ライフサイエンスコーパス: fetal

1 ha) autoantibodies have been associated with fetal abnormalities and cerebral folate deficiency-relat

2 ohol spectrum disorder (FASD), the result of fetal alcohol exposure (FAE), affects 2-11% of children

3 Fetal alcohol spectrum disorder (FASD), the result of fe

4 Zika virus (ZIKV) infects fetal and adult human brain and is associated with serio

5 we compared the chromosomal architectures of fetal and adult human erythroblasts and found that, glob

6 a of pregnancy, an important risk factor for fetal and maternal morbidity, is considered a global hea

7 nt of eutherian placentation, including both fetal and maternal signals.

8 ernal disease exacerbation and potential for fetal and neonatal complications.

9 Stock and Jenny Myers discuss approaches to fetal and neonatal growth assessment.

10 required for stem cell function in multiple fetal and neonatal tissues, including the nervous system

11 al control of a key growth factor regulating fetal and placental development.

12 e in the control of cell cycle withdrawal in fetal and postnatal myogenic stem cells, and assign to P

13 We lowered the fetal and postnatal n-6/n-3 PUFA ratio exposure in wild-

14 onal differences, which may affect maternal, fetal, and/or neonatal health and physiology.

15 remely rare and complex syndrome of numerous fetal anomalies but should always be borne in the mind d

16 HCMV) is the most common infectious cause of fetal anomalies during pregnancy, development of a vacci

17 effector responses to maintain tolerance to fetal antigens.

18 mines also allow for maintenance of a normal fetal basal metabolic rate despite low fetal insulin and

19 Fetal biometry was assessed by ultrasound at each resear

20 Serial fetal blood sampling (FBS) and intrauterine platelet tra

21 wal of ES cells cultured in media containing fetal bovine serum (FBS) and a glycogen synthase kinase-

22 This article reports the effects of fetal bovine serum (FBS), a physiologically relevant mix

23 m components, as discovered during growth in fetal bovine serum (FBS), elicit a robust increase in th

24 d in media containing human serum (group 1), fetal bovine serum (group 2), StemPro medium (group 3),

25 t a minor fraction of EDA2 was also found in fetal bovine serum.

26 (PDGFRalpha) positive progenitor cells from fetal bovine skeletal muscle and induced into adipocytes

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

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

29 Fetal brain and liver volumes were measured based on str

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

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

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

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

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

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

36 01.10 prevented PTB, neonatal mortality, and fetal brain inflammation.

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

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

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

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

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

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

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

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

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

46 wide expression profiles in the placenta and fetal brain.

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

48 d hypothesised that sildenafil also protects fetal cardiovascular function in hypoxic development.

49 Rs) of the exposure to PM10 and the risks of fetal cardiovascular malformations.

50 with CAKUT; 45% of the patients were severe fetal cases.

51 Analyses of rare human del chr 6p25 fetal cerebella demonstrate extensive phenotypic overlap

52 , diffusion anisotropy within the developing fetal cerebral cortex is longitudinally characterized in

53 y) and mean 37 weeks (late), we compared the fetal cerebral T2* in 28 fetuses without heart defects t

54 Fetal CF-conditioned media distinctly enhanced CM spread

55 Tissue patches containing fetal CFs exhibited higher velocity of action potential

56 plemented with media conditioned by adult or fetal CFs.

57 lar cartilage de novo, entirely substituting fetal chondrocytes.

58 PT) of the fetal pituitary gland, before the fetal circadian system and autonomous melatonin producti

59 ansmitted flavivirus that is associated with fetal CNS-damaging malformations during pregnancy in hum

60 Tian et al. show that cardiomyocytes in the fetal compact layer also contribute to this process, for

61 inning as early as the second trimester with fetal cord blood leptin and stronger association beginni

62 sion and delayed regression of the postnatal fetal cortex (X-zone) were detected in both the SUMOylat

63 ancy microenvironment, revealing a source of fetal CWD exposure prior to the birthing process, matern

64 icomplexan protozoan parasite that can cause fetal damage and abortion in both animals and humans.

65 transcriptome dynamics of human retina from fetal day (D) 52 to 136.

66 evere dengue infection increased the risk of fetal death by about five times (4.9, 2.3-10.2).

67 egnancy resulted in p-aHUS, one intrauterine fetal death occurred, and seven pregancies were uneventf

68 regnancy can cause congenital abnormities or fetal demise.

69 cause devastating congenital abnormities or fetal demise.

70 nal and fetal tissues, and protected against fetal demise.

71 lexes during pregnancy boosted OVA uptake by fetal dendritic cells (DCs).

72 erest as an innate-like B cell population of fetal-derived hematopoiesis, responsible for natural Ab

73 sion (P<0.0001) in the frontal cortex during fetal development and in the temporal-parietal and sub-c

74 s, exposure to FRalpha autoantibodies during fetal development and infancy could contribute to brain

75 we provide evidence that genes facilitating fetal development and nutrient transport display converg

76 long bones has been studied in-depth during fetal development but not postnatally in the epiphysis.

77 at atypical E2Fs promote angiogenesis during fetal development in mice and zebrafish.

78 exposures, including those that occur during fetal development in utero, can cause epigenetic effects

79 ues innervated by vagal motor neurons during fetal development reveal potential sites of HGF-MET inte

80 During fetal development, several cIN subtypes derive from the

81 sm through which maternal stress may disrupt fetal development.

82 terine environment could also interfere with fetal development.

83 ered to be benign with regards to effects on fetal development.

84 ZIKV's neurotropic effects in the course of fetal development.

85 are associated with considerable mortality; fetal diagnosis allows stratification of candidates for

86 They then received intraputamenal grafts of fetal dopaminergic cells, control cerebellar cells, or v

87 Current standard values of fetal dosimetry deriving from (18)F-FDG injection in pre

88 ong-term use of these medications may affect fetal drug exposure by altering BCRP expression in human

89 Fetal dyW-/- muscles display the same number of myofiber

90 RNA sequencing data from both human fetal ear and mouse second branchial arch tissue confirm

91 rly stages of development, but also in later fetal/early neonatal stages of maturation.

92 armacological similarity with drugs of known fetal effect) and empirical data (i.e., derived from Ele

93 when produced from mammalian cells, infects fetal endothelial cells much more efficiently than other

94 red for expression of Wilms' tumour 1 (Wt1), fetal EPDC activation and subsequent differentiation int

95 Disruption of fetal epigenetic programming could explain mercury's neu

96 Given the critical role of BCRP in limiting fetal exposure to drugs and xenobiotics, long-term use o

97 may not preclude the longer-term effects of fetal exposure to lower glucocorticoid levels during obe

98 his higher risk was accounted for in part by fetal exposure to lower maternal IL-8, which also predic

99 RPRETATION: Our study provides evidence that fetal exposure to oral cholera vaccine confers no signif

100 During pregnancy, semiallogeneic fetal extravillous trophoblasts (EVT) invade the uterine

101 at may arise from maternal, placental and/or fetal factors.

102 singleton pregnancies, quantitative vaginal fetal fibronectin and serial transvaginal ultrasound cer

103 ve for screening between 22 and 30 weeks for fetal fibronectin level alone was 0.59 (95% CI, 0.56-0.6

104 s women using serial measurements of vaginal fetal fibronectin levels and cervical length.

105 Fetal fibronectin levels of 50 ng/mL or greater at 16 to

106 e overload leads to the re-expression of the fetal gene program.

107 ient to promote pathological hypertrophy and fetal gene reexpression, while suppression of this pathw

108 cing (Illumina High-Seq 2500), and linked to fetal genotypes assessed by a high density single nucleo

109 silon-globin gene, physically separating the fetal globin genes from the enhancer (locus control regi

110 pression closely mimic those of deleting the fetal globin repressor BCL11A, implicating BCL11A in the

111 system of human fetal testes explants called FEtal Gonad Assay (FEGA) with tissue obtained at 10 and

112 The placenta is the main determinant of fetal growth and development in utero.

113 order to minimize confounding in studies of fetal growth and midlife health outcomes.

114 f energy homeostasis were found to relate to fetal growth and neonatal body composition and thus may

115 leptic drugs (AEDs) used during pregnancy on fetal growth and preterm delivery.

116 es all the nutrients and oxygen required for fetal growth and secretes hormones that facilitate mater

117 tion was available the greater the effect on fetal growth as shown by a reduced prevalence of SGA.

118 factor binding protein (IGFBP)-1 influences fetal growth by modifying insulin-like growth factor-I (

119 de it a high priority to provide the present fetal growth charts for estimated fetal weight (EFW) and

120 In 2006, additional benefits to fetal growth from the pregnancy-specific ration and vita

121 lin-like growth factor 2 (IGF2) is the major fetal growth hormone in mammals.

122 ating to assess impacts on preterm birth and fetal growth in all studies.

123 er interest given the mounting evidence that fetal growth in general is linked to degrees of risk of

124 spective observational longitudinal study of fetal growth in low-risk singleton pregnancies of women

125 ion of the uterine vessels and might improve fetal growth in utero.

126 evidence of the effect of refugee rations on fetal growth is limited.

127 vanced maternal age (AMA) are susceptible to fetal growth restriction (FGR) and stillbirth.

128 n of placental vessel networks in normal and fetal growth restriction (FGR) complicated pregnancies.

129 normal pregnancies and those complicated by fetal growth restriction (FGR).

130 his may be due to conditions associated with fetal growth restriction and iatrogenic preterm birth.

131 We defined fetal growth restriction as a combination of estimated f

132 Severe early-onset fetal growth restriction can lead to a range of adverse

133 Placental sO2 was lower in fetal growth restriction in an angiotensin-converting en

134 e availability causes human diseases such as fetal growth restriction, fetal malformations and cancer

135 logical conditions, including stillbirth and fetal growth restriction.

136 out resulted in reduced placental weight and fetal growth restriction.

137 ted with preterm delivery, low birth weight, fetal growth retardation and developmental defects.

138 ow maternal cobalamin may be associated with fetal growth retardation, fetal insulin resistance, and

139 ough the biological pathways associated with fetal growth to program neurodevelopment.

140 ngly associated with prematurity and reduced fetal growth, an issue of further interest given the mou

141 id hormones are also important regulators of fetal growth, and the present study tested the hypothese

142 al folate deficiency is linked to restricted fetal growth, however the underlying mechanisms remain t

143 In the fully adjusted models, impaired fetal growth, preterm birth, breech presentation and ces

144 placental nutrient transport, and therefore fetal growth, to folate availability.

145 iggered by MSU crystals and leads to reduced fetal growth.

146 and glucose concentrations while suppressing fetal growth.

147 d without known environmental constraints on fetal growth.

148 teroplacental vascular function and increase fetal growth.

149 We examined fetal head turns to visually presented upright and inver

150 inguishing effects of economic conditions on fetal health from effects of economic conditions on sele

151 differentiation and tissue formation during fetal heart development.

152 The fetal heart was visualized outside the chest through a d

153 Fetal hemoglobin (HbF) interferes with this polymerizati

154 ciated with red-blood-cell traits, including fetal hemoglobin levels.

155 More than a third of LAP+ fetal hepatocytes expressed ductal markers.

156 Fetal hepatocytes were isolated using a monoclonal antib

157 The role of fetal hepcidin in the regulation of placental iron trans

158 BAT prior to conception caused maternal and fetal hyperlipidemia, and consequently larger fetuses.

159 KEY POINTS: Chronic fetal hypoxaemia is a common pregnancy complication asso

160 ABSTRACT: Chronic fetal hypoxaemia is a common pregnancy complication that

161 ronic fetal hypoxaemia, late gestation onset fetal hypoxaemia promotes molecular regulation of fetal

162 In contrast to other models of chronic fetal hypoxaemia, late gestation onset fetal hypoxaemia

163 complications of pregnancy, such as chronic fetal hypoxia, trigger a fetal origin of cardiovascular

164 disease in pregnancy complicated by chronic fetal hypoxia.

165 Fetal immunity may play a role in controlling the infect

166 ugh immune activation may also contribute to fetal immunopathology.

167 at least 409000 (UR, 144000-573000) maternal/fetal/infant cases and 147000 (UR, 47000-273000) stillbi

168 system in simultaneously mediating maternal-fetal infection and adverse pregnancy outcomes.

169 lence data to estimate cases of maternal and fetal infection/stillbirth, and infants with invasive GB

170 ve disease in pregnant and postpartum women, fetal infection/stillbirth, and infants.

171 stpartum women, and 57000 (UR, 12000-104000) fetal infections/stillbirths.

172 ormal fetal basal metabolic rate despite low fetal insulin and glucose concentrations while suppressi

173 be associated with fetal growth retardation, fetal insulin resistance, and excess adiposity.

174 tations in pancreatic beta-cells that impair fetal insulin secretion.

175 he syncytiotrophoblast (SCT) at the maternal-fetal interface has been presumed to be the primary driv

176 of proinflammatory cytokines at the maternal-fetal interface that comprises the maternal decidua, pla

177 form for identifying factors at the maternal-fetal interface that contribute to adverse perinatal out

178 sis offers an opportunity for a intrauterine fetal intervention in potentially lethal cases.

179 and uterine hemodynamics with consequential fetal ischemia.

180 Suppression of androgen synthesis in fetal life has been associated with testis maldescent, m

181 has been linked to estrogen exposure during fetal life.

182 Before birth, B cells develop in the fetal liver (FL).

183 ed exclusively during pregnancy by the human fetal liver and initially considered as a weak estrogen.

184 increases steatosis and oxidative stress in fetal liver and is associated with lifetime disease risk

185 Tmod1 leads to enucleation defects in mouse fetal liver erythroblasts, and in CD34(+) hematopoietic

186 mal mitochondrial respiration) caused lethal fetal liver hematopoietic defects and hematopoietic stem

187 Flt3Cre+ KrasG12D fetal liver hematopoietic progenitors give rise to a mye

188 tomes of pre-HSCs, HSCs matured ex vivo, and fetal liver HSCs.

189 Comparison of adult bone marrow to fetal liver lysates demonstrated developmental silencing

190 DHT exposure, regardless of diet, decreased fetal liver Pparg mRNA expression and increased placenta

191 By taking advantage of two fetal liver-derived stromal lines with widely differing

192 tegories, focusing on two distinct outcomes: fetal loss and congenital anomalies.

193 Adverse outcomes were defined as fetal loss or a live infant with grossly abnormal clinic

194 26 (24%) of 107 mothers experienced fetal loss, but never after 29 weeks of gestation or bey

195 ld not be masked post-randomisation and that fetal losses were not divided into stillbirths and misca

196 MCH increased fetal lung expression of the anti-oxidant marker CAT and

197 hypoxaemia promotes molecular regulation of fetal lung maturation.

198 At 138 days, gene expression in fetal lung tissue was determined by quantitative RT-PCR.

199 d in placenta and cord blood at delivery, in fetal lung, and in buccal epithelium and blood during ch

200 IL-8, increased IL-1beta, IL-6, and IL-8 in fetal lung, intestine, and brain, and morphological abno

201 station promotes molecular maturation of the fetal lung, which may be an adaptive response in prepara

202 ly control the mechanical environment of the fetal lung.

203 se-dependent actin cytoskeletal signaling in fetal lungs.

204 n diseases such as fetal growth restriction, fetal malformations and cancer.

205 delay between maternal symptoms and observed fetal malformations following infection has been missing

206 e model, we found that small ruptures of the fetal membrane closed within 72 h whereas healing of lar

207 These alterations occur in normal fetal membranes during late pregnancy, in preparation fo

208 omprises the maternal decidua, placenta, and fetal membranes.

209 en together, these data demonstrate that the fetal metabolism is impacted by maternal factors (cART a

210 multi-fold increase in reported incidence of fetal microcephaly and brain malformations.

211 d with serious sequelae in fetuses, inducing fetal microcephaly and other neurodevelopment defects.

212 Using an established mating paradigm, fetal microchimeric cells present in maternal mice were

213 inic acetylcholine receptor (alpha7nAChR) in fetal microglia will augment their neuroprotective trans

214 Fetal monitoring was by intermittent auscultation.

215 We found that fetal monocyte maturation into AMs was impaired in Cre(+

216 urgery (27.5%), maternal mortality (4%), and fetal mortality (2.5%).

217 ommon, but little is known about its role in fetal mortality.

218 Alternatively, when recombined with fetal mouse lung mesenchyme, the cells recapitulated epi

219 total of 58 patient charts having at least 1 fetal MRI were reviewed.

220 l to generate enough muscle cells to sustain fetal myofiber growth.

221 tyrosine kinase physiologically expressed by fetal neural cells.

222 ylation (H3K4me2) in EPO treated and control fetal neural progenitor cells, identifying 1,150 differe

223 port the role of maternal immune activity in fetal neurodevelopment, exacerbated in part by socioecon

224 ngs form the basis for integrative models of fetal neurodevelopment, which propose that antenatal mat

225 mproved neurobehavioral outcomes and reduced fetal neuroinflammation and long-term microglial activat

226 KV infection and Guillain-Barre syndrome and fetal neurological defects, including microcephaly, has

227 trials in which the intent of treatment was fetal neuroprotection, there was a significant reduction

228 A protective effect was observed for the fetal NOG1 SNP on cleft palate only, opposite in directi

229 covery of haemopoiesis in vivo that mirrored fetal ontogeny.

230 isk of low birth weight (0.68; .29-1.57) and fetal or neonatal death (0.24; .04-1.52).

231 ead to a range of adverse outcomes including fetal or neonatal death, neurodisability, and lifelong r

232 -systemic circulations should be detected by fetal or newborn ultrasound examinations and kept in min

233 el, channelrhodopsin, were isolated from the fetal or postnatal mouse bowel and transplanted into the

234 Completed pregnancies with maternal, fetal, or infant laboratory evidence of possible recent

235 olymorphic HLA-A, -B, and -C determinants of fetal origin are selectively exposed in the ZAM to the m

236 cy, such as chronic fetal hypoxia, trigger a fetal origin of cardiovascular dysfunction and programme

237 progenitor phenotype (CD34(++) CD45(low)) of fetal origin was present in the chorion at all gestation

238 inically translatable therapy for preventing fetal origins of cardiovascular disease in pregnancy com

239 urition, we assessed the timing of birth and fetal outcome in pregnant C57BL/6J mice at 3 months (you

240 studies, demonstrating high rates of adverse fetal outcomes and commonalities in placental phenotype.

241 Maternal and fetal outcomes associated with botulism and botulinum an

242 ate Inpatient Database compared maternal and fetal outcomes between women with and without CHD by usi

243 ociated with subsequent adverse maternal and fetal outcomes, including preeclampsia.

244 tion in pregnancy is associated with adverse fetal outcomes, such as microcephaly and other congenita

245 s associated with the lowest risk of adverse fetal outcomes.

246 on in 67 first trimester human embryonic and fetal ovaries and testis and confirmed by qPCR and immun

247 liferation rates were determined in isolated fetal ovine pancreatic islets in vitro.

248 mones promote beta cell proliferation in the fetal ovine pancreatic islets, and that growth retardati

249 , PAI enables the detection of placental and fetal oxygenation during normal and pathologic pregnanci

250 Accurate analysis of placental and fetal oxygenation is critical during pregnancy.

251 ring pregnancy for normal development of the fetal pancreas.

252 Here, we reconstructed human fetal pancreatic differentiation using cell surface mark

253 The fetal pericardium was absent.

254 Fetal perturbations by OSA during pregnancy impose long-

255 s mediated by the pars tuberalis (PT) of the fetal pituitary gland, before the fetal circadian system

256 Exposure of cultured neurons to fetal plasma or to secretions from the placenta or from

257 There was no effect of MCH on fetal plasma/lung tissue cortisol concentrations, nor ge

258 emia and place it as a critical regulator of fetal programming of adult metabolic disease.

259 eration of late gestation (embryonic day 19) fetal rat hepatocytes is mitogen-independent and that me

260 We applied novel fetal resting-state functional MRI to measure brain func

261 Finally, in primary human fetal retinal pigment epithelium cells, ligand binding t

262 gnostic evaluation to determine maternal and fetal risk but also on how to manage them once they are

263 Composite fetal risk was lowest with LMWH (13%; RAR: 0.3; 95% CI:

264 No significant difference in fetal risk was observed between women taking </=5 mg dai

265 Fetal risk was similar between women taking </=5 mg warf

266 al medium following ingestion of OS by human fetal RPE and ARPE19 cells cultured on Transwell inserts

267 n and metabolite transport in cultured human fetal RPE.

268 commonly prescribed during pregnancy lack a fetal safety recommendation - called FDA 'category C' dr

269 s that are not modified by parity, latitude, fetal sex, or smoking.

270 ing modifying effects of prenatal stress and fetal sex, we found that boys born to mothers with highe

271 Hypothyroidism in fetal sheep induced by removal of the thyroid gland caus

272 , and that growth retardation in hypothyroid fetal sheep is associated with reductions in pancreatic

273 We used a preterm fetal sheep model using both sexes that reproduces the s

274 tion control (CON) (n = 8) and IUGR (n = 13) fetal sheep were catheterized with aortic and femoral ca

275 onal metabolic environment, and thus overall fetal size.

276 investigation of the potential importance of fetal-specific alloreactive immune responses within diso

277 of T regulatory cells led to an increase in fetal-specific proliferation.

278 , thromboembolism, and valve failure, and/or fetal spontaneous abortion, death, and congenital defect

279 In stark contrast, fetal steady-state hematopoiesis at embryonic day (E) 14

280 used an organotypic culture system of human fetal testes explants called FEtal Gonad Assay (FEGA) wi

281 ation, we subjected Sertoli cells from mouse fetal testes to DNaseI-seq and ChIP-seq for H3K27ac.

282 cell hormone INSL3 during culture of 8-9 GW fetal testes with concomitant reduction in expression of

283 can suppress testosterone synthesis in human fetal testicular explants to an extent greater than that

284 s direct endocrine disturbances in the human fetal testis and alteration of the germ cell biology.

285 Essential for fetal testis descent, INSL3 has been implicated in testi

286 nit increase in exposure on the ln-scale) of fetal thrombotic vasculopathy (FTV) both with increasing

287 decidual T cells proliferated in response to fetal tissue, and depletion of T regulatory cells led to

288 can penetrate the placental barrier to enter fetal tissues and is safe for use in pregnant mice.

289 tors, diminished ZIKV burden in maternal and fetal tissues, and protected against fetal demise.

290 nd mTORC2 signaling in multiple maternal and fetal tissues.

291 xygen-induced stress in the heart during the fetal-to-neonatal transition.

292 nes, which could ultimately perturb maternal-fetal tolerance during pregnancy.

293 ion (OR, 0.11; 95% CI, 0.02-0.53), difficult fetal transition (bradycardia [OR, 15.0; 95% CI, 2.19-10

294 umans to diminish the risks of ZIKV maternal-fetal transmission.

295 DNAemia may help to assess the risk of HCMV fetal transmission.

296 Fetal ultrasounds were available from 90% of the mothers

297 Variations in the fetal umbilical or porto-systemic circulations should be

298 ibit a white belly spot, all have persistent fetal vasculature in the eye, and 50% have webbed digit

299 he present fetal growth charts for estimated fetal weight (EFW) and common ultrasound biometric measu

300 th restriction as a combination of estimated fetal weight or abdominal circumference below tenth perc