+ melanoblasts that actively proliferate and colonize almost all forming hair follicles. Hence, the proliferation and/or differentiation of Mi(wh)/+ melanoblasts is not suppressed in the Mi(wh)/Mi(wh) dermis and epidermis. The Mi(wh) gene acting in melanoblasts leads to the block of their proliferation at the early stages of development in the homozygotes.
[Turning grey overnight, is it possible?].
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[The expression of the mutant gene mi in mouse aggregation chimeras].
Using aggregation of 8-cell embryos belonging to two mouse strains, we produced 17 chimeras, mi/mi<==>+/+ (3 organisms), mi/+<==>+/+ (9 organisms), and +/+<==>+/+ (5 organisms), that achieved the age of 30 days. Chimerism was identified by mosaic pigmentation of coat and retinal pigment epithelium (RPE). All mi/mi<==>+/+ chimeras suffered from microphthalmia. Disturbances of eye development in these mice were similar to those in mi/mi animals. In all three chimeras, pigmentation of RPE and choroid was represented with alternating pigmented and depigmented patches. Mosaic RPE pattern probably resulted from the effects of para-orbital mesenchyme cells of different genotypes, +/+ or mi/mi. These findings confirm our earlier data that mutant alleles of the mi locus affect ectomesenchyme (neural crest) cells playing an important role in normal RPE development. Coat pigmentation in mi/mi<==>+/+ chimeras had the same spotted pattern as in mi/+ heterozygous mice. Hence, the gene mi functions in melanoblasts, but dermal and epidermal mi/mi cells do not suppress migration, proliferation, and differentiation of +/+ melanoblasts. The mi/mi dermal cells do not interfere with the expression of the gene A. Despite the high proportion of mi/mi cells (58 to 80%), bone resorption and eruption of teeth in mi/mi<==>+/+ chimeras proceeded as in normal animals.
Targeted disruption of the trkB neurotrophin receptor gene results in nervous system lesions and neonatal death.
We have generated mice carrying a germline mutation in the tyrosine kinase catalytic domain of the trkB gene. This mutation eliminates expression of gp145trkB, a protein-tyrosine kinase that serves as the signaling receptor for two members of the nerve growth factor family of neurotrophins, brain-derived neurotrophic factor and neurotrophin-4. Mice homozygous for this mutation, trkBTK(-/-), develop to birth. However, these animals do not display feeding activity, and most die by P1. Neuroanatomical examination of trkBTK (-/-) mice revealed neuronal deficiencies in the central (facial motor nucleus and spinal cord) and peripheral (trigeminal and dorsal root ganglia) nervous systems. These findings illustrate the role of the gp145trkB protein-tyrosine kinase receptor in the ontogeny of the mammalian nervous system.
From fat yeast and nervous mice to brain myosin-V.
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Partial reversal of canities in a 22-year-old normal Chinese male.
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[Interbreed differences in cattle by "phenes"].
Significant interbreed differences (between Simmentals and Black-and-White cattle) for 16 phenotypes of molar surface structure were detected in milk-cows. In Black-and-White cattle, 15 phenotypic variants of the head colour marks correlating with the body colour were found.
Canities--reversal with chemotherapy.
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[The volumetric density of the hair pigment with different regional affiliations of the inhabitants of Asia, Africa i Latin America].
A stereometric (stereological) method has been developed for assessment of an objective quantitative parameter: volumic density of pigment in human hair. This method helped differentiate the hairs from the head, chest, armpits, and pubis in residents of Asia, Africa, Latin America, and the former USSR. The differences in this parameter were particularly evident in the aborigines of Africa and in the population of Asia, Latin America, and the former USSR (p = 0.02-0.01). Hairs of the residents of Asia, Latin America, and former USSR also differed (p = 0.05). The method is simple, available, and may be used in comparative studies of the hairs, including expert evaluations of their similarity.
[A case of vitamin B12 deficiency with broad neurologic disorders and canities].
The patient was a 48-year-old woman with gait disturbance as her initial symptom. Two years after the onset of the gait disturbance, she developed motor weakness and a sensory disturbance in her limbs, and dementia. On admission to our hospital, the patient's serum vitamin B12 and folic acid levels were low, and she was found to have normochromic anemia. She also had widespread coarse hair and canities was diagnosed. The patient's paresthesia resolved in response to injection of 500 micrograms mecobalamin every other day, and the Hasegawa dementia scale score and the patient's hand grip strength improved. Her gait also improved, and she became able to walk on tiptoe. Her hair returned to normal. Supplementation with high-dose methyl B12 appeared to be effective to some extent in treating a broad range of neurologic disorders besides subacute combined degeneration of the spinal cord. In addition, the hair abnormality may be a marker of vitamin B12 deficiency.
In vitro characterization of cocaine binding sites in human hair.
In vitro studies were performed to characterize [3H]cocaine binding to dark and light ethnic hair types. In vitro binding to hair was selective, was reversible and increased linearly with increasing hair concentration. Scatchard analyses revealed high-affinity (6-112 nM) and low-affinity (906-4433 nM) binding in hair. Competition studies demonstrated that the potencies of 3beta-(4-bromophenyl)tropane-2beta-carboxylic acid methyl ester, and 5-(4-chlorophenyl)-2,5-dihydro-3H-imidazol[2,1-alpha]isoindole-5-ol and 2beta-carbomethoxy-3beta-(4-fluorophenyl)tropane were similar to or less than that of (-)-cocaine. The potency of (-)-cocaine was 10-fold greater than that of (+)-cocaine at inhibiting radioligand specific binding to hair. Multivariate analysis indicated that significantly greater nonspecific and specific radioligand binding occurred in dark hair than in light hair. Multivariate analysis also demonstrated a significant ethnicity x sex effect on specific and nonspecific binding to hair. Greater radioligand binding occurred in male Africoid hair than in female Africoid hair and in all Caucasoid hair types. Melanin was considered the most likely binding site for cocaine in hair. Typically, the concentration of melanin is much greater in dark than in light hair. Scatchard analysis indicated that dark hair had a 5- to 43-fold greater binding capacity than light hair. Differences in radioligand binding between hair types appeared to be due to differences in the density of binding sites formed by melanin in hair.