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dc.contributor.authorRoss, Timothy Kieranen_US
dc.date.accessioned2007-05-15T19:06:04Z
dc.date.available2007-05-15T19:06:04Z
dc.date.issued1998-10-10T00:00:00Zen_US
dc.identifier.urihttp://hdl.handle.net/1993/1221
dc.description.abstractCardiac ischaemia is a condition in which there exists an imbalance between the myocardial oxygen demand and coronary arterial supply. Biochemical complications arising from cardiac ischaemia include ATP depletion, a net loss of adenine nucleotides, as well as an increase in $\rm\lbrack Ca\sp{2+}$), (P$\sb{\rm i}\rbrack,$ and $\rm\lbrack H\sp+\rbrack.$ Ironically, cells may endure a non-lethal period of ischaemia, only to succumb to reperfusion injury. Reperfusion injury is a consequence of cell reoxygenation whereby the proliferation of oxygen free radicals (and resultant oxidative stress), increased $\rm\lbrack Ca\sp{2+}\rbrack,$ continued ATP deprivation, and higher pH all contribute to the reversible formation of a non-selective permeability transition pore in the inner mitochondrial membrane. The opening of this pore results in the further decoupling the cell's oxidative phosphorylation mechanisms, resulting in a vicious cycle of pore formation and decreased cellular metabolic efficiency. Cyclosporin A(CSA), an immunosuppressant, has been found to reverse pore formation in the post-ischaemic heart. Our goal was to study the effects of the opening and closing of these pores on cardiolipin biosynthesis. (Abstract shortened by UMI.)en_US
dc.format.extent3977035 bytes
dc.format.extent184 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.language.isoengen_US
dc.rightsinfo:eu-repo/semantics/openAccess
dc.titleRegulation of polyglycerophospholipid biosynthesisen_US
dc.typeinfo:eu-repo/semantics/masterThesis
dc.typemaster thesisen_US
dc.degree.disciplineBiochemistryen_US
dc.degree.levelMaster of Science (M.Sc.)en_US


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