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You searched for +publisher:"Temple University" +contributor:("Ganea, Doina"). Showing records 1 – 14 of 14 total matches.

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Temple University

1. Kocieda, Virginia Polonia. Prostaglandin E2-induced IL-23p19 is regulated by CREB and C/EBP beta in bone marrow derived dendritic cells.

Degree: PhD, 2013, Temple University

Microbiology and Immunology

We reported previously that prostaglandin E2 (PGE2) upregulates IL-23 in vitro in bone marrow-derived dendritic cells (DC), and in vivo in models… (more)

Subjects/Keywords: Immunology; Molecular biology; C/EBP; CREB; dendritic cell; IL-23; PGE2

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APA (6th Edition):

Kocieda, V. P. (2013). Prostaglandin E2-induced IL-23p19 is regulated by CREB and C/EBP beta in bone marrow derived dendritic cells. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,214805

Chicago Manual of Style (16th Edition):

Kocieda, Virginia Polonia. “Prostaglandin E2-induced IL-23p19 is regulated by CREB and C/EBP beta in bone marrow derived dendritic cells.” 2013. Doctoral Dissertation, Temple University. Accessed July 02, 2020. http://digital.library.temple.edu/u?/p245801coll10,214805.

MLA Handbook (7th Edition):

Kocieda, Virginia Polonia. “Prostaglandin E2-induced IL-23p19 is regulated by CREB and C/EBP beta in bone marrow derived dendritic cells.” 2013. Web. 02 Jul 2020.

Vancouver:

Kocieda VP. Prostaglandin E2-induced IL-23p19 is regulated by CREB and C/EBP beta in bone marrow derived dendritic cells. [Internet] [Doctoral dissertation]. Temple University; 2013. [cited 2020 Jul 02]. Available from: http://digital.library.temple.edu/u?/p245801coll10,214805.

Council of Science Editors:

Kocieda VP. Prostaglandin E2-induced IL-23p19 is regulated by CREB and C/EBP beta in bone marrow derived dendritic cells. [Doctoral Dissertation]. Temple University; 2013. Available from: http://digital.library.temple.edu/u?/p245801coll10,214805


Temple University

2. 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 July 02, 2020. 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. 02 Jul 2020.

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 2020 Jul 02]. 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

3. 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 July 02, 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. 02 Jul 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 Jul 02]. 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

4. Roberts, Sean Anthony. A GENE THERAPY APPROACH TO THE INHIBITION OF HIV-1 REPLICATION BY RESTORATION OF INNATE ANTIVIRAL DEFENSE PATHWAYS.

Degree: PhD, 2010, Temple University

Microbiology and Immunology

Since it emerged as an infectious agent in 1981, the human immunodeficiency virus type 1 (HIV-1) is continually disseminated and remain fatal… (more)

Subjects/Keywords: Biology, Microbiology; Biology, virology

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APA (6th Edition):

Roberts, S. A. (2010). A GENE THERAPY APPROACH TO THE INHIBITION OF HIV-1 REPLICATION BY RESTORATION OF INNATE ANTIVIRAL DEFENSE PATHWAYS. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,99935

Chicago Manual of Style (16th Edition):

Roberts, Sean Anthony. “A GENE THERAPY APPROACH TO THE INHIBITION OF HIV-1 REPLICATION BY RESTORATION OF INNATE ANTIVIRAL DEFENSE PATHWAYS.” 2010. Doctoral Dissertation, Temple University. Accessed July 02, 2020. http://digital.library.temple.edu/u?/p245801coll10,99935.

MLA Handbook (7th Edition):

Roberts, Sean Anthony. “A GENE THERAPY APPROACH TO THE INHIBITION OF HIV-1 REPLICATION BY RESTORATION OF INNATE ANTIVIRAL DEFENSE PATHWAYS.” 2010. Web. 02 Jul 2020.

Vancouver:

Roberts SA. A GENE THERAPY APPROACH TO THE INHIBITION OF HIV-1 REPLICATION BY RESTORATION OF INNATE ANTIVIRAL DEFENSE PATHWAYS. [Internet] [Doctoral dissertation]. Temple University; 2010. [cited 2020 Jul 02]. Available from: http://digital.library.temple.edu/u?/p245801coll10,99935.

Council of Science Editors:

Roberts SA. A GENE THERAPY APPROACH TO THE INHIBITION OF HIV-1 REPLICATION BY RESTORATION OF INNATE ANTIVIRAL DEFENSE PATHWAYS. [Doctoral Dissertation]. Temple University; 2010. Available from: http://digital.library.temple.edu/u?/p245801coll10,99935


Temple University

5. 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 July 02, 2020. 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. 02 Jul 2020.

Vancouver:

Kong W. THE ANTI-INFLAMMATORY EFFECTS OF DOCOSAHEXAENOIC ACID ON DENDRITIC CELLS. [Internet] [Doctoral dissertation]. Temple University; 2010. [cited 2020 Jul 02]. 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

6. 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 July 02, 2020. 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. 02 Jul 2020.

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 2020 Jul 02]. 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

7. Robinson, Rebecca Hartzell. Cannabinoid Receptor 2-Selective Ligands as Immunosuppressive Compounds: Utility in Graft Rejection.

Degree: PhD, 2014, Temple University

Microbiology and Immunology

Cannabinoids are known to have anti-inflammatory and immunomodulatory properties. Cannabinoid receptor 2 (CB2) is expressed mainly on leukocytes and is the receptor… (more)

Subjects/Keywords: Immunology

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APA (6th Edition):

Robinson, R. H. (2014). Cannabinoid Receptor 2-Selective Ligands as Immunosuppressive Compounds: Utility in Graft Rejection. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,246094

Chicago Manual of Style (16th Edition):

Robinson, Rebecca Hartzell. “Cannabinoid Receptor 2-Selective Ligands as Immunosuppressive Compounds: Utility in Graft Rejection.” 2014. Doctoral Dissertation, Temple University. Accessed July 02, 2020. http://digital.library.temple.edu/u?/p245801coll10,246094.

MLA Handbook (7th Edition):

Robinson, Rebecca Hartzell. “Cannabinoid Receptor 2-Selective Ligands as Immunosuppressive Compounds: Utility in Graft Rejection.” 2014. Web. 02 Jul 2020.

Vancouver:

Robinson RH. Cannabinoid Receptor 2-Selective Ligands as Immunosuppressive Compounds: Utility in Graft Rejection. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2020 Jul 02]. Available from: http://digital.library.temple.edu/u?/p245801coll10,246094.

Council of Science Editors:

Robinson RH. Cannabinoid Receptor 2-Selective Ligands as Immunosuppressive Compounds: Utility in Graft Rejection. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,246094


Temple University

8. Rapsinski, Glenn James. Immune Recognition of S. Typhimurium Biofilms via Amyloids and Extracellular DNA.

Degree: PhD, 2016, Temple University

Microbiology and Immunology

Salmonella enterica serovar Typhimurium is an important cause of gastroenteritis in the United States and the developing world. Biofilm growth is an… (more)

Subjects/Keywords: Microbiology; Immunology;

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APA (6th Edition):

Rapsinski, G. J. (2016). Immune Recognition of S. Typhimurium Biofilms via Amyloids and Extracellular DNA. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,273605

Chicago Manual of Style (16th Edition):

Rapsinski, Glenn James. “Immune Recognition of S. Typhimurium Biofilms via Amyloids and Extracellular DNA.” 2016. Doctoral Dissertation, Temple University. Accessed July 02, 2020. http://digital.library.temple.edu/u?/p245801coll10,273605.

MLA Handbook (7th Edition):

Rapsinski, Glenn James. “Immune Recognition of S. Typhimurium Biofilms via Amyloids and Extracellular DNA.” 2016. Web. 02 Jul 2020.

Vancouver:

Rapsinski GJ. Immune Recognition of S. Typhimurium Biofilms via Amyloids and Extracellular DNA. [Internet] [Doctoral dissertation]. Temple University; 2016. [cited 2020 Jul 02]. Available from: http://digital.library.temple.edu/u?/p245801coll10,273605.

Council of Science Editors:

Rapsinski GJ. Immune Recognition of S. Typhimurium Biofilms via Amyloids and Extracellular DNA. [Doctoral Dissertation]. Temple University; 2016. Available from: http://digital.library.temple.edu/u?/p245801coll10,273605


Temple University

9. 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 July 02, 2020. 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. 02 Jul 2020.

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 2020 Jul 02]. 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

10. Tashovski, Ivan. BAG6 as a Novel HIV-1 Host Factor.

Degree: PhD, 2016, Temple University

Microbiology and Immunology

The human immunodeficiency virus type-1 (HIV-1) is the major etiological agent of acquired immunodeficiency syndrome (AIDS), the cause of over 30 million… (more)

Subjects/Keywords: Microbiology; Virology; Molecular biology;

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APA (6th Edition):

Tashovski, I. (2016). BAG6 as a Novel HIV-1 Host Factor. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,420479

Chicago Manual of Style (16th Edition):

Tashovski, Ivan. “BAG6 as a Novel HIV-1 Host Factor.” 2016. Doctoral Dissertation, Temple University. Accessed July 02, 2020. http://digital.library.temple.edu/u?/p245801coll10,420479.

MLA Handbook (7th Edition):

Tashovski, Ivan. “BAG6 as a Novel HIV-1 Host Factor.” 2016. Web. 02 Jul 2020.

Vancouver:

Tashovski I. BAG6 as a Novel HIV-1 Host Factor. [Internet] [Doctoral dissertation]. Temple University; 2016. [cited 2020 Jul 02]. Available from: http://digital.library.temple.edu/u?/p245801coll10,420479.

Council of Science Editors:

Tashovski I. BAG6 as a Novel HIV-1 Host Factor. [Doctoral Dissertation]. Temple University; 2016. Available from: http://digital.library.temple.edu/u?/p245801coll10,420479


Temple University

11. Piaggio, Eduardo. The Role of PD-1 and Its Ligands in Mercury(Hg)-induced Autoimmunity.

Degree: PhD, 2009, Temple University

Microbiology and Immunology

The development of autoimmune diseases is frequently linked to exposure to environmental factors such as chemicals, drugs or infections. In the experimental… (more)

Subjects/Keywords: Health Sciences, Immunology; Autoimmunity; Mercury; PD-1

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APA (6th Edition):

Piaggio, E. (2009). The Role of PD-1 and Its Ligands in Mercury(Hg)-induced Autoimmunity. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,52042

Chicago Manual of Style (16th Edition):

Piaggio, Eduardo. “The Role of PD-1 and Its Ligands in Mercury(Hg)-induced Autoimmunity.” 2009. Doctoral Dissertation, Temple University. Accessed July 02, 2020. http://digital.library.temple.edu/u?/p245801coll10,52042.

MLA Handbook (7th Edition):

Piaggio, Eduardo. “The Role of PD-1 and Its Ligands in Mercury(Hg)-induced Autoimmunity.” 2009. Web. 02 Jul 2020.

Vancouver:

Piaggio E. The Role of PD-1 and Its Ligands in Mercury(Hg)-induced Autoimmunity. [Internet] [Doctoral dissertation]. Temple University; 2009. [cited 2020 Jul 02]. Available from: http://digital.library.temple.edu/u?/p245801coll10,52042.

Council of Science Editors:

Piaggio E. The Role of PD-1 and Its Ligands in Mercury(Hg)-induced Autoimmunity. [Doctoral Dissertation]. Temple University; 2009. Available from: http://digital.library.temple.edu/u?/p245801coll10,52042


Temple University

12. Finley, Matthew James. Molecular Basis for Kappa-Opioid Regulation of Chemokine Receptor Function.

Degree: PhD, 2009, Temple University

Molecular Biology and Genetics

Opioid receptor-mediated regulation of chemokine receptors is vital for the host immune response, development, and neurological function. Previous studies have demonstrated… (more)

Subjects/Keywords: Biology, Molecular; Biology, Genetics; Biology, Neuroscience; Chemokine; Expression; Interferon Regulatory Factor; Opioid, Regulation; STAT3

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APA (6th Edition):

Finley, M. J. (2009). Molecular Basis for Kappa-Opioid Regulation of Chemokine Receptor Function. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,62878

Chicago Manual of Style (16th Edition):

Finley, Matthew James. “Molecular Basis for Kappa-Opioid Regulation of Chemokine Receptor Function.” 2009. Doctoral Dissertation, Temple University. Accessed July 02, 2020. http://digital.library.temple.edu/u?/p245801coll10,62878.

MLA Handbook (7th Edition):

Finley, Matthew James. “Molecular Basis for Kappa-Opioid Regulation of Chemokine Receptor Function.” 2009. Web. 02 Jul 2020.

Vancouver:

Finley MJ. Molecular Basis for Kappa-Opioid Regulation of Chemokine Receptor Function. [Internet] [Doctoral dissertation]. Temple University; 2009. [cited 2020 Jul 02]. Available from: http://digital.library.temple.edu/u?/p245801coll10,62878.

Council of Science Editors:

Finley MJ. Molecular Basis for Kappa-Opioid Regulation of Chemokine Receptor Function. [Doctoral Dissertation]. Temple University; 2009. Available from: http://digital.library.temple.edu/u?/p245801coll10,62878


Temple University

13. Hooper, Kirsten Mary. PGE2 AND IL-27: NOVEL PROINFLAMMATORY MECHANISMS INVOLVING DENDRITIC CELLS AND TYPE 1 REGULATORY T CELLS.

Degree: PhD, 2017, Temple University

Microbiology and Immunology

Interleukin-27 (p28/EBI3) is an immunomodulatory cytokine expressed by activated antigen presenting cells. Although first discovered to be involved in Th1 cell differentiation,… (more)

Subjects/Keywords: Immunology;

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APA (6th Edition):

Hooper, K. M. (2017). PGE2 AND IL-27: NOVEL PROINFLAMMATORY MECHANISMS INVOLVING DENDRITIC CELLS AND TYPE 1 REGULATORY T CELLS. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,432693

Chicago Manual of Style (16th Edition):

Hooper, Kirsten Mary. “PGE2 AND IL-27: NOVEL PROINFLAMMATORY MECHANISMS INVOLVING DENDRITIC CELLS AND TYPE 1 REGULATORY T CELLS.” 2017. Doctoral Dissertation, Temple University. Accessed July 02, 2020. http://digital.library.temple.edu/u?/p245801coll10,432693.

MLA Handbook (7th Edition):

Hooper, Kirsten Mary. “PGE2 AND IL-27: NOVEL PROINFLAMMATORY MECHANISMS INVOLVING DENDRITIC CELLS AND TYPE 1 REGULATORY T CELLS.” 2017. Web. 02 Jul 2020.

Vancouver:

Hooper KM. PGE2 AND IL-27: NOVEL PROINFLAMMATORY MECHANISMS INVOLVING DENDRITIC CELLS AND TYPE 1 REGULATORY T CELLS. [Internet] [Doctoral dissertation]. Temple University; 2017. [cited 2020 Jul 02]. Available from: http://digital.library.temple.edu/u?/p245801coll10,432693.

Council of Science Editors:

Hooper KM. PGE2 AND IL-27: NOVEL PROINFLAMMATORY MECHANISMS INVOLVING DENDRITIC CELLS AND TYPE 1 REGULATORY T CELLS. [Doctoral Dissertation]. Temple University; 2017. Available from: http://digital.library.temple.edu/u?/p245801coll10,432693


Temple University

14. Gallo, Paul Matthew. The Dendritic Cell Response to Exogenous and Endogenous Danger Signals.

Degree: PhD, 2017, Temple University

Microbiology and Immunology

Systemic lupus erythematosus (SLE) is complex autoimmune disease in which autoantibodies form against double stranded DNA (dsDNA) and nuclear antigens. Autoantigen immune… (more)

Subjects/Keywords: Biomechanics; Accounting;

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

APA (6th Edition):

Gallo, P. M. (2017). The Dendritic Cell Response to Exogenous and Endogenous Danger Signals. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,452916

Chicago Manual of Style (16th Edition):

Gallo, Paul Matthew. “The Dendritic Cell Response to Exogenous and Endogenous Danger Signals.” 2017. Doctoral Dissertation, Temple University. Accessed July 02, 2020. http://digital.library.temple.edu/u?/p245801coll10,452916.

MLA Handbook (7th Edition):

Gallo, Paul Matthew. “The Dendritic Cell Response to Exogenous and Endogenous Danger Signals.” 2017. Web. 02 Jul 2020.

Vancouver:

Gallo PM. The Dendritic Cell Response to Exogenous and Endogenous Danger Signals. [Internet] [Doctoral dissertation]. Temple University; 2017. [cited 2020 Jul 02]. Available from: http://digital.library.temple.edu/u?/p245801coll10,452916.

Council of Science Editors:

Gallo PM. The Dendritic Cell Response to Exogenous and Endogenous Danger Signals. [Doctoral Dissertation]. Temple University; 2017. Available from: http://digital.library.temple.edu/u?/p245801coll10,452916

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