Associations Between MAOA‐uVNTR Genotype, Maltreatment, MAOA Methylation, and Alcohol Consumption in Young Adult Males
Background Epigenetic mechanisms are candidate moderators of the effect of maltreatment on brain and behavior. Interactions between maltreatment and the monoamine oxidase A upstream variable number tandem repeat genotype (MAOA‐uVNTR) are associated with alcohol‐related problems. However, presently i...
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| Veröffentlicht in: | Alcoholism, clinical and experimental research clinical and experimental research, 2018-03, Vol.42 (3), p.508-519 |
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| creator | Bendre, Megha Comasco, Erika Checknita, Dave Tiihonen, Jari Hodgins, Sheilagh Nilsson, Kent W. |
| description | Background
Epigenetic mechanisms are candidate moderators of the effect of maltreatment on brain and behavior. Interactions between maltreatment and the monoamine oxidase A upstream variable number tandem repeat genotype (MAOA‐uVNTR) are associated with alcohol‐related problems. However, presently it is not known whether DNA methylation moderates this association. The study focused on 53 young adult males and aimed to determine whether MAOA methylation moderated the association of alcohol‐related problems with the interaction of MAOA‐uVNTR and maltreatment, and whether alcohol consumption moderated the association of MAOA methylation with the interaction of MAOA‐uVNTR and maltreatment.
Methods
MAOA‐uVNTR genotypes with ≤ 3 and > 3 repeats were categorized as short (S) and long (L), respectively. Data on maltreatment were obtained retrospectively, using self‐reported questionnaires. DNA methylation of 16 candidate CpGs within part of the MAOA first exon and intron was assessed and grouped based on principal component analyses. Alcohol‐related problems were assessed using the Alcohol Use Disorders Identification Test (AUDIT). Alcohol consumption was measured using AUDIT‐C. Moderation effects were assessed and probed using the moderated moderation model and Johnson–Neyman's method, respectively.
Results
Carriers of the S allele, who experienced maltreatment and displayed lower Component 1 (mean of CpGs 13–16 in the first intron) MAOA methylation levels, reported higher AUDIT score in contrast to L‐allele carriers. Carriers of the S allele, who reported higher AUDIT‐C score and experienced maltreatment, displayed lower Component 3 (mean of CpGs 2–6 in the first exon) MAOA methylation levels than L‐allele carriers.
Conclusions
Intronic methylation moderated the association of alcohol‐related problems with the interaction of MAOA‐uVNTR and maltreatment. Alcohol consumption moderated the association of exonic methylation with the interaction of MAOA‐uVNTR and maltreatment. These results suggest that epigenetic factors as well as genotype and maltreatment play a role in the development of alcohol misuse among young adult males.
The present study demonstrated that MAOA methylation moderates the association of alcohol consumption with the interaction between MAOA-uVNTR genotype and maltreatment in a sample of adolescents seeking treatment for substance misuse. Carriers of the S allele, who experienced maltreatment and displayed lower intronic MAOA methylation levels |
| doi_str_mv | 10.1111/acer.13578 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_swepu</sourceid><recordid>TN_cdi_swepub_primary_oai_swepub_ki_se_492029</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1975033990</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4698-ba53a5801a9a638f0cd11a0d8feb61a54dab73cc4c005d030490962ab2e9a81e3</originalsourceid><addsrcrecordid>eNqN0sFu0zAYB3ALgVgZXHgAZIkLQs34bMdpfAxlDKSVSdOYxMlykq9rRhJncazSG4_AM_IkOE3ZAQlELo7sn_-2rD8hzxmcsPC9MQX2J0zIRfqAzJgUEAFfLB6SGbBYRglAekSeOHcLAHGaJI_JEVecc8VgRr5lztmiMkNlW0ff4rBFbOkqu8h-fv_hrz9dXdIzbO2w63BOV6YeejRDg-0w3yO6wmGzq_fb59S0Jc3qwm5sTZchzzfduECrln6xvr2hWenrYYxB95Q8Wpva4bPDeEw-vz-9Wn6Izi_OPi6z86iIE5VGuZHCyBSYUSYR6RqKkjEDZbrGPGFGxqXJF6Io4gJAliAgVqASbnKOyqQMxTGJply3xc7nuuurxvQ7bU2lD1Nfwx_qWHHgKvj5X_276jrTtr_R3mshGU_i_-NNudGSqVQG_mriXW_vPLpBN5UrsK5Ni9Y7zdRCghBKQaAv_6C31vdteCvNARQTIW48__Wkit461-P6_gYM9NgOPbZD79sR8ItDpM8bLO_p7zoEwCawrWrc_SNKZ8vTyyn0F0-uxWk</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2009138534</pqid></control><display><type>article</type><title>Associations Between MAOA‐uVNTR Genotype, Maltreatment, MAOA Methylation, and Alcohol Consumption in Young Adult Males</title><source>Wiley Online Library Journals Frontfile Complete</source><source>Journals@Ovid Complete</source><creator>Bendre, Megha ; Comasco, Erika ; Checknita, Dave ; Tiihonen, Jari ; Hodgins, Sheilagh ; Nilsson, Kent W.</creator><creatorcontrib>Bendre, Megha ; Comasco, Erika ; Checknita, Dave ; Tiihonen, Jari ; Hodgins, Sheilagh ; Nilsson, Kent W.</creatorcontrib><description>Background
Epigenetic mechanisms are candidate moderators of the effect of maltreatment on brain and behavior. Interactions between maltreatment and the monoamine oxidase A upstream variable number tandem repeat genotype (MAOA‐uVNTR) are associated with alcohol‐related problems. However, presently it is not known whether DNA methylation moderates this association. The study focused on 53 young adult males and aimed to determine whether MAOA methylation moderated the association of alcohol‐related problems with the interaction of MAOA‐uVNTR and maltreatment, and whether alcohol consumption moderated the association of MAOA methylation with the interaction of MAOA‐uVNTR and maltreatment.
Methods
MAOA‐uVNTR genotypes with ≤ 3 and > 3 repeats were categorized as short (S) and long (L), respectively. Data on maltreatment were obtained retrospectively, using self‐reported questionnaires. DNA methylation of 16 candidate CpGs within part of the MAOA first exon and intron was assessed and grouped based on principal component analyses. Alcohol‐related problems were assessed using the Alcohol Use Disorders Identification Test (AUDIT). Alcohol consumption was measured using AUDIT‐C. Moderation effects were assessed and probed using the moderated moderation model and Johnson–Neyman's method, respectively.
Results
Carriers of the S allele, who experienced maltreatment and displayed lower Component 1 (mean of CpGs 13–16 in the first intron) MAOA methylation levels, reported higher AUDIT score in contrast to L‐allele carriers. Carriers of the S allele, who reported higher AUDIT‐C score and experienced maltreatment, displayed lower Component 3 (mean of CpGs 2–6 in the first exon) MAOA methylation levels than L‐allele carriers.
Conclusions
Intronic methylation moderated the association of alcohol‐related problems with the interaction of MAOA‐uVNTR and maltreatment. Alcohol consumption moderated the association of exonic methylation with the interaction of MAOA‐uVNTR and maltreatment. These results suggest that epigenetic factors as well as genotype and maltreatment play a role in the development of alcohol misuse among young adult males.
The present study demonstrated that MAOA methylation moderates the association of alcohol consumption with the interaction between MAOA-uVNTR genotype and maltreatment in a sample of adolescents seeking treatment for substance misuse. Carriers of the S allele, who experienced maltreatment and displayed lower intronic MAOA methylation levels, reported higher AUDIT score, in contrast to L allele carriers. The present findings suggest MAOA methylation as a putative molecular mechanism which intertwines life experiences and constitutive factors, and ultimately can influence mental health.</description><identifier>ISSN: 0145-6008</identifier><identifier>ISSN: 1530-0277</identifier><identifier>EISSN: 1530-0277</identifier><identifier>DOI: 10.1111/acer.13578</identifier><identifier>PMID: 29222910</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>Alcohol ; Alcohol use ; Alcohols ; Alleles ; Amine oxidase (flavin-containing) ; Deoxyribonucleic acid ; DNA ; DNA Methylation ; Epigenetics ; Gene by Environment ; Genotype & phenotype ; Genotypes ; Males ; Maltreatment ; MAOA ; MAOA‐ uVNTR ; Methylation ; uVNTR ; Young adults</subject><ispartof>Alcoholism, clinical and experimental research, 2018-03, Vol.42 (3), p.508-519</ispartof><rights>Copyright © 2017 by the Research Society on Alcoholism</rights><rights>Copyright © 2017 by the Research Society on Alcoholism.</rights><rights>2018 Research Society on Alcoholism</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4698-ba53a5801a9a638f0cd11a0d8feb61a54dab73cc4c005d030490962ab2e9a81e3</citedby><cites>FETCH-LOGICAL-c4698-ba53a5801a9a638f0cd11a0d8feb61a54dab73cc4c005d030490962ab2e9a81e3</cites><orcidid>0000-0002-2174-2068</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Facer.13578$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Facer.13578$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,776,780,881,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29222910$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://urn.kb.se/resolve?urn=urn:nbn:se:mdh:diva-51985$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttps://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-351264$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:137729335$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Bendre, Megha</creatorcontrib><creatorcontrib>Comasco, Erika</creatorcontrib><creatorcontrib>Checknita, Dave</creatorcontrib><creatorcontrib>Tiihonen, Jari</creatorcontrib><creatorcontrib>Hodgins, Sheilagh</creatorcontrib><creatorcontrib>Nilsson, Kent W.</creatorcontrib><title>Associations Between MAOA‐uVNTR Genotype, Maltreatment, MAOA Methylation, and Alcohol Consumption in Young Adult Males</title><title>Alcoholism, clinical and experimental research</title><addtitle>Alcohol Clin Exp Res</addtitle><description>Background
Epigenetic mechanisms are candidate moderators of the effect of maltreatment on brain and behavior. Interactions between maltreatment and the monoamine oxidase A upstream variable number tandem repeat genotype (MAOA‐uVNTR) are associated with alcohol‐related problems. However, presently it is not known whether DNA methylation moderates this association. The study focused on 53 young adult males and aimed to determine whether MAOA methylation moderated the association of alcohol‐related problems with the interaction of MAOA‐uVNTR and maltreatment, and whether alcohol consumption moderated the association of MAOA methylation with the interaction of MAOA‐uVNTR and maltreatment.
Methods
MAOA‐uVNTR genotypes with ≤ 3 and > 3 repeats were categorized as short (S) and long (L), respectively. Data on maltreatment were obtained retrospectively, using self‐reported questionnaires. DNA methylation of 16 candidate CpGs within part of the MAOA first exon and intron was assessed and grouped based on principal component analyses. Alcohol‐related problems were assessed using the Alcohol Use Disorders Identification Test (AUDIT). Alcohol consumption was measured using AUDIT‐C. Moderation effects were assessed and probed using the moderated moderation model and Johnson–Neyman's method, respectively.
Results
Carriers of the S allele, who experienced maltreatment and displayed lower Component 1 (mean of CpGs 13–16 in the first intron) MAOA methylation levels, reported higher AUDIT score in contrast to L‐allele carriers. Carriers of the S allele, who reported higher AUDIT‐C score and experienced maltreatment, displayed lower Component 3 (mean of CpGs 2–6 in the first exon) MAOA methylation levels than L‐allele carriers.
Conclusions
Intronic methylation moderated the association of alcohol‐related problems with the interaction of MAOA‐uVNTR and maltreatment. Alcohol consumption moderated the association of exonic methylation with the interaction of MAOA‐uVNTR and maltreatment. These results suggest that epigenetic factors as well as genotype and maltreatment play a role in the development of alcohol misuse among young adult males.
The present study demonstrated that MAOA methylation moderates the association of alcohol consumption with the interaction between MAOA-uVNTR genotype and maltreatment in a sample of adolescents seeking treatment for substance misuse. Carriers of the S allele, who experienced maltreatment and displayed lower intronic MAOA methylation levels, reported higher AUDIT score, in contrast to L allele carriers. The present findings suggest MAOA methylation as a putative molecular mechanism which intertwines life experiences and constitutive factors, and ultimately can influence mental health.</description><subject>Alcohol</subject><subject>Alcohol use</subject><subject>Alcohols</subject><subject>Alleles</subject><subject>Amine oxidase (flavin-containing)</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA Methylation</subject><subject>Epigenetics</subject><subject>Gene by Environment</subject><subject>Genotype & phenotype</subject><subject>Genotypes</subject><subject>Males</subject><subject>Maltreatment</subject><subject>MAOA</subject><subject>MAOA‐ uVNTR</subject><subject>Methylation</subject><subject>uVNTR</subject><subject>Young adults</subject><issn>0145-6008</issn><issn>1530-0277</issn><issn>1530-0277</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNqN0sFu0zAYB3ALgVgZXHgAZIkLQs34bMdpfAxlDKSVSdOYxMlykq9rRhJncazSG4_AM_IkOE3ZAQlELo7sn_-2rD8hzxmcsPC9MQX2J0zIRfqAzJgUEAFfLB6SGbBYRglAekSeOHcLAHGaJI_JEVecc8VgRr5lztmiMkNlW0ff4rBFbOkqu8h-fv_hrz9dXdIzbO2w63BOV6YeejRDg-0w3yO6wmGzq_fb59S0Jc3qwm5sTZchzzfduECrln6xvr2hWenrYYxB95Q8Wpva4bPDeEw-vz-9Wn6Izi_OPi6z86iIE5VGuZHCyBSYUSYR6RqKkjEDZbrGPGFGxqXJF6Io4gJAliAgVqASbnKOyqQMxTGJply3xc7nuuurxvQ7bU2lD1Nfwx_qWHHgKvj5X_276jrTtr_R3mshGU_i_-NNudGSqVQG_mriXW_vPLpBN5UrsK5Ni9Y7zdRCghBKQaAv_6C31vdteCvNARQTIW48__Wkit461-P6_gYM9NgOPbZD79sR8ItDpM8bLO_p7zoEwCawrWrc_SNKZ8vTyyn0F0-uxWk</recordid><startdate>201803</startdate><enddate>201803</enddate><creator>Bendre, Megha</creator><creator>Comasco, Erika</creator><creator>Checknita, Dave</creator><creator>Tiihonen, Jari</creator><creator>Hodgins, Sheilagh</creator><creator>Nilsson, Kent W.</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>K7.</scope><scope>K9.</scope><scope>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>DF7</scope><scope>DF2</scope><orcidid>https://orcid.org/0000-0002-2174-2068</orcidid></search><sort><creationdate>201803</creationdate><title>Associations Between MAOA‐uVNTR Genotype, Maltreatment, MAOA Methylation, and Alcohol Consumption in Young Adult Males</title><author>Bendre, Megha ; Comasco, Erika ; Checknita, Dave ; Tiihonen, Jari ; Hodgins, Sheilagh ; Nilsson, Kent W.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4698-ba53a5801a9a638f0cd11a0d8feb61a54dab73cc4c005d030490962ab2e9a81e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Alcohol</topic><topic>Alcohol use</topic><topic>Alcohols</topic><topic>Alleles</topic><topic>Amine oxidase (flavin-containing)</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA Methylation</topic><topic>Epigenetics</topic><topic>Gene by Environment</topic><topic>Genotype & phenotype</topic><topic>Genotypes</topic><topic>Males</topic><topic>Maltreatment</topic><topic>MAOA</topic><topic>MAOA‐ uVNTR</topic><topic>Methylation</topic><topic>uVNTR</topic><topic>Young adults</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bendre, Megha</creatorcontrib><creatorcontrib>Comasco, Erika</creatorcontrib><creatorcontrib>Checknita, Dave</creatorcontrib><creatorcontrib>Tiihonen, Jari</creatorcontrib><creatorcontrib>Hodgins, Sheilagh</creatorcontrib><creatorcontrib>Nilsson, Kent W.</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Criminal Justice (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Mälardalens högskola</collection><collection>SWEPUB Uppsala universitet</collection><jtitle>Alcoholism, clinical and experimental research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bendre, Megha</au><au>Comasco, Erika</au><au>Checknita, Dave</au><au>Tiihonen, Jari</au><au>Hodgins, Sheilagh</au><au>Nilsson, Kent W.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Associations Between MAOA‐uVNTR Genotype, Maltreatment, MAOA Methylation, and Alcohol Consumption in Young Adult Males</atitle><jtitle>Alcoholism, clinical and experimental research</jtitle><addtitle>Alcohol Clin Exp Res</addtitle><date>2018-03</date><risdate>2018</risdate><volume>42</volume><issue>3</issue><spage>508</spage><epage>519</epage><pages>508-519</pages><issn>0145-6008</issn><issn>1530-0277</issn><eissn>1530-0277</eissn><abstract>Background
Epigenetic mechanisms are candidate moderators of the effect of maltreatment on brain and behavior. Interactions between maltreatment and the monoamine oxidase A upstream variable number tandem repeat genotype (MAOA‐uVNTR) are associated with alcohol‐related problems. However, presently it is not known whether DNA methylation moderates this association. The study focused on 53 young adult males and aimed to determine whether MAOA methylation moderated the association of alcohol‐related problems with the interaction of MAOA‐uVNTR and maltreatment, and whether alcohol consumption moderated the association of MAOA methylation with the interaction of MAOA‐uVNTR and maltreatment.
Methods
MAOA‐uVNTR genotypes with ≤ 3 and > 3 repeats were categorized as short (S) and long (L), respectively. Data on maltreatment were obtained retrospectively, using self‐reported questionnaires. DNA methylation of 16 candidate CpGs within part of the MAOA first exon and intron was assessed and grouped based on principal component analyses. Alcohol‐related problems were assessed using the Alcohol Use Disorders Identification Test (AUDIT). Alcohol consumption was measured using AUDIT‐C. Moderation effects were assessed and probed using the moderated moderation model and Johnson–Neyman's method, respectively.
Results
Carriers of the S allele, who experienced maltreatment and displayed lower Component 1 (mean of CpGs 13–16 in the first intron) MAOA methylation levels, reported higher AUDIT score in contrast to L‐allele carriers. Carriers of the S allele, who reported higher AUDIT‐C score and experienced maltreatment, displayed lower Component 3 (mean of CpGs 2–6 in the first exon) MAOA methylation levels than L‐allele carriers.
Conclusions
Intronic methylation moderated the association of alcohol‐related problems with the interaction of MAOA‐uVNTR and maltreatment. Alcohol consumption moderated the association of exonic methylation with the interaction of MAOA‐uVNTR and maltreatment. These results suggest that epigenetic factors as well as genotype and maltreatment play a role in the development of alcohol misuse among young adult males.
The present study demonstrated that MAOA methylation moderates the association of alcohol consumption with the interaction between MAOA-uVNTR genotype and maltreatment in a sample of adolescents seeking treatment for substance misuse. Carriers of the S allele, who experienced maltreatment and displayed lower intronic MAOA methylation levels, reported higher AUDIT score, in contrast to L allele carriers. The present findings suggest MAOA methylation as a putative molecular mechanism which intertwines life experiences and constitutive factors, and ultimately can influence mental health.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>29222910</pmid><doi>10.1111/acer.13578</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-2174-2068</orcidid></addata></record> |
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| source | Wiley Online Library Journals Frontfile Complete; Journals@Ovid Complete |
| subjects | Alcohol Alcohol use Alcohols Alleles Amine oxidase (flavin-containing) Deoxyribonucleic acid DNA DNA Methylation Epigenetics Gene by Environment Genotype & phenotype Genotypes Males Maltreatment MAOA MAOA‐ uVNTR Methylation uVNTR Young adults |
| title | Associations Between MAOA‐uVNTR Genotype, Maltreatment, MAOA Methylation, and Alcohol Consumption in Young Adult Males |
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