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Träfflista för sökning "WFRF:(Fisher Helen) "

Sökning: WFRF:(Fisher Helen)

  • Resultat 1-10 av 16
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1.
  • Abbafati, Cristiana, et al. (författare)
  • 2020
  • Tidskriftsartikel (refereegranskat)
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2.
  • Beckley, Amber, 1981-, et al. (författare)
  • Childhood risk factors for adolescent victimization : A discordant twin design
  • 2016
  • Konferensbidrag (populärvet., debatt m.m.)abstract
    • In this study we considered the effect of childhood risk factors on adolescent victimization, measured at 18 years of age. We analyzed 1000 twipairs born 1994–1996 who were members of the Environmental Risk (E-Risk) Longitudinal Study, a prospective cohort study from the United Kingdom. We considered risk factors from two developmental periods (early childhood and early adolescence) and across multiple domains (individual, family, neighborhood): IQ, under controlled temperament, parent antisocial behavior, severe childhood victimization from ages 5 to 12, neighborhood socioeconomic, and neighborhood social cohesion. These childhood and early adolescence risk factors were tied to adolescent victimization. Many of these risk factors, however, are known risk factors for criminal behavior. Additionally, criminal behavior and victimization have been shown to be correlated in past research and were correlated the present sample of 18 year-olds (r = .40). We thus reanalyzed the relationship between the risk factors and victimization while controlling for adolescent offending. We found that the effect size for many of the childhood risk factors for victimization decreased and some became non-significant, suggesting that the risk factors described adolescents who were both victims and perpetrators. However, we found that one of the most robust predictors of adolescent victimization was childhood victimization, implying a continuity in victimization risk over the life-course. This presentation will include a comparison for twins discordant for severe childhood victimization.
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3.
  • Beckley, Amber L., et al. (författare)
  • The Developmental Nature of the Victim-Offender Overlap
  • 2018
  • Ingår i: Journal of Developmental and Life-Course Criminology. - : Springer Science and Business Media LLC. - 2199-4641 .- 2199-465X. ; 4:1, s. 24-49
  • Tidskriftsartikel (refereegranskat)abstract
    • Purpose It is well-established that victims and offenders are often the same people, a phenomenon known as the victim-offender overlap, but the developmental nature of this overlap remains uncertain. In this study, we drew from a developmental theoretical framework to test effects of genetics, individual characteristics, and routine-activity-based risks. Drawing from developmental literature, we additionally tested the effect of an accumulation of adverse childhood experiences (ACEs). Methods Data came from the Environmental Risk (E-Risk) Study, a representative UK birth cohort of 2232 twins born in 1994-1995 and followed to age 18 (with 93% retention). Crime victimization and offending were assessed through self-reports at age 18 (but findings replicated using crime records). We used the classical twin study method to decompose variance in the victim-offender overlap into genetic and environmental components. We used logistic regression to test the effects of childhood risk factors. Results In contrast to past twin studies, we found that environment (as well as genes) contributed to the victim-offender overlap. Our logistic regression results showed that childhood low self-control and childhood antisocial behavior nearly doubled the odds of becoming a victim-offender, compared to a victim-only or an offender-only. Each additional ACE increased the odds of becoming a victim-offender, compared to a victim-only or an offender-only, by approximately 12%, pointing to the importance of cumulative childhood adversity. Conclusions This study showed that the victim-offender overlap is, at least partially, developmental in nature and predictable from personal childhood characteristics and an accumulation of many adverse childhood experiences.
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4.
  • Beckley, Amber, 1981-, et al. (författare)
  • The developmental nature of the victim-offender overlap
  • 2018
  • Ingår i: Journal of Developmental and Life-Course Criminology. - : Springer. - 2199-4641 .- 2199-465X. ; 4:1, s. 24-49
  • Tidskriftsartikel (refereegranskat)abstract
    • Purpose: It is well-established that victims and offenders are often the same people, a phenomenon known as the victim-offender overlap, but the developmental nature of this overlap remains uncertain. In this study, we drew from a developmental theoretical framework to test effects of genetics, individual characteristics, and routine-activity-based risks. Drawing from developmental literature, we additionally tested the effect of an accumulation of adverse childhood experiences (ACEs).Methods: Data came from the Environmental Risk (E-Risk) Study, a representative UK birth cohort of 2232 twins born in 1994-1995 and followed to age 18 (with 93% retention). Crime victimization and offending were assessed through self-reports at age 18 (but findings replicated using crime records). We used the classical twin study method to decompose variance in the victim-offender overlap into genetic and environmental components. We used logistic regression to test the effects of childhood risk factors.Results: In contrast to past twin studies, we found that environment (as well as genes) contributed to the victim-offender overlap. Our logistic regression results showed that childhood low self-control and childhood antisocial behavior nearly doubled the odds of becoming a victim-offender, compared to a victim-only or an offender-only. Each additional ACE increased the odds of becoming a victim-offender, compared to a victim-only or an offender-only, by approximately 12%, pointing to the importance of cumulative childhood adversity.Conclusions: This study showed that the victim-offender overlap is, at least partially, developmental in nature and predictable from personal childhood characteristics and an accumulation of many adverse childhood experiences.
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5.
  • Clark, Andrew G., et al. (författare)
  • Evolution of genes and genomes on the Drosophila phylogeny
  • 2007
  • Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 450:7167, s. 203-218
  • Tidskriftsartikel (refereegranskat)abstract
    • Comparative analysis of multiple genomes in a phylogenetic framework dramatically improves the precision and sensitivity of evolutionary inference, producing more robust results than single-genome analyses can provide. The genomes of 12 Drosophila species, ten of which are presented here for the first time (sechellia, simulans, yakuba, erecta, ananassae, persimilis, willistoni, mojavensis, virilis and grimshawi), illustrate how rates and patterns of sequence divergence across taxa can illuminate evolutionary processes on a genomic scale. These genome sequences augment the formidable genetic tools that have made Drosophila melanogaster a pre-eminent model for animal genetics, and will further catalyse fundamental research on mechanisms of development, cell biology, genetics, disease, neurobiology, behaviour, physiology and evolution. Despite remarkable similarities among these Drosophila species, we identified many putatively non-neutral changes in protein-coding genes, non-coding RNA genes, and cis-regulatory regions. These may prove to underlie differences in the ecology and behaviour of these diverse species.
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6.
  • de las Fuentes, Lisa, et al. (författare)
  • Gene-educational attainment interactions in a multi-ancestry genome-wide meta-analysis identify novel blood pressure loci
  • 2021
  • Ingår i: Molecular Psychiatry. - : Springer Nature. - 1359-4184 .- 1476-5578. ; 26:6, s. 2111-2125
  • Tidskriftsartikel (refereegranskat)abstract
    • Educational attainment is widely used as a surrogate for socioeconomic status (SES). Low SES is a risk factor for hypertension and high blood pressure (BP). To identify novel BP loci, we performed multi-ancestry meta-analyses accounting for gene-educational attainment interactions using two variables, “Some College” (yes/no) and “Graduated College” (yes/no). Interactions were evaluated using both a 1 degree of freedom (DF) interaction term and a 2DF joint test of genetic and interaction effects. Analyses were performed for systolic BP, diastolic BP, mean arterial pressure, and pulse pressure. We pursued genome-wide interrogation in Stage 1 studies (N = 117 438) and follow-up on promising variants in Stage 2 studies (N = 293 787) in five ancestry groups. Through combined meta-analyses of Stages 1 and 2, we identified 84 known and 18 novel BP loci at genome-wide significance level (P < 5 × 10-8). Two novel loci were identified based on the 1DF test of interaction with educational attainment, while the remaining 16 loci were identified through the 2DF joint test of genetic and interaction effects. Ten novel loci were identified in individuals of African ancestry. Several novel loci show strong biological plausibility since they involve physiologic systems implicated in BP regulation. They include genes involved in the central nervous system-adrenal signaling axis (ZDHHC17, CADPS, PIK3C2G), vascular structure and function (GNB3, CDON), and renal function (HAS2 and HAS2-AS1, SLIT3). Collectively, these findings suggest a role of educational attainment or SES in further dissection of the genetic architecture of BP.
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7.
  • Feitosa, Mary F., et al. (författare)
  • Novel genetic associations for blood pressure identified via gene-alcohol interaction in up to 570K individuals across multiple ancestries
  • 2018
  • Ingår i: PLOS ONE. - : Public library science. - 1932-6203. ; 13:6
  • Tidskriftsartikel (refereegranskat)abstract
    • Heavy alcohol consumption is an established risk factor for hypertension; the mechanism by which alcohol consumption impact blood pressure (BP) regulation remains unknown. We hypothesized that a genome-wide association study accounting for gene-alcohol consumption interaction for BP might identify additional BP loci and contribute to the understanding of alcohol-related BP regulation. We conducted a large two-stage investigation incorporating joint testing of main genetic effects and single nucleotide variant (SNV)-alcohol consumption interactions. In Stage 1, genome-wide discovery meta-analyses in approximate to 131 K individuals across several ancestry groups yielded 3,514 SNVs (245 loci) with suggestive evidence of association (P <1.0 x 10(-5)). In Stage 2, these SNVs were tested for independent external replication in individuals across multiple ancestries. We identified and replicated (at Bonferroni correction threshold) five novel BP loci (380 SNVs in 21 genes) and 49 previously reported BP loci (2,159 SNVs in 109 genes) in European ancestry, and in multi-ancestry meta-analyses (P < 5.0 x 10(-8)). For African ancestry samples, we detected 18 potentially novel BP loci (P< 5.0 x 10(-8)) in Stage 1 that warrant further replication. Additionally, correlated meta-analysis identified eight novel BP loci (11 genes). Several genes in these loci (e.g., PINX1, GATA4, BLK, FTO and GABBR2 have been previously reported to be associated with alcohol consumption. These findings provide insights into the role of alcohol consumption in the genetic architecture of hypertension.
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9.
  • Fisher, Robert S., et al. (författare)
  • ILAE official report : a practical clinical definition of epilepsy
  • 2014
  • Ingår i: Epilepsia. - : Wiley-Blackwell. - 0013-9580 .- 1528-1167. ; 55:4, s. 475-482
  • Tidskriftsartikel (refereegranskat)abstract
    • Epilepsy was defined conceptually in 2005 as a disorder of the brain characterized by an enduring predisposition to generate epileptic seizures. This definition is usually practically applied as having two unprovoked seizures >24h apart. The International League Against Epilepsy (ILAE) accepted recommendations of a task force altering the practical definition for special circumstances that do not meet the two unprovoked seizures criteria. The task force proposed that epilepsy be considered to be a disease of the brain defined by any of the following conditions: (1) At least two unprovoked (or reflex) seizures occurring >24h apart; (2) one unprovoked (or reflex) seizure and a probability of further seizures similar to the general recurrence risk (at least 60%) after two unprovoked seizures, occurring over the next 10years; (3) diagnosis of an epilepsy syndrome. Epilepsy is considered to be resolved for individuals who either had an age-dependent epilepsy syndrome but are now past the applicable age or who have remained seizure-free for the last 10years and off antiseizure medicines for at least the last 5years. "Resolved" is not necessarily identical to the conventional view of "remission or "cure." Different practical definitions may be formed and used for various specific purposes. This revised definition of epilepsy brings the term in concordance with common use. A PowerPoint slide summarizing this article is available for download in the Supporting Information section.
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10.
  • Gertow, Joanna, et al. (författare)
  • Altered Protein Composition of Subcutaneous Adipose Tissue in Chronic Kidney Disease
  • 2017
  • Ingår i: Kidney International Reports. - : Elsevier BV. - 2468-0249. ; 2:6, s. 1208-1218
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction: Loss of renal function is associated with high mortality from cardiovascular disease (CVD). Patients with chronic kidney disease (CKD) have altered circulating adipokine and nonesterified fatty acid concentrations and insulin resistance, which are features of disturbed adipose tissue metabolism. Because dysfunctional adipose tissue contributes to the development of CVD, we hypothesize that adipose tissue dysfunctionality in patients with CKD could explain, at least in part, their high rates of CVD. Therefore we characterized adipose tissue from patients with CKD, in comparison to healthy controls, to search for signs of dysfunctionality. Methods: Biopsy samples of subcutaneous adipose tissue from 16 CKD patients and 11 healthy controls were analyzed for inflammation, fibrosis, and adipocyte size. Protein composition was assessed using 2dimensional gel proteomics combined with multivariate analysis. Results: Adipose tissue of CKD patients contained significantly more CD68-positive cells, but collagen content did not differ. Adipocyte size was significantly smaller in CKD patients. Proteomic analysis of adipose tissue revealed significant differences in the expression of certain proteins between the groups. Proteins whose expression differed the most were a-1-microglobulin/ bikunin precursor (AMBP, higher in CKD) and vimentin (lower in CKD). Vimentin is a lipid droplet-associated protein, and changes in its expression may impair fatty acid storage/mobilization in adipose tissue, whereas high levels of AMBP may reflect oxidative stress. Discussion: These findings demonstrate that adipose tissue of CKD patients shows signs of inflammation and disturbed functionality, thus potentially contributing to the unfavorable metabolic profile and increased risk of CVD in these patients.
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