ライフサイエンスコーパス: fetal heart

1 ssion of the alpha1D Ca channel in the human fetal heart.

2 ells contribute to normal development of the fetal heart.

3 a result most likely due to a defect in the fetal heart.

4 lette, an actin-binding protein expressed in fetal heart.

5 genes decreased to the same levels as in the fetal heart.

6 were higher in the nonfailing heart than the fetal heart.

7 es in the nonfailing heart compared with the fetal heart.

8 s preferentially expressed in both adult and fetal heart.

9 rs via the umbilical arterial route into the fetal heart.

10 substrate 1 and glucose transporter 4 in the fetal heart.

11 hondrial OXPHOS complex I, III and IV in the fetal heart.

12 IO1 mRNA expression in the non-human primate fetal heart.

13 ility profile of the non-human primate (NHP) fetal heart.

14 t spatial account of chromaffin cells in the fetal heart.

15 indow for the structural organization of the fetal heart.

16 ay indicate novel adaptive strategies in the fetal heart.

17 l capillary-level adaptations in the in vivo fetal heart.

18 glucocorticoid exposure in the Hsd11b2(-/-) fetal heart.

19 f fiber architecture in the developing human fetal heart.

20 y binding to apoptotic cardiomyocytes in the fetal heart.

21 he sex differences in SP1 methylation in the fetal heart.

22 n of chamber-specific genes was defective in fetal hearts.

23 reviously been shown to be antiarrhythmic in fetal hearts.

24 ied in the septal region of several affected fetal hearts.

25 tion and decreased coronary artery volume in fetal hearts.

26 ndance for highly expressed miRNAs in HF and fetal hearts.

27 KDR and PDGFRalpha in first-trimester human fetal hearts.

28 onatal mouse hearts compared with 16-day-old fetal hearts.

29 decreases in PKCepsilon protein and mRNA in fetal hearts.

30 was up-regulated (P<0.05) in OB maternal and fetal hearts.

31 xpression of the alpha1D Ca channel in human fetal heart, (2) inhibition of alpha1D I(Ca-L) by positi

32 Among ongoing pregnancies with fetal heart activity, the multiple gestation rate with l

33 seful therapeutic agent to protect the human fetal heart against IR injury, as may occur in complicat

34 imers flanking exon 4 and mRNA from 22 human fetal hearts (age 11-25 weeks) and 3 adult hearts.

35 In fetal hearts ages 22-25 weeks and adult heart, the 52bet

36 tabolomic profile of placentae, maternal and fetal hearts analysed using high-resolution (1)H NMR spe

37 the examiner to identify normal and complex fetal heart anatomy during the early second to the late

38 Sildenafil protects the fetal heart and circulation directly in hypoxic developm

39 ial effects of sildenafil transcend onto the fetal heart and circulation in complicated development i

40 and lung ECs in mice were conserved in human fetal heart and lung ECs.

41 nrichment in DNase I hypersensitive sites in fetal heart and lung.

42 nd quantification of blood flow in the human fetal heart and major vessels.

43 otion-corrected 3-dimensional volumes of the fetal heart and phase-contrast flow sequences gated with

44 ular pathways common between first trimester fetal heart and placenta cells which if disrupted may co

45 of shared developmental pathways between the fetal heart and placenta may play a role in PMP developm

46 n of Nfe2l2-mediated oxidative stress in the fetal heart and preservation of calcium regulatory respo

47 the hypothesis that oxidative stress in the fetal heart and vasculature underlies the molecular basi

48 RNA and protein to control levels in vivo in fetal hearts and in vitro in embryonic myocyte cells.

49 on and phenotype in fibroblasts derived from fetal hearts and lungs was investigated by Affymetrix ar

50 layer, SHISA3, primarily expressed in VCs in fetal hearts and pathological remodeling was identified.

51 ned in ex vivo hypoxic treatment of isolated fetal hearts and rat embryonic ventricular myocyte cell

52 ic conditions, we identify iFHRV in isolated fetal hearts and show that it is markedly affected by hy

53 oxide bioavailability (54.7 +/- 6.1%) in the fetal heart, and promoted peripheral endothelial dysfunc

54 ide bioavailability (115.6 +/- 22.3%) in the fetal heart, and restored endothelial function in the pe

55 cts of their cognate antibodies on the human fetal heart are unknown.

56 onsideration of technical adaptations to the fetal heart, are summarized.

57 e of the electromechanical properties of the fetal heart as well as the mechanisms of arrhythmia to f

58 iled to induce fatty acid oxidation genes in fetal hearts assessed 24 h later.

59 etabolic maturation of the growth-restricted fetal heart associated with a decreased capacity to oxid

60 -1) at Ser-307 were increased (P<0.05) in OB fetal heart associated with lower downstream PI3K-Akt ac

61 sgene, IGF-1B mRNA was not detectable in the fetal heart at the end of gestation, was present in mode

62 ally, ICA cells could be identified in human fetal hearts at a developmental stage before sympathetic

63 myocytes in vitro, was also downregulated in fetal hearts at E17.5, 24 h after dexamethasone administ

64 We show that CXCL12 is expressed in human fetal hearts at the time dominance is established.

65 eas and kidney, but was absent in samples of fetal heart, brain, liver and thymus.

66 of both the left and right ventricles of the fetal heart by day 78 of gestation.

67 We report that the fetal heart contains a reservoir of stem/progenitor cell

68 an embryonic stem cell-derived and embryonic/fetal heart-derived cardiac cells micro-dissected from s

69 ights will provide a better understanding of fetal heart development in an adverse in utero environme

70 Abnormal fetal heart development was not previously described.

71 ulation of endocardial and epicardial EMT in fetal heart development, and we summarize key literature

72 ds were administered to pregnant rats during fetal heart development.

73 differentiation and tissue formation during fetal heart development.

74 ion and gene environment interactions during fetal heart development.

75 ibited a normal contractile function vs. CON fetal hearts during basal perfusion, they developed an i

76 ophages after Langendorff perfusion of three fetal hearts dying with CHB and three healthy gestationa

77 the parallel development of the placenta and fetal heart early in pregnancy, very few studies suggest

78 measures the magnetic fields associated with fetal heart electrical activity outside of the maternal

79 We also found, in comparison with fetal heart endothelial cells, 197 commonly expressed ge

80 Although OB fetal hearts exhibited a normal contractile function vs.

81 The fetal heart expresses the slow skeletal TnI (ssTnI) isof

82 Both in vitro and in fetal hearts, EZH2 interacted with cardiac transcription

83 Isolated fetal hearts from hypoxic pregnancy exhibit a time scale

84 Age-matched fetal hearts from voluntary terminations expressed neith

85 alent to about 2% of adult or 25% of 16-week fetal heart function) in a modified working heart prepar

86 d long-term consequences of these changes in fetal heart gene expression and induction of specific ho

87 Transcripts representing most members of the fetal heart gene program remained elevated from fetal to

88 Fetal heart growth occurs through cardiomyocyte prolifer

89 Wnt and Hippo signaling during embryonic and fetal heart growth.

90 We hypothesized that the late gestation IUGR fetal heart has a lower capacity for mitochondrial oxida

91 Therefore, the isolated fetal heart has intrinsic variability and carries a memo

92 as performed on formalin-fixed sections of 4 fetal hearts identified in utero as having CHB or isolat

93 l obesity in mice induces hypertrophy of the fetal heart in association with altered expression of ge

94 d describe elevated BRG1 expression in human fetal hearts in early development.

95 Our findings relate fetal heart indices to brainstem, hypothalamic, and dACC

96 cture and function of the rapidly developing fetal heart is unknown.

97 (Flk-1) was used as a bait to screen a human fetal heart library in the yeast two-hybrid system.

98 fetal serum lipidome distinctly; (2) female fetal heart lipidomes are more sensitive to maternal obe

99 e transcriptase protein (hTERT) during human fetal heart, liver, and kidney development.

100 Bhmt2 is expressed in fetal heart, lung, liver, kidney and eye.

101 ation of preterm delivery may interfere with fetal heart maturation by downregulating the ability to

102 us glucocorticoids may interfere with normal fetal heart maturation, possibly by downregulating GR.

103 Understanding hypoxia adaptation in the fetal heart may allow development of strategies to prote

104 aternal cardiovascular system, placental and fetal heart metabolism.

105 ude new guidelines for the interpretation of fetal heart monitoring, advances in intrapartum fetal pu

106 itial use of Doppler US for the detection of fetal heart motion and the eventual use of pulsed and co

107 onsible for delivering oxygen to the anaemic fetal heart muscle using contrast-enhanced echocardiogra

108 Human fetal hearts (n = 5) between 10-19 weeks of gestation we

109 es, -346 and -268, were demonstrated in both fetal hearts of maternal hypoxia and H9c2 cells treated

110 and cross-reactive (laminin) autoantigens in fetal hearts of varied ages and in adult hearts.

111 es may be involved in the examination of the fetal heart (pediatric cardiologists, obstetricians, mat

112 ete atrioventricular (AV) block in the human fetal heart perfused by the Langendorff technique and in

113 ed a novel Langendorff, biventricular, ovine fetal heart preparation to investigate the effects of ad

114 notype explained the majority of variance in fetal heart rate (-10 beats per minute per added mutatio

115 the separate indications of a nonreassuring fetal heart rate (7.1% and 7.9%, respectively; P=0.30) a

116 l cord occlusion on the normal maturation of fetal heart rate (FHR) and mean arterial pressure (MAP)

117 The interpretation of fetal heart rate (FHR) patterns is the only available me

118 rees AVB; 3) reactive ventricular and atrial fetal heart rate (FHR) tracings at ventricular rates >56

119 to fetal mean arterial blood pressure (MAP), fetal heart rate (FHR), and fetal baro- and chemoreflexe

120 pnic hypoxia (Pa,O2, 12 +/- 0.6 mmHg) on the fetal heart rate (FHR), mean systemic arterial blood pre

121 diameter (YSD), crown rump length (CRL) and fetal heart rate (FHR), were extract from ultrasound vid

122 Our purpose was to characterize the fetal heart rate (FHR)/gestational age (GA) profile of f

123 heart rate variability (HRV) increases while fetal heart rate (HR) decreases.

124 541 (12.9%); P<0.001), and a reduced risk of fetal heart rate abnormalities (153/548 (27.9%) v 219/53

125 and by the blockade of reflex reductions in fetal heart rate after intravenous injection of phenylep

126 oke MATLAB scripts was undertaken to produce fetal heart rate and beat-to-beat rhythm strips.

127 idenced by a reduction in the variability of fetal heart rate and by the blockade of reflex reduction

128 CG has high temporal precision for measuring fetal heart rate and its variability which reflects feta

129 Strong correlations between fetal heart rate and neonatal heart rate (r=0.700; P<0.0

130 Labor complicated by a nonreassuring fetal heart rate before randomization was documented for

131 2 LQT1 founder populations, third trimester fetal heart rate discriminated between fetal genotypes a

132 white blood cell count in the 3rd trimester, fetal heart rate during labor, newborn feeding and tempe

133 Intermittent tachycardia was demonstrated on fetal heart rate graphs.

134 This finding strengthens the role of fetal heart rate in the early detection and risk stratif

135 Electronic monitoring of the fetal heart rate is commonly performed, in part to detec

136 .3%), and preterm labor (52.3%) and abnormal fetal heart rate monitoring (22.2%) were more common in

137 In terms of quality of care, intrapartum fetal heart rate monitoring decreased by 13.4% (-15.4 to

138 QTS, although the most common LQTS rhythm, a fetal heart rate of less than third percentile for gesta

139 The potential to monitor fetal heart rate over a prolonged period is an advantage

140 isk of uterine hyperstimulation and abnormal fetal heart rate patterns.

141 no association between the highest or lowest fetal heart rate recorded for each child and the risk of

142 nitoring strategies: reduced cardiotocograph fetal heart rate STV (CTG STV), early DV changes (pulsat

143 Fetal heart rate variability (FHRV) emerges from influen

144 velops during the second to third trimester, fetal heart rate variability (HRV) increases while fetal

145 roduce a technique to test whether intrinsic fetal heart rate variability (iFHRV) exists and we show

146 We discuss how circadian changes in fetal heart rate variability may offer utility as a biom

147 The fetal heart rate was compared with those measured by doc

148 bgroup of 2168 women in whom a nonreassuring fetal heart rate was detected before randomization.

149 During hypoglycaemia, an initial rise in fetal heart rate was followed by a slower fall.

150 mal findings on electronic monitoring of the fetal heart rate were associated with an increased risk

151 lar block, but sinus bradycardia, defined as fetal heart rate<3% for gestational age, is most common.

152 nce of systemic fetal hypoxia, or changes in fetal heart rate, carotid blood flow or carotid oxygen d

153 is revealed significant associations between fetal heart rate, genotype, and phenotype; mean third tr

154 liveries, epidural analgesia, non-reassuring fetal heart rate, meconium in the amniotic fluid, should

155 We investigate third trimester fetal heart rate, routinely recorded within public mater

156 allopurinol led to significant increases in fetal heart rate, umbilical blood flow and umbilical vas

157 PHSG versus HG fetuses had decreased fetal heart rate-movement coupling (P < 0.05), which may

158 aphy versus intermittent auscultation of the fetal heart rate.

159 as utilized to confirm pregnancy and measure fetal heart rate.

160 temperature, heart rate, blood pressure, and fetal heart rate.

161 tions, such as monitoring blood pressure and fetal heart rate.

162 The masked system functioned as a normal fetal heart-rate monitor.

163 junct to conventional intrapartum electronic fetal heart-rate monitoring did not improve perinatal ou

164 junct to conventional intrapartum electronic fetal heart-rate monitoring modifies intrapartum and neo

165 dditional information for use when uncertain fetal heart-rate patterns were detected.

166 Ultrasounds were performed and fetal heart rates measured on day 20-21 of gestation.

167 and phenotype; mean third trimester prelabor fetal heart rates obtained from obstetric records (gesta

168 ts, diameters, approximate fetal weights and fetal heart rates were similar to the M-P- group.

169 The fetal heart relies on carbohydrates in utero and must be

170 The human fetal heart remains highly isotropic until 14-19 weeks,

171 f Fallot (TOF) without a 22q11.2 deletion, 3 fetal heart samples, and 8 normally developing infants.

172 itted between 2012 and 2016 to participating Fetal Heart Society Research Collaborative institutions

173 had a gestational age of 22 weeks or more, a fetal heart sound at time of admission, and consented to

174 nism by which these heart defects may arise, fetal heart structure and function in these transgenic a

175 enous valves are prominent structures in the fetal heart that direct inferior vena caval flow towards

176 onin affect the functional properties of the fetal heart that lead to infantile cardiomyopathy.

177 ctors that may have an adverse effect on the fetal heart, there is a growing body of epidemiological

178 In fetal hearts, there was significantly higher abundance o

179 technique enables directly gated MRI of the fetal heart throughout the cardiac cycle, allowing for i

180 immunohistologic evaluation of CHB-affected fetal heart tissue and by determination of erythropoieti

181 iling of hiPSC-derived endocardium and human fetal heart tissue with an underdeveloped left ventricle

182 odel by transplanting second-trimester human fetal heart tissues s.c. into the ear pinna of a SCID mo

183 e-cell chromatin accessibility maps of human fetal heart tissues.

184 cells were delivered into these functioning fetal heart tissues: in contrast to traditional murine h

185 tence of sexually dimorphic responses of the fetal heart to the same in utero obesogenic environment

186 ination of the structure and function of the fetal heart together with the evaluation of other parame

187 ned by bradycardia, deceleration, or lack of fetal heart tones (FHTs).

188 xpression levels and with novel exons in the fetal heart transcriptome are known to play central role

189 window to study electrical properties of the fetal heart, unlike what has been available to date.

190 The morphology of the fetal heart was assessed by calculating the right and le

191 The fetal heart was visualized outside the chest through a d

192 respiration levels in the growth-restricted fetal heart were lower than in the normally growing fetu

193 At 10-14 weeks the fetal hearts were highly isotropic and few tracts could

194 Following exsanguination under anaesthesia, fetal hearts were mounted in the Langendorff preparation

195 Fetal hearts were studied in late gestation (embryonic d

196 m days 15 to 20 of gestational age, and term fetal hearts were studied.

197 In tissues such as fibroblasts and fetal hearts, where IGF1 levels are high, we found eithe

198 interacted with the SP1 binding sites in the fetal heart, which may explain the sex differences in SP

199 of changes in structure and function in the fetal heart with the focus on congenital heart disease m

200 by late gestation exhibit markedly enlarged fetal hearts with increased myocardial trabeculation and