• Login
    View Item 
    •   Home
    • Theses and Dissertations
    • Theses and Dissertations
    • View Item
    •   Home
    • Theses and Dissertations
    • Theses and Dissertations
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Browse

    All of TUScholarShareCommunitiesDateAuthorsTitlesSubjectsGenresThis CollectionDateAuthorsTitlesSubjectsGenres

    My Account

    LoginRegister

    Help

    AboutPeoplePoliciesHelp for DepositorsData DepositFAQs

    Statistics

    Most Popular ItemsStatistics by CountryMost Popular Authors

    DUAL INHIBITION OF CATHEPSIN G AND CHYMASE AFTER ISCHEMIA REPERFUSION: THE ROLE OF INFLAMMATORY SERINE PROTEASES IN ISCHEMIA REPERFUSION INJURY

    • CSV
    • RefMan
    • EndNote
    • BibTex
    • RefWorks
    Thumbnail
    Name:
    TETDEDXHooshdaran-temple-0225E ...
    Size:
    2.869Mb
    Format:
    PDF
    Download
    Genre
    Thesis/Dissertation
    Date
    2017
    Author
    Hooshdaran, Bahman
    Advisor
    Kiani, Mohammad F.
    Sabri, Abdelkarim
    Committee member
    Pleshko, Nancy
    Kilpatrick, Laurie
    Department
    Bioengineering
    Subject
    Engineering
    Bioengineering
    Infalmmation
    Ischemia Reperfusion
    Targeted Drug Delivery
    Permanent link to this record
    http://hdl.handle.net/20.500.12613/3023
    
    Metadata
    Show full item record
    DOI
    http://dx.doi.org/10.34944/dspace/3005
    Abstract
    Acute 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
    ADA compliance
    For Americans with Disabilities Act (ADA) accommodation, including help with reading this content, please contact scholarshare@temple.edu
    Collections
    Theses and Dissertations

    entitlement

     
    DSpace software (copyright © 2002 - 2023)  DuraSpace
    Temple University Libraries | 1900 N. 13th Street | Philadelphia, PA 19122
    (215) 204-8212 | scholarshare@temple.edu
    Open Repository is a service operated by 
    Atmire NV
     

    Export search results

    The export option will allow you to export the current search results of the entered query to a file. Different formats are available for download. To export the items, click on the button corresponding with the preferred download format.

    By default, clicking on the export buttons will result in a download of the allowed maximum amount of items.

    To select a subset of the search results, click "Selective Export" button and make a selection of the items you want to export. The amount of items that can be exported at once is similarly restricted as the full export.

    After making a selection, click one of the export format buttons. The amount of items that will be exported is indicated in the bubble next to export format.