ライフサイエンスコーパス: placental

1 contains glycyrrhizin (a potent inhibitor of placental 11beta-hydroxysteroid dehydrogenase type 2, th

2 We measured the placental 3-NTp levels of 330 mother-newborn pairs enrol

3 hat maternal SERT function impacts offspring placental 5-HT levels, forebrain 5-HT levels, and neurod

4 reterm labor, anemia complicating pregnancy, placental abnormalities, infection during labor, materna

5 ), infection (aRR, 1.85; 95% CI, 1.43-2.29), placental abruption (aRR, 1.68; 95% CI, 1.18-2.38), indu

6 Placental abruption (early separation of the placenta) i

7 Placental accumulation is mediated by P. falciparum prot

8 Placental accumulation was dose dependent, and in some c

9 nant IL-10(-/-) mice with A-1254 resulted in placental activation of the Notch/Delta-like ligand (Dll

10 function with AMA in women, with evidence of placental adaptations in normal pregnancies.

11 Because mTOR is a positive regulator of placental amino acid transport and mitochondrial functio

12 Concentrations of placental and blood vitamin D metabolites and placental

13 mice limited ZIKV vertical transmission and placental and fetal damage and overall improved placenta

14 function of CD8(+) dT that are permissive of placental and fetal development, and reversal of this dy

15 uate the effects of maternal malnutrition on placental and fetal development.

16 cental and fetal damage and overall improved placental and fetal outcomes.

17 fetal ZIKV infection and ameliorated adverse placental and fetal outcomes.

18 sitivity and accuracy of PAI for analysis of placental and fetal oxygen saturation (sO2) in mice.

19 In summary, PAI enables the detection of placental and fetal oxygenation during normal and pathol

20 Accurate analysis of placental and fetal oxygenation is critical during pregn

21 s fetal viability and increases infection of placental and fetal tissues.

22 proved for use in pregnant women, attenuated placental and fetal ZIKV infection and ameliorated adver

23 nt transport display convergent co-option by placental and mammary gland cell types to optimize offsp

24 nflammatory cytokine and chemokine levels in placental and maternal peripheral blood.

25 y complication that may arise from maternal, placental and/or fetal factors.

26 fficking of these miRNAs among the maternal, placental, and fetal compartments is unknown.

27 diminished levels of viral RNA in maternal, placental, and fetal tissues, which resulted in protecti

28 diminished levels of viral RNA in maternal, placental, and fetal tissues.

29 uss the potential contributions of maternal, placental, and fetal viral infection to pregnancy outcom

30 al liver Pparg mRNA expression and increased placental androgen receptor protein expression.

31 teins and PlGF pathways in the regulation of placental angiogenesis.

32 ly produced from trophoblasts is involved in placental angiogenesis.

33 ded evidence for pregnancy complications and placental anti-angiogenesis in response to Aroclor 1254

34 young uterine environment can restore normal placental as well as embryonic development.

35 s employed by microorganisms to overcome the placental barrier and prospects for the future.

36 Nile virus (WNV), can efficiently infect key placental barrier cells that directly contact the fetal

37 Z2 can penetrate the placental barrier to enter fetal tissues and is safe for

38 ssociated with congenital disease breach the placental barrier to transit vertically during human pre

39 ZIKV causes microcephaly by crossing the placental barrier, however, the mechanism of trans-place

40 associated with breakdown of maternal/fetal placental barrier.

41 s, the fetal-derived cells that comprise the placental barrier.

42 for discovering more about maternofetal and placental biology.

43 ent.The numerous associations of many of the placental biomarkers of vitamin D metabolism with circul

44 nancy loss, and increased IL-1beta levels in placental blood were associated with pregnancy loss and

45 gestational week 30-32, and delivery, and in placental blood, of 638 women during a longitudinal coho

46 may form a complex to functionally regulate placental cell function through modulation of target gen

47 ck a mesoderm signature and are a subtype of placental cells unlike those present at term.

48 ered hCG and PPARgamma expression in primary placental cells.

49 asmodium falciparum-infected erythrocytes to placental chondroitin sulfate A (CSA) through the PfEMP1

50 Our results implicate PTEF in regulating placental CSA binding of infected erythrocytes.

51 Oxidative stress results in reduction of placental CSE activity, decreased hydrogen sulfide produ

52 issues, which resulted in protection against placental damage and fetal demise.

53 ayer, which may partially compensate for the placental deficits.

54 s markedly enhanced angiogenic responses and placental development in DC expanded IL-10(-/-) dams.

55 Homeobox genes regulate embryonic and placental development, and are widely expressed in the h

56 egulation of a network of genes required for placental development, suggesting a central role for the

57 To understand its role in placental development, we established a novel Egfl7 knoc

58 through early gestation (to E8.5) to support placental development.

59 may play important roles in early stages of placental development.

60 is unique to eutheria, suggesting a role in placental development.

61 of a key growth factor regulating fetal and placental development.

62 ion in late gestation is required for proper placental differentiation and function.

63 These placental disruptions were associated with altered gene

64 tal barrier, however, the mechanism of trans-placental dissemination of ZIKV remains unknown.

65 few studies suggested an association between placental dysfunction and fetal CHD.

66 lation at E10 causes placental inflammation, placental dysfunction and reduces neonatal brain cortica

67 These findings highlight placental dysfunction as a potential mechanism for susce

68 rameters have the potential to help identify placental dysfunction associated with FGR and may have c

69 VSASL may serve as a potential biomarker of placental dysfunction in fetuses diagnosed with CHD.

70 hat maternal ageing is associated with utero-placental dysfunction, predisposing to adverse fetal out

71 These studies identify reduced placental efficiency and altered placental function with

72 In vitro, placental endothelial cells were deficient in migration,

73 ption is known to disrupt the ability of the placental enzyme 11beta-hydroxysteroid dehydrogenase typ

74 Finally, our results suggest the placental eQTLs may mediate the function of GWAS loci on

75 e loci of genome-wide significance, 835 were placental eSNPs (enrichment fold = 1.68, P = 7.41e-42).

76 a and IL-6, a result confirmed in human term placental explants.

77 s extruded into the maternal circulation via placental exracellular vesicles.

78 is carried into the maternal circulation via placental extracellular vesicles.

79 e recent Zika virus infection in a maternal, placental, fetal, or infant sample.

80 ween rodent and human cardiac physiology and placental-fetal development indicate a need for models i

81 g a significant driver of clinical symptoms, placental Flt1 mRNA levels strongly correlate with mater

82 f uterine morphological changes required for placental formation and fetal development.

83 androgen excess in obese dams on metabolism, placental function and fetal growth, female C57Bl6J mice

84 Effects on placental function have been suggested as a biologic bas

85 peroxia to quantitatively assess mismatch in placental function in seven monozygotic twin pairs natur

86 We evaluated the effects of phthalates on placental function in vitro by measuring relevant candid

87 with maternal hyperoxia to quantify regional placental function in vivo.

88 ify reduced placental efficiency and altered placental function with AMA in women, with evidence of p

89 olecular basis by which phthalates may alter placental function, and they provide a preliminary mecha

90 Fetal health is critically dependent on placental function, especially placental transport of ox

91 associations between maternal phthalates and placental gene expression were reproduced experimentally

92 ta are under tight genetic control, and that placental gene networks may influence postnatal risk of

93 py multiple sites in epigenetically inactive placental genes and in OCT4 Functional manipulation of G

94 otal clavicle-sternal joint in marsupial and placental gliders.

95 by HFHS feeding were related to altered feto-placental glucose metabolism and growth.

96 HS feeding was associated with impaired feto-placental glucose metabolism and growth.

97 and insulin resistance, as well as, on feto-placental glucose metabolism.

98 etabolism of the mother, in relation to feto-placental glucose utilization and growth, are unknown.

99 f preneoplastic foci in the liver (increased placental glutathione S-transferase and cytokeratin 8-18

100 The bulk of placental growth and development in the first trimester

101 nsitivity and signalling in relation to feto-placental growth and glucose utilization are unknown.

102 ution of isoforms of VEGF and of the related placental growth factor (PlGF) in the body and resulting

103 Placental growth factor (PlGF), abundantly produced from

104 r; platelet-derived growth factor AA and BB; placental growth factor; vascular endothelial growth fac

105 g, meiotic recombination hotspot choice, and placental growth.

106 a cohort of 90 preterm infants with detailed placental histology and neonatal brain magnetic resonanc

107 n had personal air exposure measurements and placental histopathology available for analysis.

108 zyme 2 knockout mouse model characterized by placental hypoxia.

109 y reduced the preterm birth rate and altered placental immune profile with decreased CD8(+) T-cell in

110 We found disturbed placental imprinting in preeclampsia and revealed potent

111 ling in WT pregnant mice enhanced ZIKV trans-placental infection although it did not result in fetal

112 ew, we first consider the pathophysiology of placental infection and transplacental transmission of t

113 ns against parasitological endpoints such as placental infection at delivery and health outcomes incl

114 ystals to rats during late gestation induced placental inflammation and was associated with fetal gro

115 Excessive placental inflammation is associated with several pathol

116 ZIKV inoculation at E10 causes placental inflammation, placental dysfunction and reduce

117 for gestation length, neonatal mortality, or placental inflammation.

118 er, these data demonstrate the novel role of placental InsRs in sex-specific neurodevelopment and rev

119 off the risk of prolonged fetal exposure to placental insufficiency against the risks of preterm del

120 nfection at embryonic day 6 (E6) resulted in placental insufficiency and fetal demise, infections at

121 Placental insufficiency and intrauterine growth restrict

122 l of these observations in sheep models with placental insufficiency are consistent with cases of hum

123 If placental insufficiency is present, the physician must t

124 When fetal growth is compromised, placental insufficiency must be distinguished from modes

125 s to reduced oxygen and nutrient supply with placental insufficiency that develop to slow hindlimb gr

126 To determine how placental insufficiency with reduced oxygen and nutrient

127 Because defective placental insulin receptor (InsR) signaling is a hallmar

128 The placental interface mediates the interaction between two

129 d regulatory aspects of maternal, fetal, and placental iron homeostasis.

130 role of fetal hepcidin in the regulation of placental iron transfer still remains to be characterize

131 kinase 1, providing biological support, as a placental isoform of this protein (sFlt-1) is implicated

132 duced BCRP mRNA up to 10-fold in human model placental JEG3 and BeWo cells and in primary human villo

133 The placental labyrinth (L) had a higher sO2 than the juncti

134 suggest that the proper organization of the placental labyrinth depends on coordinated inter-endothe

135 The placental labyrinth is the interface for gas and nutrien

136 ular mechanism underlying development of the placental labyrinth, particularly in terms of its endoth

137 sed in endothelial cells specifically in the placental labyrinth.

138 in the embryonic vasculature and heart, the placental labyrinths of these embryos exhibited aberrant

139 We fused human placental lactogen (hPL), a specific and tight binding P

140 ogenic activity ex vivo, is expressed at the placental level as revealed by in situ hybridization and

141 This maternal intervention prevented excess placental lipid deposition and hypoxia (independent of s

142 Differences in placental longitudinal R1 (1/T1) and transverse R2* (1/T

143 Pan-placental macrophages, CD4 and CD8 T cells indicate a wi

144 gestational days 85 and 135, they underwent placental magnetic resonance imaging after intravenous g

145 A mother's infection with placental malaria (PM) can affect her child's susceptibi

146 Placental malaria is caused by Plasmodium falciparum-inf

147 duced malaria incidence during pregnancy and placental malaria risk.

148 Through amplicon deep-sequencing placental malaria samples from women in Malawi and Benin

149 observed that children born to mothers with placental malaria, but not those born to mothers with pe

150 yrimethamine (SP) in preventing maternal and placental malaria.

151 in the risk of histopathologically detected placental malarial infection between the daily TMP-SMX p

152 mary outcome was detection of active or past placental malarial infection by histopathologic analysis

153 e shortest lactation periods of any group of placental mammal.

154 teleosts has evolved in a divergent manner: placental mammals have lost the monoaminergic CSF-c cell

155 They have been found in all placental mammals in which they have been searched, incl

156 Eutherians are often mistakenly termed 'placental mammals', but marsupials also have a placenta

157 w that syncytin capture is not restricted to placental mammals, but can also take place in the rare n

158 e C2H2-ZF domain in the common progenitor of placental mammals, but that extant C2H2-ZF domains typic

159 e transcriptomic study of the cervix of four placental mammals, mouse, guinea pig, rabbit and armadil

160 t, compared with the Leu(8)OXT found in most placental mammals, the Cebidae Pro(8)OXT and Saguinus Va

161 ly to have played a role in the emergence of placental mammals, with evidence for multiple, reiterate

162 alamic region of most vertebrates except for placental mammals.

163 ders within arboreal groups of marsupial and placental mammals.

164 role for these microRNAs in the evolution of placental mammals.

165 in the common stem lineage of marsupial and placental mammals.

166 ng mechanisms vary significantly, even among placental mammals.

167 he patterns of gene expression in eutherian (placental) mammals are consistent with the notion that a

168 igen was seen in the syncytiotrophoblast and placental maternal mononuclear cells by immunohistochemi

169 n (0, 300 or 1000 microg/day; GD 9 - 18) for placental measurements or perinatally (0, 100, 300 or 10

170 lacental and blood vitamin D metabolites and placental messenger RNA (mRNA) abundance of vitamin D me

171 cells (CTB) an insignificant contributor to placental metabolic activity.

172 as been presumed to be the primary driver of placental metabolism, and the underlying progenitor cyto

173 th 24,25-dihydroxyvitamin D3 Moreover, these placental metabolites were strongly correlated (r </= 0.

174 -specificity to the placental microbiota and placental microbiome studies should consider regional di

175 ggest that there is niche-specificity to the placental microbiota and placental microbiome studies sh

176 Expression and trafficking of placental microRNAs at the feto-maternal interface.

177 Our mouse models showed that placental miRNA traffic primarily to the maternal circul

178 f the IGFs and their signalling machinery on placental morphogenesis, substrate transport and hormone

179 hypoxia (10% inspired O2) from D14 to D19 on placental morphology, transport capacity and fetal growt

180 ons (P </= 0.045) were also observed between placental mRNA abundance of vitamin D metabolic componen

181 RNA-Seq of placental mRNA from Zfp36l3 knockout (KO) mice revealed

182 res of stress were associated with decreased placental mtDNAcn (all P values < 0.05).

183 ed maternal psychosocial stress with reduced placental mtDNAcn and add to literature documenting raci

184 raumatic-stress-disorder symptom scores with placental mtDNAcn in a racially/ethnically diverse sampl

185 o acid transport and mitochondrial function, placental mTOR folate sensing may constitute the mechani

186 and that maternal folate deficiency inhibits placental mTOR signaling and amino acid transporter acti

187 ty and fetal growth, involving regulation of placental mTOR signaling by folate, resulting in changes

188 Maternal folate deficiency inhibited placental mTORC1 and mTORC2 signaling and decreased trop

189 nal serum folate is positively correlated to placental mTORC1 and mTORC2 signalling activity in human

190 istinct bacterial taxa dominate in different placental niches.

191 egnancy predicts increased expression of the placental nonheme Fe transporter TfR1.

192 folate sensing in trophoblast cells matches placental nutrient transport, and therefore fetal growth

193 signaling by folate, resulting in changes in placental nutrient transport.

194 s of delta(44/42)Ca record a transition from placental nutrition to an adult-like diet and that Ca is

195 to daily TMP-SMX did not reduce the risk of placental or maternal malaria or improve birth outcomes.

196 strong immunological stimulus from prolonged placental or transplacental ZIKV shedding and potential

197 following periods of gestational hypoxia and placental oxidative stress.

198 Psychosocial stress contributes to placental oxidative stress.

199 oustic imaging for in vivo quantification of placental oxygenation in mice.

200 and loaded with a tocolytic for reducing its placental passage and sustaining its efficacy.

201 er delivery, birth weights were obtained and placental pathological evaluations were performed.

202 insight into etiological factors underlying placental pathologies associated with intrauterine growt

203 Placental pathologies of inflammatory, hypoxic, ischemic

204 Placental pathology associated with household air pollut

205 tal outcomes, we explored the association of placental pathology with household air pollution in preg

206 he association of PM2.5 and CO exposure with placental pathology.

207 -specific pregnancy syndrome associated with placental pathology.

208 ean placental TTP positively correlated with placental pathology.

209 Sildenafil treatment protects placental perfusion and fetal growth, but whether the ef

210 Evidence shows that sildenafil protects placental perfusion and fetal growth.

211 Placental perfusion imaging was performed using velocity

212 In this study, we report placental perfusion of healthy pregnancies and pregnanci

213 In pregnancies with fetal CHD, global placental perfusion significantly decreased and regional

214 ficantly decreased and regional variation of placental perfusion significantly increased with advanci

215 Also, global placental perfusion was significantly higher in fetal CH

216 Consistent with poor feto-placental perfusion, Egfl7 knockout resulted in reduced

217 , including humans, is secondary to improved placental perfusion.

218 defects are an important determinant of the placental phenotype.

219 adverse fetal outcomes and commonalities in placental phenotype.

220 y, independent of changes in the maternal or placental physiology.

221 position versus supine, and in the posterior placental position versus anterior placental position.

222 posterior placental position versus anterior placental position.

223 al, CpG density-dependent methylation in the placental progenitor.

224 dysregulated expression of many genes (e.g. placental proteins, markers of oxidative stress).

225 A functioning placental renin-angiotensin system (RAS) appears necessa

226 role of IGFs during pregnancy in regulating placental resource allocation to fetal growth is importa

227 in-like growth factors (IGFs) in controlling placental resource allocation to fetal growth, particula

228 estimates), as did P falciparum detected in placental samples (OR 1.95 [1.48-2.57]; I(2)=33.6%; 31 e

229 Malaria infections with placental sequestration have long-lasting impact on infa

230 ith peripheral infection without evidence of placental sequestration, had increased risk of malaria d

231 ring pregnancy has pointed to alterations in placental signaling, including changes in inflammatory,

232 trast to untreated C57Bl/6, L-NAME decreased placental sO2 at GD14 and GD18 vs GD10 or GD12.

233 Placental sO2 was lower in fetal growth restriction in a

234 us retroelements, as a direct repressor of a placental-specific Igf2 transcript (designated Igf2-P0)

235 l analysis, and no antigen was seen in fetal placental stromal cells or fetal organs.

236 y within the uterus, amniotic fluid, and the placental structure reveals that the developing fetus is

237 Placental structures are not restricted to mammals but a

238 responsible for the diversity of present day placental structures.

239 poietic cells, and in the case of pregnancy, placental syncytiotrophoblast cells) and several forms o

240 clampsia (PE), there is increased release of placental syncytiotrophoblast extracellular vesicles (ST

241 with or without LDA treatment on a model of placental syncytium.

242 distributed lag models, both cord blood and placental telomere length were associated with average w

243 In 641 newborns, cord blood and placental telomere length were significantly and inverse

244 lomere length as reflected by cord blood and placental telomere length.

245 and 13.2% (95% CI, -19.3% to -6.7%) shorter placental telomere length.

246 ipants with full data on both cord blood and placental telomere lengths were included, resulting in a

247 ure in vimentin knockout (VimKO) embryos and placental tissue is underdeveloped with reduced branchin

248 CaMYB31 expression analysis from placental tissue of pungent and nonpungent chili pepper

249 In the newborns, cord blood and placental tissue relative telomere length were measured.

250 along with the regulation of target genes.In placental tissue, 25-hydroxyvitamin D3 [25(OH)D3] was st

251 ancy, virus was also found in the uterus and placental tissue.

252 ring the accumulation of FM 550 compounds in placental tissue.

253 w limited contribution to the extraembryonic placental tissues in vivo.

254 The placental transcription factors Distal-less 3 (DLX3) and

255 ncy can compromise the iron availability for placental transfer and impair the efficacy of iron suppl

256 iding passive protection to newborns through placental transfer of anti-RSV antibody.

257 Placental transfer of Delta9-tetrahydrocannabinol (THC)

258 etween prenatal manganese concentrations and placental transfer of manganese with neurodevelopment in

259 Placental transfer, approximated by cord/maternal mangan

260 res during pregnancy and factors influencing placental transfer.

261 itional mother-specific factors, such as the placental transmission of antibodies, cannot be fully ru

262 dependent on placental function, especially placental transport of oxygen from mother to fetus.

263 Placental triglyceride oscillations in the third trimest

264 This protection was due to a placental trophoblast cell-autonomous effect of autophag

265 e studied the cell-cell interactome of fetal placental trophoblast cells and maternal endometrial str

266 However, the role of PRDX3 in placental trophoblast cells under ICP is not fully under

267 We hypothesized that LDA influences placental trophoblast function and reverses PE-associate

268 two models to study susceptibility of human placental trophoblast to ZIKV: cytotrophoblast and syncy

269 dult offspring were evaluated for effects of placental trophoblast-specific InsR deficiency on stress

270 Male, but not female, mice with placental trophoblast-specific InsR deficiency showed a

271 During pregnancy, placental trophoblasts at the feto-maternal interface pr

272 nt AhR agonists and can induce BCRP in human placental trophoblasts by activating AhR.

273 In this study, we show that primary human placental trophoblasts from non-exposed donors (n = 20)

274 that ZIKV-FLR strain can replicate in human placental trophoblasts without host cell destruction, th

275 onditionally target InsRs in fetally derived placental trophoblasts.

276 Mean placental TTP negatively correlated with fetal liver and

277 Mean placental TTP positively correlated with placental patho

278 chorioallantoic branching morphogenesis and placental vascular patterning.

279 mbilical arterial flow, indicating increased placental vascular resistance.

280 these data reveal that Egfl7 is crucial for placental vascularization and embryonic growth, and may

281 of microCT for ex-vivo examination of human placental vessel morphology.

282 tility of the technique in the comparison of placental vessel networks in normal and fetal growth res

283 ique for three-dimensional analyses of human placental vessels; (ii) demonstrate the utility of the t

284 hoblast and syncytiotrophoblast derived from placental villi at term and colonies of trophoblast diff

285 ver established physically in the human, the placental villi, the exocoelomic cavity, and the seconda

286 rnal uterine, endothelial, and immune cells; placental villi, which are bathed in maternal blood, and

287 ng pathologic entities representing abnormal placental villous tissue with unique genetic profiles an

288 hasizes the immunological challenge to clear placental viral infections within the immune-privileged

289 Little is known about placental vitamin D metabolism and its impact on materna

290 ught to advance the current understanding of placental vitamin D metabolism and its role in modulatin

291 These data suggest that placental VSASL may serve as a potential biomarker of pl

292 ns, 221 g [95% CI, 6-436]; P = .044) and the placental weight (difference between means, 84 g [95% CI

293 erfusion, Egfl7 knockout resulted in reduced placental weight and fetal growth restriction.

294 etal deaths, reduced fetal weight, increased placental weight and reduced fetal:placental weight rati

295 act on fetal growth, pregnancy duration, and placental weight at term.

296 increased placental weight and reduced fetal:placental weight ratio compared to 8-12 week controls.

297 t by approximately 10% compared with FA, and placental weight was reduced ( approximately 8%) on GD17

298 roup was decreased (-17%, p < 0.05), whereas placental weight, litter size and crown rump length were

299 M-1 were significantly associated with lower placental weight, thus increasing the risk of LBW.

300 enital malformations in boys born with a low placental weight.