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The March First Independence Movement of 1919 was one of the most importance turning points in the modern and contemporary history of Korea. It was the time that Korean developed modern nationalism of Western concept. At the same time, it became a incident to specify political and cultural identity of Korea. Since Korea lost her sovereignty, Korean people proclaimed their cultural identity and historical justification to become a respected member of the family of nations. The activities to request independence continued in the United States actively. The efforts to develop the sympathy for Korean independence from Japan by appealing to American public started. With this effort, Korean aimed to develop American political actions to pressure Japan to give up Korea. Fortunately, New York Times showed great interests on this issue through Korean point of view. There were over 50 reports and articles on this newspaper related to the Korean Independence. The March First Independence Movement was an incident started in Korean peninsula and it quickly developed into an Asian and international issue. The movement reflected the Korea's peace-oriented culture based on Asian and international peace through non-violent and peaceful demonstration against barbaric Japanese imperial oppression. This effort of Korean people to achieve independence from Japanese control was spread in America through New York Times. Therefore, the March First Independence Movement of 1919 was one of the most important turning point in Korean modern and contemporary history not just as an incident in Korea, but an international event to express the justification for the independence and cultural identity to the world. 1919년 3·1 독립운동을 통해 서양적 개념의 근대적 국가민족주의가 형성되었고 한국인이라는 정치적, 문화적 정체성이 만들어진 한국 근현대사의 이정표가 되는 사건이었다. 한국인은 주권을 상실한 상태에서 국제무대에서 인정받는 일원이 되기 위해서는 문화적 정체성과 역사적 정당성을 주장했다. 독립을 요구하는 활동이 미국에서도 활발히 진행되었다. 미국의 여론에 호소해 공감대를 형성하고 여론을 바탕으로 정치적 영향을 미칠 수 있는 활동이 계속되었다. 국제적인 위상을 가진 『뉴욕타임즈』는 지속적으로 한국 관련 기사를 실어 한국의 입장을 대변해 주었다. 1919년 한 해 동안 한국 관련 기사는 50여개가 게재되었고 지속적으로 한국 독립을 이슈화 했다. 3·1 독립운동은 한반도에서 일어난 사건이었으나 이는 빠르게 아시아 문제로 또 국제적 문제로 발전했다. 한국의 독립은 아시아와 세계 평화를 기반으로 하고 있는 한국의 평화 지향적 문화의 토대를 3·1 독립운동은 비폭력 평화적 시위로 전 세계에 보여 주었다. 주권회복을 통해 일제로부터 독립하려 했던 한국인의 노력은 미국에서도 『뉴욕타임즈』의 기사를 통해 확산되었다. 이로서 3·1 독립운동은 한국 독립의 당위성과 문화적 정체성을 전 세계에 알린 한국 근현대사의 가장 중요한 사건임이 다시 한 번 증명되었다.
Graft-versus-host disease (GVHD), a life-threatening complication after bone marrow transplantation (BMT), is induced by activation of alloreactive donor T cells. Our previous study demonstrated that transplantation of myeloid differentiation factor 88 (MyD88)-deficient knockout (KO) bone marrow (BM) resulted in aggravation of GVHD. Here, to understand the cellular mechanism, we performed longitudinal in vivo imaging and flow cytometric analyses followed by transcriptome and functional examination of donor MyD88-KO BM progenies in GVHD hosts, using a major histocompatibility complex-matched but minor histocompatibility antigen-mismatched C57BL/6→BALB.B model. In GVHD hosts with MyD88-KO BMT, donor BM-derived CD11b+Gr-1+ cells were found to undergo cell death, a fate significantly different from the explosive expansion shown by the wild type (WT) counterparts, and also from the moderate expansion of the WT or MyD88-KO BM-derived cells in non-GVHD hosts. It was also revealed that MyD88-KO CD11b+Gr-1+ cells preferred differentiation into CD11c+ dendritic cells (DCs) to expansion as myeloid-derived suppressor cells in GVHD hosts or in high inflammatory in vitro conditions. These CD11c+ DCs comprised the majority of MyD88-KO CD11b+Gr-1+ apoptotic cells in GVHD hosts. Their ability to cross-present alloantigens of host origin contributed to the enhancement of T cell alloreactivity, causing GVHD aggravation and eventually death through the killing function of activated T cells. These results provide insights into the roles of MyD88 in myelopoiesis of donor BM and the protective effects in GVHD hosts, helpful information for development of a strategy to control GVHD.
This study proposes basic directions for development of an evaluation model of tourist journal on the basis of literature review and an analysis of characteristics of tourist journals. The main findings are as follows: (a) The tourist journal contains a subjective description of what the tourist sees, hears, and feels. It reflects the tourist's characteristics, world view, and attitude toward tourism. (b) The tourist does not deliberate the three critical elements of tourist needs such as cultural voyeurism, pleasure seeking, and physical and/or psychological relaxation when she/he makes a decision for journey. (c) The tourist does not show a consistency of cultural reception in travel sites. The result supports that an author of a popular tourist journal is not necessarily an export on analysing and understanding local culture.
Indoleamine 2,3-dioxygenases (IDOs) are tryptophan-catabolizing enzymes with immunomodulatory functions. However, the biological role of IDO2 and its relationship with IDO1 are unknown. To assess the relationship between IDO2 and IDO1, we investigated the effects of co-expression of human (h) IDO2 on hIDO1 activity. Cells co-expressing hIDO1 and hIDO2 showed reduced tryptophan metabolic activity compared with those expressing hIDO1 only. In a proteomic analysis, hIDO1-expressing cells exhibited enhanced expression of proteins related to the cell cycle and amino acid metabolism, and decreased expression of proteins related to cell survival. However, cells co-expressing hIDO1 and hIDO2 showed enhanced expression of negative regulators of cell apoptosis compared with those expressing hIDO1 only. Co-expression of hIDO1 and hIDO2 rescued the cell death induced by tryptophan-depletion through hIDO1 activity. Cells expressing only hIDO2 exhibited no marked differences in proteome profiles or cell growth compared with mock-transfectants. Cellular tryptophan metabolic activity and cell death were restored by co-expressing the hIDO2 mutant substituting the histidine 360 residue for alanine. These results demonstrate thathIDO2 plays a novel role as a negative regulator of hIDO1 by competing for heme-binding with hIDO1, and provide information useful for development of therapeutic strategies to control cancer and immunological disorders that target IDO molecules.