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:("Wang, Hong;"). Showing records 1 – 15 of 15 total matches.

Search Limiters

Last 2 Years | English Only

No search limiters apply to these results.

▼ Search Limiters


Temple University

1. 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 October 21, 2019. 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. 21 Oct 2019.

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 2019 Oct 21]. 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

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

Degree: PhD, 2012, Temple University

Physiology

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

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

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

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

Chicago Manual of Style (16th Edition):

Wang, Fang. “DOES CALCIUM INFLUX THROUGH T-TYPE CALCIUM CHANNEL INDUCE CARDIOMYOCYTE PROLIFERATION?.” 2012. Doctoral Dissertation, Temple University. Accessed October 21, 2019. http://digital.library.temple.edu/u?/p245801coll10,214814.

MLA Handbook (7th Edition):

Wang, Fang. “DOES CALCIUM INFLUX THROUGH T-TYPE CALCIUM CHANNEL INDUCE CARDIOMYOCYTE PROLIFERATION?.” 2012. Web. 21 Oct 2019.

Vancouver:

Wang F. DOES CALCIUM INFLUX THROUGH T-TYPE CALCIUM CHANNEL INDUCE CARDIOMYOCYTE PROLIFERATION?. [Internet] [Doctoral dissertation]. Temple University; 2012. [cited 2019 Oct 21]. Available from: http://digital.library.temple.edu/u?/p245801coll10,214814.

Council of Science Editors:

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


Temple University

3. Zhang, Hongyu. INCREASING MYOCYTE CONTRACTILITY EXACERBATES CARDIAC INJURY AND PUMP DYSFUNCTION AND ABLATION OF PHOSPHORYLATION.

Degree: PhD, 2010, Temple University

Physiology

Myocardial infarction (MI) leads to heart failure (HF) and premature death. The respective roles of myocyte death and depressed myocyte contractility in the induction… (more)

Subjects/Keywords: Biology, Physiology; cardiac function; cell death; heart failure; myocardial infarction; myocyte contractility; ryanodine receptor

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Zhang, H. (2010). INCREASING MYOCYTE CONTRACTILITY EXACERBATES CARDIAC INJURY AND PUMP DYSFUNCTION AND ABLATION OF PHOSPHORYLATION. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,90859

Chicago Manual of Style (16th Edition):

Zhang, Hongyu. “INCREASING MYOCYTE CONTRACTILITY EXACERBATES CARDIAC INJURY AND PUMP DYSFUNCTION AND ABLATION OF PHOSPHORYLATION.” 2010. Doctoral Dissertation, Temple University. Accessed October 21, 2019. http://digital.library.temple.edu/u?/p245801coll10,90859.

MLA Handbook (7th Edition):

Zhang, Hongyu. “INCREASING MYOCYTE CONTRACTILITY EXACERBATES CARDIAC INJURY AND PUMP DYSFUNCTION AND ABLATION OF PHOSPHORYLATION.” 2010. Web. 21 Oct 2019.

Vancouver:

Zhang H. INCREASING MYOCYTE CONTRACTILITY EXACERBATES CARDIAC INJURY AND PUMP DYSFUNCTION AND ABLATION OF PHOSPHORYLATION. [Internet] [Doctoral dissertation]. Temple University; 2010. [cited 2019 Oct 21]. Available from: http://digital.library.temple.edu/u?/p245801coll10,90859.

Council of Science Editors:

Zhang H. INCREASING MYOCYTE CONTRACTILITY EXACERBATES CARDIAC INJURY AND PUMP DYSFUNCTION AND ABLATION OF PHOSPHORYLATION. [Doctoral Dissertation]. Temple University; 2010. Available from: http://digital.library.temple.edu/u?/p245801coll10,90859


Temple University

4. 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 October 21, 2019. 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. 21 Oct 2019.

Vancouver:

Thomas DH. Regulation of Syk activity in GPVI-mediated platelet activation. [Internet] [Doctoral dissertation]. Temple University; 2010. [cited 2019 Oct 21]. 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

5. 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 October 21, 2019. 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. 21 Oct 2019.

Vancouver:

Fang P. HYPERHOMOCYSTEINEMIA ACCELERATES ATHEROSCLEROSIS BY INDUCING INFLAMMATORY MONOCYTE DIFFERENTIATION IN A HYPERGLYCEMIC MOUSE MODEL. [Internet] [Doctoral dissertation]. Temple University; 2012. [cited 2019 Oct 21]. 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

6. 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 October 21, 2019. 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. 21 Oct 2019.

Vancouver:

Pansuria M. EFFECT AND MECHANISM OF HYPERHOMOCYSTEINEMIA ON ENDOTHELIAL INSULIN SIGNALING. [Internet] [Doctoral dissertation]. Temple University; 2013. [cited 2019 Oct 21]. 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

7. 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 October 21, 2019. 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. 21 Oct 2019.

Vancouver:

Yin Y. CASPASE-1 ACTIVATION IS CRITICAL FOR ENDOTHELIAL CELL ACTIVATION, MONOCYTE MIGRATION, AND EARLY ATHEROGENESIS. [Internet] [Doctoral dissertation]. Temple University; 2013. [cited 2019 Oct 21]. 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

8. 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 October 21, 2019. http://digital.library.temple.edu/u?/p245801coll10,264103.

MLA Handbook (7th Edition):

Jan, Michael. “Novel Mechanisms Underlying Homocysteine-Suppressed Endothelial Cell Growth.” 2014. Web. 21 Oct 2019.

Vancouver:

Jan M. Novel Mechanisms Underlying Homocysteine-Suppressed Endothelial Cell Growth. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2019 Oct 21]. 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

9. 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 October 21, 2019. 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. 21 Oct 2019.

Vancouver:

Mai J. ROLE OF INTERLEUKIN-17 IN ENDOTHELIAL CELL ACTIVATION AND VASCULAR FUNCTION. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2019 Oct 21]. 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

10. 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 October 21, 2019. 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. 21 Oct 2019.

Vancouver:

Virtue AT. The Contributions of miR-155 in Obesity, Metabolic Syndrome, and Atherosclerosis Development. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2019 Oct 21]. 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

11. 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 October 21, 2019. 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. 21 Oct 2019.

Vancouver:

Li X. Mitochondrial Reactive Oxygen Species Mediate Lysophosphatidylcholine-induced Endothelial Cell Activation. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Oct 21]. 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

12. 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 October 21, 2019. 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. 21 Oct 2019.

Vancouver:

YANG JY. CD40 monocyte differentiation mediates tissue inflammation in chronic kidney disease. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Oct 21]. 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

13. 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 October 21, 2019. 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. 21 Oct 2019.

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 2019 Oct 21]. 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

14. Kearns, Alison Catherine. A Multi-model Approach for Evaluating Caspase-1 Activation in Human Immunodeficiency Virus associated Atherosclerosis and Vascular Neurocognitive Disorders.

Degree: PhD, 2018, Temple University

Biomedical Sciences

Combination antiretroviral therapy (cART)-treated people living with human immunodeficiency virus (HIV) (PLWH) face an increased risk of atherosclerosis associated cardiovascular disease (ASCVD) even… (more)

Subjects/Keywords: Neurosciences

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Kearns, A. C. (2018). A Multi-model Approach for Evaluating Caspase-1 Activation in Human Immunodeficiency Virus associated Atherosclerosis and Vascular Neurocognitive Disorders. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,510716

Chicago Manual of Style (16th Edition):

Kearns, Alison Catherine. “A Multi-model Approach for Evaluating Caspase-1 Activation in Human Immunodeficiency Virus associated Atherosclerosis and Vascular Neurocognitive Disorders.” 2018. Doctoral Dissertation, Temple University. Accessed October 21, 2019. http://digital.library.temple.edu/u?/p245801coll10,510716.

MLA Handbook (7th Edition):

Kearns, Alison Catherine. “A Multi-model Approach for Evaluating Caspase-1 Activation in Human Immunodeficiency Virus associated Atherosclerosis and Vascular Neurocognitive Disorders.” 2018. Web. 21 Oct 2019.

Vancouver:

Kearns AC. A Multi-model Approach for Evaluating Caspase-1 Activation in Human Immunodeficiency Virus associated Atherosclerosis and Vascular Neurocognitive Disorders. [Internet] [Doctoral dissertation]. Temple University; 2018. [cited 2019 Oct 21]. Available from: http://digital.library.temple.edu/u?/p245801coll10,510716.

Council of Science Editors:

Kearns AC. A Multi-model Approach for Evaluating Caspase-1 Activation in Human Immunodeficiency Virus associated Atherosclerosis and Vascular Neurocognitive Disorders. [Doctoral Dissertation]. Temple University; 2018. Available from: http://digital.library.temple.edu/u?/p245801coll10,510716


Temple University

15. 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 October 21, 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. 21 Oct 2019.

Vancouver:

Meng S. HYPERHOMOCYSTEINEMIA ACCELERATES THROMBOSIS THROUGH ICAM-1 DEPENDENT ENDOTHELIAL ACTIVATION AND DNA HYPOMETHYLATION. [Internet] [Doctoral dissertation]. Temple University; 2013. [cited 2019 Oct 21]. 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

.