Authors attempted to examine the development of keratinocyte in the human fetal epiderrnis in term of the appearance of principal product of differentiation, the keratins. Immunohistochemical study (ABC method) using anti-prekeratin antibodies and anti-keratin antibodies was carried out on sampled skin from 9 human fetuses ranging in estirnated gestational age from 12 weeks to 27 weeks. As early as 12 weeks of embryonic life, the epidermis contained cytokeratin. At this stage of development, the embryonic epidermis consists of three-cell layer .' basal layer, intermediate layer, and periderm, all of them staining for prekeratin and keratin. A thick cornified layer developed at 24 weeks but was not stained for prekeratin and keratin. Hair germ of 12 week-fetus was recognized as bulges of basal cells that were stained for prekeratin and keratin. At 18 weeks of estimated gestational age, development has advanced to the bulbous hair peg stage at which point the primordia of nearly all the final structural components of follicles were established. In the final structureal cornponents of the follicles, outer root sheath and sebaceous gland were stained for prekeratin and keratin, whereas cortical and cuticular elements and inner root sheath were negative. There was no difference between immunostaining results for prekeratin and keratin except for the staining intensity. The appearance of these proteins early in development suggests their potential value in utero in the recognition of keratinization disorders.
Antibodies ; Epidermis* ; Fetus* ; Gestational Age ; Hair Follicle* ; Hair* ; Humans* ; Keratinocytes ; Keratins ; Sebaceous Glands ; Skin

No abstract available.
Fracture Fixation, Intramedullary

No abstract available.
Antibodies, Monoclonal* ; Mycobacterium bovis*

No abstract available.
Antifungal Agents* ; Trichophyton*

PURPOSE: The effects of pain on brain is not well known. Also, differences between somatic and visceral pains have not been fully elucidated. This study was conducted to investigate changes in the expression of c-Fos protein after somatic and visceral pains were induced by formalin. METHODS: Male rats(n=65) were underwent one of three procedures : (i) Control group, rats were left undisturbed in their cages; (ii) Somatic pain group, rats were injected subcutaneously with 0.1 ml of 10% formalin in the plantar surface of right hindpaw; (iii) Visceral pain group, rats were administered with same amount of formalin, as described above, in the rectum. Rats were sacrificed at increasing times(30 minutes, 1 hour, 2 hours, 6 hours, 1 day, 3 days and 7 days) after noxious formalin stimuli to hindpaws and rectums. Rat brains were removed and sliced in rat brain matrix. Brain slices were coronal sectioned at interaural 5.70-6.70mm. Serial sections were immunohistochemically reacted with polyclonal c-Fos antibody. The numbers of c-Fos protein immunoreactive neurons in cingulate cortex, primary somatosensory area, and hippocampus were examined and analyzed statistically with Mann-Whitney U test. RESULTS: 1) The numbers of c-For protein immunoreactive neurons in cingulate cortex, primary somatosensory area and hippocampus peaked at 2 hours after somatic pain stimuli and reached almost normal conditions at 7 days. 2) The numbers of c-Fos protein immunoreactive neurons in cingulate cortex, primary somatosensory area and hippocampus peaked at 1 day after visceral pain stimuli and reached almost normal conditions at 7 days. 3) The numbers of c-Fos protein immunoreactive neurons of somatic pain groups were higher than that of visceral groups at all times and the difference of numbers peaked at 2 hours after pain stimuli. CONCLUSION: Reactions of somatic pain stimuli influenced more changable than visceral pain stimuli to brain. Conduction velocities of somatic pain were more faster than those of visceral pain. Higher numbers of c-Fos protein immunoreactive neurons were found in specific regions. These results provide some basic knowledge in understanding the mechanism and control of pain.
Animals ; Brain* ; Formaldehyde* ; Gyrus Cinguli ; Hippocampus ; Humans ; Male ; Neurons* ; Nociceptive Pain ; Rats* ; Rectum ; Visceral Pain

KOH examination is a simple, rapid and diagnostic procedure to confirm dermatophytic infections. It is important to select a proper examination site of the lesion. To determinate the proper examination site of the lesion, mycologic studies were done with multiple specimens collected from the center, margin and out of margin of the ring-shaped dermatophytic skin lesion on the 58 patients. The results were as follows. Positive rate of KOH wet smear was 94.8% at the center and 100% at the margin of the lesions, 22.4% at the 1 cm and 5.2% at the 2 cm out of the lesions. The more hyphae were found in the lesion, the more hyphae were found out of the lesion. Culture was done on the Sabouraud's glucose agar from the highest KOH positive area and the positive culture was 48 strains (82.8%) of 58 patients. These findings suggested that the ring-shaped active margin was the best site to examine mycologic studies.
Agar ; Glucose ; Humans ; Hyphae ; Skin*

BACKGROUND: PUVA has been used effectively in the treatment of vitiligo, but the mechanism by which PUVA stimulates melanocyte proliferation in vitiligo is not known. Several mechanisms have been suggested to be involved in the process of repigmentation of vitiligo. First, UV light, with or without psoralen, directly stimulates the proliferation of melanocytes. Secondly, PUVA may act. on epidermal keratinocytes or dermal components to stimulate t,hem to release certain melanocyte growth st,inulation factors that enhance the proliferation of melanocytes in depigmented lesions. Thirdly, PUVA irnmunologically leads to the impairment of epidermal Langerhans cell function and alteration of circulating T and B cell function, which results in the suppression of the stimuli is for rnelanocyte destruction during the therapy. OBJECTIVE: To test, th hypothesis that PUVA induced repigmentation in vitiligo results from the stimulation of growth factors that induce melanocyte proliferation, and that PUVA may suppress the immune reacticin to melanocytes, especially in autoantibody synt,hesis, we examined the effects of sera on the growth of epidermal melanocytes and control cells, and the incidence of antibodies to melanocyte and melanoma cells(SK-Mel 2~3) in the sera of patients with vitiligo. We also had normal control individuals and studied the changes of the antibody titer in the sera of patients with vitiligo. METHODS: The rate of H thymidine uptake was estimat,ed in cultured melanocytes and fibroblasts t,reated by patients sera before and after PUVA treatment. SDS-PAGE and immunoblotting analysis were used to idcntify anti pigment cell autoantibodies and were compared to the titers of autoantibodies after PUVA. RESULTS: 1. Melanocyte and fibrablast proliferation was increased by PUVA treated sera. Their proliferation was in proportion to the duration of the PUVA treatment. Melanocytes proliferated more than fibroblasts. 2. Significant differences between vitiligo patients and normal controls were found in the inci dence of anti-pigment cell antibodies. The antibodies were predominantly directed to melanocyte antigens of 110 kD, 65 kD, 45 kD and melanoma cell antigens of 110 kD, 103 kD, 88kD, 70 kD, 56 kD, 41 kD. 3. The titer of anti piment cell antibodies showed a tendency to decrease after PUVA treat- ment in most patients regardless of clinical improvement. Conclusion ; PUVA treated sera induced proliferation of melanocytes and fibroblasts and the production of aut,oantibodies was suppressed against pigment cell antigens through irnmunosuppression, which might help in the repigmentation of vitiligo.
Antibodies ; Autoantibodies ; Candida* ; Classification* ; DNA* ; Electrophoresis, Polyacrylamide Gel ; Fibroblasts ; Ficusin ; Humans ; Immunoblotting ; Incidence ; Intercellular Signaling Peptides and Proteins ; Keratinocytes ; Melanocytes ; Melanoma ; Thymidine ; Ultraviolet Rays ; Vitiligo

BACKGROUND: PUVA has been used effectively in the treatment of vitiligo, but the mechanism by which PUVA stimulates melanocyte proliferation in vitiligo is not known. Several mechanisms have been suggested to be involved in the process of repigmentation of vitiligo. First, UV light, with or without psoralen, directly stimulates the proliferation of melanocytes. Secondly, PUVA may act. on epidermal keratinocytes or dermal components to stimulate t,hem to release certain melanocyte growth st,inulation factors that enhance the proliferation of melanocytes in depigmented lesions. Thirdly, PUVA irnmunologically leads to the impairment of epidermal Langerhans cell function and alteration of circulating T and B cell function, which results in the suppression of the stimuli is for rnelanocyte destruction during the therapy. OBJECTIVE: To test, th hypothesis that PUVA induced repigmentation in vitiligo results from the stimulation of growth factors that induce melanocyte proliferation, and that PUVA may suppress the immune reacticin to melanocytes, especially in autoantibody synt,hesis, we examined the effects of sera on the growth of epidermal melanocytes and control cells, and the incidence of antibodies to melanocyte and melanoma cells(SK-Mel 2~3) in the sera of patients with vitiligo. We also had normal control individuals and studied the changes of the antibody titer in the sera of patients with vitiligo. METHODS: The rate of H thymidine uptake was estimat,ed in cultured melanocytes and fibroblasts t,reated by patients sera before and after PUVA treatment. SDS-PAGE and immunoblotting analysis were used to idcntify anti pigment cell autoantibodies and were compared to the titers of autoantibodies after PUVA. RESULTS: 1. Melanocyte and fibrablast proliferation was increased by PUVA treated sera. Their proliferation was in proportion to the duration of the PUVA treatment. Melanocytes proliferated more than fibroblasts. 2. Significant differences between vitiligo patients and normal controls were found in the inci dence of anti-pigment cell antibodies. The antibodies were predominantly directed to melanocyte antigens of 110 kD, 65 kD, 45 kD and melanoma cell antigens of 110 kD, 103 kD, 88kD, 70 kD, 56 kD, 41 kD. 3. The titer of anti piment cell antibodies showed a tendency to decrease after PUVA treat- ment in most patients regardless of clinical improvement. Conclusion ; PUVA treated sera induced proliferation of melanocytes and fibroblasts and the production of aut,oantibodies was suppressed against pigment cell antigens through irnmunosuppression, which might help in the repigmentation of vitiligo.
Antibodies ; Autoantibodies ; Candida* ; Classification* ; DNA* ; Electrophoresis, Polyacrylamide Gel ; Fibroblasts ; Ficusin ; Humans ; Immunoblotting ; Incidence ; Intercellular Signaling Peptides and Proteins ; Keratinocytes ; Melanocytes ; Melanoma ; Thymidine ; Ultraviolet Rays ; Vitiligo

PURPOSE: Occupational stress is a determinant risk factor for cardiovascular disease and work disability. This study aims to describe occupational stress and identify its related factors among aged security guards. METHODS: A random sample of 76 aged security guards were interviewed by three research assistants. The criteria of the subjects were as follows : 50 or older male with 40 or more working hours a week working with colleagues ranged from 3 to 50. The data were collected in September, 2007 and analyzed by multiple regression using SAS Version 9.1. RESULTS: The mean score of occupational stress among aged security guards was 47.2. The mean scores of its sub-scales were 31.3(physical environment), 33.8(occupational demand), 80.8occupational control), 44.6(interpersonal conflict), 51.3 (occupational insecurity), 53.6(occupational system), 57.5(lack of reward), and 30.3(work environment). The scores of occupational control, interpersonal conflict, and occupational insecurity were higher than the scores of Korean average occupational stress sub-scales. Significant variables affecting occupational stress and its sub-scales were work place, work type, and employment type. CONCLUSION: In order to reduce occupational stress among security guards, sufficient occupational control and interpersonal conflict control, appropriate reward, and employment stability should be considered. Also long working hours and work shift should be improved.
Aged ; Cardiovascular Diseases ; Employment ; Humans ; Hypogonadism ; Male ; Mitochondrial Diseases ; Ophthalmoplegia ; Phenothiazines ; Reward ; Risk Factors ; Workplace

PURPOSE: Occupational stress is a determinant risk factor for cardiovascular disease and work disability. This study aims to describe occupational stress and identify its related factors among aged security guards. METHODS: A random sample of 76 aged security guards were interviewed by three research assistants. The criteria of the subjects were as follows : 50 or older male with 40 or more working hours a week working with colleagues ranged from 3 to 50. The data were collected in September, 2007 and analyzed by multiple regression using SAS Version 9.1. RESULTS: The mean score of occupational stress among aged security guards was 47.2. The mean scores of its sub-scales were 31.3(physical environment), 33.8(occupational demand), 80.8occupational control), 44.6(interpersonal conflict), 51.3 (occupational insecurity), 53.6(occupational system), 57.5(lack of reward), and 30.3(work environment). The scores of occupational control, interpersonal conflict, and occupational insecurity were higher than the scores of Korean average occupational stress sub-scales. Significant variables affecting occupational stress and its sub-scales were work place, work type, and employment type. CONCLUSION: In order to reduce occupational stress among security guards, sufficient occupational control and interpersonal conflict control, appropriate reward, and employment stability should be considered. Also long working hours and work shift should be improved.
Aged ; Cardiovascular Diseases ; Employment ; Humans ; Hypogonadism ; Male ; Mitochondrial Diseases ; Ophthalmoplegia ; Phenothiazines ; Reward ; Risk Factors ; Workplace