Gary M Shaw

University of Utah, Salt Lake City, Utah, United States

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Publications (359)1126.34 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Objective This study aims to evaluate the relationship between early-onset severe preeclampsia and first trimester serum levels of pregnancy-associated plasma protein A (PAPP-A) and total human chorionic gonadotropin (hCG). Study Design The association between early-onset severe preeclampsia and abnormal levels of first trimester PAPP-A and total hCG in maternal serum were measured in a sample of singleton pregnancies without chromosomal defects that had integrated prenatal serum screening in 2009 and 2010 (n = 129,488). Logistic binomial regression was used to estimate the relative risk (RR) of early-onset severe preeclampsia in pregnancies with abnormal levels of first trimester PAPP-A or total hCG as compared with controls. Results Regardless of parity, women with low first trimester PAPP-A or high total hCG were at increased risk for early-onset severe preeclampsia. Women with low PAPP-A (multiple of the median [MoM] ≤ the 10th percentile in nulliparous or ≤ the 5th percentile in multiparous) or high total hCG (MoM ≥ the 90th percentile in nulliparous or ≥ the 95th percentile in multiparous) were at more than a threefold increased risk for early-onset severe preeclampsia (RR, 4.2; 95% confidence interval [CI], 3.0-5.9 and RR, 3.3; 95% CI, 2.1-5.2, respectively). Conclusion Routinely collected first trimester measurements of PAPP-A and total hCG provide unique risk information for early-onset severe preeclampsia. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.
    American Journal of Perinatology 12/2014; · 1.57 Impact Factor
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    ABSTRACT: Several single nucleotide variants (SNVs) in low-density lipoprotein receptor-related protein 6 (Lrp6) cause neural tube defects (NTDs) in mice. We therefore examined LRP6 in 192 unrelated infants from California with the NTD, spina bifida, and found four heterozygous missense SNVs, three of which were predicted to be deleterious, among NTD cases and not in 190 ethnically matched non-malformed controls. Parents and siblings could not be tested because of the study design. Like Cd and rs mouse variants, the p.Tyr544Cys Lrp6 protein failed to bind the chaperone protein MESD and impaired Lrp6 subcellular localization to the plasma membrane of MDCK II cells. Only the p.Tyr544Cys Lrp6 variant down-regulated canonical Wnt signaling in a TopFlash luciferase reporter in vitro assay. In contrast, three Lrp6 mutants (p.Ala3Val, p.Tyr544Cys and p.Arg1574Leu) increased non-canonical Wnt/PCP signaling in an Ap1-luciferase assay. Thus, LRP6 variants outside of YWTD-repeats could potentially predispose embryos to NTDs, while Lrp6 modulation of Wnt/PCP signaling would be more essential than its canonical pathway role in neural tube closure.This article is protected by copyright. All rights reserved
    Human Mutation 12/2014; · 5.21 Impact Factor
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    ABSTRACT: Estrogenic endocrine disruptors acting via estrogen receptors α (ESR1) and β (ESR2) have been implicated in the etiology of hypospadias, a common congenital malformation of male external genitalia. Our objective was to determine the association of single nucleotide polymorphisms (SNPs) in ESR1 and ESR2 genes with hypospadias in a racially-ethnically diverse study population of California births. We investigated the relationship between hypospadias and 108 ESR1 and 36 ESR2 SNPs in 647 cases and 877 population-based non-malformed controls among infants born in selected California counties from 1990-2003. Subgroup analyses were performed by race/ethnicity (non-Hispanic whites, Hispanics) and by hypospadias severity (mild-moderate, severe). The odds ratios (OR) for 33 of the 108 ESR1 SNPs had p-values <0.05 (p-values: 0.05-0.007) for risk of hypospadias. However, none of the 36 ESR2 SNPs was significantly associated. In stratified analyses, the association results were consistent by disease severity, but different sets of SNPs were significantly associated with hypospadias in non-Hispanic whites and Hispanics. Due to high linkage disequilibrium across the SNPs, haplotype analyses were conducted and identified six haplotype blocks in ESR1 gene that had haplotypes significantly associated with increased risk of hypospadias (ORs: 1.3-1.8, p-values = 0.04-0.00001). Similar to SNP analysis, different ESR1 haplotypes were associated with risk for hypospadias in non-Hispanic whites and Hispanics. No significant haplotype association was observed for ESR2. The study provides evidence that ESR1 SNPs and haplotypes influence the risk of hypospadias in both whites and Hispanics and warrant further examination in other study populations. Copyright © 2014 American Urological Association Education and Research, Inc. Published by Elsevier Inc. All rights reserved.
    The Journal of urology. 11/2014;
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    ABSTRACT: Gastroschisis is unique because of its substantial risk in pregnancies of adolescent women. Adolescents may have poor diet quality, which places them at higher risk of gastroschisis.
    The Journal of nutrition. 11/2014; 144(11):1781-6.
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    ABSTRACT: The purpose of this study was to compare the performance of first-trimester nuchal translucency (NT) cutoff of ≥3.5 mm with NT percentiles that were calculated for crown-rump length to identify fetuses with critical congenital heart defects (CCHDs). This was a population-level study of singleton pregnancies in California with NT measurements performed between 11 and 14 weeks of gestation. Eligible cases were those that resulted in live births from 2009-2010 and had information about the presence or absence of CCHDs available in the hospital discharge records through age 1 year (n = 76,089). Logistic binomial regression methods were used to compare the rate of CCHDs by an NT percentile for crown-rump length and millimeter cutpoints. Compared with fetuses with an NT measurement of <90th percentile, fetuses with an NT of ≥99th percentile were >5 times as likely to have a CCHD (1.3% vs 0.2%; relative risk, 5.66; 95% confidence interval, 3.19-10.04) and fetuses with an NT measurement ≥3.5 mm were >12 times as likely to have a CCHD (2.8% vs 0.2%; relative risk, 12.28; 95% confidence interval, 5.11-29.51). NT ≥99th percentile had a sensitivity of 5.8% and a specificity of 98.9% for the detection of CCHDs compared with 2.6% and 99.8% for NT ≥3.5 mm. Results show that NT measurements of ≥99th percentile and ≥3.5 mm are not equivalent and that substantial risk for CCHD extends to the less restrictive ≥99th percentile cutpoint. Data suggest that the use of this cutpoint compared with the current standard could double the number of CCHDs that are identified based on NT risk. Copyright © 2014 Elsevier Inc. All rights reserved.
    American journal of obstetrics and gynecology. 10/2014;
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    ABSTRACT: To evaluate associations between traffic-related air pollution during pregnancy and preterm birth in births in four counties in California during years 2000 to 2006. We used logistic regression to examine the association between the highest quartile of ambient air pollutants (carbon monoxide, nitrogen dioxide, particulate matter <10 and 2.5 μm) and traffic density during pregnancy and each of five levels of prematurity based on gestational age at birth (20-23, 24-27, 28-31, 32-33, and 34-36 weeks) versus term (37-42 weeks). We examined trimester averages and the last month and the last 6 weeks of pregnancy. Models were adjusted for birthweight, maternal age, race/ethnicity, education, prenatal care, and birth costs payment. Neighborhood socioeconomic status (SES) was evaluated as a potential effect modifier. There were increased odds ratios (ORs) for early preterm birth for those exposed to the highest quartile of each pollutant during the second trimester and the end of pregnancy (adjusted OR, 1.4-2.8). Associations were stronger among mothers living in low SES neighborhoods (adjusted OR, 2.1-4.3). We observed exposure-response associations for multiple pollutant exposures and early preterm birth. Inverse associations during the first trimester were observed. The results confirm associations between traffic-related air pollution and prematurity, particularly among very early preterm births and low SES neighborhoods. Copyright © 2014 Elsevier Inc. All rights reserved.
    Annals of epidemiology. 10/2014; 24(12):888-895.e4.
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    ABSTRACT: Preterm birth is an important marker of health and has a prevalence of 12-13% in the U.S. Polycyclic aromatic hydrocarbons (PAHs) are a group of organic contaminants that form during the incomplete combustion of hydrocarbons, such as coal, diesel and gasoline. Studies suggest that exposure to PAHs during pregnancy is related to adverse birth outcomes. The aim of this study is to evaluate the association between exposure to PAHs during the pregnancy and preterm birth.
    Environmental research. 10/2014; 135C:221-226.
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    ABSTRACT: Pesticide exposures are ubiquitous and of substantial public concern. We examined the potential association of congenital heart defects with residential proximity to commercial agricultural pesticide applications in the San Joaquin Valley, California.
    Environmental research. 09/2014; 135C:133-138.
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    ABSTRACT: Background: Adverse associations between maternal pesticide exposure and neural tube defects (NTDs) have been suggested but not consistently observed. This study used data from the multisite National Birth Defects Prevention Study to examine associations between maternal periconceptional (1 month preconception through 2 months postconception) occupational pesticide exposure and NTDs. Methods: Mothers of 502 NTD cases and 2950 unaffected live-born control infants with estimated delivery dates from 1997 through 2002 were included. Duration, categorical intensity scores, and categorical frequency scores for pesticide classes (e.g., insecticides) were assigned using a modified, literature-based job-exposure matrix and maternal-reported occupational histories. Adjusted odds ratios (aORs) and 95% confidence intervals were estimated based on fitted multivariable logistic regression models that described associations between maternal periconceptional occupational pesticide exposure and NTDs. The aORs were estimated for pesticide exposure (any [yes/no] and cumulative exposure [intensity × frequency × duration] to any pesticide class, each pesticide class, or combination of pesticide classes) and all NTD cases combined and NTD subtypes. Results: Positive, but marginally significant or nonsignificant, aORs were observed for exposure to insecticides + herbicides for all NTD cases combined and for spina bifida alone. Similarly, positive aORs were observed for any exposure and cumulative exposure to insecticides + herbicides + fungicides and anencephaly alone and encephalocele alone. All other aORs were near unity. Conclusion: Pesticide exposure associations varied by NTD subtype and pesticide class. Several aORs were increased, but not significantly. Future work should continue to examine associations between pesticide classes and NTD subtypes using a detailed occupational pesticide exposure assessment and examine pesticide exposures outside the workplace. Birth Defects Research (Part A), 2014. © 2014 Wiley Periodicals, Inc.
    Birth Defects Research Part A Clinical and Molecular Teratology 08/2014; · 2.27 Impact Factor
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    ABSTRACT: Background It has been observed in several studies that infants with anotia/microtia are more common among Hispanics compared with other racial/ethnic groups. We examined the association between selected Hispanic ethnicity and acculturation factors and anotia/microtia in the National Birth Defects Prevention Study.Methods We examined data from mothers of 351 infants with isolated anotia/microtia and 8435 unaffected infants from the National Birth Defects Prevention Study with an expected delivery date from 1997 to 2007. Sociodemographic, maternal, and acculturation factors (e.g., age, maternal education, household income, body mass index, gestational diabetes, folic acid, smoking, alcohol intake, study center, parental birthplace, and years lived in the United States, maternal language) were assessed as overall risk factors and also as risk factors among subgroups of Hispanics (United States- and foreign-born) versus non-Hispanic whites.ResultsCompared with non-Hispanic whites, both United States- and foreign-born Hispanic mothers demonstrated substantially higher odds of delivering infants with anotia/microtia across nearly all strata of sociodemographic and other maternal factors (adjusted odds ratios range: 2.1–11.9). The odds of anotia/microtia was particularly elevated among Hispanic mothers who emigrated from Mexico after age five (adjusted odds ratios = 4.88; 95% confidence interval = 2.93–8.11) or who conducted the interview in Spanish (adjusted odds ratios = 4.97; 95% confidence interval = 3.00–8.24).Conclusion We observed that certain sociodemographic and acculturation factors are associated with higher risks of anotia/microtia among offspring of Hispanic mothers. Birth Defects Research (Part A), 2014. © 2014 Wiley Periodicals, Inc.
    Birth Defects Research Part A Clinical and Molecular Teratology 07/2014; · 2.27 Impact Factor
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    ABSTRACT: We used exome sequencing to study a non-consanguineous family with two children who had anterior segment dysgenesis, sclerocornea, microphthalmia, hypotonia and developmental delays. Sanger sequencing verified two Peroxidasin (PXDN) mutations in both sibs-a maternally inherited, nonsense mutation, c.1021C>T predicting p.(Arg341*), and a paternally inherited, 23-basepair deletion causing a frameshift and premature protein truncation, c.2375_2397del23, predicting p.(Leu792Hisfs*67). We re-examined exome data from 20 other patients with structural eye defects and identified two additional PXDN mutations in a sporadic male with bilateral microphthalmia, cataracts and anterior segment dysgenesis-a maternally inherited, frameshift mutation, c.1192delT, predicting p.(Tyr398Thrfs*40) and a paternally inherited, missense substitution that was predicted to be deleterious, c.947 A>C, predicting p.(Gln316Pro). Mutations in PXDN were previously reported in three families with congenital cataracts, microcornea, sclerocornea and developmental glaucoma. The gene is expressed in corneal epithelium and is secreted into the extracellular matrix. Defective peroxidasin has been shown to impair sulfilimine bond formation in collagen IV, a constituent of the basement membrane, implying that the eye defects result because of loss of basement membrane integrity in the developing eye. Our finding of a broader phenotype than previously appreciated for PXDN mutations is typical for exome-sequencing studies, which have proven to be highly effective for mutation detection in patients with atypical presentations. We conclude that PXDN sequencing should be considered in microphthalmia with anterior segment dysgenesis.European Journal of Human Genetics advance online publication, 18 June 2014; doi:10.1038/ejhg.2014.119.
    European journal of human genetics: EJHG 06/2014; · 3.56 Impact Factor
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    ABSTRACT: To examine the association between increased first trimester fetal nuchal translucency (NT) measurement and major non-cardiac structural birth defects in euploid infants.
    American journal of obstetrics and gynecology. 06/2014;
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    ABSTRACT: Background: Prevalence of gastroschisis has inexplicably been increasing over the past few decades. Our intent was to explore whether early gestational exposures to pesticides were associated with risk of gastroschisis. Methods: We used population-based data, accompanied by detailed information from maternal interviews as well as information on residential proximity to a large number of commercial pesticide applications during early pregnancy. The study population derived from the San Joaquin Valley of California (). Cases were 156 infants/fetuses with gastroschisis and controls were 785 infants without birth defects. Results: Among 22 chemical pesticide groups analyzed, none had an elevated odds ratio with an associated confidence interval that excluded 1.0, although exposure to the triazine group showed borderline significance. Among 36 specific pesticide chemicals analyzed, only exposure to petroleum distillates was associated with an elevated risk, odds ratio = 2.5 (1.1-5.6). In general, a substantially different inference was not derived when analyses were stratified by maternal age or when risk estimation included adjustment for race/ethnicity, body mass index, folic acid supplement use, and smoking. Conclusion: Our study rigorously adds to the scant literature on this topic. Our a priori expectation was that we would observe certain pesticide compounds to be particularly associated with young age owing to the disproportionate risk observed for young women to have offspring with gastroschisis. We did not observe an exposure profile unique to young women. Birth Defects Research (Part A), 2014. © 2014 Wiley Periodicals, Inc.
    Birth Defects Research Part A Clinical and Molecular Teratology 06/2014; · 2.27 Impact Factor
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    ABSTRACT: While some of the highest maternal exposures to polycyclic aromatic hydrocarbons (PAHs) occur in the workplace, there is only one previous study of occupational PAH exposure and adverse pregnancy outcomes. We sought to extend this literature using interview data combined with detailed exposure assessment.
    Occupational and environmental medicine. 06/2014;
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    ABSTRACT: Background Findings from studies examining risk of preterm birth associated with elevated prepregnancy body mass index (BMI) have been inconsistent.Methods Within a large population-based cohort, we explored associations between prepregnancy BMI and spontaneous preterm birth across a spectrum of BMI, gestational age, and racial/ethnic categories. We analysed data for 989 687 singleton births in California, 2007–09. Preterm birth was grouped as 20–23, 24–27, 28–31, or 32–36 weeks gestation (compared with 37–41 weeks). BMI was categorised as <18.5 (underweight); 18.5–24.9 (normal); 25.0–29.9 (overweight); 30.0–34.9 (obese I); 35.0–39.9 (obese II); and ≥40.0 (obese III). We assessed associations between BMI and spontaneous preterm birth of varying severity among non-Hispanic White, Hispanic, and non-Hispanic Black women.ResultsAnalyses of mothers without hypertension and diabetes, adjusted for age, education, height, and prenatal care initiation, showed obesity categories I–III to be associated with increased risk of spontaneous preterm birth at 20–23 and 24–27 weeks among those of parity 1 in each race/ethnic group. Relative risks for obese III and preterm birth at 20–23 weeks were 6.29 [95% confidence interval (CI) 3.06, 12.9], 4.34 [95% CI 2.30, 8.16], and 4.45 [95% CI 2.53, 7.82] for non-Hispanic Whites, non-Hispanic Blacks, and Hispanics, respectively. A similar, but lower risk, pattern was observed for women of parity ≥2 and preterm birth at 20–23 weeks. Underweight was associated with modest risks for preterm birth at ≥24 weeks among women in each racial/ethnic group regardless of parity.Conclusions The association between women's prepregnancy BMI and risk of spontaneous preterm birth is complex and is influenced by race/ethnicity, gestational age, and parity.
    Paediatric and Perinatal Epidemiology 06/2014; · 2.16 Impact Factor
  • American Journal of Medical Genetics Part A 06/2014; · 2.30 Impact Factor
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    ABSTRACT: The objective of the study was to determine whether pregnancies resulting in early preterm birth (PTB) (<30 weeks) were more likely than term pregnancies to have elevated midtrimester serum tumor necrosis factor alpha (TNF-α) levels combined with lipid patterns suggestive of hyperlipidemia. In 2 nested case-control samples drawn from California and Iowa cohorts, we examined the frequency of elevated midpregnancy serum TNF-α levels (in the fourth quartile [4Q]) and lipid patterns suggestive of hyperlipidemia (eg, total cholesterol, low-density-lipoproteins, or triglycerides in the 4Q, high-density lipoproteins in the first quartile) (considered independently and by co-occurrence) in pregnancies resulting in early PTB compared with those resulting in term birth (n = 108 in California and n = 734 in Iowa). Odds ratios (ORs) and 95% confidence intervals (CIs) estimated in logistic regression models were used for comparisons. Early preterm pregnancies were 2-4 times more likely than term pregnancies to have a TNF-α level in the 4Q co-occurring with indicators of hyperlipidemia (37.5% vs 13.9% in the California sample (adjusted OR, 4.0; 95% CI, 1.1-16.3) and 26.3% vs 14.9% in the Iowa sample (adjusted OR, 2.7; 95% CI, 1.1-6.3). No differences between early preterm and term pregnancies were observed when TNF-α or target lipid abnormalities occurred in isolation. Observed differences were not explicable to any maternal or infant characteristics. Pregnancies resulting in early PTB were more likely than term pregnancies to have elevated midpregnancy TNF-α levels in combination with lipid patterns suggestive of hyperlipidemia.
    American journal of obstetrics and gynecology 05/2014; · 3.28 Impact Factor
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    Pediatric Academic Societies Annual Meeting; 05/2014
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    ABSTRACT: Background We examined the association of maternal stressful life events and social support with risks of birth defects using National Birth Defects Prevention Study data, a population-based case–control study.Methods We examined seven stressful life events and three social support questions applicable to the periconceptional period, among mothers of 552 cases with neural tube defects (NTDs), 413 cleft palate (CP), 797 cleft lip ± cleft palate (CLP), 189 d-transposition of the great arteries (dTGA), 311 tetralogy of Fallot (TOF), and 2974 non-malformed controls. A stressful life events index equalled the sum of ‘yes’ responses to the seven questions. Social support questions were also summed to form an index. Data were analyzed using logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI), adjusted for maternal race-ethnicity, age, education, body mass index, smoking, drinking, and intake of vitamin supplements.ResultsAssociations with the stress index tended to be higher with higher scores, but few 95% CIs excluded one. A four-point increase in the index was moderately associated with NTDs (OR 1.5, [95% CI 1.1, 2.0]) and CLP (OR 1.3, [95% CI 1.0, 1.7]). The social support index tended to be associated with reduced risk but most 95% CIs included one, with the exception of dTGA (OR for a score of 3 vs 0 was 0.5 [95% CI 0.3, 0.8]).Conclusions Maternal periconceptional stressful life events, social support, and the two factors in combination were at most modestly, if at all, associated with risks of the studied birth defects.
    Paediatric and Perinatal Epidemiology 05/2014; · 2.16 Impact Factor
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    ABSTRACT: Epidemiologic literature suggests exposure to air pollutants is associated with fetal development. To investigate maternal exposures to air pollutants during weeks two through eight of pregnancy and congenital heart defects. Mothers from the National Birth Defects Prevention Study, a nine-state case-control study, were assigned one-week and seven-week averages of daily maximum concentrations of carbon monoxide, nitrogen dioxide, ozone, and sulfur dioxide and 24-hour measurements of fine and coarse particulate matter using the closest air monitor within 50 km to their residence during early pregnancy. Depending upon the pollutant, a maximum of 4632 live-birth controls and 3328 live-birth, fetal-death or electively terminated cases had exposure data. Hierarchical regression models, adjusted for maternal demographics, tobacco and alcohol use, were constructed. Principal component analysis was used to assess these relationships in a multipollutant context. Positive associations were observed between exposure to nitrogen dioxide and coarctation of the aorta and pulmonary valve stenosis. Exposure to fine particulate matter was positively associated with hypoplastic left heart syndrome but inversely associated with atrial septal defects. Examining individual exposure-weeks suggested associations between pollutants and defects that were not observed using the seven-week average. Associations between left ventricular outflow tract obstructions and nitrogen dioxide and hypoplastic left heart syndrome and particulate matter were supported by findings from the multipollutant analyses, although estimates were attenuated at the highest exposure levels. Utilizing daily maximum pollutant levels and exploring individual exposure-weeks revealed some positive associations between certain pollutants and defects and suggested potential windows of susceptibility during pregnancy.
    Environmental Health Perspectives 04/2014; · 7.26 Impact Factor

Publication Stats

8k Citations
1,126.34 Total Impact Points

Institutions

  • 2014
    • University of Utah
      • Department of Pediatrics
      Salt Lake City, Utah, United States
  • 2009–2014
    • Stanford Medicine
      • • Division of Neonatal and Developmental Medicine
      • • Department of Pediatrics
      Stanford, California, United States
    • Stanford University
      • • Department of Pediatrics
      • • Division of Neonatal and Developmental Medicine
      Palo Alto, California, United States
    • University of Minnesota Twin Cities
      • Division of Biostatistics
      Minneapolis, MN, United States
    • Children’s Heart Institute
      Leesburg, Virginia, United States
  • 2012–2013
    • University of Texas at Austin
      • Division of Nutritional Sciences
      Austin, Texas, United States
    • University of Arkansas for Medical Sciences
      • Department of Pediatrics
      Little Rock, AR, United States
    • University of Iowa
      • Department of Pediatrics
      Iowa City, IA, United States
  • 2008–2013
    • University of California, San Francisco
      • • Department of Epidemiology and Biostatistics
      • • Division of Pediatric Surgery
      San Francisco, CA, United States
  • 2006–2013
    • Children's Hospital & Research Center Oakland
      Oakland, California, United States
    • Radboud University Nijmegen
      • Laboratory of Pediatrics and Neurology
      Nijmegen, Provincie Gelderland, Netherlands
  • 2009–2012
    • Texas Department of State Health Services
      Austin, Texas, United States
  • 2006–2012
    • California Department of Public Health
      • Genetic Disease Screening Program
      Richmond, California, United States
  • 2005–2012
    • University of Texas Health Science Center at Houston
      • • Division of Epidemiology, Human Genetics and Environmental Sciences
      • • Human Genetics Center
      Houston, TX, United States
    • Children's Hospital Central California
      Madera, California, United States
    • Cedars-Sinai Medical Center
      • Medical Genetics Institute
      Los Angeles, CA, United States
  • 2002–2012
    • Texas A&M University System Health Science Center
      • Institute of Biosciences and Technology
      Bryan, TX, United States
  • 1996–2012
    • Centers for Disease Control and Prevention
      • • National Center on Birth Defects and Developmental Disabilities
      • • Division of Birth Defects and Developmental Disabilities
      • • National Center for Environmental Health
      Atlanta, MI, United States
  • 2008–2011
    • National Institutes of Health
      • Division of Epidemiology, Statistics and Prevention Research (DESPR)
      Bethesda, MD, United States
  • 2005–2011
    • University of North Carolina at Chapel Hill
      • Department of Epidemiology
      Chapel Hill, NC, United States
  • 2010
    • Children's Hospital Los Angeles
      Los Angeles, California, United States
    • Baylor College of Medicine
      Houston, Texas, United States
  • 2004–2010
    • Children's Hospital Oakland Research Institute
      Oakland, California, United States
  • 1990–2010
    • March of Dimes Foundation
      White Plains, New York, United States
  • 1996–2009
    • University of California, Berkeley
      • School of Public Health
      Berkeley, CA, United States
  • 2007
    • University of Houston
      Houston, Texas, United States
    • Harbor-UCLA Medical Center
      • Department of Emergency Medicine
      Torrance, CA, United States
    • CSU Mentor
      Long Beach, California, United States
  • 2002–2006
    • University of California, Los Angeles
      • Department of Epidemiology
      Los Angeles, CA, United States
  • 1998–2006
    • Texas A&M University
      • Center for Environmental and Rural Health
      College Station, TX, United States
  • 2003–2005
    • State of California
      California City, California, United States
  • 1993
    • Battelle Memorial Institute
      Columbus, Ohio, United States
  • 1991
    • California Department of Health Care Services
      Sacramento, California, United States