ライフサイエンスコーパス: fetal brain

1 hogenesis during congenital infection in the fetal brain.

2 ght junction and PLVAP protein expression in fetal brain.

3 of corticopetal interneuron migration in the fetal brain.

4 l migration of GABAergic interneurons in the fetal brain.

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

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

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

8 rcury have adverse effects on the developing fetal brain.

9 immunologically protected sites such as the fetal brain.

10 ates with early cortical neurogenesis in the fetal brain.

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

12 poxia, and neuroproliferative defects in the fetal brain.

13 al dietary choline modulates angiogenesis in fetal brain.

14 ect pharmacological effect to the developing fetal brain.

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

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

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

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

19 generalized increase in D2 mRNAs within the fetal brain.

20 produce DHEA and DHEA-sulfate (DHEAS) in the fetal brain.

21 t MAP-2c is tyrosine-phosphorylated in human fetal brain.

22 of a full length coding WNK3 cDNA from human fetal brain.

23 curin expression has been reported in murine fetal brain.

24 actor receptor 1 (HFGFR1) mRNAs in the human fetal brain.

25 isoform in muscle and paternal expression in fetal brain.

26 radiol and prostaglandin biosynthesis in the fetal brain.

27 placenta, trachea, spinal cord, stomach, and fetal brain.

28 sed in the developing cerebral cortex of the fetal brain.

29 t was very low or absent in normal adult and fetal brain.

30 holine, creatine, and N-acetylaspartate from fetal brain.

31 ry choline intake modulates apoptosis in the fetal brain.

32 rements of water diffusion anisotropy in the fetal brain.

33 icroglial and neural progenitor cells in the fetal brain.

34 tant bacteria Staphylococcus simulans in the fetal brain.

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

36 e mouse macrophages after migration into the fetal brain.

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

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

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

40 wide expression profiles in the placenta and fetal brain.

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

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

43 ic regions regulating gene expression in the fetal brain.

44 Inflammation was not detected in the fetal brain.

45 rses the murine placenta into the developing fetal brain.

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

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

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

49 he 3.0 kb mRNA is expressed at high level in fetal brain; a lower expression level was found in fetal

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

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

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

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

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

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

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

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

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

59 contrast, AC133-1 mRNA was more prominent in fetal brain and adult skeletal muscle but was not detect

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

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 From parallel screens of human fetal brain and HeLa cDNA libraries, we obtained multipl

65 of securin and FGF-2 in the developing human fetal brain and in a fetal neuronal cell line (NT 2).

66 reaction, LHX5 transcripts were detected in fetal brain and in various regions of the adult central

67 Fetal brain and liver volumes were measured based on str

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

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

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

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

72 adioisotope pharmacokinetics in maternal and fetal brain and other organs simultaneously.

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

74 (+) bone marrow precursors that colonize the fetal brain and play a key role in central nervous syste

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

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

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

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

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

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

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

82 is preferentially expressed in total brain, fetal brain, and cerebellum.

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

84 senchymal stem cells from adult bone marrow, fetal brain, and fetal liver.

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

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

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

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

89 FOXP1 and FOXP2 expression patterns in human fetal brain are strikingly similar to those in the songb

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

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

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

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

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

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

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

97 lation was observed in postnatal compared to fetal brain, but alternate polyadenylation did not corre

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

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

100 emonstrated the expression of FOXP2 in human fetal brain by RT-PCR, in the perisylvian area of the le

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

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

103 ith the catalytic domain of Raf from a human fetal brain cDNA library and also found in a variety of

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

105 he heterotrimeric G protein Galphaz, a human fetal brain cDNA library was screened for proteins that

106 ng protein of 110 kDa or Tip110 from a human fetal brain cDNA library.

107 We cloned human RGC-32 cDNA from a human fetal brain cDNA library.

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

109 ransplantation system that allows control of fetal brain cell survival and differentiation by pre-ass

110 d result in more cell death and apoptosis in fetal brain cells cultured in vitro.

111 After uterine ischemia, certain fetal brain cells die immediately, and other cells under

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

113 ultures of astrocytes or freshly dissociated fetal brain cells.

114 d cortical neurons closely resembled primary fetal brain cells.

115 actor (PBF) was not significantly altered in fetal brain compared with adult.

116 Here, it is demonstrated that the human fetal brain contains separate but overlapping epidermal

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

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

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

120 Using human fetal brain cultures, we showed that treatment of these

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

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

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

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

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

126 ve gene expression profiles similar to human fetal brain-derived neural stem cells.

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

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

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

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

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

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

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

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

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

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

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

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

139 This effect on fetal brain development might be caused by the maternal

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

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

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

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

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

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

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

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

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

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

150 dition in which there is a failure of normal fetal brain development, resulting in congenital microce

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

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

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

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

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

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

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

158 hylation is dynamically altered during human fetal brain development.

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

160 ormonal exposures in pregnancy may influence fetal brain development.

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

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

163 Gestational stress (GS) compromises fetal brain development.

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

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

166 4A expression during the second trimester of fetal brain development.

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

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

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

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

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

172 terine growth restriction including abnormal fetal brain development.

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

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

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

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

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

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

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

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

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

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

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

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

185 with inflammation and a 2.8-fold increase in fetal brain expression of IFN-gamma (P = 0.04).

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

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

188 Distribution volume ratios for maternal and fetal brain for (11)C-cocaine were calculated.

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

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

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

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

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

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

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

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

197 that (18)F accumulates in both maternal and fetal brain, heart, and bladder.

198 s minimally attached to O-glycans of NCAM in fetal brain, heart, and the myoblast cell line, C2C12.

199 Pull-down assays with SH2-Grb2 from human fetal brain homogenates, and co-immunoprecipitation of G

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

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

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

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

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

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

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

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

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

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

210 01.10 prevented PTB, neonatal mortality, and fetal brain inflammation.

211 unctions during normal development and after fetal brain injury.

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

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

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

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

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

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

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

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

220 ero hypoxia prevents associated decreases in fetal brain magnesium and suppresses alterations in both

221 Fetal brain magnesium content was decreased (P<0.05) 4 h

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

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

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

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

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

227 Fetal brain mQTLs were enriched amongst risk loci identi

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

229 6-166 d post-conception, identifying >16,000 fetal brain mQTLs.

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

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

232 5 for placental histology and measurement of fetal brain mRNA expression of tumor necrosis factor (TN

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

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

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

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

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

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

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

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

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

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

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

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

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

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

247 creases the expression of PGHS-2 in specific fetal brain regions, and that there is an interaction be

248 in endoperoxide synthase-2 (PGHS-2) in ovine fetal brain regions.

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

250 etal plasma estradiol concentration modulate fetal brain responsiveness to hypotension.

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

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

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

254 Serial fetal brain scans indicate that the immediate response o

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

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

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

258 Using microtransplantation into fetal brain slices and onto dissociated substrate cells

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

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

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

262 The fetal brain sparing response matures as the fetus approa

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

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

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

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

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

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

269 system progenitor cells, isolated from human fetal brain tissue by selective growth conditions, were

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

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

272 cal signaling pathway is altered in human DS fetal brain tissue overexpressing DSCR1, suggest that al

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

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

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

276 the presence of maternal antibodies against fetal brain tissue.

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

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

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

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

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

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

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

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

285 , whereas the Q2S transcript is prominent in fetal brain, undifferentiated neuroblastoma cells, and b

286 t, the ewe and fetus were euthanized and the fetal brain was rapidly recovered, dissected, and frozen

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

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 de that estradiol has a potent action on the fetal brain which is identifiable in the brainstem, cere

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

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

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