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You searched for +publisher:"Temple University" +contributor:("Tuma, Ronald F."). Showing records 1 – 9 of 9 total matches.

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Temple University

1. Mayanglambam, Azad. Regulation of Protein Kinases (Syk and PKC zeta) in platelets.

Degree: PhD, 2010, Temple University

Physiology

Platelets are crucial components of the hemostatic machinery of the body. When the endothelial continuity is disrupted due to injury or atherosclerotic plaque rupture,… (more)

Subjects/Keywords: Biology, Physiology; Biology, Molecular; Hemostasis; Platelets; Protein Kinase C; Signaling; Syk; Thrombosis

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

APA (6th Edition):

Mayanglambam, A. (2010). Regulation of Protein Kinases (Syk and PKC zeta) in platelets. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,91635

Chicago Manual of Style (16th Edition):

Mayanglambam, Azad. “Regulation of Protein Kinases (Syk and PKC zeta) in platelets.” 2010. Doctoral Dissertation, Temple University. Accessed September 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,91635.

MLA Handbook (7th Edition):

Mayanglambam, Azad. “Regulation of Protein Kinases (Syk and PKC zeta) in platelets.” 2010. Web. 17 Sep 2019.

Vancouver:

Mayanglambam A. Regulation of Protein Kinases (Syk and PKC zeta) in platelets. [Internet] [Doctoral dissertation]. Temple University; 2010. [cited 2019 Sep 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,91635.

Council of Science Editors:

Mayanglambam A. Regulation of Protein Kinases (Syk and PKC zeta) in platelets. [Doctoral Dissertation]. Temple University; 2010. Available from: http://digital.library.temple.edu/u?/p245801coll10,91635


Temple University

2. 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 September 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 Sep 2019.

Vancouver:

Kong W. THE ANTI-INFLAMMATORY EFFECTS OF DOCOSAHEXAENOIC ACID ON DENDRITIC CELLS. [Internet] [Doctoral dissertation]. Temple University; 2010. [cited 2019 Sep 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

3. 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 September 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 Sep 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 Sep 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

4. 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 September 17, 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. 17 Sep 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 Sep 17]. 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

5. Reichenbach, Zachary Wilmer. Modulation of the Endogenous Cannabinoid System to Attenuate Inflammation in Central Nervous System Injury.

Degree: PhD, 2015, Temple University

Physiology

In non-pathological states the central nervous system maintains a degree of immunological privilege. When illness or injury occur, this privilege can be lost and… (more)

Subjects/Keywords: Neurosciences; Immunology; Pharmacology;

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

APA (6th Edition):

Reichenbach, Z. W. (2015). Modulation of the Endogenous Cannabinoid System to Attenuate Inflammation in Central Nervous System Injury. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,253514

Chicago Manual of Style (16th Edition):

Reichenbach, Zachary Wilmer. “Modulation of the Endogenous Cannabinoid System to Attenuate Inflammation in Central Nervous System Injury.” 2015. Doctoral Dissertation, Temple University. Accessed September 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,253514.

MLA Handbook (7th Edition):

Reichenbach, Zachary Wilmer. “Modulation of the Endogenous Cannabinoid System to Attenuate Inflammation in Central Nervous System Injury.” 2015. Web. 17 Sep 2019.

Vancouver:

Reichenbach ZW. Modulation of the Endogenous Cannabinoid System to Attenuate Inflammation in Central Nervous System Injury. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Sep 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,253514.

Council of Science Editors:

Reichenbach ZW. Modulation of the Endogenous Cannabinoid System to Attenuate Inflammation in Central Nervous System Injury. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,253514


Temple University

6. Li, Hongbo. SELECTIVE CB2 RECEPTOR ACTIVATION AMELIORATES INFLAMMATION IN CENTRAL NERVOUS SYSTEM BY REDUCING TH17 CELL DIFFERENTIATION AND IMMUNE CELL ACCUMULATION.

Degree: PhD, 2014, Temple University

Physiology

Modulation of the endocannabinoid system by the administration of exogenous agonists and selective antagonists has been shown to have potential to attenuate the contribution… (more)

Subjects/Keywords: Immunology; Physiology;

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APA (6th Edition):

Li, H. (2014). SELECTIVE CB2 RECEPTOR ACTIVATION AMELIORATES INFLAMMATION IN CENTRAL NERVOUS SYSTEM BY REDUCING TH17 CELL DIFFERENTIATION AND IMMUNE CELL ACCUMULATION. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,288653

Chicago Manual of Style (16th Edition):

Li, Hongbo. “SELECTIVE CB2 RECEPTOR ACTIVATION AMELIORATES INFLAMMATION IN CENTRAL NERVOUS SYSTEM BY REDUCING TH17 CELL DIFFERENTIATION AND IMMUNE CELL ACCUMULATION.” 2014. Doctoral Dissertation, Temple University. Accessed September 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,288653.

MLA Handbook (7th Edition):

Li, Hongbo. “SELECTIVE CB2 RECEPTOR ACTIVATION AMELIORATES INFLAMMATION IN CENTRAL NERVOUS SYSTEM BY REDUCING TH17 CELL DIFFERENTIATION AND IMMUNE CELL ACCUMULATION.” 2014. Web. 17 Sep 2019.

Vancouver:

Li H. SELECTIVE CB2 RECEPTOR ACTIVATION AMELIORATES INFLAMMATION IN CENTRAL NERVOUS SYSTEM BY REDUCING TH17 CELL DIFFERENTIATION AND IMMUNE CELL ACCUMULATION. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2019 Sep 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,288653.

Council of Science Editors:

Li H. SELECTIVE CB2 RECEPTOR ACTIVATION AMELIORATES INFLAMMATION IN CENTRAL NERVOUS SYSTEM BY REDUCING TH17 CELL DIFFERENTIATION AND IMMUNE CELL ACCUMULATION. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,288653


Temple University

7. Meng, Shu. HYPERHOMOCYSTEINEMIA ACCELERATES THROMBOSIS THROUGH ICAM-1 DEPENDENT ENDOTHELIAL ACTIVATION AND DNA HYPOMETHYLATION.

Degree: PhD, 2013, Temple University

Pharmacology

Background: Hyperhomocysteinemia (HHcy) is an established risk factor for thrombotic diseases yet the underlying mechanism remain unclear. In this study we investigated the effect… (more)

Subjects/Keywords: Pharmacology;

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APA (6th Edition):

Meng, S. (2013). HYPERHOMOCYSTEINEMIA ACCELERATES THROMBOSIS THROUGH ICAM-1 DEPENDENT ENDOTHELIAL ACTIVATION AND DNA HYPOMETHYLATION. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,234268

Chicago Manual of Style (16th Edition):

Meng, Shu. “HYPERHOMOCYSTEINEMIA ACCELERATES THROMBOSIS THROUGH ICAM-1 DEPENDENT ENDOTHELIAL ACTIVATION AND DNA HYPOMETHYLATION.” 2013. Doctoral Dissertation, Temple University. Accessed September 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,234268.

MLA Handbook (7th Edition):

Meng, Shu. “HYPERHOMOCYSTEINEMIA ACCELERATES THROMBOSIS THROUGH ICAM-1 DEPENDENT ENDOTHELIAL ACTIVATION AND DNA HYPOMETHYLATION.” 2013. Web. 17 Sep 2019.

Vancouver:

Meng S. HYPERHOMOCYSTEINEMIA ACCELERATES THROMBOSIS THROUGH ICAM-1 DEPENDENT ENDOTHELIAL ACTIVATION AND DNA HYPOMETHYLATION. [Internet] [Doctoral dissertation]. Temple University; 2013. [cited 2019 Sep 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,234268.

Council of Science Editors:

Meng S. HYPERHOMOCYSTEINEMIA ACCELERATES THROMBOSIS THROUGH ICAM-1 DEPENDENT ENDOTHELIAL ACTIVATION AND DNA HYPOMETHYLATION. [Doctoral Dissertation]. Temple University; 2013. Available from: http://digital.library.temple.edu/u?/p245801coll10,234268


Temple University

8. 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 September 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 Sep 2019.

Vancouver:

Mao Y. ROLE OF PROTEASE-ACTIVATED RECEPTORS IN PLATELET ACTIVATION. [Internet] [Doctoral dissertation]. Temple University; 2009. [cited 2019 Sep 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

9. Gentile, Taylor Arthur. Investigations into the Role of Orexin (Hypocretin) and Dynorphin in Drug Seeking, Reinforcement, and Withdrawal.

Degree: PhD, 2018, Temple University

Biomedical Sciences

Psychostimulant dependence remains a major health and economic problem, leading to premature death and costing $181 billion annually in health care, crime, and… (more)

Subjects/Keywords: Neurosciences; Behavioral sciences; Pharmacology;

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APA (6th Edition):

Gentile, T. A. (2018). Investigations into the Role of Orexin (Hypocretin) and Dynorphin in Drug Seeking, Reinforcement, and Withdrawal. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,507530

Chicago Manual of Style (16th Edition):

Gentile, Taylor Arthur. “Investigations into the Role of Orexin (Hypocretin) and Dynorphin in Drug Seeking, Reinforcement, and Withdrawal.” 2018. Doctoral Dissertation, Temple University. Accessed September 17, 2019. http://digital.library.temple.edu/u?/p245801coll10,507530.

MLA Handbook (7th Edition):

Gentile, Taylor Arthur. “Investigations into the Role of Orexin (Hypocretin) and Dynorphin in Drug Seeking, Reinforcement, and Withdrawal.” 2018. Web. 17 Sep 2019.

Vancouver:

Gentile TA. Investigations into the Role of Orexin (Hypocretin) and Dynorphin in Drug Seeking, Reinforcement, and Withdrawal. [Internet] [Doctoral dissertation]. Temple University; 2018. [cited 2019 Sep 17]. Available from: http://digital.library.temple.edu/u?/p245801coll10,507530.

Council of Science Editors:

Gentile TA. Investigations into the Role of Orexin (Hypocretin) and Dynorphin in Drug Seeking, Reinforcement, and Withdrawal. [Doctoral Dissertation]. Temple University; 2018. Available from: http://digital.library.temple.edu/u?/p245801coll10,507530

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