ライフサイエンスコーパス: cardiac malformation

1 ubstantial risk for individual categories of cardiac malformation.

2 lted in embryonic lethality characterized by cardiac malformation.

3 ce of normality or a prenatal diagnosis of a cardiac malformation.

4 to first successfully repair large series of cardiac malformations.

5 are also non-genetic factors that influence cardiac malformations.

6 8-23 mo were >1.2 for 4/8 noncardiac and 3/6 cardiac malformations.

7 there was some evidence of a higher risk of cardiac malformations.

8 to maternal diabetes are related to odds of cardiac malformations.

9 as a continuous variable to odds of specific cardiac malformations.

10 active newborns without an increased risk of cardiac malformations.

11 tterning defects, midline abnormalities, and cardiac malformations.

12 enitors likely underlies many forms of human cardiac malformations.

13 ecurrent hepatopathy and encephalopathy, and cardiac malformations.

14 pathogenesis of placental insufficiency and cardiac malformations.

15 ge composition frequently is associated with cardiac malformations.

16 nly associated with pulmonary hypoplasia and cardiac malformations.

17 agmatic hernias, dilated distal airways, and cardiac malformations.

18 e somatic mutations in patients with complex cardiac malformations.

19 irrespective of patient size and associated cardiac malformations.

20 he molecular and morphogenic causes of these cardiac malformations.

21 ients with one of the most common congenital cardiac malformations.

22 putative origins of certain human congenital cardiac malformations.

23 ongenital malformation (1.24 [1.09-1.40]) or cardiac malformations (1.28 [1.11-1.47]) in babies for p

24 including splenic abnormalities and complex cardiac malformations-a distinctive subgroup commonly re

25 anscription factor Cited2 in mice results in cardiac malformation, adrenal agenesis, neural tube, pla

26 Here we show that Cited2-/- embryos die with cardiac malformations, adrenal agenesis, abnormal crania

27 0.8-2.6] and 1.9 [95% CI, 1.1-3.0]) and for cardiac malformations after chlorprothixene exposure (aR

28 The adjusted risk ratio for cardiac malformations among infants exposed to lithium a

29 We examined the risk of cardiac malformations among infants exposed to lithium d

30 Deletion of Jarid2 in mice resulted in cardiac malformation and increased endocardial Notch1 ex

31 spid aortic valve is the most common type of cardiac malformation and predisposes to aortic valve cal

32 glycemic group had 2.5 times greater risk of cardiac malformations and 3.3 times greater risk of skel

33 A dominant disease locus associated with cardiac malformations and atrioventricular conduction ab

34 al for advancing our knowledge of congenital cardiac malformations and designing new regenerative the

35 Pitx2-/- mice present with severe cardiac malformations and embryonic lethality, demonstra

36 first autosomal single-gene defect for these cardiac malformations and indicates that some cases of t

37 r use of intravenous ondansetron and risk of cardiac malformations and oral cleft in children of expo

38 fted to reducing the morbidity of congenital cardiac malformations and their treatment.

39 ective of presence of concomitant congenital cardiac malformations and time of diagnosis compared wit

40 lpha subunit die at midgestation with severe cardiac malformations and vascular regression.

41 ormation, severe cardiac malformation, other cardiac malformation, and cleft lip and palate was highe

42 l anomalies, including cognitive impairment, cardiac malformations, and craniofacial dysmorphy.

43 The absence of aortic valve or other cardiac malformations appears to markedly reduce the ris

44 ikelihood that their child will have a major cardiac malformation are given.

45 three- to fivefold increased risk for fetal cardiac malformations as a result of elevated glucose co

46 ested no substantial increase in the risk of cardiac malformations attributable to antidepressant use

47 ass of missense mutations causes significant cardiac malformations but only minor skeletal abnormalit

48 inct phenotypes: Gly80Arg caused significant cardiac malformations but only minor skeletal abnormalit

49 en knocked out die early in development with cardiac malformations by mechanisms which have yet to be

50 Syndromic cardiac malformations can result in morbidity, yet their

51 ides a potential mechanistic explanation for cardiac malformations caused by mutations in Serrate/Jag

52 notypic variability, and account for related cardiac malformations caused by other transcription fact

53 ssense variant, highly associated with extra-cardiac malformations, caused ectopic pioneer activities

54 astic left heart syndrome (HLHS) is a severe cardiac malformation characterized by left ventricle (LV

55 ith severe developmental delay, visceral and cardiac malformations, connective tissue presentations w

56 Although lower-complexity cardiac malformations constitute the majority of adult c

57 Cardiac malformations constitute the most common birth d

58 na bifida, limb reduction defects, and major cardiac malformations, detection was significantly highe

59 Cardiac malformations due to aberrant development of the

60 on (exposure during the first trimester) and cardiac malformations (exposure during any pregnancy per

61 pregnancy period or the first trimester) and cardiac malformations (exposure during the first trimest

62 We identified 1,589 infants with congenital cardiac malformations, for a live-birth prevalence rate

63 Cardiac malformations have been produced in multiple exp

64 thors' knowledge, attributable fractions for cardiac malformations have not been reported before.

65 n of AIP in mice yields embryonically lethal cardiac malformations, heterozygote, and tissue-specific

66 egulates the expression of Nkx2.5 and causes cardiac malformations; however, it is not sufficient to

67 Major congenital malformations overall and cardiac malformations identified during the first 90 day

68 s were identified: clubfoot in one twin, and cardiac malformation in a singleton birth.

69 ctional variants of MYH6 are associated with cardiac malformations in addition to ASD and provide a n

70 9, or RPS15 reduced CM proliferation, caused cardiac malformations in Drosophila, and produced hypopl

71 unction for Hex suggests an etiology for the cardiac malformations in Hex mutant mice and will make p

72 ecular defects underlying several congenital cardiac malformations in humans and may ultimately provi

73 lished factors associated with several major cardiac malformations in Maryland, the District of Colum

74 ngly in the prenatal diagnosis of congenital cardiac malformations in metropolitan Atlanta.

75 Cardiac malformations in mice lacking Cx40 in one allele

76 risk for congenital malformations overall or cardiac malformations in particular.

77 However, cardiac malformations in Zic3 deficiency occur not becau

78 the Hey2 mutant allele display a spectrum of cardiac malformations including ventricular septal defec

79 Crtl1-deficient mouse revealed a spectrum of cardiac malformations, including AV septal and myocardia

80 ter was associated with an increased risk of cardiac malformations, including Ebstein's anomaly; the

81 erotaxy syndrome, all of whom had congenital cardiac malformations, including malposition of the grea

82 he cardiac transcription factor NKX2-5 cause cardiac malformations, including muscular VSDs.

83 ibit a perinatal lethality and have multiple cardiac malformations, including ventricular and atrial

84 estational hyperoxia therapy rescued genetic cardiac malformation induced by Nkx2-5 mutation in part.

85 ntly in the prenatal diagnosis of congenital cardiac malformations, its impact on the diagnosis and s

86 obesity, retinopathy, polydactyly, renal and cardiac malformations, learning disabilities, and hypoge

87 obesity, retinopathy, polydactyly, renal and cardiac malformations, learning disabilities, and hypoge

88 obesity, retinopathy, polydactyly, renal and cardiac malformations, learning disabilities, and hypoge

89 obesity, retinopathy, polydactyly, renal and cardiac malformations, learning disabilities, hypogenita

90 mice display a high incidence of congenital cardiac malformations like ventricular septal defects, c

91 RXRalpha null mutant mice display ocular and cardiac malformations, liver developmental delay, and di

92 oplastic pulmonary and aortic arch arteries, cardiac malformations, micrognathia, thymus hypoplasia a

93 iral, and one nonspecific]) and unrecognized cardiac malformations (n = 4).

94 e 5-HTT, may lead to severe craniofacial and cardiac malformations, no obvious developmental phenotyp

95 section can occur in Turner syndrome without cardiac malformations or hypertension.

96 can be manifest at birth as life-threatening cardiac malformations or later as more subtle cardiac ab

97 Knock down of sox9a expression did not cause cardiac malformations, or defects in epicardium developm

98 mal abnormalities and concomitant congenital cardiac malformations other than atrial septal defect we

99 posure, the risk of any malformation, severe cardiac malformation, other cardiac malformation, and cl

100 Major malformations overall, cardiac malformations overall, ventricular septal defect

101 thality associated with endoderm defects and cardiac malformations, precluding an analysis of the rol

102 nockout HFOs show a phenotype reminiscent of cardiac malformations previously observed in transgenic

103 Recent studies have reported pleiotropic cardiac malformations resulting from mutations in transc

104 formations (RR, 1.26; 95% CI, 1.02-1.56) and cardiac malformations (RR, 1.26; 95% CI, 0.88-1.81) was

105 mations (RR, 2.09; 95% CI, 1.09-3.99), other cardiac malformations (RR, 1.52; 95% CI, 1.02-2.25), and

106 was associated with increased risk of severe cardiac malformations (RR, 2.09; 95% CI, 1.09-3.99), oth

107 rarely associated with chromosomal or extra cardiac malformations, so decisions about continuing a p

108 issections, 18 of 19 (95%) had an associated cardiac malformation that included a bicuspid aortic val

109 nd early cardiac differentiation but induces cardiac malformations thought to arise from a defect of

110 atal cardiovascular disease (not exclusively cardiac malformations); to benefit from educational prog

111 A complex cardiac malformation was correctly diagnosed in one fetu

112 Overall incidence of cardiac malformations was 6/33 (18%) in Cx40+/- mice and

113 Frequency of cardiac malformations was even higher in this group (44%

114 rnal blood glucose levels of infants without cardiac malformations, we observed that maternal blood g

115 Prenatally diagnosed cardiac malformations were associated with a high incide

116 Overall, 97 (6.1%) of these cases of cardiac malformations were diagnosed prenatally.

117 om crossing of Cx40+/- mice, the most common cardiac malformations were double-outlet right ventricle

118 No cardiac malformations were observed in 15 wild-type mice

119 Cardiac malformations were present in 16 of the 663 infa

120 The findings for cardiac malformations were similar.

121 ients with severe lung disease or congenital cardiac malformation who frequently have suboptimal echo

122 n anomalies with atypical antipsychotics and cardiac malformations with chlorprothixene requires conf

123 patients, these embryos had craniofacial and cardiac malformations with variable expressivity and pen

124 Nkx2-5, in contrast, manifests less profound cardiac malformations, with low disease penetrance.