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 tion, preventing zippering and causing spina bifida.

5 ants in two samples from patients with spina bifida.

6 ore closure leading to exencephaly and spina bifida.

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

8 ltimate outcome for most children with spina bifida.

9 tract reconstruction in children with spina bifida.

10 ysteine metabolic axis and the risk of spina bifida.

11 forebrain defects, facial defects, and spina bifida.

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

13 associated with an increased risk for spina bifida.

14 folic acid intake in the occurrence of spina bifida.

15 health care workers and children with spina bifida.

16 health care workers and children with spina bifida.

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

18 a risk factor for both anencepahly and spina bifida.

19 he multifactorial, neural tube defect, spina bifida.

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

21 red eligible for fetal closure of open spina bifida.

22 is, or iniencephaly) and 22 (32%) were spina bifida.

23 to open neural tube defects including spina bifida.

24 defects (NTDs) such as anencephaly and spina bifida.

25 citation during fetal surgery for open spina bifida.

26 osure, disruption of which may lead to spina bifida.

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

28 ith myelomeningocele, a severe form of spina bifida.

29 be to convergence defects that lead to spina bifida.

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

31 defects correlate with the extent of cardia bifida.

32 l closure of the gut endoderm causing cardia bifida.

33 trulation with consequent cardia and viscera bifida.

34 3' kinase (PI3K) activity resulted in spina bifida.

35 ered movement trajectories and caused cardia bifida.

36 ptor signaling in these cells leads to spina bifida.

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

38 is and demonstrated complete rescue of spina bifida.

39 ally and lack DLHPs, developing severe spina bifida.

40 cal support for the neural tube causes spina bifida.

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

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

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

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

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

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

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

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

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

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

51 ence of neural tube defects, including spina bifida and anencephaly (SBA), causing a high number of s

52 n against folic acid-preventable (FAP) spina bifida and anencephaly (SBA).

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

54 cid; only a quarter of all preventable spina bifida and anencephaly cases worldwide are currently avo

55 tion could accelerate the slow pace of spina bifida and anencephaly prevention globally, and will ass

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

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

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

59 regnancy prevents most cases of infant spina bifida and anencephaly-two major neural tube defects tha

60 d samples obtained from human cases of spina bifida and anencephaly.

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

62 nd sustainable intervention to prevent spina bifida and anencephaly.

63 ufficiency is the predominant cause of spina bifida and anencephaly.

64 age an adequate folic acid to prevent spina bifida and anencephaly.

65 lic acid to prevent the development of spina bifida and anencephaly.

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

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

68 ed, causes congenital diseases such as spina bifida and cleft palate.

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

70 e increased incidence of NTDs, such as spina bifida and exencephaly.

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

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

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

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

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

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

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

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

79 ed primary NTD (anencephaly and select spina bifida) and any NTD (primary and other NTD) were compare

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

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

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

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

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

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

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

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

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

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

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

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

92 6 and Fgf8 at the tail bud, leading to spina bifida aperta, caudal axis bending and tail truncation.

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

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

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

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

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

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

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

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

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

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

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

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

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

106 and March 2020 at a multidisciplinary spina bifida center at a single, free-standing children's hosp

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

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

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

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

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

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

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

114 lace to support fetal surgery for open spina bifida, exploring experiences and management of emergenc

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

116 n during minimally invasive fetoscopic spina bifida (fSB) repair.

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

118 mong adolescents and young adults with spina bifida, high rates of unsuccessful transition have been

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

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

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

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

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

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

125 variable significantly associated with spina bifida in multivariate analysis.

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

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

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

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

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

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

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

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

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

135 Meningomyelocele (also known as spina bifida) is considered to be a genetically complex diseas

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

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

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

139 nalysis, health literacy, age, type of spina bifida, level of education, self-administration vs compl

140 rotocol, whereas for anomalies such as spina bifida, limb reduction defects, and major cardiac malfor

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

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

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

144 12 years or older with a diagnosis of spina bifida (myelomeningocele and nonmyelomeningocele) whose

145 om posterior urethral valves (n = 49), spina bifida (n = 21), central neurogenic bladder (n = 13), bl

146 gating eight congenital anomaly types (spina bifida [n = 7,422], encephalocele [n = 1,562], oesophage

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

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

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

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

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

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

153 Survival for children with spina bifida, oesophageal atresia, biliary atresia, diaphragma

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

155 unction other than cerebral palsy (eg, spina bifida or muscle diseases) were excluded.

156 Open spina bifida or myelomeningocele (MMC) is a devastating neurol

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

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

159 pregnancy).SIGNIFICANCE STATEMENT Open spina bifida (OSB) is one of the most prevalent congenital mal

160 Open spina bifida (OSB) is one of the most prevalent congenital mal

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

162 chondrocytes did not recapitulate the spina bifida phenotype.

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

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

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

166 ry centers in 11 countries where fetal spina bifida repair is currently performed.

167 resuscitation was managed during open spina bifida repair.

168 Cardia bifida results from failed midline differentiation, even

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

170 If dorsolateral bending fails, spina bifida results.

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

172 Spina bifida (SB) is a complex disorder of failed neural tube

173 Spina bifida (SB) is a debilitating birth defect caused by mul

174 Open fetal surgery for spina bifida (SB) is safe and effective yet invasive.

175 Spina bifida (SB) patients afflicted with myelomeningocele typ

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

177 ndomized trial demonstrated that fetal spina bifida (SB) repair is safe and effective yet invasive.

178 s (PMSCs) as a potential treatment for spina bifida (SB), a neural tube defect.

179 or NTDs consistent with a diagnosis of spina bifida (SB).

180 We assembled the Spina Bifida Sequencing Consortium to identify causes.

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

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

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

184 onic genotype when evaluating putative spina bifida susceptibility loci.

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

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

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

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

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

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

191 9 cases of anencephaly and 32 cases of spina bifida were detected.

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

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

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

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

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

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