ライフサイエンスコーパス: uterine artery

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

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

3 uterus was through anastomoses with the main uterine artery.

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

5 oppler flow velocimetry of the umbilical and uterine arteries.

6 enic tone were reversed by TET2 knockdown in uterine arteries.

7 cts of hypoxia on STOCs and myogenic tone in uterine arteries.

8 nd phenylephrine-induced vasoconstriction of uterine arteries.

9 aneous transient outward currents (STOCs) in uterine arteries.

10 contractile and anti-dilatory effects on rat uterine arteries.

11 pro-contractile and anti-dilatory effects on uterine arteries.

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

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

14 and endothelial cells of chorionic villi and uterine arteries.

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

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

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

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

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

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

21 They also line uterine arteries and veins.

22 that hypoxia reduced AMPK activation in the uterine artery and placenta, and AICAR increased AMPK ac

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

24 of pregnancy-mediated vasodilatation of the uterine artery are not fully understood.

25 Dysfunction and remodelling of the uterine artery are strongly implicated in many pregnancy

26 riction (P < 0.01), due in part to increased uterine artery blood flow (P < 0.0001).

27 An increase in uterine artery blood flow (UtBF) is a common and necessa

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

29 itude (>2500 m or 8200 ft) residence reduces uterine artery blood flow during pregnancy, contributing

30 ategy for improving fetal growth and raising uterine artery blood flow in pregnancy, which may be imp

31 rivascular adipose tissue (PVAT) potentiates uterine artery blood flow in pregnant rats, although not

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

33 l growth restriction due, in part, to lesser uterine artery blood flow.

34 rug AICAR improved fetal growth and elevated uterine artery blood flow.

35 es uterine vascular resistance and decreases uterine artery blood flow.

36 vation vasodilates arteries and may increase uterine artery blood flow.

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

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

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

40 tment improved maternal metabolic health and uterine artery compliance but did not rescue obesity-ind

41 ose intolerance in pregnancy we show reduced uterine artery compliance, placental structural changes

42 intolerance during pregnancy and had reduced uterine artery compliance.

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

44 Hypoxia increased uterine artery constrictor responses to norepinephrine,

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

46 educed uterine artery diameter and increased uterine artery contractility in normoxic mice, providing

47 l inhibition of AMPK with Compound C reduced uterine artery diameter and increased uterine artery con

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

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

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

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

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

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

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

55 43 women had normal uterine artery doppler waveforms and subsequently had a

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

57 en" comprising fetal and placental size, and uterine artery Doppler.

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

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

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

61 ications during subsequent pregnancies after uterine artery embolization (UAE) for postpartum hemorrh

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

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

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

65 moral arterial access in patients undergoing uterine artery embolization for the treatment of fibroid

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

67 A total of 172 patients underwent uterine artery embolization procedures at our institute

68 acious alternative to transfemoral access in uterine artery embolization procedures.

69 often, whenever viable, as an option in the uterine artery embolization treatment of fibroids.

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

71 dy assesses the efficacy of this approach in uterine artery embolization.

72 esponse to medical treatment, myomectomy and uterine-artery embolization are therapeutic options.

73 the myomectomy group and 80.0+/-22.0 in the uterine-artery embolization group (mean adjusted differe

74 hom 105 underwent myomectomy) and 127 to the uterine-artery embolization group (of whom 98 underwent

75 mectomy group and in 24% of the women in the uterine-artery embolization group.

76 ial to evaluate myomectomy, as compared with uterine-artery embolization, in women who had symptomati

77 of life at 2 years than those who underwent uterine-artery embolization.

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

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

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

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

82 ity index) and RI (Doppler calculated in the uterine artery) for both supervised and unsupervised cla

83 presence of PVAT-conditioned media, isolated uterine arteries from both pregnant and non-pregnant rat

84 Uterine arteries from hypoxic pregnancy showed increased

85 Uterine arteries from late pregnant wildtype and LOX-1 o

86 .19 +/- 0.15 and 6.62 +/- 0.12 (P < 0.05) in uterine arteries from normoxic and chronically hypoxic s

87 .09 +/- 0.11 and 5.51 +/- 0.08 (P < 0.05) in uterine arteries from normoxic and chronically hypoxic s

88 vivo increases Ca(V)1.2 channel currents in uterine arteries from pregnant ewes.

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

90 Gestational hypoxia adversely affects uterine artery function, increasing complications.

91 ance, reduced maternal fat mass and restored uterine artery function.

92 m in inhibiting Ca(V)1.2 channel currents in uterine artery haemodynamic adaptation to pregnancy in a

93 gnant sheep, recapitulating the phenotype of uterine arteries in non-pregnant animals.

94 Selective arterial embolization of the uterine artery in PPH is a safe and effective procedure,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

110 Uterine arteries of pregnant sheep acclimatized to long-

111 at gestational hypoxia downregulated TET2 in uterine arteries of pregnant sheep and TET2 was a target

112 In uterine arteries of pregnant sheep, hypoxia significantl

113 nts by reducing steady-state inactivation in uterine arteries of pregnant sheep, recapitulating the p

114 s TET methylcytosine dioxygenase 2 (TET2) in uterine arteries of pregnant sheep.

115 ad, a monomeric G protein, is upregulated in uterine arteries of pregnant sheep.

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

117 y applying silver clips around the aorta and uterine arteries on gestational day 14, resulting in ~ 4

118 The effects of TET2 knockdown in uterine arteries on mtROS, STOCs and myogenic contractio

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

120 he group of patients with prior occlusion of uterine arteries (p = 0.025) without increasing operatin

121 onclude that temporary clamping of bilateral uterine arteries prior to laparoscopic myomectomy is a s

122 Uterine artery pulsatility index and serum placental gro

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

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

125 ratio < 5(th) centile, or abnormal umbilical/uterine artery pulsatility index; and 2) non-severe IUGR

126 xidant MitoQ in hypoxic pregnancy normalises uterine artery reactivity and prevents vascular remodell

127 n hypoxic pregnancy prevented all effects on uterine artery reactivity and remodelling.

128 Knockdown of TET2 in uterine arteries recapitulates the effect of hypoxia and

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

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

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

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

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

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

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

136 -targeted therapy against adverse changes in uterine artery structure and function in high-risk pregn

137 -targeted therapy against adverse changes in uterine artery structure and function in high-risk pregn

138 Here, we show in rodent uterine arteries that hypoxic pregnancy promotes hypertr

139 Pregnancy induces changes in uterine arteries that makes them responsive to uterine P

140 suppression of Ca(V)1.2 channel activity in uterine arteries to facilitate increased uterine blood f

141 PVAT) is a novel local mediator of UtBF and uterine artery tone during pregnancy.

142 least in part, as a result of its actions on uterine artery tone.

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

144 ivo vasoreactivity studies were conducted in uterine arteries (UtA) isolated from pregnant mice expos

145 .5, maternal nitrate/nitrite concentrations, uterine artery (UtA) blood flow and endothelial function

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

147 e hypothesis that adipose tissue surrounding uterine arteries (uterine perivascular adipose tissue; P

148 -targeted antioxidant MitoQ protects against uterine artery vascular dysfunction and remodelling, sup

149 et clinical need for therapeutics that treat uterine artery vascular dysfunction in adverse pregnancy

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

151 Uterine handling led to an acute increase in uterine artery vascular resistance, fetal peripheral vas

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

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

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

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

156 of total cardiac output flowing through the uterine artery was increased with AICAR in hypoxic mice

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

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

159 The uterine arteries were cannulated to perfuse the organ wi

160 Under local anesthesia, both uterine arteries were embolized.

161 The uterine arteries were harvested and, in one segment, con

162 Uterine arteries were isolated from non-pregnant and nea

163 Uterine arteries were obtained from pregnant patients (P

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