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- 저자 : 노성욱(Sung Wook Ro) (검색결과 5 건)
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천태종(Tae Jong Chun),노성욱(Sung Wook Ro),서성준(Seong Jun Seo),송계용(Kye Yong Song),홍창권(Chang Kwun Hong),노병인(Byung In Ro) 대한피부과학회 1999 대한피부과학회지 Vol.37 No.9
We report a case of cutaneous B cell lymphoma in a 65-year-old male who had several bizarre shaped erythematous to brownish plaques on the both shins for 2 months. An abdominal CT scan revealed gastrohepatic ligament, retroperioneal, mesenteric and bilateral external iliac lymphadenopathies. Histologic examinations revealed diffuse dense infiltration of the large arypical cells with vesicular nucleus and prominent nucleoli in the entire dermis. They showed a positiver reaction to the LCA, CD20 and kappa light chain in the immunohistochemical study, suggesting that these neoplastic lymphoid cells are B cell linage. We treated hi, with COPBLAM-V regimen. In the course of treatment, new skin lesions developed on both upper arms and herpes zoster on the left thigh. So we changed the regimen into IMVP-16. No relapses have been found up to the present date for 9 months. (Korean J Dermatol 1999;37(9) : 1330∼1334)
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배양된 정상 인체 각질형성세포에서 자외선 B 조사에 의한 아포프토시스와 p53의 발현
김명남(Myeung Nam Kim),서성준(Seong Jun Seo),홍창권(Chang Kwun Hong),노병인(Byung In Ro),노성욱(Sung Wook Ro),조성인(Sung In Cho) 대한피부과학회 2000 대한피부과학회지 Vol.38 No.4
N/A Cutaneous absorption of ultraviolet B(UVB) in the skin occurs primarily in keratinocyte, causing DNA and protein damage. p53 tumor suppressor gene appeared in the epidermis after UVB irradiation, and the wild type has been known to be responsible for apoptosis and plays an important role in excluding abnormal cells with significant DNA damage. While p53 has been implicated in both DNA repair and apoptosis, it is unclear whether the p53 protein is involved in both of these processes within the same cell. Therefore, UVB-induced apoptosis and changes in p53 expression were studied in cultured normal human keratinocyte to determine that the cellular response to UVB induced DNA damage(DNA repair or apoptosis) correlated with p53 expression. The cultured normal human keratinocytes were irradiated with the doses of UVB(25-150 mJ/cm2) and incubated for various times(3, 6, 12, 24 hour) after radiation. At UVB doses of 100 and 150 mJ/cm2, acridine orange/ethidium bromide(Ao/Eb) staining-positive cells and TUNEL (TdT mediated dUTP-biotin nick end labeling) staining-positive cells increased significantly after 3 hours and 6 hours postirradiation respectively. Twelve hour postirradiation, staining-positive cells increased at each level of UVB-radiation exposure. These results suggest that there were significant influences of UVB doses and time course after irradiation to the number of Ao/Eb and TUNEL staining-positive cells. To determine whether all Ao/Eb and TUNEL-positive cells were actually undergoing apoptosis, cellular DNA was extracted from keratinocytes at 12 hours after UVB irradiation and seperated by electrophoresis on an 2.5% agarose gel to detect the internucleosomal DNA fragmentation(DNA ladder). 'DNA ladder' occurred at every dose of UVB 12 hour after irradiation, but did not appear early after irradiation, suggesting that whether Ao/Eb and TUNEL-positive cells observed early after irradiation were not undergoing apoptosis. Activation of p53 and the response to DNA damage is not observed universally, but is dependent on tissue specificity, species specificity and type of genotoxic damage. To correlate p53 level with UVB-induced apoptosis at the dose of 100mJ/cm2 UVB, p53 levels were determined by western blot analysis. The accumulation of p53 protein was apparent after 6 hours postirradiation, and UVB irradiation caused a dramatic increase in p53 levels at 12 and 24 hours. These results demonstrate that p53 is required for UVB-induced apoptosis in cultured normal human keratinocyte and p53 has a time-dependent effect in the initiation of apoptosis. In this study, the results indicated that a low dose(25mJ/cm2) of UVB irradiation could induce apoptosis in human keratinocyte in vitro and UVB exerts a time-dependent effect on inducing apoptosis. And the results also give support to increasing evidence that p53 may play a role in UVB-induced DNA damage and the induction of apoptosis in cultured normal human keratinocyte and that p53 is involved in the decision process which determines the fate of keratinocyte after UVB -induced DNA damage. (Korean J Dermatol 2000;38(4):481~489)
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원형탈모증과 안드로겐성 탈모증 환자에서 생활사건 스트레스와 대처방식에 관한 연구
서동수,최한규,기백석,노병인,홍창권,김명남,서성준,노성욱 대한피부과학회 1999 大韓皮膚科學會誌 Vol.37 No.6
Background: Psychosocial stress and stressful events in life have been reported to be closely related to the onset and acute exacerbation of some dermatologic disorders, such as alopecia areata, psoriasis, seborrheic dermatitis and atopic dermatitis. However, the nature of the association between stress and dermatologic disorders remains unclear. Objective: The purpose of this study is to determine the relation of stress and the onset and exacerbation of dermatologic disorders. Furthermore we studied whether the coping strategies to stress are related to dermatologic disorders. Method: We examined 30 patients with alopecia areata, 30 patients with androgenetic alopecia who visited Dept. of Dermatology, Chung-Ang University Hospital and a control group of 30 who visited our clinic at the same time for tinea pedis and onychomycosis, which are supposed not to be related to stress. For the evaluation of stress we used questionares of 'Scale of Life Events' and 'Multidimensional Coping Scale'. Results: 1) The score of life event stress in the alopecia areata group was significantly higher than that of the normal control group. The score of life event stress in androgenetic alopecia was higher than that of the normal control group with no statistical significance. 2) In the aspect of coping strategies, the alopecia areata group was significantly higher than the normal control group at the passive withdrawal and fatalism, while int he normal control group, emotional pacification, positive comparison and religious seeking tended to be higher than the alopecia areata group. In the androgenetic alopecia group, no significant pathologic coping strategies were found compared with the control. Conclusion: These findings suggest that the psychosocial stress may play a role in the pathogenesis of alopecia areata and androgenetic alopecia. But to clarify the exact role of stress, further studies about biological parameters of physiologic changes to stress are needed in the future.
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