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

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*

No abstract available.
Animals ; Asian Continental Ancestry Group* ; Cricetinae ; Cricetulus* ; Female ; Humans* ; Ovary*

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

We report a case of mycosis fungoides with small follicular papules and plaques on the trunk. Histopathological findings showed lymphocytic infiltration within and around the follicular epithelium and Pautrier's microabscess in the epidermis. Immunohistochemical studies showed atypical T lymphocytes infiltrating the follicles and electron microscopic examination revealed the presence of lymphocytes with large convoluted nuclei around the follicles. These findings suggest that the follicular lesions were specific for a special variant of mycosis fungoides.
Epidermis ; Epithelium ; Lymphocytes ; Mycosis Fungoides* ; T-Lymphocytes

CTLA-4 (=CD152), a T cell activation antigen, has been known to be homologous to CD28 in its molecular and genomic structure. Both of these two molecules are sharing their counterreceptors, B7 (CDSO) and B7-2 (CD86) and are known to play a crucial role in T cell activation. In previous our study it was reported that there are 2 forms of CTLA-4 antigen in activated human T cells, 30 kD membrane-bound form and 34 kD cytosolic-sequestered form and the former was less than 5 % of total of this antigen induced. Aims of this study are to confirm previous finding by using flow cytometry and to characterize the cytoplasmic form of human CTLA-4 by using ultrafiltration and immunoprecipitation techniques. In PHA stimulated peripheral blood lymphocyte surface expression of CTLA-4 was less than 2.1% of any of CD4+, CD8+ and CD56+ subsets. And the 34 kD form of CTLA-4 was detected in CDS+ subset only. This discrepancy confirms that 34 kD antigen is the cytoplasmic form of human CTLA-4. In ultrafiltration and subsequent Western blot analysis study this 34 kD antigen was detected in >100 kD fraction only. And in non-reducing condition this antigen formed high molecular weght complex (MW > 350 kD). In immunoprecipitation study using anti-peptide A antibody it was found that this high molecular weight complex consists of the 34 kD cytoplasmic form of CTLA-4 and previously unknown 54 kD antigen and 46 kD antigen at 1:1:8-10 ratio. And none of these 3 molecules were identified in membrane fraction of activated human T cell. The result of this study implies that CTLA-4 molecule induced upon T cell activation mainly sequestered in cytoplasrn and another signal is necessary to target this antigen on the activated T cell surface.
Antigens, CD27 ; Blotting, Western ; CTLA-4 Antigen ; Cytoplasm* ; Flow Cytometry ; Humans* ; Immunoprecipitation ; Lymphocytes ; Membranes ; Molecular Weight ; T-Lymphocytes ; Ultrafiltration

We report a case of subclavian artery laceration caused by the removal of a pigtail pleural drainage catheter in a patient with a pneumothorax. The patient was successfully resuscitated through diagnostic angiography with subsequent balloon occlusion and primary repair of the injured subclavian artery. Although pigtail drainage of a pneumothorax is known to be safe and effective, proper insertion and removal techniques should be emphasized to reduce the risk of complications.
Angiography ; Balloon Occlusion ; Catheters* ; Drainage ; Hemothorax ; Humans ; Lacerations* ; Pneumothorax* ; Subclavian Artery* ; Thoracostomy

Programrned cell death (PCD), or apoptosis, is a process by which cells die in response to specific physiological and toxicological signals. This genetically programmed form of cellular suicide is intirnately involved in many biological processes including growth, metamorphosis, embryogenesis, and oncogenesis. Cells undergoing PCD in normal and neoplasmic tissues display the following biochemical and morphological features: internucleosomal DNA fragmentation, reduced cell volume, condensed chromatin in nucleus, zeiosis and generation of apoptotic bodies containing intact organelles and plasma rnembrane. Hybridoma cell production, resulting from the fusion of myeloma cells with antibody producing spleen cells, is widely used in various fields of life science. This technique requires hypoxanthine guanine phosphoribosyl transferase (HGPRT) deficient mutant myeloma cell line as a fusion partner. When these mutants cell is treated with aminopterin plus hypoxanthine-thymidine (HAT) after the cell fusion they are selectively and efficiently eliminated remaining fused hybridoma celis. But there hasn't been any report regarding the selective elimination mechanism of this HGPRT mutant myeloma cell. By using HGPRT myeloma P3-X 63-Ag8.653 (V653) as a model system, this study demonstrated that PCD was induced by aminopterin treatment of this V653 cell line. And the sequential ultrastructural changes during this death process were observed by using electron microscope. When V653 cells were incubated with 0.4 uM aminopterin, DNA fragmentation was detectable after 3 hours and peaked between 12 and 18 hours of aminopterin treatment and the cell viability decreased in a time dependant manner. V653 cells incubated with amiopterin showed following ultrastructural changes during the death process. Dilatation of rough endoplasmic reticulum (RER) and detachment of ribosomes were the earliest ultrastructural changes and first seen after 30 minute incubation. Dilatation of perinuclear cisternae began to appear after 1 hour and deformation of nucleoplasm such as decreased electron density of perinuclear heterochromatin and increased electron density of euchromatin were seen after 3 hours. Increased electron density of cytoplasm, decreased cell volume, condensation of chromatin and apoptotic bodies were observed in many cells after 9 hours but vacuolation by severe dilatation of RER was seen in some cells. 24 hours after incubation with aminopterin, many cells showed typical form of apoptosis characterized by cell shrinkage, increased electron density of cytoplasm and apoptotic bodies. On the contrary, some cells showed different type of cell death characterized by increased cell volume, decreased electron density of cytoplasm, severely dilated RER and apoptotic bodies. In both types of cells, mitochondrial cristae and limiting membrane of mitochondria are comparatively well preserved. In other cells, nuclei did not show significant changes but there were deformations of mitochondria such as markedly increased electron density and formation of lamella bodies. The death process of V653 cell was not synchronized among cells. The results of this study proved that aminopterin-induced selective elimination of fusion partner V653 myeloma cell is due to PCD. The earliest ultrastructural changes observed in this process were dilatation of RER and detachment of ribosomes. And there were two distinct morphological types in the PCD.
Aminopterin* ; Animals ; Apoptosis* ; Biological Processes ; Biological Science Disciplines ; Carcinogenesis ; Cell Death ; Cell Fusion ; Cell Line ; Cell Size ; Cell Survival ; Chromatin ; Cytoplasm ; Dilatation ; DNA Fragmentation ; Embryonic Development ; Endoplasmic Reticulum, Rough ; Euchromatin ; Female ; Guanine ; Heterochromatin ; Hybridomas ; Hypoxanthine ; Hypoxanthine Phosphoribosyltransferase ; Membranes ; Mice* ; Mitochondria ; Organelles ; Plasma ; Pregnancy ; Ribosomes ; Spleen ; Suicide ; Transferases

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

No abstract available.
Humans*