ライフサイエンスコーパス: MCAO

1 MCAO also induced significant changes in forelimb use in

2 MCAO induced significant decline in neurological score p

3 MCAO markedly downregulated fibroblast growth factor-21

4 MCAO resulted in a substantial lesion formation and a si

5 MCAO resulted in ~60% larger infarcts in PGRN(+/-) and P

6 MCAO was induced for 30, 40 or 60 min in ovariectomized

7 MCAO was performed 48 h after the last dose of E-selecti

8 MCAO-induced lesion volumes were greater in insulinopeni

9 mly assigned to Sham-operated mice (n = 10), MCAO mice receiving the vehicle (n = 15) and MCAO mice r

10 cular method for this was published in 1989, MCAO has been applied commonly to the rat, and often pai

11 ry occlusion (MCAO) in adult rats (MCAO n=9, MCAO+H(2)n=7) for comparison.

12 After MCAO, mitochondrial dysfunction was augmented more signi

13 al deficit scores were quantitated 24h after MCAO.

14 he ischemic hemisphere on Days 1 and 3 after MCAO, and were significantly restored by TubA.

15 administered thrice: 30 min, 2h and 4h after MCAO for a total dose of 3 mg/kg) on cerebral ischemia i

16 loss and similar astrocyte activation after MCAO than their wild-type littermates.

17 were sequentially acquired before and after MCAO/R.

18 did not diminish the increase in CNTF after MCAO.

19 O followed by reperfusion and then 1 d after MCAO received an intravenous injection of either PBS (co

20 reased in KI compared with WT mice 7 d after MCAO.

21 were evaluated by SPECT/CT up to 14 d after MCAO.

22 active astrocytic response is dampened after MCAO.

23 y for 2 to 4 weeks from the fourth day after MCAO induced PSD-like depressive phenotypes in mice.

24 iately after surgery, 3, 7 and 10 days after MCAO).

25 enuated cortical lesion size at 7 days after MCAO.

26 ial effects lasted at least three days after MCAO.

27 logical stress but will be exacerbated after MCAO.

28 Infarct size was measured at 22 h after MCAO in estradiol-treated OVX animals in the presence an

29 d ischemic infarct size at 24 and 72 h after MCAO surgery.

30 hemic cortex cytosolic fraction at 3 h after MCAO without affecting T-STAT3.

31 At 3 h after MCAO, ADC and CBF lesions showed similar robust correlat

32 er activity rates at both 2 h and 24 h after MCAO, associated with significant fewer apoptotic cells

33 functional neurological deficits 48 h after MCAO.

34 ificantly reduced infarct size at 24 h after MCAO.

35 ction, which remained elevated at 22 h after MCAO.

36 volume defined by TTC staining at 24 h after MCAO.

37 volumes (mm(3)) calculated At 24 hours after MCAO, and infarct volume was determined using triphenylt

38 Twenty-four hours after MCAO, apoptosis was further increased in both diabetic m

39 Notably, when given at 24 hours after MCAO, TubA still exhibited significant protection.

40 isolated cerebral microvessels in mice after MCAO.

41 dosage of 2.5 U/kg body weight 30 min after MCAO (MCAO duration=60 min) and again 24 h after reperfu

42 flow maps through the first 60 minutes after MCAO; but not after 90 minutes of occlusion.

43 eases STAT3 phosphorylation in neurons after MCAO and that STAT3 activation plays an important role i

44 ypothesized that HBO given prior to or after MCAO reduces PMN infiltration into the brain, and that d

45 nclusion, our results demonstrate that after MCAO the interaction between tPA and LRP results in NF-k

46 ice received treatment with murine tPA after MCAO.

47 Mortality at 1 week after MCAO/R in the acutobin-treated group was significantly l

48 eatment, and mice were killed 12 weeks after MCAO.

49 the ability of estradiol to protect against MCAO-induced cell death involves attenuation of c-Fos in

50 MCAO mice receiving the vehicle (n = 15) and MCAO mice receiving an anti-myostatin PINTA745 (n = 12;

51 hondrial cyt c release at 24 h post-CCI and -MCAO.

52 ary occlusion of the middle cerebral artery (MCAO) to produce ischemia.

53 lic occlusion of the middle cerebral artery (MCAO).

54 a-estradiol (E2) or vehicle (OVX) 2 h before MCAO and sacrificed 24 h after the indicated duration of

55 Administration of LPS 24 h before MCAO reduced the infarct by 68% and improved ischemic ce

56 e was injected intraperitoneally 24 h before MCAO.

57 nd 30 mg/kg, i.p. administered 15 min before MCAO) produced 43% (n = 8, p = 0.16) and 58% (n = 8, p <

58 mg/kg (n=6), or 3 mg/kg (n=7) 30 min before MCAO.

59 es in GLAST or EAAC1 mRNA expression between MCAO and sham-operated brains.

60 od/brain barrier function was compromised by MCAO in WT mice.

61 ic responses and brain infarction induced by MCAO and reperfusion.

62 ear factor (NF)-kappaB activation induced by MCAO were unaffected by lack of CD36.

63 ion in cerebrovascular regulation induced by MCAO, as demonstrated by normalization of the increase i

64 To characterize metabolic changes induced by MCAO, we have induced permanent MCAO in mice that were i

65 CD14, a co-receptor of TLR4, was induced by MCAO, while the expression of TLR4 remained unchanged.

66 these brain areas were assessed by comparing MCAO brains with sham-operated control brains.

67 In contrast, MCAO-induced microglial activation is significantly decr

68 Second, we tested in a distal MCAO model.

69 lantation was performed 14 days after distal MCAO and doublecortin (Dcx)-expressing cells in the subv

70 n-weighted magnetic resonance imaging during MCAO was similar in neonatal CD36ko and WT mice, by 24 h

71 ller in GK rats with both suture and embolic MCAO, but expanded with longer reperfusion period.

72 ith the suture model, but not in the embolic MCAO.

73 irst, we tested gemfibrozil in a filamentous MCAO model.

74 Finally, MCAO: infarct volumes were not statistically different a

75 Following MCAO, mice were treated IV with low (1000 U/kg) and high

76 s of the hippocampus were analyzed following MCAO.

77 sis of Ets-1 protein in rat brains following MCAO showed that Ets-1 was highly expressed in neurons i

78 change in cerebral ischemic damage following MCAO in rats.

79 degeneration from 10 min to 7 days following MCAO was established.

80 The neurological deficit following MCAO was lower and oxidative stress parameters were impr

81 d to prevent cortical degeneration following MCAO in SIRT5-/- mice.

82 eral Aquaporin-4 (AQP4) expression following MCAO or progesterone treatment.

83 At 24 h following MCAO, blood-brain barrier permeability (BBB), stroke inf

84 se in the contralateral hemisphere following MCAO and diminished antioxidant capacity in the brain as

85 O dramatically reduced infarctions following MCAO.

86 the volume of the ischemic lesion following MCAO in wild-type and tPA-deficient (tPA-/-) neurons and

87 the volume of the ischemic lesion following MCAO.

88 ed rats had significant protection following MCAO induced cerebral ischemia.

89 reptozotocin-induced diabetic rats following MCAO with reperfusion.

90 r therapeutic intervention in rats following MCAO.

91 ain injury and functional recovery following MCAO and tPA reperfusion was assessed in young adult and

92 By 1 week following MCAO, VEGF-positive vessels/30 microm brain slice in the

93 ateral hemisphere volumes were 34 +/- 7% for MCAO, 24 +/- 6% for isoflurane preconditioning plus MCAO

94 Furthermore, MCAO caused nuclear translocation of the intracellular d

95 Rats underwent a 1-h MCAO followed by reperfusion and then 1 d after MCAO rec

96 Reperfusion after a 2 h MCAO compared to 24 h MCAO was associated with a decreas

97 esion volume and apoptosis subsequent to 2-h MCAO followed by 24-h reperfusion.

98 apoptotic levels in animals subjected to 2-h MCAO followed by 24-h reperfusion.

99 eperfusion after a 2 h MCAO compared to 24 h MCAO was associated with a decrease in TUNEL staining an

100 and CD40L-deficient mice subjected to 1-hour MCAO and 4-hour reperfusion.

101 oflurane anesthesia) and subjected to 2-hour MCAO.

102 In MCAO in adult rats, H(2) gas therapy demonstrated a tren

103 treated group which were severely altered in MCAO group.

104 ring a muscle contraction were attenuated in MCAO rats when compared to sham rats.

105 contraction were significantly attenuated in MCAO rats when compared to sham rats.

106 esponses during static muscle contraction in MCAO rats is partly due to a reduction in nNOS expressio

107 cular responses during muscle contraction in MCAO rats may be partly due to a reduction in eNOS expre

108 tion, and ameliorated neuronal cell death in MCAO rats.

109 of tPA resulted in a significant decrease in MCAO-induced nitric oxide production and inducible nitri

110 s 1, 3, 5, 7 post-ischemia, respectively) in MCAO subjected rats.

111 e subgrouped based on amount of tissue loss, MCAO animals with only 4% tissue loss exhibited enduring

112 e of 2.5 U/kg body weight 30 min after MCAO (MCAO duration=60 min) and again 24 h after reperfusion.

113 In the 30-min MCAO group, multiple time-point analysis showed no stati

114 o implants 7 days prior to undergoing 60 min MCAO.

115 In the 60-min MCAO group, multiple time-point analysis improved specif

116 We found that a 60-minute MCAO followed by spatial restraint stress for 2 h daily

117 were serially obtained in rat stroke models (MCAO): permanent, 90 min, and 180 min temporary MCAO.

118 of cl-nanozyme in a well-characterized mouse MCAO model of I/R injury.

119 a permanent middle cerebral artery occluded (MCAO) rat model was used.

120 nt right middle cerebral arterial occlusion (MCAO) in adult male rats.

121 to 1 h of middle cerebral artery occlusion (MCAO) and 24-72 h of reperfusion.

122 transient middle cerebral artery occlusion (MCAO) and an in vitro model of excitotoxicity.

123 esponse to middle cerebral artery occlusion (MCAO) and reperfusion.

124 transient middle cerebral artery occlusion (MCAO) and reperfusion.

125 o a 2-hour middle cerebral artery occlusion (MCAO) and sacrificed at 24 hours of reperfusion.

126 ion of the middle cerebral artery occlusion (MCAO) and spatial restraint stress.

127 caused by middle cerebral artery occlusion (MCAO) and traumatic brain injury (TBI) caused by control

128 transient middle cerebral artery occlusion (MCAO) as was estrone.

129 t (45 min) middle cerebral artery occlusion (MCAO) during the hyperacute, acute and chronic phases.

130 transient middle cerebral artery occlusion (MCAO) followed by reperfusion in rats and potentiate the

131 reversible middle cerebral artery occlusion (MCAO) for 1 hour followed by 1 hour of reperfusion.

132 d to right middle cerebral artery occlusion (MCAO) for 2 h under ketamine/xylazine or isoflurane anes

133 ible right middle cerebral artery occlusion (MCAO) for 2 h was used.

134 bjected to middle cerebral artery occlusion (MCAO) for stroke induction.

135 permanent middle cerebral artery occlusion (MCAO) group, respectively.

136 ed H(2) in middle cerebral artery occlusion (MCAO) in adult rats (MCAO n=9, MCAO+H(2)n=7) for compari

137 transient middle cerebral artery occlusion (MCAO) in adult rats, expression of FosDT and Fos was ind

138 24h after Middle Cerebral Artery Occlusion (MCAO) in all 3 types of mice.

139 90 min of middle cerebral artery occlusion (MCAO) in male Wistar rats.

140 rated that middle cerebral artery occlusion (MCAO) in mice induces shedding of the LRP ectodomain, we

141 following middle cerebral artery occlusion (MCAO) in ovariectomised female mice, with a physiologica

142 ecovery to middle cerebral artery occlusion (MCAO) in rats and hMCT2 transgenic mice and of hippocamp

143 ter distal middle cerebral artery occlusion (MCAO) in rats.

144 permanent middle cerebral artery occlusion (MCAO) in SHR-SP rats and whether these effects are relat

145 line after middle cerebral artery occlusion (MCAO) in the mouse brain.

146 by embolic middle cerebral artery occlusion (MCAO) in vivo or by oxygen and glucose deprivation in br

147 transient middle cerebral artery occlusion (MCAO) increased the amount of tissue salvage compared to

148 perimental middle cerebral artery occlusion (MCAO) increases tPA activity and neuroserpin expression

149 found that middle cerebral artery occlusion (MCAO) induces microglial activation in both wild-type an

150 Middle cerebral artery occlusion (MCAO) is a popular model in experimental stroke research

151 traluminal middle cerebral artery occlusion (MCAO) method.

152 s in a rat middle cerebral artery occlusion (MCAO) model after a single intravenous (i.v.) injection.

153 sion in a permanent middle artery occlusion (MCAO) model in rats.

154 permanent middle cerebral artery occlusion (MCAO) model in the adult mouse.

155 nsient rat middle cerebral artery occlusion (MCAO) model of brain ischemia.

156 permanent middle cerebral artery occlusion (MCAO) model of focal ischemia.

157 n in a rat middle cerebral artery occlusion (MCAO) model of ischemia/reperfusion (I/R) injury (stroke

158 osis and a middle cerebral artery occlusion (MCAO) model of stroke, LSR was down-regulated, linking l

159 an in vivo middle cerebral artery occlusion (MCAO) model only the 57kDa fragment of MetAP2 was observ

160 dovascular middle cerebral artery occlusion (MCAO) model to examine the influence of NF-kappaB on neu

161 the mouse middle cerebral artery occlusion (MCAO) model.

162 permanent middle cerebral artery occlusion (MCAO) models in young adult male mice on normal diet.

163 ent distal middle cerebral artery occlusion (MCAO) on day 14 of vehicle or GCV treatment, and mice we

164 underwent middle cerebral artery occlusion (MCAO) or sham surgery.

165 a two-hour middle cerebral artery occlusion (MCAO) procedure.

166 ive in the middle cerebral artery occlusion (MCAO) rat stroke model.

167 permanent middle cerebral artery occlusion (MCAO) received three intravenous injections of either ve

168 transient middle cerebral artery occlusion (MCAO) reduced infarct volume by >50%; the protection per

169 permanent middle cerebral artery occlusion (MCAO) showed significant improvement in neurological and

170 24 h after middle cerebral artery occlusion (MCAO) stroke and gene transcription in brain tissues fol

171 the mouse middle cerebral artery occlusion (MCAO) stroke model, we have established the therapeutic

172 mice after middle cerebral artery occlusion (MCAO) strongly implicates a mixture of both pathogenic a

173 e model of middle cerebral artery occlusion (MCAO) to examine whether improvements in cerebrovascular

174 t model of middle cerebral artery occlusion (MCAO) under two anesthesia regimens.

175 bjected to middle cerebral artery occlusion (MCAO) using a genome-wide approach.

176 permanent middle cerebral artery occlusion (MCAO) was induced by intraluminal filament.

177 following middle cerebral artery occlusion (MCAO) when compared to non-diabetics.

178 underwent middle cerebral artery occlusion (MCAO) with monitoring of cerebral blood flow.

179 following middle cerebral artery occlusion (MCAO) with or without reperfusion.

180 transient middle cerebral artery occlusion (MCAO) with the suture model.

181 y utilized middle cerebral artery occlusion (MCAO) with tissue plasminogen activator (tPA) to assess

182 to 2 h of middle cerebral artery occlusion (MCAO), and phosphorylated STAT3 (P-STAT3) and total STAT

183 received a middle cerebral artery occlusion (MCAO), and T(2)-weighted MRI at 48 h post-MCAO quantifie

184 traluminal middle cerebral artery occlusion (MCAO), or SHAM surgery.

185 e model of middle cerebral artery occlusion (MCAO), p38 MAPK activation was observed in the glia scar

186 s with the middle cerebral artery occlusion (MCAO), provided the BDNF is conjugated to a blood-brain

187 transient middle cerebral artery occlusion (MCAO), we observed an initial elevation ( 1.7-fold, 1-4

188 ts against middle cerebral artery occlusion (MCAO)-induced brain injury during late phases of neurona

189 ex against middle cerebral artery occlusion (MCAO)-induced cell death.

190 P plays on middle cerebral artery occlusion (MCAO)-induced NF-kappaB-mediated inflammatory response.

191 transient middle cerebral artery occlusion (MCAO).

192 permanent middle cerebral artery occlusion (MCAO).

193 induced by middle cerebral artery occlusion (MCAO).

194 48h after middle cerebral artery occlusion (MCAO).

195 permanent middle-cerebral artery occlusion (MCAO).

196 transient middle cerebral artery occlusion (MCAO).

197 bjected to middle cerebral artery occlusion (MCAO).

198 unilateral middle cerebral artery occlusion (MCAO).

199 transient middle cerebral artery occlusion (MCAO).

200 t model of middle cerebral artery occlusion (MCAO).

201 following middle cerebral artery occlusion (MCAO).

202 90 min of middle cerebral artery occlusion (MCAO).

203 inal right middle cerebral artery occlusion (MCAO).

204 temporary middle cerebral artery occlusion (MCAO).

205 e onset of middle cerebral artery occlusion (MCAO).

206 underwent middle cerebral artery occlusion (MCAO).

207 t (90 min) middle cerebral artery occlusion (MCAO).

208 caused by middle cerebral artery occlusion (MCAO).

209 reversible middle cerebral artery occlusion (MCAO).

210 transient middle cerebral artery occlusion (MCAO).

211 45 min of middle cerebral artery occlusion (MCAO).

212 30-min of middle cerebral artery occlusion (MCAO).

213 utilizes a mouse middle cerebral occlusion (MCAO) model of embolic stroke to study neuronal degenera

214 ttenuated following transient MCA occlusion (MCAO) and reperfusion, mediated via alteration of the ne

215 ontribution of B cells to the development of MCAO by comparing infarct volumes and functional outcome

216 rificed 24 h after the indicated duration of MCAO.

217 ce were used to examine the exact effects of MCAO using Fluoro-Jade, a marker of neurodegeneration th

218 kg M40401 at 60 min of MCAO or at the end of MCAO (90 min) failed to significantly reduce lesion volu

219 ation at various survival times after 1 h of MCAO.

220 on rather than normal cerebral hemisphere of MCAO rats.

221 trophils in the affected brain hemisphere of MCAO-treated muMT(-/-) versus WT mice.

222 ours to the infarct volume after 24 hours of MCAO.

223 a single dose of 3 mg/kg M40401 at 60 min of MCAO or at the end of MCAO (90 min) failed to significan

224 ter the initial drop in rCBF at the onset of MCAO.

225 to sham rats and the right CVLM quadrant of MCAO rats, eNOS expression was significantly increased i

226 to sham rats and the right CVLM quadrant of MCAO rats, nNOS expression was significantly augmented i

227 pha expression in the ipsilateral regions of MCAO-subjected rats was reduced after MMP-12 knockdown i

228 e ability of in vivo anti-ischemic stroke of MCAO rats.

229 tective potential of NRG-1 using a permanent MCAO ischemia (pMCAO) rat model.

230 ection was also demonstrated after permanent MCAO.

231 iol increased infarct volume after permanent MCAO.

232 Following permanent MCAO, infarct size was smaller, edema was greater, and t

233 s induced by MCAO, we have induced permanent MCAO in mice that were implanted with a microdialysis pr

234 In a mouse model of permanent MCAO, no significant difference in motor function recove

235 In the permanent MCAO group, prediction with multiple time-point diffusio

236 In the permanent MCAO group, the lesion volume on the ADC maps was signif

237 recovery of skeletal muscle mass in PINTA745-MCAO mice involved an increased expression of genes enco

238 P < 0.05 for isoflurane preconditioning plus MCAO to compare with MCAO alone or with SB203580 plus is

239 B203580 plus isoflurane preconditioning plus MCAO) and mimicked by an activator of these kinases, ani

240 4 +/- 6% for isoflurane preconditioning plus MCAO, and 30 +/- 6% for SB203580 plus isoflurane precond

241 B203580 plus isoflurane preconditioning plus MCAO, n = 8, P < 0.05 for isoflurane preconditioning plu

242 ed animals compared to vehicle by day 7 post MCAO.

243 s compared to vehicle at 24 h and day 7 post MCAO.

244 l conduction velocity recovered by 21 d post MCAO in KI mice in corpus callosum.

245 ains but not in KI mouse brains at 24 h post MCAO.

246 ssion significantly increased at 1 week post MCAO in the infarcted hemisphere of IRL-1620 treated rat

247 ) and neurological score at 24h and 48h post-MCAO indicated that MCAO significantly worsened outcome

248 On day 7 post-MCAO, neurological deficit-matched rats were assigned to

249 nctional recovery was tested for 7 days post-MCAO and brains processed for histological verification

250 hemia and this increase peaks at 7 days post-MCAO.

251 d during the test period in both groups post-MCAO.

252 ency was 30+/-7 s and 103+/-9 s at 24 h post-MCAO in the animals treated with BDNF alone and the BDNF

253 n (MCAO), and T(2)-weighted MRI at 48 h post-MCAO quantified ischemic damage.

254 score performance (from 22 to 11 at 2 h post-MCAO) in the vehicle-treated animals, which was not sign

255 At 2 and 24 h post-MCAO, neurological deficits were assessed.

256 similar in cerebral hemispheres at 24 h post-MCAO.

257 d injected intravenously (i.v.) 6 hours post-MCAO with either 1 mg/kg PNU-120596 (treated group) or v

258 behavioral tests were performed 24 hrs post-MCAO.

259 In conclusion, testosterone replacement post-MCAO accelerated functional recovery in castrate rats, s

260 double labeled for SHP-1 at early times post-MCAO.

261 After 4 weeks post-MCAO, the average infarct volume was not significantly d

262 latency was >200 s at 16 RPM in all rats pre-MCAO.

263 olume and mortality in the hyperglycemic rat MCAO/R model.

264 +/-50 to 117+/-55 mm(3) in the temporary rat MCAO model (90 min), and from 216+/-58 to 127+/-57 mm(3)

265 ebral artery occlusion (MCAO) in adult rats (MCAO n=9, MCAO+H(2)n=7) for comparison.

266 esis that the ability of estradiol to reduce MCAO-induced cell death involves attenuation of expressi

267 iddle cerebral artery occlusion/reperfusion (MCAO/R) model.

268 d in rats with a temporary 90-min left-sided MCAO followed by 24 h reperfusion (n = 10).

269 left ipsilateral CVLM quadrant in left-sided MCAO rats.

270 mented in the ipsilateral CVLM in left-sided MCAO rats.

271 Left-sided MCAO significantly decreased the expression of eNOS in t

272 in rats with a temporary 90-minute one-sided MCAO followed by 24 hour reperfusion.

273 Similarly, MCAO-induced infarcts were significantly greater in IH-e

274 ransient middle cerebral artery occlusion (t-MCAO) model of stroke.

275 n vivo, using two-photon microscopy in the t-MCAO stroke model.

276 Infarct volume after temporary MCAO with a CCA clip was significantly larger and variab

277 O): permanent, 90 min, and 180 min temporary MCAO.

278 We found that MCAO increased LRP expression primarily in astrocytes an

279 We found that MCAO induces an increase in gamma-secretase activity in

280 core at 24h and 48h post-MCAO indicated that MCAO significantly worsened outcome compared with sham-o

281 The MCAO procedure resulted in a significant infarct in the

282 s undergoing MCAO alone at 14 days after the MCAO.

283 both acute and chronic insulin decreased the MCAO-induced lesion volume and apoptosis.

284 t show any significant changes following the MCAO.

285 een, liver) 3 days after IV injection in the MCAO rat.

286 ively few laboratories have investigated the MCAO method in the mouse.

287 These MCAO-induced changes were completely prevented in B-cell

288 ed after systemic administration of BMSCs to MCAO rats is likely due to the cellular changes in blood

289 by different scoring methods as compared to MCAO group.

290 or sensorimotor function in rats exposed to MCAO.

291 nhibitor; 5 mg/kg) or saline 30 min prior to MCAO.

292 ncreased apoptosis in the CNS in response to MCAO, and restoration of blood flow especially in the in

293 Transient MCAO in rats may therefore provide a pre-clinical model

294 Bax expression increased in vehicle-treated MCAO rats, these changes were attenuated (P < 0.01) by I

295 ased in IRL-1620 compared to vehicle-treated MCAO rats.

296 ane-preconditioned rats than rats undergoing MCAO alone at 14 days after the MCAO.

297 9 male mice from 33 inbred strains underwent MCAO for 6 hours (215 mice) or 24 hours (234 mice).

298 after MMP-12 knockdown compared to untreated MCAO subjected rats.

299 istar and GK rats were subjected to variable MCAO by suture or embolus occlusion.

300 ne preconditioning plus MCAO to compare with MCAO alone or with SB203580 plus isoflurane precondition