ライフサイエンスコーパス: fetal

1 Conclusion Fetal 1.5- and 3.0-T MRI examinations were found to have

2 21 (6%; 95% CI 4-9) of 336 showed fetal abnormalities, of which 12 (4%; 2-6) were adjudica

3 he maternal AChR-Ab positive plasmas reduced fetal AChR currents, but not adult AChR currents, by >80

4 beyond its recently described role in human fetal adrenocortical development.

5 Fetal alcohol exposure (FAE) is the leading preventable

6 r that contributes to the high prevalence of fetal alcohol spectrum disorder (FASD) is binge-like con

7 These include fetal alcohol spectrum disorders (FASDs) with a wide ran

8 rns globally and leads to the development of fetal alcohol spectrum disorders (FASDs).

9 period is recognized for its involvement in fetal alcohol spectrum disorders, but the lack of clear

10 the hypothalamus in a postnatal rat model of fetal alcohol spectrum disorders.

11 gistic interaction between Cdon mutation and fetal alcohol.

12 ties between the gene networks active during fetal and adult gammadelta T-cell differentiation.

13 Fetal and adult hematopoietic stem cells (HSCs) have dis

14 into the peripheral circulation during both fetal and adult life without induction of cell death or

15 atomic pathology and a functional decline in fetal and adult mice.

16 ent microglia remained suspended between the fetal and adult states.

17 cy also increases the risk for other adverse fetal and birth outcomes.

18 ribed by a two-compartment model linked to a fetal and breastmilk compartment.

19 nt study is the first to report a profile of fetal and maternal plasma FA concentrations in a baboon

20 r they were preventable, and their impact on fetal and neonatal outcomes.

21 To fill this knowledge gap, we investigated fetal and neonatal pig pancreas at multiple, crucial dev

22 s and wave 1 medullar follicles during mouse fetal and perinatal oogenesis.

23 uman skeletal muscle tissues from embryonic, fetal, and postnatal stages.

24 congenital infection and infectious cause of fetal anomaly and neurologic injury.

25 glycaemics cross the placenta, so effects on fetal anthropometry could result from direct actions on

26 of NIHF that were defined by the presence of fetal ascites, pleural or pericardial effusions, skin ed

27 ammary administration of two doses of bovine fetal AT-MSCs in healthy cows did not induce changes in

28 rily with a 2.5 x 10(7)-suspension of bovine fetal AT-MSCs on experimental days 1 and 10.

29 ression programs, and these cells acquired a fetal B-1 lymphocyte phenotype in vitro and in vivo.

30 against infection while leaving the maternal-fetal barrier intact.

31 we review the effects of glucocorticoids on fetal basal cardiovascular function and on the fetal car

32 nostic effectiveness of universal ultrasonic fetal biometry in predicting the delivery of a macrosomi

33 influences of the autonomic nervous system, fetal body and breathing movements, and from baroreflex

34 (HFD)-induced maternal obesity can regulate fetal bone development.

35 ol-block-lactide) (mPEG-LA) were unstable in fetal bovine serum, human serum and synovial fluid, with

36 The destabilizing factor in fetal bovine serum, identified as albumin, does not inte

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

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

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

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

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

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

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

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

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

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

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

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

49 200-400 mosaic SNVs per cell in three human fetal brains (15-21 wk postconception).

50 rs), altered maternal blood space, decreased fetal capillary area and an increased recruitment of per

51 r general anesthesia can impact adversely on fetal cardiometabolic health.

52 ate lncRNA, BANCR, is primarily expressed in fetal cardiomyocytes and promotes cell migration.

53 stem-cell-derived cardiomyocytes that mimic fetal cardiomyocytes in vitro to discover hundreds of ER

54 NA (lncRNA) exclusively expressed in primate fetal cardiomyocytes.

55 tal basal cardiovascular function and on the fetal cardiovascular defense responses to acute stress.

56 ate for human clinical translation to rescue fetal cardiovascular dysfunction in risky pregnancy.

57 esthetized with isofluorane and maternal and fetal catheters and flow probes were implanted to determ

58 Minor allele frequencies of two fetal CD46 SNPs were significantly higher in PE.

59 Further, complotypes consisting of fetal CD46 variants and maternal CFH/C3 variants were hi

60 enced two maternal (factor H and C3) and one fetal (CD46) complement genes and identified a total of

61 lation similar to outer radial glia (oRG), a fetal cell type that expands the stem cell niche in norm

62 brain cell types correspond well to similar fetal cell types.

63 em cells, which have several advantages over fetal cell-derived therapies.

64 nhibited Zika infection in both maternal and fetal cells.

65 MRI) techniques to determine whether reduced fetal cerebral substrate delivery impacts the brain glob

66 great arteries (TGA), diagnoses with lowest fetal cerebral substrate delivery; "CHD-other," with oth

67 Historically, fetal circadian rhythms have been considered irrelevant

68 ammatory cytokine levels in the maternal and fetal compartments and causes behavioral changes in offs

69 ploidies were detected in both placental and fetal compartments.

70 ciated with significantly increased maternal-fetal complications during the index admission [odds rat

71 Our PBK model described the measured fetal concentrations of parent compounds and metabolites

72 regional patterns of gene expression in the fetal cortex across gestation (n = 156 samples from 16 b

73 ncy outcomes, including rates of stillbirth (fetal death >=24 weeks' gestation), preterm and cesarean

74 h weight (aOR, 1.91; 95% CI, 1.33-2.76), and fetal death (aOR, 2.23; 95% CI, 1.14-4.37).

75 birth weight, small-for-gestational-age, and fetal death as well as microcephaly (i.e., overall and d

76 ne growth restriction, low birth weight, and fetal death, but findings are limited by suboptimal cont

77 birth weight, small-for-gestational-age, or fetal death.

78 Expectant management is favored if risk of fetal demise exceeded 12% or probability of biventricula

79 ppropriate patient selection and low risk of fetal demise with FAV are critical factors for obtaining

80 logical effects, including tissue damage and fetal demise.

81 GenX alters fetal development and antibody production and elicits to

82 Germ cells specified during fetal development form the foundation of the mammalian g

83 structed segment of the uterus and supported fetal development to term and live birth.

84 ne hippocampus presents many similarities in fetal development, anatomy, and physiology with human hi

85 astating consequences on pregnancy outcomes, fetal development, and maternal health.

86 are important in driving several aspects of fetal development, including muscle fibre differentiatio

87 pig placentae grow heavily, on placental and fetal development.

88 otin-transport mechanism and is critical for fetal development.

89 l environment to sperm, potentially altering fetal development.

90 lead to pregnancy complications and impaired fetal development.

91 ensatory growth of the placentae to maintain fetal development.

92 of birth, and how they are coordinated with fetal developmental programs.

93 probability of transplant-free survival from fetal diagnosis to age 6 years and postnatal restricted

94 d found that UDCA ameliorates ICP-associated fetal dyslipidemia.

95 surements of blood flow are scarcely used in fetal echocardiography due to technical assumptions and

96 nstrated on other data sets, including human fetal echocardiography, chick embryonic heart ultrasound

97 sociated with reduced birth weight through a fetal effect (p = 2.2 x 10-3).

98 We also found that fetal-enhancer regions methylated by Dnmt3a and Dnmt3b w

99 lore the contribution of shared genes and/or fetal environment to brain development.

100 l circulation significantly affects maternal-fetal exchange and thereby, fetal growth.

101 Further, it may provide a biomarker for fetal exposure to maternal smoking.

102 with surrounding maternal cells and invading fetal extravillous trophoblasts (EVT).

103 by transfer of chromatin from swine primary fetal fibroblasts, which were edited with TALENs and sin

104 ngs, stomach and liver, are derived from the fetal foregut through a series of inductive interactions

105 tion factor 4 (ATF4) as a novel regulator of fetal gamma-globin gene expression in human cells by rep

106 ion of the Clu(+) regenerative program and a fetal gene expression signature marked by Sca1, but upon

107 odelling was evident by the re-expression of fetal genes and coronary artery perivascular fibrosis, w

108 d the relative contributions of maternal and fetal genetic effects behind these observed associations

109 c instruments, we estimated the maternal and fetal genetic effects underlying the observed associatio

110 However, maternal and fetal genetic factors and the molecular mechanisms remai

111 maternal adaptation in early pregnancy than fetal genetics.

112 Fetal genotyping demonstrated that 70% of samples with H

113 entified transcriptional heterogeneity among fetal germ cells that included an apoptosis-susceptible

114 Our results indicate that the fetal germ-cell fate is based on discrete cell-heritable

115 We studied fetal germ-cell fates and discovered that both apoptosis

116 rrect a defective beta-globin gene or induce fetal globin (HbF) for patients with beta-hemoglobinopat

117 previously known to be silenced by CHD4, the fetal globin genes are exposed here as among the most se

118 we define the interactome of MIWI2 in mouse fetal gonocytes undergoing de novo genome methylation an

119 s that have been less studied in relation to fetal growth (i.e., Mo, Sb, Sn).

120 nal growth, and the importance of monitoring fetal growth and maternal glycaemic control when treatin

121 vation is a potential strategy for improving fetal growth and raising uterine artery blood flow in pr

122 ies of birth weight investigating effects of fetal growth on later-life cardiometabolic disease becau

123 es as instrument and examined the effects of fetal growth on pregnancy outcomes, maternal BP, and glu

124 Flaring and fetal growth outcomes were not significantly associated.

125 nsight into etiologic mechanisms of abnormal fetal growth outcomes.

126 Fetal growth restriction (FGR) and pre-eclampsia are sev

127 Fetal growth restriction (FGR) is a significant risk fac

128 Fetal growth restriction (FGR) is the major single cause

129 d with adverse pregnancy outcomes, including fetal growth restriction (FGR), due in part to reduction

130 by AICAR partially prevented hypoxia-induced fetal growth restriction (P < 0.01), due in part to incr

131 on effect of diabetes on oogenesis, leads to fetal growth restriction and congenital deformities.

132 he placental villous tissue occurred in both fetal growth restriction and pre-eclampsia, whereas CD79

133 Pre-eclampsia and fetal growth restriction arise from disorders of placent

134 de is associated with a greater incidence of fetal growth restriction due, in part, to lesser uterine

135 factor for preterm birth, preeclampsia, and fetal growth restriction.

136 l mechanistic link between pre-eclampsia and fetal growth restriction.

137 e outcomes of human pregnancy complicated by fetal growth restriction.

138 ms to PolyI:C during early pregnancy reduced fetal growth trajectories throughout gestation, concomit

139 a its vasoactive properties, may protect the fetal growth under hypoxic conditions by improving utero

140 se birth weight is only a crude indicator of fetal growth, and the choice of genetic instrument (mate

141 s that metal exposures contribute to reduced fetal growth, but little is known about the effects of c

142 o transfer can impair early placentation and fetal growth, but this effect normalizes by term.

143 stems A and L, thought to contribute to poor fetal growth.

144 infiltration was only apparent with reduced fetal growth.

145 affects maternal-fetal exchange and thereby, fetal growth.

146 ing essential treatment because of potential fetal harm risks a poor outcome for both mother and chil

147 seful therapeutic agent to protect the human fetal heart against IR injury, as may occur in complicat

148 nd quantification of blood flow in the human fetal heart and major vessels.

149 Therefore, the isolated fetal heart has intrinsic variability and carries a memo

150 Fetal heart rate variability (FHRV) emerges from influen

151 roduce a technique to test whether intrinsic fetal heart rate variability (iFHRV) exists and we show

152 liveries, epidural analgesia, non-reassuring fetal heart rate, meconium in the amniotic fluid, should

153 had a gestational age of 22 weeks or more, a fetal heart sound at time of admission, and consented to

154 Exclusion critiera at admission were no fetal heartbeat heard or imminent birth.

155 codes an RNA-binding protein associated with fetal hematopoietic gene expression programs, and these

156 nctions were due to an intrinsic property of fetal hematopoietic stem and precursor cells (HSPCs) cau

157 Fetal hemoglobin (HbF) can blunt the pathophysiology, te

158 aturally occurring hereditary persistence of fetal hemoglobin (HPFH) mutations, editing of transcript

159 s diminishes CHD4 levels and derepresses the fetal hemoglobin genes.

160 would be survivable once the nonpolymerizing fetal hemoglobin has been replaced by adult hemoglobin S

161 in level of 9.0 g or more per deciliter or a fetal hemoglobin level of 20% or more after 24 months.

162 O(2)-independent antisickling properties of fetal hemoglobin.

163 iogenic signaling in mouse lung EC and human fetal HPMEC.

164 itro, the addition of MC(TC)LUVA potentiated fetal human pulmonary microvascular endothelial cell int

165 rriers, for example, the placenta, enhancing fetal humoral immunity to levels similar to their mother

166 ity of clinical manifestations, ranging from fetal hydrops and symptomatic anemia requiring lifelong

167 RV originates in fetal life and that chronic fetal hypoxia significantly alters it.

168 hypothesis that iFHRV is affected by chronic fetal hypoxia, one of the most common adverse outcomes o

169 by placental insufficiency, which results in fetal hypoxia.

170 acterized by uteroplacental ischaemia and/or fetal hypoxia.

171 acterized by uteroplacental ischaemia and/or fetal hypoxia.

172 In mice, the maternal microbiome influences fetal immune development and postnatal allergic outcomes

173 High-dose HIG may prevent fetal infection and disease and is associated with the r

174 Maternal viremia predicts fetal infection and neonatal outcome.

175 nd rate of placental infection and conferred fetal infection, in contrast to ZIKV M1404, which was no

176 virus strains during pregnancy can result in fetal infection.

177 Four factors predicted fetal infection: a 1.8-fold increase (30% vs 56%) in the

178 Of all primary maternal infections and fetal infections in the first trimester, 88% (29/33) and

179 ILCs have been found at the maternal-fetal interface and we therefore investigated the potent

180 he immune population present at the maternal fetal interface by modifying the cytokine profile produc

181 t a model wherein IFNs local to the maternal-fetal interface direct novel IL-15-responsive macrophage

182 ed to respond to IL-15 at the early maternal-fetal interface have been NK cells.

183 acental syncytiotrophoblasts at the maternal-fetal interface release nanoparticles, including extrace

184 At the maternal-fetal interface, density of placental mononuclear leukoc

185 ics that mirror IFN activity at the maternal-fetal interface.

186 ental inflammatory signaling at the maternal-fetal interface.

187 Mucosal immunity develops in the human fetal intestine by 11-14 weeks of gestation, yet whether

188 ed to preserve placental iron in the face of fetal iron deficiency.

189 the fetal liver but its role in controlling fetal iron stores is not understood.

190 tal nephron and ureteric epithelium in human fetal kidney, we show here that, while existing nephron-

191 s the first evidence that iHRV originates in fetal life and that chronic fetal hypoxia significantly

192 from the predominant utilization of glucose (fetal life) to the use of lipids (postnatal life).

193 t represent a reversion of a given cell to a fetal-like epigenetic and transcriptional state.

194 HAMP is also expressed in the fetal liver but its role in controlling fetal iron store

195 Thus, fetal liver HAMP operates cell-autonomously to increase

196 in the placenta is not actively regulated by fetal liver HAMP under normal physiological conditions.

197 n of prehematopoietic stem cells (pre-HSCs), fetal liver HSCs, and adult bone marrow HSCs.

198 ent has been shown to cause a severe loss of fetal liver HSCs; however, the underlying mechanisms and

199 Manipulation of RLR expression in mouse fetal liver HSPCs indicated functional conservation amon

200 HAMP operates cell-autonomously to increase fetal liver iron stores.

201 We apply this method in mouse fetal liver, and identify de novo cell-type-specific chr

202 ith down-regulation of PU.1 and GATA2 in the fetal liver, impeding a key step required for commitment

203 state in the adult bone marrow and embryonic fetal liver, the mechanism of HSC self-renewal has remai

204 rterial clusters (IAC) before colonizing the fetal liver.

205 natal mortality (0.86 [0.73-1.00], p=0.048), fetal loss (infant death after 16 weeks' gestation and b

206 double ovulate as an insurance against early fetal loss, but to never bear twins.

207 (TC)s to affect vascular organization during fetal lung development was tested in mouse lung explant

208 n Src-1/-2 double-deficient (Src-1/-2(d/d) ) fetal lungs, compared to WT.

209 tuses, was markedly reduced in Src-1/-2(d/d) fetal lungs.

210 We applied innovative fetal magnetic resonance imaging (MRI) techniques to det

211 We reviewed the fetal magnetocardiography database from the University o

212 The purpose of our study was to use fetal magnetocardiography to characterize the electrophy

213 versus 72% (95% CI, 61%-82%) with expectant fetal management, resulting in a restricted mean transpl

214 medium-term survival benefit over expectant fetal management.

215 Here, we show that human and mouse fetal MCs phenotypically mature through pregnancy and ca

216 orphology was identified in pockets of human fetal meconium at mid-gestation by scanning electron mic

217 ved conditioned media supernatant effects on fetal membrane weakening were analyzed.

218 In human fetal membranes (FM) collected immediately after birth f

219 to congenital Zika syndrome (CZS), including fetal microcephaly.

220 ibly prevent adverse events through enhanced fetal monitoring and targeted induction of labor.

221 ro approaches are compromised by spontaneous fetal motion.

222 Loss of beta-catenin in fetal mouse mesoderm causes loss of Tbx4(+) tracheal mes

223 In the fetal mouse testis, PIWI-interacting RNAs (piRNAs) guide

224 and Methods In this retrospective study, all fetal MRI examinations performed with 1.5- and 3.0-T sca

225 A total of 3247 fetal MRI scans were included, with 2784 (86%) obtained

226 an does MRI performed at 1.5 T; however, for fetal MRI, there are concerns about the potential for gr

227 control in a manner that is detectable with fetal MRI.

228 ernal monocyte/macrophages, neutrophils, and fetal myeloid cells contained viral RNA and infectious v

229 the fetus was not the result of an impaired fetal myeloid response or breakdown of the placental bar

230 s expressed on myocytes during embryonic and fetal myogenesis and on nascent myofibers during muscle

231 ptake and signaling were measured ex vivo in fetal (n = 5-8/group) and juvenile (n = 8/group) offspri

232 To examine the effects of OSB on fetal neocortex development, we analyzed human fetuses o

233 st antimicrobials reviewed, adverse maternal/fetal/neonatal outcomes were not observed consistently.

234 abstracted data on maternal, pregnancy, and fetal/neonatal outcomes.

235 tional networks and cell types pertinent for fetal neuro-gliogenesis.

236 on of the maternal gut microbiome influences fetal neurodevelopment in mice.

237 Circulating fetal nucleated cells (CFNCs) have shown potential in no

238 ules in the maternal serum and the brains of fetal offspring.

239 Fetal or neonatal abnormalities were classified as a maj

240 ernal or perinatal outcome (either maternal, fetal, or neonatal death, or severe morbidity for the mo

241 Here we have shown that the fetal origin of asthma is orchestrated by a disrupted ai

242 d DNA methylation in Ppargc1a promoter had a fetal origin; elevated DNA methylation was also detected

243 ew model will be useful for further studying fetal outcomes and potential therapeutics for the preven

244 cribe clinical characteristics, maternal and fetal outcomes, and cardiovascular readmissions in a coh

245 , which occurs from anterior to posterior in fetal ovaries.

246 c or aplastic A1 arteries and hypoplastic or fetal PCoA, perpendicular height, width, neck diameter,

247 ned the presence of hypoplastic, aplastic or fetal PCoAs, vertebral dominance, and diameters and angl

248 heir precursors occupy distinct areas in the fetal period and that they and their progeny maintain th

249 perinatal environmental factors and maternal/fetal phenotypes.

250 Maternal progesterone administration altered fetal pituitary and testicular function in ovine male fe

251 The importance of fetal placental macrophages (Hofbauer cell [HCs]) is und

252 fetus, any compromise in the development of fetal-placental circulation significantly affects matern

253 tational age-related changes in maternal and fetal plasma FA concentrations.

254 ed obesity may be associated with decreasing fetal pre-osteoblastic cell differentiation, under epige

255 Thus, the restricted fetal preimmune repertoire contains potentially benefici

256 progesterone supplementation would increase fetal progesterone, affect progesterone target tissues i

257 er investigation as a candidate strategy for fetal protection and delay of preterm birth elicited by

258 d blood cellular folate, homocysteine, alpha fetal protein cholesterol, triglycerides, prothrombin ti

259 ia nervosa associated genes in the adult and fetal raphe and ventral tegmental areas.

260 Dissociated fetal rat testes were xenotransplanted subcutaneously in

261 rogesterone target tissues in the developing fetal reproductive system and be metabolised to other bi

262 lacentas to explore maternal, placental, and fetal responses to alterations in iron status during pre

263 at cells exhibiting characteristics of human fetal satellite cells can be produced in vitro from iPSC

264 We therefore analyzed the lipid profile of fetal serum from untreated ICP, UDCA-treated ICP and unc

265 This suggests that there may be fetal sex specific effects of the use of progesterone in

266 ochondrial biogenesis in human placenta in a fetal sex-dependent manner, including decreased histone

267 n = 11-12) and IUGR (n = 12) late gestation fetal sheep.

268 velopment could provide new insight into the fetal shifts that occur in the diseased heart and unveil

269 elivery, we collected samples from placenta (fetal side) and measured DNA methylation using Illumina

270 no acid uptake and protein synthesis in IUGR fetal skeletal muscle.

271 of mitochondrial density and ETS proteins in fetal skeletal muscle.

272 cell RNA sequencing and direct comparison to fetal specimens suggest that the skin organoids are equi

273 -1 (isolated from aborted and stillborn goat fetal spleens).

274 f the human brain occur in the embryonic and fetal stages-stages that are difficult to access and inv

275 ether dissociation and reconstitution of rat fetal testis tissue during the MPW can be used to model

276 ation in the ovary but remains absent in the fetal testis.

277 ent metabolites promoted axon outgrowth from fetal thalamic explants.

278 ow that the maternal gut microbiome promotes fetal thalamocortical axonogenesis, probably through sig

279 these metabolites abrogated deficiencies in fetal thalamocortical axons.

280 ogy of OSB and support the need for an early fetal therapy (i.e., in the first trimester of pregnancy

281 conclusion, our data indicate that the human fetal thymus generates, in an HSPC/Lin28b-dependent mann

282 Fetal thyroid hormone deficiency reduced oxidative phosp

283 ariable, in part owing to the limitations of fetal tissue as a cell source, relating to its availabil

284 However, the outcomes of fetal tissue-derived cell transplants in individuals wit

285 o compensate for the limited availability of fetal tissue.

286 Previously, VZV and HCMV models used fetal tissue; here, we developed an adult human skin mod

287 Current models rely heavily on fetal tissues, can be prohibitively expensive, and are o

288 In a small dataset of human adult and fetal tissues, RP protein levels showed development stag

289 in cardiomyocytes as the heart transits from fetal to adult states.

290 al, rather than precipitous, transition from fetal to adult transcriptional states.

291 ived myogenic progenitors to an embryonic-to-fetal transition period.

292 of an exogenous nonprimary CMV infection and fetal transmission.

293 Modeling maternal-fetal transport in FcgammaR/FcRn humanized mice confirme

294 FcRn binding as a means to improve maternal-fetal transport of IgG.

295 fter birth and in some cases before birth by fetal ultrasound.

296 e nasal sector of the optic disc, remnant of fetal vasculature on the optic disc (Bergmeister's papil

297 Here we report that the fetal version of HNF4alpha is required for HGP in the ad

298 Conclusion Assessment of intraplacental fetal vessels with other MRI descriptors improved the ab

299 Sex-dependent differences in fetal weight, placenta histoarchitecture, and the placen

300 he choice of genetic instrument (maternal or fetal) will greatly influence the interpretation of the