ライフサイエンスコーパス: uteroplacental

1 The myometrial segments of the uteroplacental arteries have a unique vascular memory an

2 intaining hemostatic balance and stabilizing uteroplacental attachment at the fibrinoid layer found a

3 of unknown origin suggests that these three uteroplacental bleeding disorders do not have a common e

4 ere was no evidence for an increased risk of uteroplacental bleeding disorders with increasing number

5 ted with reduced fetal weight, and disturbed uteroplacental blood flow and severe malnutrition were a

6 ionally, impaired placental angiogenesis and uteroplacental blood flow appears to be an early defect

7 A) remodeling is essential to ensure optimal uteroplacental blood flow during human pregnancy, yet ve

8 phoblast invasion of the decidua, leading to uteroplacental blood flow that is inadequate for the dev

9 stemic and uterine hemodynamics that reduces uteroplacental blood flow, a mechanism underlying matern

10 both) in fetuses from dams with interrupted uteroplacental blood flow, bacterial peritonitis, and ol

11 s that maternal factors, such as compromised uteroplacental blood flow, concomitant infection, and ad

12 te spiral artery remodeling, causing reduced uteroplacental blood flow.

13 maternal vascular resistance and increasing uteroplacental blood flow.

14 Uteroplacental blood hemodynamics, progression of PE fea

15 orced daily swimming, short-term clamping of uteroplacental blood vessels, restricted dietary intake,

16 ions within the physiological range regulate uteroplacental carbohydrate metabolism remains unknown.

17 ult in increased placental thrombosis in the uteroplacental circulation and may therefore contribute

18 f treatment on the fetus, via changes to the uteroplacental circulation with treatment.

19 blood flow patterns are indirect measures of uteroplacental circulation.

20 The rate of uteroplacental consumption of glucose, but not oxygen, w

21 quantified the rates of umbilical uptake and uteroplacental consumption of nutrients in preterm fetus

22 eft anterior oblique views while maintaining uteroplacental continuity.

23 clinical, laboratory, echocardiographic, and uteroplacental Doppler flow (UDF) parameters at 20 and 3

24 ncentration >75 nmol/L and a reduced risk of uteroplacental dysfunction as indicated by a composite o

25 eurological or haematological complications, uteroplacental dysfunction, or fetal growth restriction.

26 nal-age (SGA) birth, which are indicative of uteroplacental dysfunction.

27 with CHD, cardiac dysfunction may compromise uteroplacental flow and contribute to the increased inci

28 ortisol levels were positively correlated to uteroplacental glucose consumption and inversely related

29 ing stress, cortisol-dependent regulation of uteroplacental glycolysis may allow increased maternal c

30 at maternal cortisol concentrations regulate uteroplacental glycolytic metabolism, producing lactate

31 ce growth in fetal sheep, its effects on the uteroplacental handling and delivery of nutrients remain

32 n and SA remodeling, as well as with altered uteroplacental hemodynamics and placental nitrosative st

33 To address the hypothesis that maternal uteroplacental insufficiency (UPI) increases severity of

34 t intrauterine growth retardation induced by uteroplacental insufficiency 1) affects the hepatic epig

35 Uteroplacental insufficiency alone caused a significant

36 We therefore caused uteroplacental insufficiency and growth retardation by p

37 Infants suffering uteroplacental insufficiency and hypoxic ischemic injury

38 In contrast, uteroplacental insufficiency and subsequent fetal hypoxi

39 lone increased cerebral cAMP levels, whereas uteroplacental insufficiency and subsequent hypoxia decr

40 apoptosis in fetal rats exposed initially to uteroplacental insufficiency and subsequent hypoxic stre

41 he onset of hyperglycemia, and indicate that uteroplacental insufficiency causes a primary defect in

42 Uteroplacental insufficiency is induced in the pregnant

43 Uteroplacental insufficiency leads to intrauterine growt

44 Uteroplacental insufficiency resulting in fetal growth r

45 ctive was to determine the global effects of uteroplacental insufficiency upon cerebral gene expressi

46 Therefore, a rat model of uteroplacental insufficiency was developed; intrauterine

47 of maternal uterine artery ligation causing uteroplacental insufficiency with asymmetrical intrauter

48 We have developed a model of uteroplacental insufficiency, a common cause of intraute

49 nd physiological characteristics of clinical uteroplacental insufficiency.

50 ing a normalization volume 10 mm outside the uteroplacental interface and compared against the Virtua

51 ammatory granulocytes and macrophages at the uteroplacental interface and upregulation of proinflamma

52 ing in a build up of apoptotic bodies at the uteroplacental interface that elicits a local immune res

53 ume was measured on the vasculature from the uteroplacental interface to a depth 5 mm into the placen

54 e raised chronically, prolonged elevation of uteroplacental lactate production may compromise fetal w

55 Concomitantly, uteroplacental lactate production was > 2-fold greater i

56 Absolute rates of uteroplacental lactate production were lower in cortisol

57 that cortisol is physiological regulator of uteroplacental metabolism and nutrient delivery to the s

58 ternal availability, placental transport and uteroplacental metabolism of carbohydrates.

59 We hypothesized that greater maternal uteroplacental O(2) delivery would explain increased fet

60 han saline-treated ewes (P < 0.05), although uteroplacental O2 consumption was unaffected by maternal

61 cental insufficiency-FGR, in relationship to uteroplacental oxygenation.

62 rophoblast invasion, a process necessary for uteroplacental perfusion, in an extracellular signal-reg

63 imetic glyceryl trinitrate prevented altered uteroplacental perfusion, LPS-induced inflammation, plac

64 t spiral artery (SA) remodeling, and altered uteroplacental perfusion.

65 plete vascular transformation and inadequate uteroplacental perfusion.

66 d as a potential candidate for the disturbed uteroplacental remodeling, leading to hypertension and e

67 o the pharmacokinetics of narcotics while on uteroplacental support has been gained.

68 EXIT) procedure, which maintains intrapartum uteroplacental support, can be life saving.

69 Homogenates of uteroplacental tissue were incubated with immobilized re

70 Neutrophil infiltration of the uteroplacental tissues has been particularly associated

71 nges in oxygen availability to the fetus and uteroplacental tissues may contribute to the ontogenic i

72 Concomitantly, the uteroplacental tissues produced lactate at a greater rat

73 e taken up by the uterus was consumed by the uteroplacental tissues while less was transferred to the

74 psia-like symptoms, caused hypoxic injury in uteroplacental tissues, and elevated soluble fms-like ty

75 ed, a greater proportion was consumed by the uteroplacental tissues, so net fetal glucose uptake was

76 stimulating an inflammatory response of the uteroplacental tissues, while minimizing PTB in control

77 the LPS-induced inflammatory response of the uteroplacental tissues.

78 metabolism of nutrients and hormones by the uteroplacental tissues.

79 nsumption and production of nutrients by the uteroplacental tissues.

80 thophysiologic changes that occur within the uteroplacental unit and fetus is essential to identifyin

81 m as a major source of secreted IL-33 in the uteroplacental unit.

82 indices of inflammation or infection of the uteroplacental unit.

83 bsence of functional FasL affects pregnancy, uteroplacental units from homozygous matings of gld mice

84 pregnancy to enhance NO bioactivity, improve uteroplacental vascular function and increase fetal grow

85 Whilst mechanisms underpinning impaired uteroplacental vascular function are not fully understoo

86 in many experimental models of FGR, impaired uteroplacental vascular function is implicated, leading

87 l outcome of pregnancy requires an efficient uteroplacental vascular system.

88 a local renin-angiotensin system within the uteroplacental vasculature.

89 regnancy NO is not essential for maintaining uteroplacental vasodilation.