| 1. |
- Larsson, Henrik, 1975-, et al.
(författare)
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A genetic factor explains most of the variation in the psychopathic personality
- 2006
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Ingår i: Journal of Abnormal Psychology. - : American Psychological Association (APA). - 0021-843X .- 1939-1846. ; 115:2, s. 221-230
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Tidskriftsartikel (refereegranskat)abstract
- The psychopathic personality can be conceptualized as three interrelated dimensions, (a) an interpersonal style of glibness, grandiosity, and manipulation; (b) an affective disposition of callousness, lack of empathy, and unemotionality; and (c) a behavioral/lifestyle dimension of impulsivity, need for stimulation, and irresponsibility, underpinning a higher order construct, psychopathic personality. The authors used a self-report questionnaire (The Youth Psychopathic Traits Inventory) to study the importance of genetic and environmental influences on psychopathic personality traits in a sample of 1,090 monozygotic and dizygotic twin pairs, aged 16-17 years. Results showed a strong genetic influence behind the higher order "psychopathic personality" factor, underpinned by the three psychopathic personality dimensions. Over and above the effects to the higher order factor, significant unique genetic influences were also found in the callous/unemotional and in the impulsive/irresponsible dimension, but not in the grandiose/manipulative dimension. The authors propose that this latent psychopathic personality factor is a meaningful target for future etiological research.
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| 2. |
- Larsson, Henrik, et al.
(författare)
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A common genetic factor explains the association between psychopathic personality and antisocial behavior
- 2007
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Ingår i: Psychological Medicine. - 0033-2917 .- 1469-8978. ; 37:1, s. 15-26
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Tidskriftsartikel (refereegranskat)abstract
- Background: Both psychopathic personality traits and antisocial behavior are influenced by geneticas well as environmental factors. However, little is known about how genetic and environmental factors contribute to the associations between the psychopathic personality traits and antisocial behavior.Method: Data were drawn from a longitudinal population-based twin sample including all 1480 twin pairs born in Sweden between May 1985 and December 1986. The twins responded to mailed self-report questionnaires at two occasions: 1999 (twins 13–14 years old), and 2002 (twins 16–17years old).Results: A common genetic factor loaded substantially on both psychopathic personality traits and antisocial behavior, whereas a common shared environmental factor loaded exclusively on antisocial behavior.Conclusions: The genetic overlap between psychopathic personality traits and antisocial behavior may reflect a genetic vulnerability to externalizing psychopathology. The finding of shared environmental influences only in antisocial behavior suggests an etiological distinction between psychopathic personality dimensions and antisocial behavior. Knowledge about temperamental correlates to antisocial behavior is important for identification of susceptibility genes, as well as for possible prevention through identification of at-risk children early in life
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| 3. |
- Larsson, Henrik, 1975-, et al.
(författare)
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Genetic contributions to the development of ADHD subtypes from childhood to adolescence
- 2006
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Ingår i: Journal of the American Academy of Child and Adolescent Psychiatry. - : Lippincott Williams & Wilkins. - 0890-8567 .- 1527-5418. ; 45:8, s. 973-981
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: Little is known about how genes influence the development of symptoms included in the DSM-IV subtypes of attention-deficit/hyperactivity disorder (ADHD) from childhood to adolescence. The aim of this study was to examine genetic influences contributing to the development of hyperactive-impulsive symptoms and inattentive symptoms of ADHD from childhood to adolescence.METHOD: The sample included all 1,480 twin pairs born in Sweden between May 1985 and December 1986. Parents responded to mailed questionnaires on three occasions, when the twins were 8 to 9, 13 to 14, and 16 to 17 years old. The authors used dimensional scales of hyperactivity-impulsivity and inattention derived from a checklist of items based on the DSM symptoms of ADHD.RESULTS: Symptoms of hyperactivity-impulsivity declined with increasing age, whereas there was no decline in symptoms of inattention. Persistent genetic influences explain between 45% and 90% of the total genetic variance in hyperactivity-impulsivity and inattention across age. Persistent genetic variance was primarily operating across subtypes, even though persistent subtype-specific influences were also significant.CONCLUSIONS: The finding of persistent cross-subtype (i.e., combined) and persistent subtype-specific genetic influences (i.e., primarily hyperactive-impulsive and primarily inattentive) are in line with a genetic basis for the DSM-IV classification of ADHD subtypes.
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| 4. |
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| 5. |
- Larsson, Henrik, 1975-, et al.
(författare)
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Relationships between parental negativity and childhood antisocial behavior over time : a bidirectional effects model in a longitudinal genetically informative design
- 2008
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Ingår i: Journal of Abnormal Child Psychology. - : Springer. - 0091-0627 .- 1573-2835. ; 36:5, s. 633-645
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Tidskriftsartikel (refereegranskat)abstract
- This study examined the direction and etiology underlying the relationships between parental negativity and early childhood antisocial behavior using a bidirectional effects model in a longitudinal genetically informative design. We analyzed parent reports of parental negativity and early childhood antisocial behavior in 6,230 pairs of twins at 4 and 7 years of age. Results from a cross-lagged twin model contribute to the understanding of the mechanisms underlying the bidirectional processes involved in parental negativity and childhood antisocial behavior. Specifically, the findings of this study suggest that the association between parenting and child antisocial behavior is best explained by both parent-driven and child-driven effects. We found support for the notion that parent's negative feelings towards their children environmentally mediate the risk for child antisocial behavior. We also found evidence of genetically mediated child effects; in which genetically influenced antisocial behavior evoke parental negativity towards the child.
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| 6. |
- Lindskog, Henrik, 1977, et al.
(författare)
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New insights to vascular smooth muscle cell and pericyte differentiation of mouse embryonic stem cells in vitro.
- 2006
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Ingår i: Arteriosclerosis, thrombosis, and vascular biology. - 1524-4636. ; 26:7, s. 1457-64
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: The molecular mechanisms that regulate pericyte differentiation are not well understood, partly because of the lack of well-characterized in vitro systems that model this process. In this article, we develop a mouse embryonic stem (ES) cell-based angiogenesis/vasculogenesis assay and characterize the system for vascular smooth muscle cell (VSMC) and pericyte differentiation. METHODS AND RESULTS: ES cells that were cultured for 5 days on OP9 stroma cells upregulated their transcription of VSMC and pericyte selective genes. Other SMC marker genes were induced at a later time point, which suggests that vascular SMC/pericyte genes are regulated by a separate mechanism. Moreover, sequence analysis failed to identify any conserved CArG elements in the vascular SMC and pericyte gene promoters, which indicates that serum response factor is not involved in their regulation. Gleevec, a tyrosine kinase inhibitor that blocks platelet-derived growth factor (PDGF) spell-receptor signaling, and a neutralizing antibody against transforming growth factor (TGF) beta1, beta2, and beta3 failed to inhibit the induction of vascular SMC/pericyte genes. Finally, ES-derived vascular sprouts recruited cocultured MEF cells to pericyte-typical locations. The recruited cells activated expression of a VSMC- and pericyte-specific reporter gene. CONCLUSIONS: We conclude that OP9 stroma cells induce pericyte differentiation of cocultured mouse ES cells. The induction of pericyte marker genes is temporally separated from the induction of SMC genes and does not require platelet-derived growth factor B or TGFbeta1 signaling.
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| 7. |
- Petit, Marleen MR, et al.
(författare)
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Smooth muscle expression of lipoma preferred partner is mediated by an alternative intronic promoter that is regulated by serum response factor/myocardin.
- 2008
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Ingår i: Circulation research. - 1524-4571. ; 103:1, s. 61-9
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Tidskriftsartikel (refereegranskat)abstract
- Lipoma preferred partner (LPP) was recently recognized as a smooth muscle marker that plays a role in smooth muscle cell migration. In this report, we focus on the transcriptional regulation of the LPP gene. In particular, we investigate whether LPP is directly regulated by serum response factor (SRF). We show that the LPP gene contains 3 evolutionarily conserved CArG boxes and that 1 of these is part of an alternative promoter in intron 2. Quantitative RT-PCR shows that this alternative promoter directs transcription specifically to smooth muscle containing tissues in vivo. By using chromatin immunoprecipitation, we demonstrate that 2 of the CArG boxes, including the promoter-associated CArG box, bind to endogenous SRF in cultured aortic smooth muscle cells. Electrophoretic mobility-shift assays show that the conserved CArG boxes bind SRF in vitro. In reporter experiments, we show that the alternative promoter has transcriptional capacity that is dependent on SRF/myocardin and that the promoter associated CArG box is required for that activity. Finally, we show by quantitative RT-PCR that the alternative promoter is strongly downregulated in SRF-deficient embryonic stem cells and in smooth muscle tissues derived from conditional SRF knockout mice. Collectively, our data demonstrate that expression of LPP in smooth muscle is mediated by an alternative promoter that is regulated by SRF/myocardin.
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| 8. |
- Sadr Azodi, O., et al.
(författare)
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Genetic and environmental influences on the risk of acute appendicitis in twins
- 2009
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Ingår i: British Journal of Surgery. - West Sussex, United Kingdom : John Wiley & Sons. - 0007-1323 .- 1365-2168. ; 96:11, s. 1336-1340
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Tidskriftsartikel (refereegranskat)abstract
- Background: Acute appendicitis is common but the aetiology is unclear. This study examined the heritability of acute appendicitis.Methods: The study included twin pairs with known zygosity born between 1959 and 1985. Individuals with acute appendicitis were found by record linkage with the Swedish Inpatient Register. Comparing monodizygotic and dizygotic twins, the similarity and relative proportions of phenotypic variance resulting from genetic and environmental factors were analysed. Risks of acute appendicitis explained by heritability and environmental effects were estimated.Results: Some 3441 monozygotic and 2429 dizygotic twins were identified. Almost no genetic effects were found in males (8 (95 per cent confidence interval 0 to 50) per cent), but shared (31 (0 to 49) per cent) and non-shared (61 (47 to 74) per cent) environmental factors accounted for this risk. In females, the heritability was estimated as 20 (0 to 36) per cent and the remaining variation was due to non-shared environmental factors (80 (64 to 98) per cent). For the sexes combined, genetic effects accounted for 30 (5 to 40) per cent and non-shared environmental effects for 70 (60 to 81) per cent of the risk.Conclusion: Acute appendicitis has a complex aetiology with sex differences in heritability and environmental factors.
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| 9. |
- Viding, Essi, et al.
(författare)
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Quantitative genetic studies of antisocial behaviour
- 2008
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Ingår i: Philosophical Transactions of the Royal Society of London. Biological Sciences. - London, United Kingdom : The Royal Society Publishing. - 0962-8436 .- 1471-2970. ; 363:1503, s. 2519-2527
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Forskningsöversikt (refereegranskat)abstract
- This paper will broadly review the currently available twin and adoption data on antisocial behaviour (AB). It is argued that quantitative genetic research can make a significant contribution to further the understanding of how AB develops. Genetically informative study designs are particularly useful for investigating several important questions such as whether: the heritability estimates vary as a function of assessment method or gender; the relative importance of genetic and environmental influences varies for different types of AB; the environmental risk factors are truly environmental; and genetic vulnerability influences susceptibility to environmental risk. While the current data are not yet directly translatable for prevention and treatment programmes, quantitative genetic research has concrete translational potential. Quantitative genetic research can supplement neuroscience research in informing about different subtypes of AB, such as AB coupled with callous-unemotional traits. Quantitative genetic research is also important in advancing the understanding of the mechanisms by which environmental risk operates.
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