ライフサイエンスコーパス: prenatal

1 surgery clinic for evaluation of a possible prenatal abdominal mass.

2 We found the associations between maternal prenatal acetaminophen use and all the SDQ domains uncha

3 xplain the full range of reported effects of prenatal adversity on offspring growth, we propose an in

4 Here we have extended these analyses to prenatal ages and additional brain regions.

5 An association between prenatal air pollution exposure and telomere length at b

6 The observed telomere loss in newborns by prenatal air pollution exposure indicates less buffer fo

7 enetic variation modify associations between prenatal air pollution on markers of cardiovascular risk

8 c health message about the potential harm of prenatal alcohol exposure and a routine screening protoc

9 ation between dose, frequency, and timing of prenatal alcohol exposure and craniofacial phenotype in

10 t association between craniofacial shape and prenatal alcohol exposure was observed at almost any lev

11 Prenatal alcohol exposure, even at low levels, can influ

12 regnancy and children with varying levels of prenatal alcohol exposure.

13 The impact of prenatal ambient air pollution on child asthma may be mo

14 We sought to determine how prenatal and early life factors impact the gut microbiom

15 RATIONALE: Maternal depression and prenatal and early life stress may influence childhood w

16 Prenatal and early postnatal exposures to environmental

17 We examined the relationship of prenatal and early-life environmental factors to the occ

18 life and asked whether this was modified by prenatal and early-life environmental factors.

19 y components of the external exposome in the prenatal and early-life periods and their effect on atop

20 Our results suggest that prenatal and early-life tobacco smoke exposure increase

21 out a case-only analysis to explore whether prenatal and early-life tobacco smoke exposure influence

22 We investigated the association between prenatal and early-life triclosan and paraben exposure a

23 ot identify a consistent association between prenatal and early-life triclosan or paraben concentrati

24 losely associated with neurodegeneration and prenatal and neonatal mortality, which could be due to e

25 op a two-generation pharmacokinetic model of prenatal and postnatal exposure to perfluorooctanoic aci

26 nvolvement in ASD, namely dysfunction in the prenatal and postnatal periods.

27 d vaginal microbial dynamics during critical prenatal and postnatal windows, we used high-resolution

28 ests national increases in cannabis potency, prenatal and unintentional childhood exposure; and in ad

29 Contrary to our original hypothesis, prenatal and Year 1 stress and depression had significan

30 ion in schizophrenia, including (1) genetic, prenatal, and premorbid immune risk factors and (2) immu

31 earch strategy using the terms [antenatal or prenatal] and [magnesium] and [preterm or premature or n

32 Prenatal antidepressant exposure has been associated wit

33 ion at each CpG across the whole genome with prenatal arsenic exposure levels and with cancer status,

34 used as outcomes in regression models, with prenatal/birth and demographic characteristics as indepe

35 Prenatal bisphenol A (BPA) exposure has been associated

36 ylation differences associated with maternal prenatal blood mercury levels in 321 cord blood DNA samp

37 kstove randomized controlled trial examining prenatal BP.

38 We estimated the association between prenatal BPA exposure and child neurobehavior at 3 y of

39 ve been thoroughly investigated, its role in prenatal brain development remains poorly understood.

40 Prenatal caffeine exposure was common in the sample (91%

41 Prenatal cannabis exposure was not associated with globa

42 eview highlights the molecular mechanisms of prenatal cardiac growth.

43 We evaluated whether prenatal cardiovascular changes previously demonstrated

44 ortant to foetal growth and could be used in prenatal care as an additional strategy to screen women

45 ears, this screening test has revolutionized prenatal care globally and opened up new prospects for p

46 Inequalities in access to adequate prenatal care may contribute to poor outcomes associated

47 Efforts should be made by prenatal care providers to provide Tdap vaccine to pregn

48 de a growing trend towards medicalisation of prenatal care, ensuring staff are trained to treat devel

49 ects and common chromosomal anomalies during prenatal care.

50 uces reduction of Otx2 expression, increases prenatal cell death, and accordingly leads to selective

51 he deleterious neurodevelopmental effects of prenatal cocaine exposure in humans.

52 has been difficult to unravel the effects of prenatal cocaine exposure on the human fetal brain, as w

53 We reported previously that prenatal cocaine exposure to rats during the most active

54 To test this hypothesis, we manipulated the prenatal conditions (i.e., presence or absence of the ma

55 ent, and monitored the subsequent effects of prenatal conditions on offspring and parental performanc

56 g by adjusting maternal effects according to prenatal conditions.

57 udies have directly investigated the role of prenatal cytokine and chemokine profiles on neurodevelop

58 ncluding schizophrenia, may originate during prenatal development, following periods of gestational h

59 irectly influenced by the environment during prenatal development.

60 ogy, to generate phenotypic variation during prenatal development.

61 Moreover, the prenatal developmental cell death in the Mapt(+/-) VTA s

62 Differential responses to prenatal DHA supplementation on the basis of the genetic

63 Those with prenatal diagnosis had an earlier estimated gestational

64 Prenatal diagnosis of coarctation of the aorta (CoA) is

65 The relationship of prenatal diagnosis of critical congenital heart disease

66 he diagnostic accuracy and confidence of the prenatal diagnosis of fetal brain abnormalities is impro

67 Newborns with prenatal diagnosis of single ventricle physiology and tr

68 g the current status of counseling regarding prenatal diagnosis of trisomy 18 (T18) or trisomy 13 (T1

69 Prenatal diagnosis technology development is necessary t

70 trasound and fetal MRI can be used to make a prenatal diagnosis, while MRI is the imaging modality of

71 tistic traits and, consistently, neither was prenatal dietary fish intake.

72 Noninvasive prenatal DNA testing is the vanguard of genomic medicine

73 Serial prenatal electronic medical records were obtained from w

74 Early prenatal enrollment and micronutrient use during the fir

75 The prenatal environment can alter an individual's developme

76 ibutions from different risk factors such as prenatal environmental exposure to organochlorines and m

77 f1 within the embryonic brain in response to prenatal environmental stress exposure may contribute to

78 diction risk after PE.SIGNIFICANCE STATEMENT Prenatal ethanol exposure (PE) is among many adverse dev

79 Prenatal ethanol exposure (PE) leads to increased addict

80 t and how this process is altered by adverse prenatal events such as maternal inflammation.

81 wever, potential problems include harms from prenatal exposure and unintentional childhood exposure;

82 Mercury is a global pollutant, and prenatal exposure is associated with adverse health effe

83 Prenatal exposure to AEDs in WWE and WWOE was associated

84 eral studies have examined the links between prenatal exposure to antidepressants and autism spectrum

85 ntial sexual dimorphism in associations with prenatal exposure to BFRs.

86 N: Evidence from animal models suggests that prenatal exposure to bisphenol A (BPA), a ubiquitous end

87 Our aim was to determine whether prenatal exposure to brominated flame retardants (BFRs)

88 s and investigate the interaction effects of prenatal exposure to different metals on adverse birth o

89 Prenatal exposure to famine is associated with a 2-fold

90 performance among the children according to prenatal exposure to fever (odds ratio (OR) = 1.01, 95%

91 large population-based study suggested that prenatal exposure to fever and common infections does no

92 Prenatal exposure to fever and infections has been linke

93 Our aim was to estimate the association of prenatal exposure to fluoride with offspring neurocognit

94 irth year, child's sex, community income, or prenatal exposure to hazardous air pollutants, indicatin

95 : Our findings reveal a relationship between prenatal exposure to higher levels of vanadium and incre

96 Repetitive prenatal exposure to identical or similar doses of harmf

97 Prenatal exposure to infectious or inflammatory insults

98 hort study initiated in 2012 to characterize prenatal exposure to IRS insecticides and exposures' imp

99 ed blood pressure in offspring that received prenatal exposure to LPS.

100 rn about the long-term neurologic effects of prenatal exposure to maternal overweight and obesity.

101 Prenatal exposure to mercury, a known neurotoxic metal,

102 long with the potential moderating effect of prenatal exposure to methylmercury.

103 Prenatal exposure to multiple air pollutants in the firs

104 Prenatal exposure to nonylphenol (NP) and/or bisphenol A

105 oxidative/nitrative stress are a function of prenatal exposure to NP/BPA and inflammation in 241 moth

106 atial patterns persisted after adjusting for prenatal exposure to organochlorines and metals but were

107 To assess the association of prenatal exposure to particulate matter (PM) with newbor

108 ated whether there is an association between prenatal exposure to particulate matter with diameter </

109 We aimed to determine whether prenatal exposure to PCBs and OCPs influences offspring

110 Few studies have examined whether prenatal exposure to perfluoroalkyl substances (PFASs) i

111 Prenatal exposure to perfluoroalkyl substances and adipo

112 In this cohort, prenatal exposure to PFASs was associated with small inc

113 We examined associations of prenatal exposure to PFASs with adiposity in early and m

114 We aimed to study associations between prenatal exposure to phthalates and several phenols on b

115 Prenatal exposure to polyinosinic:polycytidylic acid cau

116 Our data indicate that prenatal exposure to POPs appears to be associated with

117 We aimed to assess the association of prenatal exposure to vanadium with the risk of adverse b

118 birth defects among fetuses or infants with prenatal exposure to Zika virus infection only in the se

119 For prenatal exposure, the meta-analysis on the 6 case-contr

120 ed children; yet, few studies have evaluated prenatal exposure.

121 ta are available on the relationship between prenatal exposures and asthma during later childhood.

122 ns, and human studies indicate that parental prenatal exposures may play a part in developmental vari

123 f fluoride exposure, addressed the impact of prenatal exposures or involved more than 100 participant

124 tudy was to examine the associations between prenatal exposures to POPs and allergic sensitization an

125 The relation of several prenatal factors to risk of childhood asthma supports th

126 for maternal age, race/ethnicity, education, prenatal fine particulate matter exposure, prenatal smok

127 In this study, higher prenatal fluoride exposure, in the general range of expo

128 These findings indicated that prenatal genetic or epigenetic changes influence risk of

129 Prenatal genetic testing to diagnose DS in utero, provid

130 justment for parental ethnicity and smoking, prenatal glucocorticoid administration, preeclampsia, ge

131 Prenatal glucocorticoid exposure influences the timing o

132 However, the effect of prenatal glucocorticoids exposure on AD development in t

133 by robust erythrocytic output that supports prenatal growth in the hypoxic intrauterine environment,

134 ken embryo model to determine the effects on prenatal growth, cardiovascular development and pituitar

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

136 An understanding of the relationship between prenatal iAs exposure and alterations in the neonatal me

137 olites in neonate cord serum associated with prenatal iAs exposure in participants from the Biomarker

138 Prenatal images obtained at an outside institution were

139 ent the neurodevelopmental defects caused by prenatal immune activation in a specific pregnancy time

140 Prenatal immune activation was induced by maternal treat

141 markedly influenced by the precise timing of prenatal immune activation.

142 n syndrome in different age groups including prenatal, infant and adult.

143 Some studies suggest that prenatal infection increases risk of autism spectrum dis

144 urements: Weekly and cumulative incidence of prenatal infections and microcephaly cases.

145 on and behavioral functions in subjects with prenatal infectious histories.

146 Collectively, we demonstrate that a prenatal inflammatory environment leads to inadequate Tr

147 Prenatal inflammatory mechanisms may play a role in the

148 Prenatal inorganic arsenic (iAs) exposure is associated

149 During gestation, prenatal insults including maternal infection and subseq

150 We sought to assess the association between prenatal, intrapartum, and postnatal factors and the dev

151 of antiretroviral prophylaxis or treatment (prenatal, intrapartum, and postnatal) was 22.4% in 2002-

152 tests of visual attention in pilot trials of prenatal iodine supplementation in regions of mild to mo

153 gnitive processes that might be sensitive to prenatal iodine supplementation, we examined the timing

154 hildhood, which may reflect effects of lower prenatal iron status.

155 ate the impact of the current North American prenatal iron supplementation policy, this review highli

156 e-wide significant negative association with prenatal lead exposure (-1.4% per doubling increase in l

157 ch showed a strong negative association with prenatal lead exposure among female infants (-4.3% per d

158 nome-wide methylation data for low levels of prenatal lead exposure are lacking.

159 regression models to examine associations of prenatal lead exposure with DNA methylation in cord bloo

160 rlying mechanisms for the adverse effects of prenatal lead on the offspring, but epigenome-wide methy

161 e completed to determine the relationship of prenatal licorice consumption to these outcomes.

162 findings similar to those reported in their prenatal life and childhood.

163 xecutive function score at 24 mo (P = 0.467).Prenatal LNSs, postnatal LNSs, or both, or postnatal MNP

164 Tau haploinsufficiency causes prenatal loss of dopaminergic neurons in the ventral teg

165 Prenatal low-level lead exposure was associated with new

166 Our study examines associations between prenatal manganese concentrations and placental transfer

167 concentrations in red blood cells (RBC) from prenatal maternal blood samples, and using HumanMethylat

168 ly during postnatal life, influenced by both prenatal maternal factors and postnatal developmental cu

169 model of a psychiatric disease risk factor, prenatal maternal immune activation (MIA), we found redu

170 We investigated the association between prenatal maternal lead exposure and epigenome-wide DNA m

171 Subsequently, we defined the effect of prenatal maternal lifestyle-related or immune-mediated d

172 Prenatal maternal negative life events (NLEs) were dicho

173 No associations were present between prenatal maternal RBC-Hg and %-5mC at any time point.

174 ssion analyses showed an association between prenatal maternal smoking and SDQ conduct problem scores

175 is is the first systematic review to address prenatal maternal stress (PNMS) and the subsequent risk

176 Across mammals, prenatal maternal stress (PREMS) affects many aspects of

177 It has been suggested that prenatal maternal stress may increase the risk of childh

178 Prenatal maternal stress might partly explain these asso

179 Prenatal maternal stress was indexed by a negative life

180 everal early-life factors and EoE, including prenatal (maternal fever: adjusted odds ratio [aOR], 3.1

181 Prenatal MCA pseudofeeders were a risk factor for enceph

182 psychiatric diagnoses, symptom severity, and prenatal medication usage.

183 udies have evaluated the association between prenatal mercury exposure and DNA hydroxymethylation, an

184 e sought to evaluate the association between prenatal mercury exposure and offspring global DNA methy

185 Prenatal mercury exposure was associated with lower %-5h

186 Among males, prenatal mercury levels were associated with lower regio

187 rain abnormalities reported in children with prenatal methamphetamine and/or tobacco exposure are pre

188 Exposures: Prenatal methamphetamine and/or tobacco exposure.

189 Conclusions and Relevance: Prenatal methamphetamine/tobacco exposure may lead to de

190 Their prenatal methylmercury exposure had been assessed from t

191 However, prenatal methylmercury exposure seemed to attenuate thes

192 In the group with lower prenatal methylmercury exposure, a 1 SD increase in VO2M

193 ociation was observed in the group with high prenatal methylmercury exposure.

194 dition, we compared groups with low and high prenatal methylmercury exposure.

195 l neuroinflammation and the effectiveness of prenatal MgSO4/betamethasone treatments between males an

196 esis that environmentally-induced changes in prenatal movement influence embryonic limb growth to alt

197 We assessed the effects of prenatal multiple micronutrient (MM) supplementation on

198 Maternal cigarette smoke, including prenatal nicotinic exposure (PNE), is responsible for su

199 Prenatal nicotinic exposure prolongs superior laryngeal

200 Prenatal NO3(-) exposure during distinct sensitive windo

201 nd evidence to support an association of the prenatal occurrence of fever, a common manifestation of

202 neous group of rare recessive disorders with prenatal onset, characterized by hypoplasia of pons and

203 t speech, hypotonia, growth retardation with prenatal onset, feeding difficulties, structural brain a

204 g in three unrelated individuals with severe prenatal-onset growth retardation, intellectual disabili

205 confirms previously reported associations of prenatal OP exposure among black women with decreased in

206 from four cohorts to examine associations of prenatal OP exposure with birth weight (n = 1,169), leng

207 Prenatal or early treatment, or both, may have mitigated

208 Prenatal or postnatal exposure of the IkappaBalpha degra

209 th ADHD-related behaviors and assess whether prenatal organochlorine or metal exposures, sociodemogra

210 ldhood cancer and a disease with a confirmed prenatal origin in most cases.

211 Prenatal overnutrition affects development into adulthoo

212 examined associations between coexposure to prenatal particulate matter with an aerodynamic diameter

213 ency, and foam mattress were associated with prenatal PBDE exposure.

214 environmental exposures beginning during the prenatal period) to identify modifiable factors that aff

215 ssed in neural tissue, especially during the prenatal period, and enriched for biological pathways in

216 However, treatment to the mother, in the prenatal period, may provide the possibility of preventi

217 ng critical examination of preconception and prenatal periods as vulnerable to environmental insults

218 In general, prenatal PFAS concentrations were not associated with in

219 Prenatal PFAS exposure has been associated with lower bi

220 eight and adiposity at birth associated with prenatal PFAS exposure.

221 e or no evidence of associations between low prenatal PFAS exposures and outcomes related to cardiome

222 We estimated associations between prenatal PFAS exposures and outcomes relevant to cardiom

223 Prenatal PFAS plasma concentrations were not associated

224 xceptions were positive associations between prenatal PFHxS and TGs z-score [for a doubling of exposu

225 girls, each interquartile range increment of prenatal PFOA concentrations was associated with 0.21 kg

226 Prenatal phthalate concentrations were not associated wi

227 not find evidence of an obesogenic effect of prenatal phthalate exposure.

228 Median (25-75th percentiles) prenatal plasma perfluorooctanoate (PFOA), perfluoroocta

229 ring which children concomitantly exposed to prenatal PM2.5 and maternal stress had increased risk of

230 Prenatal PM2.5 exposure during sensitive windows is asso

231 ion models to identify sensitive windows for prenatal PM2.5 exposure on children's asthma by age 6 ye

232 terquartile range [1.7 mug/m(3)] increase in prenatal PM2.5 level) during which children concomitantl

233 Both prenatal Poly I:C and postnatal LPS produced changes in

234 Here, we show that Beclin 1 is a prenatal primary cytoplasmic protein but rapidly relocat

235 by in utero vitamin D exposure, suggesting a prenatal programming role of vitamin D on the child's me

236 d endocrine cell differentiation and reduced prenatal proliferation.

237 rval (CI)] of blood %-5hmC for a doubling in prenatal RBC-Hg concentration was -0.013% (-0.029, 0.002

238 Median prenatal RBC-Hg concentration was 3.23mug/g [interquarti

239 c ratio of %-5mC to %-5hmC for a doubling in prenatal RBC-Hg concentration was 4.70% (0.04, 9.58), 22

240 d at each research visit and abstracted from prenatal records.

241 We used regression models to evaluate prenatal residential proximity to agricultural use of fi

242 We evaluated the relationship between prenatal residential proximity to agricultural use of po

243 Preeclampsia is a shared prenatal risk factor for asthma, eczema, and allergy in

244 esis reveals that CDM-relevant exons undergo prenatal RNA isoform transitions and are predicted to be

245 Observations: Extensive availability of prenatal screening and diagnostic testing has led to inc

246 s to re-examine their national approaches to prenatal screening.

247 cial environment and show that, depending on prenatal sex hormone priming, testosterone administratio

248 on analyses examined the association between prenatal smoking and NEC-associated infant mortality rat

249 , prenatal fine particulate matter exposure, prenatal smoking exposure, and the sex of the child, all

250 ants matched for gestational age, sex, race, prenatal steroid exposure, and delivery mode.

251 (66%), never smoked (80%), and reported low prenatal stress (58%); 15% of children developed asthma.

252 ion models estimated the association between prenatal stress and both conduct disorder and hyperactiv

253 When examining modifying effects of prenatal stress and fetal sex, we found that boys born t

254 The fact that a relation between maternal prenatal stress and TL was observed in the offspring but

255 Prenatal stress further demonstrated a positive, dose-re

256 Similarly, maternal Slc6a4 knock-out and prenatal stress in rodents results in offspring demonstr

257 Importantly, early prenatal stress influenced offspring bacterial community

258 serotonin transporter, SLC6A4, coupled with prenatal stress is reported to increase the risk for chi

259 together, our results demonstrate that early prenatal stress may influence offspring development thro

260 Those exposed to the highest quartile of prenatal stress were more likely to belong to the high s

261 found that boys born to mothers with higher prenatal stress were most vulnerable (19-21 weeks' gesta

262 which may function as a coping mechanism to prenatal stress.

263 examine outcomes in our mouse model of early prenatal stress.

264 seen in children born to women reporting low prenatal stress.

265 ly among boys born to mothers reporting high prenatal stress.

266 asthma in boys concurrently exposed to high prenatal stress.

267 tive was to estimate the association between prenatal stressful events and risk of offspring conduct

268 The findings suggest that prenatal stressful events may be an independent risk fac

269 Mothers self-reported 42 prenatal stressful life events at 18 weeks' gestation.

270 maternal neuroendocrine-immune responses to prenatal stressors, which adversely impact neurodevelopm

271 Here we demonstrate the existence of a prenatal sub-cortical mechanism that regulates the corti

272 hern China, we aimed to assess the effect of prenatal supplementation with multiple micronutrients (M

273 igned to receive FO and/or 5-MTHF or placebo prenatal supplementation) who were recalled for a new ex

274 Prenatal Tdap vaccination is a critical strategy for red

275 ls were used to determine the association of prenatal TDF and perinatal outcomes.

276 nd AZT/3TC/NVP (34%); 49% of pregnancies had prenatal TDF exposure and 6% used a protease inhibitor.

277 nship between adverse perinatal outcomes and prenatal TDF use.

278 fluids is a powerful method for non-invasive prenatal testing, and diagnosis of cancers and other dis

279 s carriers, assisting in genetic counseling, prenatal testing, and preimplantation genetic diagnosis

280 to arise within a narrow time window during prenatal thymic development.

281 Women (N=184) were assessed at two prenatal time points to determine psychiatric diagnoses,

282 Here, we report that prenatal to early postnatal treatment with a ciliary neu

283 ed widespread changes in the transition from prenatal to postnatal life.

284 Prenatal tobacco smoke exposure and higher maternal stre

285 uman cells are ongoing prior to pre-clinical prenatal treatment in mice.

286 Prenatal treatment with MgSO4/betamethasone confers long

287 Prenatal urinary BPA concentration was associated with s

288 inal birth cohort found associations between prenatal urinary BPA concentrations and FMI, %BF, and WC

289 All models included prenatal urinary dialkyl phosphate metabolite concentrat

290 Prenatal viral-like immune activation is capable of indu

291 Using a well-established mouse model of prenatal viral-like immune activation, we examined wheth

292 )] in maternal plasma collected at the first prenatal visit (median, 9.6 weeks gestation) and in chil

293 onsumption was obtained by interview at each prenatal visit.

294 dap vaccine to pregnant women during routine prenatal visits at the earliest opportunity between 27 a

295 o difference in benefits or harms with fewer prenatal visits but was underpowered for rare, serious o

296 important new pathway for the assessment of prenatal visual perceptual capacities.

297 eded to examine fracture risk in relation to prenatal vitamin D status in a randomized controlled set

298 Our findings indicate prenatal WD exposure leads to age-specific changes in vo

299 lag interaction models to identify sensitive prenatal windows for the influence of nitrate (NO3(-)) o

300 the effectiveness of this policy in reducing prenatal Zika virus infection has yet to be quantified.