ライフサイエンスコーパス: cardiac malformation

1 lted in embryonic lethality characterized by cardiac malformation.

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

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

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

5 tterning defects, midline abnormalities, and cardiac malformations.

6 enitors likely underlies many forms of human cardiac malformations.

7 ecurrent hepatopathy and encephalopathy, and cardiac malformations.

8 pathogenesis of placental insufficiency and cardiac malformations.

9 ge composition frequently is associated with cardiac malformations.

10 nly associated with pulmonary hypoplasia and cardiac malformations.

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

12 e somatic mutations in patients with complex cardiac malformations.

13 irrespective of patient size and associated cardiac malformations.

14 he molecular and morphogenic causes of these cardiac malformations.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

38 Cardiac malformations constitute the most common birth d

39 Cardiac malformations due to aberrant development of the

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

41 Cardiac malformations have been produced in multiple exp

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

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

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

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

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

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

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

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

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

51 Cardiac malformations in mice lacking Cx40 in one allele

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

53 However, cardiac malformations in Zic3 deficiency occur not becau

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

80 A complex cardiac malformation was correctly diagnosed in one fetu

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

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

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

84 Prenatally diagnosed cardiac malformations were associated with a high incide

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

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

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

88 Cardiac malformations were present in 16 of the 663 infa

89 The findings for cardiac malformations were similar.

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

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