Advanced search options

Advanced Search Options 🞨

Browse by author name (“Author name starts with…”).

Find ETDs with:

in
/  
in
/  
in
/  
in

Written in Published in Earliest date Latest date

Sorted by

Results per page:

Sorted by: relevance · author · university · dateNew search

You searched for +publisher:"Temple University" +contributor:("Ashby, Barrie"). Showing records 1 – 30 of 32 total matches.

[1] [2]

Search Limiters

Last 2 Years | English Only

▼ Search Limiters


Temple University

1. Giannopoulos, Phillip Fotis. THE ROLE OF 5-LIPOXYGENASE IN THE DEVELOPMENT OF TAU NEUROPATHOLOGY AND BEHAVIORAL PHENOTYPE.

Degree: PhD, 2015, Temple University

Pharmacology

5-Lipoxygenase (5LO) is a lipid-peroxidizing enzyme which inserts molecular oxygen into fatty acids leading to the biosynthesis of leukotrienes. This protein is widely expressed… (more)

Subjects/Keywords: Neurosciences;

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Giannopoulos, P. F. (2015). THE ROLE OF 5-LIPOXYGENASE IN THE DEVELOPMENT OF TAU NEUROPATHOLOGY AND BEHAVIORAL PHENOTYPE. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,315193

Chicago Manual of Style (16th Edition):

Giannopoulos, Phillip Fotis. “THE ROLE OF 5-LIPOXYGENASE IN THE DEVELOPMENT OF TAU NEUROPATHOLOGY AND BEHAVIORAL PHENOTYPE.” 2015. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,315193.

MLA Handbook (7th Edition):

Giannopoulos, Phillip Fotis. “THE ROLE OF 5-LIPOXYGENASE IN THE DEVELOPMENT OF TAU NEUROPATHOLOGY AND BEHAVIORAL PHENOTYPE.” 2015. Web. 06 Jun 2020.

Vancouver:

Giannopoulos PF. THE ROLE OF 5-LIPOXYGENASE IN THE DEVELOPMENT OF TAU NEUROPATHOLOGY AND BEHAVIORAL PHENOTYPE. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,315193.

Council of Science Editors:

Giannopoulos PF. THE ROLE OF 5-LIPOXYGENASE IN THE DEVELOPMENT OF TAU NEUROPATHOLOGY AND BEHAVIORAL PHENOTYPE. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,315193


Temple University

2. Di Donato, Francis Anthony. Determinants of compartmentalization of gene expression during sporulation in Bacillus subtilis.

Degree: 2008, Temple University

Microbiology and Immunology

Ph.D.;

Bacillus subtilis, a benign gram-positive bacterium, utilizes the strategy of sporulation, which enables it to survive stresses such as starvation, desiccation,… (more)

Subjects/Keywords: Biology; Microbiology

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Di Donato, F. A. (2008). Determinants of compartmentalization of gene expression during sporulation in Bacillus subtilis. (Thesis). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,4102

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Di Donato, Francis Anthony. “Determinants of compartmentalization of gene expression during sporulation in Bacillus subtilis.” 2008. Thesis, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,4102.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Di Donato, Francis Anthony. “Determinants of compartmentalization of gene expression during sporulation in Bacillus subtilis.” 2008. Web. 06 Jun 2020.

Vancouver:

Di Donato FA. Determinants of compartmentalization of gene expression during sporulation in Bacillus subtilis. [Internet] [Thesis]. Temple University; 2008. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,4102.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Di Donato FA. Determinants of compartmentalization of gene expression during sporulation in Bacillus subtilis. [Thesis]. Temple University; 2008. Available from: http://digital.library.temple.edu/u?/p245801coll10,4102

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


Temple University

3. Gardner, Jacob Andrew. GPCR Signaling in the Genesis and Progression of Pancreatic Cancer.

Degree: PhD, 2009, Temple University

Molecular Biology and Genetics

Ductal adenocarcinomas of the pancreas are the 4th most common cause of cancer death. The 1 and 5 year survival rates… (more)

Subjects/Keywords: Biology, Molecular; G alpha 13; GPCR; LPA; lysophosphatidic acid; Migration; Pancreatic Cancer

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Gardner, J. A. (2009). GPCR Signaling in the Genesis and Progression of Pancreatic Cancer. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,35453

Chicago Manual of Style (16th Edition):

Gardner, Jacob Andrew. “GPCR Signaling in the Genesis and Progression of Pancreatic Cancer.” 2009. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,35453.

MLA Handbook (7th Edition):

Gardner, Jacob Andrew. “GPCR Signaling in the Genesis and Progression of Pancreatic Cancer.” 2009. Web. 06 Jun 2020.

Vancouver:

Gardner JA. GPCR Signaling in the Genesis and Progression of Pancreatic Cancer. [Internet] [Doctoral dissertation]. Temple University; 2009. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,35453.

Council of Science Editors:

Gardner JA. GPCR Signaling in the Genesis and Progression of Pancreatic Cancer. [Doctoral Dissertation]. Temple University; 2009. Available from: http://digital.library.temple.edu/u?/p245801coll10,35453


Temple University

4. Pallai, Rajash. The CCAAT-box binding transcription factor, nuclear factor-Y (NF-Y) regulates transcription of human aldo-keto reductase 1C1 (AKR1C1) gene.

Degree: PhD, 2010, Temple University

Pathology

Dihydrodiol dehydrogenases are a family of aldo-keto reductases (AKR1Cs) involved in the metabolism of steroid hormones and xenobiotics. Whilst, several phase II drugs as… (more)

Subjects/Keywords: Biology, Molecular; Dihydrodiol dehydrogenase; Hydroxysteroid dehydrogenase; Liver hepatoblastoma; Lung adenocarcinoma; Ovarian carcinoma; Promoter regulation

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Pallai, R. (2010). The CCAAT-box binding transcription factor, nuclear factor-Y (NF-Y) regulates transcription of human aldo-keto reductase 1C1 (AKR1C1) gene. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,78307

Chicago Manual of Style (16th Edition):

Pallai, Rajash. “The CCAAT-box binding transcription factor, nuclear factor-Y (NF-Y) regulates transcription of human aldo-keto reductase 1C1 (AKR1C1) gene.” 2010. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,78307.

MLA Handbook (7th Edition):

Pallai, Rajash. “The CCAAT-box binding transcription factor, nuclear factor-Y (NF-Y) regulates transcription of human aldo-keto reductase 1C1 (AKR1C1) gene.” 2010. Web. 06 Jun 2020.

Vancouver:

Pallai R. The CCAAT-box binding transcription factor, nuclear factor-Y (NF-Y) regulates transcription of human aldo-keto reductase 1C1 (AKR1C1) gene. [Internet] [Doctoral dissertation]. Temple University; 2010. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,78307.

Council of Science Editors:

Pallai R. The CCAAT-box binding transcription factor, nuclear factor-Y (NF-Y) regulates transcription of human aldo-keto reductase 1C1 (AKR1C1) gene. [Doctoral Dissertation]. Temple University; 2010. Available from: http://digital.library.temple.edu/u?/p245801coll10,78307


Temple University

5. Thomas, Dafydd Huw. Regulation of Syk activity in GPVI-mediated platelet activation.

Degree: PhD, 2010, Temple University

Pharmacology

Activation of platelets is essential for hemostasis. Following damage to the vascular endothelium collagen is exposed, to which platelets stably adhere. After adhesion on… (more)

Subjects/Keywords: Health Sciences, Pharmacology; Collagen; GPVI; Phosphatase; Platelets; Syk; TULA

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Thomas, D. H. (2010). Regulation of Syk activity in GPVI-mediated platelet activation. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,92028

Chicago Manual of Style (16th Edition):

Thomas, Dafydd Huw. “Regulation of Syk activity in GPVI-mediated platelet activation.” 2010. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,92028.

MLA Handbook (7th Edition):

Thomas, Dafydd Huw. “Regulation of Syk activity in GPVI-mediated platelet activation.” 2010. Web. 06 Jun 2020.

Vancouver:

Thomas DH. Regulation of Syk activity in GPVI-mediated platelet activation. [Internet] [Doctoral dissertation]. Temple University; 2010. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,92028.

Council of Science Editors:

Thomas DH. Regulation of Syk activity in GPVI-mediated platelet activation. [Doctoral Dissertation]. Temple University; 2010. Available from: http://digital.library.temple.edu/u?/p245801coll10,92028


Temple University

6. Deliu, Elena. GPER/GPR30 Estrogen Receptor: A Target for Pain Modulation.

Degree: PhD, 2012, Temple University

Pharmacology

The G protein-coupled estrogen receptor GPER/GPER1, also known as GPR30, was originally cloned as an orphan receptor and later shown to be specifically activated… (more)

Subjects/Keywords: Pharmacology; Biochemistry; calcium imaging; estrogen; gpr30; pain; reactive oxygen species

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Deliu, E. (2012). GPER/GPR30 Estrogen Receptor: A Target for Pain Modulation. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,194862

Chicago Manual of Style (16th Edition):

Deliu, Elena. “GPER/GPR30 Estrogen Receptor: A Target for Pain Modulation.” 2012. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,194862.

MLA Handbook (7th Edition):

Deliu, Elena. “GPER/GPR30 Estrogen Receptor: A Target for Pain Modulation.” 2012. Web. 06 Jun 2020.

Vancouver:

Deliu E. GPER/GPR30 Estrogen Receptor: A Target for Pain Modulation. [Internet] [Doctoral dissertation]. Temple University; 2012. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,194862.

Council of Science Editors:

Deliu E. GPER/GPR30 Estrogen Receptor: A Target for Pain Modulation. [Doctoral Dissertation]. Temple University; 2012. Available from: http://digital.library.temple.edu/u?/p245801coll10,194862


Temple University

7. Evans, Kyle William. PPAR gamma AND eNOS CONTRIBUTE TO THE RESOLUTION OF CHRONIC INFLAMMATION.

Degree: PhD, 2011, Temple University

Microbiology and Immunology

Chronic inflammation follows defined phases of induction, inflammation, and resolution. The resolution phase requires cycloxygenase-2 (COX-2) activity. This study aims to address… (more)

Subjects/Keywords: Biology; eNOS; inflammation; PPARgamma; resolution; rheumatoid arthrits

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Evans, K. W. (2011). PPAR gamma AND eNOS CONTRIBUTE TO THE RESOLUTION OF CHRONIC INFLAMMATION. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,197871

Chicago Manual of Style (16th Edition):

Evans, Kyle William. “PPAR gamma AND eNOS CONTRIBUTE TO THE RESOLUTION OF CHRONIC INFLAMMATION.” 2011. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,197871.

MLA Handbook (7th Edition):

Evans, Kyle William. “PPAR gamma AND eNOS CONTRIBUTE TO THE RESOLUTION OF CHRONIC INFLAMMATION.” 2011. Web. 06 Jun 2020.

Vancouver:

Evans KW. PPAR gamma AND eNOS CONTRIBUTE TO THE RESOLUTION OF CHRONIC INFLAMMATION. [Internet] [Doctoral dissertation]. Temple University; 2011. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,197871.

Council of Science Editors:

Evans KW. PPAR gamma AND eNOS CONTRIBUTE TO THE RESOLUTION OF CHRONIC INFLAMMATION. [Doctoral Dissertation]. Temple University; 2011. Available from: http://digital.library.temple.edu/u?/p245801coll10,197871


Temple University

8. Fang, Pu. HYPERHOMOCYSTEINEMIA ACCELERATES ATHEROSCLEROSIS BY INDUCING INFLAMMATORY MONOCYTE DIFFERENTIATION IN A HYPERGLYCEMIC MOUSE MODEL.

Degree: PhD, 2012, Temple University

Pharmacology

Homocysteine (Hcy) is a thiol amino acid formed upon methionine de - methylation. A number of studies have revealed an association between hyperhomocysteinemia (HHcy),… (more)

Subjects/Keywords: Pharmacology

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Fang, P. (2012). HYPERHOMOCYSTEINEMIA ACCELERATES ATHEROSCLEROSIS BY INDUCING INFLAMMATORY MONOCYTE DIFFERENTIATION IN A HYPERGLYCEMIC MOUSE MODEL. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,223888

Chicago Manual of Style (16th Edition):

Fang, Pu. “HYPERHOMOCYSTEINEMIA ACCELERATES ATHEROSCLEROSIS BY INDUCING INFLAMMATORY MONOCYTE DIFFERENTIATION IN A HYPERGLYCEMIC MOUSE MODEL.” 2012. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,223888.

MLA Handbook (7th Edition):

Fang, Pu. “HYPERHOMOCYSTEINEMIA ACCELERATES ATHEROSCLEROSIS BY INDUCING INFLAMMATORY MONOCYTE DIFFERENTIATION IN A HYPERGLYCEMIC MOUSE MODEL.” 2012. Web. 06 Jun 2020.

Vancouver:

Fang P. HYPERHOMOCYSTEINEMIA ACCELERATES ATHEROSCLEROSIS BY INDUCING INFLAMMATORY MONOCYTE DIFFERENTIATION IN A HYPERGLYCEMIC MOUSE MODEL. [Internet] [Doctoral dissertation]. Temple University; 2012. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,223888.

Council of Science Editors:

Fang P. HYPERHOMOCYSTEINEMIA ACCELERATES ATHEROSCLEROSIS BY INDUCING INFLAMMATORY MONOCYTE DIFFERENTIATION IN A HYPERGLYCEMIC MOUSE MODEL. [Doctoral Dissertation]. Temple University; 2012. Available from: http://digital.library.temple.edu/u?/p245801coll10,223888


Temple University

9. Pansuria, Meghanaben. EFFECT AND MECHANISM OF HYPERHOMOCYSTEINEMIA ON ENDOTHELIAL INSULIN SIGNALING.

Degree: PhD, 2013, Temple University

Pharmacology

Hyperhomocysteinemia (HHcy) is an independent risk factor for cardiovascular disease (CVD). Both HHcy and insulin resistance (IR) are associated with atherosclerotic CVD. Recent studies… (more)

Subjects/Keywords: Pharmacology

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Pansuria, M. (2013). EFFECT AND MECHANISM OF HYPERHOMOCYSTEINEMIA ON ENDOTHELIAL INSULIN SIGNALING. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,228447

Chicago Manual of Style (16th Edition):

Pansuria, Meghanaben. “EFFECT AND MECHANISM OF HYPERHOMOCYSTEINEMIA ON ENDOTHELIAL INSULIN SIGNALING.” 2013. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,228447.

MLA Handbook (7th Edition):

Pansuria, Meghanaben. “EFFECT AND MECHANISM OF HYPERHOMOCYSTEINEMIA ON ENDOTHELIAL INSULIN SIGNALING.” 2013. Web. 06 Jun 2020.

Vancouver:

Pansuria M. EFFECT AND MECHANISM OF HYPERHOMOCYSTEINEMIA ON ENDOTHELIAL INSULIN SIGNALING. [Internet] [Doctoral dissertation]. Temple University; 2013. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,228447.

Council of Science Editors:

Pansuria M. EFFECT AND MECHANISM OF HYPERHOMOCYSTEINEMIA ON ENDOTHELIAL INSULIN SIGNALING. [Doctoral Dissertation]. Temple University; 2013. Available from: http://digital.library.temple.edu/u?/p245801coll10,228447


Temple University

10. Yin, Ying. CASPASE-1 ACTIVATION IS CRITICAL FOR ENDOTHELIAL CELL ACTIVATION, MONOCYTE MIGRATION, AND EARLY ATHEROGENESIS.

Degree: PhD, 2013, Temple University

Pharmacology

Atherosclerosis, considered a chronic inflammatory disease, is the underlying mechanism for several cardiovascular diseases. Hyperlipidemia is the number one risk factor for atherogenesis. Caspase-1… (more)

Subjects/Keywords: Pharmacology; atherosclerosis, caspase-1, vascular inflammation

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Yin, Y. (2013). CASPASE-1 ACTIVATION IS CRITICAL FOR ENDOTHELIAL CELL ACTIVATION, MONOCYTE MIGRATION, AND EARLY ATHEROGENESIS. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,252725

Chicago Manual of Style (16th Edition):

Yin, Ying. “CASPASE-1 ACTIVATION IS CRITICAL FOR ENDOTHELIAL CELL ACTIVATION, MONOCYTE MIGRATION, AND EARLY ATHEROGENESIS.” 2013. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,252725.

MLA Handbook (7th Edition):

Yin, Ying. “CASPASE-1 ACTIVATION IS CRITICAL FOR ENDOTHELIAL CELL ACTIVATION, MONOCYTE MIGRATION, AND EARLY ATHEROGENESIS.” 2013. Web. 06 Jun 2020.

Vancouver:

Yin Y. CASPASE-1 ACTIVATION IS CRITICAL FOR ENDOTHELIAL CELL ACTIVATION, MONOCYTE MIGRATION, AND EARLY ATHEROGENESIS. [Internet] [Doctoral dissertation]. Temple University; 2013. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,252725.

Council of Science Editors:

Yin Y. CASPASE-1 ACTIVATION IS CRITICAL FOR ENDOTHELIAL CELL ACTIVATION, MONOCYTE MIGRATION, AND EARLY ATHEROGENESIS. [Doctoral Dissertation]. Temple University; 2013. Available from: http://digital.library.temple.edu/u?/p245801coll10,252725


Temple University

11. Enman, Nicole Marie. Dopamine reward dysfunction and cocaine-seeking in a rat model of PTSD.

Degree: PhD, 2014, Temple University

Pharmacology

Posttraumatic stress disorder (PTSD) co-occurs with substance use disorders at high rates, but the neurobiological basis of this relationship remains largely unknown. Identifying mechanisms… (more)

Subjects/Keywords: Neurosciences; Animal behavior; Pharmacology;

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Enman, N. M. (2014). Dopamine reward dysfunction and cocaine-seeking in a rat model of PTSD. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,259963

Chicago Manual of Style (16th Edition):

Enman, Nicole Marie. “Dopamine reward dysfunction and cocaine-seeking in a rat model of PTSD.” 2014. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,259963.

MLA Handbook (7th Edition):

Enman, Nicole Marie. “Dopamine reward dysfunction and cocaine-seeking in a rat model of PTSD.” 2014. Web. 06 Jun 2020.

Vancouver:

Enman NM. Dopamine reward dysfunction and cocaine-seeking in a rat model of PTSD. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,259963.

Council of Science Editors:

Enman NM. Dopamine reward dysfunction and cocaine-seeking in a rat model of PTSD. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,259963


Temple University

12. Jan, Michael. Novel Mechanisms Underlying Homocysteine-Suppressed Endothelial Cell Growth.

Degree: PhD, 2014, Temple University

Pharmacology

Cardiovascular disease (CVD) is the leading cause of death worldwide, and is projected to remain so for at least the next decade. Ever since… (more)

Subjects/Keywords: Pharmacology;

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Jan, M. (2014). Novel Mechanisms Underlying Homocysteine-Suppressed Endothelial Cell Growth. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,264103

Chicago Manual of Style (16th Edition):

Jan, Michael. “Novel Mechanisms Underlying Homocysteine-Suppressed Endothelial Cell Growth.” 2014. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,264103.

MLA Handbook (7th Edition):

Jan, Michael. “Novel Mechanisms Underlying Homocysteine-Suppressed Endothelial Cell Growth.” 2014. Web. 06 Jun 2020.

Vancouver:

Jan M. Novel Mechanisms Underlying Homocysteine-Suppressed Endothelial Cell Growth. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,264103.

Council of Science Editors:

Jan M. Novel Mechanisms Underlying Homocysteine-Suppressed Endothelial Cell Growth. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,264103


Temple University

13. Mai, Jietang. ROLE OF INTERLEUKIN-17 IN ENDOTHELIAL CELL ACTIVATION AND VASCULAR FUNCTION.

Degree: PhD, 2014, Temple University

Pharmacology

Endothelial cell (EC) activation is a change of the endothelium from a quiescent state to one that is involved in immune reactions. Activation of… (more)

Subjects/Keywords: Immunology; Physiology; Cellular biology;

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Mai, J. (2014). ROLE OF INTERLEUKIN-17 IN ENDOTHELIAL CELL ACTIVATION AND VASCULAR FUNCTION. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,266288

Chicago Manual of Style (16th Edition):

Mai, Jietang. “ROLE OF INTERLEUKIN-17 IN ENDOTHELIAL CELL ACTIVATION AND VASCULAR FUNCTION.” 2014. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,266288.

MLA Handbook (7th Edition):

Mai, Jietang. “ROLE OF INTERLEUKIN-17 IN ENDOTHELIAL CELL ACTIVATION AND VASCULAR FUNCTION.” 2014. Web. 06 Jun 2020.

Vancouver:

Mai J. ROLE OF INTERLEUKIN-17 IN ENDOTHELIAL CELL ACTIVATION AND VASCULAR FUNCTION. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,266288.

Council of Science Editors:

Mai J. ROLE OF INTERLEUKIN-17 IN ENDOTHELIAL CELL ACTIVATION AND VASCULAR FUNCTION. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,266288


Temple University

14. Virtue, Anthony Thomas. The Contributions of miR-155 in Obesity, Metabolic Syndrome, and Atherosclerosis Development.

Degree: PhD, 2014, Temple University

Pharmacology

The global incidence of overweight and obese individuals has skyrocketed in the past few decades resulting in a new health epidemic. In 1980, 5%… (more)

Subjects/Keywords: Biology; Molecular biology;

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Virtue, A. T. (2014). The Contributions of miR-155 in Obesity, Metabolic Syndrome, and Atherosclerosis Development. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,276607

Chicago Manual of Style (16th Edition):

Virtue, Anthony Thomas. “The Contributions of miR-155 in Obesity, Metabolic Syndrome, and Atherosclerosis Development.” 2014. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,276607.

MLA Handbook (7th Edition):

Virtue, Anthony Thomas. “The Contributions of miR-155 in Obesity, Metabolic Syndrome, and Atherosclerosis Development.” 2014. Web. 06 Jun 2020.

Vancouver:

Virtue AT. The Contributions of miR-155 in Obesity, Metabolic Syndrome, and Atherosclerosis Development. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,276607.

Council of Science Editors:

Virtue AT. The Contributions of miR-155 in Obesity, Metabolic Syndrome, and Atherosclerosis Development. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,276607


Temple University

15. Joshi, Yash. The Role of 5-Lipoxygenase in the Stress-Mediated Exacerbation of the Alzheimer's Disease Phenotype.

Degree: PhD, 2015, Temple University

Pharmacology

BACKGROUND: Alzheimer's disease (AD) is the most common aging-associated neurodegenerative dementia. Current epidemiological trends indicate that a rapidly aging population, in conjunction with the… (more)

Subjects/Keywords: Neurosciences; Biology; Biochemistry;

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Joshi, Y. (2015). The Role of 5-Lipoxygenase in the Stress-Mediated Exacerbation of the Alzheimer's Disease Phenotype. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,318405

Chicago Manual of Style (16th Edition):

Joshi, Yash. “The Role of 5-Lipoxygenase in the Stress-Mediated Exacerbation of the Alzheimer's Disease Phenotype.” 2015. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,318405.

MLA Handbook (7th Edition):

Joshi, Yash. “The Role of 5-Lipoxygenase in the Stress-Mediated Exacerbation of the Alzheimer's Disease Phenotype.” 2015. Web. 06 Jun 2020.

Vancouver:

Joshi Y. The Role of 5-Lipoxygenase in the Stress-Mediated Exacerbation of the Alzheimer's Disease Phenotype. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,318405.

Council of Science Editors:

Joshi Y. The Role of 5-Lipoxygenase in the Stress-Mediated Exacerbation of the Alzheimer's Disease Phenotype. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,318405


Temple University

16. 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;

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

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 June 06, 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. 06 Jun 2020.

Vancouver:

Li X. Mitochondrial Reactive Oxygen Species Mediate Lysophosphatidylcholine-induced Endothelial Cell Activation. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2020 Jun 06]. 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

17. DiMattio, Kelly Marie. Studies on Ligands of the Kappa Opioid Receptor.

Degree: PhD, 2016, Temple University

Pharmacology

This thesis is comprised of three parts. In the first part, we investigated zyklophin, a novel selective short-acting kappa opioid receptor (KOPR) antagonist, and… (more)

Subjects/Keywords: Pharmacology; Biogeochemistry; Behavioral sciences;

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

DiMattio, K. M. (2016). Studies on Ligands of the Kappa Opioid Receptor. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,334919

Chicago Manual of Style (16th Edition):

DiMattio, Kelly Marie. “Studies on Ligands of the Kappa Opioid Receptor.” 2016. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,334919.

MLA Handbook (7th Edition):

DiMattio, Kelly Marie. “Studies on Ligands of the Kappa Opioid Receptor.” 2016. Web. 06 Jun 2020.

Vancouver:

DiMattio KM. Studies on Ligands of the Kappa Opioid Receptor. [Internet] [Doctoral dissertation]. Temple University; 2016. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,334919.

Council of Science Editors:

DiMattio KM. Studies on Ligands of the Kappa Opioid Receptor. [Doctoral Dissertation]. Temple University; 2016. Available from: http://digital.library.temple.edu/u?/p245801coll10,334919


Temple University

18. YANG, JI YEON. CD40 monocyte differentiation mediates tissue inflammation in chronic kidney disease.

Degree: PhD, 2015, Temple University

Pharmacology

Patients with chronic kidney disease (CKD) develop hyperhomocysteinemia (HHcy), have increased inflammatory monocytes (MC) and 10-times higher cardiovascular mortality than the general population. Here,… (more)

Subjects/Keywords: Medicine;

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

YANG, J. Y. (2015). CD40 monocyte differentiation mediates tissue inflammation in chronic kidney disease. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,349139

Chicago Manual of Style (16th Edition):

YANG, JI YEON. “CD40 monocyte differentiation mediates tissue inflammation in chronic kidney disease.” 2015. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,349139.

MLA Handbook (7th Edition):

YANG, JI YEON. “CD40 monocyte differentiation mediates tissue inflammation in chronic kidney disease.” 2015. Web. 06 Jun 2020.

Vancouver:

YANG JY. CD40 monocyte differentiation mediates tissue inflammation in chronic kidney disease. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,349139.

Council of Science Editors:

YANG JY. CD40 monocyte differentiation mediates tissue inflammation in chronic kidney disease. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,349139


Temple University

19. Gregg, Ryan Alexander. INVESTIGATIONS INTO THE STEREOCHEMICAL AND GLUTAMATERGIC MECHANISMS OF THE "BATH SALTS" SYNTHETIC CATHINONES MEPHEDRONE AND MDPV IN RATS.

Degree: PhD, 2015, Temple University

Pharmacology

Synthetic cathinones, commonly referred to as “bath salts”, are a subgroup of novel psychoactive substances that have seen a dramatic rise in abuse worldwide… (more)

Subjects/Keywords: Pharmacology; Neurosciences; Medicine;

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Gregg, R. A. (2015). INVESTIGATIONS INTO THE STEREOCHEMICAL AND GLUTAMATERGIC MECHANISMS OF THE "BATH SALTS" SYNTHETIC CATHINONES MEPHEDRONE AND MDPV IN RATS. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,354278

Chicago Manual of Style (16th Edition):

Gregg, Ryan Alexander. “INVESTIGATIONS INTO THE STEREOCHEMICAL AND GLUTAMATERGIC MECHANISMS OF THE "BATH SALTS" SYNTHETIC CATHINONES MEPHEDRONE AND MDPV IN RATS.” 2015. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,354278.

MLA Handbook (7th Edition):

Gregg, Ryan Alexander. “INVESTIGATIONS INTO THE STEREOCHEMICAL AND GLUTAMATERGIC MECHANISMS OF THE "BATH SALTS" SYNTHETIC CATHINONES MEPHEDRONE AND MDPV IN RATS.” 2015. Web. 06 Jun 2020.

Vancouver:

Gregg RA. INVESTIGATIONS INTO THE STEREOCHEMICAL AND GLUTAMATERGIC MECHANISMS OF THE "BATH SALTS" SYNTHETIC CATHINONES MEPHEDRONE AND MDPV IN RATS. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,354278.

Council of Science Editors:

Gregg RA. INVESTIGATIONS INTO THE STEREOCHEMICAL AND GLUTAMATERGIC MECHANISMS OF THE "BATH SALTS" SYNTHETIC CATHINONES MEPHEDRONE AND MDPV IN RATS. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,354278


Temple University

20. Whitfield, Fatima. Gamma-Delta T-Cells in Patients with Ovarian Carcinoma.

Degree: PhD, 2008, Temple University

Microbiology and Immunology

Ovarian cancer is the fifth most common cause of death from all cancers among women in the Western world and the most… (more)

Subjects/Keywords: Health Sciences, Immunology; Health Sciences, Oncology

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Whitfield, F. (2008). Gamma-Delta T-Cells in Patients with Ovarian Carcinoma. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,3422

Chicago Manual of Style (16th Edition):

Whitfield, Fatima. “Gamma-Delta T-Cells in Patients with Ovarian Carcinoma.” 2008. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,3422.

MLA Handbook (7th Edition):

Whitfield, Fatima. “Gamma-Delta T-Cells in Patients with Ovarian Carcinoma.” 2008. Web. 06 Jun 2020.

Vancouver:

Whitfield F. Gamma-Delta T-Cells in Patients with Ovarian Carcinoma. [Internet] [Doctoral dissertation]. Temple University; 2008. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,3422.

Council of Science Editors:

Whitfield F. Gamma-Delta T-Cells in Patients with Ovarian Carcinoma. [Doctoral Dissertation]. Temple University; 2008. Available from: http://digital.library.temple.edu/u?/p245801coll10,3422


Temple University

21. Miller, Jonathan S. GSK3: A Neuromodulator of Cocaine-Induced Behavioral Responses.

Degree: PhD, 2009, Temple University

Pharmacology

Cocaine is a highly abused psychostimulant with repeated use potential culminating in addiction, a disease associated with compulsive drug seeking, use and high rates… (more)

Subjects/Keywords: Health Sciences, Pharmacology; Brain; Cocaine; Dopamine; Glutamate; Glycogen Synthase Kinase-3; Mouse

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Miller, J. S. (2009). GSK3: A Neuromodulator of Cocaine-Induced Behavioral Responses. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,40192

Chicago Manual of Style (16th Edition):

Miller, Jonathan S. “GSK3: A Neuromodulator of Cocaine-Induced Behavioral Responses.” 2009. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,40192.

MLA Handbook (7th Edition):

Miller, Jonathan S. “GSK3: A Neuromodulator of Cocaine-Induced Behavioral Responses.” 2009. Web. 06 Jun 2020.

Vancouver:

Miller JS. GSK3: A Neuromodulator of Cocaine-Induced Behavioral Responses. [Internet] [Doctoral dissertation]. Temple University; 2009. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,40192.

Council of Science Editors:

Miller JS. GSK3: A Neuromodulator of Cocaine-Induced Behavioral Responses. [Doctoral Dissertation]. Temple University; 2009. Available from: http://digital.library.temple.edu/u?/p245801coll10,40192


Temple University

22. Nwaneshiudu, Chinwe A. Characterization of a functional role of the neurokinin-3 receptor in behavioral effects of cocaine.

Degree: PhD, 2011, Temple University

Pharmacology

The tachykinin NK-3 receptor is a G-protein coupled receptor activated by mammalian tachykinin neuropeptides, which can modulate dopaminergic neurotransmission, and alter dopamine-mediated behaviors. The… (more)

Subjects/Keywords: Health Sciences, Pharmacology; Behavioral Sciences; Biology, Neuroscience; CD-1; cocaine; dopamine; GSK3; NK-3; striatum

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Nwaneshiudu, C. A. (2011). Characterization of a functional role of the neurokinin-3 receptor in behavioral effects of cocaine. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,62614

Chicago Manual of Style (16th Edition):

Nwaneshiudu, Chinwe A. “Characterization of a functional role of the neurokinin-3 receptor in behavioral effects of cocaine.” 2011. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,62614.

MLA Handbook (7th Edition):

Nwaneshiudu, Chinwe A. “Characterization of a functional role of the neurokinin-3 receptor in behavioral effects of cocaine.” 2011. Web. 06 Jun 2020.

Vancouver:

Nwaneshiudu CA. Characterization of a functional role of the neurokinin-3 receptor in behavioral effects of cocaine. [Internet] [Doctoral dissertation]. Temple University; 2011. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,62614.

Council of Science Editors:

Nwaneshiudu CA. Characterization of a functional role of the neurokinin-3 receptor in behavioral effects of cocaine. [Doctoral Dissertation]. Temple University; 2011. Available from: http://digital.library.temple.edu/u?/p245801coll10,62614


Temple University

23. Khalid, Helene. S-Mephedrone: preclinical investigation of a synthetic cathinone against behavioral and neurochemical effects of cocaine and MDPV.

Degree: PhD, 2017, Temple University

Pharmacology

Synthetic cathinones are an emerging class of novel psychoactive substances whose rising rates of abuse have made them a significant public health issue. Recently,… (more)

Subjects/Keywords: Pharmacology; Neurosciences; Behavioral sciences;

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Khalid, H. (2017). S-Mephedrone: preclinical investigation of a synthetic cathinone against behavioral and neurochemical effects of cocaine and MDPV. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,434922

Chicago Manual of Style (16th Edition):

Khalid, Helene. “S-Mephedrone: preclinical investigation of a synthetic cathinone against behavioral and neurochemical effects of cocaine and MDPV.” 2017. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,434922.

MLA Handbook (7th Edition):

Khalid, Helene. “S-Mephedrone: preclinical investigation of a synthetic cathinone against behavioral and neurochemical effects of cocaine and MDPV.” 2017. Web. 06 Jun 2020.

Vancouver:

Khalid H. S-Mephedrone: preclinical investigation of a synthetic cathinone against behavioral and neurochemical effects of cocaine and MDPV. [Internet] [Doctoral dissertation]. Temple University; 2017. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,434922.

Council of Science Editors:

Khalid H. S-Mephedrone: preclinical investigation of a synthetic cathinone against behavioral and neurochemical effects of cocaine and MDPV. [Doctoral Dissertation]. Temple University; 2017. Available from: http://digital.library.temple.edu/u?/p245801coll10,434922


Temple University

24. 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;

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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 06, 2020. 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. 06 Jun 2020.

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 2020 Jun 06]. 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

25. Inan, Saadet. Pharmacological and Neuroanatomical Analysis of GNTI-Induced Repetitive Behavior in Mice.

Degree: PhD, 2010, Temple University

Pharmacology

This thesis is comprised of two parts. In the first part, we investigated a) the pharmacology of GNTI, a selective kappa opioid receptor antagonist,… (more)

Subjects/Keywords: Health Sciences, Pharmacology; Neurobiology; GNTI; Itch; Kappa opioid receptor; Muscarinic receptor; Nalfurafine; Pain

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Inan, S. (2010). Pharmacological and Neuroanatomical Analysis of GNTI-Induced Repetitive Behavior in Mice. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,75332

Chicago Manual of Style (16th Edition):

Inan, Saadet. “Pharmacological and Neuroanatomical Analysis of GNTI-Induced Repetitive Behavior in Mice.” 2010. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,75332.

MLA Handbook (7th Edition):

Inan, Saadet. “Pharmacological and Neuroanatomical Analysis of GNTI-Induced Repetitive Behavior in Mice.” 2010. Web. 06 Jun 2020.

Vancouver:

Inan S. Pharmacological and Neuroanatomical Analysis of GNTI-Induced Repetitive Behavior in Mice. [Internet] [Doctoral dissertation]. Temple University; 2010. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,75332.

Council of Science Editors:

Inan S. Pharmacological and Neuroanatomical Analysis of GNTI-Induced Repetitive Behavior in Mice. [Doctoral Dissertation]. Temple University; 2010. Available from: http://digital.library.temple.edu/u?/p245801coll10,75332


Temple University

26. Huang, Xiaofang. Functional study of amylin and regulation of amylin receptor.

Degree: PhD, 2010, Temple University

Pharmacology

Amylin, a 37 amino acid peptide secreted from pancreatic beta cells upon stimulation by meal/glucose, belongs to the family of the calcitonin or calcitonin… (more)

Subjects/Keywords: Pharmacology; amylin; antinociceptive; calcitonin receptor; RAMP; spinal cord

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Huang, X. (2010). Functional study of amylin and regulation of amylin receptor. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,114036

Chicago Manual of Style (16th Edition):

Huang, Xiaofang. “Functional study of amylin and regulation of amylin receptor.” 2010. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,114036.

MLA Handbook (7th Edition):

Huang, Xiaofang. “Functional study of amylin and regulation of amylin receptor.” 2010. Web. 06 Jun 2020.

Vancouver:

Huang X. Functional study of amylin and regulation of amylin receptor. [Internet] [Doctoral dissertation]. Temple University; 2010. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,114036.

Council of Science Editors:

Huang X. Functional study of amylin and regulation of amylin receptor. [Doctoral Dissertation]. Temple University; 2010. Available from: http://digital.library.temple.edu/u?/p245801coll10,114036


Temple University

27. 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;

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

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 June 06, 2020. 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. 06 Jun 2020.

Vancouver:

Meng S. HYPERHOMOCYSTEINEMIA ACCELERATES THROMBOSIS THROUGH ICAM-1 DEPENDENT ENDOTHELIAL ACTIVATION AND DNA HYPOMETHYLATION. [Internet] [Doctoral dissertation]. Temple University; 2013. [cited 2020 Jun 06]. 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

28. Xiong, Xinyu. Carom, a novel gene, is up-regulated by homocysteine through DNA hypomethylation to inhibit endothelial cell migration and angiogenesis.

Degree: PhD, 2014, Temple University

Pharmacology

Hyperhomocysteinemia (HHcy) is an independent risk factor for cardiovascular disease (CVD). We previously demonstrated that homocysteine (Hcy) suppresses endothelial cell (EC) proliferation, migration, and… (more)

Subjects/Keywords: Molecular biology; Biology;

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Xiong, X. (2014). Carom, a novel gene, is up-regulated by homocysteine through DNA hypomethylation to inhibit endothelial cell migration and angiogenesis. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,276456

Chicago Manual of Style (16th Edition):

Xiong, Xinyu. “Carom, a novel gene, is up-regulated by homocysteine through DNA hypomethylation to inhibit endothelial cell migration and angiogenesis.” 2014. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,276456.

MLA Handbook (7th Edition):

Xiong, Xinyu. “Carom, a novel gene, is up-regulated by homocysteine through DNA hypomethylation to inhibit endothelial cell migration and angiogenesis.” 2014. Web. 06 Jun 2020.

Vancouver:

Xiong X. Carom, a novel gene, is up-regulated by homocysteine through DNA hypomethylation to inhibit endothelial cell migration and angiogenesis. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,276456.

Council of Science Editors:

Xiong X. Carom, a novel gene, is up-regulated by homocysteine through DNA hypomethylation to inhibit endothelial cell migration and angiogenesis. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,276456


Temple University

29. 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;

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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 June 06, 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. 06 Jun 2020.

Vancouver:

Chiu Y. STUDIES ON NEURITE OUTGROWTH AND RECEPTOR PHOSPHORYLATION FOLLOWING KAPPA OPIOID RECEPTOR ACTIVATION. [Internet] [Doctoral dissertation]. Temple University; 2016. [cited 2020 Jun 06]. 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


Temple University

30. Kim, Jae Kyun. CXCL12/CXCR4 signaling in mesocorticolimbic reward pathways: relevance to cocaine reinforcement and relapse.

Degree: PhD, 2016, Temple University

Pharmacology

The role of chemokines as chemotactic cytokines and their functions in the immune system and related pathologies are well defined. Recently, strong evidence supporting… (more)

Subjects/Keywords: Pharmacology;

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Kim, J. K. (2016). CXCL12/CXCR4 signaling in mesocorticolimbic reward pathways: relevance to cocaine reinforcement and relapse. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,399036

Chicago Manual of Style (16th Edition):

Kim, Jae Kyun. “CXCL12/CXCR4 signaling in mesocorticolimbic reward pathways: relevance to cocaine reinforcement and relapse.” 2016. Doctoral Dissertation, Temple University. Accessed June 06, 2020. http://digital.library.temple.edu/u?/p245801coll10,399036.

MLA Handbook (7th Edition):

Kim, Jae Kyun. “CXCL12/CXCR4 signaling in mesocorticolimbic reward pathways: relevance to cocaine reinforcement and relapse.” 2016. Web. 06 Jun 2020.

Vancouver:

Kim JK. CXCL12/CXCR4 signaling in mesocorticolimbic reward pathways: relevance to cocaine reinforcement and relapse. [Internet] [Doctoral dissertation]. Temple University; 2016. [cited 2020 Jun 06]. Available from: http://digital.library.temple.edu/u?/p245801coll10,399036.

Council of Science Editors:

Kim JK. CXCL12/CXCR4 signaling in mesocorticolimbic reward pathways: relevance to cocaine reinforcement and relapse. [Doctoral Dissertation]. Temple University; 2016. Available from: http://digital.library.temple.edu/u?/p245801coll10,399036

[1] [2]

.