<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Quilter CR</submitter><funding>Medical Research Council</funding><funding>Bill and Melinda Gates Foundation</funding><pagination>205-230</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8019263</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>3(4)</volume><pubmed_abstract>Low birthweight and reduced height gain during infancy (stunting) may arise at least in part from adverse early life environments that trigger epigenetic reprogramming that may favor survival. We examined differential DNA methylation patterns using targeted methyl sequencing of regions regulating gene activity in groups of rural Gambian infants: (a) low and high birthweight (DNA from cord blood (&lt;i>n&lt;/i> = 16 and &lt;i>n&lt;/i> = 20, respectively), from placental trophoblast tissue (&lt;i>n&lt;/i> = 21 and &lt;i>n&lt;/i> = 20, respectively), and DNA from peripheral blood collected from infants at 12 months of age (&lt;i>n&lt;/i> = 23 and &lt;i>n&lt;/i> = 17, respectively)), and, (b) the top 10% showing rapid postnatal length gain (high, &lt;i>n&lt;/i> = 20) and the bottom 10% showing slow postnatal length gain (low, &lt;i>n&lt;/i></pubmed_abstract><journal>FASEB bioAdvances</journal><pubmed_title>Identification of methylation changes associated with positive and negative growth deviance in Gambian infants using a targeted methyl sequencing approach of genomic DNA.</pubmed_title><pmcid>PMC8019263</pmcid><funding_grant_id>MC_UU_00026/3</funding_grant_id><funding_grant_id>MC_EX_MR/M01424X/1</funding_grant_id><funding_grant_id>MC_U123292701</funding_grant_id><funding_grant_id>MC_U123292700</funding_grant_id><funding_grant_id>MR/T032863/1</funding_grant_id><funding_grant_id>MC_UP_1005/1</funding_grant_id><funding_grant_id>MR/P012019/1</funding_grant_id><funding_grant_id>MC_PC_MR/R020183/1</funding_grant_id><funding_grant_id>MC_UU_00006/2</funding_grant_id><funding_grant_id>OPP1066932</funding_grant_id><funding_grant_id>MC_UU_12015/2</funding_grant_id><pubmed_authors>Quilter CR</pubmed_authors><pubmed_authors>Bernstein RM</pubmed_authors><pubmed_authors>Prentice AM</pubmed_authors><pubmed_authors>Skinner BM</pubmed_authors><pubmed_authors>Shrivastava M</pubmed_authors><pubmed_authors>Doel AM</pubmed_authors><pubmed_authors>Affara NA</pubmed_authors><pubmed_authors>Harvey KM</pubmed_authors><pubmed_authors>Bauer J</pubmed_authors><pubmed_authors>Dunger DB</pubmed_authors><pubmed_authors>Gomez M</pubmed_authors><pubmed_authors>Ong KK</pubmed_authors><pubmed_authors>Sargent CA</pubmed_authors><pubmed_authors>Drammeh S</pubmed_authors><pubmed_authors>Moore SE</pubmed_authors></additional><is_claimable>false</is_claimable><name>Identification of methylation changes associated with positive and negative growth deviance in Gambian infants using a targeted methyl sequencing approach of genomic DNA.</name><description>Low birthweight and reduced height gain during infancy (stunting) may arise at least in part from adverse early life environments that trigger epigenetic reprogramming that may favor survival. We examined differential DNA methylation patterns using targeted methyl sequencing of regions regulating gene activity in groups of rural Gambian infants: (a) low and high birthweight (DNA from cord blood (&lt;i>n&lt;/i> = 16 and &lt;i>n&lt;/i> = 20, respectively), from placental trophoblast tissue (&lt;i>n&lt;/i> = 21 and &lt;i>n&lt;/i> = 20, respectively), and DNA from peripheral blood collected from infants at 12 months of age (&lt;i>n&lt;/i> = 23 and &lt;i>n&lt;/i> = 17, respectively)), and, (b) the top 10% showing rapid postnatal length gain (high, &lt;i>n&lt;/i> = 20) and the bottom 10% showing slow postnatal length gain (low, &lt;i>n&lt;/i></description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Apr</publication><modification>2026-04-18T01:31:24.268Z</modification><creation>2022-02-09T14:47:34.69Z</creation></dates><accession>S-EPMC8019263</accession><cross_references><pubmed>33842847</pubmed><doi>10.1096/fba.2020-00101</doi></cross_references></HashMap>