ライフサイエンスコーパス: fetal brain

1 e mouse macrophages after migration into the fetal brain.

2 from maternal l-tryptophan (TRP) reaches the fetal brain.

3 ated with ZIKV infection of the placenta and fetal brain.

4 is also dependent on maternal IL-17a, in the fetal brain.

5 tion predicts that this SNP is functional in fetal brain.

6 mplete genome of ZIKV was recovered from the fetal brain.

7 ic regions regulating gene expression in the fetal brain.

8 Inflammation was not detected in the fetal brain.

9 rses the murine placenta into the developing fetal brain.

10 ution of anatomical and diffusion MRI of the fetal brain.

11 ulted in cell apoptosis and neuronal loss in fetal brain.

12 hogenesis during congenital infection in the fetal brain.

13 ght junction and PLVAP protein expression in fetal brain.

14 of corticopetal interneuron migration in the fetal brain.

15 l migration of GABAergic interneurons in the fetal brain.

16 ceptible cell type for HCMV infection in the fetal brain.

17 l glial-like stem cell enriched in the human fetal brain.

18 rcury have adverse effects on the developing fetal brain.

19 immunologically protected sites such as the fetal brain.

20 ates with early cortical neurogenesis in the fetal brain.

21 ssed in developing neurons in the transgenic fetal brain.

22 perational in (and possibly specific to) the fetal brain.

23 poxia, and neuroproliferative defects in the fetal brain.

24 al dietary choline modulates angiogenesis in fetal brain.

25 ect pharmacological effect to the developing fetal brain.

26 mother will also affect the function of the fetal brain.

27 e detrimental impact on the developing human fetal brain.

28 etus and bound to synaptic structures in the fetal brain.

29 n several human tissues, including adult and fetal brain.

30 t two-hybrid cDNA library derived from human fetal brain.

31 uction of flow to placenta or effects on the fetal brain.

32 expression from a large number of cells from fetal brain.

33 o developmental defects in the cortex of the fetal brain.

34 es that recognize proteins in the developing fetal brain.

35 wide expression profiles in the placenta and fetal brain.

36 ated with immune responses 24 h later in the fetal brain.

37 rements of water diffusion anisotropy in the fetal brain.

38 icroglial and neural progenitor cells in the fetal brain.

39 tant bacteria Staphylococcus simulans in the fetal brain.

40 f nearby CpG sites in whole blood and in the fetal brain.

41 ion of labelled acetyl groups into gestating fetal brains.

42 from 16 human datasets, including adult and fetal brains.

43 earance of live bacteria were found in these fetal brains.

44 200-400 mosaic SNVs per cell in three human fetal brains (15-21 wk postconception).

45 enta (5.25 msec vs 11.25 msec; P < .001) and fetal brain (3.7 msec vs 7.17 msec; P = .02), whereas th

46 c temperature sensors were inserted into the fetal brain, abdomen, bladder, and amniotic fluid of min

47 eath and axonal rarefaction, which phenocopy fetal brain abnormalities in humans.

48 e of placental pathology and relationship to fetal brain abnormalities in pregnancies complicated by

49 and confidence of the prenatal diagnosis of fetal brain abnormalities is improved with iuMRI and ass

50 In utero MRI (iuMRI) detects fetal brain abnormalities more accurately than ultrasono

51 V) infection of pregnant women can result in fetal brain abnormalities.

52 iuMRI remains the optimal tool to identify fetal brain abnormalities.

53 if a future pregnancy were complicated by a fetal brain abnormality.

54 Fetal brain ADC was followed during H-I, immediate reper

55 ans was the predominant bacterial species in fetal brain after hypoxia, but was found in placenta of

56 t that bacteria from the placenta invade the fetal brain after maternal hypoxia.

57 lthough the uptake of radioactivity into the fetal brain after the injection of (11)C-cocaine is lowe

58 ays a pivotal role in the development of the fetal brain and also influences maternal brain function,

59 e developed methods were validated in rabbit fetal brain and amniotic fluid at gestational day 29.

60 signals were averaged over the placenta and fetal brain and converted to the change in R2* (DeltaR2*

61 neural progenitor cells isolated from human fetal brain and derived from human embryonic stem cells

62 NA methylation, and histone modifications in fetal brain and extra-embryonic membranes in the gray, s

63 s transcript was preferentially expressed in fetal brain and fetal sympathetic nervous tissues, and t

64 Fetal brain and liver volumes were measured based on str

65 A methylation increased in choline-deficient fetal brain and liver, and these changes in DNA methylat

66 Additionally, we use publicly available fetal brain and lung meQTL lists to assess enrichment of

67 ental barrier, resulting in infection of the fetal brain and neurological defects including microceph

68 compare in vitro systems to developing human fetal brain and observed strong conservation of in vivo

69 ansversal approaches needed to leverage both fetal brain and organoid resources promise to answer maj

70 mics, and noncoding element activity between fetal brain and organoids have helped identify gene regu

71 aled microcephaly with calcifications in the fetal brain and placenta.

72 n that organophosphate pesticides damage the fetal brain and produce cognitive and behavioral dysfunc

73 egnancy, the virus can target and damage the fetal brain and retina.

74 ulation led to histological abnormalities in fetal brain and subsequent cognitive impairments in adul

75 altered gene expression profiles in the male fetal brain and suggested delayed cortical development.

76 The effect is limited to fetal brain and to this isoform.

77 inked with changes in gene expression in the fetal brain and with human schizophrenia loci.

78 nd AS2 were also preferentially expressed in fetal brain, and all transcripts were regulated by TNFal

79 y, and NO(x) (NO and NO(2)) concentration in fetal brain, and assess neurobehavioral effects on kits

80 induction of IL-6 in the maternal plasma and fetal brain, and disrupted brain development, whereas po

81 activity in vivo, reduce NO concentration in fetal brain, and dramatically ameliorate deaths and numb

82 DL1 is differentially expressed in the human fetal brain, and there is high expression in cerebellum

83 roves diagnostic accuracy and confidence for fetal brain anomalies and leads to management changes in

84 roves diagnostic accuracy and confidence for fetal brain anomalies and leads to management changes in

85 aptively evolving, highly expressed genes in fetal brain are involved in mediating neuronal connectiv

86 ts of prenatal cocaine exposure on the human fetal brain, as well as the cellular and biochemical mec

87 multiple gene expression and DNAm levels in fetal brain at chromosomes 1 and 17 that were associated

88 its labeled metabolites) accumulates in the fetal brain at early times after injection.

89 cell sorting to isolate fetal OPCs from the fetal brain at gestational ages 16-22 weeks, we asked wh

90 cal ventricular/subventricular zone of human fetal brain at the second trimester of gestation and to

91 Naive fetal brains at 70% gestation (E22) were severely defici

92 A digital human fetal brain atlas was developed using previously obtaine

93 In human fetal brain, betaT4 cell densities peak during the latte

94 GPR110 is highly expressed in fetal brains but rapidly decreases after birth.

95 Both exons are excluded from fetal brain, but their default behavior is inclusion, su

96 sed four-dimensional atlas of the developing fetal brain by integrating symmetric diffeomorphic defor

97 If the fetal brain can be scanned at the time of insult, ADC ch

98 berrant migration of immature neurons in the fetal brain caused by maternal alcohol consumption may b

99 t that yeast two-hybrid screening of a human fetal brain cDNA library using p100 as bait revealed spe

100 lcytosine (hmC) maps revealed that hmC marks fetal brain cell genomes at putative regulatory regions

101 in supernatant obtained from virus-infected fetal brain cells were measured simultaneously in microb

102 d cortical neurons closely resembled primary fetal brain cells.

103 ultures of astrocytes or freshly dissociated fetal brain cells.

104 ry of a miR-153 antisense inhibitor to human fetal brain cultures significantly elevated APP expressi

105 elivery in both HeLa cells and primary human fetal brain cultures significantly reduced APP expressio

106 re we use transcriptional profiling of human fetal brain cultures to identify an activity-dependent s

107 Prenatal DE induced a significant fetal brain cytokine response at E18 (46-390% over FA).

108 hogenesis, given its proven association with fetal brain defects in pregnant women and acute neurolog

109 cause of congenital microcephaly and severe fetal brain defects, and it has been associated with oth

110 Fetal brain DeltaR2* was constant across all phases in h

111 Consequently, human fetal brain-derived multipotential CNS progenitor cells

112 nalysis of immunogenicity of human embryonic/fetal brain-derived neural stem cells (hNSCs) and human

113 Our findings define a mechanism that links fetal brain development and adult behavior, demonstratin

114 ommonly observed among US women could affect fetal brain development and ASD risk.

115 chanism by which maternal obesity influences fetal brain development and behavior is not well underst

116 rnal and fetal immune dysfunction may impact fetal brain development and could play a role in neurode

117 of placental function playing a key role in fetal brain development and how this process is altered

118 PPM1D is expressed during fetal brain development and in the adult brain.

119 r placental metabolic pathways in modulating fetal brain development and indicates that maternal-plac

120 Down syndrome (DS) show that alterations in fetal brain development are followed by postnatal defici

121 ignificant changes in DNA methylation across fetal brain development at >7% of sites, with an enrichm

122 m spectrum disorder (ASD), which compromises fetal brain development at critical periods of pregnancy

123 the temporal changes to the epigenome during fetal brain development has, to date, been limited.

124 erleukin-6) that has been shown to influence fetal brain development in animal models was quantified

125 Maternal thyroid hormones are essential for fetal brain development in early gestation.

126 The importance of DNA methylation in fetal brain development is highlighted by the dynamic ex

127 t the influence of steroid hormones on early fetal brain development may be one important early biolo

128 ing its anatomy at different stages of human fetal brain development not only aids in understanding t

129 riable and unpredictable negative effects on fetal brain development ranging in severity from high to

130 he HSA21 genetic factors which contribute to fetal brain development remains incomplete.

131 ensive study of DNA methylation across human fetal brain development to date, confirming the prenatal

132 elopmental changes in DNA methylation during fetal brain development were significantly underrepresen

133 present in women during gestation can alter fetal brain development, and confirm that males are pecu

134 Choline is essential for fetal brain development, and it is not known whether a t

135 ectrum disorders can be rooted very early in fetal brain development, and reinforce evidence-based co

136 ural progenitor cells (NPCs), key players in fetal brain development, are the most susceptible cell t

137 osure during pregnancy causes abnormality in fetal brain development, leading to cognitive dysfunctio

138 a type II transmembrane protein involved in fetal brain development, plays a crucial role in the inv

139 Its association with abnormal fetal brain development, sexual transmission, and lack o

140 iated signaling events at critical stages of fetal brain development, we organize histopathologic, bi

141 issection of the pathways whereby MIA alters fetal brain development, which can shed new light on the

142 terine growth restriction including abnormal fetal brain development.

143 bid methamphetamine and tobacco use on human fetal brain development.

144 ly in the cerebellum and pituitary, early in fetal brain development.

145 to recapitulate early stage, first trimester fetal brain development.

146 ety and complex genetic variations may shape fetal brain development.

147 d hormone production, which is essential for fetal brain development.

148 use easily cross the placenta and can affect fetal brain development.

149 nts and endocrine disruptors that may affect fetal brain development.

150 udy the effects of prenatal METH exposure on fetal brain development.

151 hylation is dynamically altered during human fetal brain development.

152 p to changes in DNA methylation across human fetal brain development.

153 ormonal exposures in pregnancy may influence fetal brain development.

154 and contributes to the maternal influence on fetal brain development.

155 of thyroid hormones, iodine is essential for fetal brain development.

156 Gestational stress (GS) compromises fetal brain development.

157 y a critical role in normative regulation of fetal brain development.

158 r FCDIIB based on HPV16 E6 expression during fetal brain development.

159 e enriched for changes observed during human fetal brain development.

160 4A expression during the second trimester of fetal brain development.

161 l defects and related risks to the fetus and fetal brain development.

162 emia, suggest that THs are crucial for human fetal brain development.

163 and that maternal dietary DHA can influence fetal brain development.

164 n essential nutrient that is critical during fetal brain development.

165 (NMDAR) could have a pathogenic role during fetal brain development.

166 tant life stages and tissues, such as during fetal brain development.

167 that includes highly expressed genes during fetal brain development.

168 In contrast to adults, CW-exposed fetal brains did not show any signs of inflammation or n

169 On postmortem analysis of the fetal brain, diffuse cerebral cortical thinning, high ZI

170 c characteristics of the patient fall within fetal brain disruption sequence, suggesting impaired bra

171 The developing fetal brain DTI database presented can be used for educa

172 gulate the cellular supply of THs within the fetal brain during development.

173 in the hippocampus and frontal lobes of the fetal brain during the last trimester of pregnancy.

174 and tissue destruction can occur within the fetal brain even when there is a marked maternal immune

175 njury, and oligodendroglial loss occurred in fetal brains exhibiting RepReOx than in those without.

176 Finally, we show that neurons in human fetal brain express vimentin concurrently with periods o

177 ion to integrate ADHD and ASD GWAS data with fetal brain expression and methylation quantitative trai

178 Gene expression, brain imaging and fetal brain expression quantitative trait locus studies

179 tlas of the spatiotemporal maturation of the fetal brain extending over the key developmental periods

180 and at 125 days of gestation we obtained the fetal brains for study.

181 In fetal brain from mothers fed a choline-deficient diet, D

182 nces in MRI have made it possible to examine fetal brain functional connectivity.

183 Here we examine how MIA dysregulates rat fetal brain gene expression (at a time point analogous t

184 rtium of bacteria prevented abnormalities in fetal brain gene expression and thalamocortical axonogen

185 However, it is unclear how MIA disrupts fetal brain gene expression in ways that may explain thi

186 risk for ASD by dysregulating key aspects of fetal brain gene expression that are highly relevant to

187 support for the hypothesis that the rate of fetal brain growth is related to the energy turnover of

188 These maps of fetal brain growth patterns construct a spatially specif

189 However, structural variation in the human fetal brain has not yet been investigated.

190 ids engineered to mimic the developing human fetal brain have been employed to model ZIKV-induced mic

191 However, fetal brain hypoxia is a late and sometimes fatal event

192 rowth restriction, evidence of placental and fetal brain hypoxia, and increased circulating cell free

193 perplasia as well as concomitant increase in fetal brain IFN-gamma.

194 e consequent lack of suitable algorithms for fetal brain image analysis.

195 ive KCC2 transcripts in both human adult and fetal brain in addition to the previously identified ful

196 y interconnected with the maternal brain and fetal brain in d 15 pregnant C57BL/6J mice.

197 d increase of IL-6 in response to polyI:C in fetal brain in Disc1-L100P(+/-) mice compared with WT or

198 of the damaging effects of infection on the fetal brain in prenatal studies.

199 profile transcriptional changes in the mouse fetal brain in response to maternal immune activation (M

200 ammals because of the inaccessibility of the fetal brain in the uterine environment and the challenge

201 etal growth restriction and infection of the fetal brain in WT mice.

202 pression of many of our CRS regions in human fetal brain, including 662 novel ones.

203 S-DM in adult brain cells also show DS-DM in fetal brains, indicating early onset of these epigenetic

204 01.10 prevented PTB, neonatal mortality, and fetal brain inflammation.

205 unctions during normal development and after fetal brain injury.

206 We conclude that the fetal brain is a target site for circulating steroid hor

207 influence of inflammation on the developing fetal brain is hypothesized as one potential mechanism b

208 The development of fetal brain is influenced by nutrients such as docosahex

209 The fetal brain is particularly plastic, whereby even subtle

210 The fetal brain is sensitive to a variety of teratogens, inc

211 In human but not mouse fetal brain, LAMC3 is enriched in postmitotic cortical p

212 Purpose To compare the delineation of fetal brain lamination between T2-weighted single-shot f

213 recovery sequence improves visualization of fetal brain lamination compared with the T2-weighted sin

214 We describe the development of fetal brain lesions after Zika virus (ZIKV) inoculation

215 Our observation of ZIKV-associated fetal brain lesions in a nonhuman primate provides a mod

216 gene that is expressed at moderate levels in fetal brain, liver and kidney but has widespread, low le

217 This study attempts to determine which fetal brain magnetic resonance imaging (MRI) features mi

218 tained more than 90% neurons, clustered with fetal brain messenger RNA samples by microarray criteria

219 identification of discrete sites of variable fetal brain methylation associated with schizophrenia ri

220 e the benefit of prenatal rapamycin in a new fetal brain model of TSC.

221 striatum and cerebellum), we found that most fetal brain mQTLs were developmentally stable, although

222 Fetal brain mQTLs were enriched amongst risk loci identi

223 Fetal brain mQTLs were primarily cis-acting, enriched in

224 6-166 d post-conception, identifying >16,000 fetal brain mQTLs.

225 use of this atlas and additional individual fetal brain MRI atlases for completely automatic multi-a

226 Materials and Methods Consecutive fetal brain MRI examinations performed between January 2

227 the reconstruction of three-dimensional (3D) fetal brain MRI have led to significant improvements in

228 letely automatic multi-atlas segmentation of fetal brain MRI.

229 5 for placental histology and measurement of fetal brain mRNA expression of tumor necrosis factor (TN

230 y semi-quantitative PCR from human adult and fetal brain mRNA, we demonstrated that the transcript en

231 associated with higher DNMT3B methylation in fetal brain (N=166, P=2.3 x 10(-26)) and a cis-expressio

232 oreover, knockdown of XRCC1 in primary human fetal brain neurons leads to enhanced sensitivity to men

233 xic, without cardiovascular effects, inhibit fetal brain NOS activity in vivo, reduce NO concentratio

234 ociated 2 was significantly different in the fetal brain of Foxa2 conditional knockout mice compared

235 ain development-related gene pathways in the fetal brains of MIA mice.

236 We studied 20 fetal brains of which 9 were alcohol-exposed, 11 were sa

237 ys 12 to 17 of pregnancy, and then collected fetal brains on embryonic day 17.

238 ignificant differences in DNA methylation in fetal brain or liver samples, rare IVF concepti displaye

239 ASD-associated SNPs are enriched for fetal brain (OR = 3.55; P < 0.001) and peripheral blood

240 influenced expression of ZNF804AE3E4 mRNA in fetal brain (P = .02).

241 intermediate progenitor cells-was reduced in fetal brains (P< 0.01).

242 The DHA-supplemented diet increased fetal brain Pemt(-/-) phospholipid-DHA to WT levels, and

243 tioning and cross the placenta to target the fetal brain, prenatal Hg exposure can inhibit fetal grow

244 missense mutations and mapping to predicted fetal brain promoters and embryonic stem cell enhancers.

245 ting maternal autoantibodies directed toward fetal brain proteins are highly specific for autism.

246 g the presence of autoantibodies reactive to fetal brain proteins in nearly a quarter of mothers of c

247 on, and the accompanying inflammation in the fetal brain, represent a significant risk to the develop

248 between the placenta and maternal brain and fetal brain, respectively.

249 of manifestations in the mouse model is the fetal brain's neural progenitor cell (NPC)-rich subventr

250 at approximately 400,000 sites in 179 human fetal brain samples (100 male, 79 female) spanning 23 to

251 Ls) in a large collection (n = 166) of human fetal brain samples spanning 56-166 d post-conception, i

252 Serial fetal brain scans indicate that the immediate response o

253 the placental barrier, possibly resulting in fetal brain sensitization, as indicated by studies in wh

254 Experimental data on mature human brains and fetal brains show that thicker cortices are consistently

255 ectus was evolving in response to increasing fetal brain size.

256 tion of blood flow in the fetus, part of the fetal brain sparing during acute hypoxaemic stress.

257 Now we know that major components of fetal brain sparing during acute hypoxia are triggered e

258 rmitted investigation of the dynamics of the fetal brain sparing response for the first time.

259 The fetal brain sparing response matures as the fetus approa

260 Despite intense interest into how the fetal brain sparing response may be affected by adverse

261 e decreasing-level enhancer orthologues show fetal-brain-specific enhancer activity.

262 We discover regions of the human fetal brain, such as the frontal cortex, with marked enr

263 he potential to influence rapidly developing fetal brain systems that are commonly altered in neurode

264 etus and would be 1.03-2 times higher in the fetal brain than in other fetal soft tissues.

265 utero leads to microglial activation in the fetal brain that can be monitored in vivo by (11)C-(R)-P

266 The discovery of ZIKV infection in human fetal brain tissue along with serologic confirmation pro

267 ntal disorders, the inaccessibility of human fetal brain tissue during development has hampered effor

268 electrophysiological recordings performed on fetal brain tissue obtained immediately following MRI de

269 ZIKV was found in the fetal brain tissue on reverse-transcriptase-polymerase-c

270 Analysis of human postmortem fetal brain tissue shows that the enzyme mainly responsi

271 Furthermore, in human microcephalic fetal brain tissue, ZikV-NS5 persists at the base of the

272 Particularly, fetal brain tissue-derived ECM supported long-term maint

273 opism for the brain was established in human fetal brain tissue.

274 nSpan Atlas indicate that they most resemble fetal brain tissue.

275 the presence of maternal antibodies against fetal brain tissue.

276 signaling capabilities, have been cloned in fetal brain tissue.

277 genes in lymphoblastoid cell lines and human fetal brain tissue.

278 IKV infects the subventricular zone in human fetal brain tissues and that the tissue tropism broadens

279 , direct evidence of ZIKV infection in human fetal brain tissues remains elusive.

280 or determining vulnerability of the immature fetal brain to hypoxic-ischemic injury and subsequent mo

281 erated from two different tissues (blood and fetal brain) to prioritize genes for >40 complex traits

282 these compounds were found to distribute to fetal brain, to be nontoxic, without cardiovascular effe

283 By screening a fetal brain two-hybrid library with the death domain of

284 her proportion of sequenced transcripts from fetal brain were del-miR-137 transcripts indicating neur

285 The fusion transcripts in fetal brain were enriched for genes for long-term depres

286 Strains of S. simulans from the placenta and fetal brain were equally highly resistant to multiple an

287 xia on blood oxygenation of the placenta and fetal brain were examined by using blood oxygenation lev

288 Dopamine levels in the fetal brain were increased by administering the dopamine

289 a of fixed tissues of second-trimester human fetal brains were acquired and analyzed.

290 subjected to 40-minute uterine ischemia, and fetal brains were investigated for global and focal chan

291 days 12 to 17 (E12-17) of pregnancy and then fetal brains were studied.

292 Cortical cultures derived from normal and DS fetal brains were used to study the role of ets-2 in DS

293 s, derived from a prnp 136VV/171QQ near-term fetal brain, were developed to study sheep scrapie in th

294 scripts are more abundantly expressed in the fetal brain, where, in addition to the full-length struc

295 MeCP2 protein levels are low in fetal brains, where the predominant MECP2 transcripts ha

296 Neuronatin is highly expressed in human fetal brain with gradual decrease in expression in devel

297 , in contrast, there were still areas of the fetal brain with large numbers of actively dividing, tis

298 c predictors of gene expression in the human fetal brain with which we perform transcriptome-wide ass

299 F804A allelic expression in second-trimester fetal brain, with the schizophrenia risk (T) allele asso

300 mmation demonstrated apoptotic cell death in fetal brains within the first 5 days after lipopolysacch