Studies on the physiological hair silicon content in men.
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There is increasing evidence that pro-opiomelanocortin-derived peptides have a role in controlling human skin pigmentation. In vitro, human epidermal melanocytes respond to melanocyte-stimulating hormone (MSH) with increases in melanogenesis and cell dendricity. However, in the present study, not all melanocyte cultures exhibited these changes and 24% were totally unresponsive to MSH. This unresponsiveness was limited to melanocytes from white Europeans but was particularly prevalent in cultures from individuals with red hair. Cyclic AMP, the second messenger of the melanocyte-associated MSH (MC-1) receptor, induced melanocyte dendricity, even in those cultures which were morphologically unresponsive to MSH. The cyclic nucleotide also increased melanogenesis in the cultures that responded melanogenically to MSH but its effect was reduced in those cultures that were unresponsive to MSH. Thus, while the morphological data support the hypothesis that unresponsiveness is mediated at the MSH receptor, intracellular events may also be important in determining melanogenic unresponsiveness to MSH.
Pyrolysates of tryptophan (Trp-P-2) and glutamic acid (Glu-P-1) are known mutagens in in vitro short term mutagenicity tests, and have also shown carcinogenic effects in long term animal studies. The present study demonstrates that they also produce mutations in somatic cells. This result demonstrates the ability of the test to detect carcinogenic and mutagenic compounds.
Four consecutive annual calf crops of known genotype from a single property in northern Australia were examined for the presence of stephanofilarial lesions. The animals ranged in age from 60 to 348 days at the time of examination. Initial lesions of stephanofilariasis developed adjacent to the medial canthi of the eyes; animals as young as 69 days of age were found infected. In all years, prevalence of lesions increased with age for all genotypes, and was significantly lower in genotypes with higher Bos indicus content (P less than 0.01). Males had a higher prevalence of lesions than females in only one year, and in two of the years, dark-coloured animals had a higher prevalence of lesions than light-coloured ones.
1. Beta-alanine is found in mycelial walls of mature tan, but not immature white, stage of Morchella esulenta, nor in any stage of a permanently white mutant. 2. Beta-alanine is also found in hydrolysed water-extracts of human hair, the concentration being higher in blond than in dark brown, and in pigmented than in unpigmented hair. 3. Beta-alanine, added to tyrosinase-oxidized tyrosine, dopa, or dopamine has only a slight yellowing influence on the final black pigment; but when the amino group of tyrosine is combined with leucine, added beta-alanine produces stable tan pigments. 4. With L-alanine substituted for beta-alanine in this reaction, green pigment results. 5. Gelatin filters stained with the tan pigment allow solar heating of underlaying water more quickly than do those stained with the black pigment. Unstained filters allow such heating even more quickly. 6. Beta-alanine enhances production of tan pigment when heated with the phospholipid, lecithin. Implications for pigmentary adaptation, and formation of lipofuscin-like age pigments are discussed.
Common "acquired" naevocytic naevi (moles) are often regarded as caused by ultraviolet radiation although no proof of this assumption exists. An alternative view is presented herein, describing moles as atavistic relics. When the remote ancestors of Homo sapiens lost their fur, coat colour patterns also disappeared, leaving behind small rudimentary defects of the pigmentary system. These remnants are known to us as naevocytic naevi.
An office and autopsy study was performed to see if early graying was associated with increased morbidity, earlier age at death, and specific cause of death. 195 consecutive office patients over the age of 40 were studied to see if premature graying of scalp hair (50% or more gray before age 50) was associated with increased incidence of disease before age 50 (P = ns). Their parents' mean ages at death, prematurely gray or not, were compared. For fathers, mean age at death if prematurely gray was 68.27 years; if not prematurely gray, 66.03 years (P = 0.35). For mothers, the values were 70.55 years and 70.37 years respectively (P = greater than 0.50). 874 autopsy patients dying over a 23-year period (1966-1989) were studied to see if the median age at death (of patients 50% or more gray) differed for any of the six categories of disease (myocardial infarction, congestive heart failure, cancer, stroke, pneumonia/bronchitis, or cirrhosis of the liver/GI problems) when compared to the entire autopsy sample of 19 categories of disease (P = ns for each comparison). This dual office and autopsy study provides no evidence to support the contention that early gray hair is a risk factor.
Total body irradiation (TBI) and busulfan were compared for late effects in a murine model of bone marrow transplantation (BMT). Male C57BL/6 mice were given fractionated TBI or busulfan given in 4 equal daily doses followed by infusion of 10(7) syngeneic bone marrow cells. Total doses of 16.4 Gy TBI and 3.4 mg busulfan were chosen for their equivalence in inducing near complete engraftment of allogeneic marrow from donor mice of the LP strain. The two treatment groups had a late wave of mortality starting at about 80 weeks after transplantation. Specific tissue damage was manifested in bone marrow stem cells, splenic T-cell precursors, hair greying and cataract formation for both TBI and busulfan but to varying degrees. Severe nephrotoxicity and anemia were observed only after TBI. Although both busulfan and TBI kill early marrow stem cells and are effective preparative agents in bone marrow transplantation, their effects on other stem cell and organ systems are not similar. In addition, many of the injuries seen are late to occur. The delayed expression of injury deserves careful long-term evaluation of BMT recipients before the therapeutic potential of effective preparative regimens can be fully appreciated.
Normal tissue effects in mice due to combinations of a perfluorochemical emulsion, Fluosol-DA 20%, 100% oxygen, and whole-body irradiation were investigated. Eight-to-10-week-old C57BL/6 male mice were injected via the tail vein with 10 ml/kg of Fluosol-DA with and without subsequent exposure to oxygen for 60 minutes. Animals then received graded doses of whole-body radiation (4 MV photons) at a dose rate of 2.85 +/- .015 Gy/minute. Using linear regression analysis, the lethal doses of radiation to 50% and 10% of the animals within 30 days in the absence of Fluosol-DA and oxygen were 8.35 Gy (95% c.l.:7.77-8.93 Gy) and 6.73 Gy (95% cl.:6.21-7.25 Gy), respectively, and were unaffected by Fluosol-DA and/or oxygen pre-treatment. However, Fluosol-DA given alone or in combination with oxygen produced increased balding and decreased graying incidence in mice within 60 days, and resulted in depressed weight gain 15 to 60 days post-treatment. Normal tissue effects due to administration of Fluosol-DA and oxygen in combination with whole-body irradiation have been demonstrated but appear minimal compared to other anti-tumor modalities currently under investigation.
Since Hearing Research commenced publication, 51% of reports involving the use of guinea pigs provide no information on whether the animals used were albino or pigmented. Recent evidence creates a strong suspicion that the albino mutation can influence both peripheral and central auditory function. It is concluded that information on pigmentation should always be provided in reports of auditory experiments on guinea pigs, and that the only justification for using albino animals in auditory research is to study effects of the albino mutation on hearing.
This paper reviews the methods for decontaminating hair exposed to external solutions of drugs of abuse. Exposure of hair to cocaine at 1 microgram/ml for 5 min is sufficient to contaminate hair, yet decontamination is a very slow process. Using externally contaminated hair, a number of decontamination procedures were attempted, and none removed all the contamination. The percentage of external contamination removed depended on the hair type, with thick black hair being the most resistant to decontamination. Hair treated by dying incorporated externally applied drugs differently, depending on the hair type. Thick black hair became more absorbent whereas thin brown hair became less absorbent. Kinetic wash criteria are evaluated for their ability/inability to determine if hair has been contaminated from external sources. A theoretical framework for the incorporation and removal of drugs from hair is discussed, and the hypothesis that inaccessible domains exist in hair which trap drugs is critically examined. The results presented in this paper strongly suggest that much more information on the decontamination of hair and the differentiation of exogenously and endogenously incorporated drugs is needed before hair analysis can be employed in most forensic applications. We propose that the radioactive tracer methods discussed herein are well suited for evaluating any new decontamination or extraction technique.
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In summary, without a basic knowledge of embryology and development of human hair many abnormalities that occur in early postnatal life cannot be classified. Classification of abnormalities is necessary if specific genetic or biochemical causes are to be looked for and prognosis and genetic counseling accurately assessed.
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Isolation of a gene based on its location, which depends on aligning physical landmarks with the genetic map, can yield basic information about genome structure and organization. As a first step toward isolating the mouse agouti (A) locus, we have begun to define the physical position of this gene relative to genetically linked DNA probes from the Psp, Emv-15, and Src loci. Using a combination of pulsed-field gel techniques that include partial digestion with rare-cutting restriction enzymes and analysis of polymorphic sites present in certain inbred strains, we have constructed long-range restriction maps for each of the probes that span a total of more than 3000 kb. The Src and Emv-15 probes are less than 600 kb apart, but are separated from the Psp probe by at least 1500 kb. By determining the position of a 75-kb deletion that inactivates agouti function, we have localized the A locus to within 500 kb of the Psp probe, but more than 600 kb away from the Emv-15 probe. These physical distances contrast with the known recombination frequencies, 3 +/- 3 cM for A-Psp and less than 0.3 cM for A-Emv-15, and suggest that recombination between A and Emv-15 may be suppressed.
To find a marker for the bovine "muscular hypertrophy" gene and for the "roan" locus, we have typed six cattle pedigrees totaling 540 animals for nine blood group systems, for 12 biochemical markers, for RFLPs at four loci, and with five probes revealing multilocus DNA fingerprints. Segregation analysis of the fingerprint bands showed that, in cattle, a fingerprint probe will reveal a mean of 7.6 clearly resolvable bands, behaving as simple, highly informative Mendelian entities characterized by a mean mutation rate of +/- 1/4500 gametes. For one of the bands, we observed a "mutation burst" generating germline mosaicism. Because some of the fingerprint bands were allelic or corresponded to clustered minisatellites, a mean of only 5.7 independent loci is explored per probe. Fingerprint bands revealed by different probes also show a clear propensity for close linkage, pointing toward nonrandom distribution of minisatellite sequences or the existence of minisatellite clusters. Although this reduces the power of fingerprints for linkage analysis substantially, we were able to demonstrate genetic linkage between fingerprint bands and at least three of the classical markers, to exclude the roan locus from 4.5 Morgans of the bovine genome with the DNA fingerprints and for an additional 2.5 Morgans with the classical markers, and to identify a solid candidate marker for the bovine muscular hypertrophy gene, yielding a lod score greater than or equal to 2.84 without any obliged recombinant.
Tyrosinase expression was examined in hair follicles from twenty three red- and dark-haired individuals. Tyrosinase activity was greater in the hair follicles of red-haired subjects than in those from dark-haired subjects. Tyrosinase synthesis was also greater in the red-haired subjects and this presumably accounted for their higher levels of tyrosinase activity. The levels of tyrosinase synthesis in the red-haired subjects correlated well with the phaeomelanin content in the hair but in the dark-haired individuals a better correlation was seen with eumelanin. alpha-Melanocyte stimulating hormone failed to increase tyrosinase synthesis in the hair follicles of either group of subjects and in the follicles from the redheads actually produced a decrease. 8-Bromo-cyclic AMP, on the other hand, increased tyrosinase synthesis but only in the hair follicles from dark-haired subjects. These findings contrast with those previously reported in mice and it would appear that the control mechanisms that regulate tyrosinase in human melanocytes are different in many respects from those in mice.
In a prospective study of self-reported demographic, constitutional, and life-style factors in relation to basal cell carcinoma of the skin, we followed a cohort of 73,366 nurses in the United States who were 34 to 59 years of age in 1980 and who had no previous skin or other cancer. In 4 years of follow-up, compared with women living in the Northeast, women residing in California (age-adjusted relative risk [RR] = 1.57; 95% confidence interval [CI] = 1.30 to 1.89) and Florida (RR = 2.12; 95% CI = 1.54 to 2.92) were more likely to develop basal cell carcinoma. Compared with women having naturally dark brown hair, the age-adjusted relative risk of basal cell carcinoma was increased among women with red (RR = 2.45; 95% CI = 1.89 to 3.19), blonde (RR = 1.37; 95% CI = 1.09 to 1.71), or light brown hair (RR = 1.27; 95% CI = 1.08 to 1.49) and was decreased among women with black hair (RR = 0.66; 95% CI = 0.41 to 1.06). Risk was positively associated in a dose-response manner both with tendency to sunburn as a child or adolescent and with lifetime number of severe and painful sunburns on the face or arms. These risk factors remained significant predictors of disease when included simultaneously in multivariate analyses. Tendency to tan was associated with decreased risk, although this risk was not significant after controlling for the other constitutional determinants and region. Cigarette smoking did not alter the risk of basal cell carcinoma. These prospective data emphasize the importance of sunlight, and skin response to sunlight, as determinants of basal cell carcinoma among women.