Roots of manually extracted scalp hairs among 86 healthy Koreans in different age groups were examined microscopically and the proportion of resting hairs to growing hairs were determined with the fol[owing results. 1. The proportion of resting hairs in all age groups was 10. 9% and there was no significant difference between male and female. 2. In each age group the proportion of resting hairs show's difference, being lowest (6. 8%) in below 9 years age group, increasing the rate by increasing the age group, highest (19. 7%) in over 60 years age group. 3. The proportion of resting hairs below the age of 29 years was below 10%, above 30 years to 49 years in between 10% to 15% and over 50 years in between 15% to 20%. 4. The normal range of the proportion of resting hairs among normal Koreans was below 20%.
Dermatitis, Atopic* ; Female ; Hair ; Humans ; Male ; Neutrophils* ; Reference Values ; Scalp

OBJECTIVE: The study was performed to compare the survival rate and the development of day 2 mouse embryos which had freezing procedures done. METHODS: We used three different vitrification solutions (EFS, VS14, DPS) and a ultrarapid freezing solution (UFS) for cryopreservation of day 2 mouse embryo. RESULTS: We tested toxicity by exposing embryos to vitrification solutions and a ultrarapid freezing solution. The survival rates are 100%, 97.8%, 95.6% and 100% (EFS, VS14, DPS and UFS). After cultured for 96 hours, hatching rates of each group are 93.5% (no freezing), 95.6% (EFS), 86.4% (VS14), 93.0% (DPS), and 93.0% (UFS). There is no significant differences among groups. The survival rates after thawing cryopreserved embryos are 80.2%, 91.7%, 69.5%, 0% and 91.8% (slow freezing, EFS, VS14, DPS and UFS). Also cultured for 96 hours, the hatching rates are 93.5% (no freezing), 84.1% (slow freezing), 93.9%) (EFS), 48.5% (VS14) and 70.1% (UFS). CONCLUSION:The survival rates of vitrification in EFS solution and ultrarapid freezing are higher than slow freezing (p<0.05). The hatching rate of vitrification in EFS solution cultured for 96 hours is highest, so vitrification of day 2 mouse embryos in EFS solution considered as more effective for cryopreservation.
Animals ; Cryopreservation ; Embryonic Structures* ; Freezing* ; Mice* ; Survival Rate ; Vitrification*

No abstract available.
Delivery of Health Care* ; Gyeongsangnam-do*

The use of hormonal stimulation in human in vitro fertilization and embryo transfer (IVF-ET) leads to increased production of embryos for ET. So to avoid high pregnancies and to allow conception in future, unstimulated cycles, cryopreservation of spare embryos is desirable. One of the improvement of cryopreservation methods is vitrification. We cryopreserved mouse day 3 embryos by vitrification using the three different vitrification solution (EFS40, VSll and VS3a). EFS40 solution is consisted of 40% (v/v) ethylene glycol, Ficol170 30% (w/v) and 0.5M sucrose and VSll is 6.0M ethylene glycol and 1.8M glycerol. And VS3a is 6.5M glycerol and 6% (w/v) BSA (bovine serum albumin). First we tested the toxicity of three vitrification solution by exposure to these solution during 3 min. After washing by thawing solution, the survival rates of each groups are 95.5%, 90.9% and 84.4% (EFS40, VS11 and VS3a). High percentages of them developed to expanded blastocyst and hatching embryos in culture 48hrs 94.2%, 97.7%, 100% and 97.4% (no treatment group, EFS40, VS11 and VS3a). So there is no significant differences among the each group. Second, after thawing of vitirfied embryos, the survival rates of each groups are 96.8% (slow freeze), 94.1% (EFS40), 85.5% (VS11) and 80.0% (VS3a, P vs. no freeze or EFS40 is 0.01). Vitrified embryos exhibited a high rate of development in vitro after 48hrs culture. The percentages of each group to blastocyst and hatching embryos are 88.7% (no freeze), 91.8% (slow freeze), 93.4% (EFS40), 87.7% (VS11) and 73.0% (VS3a, P vs. other group is 0.01). The results suggest that there is no significant differences in exposure of various vitrification solution and day 3 mouse embryos can be vitrified in solution EFS40 and VS11 by simple procedure.
Animals ; Blastocyst ; Cryopreservation* ; Embryo Transfer ; Embryonic Structures* ; Ethylene Glycol ; Fertilization ; Fertilization in Vitro ; Glycerol ; Humans ; Mice* ; Pregnancy ; Sucrose ; Survival Rate ; Vitrification*

When chemical agents penetrate the placenta, it is potentially hazardous to the embryo because the embryonic stage is known to be extremely sensitive to various toxic agents. It has been reported that exposure to some chemical agents during pregnancy resulted in the induction of malformation or cancer in the offspring of experimental animals (Larsen, 1947; Klein, 1952; DiPaolo, 1964; Druckrey et al. 1966; Mohr et al, 1966; DiPaolo and Elis, 1967; Spatz and Laqueus, 1967; Alexandrov, 1968; Fujii and Nishimura, 1969; Rice, 1969; Bulay and Wattenberg, 1970; Currie, 1970; Vesselinovitch et al, 1971; Swenberg et al, 1972; Nomura et al, 1973). Fraser and Fainstat (1954) and Kalter (1954) found that administration of cortisone to pregnant female mice induced the appearance of cleft palates in the offspring. The frequency with which this deformity appears was observed to depend on: I) the genotype of the treated animal (strain differences), 2) the dose of the chemical administered, 3) the time during the gestation period when the animal was treated. A single intraperitoneal injection of 5-fluorouracil at 10, 11, 12 or 13 days after copulation in mice also produced abnormalities to the feet, deft palate and deformities of the tail in a large proportion of fetuses (Dagg, 1960). Urethan has been considered to be a highly teratogenic and carcinogenic agent in experimental animals (Nishimura and Kuginuki, 1958: Nomura and Okamoto, 1972). However, they stated that accurate timing of urethan toxicity and accurate calculation of urethan dosage actually reaching the embryo make it possible to analyze the sensitivity of the developing mouse embryo to mortality, growth inhibition, malformation and neoplasm. Nomura and Okamoto (1972) reported that when pregnant mice were exposed to urethan on various days of gestation (day 5 to 19) by a single injection malformations and neoplasms were induced in their offspring. It is frequently implied that an abnormal phenotype is due to the aberration in the genotype, but it is not possible to prove the specitic causal relation. Though, the frequent association between a variety of chromosomal abnormalities solves the problem of how the genotypic and phenotypic are interreiated (Schultz, 1965). 5-bromodeoxyuridine (BUdR) and dimethylnitrosamine (DMN) induce chromosome aberrations in Chinese hamster cells cultured human lymphocytes and mouse cells in vivo (Somers and Hus, 1962; Kato, 1968; Matsuoka et al, 1979; Hahn and Kim, 1979). BUdR is a thymidine analog incorporated into only the DNA of proliferating cells and its mutagenic action is well understood (Freese, 1963). DMN is a potent carcinogen which induces tumors of the liver, lung, and kidney in rats (Magee and Bames, 1959). This agent has no teratogenic effect in rats when given in doses of different concentrations for different periods of time and by several routes of administeration during all stages of embryogeny (Alexandrov, 1967). The experiments reported in this study were undertaken to investigate the possibility that treatment of ICR inbred pregnant mice with BUdR and DMN might shows deformities or abnormalities in their offspring and also to determine whether chemical exposure during fetus will effect at 32 weeks after birth with second exposure to DMN by cytogenetical means. In this study, estrus ICR females were mated and 32 mice which had been diagnosed as pregnant were used. BUdR at the rate of 70, 100 and 150mg/kg of body weight was injected intraperitoneally at 6, 7, 8 days and 9, 11, 13 days of gestation, and DMN at the rate of 10, 20 and 30 mg/kg of body weight was injected at 8, 10, 12 days and 14, 15, 16 days of gestation, The offspring were examined macroscopicaily at time of birth for malformations. All animals were killed at 32 weeks of age and examined for liver abnormalities. The liver were cultured and treated with 1, 5 and 10 ug/ml of DMN for 18 hours. The frequencies of chromosome aberrations and sister chromatid exchanges (SCE) were analyzed. The results are summarized as follows: 1. The litter size was reduced on treated animals. 2. Among the 279 progeny from 36 BUdR treated mothers, malformations were seen in a total of 10 progeny and the group treated at the 9 to 13 gestation days stage had the most. 3. Of the 155 progeny from 24 mothers injected with DMN, none had any visible deformity. However. 37.5% of the group were found to have liver nodules after 32 weeks treated at the 8 to 12 gestation day stage. 4. Repetitive treatment with DMN of the liver culture of the previously BUdR and DMN treated progeny, showed increased chromosome aberrations and SCE frequencies. In conclusion since the exposure of the mother of BUdR and DMN during pregnancy leads to increased chromosomal abnormalities of the cultured liver cells of progeny when treated with DMN a second time, it is necessary to keep in mind that genetic damage may be occure to the progeny by exposing the mother during pregnancy.
Animals ; Body Weight ; Bromodeoxyuridine ; Chromosome Aberrations ; Cleft Palate ; Congenital Abnormalities ; Copulation ; Cortisone ; Cricetinae ; Cricetulus ; Cytogenetics ; Dimethylnitrosamine ; DNA ; Embryonic Structures ; Estrus ; Female ; Fetus ; Fluorouracil ; Foot ; Genotype ; Humans ; Injections, Intraperitoneal ; Kidney ; Litter Size ; Liver ; Lung ; Lymphocytes ; Mice ; Mortality ; Mothers ; Mutagens ; Palate ; Parturition ; Phenotype ; Placenta ; Pregnancy ; Rats ; Sister Chromatid Exchange ; Tail ; Thymidine ; Urethane

Proliferating trichilemmal tumor is one of rare benign tumors of the skin appendages, considering as hamartoma of the terminal hair follicle, isthmic segment of the outer root sheath. We report a case of numerous proliferating trichilemmal tumors admixed with ordinary trichilemmal cysts with femilial history in 64-year-old man. He has total 157 lesions, which are chiefly located in scalp (48), back (32), and also face, neck, trunk, extremities. Histologically, the tumor is composed of irregularly arranged and ansatomosed trabeculae, lobules, or sheets of proliferated trichilemmal squamous epithelium with peripheral palisading of the basaloid cells. Several layers of squamoid or ovoid cells have PAS-positive clear cytoplasm. And it also shows abrupt amorphous, trichilemmal keratinization. Some squamous eddies with mild cellular atypism are associated, but definite invasion or other evidence of the malignancy is not found. usual multiple trichilemmal cysts are admixed with tumor and occasionally exhibit connection between them.
Cysts ; Hamartoma

Porokeratosis (mibelli's disease) is a chronic, heritable disorder of the skin, which has a regular dominant limitation to the male sex. This is characterized by localized areas of faulty keratinization resulting in the cornoid lamella, the morphologic and histologic hallmakr of the disease process. Histogenesis is best explained as a mutant clonal keratosis of epidermis, these clonal cells are probably ingerited. A case of porokeratosis Mibelli is reported with its clinical, histological evaluation and review of articles.
Epidermis ; Humans ; Keratosis ; Male ; Porokeratosis* ; Skin

This study was carried out to investigate the intricate mechanisms of intraalveolar fibrosis, leading to the alveolar structural remodeling, of rat lungs treated with paraquat. Sixty-three male Sprague-Dawley rats, maintained on a stock diet, weighing 200.0 gm, average, were divided into 4 experimental groups. Group 1. Control group (10 rats). Intraperitoneal injections of 2-4 ml normal saline only. Group 2(13 rats). 10, 20, 25, 30 and 40 mg per kg of body weight was administered intraperitoneally. Animals were sacificed 5 hours. 1 and 3 days after paraquat treatment. Group 3(16 rats). 20, 25, 30 and 40 mg per kg of body weight was administered to the animal, and animals died 2-5 days after paraquat administration. Group 4(24 rats). The same amount of paraquat was administered to the animal as in the group 2. Animals were sacrificed 1, 2, 6, 8 and 10 weeks after paraquat treatment. Sacrificed animal lung was examined by gross, light-microscopic, immunohistochemical, ultrastructural observation, along with cellular and chemical analyses of bronchoalveolar lavage fluid. The results were as follows: Grossly, 6 rats of chronic stage (1-10 weeks survival) developed multiple wedge-shaped scars on both lungs. These scars were situated mainly along the bronchial trees, blood vessels and subpleural regions. Light microscopically, the salient features found of the chronic stage lungs were intraalveolar fibrosis. Intraluminal buds or polypoid masses projecting into the alveolar lumen and ducts. Elsewhere, loose connective tissue masses were found to fuse together to alveolar wall, obliterating the alveolar spaces with resultant severe alveolar structural remodeling. Immunohistochemically, fibronectin was found in the center of intraalveolar buds and polypoid mass, projecting into the alveolar lumen, and in the adjacent proliferating alveolar macrophages. An attempt to measure the amount of fibronectin in the bronchoalveolar lavage fluid failed. Electron microscopically, the chronic stage lung revealed marked proliferation of both alveolar macrophages and fibroblasts in the alveolar spaces, the latter containing actin-like microfilaments and collagen fibers arranged in bundles and spirals. In areas, myofibroblasts and smooth muscle cells also present. Cellular analysis of the bronchoalveolar lavage fluid in chronic stage lungs revealed no significant findings. It can be concluded, therefore: That intraalveolar fibrosis of the paraquat-treated lungs of the rat is probably mediated by intraalveolar migrations of the interstitial cells, the main task force being the connective tissue cells, passing through the defects created in the epithelial lining surface to its basement membrane, which were inflicted upon the alveolar wall by paraquat toxicity. Fibronectin, released by activated alveolar macrophages, may be responsible for the migrations of fibroblasts and myofibroblasts into the alveolar spaces to form the intraalveolar fibrosis with subsequent alveolar structural remodeling,
Male ; Humans ; Rats ; Animals

No abstract available.
Cytogenetics*

No abstract available.
Cytogenetics*