ライフサイエンスコーパス: cerebral ischemia

1 egenerative diseases and stroke (i.e., focal cerebral ischemia).

2 lying mechanisms in a gerbil model of global cerebral ischemia.

3 induced by treadmill exercise, in rats after cerebral ischemia.

4 hippocampal neurodegeneration after hypoxia/cerebral ischemia.

5 nd inflammatory responses prior to and after cerebral ischemia.

6 d in other conditions associated with global cerebral ischemia.

7 n injury and functional impairment caused by cerebral ischemia.

8 tion and may contribute to excitotoxicity in cerebral ischemia.

9 A pretreatment-induced tolerance in diabetic cerebral ischemia.

10 p-regulated in the injured mouse brain after cerebral ischemia.

11 nflammatory brain infarction following focal cerebral ischemia.

12 flammation contributes to neuronal injury in cerebral ischemia.

13 ed proteolytic degradation of the BBB during cerebral ischemia.

14 giogenic and neurogenic remodeling following cerebral ischemia.

15 cytokines has not been well addressed during cerebral ischemia.

16 ted tissue damage and BBB breakdown in focal cerebral ischemia.

17 oprotective effect against damage induced by cerebral ischemia.

18 l neuroprotective agents in animal models of cerebral ischemia.

19 ascular endothelial cells after induction of cerebral ischemia.

20 tly suppress pathologic glutamate release in cerebral ischemia.

21 amplifying matrix metalloproteinases during cerebral ischemia.

22 for prevention of brain injury secondary to cerebral ischemia.

23 n at both 24h and 1 week following permanent cerebral ischemia.

24 enting delayed neuronal loss after transient cerebral ischemia.

25 ed mechanistic understanding of tolerance to cerebral ischemia.

26 that inflammation enhances tissue damage in cerebral ischemia.

27 significant neuroprotection at 24h following cerebral ischemia.

28 f acidosis-induced neuronal damage following cerebral ischemia.

29 llular matrix (ECM) is highly degraded after cerebral ischemia.

30 novel therapeutic target in the treatment of cerebral ischemia.

31 d identify PK2 as a deleterious mediator for cerebral ischemia.

32 cally useful if started before initiation of cerebral ischemia.

33 ion against many cellular insults, including cerebral ischemia.

34 neurovascular remodeling and recovery after cerebral ischemia.

35 re partially protected from transient, focal cerebral ischemia.

36 ed loss of E2 neuroprotection against global cerebral ischemia.

37 ignificant protection following MCAO induced cerebral ischemia.

38 and was fully neuroprotective against global cerebral ischemia.

39 of sex chromosome dosage in the response to cerebral ischemia.

40 c (EEG) silence in anticipation of transient cerebral ischemia.

41 of the PGE2 receptor EP4 in a mouse model of cerebral ischemia.

42 thways in 2 in vitro and 2 in vivo models of cerebral ischemia.

43 fingolimod in several rodent models of focal cerebral ischemia.

44 death after local acidosis that accompanies cerebral ischemia.

45 oposed to promote neuronal death in modelled cerebral ischemia.

46 to determine the role of ET(B) receptors in cerebral ischemia.

47 edictor of eventual neuronal death following cerebral ischemia.

48 downstream adaptors during TLR signaling in cerebral ischemia.

49 stosterone increases damage following global cerebral ischemia.

50 d associated neuromigration induced by focal cerebral ischemia.

51 iled imaging for hemorrhage and overlap with cerebral ischemia.

52 olume and attenuates brain edema after focal cerebral ischemia.

53 (DWI) is a sensitive and reliable marker of cerebral ischemia.

54 creased muscle weight recovery 15 days after cerebral ischemia.

55 ral infarction in mice after transient focal cerebral ischemia.

56 rier (BBB) breakdown and neuronal loss after cerebral ischemia.

57 thophysiological and behavioral responses to cerebral ischemia.

58 hase (nNOS)-derived NO is detrimental during cerebral ischemia.

59 ay and delayed neuronal cell death following cerebral ischemia.

60 R2KO mice (1.31+/-0.02 and 2.2+/-0.32) after cerebral ischemia.

61 ptotic delayed neuronal cell death following cerebral ischemia.

62 ammation, and functional outcome after focal cerebral ischemia.

63 ly decreased MBF and increased indicators of cerebral ischemia.

64 els were not significantly changed following cerebral ischemia.

65 cal diseases such as HIV-1 AIDS dementia and cerebral ischemia.

66 ) and then decline of O-GlcNAcylation during cerebral ischemia.

67 t's susceptibility to development of delayed cerebral ischemia.

68 sue resulting from traumatic brain injury or cerebral ischemia.

69 ta frequency ratio, are surrogate markers of cerebral ischemia.

70 etection of PFO in patients with cryptogenic cerebral ischemia.

71 al bioenergetics and neuroprotection against cerebral ischemia.

72 ated with morbidity and mortality because of cerebral ischemia.

73 y of skeletal muscle mass and function after cerebral ischemia.

74 Seven of 14 patients developed delayed cerebral ischemia.

75 ditions of low energy supply, as observed in cerebral ischemia.

76 forms the basis for successful treatment of cerebral ischemia.

77 tes with the eventual development of delayed cerebral ischemia.

78 s high age and tauopathy with thromboembolic cerebral ischemia.

79 ct in reactive astrocyte proliferation after cerebral ischemia.

80 ament is a widely used model to induce focal cerebral ischemia.

81 a dramatically worsened outcome after focal cerebral ischemia.

82 ragments were identified in the blood during cerebral ischemia.

83 in an experimental model of transient focal cerebral ischemia.

84 iR-155, on brain recovery after experimental cerebral ischemia.

85 all, 23.5% of hemodialysis sessions featured cerebral ischemia; 31.9% of these events were symptomati

86 Cerebral ischemia (45 minutes) was induced by intralumin

87 group) were treated with Pam3CSK4 1 h before cerebral ischemia (60 min), followed by reperfusion (24

88 noid hemorrhage patients at risk for delayed cerebral ischemia across a wide range of hemoglobin valu

89 In animal models of cerebral ischemia, acute inhibition of JNK reduces infar

90 Fifty-two patients at risk for delayed cerebral ischemia after aneurysmal subarachnoid hemorrha

91 Acute cerebral ischemia and chronic neurovascular diseases sha

92 was the most effective treatment to prevent cerebral ischemia and could be used in anaphylactic shoc

93 However, the effects of cerebral ischemia and ex vivo stimulation of these cells

94 yloid burden directly contributes to chronic cerebral ischemia and highlights the possible utility of

95 ation that can lead to meningitis, seizures, cerebral ischemia and hydrocephalus.

96 ial ischemia, cardiovascular instability and cerebral ischemia and hyperperfusion are high, and anest

97 more, we estimated intradialytic exposure to cerebral ischemia and hypotension for each patient, and

98 ratories using two different mouse models of cerebral ischemia and in a clinically relevant large ani

99 Microglia are activated following cerebral ischemia and increase their production of the n

100 y can improve skeletal muscle recovery after cerebral ischemia and may thus represent an interesting

101 contributes to neurologic disease, including cerebral ischemia and multiple sclerosis.

102 estradiol (E2)-dependent neuroprotection in cerebral ischemia and neurodegenerative disease, most of

103 stment of established predictors for delayed cerebral ischemia and outcome: age, sex, World Federatio

104 e both independently associated with delayed cerebral ischemia and poor outcome in multivariable anal

105 hnoid hemorrhage are associated with delayed cerebral ischemia and poor outcome, suggesting that they

106 circulating lactate and glucose with delayed cerebral ischemia and poor outcome.

107 l perfusion, mitigate the harmful effects of cerebral ischemia and promote tissue restoration.

108 the animals are protected from experimental cerebral ischemia and pulmonary embolism.

109 ey rats to monitor GluA in the cortex during cerebral ischemia and reperfusion demonstrate a potentia

110 Cerebral ischemia and reperfusion increase superoxide an

111 ts injury in the acute and delayed phases of cerebral ischemia and reperfusion injury.

112 Administration of S-memantine after global cerebral ischemia and reperfusion more robustly decrease

113 complement-dependent injury following murine cerebral ischemia and reperfusion, and, based also on pr

114 In a model of cerebral ischemia and reperfusion, diabody administratio

115 ) is neuroprotective in CNS injury models of cerebral ischemia and spinal cord injury.

116 ed long-term functional motor deficits after cerebral ischemia and strongly reduced brain atrophy as

117 ne increase neuronal damage following global cerebral ischemia and that blockade of androgen receptor

118 ting apoptosis after brain injuries, such as cerebral ischemia and traumatic brain injures, but littl

119 measurements of serum S100B, a biomarker for cerebral ischemia, and computed tomography measurement o

120 infarct size following either myocardial or cerebral ischemia, and conferred survival benefit follow

121 Seizures are a common sequel of cerebral ischemia, and hyperglycemia markedly increases

122 nly results from energy shortage, such as in cerebral ischemia, and refers to the swelling of brain c

123 le sclerosis, amyotrophic lateral sclerosis, cerebral ischemia, and the prion diseases.

124 tid artery occlusion (AICAO) and hemodynamic cerebral ischemia are at high risk for subsequent stroke

125 y mechanisms of NADPH oxidase activity after cerebral ischemia are still unclear.

126 Animal models of focal cerebral ischemia are well accepted for investigating th

127 ied dipyridamole, used for the prevention of cerebral ischemia, as a potentiator of statin anticancer

128 microvascular coagulation in the brain after cerebral ischemia, as confirmed by reduced brain injury

129 loss and improved body weight recovery after cerebral ischemia, as well as muscle strength and motor

130 /3) of patients with primary ICH have active cerebral ischemia at baseline remote from the index hema

131 profile in the ischemic cortex of rats after cerebral ischemia at early time points (2 and 6 h).

132 rved after SAH is the development of delayed cerebral ischemia at sites often remote from the site of

133 CTP not only allows early detection of cerebral ischemia but also gives valuable information on

134 r (TLR) signaling plays an important role in cerebral ischemia, but downstream signaling events, whic

135 Intradialytic cerebral ischemia, but not hypotension, correlated with

136 bstantial synaptic depression during hypoxia/cerebral ischemia, but postsynaptic actions of A1Rs are

137 F isoform VEGF165b in a mouse model of focal cerebral ischemia by middle cerebral artery occlusion an

138 xendin-4 protects the CNS from damage due to cerebral ischemia by reducing oxidative stress and is in

139 elayed neuronal loss and brain atrophy after cerebral ischemia contribute to stroke and dementia path

140 ral vasospasm (CV) and the resulting delayed cerebral ischemia (DCI) significantly contribute to poor

141 Effective therapy for cerebral ischemia demands a carrier that can penetrate t

142 It results in cerebral ischemia due to a variety of mechanisms, includ

143 Cerebral ischemia due to pituitary apoplexy is very rare

144 emia and reperfusion in mice, which mimicked cerebral ischemia during cardiac arrest or forms of tran

145 ood flow such as to increase the severity of cerebral ischemia during CPR.

146 Despite cerebral ischemia during torpor and rapid reperfusion du

147 h recently symptomatic AICAO and hemodynamic cerebral ischemia, EC-IC bypass surgery plus medical the

148 In the pathophysiologic setting of cerebral ischemia, excitotoxic levels of glutamate contr

149 ngly, GluN2C knockout mice, following global cerebral ischemia, exhibit greater neuronal death in the

150 EAAC1(-/-) mice subjected to transient cerebral ischemia exhibited twice as much hippocampal ne

151 e C57BL/6 mice were subjected to 1h of focal cerebral ischemia followed by 24 or 72 h of reperfusion.

152 GlcNAcylation during the first four hours of cerebral ischemia, followed by continuous decline after

153 rebral blood flow is the hallmark of delayed cerebral ischemia following subarachnoid hemorrhage.

154 Cerebral ischemia frequently leads to long-term disabili

155 tions of oxygen-glucose deprivation to mimic cerebral ischemia, GABA(A)Rs are depleted from synapses

156 L-1620 on neurovascular remodeling following cerebral ischemia has not been established.

157 uces neuronal apoptosis and is implicated in cerebral ischemia, head trauma, and age-related neurodeg

158 Following global cerebral ischemia, hippocampal CA1 pyramidal neurons are

159 Following global cerebral ischemia, hippocampal CA1 pyramidal neurons are

160 viously undescribed therapeutic modality for cerebral ischemia/hypoxia and ischemic stroke.

161 final diagnosis of the qualifying event was cerebral ischemia in 73.3% of patients, intracranial hem

162 crovasculature before and after experimental cerebral ischemia in a mouse model of type 1 diabetes.

163 to glia and neuronal populations, following cerebral ischemia in a murine model of stroke.

164 ted imaging (DWI) provides evidence of acute cerebral ischemia in a third of TIA patients.

165 Transient focal cerebral ischemia in adult mice was induced by ligations

166 xamine the spatiotemporal dynamics of DKI in cerebral ischemia in an animal model of permanent and tr

167 Estrogen was protective against cerebral ischemia in both XX and XO mice.

168 h after MCAO for a total dose of 3 mg/kg) on cerebral ischemia in control and exendin-4 treated rats.

169 ion of IL-1alpha by microglia in response to cerebral ischemia in infected animals.

170 -mediated cytotoxic pathway on outcome after cerebral ischemia in mice.

171 ranslocated into the nuclei of neurons after cerebral ischemia in mice.

172 CARD (ARC) in in vitro and in vivo models of cerebral ischemia in mice.

173 portant to understand the pathophysiology of cerebral ischemia in pituitary apoplexy to improve manag

174 ress mediated by hypoxia in vitro and global cerebral ischemia in rats in vivo We show that pharmacol

175 rotection till 7 days after the induction of cerebral ischemia in rats.

176 rmed in an independent in vivo experiment of cerebral ischemia in rats.

177 eptor was observed 7 days after induction of cerebral ischemia in vehicle or IRL-1620 treated rats.

178 Here, we show that after focal cerebral ischemia in vivo or oxygen-glucose deprivation

179 t NMDA exposure in vitro and transient focal cerebral ischemia in vivo resulted in increased levels o

180 hypoxic conditions in vitro or experimental cerebral ischemia in vivo.

181 ployed a preterm fetal sheep model of global cerebral ischemia in which acute WMI results in selectiv

182 ment regimen to reduce cognitive decline and cerebral ischemia incidents/impact in post-menopausal wo

183 of cardiac arrest, here we show that global cerebral ischemia increases microglial activation, proin

184 Cerebral ischemia induced a time-dependent increase of b

185 e stroke-prone (SHRSP) rats protects against cerebral ischemia induced by middle cerebral artery occl

186 By using mouse models of cerebral ischemia induced by permanent and transient mid

187 fect cerebral blood flow, after experimental cerebral ischemia induced by transient middle cerebral a

188 We showed that focal cerebral ischemia induced nestin lineage neural stem cel

189 tensity of myoclonic jerks and the extent of cerebral ischemia-induced neurodegeneration in the cereb

190 These results indicate that cerebral ischemia induces a rapid increase of O-GlcNAcyl

191 After permanent focal cerebral ischemia induction, infarct volume and neurolog

192 h contribute to the damaging consequences of cerebral ischemia, inflammation, and neurodegenerative d

193 Focal cerebral ischemia initiates self-repair mechanisms that

194 protective effect of AQP4 deletion in global cerebral ischemia involves reduced astrocyte swelling an

195 Cerebral ischemia is a pathology that stems from a decre

196 rough which E2 protects the hippocampus from cerebral ischemia is by preventing the post-ischemic ele

197 therapy with a TLR2-specific agonist during cerebral ischemia is effective in reducing injury.

198 Cerebral ischemia is the major insult of stroke and indu

199 The rate of clinically silent cerebral ischemia is unknown but may be even higher.

200 Focal cerebral ischemia, known as stroke, causes serious long-

201 vivo, adult NR3A TG mice subjected to focal cerebral ischemia manifested less damage than WT mice.

202 These data show that cerebral ischemia markedly increases heparanase levels i

203 ypothesis that opening of hemichannels after cerebral ischemia may contribute to delayed evolution of

204 ell-known LVAD complication) and subclinical cerebral ischemia may result in transient or permanent c

205 After cerebral ischemia, miR-592 levels fall, with a correspon

206 the effects of increased CD39 in an in vivo cerebral ischemia model, we developed a transgenic mouse

207 emia reperfusion damage in a transient focal cerebral ischemia model.

208 lly relevant levels of progesterone prior to cerebral ischemia neither benefited nor worsened outcome

209 Delayed cerebral ischemia occurred in 84 patients (29%), and 106

210 pilot study demonstrates that intradialytic cerebral ischemia occurs frequently, is not easily predi

211 owed an independent association with delayed cerebral ischemia (odds ratio, 1.14; 95% CI, 1.01-1.28)

212 Specific knockdown of MMP-12 after focal cerebral ischemia offers neuroprotection that could be m

213 ence of preserving hypertension during focal cerebral ischemia on stroke outcome in a rat model of ch

214 association between LOC at onset and delayed cerebral ischemia or aneurysm rebleeding.

215 on of ET(B) receptors was observed following cerebral ischemia or any treatment.

216 ted with other vascular phenotypes including cerebral ischemia (OR = 1.64; P = 2.5 x 10(-3)), and art

217 7.73; CI, 2.78-21.52; P < 0.001), transient cerebral ischemia (OR, 7.67; CI, 5.31-11.07; P < 0.001),

218 auma, localized brain edema, hematoma, focal cerebral ischemia, or brain tumors.

219 atio in patients who did not develop delayed cerebral ischemia (p < 0.0001) but an overall decrease i

220 Cerebral ischemia plays a major role in the pathophysiol

221 hat MANF has neuroprotective effects against cerebral ischemia, possibly through the inhibition of ce

222 ation confers robust neuroprotection against cerebral ischemia, probably by alleviating white matter

223 on in mice lacking AQP4 in a model of global cerebral ischemia produced by transient, bilateral carot

224 lin (ET) ET(A) and ET(B) receptors following cerebral ischemia produced in rats by permanent middle c

225 io in those patients who did develop delayed cerebral ischemia (range, +11% to -31%) (p = 0.006, mult

226 In a mouse model of focal cerebral ischemia, reactive astrocytes in the peri-infar

227 fined as grade 3 or 2b modified Treatment in Cerebral Ischemia recanalization accomplished in up to t

228 Here, we report that cerebral ischemia recruits death-associated protein kina

229 In mice, transient focal cerebral ischemia reduced endogenous ARC protein in neur

230 -dimer (3 nmol/g) to mice subjected to focal cerebral ischemia reduces infarct volume with 40% and re

231 actate and glucose were related with delayed cerebral ischemia-related infarction and poor outcome (a

232 -enhanced local therapeutic gas delivery for cerebral ischemia-related injury while minimizing system

233 We examined the relationship between BP and cerebral ischemia (relative drop in cerebral saturation

234 In addition, MB significantly reduced cerebral ischemia reperfusion damage in a transient foca

235 Meta-analysis for argon was only possible in cerebral ischemia reperfusion injury and did not show ne

236 ingle Ab reactivity is sufficient to develop cerebral ischemia reperfusion injury in the context of a

237 s are key contributors to the acute phase of cerebral ischemia reperfusion injury, but the relevant T

238 d in hippocampus CA1 at 10 min to 72 h after cerebral ischemia reperfusion, with peak levels 30 min t

239 osis of hippocampal neurons following global cerebral ischemia-reperfusion (I/R) injury, in a rat mod

240 ctor (bFGF) may protect stroke patients from cerebral ischemia-reperfusion (I/R) injury.

241 The inflammatory response initiated by cerebral ischemia-reperfusion contributes to ischemic br

242 impact of acetaminophen on acute injury from cerebral ischemia-reperfusion has not been studied.

243 derzone vascular density 10 days after focal cerebral ischemia-reperfusion in rats.

244 ylation by pharmacological means ameliorated cerebral ischemia-reperfusion injury and the consequent

245 his study reveals an important regulation of cerebral ischemia-reperfusion injury by O-GlcNAcylation

246 Ps) and tested their efficacy in a rat focal cerebral ischemia-reperfusion injury model.

247 (C1q/MBL deficient) were also protected from cerebral ischemia-reperfusion injury, and there was no d

248 t role for complement in the pathogenesis of cerebral ischemia-reperfusion injury, or ischemic stroke

249 ) are protected from arterial thrombosis and cerebral ischemia-reperfusion injury.

250 investigated the effects of acetaminophen on cerebral ischemia-reperfusion-induced injury using a tra

251 al-mediated mechanism in an in vivo model of cerebral ischemia-reperfusion.

252 Cerebral ischemia/reperfusion (I/R) injury, expression o

253 ivation by its specific ligand, Pam3CSK4, on cerebral ischemia/reperfusion (I/R) injury.

254 water soluble compound from garlic, against cerebral ischemia/reperfusion (I/R)-induced mitochondria

255 ne, on the behavioral dysfunction induced by cerebral ischemia/reperfusion injury in gerbils.

256 In a transient cerebral ischemia/reperfusion injury model, Apoe(-/-) mi

257 Using intravital microscopy, we found that cerebral ischemia/reperfusion injury was accompanied by

258 age and subsequent neuronal death induced by cerebral ischemia/reperfusion injury, and also can contr

259 eviated neurological deficits than sTM after cerebral ischemia/reperfusion injury.

260 oresolving, anti-inflammatory pathways after cerebral ischemia/reperfusion injury.

261 ptor) evoked neuroprotective functions after cerebral ischemia/reperfusion injury.

262 t could contribute to neuronal injury in the cerebral ischemia/reperfusion pathology.

263 Global cerebral ischemia results in oxygen and glucose deprivat

264 Whether cerebral ischemia results in POCD after ablation for AF

265 These data suggest that global cerebral ischemia results in significant declines in cen

266 tudy was to compare the prevalence of silent cerebral ischemia (SCI) and cognitive performance in pat

267 substantial recanalization (Thrombolysis in Cerebral Ischemia scores 2B to 3; drip and ship, 84 [84.

268 citotoxicity is a condition occurring during cerebral ischemia, seizures, and chronic neurodegenerati

269 ]-fluorodeoxyglucose immediately after focal cerebral ischemia showed increased glucose uptake in Lys

270 as long as 6 hours after the onset of focal cerebral ischemia significantly reduces brain injury and

271 l cortex following traumatic brain injury or cerebral ischemia, significantly aggravates brain damage

272 A experience ongoing (chronic, intermittent) cerebral ischemia, sometimes reversible, far more freque

273 death, as seen in neurodegenerative disease, cerebral ischemia (stroke) and traumatic brain injury (T

274 (2)(*-) overproduction after transient focal cerebral ischemia (tFCI).

275 age after acute excitotoxicity and transient cerebral ischemia than do control mice.

276 ational studies of patients with cryptogenic cerebral ischemia that provided both sensitivity and spe

277 cularly during acute brain injuries, such as cerebral ischemia, trauma, and seizures.

278 ress, is neuroprotective in animal models of cerebral ischemia, traumatic brain injury, subarachnoid

279 ed in up to 43% of patients with cryptogenic cerebral ischemia undergoing investigation with transeso

280 that chronic SEH inhibition protects against cerebral ischemia via vascular protection in SHRSP rats

281 Periprocedural apparent and silent cerebral ischemia was assessed by neurological testing a

282 Cerebral ischemia was induced by 30 minutes of middle ce

283 Focal cerebral ischemia was induced by a transient (90 min) mi

284 Cerebral ischemia was induced by middle cerebral artery

285 Focal cerebral ischemia was induced by permanent distal middle

286 Focal cerebral ischemia was induced by transient (1h) occlusio

287 ours after the end of EA pretreatment, focal cerebral ischemia was induced following 24h reperfusion.

288 Focal cerebral ischemia was induced in mice (by permanent or t

289 Transient cerebral ischemia was induced in mice by middle cerebral

290 BQ123 induced protection from cerebral ischemia was similar in vehicle or exendin-4 tr

291 on of TNF from this cellular source in focal cerebral ischemia we used TNF conditional knock out mice

292 n and glucose deprivation (in vitro model of cerebral ischemia), we observed an increased expression

293 central nervous system (CNS) are involved in cerebral ischemia, we determined the effect of a specifi

294 e of some of these mediators in outcome from cerebral ischemia, we treated rats with the growth-inhib

295 ts from garlic clove (GCE) and skin (GSE) on cerebral ischemia were evaluated by administering extrac

296 L-1620 is not known in the subacute phase of cerebral ischemia, where development of cerebral edema f

297 eptors was significantly increased following cerebral ischemia which was not affected by exendin-4 tr

298 R4 in the pathogenesis of seizures following cerebral ischemia with hyperglycemia.

299 aircase task and subsequently underwent left cerebral ischemia with the 3-vessel occlusion model.

300 of a clinically validated biomarker of acute cerebral ischemia would have the potential to facilitate