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You searched for +publisher:"Temple University" +contributor:("Tilley, Douglas;"). Showing records 1 – 5 of 5 total matches.

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Temple University

1. Wasilewski, Melissa Anne. ABSENCE OF V1AR ALTERS CARDIAC FUNCTION AT BASELINE AND FOLLOWING ACUTE CARDIAC INJURY.

Degree: PhD, 2018, Temple University

Biomedical Sciences

Heart failure (HF) is a prevalent disease affecting over 5.1 million people in the United States and over 23 million people worldwide. Many… (more)

Subjects/Keywords: Molecular biology; Cellular biology

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APA (6th Edition):

Wasilewski, M. A. (2018). ABSENCE OF V1AR ALTERS CARDIAC FUNCTION AT BASELINE AND FOLLOWING ACUTE CARDIAC INJURY. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,525634

Chicago Manual of Style (16th Edition):

Wasilewski, Melissa Anne. “ABSENCE OF V1AR ALTERS CARDIAC FUNCTION AT BASELINE AND FOLLOWING ACUTE CARDIAC INJURY.” 2018. Doctoral Dissertation, Temple University. Accessed July 02, 2020. http://digital.library.temple.edu/u?/p245801coll10,525634.

MLA Handbook (7th Edition):

Wasilewski, Melissa Anne. “ABSENCE OF V1AR ALTERS CARDIAC FUNCTION AT BASELINE AND FOLLOWING ACUTE CARDIAC INJURY.” 2018. Web. 02 Jul 2020.

Vancouver:

Wasilewski MA. ABSENCE OF V1AR ALTERS CARDIAC FUNCTION AT BASELINE AND FOLLOWING ACUTE CARDIAC INJURY. [Internet] [Doctoral dissertation]. Temple University; 2018. [cited 2020 Jul 02]. Available from: http://digital.library.temple.edu/u?/p245801coll10,525634.

Council of Science Editors:

Wasilewski MA. ABSENCE OF V1AR ALTERS CARDIAC FUNCTION AT BASELINE AND FOLLOWING ACUTE CARDIAC INJURY. [Doctoral Dissertation]. Temple University; 2018. Available from: http://digital.library.temple.edu/u?/p245801coll10,525634


Temple University

2. Li, Xinyuan. Mitochondrial Reactive Oxygen Species Mediate Lysophosphatidylcholine-induced Endothelial Cell Activation.

Degree: PhD, 2015, Temple University

Pharmacology

Lysophosphatidylcholines (LPCs) are a class of pro-inflammatory lipids that play important roles in atherogenesis. LPC activates endothelial cells (ECs) to upregulate adhesion molecules, cytokines… (more)

Subjects/Keywords: Pharmacology; Immunology; Cellular biology;

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APA (6th Edition):

Li, X. (2015). Mitochondrial Reactive Oxygen Species Mediate Lysophosphatidylcholine-induced Endothelial Cell Activation. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,320473

Chicago Manual of Style (16th Edition):

Li, Xinyuan. “Mitochondrial Reactive Oxygen Species Mediate Lysophosphatidylcholine-induced Endothelial Cell Activation.” 2015. Doctoral Dissertation, Temple University. Accessed July 02, 2020. http://digital.library.temple.edu/u?/p245801coll10,320473.

MLA Handbook (7th Edition):

Li, Xinyuan. “Mitochondrial Reactive Oxygen Species Mediate Lysophosphatidylcholine-induced Endothelial Cell Activation.” 2015. Web. 02 Jul 2020.

Vancouver:

Li X. Mitochondrial Reactive Oxygen Species Mediate Lysophosphatidylcholine-induced Endothelial Cell Activation. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2020 Jul 02]. Available from: http://digital.library.temple.edu/u?/p245801coll10,320473.

Council of Science Editors:

Li X. Mitochondrial Reactive Oxygen Species Mediate Lysophosphatidylcholine-induced Endothelial Cell Activation. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,320473


Temple University

3. Woodall, Benjamin Philip. NOVEL ROLES FOR GRK2 IN METABOLIC HOMEOSTASIS AND SKELETAL MUSCLE PHYSIOLOGY.

Degree: PhD, 2016, Temple University

Biomedical Sciences

Over the past two decades, a vast body of research has demonstrated the importance of G protein-coupled receptor kinase 2 (GRK2) in the… (more)

Subjects/Keywords: Molecular biology;

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APA (6th Edition):

Woodall, B. P. (2016). NOVEL ROLES FOR GRK2 IN METABOLIC HOMEOSTASIS AND SKELETAL MUSCLE PHYSIOLOGY. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,391153

Chicago Manual of Style (16th Edition):

Woodall, Benjamin Philip. “NOVEL ROLES FOR GRK2 IN METABOLIC HOMEOSTASIS AND SKELETAL MUSCLE PHYSIOLOGY.” 2016. Doctoral Dissertation, Temple University. Accessed July 02, 2020. http://digital.library.temple.edu/u?/p245801coll10,391153.

MLA Handbook (7th Edition):

Woodall, Benjamin Philip. “NOVEL ROLES FOR GRK2 IN METABOLIC HOMEOSTASIS AND SKELETAL MUSCLE PHYSIOLOGY.” 2016. Web. 02 Jul 2020.

Vancouver:

Woodall BP. NOVEL ROLES FOR GRK2 IN METABOLIC HOMEOSTASIS AND SKELETAL MUSCLE PHYSIOLOGY. [Internet] [Doctoral dissertation]. Temple University; 2016. [cited 2020 Jul 02]. Available from: http://digital.library.temple.edu/u?/p245801coll10,391153.

Council of Science Editors:

Woodall BP. NOVEL ROLES FOR GRK2 IN METABOLIC HOMEOSTASIS AND SKELETAL MUSCLE PHYSIOLOGY. [Doctoral Dissertation]. Temple University; 2016. Available from: http://digital.library.temple.edu/u?/p245801coll10,391153


Temple University

4. Myers, Valerie. The Role of BAG3 in the Failing Heart.

Degree: PhD, 2018, Temple University

Biomedical Sciences

Heart disease has been the leading cause of death in the United States for more than 90 years. The leading cause of death… (more)

Subjects/Keywords: Cellular biology;

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

APA (6th Edition):

Myers, V. (2018). The Role of BAG3 in the Failing Heart. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,490584

Chicago Manual of Style (16th Edition):

Myers, Valerie. “The Role of BAG3 in the Failing Heart.” 2018. Doctoral Dissertation, Temple University. Accessed July 02, 2020. http://digital.library.temple.edu/u?/p245801coll10,490584.

MLA Handbook (7th Edition):

Myers, Valerie. “The Role of BAG3 in the Failing Heart.” 2018. Web. 02 Jul 2020.

Vancouver:

Myers V. The Role of BAG3 in the Failing Heart. [Internet] [Doctoral dissertation]. Temple University; 2018. [cited 2020 Jul 02]. Available from: http://digital.library.temple.edu/u?/p245801coll10,490584.

Council of Science Editors:

Myers V. The Role of BAG3 in the Failing Heart. [Doctoral Dissertation]. Temple University; 2018. Available from: http://digital.library.temple.edu/u?/p245801coll10,490584


Temple University

5. Chiu, Yi-Ting. STUDIES ON NEURITE OUTGROWTH AND RECEPTOR PHOSPHORYLATION FOLLOWING KAPPA OPIOID RECEPTOR ACTIVATION.

Degree: PhD, 2016, Temple University

Pharmacology

Kappa opioid receptor (KOPR) is involved in many physiological functions and pharmacological responses such as analgesia, anti-pruritic effect, sedation, motor incoordination and aversion (Simonin… (more)

Subjects/Keywords: Pharmacology;

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

APA (6th Edition):

Chiu, Y. (2016). STUDIES ON NEURITE OUTGROWTH AND RECEPTOR PHOSPHORYLATION FOLLOWING KAPPA OPIOID RECEPTOR ACTIVATION. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,384383

Chicago Manual of Style (16th Edition):

Chiu, Yi-Ting. “STUDIES ON NEURITE OUTGROWTH AND RECEPTOR PHOSPHORYLATION FOLLOWING KAPPA OPIOID RECEPTOR ACTIVATION.” 2016. Doctoral Dissertation, Temple University. Accessed July 02, 2020. http://digital.library.temple.edu/u?/p245801coll10,384383.

MLA Handbook (7th Edition):

Chiu, Yi-Ting. “STUDIES ON NEURITE OUTGROWTH AND RECEPTOR PHOSPHORYLATION FOLLOWING KAPPA OPIOID RECEPTOR ACTIVATION.” 2016. Web. 02 Jul 2020.

Vancouver:

Chiu Y. STUDIES ON NEURITE OUTGROWTH AND RECEPTOR PHOSPHORYLATION FOLLOWING KAPPA OPIOID RECEPTOR ACTIVATION. [Internet] [Doctoral dissertation]. Temple University; 2016. [cited 2020 Jul 02]. Available from: http://digital.library.temple.edu/u?/p245801coll10,384383.

Council of Science Editors:

Chiu Y. STUDIES ON NEURITE OUTGROWTH AND RECEPTOR PHOSPHORYLATION FOLLOWING KAPPA OPIOID RECEPTOR ACTIVATION. [Doctoral Dissertation]. Temple University; 2016. Available from: http://digital.library.temple.edu/u?/p245801coll10,384383

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