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You searched for +publisher:"Temple University" +contributor:("Autieri, Michael V."). Showing records 1 – 29 of 29 total matches.

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Temple University

1. Sommerville, Laura Jean. The Role of Allograft Inflammatory Factor-1 in Vascular Smooth Muscle Cell Activation and Development of Vascular Proliferative Disease.

Degree: PhD, 2010, Temple University

Molecular and Cellular Physiology

The underlying cause of all vascular proliferative diseases is injury-induced activation of vascular endothelium and vascular smooth muscle cells (VSMC). Activated… (more)

Subjects/Keywords: Biology, Physiology; Allograft Inflammatory Factor-1; Atherosclerosis; Smooth Muscle Cell Activation; Vascular Proliferative Disease

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APA (6th Edition):

Sommerville, L. J. (2010). The Role of Allograft Inflammatory Factor-1 in Vascular Smooth Muscle Cell Activation and Development of Vascular Proliferative Disease. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,76756

Chicago Manual of Style (16th Edition):

Sommerville, Laura Jean. “The Role of Allograft Inflammatory Factor-1 in Vascular Smooth Muscle Cell Activation and Development of Vascular Proliferative Disease.” 2010. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,76756.

MLA Handbook (7th Edition):

Sommerville, Laura Jean. “The Role of Allograft Inflammatory Factor-1 in Vascular Smooth Muscle Cell Activation and Development of Vascular Proliferative Disease.” 2010. Web. 17 Aug 2019.

Vancouver:

Sommerville LJ. The Role of Allograft Inflammatory Factor-1 in Vascular Smooth Muscle Cell Activation and Development of Vascular Proliferative Disease. [Internet] [Doctoral dissertation]. Temple University; 2010. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,76756.

Council of Science Editors:

Sommerville LJ. The Role of Allograft Inflammatory Factor-1 in Vascular Smooth Muscle Cell Activation and Development of Vascular Proliferative Disease. [Doctoral Dissertation]. Temple University; 2010. Available from: http://digital.library.temple.edu/u?/p245801coll10,76756


Temple University

2. Cuneo, Anthony. THERAPEUTIC MECHANISMS OF INTERLEUKIN-19 FOR VASCULAR PROLIFERATIVE DISEASES.

Degree: PhD, 2012, Temple University

Molecular and Cellular Physiology

Cardiovascular disease is the leading cause of mortality in the western world. The pro-inflammatory and pro-proliferative etiology of vascular proliferative diseases… (more)

Subjects/Keywords: Biology, Molecular; Biology, General; Biology, Cell; Atherosclerosis; Human antigen R (HuR); Interleukin-19 (IL-19); oxidized LDL (ox-LDL); Vascular Proliferative Diseases; Vascular Smooth Muscle Cells (VSMC)

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APA (6th Edition):

Cuneo, A. (2012). THERAPEUTIC MECHANISMS OF INTERLEUKIN-19 FOR VASCULAR PROLIFERATIVE DISEASES. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,78032

Chicago Manual of Style (16th Edition):

Cuneo, Anthony. “THERAPEUTIC MECHANISMS OF INTERLEUKIN-19 FOR VASCULAR PROLIFERATIVE DISEASES.” 2012. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,78032.

MLA Handbook (7th Edition):

Cuneo, Anthony. “THERAPEUTIC MECHANISMS OF INTERLEUKIN-19 FOR VASCULAR PROLIFERATIVE DISEASES.” 2012. Web. 17 Aug 2019.

Vancouver:

Cuneo A. THERAPEUTIC MECHANISMS OF INTERLEUKIN-19 FOR VASCULAR PROLIFERATIVE DISEASES. [Internet] [Doctoral dissertation]. Temple University; 2012. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,78032.

Council of Science Editors:

Cuneo A. THERAPEUTIC MECHANISMS OF INTERLEUKIN-19 FOR VASCULAR PROLIFERATIVE DISEASES. [Doctoral Dissertation]. Temple University; 2012. Available from: http://digital.library.temple.edu/u?/p245801coll10,78032


Temple University

3. Jaleel, Naser. Re-Expression of T-Type Calcium Channels Minimally Affects Cardiac Contractility and Activates Pro-Survival Signaling Pathways in the Myocardium.

Degree: PhD, 2010, Temple University

Physiology

The role of T-type calcium channels (TTCCs) in the heart is unclear. TTCCs are transiently expressed throughout the neonatal heart during a period of… (more)

Subjects/Keywords: Biology, Physiology; Biology, General; Cardiac Electrophysiology; Cardiac Hypertrophy; Excitation Contraction Coupling; L-Type Calcium Channels; T-type Calcium Channels

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APA (6th Edition):

Jaleel, N. (2010). Re-Expression of T-Type Calcium Channels Minimally Affects Cardiac Contractility and Activates Pro-Survival Signaling Pathways in the Myocardium. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,83093

Chicago Manual of Style (16th Edition):

Jaleel, Naser. “Re-Expression of T-Type Calcium Channels Minimally Affects Cardiac Contractility and Activates Pro-Survival Signaling Pathways in the Myocardium.” 2010. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,83093.

MLA Handbook (7th Edition):

Jaleel, Naser. “Re-Expression of T-Type Calcium Channels Minimally Affects Cardiac Contractility and Activates Pro-Survival Signaling Pathways in the Myocardium.” 2010. Web. 17 Aug 2019.

Vancouver:

Jaleel N. Re-Expression of T-Type Calcium Channels Minimally Affects Cardiac Contractility and Activates Pro-Survival Signaling Pathways in the Myocardium. [Internet] [Doctoral dissertation]. Temple University; 2010. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,83093.

Council of Science Editors:

Jaleel N. Re-Expression of T-Type Calcium Channels Minimally Affects Cardiac Contractility and Activates Pro-Survival Signaling Pathways in the Myocardium. [Doctoral Dissertation]. Temple University; 2010. Available from: http://digital.library.temple.edu/u?/p245801coll10,83093


Temple University

4. Kong, Weimin. THE ANTI-INFLAMMATORY EFFECTS OF DOCOSAHEXAENOIC ACID ON DENDRITIC CELLS.

Degree: PhD, 2010, Temple University

Physiology

Dendritic cells (DC) are professional antigen presenting cells which link innate and adaptive immunity through recognition and processing of pathogens, migration to secondary lymph… (more)

Subjects/Keywords: Immunology

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APA (6th Edition):

Kong, W. (2010). THE ANTI-INFLAMMATORY EFFECTS OF DOCOSAHEXAENOIC ACID ON DENDRITIC CELLS. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,119523

Chicago Manual of Style (16th Edition):

Kong, Weimin. “THE ANTI-INFLAMMATORY EFFECTS OF DOCOSAHEXAENOIC ACID ON DENDRITIC CELLS.” 2010. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,119523.

MLA Handbook (7th Edition):

Kong, Weimin. “THE ANTI-INFLAMMATORY EFFECTS OF DOCOSAHEXAENOIC ACID ON DENDRITIC CELLS.” 2010. Web. 17 Aug 2019.

Vancouver:

Kong W. THE ANTI-INFLAMMATORY EFFECTS OF DOCOSAHEXAENOIC ACID ON DENDRITIC CELLS. [Internet] [Doctoral dissertation]. Temple University; 2010. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,119523.

Council of Science Editors:

Kong W. THE ANTI-INFLAMMATORY EFFECTS OF DOCOSAHEXAENOIC ACID ON DENDRITIC CELLS. [Doctoral Dissertation]. Temple University; 2010. Available from: http://digital.library.temple.edu/u?/p245801coll10,119523


Temple University

5. Angert, David W. Repair of the Injured Adult Heart Involves Resident Cardiac Stem Cell Derived New Myocytes.

Degree: PhD, 2011, Temple University

Physiology

The ability of the adult heart to generate new myocytes after injury is not established. Our purpose was to determine if the adult heart… (more)

Subjects/Keywords: Physiology; Cardiac; Catecholamine; Endogenous; Injury; Isoproterenol; Regeneration

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APA (6th Edition):

Angert, D. W. (2011). Repair of the Injured Adult Heart Involves Resident Cardiac Stem Cell Derived New Myocytes. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,125347

Chicago Manual of Style (16th Edition):

Angert, David W. “Repair of the Injured Adult Heart Involves Resident Cardiac Stem Cell Derived New Myocytes.” 2011. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,125347.

MLA Handbook (7th Edition):

Angert, David W. “Repair of the Injured Adult Heart Involves Resident Cardiac Stem Cell Derived New Myocytes.” 2011. Web. 17 Aug 2019.

Vancouver:

Angert DW. Repair of the Injured Adult Heart Involves Resident Cardiac Stem Cell Derived New Myocytes. [Internet] [Doctoral dissertation]. Temple University; 2011. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,125347.

Council of Science Editors:

Angert DW. Repair of the Injured Adult Heart Involves Resident Cardiac Stem Cell Derived New Myocytes. [Doctoral Dissertation]. Temple University; 2011. Available from: http://digital.library.temple.edu/u?/p245801coll10,125347


Temple University

6. Getz, Todd Michael. The Regulation of Phosphorylation Events in Platelets.

Degree: PhD, 2012, Temple University

Physiology

Platelets play a vital role in processes of hemostasis and thrombosis under physiological and pathological conditions. Following vascular damage, platelets will accumulate and stably… (more)

Subjects/Keywords: Physiology; Biology; Biochemistry; Dextran sulfate; Myosin light chain; Phosphorylation; Platelets; signal transduction; Syk kinase

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APA (6th Edition):

Getz, T. M. (2012). The Regulation of Phosphorylation Events in Platelets. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,213114

Chicago Manual of Style (16th Edition):

Getz, Todd Michael. “The Regulation of Phosphorylation Events in Platelets.” 2012. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,213114.

MLA Handbook (7th Edition):

Getz, Todd Michael. “The Regulation of Phosphorylation Events in Platelets.” 2012. Web. 17 Aug 2019.

Vancouver:

Getz TM. The Regulation of Phosphorylation Events in Platelets. [Internet] [Doctoral dissertation]. Temple University; 2012. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,213114.

Council of Science Editors:

Getz TM. The Regulation of Phosphorylation Events in Platelets. [Doctoral Dissertation]. Temple University; 2012. Available from: http://digital.library.temple.edu/u?/p245801coll10,213114


Temple University

7. Adhikary, Sabina. CANNABINOID RECEPTOR 2 AGONIST REDUCES IMMUNE CELL MIGRATION IN NEUROINFLAMMATION VIA INHIBITION OF MATRIX METALLOPROTEINASE-9.

Degree: PhD, 2013, Temple University

Physiology

Several studies have reported that administration of cannabinoid receptor agonists in inflammatory/autoimmune and CNS injury models resulted in significant attenuation of clinical disease. The… (more)

Subjects/Keywords: Immunology; Cannabinoid Receptor 2; Chemokines; Dendritic cell migration; Matrix Metalloproteinase 9; Multiple sclerosis; Spinal cord injury

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APA (6th Edition):

Adhikary, S. (2013). CANNABINOID RECEPTOR 2 AGONIST REDUCES IMMUNE CELL MIGRATION IN NEUROINFLAMMATION VIA INHIBITION OF MATRIX METALLOPROTEINASE-9. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,214799

Chicago Manual of Style (16th Edition):

Adhikary, Sabina. “CANNABINOID RECEPTOR 2 AGONIST REDUCES IMMUNE CELL MIGRATION IN NEUROINFLAMMATION VIA INHIBITION OF MATRIX METALLOPROTEINASE-9.” 2013. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,214799.

MLA Handbook (7th Edition):

Adhikary, Sabina. “CANNABINOID RECEPTOR 2 AGONIST REDUCES IMMUNE CELL MIGRATION IN NEUROINFLAMMATION VIA INHIBITION OF MATRIX METALLOPROTEINASE-9.” 2013. Web. 17 Aug 2019.

Vancouver:

Adhikary S. CANNABINOID RECEPTOR 2 AGONIST REDUCES IMMUNE CELL MIGRATION IN NEUROINFLAMMATION VIA INHIBITION OF MATRIX METALLOPROTEINASE-9. [Internet] [Doctoral dissertation]. Temple University; 2013. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,214799.

Council of Science Editors:

Adhikary S. CANNABINOID RECEPTOR 2 AGONIST REDUCES IMMUNE CELL MIGRATION IN NEUROINFLAMMATION VIA INHIBITION OF MATRIX METALLOPROTEINASE-9. [Doctoral Dissertation]. Temple University; 2013. Available from: http://digital.library.temple.edu/u?/p245801coll10,214799


Temple University

8. England, Ross N. Cellular Mechanisms of the Anti-Inflammatory Effects of Interleukin-19.

Degree: PhD, 2015, Temple University

Physiology

BACKGROUND: Atherosclerotic vascular disease is a significant medical and socioeconomic problem and contributes to mortality in multiple diseases including myocardial infarction (MI), stroke, renal… (more)

Subjects/Keywords: Physiology; Pathology; Molecular biology;

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APA (6th Edition):

England, R. N. (2015). Cellular Mechanisms of the Anti-Inflammatory Effects of Interleukin-19. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,216875

Chicago Manual of Style (16th Edition):

England, Ross N. “Cellular Mechanisms of the Anti-Inflammatory Effects of Interleukin-19.” 2015. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,216875.

MLA Handbook (7th Edition):

England, Ross N. “Cellular Mechanisms of the Anti-Inflammatory Effects of Interleukin-19.” 2015. Web. 17 Aug 2019.

Vancouver:

England RN. Cellular Mechanisms of the Anti-Inflammatory Effects of Interleukin-19. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,216875.

Council of Science Editors:

England RN. Cellular Mechanisms of the Anti-Inflammatory Effects of Interleukin-19. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,216875


Temple University

9. Fang, Pu. HYPERHOMOCYSTEINEMIA ACCELERATES ATHEROSCLEROSIS BY INDUCING INFLAMMATORY MONOCYTE DIFFERENTIATION IN A HYPERGLYCEMIC MOUSE MODEL.

Degree: PhD, 2012, Temple University

Pharmacology

Homocysteine (Hcy) is a thiol amino acid formed upon methionine de - methylation. A number of studies have revealed an association between hyperhomocysteinemia (HHcy),… (more)

Subjects/Keywords: Pharmacology

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APA (6th Edition):

Fang, P. (2012). HYPERHOMOCYSTEINEMIA ACCELERATES ATHEROSCLEROSIS BY INDUCING INFLAMMATORY MONOCYTE DIFFERENTIATION IN A HYPERGLYCEMIC MOUSE MODEL. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,223888

Chicago Manual of Style (16th Edition):

Fang, Pu. “HYPERHOMOCYSTEINEMIA ACCELERATES ATHEROSCLEROSIS BY INDUCING INFLAMMATORY MONOCYTE DIFFERENTIATION IN A HYPERGLYCEMIC MOUSE MODEL.” 2012. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,223888.

MLA Handbook (7th Edition):

Fang, Pu. “HYPERHOMOCYSTEINEMIA ACCELERATES ATHEROSCLEROSIS BY INDUCING INFLAMMATORY MONOCYTE DIFFERENTIATION IN A HYPERGLYCEMIC MOUSE MODEL.” 2012. Web. 17 Aug 2019.

Vancouver:

Fang P. HYPERHOMOCYSTEINEMIA ACCELERATES ATHEROSCLEROSIS BY INDUCING INFLAMMATORY MONOCYTE DIFFERENTIATION IN A HYPERGLYCEMIC MOUSE MODEL. [Internet] [Doctoral dissertation]. Temple University; 2012. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,223888.

Council of Science Editors:

Fang P. HYPERHOMOCYSTEINEMIA ACCELERATES ATHEROSCLEROSIS BY INDUCING INFLAMMATORY MONOCYTE DIFFERENTIATION IN A HYPERGLYCEMIC MOUSE MODEL. [Doctoral Dissertation]. Temple University; 2012. Available from: http://digital.library.temple.edu/u?/p245801coll10,223888


Temple University

10. Hemmasizadeh, Ali. Characterization of Heterogeneous Material Properties of Aorta Using Nanoindentation.

Degree: PhD, 2013, Temple University

Mechanical Engineering

Arterial mechanical properties have received increasing attention in the past few decades due to their vast effect on predicting cardiovascular diseases and injuries.… (more)

Subjects/Keywords: Engineering; Mechanical engineering; Biomechanics;

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APA (6th Edition):

Hemmasizadeh, A. (2013). Characterization of Heterogeneous Material Properties of Aorta Using Nanoindentation. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,240046

Chicago Manual of Style (16th Edition):

Hemmasizadeh, Ali. “Characterization of Heterogeneous Material Properties of Aorta Using Nanoindentation.” 2013. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,240046.

MLA Handbook (7th Edition):

Hemmasizadeh, Ali. “Characterization of Heterogeneous Material Properties of Aorta Using Nanoindentation.” 2013. Web. 17 Aug 2019.

Vancouver:

Hemmasizadeh A. Characterization of Heterogeneous Material Properties of Aorta Using Nanoindentation. [Internet] [Doctoral dissertation]. Temple University; 2013. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,240046.

Council of Science Editors:

Hemmasizadeh A. Characterization of Heterogeneous Material Properties of Aorta Using Nanoindentation. [Doctoral Dissertation]. Temple University; 2013. Available from: http://digital.library.temple.edu/u?/p245801coll10,240046


Temple University

11. Hubert, Terrence L. Effect of rhCC10 on the Pro/Anti-Inflammatory Profile of the Immature Lung.

Degree: PhD, 2014, Temple University

Physiology

There is a gap in the treatment of preterm infants with respiratory distress syndrome. Despite addressing surfactant insufficiency and mechanical instability, currently available exogenous… (more)

Subjects/Keywords: Physiology;

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APA (6th Edition):

Hubert, T. L. (2014). Effect of rhCC10 on the Pro/Anti-Inflammatory Profile of the Immature Lung. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,240379

Chicago Manual of Style (16th Edition):

Hubert, Terrence L. “Effect of rhCC10 on the Pro/Anti-Inflammatory Profile of the Immature Lung.” 2014. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,240379.

MLA Handbook (7th Edition):

Hubert, Terrence L. “Effect of rhCC10 on the Pro/Anti-Inflammatory Profile of the Immature Lung.” 2014. Web. 17 Aug 2019.

Vancouver:

Hubert TL. Effect of rhCC10 on the Pro/Anti-Inflammatory Profile of the Immature Lung. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,240379.

Council of Science Editors:

Hubert TL. Effect of rhCC10 on the Pro/Anti-Inflammatory Profile of the Immature Lung. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,240379


Temple University

12. Yin, Ying. CASPASE-1 ACTIVATION IS CRITICAL FOR ENDOTHELIAL CELL ACTIVATION, MONOCYTE MIGRATION, AND EARLY ATHEROGENESIS.

Degree: PhD, 2013, Temple University

Pharmacology

Atherosclerosis, considered a chronic inflammatory disease, is the underlying mechanism for several cardiovascular diseases. Hyperlipidemia is the number one risk factor for atherogenesis. Caspase-1… (more)

Subjects/Keywords: Pharmacology; atherosclerosis, caspase-1, vascular inflammation

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APA (6th Edition):

Yin, Y. (2013). CASPASE-1 ACTIVATION IS CRITICAL FOR ENDOTHELIAL CELL ACTIVATION, MONOCYTE MIGRATION, AND EARLY ATHEROGENESIS. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,252725

Chicago Manual of Style (16th Edition):

Yin, Ying. “CASPASE-1 ACTIVATION IS CRITICAL FOR ENDOTHELIAL CELL ACTIVATION, MONOCYTE MIGRATION, AND EARLY ATHEROGENESIS.” 2013. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,252725.

MLA Handbook (7th Edition):

Yin, Ying. “CASPASE-1 ACTIVATION IS CRITICAL FOR ENDOTHELIAL CELL ACTIVATION, MONOCYTE MIGRATION, AND EARLY ATHEROGENESIS.” 2013. Web. 17 Aug 2019.

Vancouver:

Yin Y. CASPASE-1 ACTIVATION IS CRITICAL FOR ENDOTHELIAL CELL ACTIVATION, MONOCYTE MIGRATION, AND EARLY ATHEROGENESIS. [Internet] [Doctoral dissertation]. Temple University; 2013. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,252725.

Council of Science Editors:

Yin Y. CASPASE-1 ACTIVATION IS CRITICAL FOR ENDOTHELIAL CELL ACTIVATION, MONOCYTE MIGRATION, AND EARLY ATHEROGENESIS. [Doctoral Dissertation]. Temple University; 2013. Available from: http://digital.library.temple.edu/u?/p245801coll10,252725


Temple University

13. Duran, Jason Mathew. Bone-derived stem cells repair the heart after myocardial infarction through transdifferentiation and paracrine signaling mechanisms.

Degree: PhD, 2015, Temple University

Physiology

Rationale: Autologous bone marrow- or cardiac-derived stem cell therapy for heart disease has demonstrated safety and efficacy in clinical trials but has only offered… (more)

Subjects/Keywords: Physiology; myocardial infarction; paracrine factors; regeneration; stem cells; transdifferentiation

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APA (6th Edition):

Duran, J. M. (2015). Bone-derived stem cells repair the heart after myocardial infarction through transdifferentiation and paracrine signaling mechanisms. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,253042

Chicago Manual of Style (16th Edition):

Duran, Jason Mathew. “Bone-derived stem cells repair the heart after myocardial infarction through transdifferentiation and paracrine signaling mechanisms.” 2015. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,253042.

MLA Handbook (7th Edition):

Duran, Jason Mathew. “Bone-derived stem cells repair the heart after myocardial infarction through transdifferentiation and paracrine signaling mechanisms.” 2015. Web. 17 Aug 2019.

Vancouver:

Duran JM. Bone-derived stem cells repair the heart after myocardial infarction through transdifferentiation and paracrine signaling mechanisms. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,253042.

Council of Science Editors:

Duran JM. Bone-derived stem cells repair the heart after myocardial infarction through transdifferentiation and paracrine signaling mechanisms. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,253042


Temple University

14. Ellison, Stephen Patrick. THE EFFECTS OF INTERLEUKIN-19 ON ATTENUATION OF THE VASCULAR RESPONSE TO INJURY.

Degree: PhD, 2015, Temple University

Physiology

BACKGROUND: Despite aggressive dietary modification, lipid lowering medications, and other medical therapy, vascular proliferative diseases continue to account for 50% of all mortality in… (more)

Subjects/Keywords: Physiology;

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APA (6th Edition):

Ellison, S. P. (2015). THE EFFECTS OF INTERLEUKIN-19 ON ATTENUATION OF THE VASCULAR RESPONSE TO INJURY. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,253270

Chicago Manual of Style (16th Edition):

Ellison, Stephen Patrick. “THE EFFECTS OF INTERLEUKIN-19 ON ATTENUATION OF THE VASCULAR RESPONSE TO INJURY.” 2015. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,253270.

MLA Handbook (7th Edition):

Ellison, Stephen Patrick. “THE EFFECTS OF INTERLEUKIN-19 ON ATTENUATION OF THE VASCULAR RESPONSE TO INJURY.” 2015. Web. 17 Aug 2019.

Vancouver:

Ellison SP. THE EFFECTS OF INTERLEUKIN-19 ON ATTENUATION OF THE VASCULAR RESPONSE TO INJURY. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,253270.

Council of Science Editors:

Ellison SP. THE EFFECTS OF INTERLEUKIN-19 ON ATTENUATION OF THE VASCULAR RESPONSE TO INJURY. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,253270


Temple University

15. Jan, Michael. Novel Mechanisms Underlying Homocysteine-Suppressed Endothelial Cell Growth.

Degree: PhD, 2014, Temple University

Pharmacology

Cardiovascular disease (CVD) is the leading cause of death worldwide, and is projected to remain so for at least the next decade. Ever since… (more)

Subjects/Keywords: Pharmacology;

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APA (6th Edition):

Jan, M. (2014). Novel Mechanisms Underlying Homocysteine-Suppressed Endothelial Cell Growth. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,264103

Chicago Manual of Style (16th Edition):

Jan, Michael. “Novel Mechanisms Underlying Homocysteine-Suppressed Endothelial Cell Growth.” 2014. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,264103.

MLA Handbook (7th Edition):

Jan, Michael. “Novel Mechanisms Underlying Homocysteine-Suppressed Endothelial Cell Growth.” 2014. Web. 17 Aug 2019.

Vancouver:

Jan M. Novel Mechanisms Underlying Homocysteine-Suppressed Endothelial Cell Growth. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,264103.

Council of Science Editors:

Jan M. Novel Mechanisms Underlying Homocysteine-Suppressed Endothelial Cell Growth. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,264103


Temple University

16. Mai, Jietang. ROLE OF INTERLEUKIN-17 IN ENDOTHELIAL CELL ACTIVATION AND VASCULAR FUNCTION.

Degree: PhD, 2014, Temple University

Pharmacology

Endothelial cell (EC) activation is a change of the endothelium from a quiescent state to one that is involved in immune reactions. Activation of… (more)

Subjects/Keywords: Immunology; Physiology; Cellular biology;

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APA (6th Edition):

Mai, J. (2014). ROLE OF INTERLEUKIN-17 IN ENDOTHELIAL CELL ACTIVATION AND VASCULAR FUNCTION. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,266288

Chicago Manual of Style (16th Edition):

Mai, Jietang. “ROLE OF INTERLEUKIN-17 IN ENDOTHELIAL CELL ACTIVATION AND VASCULAR FUNCTION.” 2014. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,266288.

MLA Handbook (7th Edition):

Mai, Jietang. “ROLE OF INTERLEUKIN-17 IN ENDOTHELIAL CELL ACTIVATION AND VASCULAR FUNCTION.” 2014. Web. 17 Aug 2019.

Vancouver:

Mai J. ROLE OF INTERLEUKIN-17 IN ENDOTHELIAL CELL ACTIVATION AND VASCULAR FUNCTION. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,266288.

Council of Science Editors:

Mai J. ROLE OF INTERLEUKIN-17 IN ENDOTHELIAL CELL ACTIVATION AND VASCULAR FUNCTION. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,266288


Temple University

17. Virtue, Anthony Thomas. The Contributions of miR-155 in Obesity, Metabolic Syndrome, and Atherosclerosis Development.

Degree: PhD, 2014, Temple University

Pharmacology

The global incidence of overweight and obese individuals has skyrocketed in the past few decades resulting in a new health epidemic. In 1980, 5%… (more)

Subjects/Keywords: Biology; Molecular biology;

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APA (6th Edition):

Virtue, A. T. (2014). The Contributions of miR-155 in Obesity, Metabolic Syndrome, and Atherosclerosis Development. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,276607

Chicago Manual of Style (16th Edition):

Virtue, Anthony Thomas. “The Contributions of miR-155 in Obesity, Metabolic Syndrome, and Atherosclerosis Development.” 2014. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,276607.

MLA Handbook (7th Edition):

Virtue, Anthony Thomas. “The Contributions of miR-155 in Obesity, Metabolic Syndrome, and Atherosclerosis Development.” 2014. Web. 17 Aug 2019.

Vancouver:

Virtue AT. The Contributions of miR-155 in Obesity, Metabolic Syndrome, and Atherosclerosis Development. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,276607.

Council of Science Editors:

Virtue AT. The Contributions of miR-155 in Obesity, Metabolic Syndrome, and Atherosclerosis Development. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,276607


Temple University

18. Crawford, Kevin John. THE ROLE OF CAVEOLAE IN THE FORMATION OF ABDOMINAL AORTIC ANEURYSMS.

Degree: PhD, 2015, Temple University

Cell Biology

Abdominal aortic aneurysm (AAA) is a major cardiovascular disease and involves enhancement of renin-angiotensin system and recruitment/activation of inflammatory factors such as matrix… (more)

Subjects/Keywords: Cellular biology;

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APA (6th Edition):

Crawford, K. J. (2015). THE ROLE OF CAVEOLAE IN THE FORMATION OF ABDOMINAL AORTIC ANEURYSMS. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,312992

Chicago Manual of Style (16th Edition):

Crawford, Kevin John. “THE ROLE OF CAVEOLAE IN THE FORMATION OF ABDOMINAL AORTIC ANEURYSMS.” 2015. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,312992.

MLA Handbook (7th Edition):

Crawford, Kevin John. “THE ROLE OF CAVEOLAE IN THE FORMATION OF ABDOMINAL AORTIC ANEURYSMS.” 2015. Web. 17 Aug 2019.

Vancouver:

Crawford KJ. THE ROLE OF CAVEOLAE IN THE FORMATION OF ABDOMINAL AORTIC ANEURYSMS. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,312992.

Council of Science Editors:

Crawford KJ. THE ROLE OF CAVEOLAE IN THE FORMATION OF ABDOMINAL AORTIC ANEURYSMS. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,312992


Temple University

19. Richards, Jamie Madison. The Potential of IL-19 As a Therapeutic Anti-inflammatory and Angiogenic Cytokine.

Degree: PhD, 2015, Temple University

Physiology

Our lab has recently shown that IL-19 is expressed in angiogenic ECs, opening the possibility for its use as a medicine to increase perfusion… (more)

Subjects/Keywords: Physiology; Health sciences; Medicine;

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APA (6th Edition):

Richards, J. M. (2015). The Potential of IL-19 As a Therapeutic Anti-inflammatory and Angiogenic Cytokine. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,345114

Chicago Manual of Style (16th Edition):

Richards, Jamie Madison. “The Potential of IL-19 As a Therapeutic Anti-inflammatory and Angiogenic Cytokine.” 2015. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,345114.

MLA Handbook (7th Edition):

Richards, Jamie Madison. “The Potential of IL-19 As a Therapeutic Anti-inflammatory and Angiogenic Cytokine.” 2015. Web. 17 Aug 2019.

Vancouver:

Richards JM. The Potential of IL-19 As a Therapeutic Anti-inflammatory and Angiogenic Cytokine. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,345114.

Council of Science Editors:

Richards JM. The Potential of IL-19 As a Therapeutic Anti-inflammatory and Angiogenic Cytokine. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,345114


Temple University

20. Chang, Jen-Kuan. The Biochemical Basis of The miR-21 Expression by The Mu-Opioid Receptor.

Degree: PhD, 2015, Temple University

Molecular Biology and Genetics

Opioid receptors are members of the superfamily of seven transmembrane G protein-coupled receptors (GPCRs) which share several structural and functional characteristics.… (more)

Subjects/Keywords: Molecular biology; Genetics; Immunology;

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APA (6th Edition):

Chang, J. (2015). The Biochemical Basis of The miR-21 Expression by The Mu-Opioid Receptor. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,352105

Chicago Manual of Style (16th Edition):

Chang, Jen-Kuan. “The Biochemical Basis of The miR-21 Expression by The Mu-Opioid Receptor.” 2015. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,352105.

MLA Handbook (7th Edition):

Chang, Jen-Kuan. “The Biochemical Basis of The miR-21 Expression by The Mu-Opioid Receptor.” 2015. Web. 17 Aug 2019.

Vancouver:

Chang J. The Biochemical Basis of The miR-21 Expression by The Mu-Opioid Receptor. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,352105.

Council of Science Editors:

Chang J. The Biochemical Basis of The miR-21 Expression by The Mu-Opioid Receptor. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,352105


Temple University

21. Preston, Kyle J. Macronutrient Activation of Endothelium Dependent Leukocyte Trafficking: Metabolic Implications.

Degree: PhD, 2015, Temple University

Physiology

Obesity and insulin resistance are characterized by elevated pro-inflammatory proteins in the blood and immune cell accumulation in the visceral adipose tissue. Resident leukocytes… (more)

Subjects/Keywords: Physiology;

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APA (6th Edition):

Preston, K. J. (2015). Macronutrient Activation of Endothelium Dependent Leukocyte Trafficking: Metabolic Implications. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,361365

Chicago Manual of Style (16th Edition):

Preston, Kyle J. “Macronutrient Activation of Endothelium Dependent Leukocyte Trafficking: Metabolic Implications.” 2015. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,361365.

MLA Handbook (7th Edition):

Preston, Kyle J. “Macronutrient Activation of Endothelium Dependent Leukocyte Trafficking: Metabolic Implications.” 2015. Web. 17 Aug 2019.

Vancouver:

Preston KJ. Macronutrient Activation of Endothelium Dependent Leukocyte Trafficking: Metabolic Implications. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,361365.

Council of Science Editors:

Preston KJ. Macronutrient Activation of Endothelium Dependent Leukocyte Trafficking: Metabolic Implications. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,361365


Temple University

22. Kermani, Golriz. Characterization of Rate Dependency and Inhomogeneity of Aortic Tissue.

Degree: PhD, 2016, Temple University

Mechanical Engineering

Traumatic aortic rupture (TAR) is one of the leading causes of morbidity and mortality in motor-vehicle accidents with the majority of injuries occurring… (more)

Subjects/Keywords: Engineering; Mechanical engineering; Biomechanics

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APA (6th Edition):

Kermani, G. (2016). Characterization of Rate Dependency and Inhomogeneity of Aortic Tissue. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,412554

Chicago Manual of Style (16th Edition):

Kermani, Golriz. “Characterization of Rate Dependency and Inhomogeneity of Aortic Tissue.” 2016. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,412554.

MLA Handbook (7th Edition):

Kermani, Golriz. “Characterization of Rate Dependency and Inhomogeneity of Aortic Tissue.” 2016. Web. 17 Aug 2019.

Vancouver:

Kermani G. Characterization of Rate Dependency and Inhomogeneity of Aortic Tissue. [Internet] [Doctoral dissertation]. Temple University; 2016. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,412554.

Council of Science Editors:

Kermani G. Characterization of Rate Dependency and Inhomogeneity of Aortic Tissue. [Doctoral Dissertation]. Temple University; 2016. Available from: http://digital.library.temple.edu/u?/p245801coll10,412554


Temple University

23. Malone, Daniel Joseph. PERFLUOROCHEMICAL AUGMENTED INTRATRACHEAL DELIVERY OF ANTIOXIDANT ENZYMES AND GENES TO ATTENUATE OXIDATIVE STRESS-INDUCED LUNG AND RESPIRATORY MUSCLE ALTERATIONS.

Degree: PhD, 2009, Temple University

Physiology

Supraphysiologic concentrations of oxygen are used in the management of critically ill patients across the lifespan. However, hyperoxia (HO) results in alveolar- capillary membrane… (more)

Subjects/Keywords: Biology, Physiology; Health Sciences, Medicine and Surgery; diaphragm; hyperoxia; lung injury

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APA (6th Edition):

Malone, D. J. (2009). PERFLUOROCHEMICAL AUGMENTED INTRATRACHEAL DELIVERY OF ANTIOXIDANT ENZYMES AND GENES TO ATTENUATE OXIDATIVE STRESS-INDUCED LUNG AND RESPIRATORY MUSCLE ALTERATIONS. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,24041

Chicago Manual of Style (16th Edition):

Malone, Daniel Joseph. “PERFLUOROCHEMICAL AUGMENTED INTRATRACHEAL DELIVERY OF ANTIOXIDANT ENZYMES AND GENES TO ATTENUATE OXIDATIVE STRESS-INDUCED LUNG AND RESPIRATORY MUSCLE ALTERATIONS.” 2009. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,24041.

MLA Handbook (7th Edition):

Malone, Daniel Joseph. “PERFLUOROCHEMICAL AUGMENTED INTRATRACHEAL DELIVERY OF ANTIOXIDANT ENZYMES AND GENES TO ATTENUATE OXIDATIVE STRESS-INDUCED LUNG AND RESPIRATORY MUSCLE ALTERATIONS.” 2009. Web. 17 Aug 2019.

Vancouver:

Malone DJ. PERFLUOROCHEMICAL AUGMENTED INTRATRACHEAL DELIVERY OF ANTIOXIDANT ENZYMES AND GENES TO ATTENUATE OXIDATIVE STRESS-INDUCED LUNG AND RESPIRATORY MUSCLE ALTERATIONS. [Internet] [Doctoral dissertation]. Temple University; 2009. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,24041.

Council of Science Editors:

Malone DJ. PERFLUOROCHEMICAL AUGMENTED INTRATRACHEAL DELIVERY OF ANTIOXIDANT ENZYMES AND GENES TO ATTENUATE OXIDATIVE STRESS-INDUCED LUNG AND RESPIRATORY MUSCLE ALTERATIONS. [Doctoral Dissertation]. Temple University; 2009. Available from: http://digital.library.temple.edu/u?/p245801coll10,24041


Temple University

24. JAIN,SURBHI. ROLE OF INTERLEUKIN-19 AND ALLOGRAFT INFLAMMATORY FACTOR-1 IN ENDOTHELIAL CELL PROLIFERATION, ACTIVATION, MIGRATION AND ANGIOGENIC POTENTIAL.

Degree: PhD, 2009, Temple University

Microbiology and Immunology

Angiogenesis is an important process in maintaining normal physiology as well as in the pathology of many diseases. Angiogenesis based therapies have… (more)

Subjects/Keywords: Biology, Microbiology; Health Sciences, Immunology; Allograft Inflammatory Factor-1; Angiogenesis; Endothelial Cell; Interleukin-19; Migration; Proliferation

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APA (6th Edition):

JAIN,SURBHI. (2009). ROLE OF INTERLEUKIN-19 AND ALLOGRAFT INFLAMMATORY FACTOR-1 IN ENDOTHELIAL CELL PROLIFERATION, ACTIVATION, MIGRATION AND ANGIOGENIC POTENTIAL. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,25799

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Chicago Manual of Style (16th Edition):

JAIN,SURBHI. “ROLE OF INTERLEUKIN-19 AND ALLOGRAFT INFLAMMATORY FACTOR-1 IN ENDOTHELIAL CELL PROLIFERATION, ACTIVATION, MIGRATION AND ANGIOGENIC POTENTIAL.” 2009. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,25799.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

MLA Handbook (7th Edition):

JAIN,SURBHI. “ROLE OF INTERLEUKIN-19 AND ALLOGRAFT INFLAMMATORY FACTOR-1 IN ENDOTHELIAL CELL PROLIFERATION, ACTIVATION, MIGRATION AND ANGIOGENIC POTENTIAL.” 2009. Web. 17 Aug 2019.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

JAIN,SURBHI. ROLE OF INTERLEUKIN-19 AND ALLOGRAFT INFLAMMATORY FACTOR-1 IN ENDOTHELIAL CELL PROLIFERATION, ACTIVATION, MIGRATION AND ANGIOGENIC POTENTIAL. [Internet] [Doctoral dissertation]. Temple University; 2009. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,25799.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Council of Science Editors:

JAIN,SURBHI. ROLE OF INTERLEUKIN-19 AND ALLOGRAFT INFLAMMATORY FACTOR-1 IN ENDOTHELIAL CELL PROLIFERATION, ACTIVATION, MIGRATION AND ANGIOGENIC POTENTIAL. [Doctoral Dissertation]. Temple University; 2009. Available from: http://digital.library.temple.edu/u?/p245801coll10,25799

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete


Temple University

25. Mao, Yingying. ROLE OF PROTEASE-ACTIVATED RECEPTORS IN PLATELET ACTIVATION.

Degree: PhD, 2009, Temple University

Physiology

Platelets act as a fundamental component of the hemostatic process and their activation leads to the formation of a stable clot at the injured… (more)

Subjects/Keywords: Biology, Physiology; ischemic injury; PAR1 agonist; plasmin; platelet; protease-activated receptor

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APA (6th Edition):

Mao, Y. (2009). ROLE OF PROTEASE-ACTIVATED RECEPTORS IN PLATELET ACTIVATION. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,47279

Chicago Manual of Style (16th Edition):

Mao, Yingying. “ROLE OF PROTEASE-ACTIVATED RECEPTORS IN PLATELET ACTIVATION.” 2009. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,47279.

MLA Handbook (7th Edition):

Mao, Yingying. “ROLE OF PROTEASE-ACTIVATED RECEPTORS IN PLATELET ACTIVATION.” 2009. Web. 17 Aug 2019.

Vancouver:

Mao Y. ROLE OF PROTEASE-ACTIVATED RECEPTORS IN PLATELET ACTIVATION. [Internet] [Doctoral dissertation]. Temple University; 2009. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,47279.

Council of Science Editors:

Mao Y. ROLE OF PROTEASE-ACTIVATED RECEPTORS IN PLATELET ACTIVATION. [Doctoral Dissertation]. Temple University; 2009. Available from: http://digital.library.temple.edu/u?/p245801coll10,47279


Temple University

26. Forrester, Steven James. MITOCHONDRIA FACILITATE VASCULAR INFLAMMATION: THE ROLE OF CANONICAL INFLAMMATORY SIGNALING IN THE REGULATION OF MITOCHONDRIAL MORPHOLOGY.

Degree: PhD, 2017, Temple University

Kinesiology

Vascular inflammation is an underlying cause to numerous diseases and is characterized by classical NF-κB activation and downstream physiological responses including inflammatory gene induction… (more)

Subjects/Keywords: Physiology; Cellular biology; Medicine

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APA (6th Edition):

Forrester, S. J. (2017). MITOCHONDRIA FACILITATE VASCULAR INFLAMMATION: THE ROLE OF CANONICAL INFLAMMATORY SIGNALING IN THE REGULATION OF MITOCHONDRIAL MORPHOLOGY. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,429386

Chicago Manual of Style (16th Edition):

Forrester, Steven James. “MITOCHONDRIA FACILITATE VASCULAR INFLAMMATION: THE ROLE OF CANONICAL INFLAMMATORY SIGNALING IN THE REGULATION OF MITOCHONDRIAL MORPHOLOGY.” 2017. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,429386.

MLA Handbook (7th Edition):

Forrester, Steven James. “MITOCHONDRIA FACILITATE VASCULAR INFLAMMATION: THE ROLE OF CANONICAL INFLAMMATORY SIGNALING IN THE REGULATION OF MITOCHONDRIAL MORPHOLOGY.” 2017. Web. 17 Aug 2019.

Vancouver:

Forrester SJ. MITOCHONDRIA FACILITATE VASCULAR INFLAMMATION: THE ROLE OF CANONICAL INFLAMMATORY SIGNALING IN THE REGULATION OF MITOCHONDRIAL MORPHOLOGY. [Internet] [Doctoral dissertation]. Temple University; 2017. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,429386.

Council of Science Editors:

Forrester SJ. MITOCHONDRIA FACILITATE VASCULAR INFLAMMATION: THE ROLE OF CANONICAL INFLAMMATORY SIGNALING IN THE REGULATION OF MITOCHONDRIAL MORPHOLOGY. [Doctoral Dissertation]. Temple University; 2017. Available from: http://digital.library.temple.edu/u?/p245801coll10,429386


Temple University

27. Ray, Mitali. Genetic Deletion of Interleukin-19 Exacerbates Atherogenesis in Double Knockout Mice by Modulation of mRNA Stability Protein HuR.

Degree: PhD, 2018, Temple University

Biomedical Sciences

Objective: To test the hypothesis that loss of IL-19 exacerbates atherosclerosis. Approach and Results: Il19-/- mice were crossed into Ldlr-/- mice. Double knockout… (more)

Subjects/Keywords: Biology;

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APA (6th Edition):

Ray, M. (2018). Genetic Deletion of Interleukin-19 Exacerbates Atherogenesis in Double Knockout Mice by Modulation of mRNA Stability Protein HuR. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,491387

Chicago Manual of Style (16th Edition):

Ray, Mitali. “Genetic Deletion of Interleukin-19 Exacerbates Atherogenesis in Double Knockout Mice by Modulation of mRNA Stability Protein HuR.” 2018. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,491387.

MLA Handbook (7th Edition):

Ray, Mitali. “Genetic Deletion of Interleukin-19 Exacerbates Atherogenesis in Double Knockout Mice by Modulation of mRNA Stability Protein HuR.” 2018. Web. 17 Aug 2019.

Vancouver:

Ray M. Genetic Deletion of Interleukin-19 Exacerbates Atherogenesis in Double Knockout Mice by Modulation of mRNA Stability Protein HuR. [Internet] [Doctoral dissertation]. Temple University; 2018. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,491387.

Council of Science Editors:

Ray M. Genetic Deletion of Interleukin-19 Exacerbates Atherogenesis in Double Knockout Mice by Modulation of mRNA Stability Protein HuR. [Doctoral Dissertation]. Temple University; 2018. Available from: http://digital.library.temple.edu/u?/p245801coll10,491387


Temple University

28. Harper, Shavonn Christine. The Effects of Growth Differentiation Factor 11 on Pathological Cardiac Hypertrophy.

Degree: PhD, 2018, Temple University

Biomedical Sciences

Pathological cardiac hypertrophy (PCH) occurs in response to pathological stimuli affecting the heart such as coronary artery disease, myocardial infarction, or hypertension. PCH… (more)

Subjects/Keywords: Physiology;

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APA (6th Edition):

Harper, S. C. (2018). The Effects of Growth Differentiation Factor 11 on Pathological Cardiac Hypertrophy. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,498061

Chicago Manual of Style (16th Edition):

Harper, Shavonn Christine. “The Effects of Growth Differentiation Factor 11 on Pathological Cardiac Hypertrophy.” 2018. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,498061.

MLA Handbook (7th Edition):

Harper, Shavonn Christine. “The Effects of Growth Differentiation Factor 11 on Pathological Cardiac Hypertrophy.” 2018. Web. 17 Aug 2019.

Vancouver:

Harper SC. The Effects of Growth Differentiation Factor 11 on Pathological Cardiac Hypertrophy. [Internet] [Doctoral dissertation]. Temple University; 2018. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,498061.

Council of Science Editors:

Harper SC. The Effects of Growth Differentiation Factor 11 on Pathological Cardiac Hypertrophy. [Doctoral Dissertation]. Temple University; 2018. Available from: http://digital.library.temple.edu/u?/p245801coll10,498061


Temple University

29. Etwebi, Zienab. MYELOPEROXIDASE INDUCES ENDOTHELIAL DYSFUNCTION VIA ACTIVATION OF THE CALCIUM DEPENDENT PROTEASE CALPAIN.

Degree: PhD, 2018, Temple University

Biomedical Sciences

Cardiovascular disease and the associated endothelial dysfunction are characterized by leukocyte activation, decrease endothelial nitric oxide synthase (eNOS) activity, and increased endothelial cell… (more)

Subjects/Keywords: Physiology; Cellular biology;

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

APA (6th Edition):

Etwebi, Z. (2018). MYELOPEROXIDASE INDUCES ENDOTHELIAL DYSFUNCTION VIA ACTIVATION OF THE CALCIUM DEPENDENT PROTEASE CALPAIN. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,508536

Chicago Manual of Style (16th Edition):

Etwebi, Zienab. “MYELOPEROXIDASE INDUCES ENDOTHELIAL DYSFUNCTION VIA ACTIVATION OF THE CALCIUM DEPENDENT PROTEASE CALPAIN.” 2018. Doctoral Dissertation, Temple University. Accessed August 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,508536.

MLA Handbook (7th Edition):

Etwebi, Zienab. “MYELOPEROXIDASE INDUCES ENDOTHELIAL DYSFUNCTION VIA ACTIVATION OF THE CALCIUM DEPENDENT PROTEASE CALPAIN.” 2018. Web. 17 Aug 2019.

Vancouver:

Etwebi Z. MYELOPEROXIDASE INDUCES ENDOTHELIAL DYSFUNCTION VIA ACTIVATION OF THE CALCIUM DEPENDENT PROTEASE CALPAIN. [Internet] [Doctoral dissertation]. Temple University; 2018. [cited 2019 Aug 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,508536.

Council of Science Editors:

Etwebi Z. MYELOPEROXIDASE INDUCES ENDOTHELIAL DYSFUNCTION VIA ACTIVATION OF THE CALCIUM DEPENDENT PROTEASE CALPAIN. [Doctoral Dissertation]. Temple University; 2018. Available from: http://digital.library.temple.edu/u?/p245801coll10,508536

.