ライフサイエンスコーパス: uterine artery

1 major blood supply to the ovary was from the uterine artery.

2 uterus was through anastomoses with the main uterine artery.

3 expression of NO synthase (NOS) in the human uterine artery.

4 fects of hypoxia on BKCa channel currents in uterine arteries.

5 and endothelial cells of chorionic villi and uterine arteries.

6 a-mediated, pregnancy-induced remodelling of uterine arteries.

7 at 2 and 6 months after embolization of the uterine arteries.

8 embolization had bilateral ovarian artery-to-uterine artery anastomoses that were classified as high

9 Angiographic ovarian artery-to-uterine artery anastomoses were studied in 76 consecutiv

10 Delineation of ovarian artery-to-uterine artery anastomosis is of practical relevance in

11 = 8) ewes had flow probes implanted on main uterine arteries and catheters in branches of the uterin

12 d inhibition of the BKCa channel activity in uterine arteries and new insights in understanding and a

13 tal growth parameters and blood flows of the uterine arteries and umbilical cord were normal througho

14 They also line uterine arteries and veins.

15 rioles, superficial epigastric, femoral, and uterine arteries, and foot skin.

16 ient reduction and irregular fluctuations in uterine artery blood flow associated with cardiac arrhyt

17 were surgically instrumented with bilateral uterine artery blood flow transducers, and uterine and f

18 d maternal dietary intake or modification of uterine artery blood flow.

19 adequate invasion and remodeling of maternal uterine arteries by extravillous trophoblasts (EVTs) in

20 ses pharmacomechanical coupling of the ovine uterine artery by inhibiting the efficiency of receptor-

21 esence of various types of ovarian artery-to-uterine artery connections.

22 Chronic hypoxia significantly decreased uterine artery contractile sensitivity in that pD2 (-log

23 Altitude was associated with decreased uterine artery diameter, volumetric blood flow and O(2)

24 A uterine artery Doppler resistance index (RI) in the firs

25 High uterine artery Doppler resistance indexes (RIs) are pred

26 erefore, by characterizing pregnancies using uterine artery Doppler RI before dNK cell isolation, we

27 n the first trimester, pregnancies with high uterine artery Doppler RI demonstrate alterations in pla

28 Treatment and close monitoring including uterine artery Doppler scans and timely delivery may imp

29 Tail cuff blood pressure and uterine artery Doppler ultrasound were measured on GD 15

30 43 women had normal uterine artery doppler waveforms and subsequently had a

31 We assessed uterine artery doppler waveforms in 86 women at 23-25 we

32 risk of pre-eclampsia by abnormal two-stage uterine-artery doppler analysis or a previous history of

33 phoblast (EVT) cells to remodel the maternal uterine arteries during the first and second trimesters

34 increased NO synthesis/release in the human uterine artery during pregnancy.

35 es are available in the literature regarding uterine artery embolization (UAE).

36 reintervention (compared with myomectomy or uterine artery embolization [UAE]), but rates of more se

37 o hundred consecutive patients who underwent uterine artery embolization at one institution were pros

38 ntification of those who would be at risk of uterine artery embolization or ovarian failure, and in t

39 ure fertility; new treatment options include uterine artery embolization via interventional radiologi

40 ate proliferation of pregnancy-derived ovine uterine artery endothelial cells (P-UAECs) through beta-

41 timulate pregnancy-specific proliferation of uterine artery endothelial cells derived from pregnant (

42 S3 expression in human umbilical vein EC and uterine artery endothelial cells.

43 CI 182 780 (0.1-3.0 microg min(-1)) into one uterine artery for 10 min before and 50 min after E2beta

44 .19 +/- 0.15 and 6.62 +/- 0.12 (P < 0.05) in uterine arteries from normoxic and chronically hypoxic s

45 .09 +/- 0.11 and 5.51 +/- 0.08 (P < 0.05) in uterine arteries from normoxic and chronically hypoxic s

46 bundance and BKCa channel current density in uterine arteries from pregnant sheep exposed to high-alt

47 th profound structural alterations of murine uterine arteries, including the occurrence of outward hy

48 from control and IUGR (induced by bilateral uterine artery ligation at day 18 of fetal life) animals

49 nant Sprague-Dawley rats underwent bilateral uterine artery ligation causing IUGR in F1.

50 ysis, we investigated the effect of maternal uterine artery ligation causing uteroplacental insuffici

51 With the use of the same grandparental uterine artery ligation model, we profiled the F2 serum

52 IUGR was induced through a bilateral uterine artery ligation of the pregnant rat, a well-char

53 ough a well-characterized model of bilateral uterine artery ligation of the pregnant rat.

54 nant Sprague-Dawley dams underwent bilateral uterine artery ligation or anesthesia (control) at e19.5

55 d growth retardation by performing bilateral uterine artery ligation upon pregnant rats 2 days prior

56 Bilateral uterine artery ligation was performed on day 19 of gesta

57 A surgical model of IUGR (bilateral uterine artery ligation) in Sprague-Dawley rats with sha

58 ine blood flow)-1; 60 min infusion) into one uterine artery (n = 8 sheep).

59 Uterine artery O(2) delivery in these pregnancies was 99

60 T) caused by chronic hypoxia was examined in uterine arteries obtained from normoxic (control) and ch

61 In uterine arteries of non-pregnant animals, hypoxia inhibi

62 Uterine arteries of pregnant sheep acclimatized to long-

63 In uterine arteries of pregnant sheep, hypoxia significantl

64 and inhibiting the BKCa channel activity in uterine arteries of pregnant sheep.

65 nsity of superficial epigastric, femoral, or uterine arteries, or foot skin.

66 At 23 to 25 weeks, uterine artery pulsatility index correlated with serum s

67 Maternal mean arterial pressure, uterine artery pulsatility index, brachial artery flow-m

68 Umbilical artery pulsatility index and uterine artery resistance index and fetal growth were me

69 and third trimesters were 0.50 and 0.32 for uterine artery resistance index and umbilical artery pul

70 rs and persistence in the highest tertile of uterine artery resistance index from the second trimeste

71 We examined whether umbilical and uterine artery resistance indices, as measures of feto-p

72 udy, we correlated increased first trimester uterine artery resistance with a biological abnormality

73 ctivator inhibitor (PAI) 1 to PAI-2 and mean uterine-artery resistance index (UtARI)] and placental a

74 (14)C-MeAIB and (3)H-taurine was reduced and uterine arteries showed increased relaxation.

75 versus VSM ERalpha and ERbeta expression in uterine arteries (UAs) during the ovarian cycle, pregnan

76 (PRKAA1) have been implicated in the greater uterine artery (UtA) blood flow and relative protection

77 Higher third trimester umbilical and uterine artery vascular resistance were associated with

78 mbilical artery vascular resistance, but not uterine artery vascular resistance, was associated with

79 a in inhibiting the BKCa channel activity in uterine arteries via increased oxidative stress.

80 ss and improved glucose tolerance, increased uterine artery volume blood flow, and decreased placenta

81 onse of 5-HT-induced InsP3 generation in the uterine artery was decreased from 251.3 +/- 24.2 pmol (m

82 though 5-HT2A receptor density (Bmax) in the uterine artery was not changed in chronically hypoxic sh

83 nsP3 generated, the contractile force of the uterine artery was significantly less in chronically hyp

84 The uterine arteries were cannulated to perfuse the organ wi

85 Under local anesthesia, both uterine arteries were embolized.

86 Uterine arteries were isolated from non-pregnant and nea

87 Uterine arteries were obtained from pregnant patients (P

88 the production of reactive oxygen species in uterine arteries, which was blocked by N-acetylcysteine.