ライフサイエンスコーパス: maternal blood

1 Percentage of free fetal DNA in samples of maternal blood.

2 ld be a leading factor for thrombosis in GDM maternal blood.

3 Rare nucleated fetal cells circulate within maternal blood.

4 ome the need for direct sampling of fetal or maternal blood.

5 e assessment of the entire fetal genome from maternal blood.

6 tudy variability, performance was high using maternal blood.

7 croparticles released from the placenta into maternal blood.

8 in contact with immune cells circulating in maternal blood.

9 syncytiotrophoblast interacts directly with maternal blood.

10 sions were significantly higher in cord than maternal blood.

11 prenatal identification of fetal alleles in maternal blood.

12 nd dimethylglycine (r = 0.30, P < 0.0001) in maternal blood.

13 We found no evidence that maternal blood 25(OH)D concentration in pregnancy is ass

14 AEA was analyzed in cord and maternal blood, amniotic fluid, placenta, and fetal memb

15 Maternal blood and breast milk lead levels were measured

16 oxia limits the transport of substances from maternal blood and contributes to fetal growth restricti

17 imethamine and sulfadiazine concentration in maternal blood and observation of possible adverse effec

18 Maternal blood and placental samples were retrieved at d

19 of fetal cells, such as erythroblasts, from maternal blood and progress has been made in the diagnos

20 The maternal blood and the placentas were obtained at the ti

21 rmed the residual presence of fetal cells in maternal blood and tissues following pregnancy.

22 The presence of the Y chromosome in maternal blood and tissues was assessed using real-time

23 placental cells that interface directly with maternal blood and tissues.

24 ion of skin tests, foetal Rh genotyping from maternal blood and, in some cases, anti-D challenges.

25 revalence of malaria infection in 102 paired maternal-blood and umbilical cord-blood samples was asse

26 asma during pregnancy, parturition (cord and maternal blood), and lactation.

27 Levels of Mn in prenatal dentin, prenatal maternal blood, and 24 month urine were higher (p < 0.05

28 rnal platelet aggregation, thrombosis of the maternal blood, and death of the embryo.

29 cells; placental villi, which are bathed in maternal blood, and fetal membranes, which encapsulate t

30 lasts, cells that lie in direct contact with maternal blood, and show that these cells recapitulate t

31 Fetal cells in maternal blood are a noninvasive source of fetal genetic

32 We estimated negative associations between maternal blood arsenic concentrations and birth outcomes

33 anganese, an interquartile range increase in maternal blood arsenic was associated with -77.5 g (95%

34 vels similar to the U.S. general population, maternal blood arsenic was negatively associated with fe

35 l cell layer that is continuously exposed to maternal blood, as well as in macrophage-like placental

36 mean (GM) = 0.51 vs 0.16 Mn:Ca, p < 0.001), maternal blood at delivery than 26 weeks gestation (GM =

37 d antenatally or contamination with infected maternal blood at delivery.

38 in P0 fetal blood compared with both WT and maternal blood at E17 and E19, reflecting a reversal of

39 (trophoblasts): (i) the villous region where maternal blood bathes syncytialized trophoblasts for nut

40 , and antibody to pertactin were measured in maternal blood before and after vaccination and at both

41 atal diagnosis by enriching fetal cells from maternal blood by magnetic cell sorting followed by isol

42 sion, reduced arterial invasion, the size of maternal blood canals by 30-40% and placental perfusion

43 tus indicators and isotopes were measured in maternal blood collected 2 wk postdosing with oral (57Fe

44 as done on CD34 and CD34 cells isolated from maternal blood collected at select time points during ge

45 cental CRH concentrations were quantified in maternal blood collected serially over the course of ges

46 in utero exposure being approximately 71% of maternal blood concentrations.

47 , circulating tumor cells and fetal cells in maternal blood), detection of cells/particles in large d

48 B19V-IgG levels in maternal blood did not correlate with the likelihood of

49 In the human hemochorial placenta, maternal blood directly contacts syncytiotrophoblasts th

50 ties of cell-free fetal DNA circulate in the maternal blood during human pregnancy, but the origin of

51 Fetal cells enter maternal blood during pregnancy and persist in women wit

52 d miR-223 together with Treg cell numbers in maternal blood during pregnancy, as well as in cord bloo

53 clude that fetal stem cells transferred into maternal blood engraft in marrow, where they remain thro

54 ctively 31-32 days after negativation of the maternal blood EVD-polymerase chain reaction (PCR) both

55 NOx concentrations in maternal blood expressed a biphasic pattern with NOx con

56 Our results also suggest the time when maternal blood first flows into the placenta is a high-r

57 tions with uterine blood vessels that divert maternal blood flow to the placenta, a critical hurdle i

58 ificant amounts of shear stress generated by maternal blood flow.

59 lated to embryonic folate concentration, not maternal blood folate concentration.

60 ietary folate restriction results in reduced maternal blood folate, elevated plasma homocysteine and

61 studies indicate that fetal cells persist in maternal blood for decades after pregnancy.

62 al urinary TCS and cord blood FT3 as well as maternal blood FT4 concentrations at third trimester.

63 Elevated maternal blood glucose concentrations may contribute to

64 f the association being altered depending on maternal blood glucose level.

65 hout cardiac malformations, we observed that maternal blood glucose levels in models including insuli

66 Relative to maternal blood glucose levels of infants without cardiac

67 Moreover, lead concentration in maternal blood has been shown to increase during pregnan

68 Maternal blood hemoglobin A1C was inversely related to p

69 Midpregnancy biomarkers from maternal blood (i.e., C-reactive protein (CRP), corticot

70 Plasma leptin was analyzed in maternal blood in late pregnancy, in cord blood, and at

71 the early postimplantation period by pooling maternal blood in the implantation site in order to secu

72 Yet lactational transfer of lead from maternal blood into breast milk and its contribution to

73 The interface with maternal blood is the lining of the placenta, that is a

74 rom 1999 to 2007 correlated with proxies for maternal blood lead including the geometric mean blood l

75 Maternal blood manganese concentrations were negatively

76 refore, measurement of DLK1 concentration in maternal blood may be a valuable method for diagnosing h

77 ssociated with decreased cord blood, but not maternal blood, miR-155 expression.

78 nzymes, and quantification of metabolites in maternal blood, neither the protective mechanism nor the

79 RNA was measured by two assays in samples of maternal blood obtained at study entry and at delivery.

80 al DNA in 69 formaldehyde-treated samples of maternal blood obtained from a network of 27 US clinical

81 etween Mn in dentin and Mn concentrations in maternal blood or maternal or child urine.

82 was designed to examine associations between maternal blood PBDEs and PCBs in early pregnancy and lev

83 In fetal and maternal lungs, and in maternal blood plasma from pregnant rats exposed to envi

84 We measured lead in 81 maternal blood, plasma, and breast milk samples at 1 mon

85 ored the dose-response relationships between maternal blood, plasma, and breast milk to better unders

86 females were abnormal and contained numerous maternal blood pools in the labyrinth.

87 We examined the associations of maternal blood pressure development and hypertensive dis

88 Our results suggest that higher maternal blood pressure during pregnancy is associated w

89 owever, the influence on fetal growth of the maternal blood pressure during pregnancy is not well def

90 ildren for whom information was available on maternal blood pressure in different periods of pregnanc

91 Maternal blood pressure may be an important confounding

92 iation between prenatal arsenic exposure and maternal blood pressure over the course of pregnancy in

93 inverse association between fetal growth and maternal blood pressure, throughout the range seen in no

94 tal Flt1 mRNA levels strongly correlate with maternal blood pressure.

95 -tidal carbon dioxide between 32-34 mmHg and maternal blood pressures within 20% of baseline, and lim

96 The median gestational age when the maternal blood sample was obtained was 16 weeks (interqu

97 ripts from a variety of fetal tissues in the maternal blood sample.

98 osome abnormalities across the genome from a maternal blood sample.

99 In this study, we collected maternal blood samples from 125 pregnant women between 2

100 PFOS and PFOA were measured in maternal blood samples taken early in pregnancy.

101 At the time of amniocentesis, maternal blood samples were collected and analyzed by me

102 Maternal blood samples were obtained during the first tr

103 Cord blood samples and matching maternal blood samples were taken at delivery.

104 tions in red blood cells (RBC) from prenatal maternal blood samples, and using HumanMethylation450 Be

105 Addition of formaldehyde to maternal blood samples, coupled with careful processing

106 was obtained for the 69 formaldehyde-treated maternal blood samples.

107 B19V-IgM was detected in 95% of maternal blood samples.

108 determine the number of fetal chromosomes-in maternal blood samples.

109 od samples were 10-fold higher than those in maternal-blood samples (n=9).

110 ies infections were observed in 11 cord- and maternal-blood samples at a 5.5-fold greater frequency t

111 her absence of infection was noted in paired maternal-blood samples at delivery (n=16) or amplicon le

112 In contrast, maternal-blood samples showed a PCR prevalence of 48% fo

113 om sequential live births, analyzing matched maternal-blood samples to estimate the de novo mutation

114 Similar decreases (P=0.04) were detected in maternal blood sFLT1 protein concentrations.

115 Last, variably penetrant maternal blood sinus dilation in Muc1-deficient placenta

116 rface of the labyrinthine trophoblast around maternal blood sinuses, resembling its luminal localizat

117 of labyrinthine development, the dilation of maternal blood sinuses, the massive erythrophagocytosis

118 ntal disruption, with fibrin thrombi in some maternal blood sinusoids.

119 ontacts of layer I trophoblasts spanning the maternal blood space between adjacent trabeculae.

120 ted to placental trophoblast cells bordering maternal blood spaces and fetal placental endothelial ce

121 alyses revealed an increase in the volume of maternal blood spaces in the placenta, consistent with i

122 form a hybrid vasculature that amplifies the maternal blood supply for fetal development.

123 the uterine implantation site and secondly, maternal blood surrounding the syncytiotrophoblast (SYN)

124 atus, parity, lactation, supplement use, and maternal blood T cell populations.

125 on with the improved safety of a noninvasive maternal blood test.

126 t in the HDL fraction (P < 0.05), whereas in maternal blood they were greatest in the LDL fraction (P

127 Oxygen transport from maternal blood to fetal blood is a primary function of t

128 hors the placenta to the uterus and supplies maternal blood to the fetus.

129 , which involves vascular mimicry, re-routes maternal blood to the placenta, but fails in pre-eclamps

130 that line uterine vessels, thereby diverting maternal blood to the placenta.

131 s to the uterine wall and starts the flow of maternal blood to the placenta.

132 ulature, anchoring the progeny and rerouting maternal blood to the placenta.

133 lar, we review the potential contribution of maternal blood total cholesterol levels during pregnancy

134 ophoblast giant cells (SpA-TGCs) surrounding maternal blood vessels and severely compromises the abil

135 factors to influence the angiogenic state of maternal blood vessels and that this cross talk plays an

136 In the uterus, the formation of new maternal blood vessels in the stromal compartment at the

137 cytotrophoblasts invade the decidua, breach maternal blood vessels, and form heterotypic contacts wi

138 rate the uterine stroma to make contact with maternal blood vessels.

139 ant cells (SpA-TGCs) that invade and remodel maternal blood vessels.

140 The development of embryonic, but not maternal, blood vessels in the placentas of Map3k3-/- em

141 ncy outcome was accompanied by reductions in maternal blood viral load, measured by real-time polymer

142 ring pregnancy to support rapid expansion of maternal blood volume.

143 The median ratio of maraviroc cord blood to maternal blood was 0.33 (range, 0.03-0.56).

144 The median ratio of raltegravir cord to maternal blood was 1.21 (interquartile range, 1.02-2.17;

145 Maternal blood was assayed for 8-isoprostane concentrati

146 Maternal blood was obtained before dosing, at hospital a

147 After delivery, newborn cord and maternal blood were assayed for IgE and mononuclear cell

148 At delivery, high IL-10 levels in maternal blood were associated with an increase in pregn

149 sixfold elevation of fetal cells observed in maternal blood when the fetus had trisomy 21 indicates t

150 More fetal cells were detected in maternal blood when the fetus was aneuploid.

151 Rare fetal cells can be recovered from maternal blood, which suggests that non-invasive prenata

152 rd-blood samples, as markers of admixture of maternal blood with cord blood.

153 omparison of tacrolimus concentration in the maternal blood with different combinations of cord and i