ライフサイエンスコーパス: spina bifida

1 isk for neural tube defects (anencephaly and spina bifida).

2 NTDs, both cranial (exencephaly) and spinal (spina bifida).

3 ernal folic acid intake in the occurrence of spina bifida.

4 among health care workers and children with spina bifida.

5 cially health care workers and children with spina bifida.

6 terminations) for anencephaly and 70.2% for spina bifida.

7 t was a risk factor for both anencepahly and spina bifida.

8 y to the multifactorial, neural tube defect, spina bifida.

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

10 leads to open neural tube defects including spina bifida.

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

12 f receptor signaling in these cells leads to spina bifida.

13 sgenesis and demonstrated complete rescue of spina bifida.

14 s dorsally and lack DLHPs, developing severe spina bifida.

15 ght in meters squared, of >/=30 vs. <30) and spina bifida.

16 echanical support for the neural tube causes spina bifida.

17 similar to the human open neural tube defect spina bifida.

18 neuropore closure leading to exencephaly and spina bifida.

19 d posterior to the forelimb buds and lead to spina bifida.

20 the ultimate outcome for most children with spina bifida.

21 rinary tract reconstruction in children with spina bifida.

22 -homocysteine metabolic axis and the risk of spina bifida.

23 duces forebrain defects, facial defects, and spina bifida.

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

25 uld be associated with an increased risk for spina bifida.

26 included 73 cases with anencephaly, 123 with spina bifida, 277 with CLP, and 117 with cleft palate on

27 ere prenatally diagnosed: anencephaly (87%), spina bifida (62%), encephalocele (83%), cleft palate (0

28 ailure of this closure process leads to open spina bifida, a common cause of severe neurologic disabi

29 progenitor cell death in the pathogenesis of spina bifida-a common human congenital malformation.

30 s exencephaly, acrania, facial clefting, and spina bifida, all of which can be attributed to failed n

31 nia study found a modestly increased risk of spina bifida among infants who were homozygous for the C

32 s of MTHFR in 214 liveborn case infants with spina bifida and 503 control infants for whom informatio

33 Birth certificate reports of spina bifida and anencephaly before fortification (Octob

34 ren born with serious malformations (such as spina bifida and anencephaly) could be reduced by half.

35 Neural tube defects (NTDs), including spina bifida and anencephaly, are severe birth defects o

36 ss results in neural tube defects, including spina bifida and anencephaly, which are among the most c

37 e embryos presenting with varying degrees of spina bifida and anencephaly.

38 in human embryos leads to defects including spina bifida and anencephaly.

39 ations in SCRIB SADH domains associated with spina bifida and cancer impact the stability of SCRIB at

40 the etiology of human birth defects, such as spina bifida and congenital kidney cysts.

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

42 (4) Children with spina bifida and fecal incontinence may benefit from tec

43 ciated with maternal obesity was greater for spina bifida and for other less prevalent NTDs than for

44 ants exhibit NTDs consisting of exencephaly, spina bifida and forebrain truncations, while Fpn1(ffe/K

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

46 fects, and homozygous mutant embryos develop spina bifida and sometimes exencephaly.

47 background, 12% of mid-gestation embryos had spina bifida and/or exencephaly, whereas wild-type anima

48 logies: failure of the neural tube to close (spina bifida) and multiple neural tubes (diastematomyeli

49 re were 87 cases of anencephaly, 96 cases of spina bifida, and 14 cases of encephalocele for respecti

50 ncephaly, hydroxybenzonitrile herbicides for spina bifida, and 2,6-dinitroaniline herbicides and dith

51 ral tube defects show that anencephaly, open spina bifida, and craniorachischisis result from failure

52 mutant embryos lack caudal somites, develop spina bifida, and die at 9.5-12.5 days of embryonic deve

53 is a lifelong necessity for individuals with spina bifida, and should be provided by a multidisciplin

54 efects observed include both exencephaly and spina bifida, and the phenotype exhibits partial penetra

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

56 ey compared data on 1,242 infants with NTDs (spina bifida, anencephaly, and encephalocele) with data

57 her percentages of maternal diabetes-induced spina bifida aperta but not exencephaly, and this increa

58 T, Tbx6 and Fgf8 at the tail bud, leading to spina bifida aperta, caudal axis bending and tail trunca

59 th variants, the risk of having a child with spina bifida appears to increase with the number of high

60 Neural tube defects (NTDs), such as spina bifida, are common and severe birth defects in hum

61 vitamins containing folic acid, the risk of spina bifida, as measured by the odds ratio, was 1.6 (95

62 Some data suggest that the risk for spina bifida associated with C677T homozygosity may depe

63 on removed 27 genes, including PAX3, a known spina bifida-associated gene.

64 hunt-dependent hydrocephalus in infants with spina bifida, but increases the incidence of premature d

65 wth factor receptor (PDGFR) alpha results in spina bifida, but the underlying mechanism has not been

66 ernal and embryonic genetic risk factors for spina bifida by use of the two-step transmission/disequi

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

68 Up to 70% of spina bifida cases can be prevented by maternal, pericon

69 Among 180 anencephalic cases, 385 spina bifida cases, and 3, 963 controls, 21.1%, 25.2%, a

70 ion of the neural tube, tail distortion, and spina bifida caused by the amplification of neural tissu

71 orth American studies: a study of mothers of spina bifida children and control mothers (1995-1996; n

72 iated with an increased risk of anencephaly, spina bifida, cleft lip with or without cleft palate (CL

73 ure to inhaled beta2-agonists were found for spina bifida, cleft lip, anal atresia, severe congenital

74 All Noggin-/- pups are born with lumbar spina bifida; depending on genetic background, they may

75 that generates a complex phenotype including spina bifida, exencephaly and cardiac outflow tract abno

76 ance and penetrance to analyse data from the spina bifida families.

77 clinical trial to assess in utero closure of spina bifida has been initiated in the USA.

78 of epilepsy and bipolar disorder but causes spina bifida if taken during pregnancy.

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

80 nic defect that is known to lead directly to spina bifida in curly tail embryos.

81 In order to test the hypothesis that spina bifida in curly tail mice results from insufficien

82 Spina bifida in curly tail results from a cell type-spec

83 n chromosomal location and the occurrence of spina bifida in Grhl3 null mice.

84 study variable significantly associated with spina bifida in multivariate analysis.

85 DGFR inhibitor imatinib mesylate resulted in spina bifida in the absence of NTDs.

86 The pathogenesis and etiology of spina bifida in the curly tail mouse closely resemble de

87 yos homozygous for the Pax3Sp-d gene develop spina bifida in the lumbosacral region of the neuraxis.

88 ing that these loci were not major genes for spina bifida in these families.

89 but they display striking features of human spina bifida, including a dysplastic spinal cord, open n

90 Spina bifida is a NTD where the spinal cord is dysplasti

91 improves neurologic outcome in infants with spina bifida is not known.

92 Adult ambulatory status in spina bifida is significantly predictive (89% accurate)

93 efects (NTDs), specifically, anencephaly and spina bifida, is now well recognized, having been establ

94 s come from the finding that closure of open spina bifida lesions in utero can diminish neurological

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

96 of myelomeningocele, the most common form of spina bifida, may result in better neurologic function t

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

98 the profound craniofacial abnormalities and spina bifida observed in PDGFRalpha knockout mice and pr

99 nts develop polyhydramnios, hydrops fetalis, spina bifida occulta and osteochondrodysplasia.

100 formation of the spinous process, mimicking spina bifida occulta, a common malformation in humans.

101 e defects consisting of both exencephaly and spina bifida occulta, an unusual combination.

102 ect produces one of very few mouse models of spina bifida occulta.

103 eural-tube closure similar to those in human spina bifida, one of the most serious congenital birth d

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

105 Spina bifida, or failure of the vertebrae to close at th

106 Fifty-six percent of spina bifida patients and 92% of health care workers wit

107 r from chondrocytes did not recapitulate the spina bifida phenotype.

108 ociated with a moderately increased risk for spina bifida (pooled odds ratio = 1.8; 95% confidence in

109 e anencephaly rate (4.9 per 10,000) than the spina bifida rate (6.7 per 10,000).

110 ay genetically co-segregated exencephaly and spina bifida, recapitulating the phenotypes observed in

111 Spina bifida results from failure of fusion of the cauda

112 If dorsolateral bending fails, spina bifida results.

113 hors investigated whether an interaction for spina bifida risk existed between infant MTHFR C677T gen

114 Spina bifida (SB) patients afflicted with myelomeningoce

115 latex-allergic health care workers (HCW) and spina bifida (SB) patients.

116 e of gastrulation-specific defects including spina bifida, shortened anteroposterior axis, and reduce

117 A review of new developments in spina bifida shows that many cases are preventable by ad

118 Elevated risks of NTDs and anencephaly or spina bifida subtypes were also associated with exposure

119 embryonic genotype when evaluating putative spina bifida susceptibility loci.

120 ers than in those with spinal cord injury or spina bifida; this difference in morbidity is taken into

121 in birth defects, with severity ranging from spina bifida to lethal anencephaly.

122 nce that both variants influence the risk of spina bifida via the maternal rather than the embryonic

123 association between prepregnancy obesity and spina bifida was 1.48 (95% confidence interval: 1.26, 1.

124 The frequency of spina bifida was not altered in either backcross, emphas

125 s the referent group, mothers of babies with spina bifida were 2.0 times more likely (95% CI: 1.3, 3.

126 ods, 59 cases of anencephaly and 32 cases of spina bifida were detected.

127 hat has an isolated and completely penetrant spina bifida, which is folate- and inositol-resistant.

128 2-3% of Dvl2(-/-) embryos displayed thoracic spina bifida, while virtually all Dvl1/2 double mutant e

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