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You searched for +publisher:"Temple University" +contributor:("Scalia, Rosario;"). Showing records 1 – 18 of 18 total matches.

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Temple University

1. Buitrago Murcia, Claudia Lorena. Cbl proteins in platelet functional responses.

Degree: PhD, 2012, Temple University

Physiology

c-Cbl protein functions as an E3 ligase and scaffolding protein, where three residues, Y700, Y731, and Y774, upon phosphorylation, have been shown to initiate… (more)

Subjects/Keywords: Physiology; Cellular biology; Cbl; hemostasis; kinases; platelets; signaling

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APA (6th Edition):

Buitrago Murcia, C. L. (2012). Cbl proteins in platelet functional responses. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,198139

Chicago Manual of Style (16th Edition):

Buitrago Murcia, Claudia Lorena. “Cbl proteins in platelet functional responses.” 2012. Doctoral Dissertation, Temple University. Accessed October 16, 2019. http://digital.library.temple.edu/u?/p245801coll10,198139.

MLA Handbook (7th Edition):

Buitrago Murcia, Claudia Lorena. “Cbl proteins in platelet functional responses.” 2012. Web. 16 Oct 2019.

Vancouver:

Buitrago Murcia CL. Cbl proteins in platelet functional responses. [Internet] [Doctoral dissertation]. Temple University; 2012. [cited 2019 Oct 16]. Available from: http://digital.library.temple.edu/u?/p245801coll10,198139.

Council of Science Editors:

Buitrago Murcia CL. Cbl proteins in platelet functional responses. [Doctoral Dissertation]. Temple University; 2012. Available from: http://digital.library.temple.edu/u?/p245801coll10,198139


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

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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 16, 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. 16 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 16]. 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. England, Ross N. Cellular Mechanisms of the Anti-Inflammatory Effects of Interleukin-19.

Degree: PhD, 2015, Temple University

Physiology

BACKGROUND: Atherosclerotic vascular disease is a significant medical and socioeconomic problem and contributes to mortality in multiple diseases including myocardial infarction (MI), stroke, renal… (more)

Subjects/Keywords: Physiology; Pathology; Molecular biology;

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APA (6th Edition):

England, R. N. (2015). Cellular Mechanisms of the Anti-Inflammatory Effects of Interleukin-19. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,216875

Chicago Manual of Style (16th Edition):

England, Ross N. “Cellular Mechanisms of the Anti-Inflammatory Effects of Interleukin-19.” 2015. Doctoral Dissertation, Temple University. Accessed October 16, 2019. http://digital.library.temple.edu/u?/p245801coll10,216875.

MLA Handbook (7th Edition):

England, Ross N. “Cellular Mechanisms of the Anti-Inflammatory Effects of Interleukin-19.” 2015. Web. 16 Oct 2019.

Vancouver:

England RN. Cellular Mechanisms of the Anti-Inflammatory Effects of Interleukin-19. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Oct 16]. Available from: http://digital.library.temple.edu/u?/p245801coll10,216875.

Council of Science Editors:

England RN. Cellular Mechanisms of the Anti-Inflammatory Effects of Interleukin-19. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,216875


Temple University

4. Singh, Harinder. CAVEOLAE AS SPATIO-TEMPORAL COMPARTMENTS FOR ROS/RNS GENERATION AND NITROXIDATIVE STRESS SIGNALING.

Degree: PhD, 2014, Temple University

Cell Biology

During inflammatory conditions excessive production of reactive oxygen (ROS) and nitrogen species (RNS), peroxynitrite, is implicated in the development of vascular pathologies. Our… (more)

Subjects/Keywords: Biology; Cellular biology

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APA (6th Edition):

Singh, H. (2014). CAVEOLAE AS SPATIO-TEMPORAL COMPARTMENTS FOR ROS/RNS GENERATION AND NITROXIDATIVE STRESS SIGNALING. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,275561

Chicago Manual of Style (16th Edition):

Singh, Harinder. “CAVEOLAE AS SPATIO-TEMPORAL COMPARTMENTS FOR ROS/RNS GENERATION AND NITROXIDATIVE STRESS SIGNALING.” 2014. Doctoral Dissertation, Temple University. Accessed October 16, 2019. http://digital.library.temple.edu/u?/p245801coll10,275561.

MLA Handbook (7th Edition):

Singh, Harinder. “CAVEOLAE AS SPATIO-TEMPORAL COMPARTMENTS FOR ROS/RNS GENERATION AND NITROXIDATIVE STRESS SIGNALING.” 2014. Web. 16 Oct 2019.

Vancouver:

Singh H. CAVEOLAE AS SPATIO-TEMPORAL COMPARTMENTS FOR ROS/RNS GENERATION AND NITROXIDATIVE STRESS SIGNALING. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2019 Oct 16]. Available from: http://digital.library.temple.edu/u?/p245801coll10,275561.

Council of Science Editors:

Singh H. CAVEOLAE AS SPATIO-TEMPORAL COMPARTMENTS FOR ROS/RNS GENERATION AND NITROXIDATIVE STRESS SIGNALING. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,275561


Temple University

5. BADOLIA, RACHIT. MOLECULAR PHYSIOLOGY OF p21-ACTIVATED KINASES.

Degree: PhD, 2015, Temple University

Organ Systems & Translational Medicine

Platelets are involved in many processes ranging from fighting microbial infections and triggering inflammation to promoting tumor angiogenesis and metastasis.… (more)

Subjects/Keywords: Physiology;

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APA (6th Edition):

BADOLIA, R. (2015). MOLECULAR PHYSIOLOGY OF p21-ACTIVATED KINASES. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,368893

Chicago Manual of Style (16th Edition):

BADOLIA, RACHIT. “MOLECULAR PHYSIOLOGY OF p21-ACTIVATED KINASES.” 2015. Doctoral Dissertation, Temple University. Accessed October 16, 2019. http://digital.library.temple.edu/u?/p245801coll10,368893.

MLA Handbook (7th Edition):

BADOLIA, RACHIT. “MOLECULAR PHYSIOLOGY OF p21-ACTIVATED KINASES.” 2015. Web. 16 Oct 2019.

Vancouver:

BADOLIA R. MOLECULAR PHYSIOLOGY OF p21-ACTIVATED KINASES. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Oct 16]. Available from: http://digital.library.temple.edu/u?/p245801coll10,368893.

Council of Science Editors:

BADOLIA R. MOLECULAR PHYSIOLOGY OF p21-ACTIVATED KINASES. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,368893


Temple University

6. Ray, Mitali. Genetic Deletion of Interleukin-19 Exacerbates Atherogenesis in Double Knockout Mice by Modulation of mRNA Stability Protein HuR.

Degree: PhD, 2018, Temple University

Biomedical Sciences

Objective: To test the hypothesis that loss of IL-19 exacerbates atherosclerosis. Approach and Results: Il19-/- mice were crossed into Ldlr-/- mice. Double knockout… (more)

Subjects/Keywords: Biology;

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APA (6th Edition):

Ray, M. (2018). Genetic Deletion of Interleukin-19 Exacerbates Atherogenesis in Double Knockout Mice by Modulation of mRNA Stability Protein HuR. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,491387

Chicago Manual of Style (16th Edition):

Ray, Mitali. “Genetic Deletion of Interleukin-19 Exacerbates Atherogenesis in Double Knockout Mice by Modulation of mRNA Stability Protein HuR.” 2018. Doctoral Dissertation, Temple University. Accessed October 16, 2019. http://digital.library.temple.edu/u?/p245801coll10,491387.

MLA Handbook (7th Edition):

Ray, Mitali. “Genetic Deletion of Interleukin-19 Exacerbates Atherogenesis in Double Knockout Mice by Modulation of mRNA Stability Protein HuR.” 2018. Web. 16 Oct 2019.

Vancouver:

Ray M. Genetic Deletion of Interleukin-19 Exacerbates Atherogenesis in Double Knockout Mice by Modulation of mRNA Stability Protein HuR. [Internet] [Doctoral dissertation]. Temple University; 2018. [cited 2019 Oct 16]. Available from: http://digital.library.temple.edu/u?/p245801coll10,491387.

Council of Science Editors:

Ray M. Genetic Deletion of Interleukin-19 Exacerbates Atherogenesis in Double Knockout Mice by Modulation of mRNA Stability Protein HuR. [Doctoral Dissertation]. Temple University; 2018. Available from: http://digital.library.temple.edu/u?/p245801coll10,491387


Temple University

7. 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 October 16, 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. 16 Oct 2019.

Vancouver:

Pansuria M. EFFECT AND MECHANISM OF HYPERHOMOCYSTEINEMIA ON ENDOTHELIAL INSULIN SIGNALING. [Internet] [Doctoral dissertation]. Temple University; 2013. [cited 2019 Oct 16]. 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

8. Duran, Jason Mathew. Bone-derived stem cells repair the heart after myocardial infarction through transdifferentiation and paracrine signaling mechanisms.

Degree: PhD, 2015, Temple University

Physiology

Rationale: Autologous bone marrow- or cardiac-derived stem cell therapy for heart disease has demonstrated safety and efficacy in clinical trials but has only offered… (more)

Subjects/Keywords: Physiology; myocardial infarction; paracrine factors; regeneration; stem cells; transdifferentiation

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APA (6th Edition):

Duran, J. M. (2015). Bone-derived stem cells repair the heart after myocardial infarction through transdifferentiation and paracrine signaling mechanisms. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,253042

Chicago Manual of Style (16th Edition):

Duran, Jason Mathew. “Bone-derived stem cells repair the heart after myocardial infarction through transdifferentiation and paracrine signaling mechanisms.” 2015. Doctoral Dissertation, Temple University. Accessed October 16, 2019. http://digital.library.temple.edu/u?/p245801coll10,253042.

MLA Handbook (7th Edition):

Duran, Jason Mathew. “Bone-derived stem cells repair the heart after myocardial infarction through transdifferentiation and paracrine signaling mechanisms.” 2015. Web. 16 Oct 2019.

Vancouver:

Duran JM. Bone-derived stem cells repair the heart after myocardial infarction through transdifferentiation and paracrine signaling mechanisms. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Oct 16]. Available from: http://digital.library.temple.edu/u?/p245801coll10,253042.

Council of Science Editors:

Duran JM. Bone-derived stem cells repair the heart after myocardial infarction through transdifferentiation and paracrine signaling mechanisms. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,253042


Temple University

9. Ellison, Stephen Patrick. THE EFFECTS OF INTERLEUKIN-19 ON ATTENUATION OF THE VASCULAR RESPONSE TO INJURY.

Degree: PhD, 2015, Temple University

Physiology

BACKGROUND: Despite aggressive dietary modification, lipid lowering medications, and other medical therapy, vascular proliferative diseases continue to account for 50% of all mortality in… (more)

Subjects/Keywords: Physiology;

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APA (6th Edition):

Ellison, S. P. (2015). THE EFFECTS OF INTERLEUKIN-19 ON ATTENUATION OF THE VASCULAR RESPONSE TO INJURY. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,253270

Chicago Manual of Style (16th Edition):

Ellison, Stephen Patrick. “THE EFFECTS OF INTERLEUKIN-19 ON ATTENUATION OF THE VASCULAR RESPONSE TO INJURY.” 2015. Doctoral Dissertation, Temple University. Accessed October 16, 2019. http://digital.library.temple.edu/u?/p245801coll10,253270.

MLA Handbook (7th Edition):

Ellison, Stephen Patrick. “THE EFFECTS OF INTERLEUKIN-19 ON ATTENUATION OF THE VASCULAR RESPONSE TO INJURY.” 2015. Web. 16 Oct 2019.

Vancouver:

Ellison SP. THE EFFECTS OF INTERLEUKIN-19 ON ATTENUATION OF THE VASCULAR RESPONSE TO INJURY. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Oct 16]. Available from: http://digital.library.temple.edu/u?/p245801coll10,253270.

Council of Science Editors:

Ellison SP. THE EFFECTS OF INTERLEUKIN-19 ON ATTENUATION OF THE VASCULAR RESPONSE TO INJURY. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,253270


Temple University

10. Reichenbach, Zachary Wilmer. Modulation of the Endogenous Cannabinoid System to Attenuate Inflammation in Central Nervous System Injury.

Degree: PhD, 2015, Temple University

Physiology

In non-pathological states the central nervous system maintains a degree of immunological privilege. When illness or injury occur, this privilege can be lost and… (more)

Subjects/Keywords: Neurosciences; Immunology; Pharmacology;

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APA (6th Edition):

Reichenbach, Z. W. (2015). Modulation of the Endogenous Cannabinoid System to Attenuate Inflammation in Central Nervous System Injury. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,253514

Chicago Manual of Style (16th Edition):

Reichenbach, Zachary Wilmer. “Modulation of the Endogenous Cannabinoid System to Attenuate Inflammation in Central Nervous System Injury.” 2015. Doctoral Dissertation, Temple University. Accessed October 16, 2019. http://digital.library.temple.edu/u?/p245801coll10,253514.

MLA Handbook (7th Edition):

Reichenbach, Zachary Wilmer. “Modulation of the Endogenous Cannabinoid System to Attenuate Inflammation in Central Nervous System Injury.” 2015. Web. 16 Oct 2019.

Vancouver:

Reichenbach ZW. Modulation of the Endogenous Cannabinoid System to Attenuate Inflammation in Central Nervous System Injury. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Oct 16]. Available from: http://digital.library.temple.edu/u?/p245801coll10,253514.

Council of Science Editors:

Reichenbach ZW. Modulation of the Endogenous Cannabinoid System to Attenuate Inflammation in Central Nervous System Injury. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,253514


Temple University

11. Heayn, Michelle Diane. The Role of Caveolae in PECAM-1 Mechanotransduction.

Degree: PhD, 2014, Temple University

Physiology

Altered fluid flow, which is found in branches and curvatures of arteries, results in abnormal forces on the endothelial cells (EC). These forces have… (more)

Subjects/Keywords: Cellular biology; Molecular biology; Biomechanics;

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APA (6th Edition):

Heayn, M. D. (2014). The Role of Caveolae in PECAM-1 Mechanotransduction. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,263778

Chicago Manual of Style (16th Edition):

Heayn, Michelle Diane. “The Role of Caveolae in PECAM-1 Mechanotransduction.” 2014. Doctoral Dissertation, Temple University. Accessed October 16, 2019. http://digital.library.temple.edu/u?/p245801coll10,263778.

MLA Handbook (7th Edition):

Heayn, Michelle Diane. “The Role of Caveolae in PECAM-1 Mechanotransduction.” 2014. Web. 16 Oct 2019.

Vancouver:

Heayn MD. The Role of Caveolae in PECAM-1 Mechanotransduction. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2019 Oct 16]. Available from: http://digital.library.temple.edu/u?/p245801coll10,263778.

Council of Science Editors:

Heayn MD. The Role of Caveolae in PECAM-1 Mechanotransduction. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,263778


Temple University

12. Manne, Bhanu Kanth. CLEC-2 SIGNAL TRANSDUCTION IN PLATELET ACTIVATION.

Degree: PhD, 2015, Temple University

Physiology

Platelets are involved in many processes ranging from fighting microbial infections and triggering inflammation to promoting tumor angiogenesis and metastasis. Nevertheless, the primary physiological… (more)

Subjects/Keywords: Physiology; Cellular biology;

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APA (6th Edition):

Manne, B. K. (2015). CLEC-2 SIGNAL TRANSDUCTION IN PLATELET ACTIVATION. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,340495

Chicago Manual of Style (16th Edition):

Manne, Bhanu Kanth. “CLEC-2 SIGNAL TRANSDUCTION IN PLATELET ACTIVATION.” 2015. Doctoral Dissertation, Temple University. Accessed October 16, 2019. http://digital.library.temple.edu/u?/p245801coll10,340495.

MLA Handbook (7th Edition):

Manne, Bhanu Kanth. “CLEC-2 SIGNAL TRANSDUCTION IN PLATELET ACTIVATION.” 2015. Web. 16 Oct 2019.

Vancouver:

Manne BK. CLEC-2 SIGNAL TRANSDUCTION IN PLATELET ACTIVATION. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Oct 16]. Available from: http://digital.library.temple.edu/u?/p245801coll10,340495.

Council of Science Editors:

Manne BK. CLEC-2 SIGNAL TRANSDUCTION IN PLATELET ACTIVATION. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,340495


Temple University

13. 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 October 16, 2019. 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. 16 Oct 2019.

Vancouver:

Richards JM. The Potential of IL-19 As a Therapeutic Anti-inflammatory and Angiogenic Cytokine. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Oct 16]. 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

14. Preston, Kyle J. Macronutrient Activation of Endothelium Dependent Leukocyte Trafficking: Metabolic Implications.

Degree: PhD, 2015, Temple University

Physiology

Obesity and insulin resistance are characterized by elevated pro-inflammatory proteins in the blood and immune cell accumulation in the visceral adipose tissue. Resident leukocytes… (more)

Subjects/Keywords: Physiology;

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APA (6th Edition):

Preston, K. J. (2015). Macronutrient Activation of Endothelium Dependent Leukocyte Trafficking: Metabolic Implications. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,361365

Chicago Manual of Style (16th Edition):

Preston, Kyle J. “Macronutrient Activation of Endothelium Dependent Leukocyte Trafficking: Metabolic Implications.” 2015. Doctoral Dissertation, Temple University. Accessed October 16, 2019. http://digital.library.temple.edu/u?/p245801coll10,361365.

MLA Handbook (7th Edition):

Preston, Kyle J. “Macronutrient Activation of Endothelium Dependent Leukocyte Trafficking: Metabolic Implications.” 2015. Web. 16 Oct 2019.

Vancouver:

Preston KJ. Macronutrient Activation of Endothelium Dependent Leukocyte Trafficking: Metabolic Implications. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Oct 16]. Available from: http://digital.library.temple.edu/u?/p245801coll10,361365.

Council of Science Editors:

Preston KJ. Macronutrient Activation of Endothelium Dependent Leukocyte Trafficking: Metabolic Implications. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,361365


Temple University

15. Etwebi, Zienab. MYELOPEROXIDASE INDUCES ENDOTHELIAL DYSFUNCTION VIA ACTIVATION OF THE CALCIUM DEPENDENT PROTEASE CALPAIN.

Degree: PhD, 2018, Temple University

Biomedical Sciences

Cardiovascular disease and the associated endothelial dysfunction are characterized by leukocyte activation, decrease endothelial nitric oxide synthase (eNOS) activity, and increased endothelial cell… (more)

Subjects/Keywords: Physiology; Cellular biology;

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APA (6th Edition):

Etwebi, Z. (2018). MYELOPEROXIDASE INDUCES ENDOTHELIAL DYSFUNCTION VIA ACTIVATION OF THE CALCIUM DEPENDENT PROTEASE CALPAIN. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,508536

Chicago Manual of Style (16th Edition):

Etwebi, Zienab. “MYELOPEROXIDASE INDUCES ENDOTHELIAL DYSFUNCTION VIA ACTIVATION OF THE CALCIUM DEPENDENT PROTEASE CALPAIN.” 2018. Doctoral Dissertation, Temple University. Accessed October 16, 2019. http://digital.library.temple.edu/u?/p245801coll10,508536.

MLA Handbook (7th Edition):

Etwebi, Zienab. “MYELOPEROXIDASE INDUCES ENDOTHELIAL DYSFUNCTION VIA ACTIVATION OF THE CALCIUM DEPENDENT PROTEASE CALPAIN.” 2018. Web. 16 Oct 2019.

Vancouver:

Etwebi Z. MYELOPEROXIDASE INDUCES ENDOTHELIAL DYSFUNCTION VIA ACTIVATION OF THE CALCIUM DEPENDENT PROTEASE CALPAIN. [Internet] [Doctoral dissertation]. Temple University; 2018. [cited 2019 Oct 16]. Available from: http://digital.library.temple.edu/u?/p245801coll10,508536.

Council of Science Editors:

Etwebi Z. MYELOPEROXIDASE INDUCES ENDOTHELIAL DYSFUNCTION VIA ACTIVATION OF THE CALCIUM DEPENDENT PROTEASE CALPAIN. [Doctoral Dissertation]. Temple University; 2018. Available from: http://digital.library.temple.edu/u?/p245801coll10,508536


Temple University

16. Inamdar, Vaishali Vijay. FUNCTIONAL PROTEIN TYROSINE PHOSPHATASES IN PLATELETS.

Degree: PhD, 2017, Temple University

Biomedical Sciences

Platelets are small anucleate cells in blood that are derived from megakaryocytes and their primary function is to prevent bleeding. Upon vascular injury,… (more)

Subjects/Keywords: Physiology

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

APA (6th Edition):

Inamdar, V. V. (2017). FUNCTIONAL PROTEIN TYROSINE PHOSPHATASES IN PLATELETS. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,473257

Chicago Manual of Style (16th Edition):

Inamdar, Vaishali Vijay. “FUNCTIONAL PROTEIN TYROSINE PHOSPHATASES IN PLATELETS.” 2017. Doctoral Dissertation, Temple University. Accessed October 16, 2019. http://digital.library.temple.edu/u?/p245801coll10,473257.

MLA Handbook (7th Edition):

Inamdar, Vaishali Vijay. “FUNCTIONAL PROTEIN TYROSINE PHOSPHATASES IN PLATELETS.” 2017. Web. 16 Oct 2019.

Vancouver:

Inamdar VV. FUNCTIONAL PROTEIN TYROSINE PHOSPHATASES IN PLATELETS. [Internet] [Doctoral dissertation]. Temple University; 2017. [cited 2019 Oct 16]. Available from: http://digital.library.temple.edu/u?/p245801coll10,473257.

Council of Science Editors:

Inamdar VV. FUNCTIONAL PROTEIN TYROSINE PHOSPHATASES IN PLATELETS. [Doctoral Dissertation]. Temple University; 2017. Available from: http://digital.library.temple.edu/u?/p245801coll10,473257


Temple University

17. Patel, Akruti. NOVEL REGULATORS OF GPVI-MEDIATED PLATELET ACTIVATION.

Degree: PhD, 2017, Temple University

Biomedical Sciences

Platelets are anucleate cells that are crucial mediators of hemostasis and thrombosis. Under physiological conditions, platelets are maintained in a quiescent state within… (more)

Subjects/Keywords: Physiology

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

APA (6th Edition):

Patel, A. (2017). NOVEL REGULATORS OF GPVI-MEDIATED PLATELET ACTIVATION. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,473397

Chicago Manual of Style (16th Edition):

Patel, Akruti. “NOVEL REGULATORS OF GPVI-MEDIATED PLATELET ACTIVATION.” 2017. Doctoral Dissertation, Temple University. Accessed October 16, 2019. http://digital.library.temple.edu/u?/p245801coll10,473397.

MLA Handbook (7th Edition):

Patel, Akruti. “NOVEL REGULATORS OF GPVI-MEDIATED PLATELET ACTIVATION.” 2017. Web. 16 Oct 2019.

Vancouver:

Patel A. NOVEL REGULATORS OF GPVI-MEDIATED PLATELET ACTIVATION. [Internet] [Doctoral dissertation]. Temple University; 2017. [cited 2019 Oct 16]. Available from: http://digital.library.temple.edu/u?/p245801coll10,473397.

Council of Science Editors:

Patel A. NOVEL REGULATORS OF GPVI-MEDIATED PLATELET ACTIVATION. [Doctoral Dissertation]. Temple University; 2017. Available from: http://digital.library.temple.edu/u?/p245801coll10,473397


Temple University

18. Forrester, Steven James. MITOCHONDRIA FACILITATE VASCULAR INFLAMMATION: THE ROLE OF CANONICAL INFLAMMATORY SIGNALING IN THE REGULATION OF MITOCHONDRIAL MORPHOLOGY.

Degree: PhD, 2017, Temple University

Kinesiology

Vascular inflammation is an underlying cause to numerous diseases and is characterized by classical NF-κB activation and downstream physiological responses including inflammatory gene induction… (more)

Subjects/Keywords: Physiology; Cellular biology; Medicine

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

APA (6th Edition):

Forrester, S. J. (2017). MITOCHONDRIA FACILITATE VASCULAR INFLAMMATION: THE ROLE OF CANONICAL INFLAMMATORY SIGNALING IN THE REGULATION OF MITOCHONDRIAL MORPHOLOGY. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,429386

Chicago Manual of Style (16th Edition):

Forrester, Steven James. “MITOCHONDRIA FACILITATE VASCULAR INFLAMMATION: THE ROLE OF CANONICAL INFLAMMATORY SIGNALING IN THE REGULATION OF MITOCHONDRIAL MORPHOLOGY.” 2017. Doctoral Dissertation, Temple University. Accessed October 16, 2019. http://digital.library.temple.edu/u?/p245801coll10,429386.

MLA Handbook (7th Edition):

Forrester, Steven James. “MITOCHONDRIA FACILITATE VASCULAR INFLAMMATION: THE ROLE OF CANONICAL INFLAMMATORY SIGNALING IN THE REGULATION OF MITOCHONDRIAL MORPHOLOGY.” 2017. Web. 16 Oct 2019.

Vancouver:

Forrester SJ. MITOCHONDRIA FACILITATE VASCULAR INFLAMMATION: THE ROLE OF CANONICAL INFLAMMATORY SIGNALING IN THE REGULATION OF MITOCHONDRIAL MORPHOLOGY. [Internet] [Doctoral dissertation]. Temple University; 2017. [cited 2019 Oct 16]. Available from: http://digital.library.temple.edu/u?/p245801coll10,429386.

Council of Science Editors:

Forrester SJ. MITOCHONDRIA FACILITATE VASCULAR INFLAMMATION: THE ROLE OF CANONICAL INFLAMMATORY SIGNALING IN THE REGULATION OF MITOCHONDRIAL MORPHOLOGY. [Doctoral Dissertation]. Temple University; 2017. Available from: http://digital.library.temple.edu/u?/p245801coll10,429386

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