Antecedent hydrogen sulfide elicits an anti-inflammatory phenotype in postischemic murine small intestine

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Antecedent hydrogen sulfide elicits an anti-inflammatory phenotype in postischemic murine small intestine

Please use this identifier to cite or link to this item: http://hdl.handle.net/10355/4779

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dc.contributor.advisor Korthuis, Ronald J. en
dc.contributor.author Yusof, Mozow, 1976- en_US
dc.date.accessioned 2010-01-12T18:42:21Z
dc.date.available 2010-01-12T18:42:21Z
dc.date.issued 2007 en_US
dc.date.submitted 2007 Fall en
dc.identifier.other YusofM-030309-D9190 en_US
dc.identifier.uri http://hdl.handle.net/10355/4779
dc.description The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. en_US
dc.description Thesis (Ph. D.) University of Missouri-Columbia 2007. en_US
dc.description Vita. en_US
dc.description Includes bibliographical references. en_US
dc.description Dissertations, Academic -- University of Missouri--Columbia -- pharmacology. en_US
dc.description.abstract Ischemia followed by reperfusion (I/R) is now well-recognized as one form of acute inflammation in which leukocytes play a key role. Preconditioning is a phenomenon through which antecedent exposure to a particular stimulus confers protection against a subsequent prolonged ischemic event. The development of a protected phenotype occurs in response to a diverse array of preconditioning stimuli; each of these preconditioning stimuli appears to promote the production of the gaseous monoxide, nitric oxide (NO), as an initial triggering event in the acquisition of tolerance to I/R. Recent work has shown that NO acts as an endogenous regulator of a second gaseous signaling molecule with vasorelaxant properties, hydrogen sulfide (H₂S). Similar to NO, H₂S has the ability to fulfill a physiologic role in regulating cardiovascular function, distinct from its toxicologic effect. This dissertation shows that H₂S inhibits inflammation after I/R injury, through four separate, yet not necessarily distinct, mechanisms. The aims of this dissertation addressed the hypothesis that H₂S elicits a preconditioning stimulus and protects against I/R injury through an eNOS-/p38 MAPK-/K channel-/HO-1 dependent mechanism. en_US
dc.language.iso en_US en_US
dc.publisher University of Missouri--Columbia en_US
dc.relation.ispartof 2007 Freely available dissertations (MU) en_US
dc.subject.mesh Anti-inflammatory agents en_US
dc.subject.mesh Nitric Oxide -- metabolism en_US
dc.subject.mesh Ischemic Preconditioning en_US
dc.subject.mesh Hydrogen Sulfide -- pharmacology en_US
dc.subject.mesh Ischemia -- prevention & control en_US
dc.title Antecedent hydrogen sulfide elicits an anti-inflammatory phenotype in postischemic murine small intestine en_US
dc.type Thesis en_US
thesis.degree.discipline Pharmacology en_US
thesis.degree.grantor University of Missouri--Columbia en_US
thesis.degree.name Ph. D. en_US
thesis.degree.level Doctoral en_US
dc.identifier.merlin .b66635627 en_US
dc.identifier.oclc 314399271 en_US
dc.relation.ispartofcommunity University of Missouri-Columbia. Graduate School. Theses and Dissertations. Dissertations. 2007 Dissertations


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