FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2018502531> ?p ?o ?g. }

• W2018502531 endingPage "840" @default.
• W2018502531 startingPage "830" @default.
• W2018502531 abstract "Objective Bullying is the act of intentionally and repeatedly causing harm to someone who has difficulty defending him- or herself, and is a relatively widespread school-age phenomenon. Being the victim of bullying is associated with a broad spectrum of emotional problems; however, not all children who are bullied go on to develop such problems. Method We tested the hypothesis that the relationship between bullying victimization and emotional problems was moderated by variation in the serotonin transporter (5-HTT) gene in 2,232 British children comprising the Environmental Risk (E-Risk) study cohort. Results Our data supported the hypothesis that children's bullying victimization leads to their developing emotional problems, and that genetic variation in the 5-HTTLPR moderates this relationship. Specifically, frequently bullied children with the SS genotype were at greater risk for developing emotional problems at age 12 than were children with the SL or LL genotype. Furthermore, we demonstrated that this genetic moderation persisted (a) after controlling for children's previctimization emotional problems by assessing intraindividual change in problems between ages 5 and 12 years, and (b) after controlling for other risk factors shared by children growing up in the same family by comparing emotional problems in twins discordant for bullying victimization. Conclusions These findings are further evidence that the 5-HTTLPR moderates the risk of emotional disturbance after exposure to stressful events. Bullying is the act of intentionally and repeatedly causing harm to someone who has difficulty defending him- or herself, and is a relatively widespread school-age phenomenon. Being the victim of bullying is associated with a broad spectrum of emotional problems; however, not all children who are bullied go on to develop such problems. We tested the hypothesis that the relationship between bullying victimization and emotional problems was moderated by variation in the serotonin transporter (5-HTT) gene in 2,232 British children comprising the Environmental Risk (E-Risk) study cohort. Our data supported the hypothesis that children's bullying victimization leads to their developing emotional problems, and that genetic variation in the 5-HTTLPR moderates this relationship. Specifically, frequently bullied children with the SS genotype were at greater risk for developing emotional problems at age 12 than were children with the SL or LL genotype. Furthermore, we demonstrated that this genetic moderation persisted (a) after controlling for children's previctimization emotional problems by assessing intraindividual change in problems between ages 5 and 12 years, and (b) after controlling for other risk factors shared by children growing up in the same family by comparing emotional problems in twins discordant for bullying victimization. These findings are further evidence that the 5-HTTLPR moderates the risk of emotional disturbance after exposure to stressful events." @default.
• W2018502531 created "2016-06-24" @default.
• W2018502531 creator A5000891136 @default.
• W2018502531 creator A5026594853 @default.
• W2018502531 creator A5030654040 @default.
• W2018502531 creator A5052194471 @default.
• W2018502531 creator A5081542021 @default.
• W2018502531 creator A5083095072 @default.
• W2018502531 date "2010-08-01" @default.
• W2018502531 modified "2023-10-18" @default.
• W2018502531 title "Serotonin Transporter Gene Moderates the Development of Emotional Problems Among Children Following Bullying Victimization" @default.
• W2018502531 cites W1517585079 @default.
• W2018502531 cites W1750337463 @default.
• W2018502531 cites W1971231611 @default.
• W2018502531 cites W1979073775 @default.
• W2018502531 cites W1980207569 @default.
• W2018502531 cites W1981062734 @default.
• W2018502531 cites W1983164128 @default.
• W2018502531 cites W1984230889 @default.
• W2018502531 cites W1993687344 @default.
• W2018502531 cites W1994628299 @default.
• W2018502531 cites W2005445801 @default.
• W2018502531 cites W2006018937 @default.
• W2018502531 cites W2030081504 @default.
• W2018502531 cites W2034109146 @default.
• W2018502531 cites W2042170262 @default.
• W2018502531 cites W2059997499 @default.
• W2018502531 cites W2064779084 @default.
• W2018502531 cites W2066397039 @default.
• W2018502531 cites W2078392373 @default.
• W2018502531 cites W2084306651 @default.
• W2018502531 cites W2084665828 @default.
• W2018502531 cites W2094588342 @default.
• W2018502531 cites W2094961948 @default.
• W2018502531 cites W2102292415 @default.
• W2018502531 cites W2104843739 @default.
• W2018502531 cites W2105874139 @default.
• W2018502531 cites W2106888773 @default.
• W2018502531 cites W2108240300 @default.
• W2018502531 cites W2114162219 @default.
• W2018502531 cites W2115087214 @default.
• W2018502531 cites W2116903168 @default.
• W2018502531 cites W2117527509 @default.
• W2018502531 cites W2119844886 @default.
• W2018502531 cites W2121488984 @default.
• W2018502531 cites W2125464838 @default.
• W2018502531 cites W2126548787 @default.
• W2018502531 cites W2128833514 @default.
• W2018502531 cites W2145430042 @default.
• W2018502531 cites W2147351252 @default.
• W2018502531 cites W2149823098 @default.
• W2018502531 cites W2150523152 @default.
• W2018502531 cites W2161085199 @default.
• W2018502531 cites W2162196924 @default.
• W2018502531 cites W2162576395 @default.
• W2018502531 doi "https://doi.org/10.1016/j.jaac.2010.01.024" @default.
• W2018502531 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2908591" @default.
• W2018502531 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20643316" @default.
• W2018502531 hasPublicationYear "2010" @default.
• W2018502531 type Work @default.
• W2018502531 sameAs 2018502531 @default.
• W2018502531 citedByCount "108" @default.
• W2018502531 countsByYear W20185025312012 @default.
• W2018502531 countsByYear W20185025312013 @default.
• W2018502531 countsByYear W20185025312014 @default.
• W2018502531 countsByYear W20185025312015 @default.
• W2018502531 countsByYear W20185025312016 @default.
• W2018502531 countsByYear W20185025312017 @default.
• W2018502531 countsByYear W20185025312018 @default.
• W2018502531 countsByYear W20185025312019 @default.
• W2018502531 countsByYear W20185025312020 @default.
• W2018502531 countsByYear W20185025312021 @default.
• W2018502531 countsByYear W20185025312022 @default.
• W2018502531 countsByYear W20185025312023 @default.
• W2018502531 crossrefType "journal-article" @default.
• W2018502531 hasAuthorship W2018502531A5000891136 @default.
• W2018502531 hasAuthorship W2018502531A5026594853 @default.
• W2018502531 hasAuthorship W2018502531A5030654040 @default.
• W2018502531 hasAuthorship W2018502531A5052194471 @default.
• W2018502531 hasAuthorship W2018502531A5081542021 @default.
• W2018502531 hasAuthorship W2018502531A5083095072 @default.
• W2018502531 hasBestOaLocation W20185025312 @default.
• W2018502531 hasConcept C126322002 @default.
• W2018502531 hasConcept C138496976 @default.
• W2018502531 hasConcept C15744967 @default.
• W2018502531 hasConcept C170493617 @default.
• W2018502531 hasConcept C2775864247 @default.
• W2018502531 hasConcept C2777363581 @default.
• W2018502531 hasConcept C2778794976 @default.
• W2018502531 hasConcept C2778897192 @default.
• W2018502531 hasConcept C5284366 @default.
• W2018502531 hasConcept C70410870 @default.
• W2018502531 hasConcept C71924100 @default.
• W2018502531 hasConcept C77805123 @default.
• W2018502531 hasConcept C93225998 @default.
• W2018502531 hasConceptScore W2018502531C126322002 @default.
• W2018502531 hasConceptScore W2018502531C138496976 @default.
• W2018502531 hasConceptScore W2018502531C15744967 @default.

• next