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Chang-Min Kim,Seongkook Heo,Kyeongah Jeong,Youn-Kyung Lim 한국HCI학회 2016 한국HCI학회 학술대회 Vol.2016 No.1
As computers are becoming more wearable and ubiquitous, design methods using interactive prototypes have also been evolved to support in-the-wild design and evaluation in the early design stage. However, current prototype-based design methods are still complex and difficult to use for designers without programming knowledge. It is even more challenging to bring out those prototypes in the actual inthe- wild situation. In this paper, we propose a novel design method called Formula One, which supports quick and easy development of interactive prototype by using the video call functionalities of consumer smart mobile appliances. The Formula One method consists of two-stages, which are Pit Stop and Drive that a user and designers design and modify a prototype and test it, respectively. Through a pilot study, we observed potential benefits of our method in exploring different interaction modalities, finding usability concerns that can be raised while in the wild to define design guidelines.
Liang, Zhe Long,Kang, Kyeongah,Yoon, Sukjoon,Huang, Song Mei,Lim, Jae Sung,Kim, Jin Man,Lim, Jong-Seok,Lee, Hyo Jin Raven Press 2012 Annals of Surgical Oncology Vol.19 No.8
<P>Although NDRG2 is a candidate tumor suppressor, its exact role in renal cell carcinoma (RCC) is not fully understood. We investigated the functional role of NDRG2 and its clinical relevance in RCC tumorigenesis.</P>
Nam, Sorim,Kang, Kyeongah,Cha, Jae Seon,Kim, Jung Woo,Lee, Hee Gu,Kim, Yonghwan,Yang, Young,Lee, Myeong-Sok,Lim, Jong-Seok Society for Leukocyte Biology 2016 Journal of leukocyte biology Vol.100 No.6
<P>Myeloid-derived suppressor cells (MDSCs) are immature cells that do not differentiate into mature myeloid cells. Two major populations of PMN-MDSCs (Ly6G(high)Ly6C(low)Gr1(high)CD11b(+)) andMO-MDSCs (Ly6G(-)Ly6C(high)Gr-1(int)CD11b(+)) have an immune suppressive function. Interferon regulatory factor 4 (IRF4) has a role in the negative regulation of TLR signaling and is associated with lymphoid cell development. However, the roles of IRF4 in myeloid cell differentiation are unclear. In this study, we found that IRF4 expression was remarkably suppressed during the development of MDSCs in the tumor microenvironment. Both the mRNA and protein levels of IRF4 in MDSCs were gradually reduced, depending on the development of tumors in the 4T1 model. siRNA-mediated knockdown of IRF4 in bone marrow cells promoted the differentiation of PMN-MDSCs. Similarly, IRF4 inhibition in bone marrow cells using simvastatin, which has been known to inhibit IRF4 expression, increased PMN-MDSC numbers. In contrast, IRF4 overexpression in bone marrow cells inhibited the total numbers of MDSCs, especially PMN-MDSCs. Notably, treatment with IL-4, an upstream regulator of IRF4, induced IRF4 expression in the bone marrow cells, and consequently, IL-4-induced IRF4 expression resulted in a decrease in PMN-MDSC numbers. Finally, we confirmed that IRF4 expression in MDSCs can modulate their activity to inhibit T cell proliferation through IL-10 production and ROS generation, and myeloid-specific deletion of IRF4 leads to the increase of MDSC differentiation. Our present findings indicate that IRF4 reduction induced by tumor formation can increase the number of MDSCs, and increases in the IRF4 expression in MDSCs may infringe on the immune-suppressive function of MDSCs.</P>