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1 eks 12-25 for cord blood and weeks 15-27 for placenta).
2 ed TB cell lines and primary cells from term placenta.
3 hrough the endothelium of brain, retina, and placenta.
4 us CTBs normally upregulate as they exit the placenta.
5 itor cells for both the new organism and the placenta.
6 give rise to complex structures such as the placenta.
7 lobal metabolism in the late gestation human placenta.
8 orphological and functional phenotype of the placenta.
9 th the Igf2r cluster extending over 10 Mb in placenta.
10 ed by preserving PPARgamma expression in the placenta.
11 the transport capacity and metabolism of the placenta.
12 iral infections within the immune-privileged placenta.
13 ssion plasmids, which we tested in the mouse placenta.
14 e the risk of LBW by transmission across the placenta.
15 xposure by altering BCRP expression in human placenta.
16 xtravillous trophoblast lineage in the human placenta.
17 he first single-cell RNA-seq analysis of the placenta.
18 xtraembryonic lineage that gives rise to the placenta.
19 entiate into all trophoblast subtypes of the placenta.
20 l ends of mutant ovaries and thinning of the placenta.
21 to the plasma membrane of the trophoblast in placenta.
22 ed in regulating HOX genes expression in the placenta.
23 rophoblast giant cells (p-TGCs) of the mouse placenta.
24 he pregnant mother affects metabolism of the placenta.
25 ion to form the yolk sac, umbilical cord and placenta.
26 the organism being detected in the diseased placenta.
27 eeclamptic placenta as well as uncomplicated placenta.
28 ion enables confirmation that it crosses the placenta.
29 in primary human trophoblasts isolated from placenta.
30 ransferred from mother to neonate across the placenta.
31 y with calcifications in the fetal brain and placenta.
32 the normal immunoprotective responses of the placenta.
33 elatively very low levels in adult brain and placenta.
34 or listeriosis with a strong tropism for the placenta.
35 the chorion and labyrinth layer of the mouse placenta.
36 micals may sex-dependently accumulate in the placenta.
37 to Plasmodium falciparum accumulation in the placenta.
38 ve rise to specialized cell types within the placenta.
39 press C19MC miRNA members selectively in the placenta.
40 which is expressed nearly exclusively in the placenta.
41 during gestation, while some only infect the placenta.
42 anti-angiogenic factors originating from the placenta.
43 (CSE) is down-regulated in growth-restricted placentas.
44 DLX5 was upregulated in 69% of preeclamptic placentas.
45 n the high- compared with low-altitude human placentas.
46 OPA1 mRNA and protein expression in the eoPE placentas.
47 hway genes-HSD11B2, NR3C1, and FKBP5-in term placentas.
48 horionic villi of one of the first trimester placentas.
49 , Mmrn1, were temporally dysregulated in the placentas.
50 lls mimics the transcriptome of preeclamptic placentas.
51 iscrepancies in vessel length density in FGR placentas.
52 ut wall thickness remained unchanged in IUGR placentas.
53 QTLs at </=10% false discovery rate in human placentas.
54 us for IGF2 and H19 methylation levels of 48 placentas.
55 rebrain, suggesting that altered maternal or placenta 5-HT system function could impact the developin
57 ithin the uterine environment depends on the placenta, a highly complex vascularized organ comprised
58 t is the primary epithelial cell type in the placenta, a transient organ required for proper fetal gr
59 are epithelial stem cells of the early human placenta, able to differentiate either into syncytiotrop
60 ult bloodstream by lipoproteins and that the placenta acquires, assembles, and secretes lipoproteins,
62 spite its defective development, the alpha/+ placenta adapted functionally to increase the supply of
66 rofiles depending on the location within the placenta and (2) "semi-composite" 16S profiles using mul
67 me-wide assessment of DNA methylation in the placenta and arsenic exposure in the New Hampshire Birth
71 king during pregnancy have been described in placenta and cord blood at delivery, in fetal lung, and
72 nd lipid metabolism) were hypermethylated in placenta and cord blood from SGA newborns, whereas GPR12
73 d differences in regulation of imprinting in placenta and cord blood; a lack of correlation of the me
75 Ala56 genotypes to examine effects on blood, placenta and embryo serotonin levels and neurodevelopmen
77 Ala56 genotype was associated with decreased placenta and embryonic forebrain 5-HT levels at E14.5.
83 , Il6, Ccl2, Pghs2, and Mpges1 expression in placenta and fetal membranes, and it elevated amniotic f
85 rnal immunity required for protection of the placenta and fetus against congenital cytomegalovirus (C
86 IKV transmission in utero, we found that the placenta and fetus were more susceptible to ZIKV infecti
87 naling had increased ZIKV replication in the placenta and fetus when infected at E12, and reciprocall
90 arisons with microarray datasets from mutant placenta and in vitro differentiated trophoblast stem ce
91 o identify novel imprinted DMRs in the human placenta and investigated the dynamics of these imprinte
94 we performed yeast-two-hybrid screenings of placenta and lung cancer cDNA libraries, which demonstra
96 ping preventative treatments that target the placenta and not the fetus to reduce risk of psychiatric
97 ancy, we sequenced miRNAs in triads of human placenta and of maternal and fetal blood and found large
99 ns in fruit development: while TAG1 controls placenta and seed formation, TAGL1 participates in cutic
101 methylation status of specific genes in the placenta and thus supports a potentially novel mechanism
103 in the accumulation of target transcripts in placenta and/or yolk sac, and that some of these would b
104 of imprinting (LOI) of IGF2 and H19 genes in placentas and cord blood of 90 mother-child dyads in ass
105 ong 47 placentas heterozygous for H19 and 37 placentas and cord blood tissues heterozygous for IGF2 a
106 mary cell types from mid- and late-gestation placentas and explants from first-trimester chorionic vi
107 Guided by these studies, we analyzed mouse placentas and identified a population with this phenotyp
108 fferentially expressed genes in preeclamptic placentas and intersected them with the list of human im
111 in trophoblast and endothelial cells in the placenta, and endothelial, microglial and neural progeni
113 y in the gastrointestinal tract, kidney, and placenta, and glycosylation seems essential for reaching
114 ating AMPK) were present in murine and human placenta, and hypoxia increased LKB1 and AMPK-alpha1 and
115 urified neurons and glia, T lymphocytes, and placenta, and identify 795 hap-ASM differentially methyl
117 demonstrated in vertebrate-specific tissues, placenta, and parathyroid glands, begging questions on t
118 (+)-naloxone, and cytokine expression in the placenta, and uterine myometrium and decidua, was also a
119 ant vasculogenesis in embryos, yolk sacs and placentas, and die between embryonic day 10.5 and 11.5.
121 morphology, reduced junctional zone, smaller placentas, and impaired spiral artery remodeling with fe
122 The ZFP36L3 protein is a rodent-specific, placenta- and yolk sac-specific member of the tristetrap
123 estration and consequent inflammation in the placenta are common attributes of placental malaria.
125 r network of large organs, such as the human placenta are limited, preventing adequate comparison of
126 Two hypotheses regarding the role of the placenta are possible: one is that the placenta directly
128 isolated from early-gestation (6-8 wk) human placentas are bipotential, a phenotype that is lost with
131 acental growth and function and identify the placenta as critical in integrating both intrinsic and e
132 persist in the mid- to late- gestation mouse placenta as well as a cell surface protein that can be u
133 LTR, with sites of expression including the placenta as well as other tissues and rather unexpectedl
136 s an enigmatic inflammatory condition of the placenta associated with fetal growth restriction and st
137 lopment of methods for detecting fetuses and placentas at risk as a means of reducing preterm brain i
138 sh border of syncytiotrophoblast of infected placentas; (b) amounts of megalin and Dab2 were strongly
143 or megalin, which is abundantly expressed in placenta but was not previously analyzed in pregnancy ou
144 e proliferation or increase apoptosis in the placentas but induced extensive apoptosis in the brain.
145 pment, and are widely expressed in the human placenta, but their regulatory control by DNA methylatio
146 Viruses can gain access to the decidua and placenta by ascending from the lower reproductive tract
147 man IgGs are actively transferred across the placenta by binding the neonatal Fc receptor (FcRn) expr
148 imprinted DMRs were identified in the human placenta by comparing methylation between diandric and d
149 ely activated in either the pituitary or the placenta by distinct components of a remote locus contro
150 onfirm that preeclampsia is a disease of the placenta by generating and analyzing genome-wide molecul
153 n Time-To-Plateau (TTP) were obtained in the placentas by voxel-wise fitting of the time series.
154 rall, the present study shows that the mouse placenta can integrate signals of oxygen and nutrient av
155 Maternal antibodies transported across the placenta can provide vital immunity against infectious p
157 rations of Cd, Pb, Hg, Mn, Se, and Zn in 750 placentas collected from women enrolled in the New Hamps
160 (>40-fold) expression of C19MC miRNA in the placenta, compared with other organs, that resembled C19
161 ithin trophoblasts of the maternal and fetal placenta, consistent with a trans-placental infection ro
163 te sequencing was performed with a subset of placentas, cord blood samples, and buccal samples collec
166 nificant interest in elucidating the role of placenta-derived exosomes (PdEs) during pregnancy, the e
167 ceptor mRNA was unexpectedly decreased in KO placentas, despite an increase in its stability in KO st
169 ssor Prdm1/Blimp1, an essential regulator of placenta development, were identified in ChIP-seq experi
170 f the placenta are possible: one is that the placenta directly conveys the Zika virus to the early em
172 regnancy is relatively short, and although a placenta does form, it is present for only a few days be
173 sexual transmission, an ability to cross the placenta during pregnancy and infect the developing fetu
174 d ESCs contributed to the development of the placenta, embryolemma and umbilical cord at 13.5 dpc and
175 ssion of TCblR/CD320 in the labyrinth of the placenta, embryonic brain, and spinal column in wild-typ
176 rted in extragonadal tissues including bone, placenta, endometrium, liver, and blood vessels from a n
177 another member of this small group of genes, Placenta Expressed Transcript 1 (Plet1), for its functio
178 onstrate that the anatomically simple tammar placenta expresses a dynamic molecular program that is r
182 amniochorionic membranes from mid-gestation placentas formed foci of infection, and interferon-beta
183 lopment, serotonin (5-HT) synthesized in the placenta from maternal l-tryptophan (TRP) reaches the fe
188 at epithelial cells in amniotic membranes of placentas from newborns with intrauterine growth restric
190 riglyceride patterns were disrupted in human placentas from pregnancies with large-for-gestational ag
192 y after birth, one 2-month-old baby, and two placentas from spontaneous abortions, from Brazil were s
194 we immunostained amniotic membranes from 51 placentas from symptomatic and asymptomatic congenital i
195 ed a genome-wide DNA methylation analysis in placentas from term infants born appropriate-for-gestati
198 Previous studies showed that high levels of placenta growth factor (PlGF) correlated with increased
203 viation from monoallelic expression among 47 placentas heterozygous for H19 and 37 placentas and cord
204 o-hematopoietic transition in the embryo and placenta; however, the precursor cells to hemogenic endo
205 nd macrophages were increased throughout the placenta in stillbirths; pan-placental CD4(+) and CD8(+)
206 Here we review the novel involvement of the placenta in the transmission of the maternal adverse env
208 Primary AmEpCs isolated from mid-gestation placentas infected with pathogenic VR1814 proliferated a
210 rome (APS) does not prevent life-threatening placenta insufficiency-associated complications such as
212 These results suggest that bacteria from the placenta invade the fetal brain after maternal hypoxia.
213 ulthood may have an in utero origin, and the placenta is a key organ that plays a pivotal role in fet
215 site of materno-fetal nutrient transfer, the placenta is central to this interplay; however, the rela
217 We propose that although a choriovitelline placenta is never established physically in the human, t
224 Placental abruption (early separation of the placenta) is associated with preterm birth and perinatal
225 sical HLA molecule uniquely expressed in the placenta, is a central component of fetus-induced immune
229 ging revealed patchy perfusion of Egfl7(-/-) placentas marked by impeded blood conductance through si
230 lites, especially 25(OH)D3, suggest that the placenta may play an active role in modulating the vitam
231 ailability is mediated by coordinated muscle-placenta metabolic adjustments linked to internal clocks
232 ue plastic vessel networks of normal and FGR placentas (n = 12/group) were created by filling the ves
233 CXCL14) to test with qPCR in a larger set of placentas (n = 475) and found no differences between the
234 xation of imprinting (ROI) and LOI of H19 in placentas not associated with differences in methylation
236 locytic MDSCs (GR-MDSCs) accumulate in human placenta of healthy pregnancies but are diminished in pa
238 lipid content was significantly lower in the placentas of overweight and obese women supplemented wit
239 ns to fetal plasma or to secretions from the placenta or from model trophoblast barriers that had bee
246 inflammasome activation specifically in the placenta, pharmacological inhibition of inflammasome or
250 ynamic than previously reported and that the placenta preferentially maintains maternal germline-deri
253 d in numerous fetal tissues, 2) ex vivo, the placenta released high amounts of apelin in late gestati
254 ly that trophoblasts isolated from full-term placentas resist infection by diverse viruses, including
256 describe the innate mechanisms by which the placenta restricts microbial access to the intrauterine
258 l structure of aromatase purified from human placenta, revealing an androgen-specific active site.
262 hroughput transcriptome analyses of multiple placenta samples from healthy controls and patients with
263 ion and had serum, urine, amniotic fluid, or placenta samples tested by real-time polymerase chain re
266 stational diabetes mellitus (GDM)-associated placenta, SERT is found entrapped in the cytoplasm of th
269 f STBEVs into primary HCAEC, and transfer of placenta specific miRNAs from STBEVs into the endoplasmi
272 associated with altered miRNA expression in placenta, suggesting a potential mechanism of EDC toxici
274 ved between GWAS SNPs and gene expression in placentas than what has been reported in other tissues,
275 ypoxia promotes damaging secretions from the placenta that affect fetal development and whether a mit
276 experimental models with a small, defective placenta that restricts delivery of nutrients and oxygen
277 al milieu are conveyed to the embryo via the placenta, the maternal-fetal intermediary responsible fo
278 removing a toxic aggregated protein from the placenta, they may also be delivering aggregated transth
281 tene induces a feed-forward mechanism in the placenta to enhance the assimilation of beta-carotene fo
286 d high-throughput RNA sequencing of a Mabuya placenta transcriptome and screened for the presence of
292 of abnormal placental development; abnormal placentas were observed predominantly in abnormally deve
294 r was not associated with methylation in the placenta, whereas arsenic levels quantified through mate
295 the effects of hypoxia on the growth of the placenta, which is the organ that interfaces between the
296 to form properly in the majority of abnormal placentas, which compromised the integration of the mate
297 ed genes were found in late-onset PE and GDM placentas, which may suggest that these conditions could
299 ll as Mel 624 parental cells, and human term placenta whole tissue sections were used as controls and
300 e demonstrate that (1) both agents cross the placenta with rapidly detectable fetal serum concentrati
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