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dc.contributor.advisorCampanucci, Veronica
dc.contributor.advisorIanowski, Juan
dc.creatorG Baskaran, Manoj Nair 1984-
dc.date.accessioned2016-12-19T15:41:17Z
dc.date.available2016-12-19T15:41:17Z
dc.date.created2016-12
dc.date.issued2016-12-19
dc.date.submittedDecember 2016
dc.identifier.urihttp://hdl.handle.net/10388/7630
dc.description.abstractVarious airway inflammatory diseases progress as a result of chronic inflammation, specifically neurogenic inflammation. One factor known to be involved in this is RAGE. This work has established RAGE as a key mediator in LPS-induced sensitization of afferent thoracic dorsal root ganglia neurons of the upper airway in mice. This was demonstrated from electrophysiological data showing the failure of LPS to potentiate capsaicin-evoked TRPV1 currents and increase action potential generation in RAGE KO relative to wild-type thoracic neurons. Mass spectrometry analysis for protein identification represents a step forward in biochemistry, allowing to obtain a global picture of the proteins expressed in a cell, including isoforms, post-translational modifications and downstream signalling pathways.
dc.format.mimetypeapplication/pdf
dc.subjectRAGE, RAGE isoforms, RAGE KO, thoracic dorsal root ganglia, LPS, airway inflammatory disease, neurogenic inflammation, sensory neuron sensitization
dc.titleRAGE-DEPENDENT SENSITIZATION OF THORACIC SENSORY NEURONS DURING INFLAMMATORY CONDITIONS
dc.typeThesis
dc.date.updated2016-12-19T15:41:17Z
thesis.degree.departmentPhysiology
thesis.degree.disciplinePhysiology
thesis.degree.grantorUniversity of Saskatchewan
thesis.degree.levelMasters
thesis.degree.nameMaster of Science (M.Sc.)
dc.type.materialtext
dc.contributor.committeeMemberMulligan, Sean
dc.contributor.committeeMemberChlan-Fourney, Jennifer
dc.contributor.committeeMemberCayabyab, Francisco


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