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You searched for +publisher:"Dalhousie University" +contributor:("Dr. Elizabeth Cowley"). Showing records 1 – 15 of 15 total matches.

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Dalhousie University

1. Ismaiel, Nada. Protective Ventilation vs. Hypercapnia for the Attenuation of Ventilator-Associated Lung Injury.

Degree: MS, Department of Physiology & Biophysics, 2011, Dalhousie University

 Mechanically ventilated patients are at risk of developing Ventilator-Associated Lung Injury (VALI). Improved ventilation strategies by lung-protective settings may cause hypercapnia. This study investigated whether… (more)

Subjects/Keywords: Acute Lung Injury; Mechanical Ventilation; Hypercapnia; Inflammation; Carbon Dioxide

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APA (6th Edition):

Ismaiel, N. (2011). Protective Ventilation vs. Hypercapnia for the Attenuation of Ventilator-Associated Lung Injury. (Masters Thesis). Dalhousie University. Retrieved from http://hdl.handle.net/10222/14227

Chicago Manual of Style (16th Edition):

Ismaiel, Nada. “Protective Ventilation vs. Hypercapnia for the Attenuation of Ventilator-Associated Lung Injury.” 2011. Masters Thesis, Dalhousie University. Accessed April 13, 2021. http://hdl.handle.net/10222/14227.

MLA Handbook (7th Edition):

Ismaiel, Nada. “Protective Ventilation vs. Hypercapnia for the Attenuation of Ventilator-Associated Lung Injury.” 2011. Web. 13 Apr 2021.

Vancouver:

Ismaiel N. Protective Ventilation vs. Hypercapnia for the Attenuation of Ventilator-Associated Lung Injury. [Internet] [Masters thesis]. Dalhousie University; 2011. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/10222/14227.

Council of Science Editors:

Ismaiel N. Protective Ventilation vs. Hypercapnia for the Attenuation of Ventilator-Associated Lung Injury. [Masters Thesis]. Dalhousie University; 2011. Available from: http://hdl.handle.net/10222/14227


Dalhousie University

2. Kalbfleisch, Emma R. ACTIVATION OF THE PGE2 RECEPTOR EP4 PROTECTS AGAINST OXIDANT-INDUCED APOPTOSIS IN AIRWAY EPITHELIAL CELLS.

Degree: MS, Department of Physiology & Biophysics, 2012, Dalhousie University

 Heme oxygenase (HO)-1 expression is induced in pulmonary diseases characterized by oxidative stress, including CF, and is cytoprotective in nature. Prostaglanin (PG) E2 can protect… (more)

Subjects/Keywords: Subject Not Available

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APA (6th Edition):

Kalbfleisch, E. R. (2012). ACTIVATION OF THE PGE2 RECEPTOR EP4 PROTECTS AGAINST OXIDANT-INDUCED APOPTOSIS IN AIRWAY EPITHELIAL CELLS. (Masters Thesis). Dalhousie University. Retrieved from http://hdl.handle.net/10222/15417

Chicago Manual of Style (16th Edition):

Kalbfleisch, Emma R. “ACTIVATION OF THE PGE2 RECEPTOR EP4 PROTECTS AGAINST OXIDANT-INDUCED APOPTOSIS IN AIRWAY EPITHELIAL CELLS.” 2012. Masters Thesis, Dalhousie University. Accessed April 13, 2021. http://hdl.handle.net/10222/15417.

MLA Handbook (7th Edition):

Kalbfleisch, Emma R. “ACTIVATION OF THE PGE2 RECEPTOR EP4 PROTECTS AGAINST OXIDANT-INDUCED APOPTOSIS IN AIRWAY EPITHELIAL CELLS.” 2012. Web. 13 Apr 2021.

Vancouver:

Kalbfleisch ER. ACTIVATION OF THE PGE2 RECEPTOR EP4 PROTECTS AGAINST OXIDANT-INDUCED APOPTOSIS IN AIRWAY EPITHELIAL CELLS. [Internet] [Masters thesis]. Dalhousie University; 2012. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/10222/15417.

Council of Science Editors:

Kalbfleisch ER. ACTIVATION OF THE PGE2 RECEPTOR EP4 PROTECTS AGAINST OXIDANT-INDUCED APOPTOSIS IN AIRWAY EPITHELIAL CELLS. [Masters Thesis]. Dalhousie University; 2012. Available from: http://hdl.handle.net/10222/15417


Dalhousie University

3. Braubach, Oliver Robert. Development, Organization and Plasticity of the Zebrafish Olfactory System.

Degree: PhD, Department of Physiology & Biophysics with Neuroscience, 2011, Dalhousie University

 Olfaction is vitally important to animals in all environments and is used to identify food, habitat, conspecifics and predators. Some odors, like pheromones or the… (more)

Subjects/Keywords: In vivo; neuroscience; sensory system; zebrafish; anatomy; transgenic; plasticity; development; olfaction

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APA (6th Edition):

Braubach, O. R. (2011). Development, Organization and Plasticity of the Zebrafish Olfactory System. (Doctoral Dissertation). Dalhousie University. Retrieved from http://hdl.handle.net/10222/13342

Chicago Manual of Style (16th Edition):

Braubach, Oliver Robert. “Development, Organization and Plasticity of the Zebrafish Olfactory System.” 2011. Doctoral Dissertation, Dalhousie University. Accessed April 13, 2021. http://hdl.handle.net/10222/13342.

MLA Handbook (7th Edition):

Braubach, Oliver Robert. “Development, Organization and Plasticity of the Zebrafish Olfactory System.” 2011. Web. 13 Apr 2021.

Vancouver:

Braubach OR. Development, Organization and Plasticity of the Zebrafish Olfactory System. [Internet] [Doctoral dissertation]. Dalhousie University; 2011. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/10222/13342.

Council of Science Editors:

Braubach OR. Development, Organization and Plasticity of the Zebrafish Olfactory System. [Doctoral Dissertation]. Dalhousie University; 2011. Available from: http://hdl.handle.net/10222/13342


Dalhousie University

4. Adamczyk, Andrew. CHARACTERIZATION OF THE PHOSPHODIESTERASE SUBTYPES THAT REGULATE MOUSE ATRIAL MYOCYTE ELECTROPHYSIOLOGY.

Degree: MS, Department of Physiology & Biophysics, 2012, Dalhousie University

 Phosphodiesterases (PDEs) are the enzymes responsible for the hydrolysis of cyclic nucleotides including cAMP and cGMP. We recently discovered that natriuretic peptides elicit effects in… (more)

Subjects/Keywords: Electrophysiology; Cardiomyocyte; Action Potential; Calcium Current; Phosphodiesterase

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APA (6th Edition):

Adamczyk, A. (2012). CHARACTERIZATION OF THE PHOSPHODIESTERASE SUBTYPES THAT REGULATE MOUSE ATRIAL MYOCYTE ELECTROPHYSIOLOGY. (Masters Thesis). Dalhousie University. Retrieved from http://hdl.handle.net/10222/15708

Chicago Manual of Style (16th Edition):

Adamczyk, Andrew. “CHARACTERIZATION OF THE PHOSPHODIESTERASE SUBTYPES THAT REGULATE MOUSE ATRIAL MYOCYTE ELECTROPHYSIOLOGY.” 2012. Masters Thesis, Dalhousie University. Accessed April 13, 2021. http://hdl.handle.net/10222/15708.

MLA Handbook (7th Edition):

Adamczyk, Andrew. “CHARACTERIZATION OF THE PHOSPHODIESTERASE SUBTYPES THAT REGULATE MOUSE ATRIAL MYOCYTE ELECTROPHYSIOLOGY.” 2012. Web. 13 Apr 2021.

Vancouver:

Adamczyk A. CHARACTERIZATION OF THE PHOSPHODIESTERASE SUBTYPES THAT REGULATE MOUSE ATRIAL MYOCYTE ELECTROPHYSIOLOGY. [Internet] [Masters thesis]. Dalhousie University; 2012. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/10222/15708.

Council of Science Editors:

Adamczyk A. CHARACTERIZATION OF THE PHOSPHODIESTERASE SUBTYPES THAT REGULATE MOUSE ATRIAL MYOCYTE ELECTROPHYSIOLOGY. [Masters Thesis]. Dalhousie University; 2012. Available from: http://hdl.handle.net/10222/15708


Dalhousie University

5. Cao, Qi. Expression and Role of Anaphylatoxin Receptors on Human Colonic Epithelial Cells.

Degree: MS, Department of Microbiology & Immunology, 2013, Dalhousie University

 Human colonic epithelial cell lines (T84, Caco2 and HT-29) were used to address the question of whether intestinal epithelial cells can detect and respond to… (more)

Subjects/Keywords: Anaphylatoxin; Anaphylatoxin receptor; Chemokine; Human colonic epithelial cell

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APA (6th Edition):

Cao, Q. (2013). Expression and Role of Anaphylatoxin Receptors on Human Colonic Epithelial Cells. (Masters Thesis). Dalhousie University. Retrieved from http://hdl.handle.net/10222/21905

Chicago Manual of Style (16th Edition):

Cao, Qi. “Expression and Role of Anaphylatoxin Receptors on Human Colonic Epithelial Cells.” 2013. Masters Thesis, Dalhousie University. Accessed April 13, 2021. http://hdl.handle.net/10222/21905.

MLA Handbook (7th Edition):

Cao, Qi. “Expression and Role of Anaphylatoxin Receptors on Human Colonic Epithelial Cells.” 2013. Web. 13 Apr 2021.

Vancouver:

Cao Q. Expression and Role of Anaphylatoxin Receptors on Human Colonic Epithelial Cells. [Internet] [Masters thesis]. Dalhousie University; 2013. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/10222/21905.

Council of Science Editors:

Cao Q. Expression and Role of Anaphylatoxin Receptors on Human Colonic Epithelial Cells. [Masters Thesis]. Dalhousie University; 2013. Available from: http://hdl.handle.net/10222/21905


Dalhousie University

6. Whitehouse, Scott David. THE EFFECTS OF P22PHOX GENETIC POLYMORPHISMS AND NATURAL COMPOUNDS ON REACTIVE OXYGEN SPECIES FORMATION.

Degree: MS, Department of Pathology, 2013, Dalhousie University

 Reactive oxygen species (ROS) have a role in cardiovascular health and disease. This study was undertaken to determine if ROS formation is influenced by either… (more)

Subjects/Keywords: NOX; ROS; Reactive oxygen species; p22; NADPH oxidase; Celastrol; Resveratrol; NOX1; NOX2; p22phox; CYBA

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APA (6th Edition):

Whitehouse, S. D. (2013). THE EFFECTS OF P22PHOX GENETIC POLYMORPHISMS AND NATURAL COMPOUNDS ON REACTIVE OXYGEN SPECIES FORMATION. (Masters Thesis). Dalhousie University. Retrieved from http://hdl.handle.net/10222/21436

Chicago Manual of Style (16th Edition):

Whitehouse, Scott David. “THE EFFECTS OF P22PHOX GENETIC POLYMORPHISMS AND NATURAL COMPOUNDS ON REACTIVE OXYGEN SPECIES FORMATION.” 2013. Masters Thesis, Dalhousie University. Accessed April 13, 2021. http://hdl.handle.net/10222/21436.

MLA Handbook (7th Edition):

Whitehouse, Scott David. “THE EFFECTS OF P22PHOX GENETIC POLYMORPHISMS AND NATURAL COMPOUNDS ON REACTIVE OXYGEN SPECIES FORMATION.” 2013. Web. 13 Apr 2021.

Vancouver:

Whitehouse SD. THE EFFECTS OF P22PHOX GENETIC POLYMORPHISMS AND NATURAL COMPOUNDS ON REACTIVE OXYGEN SPECIES FORMATION. [Internet] [Masters thesis]. Dalhousie University; 2013. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/10222/21436.

Council of Science Editors:

Whitehouse SD. THE EFFECTS OF P22PHOX GENETIC POLYMORPHISMS AND NATURAL COMPOUNDS ON REACTIVE OXYGEN SPECIES FORMATION. [Masters Thesis]. Dalhousie University; 2013. Available from: http://hdl.handle.net/10222/21436


Dalhousie University

7. Gagnon, Jeffrey. Unravelling the mechanism of ghrelin secretion and the effects of ghrelin reduction using a receptor decoy approach.

Degree: PhD, Department of Physiology & Biophysics, 2013, Dalhousie University

 The incidence of obesity, and the associated morbidities and mortality are increasing. Strategies to manage this disease hinge on the balance of caloric intake and… (more)

Subjects/Keywords: diabetes; ghrelin; hormones

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APA (6th Edition):

Gagnon, J. (2013). Unravelling the mechanism of ghrelin secretion and the effects of ghrelin reduction using a receptor decoy approach. (Doctoral Dissertation). Dalhousie University. Retrieved from http://hdl.handle.net/10222/21435

Chicago Manual of Style (16th Edition):

Gagnon, Jeffrey. “Unravelling the mechanism of ghrelin secretion and the effects of ghrelin reduction using a receptor decoy approach.” 2013. Doctoral Dissertation, Dalhousie University. Accessed April 13, 2021. http://hdl.handle.net/10222/21435.

MLA Handbook (7th Edition):

Gagnon, Jeffrey. “Unravelling the mechanism of ghrelin secretion and the effects of ghrelin reduction using a receptor decoy approach.” 2013. Web. 13 Apr 2021.

Vancouver:

Gagnon J. Unravelling the mechanism of ghrelin secretion and the effects of ghrelin reduction using a receptor decoy approach. [Internet] [Doctoral dissertation]. Dalhousie University; 2013. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/10222/21435.

Council of Science Editors:

Gagnon J. Unravelling the mechanism of ghrelin secretion and the effects of ghrelin reduction using a receptor decoy approach. [Doctoral Dissertation]. Dalhousie University; 2013. Available from: http://hdl.handle.net/10222/21435


Dalhousie University

8. Nelson, Stephanie. Regulation of Pancreatic Beta Cell Mass and Function by Proghrelin Derived Peptides.

Degree: MS, Department of Physiology & Biophysics, 2010, Dalhousie University

 Proghrelin produces three proghrelin derived peptides (PGDP) known for their roles in glucose homeostasis: acylated ghrelin (AG), unacylated ghrelin (UAG), and obestatin (Ob). Only the… (more)

Subjects/Keywords: Ghrelin; Diabetes; insulin; obestatin

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APA (6th Edition):

Nelson, S. (2010). Regulation of Pancreatic Beta Cell Mass and Function by Proghrelin Derived Peptides. (Masters Thesis). Dalhousie University. Retrieved from http://hdl.handle.net/10222/13014

Chicago Manual of Style (16th Edition):

Nelson, Stephanie. “Regulation of Pancreatic Beta Cell Mass and Function by Proghrelin Derived Peptides.” 2010. Masters Thesis, Dalhousie University. Accessed April 13, 2021. http://hdl.handle.net/10222/13014.

MLA Handbook (7th Edition):

Nelson, Stephanie. “Regulation of Pancreatic Beta Cell Mass and Function by Proghrelin Derived Peptides.” 2010. Web. 13 Apr 2021.

Vancouver:

Nelson S. Regulation of Pancreatic Beta Cell Mass and Function by Proghrelin Derived Peptides. [Internet] [Masters thesis]. Dalhousie University; 2010. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/10222/13014.

Council of Science Editors:

Nelson S. Regulation of Pancreatic Beta Cell Mass and Function by Proghrelin Derived Peptides. [Masters Thesis]. Dalhousie University; 2010. Available from: http://hdl.handle.net/10222/13014


Dalhousie University

9. Springer, Jeremy. Brain type natriuretic peptide increases L-type Ca2+ current in atrial myocytes by activating natriuretic peptide receptor A.

Degree: MS, Department of Physiology & Biophysics, 2012, Dalhousie University

 Natriuretic peptides are a group of hormones, including atrial-, brain-, and C-type- natriuretic peptides (ANP, BNP, CNP). BNP can bind to two NP receptors (NPRs)… (more)

Subjects/Keywords: Brain type natriuretic peptide; phosphodiesterase; electrophysiology; cardiac; cGMP; atrial

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APA (6th Edition):

Springer, J. (2012). Brain type natriuretic peptide increases L-type Ca2+ current in atrial myocytes by activating natriuretic peptide receptor A. (Masters Thesis). Dalhousie University. Retrieved from http://hdl.handle.net/10222/15721

Chicago Manual of Style (16th Edition):

Springer, Jeremy. “Brain type natriuretic peptide increases L-type Ca2+ current in atrial myocytes by activating natriuretic peptide receptor A.” 2012. Masters Thesis, Dalhousie University. Accessed April 13, 2021. http://hdl.handle.net/10222/15721.

MLA Handbook (7th Edition):

Springer, Jeremy. “Brain type natriuretic peptide increases L-type Ca2+ current in atrial myocytes by activating natriuretic peptide receptor A.” 2012. Web. 13 Apr 2021.

Vancouver:

Springer J. Brain type natriuretic peptide increases L-type Ca2+ current in atrial myocytes by activating natriuretic peptide receptor A. [Internet] [Masters thesis]. Dalhousie University; 2012. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/10222/15721.

Council of Science Editors:

Springer J. Brain type natriuretic peptide increases L-type Ca2+ current in atrial myocytes by activating natriuretic peptide receptor A. [Masters Thesis]. Dalhousie University; 2012. Available from: http://hdl.handle.net/10222/15721


Dalhousie University

10. MacLeod, Katie. The Role of K+ Channels in Cell Proliferation and Cell Volume Regulation in Human Bronchial Epithelial Cells.

Degree: MS, Department of Physiology & Biophysics, 2011, Dalhousie University

 K+ channels are expressed in a wide variety of cell types, including airway epithelial cells. The purpose of this study was to investigate the role… (more)

Subjects/Keywords: Subject Not Available

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APA (6th Edition):

MacLeod, K. (2011). The Role of K+ Channels in Cell Proliferation and Cell Volume Regulation in Human Bronchial Epithelial Cells. (Masters Thesis). Dalhousie University. Retrieved from http://hdl.handle.net/10222/14077

Chicago Manual of Style (16th Edition):

MacLeod, Katie. “The Role of K+ Channels in Cell Proliferation and Cell Volume Regulation in Human Bronchial Epithelial Cells.” 2011. Masters Thesis, Dalhousie University. Accessed April 13, 2021. http://hdl.handle.net/10222/14077.

MLA Handbook (7th Edition):

MacLeod, Katie. “The Role of K+ Channels in Cell Proliferation and Cell Volume Regulation in Human Bronchial Epithelial Cells.” 2011. Web. 13 Apr 2021.

Vancouver:

MacLeod K. The Role of K+ Channels in Cell Proliferation and Cell Volume Regulation in Human Bronchial Epithelial Cells. [Internet] [Masters thesis]. Dalhousie University; 2011. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/10222/14077.

Council of Science Editors:

MacLeod K. The Role of K+ Channels in Cell Proliferation and Cell Volume Regulation in Human Bronchial Epithelial Cells. [Masters Thesis]. Dalhousie University; 2011. Available from: http://hdl.handle.net/10222/14077


Dalhousie University

11. Conrad, Dustin. Increased VIP Receptor Expression Mediates CFTR Membrane Localization in Response to VIP Treatment in VIP Knockout Mice.

Degree: MS, Department of Physiology & Biophysics, 2011, Dalhousie University

 Cystic Fibrosis (CF) is caused by mutations in CFTR, a protein for chloride efflux in epithelial cells. VIP is a peptide that activates CFTR and… (more)

Subjects/Keywords: VIP; CFTR; VIPKO; Cystic Fibrosis; VPAC1; VPAC2; PAC1; Lung; Duodenum

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APA (6th Edition):

Conrad, D. (2011). Increased VIP Receptor Expression Mediates CFTR Membrane Localization in Response to VIP Treatment in VIP Knockout Mice. (Masters Thesis). Dalhousie University. Retrieved from http://hdl.handle.net/10222/14231

Chicago Manual of Style (16th Edition):

Conrad, Dustin. “Increased VIP Receptor Expression Mediates CFTR Membrane Localization in Response to VIP Treatment in VIP Knockout Mice.” 2011. Masters Thesis, Dalhousie University. Accessed April 13, 2021. http://hdl.handle.net/10222/14231.

MLA Handbook (7th Edition):

Conrad, Dustin. “Increased VIP Receptor Expression Mediates CFTR Membrane Localization in Response to VIP Treatment in VIP Knockout Mice.” 2011. Web. 13 Apr 2021.

Vancouver:

Conrad D. Increased VIP Receptor Expression Mediates CFTR Membrane Localization in Response to VIP Treatment in VIP Knockout Mice. [Internet] [Masters thesis]. Dalhousie University; 2011. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/10222/14231.

Council of Science Editors:

Conrad D. Increased VIP Receptor Expression Mediates CFTR Membrane Localization in Response to VIP Treatment in VIP Knockout Mice. [Masters Thesis]. Dalhousie University; 2011. Available from: http://hdl.handle.net/10222/14231


Dalhousie University

12. Holland, Patrick. DRUGS, DIMERS, AND MUTATIONS: INVESTIGATING THE EFFECTS OF LIGANDS AND A ?2-ADRENERGIC POLYMORPHISM ON HOMO/HETERODIMERIZATION OF ?2-ADRENERGIC AND ANGIOTENSIN II TYPE 1 RECEPTORS.

Degree: MS, Department of Pharmacology, 2012, Dalhousie University

 GPCRs are known to form dimeric structures, and this affects their pharmacological properties. The ?2AR and AT1aR are GPCRs that are involved the regulation of… (more)

Subjects/Keywords: GPCRs; Signalling; Polymorphism; Dimerization; Receptor Pharmacology

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APA (6th Edition):

Holland, P. (2012). DRUGS, DIMERS, AND MUTATIONS: INVESTIGATING THE EFFECTS OF LIGANDS AND A ?2-ADRENERGIC POLYMORPHISM ON HOMO/HETERODIMERIZATION OF ?2-ADRENERGIC AND ANGIOTENSIN II TYPE 1 RECEPTORS. (Masters Thesis). Dalhousie University. Retrieved from http://hdl.handle.net/10222/15245

Chicago Manual of Style (16th Edition):

Holland, Patrick. “DRUGS, DIMERS, AND MUTATIONS: INVESTIGATING THE EFFECTS OF LIGANDS AND A ?2-ADRENERGIC POLYMORPHISM ON HOMO/HETERODIMERIZATION OF ?2-ADRENERGIC AND ANGIOTENSIN II TYPE 1 RECEPTORS.” 2012. Masters Thesis, Dalhousie University. Accessed April 13, 2021. http://hdl.handle.net/10222/15245.

MLA Handbook (7th Edition):

Holland, Patrick. “DRUGS, DIMERS, AND MUTATIONS: INVESTIGATING THE EFFECTS OF LIGANDS AND A ?2-ADRENERGIC POLYMORPHISM ON HOMO/HETERODIMERIZATION OF ?2-ADRENERGIC AND ANGIOTENSIN II TYPE 1 RECEPTORS.” 2012. Web. 13 Apr 2021.

Vancouver:

Holland P. DRUGS, DIMERS, AND MUTATIONS: INVESTIGATING THE EFFECTS OF LIGANDS AND A ?2-ADRENERGIC POLYMORPHISM ON HOMO/HETERODIMERIZATION OF ?2-ADRENERGIC AND ANGIOTENSIN II TYPE 1 RECEPTORS. [Internet] [Masters thesis]. Dalhousie University; 2012. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/10222/15245.

Council of Science Editors:

Holland P. DRUGS, DIMERS, AND MUTATIONS: INVESTIGATING THE EFFECTS OF LIGANDS AND A ?2-ADRENERGIC POLYMORPHISM ON HOMO/HETERODIMERIZATION OF ?2-ADRENERGIC AND ANGIOTENSIN II TYPE 1 RECEPTORS. [Masters Thesis]. Dalhousie University; 2012. Available from: http://hdl.handle.net/10222/15245


Dalhousie University

13. Levesque, Julie. The Analysis of Brn3a and Thy1-CFP as Potential Markers of Retinal Ganglion Cells after Optic Nerve Injury in Mice.

Degree: MS, Department of Physiology & Biophysics with Neuroscience, 2013, Dalhousie University

 Purpose: Retinal ganglion cell (RGC) loss is a measure of the progression of many visual disorders. It is important to identify RGCs with good specificity,… (more)

Subjects/Keywords: retinal ganglion cell; retina; Thy1-CFP; optic nerve crush; optic nerve transection; mouse; transgenic; Brn3a

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APA (6th Edition):

Levesque, J. (2013). The Analysis of Brn3a and Thy1-CFP as Potential Markers of Retinal Ganglion Cells after Optic Nerve Injury in Mice. (Masters Thesis). Dalhousie University. Retrieved from http://hdl.handle.net/10222/31129

Chicago Manual of Style (16th Edition):

Levesque, Julie. “The Analysis of Brn3a and Thy1-CFP as Potential Markers of Retinal Ganglion Cells after Optic Nerve Injury in Mice.” 2013. Masters Thesis, Dalhousie University. Accessed April 13, 2021. http://hdl.handle.net/10222/31129.

MLA Handbook (7th Edition):

Levesque, Julie. “The Analysis of Brn3a and Thy1-CFP as Potential Markers of Retinal Ganglion Cells after Optic Nerve Injury in Mice.” 2013. Web. 13 Apr 2021.

Vancouver:

Levesque J. The Analysis of Brn3a and Thy1-CFP as Potential Markers of Retinal Ganglion Cells after Optic Nerve Injury in Mice. [Internet] [Masters thesis]. Dalhousie University; 2013. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/10222/31129.

Council of Science Editors:

Levesque J. The Analysis of Brn3a and Thy1-CFP as Potential Markers of Retinal Ganglion Cells after Optic Nerve Injury in Mice. [Masters Thesis]. Dalhousie University; 2013. Available from: http://hdl.handle.net/10222/31129

14. Zaman, Nishat. Influence of loading and matrix stiffness on airway smooth muscle contractile function and phenotype within a 3D microtissue culture model.

Degree: Master of Applied Science, Department of Biomedical Engineering, 2013, Dalhousie University

 Airway remodeling characteristic of asthma involves structural changes altering the elasticity of the airway smooth muscle (ASM) microenvironment potentially leading to ASM dysfunction. This effect… (more)

Subjects/Keywords: tissue culture; tissue engineering; cellular mechanics

…committee members, Dr. Paul Gratzer and Dr. Elizabeth Cowley for their guidance, review of my… 

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APA (6th Edition):

Zaman, N. (2013). Influence of loading and matrix stiffness on airway smooth muscle contractile function and phenotype within a 3D microtissue culture model. (Masters Thesis). Dalhousie University. Retrieved from http://hdl.handle.net/10222/42709

Chicago Manual of Style (16th Edition):

Zaman, Nishat. “Influence of loading and matrix stiffness on airway smooth muscle contractile function and phenotype within a 3D microtissue culture model.” 2013. Masters Thesis, Dalhousie University. Accessed April 13, 2021. http://hdl.handle.net/10222/42709.

MLA Handbook (7th Edition):

Zaman, Nishat. “Influence of loading and matrix stiffness on airway smooth muscle contractile function and phenotype within a 3D microtissue culture model.” 2013. Web. 13 Apr 2021.

Vancouver:

Zaman N. Influence of loading and matrix stiffness on airway smooth muscle contractile function and phenotype within a 3D microtissue culture model. [Internet] [Masters thesis]. Dalhousie University; 2013. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/10222/42709.

Council of Science Editors:

Zaman N. Influence of loading and matrix stiffness on airway smooth muscle contractile function and phenotype within a 3D microtissue culture model. [Masters Thesis]. Dalhousie University; 2013. Available from: http://hdl.handle.net/10222/42709

15. Hogel, Matthew. INVESTIGATING THE MECHANISM OF PROMOTER-SPECIFIC N-TERMINAL MUTANT HUNTINGTIN-MEDIATED TRANSCRIPTIONAL DYSREGULATION.

Degree: PhD, Department of Pharmacology with Neuroscience, 2012, Dalhousie University

 Huntington’s disease (HD) is a neurodegenerative disorder caused by the inheritance of one mutant copy of the huntingtin gene. Mutant huntingtin protein (mHtt) contains an… (more)

Subjects/Keywords: Huntington's; Transcription; Repression; Huntingtin; Polyglutamine; Transcriptional Dysregulation; in vitro transcription; N548; ST14A; Dual-luciferase assay; Chromatin Immunoprecipitation; Promoter Deletion; Linker Scanning Mutagenesis; Quantitative PCR; Promoter binding assay; TBP; RAP30

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

APA (6th Edition):

Hogel, M. (2012). INVESTIGATING THE MECHANISM OF PROMOTER-SPECIFIC N-TERMINAL MUTANT HUNTINGTIN-MEDIATED TRANSCRIPTIONAL DYSREGULATION. (Doctoral Dissertation). Dalhousie University. Retrieved from http://hdl.handle.net/10222/15723

Chicago Manual of Style (16th Edition):

Hogel, Matthew. “INVESTIGATING THE MECHANISM OF PROMOTER-SPECIFIC N-TERMINAL MUTANT HUNTINGTIN-MEDIATED TRANSCRIPTIONAL DYSREGULATION.” 2012. Doctoral Dissertation, Dalhousie University. Accessed April 13, 2021. http://hdl.handle.net/10222/15723.

MLA Handbook (7th Edition):

Hogel, Matthew. “INVESTIGATING THE MECHANISM OF PROMOTER-SPECIFIC N-TERMINAL MUTANT HUNTINGTIN-MEDIATED TRANSCRIPTIONAL DYSREGULATION.” 2012. Web. 13 Apr 2021.

Vancouver:

Hogel M. INVESTIGATING THE MECHANISM OF PROMOTER-SPECIFIC N-TERMINAL MUTANT HUNTINGTIN-MEDIATED TRANSCRIPTIONAL DYSREGULATION. [Internet] [Doctoral dissertation]. Dalhousie University; 2012. [cited 2021 Apr 13]. Available from: http://hdl.handle.net/10222/15723.

Council of Science Editors:

Hogel M. INVESTIGATING THE MECHANISM OF PROMOTER-SPECIFIC N-TERMINAL MUTANT HUNTINGTIN-MEDIATED TRANSCRIPTIONAL DYSREGULATION. [Doctoral Dissertation]. Dalhousie University; 2012. Available from: http://hdl.handle.net/10222/15723

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