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You searched for +publisher:"University of North Carolina" +contributor:("Goy, Michael F."). Showing records 1 – 2 of 2 total matches.

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University of North Carolina

1. Fellner, Robert C. Prouroguanylin’s role in the homeostatic response to dietary sodium: hormone precursor or active signaling agent?.

Degree: Cell Biology and Physiology, 2010, University of North Carolina

High blood pressure affects more than 70 million Americans, putting them at a much greater risk for heart disease or a stroke. Sodium (Na+) is a major determinant of blood osmolarity and volume, and therefore plays a critical role in blood pressure regulation. Prouroguanylin (proUgn) has been implicated as a signal being sent from the small intestine to the kidney, in response to oral Na+ intake, that intestinal Na+ adsorption is eminent and renal Na+ excretion is necessary to maintain homeostasis. This concept, known as post-prandial natriuresis, is based on past observations of a faster natriuretic response from an oral salt load than from an equimolar intravenous infusion of NaCl. This role for proUgn is contentious however, as it has not been clearly shown if the role played by proUgn is that of a primary messenger from the intestine to the kidney in response to salt, if it is a intrarenal paracrine mechanism secondary to some other extrarenal signal in response to oral Na+ or even if it is proUgn itself or one of its' metabolites that are acting in the kidney. My studies address identification and quantification of proUgn and Ugn in relevant tissue compartments and additionally, I look at the effects of dietary Na+ on changes in the expression of proUgn and Ugn in these tissues. A novel adaptation of a binding assay technique allowed for urinary Ugn measurements that were found to directly correlate with dietary Na+ intake on a time scale that the prior techniques were insufficiently sensitive to achieve. Enteric and plasma proUgn do not change in response to dietary Na+, however a renal proUgn expression and Ugn in the urine do. Changes in plasma proUgn elicit a greater natriuretic response with a lower urinary Ugn concentration than urinary Ugn concentrations from infusions of Ugn in the blood. My conclusion is that proUgn is a secondary agent involved in volume and Na+ homeostasis, acting though some as yet unidentified renal metabolite/receptor mechanism. Further studies should focus on if there is another active cleavage product of proUgn and what receptor it (proUgn or Ugn) acts through. Advisors/Committee Members: Fellner, Robert C., Goy, Michael F..

Subjects/Keywords: School of Medicine; Department of Cell Biology and Physiology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Fellner, R. C. (2010). Prouroguanylin’s role in the homeostatic response to dietary sodium: hormone precursor or active signaling agent?. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:58233f79-43ae-4eb6-81c7-d73394886510

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Fellner, Robert C. “Prouroguanylin’s role in the homeostatic response to dietary sodium: hormone precursor or active signaling agent?.” 2010. Thesis, University of North Carolina. Accessed September 24, 2020. https://cdr.lib.unc.edu/record/uuid:58233f79-43ae-4eb6-81c7-d73394886510.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Fellner, Robert C. “Prouroguanylin’s role in the homeostatic response to dietary sodium: hormone precursor or active signaling agent?.” 2010. Web. 24 Sep 2020.

Vancouver:

Fellner RC. Prouroguanylin’s role in the homeostatic response to dietary sodium: hormone precursor or active signaling agent?. [Internet] [Thesis]. University of North Carolina; 2010. [cited 2020 Sep 24]. Available from: https://cdr.lib.unc.edu/record/uuid:58233f79-43ae-4eb6-81c7-d73394886510.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Fellner RC. Prouroguanylin’s role in the homeostatic response to dietary sodium: hormone precursor or active signaling agent?. [Thesis]. University of North Carolina; 2010. Available from: https://cdr.lib.unc.edu/record/uuid:58233f79-43ae-4eb6-81c7-d73394886510

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


University of North Carolina

2. Roche, Kyle. Intrinsic regulation of quiescence and radioresistance in intestinal stem cells.

Degree: Cell Biology and Physiology, 2016, University of North Carolina

The intestinal epithelium regenerates every 5-7 days, a process that is facilitated by a pool of intestinal stem cells. Over the past decade, it has become apparent that the intestinal stem cell pool is diverse, containing at least two populations. Active stem cells (aISCs) are moderately proliferative and contribute to homeostatic regeneration, while reserve stem cells (rISCs) are slowly proliferative and facilitate regeneration following damage-induced loss of the aISC population. The genetic mechanisms required for the production and maintenance of rISCs are unknown. Sox9 is a transcription factor that has been shown to maintain stem cell populations in various tissues. In the intestinal epithelium, Sox9 is expressed in a gradient that negatively correlates with proliferative capacity. Transit-amplifying progenitors express the lowest levels of Sox9, while aISCs express intermediate levels, and cells expressing the highest levels of Sox9 are consistent with slowly cycling rISCs. In this dissertation, I will address the role that Sox9 plays in maintaining rISC function within the intestinal epithelium. I find that Sox9 is not only necessary for the production of a quiescent rISCs, but that it is also uniformly necessary for maintaining radioresistance within the rISC pool. This work identifies Sox9 as a novel intrinsic regulator of the rISC state. Advisors/Committee Members: Roche, Kyle, Otey, Carol, Magness, Scott, Sheikh, Shehzad, Goy, Michael F., Henning, Susan.

Subjects/Keywords: School of Medicine; Department of Cell Biology and Physiology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Roche, K. (2016). Intrinsic regulation of quiescence and radioresistance in intestinal stem cells. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:91534062-64fa-4881-9c13-92b57864f0e7

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Roche, Kyle. “Intrinsic regulation of quiescence and radioresistance in intestinal stem cells.” 2016. Thesis, University of North Carolina. Accessed September 24, 2020. https://cdr.lib.unc.edu/record/uuid:91534062-64fa-4881-9c13-92b57864f0e7.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Roche, Kyle. “Intrinsic regulation of quiescence and radioresistance in intestinal stem cells.” 2016. Web. 24 Sep 2020.

Vancouver:

Roche K. Intrinsic regulation of quiescence and radioresistance in intestinal stem cells. [Internet] [Thesis]. University of North Carolina; 2016. [cited 2020 Sep 24]. Available from: https://cdr.lib.unc.edu/record/uuid:91534062-64fa-4881-9c13-92b57864f0e7.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Roche K. Intrinsic regulation of quiescence and radioresistance in intestinal stem cells. [Thesis]. University of North Carolina; 2016. Available from: https://cdr.lib.unc.edu/record/uuid:91534062-64fa-4881-9c13-92b57864f0e7

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

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