Genetics Research
rs3025382
Population Frequencies12
African
G 0.73687A 0.26313GG 0.5472GA/AG 0.379331AA 0.073469pop=42,712
African American
G 0.73814A 0.26186GG 0.549286GA/AG 0.37771AA 0.073005pop=41,148
African Others
G 0.7033A 0.2967GG 0.492327GA/AG 0.421995AA 0.085678pop=1,564
Asian
G 0.9737A 0.0263GG 0.948436GA/AG 0.050437AA 0.001127pop=7,098
East Asian
G 0.9744A 0.0256GG 0.950169GA/AG 0.048475AA 0.001356pop=5,900
European
G 0.875958A 0.124042GG 0.767929GA/AG 0.21606AA 0.016012pop=342,498
Latin American 1
G 0.8548A 0.1452GG 0.732872GA/AG 0.243872AA 0.023256pop=6,364
Latin American 2
G 0.93006A 0.06994GG 0.865248GA/AG 0.12963AA 0.005122pop=10,152
Other
G 0.8745A 0.1255GG 0.76663GA/AG 0.215691AA 0.01768pop=9,050
Other Asian
G 0.9699A 0.0301GG 0.9399GA/AG 0.0601AA 0pop=1,198
South Asian
G 0.925A 0.075GG 0.857355GA/AG 0.135235AA 0.00741pop=5,398
Studies10
Unread Studies10 ▼
1
Нікотинова залежність‒це розлад вживання нікотину, який міститься в тютюновому димі. Характерною рисою цього розладу є потужний внутрішній потяг до тютюнокуріння, …
2
This study investigated neuroanatomic, genetic, cognitive, sociodemographic and emotional underpinnings of the Negative Urgency subscale of the Urgency, Premeditation, Perseverance, Sensation-Seeking and Positive Urgency Impulsive Behavior Scale in a healthy developmental sample. The goal of the investigation is to contribute to the harmonisation of behavioural, brain and neurogenetic aspects of behavioural self-control. Three domains – (1) Demographic, developmental, psychiatric and cognitive ability; (2) Regional brain volumes (neurobiological); and (3) Genetic variability (single nucleotide polymorphisms) – were examined, and models with relevant predictor variables were selected. Least absolute shrinkage and selection operator and best subset regressions were used to identify sparse models predicting negative urgency scores, which revealed that variables related to emotional regulation and right cingulate volume, as well as single nucleotide polymorphisms in CADM2 and SLC6A4, were associated with negative urgency. Our results contribute to the construct and criterion validity of negative urgency and support the hypothesis that negative urgency is a result of a complex array of influences across domains whose integration furthers developmental psychopathology research.
3
Teaching creativity is a substantial quality improvement in higher education. To demonstrate cross-functional thinking is a must for degree holders to be able to solve solutions useful for the society. Such a demand must be underlined by rational arguments. The neurobiology of creative behavior provides important information how the brain processes such activities. The subcortical mesolimbic brain areas, specifically the dopaminergic system, are of interest. The mentioned system and its two class receptors, D1 and D2 types, seem to be key players to mediate pleasure associated with predictive, motivational, or attentional sensations linked to learning processes and creativity. In this work a comparative biological approach was used to analyze genetic polymorphisms of SNPs in humans and nonhuman primates based on phenotypical expressions of creativity in humans. This methodology was used to get a view of the phylogenetic dimension of this trait in the order of primates. 13 out of 50 chosen SNPs showed accelerated selection processes shared by humans and nonhuman primates. The results of this study confirmed the assumption that phenotypical expression of creativity is a genetically inherited feature in primates. It is suggested that such a phylogenetic approach justifies a consideration of teaching creativity in higher education. It is suggested that creativity represents an old trait in primates because the most distant relative primate used in this study diverged 25 Mya ago from humans.
4
Las hipotesis actuales sobre la etiopatogenia del Trastorno Limite de la Personalidad (TLP) plantean que en el desarrollo del trastorno intervendrian tanto factores geneticos como ambientales que interaccionarian entre si. Entre los factores ambientales destacan los antecedentes de traumas en la infancia. Entre los geneticos, se han estudiado principalmente los sistemas monoaminergicos con resultados poco concluyentes, con lo que seria interesante investigar genes relacionados con el eje hipotalamico-hipofisario-adrenal (HHA) y otros sistemas implicados en la respuesta del organismo al estres, dado que se han descrito alteraciones en el funcionamiento de estos sistemas en relacion con el TLP y con los traumas infantiles. El objetivo principal de esta tesis, por tanto, es identificar asociaciones entre variantes de genes de los sistemas de respuesta al estres (eje HHA y sistema noradrenergico) y el TLP, asi como evaluar la posible modulacion de dichas asociaciones por los antecedentes de traumas en la infancia. Los objetivos secundarios son evaluar si existe asociacion entre los antecedentes de traumas infantiles y la gravedad del TLP, y si dicha asociacion esta mediada por los rasgos temperamentales, e investigar si los traumas infantiles y/o la gravedad del trastorno se asocian con una mayor metilacion de un gen del eje HHA, el receptor de glucocorticoides (GR), en sujetos con TLP. Los resultados de este trabajo sugieren la implicacion en el desarrollo del TLP de genes de estos sistemas (FKBP5, CRHR1, COMT, DBH y SLC6A2) y su modulacion por la presencia de traumas en la infancia. Tambien muestran que el haber sufrido abuso emocional en la infancia se asociaria con una mayor gravedad del TLP, principalmente en aquellos sujetos con un elevado neuroticismo. Y, por ultimo, que tanto los antecedentes de abuso fisico como una mayor gravedad del trastorno se asociarian con un aumento de la metilacion del GR en individuos con TLP. Por tanto, los resultados observados apoyan la implicacion de factores geneticos y ambientales tanto en la etiologia del TLP como en su gravedad, y sugieren que los genes de los sistemas de respuesta al estres, sujetos a la modulacion por parte de los sucesos traumaticos en la infancia, se asociarian con el riesgo de padecer este trastorno. Ademas, abren las puertas a profundizar en el estudio del papel que juegan estas interacciones en el TLP y, en caso de confirmarse en muestras independientes, a disenar estrategias terapeuticas o incluso preventivas centradas en estos factores.
5
Parenting influences many aspects of child development, including socio-emotional, cognitive, and behavioral outcomes. Yet most studies report only modest effect sizes. An increasingly likely explanation is that not all children are equally affected by environmental factors, including parenting. The differential susceptibility theory proposes that some children might be more susceptible to both positive and negative environmental influences, compared to other children. Such differences in susceptibility are thought to be due to genetic, temperamental, or physiological susceptibility factors. In the current thesis, we tested the theory of differential susceptibility of children to the effects of parenting in a large population-based cohort, the Generation R Study. Doing so, we went beyond common methods. First, we investigated differential susceptibility from a developmental perspective by including multiple measures over time. Second, we went beyond single-gene/polymorphisms in the investigation of gene-environment interplay by aggregating genetic variation in a set of dopamine genes. Third, we extended previous research on mild perinatal adversity as a susceptibility factor by examining its moderating role in the association between harsh parenting and hair cortisol levels, taking into account background factors that we demonstrated to be of influence on hair cortisol levels.
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This study investigated the possible association of 40 polymorphisms within 4 noradrenergic genes with BPD risk and the modulating effect of childhood trauma on these associations in 481 BPD subjects and 442 controls. COMT rs5993882, DBH rs77905 and SLC6A2 rs1814270 showed associations with BPD, which were modulated by childhood trauma. However, none of these findings survived Bonferroni correction. Further investigation is needed to clarify the involvement of these genes in BPD pathogenesis.
7
Nicotine dependence is moderately heritable, but identified genetic associations explain only modest portions of this heritability. We analyzed 3369 SNPs from 349 candidate genes …
8
Nicotine dependence is moderately heritable, but identified genetic associations explain only modest portions of this heritability. We analyzed 3,369 SNPs from 349 candidate genes, and investigated whether incorporation of SNP-by-environment interaction into association analyses might bolster gene discovery efforts and prediction of nicotine dependence. Specifically, we incorporated the interaction between allele count and age-at-onset of regular smoking (AOS) into association analyses of nicotine dependence. Subjects were from the Collaborative Genetic Study of Nicotine Dependence, and included 797 cases ascertained for Fagerstrom nicotine dependence, and 811 non-nicotine dependent smokers as controls, all of European descent. Compared with main-effect models, SNP x AOS interaction models resulted in higher numbers of nominally significant tests, increased predictive utility at individual SNPs, and higher predictive utility in a multi-locus model. Some SNPs previously documented in main-effect analyses exhibited improved fits in the joint-analysis, including rs16969968 from CHRNA5 and rs2314379 from MAP3K4. CHRNA5 exhibited larger effects in later-onset smokers, in contrast with a previous report that suggested the opposite interaction (Weiss et al, PLOS Genetics, 4: e1000125, 2008). However, a number of SNPs that did not emerge in main-effect analyses were among the strongest findings in the interaction analyses. These include SNPs located in GRIN2B (p=1.5 × 10−5), which encodes a subunit of the NMDA receptor channel, a key molecule in mediating age-dependent synaptic plasticity. Incorporation of logically chosen interaction parameters, such as AOS, into genetic models of substance-use disorders may increase the degree of explained phenotypic variation, and constitutes a promising avenue for gene-discovery.
9
Nicotine dependence is one of the world's leading causes of preventable death. To discover genetic variants that influence risk for nicotine dependence, we targeted over 300 candidate genes and analyzed 3713 single nucleotide polymorphisms (SNPs) in 1050 cases and 879 controls. The Fagerström test for nicotine dependence (FTND) was used to assess dependence, in which cases were required to have an FTND of 4 or more. The control criterion was strict: control subjects must have smoked at least 100 cigarettes in their lifetimes and had an FTND of 0 during the heaviest period of smoking. After correcting for multiple testing by controlling the false discovery rate, several cholinergic nicotinic receptor genes dominated the top signals. The strongest association was from an SNP representing CHRNB3, the beta3 nicotinic receptor subunit gene (P = 9.4 x 10(-5)). Biologically, the most compelling evidence for a risk variant came from a non-synonymous SNP in the alpha5 nicotinic receptor subunit gene CHRNA5 (P = 6.4 x 10(-4)). This SNP exhibited evidence of a recessive mode of inheritance, resulting in individuals having a 2-fold increase in risk of developing nicotine dependence once exposed to cigarette smoking. Other genes among the top signals were KCNJ6 and GABRA4. This study represents one of the most powerful and extensive studies of nicotine dependence to date and has found novel risk loci that require confirmation by replication studies.
10
This research is built upon representation and cultural identity frameworks, implying that cultural products such as Internet portals' news coverage are valuable to understand the relationship between culture and ideology.
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