ライフサイエンスコーパス: fetal growth

1 rs are the time windows of interest for SGA (fetal growth).

2 possibility of worsening race disparities in fetal growth.

3 aria during both early and late pregnancy on fetal growth.

4 blood arsenic was negatively associated with fetal growth.

5 ake in pregnancy has been shown to influence fetal growth.

6 ard for size for gestational age for healthy fetal growth.

7 in and associated complications, but affects fetal growth.

8 e effects of prenatal LNS supplementation on fetal growth.

9 f maternal obesity on placental function and fetal growth.

10 ction and, in turn, for appropriate in utero fetal growth.

11 t with Sildenafil, a treatment which rescues fetal growth.

12 ations, it might have detrimental effects on fetal growth.

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

14 and during (36 wk) the time frame of slowed fetal growth.

15 of urban air pollution exposure with reduced fetal growth.

16 sed uterine arterial remodelling and reduced fetal growth.

17 ationship of epigenome-wide methylation with fetal growth.

18 confounding characteristics affecting normal fetal growth.

19 villous and basal plasma membranes regulates fetal growth.

20 ired transport has been associated with poor fetal growth.

21 that developmental exposure to PFOA reduces fetal growth.

22 tional-age (SGA) births and other aspects of fetal growth.

23 cient vitamin D, has an adverse influence on fetal growth.

24 ntial insights into epigenetic mechanisms of fetal growth.

25 and glucose concentrations while suppressing fetal growth.

26 -programming associated with the extremes of fetal growth.

27 no acids, and lactate were unaffected) or on fetal growth.

28 Stillbirth is strongly related to impaired fetal growth.

29 on during gestation to support embryonic and fetal growth.

30 genomic imprinting the driving force of the fetal growth.

31 d with both growth restriction and excessive fetal growth.

32 ment, as these genes often directly regulate fetal growth.

33 representing the international standards for fetal growth.

34 maternal vascular dysfunction and diminished fetal growth.

35 d without known environmental constraints on fetal growth.

36 n the impact these medications might have on fetal growth.

37 D status may or may not adversely influence fetal growth.

38 y link maternal undernutrition to restricted fetal growth.

39 uring adulthood in individuals with impaired fetal growth.

40 and chronic hypoxia during pregnancy impairs fetal growth.

41 mportant role in the development of abnormal fetal growth.

42 pregnant women are inversely associated with fetal growth.

43 teroplacental vascular function and increase fetal growth.

44 scularization in the placenta, and decreased fetal growth.

45 sildenafil protects placental perfusion and fetal growth.

46 stic link between maternal folate status and fetal growth.

47 quences for maternal nutrient allocation for fetal growth.

48 one exposure during gestation may compromise fetal growth.

49 ss mediators (e.g., glucocorticoids) or with fetal growth.

50 ASD risk increased with fetal growth 1.50 standard deviations below and >2.00 st

51 Fetal growth abnormalities were categorized as small for

52 hat the intrauterine signals that compromise fetal growth also act to "program" tissue differentiatio

53 Fetal growth also predicts the risk for later psychopath

54 ring pregnancy is associated with restricted fetal growth, although the underlying mechanisms are poo

55 Prenatal LNS supplementation can improve fetal growth among vulnerable women in Ghana, particular

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

57 Finally, while the observed relation between fetal growth and adult health has garnered considerable

58 Nutrition plays a fundamental role in fetal growth and birth outcomes.

59 cant remodeling and alterations to allow for fetal growth and birth.

60 pring, maternal myostatin deficiency altered fetal growth and calvarial collagen content of newborn m

61 Careful monitoring of fetal growth and cautious decision making on preterm del

62 ntification of early life factors related to fetal growth and childhood obesity is warranted.

63 etal brain, prenatal Hg exposure can inhibit fetal growth and development directly and indirectly.

64 The placenta is a vital organ for fetal growth and development during pregnancy.

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

66 The quality of fetal growth and development predicts the risk for a ran

67 The placenta plays a crucial role in fetal growth and development through adaptive responses

68 sis during pregnancy is essential for normal fetal growth and development.

69 is a key organ that plays a pivotal role in fetal growth and development.

70 centa, a transient organ required for proper fetal growth and development.

71 Fetal growth and fetal androgen exposure can also predet

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

73 ancies were unsuccessful because of retarded fetal growth and miscarriage.

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

75 l-age (SGA) to identify new genes related to fetal growth and neonatal body composition.

76 and thyroid hormones play a critical role in fetal growth and neurodevelopment.

77 Fetal growth and newborn length are similar across diver

78 various references are often used to assess fetal growth and newborn size across populations and eth

79 is a population-based project that assessed fetal growth and newborn size in eight geographically de

80 GROWTH-21(st) Project, our aim was to assess fetal growth and newborn size in eight geographically de

81 For this study, fetal growth and newborn size were measured in two INTER

82 nal circulating ouabain in the regulation of fetal growth and organ development.

83 in maintaining ER homeostasis during normal fetal growth and postnatal adaptation to metabolic stres

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

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

86 However, the relationship between fetal growth and stillbirth is difficult to determine be

87 h intake during pregnancy is associated with fetal growth and the length of gestation in a panel of E

88 ay be associated with inflammatory response, fetal growth, and adiposity later in life.

89 ich is a key mediator of embryonic survival, fetal growth, and pregnancy maintenance.

90 Low-level arsenic exposure may affect fetal growth, and the associations may be modified by ma

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

92 The association with high fetal growth appeared to involve pilocytic astrocytomas,

93 Fetal growth appears to be under matriline influence, an

94 Prenatal factors affecting fetal growth are believed important, but the underlying

95 al nutrient restriction (MNR) causes reduced fetal growth are poorly understood.

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

97 to assess the relationship between MeHg and fetal growth as well as the potential for confounding or

98 nfected pregnant women carrying fetuses with fetal growth-associated malformations.

99 13, 14 to 20, 21 to 27, and 28 to 34 wk and fetal growth at the subsequent week (i.e., 14, 21, 28, a

100 aternal insulin resistance occurs to support fetal growth, but little is known about insulin-glucose

101 l treatment protects placental perfusion and fetal growth, but whether the effects of sildenafil tran

102 expression of sFRP1 seen in smokers impairs fetal growth by inhibiting WNT signaling and trophoblast

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

104 ine link between maternal adipose tissue and fetal growth by regulating placental function.

105 This study evaluated fetal growth by ultrasonography and birth outcomes in wo

106 are before 14 weeks' gestation and monitored fetal growth by ultrasonography.

107 posure included sperm abnormalities, reduced fetal growth, cardiovascular disease, respiratory dysfun

108 This study provides WHO fetal growth charts for EFW and common ultrasound biomet

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

110 sing maternal exposure to air pollutants and fetal growth during gestation as assessed by ultrasound

111 and optimize maternal resource allocation to fetal growth during late pregnancy.

112 the characteristics used for individualized fetal growth estimates were missing and were replaced wi

113 -like growth factor 2 (IGF2) is an important fetal growth factor.

114 e dams on metabolism, placental function and fetal growth, female C57Bl6J mice were fed a control (CD

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

116 The five primary ultrasound measures of fetal growth--head circumference, biparietal diameter, o

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

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

119 Methylmercury (MeHg) may affect fetal growth; however, prior research often lacked asses

120 conclusions on the role of TFAs in modifying fetal growth; however, TFA exposure may be a confounding

121 However, poor fetal growth (i.e., growth below the mean) was more stro

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

123 uorooctanoic acid (PFOA) or its salts affect fetal growth in animals ?" and to rate the strength of t

124 (OP) pesticides are associated with reduced fetal growth in animals, but human studies are inconsist

125 fetal developmental exposure to PFOA reduces fetal growth in animals.

126 nt based on sufficient evidence of decreased fetal growth in both human and nonhuman mammalian specie

127 th based on sufficient evidence of decreased fetal growth in both human and nonhuman mammalian specie

128 the association of maternal weight gain and fetal growth in dichorionic twins throughout pregnancy.T

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

130 multicentre, population-based FGLS assessed fetal growth in geographically defined urban populations

131 on are implicated in normal placentation and fetal growth in humans, our findings suggest that abnorm

132 ure to perfluorooctanoic acid (PFOA) affects fetal growth in humans.

133 sure to perfluorooctanoic acid (PFOA) affect fetal growth in humans?" METHODS: We developed and appli

134 In conclusion, PBDEs may impair fetal growth in late pregnancy and reduce birth size.

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

136 e-1 and soluble endoglin levels and restored fetal growth in mice that was compromised by DL-propargy

137 ht gain was associated with dichorionic twin fetal growth in the second trimester only, driven by an

138 2.96) for intubation, despite more favorable fetal growth in those born to noninjured women (adjusted

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

140 risk factors for brain tumors included high fetal growth [incidence rate ratio (IRR) per additional

141 edict infant morbidity, mortality, and other fetal growth indicators.

142 The findings are consistent with extreme fetal growth interacting with variable fetal susceptibil

143 ink between maternal folate availability and fetal growth, involving regulation of placental mTOR sig

144 Restriction in fetal growth is associated with cardiovascular disease i

145 As altered fetal growth is associated with increased perinatal morb

146 Extreme fetal growth is associated with increased susceptibility

147 When fetal growth is compromised, placental insufficiency mus

148 Fetal growth is critically dependent on energy metabolis

149 regulating placental resource allocation to fetal growth is important for identifying the mechanisms

150 r haloacetic acid (HAA) exposure and adverse fetal growth is inconsistent.

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

152 egnant women and their children, we measured fetal growth, kidney volumes, and umbilical and cerebral

153 ria for a population at low risk of impaired fetal growth (labelled the NCSS prescriptive subpopulati

154 he same methods and conceptual approach, the Fetal Growth Longitudinal Study (FGLS), part of the INTE

155 In the Fetal Growth Longitudinal Study (FGLS), we studied educa

156 From these populations, the Fetal Growth Longitudinal Study selected low-risk women

157 Hypoxic pregnancy sufficient to restrict fetal growth markedly augmented the UtA vasodilator effe

158 rved association between maternal height and fetal growth measures (i.e., birth length and birth weig

159 e strong association of maternal height with fetal growth measures (i.e., birth length and birth weig

160 associated with gestational age at birth and fetal growth measures (i.e., shorter mothers deliver inf

161 For each of the five fetal growth measures, the mean differences between the

162 ing a major fetal genetic influence on these fetal growth measures.

163 Notably, reduced fetal growth occurs irrespectively of the parental origi

164 placental morphology, transport capacity and fetal growth on D16 and D19 (term approximately D20.5),

165 bout how the level of celiac disease affects fetal growth or birth outcomes.

166 hat observational studies associating either fetal growth or maternal mental health with neurodevelop

167 o investigate the relation between PBDEs and fetal growth or newborn anthropometry in a Spanish cohor

168 role of uterine NK cells in placentation and fetal growth, other uterine ILCs (uILCs) are likely to p

169 term ozone inhalation during implantation on fetal growth outcomes and to explore the potential for a

170 Dose-response curves for smoking versus fetal growth parameters (abscissa: log2 cotinine) were l

171 Fetal growth parameters and blood flows of the uterine a

172 that maternal glucocorticoid excess reduces fetal growth partially by altering placental glucose tra

173 controlling placental resource allocation to fetal growth, particularly in response to adverse gestat

174 data exist on prenatal arsenic exposure and fetal growth, particularly in the context of co-exposure

175 [25(OH)D] concentrations in pregnancy affect fetal growth patterns and birth outcomes.

176 tes, whereas HIF-2alpha is not necessary for fetal growth plate development.

177 Fetal growth plays a role in programming of adult cardio

178 exposure to organophosphorous pesticides and fetal growth: pooled results from four longitudinal birt

179 control strategies, has a profound impact on fetal growth, pregnancy duration, and placental weight a

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

181 erine growth restriction on the basis of the fetal growth rate, rather than just the small-for-gestat

182 cular resistance, was associated with slower fetal growth rates and cardiovascular adaptations in chi

183 an birth weight of 1200 g, who achieved near-fetal growth rates.

184 inverse correlation between maternal ADN and fetal growth reflects a cause-and-effect relationship.

185 pecific contributions of gestational age and fetal growth remain unknown, and these issues have never

186 that the protective effect of sildenafil on fetal growth reported in mammalian studies, including hu

187 Both low birth weight (BW), as a marker of fetal growth restraint, and high birth weight (BW), espe

188 f gestation; 1.16, 1.01-1.34; I(2)=64%), and fetal growth restriction (1.26, 1.20-1.33; I(2)=1%).

189 An atmosphere of 13% oxygen induced fetal growth restriction (1182 +/- 9 mg, n = 90 vs. 1044

190 Fetal growth restriction (FGR) affects 5% to 10% of newb

191 Fetal growth restriction (FGR) affects around 5% of preg

192 Fetal growth restriction (FGR) and preeclampsia (PE) are

193 eenage motherhood and short birth intervals, fetal growth restriction (FGR) and preterm birth, child

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

195 Preeclampsia (PE) and fetal growth restriction (FGR) are serious complications

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

197 Fetal growth restriction (FGR) is associated with global

198 Fetal growth restriction (FGR) results from placental in

199 of the most common and preventable causes of fetal growth restriction (FGR), a condition in which a f

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

201 putative aetiologies in the pathogenesis of fetal growth restriction (FGR); however, the regulating

202 6-32 weeks of gestation who had very preterm fetal growth restriction (ie, low abdominal circumferenc

203 Intrauterine fetal growth restriction (IUGR) is often associated with

204 example, maternal smoking (Z) is a cause of fetal growth restriction (X), which subsequently affects

205 d with incident CHF, atrial arrhythmias, and fetal growth restriction and complex CHD was associated

206 nd JZ+D at GD14 and GD18 in association with fetal growth restriction and higher blood pressure.

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

208 pregnant dams during early pregnancy led to fetal growth restriction and infection of the fetal brai

209 Here we show that both fetal growth restriction and over-growth are associated

210 ry condition of the placenta associated with fetal growth restriction and stillbirth.

211 posure is a significant mechanism underlying fetal growth restriction and the programming of adverse

212 tudies have suggested an association between fetal growth restriction and the risk of spontaneous pre

213 ove pregnancy outcomes in severe early-onset fetal growth restriction and therefore it should not be

214 centrations are associated with proportional fetal growth restriction and with an increased risk of p

215 Increased morbidity and fetal growth restriction are reported in uninfected chil

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

217 revious understanding and interpretations of fetal growth restriction as represented by small for ges

218 Hypoxia-related fetal growth restriction becomes apparent between 25 and

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

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

221 mplex (OR, 31.8; 95% CI, 4.3-236.3) CHD, for fetal growth restriction in noncomplex (OR, 1.6; 95% CI,

222 ability; Sildenafil does not protect against fetal growth restriction in the chick embryo, supporting

223 Markers of fetal growth restriction included biometric ratios, uter

224 onatal glucose homeostasis and is altered by fetal growth restriction induced by maternal undernutrit

225 Fetal growth restriction is a major determinant of adver

226 Screening procedures for fetal growth restriction need to identify small babies a

227 lve impaired placental function, either with fetal growth restriction or preterm labour, or both.

228 UtA) blood flow and relative protection from fetal growth restriction seen in altitude-adapted Andean

229 and 6 days' gestation and severe early-onset fetal growth restriction to receive either sildenafil 25

230 he fetus and is associated with fetal death, fetal growth restriction, and a spectrum of central nerv

231 se obstetric outcomes such as pre-eclampsia, fetal growth restriction, and preterm birth.

232 ications of pregnancy, such as preeclampsia, fetal growth restriction, and stillbirth.

233 egnancy complications, such as preeclampsia, fetal growth restriction, and stillbirth.

234 late levels in pregnancy are associated with fetal growth restriction, but the underlying mechanisms

235 ro tobacco exposure has been associated with fetal growth restriction, but uncertainty remains about

236 e consumption led to placental inefficiency, fetal growth restriction, elevated fetal serum glucose a

237 folate availability causes diseases such as fetal growth restriction, fetal malformations and cancer

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

239 quartiles had offspring with third-trimester fetal growth restriction, leading to a smaller head circ

240 l-recessive disorder characterized by severe fetal growth restriction, microcephaly, a distinct facia

241 gestation without congenital malformations, fetal growth restriction, or severe postnatal morbidity.

242 GT/GT) mice died perinatally associated with fetal growth restriction, reduced hepatic glycogen store

243 t undernutrition in the aggregate--including fetal growth restriction, stunting, wasting, and deficie

244 e than placental malaria per se, might cause fetal growth restriction, through impaired transplacenta

245 Maternal undernutrition contributes to fetal growth restriction, which increases the risk of ne

246 omplications, uteroplacental dysfunction, or fetal growth restriction.

247 ies and preterm newborns without evidence of fetal growth restriction.

248 logical conditions, including stillbirth and fetal growth restriction.

249 ype in response to hypoxia, a major cause of fetal growth restriction.

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

251 , and impaired spiral artery remodeling with fetal growth restriction.

252 hi women, especially those at higher risk of fetal growth restriction.

253 estational hypoxia such as pre-eclampsia and fetal growth restriction.

254 ances from maternal blood and contributes to fetal growth restriction.

255 presence or absence of ultrasonic markers of fetal growth restriction.

256 o trigger delivery in mothers of babies with fetal growth restriction.

257 complicated with intervillositis, can cause fetal growth restriction.

258 sed to play a role in the pathophysiology of fetal growth restriction.

259 ), several are of pathological relevance for fetal growth restriction.

260 ancies worldwide and is often complicated by fetal growth restriction.

261 oteinuria, and edema) and, in some patients, fetal growth restriction.

262 egnancy disorders including preeclampsia and fetal growth restriction.

263 acental inflammation and was associated with fetal growth restriction.

264 d amino acid transporter activity and causes fetal growth restriction.

265 Here, we developed a mouse model of fetal-growth restriction and placental insufficiency tha

266 cells is supported by Hmox1 and ameliorates fetal-growth restriction in Hmox1 deficiency.

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

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

269 range of birth weight (<2500 g), restricted fetal growth seems to be a common contributing factor to

270 risks of gestational diabetes and excessive fetal growth, shorter gestation, an increased risk of sm

271 We recommend these international fetal growth standards for the clinical interpretation o

272 o our knowledge, this is the largest DBP and fetal growth study to date with individual water use dat

273 r gestational age; the greatest risk was for fetal growth that was less than 2.00 standard deviations

274 signals in linking resource availability to fetal growth through changes in the morphological and fu

275 cal function of the placenta, which supports fetal growth through transplacental exchange, nutritiona

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

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

278 r epidemiology became available that tie the fetal growth trajectory to genomic imprinting in respons

279 l critical information on alterations of the fetal growth trajectory.

280 ds to environmental stimuli to determine the fetal growth trajectory.

281 -gestational age z score (n = 735 women) and fetal growth velocity (n = 664), defined as a change in

282 Combined analysis of fetal biometry and fetal growth velocity identified a subset of SGA fetuses

283 Fetal growth velocity was negative overall, decreasing f

284 Fetal growth velocity was quantified by change in z scor

285 pregnancy was associated with a reduction in fetal growth velocity, which occurred either immediately

286 ometric ratios, utero-placental Doppler, and fetal growth velocity.

287 In this large cohort study, high fetal growth was associated with an increased risk of br

288 Fetal growth was compared across groups by using intenti

289 of gestational exposure of the new ration on fetal growth was compared with birth outcomes [small for

290 Consequently, fetal growth was only marginally affected in 13% O2 (unc

291 Given race disparities in fetal growth, we explored race-specific trends in birth

292 ndex and uterine artery resistance index and fetal growth were measured in third trimester.

293 ertain subtypes, the described deviations in fetal growth were reduced by up to two-thirds after adju

294 ther-child cohort ultrasound measurements of fetal growth were related to bronchial hyperreactivity,

295 The primary markers of fetal growth were ultrasound measurements of fetal crown

296 ollution has been associated with restricted fetal growth, which is linked with adverse respiratory h

297 PPARalpha signaling, nutrient transport, and fetal growth without affecting maternal fat mass.

298 st in size at birth and in rates of impaired fetal growth worldwide.

299 for-gestational-age z scores and conditional fetal growth z scores (reflecting growth between 25 week

300 In univariable analyses, conditional fetal growth z scores were positively associated with z