BACKGROUND: Each kind of human cell has its own characteristic morphological and functional property. In the skin, epidermal cells, including keratinocyte and melanocyte, also have their own functional characteristics. Thus, it is expected that there are some different responses to external stimuli, such as ionizing radiatio,, free radicals, and cytokines between these cells. OBJECTIVE AND METHODS: To im estigate whether there are different effects of UV light on the viability of cultured human ker tinocytes and rnelanocytes. Cultured human keratinocytes and melanocytes are irradiated by UVB at 5, 25, 50, and 100mJ/cm, and examined by Methylthiazole tetrazollium assay at 0, 1, 3, 6, 24, 48, and 72 hours after UVB exposure. RESULTS: 1. The effects on viability according to the doses of UVB are as follows: 1) In the keratinocytes, the viability was increased in most of the UVB exposure groups within 24 hours after UVB exposure, and was significantly increased at 25, 50, and 100mJ/cm of UVB at 3 hours after UVB exposur.(p<0.05). However, the viability was significantly decreased at relatively high doses of UVB (50, 100mJ/cm) from 48 hours after UVB exposure (p<0.05). 2) In the melanocytes, the viability was decreased in all of the UVB exposure groups within 3 hours, and was significantly decreased in all of the UVB exposure groups at, 1 hour after UVB exposure (p<0.05). The viability was increased from 6 to 24 hours, which was significantly decreased at 100mJ/cm of UVB from 48 hours after UVB exposure (p<0.05). 2. The effects on viability according to the time after UVB exposure at the same dose of UUB In both cells, the viability was increased as time went by. The slopes of the viability curve gradually decreased according to the increment of UVB doses. CONCLUSION: The viability of keratinocyte was decreased at 50mJ/cm of UVB which melanocyte did not show decrease. Melanocyte was more easily damaged than keratinocyte in relatively earlier time period after UVB exposure. These results suggest that the change of viability in cultured keratinocyte and melanocyte after UVB exposure at the dose of less than 100mJ/cm is related to the time course after UVB exposure as well as to the UVB dose.
Cytokines ; Free Radicals ; Humans* ; Keratinocytes* ; Melanocytes* ; Skin ; Ultraviolet Rays

No abstract available.
Incisor*

Vitiligo is an acquired systemic disease of the skin characterized by circumscribed patches of complete pigment loss due to destruction of melanocytes. A 28-year old male patient presented with generalized depigmented patchs. We performed microscopic studies of cultured melanocytes from this patient and compared them with those of normal neonatal foreskin. Phase contrast microscopic findings revealed no difference between the two groups of melanocytes, but transmission electron microscopic findings showed dilated circular rough endoplasmic reticulum in cultured melanocytes from our vitiligo patient. We could observe the innate cellular structural aberration of melanocytes from the vitiligo subject.
Adult ; Endoplasmic Reticulum, Rough ; Foreskin ; Humans* ; Male ; Melanocytes* ; Skin ; Vitiligo*

Pityriasis Rubra Pilaris is a rare, chronic, mildly inflammatory disease characterized by fine acuminate follicular papules with orange-red to salmon-colored scaling of the skin and erythroderma that surround islands of normal, uninvolved skin, particular in the trunk. Most patients also develop palmoplantar hyperkeratosis in the early course of the disease. Focal acantholysis occurring in pityriasis rubra pilaris is an unusual and incidental histologic finding within the spectrum of histologic change of the disease. No case featuring this concomitant histologic finding has been reported in the Korean literatures up to date. We report a case of focal acantholysis occurring in a patient with the clinical features of pityriasis rubra pilaris which may be considered as an incidental finding.
Acantholysis* ; Dermatitis, Exfoliative ; Humans ; Incidental Findings ; Islands ; Pityriasis Rubra Pilaris* ; Pityriasis* ; Skin

No abstract available.
Embryonic Structures* ; Extremities*

BACKGROUND: Human growth hormone(hGH) plays a central role in linear bone growth and body metabolism. Its mitogenic effect in human tissues is mediated via direct and indirect actions. As proposed by the "somatomedin hypothesis", many circulating GH-mediated effects are exerted indirectly and systemically via stimulation of hepatic synthesis of insulin-like growth factor 1(IGF-1). Given additional evidences for the expression of growth hormone receptor(GH-R) and IGF-1 receptor(IGF-1R) on many target tissues including keratinocytes, melanocytes, and fibroblasts, it is now evident that the GH can act via systemic IGF-1 secreted by the liver and locally produced IGF-1, as well as directly through the GH receptor. OBJECTIVE: The purpose of this study was to investigate not only the effect of IGF-1 on the morphologic changes, proliferation, and melanization of cultured human melanocytes but also on its signal transduction pathway through the IGF-1R. METHODS: Melanocytes were exposed to IGF-1 at 10, 25, 50, 75, 100ng/ml and we examined the changes of cell morphology, number of cells, [3H]-thymidine incorporation, MTS assay, and melanization according to the concentrations and exposure times of IGF-1. Also, the activity of p44/42 MAPK/ERK according to the various exposure times of IGF-1(25ng/ml) was examined using the Western blotting method to find out about the signal transdution pathway of IGF-1. RESULTS: The results were as follows: 1. There were no significant morphological changes of cells between the control and experimental groups according to the concentrations and exposure times of IGF-1. 2. The effects on melanocytes according to the concentrations of IGF-1 5 days after adding IGF-1 : 1) The number of cells, [3H]-thymidine incorporation, and MTS assay were significantly higher than those of control group in all experimental groups(p<0.05). 2) The melanin content showed an insignificant decrease in all experimental groups. 3) The melanocytes responded independent of the IGF-1 concentration in the assay of cell number, [3H]-thymidine incorporation and MTS. 3. The effects on melanocytes according to the exposure times(3 days, 5 days, 7 days) of IGF-1(25 ng/ml) : 1) The number of cells, [3H]-thymidine incorporation, and MTS assay increased as time went by, and was significantly higher than those of control group at all exposure times(p<0.05). 2) The melanin content decreased after exposure of IGF-1, especially that of 3 days exposure group showed a significant decrease(p<0.05). 4. The activities of p44/42 MAPK/ERK increased suddenly at 5 minutes with a peak at 60 minutes and then abruptly decreased at 120 minutes after adding IGF-1 CONCLUSION: In summary, this study demonstrates that IGF-1 has no effect on the morphology, but it does increase the proliferation and slightly decrease the melanization of cultured human melanocytes. In addition, it is suggested that IGF-1 plays a role in regulation of proliferation of melanocytes via the receptor PTK pathway with activation of p44/42 MAPK/ERK.
Blotting, Western ; Bone Development ; Cell Count ; Fibroblasts ; Growth Hormone ; Humans* ; Insulin-Like Growth Factor I* ; Keratinocytes ; Liver ; Melanins ; Melanocytes* ; Metabolism ; Signal Transduction

The authors investigated the antiproliferative effect and expression of HLA-DR an- tigen by recombinant gamma-interferon (r-IFN-y) on cultured human keratinocytes (KC). The results were as follows, 1. From 10l.J/ml of r-1FN-p exposure, the proliferation of KC decreased in a concentration dependent fashion. But there was little difference of antiproliferative effect above 30U/ml of r-IFN-y exposure. 2. The expression of HLA-DR antigen on KC increased in a concentration and time dependent fashion of r-IFN-p exposure. E3ut t,here was little difference of HLA-DR antigen expression on KC above 30tJ/ml and most of HLA-DR antigen were expressed within 48hr. 3. The opt,imal condition for HLA-DR antigen induction on KC by r-IFN-p was likely t,hat HLA-DR KC was observed at 48hr under the our exposure of 30U/ml of r-IFN p. 4. After 4hr exposure of 30U/ml of r-IFN-p, KC expresed HLA-BR. antigen, reaching a maximum intensity at 3 days. At, 7 days, the loss of HI A-DR KC showed over 90% of maximum intensity.
HLA-DR Antigens* ; Humans* ; Interferon-gamma ; Interferons* ; Keratinocytes*

No abstract available.

Addison's disease is a rare disorder resulted from a chronic deficiency of the adreanl cortical hormone. The clinical manifestations are general weakness, weight loss, hyperpigmentation, hypovolemia with hyponatremia and hyperkalemia. We report a case of Addison's disease in a 60-year-old woman who has experienced slowly progressive weakness, weight loss and generalized cutaneous pigmentation, especially sun exposed area, extensor surface and nail bed for the last, 2 years. On a hormonal assay of the adrenal glands, basal plasma cortisol level was decreased and basal plasma ACTH level was markedly elevated. A chest X-ray showed streaky tuberculous infiltration in left, upper lobe field and adrenal CT scan showed calcific densities of both adrenal glands with nodular enlargement of right adrenal gland. There was a clinical improvement with steroid replacement therapy and anti-tuber- culosis chemotherapy. A nearly normal appearance was obtained after 5 months' treatment.
Addison Disease ; Adrenal Glands ; Adrenocorticotropic Hormone ; Drug Therapy ; Female ; Humans ; Hydrocortisone ; Hyperkalemia ; Hyperpigmentation ; Hyponatremia ; Hypovolemia ; Middle Aged ; Pigmentation ; Plasma ; Solar System ; Thorax ; Tomography, X-Ray Computed ; Weight Loss

Background and purpose: Transient global amnesia (TGA) is a rare amnestic syndrome characterized by the sudden onset of a selective anterograde and retrograde amnesia with a time course of up to 24 hours. Recent studies have found a high frequency of small high-signal abnormalities in the hippocampus on diffusion-weighted imaging (DWI), and accordingly ischemia has been proposed as an etiology of TGA. We hypothesized that TGA lesions occur preferentially in the CA1 region of the hippocampus, which is known to be susceptible to ischemia. Methods: Twenty consecutive patients with a clinical diagnosis of TGA underwent DWI both within 24 hours of symptom onset and 3 days later. Twenty patients with high-signal abnormalities in the hippocampus on the initial DWI underwent subsequent DWI and T2-weighted imaging in the coronal plane to precisely localize the lesions. Results: Seventeen patients had small high-signal abnormalities (with diameters of 1-3 mm) in the hippocampus unilaterally on DWI. One of these patients had two lesions in one hippocampus. Three of the 20 patients had lesions bilaterally in the hippocampus, 1 of whom had 3 bilateral lesions. A total of 25 lesions were identified: 5 in the hippocampal head, 19 in the body, and 1 in the tail. Six patients had unilateral lesions on the left,11 patients had them on the right, and 3 patients had bilateral lesions. Conclusions: In this study, lesions associated with TGA were localized mostly to the lateral portion of the hippocampus, corresponding to CA1. This finding supports the ischemic etiology of TGA, but the underlying pathophysiologic mechanism requires further investigation.
Amnesia, Retrograde ; Amnesia, Transient Global ; Head ; Hippocampus ; Humans ; Ischemia