+publisher:"University of North Carolina" +contributor:("Wolberg, Alisa")

University of North Carolina

1. Weise Cross, Laura. Regulation of Smooth Muscle Cell Phenotype by the RhoA Effectors mDia1 and mDia2.

Degree: Pathology and Laboratory Medicine, 2015, University of North Carolina

URL: https://cdr.lib.unc.edu/record/uuid:b656650d-84e2-48f7-ac8b-4135ba45a063

► Smooth muscle cells (SMCs) play an important role in vascular development and disease. Vascular SMCs undergo profound changes in phenotype in response to environmental cues… (more)

▼ Smooth muscle cells (SMCs) play an important role in vascular development and disease. Vascular SMCs undergo profound changes in phenotype in response to environmental cues that aid in development and vascular repair, but perturbations in the process contribute to many cardiovascular diseases, including atherosclerosis, restenosis, and hypertension. Therefore, it is critical to determine the mechanisms that control their phenotype. We have previously shown that the small GTPase RhoA promotes SMC differentiation through an SRF-dependent mechanism, and the RhoA effectors mDia1 and mDia2 mediate this effect through actin polymerization-dependent localization of the myocardin-related transcription factors (MRTFs). The primary aim of this dissertation is to further dissect the contributions of mDia signaling to SMC phenotype in vivo and in the nuclear compartment of the cell. Using a Cre-based approach, we overexpressed a dominant-negative mDia variant specifically in SMCs in a mouse model. We determined that inhibition of mDia signaling impaired cardiac structure and normal vessel morphology in a subset of developing mice. Adult mice exhibited altered SMC marker gene expression and abnormal SMC migration, indicating that mDia signaling has roles in both SMC differentiation and migration. In vitro studies revealed that mDia variants that preferentially localized to the nucleus significantly enhanced SMC-specific transcription, while those that were less nuclear exhibited reduced SMC transcriptional activity. These observations were also recapitulated with other RhoA signaling genes, implicating a model whereby nuclear RhoA signaling promotes SMC differentiation. Finally, little is known about the mechanisms regulating the expression of the RhoA signaling gene program. Using DNase I hypersensitivity methods coupled to high-throughput sequecing, deletion and mutation analysis, and a transgenic LacZ approach, we present novel evidence that this signaling pathway, including mDia2, may be regulated in an SRF-dependent manner. Because RhoA signaling promotes SRF-dependent transcription, we hypothesize that this mechanism serves as an auto-regulatory feed-forward circuit to promote SMC differentiation. Advisors/Committee Members: Weise Cross, Laura, Mack, Christopher P., Burridge, Keith, Furey, Terrence, Homeister, Jonathon, Wolberg, Alisa.

Subjects/Keywords: Pathology; Cytology; Molecular biology; School of Medicine; Department of Pathology and Laboratory Medicine

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APA (6^th Edition):

Weise Cross, L. (2015). Regulation of Smooth Muscle Cell Phenotype by the RhoA Effectors mDia1 and mDia2. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:b656650d-84e2-48f7-ac8b-4135ba45a063

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

Chicago Manual of Style (16^th Edition):

Weise Cross, Laura. “Regulation of Smooth Muscle Cell Phenotype by the RhoA Effectors mDia1 and mDia2.” 2015. Thesis, University of North Carolina. Accessed January 22, 2021. https://cdr.lib.unc.edu/record/uuid:b656650d-84e2-48f7-ac8b-4135ba45a063.

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

MLA Handbook (7^th Edition):

Weise Cross, Laura. “Regulation of Smooth Muscle Cell Phenotype by the RhoA Effectors mDia1 and mDia2.” 2015. Web. 22 Jan 2021.

Vancouver:

Weise Cross L. Regulation of Smooth Muscle Cell Phenotype by the RhoA Effectors mDia1 and mDia2. [Internet] [Thesis]. University of North Carolina; 2015. [cited 2021 Jan 22]. Available from: https://cdr.lib.unc.edu/record/uuid:b656650d-84e2-48f7-ac8b-4135ba45a063.

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

Council of Science Editors:

Weise Cross L. Regulation of Smooth Muscle Cell Phenotype by the RhoA Effectors mDia1 and mDia2. [Thesis]. University of North Carolina; 2015. Available from: https://cdr.lib.unc.edu/record/uuid:b656650d-84e2-48f7-ac8b-4135ba45a063

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

University of North Carolina

2. Walton, Bethany. The Contribution of Fibrinogen and Red Blood Cells to Arterial Thrombosis.

Degree: Pathology and Laboratory Medicine, 2015, University of North Carolina

URL: https://cdr.lib.unc.edu/record/uuid:e1274003-847a-4104-b897-27df33ada89c

► Cardiovascular disease is the leading cause of death and disability worldwide. This dissertation explores the role of the clotting factor fibrinogen and red blood cells… (more)

▼ Cardiovascular disease is the leading cause of death and disability worldwide. This dissertation explores the role of the clotting factor fibrinogen and red blood cells (RBCs) to arterial thrombosis. Elevated plasma fibrinogen is associated with arterial thrombosis in humans and directly promotes thrombosis in mice, but the contribution of the γA/γ′ fibrinogen isoform to thrombosis is controversial. To determine if γA/γ′ is prothrombotic, we separated γA/γA and γA/γ′ from human plasma and determined the effects on in vitro clot formation and on in vivo thrombus formation. Both γA/γA and γA/γ′ were cleaved by murine and human thrombin and were incorporated into murine and human clots. When γA/γA or γA/γ′ was spiked into plasma, γA/γA increased the fibrin formation rate to a greater extent than γA/γ′. In mice, compared to controls, γA/γA infusion shortened the time to carotid artery occlusion, whereas γA/γ′ infusion did not. Additionally, γA/γ′ infusion led to lower levels of plasma thrombin-antithrombin complexes following arterial injury, whereas γA/γA infusion did not. These data suggest that γA/γ′ binds thrombin in vivo and decreases prothrombotic activity. Together, these findings indicate that elevated levels of γA/γA promote arterial thrombosis in vivo, whereas γA/γ′ does not. RBCs are the most abundant cell type in blood and increased hematocrit is associated with thrombosis. While it is known that RBCs support thrombin generation and increase platelet activation and aggregation, the specific mechanism by which RBCs influence clotting is unclear. In reconstituted human blood ex vivo, RBCs dose-dependently increased thrombin generation in the absence of platelets, although effects were blunted or absent in the presence of platelets. Compared to controls, mice infused with RBCs formed thrombi at a faster rate and had a shortened time to vessel occlusion in a carotid artery injury model. Interestingly, there was no difference in circulating thrombin-antithrombin complexes between RBCHIGH and control mice, and thrombi did not differ in size or fibrin content, suggesting elevated hematocrit promotes arterial thrombosis by a thrombin-independent mechanism. Our data suggest that reducing hematocrit may reduce arterial thrombosis in humans. Future experiments will investigate the RBC effect on platelets to thrombosis. Advisors/Committee Members: Walton, Bethany, Wolberg, Alisa, Coleman, William, Cooley, Brian, Key, Nigel, Parise, Leslie, Wolberg, Alisa.

Subjects/Keywords: Pathology; School of Medicine; Department of Pathology and Laboratory Medicine

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

APA (6^th Edition):

Walton, B. (2015). The Contribution of Fibrinogen and Red Blood Cells to Arterial Thrombosis. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:e1274003-847a-4104-b897-27df33ada89c

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

Chicago Manual of Style (16^th Edition):

Walton, Bethany. “The Contribution of Fibrinogen and Red Blood Cells to Arterial Thrombosis.” 2015. Thesis, University of North Carolina. Accessed January 22, 2021. https://cdr.lib.unc.edu/record/uuid:e1274003-847a-4104-b897-27df33ada89c.

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

MLA Handbook (7^th Edition):

Walton, Bethany. “The Contribution of Fibrinogen and Red Blood Cells to Arterial Thrombosis.” 2015. Web. 22 Jan 2021.

Vancouver:

Walton B. The Contribution of Fibrinogen and Red Blood Cells to Arterial Thrombosis. [Internet] [Thesis]. University of North Carolina; 2015. [cited 2021 Jan 22]. Available from: https://cdr.lib.unc.edu/record/uuid:e1274003-847a-4104-b897-27df33ada89c.

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

Council of Science Editors:

Walton B. The Contribution of Fibrinogen and Red Blood Cells to Arterial Thrombosis. [Thesis]. University of North Carolina; 2015. Available from: https://cdr.lib.unc.edu/record/uuid:e1274003-847a-4104-b897-27df33ada89c

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

University of North Carolina

3. Aleman, Maria M. Cellular and Plasma Protein Crosstalk in Arterial and Venous Thrombosis.

Degree: Pathology and Laboratory Medicine, 2014, University of North Carolina

URL: https://cdr.lib.unc.edu/record/uuid:999c7bac-bb86-4ec6-bc5a-9a73e819870b

► Coagulation is an enzymatic cascade culminating in the formation of a clot. Intravascular coagulation is termed thrombosis. Studies using platelet-rich plasma, whole blood, and animal… (more)

▼ Coagulation is an enzymatic cascade culminating in the formation of a clot. Intravascular coagulation is termed thrombosis. Studies using platelet-rich plasma, whole blood, and animal models reveal the complex crosstalk between clotting factors and the cellular environment that promote thrombosis. Three distinct, yet related, studies included in this dissertation exemplify this crosstalk. First, the vascular bed-dependent prothrombotic effects of elevated prothrombin were examined. We found that elevated prothrombin increased venous, but not arterial, thrombosis in mice. The prothrombotic effects of elevated prothrombin were manifested by increased fibrin deposition but no significant increase in platelet accumulation. These data show that elevated prothrombin would not be expected to contribute to platelet-dominated arterial thrombosis. Second, the procoagulant properties of microparticles from different cell types were investigated. We found that monocyte-derived microparticles contributed to initiation and propagation of clotting via the extrinsic coagulation pathway, while platelet-derived microparticles contributed to primarily to propagation of clotting via the intrinsic coagulation pathway. These data suggest monocyte-derived microparticles may contribute to the initiation of a thrombotic event, while platelet-derived microparticles may propagate an existing thrombotic event. Third, the role of fibrinogen and factor XIII (FXIII) in venous thrombosis was studied. We discovered the binding site of FXIII on fibrinogen, the necessity for FXIII activity for red blood cell retention in clots, and that reduction or deficiency of FXIII activity reduces venous thrombus size. These data indicate a novel role for FXIII in the pathogenesis of thrombosis and implicate FXIII as a novel therapeutic target. Together, these studies emphasize the importance of complementary in vitro and in vivo studies of coagulation and thrombosis to properly elucidate the pathophysiological relevance of clotting factor and cell function. Advisors/Committee Members: Aleman, Maria M., Wolberg, Alisa.

Subjects/Keywords: School of Medicine; Department of Pathology and Laboratory Medicine

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

APA (6^th Edition):

Aleman, M. M. (2014). Cellular and Plasma Protein Crosstalk in Arterial and Venous Thrombosis. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:999c7bac-bb86-4ec6-bc5a-9a73e819870b

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

Chicago Manual of Style (16^th Edition):

Aleman, Maria M. “Cellular and Plasma Protein Crosstalk in Arterial and Venous Thrombosis.” 2014. Thesis, University of North Carolina. Accessed January 22, 2021. https://cdr.lib.unc.edu/record/uuid:999c7bac-bb86-4ec6-bc5a-9a73e819870b.

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

MLA Handbook (7^th Edition):

Aleman, Maria M. “Cellular and Plasma Protein Crosstalk in Arterial and Venous Thrombosis.” 2014. Web. 22 Jan 2021.

Vancouver:

Aleman MM. Cellular and Plasma Protein Crosstalk in Arterial and Venous Thrombosis. [Internet] [Thesis]. University of North Carolina; 2014. [cited 2021 Jan 22]. Available from: https://cdr.lib.unc.edu/record/uuid:999c7bac-bb86-4ec6-bc5a-9a73e819870b.

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

Council of Science Editors:

Aleman MM. Cellular and Plasma Protein Crosstalk in Arterial and Venous Thrombosis. [Thesis]. University of North Carolina; 2014. Available from: https://cdr.lib.unc.edu/record/uuid:999c7bac-bb86-4ec6-bc5a-9a73e819870b

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

University of North Carolina

4. Machlus, Kellie R. Pathophysiology of plasma hypercoagulability in thrombosis.

Degree: Pathology and Laboratory Medicine, 2011, University of North Carolina

URL: https://cdr.lib.unc.edu/record/uuid:467a5300-943d-418b-9bb9-f72db83251c8

► Blood coagulation abnormalities are the leading cause of death world-wide. Elevated procoagulant factor levels (hypercoagulability) have been correlated with increased thrombin generation and increased risk… (more)

▼ Blood coagulation abnormalities are the leading cause of death world-wide. Elevated procoagulant factor levels (hypercoagulability) have been correlated with increased thrombin generation and increased risk of arterial and venous thrombosis. This dissertation explores the role of hypercoagulability on various aspects of coagulation and thrombosis in vitro and in vivo. Thrombin generation tests are increasingly being employed as a high throughput, global measure of procoagulant activity. Thrombin generation was measured using calibrated automated thrombography (CAT) in platelet-free plasma (PFP) and platelet-rich plasma (PRP). The relative sensitivity of CAT parameters to elevated factors XI, IX, VIII, X, and prothrombin was: PFP initiated with 1 pM tissue factor (TF) > PFP initiated with 5 pM TF > PRP initiated with 1 pM TF. Monitoring the peak height following initiation with 1 pM TF in PFP was most likely to detect hypercoagulability (increased procoagulant factors). Epidemiologic studies have correlated elevated plasma fibrinogen (hyperfibrinogenemia) with risk of arterial and venous thrombosis. However, it is unknown whether hyperfibrinogenemia is a biomarker of disease or causative in the etiology. In mice, hyperfibrinogenemia significantly shortened the time to occlusion (TTO) after FeCl3 injury to the saphenous vein and carotid artery. Hyperfibrinogenemia increased thrombus fibrin content, promoted faster fibrin formation, and increased fibrin network density, strength, and stability and increased thrombus thrombolysis resistance in vivo. These data indicate hyperfibrinogenemia directly promotes thrombosis and thrombolysis resistance via enhanced fibrin formation and stability. Studies have correlated elevated plasma factor VIII (FVIII) with thrombosis. However, like hyperfibrinogenemia, it is unclear whether elevated FVIII is a biomarker or causative agent. In mice, elevated FVIII had no effect on 3-minute FeCl3 carotid artery injury, but shortened the TTO after 2-minute injury. Additionally, elevated FVIII increased circulating thrombin-antithrombin complexes and stabilized clots after 2- but not 3-minute FeCl3 injury. In vitro, elevated FVIII increased thrombin generation and accelerated platelet aggregation only when initiated by low TF. These results demonstrate dependence of FVIII thrombogenicity on extent of vascular injury. These findings provide a better understanding of how plasma hypercoagulability impacts thrombogenesis. Specifically, these data suggest causative yet differential roles for hyperfibrinogenemia and elevated FVIII in thrombosis. Advisors/Committee Members: Machlus, Kellie R., Wolberg, Alisa.

Subjects/Keywords: School of Medicine; Department of Pathology and Laboratory Medicine

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

APA (6^th Edition):

Machlus, K. R. (2011). Pathophysiology of plasma hypercoagulability in thrombosis. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:467a5300-943d-418b-9bb9-f72db83251c8

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

Chicago Manual of Style (16^th Edition):

Machlus, Kellie R. “Pathophysiology of plasma hypercoagulability in thrombosis.” 2011. Thesis, University of North Carolina. Accessed January 22, 2021. https://cdr.lib.unc.edu/record/uuid:467a5300-943d-418b-9bb9-f72db83251c8.

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

MLA Handbook (7^th Edition):

Machlus, Kellie R. “Pathophysiology of plasma hypercoagulability in thrombosis.” 2011. Web. 22 Jan 2021.

Vancouver:

Machlus KR. Pathophysiology of plasma hypercoagulability in thrombosis. [Internet] [Thesis]. University of North Carolina; 2011. [cited 2021 Jan 22]. Available from: https://cdr.lib.unc.edu/record/uuid:467a5300-943d-418b-9bb9-f72db83251c8.

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

Council of Science Editors:

Machlus KR. Pathophysiology of plasma hypercoagulability in thrombosis. [Thesis]. University of North Carolina; 2011. Available from: https://cdr.lib.unc.edu/record/uuid:467a5300-943d-418b-9bb9-f72db83251c8

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

University of North Carolina

5. Spero, Richard. Small Particle Transport in Fibrin Gels and High Throughput Clot Characterization.

Degree: Physics and Astronomy, 2010, University of North Carolina

URL: https://cdr.lib.unc.edu/record/uuid:56b1a8f5-914c-49d9-930d-73ede3675796

► The formation, function, and lysis of blood clots is largely governed by the transport of nano- and micro-scale particles. Yet there is not fully established… (more)

Subjects/Keywords: College of Arts and Sciences; Department of Physics and Astronomy

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APA (6^th Edition):

Spero, R. (2010). Small Particle Transport in Fibrin Gels and High Throughput Clot Characterization. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:56b1a8f5-914c-49d9-930d-73ede3675796

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

Chicago Manual of Style (16^th Edition):

Spero, Richard. “Small Particle Transport in Fibrin Gels and High Throughput Clot Characterization.” 2010. Thesis, University of North Carolina. Accessed January 22, 2021. https://cdr.lib.unc.edu/record/uuid:56b1a8f5-914c-49d9-930d-73ede3675796.

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

MLA Handbook (7^th Edition):

Spero, Richard. “Small Particle Transport in Fibrin Gels and High Throughput Clot Characterization.” 2010. Web. 22 Jan 2021.

Vancouver:

Spero R. Small Particle Transport in Fibrin Gels and High Throughput Clot Characterization. [Internet] [Thesis]. University of North Carolina; 2010. [cited 2021 Jan 22]. Available from: https://cdr.lib.unc.edu/record/uuid:56b1a8f5-914c-49d9-930d-73ede3675796.

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

Council of Science Editors:

Spero R. Small Particle Transport in Fibrin Gels and High Throughput Clot Characterization. [Thesis]. University of North Carolina; 2010. Available from: https://cdr.lib.unc.edu/record/uuid:56b1a8f5-914c-49d9-930d-73ede3675796

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

University of North Carolina

6. Campbell, Robert A. The Role of Different Cell Types on Thrombin Generation and Fibrin Clot Formation and Structure.

Degree: Pathology and Laboratory Medicine, 2009, University of North Carolina

URL: https://cdr.lib.unc.edu/record/uuid:8234e04a-57c3-4744-b1c1-1a6d5aa557eb

► Previous studies have demonstrated that fibrin clot quality is dictated by the concentration of thrombin at the time of gelation. These studies were conducted by… (more)

▼ Previous studies have demonstrated that fibrin clot quality is dictated by the concentration of thrombin at the time of gelation. These studies were conducted by adding a single concentration of thrombin to a solution of fibrinogen; however, in vivo, thrombin generation proceeds on a cell surface, where the concentration of thrombin changes during the reaction. Surprisingly, few studies have examined how thrombin generation on a cell surface influences clot formation, structure, and stability. The present work is a study of the cellular properties that influence thrombin generation and the ways in which these properties contribute to clot formation and stability. Patients with hemophilia form clots that have increased fibrinolytic susceptibility due to reduced rates of thrombin generation. With the goal of improving the rate of thrombin generation in these patients, we explored whether the combination of rehydrated, lyophilized (RL) platelets (a cellular component) and recombinant factor VIIa (rFVIIa, a drug used to treat hemophilia) improved thrombin generation and the quality of the fibrin network over rFVIIa alone. Using an in vitro model of coagulation, we determined that RL platelets combined with 10 nM rFVIIa improved thrombin generation and clot stability to levels seen with 50 nM of rFVIIa alone. We further determined that the mechanism responsible for this improvement involved the procoagulant nature of RL platelets, suggesting cellular procoagulant activity can play a significant role in thrombin generation and the quality of the fibrin network. We next focused on the role of vascular cells in thrombin generation and demonstrated that intravascular endothelial cells support low levels of thrombin generation, which results in the formation of a loose network of fibrin. However, extravascular cells (fibroblasts and smooth muscle cells), support significantly higher rates of thrombin generation, which produce tighter fibrin networks. Modulation of the endothelial cell procoagulant phenotype through cytokine stimulation caused thrombin generation and clot quality to shift to that observed for extravascular cells, suggesting a novel link between inflammation and thrombosis. These studies provide a better understanding of the mechanisms through which thrombin generation on a cell surface ultimately affects the quality of the fibrin clot. Our findings will likely enhance our ability to design therapeutics for bleeding and thrombotic disorders. Advisors/Committee Members: Campbell, Robert A., Wolberg, Alisa, University of North Carolina at Chapel Hill.

Subjects/Keywords: School of Medicine; Department of Pathology and Laboratory Medicine

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

APA (6^th Edition):

Campbell, R. A. (2009). The Role of Different Cell Types on Thrombin Generation and Fibrin Clot Formation and Structure. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:8234e04a-57c3-4744-b1c1-1a6d5aa557eb

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

Chicago Manual of Style (16^th Edition):

Campbell, Robert A. “The Role of Different Cell Types on Thrombin Generation and Fibrin Clot Formation and Structure.” 2009. Thesis, University of North Carolina. Accessed January 22, 2021. https://cdr.lib.unc.edu/record/uuid:8234e04a-57c3-4744-b1c1-1a6d5aa557eb.

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

MLA Handbook (7^th Edition):

Campbell, Robert A. “The Role of Different Cell Types on Thrombin Generation and Fibrin Clot Formation and Structure.” 2009. Web. 22 Jan 2021.

Vancouver:

Campbell RA. The Role of Different Cell Types on Thrombin Generation and Fibrin Clot Formation and Structure. [Internet] [Thesis]. University of North Carolina; 2009. [cited 2021 Jan 22]. Available from: https://cdr.lib.unc.edu/record/uuid:8234e04a-57c3-4744-b1c1-1a6d5aa557eb.

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

Council of Science Editors:

Campbell RA. The Role of Different Cell Types on Thrombin Generation and Fibrin Clot Formation and Structure. [Thesis]. University of North Carolina; 2009. Available from: https://cdr.lib.unc.edu/record/uuid:8234e04a-57c3-4744-b1c1-1a6d5aa557eb

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

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