ライフサイエンスコーパス: neural tube defect

1 y and the development of birth defects (e.g. neural tube defects).

2 the risk of having a pregnancy affected by a neural tube defect.

3 potential molecular mechanism underlying the neural tube defect.

4 e associated with pregnancy complicated by a neural-tube defect.

5 es a woman's risk of having an infant with a neural-tube defect.

6 an's risk of having a fetus or infant with a neural-tube defect.

7 ted with modification of disease and risk of neural tube defects.

8 m retinal degeneration and cystic kidneys to neural tube defects.

9 ed cross-midline cell divisions, and similar neural tube defects.

10 men and causes many complications, including neural tube defects.

11 n in the periconceptional period can prevent neural tube defects.

12 folate was not significantly associated with neural tube defects.

13 duced the occurrence of folic acid-sensitive neural tube defects.

14 who remain at increased risk of preventable neural tube defects.

15 sociation of folic acid supplementation with neural tube defects.

16 itute of Medicine to reduce the frequency of neural tube defects.

17 Its deficiency can lead to neural tube defects.

18 ation in the treatment of homocystinuria and neural tube defects.

19 ed as candidate susceptibility gene in human neural tube defects.

20 lethality with embryos manifesting heart and neural tube defects.

21 hey were proven to prevent the occurrence of neural tube defects.

22 c kidney disease, Bardet-Biedl syndrome, and neural tube defects.

23 the risk that women will have children with neural tube defects.

24 n between Wnt signaling and folate rescue of neural tube defects.

25 th as a result of skeletal malformations and neural tube defects.

26 e, Alzheimer's and Parkinson's diseases, and neural tube defects.

27 is well established that folic acid prevents neural tube defects.

28 kappa B activity leads to prenatal death and neural tube defects.

29 oronary artery disease, Down's syndrome, and neural tube defects.

30 dreher(J) (dr(J)), all of which cause dorsal neural tube defects.

31 dy on folic acid supplementation and risk of neural tube defects.

32 supplementation provided protection against neural tube defects.

33 lar diseases and Alzheimers disease and with neural tube defects.

34 occurring mouse mutant that develops severe neural tube defects.

35 e was not associated with increased risk for neural tube defects.

36 te from drinking water and diet and risk for neural tube defects.

37 st occurrence, as well as the recurrence, of neural tube defects.

38 n disorders ranging from vascular disease to neural tube defects.

39 produces tail deformities and, rarely, open neural tube defects.

40 candidate risk factor for susceptibility to neural tube defects.

41 ormations, including craniofacial, heart and neural tube defects.

42 dify the incidence of spina bifida and other neural tube defects.

43 pendent risk factor for vascular disease and neural tube defects.

44 with a phenocopy of DGS, or neonatally with neural tube defects.

45 g either protein exhibit a high frequency of neural tube defects.

46 in the prevention of many diseases including neural tube defects.

47 ociated with a low risk of folate-responsive neural tube defects.

48 imal for the prevention of folate-responsive neural tube defects.

49 ood fortification are recommended to prevent neural tube defects.

50 s in lamin B1 are susceptibility factors for neural tube defects.

51 genetic basis underlying the pathogenesis of neural tube defects.

52 implications for a population-level risk of neural tube defects.

53 utations in Vangl2 are associated with human neural tube defects.

54 FR) 677C>T polymorphism is a risk factor for neural tube defects.

55 Ozone was associated with decreased odds of neural tube defects.

56 uring pregnancy to decrease the incidence of neural tube defects.

57 e identified 102 and 173, respectively, with neural-tube defects.

58 nd was highest for the nine stillbirths with neural-tube defects.

59 tified with folic acid to prevent congenital neural-tube defects.

60 n: Does fortification prevent folate-related neural tube defects?

61 heart disease, Alzheimer's disease (3), and neural tube defects (4).

62 a spectrum of birth malformations, including neural tube defects, a shortened and/or curly tail, no g

63 ouse mutant with multiple defects, including neural tube defects, abnormal dorsal-ventral patterning

64 nitrogen oxide exposure was associated with neural tube defects (adjusted odds ratio = 1.8, 95% conf

65 after conception in 1,223 case mothers with neural tube defect-affected pregnancies and 6,807 contro

66 us pathologies, including vascular diseases, neural tube defects, Alzheimer disease, and pregnancy co

67 Nevertheless, the high incidence of neural tube defects among North Indian women, who chroni

68 The adjusted odds ratio for neural tube defects among those with the highest carbon

69 ously affected child and the occurrence of a neural tube defect and possibly other birth defects in t

70 Inadequate folate status is associated with neural tube defect and some cancers.

71 Pax3-deficient Splotch mice display neural tube defects and an array of neural crest related

72 tural pesticide use has been associated with neural tube defects and autism, but more subtle outcomes

73 methylation reactions, and increase risk for neural tube defects and cancer.

74 h increased risk for cardiovascular disease, neural tube defects and cognitive deficits.

75 similar to the testing/screening method for neural tube defects and common chromosomal anomalies dur

76 All compound homozygotes had severe neural tube defects and died earlier in embryogenesis th

77 pes with PCP mutants including open eyelids, neural tube defects and disrupted cochlear stereociliary

78 Association of folate deficiency with neural tube defects and impact of fortification programs

79 an essential nutrient, increase the risk of neural tube defects and lead to low performance on cogni

80 gene (Sufu) led to a phenotype that included neural tube defects and lethality at mid-gestation (9.0-

81 ucture and function and influencing risk for neural tube defects and lifelong memory function.

82 ive was to evaluate the associations between neural tube defects and maternal folic acid intake among

83 nd little evidence of an association between neural tube defects and maternal folic acid intake.

84 late homeostasis can reduce the incidence of neural tube defects and may decrease the risk of Alzheim

85 rtification of food is effective in reducing neural tube defects and may even reduce stroke-related m

86 s recently associated with increased risk of neural tube defects and might also contribute to increas

87 Neural tube defects and other developmental anomalies ar

88 abnormalities with or without microcephaly, neural tube defects and other early brain malformations,

89 Folate deficiency leads to neural tube defects and other human diseases, and is a g

90 tic studies in other groups of patients with neural tube defects and other neurodevelopmental abnorma

91 ously reported positive associations between neural tube defects and periconceptional exposure to NSD

92 birth defects, including holoprosencephaly, neural tube defects and polydactyly, and in adults resul

93 lly lethal and recapitulates JBTS, including neural tube defects and polydactyly; however, the underl

94 arkers in the caudal spinal cord, as well as neural tube defects and preaxial polydactyly, consistent

95 during the periconception period to prevent neural tube defects and to ensure normal brain developme

96 of its beneficial role in the prevention of neural tube defects and yet possible deleterious effects

97 ere or had been pregnant with a fetus with a neural-tube defect and from 24 control women (20 with cu

98 r understanding certain birth defects (e.g., neural tube defects) and the long-term consequences of e

99 h defects that includes heart abnormalities, neural tube defects, and caudal dysgenesis syndromes.

100 re a risk factor for cardiovascular disease, neural tube defects, and colon and breast cancer; low le

101 ates, have multiple malformations, including neural tube defects, and die due to failure of chorioall

102 disposition accounts for most of the risk of neural tube defects, and genes that regulate folate one-

103 is an established model of folate-sensitive neural tube defects, and homozygous mutant embryos devel

104 e characterized by late embryonic lethality, neural tube defects, and intrauterine growth retardation

105 ngl2 loss is embryonically lethal because of neural tube defects, and mutations in Vangl2 are associa

106 disease, retinal degeneration, polydactyly, neural tube defects, and obesity (ciliopathies).

107 ardiovascular diseases, Alzheimer's disease, neural tube defects, and osteoporosis.

108 2, which had been previously associated with neural tube defects, and vitamin B-12 status, as well as

109 during the periconceptional period prevents neural tube defects, animal data suggest that higher sup

110 Approximately 30% of neural tube defects appear resistant to folic acid and r

111 blood levels of women who had a fetus with a neural tube defect are low for several micronutrients, p

112 Neural tube defects are among the most common congenital

113 Neural tube defects are among the most common major cong

114 Neural tube defects are common and serious human congeni

115 Few genetic risk factors for neural tube defects are known in humans, highlighting th

116 pment is grossly normal in heterozygotes and neural tube defects are not seen.

117 Neural tube defects are serious birth defects of the bra

118 Neural tube defects are severe congenital malformations

119 embryos (whose phenotype is characterized by neural tube defects) as compared with Pax3(+/+) litterma

120 oth chick and mouse results in a spectrum of neural tube defects associated with neuroepithelial diso

121 lted in a high prevalence of severe anterior neural tube defect-associated congenital malformations.

122 se of folic acid supplements reduces risk of neural tube defects but a proportion of cases are not pr

123 ike talpid(3) chicken embryos, have face and neural tube defects but also defects in left/right asymm

124 y because of its proven effect in preventing neural tube defects, but the role of FA after the 12th g

125 primidone, may increase the risk not only of neural-tube defects, but also of cardiovascular defects,

126 This neural tube defect can be attributed to a lack of proper

127 Neural tube defects can be prevented by folic acid, alth

128 Up to 70% of neural tube defects can be prevented by the consumption

129 Many neural tube defects can be prevented if women take folic

130 Prevention of neural-tube defects can be achieved with preconceptional

131 or B12 homeostasis have been associated with neural tube defects, cardiovascular disease, and cancer.

132 y by E11 of Hif1a-/- embryos that manifested neural tube defects, cardiovascular malformations, and m

133 aternal periconceptional NSD use between 334 neural tube defect cases and 7,619 nonmalformed controls

134 Caudal regression syndrome is a rare, neural tube defect characterized by an abnormal developm

135 lation defects, axial patterning defects and neural tube defects complicating an assessment of the ro

136 Most that survived to term had neural tube defects consisting of both exencephaly and s

137 from women with a pregnancy complicated by a neural-tube defect contains autoantibodies that bind to

138 mouse mutant that exhibits a severe form of neural tube defect, craniorachischisis, in which almost

139 ciated with a variety of disorders including neural tube defects (during pregnancy) and heart disease

140 in development at mid-gestation and exhibit neural tube defects, enlargement of the pericardial sac

141 nitrosatable drugs may increase the risk of neural tube defects, especially in conjunction with a mo

142 Hectd1 mutant mouse embryos exhibit the neural tube defect exencephaly associated with abnormal

143 from Hungary initiated in 1984, incidence of neural tube defects for folic acid supplementation compa

144 Pax3 mutants develop muscular and neural tube defects; furthermore, Pax3 is essential for

145 Neural tube defects, harms of treatment (twinning, respi

146 was sufficient to prevent all folate-related neural tube defects has been hotly debated.

147 ular disease, stroke, cognitive decline, and neural tube defects have been completed or are underway.

148 Rates of neural tube defects have decreased since folic acid fort

149 The presence of neural tube defects identifies a previously unsuspected

150 A cranial neural tube defect in Crooked tail (Cd) mice is prevente

151 The timing of the neural tube defect in ski -/- embryos coincides with exc

152 fortification of flour for the prevention of neural tube defects in addition to the existing extensiv

153 -nitroso compounds have been associated with neural tube defects in animal models.

154 al folic acid supplements reduce the risk of neural tube defects in children, but it has not been det

155 apoptotic cells were also found at sites of neural tube defects in embryos carrying null mutation of

156 This low penetrance of neural tube defects in embryos heterozygous for Hectd1 m

157 Hectd1 alleles cause incompletely penetrant neural tube defects in heterozygous animals, indicating

158 In contrast, we found a low incidence of neural tube defects in heterozygous Splotch mice that al

159 nd are associated with esophageal cancer and neural tube defects in humans.

160 en of childbearing age for the prevention of neural tube defects in infants.

161 orrhage; and vasculogenic, craniofacial, and neural tube defects in mice.

162 ycero-3-phosphocholine (ET-18-OCH3), produce neural tube defects in mouse embryos grown in vitro.

163 ant dam's drinking water on the incidence of neural tube defects in some genetic models.

164 nvironmental factors affect the incidence of neural tube defects in Splotch mice, these results estab

165 the first known gene to act as a modifier of neural tube defects in Splotch.

166 Rho kinase, during the development of severe neural tube defects in the mouse.

167 d containing supplements decreased recurrent neural tube defects in the offspring of women with a pre

168 sufficiency on the basis of elevated risk of neural tube defects in women 12-49 y old (e.g., RBC fola

169 g of folic acid daily can reduce the risk of neural-tube defects in areas with high rates of these de

170 tified with folic acid to reduce the risk of neural-tube defects in newborns.

171 g and tail morphogenesis, but did not induce neural tube defects, in zebrafish.

172 fold fusion during neurulation leads to open neural tube defects including spina bifida.

173 Failure of this process results in neural tube defects, including spina bifida and anenceph

174 use or dietary folate intake was related to neural tube defects, indicating that fortified food is p

175 with folic acid in reducing the incidence of neural tube defects is a major success story for public

176 In this system, the rate of neural tube defects is about three times higher in embry

177 in attempts to ameliorate homocystinuria and neural tube defects is supplementation of the diet with

178 eatment-specific effects on the incidence of neural tube defects, left-right patterning defects and a

179 itionally been associated with prevention of neural tube defects; more recent work suggests that it m

180 Some relate to birth defects other than neural tube defects, neurological functions or varied as

181 y reduce their risk of having a child with a neural tube defect (NTD) by >50%.

182 ms produced offspring at a rate of 11.3% for neural tube defect (NTD) formation, whereas no embryos i

183 fortification and to estimate the effect on neural tube defect (NTD) occurrence.

184 in Cameron County, Texas, a surveillance and neural tube defect (NTD) recurrence prevention project f

185 ing behaviors were associated with increased neural tube defect (NTD) risk among offspring, using pop

186 mutants that exhibit the most severe form of neural tube defect (NTD), termed craniorachischisis.

187 mation and the most common form of syndromic neural tube defect (NTD).

188 increased risk for a pregnancy affected by a neural tube defect (NTD).

189 SWV mice strain, susceptible to VPA-induced neural tube defect (NTD).

190 ay be risk factors for having a child with a neural tube defect (NTD); however, the data are inconsis

191 Neural tube defects (NTD) are clinically important conge

192 ve been associated with an increased risk of neural tube defects (NTD), possibly due to a sustained s

193 a causal event in maternal diabetes-induced neural tube defects (NTD).

194 uces a woman's risk for having a baby with a neural-tube defect (NTD), the effects of such supplement

195 udied the association of these patterns with neural tube defects (NTDs) and congenital heart defects

196 se-control study populations of infants with neural tube defects (NTDs) and nonmalformed controls del

197 mely effective in reducing the occurrence of neural tube defects (NTDs) and other congenital abnormal

198 Vangl genes encoding core PCP proteins cause neural tube defects (NTDs) and Vangl2 mutations also imp

199 Neural tube defects (NTDs) are birth defects that can be

200 Neural tube defects (NTDs) are common birth defects of c

201 Neural tube defects (NTDs) are common, severe congenital

202 Neural tube defects (NTDs) are prevalent human birth def

203 Previously, we demonstrated that neural tube defects (NTDs) are significantly increased i

204 Neural tube defects (NTDs) are some of the most common b

205 Neural tube defects (NTDs) are the most severe congenita

206 Neural tube defects (NTDs) are the second most common bi

207 Neural tube defects (NTDs) arise from a complex combinat

208 Folic acid prevents 70 percent of human neural tube defects (NTDs) but its mode of action is unc

209 lic acid is known to reduce the incidence of neural tube defects (NTDs) by as much as 70%.

210 A proportion of neural tube defects (NTDs) can be prevented by maternal

211 Folic acid can prevent up to 70% of neural tube defects (NTDs) if taken before pregnancy.

212 lemental and dietary zinc intake and risk of neural tube defects (NTDs) in a population-based case-co

213 abetes mellitus in early pregnancy can cause neural tube defects (NTDs) in embryos by perturbing prot

214 ke has been proposed to increase the risk of neural tube defects (NTDs) in human populations.

215 rhl2 loss results in fully penetrant cranial neural tube defects (NTDs) in mice.

216 ncreased FGR frequency and caused occasional neural tube defects (NTDs) in Mthfd1(gt/+) embryos.

217 ART has been reported to be associated with neural tube defects (NTDs) in offspring.

218 sly showed that apoptosis is associated with neural tube defects (NTDs) in Pax-3-deficient Splotch (S

219 resulting from homozygous matings uncovered neural tube defects (NTDs) in some animals and axial ske

220 folic acid substantially reduces the risk of neural tube defects (NTDs) in the offspring.

221 Mouse models of folate-responsive neural tube defects (NTDs) indicate that impaired de nov

222 Risk of neural tube defects (NTDs) is determined by genetic and

223 The risk of neural tube defects (NTDs) is significantly reduced by s

224 Genetic correlation of human neural tube defects (NTDs) with NTD genes identified in

225 Neural tube defects (NTDs), a common birth defect in hum

226 ess is susceptible to disruption, leading to neural tube defects (NTDs), a common birth defect.

227 supplementation can reduce the prevalence of neural tube defects (NTDs), although just how folates be

228 supplementation prevents up to 70% of human neural tube defects (NTDs), although the precise cellula

229 Congenital malformations, including neural tube defects (NTDs), are significantly increased

230 on prevents the occurrence and recurrence of neural tube defects (NTDs), but the causal metabolic pat

231 ortant role in determining susceptibility to neural tube defects (NTDs), for example between differen

232 array of congenital malformations, including neural tube defects (NTDs), in humans.

233 Neural tube defects (NTDs), including spina bifida and a

234 he risk in infants of birth defects, such as neural tube defects (NTDs), known as diabetic embryopath

235 ation reduces the occurrence and severity of neural tube defects (NTDs), many cases are resistant to

236 canonical WNT signaling, and are a model of neural tube defects (NTDs), preventable with dietary fol

237 letion-induced autophagy deficiency leads to neural tube defects (NTDs), similar to those in diabetic

238 effect of folate against the development of neural tube defects (NTDs), specifically, anencephaly an

239 Neural tube defects (NTDs), such as spina bifida, are co

240 al ventricles, which is seen in fetuses with neural tube defects (NTDs), was present on review of MR

241 id supplementation can prevent many cases of neural tube defects (NTDs), whereas suboptimal maternal

242 vere anomalies of the nervous system, called neural tube defects (NTDs), which are among the most com

243 Folate supplementation prevents up to 70% of neural tube defects (NTDs), which result from a failure

244 mouse mutant causes congenital cataracts and neural tube defects (NTDs), with the NTDs being caused b

245 tion in humans that is often synonymous with neural tube defects (NTDs).

246 ceptional intake of folic acid prevents some neural tube defects (NTDs).

247 nancy dramatically reduces the occurrence of neural tube defects (NTDs).

248 lic acid supplementation reduces the risk of neural tube defects (NTDs).

249 or the prevention of the first occurrence of neural tube defects (NTDs).

250 of Mexican descent have high occurrences of neural tube defects (NTDs).

251 folic acid, a B vitamin, reduces the risk of neural tube defects (NTDs).

252 ly pregnancy causes birth defects, including neural tube defects (NTDs).

253 High glucose in vivo and in vitro induces neural tube defects (NTDs).

254 PCP signaling gene mutations cause severe neural tube defects (NTDs).

255 pase activation, and apoptosis, resulting in neural tube defects (NTDs).

256 to diabetes and obesity as a risk factor for neural tube defects (NTDs).

257 suboptimal RBC folate for protection against neural tube defects (NTDs); among nonconsumers of folic

258 s have also been identified in patients with neural tube defects (NTDs); however, the relationship be

259 Folic acid is known to prevent neural-tube defects (NTDs) but the size of the effect fo

260 within 3 km of a landfill site was found for neural-tube defects (odds ratio 1.86 [1.24-2.79]), malfo

261 nd elective termination on the prevalence of neural tube defects, oral clefts, abdominal wall defects

262 responsible for several diseases, including neural tube defects, polycystic kidney disease, retinal

263 been implicated in adverse outcomes such as neural tube defects, preeclampsia, spontaneous abortion,

264 including some evidence that a proportion of neural tube defect pregnancies may be the result of vita

265 n in the primary prevention or recurrence of neural tube defect pregnancies, as was the case with fol

266 o an increased intake of folic acid for each neural tube defect pregnancy that is prevented.

267 bserved in other common disorders, including neural tube defects, pregnancy complications, and Alzhei

268 death, pneumonia, congenital heart disease, neural tube defects, preterm birth and low birth weight,

269 tus and have resulted in a major decrease in neural tube defect prevalence.

270 yos, consistent with a proposed mechanism of neural tube defect prevention through stimulation of cel

271 perturbed choline metabolism contributes to neural tube defects produced by DMAE and ET-18-OCH3.

272 e large number of mouse genes known to cause neural tube defects provide a starting point for identif

273 without the potential for childbearing, and neural tube defect recurrence; and studies conducted in

274 autoantibodies against folate receptors and neural-tube defects reflects a causal relation.

275 NGL2 are found to cause Robinow syndrome and neural tube defects, respectively, our results further s

276 The spinal neural tube defect results from a different mechanism: i

277 Further analysis of neural tube defects revealed the absence of lateral floo

278 Neural tube defect risk was associated with maternal per

279 ontroversial, but studies of mouse models of neural tube defects show that anencephaly, open spina bi

280 urthermore, because folate deficiency causes neural tube defects, some birth defects unexplained by o

281 ing in a phenotype similar to the human open neural tube defect spina bifida.

282 ice cause recessive embryonic lethality with neural-tube defects, suggesting a species difference in

283 ans to prevent a greater proportion of human neural tube defects than can be achieved by folic acid a

284 hese findings, Ski-/- mice display a cranial neural tube defect that results in exencephaly and a mar

285 The reduced PKA activity results in neural tube defects that are specifically localized post

286 s that carry null mutations in Pax-3 develop neural tube defects that resemble the malformations that

287 ew of the severe congenital malformations - 'neural tube defects' - that result when closure fails.

288 1995 in an area of China with high rates of neural-tube defects (the northern region) and one with l

289 between FGFR-1-mediated signal pathways and neural tube defects, the most common malformations in th

290 e principal change involving a switch from a neural tube defect to midline facial clefting.

291 on folic acid supplementation for preventing neural tube defects to inform the US Preventive Services

292 tal abnormalities in the fetus, ranging from neural tube defects to neurocristopathies such as cleft-

293 e 20 individual malformation categories, eg, neural tube defects, transposition of great vessels, ven

294 food with folic acid to reduce the number of neural tube defects was introduced 10 y ago in North Ame

295 Furthermore, risk of neural tube defects was related to high color (adjusted

296 of the role of folate in protecting against neural tube defects, we propose that NAT1 is a candidate

297 use model that exhibits folic acid-resistant neural tube defects, we tested the effect of specific co

298 However, neural tube defects were detected in HAI2-deficient mice

299 ho did not take any folic acid, the rates of neural-tube defects were 4.8 per 1000 pregnancies of at

300 We observed increased odds of neural tube defects when comparing the highest with the