15 research outputs found

    Sketching women in court: The visual construction of co-accused women in court drawings

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    This paper explores the visual construction and representation of co-accused women offenders in court drawings. It utilises three case studies of female co-defendants who appeared in the England and Wales court system between 2003 and 2013. In doing so this paper falls into three parts. The first part considers the emergence of the sub-discipline, visual criminology and examines what is known about the visual representation of female offenders. The second part presents the findings of an empirical investigation, which involved engaging in a critical, reflexive visual analysis of a selection of court drawings of three female co-offenders. The third part discusses the ways in which the court artists' interpretation, the conventions of court sketching, and motifs of female offenders as secondary actors, drew on existing myths and prejudices by representing the women as listening, remorseless ‘others’

    Identification of a gene (<i>FMR-1</i>) containing a CGG repeat coincident with a breakpoint cluster region exhibiting length variation in fragile X syndrome

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    Fragile X syndrome is the most frequent form of inherited mental retardation and is associated with a fragile site at Xq27.3. We identified human YAC clones that span fragile X site-induced translocation breakpoints coincident with the fragile X site. A gene (FMR-1) was identified within a four cosmid contig of YAC DNA that expresses a 4.8 kb message in human brain. Within a 7.4 kb EcoRI genomic fragment, containing FMR-1 exonic sequences distal to a CpG island previously shown to be hypermethylated in fragile X patients, is a fragile X site-induced breakpoint cluster region that exhibits length variation in fragile X chromosomes. This fragment contains a lengthy CGG repeat that is 250 bp distal of the CpG island and maps within a FMR-1 axon. Localization of the brain-expressed FMR-1 gene to this EcoRI fragment suggests the involvement of this gene in the phenotypic expression of the fragile X syndrome.</p

    Identification of a gene (<i>FMR-1</i>) containing a CGG repeat coincident with a breakpoint cluster region exhibiting length variation in fragile X syndrome

    No full text
    Fragile X syndrome is the most frequent form of inherited mental retardation and is associated with a fragile site at Xq27.3. We identified human YAC clones that span fragile X site-induced translocation breakpoints coincident with the fragile X site. A gene (FMR-1) was identified within a four cosmid contig of YAC DNA that expresses a 4.8 kb message in human brain. Within a 7.4 kb EcoRI genomic fragment, containing FMR-1 exonic sequences distal to a CpG island previously shown to be hypermethylated in fragile X patients, is a fragile X site-induced breakpoint cluster region that exhibits length variation in fragile X chromosomes. This fragment contains a lengthy CGG repeat that is 250 bp distal of the CpG island and maps within a FMR-1 axon. Localization of the brain-expressed FMR-1 gene to this EcoRI fragment suggests the involvement of this gene in the phenotypic expression of the fragile X syndrome.</p

    The Genetic Landscape of the Childhood Cancer Medulloblastoma

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    Medulloblastoma (MB) is the most common malignant brain tumor of children. To identify the genetic alterations in this tumor type, we searched for copy number alterations using high-density microarrays and sequenced all known protein-coding genes and microRNA genes using Sanger sequencing in a set of 22 MBs. We found that, on average, each tumor had 11 gene alterations, fewer by a factor of 5 to 10 than in the adult solid tumors that have been sequenced to date. In addition to alterations in the Hedgehog and Wnt pathways, our analysis led to the discovery of genes not previously known to be altered in MBs. Most notably, inactivating mutations of the histone-lysine N-methyltransferase genes MLL2 or MLL3 were identified in 16% of MB patients. These results demonstrate key differences between the genetic landscapes of adult and childhood cancers, highlight dysregulation of developmental pathways as an important mechanism underlying MBs, and identify a role for a specific type of histone methylation in human tumorigenesis.National Cancer Institute, National Institutes of Health (NIH)[HHSN261200800001E]Virginia and D. K. Ludwig Fund for Cancer ResearchAlex`s Lemonade Stand FoundationAmerican Brain Tumor AssociationBrain Tumor Research Fund at Johns HopkinsHoglund FoundationReady or Not FoundationChildren`s Brain Tumor FoundationPediatric Brain Tumor Foundation InstituteDavid and Barbara B. Hirschhorn FoundationAmerican Association for Cancer ResearchJohns Hopkins Sommer Scholar ProgramNIH[CA121113]NIH[CA096832]NIH[CA057345]NIH[CA118822]NIH[CA135877]NIH[GM074906-01A1/B7BSCW]NSF[DBI 0845275]DOD NDSEG[32 CFR 168a
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