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RF-스퍼터링 기법으로 제작한 Fe<SUB>3</SUB>O<SUB>4</SUB> 박막에 Ta 기저층이 미치는 효과
국지현(Jihyeon Gook),이년종(Nyun Jong Lee),배유정(Yu Jeong Bae),김태희(Tae Hee Kim) 한국자기학회 2015 韓國磁氣學會誌 Vol.25 No.2
Si(100)\200 nm SiO<SUB>2</SUB>\5 nm Ta\5 nm MgO\35 nm Fe<SUB>3</SUB>O<SUB>4</SUB> multi-layers were prepared by using RF-sputtering and ultra-high vacuum molecular beam epitaxy (UHV-MBE) techniques. After post-annealing the multi-layers at 500℃ for 1 hour under the high vacuum of~1 × 10<SUP>?6</SUP> Torr, we observed ferromagnetic properties at room temperature as well as the Verwey transition which is the typical features of magnetite crystals formed. We have carried out a comparative study of the effect of Ta buffered layer on the crystallinity and magnetic properties of Fe<SUB>3</SUB>O<SUB>4</SUB> thin films prepared under different growth and annealing conditions.
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생쥐에서 Pilocarpine에 의한 경련이 해마의 신경세포사멸, 이끼섬유발아 및 신경발생에 미치는 영향
이상현(Sang-Hyeon Lee),국지현(Ji-Hyun Kook),황신애(Shinae Hwang),김종근(Jong-Keun Kim),배춘상(Choon-Sang Bae) 대한체질인류학회 2011 해부·생물인류학 (Anat Biol Anthropol) Vol.24 No.4
해마 치아이랑은 지속적인 경련 후 이끼섬유발아(mossy fiber sprouting)가 일어나는 부위일 뿐만 아니라 성체 뇌의 신경발생(neurogenesis)이 일어나는 부위로 많은 연구의 대상이 되고 있다. 본 논문은 pilocarpine에 의한 발작을 이용한 해마 및 치아이랑에서 신경세포사멸, 이끼섬유발아 및 신경발생의 변동을 조사하여 이들 3자간의 상관관계를 규명하고자 하였다. 수컷 ICR 생쥐와 C57BL/6 생쥐에 pilocarpine을 처리하여 발작을 유발하였으며 처음 4시간 동안 발작양상을 관찰하여 Racine의 5등급 scale에 중 적어도 3등급 이상인 동물을 실험에 사용하였다. 신경세포사멸은 Fluoro-Jade C(FJC) 염색으로, 이끼섬유발아는 NeoTimm 염색으로, 신경발생은 bromodeoxyuridine(BrdU) 주사 후 이에 대한 면역조직염색으로 평가하였다. 본 실험에서 사용한 모든 동물에서 pilocarpine(300 mg/kg, ip) 투여에 의해 3등급 이상의 발작을 일으켰으며 발작 반응은 ICR 생쥐에서 C57BL/6 생쥐에서 보다 더 강하게 나타났다. 즉 ICR 생쥐의 평균 발작 등급이 4.37로 C57BL/6 생쥐의 3.22보다 유의하게 강하였다. 그러나 3등급 이상의 발작이 시작하는데 걸린 시간은 15~20분 사이로 차이가 없었다. 약물주입 4시간 후 ICR 생쥐에서는 FJC염색 상 해마 문(hilus)에서 사멸세포가 관찰되었으나, C57BL/6 생쥐에서는 관찰되지 않았다. 24시간 이후부터는 두 strain 모두에서 CA1 및 CA3 피라밋세포의 사멸도 관찰되었다. 이 세포사멸은 약물투여 후 3일에 가장 강하였으며 l주일 후에는 거의 관찰할 수 없었다. 신경발생을 나타내는 해마의 BrdU 양성세포수는 대조동물의 경우 C57BL/6 생쥐가 ICR 생쥐보다 유의하게 많았다. BrdU 양성세포수는 약물투여 2일 후에 대조군에 비해 유의하게 증가하였으며, 8일 후에는 더 큰 증가를 보인 후 15일 후에는 대조군 수준으로 돌아왔다. 두 strain 모두에서 약물투여 후 해마 신경발생의 증가를 보였으나 대조동물과의 비로 비교하면 ICR 생쥐가 C57BL/6 생쥐에 비해 더 큰 증가를 보였다. 이끼섬유발아는 약물투여 2주 후에 약하게 나타나서 4주 후에는 더 강해졌으며 두 strain 간에 차이는 관찰 할 수 없었다. 이상의 성적은 pilocarpine에 의한 발작의 정도와 신경세포사멸 및 신경발생 간에는 서로 상관관계가 있지만 이들과 이끼섬유발아 간에는 직접적인 상관관계가 없음을 시사한다. Present study was performed to delineate the inter-relationship among neuronal death, mossy fiber sprouting (MFS) and neurogenesis in hippocampal formation of pilocarpine-treated mice. Status epilepticus was induced by intraperitoneal administration of 300 mg/kg pilocarpine in male ICR and C57BL/6 mouse. The severity of seizure was evaluated using 5 grades of Racine scales for first 4 hr after pilocarpine injection. Fluro-Jade C (FJC) staing, NeoTimm"s staining and immunohistochemistry for BrdU were employed to evaluate neuronal cell death, MFS and neurogenesis, respectively. All animals in the present study induced seizures over grade 3 of Racine scale by pilocarpine injection. ICR mice show higher seizure severity (mean Racine scale; 4.37) than C57BL/6 mice do (mean Racine scale; 3.22), while the latency times for the first seizure over Racine scale grade 3 are from 15 min to 20 min and showed no difference between the 2 strains. In ICR mouse, numerous FJC-positive cells in hilus of hippocampus were detected at 4 h after pilocarpine injection, while they were not detected at that time in C57BL/6 mouse. The number of FJC-positive neuronal cells, which were densely found in the pyramidal layer of CA1, CA3 and hilus polymorphic regions of hippocampus, reached peak at 3 days after injection and then few cells were found at 7 days after injection in both strains. In control animals, BrdU positive cells in dentate subgranular layer which represent the hippocampal neurogenesis were more numerous in C57BL/6 than in ICR. The number of BrdU positive cells significantly increased at 2 days after pilocarpine injection and reached the peak at 8 days after injection and returned to control level at 15 day after injection in both strains. The percent increase of the BrdU positive cell was more prominent in ICR mouse. MFS was found at 2 weeks after the injection and the intensity of MFS was getting strong at 4 weeks after injection. There was no differences in MFS grading between 2 strains. These results suggest that there are some inter-relationships among the seizure severity, hippocampal neuronal cell death and hippocampal neurogenesis, but they don"t have any significant relationships with the mossy fiber sprouting from dentate granule cells.
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Neuroprotection by Valproic Acid in Mouse Models of Permanent and Transient Focal Cerebral Ischemia
Yong Ri Qian,김종근,이무진,황신아,국지현,김종근,배춘성 대한약리학회 2010 The Korean Journal of Physiology & Pharmacology Vol.14 No.6
Valproic acid (VPA) is a well-known anti-epileptic and mood stabilizing drug. A growing number of reports demonstrate that VPA is neuroprotective against various insults. Despite intensive efforts to develop new therapeutics for stroke over the past two decades, all treatments have thus far failed to show clinical effect because of treatment-limiting side effects of the drugs. Therefore, a safety-validated drug like VPA would be an attractive candidate if it has neuroprotective effects against ischemic insults. The present study was undertaken to examine whether pre- and post-insult treatments with VPA protect against brain infarct and neurological deficits in mouse transient (tMCAO) and permanent middle cerebral artery occlusion (pMCAO) models. In the tMCAO (2 hr MCAO and 22 hr reperfusion) model, intraperitoneal injection of VPA (300 mg/kg, i.p.) 30 min prior to MCAO significantly reduced the infarct size and the neurological deficit. VPA treatment immediately after reperfusion significantly reduced the infarct size. The administration of VPA at 4 hr after reperfusion failed to reduce the infarct size and the neurological deficit. In the pMCAO model, treatment with VPA (300 mg/kg, i.p.) 30 min prior to MCAO significantly attenuated the infarct size, but did not affect the neurological deficit. Western blot analysis of acetylated H3 and H4 protein levels in extracts from the ischemic cortical area showed that treatment with VPA increased the expression of acetylated H3 and H4 at 2 hrs after MCAO. These results demonstrated that treatment with VPA prior to ischemia attenuated ischemic brain damage in both mice tMCAO and pMCAO models and treatment with VPA immediately after reperfusion reduced the infarct area in the tMCAO model. VPA could therefore be evaluated for clinical use in stroke patients.
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