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You searched for +publisher:"Temple University" +contributor:("Houser, Steven R.;"). Showing records 1 – 17 of 17 total matches.

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Temple University

1. 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 October 30, 2020. 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. 30 Oct 2020.

Vancouver:

Angert DW. Repair of the Injured Adult Heart Involves Resident Cardiac Stem Cell Derived New Myocytes. [Internet] [Doctoral dissertation]. Temple University; 2011. [cited 2020 Oct 30]. 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

2. Barr, Larry A. The Role of Calcium in the Regulation of Pathological Hypertrophy.

Degree: PhD, 2014, Temple University

Physiology

Pathological hypertrophy leads to cardiac dysfunction and heart failure. It is not clearly defined how this process occurs in the cardiomyocyte, or how the… (more)

Subjects/Keywords: Physiology; Molecular biology; Pharmacology;

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APA (6th Edition):

Barr, L. A. (2014). The Role of Calcium in the Regulation of Pathological Hypertrophy. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,254617

Chicago Manual of Style (16th Edition):

Barr, Larry A. “The Role of Calcium in the Regulation of Pathological Hypertrophy.” 2014. Doctoral Dissertation, Temple University. Accessed October 30, 2020. http://digital.library.temple.edu/u?/p245801coll10,254617.

MLA Handbook (7th Edition):

Barr, Larry A. “The Role of Calcium in the Regulation of Pathological Hypertrophy.” 2014. Web. 30 Oct 2020.

Vancouver:

Barr LA. The Role of Calcium in the Regulation of Pathological Hypertrophy. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2020 Oct 30]. Available from: http://digital.library.temple.edu/u?/p245801coll10,254617.

Council of Science Editors:

Barr LA. The Role of Calcium in the Regulation of Pathological Hypertrophy. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,254617


Temple University

3. 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 October 30, 2020. 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. 30 Oct 2020.

Vancouver:

Cuneo A. THERAPEUTIC MECHANISMS OF INTERLEUKIN-19 FOR VASCULAR PROLIFERATIVE DISEASES. [Internet] [Doctoral dissertation]. Temple University; 2012. [cited 2020 Oct 30]. 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

4. 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 October 30, 2020. 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. 30 Oct 2020.

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 2020 Oct 30]. 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

5. 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 October 30, 2020. 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. 30 Oct 2020.

Vancouver:

Ellison SP. THE EFFECTS OF INTERLEUKIN-19 ON ATTENUATION OF THE VASCULAR RESPONSE TO INJURY. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2020 Oct 30]. 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

6. 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 October 30, 2020. 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. 30 Oct 2020.

Vancouver:

Harper SC. The Effects of Growth Differentiation Factor 11 on Pathological Cardiac Hypertrophy. [Internet] [Doctoral dissertation]. Temple University; 2018. [cited 2020 Oct 30]. 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

7. 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 October 30, 2020. 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. 30 Oct 2020.

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 2020 Oct 30]. 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

8. Li, Yingxin. THE ROLES OF Cav3.1/a1G T-TYPE CALCIUM CHANNEL IN HEART RATE GENERATION, REGULATION AND CARDIAC ARRHYTHMIAS.

Degree: PhD, 2011, Temple University

Physiology

T-type Ca²+ channels (TTCCs) are expressed in cardiac pacemaker cells and conduction system of mammals. However, the roles of TTCCs in heart rate (HR)… (more)

Subjects/Keywords: Physiology; arrhythmia; Cav3.1/a1G; heart rate

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APA (6th Edition):

Li, Y. (2011). THE ROLES OF Cav3.1/a1G T-TYPE CALCIUM CHANNEL IN HEART RATE GENERATION, REGULATION AND CARDIAC ARRHYTHMIAS. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,151806

Chicago Manual of Style (16th Edition):

Li, Yingxin. “THE ROLES OF Cav3.1/a1G T-TYPE CALCIUM CHANNEL IN HEART RATE GENERATION, REGULATION AND CARDIAC ARRHYTHMIAS.” 2011. Doctoral Dissertation, Temple University. Accessed October 30, 2020. http://digital.library.temple.edu/u?/p245801coll10,151806.

MLA Handbook (7th Edition):

Li, Yingxin. “THE ROLES OF Cav3.1/a1G T-TYPE CALCIUM CHANNEL IN HEART RATE GENERATION, REGULATION AND CARDIAC ARRHYTHMIAS.” 2011. Web. 30 Oct 2020.

Vancouver:

Li Y. THE ROLES OF Cav3.1/a1G T-TYPE CALCIUM CHANNEL IN HEART RATE GENERATION, REGULATION AND CARDIAC ARRHYTHMIAS. [Internet] [Doctoral dissertation]. Temple University; 2011. [cited 2020 Oct 30]. Available from: http://digital.library.temple.edu/u?/p245801coll10,151806.

Council of Science Editors:

Li Y. THE ROLES OF Cav3.1/a1G T-TYPE CALCIUM CHANNEL IN HEART RATE GENERATION, REGULATION AND CARDIAC ARRHYTHMIAS. [Doctoral Dissertation]. Temple University; 2011. Available from: http://digital.library.temple.edu/u?/p245801coll10,151806


Temple University

9. Luongo, Timothy Scott. The Role of Mitochondrial Calcium Exchange in Cardiac Physiology and Disease.

Degree: PhD, 2017, Temple University

Biomedical Sciences

The high metabolic demand of the heart makes it essential that an efficient and tightly controlled system be in place to regulate energy… (more)

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

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APA (6th Edition):

Luongo, T. S. (2017). The Role of Mitochondrial Calcium Exchange in Cardiac Physiology and Disease. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,437718

Chicago Manual of Style (16th Edition):

Luongo, Timothy Scott. “The Role of Mitochondrial Calcium Exchange in Cardiac Physiology and Disease.” 2017. Doctoral Dissertation, Temple University. Accessed October 30, 2020. http://digital.library.temple.edu/u?/p245801coll10,437718.

MLA Handbook (7th Edition):

Luongo, Timothy Scott. “The Role of Mitochondrial Calcium Exchange in Cardiac Physiology and Disease.” 2017. Web. 30 Oct 2020.

Vancouver:

Luongo TS. The Role of Mitochondrial Calcium Exchange in Cardiac Physiology and Disease. [Internet] [Doctoral dissertation]. Temple University; 2017. [cited 2020 Oct 30]. Available from: http://digital.library.temple.edu/u?/p245801coll10,437718.

Council of Science Editors:

Luongo TS. The Role of Mitochondrial Calcium Exchange in Cardiac Physiology and Disease. [Doctoral Dissertation]. Temple University; 2017. Available from: http://digital.library.temple.edu/u?/p245801coll10,437718


Temple University

10. Makarewich, Catherine Anne. MICRODOMAIN BASED CALCIUM INFLUX PATHWAYS THAT REGULATE PATHOLOGICAL CARDIAC HYPERTROPHY AND CONTRACTILITY.

Degree: PhD, 2014, Temple University

Molecular and Cellular Physiology

Pathological cardiac stressors, including persistent hypertension or damage from ischemic heart disease, induce a chronic demand for enhanced contractile performance of… (more)

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

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APA (6th Edition):

Makarewich, C. A. (2014). MICRODOMAIN BASED CALCIUM INFLUX PATHWAYS THAT REGULATE PATHOLOGICAL CARDIAC HYPERTROPHY AND CONTRACTILITY. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,266828

Chicago Manual of Style (16th Edition):

Makarewich, Catherine Anne. “MICRODOMAIN BASED CALCIUM INFLUX PATHWAYS THAT REGULATE PATHOLOGICAL CARDIAC HYPERTROPHY AND CONTRACTILITY.” 2014. Doctoral Dissertation, Temple University. Accessed October 30, 2020. http://digital.library.temple.edu/u?/p245801coll10,266828.

MLA Handbook (7th Edition):

Makarewich, Catherine Anne. “MICRODOMAIN BASED CALCIUM INFLUX PATHWAYS THAT REGULATE PATHOLOGICAL CARDIAC HYPERTROPHY AND CONTRACTILITY.” 2014. Web. 30 Oct 2020.

Vancouver:

Makarewich CA. MICRODOMAIN BASED CALCIUM INFLUX PATHWAYS THAT REGULATE PATHOLOGICAL CARDIAC HYPERTROPHY AND CONTRACTILITY. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2020 Oct 30]. Available from: http://digital.library.temple.edu/u?/p245801coll10,266828.

Council of Science Editors:

Makarewich CA. MICRODOMAIN BASED CALCIUM INFLUX PATHWAYS THAT REGULATE PATHOLOGICAL CARDIAC HYPERTROPHY AND CONTRACTILITY. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,266828


Temple University

11. Powers, Jeffery. microRNA-21 as a Pro-Fibrotic Mediator in Right Ventricular Failure.

Degree: PhD, 2016, Temple University

Physiology

Historical emphasis on the left ventricle (LV) has left clinicians with a lack of efficacious right ventricle (RV)-specific therapies, and classical pharmacological interventions for… (more)

Subjects/Keywords: Physiology

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APA (6th Edition):

Powers, J. (2016). microRNA-21 as a Pro-Fibrotic Mediator in Right Ventricular Failure. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,417461

Chicago Manual of Style (16th Edition):

Powers, Jeffery. “microRNA-21 as a Pro-Fibrotic Mediator in Right Ventricular Failure.” 2016. Doctoral Dissertation, Temple University. Accessed October 30, 2020. http://digital.library.temple.edu/u?/p245801coll10,417461.

MLA Handbook (7th Edition):

Powers, Jeffery. “microRNA-21 as a Pro-Fibrotic Mediator in Right Ventricular Failure.” 2016. Web. 30 Oct 2020.

Vancouver:

Powers J. microRNA-21 as a Pro-Fibrotic Mediator in Right Ventricular Failure. [Internet] [Doctoral dissertation]. Temple University; 2016. [cited 2020 Oct 30]. Available from: http://digital.library.temple.edu/u?/p245801coll10,417461.

Council of Science Editors:

Powers J. microRNA-21 as a Pro-Fibrotic Mediator in Right Ventricular Failure. [Doctoral Dissertation]. Temple University; 2016. Available from: http://digital.library.temple.edu/u?/p245801coll10,417461


Temple University

12. 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 October 30, 2020. 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. 30 Oct 2020.

Vancouver:

Preston KJ. Macronutrient Activation of Endothelium Dependent Leukocyte Trafficking: Metabolic Implications. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2020 Oct 30]. 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

13. Sharp III, Thomas E. DRUG AND CELL–BASED THERAPIES TO REDUCE PATHOLOGICAL REMODELING AND CARDIAC DYSFUNCTION AFTER ACUTE MYOCARDIAL INFARCTION.

Degree: PhD, 2017, Temple University

Physiology

Remarkable advances have been made in the treatment of cardiovascular diseases (CVD), however, CVD still accounts for the most deaths in industrialized nations. Ischemic… (more)

Subjects/Keywords: Physiology;

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APA (6th Edition):

Sharp III, T. E. (2017). DRUG AND CELL–BASED THERAPIES TO REDUCE PATHOLOGICAL REMODELING AND CARDIAC DYSFUNCTION AFTER ACUTE MYOCARDIAL INFARCTION. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,445275

Chicago Manual of Style (16th Edition):

Sharp III, Thomas E. “DRUG AND CELL–BASED THERAPIES TO REDUCE PATHOLOGICAL REMODELING AND CARDIAC DYSFUNCTION AFTER ACUTE MYOCARDIAL INFARCTION.” 2017. Doctoral Dissertation, Temple University. Accessed October 30, 2020. http://digital.library.temple.edu/u?/p245801coll10,445275.

MLA Handbook (7th Edition):

Sharp III, Thomas E. “DRUG AND CELL–BASED THERAPIES TO REDUCE PATHOLOGICAL REMODELING AND CARDIAC DYSFUNCTION AFTER ACUTE MYOCARDIAL INFARCTION.” 2017. Web. 30 Oct 2020.

Vancouver:

Sharp III TE. DRUG AND CELL–BASED THERAPIES TO REDUCE PATHOLOGICAL REMODELING AND CARDIAC DYSFUNCTION AFTER ACUTE MYOCARDIAL INFARCTION. [Internet] [Doctoral dissertation]. Temple University; 2017. [cited 2020 Oct 30]. Available from: http://digital.library.temple.edu/u?/p245801coll10,445275.

Council of Science Editors:

Sharp III TE. DRUG AND CELL–BASED THERAPIES TO REDUCE PATHOLOGICAL REMODELING AND CARDIAC DYSFUNCTION AFTER ACUTE MYOCARDIAL INFARCTION. [Doctoral Dissertation]. Temple University; 2017. Available from: http://digital.library.temple.edu/u?/p245801coll10,445275


Temple University

14. 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 October 30, 2020. 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. 30 Oct 2020.

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 2020 Oct 30]. 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

15. Troupes, Constantine. The Role of STIM1 in Hypertrophy-Related Contractile Dysfunction.

Degree: PhD, 2016, Temple University

Biomedical Sciences

Increases in cardiac afterload caused by disease conditions results in remodeling of heart structure by hypertrophy and alterations in the molecular regulation of… (more)

Subjects/Keywords: Physiology;

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

APA (6th Edition):

Troupes, C. (2016). The Role of STIM1 in Hypertrophy-Related Contractile Dysfunction. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,403786

Chicago Manual of Style (16th Edition):

Troupes, Constantine. “The Role of STIM1 in Hypertrophy-Related Contractile Dysfunction.” 2016. Doctoral Dissertation, Temple University. Accessed October 30, 2020. http://digital.library.temple.edu/u?/p245801coll10,403786.

MLA Handbook (7th Edition):

Troupes, Constantine. “The Role of STIM1 in Hypertrophy-Related Contractile Dysfunction.” 2016. Web. 30 Oct 2020.

Vancouver:

Troupes C. The Role of STIM1 in Hypertrophy-Related Contractile Dysfunction. [Internet] [Doctoral dissertation]. Temple University; 2016. [cited 2020 Oct 30]. Available from: http://digital.library.temple.edu/u?/p245801coll10,403786.

Council of Science Editors:

Troupes C. The Role of STIM1 in Hypertrophy-Related Contractile Dysfunction. [Doctoral Dissertation]. Temple University; 2016. Available from: http://digital.library.temple.edu/u?/p245801coll10,403786


Temple University

16. Wang, Fang. DOES CALCIUM INFLUX THROUGH T-TYPE CALCIUM CHANNEL INDUCE CARDIOMYOCYTE PROLIFERATION?.

Degree: PhD, 2012, Temple University

Physiology

Cardiovascular disease remains the number one cause or mortally in the western world. Heart failure is the most rapidly growing cardiovascular disease (Hobbs, 2004;… (more)

Subjects/Keywords: Physiology; Calcium Current; Cardiomyocyte Proliferation; Electrophysiology; Flow Cytometry; Neonatal Mice Ventricular Cardiomyocyte; T-type calcium channel

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

APA (6th Edition):

Wang, F. (2012). DOES CALCIUM INFLUX THROUGH T-TYPE CALCIUM CHANNEL INDUCE CARDIOMYOCYTE PROLIFERATION?. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,214814

Chicago Manual of Style (16th Edition):

Wang, Fang. “DOES CALCIUM INFLUX THROUGH T-TYPE CALCIUM CHANNEL INDUCE CARDIOMYOCYTE PROLIFERATION?.” 2012. Doctoral Dissertation, Temple University. Accessed October 30, 2020. http://digital.library.temple.edu/u?/p245801coll10,214814.

MLA Handbook (7th Edition):

Wang, Fang. “DOES CALCIUM INFLUX THROUGH T-TYPE CALCIUM CHANNEL INDUCE CARDIOMYOCYTE PROLIFERATION?.” 2012. Web. 30 Oct 2020.

Vancouver:

Wang F. DOES CALCIUM INFLUX THROUGH T-TYPE CALCIUM CHANNEL INDUCE CARDIOMYOCYTE PROLIFERATION?. [Internet] [Doctoral dissertation]. Temple University; 2012. [cited 2020 Oct 30]. Available from: http://digital.library.temple.edu/u?/p245801coll10,214814.

Council of Science Editors:

Wang F. DOES CALCIUM INFLUX THROUGH T-TYPE CALCIUM CHANNEL INDUCE CARDIOMYOCYTE PROLIFERATION?. [Doctoral Dissertation]. Temple University; 2012. Available from: http://digital.library.temple.edu/u?/p245801coll10,214814


Temple University

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

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 October 30, 2020. 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. 30 Oct 2020.

Vancouver:

Zhang H. INCREASING MYOCYTE CONTRACTILITY EXACERBATES CARDIAC INJURY AND PUMP DYSFUNCTION AND ABLATION OF PHOSPHORYLATION. [Internet] [Doctoral dissertation]. Temple University; 2010. [cited 2020 Oct 30]. 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

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