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하이퍼텍스트형 조직구조가 지식의 창조와 공유에 미치는 영향
권정미(Jeoung Mi Kweon),최만기(Man Kee Choe) 한국인사조직학회 2004 인사조직연구 Vol.12 No.특별
Nonaka 등의 지식경영이론에 따르면, 지식창조와 지식공유를 유발하기 위한 효과적인 조직은 하이퍼텍스트형 구조를 갖추고 있다. 이는 하이퍼텍스트형 조직구조가 지식의 창조와 공유에 영향을 미침을 의미한다. 그러나 하이퍼텍스트형 조직구조가 지식창조와 공유에 어떠한 영향을 미치는 지를 실증적으로 규명한 연구는 아직 없다. 따라서 본 연구에서는 이의 실증적 규명을 위하여 107개 조직 1,034명에 대한 설문조사 결과를 조직수준에서 구조분석 하였다. 그 결과, 하이퍼텍스트형 조직구조는 지식창조는 물론 지식공윽에 유의한 영향을 미쳤으며, 특히 지식공유에 더 큰 영향을 미치는 것으로 나타났다. 보다 구체적으로는 하이퍼텍스트형 조직구조의 특성중 지식창조를 위해서는 개방된 입체적 구조가, 지식공유를 위해서는 지식영역과의 상호작용이 더욱 요구되는 경향을 보였다. 본 연구에서는 이 결과의 학문적, 실무적 시사점들을 논의하고 있다. According to Nonaka's theories of knowledge management, hypertext organizational structure is effective for creating and sharing knowledge in organizations. Very little empirical research on this however, has been conducted so far. In addition, a model of organizational structure and knowledge management and a measurement tool for empirical investigation. Therefore, this study proposes a model to analyze relationship's between hypertext organizational structure and knowledge creation and sharing based on existing studies and logical extensions. This study also generates hypotheses about the relations based on the model. This study finally collected data trom 1,034 members of 107 companies through a questionnaire survey. According to the analyses of the data, hypertext organizational structure has significantly positive influence on both knowledge creation and sharing. Expecially, the construction of open cubical structure tends to affect strongly to knowledge creation whereas the interaction with knowledge field affects mighty to knowledge sharing. This study discusses the implications of such findings future research ideas and provides.
Lim, Seong-in,Choe, SeEun,Kim, Ki-Sun,Jeoung, Hye-Young,Cha, Ra Mi,Park, Gil-Soon,Shin, Jihye,Park, Gyu-Nam,Cho, In-Soo,Song, Jae-Young,Hyun, Bang-Hun,Park, Bong-Kyun,An, Dong-Jun Elsevier Ltd. 2019 Vaccine Vol.37 No.27
<P><B>Abstract</B></P> <P>Here, we constructed an attenuated live marker classical swine fever (CSF) vaccine (Flc-LOM-BE<SUP>rns</SUP>) to eradicate CSF. This was done by taking infectious clone Flc-LOM, which is based on an attenuated live CSF vaccine virus (LOM strain), and removing the full-length classical swine fever virus (CSFV) E<SUP>rns</SUP> sequences and the 3′ end (52 base pairs) of the CSFV capsid. These regions were substituted with the full-length bovine viral diarrhoea virus (BVDV) E<SUP>rns</SUP> gene sequence and the 3′ end (52 base pairs) of the BVDV capsid gene. Sows were vaccinated with the Flc-LOM-BE<SUP>rns</SUP> vaccine 3 weeks before insemination and then challenged with virulent CSFV at the early, mid- or late stages of pregnancy. We then examined transplacental transmission to the foetuses. Piglets born to sows vaccinated with Flc-LOM-BE<SUP>rns</SUP> did not show vertical infection, regardless of challenge time. In addition, CSFV challenge did not affect the delivery date, weight or length of the foetus. Pregnant sows inoculated with the Flc-LOM-BE<SUP>rns</SUP> vaccine were anti-CSF E<SUP>rns</SUP> antibody-negative and anti-BVDV E<SUP>rns</SUP> antibody-positive. Challenge of pregnant sows with virulent CSFV resulted in anti-CSF E<SUP>rns</SUP> antibody positivity. These results strongly indicate that differential diagnosis can be conducted between the Flc-LOM-BE<SUP>rns</SUP> vaccinated animal and virulent CSFV affected animal by detecting antibody against BVDV E<SUP>rns</SUP> or CSF E<SUP>rns</SUP> gene. Therefore, the Flc-LOM-BE<SUP>rns</SUP> vaccine may fulfil the function of differential diagnosis which required for DIVA vaccine.</P> <P><B>Highlights</B></P> <P> <UL> <LI> The Flc-LOM-BE<SUP>rns</SUP> is live attenuated DIVA vaccine for CSFV. </LI> <LI> The Flc-LOM-BE<SUP>rns</SUP> vaccine protected foetuses from vertical transmission. </LI> <LI> The Flc-LOM-BE<SUP>rns</SUP> vaccine enables differential identification of serum antibodies. </LI> </UL> </P>
Lee, In Yong,Ko, Eun-Mi,Kim, Sang-Hyun,Jeoung, Doo-Il,Choe, Jongseon Williams Wilkins 2005 JOURNAL OF IMMUNOLOGY Vol.175 No.3
<P>Stromal cells in the lymphoid organs provide a microenvironment where lymphocytes undergo various biological processes such as development, homing, clonal expansion, and differentiation. Follicular dendritic cells (FDCs) in the primary and secondary follicles of the peripheral lymphoid tissues interact with lymphocytes by contacting directly or producing diffusible molecules. To understand the biological role of human FDC at the molecular level, we developed a mAb, 3C8, that recognizes FDC but not bone marrow-derived cells. Through expression cloning and proteome analysis, we identified the protein that is recognized by 3C8 mAb, which revealed that FDC expresses prostacyclin synthase. The 3C8 protein purified from FDC-like cells indeed displayed the enzymatic activity of prostacyclin synthase and converted PGH2 into prostacyclin. In addition, prostacyclin significantly inhibited proliferation of T cells but delayed their spontaneous apoptosis. These findings may help explain why T cells constitute only a minor population compared with B cells in the germinal center.</P>
Cho, Wha-Jung,Ko, Eun-Mi,Cheon, In-Su,Jeoung, Doo-Il,Kim, Young-Myeong,Choe, Jong-Seon The Korean Association of Immunobiologists 2008 Immune Network Vol.8 No.3
Background: Platelets take part in repairing the lesions of endothelial damage. To understand the molecular mechanism of this process, we tested the hypothesis that CD154 expressed on activated platelets stimulates proliferation of human endothelial cells. Methods: The expression levels of CD154 and CD40 on platelets and endothelial cells, respectively, were measured by flow cytometry and confocal microscopy. Function-blocking monoclonal antibody against CD154 was developed after immunization with CD154-transfected L cells. Results: An anti-CD40 agonist antibody and soluble CD154 both induced significant proliferation of endothelial cells. In addition, a function-blocking anti-CD154 antibody inhibited the platelet-induced proliferation of endothelial cells, indicating that the CD154-CD40 pathway is involved in these cellular interactions. An anti-VEGF antibody failed to inhibit the proliferation. This, in addition to the fact that very small amounts of VEGF are released from platelets or endothelial cells, suggests that VEGF does not play an important role in the platelet-stimulated proliferation of endothelial cells. Conclusion: Our results indicate that platelets induce proliferation of endothelial cells by CD154-CD40 interactions independently of VEGF.
In Yong Lee,Euh Jun Jeoung,권영근,Jongseon Choe,Jinkoo Kim,Eun-Mi Ko 한국분자세포생물학회 2002 Molecules and cells Vol.14 No.1
The role of interleukin-4 (IL-4) in the inflammatory process has emerged recently. In this study, we investi-gated the effect of IL-4 on the angiogenic process in an in vitro experimental system. IL-4 significantly inhib-ited the proliferation of human umbilical vein endo-thelial cells (HUVEC) that was induced by the vascu-lar endothelial growth factor (VEGF) and basic fibro-blast growth factor (bFGF). VEGF- or bFGF-induced HUVEC chemotaxis was abrogated by the IL-4 treat-ment. In addition, the formation of tube-like struc-tures by HUVEC in the presence of VEGF or bFGF was also severely down-regulated by IL-4. The inhibi-tory effects on the critical steps of angiogenesis were not observed with IL-6 that is abundantly found in the inflamed tissue. Our results suggest that IL-4 may play a regulatory role in normal physiology and provide the potential possibility for IL-4 as a therapeutic agent in the intervention of angiogenesis-related diseases.
Pyruvate dehydrogenase kinase 4 deficiency attenuates cisplatin-induced acute kidney injury
Oh, Chang Joo,Ha, Chae-Myeong,Choi, Young-Keun,Park, Sungmi,Choe, Mi Sun,Jeoung, Nam Ho,Huh, Yang Hoon,Kim, Hyo-Jeong,Kweon, Hee-Seok,Lee, Ji-min,Lee, Sun Joo,Jeon, Jae-Han,Harris, Robert A.,Park, Keu Springer-Verlag 2017 Kidney international Vol.91 No.4
<P>Clinical prescription of cisplatin, one of the most widely used chemotherapeutic agents, is limited by its side effects, particularly tubular injury-associated nephrotoxicity. Since details of the underlying mechanisms are not fully understood, we investigated the role of pyruvate dehydrogenase kinase (PDK) in cisplatin-induced acute kidney injury. Among the PDK isoforms, PDK4 mRNA and protein levels were markedly increased in the kidneys of mice treated with cisplatin, and c-Jun N-terminal kinase activation was involved in cisplatin-induced renal PDK4 expression. Treatment with the PDK inhibitor sodium dichloroacetate (DCA) or genetic knockout of PDK4 attenuated the signs of cisplatin-induced acute kidney injury, including apoptotic morphology of the kidney tubules along with numbers of TUNEL-positive cells, cleaved caspase-3, and renal tubular injury markers. Cisplatin-induced suppression of the mitochondria! membrane potential, oxygen consumption rate, expression of electron transport chain components, cytochrome c oxidase activity, and disruption of mitochondrial morphology were noticeably improved in the kidneys of DCA-treated or PDK4 knockout mice. Additionally, levels of the oxidative stress marker 4-hydroxynonenal and mitochondria! reactive oxygen species were attenuated, whereas superoxide dismutase 2 and catalase expression and glutathione synthetase and glutathione levels were recovered in DCA-treated or PDK4 knockout mice. Interestingly, lipid accumulation was considerably OCrossMark attenuated in DCA-treated or PDK4 knockout mice via recovered expression of peroxisome proliferator-activated receptor-a and coactivator PGC-1 alpha, which was accompanied by recovery of mitochondria! biogenesis. Thus, PDK4 mediates cisplatin-induced acute kidney injury, suggesting that PDK4 might be a therapeutic target for attenuating cisplatin-induced acute kidney injury.</P>