ライフサイエンスコーパス: fetus

1 placental transport of oxygen from mother to fetus.

2 transplacental transfer of antibodies to the fetus.

3 s bacterial transmission to the placenta and fetus.

4 ate to high risk for both the mother and her fetus.

5 of neural precursor cells in the developing fetus.

6 mentally similar to a second-trimester human fetus.

7 ry of oxygen and nutrients to the developing fetus.

8 anges in maternal resource allocation to the fetus.

9 pregnancy could increase virus spread to the fetus.

10 ility to protect against transmission to the fetus.

11 enatally passed from a pregnant woman to her fetus.

12 emain poorly characterized in the developing fetus.

13 prospects for personalized medicine for the fetus.

14 sely impact pregnancy and development of the fetus.

15 dative stress in the placenta but not in the fetus.

16 l effect of PM2.5 exposure on the developing fetus.

17 n that interfaces between the mother and her fetus.

18 feron gamma production in these Tregs in the fetus.

19 erm consequences for both the mother and the fetus.

20 placental transfer of cobalamin (Cbl) to the fetus.

21 ly of maternal glucose and amino acid to the fetus.

22 s during their first trimester with a viable fetus.

23 valve thrombosis, but they pose risks to the fetus.

24 onveys the Zika virus to the early embryo or fetus.

25 the risks and the benefits to the mother and fetus.

26 the prevention of virus transmission to the fetus.

27 e barriers, assist ZIKV dissemination to the fetus.

28 alter the hormonal environment of the female fetus.

29 anisms appear to provide adequate B12 to the fetus.

30 tate maternal allocation of nutrients to the fetus.

31 te, which pose known or unknown risks to the fetus.

32 le to deliver specific visual stimuli to the fetus.

33 ion or treatment that might pose harm to the fetus.

34 low and oxygen consumption rates in the IUGR fetus.

35 ects from cholera for both mothers and their fetuses.

36 essation of catecholamine signalling in IUGR fetuses.

37 its link to brain damage in developing human fetuses.

38 isclassified 15% of the large-for-gestation fetuses.

39 nized concern for infected mothers and their fetuses.

40 fusion into myotubes are misregulated in LOS fetuses.

41 ound ocular deformities in a minority of the fetuses.

42 conducted in Gestational Day 14 FVB/N mouse fetuses.

43 nd associated with reduced growth of alpha/+ fetuses.

44 c polyhydramnios who were pregnant with male fetuses.

45 etal hyperlipidemia, and consequently larger fetuses.

46 ger mothers, less educated mothers, and male fetuses.

47 velopment of female fetuses relative to male fetuses.

48 cephaly and other neuropathies in developing fetuses.

49 bjective models for risk assessment in these fetuses.

50 V) crosses the placenta and begins to infect fetuses.

51 gle cells from the forebrains of three human fetuses (15 to 21 weeks postconception) using clonal cel

52 Nine fetuses (16%) had encephalomalacia.

53 Ocular tissue samples from the 4 deceased fetuses (2 female, 2 male) ranging from 21.5 to 29 weeks

54 Twenty-six fetuses (45%) had prenatal hydrocephalus.

55 Thirty-one fetuses (53%) had MCA pseudofeeders.

56 The fetus acquires a small amount of maternal cells and DNA

57 cation of 6% (95% CI, 4%-8%) of hypothetical fetuses affected for East Asian couples to 87% (95% CI,

58 ntrauterine growth restriction (IUGR) of the fetus affects approximately 8% of all pregnancies and is

59 th reduced oxygen and nutrient supply to the fetus affects hindlimb blood flow, substrate uptake and

60 exposure controls to protect the mother and fetus allowing for development of safety by design for e

61 However, human fetuses already show considerable asymmetries in arm mov

62 bs cross the placenta from the mother to the fetus and can cause fetal or neonatal hyperthyroidism.

63 l infection acquired by the developing human fetus and can result in damage to the developing central

64 mmon viral infection of the developing human fetus and can result in neurodevelopmental sequelae.

65 picted as a linear process initiating in the fetus and continuing postnatally.

66 effects of pregnant women's distress on the fetus and epigenetic changes in placental genes.

67 birth is essential for normal growth of the fetus and for long-term control of carbohydrate metaboli

68 ole of dendritic cells within the developing fetus and indicate that they mediate homeostatic immune-

69 n and mass observed in the hypothyroid sheep fetus and may have consequences for pancreatic function

70 ale reproductive systems, and the developing fetus and neonate.

71 Adverse perinatal outcomes for the fetus and newborn include intrauterine growth restrictio

72 sequelae for the mother, but the risk to the fetus and newborn is substantial.

73 Family 1 had one fetus and one deceased child with heterotaxy and complex

74 ymphoid tissue inducer cells may form in the fetus and persist throughout life, as hypothesized in ro

75 ld avoid direct mechanical engagement of the fetus and present an external reservoir of drug.

76 at 20 weeks' gestation or later with a live fetus and required delivery as a result of pre-eclampsia

77 period of enhanced tissue plasticity for the fetus and the mother and may be a critical window of PFA

78 ion as well as block folate transport to the fetus and to the developing brain to produce the functio

79 skeletal muscle TL (MTL) were measured in 28 fetuses and 73 children.

80 Ds) later in pregnancy and on the outcome of fetuses and children born alive with a CHD.

81 idoamine (PAMAM) dendrimers were absorbed by fetuses and demonstrated bi-directional transport betwee

82 kidney, and brain of control and LOS bovine fetuses and found that different tissues within LOS fetu

83 asite that causes disseminated infections in fetuses and immunocompromised individuals.

84 ts and congenital microcephaly in developing fetuses and infants.

85 emonstrated bi-directional transport between fetuses and mother.

86 has resulted in congenital abnormalities in fetuses and neonates.

87 ding diagnostic criteria for microcephaly in fetuses and newborns exposed to the virus.

88 Fetuses and newborns were evaluated for the presence of

89 on the development of methods for detecting fetuses and placentas at risk as a means of reducing pre

90 and abnormal hippocampal development in rat fetuses and pups, there has been little research on the

91 thoracal spinal cord segments of five human fetuses and show development-dependent gene expression a

92 ectable virus in brain and/or lymph nodes of fetuses and/or pups.

93 women (15 transmitting the infection to the fetus) and 8 pregnant women with remote infection.

94 Amniotic fluid (AF) surrounds the growing fetus, and cells derived from AF are commonly used for d

95 emiallogenic individuals, the mother and the fetus, and is thus the epitome of cell interactions.

96 an have long-term detrimental effects on the fetus, and lead to persistent metabolic dysfunction in a

97 st common pathway for GBS disease in mother, fetus, and newborn.

98 cine could reduce disease in the mother, the fetus, and the infant.

99 from women who had CHD-possessing or normal fetuses, and 47 proteins displayed significant different

100 body size is apparent in embryonic day 15.5 fetuses, and persists until postnatal day 30 in cerebell

101 sequences of this exposure on the developing fetus are largely unknown, although in animal models we

102 The majority of aneuploid fetuses are spontaneously miscarried.

103 ood flow, and hence nutrient transfer to the fetus, are unknown.

104 Male fetuses were larger than female fetuses as measured by EFW, but the disparity was smalle

105 erature identifying pregnant women and their fetuses as subgroups vulnerable to heat exposure.

106 enhances the ability to communicate with the fetus, as most of the receptors and ligands up-regulated

107 led to more severe microcephaly in the mouse fetus, as well as higher mortality rates in neonatal mic

108 tial circulations in the chronically hypoxic fetus, associated with increases in xanthine oxidase-der

109 Some viruses can directly infect the fetus at specific times during gestation, while some onl

110 increased size of the pancreas in Ucp2(-/-) fetuses at embryonic day 16.5, associated with a higher

111 mated with naive female mice, the weight of fetuses at embryonic day 18.5 was significantly reduced

112 s distinction is crucial to the diagnosis of fetuses at risk and the design of therapeutic strategies

113 y-four articles were identified, and 12 (922 fetuses at risk for CoA) articles were included.

114 carrier screening modeled more hypothetical fetuses at risk for severe or profound conditions than d

115 for maternal height and parity) to identify fetuses at risk.

116 Among all fetuses, blood O2 saturation and plasma glucose, insulin

117 arent increased incidence of microcephaly in fetuses born to mothers infected with ZIKV.

118 cortisol, alters metabolism in the adult and fetus but it is not known whether cortisol in the pregna

119 ody composition that replicates the in utero fetus, but intrauterine body composition reference chart

120 infection is associated with microcephaly in fetuses, but the pathogenesis of ZIKV-related microcepha

121 f PCV3 nucleic acid were observed in aborted fetuses by quantitative PCR, and PCV3 antigen was locali

122 In fetuses, chronic anaemia stimulates cardiac growth; simu

123 ohort (n=369) and into the 24 weeks or older fetus cohort (n=201).

124 tion into the 18 weeks to less than 24 weeks fetus cohort (n=369) and into the 24 weeks or older fetu

125 Here we show that mammalian C. fetus consists of distinct evolutionary lineages, primar

126 fined as the probability that a hypothetical fetus created from a random pairing of individuals (with

127 hrough the uterine wall and perceived by the fetus, dependent on how light interfaces with maternal t

128 similar to the mean values for the reference fetus derived from chemical analysis previously.

129 Second-trimester fetuses diagnosed with a CHD between 2007 and 2013 were

130 2013 were also compared with Group III (532 fetuses diagnosed with a CHD in the second trimester fro

131 ential biomarker of placental dysfunction in fetuses diagnosed with CHD.

132 ion (P<0.0001) were identified compared with fetuses diagnosed with CHDs in the second trimester betw

133 mbilical vein blood velocity in Hsd11b2(-/-) fetuses did not undergo the normal gestational increase

134 One fetus died; the other two had transient massive salt-was

135 lacenta is the principal organ nurturing the fetus during pregnancy and was traditionally considered

136 ction, testis damage and transmission to the fetus during pregnancy in different animal models.

137 indicate that AHR activation by TCDD in the fetus during pregnancy leads to impairment of long-term

138 ndii that can lead to severe sequelae in the fetus during pregnancy.

139 ficiency virus (HIV)-infected pregnant woman/fetus dyads in Cape Town, South Africa.

140 ould represent healthy appropriately growing fetuses (e.g., singleton, birth weight appropriate for t

141 Ds, associated comorbidities, and outcome of fetuses, either diagnosed with a CHD in the first trimes

142 ed evolutionary framework will facilitate C. fetus epidemiology research and the development of impro

143 sia involves stabilisation of the mother and fetus, followed by delivery at an optimal time.

144 has been replicated in normally grown sheep fetuses following a 7-day noradrenaline (norepinephrine)

145 roliferation and mass were examined in sheep fetuses following removal of the thyroid gland in utero.

146 oximate the body composition of the in utero fetus from 30 to 36 wk of gestation.

147 Protecting the fetus from the hematogenous spread of viruses requires m

148 Fetuses from HF/HS-Veh dams had lower liver triglyceride

149 s, and pooled subsets of 3 male and 3 female fetuses from litters exposed to 0.8 ppm ozone had lower

150 Aborted fetuses from sows with PDNS contained high levels of PCV

151 We randomly assigned fetuses from women who were expected to deliver before 3

152 in utero MRI measurements of rhesus macaque fetuses, from which macroscopic and cellular information

153 We detect C. fetus genomes in 8% of healthy human fecal metagenomes,

154 pregnant women aged 16 years or older whose fetus had a brain abnormality detected by ultrasound at

155 hirty-one women had a miscarriage, and three fetuses had intrauterine death.

156 women in their 36th week of pregnancy whose fetuses had preserved head circumference at birth and fi

157 the third trimester of pregnancy, the human fetus has the capacity to process perceptual information

158 Importantly, HA fetuses have a marked reduction in umbilical blood flow

159 and found that different tissues within LOS fetuses have perturbations of distinct gene pathways.

160 er of maternal immunoglobulin G (IgG) to the fetus helps to protect against malaria and other infecti

161 syndrome in adults and CNS abnormalities in fetuses, highlights the importance in understanding the

162 often with grave outcomes to the developing fetus (i.e., Zika virus, brucella, cytomegalovirus, and

163 ht below 10th centile) and 94 normally grown fetuses identified in utero and followed-up into preadol

164 t therapy to protect the chronically hypoxic fetus in adverse pregnancy.

165 Fetus in fetu (FIF) is a rare entity in which a malforme

166 This case report describes a retroperitoneal fetus in fetu and discusses its clinical presentation, d

167 Histopathology confirmed the presence of a fetus in fetu.

168 ative interaction between the mother and the fetus in the allocation of resources.

169 fects of low maternal glucocorticoids on the fetus in the short-term.

170 Here we show that the fetus in the third trimester of pregnancy is more likely

171 al MRI to measure brain function in 32 human fetuses in utero and found that systems-level neural fun

172 d in the placenta, is a central component of fetus-induced immune tolerance during pregnancy.

173 e the center of the present understanding of fetus-induced immune tolerance.

174 causally associated with serious sequelae in fetuses, inducing fetal microcephaly and other neurodeve

175 syndrome in 4 different age groups including fetus, infant, early childhood and adult.

176 It is often assumed that C. fetus infection occurs in humans as a zoonosis through f

177 2016, a cluster of 13 cases of Campylobacter fetus intestinal and extraintestinal infections, includi

178 Campylobacter fetus is a venereal pathogen of cattle and sheep, and an

179 Thus, our work suggests that C. fetus is an unappreciated human intestinal pathobiont li

180 ogical cross talk between the mother and her fetus is critical for the maintenance of pregnancy and t

181 olerance induction toward the semiallogeneic fetus is crucial to enable a successful pregnancy; its f

182 During gestation the developing human fetus is exposed to a diverse range of potentially immun

183 cental structure reveals that the developing fetus is exposed to a source of prions long before expos

184 mode of vertical transmission from mother to fetus is presumptively transplacental, although a causal

185 denafil transcend the placenta to affect the fetus is unknown.

186 modifying the allocation of resources to the fetus is unknown.

187 ate if the survival probability of aneuploid fetuses is affected by the genome-wide burden of slightl

188 This PDX1(-/-) fetus lacked a pancreas and provides the basis for the p

189 In addition, we found that fetuses lacking type III IFN-lambda signaling had increa

190 to inactivate cortisol before it reaches the fetus, leading to higher levels of cortisol exposure.

191 se medications can cross the placenta to the fetus, leading to postpartum neonatal abstinence syndrom

192 od was able to quantify total Cot and Cbl in fetus liver, and it was sensitive and precise enough to

193 rom 17 countries to provide evidence that C. fetus may have originated in humans around 10,500 years

194 In addition, infection of a developing fetus may result in lifelong complications such as deafn

195 essary for the growth and development of the fetus, mediated by reproductive signals acting on metabo

196 Our data suggest that the developing fetus might be most vulnerable to ZIKV early in the firs

197 The (18)F-FDG doses to the fetus (n = 19; 5-34 wk of pregnancy) were calculated wit

198 ause of severe neurological complications in fetuses, neonates, and adults.

199 pumpless oxygenator circuit connected to the fetus of a lamb via an umbilical cord interface that is

200 ogic studies to evaluate the benefits to the fetus of maternal influenza vaccination because the caus

201 0.6 mmHg) similar to those measured in human fetuses of hypoxic pregnancy.

202 cal manifestations including microcephaly in fetuses of infected pregnant women and Guillian-Barre sy

203 ection in the brains, testes, placentas, and fetuses of mice.

204 GFP cells in the extraembryonic tissues and fetuses of tetraploid ESC chimeras were tetraploid as de

205 wever, very less GFP cells were found in the fetuses of tetraploid ESC chimeras.

206 eable interface that sustains the developing fetus, of CWD-infected dams.

207 w rates in IUGR that were similar to control fetuses on a weight-specific basis.

208 ssociated with increased risk of harm to the fetus or in early childhood.

209 nce of possible recent Zika infection, 6% of fetuses or infants had evidence of Zika-associated birth

210 with first-trimester Zika infection, 11% of fetuses or infants had evidence of Zika-associated birth

211 To estimate the preliminary proportion of fetuses or infants with birth defects after maternal Zik

212 iod), with no reports of birth defects among fetuses or infants with prenatal exposure to Zika virus

213 reports of congenital anomalies occurring in fetuses or infants with presumed or laboratory-confirmed

214 Of the 26 affected fetuses or infants, 4 had microcephaly and no reported n

215 us were identified in 26 (6%; 95% CI, 4%-8%) fetuses or infants.

216 tic infection occurred in 6 (42.9%) infected fetuses or newborns from women with and in 9 (21.4%) fro

217 h a CHD in the first trimester (Group I, 127 fetuses) or only in the second-trimester screening (Grou

218 gnancy and its consequences on pregnancy and fetus outcome.

219 as lower in fetuses with CoA than in healthy fetuses (P</=0.001), but the ascending aorta diameter, e

220 ure to NP/BPA and inflammation in 241 mother-fetus pairs.

221 vation in circulating catecholamines in IUGR fetuses persistently inhibits insulin concentrations and

222 hnic categories, the calculated frequency of fetuses potentially affected by a profound or severe con

223 Sox6-null mouse fetuses present misshapen and nucleated erythrocytes, du

224 holamine concentrations observed in the IUGR fetus produce developmental adaptations in pancreatic be

225 ium, the exchange surface between mother and fetus, progenitors develop into extravillous trophoblast

226 infections resulting in transmission to the fetus provide instructive lessons that can be applied to

227 rdize the health of the either the mother or fetus, providers continue to recommend the women with HI

228 VTx of ZIKV was stochastic, in that not all fetuses/pups within the same dam had detectable virus an

229 t were highly correlated within individuals (fetuses, r = 0.76, P < 0.0001; children, r = 0.87, P < 0

230 omic information on pregnant women and their fetuses raise ethical issues regarding consent for futur

231 In this study, CD163-positive fetuses, recovered between 109 days of gestation or 20 d

232 During acute superimposed hypoxia, LA fetuses redistributed blood flow favouring the brain, he

233 terine position during development of female fetuses relative to male fetuses.

234 ct of microbial infections on the developing fetus, relatively little is known about how pathogens as

235 e harmful effects of alcohol on a developing fetus represent many cases of preventable disability, an

236 icts delivery of nutrients and oxygen to the fetus result in IUGR.

237 Hypothyroidism in the sheep fetus resulted in an asymmetric pattern of organ growth,

238 ncement in the resolution in determining the fetus's maternal inheritance.

239 a spatiotemporal atlas from MRI of 81 normal fetuses scanned between 19 and 39 weeks of gestation and

240 ng the brain, heart and adrenals, whereas HA fetuses showed a blunted cardiovascular response.

241 Isolated cerebral arteries from HA fetuses showed a higher contractile capacity but a dimin

242 In contrast, femoral arteries from HA fetuses showed decreased contractile capacity and increa

243 e ratio was reduced at E17.5 in Hsd11b2(-/-) fetuses, suggesting impaired cardiac function.

244 Women carrying a fetus suspected of having a brain anomaly on ultrasound

245 The LTL-MTL gap was smaller in fetuses than children.

246 Parous women had heavier fetuses than nulliparous women, with the disparity being

247 l utility in correctly identifying FGR among fetuses that are small for gestational age.

248 Of 1634 fetuses that underwent randomization, 1566 were born ali

249 al functional connectivity was diminished in fetuses that would subsequently be born preterm.

250 malformations (VGAM) can be diagnosed in the fetus, the challenge is predicting the occurrence of its

251 ngle sgRNA was efficient at inducing mutated fetuses, the lack of complete gene inactivation resulted

252 ing HCMV transmission from the mother to the fetus, thereby mitigating severe developmental disabilit

253 n have immunologic effects on the developing fetus through several anti-inflammatory pathways.

254 a during pregnancy and infect the developing fetus to cause congenital malformations, and its associa

255 of pregnancy that results in failure of the fetus to reach its genetically determined growth potenti

256 atments that target the placenta and not the fetus to reduce risk of psychiatric disease in later lif

257 thousands of pregnant women to expose their fetuses to an infection that causes birth defects and ot

258 emiological studies suggest that exposure of fetuses to maternal inflammation increases the likelihoo

259 inked to severe birth defects, but mother-to-fetus transmission routes are unknown.

260 plications such as loss of vision, mother-to-fetus transmission, and fatal cases can occur.

261 ated the direct effects of sildenafil on the fetus using the chick embryo and hypothesised that silde

262 nished splenic Treg frequency in LPS-exposed fetuses was associated with inadequate Treg generation i

263 The Gd content of excised placentae and fetuses was measured, using inductively coupled plasma m

264 ion in utero, we found that the placenta and fetus were more susceptible to ZIKV infection at earlier

265 Fetuses were delivered surgically 3 or 7 days later.

266 Placentas from male fetuses were heavier (1082 +/- 2 mg, n = 30 vs. 928 +/-

267 Pregnant ewes and fetuses were instrumented for cardiovascular investigati

268 Male fetuses were larger than female fetuses as measured by E

269 Chronically instrumented fetuses were randomized to a control group (n = 11) or w

270 he second-trimester screening (Group II, 344 fetuses), were analyzed retrospectively between 2007 and

271 creased ZIKV replication in the placenta and fetus when infected at E12, and reciprocally, treatment

272 acceptability, leads us to propose that any fetus with a suspected brain abnormality on ultrasound s

273 BSTRACT: Reduced skeletal muscle mass in the fetus with intrauterine growth restriction (IUGR) persis

274 mmunolabeling on brain tissue from a 20-week fetus with intrauterine ZIKV infection.

275 n-interacting protein was impaired in a male fetus with IP, leading to defective linear ubiquitinatio

276 7068), found in the brain tissue of infected fetus with neonatal microcephaly, is located at the dime

277 2017, ocular tissue samples from 4 deceased fetuses with a diagnosis of CZS from the National Instit

278 All studies selected isolated severe CDH fetuses with a lung-to-head ratio 1.0 or less and liver

279 f both overall growth and cerebral growth in fetuses with all subtypes of CHD.

280 th birth defects among 395 live births and 5 fetuses with birth defects among 47 pregnancy losses.

281 <0.001, P=0.02, and P=0.02, respectively) in fetuses with CoA in comparison with controls, although a

282 d aortic arch hypoplasia were more common in fetuses with CoA than in controls (odds ratio, 26.0; 95%

283 n aortic valve diameter z score was lower in fetuses with CoA than in healthy fetuses (P</=0.001), bu

284 us/arterial duct diameter ratio was lower in fetuses with CoA than in those without CoA (P<0.001).

285 icuspid valve diameter z score was higher in fetuses with CoA than in those without CoA (P=0.01).

286 -vessel trachea view (P<0.001) were lower in fetuses with CoA.

287 ed in cell types/tissues obtained from human fetuses with DS and mouse embryos.

288 ved in ZIKV-infected pregnant women carrying fetuses with fetal growth-associated malformations.

289 er (mean 14 ms; 95% CI, 6-22; P<0.001) among fetuses with heart defects 143 ms (95% CI, 136-150) earl

290 Both pregnant women carrying fetuses with heart defects and women with hypertensive d

291 ssue oxygenation measured by T2* is lower in fetuses with heart defects compared with fetuses without

292 r that possibly affects brain development in fetuses with heart defects.

293 o compare the cerebral tissue oxygenation of fetuses with major heart defects to that of fetuses with

294 fetuses without heart defects to that of 15 fetuses with major heart defects: transposition of the g

295 fetuses with major heart defects to that of fetuses without heart defects as estimated by the magnet

296 e), we compared the fetal cerebral T2* in 28 fetuses without heart defects to that of 15 fetuses with

297 Among fetuses without heart defects, the mean T2* value was 15

298 in fetuses with heart defects compared with fetuses without heart defects.

299 How the fetus withstands an environment of reduced oxygenation d

300 stosterone was not suppressed in testes from fetuses younger than 8 GW, older than 10-12 GW, or in se