Neural Tube Malformations Research Articles

Melatonin alleviates valproic acid-induced neural tube defects by modulating Src/PI3K/ERK signaling and oxidative stress.

Neural tube defects (NTDs) represent a developmental disorder of the nervous system that can lead to significant disability in children and impose substantial social burdens. Valproic acid (VPA), a widely prescribed first-line antiepileptic drug for epilepsy and various neurological conditions, has been associated with a 4-fold increase in the risk of NTDs when used during pregnancy. Consequently, urgent efforts are required to identify innovative prevention and treatment approaches for VPA-induced NTDs. Studies have demonstrated that the disruption in the delicate balance between cell proliferation and apoptosis is a crucial factor contributing to NTDs induced by VPA. Encouragingly, our current data reveal that melatonin (MT) significantly inhibits apoptosis while promoting the restoration of neuroepithelial cell proliferation impaired by VPA. Moreover, further investigations demonstrate that MT substantially reduces the incidence of neural tube malformations resulted from VPA exposure, primarily by suppressing apoptosis through the modulation of intracellular reactive oxygen species levels. In addition, the Src/PI3K/ERK signaling pathway appears to play a pivotal role in VPA-induced NTDs, with significant inhibition observed in the affected samples. Notably, MT treatment successfully reinstates Src/PI3K/ERK signaling, thereby offering a potential underlying mechanism for the protective effects of MT against VPA-induced NTDs. In summary, our current study substantiates the considerable protective potential of MT in mitigating VPA-triggered NTDs, thereby offering valuable strategies for the clinical management of VPA-related birth defects.

Embryonic exposure to decitabine induces multiple neural tube defects in developing zebrafish.

Neural tube defects are severe congenital disorders of the central nervous system that originate during embryonic development when the neural tube fails to close completely. It affects one to two infants per 1000 births. The aetiology is multifactorial with contributions from both genetic and environmental factors. Dysregulated epigenetic mechanisms, in particular the abnormal genome-wide methylation during embryogenesis, have been linked to developmental abnormalities including neural tube defects. The current study investigated the influence of decitabine (DCT), a DNA methylation inhibitor, on embryonic development in zebrafish, with a focus on neural tube formation. The developing zebrafish embryos were exposed to graded concentrations of decitabine (from 13.69 μM to 1 mM) before the onset of neurulation. The developmental process was monitored at regular time intervals post fertilization. At 120 h post fertilization, the developing embryos were inspected individually to determine the incidence and severity of neural tube defects. Using alizarin red staining, the cranial and caudal neural tube morphology was examined in formaldehyde fixed larvae. Anomalies in neural tube and somite development, as well as a delay in hatching, were discovered at an early stage of development. As development continued, neural tube defects became increasingly evident, and there was a concentration-dependent rise in the prevalence and severity of various neural tube defects. 90% of growing embryos in the group exposed to decitabine 1 mM had multiple neural tube malformations, and 10% had isolated neural tube defects. With several abnormalities, the caudal region of the neural tube was seriously compromised. The histopathological studies supported the malformations in neural tube. Our study revealed the harmful impact of decitabine on the development of the neural tube in growing zebrafish. Moreover, these findings support the hypothesis that the hypomethylation during embryonic development causes neural tube defects.

An interaction between OTULIN and SCRIB uncovers roles for linear ubiquitination in planar cell polarity.

Planar cell polarity (PCP) plays critical roles in developmental and homeostatic processes. Membrane presentation of PCP complexes containing Van Gogh-like (VANGL) transmembrane proteins is central to PCP and can be directed by the scaffold protein scribble (SCRIB). The role atypical linear ubiquitin (Met1-Ub) chains might play in PCP is unknown. Here, HEK293 cell-based interactomic analyses of the Met1-Ub deubiquitinase OTULIN revealed that OTULIN can interact with SCRIB. Moreover, Met1-Ub chains associated with VANGL2 and PRICKLE1, but not SCRIB, can direct VANGL2 surface presentation. Mouse embryos lacking Otulin showed variable neural tube malformations, including rare open neural tubes, a deficit associated with PCP disruption in mice. In Madin-Darby canine kidney cells, in which the enrichment of VANGL2-GFP proteins at cell-cell contacts represents activated PCP complexes, endogenous OTULIN was recruited to these sites. In the human MDA-MB-231 breast cancer cell model, OTULIN loss caused deficits in Wnt5a-induced filopodia extension and trafficking of transfected HA-VANGL2. Taken together, these findings support a role for linear (de)ubiquitination in PCP signaling. The association of Met1-Ub chains with PCP complex components offers new opportunities for integrating PCP signaling with OTULIN-dependent immune and inflammatory pathways.

MAP4K4 is involved in the neuronal development of retinal photoreceptors

Mitogen-activated protein kinase kinase kinase kinase-4 (MAP4K4) is a potential regulator of photoreceptor development. To investigate the mechanisms underlying MAP4K4 during the neuronal development of retinal photoreceptors, we generated knockout models of C57BL/6j mice in vivo and 661 W cells in vitro. Our findings revealed homozygous lethality and neural tube malformation in mice subjected to Map4k4 DNA ablation, providing evidence for the involvement of MAP4K4 in early stage embryonic neural formation. Furthermore, our study demonstrated that the ablation of Map4k4 DNA led to the vulnerability of photoreceptor neurites during induced neuronal development. By monitoring transcriptional and protein variations in mitogen-activated protein kinase (MAPK) signaling pathway-related factors, we discovered an imbalance in neurogenesis-related factors in Map4k4 −/− cells. Specifically, MAP4K4 promotes jun proto-oncogene (c-JUN) phosphorylation and recruits other factors related to nerve growth, ultimately leading to the robust formation of photoreceptor neurites. These data suggest that MAP4K4 plays a decisive role in regulating the fate of retinal photoreceptors through molecular modulation and contributes to our understanding of vision formation.

Deficiency of Wdr60 and Wdr34 cause distinct neural tube malformation phenotypes in early embryos.

Cilia are specialized organelles that extend from plasma membrane, functioning as antennas for signal transduction and are involved in embryonic morphogenesis. Dysfunction of cilia lead to many developmental defects, including neural tube defects (NTDs). Heterodimer WDR60-WDR34 (WD repeat domain 60 and 34) are intermediate chains of motor protein dynein-2, which play important roles in ciliary retrograde transport. It has been reported that disruption of Wdr34 in mouse model results in NTDs and defects of Sonic Hedgehog (SHH) signaling. However, no Wdr60 deficiency mouse model has been reported yet. In this study, piggyBac (PB) transposon is used to interfere Wdr60 and Wdr34 expression respectively to establish Wdr60 PB/PB and Wdr34 PB/PB mouse models. We found that the expression of Wdr60 or Wdr34 is significantly decreased in the homozygote mice. Wdr60 homozygote mice die around E13.5 to E14.5, while Wdr34 homozygote mice die around E10.5 to E11.5. WDR60 is highly expressed in the head region at E10.5 and Wdr60 PB/PB embryos have head malformation. RNAseq and qRT-PCR experiments revealed that Sonic Hedgehog signaling is also downregulated in Wdr60 PB/PB head tissue, demonstrating that WDR60 is also required for promoting SHH signaling. Further experiments on mouse embryos also revealed that the expression levels of planar cell polarity (PCP) components such as CELSR1 and downstream signal molecule c-Jun were downregulated in WDR34 homozygotes compared to wildtype littermates. Coincidently, we observed much higher ratio of open cranial and caudal neural tube in Wdr34 PB/PB mice. CO-IP experiment showed that WDR60 and WDR34 both interact with IFT88, but only WDR34 interacts with IFT140. Taken together, WDR60 and WDR34 play overlapped and distinct functions in modulating neural tube development.

Fetal Tethered Spinal Cord: Diagnostic Features and Its Association with Congenital Anomalies

Objective We assessed the frequency and type of associated congenital anomalies encountered with fetal tethered spinal cord (TSC) determined prenatally. Method A retrospective review was conducted based on the associated fetal abnormalities following diagnosis of low-lying fetal conus medullaris during the prenatal ultrasound. Results Of the 26 fetuses with low-lying conus medullaris, four were solitary TSC and 22 had TSC combined with associated congenital malformations, including four cases with spina bifida occulta, four cases with spina bifida aperta, one case with severe hydrocephalus, and 13 cases with multisystem congenital malformations. Among all the 13 cases with combined multisystem congenital malformations, four cases had vertebral defects, anal anomalies, cardiac defects, trachea-esophageal fistula, renal anomalies, and limb anomalies (VACTERL) syndrome, two cases had combined kidney development abnormalities, one case had cloacal exstrophy (OEIS syndrome), and six cases had chromosomal abnormalities (one case of chromosome 7q deletion, two cases of trisomy 13 syndrome, one case of trisomy 18 syndrome, one case of trisomy 9 syndrome, and one case of chromosome 4p deletion). Conclusions Low-lying conus medullaris found during prenatal ultrasound examination were often associated with neural tube malformations or multi-systemic complex developmental malformations. The frequency of chromosomal abnormalities was 23.1%.

Transcriptome sequencing reveals neurotoxicity in embryonic neural stem/progenitor cells under heat stress

Neural tube malformation is a common kind of human birth defect. High temperature is one of the most common physical teratogenic factors. Several studies have suggested that heat stress may cause neurotoxicity during brain development, but more studies are warranted to reveal the mechanism and draw consistent conclusions. The current study used a cell model of primary mouse embryonic neural stem/progenitor cells (NSPCs) subjected to heat stress of 43 °C for 20 min. Our study investigated the changes in the NSPCs transcriptome under heat stress using high-throughput mRNA-seq. The NSPCs showed remarkably altered genes associated with cell growth, proliferation, cell cycle, and survival when exposed to heat stress. Heat stress reduced cell viability, proliferation, and neurosphere formation and caused cell cycle arrest and apoptosis in cultured NSPCs. PCR arrays confirmed that the TNF receptor family plays an important role in the apoptosis of NSPCs during heat stress. The results of real-time PCR confirmed that heat stress affects the expression of critical genes. We provide transcriptomic insight into heat stress-induced developmental neurotoxic effects and the underlying mechanisms.

Trends and influencing factors of perinatal birth defects in Huai'an from 2008 to 2020.

To analyze the incidence, trends and related factors of birth defects in Huai'an from 2008 to 2020. The surveillance data from maternal and child health system of Huai'an from 2008 to 2020 and Huai'an Statistical Yearbook were used for analysis. Taking the annual change percentage and average annual change percentage (AAPC) as the main outcome indicators, the JoinPoint regression analysis was performed to estimate the changing trend of birth defects from 2008 to 2020. Spearman correlation analysis was used to examine the association between birth defects and birth rate, marriage rate, proportion of women with advanced maternal age. During 2008 to 2020, a total of 3414 cases of neonatal birth defects occurred in Huai'an, with an incidence of 4.6‰ (3414/736 608). The rate of perinatal birth defects in Huai'an showed an increasing trend (AAPC=8.8%, t=3.2, P<0.01), and the year of 2016 was a significant changing point. Among 24 types of birth defects, the incidence of congenital heart disease rose and became the most prevalent defect, while the incidence of neural tube malformations such as anencephaly, encephalocele and spina bifida was declined. The incidence of birth defect was negatively correlated with the birth rate ( r=-0.751, P<0.01), not correlated with marriage rate ( r=-0.516, P>0.05), and positively correlated with the proportion of women with advanced maternal age ( r=0.726, P<0.01). The incidence of birth defects in Huai'an shows an increasing trend from 2008 to 2020 with congenital heart disease as the most common type of birth defect, and the increase of birth defects incidence is closely related with the increase of the proportion of women with advanced maternal age.

Anencephaly: a rare clinical image.

Anencephaly is a lethal fetal neurological malformation. This malformation accounts for 40% of neural tube malformations. The diagnosis is based on the ultrasound of the first trimester between the 11th and the 14th weeks of amenorrhea by discovering an exencephaly which results in the visualisation of the ossification of the cranial box and, therefore, the impossibility of measuring the biparietal diameter. Here we present the case of anencephaly; a female patient comes to the gynaecology department for the delivery on the utrasound sonography test (USG) examination to know the health status of the fetus show anencephaly. On the second day, patient delivery was done, and the patient´s newborn child was seen with low set ears and protruded eyeballs.

Closed spinal dysraphism in a 6-month-old mixed breed dog

The term spinal dysraphism defines an incomplete fusion or a bone defect that affects the neural structures of the spinal cord due to a neural tube malformation. A 6-month-old, male, mixed-breed dog, was evaluated for paraparesis, pelvic limb proprioceptive ataxia, faecal and urinary incontinence. A neurological examination indicated an L4-S3 spinal cord segment lesion. A thoracolumbar and lumbosacral spine magnetic resonance imaging was performed and a closed spinal dysraphism, with the presence of a lipomyelomeningocele, was detected. The magnetic resonance imaging showed an entire narrowing passage and a fibrous mass stemming from a wedge-shaped gap in the caudal region of the dorsal lamina of the L4 vertebra, leaving the spinal canal towards the skin surface in the region where the skin stigma was observed. A dorsal laminectomy was performed, the spinal cord was exposed, and the entire fibrous mass was excised. Three months postoperatively, the patient had a complete resolution of the urinary and faecal incontinence showing only a residual mild paraparesis, which remained six months after surgery. The surgical procedure resulted in the satisfactory recovery of the neurological signs.

Early Prenatal Diagnosis And Prevention Of Birth Damage Development In Children (Spina Bifida - A Defect In The Development Of The Nervous System)

Spina bifida-is a defect in the development of the neural tube, which is a splittinq of the spinal canal and is one of the most common conqenital malformation of the fetus. Worldwidt, the incidence of fetal neural tube defects ranqes from 0,17 to 6,39 per 1000 newborns. This article describes methods for early diaqnosis of fetal neural tube malformation in earle preqnancy and the results of studies of preqnant woman at different staqes of preqnancy.

MAP4K4 is Involved in the Neuronal Development of Retinal Photoreceptors

Differentiated from multipotent neural progenitors, the development of retinal photoreceptors is under sophisticated programming of multiple genes. Mitogen-activated protein kinase kinase kinase kinase-4 (MAP4K4) is one of the upstream regulators in the mitogen-activated protein kinase (MAPK) signaling pathway, associated to neurodegeneration. However the role of MAP4K4 in retina—an extension of neural system—remains unknown. In the present study, we generated knockout models of C57BL/6j mice in vivo and 661W cells in vitro to unfold the mechanism of MAP4K4 during neuronal development of retinal photoreceptors. We identified the linkage between the Map4k4 ablation induced murine homozygous lethality and neural tube malformation during the embryonic phase from EM9.5 to EM10.5, providing a collateral evidence for the involvement of MAP4K4 in early stage embryonic neural formation. To further clarify the participation of MAP4K4 in neurogenesis of photoreceptors, we subjected 661W cells of both Map4k4 +/+ and Map4k4 -/- to staurosporine. Later, spatiotemporal development and remodeling of photoreceptor cells were detected. Ablation of Map4k4 leaded to vulnerability of photoreceptor nerites during induced neuronal development. By monitoring transcriptional and protein variation of MAPK signaling pathway targeted factors, we discovered the imbalanced neurogenesis factors occurring in Map4k4 -/- cells. MAP4K4 promoted jun proto-oncogene (c-JUN) phosphorylation and recruited other factors related to nerve growth, convoying the photoreceptors to robust formation of neurites. Together, MAP4K4 showed decisiveness in the programming fate of retinal photoreceptors through molecular modulations, which may be providing a new insight into the blueprint of visual formation. Funding Statement: This study was supported by the National Natural Science Foundation of China (81670874 and 81670885), the Natural Science Foundation of Gurangdong Province of China (2020A1515010144), the Fundamental Research Funds and the Open Research Funds of the State Key Laboratory of Ophthalmology. Declaration of Interests: The authors declare no conflicts of interest. Ethics Approval Statement: All animal experiments in this study were approved by and in compliance with the guides of the Animal Experimentation Ethics Committee of State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China (Approval Number: 2017-083). All animal experiments were performed in accordance with the Association for Research in Vision and Ophthalmology (ARVO) Statement for the Use and Care of Animals in Ophthalmic and Vision Research.

Turbulent Cerebrospinal Fluid Flow in Enlarging Terminal Myelocystocele

Terminal myelocystocele is a rare type of neural tube malformation, consisting of a skin-covered lumbosacral mass, highly associated with other complex abdominal malformations within the OIES complex (omphalocele, imperforate anus, exstrophy of the cloaca and spinal defects). We present a case of a premature female with an extensive lumbosacral mass at birth, as well as an omphalocele, cloacal exstrophy, renal abnormalities, and sacral agenesis. Lumbar magnetic resonance imaging revealed a meningocele sac herniating through the bone defects and containing a syringocele sac. Advanced imaging techniques showed turbulent cerebrospinal fluid flow. At control, 4 weeks later, the defect doubled in size. The myelocystocele sac was evacuated and closed, and the patient persisted with paraparesis. The role of cerebrospinal fluid flow analysis is well established in Chiari-type malformations, in which turbulent flow within the syrinx is related to a better outcome after surgery. It is possible that the same principle could be applied to other spinal malformations, as shown in this case of terminal myelocystocele.

A molecular-beacon-based asymmetric PCR assay for detecting polymorphisms related to folate metabolism.

BackgroundPolymorphisms (rs1801133 or C677T; rs1801131 or A1298C) of the MTHFR gene and rs1801394 (A66G) of the MTRR gene are important genetic determinants of folate metabolism. A convenient, sensitive, and reliable method is required to detect polymorphisms for the precise supplementation of folate.MethodsA rapid detection method based on molecular beacon probes that can detect rs1801133, rs1801131, and rs1801394 simultaneously was developed in this study. Specific primers and probes were designed, and the amplification system and conditions were optimized. We applied our method to a group of 500 unrelated women of gestational age in the Dongguan region of Guangdong Province in China. The clinical performance of this assay was evaluated by testing 94 samples in comparison with Sanger sequencing.ResultsThe molecular‐beacon‐based PCR assay we established is extremely sensitive, with a detection limit of 2 ng/μL of genomic DNA, and validated by direct sequencing in a blind study with 100% concordance.ConclusionThe results demonstrate that our molecular‐beacon‐based asymmetric PCR assay is an easy, reliable, high‐yield, and cost‐effective method for the simultaneous detection of three polymorphisms related to folate metabolism. It could help evaluate the risk of perinatal‐neonatal neural tube malformation, pregnancy hypertension, and other diseases and guide the individualized supplementation of folic acid. Data on the spectrum of mutations in the Dongguan District in this study are beneficial for guiding the supplementation of folic acid.

A rare case of a fetal neural tube defect: Iniencephaly

Iniencephaly is characterized by severe retro flexion of the head with the absence of neck due to spinal vertebrae deformities, it is considered as uncommon anomaly. Prevalence: 0.1-10:10,000, M:F. Etiology: Unknown, but genetic, environmental factors are implicated. Pathogenesis: Unknown. Recurrence risk: 1-4%. Associated anomalies: Anencephaly, encephalocele, cyclopedia, lack of lower jaw bone, cleft palate, arthrogryposis, clubfeet, holoprosencephaly, spina bifida, lung hypoplasia, omphalocele, gastroschisis, cardiovascular disorders, Congenital diaphragmatic hernias, gastrointestinal atresia, single umbilical artery and renal abnormalities. Conclusion: Iniencephaly is a lethal congenital neural tube malformation. It is characterized by occipital bone defect, fixed retroflexion of the fetal head and severe lordosis of the cervicothoracic spine. Differential diagnosis: Include anencephaly with cervical spinal retro flexion and Klippel-Fiel syndrome

Neural Tube Malformations Diagnosed at Prenatal Ultrasound in Abidjan

Objective To describe the morphological abnormalities of the neural tube discovered at ultrasound in Abidjan Patients and methods A retrospective multicenter study carried out over a year period in C ocirc te d Ivoire January to December All obstetric ultrasound reports were re read Cases of neural tube defects have been recurrent Then their types seating associated signs and socio demographic and epidemiological characteristics were described Results obstetric ultrasound scans of the first second and third trimesters were reviewed cases of fetal malformation were identified of the malformations concerned the neural tube The major morphological abnormality was lethal in cases and minor non lethal in cases The major morphological abnormalities were all anencephaly Minor morphological abnormalities included cases of myelomeningocele cases of lumbosacral spinabifida and cases of hydrocephalus Hydramnios were associated in cases Discussion The rate of malformation of the neural tube would be high in our context for reasons a nbsp nbsp nbsp The high prevalence of infectious diseases such as rubella and toxoplasmosis which have a high tropism for the neural tube b nbsp nbsp nbsp Poverty with a lack of folic acid supplementation necessary for the good development of the neural tube c nbsp nbsp nbsp A frequent association with a hydramnios cases or a sign of specificity and high sensitivity and respectively for the detection of fetal malformations in particular of the neural tube Conclusion Malformations of neural tube are not seldom and when they occur they are serious The most frequent is anencephaly They are the easiest morphological abnormalities to detect during the prenatal period because they are often associated with an hydramnios which is a sign of high sensitivity alert for antenatal diagnosis concerning fetal malformation

Dose-dependent effect of Hyperglycemia during Cardiac Development

Congenital heart disease (CHD) constitutes a major proportion of birth defects among infants. It has a complex etiology, involving both genetic and environmental determinants. Pre-existing maternal diabetes mellitus (DM) is one environmental risk factor associated with increased risk of CHDs. Previous studies have reported a direct correlation between maternal glucose level and the onset of specific cardiac malformations. Hyperglycemia (HG) is the primary teratogen in DM mediated complications and results in increased levels of reactive oxygen species (ROS) and reduced nitric oxide (NO) bioavailability. However, the exact molecular mechanism underlying the influence of altered redox homeostasis on the development of CHD is unclear. In this study, we hypothesized that in response to various concentrations of glycemic stress in utero, there is dose-dependent change in ROS regulating enzymes. We utilized a Streptozotocin induced type1 DM mouse model as well as atrioventricular cushion mesenchymal cells (AVM), an embryonic cardiac cell line for our study. AVM cells were cultured for 6, 24 and 48-hours in normal glucose (NG, 5.5mM) and three different concentrations of D-glucose (HG; 10mM, 20mM and 30mM). Our preliminary data indicated that mitochondrial ROS generation constituted more than 70% of total ROS across HG concentrations compared to NG after 24hr exposure. ROS regulating genes did not show a linear trend in expression across different time points: Sod1 (p=0.0004) and Sod2 (p=0.0108) gene expression was found to be significantly increased after 24hr and 48hr exposure with HG (30mM)while Nox1 (p=0.0004) showed an opposite trend after 24hr exposure (30mM)). In addition, E13.5 embryos from chemically induced maternal type 1 model revealed a spectrum of CHD’s, including septal and outflow tract defects, and neural tube malformations with increased glucose levels. Further histologic and molecular characterization in vivo will provide a better understanding of the mechanism of how maternal hyperglycemic dose influences cardiac development.

Impact of protein O-GlcNAcylation on neural tube malformation in diabetic embryopathy

Diabetes mellitus in early pregnancy can cause neural tube defects (NTDs) in embryos by perturbing protein activity, causing cellular stress, and increasing programmed cell death (apoptosis) in the tissues required for neurulation. Hyperglycemia augments a branch pathway in glycolysis, the hexosamine biosynthetic pathway (HBP), to increase uridine diphosphate-N-acetylglucosamine (UDP-GlcNAc). GlcNAc can be added to proteins by O-GlcNAc transferase (OGT) to regulate protein activity. In the embryos of diabetic mice, OGT is highly activated in association with increases in global protein O-GlcNAcylation. In neural stem cells in vitro, high glucose elevates O-GlcNAcylation and reactive oxygen species, but the elevations can be suppressed by an OGT inhibitor. Inhibition of OGT in diabetic pregnant mice in vivo decreases NTD rate in the embryos. This effect is associated with reduction in global O-GlcNAcylation, alleviation of intracellular stress, and decreases in apoptosis in the embryos. These suggest that OGT plays an important role in diabetic embryopathy via increasing protein O-GlcNAcylation, and that inhibiting OGT could be a candidate approach to prevent birth defects in diabetic pregnancies.

Preventing malformations

Damage of the central nervous system of the fetus is one of crucial issues in the modern healthcare as it represents a severe congenital disease with a poor prognosis accompanied by fetal death or severe disability of the newborn. Administration of folic acid or multivitamins during the periconceptual period is an effective method for primary prevention of neural tube malformation.

Application effect of nursing intervention on anxiety of pregnant women with fetal neural tube malformation before and after induced labor

Objective To discuss the relaxation effect of nursing intervention on anxiety of pregnant women with fetal neural tube malformation before and after induced labor..Methods Totaled of 24 pregnant women with fetal neural tube malformation undergoing AFP detection and three-dimensional ultrasound detection were selected and randomly divided into intervention group and control group with 12 cases in each.Through nursing intervention pregnant women understood the factors of leading to fetal neural tube malformation to reduce anxiety.SAS and SDS were used to assess anxiety and depress on the second day when hospitalization,1 day and 3 hours before delivery,delivery end immediately and the second day after delivery.Results Compared with control group,the scores of anxiety and depress of intervention group were all lower (P ＜ 0.05),the scores of SAS and SDS were all rose,while there was no difference in the intervention group.Conclusions Nursing intervention can ease anxiety significantly,make the pregnant women understand the factors of fetal neural tube malformation and the next time pregnancy matters needing attention.It was worth clinical further popularization and application. Key words: Neural tube malformation; Pregnant women; Anxiety; Nursing intervention