Shared more. Cited more. Safe forever.
    • advanced search
    • submit works
    • about
    • help
    • contact us
    • login
    View Item 
    •   MOspace Home
    • University of Missouri-Columbia
    • Health Sciences Research Day (MU)
    • 2009 Health Sciences Research Day (MU)
    • View Item
    •   MOspace Home
    • University of Missouri-Columbia
    • Health Sciences Research Day (MU)
    • 2009 Health Sciences Research Day (MU)
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.
    advanced searchsubmit worksabouthelpcontact us

    Browse

    All of MOspaceCommunities & CollectionsDate IssuedAuthor/ContributorTitleIdentifierThesis DepartmentThesis AdvisorThesis SemesterThis CollectionDate IssuedAuthor/ContributorTitleIdentifierThesis DepartmentThesis AdvisorThesis Semester

    Statistics

    Most Popular ItemsStatistics by CountryMost Popular AuthorsStatistics by Referrer

    Brain phenotypes in two FGFR2 mouse models for apert syndrome [abstract]

    Austin, Jordan
    View/Open
    [PDF] BrainPhenotypesTwoFGFR2[abstract].pdf (16.07Kb)
    Date
    2010-02
    Contributor
    University of Missouri--Columbia. School of Medicine
    Format
    Abstract
    Metadata
    [+] Show full item record
    Abstract
    Apert syndrome (AS) is one of at least nine disorders considered members of the FGFR-1, -2, and -3-related craniosynostosis syndromes. Nearly 100% of individuals diagnosed with AS have one of two neighboring mutations on Fgfr2. The cranial phenotype associated with these two mutations includes coronal suture synostosis, either unilateral (unicoronal synostosis) or bilateral (bicoronal synostosis). Brain dysmorphology associated with AS is thought to be secondary to cranial vault or base alterations, but the variation in brain phenotypes within Apert syndrome is unexplained. Here we present novel 3D data on brain phenotypes of mice each carrying one of the two Fgfr2 mutations associated with Apert syndrome. Our data suggest that the brain is primarily affected, rather than secondarily responding to skull dysmorphogenesis. Our hypothesis is that the skull and brain are both primarily affected in craniosynostosis and that shared phenogenetic developmental processes affect both tissues in craniosynostosis phenotypes.
    URI
    http://hdl.handle.net/10355/6192
    Rights
    OpenAccess.
    This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 License.
    Collections
    • 2009 Health Sciences Research Day (MU)

    Send Feedback
    hosted by University of Missouri Library Systems
     

     


    Send Feedback
    hosted by University of Missouri Library Systems