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of special interest. Suggestion that the nature of death induced in cultured rat cortical neurons by NMDA depends on insult severity, with mild excitotoxic insults inducing apoptosis (defined by descriptive criteria only) and more severe insults inducing necrosis. The general principle of insult severity determining whether a cell dies by apoptosis or necrosis is attractive and consistent with multiple precedents (see Figure 1), although my laboratory has been more impressed with the predilection of even low intensity excitotoxic insults to induce necrosis in a similar rat cortical cell culture system - albeit a necrosis associated with transient DNA laddering (see [22]).
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of special interest Bonfoco E, Krainc D, Ankarcrona M, Nicotera P, lipton SA. Apoptosis and necrosis: two distinct events induced, respectively, by mild and intense insults with N-methyl-D-aspartate or nitric oxide/superoxide in cortical cell cultures. Proc Natl Acad Sci USA. 92:1995;7162-7166 Suggestion that the nature of death induced in cultured rat cortical neurons by NMDA depends on insult severity, with mild excitotoxic insults inducing apoptosis (defined by descriptive criteria only) and more severe insults inducing necrosis. The general principle of insult severity determining whether a cell dies by apoptosis or necrosis is attractive and consistent with multiple precedents (see Figure 1), although my laboratory has been more impressed with the predilection of even low intensity excitotoxic insults to induce necrosis in a similar rat cortical cell culture system - albeit a necrosis associated with transient DNA laddering (see [22]).
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of special interest. Although conventional wisdom has it that tissue injury is fully apparent within a day after focal ischemic insults, our search for delayed forms of focal ischemic infarction was productive. Most of the tissue damage after mild transient focal ischemia in this model developed more than three days after the insult. Does such very delayed infarction ever happen in humans? Is there also an extended window of therapeutic opportunity?
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of special interest Du C, Hu R, Csernansky CA, Hsu CY, Choi DW. Very delayed infarction after mild focal cerebral ischemia: a role for apoptosis? J Cereb Blood Flow Metab. 16:1996;195-201 Although conventional wisdom has it that tissue injury is fully apparent within a day after focal ischemic insults, our search for delayed forms of focal ischemic infarction was productive. Most of the tissue damage after mild transient focal ischemia in this model developed more than three days after the insult. Does such very delayed infarction ever happen in humans? Is there also an extended window of therapeutic opportunity?
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Du, C.1
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Choi, D.W.5
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47
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0027944004
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Overexpression of BCL-2 in transgenic mice protects neurons from naturally occurring cell death and experimental ischemia
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of special interest. of outstanding interest. The first demonstration that Bcl-2 is neuroprotective against ischemic insults, and important evidence favoring the existence of ischemia-induced neuronal apoptosis. See annotation [49].
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of special interest Martinou J-C, Dubois-Dauphin M, Staple JK, Rodriguez I, Frankowski H, Missotten M, Albertini P, Talabot D, Catsicas S, Pietra C, Huarte J. Overexpression of BCL-2 in transgenic mice protects neurons from naturally occurring cell death and experimental ischemia. of outstanding interest Neuron. 13:1994;1017-1030 The first demonstration that Bcl-2 is neuroprotective against ischemic insults, and important evidence favoring the existence of ischemia-induced neuronal apoptosis. See annotation [49].
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Albertini, P.7
Talabot, D.8
Catsicas, S.9
Pietra, C.10
Huarte, J.11
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48
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0028981908
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Expression of bcl-2 from a defective herpes simplex virus-1 vector limits neuronal death in focal cerebral ischemia
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of special interest. Interesting study probing the possibility of administering the bcl-2 gene exogenously as therapy for focal cerebral ischemia.
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of special interest Linnik MD, Zahos P, Geschwind MD, Federoff HJ. Expression of bcl-2 from a defective herpes simplex virus-1 vector limits neuronal death in focal cerebral ischemia. Stroke. 26:1995;1670-1674 Interesting study probing the possibility of administering the bcl-2 gene exogenously as therapy for focal cerebral ischemia.
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Linnik, M.D.1
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Expression of bcl-2 inhibits necrotic neuronal cell death
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of special interest. Cautionary note regarding the specificity of bcl-2-induced neuroprotection as evidence in favor of apoptosis.
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of special interest Kane DJ, Ord T, Anton R, Bredesen DE. Expression of bcl-2 inhibits necrotic neuronal cell death. J Neurosci Res. 40:1995;269-275 Cautionary note regarding the specificity of bcl-2-induced neuroprotection as evidence in favor of apoptosis.
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Kane, D.J.1
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50
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0027985453
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Attenuation of p53 expression protects against focal ischemic damage in transgenic mice
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of special interest. Protein p53 may be a two-edged sword in the ischemic brain, assisting with necessary DNA repair, but also triggering apoptosis.
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of special interest Crumrine RC, Thomas AL, Morgan PF. Attenuation of p53 expression protects against focal ischemic damage in transgenic mice. J Cereb Blood Flow Metab. 14:1994;887-891 Protein p53 may be a two-edged sword in the ischemic brain, assisting with necessary DNA repair, but also triggering apoptosis.
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Crumrine, R.C.1
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51
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0029048295
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Blockade of glutamate receptors unmasks neuronal apoptosis after oxygen-glucose deprivation in vitro
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of special interest. Death in cultured cortical neurons exposed to oxygen/glucose deprivation occurs in layers, with NMDA-receptor-mediated excitotoxic necrosis the dominant layer. Peel back that, as well as an underlying slowly triggered AMPA/kainate receptor-mediated excitotoxic necrosis, and neuronal death then occurs mainly by apoptosis. We are currently exploring our theory that this in vitro model of blocked oxygen/glucose deprivation captures key elements of ischemic apoptosis in vivo.
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of special interest Gwag BJ, Lobner D, Koh JY, Wie MB, Choi DW. Blockade of glutamate receptors unmasks neuronal apoptosis after oxygen-glucose deprivation in vitro. Neuroscience. 68:1995;615-619 Death in cultured cortical neurons exposed to oxygen/glucose deprivation occurs in layers, with NMDA-receptor-mediated excitotoxic necrosis the dominant layer. Peel back that, as well as an underlying slowly triggered AMPA/kainate receptor-mediated excitotoxic necrosis, and neuronal death then occurs mainly by apoptosis. We are currently exploring our theory that this in vitro model of blocked oxygen/glucose deprivation captures key elements of ischemic apoptosis in vivo.
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Neuroscience
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Gwag, B.J.1
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Additive neuroprotective effects of dextrophan and cycloheximide in rats subjected to transient focal cerebral ischemia
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Du C, Hu R, Csernansky CA, Liu XZ, Hsu CY, Choi DW. Additive neuroprotective effects of dextrophan and cycloheximide in rats subjected to transient focal cerebral ischemia. Brain Res. 718:1996;233-236.
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Buckministerfullerenol free radical scavengers reduce excitotoxic and apoptotic death of cultured cortical neurons
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Dugan L, Gabrielsen JK, Yu SP, Lin TS, Choi DW. Buckministerfullerenol free radical scavengers reduce excitotoxic and apoptotic death of cultured cortical neurons. Neurobiol Dis. 3:1996;129-135.
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Choi DW. Calcium: still center-stage in hypoxic-ischemic neuronal death. Trends Neurosci. 18:1995;58-60.
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