ライフサイエンスコーパス: prenatal

1 ependent t tests to analyze the influence of prenatal 25(OH)D levels in YKD AN mothers on S-ECC in th

2 0%-30% higher risk of ADHD and ASD following prenatal acetaminophen exposure.

3 n some ways opposite to-those seen following prenatal activation of TLR3 and/or TLR4.

4 Here, we characterize the effects of prenatal activation of TLR7, which is implicated in the

5 Our study indicates that prenatal AED exposure does not increase the burden of de

6 to environmental agents, in the influence of prenatal air pollution exposure on neurodevelopment and

7 Prenatal alcohol exposure (PAE) affects at least 10% of

8 Prenatal alcohol exposure (PAE) leads to profound defici

9 A new study shows that moderate prenatal alcohol exposure alters multiple features of hi

10 Prenatal alcohol exposure of any severity was associated

11 l mediation models were used to test whether prenatal alcohol exposure was associated with psychologi

12 Children with prenatal alcohol exposure, compared with those without,

13 d for associations between reported maternal prenatal alcohol use and psychological, behavioral, and

14 We show that within the native prenatal and adult environments, the frequency and rate

15 into reference transcriptomic atlases of the prenatal and adult human brain to determine where these

16 sequenced both RNA fractions from homogenate prenatal and adult human postmortem cortex using poly(A)

17 Furthermore, prenatal and age-dependent differentially expressed gene

18 include additional outcomes associated with prenatal and childhood exposure to ambient fine particul

19 Exposures from the prenatal and early postnatal (2-month) visits were evalu

20 Latent class analysis was performed with prenatal and early postnatal farm-exposure variables to

21 higher-than-average temperatures during the prenatal and early-life period is associated with fewer

22 r retinopathy of prematurity are to optimize prenatal and perinatal care, improve diagnostic acumen w

23 ort with atopic children with adjustment for prenatal and postnatal confounders.

24 We find that exons biased toward prenatal and postnatal expression preferentially contrib

25 n a dynamic settling process, generating all prenatal and postnatal granule neurons in defined spatio

26 The correlates of prenatal and postnatal growth on Intelligence Quotient (

27 KAP1 is broadly and highly expressed in both prenatal and postnatal periods and demostrate enriched e

28 The enhancer cluster was essential for prenatal and postnatal ventricular expression of Nppa an

29 atter ([Formula: see text]) during different prenatal and postnatal windows may play in children's co

30 urth digit length ratio (2D:4D), a proxy for prenatal androgen load, and transgender identity have be

31 entity and 2D:4D indicating the influence of prenatal androgen on the development of gender identity

32 eveloping male ovine fetuses to model excess prenatal androgenic overexposure associated with conditi

33 c fluid of autistic boys, based on measuring prenatal androgens and other steroid hormones.

34 same Danish Historic Birth Cohort, in which prenatal androgens were measured, using univariate logis

35 ata from 2,208 samples sent for non-invasive prenatal aneuploidy screening to detect CMV and precisel

36 n a meta-analysis of the association between prenatal antidepressant exposure and autism risk, the au

37 ing designs supported an association between prenatal antidepressant exposure and autism.

38 observational studies of the association of prenatal antidepressant exposure with autism.

39 Observational studies of prenatal antidepressant safety are hindered by methodolo

40 n birth defects or pup deaths resulting from prenatal apigenin treatment.

41 n, a defect in folate metabolism can lead to prenatal aqueduct stenosis and resultant hydrocephalus.

42 Sex-specific effects of prenatal BPA exposure on the susceptibility of AD deserv

43 Thus, the role of genes in prenatal brain development is more pronounced for childh

44 d interest in understanding the relevance of prenatal brain development to common neurological diseas

45 During prenatal brain development, ion channels are ubiquitous

46 e-bias by sex-differentially impacting early prenatal brain development, particularly neural circuits

47 rovided insight into the staged processes of prenatal brain development.

48 d 4) evaluate opportunities to link specific prenatal brain developmental processes to the forms of a

49 rt a role for altered gene regulation in the prenatal brain in susceptibility to various neuropsychia

50 pecific methodologies for studying the human prenatal brain, 2) summarize large-scale human prenatal

51 ATRT(5,6), B7-H3 is highly expressed on the prenatal, but not postnatal, brain.

52 Prenatal cannabis exposure (PCE) influences human brain

53 this association is mediated by adequacy of prenatal care (PNC).

54 eving centers to promote early initiation of prenatal care among medically vulnerable and underserved

55 o 24 years) and target (more total patients, prenatal care by referral only, a larger proportion of p

56 PrOMIS cohort (N = 3308) was recruited from prenatal care clinics at the Instituto Nacional Materno

57 7.1%) and target (84.8%) for women receiving prenatal care in the first trimester (Maternal, Infant,

58 rserved populations are less likely to begin prenatal care in the first trimester.

59 h centers tracked whether patients initiated prenatal care in their first trimester of pregnancy.

60 Early prenatal care is vital for improving maternal health out

61 , location outside New England, provision of prenatal care to women living with HIV, and more uninsur

62 nformation on timing or quality of follow-up prenatal care.

63 arital status, infant sex, and initiation of prenatal care.

64 may help shape future guidelines on maternal prenatal care.

65 95% CI: 1.11, 1.24), women with fewer than 5 prenatal-care visits (OR = 1.85, 95% CI: 1.60, 2.16), an

66 We aimed to examine whether prenatal Cd associates with the expression of imprinted

67 arly DLX5, H19, and NDN, in association with prenatal Cd exposure may be involved in overall developm

68 tivation of apoptotic cellular events in the prenatal cerebellum.

69 ify the differential sex-specific effects of prenatal challenges on lung function, immune response, a

70 Prenatal challenges such as maternal stress perception i

71 understanding of the mechanisms influencing prenatal characteristics is fundamental to comprehend th

72 We identify prenatal cis-regulatory effects on 63 genes and 166 indi

73 We also examined prenatal correlates of cord UMFA concentrations.

74 irth were lower in infants exposed to repeat prenatal corticosteroids.

75 standardization and quality improvement for prenatal counseling and delivery planning.

76 ion of staff/patients by opinion leaders and prenatal counseling for women and partners, although cli

77 rated poor because of inadequate control for prenatal depression and maternal ethnicity.

78 disorder (MDD) and preterm birth (PTB), and prenatal depression associates with PTB.

79 e is a possible mechanism via which maternal prenatal depression impacts children's behavior.

80 Prenatal depression is common, underrecognized, and unde

81 s higher in mothers with positive history of prenatal depression, and in divorced or widowed mothers.

82 ain development, yet the relationships among prenatal depression, child behavior, and children's brai

83 ance of both recognition and intervention in prenatal depression.SIGNIFICANCE STATEMENT Understanding

84 mean diffusivity and analyzed with maternal prenatal depressive symptoms as well as child behavior.

85 red brain structure is a mechanism via which prenatal depressive symptoms can impact child behavior,

86 hanges in young children exposed to maternal prenatal depressive symptoms.

87 Prenatal detection of congenital heart disease facilitat

88 ther the prevalence nor extent of CIN during prenatal development and at birth, following IVF treatme

89 with autism with macrocephaly also indicate prenatal development as a critical period for this condi

90 Ethanol exposure during prenatal development causes fetal alcohol spectrum disor

91 we examined fetal microglial activity during prenatal development in response to maternal infection w

92 rtem brain studies have indicated that early prenatal development may be altered in autism.

93 shaping the human genome and is involved in prenatal development, disease and aging.

94 in synaptogenesis and corticogenesis during prenatal development, in both males and females.

95 iagnosis after birth, but its usefulness for prenatal diagnosis is still emerging.

96 ch includes prepregnancy genetic counseling, prenatal diagnostic procedures, and a treatment plan for

97 We also review the advances made in prenatal diagnostics of clefts through imaging and genom

98 (CFNCs) have shown potential in noninvasive prenatal diagnostics.

99 We created a prenatal diet quality index (PDQI) based on adherence to

100 0%)-these differences were largely driven by prenatal differences that were enriched for pathways pre

101 der (ASD) is a largely heritable, multistage prenatal disorder that impacts a child's ability to perc

102 gated the effects of different dimensions of prenatal distress in pregnant adolescents, a population

103 Nevertheless, most prenatal distress studies do not focus on multiple dimen

104 the hippocampus displays alterations due to prenatal distress.

105 CVI and a history of perinatal distress have prenatal dysgenesis of the developing brain.

106 ated the association between exposure to any prenatal environmental adversity and child neurodevelopm

107 evelopmental delay and mediate the effect of prenatal environmental adversity on child neurodevelopme

108 time points also mediated the effect of any prenatal environmental adversity on child neurodevelopme

109 g that the visual loss was attributable to a prenatal etiology with secondary birth complications.

110 lection phases jointly, and for the averaged prenatal exposure across pregnancy.

111 We used prenatal exposure biomarker data from the NBC, a populat

112 explained reasonable amounts of variance in prenatal exposure biomarkers.

113 al and postnatal DNA damage are prevented by prenatal exposure of the placenta to a mitochondrially-t

114 Autism risk estimates after prenatal exposure to any antidepressant were decidedly d

115 Our recent study revealed that prenatal exposure to bisphenol A (BPA) disrupted the tra

116 Results suggest that prenatal exposure to DDT is related to elevated birth si

117 perimental model increases the evidence that prenatal exposure to EDC mixtures impacts later life bra

118 Prenatal exposure to environmental adversities, includin

119 In adjusted analyses, prenatal exposure to H1N1 vaccination was not associated

120 hallmarks of congenital conditions caused by prenatal exposure to harmful agents.

121 We assessed the effects of prenatal exposure to mixtures of air pollutants of parti

122 Prenatal exposure to per- and polyfluoroalkyl substances

123 l, 1.21-1.92) that was characterized by high prenatal exposure to PFAS and increased serum levels of

124 We evaluated how prenatal exposure to PFAS associates with established se

125 iations of altered pubertal development with prenatal exposure to PFASs.

126 Our results suggest that prenatal exposure to PM(2.5) disrupts neurodevelopment a

127 Shifts in birthweight z-scores from prenatal exposure to PM(2.5), PM(10), and NO(2) were med

128 Findings for prenatal exposure to selective serotonin reuptake inhibi

129 Prenatal exposure to streptomycin and TMP-SMX was associ

130 00.0%, P = 0.029) of the association between prenatal exposure to the Chinese great famine and adulth

131 at INSR and IGF2 mediated the association of prenatal exposure to the Chinese great famine with adult

132 f DNA methylation on the association between prenatal exposure to the famine and adult WC and BMI.

133 Maternal smoking was the only prenatal exposure variable associated with higher child

134 s vitamin D (VD) has emerged as a modifiable prenatal exposure.

135 ss, anxiety, and depression-is a substantial prenatal exposure.

136 We estimated 77 prenatal exposures and 96 childhood exposures (cross-sec

137 case reports were included, totaling 27 751 prenatal exposures to amikacin (n = 9), gentamicin (n =

138 Prenatal exposures to phthalates and bisphenols are asso

139 tion in reproductive females might influence prenatal factors such as fetal development and sex alloc

140 the INSR might mediate the adverse effect of prenatal famine exposure on WC in adulthood.

141 The results showed that prenatal famine exposure was significantly associated wi

142 Prenatal fetal immune priming may have an important role

143 7; n = 258) and among children who had lower prenatal folic acid supplementation ( < 400 mug/d) (beta

144 scovery rate (FDR) [Formula: see text]] with prenatal [Formula: see text] and 14 with [Formula: see t

145 Prenatal [Formula: see text] was nonsignificantly associ

146 posure to conditions associated with altered prenatal GCs in newborn's cord blood DNA.

147 ukemias (pB-ALLs) caused by a combination of prenatal genetic predispositions and oncogenic events oc

148 re, we examined whether XCD extends to human prenatal germ cells given their similarities to naive pl

149 mosome dosage compensation mechanisms in the prenatal germline.

150 These findings emphasize the importance of prenatal growth on ROP development.

151 nopathy of prematurity (ROP) but the role of prenatal growth patterns in ROP remains inconclusive.

152 SPSTF) previously found strong evidence that prenatal HIV screening reduced risk of mother-to-child t

153 g situations due to organizational effect of prenatal hormonal milieu on adult endocrine functioning.

154 ng mammary bud, it is essential for both the prenatal hormone-independent as well as the pubertal hor

155 - yet data now support a surprising role in prenatal human brain disorders as well.

156 omical regions and axon tract orientation in prenatal human brain tissue sections that are not visibl

157 ing pregnancy affects gene expression in the prenatal human cortex.

158 es to an external set of tissue samples from prenatal human hippocampi.

159 Background Prenatal identification of placenta accreta spectrum (PA

160 Our findings demonstrate that prenatal immune activation can promote a wide range of d

161 The mechanisms by which prenatal immune activation increase the risk for neurops

162 Mouse models of prenatal immune activation often involve maternal admini

163 Previous studies suggest that prenatal immune challenges may elevate the risk of schiz

164 Prenatal infection during pregnancy increases the risk f

165 ATEMENT In autism spectrum disorders (ASDs), prenatal infection or maternal immune activation (MIA) m

166 Human studies show the deleterious impact of prenatal inflammation and low n-3 polyunsaturated fatty

167 Androgens have male-specific prenatal influence over social brain circuitry in humans

168 al carriage in a community-based, randomized prenatal influenza vaccination trial in Nepal with weekl

169 r understanding of basic mechanisms by which prenatal insults impact offspring brain function, and su

170 te development is necessary to pioneer novel prenatal interventions.

171 tion of myoblasts, developmental failure and prenatal lethality.

172 une systems develop in parallel during early prenatal life.

173 nal smoking on human cortical biology during prenatal life.

174 a (PE) would allow providers to tailor their prenatal management and adopt preventive strategies, suc

175 ion.SIGNIFICANCE STATEMENT Understanding how prenatal maternal depression impacts child behavior is c

176 connectivity mediates relationships between prenatal maternal depressive symptoms and child behavior

177 s considered relevant confounders, including prenatal maternal depressive symptoms.

178 Different dimensions of prenatal maternal distress likely contribute shared and

179 Prenatal maternal distress-an umbrella concept encompass

180 that the epigenetic impact of a dysglycaemic prenatal maternal environment appeared to be modified by

181 avior is critical for appropriately treating prenatal maternal mental health problems and improving c

182 unity of offspring when exposed to direct or prenatal maternal stress, but little is known in humans.

183 quencing (scRNA-seq) to study the effects of prenatal METH exposure on fetal brain development.

184 Brain imaging studies in children with prenatal methamphetamine exposure (PME) suggest structur

185 for systemic lymphatic vessel development in prenatal mice and it is critical for their survival post

186 rgans examined, highlighting tissue-specific prenatal molecular phenotypes in SMA.

187 xamine systemic pre-symptomatic changes in a prenatal mouse model of SMA.

188 n analysis using RNA sequencing (RNA-seq) on prenatal (N = 33; 16 smoking-exposed) as well as adult (

189 Much of the available literature on human prenatal neural development comes from cross-sectional o

190 enatal brain, 2) summarize large-scale human prenatal neural network development, integrating finding

191 In summary, Myo10 is important for both prenatal (neural tube closure and digit formation) and p

192 role for this molecule in the regulation of prenatal neurogenesis.

193 Although genetic and prenatal non-genetic causes have been described, no syst

194 Here we test whether levels of prenatal oestriol, oestradiol, oestrone and oestrone sul

195 onment of high prenatal testosterone and low prenatal oestrogen inhibits lung development and may pre

196 relate of high prenatal testosterone and low prenatal oestrogen) and the age of lung cancer diagnosis

197 o make a like-to-like comparison between the prenatal oestrogens and androgens.

198 These results for the first time show that prenatal oestrogens contribute to autism likelihood, ext

199 Prenatal oestrogens need to be investigated, as they pla

200 res include congenital cataracts, hypotonia, prenatal-onset ventriculomegaly, white-matter abnormalit

201 We also found that prenatal OP exposure was associated with sex differences

202 amming, to windows of plasticity, and to the prenatal origin of disorders of childhood that involve d

203 hlight the persistent negative influences of prenatal parental smoking and youth substance use as the

204 ations were observed at both time points for prenatal parental smoking, life events, and negative aff

205 aternal education, smoking in pregnancy, and prenatal particulate matter with diameter of <2.5 microm

206 We consider the implications of prenatal pathological changes for the onset and progress

207 n in a rural area, and a large proportion of prenatal patients aged <15 years) and target (more prena

208 h meeting the baseline (larger proportion of prenatal patients aged 20 to 24 years) and target (more

209 are by referral only, a larger proportion of prenatal patients aged 25 to 44 or >=45 years, and a lar

210 e than 27 million persons, including 573 026 prenatal patients, at approximately 12 000 sites across

211 al patients aged <15 years) and target (more prenatal patients, location outside New England, provisi

212 Vitamin D supplementation during the prenatal period alone did not influence the 6-year incid

213 e farm animals, feed, and bedding during the prenatal period and in early infancy reduce the risk of

214 ts from exposure to air pollution during the prenatal period have not been not fully elucidated, espe

215 ntestinal microbiome affects health from the prenatal period throughout childhood, and many diseases

216 Smoking exposure during the prenatal period was directly associated with differentia

217 ns of mouse fetuses following MIA during the prenatal period, and evaluated the behavioral and bioche

218 ents presented with BRA, detected during the prenatal period, without additional recognizable malform

219 influences neurodevelopment during critical prenatal periods and in the absence of environmental cha

220 Prenatal PFAA were positively associated with longitudin

221 that DNA methylation changes may result from prenatal PFAS exposure and may be linked to offspring ca

222 Prenatal PFAS exposure is associated with adverse health

223 ylation changes mediate associations between prenatal PFAS exposures and child health outcomes.

224 We estimated associations of prenatal PFAS with DNA methylation in umbilical cord blo

225 ycerophospholipid metabolism associated with prenatal PFAS.

226 s, suggesting a possible association between prenatal PFBS exposure and adverse placentation.

227 tudies investigating the association between prenatal phthalate or bisphenol exposure and cognition h

228 specially regarding intertwin concordance of prenatal, placental, and infant outcomes.

229 Prenatal PM(2.5) exposure influenced mitochondrial respi

230 ) and 10% (SD = 2%) of the effect of average prenatal PM(2.5) exposure on neurodevelopment and behavi

231 neurodevelopment but directly influenced by prenatal PM(2.5).

232 Prenatal polybrominated diphenyl ether (PBDE) exposures

233 's Environmental Health to determine whether prenatal polycyclic aromatic hydrocarbons interacts with

234 Findings on prenatal polyunsaturated fatty acid (PUFA) intake and ch

235 e work from the past several decades linking prenatal preeclampsia to altered neurodevelopment.

236 nal immune activation contributes in part to prenatal programming of risk.

237 We sought to examine associations between prenatal PUFA status and child wheeze/asthma and modifyi

238 Associations between prenatal PUFA status and childhood wheeze/asthma were mo

239 DNA methylation as a key regulatory event of prenatal renal programming, which possibly represents a

240 Prenatal risk factors may interfere with early trajector

241 Prenatal risk factors were frequently found among indivi

242 Both passive and active prenatal sensitization conferred allergen sensitivity, r

243 enome-wide next-generation sequencing in the prenatal setting.

244 preference, readily available technology of prenatal sex determination, and fertility decline.

245 A prenatal sex steroid environment of high prenatal testos

246 n between right and left 2D:4D (biomarker of prenatal sex steroids exposure) and primary lung cancer

247 said to be a potential marker of exposure to prenatal sex steroids.

248 spliceQTL (sQTL), including several thousand prenatal-specific regulatory regions.

249 s prior to birth and is punctuated by a late prenatal spike in type I interferon signaling that promo

250 , which potentially refines estimates of its prenatal stage.

251 n about early altered cellular events during prenatal stages in autism.

252 vented both ventriculomegaly, as assessed at prenatal stages, and postnatal development of hydrocepha

253 s expressed in the heart during development, prenatal stages, lost in the neonate, and adult heart co

254 ated with autism may be established at early prenatal stages.

255 Elevated latent prenatal steroidogenic activity has been found in the am

256 ikelihood, extending the finding of elevated prenatal steroidogenic activity in autism.

257 To date, it is unclear if other prenatal steroids also contribute to autism likelihood.

258 en and 17/109 (16%) pregnant women following prenatal streptomycin exposure.

259 Lead (Pb) exposure and prenatal stress (PS) during development are co-occurring

260 ies have demonstrated an association between prenatal stress and neurodevelopmental disorders.

261 Maternal prenatal stress exposure (PNSE) increases risk for adver

262 Prenatal stress exposure is associated with risk for psy

263 re were obtained, along with demographic and prenatal stress measures.

264 esults emerge to suggest that the effects of prenatal stress on various aspects of brain development

265 Prenatal stress-induced fetal neuroinflammation is thoug

266 lammatory and metabolic dysregulation during prenatal stress.

267 unting for maternal postnatal depression and prenatal stress.

268 gs and the immune system had been exposed to prenatal stress.

269 provided non-fasting plasma samples during 3 prenatal study visits (at median 11, 25, and 35 weeks ge

270 We found no effects of prenatal supplementation on spirometric indexes.

271 ted with reduction of early preterm birth in prenatal supplementation trials.

272 rnal steroids in the setting of hydrops, and prenatal surgical intervention was uncommon (1.7%).

273 rain as well as potential sex differences in prenatal susceptibility, and 4) evaluate opportunities t

274 usted analyses showed no association between prenatal Tdap vaccination and ADHD in offspring (hazard

275 In this study, prenatal Tdap vaccination was not associated with ADHD r

276 A prenatal sex steroid environment of high prenatal testosterone and low prenatal oestrogen inhibit

277 4D (Delta2D:4D, a negative correlate of high prenatal testosterone and low prenatal oestrogen) and th

278 es, chromosomal females passively exposed to prenatal testosterone from male littermates exhibit alte

279 Here, we find that increasing prenatal testosterone in humans is associated with later

280 014, we investigated the association between prenatal tetanus, diphtheria, and acellular pertussis (T

281 use models we can discover novel targets for prenatal therapy.

282 ar evidence for context-dependent effects of prenatal THs related to postnatal temperature on growth,

283 ow initial ADC values, indicating an earlier prenatal time course of development.

284 ons such as polymicrogyria consistent with a prenatal timing of CNS injury.

285 hanges in microglial markers, indicates that prenatal TLR7 activation induces differential expression

286 Prenatal TLR7 activation via administration of the selec

287 Prenatal TLR7-activated mice have normal baseline locomo

288 antibiotic use, especially during the early prenatal to adolescent periods of life.

289 ectors were identified, including ethnicity, prenatal tobacco smoke exposure, history of allergies be

290 affected foetuses might be improved through prenatal treatment.

291 Prenatal ultrasounds were completed for each twin, and h

292 As prenatal vaccinations become more prevalent, it is impor

293 hma versus among mothers with early and late prenatal VD insufficiency, those with early or late VD s

294 We also examined the effect of prenatal VD level on early life asthma or recurrent whee

295 xamine the combined effect of early and late prenatal VD status in during pregnancies in women with a

296 ordered variable representing early and late prenatal VD sufficiency (25(OH)D level >= 30 ng/mL) stat

297 There was no effect of prenatal vitamin D supplementation on most of the prespe

298 reviously reported the results of a trial of prenatal vitamin D supplementation to prevent asthma and

299 Along these behavioral deficits, prenatal VPA exposure downregulated prefrontal cortex va

300 ical evidence supports a causal link between prenatal Zika Virus (ZIKV) infection and congenital brai