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3- https://doi.org/10.1002/bdr2.1000
Papers from the Ninth International Conference on Neural Tube Defects.
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Take Notes Papers from the Ninth International Conference on Neural Tube Defects.
- 611
- 10.1002/bdra.20294
- Oct 18, 2006
- Birth Defects Research Part A: Clinical and Molecular Teratology
- 435
- 10.1001/archpedi.161.8.745
- Aug 1, 2007
- Archives of Pediatrics & Adolescent Medicine
- 156
- 10.1002/bdra.20360
- Mar 2, 2007
- Birth Defects Research Part A: Clinical and Molecular Teratology
- 607
- 10.1016/j.ajog.2008.06.028
- Jul 31, 2008
- American Journal of Obstetrics and Gynecology
- Research Article
- 1
- 10.1038/s41419-025-07343-3
- Jan 19, 2025
- Cell Death & Disease
Research on the aetiology of neural tube defects (NTDs) has made progress in recent years. However, the molecular mechanism of apolipoproteins underlying NTDs development remains unclear. This study aimed to investigate the function of apolipoprotein M (ApoM) in the pathogenesis of NTDs and its underlying mechanisms. We demonstrated that ApoM expression was reduced in the spinal cord samples of rat models and human fetuses with NTDs respectively. Specifically, lack of ApoM resulted in reduced cytosolic localization of Elavl2 and caused Nnt mRNA degradation, which further led to impaired cell homeostasis by suppressing PINK1-PRKN-mediated mitophagy and promoting apoptosis and subsequent NTDs formation. Moreover, Zic3 directly interacted with the promoter of ApoM and activated its transcription. Lastly, intra-amniotic delivery of adenoviral recombinant Zic3 or ApoM could promote mitophagy and alleviate apoptosis in spinal cords of NTDs. Collectively, these findings highlight the important role of the Zic3-ApoM-Elavl2-Nnt axis in cellular homeostasis during neural tube development, thereby revealing an intracellular molecular regulatory mechanism of ApoM, providing a mechanistic basis for understanding embryonic neural development, and offering experimental evidence for potential therapeutic targets for NTDs.
- Research Article
- 18
- 10.1111/nyas.14443
- Aug 5, 2020
- Annals of the New York Academy of Sciences
Neural tube defects (NTDs) are serious congenital malformations. In this study, we aimed to identify more specific and sensitive maternal serum biomarkers for noninvasive NTD screenings. We collected serum from 37 pregnant women carrying fetuses with NTDs and 38 pregnant women carrying normal fetuses. Isobaric tags for relative and absolute quantitation were conducted for differential proteomic analysis, and an enzyme-linked immunosorbent assay was used to validate the results. We then used a support vector machine (SVM) classifier to establish a disease prediction model for NTD diagnosis. We identified 113 differentially expressed proteins; of these, 23 were either up- or downregulated 1.5-fold or more, including five complement proteins (C1QA, C1S, C1R, C9, and C3); C3 and C9 were downregulated significantly in NTD groups. The accuracy rate of the SVM model of the complement factors (including C1QA, C1S, and C3) was 62.5%, with 60% sensitivity and 67% specificity, while the accuracy rate of the SVM model of alpha-fetoprotein (AFP, an established biomarker for NTDs) was 62.5%, with 75% sensitivity and 50% specificity. Combination of the complement factor and AFP data resulted in the SVM model accuracy of 75%, and receiver operating characteristic curve analysis showed 75% sensitivity and 75% specificity. These data suggest that a disease prediction model based on combined complement factor and AFP data could serve as a more accurate method of noninvasive prenatal NTD diagnosis.
- Research Article
- 24
- 10.1111/1471-0528.15342
- Jul 18, 2018
- BJOG: An International Journal of Obstetrics & Gynaecology
Controversy exists regarding the optimal mode of delivery for fetuses with open neural tube defects. To compare neurological outcomes among infants with open neural tube defects who underwent vaginal compared with caesarean delivery. Electronic databases MEDLINE, EMBASE, Scopus, and Clinicaltrials.gov were searched from inception to November 2017. Eligible studies included observational or randomised studies comparing vaginal and caesarean delivery in pregnancies with fetal open neural tube defects who did not undergo prenatal repair. Two reviewers independently reviewed abstracts and full-text articles. Outcomes were compared between vaginal and caesarean delivery and prelabour caesarean versus exposure to labour. The primary outcome was motor-anatomic level difference. Secondary outcomes included shunt requirement, sac disruption, meningitis, and ambulation at 2years. Meta-analysis was performed and mean difference or odds ratios with 95% CI were calculated. Of 201 abstracts identified in the primary search, nine studies (672 women) met the eligibility criteria. Comparing vaginal and caesarean delivery, there was no significant difference in motor-anatomic level difference (mean difference -0.10, 95% CI -0.58 to 0.38; I2 =57%). The vaginal delivery group was less likely to require a shunt or have sac disruption [odds ratio (OR) 0.37, 95% CI 0.14-0.95 and OR 0.46, 95% CI 0.23-0.90, respectively]. Comparisons by prelabour caesarean versus exposure to labour showed no significant difference in motor-anatomic level difference (OR 1.29, 95% CI 0.63-3.21) or ambulation at 2years (OR 2.13, 95% CI 0.35-13.12). Caesarean delivery was not associated with improved neurological outcomes among fetuses with open neural tube defects. Available evidence does not support routine caesarean delivery for fetuses with open neural tube defects.
- Addendum
- 10.1038/s41436-021-01226-6
- Dec 1, 2021
- Genetics in Medicine
Focused Revision: Policy statement on folic acid and neural tube defects
- Research Article
- 3
- 10.1111/j.1471-4159.2012.07800.x
- Jul 9, 2012
- Journal of Neurochemistry
Could microRNAs be biomarkers for neural tube defects?
- Front Matter
- 6
- 10.1053/j.ajkd.2015.02.320
- Apr 22, 2015
- American Journal of Kidney Diseases
Diabetes-Induced Congenital Anomalies of the Kidney and Urinary Tract (CAKUT): Nurture and Nature at Work?
- Research Article
- 159
- 10.1007/s00125-003-1063-2
- Mar 26, 2003
- Diabetologia
Maternal diabetes increases oxidative stress in embryos. Maternal diabetes also inhibits expression of embryonic genes, most notably, Pax-3, which is required for neural tube closure. Here we tested the hypothesis that oxidative stress inhibits expression of Pax-3, thereby providing a molecular basis for neural tube defects induced by diabetic pregnancy. Maternal diabetes-induced oxidative stress was blocked with alpha-tocopherol (vitamin E), and oxidative stress was induced with the complex III electron transport inhibitor, antimycin A, using pregnant diabetic or non-diabetic mice, primary cultures of neurulating mouse embryo tissues, or differentiating P19 embryonal carcinoma cells. Pax-3 expression was assayed by quantitative RT-PCR, and neural tube defects were scored by visual inspection. Oxidation-induced DNA fragmentation in P19 cells was assayed by electrophoretic analysis. Maternal diabetes inhibited Pax-3 expression and increased neural tube defects, and alpha-tocopherol blocked these effects. In addition, induction of oxidative stress with antimycin A inhibited Pax-3 expression and increased neural tube defects. In cultured embryo tissues, high glucose-inhibited Pax-3 expression, and this effect was blocked by alpha-tocopherol and GSH-ethyl ester, and Pax-3 expression was inhibited by culture with antimycin A. In differentiating P19 cells, antimycin A inhibited Pax-3 induction but did not induce DNA strand breaks. Oxidative stress inhibits expression of Pax-3, a gene that is essential for neural tube closure. Impaired expression of essential developmental control genes could be the central mechanism by which neural tube defects occur during diabetic pregnancy, as well as other sources of oxidative stress.
- News Article
- 3
- 10.4300/jgme-d-21-01177.1
- Feb 1, 2022
- Journal of Graduate Medical Education
Pursuing Excellence: Innovations in Designing an Interprofessional Clinical Learning Environment.
- Research Article
- 23
- 10.1016/j.jen.2010.08.013
- Jan 22, 2011
- Journal of Emergency Nursing
Outcomes of Implementing Rapid Triage in the Pediatric Emergency Department
- Front Matter
- 30
- 10.1016/j.jogc.2022.04.004
- Jun 1, 2022
- Journal of Obstetrics and Gynaecology Canada
Guideline No. 427: Folic Acid and Multivitamin Supplementation for Prevention of Folic Acid–Sensitive Congenital Anomalies
- Research Article
- 10.1176/appi.ps.58.1.12-a
- Jan 1, 2007
- Psychiatric Services
Innovations: Child & Adolescent Psychiatry Training in Developmental Responses to Trauma for Child Service Providers
- Research Article
- 4
- 10.1176/appi.ps.58.1.12
- Jan 1, 2007
- Psychiatric Services
Innovations: Child & Adolescent Psychiatry Training in Developmental Responses to Trauma for Child Service Providers
- Research Article
- 31
- 10.1016/j.jpeds.2010.12.037
- Feb 23, 2011
- The Journal of Pediatrics
Long Term Maintenance of Neural Tube Defects Prevention in a High Prevalence State
- Discussion
- 23
- 10.1016/s0140-6736(05)63358-2
- Aug 1, 1997
- The Lancet
Folic acid and prevention of neural-tube defects
- Front Matter
- 10.1002/jhrm.21552
- Jun 16, 2023
- Journal of Healthcare Risk Management
Journal of Healthcare Risk ManagementEarly View PRESIDENT'S MESSAGE President's Message Rebecca Cady Esq., BSN, CPHRM, DFASHRM, FACHE, Corresponding Author Rebecca Cady Esq., BSN, CPHRM, DFASHRM, FACHE [email protected] orcid.org/0009-0005-5468-9557 Children's National Medical Center, Washington, District of Columbia, USA Correspondence Rebecca Cady, Esq., BSN, CPHRM, DFASHRM, FACHE, Children's National Medical Center, Washington, DC, USA. Email: [email protected]Search for more papers by this author Rebecca Cady Esq., BSN, CPHRM, DFASHRM, FACHE, Corresponding Author Rebecca Cady Esq., BSN, CPHRM, DFASHRM, FACHE [email protected] orcid.org/0009-0005-5468-9557 Children's National Medical Center, Washington, District of Columbia, USA Correspondence Rebecca Cady, Esq., BSN, CPHRM, DFASHRM, FACHE, Children's National Medical Center, Washington, DC, USA. Email: [email protected]Search for more papers by this author First published: 16 June 2023 https://doi.org/10.1002/jhrm.21552Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article. Early ViewOnline Version of Record before inclusion in an issue RelatedInformation
- Research Article
- 10.1111/jocs.13730
- Jun 13, 2018
- Journal of cardiac surgery
Journal of Cardiac SurgeryVolume 33, Issue 7 p. 402-402 INVITED COMMENTARY The risk of overzealous application of hybrid strategies for patients with biventricular cardiac anomalies Invited commentary regarding: “Hybrid Strategies for High-Risk Non-Hypoplastic Left Heart Syndrome Patients” Richard A. Jonas MD, Corresponding Author Richard A. Jonas MD rjonas@childrensnational.org orcid.org/0000-0002-8379-4824 Children's National Heart Institute, Children's National Medical Center, Washington, District of Columbia Correspondence Richard A. Jonas MD, Children's National Heart Institute, Children's National Medical Center, 111 Michigan Avenue NW, Washington, DC 20010. Email: rjonas@childrensnational.orgSearch for more papers by this author Richard A. Jonas MD, Corresponding Author Richard A. Jonas MD rjonas@childrensnational.org orcid.org/0000-0002-8379-4824 Children's National Heart Institute, Children's National Medical Center, Washington, District of Columbia Correspondence Richard A. Jonas MD, Children's National Heart Institute, Children's National Medical Center, 111 Michigan Avenue NW, Washington, DC 20010. Email: rjonas@childrensnational.orgSearch for more papers by this author First published: 13 June 2018 https://doi.org/10.1111/jocs.13730Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume33, Issue7July 2018Pages 402-402 RelatedInformation
- Research Article
- 10.1002/(sici)1096-911x(199806)30:6<330::aid-mpo4>3.3.co;2-j
- Jun 1, 1998
- Medical and Pediatric Oncology
Medical and Pediatric OncologyVolume 30, Issue 6 p. 330-330 Comment Comment: Intracranial ependymomas in children Roger Packer, Corresponding Author Roger Packer Department of Neurology, Children's National Medical Center, Washington, D.C.Department of Neurology, Children's National Medical Center, Washington, D.C.Search for more papers by this author Roger Packer, Corresponding Author Roger Packer Department of Neurology, Children's National Medical Center, Washington, D.C.Department of Neurology, Children's National Medical Center, Washington, D.C.Search for more papers by this author First published: 07 December 1998 https://doi.org/10.1002/(SICI)1096-911X(199806)30:6<330::AID-MPO4>3.0.CO;2-FAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Volume30, Issue6June 1998Pages 330-330 RelatedInformation
- Front Matter
- 1
- 10.1002/pbc.30235
- Feb 20, 2023
- Pediatric blood & cancer
Pediatric Blood & CancerEarly View e30235 HIGHLIGHT Introduction to fertility preservation in pediatric patients with cancer: A report from the Children's Oncology Group Jennifer M Levine, Corresponding Author Jennifer M Levine [email protected] orcid.org/0000-0003-1417-0169 Pediatric Oncology, Center for Cancer and Blood Disorders, Children's National Medical Center, Washington, District of Columbia, USA Correspondence Jennifer M Levine, 111 Michigan Ave, NW, 4th Floor, Pediatric Oncology, Center for Cancer and Blood Disorders, Children's National Medical Center, Washington, DC 20010, USA. Email: [email protected]Search for more papers by this author Jennifer M Levine, Corresponding Author Jennifer M Levine [email protected] orcid.org/0000-0003-1417-0169 Pediatric Oncology, Center for Cancer and Blood Disorders, Children's National Medical Center, Washington, District of Columbia, USA Correspondence Jennifer M Levine, 111 Michigan Ave, NW, 4th Floor, Pediatric Oncology, Center for Cancer and Blood Disorders, Children's National Medical Center, Washington, DC 20010, USA. Email: [email protected]Search for more papers by this author First published: 20 February 2023 https://doi.org/10.1002/pbc.30235Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Early ViewOnline Version of Record before inclusion in an issuee30235 RelatedInformation
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