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dc.contributor.advisorTibbles, Lee Anne
dc.contributor.authorPolukoshko, Andrew James
dc.date.accessioned2005-08-16T17:19:10Z
dc.date.available2005-08-16T17:19:10Z
dc.date.issued2004
dc.identifier.citationPolukoshko, A. J. (2004). Ischemia/reperfusion injury model development (Unpublished master's thesis). University of Calgary, Calgary, AB. doi:10.11575/PRISM/19081en_US
dc.identifier.isbn0494057025en
dc.identifier.urihttp://hdl.handle.net/1880/41898
dc.descriptionBibliography: p. 137-167en
dc.descriptionSome pages are in colour.en
dc.description.abstractA major barrier to the success of renal organ transplantation is the recognition by the recipient's immune system of the graft as foreign. This, ultimately, culminates in rejection. The process of transplantation itself facilitates this outcome by priming the organ for injury and subsequent inflammation through a process known as ischemia/reperfusion (1/R). The Stress Activated Protein Kinases (SAPKs) are a group of intracellular signalling molecules well known to be active under 1/R conditions. However, the mechanism of SAPK activation in response to I/R is, as yet, unknown, as well as its importance. Here, both in vitro and in vivo model systems have been developed for the purpose of understanding the effect of inhibition of the SAPK pathway in response to 1/R injury through the use of recombinant adenoviral vectors carrying dominant/negative transgenes. Two in vitro model systems demonstrate both SAPK activation and leukocyte recruitment to endothelium with the inhibition of SAPK significantly reducing the number of binding leukocytes. In vivo, injury to murine kidneys is produced in response to 1/R, but a renal gene therapy approach requires ex vivo perfusion of the adenoviral vectors to achieve high levels of transfection.
dc.format.extentxx, 177 leaves : ill. ; 30 cm.en
dc.language.isoeng
dc.rightsUniversity of Calgary graduate students retain copyright ownership and moral rights for their thesis. You may use this material in any way that is permitted by the Copyright Act or through licensing that has been assigned to the document. For uses that are not allowable under copyright legislation or licensing, you are required to seek permission.
dc.titleIschemia/reperfusion injury model development
dc.typemaster thesis
dc.publisher.institutionUniversity of Calgaryen
dc.identifier.doihttp://dx.doi.org/10.11575/PRISM/19081
thesis.degree.nameMaster of Science
thesis.degree.nameMS
thesis.degree.nameMSc
thesis.degree.disciplineMedical Science
thesis.degree.grantorUniversity of Calgary
dc.identifier.lccAC1 .T484 2004 P65en
dc.publisher.placeCalgaryen
ucalgary.thesis.notesUARCen
ucalgary.thesis.uarcreleaseyen
ucalgary.item.requestcopytrue


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University of Calgary graduate students retain copyright ownership and moral rights for their thesis. You may use this material in any way that is permitted by the Copyright Act or through licensing that has been assigned to the document. For uses that are not allowable under copyright legislation or licensing, you are required to seek permission.