ライフサイエンスコーパス: middle cerebral artery

1 sion at any level of the internal carotid or middle cerebral artery.

2 ociated with changes in flow velocity in the middle cerebral artery.

3 n adult Sprague Dawley rats by occluding the middle cerebral artery.

4 underwent 90 min transient occlusions of the middle cerebral artery.

5 ombosis in the murine carotid artery and the middle cerebral artery.

6 s in layer 2/3 located just posterior to the middle cerebral artery.

7 tonin-evoked constriction of pressurized rat middle cerebral arteries.

8 rial lesions were frequently detected in the middle cerebral artery (23%), internal carotid artery (1

9 ral artery (39 vs 109 cm3; P = .004), and M2 middle cerebral artery (33 vs 59 cm3; P = .04) occlusion

10 Most aneurysms were in the middle cerebral arteries (36%) and the internal carotid

11 rtery terminus (75 vs 190 cm3; P < .001), M1 middle cerebral artery (39 vs 109 cm3; P = .004), and M2

12 set of vasospasm was 4 days (+/- 2 d) in the middle cerebral arteries and 5 days (+/- 2.5 d) in the b

13 Changes of middle cerebral arteries and basilar arteries were extre

14 flow velocities (transcranial Doppler) from middle cerebral artery and blood pressure (Finometer) we

15 nts had occlusion of the internal carotid or middle cerebral artery and evidence of salvageable brain

16 2017 from patients with an occlusion in the middle cerebral artery and from an additional cohort of

17 hed infarcts in the anterior cerebral artery-middle cerebral artery and middle cerebral artery-poster

18 intracranial aneurysms of the right and left middle cerebral artery and right internal carotid artery

19 rminal internal carotid artery [ICA] with M1 middle cerebral artery and/or A1 anterior cerebral arter

20 d spectroscopy, blood flow velocities of the middle cerebral artery, and cardiac output at baseline,

21 Three months later the right middle cerebral artery aneurysm was embolised and the wo

22 Endovascular treatment of small unruptured middle cerebral artery aneurysms is feasible and effecti

23 using near-infrared spectroscopy along with middle cerebral artery blood flow measured using transcr

24 In the middle cerebral artery blood flow velocities and vasomot

25 Beat-by-beat measurements of middle cerebral artery blood flow velocity (MCAv; transc

26 Mean middle cerebral artery blood velocity (MCA V(mean)), mea

27 cerebrovascular control were measured using middle cerebral artery blood velocity (MCAv(mean) ) and

28 al, prefrontal cortex tissue oxygenation and middle cerebral artery blood velocity (MCAV) were assess

29 s of superficial temporal artery branch to a middle cerebral artery cortical branch for the surgical

30 Patients with significant carotid or middle-cerebral artery disease or impaired vasoreactivit

31 monitored by near-infrared spectroscopy and middle cerebral artery Doppler.Measurements and Main Res

32 s induced by transient (1h) occlusion of the middle cerebral artery, during which mean arterial blood

33 Bilateral transcranial middle cerebral artery flow velocities using Doppler and

34 that the raw recordings from left and right middle cerebral arteries had higher content of mutual in

35 ces of ET-1-mediated vasoconstriction of the middle cerebral artery in a rat model.

36 The relatively low mean flow velocity in the middle cerebral artery in combination with normal jugula

37 between 2010 and 2018 with occlusion of the middle cerebral artery in the M1-/proximal M2-segment or

38 The angio-CT revealed an aneurysm of the middle cerebral artery, in its distal branch.

39 d ADC maps obtained less than 12 hours after middle cerebral artery infarct.

40 ntal and parietal cortex is common following middle cerebral artery infarction, leading to upper extr

41 n, 70 years; range, 61 to 82) with malignant middle-cerebral-artery infarction to either conservative

42 er with complete or subtotal space-occupying middle-cerebral-artery infarction.

43 ts 61 years of age or older with a malignant middle-cerebral-artery infarction.

44 Survival after malignant middle cerebral artery infarcts is dismal.

45 Consecutive patients with M1 segment middle cerebral artery +/- intracranial internal carotid

46 t of middle cerebral artery vs M2 segment of middle cerebral artery), intravenous alteplase (yes vs n

47 ed 30 to 83 years, with confirmed first-time middle cerebral artery ischemic stroke with modified Ran

48 10 patients, 18 to 80 years old, with acute middle cerebral artery ischemic stroke.

49 al and stroke volume after femoral artery or middle cerebral artery ligation, respectively.

50 ified for endovascular treatment of the left middle cerebral artery (LMCA) aneurysm because it posed

51 idence interval [CI]: 1.1, 2.8; P = .02) and middle cerebral artery location (OR, 1.9; 95% CI: 1.2, 3

52 or thromboembolic events were female sex and middle cerebral artery location.

53 (intracranial internal carotid artery and/or middle cerebral artery M1 and/or M2) on computed tomogra

54 h after stroke induction by occlusion of the middle cerebral artery markedly reduced infarct size, an

55 .3 hyperpolarization was investigated in rat middle cerebral arteries (MCA).

56 ain parenchyma, hydrocephalus, and so-called middle cerebral artery (MCA) "pseudofeeders" were correl

57 t mice was induced by ligations of the right middle cerebral artery (MCA) and both common carotid art

58 The risk of seizures after malignant middle cerebral artery (MCA) infarction with decompressi

59 The middle cerebral artery (MCA) is the second most common l

60 stoperatively, by recording 1-hour bilateral middle cerebral artery (MCA) microembolic signals (MES).

61 ars) with acute ischemic stroke (AIS) due to middle cerebral artery (MCA) occlusion were enrolled; 75

62 generated occlusive VWF-rich thrombi in the middle cerebral artery (MCA) of mice.

63 A), anterior cerebral artery (ACA), and / or middle cerebral artery (MCA) secondary to SAH due to an

64 in patients with internal carotid artery or middle cerebral artery (MCA) stroke and to evaluate the

65 am, n = 10), rats were sacrificed for either middle cerebral artery (MCA) structure and function asse

66 of the GPIIb/IIIa antagonist tirofiban, in a middle cerebral artery (MCA) thrombosis model in guinea

67 Occlusion of the middle cerebral artery (MCA) with an endovascular filame

68 -HAs defined by location (at proximal/distal middle cerebral artery (MCA), within/beyond diffusion-we

69 nduced following photochemical injury to the middle cerebral artery (MCA).

70 ertebral artery (VA) and CBF velocity at the middle cerebral artery (MCA).

71 arterial transcranial Doppler (aTCD) on the middle cerebral artery (MCA): MCA pulsatility index (PIa

72 l carotid artery (ICA), basilar artery (BA), middle cerebral artery (MCA)], the submandibular gland (

73 lower in Eln(+/-) than Eln(+/+) mice in the middle cerebral artery (MCA, P < 0.001), but was similar

74 tile range, 5-17]), of the M1 segment of the middle cerebral artery (MCA; 52 patients: median NIHSS s

75 re were compared in isolated and pressurized middle cerebral arteries (MCAs) and PAs taken from the s

76 Cerebral blood velocity in the middle cerebral artery (MCAv) was obtained by transcrani

77 +/- 5 mm Hg vs. 41 +/- 2 mm Hg; p < .05) and middle cerebral artery mean flow velocity (37 +/- 9 cm.s

78 < .05), and higher mean arterial pressure-to-middle cerebral artery mean flow velocity phase differen

79 ation, endotoxemia was associated with lower middle cerebral artery mean flow velocity variability (1

80 Systemic hemodynamics, middle cerebral artery mean flow velocity, and dynamic c

81 Malignant middle cerebral artery [MMCA] infarction has a different

82 We included 67 patients with malignant middle cerebral artery [MMCA] stroke who underwent decom

83 In this study, a permanent middle cerebral artery occluded (MCAO) rat model was use

84 to be useful in infarct volume reduction in middle cerebral artery occluded rat brain.

85 Vehicle-treated middle cerebral artery occluded rats demonstrated high l

86 Results CT scans from 100 patients with middle cerebral artery occlusion (44 women [mean age +/-

87 urs was calculated in patients with proximal middle cerebral artery occlusion (derivation cohort) wit

88 h, 1, 3, 5 and 7 days after permanent distal middle cerebral artery occlusion (dMCAO) in mice compare

89 or were initiated at 48 h after mouse distal middle cerebral artery occlusion (dMCAO).

90 ult male rats received a 90-min right distal middle cerebral artery occlusion (dMCAo).

91 and wild-type mice were subjected to 1 h of middle cerebral artery occlusion (MCAO) and 24-72 h of r

92 HDAC6 inhibitor, in a rat model of transient middle cerebral artery occlusion (MCAO) and an in vitro

93 equent severe ischemic injury, as induced by middle cerebral artery occlusion (MCAo) and if this prot

94 eeks, the animals were subjected to a 2-hour middle cerebral artery occlusion (MCAO) and sacrificed a

95 nimal model encompasses a combination of the middle cerebral artery occlusion (MCAO) and spatial rest

96 al model of permanent and transient (45 min) middle cerebral artery occlusion (MCAO) during the hyper

97 homing to the ischemic site after transient middle cerebral artery occlusion (MCAO) followed by repe

98 present study, the model of reversible right middle cerebral artery occlusion (MCAO) for 2 h was used

99 Adult male C57BL/6 mice were subjected to middle cerebral artery occlusion (MCAO) for stroke induc

100 BF data for the 30-min, 60-min and permanent middle cerebral artery occlusion (MCAO) group, respectiv

101 Following transient middle cerebral artery occlusion (MCAO) in adult rats, e

102 in ischemia and 2) infarct volumes 24h after Middle Cerebral Artery Occlusion (MCAO) in all 3 types o

103 In addition, the functional recovery to middle cerebral artery occlusion (MCAO) in rats and hMCT

104 chemia, followed by continuous decline after middle cerebral artery occlusion (MCAO) in the mouse bra

105 Ischemia induced either by embolic middle cerebral artery occlusion (MCAO) in vivo or by ox

106 inistration of Ang-(1-7) following transient middle cerebral artery occlusion (MCAO) increased the am

107 and improve sensorimotor functions in a rat middle cerebral artery occlusion (MCAO) model after a si

108 he vehicle-treated groups in a 12h permanent middle cerebral artery occlusion (MCAO) model of focal i

109 a single intravenous (IV) injection in a rat middle cerebral artery occlusion (MCAO) model of ischemi

110 itis (EAE) model of multiple sclerosis and a middle cerebral artery occlusion (MCAO) model of stroke,

111 Using an in vivo middle cerebral artery occlusion (MCAO) model only the 5

112 ed brain injury in mouse photothrombotic and middle cerebral artery occlusion (MCAo) models.

113 ral ischemia was induced by permanent distal middle cerebral artery occlusion (MCAO) on day 14 of veh

114 UCHL1 C152A KI and WT mice underwent middle cerebral artery occlusion (MCAO) or sham surgery.

115 Male rats were subjected to a two-hour middle cerebral artery occlusion (MCAO) procedure.

116 ale Sprague-Dawley rats undergoing permanent middle cerebral artery occlusion (MCAO) received three i

117 IRL-1620-treated rats following permanent middle cerebral artery occlusion (MCAO) showed significa

118 this study, rats were sacrificed 24 h after middle cerebral artery occlusion (MCAO) stroke and gene

119 Using the mouse middle cerebral artery occlusion (MCAO) stroke model, we

120 rating immune cell populations in mice after middle cerebral artery occlusion (MCAO) strongly implica

121 of the size of penumbra in mice subjected to middle cerebral artery occlusion (MCAO) using a genome-w

122 Infarct sizes 72 h after 60 min middle cerebral artery occlusion (MCAo) were on average

123 PGRN(+/-) and PGRN(-/-) mice underwent middle cerebral artery occlusion (MCAO) with monitoring

124 cit despite smaller infarcts after transient middle cerebral artery occlusion (MCAO) with the suture

125 In a mouse model of middle cerebral artery occlusion (MCAO), p38 MAPK activa

126 ischemia induced by permanent and transient middle cerebral artery occlusion (MCAO), we observed an

127 Rats in the model groups underwent middle cerebral artery occlusion (MCAO).

128 of reperfusion after a 90-minute unilateral middle cerebral artery occlusion (MCAO).

129 ischemia was induced by a transient (90 min) middle cerebral artery occlusion (MCAO).

130 n to rats with experimental stroke caused by middle cerebral artery occlusion (MCAO).

131 fusion proteins, following a 1-h reversible middle cerebral artery occlusion (MCAO).

132 type (WT) mice were subjected to a transient middle cerebral artery occlusion (MCAO).

133 (WT) littermate were subjected to 45 min of middle cerebral artery occlusion (MCAO).

134 subjected to permanent, 60-min and 30-min of middle cerebral artery occlusion (MCAO).

135 ted neurological deficits after the onset of middle cerebral artery occlusion (MCAO).

136 llowing a focal stroke caused by a transient middle cerebral artery occlusion (MCAO).

137 ebral ischemia produced in rats by permanent middle cerebral artery occlusion (MCAO).

138 se model of focal ischemic stroke induced by middle cerebral artery occlusion (MCAO).

139 5 minutes) was induced by intraluminal right middle cerebral artery occlusion (MCAO).

140 Male 129/SV mice were subjected to 30-min middle cerebral artery occlusion (MCAo)/reperfusion and

141 Cx43(S255/262/279/282A) (MK4) on a permanent middle cerebral artery occlusion (pMCAO) stroke model.

142 e and excitatory neurotoxicity in reversible middle cerebral artery occlusion (rMCAO) model in vivo.

143 erebral infarction using a stroke model with middle cerebral artery occlusion (see figure).

144 further evaluated in vivo using a transient middle cerebral artery occlusion (t-MCAO) model of strok

145 s) from mouse brains following 1 h transient middle cerebral artery occlusion (tMCAO) and measured re

146 P-infiltrating myeloid cells after transient middle cerebral artery occlusion (tMCAO) in neonatal mic

147 Furthermore, by transient middle cerebral artery occlusion (tMCAO) in rats, the tr

148 We induced transient middle cerebral artery occlusion (tMCAO) in T2D/obese mi

149 A transient middle cerebral artery occlusion (tMCAO) model was used

150 e in chronic diaschisis by using a transient middle cerebral artery occlusion (tMCAO) rat model.

151 nt arterial thrombosis models: the transient middle cerebral artery occlusion (tMCAO) stroke model an

152 ed infarct volumes 3 and 7 d after transient middle cerebral artery occlusion (tMCAo), independent of

153 ng, and corresponding controls, to transient middle cerebral artery occlusion (tMCAO).

154 r CR2-fH have improved outcomes after 60-min middle cerebral artery occlusion and 24-h reperfusion.

155 We used rodent models of middle cerebral artery occlusion and cell-culture models

156 mice were subjected to 60 min of reversible middle cerebral artery occlusion and evaluated for infar

157 Imaging revealed left middle cerebral artery occlusion and left transverse and

158 ocument Adipor gene expression in mice after middle cerebral artery occlusion and lipopolysaccharide

159 a mouse model of focal cerebral ischemia by middle cerebral artery occlusion and reperfusion (I/R) i

160 In vivo, transient middle cerebral artery occlusion and reperfusion in kina

161 Ab-deficient Rag1(-/-) mice after 60 min of middle cerebral artery occlusion and reperfusion.

162 cium ions, while applying a remote transient middle cerebral artery occlusion as a model for ischemic

163 Using the EcoHIV infection model and the middle cerebral artery occlusion as the ischemic stroke

164 l deficits and poststroke inflammation after middle cerebral artery occlusion by preventing microglia

165 ke Scale scores at those times, and proximal middle cerebral artery occlusion demonstrated prior to t

166 -) mice of either sex subjected to transient middle cerebral artery occlusion developed dramatically

167 mice of either sex challenged with transient middle cerebral artery occlusion developed significantly

168 nfarct volume of mice subjected to transient middle cerebral artery occlusion even up to 3 to 5 hours

169 littermate controls were subjected to 1 hour middle cerebral artery occlusion followed by 28-day repe

170 Male Swiss Webster mice underwent middle cerebral artery occlusion for 1 h followed by rep

171 We performed right middle cerebral artery occlusion for 3 hours, administer

172 Mice were subjected to middle cerebral artery occlusion for 40 min, followed by

173 ent cerebral ischemia was induced in mice by middle cerebral artery occlusion for 60 minutes and s-NS

174 and endothelin receptors following permanent middle cerebral artery occlusion for 7 days.

175 Male Sprague-Dawley rats were subjected to middle cerebral artery occlusion for 70 min followed by

176 Animals were subjected to transient middle cerebral artery occlusion for 90 mins.

177 To define the role of AhR in stroke, we used middle cerebral artery occlusion in mice and oxygen-gluc

178 g-term spontaneous functional recovery after middle cerebral artery occlusion in mice.

179 c injury, and cerebral edema formation after middle cerebral artery occlusion in mice.

180 creased the severity of stroke in a model of middle cerebral artery occlusion in mice.

181 ic penumbra when administered six hours post middle cerebral artery occlusion in rats.

182 ting the ET(B) receptors following permanent middle cerebral artery occlusion in rats.

183 onset and until completion of 15 min distal middle cerebral artery occlusion in spontaneously hypert

184 Middle cerebral artery occlusion in the rat brain result

185 human umbilical cord blood cells 48 h after middle cerebral artery occlusion increased Akt phosphory

186 ental cerebral ischemia induced by transient middle cerebral artery occlusion it selectively dilates

187 stasis in the ischemic brain after transient middle cerebral artery occlusion leading to increased in

188 We used a transient middle cerebral artery occlusion model to induce stroke

189 A transient middle cerebral artery occlusion model was used to inves

190 In the middle cerebral artery occlusion model, the volume and f

191 diated cerebrovascular protection in a mouse middle cerebral artery occlusion model.

192 in male C57BL/6 mice using the intraluminal middle cerebral artery occlusion model.

193 We then used the murine suture and embolic middle cerebral artery occlusion models of stroke to inv

194 of microglial activation in infarcted distal middle cerebral artery occlusion mouse brain tissue more

195 e-Dawley rats (12 months old) with permanent middle cerebral artery occlusion or sham operations on m

196 Methods: After distal middle cerebral artery occlusion or sham surgery, mice u

197 normotensive rats and were subjected to 1-h middle cerebral artery occlusion or sham surgery.

198 tion of TAT-C1aB in mice following transient middle cerebral artery occlusion significantly reduced i

199 In the model of transient middle cerebral artery occlusion stroke Gna(i2)(fl/fl)/P

200 In this study, using a murine transient middle cerebral artery occlusion stroke model, a novel t

201 assessment of blood flow anomaly in a mouse middle cerebral artery occlusion stroke model.

202 in rats implanted with CTX-DP 4 weeks after middle cerebral artery occlusion stroke prompted investi

203 We investigated in a murine model of middle cerebral artery occlusion the effect of blocking

204 Following middle cerebral artery occlusion to induce stroke in mic

205 rformed fecal transplant gavage 3 days after middle cerebral artery occlusion using young donor biome

206 hemisphere reperfusion after photothrombolic middle cerebral artery occlusion was increased in Klkb1(

207 tion volumes following a 60-minute transient middle cerebral artery occlusion were determined in adul

208 icits following experimental stroke, using a middle cerebral artery occlusion with reperfusion model.

209 Middle cerebral artery occlusion with reperfusion was pe

210 s induced in mice (by permanent or transient middle cerebral artery occlusion) and rats (by 3-vessel

211 rotid artery occlusion and 360 with isolated middle cerebral artery occlusion).

212 of amyotrophic lateral sclerosis (SOD1G93A), middle cerebral artery occlusion, and multiple mini-stro

213 Following transient middle cerebral artery occlusion, ck2beta(-/-) mice disp

214 s in various microvascular settings, such as middle cerebral artery occlusion, femoral artery clippin

215 We found that after transient middle cerebral artery occlusion, inhibiting PlexinD1 si

216 ith ischemic stroke and in mice subjected to middle cerebral artery occlusion, natural killer (NK) ce

217 g photothrombotic cortical injury, transient middle cerebral artery occlusion, or neonatal hypoxic-is

218 Following transient middle cerebral artery occlusion, progesterone was admin

219 In a mouse model of thrombin-induced middle cerebral artery occlusion, the efficacy of the di

220 marrow (BM) chimeras subjected to transient middle cerebral artery occlusion, we found that CD36(-/-

221 Following middle cerebral artery occlusion, we observed a rapid in

222 However, using a mouse model of transient middle cerebral artery occlusion, we observed that cereb

223 Using two distinct models of acute middle cerebral artery occlusion, we show by next-genera

224 pharmacologically induced excitotoxicity and middle cerebral artery occlusion-induced brain damage.

225 vivo against NMDA-induced excitotoxicity and middle cerebral artery occlusion-induced stroke in mice.

226 cerebral vascular endothelial cell death and middle cerebral artery occlusion-triggered cerebrovascul

227 and functional recovery following permanent middle cerebral artery occlusion.

228 rebral ischemia was induced by 30 minutes of middle cerebral artery occlusion.

229 sponses in the brains of 2D2 mice 14 d after middle cerebral artery occlusion.

230 t mediates AhR activation in the brain after middle cerebral artery occlusion.

231 (M/M) littermates received sham or transient middle cerebral artery occlusion.

232 months) were subjected to ischemic stroke by middle cerebral artery occlusion.

233 d at 4 weeks into the treatment by transient middle cerebral artery occlusion.

234 e penumbra using a mouse model of reversible middle cerebral artery occlusion.

235 e matter bundles from degeneration following middle cerebral artery occlusion.

236 o mouse brains 6 h or 7 days after transient middle cerebral artery occlusion.

237 ntly in neonatal and adult rats by transient middle cerebral artery occlusion.

238 infarct cavity for 7 d, beginning 7 d after middle cerebral artery occlusion.

239 splanted into rat brains 6 h after transient middle cerebral artery occlusion.

240 r regional infarcts such as those induced by middle cerebral artery occlusion.

241 80 male rats underwent 90-min middle cerebral artery occlusion.

242 e induced ischemia by transient or permanent middle cerebral artery occlusion.

243 Cerebral ischemia was induced by middle cerebral artery occlusion.

244 ow and 85% reduction of infarct volume after middle cerebral artery occlusion; 54% rescue of low skel

245 stroke groups: 30-min, 60-min, and permanent middle cerebral-artery occlusion (n=12 rats for each gro

246 star rats were subjected to right hemisphere middle-cerebral artery occlusion and reperfusion.

247 ive patients with internal carotid artery or middle cerebral artery occlusions transferred over an 11

248 inal internal carotid artery or the proximal middle cerebral artery occlusions we found that an infar

249 acranial carotid, basilar, and M1 segment of middle cerebral artery occlusions).

250 ly constant with a mean flow velocity in the middle cerebral artery of 71.5 (56.0-78.5) at 108 hrs (p

251 Under anaesthesia, the middle cerebral artery of adult rats was occluded for 60

252 areas of the internal carotid, basilar, and middle cerebral arteries on the first day at high altitu

253 cerebral artery sign is an appearance of the middle cerebral artery on non-contrast-enhanced computed

254 artery occlusion (internal carotid artery or middle cerebral artery) on outcomes.

255 between 2013 and 2014 for occlusions in the middle cerebral artery or carotid terminus by using a st

256 ve cohort study, we studied 72 patients with middle cerebral artery or terminal internal carotid arte

257 viscosity and the mean flow velocity in the middle cerebral artery (p = 0.0008).

258 ebral artery, anterior communicating artery, middle cerebral artery, persistent stapedial artery and

259 r cerebral artery-middle cerebral artery and middle cerebral artery-posterior cerebral artery watersh

260 no differences in mean flow velocity in the middle cerebral artery, pulsatility index, and jugular b

261 pon rewarming, the mean flow velocity in the middle cerebral artery remained relatively constant with

262 gional oxygen saturation (P = 0.007) and low middle cerebral artery resistive index (P = 0.04) were a

263 g localized the clot in the internal carotid/middle cerebral artery segment of all rats.

264 r-old female patient who had both hyperdense middle cerebral artery sign and pulmonary thromboembolis

265 Coexistence of hyperdense middle cerebral artery sign and pulmonary thromboembolis

266 Hyperdense middle cerebral artery sign is an appearance of the midd

267 e at 22 to 36 hours of a baseline hyperdense middle cerebral artery sign was increased (63% [124 of 1

268 ood pressures and systolic velocities of the middle cerebral artery significantly decreased (p < 0.01

269 s In this retrospective study, patients with middle cerebral artery stroke due to proximal occlusion

270 w-derived ALD-401 in patients with disabling middle cerebral artery stroke in comparison with sham ha

271 onclusion In this study, patients with acute middle cerebral artery stroke with absence of cortical v

272 malignant infarction in the territory of the middle cerebral artery, TAT.ARC salvages brain tissue wh

273 children had low or uninterpretable baseline middle cerebral artery TCD velocities, which were associ

274 fected white matter tracts, and involved the middle cerebral artery territory for 112 patients (73%).

275 rast computed tomography (ie, over one-third middle cerebral artery territory hypodensity).

276 Three weeks after right middle cerebral artery territory injury, rats treated wi

277 33 subjects with chronic infarctions in the middle cerebral artery territory, and 109 age-matched no

278 Conclusion In acute stroke of the middle cerebral artery, the Alberta Stroke Program Early

279 odel was generated by occlusion of the right middle cerebral artery, then 90 min later, stroke rats w

280 As compared with aneurysms in the middle cerebral arteries, those in the posterior and ant

281 e cerebral artery was a ratio of flow in the middle cerebral artery to extracranial internal carotid

282 In mice with thrombotic occlusion of the middle cerebral artery, tPA administration increased bra

283 ilateral CBFV recordings from left and right middle cerebral arteries using 20 healthy subjects (10 f

284 al-to-contralateral ratio of the activity in middle cerebral artery-vascularized territories in each

285 The prevalence of middle cerebral artery vasospasm in children with modera

286 cative of CBF and extra-cranial blood flow), middle cerebral artery velocity (MCA Vmean), arterial-ve

287 sodilatation, blood pressure, heart rate and middle cerebral artery velocity (MCAv) were measured dur

288 on (internal carotid artery vs M1 segment of middle cerebral artery vs M2 segment of middle cerebral

289 cranial Doppler ultrasound monitoring of the middle cerebral arteries was performed whenever possible

290 Mean duration of vasospasm in the middle cerebral artery was 2 days (+/- 2 d) and 1.5 days

291 eria required for vasospasm diagnosis in the middle cerebral artery was a ratio of flow in the middle

292 Mean flow velocity in the middle cerebral artery was low (26.5 (18.7-48.0) cm/sec)

293 Median mean flow velocity in the middle cerebral artery was low (27.0 cm/s [23.8-30.5 cm/

294 Mean flow velocity in the middle cerebral artery was measured by transcranial Dopp

295 bone marrow (BM) chimeric mice in which the middle cerebral artery was occluded and infarct volume w

296 Middle cerebral artery was occluded for 12 to 60 minutes

297 Cerebral emboli entering the middle cerebral arteries were counted at baseline and ev

298 intracranial internal carotid, \basilar, or middle cerebral artery were included less than 4.5 hours

299 acranial internal carotid artery or proximal middle cerebral artery who had last been known to be wel

300 ia was induced by temporary occlusion of the middle cerebral artery with a microfilament.