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박민정,하세운,배혜란,김상호,Park Min-Jeong,Ha Se-Un,Bae Hae-Rahn,Kim Sang-Ho Korean Society of Life Science 2005 생명과학회지 Vol.15 No.3
신경흥분독성과 간질발작발현은 glutamate 수용체활성과 연관이 있다고 알려져 있다. a-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA), kainate 수용체에 대한 glutamate 활성을 포함하는 다양한 기전을 가진 항전간제인 Topiramate는 신경보호작용을 가진다는 증거가 제시되어 Topiramate가 간질발작 후 해마의 glutamate 수용체 발현에 미치는 효과를 관찰하였다. 흰쥐에 kainate를 복강 내 주사하여 간질중첩증을 유발시킨 후 Topiramate를 1주일 주사하였다 Apop tag in situ detection kit를 이용하여 세포손상을 관찰한 결과 kainate 유발 간질중첩증 1주일 후 해마의 CA1, CA3에서 심각한 세포사를 보였으나, Topiramte 처리 군에서는 세포사가 현저히 감소하였다. 간질중첩증 이후 NMDA 수용체 아형 1,2a, 2b 발현이 현저히 증가했으나 Topiramate 처치에 의해 NMDA수용체의 발현에는 뚜렷한 변화가 없었다. AMPA수용체에서는 GluR1이 간질중첩증 이후 현저히 상향 조정되었고 GluR2는 현저히 하향조정 되었다 Topiramate 1주일 처리 시 간질중첩증으로 인해 변화된 CluR1과 GluR2의 발현이 역전되었다. 결론적으로 Topiramate는 간질중침증에 의한 CluR1/CluR2 발현비의 증가로 유발되는 흥분성 신경세포사를 억제시킴으로써 신경보호작용이 있는 것으로 보인다. Excitotoxicity and epileptogenesis have often been associated with glutamate receptor activation. Accumulating evidences indicates that topiramate (TPM), an antiepileptic drug with multiple mechanisms of action has neuroprotective activity. We explored the neuroprotective effect of TPM on the status epilepticus (SE)-induced hippocampal neuronal death. After development of SE by kainite injection (15 mg/Kg), rats were treated with TPM (10mg/kg) for 1 week. The neuronal death was detected by Apop tag in situ detection kit, and the expression levels of glutamate receptors were semi-quantitatively analyzed by immunoblot. Kainate-induced SE caused a significant neuronal death and cell loss in CAI and CA3 regions of hippocampus at 1 week. However, treatment of TPM for 1 week after SE markedly reduced hippocampal neuronal death. The expression of N-methyl-D-aspartate (NMDA) receptor subunit 1, was increased by SE, but was not affected by 1 week treatment of TPM. The expressions of NMDA receptor subunit 2a and 2b were not changed by either SE or TPM. As for ${\alpha}-amino-3-hydroxy-5-methyl-4-isoxazole-propionate$ (AMPA) glutamate receptors (GluR), kainate-induced SE markedly up-regulated GluR1 expression but down-regulated GluR2 expression, leading to increased formation of $Ca^{2+}$ permeable GluR2- lacking AMPA receptors. TPM administration for 1 week attenuated SE-induced expression of both the up-regulation of GluR1 and down-regulation of GluR2, reversing the ratio of GluR1/GluR2 to the control value. In conclusion, TPM protects neuronal cell death against glutamate induced excitotoxicity in kainate-induced SE model, supporting the potential of TPM as a neuroprotective agent.
Peritoneal dialysis-related peritonitis due to <i>Halomonas hamiltonii</i> : A first case report
Yeo, Se Hwan,Kwak, Jae Hoon,Kim, Yeo Un,Lee, Jin Suk,Kim, Hyo Jin,Park, Kyoung Hwa,Lee, Jung Sook,Ha, Gyoung Yim,Lee, Jeong Ho,Lee, Jun Yeop,Yoo, Kyung Don Williams & Wilkins Co 2016 Medicine Vol.95 No.47
<P><B>Abstract</B></P><P><B>Introduction:</B></P><P><I>Halomonas hamiltonii</I> is a Gram-negative, halophilic, motile, and nonspore-forming rod bacterium. Although most <I>Halomonas</I> sp. are commonly found in saline environments, it has rarely been implicated as a cause of human infection. Herein, the authors present a case report of continuous ambulatory peritoneal dialysis (CAPD)-related peritonitis attributed to <I>H hamiltonii</I>.</P><P><B>Case presentation:</B></P><P>An 82-year-old male patient who had been receiving CAPD therapy presented to an emergency department with complaints of abdominal pain and cloudy dialysate that had persisted for 2 days. The peritoneal dialysate was compatible with CAPD peritonitis, with white blood cell count of peritoneal effluent of 810/mm<SUP>3</SUP> and neutrophils predominated (60%). Two days after culture on blood agar medium, nonhemolytic pink mucoid colonies showed, with cells showing Gram-negative, nonspore-forming rods with a few longer and larger bacilli than usual were found. We also performed biochemical tests and found negative responses in K/K on the triple sugar iron test and H<SUB>2</SUB>S and equivocal (very weak) response in the motility test, but positive responses to catalase, oxidase, and urease tests. The partial sequence of the 16S rRNA gene of a bacterium detected by peritoneal fluid culture was utilized for a Basic Local Alignment Search Tool search, which revealed that the organism was <I>H hamiltonii</I>. Intraperitoneal antibiotics were administered for 21 days, and the patient was discharged without clinical problems.</P><P><B>Conclusion:</B></P><P>We present here the first case report of CAPD-related peritonitis caused by <I>H hamiltonii</I>, which was identified using molecular biological techniques. Although guidelines do not exist for the treatment of infections caused by this organism, conventional treatment for Gram-negative organisms could be effective.</P>
Endothelial Cell Products as a Key Player in Hypoxia-Induced Nerve Cell Injury after Stroke
Cho, Chul-Min,Ha, Se-Un,Bae, Hae-Rahn,Huh, Jae-Taeck The Korean Neurosurgical Society 2006 Journal of Korean neurosurgical society Vol.40 No.2
Objective : Activated endothelial cells mediate the cascade of reactions in response to hypoxia for adaptation to the stress. It has been suggested that hypoxia, by itself, without reperfusion, can activate the endothelial cells and initiate complex responses. In this study, we investigated whether hypoxia-induced endothelial products alter the endothelial permeability and have a direct cytotoxic effect on nerve cells. Methods : Hypoxic condition of primary human umbilical vein endothelial cells[HUVEC] was induced by $CoCl_2$ treatment in culture medium. Cell growth was evaluated by 3,4,5-dimethyl thiazole-3,5-diphenyl tetrazolium bromide [MTT] assay Hypoxia-induced products [$IL-1{\beta},\;TGF-{\beta}1,\;IFN-{\gamma},\;TNF-{\alpha}$, IL-10, IL-6, IL-8, MCP-l and VEGF] were assessed by enzyme-linked immunosorbent assay. Endothelial permeability was evaluated by Western blotting. Results : Prolonged hypoxia caused endothelial cells to secrete IL -6, IL -8, MCP-1 and VEGF. However, the levels of IL -1, IL -10, $TNF-{\alpha},\;TGF-{\beta},\;IFN-{\gamma}$ and nitric oxide remained unchanged over 48 h hypoxia. Hypoxic exposure to endothelial cells induced the time-dependent down regulation of the expression of cadherin and catenin protein. The conditioned medium taken from hypoxic HUVECs had the cytotoxic effect selectively on neuroblastoma cells, but not on astroglioma cells. Conclusion : These results suggest the possibility that endothelial cell derived cytokines or other secreted products with the increased endothelial permeability might directly contribute to nerve cell injury followed by hypoxia.