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Roles and Regulation of Gastrointestinal Eosinophils in Immunity and Disease
Jung, YunJae,Rothenberg, Marc E. American Association of Immunologists 2014 Journal of Immunology Vol. No.
<P>Eosinophils have historically been considered to be destructive end-stage effector cells that have a role in parasitic infections and allergic reactions by the release of their granule-derived cytotoxic proteins. However, an increasing number of experimental observations indicate that eosinophils also are multifunctional leukocytes involved in diverse inflammatory and physiologic immune responses. Under homeostatic conditions, eosinophils are particularly abundant in the lamina propria of the gastrointestinal tract, where their involvement in various biological processes within the gastrointestinal tract has been posited. In this review, we summarize the molecular steps involved in eosinophil development and describe eosinophil trafficking to the gastrointestinal tract. We synthesize the current findings on the phenotypic and functional properties of gastrointestinal eosinophils and the accumulating evidence that they have a contributory role in gastrointestinal disorders, with a focus on primary eosinophilic gastrointestinal disorders. Finally, we discuss the potential role of eosinophils as modulators of the intestinal immune system.</P>
Jung, YunJae The Korean Society for Microbiology 2016 Journal of Bacteriology and Virology Vol.46 No.1
Brown adipose generates heat via oxidation of fatty acids by a mitochondrial uncoupling protein 1 (UCP1)-dependent process. In addition, a subpopulation of cells within subcutaneous white adipose tissue, known as beige adipocytes, also plays a role in thermogenesis. The biogenesis of beige adipocytes is induced by thermogenic signals, such as chronic cold exposure. Recently, it has been reported that eosinophils, type 2 cytokines of IL-4/13, and alternatively activated macrophages control the thermogenic cycle of beige adipocytes. Alternatively, activated macrophages induce $UCP1^+$ beige adipocytes through secretion of catecholamines. These results define the role of type 2 immune responses in the regulation of energy homeostasis.
씬 클라이언트 환경에서 터미널 서비스를 위한 적응적 서버 클러스터링
정윤재(Yunjae Jung),곽후근(Hukeun Kwak),정규식(Kyusik Chung) 한국정보과학회 2004 한국정보과학회 학술발표논문집 Vol.31 No.1A
수십 대의 PC들로 구성된 학교 PC 실 또는 교육 목적 PC 실에서는 컴퓨터들이 분산 구조로 되어 있어서 각 컴퓨터별로 셋업, 유지보수, 업그레이드가 각각 따로따로 수행된다. 이러한 분산 구조에 대한 대안으로 씬 클라이언트 컴퓨팅 환경을 고려해 볼 수 있다. 씬 클라이언트 컴퓨팅 환경에서, 클라이언트 쪽 장치는 사용자에게 친숙한 GUI 와 멀티미디어 지원과 함께 주로 IO 기능들을 제공하는 반면에 터미널 서버라 불리는 원격 서버들은 컴퓨팅 파워를 제공한다. 이 환경에서는 많은 클라이언트를 지원하기 위해서 터미널 서버들을 클러스터로 구성할 수 있다. 그러나 이러한 구조에서는 터미널 세션의 유지와 사용자의 다양한 컴퓨팅 사용 패턴 요인으로 부하 분산이 어렵고 결과적으로 터미널 서버 자원의 활용도가 낮아지는 단점을 가진다. 이러한 단점을 보완하기 위해 본 논문에서는 적응적 터미널 클러스터를 제안한다. 이 구조에서는 부하가 적은 그룹에 속한 터미널 서버가 부하가 큰 그룹으로 실시간에 동적으로 재 할당될 수 있다. 제안된 적응적 터미널 클러스터를 일반적인 터미널 클러스터와 그룹 기반 비적응적 터미널 클러스터와 비교하고 실험을 통해 제안된 방법의 유효성을 검증하였다.
씬 - 클라이언트 환경에서의 터미널 서비스를 위한 적응적 서버 클러스터링
정윤재(Yunjae Jung),곽후근(Hukeun Kwak),정규식(Kyusik Chung) 한국정보과학회 2004 정보과학회논문지 : 정보통신 Vol.31 No.6
수십 대의 PC들로 구성된 학교 PC실 또는 교육 목적 PC실에서는 컴퓨터들이 분산 구조로 되어 있어서 각 컴퓨터별로 셋업, 유지보수, 업그레이드가 각각 따로따로 수행된다. 이러한 분산 구조에 대한 대안으로 씬 클라이언트 컴퓨팅 환경을 고려해 볼 수 있다. 씬 클라이언트 컴퓨팅 환경에서, 클라이언트 쪽 장치는 사용자에게 친숙한 GUI와 멀티미디어 지원과 함께 주로 IO 기능들을 제공하는 반면에 터미널 서버라 불리는 원격 서버들은 컴퓨팅 파워를 제공한다. 이 환경에서는 많은 클라이언트를 지원하기 위해서 터미널 서버들을 클러스터로 구성할 수 있다. 그러나 이러한 구조에서는 터미널 세션의 유지와 사용자의 다양한 컴퓨팅 사용 패턴 요인으로 부하 분산이 어렵고 결과적으로 터미널 서버 자원의 활용도가 낮아지는 단점을 가진다. 이러한 단점을 보완하기 위해 본 논문에서는 적응적 터미널 클러스터를 제안한다. 이 구조에서는 부하가 적은 그룹에 속한 터미널 서버가 부하가 큰 그룹으로 실시간에 동적으로 재 할당될 수 있다. 제안된 적응적 터미널 클러스터를 일반적인 터미널 클러스터와 그룹 기반 비적응적 터미널 클러스터와 비교하고 실험을 통해 제안된 방법의 유효성을 검증하였다. In school PC labs or other educational purpose PC labs with a few dozens of PCs, computers are configured in a distributed architecture so that they are set up, maintained and upgraded separately. As an alternative to the distributed architecture, we can consider a thin-client computing environment. In a thin-client computing environment, client side devices provide mainly I/O functions with user friendly GUI and multimedia processing support whereas remote servers called terminal server provide computing power. In order to support many clients in the environment, a cluster of terminal servers can be configured. In this architecture, it is difficult due to the characteristics of terminal session persistence and different pattern of computing usage of users so that the utilization of terminal server resources becomes low. To overcome this disadvantage, we propose an adaptive terminal cluster where terminal servers are partitioned into groups and a terminal server in a light-loaded group can be dynamically reassigned to a heavy-loaded group at run time. The proposed adaptive scheme is compared with a generic terminal service cluster and a group based non-adaptive terminal server cluster. Experimental results show the effectiveness of the proposed scheme.
Small intestinal eosinophils regulate Th17 cells by producing IL-1 receptor antagonist
Sugawara, Reiko,Lee, Eun-Jung,Jang, Min Seong,Jeun, Eun-Ji,Hong, Chun-Pyo,Kim, Jung-Hwan,Park, Areum,Yun, Chang Ho,Hong, Sung-Wook,Kim, You-Me,Seoh, Ju-Young,Jung, YunJae,Surh, Charles D.,Miyasaka, Ma The Rockefeller University Press 2016 The Journal of experimental medicine Vol.213 No.4
<▼1><P>Jang et al. show that eosinophils in the small intestine can suppress Th17 cell differentiation through the secretion of the IL-1 receptor antagonist.</P></▼1><▼2><P>Eosinophils play proinflammatory roles in helminth infections and allergic diseases. Under steady-state conditions, eosinophils are abundantly found in the small intestinal lamina propria, but their physiological function is largely unexplored. In this study, we found that small intestinal eosinophils down-regulate Th17 cells. Th17 cells in the small intestine were markedly increased in the ΔdblGATA-1 mice lacking eosinophils, and an inverse correlation was observed between the number of eosinophils and that of Th17 cells in the small intestine of wild-type mice. In addition, small intestinal eosinophils suppressed the in vitro differentiation of Th17 cells, as well as IL-17 production by small intestinal CD4<SUP>+</SUP> T cells. Unlike other small intestinal immune cells or circulating eosinophils, we found that small intestinal eosinophils have a unique ability to constitutively secrete high levels of IL-1 receptor antagonist (IL-1Ra), a natural inhibitor of IL-1β. Moreover, small intestinal eosinophils isolated from IL-1Ra−deficient mice failed to suppress Th17 cells. Collectively, our results demonstrate that small intestinal eosinophils play a pivotal role in the maintenance of intestinal homeostasis by regulating Th17 cells via production of IL-1Ra.</P></▼2>
The Korean Association of Immunologists 2015 Immune Network Vol.15 No.6
<P>Purification of enough numbers of circulating eosinophils is difficult because eosinophils account for less than 5% peripheral blood leukocytes. Human eosinophilic leukemia EoL-1 cells have been considered an <I>in vitro</I> source of eosinophils as they can differentiate into mature eosinophil-like cells when incubated with dibutyryl cAMP (dbcAMP) or butyric acid. In this study, the viability and phenotypic maturation of EoL-1 cells stimulated by either dbcAMP or butyric acid were comparatively analyzed. After treatment with 100 µM dbcAMP or 0.5 µM butyric acid, EoL-1 cells showed morphological signs of differentiation, although the number of nonviable EoL-1 cells was significantly increased following butyric acid treatment. Stimulation of EoL-1 cells with 0.5 µM butyric acid more effectively induced the expression of mature eosinophil markers than stimulation with dbcAMP. These results suggest that treatment of EoL-1 cells with 0.5 µM butyric acid for limited duration could be an effective strategy for inducing their differentiation. Considering that expression of CCR3 was not sufficient in EoL-1 cells stimulated with 0.5 µM butyric acid, treatment of the chemically stimulated EoL-1 cells with cytokines, which primarily support eosinophil maturation, would help to obtain differentiated EoL-1 cells with greater functional maturity.</P>