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href="https://www.academia.edu/23337368/A_genome_wide_identified_risk_variant_for_PTSD_is_a_methylation_quantitative_trait_locus_and_confers_decreased_cortical_activation_to_fearful_faces"><img alt="Research paper thumbnail of A genome-wide identified risk variant for PTSD is a methylation quantitative trait locus and confers decreased cortical activation to fearful faces" class="work-thumbnail" src="https://attachments.academia-assets.com/43794249/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23337368/A_genome_wide_identified_risk_variant_for_PTSD_is_a_methylation_quantitative_trait_locus_and_confers_decreased_cortical_activation_to_fearful_faces">A genome-wide identified risk variant for PTSD is a methylation quantitative trait locus and confers decreased cortical activation to fearful faces</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/LynnAlmli">Lynn Almli</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/AliciaSmith34">Alicia Smith</a></span></div><div class="wp-workCard_item"><span>American Journal of Medical Genetics Part B: Neuropsychiatric Genetics</span><span>, 2015</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="db51d42832544fe35502ec581c3ca6e1" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":43794249,"asset_id":23337368,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/43794249/download_file?st=MTczMjc3ODAwNyw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa 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data-work-id="23451273"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451273/Ancestry_Dependent_DNA_Methylation_and_Influence_of_Maternal_Nutrition"><img alt="Research paper thumbnail of Ancestry Dependent DNA Methylation and Influence of Maternal Nutrition" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451273/Ancestry_Dependent_DNA_Methylation_and_Influence_of_Maternal_Nutrition">Ancestry Dependent DNA Methylation and Influence of Maternal Nutrition</a></div><div class="wp-workCard_item"><span>PLOS ONE</span><span>, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">There is extensive variation in DNA methylation between individuals and ethnic groups. These diff...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">There is extensive variation in DNA methylation between individuals and ethnic groups. These differences arise from a combination of genetic and non-genetic influences and potential modifiers include nutritional cues, early life experience, and social and physical environments. Here we compare genome-wide DNA methylation in neonatal cord blood from African American (AA; N = 112) and European American (EA; N = 91) participants of the CANDLE Study (Conditions Affecting Neurocognitive Development and Learning in Early Childhood). Our goal is to determine if there are replicable ancestry-specific methylation patterns that may implicate risk factors for diseases that have differential prevalence between populations. To identify the most robust ancestry-specific CpG sites, we replicate our results in lymphoblastoid cell lines from Yoruba African and CEPH European panels of HapMap. We also evaluate the influence of maternal nutrition-specifically, plasma levels of vitamin D and folate during pregnancy-on methylation in newborns. We define stable ancestry-dependent methylation of genes that include tumor suppressors and cell cycle regulators (e.g., APC, BRCA1, MCC). Overall, there is lower global methylation in African ancestral groups. Plasma levels of 25-hydroxy vitamin D are also considerably lower among AA mothers and about 60% of AA and 40% of EA mothers have concentrations below 20 ng/ml. Using a weighted correlation analysis, we define a network of CpG sites that is jointly modulated by ancestry and maternal vitamin D. Our results show that differences in DNA methylation patterns are remarkably stable and maternal micronutrients can exert an influence on the child epigenome.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451273"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451273"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451273; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=23451273]").text(description); $(".js-view-count[data-work-id=23451273]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 23451273; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='23451273']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 23451273, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=23451273]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":23451273,"title":"Ancestry Dependent DNA Methylation and Influence of Maternal Nutrition","translated_title":"","metadata":{"abstract":"There is extensive variation in DNA methylation between individuals and ethnic groups. These differences arise from a combination of genetic and non-genetic influences and potential modifiers include nutritional cues, early life experience, and social and physical environments. Here we compare genome-wide DNA methylation in neonatal cord blood from African American (AA; N = 112) and European American (EA; N = 91) participants of the CANDLE Study (Conditions Affecting Neurocognitive Development and Learning in Early Childhood). Our goal is to determine if there are replicable ancestry-specific methylation patterns that may implicate risk factors for diseases that have differential prevalence between populations. To identify the most robust ancestry-specific CpG sites, we replicate our results in lymphoblastoid cell lines from Yoruba African and CEPH European panels of HapMap. We also evaluate the influence of maternal nutrition-specifically, plasma levels of vitamin D and folate during pregnancy-on methylation in newborns. We define stable ancestry-dependent methylation of genes that include tumor suppressors and cell cycle regulators (e.g., APC, BRCA1, MCC). Overall, there is lower global methylation in African ancestral groups. Plasma levels of 25-hydroxy vitamin D are also considerably lower among AA mothers and about 60% of AA and 40% of EA mothers have concentrations below 20 ng/ml. Using a weighted correlation analysis, we define a network of CpG sites that is jointly modulated by ancestry and maternal vitamin D. Our results show that differences in DNA methylation patterns are remarkably stable and maternal micronutrients can exert an influence on the child epigenome.","publication_date":{"day":null,"month":null,"year":2015,"errors":{}},"publication_name":"PLOS ONE"},"translated_abstract":"There is extensive variation in DNA methylation between individuals and ethnic groups. These differences arise from a combination of genetic and non-genetic influences and potential modifiers include nutritional cues, early life experience, and social and physical environments. Here we compare genome-wide DNA methylation in neonatal cord blood from African American (AA; N = 112) and European American (EA; N = 91) participants of the CANDLE Study (Conditions Affecting Neurocognitive Development and Learning in Early Childhood). Our goal is to determine if there are replicable ancestry-specific methylation patterns that may implicate risk factors for diseases that have differential prevalence between populations. To identify the most robust ancestry-specific CpG sites, we replicate our results in lymphoblastoid cell lines from Yoruba African and CEPH European panels of HapMap. We also evaluate the influence of maternal nutrition-specifically, plasma levels of vitamin D and folate during pregnancy-on methylation in newborns. We define stable ancestry-dependent methylation of genes that include tumor suppressors and cell cycle regulators (e.g., APC, BRCA1, MCC). Overall, there is lower global methylation in African ancestral groups. Plasma levels of 25-hydroxy vitamin D are also considerably lower among AA mothers and about 60% of AA and 40% of EA mothers have concentrations below 20 ng/ml. Using a weighted correlation analysis, we define a network of CpG sites that is jointly modulated by ancestry and maternal vitamin D. Our results show that differences in DNA methylation patterns are remarkably stable and maternal micronutrients can exert an influence on the child epigenome.","internal_url":"https://www.academia.edu/23451273/Ancestry_Dependent_DNA_Methylation_and_Influence_of_Maternal_Nutrition","translated_internal_url":"","created_at":"2016-03-19T08:31:47.176-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":45422374,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":17587460,"work_id":23451273,"tagging_user_id":45422374,"tagged_user_id":37586952,"co_author_invite_id":null,"email":"f***k@uthsc.edu","display_order":0,"name":"Frances Tylavsky","title":"Ancestry Dependent DNA Methylation and Influence of Maternal Nutrition"}],"downloadable_attachments":[],"slug":"Ancestry_Dependent_DNA_Methylation_and_Influence_of_Maternal_Nutrition","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":45422374,"first_name":"Alicia","middle_initials":null,"last_name":"Smith","page_name":"AliciaSmith34","domain_name":"independent","created_at":"2016-03-19T07:49:15.587-07:00","display_name":"Alicia Smith","url":"https://independent.academia.edu/AliciaSmith34"},"attachments":[],"research_interests":[{"id":28235,"name":"Multidisciplinary","url":"https://www.academia.edu/Documents/in/Multidisciplinary"},{"id":220780,"name":"PLoS one","url":"https://www.academia.edu/Documents/in/PLoS_one"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="23451272"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451272/Oxytocin_vasopressin_and_Williams_syndrome_epigenetic_effects_on_abnormal_social_behavior"><img alt="Research paper thumbnail of Oxytocin, vasopressin, and Williams syndrome: epigenetic effects on abnormal social behavior" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451272/Oxytocin_vasopressin_and_Williams_syndrome_epigenetic_effects_on_abnormal_social_behavior">Oxytocin, vasopressin, and Williams syndrome: epigenetic effects on abnormal social behavior</a></div><div class="wp-workCard_item"><span>Frontiers in Genetics</span><span>, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Williams syndrome (WS) is a condition caused by a deletion of ∼26-28 genes on chromosome 7q11.23 ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Williams syndrome (WS) is a condition caused by a deletion of ∼26-28 genes on chromosome 7q11.23 often characterized by abnormal social behavior and disrupted oxytocin (OT) and vasopressin (AVP) functioning. The observation that individuals with WS exhibit OT and AVP dysregulation is compelling. There is currently a lack of evidence that any of the genes typically deleted in WS have any direct effect on either OT or AVP. In this perspective article, we present a novel epigenetic model describing how DNA methylation may impact the expression of key genes within the OT and AVP systems, which may ultimately influence the social behavior observed in WS. We draw support from data pooled from a prior empirical research study (Henrichsen et al., 2011), demonstrating that OXTR is overexpressed in WS. These preliminary findings may create new opportunities to target the OT and AVP systems with the specific goal of improving outcomes in WS and other psychiatric conditions.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451272"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451272"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451272; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=23451272]").text(description); $(".js-view-count[data-work-id=23451272]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 23451272; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='23451272']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 23451272, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=23451272]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":23451272,"title":"Oxytocin, vasopressin, and Williams syndrome: epigenetic effects on abnormal social behavior","translated_title":"","metadata":{"abstract":"Williams syndrome (WS) is a condition caused by a deletion of ∼26-28 genes on chromosome 7q11.23 often characterized by abnormal social behavior and disrupted oxytocin (OT) and vasopressin (AVP) functioning. The observation that individuals with WS exhibit OT and AVP dysregulation is compelling. There is currently a lack of evidence that any of the genes typically deleted in WS have any direct effect on either OT or AVP. In this perspective article, we present a novel epigenetic model describing how DNA methylation may impact the expression of key genes within the OT and AVP systems, which may ultimately influence the social behavior observed in WS. We draw support from data pooled from a prior empirical research study (Henrichsen et al., 2011), demonstrating that OXTR is overexpressed in WS. These preliminary findings may create new opportunities to target the OT and AVP systems with the specific goal of improving outcomes in WS and other psychiatric conditions.","publication_date":{"day":null,"month":null,"year":2015,"errors":{}},"publication_name":"Frontiers in Genetics"},"translated_abstract":"Williams syndrome (WS) is a condition caused by a deletion of ∼26-28 genes on chromosome 7q11.23 often characterized by abnormal social behavior and disrupted oxytocin (OT) and vasopressin (AVP) functioning. The observation that individuals with WS exhibit OT and AVP dysregulation is compelling. There is currently a lack of evidence that any of the genes typically deleted in WS have any direct effect on either OT or AVP. In this perspective article, we present a novel epigenetic model describing how DNA methylation may impact the expression of key genes within the OT and AVP systems, which may ultimately influence the social behavior observed in WS. We draw support from data pooled from a prior empirical research study (Henrichsen et al., 2011), demonstrating that OXTR is overexpressed in WS. These preliminary findings may create new opportunities to target the OT and AVP systems with the specific goal of improving outcomes in WS and other psychiatric conditions.","internal_url":"https://www.academia.edu/23451272/Oxytocin_vasopressin_and_Williams_syndrome_epigenetic_effects_on_abnormal_social_behavior","translated_internal_url":"","created_at":"2016-03-19T08:31:47.027-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":45422374,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":17587459,"work_id":23451272,"tagging_user_id":45422374,"tagged_user_id":33569643,"co_author_invite_id":null,"email":"b***s@uga.edu","display_order":0,"name":"Brian Haas","title":"Oxytocin, vasopressin, and Williams syndrome: epigenetic effects on abnormal social behavior"}],"downloadable_attachments":[],"slug":"Oxytocin_vasopressin_and_Williams_syndrome_epigenetic_effects_on_abnormal_social_behavior","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":45422374,"first_name":"Alicia","middle_initials":null,"last_name":"Smith","page_name":"AliciaSmith34","domain_name":"independent","created_at":"2016-03-19T07:49:15.587-07:00","display_name":"Alicia Smith","url":"https://independent.academia.edu/AliciaSmith34"},"attachments":[],"research_interests":[],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="23451271"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451271/Fetal_DNA_Methylation_of_Autism_Spectrum_Disorders_ASD_Candidate_Genes_Association_with_Spontaneous_Preterm_Birth"><img alt="Research paper thumbnail of Fetal DNA Methylation of Autism Spectrum Disorders (ASD) Candidate Genes: Association with Spontaneous Preterm Birth" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451271/Fetal_DNA_Methylation_of_Autism_Spectrum_Disorders_ASD_Candidate_Genes_Association_with_Spontaneous_Preterm_Birth">Fetal DNA Methylation of Autism Spectrum Disorders (ASD) Candidate Genes: Association with Spontaneous Preterm Birth</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/AliciaSmith34">Alicia Smith</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/SashaParets">Sasha Parets</a></span></div><div class="wp-workCard_item"><span>American journal of obstetrics and gynecology</span><span>, Jan 13, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Autism Spectrum Disorder (ASD) is associated with preterm birth (PTB); though the reason underlyi...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Autism Spectrum Disorder (ASD) is associated with preterm birth (PTB); though the reason underlying this relationship is still unclear. Our objective was to examine DNA methylation patterns of four ASD candidate genes in human fetal membranes from spontaneous PTB and uncomplicated term birth (TB). A literature search for genes implicated in ASD yielded 14 candidate genes (OXTR, SHANK3, BCL2, RORA, EN2, RELN, MECP2, AUTS2, NLGN3, NRXN1, SLC6A4, UBE3A, GABA, AFF2) that were epigenetically modified in relation to ASD. DNA methylation in fetal leukocyte DNA in four of these genes (OXTR, SHANK3, BCL2 and RORA) associated with PTB in a previous study. This study evaluated DNA methylation, transcription (qPCR) and translation patterns (immunostaining and western blot) in fetal membrane from term labor (TL; n=14), term not in labor (TNIL; n=29) and spontaneous preterm birth (PTB; n=27). Statistical analysis was performed using ANOVA and a p-value of &lt; 0.05 was significant. Higher methyla...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451271"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451271"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451271; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=23451271]").text(description); $(".js-view-count[data-work-id=23451271]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 23451271; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='23451271']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 23451271, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=23451271]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":23451271,"title":"Fetal DNA Methylation of Autism Spectrum Disorders (ASD) Candidate Genes: Association with Spontaneous Preterm Birth","translated_title":"","metadata":{"abstract":"Autism Spectrum Disorder (ASD) is associated with preterm birth (PTB); though the reason underlying this relationship is still unclear. Our objective was to examine DNA methylation patterns of four ASD candidate genes in human fetal membranes from spontaneous PTB and uncomplicated term birth (TB). A literature search for genes implicated in ASD yielded 14 candidate genes (OXTR, SHANK3, BCL2, RORA, EN2, RELN, MECP2, AUTS2, NLGN3, NRXN1, SLC6A4, UBE3A, GABA, AFF2) that were epigenetically modified in relation to ASD. DNA methylation in fetal leukocyte DNA in four of these genes (OXTR, SHANK3, BCL2 and RORA) associated with PTB in a previous study. This study evaluated DNA methylation, transcription (qPCR) and translation patterns (immunostaining and western blot) in fetal membrane from term labor (TL; n=14), term not in labor (TNIL; n=29) and spontaneous preterm birth (PTB; n=27). Statistical analysis was performed using ANOVA and a p-value of \u0026lt; 0.05 was significant. Higher methyla...","publication_date":{"day":13,"month":1,"year":2015,"errors":{}},"publication_name":"American journal of obstetrics and gynecology"},"translated_abstract":"Autism Spectrum Disorder (ASD) is associated with preterm birth (PTB); though the reason underlying this relationship is still unclear. Our objective was to examine DNA methylation patterns of four ASD candidate genes in human fetal membranes from spontaneous PTB and uncomplicated term birth (TB). A literature search for genes implicated in ASD yielded 14 candidate genes (OXTR, SHANK3, BCL2, RORA, EN2, RELN, MECP2, AUTS2, NLGN3, NRXN1, SLC6A4, UBE3A, GABA, AFF2) that were epigenetically modified in relation to ASD. DNA methylation in fetal leukocyte DNA in four of these genes (OXTR, SHANK3, BCL2 and RORA) associated with PTB in a previous study. This study evaluated DNA methylation, transcription (qPCR) and translation patterns (immunostaining and western blot) in fetal membrane from term labor (TL; n=14), term not in labor (TNIL; n=29) and spontaneous preterm birth (PTB; n=27). Statistical analysis was performed using ANOVA and a p-value of \u0026lt; 0.05 was significant. Higher methyla...","internal_url":"https://www.academia.edu/23451271/Fetal_DNA_Methylation_of_Autism_Spectrum_Disorders_ASD_Candidate_Genes_Association_with_Spontaneous_Preterm_Birth","translated_internal_url":"","created_at":"2016-03-19T08:31:46.877-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":45422374,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":17587457,"work_id":23451271,"tagging_user_id":45422374,"tagged_user_id":45482666,"co_author_invite_id":3996871,"email":"s***s@emory.edu","display_order":0,"name":"Sasha Parets","title":"Fetal DNA Methylation of Autism Spectrum Disorders (ASD) Candidate Genes: Association with Spontaneous Preterm Birth"},{"id":17587458,"work_id":23451271,"tagging_user_id":45422374,"tagged_user_id":null,"co_author_invite_id":440339,"email":"r***n@utmb.edu","display_order":4194304,"name":"Ramkumar Menon","title":"Fetal DNA Methylation of Autism Spectrum Disorders (ASD) Candidate Genes: Association with Spontaneous Preterm Birth"},{"id":17587466,"work_id":23451271,"tagging_user_id":45422374,"tagged_user_id":null,"co_author_invite_id":399883,"email":"g***e@utmb.edu","display_order":6291456,"name":"George Saade","title":"Fetal DNA Methylation of Autism Spectrum Disorders (ASD) Candidate Genes: Association with Spontaneous Preterm Birth"}],"downloadable_attachments":[],"slug":"Fetal_DNA_Methylation_of_Autism_Spectrum_Disorders_ASD_Candidate_Genes_Association_with_Spontaneous_Preterm_Birth","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":45422374,"first_name":"Alicia","middle_initials":null,"last_name":"Smith","page_name":"AliciaSmith34","domain_name":"independent","created_at":"2016-03-19T07:49:15.587-07:00","display_name":"Alicia Smith","url":"https://independent.academia.edu/AliciaSmith34"},"attachments":[],"research_interests":[{"id":22506,"name":"Adolescent","url":"https://www.academia.edu/Documents/in/Adolescent"},{"id":37834,"name":"Western blotting","url":"https://www.academia.edu/Documents/in/Western_blotting"},{"id":62550,"name":"Pregnancy","url":"https://www.academia.edu/Documents/in/Pregnancy"},{"id":121665,"name":"DNA methylation","url":"https://www.academia.edu/Documents/in/DNA_methylation"},{"id":133057,"name":"Young Adult","url":"https://www.academia.edu/Documents/in/Young_Adult"},{"id":1034181,"name":"Cross Sectional Studies","url":"https://www.academia.edu/Documents/in/Cross_Sectional_Studies"},{"id":1232430,"name":"Genetic Markers","url":"https://www.academia.edu/Documents/in/Genetic_Markers"},{"id":1399301,"name":"Premature Birth","url":"https://www.academia.edu/Documents/in/Premature_Birth"},{"id":1819399,"name":"Case Control Studies","url":"https://www.academia.edu/Documents/in/Case_Control_Studies"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="23451270"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451270/An_angiotensin_1_converting_enzyme_polymorphism_is_associated_with_allostatic_load_mediated_by_C_reactive_protein_interleukin_6_and_cortisol"><img alt="Research paper thumbnail of An angiotensin-1 converting enzyme polymorphism is associated with allostatic load mediated by C-reactive protein, interleukin-6 and cortisol" class="work-thumbnail" src="https://attachments.academia-assets.com/43891702/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451270/An_angiotensin_1_converting_enzyme_polymorphism_is_associated_with_allostatic_load_mediated_by_C_reactive_protein_interleukin_6_and_cortisol">An angiotensin-1 converting enzyme polymorphism is associated with allostatic load mediated by C-reactive protein, interleukin-6 and cortisol</a></div><div class="wp-workCard_item"><span>Psychoneuroendocrinology</span><span>, 2009</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Allostatic load (AL) is a theoretical framework that describes the cumulative physiologic effects...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Allostatic load (AL) is a theoretical framework that describes the cumulative physiologic effects of adaptation to change or stress throughout the lifespan. AL is operationalized by a composite index of multiple biomarkers. Accordingly, genes, behavior and environment contribute to AL. To determine if individual differences in AL may be influenced by inherent genetic variation, we calculated an allostatic load index (ALI) for 182 Caucasian subjects derived from a population-based study of chronic fatigue syndrome. Nearly 65% of the subjects in this study sample reported fatiguing illness. ALI was calculated based on 11 measures representing metabolic, cardiovascular, inflammatory, hypothalamic-pituitary-adrenal (HPA) axis and sympathetic nervous system (SNS) activities. Subjects were dichotomized into high (ALI &gt; or = 3) or low (ALI &lt; 3) AL groups, and the association between high AL and 129 polymorphisms in 32 genes related to the HPA axis, neurotransmission, inflammation, ca...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="bf18c58837692329cbfc75674095f237" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":43891702,"asset_id":23451270,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/43891702/download_file?st=MTczMjc3ODAwNyw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451270"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451270"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451270; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=23451270]").text(description); $(".js-view-count[data-work-id=23451270]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 23451270; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='23451270']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 23451270, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "bf18c58837692329cbfc75674095f237" } } $('.js-work-strip[data-work-id=23451270]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":23451270,"title":"An angiotensin-1 converting enzyme polymorphism is associated with allostatic load mediated by C-reactive protein, interleukin-6 and cortisol","translated_title":"","metadata":{"abstract":"Allostatic load (AL) is a theoretical framework that describes the cumulative physiologic effects of adaptation to change or stress throughout the lifespan. 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profile--work_container" data-work-id="23451269"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451269/Biomarker_Development_for_Brain_Based_Disorders_Recent_Progress_in_Psychiatry"><img alt="Research paper thumbnail of Biomarker Development for Brain-Based Disorders: Recent Progress in Psychiatry" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451269/Biomarker_Development_for_Brain_Based_Disorders_Recent_Progress_in_Psychiatry">Biomarker Development for Brain-Based Disorders: Recent Progress in Psychiatry</a></div><div class="wp-workCard_item"><span>Journal of neurology and psychology</span><span>, 2013</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Biomarkers are biological measures that are indicative of a specific disorder, its severity or re...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Biomarkers are biological measures that are indicative of a specific disorder, its severity or response to treatment. They are widely used in many areas of medicine, but biomarker development for brain-based disorders lags behind. Using examples from the field of psychiatry, this article reviews the concepts of biomarkers, challenges to their development and the recent progress along those lines. In addition to discussing historical biomarker candidates such as cortisol or catecholamine levels, we include progress from recent genetic, epigenetic, proteomic, neuroimaging and EEG studies. Successful identification of biomarkers will advance the field of psychiatry towards the goal of biological tests for diagnosis, symptom management and treatment response.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451269"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451269"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451269; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=23451269]").text(description); $(".js-view-count[data-work-id=23451269]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 23451269; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='23451269']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 23451269, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=23451269]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":23451269,"title":"Biomarker Development for Brain-Based Disorders: Recent Progress in Psychiatry","translated_title":"","metadata":{"abstract":"Biomarkers are biological measures that are indicative of a specific disorder, its severity or response to treatment. 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They are widely used in many areas of medicine, but biomarker development for brain-based disorders lags behind. Using examples from the field of psychiatry, this article reviews the concepts of biomarkers, challenges to their development and the recent progress along those lines. In addition to discussing historical biomarker candidates such as cortisol or catecholamine levels, we include progress from recent genetic, epigenetic, proteomic, neuroimaging and EEG studies. Successful identification of biomarkers will advance the field of psychiatry towards the goal of biological tests for diagnosis, symptom management and treatment response.","internal_url":"https://www.academia.edu/23451269/Biomarker_Development_for_Brain_Based_Disorders_Recent_Progress_in_Psychiatry","translated_internal_url":"","created_at":"2016-03-19T08:31:46.595-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":45422374,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[],"slug":"Biomarker_Development_for_Brain_Based_Disorders_Recent_Progress_in_Psychiatry","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":45422374,"first_name":"Alicia","middle_initials":null,"last_name":"Smith","page_name":"AliciaSmith34","domain_name":"independent","created_at":"2016-03-19T07:49:15.587-07:00","display_name":"Alicia Smith","url":"https://independent.academia.edu/AliciaSmith34"},"attachments":[],"research_interests":[],"urls":[]}, dispatcherData: dispatcherData }); 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window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=23451267]").text(description); $(".js-view-count[data-work-id=23451267]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 23451267; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='23451267']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 23451267, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); 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Although family, twin, and adoption studies demonstrate that ADHD is a highly heritable condition, studies also suggest that genetic architecture is complex, prompting the use of more advanced methodologies such as genome-wide linkage and association studies. Although such studies are theoretically compelling, replication of these results has been inconsistent. Meta-analyses have produced more reliable results, but the associations identifi ed to date account for only a small percentage of the genetic component of ADHD. Approaches such as neuroimaging genetics and epigenetic studies are being explored to probe further the etiologic complexity of this disorder.","publication_date":{"day":null,"month":null,"year":2009,"errors":{}},"publication_name":"Current Psychiatry Reports","grobid_abstract_attachment_id":43891697},"translated_abstract":null,"internal_url":"https://www.academia.edu/23451267/Advances_in_genetic_studies_of_attention_deficit_hyperactivity_disorder","translated_internal_url":"","created_at":"2016-03-19T08:31:46.412-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":45422374,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":17587455,"work_id":23451267,"tagging_user_id":45422374,"tagged_user_id":32671888,"co_author_invite_id":null,"email":"f***s@upstate.edu","affiliation":"SUNY: Upstate Medical University","display_order":0,"name":"Stephen V Faraone","title":"Advances in genetic studies of attention-deficit/hyperactivity disorder"}],"downloadable_attachments":[{"id":43891697,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/43891697/thumbnails/1.jpg","file_name":"Advances_in_genetic_studies_of_attention20160319-22462-yr8y1t.pdf","download_url":"https://www.academia.edu/attachments/43891697/download_file?st=MTczMjc3ODAwNyw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Advances_in_genetic_studies_of_attention.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/43891697/Advances_in_genetic_studies_of_attention20160319-22462-yr8y1t-libre.pdf?1458401614=\u0026response-content-disposition=attachment%3B+filename%3DAdvances_in_genetic_studies_of_attention.pdf\u0026Expires=1732781607\u0026Signature=DxckELlCSB9tm4AMFDx9rRpRY6FjT~WWRCD5e5h5cN6cUN3FiqQ07TT2scD~VUyQF6EmGkICZCW1kdinZGMmxl0nL3f8Upxxrdeyi1uaLQD-cqJE7GzwZN0D9Nuu96AOO-edl4L833j8gGexU1C0P6mhnAKS07cJMJeZJMzQsQsliCrQIZg4udO2F993-r8K4jpId2en60EdGRtH6asRnUUXCPaRBMOld-COlPtSHW8t~sVX~KHddBD9YkSg~QCX49SMOgXOphEqD3WBo8egnyR79WZPzfwnRoxnN28tguRtFrzmF-OiTK5eqFBKG79ScHfRu1oCE6KnWq4dLzHDEw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Advances_in_genetic_studies_of_attention_deficit_hyperactivity_disorder","translated_slug":"","page_count":6,"language":"en","content_type":"Work","owner":{"id":45422374,"first_name":"Alicia","middle_initials":null,"last_name":"Smith","page_name":"AliciaSmith34","domain_name":"independent","created_at":"2016-03-19T07:49:15.587-07:00","display_name":"Alicia Smith","url":"https://independent.academia.edu/AliciaSmith34"},"attachments":[{"id":43891697,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/43891697/thumbnails/1.jpg","file_name":"Advances_in_genetic_studies_of_attention20160319-22462-yr8y1t.pdf","download_url":"https://www.academia.edu/attachments/43891697/download_file?st=MTczMjc3ODAwNyw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Advances_in_genetic_studies_of_attention.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/43891697/Advances_in_genetic_studies_of_attention20160319-22462-yr8y1t-libre.pdf?1458401614=\u0026response-content-disposition=attachment%3B+filename%3DAdvances_in_genetic_studies_of_attention.pdf\u0026Expires=1732781607\u0026Signature=DxckELlCSB9tm4AMFDx9rRpRY6FjT~WWRCD5e5h5cN6cUN3FiqQ07TT2scD~VUyQF6EmGkICZCW1kdinZGMmxl0nL3f8Upxxrdeyi1uaLQD-cqJE7GzwZN0D9Nuu96AOO-edl4L833j8gGexU1C0P6mhnAKS07cJMJeZJMzQsQsliCrQIZg4udO2F993-r8K4jpId2en60EdGRtH6asRnUUXCPaRBMOld-COlPtSHW8t~sVX~KHddBD9YkSg~QCX49SMOgXOphEqD3WBo8egnyR79WZPzfwnRoxnN28tguRtFrzmF-OiTK5eqFBKG79ScHfRu1oCE6KnWq4dLzHDEw__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":2513,"name":"Molecular Biology","url":"https://www.academia.edu/Documents/in/Molecular_Biology"},{"id":87626,"name":"Psychological","url":"https://www.academia.edu/Documents/in/Psychological"},{"id":174464,"name":"Social Environment","url":"https://www.academia.edu/Documents/in/Social_Environment"},{"id":176486,"name":"Genome","url":"https://www.academia.edu/Documents/in/Genome"},{"id":224794,"name":"Genetic linkage analysis","url":"https://www.academia.edu/Documents/in/Genetic_linkage_analysis"},{"id":372410,"name":"Genotype","url":"https://www.academia.edu/Documents/in/Genotype"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="23451266"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451266/HPA_Axis_Evidence_of_Transgenerational_Effects_of_Maternal_Early_Life_Trauma_in_6_Month_Old_Infants"><img alt="Research paper thumbnail of HPA Axis Evidence of Transgenerational Effects of Maternal Early-Life Trauma in 6-Month-Old Infants" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451266/HPA_Axis_Evidence_of_Transgenerational_Effects_of_Maternal_Early_Life_Trauma_in_6_Month_Old_Infants">HPA Axis Evidence of Transgenerational Effects of Maternal Early-Life Trauma in 6-Month-Old Infants</a></div><div class="wp-workCard_item"><span>PsycEXTRA Dataset</span><span>, 2000</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451266"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451266"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451266; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="23451265"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451265/The_impact_of_maternal_childhood_abuse_on_maternal_and_infant_HPA_axis_function_in_the_postpartum_period"><img alt="Research paper thumbnail of The impact of maternal childhood abuse on maternal and infant HPA axis function in the postpartum period" class="work-thumbnail" src="https://attachments.academia-assets.com/43891701/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451265/The_impact_of_maternal_childhood_abuse_on_maternal_and_infant_HPA_axis_function_in_the_postpartum_period">The impact of maternal childhood abuse on maternal and infant HPA axis function in the postpartum period</a></div><div class="wp-workCard_item"><span>Psychoneuroendocrinology</span><span>, 2010</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="c5a2caa35a7c2fb41e263e1182cd0d3d" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":43891701,"asset_id":23451265,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/43891701/download_file?st=MTczMjc3ODAwNyw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451265"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451265"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451265; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="23451264"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451264/Genetic_evaluation_of_the_serotonergic_system_in_chronic_fatigue_syndrome"><img alt="Research paper thumbnail of Genetic evaluation of the serotonergic system in chronic fatigue syndrome" class="work-thumbnail" src="https://attachments.academia-assets.com/43891699/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451264/Genetic_evaluation_of_the_serotonergic_system_in_chronic_fatigue_syndrome">Genetic evaluation of the serotonergic system in chronic fatigue syndrome</a></div><div class="wp-workCard_item"><span>Psychoneuroendocrinology</span><span>, 2008</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="948e02ef53a57b866daaf90e96152ceb" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":43891699,"asset_id":23451264,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/43891699/download_file?st=MTczMjc3ODAwOCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451264"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451264"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451264; 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The pathophysiology of CFS remains elusive, although abnormalities in the central nervous system (CNS) have been implicated, particularly hyperactivity of the serotonergic (5-hydroxytryptamine; 5-HT) system and hypoactivity of the hypothalamic-pituitary-adrenal (HPA) axis. Since alterations in 5-HT signaling can lead to physiologic and behavioral changes, a genetic evaluation of the 5-HT system was undertaken to identify serotonergic markers associated with CFS and potential mechanisms for CNS abnormality. A total of 77 polymorphisms in genes related to serotonin synthesis (TPH2), signaling (HTR1A, HTR1E, HTR2A, HTR2B, HTR2C, HTR3A, HTR3B, HTR4, HTR5A, HTR6, and HTR7), transport (SLC6A4), and catabolism (MAOA) were examined in 137 clinically evaluated subjects (40 CFS, 55 with insufficient fatigue, and 42 non-fatigued, NF, controls) derived from a population-based CFS surveillance study in Wichita, Kansas. Of the polymorphisms examined, three markers (À1438G/A, C102T, and rs1923884) all located in the 5-HT receptor subtype HTR2A were associated with CFS when compared to NF controls. Additionally, consistent associations were observed between HTR2A variants and quantitative measures of disability and fatigue in all subjects. The most compelling of these associations was with the A allele of À1438G/A (rs6311) which is suggested to have increased promoter activity in functional studies. Further, in silico analysis revealed that the À1438 A allele creates a consensus binding site for Th1/E47, a transcription factor implicated in the development of the nervous system. 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}); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="23451263"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451263/Polymorphisms_in_genes_regulating_the_HPA_axis_associated_with_empirically_delineated_classes_of_unexplained_chronic_fatigue"><img alt="Research paper thumbnail of Polymorphisms in genes regulating the HPA axis associated with empirically delineated classes of unexplained chronic fatigue" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451263/Polymorphisms_in_genes_regulating_the_HPA_axis_associated_with_empirically_delineated_classes_of_unexplained_chronic_fatigue">Polymorphisms in genes regulating the HPA axis associated with empirically delineated classes of unexplained chronic fatigue</a></div><div class="wp-workCard_item"><span>Pharmacogenomics</span><span>, 2006</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Chronic fatigue syndrome (CFS) is characterized by persistent or relapsing fatigue that is not al...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Chronic fatigue syndrome (CFS) is characterized by persistent or relapsing fatigue that is not alleviated by rest, causes substantial reduction in activities and is accompanied by a variety of symptoms. Its unknown etiology may reflect that CFS is heterogeneous. Latent class analyses of symptoms and physiological systems were used to delineate subgroups within a population-based sample of fatigued and nonfatigued subjects [1] . This study examined whether genetic differences underlie the individual subgroups of the latent class solution. Polymorphisms in 11 candidate genes related to both hypothalamic-pituitary-adrenal (HPA) axis function and mood-related neurotransmitter systems were evaluated by comparing each of the five ill classes (Class 1, n = 33; Class 3, n = 22; Class 4, n = 22; Class 5, n = 17; Class 6, n = 11) of fatigued subjects with subjects defined as well (Class 2, n = 35). Of the five classes of subjects with unexplained fatigue, three classes were distinguished by gene polymorphsims involved in either HPA axis function or neurotransmitter systems, including proopiomelanocortin (POMC), nuclear receptor subfamily 3, group C, member 1 (NR3C1), monoamine oxidase A (MAOA), monoamine oxidase B (MAOB), and tryptophan hydroxylase 2 (TPH2). These data support the hypothesis that medically unexplained chronic fatigue is heterogeneous and presents preliminary evidence of the genetic mechanisms underlying some of the putative conditions.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451263"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451263"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451263; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=23451263]").text(description); $(".js-view-count[data-work-id=23451263]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 23451263; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='23451263']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 23451263, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=23451263]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":23451263,"title":"Polymorphisms in genes regulating the HPA axis associated with empirically delineated classes of unexplained chronic fatigue","translated_title":"","metadata":{"abstract":"Chronic fatigue syndrome (CFS) is characterized by persistent or relapsing fatigue that is not alleviated by rest, causes substantial reduction in activities and is accompanied by a variety of symptoms. Its unknown etiology may reflect that CFS is heterogeneous. Latent class analyses of symptoms and physiological systems were used to delineate subgroups within a population-based sample of fatigued and nonfatigued subjects [1] . This study examined whether genetic differences underlie the individual subgroups of the latent class solution. Polymorphisms in 11 candidate genes related to both hypothalamic-pituitary-adrenal (HPA) axis function and mood-related neurotransmitter systems were evaluated by comparing each of the five ill classes (Class 1, n = 33; Class 3, n = 22; Class 4, n = 22; Class 5, n = 17; Class 6, n = 11) of fatigued subjects with subjects defined as well (Class 2, n = 35). Of the five classes of subjects with unexplained fatigue, three classes were distinguished by gene polymorphsims involved in either HPA axis function or neurotransmitter systems, including proopiomelanocortin (POMC), nuclear receptor subfamily 3, group C, member 1 (NR3C1), monoamine oxidase A (MAOA), monoamine oxidase B (MAOB), and tryptophan hydroxylase 2 (TPH2). These data support the hypothesis that medically unexplained chronic fatigue is heterogeneous and presents preliminary evidence of the genetic mechanisms underlying some of the putative conditions.","publication_date":{"day":null,"month":null,"year":2006,"errors":{}},"publication_name":"Pharmacogenomics"},"translated_abstract":"Chronic fatigue syndrome (CFS) is characterized by persistent or relapsing fatigue that is not alleviated by rest, causes substantial reduction in activities and is accompanied by a variety of symptoms. Its unknown etiology may reflect that CFS is heterogeneous. Latent class analyses of symptoms and physiological systems were used to delineate subgroups within a population-based sample of fatigued and nonfatigued subjects [1] . This study examined whether genetic differences underlie the individual subgroups of the latent class solution. Polymorphisms in 11 candidate genes related to both hypothalamic-pituitary-adrenal (HPA) axis function and mood-related neurotransmitter systems were evaluated by comparing each of the five ill classes (Class 1, n = 33; Class 3, n = 22; Class 4, n = 22; Class 5, n = 17; Class 6, n = 11) of fatigued subjects with subjects defined as well (Class 2, n = 35). Of the five classes of subjects with unexplained fatigue, three classes were distinguished by gene polymorphsims involved in either HPA axis function or neurotransmitter systems, including proopiomelanocortin (POMC), nuclear receptor subfamily 3, group C, member 1 (NR3C1), monoamine oxidase A (MAOA), monoamine oxidase B (MAOB), and tryptophan hydroxylase 2 (TPH2). These data support the hypothesis that medically unexplained chronic fatigue is heterogeneous and presents preliminary evidence of the genetic mechanisms underlying some of the putative conditions.","internal_url":"https://www.academia.edu/23451263/Polymorphisms_in_genes_regulating_the_HPA_axis_associated_with_empirically_delineated_classes_of_unexplained_chronic_fatigue","translated_internal_url":"","created_at":"2016-03-19T08:31:45.862-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":45422374,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":17587451,"work_id":23451263,"tagging_user_id":45422374,"tagged_user_id":255601877,"co_author_invite_id":2188190,"email":"u***a@unsw.edu.au","display_order":0,"name":"Ute Vollmer-conna","title":"Polymorphisms in genes regulating the HPA axis associated with empirically delineated classes of unexplained chronic fatigue"},{"id":17587452,"work_id":23451263,"tagging_user_id":45422374,"tagged_user_id":null,"co_author_invite_id":4031374,"email":"d***2@emory.edu","display_order":4194304,"name":"Peter White","title":"Polymorphisms in genes regulating the HPA axis associated with empirically delineated classes of unexplained chronic fatigue"}],"downloadable_attachments":[],"slug":"Polymorphisms_in_genes_regulating_the_HPA_axis_associated_with_empirically_delineated_classes_of_unexplained_chronic_fatigue","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":45422374,"first_name":"Alicia","middle_initials":null,"last_name":"Smith","page_name":"AliciaSmith34","domain_name":"independent","created_at":"2016-03-19T07:49:15.587-07:00","display_name":"Alicia Smith","url":"https://independent.academia.edu/AliciaSmith34"},"attachments":[],"research_interests":[{"id":2629,"name":"Pharmacogenomics","url":"https://www.academia.edu/Documents/in/Pharmacogenomics"},{"id":3855,"name":"Polymorphism","url":"https://www.academia.edu/Documents/in/Polymorphism"},{"id":4338,"name":"Gene regulation","url":"https://www.academia.edu/Documents/in/Gene_regulation"},{"id":17804,"name":"Chronic Fatigue Syndrome","url":"https://www.academia.edu/Documents/in/Chronic_Fatigue_Syndrome"},{"id":48057,"name":"DNA","url":"https://www.academia.edu/Documents/in/DNA"},{"id":50238,"name":"Affect","url":"https://www.academia.edu/Documents/in/Affect"},{"id":86952,"name":"Haplotypes","url":"https://www.academia.edu/Documents/in/Haplotypes"},{"id":131835,"name":"HPA axis","url":"https://www.academia.edu/Documents/in/HPA_axis"},{"id":372410,"name":"Genotype","url":"https://www.academia.edu/Documents/in/Genotype"},{"id":1252054,"name":"Pituitary Hormones","url":"https://www.academia.edu/Documents/in/Pituitary_Hormones"},{"id":1763968,"name":"Gene Expression Regulation","url":"https://www.academia.edu/Documents/in/Gene_Expression_Regulation"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="23451262"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451262/Convergent_Genomic_Studies_Identify_Association_of_i_GRIK2_i_and_i_NPAS2_i_with_Chronic_Fatigue_Syndrome"><img alt="Research paper thumbnail of Convergent Genomic Studies Identify Association of <i>GRIK2</i> and <i>NPAS2</i> with Chronic Fatigue Syndrome" class="work-thumbnail" src="https://attachments.academia-assets.com/43891695/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451262/Convergent_Genomic_Studies_Identify_Association_of_i_GRIK2_i_and_i_NPAS2_i_with_Chronic_Fatigue_Syndrome">Convergent Genomic Studies Identify Association of <i>GRIK2</i> and <i>NPAS2</i> with Chronic Fatigue Syndrome</a></div><div class="wp-workCard_item"><span>Neuropsychobiology</span><span>, 2011</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="55e2271cc72b7059136647e3d1940877" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":43891695,"asset_id":23451262,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/43891695/download_file?st=MTczMjc3ODAwOCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451262"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451262"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451262; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=23451262]").text(description); $(".js-view-count[data-work-id=23451262]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 23451262; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='23451262']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 23451262, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "55e2271cc72b7059136647e3d1940877" } } $('.js-work-strip[data-work-id=23451262]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":23451262,"title":"Convergent Genomic Studies Identify Association of \u003ci\u003eGRIK2\u003c/i\u003e and \u003ci\u003eNPAS2\u003c/i\u003e with Chronic Fatigue Syndrome","translated_title":"","metadata":{"grobid_abstract":"sion of 20,160 genes in a subset of these subjects (35 CFS subjects and 27 controls) derived from a population-based study. Results: Sixty-five SNPs were nominally associated with CFS (p ! 0.001), and 165 genes were differentially expressed ( 6 4-fold; p ^ 0.05) in peripheral blood mononuclear cells of CFS subjects. Two genes, glutamate receptor, ionotropic, kinase 2 (GRIK2) and neuronal PAS domain protein 2 (NPAS2), were identified by both SNP and gene expression analyses. Subjects with the G allele of rs2247215 (GRIK2) were more likely to have CFS (p = 0.0005), and CFS subjects showed decreased GRIK2 expression (10-fold; p = 0.015). Subjects with the T allele of rs356653 (NPAS2) were more likely to have CFS (p = 0.0007), and NPAS2 expression was increased (10-fold; p = 0.027) in those with CFS. Conclusion: Using an integrated genomic strategy, this study suggests a possible role for genes involved in glutamatergic neurotransmission and circadian rhythm in CFS and supports further study of novel candidate genes in independent populations of CFS subjects.","publication_date":{"day":null,"month":null,"year":2011,"errors":{}},"publication_name":"Neuropsychobiology","grobid_abstract_attachment_id":43891695},"translated_abstract":null,"internal_url":"https://www.academia.edu/23451262/Convergent_Genomic_Studies_Identify_Association_of_i_GRIK2_i_and_i_NPAS2_i_with_Chronic_Fatigue_Syndrome","translated_internal_url":"","created_at":"2016-03-19T08:31:45.692-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":45422374,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":17587449,"work_id":23451262,"tagging_user_id":45422374,"tagged_user_id":null,"co_author_invite_id":2191941,"email":"t***r@cdc.gov","display_order":0,"name":"Toni Whistler","title":"Convergent Genomic Studies Identify Association of \u003ci\u003eGRIK2\u003c/i\u003e and \u003ci\u003eNPAS2\u003c/i\u003e with Chronic Fatigue 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wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451260/Posttraumatic_stress_disorder_is_a_risk_factor_for_metabolic_syndrome_in_an_impoverished_urban_population">Posttraumatic stress disorder is a risk factor for metabolic syndrome in an impoverished urban population</a></div><div class="wp-workCard_item"><span>General Hospital Psychiatry</span><span>, 2011</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="71a24fff3076582fe20dae8f74ce7942" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":43891696,"asset_id":23451260,"asset_type":"Work","button_location":"profile"}" 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href="https://www.academia.edu/23451259/Predictors_of_neonatal_hypothalamic_pituitary_adrenal_axis_activity_at_delivery"><img alt="Research paper thumbnail of Predictors of neonatal hypothalamic-pituitary-adrenal axis activity at delivery" class="work-thumbnail" src="https://attachments.academia-assets.com/43891698/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451259/Predictors_of_neonatal_hypothalamic_pituitary_adrenal_axis_activity_at_delivery">Predictors of neonatal hypothalamic-pituitary-adrenal axis activity at delivery</a></div><div class="wp-workCard_item"><span>Clinical Endocrinology</span><span>, 2011</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="e3879b2bbaa4485eada35ff09834dc8f" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":43891698,"asset_id":23451259,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/43891698/download_file?st=MTczMjc3ODAwOCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451259"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451259"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451259; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=23451259]").text(description); $(".js-view-count[data-work-id=23451259]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 23451259; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='23451259']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 23451259, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "e3879b2bbaa4485eada35ff09834dc8f" } } $('.js-work-strip[data-work-id=23451259]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":23451259,"title":"Predictors of neonatal hypothalamic-pituitary-adrenal axis activity at delivery","translated_title":"","metadata":{"grobid_abstract":"Objective Clinical and preclinical studies indicate that maternal stress during pregnancy may exert long-lasting adverse effects on offspring. This investigation sought to identify factors mediating the relationship between maternal and neonatal hypothalamicpituitary-adrenal (HPA) axes in pregnant women with past or family psychiatric history. Patients Two hundred and five pairs of maternal and umbilical cord blood samples from a clinical population were collected at delivery. Measurements Maternal and neonatal HPA axis activity measures were plasma adrenocorticotrophic hormone (ACTH), total cortisol, free cortisol and cortisol-binding globulin concentrations. The effects of maternal race, age, body mass index, psychiatric diagnosis (DSM-IV), birth weight, delivery method and estimated gestational age (EGA) at delivery on both maternal and neonatal HPA axis measures were also examined. Incorporating these independent predictors as covariates where necessary, we evaluated whether neonatal HPA axis activity measures could be predicted by the same maternal measure using linear regression. Results Delivery method was associated with umbilical cord plasma ACTH and both total and free cord cortisol concentrations (T = 10AE53-4AE21; P \u003c 0AE0001-0AE010). After accounting for method of delivery and EGA, we found that maternal plasma ACTH concentrations predicted 23AE9% of the variance in foetal plasma ACTH concentrations (T = 6AE76; P \u003c 0AE0001), and maternal free and total plasma cortisol concentrations predicted 39AE8% and 32AE3% of the variance in foetal plasma free and total cortisol concentrations (T = 5AE37-6AE90; P \u003c 0AE0001), respectively. Conclusion These data suggest that neonatal response is coupled with maternal HPA axis activity at delivery. Future investigations will scrutinize the potential long-term sequelae for the offspring.","publication_date":{"day":null,"month":null,"year":2011,"errors":{}},"publication_name":"Clinical Endocrinology","grobid_abstract_attachment_id":43891698},"translated_abstract":null,"internal_url":"https://www.academia.edu/23451259/Predictors_of_neonatal_hypothalamic_pituitary_adrenal_axis_activity_at_delivery","translated_internal_url":"","created_at":"2016-03-19T08:31:45.084-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":45422374,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":43891698,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/43891698/thumbnails/1.jpg","file_name":"Predictors_of_Neonatal_Hypothalamic-Pitu20160319-28582-1erw3g6.pdf","download_url":"https://www.academia.edu/attachments/43891698/download_file?st=MTczMjc3ODAwOCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Predictors_of_neonatal_hypothalamic_pitu.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/43891698/Predictors_of_Neonatal_Hypothalamic-Pitu20160319-28582-1erw3g6-libre.pdf?1458401613=\u0026response-content-disposition=attachment%3B+filename%3DPredictors_of_neonatal_hypothalamic_pitu.pdf\u0026Expires=1732781608\u0026Signature=a9OjtaUAjMcN3n5g9dIeI26rWozf7nlTAIdjuCSGfLPlsQHu6YpMD8WRF5kCrOEbv5lIwdf8dNn2DWAAd5mXxiK5XOUZ37ll2-HjyfmBSBuS7ONL2ks8lpCCAgzLeJ0wwAdv9h77Kx9JW2VtcFOMAclN3pgwJiRgg0me~JtumAmEY-TDqc5WL2kSVeA5pvMQXDP4b~h6eWTRpxCP4lZLvUWP1vc14CW2z262VZOdHU6M~B0OTrMDeM4hiN~cEwiazsvzpD0e7vWqDtz6w6amXttwATWPenpY12bCfYW0GEuPlv0vEaOpQy-HBcvS87NdSsu3GwAxpNxjSFNqf6ZwUA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Predictors_of_neonatal_hypothalamic_pituitary_adrenal_axis_activity_at_delivery","translated_slug":"","page_count":6,"language":"en","content_type":"Work","owner":{"id":45422374,"first_name":"Alicia","middle_initials":null,"last_name":"Smith","page_name":"AliciaSmith34","domain_name":"independent","created_at":"2016-03-19T07:49:15.587-07:00","display_name":"Alicia Smith","url":"https://independent.academia.edu/AliciaSmith34"},"attachments":[{"id":43891698,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/43891698/thumbnails/1.jpg","file_name":"Predictors_of_Neonatal_Hypothalamic-Pitu20160319-28582-1erw3g6.pdf","download_url":"https://www.academia.edu/attachments/43891698/download_file?st=MTczMjc3ODAwOCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Predictors_of_neonatal_hypothalamic_pitu.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/43891698/Predictors_of_Neonatal_Hypothalamic-Pitu20160319-28582-1erw3g6-libre.pdf?1458401613=\u0026response-content-disposition=attachment%3B+filename%3DPredictors_of_neonatal_hypothalamic_pitu.pdf\u0026Expires=1732781608\u0026Signature=a9OjtaUAjMcN3n5g9dIeI26rWozf7nlTAIdjuCSGfLPlsQHu6YpMD8WRF5kCrOEbv5lIwdf8dNn2DWAAd5mXxiK5XOUZ37ll2-HjyfmBSBuS7ONL2ks8lpCCAgzLeJ0wwAdv9h77Kx9JW2VtcFOMAclN3pgwJiRgg0me~JtumAmEY-TDqc5WL2kSVeA5pvMQXDP4b~h6eWTRpxCP4lZLvUWP1vc14CW2z262VZOdHU6M~B0OTrMDeM4hiN~cEwiazsvzpD0e7vWqDtz6w6amXttwATWPenpY12bCfYW0GEuPlv0vEaOpQy-HBcvS87NdSsu3GwAxpNxjSFNqf6ZwUA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":62550,"name":"Pregnancy","url":"https://www.academia.edu/Documents/in/Pregnancy"},{"id":99708,"name":"Clinical","url":"https://www.academia.edu/Documents/in/Clinical"},{"id":171144,"name":"Mental Disorders","url":"https://www.academia.edu/Documents/in/Mental_Disorders"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":253560,"name":"Newborn Infant","url":"https://www.academia.edu/Documents/in/Newborn_Infant"},{"id":489727,"name":"Prognosis","url":"https://www.academia.edu/Documents/in/Prognosis"},{"id":564888,"name":"Adrenocorticotropic Hormone","url":"https://www.academia.edu/Documents/in/Adrenocorticotropic_Hormone"},{"id":923234,"name":"Clinical Endocrinology","url":"https://www.academia.edu/Documents/in/Clinical_Endocrinology"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="23451258"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451258/Association_of_polymorphisms_in_CASP10_and_CASP8_with_FEV_1_FVC_and_bronchial_hyperresponsiveness_in_ethnically_diverse_asthmatics"><img alt="Research paper thumbnail of Association of polymorphisms in CASP10 and CASP8 with FEV 1 /FVC and bronchial hyperresponsiveness in ethnically diverse asthmatics" class="work-thumbnail" src="https://attachments.academia-assets.com/43891700/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451258/Association_of_polymorphisms_in_CASP10_and_CASP8_with_FEV_1_FVC_and_bronchial_hyperresponsiveness_in_ethnically_diverse_asthmatics">Association of polymorphisms in CASP10 and CASP8 with FEV 1 /FVC and bronchial hyperresponsiveness in ethnically diverse asthmatics</a></div><div class="wp-workCard_item"><span>Clinical & Experimental Allergy</span><span>, 2008</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="c4f0f152678dbe92dcced99b8a32e9cb" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":43891700,"asset_id":23451258,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/43891700/download_file?st=MTczMjc3ODAwOCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451258"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451258"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451258; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=23451258]").text(description); $(".js-view-count[data-work-id=23451258]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 23451258; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='23451258']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 23451258, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "c4f0f152678dbe92dcced99b8a32e9cb" } } $('.js-work-strip[data-work-id=23451258]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":23451258,"title":"Association of polymorphisms in CASP10 and CASP8 with FEV 1 /FVC and bronchial hyperresponsiveness in ethnically diverse asthmatics","translated_title":"","metadata":{"grobid_abstract":"Background Several chromosomal regions have been identified using family-based linkage analysis to contain genes contributing to the development of asthma and allergic disorders. One of these regions, chromosome 2q32-q33, contains a gene cluster containing CFLAR, CASP10 and CASP8. These genes regulate the extrinsic apoptosis pathway utilized by several types of immune and structural cells that have been implicated in the pathogenesis of asthma. Objective To assess the role of genetic variation in CFLAR, CASP10 and CASP8 in asthma and related phenotypes in individuals of diverse ethnic backgrounds. Methods We tested 26 single nucleotide polymorphisms (SNPs) in the CFLAR, CASP10 and CASP8 gene cluster for association with asthma and related phenotypes in African-American, non-Hispanic whites, and Hispanic case-control populations (cases, N = 517, controls, N = 644). Results Five CASP10 SNPS were associated with forced expiratory volume in 1 s (FEV 1 )/ forced expiration volume capacity (FVC) in the African-American subjects with asthma (P = 0.0009-0.047). Nine SNPs, seven in CASP10 and two in CASP8, were also associated with the degree of bronchial hyperresponsiveness (BHR) (as determined by PC 20 ) in race-specific analysis, predominately in the Non-Hispanic white cases. Two SNPs, rs6750157 in CASP10 and rs1045485 in CASP8 were modestly associated with asthma in the African-American (P = 0.025) and Hispanic (P = 0.033) populations, respectively. Conclusion These data suggest a role for CASP10 as a potential modifier of the asthma phenotype, specifically with measures of airway obstruction and BHR. Caspase 8 and 10 polymorphisms and pulmonary phenotypes 1739 Ã Indicates deviation from expected values of Hardy-Weinberg equilibrium (Po0.05).","publication_date":{"day":null,"month":null,"year":2008,"errors":{}},"publication_name":"Clinical \u0026 Experimental Allergy","grobid_abstract_attachment_id":43891700},"translated_abstract":null,"internal_url":"https://www.academia.edu/23451258/Association_of_polymorphisms_in_CASP10_and_CASP8_with_FEV_1_FVC_and_bronchial_hyperresponsiveness_in_ethnically_diverse_asthmatics","translated_internal_url":"","created_at":"2016-03-19T08:31:44.912-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":45422374,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":17587446,"work_id":23451258,"tagging_user_id":45422374,"tagged_user_id":null,"co_author_invite_id":296647,"email":"e***k@wakehealth.edu","display_order":0,"name":"Eugene Bleecker","title":"Association of polymorphisms in CASP10 and CASP8 with FEV 1 /FVC and bronchial hyperresponsiveness in ethnically diverse asthmatics"},{"id":17587447,"work_id":23451258,"tagging_user_id":45422374,"tagged_user_id":null,"co_author_invite_id":311439,"email":"t***d@wfubmc.edu","display_order":4194304,"name":"Timothy Howard","title":"Association of polymorphisms in CASP10 and CASP8 with FEV 1 /FVC and bronchial hyperresponsiveness in ethnically diverse asthmatics"},{"id":17587477,"work_id":23451258,"tagging_user_id":45422374,"tagged_user_id":null,"co_author_invite_id":296645,"email":"d***s@wfubmc.edu","display_order":6291456,"name":"Deborah Meyers","title":"Association of polymorphisms in CASP10 and CASP8 with FEV 1 /FVC and bronchial hyperresponsiveness in ethnically diverse asthmatics"}],"downloadable_attachments":[{"id":43891700,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/43891700/thumbnails/1.jpg","file_name":"j.1365-2222.2008.03095.x.pdf20160319-21707-1wjqj2v","download_url":"https://www.academia.edu/attachments/43891700/download_file?st=MTczMjc3ODAwOCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Association_of_polymorphisms_in_CASP10_a.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/43891700/j.1365-2222.2008.03095.x-libre.pdf20160319-21707-1wjqj2v?1458401641=\u0026response-content-disposition=attachment%3B+filename%3DAssociation_of_polymorphisms_in_CASP10_a.pdf\u0026Expires=1732781608\u0026Signature=GSwWqRoENgL6DMu4SkWNpelAzfJg~fnM2Y3bJfgCR-p-yGyUQ2bV3TOD5Vv-LvZrvW9wKu3DRp0SP5TlyoigaGD0YWVnjgN7KaN5fQ5eyZMdFbATn1vWlSVocKMHBnSWSpx1ILXfD586x3~FEhRClXZ37ih4YldMw349kBskfXR0T~aEr7g2PcCT6HrfZ3MuDjyqadMIloEpUojV7Gs0lOBOAjtA0OuaPiWkAHQLlAhMqyW14bd~CIMp0lqIzXcETDaNb3h3~tO8NDho0VTI-TOaMCarNTTs~fg4p0vpfpcRL6hvrtMObfN~hM3GydHzgA08I4xC7BtFEwJOAXuxQA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Association_of_polymorphisms_in_CASP10_and_CASP8_with_FEV_1_FVC_and_bronchial_hyperresponsiveness_in_ethnically_diverse_asthmatics","translated_slug":"","page_count":7,"language":"en","content_type":"Work","owner":{"id":45422374,"first_name":"Alicia","middle_initials":null,"last_name":"Smith","page_name":"AliciaSmith34","domain_name":"independent","created_at":"2016-03-19T07:49:15.587-07:00","display_name":"Alicia 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Adult","url":"https://www.academia.edu/Documents/in/Young_Adult"},{"id":233800,"name":"African Americans","url":"https://www.academia.edu/Documents/in/African_Americans"},{"id":247477,"name":"Caspase","url":"https://www.academia.edu/Documents/in/Caspase"},{"id":390808,"name":"Vital Capacity","url":"https://www.academia.edu/Documents/in/Vital_Capacity"},{"id":410370,"name":"Public health systems and services research","url":"https://www.academia.edu/Documents/in/Public_health_systems_and_services_research-1"},{"id":489736,"name":"Linkage Disequilibrium","url":"https://www.academia.edu/Documents/in/Linkage_Disequilibrium"},{"id":502712,"name":"Ethnic diversity","url":"https://www.academia.edu/Documents/in/Ethnic_diversity"},{"id":561981,"name":"European Continental Ancestry Group","url":"https://www.academia.edu/Documents/in/European_Continental_Ancestry_Group"},{"id":1635839,"name":"bronchial hyperreactivity (BHR)","url":"https://www.academia.edu/Documents/in/bronchial_hyperreactivity_BHR_"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="23451257"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451257/Posttraumatic_stress_disorder_is_associated_with_an_enhanced_spontaneous_production_of_pro_inflammatory_cytokines_by_peripheral_blood_mononuclear_cells"><img alt="Research paper thumbnail of Posttraumatic stress disorder is associated with an enhanced spontaneous production of pro-inflammatory cytokines by peripheral blood mononuclear cells" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451257/Posttraumatic_stress_disorder_is_associated_with_an_enhanced_spontaneous_production_of_pro_inflammatory_cytokines_by_peripheral_blood_mononuclear_cells">Posttraumatic stress disorder is associated with an enhanced spontaneous production of pro-inflammatory cytokines by peripheral blood mononuclear cells</a></div><div class="wp-workCard_item"><span>BMC Psychiatry</span><span>, 2013</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Posttraumatic stress disorder (PTSD) is associated with an enhanced risk for cardiovascular and o...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Posttraumatic stress disorder (PTSD) is associated with an enhanced risk for cardiovascular and other inflammatory diseases. Chronic low-level inflammation has been suggested as a potential mechanism linking these conditions. We investigated plasma cytokine levels as well as spontaneous and lipopolysaccharide (LPS)-stimulated cytokine production by peripheral blood mononuclear cells (PBMCs) in a group of 35 severely traumatized PTSD patients compared to 25 healthy controls. Spontaneous production of interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α by isolated PBMCs was significantly higher in the PTSD compared to the control group and even correlated with PTSD symptom severity within the PTSD group. In contrast, circulating plasma levels of pro- and anti-inflammatory cytokines such as IL-6, IL-8, IL-10, TNF-α, or monocyte chemotactic protein (MCP)-1 were not significantly altered in PTSD patients compared to healthy controls. Our findings indicate that PBMCs of PTSD patients are already pre-activated in vivo, providing further evidence for low-grade inflammation in PTSD. This might possibly represent one psychobiological pathway from PTSD to poor physical health.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451257"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451257"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451257; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=23451257]").text(description); $(".js-view-count[data-work-id=23451257]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 23451257; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='23451257']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 23451257, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=23451257]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":23451257,"title":"Posttraumatic stress disorder is associated with an enhanced spontaneous production of pro-inflammatory cytokines by peripheral blood mononuclear cells","translated_title":"","metadata":{"abstract":"Posttraumatic stress disorder (PTSD) is associated with an enhanced risk for cardiovascular and other inflammatory diseases. Chronic low-level inflammation has been suggested as a potential mechanism linking these conditions. We investigated plasma cytokine levels as well as spontaneous and lipopolysaccharide (LPS)-stimulated cytokine production by peripheral blood mononuclear cells (PBMCs) in a group of 35 severely traumatized PTSD patients compared to 25 healthy controls. Spontaneous production of interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α by isolated PBMCs was significantly higher in the PTSD compared to the control group and even correlated with PTSD symptom severity within the PTSD group. In contrast, circulating plasma levels of pro- and anti-inflammatory cytokines such as IL-6, IL-8, IL-10, TNF-α, or monocyte chemotactic protein (MCP)-1 were not significantly altered in PTSD patients compared to healthy controls. Our findings indicate that PBMCs of PTSD patients are already pre-activated in vivo, providing further evidence for low-grade inflammation in PTSD. This might possibly represent one psychobiological pathway from PTSD to poor physical health.","publication_date":{"day":null,"month":null,"year":2013,"errors":{}},"publication_name":"BMC Psychiatry"},"translated_abstract":"Posttraumatic stress disorder (PTSD) is associated with an enhanced risk for cardiovascular and other inflammatory diseases. Chronic low-level inflammation has been suggested as a potential mechanism linking these conditions. We investigated plasma cytokine levels as well as spontaneous and lipopolysaccharide (LPS)-stimulated cytokine production by peripheral blood mononuclear cells (PBMCs) in a group of 35 severely traumatized PTSD patients compared to 25 healthy controls. Spontaneous production of interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α by isolated PBMCs was significantly higher in the PTSD compared to the control group and even correlated with PTSD symptom severity within the PTSD group. In contrast, circulating plasma levels of pro- and anti-inflammatory cytokines such as IL-6, IL-8, IL-10, TNF-α, or monocyte chemotactic protein (MCP)-1 were not significantly altered in PTSD patients compared to healthy controls. Our findings indicate that PBMCs of PTSD patients are already pre-activated in vivo, providing further evidence for low-grade inflammation in PTSD. This might possibly represent one psychobiological pathway from PTSD to poor physical health.","internal_url":"https://www.academia.edu/23451257/Posttraumatic_stress_disorder_is_associated_with_an_enhanced_spontaneous_production_of_pro_inflammatory_cytokines_by_peripheral_blood_mononuclear_cells","translated_internal_url":"","created_at":"2016-03-19T08:31:44.751-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":45422374,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":17587438,"work_id":23451257,"tagging_user_id":45422374,"tagged_user_id":21316286,"co_author_invite_id":null,"email":"m***n@illinois.edu","affiliation":"University of Illinois at Urbana-Champaign","display_order":0,"name":"Monica Uddin","title":"Posttraumatic stress disorder is associated with an enhanced spontaneous production of pro-inflammatory cytokines by peripheral blood mononuclear cells"},{"id":17587439,"work_id":23451257,"tagging_user_id":45422374,"tagged_user_id":null,"co_author_invite_id":1007428,"email":"v***u@emory.edu","display_order":4194304,"name":"Varun Kilaru","title":"Posttraumatic stress disorder is associated with an enhanced spontaneous production of pro-inflammatory cytokines by peripheral blood mononuclear cells"},{"id":17587440,"work_id":23451257,"tagging_user_id":45422374,"tagged_user_id":null,"co_author_invite_id":344990,"email":"a***s@med.miami.edu","display_order":6291456,"name":"Amanda Myers","title":"Posttraumatic stress disorder is associated with an enhanced spontaneous production of pro-inflammatory cytokines by peripheral blood mononuclear cells"},{"id":17587441,"work_id":23451257,"tagging_user_id":45422374,"tagged_user_id":null,"co_author_invite_id":560738,"email":"s***k@uvm.edu","display_order":7340032,"name":"Sayamwong Hammack","title":"Posttraumatic stress disorder is associated with an enhanced spontaneous production of pro-inflammatory cytokines by peripheral blood mononuclear cells"},{"id":17587442,"work_id":23451257,"tagging_user_id":45422374,"tagged_user_id":null,"co_author_invite_id":47312,"email":"s***2@columbia.edu","display_order":7864320,"name":"Sandro Galea","title":"Posttraumatic stress disorder is associated with an enhanced spontaneous production of pro-inflammatory cytokines by peripheral blood mononuclear cells"},{"id":17587443,"work_id":23451257,"tagging_user_id":45422374,"tagged_user_id":null,"co_author_invite_id":254648,"email":"k***5@mail.cumc.columbia.edu","display_order":8126464,"name":"Karestan Koenen","title":"Posttraumatic stress disorder is associated with an enhanced spontaneous production of pro-inflammatory cytokines by peripheral blood mononuclear cells"},{"id":17587444,"work_id":23451257,"tagging_user_id":45422374,"tagged_user_id":null,"co_author_invite_id":4031373,"email":"a***5@emory.edu","display_order":8257536,"name":"A. King","title":"Posttraumatic stress disorder is associated with an enhanced spontaneous production of pro-inflammatory cytokines by peripheral blood mononuclear cells"},{"id":17587445,"work_id":23451257,"tagging_user_id":45422374,"tagged_user_id":31010066,"co_author_invite_id":null,"email":"r***4@gmail.com","display_order":8323072,"name":"Rachel Yehuda","title":"Posttraumatic stress disorder is associated with an enhanced spontaneous production of pro-inflammatory cytokines by peripheral blood mononuclear cells"},{"id":17587464,"work_id":23451257,"tagging_user_id":45422374,"tagged_user_id":31705180,"co_author_invite_id":null,"email":"l***n@umich.edu","display_order":8355840,"name":"Israel Liberzon","title":"Posttraumatic stress disorder is associated with an enhanced spontaneous production of pro-inflammatory cytokines by peripheral blood mononuclear cells"},{"id":17587468,"work_id":23451257,"tagging_user_id":45422374,"tagged_user_id":45487326,"co_author_invite_id":312264,"email":"s***o@emory.edu","display_order":8372224,"name":"Seth Norrholm","title":"Posttraumatic stress disorder is associated with an enhanced spontaneous production of pro-inflammatory cytokines by peripheral blood mononuclear cells"},{"id":17587472,"work_id":23451257,"tagging_user_id":45422374,"tagged_user_id":null,"co_author_invite_id":415593,"email":"e***r@emory.edu","display_order":8380416,"name":"Elisabeth Binder","title":"Posttraumatic stress disorder is associated with an enhanced spontaneous production of pro-inflammatory cytokines by peripheral blood mononuclear cells"},{"id":17587475,"work_id":23451257,"tagging_user_id":45422374,"tagged_user_id":null,"co_author_invite_id":4031376,"email":"b***2@emory.edu","display_order":8384512,"name":"Bekh Bradley","title":"Posttraumatic stress disorder is associated with an enhanced spontaneous production of pro-inflammatory cytokines by peripheral blood mononuclear cells"},{"id":17587485,"work_id":23451257,"tagging_user_id":45422374,"tagged_user_id":null,"co_author_invite_id":716841,"email":"k***e@emory.edu","display_order":8386560,"name":"Kerry Ressler","title":"Posttraumatic stress disorder is associated with an enhanced spontaneous production of pro-inflammatory cytokines by peripheral blood mononuclear cells"}],"downloadable_attachments":[],"slug":"Posttraumatic_stress_disorder_is_associated_with_an_enhanced_spontaneous_production_of_pro_inflammatory_cytokines_by_peripheral_blood_mononuclear_cells","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":45422374,"first_name":"Alicia","middle_initials":null,"last_name":"Smith","page_name":"AliciaSmith34","domain_name":"independent","created_at":"2016-03-19T07:49:15.587-07:00","display_name":"Alicia Smith","url":"https://independent.academia.edu/AliciaSmith34"},"attachments":[],"research_interests":[{"id":9111,"name":"Cytokines","url":"https://www.academia.edu/Documents/in/Cytokines"},{"id":22506,"name":"Adolescent","url":"https://www.academia.edu/Documents/in/Adolescent"},{"id":133057,"name":"Young Adult","url":"https://www.academia.edu/Documents/in/Young_Adult"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":474029,"name":"Tumor necrosis factor-alpha","url":"https://www.academia.edu/Documents/in/Tumor_necrosis_factor-alpha"},{"id":1819399,"name":"Case Control Studies","url":"https://www.academia.edu/Documents/in/Case_Control_Studies"},{"id":1924712,"name":"Interleukin","url":"https://www.academia.edu/Documents/in/Interleukin"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="23451256"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451256/Interactions_between_the_COMT_Val108_158Met_polymorphism_and_maternal_prenatal_smoking_predict_aggressive_behavior_outcomes"><img alt="Research paper thumbnail of Interactions between the COMT Val108/158Met polymorphism and maternal prenatal smoking predict aggressive behavior outcomes" class="work-thumbnail" src="https://attachments.academia-assets.com/43891693/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451256/Interactions_between_the_COMT_Val108_158Met_polymorphism_and_maternal_prenatal_smoking_predict_aggressive_behavior_outcomes">Interactions between the COMT Val108/158Met polymorphism and maternal prenatal smoking predict aggressive behavior outcomes</a></div><div class="wp-workCard_item"><span>Biological Psychology</span><span>, 2011</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="2f2f40ef8fc64fc7c20c4b672f2861bf" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":43891693,"asset_id":23451256,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/43891693/download_file?st=MTczMjc3ODAwOCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451256"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451256"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451256; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=23451256]").text(description); $(".js-view-count[data-work-id=23451256]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 23451256; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='23451256']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 23451256, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "2f2f40ef8fc64fc7c20c4b672f2861bf" } } $('.js-work-strip[data-work-id=23451256]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":23451256,"title":"Interactions between the COMT Val108/158Met polymorphism and maternal prenatal smoking predict aggressive behavior outcomes","translated_title":"","metadata":{"grobid_abstract":"The purpose of the current study is to examine the moderating influence of the catechol O methyltransferase gene (COMT) on the maternal prenatal smoking/offspring externalizing disorder relationship. The sample consisted of 430 young adults born between 1981 and 1984 at the Mater Misericordiae Mother's Hospital in Brisbane, Australia, as well as their mothers and peers. Mothers reported their prenatal smoking status during pregnancy, and genetic data was obtained from the youth at a later follow-up in adulthood. The outcome measures in this study were mother and teacher reports of youth attention problems and aggression at age 15, and youth, mother and peer reports of youth attention problems and aggression at age 20 (combined to create latent factors of attention problems and aggression at each age). The COMT Val108/158Met polymorphism (rs4680) significantly interacted with maternal cigarette smoking during pregnancy to predict youth aggressive behavior at ages 15 and 20. This gene-environment interaction was not significant for youth attention problems.","publication_date":{"day":null,"month":null,"year":2011,"errors":{}},"publication_name":"Biological Psychology","grobid_abstract_attachment_id":43891693},"translated_abstract":null,"internal_url":"https://www.academia.edu/23451256/Interactions_between_the_COMT_Val108_158Met_polymorphism_and_maternal_prenatal_smoking_predict_aggressive_behavior_outcomes","translated_internal_url":"","created_at":"2016-03-19T08:31:44.603-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":45422374,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":17587436,"work_id":23451256,"tagging_user_id":45422374,"tagged_user_id":6138223,"co_author_invite_id":null,"email":"p***d@qimrberghofer.edu.au","affiliation":"Queensland Institute of Medical Research","display_order":0,"name":"Penelope Lind","title":"Interactions between the COMT Val108/158Met polymorphism and maternal prenatal smoking predict aggressive behavior outcomes"},{"id":17587437,"work_id":23451256,"tagging_user_id":45422374,"tagged_user_id":32210390,"co_author_invite_id":null,"email":"h***n@psych.ucla.edu","affiliation":"University of California, Los Angeles","display_order":4194304,"name":"Constance Hammen","title":"Interactions between the COMT Val108/158Met polymorphism and maternal prenatal smoking predict aggressive behavior outcomes"},{"id":17587473,"work_id":23451256,"tagging_user_id":45422374,"tagged_user_id":5846287,"co_author_invite_id":null,"email":"p***1@emory.edu","affiliation":"Emory University","display_order":6291456,"name":"Patricia Brennan","title":"Interactions between the COMT Val108/158Met polymorphism and maternal prenatal smoking predict aggressive behavior 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$a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="23335209"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23335209/Differential_immune_system_DNA_methylation_and_cytokine_regulation_in_post_traumatic_stress_disorder"><img alt="Research paper thumbnail of Differential immune system DNA methylation and cytokine regulation in post-traumatic stress disorder" class="work-thumbnail" src="https://attachments.academia-assets.com/43792465/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23335209/Differential_immune_system_DNA_methylation_and_cytokine_regulation_in_post_traumatic_stress_disorder">Differential immune system DNA methylation and cytokine regulation in post-traumatic stress disorder</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/KarenConneely">Karen Conneely</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/AliciaSmith34">Alicia Smith</a></span></div><div class="wp-workCard_item"><span>American Journal of Medical Genetics Part B: Neuropsychiatric Genetics</span><span>, 2011</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="dc401c63909a973334250f6b3b6f4035" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" 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To examine this hypothesis, we evaluated African American subjects matched by age and sex, and stratified into four groups by post-traumatic stress disorder (PTSD) diagnosis and history of child abuse. Total Life Stress (TLS) was also assessed in all subjects. We evaluated DNA extracted from peripheral blood using the HumanMethylation27 BeadChip and analyzed both global and site-specific methylation. Methylation levels were examined for association with PTSD, child abuse history, and TLS using a linear mixed model adjusted for age, sex, and chip effects. Global methylation was increased in subjects with PTSD. CpG sites in five genes (TPR, CLEC9A, APC5, ANXA2, and TLR8) were differentially methylated in subjects with PTSD. Additionally, a CpG site in NPFFR2 was associated with TLS after adjustment for multiple testing. Notably, many of these genes have been previously associated with inflammation. Given these results and reports of immune dysregulation associated with trauma history, we compared plasma cytokine levels in these subjects and found IL4, IL2, and TNFa levels associated with PTSD, child abuse, and TLS. Together, these results suggest that psychosocial stress may alter global and gene-specific DNA methylation patterns potentially associated with peripheral immune dysregulation. 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class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23337368/A_genome_wide_identified_risk_variant_for_PTSD_is_a_methylation_quantitative_trait_locus_and_confers_decreased_cortical_activation_to_fearful_faces"><img alt="Research paper thumbnail of A genome-wide identified risk variant for PTSD is a methylation quantitative trait locus and confers decreased cortical activation to fearful faces" class="work-thumbnail" src="https://attachments.academia-assets.com/43794249/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23337368/A_genome_wide_identified_risk_variant_for_PTSD_is_a_methylation_quantitative_trait_locus_and_confers_decreased_cortical_activation_to_fearful_faces">A genome-wide identified risk variant for PTSD is a methylation quantitative trait locus and confers decreased cortical activation to fearful faces</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/LynnAlmli">Lynn Almli</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/AliciaSmith34">Alicia Smith</a></span></div><div class="wp-workCard_item"><span>American Journal of Medical Genetics Part B: Neuropsychiatric Genetics</span><span>, 2015</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="db51d42832544fe35502ec581c3ca6e1" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":43794249,"asset_id":23337368,"asset_type":"Work","button_location":"profile"}" 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})(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "db51d42832544fe35502ec581c3ca6e1" } } $('.js-work-strip[data-work-id=23337368]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":23337368,"title":"A genome-wide identified risk variant for PTSD is a methylation quantitative trait locus and confers decreased cortical activation to fearful faces","translated_title":"","metadata":{"grobid_abstract":"R, Marmar CR, Ressler KJ. 2015. A genome-wide identified risk variant for PTSD is a methylation quantitative trait locus and confers decreased cortical activation to fearful faces. Am J Med Genet Part B 9999:1-10.","publication_date":{"day":null,"month":null,"year":2015,"errors":{}},"publication_name":"American Journal of Medical Genetics Part B: Neuropsychiatric Genetics","grobid_abstract_attachment_id":43794249},"translated_abstract":null,"internal_url":"https://www.academia.edu/23337368/A_genome_wide_identified_risk_variant_for_PTSD_is_a_methylation_quantitative_trait_locus_and_confers_decreased_cortical_activation_to_fearful_faces","translated_internal_url":"","created_at":"2016-03-16T13:51:54.275-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":45255247,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":17428989,"work_id":23337368,"tagging_user_id":45255247,"tagged_user_id":null,"co_author_invite_id":1521894,"email":"r***2@emory.edu","display_order":0,"name":"Bekh Bradley","title":"A genome-wide identified risk variant for PTSD is a methylation quantitative trait locus and confers decreased 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data-work-id="23451273"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451273/Ancestry_Dependent_DNA_Methylation_and_Influence_of_Maternal_Nutrition"><img alt="Research paper thumbnail of Ancestry Dependent DNA Methylation and Influence of Maternal Nutrition" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451273/Ancestry_Dependent_DNA_Methylation_and_Influence_of_Maternal_Nutrition">Ancestry Dependent DNA Methylation and Influence of Maternal Nutrition</a></div><div class="wp-workCard_item"><span>PLOS ONE</span><span>, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">There is extensive variation in DNA methylation between individuals and ethnic groups. These diff...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">There is extensive variation in DNA methylation between individuals and ethnic groups. These differences arise from a combination of genetic and non-genetic influences and potential modifiers include nutritional cues, early life experience, and social and physical environments. Here we compare genome-wide DNA methylation in neonatal cord blood from African American (AA; N = 112) and European American (EA; N = 91) participants of the CANDLE Study (Conditions Affecting Neurocognitive Development and Learning in Early Childhood). Our goal is to determine if there are replicable ancestry-specific methylation patterns that may implicate risk factors for diseases that have differential prevalence between populations. To identify the most robust ancestry-specific CpG sites, we replicate our results in lymphoblastoid cell lines from Yoruba African and CEPH European panels of HapMap. We also evaluate the influence of maternal nutrition-specifically, plasma levels of vitamin D and folate during pregnancy-on methylation in newborns. We define stable ancestry-dependent methylation of genes that include tumor suppressors and cell cycle regulators (e.g., APC, BRCA1, MCC). Overall, there is lower global methylation in African ancestral groups. Plasma levels of 25-hydroxy vitamin D are also considerably lower among AA mothers and about 60% of AA and 40% of EA mothers have concentrations below 20 ng/ml. Using a weighted correlation analysis, we define a network of CpG sites that is jointly modulated by ancestry and maternal vitamin D. Our results show that differences in DNA methylation patterns are remarkably stable and maternal micronutrients can exert an influence on the child epigenome.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451273"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451273"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451273; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=23451273]").text(description); $(".js-view-count[data-work-id=23451273]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 23451273; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='23451273']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 23451273, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=23451273]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":23451273,"title":"Ancestry Dependent DNA Methylation and Influence of Maternal Nutrition","translated_title":"","metadata":{"abstract":"There is extensive variation in DNA methylation between individuals and ethnic groups. These differences arise from a combination of genetic and non-genetic influences and potential modifiers include nutritional cues, early life experience, and social and physical environments. Here we compare genome-wide DNA methylation in neonatal cord blood from African American (AA; N = 112) and European American (EA; N = 91) participants of the CANDLE Study (Conditions Affecting Neurocognitive Development and Learning in Early Childhood). Our goal is to determine if there are replicable ancestry-specific methylation patterns that may implicate risk factors for diseases that have differential prevalence between populations. To identify the most robust ancestry-specific CpG sites, we replicate our results in lymphoblastoid cell lines from Yoruba African and CEPH European panels of HapMap. We also evaluate the influence of maternal nutrition-specifically, plasma levels of vitamin D and folate during pregnancy-on methylation in newborns. We define stable ancestry-dependent methylation of genes that include tumor suppressors and cell cycle regulators (e.g., APC, BRCA1, MCC). Overall, there is lower global methylation in African ancestral groups. Plasma levels of 25-hydroxy vitamin D are also considerably lower among AA mothers and about 60% of AA and 40% of EA mothers have concentrations below 20 ng/ml. Using a weighted correlation analysis, we define a network of CpG sites that is jointly modulated by ancestry and maternal vitamin D. Our results show that differences in DNA methylation patterns are remarkably stable and maternal micronutrients can exert an influence on the child epigenome.","publication_date":{"day":null,"month":null,"year":2015,"errors":{}},"publication_name":"PLOS ONE"},"translated_abstract":"There is extensive variation in DNA methylation between individuals and ethnic groups. These differences arise from a combination of genetic and non-genetic influences and potential modifiers include nutritional cues, early life experience, and social and physical environments. Here we compare genome-wide DNA methylation in neonatal cord blood from African American (AA; N = 112) and European American (EA; N = 91) participants of the CANDLE Study (Conditions Affecting Neurocognitive Development and Learning in Early Childhood). Our goal is to determine if there are replicable ancestry-specific methylation patterns that may implicate risk factors for diseases that have differential prevalence between populations. To identify the most robust ancestry-specific CpG sites, we replicate our results in lymphoblastoid cell lines from Yoruba African and CEPH European panels of HapMap. We also evaluate the influence of maternal nutrition-specifically, plasma levels of vitamin D and folate during pregnancy-on methylation in newborns. We define stable ancestry-dependent methylation of genes that include tumor suppressors and cell cycle regulators (e.g., APC, BRCA1, MCC). Overall, there is lower global methylation in African ancestral groups. Plasma levels of 25-hydroxy vitamin D are also considerably lower among AA mothers and about 60% of AA and 40% of EA mothers have concentrations below 20 ng/ml. Using a weighted correlation analysis, we define a network of CpG sites that is jointly modulated by ancestry and maternal vitamin D. Our results show that differences in DNA methylation patterns are remarkably stable and maternal micronutrients can exert an influence on the child epigenome.","internal_url":"https://www.academia.edu/23451273/Ancestry_Dependent_DNA_Methylation_and_Influence_of_Maternal_Nutrition","translated_internal_url":"","created_at":"2016-03-19T08:31:47.176-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":45422374,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":17587460,"work_id":23451273,"tagging_user_id":45422374,"tagged_user_id":37586952,"co_author_invite_id":null,"email":"f***k@uthsc.edu","display_order":0,"name":"Frances Tylavsky","title":"Ancestry Dependent DNA Methylation and Influence of Maternal Nutrition"}],"downloadable_attachments":[],"slug":"Ancestry_Dependent_DNA_Methylation_and_Influence_of_Maternal_Nutrition","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":45422374,"first_name":"Alicia","middle_initials":null,"last_name":"Smith","page_name":"AliciaSmith34","domain_name":"independent","created_at":"2016-03-19T07:49:15.587-07:00","display_name":"Alicia Smith","url":"https://independent.academia.edu/AliciaSmith34"},"attachments":[],"research_interests":[{"id":28235,"name":"Multidisciplinary","url":"https://www.academia.edu/Documents/in/Multidisciplinary"},{"id":220780,"name":"PLoS one","url":"https://www.academia.edu/Documents/in/PLoS_one"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="23451272"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451272/Oxytocin_vasopressin_and_Williams_syndrome_epigenetic_effects_on_abnormal_social_behavior"><img alt="Research paper thumbnail of Oxytocin, vasopressin, and Williams syndrome: epigenetic effects on abnormal social behavior" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451272/Oxytocin_vasopressin_and_Williams_syndrome_epigenetic_effects_on_abnormal_social_behavior">Oxytocin, vasopressin, and Williams syndrome: epigenetic effects on abnormal social behavior</a></div><div class="wp-workCard_item"><span>Frontiers in Genetics</span><span>, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Williams syndrome (WS) is a condition caused by a deletion of ∼26-28 genes on chromosome 7q11.23 ...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Williams syndrome (WS) is a condition caused by a deletion of ∼26-28 genes on chromosome 7q11.23 often characterized by abnormal social behavior and disrupted oxytocin (OT) and vasopressin (AVP) functioning. The observation that individuals with WS exhibit OT and AVP dysregulation is compelling. There is currently a lack of evidence that any of the genes typically deleted in WS have any direct effect on either OT or AVP. In this perspective article, we present a novel epigenetic model describing how DNA methylation may impact the expression of key genes within the OT and AVP systems, which may ultimately influence the social behavior observed in WS. We draw support from data pooled from a prior empirical research study (Henrichsen et al., 2011), demonstrating that OXTR is overexpressed in WS. These preliminary findings may create new opportunities to target the OT and AVP systems with the specific goal of improving outcomes in WS and other psychiatric conditions.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451272"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451272"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451272; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=23451272]").text(description); $(".js-view-count[data-work-id=23451272]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 23451272; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='23451272']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 23451272, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=23451272]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":23451272,"title":"Oxytocin, vasopressin, and Williams syndrome: epigenetic effects on abnormal social behavior","translated_title":"","metadata":{"abstract":"Williams syndrome (WS) is a condition caused by a deletion of ∼26-28 genes on chromosome 7q11.23 often characterized by abnormal social behavior and disrupted oxytocin (OT) and vasopressin (AVP) functioning. The observation that individuals with WS exhibit OT and AVP dysregulation is compelling. There is currently a lack of evidence that any of the genes typically deleted in WS have any direct effect on either OT or AVP. In this perspective article, we present a novel epigenetic model describing how DNA methylation may impact the expression of key genes within the OT and AVP systems, which may ultimately influence the social behavior observed in WS. We draw support from data pooled from a prior empirical research study (Henrichsen et al., 2011), demonstrating that OXTR is overexpressed in WS. These preliminary findings may create new opportunities to target the OT and AVP systems with the specific goal of improving outcomes in WS and other psychiatric conditions.","publication_date":{"day":null,"month":null,"year":2015,"errors":{}},"publication_name":"Frontiers in Genetics"},"translated_abstract":"Williams syndrome (WS) is a condition caused by a deletion of ∼26-28 genes on chromosome 7q11.23 often characterized by abnormal social behavior and disrupted oxytocin (OT) and vasopressin (AVP) functioning. The observation that individuals with WS exhibit OT and AVP dysregulation is compelling. There is currently a lack of evidence that any of the genes typically deleted in WS have any direct effect on either OT or AVP. In this perspective article, we present a novel epigenetic model describing how DNA methylation may impact the expression of key genes within the OT and AVP systems, which may ultimately influence the social behavior observed in WS. We draw support from data pooled from a prior empirical research study (Henrichsen et al., 2011), demonstrating that OXTR is overexpressed in WS. These preliminary findings may create new opportunities to target the OT and AVP systems with the specific goal of improving outcomes in WS and other psychiatric conditions.","internal_url":"https://www.academia.edu/23451272/Oxytocin_vasopressin_and_Williams_syndrome_epigenetic_effects_on_abnormal_social_behavior","translated_internal_url":"","created_at":"2016-03-19T08:31:47.027-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":45422374,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":17587459,"work_id":23451272,"tagging_user_id":45422374,"tagged_user_id":33569643,"co_author_invite_id":null,"email":"b***s@uga.edu","display_order":0,"name":"Brian Haas","title":"Oxytocin, vasopressin, and Williams syndrome: epigenetic effects on abnormal social behavior"}],"downloadable_attachments":[],"slug":"Oxytocin_vasopressin_and_Williams_syndrome_epigenetic_effects_on_abnormal_social_behavior","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":45422374,"first_name":"Alicia","middle_initials":null,"last_name":"Smith","page_name":"AliciaSmith34","domain_name":"independent","created_at":"2016-03-19T07:49:15.587-07:00","display_name":"Alicia Smith","url":"https://independent.academia.edu/AliciaSmith34"},"attachments":[],"research_interests":[],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="23451271"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451271/Fetal_DNA_Methylation_of_Autism_Spectrum_Disorders_ASD_Candidate_Genes_Association_with_Spontaneous_Preterm_Birth"><img alt="Research paper thumbnail of Fetal DNA Methylation of Autism Spectrum Disorders (ASD) Candidate Genes: Association with Spontaneous Preterm Birth" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451271/Fetal_DNA_Methylation_of_Autism_Spectrum_Disorders_ASD_Candidate_Genes_Association_with_Spontaneous_Preterm_Birth">Fetal DNA Methylation of Autism Spectrum Disorders (ASD) Candidate Genes: Association with Spontaneous Preterm Birth</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/AliciaSmith34">Alicia Smith</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/SashaParets">Sasha Parets</a></span></div><div class="wp-workCard_item"><span>American journal of obstetrics and gynecology</span><span>, Jan 13, 2015</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Autism Spectrum Disorder (ASD) is associated with preterm birth (PTB); though the reason underlyi...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Autism Spectrum Disorder (ASD) is associated with preterm birth (PTB); though the reason underlying this relationship is still unclear. Our objective was to examine DNA methylation patterns of four ASD candidate genes in human fetal membranes from spontaneous PTB and uncomplicated term birth (TB). A literature search for genes implicated in ASD yielded 14 candidate genes (OXTR, SHANK3, BCL2, RORA, EN2, RELN, MECP2, AUTS2, NLGN3, NRXN1, SLC6A4, UBE3A, GABA, AFF2) that were epigenetically modified in relation to ASD. DNA methylation in fetal leukocyte DNA in four of these genes (OXTR, SHANK3, BCL2 and RORA) associated with PTB in a previous study. This study evaluated DNA methylation, transcription (qPCR) and translation patterns (immunostaining and western blot) in fetal membrane from term labor (TL; n=14), term not in labor (TNIL; n=29) and spontaneous preterm birth (PTB; n=27). Statistical analysis was performed using ANOVA and a p-value of &lt; 0.05 was significant. Higher methyla...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451271"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451271"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451271; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=23451271]").text(description); $(".js-view-count[data-work-id=23451271]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 23451271; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='23451271']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 23451271, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=23451271]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":23451271,"title":"Fetal DNA Methylation of Autism Spectrum Disorders (ASD) Candidate Genes: Association with Spontaneous Preterm Birth","translated_title":"","metadata":{"abstract":"Autism Spectrum Disorder (ASD) is associated with preterm birth (PTB); though the reason underlying this relationship is still unclear. Our objective was to examine DNA methylation patterns of four ASD candidate genes in human fetal membranes from spontaneous PTB and uncomplicated term birth (TB). A literature search for genes implicated in ASD yielded 14 candidate genes (OXTR, SHANK3, BCL2, RORA, EN2, RELN, MECP2, AUTS2, NLGN3, NRXN1, SLC6A4, UBE3A, GABA, AFF2) that were epigenetically modified in relation to ASD. DNA methylation in fetal leukocyte DNA in four of these genes (OXTR, SHANK3, BCL2 and RORA) associated with PTB in a previous study. This study evaluated DNA methylation, transcription (qPCR) and translation patterns (immunostaining and western blot) in fetal membrane from term labor (TL; n=14), term not in labor (TNIL; n=29) and spontaneous preterm birth (PTB; n=27). Statistical analysis was performed using ANOVA and a p-value of \u0026lt; 0.05 was significant. Higher methyla...","publication_date":{"day":13,"month":1,"year":2015,"errors":{}},"publication_name":"American journal of obstetrics and gynecology"},"translated_abstract":"Autism Spectrum Disorder (ASD) is associated with preterm birth (PTB); though the reason underlying this relationship is still unclear. Our objective was to examine DNA methylation patterns of four ASD candidate genes in human fetal membranes from spontaneous PTB and uncomplicated term birth (TB). A literature search for genes implicated in ASD yielded 14 candidate genes (OXTR, SHANK3, BCL2, RORA, EN2, RELN, MECP2, AUTS2, NLGN3, NRXN1, SLC6A4, UBE3A, GABA, AFF2) that were epigenetically modified in relation to ASD. DNA methylation in fetal leukocyte DNA in four of these genes (OXTR, SHANK3, BCL2 and RORA) associated with PTB in a previous study. This study evaluated DNA methylation, transcription (qPCR) and translation patterns (immunostaining and western blot) in fetal membrane from term labor (TL; n=14), term not in labor (TNIL; n=29) and spontaneous preterm birth (PTB; n=27). Statistical analysis was performed using ANOVA and a p-value of \u0026lt; 0.05 was significant. 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AL is operationalized by a composite index of multiple biomarkers. Accordingly, genes, behavior and environment contribute to AL. To determine if individual differences in AL may be influenced by inherent genetic variation, we calculated an allostatic load index (ALI) for 182 Caucasian subjects derived from a population-based study of chronic fatigue syndrome. Nearly 65% of the subjects in this study sample reported fatiguing illness. ALI was calculated based on 11 measures representing metabolic, cardiovascular, inflammatory, hypothalamic-pituitary-adrenal (HPA) axis and sympathetic nervous system (SNS) activities. Subjects were dichotomized into high (ALI &gt; or = 3) or low (ALI &lt; 3) AL groups, and the association between high AL and 129 polymorphisms in 32 genes related to the HPA axis, neurotransmission, inflammation, ca...</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="bf18c58837692329cbfc75674095f237" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":43891702,"asset_id":23451270,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/43891702/download_file?st=MTczMjc3ODAwOCw4LjIyMi4yMDguMTQ2&st=MTczMjc3ODAwNyw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451270"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451270"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451270; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=23451270]").text(description); $(".js-view-count[data-work-id=23451270]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 23451270; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='23451270']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 23451270, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "bf18c58837692329cbfc75674095f237" } } $('.js-work-strip[data-work-id=23451270]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":23451270,"title":"An angiotensin-1 converting enzyme polymorphism is associated with allostatic load mediated by C-reactive protein, interleukin-6 and cortisol","translated_title":"","metadata":{"abstract":"Allostatic load (AL) is a theoretical framework that describes the cumulative physiologic effects of adaptation to change or stress throughout the lifespan. 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profile--work_container" data-work-id="23451269"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451269/Biomarker_Development_for_Brain_Based_Disorders_Recent_Progress_in_Psychiatry"><img alt="Research paper thumbnail of Biomarker Development for Brain-Based Disorders: Recent Progress in Psychiatry" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451269/Biomarker_Development_for_Brain_Based_Disorders_Recent_Progress_in_Psychiatry">Biomarker Development for Brain-Based Disorders: Recent Progress in Psychiatry</a></div><div class="wp-workCard_item"><span>Journal of neurology and psychology</span><span>, 2013</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Biomarkers are biological measures that are indicative of a specific disorder, its severity or re...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Biomarkers are biological measures that are indicative of a specific disorder, its severity or response to treatment. They are widely used in many areas of medicine, but biomarker development for brain-based disorders lags behind. Using examples from the field of psychiatry, this article reviews the concepts of biomarkers, challenges to their development and the recent progress along those lines. In addition to discussing historical biomarker candidates such as cortisol or catecholamine levels, we include progress from recent genetic, epigenetic, proteomic, neuroimaging and EEG studies. Successful identification of biomarkers will advance the field of psychiatry towards the goal of biological tests for diagnosis, symptom management and treatment response.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451269"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451269"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451269; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=23451269]").text(description); $(".js-view-count[data-work-id=23451269]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 23451269; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='23451269']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 23451269, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=23451269]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":23451269,"title":"Biomarker Development for Brain-Based Disorders: Recent Progress in Psychiatry","translated_title":"","metadata":{"abstract":"Biomarkers are biological measures that are indicative of a specific disorder, its severity or response to treatment. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="23451266"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451266/HPA_Axis_Evidence_of_Transgenerational_Effects_of_Maternal_Early_Life_Trauma_in_6_Month_Old_Infants"><img alt="Research paper thumbnail of HPA Axis Evidence of Transgenerational Effects of Maternal Early-Life Trauma in 6-Month-Old Infants" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451266/HPA_Axis_Evidence_of_Transgenerational_Effects_of_Maternal_Early_Life_Trauma_in_6_Month_Old_Infants">HPA Axis Evidence of Transgenerational Effects of Maternal Early-Life Trauma in 6-Month-Old Infants</a></div><div class="wp-workCard_item"><span>PsycEXTRA Dataset</span><span>, 2000</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451266"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451266"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451266; 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="23451264"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451264/Genetic_evaluation_of_the_serotonergic_system_in_chronic_fatigue_syndrome"><img alt="Research paper thumbnail of Genetic evaluation of the serotonergic system in chronic fatigue syndrome" class="work-thumbnail" src="https://attachments.academia-assets.com/43891699/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451264/Genetic_evaluation_of_the_serotonergic_system_in_chronic_fatigue_syndrome">Genetic evaluation of the serotonergic system in chronic fatigue syndrome</a></div><div class="wp-workCard_item"><span>Psychoneuroendocrinology</span><span>, 2008</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="948e02ef53a57b866daaf90e96152ceb" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":43891699,"asset_id":23451264,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/43891699/download_file?st=MTczMjc3ODAwOCw4LjIyMi4yMDguMTQ2&st=MTczMjc3ODAwOCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451264"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451264"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451264; 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The pathophysiology of CFS remains elusive, although abnormalities in the central nervous system (CNS) have been implicated, particularly hyperactivity of the serotonergic (5-hydroxytryptamine; 5-HT) system and hypoactivity of the hypothalamic-pituitary-adrenal (HPA) axis. Since alterations in 5-HT signaling can lead to physiologic and behavioral changes, a genetic evaluation of the 5-HT system was undertaken to identify serotonergic markers associated with CFS and potential mechanisms for CNS abnormality. A total of 77 polymorphisms in genes related to serotonin synthesis (TPH2), signaling (HTR1A, HTR1E, HTR2A, HTR2B, HTR2C, HTR3A, HTR3B, HTR4, HTR5A, HTR6, and HTR7), transport (SLC6A4), and catabolism (MAOA) were examined in 137 clinically evaluated subjects (40 CFS, 55 with insufficient fatigue, and 42 non-fatigued, NF, controls) derived from a population-based CFS surveillance study in Wichita, Kansas. Of the polymorphisms examined, three markers (À1438G/A, C102T, and rs1923884) all located in the 5-HT receptor subtype HTR2A were associated with CFS when compared to NF controls. Additionally, consistent associations were observed between HTR2A variants and quantitative measures of disability and fatigue in all subjects. The most compelling of these associations was with the A allele of À1438G/A (rs6311) which is suggested to have increased promoter activity in functional studies. Further, in silico analysis revealed that the À1438 A allele creates a consensus binding site for Th1/E47, a transcription factor implicated in the development of the nervous system. 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}); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="23451263"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451263/Polymorphisms_in_genes_regulating_the_HPA_axis_associated_with_empirically_delineated_classes_of_unexplained_chronic_fatigue"><img alt="Research paper thumbnail of Polymorphisms in genes regulating the HPA axis associated with empirically delineated classes of unexplained chronic fatigue" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451263/Polymorphisms_in_genes_regulating_the_HPA_axis_associated_with_empirically_delineated_classes_of_unexplained_chronic_fatigue">Polymorphisms in genes regulating the HPA axis associated with empirically delineated classes of unexplained chronic fatigue</a></div><div class="wp-workCard_item"><span>Pharmacogenomics</span><span>, 2006</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Chronic fatigue syndrome (CFS) is characterized by persistent or relapsing fatigue that is not al...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Chronic fatigue syndrome (CFS) is characterized by persistent or relapsing fatigue that is not alleviated by rest, causes substantial reduction in activities and is accompanied by a variety of symptoms. Its unknown etiology may reflect that CFS is heterogeneous. Latent class analyses of symptoms and physiological systems were used to delineate subgroups within a population-based sample of fatigued and nonfatigued subjects [1] . This study examined whether genetic differences underlie the individual subgroups of the latent class solution. Polymorphisms in 11 candidate genes related to both hypothalamic-pituitary-adrenal (HPA) axis function and mood-related neurotransmitter systems were evaluated by comparing each of the five ill classes (Class 1, n = 33; Class 3, n = 22; Class 4, n = 22; Class 5, n = 17; Class 6, n = 11) of fatigued subjects with subjects defined as well (Class 2, n = 35). Of the five classes of subjects with unexplained fatigue, three classes were distinguished by gene polymorphsims involved in either HPA axis function or neurotransmitter systems, including proopiomelanocortin (POMC), nuclear receptor subfamily 3, group C, member 1 (NR3C1), monoamine oxidase A (MAOA), monoamine oxidase B (MAOB), and tryptophan hydroxylase 2 (TPH2). These data support the hypothesis that medically unexplained chronic fatigue is heterogeneous and presents preliminary evidence of the genetic mechanisms underlying some of the putative conditions.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451263"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451263"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451263; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=23451263]").text(description); $(".js-view-count[data-work-id=23451263]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 23451263; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='23451263']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 23451263, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=23451263]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":23451263,"title":"Polymorphisms in genes regulating the HPA axis associated with empirically delineated classes of unexplained chronic fatigue","translated_title":"","metadata":{"abstract":"Chronic fatigue syndrome (CFS) is characterized by persistent or relapsing fatigue that is not alleviated by rest, causes substantial reduction in activities and is accompanied by a variety of symptoms. Its unknown etiology may reflect that CFS is heterogeneous. Latent class analyses of symptoms and physiological systems were used to delineate subgroups within a population-based sample of fatigued and nonfatigued subjects [1] . This study examined whether genetic differences underlie the individual subgroups of the latent class solution. Polymorphisms in 11 candidate genes related to both hypothalamic-pituitary-adrenal (HPA) axis function and mood-related neurotransmitter systems were evaluated by comparing each of the five ill classes (Class 1, n = 33; Class 3, n = 22; Class 4, n = 22; Class 5, n = 17; Class 6, n = 11) of fatigued subjects with subjects defined as well (Class 2, n = 35). Of the five classes of subjects with unexplained fatigue, three classes were distinguished by gene polymorphsims involved in either HPA axis function or neurotransmitter systems, including proopiomelanocortin (POMC), nuclear receptor subfamily 3, group C, member 1 (NR3C1), monoamine oxidase A (MAOA), monoamine oxidase B (MAOB), and tryptophan hydroxylase 2 (TPH2). These data support the hypothesis that medically unexplained chronic fatigue is heterogeneous and presents preliminary evidence of the genetic mechanisms underlying some of the putative conditions.","publication_date":{"day":null,"month":null,"year":2006,"errors":{}},"publication_name":"Pharmacogenomics"},"translated_abstract":"Chronic fatigue syndrome (CFS) is characterized by persistent or relapsing fatigue that is not alleviated by rest, causes substantial reduction in activities and is accompanied by a variety of symptoms. Its unknown etiology may reflect that CFS is heterogeneous. Latent class analyses of symptoms and physiological systems were used to delineate subgroups within a population-based sample of fatigued and nonfatigued subjects [1] . This study examined whether genetic differences underlie the individual subgroups of the latent class solution. Polymorphisms in 11 candidate genes related to both hypothalamic-pituitary-adrenal (HPA) axis function and mood-related neurotransmitter systems were evaluated by comparing each of the five ill classes (Class 1, n = 33; Class 3, n = 22; Class 4, n = 22; Class 5, n = 17; Class 6, n = 11) of fatigued subjects with subjects defined as well (Class 2, n = 35). Of the five classes of subjects with unexplained fatigue, three classes were distinguished by gene polymorphsims involved in either HPA axis function or neurotransmitter systems, including proopiomelanocortin (POMC), nuclear receptor subfamily 3, group C, member 1 (NR3C1), monoamine oxidase A (MAOA), monoamine oxidase B (MAOB), and tryptophan hydroxylase 2 (TPH2). These data support the hypothesis that medically unexplained chronic fatigue is heterogeneous and presents preliminary evidence of the genetic mechanisms underlying some of the putative conditions.","internal_url":"https://www.academia.edu/23451263/Polymorphisms_in_genes_regulating_the_HPA_axis_associated_with_empirically_delineated_classes_of_unexplained_chronic_fatigue","translated_internal_url":"","created_at":"2016-03-19T08:31:45.862-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":45422374,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":17587451,"work_id":23451263,"tagging_user_id":45422374,"tagged_user_id":255601877,"co_author_invite_id":2188190,"email":"u***a@unsw.edu.au","display_order":0,"name":"Ute Vollmer-conna","title":"Polymorphisms in genes regulating the HPA axis associated with empirically delineated classes of unexplained chronic fatigue"},{"id":17587452,"work_id":23451263,"tagging_user_id":45422374,"tagged_user_id":null,"co_author_invite_id":4031374,"email":"d***2@emory.edu","display_order":4194304,"name":"Peter White","title":"Polymorphisms in genes regulating the HPA axis associated with empirically delineated classes of unexplained chronic fatigue"}],"downloadable_attachments":[],"slug":"Polymorphisms_in_genes_regulating_the_HPA_axis_associated_with_empirically_delineated_classes_of_unexplained_chronic_fatigue","translated_slug":"","page_count":null,"language":"en","content_type":"Work","owner":{"id":45422374,"first_name":"Alicia","middle_initials":null,"last_name":"Smith","page_name":"AliciaSmith34","domain_name":"independent","created_at":"2016-03-19T07:49:15.587-07:00","display_name":"Alicia Smith","url":"https://independent.academia.edu/AliciaSmith34"},"attachments":[],"research_interests":[{"id":2629,"name":"Pharmacogenomics","url":"https://www.academia.edu/Documents/in/Pharmacogenomics"},{"id":3855,"name":"Polymorphism","url":"https://www.academia.edu/Documents/in/Polymorphism"},{"id":4338,"name":"Gene regulation","url":"https://www.academia.edu/Documents/in/Gene_regulation"},{"id":17804,"name":"Chronic Fatigue Syndrome","url":"https://www.academia.edu/Documents/in/Chronic_Fatigue_Syndrome"},{"id":48057,"name":"DNA","url":"https://www.academia.edu/Documents/in/DNA"},{"id":50238,"name":"Affect","url":"https://www.academia.edu/Documents/in/Affect"},{"id":86952,"name":"Haplotypes","url":"https://www.academia.edu/Documents/in/Haplotypes"},{"id":131835,"name":"HPA axis","url":"https://www.academia.edu/Documents/in/HPA_axis"},{"id":372410,"name":"Genotype","url":"https://www.academia.edu/Documents/in/Genotype"},{"id":1252054,"name":"Pituitary Hormones","url":"https://www.academia.edu/Documents/in/Pituitary_Hormones"},{"id":1763968,"name":"Gene Expression Regulation","url":"https://www.academia.edu/Documents/in/Gene_Expression_Regulation"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="23451262"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451262/Convergent_Genomic_Studies_Identify_Association_of_i_GRIK2_i_and_i_NPAS2_i_with_Chronic_Fatigue_Syndrome"><img alt="Research paper thumbnail of Convergent Genomic Studies Identify Association of <i>GRIK2</i> and <i>NPAS2</i> with Chronic Fatigue Syndrome" class="work-thumbnail" src="https://attachments.academia-assets.com/43891695/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451262/Convergent_Genomic_Studies_Identify_Association_of_i_GRIK2_i_and_i_NPAS2_i_with_Chronic_Fatigue_Syndrome">Convergent Genomic Studies Identify Association of <i>GRIK2</i> and <i>NPAS2</i> with Chronic Fatigue Syndrome</a></div><div class="wp-workCard_item"><span>Neuropsychobiology</span><span>, 2011</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="55e2271cc72b7059136647e3d1940877" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":43891695,"asset_id":23451262,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/43891695/download_file?st=MTczMjc3ODAwOCw4LjIyMi4yMDguMTQ2&st=MTczMjc3ODAwOCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451262"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451262"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451262; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=23451262]").text(description); $(".js-view-count[data-work-id=23451262]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 23451262; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='23451262']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 23451262, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "55e2271cc72b7059136647e3d1940877" } } $('.js-work-strip[data-work-id=23451262]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":23451262,"title":"Convergent Genomic Studies Identify Association of \u003ci\u003eGRIK2\u003c/i\u003e and \u003ci\u003eNPAS2\u003c/i\u003e with Chronic Fatigue Syndrome","translated_title":"","metadata":{"grobid_abstract":"sion of 20,160 genes in a subset of these subjects (35 CFS subjects and 27 controls) derived from a population-based study. Results: Sixty-five SNPs were nominally associated with CFS (p ! 0.001), and 165 genes were differentially expressed ( 6 4-fold; p ^ 0.05) in peripheral blood mononuclear cells of CFS subjects. Two genes, glutamate receptor, ionotropic, kinase 2 (GRIK2) and neuronal PAS domain protein 2 (NPAS2), were identified by both SNP and gene expression analyses. Subjects with the G allele of rs2247215 (GRIK2) were more likely to have CFS (p = 0.0005), and CFS subjects showed decreased GRIK2 expression (10-fold; p = 0.015). Subjects with the T allele of rs356653 (NPAS2) were more likely to have CFS (p = 0.0007), and NPAS2 expression was increased (10-fold; p = 0.027) in those with CFS. Conclusion: Using an integrated genomic strategy, this study suggests a possible role for genes involved in glutamatergic neurotransmission and circadian rhythm in CFS and supports further study of novel candidate genes in independent populations of CFS 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container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "e3879b2bbaa4485eada35ff09834dc8f" } } $('.js-work-strip[data-work-id=23451259]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":23451259,"title":"Predictors of neonatal hypothalamic-pituitary-adrenal axis activity at delivery","translated_title":"","metadata":{"grobid_abstract":"Objective Clinical and preclinical studies indicate that maternal stress during pregnancy may exert long-lasting adverse effects on offspring. This investigation sought to identify factors mediating the relationship between maternal and neonatal hypothalamicpituitary-adrenal (HPA) axes in pregnant women with past or family psychiatric history. Patients Two hundred and five pairs of maternal and umbilical cord blood samples from a clinical population were collected at delivery. Measurements Maternal and neonatal HPA axis activity measures were plasma adrenocorticotrophic hormone (ACTH), total cortisol, free cortisol and cortisol-binding globulin concentrations. The effects of maternal race, age, body mass index, psychiatric diagnosis (DSM-IV), birth weight, delivery method and estimated gestational age (EGA) at delivery on both maternal and neonatal HPA axis measures were also examined. Incorporating these independent predictors as covariates where necessary, we evaluated whether neonatal HPA axis activity measures could be predicted by the same maternal measure using linear regression. Results Delivery method was associated with umbilical cord plasma ACTH and both total and free cord cortisol concentrations (T = 10AE53-4AE21; P \u003c 0AE0001-0AE010). After accounting for method of delivery and EGA, we found that maternal plasma ACTH concentrations predicted 23AE9% of the variance in foetal plasma ACTH concentrations (T = 6AE76; P \u003c 0AE0001), and maternal free and total plasma cortisol concentrations predicted 39AE8% and 32AE3% of the variance in foetal plasma free and total cortisol concentrations (T = 5AE37-6AE90; P \u003c 0AE0001), respectively. Conclusion These data suggest that neonatal response is coupled with maternal HPA axis activity at delivery. Future investigations will scrutinize the potential long-term sequelae for the offspring.","publication_date":{"day":null,"month":null,"year":2011,"errors":{}},"publication_name":"Clinical Endocrinology","grobid_abstract_attachment_id":43891698},"translated_abstract":null,"internal_url":"https://www.academia.edu/23451259/Predictors_of_neonatal_hypothalamic_pituitary_adrenal_axis_activity_at_delivery","translated_internal_url":"","created_at":"2016-03-19T08:31:45.084-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":45422374,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[],"downloadable_attachments":[{"id":43891698,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/43891698/thumbnails/1.jpg","file_name":"Predictors_of_Neonatal_Hypothalamic-Pitu20160319-28582-1erw3g6.pdf","download_url":"https://www.academia.edu/attachments/43891698/download_file?st=MTczMjc3ODAwOCw4LjIyMi4yMDguMTQ2&st=MTczMjc3ODAwOCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Predictors_of_neonatal_hypothalamic_pitu.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/43891698/Predictors_of_Neonatal_Hypothalamic-Pitu20160319-28582-1erw3g6-libre.pdf?1458401613=\u0026response-content-disposition=attachment%3B+filename%3DPredictors_of_neonatal_hypothalamic_pitu.pdf\u0026Expires=1732781608\u0026Signature=a9OjtaUAjMcN3n5g9dIeI26rWozf7nlTAIdjuCSGfLPlsQHu6YpMD8WRF5kCrOEbv5lIwdf8dNn2DWAAd5mXxiK5XOUZ37ll2-HjyfmBSBuS7ONL2ks8lpCCAgzLeJ0wwAdv9h77Kx9JW2VtcFOMAclN3pgwJiRgg0me~JtumAmEY-TDqc5WL2kSVeA5pvMQXDP4b~h6eWTRpxCP4lZLvUWP1vc14CW2z262VZOdHU6M~B0OTrMDeM4hiN~cEwiazsvzpD0e7vWqDtz6w6amXttwATWPenpY12bCfYW0GEuPlv0vEaOpQy-HBcvS87NdSsu3GwAxpNxjSFNqf6ZwUA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"slug":"Predictors_of_neonatal_hypothalamic_pituitary_adrenal_axis_activity_at_delivery","translated_slug":"","page_count":6,"language":"en","content_type":"Work","owner":{"id":45422374,"first_name":"Alicia","middle_initials":null,"last_name":"Smith","page_name":"AliciaSmith34","domain_name":"independent","created_at":"2016-03-19T07:49:15.587-07:00","display_name":"Alicia Smith","url":"https://independent.academia.edu/AliciaSmith34"},"attachments":[{"id":43891698,"title":"","file_type":"pdf","scribd_thumbnail_url":"https://attachments.academia-assets.com/43891698/thumbnails/1.jpg","file_name":"Predictors_of_Neonatal_Hypothalamic-Pitu20160319-28582-1erw3g6.pdf","download_url":"https://www.academia.edu/attachments/43891698/download_file?st=MTczMjc3ODAwOCw4LjIyMi4yMDguMTQ2&st=MTczMjc3ODAwOCw4LjIyMi4yMDguMTQ2&","bulk_download_file_name":"Predictors_of_neonatal_hypothalamic_pitu.pdf","bulk_download_url":"https://d1wqtxts1xzle7.cloudfront.net/43891698/Predictors_of_Neonatal_Hypothalamic-Pitu20160319-28582-1erw3g6-libre.pdf?1458401613=\u0026response-content-disposition=attachment%3B+filename%3DPredictors_of_neonatal_hypothalamic_pitu.pdf\u0026Expires=1732781608\u0026Signature=a9OjtaUAjMcN3n5g9dIeI26rWozf7nlTAIdjuCSGfLPlsQHu6YpMD8WRF5kCrOEbv5lIwdf8dNn2DWAAd5mXxiK5XOUZ37ll2-HjyfmBSBuS7ONL2ks8lpCCAgzLeJ0wwAdv9h77Kx9JW2VtcFOMAclN3pgwJiRgg0me~JtumAmEY-TDqc5WL2kSVeA5pvMQXDP4b~h6eWTRpxCP4lZLvUWP1vc14CW2z262VZOdHU6M~B0OTrMDeM4hiN~cEwiazsvzpD0e7vWqDtz6w6amXttwATWPenpY12bCfYW0GEuPlv0vEaOpQy-HBcvS87NdSsu3GwAxpNxjSFNqf6ZwUA__\u0026Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA"}],"research_interests":[{"id":62550,"name":"Pregnancy","url":"https://www.academia.edu/Documents/in/Pregnancy"},{"id":99708,"name":"Clinical","url":"https://www.academia.edu/Documents/in/Clinical"},{"id":171144,"name":"Mental Disorders","url":"https://www.academia.edu/Documents/in/Mental_Disorders"},{"id":244814,"name":"Clinical Sciences","url":"https://www.academia.edu/Documents/in/Clinical_Sciences"},{"id":253560,"name":"Newborn Infant","url":"https://www.academia.edu/Documents/in/Newborn_Infant"},{"id":489727,"name":"Prognosis","url":"https://www.academia.edu/Documents/in/Prognosis"},{"id":564888,"name":"Adrenocorticotropic Hormone","url":"https://www.academia.edu/Documents/in/Adrenocorticotropic_Hormone"},{"id":923234,"name":"Clinical Endocrinology","url":"https://www.academia.edu/Documents/in/Clinical_Endocrinology"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="23451258"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451258/Association_of_polymorphisms_in_CASP10_and_CASP8_with_FEV_1_FVC_and_bronchial_hyperresponsiveness_in_ethnically_diverse_asthmatics"><img alt="Research paper thumbnail of Association of polymorphisms in CASP10 and CASP8 with FEV 1 /FVC and bronchial hyperresponsiveness in ethnically diverse asthmatics" class="work-thumbnail" src="https://attachments.academia-assets.com/43891700/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451258/Association_of_polymorphisms_in_CASP10_and_CASP8_with_FEV_1_FVC_and_bronchial_hyperresponsiveness_in_ethnically_diverse_asthmatics">Association of polymorphisms in CASP10 and CASP8 with FEV 1 /FVC and bronchial hyperresponsiveness in ethnically diverse asthmatics</a></div><div class="wp-workCard_item"><span>Clinical & Experimental Allergy</span><span>, 2008</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="c4f0f152678dbe92dcced99b8a32e9cb" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":43891700,"asset_id":23451258,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/43891700/download_file?st=MTczMjc3ODAwOCw4LjIyMi4yMDguMTQ2&st=MTczMjc3ODAwOCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451258"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451258"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451258; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=23451258]").text(description); $(".js-view-count[data-work-id=23451258]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 23451258; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='23451258']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 23451258, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (true){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "c4f0f152678dbe92dcced99b8a32e9cb" } } $('.js-work-strip[data-work-id=23451258]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":23451258,"title":"Association of polymorphisms in CASP10 and CASP8 with FEV 1 /FVC and bronchial hyperresponsiveness in ethnically diverse asthmatics","translated_title":"","metadata":{"grobid_abstract":"Background Several chromosomal regions have been identified using family-based linkage analysis to contain genes contributing to the development of asthma and allergic disorders. One of these regions, chromosome 2q32-q33, contains a gene cluster containing CFLAR, CASP10 and CASP8. These genes regulate the extrinsic apoptosis pathway utilized by several types of immune and structural cells that have been implicated in the pathogenesis of asthma. Objective To assess the role of genetic variation in CFLAR, CASP10 and CASP8 in asthma and related phenotypes in individuals of diverse ethnic backgrounds. Methods We tested 26 single nucleotide polymorphisms (SNPs) in the CFLAR, CASP10 and CASP8 gene cluster for association with asthma and related phenotypes in African-American, non-Hispanic whites, and Hispanic case-control populations (cases, N = 517, controls, N = 644). Results Five CASP10 SNPS were associated with forced expiratory volume in 1 s (FEV 1 )/ forced expiration volume capacity (FVC) in the African-American subjects with asthma (P = 0.0009-0.047). Nine SNPs, seven in CASP10 and two in CASP8, were also associated with the degree of bronchial hyperresponsiveness (BHR) (as determined by PC 20 ) in race-specific analysis, predominately in the Non-Hispanic white cases. Two SNPs, rs6750157 in CASP10 and rs1045485 in CASP8 were modestly associated with asthma in the African-American (P = 0.025) and Hispanic (P = 0.033) populations, respectively. Conclusion These data suggest a role for CASP10 as a potential modifier of the asthma phenotype, specifically with measures of airway obstruction and BHR. Caspase 8 and 10 polymorphisms and pulmonary phenotypes 1739 Ã Indicates deviation from expected values of Hardy-Weinberg equilibrium (Po0.05).","publication_date":{"day":null,"month":null,"year":2008,"errors":{}},"publication_name":"Clinical \u0026 Experimental Allergy","grobid_abstract_attachment_id":43891700},"translated_abstract":null,"internal_url":"https://www.academia.edu/23451258/Association_of_polymorphisms_in_CASP10_and_CASP8_with_FEV_1_FVC_and_bronchial_hyperresponsiveness_in_ethnically_diverse_asthmatics","translated_internal_url":"","created_at":"2016-03-19T08:31:44.912-07:00","preview_url":null,"current_user_can_edit":null,"current_user_is_owner":null,"owner_id":45422374,"coauthors_can_edit":true,"document_type":"paper","co_author_tags":[{"id":17587446,"work_id":23451258,"tagging_user_id":45422374,"tagged_user_id":null,"co_author_invite_id":296647,"email":"e***k@wakehealth.edu","display_order":0,"name":"Eugene Bleecker","title":"Association of polymorphisms in CASP10 and CASP8 with FEV 1 /FVC and bronchial hyperresponsiveness in ethnically diverse asthmatics"},{"id":17587447,"work_id":23451258,"tagging_user_id":45422374,"tagged_user_id":null,"co_author_invite_id":311439,"email":"t***d@wfubmc.edu","display_order":4194304,"name":"Timothy Howard","title":"Association of polymorphisms in CASP10 and CASP8 with FEV 1 /FVC and bronchial hyperresponsiveness in ethnically diverse asthmatics"},{"id":17587477,"work_id":23451258,"tagging_user_id":45422374,"tagged_user_id":null,"co_author_invite_id":296645,"email":"d***s@wfubmc.edu","display_order":6291456,"name":"Deborah Meyers","title":"Association of polymorphisms in CASP10 and CASP8 with FEV 1 /FVC and bronchial hyperresponsiveness in ethnically diverse 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(BHR)","url":"https://www.academia.edu/Documents/in/bronchial_hyperreactivity_BHR_"}],"urls":[]}, dispatcherData: dispatcherData }); $(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="23451257"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451257/Posttraumatic_stress_disorder_is_associated_with_an_enhanced_spontaneous_production_of_pro_inflammatory_cytokines_by_peripheral_blood_mononuclear_cells"><img alt="Research paper thumbnail of Posttraumatic stress disorder is associated with an enhanced spontaneous production of pro-inflammatory cytokines by peripheral blood mononuclear cells" class="work-thumbnail" src="https://a.academia-assets.com/images/blank-paper.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451257/Posttraumatic_stress_disorder_is_associated_with_an_enhanced_spontaneous_production_of_pro_inflammatory_cytokines_by_peripheral_blood_mononuclear_cells">Posttraumatic stress disorder is associated with an enhanced spontaneous production of pro-inflammatory cytokines by peripheral blood mononuclear cells</a></div><div class="wp-workCard_item"><span>BMC Psychiatry</span><span>, 2013</span></div><div class="wp-workCard_item"><span class="js-work-more-abstract-truncated">Posttraumatic stress disorder (PTSD) is associated with an enhanced risk for cardiovascular and o...</span><a class="js-work-more-abstract" data-broccoli-component="work_strip.more_abstract" data-click-track="profile-work-strip-more-abstract" href="javascript:;"><span> more </span><span><i class="fa fa-caret-down"></i></span></a><span class="js-work-more-abstract-untruncated hidden">Posttraumatic stress disorder (PTSD) is associated with an enhanced risk for cardiovascular and other inflammatory diseases. Chronic low-level inflammation has been suggested as a potential mechanism linking these conditions. We investigated plasma cytokine levels as well as spontaneous and lipopolysaccharide (LPS)-stimulated cytokine production by peripheral blood mononuclear cells (PBMCs) in a group of 35 severely traumatized PTSD patients compared to 25 healthy controls. Spontaneous production of interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α by isolated PBMCs was significantly higher in the PTSD compared to the control group and even correlated with PTSD symptom severity within the PTSD group. In contrast, circulating plasma levels of pro- and anti-inflammatory cytokines such as IL-6, IL-8, IL-10, TNF-α, or monocyte chemotactic protein (MCP)-1 were not significantly altered in PTSD patients compared to healthy controls. Our findings indicate that PBMCs of PTSD patients are already pre-activated in vivo, providing further evidence for low-grade inflammation in PTSD. This might possibly represent one psychobiological pathway from PTSD to poor physical health.</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451257"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451257"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451257; window.Academia.workViewCountsFetcher.queue(workId, function (count) { var description = window.$h.commaizeInt(count) + " " + window.$h.pluralize(count, 'View'); $(".js-view-count[data-work-id=23451257]").text(description); $(".js-view-count[data-work-id=23451257]").attr('title', description).tooltip(); }); });</script></span></span><span><span class="percentile-widget hidden"><span class="u-mr2x work-percentile"></span></span><script>$(function () { var workId = 23451257; window.Academia.workPercentilesFetcher.queue(workId, function (percentileText) { var container = $(".js-work-strip[data-work-id='23451257']"); container.find('.work-percentile').text(percentileText.charAt(0).toUpperCase() + percentileText.slice(1)); container.find('.percentile-widget').show(); container.find('.percentile-widget').removeClass('hidden'); }); });</script></span><span><script>$(function() { new Works.PaperRankView({ workId: 23451257, container: "", }); });</script></span></div><div id="work-strip-premium-row-container"></div></div></div><script> require.config({ waitSeconds: 90 })(["https://a.academia-assets.com/assets/wow_profile-f77ea15d77ce96025a6048a514272ad8becbad23c641fc2b3bd6e24ca6ff1932.js","https://a.academia-assets.com/assets/work_edit-ad038b8c047c1a8d4fa01b402d530ff93c45fee2137a149a4a5398bc8ad67560.js"], function() { // from javascript_helper.rb var dispatcherData = {} if (false){ window.WowProfile.dispatcher = window.WowProfile.dispatcher || _.clone(Backbone.Events); dispatcherData = { dispatcher: window.WowProfile.dispatcher, downloadLinkId: "-1" } } $('.js-work-strip[data-work-id=23451257]').each(function() { if (!$(this).data('initialized')) { new WowProfile.WorkStripView({ el: this, workJSON: {"id":23451257,"title":"Posttraumatic stress disorder is associated with an enhanced spontaneous production of pro-inflammatory cytokines by peripheral blood mononuclear cells","translated_title":"","metadata":{"abstract":"Posttraumatic stress disorder (PTSD) is associated with an enhanced risk for cardiovascular and other inflammatory diseases. Chronic low-level inflammation has been suggested as a potential mechanism linking these conditions. We investigated plasma cytokine levels as well as spontaneous and lipopolysaccharide (LPS)-stimulated cytokine production by peripheral blood mononuclear cells (PBMCs) in a group of 35 severely traumatized PTSD patients compared to 25 healthy controls. Spontaneous production of interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α by isolated PBMCs was significantly higher in the PTSD compared to the control group and even correlated with PTSD symptom severity within the PTSD group. In contrast, circulating plasma levels of pro- and anti-inflammatory cytokines such as IL-6, IL-8, IL-10, TNF-α, or monocyte chemotactic protein (MCP)-1 were not significantly altered in PTSD patients compared to healthy controls. Our findings indicate that PBMCs of PTSD patients are already pre-activated in vivo, providing further evidence for low-grade inflammation in PTSD. This might possibly represent one psychobiological pathway from PTSD to poor physical health.","publication_date":{"day":null,"month":null,"year":2013,"errors":{}},"publication_name":"BMC Psychiatry"},"translated_abstract":"Posttraumatic stress disorder (PTSD) is associated with an enhanced risk for cardiovascular and other inflammatory diseases. Chronic low-level inflammation has been suggested as a potential mechanism linking these conditions. We investigated plasma cytokine levels as well as spontaneous and lipopolysaccharide (LPS)-stimulated cytokine production by peripheral blood mononuclear cells (PBMCs) in a group of 35 severely traumatized PTSD patients compared to 25 healthy controls. Spontaneous production of interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α by isolated PBMCs was significantly higher in the PTSD compared to the control group and even correlated with PTSD symptom severity within the PTSD group. In contrast, circulating plasma levels of pro- and anti-inflammatory cytokines such as IL-6, IL-8, IL-10, TNF-α, or monocyte chemotactic protein (MCP)-1 were not significantly altered in PTSD patients compared to healthy controls. Our findings indicate that PBMCs of PTSD patients are already pre-activated in vivo, providing further evidence for low-grade inflammation in PTSD. 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$(this).data('initialized', true); } }); $a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="23451256"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23451256/Interactions_between_the_COMT_Val108_158Met_polymorphism_and_maternal_prenatal_smoking_predict_aggressive_behavior_outcomes"><img alt="Research paper thumbnail of Interactions between the COMT Val108/158Met polymorphism and maternal prenatal smoking predict aggressive behavior outcomes" class="work-thumbnail" src="https://attachments.academia-assets.com/43891693/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23451256/Interactions_between_the_COMT_Val108_158Met_polymorphism_and_maternal_prenatal_smoking_predict_aggressive_behavior_outcomes">Interactions between the COMT Val108/158Met polymorphism and maternal prenatal smoking predict aggressive behavior outcomes</a></div><div class="wp-workCard_item"><span>Biological Psychology</span><span>, 2011</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="2f2f40ef8fc64fc7c20c4b672f2861bf" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" data-download="{"attachment_id":43891693,"asset_id":23451256,"asset_type":"Work","button_location":"profile"}" href="https://www.academia.edu/attachments/43891693/download_file?st=MTczMjc3ODAwOCw4LjIyMi4yMDguMTQ2&st=MTczMjc3ODAwOCw4LjIyMi4yMDguMTQ2&s=profile"><span><i class="fa fa-arrow-down"></i></span><span>Download</span></a><span class="wp-workCard--action visible-if-viewed-by-owner inline-block" style="display: none;"><span class="js-profile-work-strip-edit-button-wrapper profile-work-strip-edit-button-wrapper" data-work-id="23451256"><a class="js-profile-work-strip-edit-button" tabindex="0"><span><i class="fa fa-pencil"></i></span><span>Edit</span></a></span></span><span id="work-strip-rankings-button-container"></span></div><div class="wp-workCard_item wp-workCard--stats"><span><span><span class="js-view-count view-count u-mr2x" data-work-id="23451256"><i class="fa fa-spinner fa-spin"></i></span><script>$(function () { var workId = 23451256; 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The sample consisted of 430 young adults born between 1981 and 1984 at the Mater Misericordiae Mother's Hospital in Brisbane, Australia, as well as their mothers and peers. Mothers reported their prenatal smoking status during pregnancy, and genetic data was obtained from the youth at a later follow-up in adulthood. The outcome measures in this study were mother and teacher reports of youth attention problems and aggression at age 15, and youth, mother and peer reports of youth attention problems and aggression at age 20 (combined to create latent factors of attention problems and aggression at each age). The COMT Val108/158Met polymorphism (rs4680) significantly interacted with maternal cigarette smoking during pregnancy to predict youth aggressive behavior at ages 15 and 20. 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$a.trackClickSource(".js-work-strip-work-link", "profile_work_strip") }); </script> <div class="js-work-strip profile--work_container" data-work-id="23335209"><div class="profile--work_thumbnail hidden-xs"><a class="js-work-strip-work-link" data-click-track="profile-work-strip-thumbnail" href="https://www.academia.edu/23335209/Differential_immune_system_DNA_methylation_and_cytokine_regulation_in_post_traumatic_stress_disorder"><img alt="Research paper thumbnail of Differential immune system DNA methylation and cytokine regulation in post-traumatic stress disorder" class="work-thumbnail" src="https://attachments.academia-assets.com/43792465/thumbnails/1.jpg" /></a></div><div class="wp-workCard wp-workCard_itemContainer"><div class="wp-workCard_item wp-workCard--title"><a class="js-work-strip-work-link text-gray-darker" data-click-track="profile-work-strip-title" href="https://www.academia.edu/23335209/Differential_immune_system_DNA_methylation_and_cytokine_regulation_in_post_traumatic_stress_disorder">Differential immune system DNA methylation and cytokine regulation in post-traumatic stress disorder</a></div><div class="wp-workCard_item wp-workCard--coauthors"><span>by </span><span><a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/KarenConneely">Karen Conneely</a> and <a class="" data-click-track="profile-work-strip-authors" href="https://independent.academia.edu/AliciaSmith34">Alicia Smith</a></span></div><div class="wp-workCard_item"><span>American Journal of Medical Genetics Part B: Neuropsychiatric Genetics</span><span>, 2011</span></div><div class="wp-workCard_item wp-workCard--actions"><span class="work-strip-bookmark-button-container"></span><a id="dc401c63909a973334250f6b3b6f4035" class="wp-workCard--action" rel="nofollow" data-click-track="profile-work-strip-download" 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To examine this hypothesis, we evaluated African American subjects matched by age and sex, and stratified into four groups by post-traumatic stress disorder (PTSD) diagnosis and history of child abuse. Total Life Stress (TLS) was also assessed in all subjects. We evaluated DNA extracted from peripheral blood using the HumanMethylation27 BeadChip and analyzed both global and site-specific methylation. Methylation levels were examined for association with PTSD, child abuse history, and TLS using a linear mixed model adjusted for age, sex, and chip effects. Global methylation was increased in subjects with PTSD. CpG sites in five genes (TPR, CLEC9A, APC5, ANXA2, and TLR8) were differentially methylated in subjects with PTSD. Additionally, a CpG site in NPFFR2 was associated with TLS after adjustment for multiple testing. Notably, many of these genes have been previously associated with inflammation. Given these results and reports of immune dysregulation associated with trauma history, we compared plasma cytokine levels in these subjects and found IL4, IL2, and TNFa levels associated with PTSD, child abuse, and TLS. Together, these results suggest that psychosocial stress may alter global and gene-specific DNA methylation patterns potentially associated with peripheral immune dysregulation. 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