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PKCδ-dependent p47<i>phox</i> activation mediates methamphetamine-induced dopaminergic neurotoxicity
Dang, Duy-Khanh,Shin, Eun-Joo,Kim, Dae-Joong,Tran, Hai-Quyen,Jeong, Ji Hoon,Jang, Choon-Gon,Ottersen, Ole Petter,Nah, Seung-Yeol,Hong, Jau-Shyong,Nabeshima, Toshitaka,Kim, Hyoung-Chun PERGAMON PRESS 2018 FREE RADICAL BIOLOGY AND MEDICINE Vol.115 No.-
<P><B>Abstract</B></P> <P>Protein kinase C (PKC) has been recognized to activate NADPH oxidase (PHOX). However, the interaction between PKC and PHOX <I>in vivo</I> remains elusive. Treatment with methamphetamine (MA) resulted in a selective increase in PKCδ expression out of PKC isoforms. PKCδ co-immunoprecipitated with p47<I>phox</I>, and facilitated phosphorylation and membrane translocation of p47<I>phox</I>. MA-induced increases in PHOX activity and reactive oxygen species were attenuated by knockout of p47<I>phox</I> or PKCδ. In addition, MA-induced impairments in the Nrf-2-related glutathione synthetic system were also mitigated by knockout of p47<I>phox</I> or PKCδ. Glutathione-immunoreactivity was co-localized in Iba-1-labeled microglial cells and in NeuN-labeled neurons, but not in GFAP-labeled astrocytes, reflecting the necessity for self-protection against oxidative stress by mainly microglia. Buthionine-sulfoximine, an inhibitor of glutathione biosynthesis, potentiated microglial activation and pro-apoptotic changes, leading to dopaminergic losses. These neurotoxic processes were attenuated by rottlerin, a pharmacological inhibitor of PKCδ, genetic inhibitions of PKCδ <B>[</B>i.e., PKCδ knockout mice (KO) and PKCδ antisense oligonucleotide (ASO)<B>]</B>, or genetic inhibition of p47<I>phox</I> (i.e., p47<I>phox</I> KO or p47<I>phox</I> ASO). Rottlerin did not exhibit any additive effects against the protective activity offered by genetic inhibition of p47<I>phox</I>. Therefore, we suggest that PKCδ is a critical regulator for p47<I>phox</I> activation induced by MA, and that Nrf-2-dependent GSH induction via inhibition of PKCδ or p47<I>phox</I>, is important for dopaminergic protection against MA insult.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Interplay between PKC and PHOX <I>in vivo</I> in the neurotoxic condition remains unclear. </LI> <LI> PKCδ co-immunoprecipitated with p47<I>phox</I> and facilitated the potential of p47<I>phox.</I> </LI> <LI> Methamphetamine-induced Nrf-2 system was mitigated by inhibition of p47<I>phox</I> or PKCδ. </LI> <LI> BSO potentiated microgliosis and apoptotic changes, leading to dopaminergic losses. </LI> <LI> PKCδ is a critical regulator for p47<I>phox</I> activation induced by methamphetamine. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Dang Quoc Khanh,Young-Soo Suh 대한전기학회 2013 Journal of Electrical Engineering & Technology Vol.8 No.3
A new remote control algorithm for a mobile robot is proposed, where a remote controller consists of a camera and inertial sensors. Initially the relative position and orientation of a robot is estimated by capturing four circle landmarks on the plate of the robot. When the remote controller moves to point to the destination, the camera pointing trajectory is estimated using an inertial navigation algorithm. The destination is transmitted wirelessly to the robot and then the robot is controlled to move to the destination. A quick movement of the remote controller is possible since the destination is estimated using inertial sensors. Also unlike the vision only control, the robot can be out of camera’s range of view.
A Study on the Development of the Position Detection System of Small Vessels for Collision Avoidance
Dang-Khanh Le,Teak-Kun Nam 해양환경안전학회 2014 海洋環境安全學會誌 Vol.20 No.2
본 연구에서는 단거리 영역 내에서 대상물표의 정확한 위치를 파악하여 물표와의 충돌을 방지하기 위한 시스템을 개발하였다. 이를 위해 먼저 물표를 속도 모델과 가속도 모델로 표현하여 초기위치로부터의 움직임을 프로세스 잡음과 측정 잡음이 있는 상태에서 위치, 속도 및 가속도를 추정하였다. 추정기법으로는 칼만필터를 적용하였고 시뮬레이션을 통해 제안기법의 유용성을 확인하였다. 다음으로는 레이저센서를 적용하여 이동하는 물표와의 거리를 계측할 수 있는 시스템을 제작하여 물표의 이동 정보를 검출하였다. 이동 물표를 대상으로 속도 모델과 가속도 모델을 적용하여 실험을 수행하였고, 각각의 실험을 통해 불연속적인 측정데이터가 필터링을 통해 매끄럽고 연속적인 측정값으로 얻어지는 것을 확인하였다. 또한 물표 데이터의 계측과 디스플레이를 위한 UI를 구축하였으며, 물표가 일정거리 영역이내에 접근했을 경우 시각, 청각적인 경보를 울릴 수 있는 기능을 부가하였다. 본 연구결과를 통해 저가의 장비로 물표 위치의 추정 성능이 뛰어난 시스템을 구축할 수 있었다. In this paper, a developed device for detecting target’s location and avoiding collision is proposed. Velocity and acceleration model of target are derived to estimate target's information, i.e. position, velocity and acceleration considering process and measurement noise. Kalman filtering method applied to the estimation process and its results was confirmed by simulation. The distance measurements system using laser sensor for moving target system is also developed to confirm the effectiveness of the proposed scheme. Experiments to get information of moving target with velocity and acceleration model was executed. The data with filtering and without filtering was compared by experiments. Discontinuous measured data was changed to smooth and continuous data by Kalman filtering. It is confirmed that desired data was obtained by applying proposed scheme.. UI for measuring and monitoring the target data is developed and visual and auditory alarm function is attached on the system Finally, position estimation system of moving target with good performance is achieved by low price equipments.
Dang, Duy-Khanh,Shin, Eun-Joo,Mai, Anh-Thu,Jang, Choon-Gon,Nah, Seung-Yeol,Jeong, Ji Hoon,Ledent, Catherine,Yamamoto, Tsuneyuki,Nabeshima, Toshitaka,Onaivi, Emmanuel S.,Kim, Hyoung-Chun Elsevier 2017 FREE RADICAL BIOLOGY AND MEDICINE Vol.108 No.-
<P><B>Abstract</B></P> <P>Accumulating evidence suggests that cannabinoid ligands play delicate roles in cell survival and apoptosis decisions, and that cannabinoid CB1 receptors (CB1R) modulate dopaminergic function. However, the role of CB1R in methamphetamine (MA)-induced dopaminergic neurotoxicity in vivo remains elusive. Multiple high doses of MA increased phospho-ERK and CB1R mRNA expressions in the striatum of CB1R (+/+) mice. These increases were attenuated by CB1R antagonists (i.e., AM251 and rimonabant), an ERK inhibitor (U0126), or dopamine D2R antagonist (sulpiride). In addition, treatment with MA resulted in dopaminergic impairments, which were attenuated by CB1R knockout or CB1R antagonists (i.e., AM251 and rimonabant). Consistently, MA-induced oxidative stresses (i.e., protein oxidation, lipid peroxidation and reactive oxygen species) and pro-apoptotic changes (i.e., increases in Bax, cleaved PKCδ- and cleaved caspase 3-expression and decrease in Bcl-2 expression) were observed in the striatum of CB1R (+/+) mice. These toxic effects were attenuated by CB1R knockout or CB1R antagonists. Consistently, treatment with four high doses of CB1R agonists (i.e., WIN 55,212-2 36mg/kg and ACEA 16mg/kg) also resulted in significant oxidative stresses, pro-apoptotic changes, and dopaminergic impairments. Since CB1R co-immunoprecipitates PKCδ in the presence of MA or CB1R agonists, we applied PKCδ knockout mice to clarify the role of PKCδ in the neurotoxicity elicited by CB1Rs. CB1R agonist-induced toxic effects were significantly attenuated by CB1R knockout, CB1R antagonists or PKCδ knockout. Therefore, our results suggest that interaction between D2R, ERK and CB1R is critical for MA-induced dopaminergic neurotoxicity and that PKCδ mediates dopaminergic damage induced by high-doses of CB1R agonist.</P> <P><B>Highlights</B></P> <P> <UL> <LI> MA or CB1R agonists increased CB1R mRNA level in the striatum of wild type mice. </LI> <LI> Inhibition of CB1R attenuated dopaminergic degeneration induced by MA. </LI> <LI> CB1R co-immunoprecipitated PKCδ in the presence of MA or CB1R agonists. </LI> <LI> Oxidative burdens contributed to PKCδ cleavage and apoptotic activity. </LI> <LI> CB1R agonists-induced dopaminergic degeneration was protected by PKCδ inhibition. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>