ライフサイエンスコーパス: global ischemia

1 ntrol group received 0% low flow (20 mins of global ischemia).

2 subjected to 30 minutes of global ischemia (global ischemia).

3 y impaired after 10 min of reperfusion after global ischemia.

4 when CSIL therapy was initiated at 20 min of global ischemia.

5 study, CD-1 mice were subjected to transient global ischemia.

6 vioral performance of gerbils after cerebral global ischemia.

7 n the delayed neuronal death associated with global ischemia.

8 rtex (Pir) and hypothalamic nuclei following global ischemia.

9 to 7 min of cardiac arrest-induced transient global ischemia.

10 to necrosis or apoptosis following transient global ischemia.

11 tent of rab4 immunoreactivity in response to global ischemia.

12 tischemic function, compared with continuous global ischemia.

13 njury in the hippocampal CA1 subregion after global ischemia.

14 cell death in hippocampal CA1 neurons after global ischemia.

15 njury and cognitive deficits associated with global ischemia.

16 injection of CsA reduces brain damage after global ischemia.

17 uroprotective effects in the gerbil model of global ischemia.

18 hearts were subjected to 20 to 30 minutes of global ischemia.

19 h after certain insults, including transient global ischemia.

20 ltered in control hearts after 20 minutes of global ischemia.

21 to occur in a delayed manner after transient global ischemia.

22 to selective neuronal death after transient global ischemia.

23 o exert neuroprotection in rats subjected to global ischemia.

24 pocampal CA1 neurons in rats after transient global ischemia.

25 the hippocampus in a rat model of transient global ischemia.

26 es CA1 neuron loss produced by 10 minutes of global ischemia.

27 sensation and cognition following transient global ischemia.

28 in selective neuronal death after transient global ischemia.

29 eceptor subunits in gerbil hippocampus after global ischemia.

30 vity contributes to CA1 neuronal death after global ischemia.

31 ly susceptible to short periods of transient global ischemia.

32 t therapeutic targets in an in vivo model of global ischemia.

33 l pyramidal CA1 neurons induced by transient global ischemia.

34 ntribute to the delayed neuronal death after global ischemia.

35 e (i.v.) prior to KCl-induced cardiac arrest global ischemia.

36 o deep prepiriform cortex prior to 10 min of global ischemia.

37 neuronal death in animal models of focal and global ischemia.

38 ddle-aged and young female rats subjected to global ischemia.

39 to promote neuronal survival in the face of global ischemia.

40 ampal CA1 neuronal death following transient global ischemia.

41 pocampus of adult mice 1 day after transient global ischemia.

42 A1 neurons in a clinically-relevant model of global ischemia.

43 eprivation and in the rat model of transient global ischemia.

44 y of hippocampal CA1 synapses in the face of global ischemia.

45 d in hippocampal CA1 neurons after transient global ischemia.

46 mRNA levels in the rat brain after transient global ischemia.

47 n of CRH in discrete brain regions following global ischemia.

48 ent ischemic attack (45%), post-stroke (7%), global ischemia (10%), and asymptomatic severe occlusive

49 crease in core area was observed both during global ischemia (13.6+/-1.7 mm2; P<0.001) and TTX perfus

50 y utilized a rat model of transient (15 min) global ischemia (2-vessel occlusion) to investigate the

51 at hearts (n = 8) using a model of transient global ischemia (20 min) followed by reperfusion (20 min

52 rfused isolated rat hearts were subjected to global ischemia (25 min).

53 Isolated rat hearts were subjected to global ischemia (25 minutes; 37 degrees C) and reperfusi

54 m rats treated with PD98059 and subjected to global ischemia (30 minutes)/reoxygenation (1 hour) show

55 reconditioning (ie, three cycles of 5-minute global ischemia+5-minute reperfusion) prevented the impa

56 sted of 10 mins of baseline flow, 15 mins of global ischemia, 5 mins of low flow ischemia, and 30 min

57 level, before 2 cycles of IPC (5 minutes of global ischemia/5 minutes of reperfusion, n=6) or PPC by

58 In nontransgenic hearts following 30 min of global ischemia a reperfusion-associated burst of supero

59 ed and released in response to the stress of global ischemia accompanying cardiac arrest, play a role

60 GluR2 antisense and brief sublethal global ischemia acted synergistically to cause degenerat

61 us, protects CA1 neurons in the rat model of global ischemia, albeit transiently.

62 Global ischemia also induced a marked downregulation of

63 Neurological diseases, including global ischemia, Alzheimer's disease and amyotrophic lat

64 jected to either IPC, consisting of 5-minute global ischemia and 10-minute reperfusion, or high-Ca2+

65 3+/+ mouse hearts subjected to 30 minutes of global ischemia and 120 minutes of reperfusion, infarcti

66 23) reduced infarct size after 25 minutes of global ischemia and 120 minutes of reperfusion, maintain

67 sed mouse heart in response to 30 minutes of global ischemia and 120 minutes of reperfusion.

68 After 20 minutes of global ischemia and 20 minutes of reflow, hearts perfuse

69 up) or for 10 minutes, followed by 20-minute global ischemia and 20-minute reperfusion (stunned group

70 After 30-minute global ischemia and 20-minute reperfusion, HCVD was decr

71 Isolated hearts underwent 25 min global ischemia and 30 min reperfusion without additiona

72 olated rat hearts subjected to 25 minutes of global ischemia and 30 minutes of reperfusion.

73 osed to 40-minute normothermic, cardioplegic global ischemia and 30 minutes of reperfusion.

74 This was followed by 30 minutes of global ischemia and 35 minutes of reperfusion.

75 eveloped pressure (LVDP) after 20 minutes of global ischemia and 40 minutes of reperfusion in untreat

76 usion (IPC group) before 30 or 45 minutes of global ischemia and 40 minutes of reperfusion.

77 rfused rat hearts subjected to 20 minutes of global ischemia and 45 minutes of reperfusion.

78 lated guinea pig hearts undergoing 20-minute global ischemia and 45-minute reperfusion was attenuated

79 reductase, for 10 min, followed by 20 min of global ischemia and 60 min of reperfusion in the absence

80 ne-negative littermates exposed to 10 min of global ischemia and 90 min of reperfusion, HSP70 transge

81 otection in experimental models of focal and global ischemia and ameliorates the cognitive deficits a

82 ure worsens injury in experimental focal and global ischemia and brain trauma.

83 A1 neurons degenerating preferentially after global ischemia and CA3 neurons after limbic seizures.

84 In this model, global ischemia and cardiopulmonary resuscitation were a

85 seek to validate a mouse model of transient global ischemia and evaluate the effects of estradiol on

86 from neuronal cell death following transient global ischemia and excitotoxic injury.

87 ased neuronal cell death following transient global ischemia and excitotoxicity.

88 uring the period beginning with induction of global ischemia and extending after reperfusion using tr

89 ampal extracts prepared from rats exposed to global ischemia and found an up-regulated transcript, cl

90 iR-132 in the neuronal death associated with global ischemia and identify a novel therapeutic target

91 in of patients who experienced an episode of global ischemia and in controls.

92 the hippocampus in a rat model of transient global ischemia and in primary neuronal cultures under i

93 emic recovery in the rat hearts subjected to global ischemia and increased the infarct size when give

94 te postoperative cardiovascular dysfunction, global ischemia and metabolic dysfunction, and anemia be

95 PV inhibitory neurons was suppressed during global ischemia and rapidly recovered during reperfusion

96 serves myofilament Ca2+ responsiveness after global ischemia and reflow.

97 sed mouse hearts were subjected to 35 min of global ischemia and reperfused for 30 min in the presenc

98 (1) or B(2) receptors subjected to zero-flow global ischemia and reperfusion in a Langendorff model.

99 n (PV) interneurons during a 5 min period of global ischemia and reperfusion in mice, which mimicked

100 and improve left ventricular function after global ischemia and reperfusion in the isolated blood-pe

101 at undergo changes in phosphorylation during global ischemia and reperfusion in the isolated rabbit h

102 ed perfused adult rabbit hearts subjected to global ischemia and reperfusion were studied.

103 olated perfused rat hearts were subjected to global ischemia and reperfusion with rat PMNs (10(8) cel

104 as cardioprotective when administered before global ischemia and reperfusion.

105 king ethanol for 3-12 weeks and subjected to global ischemia and reperfusion.

106 ry and decreased infarct size in vitro after global ischemia and reperfusion.

107 isolated-perfused mouse hearts subjected to global ischemia and reperfusion.

108 ically protected in an intact heart model of global ischemia and reperfusion.

109 the neuronal death associated with transient global ischemia and sustained seizures, as well as perha

110 ive neuronal death associated with transient global ischemia and sustained seizures.

111 kt are involved in the molecular response to global ischemia and that age influences the status of CR

112 tosol from mitochondria in CA1 neurons after global ischemia and that the release preceded DNA fragme

113 /ml) during a four vessel occlusion model of global ischemia and the release of amino acids, especial

114 the resistance of CA3 hippocampal neurons to global ischemia and the tolerance conferred by ischemic

115 erative therapy to ameliorate splanchnic and global ischemia, and avoidance of anemia to improve the

116 delayed death of CA1 neurons after transient global ischemia, and block of GluR2 down-regulation may

117 for clinical risk score, ejection fraction, global ischemia, and early revascularization, CFR and CA

118 of hearts was treated with anisomycin before global ischemia, and in these, JNK activity increased by

119 surgery or transplantation generally involve global ischemia, and techniques have been developed to p

120 e and at selected times during 60 minutes of global ischemia, and the tissue was assayed for PP1 and

121 incubation with 10 mM ethanol 20 min before global ischemia; and (iv) ethanol-induced cardioprotecti

122 hanisms underlying neuronal cell death after global ischemia are as yet unknown.

123 Global ischemia arising during cardiac arrest or cardiac

124 Transient global ischemia, as with cardiac arrest, causes loss of

125 All hearts underwent 2 hours of global ischemia at 34 degrees C.

126 (1) control; (2) IP of 2x 5 minutes each of global ischemia before lethal ischemia; or pretreatment

127 At 10% flow, following global ischemia, both left ventricular function and bioe

128 Following global ischemia but before full reperfusion, a period of

129 educed in gerbil CA1 pyramidal neurons after global ischemia but before the onset of neurodegeneratio

130 layers was rapidly swollen and beaded during global ischemia, but recovered within 5-10 min following

131 Rats underwent 10 min of global ischemia by bilateral carotid artery occlusions p

132 hetized by chloral hydrate were subjected to global ischemia by bilateral common carotid artery occlu

133 beginning 25 mins before 12 mins of cerebral global ischemia (by aortic occlusion).

134 Acute global ischemia caused a threefold increase in the width

135 In isolated perfused rat hearts, global ischemia caused a time-dependent irreversible inj

136 ent with the hypothesis that the exposure to global ischemia caused an upregulation of the potassium-

137 ether, these findings suggest that 15 min of global ischemia causes extensive hippocampal neurodegene

138 These findings suggest that global ischemia causes impairments in performance on the

139 Transient global ischemia causes selective, delayed death of hippo

140 inimizes cellular energy requirements during global ischemia compared with traditional, hyperkalemic

141 [(4-fluoro)phenyl] pyrazole] before or after global ischemia compared with vehicle controls.

142 mprovement in neurobehavioral outcomes after global ischemia complicated by mild hyperglycemia, but n

143 antly improved functional recovery following global ischemia, demonstrating the specificity of the bi

144 Global ischemia did not significantly alter Cx32 and Cx3

145 he isolated perfused rat heart, we show that global ischemia does not activate the 42- and 44-kD extr

146 hen partial nephrectomy is performed without global ischemia, even after correcting for volume loss.

147 itol accumulation in rat hearts subjected to global ischemia ex vivo or coronary ligation in situ, wh

148 rnosinylated proteins in hearts subjected to global ischemia ex vivo.

149 type littermates were subjected to 10 min of global ischemia followed by 1 and 3 d of reperfusion.

150 fused hearts were subjected to 20 minutes of global ischemia followed by 2 hours of reperfusion, duri

151 were subjected to 30 minutes of normothermic global ischemia followed by 2 hours of reperfusion.

152 control mice were subjected to 30 minutes of global ischemia followed by 2 hours of reperfusion.

153 ration in a protocol consisting of 20 min of global ischemia followed by 2 hr of reperfusion.

154 ere then subjected to 20 min of normothermic global ischemia followed by 25 min of reperfusion.

155 perfusion (control, n=5) or to 25 minutes of global ischemia followed by 30 minutes of reperfusion (n

156 gendorff mode and subjected to 30 minutes of global ischemia followed by 30 minutes of reperfusion.

157 sed in vitro, and subjected to 25 minutes of global ischemia followed by 30 minutes of reperfusion.

158 d rat hearts were subjected to 40 minutes of global ischemia followed by 30 minutes of reperfusion.

159 fused rat hearts were subjected to 40-minute global ischemia followed by 30-minute reperfusion (I/R).

160 isolated-perfused rat heart model, 20 min of global ischemia followed by 40 min of reflow resulted in

161 e they were subjected to 30 or 45 minutes of global ischemia followed by 40 minutes of reperfusion (c

162 hearts were isolated and subjected to 30 min global ischemia followed by 60 min reperfusion in a Lang

163 se of 2 protocols: (1) 15 minutes of no-flow global ischemia followed by reperfusion (n=7) and (2) de

164 ermates (WT) were subjected to 24 minutes of global ischemia followed by reperfusion.

165 d perfused hearts subjected to 30 minutes of global ischemia followed by reperfusion.

166 guinea pig hearts subjected to 30 minutes of global ischemia followed by reperfusion.

167 Preparations were subjected to 30 minutes of global ischemia, followed by 30 minutes of reperfusion.

168 Rats were subjected to transient global ischemia (four vessel occlusion) and time-related

169 In a model of global ischemia, gerbils were infused with clomethiazole

170 r 30 minutes then subjected to 30 minutes of global ischemia (global ischemia).

171 During global ischemia, hearts with coronary disease had shorte

172 Similarly, global ischemia (I) for 20 minutes followed by 45 minute

173 Global ischemia impairs basal synaptic transmission, ass

174 dentate gyrus were examined after transient global ischemia in adult gerbils.

175 R was significantly increased (P<.05) during global ischemia in AGE but not in MAT.

176 ction was determined after brief episodes of global ischemia in an isolated Langendorff heart.

177 est decline in activity during 30 minutes of global ischemia in both groups.

178 Following global ischemia in gerbils, levels of caspase-3 enzyme a

179 Recovery of function (LVDP) after global ischemia in hearts from COX-1(-/-) and COX-2(-/-)

180 Global ischemia in humans or induced experimentally in a

181 We found that global ischemia in intact rats triggered expression and

182 Ca2+ channel activity is decreased during global ischemia in mature but increased in the aged hear

183 terns of neuronal death in hippocampus after global ischemia in mice.

184 tradiol treatment initiated 14 days prior to global ischemia in ovariectomized female rats acts via t

185 Global ischemia in rats and gerbils induces down-regulat

186 We further show that global ischemia in rats in vivo triggers a decrease in C

187 Transient global ischemia in rats induces delayed death of hippoca

188 Induction of global ischemia in rats resulted in JAK2 activation foll

189 ocampal CA1 neurons from delayed death after global ischemia in rats, suggesting that Cav3.1, Cav3.2,

190 water (ADCw) during the first few minutes of global ischemia in rats.

191 earning impairments resulting from transient global ischemia in rats.

192 ibutes to CA1 hippocampal neuron damage from global ischemia in rodents, raising the possibility that

193 ), c-jun, junB and c-fos are expressed after global ischemia in the gerbil.

194 maximal and half maximal ADCw drop following global ischemia in the hyperglycemic group were 3.96 and

195 8% hypoxia has been used to study focal and global ischemia in the newborn, and recently a filament

196 on of neuroglobin expression after transient global ischemia in the rat brain using mRNA in situ hybr

197 ilar results were observed in vivo following global ischemia in the rat.

198 cess involving excitatory neurotransmission: global ischemia in the rat.

199 Finally, calpain inhibition following global ischemia in vivo blocked decreases in eIF4G1, fac

200 Global ischemia increased myocardial SDH activity by app

201 Injury of control hearts during global ischemia, indexed by time-to-ischemic contracture

202 Transient global ischemia induced a fourfold increase in MCM mRNA

203 Global ischemia induced a marked increase in activated c

204 Global ischemia induced a marked upregulation of the pro

205 Global ischemia induced a selective increase in Cx32 and

206 n in the rat cerebral cortex after transient global ischemia induced by cardiac arrest and resuscitat

207 tered after the ischemic event intervenes in global ischemia-induced apoptotic cell death are unclear

208 17 can offer considerable protection against global ischemia-induced cell death in the hippocampus wi

209 Exogenous estradiol ameliorates global ischemia-induced neuronal death and cognitive imp

210 tmenopausal women affords protection against global ischemia-induced neuronal death and prevents acti

211 ) exhibit neuroprotection against subsequent global ischemia-induced neuronal death in the hippocampa

212 , thereby defining cell-specific patterns of global ischemia-induced neuronal death.

213 Eliminating elevations in preload after global ischemia-induced stunning also prevented TnI degr

214 Transient global ischemia induces a delayed rise in intracellular

215 Global ischemia induces a marked decrease in MOR-1 mRNA

216 Transient forebrain or global ischemia induces delayed neuronal death in vulner

217 Transient global ischemia induces selective, delayed neuronal deat

218 Although global ischemia induces troponin I (TnI) degradation, re

219 Global ischemia is a neuronal insult that induces delaye

220 Transient global ischemia is a neuronal insult that induces delaye

221 use hearts activation of AR during 15 min of global ischemia is completely reversed by 30 min of repe

222 osolic calcium ([Ca2+]i) accumulation during global ischemia is increased 30% more in the aged compar

223 Elimination of global ischemia is made possible through novel technical

224 (Sch-CA1) pyramidal cell synapses following global ischemia is not clear.

225 ia on arrhythmia susceptibility during acute global ischemia is not well understood.

226 A new model for mouse global ischemia is presented, and the relationship of is

227 Animals subjected to sublethal transient global ischemia (ischemic preconditioning) exhibit neuro

228 HIT could improve myocardial recovery after global ischemia, isolated rabbit hearts received either

229 After 20 mins of global ischemia, isolated rat hearts were reperfused for

230 Before 20 minutes of global ischemia, Langendorff-perfused rat hearts were pe

231 Transient, severe forebrain or global ischemia leads to delayed cell death of pyramidal

232 chemia-reperfusion injury, in both focal and global ischemia models.

233 Prior to 20 min of global ischemia, mouse hearts were either perfused for 3

234 Global ischemia: neuronal survival was similar in all 3

235 Global ischemia of a 30-min duration was induced in the

236 tential to greatly improve survival from the global ischemia of cardiac arrest.

237 mammalian central nervous system, transient global ischemia of specific duration causes selective de

238 Ventricular fibrillation (VF) leads to global ischemia of the heart.

239 ve dogs underwent 15 minutes of 37 degrees C global ischemia on cardiopulmonary bypass, followed by 7

240 udy were to determine the effects of no-flow global ischemia on nonlinear wave dynamics and establish

241 This study investigated the effects of acute global ischemia on the vulnerable window, the upper limi

242 isolated rat hearts subjected to periods of global ischemia or ischemia followed by reperfusion.

243 Density of wave fronts decreased during both global ischemia (P<0.002) and TTX perfusion (P<0.002) co

244 ring control to 9.3+/-1.4 Hz at 5 minutes of global ischemia (P<0.02).

245 ion model is one of the most frequently used global ischemia paradigms in rodents.

246 hanges in arterial Po2; and c) during severe global ischemia, Pbto2 decreased to 0 and remained at 0,

247 f preconditioning consisting of 5 minutes of global ischemia plus 10 minutes of reperfusion.

248 l cells and their loss of function following global ischemia, prior to their eventual death.

249 We demonstrate that global ischemia promotes early activation of glycogen sy

250 We further show that global ischemia promotes expression of the pro-survival

251 target genes in estradiol neuroprotection in global ischemia remains unclear.

252 Global ischemia-reperfusion increased left ventricle (LV

253 FA (4.5x10(-6) mol/L i.c.) pretreatment and global ischemia/reperfusion (30 minutes/30 minutes) also

254 Isolated mouse hearts subjected to global ischemia/reperfusion demonstrated cleavage of PKC

255 an injury and inflammation in the setting of global ischemia/reperfusion elicited by trauma/hemorrhag

256 f an important role of fibrin derivatives in global ischemia/reperfusion injury, which can be attenua

257 herapy may improve outcomes after the unique global ischemia/reperfusion insult of cardiopulmonary ar

258 rdiac efficiency and function in a rat heart global ischemia/reperfusion model, suggesting MCD inhibi

259 emorrhagic shock and resuscitation trigger a global ischemia/reperfusion phenomenon, in which various

260 These data indicate that HS/R, a global ischemia/reperfusion stimulus, regulates PMN mobi

261 dial metabolic reserve and flexibility after global ischemia/reperfusion stress in the setting of car

262 (MLA35 or MLA350) or vehicle 24 hours before global ischemia/reperfusion, which was carried out in a

263 assay rat hearts subjected to 30/120 minutes global ischemia/reperfusion.

264 dding Ran to cardioplegia (CP) in a model of global ischemia/reperfusion.

265 icosatrienoic acid to the perfusate prior to global ischemia resulted in a significant 1.6-fold impro

266 fore and for 6 days (but not 2 months) after global ischemia showed significantly better preservation

267 Global ischemia significantly decreased RyR activity in

268 -dose albumin therapy instituted 5 min after global ischemia significantly improves neurological scor

269 etabolic acidosis following brief periods of global ischemia sufficient to induce sustained abnormali

270 Global ischemia suppresses mRNA and protein expression o

271 stigated a non-human primate (NHP) transient global ischemia (TGI) model which was induced by clippin

272 ported in a rat model of transient forebrain global ischemia that activation and nuclear localization

273 d alterations in the endocytic pathway after global ischemia that are dependent on APOE genotype.

274 During 150 seconds of global ischemia the dominant frequency of activation dec

275 After global ischemia there was a marked increase in immunorea

276 After global ischemia, there was no influence of APOE genotype

277 Here we show that global ischemia triggers REST mRNA and protein expressio

278 These impairments after cerebral global ischemia under conditions of reduced neurogenesis

279 ful model to study the detailed mechanism of global ischemia using transgenic or knockout mutant mice

280 electrical function after complete transient global ischemia via mechanisms unrelated to cerebral cir

281 Neuronal apoptosis after global ischemia was also characterized by terminal deoxy

282 Apoptosis after global ischemia was also characterized by terminal deoxy

283 h of hippocampal CA1 neurons after transient global ischemia was examined.

284 icant increase in CRH release in response to global ischemia was found at the CeA with no alterations

285 Global ischemia was induced by 10 min of bilateral commo

286 ral regeneration, and 2 weeks later cerebral global ischemia was induced by bilateral common carotid

287 Seven-minute global ischemia was induced by cardiac arrest, followed

288 Five minutes of global ischemia was induced in male SOD1-transgenic (Tg)

289 Fifteen minutes of global ischemia was produced in adult Wistar rats using

290 tissue perfusion under this condition 10 min global ischemia was produced in two groups of isoflurane

291 activity and neuronal damage after transient global ischemia were also significantly reduced in MMP-9

292 l prostaglandin E2 concentrations 24 h after global ischemia were decreased in drug-treated animals c

293 bitor on neuronal survival in a rat model of global ischemia were determined.

294 Oxygenated rats subjected to global ischemia were prepared for comparison.

295 Rodent models of focal and global ischemia were used to examine caspase activation.

296 neostriatum die within 24 hr after transient global ischemia, whereas large aspiny (LA) neurons remai

297 We induced 10 min of global ischemia with 2-vessel occlusion and various seve

298 lobal ischemia without treatment (GI, n=49), global ischemia with G-CSF treatment (GI+G-CSF, n=42), a

299 athway is associated with seizures following global ischemia with hyperglycemia, which provides a new

300 Three groups of animals were used: global ischemia without treatment (GI, n=49), global isc