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You searched for +publisher:"Vanderbilt University" +contributor:("Kevin C. Ess"). Showing records 1 – 8 of 8 total matches.

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Vanderbilt University

1. Shen, Dingding. Characterization of GABAA receptor subunit mutations associated with epileptic encephalopathies.

Degree: PhD, Neuroscience, 2017, Vanderbilt University

 Epileptic encephalopathies (EEs) are a devastating group of severe childhood onset epilepsies with medication resistant seizures and poor developmental outcomes. Many EEs have a genetic… (more)

Subjects/Keywords: Epileptic encephalopathies; GABAA receptor

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APA (6th Edition):

Shen, D. (2017). Characterization of GABAA receptor subunit mutations associated with epileptic encephalopathies. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14271

Chicago Manual of Style (16th Edition):

Shen, Dingding. “Characterization of GABAA receptor subunit mutations associated with epileptic encephalopathies.” 2017. Doctoral Dissertation, Vanderbilt University. Accessed November 26, 2020. http://hdl.handle.net/1803/14271.

MLA Handbook (7th Edition):

Shen, Dingding. “Characterization of GABAA receptor subunit mutations associated with epileptic encephalopathies.” 2017. Web. 26 Nov 2020.

Vancouver:

Shen D. Characterization of GABAA receptor subunit mutations associated with epileptic encephalopathies. [Internet] [Doctoral dissertation]. Vanderbilt University; 2017. [cited 2020 Nov 26]. Available from: http://hdl.handle.net/1803/14271.

Council of Science Editors:

Shen D. Characterization of GABAA receptor subunit mutations associated with epileptic encephalopathies. [Doctoral Dissertation]. Vanderbilt University; 2017. Available from: http://hdl.handle.net/1803/14271


Vanderbilt University

2. Armour, Eric Andrew. Dysregulated mTOR signaling and tissue-specific phenotypes in Tuberous Sclerosis Complex.

Degree: PhD, Cell and Developmental Biology, 2013, Vanderbilt University

 Tuberous Sclerosis Complex (TSC) is a multi-organ hamartomatous disease caused by loss of function mutations in either the TSC1 or TSC2 genes. Despite involvement of… (more)

Subjects/Keywords: TSC; pluripotency; Tuberous Sclerosis; cilia; cystogenesis; mTOR

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APA (6th Edition):

Armour, E. A. (2013). Dysregulated mTOR signaling and tissue-specific phenotypes in Tuberous Sclerosis Complex. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14546

Chicago Manual of Style (16th Edition):

Armour, Eric Andrew. “Dysregulated mTOR signaling and tissue-specific phenotypes in Tuberous Sclerosis Complex.” 2013. Doctoral Dissertation, Vanderbilt University. Accessed November 26, 2020. http://hdl.handle.net/1803/14546.

MLA Handbook (7th Edition):

Armour, Eric Andrew. “Dysregulated mTOR signaling and tissue-specific phenotypes in Tuberous Sclerosis Complex.” 2013. Web. 26 Nov 2020.

Vancouver:

Armour EA. Dysregulated mTOR signaling and tissue-specific phenotypes in Tuberous Sclerosis Complex. [Internet] [Doctoral dissertation]. Vanderbilt University; 2013. [cited 2020 Nov 26]. Available from: http://hdl.handle.net/1803/14546.

Council of Science Editors:

Armour EA. Dysregulated mTOR signaling and tissue-specific phenotypes in Tuberous Sclerosis Complex. [Doctoral Dissertation]. Vanderbilt University; 2013. Available from: http://hdl.handle.net/1803/14546


Vanderbilt University

3. Tidball, Andrew Martin. A Manganese-Handling Deficit in Huntington’s Disease Selectively Impairs ATM-p53 Signaling.

Degree: PhD, Neuroscience, 2014, Vanderbilt University

 The essential micronutrient manganese is enriched in brain, especially the basal ganglia. We sought to identify neuronal signaling pathways responsive to neurologically relevant manganese levels,… (more)

Subjects/Keywords: manganese; induced-pluripotent stem cells; ATM; p53; cell signaling; cytotoxicity; genomic instability; Huntingtons disease

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APA (6th Edition):

Tidball, A. M. (2014). A Manganese-Handling Deficit in Huntington’s Disease Selectively Impairs ATM-p53 Signaling. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14230

Chicago Manual of Style (16th Edition):

Tidball, Andrew Martin. “A Manganese-Handling Deficit in Huntington’s Disease Selectively Impairs ATM-p53 Signaling.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed November 26, 2020. http://hdl.handle.net/1803/14230.

MLA Handbook (7th Edition):

Tidball, Andrew Martin. “A Manganese-Handling Deficit in Huntington’s Disease Selectively Impairs ATM-p53 Signaling.” 2014. Web. 26 Nov 2020.

Vancouver:

Tidball AM. A Manganese-Handling Deficit in Huntington’s Disease Selectively Impairs ATM-p53 Signaling. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2020 Nov 26]. Available from: http://hdl.handle.net/1803/14230.

Council of Science Editors:

Tidball AM. A Manganese-Handling Deficit in Huntington’s Disease Selectively Impairs ATM-p53 Signaling. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/14230


Vanderbilt University

4. Kumar, Kevin Krishan. Investigation of Neuronal Manganese Regulation in Physiology and Disease Using High Throughput Screening, Induced Pluripotent Stem Cells, and Chemical Biology Approaches.

Degree: PhD, Neuroscience, 2014, Vanderbilt University

 Manganese (Mn) is both an essential biological cofactor and neurotoxicant. Disruption of Mn biology in the basal ganglia has been implicated in the pathogenesis of… (more)

Subjects/Keywords: High Throughput Screening; Manganese; Neurodegenerative diseases; Human Induced Pluripotent Stem Cells; Metabolomics

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APA (6th Edition):

Kumar, K. K. (2014). Investigation of Neuronal Manganese Regulation in Physiology and Disease Using High Throughput Screening, Induced Pluripotent Stem Cells, and Chemical Biology Approaches. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14021

Chicago Manual of Style (16th Edition):

Kumar, Kevin Krishan. “Investigation of Neuronal Manganese Regulation in Physiology and Disease Using High Throughput Screening, Induced Pluripotent Stem Cells, and Chemical Biology Approaches.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed November 26, 2020. http://hdl.handle.net/1803/14021.

MLA Handbook (7th Edition):

Kumar, Kevin Krishan. “Investigation of Neuronal Manganese Regulation in Physiology and Disease Using High Throughput Screening, Induced Pluripotent Stem Cells, and Chemical Biology Approaches.” 2014. Web. 26 Nov 2020.

Vancouver:

Kumar KK. Investigation of Neuronal Manganese Regulation in Physiology and Disease Using High Throughput Screening, Induced Pluripotent Stem Cells, and Chemical Biology Approaches. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2020 Nov 26]. Available from: http://hdl.handle.net/1803/14021.

Council of Science Editors:

Kumar KK. Investigation of Neuronal Manganese Regulation in Physiology and Disease Using High Throughput Screening, Induced Pluripotent Stem Cells, and Chemical Biology Approaches. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/14021


Vanderbilt University

5. Bruntz, Ronald Chase. Insights into the Molecular Mechanisms of Phospholipase D-Mediated Cancer Cell Survival.

Degree: PhD, Pharmacology, 2014, Vanderbilt University

 The production of bioactive lipids by phospholipases has long been appreciated as an important mode of cellular communication. Phospholipase D (PLD) enzymes hydrolyze phosphatidylcholine to… (more)

Subjects/Keywords: phospholipase D; phosphatidic acid; cancer; Akt; cell signaling; autophagy

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APA (6th Edition):

Bruntz, R. C. (2014). Insights into the Molecular Mechanisms of Phospholipase D-Mediated Cancer Cell Survival. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/10427

Chicago Manual of Style (16th Edition):

Bruntz, Ronald Chase. “Insights into the Molecular Mechanisms of Phospholipase D-Mediated Cancer Cell Survival.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed November 26, 2020. http://hdl.handle.net/1803/10427.

MLA Handbook (7th Edition):

Bruntz, Ronald Chase. “Insights into the Molecular Mechanisms of Phospholipase D-Mediated Cancer Cell Survival.” 2014. Web. 26 Nov 2020.

Vancouver:

Bruntz RC. Insights into the Molecular Mechanisms of Phospholipase D-Mediated Cancer Cell Survival. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2020 Nov 26]. Available from: http://hdl.handle.net/1803/10427.

Council of Science Editors:

Bruntz RC. Insights into the Molecular Mechanisms of Phospholipase D-Mediated Cancer Cell Survival. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/10427


Vanderbilt University

6. Jorge, Benjamin S. Genetic Variation in the Voltage-gated Potassium Channel Genes KCNV2 and KCNB1 Contributes to Epilepsy Susceptibility.

Degree: PhD, Neuroscience, 2014, Vanderbilt University

 Epilepsy is a common neurological disease characterized by an enduring predisposition to generate seizures. Although multiple factors contribute to epilepsy, the majority of cases are… (more)

Subjects/Keywords: potassium channel; epileptic encephalopathy; mouse model; genetics; whole-exome sequencing; epilepsy

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APA (6th Edition):

Jorge, B. S. (2014). Genetic Variation in the Voltage-gated Potassium Channel Genes KCNV2 and KCNB1 Contributes to Epilepsy Susceptibility. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14387

Chicago Manual of Style (16th Edition):

Jorge, Benjamin S. “Genetic Variation in the Voltage-gated Potassium Channel Genes KCNV2 and KCNB1 Contributes to Epilepsy Susceptibility.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed November 26, 2020. http://hdl.handle.net/1803/14387.

MLA Handbook (7th Edition):

Jorge, Benjamin S. “Genetic Variation in the Voltage-gated Potassium Channel Genes KCNV2 and KCNB1 Contributes to Epilepsy Susceptibility.” 2014. Web. 26 Nov 2020.

Vancouver:

Jorge BS. Genetic Variation in the Voltage-gated Potassium Channel Genes KCNV2 and KCNB1 Contributes to Epilepsy Susceptibility. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2020 Nov 26]. Available from: http://hdl.handle.net/1803/14387.

Council of Science Editors:

Jorge BS. Genetic Variation in the Voltage-gated Potassium Channel Genes KCNV2 and KCNB1 Contributes to Epilepsy Susceptibility. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/14387


Vanderbilt University

7. West, Kathryn Louise. Development and Evaluation of Relaxation-Based Measures of Myelin Content and Microstructure in Rodent Brains.

Degree: PhD, Biomedical Engineering, 2016, Vanderbilt University

 Advanced neuroimaging techniques provide the possibility to non-invasively understand and monitor white matter during development and disease. While data from quantitative MRI techniques, such as… (more)

Subjects/Keywords: magnetization transfer; multiexponential T2; myelin; MRI; neuroimaging; histology; g-ratio

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APA (6th Edition):

West, K. L. (2016). Development and Evaluation of Relaxation-Based Measures of Myelin Content and Microstructure in Rodent Brains. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14525

Chicago Manual of Style (16th Edition):

West, Kathryn Louise. “Development and Evaluation of Relaxation-Based Measures of Myelin Content and Microstructure in Rodent Brains.” 2016. Doctoral Dissertation, Vanderbilt University. Accessed November 26, 2020. http://hdl.handle.net/1803/14525.

MLA Handbook (7th Edition):

West, Kathryn Louise. “Development and Evaluation of Relaxation-Based Measures of Myelin Content and Microstructure in Rodent Brains.” 2016. Web. 26 Nov 2020.

Vancouver:

West KL. Development and Evaluation of Relaxation-Based Measures of Myelin Content and Microstructure in Rodent Brains. [Internet] [Doctoral dissertation]. Vanderbilt University; 2016. [cited 2020 Nov 26]. Available from: http://hdl.handle.net/1803/14525.

Council of Science Editors:

West KL. Development and Evaluation of Relaxation-Based Measures of Myelin Content and Microstructure in Rodent Brains. [Doctoral Dissertation]. Vanderbilt University; 2016. Available from: http://hdl.handle.net/1803/14525


Vanderbilt University

8. Huang, Xuan. Epilepsy-associated mutations in GABRG2: characterization and therapeutic opportunities.

Degree: PhD, Neuroscience, 2014, Vanderbilt University

 Epilepsy is a neurological disorder affecting almost one percent of the population, and genetic epilepsy are those caused by a presumed or unknown genetic factor(s).… (more)

Subjects/Keywords: GABA(A) receptors; GABRG2; genetic epilepsy; mutation; therapy

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APA (6th Edition):

Huang, X. (2014). Epilepsy-associated mutations in GABRG2: characterization and therapeutic opportunities. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14755

Chicago Manual of Style (16th Edition):

Huang, Xuan. “Epilepsy-associated mutations in GABRG2: characterization and therapeutic opportunities.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed November 26, 2020. http://hdl.handle.net/1803/14755.

MLA Handbook (7th Edition):

Huang, Xuan. “Epilepsy-associated mutations in GABRG2: characterization and therapeutic opportunities.” 2014. Web. 26 Nov 2020.

Vancouver:

Huang X. Epilepsy-associated mutations in GABRG2: characterization and therapeutic opportunities. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2020 Nov 26]. Available from: http://hdl.handle.net/1803/14755.

Council of Science Editors:

Huang X. Epilepsy-associated mutations in GABRG2: characterization and therapeutic opportunities. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/14755

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