ライフサイエンスコーパス: bifida

1 both cranial (exencephaly) and spinal (spina bifida).

2 r neural tube defects (anencephaly and spina bifida).

3 on of two bilaterally located hearts (cardia bifida).

4 forebrain defects, facial defects, and spina bifida.

5 interval (CI): 1.0, 15.4), but not for spina bifida.

6 associated with an increased risk for spina bifida.

7 folic acid intake in the occurrence of spina bifida.

8 health care workers and children with spina bifida.

9 health care workers and children with spina bifida.

10 nations) for anencephaly and 70.2% for spina bifida.

11 a risk factor for both anencepahly and spina bifida.

12 he multifactorial, neural tube defect, spina bifida.

13 TIVS7-2 allele of the human T gene and spina bifida.

14 defects correlate with the extent of cardia bifida.

15 l closure of the gut endoderm causing cardia bifida.

16 to open neural tube defects including spina bifida.

17 trulation with consequent cardia and viscera bifida.

18 n and epidermal zippering, as well as cardia bifida.

19 3' kinase (PI3K) activity resulted in spina bifida.

20 ered movement trajectories and caused cardia bifida.

21 ptor signaling in these cells leads to spina bifida.

22 ventral body wall to fuse, leading to cardia bifida.

23 meters squared, of >/=30 vs. <30) and spina bifida.

24 is and demonstrated complete rescue of spina bifida.

25 ally and lack DLHPs, developing severe spina bifida.

26 cal support for the neural tube causes spina bifida.

27 r to the human open neural tube defect spina bifida.

28 ore closure leading to exencephaly and spina bifida.

29 erior to the forelimb buds and lead to spina bifida.

30 ltimate outcome for most children with spina bifida.

31 tract reconstruction in children with spina bifida.

32 ysteine metabolic axis and the risk of spina bifida.

33 ed 73 cases with anencephaly, 123 with spina bifida, 277 with CLP, and 117 with cleft palate only in

34 enatally diagnosed: anencephaly (87%), spina bifida (62%), encephalocele (83%), cleft palate (0%), cl

35 of this closure process leads to open spina bifida, a common cause of severe neurologic disability i

36 function of Mtx1 in the YSL leads to cardia bifida, a phenotype in which the myocardial cells fail t

37 itor cell death in the pathogenesis of spina bifida-a common human congenital malformation.

38 cephaly, acrania, facial clefting, and spina bifida, all of which can be attributed to failed neural

39 udy found a modestly increased risk of spina bifida among infants who were homozygous for the C677T g

40 THFR in 214 liveborn case infants with spina bifida and 503 control infants for whom information on m

41 bbistatin treatment often resulted in cardia bifida and abnormal foregut morphogenesis.

42 Birth certificate reports of spina bifida and anencephaly before fortification (October 199

43 rn with serious malformations (such as spina bifida and anencephaly) could be reduced by half.

44 Neural tube defects (NTDs), including spina bifida and anencephaly, are severe birth defects of the

45 ults in neural tube defects, including spina bifida and anencephaly, which are among the most common

46 yos presenting with varying degrees of spina bifida and anencephaly.

47 man embryos leads to defects including spina bifida and anencephaly.

48 in SCRIB SADH domains associated with spina bifida and cancer impact the stability of SCRIB at the p

49 iology of human birth defects, such as spina bifida and congenital kidney cysts.

50 Mortality was lowest (<3%) in spina bifida and facial cleft procedures, and highest (>50%) i

51 (4) Children with spina bifida and fecal incontinence may benefit from technique

52 with maternal obesity was greater for spina bifida and for other less prevalent NTDs than for anence

53 xhibit NTDs consisting of exencephaly, spina bifida and forebrain truncations, while Fpn1(ffe/KI) mut

54 to predict and modify the incidence of spina bifida and other neural tube defects.

55 and homozygous mutant embryos develop spina bifida and sometimes exencephaly.

56 ng zygotic oep (Zoep mutants) display cardia bifida and, as we show here, also display reduced or abs

57 ound, 12% of mid-gestation embryos had spina bifida and/or exencephaly, whereas wild-type animals of

58 : failure of the neural tube to close (spina bifida) and multiple neural tubes (diastematomyelia).

59 be, fail to form a single heart tube (cardia bifida), and show delayed migration of endoderm and meso

60 e 87 cases of anencephaly, 96 cases of spina bifida, and 14 cases of encephalocele for respective rat

61 ly, hydroxybenzonitrile herbicides for spina bifida, and 2,6-dinitroaniline herbicides and dithiocarb

62 be defects show that anencephaly, open spina bifida, and craniorachischisis result from failure of pr

63 t embryos lack caudal somites, develop spina bifida, and die at 9.5-12.5 days of embryonic developmen

64 ifelong necessity for individuals with spina bifida, and should be provided by a multidisciplinary te

65 observed include both exencephaly and spina bifida, and the phenotype exhibits partial penetrance wi

66 e the endoderm convergence defect and cardia bifida, and, conversely, that the presence of anterior e

67 the herbicide bromoxynil octanoate for spina bifida; and trifluralin and maneb for CLP.

68 pared data on 1,242 infants with NTDs (spina bifida, anencephaly, and encephalocele) with data from a

69 rcentages of maternal diabetes-induced spina bifida aperta but not exencephaly, and this increase was

70 6 and Fgf8 at the tail bud, leading to spina bifida aperta, caudal axis bending and tail truncation.

71 iants, the risk of having a child with spina bifida appears to increase with the number of high-risk

72 Neural tube defects (NTDs), such as spina bifida, are common and severe birth defects in humans bu

73 ins containing folic acid, the risk of spina bifida, as measured by the odds ratio, was 1.6 (95% conf

74 ng phenotype is strikingly similar to cardia bifida, as observed in vertebrate embryos when endoderm

75 Some data suggest that the risk for spina bifida associated with C677T homozygosity may depend on

76 oved 27 genes, including PAX3, a known spina bifida-associated gene.

77 ependent hydrocephalus in infants with spina bifida, but increases the incidence of premature deliver

78 ctor receptor (PDGFR) alpha results in spina bifida, but the underlying mechanism has not been identi

79 and embryonic genetic risk factors for spina bifida by use of the two-step transmission/disequilibriu

80 rates of congenital malformations (eg, spina bifida, cardiac anomalies).

81 Up to 70% of spina bifida cases can be prevented by maternal, periconceptio

82 Among 180 anencephalic cases, 385 spina bifida cases, and 3, 963 controls, 21.1%, 25.2%, and 26.

83 the neural tube, tail distortion, and spina bifida caused by the amplification of neural tissue in t

84 merican studies: a study of mothers of spina bifida children and control mothers (1995-1996; n = 136)

85 with an increased risk of anencephaly, spina bifida, cleft lip with or without cleft palate (CLP), or

86 inhaled beta2-agonists were found for spina bifida, cleft lip, anal atresia, severe congenital heart

87 Analyses of mutations that cause cardia bifida demonstrate that the achievement of a proper card

88 ll Noggin-/- pups are born with lumbar spina bifida; depending on genetic background, they may also h

89 e molecular mechanisms underlying the spinal bifida development are largely unknown.

90 enerates a complex phenotype including spina bifida, exencephaly and cardiac outflow tract abnormalit

91 nd penetrance to analyse data from the spina bifida families.

92 al trial to assess in utero closure of spina bifida has been initiated in the USA.

93 ilepsy and bipolar disorder but causes spina bifida if taken during pregnancy.

94 closure and developed exencephaly and spina bifida, important human congenital anomalies.

95 fect that is known to lead directly to spina bifida in curly tail embryos.

96 In order to test the hypothesis that spina bifida in curly tail mice results from insufficient expr

97 Spina bifida in curly tail results from a cell type-specific p

98 mosomal location and the occurrence of spina bifida in Grhl3 null mice.

99 variable significantly associated with spina bifida in multivariate analysis.

100 nhibitor imatinib mesylate resulted in spina bifida in the absence of NTDs.

101 ression of Galpha(13) fails to rescue cardia bifida in the context of global Galpha(13) inhibition.

102 The pathogenesis and etiology of spina bifida in the curly tail mouse closely resemble defects

103 mozygous for the Pax3Sp-d gene develop spina bifida in the lumbosacral region of the neuraxis.

104 at these loci were not major genes for spina bifida in these families.

105 hey display striking features of human spina bifida, including a dysplastic spinal cord, open neural

106 Spina bifida is a NTD where the spinal cord is dysplastic, and

107 ves neurologic outcome in infants with spina bifida is not known.

108 Adult ambulatory status in spina bifida is significantly predictive (89% accurate) by two

109 (NTDs), specifically, anencephaly and spina bifida, is now well recognized, having been established

110 wo independent bilateral heart tubes (cardia bifida), lacked a foregut, and died around embryonic day

111 from the finding that closure of open spina bifida lesions in utero can diminish neurological dysfun

112 Mutant analyses indicate that the cardia bifida locus natter (nat) is required for the integrity

113 children with certain conditions (e.g. spina bifida), may adversely affect parental health.

114 lomeningocele, the most common form of spina bifida, may result in better neurologic function than re

115 Individuals with spina bifida need both surgical and medical management.

116 rofound craniofacial abnormalities and spina bifida observed in PDGFRalpha knockout mice and prolonge

117 velop polyhydramnios, hydrops fetalis, spina bifida occulta and osteochondrodysplasia.

118 tion of the spinous process, mimicking spina bifida occulta, a common malformation in humans.

119 cts consisting of both exencephaly and spina bifida occulta, an unusual combination.

120 oduces one of very few mouse models of spina bifida occulta.

121 tube closure similar to those in human spina bifida, one of the most serious congenital birth defects

122 haly (OR = 2.58, 95% CI 1.19-5.61) and spina bifida (OR = 3.71, 95% CI 1.48-9.31).

123 Spina bifida, or failure of the vertebrae to close at the midl

124 Fifty-six percent of spina bifida patients and 92% of health care workers with late

125 chondrocytes did not recapitulate the spina bifida phenotype.

126 d with a moderately increased risk for spina bifida (pooled odds ratio = 1.8; 95% confidence interval

127 cephaly rate (4.9 per 10,000) than the spina bifida rate (6.7 per 10,000).

128 etically co-segregated exencephaly and spina bifida, recapitulating the phenotypes observed in human

129 Cardia bifida results from failed midline differentiation, even

130 Spina bifida results from failure of fusion of the caudal neur

131 If dorsolateral bending fails, spina bifida results.

132 nvestigated whether an interaction for spina bifida risk existed between infant MTHFR C677T genotype

133 Spina bifida (SB) patients afflicted with myelomeningocele typ

134 allergic health care workers (HCW) and spina bifida (SB) patients.

135 astrulation-specific defects including spina bifida, shortened anteroposterior axis, and reduced ante

136 A review of new developments in spina bifida shows that many cases are preventable by administ

137 vated risks of NTDs and anencephaly or spina bifida subtypes were also associated with exposures to c

138 onic genotype when evaluating putative spina bifida susceptibility loci.

139 an in those with spinal cord injury or spina bifida; this difference in morbidity is taken into accou

140 th defects, with severity ranging from spina bifida to lethal anencephaly.

141 at both variants influence the risk of spina bifida via the maternal rather than the embryonic genoty

142 ation between prepregnancy obesity and spina bifida was 1.48 (95% confidence interval: 1.26, 1.73), a

143 The frequency of spina bifida was not altered in either backcross, emphasizing

144 referent group, mothers of babies with spina bifida were 2.0 times more likely (95% CI: 1.3, 3.2) to

145 9 cases of anencephaly and 32 cases of spina bifida were detected.

146 ilure of ventral foregut closure and cardiac bifida, whereas GATA6 is essential for development of th

147 syndrome, Brachydactyly Type B1, and spinal bifida which are caused by mutations in human ROR2, WNT5

148 s an isolated and completely penetrant spina bifida, which is folate- and inositol-resistant.

149 f Dvl2(-/-) embryos displayed thoracic spina bifida, while virtually all Dvl1/2 double mutant embryos

150 n of miles apart or casanova leads to cardia bifida with each bilateral heart associated with its own

151 Failure of spinal closure in pre-spina bifida Zic2(Ku) mutant embryos is associated with altere