Birth Defects Research Part A: Clinical and Molecular TeratologyThis is an RSS file. You can use it to subscribe to this data in your favourite RSS reader, such as GoogleReader, or to display this data on your own website or blog. Subscribe to this data using MyMedWorm.Subscribe to this data using GoogleReader.Subscribe to this data using Bloglines.Subscribe to this data using MyYahoo.

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Methods for developing useful estimates of the costs associated with birth defectsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Cost estimates for birth defects are useful to policy makers in deciding the best use of resources to prevent these conditions. Much of the effort in this area has focused on spina bifida, in part because cost savings can be estimated from folic acid-preventable cases. However, comprehensive cost-of-illness estimates for this condition may be too outdated, too general, or not applicable to individual states' environments.Using the live birth prevalence for spina bifida in Texas, we applied recent spina bifida cost estimates to approximate total lifetime medical and other costs for an average live birth cohort of spina bifi...
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - October 14, 2009 Category: Perinatology & Neonatology Authors: Amy P. Case, Mark A. Canfield Source Type: journals

Hospital use and associated costs of children aged zero-to-two years with craniofacial malformations in MassachusettsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Craniofacial malformations (CFMs) are among the most common and correctable birth defects in the United States, often requiring multiple medical and surgical treatments. However, population-based data on hospital utilization and costs are sparse.This retrospective cohort study used linked data from the Massachusetts Pregnancy to Early Life Longitudinal Data System. Cases were children born during 1998-2002 in Massachusetts hospitals to Massachusetts residents, alive at age two years, and ascertained by the Massachusetts Birth Defects Monitoring Program as having a CFM (orofacial cleft, craniosynostosis, microtia/anotia). M...
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - October 13, 2009 Category: Perinatology & Neonatology Authors: Judith Weiss, Milton Kotelchuck, Scott D. Grosse, Susan E. Manning, Marlene Anderka, Diego F. Wyszynski, Howard Cabral, Wanda Barfield, Raul Garcia, Emily Lu, Cathy Higgins Source Type: journals

Birth defects surveillance, epidemiology, and significance in public healthEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
No abstract. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - October 12, 2009 Category: Perinatology & Neonatology Authors: Julianne S. Collins, Russell S. Kirby Source Type: journals

The genetic background of the curly tail strain confers susceptibility to folate-deficiency-induced exencephalyEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CONCLUSIONS: Dietary folate deficiency can induce cranial NTDs in nonmutant mice with a permissive genetic background, a situation that likely parallels gene-nutrient interactions in human NTDs. Our findings suggest that inositol supplementation may ameliorate NTDs resulting from insufficient dietary folate. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - October 11, 2009 Category: Perinatology & Neonatology Authors: Katie A. Burren, John M. Scott, Andrew J. Copp, Nicholas D. E. Greene Source Type: journals

Birth defects and preterm birth: Overlapping outcomes with a shared strategy for research and preventionEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
No abstract. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - October 11, 2009 Category: Perinatology & Neonatology Authors: Siobhan M. Dolan, William M. Callaghan, Sonja A. Rasmussen Source Type: journals

Interstitial deletion of 18q: Comparative genomic hybridization array analysis of 46, XX,del(18)(q21.2.q21.33)Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CONCLUSIONS: The deletion of the transcription factor 4 gene suggested a possible contribution of the deletion to the patient's facial abnormalities, as observed in Pitt-Hopkins syndrome. Together with other reported cases with interstitial deletion of 18q, a possible contribution of haploinsufficiency in both MBD1 and MBD2 genes to a Rett syndrome-like phenotype was suggested, but further genetic studies on other cases are necessary to clarify the genotype-phenotype correlation. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - October 7, 2009 Category: Perinatology & Neonatology Authors: Zenichiro Kato, Wataru Morimoto, Takeshi Kimura, Akihiro Matsushima, Naomi Kondo Source Type: journals

Gene expression profiling in the fetal cardiac tissue after folate and low-dose trichloroethylene exposureEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CONCLUSIONS: A mechanism by which TCE induces a folate deficiency does not explain altered gene expression patterns in the embryonic mouse heart. The data further suggest that use of folate supplementation, in the presence of this toxin, may be detrimental and not protective of the developing embryo Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - October 6, 2009 Category: Perinatology & Neonatology Authors: Patricia T. Caldwell, Ann Manziello, Jamie Howard, Brittany Palbykin, Raymond B. Runyan, Ornella Selmin Source Type: journals

Variants of folate metabolism genes and risk of left-sided cardiac defectsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Congenital heart defects (CHDs) are the most common, serious group of birth defects. Although relatively little is known about the causes of these conditions and there are no established prevention strategies, evidence suggests that the risk of CHDs may be related to maternal folate status as well as genetic variants in folate-related genes. Efforts to establish the relationships between these factors and CHD risk have, however, been hampered by a number of factors, including small study sample sizes and phenotypic heterogeneity.The present study examined the relationship between nine genetic variants in eight folate-relat...
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - September 23, 2009 Category: Perinatology & Neonatology Authors: Laura E. Mitchell, Jin Long, Jennifer Garbarini, Prasuna Paluru, Elizabeth Goldmuntz Source Type: journals

False positive reporting of Hirschsprung's disease in Alaska: An evaluation of Hirschsprung's disease surveillance, birth years 1996-2007Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Hirschsprung's disease (HSCR) is a potentially fatal congenital intestinal obstruction syndrome. For birth years 1996-2002, reported HSCR prevalence in Alaska was approximately six times higher than the national estimate of two per 10,000 live births. In 2008 we completed a case verification study of HSCR reported to the Alaska Birth Defects Registry (ABDR) to verify prevalence and evaluate sensitivity and predictive value of HSCR surveillance.We abstracted medical records for children reported with HSCR who were born in 1996-2007 and matched to an Alaska birth certificate. We categorized reports as confirmed, ruled out, o...
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - September 22, 2009 Category: Perinatology & Neonatology Authors: Janine Schoellhorn, Sandra Collins Source Type: journals

Association of congenital cardiovascular malformations with 33 single nucleotide polymorphisms of selected cardiovascular disease-related genesEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CONCLUSIONS: Genes affecting vascular function and coagulation appear to be promising candidates for the etiology of cardiac malformations and warrant further study. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - September 17, 2009 Category: Perinatology & Neonatology Authors: Karen Kuehl, Christopher Loffredo, Edward J. Lammer, David M. Iovannisci, Gary M. Shaw Source Type: journals

Polymicrogyria in fetal alcohol syndromeEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CONCLUSION: Our observation represents only the second patient of PMG in FAS and confirms the phenotypic variability of cerebral malformations associated with maternal alcohol abuse during pregnancy. In patients with clinical features of FAS and neurologic deficits or seizures neuroimaging is recommended. Furthermore, FAS should be considered as a differential diagnosis for PMG. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - September 16, 2009 Category: Perinatology & Neonatology Authors: Konstanze Reinhardt, Alexander Mohr, Jutta Gärtner, Hans-Ludwig Spohr, Knut Brockmann Source Type: journals

Epidemiologic features and clinical subgroups of anotia/microtia in TexasEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Few studies have investigated the epidemiologic features of clinically defined subgroups of anotia/microtia.Data on cases of anotia and/or microtia among 1999-2005 deliveries were obtained from the Texas Birth Defects Registry, a population-based active surveillance system. We determined crude and adjusted associations between selected factors and seven clinical subgroups of anotia/microtia.In total, 742 cases were diagnosed with anotia and/or microtia, corresponding to a prevalence of 2.86 per 10,000 live births. Of those, 45% had no other major birth defect ("isolated"), 77% were unilateral, and 22% bilateral. Anotia alo...
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - September 16, 2009 Category: Perinatology & Neonatology Authors: Mark A. Canfield, Peter H. Langlois, Ly M. Nguyen, Angela E. Scheuerle Source Type: journals

First trimester paroxetine use and the prevalence of congenital, specifically cardiac, defects: A meta-analysis of epidemiological studiesEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CONCLUSIONS: This meta-analysis found little evidence of publication bias or overall statistical heterogeneity and only weak evidence of associations with some study characteristics. Although subject to limitations, the summary estimate indicates an increased prevalence of combined cardiac defects with first trimester paroxetine use. The summary estimate also indicates an increased prevalence of aggregated congenital defects with paroxetine; however, this association may be explained, in part, by the increased prevalence of combined cardiac defects. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. (Source: B...
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - September 8, 2009 Category: Perinatology & Neonatology Authors: Keele E. Wurst, Charles Poole, Sara A. Ephross, Andrew F. Olshan Source Type: journals

Arsenate-induced apoptosis in murine embryonic maxillary mesenchymal cells via mitochondrial-mediated oxidative injuryEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CONCLUSIONS: Taken together, these findings suggest that in MEMM cells arsenate-mediated oxidative injury acts as an early and upstream initiator of the cell death cascade, triggering cytotoxicity, mitochondrial dysfunction, altered Bcl/Bax protein ratios, and activation of caspase-9. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - September 7, 2009 Category: Perinatology & Neonatology Authors: Saurabh Singh, Robert M. Greene, M. Michele Pisano Source Type: journals

Maternal obesity and morbid obesity: The risk for birth defects in the offspringEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CONCLUSION: The risk for a morbidly obese pregnant woman to have an infant with a congenital birth defect is small, but for society the association is important in the light of the ongoing obesity epidemic. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - August 26, 2009 Category: Perinatology & Neonatology Authors: Marie I. Blomberg, Bengt Källén Source Type: journals

Early development of the primordial mammalian diaphragm and cellular mechanisms of nitrofen-induced congenital diaphragmatic herniaEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
This study provides novel insight into the embryogenesis of the PPF in rats and humans, and it indicates that impaired cell proliferation might contribute to abnormal diaphragm development in the nitrofen model of CDH. Birth Defects Research (Part A) 2009. © 2009 Wiley-Liss, Inc. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - August 25, 2009 Category: Perinatology & Neonatology Authors: Robin D. Clugston, Wei Zhang, John J. Greer Source Type: journals

Maternal caffeine consumption and risk of neural tube defectsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Animal studies demonstrate teratogenic effects of caffeine, whereas human studies are inconclusive.Associations between maternal caffeine consumption and neural tube defects (NTDs) by type of NTD (anencephaly, spina bifida, or encephalocele) were examined using data from the National Birth Defects Prevention Study (NBDPS). Total average daily caffeine from coffee, tea, soda, and chocolate consumption during the year before pregnancy was estimated for 768 mothers of infants with NTDs and 4143 mothers of infants without birth defects who gave birth during 1997 through 2002. Periconceptional use of caffeine-containing medicat...
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - August 25, 2009 Category: Perinatology & Neonatology Authors: Rebecca J. Schmidt, Paul A. Romitti, Trudy L. Burns, Marilyn L. Browne, Charlotte M. Druschel, Richard S. Olney, the National Birth Defects Prevention Study Source Type: journals

Multistate study of the epidemiology of clubfootEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CONCLUSIONS: We estimated the prevalence of clubfoot using data from several birth defects programs, representing one-quarter of all births in the United States. Our findings underline the importanceof birth defects surveillance programs and their utility in monitoring population-based prevalence and investigating risk factors. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - August 20, 2009 Category: Perinatology & Neonatology Authors: Samantha E. Parker, Cara T. Mai, Matthew J. Strickland, Richard S. Olney, Russel Rickard, Lisa Marengo, Ying Wang, S. Shahrukh Hashmi, Robert E. Meyer, National Birth Defects Prevention Network Source Type: journals

An update on cardiovascular malformations in congenital rubella syndromeEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CONCLUSION: Among children with suspected CRS, clinical evaluations for the presence of CVMs should include examinations for both branch pulmonary artery stenosis and PDA. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - August 19, 2009 Category: Perinatology & Neonatology Authors: Matthew E. Oster, Tiffany Riehle-Colarusso, Adolfo Correa Source Type: journals

Neurofibromatosis type 1 is a disorder of dysplasia: The importance of distinguishing features, consequences, and complicationsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CONCLUSIONS: NF1 is a histogenesis control gene that also has properties that overlap with those of a tumor suppressor gene. Both its neoplastic and dysplastic manifestations become more amenable to understanding and treatment if they are differentiated at three levels - specifically, features, consequences and complications. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - August 18, 2009 Category: Perinatology & Neonatology Authors: Vincent Michael Riccardi Source Type: journals

Time trends in oral clefts in Chinese newborns: Data from the Chinese National Birth Defects Monitoring NetworkEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CONCLUSIONS: The observed complex patterns of prevalence of oral clefts from the Chinese national birth defects registry indicate that oral cleft subtypes by either cleft location or syndromic status should be considered in the development of intervention measures and in future analytical studies. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - August 17, 2009 Category: Perinatology & Neonatology Authors: Li Dai, Jun Zhu, Meng Mao, Yanhua Li, Ying Deng, Yanping Wang, Juan Liang, Liu Tang, He Wang, Briseis A. Kilfoy, Tongzhang Zheng, Yawei Zhang Source Type: journals

Are selective serotonin reuptake inhibitors cardiac teratogens? Echocardiographic screening of newborns with persistent heart murmurEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CONCLUSIONS: Newborns exposed in utero to SSRIs, have a twofold higher risk of mild nonsyndromic heart defects than unexposed infants. The data suggest that women who require SSRI treatment during pregnancy can be reassured that the fetal risk is low and possible cardiac malformations will probably be mild. Late-targeted ultrasound and fetal echocardiography at 22 to 23 weeks' gestation are recommended in this patient group. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - August 17, 2009 Category: Perinatology & Neonatology Authors: Paul Merlob, Einat Birk, Lea Sirota, Nehama Linder, Michael Berant, Bracha Stahl, Gil Klinger Source Type: journals

Pena-Shokeir phenotype (Fetal akinesia deformation sequence) revisitedEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CONCLUSION: Lack of fetal movement (fetal akinesia) in humans produces a recognizable sequence of deformations. Many developmental processes must be accomplished for fetal movement to be normal, and for extra-uterine life to be sustainable. Prenatal diagnosis is possible through real-time ultrasound studies as early as 12 weeks. Most reported cases die in utero, at birth, or in the newborn period. Advances in embryo/fetus pathology have led to the recognition of the many familial subtypes, allowing improved genetic counseling and early recognition in subsequent pregnancies. Birth Defects Research (Part A), 2009. © 2009 Wi...
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - July 30, 2009 Category: Perinatology & Neonatology Authors: Judith G. Hall Source Type: journals

Single nucleotide polymorphism discovery in TBX1 in individuals with and without 22q11.2 deletion syndromeEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Children with 22q11.2 deletion syndrome (22q11.2DS) have a wide range of clinical features. TBX1 has been proposed as a candidate gene for some of the features in this condition. Polymorphisms in the nondeleted TBX1, which may affect the function of the sole TBX1 gene in individuals with the 22q11.2DS, may be a key to understanding the phenotypic variability among individuals with a shared deletion. Comprehensive single nucleotide polymorphism (SNP) discovery by resequencing candidate genes can identify genetic variants that influence a given phenotype. The purpose of this study was to further characterize the sequence var...
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - July 29, 2009 Category: Perinatology & Neonatology Authors: Carrie L. Heike, Jacqueline R. Starr, Mark J. Rieder, Michael L. Cunningham, Karen L. Edwards, Ian B. Stanway, Dana C. Crawford Source Type: journals

The effect of thalidomide in chicken embryosEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Early in the history of the thalidomide disaster, chick embryos were "eliminated" as useful in the study of thalidomide. One reason for that conclusion was that many of the early experiments were flawed. We employed a number of experiments to expose chick embryos to thalidomide. Our data show that thalidomide does cause limb reduction defects in chick embryos as long as the embryos are directly exposed to the drug. The most useful techniques are implanting thalidomide-soaked beads into the embryo immediately adjacent to the limb territory or soaking presumptive chick limb territories in thalidomide and then grafting the ex...
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - July 29, 2009 Category: Perinatology & Neonatology Authors: Trent D. Stephens Source Type: journals

Developmental control of inositol phosphate biosynthesis is altered in the brain of both curly and phenotypically normal straight tail mutant miceEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CONCLUSIONS: These findings implicate a role for MIP in the maturation of the CNS and evoke a hypothesis regarding the regulation of inositol phosphate biosynthesis in brain development. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - July 29, 2009 Category: Perinatology & Neonatology Authors: Hana Dawood Ali Alebous, Robert Cartee, David Vaccari, Oneil A. Wright, Altan Ahmed, Ronald D. Hood, Margaret Dean Johnson Source Type: journals

Maternal nativity as a risk factor for gastroschisis: A population-based studyEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CONCLUSIONS: Although young maternal age remains a strong significant risk factor for gastroschisis in Florida, other factors such as maternal race/ethnicity and nativity could be important in explaining the increasing prevalence of gastroschisis. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - July 29, 2009 Category: Perinatology & Neonatology Authors: Jason L. Salemi, Marie Pierre, Jean Paul Tanner, Jennifer L. Kornosky, Kimberlea W. Hauser, Russell S. Kirby, Jane D. Carver Source Type: journals

Socioeconomic measures, orofacial clefts, and conotruncal heart defects in CaliforniaEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CONCLUSIONS: This detailed analysis of SES and selected birth defects did not suggest worse SES was associated with increased risk of the studied defects, with the possible exception of cleft lip with or without cleft palate. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - July 29, 2009 Category: Perinatology & Neonatology Authors: Suzan L. Carmichael, Chen Ma, Gary M. Shaw Source Type: journals

Thalidomide and misoprostol: Ophthalmologic manifestations and associations both expected and unexpectedEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Thalidomide is a very potent teratogen capable of causing severe systemic malformations if the fetus is exposed during the sensitive period. Although structural anomalies of the eye can occur from thalidomide exposure, the most frequent eye complication is secondary to damage to the cranial nuclei in the brain stem, resulting in aberrant neurologic connections causing a condition of abnormal ocular movement, Duane syndrome. A less frequent anomalous neurologic complication is tearing when eating (paradoxical gustolacrimal tearing or "crocodile tears") or lack of emotional tearing. The involvement of the 6th and 7th cranial...
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - July 27, 2009 Category: Perinatology & Neonatology Authors: Marilyn T. Miller, Liana Ventura, Kerstin Strömland Source Type: journals

Inducible 70 kDa heat shock proteins protect embryos from teratogen-induced exencephaly: Analysis using Hspa1a/a1b knockout miceEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
It is well known that a variety of teratogens induce neural tube defects in animals; however, less is known about proteins that play a role in protecting embryos from teratogen-induced neural tube defects. Previously, our laboratory has shown that embryos overexpressing the 70-Da heat shock proteins (HSPs) Hspa1a and Hspa1b were partially protected from the deleterious effects of exposure to hyperthermia in vitro.In the present studies, we have used a transgenic mouse in which both of the stress-inducible HSPs Hspa1a and Hspa1b were deleted by homologous recombination. Time-mated Hspa1a/a1b-/- (KO) and wildtype (WT) mice w...
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - July 27, 2009 Category: Perinatology & Neonatology Authors: Marianne Barrier, David J. Dix, Philip E. Mirkes Source Type: journals

Women's perspectives on counseling about risks for medication-induced birth defectsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CONCLUSIONS: Women of reproductive age think that providing information about the possible teratogenic effects of medications could be improved by routine discussions of teratogenic risks at the time medications are prescribed. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - July 27, 2009 Category: Perinatology & Neonatology Authors: Aimee K. Santucci, Melanie A. Gold, Aletha Y. Akers, Sonya Borrero, Eleanor Bimla Schwarz Source Type: journals

Genetic skeletal disorders of the fetus and infant: Pathologic and molecular findings in a series of 41 casesEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CONCLUSIONS: The central role of the perinatal pathologist in collaboration with specialized services is essential for the correct interpretation of the radiologic, physical, and histopathologic findings, to accurately classify specific types of genetic skeletal disorders and enable genetic counseling. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - July 26, 2009 Category: Perinatology & Neonatology Authors: Anastasia E. Konstantinidou, Georgios Agrogiannis, Stavros Sifakis, Apostolos Karantanas, Vassileios Harakoglou, Petros Kaminopetros, Angeliki Hatzaki, Michael B. Petersen, Charalampos Karadimas, Voula Velissariou, Stylianos Velonis, Nikolaos Papantoniou, Source Type: journals

Public health projects for preventing the recurrence of neural tube defects in the United StatesEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CONCLUSIONS: Only 15 states and Puerto Rico had or were planning NTD recurrence prevention projects. An NTD recurrence prevention project using minimal resources should consist of timely case ascertainment, educational materials, and mechanisms for disseminating these materials. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - July 22, 2009 Category: Perinatology & Neonatology Authors: Julianne S. Collins, Mark A. Canfield, Kay Pearson, Russell S. Kirby, Amy P. Case, Cara T. Mai, Judy Major, Joe Mulinare, for the National Birth Defects Prevention Network Source Type: journals

Variability in human embryonic development and its implications for the susceptibility to environmental teratogenesisEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Considerable variability is observed in the size and developmental stage among human embryos at a given gestational age, suggesting that prenatal development does not proceed at the same speed in every embryo. Such variability in embryonic development seems to occur in many (probably all) animal species, and is probably a normal "biologic" phenomenon to some extent. In the case of humans, some other factors (e.g., maternal memory bias, difficulty in assessing the timing of ovulation and fertilization) make it more difficult to assess the developmental stage of embryos in utero. Such facts related to human embryonic develop...
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - July 15, 2009 Category: Perinatology & Neonatology Authors: Kohei Shiota Source Type: journals

Maternal caffeine intake during pregnancy and orofacial cleftsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CONCLUSIONS: Our data do not suggest an association between maternal dietary caffeine intake and orofacial clefts, but caffeine-containing medications merit further study. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - July 8, 2009 Category: Perinatology & Neonatology Authors: Sarah A. Collier, Marilyn L. Browne, Sonja A. Rasmussen, Margaret A. Honein, National Birth Defects Prevention Study Source Type: journals

Perspectives of primary care clinicians on teratogenic risk counselingEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CONCLUSIONS: PCPs perceive themselves as playing an important role in providing their patients information on risk of medication-induced birth defects. To ensure safe prescription of teratogenic medications, PCPs suggest interventions at both the clinic and healthcare system levels. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - July 7, 2009 Category: Perinatology & Neonatology Authors: Eleanor Bimla Schwarz, Aimee Santucci, Sonya Borrero, Aletha Y. Akers, Cara Nikolajski, Melanie A. Gold Source Type: journals

Big risks in small groups: The difference between epidemiology and counsellingEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Congenital anomalies do not occur in all babies born after a teratogenic exposure. Whether a given exposure is teratogenic depends on the chemical nature and physical properties of the agent, the dose and route of exposure, when in pregnancy the exposure occurs, and genetic and other factors that affect susceptibility. Teratogenic birth defects are inherently multifactorial. Absolute risk, relative risk, and population attributable risk provide useful but different information regarding teratogenic effects. Statistical significance and clinical significance also are important considerations, but they may not be concordant....
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - July 4, 2009 Category: Perinatology & Neonatology Authors: J. M. Friedman Source Type: journals

Response to Charlton et al.Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
No abstract. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - June 30, 2009 Category: Perinatology & Neonatology Authors: Angela Scheuerle, Vani X. Vannappagari, Mary K. Miller Source Type: journals

Developmental exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin alters postnatal T cell phenotypes and T cell function and exacerbates autoimmune lupus in 24-week-old SNF1 miceEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Untreated, more than 95% of female SWR x NZB: F1 (SNF1) mice spontaneously develop a fatal lupus-like glomerulonephritis by 8 months-of-age, while disease onset in males is much slower.Timed-pregnant SNF1 mice (10 per treatment) were exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on gestational day (GD) 12 by oral maternal gavage with 0, 40, or 80 [mu]g/kg TCDD.Offspring of the TCDD-exposed dams showed numerous alterations in T lineage cells at 24 weeks-of-age. Females but not males showed decreased CD4+8+ and increased CD4-8- thymocytes. Females also showed increased autoreactive CD4+V[beta]17a+ axillary and inguin...
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - June 30, 2009 Category: Perinatology & Neonatology Authors: Amjad Mustafa, Steven D. Holladay, Matthew Goff, Sharon Witonsky, Richard Kerr, Danielle A. Weinstein, Ebru Karpuzoglu-Belgin, Robert M. Gogal Jr Source Type: journals

New and improved: The role of text augmentation and the application of response interpretation standards (coding schemes) in a final iteration of birth defects warnings developmentEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Several birth defects warning symbols identified as most successful in an earlier study (Mayhorn and Goldsworthy, 2007) were further modified and then evaluated within a nationally distributed field trial (n = 2773). The purpose for the current research was to determine whether symbol warning components could be improved further, whether the addition of text enhanced comprehension uniformly across symbols, and whether results varied by the application of different interpretation standards (coding schemes).A total of 11 warning labels were examined: four new symbols plus the existing baseline symbol, each in versions with a...
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - June 24, 2009 Category: Perinatology & Neonatology Authors: Christopher B. Mayhorn, Richard C. Goldsworthy Source Type: journals

Familial recurrence of urethral stenosis/atresiaEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CONCLUSIONS: A microdeletion of 6p25.3, identified in mother and one fetus, is not associated with a gene known to be involved in urethral development and therefore of unknown significance. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - June 22, 2009 Category: Perinatology & Neonatology Authors: Joseph R. Siebert, Martin P. R. Walker Source Type: journals

Regarding the need, or lack thereof, of a comparator group for pregnancy registriesEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
No abstract. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - June 22, 2009 Category: Perinatology & Neonatology Authors: Rachel Charlton, Marianne Cunnington, John Weil, Corinne de Vries Source Type: journals

The impact of human superoxide dismutase 1 expression in a mouse model on the embryotoxicity of hydroxyureaEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Oxidative stress is hypothesized to mediate embryotoxicity during organogenesis, yet the reactive oxygen species involved are not defined. The superoxide oxygen radical is converted to hydrogen peroxide, a less reactive species, by superoxide dismutases (SODs). If superoxide is important in mediating embryotoxicity, increased SOD expression should protect embryos against insult. Exposure to hydroxyurea during organogenesis causes brain defects, cleft palate, tail anomalies, and limb defects; administration of D-mannitol, a free radical scavenger, ameliorates hydroxyurea embryotoxicity, suggesting that oxidative stress is i...
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - June 5, 2009 Category: Perinatology & Neonatology Authors: Geneviève Larouche, Barbara F. Hales Source Type: journals

Tribute to Thomas H. Shepard: Scholar, mentor, friendEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
No abstract. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - May 19, 2009 Category: Perinatology & Neonatology Authors: Alan G. Fantel Source Type: journals

Genetic and environmental factors in the etiology of esophageal atresia and/or tracheoesophageal fistula: An overview of the current conceptsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Esophageal atresia and/or tracheoesophageal fistula (EA/TEF) are severe congenital anomalies. Although recent years have brought significant improvement in clinical treatment, our understanding of the etiology of these defects is lagging. Many genes and genetic pathways have been implicated in the development of EA/TEF, but only a few genes have been shown to be involved in humans, in animals, or in both. Extrapolating data from animal models to humans is not always straightforward. Environmental factors may also carry a risk, but the mechanisms are yet to be elucidated. This review gives an overview of the current state o...
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - May 18, 2009 Category: Perinatology & Neonatology Authors: Janine F. Felix, Elisabeth M. de Jong, Claudine P. Torfs, A. de Klein, Robbert J. Rottier, Dick Tibboel Source Type: journals

The effects of prenatal alcohol exposure on the morphological characteristics of spinal motoneuronsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In this study, the morphometric alterations in spinal motoneurons were assessed as a result of prenatal alcohol exposure.Pregnant Sprague Dawley rats were administered with 1.0 ml of 20% ethyl alcohol per 100 gm body weight via intraperitoneal injections, and unexposed rats served as controls. Rats were perfused through the left cardiac ventricle and a complete laminectomy was performed. Spinal cord sections from the L4-5 segments were cut serially and stained for cresyl fast violet. Sections were also subjected to TUNEL assay for detection of apoptosis. Observations were made between 1 and 4 weeks after birth.Morphologic ...
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - May 18, 2009 Category: Perinatology & Neonatology Authors: Pamela David, Krishnan Subramaniam Source Type: journals

The long arms of anencephaly: A refutationEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
A paper published in 1925 reported that human fetuses with anencephaly have arms that are longer than normal. This finding was accepted as true through the early 1990s. An analysis of body dimensions done in 1996 and enlarged and updated here shows that the arms of human fetuses with anencephaly are appropriate for gestational age and normal in proportion to their leg lengths. A subtle difference in measurement technique was found to explain the discordant findings. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. (Source: Birth Defects Research Part A: Clinical and Molecular Teratology)
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - May 15, 2009 Category: Perinatology & Neonatology Authors: Mason Barr Jr. Source Type: journals

Normal and abnormal anatomy of the cerebellar vermis in midgestational human fetusesEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Evaluation of the cerebellar vermis is an important component of fetal autopsy, but lack of an established approach, inadequate normal anatomic data, and the subtle nature of some cerebellar malformations negatively affect concordance between prenatal ultrasound and autopsy diagnoses.Gross anatomy and sagittal histologic sections of vermis from 26 midgestation fetuses with no posterior fossa anomalies detected by prenatal ultrasound or autopsy were examined to establish stage-specific norms. These were compared to data from three fetuses with prenatal ultrasound diagnoses of hypoplasia or absence of the cerebellar vermis, ...
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - May 13, 2009 Category: Perinatology & Neonatology Authors: Raj P. Kapur, Barry S. Mahony, Lisa Finch, Joseph R. Siebert Source Type: journals

Smad2/3 is involved in growth inhibition of mouse embryonic palate mesenchymal cells induced by all-trans retinoic acidEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Cleft palate is one of the major malformations induced by retinoic acid in both rodents and humans. The purpose of the present study was to elucidate the mechanism by which all-trans retinoic acid (atRA) induces the cleft palate.The cell cycle distribution of mouse embryonic palate mesenchymal (MEPM) cells under atRA (100 mg/kg) treatment on gestation day (GD) 10 or GD 12 were measured by immunohistochemistry and flow cytometry. The p21, phospho-Rb, Smad2/3, phospho-Smad2 and phospho-Smad3 protein expression levels were detected by western blot, respectively. Quantitative real-time PCR was performed for p21, Smad2, and Sma...
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - April 24, 2009 Category: Perinatology & Neonatology Authors: Miao Wang, Hongzhang Huang, Yiyang Chen Source Type: journals

Urban versus rural residence and occurrence of septal heart defects in TexasEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
There is conflicting information on the association between urban/rural residence of mothers and atrial septal defect (ASD) or ventricular septal defect (VSD) in their offspring. Few studies have compared multiple measures of urban/rural residence.Data were taken from the Texas Birth Defects Registry, 1999-2003. Poisson regression was used to compare crude and adjusted birth prevalence.Three broad urban/rural measures, namely, the rural urban continuum code (RUCC), urban influence code (UIC), and rural urban commuting area (RUCA), were correlated with each other, but much less correlated with percentage of land in crops. A...
Source: Birth Defects Research Part A: Clinical and Molecular Teratology - April 12, 2009 Category: Perinatology & Neonatology Authors: Peter H. Langlois, Angela Scheuerle, Scott A. Horel, Susan E. Carozza Source Type: journals