ライフサイエンスコーパス: OGD

1 OGD also increased lipid peroxidation levels and this ef

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

3 OGD does not cause GluA2 endocytosis in cortical neurons

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

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

6 OGD induced a transient decrease in fluorescence resonan

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

8 OGD progressively decreased neuronal survival over 48 h

9 OGD resulted in delayed degeneration of YFP-positive axo

10 OGD-induced accumulation of reactive oxygen species (ROS

11 OGD-induced synaptic depression was ameliorated by funct

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

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

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

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

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

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

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

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

20 Adjusted models showed exposure to active OGD was associated with adverse birth outcomes in rural

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

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

23 ndication of increased NKCC-1 activity after OGD.

24 K1-dependent internalization of AMPARs after OGD.

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

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

27 emia-gated currents or neuronal damage after OGD.

28 schemia-gated currents and cell damage after OGD.

29 ischemia-gated currents and cell death after OGD.

30 ut did not prevent axonal degeneration after OGD.

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

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

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

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

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

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

37 ncreased during reperfusion, even 24 h after OGD.

38 Cell death was assessed 48 h after OGD.

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

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

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

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

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

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

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

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

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

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

49 ecules at the onset of recovery period after OGD and showed that most of these QNs, but not the azo m

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

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

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

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

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

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

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

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

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

59 ubunits in affording neuroprotection against OGD/R injury.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 the effect of melatonin on Bmal1 after both OGD in vitro and focal cerebral ischemia in vivo.

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

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

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

81 sure to CSE worsens BBB disruption caused by OGD + RO, however, this is not linked to elevated ROS le

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

118 e (LPS), KCl and oxygen/glucose deprivation (OGD) that reflect inflammation, depolarization and ische

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 r survival after oxygen glucose deprivation (OGD) while the inhibition of Bmal1 resulted in the decre

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

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

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

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

128 res subjected to oxygen-glucose deprivation (OGD), as experimental model for ischemic conditions, wer

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

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

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

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

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

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

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

136 /16-1 diminished oxygen-glucose deprivation (OGD)-induced down-regulation of claudin-5 mRNA and prote

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

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

139 ondria following oxygen-glucose deprivation (OGD).

140 ltures following oxygen glucose deprivation (OGD).

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

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

143 OL cultures from oxygen glucose deprivation (OGD).

144 exposed to hypoxia and glucose deprivation (OGD).

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

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

147 eurons following oxygen-glucose deprivation (OGD).

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

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

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

151 simulated by oxygen and glucose deprivation (OGD).

152 lutamate and oxygen and glucose deprivation (OGD).

153 breakdown after oxygen-glucose deprivation (OGD).

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

155 usceptibility to oxygen glucose deprivation (OGD).

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

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

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

159 apoptosis after oxygen-glucose deprivation (OGD).

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

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

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

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

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

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

166 suggest exposure to oil and gas development (OGD) adversely affects birth outcomes, but no studies ha

167 ssociations between oil and gas development (OGD) and adverse birth outcomes, but few epidemiological

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

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

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

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

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

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

174 d increases in fluorescence intensity during OGD and reperfusion.

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

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

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

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

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

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

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

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

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

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

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

186 ng is affected in cortical neurons following OGD.

187 pharmacological inhibition of NHE1 following OGD/REOX.

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

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

190 abrogated the loss of water uptake following OGD.

191 Our study suggests exposure to flaring from OGD is associated with an increased risk of preterm birt

192 hether residential proximity to flaring from OGD was associated with shorter gestation and reduced fe

193 ring-the open combustion of natural gas-from OGD.

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

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

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

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

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

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

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

201 ed by 24 hour reoxygenation prior to 6 hours OGD (0.3% O(2)) significantly reduced LDH release and in

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

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

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

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

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

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

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

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

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

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

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

213 s spectrometry (MS) reveals that the modular OGD architecture offers the ability to control protein p

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

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

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

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

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

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

220 2 internalization is a critical component of OGD-induced cell death in hippocampal neurons.

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

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

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

224 The effects of OGD were mimicked by NMDA.

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

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

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

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

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

230 120 min of glutamate incubation or 3-6 hr of OGD treatment.

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

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

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

236 -207 was applied either 1 or 2 h before OGD, OGD-induced LDH release was significantly reduced.

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

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

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

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

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

242 sequent exposure to lethal levels of NMDA or OGD.

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

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

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

246 2 cells, treatment with premiR-29c prevented OGD-induced cell death (by 58 +/- 6%; p<0.05).

247 Proximity to higher production OGD in California was associated with adverse birth outc

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

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

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

251 xygen glucose deprivation and reoxygenation (OGD + RO).

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

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

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

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

256 intestinal transplant underwent simultaneous OGD and EUS.

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

258 tions between overall and trimester-specific OGD exposures and term birth weight (tBW), low birth wei

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 tophagy, and protect cells from a subsequent OGD insult.

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

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

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

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

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

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

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

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

272 1 or HOE 642 treatment had no effects on the OGD-mediated initial Na+(i) rise but reduced the second

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

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

275 ncrease in primary neuronal cells exposed to OGD condition.

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

277 modulate the survival of neurons exposed to OGD.

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

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

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

281 elationship between residential proximity to OGD and birth outcomes in California.

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.