ISDN2012_0272: Tortillas and toxins: Gene–environment interactions in fumonisin‐induced neural tube defects

2012 ◽  
Vol 30 (8) ◽  
pp. 636-636
Author(s):  
J. Gelineau‐van Waes ◽  
J. Maddox ◽  
M. Rainey ◽  
N. Gardner ◽  
A. Sachs ◽  
...  
Keyword(s):  
Neural Tube ◽  
Neural Tube Defects ◽  
Gene Environment

scholarly journals Gene-environment interactions in the causation of neural tube defects: folate deficiency increases susceptibility conferred by loss of Pax3 function

2008 ◽  
Vol 17 (23) ◽  
pp. 3675-3685 ◽  
Author(s):  
K. A. Burren ◽  
D. Savery ◽  
V. Massa ◽  
R. M. Kok ◽  
J. M. Scott ◽  
...  
Keyword(s):  
Neural Tube ◽  
Neural Tube Defects ◽  
Folate Deficiency ◽  
Gene Environment

scholarly journals Neural Tube Defects and Folate Pathway Genes: Family-Based Association Tests of Gene–Gene and Gene–Environment Interactions

2006 ◽  
Vol 114 (10) ◽  
pp. 1547-1552 ◽  
Author(s):  
Abee L. Boyles ◽  
Ashley V. Billups ◽  
Kristen L. Deak ◽  
Deborah G. Siegel ◽  
Lorraine Mehltretter ◽  
...  
Keyword(s):  
Neural Tube ◽  
Neural Tube Defects ◽  
Association Tests ◽  
Gene Environment ◽  
Folate Pathway ◽  
Family Based

Spina Bifida and Related Conditions

2017 ◽  
Author(s):  
Stephen L. Kinsman
Keyword(s):  
Spinal Cord ◽  
Spina Bifida ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
Spinal Dysraphism ◽  
Gene Interactions ◽  
Tethered Spinal Cord ◽  
Spinal Lesion ◽  
Gene Environment ◽  
Spina Bifida Aperta

The term “spinal dysraphism” encompasses the broadest array of the conditions known as the neural tube defects. The open neural tube defects (spina bifida aperta and cystica) include both disorders of primary and/or secondary neuralation and are best defined as myelomeningocele complex (MMC) due to their protean nervous system manifestations beyond the spinal lesion. Closed spinal dysraphisms (so-called spina bifida occulta) include lipomatous lesions, forms of tethered spinal cord, sinus tracts, and forms of split spinal cord (diastematomyelia). Both genetic and environmental etiologies have been identified. Gene-environment and gene-gene interactions are also important in the pathobiology of these conditions.

Neural tube defects in curly-tail mice. II. Effect of maternal administration of vitamin A

1979 ◽  
Vol 206 (1162) ◽  
pp. 95-107 ◽  
Keyword(s):  
Vitamin A ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
Neural Tube Closure ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Curly Tail ◽  
The Central Nervous System ◽  
Maternal Administration

Vitamin A, a known teratogen of the central nervous system, was administered in various doses, at the time of active neural tube closure, to pregnant curly-tail mice which have a genetic predisposition to neural tube defects (n. t. d. ), and to A Strong mice, which are not so predisposed. The curly-tail mice showed an enhanced susceptibility to the terato­genic effect of vitamin A given on day 8 of gestation, demonstrating a clear gene─environment interaction. There was a differential response by the two sexes. Females seemed to be more affected by the vitamin A than males. When vitamin A was administered on day 9, instead of day 8, of gestation, the incidence of n. t. d. decreased rather than increased. Furthermore, the number of mice affected by n. t. d. was markedly lower even than that found spontaneously in untreated curly-tail mice.

scholarly journals Gene Environment Interactions in the Etiology of Neural Tube Defects

2021 ◽  
Vol 12 ◽  
Author(s):  
Richard H. Finnell ◽  
Carlo Donato Caiaffa ◽  
Sung-Eun Kim ◽  
Yunping Lei ◽  
John Steele ◽  
...  
Keyword(s):  
United States ◽  
Folic Acid ◽  
Spina Bifida ◽  
Birth Defects ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
The United States ◽  
Model Systems ◽  
Posterior Portion ◽  
Gene Environment

Human structural congenital malformations are the leading cause of infant mortality in the United States. Estimates from the United States Center for Disease Control and Prevention (CDC) determine that close to 3% of all United States newborns present with birth defects; the worldwide estimate approaches 6% of infants presenting with congenital anomalies. The scientific community has recognized for decades that the majority of birth defects have undetermined etiologies, although we propose that environmental agents interacting with inherited susceptibility genes are the major contributing factors. Neural tube defects (NTDs) are among the most prevalent human birth defects and as such, these malformations will be the primary focus of this review. NTDs result from failures in embryonic central nervous system development and are classified by their anatomical locations. Defects in the posterior portion of the neural tube are referred to as meningomyeloceles (spina bifida), while the more anterior defects are differentiated as anencephaly, encephalocele, or iniencephaly. Craniorachischisis involves a failure of the neural folds to elevate and thus disrupt the entire length of the neural tube. Worldwide NTDs have a prevalence of approximately 18.6 per 10,000 live births. It is widely believed that genetic factors are responsible for some 70% of NTDs, while the intrauterine environment tips the balance toward neurulation failure in at risk individuals. Despite aggressive educational campaigns to inform the public about folic acid supplementation and the benefits of providing mandatory folic acid food fortification in the United States, NTDs still affect up to 2,300 United States births annually and some 166,000 spina bifida patients currently live in the United States, more than half of whom are now adults. Within the context of this review, we will consider the role of maternal nutritional status (deficiency states involving B vitamins and one carbon analytes) and the potential modifiers of NTD risk beyond folic acid. There are several well-established human teratogens that contribute to the population burden of NTDs, including: industrial waste and pollutants [e.g., arsenic, pesticides, and polycyclic aromatic hydrocarbons (PAHs)], pharmaceuticals (e.g., anti-epileptic medications), and maternal hyperthermia during the first trimester. Animal models for these teratogens are described with attention focused on valproic acid (VPA; Depakote). Genetic interrogation of model systems involving VPA will be used as a model approach to discerning susceptibility factors that define the gene-environment interactions contributing to the etiology of NTDs.

Lessons from dolutegravir and neural tube defects

2021 ◽  
Vol 8 (1) ◽  
pp. e3-e4
Author(s):  
Elaine Abrams ◽  
Landon Myer
Keyword(s):  
Neural Tube ◽  
Neural Tube Defects

A Public Health Success Story: Folic Acid Fortification and Supplementation for Prevention of Neural Tube Defects

2004 ◽  
Author(s):  
Linda Longerich ◽  
Roy West ◽  
Ed Randell ◽  
Marian Crowley ◽  
Shiliang Liu ◽  
...  
Keyword(s):  
Public Health ◽  
Folic Acid ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
Success Story ◽  
Folic Acid Fortification
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