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김동희,정경채,김민희,황돈하,이달해 嶺南大學校 工業技術硏究所 1994 工業技術硏究所論文集 Vol.22 No.1
Recently, the vector controlled induction motors are widely used in the industrial AC servo system requiring high accuracy and fast response. However, in the conventional vector control, by using of speed sensors for speed information of the motor, the system design has been restricted. This paper proposes te vector control system based on speed estimation controls motor speed by estimating angular speed of secondary flux linkages from voltage equations of induction motor without speed and voltage sensor. To stabilize the control system for estimation, the ??-axis flux keeps to zero by the compensation control method with state feedback. In addition, the whole control system is designed to be controlled by software in microcomputer. Computer simulations domonstrates that the control characteristics of the proposed vector control system based on speed estimation are satisfactory in both dynamic performance and accuracy.
고속전철 추진 시스템의 미끄럼 방지 제어기법에 관한 연구
황돈하,김동희,노채균,심광열,조규판,정원영 영남대학교 공업기술연구소 1999 工業技術硏究所論文集 Vol.27 No.2
Induction motor drive with PWM inverter control has been developed for Korean High Speed Railways. To improve traction performance, the anti-slip control(ASC) to recover adhesion must be considered. This paper describes a novel hybrid anti-slip control method for the induction motor drive. By introducing the vector control for drive system, quick response of the motor torque can be achieved when wheels are going to slip. A hybrid control scheme by mixing two conventional control methods (slip velocity feedback control and slip detection pattern control) for wheel slip and re-adhesion is proposed. This control method is simulated by motor drive, train load, and friction-creep models. The train running simulation results based on induction motor vector control with PWM inverter show that good re-adhesion characteristics are obtained.
電壓形 PWM Inverter에 依한 誘導電動機의 精密 速度制御
金玟會,鄭瓊採,金東熙,李達海,黃敦夏 嶺南大學校 工業技術硏究所 1992 연구보고 Vol.20 No.1
For precision control of Induction Motor with Voltage Source PWM Inverter, the current component should be converted into the voltage one. We are in difficulties for precision control with simple current feedback control because of the oscillation in system and torque ripple on high speed rotation and transient switching resulted from the disturbance which is generated by the mutual interference between d-axis and q-axis during conversion. This paper propose linearized Decoupling Control Theory in Field-Oriented Control and presents controllable system with Microcomputer software in the whole control system. In addition, by experiment it is proved that the system is controlled well in both steady and transient states. The proposed system is expected to be applied in industrial AC Servo System.
Chae, Hee-Don,Choi, Tae-Saeng,Kim, Byeong-Mo,Jung, Jee H.,Bang, Yung-Jue,Shin, Deug Y. 이화여자대학교 세포신호전달연구센터 2004 고사리 세포신호전달 심포지움 Vol. No.6
In this study, we demonstrate that p53-deficient cancer cells have enhanced chemosensitivity to an actin inhibitor, pectenotoxin-2(PTX-2), both in vitro and in vivo. While p53-positive cells lead to tetraploid G1 arrest after PTX-2 treatment, p53-deficient cells fail to sustain cell cycle arrest and reenter S and M phases, resulting in hyperploid and multinucleate cells. We found that PTX-2 and other actin inhibitors activate the p53-p21 pathway. Thus, PTX-2 treatment causes inactivation of both cdk2 and cdc2 in p53-positive cells, but leaves both of them active in p53-deficient cells. The enhanced chemosensitivity of p53-deficient cells to actin inhibitors is a result of p53-independent apoptosis, which is mediated by mitochondrial translocation of Bax proteins, loss of mitochondrial membrane potential, and subsequent cytochrome c release and caspase-3 activation. Moreover, Bel-X_(L), which antagonizes Bax, was found to inhibit p53-independent apoptosis and to enhance polyploidy. Based on these results, we examined whether CDKs remaining active in p53-deficient cells are responsible for the Bax-mediated apoptosis as well as perturbations of tetraploid G1 arrest. CDK inhibitors, such as roscovitine and olomoucine, were found to block apoptosis induction and mitochondrial translocation of Bax protein. Therefore, these results suggest that CDKs remaining active in p53-deficient cells trigger Bax-mediated apoptosis and therefore results in the enhanced chemosensitivity to actin inhibitors. These results also suggest that actin inhibitors be potent chemotherap! eutic agents against p53-deficient tumors.
( Hee Don Chae ),( Jung Bin Kim ),( Deug Y. Shin ) 생화학분자생물학회(구 한국생화학분자생물학회) 2011 BMB Reports Vol.44 No.8
We previously reported that CDK2/Cyclin A can phosphorylate and activate the transcription factor NF-Y. In this study, we investigated a potential regulatory role for NF-Y in the transcription of Cyclin A and other cell cycle regulatory genes. Gel-shift assays demonstrate that NF-Y binds to CCAAT sequences in the Cyclin A promoter, as well as to those in the promoters of cell cycle G2 regulators such as CDC2, Cyclin B and CDC25C. Furthermore, expression of Cyclin A increases NF-Y`s affinity for CCAAT sequences in the CDC2 promoter; however, Cyclin A`s induction of CDC2 transcription is antagonized by p21, an inhibitor of CDK2/Cyclin A. These results suggest a model wherein NF-Y binds to and activates transcription from the Cyclin A promoter, increasing cellular levels of Cyclin A/CDK2 and potentiating NF-Y`s capacity for transcriptional transactivation, and imply a positive feedback loop between NF-Y and Cyclin A/CDK2. Our findings are additionally indicative of a role for Cyclin A in activating Cyclin B/CDK1 through promoting NF-Y dependent transcription of Cyclin B and CDC2; NF-Y mediated crosstalk may therefore help to orchestrate cell-cycle progression. [BMB reports 2011; 44(8): 553-557]
Hee-Don Chae,So Youn Kim,Sang Eun Park,김정빈,Deug Y Shin 생화학분자생물학회 2012 Experimental and molecular medicine Vol.44 No.3
We previously reported that the p53 tumor suppressor protein plays an essential role in the induction of tetraploid G1 arrest in response to perturbation of the actin cytoskeleton, termed actin damage. In this study, we investigated the role of p53, ataxia telangiectasia mutated protein (ATM), and catalytic subunit of DNA-dependent protein kinase (DNA-PKcs) in tetraploid G1 arrest induced by actin damage. Treatment with actin-damaging agents including pectenotoxin-2 (PTX-2)increases phosphorylation of Ser-15 and Ser-37 residues of p53, but not Ser-20 residue. Knockdown of ATM and DNA-PKcs do not affect p53 phosphorylation induced by actin damage. However, while ATM knockdown does not affect tetraploid G1 arrest, knockdown of DNA-PKcs not only perturbs tetraploid G1 arrest, but also results in formation of polyploidy and induction of apoptosis. These results indicate that DNA-PKcs is essential for the maintenance of actin damage induced-tetraploid G1 arrest in a p53-independent manner. Furthermore, actin damage-induced p53 expression is not observed in cells synchronized at G1/S of the cell cycle, implying that p53 induction is due to actin damage-induced tetraploidy rather than perturbation of actin cytoskeleton. Therefore, these results suggest that p53 and DNA- PKcs independently function for tetraploid G1 arrest and preventing polyploidy formation.
Don-Ha Hwang,Dong-Sik Kang,Yong-Joo Kim Tae-Hoon Lim,Sung-Woo Bae,Dong-Hee Kim,Chae-Cyun Ro 전력전자학회 2003 JOURNAL OF POWER ELECTRONICS Vol.3 No.3
The winding insulation of low-voltage induction motors in adjustable-speed drive system with voltage-fed Inverters is substantially stressed due to the uneven voltage distribution and excessive voltage stress (dv/dt), which result in the premature insulation breakdown In this paper, the detailed insulation test results of 26 low-voltage induction motors are presented. Six different types of insulation techniques are applied to 26 motors. The insulation characteristics are analyzed with partial discharge, discharge inception voltage, AC current, and dissipation factor tests Also, insulation breakdown tests by high voltage pulses are performed, and the corresponding breakdown voltages obtained.