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1                                          The uteroplacental and umbilical venoarterial concentration
2               The myometrial segments of the uteroplacental arteries have a unique vascular memory an
3 intaining hemostatic balance and stabilizing uteroplacental attachment at the fibrinoid layer found a
4  of unknown origin suggests that these three uteroplacental bleeding disorders do not have a common e
5 ere was no evidence for an increased risk of uteroplacental bleeding disorders with increasing number
6  proteinuria in pregnant rats, and decreased uteroplacental blood flow and fetal and placental growth
7 ted with reduced fetal weight, and disturbed uteroplacental blood flow and severe malnutrition were a
8 potential therapeutic targets for augmenting uteroplacental blood flow and, in turn, preserving fetal
9 ionally, impaired placental angiogenesis and uteroplacental blood flow appears to be an early defect
10 E increased proteinuria by 50% and decreased uteroplacental blood flow by 26%.
11 A) remodeling is essential to ensure optimal uteroplacental blood flow during human pregnancy, yet ve
12 phoblast invasion of the decidua, leading to uteroplacental blood flow that is inadequate for the dev
13                              Proteinuria and uteroplacental blood flow were monitored on GD20.
14 stemic and uterine hemodynamics that reduces uteroplacental blood flow, a mechanism underlying matern
15  both) in fetuses from dams with interrupted uteroplacental blood flow, bacterial peritonitis, and ol
16 s that maternal factors, such as compromised uteroplacental blood flow, concomitant infection, and ad
17              Sildenafil citrate may increase uteroplacental blood flow.
18 te spiral artery remodeling, causing reduced uteroplacental blood flow.
19  maternal vascular resistance and increasing uteroplacental blood flow.
20 creased peripheral resistance, and increased uteroplacental blood flow.
21                                              Uteroplacental blood hemodynamics, progression of PE fea
22 orced daily swimming, short-term clamping of uteroplacental blood vessels, restricted dietary intake,
23 ions within the physiological range regulate uteroplacental carbohydrate metabolism remains unknown.
24                  Finally, we reconstruct the uteroplacental cell-cell communication networks of extin
25 ult in increased placental thrombosis in the uteroplacental circulation and may therefore contribute
26 f treatment on the fetus, via changes to the uteroplacental circulation with treatment.
27 be attributed to vasodilatory effects in the uteroplacental circulation.
28 blood flow patterns are indirect measures of uteroplacental circulation.
29                                  The rate of uteroplacental consumption of glucose, but not oxygen, w
30 quantified the rates of umbilical uptake and uteroplacental consumption of nutrients in preterm fetus
31 eft anterior oblique views while maintaining uteroplacental continuity.
32 clinical, laboratory, echocardiographic, and uteroplacental Doppler flow (UDF) parameters at 20 and 3
33 cardiorespiratory, renal, hepatic, etc.), or uteroplacental dysfunction (e.g., placental abruption).
34 ncentration >75 nmol/L and a reduced risk of uteroplacental dysfunction as indicated by a composite o
35 eurological or haematological complications, uteroplacental dysfunction, or fetal growth restriction.
36 g proteinuria, maternal organ dysfunction or uteroplacental dysfunction.
37 nal-age (SGA) birth, which are indicative of uteroplacental dysfunction.
38 with CHD, cardiac dysfunction may compromise uteroplacental flow and contribute to the increased inci
39 ortisol levels were positively correlated to uteroplacental glucose consumption and inversely related
40 ing stress, cortisol-dependent regulation of uteroplacental glycolysis may allow increased maternal c
41 at maternal cortisol concentrations regulate uteroplacental glycolytic metabolism, producing lactate
42 ce growth in fetal sheep, its effects on the uteroplacental handling and delivery of nutrients remain
43 n and SA remodeling, as well as with altered uteroplacental hemodynamics and placental nitrosative st
44 in turn, preserving fetal growth in cases of uteroplacental hypoperfusion.
45                                              Uteroplacental hypoxia is associated with pregnancy diso
46 tery transformation resulting in progressive uteroplacental hypoxia.
47      To address the hypothesis that maternal uteroplacental insufficiency (UPI) increases severity of
48 t intrauterine growth retardation induced by uteroplacental insufficiency 1) affects the hepatic epig
49                                              Uteroplacental insufficiency alone caused a significant
50                          We therefore caused uteroplacental insufficiency and growth retardation by p
51                            Infants suffering uteroplacental insufficiency and hypoxic ischemic injury
52                                 In contrast, uteroplacental insufficiency and subsequent fetal hypoxi
53 lone increased cerebral cAMP levels, whereas uteroplacental insufficiency and subsequent hypoxia decr
54 apoptosis in fetal rats exposed initially to uteroplacental insufficiency and subsequent hypoxic stre
55 he onset of hyperglycemia, and indicate that uteroplacental insufficiency causes a primary defect in
56                                              Uteroplacental insufficiency is induced in the pregnant
57                                              Uteroplacental insufficiency leads to intrauterine growt
58                                              Uteroplacental insufficiency resulting in fetal growth r
59 ctive was to determine the global effects of uteroplacental insufficiency upon cerebral gene expressi
60                    Therefore, a rat model of uteroplacental insufficiency was developed; intrauterine
61  of maternal uterine artery ligation causing uteroplacental insufficiency with asymmetrical intrauter
62                 We have developed a model of uteroplacental insufficiency, a common cause of intraute
63 nd physiological characteristics of clinical uteroplacental insufficiency.
64 ing a normalization volume 10 mm outside the uteroplacental interface and compared against the Virtua
65 ammatory granulocytes and macrophages at the uteroplacental interface and upregulation of proinflamma
66 acterize the complex cellular changes at the uteroplacental interface in placenta accreta spectrum.
67 ing in a build up of apoptotic bodies at the uteroplacental interface that elicits a local immune res
68 ume was measured on the vasculature from the uteroplacental interface to a depth 5 mm into the placen
69 and preeclampsia, which are characterized by uteroplacental ischaemia and/or fetal hypoxia.
70 tant in pregnancy disorders characterized by uteroplacental ischaemia and/or fetal hypoxia.
71 , maternal hyperoxia in the setting of acute uteroplacental ischemia-hypoxia does not appear to cause
72 e raised chronically, prolonged elevation of uteroplacental lactate production may compromise fetal w
73                               Concomitantly, uteroplacental lactate production was > 2-fold greater i
74                            Absolute rates of uteroplacental lactate production were lower in cortisol
75  that cortisol is physiological regulator of uteroplacental metabolism and nutrient delivery to the s
76 ternal availability, placental transport and uteroplacental metabolism of carbohydrates.
77        We hypothesized that greater maternal uteroplacental O(2) delivery would explain increased fet
78 han saline-treated ewes (P < 0.05), although uteroplacental O2 consumption was unaffected by maternal
79 cental insufficiency-FGR, in relationship to uteroplacental oxygenation.
80 growth under hypoxic conditions by improving uteroplacental perfusion and thereby justify further inv
81 potential therapeutic strategy for restoring uteroplacental perfusion in pregnancy disorders.
82                             In a rat reduced uteroplacental perfusion pressure (RUPP) model of chroni
83 tions facilitate the progressive increase in uteroplacental perfusion that is required for normal fet
84 rophoblast invasion, a process necessary for uteroplacental perfusion, in an extracellular signal-reg
85 imetic glyceryl trinitrate prevented altered uteroplacental perfusion, LPS-induced inflammation, plac
86 restriction and preterm birth due to altered uteroplacental perfusion.
87 t spiral artery (SA) remodeling, and altered uteroplacental perfusion.
88 plete vascular transformation and inadequate uteroplacental perfusion.
89 by placental ischemia resulting from reduced uteroplacental perfusion.
90 the offspring or secondary to alterations in uteroplacental physiology is unclear.
91 d as a potential candidate for the disturbed uteroplacental remodeling, leading to hypertension and e
92 o the pharmacokinetics of narcotics while on uteroplacental support has been gained.
93 EXIT) procedure, which maintains intrapartum uteroplacental support, can be life saving.
94                               Homogenates of uteroplacental tissue were incubated with immobilized re
95               Neutrophil infiltration of the uteroplacental tissues has been particularly associated
96 nges in oxygen availability to the fetus and uteroplacental tissues may contribute to the ontogenic i
97 rd a more anti-inflammatory phenotype in the uteroplacental tissues of infected mice contributed to b
98                           Concomitantly, the uteroplacental tissues produced lactate at a greater rat
99 e taken up by the uterus was consumed by the uteroplacental tissues while less was transferred to the
100 psia-like symptoms, caused hypoxic injury in uteroplacental tissues, and elevated soluble fms-like ty
101 ed, a greater proportion was consumed by the uteroplacental tissues, so net fetal glucose uptake was
102  stimulating an inflammatory response of the uteroplacental tissues, while minimizing PTB in control
103 the LPS-induced inflammatory response of the uteroplacental tissues.
104  metabolism of nutrients and hormones by the uteroplacental tissues.
105 nsumption and production of nutrients by the uteroplacental tissues.
106 thophysiologic changes that occur within the uteroplacental unit and fetus is essential to identifyin
107 m as a major source of secreted IL-33 in the uteroplacental unit.
108  indices of inflammation or infection of the uteroplacental unit.
109 bsence of functional FasL affects pregnancy, uteroplacental units from homozygous matings of gld mice
110 ma (PPAR-gamma) is an important regulator of uteroplacental vascular development and function and has
111 pregnancy to enhance NO bioactivity, improve uteroplacental vascular function and increase fetal grow
112      Whilst mechanisms underpinning impaired uteroplacental vascular function are not fully understoo
113 in many experimental models of FGR, impaired uteroplacental vascular function is implicated, leading
114 l outcome of pregnancy requires an efficient uteroplacental vascular system.
115  a local renin-angiotensin system within the uteroplacental vasculature.
116 regnancy NO is not essential for maintaining uteroplacental vasodilation.

 
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