Gary M Shaw

Stanford Medicine, Stanford, California, United States

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Publications (389)1386.68 Total impact

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    ABSTRACT: An inter-alpha-trypsin inhibitor heavy chain 4 (ITIH4) peptide (QLGLPGPPDVPDHAAYHPF) was previously identified as a preterm birth biomarker from a predominantly (∼75%) African-American cohort. Because there is a single nucleotide polymorphism (SNP) at position 669 of interalpha-trypsin inhibitor heavy chain 4 (ITIH4), we hypothesized that the "L" peptide isoform (LLGLPGPPDVPDHAAYHPF) would be found in the sera of patients of different ethnic backgrounds and that reduction of the "L" isoform serum abundance would also be associated with human preterm birth (<37 weeks gestation), similar to the reported "Q" isoform. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) profiling of term pregnancies (n=14) identified the "L" isoform peptide, which remained largely unchanged throughout gestation. Subsequent quantitative proteomics based on stable isotope dilution (SID) quantified the ITIH4 "L" isoform peptide serum abundance in a cohort of uncomplicated term pregnancies (n=14) and pregnancies complicated by preterm birth (n=11) subjects.Our results showed that the reduction of the "L" peptide's serum quantity is associated with the clinical state of preterm birth (p value < 0.001). We concluded that the "L" ITIH4 peptide is a potential biomarker predictive of preterm birth and the validation of the L isoform in a prospective series of pregnancies should be performed.
    Journal of Genetics and Genomics 06/2015; DOI:10.1016/j.jgg.2015.06.001 · 2.92 Impact Factor
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    ABSTRACT: The National Birth Defects Prevention Study (NBDPS) is a large population-based multicenter case-control study of major birth defects in the United States. Data collection took place from 1998 through 2013 on pregnancies ending between October 1997 and December 2011. Cases could be live born, stillborn, or induced terminations, and were identified from birth defects surveillance programs in Arkansas, California, Georgia, Iowa, Massachusetts, New Jersey, New York, North Carolina, Texas, and Utah. Controls were live born infants without major birth defects identified from the same geographical regions and time periods as cases by means of either vital records or birth hospitals. Computer-assisted telephone interviews were completed with women between 6 weeks and 24 months after the estimated date of delivery. After completion of interviews, families received buccal cell collection kits for the mother, father, and infant (if living). There were 47,832 eligible cases and 18,272 eligible controls. Among these, 32,187 (67%) and 11,814 (65%), respectively, provided interview information about their pregnancies. Buccal cell collection kits with a cytobrush for at least one family member were returned by 19,065 case and 6,211 control families (65% and 59% of those who were sent a kit). More than 500 projects have been proposed by the collaborators and over 200 manuscripts published using data from the NBDPS through December 2014. The NBDPS has made substantial contributions to the field of birth defects epidemiology through its rigorous design, including case classification, detailed questionnaire and specimen collection, large study population, and collaborative activities across Centers. Birth Defects Research (Part A), 2015. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.
    Birth Defects Research Part A Clinical and Molecular Teratology 06/2015; DOI:10.1002/bdra.23384 · 2.21 Impact Factor
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    ABSTRACT: Bronchopulmonary dysplasia (BPD) has a strong heritable component yet large-scale genome-wide association studies for common variants have not revealed its genetic basis. Given the historical high mortality rate of extremely preterm infants who now survive and develop BPD, we hypothesized that risk loci underlying this disease are under severe purifying selection during evolution and that rare variants may explain greater risk of the disease. We performed exome-sequencing on 50 BPD affected and unaffected twin pairs using DNA isolated from neonatal blood spots, and identified genes affected by extremely rare nonsynonymous mutations. Functional genomic approaches were then employed to systematically compare these affected genes between cases and controls. We identified 258 genes with rare nonsynonymous mutations in BPD patients. These genes were highly enriched for processes that are expected to be involved in pulmonary structure and function including collagen fibril organization, morphogenesis of embryonic epithelium and regulation of Wnt signaling pathway, displayed significantly elevated expression in fetal and adult lungs, and were substantially up-regulated in a murine model of BPD. Analyses of mouse mutants revealed their phenotypic enrichment for embryonic development and the cyanosis phenotype, a clinical manifestation of BPD. Our study supports the role of rare variants in BPD and is the first to sequence BPD exomes from newborn blood spot samples and identify with high confidence genes implicated in BPD thereby providing important insights into its biology and molecular etiology.
    American Journal of Respiratory and Critical Care Medicine 06/2015; DOI:10.1164/rccm.201501-0168OC · 11.99 Impact Factor
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    ABSTRACT: Background The National Birth Defects Prevention Study (NBDPS) contains a wealth of information on affected and unaffected family triads, and thus provides numerous opportunities to study gene–environment interactions (G×E) in the etiology of birth defect outcomes. Depending on the research objective, several analytic options exist to estimate G×E effects that use varying combinations of individuals drawn from available triads.Methods In this study, we discuss important considerations in the collection of genetic data and environmental exposures.ResultsWe will also present several population- and family-based approaches that can be applied to data from the NBDPS including case–control, case-only, family-based trio, and maternal versus fetal effects. For each, we describe the data requirements, applicable statistical methods, advantages, and disadvantages.ConclusionA range of approaches can be used to evaluate potentially important G×E effects in the NBDPS. Investigators should be aware of the limitations inherent to each approach when choosing a study design and interpreting results. Birth Defects Research (Part A), 2015. © 2015 Wiley Periodicals, Inc.
    Birth Defects Research Part A Clinical and Molecular Teratology 05/2015; DOI:10.1002/bdra.23382 · 2.21 Impact Factor
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    ABSTRACT: http://onlinelibrary.wiley.com/enhanced/doi/10.1002/bdra.23385/ Birth defects are a major cause of morbidity and mortality worldwide. There has been much progress in understanding the genetic basis of familial and syndromic forms of birth defects. However, the etiology of nonsydromic birth defects is not well-understood. Although there is still much work to be done, we have many of the tools needed to accomplish the task. Advances in next-generation sequencing have introduced a sea of possibilities, from disease-gene discovery to clinical screening and diagnosis. These advances have been fruitful in identifying a host of candidate disease genes, spanning the spectrum of birth defects. With the advent of CRISPR-Cas9 gene editing, researchers now have a precise tool for characterizing this genetic variation in model systems. Work in model organisms has also illustrated the importance of epigenetics in human development and birth defects etiology. Here we review past and current knowledge in birth defects genetics. We describe genotyping and sequencing methods for the detection and analysis of rare and common variants. We remark on the utility of model organisms and explore epigenetics in the context of structural malformation. We conclude by highlighting approaches that may provide insight into the complex genetics of birth defects.
    Birth Defects Research Part A Clinical and Molecular Teratology 05/2015; DOI:10.1002/bdra.23385 · 2.21 Impact Factor
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    ABSTRACT: Background Maternal nutritional status has been recognized as a contributor to conotruncal heart defects, but there is limited understanding of the specific nutrition-related factors involved. In this California case-control study of 296 conotruncal cases and 695 nonmalformed controls we explored whether weight loss during early pregnancy was associated with an increased risk of d-transposition of the great arteries (dTGA) and tetralogy of Fallot (TOF) conotruncal defects.Methods During telephone interviews women were asked whether they were dieting to lose weight or using weight loss remedies during 2 months before or 2 months after conception, and how much weight they gained or lost in the first 2 months of pregnancy or during the year before pregnancy.ResultsOdds ratios for dieting to lose weight and use of weight loss remedies for dTGA and TOF were not substantially elevated and all had confidence intervals that included 1.0. Mothers who had a loss of >5 lbs in the first 2 months of pregnancy as well as mothers who lost and gained >5 lbs in the first 2 months of pregnancy also did not show a significant increased risk of delivering case infants when compared with women with no weight change in the year before pregnancy.Conclusion Given current recommendations about limited weight gain for obese pregnant women, these data indicate that dieting may not substantially increase a fetus' risk of having a conotruncal defect. Birth Defects Research (Part A), 2015. © 2015 Wiley Periodicals, Inc.
    Birth Defects Research Part A Clinical and Molecular Teratology 05/2015; DOI:10.1002/bdra.23381 · 2.21 Impact Factor
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    ABSTRACT: To examine associations with morbidly adherent placenta (MAP) among women with placenta previa. Women with MAP (cases) and previa alone (controls) were identified from a cohort of 236 714 singleton pregnancies with both first and second trimester prenatal screening, and live birth and hospital discharge records; pregnancies with aneuploidies and neural tube or abdominal wall defects were excluded. Logistic binomial regression was used to compare cases with controls. In all, 37 cases with MAP and 699 controls with previa alone were included. Risk for MAP was increased among multiparous women with pregnancy-associated plasma protein-A (PAPP-A) ⩾95th percentile (⩾2.63 multiple of the median (MoM); adjusted OR (aOR) 8.7, 95% confidence interval (CI) 2.8 to 27.4), maternal-serum alpha fetoprotein (MS-AFP) ⩾95th percentile (⩾1.79 MoM; aOR 2.8, 95% CI 1.0 to 8.0), and 1 and ⩾2 prior cesarean deliveries (CDs; aORs 4.4, 95% CI 1.5 to 13.6 and 18.4, 95% CI 5.9 to 57.5, respectively). Elevated PAPP-A, elevated MS-AFP and prior CDs are associated with MAP among women with previa.Journal of Perinatology advance online publication, 30 April 2015; doi:10.1038/jp.2015.40.
    Journal of perinatology: official journal of the California Perinatal Association 04/2015; DOI:10.1038/jp.2015.40 · 2.35 Impact Factor
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    ABSTRACT: Gastroschisis is a birth defect where loops of bowel are protruding from the abdominal wall at birth. Previous research has suggested that gastroschisis cases can occur in clusters. The objective of this study was to identify if there were areas of elevated gastroschisis risk using data from the National Birth Defects Prevention Study (NBDPS), 1997 through 2007. We obtained data on cases (n = 371) through population-based birth defects surveillance systems in Arkansas, California, and Utah; controls (n = 2359) were selected from the same geographic areas as cases. Mothers were interviewed on demographic information and exposures during pregnancy, including residential history. We used first trimester maternal addresses and generalized additive models to create a continuous map surface of odds ratios (OR) by smoothing over latitude and longitude. Permutation tests were used to assess whether location of maternal residence was important and identify locations with statistically significant ORs. In Arkansas, adjusted ORs in the southwest corner were 2.0 and the global deviance was not statistically significant (p-value: 0.57). Adjusted ORs for California indicated areas of increased risk with ORs 1.3 (p-value: 0.34). In Utah, the adjusted ORs were elevated (OR: 2.4) in the south-eastern corner of the study area (p-value: 0.34). The results of this study, while not statistically significant, suggest there were spatial variations in gastroschisis births. We cannot rule out that these variations were due to edge effects or residual confounding. Birth Defects Research (Part A), 2015. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.
    Birth Defects Research Part A Clinical and Molecular Teratology 04/2015; 103(6). DOI:10.1002/bdra.23375 · 2.21 Impact Factor
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    ABSTRACT: We sought to identify age group specific maternal risk factors for gastroschisis. Maternal characteristics and prenatal factors were compared for 1,279 live born infants with gastroschisis and 3,069,678 without. Data were obtained using the California database containing linked hospital discharge, birth certificate and death records from 1 year prior to the birth to 1 year after the birth. Backwards-stepwise logistic regression models were used with maternal factors where initial inclusion was determined by a threshold of p < 0.10 on initial crude analyses. Due to the strong association of gastroschisis with young maternal age, models were stratified by age groups and odds ratios were calculated. These final models identified maternal infection as the only risk factor common to all age groups and a protective effect of obesity and gestational hypertension. In addition, age specific risk factors were identified. Although gestation at the time of infection was not available, a sexually transmitted disease complicating pregnancy was associated with increased risk in the less than 20 years of age grouping whereas viral infection was associated with increased risk only in the 20-24 and more than 24 years of age groupings. Urinary tract infection remained in the final logistic model for women less than 20 years. Short interpregnancy interval was not found to be a risk factor for any age group. Our findings support the need to explore maternal infection by type and gestational timing. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.
    American Journal of Medical Genetics Part A 04/2015; DOI:10.1002/ajmg.a.37016 · 2.05 Impact Factor
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    ABSTRACT: Right-sided and left-sided obstructive heart defects (OHDs) are subtypes of congenital heart defects, in which the heart valves, arteries, or veins are abnormally narrow or blocked. Previous studies have suggested that the development of OHDs involved a complex interplay between genetic variants and maternal factors. Using the data from 569 OHD case families and 1,644 control families enrolled in the National Birth Defects Prevention Study (NBDPS) between 1997 and 2008, we conducted an analysis to investigate the genetic effects of 877 single nucleotide polymorphisms (SNPs) in 60 candidate genes for association with the risk of OHDs, and their interactions with maternal use of folic acid supplements, and pre-pregnancy obesity. Applying log-linear models based on the hybrid design, we identified a SNP in methylenetetrahydrofolate reductase (MTHFR) gene (C677T polymorphism) with a main genetic effect on the occurrence of OHDs. In addition, multiple SNPs in betaine-homocysteine methyltransferase (BHMT and BHMT2) were also identified to be associated with the occurrence of OHDs through significant main infant genetic effects and interaction effects with maternal use of folic acid supplements. We also identified multiple SNPs in glutamate-cysteine ligase, catalytic subunit (GCLC) and DNA (cytosine-5-)-methyltransferase 3 beta (DNMT3B) that were associated with elevated risk of OHDs among obese women. Our findings suggested that the risk of OHDs was closely related to a combined effect of variations in genes in the folate, homocysteine, or glutathione/transsulfuration pathways, maternal use of folic acid supplements and pre-pregnancy obesity. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.
    American Journal of Medical Genetics Part A 04/2015; 167(6). DOI:10.1002/ajmg.a.36867 · 2.05 Impact Factor
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    ABSTRACT: Despite years of research, the etiologies of preterm birth remain unclear. In order to help generate new research hypotheses, this study explored spatial and temporal patterns of preterm birth in a large, total-population dataset. Data on 145 million U.S. births in 3,000 counties from the Natality Files of the National Center for Health Statistics for 1971-2011 were examined. State trends in early (<34 weeks) and late (34-36 weeks) preterm birth rates were compared. K-means cluster analyses were conducted to identify gestational age distribution patterns for all US counties over time. A weak association was observed between state trends in <34 weeks birth rates and the initial absolute <34 weeks birth rate. Significant associations were observed between trends in <34 weeks and 34-36 weeks birth rates and between white and African American <34 weeks births. Periodicity was observed in county-level trends in <34 weeks birth rates. Cluster analyses identified periods of significant heterogeneity and homogeneity in gestational age distributional trends for U.S. counties. The observed geographic and temporal patterns suggest periodicity and complex, shared influences among preterm birth rates in the United States. These patterns could provide insight into promising hypotheses for further research.Pediatric Research (2015); doi:10.1038/pr.2015.55.
    Pediatric Research 03/2015; 77(6). DOI:10.1038/pr.2015.55 · 2.84 Impact Factor
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    ABSTRACT: Objective Preterm birth (PTB) is the leading cause of neonatal morbidity and mortality. Short stature and obesity have each been associated with increased risk for PTB. However, the effect of short height on PTB risk, across BMI categories has not been studied. Our objective was to determine the influence of maternal height on the risk for PTB within BMI categories. Study Design Included for analysis were California singleton, live births between 2007-2010, linked to hospital discharge data. Maternal height was categorized into quintiles. Pre-pregnancy BMI was categorized as normal (18.5-24.9); overweight (25.0-29.9) or obese (≥30.0). Poisson regression models were used to estimate odds ratios for the association between maternal height and risk of PTB (less than 37 weeks) for each category, with the middle quintile serving as reference. Models were further stratified by maternal age, parity, race/ethnicity, education and prenatal care. Results Short stature (1st height quintile) was found to be associated with increased risk for spontaneous PTB across BMI categories with odds of 1.22 (1.13:1.31), 1.20 (1.06,1.35) and 1.17 (1.03,1.33) for normal, overweight and obese categories, respectively. Tall stature (5th quintile) was associated with reduced risk for spontaneous PTB with odds of 0.83 (0.78,0.89), 0.81 (0.73,0.91) and 0.85 (0.75,0.97) for normal, overweight and obese categories, respectively. Patterns of association were similar after stratification by maternal age, parity, race/ethnicity, education and prenatal care. Conclusion While maternal height is a component of the BMI calculation, we found that maternal stature is associated with risk for spontaneous PTB across different BMI categories. Identifying different risk profiles based on maternal anthropometric measures are important for directing intervention efforts for reducing PTB.
    SMFM; 02/2015
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    ABSTRACT: First, create a clinical severity score for patients with chronic lung disease of infancy (CLDi) following neonatal intensive care unit (NICU) stay. Second, using California wide population-based data, identify factors associated with clinical severity of CLDi at 4-9 months corrected gestational age (CGA). Pediatric pulmonologists ranked and weighted eight factors reflecting clinical severity of CLDi. Utilizing these data we scored and assigned these to 4-9 month old CGA moderate/severe bronchopulmonary dysplasia (BPD) infants, born<30 weeks gestational age (GA), within the California High Risk Infant Follow up (HRIF) program. Infants were studied relative to factors from the California Perinatal Quality Care Collaborative (CPQCC). We received survey responses from 43/88 pediatric pulmonologists from 28/53 North American training centers who are experts in CLDi. Strong agreement between ranking (72-100%) of respiratory system parameters and weighting (out of 100 points weighting was within 20 points) was observed with severity of CLDi. Data from 940 CLDi premature infants <30 weeks GA were obtained. Infants with severe CLDi scores at 4-9 months CGA (relative to a zero score) showed positive associations with being male, odds ratio[OR] = 2.45[confidence interval (CI) 1.26-4.77]), >30 ventilator days, OR = 3.82 (1.30-11.2), postnatal steroids OR = 3.94 (1.94-7.84), and a surprising inverse association with retinopathy of prematurity stage 3-4, OR = 0.24 (0.09-0.67) CONCLUSIONS: The CLDi clinical severity score allowed for standardized assessment of pulmonary morbidity, and evaluation of risk factors in the NICU for CLDi following NICU discharge. These observations point to risk factors associated with CLDi outcomes at 4-9 months CGA. Pediatr Pulmonol. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.
    Pediatric Pulmonology 02/2015; DOI:10.1002/ppul.23148 · 2.30 Impact Factor
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    ABSTRACT: Bronchopulmonary dysplasia (BPD) remains a serious morbidity in very low-birth-weight (VLBW) infants (<1500 g). Deregionalization of neonatal care has resulted in an increasing number of VLBW infants treated in community hospitals with unknown impact on the development of BPD. To identify individual risk factors for BPD development and hospital variation of BPD rates across all levels of neonatal intensive care units (NICUs) within the California Perinatal Quality Care Collaborative. Retrospective cohort study (January 2007 to December 2011) from the California Perinatal Quality Care Collaborative including more than 90% of California's NICUs. Eligible VLBW infants born between 22 to 29 weeks' gestational age. Varying levels of intensive care. Bronchopulmonary dysplasia was defined as continuous supplemental oxygen use at 36 weeks' postmenstrual age. A combined outcome of BPD or mortality prior to 36 weeks was used. Multivariable logistic regression accounting for hospital as a random effect and gestational age as a risk factor was used to assess individual risk factors for BPD. This model was applied to determine risk-adjusted rates of BPD across hospitals and assess associations between levels of care and BPD rates. The study cohort included 15 779 infants, of which 1534 infants died prior to 36 weeks' postmenstrual age. A total of 7081 infants, or 44.8%, met the primary outcome of BPD or death prior to 36 weeks. Combined BPD or death rates across 116 NICUs varied from 17.7% to 73.4% (interquartile range, 38.7%-54.1%). Compared with level IV NICUs, the risk for developing BPD was higher for level II NICUs (odds ratio, 1.23; 95% CI, 1.02-1.49) and similar for level III NICUs (odds ratio, 1.04; 95% CI, 0.95-1.14). Bronchopulmonary dysplasia or death prior to 36 weeks' postmenstrual age affects approximately 45% of VLBW infants across California. The wide variability in BPD occurrence across hospitals could offer insights into potential risk or preventive factors. Additionally, our findings suggest that increased regionalization of NICU care may reduce BPD among VLBW infants.
    JAMA Pediatrics 02/2015; 169(2):e143676. DOI:10.1001/jamapediatrics.2014.3676 · 4.25 Impact Factor
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    ABSTRACT: Approximately 6.3 million live births and fetal deaths occurred during the ascertainment period in the California Birth Defects Monitoring Program registry. American-Indian and non-Hispanic white women delivered 40,268 and 2,044,118 births, respectively. While much information has been published about non-Hispanic white infants, little is known regarding the risks of birth defects among infants born to American-Indian women. This study used data from the California Birth Defects Monitoring Program to explore risks of selected birth defects in offspring of American-Indian relative to non-Hispanic white women in California. The study population included all live births and fetal deaths 20 weeks or greater from 1983 to 2010. Prevalence ratios and corresponding 95% confidence intervals (CI) were computed using Poisson regression for 51 groupings of birth defects. Prevalence ratios were estimated for 51 groupings of birth defects. Of the 51, nine had statistically precise results ranging from 0.78 to 1.85. The eight groups with elevated risks for American-Indian births were reduction deformities of brain, anomalies of anterior segments, specified anomalies of ear, ostium secundum type atrial septal defect, specified anomalies of heart, anomalies of the aorta, anomalies of great veins, and cleft lip with cleft palate. Our results suggest that American-Indian women having babies in California may be at higher risk for eight birth defect phenotypes compared with non-Hispanic whites. Further research is needed to determine whether these risks are observed among other populations of American-Indian women or when adjusted for potential covariates. Birth Defects Research (Part A) 103:105-110, 2015 © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.
    Birth Defects Research Part A Clinical and Molecular Teratology 02/2015; 103(2):105-10. DOI:10.1002/bdra.23341 · 2.21 Impact Factor
  • American Journal of Obstetrics and Gynecology 01/2015; 212(1):S292. DOI:10.1016/j.ajog.2014.10.792 · 3.97 Impact Factor
  • American Journal of Obstetrics and Gynecology 01/2015; 212(1):S82. DOI:10.1016/j.ajog.2014.10.177 · 3.97 Impact Factor
  • American Journal of Obstetrics and Gynecology 01/2015; 212(1):S142. DOI:10.1016/j.ajog.2014.10.305 · 3.97 Impact Factor
  • Journal of Investigative Medicine 01/2015; 63(1):176-176. · 1.50 Impact Factor
  • Journal of Investigative Medicine 01/2015; 63(1):177-177. · 1.50 Impact Factor

Publication Stats

10k Citations
1,386.68 Total Impact Points

Institutions

  • 2009–2015
    • Stanford Medicine
      • • Division of Neonatal and Developmental Medicine
      • • Department of Pediatrics
      • • Pediatric Neurology Clinic
      Stanford, California, United States
    • Stanford University
      • Department of Pediatrics
      Palo Alto, California, United States
  • 2012–2013
    • University of Texas at Austin
      • Division of Nutritional Sciences
      Austin, Texas, United States
  • 2005–2009
    • Children's Hospital Oakland Research Institute
      Oakland, California, United States
  • 1996–2009
    • University of California, Berkeley
      • School of Public Health
      Berkeley, California, United States
  • 1995–2009
    • Children's Hospital & Research Center Oakland
      Oakland, California, United States
    • Oakland University
      Рочестер, Michigan, United States
  • 1990–2009
    • March of Dimes Foundation
      White Plains, New York, United States
  • 2008
    • Texas A&M University System Health Science Center
      • Institute of Biosciences and Technology
      Bryan, TX, United States
  • 2007
    • University of Arkansas at Little Rock
      Little Rock, Arkansas, United States
    • Harbor-UCLA Medical Center
      • Department of Emergency Medicine
      Torrance, CA, United States
  • 2002–2006
    • University of California, Los Angeles
      • • Department of Epidemiology
      • • School of Public Health
      Los Angeles, CA, United States
  • 2004
    • University of Nebraska at Omaha
      Omaha, Nebraska, United States
  • 2003
    • Centers for Disease Control and Prevention
      • National Center on Birth Defects and Developmental Disabilities
      Druid Hills, GA, United States
  • 1999
    • Washington State Department of Health
      Olympia, Washington, United States
    • University of Oklahoma Health Sciences Center
      Oklahoma City, Oklahoma, United States
  • 1996–1999
    • Kaiser Permanente
      Oakland, California, United States
  • 1998
    • Texas A&M University
      College Station, Texas, United States
  • 1993
    • Battelle Memorial Institute
      Columbus, Ohio, United States
  • 1991
    • Berkeley Earth
      Washington, Washington, D.C., United States