ライフサイエンスコーパス: neurogenic

1 We disclose a basal level of adult neurogenic activity characterized by glial invasion of t

2 Consistent adult neurogenic activity in humans is observed in specific ni

3 llenged by accumulating evidence for ectopic neurogenic activity in other cerebral locations.

4 Most of the neurogenic activity induced by PUFAs resulted in increas

5 this process is sustained by the persistent neurogenic activity of individual pallial neural stem ce

6 nt contributions by activating or inhibiting neurogenic activity with veratridine and tetrodotoxin, r

7 letion extends the response and rescues both neurogenic and behavioral deficits in mice lacking TrkB.

8 There are significant neurogenic and inflammatory influences on blood pressure

9 , revealing three VNC cell clusters (neural, neurogenic and mesenchymal), each predetermined epigenet

10 ay be eosinophilic and steroid-responsive or neurogenic and non- inflammatory.

11 Such a generator could be targeted to treat neurogenic and non-neurogenic ejaculatory disorders.

12 We demonstrate Dmrt5 to be neurogenic, and reciprocally regulated by Lhx2: loss of

13 Genetic perturbations revealed that the neurogenic/apoptotic fate switch was mediated through ce

14 ein Sam68 (Khdrbs1) is strongly expressed in neurogenic areas of the neocortex and supports the self-

15 od stabilizer, has both neuroprotective, pro-neurogenic as well as antitumor effects, and in the curr

16 premature senescence of adult NSCs into non-neurogenic astrocytes in mice lacking alpha-SYN resemble

17 g premature differentiation of NSCs into non-neurogenic astrocytes.

18 that the muscle of FE women has significant neurogenic atrophy, whereas MA muscle exhibit superior r

19 ves (n = 49), spina bifida (n = 21), central neurogenic bladder (n = 13), bladder exstrophy (n = 14),

20 bidity and hospitalisations in subjects with neurogenic bladder (NB) due to spinal cord injury (SCI).

21 bidity and hospitalizations in subjects with neurogenic bladder (NB) due to spinal cord injury (SCI).

22 ting neurodegeneration on the development of neurogenic bladder dysfunction in mice with corona-virus

23 e previously characterized a murine model of neurogenic bladder dysfunction induced by a neurotropic

24 s and showed differential mechanisms driving neurogenic bladder dysfunction.

25 The outlook for patients with neurogenic bladder has been transformed by a combination

26 onditions such as posterior urethral valves, neurogenic bladder, ureteral ectopy, or bladder exstroph

27 method was also applied on 16 patients with neurogenic bladders (10 compliant and 6 non-compliant su

28 iomarker for management of the patients with neurogenic bladders.

29 We identified LLC in meningeal, cortical and neurogenic brain regions.

30 in vivo experiments confirmed gliogenic and neurogenic capacities of human neural pericytes.

31 e exploring the links between alterations in neurogenic capacity and changes in behavioural ability.

32 Loss of neurogenic capacity in mature MG is accompanied by reduc

33 rm maintenance of the stem cell pool and the neurogenic capacity of the aging brain.

34 However, by postnatal day 16, mouse MG lose neurogenic capacity, despite Ascl1 overexpression.

35 amic neuronal activity during this prevalent neurogenic cardiovascular disease.

36 o altered neuronal activity during prevalent neurogenic cardiovascular diseases.

37 ave sequenced the transcriptomes of purified neurogenic cell types across consecutive time points cov

38 gnatures for hundreds of genes among diverse neurogenic cell types, most of which remain unstudied.

39 nd demarcates specific subpopulations within neurogenic cell types.

40 studies confirmed axonal damage with chronic neurogenic changes.

41 enitors and identified RET as a regulator of neurogenic commitment.

42 ted Wnt signaling accompanying an incomplete neurogenic commitment.

43 reas in mice, a dedicated network suppresses neurogenic competence and restores quiescence.

44 sses differentiation without affecting their neurogenic competence.

45 osed that obesity-related hypertension has a neurogenic component which is characterized by sympathet

46 model of allergic asthma, which has a strong neurogenic component.

47 NSI-189 is a novel neurogenic compound independent of monoamine reuptake pa

48 The data obtained suggest that constitutive neurogenic control of cardiomyocyte trophism occurs thro

49 Acute neurogenic control of heart rate is achieved locally thr

50 Surprisingly, in the non-neurogenic cortex, Notch-depleted astrocytes also initia

51 enic enhancement that attenuates age-related neurogenic decay has not been described.

52 YN and DA as potential targets to ameliorate neurogenic defects in the aging and diseased brain.SIGNI

53 zing Ascl-1(null) mutants we dissociated the neurogenic defects observed in Gli3 mutants from lack of

54 Neurogenic detrusor overactivity (NDO) is among the most

55 al stages of migration, transcription factor Neurogenic Differentiation 2 (Neurod2) contributes to te

56 ute homologue 1 (ASCL1; also known as ASH1), neurogenic differentiation factor 1 (NeuroD1), yes-assoc

57 basic helix-loop-helix transcription factor, Neurogenic Differentiation Factor-6 (NEUROD6).

58 ogenic differentiation, but not during early neurogenic differentiation, and is transcriptionally upr

59 away from the nuclear periphery during early neurogenic differentiation, but not during early cardiog

60 specificity protein 2 (Sp2) in expansive and neurogenic divisions of the developing cerebral cortex b

61 d that loss of Sp2 in progenitors undergoing neurogenic divisions results in prolonged mitosis due to

62 owed normal cell cycle progression, although neurogenic divisions were severely reduced.

63 e found that BC progenitors undergo terminal neurogenic divisions while in markedly disparate stages

64 rative replenishment divisions and consuming neurogenic divisions.

65 both early proliferative divisions and later neurogenic divisions.

66 ric NPC-NPC divisions, but not in asymmetric neurogenic divisions.

67 cover the construction of the zebrafish otic neurogenic domain.

68 e relevant to future clinical application in neurogenic dysphagia.

69 EGFR is activated in the ventral midline and neurogenic ectoderm by the Spitz ligand, which is proces

70 oundary between the presumptive mesoderm and neurogenic ectoderm of early Drosophila embryos.

71 Surprisingly, the neurogenic ectoderm, not the ventral midline, was found

72 ing activity from the ventral midline to the neurogenic ectoderm.

73 t in vitro neurogenesis, indicating that the neurogenic effect of 24,25-EC on mDA neurons is specific

74 ibition of GPR40 was capable of reducing the neurogenic effect of a PUFA, while the inhibition of BDN

75 The neurogenic effect of Wnt agonists on ENS progenitors sup

76 This neurogenic effect was more pronounced after high-thoraci

77 Behavioral and neurogenic effects of chronic treatment with the SSRI, f

78 can lead to olfactory deficits and that the neurogenic effects of selective serotonin reuptake inhib

79 SF) was chosen, due to its clinically proven neurogenic effects.

80 myloid-beta (Abeta), and proinflammatory and neurogenic effects.

81 ould be targeted to treat neurogenic and non-neurogenic ejaculatory disorders.

82 Neurogenic enhancement by VEGF preconditioning was, in p

83 a factor capable of inducing a long-lasting neurogenic enhancement that attenuates age-related neuro

84 ultipotent progenitor divisions that lead to neurogenic entry and the factors that regulate them are

85 igher dose converted most of the embryo to a neurogenic epithelial sphere expressing the Hnf6 ciliary

86 that the dog may be better representative of neurogenic events in humans, compared with rodents.

87 tential therapeutic target for reversing the neurogenic exhaustion characteristic of the aged OE.

88 nic eminence (LGE), despite upregulating the neurogenic factor Ascl1.

89 elial cells, and identify Decorin as a novel neurogenic factor in the central nervous system.

90 strate a novel function of Dmrt5/Dmrta2 as a neurogenic factor in the developing hippocampus.

91 We show that Dmrt5, as well as known neurogenic factors Neurog2 and Pax6, can each not only m

92 Whether neurogenic fate progression necessarily implies fate res

93 Overall, our analysis indicates a loss of neurogenic gene expression and motif accessibility durin

94 ess, activation of pro-proliferative and pro-neurogenic genes (KI67, Nestin, Sox2, and PAX6), reducti

95 ogether with globally enhanced expression of neurogenic genes in undifferentiated hESCs.

96 development, transcription of most essential neurogenic genes is dependent on ARID1A, which can inter

97 ARID1A, whereas transcriptional activity of neurogenic genes is under control by ARID1A, possibly th

98 h factor has opposing effects on established neurogenic genes Neurog2 and Pax6 Dmrt5 is known to supp

99 n, at a subset of genomic regions, including neurogenic genes.

100 d off were rich in transcription factors and neurogenic genes.

101 tin between progenitors and MG, primarily in neurogenic genes.

102 stablished contributor to the progression of neurogenic hypertension and heart failure, yet the under

103 RATIONALE: Neurogenic hypertension is characterized by an increase

104 tem have been involved in the development of neurogenic hypertension, the contribution of ADAM17 has

105 SI, an increased hypothermia is observed in neurogenic hypertension, which is caused by reduced hypo

106 ng to a loss in compensatory activity during neurogenic hypertension.

107 m contributing to neurohumoral activation in neurogenic hypertension.

108 l respiratory drive or during development of neurogenic hypertension.

109 halamus and suggests new strategies to treat neurogenic hypertension.

110 system may be beneficial in the treatment of neurogenic hypertension.

111 The neurogenic hypothesis proposes that MDD is linked to imp

112 e investigate whether a secondary functional neurogenic immune deficiency (spinal cord injury-induced

113 Based upon evidence that susceptibility to neurogenic impact is an important determinant of the sev

114 In MO-treated rats, acupoints showing neurogenic inflammation (termed "neurogenic spots" or Ne

115 precise mechanism underlying this so-called neurogenic inflammation and associated pain has remained

116 l vanilloid 1 (TRPV1) channel contributes to neurogenic inflammation and pain hypersensitivity, in pa

117 ation elicits robust pain behaviours without neurogenic inflammation and produces profound hypersensi

118 ere, we show that an acupoint is one form of neurogenic inflammation on the skin.

119 rigger efferent release of neuropeptides and neurogenic inflammation typically produced by noxious el

120 conduction of these spikes may contribute to neurogenic inflammation while orthodromic (centripetal)

121 llary permeability and blood flow to produce neurogenic inflammation(1,2), but whether nociceptors al

122 inflammatory diseases such as periodontitis, neurogenic inflammation, and inflammatory pain likely vi

123 activation may contribute to periodontitis, neurogenic inflammation, and inflammatory pain.

124 fection, wound healing, periodontal disease, neurogenic inflammation, and inflammatory pain.

125 skin (neurogenic spots), caused by cutaneous neurogenic inflammation, in the dermatome that overlaps

126 fense, drug-induced anaphylactoid reactions, neurogenic inflammation, pain, itch, and chronic inflamm

127 lows bidirectional communication, leading to neurogenic inflammation.

128 nd neuropeptide release, leading to pain and neurogenic inflammation.

129 uous airway inflammation, a process known as neurogenic inflammation.

130 Increased number and size of neurogenic inflammatory acupoints following MO treatment

131 byproducts produces AIMSS-like behaviors and neurogenic inflammatory responses in mice.

132 ted with internal organs may be identical to neurogenic inflammatory spots on the skin, which are pro

133 us the periphery, and targeted inhibition of neurogenic innervation limits post-stroke infection.

134 enteric glia significantly contribute to the neurogenic ion transport while glial activity does not a

135 an extent equal to the direct activation of neurogenic ion transport with veratridine and glial driv

136 an extent equal to the direct activation of neurogenic ion transport.

137 T2+/-) /Cx43(f/f) mice significantly reduced neurogenic ion transport.

138 suppression was sufficient to rescue poorly neurogenic iPSC lines.

139 We show that the adult hippocampal neurogenic lineage is critically dependent on the mitoch

140 lly and transitorily expressed in the dorsal neurogenic lineage that generates glutamatergic juxtaglo

141 The neurogenic locus notch homolog protein (Notch)-2 recepto

142 Lower levels of laminin and neurogenic locus notch homolog protein 1 but higher expr

143 nal cord injury could prevent development of neurogenic lower urinary tract dysfunction, in particula

144 with severe SCI could prevent development of neurogenic lower urinary tract dysfunction.

145 oon be the first causal treatment option for neurogenic lower urinary tract dysfunction.

146 However, the blockade of common sensory neurogenic mechanisms for transient receptor potential (

147 sion, which appears to rely on sodium-driven neurogenic mechanisms.

148 communication route explains how circulatory neurogenic mediators are 'sensed' by NSCs.

149 The lack of convenient neurogenic molecules and neurotransmitters suggests an e

150 hospholipase A(2) (cPLA(2)) derived LOOHs in neurogenic muscle atrophy.

151 proteostasis and contractility properties in neurogenic myopathy in mice.

152 g kg(-1) day(-1) ), starting at the onset of neurogenic myopathy, prevents disruption of autophagic f

153 (2) -adrenoceptor activation in rodents with neurogenic myopathy, which display impaired skeletal mus

154 ophagic flux and contractility properties in neurogenic myopathy, without affecting the cross-section

155 proteostasis and contractility properties in neurogenic myopathy.

156 A specialized neurogenic niche along the ventricles accumulates millio

157 ish a causal role for JNK in the hippocampal neurogenic niche and anxiety behaviour, and advocate tar

158 from dentate CCK interneurons, in regulating neurogenic niche cells and NSCs.

159 s that couples dynamic brain activity to the neurogenic niche in controlling NSC quiescence and hippo

160 thinking, recent evidence suggests that the neurogenic niche in the crayfish DPS lacks self-renewing

161 However, the notion of an adult neurogenic niche is challenged by accumulating evidence

162 te immune system reside in the dentate gyrus neurogenic niche of aged brains in humans and mice.

163 analysis of cell kinetics in the cerebellar neurogenic niche of normal young adult male zebrafish, w

164 Increasing evidence indicates that the adult neurogenic niche of the ventricular-subventricular zone

165 Sox2 signaling pathway as a key component of neurogenic niche sensing, contributing to the regulation

166 Ls, progenitors, and adult-born DGCs via the neurogenic niche that is composed of diverse cell types,

167 contacts with the cellular components of the neurogenic niche that may play a crucial role in the reg

168 cumulation of apoptotic newborn cells in the neurogenic niche that was due not to decreased survival

169 ce between proliferation and survival in the neurogenic niche through the phagocytosis secretome, the

170 newborn neurons within the adult hippocampal neurogenic niche, respectively.

171 and disinhibiting neural circuits within the neurogenic niche, suggesting a potential of GABAergic po

172 nal phagocytes and, in the adult hippocampal neurogenic niche, they remove newborn cells naturally un

173 ndings suggest that in the adult hippocampal neurogenic niche, where the excess of newborn cells unde

174 extracellular matrix (ECM) components in the neurogenic niche.

175 These neurogenic niches are important because they are associa

176 indications from the proteomic analyses that neurogenic niches are significantly stiffer than non-neu

177 Neurogenic niches become less functional with age, but h

178 The presence of active neurogenic niches in adult humans is controversial.

179 single-cell RNA sequencing of young and old neurogenic niches in mice.

180 stages of neuronal differentiation and (ii) neurogenic niches in the brain may constitute additional

181 Differences between neurogenic niches in the phase and degree of S-phase ent

182 Common to neurogenic niches located in diverse brain regions is da

183 the cell division cycle (CDC) in 5 of the 16 neurogenic niches of adult brain, the dorsal telencephal

184 NCE STATEMENT This study establishes that in neurogenic niches of an adult diurnal vertebrate, the ce

185 We conclude that, in neurogenic niches of an adult diurnal vertebrate, the ci

186 demonstrates clonal T cell expansion within neurogenic niches of the aged brain, impairing neurogene

187 tion of HSV-1 with NPCs, which reside in the neurogenic niches of the CNS and play a fundamental role

188 ngly expressed in ependymal cells located in neurogenic niches revealed by the BLBP and PCNA immunost

189 The mammalian brain contains neurogenic niches that comprise neural stem cells and ot

190 o decreased brain cell proliferation in most neurogenic niches throughout the forebrain and the midbr

191 quires understanding of cell kinetics within neurogenic niches using a high-throughput quantitative a

192 ncomitant angiogenesis, a signature of adult neurogenic niches, accelerates the rate of neurogenesis

193 echanisms or by modifying the environment of neurogenic niches, with daily variation in growth factor

194 oglia, and an infiltration of T cells in old neurogenic niches.

195 progenitors during development and in adult neurogenic niches.

196 source for unraveling unique compositions of neurogenic niches.

197 potential of GABAergic potentiators for pro-neurogenic or cell therapies of AD.

198 on, which might explain its problematic anti-neurogenic or cognitive side-effect.

199 Considering that neurogenic oropharyngeal dysphagia is a prevalent condit

200 jects aged between 41 and 75 years old] with neurogenic oropharyngeal dysphagia regardless of gender.

201 eart rate variability (HRV) in subjects with neurogenic oropharyngeal dysphagia.

202 rtensive therapy in patients with coexistent neurogenic orthostatic hypotension and supine hypertensi

203 ist for outcomes in patients with coexistent neurogenic orthostatic hypotension and supine hypertensi

204 otential immediate benefits of treatment for neurogenic orthostatic hypotension and the long-term ris

205 Whereas neurogenic orthostatic hypotension poses risks for falls

206 e, and therapeutic requirements for managing neurogenic orthostatic hypotension that manifests with f

207 degree of supine hypertension when treating neurogenic orthostatic hypotension; the effectiveness of

208 ad antinociceptive activity in both phase 1 (neurogenic pain) and phase 2 (inflammatory pain) of the

209 lin-induced tonic pain, in capsaicin-induced neurogenic pain, and notably in oxaliplatin-induced neur

210 ic niches are significantly stiffer than non-neurogenic parenchyma.

211 These results suggests that non-neurogenic, parenchymal structural plasticity might be m

212 els at which this influence occurs and which neurogenic pathways are involved are not well defined.

213 ted antidepressant effects likely acting via neurogenic pathways, supporting their utility for depres

214 with at least 694 common targets in multiple neurogenic pathways.

215 ortical progenitors and in the length of the neurogenic period during development.

216 rences between the early expansive and later neurogenic periods of cortical development.This article

217 in, Phf21b, which is highly expressed in the neurogenic phase of cortical development and gets induce

218 LGMD2H pathogenesis has proven difficult, as neurogenic phenotypes, independent of LGMD2H pathology,

219 gh SARA knockdown did not lead to detectable neurogenic phenotypes, SARA-suppressed neurons exhibited

220 m cell lines exhibited reproducible aberrant neurogenic phenotypes.

221 ical neurons, but factors that control their neurogenic plasticity remain elusive.

222 tegrity of NSCs, which is critical for their neurogenic potency.

223 ese miRNAs are relevant to the difference in neurogenic potential between these two cell types, we te

224 hNSCs) and human mesenchymal stem cells with neurogenic potential from umbilical cord (UC-MSCs) and p

225 equired for stemness and the preservation of neurogenic potential in concert with dopamine.

226 d iPSCs into neurons and by the reduction of neurogenic potential in control NPCs-expressing shIMPA1.

227 entricular zone (V-SVZ) presents the highest neurogenic potential in the brain of the adult individua

228 The neurogenic potential of adipose tissue - derived human m

229 ne, acts as a niche component to sustain the neurogenic potential of adult NSCs and identify alpha-SY

230 e assay the morphology, cytoarchitecture and neurogenic potential of cV-SVZ.

231 progenitors (mFPPs) that retain efficient DA neurogenic potential over multiple passages and can be c

232 G and RPCs contribute to their difference in neurogenic potential, and that manipulations in miRNAs p

233 ture of canine V-SVZ (cV-SVZ), to assess its neurogenic potential, and to compare our results with th

234 Each part's neurogenic potential, radial glia-like neural stem cells

235 that may be relevant to their differences in neurogenic potential.

236 fferentiation of NSCs without changing their neurogenic potential.

237 ed substantial deficits in proliferation and neurogenic potential.

238 he larval intestine appears to lack resident neurogenic precursors or classical glia marked by sox10,

239 g DG development produces an increase in the neurogenic process, increasing NPCs numbers.

240 ired memory capacity, neural plasticity, and neurogenic processes.

241 ations of crucially important 5-HT-dependent neurogenic processes.

242 We show that early neurogenic progenitors arise from asymmetric divisions.

243 es of perinatal mice contain a population of neurogenic progenitors formed during embryonic developme

244 ppress the reprogramming of Muller glia into neurogenic progenitors is key to harnessing the regenera

245 inhibited, symmetric divisions producing two neurogenic progenitors occur.

246 Further, the resulting neurogenic progenitors show cell biological features dif

247 The generation of neurogenic progeny involves translational repression of

248 cells, progressing through a near-identical neurogenic program.

249 ctors, such as diet and microbiota, regulate neurogenic programs of gut motility(2-5), but the underl

250 urogenesis and differentiation could provide neurogenic programs with flexibility, while allowing for

251 astrocytes, which correlates with decreased neurogenic proliferation of NSCs and upregulation of gen

252 ecifically, stimulating CCK release supports neurogenic proliferation of NSCs through a dominant astr

253 specialized local niche that supports their neurogenic proliferation to produce adult-born neurons t

254 functionally exhibit intrinsic stem-like and neurogenic properties with enhanced rRNA transcription a

255 stabilizer and displays neuroprotective and neurogenic properties.

256 dies have suggested that naloxone attenuates neurogenic pulmonary edema and reverses hypoxemia after

257 anscriptome signatures characteristic of (1) neurogenic radial glia-like cells (resembling neural ste

258 here the expansive neuroepithelial cells and neurogenic radial glial progenitors are coexisting.

259 ons in the adult spinal cord, a noncanonical neurogenic region.

260 We found that Li accumulated in neurogenic regions and investigated the effects on hippo

261 Slc7a5 is present within neurogenic regions during embryogenesis, is found in cul

262 ism by which NSC number is controlled in the neurogenic regions of the adult brain is not fully under

263 umulation of apoptotic cells specifically in neurogenic regions of the CNS, and that microglial phago

264 brain except for ependymal cells and in the neurogenic regions, where SOX9 is also expressed by neur

265 in all major areas of the CNS outside of the neurogenic regions.

266 ession in regions shared with fish including neurogenic regions.

267 The prevailing dogma about neurogenic regulation of vascular tone consists of major

268 Brn1/2/4, which function sequentially in the neurogenic regulatory pathway and are also required for

269 a also suggests that vascular EphA4-mediated neurogenic remodeling adversely affects learning and mem

270 cells using Gi-DREADD impairs behavioral and neurogenic responses to chronic administration of SSRI.

271 In addition, the stimulation of neurogenic spots by electrical, mechanical, or chemical

272 nt study provides experimental evidence that neurogenic spots exhibit all the characteristics of the

273 nts showing neurogenic inflammation (termed "neurogenic spots" or Neuro-Sps) were found both bilatera

274 ns produce hypersensitive spots on the skin (neurogenic spots), caused by cutaneous neurogenic inflam

275 ssion can modulate stem-cell competence in a neurogenic-stage-specific manner to shift neuron product

276 ed expression of Ascl1 in mouse MG induces a neurogenic state in vitro and in vivo after NMDA (N-meth

277 ter past molecular, electrophysiological and neurogenic states when exposed to an earlier-stage envir

278 Idh1(R132H) mutation in the major adult neurogenic stem cell niche causes a phenotype resembling

279 GNIFICANCE STATEMENT The subventricular zone neurogenic stem cell niche generates highly migratory ne

280 ss, identifying them as potential sources of neurogenic stress-induced recruitment of PPG neurons.

281 The neurogenic system promoted effective regeneration by inc

282 As a result, the niche shifted from neurogenic to neuro/astrogenic with increased age.

283 l stage when retinal progenitors switch from neurogenic to terminal patterns of cell division.

284 cently showed that MEIS2 cooperates with the neurogenic transcription factor PAX6 in the control of a

285 rived CMs (PSC-CMs) were transduced with the neurogenic transcription factors Brn2, Ascl1, Myt1l and

286 ecific trajectories reveal the expression of neurogenic transcription factors in early radial glia an

287 rtical neurogenesis, acts as a driver of the neurogenic transition through direct silencing of a sele

288 lved in myogenic, endothelial, metabolic and neurogenic vascular responses to injury.

289 Moreover, this mouthless, neurogenic ventral ectoderm displayed a medial-to-latera

290 on, BP proliferation, neuron production, and neurogenic vs. gliogenic BP cell fate, suggesting that S

291 (E9.5) to E10.5] or late-born (E11.5-E12.5) neurogenic waves, where late-born V3 INs display increas

292 (E9.5) to E10.5] or late-born (E11.5-E12.5) neurogenic waves.

293 iency delays IPC production and prolongs the neurogenic window, resulting in an increased number of n

294 dispersion of newly generated neurons in the neurogenic zone and observe that cells that are physical

295 newly generated dentate granule cells in the neurogenic zone is a required developmental stage for ci

296 e dispersion of newly generated cells in the neurogenic zone is restricted when this coupling is disr

297 l simplicity of accessible human dental pulp neurogenic zone to address this conflict.

298 er birth, by which time most neurites in the neurogenic zone were eliminated, a compact Golgi apparat

299 at this stage, with several neurites in the neurogenic zone.

300 tial patterning of neurogenesis in which non-neurogenic zones form at boundaries and segment centres,