ライフサイエンスコーパス: pial

1 Blood flow velocity in pial and cortical penetrating vessels measuring <20 micr

2 emarkably, these antibodies also labeled rat pial and ependymal cells as well as reactive astrocytes

3 vascular smooth muscle cells (VSMC) in small pial and intracerebral arteries, which are critical for

4 that neuronal excitation modulates both the pial and meningeal circulation through a critical intera

5 In control brains, pial and parenchymal blood vessels of all sizes were dis

6 ase (SVD) is characterized by changes in the pial and parenchymal microcirculations.

7 structure of the junctional complex between pial and parenchymal vessels and involvement of MMP acti

8 Moreover, the timing of MMP activity in pial and parenchymal vessels correlated with the timing

9 Both pial and parenchymal vessels from mock infected animals

10 pathology is also evident at cerebral cortex pial and ventricular ependymal surfaces in ASD.

11 a pial artery would (1) attenuate changes in pial arterial diameter during acute hypertension and (2)

12 easurement of blood pressure, heart rate and pial arterial diameter through a cranial window.

13 Pial arterial filling was scored on a six-point ordinal

14 d prominent autofluorescent particles in the pial arterial wall and in neocortical parenchyma of youn

15 ignaling and transport between brain and the pial arteries and cerebrospinal fluid in the subarachnoi

16 ssion brain injury (FPI) in the newborn pig, pial arteries constrict and responses to dilator stimuli

17 myogenic responses were similarly altered in pial arteries from TgNotch3(R169C) mice, but not in mese

18 MYOCD in vivo gene transfer to mouse pial arteries increased contractile protein content and

19 remanezumab, it did not induce dilatation in pial arteries, pial veins, or dural veins.

20 ief dilatation and prolonged constriction of pial arteries, prolonged dilatation of dural arteries an

21 Brain parenchymal arterioles (PAs), but not pial arteries, undergo hypotrophic outward remodeling du

22 ngiography generates time-resolved images of pial arteries.

23 followed by delayed, active constriction of pial arteries.

24 One important mechanism to dilate cerebral (pial) arteries is by activation of large-conductance, ca

25 IL, revealed functional defects in cerebral (pial) arteries on the surface of the brain at an early s

26 ion of EphA4 resulted in acceleration of the pial arteriogenic response.

27 ociated with marked decreases (mean: 60%) of pial arteriolar blood flow attributable to vasoconstrict

28 nsitive (KATP) potassium channel blockers on pial arteriolar CO2 reactivity, in vivo, were evaluated

29 Pial arteriolar diameter changes in hypercapnia were mea

30 Sco2 and pial arteriolar diameter decreased to hypocapnia (Paco2,

31 d similar decreases in Sco2 and increases in pial arteriolar diameter in response to moderate and sev

32 ges in cerebral oxygen saturation (Sco2) and pial arteriolar diameter measured by near- infrared spec

33 Pial arteriolar diameter to hypercapnia increased in the

34 rin (SnPP), on brain electrical activity and pial arteriolar diameter were examined using quantitativ

35 In anesthetized piglets, pial arteriolar diameters were determined using intravit

36 NOC/oFQ (10(-8), 10(-6) M) induced pial arteriole dilation was decreased by the protein kin

37 We have applied P2 receptor drugs to rat pial arterioles and measured changes in arteriole diamet

38 urface is consistent with diffusion of NO to pial arterioles as the mechanism of dilation to NMDA.

39 and progressively worsening to involve most pial arterioles by 18 months; soluble Abeta levels are e

40 th compound 48/80 (25 microg/ml) constricted pial arterioles by 26+/-9% at 80 min.

41 to 100 nmol/L) dose-dependently constricted pial arterioles from SHR and WKY rats (n = 6 to 8).

42 Dilation of pial arterioles in response to hypoxia and hypercapnia w

43 hibits Ca2+ sparks, abolished CO dilation of pial arterioles in vivo.

44 nitroprusside (SNP, 10(-4) M) still dilated pial arterioles normally.

45 ffects of ministrokes targeted to individual pial arterioles on motor function in Thy-1 line 18 chann

46 In addition, diameter of pial arterioles remained constant (32+/-5 microm) while

47 K and NaFl from pial vessels and diameter of pial arterioles remained constant.

48 om pial vessels was minimal, and diameter of pial arterioles remained constant.

49 extran-10K from pial vessels and diameter of pial arterioles remained relatively constant during the

50 th or without alcohol, responses of parietal pial arterioles to systemic hypoxia and hypercapnia were

51 y of the blood-brain barrier and diameter of pial arterioles via the activation of inducible nitric o

52 10,000 Da; FITC-dextran-10K) and diameter of pial arterioles were measured in the absence and presenc

53 led sustained MA-induced vasoconstriction of pial arterioles, consistent with laser Doppler flowmetry

54 plication of L-NMMA produced constriction of pial arterioles, L-NMMA did not alter the permeability c

55 l expression was assessed in SHR and WKY rat pial arterioles, which were monitored by intravital micr

56 ytosis in penetrating arterioles, but not in pial arterioles.

57 nd produced a rapid, sustained dilatation of pial arterioles.

58 noic acid (20-HETE), a potent constrictor of pial arterioles.

59 in clearance of FITC-dextran-10K and dilated pial arterioles.

60 n presenting at least one cerebral or spinal pial arteriovenous fistula (AVF), and to describe their

61 a closed cranial window was used to measure pial artery diameter and to collect cortical periarachno

62 Topical NOC/oFQ (10(-10) M) had no effect on pial artery diameter by itself but attenuated NMDA (10(-

63 Reductions in pial artery diameter, cerebral blood flow, cerebral perf

64 Reductions in pial artery diameter, cortical CBF, and cerebral perfusi

65 Cerebral blood flow, pial artery diameter, intracranial pressure, and autoreg

66 tive analogue mastoparan-17 had no effect on pial artery diameter.

67 During hypotension, pial artery dilation (PAD) was impaired more in the male

68 nists, partially restored attenuated NOC/oFQ pial artery dilation 1 h after I+R (9+/-1 and 18+/-1 vs.

69 lephrine decreased impairment of hypotensive pial artery dilation after fluid percussion brain injury

70 ed the effect of H/I on Katp and Kca induced pial artery dilation and the roles of tPA and ERK during

71 These data show that pial artery dilation by Kca channel activation is not me

72 f SB 203580 did not prevent impairment of PG pial artery dilation by NOC/oFQ.

73 Since recent studies show that pial artery dilation during a 20 or 40 min hypoxic expos

74 These data suggest that diminished pial artery dilation during longer hypoxic exposure resu

75 el activation and cAMP contribute to hypoxic pial artery dilation in a stimulus duration-dependent ma

76 K(ca) channel activation in NOC/oFQ-induced pial artery dilation in newborn pigs equipped with a clo

77 a) channel activation in hypotension induced pial artery dilation in newborn pigs equipped with a clo

78 ion and cAMP-dependent mechanisms to hypoxic pial artery dilation in piglets equipped with a closed c

79 However, tPA potentiates impairment of pial artery dilation in response to hypotension after hy

80 annel (Kca) activation contribute to hypoxic pial artery dilation in the piglet, responses to the NO

81 Hypotension induced pial artery dilation is prostaglandin-dependent in the n

82 ve (K(ca)) K channels and cAMP contribute to pial artery dilation observed during a 10-min exposure t

83 generating system blunted mastoparan induced pial artery dilation similar to FPI (10+/-1 and 17+/-1 v

84 Mastoparan (10(-8), 10(-6) M) elicited pial artery dilation that was blunted by FPI and partial

85 acterize the role of vasopressin in impaired pial artery dilation to activators of the ATP sensitive

86 se of prostaglandins contributes to impaired pial artery dilation to the newly described opioid, noci

87 (+) channel-dependent mechanisms in impaired pial artery dilation to the newly described opioid, noci

88 NOC/oFQ), which contributes to impairment of pial artery dilation to the prostaglandins (PG) PGE2 and

89 Vasopressin so administered attenuated pial artery dilation to these K(+) channel activators un

90 ersal of N-methyl-D-aspartate (NMDA)-induced pial artery dilation to vasoconstriction.

91 kephalin (10(-10), 10(-8), 10(-6) M)-induced pial artery dilation was also inhibited within 1 h of FP

92 NMDA induced pial artery dilation was attenuated by I+R or H+I+R; but

93 Cromakalim and NS1619 induced pial artery dilation was attenuated following FPI and ME

94 Cromakalim and NS1619 induced pial artery dilation was attenuated following FPI, while

95 studies in piglets show that opioid-induced pial artery dilation was impaired following fluid percus

96 potension and fluid percussion brain injury, pial artery dilation was impaired more in males.

97 Leucine enkephalin and dynorphin-induced pial artery dilation were similarly altered by FPI and p

98 These data show that NOC/oFQ elicits pial artery dilation, at least in part, via cAMP, K(ATP)

99 FPI blunted PGE2 pial artery dilation, but U 0126 and SP 600125 (10(-6) M

100 tenuated N-methyl-D-aspartate (NMDA)-induced pial artery dilation.

101 oxic/ischemic impairment of NOC/oFQ-mediated pial artery dilation.

102 nteraction between opioids and NO in hypoxic pial artery dilation.

103 hese opioids, in turn, contribute to hypoxic pial artery dilation.

104 rent sites in their contributions to hypoxic pial artery dilation.

105 Kca+2 channels contribute to opioid-induced pial artery dilation.

106 s designed to determine if hyperoxia elicits pial artery vasoconstriction and to characterize the con

107 Hyperoxia also elicited pial artery vasoconstriction that was attenuated by BQ12

108 indicate that ET-1 contributes to hyperoxic pial artery vasoconstriction.

109 Papaverine-induced pial artery vasodilation was unchanged by fluid percussi

110 delivered directly to the outer surface of a pial artery would (1) attenuate changes in pial arterial

111 Pial artrioles of rats were monitored in vivo and found

112 atients with at least one cerebral or spinal pial AVF were screened for genetic disease.

113 The disruption of the pial basal lamina caused the neuroepithelial cells to re

114 The present experiments demonstrate that the pial basal lamina has an important function during brain

115 ablished at later stages of development, the pial basal lamina of the newly developing neuroepitheliu

116 By correlating the disruptions in the pial basal lamina with changes in the morphology of radi

117 revealed that the collagenase disrupted the pial basal lamina, which was evident by the fragmented d

118 The disruption of pial basal membranes underlying the heterotopias and poo

119 of radial glia/progenitor fibers toward the pial/basal surface.

120 ment of cobblestone cortex, namely defective pial basement membrane (BM), abnormal anchorage of radia

121 ral cortex in the knockout mice, breaches in pial basement membrane allowed emigration of overmigrate

122 exhibit overmigration of neurons beyond the pial basement membrane and a cobblestone-like cortical m

123 This along with the pial basement membrane defects, contributed to the abnor

124 We hypothesize that breaches in pial basement membrane disrupt the neural-meningeal boun

125 olecules and major protein components of the pial basement membrane during normal brain development.

126 amma1 were used to study the function of the pial basement membrane in cortical histogenesis.

127 The pial basement membrane in the mutant embryos assembled b

128 t detect penetration of OSN axons across the pial basement membrane surrounding the olfactory bulb, s

129 Disruptions in the pial basement membrane underlie neural ectopia seen in t

130 The pial basement membrane was normal in the knockout mouse

131 LAMB1 is localized to the pial basement membrane, suggesting that defective connec

132 f neurons and glia, and fragmentation of the pial basement membrane.

133 ion to extracellular matrix molecules of the pial basement membrane.

134 eye-brain disease, caused by breaches in the pial basement membrane.

135 histogenesis with the presence of an intact pial basement membrane.

136 rized by overmigration of neurons beyond the pial basement membrane.

137 e closely associated with disruptions in the pial basement membrane.

138 imodipine induced vasodilation and increased pial blood flow.

139 evidence that GPR56 functions in regulating pial BM integrity during cortical development.

140 causal events are likely the breaches in the pial BM.

141 er microstructure, The gray/white matter and pial boundaries were identified on the high-resolution s

142 oint, half way between gray/white matter and pial boundaries.

143 ce imaging of transport gradients across the pial brain surface following controlled intracisternal i

144 artery-infusion of HENA (45 muM) dilated the pial cerebral arterioles via selective BK-channel target

145 tor of Tie2 receptor signaling, which limits pial collateral arteriogenesis following cerebrovascular

146 congenic mice as follows: 83% rescue of low pial collateral extent and 4.5-fold increase in blood fl

147 Pial collateral remodeling is limited by the crosstalk b

148 tor tyrosine kinase as a major suppressor of pial collateral remodeling, CBF, and functional recovery

149 Leptomeningeal anastomoses or pial collateral vessels play a critical role in cerebral

150 Pial collaterals begin forming between embryonic day 13.

151 Formation of pial collaterals occurs during a narrow developmental wi

152 e differences were confirmed in the cerebral pial cortical circulation where, compared to VEGF(hi/+)

153 evelopment, SC1 localizes to radial glia and pial-derived structures, including the vasculature, chor

154 t attenuated NMDA (10(-8), 10(-6) M) induced pial dilation (control, 9+/-1 and 16+/-1; coadministered

155 with iberiotoxin further decremented hypoxic pial dilation and blocked the hypoxia-associated rise in

156 l antagonist iberiotoxin had no influence on pial dilation during 5 min of hypoxia (pO(2) approximate

157 agonist Rp 8-Bromo cAMPs had no influence on pial dilation during 5 min of hypoxia, decremented the d

158 Recent studies show that pial dilation during a 20- or 40-min hypoxic exposure wa

159 NS1619, a K(ca) channel agonist, induced pial dilation during hypoxia that was attenuated by 20-

160 Met-induced pial dilation during hypoxia was also stimulus duration

161 Decremented hypoxic pial dilation during longer exposure periods results, at

162 indicate that the diminished role of Met in pial dilation during longer hypoxic exposure periods res

163 halin (10(-10), 10(-8), 10(-6) M) attenuated pial dilation induced by this opioid (7+/-1, 13+/-2, and

164 nteraction between opioids and NO in hypoxic pial dilation using newborn pigs equipped with a closed

165 t studies have observed that NOC/oFQ elicits pial dilation via release of cAMP, which, in turn, activ

166 Topical 8-Bromo cAMP (10(-8), 10(-6) M) pial dilation was unchanged by I+R but blunted by H+I+R

167 d the neuroepithelial cells to retract their pial end feet and caused tectal axons to exit the brain

168 tained throughout its depth, even though the pial half appeared darker during epi-illumination and li

169 es are tectal foliation and the formation of pial holes.

170 by investigating the molecular properties of pial ILA and confirming their astrocytic nature.

171 have been referred to as ILA, that we termed pial ILA and supial ILA.

172 We focused on the properties of pial ILA by investigating the molecular properties of pi

173 We found that while the density of pial ILA somata only varied slightly, the complexity of

174 Pial ILA were present in all mammalian species analyzed,

175 chimpanzee, orangutan, and human, exhibited pial ILA with the highest complexity.

176 ligand, collagen, which is localized to the pial layer of the developing cerebellum, thereby leading

177 ity at the surface of the cortex (meningeal, pial layer, vasculature) and around the ventricular wall

178 The vertical migration of neuroblasts to the pial layers of the tectum was inhibited, leading to a di

179 Arteriolar segments were isolated from pial membrane and studied within 10 h.

180 yelinated axon tracts but even ependymal and pial membranes.

181 cluding the vasculature, choroid plexus, and pial membranes.

182 urogenic zone intimately associated with the pial meningeal surface lining the outer edge of the form

183 ) /Iba1(+) macrophages were prominent in the pial meninges and ventricle lining, mainly at P1-P5.

184 particular, the basement membrane below the pial meninx (pBM) is required for correct cortical devel

185 We examined the pial microcirculation in rats using intravital fluoresce

186 Using intravital microscopy to assess the pial microvasculature through a closed cranial window in

187 r endothelial cells, as well as occluded rat pial microvessels, showed that luminal but not abluminal

188 We examined the pial network of the middle cerebral artery, which distri

189 the present and prior studies imply that the pial network reallocates blood in response to changing m

190 ecular identities distinct from those of the pial network.

191 The soma translocated within the pial process toward the pial surface and could also tran

192 hrough its neurites, which sprouted from the pial process.

193 uron maintains its primitive ventricular and pial processes, through which the cell body moves.

194 region of the optic nerve was present in the pial septa that divide the nerve fiber bundles, in the p

195 embrane, lamina cribrosa, optic nerve septa, pial sheath, and vasculature were delineated as unique o

196 7 and P2Y1,2,6 RNA can be amplified from the pial sheet.

197 se cloned with differentiated neurons in the pial side did so.

198 postmitotic-differentiated neurons from the pial side of the cortex were used for cloning.

199 regions and identify a regionally localized pial subpopulation marked by the expression of mu-crysta

200 Its filamentous pial, subventricular, and perivascular immunostaining pa

201 gradient, netrin1 protein accumulates on the pial surface adjacent to the path of commissural axon ex

202 nslocated within the pial process toward the pial surface and could also translocate through its neur

203 kinje cell (PC) dendrites extend towards the pial surface and progressively contact immature granule

204 ly postnatal ages, which migrates toward the pial surface and proliferates in situ.

205 ed past microknife cuts which started at the pial surface and sectioned layers I-IV.

206 Pial surface arteries in cats, as well as surface arteri

207 in laminin, and shows discontinuities in the pial surface basal lamina (glia limitans) that probably

208 nd into the telencephalon and grow along the pial surface but not more deeply into this tissue.

209 an extracellular protein expressed near the pial surface during embryonic development that is absent

210 We also found that the BL located at the pial surface formed labyrinthine tube-like structures en

211 rtical CR cells were distributed beneath the pial surface in control mice, but were virtually absent

212 tion seem to include the molecular layer and pial surface in neonates and blood vessels from P7 until

213 t the growth of apical dendrites towards the pial surface is regulated by a diffusible chemoattractan

214 onnection between radial glial cells and the pial surface mediated by LAMB1 leads to this malformatio

215 idase, Diamidino yellow, or fast blue to the pial surface of SI labeled a characteristic pattern of n

216 ray matter was confined to astrocytes at the pial surface of the brain.

217 urons beyond the first cortical layer at the pial surface of the brain.

218 oriented from the ventricular surface to the pial surface of the brain.

219 d population of neurons situated beneath the pial surface of the human embryonic forebrain even befor

220 distribution of basal lamina proteins at the pial surface of the midbrain and the brainstem.

221 ons underwent normal radial migration to the pial surface of the neural tube.

222 y anchoring the neuroepithelial cells to the pial surface of the retina, has an important function in

223 thalamic axons abnormally migrate toward the pial surface of the ventral telencephalon (VT).

224 amidino yellow (DY), applied directly to the pial surface on rostral or caudal areas of rat M2 (RM2 a

225 e cortical sections, cut tangentially to the pial surface or in the coronal plane, were stained for C

226 minals in cortex sectioned tangential to the pial surface revealed several consistent findings.

227 ciated directional blood pooling towards the pial surface strongly influence the cortical depth-depen

228 First, during radial migration toward the pial surface the A13 cells differentiate into dopaminerg

229 loss that in most animals extended from the pial surface through layer V.

230 vascular; Type III lesions extended from the pial surface to cortical layer 3 or 4.

231 ctivation was present in a gradient from the pial surface to deeper cortical layers.

232 Lateral MN dendrites proliferated under the pial surface to form a dense, thin (1-2 microm) plexus i

233 ve, migrate through the claustrum toward the pial surface to form layers (2-6a) of the insular cortex

234 hey migrate radially in the direction of the pial surface to take up positions in the cortical plate.

235 laminae and microknife cuts parallel to the pial surface were used to interrupt propagation or to is

236 fuse pattern of laminin deposition below the pial surface which correlated with an abrupt termination

237 loping brain and extend radial fibres to the pial surface, along which embryonic neurons migrate to r

238 nchoring of the neuroepithelial cells to the pial surface, and allowing the formation of a defined cy

239 e, radial glia cells were retracted from the pial surface, and radially migrating neurons, including

240 s as a sharp wave front perpendicular to the pial surface, at speeds ranging between 50 and 300 m/sec

241 -treated tecta outpaces the expansion of the pial surface, creating abnormal mechanical stresses.

242 ls, prominently residing in proximity of the pial surface, do not, in this case, hinder the ability o

243 ere usually made 1.2 to 1.5 mm down from the pial surface, in or around layer III.

244 domly rotated sections cut orthogonal to the pial surface, within the region of interest.

245 rbB2 antibody also immunostained glia at the pial surface.

246 atterning as they weave a course towards the pial surface.

247 cones, especially those oriented toward the pial surface.

248 .5%), located approximately 1.4 mm below the pial surface.

249 xtend an apical dendrite directed toward the pial surface.

250 also varied with the cortical depth from the pial surface.

251 ive astroglia were aberrantly present on the pial surface.

252 rectangular network oriented parallel to the pial surface.

253 aps were sampled at 25%, 50%, 75% depth from pial surface.

254 ortical pathological process driven from the pial surface.

255 pling T2* at 25%, 50% and 75% depth from the pial surface.

256 sometimes extending barely 100 mum below the pial surface.

257 tex at depths of up to -900 microm below the pial surface.

258 o vertical microcolumns perpendicular to the pial surface.

259 the brainstem to form a motor nucleus at the pial surface.

260 rodes implanted in Heschl's gyrus (HG), from pial-surface electrodes placed on the lateral superior t

261 maintain contact both at the ventricular and pial surfaces throughout mitotic division, and (2) short

262 tion MRI scans, models of the gray-white and pial surfaces were generated for each individual's corte

263 and no link was found with distance from the pial surfaces.

264 ctivity increase previously seen in the glio-pial tissue of diabetic rats may be due to the selective

265 Conversely, in glio-pial tissue, PKC-alpha and RACK1 were upregulated, where

266 ffer when comparing cerebral cortex and glio-pial tissue.

267 out passively into the brain parenchyma from pial vascular plexuses to meet metabolic needs of growin

268 SE BOLD iso-orientation maps excluding large pial vascular regions were significantly correlated to m

269 Pial vasodilation to a cAMP analogue during hypoxia was

270 SQ 29,548 similarly partially restored such pial vasodilation.

271 ief constriction and prolonged dilatation of pial veins are affected.

272 did not induce dilatation in pial arteries, pial veins, or dural veins.

273 d is found in endothelial cells (ECs) of the pial venous plexus.

274 ity-increasing effect of arachidonic acid on pial venular capillaries in vivo using the single microv

275 The permeability response of slightly leaky pial venular capillaries to histamine was investigated u

276 Permeability of pial venular capillaries to Lucifer Yellow (PLY) was mea

277 iocyanate-BSA infusion was used to determine pial-venular permeability.

278 Finally, in a pial vessel disruption cortical stroke model, a unilater

279 nges differed between both types of vessels (pial vessel disruption within days versus weeks for pare

280 f smooth muscle cells (SMCs) in the walls of pial vessels affected by amyloid deposition in the Tg257

281 es in permeability and leukocyte adhesion in pial vessels after a localized, single dose of 20 Gy.

282 While adaptive arteriogenesis of the pial vessels and angiogenesis at the capillary level may

283 FITC-albumin, FITC-dextran-10K and NaFl from pial vessels and diameter of pial arterioles remained co

284 vehicle, clearance of FITC-dextran-10K from pial vessels and diameter of pial arterioles remained re

285 tly attenuated leukocyte adhesion in surface pial vessels and in deep ascending cortical postcapillar

286 sults showed that fast flows up to 3 cm/s in pial vessels and minute flows down to 0.3 mm/s in arteri

287 nicotine blunted NO-induced vasodilation of pial vessels and the increase in cortical blood flow mea

288 ere identified in immune cells extravasating pial vessels as early as 1 day post infection.

289 Thermocoagulation (TCL) of pial vessels has been shown to result in the same degree

290 ure the diameter changes of single dural and pial vessels in the awake mouse during voluntary locomot

291 vasoconstriction and improved blood flow in pial vessels of PbA-infected mice.

292 radiation did not affect the permeability of pial vessels to the 150-kDa molecule.

293 vehicle, clearance of FITC-dextran-10K from pial vessels was minimal, and diameter of pial arteriole

294 saline), clearance of FITC-dextran-10 K from pial vessels was modest and remained relatively constant

295 d in blood vessels located in leptomeninges (pial vessels) and brain parenchyma (parenchymal vessels)

296 imarily of the superficial glia limitans and pial vessels, but trended toward a decrease in cerebral

297 ml) was required to increase permeability in pial vessels, suggesting that different tissues exhibit

298 I ganglionic cells in the SPG send fibers to pial vessels.

299 CGRP dilated dural, but not pial, vessels and significantly reduced spontaneous loco

300 In pial window preparations, chronic nicotine blunted NO-in