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모델링 기반 가상현실 활용 방안 연구 : 디자인 프리젠테이션을 중심으로
나인용,김영숙,계재영 대구보건대학 2005 대구보건대학 論文集 Vol.25 No.-
These days many informations are delivered through web by the development of internet. But those are delivered only limited informations by two dimensional informations. Recently three dimensional virtual reality is applied to many parts in order to overcome these points. The development of virtual reality technology based on web shows several possibilities through design department. The three dimension virtual reality model which can help good understandings through design development process and presentation. Also it can be used as a tool of decision making. So I classified the virtual reality into the modeling based virtual reality, surveyed the characters and the application cases of them, and compared the characters of them. And I'm going to discuss the utility of virtual reality technology based on modeling through environmental and interior design department.
Kim, Ju Young,Lee, Ra Ham,Kim, Tae Min,Kim, Dong-Wook,Jeon, Young-Joo,Huh, Sung-Ho,Oh, Se-Yeong,Kyba, Michael,Kataoka, Hiroshi,Choi, Kyunghee,Ornitz, David M.,Chae, Jung-Il,Park, Changwon American Society of Hematology 2014 Blood Vol.124 No.19
<P>In this study, we report that OVOL2, a C<SUB>2</SUB>H<SUB>2</SUB> zinc finger protein, is a novel binding protein of ER71, which is a critical transcription factor for blood and vessel development. OVOL2 directly interacted with ER71, but not with ETS1 or ETS2, in the nucleus. ER71-mediated activation of the <I>Flk1</I> promoter was further enhanced by OVOL2, although OVOL2 alone failed to activate it. Consistently, coexpression of ER71 and OVOL2 in differentiating embryonic stem cells led to a significant augmentation of FLK1<SUP>+</SUP>, endothelial, and hematopoietic cells. Such cooperative effects were impaired by the short hairpin RNA-mediated inhibition of <I>Ovol2</I>. Collectively, we show that ER71 directly interacts with OVOL2 and that such interaction is critical for FLK1<SUP>+</SUP> cell generation and their differentiation into downstream cell lineages.</P>
놀이치료자의 평가염려 완벽주의가 수퍼비전 만족도에 미치는 영향에서 수퍼비전 관계에 의해 조절된 수치심의 매개효과
김라영(Ra-Yeong Kim),진미경(Mi-Kyoung Jin) 한국아동심리치료학회 2024 한국아동심리치료학회지 Vol.19 No.1
This study aims to examine the mediating effect of shame, moderated by subfactors of the supervisory relationship (i.e., safe base, reflective education, and structure), on the causational relationship between evaluative concerns perfectionism and supervisory satisfaction of play therapists. The subjects of this study is 197 play therapists with experience of working at child counseling centers in South Korea, each with the minimum of three supervision sessions. Data analysis was conducted using SPSS 26.0 and Hayes’s Process Macro ver. 4.2. The results revealed a significant correlation of evaluative concerns perfectionism, shame, supervisory relationship (i.e., safe base, reflective education, structure), and supervisory satisfaction. The study also found that shame, moderated by subfactors of the supervisory relationship, mediated the relationship between evaluative concerns perfectionism and supervisory satisfaction. Furthermore, reflective education and structure of the supervisory relationship demonstrated an essential moderated mediating effect. This study suggests that to mitigate the adverse impact of evaluative concerns perfectionism on supervisory satisfaction through shame, it is imperative to provide systematic and structured supervision, accompanied by appropriate feedback that fosters internal reflection.
풀무치 유래 항균 펩타이드 locustacin의 항염증 활성
최라영(Ra-Yeong Choi),이준하(Joon Ha Lee),서민철(Minchul Seo),김인우(In-Woo Kim),황재삼(Jae-Sam Hwang),김미애(Mi-Ae Kim) 한국생명과학회 2021 생명과학회지 Vol.31 No.10
본 연구는 lipopolysaccharide (LPS)로 자극된 RAW264.7 세포에 대한 풀무치 유래 항균 펩타이드 locustacin의 항염증 메커니즘을 조사하였다. Locustacin (50, 100, 200 μg/ml)은 세포 독성 없이 LPS로 자극된 대식세포의 nitric oxide (NO) 생성을 유의하게 감소시켰고, 단백질과 mRNA 수준에서 inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2)와 같은 전염증 매개체의 발현을 억제하였다. Locustacin은 LPS 처리로 증가된 염증성 사이토카인인 interleukin (IL)-6 및 IL-1β 함량과 이들의 유전자 발현을 모든 처리 농도에서 농도의존적으로 감소시켰다. 한편, LPS에 의해 인산화된 extracellular signal regulated kinase (ERK), p38 및 c-Jun N-terminal kinase (JNK)는 locustacin (100, 200 μg/ml) 처리로 억제되었다. 또한, LPS에 의해 유도된 inhibitory kappa B alpha (IκB-α)의 분해를 locustacin이 단백질 수준에서 억제한다는 것을 발견했다. 결론적으로, locustacin은 LPS 처리된 대식세포에서 mitogen-activated protein kinases (MAPKs) 인산화, nuclear factor kappa B (NF-κB) 활성화 및 하위 염증매개체를 억제함으로써 항염증 효과를 가지고 있음을 확인하였다. 이러한 결과들은 풀무치 전사체 분석을 통해 확인된 locustacin이 항염증제 후보물질로서 개발 가능성이 있음을 제시한다. Locusta migratoria is a widespread locust species in many parts of the world and is considered an alternative source for the production of protein for value-added ingredients. We previously identified putative antimicrobial peptides derived from L. migratoria through an in silico analysis of its transcriptome. However, its anti-inflammatory effect has not been studied. In this study, we investigated the anti-inflammatory activities of the antimicrobial peptide locustacin (KTHILSFFPSFLPLFLKK-NH₂) derived from L. migratoria on lipopolysaccharide (LPS)-stimulated RAW264.7 macrophage cells. Locustacin (50, 100, and 200 μg/ml) significantly reduced the production of nitric oxide (NO) in LPS-stimulated macrophages without any cytotoxicity. Locustacin also inhibited the mRNA and protein expression of pro-inflammatory mediators, such as inducible NO synthase and cyclooxygenase-2, in contrast to the presence of LPS alone. Locustacin decreased the release of LPS-induced pro-inflammatory cytokines, including interleukin (IL)-6 and IL-1β, and their gene expression in a dose-dependent manner. Furthermore, locustacin (100 and/or 200 μg/ml) inhibited phosphorylation levels of extracellular signal regulated kinase, p38, and c-Jun N-terminal kinase. Locustacin also suppressed the degradation of inhibitory kappa B alpha, which was considered to be an inhibitor of nuclear factor kappa B (NF-κB). Collectively, these results demonstrate that locustacin can exert anti-inflammatory effects through the inhibition of mitogen-activated protein kinase (MAPK) phosphorylation, activation of NF-κB, and downstream inflammatory mediators in LPS-stimulated macrophage cells.