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Bcl-2、fas蛋白在颞叶癫痫病灶内的表达与神经元凋亡 被引量:6

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出处 《中华神经外科杂志》 CSCD 北大核心 2005年第10期630-632,共3页 Chinese Journal of Neurosurgery
基金 山东省自然科学基金项目(编号:Y2000C11)
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  • 1Zhang LX, Smith MA, Li XL, et al. Apoptosis of hippocampal neurons after amygdala kindled seizures. Brain Res Mol Brain Res, 1998, 55: 198-208.
  • 2Tuunanen J, Lukasiuk K, Halonen T, et al. Status epilepticus-induced neuronal damage in the rat amygdaloid complex: distribution, time-course and mechanisms. Neurosciene, 1999, 94:473-495.
  • 3Fujkawa DG, Shinmei SS, Cai B. Lithium-pilocarpine-induced status epilepticus produces necrotic neurons with internucleo-somal DNA fragmentation in adult rats. Eur J Neurosci, 1999,11: 1605-1614.
  • 4Fujkawa DG, Shinmei SS, Cai B. Kainic acid-induced seizures produce necrotic, not apoptotic, neurons with internucleosomal DNA cleavage: implications for programmed cell death mechanisms. Neuroscience, 2000, 98: 41-53.
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  • 6Bengzon J, Mohapel P, Ekdahl CT, et al. Neuronal apoptosis after brief and prolonged seizures. Prog Brain Res, 2002, 135:111-119.
  • 7Uysal H, Cevik IU, Soylemezoglu F, et al. Is the cell death in mesial temporal sclerosis apoptotic? Epilepsia, 2003, 44: 778-784.
  • 8Yi X, Yin XM, Dong Z. Inhibition of bid-induced apoptosis by bcl-2: tbid insertion, bax translocation and bax/bak oligomerization suppressed. J Biol Chem, 2003, 278:16992-16999.
  • 9Tan Z, Levid J, Schreiber SS. Increased expression of Fas (CD95/APO-1) in adult rat brain after kainite-induced seizures.Neuroreport, 2001, 12: 1979-1982.

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