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You searched for +publisher:"Temple University" +contributor:("Merali, Salim"). Showing records 1 – 6 of 6 total matches.

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Temple University

1. Moncada Benavides, Camilo Andres. EFFECT OF NICOTINE ON LUNG S-ADENOSYLMETHIONINE AND PNEUMOCYSTIS PNEUMONIA DEVELOPMENT.

Degree: PhD, 2012, Temple University

Biochemistry

Infection with "Pneumocystis" causes a ≥ 99% depletion of plasma S-adenosylmethionine (AdoMet) levels in both "Pneumocystis" pneumonia (PcP) animal models and patients. AdoMet is… (more)

Subjects/Keywords: Biochemistry; Laser Capture Microdissection; Lung; Nicotine; Pneumocystis; Polyamines; S-Adenosylmethionine

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APA (6th Edition):

Moncada Benavides, C. A. (2012). EFFECT OF NICOTINE ON LUNG S-ADENOSYLMETHIONINE AND PNEUMOCYSTIS PNEUMONIA DEVELOPMENT. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,206623

Chicago Manual of Style (16th Edition):

Moncada Benavides, Camilo Andres. “EFFECT OF NICOTINE ON LUNG S-ADENOSYLMETHIONINE AND PNEUMOCYSTIS PNEUMONIA DEVELOPMENT.” 2012. Doctoral Dissertation, Temple University. Accessed September 24, 2020. http://digital.library.temple.edu/u?/p245801coll10,206623.

MLA Handbook (7th Edition):

Moncada Benavides, Camilo Andres. “EFFECT OF NICOTINE ON LUNG S-ADENOSYLMETHIONINE AND PNEUMOCYSTIS PNEUMONIA DEVELOPMENT.” 2012. Web. 24 Sep 2020.

Vancouver:

Moncada Benavides CA. EFFECT OF NICOTINE ON LUNG S-ADENOSYLMETHIONINE AND PNEUMOCYSTIS PNEUMONIA DEVELOPMENT. [Internet] [Doctoral dissertation]. Temple University; 2012. [cited 2020 Sep 24]. Available from: http://digital.library.temple.edu/u?/p245801coll10,206623.

Council of Science Editors:

Moncada Benavides CA. EFFECT OF NICOTINE ON LUNG S-ADENOSYLMETHIONINE AND PNEUMOCYSTIS PNEUMONIA DEVELOPMENT. [Doctoral Dissertation]. Temple University; 2012. Available from: http://digital.library.temple.edu/u?/p245801coll10,206623


Temple University

2. Liu, Chunli. THE ROLE OF POLYAMINE ACETYLATION IN REGULATING ADIPOSE TISSUE METABOLISM.

Degree: PhD, 2011, Temple University

Biochemistry

Because excessive body weight is a major health issue, there is an urgent need to understand all physiological mechanisms relating to control of fat… (more)

Subjects/Keywords: Biochemistry; adipose tissue; metabolism; polyamine acetylation; SSAT

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APA (6th Edition):

Liu, C. (2011). THE ROLE OF POLYAMINE ACETYLATION IN REGULATING ADIPOSE TISSUE METABOLISM. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,213123

Chicago Manual of Style (16th Edition):

Liu, Chunli. “THE ROLE OF POLYAMINE ACETYLATION IN REGULATING ADIPOSE TISSUE METABOLISM.” 2011. Doctoral Dissertation, Temple University. Accessed September 24, 2020. http://digital.library.temple.edu/u?/p245801coll10,213123.

MLA Handbook (7th Edition):

Liu, Chunli. “THE ROLE OF POLYAMINE ACETYLATION IN REGULATING ADIPOSE TISSUE METABOLISM.” 2011. Web. 24 Sep 2020.

Vancouver:

Liu C. THE ROLE OF POLYAMINE ACETYLATION IN REGULATING ADIPOSE TISSUE METABOLISM. [Internet] [Doctoral dissertation]. Temple University; 2011. [cited 2020 Sep 24]. Available from: http://digital.library.temple.edu/u?/p245801coll10,213123.

Council of Science Editors:

Liu C. THE ROLE OF POLYAMINE ACETYLATION IN REGULATING ADIPOSE TISSUE METABOLISM. [Doctoral Dissertation]. Temple University; 2011. Available from: http://digital.library.temple.edu/u?/p245801coll10,213123


Temple University

3. 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 September 24, 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. 24 Sep 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 Sep 24]. 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

4. 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 September 24, 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. 24 Sep 2020.

Vancouver:

Jan M. Novel Mechanisms Underlying Homocysteine-Suppressed Endothelial Cell Growth. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2020 Sep 24]. 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

5. 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 September 24, 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. 24 Sep 2020.

Vancouver:

YANG JY. CD40 monocyte differentiation mediates tissue inflammation in chronic kidney disease. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2020 Sep 24]. 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

6. 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 · 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 September 24, 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. 24 Sep 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 Sep 24]. 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

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