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 potential molecular mechanism underlying the neural tube defect.

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

4 potential treatment for spina bifida (SB), a neural tube defect.

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

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

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

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

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

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

11 men and causes many complications, including 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 itute of Medicine to reduce the frequency of neural tube defects.

16 Its deficiency can lead to neural tube defects.

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

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

19 lethality with embryos manifesting heart and neural tube defects.

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

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

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

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

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

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

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

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

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

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

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

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

32 occurring mouse mutant that develops severe neural tube defects.

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

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

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

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

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

38 candidate risk factor for susceptibility to neural tube defects.

39 nesis in the neuroepithelium and ameliorated neural tube defects.

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

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

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

43 sociation of folic acid supplementation with neural tube defects.

44 supplementation provided protection against neural tube defects.

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

46 ood fortification are recommended to prevent neural tube defects.

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

48 genetic basis underlying the pathogenesis of neural tube defects.

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

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

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

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

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

54 is an indicator of folate status and risk of neural-tube defects.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

72 ulthood, heterotaxia, pre-axial polydactyly, neural tube defects and hydrocephalus.

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

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

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

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

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

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

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

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

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

82 tes to delineate the genetic architecture of neural tube defects and new therapeutic targets to preve

83 Neural tube defects and other developmental anomalies ar

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

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

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

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

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

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

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

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

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

93 The prevalence of neural-tube defects and major external structural defect

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

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

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

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

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

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

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

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

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

103 2, which had been previously associated with neural tube defects, and vitamin B-12 status, as well as

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

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

106 Neural tube defects are among the most common congenital

107 Neural tube defects are among the most common major cong

108 Neural tube defects are common and serious human congeni

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

110 Neural tube defects are serious birth defects of the bra

111 Neural tube defects are severe congenital malformations

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 r Down syndrome, fetal alcohol syndrome, and neural tube defects combined.

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

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

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

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

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

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

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

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

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

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

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

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

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

140 tudies such as Tsepamo are critically needed.Neural tube defects have been reported among infants bor

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

142 The presence of neural tube defects identifies a previously unsuspected

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

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

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

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

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

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

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

150 ance spread and a possible increased risk of neural tube defects in infants if used in women at the t

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

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

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

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

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

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

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

158 dults to consider information on the risk of neural tube defects in women taking dolutegravir at time

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

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

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

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

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

164 assuming that a woman having a child with a neural tube defect incurs an extra DALY per year for the

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

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

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

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

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

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

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

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

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

174 nd B12, choline, betaine, and methionine and neural tube defect (NTD) outcomes among mothers meeting

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

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

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

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

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

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

181 Neural tube defects (NTD) are clinically important conge

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

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

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

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

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

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

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

189 Neural tube defects (NTDs) are a group of severe congeni

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

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

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

193 Planar cell polarity (PCP) and neural tube defects (NTDs) are linked, with a subset of

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

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

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

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

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

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

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

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

202 Lin28a/b double knockout (dKO) mice display neural tube defects (NTDs) coupled with reduced prolifer

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

204 The Botswana Tsepamo study reported neural tube defects (NTDs) in 4 of 426 (0.94%) infants o

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

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

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

208 Gpr161 null and hypomorphic mutations cause neural tube defects (NTDs) in mouse models.

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

210 may be associated with an increased risk for neural tube defects (NTDs) in newborns if used by women

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

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

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

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

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

216 The risk of neural tube defects (NTDs) is influenced by nutritional

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

218 Neural tube defects (NTDs) represent a failure of the ne

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

238 ptions in neural tube (NT) closure result in neural tube defects (NTDs).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

253 Neural tube defects occur frequently, yet underlying gen

254 6, 0.43), and a 41% reduction in the odds of neural tube defects (OR: 0.59; 95% CI: 0.49, 0.70).

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

256 MP-SMX was associated with increased risk of neural tube defects (pooled OR 2.5, 95% CI 1.4-4.3), spo

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

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

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

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

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

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

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

264 become an obstacle to the wider adoption of neural tube defect prevention programs and have called f

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

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

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

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

269 supplementation and birth defects other than neural tube defects remains unclear.

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

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

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

273 rol this process is expected to reveal novel neural tube defect risk factors and increase our underst

274 Neural tube defect risk was associated with maternal per

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

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

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

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

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

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

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

282 1995 in an area of China with high rates of neural-tube defects (the northern region) and one with l

283 ession of Irf6 caused exencephaly, a rostral neural tube defect, through suppression of Tfap2a and Gr

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

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

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

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

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

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

290 The prevalence of neural-tube defects was higher in association with dolut

291 A preliminary safety signal for neural-tube defects was previously reported in associati

292 The prevalence of neural-tube defects was slightly higher in association w

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

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

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

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

297 her was taking dolutegravir at conception, 5 neural-tube defects were found (0.30% of deliveries); th

298 In comparison, 15 neural-tube defects were found among 14,792 deliveries (

299 examination that could be evaluated, and 98 neural-tube defects were identified (0.08% of deliveries

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