ライフサイエンスコーパス: periventricular

1 rojection pattern: superficial, central, and periventricular.

2 dilated ventricle margin were classified as periventricular.

3 These results indicate that periventricular abnormalities arising from abnormal migr

4 rtal, sex differentiation in ventricular and periventricular anatomy and associated behavior, affecti

5 Immunoreactivity was seen in several periventricular and a few magnocellular neurons, and in

6 show that Kiss1 neurons in the anteroventral periventricular and anterior periventricular nuclei (AVP

7 These features closely mimic the periventricular and cortical pathology described in MS p

8 ies with multifocal small cavitations in the periventricular and deep cerebral white matter.

9 ion of white matter hyperintensities in both periventricular and deep white matter areas was found.

10 Periventricular and deep WMH volumes were measured with

11 arabrachial nucleus), neuroendocrine system (periventricular and paraventricular hypothalamic nuclei,

12 queductal gray, dorsal parabrachial nucleus, periventricular and rhomboid nuclei of the thalamus, and

13 ra of diseases that includes polymicrogyria, periventricular and subcortical heterotopia and lissence

14 ll infiltration and microglial activation in periventricular and superficial white matter structures

15 C-PK11195 was significantly increased in the periventricular and total NAWM (P = 0.016 and P < 0.001,

16 k was seen in the facial and vagal lobes and periventricular and ventral regions of the medulla oblon

17 including the medial preoptic, anteroventral periventricular, arcuate, and ventromedial nuclei.

18 and left medial prefrontal cortex and in the periventricular area in the patient group regardless of

19 urons were scattered throughout the preoptic periventricular areas (PV), but the vast majority of Kis

20 ghly vascularized compared to non-neurogenic periventricular areas, within which NSCs and precursors

21 CR-ir cell bodies were mainly distributed in periventricular areas.

22 oestradiol in the hypothalamic anteroventral periventricular (AVPV) and arcuate (ARC) nuclei, while t

23 ding kisspeptin neurons in the anteroventral periventricular (AVPV) and arcuate nuclei, providing hom

24 The first periventricular band was excluded from analysis to mitig

25 Here we show that periventricular blood vessels selectively influence neoc

26 The combination of microencephaly and periventricular calcifications was the most common neuro

27 aging abnormalities included microencephaly, periventricular calcifications, ventriculomegaly, pachyg

28 vious hypotheses concerning the aetiology of periventricular CBF reduction in NPH.

29 duction of constitutively active Notch3 into periventricular cells of embryonic day 9.5 mice causes t

30 teral ventricular dilatation, necrotic foci, periventricular cysts and intraventricular hemorrhages w

31 cerebellar hypoplasia, porencephalic cysts, periventricular cysts, and hydrocephalus.

32 , including any of the following: persistent periventricular echogenicity or echolucency on neuroimag

33 dymal cell microvilli and the development of periventricular edema.

34 Our data suggest that periventricular endothelial cells have intrinsic program

35 urons occur in the white matter distant from periventricular foci, including the subplate region, in

36 ted in the subcortical frontal lobe, and the periventricular frontal and parietal caps of the brain.

37 fically in the subcortical frontal lobe, and periventricular frontal and parietal caps.

38 the generation of neural progenitors in the periventricular germinal zones, cell proliferation chara

39 17.5, donor cells formed discrete spheres in periventricular germinal zones, suggesting preferential

40 ile AF64A damaged septal cholinergic fibers, periventricular GnRH-immunoreactive fibers remained inta

41 glutamatergic neurons were found within the periventricular gray layer throughout the brainstem, wit

42 well as in the locus coeruleus (LC) and the periventricular gray substance (PVG) in post-hypoxic rat

43 cortex, medial thalamus, and periaqueductal/periventricular gray.

44 Preterm individuals who had experienced periventricular haemorrhage and ventricular dilatation i

45 VPT individuals with evidence of periventricular haemorrhage and ventricular dilatation o

46 Neonatal periventricular haemorrhage with ventricular dilatation

47 e onset of neuroblast migration give rise to periventricular heterotopia (clusters of neurons along t

48 Periventricular heterotopia (PH) is a disorder character

49 Periventricular heterotopia (PH) is a human malformation

50 Periventricular heterotopia (PH) is a malformation of co

51 ne filamin A (FlnA) cause the human disorder periventricular heterotopia (PH).

52 ity gene lgl, exhibit MCCs resembling severe periventricular heterotopia (PH).

53 Periventricular heterotopia (PVH) is a congenital malfor

54 iferative zones near the lateral ventricles (periventricular heterotopia).

55 yonic mouse forebrain frequently resulted in periventricular heterotopia, developmental abnormalities

56 he reeler mouse, double cortex syndrome, and periventricular heterotopia.

57 Periventricular heterotopias is a malformation of cortic

58 nd one child with cerebral ventriculomegaly, periventricular heterotopias, echogenic kidneys, and ren

59 tions in FLNA, the gene for filamin A, cause periventricular heterotopias.

60 cumulation of neural progenitor cells in the periventricular, hippocampal, cerebellar and olfactory b

61 0.24), and cholesterol (r = 0.20), and with periventricular hyperintensities for glycated hemoglobin

62 nts, showing ventricular enlargement in one, periventricular hyperintensities in another and frontal

63 factors and scores for deep white matter and periventricular hyperintensities, and stepwise multiple

64 interval, 1.64-3.79; P = 2 x 10(-5)) but not periventricular hyperintensities.

65 y for deep white matter hyperintensities and periventricular hyperintensities.

66 dibular (TIDA), tuberohypophyseal (THDA) and periventricular hypophyseal DAergic (PHDA) neurons regul

67 ic nucleus, accessory neurosecretory nuclei, periventricular hypothalamic nucleus, dorsomedial hypoth

68 xpressing neurons are located in the ventral periventricular hypothalamus (the equivalent of the mamm

69 , an array of cells extending throughout the periventricular hypothalamus and ventral thalamus were e

70 essing neurons (located in the anteroventral periventricular hypothalamus, Kiss1(AVPV), and arcuate h

71 found in discrete populations in the ventral periventricular hypothalamus, the proposed arcuate homol

72 the preoptic area and in rostral and caudal periventricular hypothalamus.

73 patients, the increases in FMZ binding were periventricular, in locations normally seen in periventr

74 ing lesions with macrophages and lymphocytic periventricular infiltrates, and chronic, inactive demye

75 While immunohistochemical analysis revealed periventricular inflammation and a loss of integrity of

76 least two of four locations (juxtacortical, periventricular, infratentorial, and spinal-cord) and DI

77 sing an automated method) were determined in periventricular, intermediate, and subcortical regions o

78 y low-gestational-age infants with low-grade periventricular-intraventricular hemorrhage are not sign

79 igher rates of early-onset sepsis and severe periventricular-intraventricular hemorrhage as compared

80 Low-grade periventricular-intraventricular hemorrhage is a common

81 Low-grade periventricular-intraventricular hemorrhage.

82 val/death, bronchopulmonary dysplasia (BPD), periventricular/intraventricular hemorrhage or periventr

83 suggest that needing three lesions to define periventricular involvement might slightly increase spec

84 asing the number of lesions needed to define periventricular involvement to three, combining cortical

85 The correlation between increased periventricular lesion burden and decreased CMT indicati

86 To quantify periventricular lesion load (PV-LL), we generated ventri

87 ular volume and total lesion load, increased periventricular lesion occupancy (percentage of PV-LL) s

88 ike phenotype that recapitulates the primary periventricular lesion, ventricular enlargement, and the

89 rise to abnormal astroglial cells and induce periventricular lesions and hemorrhage that leads to cer

90 Periventricular lesions developed within 10 d and evolve

91 Requirement of three periventricular lesions resulted in slightly lower sensi

92 scores for cortical, deep white matter, and periventricular lesions were 0.93 +/- 0.05, 0.97 +/- 0.0

93 es in compartments close to the CSF, such as periventricular lesions, might correlate with cortical p

94 ne-derived cells contribute to the repair of periventricular lesions.

95 vere intraventricular haemorrhage (IVH), and periventricular leucomalacia (PVL) in preterm neonates.

96 g enterocolitis, bronchopulmonary dysplasia, periventricular leucomalacia, and retinopathy of prematu

97 cases but without classic cystic lesions of periventricular leucomalacia.

98 epsis, intraventricular hemorrhage >grade 2, periventricular leukomalacia >grade 1, or necrotizing en

99 riventricular/intraventricular hemorrhage or periventricular leukomalacia (PIVH/PVL), retinopathy of

100 tributes to mental or physical impairment in periventricular leukomalacia (pre- or perinatal white ma

101 brain injuries, including the development of periventricular leukomalacia (PVL) and cerebral palsy (C

102 causes of perinatal brain injury leading to periventricular leukomalacia (PVL) and cerebral palsy.

103 nitive abnormalities in preterm infants with periventricular leukomalacia (PVL) is uncertain.

104 te of cerebral palsy in premature infants is periventricular leukomalacia (PVL), a disorder of the im

105 is generally thought to consist primarily of periventricular leukomalacia (PVL), a distinctive form o

106 lying cerebral palsy in premature infants is periventricular leukomalacia (PVL), a lesion of the imma

107 ellular models of Huntington's disease (HD), periventricular leukomalacia (PVL), and kidney dysfuncti

108 e infant leads to white matter injury termed periventricular leukomalacia (PVL), the leading cause of

109 d and one coinciding with the peak period of periventricular leukomalacia (PVL), the major disorder u

110 e matter is important in the pathogenesis of periventricular leukomalacia (PVL), the major pathologic

111 white-matter damage of immaturity, including periventricular leukomalacia (PVL), was the most common

112 ctor for multiple brain pathologies, notably periventricular leukomalacia (PVL), which is distinguish

113 lnerability for white matter injury, such as periventricular leukomalacia (PVL).

114 ndroglial injury and loss, a disorder termed periventricular leukomalacia (PVL).

115 7.5 percent vs. 23.9 percent, P=0.03) and of periventricular leukomalacia alone (5.2 percent vs. 9.0

116 n lesions of white matter disorders, such as periventricular leukomalacia and multiple sclerosis.

117 hogenesis of white matter disorders, such as periventricular leukomalacia and multiple sclerosis.

118 tial failure of recovery in insults, such as periventricular leukomalacia and multiple sclerosis.

119 or translation as a therapeutic strategy for periventricular leukomalacia and that the mechanism of p

120 In animal models, features of periventricular leukomalacia can be induced by hypoxia a

121 associated with BAS; however, neonates with periventricular leukomalacia had lower preoperative oxyg

122 plications with respect to the mechanisms of periventricular leukomalacia in infants and of persisten

123 se and severe intraventricular hemorrhage or periventricular leukomalacia in premature infants are as

124 severe intracranial hemorrhage and/or cystic periventricular leukomalacia in the neonatal period.

125 ith clinical potential for disorders such as periventricular leukomalacia in the preterm and neonatal

126 Periventricular leukomalacia is a form of hypoxic-ischem

127 Periventricular leukomalacia is characterized by a reduc

128 Periventricular leukomalacia is the predominant injury i

129 mes of myelination or remyelination, such as periventricular leukomalacia leading to cerebral palsy,

130 elination is also noted in children with the periventricular leukomalacia of cerebral palsy, another

131 In preterm infants (n = 44), periventricular leukomalacia was associated with larger

132 Periventricular leukomalacia was not associated with BAS

133 ncluding multiple sclerosis, cerebral palsy (periventricular leukomalacia), and spinal cord injury.

134 lasia, sepsis, intraventricular haemorrhage, periventricular leukomalacia, and necrotising enterocoli

135 mes included severe intracranial hemorrhage, periventricular leukomalacia, and ventriculomegaly.

136 asia, severe intracranial hemorrhage, cystic periventricular leukomalacia, and/or severe retinopathy

137 on, length of stay, intracranial hemorrhage, periventricular leukomalacia, chronic lung disease, pate

138 alence of structural brain abnormalities and periventricular leukomalacia, fetal and postnatal cerebr

139 mbined end point of intracranial hemorrhage, periventricular leukomalacia, or ventriculomegaly (17.5

140 II or IV intraventricular hemorrhage, cystic periventricular leukomalacia, severe bronchopulmonary dy

141 lar hemorrhage grade of 3 or greater, cystic periventricular leukomalacia, surgical necrotizing enter

142 ing diseases, such as multiple sclerosis and periventricular leukomalacia.

143 prematurity, necrotizing enterocolitis, and periventricular leukomalacia.

144 to have hypoxic brain injury in the form of periventricular leukomalacia.

145 time to surgery (P=0.028) than those without periventricular leukomalacia.

146 r hemorrhage grade of 3 or greater or cystic periventricular leukomalacia.

147 e rates of severe intracranial hemorrhage or periventricular leukomalacia.

148 se and severe intraventricular hemorrhage or periventricular leukomalacia.

149 ll as severe intraventricular hemorrhage and periventricular leukomalacia.

150 ks gestation, the period of highest risk for periventricular leukomalacia.

151 amate receptor blockade in a rodent model of periventricular leukomalacia.

152 severe intracranial hemorrhage and/or cystic periventricular leukomalacia.

153 eath; death, intraventricular hemorrhage, or periventricular leukomalacia; and death or necrotizing e

154 An abnormal periventricular magnetization transfer ratio gradient oc

155 nal migration, resulting in the formation of periventricular masses.

156 d the expression and function of OCTs in the periventricular medial hypothalamus of male Sprague Dawl

157 In control patients, periventricular NAWM regions had significantly higher CB

158 up showed prolonged mean transit time in the periventricular NAWM, as compared with the control group

159 of ganglionic eminence vessels and resultant periventricular neural apoptosis resulted in a PVL-like

160 differentiation and overexpression produces periventricular neuronal masses, demonstrating its funct

161 lamin function, leading to the generation of periventricular neurons independent of normal neocortica

162 a model for how temporal dynamics in tectal periventricular neurons might arise from computations be

163 we found transgene expression in subsets of periventricular neurons of the hypothalamus, Purkinje ce

164 and their subventricular dispersion from the periventricular niche during neocortical development.

165 s), polymicrogyria with megalencephaly (20), periventricular nodular heterotopia (61), and pachygyria

166 und mutations in DCX and LIS1), persons with periventricular nodular heterotopia (FLNA), and persons

167 ear their site of origin and form persistent periventricular nodular heterotopia (PH).

168 Neurodevelopmental disorders with periventricular nodular heterotopia (PNH) are etiologica

169 Polymicrogyria (PMG) and periventricular nodular heterotopia (PNH) are two develo

170 gate whether it is possible in patients with periventricular nodular heterotopia (PVNH) to detect abn

171 ocalized neuronal migration disorder, called periventricular nodular heterotopia (PVNH; refs. 3-6).

172 eral cortical malformations, polymicrogyria, periventricular nodular heterotopia and diffuse megalenc

173 and Melnick-Needles syndrome, with X-linked periventricular nodular heterotopia and FG syndrome (Omi

174 ) recording in 8 patients with epilepsy from periventricular nodular heterotopia and matched healthy

175 zygous loss of function of human FLNA causes periventricular nodular heterotopia in females and is ge

176 riventricular, in locations normally seen in periventricular nodular heterotopia on MRI.

177 inct neuronal migration disorders, including periventricular nodular heterotopia, subcortical band he

178 ree cases of schizencephaly, and 15 cases of periventricular nodular heterotopia.

179 indirect interactor with FlnA, also lead to periventricular nodule formation in mice.

180 enudation of the neuroepithelium, leading to periventricular nodule formation.

181 migrated appropriately into the cortex, that periventricular nodules were primarily composed of later

182 but an investigation of the relationship of periventricular normal-appearing white matter abnormalit

183 e anteroventral periventricular and anterior periventricular nuclei (AVPV/PeN) of males and females e

184 roducing oxytocin in the paraventricular and periventricular nuclei (PVN and PeVN, respectively) are

185 tin neurons in the arcuate and anteroventral periventricular nuclei are postulated to mediate negativ

186 lei of the thalamus, and paraventricular and periventricular nuclei of the hypothalamus.

187 araventricular, suprachiasmatic, arcuate and periventricular nuclei.

188 ventricular nucleus (PVH), the anteroventral periventricular nucleus (AVPe), and the central nucleus

189 itive afferents located in the anteroventral periventricular nucleus (AVPV) are either absent or disa

190 vation of Kiss1 neurons in the anteroventral periventricular nucleus (AVPV) is linked to the inductio

191 In rodents, the hypothalamic anteroventral periventricular nucleus (AVPV) is sexually differentiate

192 The expression of Kiss1 in the anteroventral periventricular nucleus (AVPV) is sexually dimorphic, an

193 ese studies, we focused on the anteroventral periventricular nucleus (AVPV), a nucleus that is larger

194 riodic signals converge in the anteroventral periventricular nucleus (AVPV), but it is unclear how th

195 pha, ERbeta, and Kiss1 in the anterioventral periventricular nucleus (AVPV), medial preoptic area (MP

196 creased NOP mRNA expression in anteroventral periventricular nucleus (AVPV), median preoptic nucleus,

197 urons than do females, and the anteroventral periventricular nucleus (AVPV), where females have more

198 the expression of Kiss1 in the anteroventral periventricular nucleus (AVPV).

199 erifornical area (LH/PFA), and anteroventral periventricular nucleus (AVPV).

200 ll bodies were localized in the intermediate periventricular nucleus (IPe) in the hypothalamus, as de

201 lamic cells in the posterior division of the periventricular nucleus (RPPp), the nucleus hypothalamus

202 i of male Sprague-Dawley rats (anteroventral periventricular nucleus [AVPV], median preoptic area [Me

203 mRNA-containing neurons in the anteroventral periventricular nucleus and likewise possessed fewer mot

204 raventricular hypothalamic nucleus (PVN) and periventricular nucleus in the BK-treated animals.

205 ex difference was found in the anteroventral periventricular nucleus of P21, but not P0 or P4, mice,

206 Neurons in the anteroventral periventricular nucleus of the hypothalamus (AVPV) media

207 n was increased in the subfornical organ and periventricular nucleus of the hypothalamus, but not in

208 ion of dopamine neurons in the anteroventral periventricular nucleus of the preoptic region of the hy

209 lamus (VMN-VL) in males and females, and the periventricular nucleus of the thalamus in males only.

210 ut3 and Nmur2 genes, and placed these in the periventricular nucleus with many synaptic afferents ari

211 area, median preoptic nucleus, anteroventral periventricular nucleus, and bed nucleus of the stria te

212 was detected in the retrochiasmatic nucleus, periventricular nucleus, arcuate nucleus and restricted

213 hypothalamus, arcuate nucleus, anteroventral periventricular nucleus, medial preoptic nucleus, parave

214 n the medial preoptic area and anteroventral periventricular nucleus, regions important for generatio

215 alamic cells in the anterior division of the periventricular nucleus, the suprachiasmatic nucleus, an

216 ales' medial preoptic nucleus, anteroventral periventricular nucleus, ventromedial hypothalamus, and

217 matter tracts in the corpus callosum and the periventricular optic radiations.

218 erebral hemorrhage, seizure, cardiomyopathy, periventricular or intraventricular hemorrhage, necrotiz

219 Open-ring lesions were periventricular or juxtacortical and enhanced centripeta

220 particular, the dopaminergic nucleus of the periventricular organ was evidenced with dopamine antibo

221 Axons from neurons of the suprachiasmatic, periventricular organ-associated, and posterior tuberal

222 clei, the hypothalamus including supraoptic, periventricular, paraventricular (PVN), arcuate nuclei a

223 Minocycline treatment decreases cortical and periventricular pathology in the chronic phase of EAE, i

224 f EC stability, ependymal cell function, and periventricular permeability.

225 Diencephalic TH-ir neurons in the periventricular posterior tuberculum, known to be dopami

226 tments like the fetal cortex, but low in the periventricular progenitor cell regions.

227 We found that periventricular PV-immunofluorescence showed positive co

228 e third ventricle (RP3V) and in the anterior periventricular (PVa), arcuate, and dorsomedial hypothal

229 ons of the arcuate nucleus and anteroventral-periventricular region (AVPV) may differentially regulat

230 eased number and morphologic changes) in the periventricular region and hippocampus of the brain of n

231 e suprachiasmatic nucleus terminating in the periventricular region immediately dorsal to the nucleus

232 d in medial HVC and pvMSt, a newly described periventricular region in the medial striatum.

233 es of immunoreactive fibers were seen in the periventricular region in the thalamus, hypothalamus, an

234 n-ir cell bodies are detected in the rostral periventricular region of the third ventricle (RP3V) and

235 of kisspeptin neurons located in the rostral periventricular region of the third ventricle (RP3V) of

236 vior control column, and to the hypothalamic periventricular region, which controls patterned neuroen

237 and white matter hyperintensities, including periventricular regions and both frontal and temporal su

238 over, recombinant GALC was found not only in periventricular regions but also at sites distant to the

239 n in association with ependymal surfaces and periventricular regions of formalin-fixed brain tissue,

240 xpression in the ventromedial telencephalon, periventricular regions of the thalamus and anterior hyp

241 sion recovery sequences predominantly in the periventricular regions, the posterior limb of the inter

242 rpus callosum, olfactory bulbs, subpial, and periventricular regions.

243 layer separating the ependymal lining from a periventricular ribbon of astrocytes.

244 The early targeting of visual and periventricular structures followed by more widespread C

245 Here we describe cortical, periventricular subcortical lesions and callosal demyeli

246 bes and were mostly confluent, affecting the periventricular subcortical white matter and U-fibers.

247 Neuronal specification occurs at the periventricular surface of the embryonic central nervous

248 ce of brain lesions [T2 lesions (P = 0.918), periventricular T2 lesions (P = 0.580) or gadolinium-enh

249 Central neurocytoma (CN) is a rare periventricular tumor, whose derivation, lineage potenti

250 Endothelial cells of the periventricular vascular network have molecular identiti

251 perinatal ischemic stroke (APPIS), or fetal periventricular venous infarction (PVI) were recruited.

252 the hypothalamus included the anteroventral periventricular, ventromedial preoptic, median preoptic,

253 ridization was observed in the anteroventral periventricular, ventromedial preoptic, suprachiasmatic,

254 r and exit from a VEGF-dependent phase, with periventricular vessels being the last to mature.

255 cate that damage to VEGF-dependent, immature periventricular vessels contributes to PVL development.

256 ght a prominent interaction between RGPs and periventricular vessels important for proper production

257 ntal program permitted selective ablation of periventricular vessels via episodic VEGF blockade withi

258 ssively grow radial glial fibers anchored to periventricular vessels.

259 xhibited meningeal, subpial neocortical, and periventricular virus.

260 Volumetric WML measures (deep and periventricular) were obtained with 1.5T magnetic resona

261 rvival of oligodendrocytes in intragyral and periventricular white matter (p < 0.05) and increased br

262 Basal flow in the periventricular white matter (PVWM) was significantly lo

263 mine cerebral hypoxemia in specific regions (periventricular white matter and both hippocampi).

264 and NAA/Cho ratios measured in the posterior periventricular white matter at term-equivalent age is p

265 analysis in neonatal rodent optic nerve and periventricular white matter axons studied under modeled

266 tes similar to the astrocyte ribbon in human periventricular white matter biopsies that is reported t

267 ignificant cerebral white matter hypoplasia, periventricular white matter gliosis, and axonal and epe

268 cerebral leukoencephalopathy that harboured periventricular white matter hyperintensities were selec

269 Periventricular white matter injury (PVWMI) in premature

270 Periventricular white matter injury (PWMI) is the leadin

271 Although periventricular white matter injury (PWMI) is the leadin

272 Periventricular white matter injury (PWMI) is the leadin

273 Periventricular white matter injury (PWMI) is the major

274 in premature infants frequently arises from periventricular white matter injury (PWMI), a condition

275 form of injury in the preterm population is periventricular white matter injury (PWMI), a pathology

276 n is a major pathological sequela of chronic periventricular white matter injury in survivors of prem

277 failure in chronic hypoxia-ischemia-induced periventricular white matter injury is related to persis

278 /88]; adjusted RR, 0.20; 95% CI, 0.05-0.90), periventricular white matter loss (18% [14/77] vs 33% [2

279 ing corpus callosum atrophy (7/7 [100%]) and periventricular white matter loss (6/7 [85%]).

280 ther posthemorrhagic ventricular dilation or periventricular white matter loss.

281 Additionally, Cho/Cr ratio in the periventricular white matter region of OSA group was hig

282 elopment of IVH leads to inflammation of the periventricular white matter, apoptosis and arrested mat

283 ns in the ventricular/subventricular region, periventricular white matter, central white matter, and

284 In the periventricular white matter, NAA/Cho ratio in OSA patie

285 The onset of IVH induces inflammation of the periventricular white matter, which results in arrested

286 ory lesions that have a predilection for the periventricular white matter.

287 om a 2-cm(3) voxel centered in the posterior periventricular white matter.

288 had positive correlations with the total and periventricular WMH volume (r = 0.55 and 0.59, P < 0.01)

289 d with an increasing load of subcortical and periventricular WMHs.

290 rosphere morphology of NPCs derived from the periventricular zone of mice brain.

291 The BSTp sends its strongest outputs to the periventricular zone of the hypothalamus and innervates

292 arily innervate neuroendocrine nuclei in the periventricular zone of the hypothalamus, including the

293 ng to the median eminence and throughout the periventricular zone of the hypothalamus.

294 feration of neuroprogenitors in the germinal periventricular zone.

295 ivation cells, preferentially lie within the periventricular zone; the other cell types are distribut

296 rative study of six (D, Vd, Vv, Dm, Dl, Ppa) periventricular zones (PVZs) harboring proliferative cel

297 amine (DA) and serotonin (5-HT) occur in the periventricular zones of the hypothalamic region of most

298 is and stroke, T-cell infiltration occurs in periventricular zones where NPCs are located and is asso

299 and located preferentially in white matter, periventricular zones, and meninges.

300 nhanced radial migration of NSPCs out of the periventricular zones, possibly by epithelial-mesenchyma