Objectimage 실험연구

오재희(Oh, Jae-Hee),김지현(Jeehyun Kim) 한국타이포그라피학회 2011 글짜씨 Vol.3 No.1

A Study on the Post-Receptor Mechanism of Adenosine Receptor on Acetylcholine Release in the Rat Hippocampus

최봉규,오재희,Choi, Bong-Kyu,Oh, Jae-Hee The Korean Society of Pharmacology 1994 대한약리학잡지 Vol.30 No.3

흰쥐 해마(hippocampus)에서 acetylcholine (ACh) 유리에 미치는 $A_{1}-adenosine$ 수용체의 post-receptor 기전에 관한 지견을 얻고자 하여 $^3H-choline$으로 평형시킨 해마 slice를 사용하여 $^3H-ACh$ 유리에 미치는 여러가지 약물들의 영향을 관찰하였다. Adenosine $(0.3{\sim}300\;{\mu}M)$은 전기자극(3Hz, 2 ms, 5 $VCm^{-1}$, 구형파)에 의한 ACh 유리를 용량 의존적으로 감소 시켰으며, 이러한 효과는 $A_1-adenosine$ 수용체의 선택적 차단제인 8-cyclopentyl-1, 3-dipropylxanthine $(2\;{\mu}M)$에 의해 차단됨을 볼 수 있었다. G-단백 억제제인 N-ethylmaleimide (NEM, 10과 $30\;{\mu}M$)는 그 자체에 의하여 자극유발성 ACh 유리를 증가시켰으며, adenosine의 효과는 NEM 전처리에 의하여 완전히 소실되었다. Protein kinase C 활성화제인 $4{\beta}-phorbol$ 12, 13-dibutyrate (PDB, $1{\sim}10\;{\mu}M$)는 ACh 유리 증가를 일으켰으며 억제제인 polymyxin B (PMB, $0.03{\sim}1\;mg$)는 감소를 일으켰으나, adenosine에 의한 ACh 유리 감소효과는 PDB 및 PMB에 의해 영향을 받지 않았다. $Ca^{++}$-통로 차단제인 nifedipine $(1\;{\mu}M)$은 adenosine의 효과를 길항함을 볼 수 있었으나 $K{^+}$-통로 차단제인 glibenclamide는 adenosine의 효과에 영향을 미치지 못하였다. 8-Bromo-cAMP (100과 $300{\mu}M$) 그 자체로는 ACh 유리에 별다른 영향을 미치치 못하였으나 $300\;{\mu}M$ 8-bromo-cAMP 전처리에 의하여 $30\;{\mu}M\;adenosine$의 효과가 억제됨을 볼 수 있었다. 이상의 실험결과로 흰쥐 해마에서 $A_1-adenosine$ 수용체를 통한 adenosine의 ACh유리 감소는 G-단백에 의존적이며, 이러한 효과에 nifedipine에 예민한 $Ca^{++}$-통로와 adenylate cyclase계가 일부 관여함은 확실하나 proteinkinase C 및 glibenclamide에 예민한 $K{^+}$통로는 관여하지 않는 것으로 사료된다. Since it was been reported that the depolarization-induced ACh release is inhibited by activation of presynaptic $A_1-adenosine$ heteroreceptor in hippocampus, a large body of experimental data on the post-receptor mechanism of this process has been accumulated. But, the post-receptor mechanism of presynaptic $A_1-adenosine$ receptor on the ACh release has not been clearly elucidated yet. Therefore, it was attempted to clarify the post-receptor mechanisms of the $A_1-adenosine$ receptor-mediated control of ACh release in this study. Slices from rat hippocampus were equilibrated with $^3H-choline$ and the release of the labelled products was evoked by electrical stimulation (3 Hz, 5 $VCm^{-1}$, 2ms, rectangular pulses), and the influence of various agents on the evoked tritium-outflow was investigated. Adenosine, in concentrations ranging from $0.3{\sim}300\;{\mu}M$, decreased the ACh release in a dose-dependent manner, without affecting the basal rate of release. The adenosine effects were significantly inhibited by $DPCPX\;(2\;{\mu}M)$, a selective $A_1-receptor$ antagonist. The responses to N-ethylmaleimide $(10&30{\mu}M)$, a SH-alkylating agent of G-protein, were characterized by increments of the evoked ACh-release and the basal release, and the adenosine effects were completely abolished by NEM pretreatment. PDB $(1{\sim}10\;{\mu}M)$, a specific protein kinase C (PKC) activator, increased, whereas PMB $(0.03{\sim}1\;mg)$, a PKC inhibitor, decreased the evoked ACh-release, and the adenosine effects were not affected by these agents. Nifedipine $(1\;{\mu}M)$, a $Ca^{2+}\;-channel$ blocker of dihydropyridine analogue, significantly inhibited the adenosine effect, but glibenclamide, a $K^+-channel$ blocker, did not. Finally, 8-bromo cyclic AMP $(100\;&\;300{\mu}M)$, a membrane-permeable analogue of cAMP, did not alter the ACh release, but adenosine effects were inhibited by pretreatment with large dose of 8-br-cAMP $(300\;{\mu}M)$. These results indicate that the decrement of the evoked ACh-release by $A_1-adenosine$ receptor is mediated by the G-protein, and nifedipine-sensitive $Ca^{2+}-channel$ and adenylate cyclase system are coupled partly to this effect, and that protein kinase C and glibenclamide-sensitive $K{^+}-channel$ are not involved in this process.

공증발과 열산화로 제조한 Ag-CuO-SnO₂ 박막에서 미세조직과 CO 가스 감지특성

지인걸,한규석,오재희,고태경,Ji, In-Geol,Han, Kyu-Suk,Oh, Jae-Hee,Ko, Tae-Gyung 한국세라믹학회 2009 한국세라믹학회지 Vol.46 No.4

In this study, we investigated microstructure and the CO gas sensing properties of Ag-CuO-$SnO_2$ thin films prepared by co-evaporation and subsequently thermal oxidation at air atmosphere. The sensitivity of a Cu-Sn films, thermally oxidized at $600^{\circ}C$, is strongly affected by the amount of Cu. At Cu:7 wt%-Sn:93 wt%, the film exhibited a maximum sensitivity of ${\sim}2.3$ to CO gas of 1000 ppm at $300^{\circ}C$. In contrast, the sensitivity of a Sn-Ag film did not change significantly with the amount of Ag. An enhanced sensitivity of ${\sim}3.7$ was observed in the film with a composition of Ag:3 wt%-Cu:4 wt%-Sn:93 wt%, when thermally oxidized at $600^{\circ}C$. In addition, this thin film shows a response time of ${\sim}80$ sec and a recovery time of ${\sim}450$ sec to 1000 ppm CO gas. The results demonstrate that the CO sensitivity of the Ag-CuO-$SnO_2$ thin films may be closely associated with coexistence of $SnO_2$ and SnO phase, decrease in average particle size, and a porous microstructure. We also suggest that co-evaporation and followed by thermal oxidation is a very simple and effective method to prepare oxide gas sensor thin films.

NiCuZn계 페라이트의 조성에 따른 복소투자율 변화 해석

남중희(Joong-Hee Nam),오재희(Jae-Hee Oh) 한국자기학회 1996 韓國磁氣學會誌 Vol.6 No.6

The characteristics of the complex permeability of (Ni_xCu_(0.2)Zn_(0.8-x)O)_(1-w) (Fe₂O₃)_(1+w) with various Ni and Co₃O₄ contents were investigated in this work. It is found that the NiCuZn ferrites with x≥0.6 have a relatively small peak width of the imaginary part of permeability μ″. The resonance frequency is increased as Ni content becomes higher, where the loss is low. The μ″ value decreases with increasing Fe₂O₃ deficiency, but the resonance frequency(fμㆍmax) is only slightly affected by Fe₂O₃ deficiency. In case of Co₃O₄ addition to the NiCuZn ferrites, the fμㆍmax increases since the initial permeability decreases with the amount of Co₃O₄. It is concluded that the Ni content in the NiCuZn ferrite is a dominant factor for the total loss of these spinel ferrites.

이산화탄소 분해용 페라이트 담지 다공성 세라믹 섬유복합체 제조와 물성

이봉수,김명수,최승철,오재희,이재춘,Lee, Bong-Soo,Kim, Myung-Soo,Choi, Seung-Chul,Oh, Jae-Hee,Lee, Jae-Chun 한국세라믹학회 2002 한국세라믹학회지 Vol.39 No.8

대기중에 방출되는 이산화탄소 저감을 위해서 산소결핍 페라이트를 이용한 이산화탄소의 탄소 전환에 대한 연구가 이루어지고 있다. 본 연구에서는 우레아 분해를 이용한 균일침전법에 의해 Ni 페라이트 $Ni_{0.4}Fe_{2.6}O_4$를 다공성 세라믹섬유 지지체(지름 50mm, 두께 10mm)에 in-situ 하게 담지하였다. 페라이트를 다공성 세라믹섬유 지지체에 담지하는 방법이 이산화탄소 분해효율에 미치는 영향을 조사하였다. 페라이트가 담지된 시편으로부터 잔류 염소이온과 우레아를 제거하면 주 결정상으로 스피넬 구조의 페라이트를 얻을 수 있었으나 이산화탄소 분해효율이 크게 향상되지는 않았다. 페라이트가 중량 분율로 20% (1g) 담지된 다공성 세라믹섬유 복합체 시편의 경우, 초기 3분 까지는 100% 이산화탄소 분해효율을 나타내었으나 10분 경과 후에는 급격하게 감소하였다. 이산화탄소 분해효율 감쇄 특성시간은 약 3∼7분 사이로 나타났다. The decomposition and/or conversion of carbon dioxide to carbon have been studied using oxygen-deficient ferrites for the reduction of $CO_2$ emission to the atmosphere. In this work, the homogeneous precipitation method using urea decomposition was employed to induce in situ precipitation of Ni ferrite($Ni_{0.4}Fe_{2.6}O_4$) on the porous ceramic fiber support (50 mm diameter${\times}$10 mm thickness). Effects of ferrite loading conditions on the CO2 decomposition efficiency were discussed in this paper. Removal of residual chloride ions and urea by solvent exchange from the porous media after ferrite deposition apparently helps to form spinel ferrite, but does not increase the efficiency of $CO_2$ decomposition. Porous ceramic fiber composites containing 20 wt% (1g) ferrite samples showed 100% efficiency for $CO_2$decomposition during the first three minutes, but the efficiency decreased rapidly after the elapsed time of ten minutes. The characteristic reduction time for the $CO_2$ decomposition efficiency was estimated as about 3∼7 min.

결핵균에 감염된 숙주 면역세포의 저산소 조건 배양 시 발현되는 유전자군 발굴 및 기능분석

이지숙(Ji-Sook Lee),오재희(Jae-Hee Oh),손지웅(Ji Woong Son),송창화(Chang-Hwa Song),김화중(Hwa-Jung Kim),박정규(Jung-Kyu Park),백태현(Tae-Hyun Paik),조은경(Eun-Kyeong Jo) 대한미생물학회 2007 Journal of Bacteriology and Virology Vol.37 No.2

Ni - ferrite를 코팅한 Moly - permalloy 분말의 제조 및 특성 평가

박현규(Hyun-Kyu Park),오재희(Jae-Hee Oh) 한국자기학회 2004 한국자기학회 학술연구발표회 논문개요집 Vol.14 No.2

시각 장애인을 위한 착용형 보조 장치의 새로운 디자인 설계

이정현(Jeong-Hyeon Lee),오재희(Jae-Hee Oh),차현준(Hyeon-Jun Cha),허준영(Jun-Young Heo),송규원(Gyu-Won Song),이승환(Seung-Hwan Lee) 한국정보기술학회 2021 Proceedings of KIIT Conference Vol.2021 No.11

본 논문에서는 시각장애인의 안정적인 보행을 보조하기 위한 착용형 장치의 새로운 디자인 설계를 제안한다. 착용형 보행 보조 장치는 LiDAR, IMU, 진동모터 및 임베디드 보드로 구성되어있다. LiDAR는 시각장애인 주변의 클라우드 포인트를 검출하였고, 이를 토대로 장애물 탐지를 수행하기 위해 ROS Obstacle Detector Package가 이용되었다. 탐지된 장애물 정보는 진동모터를 통해 시각장애인에게 표현/전달되고, 시각장애인은 이를 이용하여 다가오는 물체를 회피하여 안정적으로 보행할 수 있게 된다. 현재 모듈 단위로 구현 및 테스트를 진행하고 있으며, 향후 설계가 완료된 후, 실제 시각장애인을 대상으로 실험을 진행할 예정이다. In this study, we propose a new design of wearable walking assistive device for the blind. The wearable walking assistive device is composed of LiDAR, IMU, vibration motor and an embedded board. LiDAR detects point cloud around the blind and ROS Obstacle Detector Package is performed using it. The detected obstacle information is expressed/transmitted to the blind through the vibration motor, and finally the blind can walk stably by avoiding approaching objects. Currently, we are implementing and testing modules of the wearable assistive device. In future work, we plan to conduct experiments practically for the blind.

흰쥐 해마에서 Acetylcholine 유리에 관여하는 Adenosine Receptor의 Post-Receptor 기전에 관한 연구

최봉규(Bong Kyu Choi),오재희(Jae Hee Oh) 대한약리학회 1994 대한약리학잡지 Vol.30 No.3

흰쥐 해마(hippocampus)에서 acetylcholine (ACh) 유리에 미치는 A₁-adenosine 수용체의 post-receptor 기전에 관한 지견을 얻고자 하여 ³H-choline으로 평형시킨 해마 slice를 사용하여 ³H-ACh 유리에 미치는 여러가지 약물들의 영향을 관찰하였다. Adenosine (0.3 ~ 300μM)은 전기자극(3Hz, 2 ms, 5 VCm^-1, 구형파)에 의한 ACh 유리를 용량 의존적으로 감소 시켰으며, 이러한 효과는 A₁-adenosine 수용체의 선택적 차단제인 8-cyclopentyl-1, 3-dipropylxanthine (2μM)에 의해 차단됨을 볼 수 있었다. G-단백 억제제인 N-ethylmaleimide (NEM, 10과 30μM)는 그 자체에 의하여 자극유발성 ACh 유리를 증가시켰으며, adenosine의 효과는 NEM 전처리에 의하여 완전히 소실되었다. Protein kinase C 활성화제인 4β-phorbol 12, 13-dibutyrate (PDB, 1 ~ 10μM)는 ACh 유리 증가를 일으켰으며 억제제인 polymyxin B (PMB, 0.03 ~ 1 mg)는 감소를 일으켰으나, adenosine에 의한 ACh 유리 감소효과는 PDB 및 PMB에 의해 영향을 받지 않았다. Ca⁺⁺-통로 차단제인 nifedipine (1μM)은 adenosine의 효과를 길항함을 볼 수 있었으나 K⁺-통로 차단제인 glibenclamide는 adenosine의 효과에 영향을 미치지 못하였다. 8-Bromo-cAMP (100과 300μM) 그 자체로는 ACh 유리에 별다른 영향을 미치치 못하였으나 300μM 8-bromo-cAMP 전처리에 의하여 30μM adenosine의 효과가 억제됨을 볼 수 있었다. 이상의 실험결과로 흰쥐 해마에서 A₁-adenosine 수용체를 통한 adenosine의 ACh유리 감소는 G-단백에 의존적이며, 이러한 효과에 nifedipine에 예민한 Ca⁺⁺-통로와 adenylate cyclase계가 일부 관여함은 확실하나 proteinkinase C 및 glibenclamide에 예민한 K⁺통로는 관여하지 않는 것으로 사료된다. Since it was been reported that the depolarization-induced ACh release is inhibited by activation of presynaptic A₁-adenosine heteroreceptor in hippocampus, a large body of experimental data on the post-receptor mechanism of this process has been accumulated. But, the post-receptor mechanism of presynaptic A₁-adenosine receptor on the ACh release has not been clearly elucidated yet. Therefore, it was attempted to clarify the post-receptor mechanisms of the A₁-adenosine receptor-mediated control of ACh release in this study. Slices from rat hippocampus were equilibrated with ³H-choline and the release of the labelled products was evoked by electrical stimulation (3 Hz, 5 VCm^-1, 2ms, rectangular pulses), and the influence of various agents on the evoked tritium-outflow was investigated. Adenosine, in concentrations ranging from 0.3 ~ 300μM, decreased the ACh release in a dose-dependent manner, without affecting the basal rate of release. The adenosine effects were significantly inhibited by DPCPX (2μM), a selective A₁-receptor antagonist. The responses to N-ethylmaleimide (10&30μM), a SH-alkylating agent of G-protein, were characterized by increments of the evoked ACh-release and the basal release, and the adenosine effects were completely abolished by NEM pretreatment. PDB (1 ~ 10μM), a specific protein kinase C (PKC) activator, increased, whereas PMB (0.03 ~ 1 mg), a PKC inhibitor, decreased the evoked ACh-release, and the adenosine effects were not affected by these agents. Nifedipine (1μM), a Ca²⁺ -channel blocker of dihydropyridine analogue, significantly inhibited the adenosine effect, but glibenclamide, a K⁺-channel blocker, did not. Finally, 8-bromo cyclic AMP (100 & 300μM), a membrane-permeable analogue of cAMP, did not alter the ACh release, but adenosine effects were inhibited by pretreatment with large dose of 8-br-cAMP (300μM). These results indicate that the decrement of the evoked ACh-release by A₁-adenosine receptor is mediated by the G-protein, and nifedipine-sensitive Ca²⁺-channel and adenylate cyclase system are coupled partly to this effect, and that protein kinase C and glibenclamide-sensitive K⁺-channel are not involved in this process.

초음파 여기 페라이트 플레이팅 법에 의한 Fe₃O₄ / BaTiO₃ 복합 분말의 제조 및 특성

최성현(Sung Hyun Choi),오재희(Jae Hee Oh) 한국자기학회 2002 한국자기학회 학술연구발표회 논문개요집 Vol.12 No.2