{"id":{"repo_id":"ncsu","oai_identifier":"oai:repository.lib.ncsu.edu:1840.16/4530"},"canonical_url":"https://search.dev.ndltd.org/etd/ncsu/oai:repository.lib.ncsu.edu:1840.16/4530","repository":{"repo_id":"ncsu","name":"North Carolina State University","base_url":"https://repository.lib.ncsu.edu/server/oai/request"},"display":{"title":"Mechanisms of Prostaglandin-Stimulated Recovery of Mucosal Barrier Function in the Ischemia-Injured Porcine Intestine: Role of Intestinal Ion Transport","abstract":"A series of experiments were conducted to determine physiologic mechanisms of mucosal repair in the ischemia-injured intestine. The first experiment (Chapter III) investigated the contributory role of individual Cl- channels in the recovery of barrier function in ischemia-injured porcine ileum. Ischemia-injured porcine ileal mucosa was mounted in Ussing chambers. Short circuit current (Isc) and transepithelial resistance (TER) were measured in response to PGE2 and pharmacologic inhibitors of epithelial Cl- channels. Overall, results from these studies demonstrate that ClC-2-mediated intestinal Cl- secretion restores TER in ischemia-injured intestine. Chapter IV entails a study aimed at more directly investigating the role of ClC-2 in mucosal repair by evaluating mucosal repair in ischemia-injured intestinal mucosa mounted on Ussing chambers treated with the selective ClC-2 agonist, lubiprostone. Results from this suggest that activation of ClC-2 with the selective agonist, lubiprostone, stimulated elevations in TER and reduction in mannitol flux in the Ischemia-injured intestine. In Chapter V, experiments focused on the role of individual NHE isoforms in the recovery of barrier function in ischemia-injured porcine ileum. Results from this study demonstrate that inhibition of NHE2 activity, possibly via EBP50, induces recovery of barrier function in ischemic-injured intestine","abstract_html":"A series of experiments were conducted to determine physiologic mechanisms of mucosal repair in the ischemia-injured intestine. The first experiment (Chapter III) investigated the contributory role of individual Cl- channels in the recovery of barrier function in ischemia-injured porcine ileum. Ischemia-injured porcine ileal mucosa was mounted in Ussing chambers. Short circuit current (Isc) and transepithelial resistance (TER) were measured in response to PGE2 and pharmacologic inhibitors of epithelial Cl- channels. Overall, results from these studies demonstrate that ClC-2-mediated intestinal Cl- secretion restores TER in ischemia-injured intestine. Chapter IV entails a study aimed at more directly investigating the role of ClC-2 in mucosal repair by evaluating mucosal repair in ischemia-injured intestinal mucosa mounted on Ussing chambers treated with the selective ClC-2 agonist, lubiprostone. Results from this suggest that activation of ClC-2 with the selective agonist, lubiprostone, stimulated elevations in TER and reduction in mannitol flux in the Ischemia-injured intestine. In Chapter V, experiments focused on the role of individual NHE isoforms in the recovery of barrier function in ischemia-injured porcine ileum. Results from this study demonstrate that inhibition of NHE2 activity, possibly via EBP50, induces recovery of barrier function in ischemic-injured intestine","abstract_has_math":false,"creators":["Moeser, Adam James"],"institution":null,"degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":["Anthony Blikslager, Committee Chair","Glen Almond, Committee Member","Jody Gookin, Committee Member","Jack Odle, Committee Member"],"committee_chairs":[],"committee_members":[],"year":2006,"date_issued":"2006-05-16","date_published":"2006-05-16","updated_at":"2026-08-21T22:21:56Z","subjects":["ion transport","porcine","barrier function","Intestine"],"languages":[],"rights":["I hereby certify that, if appropriate, I have obtained and attached hereto a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to NC State University or its agents the non-exclusive license to archive and make accessible, under the conditions specified below, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report."],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier.other","label":"Dc Identifier Other","values":["etd-04252006-123724"],"render_values":[{"text":"etd-04252006-123724","href":null,"code":true}]}]},"links":{"outbound_url":"http://www.lib.ncsu.edu/resolver/1840.16/4530","outbound_label":"Repository record","outbound_source":"dc:identifier.uri"},"source_record":{"url":"https://repository.lib.ncsu.edu/server/oai/request?verb=GetRecord&metadataPrefix=dim&identifier=oai%3Arepository.lib.ncsu.edu%3A1840.16%2F4530","prefix":"dim"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Anthony Blikslager, Committee Chair","Glen Almond, Committee Member","Jody Gookin, Committee Member","Jack Odle, Committee Member"]},{"key":"dc:creator","label":"Author","values":["Moeser, Adam James"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2010-04-02T18:55:36Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2010-04-02T18:55:36Z"]},{"key":"dc:date.issued","label":"Date","values":["2006-05-16"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["ion transport","porcine","barrier function","Intestine"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:rights","label":"Dc Rights","values":["I hereby certify that, if appropriate, I have obtained and attached hereto a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to NC State University or its agents the non-exclusive license to archive and make accessible, under the conditions specified below, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.other","label":"Dc Identifier Other","values":["etd-04252006-123724"]},{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://www.lib.ncsu.edu/resolver/1840.16/4530"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["North Carolina State University Theses Physiology."]},{"key":"dc:description.abstract","label":"Abstract","values":["A series of experiments were conducted to determine physiologic mechanisms of mucosal repair in the ischemia-injured intestine. The first experiment (Chapter III) investigated the contributory role of individual Cl- channels in the recovery of barrier function in ischemia-injured porcine ileum. Ischemia-injured porcine ileal mucosa was mounted in Ussing chambers. Short circuit current (Isc) and transepithelial resistance (TER) were measured in response to PGE2 and pharmacologic inhibitors of epithelial Cl- channels. Overall, results from these studies demonstrate that ClC-2-mediated intestinal Cl- secretion restores TER in ischemia-injured intestine. Chapter IV entails a study aimed at more directly investigating the role of ClC-2 in mucosal repair by evaluating mucosal repair in ischemia-injured intestinal mucosa mounted on Ussing chambers treated with the selective ClC-2 agonist, lubiprostone. Results from this suggest that activation of ClC-2 with the selective agonist, lubiprostone, stimulated elevations in TER and reduction in mannitol flux in the Ischemia-injured intestine. In Chapter V, experiments focused on the role of individual NHE isoforms in the recovery of barrier function in ischemia-injured porcine ileum. Results from this study demonstrate that inhibition of NHE2 activity, possibly via EBP50, induces recovery of barrier function in ischemic-injured intestine"]},{"key":"dc:format","label":"Dc Format","values":["Thesis (Ph.D.)--North Carolina State University."]},{"key":"dc:title","label":"Title","values":["Mechanisms of Prostaglandin-Stimulated Recovery of Mucosal Barrier Function in the Ischemia-Injured Porcine Intestine: Role of Intestinal Ion Transport"]}]}],"canonical_facts":{"dc:contributor.advisor":["Anthony Blikslager, Committee Chair","Glen Almond, Committee Member","Jody Gookin, Committee Member","Jack Odle, Committee Member"],"dc:creator":["Moeser, Adam James"],"dc:date.accessioned":["2010-04-02T18:55:36Z"],"dc:date.available":["2010-04-02T18:55:36Z"],"dc:date.issued":["2006-05-16"],"dc:description":["North Carolina State University Theses Physiology."],"dc:description.abstract":["A series of experiments were conducted to determine physiologic mechanisms of mucosal repair in the ischemia-injured intestine. The first experiment (Chapter III) investigated the contributory role of individual Cl- channels in the recovery of barrier function in ischemia-injured porcine ileum. Ischemia-injured porcine ileal mucosa was mounted in Ussing chambers. Short circuit current (Isc) and transepithelial resistance (TER) were measured in response to PGE2 and pharmacologic inhibitors of epithelial Cl- channels. Overall, results from these studies demonstrate that ClC-2-mediated intestinal Cl- secretion restores TER in ischemia-injured intestine. Chapter IV entails a study aimed at more directly investigating the role of ClC-2 in mucosal repair by evaluating mucosal repair in ischemia-injured intestinal mucosa mounted on Ussing chambers treated with the selective ClC-2 agonist, lubiprostone. Results from this suggest that activation of ClC-2 with the selective agonist, lubiprostone, stimulated elevations in TER and reduction in mannitol flux in the Ischemia-injured intestine. In Chapter V, experiments focused on the role of individual NHE isoforms in the recovery of barrier function in ischemia-injured porcine ileum. Results from this study demonstrate that inhibition of NHE2 activity, possibly via EBP50, induces recovery of barrier function in ischemic-injured intestine"],"dc:format":["Thesis (Ph.D.)--North Carolina State University."],"dc:identifier.other":["etd-04252006-123724"],"dc:identifier.uri":["http://www.lib.ncsu.edu/resolver/1840.16/4530"],"dc:rights":["I hereby certify that, if appropriate, I have obtained and attached hereto a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to NC State University or its agents the non-exclusive license to archive and make accessible, under the conditions specified below, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report."],"dc:subject":["ion transport","porcine","barrier function","Intestine"],"dc:title":["Mechanisms of Prostaglandin-Stimulated Recovery of Mucosal Barrier Function in the Ischemia-Injured Porcine Intestine: Role of Intestinal Ion Transport"]},"updated_at":"2026-08-21T22:21:56Z"}