Advanced search options

Advanced Search Options 🞨

Browse by author name (“Author name starts with…”).

Find ETDs with:

in
/  
in
/  
in
/  
in

Written in Published in Earliest date Latest date

Sorted by

Results per page:

Sorted by: relevance · author · university · date | New search

You searched for +publisher:"Georgia Tech" +contributor:("Dr. Larry V. McIntire"). Showing records 1 – 3 of 3 total matches.

Search Limiters

Last 2 Years | English Only

No search limiters apply to these results.

▼ Search Limiters


Georgia Tech

1. 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

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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 March 01, 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. 01 Mar 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 Mar 01]. 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

2. 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

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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 March 01, 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. 01 Mar 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 Mar 01]. 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


Georgia Tech

3. Flannery, Conor James. Thrombus Formation under High Shear in Arterial Stenotic Flow.

Degree: MS, Mechanical Engineering, 2005, Georgia Tech

Acute thrombotic and thromboembolic occlusion of atherosclerotic vessels are events that precipitate most heart attacks and strokes. In arterial stenotic flow, thrombus formation is shear dependent and may or may not lead to complete occlusion of the vessel. Platelets in whole blood adhere to collagen-coated surfaces and as they accumulate the resistance of the stenosis increases because of the decreasing passageway of the occluded stenosis. As a model of blood clotting in stenoses, porcine blood is heparinized and perfused over tubular glass test sections that are coated with collagen type I. Each test section has a preexisting stenosis and its severity varies so that higher percent stenoses produce higher shear rates on the blood. The hypothesis of this thesis is that high shear rates due to stenosis in arteries are a necessary feature for occlusive thrombosis. Advisors/Committee Members: Dr. David N. Ku (Committee Chair), Dr. Andres J. Garcia (Committee Member), Dr. Larry V. McIntire (Committee Member).

Subjects/Keywords: Stenosis; Shear; Blood; Thrombosis

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Flannery, C. J. (2005). Thrombus Formation under High Shear in Arterial Stenotic Flow. (Masters Thesis). Georgia Tech. Retrieved from http://hdl.handle.net/1853/6943

Chicago Manual of Style (16th Edition):

Flannery, Conor James. “Thrombus Formation under High Shear in Arterial Stenotic Flow.” 2005. Masters Thesis, Georgia Tech. Accessed March 01, 2021. http://hdl.handle.net/1853/6943.

MLA Handbook (7th Edition):

Flannery, Conor James. “Thrombus Formation under High Shear in Arterial Stenotic Flow.” 2005. Web. 01 Mar 2021.

Vancouver:

Flannery CJ. Thrombus Formation under High Shear in Arterial Stenotic Flow. [Internet] [Masters thesis]. Georgia Tech; 2005. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/1853/6943.

Council of Science Editors:

Flannery CJ. Thrombus Formation under High Shear in Arterial Stenotic Flow. [Masters Thesis]. Georgia Tech; 2005. Available from: http://hdl.handle.net/1853/6943

.