ライフサイエンスコーパス: OGD

1 OGD also caused widespread oligodendrocyte death, demons

2 OGD also increased lipid peroxidation levels and this ef

3 OGD causes an NMDAR- and Ca(2+)-permeable AMPAR-dependen

4 OGD does not cause GluA2 endocytosis in cortical neurons

5 OGD enhanced TNF-alpha/IFN-gamma toxicity in both neuron

6 OGD evoked long-lasting cytosolic Ca(2+) elevations that

7 OGD for 30 min resulted in an irreversible loss of the C

8 OGD induced a transient decrease in fluorescence resonan

9 OGD markedly activated AMPK as early as 30 min, and AMPK

10 OGD progressively decreased neuronal survival over 48 h

11 OGD resulted in delayed degeneration of YFP-positive axo

12 OGD-induced accumulation of reactive oxygen species (ROS

13 OGD-induced synaptic depression was ameliorated by funct

14 OGD/REOX not only increased the V(max) for NHE1 but also

15 OGD/REOX-mediated Ca2+ accumulation in ER Ca2+ stores wa

16 OGD/REOX-mediated mitochondrial Ca2+ accumulation and cy

17 te prevented the loss of HT22 cells after 3h OGD+/-rtPA.

18 In endothelial cell monolayers, 3h OGD and 24h reoxygenation increased FITC-dextran leakage

19 After 6h OGD, rtPA sharply lowered cell viability; pyruvate dampe

20 After 3 or 6h OGD, cells were reoxygenated with 11mmol/L glucose+/-pyr

21 ive inhibition of NF-kappaB, which abolished OGD-enhanced expression of Bcl-2 and Survivin, accentuat

22 After OGD (12 min), perfusion of hippocampal slices with contr

23 found neuronal rescue provided by F-68 after OGD and the high level of efficacy with delayed administ

24 CC1 activity leads to Na+ accumulation after OGD/REOX and that subsequent reverse-mode operation of N

25 ndication of increased NKCC-1 activity after OGD.

26 K1-dependent internalization of AMPARs after OGD.

27 tors on the rises in [Cl-]i during and after OGD.

28 els were found in cultured mouse BMECs after OGD as well as in isolated cerebral microvessels in mice

29 emia-gated currents or neuronal damage after OGD.

30 schemia-gated currents and cell damage after OGD.

31 ischemia-gated currents and cell death after OGD.

32 ut did not prevent axonal degeneration after OGD.

33 A rise in [Ca2+]i was detected after OGD/REOX in the presence of a sarcoplasmic-endoplasmic r

34 that MAP2 breakdown occurs very early after OGD, with the first statistical decrease in MAP2 levels

35 Administration of F-68 for 48 h after OGD rescued neurons from death in a dose-dependent manne

36 ducing factor (AIF) were increased 3 h after OGD, and the translocation of AIF from mitochondria to n

37 When measured 3 h after OGD, increased ROS levels were significantly reduced by

38 ncreased during reperfusion, even 24 h after OGD.

39 Cell death was assessed 48 h after OGD.

40 s changed by approximately 2-fold 24 h after OGD.

41 n F-68 administration was delayed 12 h after OGD.

42 ity of cell death occurring after 12 h after OGD.

43 t would have died after the first hour after OGD.

44 t inhibit the secondary rise in [Cl-]i after OGD.

45 Treatment with NRG-1 immediately after OGD significantly increased neuronal survival.

46 surface and total AMPAR protein levels after OGD was prevented by mGluR1 or A(3) receptor antagonists

47 y]-l-aspartate increased neuronal loss after OGD or NMDA, and blocked the loss of astrocytic mitochon

48 c Zn(2+) rises persisted for 10-30 min after OGD, followed by recovery over approximately 40-60 min.

49 n, JSTx) administered either during or after OGD.

50 imulated the neurite outgrowth of PCNs after OGD, which was attenuated by LY294002 and enhanced by li

51 ONs) showed better functional recovery after OGD than the non-preconditioned MONs (31 +/- 3 vs 17 +/-

52 levels recover following reoxygenation after OGD allowing deSUMOylation of Drp1, which facilitates Dr

53 ed to a dose-dependent better survival after OGD.

54 significantly attenuated cell swelling after OGD or NMDA receptor activation.

55 HNG increased cell viability after OGD in primary cortical neurons, whereas the PI3K/Akt in

56 ased TG2 expression protects neurons against OGD-induced cell death independent of its transamidating

57 KCC1 did not protect DIV 7-8 neurons against OGD-mediated cell death.

58 uated IL-10 mediated neuroprotection against OGD and glutamate.

59 on, EUK-207 provides neuroprotection against OGD-induced cell death in cultured hippocampal slices.

60 ubunits in affording neuroprotection against OGD/R injury.

61 his LG3, in turn, is neuroprotective against OGD, and may therefore represent one of the brain's defe

62 However, it did not protect against OGD- or kainic-acid-induced toxicity.

63 for the first time that TG2 protects against OGD, interacts with HIF1beta, and attenuates the HIF1 hy

64 rgeted to microglia (DNMSR) protects against OGD-induced synaptic impairment in an amyloid-enriched e

65 s sufficient to protect brain slices against OGD, whereas downstream activation of TrkB receptors for

66 cing of Malat1 also significantly aggravated OGD-induced expression of the proapoptotic factor Bim an

67 ces from both young and adult rats, although OGD-induced toxicity was attenuated by MK-801 only in sl

68 nucleotide exchange factor Tiam1 mediates an OGD-induced increase in Rac1 activity in hippocampal neu

69 ultured cortical neurons are resistant to an OGD insult that causes cell death in hippocampal neurons

70 In vitro, inflammatory cytokines and OGD treatment significantly induced mRNAs for TRAIL, DR5

71 nd its receptors after cytokine exposure and OGD in primary neurons and OPCs were similar to those fo

72 inhibition of NKCC1 by bumetanide-attenuated OGD-mediated swelling.

73 When EUK-207 was applied 1 h before OGD and during 24 h recovery, PI uptake was also reduced

74 n EUK-207 was applied either 1 or 2 h before OGD, OGD-induced LDH release was significantly reduced.

75 utathione-related cellular metabolism before OGD, oxytocin modulated the expression levels of GABAAR

76 ell as a dominant negative mutant Ras, block OGD preconditioning whereas a constitutively active form

77 Furthermore, NBQX or JSTx blocked OGD-induced Ca2+ influx.

78 interaction with a fragment of Tiam1 blocks OGD-induced Tiam1 activation but has no effect on the de

79 AMPARs, and that PICK1 is required for both OGD-induced GluA2 endocytosis and lysosomal sorting.

80 e hydrogen maleate (1 microm) prevented both OGD- and glutamate-mediated cell death.

81 d at different time points following a brief OGD (3, 6 and 12 h) and used to probe genome-wide expres

82 pressed endothelial cell apoptosis caused by OGD.

83 accentuated endothelial apoptosis caused by OGD.

84 Increased Rac1 activity caused by OGD/ischemia contributes to neuronal death in hippocampa

85 to the endocytic adaptor AP2 is enhanced by OGD in hippocampal, but not cortical neurons.

86 extracellular signal-related kinase (ERK) by OGD was dependent on alpha-dystroglycan binding, and inh

87 reconditioning against cell death induced by OGD/R.

88 ML-090 decreased the ROS burst stimulated by OGD, which was associated with a decreased level of RGC

89 In contrast, OGD causes a rapid endocytosis of GluA2 in hippocampal n

90 In contrast, OGD-induced edema observed in brain slices was not affec

91 Corneal OGD permeability, surface irregularity, and the number o

92 In the microglia/neuron co-cultures, OGD induced neuronal damage was reduced markedly in the

93 nzo[f]quinoxaline-2,3-dione (NBQX) decreased OGD-induced axonal degeneration and oligodendrocyte loss

94 before 16 h oxygen and glucose depravation (OGD).

95 subjected to oxygen and glucose deprivation (OGD) (3 h) plus reoxygenation (RX) (24 h), the neuroprot

96 cted to 8 min of oxygen-glucose deprivation (OGD) (an in vitro model for ischemia) and reoxygenated i

97 24h before a 1h oxygen-glucose deprivation (OGD) and a 24h simulated reperfusion had a reduced lacta

98 a results in oxygen and glucose deprivation (OGD) and consequent delayed cell death of vulnerable neu

99 assay under both oxygen/glucose deprivation (OGD) and direct antibody-mediated blockade of alpha-dyst

100 death following oxygen glucose deprivation (OGD) and ischemia.

101 with neurons to oxygen-glucose deprivation (OGD) and monitored psi(m) using tetramethylrhodamine eth

102 lls subjected to oxygen glucose deprivation (OGD) and re-oxygenation.

103 tical neurons by oxygen-glucose deprivation (OGD) and reoxygenation.

104 response to oxygen and glucose deprivation (OGD) as a real-time glutamate sensor to identify the sou

105 were exposed to oxygen glucose deprivation (OGD) conditions and we observed that hippocampal water c

106 osure to NMDA or oxygen glucose deprivation (OGD) exhibited enhanced Lck kinase activity, and were re

107 ree hours of oxygen and glucose deprivation (OGD) followed by 21 h of reoxygenation (REOX) led to 68

108 used a model of oxygen-glucose deprivation (OGD) followed by flow cytometric analysis to determine:1

109 ere subjected to oxygen glucose deprivation (OGD) followed by various treatments.

110 hemia causes oxygen and glucose deprivation (OGD) in neurons, triggering a cascade of events leading

111 es evoked by oxygen and glucose deprivation (OGD) in the cytosol and in the mitochondria of PC12 cell

112 lic stress using oxygen/glucose deprivation (OGD) increases GABAB1 but decreases GABAB2 surface expre

113 We show that oxygen-glucose deprivation (OGD) induced microglia proliferation, migration, and sec

114 NMDA treatment, oxygen/glucose deprivation (OGD) induced neurotoxicity in slices from both young and

115 lices damaged by oxygen-glucose deprivation (OGD) is mediated by BDNF.

116 fter exposure to oxygen-glucose deprivation (OGD) or glutamate toxicity.

117 on following oxygen and glucose deprivation (OGD) protected SH-SY5Y cells and murine primary cortical

118 ces to transient oxygen/glucose deprivation (OGD) that causes delayed excitotoxic death of CA1 pyrami

119 to mimic the oxygen and glucose deprivation (OGD) that usually results from ischemia.

120 icity induced by oxygen-glucose deprivation (OGD) to simulate brain ischemia.

121 ssion induced by oxygen glucose deprivation (OGD) was enhanced in EC slices either in presence of syn

122 Oxygen-glucose deprivation (OGD) was performed in cultured mouse primary cortical ne

123 degraded during oxygen/glucose deprivation (OGD), an in vitro model of ischaemia, via a pathway invo

124 HSCs) exposed to oxygen glucose deprivation (OGD), and dissociated cultures of hippocampal pyramidal

125 s exposed to oxygen and glucose deprivation (OGD), and increased TG2 expression protects neurons agai

126 death induced by oxygen glucose deprivation (OGD), and whether the protection is through thrombin rec

127 hemia induced by oxygen-glucose deprivation (OGD), caused cellular edema formation as indicated by an

128 del of ischemia, oxygen/glucose deprivation (OGD), leads to an enhanced permeability of AMPARs to Ca(

129 er 3-8 hr of oxygen and glucose deprivation (OGD), NKCC1-mediated 86Rb influx was significantly incre

130 a period of oxygen and glucose deprivation (OGD), promote functional recovery of axons and preserve

131 been shown that oxygen-glucose deprivation (OGD), reperfusion and interleukin-1 alpha (IL-1alpha) st

132 n vitro model of oxygen-glucose deprivation (OGD), we studied the role of HIF-1alpha and HIF-2alpha i

133 to transient oxygen and glucose deprivation (OGD), white matter injury was assessed by electrophysiol

134 ts of EUK-207 on oxygen/glucose deprivation (OGD)-induced cell death in cultured hippocampal slices a

135 antly reduced in oxygen-glucose deprivation (OGD)-induced mouse CEC death.

136 s to study acute oxygen glucose deprivation (OGD)-triggered neurodegeneration, we found evidence for

137 lu) exposure and oxygen glucose deprivation (OGD).

138 e exposed to oxygen and glucose deprivation (OGD).

139 OL cultures from oxygen glucose deprivation (OGD).

140 exposed to hypoxia and glucose deprivation (OGD).

141 tures by a brief oxygen-glucose deprivation (OGD).

142 ces subjected to oxygen-glucose deprivation (OGD).

143 X) after 2-h oxygen and glucose deprivation (OGD).

144 was simulated by oxygen-glucose deprivation (OGD).

145 , kainic acid or oxygen glucose deprivation (OGD).

146 simulated by oxygen and glucose deprivation (OGD).

147 lutamate and oxygen and glucose deprivation (OGD).

148 breakdown after oxygen-glucose deprivation (OGD).

149 d periods of oxygen and glucose deprivation (OGD).

150 usceptibility to oxygen glucose deprivation (OGD).

151 eled in vitro by oxygen-glucose deprivation (OGD).

152 tment and/or oxygen and glucose deprivation (OGD).

153 , leading to oxygen and glucose deprivation (OGD).

154 lso increased by oxygen-glucose deprivation (OGD).

155 apoptosis after oxygen-glucose deprivation (OGD).

156 ondria following oxygen-glucose deprivation (OGD).

157 ltures following oxygen glucose deprivation (OGD).

158 ere subjected to oxygen glucose deprivation (OGD)/reoxygenation or glutamate, widespread neuronal dea

159 astrocytes from oxygen glucose deprivation (OGD)/reoxygenation stress and rtPA cytotoxicity.

160 c vulnerability [oxygen-glucose deprivation (OGD)] 72 h later, using acutely isolated optic nerves (C

161 rebral ischemia [oxygen-glucose deprivation (OGD)] when present both during OGD and for the first 3 h

162 , we showed that oxygen-glucose deprivation (OGD, to simulate ischemia in vitro) increased extracellu

163 of ischemia (oxygen and glucose deprivation; OGD).

164 orneal permeability to Oregon green dextran (OGD) and sodium fluorescein was measured.

165 Corneal smoothness and Oregon green dextran (OGD) permeability were assessed.

166 ed and reduced glutamate accumulation during OGD, preservation of axonal mitochondria and oligodendro

167 g delayed the decline of cellular ATP during OGD, consistent with a reduction in the Ca(2+) load acti

168 deprivation (OGD)] when present both during OGD and for the first 3 hr of reperfusion.

169 e release of high mobility group box1 during OGD/R.

170 ncubated at 31 degreesC (hypothermia) during OGD/reoxygenation, neuronal dysfunction and elemental de

171 d increases in fluorescence intensity during OGD and reperfusion.

172 perlecan may be exocytosed by neurons during OGD and de novo synthesis of perlecan is increased durin

173 cytosolic Ca(2+) elevations occurring during OGD directly correlated to the extent of cell death meas

174 However, introduction of oxytocin during OGD/R did not induce neuroprotection.

175 nd the VSCC blocker Gd3+ were present during OGD, the presence of either the Ca-A/K channel blocker 1

176 found that blocking the NMDA receptor during OGD does not significantly inhibit IPC in this model or

177 a critical player in Rac1 regulation during OGD in hippocampal neurons.

178 Astrocyte psi(m) was rescued during OGD by cyclosporin A, a permeability transition pore blo

179 rescence in slices increased steadily during OGD treatment, rapidly disappeared following return to r

180 and dentate region death by 64-86% following OGD, more than HPC or APC alone (P<0.01).

181 ct was also reduced by EUK-207 6 h following OGD.

182 o generate increased levels of LG3 following OGD and reperfusion.

183 of AMPARs in CA3 pyramidal neurons following OGD that has the potential to reduce excitotoxicity and

184 ng is affected in cortical neurons following OGD.

185 pharmacological inhibition of NHE1 following OGD/REOX.

186 verified that protein translation following OGD is necessary for IPC.

187 epression of synaptic transmission following OGD was prevented by metabotropic glutamate receptor 1 (

188 abrogated the loss of water uptake following OGD.

189 atidyl inositol 3-kinase is not required for OGD preconditioning because inhibition of phosphatidyl i

190 lar regulated kinase cascade is required for OGD preconditioning.

191 Ras activity is necessary and sufficient for OGD tolerance in neurons.

192 ith reduced sEH activity and protection from OGD-induced neuronal cell death.

193 Furthermore, OGD preconditioning resulted in a down-regulation of the

194 rices (GOV) at oesophago-gastroduodenoscopy (OGD) has been an indication for combined transplantation

195 cultures were deprived of O(2) and glucose (OGD) to produce neuronal injury.

196 red hippocampal slices were subjected to 1 h OGD followed by 3 or 24 h recovery in regular medium wit

197 f phosphorylated ERK1/2 (p-ERK1/2) after 2 h OGD.

198 ak levels ( approximately 10 fold) after 6 h OGD.

199 Three hours OGD and 4h reoxygenation with rtPA increased ROS formati

200 reater effect in decreasing water content in OGD-exposed hippocampal slices, compared with mu, delta,

201 ytic cleavage of dystroglycan that occurs in OGD abrogated the effect of OGD, but not direct blockade

202 clude that NKCC-1 plays an important role in OGD-induced Cl- accumulation and subsequent neuronal dam

203 unction can significantly reduce or increase OGD-induced CEC death, respectively.

204 at1 by Malat1 GapmeR significantly increased OGD-induced cell death and Caspase 3 activity in BMECs.

205 Ras promotes neuroprotection against lethal OGD insults.

206 Sumo-2/3-ylation following 120 min OGD was reduced when cultures were preconditioned with n

207 Following harmful ischemia (120 min OGD), we observed a significant increase in the sumo-2/3

208 Following a 15 min OGD protocol, a substantial depression of AMPAR-mediated

209 were preconditioned with non-harmful 30 min OGD 24 h earlier (delayed ischemic tolerance).

210 experiments, slices were subjected to 5 min OGD exposures as described above, followed 4 hr later by

211 Moreover, OGD/REOX led to a significant increase in Ca2+ release f

212 In hippocampal CA1 neurons, OGD causes the synaptic expression of GluA2-lacking Ca(2

213 In NHE1(+/+) neurons, OGD caused a twofold increase in [Na+]i, and 60 min REOX

214 e conditions prevented NMDA-induced, but not OGD-induced, water influx.

215 BCR knockdown occludes OGD-induced Rac1 activation in hippocampal neurons.

216 This strongly suggests that the absence of OGD-induced GluA2 trafficking contributes to the relativ

217 2 internalization is a critical component of OGD-induced cell death in hippocampal neurons.

218 Here, we investigated the consequences of OGD for AMPAR function in CA3 neurons using electrophysi

219 a critical mechanism for the development of OGD tolerance in cortical neurons, which may also play a

220 es not have any effect on the development of OGD tolerance.

221 and Zn(2+) markedly extended the duration of OGD tolerated.

222 n that occurs in OGD abrogated the effect of OGD, but not direct blockade of alpha-dystroglycan, indi

223 The effects of OGD were mimicked by NMDA.

224 lial apoptosis was not detected until 2 h of OGD but became markedly elevated at 6 h of OGD treatment

225 f OGD but became markedly elevated at 6 h of OGD treatment.

226 and AMPK activity reached maximal at 2 h of OGD.

227 Two hours of OGD and 1 hr of reoxygenation (OGD/REOX) triggered an 3.

228 Three hours of OGD followed by 21 hr of reoxygenation led to 70% cell d

229 120 min of glutamate incubation or 3-6 hr of OGD treatment.

230 increased in NKCC1+/+ astrocytes at 2 hr of OGD.

231 a levels increased during the first 5 min of OGD and then decreased over the remaining experimental p

232 However, 15 min of OGD resulted in marked labeling in both regions.

233 ocytes swelled by 10-30% during 20-60 min of OGD.

234 d profound loss of psi(m) after 45-60 min of OGD.

235 after several (approximately 6-8) minutes of OGD, followed shortly by sharp somatic signals, which we

236 In 9 of 16 patients the results of OGD and EUS were concordant, that is, both positive (2)

237 -207 was applied either 1 or 2 h before OGD, OGD-induced LDH release was significantly reduced.

238 The effect of HNG and PI3K/Akt inhibitors on OGD-induced cell death was examined at 24 h after reperf

239 d vulnerability to subsequent excitotoxic or OGD-induced injury associated with an increased Ca2+ inf

240 ological conditions such as excessive Glu or OGD exposure, is able to counteract neuronal cell death

241 tanide (5-10 microm) abolished glutamate- or OGD-induced neurotoxicity.

242 vated either by lipopolysaccharides (LPS) or OGD, the levels of phosphorylated ERK1/2, JNK and p38 we

243 sequent exposure to lethal levels of NMDA or OGD.

244 ed the water content nearly back to original OGD values for all opioid agonist treatments, supporting

245 nd subjected to ischemic preconditioning (PC+OGD/RX), the neurotoxic effect of p300 inhibitor C646 wa

246 atment also significantly curtailed the post-OGD cell death in PC12 cells (by 54 +/- 6%; p<0.05) and

247 2 cells, treatment with premiR-29c prevented OGD-induced cell death (by 58 +/- 6%; p<0.05).

248 ve antagonist 30 microm GYKI 52466 prevented OGD-induced oligodendrocyte death.

249 NBQX prevented OGD-induced CAP loss and preserved axonal structure.

250 mimicked the effects of thrombin and reduced OGD-induced neuronal death.

251 HOE 642) or genetic ablation of NHE1 reduced OGD-induced cell death by approximately 40-50% (p < 0.05

252 TPC reduced OGD-induced neuronal death (e.g. dead cells: 52.5 +/- 5.

253 xygen-glucose deprivation and reoxygenation (OGD/R) model in PC12 cells, we show that 2-day pretreatm

254 Two hours of OGD and 1 hr of reoxygenation (OGD/REOX) triggered an 3.6-fold increase in intracellula

255 via oxygen-glucose deprivation-reperfusion (OGD/R) injury.

256 suggest that GluA1-containing AMPARs resist OGD-induced endocytosis.

257 intestinal transplant underwent simultaneous OGD and EUS.

258 accumulates rapidly in neurons during slice OGD, is taken up by mitochondria, and contributes to con

259 BQX or JSTx either during or after sublethal OGD prevented its priming effect.

260 dium from astrocytes challenged by sublethal OGD improved neuronal survival to OGD; however, this eff

261 matter, we examined the effects of sublethal OGD preconditioning.

262 A prior exposure of OPCs to sublethal OGD resulted in enhanced vulnerability to subsequent exc

263 llate (EGCG), protects cells from subsequent OGD/R-induced cell death.

264 ingly, PPARdelta overexpression can suppress OGD-induced caspase-3 activity, Golgi fragmentation, and

265 e AMPKalpha1, but not AMPKalpha2, suppressed OGD-enhanced NF-kappaB activation, the expression of Bcl

266 We show here that OGD causes endocytosis, lysosomal targeting and conseque

267 We report here that OGD preconditioning induces p21(ras) (Ras) activation in

268 isingly long period (>1 hr), suggesting that OGD caused specific, reversible changes in astrocyte mit

269 reverse-mode operation of NCX, abolished the OGD/REOX-induced enhancement in filling of ER Ca2+ store

270 y relevant concentrations did not affect the OGD-induced extracellular glutamate accumulation from br

271 Isoflurane also did not change the OGD-induced extracellular glutamate accumulation from br

272 e A2A receptors resulted in reduction of the OGD and simulated reperfusion-induced cell injury.

273 1 or HOE 642 treatment had no effects on the OGD-mediated initial Na+(i) rise but reduced the second

274 These results suggest that the OGD-induced glutamate accumulation involves reversed tra

275 Similarly, this OGD and simulated reperfusion-induced lactate dehydrogen

276 ncrease in primary neuronal cells exposed to OGD condition.

277 e conditioned medium of BV2 cells exposed to OGD contained increased Gal-3 levels, and promoted the f

278 modulate the survival of neurons exposed to OGD.

279 a crucial aspect of the mechanism leading to OGD-induced cell death is absent in cortical neurons.

280 EDE increased corneal permeability to OGD and fluorescein and corneal surface irregularity.

281 doxycycline reduced corneal permeability to OGD, improved corneal smoothness, and decreased involucr

282 pression of hamartin increased resistance to OGD by inducing productive autophagy through an mTORC1-d

283 Cultured hippocampal neurons respond to OGD with a rapid internalization of AMPA receptor (AMPAR

284 ndent proapoptotic gene Bnip3 in response to OGD but had no effect on the expression of VEGF, which h

285 tical and hippocampal neurons in response to OGD.

286 larization and neuronal death in response to OGD.

287 s differentially dysregulated in response to OGD/ischemia in hippocampal and cortical neurons.

288 OPCs were more sensitive to OGD-induced toxicity than mature oligodendrocytes, and O

289 f RNA prepared from OL cultures subjected to OGD and treated with HUCB cells showed an increase in th

290 EUS is superior to OGD for detecting GOV in children with intestinal failur

291 sublethal OGD improved neuronal survival to OGD; however, this effect was abolished during the downr

292 of neurons with different vulnerabilities to OGD recruit distinct cell biological mechanisms in respo

293 potential and of field EPSPs after transient OGD, and combined removal of Ca(2+) and Zn(2+) markedly

294 d Akt, in JEG-3 cells diminished tunicamycin-OGD reoxygenation-induced apoptosis.

295 e intracellular Zn(2+) accumulation, we used OGD exposures slightly shorter than those causing acute

296 Using OGD in the adult rat hippocampal slice as a model system

297 Whereas OGD stimulated robust increases in PGHS-2 mRNA abundance

298 NMDA-induced edema were reduced by 64% while OGD-induced edema were unaffected.

299 xerted toxicity alone or in combination with OGD and TNF-alpha/IFN-gamma in primary neurons but not i

300 mouse common carotid artery with or without OGD treatment.