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You searched for +publisher:"Temple University" +contributor:("Yang, Xiao-Feng;"). Showing records 1 – 16 of 16 total matches.

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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;

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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 July 02, 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. 02 Jul 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 Jul 02]. 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. Xu, Jun. Regulation of type I interferons in murine dendritic cells.

Degree: PhD, 2014, Temple University

Microbiology and Immunology

Conventional Dendritic cells (cDCs), a specialized group of immunological sentinels with tree-like or dendritic shapes, are critical for recognition of danger signals,… (more)

Subjects/Keywords: Immunology; Microbiology;

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APA (6th Edition):

Xu, J. (2014). Regulation of type I interferons in murine dendritic cells. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,308946

Chicago Manual of Style (16th Edition):

Xu, Jun. “Regulation of type I interferons in murine dendritic cells.” 2014. Doctoral Dissertation, Temple University. Accessed July 02, 2020. http://digital.library.temple.edu/u?/p245801coll10,308946.

MLA Handbook (7th Edition):

Xu, Jun. “Regulation of type I interferons in murine dendritic cells.” 2014. Web. 02 Jul 2020.

Vancouver:

Xu J. Regulation of type I interferons in murine dendritic cells. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2020 Jul 02]. Available from: http://digital.library.temple.edu/u?/p245801coll10,308946.

Council of Science Editors:

Xu J. Regulation of type I interferons in murine dendritic cells. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,308946


Temple University

3. Pokiniewski, Katie Ann. Understanding the cellular mechanism of Adeno-Associated Virus genome stabilization.

Degree: PhD, 2016, Temple University

Microbiology and Immunology

The Adeno-Associated Virus(AAV) is a small, single stranded DNA virus that has been developed as a gene transfer vector. Early clinical trials… (more)

Subjects/Keywords: Virology; Microbiology;

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APA (6th Edition):

Pokiniewski, K. A. (2016). Understanding the cellular mechanism of Adeno-Associated Virus genome stabilization. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,385837

Chicago Manual of Style (16th Edition):

Pokiniewski, Katie Ann. “Understanding the cellular mechanism of Adeno-Associated Virus genome stabilization.” 2016. Doctoral Dissertation, Temple University. Accessed July 02, 2020. http://digital.library.temple.edu/u?/p245801coll10,385837.

MLA Handbook (7th Edition):

Pokiniewski, Katie Ann. “Understanding the cellular mechanism of Adeno-Associated Virus genome stabilization.” 2016. Web. 02 Jul 2020.

Vancouver:

Pokiniewski KA. Understanding the cellular mechanism of Adeno-Associated Virus genome stabilization. [Internet] [Doctoral dissertation]. Temple University; 2016. [cited 2020 Jul 02]. Available from: http://digital.library.temple.edu/u?/p245801coll10,385837.

Council of Science Editors:

Pokiniewski KA. Understanding the cellular mechanism of Adeno-Associated Virus genome stabilization. [Doctoral Dissertation]. Temple University; 2016. Available from: http://digital.library.temple.edu/u?/p245801coll10,385837


Temple University

4. 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

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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 July 02, 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. 02 Jul 2020.

Vancouver:

Evans KW. PPAR gamma AND eNOS CONTRIBUTE TO THE RESOLUTION OF CHRONIC INFLAMMATION. [Internet] [Doctoral dissertation]. Temple University; 2011. [cited 2020 Jul 02]. 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

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

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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 July 02, 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. 02 Jul 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 Jul 02]. 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

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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 July 02, 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. 02 Jul 2020.

Vancouver:

Pansuria M. EFFECT AND MECHANISM OF HYPERHOMOCYSTEINEMIA ON ENDOTHELIAL INSULIN SIGNALING. [Internet] [Doctoral dissertation]. Temple University; 2013. [cited 2020 Jul 02]. 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

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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 July 02, 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. 02 Jul 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 Jul 02]. 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;

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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 July 02, 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. 02 Jul 2020.

Vancouver:

Jan M. Novel Mechanisms Underlying Homocysteine-Suppressed Endothelial Cell Growth. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2020 Jul 02]. 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;

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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 July 02, 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. 02 Jul 2020.

Vancouver:

Mai J. ROLE OF INTERLEUKIN-17 IN ENDOTHELIAL CELL ACTIVATION AND VASCULAR FUNCTION. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2020 Jul 02]. 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;

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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 July 02, 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. 02 Jul 2020.

Vancouver:

Virtue AT. The Contributions of miR-155 in Obesity, Metabolic Syndrome, and Atherosclerosis Development. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2020 Jul 02]. 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;

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APA (6th Edition):

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

Chicago Manual of Style (16th Edition):

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

MLA Handbook (7th Edition):

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

Vancouver:

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

Council of Science Editors:

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


Temple University

12. Richards, Jamie Madison. The Potential of IL-19 As a Therapeutic Anti-inflammatory and Angiogenic Cytokine.

Degree: PhD, 2015, Temple University

Physiology

Our lab has recently shown that IL-19 is expressed in angiogenic ECs, opening the possibility for its use as a medicine to increase perfusion… (more)

Subjects/Keywords: Physiology; Health sciences; Medicine;

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APA (6th Edition):

Richards, J. M. (2015). The Potential of IL-19 As a Therapeutic Anti-inflammatory and Angiogenic Cytokine. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,345114

Chicago Manual of Style (16th Edition):

Richards, Jamie Madison. “The Potential of IL-19 As a Therapeutic Anti-inflammatory and Angiogenic Cytokine.” 2015. Doctoral Dissertation, Temple University. Accessed July 02, 2020. http://digital.library.temple.edu/u?/p245801coll10,345114.

MLA Handbook (7th Edition):

Richards, Jamie Madison. “The Potential of IL-19 As a Therapeutic Anti-inflammatory and Angiogenic Cytokine.” 2015. Web. 02 Jul 2020.

Vancouver:

Richards JM. The Potential of IL-19 As a Therapeutic Anti-inflammatory and Angiogenic Cytokine. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2020 Jul 02]. Available from: http://digital.library.temple.edu/u?/p245801coll10,345114.

Council of Science Editors:

Richards JM. The Potential of IL-19 As a Therapeutic Anti-inflammatory and Angiogenic Cytokine. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,345114


Temple University

13. 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;

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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 July 02, 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. 02 Jul 2020.

Vancouver:

YANG JY. CD40 monocyte differentiation mediates tissue inflammation in chronic kidney disease. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2020 Jul 02]. 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

14. 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

15. 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;

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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 July 02, 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. 02 Jul 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 Jul 02]. 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

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

Degree: PhD, 2013, Temple University

Pharmacology

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

Subjects/Keywords: Pharmacology;

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APA · 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 July 02, 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. 02 Jul 2020.

Vancouver:

Meng S. HYPERHOMOCYSTEINEMIA ACCELERATES THROMBOSIS THROUGH ICAM-1 DEPENDENT ENDOTHELIAL ACTIVATION AND DNA HYPOMETHYLATION. [Internet] [Doctoral dissertation]. Temple University; 2013. [cited 2020 Jul 02]. 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

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