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dc.contributor.advisorKiani, Mohammad F.
dc.contributor.advisorSabri, Abdelkarim
dc.creatorHooshdaran, Bahman
dc.date.accessioned2020-11-04T15:20:06Z
dc.date.available2020-11-04T15:20:06Z
dc.date.issued2017
dc.identifier.urihttp://hdl.handle.net/20.500.12613/3023
dc.description.abstractAcute myocardial infarction (AMI) is a leading cause of morbidity and mortality in the world (4). Restoration of coronary flow to the ischemic myocardium by interventions such as angioplasty, thrombolytic treatment or coronary bypass surgery is the current standard therapy for AMI (5). However, reperfusion of the ischemic myocardium may result in paradoxical cardiomyocyte dysfunction and worsen tissue damage, in a process known as “reperfusion injury” (6). Ischemic reperfusion (IR) injury may intensify pathological processes that contribute to the generation of oxyradicals, disturbances in cation homeostasis, and depletion of cellular energy stores, which may elicit arrhythmias, contractile dysfunction, and ultrastructural damage of the myocardium. These changes can lead to heart failure and ultimately sudden death. The exact mechanisms of IR injury are not fully known (7). Molecular, cellular, and tissue alterations such as cell death, inflammation, neurohumoral activation, and oxidat
dc.format.extent139 pages
dc.language.isoeng
dc.publisherTemple University. Libraries
dc.relation.ispartofTheses and Dissertations
dc.rightsIN COPYRIGHT- This Rights Statement can be used for an Item that is in copyright. Using this statement implies that the organization making this Item available has determined that the Item is in copyright and either is the rights-holder, has obtained permission from the rights-holder(s) to make their Work(s) available, or makes the Item available under an exception or limitation to copyright (including Fair Use) that entitles it to make the Item available.
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/
dc.subjectEngineering
dc.subjectBioengineering
dc.subjectInfalmmation
dc.subjectIschemia Reperfusion
dc.subjectTargeted Drug Delivery
dc.titleDUAL INHIBITION OF CATHEPSIN G AND CHYMASE AFTER ISCHEMIA REPERFUSION: THE ROLE OF INFLAMMATORY SERINE PROTEASES IN ISCHEMIA REPERFUSION INJURY
dc.typeText
dc.type.genreThesis/Dissertation
dc.contributor.committeememberPleshko, Nancy
dc.contributor.committeememberKilpatrick, Laurie
dc.description.departmentBioengineering
dc.relation.doihttp://dx.doi.org/10.34944/dspace/3005
dc.ada.noteFor Americans with Disabilities Act (ADA) accommodation, including help with reading this content, please contact scholarshare@temple.edu
dc.description.degreePh.D.
refterms.dateFOA2020-11-04T15:20:06Z


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