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Identification of a key regulatory pathway in bone regeneration using a novel mouse fracture model

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TitleInfo (displayLabel = Citation Title); (type = uniform)
Title
Identification of a key regulatory pathway in bone regeneration using a novel mouse fracture model
Name (ID = NAME001); (type = personal)
NamePart (type = family)
Manigrasso
NamePart (type = given)
Michaele Beth
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Michaele Beth Manigrasso
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author
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O'Connor
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James
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Advisory Committee
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James Patrick O'Connor
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chair
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Parsons
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John
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Advisory Committee
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John Russell Parsons
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internal member
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Denhardt
NamePart (type = given)
David
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Advisory Committee
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David Denhardt
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internal member
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Harten
NamePart (type = given)
Robert
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Advisory Committee
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Robert Harten
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outside member
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Gaussin
NamePart (type = given)
Vinciane
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Advisory Committee
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Vinciane Gaussin
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outside member
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Rutgers University
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degree grantor
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Graduate School - New Brunswick
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Text
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theses
OriginInfo
DateCreated (qualifier = exact)
2007
DateOther (qualifier = exact); (type = degree)
2007
Language
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English
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electronic
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application/pdf
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text/xml
Extent
xv, 176 pages
Abstract
Fracture healing is the complex biological process that restores broken bones to their original shape and function. While the fracture repair process follows a definitive sequence of events, not all the molecular or chemical pathways are completely understood. The development of animals with targeted mutations has allowed for the examination of specific fracture healing pathways, making the use of the mouse model an increasingly valuable tool in the field of orthopaedics. Additionally, evaluating the healing tissues using a torsional mechanical testing protocol is more reproducible and provides a better estimate of the biomechanical properties. Therefore, the first section of this dissertation is focused on the development and characterization of a murine femoral fracture model suitable for torsional mechanical testing. The model developed was tested using radiography, histology and mechanical testing and was shown to be comparable to other published femoral fracture models. After validation of this model, the next experiment focused on exploring how a complex phenotype, such as bone mineral density, may affect bone healing. Using inbred strains of mice with established bone mineral density values, the radiographic, histologic and biomechanical analyses of the healing femurs were evaluated. This data showed that having a high bone mineral density actually results in lower mechanical properties and therefore may be deleterious to fracture repair. Finally, this mouse fracture model was used to see how altering the arachidonic acid pathway affects fracture healing. Using genetically modified mice and the fracture and mechanical testing protocols as described, the role of the arachidonic acid pathway in fracture repair was examined. This data showed that either inhibition or acceleration of fracture repair is achieved by manipulating this pathway.
Note (type = degree)
Ph.D.
Note (type = bibliography)
Includes bibliographical references (p. 154-175).
Subject (ID = SUBJ1); (authority = RUETD)
Topic
Biomedical Engineering
Subject (ID = SUBJ2); (authority = ETD-LCSH)
Topic
Bone regeneration
Subject (ID = SUBJ3); (authority = ETD-LCSH)
Topic
Bones--Wounds and injuries--Treatment
RelatedItem (type = host)
TitleInfo
Title
Graduate School - New Brunswick Electronic Theses and Dissertations
Identifier (type = local)
rucore19991600001
Identifier (type = hdl)
http://hdl.rutgers.edu/1782.2/rucore10001600001.ETD.16740
Identifier
ETD_548
Location
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NjNbRU
Identifier (type = doi)
doi:10.7282/T3GQ6Z4B
Genre (authority = ExL-Esploro)
ETD doctoral
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The author owns the copyright to this work.
Copyright
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Copyright protected
Availability
Status
Open
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Name
Michaele Manigrasso
Role
Copyright holder
Affiliation
Rutgers University. Graduate School - New Brunswick
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Non-exclusive ETD license
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Author Agreement License
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I hereby grant to the Rutgers University Libraries and to my school the non-exclusive right to archive, reproduce and distribute my thesis or dissertation, in whole or in part, and/or my abstract, in whole or in part, in and from an electronic format, subject to the release date subsequently stipulated in this submittal form and approved by my school. I represent and stipulate that the thesis or dissertation and its abstract are my original work, that they do not infringe or violate any rights of others, and that I make these grants as the sole owner of the rights to my thesis or dissertation and its abstract. I represent that I have obtained written permissions, when necessary, from the owner(s) of each third party copyrighted matter to be included in my thesis or dissertation and will supply copies of such upon request by my school. I acknowledge that RU ETD and my school will not distribute my thesis or dissertation or its abstract if, in their reasonable judgment, they believe all such rights have not been secured. I acknowledge that I retain ownership rights to the copyright of my work. I also retain the right to use all or part of this thesis or dissertation in future works, such as articles or books.
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