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Mitochondrial dysfunction and calcium deregulation by the RanBP9-cofilin pathway
Roh, Seung-Eon,Woo, Jung A.,Lakshmana, Madepalli K.,Uhlar, Courtney,Ankala, Vinishaa,Boggess, Taylor,Liu, Tian,Hong, Yun-Hwa,Mook-Jung, Inhee,Kim, Sang Jeong,Kang, David E. The Federation of American Societies for Experimen 2013 The FASEB Journal Vol.27 No.12
<P>Mitochondrial dysfunction and synaptic damage are important features of Alzheimer's disease (AD) associated with amyloid β (Aβ) and tau. We reported previously that the scaffolding protein RanBP9, which is overall increased in brains of patients with AD and in mutant APP transgenic mice, simultaneously promotes Aβ generation and focal adhesion disruption by accelerating the endocytosis of APP and β1-integrin, respectively. Moreover, RanBP9 induces neurodegeneration <I>in vitro</I> and <I>in vivo</I> and mediates Aβ-induced neurotoxicity. Here we show in primary hippocampal neurons that RanBP9 potentiates Aβ-induced reactive oxygen species (ROS) overproduction, apoptosis, and calcium deregulation. Analyses of calcium-handling measures demonstrate that RanBP9 selectively delays the clearance of cytosolic Ca<SUP>2+</SUP> mediated by the mitochondrial calcium uniporter through a process involving the translocation of cofilin into mitochondria and oxidative mechanisms. Further, RanBP9 retards the anterograde axonal transport of mitochondria in primary neurons and decreases synaptic mitochondrial activity in brain. These data indicate that RanBP9, cofilin, and Aβ mimic and potentiate each other to produce mitochondrial dysfunction, ROS overproduction, and calcium deregulation, which leads to neurodegenerative changes reminiscent of those seen in AD.—Roh. S.-E., Woo, J. A., Lakshmana, M. K., Uhlar, C., Ankala, V., Boggess, T., Liu, T., Hong, Y.-H., Mook-Jung, I., Kim, S. J., Kang, D. E. Mitochondrial dysfunction and calcium deregulation by the RanBP9-cofilin pathway.</P>
MathML 수식 편집을 포함한 XML문서편집 시스템의 설계 및 구현
윤화묵(Hwa-Mook Yoon),김철수(Coeol-Soon Kim),정희경(Hoe-Kyoung Jung) 한국정보과학회 2002 한국정보과학회 학술발표논문집 Vol.29 No.2Ⅲ
정보화 사회로 발전해 나아감에 따라 컴퓨터를 이용한 문서처리의 중요성이 날로 증가해가면서, 문서를 전자적으로 처리하기 위한 전자문서처리 시스템이 널리 이용되고 있는 설정이다. 하지만 기존의 문서편집 시스템들에서 수학식의 표현은 이미지나 텍스트 등의 비 구조적인 방법에 의해 표현되거나 처리됨에 따라 사용자가 읽거나 표현하는데 어려움이 있다. 따라서 이러한 단점을 보완하면서 최소한의 노력으로 효과적으로 수학식을 표현하는 구조적인 문서생성을 위한 노력이 필요하다. 이에 본 논문에서는 수학식 표현을 구조적으로 생성해주는 MathML(Mathematical Markup Language)의 적용이 가능한 XML(eXtensible Markup Language)기반의 구조적 문서생성을 위한 문서 편집 시스템을 설계 및 구현하였다.
Sang-Mook Kim,Hwa Sub Oh,Jong Hyeob Baek,Kwang-Ho Lee,Gun Young Jung,Jae-Ho Song,Ho-Jong Kim,Byung-Jun Ahn,Dong Yanqun,Jung-Hoon Song IEEE 2010 IEEE electron device letters Vol.31 No.8
<P>The strain and piezoelectric fields in InGaN blue light-emitting diodes on a GaN layer, which is grown on a planar sapphire substrate or patterned sapphire substrates (PSSs), such as a microsized PSS and a nanosized PSS (NPSS), are investigated by micro-Raman spectroscopy and electroreflectance (ER) spectroscopy. The obtained piezoelectric field in InGaN multiple quantum wells (QWs) grown on the planar substrate is 0.83 MV/cm, and it is 0.70 MV/cm for the case of the NPSS. These results are attributed to the fact that the GaN layers on the PSSs have a smaller residual strain compared to that on the planar sapphire, and thus, strain reduction in the GaN layer can reduce the piezoelectric field in the InGaN QWs grown on top of it.</P>
Sun Hwa Park,Ami Kim,Jieun An,Hyun Sung Cho,Tong Mook Kang 대한생리학회-대한약리학회 2020 The Korean Journal of Physiology & Pharmacology Vol.24 No.6
In contrast to ventricular myocytes, the structural and functional importance of atrial transverse tubules (T-tubules) is not fully understood. Therefore, we investigated the ultrastructure of T-tubules of living rat atrial myocytes in comparison with ventricular myocytes. Nanoscale cell surface imaging by scanning ion conductance microscopy (SICM) was accompanied by confocal imaging of intracellular T-tubule network, and the effect of removal of T-tubules on atrial excitation-contraction coupling (EC-coupling) was observed. By SICM imaging, we classified atrial cell surface into 4 subtypes. About 38% of atrial myocytes had smooth cell surface with no clear T-tubule openings and intracellular T-tubules (smooth-type). In 33% of cells, we found a novel membrane nanostructure running in the direction of cell length and named it longitudinal fissures (LFs-type). Interestingly, T-tubule openings were often found inside the LFs. About 17% of atrial cells resembled ventricular myocytes, but they had smaller T-tubule openings and a lower Z-groove ratio than the ventricle (ventricular-type). The remaining 12% of cells showed a mixed structure of each subtype (mixed-type). The LFs-, ventricular-, and mixed-type had an appreciable amount of reticular form of intracellular T-tubules. Formamide-induced detubulation effectively removed atrial T-tubules, which was confirmed by both confocal images and decreased cell capacitance. However, the LFs remained intact after detubulation. Detubulation reduced action potential duration and L-type Ca2+ channel (LTCC) density, and prolonged relaxation time of the myocytes. Taken together, we observed heterogeneity of rat atrial T-tubules and membranous ultrastructure, and the alteration of atrial EC-coupling by disruption of T-tubules.