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김재실,안승국,이재환,안대균,최헌오 창원대학교 산업기술연구소 2001 産技硏論文集 Vol.15 No.-
This article describes (1) 2 and 3 dimensional electromagnetic finite element models for an active heteropolar radial magnetic bearing, (2) the procedure for obtaining the bearing stiffnesses by simulating the models and (3) the reviews of the models by comparing an experimental test to the ideal closed loop analysis with the stiffnesses calculated from(2). The 3 dimensional model for the magnetic bearing may be very effectively applied to several types of magnetic bearings.
김재실,배철용,이재환,안대균,최헌오 창원대학교 산업기술연구소 2001 産技硏論文集 Vol.15 No.-
자기베어링의 회전정밀도에 영향을 미치는 인자로 PWM 전력증폭기, 위치 센서 등과 같은 자기베어링 구성 장치의 동특성 및 정밀도, 시스템의 정확한 모델링, 제어기법, 런아웃 등이 있다. 본 연구에서는 능동 자기베어링을 제어하기 위해 자기베어링의 PWM 전력증폭기와 회전축을 모델링하고 이를 바탕으로 능동 자기베어링 제어를 위한 PID 제어기를 구성하였으며, 변위 센서의 부착위치 및 회전축의 진원도의 영향으로 발생하는 주기적인 런아웃 요소를 첨가하여 런아웃의 영향을 확인하였으며, 런아웃(Runout)에 의해 발생하는 에러(Error)를 효과적으로 제어하여 자기베어링의 제어 정밀도를 향상시키기 위한 방법으로 기본적인 PID 제어기에 최소평균자승(Least Mean Square, LMS) 알고리즘을 적용한 적응 피드포워드 제어기를 구성하여 자기베어링의 능동 제어에서 발생하는 주기적인 런아웃을 효과적으로 제어할 수 있음을 MATLAB을 통한 시뮬레이션을 통해 확인하였다.
ULSI DRAM의 BIST 알고리즘을 위한 제어회로 설계
온정근,김대익,도경주,이영훈,이창기,전병실 전북대학교 전자산업개발연구소 1991 전자산업연구 Vol.2 No.-
Lately, more developed semiconductor technolgy is, higher integration per one chip is rapidly. Mow 64 Mb DRAM is used 0.3㎛ techonology. This very large integration is caused faults of new type, and exhaused much time for test. So algorithms which distiguish at higher faults coverage. less time and cost of test is reported. In this paper control circuit of Built-In Self Test(BIST) Algorithm was designed for ULSI DRAM and simulated with MYCAD. This control circuit is carried out steps of algorithm, controlled generation of test patterns and data, generated control signals of parallel test.
ULSI DRAM의 BIST 알고리즘을 위한 패턴발생회로 설계
온정근,김대익,도경주,이영훈,이창기,전병실 전북대학교 전자산업개발연구소 1991 전자산업연구 Vol.2 No.-
Lately, more developed semiconductor technolgy is, higher integration per one chip is rapidly. Mow 64 Mb DRAM is used 0.3㎛ techonology. This very large integration is caused faults of new type, and exhaused much time for test. So algorithms which distiguish at higher faults coverage. less time and cost of test is reported. In this paper control circuit of Built-In Self Test(BIST) Algorithm was designed for ULSI DRAM. This circuit generates patterns of the algorithm by input clocks.
남성화를 보이는 여성에서 발견된 난소의 Steroid Cell Tumor 1예
조인호,정대훈,박영미,서영진,손영실,정철회,강영미,정수전,김영남,이경복,성문수,김기태 인제대학교 2006 仁濟醫學 Vol.27 No.-
Steroid cell tumor is a rare ovarian sex cord-stromal tumor which accounts for 0.1% of all ovarian tumors. Until now, only 4 cases have been reported in domestic literatures. Steroid cell tumor often secrets testosterone and presents virilization in adult women or precocious puberty in children. Treatment is often performed by surgical removal, adjuvant chemotherapy and radiation, but completely accepted treatment was not existed. We experienced a case of steroid cell tumor, which was manifested by typical virilization in a 43-year old patient, who was previously performed hysterectomy and unilateral oophorectomy. So, we present with a brief review of the literatures.
대장균에서 Thermus caldophilus GK24의 DNA Polymerase유전자의 고발현
권석태,김현규,김중수,이대실 성균관대학교 생명과학자원연구소 1997 生命資源科學硏究 Vol.4 No.2
Thermus caldophilus GK24 (Tca) DNA polymerase is highly useful enzyme for amplifying DNA fragments by polymerase chain reaction (PCR). A plasmid, pTCA, is expression vector for Tca DNA polymerase gene in Escherichia coli under the control of tac promoter and its expression level is low. For the high expression, the DNA sequence coding for NH_2-amino acid sequence of Tca DNA polymerase was changed by PCR, and then an expression vector pTCAM was constructed. The activity of Tca DNA polymerase in E. coli harboring for pTCAM has enhanced nearly 6-fold/ml than that for E. coli harboring pTCA.
HSP25 Inhibits Protein Kinase Cδ-mediated Cell Death through Direct Interaction
Lee, Yoon-Jin,Lee, Dae-Hoon,Cho, Chul-Koo,Bae, Sangwoo,Jhon, Gil-Ja,Lee, Su-Jae,Soh, Jae-Won,Lee, Yun-Sil American Society for Biochemistry and Molecular Bi 2005 The Journal of biological chemistry Vol.280 No.18
<P>Heat shock protein 25 (HSP25) interferes negatively with apoptosis through several pathways that involve its direct interaction with cytochrome c or Akt. Here we show that HSP25 inhibits protein kinase C (PKC) delta-mediated cell death through direct interaction. HSP25 binds to kinase-active PKCdelta to inhibit its kinase activity and translocation to the membrane, which results in reduced cell death. Deletion constructs of HSP25 and PKCdelta identified amino acids 90-103 of HSP25 and the C-terminal V5 region of PKCdelta as binding sites. In addition, the interaction between HSP25 and PKCdelta induced HSP25 phosphorylation at Ser-15 and Ser-86, and these phosphorylations permitted HSP25 release from PKCdelta. Based on these observations, we propose that after PKCdelta activation, HSP25 binds to the exposed V5 region of PKCdelta. This novel function of HSP25 accounts for its cytoprotective properties via the inhibition of PKCdelta and the enhancement of HSP25 phosphorylation.</P>
Responses of Nitrogen Oxide to High‐Speed Solar Wind Stream in the Polar Middle Atmosphere
Lee, Ji‐,Hee,Jee, Geonhwa,Kwak, Young‐,Sil,Hong, Sang‐,bum,Hwang, Heejin,Song, In‐,Sun,Lee, Young‐,Sook,Turunen, Esa,Lee, Dae‐,Young American Geophysical Union 2018 JOURNAL OF GEOPHYSICAL RESEARCH. SPACE PHYSICS Vol.123 No.11
HSP25 inhibits radiation-induced apoptosis through reduction of PKCδ-mediated ROS production
Lee, Yoon-Jin,Lee, Dae-Hoon,Cho, Chul-Koo,Chung, Hee-Yong,Bae, Sangwoo,Jhon, Gil-Ja,Soh, Jae-Won,Jeoung, Doo-Il,Lee, Su-Jae,Lee, Yun-Sil Nature Publishing Group 2005 Oncogene Vol.24 No.23
Since radiation-induced caspase-dependent apoptosis and ROS generation were partially prevented by HSP25 overexpression, similar to the treatment of control cells with antioxidant agents such as DPI and tiron, questions arise whether radiation-mediated ROS generation contributes to the apoptotic cell death, and also whether HSP25 overexpression can reduce ROS mediated apoptotic cell death. In the present study, radiation-induced cytochrome c release from mitochondria and activation of caspases accompanied by a decrease of mitochondrial membrane potential in Jurkat T cells were shown to be inhibited by mitochondrial complex I inhibitor rotenone, suggesting that mitochondrial ROS might be important in radiation-induced caspase-dependent apoptosis. When HSP25 was overexpressed, effects similar to the treatment of cells with the antioxidants were obtained, indicating that HSP25 suppressed radiation-induced mitochondrial alteration that resulted in apoptosis. Furthermore, activation of p38 MAP kinase by radiation was associated with radiation-induced cell death and ROS production and PKCδ was an upstream molecule for p38 MAP kinase activation, ROS generation and subsequent caspase-dependent apoptotic events. However, in the HSP25 overexpressed cells, the above-described effects were blocked. In fact, radiation-induced membrane translocation of PKCδ and tyrosine phosphorylation were inhibited by HSP25. Based on the above data, we suggest that HSP25 downregulates PKCδ, which is a key molecule for radiation-induced ROS generation and mitochondrial-mediated caspase-dependent apoptotic events.Oncogene (2005) 24, 3715–3725. doi:10.1038/sj.onc.1208440 Published online 4 April 2005
Lee, Young-Sun,Kim, Yeong-Seok,Kim, Dae-Jin,Hur, Dae-Young,Kang, Jae-Seung,Kim, Young-In,Hahm, Eun-Sil,Cho, Dae-Ho,Hwang, Young-Il,Lee, Wang-Jae The Korean Association of Immunobiologists 2006 Immune Network Vol.6 No.2
Background: CM1 (Centrocyte/-blast Marker I) defined by a mAb developed against concanavalin-A activated PBMC, is expressed specifically on a subpopulation of centroblasts and centrocytes of human germinal center (GC) B cells. Burkitt lymphoma (BL) is a tumor consisting of tumor cells with the characteristics of GC B cell. Previously we reported that CM1 ligation with anti-CM1 mAb induced apoptosis in Ramos $(IgM^{high})$ and Raji $(IgM^{low})$ cells. Methods & Results: In the present study, we observed that CM1 ligation with anti-CM1 mAb induced Fas ligand and Fas expression in Ramos cells, but not in Raji cells. Furthermore, anti-Fas blocking antibody, ZB4, blocked CM1-mediated apoptosis effectively in Ramos cells, but not in Raji cells. Increased mitochondrial membrane permeabilization, which was measured by $DiOC_6$, was observed only in Raji cells. In contrast to no significant change of Bax known as pro-apoptotic protein, anti-apoptotic protein Bcl-2 was significantly decreased in Raji cells. In addition, we observed that CM1 ligation increased release of mitochondrial cytochrome c and upregulated caspase-9 activity in Raji cells. Conclusion: These results suggest that apoptosis induced by CM1-ligation is mediated by Fas-Fas ligand interaction in Ramos cells, whereas apoptosis is mediated by down-regulation of Bcl-2 and subsequent decrease of mitochondrial membrane potential in Raji cells.