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You searched for +publisher:"Georgia Tech" +contributor:("Dr. Timothy M. Wick"). Showing records 1 – 3 of 3 total matches.

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Georgia Tech

1. Konduri, Suchitra. The Influence of Normal Physiological Forces on Porcine Aortic Heart Valves in a Sterile Ex Vivo Pulsatile Organ Culture System.

Degree: MS, Chemical Engineering, 2005, Georgia Tech

The aortic valve functions in a complex mechanical environment which leads to force dependent cellular and tissue responses. Characterization of these responses provides a fundamental understanding of valve pathogenesis. The aim of this work was to develop an ex vivo organ culture system capable of simulating physiological aortic pressures and flow rates, and study the biological characteristics of native porcine aortic valves cultured in the system. Collagen, sGAG and elastin content of the valve leaflets were measured and cusp morphology, cell phenotype, cell proliferation and apoptosis were examined. Presence of endothelial cells (ECs) on the leaflet surface was also evaluated. The differences in collagen, sGAG and elastin contents were not significant (p greater than0.05) between the cultured and fresh valve leaflets. The cultured valves maintained the structural integrity of the leaflets while preserving the native morphology and cell phenotype. Cell phenotype in leaflets incubated statically under atmospheric conditions decreased compared to fresh and cultured valve leaflets, indicating the importance of mechanical forces in maintaining the natural biology of the valve leaflets. ECs were retained on the surfaces of cultured leaflets with no remodeling of the leaflets. The number of apoptotic cells in the cultured leaflets was significantly (p less than 0.05) less than in the statically incubated leaflets and comparable to fresh leaflets. The sterile ex vivo organ culture system thus maintained the viability and native biological characteristics of the aortic valves that were cultured under dynamic conditions for a period of 48 hours. Advisors/Committee Members: Dr. Ajit P.Yoganathan (Committee Chair), Dr. Athanassios Sambanis (Committee Member), Dr. Timothy M. Wick (Committee Member).

Subjects/Keywords: Flow and pressure waveforms; Porcine aortic valve leaflets; Extracellular matrix components; Cell phenotype; Endothelial cells; Organ culture system; Tissue morphology

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APA (6th Edition):

Konduri, S. (2005). The Influence of Normal Physiological Forces on Porcine Aortic Heart Valves in a Sterile Ex Vivo Pulsatile Organ Culture System. (Masters Thesis). Georgia Tech. Retrieved from http://hdl.handle.net/1853/6999

Chicago Manual of Style (16th Edition):

Konduri, Suchitra. “The Influence of Normal Physiological Forces on Porcine Aortic Heart Valves in a Sterile Ex Vivo Pulsatile Organ Culture System.” 2005. Masters Thesis, Georgia Tech. Accessed January 19, 2021. http://hdl.handle.net/1853/6999.

MLA Handbook (7th Edition):

Konduri, Suchitra. “The Influence of Normal Physiological Forces on Porcine Aortic Heart Valves in a Sterile Ex Vivo Pulsatile Organ Culture System.” 2005. Web. 19 Jan 2021.

Vancouver:

Konduri S. The Influence of Normal Physiological Forces on Porcine Aortic Heart Valves in a Sterile Ex Vivo Pulsatile Organ Culture System. [Internet] [Masters thesis]. Georgia Tech; 2005. [cited 2021 Jan 19]. Available from: http://hdl.handle.net/1853/6999.

Council of Science Editors:

Konduri S. The Influence of Normal Physiological Forces on Porcine Aortic Heart Valves in a Sterile Ex Vivo Pulsatile Organ Culture System. [Masters Thesis]. Georgia Tech; 2005. Available from: http://hdl.handle.net/1853/6999


Georgia Tech

2. Wagner, Matthew Christian. Histamine as a Potential Initiator of Sickle Pain crisis by Mediation of Sickle Erythrocyte Adherence in a Shear-Dependent Manner.

Degree: PhD, Chemical Engineering, 2006, Georgia Tech

The genetic disorder sickle cell anemia causes hemolytic anemia and sickle pain crisis, episodes of microvascular occlusion resulting in painful ischemic tissue damage. Pain crisis is thought to occur when sickle erythrocytes adhere in the post-capillary venule, partially occluding the vessel. The resulting slowed blood flow causes more extensive cell adherence and entrapment of rigid, deoxygenated erythrocytes until the vessel is entirely occluded. It was hypothesized that the inflammatory mediators histamine and tumor necrosis factor-, factors known to cause endothelial expression of adhesive ligands, might significantly increase sickle erythrocyte adhesion, and thus be capable of initiating sickle pain crisis. It was also hypothesized that the perfusion shear stress environment of the endothelium, known to be oscillatory and reduced in sickle cell patients, was a significant mediating factor of sickle cell adhesion. An in-vitro flow chamber using cultured endothelial cells and erythrocytes from blood samples of sickle cell anemic patients was used to quantify sickle erythrocyte adherence to stimulated and unstimulated endothelial cells under shear stresses from 1.0 to 0.1 dyne/cm2. Results showed that both endothelial stimulation and reduction of the perfusion shear stress increased sickle erythrocyte adherence. In combination, the use of inflammatory stimulation with reduced shear stress resulted in further increased adhesion, but only when above the range of 0.1 V 0.2 or 0.4 dyne/cm2, depending on the inflammatory mediator. Adhesion below this level of shear is not significantly increased by endothelial stimulation. The mechanism by which histamine mediates adhesion was investigated, and found to involve the endothelial H2 and H4 receptors and expression of the P-selectin ligand. These data suggest that irregular flow, typical of sickle microvasculature, may act in conjunction with the pro-inflammatory state of sickle vasculature and the histaminergic nature of some pain treatments to initiate or propagate sickle vaso-occlusion. Findings concerning histamine, tumor necrosis factor-alpha, and shear stress effects on adherence are discussed in relation to their possible applicability to patient health, future studies are outlined to confirm the relation of in vitro data to in vivo patient condition, and proposals are made for applying these methodologies to other potential mediators of sickle erythrocyte adhesion. Advisors/Committee Members: Dr. Timothy M. Wick (Committee Chair), Dr. Athanassios Sambanis (Committee Member), Dr. James R. Eckman (Committee Member), Dr. Larry V. McIntire (Committee Member), Dr. Lewis L. Hsu (Committee Member).

Subjects/Keywords: Sickle cell anemia; Inflammation; Shear stress; Vaso-occlusive crisis; Cell adhesion; Histamine; Shear (Mechanics); Sickle cell anemia; Cell adhesion; Erythrocytes

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

APA (6th Edition):

Wagner, M. C. (2006). Histamine as a Potential Initiator of Sickle Pain crisis by Mediation of Sickle Erythrocyte Adherence in a Shear-Dependent Manner. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/14478

Chicago Manual of Style (16th Edition):

Wagner, Matthew Christian. “Histamine as a Potential Initiator of Sickle Pain crisis by Mediation of Sickle Erythrocyte Adherence in a Shear-Dependent Manner.” 2006. Doctoral Dissertation, Georgia Tech. Accessed January 19, 2021. http://hdl.handle.net/1853/14478.

MLA Handbook (7th Edition):

Wagner, Matthew Christian. “Histamine as a Potential Initiator of Sickle Pain crisis by Mediation of Sickle Erythrocyte Adherence in a Shear-Dependent Manner.” 2006. Web. 19 Jan 2021.

Vancouver:

Wagner MC. Histamine as a Potential Initiator of Sickle Pain crisis by Mediation of Sickle Erythrocyte Adherence in a Shear-Dependent Manner. [Internet] [Doctoral dissertation]. Georgia Tech; 2006. [cited 2021 Jan 19]. Available from: http://hdl.handle.net/1853/14478.

Council of Science Editors:

Wagner MC. Histamine as a Potential Initiator of Sickle Pain crisis by Mediation of Sickle Erythrocyte Adherence in a Shear-Dependent Manner. [Doctoral Dissertation]. Georgia Tech; 2006. Available from: http://hdl.handle.net/1853/14478


Georgia Tech

3. Amos, Amanda Owings. Regulation of Cytokine-Induced Adhesion Molecule Expression and Sickle Erythrocyte Adhesion to Microvascular Endothelial Cells by Intracellular Adenosine 3',5'-Cyclic Monophosphate and Nitric Oxide.

Degree: PhD, Chemical Engineering, 2006, Georgia Tech

Adhesion of sickle erythrocytes to vascular endothelium may initiate or propagate occlusive events in sickle cell anemia, many of which are accompanied by infection and the associated inflammatory response. Inflammatory markers are also present in sickle patients during asymptomatic periods. Inflammatory cytokines upregulate expression of endothelial adhesion molecules that promote adhesion of sickle erythrocytes. The data in this work demonstrate that after 2 hrs of stimulation with the cytokine TNF- and alpha;, E-selectin, but not VCAM-1 is upregulated on human dermal microvascular endothelial cells. After 6 hrs of TNF- and alpha; stimulation, both VCAM-1 and E-selectin expression are upregulated on MECs, and sickle erythrocytes bind to both receptors. Because strategies to control inflammation-associated adhesion in vivo may need to account for both VCAM-1 and E-selectin mediated events, control of intracellular signaling pathways leading to receptor expression is an attractive strategy for inhibiting adhesion. Cyclic AMP and nitric oxide are two intracellular signaling molecules important to cytokine-induced receptor expression. The data in this work demonstrate that TNF- and alpha; induced VCAM-1 and E-selectin expression on endothelial cells and sickle erythrocyte adhesion are abated by increasing endothelial cyclic AMP concentrations using Forskolin, IBMX, or Bt2cAMP. Conversely, when sickle erythrocytes, rather than endothelial cells, are treated with reagents that increase intracellular cAMP, adhesion to unstimulated endothelial cells is increased in some patients. Treatment of endothelial cells with reagents such as SNP and DETA-NO that increase nitric oxide significantly inhibits VCAM-1, but not E-selectin expression, induced by TNF- and alpha; stimulation and significantly inhibits sickle erythrocyte adhesion. Treatment of sickle erythrocytes directly with these reagents may also inhibit adhesion. Together these data suggest that cAMP- and nitric oxide-dependent signaling are useful therapeutic targets to inhibit cytokine-induced sickle erythrocyte adhesion to endothelium. Advisors/Committee Members: Dr. Timothy M. Wick (Committee Chair), Dr. James R. Eckman (Committee Member), Dr. Larry V. McIntire (Committee Member), Dr. Peter A. Lane (Committee Member), Dr. Ronald W. Rousseau (Committee Member).

Subjects/Keywords: Cyclic AMP; Adhesion; Sickle cell anemia; Nitric oxide; Sickle cell anemia; Vascular endothelium; Cell adhesion molecules; Cytokines; Erythrocytes; Inflammation

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

APA (6th Edition):

Amos, A. O. (2006). Regulation of Cytokine-Induced Adhesion Molecule Expression and Sickle Erythrocyte Adhesion to Microvascular Endothelial Cells by Intracellular Adenosine 3',5'-Cyclic Monophosphate and Nitric Oxide. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/14621

Chicago Manual of Style (16th Edition):

Amos, Amanda Owings. “Regulation of Cytokine-Induced Adhesion Molecule Expression and Sickle Erythrocyte Adhesion to Microvascular Endothelial Cells by Intracellular Adenosine 3',5'-Cyclic Monophosphate and Nitric Oxide.” 2006. Doctoral Dissertation, Georgia Tech. Accessed January 19, 2021. http://hdl.handle.net/1853/14621.

MLA Handbook (7th Edition):

Amos, Amanda Owings. “Regulation of Cytokine-Induced Adhesion Molecule Expression and Sickle Erythrocyte Adhesion to Microvascular Endothelial Cells by Intracellular Adenosine 3',5'-Cyclic Monophosphate and Nitric Oxide.” 2006. Web. 19 Jan 2021.

Vancouver:

Amos AO. Regulation of Cytokine-Induced Adhesion Molecule Expression and Sickle Erythrocyte Adhesion to Microvascular Endothelial Cells by Intracellular Adenosine 3',5'-Cyclic Monophosphate and Nitric Oxide. [Internet] [Doctoral dissertation]. Georgia Tech; 2006. [cited 2021 Jan 19]. Available from: http://hdl.handle.net/1853/14621.

Council of Science Editors:

Amos AO. Regulation of Cytokine-Induced Adhesion Molecule Expression and Sickle Erythrocyte Adhesion to Microvascular Endothelial Cells by Intracellular Adenosine 3',5'-Cyclic Monophosphate and Nitric Oxide. [Doctoral Dissertation]. Georgia Tech; 2006. Available from: http://hdl.handle.net/1853/14621

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