ライフサイエンスコーパス: fetus

1 1 were twins, and 2 were triplets (304 total fetuses).

2 enta is essential for the development of the fetus.

3 g devastating consequences to the mother and fetus.

4 vertical transmission of virus occurs to the fetus.

5 ot linked to structural abnormalities in the fetus.

6 cts the delivery of iron to the placenta and fetus.

7 egnancy loss or vertical transmission to the fetus.

8 and mortality incurred on the mother and the fetus.

9 y impact every maternal organ system and the fetus.

10 genomic features linked with survival in the fetus.

11 nd its management might adversely affect the fetus.

12 PUFAs from maternal liver to the developing fetus.

13 that may be pro-arrhythmic in the developing fetus.

14 tes during pregnancy for both the mother and fetus.

15 ells (NPCs), the major cells infected in the fetus.

16 resulted in increased ZIKV infection in the fetus.

17 t have adverse consequences for a developing fetus.

18 fit cells proceed through development of the fetus.

19 efficient delivery of oxygen from mother to fetus.

20 sporting oxygen and nutrients to the growing fetus.

21 ct development of the decidua, placenta, and fetus.

22 ancy and ensuring adequate blood flow to the fetus.

23 jor pro-inflammatory cells in the developing fetus.

24 onatal immunity via antibody transfer to the fetus.

25 contributors to placental FA transfer to the fetus.

26 ble pre-thymic precursors in the early human fetus.

27 erms of ability to transfer nutrients to the fetus.

28 vels may be insufficient for both mother and fetus.

29 A), but it is not clear if UDCA protects the fetus.

30 involve radiation exposure to the mother and fetus.

31 ced accumulation of maternal antibody in the fetus.

32 yndrome (PAPPAS) in one available homozygous fetus.

33 by increasing the delivery of glucose to the fetus.

34 nancy is harmful for both the mother and her fetus.

35 sses critical blood flow to the placenta and fetus.

36 tercellular signaling networks in the unborn fetus.

37 lacentas, inducing defects in the developing fetus.

38 ysician concerns about potential risk to the fetus.

39 chanism for IgG from maternal circulation to fetus.

40 d purpose: the development and growth of the fetus.

41 and oxygen can be extracted for the growing fetus.

42 ibility of chromatin in the developing mouse fetus.

43 tabolised to other bioactive steroids in the fetus.

44 placental-brain axis of the developing mouse fetus.

45 ower in hindlimb skeletal muscle of the IUGR fetus.

46 noculated pregnant rhesus macaques and their fetuses.

47 ng gestation to improve outcomes in affected fetuses.

48 oitum (dpc) Src-1(-/-) /-2(-/-) (dKO) vs. WT fetuses.

49 l data on neocortex development of human OSB fetuses.

50 circulating 11-dehydrocorticosterone in male fetuses.

51 y (5 of 9, 56%) of animals and some of their fetuses.

52 oncentrations were lower in male than female fetuses.

53 age, and both MCs and IgE are detectable in fetuses.

54 esis underlying the neuronal decrease in OSB fetuses.

55 nvestigated such light exposure on gestating fetuses.

56 est hinders the formation of highly chimeric fetuses.

57 in relation to the growth of female and male fetuses.

58 nes were upregulated in female, but not male fetuses.

59 were more likely to have female versus male fetuses.

60 ndent protein kinase II-were activated in MO fetuses.

61 l cyclopic trisomy 18 and anencephalic human fetuses.

62 uitary and testicular function in ovine male fetuses.

63 ast to ZIKV M1404, which was not detected in fetuses.

64 nesis underlies the neuronal decrease in OSB fetuses.

65 etection of chromosomal abnormalities in the fetus(1,2).

66 ally the case, we examined tissue from human fetuses (13 weeks gestation) that carried the Huntington

67 ch outcomes had been reported, 93 infants or fetuses (2%) had brain or eye defects.

68 spective study, BOLD MRI was performed in 86 fetuses (56 healthy fetuses and 30 fetuses diagnosed wit

69 st one DNA sample (from either parent or the fetus), 69 (13%) trios had a clinically relevant abnorma

70 ling to meet the ever-growing demands of the fetus - a process which is deficient in preeclampsia.

71 of trophoblast p110alpha resulted in viable fetuses, abnormal placental development and a failure of

72 Stillbirth is the loss of a fetus after 22 weeks of gestation, of which almost half

73 rnal neutralizing antibodies in utero to the fetus after maternal immunization.

74 g mice, particularly pregnant mice and their fetuses, against high-dose lethal ZIKV challenge.

75 nique must account for potential risk to the fetus and altered test accuracy (sensitivity and specifi

76 eased transfer of maternal bile acids to the fetus and an increased incidence of sudden fetal death.

77 Transferred NR1 ABs enriched in the fetus and bound to synaptic structures in the fetal brai

78 by certain bacteria, viruses, parasites, the fetus and cancer cells to induce tolerance to allogeneic

79 report a role for MCs within the developing fetus and demonstrate that fetal MCs may contribute to a

80 he interface of the transplanted uterus, the fetus and maternal circulation might provide valuable no

81 Dietary protein is vital for fetus and mother but the effects of protein undernutriti

82 ophylaxis prevents haemolytic disease of the fetus and newborn.

83 tially resulting in hemolytic disease of the fetus and newborn.

84 ts are known to pose risks to the developing fetus and only limited safety data are available for oth

85 nocytogenes colonization of the placenta and fetus and that this protection is due to both maternal a

86 facilitate communication between the embryo/fetus and the mother.

87 innate immune cells within the placenta and fetus and whether these cells influenced virus vertical

88 etry could result from direct actions on the fetus and/or placenta.

89 MRI was performed in 86 fetuses (56 healthy fetuses and 30 fetuses diagnosed with CHD) between 22 an

90 ansfer resulted in similar incidence of live fetuses and abortions, and no changes in placental size.

91 across a wide range of exposures; developing fetuses and breastfeeding infants may be particularly vu

92 creased during maternal hyperoxia in healthy fetuses and fetuses with CHD, but it was higher in SV CH

93 a increased placental oxygenation in healthy fetuses and fetuses with congenital heart disease, and i

94 hyperoxia changed with GA in healthy control fetuses and fetuses with SV or AO CHD (DeltaR2* per week

95 onstant across all phases in healthy control fetuses and fetuses with TV CHD but increased during mat

96 he contributory causes of death in stillborn fetuses and in deceased neonates and children younger th

97 sis approaches in living and nonliving human fetuses and in prematurely born neonates have provided i

98 th or neonatal death occurred in 393 of 1532 fetuses and infants (25.7%) and in 444 of 1519 fetuses a

99 tuses and infants (25.7%) and in 444 of 1519 fetuses and infants (29.2%), respectively (relative risk

100 The placenta mediates nutrient delivery to fetuses and its function is impaired as a result of MO.

101 ta-cell areas were observed in pancreases of fetuses and neonates from prepregnant HF-fed dams.

102 natal hepatic inflammation in late gestation fetuses and neonates.

103 Brain or eye defects in infants and fetuses and other adverse pregnancy outcomes were identi

104 By use of WES of the fetuses and parents (parent-fetus trios), we identified

105 In the embryo, fetus, and adult, intestinal Hh signaling is paracrine:

106 s required for sexual differentiation in the fetus, and in adult females AMH is produced by growing o

107 e pluripotent inner cell mass that forms the fetus, and the outer trophectoderm layer that forms the

108 l cyclopic trisomy 18 and anencephalic human fetuses, and of normal fetal, newborn, and adult humans.

109 sed in areas of active neurogenesis in human fetuses, and sox4 knockdown in Xenopus embryos diminishe

110 ation similarly in IGF-1-treated and Control fetuses, and the relationships between coronary flow and

111 fer oxygen and nutrients from mother, to the fetus, any compromise in the development of fetal-placen

112 ctively; alleles raising birth weight in the fetus are associated with shorter gestational duration a

113 Morbidity and mortality for mother and fetus are strongly associated with etiology of liver fai

114 l identity and axonal selectivity when mouse fetuses are exposed to excess omega-6 PUFAs in utero.

115 nt and surfactant synthesis in Src-1/-2(d/d) fetuses are likely caused, in part, by decreased GR and

116 thway androgen biosynthesis is active in the fetus, as assessed by liquid chromatography-tandem mass

117 ch, MRI data were acquired in 85 consecutive fetuses, as overlapping stacks of 2D images.

118 tic were also evaluated; 46 (20%) of the 234 fetuses assessed were found to have such signatures.

119 er radiofrequency energy administered to the fetus at 3.0-T MRI.

120 y ionization (DESI) - MS of a complete swine fetus at 50 days of gestation.

121 m were competent to implant and develop into fetuses at a similar rate as embryos produced in the con

122 ferences between ethanol-exposed and control fetuses at gestation day 135 (G135), but not G110 or G85

123 c calvarial cells (EOCCs) were isolated from fetuses at gestational day 18.5 (E18.5) of HFD-induced o

124 onal study, an initial CVR <= 1.4 identifies fetuses at very low risk for hydrops, and a maximum CVR

125 X (hFIX) or X (hFX) into Macaca fascicularis fetuses at ~0.4 gestation.

126 reviously obtained MRI imaging of 81 healthy fetuses between gestational ages 21 and 38 weeks.

127 ) compromises growth of both female and male fetuses but affects the placental phenotype sex-specific

128 sed the ability of the virus to infect mouse fetuses but decreased its capacity to produce high level

129 through the same mechanism in the developing fetus by establishing a link between the biophysical pro

130 ar a bacterial infection from the developing fetus by infusion of granulysin into placental trophobla

131 n offspring share a womb, interactions among fetuses can impart lasting impressions on phenotypic out

132 However, fetuses carried by diabetic recipients were smaller comp

133 l abnormalities were observed only among the fetuses carried by diabetic recipients.

134 ampal volumes were reduced in both Hx and HI fetuses compared with controls.

135 The presence of the fetus compounds the situation because both the cardiomet

136 Acer2 deficiency in both the mother and fetus decreases the placental levels of sphingolipids, i

137 Masculinization of the human fetus depends, therefore, on testosterone and androstero

138 nancies exposed to HCQ alone, 4 of 54 (7.4%) fetuses developed a primary outcome as in the ITT.

139 all three-fold increase in weight, while the fetus develops from a single cell into a viable infant i

140 med in 86 fetuses (56 healthy fetuses and 30 fetuses diagnosed with CHD) between 22 and 39 weeks gest

141 ning of life, inexperienced babies and human fetuses, domestic chicks, and monkeys exhibit a preferen

142 ZIKV can be transmitted from mother to fetus during pregnancy and can cause microcephaly and ot

143 erface between the mother and the developing fetus during pregnancy, and is a target for investigatin

144 and progesterone (P4), which impregnate the fetus during pregnancy, on GBS neonatal infection in cel

145 ratio was significantly reduced in sham-CDH fetuses either (1.2 +/- 0.3% vs 2.3 +/- 0.3% in controls

146 Compared to TN fetuses, ET fetuses had increased (P = 0.041) placental

147 In Montevideo (2013-2018), 8 Campylobacter fetus extraintestinal infections were reported.

148 +/- 0.3 [P < .01], respectively, for control fetuses, fetuses with SV CHD, and fetuses with TV CHD).

149 Tissues were harvested at E21 and fetuses fixed overnight in 4% paraformaldehyde/phosphate

150 anscriptional changes in the brains of mouse fetuses following MIA during the prenatal period, and ev

151 ral role of glucocorticoids in preparing the fetus for life after birth.

152 he possibility of lung clocks in priming the fetus for postnatal life.

153 alovirus (CMV) immunity does not protect the fetus from acquiring congenital CMV infection (cCMV).

154 tic mechanisms that protect the placenta and fetus from maternal iron excess.

155 respiration, thus ultimately protecting the fetus from the potentially dire consequences of generali

156 Fetuses from ET pigs had reduced (P = 0.032) M. longissi

157 A total of 2852 women (and their 3070 fetuses) from 29 secondary- and tertiary-level hospitals

158 PHSG versus HG fetuses had decreased fetal heart rate-movement coupling

159 Compared to TN fetuses, ET fetuses had increased (P = 0.041) placental weights and

160 ous system development, and PSYG versus PHSG fetuses had more birth complications, consistent with pr

161 shelf elevation, whereas Has2(f/f);Osr2-Cre fetuses had normal mandibles and delayed palatal shelf e

162 Thirty-nine fetuses had pathogenic variants in LQTS genes: 27 carrie

163 MIA fetuses had reduced brain weights at 21 dpi compared to

164 At G135, ethanol-exposed fetuses had reduced brainstem and cerebellum volume and

165 These fetuses had reduced liver iron stores and hemoglobin, an

166 ered maternal iron homeostasis, we generated fetuses harboring a paternally-inherited ubiquitous knoc

167 eas Acer2 deficiency in either the mother or fetus has no such effects.

168 , protection encompasses both the mother and fetus; however, during worsening conditions, protection

169 04 in 9 additional macaque mothers and their fetuses identified M1404I at a subconsensus frequency in

170 placenta is the interface between mother and fetus in all eutherian species.

171 y more altered than the placenta with a male fetus in FOXA2 cKO dams.

172 UDCA may protect the fetus in ICP by inhibiting OATP4A1-mediated bile acid tr

173 providing for the growth requirements of the fetus in later pregnancy, without exerting undue stress

174 is protective either for both the mother and fetus in milder infections or exclusively for the mother

175 eproductive tract, which regress in the male fetus in response to MIS.

176 o prepartum while still carrying a full-term fetus in the contralateral uterus.

177 ventions to be designed specifically for the fetus in the future.

178 hree hypotheses of how a mother supports her fetus in utero, now known as "Medawar's Paradox." The me

179 s are equivalent to the facial skin of human fetuses in the second trimester of development.

180 o be at risk of preterm birth, the number of fetuses in utero, the gestational age when first trial t

181 l-fetal interface, in the mother, and in the fetus, inducing preterm labor and birth and adverse neon

182 (ZIKV) to cross the placenta and infect the fetus is a key mechanism by which ZIKV causes microcepha

183 tatins affect cardiovascular function in the fetus is completely unknown.

184 ng the perinatal period, especially when the fetus is known to have a neurodevelopmental disorder suc

185 a indicate that neocortex development in OSB fetuses is altered as early as 11 weeks of gestation.

186 Hearts of fetuses isolated from hypoxic pregnancy showed approxima

187 eled during pregnancy to protect the growing fetus it contains, and it is particularly dynamic just b

188 mma9Vdelta2 T cells find their origin in the fetus like it is established for mouse innate gammadelta

189 Sulfatides were highly concentrated in the fetus liver, while hexoses were barely detected at this

190 ized to restrict growth, and male and female fetuses may have differential susceptibility to the deve

191 In women carrying multiple fetuses, neonatal hepcidin explained a significant amoun

192 We included 255 women and their 260 fetuses/neonates.

193 tal neocortex development, we analyzed human fetuses of both sexes diagnosed with OSB between 11 and

194 ccine is to prevent a congenital syndrome in fetuses of pregnant women, but studies directly evaluati

195 Ultrasound-guided IUCT was conducted in rat fetuses on embryonic day 16.

196 sue rejection response to the haploidentical fetus or from an undiagnosed infection.

197 cts on the cardiometabolic physiology of the fetus or mother in response to uterine manipulation in o

198 for absorbed iron that is transferred to the fetus or retained within the placenta.

199 d to lead at levels that may harm developing fetuses or breastfeeding infants.

200 ade inflammation in the mother, placenta, or fetus (or a combination of the 3) in pregnancies complic

201 l trios, including two sets of twins, and 14 fetus-parent dyads) were analysed by WES.

202 02 matched parental samples (analysed as 596 fetus-parental trios, including two sets of twins, and 1

203 resembles organ transplantation in that the fetus, possessing paternal antigens, is a semi-allogenei

204 gnificant role in inhibiting ZIKV VTx to the fetus, possibly through phagocytosis of virus or virus-i

205 Androgen biosynthesis in the human fetus proceeds through the adrenal sex steroid precursor

206 Unlike neonatal pups, late gestation fetuses proved to be resistant to rhesus rotavirus (RRV)

207 Resolving the degree of risk for human fetuses requires comprehensive knowledge of the pathways

208 helf elevation in Has2(f/f);Hand2-Cre mutant fetuses resulted from physical obstruction by the malfor

209 simulate concentrations of chemicals in the fetus resulting from maternal dosing.

210 ion of neurodevelopmental deformities in the fetus resulting in a disease termed congenital Zika synd

211 ion of neurodevelopmental deformities in the fetus resulting in a disease termed congenital Zika synd

212 d of pregnancy as well as transiently in the fetus several days before birth.

213 complete penetrance, the Has2(f/f); Wnt1-Cre fetuses showed dramatically reduced mandible size and co

214 management simultaneously affect mother and fetus, sometimes putting their well-being at odds with e

215 nced Zika virus (ZIKV) from a rhesus macaque fetus that died after inoculation and identified a singl

216 targeted immune protection of the developing fetus that maintains tolerance at the maternal-fetal int

217 d at least 18 years; they were pregnant with fetuses that had reached a gestational age of at least 2

218 odel using both sexes in twin 0.65 gestation fetuses that reproduces the spectrum of injury and abnor

219 birth size through maternal effects; in the fetus, the height- and metabolic-risk-increasing alleles

220 is undetectable (<1 ng/mL), while in female fetuses, there are significantly lower levels of androst

221 causes epigenetic change in the placenta and fetus; therefore, we utilized these patients as a unique

222 go a shift from a proliferative state in the fetus to a more mature but quiescent state after birth.

223 nd transporter activity without exposing the fetus to contrast media.

224 ca and frequently results in exposure of the fetus to malaria antigens in utero, while the immune sys

225 T) to benefit was 21 (95% CI 14 to 41) women/fetus to prevent one infant from needing respiratory sup

226 Maternal stress during pregnancy exposes fetuses to hyperglucocorticoids, which increases the ris

227 rectly administered to developing male ovine fetuses to model excess prenatal androgenic overexposure

228 rarer infection routes, including mother-to-fetus transmission, sexual contact and blood transfusion

229 Vitamin H (biotin) is delivered to the fetus transplacentally by an active biotin-transport mec

230 Both CDH-sham and CDH-TO fetuses treated with placebo had an increased medial wal

231 CDH fetuses treated with sildenafil, either with or without

232 se of WES of the fetuses and parents (parent-fetus trios), we identified genetic variants that indica

233 8), but both effects were more pronounced in fetuses undergoing additional TO (2.1 +/- 0.8 br/mm, P=0

234 l had no effect on this parameter, while CDH fetuses undergoing TO had a lung-to-body-weight ratio co

235 mmation and mechanical damage to protect the fetus until parturition.

236 ndogenous steroids in second trimester human fetuses using multidimensional and high-resolution mass

237 transcriptome of the placenta with a female fetus was considerably more altered than the placenta wi

238 The affected fetus was homozygous for the variant.

239 Thus, the increased virus infection in the fetus was not the result of an impaired fetal myeloid re

240 allenge and ZIKV-associated abnormalities in fetuses was confirmed.

241 A family with recurrent anencephalic fetuses was investigated to understand its etiology and

242 tically increased toward term in lungs of WT fetuses, was markedly reduced in Src-1/-2(d/d) fetal lun

243 primary endpoint, which was assessed in all fetuses, was the detection of diagnostic genetic variant

244 wever, the glucose-increasing alleles in the fetus were associated with reduced birth weight through

245 Myeloid cells in the fetus were not depleted in this experiment, likely becau

246 en who were pregnant with single or multiple fetuses were assigned to receive either fish-oil capsule

247 At term (GD30) fetuses were delivered, ventilated, and finally harveste

248 rats was removed by cesarean section and the fetuses were exposed to hypoxia by immersion in water (1

249 ly catheterized ewes carrying male singleton fetuses were exposed to normoxia (n = 6) or hypoxia (10%

250 Fifteen (5.5%) fetuses were managed with maternal steroids in the setti

251 rmed ZVD, brain or eye defects in infants or fetuses were more common during the Zika virus outbreak

252 Fetuses were obtained by cesarean sections performed 7 a

253 On GD28, fetuses were randomly assigned to TO or sham neck dissec

254 Viable fetuses were reduced in FOXA2 cKO mice on gestational da

255 ted with BrdU at embryonic day 13, and their fetuses were sacrificed from 5 to 35 hr after exposure.

256 At GD18.5, eNOS(-/-) fetuses were significantly smaller than WT animals (P <

257 tal liver inflammation in the late gestation fetus, where there is a physiologic expansion of non-cla

258 ations occur in order to support the growing fetus which are further exacerbated by gestational diabe

259 We performed a retrospective analysis of 143 fetuses who underwent FAV from 2000 to 2017 and a second

260 stasis of pregnancy, and their impact on the fetus, will be reviewed.

261 ion with T. gondii can be transmitted to the fetus with potentially lethal outcomes.

262 red placental iron homeostasis, we generated fetuses with a liver-specific knock-in of fpnC326Y or kn

263 ally identified pregnant women found to have fetuses with a structural anomaly were screened for thei

264 After exclusion of fetuses with aneuploidy and CNVs, 610 fetuses with struc

265 etal structural anomaly), nine (11.1%) of 81 fetuses with cardiac anomalies, and ten (15.4%) of 65 fe

266 ) +/- 0 [P = .01], respectively), but not in fetuses with CHD and TV or non-AO.

267 Fetuses with CHD were categorized into those with a sing

268 The brains of fetuses with CHD were more similar to those of CHD-relat

269 ng maternal hyperoxia in healthy fetuses and fetuses with CHD, but it was higher in SV CHD (mean Delt

270 Fetuses with CHD, especially those with lowest cerebral

271 Fetuses with confirmed aneuploidy or a causal pathogenic

272 ity of Wisconsin Biomagnetism Laboratory for fetuses with confirmed LQTS.

273 Background Impaired brain development in fetuses with congenital heart disease (CHD) may result f

274 placental oxygenation in healthy fetuses and fetuses with congenital heart disease, and it selectivel

275 e electrophysiology and rhythm phenotypes of fetuses with de novo and inherited LQTS variants and ide

276 Fetuses with familial variants showed a lower incidence

277 FAV was technically successful in 84% of 143 fetuses with fetal demise in 8%.

278 of early developmental arrest, interspecies fetuses with high levels of organ chimerism can be gener

279 179 pregnant women into 4 groups: "HLHS/TGA" fetuses with hypoplastic left heart syndrome (HLHS) or t

280 Fetuses with intrauterine growth restriction (IUGR) have

281 Fetuses with intrauterine growth restriction (IUGR) have

282 Previous studies in fetuses with intrauterine growth restriction (IUGR) have

283 c variants were present in 22 (15.4%) of 143 fetuses with multisystem anomalies (ie, more than one fe

284 e we report the etiology and outcome of 1004 fetuses with NIHF, in a large single Maternal and Childr

285 Etiologies were identified for 72% of 1004 fetuses with NIHF.

286 vely increased cerebral blood oxygenation in fetuses with single ventricle or aortic obstruction.

287 ith cardiac anomalies, and ten (15.4%) of 65 fetuses with skeletal anomalies; these phenotypes were m

288 herefore aimed to evaluate the proportion of fetuses with structural abnormalities that had identifia

289 ion of fetuses with aneuploidy and CNVs, 610 fetuses with structural anomalies and 1202 matched paren

290 S data in a prospective cohort of unselected fetuses with structural anomalies shows the value added

291 P < .01], respectively, for control fetuses, fetuses with SV CHD, and fetuses with TV CHD).

292 anged with GA in healthy control fetuses and fetuses with SV or AO CHD (DeltaR2* per week, 0.1 sec(-1

293 D but increased during maternal hyperoxia in fetuses with SV or AO CHD (mean DeltaR2*, 0.7 sec(-1) +/

294 this approach, in both human amniocytes from fetuses with T21 and in the Ts1Cje mouse model.

295 Human fetuses with trisomy 21 (T21) have atypical brain develo

296 ss all phases in healthy control fetuses and fetuses with TV CHD but increased during maternal hypero

297 or control fetuses, fetuses with SV CHD, and fetuses with TV CHD).

298 In this large case series of 127 fetuses with unexplained NIHF, we identified a diagnosti

299 intaining the ability to support growth of a fetus without rejection.

300 We hypothesized that androgens from male fetuses would mediate developmental differences across l