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You searched for +publisher:"University of Alabama – Birmingham" +contributor:("Murphy-Ullrich, Joanne<br>"). Showing records 1 – 9 of 9 total matches.

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1. Nilo, Michael P. Effects of cyclic strain on TGF-[Beta]1 activation and phenotype modulation [of] the aortic valve interstitial cells.

Degree: MS, 2009, University of Alabama – Birmingham

Aortic valve interstitial cells (AVICs) are responsible for maintaining tissue structure and function within the highly dynamic mechanical environment of the aortic valve leaflets. AVICs… (more)

Subjects/Keywords: Aortic valve  – Diseases  – Etiology <; br>; Aortic valve  – Effect of stress on <; br>; Phenotypic plasticity <; br>; Myofibroblasts <; br>; Transforming growth factors-beta <; br>; Heart cells

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APA (6th Edition):

Nilo, M. P. (2009). Effects of cyclic strain on TGF-[Beta]1 activation and phenotype modulation [of] the aortic valve interstitial cells. (Masters Thesis). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,801

Chicago Manual of Style (16th Edition):

Nilo, Michael P. “Effects of cyclic strain on TGF-[Beta]1 activation and phenotype modulation [of] the aortic valve interstitial cells.” 2009. Masters Thesis, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,801.

MLA Handbook (7th Edition):

Nilo, Michael P. “Effects of cyclic strain on TGF-[Beta]1 activation and phenotype modulation [of] the aortic valve interstitial cells.” 2009. Web. 22 Feb 2020.

Vancouver:

Nilo MP. Effects of cyclic strain on TGF-[Beta]1 activation and phenotype modulation [of] the aortic valve interstitial cells. [Internet] [Masters thesis]. University of Alabama – Birmingham; 2009. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,801.

Council of Science Editors:

Nilo MP. Effects of cyclic strain on TGF-[Beta]1 activation and phenotype modulation [of] the aortic valve interstitial cells. [Masters Thesis]. University of Alabama – Birmingham; 2009. Available from: http://contentdm.mhsl.uab.edu/u?/etd,801

2. Saxena, Ritu. Mechanisms and countermeasures of microgravity-induced bone loss: in vitro and in vivo model systems.

Degree: PhD, 2009, University of Alabama – Birmingham

Rapid bone loss occurs during prolonged periods of weightlessness experienced by astronauts during spaceflights which leads to osteopenia and increased fracture risk upon return to… (more)

Subjects/Keywords: Bone Resorption<; br>; Cell Differentiation<; br>; Osteoblasts  – cytology<; br>; Osteoclasts  – cytology<; br>; Parathyroid Hormone<; br>; Weightlessness

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APA (6th Edition):

Saxena, R. (2009). Mechanisms and countermeasures of microgravity-induced bone loss: in vitro and in vivo model systems. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,689

Chicago Manual of Style (16th Edition):

Saxena, Ritu. “Mechanisms and countermeasures of microgravity-induced bone loss: in vitro and in vivo model systems.” 2009. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,689.

MLA Handbook (7th Edition):

Saxena, Ritu. “Mechanisms and countermeasures of microgravity-induced bone loss: in vitro and in vivo model systems.” 2009. Web. 22 Feb 2020.

Vancouver:

Saxena R. Mechanisms and countermeasures of microgravity-induced bone loss: in vitro and in vivo model systems. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2009. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,689.

Council of Science Editors:

Saxena R. Mechanisms and countermeasures of microgravity-induced bone loss: in vitro and in vivo model systems. [Doctoral Dissertation]. University of Alabama – Birmingham; 2009. Available from: http://contentdm.mhsl.uab.edu/u?/etd,689

3. Khaled, Saman (Saman Fatima). Low and high LET irradiation of human aortic endothelial cells induces dose and time dependent adhesion of monocytes which is mediated by chemokines expressed by the irradiated endothelium.

Degree: PhD, 2011, University of Alabama – Birmingham

Exposure to radiation from a variety of sources is associated with increased risk of heart disease and stroke. Since radiation also induces inflammation, a possible… (more)

Subjects/Keywords: Aortic Diseases  – etiology<; br>; Heavy Ions  – adverse effects<; br>; Iron<; br>; Leukocytes<; br>; Radiation Dosage

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APA (6th Edition):

Khaled, S. (. F. (2011). Low and high LET irradiation of human aortic endothelial cells induces dose and time dependent adhesion of monocytes which is mediated by chemokines expressed by the irradiated endothelium. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1159

Chicago Manual of Style (16th Edition):

Khaled, Saman (Saman Fatima). “Low and high LET irradiation of human aortic endothelial cells induces dose and time dependent adhesion of monocytes which is mediated by chemokines expressed by the irradiated endothelium.” 2011. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,1159.

MLA Handbook (7th Edition):

Khaled, Saman (Saman Fatima). “Low and high LET irradiation of human aortic endothelial cells induces dose and time dependent adhesion of monocytes which is mediated by chemokines expressed by the irradiated endothelium.” 2011. Web. 22 Feb 2020.

Vancouver:

Khaled S(F. Low and high LET irradiation of human aortic endothelial cells induces dose and time dependent adhesion of monocytes which is mediated by chemokines expressed by the irradiated endothelium. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2011. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1159.

Council of Science Editors:

Khaled S(F. Low and high LET irradiation of human aortic endothelial cells induces dose and time dependent adhesion of monocytes which is mediated by chemokines expressed by the irradiated endothelium. [Doctoral Dissertation]. University of Alabama – Birmingham; 2011. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1159

4. Edmonds, Mick D. Brms1 Coordinately Regulates Microrna To Suppress Breast.

Degree: PhD, 2010, University of Alabama – Birmingham

The majority of cancer related mortality is attributed to complications associated with metastatic disease. Breast cancer metastasis suppressor 1 (BRMS1) suppresses metastasis of multiple cancer… (more)

Subjects/Keywords: Antineoplastic Agents – pharmacology<; br>; Colonic Neoplasms – pathology<; br>; Cyclic Nucleotide Phosphodiesterases, Type 5 – metabolism.<; br>; Phosphodiesterase 5 Inhibitors – pharmacology.<; br>; Sulindac – pharmacology.<; br>; Transcriptional Activation – drug effects.<; br>; beta Catenin – genetics.

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APA (6th Edition):

Edmonds, M. D. (2010). Brms1 Coordinately Regulates Microrna To Suppress Breast. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1417

Chicago Manual of Style (16th Edition):

Edmonds, Mick D. “Brms1 Coordinately Regulates Microrna To Suppress Breast.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,1417.

MLA Handbook (7th Edition):

Edmonds, Mick D. “Brms1 Coordinately Regulates Microrna To Suppress Breast.” 2010. Web. 22 Feb 2020.

Vancouver:

Edmonds MD. Brms1 Coordinately Regulates Microrna To Suppress Breast. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1417.

Council of Science Editors:

Edmonds MD. Brms1 Coordinately Regulates Microrna To Suppress Breast. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1417

5. Hovater, Michael (Michael Brian). Underlying purinergic signaling important for monocilium-dependent signaling in ductal epithelia: implications for polycystic kidney disease.

Degree: MS, 2006, University of Alabama – Birmingham

This thesis concerns purinergic signaling in renal epithelial cells of normal and polycystic kidneys. The first section discusses first principles of “purinergic signaling” as they… (more)

Subjects/Keywords: Epithelial Cells  – physiology <; br>; Kidney Tubules  – physiology <; br>; Polycystic Kidney Diseases  – pathology <; br>; Receptors, Purinergic P2  – metabolism <; br>; Signal Transduction  – physiology

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APA (6th Edition):

Hovater, M. (. B. (2006). Underlying purinergic signaling important for monocilium-dependent signaling in ductal epithelia: implications for polycystic kidney disease. (Masters Thesis). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,30

Chicago Manual of Style (16th Edition):

Hovater, Michael (Michael Brian). “Underlying purinergic signaling important for monocilium-dependent signaling in ductal epithelia: implications for polycystic kidney disease.” 2006. Masters Thesis, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,30.

MLA Handbook (7th Edition):

Hovater, Michael (Michael Brian). “Underlying purinergic signaling important for monocilium-dependent signaling in ductal epithelia: implications for polycystic kidney disease.” 2006. Web. 22 Feb 2020.

Vancouver:

Hovater M(B. Underlying purinergic signaling important for monocilium-dependent signaling in ductal epithelia: implications for polycystic kidney disease. [Internet] [Masters thesis]. University of Alabama – Birmingham; 2006. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,30.

Council of Science Editors:

Hovater M(B. Underlying purinergic signaling important for monocilium-dependent signaling in ductal epithelia: implications for polycystic kidney disease. [Masters Thesis]. University of Alabama – Birmingham; 2006. Available from: http://contentdm.mhsl.uab.edu/u?/etd,30

6. Nash, Kevin T. (Kevin Tyler). KISS1 metastasis suppressor secretion is required for metastasis suppression.

Degree: PhD, 2006, University of Alabama – Birmingham

Failure to reduce the number of cancer deaths over the last 50 years is due to the inability to selectively target metastatic disease. Recently, the… (more)

Subjects/Keywords: Gene Expression Regulation, Neoplastic <; br>; Melanoma  – metabolism <; br>; Melanoma  – secretion <; br>; Neoplasm Metastasis  – prevention & control <; br>; Proteins  – physiology <; br>; Receptors, G-Protein-Coupled  – metabolism <; br>; Tumor Suppressor Proteins  – secretion

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APA (6th Edition):

Nash, K. T. (. T. (2006). KISS1 metastasis suppressor secretion is required for metastasis suppression. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,380

Chicago Manual of Style (16th Edition):

Nash, Kevin T (Kevin Tyler). “KISS1 metastasis suppressor secretion is required for metastasis suppression.” 2006. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,380.

MLA Handbook (7th Edition):

Nash, Kevin T (Kevin Tyler). “KISS1 metastasis suppressor secretion is required for metastasis suppression.” 2006. Web. 22 Feb 2020.

Vancouver:

Nash KT(T. KISS1 metastasis suppressor secretion is required for metastasis suppression. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2006. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,380.

Council of Science Editors:

Nash KT(T. KISS1 metastasis suppressor secretion is required for metastasis suppression. [Doctoral Dissertation]. University of Alabama – Birmingham; 2006. Available from: http://contentdm.mhsl.uab.edu/u?/etd,380

7. Woodard-Grice, Alencia V. (Alencia Vanay). Hyposialylation regulates [alpha]4[beta]1 integrin binding to VCAM-1.

Degree: PhD, 2008, University of Alabama – Birmingham

During monocyte activation and differentiation along the macrophage lineage, the activity of [alpha]4[beta]1 integrins is upregulated, which promotes extravasation from the vasculature and migration through… (more)

Subjects/Keywords: Amyloid Precursor Protein Secretases  – metabolism<; br>; Antigens, CD  – biosynthesis<; br>; Aspartic Endopeptidases  – metabolism<; br>; Cell Differentiation  – physiology<; br>; Integrin alpha4beta1  – metabolism<; br>; Macrophages  – enzymology<; br>; Monocytes  – enzymology<; br>; Protein Modification, Translational  – physiology<; br>; Sialyltransferases  – biosynthesis

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APA (6th Edition):

Woodard-Grice, A. V. (. V. (2008). Hyposialylation regulates [alpha]4[beta]1 integrin binding to VCAM-1. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,473

Chicago Manual of Style (16th Edition):

Woodard-Grice, Alencia V (Alencia Vanay). “Hyposialylation regulates [alpha]4[beta]1 integrin binding to VCAM-1.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,473.

MLA Handbook (7th Edition):

Woodard-Grice, Alencia V (Alencia Vanay). “Hyposialylation regulates [alpha]4[beta]1 integrin binding to VCAM-1.” 2008. Web. 22 Feb 2020.

Vancouver:

Woodard-Grice AV(V. Hyposialylation regulates [alpha]4[beta]1 integrin binding to VCAM-1. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,473.

Council of Science Editors:

Woodard-Grice AV(V. Hyposialylation regulates [alpha]4[beta]1 integrin binding to VCAM-1. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,473

8. Ashley, Jason Waid. Significance and regulation of CD68 expression in the osteoclast.

Degree: PhD, 2011, University of Alabama – Birmingham

The mucin-like Lysosome Associated Membrane Protein (LAMP) family member CD68 is a primarily myeloid lineage restricted transmembrane protein that is expressed in macrophages and osteoclasts.… (more)

Subjects/Keywords: Antigens, CD  – genetics<; br>; Antigens, Differentiation, Myelomonocytic  – genetics<; br>; Biological Assay  – methods<; br>; Bone and Bones<; br>; Drug Evaluation, Preclinical  – methods<; br>; Gene Deletion<; br>; High-Throughput Screening Assays  – methods<; br>; Macrophages  – drug effects<; br>; Osteoclasts<; br>; Receptor Activator of Nuclear Factor-kappa B  – metabolism<; br>; Signal Transduction  – physiology

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APA (6th Edition):

Ashley, J. W. (2011). Significance and regulation of CD68 expression in the osteoclast. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1033

Chicago Manual of Style (16th Edition):

Ashley, Jason Waid. “Significance and regulation of CD68 expression in the osteoclast.” 2011. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,1033.

MLA Handbook (7th Edition):

Ashley, Jason Waid. “Significance and regulation of CD68 expression in the osteoclast.” 2011. Web. 22 Feb 2020.

Vancouver:

Ashley JW. Significance and regulation of CD68 expression in the osteoclast. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2011. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1033.

Council of Science Editors:

Ashley JW. Significance and regulation of CD68 expression in the osteoclast. [Doctoral Dissertation]. University of Alabama – Birmingham; 2011. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1033

9. Reily, Colin. Targeting Mitochondrial Function In Diabetic Nephropathy.

Degree: PhD, 2012, University of Alabama – Birmingham

TARGETING MITOCHONDRIAL FUNCTION IN DIABETIC NEPHROPATHYThe incidence of diabetes has increased to epidemic proportions over the last 50 years, due to a complex interaction of… (more)

Subjects/Keywords: Antioxidants<; br>; Diabetic Nephropathies – prevention & control<; br>; Fibrosis – prevention & control.<; br>; Hyperglycemia<; br>; Insulin – deficiency.<; br>; Mitochondria – drug effects<; br>; Proteomics – methods<; br>; Sulfhydryl Compounds

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APA (6th Edition):

Reily, C. (2012). Targeting Mitochondrial Function In Diabetic Nephropathy. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1403

Chicago Manual of Style (16th Edition):

Reily, Colin. “Targeting Mitochondrial Function In Diabetic Nephropathy.” 2012. Doctoral Dissertation, University of Alabama – Birmingham. Accessed February 22, 2020. http://contentdm.mhsl.uab.edu/u?/etd,1403.

MLA Handbook (7th Edition):

Reily, Colin. “Targeting Mitochondrial Function In Diabetic Nephropathy.” 2012. Web. 22 Feb 2020.

Vancouver:

Reily C. Targeting Mitochondrial Function In Diabetic Nephropathy. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2012. [cited 2020 Feb 22]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1403.

Council of Science Editors:

Reily C. Targeting Mitochondrial Function In Diabetic Nephropathy. [Doctoral Dissertation]. University of Alabama – Birmingham; 2012. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1403

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