@article{jima_skaar_planchart_motsinger-reif_cevik_park_cowley_wright_house_liu_et al._2022, title={Genomic map of candidate human imprint control regions: the imprintome}, volume={6}, ISSN={["1559-2308"]}, url={https://doi.org/10.1080/15592294.2022.2091815}, DOI={10.1080/15592294.2022.2091815}, abstractNote={ABSTRACT Imprinted genes – critical for growth, metabolism, and neuronal function – are expressed from one parental allele. Parent-of-origin-dependent CpG methylation regulates this expression at imprint control regions (ICRs). Since ICRs are established before tissue specification, these methylation marks are similar across cell types. Thus, they are attractive for investigating the developmental origins of adult diseases using accessible tissues, but remain unknown. We determined genome-wide candidate ICRs in humans by performing whole-genome bisulphite sequencing (WGBS) of DNA derived from the three germ layers and from gametes. We identified 1,488 hemi-methylated candidate ICRs, including 19 of 25 previously characterized ICRs (https://humanicr.org/). Gamete methylation approached 0% or 100% in 332 ICRs (178 paternally and 154 maternally methylated), supporting parent-of-origin-specific methylation, and 65% were in well-described CTCF-binding or DNaseI hypersensitive regions. This draft of the human imprintome will allow for the systematic determination of the role of early-acquired imprinting dysregulation in the pathogenesis of human diseases and developmental and behavioural disorders.}, journal={EPIGENETICS}, author={Jima, Dereje D. and Skaar, David A. and Planchart, Antonio and Motsinger-Reif, Alison and Cevik, Sebnem E. and Park, Sarah S. and Cowley, Michael and Wright, Fred and House, John and Liu, Andy and et al.}, year={2022}, month={Jun} }
 @article{maguire_house_lloyd_skinner_allen_raffi_skaar_park_mccullough_kollins_et al._2021, title={Associations between maternal obesity, gestational cytokine levels and child obesity in the NEST cohort}, volume={16}, ISSN={["2047-6302"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-85098446153&partnerID=MN8TOARS}, DOI={10.1111/ijpo.12763}, abstractNote={SummaryBackgroundAlthough maternal systemic inflammation is hypothesized to link maternal pre‐pregnancy obesity to offspring metabolic dysfunction, patient empirical data are limited.ObjectivesIn this study, we hypothesized that pre‐pregnancy obesity alters systemic chemo/cytokines concentrations in pregnancy, and this alteration contributes to obesity in children.MethodsIn a multi‐ethnic cohort of 361 mother‐child pairs, we measured prenatal concentrations of plasma TNF‐α, IL‐6, IL‐8, IL‐1β, IL‐4, IFN‐γ, IL‐12 p70 subunit, and IL‐17A using a multiplex ELISA and examined associations of pre‐pregnancy obesity on maternal chemo/cytokine levels, and associations of these cytokine levels with offspring body mass index z score (BMI‐z) at age 2–6 years using linear regression.ResultsAfter adjusting for maternal smoking, ethnicity, age, and education, pre‐pregnancy obesity was associated with increased concentrations of TNF‐α (P = .026) and IFN‐γ (P = .06). While we found no evidence for associations between TNF‐α concentrations and offspring BMI‐z, increased IFN‐γ concentrations were associated with decreased BMI‐z (P = .0002), primarily in Whites (P = .0011). In addition, increased maternal IL‐17A concentrations were associated with increased BMI‐z in offspring (P = .0005) with stronger associations in African Americans (P = .0042) than Whites (P = .24).ConclusionsData from this study are consistent with maternal obesity‐related inflammation during pregnancy, increasing the risk of childhood obesity in an ethnic‐specific manner.}, number={7}, journal={PEDIATRIC OBESITY}, author={Maguire, Rachel L. and House, John S. and Lloyd, Dillon T. and Skinner, Harlyn G. and Allen, Terrence K. and Raffi, Asifa Mohamed and Skaar, David A. and Park, Sarah S. and McCullough, Lauren E. and Kollins, Scott H. and et al.}, year={2021}, month={Jul} }
 @article{martin_jima_sharp_mccullough_park_gowdy_skaar_cowley_maguire_fuemmeler_et al._2019, title={Maternal pre-pregnancy obesity, offspring cord blood DNA methylation, and offspring cardiometabolic health in early childhood: an epigenome-wide association study}, volume={14}, ISSN={["1559-2308"]}, url={https://doi.org/10.1080/15592294.2019.1581594}, DOI={10.1080/15592294.2019.1581594}, abstractNote={ABSTRACT Pre-pregnancy obesity is an established risk factor for adverse sex-specific cardiometabolic health in offspring. Epigenetic alterations, such as in DNA methylation (DNAm), are a hypothesized link; however, sex-specific epigenomic targets remain unclear. Leveraging data from the Newborn Epigenetics Study (NEST) cohort, linear regression models were used to identify CpG sites in cord blood leukocytes associated with pre-pregnancy obesity in 187 mother-female and 173 mother-male offsprings. DNAm in cord blood was measured using the Illumina HumanMethylation450k BeadChip. Replication analysis was conducted among the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort. Associations between pre-pregnancy obesity-associated CpG sites and offspring BMI z-score (BMIz) and blood pressure (BP) percentiles at 4–5-years of age were also examined. Maternal pre-pregnacy obesity was associated with 876 CpGs in female and 293 CpGs in male offspring (false discovery rate <5%). Among female offspring, 57 CpG sites, including the top 18, mapped to the TAPBP gene (range of effect estimates: −0.83% decrease to 4.02% increase in methylation). CpG methylation differences in the TAPBP gene were also observed among males (range of effect estimates: −0.30% decrease to 2.59% increase in methylation). While technically validated, none of the TAPBP CpG sites were replicated in ALSPAC. In NEST, methylation differences at CpG sites of the TAPBP gene were associated with BMI z-score (cg23922433 and cg17621507) and systolic BP percentile (cg06230948) in female and systolic (cg06230948) and diastolic (cg03780271) BP percentile in male offspring. Together, these findings suggest sex-specific effects, which, if causal, may explain observed sex-specific effects of maternal obesity.}, number={4}, journal={EPIGENETICS}, author={Martin, Chantel L. and Jima, Dereje and Sharp, Gemma C. and McCullough, Lauren E. and Park, Sarah S. and Gowdy, Kymberly M. and Skaar, David and Cowley, Michael and Maguire, Rachel L. and Fuemmeler, Bernard and et al.}, year={2019}, month={Apr}, pages={325–340} }
 @article{hoyo_skaar_park_sorrow_2018, title={EPIGENOMICS AND HUMAN OBESITY}, volume={6}, ISBN={["978-0-12-812215-0"]}, DOI={10.1016/B978-0-12-812215-0.00014-5}, abstractNote={Obesity has become one of the most urgent public health problems globally with the steepest increases in prevalence reported among socioeconomically disadvantaged and ethnic minorities. Obesity is associated with sizable reductions in life expectancy and quality of life. Although evidence from model systems supports that epigenetic dysregulation may cause obesity, the affected pathways are still unclear. This chapter summarizes human data on CpG methylation, the most studied epigenetic mechanism in humans, in the context of causal inference, in adults and children. Recent technological advances in the measurement of CpG methylation have led to the identification of multiple obesity-related sequence regions. Still limited are data on the temporal stability of regions identified thus far, and the extent to which obesity-related sequence regions remain significant in ethnic minorities. We conclude with a call for sex- and ethnic-specific data, together with data demonstrating that obesity-associated DNA methylation marks identified precede obesity.}, journal={EPIGENETICS IN HUMAN DISEASE, 2ND EDITION}, author={Hoyo, Cathrine and Skaar, David A. and Park, Sarah S. and Sorrow, Patricia}, year={2018}, pages={409–426} }
 @article{cowley_skaar_jima_maguire_hudson_park_sorrow_hoyo_2018, title={Effects of cadmium exposure on DNA methylation at imprinting control regions and genome-wide in mothers and newborn children}, volume={126}, number={3}, journal={Environmental Health Perspectives}, author={Cowley, M. and Skaar, D. A. and Jima, D. D. and Maguire, R. L. and Hudson, K. M. and Park, S. S. and Sorrow, P. and Hoyo, C.}, year={2018} }
 @article{golden_yu_meilleur_blakeley_duff_karton_vrielink_2017, title={An Extended n-h bond, driven by a conserved second-order interaction, orients the flavin n5 orbital in cholesterol oxidase}, volume={7}, journal={Scientific Reports}, author={Golden, E. and Yu, L. J. and Meilleur, F. and Blakeley, M. P. and Duff, A. P. and Karton, A. and Vrielink, A.}, year={2017} }