<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Padilla-Valdez MM</submitter><funding>Universidad de Guadalajara</funding><funding>Consejo Nacional de Humanidades, Ciencias y Tecnologías</funding><pagination>1920</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11900973</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>26(5)</volume><pubmed_abstract>Prenatal alcohol exposure (PAE) affects around 40,000 newborns every year and poses a significant health risk. Although much is already known about the neurotoxic mechanisms of PAE, new findings continue to emerge. Studies with mouse models show that PAE leads to overexpression of proinflammatory cytokines and chemokines in the brain, which disrupts important neurodevelopmental processes such as cell migration, survival and proliferation of neurons. The chemokine CXCL16 is overexpressed in the brain following various impairments, including PAE. This study shows that CXCL16 expression varies by developmental stage and sex, consistent with known sexual dimorphism in immune responses. In females, CXCL16 expression may be influenced by estrogen-related mechanisms, possibly related to the alcoh</pubmed_abstract><journal>International journal of molecular sciences</journal><pubmed_title>Prenatal Alcohol Exposure Disrupts CXCL16 Expression in Rat Hippocampus: Temporal and Sex Differences.</pubmed_title><pmcid>PMC11900973</pmcid><funding_grant_id>2020-552265</funding_grant_id><funding_grant_id>948559</funding_grant_id><funding_grant_id>APPAC-VII</funding_grant_id><pubmed_authors>Santana-Bejarano MB</pubmed_authors><pubmed_authors>Rojas-Mayorquin AE</pubmed_authors><pubmed_authors>Ortuno-Sahagun D</pubmed_authors><pubmed_authors>Godinez-Rubi M</pubmed_authors><pubmed_authors>Padilla-Valdez MM</pubmed_authors></additional><is_claimable>false</is_claimable><name>Prenatal Alcohol Exposure Disrupts CXCL16 Expression in Rat Hippocampus: Temporal and Sex Differences.</name><description>Prenatal alcohol exposure (PAE) affects around 40,000 newborns every year and poses a significant health risk. Although much is already known about the neurotoxic mechanisms of PAE, new findings continue to emerge. Studies with mouse models show that PAE leads to overexpression of proinflammatory cytokines and chemokines in the brain, which disrupts important neurodevelopmental processes such as cell migration, survival and proliferation of neurons. The chemokine CXCL16 is overexpressed in the brain following various impairments, including PAE. This study shows that CXCL16 expression varies by developmental stage and sex, consistent with known sexual dimorphism in immune responses. In females, CXCL16 expression may be influenced by estrogen-related mechanisms, possibly related to the alcoh</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Feb</publication><modification>2025-04-04T01:28:31.589Z</modification><creation>2025-04-04T01:28:31.589Z</creation></dates><accession>S-EPMC11900973</accession><cross_references><pubmed>40076549</pubmed><doi>10.3390/ijms26051920</doi></cross_references></HashMap>