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You searched for subject:(Department of Pathology AND Laboratory Medicine). Showing records 1 – 30 of 122 total matches.

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University of North Carolina

1. Monk, Justine. Inflammatory Responses Induced by Cigarette Smoke in Healthy Mice and in Mice with Chronic Bronchitis.

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

 Mice overexpressing the beta-epithelial sodium channel (betaENaC) in pulmonary epithelial cells have hyperconcentrated airway mucus and develop chronic bronchitis. These mice may serve as a… (more)

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

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APA (6th Edition):

Monk, J. (2015). Inflammatory Responses Induced by Cigarette Smoke in Healthy Mice and in Mice with Chronic Bronchitis. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:6ca57af1-2cad-4d8b-9423-3564355459cf

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):

Monk, Justine. “Inflammatory Responses Induced by Cigarette Smoke in Healthy Mice and in Mice with Chronic Bronchitis.” 2015. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:6ca57af1-2cad-4d8b-9423-3564355459cf.

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

MLA Handbook (7th Edition):

Monk, Justine. “Inflammatory Responses Induced by Cigarette Smoke in Healthy Mice and in Mice with Chronic Bronchitis.” 2015. Web. 22 Sep 2020.

Vancouver:

Monk J. Inflammatory Responses Induced by Cigarette Smoke in Healthy Mice and in Mice with Chronic Bronchitis. [Internet] [Thesis]. University of North Carolina; 2015. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:6ca57af1-2cad-4d8b-9423-3564355459cf.

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

Council of Science Editors:

Monk J. Inflammatory Responses Induced by Cigarette Smoke in Healthy Mice and in Mice with Chronic Bronchitis. [Thesis]. University of North Carolina; 2015. Available from: https://cdr.lib.unc.edu/record/uuid:6ca57af1-2cad-4d8b-9423-3564355459cf

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

 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)

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

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APA (6th 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 (16th Edition):

Walton, Bethany. “The Contribution of Fibrinogen and Red Blood Cells to Arterial Thrombosis.” 2015. Thesis, University of North Carolina. Accessed September 22, 2020. 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 (7th Edition):

Walton, Bethany. “The Contribution of Fibrinogen and Red Blood Cells to Arterial Thrombosis.” 2015. Web. 22 Sep 2020.

Vancouver:

Walton B. The Contribution of Fibrinogen and Red Blood Cells to Arterial Thrombosis. [Internet] [Thesis]. University of North Carolina; 2015. [cited 2020 Sep 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. Merricks, Elizabeth Parker. Cardiovascular Disease, Endothelial Cell Gene Expression, and Renal Dysfunction in Insulin Resistant, Hyperlipidemic Swine.

Degree: Pathology and Laboratory Medicine, 2010, University of North Carolina

 Globally, the prevalence of insulin resistant (IR), type-2 diabetes mellitus (DM) is increasing. Both IR and DM are associated with an increase in cardiovascular events… (more)

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

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APA (6th Edition):

Merricks, E. P. (2010). Cardiovascular Disease, Endothelial Cell Gene Expression, and Renal Dysfunction in Insulin Resistant, Hyperlipidemic Swine. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:c1cda3b8-eb6b-47fa-b626-f80e32a5a03f

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):

Merricks, Elizabeth Parker. “Cardiovascular Disease, Endothelial Cell Gene Expression, and Renal Dysfunction in Insulin Resistant, Hyperlipidemic Swine.” 2010. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:c1cda3b8-eb6b-47fa-b626-f80e32a5a03f.

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

MLA Handbook (7th Edition):

Merricks, Elizabeth Parker. “Cardiovascular Disease, Endothelial Cell Gene Expression, and Renal Dysfunction in Insulin Resistant, Hyperlipidemic Swine.” 2010. Web. 22 Sep 2020.

Vancouver:

Merricks EP. Cardiovascular Disease, Endothelial Cell Gene Expression, and Renal Dysfunction in Insulin Resistant, Hyperlipidemic Swine. [Internet] [Thesis]. University of North Carolina; 2010. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:c1cda3b8-eb6b-47fa-b626-f80e32a5a03f.

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

Council of Science Editors:

Merricks EP. Cardiovascular Disease, Endothelial Cell Gene Expression, and Renal Dysfunction in Insulin Resistant, Hyperlipidemic Swine. [Thesis]. University of North Carolina; 2010. Available from: https://cdr.lib.unc.edu/record/uuid:c1cda3b8-eb6b-47fa-b626-f80e32a5a03f

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


University of North Carolina

4. Medlin, Matthew Douglas. Sphingosine-1-phosphate and the RGS RhoGEFs regulate vascular smooth muscle phenotype.

Degree: Pathology and Laboratory Medicine, 2010, University of North Carolina

 The regulation of smooth muscle cell (SMC) differentiation is critical during vascular development, and perturbations in this process contribute to a number of cardiovascular pathologies… (more)

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

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APA (6th Edition):

Medlin, M. D. (2010). Sphingosine-1-phosphate and the RGS RhoGEFs regulate vascular smooth muscle phenotype. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:2d9e6b49-a8a7-4337-a948-9e4b380d322e

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):

Medlin, Matthew Douglas. “Sphingosine-1-phosphate and the RGS RhoGEFs regulate vascular smooth muscle phenotype.” 2010. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:2d9e6b49-a8a7-4337-a948-9e4b380d322e.

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

MLA Handbook (7th Edition):

Medlin, Matthew Douglas. “Sphingosine-1-phosphate and the RGS RhoGEFs regulate vascular smooth muscle phenotype.” 2010. Web. 22 Sep 2020.

Vancouver:

Medlin MD. Sphingosine-1-phosphate and the RGS RhoGEFs regulate vascular smooth muscle phenotype. [Internet] [Thesis]. University of North Carolina; 2010. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:2d9e6b49-a8a7-4337-a948-9e4b380d322e.

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

Council of Science Editors:

Medlin MD. Sphingosine-1-phosphate and the RGS RhoGEFs regulate vascular smooth muscle phenotype. [Thesis]. University of North Carolina; 2010. Available from: https://cdr.lib.unc.edu/record/uuid:2d9e6b49-a8a7-4337-a948-9e4b380d322e

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


University of North Carolina

5. Gramling, Mark W. Serine proteases and serine protease inhibitors in breast cancer cell pathophysiology.

Degree: Pathology and Laboratory Medicine, 2010, University of North Carolina

 Hemostasis and fibrinolysis are mediated by serine proteases and regulated by serine protease inhibitors, or serpins. There is a growing body of evidence that a… (more)

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

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APA (6th Edition):

Gramling, M. W. (2010). Serine proteases and serine protease inhibitors in breast cancer cell pathophysiology. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:5f59fb2d-eb97-4230-8721-1a7a461d2d02

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):

Gramling, Mark W. “Serine proteases and serine protease inhibitors in breast cancer cell pathophysiology.” 2010. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:5f59fb2d-eb97-4230-8721-1a7a461d2d02.

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

MLA Handbook (7th Edition):

Gramling, Mark W. “Serine proteases and serine protease inhibitors in breast cancer cell pathophysiology.” 2010. Web. 22 Sep 2020.

Vancouver:

Gramling MW. Serine proteases and serine protease inhibitors in breast cancer cell pathophysiology. [Internet] [Thesis]. University of North Carolina; 2010. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:5f59fb2d-eb97-4230-8721-1a7a461d2d02.

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

Council of Science Editors:

Gramling MW. Serine proteases and serine protease inhibitors in breast cancer cell pathophysiology. [Thesis]. University of North Carolina; 2010. Available from: https://cdr.lib.unc.edu/record/uuid:5f59fb2d-eb97-4230-8721-1a7a461d2d02

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


University of North Carolina

6. Johnson, Lance A. Apolipoprotein E in Diabetic Dyslipidemia and Atherosclerosis.

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

 Each year, cardiovascular disease (CVD) kills more Americans than any other cause of death. The majority of the diseases contributing to CVD can be traced… (more)

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

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APA (6th Edition):

Johnson, L. A. (2011). Apolipoprotein E in Diabetic Dyslipidemia and Atherosclerosis. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:eb1e9951-a82b-46e2-8eca-6ab4e95d2f83

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):

Johnson, Lance A. “Apolipoprotein E in Diabetic Dyslipidemia and Atherosclerosis.” 2011. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:eb1e9951-a82b-46e2-8eca-6ab4e95d2f83.

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

MLA Handbook (7th Edition):

Johnson, Lance A. “Apolipoprotein E in Diabetic Dyslipidemia and Atherosclerosis.” 2011. Web. 22 Sep 2020.

Vancouver:

Johnson LA. Apolipoprotein E in Diabetic Dyslipidemia and Atherosclerosis. [Internet] [Thesis]. University of North Carolina; 2011. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:eb1e9951-a82b-46e2-8eca-6ab4e95d2f83.

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

Council of Science Editors:

Johnson LA. Apolipoprotein E in Diabetic Dyslipidemia and Atherosclerosis. [Thesis]. University of North Carolina; 2011. Available from: https://cdr.lib.unc.edu/record/uuid:eb1e9951-a82b-46e2-8eca-6ab4e95d2f83

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


University of North Carolina

7. Sandhu, Rupninder. Hypermethylator phenotype in human breast cancer: therapeutic target and mechanism of DNMT3b regulation.

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

 A subset of primary breast cancers and breast cancer cell lines express a hypermethylation defect characterized by DNMT hyperactivity and DNMT3b overexpression. The objectives of… (more)

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

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APA (6th Edition):

Sandhu, R. (2011). Hypermethylator phenotype in human breast cancer: therapeutic target and mechanism of DNMT3b regulation. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:30379454-98cb-445a-b6e6-7c01eaf7f971

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):

Sandhu, Rupninder. “Hypermethylator phenotype in human breast cancer: therapeutic target and mechanism of DNMT3b regulation.” 2011. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:30379454-98cb-445a-b6e6-7c01eaf7f971.

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

MLA Handbook (7th Edition):

Sandhu, Rupninder. “Hypermethylator phenotype in human breast cancer: therapeutic target and mechanism of DNMT3b regulation.” 2011. Web. 22 Sep 2020.

Vancouver:

Sandhu R. Hypermethylator phenotype in human breast cancer: therapeutic target and mechanism of DNMT3b regulation. [Internet] [Thesis]. University of North Carolina; 2011. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:30379454-98cb-445a-b6e6-7c01eaf7f971.

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

Council of Science Editors:

Sandhu R. Hypermethylator phenotype in human breast cancer: therapeutic target and mechanism of DNMT3b regulation. [Thesis]. University of North Carolina; 2011. Available from: https://cdr.lib.unc.edu/record/uuid:30379454-98cb-445a-b6e6-7c01eaf7f971

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


University of North Carolina

8. Doherty, Jason Thomas. Focal adhesion kinase and ARHGAP26 in cardiac and skeletal muscle development.

Degree: Pathology and Laboratory Medicine, 2010, University of North Carolina

 Cardiac and skeletal muscle are highly specialized tissue types and the normal development of these striated muscles during embryogenesis requires very tightly regulated processes such… (more)

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

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APA (6th Edition):

Doherty, J. T. (2010). Focal adhesion kinase and ARHGAP26 in cardiac and skeletal muscle development. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:191f2943-033e-42ff-9982-c89a9c93a6f9

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):

Doherty, Jason Thomas. “Focal adhesion kinase and ARHGAP26 in cardiac and skeletal muscle development.” 2010. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:191f2943-033e-42ff-9982-c89a9c93a6f9.

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

MLA Handbook (7th Edition):

Doherty, Jason Thomas. “Focal adhesion kinase and ARHGAP26 in cardiac and skeletal muscle development.” 2010. Web. 22 Sep 2020.

Vancouver:

Doherty JT. Focal adhesion kinase and ARHGAP26 in cardiac and skeletal muscle development. [Internet] [Thesis]. University of North Carolina; 2010. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:191f2943-033e-42ff-9982-c89a9c93a6f9.

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

Council of Science Editors:

Doherty JT. Focal adhesion kinase and ARHGAP26 in cardiac and skeletal muscle development. [Thesis]. University of North Carolina; 2010. Available from: https://cdr.lib.unc.edu/record/uuid:191f2943-033e-42ff-9982-c89a9c93a6f9

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


University of North Carolina

9. Karaca, Mehmet. Regulation of androgen receptor function by tyrosine phosphorylation.

Degree: Pathology and Laboratory Medicine, 2010, University of North Carolina

 Androgen receptor (AR) re-activation under low androgen environment is the hallmark of castration resistant or hormone refractory prostate cancer (HRPC). Non-receptor tyrosine kinases phosphorylate AR… (more)

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

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APA (6th Edition):

Karaca, M. (2010). Regulation of androgen receptor function by tyrosine phosphorylation. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:d0608295-ede7-41ce-a969-af31f3af12ea

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):

Karaca, Mehmet. “Regulation of androgen receptor function by tyrosine phosphorylation.” 2010. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:d0608295-ede7-41ce-a969-af31f3af12ea.

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

MLA Handbook (7th Edition):

Karaca, Mehmet. “Regulation of androgen receptor function by tyrosine phosphorylation.” 2010. Web. 22 Sep 2020.

Vancouver:

Karaca M. Regulation of androgen receptor function by tyrosine phosphorylation. [Internet] [Thesis]. University of North Carolina; 2010. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:d0608295-ede7-41ce-a969-af31f3af12ea.

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

Council of Science Editors:

Karaca M. Regulation of androgen receptor function by tyrosine phosphorylation. [Thesis]. University of North Carolina; 2010. Available from: https://cdr.lib.unc.edu/record/uuid:d0608295-ede7-41ce-a969-af31f3af12ea

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


University of North Carolina

10. McEachron, Troy Anthony. Regulation of urokinase plasminogen activator and plasminogen activator inhibitor-1 in murine breast cancer cells.

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

 Proteases are indispensable for tumor growth, angiogenesis, and metastasis. These proteases are produced by tumor cells, stromal cells, and by the host coagulation cascade. Protease-activated… (more)

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

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APA (6th Edition):

McEachron, T. A. (2011). Regulation of urokinase plasminogen activator and plasminogen activator inhibitor-1 in murine breast cancer cells. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:fa79f55d-2f3c-432c-aea1-cd55446f04c9

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):

McEachron, Troy Anthony. “Regulation of urokinase plasminogen activator and plasminogen activator inhibitor-1 in murine breast cancer cells.” 2011. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:fa79f55d-2f3c-432c-aea1-cd55446f04c9.

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

MLA Handbook (7th Edition):

McEachron, Troy Anthony. “Regulation of urokinase plasminogen activator and plasminogen activator inhibitor-1 in murine breast cancer cells.” 2011. Web. 22 Sep 2020.

Vancouver:

McEachron TA. Regulation of urokinase plasminogen activator and plasminogen activator inhibitor-1 in murine breast cancer cells. [Internet] [Thesis]. University of North Carolina; 2011. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:fa79f55d-2f3c-432c-aea1-cd55446f04c9.

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

Council of Science Editors:

McEachron TA. Regulation of urokinase plasminogen activator and plasminogen activator inhibitor-1 in murine breast cancer cells. [Thesis]. University of North Carolina; 2011. Available from: https://cdr.lib.unc.edu/record/uuid:fa79f55d-2f3c-432c-aea1-cd55446f04c9

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


University of North Carolina

11. Samuelson, Lisa L. Sca-1 positive pancreatic progenitor cells: a replacement for transplanted islets.

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

 A major challenge in the treatment of Type I diabetes is the lack of a restorative therapy to replace lost islet mass. Islet or pancreas… (more)

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

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APA (6th Edition):

Samuelson, L. L. (2011). Sca-1 positive pancreatic progenitor cells: a replacement for transplanted islets. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:da5244e4-4a97-44c9-8fc9-0498e221507a

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):

Samuelson, Lisa L. “Sca-1 positive pancreatic progenitor cells: a replacement for transplanted islets.” 2011. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:da5244e4-4a97-44c9-8fc9-0498e221507a.

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

MLA Handbook (7th Edition):

Samuelson, Lisa L. “Sca-1 positive pancreatic progenitor cells: a replacement for transplanted islets.” 2011. Web. 22 Sep 2020.

Vancouver:

Samuelson LL. Sca-1 positive pancreatic progenitor cells: a replacement for transplanted islets. [Internet] [Thesis]. University of North Carolina; 2011. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:da5244e4-4a97-44c9-8fc9-0498e221507a.

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

Council of Science Editors:

Samuelson LL. Sca-1 positive pancreatic progenitor cells: a replacement for transplanted islets. [Thesis]. University of North Carolina; 2011. Available from: https://cdr.lib.unc.edu/record/uuid:da5244e4-4a97-44c9-8fc9-0498e221507a

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


University of North Carolina

12. Goldsmith, Rachel B. Detection and Mechanistic Comparison of Two Anti-Trypanosomal Diamidines in a Rat Renal Model.

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

 There is an urgent need for new treatments for human African trypanosomiasis (HAT), a neglected parasitic disease indigenous to sub-Saharan Africa. HAT progresses in two… (more)

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

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APA (6th Edition):

Goldsmith, R. B. (2011). Detection and Mechanistic Comparison of Two Anti-Trypanosomal Diamidines in a Rat Renal Model. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:c81d7310-8784-4019-adbc-0e8c7fc7021b

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):

Goldsmith, Rachel B. “Detection and Mechanistic Comparison of Two Anti-Trypanosomal Diamidines in a Rat Renal Model.” 2011. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:c81d7310-8784-4019-adbc-0e8c7fc7021b.

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

MLA Handbook (7th Edition):

Goldsmith, Rachel B. “Detection and Mechanistic Comparison of Two Anti-Trypanosomal Diamidines in a Rat Renal Model.” 2011. Web. 22 Sep 2020.

Vancouver:

Goldsmith RB. Detection and Mechanistic Comparison of Two Anti-Trypanosomal Diamidines in a Rat Renal Model. [Internet] [Thesis]. University of North Carolina; 2011. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:c81d7310-8784-4019-adbc-0e8c7fc7021b.

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

Council of Science Editors:

Goldsmith RB. Detection and Mechanistic Comparison of Two Anti-Trypanosomal Diamidines in a Rat Renal Model. [Thesis]. University of North Carolina; 2011. Available from: https://cdr.lib.unc.edu/record/uuid:c81d7310-8784-4019-adbc-0e8c7fc7021b

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


University of North Carolina

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

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

 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)

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

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APA (6th 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 (16th Edition):

Machlus, Kellie R. “Pathophysiology of plasma hypercoagulability in thrombosis.” 2011. Thesis, University of North Carolina. Accessed September 22, 2020. 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 (7th Edition):

Machlus, Kellie R. “Pathophysiology of plasma hypercoagulability in thrombosis.” 2011. Web. 22 Sep 2020.

Vancouver:

Machlus KR. Pathophysiology of plasma hypercoagulability in thrombosis. [Internet] [Thesis]. University of North Carolina; 2011. [cited 2020 Sep 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

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

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

 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)

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

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APA (6th 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 (16th Edition):

Aleman, Maria M. “Cellular and Plasma Protein Crosstalk in Arterial and Venous Thrombosis.” 2014. Thesis, University of North Carolina. Accessed September 22, 2020. 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 (7th Edition):

Aleman, Maria M. “Cellular and Plasma Protein Crosstalk in Arterial and Venous Thrombosis.” 2014. Web. 22 Sep 2020.

Vancouver:

Aleman MM. Cellular and Plasma Protein Crosstalk in Arterial and Venous Thrombosis. [Internet] [Thesis]. University of North Carolina; 2014. [cited 2020 Sep 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

15. Lenhart, Kaitlin Christine. The Rho-GAP GRAF1 Regulates Skeletal Muscle Maturation and Repair.

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

 Skeletal muscle is a large and highly specialized tissue requiring tightly regulated processes during development and maintenance to prevent the manifestation of debilitating myopathies. The… (more)

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

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APA (6th Edition):

Lenhart, K. C. (2014). The Rho-GAP GRAF1 Regulates Skeletal Muscle Maturation and Repair. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:3fe923ca-2417-4fe3-ab7f-ef1d0539f23d

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):

Lenhart, Kaitlin Christine. “The Rho-GAP GRAF1 Regulates Skeletal Muscle Maturation and Repair.” 2014. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:3fe923ca-2417-4fe3-ab7f-ef1d0539f23d.

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

MLA Handbook (7th Edition):

Lenhart, Kaitlin Christine. “The Rho-GAP GRAF1 Regulates Skeletal Muscle Maturation and Repair.” 2014. Web. 22 Sep 2020.

Vancouver:

Lenhart KC. The Rho-GAP GRAF1 Regulates Skeletal Muscle Maturation and Repair. [Internet] [Thesis]. University of North Carolina; 2014. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:3fe923ca-2417-4fe3-ab7f-ef1d0539f23d.

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

Council of Science Editors:

Lenhart KC. The Rho-GAP GRAF1 Regulates Skeletal Muscle Maturation and Repair. [Thesis]. University of North Carolina; 2014. Available from: https://cdr.lib.unc.edu/record/uuid:3fe923ca-2417-4fe3-ab7f-ef1d0539f23d

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


University of North Carolina

16. Pfefferle, Adam. Genetically engineered mouse models of breast carcinoma: a translational resource for highlighting human breast subtype etiology and developing personalized therapeutic approaches.

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

 Approximately one in eight women will be diagnosed with breast cancer during their lifetime. While increased public awareness has led to earlier detection of this… (more)

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

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APA (6th Edition):

Pfefferle, A. (2015). Genetically engineered mouse models of breast carcinoma: a translational resource for highlighting human breast subtype etiology and developing personalized therapeutic approaches. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:a46f7d8c-90c5-4647-9142-6abde9f544b1

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):

Pfefferle, Adam. “Genetically engineered mouse models of breast carcinoma: a translational resource for highlighting human breast subtype etiology and developing personalized therapeutic approaches.” 2015. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:a46f7d8c-90c5-4647-9142-6abde9f544b1.

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

MLA Handbook (7th Edition):

Pfefferle, Adam. “Genetically engineered mouse models of breast carcinoma: a translational resource for highlighting human breast subtype etiology and developing personalized therapeutic approaches.” 2015. Web. 22 Sep 2020.

Vancouver:

Pfefferle A. Genetically engineered mouse models of breast carcinoma: a translational resource for highlighting human breast subtype etiology and developing personalized therapeutic approaches. [Internet] [Thesis]. University of North Carolina; 2015. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:a46f7d8c-90c5-4647-9142-6abde9f544b1.

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

Council of Science Editors:

Pfefferle A. Genetically engineered mouse models of breast carcinoma: a translational resource for highlighting human breast subtype etiology and developing personalized therapeutic approaches. [Thesis]. University of North Carolina; 2015. Available from: https://cdr.lib.unc.edu/record/uuid:a46f7d8c-90c5-4647-9142-6abde9f544b1

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


University of North Carolina

17. Jones, Britta. DNA Methylation Patterns as a Biomarker of Disease Relapse and Remission in Patients with ANCA-Associated Vasculitis.

Degree: Pathology and Laboratory Medicine, 2016, University of North Carolina

 This dissertation is focused on the role of DNA methylation in anti-neutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis (AAV), an autoimmune condition characterized by vascular inflammation and… (more)

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

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APA (6th Edition):

Jones, B. (2016). DNA Methylation Patterns as a Biomarker of Disease Relapse and Remission in Patients with ANCA-Associated Vasculitis. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:1dbd20cb-3f1f-47a3-bc13-89ab6b26cb64

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):

Jones, Britta. “DNA Methylation Patterns as a Biomarker of Disease Relapse and Remission in Patients with ANCA-Associated Vasculitis.” 2016. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:1dbd20cb-3f1f-47a3-bc13-89ab6b26cb64.

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

MLA Handbook (7th Edition):

Jones, Britta. “DNA Methylation Patterns as a Biomarker of Disease Relapse and Remission in Patients with ANCA-Associated Vasculitis.” 2016. Web. 22 Sep 2020.

Vancouver:

Jones B. DNA Methylation Patterns as a Biomarker of Disease Relapse and Remission in Patients with ANCA-Associated Vasculitis. [Internet] [Thesis]. University of North Carolina; 2016. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:1dbd20cb-3f1f-47a3-bc13-89ab6b26cb64.

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

Council of Science Editors:

Jones B. DNA Methylation Patterns as a Biomarker of Disease Relapse and Remission in Patients with ANCA-Associated Vasculitis. [Thesis]. University of North Carolina; 2016. Available from: https://cdr.lib.unc.edu/record/uuid:1dbd20cb-3f1f-47a3-bc13-89ab6b26cb64

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


University of North Carolina

18. Rinkenbaugh, Amanda. Roles of the NF-kappaB Pathway in Glioblastoma Stem Cells and Chordoma.

Degree: Pathology and Laboratory Medicine, 2016, University of North Carolina

 The NF-κB pathway consists of a family of five transcription factors: RelA/p65, RelB, c-Rel, p100/p52, and p105/p50. Originally discovered for its involvement in inflammation and… (more)

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

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APA (6th Edition):

Rinkenbaugh, A. (2016). Roles of the NF-kappaB Pathway in Glioblastoma Stem Cells and Chordoma. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:4046c94e-b8aa-4bba-93e0-ac8d1490b55d

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):

Rinkenbaugh, Amanda. “Roles of the NF-kappaB Pathway in Glioblastoma Stem Cells and Chordoma.” 2016. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:4046c94e-b8aa-4bba-93e0-ac8d1490b55d.

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

MLA Handbook (7th Edition):

Rinkenbaugh, Amanda. “Roles of the NF-kappaB Pathway in Glioblastoma Stem Cells and Chordoma.” 2016. Web. 22 Sep 2020.

Vancouver:

Rinkenbaugh A. Roles of the NF-kappaB Pathway in Glioblastoma Stem Cells and Chordoma. [Internet] [Thesis]. University of North Carolina; 2016. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:4046c94e-b8aa-4bba-93e0-ac8d1490b55d.

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

Council of Science Editors:

Rinkenbaugh A. Roles of the NF-kappaB Pathway in Glioblastoma Stem Cells and Chordoma. [Thesis]. University of North Carolina; 2016. Available from: https://cdr.lib.unc.edu/record/uuid:4046c94e-b8aa-4bba-93e0-ac8d1490b55d

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


University of North Carolina

19. Mangum, Kevin. Genetic and Epigenetic Mechanisms Regulating Smooth Muscle Cell Differentiation.

Degree: Pathology and Laboratory Medicine, 2017, University of North Carolina

 Smooth muscle differentiation is a complex process, involving numerous molecular, genetic, and epigenetic mechanisms. Notably, smooth muscle cells (SMCs) retain marked plasticity in their ability… (more)

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

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APA (6th Edition):

Mangum, K. (2017). Genetic and Epigenetic Mechanisms Regulating Smooth Muscle Cell Differentiation. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:3e390865-999e-44be-b0f8-91bcda14f410

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):

Mangum, Kevin. “Genetic and Epigenetic Mechanisms Regulating Smooth Muscle Cell Differentiation.” 2017. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:3e390865-999e-44be-b0f8-91bcda14f410.

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

MLA Handbook (7th Edition):

Mangum, Kevin. “Genetic and Epigenetic Mechanisms Regulating Smooth Muscle Cell Differentiation.” 2017. Web. 22 Sep 2020.

Vancouver:

Mangum K. Genetic and Epigenetic Mechanisms Regulating Smooth Muscle Cell Differentiation. [Internet] [Thesis]. University of North Carolina; 2017. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:3e390865-999e-44be-b0f8-91bcda14f410.

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

Council of Science Editors:

Mangum K. Genetic and Epigenetic Mechanisms Regulating Smooth Muscle Cell Differentiation. [Thesis]. University of North Carolina; 2017. Available from: https://cdr.lib.unc.edu/record/uuid:3e390865-999e-44be-b0f8-91bcda14f410

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


University of North Carolina

20. Lockyer, Pamela. Bone Morphogenetic Protein Binding Endothelial Regulator (BMPER) Regulates Vascular Inflammatory Responses in Endothelial Cells.

Degree: Pathology and Laboratory Medicine, 2017, University of North Carolina

 ABSTRACT Pamela P. Lockyer: Bone Morphogenetic Protein Binding Endothelial Regulator (BMPER) Regulates Vascular Inflammatory Responses in Endothelial Cells (Under the direction of Xinchun Pi) Dysfunction… (more)

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

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APA (6th Edition):

Lockyer, P. (2017). Bone Morphogenetic Protein Binding Endothelial Regulator (BMPER) Regulates Vascular Inflammatory Responses in Endothelial Cells. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:a3fcbc9c-116b-4279-8026-f03a8372ddfd

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):

Lockyer, Pamela. “Bone Morphogenetic Protein Binding Endothelial Regulator (BMPER) Regulates Vascular Inflammatory Responses in Endothelial Cells.” 2017. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:a3fcbc9c-116b-4279-8026-f03a8372ddfd.

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

MLA Handbook (7th Edition):

Lockyer, Pamela. “Bone Morphogenetic Protein Binding Endothelial Regulator (BMPER) Regulates Vascular Inflammatory Responses in Endothelial Cells.” 2017. Web. 22 Sep 2020.

Vancouver:

Lockyer P. Bone Morphogenetic Protein Binding Endothelial Regulator (BMPER) Regulates Vascular Inflammatory Responses in Endothelial Cells. [Internet] [Thesis]. University of North Carolina; 2017. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:a3fcbc9c-116b-4279-8026-f03a8372ddfd.

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

Council of Science Editors:

Lockyer P. Bone Morphogenetic Protein Binding Endothelial Regulator (BMPER) Regulates Vascular Inflammatory Responses in Endothelial Cells. [Thesis]. University of North Carolina; 2017. Available from: https://cdr.lib.unc.edu/record/uuid:a3fcbc9c-116b-4279-8026-f03a8372ddfd

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


University of North Carolina

21. Cardenas, Jessica Caroline. The Role of p16INK4a Expression in the Age-related Risk of Venous Thromboembolism.

Degree: Pathology and Laboratory Medicine, 2012, University of North Carolina

 Venous thromboembolism (VTE) is a pathophysiologically complex disease involving dysregulation of pro and anticoagulant processes in the vasculature. Aging is the strongest risk factor for… (more)

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

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APA (6th Edition):

Cardenas, J. C. (2012). The Role of p16INK4a Expression in the Age-related Risk of Venous Thromboembolism. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:8515c744-d71e-42af-a5e2-257a7fae9485

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):

Cardenas, Jessica Caroline. “The Role of p16INK4a Expression in the Age-related Risk of Venous Thromboembolism.” 2012. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:8515c744-d71e-42af-a5e2-257a7fae9485.

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

MLA Handbook (7th Edition):

Cardenas, Jessica Caroline. “The Role of p16INK4a Expression in the Age-related Risk of Venous Thromboembolism.” 2012. Web. 22 Sep 2020.

Vancouver:

Cardenas JC. The Role of p16INK4a Expression in the Age-related Risk of Venous Thromboembolism. [Internet] [Thesis]. University of North Carolina; 2012. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:8515c744-d71e-42af-a5e2-257a7fae9485.

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

Council of Science Editors:

Cardenas JC. The Role of p16INK4a Expression in the Age-related Risk of Venous Thromboembolism. [Thesis]. University of North Carolina; 2012. Available from: https://cdr.lib.unc.edu/record/uuid:8515c744-d71e-42af-a5e2-257a7fae9485

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


University of North Carolina

22. Durando, Michael Luca. Novel Mechanisms through which translesion synthesis protects genome integrity.

Degree: Pathology and Laboratory Medicine, 2013, University of North Carolina

 Exposure to ubiquitous environmental carcinogens, such as polycyclic aromatic hydrocarbons and UV light, is a major cause of human disease. It is well accepted that… (more)

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

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APA (6th Edition):

Durando, M. L. (2013). Novel Mechanisms through which translesion synthesis protects genome integrity. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:854d9fe8-4dd9-495e-a39e-c7ac048299bf

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):

Durando, Michael Luca. “Novel Mechanisms through which translesion synthesis protects genome integrity.” 2013. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:854d9fe8-4dd9-495e-a39e-c7ac048299bf.

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

MLA Handbook (7th Edition):

Durando, Michael Luca. “Novel Mechanisms through which translesion synthesis protects genome integrity.” 2013. Web. 22 Sep 2020.

Vancouver:

Durando ML. Novel Mechanisms through which translesion synthesis protects genome integrity. [Internet] [Thesis]. University of North Carolina; 2013. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:854d9fe8-4dd9-495e-a39e-c7ac048299bf.

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

Council of Science Editors:

Durando ML. Novel Mechanisms through which translesion synthesis protects genome integrity. [Thesis]. University of North Carolina; 2013. Available from: https://cdr.lib.unc.edu/record/uuid:854d9fe8-4dd9-495e-a39e-c7ac048299bf

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


University of North Carolina

23. De Silva, Dinuka. Role of androgen receptor co-repressor SLIRP in cell cycle regulation.

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

 Androgen receptor (AR) reactivation is a hallmark of castration resistant prostate cancer (CRPC). One mechanism is tyrosine kinase Ack1 mediated activation phosphorylation of Tyr-267 and… (more)

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

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APA (6th Edition):

De Silva, D. (2014). Role of androgen receptor co-repressor SLIRP in cell cycle regulation. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:9598b80e-a902-40ef-bf46-0b974f8d120d

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):

De Silva, Dinuka. “Role of androgen receptor co-repressor SLIRP in cell cycle regulation.” 2014. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:9598b80e-a902-40ef-bf46-0b974f8d120d.

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

MLA Handbook (7th Edition):

De Silva, Dinuka. “Role of androgen receptor co-repressor SLIRP in cell cycle regulation.” 2014. Web. 22 Sep 2020.

Vancouver:

De Silva D. Role of androgen receptor co-repressor SLIRP in cell cycle regulation. [Internet] [Thesis]. University of North Carolina; 2014. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:9598b80e-a902-40ef-bf46-0b974f8d120d.

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

Council of Science Editors:

De Silva D. Role of androgen receptor co-repressor SLIRP in cell cycle regulation. [Thesis]. University of North Carolina; 2014. Available from: https://cdr.lib.unc.edu/record/uuid:9598b80e-a902-40ef-bf46-0b974f8d120d

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


University of North Carolina

24. Free, Meghan Elizabeth. Role of circulating T cells in autoimmune kidney disease: implications for ANCA disease and minimal change disease.

Degree: Pathology and Laboratory Medicine, 2013, University of North Carolina

 This dissertation is focused on circulating T cells and the role they play in the immunopathogenesis of two autoimmune kidney diseases: anti-neutrophil cytoplasmic autoantibody (ANCA)… (more)

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

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APA (6th Edition):

Free, M. E. (2013). Role of circulating T cells in autoimmune kidney disease: implications for ANCA disease and minimal change disease. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:7f7fbfb8-3e7b-4820-b4d8-dd22bb143a15

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):

Free, Meghan Elizabeth. “Role of circulating T cells in autoimmune kidney disease: implications for ANCA disease and minimal change disease.” 2013. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:7f7fbfb8-3e7b-4820-b4d8-dd22bb143a15.

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

MLA Handbook (7th Edition):

Free, Meghan Elizabeth. “Role of circulating T cells in autoimmune kidney disease: implications for ANCA disease and minimal change disease.” 2013. Web. 22 Sep 2020.

Vancouver:

Free ME. Role of circulating T cells in autoimmune kidney disease: implications for ANCA disease and minimal change disease. [Internet] [Thesis]. University of North Carolina; 2013. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:7f7fbfb8-3e7b-4820-b4d8-dd22bb143a15.

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

Council of Science Editors:

Free ME. Role of circulating T cells in autoimmune kidney disease: implications for ANCA disease and minimal change disease. [Thesis]. University of North Carolina; 2013. Available from: https://cdr.lib.unc.edu/record/uuid:7f7fbfb8-3e7b-4820-b4d8-dd22bb143a15

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


University of North Carolina

25. Casbas-Hernandez, Patricia. In vitro coculture models to study heterotypic interactions in breast cancer microenvironments.

Degree: Pathology and Laboratory Medicine, 2013, University of North Carolina

 Epithelial-stromal interactions are fundamental to tissue homeostasis and may alter breast cancer (BC) initiation and progression. Co-evolution of the neoplastic epithelium and the stroma implies… (more)

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

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APA (6th Edition):

Casbas-Hernandez, P. (2013). In vitro coculture models to study heterotypic interactions in breast cancer microenvironments. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:727f1978-2942-46d3-8df5-52eef1afd7d7

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):

Casbas-Hernandez, Patricia. “In vitro coculture models to study heterotypic interactions in breast cancer microenvironments.” 2013. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:727f1978-2942-46d3-8df5-52eef1afd7d7.

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

MLA Handbook (7th Edition):

Casbas-Hernandez, Patricia. “In vitro coculture models to study heterotypic interactions in breast cancer microenvironments.” 2013. Web. 22 Sep 2020.

Vancouver:

Casbas-Hernandez P. In vitro coculture models to study heterotypic interactions in breast cancer microenvironments. [Internet] [Thesis]. University of North Carolina; 2013. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:727f1978-2942-46d3-8df5-52eef1afd7d7.

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

Council of Science Editors:

Casbas-Hernandez P. In vitro coculture models to study heterotypic interactions in breast cancer microenvironments. [Thesis]. University of North Carolina; 2013. Available from: https://cdr.lib.unc.edu/record/uuid:727f1978-2942-46d3-8df5-52eef1afd7d7

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


University of North Carolina

26. Detwiler, David A. Isolation of Primary Canine Satellite Cells.

Degree: Pathology and Laboratory Medicine, 2012, University of North Carolina

 Duchenne muscular dystrophy (DMD) is a debilitating disease that principally affects striated muscles (skeletal and cardiac) and is the most severe form of muscular dystrophy.… (more)

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

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APA (6th Edition):

Detwiler, D. A. (2012). Isolation of Primary Canine Satellite Cells. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:6344c9c0-bdc8-4fb7-a5ad-b1a2ec5df8c5

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):

Detwiler, David A. “Isolation of Primary Canine Satellite Cells.” 2012. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:6344c9c0-bdc8-4fb7-a5ad-b1a2ec5df8c5.

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

MLA Handbook (7th Edition):

Detwiler, David A. “Isolation of Primary Canine Satellite Cells.” 2012. Web. 22 Sep 2020.

Vancouver:

Detwiler DA. Isolation of Primary Canine Satellite Cells. [Internet] [Thesis]. University of North Carolina; 2012. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:6344c9c0-bdc8-4fb7-a5ad-b1a2ec5df8c5.

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

Council of Science Editors:

Detwiler DA. Isolation of Primary Canine Satellite Cells. [Thesis]. University of North Carolina; 2012. Available from: https://cdr.lib.unc.edu/record/uuid:6344c9c0-bdc8-4fb7-a5ad-b1a2ec5df8c5

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


University of North Carolina

27. Wang, Chih-Hong. Inhibition of Renin Angiotensin System Improves Leptin and Insulin Sensitivity, but Causes Severe Anemia Due to Hypothyroidism.

Degree: Pathology and Laboratory Medicine, 2010, University of North Carolina

 An overactive Renin-Angiotensin System (RAS) is associated with the metabolic syndrome, and inhibiting RAS causes severe anemia. Our previous study has demonstrated that mice lacking… (more)

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

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APA (6th Edition):

Wang, C. (2010). Inhibition of Renin Angiotensin System Improves Leptin and Insulin Sensitivity, but Causes Severe Anemia Due to Hypothyroidism. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:9d6c7dd5-574a-47cd-8e27-219f367a286f

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):

Wang, Chih-Hong. “Inhibition of Renin Angiotensin System Improves Leptin and Insulin Sensitivity, but Causes Severe Anemia Due to Hypothyroidism.” 2010. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:9d6c7dd5-574a-47cd-8e27-219f367a286f.

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

MLA Handbook (7th Edition):

Wang, Chih-Hong. “Inhibition of Renin Angiotensin System Improves Leptin and Insulin Sensitivity, but Causes Severe Anemia Due to Hypothyroidism.” 2010. Web. 22 Sep 2020.

Vancouver:

Wang C. Inhibition of Renin Angiotensin System Improves Leptin and Insulin Sensitivity, but Causes Severe Anemia Due to Hypothyroidism. [Internet] [Thesis]. University of North Carolina; 2010. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:9d6c7dd5-574a-47cd-8e27-219f367a286f.

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

Council of Science Editors:

Wang C. Inhibition of Renin Angiotensin System Improves Leptin and Insulin Sensitivity, but Causes Severe Anemia Due to Hypothyroidism. [Thesis]. University of North Carolina; 2010. Available from: https://cdr.lib.unc.edu/record/uuid:9d6c7dd5-574a-47cd-8e27-219f367a286f

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


University of North Carolina

28. Geddings, Julia. The Role of Tumor Microvesicles in Cancer-Associated Thrombosis.

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

 Cancer patients have a ~4 -fold increased risk of venous thromboembolism (VTE) compared with the general population, and cancer patients with VTE have reduced survival… (more)

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

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APA (6th Edition):

Geddings, J. (2015). The Role of Tumor Microvesicles in Cancer-Associated Thrombosis. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:3d55e13e-65a0-47b3-885e-91787f00f01f

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):

Geddings, Julia. “The Role of Tumor Microvesicles in Cancer-Associated Thrombosis.” 2015. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:3d55e13e-65a0-47b3-885e-91787f00f01f.

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

MLA Handbook (7th Edition):

Geddings, Julia. “The Role of Tumor Microvesicles in Cancer-Associated Thrombosis.” 2015. Web. 22 Sep 2020.

Vancouver:

Geddings J. The Role of Tumor Microvesicles in Cancer-Associated Thrombosis. [Internet] [Thesis]. University of North Carolina; 2015. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:3d55e13e-65a0-47b3-885e-91787f00f01f.

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

Council of Science Editors:

Geddings J. The Role of Tumor Microvesicles in Cancer-Associated Thrombosis. [Thesis]. University of North Carolina; 2015. Available from: https://cdr.lib.unc.edu/record/uuid:3d55e13e-65a0-47b3-885e-91787f00f01f

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


University of North Carolina

29. 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

 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)

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

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APA (6th 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 (16th Edition):

Weise Cross, Laura. “Regulation of Smooth Muscle Cell Phenotype by the RhoA Effectors mDia1 and mDia2.” 2015. Thesis, University of North Carolina. Accessed September 22, 2020. 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 (7th Edition):

Weise Cross, Laura. “Regulation of Smooth Muscle Cell Phenotype by the RhoA Effectors mDia1 and mDia2.” 2015. Web. 22 Sep 2020.

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 2020 Sep 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

30. Mackey, Lantz. The Role of α(1,3)-Fucosylated Glycans in Homeostatic Immunity, Granulopoiesis, and Mucosal Injury.

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

 The mechanisms that control granulopoiesis are poorly understood. Mice deficient in α(1,3)-fucosyltransferases (FUT) 4 and 7 (Fut-/-) lack selectin ligand activity and selectin-dependent leukocyte trafficking,… (more)

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

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APA (6th Edition):

Mackey, L. (2014). The Role of α(1,3)-Fucosylated Glycans in Homeostatic Immunity, Granulopoiesis, and Mucosal Injury. (Thesis). University of North Carolina. Retrieved from https://cdr.lib.unc.edu/record/uuid:532275af-f63a-4934-97d0-2ee6c141ded0

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):

Mackey, Lantz. “The Role of α(1,3)-Fucosylated Glycans in Homeostatic Immunity, Granulopoiesis, and Mucosal Injury.” 2014. Thesis, University of North Carolina. Accessed September 22, 2020. https://cdr.lib.unc.edu/record/uuid:532275af-f63a-4934-97d0-2ee6c141ded0.

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

MLA Handbook (7th Edition):

Mackey, Lantz. “The Role of α(1,3)-Fucosylated Glycans in Homeostatic Immunity, Granulopoiesis, and Mucosal Injury.” 2014. Web. 22 Sep 2020.

Vancouver:

Mackey L. The Role of α(1,3)-Fucosylated Glycans in Homeostatic Immunity, Granulopoiesis, and Mucosal Injury. [Internet] [Thesis]. University of North Carolina; 2014. [cited 2020 Sep 22]. Available from: https://cdr.lib.unc.edu/record/uuid:532275af-f63a-4934-97d0-2ee6c141ded0.

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

Council of Science Editors:

Mackey L. The Role of α(1,3)-Fucosylated Glycans in Homeostatic Immunity, Granulopoiesis, and Mucosal Injury. [Thesis]. University of North Carolina; 2014. Available from: https://cdr.lib.unc.edu/record/uuid:532275af-f63a-4934-97d0-2ee6c141ded0

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

[1] [2] [3] [4] [5]

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