脑缺血与神经细胞凋亡

[1] Apoptosis; a basic blologi-calphenomenon with wide-ranging implications in tissue kinetics. Kerr JFR,Wyllie AH,Currie AR. Br JCance . 1972

[2] Choi DW Excitotoxic cell death. Journal of Neurobiology . 1992

[3] Choi DW Preincubation with protein synthesis inhibitorsprotects conical neurons against oxygen-glucose deprtvstion-induceddeath. Lobner D. Neuroscience . 1 996

[4] Saya H et al.evidence for p53-mediatedmodulation of neuronal viability. Xiang H,Hochman DW. The Journal of Neuroscience . 1 996

[5] Expression of the apoptosisefftctor gene.bax, is up regulated in vulnerable hippocampel CA1neurons following global ischemia. Chen J,Zhu RL,Nakayama M et al. Journal of Neurochemistry . 1996

[6] Apoptosis and necrosis: twodistinct events induced, respectively, by mild and intense insults withN-methyl-D-aspahate or nitric oxide/super-oxide in conical cellcultures. Bonfoco E,Krainc D,Ankarerona M et al. Proceedings of the National Academy of Sciences of the United States of America . 1995

[7] Induction of c-fos and c--jungene-products and heat shock protein after brief and prolonged cerebralischemia in gerbils. Takemoto O,Tomimoto H,Yanagihara T. Stroke . 1995

[8] Blockade of glutamate receptorsunmasks neuronal apoptosis after oxygen-glucose depnvation in vitro. Gwag BJ,Lobner D,Koh JY et al. Neuroscience . 1995

[9] Wenzel HJ, Kinoshita Y et al Loss of the p53 tumorsuppressor gene protects neurons from kainate-induced cell death. Morrison RS. The Journal of Neuroscience . 1996

[10] Apoptosis receptor genes bcl2 and bcl-x-long are expressed in the rat blain following globalischemia. Chen J,Graham SH,Nakayama M et al. Journal of Cerebral Blood Flow and Metabolism . 1997

[1] Apoptosis; a basic blologi-calphenomenon with wide-ranging implications in tissue kinetics. Kerr JFR,Wyllie AH,Currie AR. Br JCance . 1972

[2] Choi DW Excitotoxic cell death. Journal of Neurobiology . 1992

[3] Choi DW Preincubation with protein synthesis inhibitorsprotects conical neurons against oxygen-glucose deprtvstion-induceddeath. Lobner D. Neuroscience . 1 996

[4] Saya H et al.evidence for p53-mediatedmodulation of neuronal viability. Xiang H,Hochman DW. The Journal of Neuroscience . 1 996

[5] Expression of the apoptosisefftctor gene.bax, is up regulated in vulnerable hippocampel CA1neurons following global ischemia. Chen J,Zhu RL,Nakayama M et al. Journal of Neurochemistry . 1996

[6] Apoptosis and necrosis: twodistinct events induced, respectively, by mild and intense insults withN-methyl-D-aspahate or nitric oxide/super-oxide in conical cellcultures. Bonfoco E,Krainc D,Ankarerona M et al. Proceedings of the National Academy of Sciences of the United States of America . 1995

[7] Induction of c-fos and c--jungene-products and heat shock protein after brief and prolonged cerebralischemia in gerbils. Takemoto O,Tomimoto H,Yanagihara T. Stroke . 1995

[8] Blockade of glutamate receptorsunmasks neuronal apoptosis after oxygen-glucose depnvation in vitro. Gwag BJ,Lobner D,Koh JY et al. Neuroscience . 1995

[9] Wenzel HJ, Kinoshita Y et al Loss of the p53 tumorsuppressor gene protects neurons from kainate-induced cell death. Morrison RS. The Journal of Neuroscience . 1996

[10] Apoptosis receptor genes bcl2 and bcl-x-long are expressed in the rat blain following globalischemia. Chen J,Graham SH,Nakayama M et al. Journal of Cerebral Blood Flow and Metabolism . 1997