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1 reater at each gestational age compared with normal pregnancies).
2  or placental bed in PE or FGR compared with normal pregnancy.
3 V and V and alpha6-fucosyltransferase during normal pregnancy.
4 > 100 kDa) were similar in pre-eclampsia and normal pregnancy.
5 blood pressure, throughout the range seen in normal pregnancy.
6 hes in order to characterize this process in normal pregnancy.
7 lacenta and chorioamniotic membranes) during normal pregnancy.
8 ppear to achieve appropriate fetal growth in normal pregnancy.
9  maternal-fetal-placental circulation during normal pregnancy.
10 tate of relative immunosuppression exists in normal pregnancy.
11 two subsets also changed in PE compared with normal pregnancy.
12 under conditions of preeclampsia compared to normal pregnancy.
13 that is fundamental for the maintenance of a normal pregnancy.
14 onic gonadotropin between days 40 and 120 of normal pregnancy.
15 n their DNA methylation status compared with normal pregnancy.
16 ee DNA reach the maternal circulation during normal pregnancy.
17  expression of angiogenic factors throughout normal pregnancy.
18 ibute to the physiologic sodium retention of normal pregnancy.
19 antly raised in PE and IUGR as compared with normal pregnancy.
20 aternal insulin resistance, which occurs in "normal" pregnancy.
21  than it does among women with chromosomally normal pregnancies.
22 counts>400/mm3, no AIDS-defining illness and normal pregnancies.
23 FBP-1 levels were higher in diabetic than in normal pregnancies.
24 analyzed these glycosylation changes in five normal pregnancies.
25  had higher PLAP levels per EV particle than normal pregnancies.
26 n, with evidence of placental adaptations in normal pregnancies.
27 as significantly higher than in samples from normal pregnancies.
28 levels were significantly lower than that in normal pregnancies.
29 lampsia compared with plasma from women with normal pregnancies.
30  mannose across the umbilical circulation in normal pregnancies.
31 n artery resistance between preeclamptic and normal pregnancies.
32  respectively, in preeclampsia compared with normal pregnancies.
33 s 1 in 300 or higher in 7907 (8.3%) of 95476 normal pregnancies, 268 (82-2%) of 326 with trisomy 21,
34 in-1 level was not different in women during normal pregnancy (57 37-85 microg/L) compared to the unc
35 sitive to increased insulin concentration in normal pregnancy (96% suppression), but is less sensitiv
36                                           In normal pregnancy, a subpopulation of placental cytotroph
37  of developing complications from those with normal pregnancies, achieving 80% sensitivity, 90% speci
38 mmune and metabolic changes occurring during normal pregnancy also describe metabolic syndrome.
39 m 24 control women (20 with current or prior normal pregnancies and 4 who were nulligravid) was analy
40 mes of platelet activation and early in both normal pregnancies and in pregnancy-induced hypertension
41 nts were done on six healthy volunteers with normal pregnancies and nine with pregnancies complicated
42  preeclampsia plasma and plasma samples from normal pregnancies and nonpregnant women (294+/-110, 186
43 agnetic resonance (MR) imaging parameters in normal pregnancies and those complicated by fetal growth
44 eltaPo2 were significantly different between normal pregnancies and those complicated by severe FGR.
45 ofile of PdEs in maternal plasma of GDM with normal pregnancies and to determine the effect of exosom
46 tanes for placentas obtained from women with normal pregnancies and women with preeclampsia, a hypert
47 ons about physiologic changes present during normal pregnancy and after brain death, and the critical
48 describes the routine over-medicalisation of normal pregnancy and birth.
49  Insulin resistance is a cardinal feature of normal pregnancy and excess growth hormone (GH) states,
50 y modulator of TGF, we evaluated its role in normal pregnancy and gestational hypertension in a mouse
51  We hypothesized that NHGU is reduced during normal pregnancy and in a pregnant diet-induced model of
52 accommodating fetal nutrient requirements in normal pregnancy and in gestational diabetes mellitus (G
53 les (STBM), into the maternal circulation in normal pregnancy and in increased amounts in pre-eclamps
54 y modulate the maternal immune system during normal pregnancy and in the presence of an intrauterine
55 a preparation of freshly isolated CPASMCs of normal pregnancy and investigated K(+) channel expressio
56 endocrine zones of the mouse placenta during normal pregnancy and maternal inhalation hypoxia.
57 53.7% and 56.8% of plasma S-nitrosothiols in normal pregnancy and preeclampsia, respectively.
58 uman chorionic gonadotropin, produced during normal pregnancy and that secreted by three human chorio
59 linical features and laboratory data between normal pregnancy and the many potential causes of thromb
60 mpathetic output was increased in women with normal pregnancy and was even greater in the hypertensiv
61 ased as gestation progressed in women with a normal pregnancy and women experiencing SCH.
62 artum hemorrhage, 2) uncomplicated labor, 3) normal pregnancy, and 4) non-pregnant patients with acut
63 rovide clear evidence for placental aging in normal pregnancy, and demonstrate how HIF-1 signaling in
64 e metabolism, and FXR activity is reduced in normal pregnancy, and further in ICP.
65 tive pathway of complement in facilitating a normal pregnancy, and its detrimental participation in p
66 21 women with preeclampsia and 21 women with normal pregnancy, and plasma samples were also obtained
67 of SHG endomicroscopy technology for staging normal pregnancy, and suggest its potential application
68 metabolic profile that develops as a part of normal pregnancy, and that when lactation does not occur
69 e pulsatile arterial load alterations during normal pregnancy are adaptive in that they help to accom
70 n maternal O(2) transport in third trimester normal pregnancy are unlikely to be causally associated
71 5 women at PE diagnosis and in 64 women with normal pregnancies at a similar stage.
72  its regulatory mechanisms in placentas from normal pregnancies at high (3100 m), moderate (1600 m),
73  into the maternal and fetal circulations in normal pregnancy based on 4-vessel sampling.
74 ined from non-pregnant women, and women with normal pregnancies, before or after the spontaneous onse
75 nt in induced regulatory T cells (iTregs) in normal pregnancy but not in preeclampsia, implicating iT
76 EVs reduced angiotensin II responsiveness in normal pregnancy, but not in conditions of increased LOX
77 r resistance measured in vivo and ex vivo in normal pregnancy, but not in FGR.
78 loss of VSMCs from SpAs during remodeling in normal pregnancy, but VSMCs appear to migrate away from
79 -dependent changes in the AF proteome during normal pregnancy by using an omics platform.
80 ion between pregnancy complicated by FGR and normal pregnancy by using DeltaPo2, baseline R1, and bas
81                                              Normal pregnancy can be associated with a decline in ene
82 ly higher level of IgM-AECA was found during normal pregnancy compared with that in healthy nonpregna
83                This review examines sleep in normal pregnancy; discusses the physiologic bases for al
84 ospective outpatient study of 90 consecutive normal pregnancies during routine obstetric services at
85 vasion is essential for the establishment of normal pregnancy, dysregulation of this process may cont
86                                       During normal pregnancy, elevated angiotensin II (Ang II) conce
87            This finding has implications for normal pregnancy, for obstetric complications that incre
88 Only rabbits with cell-seeded constructs had normal pregnancies (four in ten) in the reconstructed se
89 t was generally 61.5% lower than that in the normal pregnancy group (P = .003).
90 evels, circulating maternal cytokines during normal pregnancies have not been considered to play a ro
91 plicated by IUGR differed significantly from normal pregnancies in patterns of perfusion within the p
92 women with SCH when compared to women with a normal pregnancy, in the second trimester.
93 s in sTNFR-I levels during the later half of normal pregnancies indicate that sTNFR-I may be importan
94 d 1 year postpartum compared with women with normal pregnancies, indicating increased cardiovascular
95 rcinoma initiation, but does not perturb the normal pregnancy-induced epigenomic landscape.
96 ntly higher in pre-eclampsia than in control normal pregnancy (inhibin A 3.05 [1.8] vs 0.36 [0.14] ng
97 t have indicated that insulin action in late normal pregnancy is 50-70% lower than in nonpregnant wom
98                           The discovery that normal pregnancy is a controlled state of inflammation,
99                                              Normal pregnancy is also accompanied by sodium retention
100                                              Normal pregnancy is associated with a reversible fall in
101                                              Normal pregnancy is characterized by an early expansion
102                                              Normal pregnancy is characterized by decreased venous se
103                                              Normal pregnancy is characterized by the presence of inn
104 t of glutamine and glutamate between FGR and normal pregnancy is currently lacking.
105 ), which is expressed in the placenta during normal pregnancy, is down regulated in pre-eclampsia, a
106 facilitating role in many of the stages of a normal pregnancy, it is also important that any necessar
107 g finding was that while P(4) at higher than normal pregnancy levels conferred PR signaling sufficien
108 ne conflict between mother and fetus, yet in normal pregnancy maternal immunity against infection is
109 ic hyperactivity during the latter months of normal pregnancy may help to return the arterial pressur
110  thinner media, and higher I/M ratio than in normal pregnancy (mean I/M difference, 0.21; 95% confide
111 ous clinical acumen because many symptoms of normal pregnancy mimic those of VTE and algorithmic tool
112  and their wild-type (WT) littermates as the normal pregnancy model.
113                   Resistance was measured in normal pregnancies (n = 10) and FGR (n = 10) both in viv
114 tained at term (37-39 weeks) from women with normal pregnancies (n = 5) or carrying fetuses with CDH
115  and Normal Pregnancy (NP; n = 12; carried a normal pregnancy; no surgery).
116 (preeclamptic plasma, N = 12) or plasma from normal pregnancies (normal plasma, N = 12).
117  women with late-onset preeclampsia (LPE) or normal pregnancy (NP) and investigated its underlying me
118 uring pregnancy and postpartum in women with normal pregnancy (NP) and PIH and in normotensive nonpre
119 12; underwent embryo relocation surgery) and Normal Pregnancy (NP; n = 12; carried a normal pregnancy
120     Symptoms of heart failure mimic those of normal pregnancy, often resulting in a delay in diagnosi
121 s of plasma from women with preeclamptic and normal pregnancies on the transcriptome of an immortaliz
122                                           In normal pregnancies only, the highest level of ex vivo FM
123 etuses with Hb Bart's hydrops and those with normal pregnancies or placenta-associated complications.
124 iated specifically with malaria and not with normal pregnancy or even pregnancy with low birth weight
125 significantly higher in preeclampsia than in normal pregnancy or nonpregnancy plasma (6.3+/-1.4, 5.1+
126 y BP monitoring, to determine the effects of normal pregnancy or reduced uterine perfusion pressure (
127 the transient hypotension that occurs during normal pregnancy or that is induced by treatment with li
128 ailable for metabolic signature: (1) SLE and normal pregnancy outcome (Group 1, n = 21); (2) SLE with
129 of NKG2D in poly(I:C)-treated WT mice led to normal pregnancy outcome.
130 nd/or localization may have consequences for normal pregnancy outcome.
131 ied 109 amniotic fluid samples of women with normal pregnancy outcomes (n = 28) and women with (n = 3
132 e plastic for induced Foxp3 expression, with normal pregnancy outcomes.
133 th restriction vs. placentas from women with normal pregnancies, particularly in fetal growth restric
134 creased in FGR vs. placentas from women with normal pregnancies, particularly in FGR associated with
135 were exposed for 24 hours to preeclamptic or normal pregnancy plasma and their transcriptome was anal
136 d 186% compared with normal nonpregnancy and normal pregnancy plasma, respectively).
137 t variation of GPBB concentrations occurs in normal pregnancy, pre-eclampsia, and SGA pregnancies.
138  and second trimester placental tissues from normal pregnancies predominantly expressed IL-10, wherea
139  cell-free RNA (cfRNA) to reveal patterns of normal pregnancy progression and determine the risk of d
140                          cfRNA signatures of normal pregnancy progression and pre-eclampsia are indep
141 Fms-related tyrosine kinase 3 ligand, led to normal pregnancy rates in a spontaneous abortion-prone m
142 reased excretion of 3-HIA seen frequently in normal pregnancy reflects reduced biotin status.
143 but the exact nature of the differences from normal pregnancy remain elusive.
144 ority of the women with eating disorders had normal pregnancies, resulting in healthy babies.
145 vical tissue sections at different stages of normal pregnancy reveal progressive, quantifiable change
146 al S-nitrosothiols (11.1+/-2.9 nmol/mL) than normal pregnancy samples (9.4+/-1.5 nmol/mL).
147 showed a four-fold increase in sVEGFR-1 than normal pregnancies, suggesting that villous explants in
148 nd greater aldosterone concentrations during normal pregnancy than Caucasians.
149 the uterus stays remarkably quiescent during normal pregnancy to allow sufficient time for developmen
150                                          For normal pregnancy, tumor necrosis factor-alpha and deplet
151                                              Normal pregnancy was associated with a lower preference
152  mimic aspects of the uterine environment in normal pregnancy, we added PRL and IGFBP1, which enhance
153              Placentae from preeclamptic and normal pregnancies were analyzed by western-blot and tra
154 sts specific to the standard monitoring of a normal pregnancy were covered.
155                Differentiating features from normal pregnancy were left ventricular wall thickness of
156 nown whether sympathetic drive is altered in normal pregnancy, when arterial blood pressure can be no
157 tochondria leads to oxidative stress even in normal pregnancy which is exacerbated further in IUGR, d
158  exhibited reduced neutrophil activation and normal pregnancies, which indicates that PAR2 plays an i
159  as the relative amounts of these glycans in normal pregnancy will be determined by gestational age.
160                                  Forty-eight normal pregnancies with a gestational age (GA) of 25 to
161 ectory patterns over 18 gestational weeks in normal pregnancies with repeated measures.
162 tprandial state is delayed and suppressed in normal pregnancy, with concomitant reduction in glycogen

 
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