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RISS 인기검색어
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- 발행기관 : Macmillan ; Oxford University Press (검색결과 3 건)
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Lee, Soon-Tae,Chu, Kon,Jung, Keun-Hwa,Kim, Se-Jeong,Kim, Dong-Hyun,Kang, Kyung-Mook,Hong, Nan Hyung,Kim, Jin-Hee,Ban, Jae-Joon,Park, Hee-Kwon,Kim, Seung U,Park, Chung-Gyu,Lee, Sang Kun,Kim, Manho,Roh, Macmillan ; Oxford University Press 2008 Brain Vol.131 No.3
<P>Neural stem cell (NSC) transplantation has been investigated as a means to reconstitute the damaged brain after stroke. In this study, however, we investigated the effect on acute cerebral and peripheral inflammation after intracerebral haemorrhage (ICH). NSCs (H1 clone) from fetal human brain were injected intravenously (NSCs-iv, 5 million cells) or intracerebrally (NSCs-ic, 1 million cells) at 2 or 24 h after collagenase-induced ICH in a rat model. Only NSCs-iv-2 h resulted in fewer initial neurologic deteriorations and reduced brain oedema formation, inflammatory infiltrations (OX-42, myeloperoxidase) and apoptosis (activated caspase-3, TUNEL) compared to the vehicle-injected control animals. Rat neurosphere-iv-2 h, but not human fibroblast-iv-2 h, also reduced the brain oedema and the initial neurologic deficits. Human NSCs-iv-2 h also attenuated both cerebral and splenic activations of tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and nuclear factor-kappa B (NF-kappaB). However, we observed only a few stem cells in brain sections of the NSCs-iv-2 h group; in the main, they were detected in marginal zone of spleens. To investigate whether NSCs interact with spleen to reduce cerebral inflammation, we performed a splenectomy prior to ICH induction, which eliminated the effect of NSCs-iv-2 h transplantation on brain water content and inflammatory infiltrations. NSCs also inhibited in vitro macrophage activations after lipopolysaccharide stimulation in a cell-to-cell contact dependent manner. In summary, early intravenous NSC injection displayed anti-inflammatory functionality that promoted neuroprotection, mainly by interrupting splenic inflammatory responses after ICH.</P>
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Speech experience shapes the speechreading network and subsequent deafness facilitates it.
Suh, Myung-Whan,Lee, Hyo-Jeong,Kim, June Sic,Chung, Chun Kee,Oh, Seung-Ha Macmillan ; Oxford University Press 2009 Brain Vol.132 No.10
<P>Speechreading is a visual communicative skill for perceiving speech. In this study, we tested the effects of speech experience and deafness on the speechreading neural network in normal hearing controls and in two groups of deaf patients who became deaf either before (prelingual deafness) or after (postlingual deafness) auditory language acquisition. Magnetic signals from the cerebral cortex were recorded using a 306-channel magnetoencephalographic system. During magnetoencephalographic measurements, subjects were asked to perform a speechreading task from video clips of a female speaker either pronouncing syllables (speechreading condition) or showing closed-mouth movement. The sources of the evoked fields were modelled using equivalent current dipoles, the origins of which were fitted to the intracranial space based on magnetic resonance imaging findings. During the speechreading condition, the latency of auditory cortex activation was shorter in the postlingual deafness group than in the normal hearing control group. This parameter negatively correlated with speechreading scores measured clinically. Furthermore, as the duration of deafness increased, the latency of auditory cortex activation decreased exponentially. However, no such correlation was found in the prelingual deafness group which differed significantly from the two other groups in this respect. The latency of auditory cortex activation was significantly longer in the prelingual deafness group than in the two other groups. Thus, auditory experience may be crucial for the development of a normal neural network for speechreading. The pre-existing speechreading network in the postlingual deafness group is made more efficient by speeding up the neural response.</P>
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Only tetracaine and not other local anaesthetics induce apoptosis in rat cortical astrocytes.
Lee, W Y,Park, C J,Shin, T J,Yum, K W,Yoon, T G,Seo, K S,Kim, H J Macmillan Journals ; Oxford University Press 2009 British journal of anaesthesia Vol.103 No.5
<P>BACKGROUND: The potential risks of neurotoxicity due to local anaesthetics after regional anaesthesia have been suggested recently. To evaluate the neurotoxicity of commonly used local anaesthetics, primary cultured rat cortical astrocytes were treated with lidocaine, ropivacaine, bupivacaine, levobupivacaine, and tetracaine. METHODS: Cell death after local anaesthetic treatment was evaluated with a lactate dehydrogenase (LDH) assay. To examine the mechanisms of cell death, reactive oxygen species (ROS) measurement and western blots of poly-ADP ribose polymerase (PARP), procaspase-3, and mitogen-activated protein kinases family members were performed. RESULTS: Of the local anaesthetics, which were applied at <1 mM for 18 h, only tetracaine significantly increased LDH leakage (P<0.05) and cell death in a dose- and time-dependent manner. Hoechst 33258-propidium iodide staining and western blots with PARP and procaspase-3 antibodies suggested that tetracaine induced apoptosis. ROS levels increased 2-fold at 30 min after tetracaine treatment compared with the control and then decreased. The antioxidants, N-acetylcysteine and trolox, markedly inhibited tetracaine-induced apoptosis. CONCLUSIONS: Tetracaine induced apoptosis through ROS generation. Further studies focusing on the neurotoxicity of tetracaine are needed.</P>
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