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You searched for +publisher:"Temple University" +contributor:("Eguchi, Satoru;"). Showing records 1 – 18 of 18 total matches.

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Temple University

1. 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 June 20, 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. 20 Jun 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 Jun 20]. 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

2. Bhavaraju, Kamala. MOLECULAR PHYSIOLOGY OF THROMBOXANE A2 GENERATION IN PLATELETS.

Degree: PhD, 2010, Temple University

Molecular and Cellular Physiology

Cardiovascular diseases are a major cause of mortality and morbidity in the developed countries. Anti-platelet therapy is a cornerstone treatment for… (more)

Subjects/Keywords: Biology, Physiology; ADP Receptors; Anti-platelet Therapy; G12/13 Pathways; Platelets; Serum Thromboxane; Thrombin

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APA (6th Edition):

Bhavaraju, K. (2010). MOLECULAR PHYSIOLOGY OF THROMBOXANE A2 GENERATION IN PLATELETS. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,92746

Chicago Manual of Style (16th Edition):

Bhavaraju, Kamala. “MOLECULAR PHYSIOLOGY OF THROMBOXANE A2 GENERATION IN PLATELETS.” 2010. Doctoral Dissertation, Temple University. Accessed June 20, 2019. http://digital.library.temple.edu/u?/p245801coll10,92746.

MLA Handbook (7th Edition):

Bhavaraju, Kamala. “MOLECULAR PHYSIOLOGY OF THROMBOXANE A2 GENERATION IN PLATELETS.” 2010. Web. 20 Jun 2019.

Vancouver:

Bhavaraju K. MOLECULAR PHYSIOLOGY OF THROMBOXANE A2 GENERATION IN PLATELETS. [Internet] [Doctoral dissertation]. Temple University; 2010. [cited 2019 Jun 20]. Available from: http://digital.library.temple.edu/u?/p245801coll10,92746.

Council of Science Editors:

Bhavaraju K. MOLECULAR PHYSIOLOGY OF THROMBOXANE A2 GENERATION IN PLATELETS. [Doctoral Dissertation]. Temple University; 2010. Available from: http://digital.library.temple.edu/u?/p245801coll10,92746


Temple University

3. 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 June 20, 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. 20 Jun 2019.

Vancouver:

England RN. Cellular Mechanisms of the Anti-Inflammatory Effects of Interleukin-19. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Jun 20]. 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

4. Chari, Ramya. Molecular Mechanisms Underlying Differential Regulation of Platelet Dense Granule Secretion by Protein Kinase C delta.

Degree: PhD, 2010, Temple University

Physiology

Protein Kinase C delta (PKCδ) is expressed in platelets and activated downstream of protease-activated receptors (PAR)s and glycoprotein VI (GPVI) receptors. We evaluated the… (more)

Subjects/Keywords: Biology, Physiology; Biology, Cell; Biology, Molecular; Dense Granule Secretion; Phosphorylation; Platelets; Protein Kinase C; Signaling; Thrombosis

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APA (6th Edition):

Chari, R. (2010). Molecular Mechanisms Underlying Differential Regulation of Platelet Dense Granule Secretion by Protein Kinase C delta. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,77283

Chicago Manual of Style (16th Edition):

Chari, Ramya. “Molecular Mechanisms Underlying Differential Regulation of Platelet Dense Granule Secretion by Protein Kinase C delta.” 2010. Doctoral Dissertation, Temple University. Accessed June 20, 2019. http://digital.library.temple.edu/u?/p245801coll10,77283.

MLA Handbook (7th Edition):

Chari, Ramya. “Molecular Mechanisms Underlying Differential Regulation of Platelet Dense Granule Secretion by Protein Kinase C delta.” 2010. Web. 20 Jun 2019.

Vancouver:

Chari R. Molecular Mechanisms Underlying Differential Regulation of Platelet Dense Granule Secretion by Protein Kinase C delta. [Internet] [Doctoral dissertation]. Temple University; 2010. [cited 2019 Jun 20]. Available from: http://digital.library.temple.edu/u?/p245801coll10,77283.

Council of Science Editors:

Chari R. Molecular Mechanisms Underlying Differential Regulation of Platelet Dense Granule Secretion by Protein Kinase C delta. [Doctoral Dissertation]. Temple University; 2010. Available from: http://digital.library.temple.edu/u?/p245801coll10,77283


Temple University

5. 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 June 20, 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. 20 Jun 2019.

Vancouver:

Cuneo A. THERAPEUTIC MECHANISMS OF INTERLEUKIN-19 FOR VASCULAR PROLIFERATIVE DISEASES. [Internet] [Doctoral dissertation]. Temple University; 2012. [cited 2019 Jun 20]. 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

6. 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 June 20, 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. 20 Jun 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 Jun 20]. 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

7. Zhang, Hongyu. INCREASING MYOCYTE CONTRACTILITY EXACERBATES CARDIAC INJURY AND PUMP DYSFUNCTION AND ABLATION OF PHOSPHORYLATION.

Degree: PhD, 2010, Temple University

Physiology

Myocardial infarction (MI) leads to heart failure (HF) and premature death. The respective roles of myocyte death and depressed myocyte contractility in the induction… (more)

Subjects/Keywords: Biology, Physiology; cardiac function; cell death; heart failure; myocardial infarction; myocyte contractility; ryanodine receptor

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APA (6th Edition):

Zhang, H. (2010). INCREASING MYOCYTE CONTRACTILITY EXACERBATES CARDIAC INJURY AND PUMP DYSFUNCTION AND ABLATION OF PHOSPHORYLATION. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,90859

Chicago Manual of Style (16th Edition):

Zhang, Hongyu. “INCREASING MYOCYTE CONTRACTILITY EXACERBATES CARDIAC INJURY AND PUMP DYSFUNCTION AND ABLATION OF PHOSPHORYLATION.” 2010. Doctoral Dissertation, Temple University. Accessed June 20, 2019. http://digital.library.temple.edu/u?/p245801coll10,90859.

MLA Handbook (7th Edition):

Zhang, Hongyu. “INCREASING MYOCYTE CONTRACTILITY EXACERBATES CARDIAC INJURY AND PUMP DYSFUNCTION AND ABLATION OF PHOSPHORYLATION.” 2010. Web. 20 Jun 2019.

Vancouver:

Zhang H. INCREASING MYOCYTE CONTRACTILITY EXACERBATES CARDIAC INJURY AND PUMP DYSFUNCTION AND ABLATION OF PHOSPHORYLATION. [Internet] [Doctoral dissertation]. Temple University; 2010. [cited 2019 Jun 20]. Available from: http://digital.library.temple.edu/u?/p245801coll10,90859.

Council of Science Editors:

Zhang H. INCREASING MYOCYTE CONTRACTILITY EXACERBATES CARDIAC INJURY AND PUMP DYSFUNCTION AND ABLATION OF PHOSPHORYLATION. [Doctoral Dissertation]. Temple University; 2010. Available from: http://digital.library.temple.edu/u?/p245801coll10,90859


Temple University

8. Bynagari, Yamini Saraswathy. Molecular Physiology of Novel Class of Protein Kinase C isoforms in Platelets.

Degree: PhD, 2010, Temple University

Molecular and Cellular Physiology

Platelets are primary components of hemostasis. However, incongruous activation of platelets lead to thrombosis, which result in multiple cardio-vascular and cerebrovascular… (more)

Subjects/Keywords: Biology, Cell; Biology, Physiology; ADP receptors; Phosphatases; Platelet signaling; Protein Kinase C; thromboxane

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APA (6th Edition):

Bynagari, Y. S. (2010). Molecular Physiology of Novel Class of Protein Kinase C isoforms in Platelets. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,103230

Chicago Manual of Style (16th Edition):

Bynagari, Yamini Saraswathy. “Molecular Physiology of Novel Class of Protein Kinase C isoforms in Platelets.” 2010. Doctoral Dissertation, Temple University. Accessed June 20, 2019. http://digital.library.temple.edu/u?/p245801coll10,103230.

MLA Handbook (7th Edition):

Bynagari, Yamini Saraswathy. “Molecular Physiology of Novel Class of Protein Kinase C isoforms in Platelets.” 2010. Web. 20 Jun 2019.

Vancouver:

Bynagari YS. Molecular Physiology of Novel Class of Protein Kinase C isoforms in Platelets. [Internet] [Doctoral dissertation]. Temple University; 2010. [cited 2019 Jun 20]. Available from: http://digital.library.temple.edu/u?/p245801coll10,103230.

Council of Science Editors:

Bynagari YS. Molecular Physiology of Novel Class of Protein Kinase C isoforms in Platelets. [Doctoral Dissertation]. Temple University; 2010. Available from: http://digital.library.temple.edu/u?/p245801coll10,103230


Temple University

9. 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 June 20, 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. 20 Jun 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 Jun 20]. 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

10. 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 June 20, 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. 20 Jun 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 Jun 20]. 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

11. Ronca, Rich Daniel. The Cannabinoid-2 Receptor Agonist O-1966 Reverses Postischemic Learning and Memory Deficits Through Anti-Inflammatory Processes.

Degree: PhD, 2013, Temple University

Pharmacology

Ischemic stroke is the third leading cause of death and the leading cause of morbidity in the United States. Cognitive deficits, specifically with respect… (more)

Subjects/Keywords: Physiology

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APA (6th Edition):

Ronca, R. D. (2013). The Cannabinoid-2 Receptor Agonist O-1966 Reverses Postischemic Learning and Memory Deficits Through Anti-Inflammatory Processes. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,253154

Chicago Manual of Style (16th Edition):

Ronca, Rich Daniel. “The Cannabinoid-2 Receptor Agonist O-1966 Reverses Postischemic Learning and Memory Deficits Through Anti-Inflammatory Processes.” 2013. Doctoral Dissertation, Temple University. Accessed June 20, 2019. http://digital.library.temple.edu/u?/p245801coll10,253154.

MLA Handbook (7th Edition):

Ronca, Rich Daniel. “The Cannabinoid-2 Receptor Agonist O-1966 Reverses Postischemic Learning and Memory Deficits Through Anti-Inflammatory Processes.” 2013. Web. 20 Jun 2019.

Vancouver:

Ronca RD. The Cannabinoid-2 Receptor Agonist O-1966 Reverses Postischemic Learning and Memory Deficits Through Anti-Inflammatory Processes. [Internet] [Doctoral dissertation]. Temple University; 2013. [cited 2019 Jun 20]. Available from: http://digital.library.temple.edu/u?/p245801coll10,253154.

Council of Science Editors:

Ronca RD. The Cannabinoid-2 Receptor Agonist O-1966 Reverses Postischemic Learning and Memory Deficits Through Anti-Inflammatory Processes. [Doctoral Dissertation]. Temple University; 2013. Available from: http://digital.library.temple.edu/u?/p245801coll10,253154


Temple University

12. 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 June 20, 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. 20 Jun 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 Jun 20]. 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

13. Heayn, Michelle Diane. The Role of Caveolae in PECAM-1 Mechanotransduction.

Degree: PhD, 2014, Temple University

Physiology

Altered fluid flow, which is found in branches and curvatures of arteries, results in abnormal forces on the endothelial cells (EC). These forces have… (more)

Subjects/Keywords: Cellular biology; Molecular biology; Biomechanics;

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APA (6th Edition):

Heayn, M. D. (2014). The Role of Caveolae in PECAM-1 Mechanotransduction. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,263778

Chicago Manual of Style (16th Edition):

Heayn, Michelle Diane. “The Role of Caveolae in PECAM-1 Mechanotransduction.” 2014. Doctoral Dissertation, Temple University. Accessed June 20, 2019. http://digital.library.temple.edu/u?/p245801coll10,263778.

MLA Handbook (7th Edition):

Heayn, Michelle Diane. “The Role of Caveolae in PECAM-1 Mechanotransduction.” 2014. Web. 20 Jun 2019.

Vancouver:

Heayn MD. The Role of Caveolae in PECAM-1 Mechanotransduction. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2019 Jun 20]. Available from: http://digital.library.temple.edu/u?/p245801coll10,263778.

Council of Science Editors:

Heayn MD. The Role of Caveolae in PECAM-1 Mechanotransduction. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,263778


Temple University

14. Kim, Boa. EFFECTS OF LAMINAR SHEAR STRESS ON MITOCHONDRIAL DNA INTEGRITY IN ENDOTHELIAL CELLS.

Degree: PhD, 2014, Temple University

Kinesiology

Purpose/hypothesis: Regular practice of exercise is the most effective non-pharmacological intervention that improves vascular health, which is thought to be mediated by a repeated… (more)

Subjects/Keywords: Kinesiology; Physiology; Biology;

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APA (6th Edition):

Kim, B. (2014). EFFECTS OF LAMINAR SHEAR STRESS ON MITOCHONDRIAL DNA INTEGRITY IN ENDOTHELIAL CELLS. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,266464

Chicago Manual of Style (16th Edition):

Kim, Boa. “EFFECTS OF LAMINAR SHEAR STRESS ON MITOCHONDRIAL DNA INTEGRITY IN ENDOTHELIAL CELLS.” 2014. Doctoral Dissertation, Temple University. Accessed June 20, 2019. http://digital.library.temple.edu/u?/p245801coll10,266464.

MLA Handbook (7th Edition):

Kim, Boa. “EFFECTS OF LAMINAR SHEAR STRESS ON MITOCHONDRIAL DNA INTEGRITY IN ENDOTHELIAL CELLS.” 2014. Web. 20 Jun 2019.

Vancouver:

Kim B. EFFECTS OF LAMINAR SHEAR STRESS ON MITOCHONDRIAL DNA INTEGRITY IN ENDOTHELIAL CELLS. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2019 Jun 20]. Available from: http://digital.library.temple.edu/u?/p245801coll10,266464.

Council of Science Editors:

Kim B. EFFECTS OF LAMINAR SHEAR STRESS ON MITOCHONDRIAL DNA INTEGRITY IN ENDOTHELIAL CELLS. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,266464


Temple University

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

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 June 20, 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. 20 Jun 2019.

Vancouver:

Crawford KJ. THE ROLE OF CAVEOLAE IN THE FORMATION OF ABDOMINAL AORTIC ANEURYSMS. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Jun 20]. 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

16. Kim, Ji-Seok. Shear Stress-Induced SIRT1 Activation: Effects on Mitochondrial Biogenesis and Endothelial Senescence.

Degree: PhD, 2015, Temple University

Kinesiology

Vascular aging has been implicated in the etiology of many vascular diseases. A common process linking the vascular aging to the development of vascular… (more)

Subjects/Keywords: Kinesiology

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

APA (6th Edition):

Kim, J. (2015). Shear Stress-Induced SIRT1 Activation: Effects on Mitochondrial Biogenesis and Endothelial Senescence. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,356508

Chicago Manual of Style (16th Edition):

Kim, Ji-Seok. “Shear Stress-Induced SIRT1 Activation: Effects on Mitochondrial Biogenesis and Endothelial Senescence.” 2015. Doctoral Dissertation, Temple University. Accessed June 20, 2019. http://digital.library.temple.edu/u?/p245801coll10,356508.

MLA Handbook (7th Edition):

Kim, Ji-Seok. “Shear Stress-Induced SIRT1 Activation: Effects on Mitochondrial Biogenesis and Endothelial Senescence.” 2015. Web. 20 Jun 2019.

Vancouver:

Kim J. Shear Stress-Induced SIRT1 Activation: Effects on Mitochondrial Biogenesis and Endothelial Senescence. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Jun 20]. Available from: http://digital.library.temple.edu/u?/p245801coll10,356508.

Council of Science Editors:

Kim J. Shear Stress-Induced SIRT1 Activation: Effects on Mitochondrial Biogenesis and Endothelial Senescence. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,356508


Temple University

17. Zhang, Lixiao. HYPERHOMOCYSTEINEMIA ACCELERATES STROKE-INDUCED BRAIN INJURY VIA PROMOTING ENDOTHELIAL ACTIVATION AND INFLAMMATORY CELL INFILTRATION: THE ROLE OF ICAM1-MEDIATED NEUTROPHIL AND MONOCYTE INFILTRATION.

Degree: PhD, 2017, Temple University

Pharmacology

Background: Epidemiology, clinical trials and meta-analysis studies have established that Hyperhomocysteinemia (HHcy) is an independent risk factor for stroke. However, the exact molecular mechanism… (more)

Subjects/Keywords: Health sciences; Pharmacology; Biology;

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

APA (6th Edition):

Zhang, L. (2017). HYPERHOMOCYSTEINEMIA ACCELERATES STROKE-INDUCED BRAIN INJURY VIA PROMOTING ENDOTHELIAL ACTIVATION AND INFLAMMATORY CELL INFILTRATION: THE ROLE OF ICAM1-MEDIATED NEUTROPHIL AND MONOCYTE INFILTRATION. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,450002

Chicago Manual of Style (16th Edition):

Zhang, Lixiao. “HYPERHOMOCYSTEINEMIA ACCELERATES STROKE-INDUCED BRAIN INJURY VIA PROMOTING ENDOTHELIAL ACTIVATION AND INFLAMMATORY CELL INFILTRATION: THE ROLE OF ICAM1-MEDIATED NEUTROPHIL AND MONOCYTE INFILTRATION.” 2017. Doctoral Dissertation, Temple University. Accessed June 20, 2019. http://digital.library.temple.edu/u?/p245801coll10,450002.

MLA Handbook (7th Edition):

Zhang, Lixiao. “HYPERHOMOCYSTEINEMIA ACCELERATES STROKE-INDUCED BRAIN INJURY VIA PROMOTING ENDOTHELIAL ACTIVATION AND INFLAMMATORY CELL INFILTRATION: THE ROLE OF ICAM1-MEDIATED NEUTROPHIL AND MONOCYTE INFILTRATION.” 2017. Web. 20 Jun 2019.

Vancouver:

Zhang L. HYPERHOMOCYSTEINEMIA ACCELERATES STROKE-INDUCED BRAIN INJURY VIA PROMOTING ENDOTHELIAL ACTIVATION AND INFLAMMATORY CELL INFILTRATION: THE ROLE OF ICAM1-MEDIATED NEUTROPHIL AND MONOCYTE INFILTRATION. [Internet] [Doctoral dissertation]. Temple University; 2017. [cited 2019 Jun 20]. Available from: http://digital.library.temple.edu/u?/p245801coll10,450002.

Council of Science Editors:

Zhang L. HYPERHOMOCYSTEINEMIA ACCELERATES STROKE-INDUCED BRAIN INJURY VIA PROMOTING ENDOTHELIAL ACTIVATION AND INFLAMMATORY CELL INFILTRATION: THE ROLE OF ICAM1-MEDIATED NEUTROPHIL AND MONOCYTE INFILTRATION. [Doctoral Dissertation]. Temple University; 2017. Available from: http://digital.library.temple.edu/u?/p245801coll10,450002


Temple University

18. 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 June 20, 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. 20 Jun 2019.

Vancouver:

Etwebi Z. MYELOPEROXIDASE INDUCES ENDOTHELIAL DYSFUNCTION VIA ACTIVATION OF THE CALCIUM DEPENDENT PROTEASE CALPAIN. [Internet] [Doctoral dissertation]. Temple University; 2018. [cited 2019 Jun 20]. 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

.