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A Novel Control Algorithm for Two-axis Motion in 3-DOF TVC Nozzle
Sungjin Cho,Eulgon Kim,HyungSik Lee 제어로봇시스템학회 2010 제어로봇시스템학회 국제학술대회 논문집 Vol.2010 No.10
To control pitch and yaw motion of a TVC(Thrust Vector Control) nozzle with 3-DOF(Degree Of Freedom), additional apparatuses are usually required to prevent induced rolling motion. However, the supplemental devices bring hardware designers many difficulties related to the spatial arrangement of TVC nozzle and actuators. In this paper, in order to solve the problem, the type of two joints linked between the nozzle and two actuators are proposed. And, by using the proposed type of two joints, new kinematic model to restrict the rolling motion is established. Moreover, a novel control algorithm based on the analytic solution for the kinematic model is suggested. The usefulness of this algorithm is verified through simulation study.
The Feasible Bias Set of BPNG Law for Single-Lag System
Sungjin Cho,Ick-Ho Whang,Young-In Lee,Dong-Kyun Choe,Dae-gyu Sang 제어로봇시스템학회 2011 제어로봇시스템학회 국제학술대회 논문집 Vol.2011 No.10
In this paper, we suggest the feasible bias set of BPNG(Biased Proportional Navigation Guidance) law for single-lag strap-down imaging sensor homing loop design. The pitch angle is analytically derived from the turning rate dynamics based on analytic solution of the BPNG single-lag homing system. Moreover, the appropriate bias range which guarantees the FOV(Field-Of-View) limit of strap-down imaging sensor is obtained.
Storage Logic Primitives Based on Stacked Memristor-CMOS Technology
Cho, Sung-Wan,Eshraghian, Jason,Eom, Ju-Song,Kim, Sungjin,Cho, Kyoungrok American Scientific Publishers 2016 Journal of Nanoscience and Nanotechnology Vol.16 No.12
<P>A newer and higher standard of circuits is emerging with the advent of memristive logic components. In the present paper memristor-CMOS (MCM)-based storage primitives are presented by exploiting the resistive switching property of the memristor. Practical implementation and fabrication of MCM-based logic circuits were verified by way of SPICE modeling, related simulations, and device characterization. The logic structure was designed by combining memristors with CMOS, and fabrication was performed by atomic layer deposition and an aluminum evaporation process in the form of a memristor on 350-nm CMOS technology. The proposed design method realized more efficient area utilization compared with current CMOS technology. As a result, the presented memristor-CMOS-based SR flip-flop and JK master slave flip-flop decreased the area by a factor of 31.2-52.2% with respect to the equivalent state memory CMOS circuits. The proposed memristor-CMOS technology allows for significant reduction of the silicon area, sustainability of Moore's law, and can be applied to increase the density of microchips.</P>
GOLGA2 loss causes fibrosis with autophagy in the mouse lung and liver
Park, Sungjin,Kim, Sanghwa,Kim, Min Jung,Hong, Youngeun,Lee, Ah Young,Lee, Hyunji,Tran, Quangdon,Kim, Minhee,Cho, Hyeonjeong,Park, Jisoo,Kim, Kwang Pyo,Park, Jongsun,Cho, Myung-Haing Elsevier 2018 Biochemical and biophysical research communication Vol.495 No.1
<P><B>Abstract</B></P> <P>Autophagy is a biological recycling process via the self-digestion of organelles, proteins, and lipids for energy-consuming differentiation and homeostasis. The Golgi serves as a donor of the double-membraned phagophore for autophagosome assembly. In addition, recent studies have demonstrated that pulmonary and hepatic fibrosis is accompanied by autophagy. However, the relationships among Golgi function, autophagy, and fibrosis are unclear. Here, we show that the deletion of <I>GOLGA2</I>, encoding a cis-Golgi protein, induces autophagy with Golgi disruption. The induction of autophagy leads to fibrosis along with the reduction of subcellular lipid storage (lipid droplets and lamellar bodies) by autophagy in the lung and liver. <I>GOLGA2</I> knockout mice clearly demonstrated fibrosis features such as autophagy-activated cells, densely packed hepatocytes, increase of alveolar macrophages, and decrease of alveolar surfactant lipids (dipalmitoylphosphatidylcholine). Therefore, we confirmed the associations among Golgi function, fibrosis, and autophagy. Moreover, <I>GOLGA2</I> knockout mice may be a potentially valuable animal model for studying autophagy-induced fibrosis.</P> <P><B>Highlights</B></P> <P> <UL> <LI> GOLGA2/GM130 loss induces autophagy with Golgi disruption in liver cells and transgenic mice. </LI> <LI> GOLGA2/GM130 loss leads to degradation of lipid structures (LBs and LDs) by autophagy. </LI> <LI> GOLGA2/GM130 loss causes liver and lung fibrosis. </LI> </UL> </P>