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1 tudy variability, performance was high using maternal blood.
2 croparticles released from the placenta into maternal blood.
3  in contact with immune cells circulating in maternal blood.
4  syncytiotrophoblast interacts directly with maternal blood.
5  prenatal identification of fetal alleles in maternal blood.
6 nd dimethylglycine (r = 0.30, P < 0.0001) in maternal blood.
7   Percentage of free fetal DNA in samples of maternal blood.
8  Rare nucleated fetal cells circulate within maternal blood.
9 res had shorter CDR3s compared with those in maternal blood.
10 e placenta are present in EVs circulating in maternal blood.
11 brain are also present in EVs circulating in maternal blood.
12 imally impacted by antibody glycosylation in maternal blood.
13 exane sulfonate, and perfluoroundecanoate in maternal blood.
14 sions were significantly higher in cord than maternal blood.
15 ld be a leading factor for thrombosis in GDM maternal blood.
16 ome the need for direct sampling of fetal or maternal blood.
17 e assessment of the entire fetal genome from maternal blood.
18                    We found no evidence that maternal blood 25(OH)D concentration in pregnancy is ass
19                 AEA was analyzed in cord and maternal blood, amniotic fluid, placenta, and fetal memb
20 sive prenatal diagnostic approaches based on maternal blood analysis is confined.
21                                              Maternal blood and breast milk lead levels were measured
22 oxia limits the transport of substances from maternal blood and contributes to fetal growth restricti
23 e mtDNAcn and TL measured in first trimester maternal blood and cord blood.
24 tor 1 [CRHR1]) in isolated immune cells from maternal blood and neonatal umbilical cord blood.
25 imethamine and sulfadiazine concentration in maternal blood and observation of possible adverse effec
26                                              Maternal blood and placental samples were retrieved at d
27  of fetal cells, such as erythroblasts, from maternal blood and progress has been made in the diagnos
28 cing infected or uninfected blood simulating maternal blood and termed "trophoblast side") and human
29                                          The maternal blood and the placentas were obtained at the ti
30 rmed the residual presence of fetal cells in maternal blood and tissues following pregnancy.
31          The presence of the Y chromosome in maternal blood and tissues was assessed using real-time
32 placental cells that interface directly with maternal blood and tissues.
33                                              Maternal blood and urine were collected at 5-time points
34 ion of skin tests, foetal Rh genotyping from maternal blood and, in some cases, anti-D challenges.
35 revalence of malaria infection in 102 paired maternal-blood and umbilical cord-blood samples was asse
36 asma during pregnancy, parturition (cord and maternal blood), and lactation.
37    Levels of Mn in prenatal dentin, prenatal maternal blood, and 24 month urine were higher (p < 0.05
38 rnal platelet aggregation, thrombosis of the maternal blood, and death of the embryo.
39  cells; placental villi, which are bathed in maternal blood, and fetal membranes, which encapsulate t
40 lasts, cells that lie in direct contact with maternal blood, and show that these cells recapitulate t
41 ion contributed more to cord than peripheral maternal blood antibody functional potency.
42                               Fetal cells in maternal blood are a noninvasive source of fetal genetic
43     We confirmed that higher GDF15 levels in maternal blood are associated with vomiting in pregnancy
44   We estimated negative associations between maternal blood arsenic concentrations and birth outcomes
45 anganese, an interquartile range increase in maternal blood arsenic was associated with -77.5 g (95%
46 vels similar to the U.S. general population, maternal blood arsenic was negatively associated with fe
47 rculating DNA (cirDNA) samples isolated from maternal blood, as early as the first gestational trimes
48 l cell layer that is continuously exposed to maternal blood, as well as in macrophage-like placental
49 humoral and cellular immune responses in the maternal blood, as well as with a mild cytokine response
50             IgG and IgA Abs were detected in maternal blood at delivery and 42 d postpartum using ELI
51  mean (GM) = 0.51 vs 0.16 Mn:Ca, p < 0.001), maternal blood at delivery than 26 weeks gestation (GM =
52              Detection of IgG and IgA Abs in maternal blood at delivery was independently associated
53 d antenatally or contamination with infected maternal blood at delivery.
54  in P0 fetal blood compared with both WT and maternal blood at E17 and E19, reflecting a reversal of
55 (trophoblasts): (i) the villous region where maternal blood bathes syncytialized trophoblasts for nut
56 ruption of maternal blood vessels results in maternal blood bathing the syncytial maternofetal interf
57 , and antibody to pertactin were measured in maternal blood before and after vaccination and at both
58 ons, which were measured in maternal plasma, maternal blood, breastmilk, infant plasma, and infant bl
59 esterol biosynthesis and accumulation in the maternal blood (but not amniotic fluid) of women with pr
60 atal diagnosis by enriching fetal cells from maternal blood by magnetic cell sorting followed by isol
61                         To determine whether maternal blood can be used to identify LOS, leukocyte mR
62 sion, reduced arterial invasion, the size of maternal blood canals by 30-40% and placental perfusion
63 tional placenta, which releases factors into maternal blood causing systemic inflammation and widespr
64 ed a significant inverse correlation between maternal blood cholesterol levels and cord blood bone fo
65                                              Maternal blood cirDNA profiles accurately detects early
66 tus indicators and isotopes were measured in maternal blood collected 2 wk postdosing with oral (57Fe
67 as done on CD34 and CD34 cells isolated from maternal blood collected at select time points during ge
68 cental CRH concentrations were quantified in maternal blood collected serially over the course of ges
69 in utero exposure being approximately 71% of maternal blood concentrations.
70 ic analysis of fetal or trophoblast cells in maternal blood could revolutionize prenatal diagnosis.
71  methylated regions (DMRs) from longitudinal maternal blood-derived cell-free fetal DNA (cffDNA) sign
72 , circulating tumor cells and fetal cells in maternal blood), detection of cells/particles in large d
73                                 Increases in maternal blood DHA concentration in pregnancy were relat
74                                              Maternal blood DHA concentrations at delivery were unrel
75                                 Increases in maternal blood DHA during pregnancy were related to verb
76                           B19V-IgG levels in maternal blood did not correlate with the likelihood of
77           In the human hemochorial placenta, maternal blood directly contacts syncytiotrophoblasts th
78 rowth Factor-Like domain 7 (EGFL7) dosage in maternal blood discriminates between isolated IUGR and P
79 ties of cell-free fetal DNA circulate in the maternal blood during human pregnancy, but the origin of
80              We measured Hg concentration in maternal blood during pregnancy (median, 2.0 ug/L; IQR,
81                            Fetal cells enter maternal blood during pregnancy and persist in women wit
82 re either exclusively or highly expressed in maternal blood during pregnancy only and not in the post
83 d miR-223 together with Treg cell numbers in maternal blood during pregnancy, as well as in cord bloo
84 luding extracellular microvesicles, into the maternal blood during pregnancy.
85 clude that fetal stem cells transferred into maternal blood engraft in marrow, where they remain thro
86 ctively 31-32 days after negativation of the maternal blood EVD-polymerase chain reaction (PCR) both
87                        NOx concentrations in maternal blood expressed a biphasic pattern with NOx con
88  Importantly, our data reveal defects in the maternal blood-facing syncytiotrophoblast layer as a sha
89       Our results also suggest the time when maternal blood first flows into the placenta is a high-r
90 tions with uterine blood vessels that divert maternal blood flow to the placenta, a critical hurdle i
91 r decidual vessel remodeling and adaption of maternal blood flow to the placenta.
92 ificant amounts of shear stress generated by maternal blood flow.
93 lated to embryonic folate concentration, not maternal blood folate concentration.
94 ietary folate restriction results in reduced maternal blood folate, elevated plasma homocysteine and
95 studies indicate that fetal cells persist in maternal blood for decades after pregnancy.
96 ustered circulating trophoblasts (cTBs) from maternal blood for detecting PAS.
97 gh levels of soluble CORIN were confirmed in maternal blood from preeclamptic pregnancies compared wi
98 ndently of the rest of the uterus, expelling maternal blood from the intervillous space.
99 al urinary TCS and cord blood FT3 as well as maternal blood FT4 concentrations at third trimester.
100 nal stature, higher maternal BMI, and higher maternal blood glucose are associated with larger birth
101                                     Elevated maternal blood glucose concentrations may contribute to
102   However, studies seldom focus precisely on maternal blood glucose level prior to pregnancy.
103 f the association being altered depending on maternal blood glucose level.
104 hout cardiac malformations, we observed that maternal blood glucose levels in models including insuli
105                                  Relative to maternal blood glucose levels of infants without cardiac
106                                      Lack of maternal blood group checks during pregnancy was associa
107              Moreover, lead concentration in maternal blood has been shown to increase during pregnan
108 lication of omic methods to the placenta and maternal blood has yielded promising results, but comes
109 uring fetal or placental mRNA transcripts in maternal blood, has the potential to more precisely dete
110                                              Maternal blood hemoglobin A1C was inversely related to p
111  nutrients are delivered to the placenta via maternal blood (hemotrophic nutrition).
112                 Midpregnancy biomarkers from maternal blood (i.e., C-reactive protein (CRP), corticot
113 rresponding mRNAs previously reported in the maternal blood identified neutrophil-related protein/mRN
114                Plasma leptin was analyzed in maternal blood in late pregnancy, in cord blood, and at
115 the early postimplantation period by pooling maternal blood in the implantation site in order to secu
116        Yet lactational transfer of lead from maternal blood into breast milk and its contribution to
117 y remodeling that leads to decreased flow of maternal blood into the placenta, fetal growth restricti
118 decidua and remodel spiral arteries to bring maternal blood into the placenta.
119                           The interface with maternal blood is the lining of the placenta, that is a
120 rom 1999 to 2007 correlated with proxies for maternal blood lead including the geometric mean blood l
121  Hong Kong for the discovery of fetal DNA in maternal blood, leading to development of noninvasive pr
122 erative day 1, which was used as a proxy for maternal blood loss.
123                                              Maternal blood manganese concentrations were negatively
124 pothesized that fetal ultrasonography and/or maternal blood markers are useful to identify LOS.
125 refore, measurement of DLK1 concentration in maternal blood may be a valuable method for diagnosing h
126 mpal lipidomic and metabolomic profiles, and maternal blood measurements of DUX4 cffDNA methylation,
127 uplicate teeth, and assess associations with maternal blood metal concentrations during pregnancy, wh
128 ssociated with decreased cord blood, but not maternal blood, miR-155 expression.
129 nzymes, and quantification of metabolites in maternal blood, neither the protective mechanism nor the
130 RNA was measured by two assays in samples of maternal blood obtained at study entry and at delivery.
131 al DNA in 69 formaldehyde-treated samples of maternal blood obtained from a network of 27 US clinical
132 etween Mn in dentin and Mn concentrations in maternal blood or maternal or child urine.
133 chemical group among the 45 EDCs measured in maternal blood or urine samples collected in pregnancy w
134 d in the peripheral (maternal) or placental (maternal) blood or tissue by PCR, microscopy, rapid diag
135 mmonly used to detect uterine contractility, maternal blood oxygenation, temperature, heart rate, blo
136                                           In maternal blood, patients in Group 1 had significantly hi
137 was designed to examine associations between maternal blood PBDEs and PCBs in early pregnancy and lev
138 ice, we compare directly the effects, on the maternal blood, placenta and the embryonic brain, of mat
139 find no evidence of mRNA vaccine products in maternal blood, placenta tissue, or cord blood at delive
140  Paenibacillus spp were detected in vaginal, maternal blood, placental, or cord blood specimens from
141          In fetal and maternal lungs, and in maternal blood plasma from pregnant rats exposed to envi
142                       We measured lead in 81 maternal blood, plasma, and breast milk samples at 1 mon
143 ored the dose-response relationships between maternal blood, plasma, and breast milk to better unders
144 females were abnormal and contained numerous maternal blood pools in the labyrinth.
145      An endogenous AhR ligand (ITE) elevated maternal blood pressure and proteinuria in pregnant rats
146  in the placenta, which results in increased maternal blood pressure and restricted fetal growth.
147                                              Maternal blood pressure and weight gain and infant ponde
148              We examined the associations of maternal blood pressure development and hypertensive dis
149              Our results suggest that higher maternal blood pressure during pregnancy is associated w
150 owever, the influence on fetal growth of the maternal blood pressure during pregnancy is not well def
151 ildren for whom information was available on maternal blood pressure in different periods of pregnanc
152 Among 5,532 eligible women, we observed that maternal blood pressure in early gestation was significa
153                                              Maternal blood pressure may be an important confounding
154 iation between prenatal arsenic exposure and maternal blood pressure over the course of pregnancy in
155 very, low or high birth weight, and elevated maternal blood pressure, lipids, glucose, and gestationa
156 inverse association between fetal growth and maternal blood pressure, throughout the range seen in no
157 irth weight and higher later blood pressure: maternal blood pressure-raising alleles reduce offspring
158  significantly associated with a decrease in maternal blood pressure.
159 tal Flt1 mRNA levels strongly correlate with maternal blood pressure.
160 -tidal carbon dioxide between 32-34 mmHg and maternal blood pressures within 20% of baseline, and lim
161  this study reveals distinct RNA subtypes in maternal blood, reclassifying clinical HDP phenotypes li
162                                              Maternal blood, saliva, and cervicovaginal wash (CVW) sa
163          The median gestational age when the maternal blood sample was obtained was 16 weeks (interqu
164 ripts from a variety of fetal tissues in the maternal blood sample.
165 osome abnormalities across the genome from a maternal blood sample.
166 o study the immune phenotype in neonatal and maternal blood samples and mixed lymphocyte reactions to
167 ometry to detect circulating fRBCs in paired maternal blood samples before and after induced first-tr
168                                              Maternal blood samples collected at 12, 28, and 36 GW an
169 sectional analysis was conducted using 1,366 maternal blood samples collected between gestational wee
170 dation of sgNIPTs was further performed with maternal blood samples collected during pregnancy, and s
171               Using human umbilical cord and maternal blood samples collected from mid- to late-gesta
172                  In this study, we collected maternal blood samples from 125 pregnant women between 2
173 d Fy(a) (Duffy) fetal antigen genotypes from maternal blood samples in the ethnically diverse U.S. po
174               PFOS and PFOA were measured in maternal blood samples taken early in pregnancy.
175                At the time of amniocentesis, maternal blood samples were collected and analyzed by me
176                                              Maternal blood samples were obtained during the first tr
177              Cord blood samples and matching maternal blood samples were taken at delivery.
178    Malaria microscopy was carried out on the maternal blood samples, and the corresponding newborns'
179 tions in red blood cells (RBC) from prenatal maternal blood samples, and using HumanMethylation450 Be
180                  Addition of formaldehyde to maternal blood samples, coupled with careful processing
181              B19V-IgM was detected in 95% of maternal blood samples.
182 determine the number of fetal chromosomes-in maternal blood samples.
183 was obtained for the 69 formaldehyde-treated maternal blood samples.
184 nguish between true and false labor by using maternal blood samples.
185 cules in human placental villous tissues and maternal blood samples.
186  aflatoxin exposure was observed in 86.6% of maternal blood samples.
187 od samples were 10-fold higher than those in maternal-blood samples (n=9).
188 ies infections were observed in 11 cord- and maternal-blood samples at a 5.5-fold greater frequency t
189 her absence of infection was noted in paired maternal-blood samples at delivery (n=16) or amplicon le
190                                 In contrast, maternal-blood samples showed a PCR prevalence of 48% fo
191 om sequential live births, analyzing matched maternal-blood samples to estimate the de novo mutation
192                                              Maternal blood sampling was done before and 2 weeks afte
193  Similar decreases (P=0.04) were detected in maternal blood sFLT1 protein concentrations.
194 amples may yield progress: omics analyses of maternal blood show promise in identifying better predic
195                     Last, variably penetrant maternal blood sinus dilation in Muc1-deficient placenta
196 rface of the labyrinthine trophoblast around maternal blood sinuses, resembling its luminal localizat
197 of labyrinthine development, the dilation of maternal blood sinuses, the massive erythrophagocytosis
198 ntal disruption, with fibrin thrombi in some maternal blood sinusoids.
199 ontacts of layer I trophoblasts spanning the maternal blood space between adjacent trabeculae.
200  labyrinth trophoblast progenitors), altered maternal blood space, decreased fetal capillary area and
201 ted to placental trophoblast cells bordering maternal blood spaces and fetal placental endothelial ce
202 ancestry deer mice expand their placenta and maternal blood spaces in the placenta in response to env
203 alyses revealed an increase in the volume of maternal blood spaces in the placenta, consistent with i
204 igh-elevation ancestry increased the size of maternal blood spaces in the placenta, especially under
205  deer mice produce even larger placentas and maternal blood spaces, suggesting that these hypoxia-dri
206                       Each group had 118-239 maternal blood specimens and 100-201 cord blood samples
207 form a hybrid vasculature that amplifies the maternal blood supply for fetal development.
208  the uterine implantation site and secondly, maternal blood surrounding the syncytiotrophoblast (SYN)
209 atus, parity, lactation, supplement use, and maternal blood T cell populations.
210 d in 205 samples of placenta, cord blood, or maternal blood taken at birth from 54 mothers in the ser
211  of formate in cord blood in comparison with maternal blood taken earlier in pregnancy and at deliver
212                                We found that maternal blood TCM concentrations were significantly hig
213 on with the improved safety of a noninvasive maternal blood test.
214 ances, fetal growth restriction, or abnormal maternal blood tests that were suggestive of disease (su
215                  Obesity impairs the rise of maternal blood TG concentrations by reducing ANGPTL4 exp
216 hat ANGPTL4 plays a vital role in increasing maternal blood TG concentrations during pregnancy.
217           Interestingly, a lower increase in maternal blood TG concentrations has been observed in so
218                       We found not only that maternal blood TG concentrations in ppHF dams were remar
219 , ectopic overexpression of ANGPTL4 restored maternal blood TG concentrations in ppHF dams.
220 eding during pregnancy significantly reduces maternal blood TG levels.
221 udy to investigate if and how obesity alters maternal blood TG levels.
222 t in the HDL fraction (P < 0.05), whereas in maternal blood they were greatest in the LDL fraction (P
223 THg that was transferred to eggs at the same maternal blood THg concentration differed among taxonomi
224  (THg) concentrations in eggs increased with maternal blood THg concentrations; however, the proporti
225                        Oxygen transport from maternal blood to fetal blood is a primary function of t
226                    PFAS are transferred from maternal blood to human milk, an important exposure sour
227 hors the placenta to the uterus and supplies maternal blood to the fetus.
228 , which involves vascular mimicry, re-routes maternal blood to the placenta, but fails in pre-eclamps
229 that line uterine vessels, thereby diverting maternal blood to the placenta.
230 s to the uterine wall and starts the flow of maternal blood to the placenta.
231 ulature, anchoring the progeny and rerouting maternal blood to the placenta.
232 lar, we review the potential contribution of maternal blood total cholesterol levels during pregnancy
233                               Development of maternal blood transcriptomic markers to monitor placent
234 ifications to this index (e.g., exclusion of maternal blood transfusion) have been proposed; some res
235 res; maternal intensive care unit admission; maternal blood transfusion; and severe perineal lacerati
236                To ensure fetal lipid supply, maternal blood triglyceride (TG) concentrations are robu
237 le iron isotopic enrichment were measured in maternal blood, umbilical cord blood, and placental tiss
238                                 We collected maternal blood, vaginal swabs, and placental samples and
239  in the scar tissue, with higher-than-normal maternal blood velocity entering the intervillous space
240 ophoblast giant cells (SpA-TGCs) surrounding maternal blood vessels and severely compromises the abil
241 factors to influence the angiogenic state of maternal blood vessels and that this cross talk plays an
242          In the uterus, the formation of new maternal blood vessels in the stromal compartment at the
243 nta, as found in humans, where disruption of maternal blood vessels results in maternal blood bathing
244  cytotrophoblasts invade the decidua, breach maternal blood vessels, and form heterotypic contacts wi
245  pregnant mice, virus dissemination to major maternal blood vessels, including the aorta, resulted in
246 rate the uterine stroma to make contact with maternal blood vessels.
247 ant cells (SpA-TGCs) that invade and remodel maternal blood vessels.
248        The development of embryonic, but not maternal, blood vessels in the placentas of Map3k3-/- em
249 ncy outcome was accompanied by reductions in maternal blood viral load, measured by real-time polymer
250 ring pregnancy to support rapid expansion of maternal blood volume.
251  The median ratio of maraviroc cord blood to maternal blood was 0.33 (range, 0.03-0.56).
252      The median ratio of raltegravir cord to maternal blood was 1.21 (interquartile range, 1.02-2.17;
253                                              Maternal blood was assayed for 8-isoprostane concentrati
254                                              Maternal blood was drawn pre-treatment, CD14 + monocytes
255                                              Maternal blood was obtained before dosing, at hospital a
256 osed in utero to high levels of estrogens in maternal blood, we discuss how remyelinating properties
257             After delivery, newborn cord and maternal blood were assayed for IgE and mononuclear cell
258            At delivery, high IL-10 levels in maternal blood were associated with an increase in pregn
259                                     Cord and maternal blood were collected at delivery.
260  Phenotypic distances between cord blood and maternal blood were high at birth but decreased sharply
261 sixfold elevation of fetal cells observed in maternal blood when the fetus had trisomy 21 indicates t
262            More fetal cells were detected in maternal blood when the fetus was aneuploid.
263       Rare fetal cells can be recovered from maternal blood, which suggests that non-invasive prenata
264 rd-blood samples, as markers of admixture of maternal blood with cord blood.
265 omparison of tacrolimus concentration in the maternal blood with different combinations of cord and i

 
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