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1 protective in paradigms of NMDA toxicity and oxygen glucose deprivation.
2 otoxic insult (50 microM kainic acid) or 6-h oxygen glucose deprivation.
3 termination of SD caused by K+ perfusion and oxygen-glucose deprivation.
4 ng both middle cerebral artery occlusion and oxygen-glucose deprivation.
5 amplified by RT-PCR 24-48 hr after sublethal oxygen-glucose deprivation.
6 horylation promotes neuronal death following oxygen-glucose deprivation.
7 cal C1q(-/-) neurons exhibited resistance to oxygen-glucose deprivation.
8 protect against glutamate excitotoxicity or oxygen-glucose deprivation.
9 s monitored in hippocampal slices exposed to oxygen-glucose deprivation.
10 res, IPC and lethal ischemia were induced by oxygen-glucose deprivation.
11 t to calpain cleavage was not released after oxygen-glucose deprivation.
12 protein kinase C inhibition, DNA damage, or oxygen- glucose deprivation.
15 s in vitro 13-15) were exposed to periods of oxygen-glucose deprivation (5-30 min) too brief to induc
16 otypic hippocampal slice cultures exposed to oxygen glucose deprivation (a model of ischaemic stroke)
17 d in primary neurons subjected to hypoxia or oxygen-glucose deprivation, an in vitro model of ischemi
19 RNA interference reduced cell survival under oxygen glucose deprivation and after transplantation.
20 ates brain injury induced by excitotoxicity, oxygen glucose deprivation and middle cerebral artery (M
21 angiogenesis, and neutrophil migration using oxygen glucose deprivation and reoxygenation as in vitro
22 d P0-CNS optic nerves were more sensitive to oxygen-glucose deprivation and contained less adenosine
24 dium method in cultured neurons treated with oxygen-glucose deprivation and in mice treated with fore
25 release in neuronal cultures challenged with oxygen-glucose deprivation and in the rat model of trans
26 e used murine cells to demonstrate that both oxygen-glucose deprivation and pharmacologic unfolded pr
28 ected primary neuronal cultures subjected to oxygen-glucose deprivation and reduced infarct size and
29 hr after termination of agonist exposure or oxygen-glucose deprivation and remained stable over the
32 nificantly reduced ischemic cell death after oxygen-glucose deprivation, and this effect was abolishe
33 ions of S100B decreased neuronal death after oxygen-glucose deprivation, and this effect was abolishe
34 d(-/-) neurons were resistant to death after oxygen/glucose deprivation, and caspase 3 cleavage was s
35 ral vascular endothelial cell cultures after oxygen-glucose deprivation, as well as pioglitazone-medi
38 (2+) chelation could prevent SD triggered by oxygen/glucose deprivation but Zn(2+) accumulation did n
39 -methyl-4-isoxazolepropionic acid (AMPA), or oxygen-glucose deprivation, but the C3 regioisomer was m
41 urvival of preconditioned Sca-1+ cells under oxygen glucose deprivation compared with nonprecondition
42 ell swelling and cytotoxicity in response to oxygen-glucose deprivation, compared with slices from AQ
43 ition, Zn(2+)-mediated neuronal injury under oxygen-glucose deprivation conditions was also diminishe
44 eater neuroprotection from damage induced by oxygen glucose deprivation, consistent with the idea tha
45 obilizing ER stress (thapsigargin treatment, oxygen-glucose deprivation) critically depended upon sti
47 ed whether glutamate receptor ligands affect oxygen-glucose deprivation-evoked L-glutamate efflux fro
50 death of primary cortical neurons exposed to oxygen-glucose deprivation followed by reoxygenation.
51 drug-free period, and then were subjected to oxygen-glucose deprivation for 10 min at 37 degrees C.
52 esent study of events during and after acute oxygen glucose deprivation highlights a possible importa
54 ll protect cultured hippocampal neurons from oxygen/glucose deprivation if introduced following an in
55 eptor agonist FTY720 did not protect against oxygen glucose deprivation in cultured neurons and did n
57 hat after focal cerebral ischemia in vivo or oxygen-glucose deprivation in organotypic hippocampal sl
60 ion could be triggered in vitro by sublethal oxygen-glucose deprivation in rat hippocampal neuronal c
61 middle cerebral artery occlusion in vivo and oxygen-glucose deprivation in vitro, to delineate change
62 uroprotection against excitotoxic injury and oxygen/glucose deprivation in mouse neocortical neuron c
64 uN2B resulted in more reduction of NMDA- and oxygen glucose deprivation-induced excitotoxicity as wel
65 urthermore PMNs exacerbated kainic acid- and oxygen glucose deprivation-induced neuron death by 20-30
66 by pioglitazone significantly inhibited both oxygen-glucose deprivation-induced cerebral vascular end
67 soflurane preconditioning did not change the oxygen-glucose deprivation-induced glutamate accumulatio
68 ective concentration [EC(50)] = 27 +/- 3 nM) oxygen/glucose deprivation-induced BBB breakdown, as dem
69 creased staurosporine-, excitotoxicity-, and oxygen/glucose deprivation-induced cell death in bax-def
71 bok-deficient neurons were more sensitive to oxygen/glucose deprivation-induced injury in vitro and s
73 relevant, as a decrease in apoptosis, after oxygen-glucose deprivation, is observed in hippocampal n
74 hypoxia-induced oxidative stress, we used an oxygen/glucose deprivation neurodegeneration model that
75 e markedly protected from 60 min of combined oxygen-glucose deprivation neurotoxicity compared with w
78 iability of microglia BV2 cells subjected to oxygen glucose deprivation (OGD) and re-oxygenation.
79 ischemia, hippocampal slices were exposed to oxygen glucose deprivation (OGD) conditions and we obser
80 nditioned with sublethal exposure to NMDA or oxygen glucose deprivation (OGD) exhibited enhanced Lck
81 ry cortical neurons (PCNs) were subjected to oxygen glucose deprivation (OGD) followed by various tre
82 We found that synaptic depression induced by oxygen glucose deprivation (OGD) was enhanced in EC slic
83 ippocampal slice cultures (OHSCs) exposed to oxygen glucose deprivation (OGD), and dissociated cultur
84 otects against the neuronal death induced by oxygen glucose deprivation (OGD), and whether the protec
85 sing mouse hippocampal slices to study acute oxygen glucose deprivation (OGD)-triggered neurodegenera
92 lls co-cultured with primary astrocytes from oxygen glucose deprivation (OGD)/reoxygenation stress an
93 ppocampal neurons were subjected to 8 min of oxygen-glucose deprivation (OGD) (an in vitro model for
94 o 2% isoflurane for 30min at 24h before a 1h oxygen-glucose deprivation (OGD) and a 24h simulated rep
95 astrocytes cultured alone or with neurons to oxygen-glucose deprivation (OGD) and monitored psi(m) us
97 For in vitro studies, we used a model of oxygen-glucose deprivation (OGD) followed by flow cytome
99 by PBI-05204 to rat brain slices damaged by oxygen-glucose deprivation (OGD) is mediated by BDNF.
100 ncreased neuronal survival after exposure to oxygen-glucose deprivation (OGD) or glutamate toxicity.
101 he mechanism of cellular toxicity induced by oxygen-glucose deprivation (OGD) to simulate brain ische
103 300 microM), as well as ischemia induced by oxygen-glucose deprivation (OGD), caused cellular edema
105 In addition, using an in vitro model of oxygen-glucose deprivation (OGD), we studied the role of
106 e that PPARdelta is significantly reduced in oxygen-glucose deprivation (OGD)-induced mouse CEC death
115 ce and determined WM ischemic vulnerability [oxygen-glucose deprivation (OGD)] 72 h later, using acut
116 ippocampal slice model of cerebral ischemia [oxygen-glucose deprivation (OGD)] when present both duri
118 fluorescence self-quenching assay under both oxygen/glucose deprivation (OGD) and direct antibody-med
119 ng neurons to extreme metabolic stress using oxygen/glucose deprivation (OGD) increases GABAB1 but de
122 opy, and subjected these slices to transient oxygen/glucose deprivation (OGD) that causes delayed exc
123 3-specific protease SENP3 is degraded during oxygen/glucose deprivation (OGD), an in vitro model of i
124 eurons during an in vitro model of ischemia, oxygen/glucose deprivation (OGD), leads to an enhanced p
125 riments, we tested the effects of EUK-207 on oxygen/glucose deprivation (OGD)-induced cell death in c
126 preconditioning protected against subsequent oxygen glucose deprivation or glutamate injury, whereas
127 ted in primary cortical neurons subjected to oxygen glucose deprivation or N-methyl-D-aspartate (NMDA
129 ction of experimental acute stroke model via oxygen-glucose deprivation-reperfusion (OGD/R) injury.
130 ffect of ischemic preconditioning induced by oxygen-glucose deprivation requires K(ATP) and NO syntha
132 B cells to oligodendrocyte cultures prior to oxygen glucose deprivation significantly enhanced oligod
133 ceptor mutants are challenged with transient oxygen-glucose deprivation, they show a reduced function
134 cell injury in an oxidative stress model of oxygen-glucose deprivation through phosphatidylinositol-
135 IGF-1 for 30 minutes followed by 8 hours of oxygen glucose deprivation to assess the cytoprotective
136 rons, we also show that, under conditions of oxygen-glucose deprivation to mimic cerebral ischemia, G
137 used an in vitro model of cerebral ischemia (oxygen-glucose deprivation) to examine changes in [Cl-]i
139 n-mediated decreases in cell death following oxygen-glucose deprivation were abolished in cortical cu
140 l brain slices exposed to ischemic injury by oxygen-glucose deprivation were treated with human amnio
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