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 5, inadequate: -4.5+/-0.5, P<0.001), but not fetal growth.

3 ay to regulate placental nutrient supply and fetal growth.

4 h factor signaling to placental function and fetal growth.

5 t at E18.5; this may contribute to decreased fetal growth.

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

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

8 and glucose concentrations while suppressing fetal growth.

9 d without known environmental constraints on fetal growth.

10 teroplacental vascular function and increase fetal growth.

11 infiltration was only apparent with reduced fetal growth.

12 sildenafil protects placental perfusion and fetal growth.

13 stic link between maternal folate status and fetal growth.

14 quences for maternal nutrient allocation for fetal growth.

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

16 one exposure during gestation may compromise fetal growth.

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

18 possibility of worsening race disparities in fetal growth.

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

20 blood arsenic was negatively associated with fetal growth.

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

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

23 in and associated complications, but affects fetal growth.

24 e effects of prenatal LNS supplementation on fetal growth.

25 f maternal obesity on placental function and fetal growth.

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

27 due to placental insufficiency and impaired fetal growth.

28 reduce fetal growth, whereas Ni may promote fetal growth.

29 ses latent placental development and reduced fetal growth.

30 longitudinal ultrasound measures to estimate fetal growth.

31 uring pregnancy is hypothesized to influence fetal growth.

32 nce that partner smoking was associated with fetal growth.

33 se birth weights did not indicate suboptimal fetal growth.

34 ed prenatal risk factors of PTB and impaired fetal growth.

35 for its reduced size and maintaining normal fetal growth.

36 utcomes (intrauterine death/stillbirth, poor fetal growth, abortion, preterm delivery, C-section, obs

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

38 Fetal growth also predicts the risk for later psychopath

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

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

41 mmediate pregnancy outcomes, reducing excess fetal growth and adiposity and pregnancy-related hyperte

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

43 before and during pregnancy could influence fetal growth and birth outcomes.

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

45 intain delivery of critically needed FAs for fetal growth and brain development.

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

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

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

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

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

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

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

53 n of these genes is particularly critical to fetal growth and development, and some are expressed in

54 cental perfusion that is required for normal fetal growth and development, prevent the development of

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

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

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

58 trimental to pregnancy and negatively affect fetal growth and development.

59 ritional support and increased monitoring of fetal growth and development.

60 tion of our proposed algorithm with targeted fetal growth and Doppler surveillance, compared with uni

61 ctivation of AMPK by the drug AICAR improved fetal growth and elevated uterine artery blood flow.

62 are critical placental functions influencing fetal growth and long-term health.

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

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

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

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

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

68 chondria in the placenta, an organ vital for fetal growth and pregnancy maintenance in eutherian mamm

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

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

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

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

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

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

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

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

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

78 Fetal growth appears to be under matriline influence, an

79 onal duration, whereas alleles that increase fetal growth are associated with shorter gestational dur

80 We found that both maternal height and fetal growth are important factors in shaping the durati

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

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

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

84 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

85 occurs due to high calcium requirements for fetal growth but skeletal recovery is normally achieved

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

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

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

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

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

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

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

93 g smoking during pregnancy with longitudinal fetal growth by triangulating evidence from 3 analytical

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

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

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

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

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

99 d paternal (1.38 [1.27-1.51]) education; and fetal growth (eg, low birthweight 1.30 [1.09-1.55] and s

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

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

102 to full-term infants to separate effects of fetal growth from those of prematurity.

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

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

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

106 previously been associated individually with fetal growth (i.e., As, Cd, Co, Hg, Ni, Pb, Tl) (n = 262

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

108 small-for-gestational age (SGA), a proxy for fetal growth impairment, on risk of malaria during infan

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

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

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

112 (BPA) is an endocrine disruptor that affects fetal growth in experimental studies.

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

114 Fetal growth in gestational diabetes mellitus (GDM) is d

115 However, the effects of BPF and BPS on fetal growth in humans are unknown.

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

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

118 e association of the genetic instrument with fetal growth in non-smokers suggests that genetic pleiot

119 or small size, appear to achieve appropriate fetal growth in normal pregnancy.

120 SBP), improve vascular function and increase fetal growth in pregnant endothelial NO synthase knockou

121 sed maternal-fetal lipid transfer and excess fetal growth in some DM pregnancies.

122 ssociated with shorter gestation and reduced fetal growth in the Eagle Ford Shale of south Texas.

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

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

125 ing reduction can lower the risk of impaired fetal growth in women who struggle to quit.

126 Reduced fetal growth increases the risk for adverse health outco

127 ve are causal or explained by confounding or fetal growth influencing DNA methylation (i.e. reverse c

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

129 Restriction in fetal growth is associated with cardiovascular disease i

130 As altered fetal growth is associated with increased perinatal morb

131 When fetal growth is compromised, placental insufficiency mus

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

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

134 Fetal growth is influenced by both maternal and fetal ef

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

136 key amino acids for placental metabolism and fetal growth, is unknown.

137 culature of the placenta, which could impact fetal growth later in pregnancy.

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

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

140 Fetal growth may contribute to shaping later life risk f

141 Perturbations in fetal growth may have adverse consequences for childhood

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

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

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

145 m exposure has been associated with impaired fetal growth; much less is known about the impact during

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

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

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

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

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

151 on with hypertensive disorders of pregnancy, fetal growth, or gestational age, the prevalence of dete

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

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

154 Flaring and fetal growth outcomes were not significantly associated.

155 nsight into etiologic mechanisms of abnormal fetal growth outcomes.

156 No studies reported fetal growth parameters.

157 No studies reported fetal growth parameters; 19 studies (n = 3,723 neonates)

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

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

160 [25(OH)D] concentrations in pregnancy affect fetal growth patterns and birth outcomes.

161 Although PIO was beneficial for fetal growth, PIO treatment reduced placental vascular d

162 We tested this hypothesis in the fetal growth plate, which is hypoxic.

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

164 s, cesarean delivery, preterm delivery, poor fetal growth, preeclampsia, chorioamnionitis, postpartum

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

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

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

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

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

170 h-fat diet (HFD) exposure results in reduced fetal growth regardless of maternal genotype.

171 In low-resource populations, benefits on fetal growth-related birth outcomes were derived from nu

172 early-life exposure to maternal obesity- and fetal growth-related factors in childhood cancer develop

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

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

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

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

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

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

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

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

181 was to identify metabolites associated with fetal growth restriction (FGR) by examining early and la

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

183 Fetal growth restriction (FGR) is a major risk factor fo

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

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

186 d pre-eclamptic pregnancies complicated with fetal growth restriction (FGR) with and without villitis

187 Fetal growth restriction (FGR), a major risk factor for

188 They are associated with fetal growth restriction (FGR), but previous studies hav

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

190 that may be indicative of local ischemia or fetal growth restriction (FGR).

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

192 ral artery remodeling (ISAR) with or without fetal growth restriction (FGR).

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

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

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

196 ht into mechanisms and interventions against fetal growth restriction and adult-onset programmed hype

197 ion; PIO prevented approximately half of the fetal growth restriction and attenuated placental insuff

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

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

200 Hypoxic pregnancy induced fetal growth restriction and fetal oxidative stress.

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

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

203 death, whilst heterozygous loss resulted in fetal growth restriction and impaired placental formatio

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

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

206 itigation of pregnancy complications such as fetal growth restriction and preeclampsia.

207 treatment with antioxidants protects against fetal growth restriction and programmed hypertension in

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

209 Placental insufficiency can cause fetal growth restriction and stillbirth.

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

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

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

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

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

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

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

217 men with normal pregnancies, particularly in fetal growth restriction associated with pre-eclampsia.

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

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

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 e on critical exposure windows and timing of fetal growth restriction is limited.

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

227 et and provide a potential mechanism for the fetal growth restriction observed in women who use canna

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

229 in mice to determine whether hypoxia-induced fetal growth restriction reduces placental PPAR-gamma pr

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

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

232 in placental villous tissue are increased in fetal growth restriction vs. placentas from women with n

233 l dilation, intra-amniotic inflammation, and fetal growth restriction, all of which are clinical sign

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

235 ce significantly increased placental damage, fetal growth restriction, and fetal resorption.

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

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

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

239 ed rates of pregnancy pathologies, including fetal growth restriction, due at least in part to reduct

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

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

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

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

244 ant pain, headache with visual disturbances, fetal growth restriction, or abnormal maternal blood tes

245 psychoactive ingredient in cannabis, causes fetal growth restriction, though the mechanisms are not

246 Maternal exposure to Cd is associated with fetal growth restriction, trace element deficiencies, an

247 osure resulted in pups born with symmetrical fetal growth restriction, with catch up growth by post-n

248 R-gamma) protects against hypoxia-associated fetal growth restriction.

249 logical characteristics of preeclampsia with fetal growth restriction.

250 ction are associated with poor outcomes like fetal growth restriction.

251 logical conditions, including stillbirth and fetal growth restriction.

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

253 acental inflammation and was associated with fetal growth restriction.

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

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

256 omplications, uteroplacental dysfunction, or fetal growth restriction.

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

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

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

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

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

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

263 e the association between race/ethnicity and fetal growth restriction.

264 macological AMPK activation for treatment of fetal growth restriction.

265 regnancy disorders such as pre-eclampsia and fetal growth restriction.

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

267 GFR3 signaling contributed to late-gestation fetal growth restriction.

268 ; and previous pre-eclampsia or intrauterine fetal growth restriction.

269 sociated disorders, such as preeclampsia and fetal growth restriction.

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

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

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

273 f Child Health and Human Development (NICHD) Fetal Growth Studies-Singleton Cohort (n = 2,802), indiv

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

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

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

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

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

279 The fetal growth trajectory in women who quit smoking in ear

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

281 PIO did not affect fetal growth under normoxia.

282 udinal analysis of placental development and fetal growth using a mouse model to investigate the effe

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

284 Fetal growth velocity was negative overall, decreasing f

285 Fetal growth velocity was quantified by change in z scor

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

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

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 pendent association of maternal smoking with fetal growth was observed from the early second trimeste

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

292 glutamine and glutamate, key amino acids for fetal growth, was assessed in normal mice and those with

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

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

295 this understudied population, Hg may reduce fetal growth, whereas Ni may promote fetal growth.

296 , suggesting that these exposures accelerate fetal growth, which is consistent with the known estroge

297 posure to Delta9-THC effectively compromised fetal growth, which may be a result of the adversely aff

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

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