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여현구,홍정주,이영전,이경식,전창엽,박정형,원진영,서진철,안유진,김건우,백승호,황은하,김그린,진영배,정강진,구본상,강필용,임경섭,김선욱,허재원,김영현,손영훈,김지수,최치훈,차상훈,이상래 한국뇌신경과학회 2019 Experimental Neurobiology Vol.28 No.4
The function of microglia/macrophages after ischemic stroke is poorly understood. This study examines the role of microglia/macrophages in the focal infarct area after transient middle cerebral artery occlusion (MCAO) in rhesus monkeys. We measured infarct volume and neurological function by magnetic resonance imaging (MRI) and non-human primate stroke scale (NHPSS), respectively, to assess temporal changes following MCAO. Activated phagocytic microglia/macrophages were examined by immunohistochemistry in post-mortem brains (n=6 MCAO, n=2 controls) at 3 and 24 hours (acute stage), 2 and 4 weeks (subacute stage), and 4, and 20 months (chronic stage) following MCAO. We found that the infarct volume progressively decreased between 1 and 4 weeks following MCAO, in parallel with the neurological recovery. Greater presence of cluster of differentiation 68 (CD68)-expressing microglia/macrophages was detected in the infarct lesion in the subacute and chronic stage, compared to the acute stage. Surprisingly, 98~99% of transforming growth factor beta (TGFβ) was found co-localized with CD68-expressing cells. CD68-expressing microglia/macrophages, rather than CD206+ cells, may exert anti-inflammatory effects by secreting TGFβ after the subacute stage of ischemic stroke. CD68+ microglia/macrophages can therefore be used as a potential therapeutic target.
박준형,서진철,원진영,Hyeon-Gu Yeo,안유진,Keonwoo Kim,진영배,구본상,임경섭,Kang-Jin Jeong,Philyong Kang,Hwal-Yong Lee,Seung Ho Baek,Chang-Yeop Jeon,홍정주,허재원,김영현,Sang-Je Park,김선욱,이동석,이상래,이영전 한국뇌신경과학회 2019 Experimental Neurobiology Vol.28 No.3
Mitochondria continuously fuse and divide to maintain homeostasis. An impairment in the balance between the fusion and fission processes can trigger mitochondrial dysfunction. Accumulating evidence suggests that mitochondrial dysfunction is related to neurodegenerative diseases such as Parkinson’s disease (PD), with excessive mitochondrial fission in dopaminergic neurons being one of the pathological mechanisms of PD. Here, we investigated the balance between mitochondrial fusion and fission in the substantia nigra of a non-human primate model of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD. We found that MPTP induced shorter and abnormally distributed mitochondria. This phenomenon was accompanied by the activation of dynamin-related protein 1 (Drp1), a mitochondrial fission protein, through increased phosphorylation at S616. Thereafter, we assessed for activation of the components of the cyclin-dependent kinase 5 (CDK5) and extracellular signal-regulated kinase (ERK) signaling cascades, which are known regulators of Drp1(S616) phosphorylation. MPTP induced an increase in p25 and p35, which are required for CDK5 activation. Together, these findings suggest that the phosphorylation of Drp1(S616) by CDK5 is involved in mitochondrial fission in the substantia nigra of a non-human primate model of MPTP-induced PD.
실시간 영상에서 모션 벡터 차이를 이용한 정면얼굴 이미지 탐지
김동현 ( Dong-hyun Kim ),정주신 ( Ju-sin Jung ),김현정 ( Hyun-jung Kim ),원일용 ( Il-young Won ) 한국정보처리학회 2012 한국정보처리학회 학술대회논문집 Vol.19 No.2
본 연구는 실시간 영상에서 정면 얼굴을 가지고 있는 이미지를 탐지하는 방법에 대한 것이다. 모든 프레임마다 얼굴 인식 등의 연산을 수행한다면 계산량과 시간이 문제이다. 우리가 제안하는 방법은 동일인이 등장하는 영상 중 동일한 얼굴을 추적하여 움직임의 차이를 이용하여 정면 이미지를 판단하는 것이다. Gaussian Mixture Model 과 Motion template 을 이용하였으며, 실험을 통해 도출된 결과는 제안 알고리즘의 유용성을 어느 정도 증명할 수 있었다.