+publisher:"Georgia Tech" +contributor:("Timothy M. Wick")

Georgia Tech

1. Williams, Chrysanthi. Perfusion bioreactor for tissue-engineered blood vessels.

Degree: PhD, Bioengineering, 2003, Georgia Tech

Subjects/Keywords: Tissue engineering; Bioreactors Design and construction; Vascular grafts; Vascular grafts; Tissue engineering; Bioreactors Design and construction

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APA (6^th Edition):

Williams, C. (2003). Perfusion bioreactor for tissue-engineered blood vessels. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/9455

Chicago Manual of Style (16^th Edition):

Williams, Chrysanthi. “Perfusion bioreactor for tissue-engineered blood vessels.” 2003. Doctoral Dissertation, Georgia Tech. Accessed January 24, 2021. http://hdl.handle.net/1853/9455.

MLA Handbook (7^th Edition):

Williams, Chrysanthi. “Perfusion bioreactor for tissue-engineered blood vessels.” 2003. Web. 24 Jan 2021.

Vancouver:

Williams C. Perfusion bioreactor for tissue-engineered blood vessels. [Internet] [Doctoral dissertation]. Georgia Tech; 2003. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/1853/9455.

Council of Science Editors:

Williams C. Perfusion bioreactor for tissue-engineered blood vessels. [Doctoral Dissertation]. Georgia Tech; 2003. Available from: http://hdl.handle.net/1853/9455

Georgia Tech

2. 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

URL: http://hdl.handle.net/1853/6999

► 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… (more)

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 (6^th 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 (16^th 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 24, 2021. http://hdl.handle.net/1853/6999.

MLA Handbook (7^th 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. 24 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 24]. 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

3. Bartling, Karsten. Apoferritin Crystallization in relation to Eye Cataract.

Degree: PhD, Bioengineering, 2006, Georgia Tech

URL: http://hdl.handle.net/1853/14111

► Protein crystallization is significant in both biotechnology and biomedical applications. In biotechnology, crystallization is essential for determining the structure of both native and synthesized therapeutically… (more)

▼ Protein crystallization is significant in both biotechnology and biomedical applications. In biotechnology, crystallization is essential for determining the structure of both native and synthesized therapeutically important proteins. It can also be used as a final purification step and as a stable form for protein storage. With regard to biomedical systems, protein crystallization appears to be involved in the development and manifestation of certain human diseases. In particular, there exists evidence that L-rich ferritin crystals are involved in Hereditary Hyperferritinemia Cataract Syndrome (HHCS). In the current research a microbatch crystallization apparatus has been introduced that enables (1) multiple batch crystallization experiments at various temperatures and solution conditions in parallel and (2) quantitative monitoring of crystal growth without disturbing the progress of an experiment for observation. The primary application of the apparatus is, but not limited to, screening of protein crystallization conditions, although the system can also be used for other macromolecular and small-molecule crystallization experiments. Multiwell microbatch experiments demonstrated the dependence of apoferritin crystal growth kinetics and final crystal size on temperature and cadmium concentration. Although the solubility of apoferritin might be independent of temperature, the results of this study show that the crystal growth kinetics are affected by temperature, profoundly under some conditions. For apoferritin under near physiological conditions the solution thermodynamics in the form of the second virial coefficient have proofed to be a valuable predictor for the crystallization outcome. Furthermore, the significance of the elevated level of some divalent cations in cataractous lenses has been studied both in dilute solutions and under crystallization conditions and cadmium seems to be sole menace in apoferritin condensation. Advisors/Committee Members: Ronald W. Rousseau (Committee Chair), Athanassios Sambanis (Committee Co-Chair), Joe LeDoux (Committee Member), Timothy M. Wick (Committee Member), Victor Breedveld (Committee Member).

Subjects/Keywords: Activation energy for crystallization; Cataract; Apoferritin; Second virial coefficient; Crystallization; Thermal gradient; Light Scattering; Microbatch

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APA (6^th Edition):

Bartling, K. (2006). Apoferritin Crystallization in relation to Eye Cataract. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/14111

Chicago Manual of Style (16^th Edition):

Bartling, Karsten. “Apoferritin Crystallization in relation to Eye Cataract.” 2006. Doctoral Dissertation, Georgia Tech. Accessed January 24, 2021. http://hdl.handle.net/1853/14111.

MLA Handbook (7^th Edition):

Bartling, Karsten. “Apoferritin Crystallization in relation to Eye Cataract.” 2006. Web. 24 Jan 2021.

Vancouver:

Bartling K. Apoferritin Crystallization in relation to Eye Cataract. [Internet] [Doctoral dissertation]. Georgia Tech; 2006. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/1853/14111.

Council of Science Editors:

Bartling K. Apoferritin Crystallization in relation to Eye Cataract. [Doctoral Dissertation]. Georgia Tech; 2006. Available from: http://hdl.handle.net/1853/14111

Georgia Tech

4. Fallon, Anna Marie. The Development of a Novel in vitro Flow System to Evaluate Platelet Activation and Procoagulant Potential Induced by Bileaflet Mechanical Heart Valve Leakage Jets.

Degree: PhD, Chemical Engineering, 2006, Georgia Tech

URL: http://hdl.handle.net/1853/10451

► Bileaflet mechanical heart valves (BMHVs) are prone to thrombus formation in the hinge region due to high shear stress combined with stagnation regions. This thesis… (more)

▼ Bileaflet mechanical heart valves (BMHVs) are prone to thrombus formation in the hinge region due to high shear stress combined with stagnation regions. This thesis research addresses the hypothesis that models that isolate and mimic BMHV hinge geometries can be used to quantitatively characterize procoagulant potential using a novel in vitro blood flow system. Furthermore, these results can be correlated with digital particle image velocimetry (DPIV) measurements detailing flow fields for the same models. The significant findings were that: 1) recalcification of recirculating citrated blood markedly increases the magnitude of thrombus forming reactions and the sensitivity for their detection; 2) platelet activation, and the presence of adequate platelet numbers are essential for the activation of coagulation under conditions of high shear; and 3) thrombin formation can be inhibited by blocking the platelet receptors that facilitate platelet aggregation. The DPIV studies give some insight into why different channel geometries resulted in varying propensities for coagulation. The channel geometries with abrupt changes in diameter induced significantly higher levels of TAT and also formed jets that were subject to increased entrainment of the stagnant fluid in the chamber. This entrainment enables more mixing of the shear-activated platelets with the surrounding flow, which can propagate the coagulation cascade, thus increasing the chance for thrombus formation. The influence of abrupt changes in diameter was also evident in the BMHV human blood studies. The MP valve, which has a tortuous hinge pathway, induced significantly more TAT formation than the SJM Standard valve with a smoother hinge channel. Thus, BMHV hinge geometry should be as smooth and free of diameter changes as possible to eliminate stagnation regions that enable activated platelets to congregate and propagate the coagulation cascade. Leakage gap width also had a significant effect not only on procoagulant potential but also on platelet activation. Both the low and high leaker prototype valves had significantly higher levels of platelet activation compared to the SJM Standard valve, but only the low leaker valve demonstrated a higher propensity for coagulation. Thus, to minimize both platelet activation and thromboemboli formation, an optimal gap width should be maintained for BMHVs. Advisors/Committee Members: Ajit P. Yoganathan (Committee Chair), Dale E. Edmondson (Committee Member), Peter J. Ludovice (Committee Member), Stephen R. Hanson (Committee Member), Timothy M. Wick (Committee Member).

Subjects/Keywords: Blood; Thrombosis; Mechanical heart valves; Platelets; Shear stress

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APA (6^th Edition):

Fallon, A. M. (2006). The Development of a Novel in vitro Flow System to Evaluate Platelet Activation and Procoagulant Potential Induced by Bileaflet Mechanical Heart Valve Leakage Jets. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/10451

Chicago Manual of Style (16^th Edition):

Fallon, Anna Marie. “The Development of a Novel in vitro Flow System to Evaluate Platelet Activation and Procoagulant Potential Induced by Bileaflet Mechanical Heart Valve Leakage Jets.” 2006. Doctoral Dissertation, Georgia Tech. Accessed January 24, 2021. http://hdl.handle.net/1853/10451.

MLA Handbook (7^th Edition):

Fallon, Anna Marie. “The Development of a Novel in vitro Flow System to Evaluate Platelet Activation and Procoagulant Potential Induced by Bileaflet Mechanical Heart Valve Leakage Jets.” 2006. Web. 24 Jan 2021.

Vancouver:

Fallon AM. The Development of a Novel in vitro Flow System to Evaluate Platelet Activation and Procoagulant Potential Induced by Bileaflet Mechanical Heart Valve Leakage Jets. [Internet] [Doctoral dissertation]. Georgia Tech; 2006. [cited 2021 Jan 24]. Available from: http://hdl.handle.net/1853/10451.

Council of Science Editors:

Fallon AM. The Development of a Novel in vitro Flow System to Evaluate Platelet Activation and Procoagulant Potential Induced by Bileaflet Mechanical Heart Valve Leakage Jets. [Doctoral Dissertation]. Georgia Tech; 2006. Available from: http://hdl.handle.net/1853/10451

Georgia Tech

5. 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

URL: http://hdl.handle.net/1853/14478

► 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… (more)

▼ 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 (6^th 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 (16^th 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 24, 2021. http://hdl.handle.net/1853/14478.

MLA Handbook (7^th 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. 24 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 24]. 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

6. 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

URL: http://hdl.handle.net/1853/14621

► 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… (more)

▼ 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 (6^th 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 (16^th 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 24, 2021. http://hdl.handle.net/1853/14621.

MLA Handbook (7^th 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. 24 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 24]. 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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