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인공망막칩과 형상기억합금을 이용한 평활 안구운동시스템 구현
김원철,김현수,박종호,박대식,이민호,신장규 한국뇌학회 2001 한국뇌학회지 Vol.1 No.2
본 논문에서는 인간의 평활 추적안구운동을 모방하는 능동시각시스템(active vision system)을 구현하였다. 평활 추적 안구운동을 모방하는 능동시각시스템을 구현하기 위해 인간의 안구운동 중에 관찰되는 신경생리학적인 특징들을 이해하고, 다양한 안구운동 중에서 평활 추적안구운동 중에 관찰되는 중측관자(medial temporal) 세포의 역할을 자기조직화 형상지도(self-organizing feature map)와 승자독점(winner take all)을 이용하여 구현하였다. 회전속도계 궤환 모델(tachometer feedback model)로 중상측관자(medial superior temporal) 세포의 역할을 모델하였다. 그리고 인공망막칩으로 인공 안구를 구성하고 형상기억합금 구동기(actuator)를 이용하여 인공 안근육을 구성하여, 빛의 밝기 변화인 윤곽(edge) 정보에 반응하는 인공 안구모형을 제작하였으며, 실험을 통하여 시스템의 동작성능을 보였다. In this paper, we proposed a model of smooth pursuit eye movement, and developed a human-like active vision system using a retina chip and a shape memory alloy actuator. The model of smooth pursuit eye movement is to imitate the role of MT and MST area of human brain in smooth pursuit eye movements. We fabricated the 8×8 retina chip for the edge detection. The developed retina chip is an image sensor to extract edge information and the shape memory alloy actuator is a driver to imitate the role of eye muscles to follow a moving object.
정원봉,이민호,강신원 경북대학교 센서기술연구소 1998 센서技術學術大會論文集 Vol.9 No.1
A LAPS (Light Addressable Potentiometric Sensor) system using a neural network was proposed for the sensing a hydrogen ion concentration. A multilayer neural network is used for enhancing a resolution of LAPS which is limited by a hardware device including a AD converter, low-pass filter etc. Also, an experimental results is compared and analyzed with an analytic result.
Lnx2 ubiquitin ligase is essential for exocrine cell differentiation in the early zebrafish pancreas
Won, Minho,Ro, Hyunju,Dawid, Igor B. National Academy of Sciences 2015 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.112 No.40
<P><B>Significance</B></P><P>Pancreas differentiation is of interest as an example of organogenesis and for its medical implications. We report here that regulation of protein stability is a player in the differentiation of certain cell lineages in the early zebrafish pancreas. The related E3 ubiquitin ligases Ligand of Numb protein-X (Lnx)2a and Lnx2b affect differentiation of exocrine cells, apparently by destabilizing Numb in exocrine progenitor cells. Numb is an inhibitor of Notch, a key regulator of pancreatic development. We suggest that Lnx2a/b destabilize Numb to derepress Notch, allowing precursors to proliferate and support subsequent differentiation. This study also highlights the fact that detailed analysis of morpholino versus mutant phenotypes may be required for a full understanding of their relationship.</P><P>The gene encoding the E3 ubiquitin ligase Ligand of Numb protein-X (Lnx)2a is expressed in the ventral-anterior pancreatic bud of zebrafish embryos in addition to its expression in the brain. Knockdown of Lnx2a by using an exon 2/intron 2 splice morpholino resulted in specific inhibition of the differentiation of ventral bud derived exocrine cell types, with little effect on endocrine cell types. A frame shifting null mutation in <I>lnx2a</I> did not mimic this phenotype, but a mutation that removed the exon 2 splice donor site did. We found that Lnx2b functions in a redundant manner with its paralog Lnx2a. Inhibition of <I>lnx2a</I> exon 2/3 splicing causes exon 2 skipping and leads to the production of an N-truncated protein that acts as an interfering molecule. Thus, the phenotype characterized by inhibition of exocrine cell differentiation requires inactivation of both Lnx2a and Lnx2b. Human LNX1 is known to destabilize Numb, and we show that inhibition of Numb expression rescues the Lnx2a/b-deficient phenotype. Further, Lnx2a/b inhibition leads to a reduction in the number of Notch active cells in the pancreas. We suggest that Lnx2a/b function to fine tune the regulation of Notch through Numb in the differentiation of cell types in the early zebrafish pancreas. Further, the complex relationships among genotype, phenotype, and morpholino effect in this case may be instructive in the ongoing consideration of morpholino use.</P>
Won, Minho,Ro, Hyunju,Park, Hae-Chul,Kim, Kyoon E.,Huh, Tae-Lin,Kim, Cheol-Hee,Rhee, Myungchull Wiley-Liss, Inc. 2006 Developmental dynamics Vol.235 No.3
<P>Evolutionarily well-conserved Ca<SUP>2+</SUP>/calmodulin-dependent protein kinase (CaMK) proteins are known for their role as Ca<SUP>2+</SUP> signaling mediators. 1G5 encodes a CaMK like protein, which belongs to a calmodulin (CaM) kinase gene family. Here, we report the isolation of zebrafish homologue of mammalian 1G5, which we named 1G5z. 1G5z is composed of three major domains: (1) an N-terminal serine/threonine kinase domain, (2) a central calmodulin-binding domain, and (3) a C-terminal alanine-rich domain, the 1G5z-specific domain. 1G5z shares 83∼84% homology with other vertebrate 1G5 proteins. Spatiotemporal expression studies found that 1G5z is expressed by means of zygotic transcription and appears in various neuronal tissues from the 20-somite stage. 1G5z transcripts are more regionalized in the brain and spinal cord at 24 hr postfertilization (hpf). At 35 hpf, 1G5z transcripts are exclusively present in the anterior trunk spinal cord as well as in the hindbrain, tegmentum, hypothalamus, and telencephalon. This expression pattern lasts until 48 hpf but ceases in the trunk. At 72 hpf, 1G5z is abundantly transcribed particularly in the specific region of the tectum and eye. We further observed that the number of 1G5z-positive cells is dramatically increased in the mindbomb mutant embryos but abolished in the trigeminal ganglion and caudal trunk sensory neuron of the neurogenin1 morphant at 24 hpf. In addition, bromodeoxyuridine staining further confirmed that the 1G5z-positive cells were postmitotic sensory and interneurons. Developmental Dynamics 235:835–842, 2006. © 2006 Wiley-Liss, Inc.</P>
Role of A20 on the TNF Receptor Death Signaling Pathway through the Suppression of JNK Activation
Won, Minho,Byun, Hee Sun,Park, Kyeong Ah,Kim, Young-Rae,Choil, Byung Lyul,Lee, Hyunji,Yang, Keum-Jin,Shin, Sanghee,Piao, Longzhen,Shin, Eulsoon,Park, Jongsun,Seok, Jeong Ho,Hur, Gang Min 충남대학교 형질전환복제돼지연구센터 2007 논문집 Vol. No.10
Zhang, Tiejun,Li, Yuwen,Park, Kyeong Ah,Byun, Hee Sun,Won, Minho,Jeon, Juhee,Lee, Yoonjung,Seok, Jeong Ho,Choi, Seung-Won,Lee, Sang-Hee,Man Kim, Jin,Lee, Ji Hoon,Son, Chang Gue,Lee, Zee-Won,Shen, Han- Landes Bioscience 2012 AUTOPHAGY Vol.8 No.4
<P>Targeted disruption of STAT3 function has proven to be a useful cancer therapeutic approach by inducing apoptotic cell death. Cucurbitacin is currently under development as a small molecule of STAT3 inhibitor to trigger cell death in many cancers. Here, we systematically studied the molecular mechanisms underlying cucurbitacin-induced cell death, in particular the involvement of autophagy. Treatment with cucurbitacin resulted in non-apoptotic cell death in a caspase-independent manner. Notably, cucurbitacin enhanced excessive conversion of lipidated LC3 (LC3-II) and accumulation of autophagosomes in many cell types. Such autophagy and cell death induced by cucurbitacin were independent of its ability to inhibit STAT3 function, but mainly mediated by enhanced production of mitochondrial-derived reactive oxygen species (ROS), and subsequently activation of extracellular signal-regulated kinase (ERK) and c-jun NH2-terminal kinase (JNK). Interestingly, both the autophagy inhibitor wortmannin and knockdown of Atg5 or Beclin 1 failed to rescue the cells from cucurbitacin-induced cell death, as suppression of autophagy induced the mode of cell death to shift from autophagic cell death to caspase-dependent apoptosis. Thus the present study provides new insights into the molecular mechanisms underlying cucurbitacin-mediated cell death and supports cucurbitacin as a potential anti-cancer drug through modulating the balance between autophagic and apoptotic modes of cell death.</P>