{"id":{"repo_id":"cape-town","oai_identifier":"oai:open.uct.ac.za:11427/3414"},"canonical_url":"https://search.dev.ndltd.org/etd/cape-town/oai:open.uct.ac.za:11427/3414","repository":{"repo_id":"cape-town","name":"University of Cape Town","base_url":"https://open.uct.ac.za/oai/request"},"display":{"title":"Signalling pathways involved in TNFα-induced cytoprotection : role of reactive oxygen species","abstract":"Tumour necrosis factor alpha (TNFa) is a pleiotropic cytokine which has both beneficial and deleterious effects. It has previously been shown in our laboratory that TNFa can mimic ischemic preconditioning (IPC). However, the signalling pathways involved in this protection remain incompletely understood. One potential protective pathway involves the generation of reactive oxygen species (ROS), which are known to be activated by TNFa. It was therefore hypothesized that TNFa-induced cytoprotection requires the generation of ROS. In addition, it was postulated that this ROS generation originates in the mitochondria.","abstract_html":"Tumour necrosis factor alpha (TNFa) is a pleiotropic cytokine which has both beneficial and deleterious effects. It has previously been shown in our laboratory that TNFa can mimic ischemic preconditioning (IPC). However, the signalling pathways involved in this protection remain incompletely understood. One potential protective pathway involves the generation of reactive oxygen species (ROS), which are known to be activated by TNFa. It was therefore hypothesized that TNFa-induced cytoprotection requires the generation of ROS. In addition, it was postulated that this ROS generation originates in the mitochondria.","abstract_has_math":false,"creators":["Lacerda, Lydia"],"institution":"Department of Medicine","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":["Lecour, Sandrine","Opie, Lionel H"],"committee_chairs":[],"committee_members":[],"year":2005,"date_issued":"2005","date_published":"2005","updated_at":"2026-07-22T22:22:37Z","subjects":[],"languages":["eng"],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/11427/3414","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Lecour, Sandrine","Opie, Lionel H"]},{"key":"dc:creator","label":"Author","values":["Lacerda, Lydia"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2014-07-29T09:04:19Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2014-07-29T09:04:19Z"]},{"key":"dc:date.issued","label":"Date","values":["2005"]},{"key":"dc:publisher.department","label":"Dc Publisher Department","values":["Department of Medicine"]},{"key":"dc:publisher.institution","label":"Dc Publisher Institution","values":["University of Cape Town"]},{"key":"dc:type","label":"Dc Type","values":["Master Thesis"]},{"key":"dc:type.qualificationlevel","label":"Dc Type Qualificationlevel","values":["Masters"]},{"key":"dc:type.qualificationname","label":"Dc Type Qualificationname","values":["MSc"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["eng"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/11427/3414"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Includes bibliographical references (leaves 73-89)."]},{"key":"dc:description.abstract","label":"Abstract","values":["Tumour necrosis factor alpha (TNFa) is a pleiotropic cytokine which has both beneficial and deleterious effects. It has previously been shown in our laboratory that TNFa can mimic ischemic preconditioning (IPC). However, the signalling pathways involved in this protection remain incompletely understood. One potential protective pathway involves the generation of reactive oxygen species (ROS), which are known to be activated by TNFa. It was therefore hypothesized that TNFa-induced cytoprotection requires the generation of ROS. In addition, it was postulated that this ROS generation originates in the mitochondria."]},{"key":"dc:title","label":"Title","values":["Signalling pathways involved in TNFα-induced cytoprotection : role of reactive oxygen species"]}]}],"canonical_facts":{"dc:contributor.advisor":["Lecour, Sandrine","Opie, Lionel H"],"dc:creator":["Lacerda, Lydia"],"dc:date.accessioned":["2014-07-29T09:04:19Z"],"dc:date.available":["2014-07-29T09:04:19Z"],"dc:date.issued":["2005"],"dc:description":["Includes bibliographical references (leaves 73-89)."],"dc:description.abstract":["Tumour necrosis factor alpha (TNFa) is a pleiotropic cytokine which has both beneficial and deleterious effects. It has previously been shown in our laboratory that TNFa can mimic ischemic preconditioning (IPC). However, the signalling pathways involved in this protection remain incompletely understood. One potential protective pathway involves the generation of reactive oxygen species (ROS), which are known to be activated by TNFa. It was therefore hypothesized that TNFa-induced cytoprotection requires the generation of ROS. In addition, it was postulated that this ROS generation originates in the mitochondria."],"dc:identifier.uri":["http://hdl.handle.net/11427/3414"],"dc:language.iso":["eng"],"dc:publisher.department":["Department of Medicine"],"dc:publisher.institution":["University of Cape Town"],"dc:title":["Signalling pathways involved in TNFα-induced cytoprotection : role of reactive oxygen species"],"dc:type":["Master Thesis"],"dc:type.qualificationlevel":["Masters"],"dc:type.qualificationname":["MSc"]},"updated_at":"2026-07-22T22:22:37Z"}