ライフサイエンスコーパス: cerebral blood flow

1 t (LSC) channel for imaging perfusion (i.e., cerebral blood flow).

2 matter tracts and a colocalized increase in cerebral blood flow.

3 lature in response to changes in pressure or cerebral blood flow.

4 on choice of reference region and changes in cerebral blood flow.

5 ribes the link between neuronal activity and cerebral blood flow.

6 ion of blood pressure, body temperature, and cerebral blood flow.

7 5)O-H2O PET showed no significant changes in cerebral blood flow.

8 vessels could be used as a means to increase cerebral blood flow.

9 es in cutaneous vasodilatation, sweating and cerebral blood flow.

10 g of basilar and carotid arteries to measure cerebral blood flow.

11 tionary expansion, cortical myelination, and cerebral blood flow.

12 eGFR is independently associated with lower cerebral blood flow.

13 ions cause vasoconstriction that would limit cerebral blood flow.

14 zheimer's disease is associated with reduced cerebral blood flow.

15 yelin content, inflammation, and edema), and cerebral blood flow.

16 e areas of high or low metabolic activity or cerebral blood flow.

17 n, which assume that only arterioles control cerebral blood flow.

18 relation between blood pressure and regional cerebral blood flow.

19 ional vessels, and increases the ipsilateral cerebral blood flow.

20 roinfarcts, cerebral hemorrhage, and reduced cerebral blood flow.

21 gnetic resonance imaging to measure regional cerebral blood flow.

22 sis, is one of the most potent regulators of cerebral blood flow.

23 pivotal role in coupling neural activity and cerebral blood flow.

24 was reduced in female mice independently of cerebral blood flow.

25 ratio of mean arterial pressure to regional cerebral blood flow.

26 t, the HBV compartment showed similar median cerebral blood flow (17 [range, 11-40] vs 14 [range, 6-2

27 0) relative to controls (interquartile range cerebral blood flow = 40.8-46.3 ml/100 g/min; oxygen ext

28 thly blood transfusions (interquartile range cerebral blood flow = 46.2-56.8 ml/100 g/min; oxygen ext

29 associated with 0.42 ml/min per 100 ml lower cerebral blood flow (95% confidence interval, 0.01 to 0.

30 is closely followed by a localised change in cerebral blood flow, a process termed neurovascular coup

31 Furthermore, despite an increase in cerebral blood flow after 2 hours of hypoxia (hypoxia vs

32 Levosimendan increased cerebral blood flow after experimental cardiac arrest/ca

33 eater number of brain regions than those for cerebral blood flow alone.

34 d associations with Alzheimer's disease than cerebral blood flow alone.

35 By contrast, in the range 0.03-0.10 Hz, both cerebral blood flow and arterial pressure power more tha

36 erebrovascular abnormalities such as altered cerebral blood flow and cerebral microinfarcts.

37 Hence, cerebral blood flow and cerebral oxygenation are importa

38 was associated with a mild increase in both cerebral blood flow and femoral blood flow (P<0.05 versu

39 [(18)F]-fluorodeoxyglucose, to map regional cerebral blood flow and glucose metabolism, and with [(1

40 amyloid-beta had different associations with cerebral blood flow and grey matter volume.

41 SVD produces reductions in cerebral blood flow and impaired blood-brain barrier fun

42 Moreover, we observed higher cerebral blood flow and lower oxygen saturation in femal

43 ess the effects of kidney transplantation on cerebral blood flow and magnetic resonance spectroscopic

44 cosity early after cardiac arrest may reduce cerebral blood flow and may contribute to secondary brai

45 ted cancer survivors had significantly lower cerebral blood flow and metabolic activity in key brain

46 aemic penumbra suggested imaging of regional cerebral blood flow and metabolism would be required to

47 entration, oxygen saturation, and indices of cerebral blood flow and metabolism.

48 brain function is the tight coupling between cerebral blood flow and neuronal activity.

49 the long-term impact of low-grade GM-IVH on cerebral blood flow and neuronal health have not been fu

50 Prospective study measuring cerebral blood flow and oxygen extraction fraction using

51 Cerebral blood flow and oxygen extraction fraction were

52 lly undermine the capacity for regulation of cerebral blood flow and probably underlie several cerebr

53 all parameters had decreased in both groups, cerebral blood flow and regional cerebral blood flow (in

54 The changes in regional cerebral blood flow and regional metabolism can be asses

55 e was associated with sustained reduction in cerebral blood flow and restored DMN thalamo-cortical fu

56 The influence of reproductive hormones on cerebral blood flow and sex differences in the ability o

57 apnoea and hypopnoea, along with changes in cerebral blood flow and sleep fragmentation.

58 ed a significant inverse association between cerebral blood flow and the expected age of symptom onse

59 ive metabolism, measured from the product of cerebral blood flow and the radial artery-jugular venous

60 ral activity is correlated with increases of cerebral blood flow and tissue oxygenation.

61 lities are combined with long periods of low cerebral blood flow and/or circulatory arrest.

62 Brain hemodynamics (cerebral and regional cerebral blood flow) and cerebral oxygen metabolism (cer

63 termined by transcranial Doppler ultrasound (cerebral blood flow) and constant infusion thermodilutio

64 rea around intracranial monitoring (regional cerebral blood flow) and in bilateral supra-ventricular

65 ateral supra-ventricular brain areas (global cerebral blood flow) and was matched to cerebral physiol

66 reased cerebral vascular resistance, reduced cerebral blood flow, and a higher incidence of lacunar t

67 ional connection strength that is related to cerebral blood flow, and a phase shift parameter that is

68 MCA pseudofeeders are the result of impaired cerebral blood flow, and are thus a risk factor for furt

69 ionships between oxygen extraction fraction, cerebral blood flow, and clinical markers of cerebrovasc

70 ated with lower cognitive performance, lower cerebral blood flow, and greater white matter hyperinten

71 time, reproducibility and quantification of cerebral blood flow, and to measure cerebrovascular rese

72 ion tomography scans with H2(15)O to measure cerebral blood flow as a marker of neuronal activity.

73 ce software segmentation was used to compare cerebral blood flow as measured with ASL.

74 CA) is a protective mechanism that maintains cerebral blood flow at a relatively constant level despi

75 l that different signaling cascades regulate cerebral blood flow at the capillary and arteriole level

76 erences in arterial spin labelling MRI-based cerebral blood flow between presymptomatic C9orf72, GRN

77 with increased blood pressure and decreased cerebral blood flow both linked to in vivo biomarkers an

78 tly more accurate in predicting low regional cerebral blood flow (both p < 0.05).

79 imilar to those in the general population on cerebral blood flow, brain volumes, and dementia.

80 ght link between neuronal activity and local cerebral blood flow, but their precise identity, cellula

81 Between 2005 and 2012, we measured cerebral blood flow by 2-dimensional phase-contrast magn

82 tentials by electrophysiological recordings, cerebral blood flow by laser Doppler flowmetry, and oxyg

83 Little attention has been paid to cerebral blood flow (CBF) alterations in IGE detected by

84 Here, cerebral blood flow (CBF) and blood oxygen-level depende

85 responses in rat barrel cortex, measured by cerebral blood flow (CBF) and neurophysiological recordi

86 The role of pericytes in the regulation of cerebral blood flow (CBF) and neurovascular coupling rem

87 Cerebral blood flow (CBF) and oxygen extraction fraction

88 This pilot study aims to evaluate cerebral blood flow (CBF) and oxygen metabolism (CMRO2)

89 and to assess potential correlations between cerebral blood flow (CBF) and quantitative histologic mi

90 d transcranial Doppler ultrasound to measure cerebral blood flow (CBF) and reactivity.

91 We determined whether cerebral blood flow (CBF) and regional brain volumes wer

92 o produce spatial maps displaying changes in cerebral blood flow (CBF) and RSFC after MDMA administra

93 Resting cerebral blood flow (CBF) and task-related activation of

94 by conducting voxelwise comparisons between cerebral blood flow (CBF) and tau positron emission tomo

95 nknown Core cooling by 1.0 degrees C reduced cerebral blood flow (CBF) by 20-30% and cerebral oxygen

96 nerve induces pressor response and improves cerebral blood flow (CBF) by activating the rostral vent

97 Resting-state regional cerebral blood flow (CBF) can be measured noninvasively

98 brain voxelwise analysis of the ASL relative cerebral blood flow (CBF) data, receiver operating chara

99 Disease-related phenotypes, including cerebral blood flow (CBF) deficits, white matter lesions

100 heimer's disease, attenuates the increase in cerebral blood flow (CBF) evoked by neural activity (fun

101 ental properties of brain physiology such as cerebral blood flow (CBF) have never been investigated.

102 wever, it is unknown whether acutely-reduced cerebral blood flow (CBF) impairs cognition in healthy a

103 (ASL) MRI, nonresponders exhibited increased cerebral blood flow (CBF) in bilateral anterior hippocam

104 e first study to show regional reductions in cerebral blood flow (CBF) in response to decreased oxyge

105 re vasoconstriction and marked reductions in cerebral blood flow (CBF) in the PFC, which were exacerb

106 O2, which has previously been shown to evoke cerebral blood flow (CBF) increases via the release of t

107 In our study, we found that Cerebral Blood Flow (CBF) is 90.91% sensitive and 100% s

108 Cerebral blood flow (CBF) is controlled by arterial bloo

109 Animal models suggest that reduced cerebral blood flow (CBF) is one of the most enduring ph

110 Cessation of cerebral blood flow (CBF) leads to cell death in the inf

111 resonance imaging tracks absolute changes in cerebral blood flow (CBF) linked with brain function and

112 Changes in cerebral blood flow (CBF) may occur with acute exposure

113 ional anisotropy (FA), fiber number (FN) and cerebral blood flow (CBF) measurements.

114 hest OEF falls within the border zone, where cerebral blood flow (CBF) nadirs; OEF in this region was

115 his approach may be influenced by changes in cerebral blood flow (CBF) or radiotracer clearance.

116 (CA) is expressed by the temporal pattern of cerebral blood flow (CBF) recovery following a sudden ch

117 Cerebral blood flow (CBF) reductions are an early featur

118 Cerebral blood flow (CBF) reductions in Alzheimer's dise

119 determine whether cocaine-induced changes in cerebral blood flow (CBF) reflect neuronal activation or

120 ed by the mean arterial blood pressure (MAP)-cerebral blood flow (CBF) relationship, with little atte

121 nkage between elevated TIMP3 and compromised cerebral blood flow (CBF) remains unknown.

122 important determinant of CVR, to explain the cerebral blood flow (CBF) response to a sudden change in

123 l collateral vessels play a critical role in cerebral blood flow (CBF) restoration following ischemic

124 Cerebral blood flow (CBF) significantly improved in IRL-

125 ronal activity leads to an increase in local cerebral blood flow (CBF) to allow adequate supply of ox

126 which dilate arterioles, increasing in turn cerebral blood flow (CBF) to areas with increased metabo

127 Cerebral blood flow (CBF) was measured at the internal c

128 Following this training period, hippocampal cerebral blood flow (CBF) was measured by functional mag

129 Cerebral blood flow (CBF) was measured using colour-code

130 indicators: (1) global and regional resting cerebral blood flow (CBF), (2) oxygen extraction fractio

131 vel in vivo evidence of associations between cerebral blood flow (CBF), an MRI measure of vascular he

132 were used to study structural connectivity, cerebral blood flow (CBF), and corticospinal excitabilit

133 r Hb, higher brain blood density, lower mean cerebral blood flow (CBF), and significant cerebral circ

134 Aerobic exercise elicits increases in cerebral blood flow (CBF), as well as core body temperat

135 ated the local relationships between DVR and cerebral blood flow (CBF), as well as relative CBF (R1),

136 e exercise is associated with a reduction in cerebral blood flow (CBF), but regulation of CBF during

137 opathy have abnormal vascular reactivity and cerebral blood flow (CBF), but, to our knowledge, abnorm

138 Increased visual cortex cerebral blood flow (CBF), decreased visual cortex alpha

139 Penumbra as defined by (15) O-PET cerebral blood flow (CBF), oxygen extraction fraction, a

140 DWLS enabled rapid identification of cerebral blood flow (CBF), prediction of infarct area an

141 very (R1) parameters as surrogate indices of cerebral blood flow (CBF), with a secondary goal of dire

142 ffusivity), white matter lesions (WMLs), and cerebral blood flow (CBF).

143 er (BBB) disruption, cerebral apoptosis, and cerebral blood flow (CBF).

144 ystem that conducts continuous monitoring of cerebral blood flow (CBF).

145 erstitial brain tissue (Pbto2), and regional cerebral blood flow (CBF).

146 We measured cerebral blood flow (CBF, duplex ultrasound), cerebral o

147 degrees C); however, such exercise increases cerebral blood flow (CBF; +10-20%) mediated via small el

148 is a neuroimaging technique used to measure cerebral blood flow (CBF; perfusion) to understand brain

149 n vivo validation was performed, in which 3D cerebral-blood-flow (CBF) networks in mouse brain over a

150 bral oxygen saturation (SO2) and an index of cerebral blood flow (CBFi) at the infant's bedside and c

151 ume ratios, apparent diffusion coefficients, cerebral blood flow, cerebral blood volume, and intratum

152 ence standard were 4.5%, 5.0%, and 1.9%, for cerebral blood flow, cerebral blood volume, and mean tra

153 Cerebral blood flow, cerebral blood volume, cerebral oxy

154 CKD is associated with abnormalities in cerebral blood flow, cerebral neurochemical concentratio

155 ress syndrome, cerebral blood flow, regional cerebral blood flow, cerebral oxygen delivery, and cereb

156 ct diagnosis, APOE epsilon4 carriage status, cerebral blood flow, cerebrospinal fluid total-tau and p

157 TMPAP expression had no effect on resting cerebral blood flow, cerebrovascular reactivity, and neu

158 Basal and activity-dependent cerebral blood flow changes are coordinated by the actio

159 Insufficient cerebral blood flow contributes to brain dysfunction and

160 Here, we reveal a mechanism for cerebral blood flow control, a precapillary sphincter at

161 Regional cerebral blood flow correlated significantly with global

162 hemodialysis experience transient decline in cerebral blood flow, correlating with intradialytic cogn

163 educed intracerebral thrombosis and improved cerebral blood flow could be identified as underlying me

164 sess whole-brain oxygen extraction fraction, cerebral blood flow, degree of vasculopathy, severity of

165 gies in different trajectories, we tested if cerebral blood flow differed between amyloid-beta-negati

166 No cerebral blood flow differences between groups were foun

167 relative to both non-demented groups, but no cerebral blood flow differences between non-demented amy

168 These cerebral blood flow differences first appeared approxima

169 we measured arterial blood gases and global cerebral blood flow (duplex ultrasound) during a 9 day a

170 rest and coupled with volumetric measures of cerebral blood flow (duplex ultrasound) to quantify rest

171 in cutaneous vasodilatation, sweat rate and cerebral blood flow during a hot flush.

172 sodilatation, sweating and the reductions in cerebral blood flow during a hot flush.

173 The precise modulation of regional cerebral blood flow during neural activation is importan

174 ted multiple IHRs, and a limited increase in cerebral blood flow during SE with a high degree of mome

175 ministration in terms of effects on regional cerebral blood flow during two hours post-dosing.

176 e last two decades, physiological studies of cerebral blood flow dynamics have demonstrated that subs

177 ed diminished inferior parietal and temporal cerebral blood flow for patients with Alzheimer's diseas

178 (5% CO2 ) confirmed that these reductions in cerebral blood flow from hypoxia were related to vasocon

179 lowing 4-6 days at high altitude (HA) global cerebral blood flow (gCBF) increases to preserve cerebra

180 ovascular function (measured via grey-matter cerebral blood flow (gmCBF)) is altered in young individ

181 While the effect of neural activity on cerebral blood flow has been extensively studied, whethe

182 the association between kidney function and cerebral blood flow has yet to be determined.

183 BF), but, to our knowledge, abnormalities in cerebral blood flow have not been reported for healthy i

184 Reduced cerebral blood flow impairs cognitive function and ultim

185 plt-/-mice) exhibited significantly enhanced cerebral blood flow, improved neurological and motor fun

186 LDL-C variability was associated with lower cerebral blood flow in both trial arms (P=0.031 and P=0.

187 e hyperactivity and hypoactivity of regional cerebral blood flow in brain regions in cocaine-dependen

188 gnetic resonance imaging to measure regional cerebral blood flow in brain regions susceptible to agei

189 oost was conveyed by CE-induced increases in cerebral blood flow in frontal brain regions and changes

190 ositron emission topographic measurements of cerebral blood flow in humans have consistently reported

191 in the brain to couple neuronal activity and cerebral blood flow in normal and pathologic states.

192 t could account in part for the reduction in cerebral blood flow in patients with Alzheimer's disease

193 cytes are not contractile, and regulation of cerebral blood flow in physiological and pathological co

194 technology that provides a direct measure of cerebral blood flow in response to cognitive activity.

195 vent of transcranial Doppler, measurement of cerebral blood flow in response to transient changes in

196 r) and function (functional connectivity and cerebral blood flow in resting state).

197 igher amyloid-beta load was related to lower cerebral blood flow in several regions, independent of d

198 , while there is reliably increased regional cerebral blood flow in sgPFC in MDD, no such abnormality

199 approximately 100 mL min(-1) (~17-34%) lower cerebral blood flow in Sherpa compared to lowlanders acr

200 level, diabetes is associated with abnormal cerebral blood flow in surviving brain regions and great

201 h muscle cells are key players in regulating cerebral blood flow in the healthy state and contribute

202 ntional individuals showed increased resting cerebral blood flow in the ventral striatum and ventrome

203 Cerebral blood flow in these brain regions correlated wi

204 oth groups, cerebral blood flow and regional cerebral blood flow (in inner and cerebellum brainstem r

205 hanisms must be playing hand in hand, namely cerebral blood flow increase and microvascular flow homo

206 Similar to seizures, cerebral blood flow increases in patients with PDs to co

207 ctive suppression of neural activity-induced cerebral blood flow increases that precedes tau patholog

208 that an elevated ratio of blood pressure to cerebral blood flow, indicative of cerebrovascular resis

209 The precise regulation of cerebral blood flow is critical for normal brain functio

210 Precise regulation of cerebral blood flow is critical for normal brain functio

211 Continuous cerebral blood flow is essential for neuronal survival,

212 Cerebral blood flow is highly sensitive to changes in CO

213 Cerebral blood flow is one brain phenotype that is known

214 Cerebral blood flow is reduced early in the onset of Alz

215 Impaired oxygen delivery due to reduced cerebral blood flow is the hallmark of delayed cerebral

216 appropriately matched increases in regional cerebral blood flow) is preserved during both exercise a

217 erval: 0.92, 0.98]) and with delay-corrected cerebral blood flow less than 30% in patients with compl

218 standard medical therapy, by CTP as relative cerebral blood flow less than 30% of normal brain blood

219 mm (P = .04) and the core volume measured as cerebral blood flow less than 30% was underestimated whe

220 o-creatinine ratio was associated with lower cerebral blood flow level (difference in cerebral blood

221 poperfusion (defined as an oligemic regional cerebral blood flow < 35 mL/100 g/min) was examined usin

222 ke Program Early CT Score >= 6, CTP:regional cerebral blood flow (<30%) < 70ml with mismatch ratio >=

223 tients with Alzheimer's disease have reduced cerebral blood flow measured by arterial spin labelling

224 obe, apparently normal tissue) combined with cerebral blood flow measurements using perfusion CT.

225 ted whether developmental sex differences in cerebral blood flow mediated sex differences in anxiety

226 wer cerebral blood flow level (difference in cerebral blood flow [milliliters per minute per 100 ml]

227 l cerebral blood flow (n = 16), low regional cerebral blood flow (n = 14) measurements had a higher p

228 Compared with normal regional cerebral blood flow (n = 16), low regional cerebral bloo

229 onance (MR) imaging technique used to assess cerebral blood flow noninvasively by magnetically labeli

230 ume (nrCBV) and Gaussian-normalized relative cerebral blood flow (nrCBF) maps.

231 s greater than 3 seconds and delay-corrected cerebral blood flow of less than 30% (P = .34 and .33, r

232 dialysis-related factors, such as changes in cerebral blood flow or cardiac structure, are also postu

233 l reconstruction and their relationship with cerebral blood flow, oxygen delivery, and carbon dioxide

234 icit, intracellular pH (P < 0.0001), but not cerebral blood flow (P = 0.31), differed between tissue

235 44%, respectively) with increasing amount of cerebral blood flow (P<0.05).

236 od flow correlated significantly with global cerebral blood flow (Pearson r = 0.70, p < 0.01).

237 t was obtained with oxygen-15 water regional cerebral blood flow PET in 39 healthy women genotyped fo

238 d by quantifying metabolic RSN expression in cerebral blood flow PET scans acquired at rest and durin

239 that long-duration spaceflight may increase cerebral blood flow, possibly due to reduced haemoglobin

240 with oscillatory LBP, there was no change in cerebral blood flow power, indicating near perfect count

241 In response to whisker stimulation, regional cerebral blood flow (rCBF) and hemodynamic responses wer

242 Regional cerebral blood flow (rCBF) and volume (rCBV) were measur

243 Using regional cerebral blood flow (rCBF) as a marker of basal neuronal

244 re IN-OT-induced changes in resting regional cerebral blood flow (rCBF) in 32 healthy men.

245 imaging was used to measure resting regional cerebral blood flow (rCBF) in 52 individuals at ultra-hi

246 effect of age and diagnosis on glutamate and cerebral blood flow (rCBF) in adults with SZ and healthy

247 Our aim was to assess resting cerebral blood flow (rCBF) in children and adults with a

248 face area, subcortical volumes, and regional cerebral blood flow (rCBF) in healthy controls (HC) (n =

249 itivity and high resolution, and of regional cerebral blood flow (rCBF) in the brain of transgenic AP

250 We measured regional cerebral blood flow (rCBF) using pseudo-continuous arter

251 ting for an AD-related reduction in regional cerebral blood flow (rCBF).

252 rier maintenance, and regulation of regional cerebral blood flow (rCBF).

253 g the previously validated measure (relative cerebral blood flow [rCBF], <30%), thrombectomy patients

254 nesis marker Endoglin, vascular density, and cerebral blood flow recovery, are all decreased in brain

255 gside ventricular and venous vessel volumes, cerebral blood flow, regional brain volumes, and intracr

256 rm lambs with respiratory distress syndrome, cerebral blood flow, regional cerebral blood flow, cereb

257 of stroke, cognitive decline and diminished cerebral blood flow regulation.

258 eable binding potential [BPND]) and relative cerebral blood flow (relative delivery [R1]) at voxel le

259 Change in the cerebral blood flow response to an acute challenge with

260 s of methylphenidate treatment increased the cerebral blood flow response to methylphenidate within t

261 To test this, we measured NBG, BOLD, and cerebral blood flow responses to stimuli that either cor

262 ippocampus-dependent behavioral deficits and cerebral blood flow responses, improved cerebrovascular

263 otective effects in morality, fluctuation of cerebral blood flow, SAH grade, and cerebral vasospasm o

264 While cerebral blood flow shows differences between frontotemp

265 This study aimed to delineate the cerebral blood flow signature of presymptomatic, genetic

266 untreated hypertensive patients (n=20) had a cerebral blood flow similar to age-matched controls (n=2

267 hial artery flow-mediated dilation, abnormal cerebral blood flow, skeletal myopathy, and intrinsic ki

268 associated with a pathological reduction in cerebral blood flow termed the inverse hemodynamic respo

269 y demonstrated that BDG patients had greater cerebral blood flow than did Fontan patients and that an

270 BDG patients had significantly higher cerebral blood flow than did Fontan patients.

271 temperature, an effect capable of affecting cerebral blood flow, the properties of the oxygen sensor

272 PET allows the quantification of regional cerebral blood flow, the regional oxygen extraction frac

273 ain brain homeostasis, and the regulation of cerebral blood flow to adequately couple energy supply t

274 the CMRO2 was calculated from the product of cerebral blood flow (ultrasound) and the radial artery-i

275 , CMRO(2) was calculated from the product of cerebral blood flow (ultrasound) and the radial artery-j

276 oride application followed by measurement of cerebral blood flow using a combination of laser Doppler

277 sham procedure with continuous monitoring of cerebral blood flow using laser Doppler, NIRS and ICP.

278 the acetazolamide-induced change in regional cerebral blood flow using SPECT with (99m)Tc-labeled hex

279 lood volume and Gaussian-normalized relative cerebral blood flow values (area under the receiver oper

280 Using a set of artificial cerebral blood flow velocities (CBFV) generated from a w

281 Cerebral blood flow velocities (transcranial Doppler) fr

282 analysis of arterial blood pressure (BP) and cerebral blood flow velocity (CBFV).

283 In contrast, cerebral-blood-flow velocity (CBFv) in arteries and vein

284 moglobin was 9.7 g/dL (range, 6.9-12.9), and cerebral blood flow was 43 +/- 11 mL/100 g/min.

285 gen extraction fraction (P < 0.0001) but not cerebral blood flow was increased in participants with h

286 Cerebral blood flow was lower in presymptomatic mutation

287 s to the motor cortex of mice, post-ischemic cerebral blood flow was measured using multi-exposure sp

288 Cerebral blood flow was measured using perfusion CT in t

289 with subdural electrode strips and regional cerebral blood flow was measured with a parenchymal ther

290 y 10 hours, when AMS symptoms had developed, cerebral blood flow was normal (Delta-51ml/min(-1) , 95%

291 In addition, (15)O-H2O scans to measure cerebral blood flow were acquired before each (11)C-erlo

292 Protocol B: Myocardial and cerebral blood flow were measured in seven pigs before v

293 ness, cerebral metabolic rate of glucose and cerebral blood flow were preferentially decreased in the

294 , pro-inflammatory signalling, and protected cerebral blood flow, when determined 1 to 3 days post-in

295 STRACT: Hypoxia causes an increase in global cerebral blood flow, which maintains global cerebral oxy

296 Hypoxia causes an increase in global cerebral blood flow, which maintains global cerebral oxy

297 Cerebral blood flow, which was higher in patients pretra

298 rse association exists of various indexes of cerebral blood flow with these brain lesions.

299 tistically significant decreases in regional cerebral blood flow within areas dense in insulin recept

300 Cerebral blood flow within regions of interest derived f