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 pathophysiologic pathways undergoing during cerebral ischemia.

3 Seven of 14 patients developed delayed cerebral ischemia.

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

5 forms the basis for successful treatment of cerebral ischemia.

6 and worse cognitive dysfunction after global cerebral ischemia.

7 tes with the eventual development of delayed cerebral ischemia.

8 sorders, focusing on Parkinson's disease and cerebral ischemia.

9 s high age and tauopathy with thromboembolic cerebral ischemia.

10 ct in reactive astrocyte proliferation after cerebral ischemia.

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

12 a dramatically worsened outcome after focal cerebral ischemia.

13 in an experimental model of transient focal cerebral ischemia.

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

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

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

17 hippocampal neurodegeneration after hypoxia/cerebral ischemia.

18 nd inflammatory responses prior to and after cerebral ischemia.

19 d in other conditions associated with global cerebral ischemia.

20 n injury and functional impairment caused by cerebral ischemia.

21 tion and may contribute to excitotoxicity in cerebral ischemia.

22 A pretreatment-induced tolerance in diabetic cerebral ischemia.

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

24 nflammatory brain infarction following focal cerebral ischemia.

25 flammation contributes to neuronal injury in cerebral ischemia.

26 giogenic and neurogenic remodeling following cerebral ischemia.

27 cytokines has not been well addressed during cerebral ischemia.

28 mmune-system-mediated defense response after cerebral ischemia.

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

30 oprotective effect against damage induced by cerebral ischemia.

31 l neuroprotective agents in animal models of cerebral ischemia.

32 ascular endothelial cells after induction of cerebral ischemia.

33 tly suppress pathologic glutamate release in cerebral ischemia.

34 amplifying matrix metalloproteinases during cerebral ischemia.

35 for prevention of brain injury secondary to cerebral ischemia.

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

37 uronal damage like stroke, brain trauma, and cerebral ischemia.

38 enting delayed neuronal loss after transient cerebral ischemia.

39 ed mechanistic understanding of tolerance to cerebral ischemia.

40 that inflammation enhances tissue damage in cerebral ischemia.

41 significant neuroprotection at 24h following cerebral ischemia.

42 oglial activation, and neuroprotection after cerebral ischemia.

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

44 novel therapeutic target in the treatment of cerebral ischemia.

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

46 cally useful if started before initiation of cerebral ischemia.

47 ion against many cellular insults, including cerebral ischemia.

48 neurovascular remodeling and recovery after cerebral ischemia.

49 re partially protected from transient, focal cerebral ischemia.

50 ed loss of E2 neuroprotection against global cerebral ischemia.

51 ignificant protection following MCAO induced cerebral ischemia.

52 and was fully neuroprotective against global cerebral ischemia.

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

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

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

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

57 fingolimod in several rodent models of focal cerebral ischemia.

58 death after local acidosis that accompanies cerebral ischemia.

59 oposed to promote neuronal death in modelled cerebral ischemia.

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

61 edictor of eventual neuronal death following cerebral ischemia.

62 downstream adaptors during TLR signaling in cerebral ischemia.

63 osis and autophagy following transient focal cerebral ischemia.

64 significantly reduces infarction after focal cerebral ischemia.

65 ulation to the benefit of S1PR modulation in cerebral ischemia.

66 lopment of targeted treatment strategies for cerebral ischemia.

67 ly, worsened neurological function following cerebral ischemia.

68 rebrain and determine its roles after global cerebral ischemia.

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

70 ragments were identified in the blood during cerebral ischemia.

71 ed proteolytic degradation of the BBB during cerebral ischemia.

72 l molecule CGRP receptor antagonists, worsen cerebral ischemia.

73 f acidosis-induced neuronal damage following cerebral ischemia.

74 creased muscle weight recovery 15 days after cerebral ischemia.

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

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

77 sue resulting from traumatic brain injury or cerebral ischemia.

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

79 etection of PFO in patients with cryptogenic cerebral ischemia.

80 al bioenergetics and neuroprotection against cerebral ischemia.

81 ated with morbidity and mortality because of cerebral ischemia.

82 SR was defined as modified thrombolysis in cerebral ischemia 2b to 3.

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

84 Cerebral ischemia (45 minutes) was induced by intralumin

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

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

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

88 1.36; 95% CI, 1.20-1.54; p < 0.001), delayed cerebral ischemia (adjusted odds ratio, 1.31; 95% CI, 1.

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

90 patient in the caplacizumab group died from cerebral ischemia after the end of the treatment period.

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

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

103 ay ameliorate the functional consequences of cerebral ischemia and point to be a potential new therap

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

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

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

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

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

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

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

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

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

116 tion (viral and fungal), multiple sclerosis, cerebral ischemia, and cerebral malaria.

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

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

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

120 NPCs and mitochondrial fate determination in cerebral ischemia, and in improving neurological deficit

121 shown SAAs are elevated following stroke and cerebral ischemia, and our studies demonstrated that SAA

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

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

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

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

129 o the brain.SIGNIFICANCE STATEMENT Following cerebral ischemia, astrocytes become highly reactive and

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 favorable performance for predicting delayed cerebral ischemia (DCI) (area under curve (AUC) > 0.750)

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

142 d Rankin Scale (mRS), mortality, and delayed cerebral ischemia (DCI).

143 rotection induction in two in vivo models of cerebral ischemia, decreasing neuronal death and reducin

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

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

146 Cerebral ischemia due to pituitary apoplexy is very rare

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

148 Despite cerebral ischemia during torpor and rapid reperfusion du

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

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

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

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

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

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

155 Cerebral ischemia frequently leads to long-term disabili

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

157 e brain and determine its roles after global cerebral ischemia (GCI) in male and female mice.

158 ived E2 and elucidate its roles after global cerebral ischemia (GCI).

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

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

161 Following global cerebral ischemia, hippocampal CA1 pyramidal neurons are

162 Following global cerebral ischemia, hippocampal CA1 pyramidal neurons are

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

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

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

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

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

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

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

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

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

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

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

174 ation at acute and chronic time points after cerebral ischemia in mice.

175 pair and reduces neurological deficits after cerebral ischemia in mice.

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

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

178 ctive and attenuates neural damage following cerebral ischemia in rats by increasing CBF and reducing

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

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

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

182 ovides significant neuroprotection following cerebral ischemia in rats.

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

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

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

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

187 n on Bmal1 after both OGD in vitro and focal cerebral ischemia in vivo.

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

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

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

191 Cerebral ischemia induced a time-dependent increase of b

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

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

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

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

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

197 Breakdown of BBB integrity during cerebral ischemia initiates a devastating cascade of eve

198 Focal cerebral ischemia initiates self-repair mechanisms that

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

200 Cerebral ischemia is a pathology that stems from a decre

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

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

203 ke is a multiphasic process in which initial cerebral ischemia is followed by secondary injury from i

204 Cerebral ischemia is one of the leading causes of mortal

205 Cerebral ischemia is the major insult of stroke and indu

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

207 In rats subjected to focal cerebral ischemia, lymphatic endothelial cells prolifera

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

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

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

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

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

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

214 ls in the context of Alzheimer's disease and cerebral ischemia mouse models.

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

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

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

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

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

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

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

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

223 7.73; CI, 2.78-21.52; P < 0.001), transient cerebral ischemia (OR, 7.67; CI, 5.31-11.07; P < 0.001),

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

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

226 Cerebral ischemia plays a major role in the pathophysiol

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

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

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

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

231 o the brain.SIGNIFICANCE STATEMENT Following cerebral ischemia, reactive astrocytes express the enzym

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

250 reduced ischemic stroke infarct volume after cerebral ischemia-reperfusion injury.

251 Cerebral ischemia/reperfusion (I/R) injury was significa

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

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

254 Here we used cerebral ischemia/reperfusion as a model to investigate

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 Cerebral ischemia/reperfusion insult rapidly activates n

263 tion of ATF6 is also protective in renal and cerebral ischemia/reperfusion models, demonstrating its

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

265 Global cerebral ischemia results in oxygen and glucose deprivat

266 Whether cerebral ischemia results in POCD after ablation for AF

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

268 A biomarker of cerebral ischemia, S100b, remained unchanged, suggesting

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

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

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

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

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

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

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

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

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

278 )methanimine oxide (17) is a novel agent for cerebral ischemia therapy as it is able to scavenge diff

279 After permanent focal cerebral ischemia, tPA knockout mice developed more seve

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

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

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

283 Cerebral ischemia was induced by 30 minutes of middle ce

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

285 Cerebral ischemia was induced by middle cerebral artery

286 Focal cerebral ischemia was induced by permanent distal middle

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

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

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

290 Transient cerebral ischemia was induced in mice by middle cerebral

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

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

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

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

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

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

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

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

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

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