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안성훈,김은옥,고대곤 한국컴퓨터교육학회 2004 컴퓨터교육학회 논문지 Vol.7 No.2
본 연구에서는 ICT 교유그의 효과를 높이고자 ICT 활용 학습 과정 시 학습자에게서 나타나는 오류의 사례들을 분석하여 오류 유형을 설정하고 그에 대한 효과적인 처치 방안을 탐색하였다. 관찰, 면담, 설문 조사 등의 방법을 이용하여 오류 사례를 탐색한 결과 기능 혼동 오류, 개념 혼동 오류, 인터페이스 해석 장애 오류, 심리적 불안으로 인한 오류, 학습자 성격 유형에 의한 오류, 습관적인 오류 등 6가지 오류 유형을 설정하였다. 그중 가장 많은 빈도를 차지하는 기능 혼동 오류와 개념 혼동 오류 중심으로 웹 기반 Q&A 학습 시스템을 개발하고 이용한 오류 처치 방안을 제안하였다. 또한 제안한 오류 처치 방안을 현장에 적용하고 그 효과를 검증하였다. In this paper, I analyze error cases a learner made during learning using ICT, set up error types, and search for effective treatment methods in order to enhance the effects of ICT education. I search for error case to use the methodology of the study which is observation, interviews, and survey. I set up the error types which is the error type of confusion with functions, that of confusion with concepts, that of barriers in interface interpretation, that caused by psychological anxiety, that according to learner personality patterns, and habitual error type. The biggest frequency of errors was found in the error type of confusion with function and that of confusion with concepts, whose treatment methods were searched for using the web-based Q&A learning. Also, I apply the error treatment methods on the classroom and prove the effect.
Basic : A case of propylthiouracil-induced acute hepatic failure (초)
( Dae Seon Ahn ),( In Hee Kim ),( Ji Youn Sohn ),( Dae Hun Kwon ),( Kang Hun Koh ),( Bum Soo Jeong ),( Seong Hun Kim ),( Sang Wook Kim ),( Seung Ok Lee ),( Soo Teik Lee ),( Dae Ghon Kim ),( Hee Chul Y 대한간학회 2011 Clinical and Molecular Hepatology(대한간학회지) Vol.17 No.3(S)
Functional Role of BclXL during Parthenolide Induced Apoptosis in Cholangiocarcinoma Cells
( Dae Ghon Kim ),( In Hee Kim ),( Sung Hoon Kim ),( Kyung Ran You ),( Seung Ok Lee ),( Yong Tae Kim ) 대한간학회 2005 Clinical and Molecular Hepatology(대한간학회지) Vol.11 No.3(S)
Aims: Cholangiocarcinomas (CC) are intrahepatic bile duct carcinomas that are known to have a poor prognosis. Sesquiterpene lactone parthenolide, which is the principal active component in medicinal plants, has been used to treat tumors. Parthenolide effe
Shin, Hye-Jun,Park, Young-Ho,Kim, Sun-Uk,Moon, Hyung-Bae,Park, Do Sim,Han, Ying-Hao,Lee, Chul-Ho,Lee, Dong-Seok,Song, In-Sung,Lee, Dae Ho,Kim, Minhye,Kim, Nam-Soon,Kim, Dae-Ghon,Kim, Jin-Man,Kim, Sang American Society for Biochemistry and Molecular Bi 2011 The Journal of biological chemistry Vol.286 No.34
<P>Dysregulation of liver functions leads to insulin resistance causing type 2 diabetes mellitus and is often found in chronic liver diseases. However, the mechanisms of hepatic dysfunction leading to hepatic metabolic disorder are still poorly understood in chronic liver diseases. The current work investigated the role of hepatitis B virus X protein (<I>HBx</I>) in regulating glucose metabolism. We studied HBx-overexpressing (<I>HBx</I>Tg) mice and <I>HBx</I>Tg mice lacking inducible nitric oxide synthase (iNOS). Here we show that gene expressions of the key gluconeogenic enzymes were significantly increased in HepG2 cells expressing HBx (HepG2-<I>HBx</I>) and in non-tumor liver tissues of hepatitis B virus patients with high levels of <I>HBx</I> expression. In the liver of <I>HBx</I>Tg mice, the expressions of gluconeogenic genes were also elevated, leading to hyperglycemia by increasing hepatic glucose production. However, this effect was insufficient to cause systemic insulin resistance. Importantly, the actions of HBx on hepatic glucose metabolism are thought to be mediated via iNOS signaling, as evidenced by the fact that deficiency of <I>iNOS</I> restored HBx-induced hyperglycemia by suppressing the gene expression of gluconeogenic enzymes. Treatment of HepG2-<I>HBx</I> cells with nitric oxide (NO) caused a significant increase in the expression of gluconeogenic genes, but JNK1 inhibition was completely normalized. Furthermore, hyperactivation of JNK1 in the liver of <I>HBx</I>Tg mice was also suppressed in the absence of iNOS, indicating the critical role for JNK in the mutual regulation of HBx- and iNOS-mediated glucose metabolism. These findings establish a novel mechanism of HBx-driven hepatic metabolic disorder that is modulated by iNOS-mediated activation of JNK.</P>
대한간학회지 제8차 춘계학술대회 초록집 : 구연 ; 담관세포암 육종성변화 관련 발현유전자 cDNA Microarray 분석
( Dae Ghon Kim ),( Young Tae Kim ),( Kyung Ran You ),( Win Jing ),( Deuk Soo Ahn ),( Jung Min Lee ),( Jeong Min Lee ),( Hee Chul You ),( Baik Whan Cho ),( Jung Kyoon Choi ),( Sang Soo Kim ) 대한간학회 2002 Clinical and Molecular Hepatology(대한간학회지) Vol.8 No.2(S)
구연 : 간세포암에서 암세포 증식에 관련된 RPL36A 유전자 과발현
( Dae Ghon Kim ),( Kyung Ran You ),( Seung Ok Lee ),( Soo Taek Lee ),( Deuk Soo Ahn ),( Baik Whan Cho ),( Myung Ja Jung ) 대한간학회 2003 Clinical and Molecular Hepatology(대한간학회지) Vol.9 No.3(S)
Background/Aims: Hepatocellular carcinoma (HCC) is a worldwide major malignancy with an increasing incidence. Altered gene expression caused either by mutations or by changes in the regulatory characteristics of HCC compared with corresponding nontumor tissues have been reported. However, these genetic changes reported do not precisely reflect the biological nature or clinical characteristics of all HCCs. Methods: Previously, we identified and reported genes that were differentially expressed in HCC cells using the differential-display PCR method. Among them, we focused preferentially on an up-regulated gene in human HCC in comparison with the nontumor surrounding tissues. We identified a single fragment cDNA (HG23T1) that was over-expressed in a hepatocellular carcinoma (HCC) specimen. We cloned the full-length HG23T1 gene by the rapid amplification of cDNA end (RACE) PCR method. Results: It perfectly matched the gene encoding human ribosomal protein L36A (RPL36A or referred to RPL44). RPL36A mRNA was preferentially over-expressed in 34 of 40 HCC cases (85%, P <0.001) and in all 8 HCC cell lines. Ectotopically over-expressed L36A ribosomal protein localized in the nucleoli of cells and this localization seemed to be controlled by the N-terminal or the internal tetrapeptide consensus with its adjacent N-terminal domain. Over-expression of L36A led to enhanced colony formation and cell proliferation, which may have resulted from rapid cell cycling, and an antisense cDNA effectively reversed these alterations. Conclusions: These results suggest that RPL36A plays a role in tumor cell proliferation and may be a potential target for anticancer therapy of HCC.