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You searched for subject:(Mitochondrial disease). Showing records 1 – 30 of 122 total matches.

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University of Sydney

1. Liang, Christina Luh-Unn. The Australian Mitochondrial Disease Study – Recognising and improving the diagnosis and management outcomes of adult patients with mitochondrial diseases .

Degree: 2016, University of Sydney

 Background: Mitochondrial diseases are one of the most common hereditary neuromuscular conditions. Late-onset presentations are common. Genotype-phenotype correlations are poor, making the diagnosis difficult and… (more)

Subjects/Keywords: Mitochondrial; Mitochondrial disease; Database; Adult

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APA (6th Edition):

Liang, C. L. (2016). The Australian Mitochondrial Disease Study – Recognising and improving the diagnosis and management outcomes of adult patients with mitochondrial diseases . (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/16723

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Liang, Christina Luh-Unn. “The Australian Mitochondrial Disease Study – Recognising and improving the diagnosis and management outcomes of adult patients with mitochondrial diseases .” 2016. Thesis, University of Sydney. Accessed November 27, 2020. http://hdl.handle.net/2123/16723.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Liang, Christina Luh-Unn. “The Australian Mitochondrial Disease Study – Recognising and improving the diagnosis and management outcomes of adult patients with mitochondrial diseases .” 2016. Web. 27 Nov 2020.

Vancouver:

Liang CL. The Australian Mitochondrial Disease Study – Recognising and improving the diagnosis and management outcomes of adult patients with mitochondrial diseases . [Internet] [Thesis]. University of Sydney; 2016. [cited 2020 Nov 27]. Available from: http://hdl.handle.net/2123/16723.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Liang CL. The Australian Mitochondrial Disease Study – Recognising and improving the diagnosis and management outcomes of adult patients with mitochondrial diseases . [Thesis]. University of Sydney; 2016. Available from: http://hdl.handle.net/2123/16723

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

2. Berg Alonso, Laetitia. Déficits de la chaîne respiratoire mitochondriale avec instabilité de l’ADN mitochondrial : identification de nouveaux gènes et mécanismes : Non communiqué.

Degree: Docteur es, Interactions moléculaires et cellulaires, 2016, Université Côte d'Azur (ComUE)

Les maladies mitochondriales regroupent un ensemble de pathologies liées à un déficit de la chaînerespiratoire mitochondriale. Au laboratoire, nous focalisons notre intérêt sur les mitochondriopathies… (more)

Subjects/Keywords: Maladie mitochondriale; ADNmt; Mitochondrial disease; Mitochondrial DNA

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APA (6th Edition):

Berg Alonso, L. (2016). Déficits de la chaîne respiratoire mitochondriale avec instabilité de l’ADN mitochondrial : identification de nouveaux gènes et mécanismes : Non communiqué. (Doctoral Dissertation). Université Côte d'Azur (ComUE). Retrieved from http://www.theses.fr/2016AZUR4101

Chicago Manual of Style (16th Edition):

Berg Alonso, Laetitia. “Déficits de la chaîne respiratoire mitochondriale avec instabilité de l’ADN mitochondrial : identification de nouveaux gènes et mécanismes : Non communiqué.” 2016. Doctoral Dissertation, Université Côte d'Azur (ComUE). Accessed November 27, 2020. http://www.theses.fr/2016AZUR4101.

MLA Handbook (7th Edition):

Berg Alonso, Laetitia. “Déficits de la chaîne respiratoire mitochondriale avec instabilité de l’ADN mitochondrial : identification de nouveaux gènes et mécanismes : Non communiqué.” 2016. Web. 27 Nov 2020.

Vancouver:

Berg Alonso L. Déficits de la chaîne respiratoire mitochondriale avec instabilité de l’ADN mitochondrial : identification de nouveaux gènes et mécanismes : Non communiqué. [Internet] [Doctoral dissertation]. Université Côte d'Azur (ComUE); 2016. [cited 2020 Nov 27]. Available from: http://www.theses.fr/2016AZUR4101.

Council of Science Editors:

Berg Alonso L. Déficits de la chaîne respiratoire mitochondriale avec instabilité de l’ADN mitochondrial : identification de nouveaux gènes et mécanismes : Non communiqué. [Doctoral Dissertation]. Université Côte d'Azur (ComUE); 2016. Available from: http://www.theses.fr/2016AZUR4101


University of California – Irvine

3. Fiss, Ashlynn Nicole. An Assessment of the Mitochondrial Disease Community’s Knowledge and Perception of the “Three-Person Baby,” or MRT, and the Impact of the Media Debate that Surrounds this Technique.

Degree: Genetic Counseling, 2016, University of California – Irvine

 This study was designed to assess the mitochondrial disease community’s knowledge, attitude and perception of mitochondrial replacement therapy (MRT) and determine how the media can… (more)

Subjects/Keywords: Genetics; Assisted reproductive technology; Mitochondrial disease; Mitochondrial Replacement Therapy

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APA (6th Edition):

Fiss, A. N. (2016). An Assessment of the Mitochondrial Disease Community’s Knowledge and Perception of the “Three-Person Baby,” or MRT, and the Impact of the Media Debate that Surrounds this Technique. (Thesis). University of California – Irvine. Retrieved from http://www.escholarship.org/uc/item/75r0w31g

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Fiss, Ashlynn Nicole. “An Assessment of the Mitochondrial Disease Community’s Knowledge and Perception of the “Three-Person Baby,” or MRT, and the Impact of the Media Debate that Surrounds this Technique.” 2016. Thesis, University of California – Irvine. Accessed November 27, 2020. http://www.escholarship.org/uc/item/75r0w31g.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Fiss, Ashlynn Nicole. “An Assessment of the Mitochondrial Disease Community’s Knowledge and Perception of the “Three-Person Baby,” or MRT, and the Impact of the Media Debate that Surrounds this Technique.” 2016. Web. 27 Nov 2020.

Vancouver:

Fiss AN. An Assessment of the Mitochondrial Disease Community’s Knowledge and Perception of the “Three-Person Baby,” or MRT, and the Impact of the Media Debate that Surrounds this Technique. [Internet] [Thesis]. University of California – Irvine; 2016. [cited 2020 Nov 27]. Available from: http://www.escholarship.org/uc/item/75r0w31g.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Fiss AN. An Assessment of the Mitochondrial Disease Community’s Knowledge and Perception of the “Three-Person Baby,” or MRT, and the Impact of the Media Debate that Surrounds this Technique. [Thesis]. University of California – Irvine; 2016. Available from: http://www.escholarship.org/uc/item/75r0w31g

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


University of California – Irvine

4. Simon, Mariella T. Mitochondrial Metabolism and Morphology in Mitochondrial Disease States.

Degree: Biological Sciences, 2016, University of California – Irvine

 ABSTRACT OF THE DISSERTATIONMitochondrial Metabolism and Morphologyin Mitochondrial Disease StatesByMariella Theresa SimonDoctor of Philosophy in Biological SciencesUniversity of California, Irvine, 2016Professor Susanne Rafelski, ChairMitochondria are… (more)

Subjects/Keywords: Cellular biology; Genetics; Leigh Syndrome; LonP1; Mitochondrial Disease; Mitochondrial Myopathy; Nars2

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APA (6th Edition):

Simon, M. T. (2016). Mitochondrial Metabolism and Morphology in Mitochondrial Disease States. (Thesis). University of California – Irvine. Retrieved from http://www.escholarship.org/uc/item/7ss5250z

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Simon, Mariella T. “Mitochondrial Metabolism and Morphology in Mitochondrial Disease States.” 2016. Thesis, University of California – Irvine. Accessed November 27, 2020. http://www.escholarship.org/uc/item/7ss5250z.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Simon, Mariella T. “Mitochondrial Metabolism and Morphology in Mitochondrial Disease States.” 2016. Web. 27 Nov 2020.

Vancouver:

Simon MT. Mitochondrial Metabolism and Morphology in Mitochondrial Disease States. [Internet] [Thesis]. University of California – Irvine; 2016. [cited 2020 Nov 27]. Available from: http://www.escholarship.org/uc/item/7ss5250z.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Simon MT. Mitochondrial Metabolism and Morphology in Mitochondrial Disease States. [Thesis]. University of California – Irvine; 2016. Available from: http://www.escholarship.org/uc/item/7ss5250z

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


Boston University

5. Monson, Samantha. Mitochondrial dysfunction as an underlying cause of bipolar disorder.

Degree: MS, Medical Sciences, 2017, Boston University

 Bipolar disorder is a psychiatric disorder with alarming rates of morbidity and mortality. Since the pathophysiology of the disease is not well understood, it is… (more)

Subjects/Keywords: Medicine; Bipolar disorder; Genetics; Mitochondrial disease; Mitochondrial dysfunction; Psychiatry

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APA (6th Edition):

Monson, S. (2017). Mitochondrial dysfunction as an underlying cause of bipolar disorder. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/26896

Chicago Manual of Style (16th Edition):

Monson, Samantha. “Mitochondrial dysfunction as an underlying cause of bipolar disorder.” 2017. Masters Thesis, Boston University. Accessed November 27, 2020. http://hdl.handle.net/2144/26896.

MLA Handbook (7th Edition):

Monson, Samantha. “Mitochondrial dysfunction as an underlying cause of bipolar disorder.” 2017. Web. 27 Nov 2020.

Vancouver:

Monson S. Mitochondrial dysfunction as an underlying cause of bipolar disorder. [Internet] [Masters thesis]. Boston University; 2017. [cited 2020 Nov 27]. Available from: http://hdl.handle.net/2144/26896.

Council of Science Editors:

Monson S. Mitochondrial dysfunction as an underlying cause of bipolar disorder. [Masters Thesis]. Boston University; 2017. Available from: http://hdl.handle.net/2144/26896


Harvard University

6. GILBERT, JASON A. RNAi Mediated Knock Down of Prolyl Hydroxylase II in Liver Tissue Enhances Lactate Clearance in Mice.

Degree: ALM, 2019, Harvard University

Patients with respiratory chain disorders can present with lactic acidosis (Jain et al., 2016). At present, mitochondrial diseases caused by mutant mtDNAs remain largely untreatable… (more)

Subjects/Keywords: Mitochondrial disease; siRNA; PHD2; Egln1; lactate clearance

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APA (6th Edition):

GILBERT, J. A. (2019). RNAi Mediated Knock Down of Prolyl Hydroxylase II in Liver Tissue Enhances Lactate Clearance in Mice. (Masters Thesis). Harvard University. Retrieved from http://nrs.harvard.edu/urn-3:HUL.InstRepos:42006728

Chicago Manual of Style (16th Edition):

GILBERT, JASON A. “RNAi Mediated Knock Down of Prolyl Hydroxylase II in Liver Tissue Enhances Lactate Clearance in Mice.” 2019. Masters Thesis, Harvard University. Accessed November 27, 2020. http://nrs.harvard.edu/urn-3:HUL.InstRepos:42006728.

MLA Handbook (7th Edition):

GILBERT, JASON A. “RNAi Mediated Knock Down of Prolyl Hydroxylase II in Liver Tissue Enhances Lactate Clearance in Mice.” 2019. Web. 27 Nov 2020.

Vancouver:

GILBERT JA. RNAi Mediated Knock Down of Prolyl Hydroxylase II in Liver Tissue Enhances Lactate Clearance in Mice. [Internet] [Masters thesis]. Harvard University; 2019. [cited 2020 Nov 27]. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:42006728.

Council of Science Editors:

GILBERT JA. RNAi Mediated Knock Down of Prolyl Hydroxylase II in Liver Tissue Enhances Lactate Clearance in Mice. [Masters Thesis]. Harvard University; 2019. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:42006728


University of Melbourne

7. Thirukeswaran, Shalini. Determining the genetic basis of mitochondrial complex I deficiency in children using massively parallel sequencing.

Degree: 2019, University of Melbourne

Mitochondrial oxidative phosphorylation (OXPHOS) disorders constitute the largest group of inborn errors of metabolism. Complex I (CI) deficiency is the most common enzymatic defect identified… (more)

Subjects/Keywords: mitochondrial disease; complex I; massively parallel sequencing

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APA (6th Edition):

Thirukeswaran, S. (2019). Determining the genetic basis of mitochondrial complex I deficiency in children using massively parallel sequencing. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/225852

Chicago Manual of Style (16th Edition):

Thirukeswaran, Shalini. “Determining the genetic basis of mitochondrial complex I deficiency in children using massively parallel sequencing.” 2019. Doctoral Dissertation, University of Melbourne. Accessed November 27, 2020. http://hdl.handle.net/11343/225852.

MLA Handbook (7th Edition):

Thirukeswaran, Shalini. “Determining the genetic basis of mitochondrial complex I deficiency in children using massively parallel sequencing.” 2019. Web. 27 Nov 2020.

Vancouver:

Thirukeswaran S. Determining the genetic basis of mitochondrial complex I deficiency in children using massively parallel sequencing. [Internet] [Doctoral dissertation]. University of Melbourne; 2019. [cited 2020 Nov 27]. Available from: http://hdl.handle.net/11343/225852.

Council of Science Editors:

Thirukeswaran S. Determining the genetic basis of mitochondrial complex I deficiency in children using massively parallel sequencing. [Doctoral Dissertation]. University of Melbourne; 2019. Available from: http://hdl.handle.net/11343/225852


University of Melbourne

8. Lake, Nicole Janet. Using massively parallel sequencing to determine the genetic basis of Leigh Syndrome, the most common mitochondrial disorder affecting children.

Degree: 2018, University of Melbourne

Mitochondrial diseases are debilitating illnesses caused by mutations that impair mitochondrial energy generation. The most common clinical presentation of mitochondrial disease in children is Leigh… (more)

Subjects/Keywords: mitochondrial disease; Leigh syndrome; massively parallel sequencing

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APA (6th Edition):

Lake, N. J. (2018). Using massively parallel sequencing to determine the genetic basis of Leigh Syndrome, the most common mitochondrial disorder affecting children. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/212134

Chicago Manual of Style (16th Edition):

Lake, Nicole Janet. “Using massively parallel sequencing to determine the genetic basis of Leigh Syndrome, the most common mitochondrial disorder affecting children.” 2018. Doctoral Dissertation, University of Melbourne. Accessed November 27, 2020. http://hdl.handle.net/11343/212134.

MLA Handbook (7th Edition):

Lake, Nicole Janet. “Using massively parallel sequencing to determine the genetic basis of Leigh Syndrome, the most common mitochondrial disorder affecting children.” 2018. Web. 27 Nov 2020.

Vancouver:

Lake NJ. Using massively parallel sequencing to determine the genetic basis of Leigh Syndrome, the most common mitochondrial disorder affecting children. [Internet] [Doctoral dissertation]. University of Melbourne; 2018. [cited 2020 Nov 27]. Available from: http://hdl.handle.net/11343/212134.

Council of Science Editors:

Lake NJ. Using massively parallel sequencing to determine the genetic basis of Leigh Syndrome, the most common mitochondrial disorder affecting children. [Doctoral Dissertation]. University of Melbourne; 2018. Available from: http://hdl.handle.net/11343/212134


University of Melbourne

9. Frentz, Sophia-Louise. Development, characterisation and nicotinamide riboside treatment of Complex I-deficient model systems.

Degree: 2018, University of Melbourne

Mitochondrial disorders are the most common inborn error of metabolism, affecting 1 in 5000 live births. Complex I (CI) de ciency is the most common… (more)

Subjects/Keywords: mitochondrial disease; mitochondria; complex I; nicotinamide riboside

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APA (6th Edition):

Frentz, S. (2018). Development, characterisation and nicotinamide riboside treatment of Complex I-deficient model systems. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/213470

Chicago Manual of Style (16th Edition):

Frentz, Sophia-Louise. “Development, characterisation and nicotinamide riboside treatment of Complex I-deficient model systems.” 2018. Doctoral Dissertation, University of Melbourne. Accessed November 27, 2020. http://hdl.handle.net/11343/213470.

MLA Handbook (7th Edition):

Frentz, Sophia-Louise. “Development, characterisation and nicotinamide riboside treatment of Complex I-deficient model systems.” 2018. Web. 27 Nov 2020.

Vancouver:

Frentz S. Development, characterisation and nicotinamide riboside treatment of Complex I-deficient model systems. [Internet] [Doctoral dissertation]. University of Melbourne; 2018. [cited 2020 Nov 27]. Available from: http://hdl.handle.net/11343/213470.

Council of Science Editors:

Frentz S. Development, characterisation and nicotinamide riboside treatment of Complex I-deficient model systems. [Doctoral Dissertation]. University of Melbourne; 2018. Available from: http://hdl.handle.net/11343/213470


University of Cambridge

10. Smith, Alexander. Computer modelling of metabolic adaptions during mitochondrial dysfunction and machine learning to predict novel mitochondrial disease genes.

Degree: PhD, 2019, University of Cambridge

 Mitochondria are organelles found in almost every eukaryote and are primarily responsible for generating chemical energy in the form of adenosine triphosphate. This thesis investigates… (more)

Subjects/Keywords: Machine learning; Modelling; Mitochondria; Mitochondrial disease; Metabolomics

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APA (6th Edition):

Smith, A. (2019). Computer modelling of metabolic adaptions during mitochondrial dysfunction and machine learning to predict novel mitochondrial disease genes. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/306916

Chicago Manual of Style (16th Edition):

Smith, Alexander. “Computer modelling of metabolic adaptions during mitochondrial dysfunction and machine learning to predict novel mitochondrial disease genes.” 2019. Doctoral Dissertation, University of Cambridge. Accessed November 27, 2020. https://www.repository.cam.ac.uk/handle/1810/306916.

MLA Handbook (7th Edition):

Smith, Alexander. “Computer modelling of metabolic adaptions during mitochondrial dysfunction and machine learning to predict novel mitochondrial disease genes.” 2019. Web. 27 Nov 2020.

Vancouver:

Smith A. Computer modelling of metabolic adaptions during mitochondrial dysfunction and machine learning to predict novel mitochondrial disease genes. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2020 Nov 27]. Available from: https://www.repository.cam.ac.uk/handle/1810/306916.

Council of Science Editors:

Smith A. Computer modelling of metabolic adaptions during mitochondrial dysfunction and machine learning to predict novel mitochondrial disease genes. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://www.repository.cam.ac.uk/handle/1810/306916


University of Cambridge

11. Kullar, Peter John. Defining the cellular and molecular mechanism of maternally inherited hearing loss.

Degree: PhD, 2018, University of Cambridge

Mitochondrial dysfunction causes moderate to profound hearing loss both in isolation and as a feature of multi-systemic mitochondrial disease. The m.1555A > G mitochondrial DNA… (more)

Subjects/Keywords: 616.07; mitochondria; hearing loss; mitochondrial disease

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APA (6th Edition):

Kullar, P. J. (2018). Defining the cellular and molecular mechanism of maternally inherited hearing loss. (Doctoral Dissertation). University of Cambridge. Retrieved from https://doi.org/10.17863/CAM.17440 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.744444

Chicago Manual of Style (16th Edition):

Kullar, Peter John. “Defining the cellular and molecular mechanism of maternally inherited hearing loss.” 2018. Doctoral Dissertation, University of Cambridge. Accessed November 27, 2020. https://doi.org/10.17863/CAM.17440 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.744444.

MLA Handbook (7th Edition):

Kullar, Peter John. “Defining the cellular and molecular mechanism of maternally inherited hearing loss.” 2018. Web. 27 Nov 2020.

Vancouver:

Kullar PJ. Defining the cellular and molecular mechanism of maternally inherited hearing loss. [Internet] [Doctoral dissertation]. University of Cambridge; 2018. [cited 2020 Nov 27]. Available from: https://doi.org/10.17863/CAM.17440 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.744444.

Council of Science Editors:

Kullar PJ. Defining the cellular and molecular mechanism of maternally inherited hearing loss. [Doctoral Dissertation]. University of Cambridge; 2018. Available from: https://doi.org/10.17863/CAM.17440 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.744444


University of Cincinnati

12. Collier, Sarah E. Perspectives from Adolescents with Secondary Mitochondrial Disease.

Degree: MS, Medicine: Genetic Counseling, 2017, University of Cincinnati

Mitochondrial diseases are a diverse group of disorders that can affect multiple high energy body systems, creating many chronic health issues. There are two types… (more)

Subjects/Keywords: Genetics; secondary mitochondrial disease; mitochondrial disease; qualitative interviews; phenomenology; patient perspective; physician-patient relationship

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APA (6th Edition):

Collier, S. E. (2017). Perspectives from Adolescents with Secondary Mitochondrial Disease. (Masters Thesis). University of Cincinnati. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ucin1491317275179069

Chicago Manual of Style (16th Edition):

Collier, Sarah E. “Perspectives from Adolescents with Secondary Mitochondrial Disease.” 2017. Masters Thesis, University of Cincinnati. Accessed November 27, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1491317275179069.

MLA Handbook (7th Edition):

Collier, Sarah E. “Perspectives from Adolescents with Secondary Mitochondrial Disease.” 2017. Web. 27 Nov 2020.

Vancouver:

Collier SE. Perspectives from Adolescents with Secondary Mitochondrial Disease. [Internet] [Masters thesis]. University of Cincinnati; 2017. [cited 2020 Nov 27]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1491317275179069.

Council of Science Editors:

Collier SE. Perspectives from Adolescents with Secondary Mitochondrial Disease. [Masters Thesis]. University of Cincinnati; 2017. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1491317275179069


Universidade do Minho

13. Carmo, Catarina Sofia Rodrigues do. Role of sirtuin 3 on mitochondrial dynamics in Huntington's disease striatal cells .

Degree: 2015, Universidade do Minho

 Altered mitochondrial dynamics has been implicated in the pathogenesis of several neurodegenerative disorders, including Huntington’s disease (HD). Sirtuins, NAD+-dependent lysine deacetylases, have emerged as important… (more)

Subjects/Keywords: Huntington’s disease; Mitochondrial dysfunction; Mitochondrial dynamics; Fission / fusion balance; Mitophagy; Sirtuin 3

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APA (6th Edition):

Carmo, C. S. R. d. (2015). Role of sirtuin 3 on mitochondrial dynamics in Huntington's disease striatal cells . (Masters Thesis). Universidade do Minho. Retrieved from http://hdl.handle.net/1822/41212

Chicago Manual of Style (16th Edition):

Carmo, Catarina Sofia Rodrigues do. “Role of sirtuin 3 on mitochondrial dynamics in Huntington's disease striatal cells .” 2015. Masters Thesis, Universidade do Minho. Accessed November 27, 2020. http://hdl.handle.net/1822/41212.

MLA Handbook (7th Edition):

Carmo, Catarina Sofia Rodrigues do. “Role of sirtuin 3 on mitochondrial dynamics in Huntington's disease striatal cells .” 2015. Web. 27 Nov 2020.

Vancouver:

Carmo CSRd. Role of sirtuin 3 on mitochondrial dynamics in Huntington's disease striatal cells . [Internet] [Masters thesis]. Universidade do Minho; 2015. [cited 2020 Nov 27]. Available from: http://hdl.handle.net/1822/41212.

Council of Science Editors:

Carmo CSRd. Role of sirtuin 3 on mitochondrial dynamics in Huntington's disease striatal cells . [Masters Thesis]. Universidade do Minho; 2015. Available from: http://hdl.handle.net/1822/41212


Brigham Young University

14. Ridge, Perry Gene. Mitochondrial Genetics of Alzheimer's Disease and Aging.

Degree: PhD, 2013, Brigham Young University

 Mitochondria are essential cellular organelles and the location of the electron transport chain, the site of the majority of energy production in the cell. Mitochondria… (more)

Subjects/Keywords: mitochondrial genetics; haplotypes; mitochondrial copy number; Alzheimer's disease; whole genomes; endophenotypes; Biology

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APA (6th Edition):

Ridge, P. G. (2013). Mitochondrial Genetics of Alzheimer's Disease and Aging. (Doctoral Dissertation). Brigham Young University. Retrieved from https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=4520&context=etd

Chicago Manual of Style (16th Edition):

Ridge, Perry Gene. “Mitochondrial Genetics of Alzheimer's Disease and Aging.” 2013. Doctoral Dissertation, Brigham Young University. Accessed November 27, 2020. https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=4520&context=etd.

MLA Handbook (7th Edition):

Ridge, Perry Gene. “Mitochondrial Genetics of Alzheimer's Disease and Aging.” 2013. Web. 27 Nov 2020.

Vancouver:

Ridge PG. Mitochondrial Genetics of Alzheimer's Disease and Aging. [Internet] [Doctoral dissertation]. Brigham Young University; 2013. [cited 2020 Nov 27]. Available from: https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=4520&context=etd.

Council of Science Editors:

Ridge PG. Mitochondrial Genetics of Alzheimer's Disease and Aging. [Doctoral Dissertation]. Brigham Young University; 2013. Available from: https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=4520&context=etd


University of Oxford

15. Johnson, Andrew William. Metabolic control of energetics in human heart and skeletal muscle.

Degree: PhD, 2012, University of Oxford

 Myocardial and skeletal muscle high energy phosphate metabolism is abnormal in heart failure, but the pathophysiology is not understood. Plasma non-esterified fatty acids (NEFA) increase… (more)

Subjects/Keywords: 612.74045; Metabolism; Cardiovascular disease; heart failure; mitochondrial function; mitochondrial uncoupling protein-3

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APA (6th Edition):

Johnson, A. W. (2012). Metabolic control of energetics in human heart and skeletal muscle. (Doctoral Dissertation). University of Oxford. Retrieved from http://ora.ox.ac.uk/objects/uuid:82c0dce6-a162-4c08-b061-3ea7f2e35134 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.565959

Chicago Manual of Style (16th Edition):

Johnson, Andrew William. “Metabolic control of energetics in human heart and skeletal muscle.” 2012. Doctoral Dissertation, University of Oxford. Accessed November 27, 2020. http://ora.ox.ac.uk/objects/uuid:82c0dce6-a162-4c08-b061-3ea7f2e35134 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.565959.

MLA Handbook (7th Edition):

Johnson, Andrew William. “Metabolic control of energetics in human heart and skeletal muscle.” 2012. Web. 27 Nov 2020.

Vancouver:

Johnson AW. Metabolic control of energetics in human heart and skeletal muscle. [Internet] [Doctoral dissertation]. University of Oxford; 2012. [cited 2020 Nov 27]. Available from: http://ora.ox.ac.uk/objects/uuid:82c0dce6-a162-4c08-b061-3ea7f2e35134 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.565959.

Council of Science Editors:

Johnson AW. Metabolic control of energetics in human heart and skeletal muscle. [Doctoral Dissertation]. University of Oxford; 2012. Available from: http://ora.ox.ac.uk/objects/uuid:82c0dce6-a162-4c08-b061-3ea7f2e35134 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.565959


University of Washington

16. Itsara, Leslie. Characterization of Mitochondrial DNA Mutations in Drosophila melanogaster.

Degree: PhD, 2014, University of Washington

 Mitochondria are vital organelles as they produce the majority of cellular energy in the form of ATP through oxidative phosphorylation (OXPHOS). Mitochondria contain their own… (more)

Subjects/Keywords: Drosophila; Mitochondrial disease; Mitochondrial DNA mutations; Oxidative stress; Genetics; molecular and cellular biology

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APA (6th Edition):

Itsara, L. (2014). Characterization of Mitochondrial DNA Mutations in Drosophila melanogaster. (Doctoral Dissertation). University of Washington. Retrieved from http://hdl.handle.net/1773/25400

Chicago Manual of Style (16th Edition):

Itsara, Leslie. “Characterization of Mitochondrial DNA Mutations in Drosophila melanogaster.” 2014. Doctoral Dissertation, University of Washington. Accessed November 27, 2020. http://hdl.handle.net/1773/25400.

MLA Handbook (7th Edition):

Itsara, Leslie. “Characterization of Mitochondrial DNA Mutations in Drosophila melanogaster.” 2014. Web. 27 Nov 2020.

Vancouver:

Itsara L. Characterization of Mitochondrial DNA Mutations in Drosophila melanogaster. [Internet] [Doctoral dissertation]. University of Washington; 2014. [cited 2020 Nov 27]. Available from: http://hdl.handle.net/1773/25400.

Council of Science Editors:

Itsara L. Characterization of Mitochondrial DNA Mutations in Drosophila melanogaster. [Doctoral Dissertation]. University of Washington; 2014. Available from: http://hdl.handle.net/1773/25400

17. Smith, Cassandra Lauren. Comparative phylogenetic exploration of the human mitochondrial proteome : insights into disease and metabolism.

Degree: PhD, 2019, University of Cambridge

 Mitochondria are a key organelle within human cells, with functions ranging from ATP synthesis to apoptosis. Changes in mitochondrial function are associated with many diseases,… (more)

Subjects/Keywords: Mitochondria; Phylogenetic profiling; Mitochondrial disease; Mitochondrial carriers; Non-enzymatic acetylation; Mammalian ageing

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APA (6th Edition):

Smith, C. L. (2019). Comparative phylogenetic exploration of the human mitochondrial proteome : insights into disease and metabolism. (Doctoral Dissertation). University of Cambridge. Retrieved from https://doi.org/10.17863/CAM.31654 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.763757

Chicago Manual of Style (16th Edition):

Smith, Cassandra Lauren. “Comparative phylogenetic exploration of the human mitochondrial proteome : insights into disease and metabolism.” 2019. Doctoral Dissertation, University of Cambridge. Accessed November 27, 2020. https://doi.org/10.17863/CAM.31654 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.763757.

MLA Handbook (7th Edition):

Smith, Cassandra Lauren. “Comparative phylogenetic exploration of the human mitochondrial proteome : insights into disease and metabolism.” 2019. Web. 27 Nov 2020.

Vancouver:

Smith CL. Comparative phylogenetic exploration of the human mitochondrial proteome : insights into disease and metabolism. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2020 Nov 27]. Available from: https://doi.org/10.17863/CAM.31654 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.763757.

Council of Science Editors:

Smith CL. Comparative phylogenetic exploration of the human mitochondrial proteome : insights into disease and metabolism. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://doi.org/10.17863/CAM.31654 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.763757


George Mason University

18. Jeiran, Kianoush. Mitochondrial Haplogroups in Obese Patients Predisposed to Non-Alcoholic Fatty Liver Disease (NAFLD) .

Degree: 2014, George Mason University

 Liver diseases are considered a significant health problem worldwide. Non-alcoholic fatty liver disease (NAFLD), which is widely considered the hepatic manifestation of the metabolic syndrome,… (more)

Subjects/Keywords: non-alcoholic fatty liver disease; mitochondrial haplogroups; obesity and fatty liver disease; metabolic syndrome and fatty liver disease; mitochondrial genotype and fatty liver disease

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APA (6th Edition):

Jeiran, K. (2014). Mitochondrial Haplogroups in Obese Patients Predisposed to Non-Alcoholic Fatty Liver Disease (NAFLD) . (Thesis). George Mason University. Retrieved from http://hdl.handle.net/1920/9083

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Jeiran, Kianoush. “Mitochondrial Haplogroups in Obese Patients Predisposed to Non-Alcoholic Fatty Liver Disease (NAFLD) .” 2014. Thesis, George Mason University. Accessed November 27, 2020. http://hdl.handle.net/1920/9083.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Jeiran, Kianoush. “Mitochondrial Haplogroups in Obese Patients Predisposed to Non-Alcoholic Fatty Liver Disease (NAFLD) .” 2014. Web. 27 Nov 2020.

Vancouver:

Jeiran K. Mitochondrial Haplogroups in Obese Patients Predisposed to Non-Alcoholic Fatty Liver Disease (NAFLD) . [Internet] [Thesis]. George Mason University; 2014. [cited 2020 Nov 27]. Available from: http://hdl.handle.net/1920/9083.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Jeiran K. Mitochondrial Haplogroups in Obese Patients Predisposed to Non-Alcoholic Fatty Liver Disease (NAFLD) . [Thesis]. George Mason University; 2014. Available from: http://hdl.handle.net/1920/9083

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

19. Rafiei, Hossein 1981-. Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease.

Degree: 2017, University of Saskatchewan

 Non-alcoholic fatty liver disease (NAFLD) is a public health burden. Steatosis as the “first hit”, and oxidative stress, inflammation, mitochondrial dysfunction, and endoplasmic reticulum stress… (more)

Subjects/Keywords: Non-alcoholic fatty liver disease; Mitochondrial dysfunction; endoplasmic reticulum stress; Steatosis

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APA (6th Edition):

Rafiei, H. 1. (2017). Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease. (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/7946

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Rafiei, Hossein 1981-. “Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease.” 2017. Thesis, University of Saskatchewan. Accessed November 27, 2020. http://hdl.handle.net/10388/7946.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Rafiei, Hossein 1981-. “Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease.” 2017. Web. 27 Nov 2020.

Vancouver:

Rafiei H1. Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease. [Internet] [Thesis]. University of Saskatchewan; 2017. [cited 2020 Nov 27]. Available from: http://hdl.handle.net/10388/7946.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Rafiei H1. Molecular mechanisms of protection by dietary polyphenols against free fatty acid-induced mitochondrial dysfunction and endoplasmic reticulum stress in an in vitro model of non-alcoholic fatty liver disease. [Thesis]. University of Saskatchewan; 2017. Available from: http://hdl.handle.net/10388/7946

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


Texas A&M University

20. Tripathi, Utkarsh. PARTIAL INHIBITION OF MITOCHONDRIAL COMPLEX I ACTIVATES STRESS RESPONSE PATHWAYS INDUCING A PROTECTION AGAINST OXIDATIVE STRESS.

Degree: MS, Biochemistry, 2017, Texas A&M University

 We have previously shown that partial inhibition of mitochondrial complex I activity with a small molecule tricycle pyrone compound (code name CP2) averted the development… (more)

Subjects/Keywords: mitohormesis; mitochondrial complex I inhibitor; Alzheimer's Disease; oxidative stress

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APA (6th Edition):

Tripathi, U. (2017). PARTIAL INHIBITION OF MITOCHONDRIAL COMPLEX I ACTIVATES STRESS RESPONSE PATHWAYS INDUCING A PROTECTION AGAINST OXIDATIVE STRESS. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/187299

Chicago Manual of Style (16th Edition):

Tripathi, Utkarsh. “PARTIAL INHIBITION OF MITOCHONDRIAL COMPLEX I ACTIVATES STRESS RESPONSE PATHWAYS INDUCING A PROTECTION AGAINST OXIDATIVE STRESS.” 2017. Masters Thesis, Texas A&M University. Accessed November 27, 2020. http://hdl.handle.net/1969.1/187299.

MLA Handbook (7th Edition):

Tripathi, Utkarsh. “PARTIAL INHIBITION OF MITOCHONDRIAL COMPLEX I ACTIVATES STRESS RESPONSE PATHWAYS INDUCING A PROTECTION AGAINST OXIDATIVE STRESS.” 2017. Web. 27 Nov 2020.

Vancouver:

Tripathi U. PARTIAL INHIBITION OF MITOCHONDRIAL COMPLEX I ACTIVATES STRESS RESPONSE PATHWAYS INDUCING A PROTECTION AGAINST OXIDATIVE STRESS. [Internet] [Masters thesis]. Texas A&M University; 2017. [cited 2020 Nov 27]. Available from: http://hdl.handle.net/1969.1/187299.

Council of Science Editors:

Tripathi U. PARTIAL INHIBITION OF MITOCHONDRIAL COMPLEX I ACTIVATES STRESS RESPONSE PATHWAYS INDUCING A PROTECTION AGAINST OXIDATIVE STRESS. [Masters Thesis]. Texas A&M University; 2017. Available from: http://hdl.handle.net/1969.1/187299


Boston University

21. Mukerji, Shivali. Mitochondrial dysfunction in C. elegans model of Parkinson's disease.

Degree: MS, Medical Sciences, 2019, Boston University

 Parkinson’s disease (PD) is a devastating neurodegenerative disease and the second most prevalent after Alzheimer’s disease. The most characteristic hallmark of Parkinson’s is the presence… (more)

Subjects/Keywords: Neurosciences; C. elegans; L-DOPA; Mitochondrial dysregulation; Oxidative stress; Parkinson's disease

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APA (6th Edition):

Mukerji, S. (2019). Mitochondrial dysfunction in C. elegans model of Parkinson's disease. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/38668

Chicago Manual of Style (16th Edition):

Mukerji, Shivali. “Mitochondrial dysfunction in C. elegans model of Parkinson's disease.” 2019. Masters Thesis, Boston University. Accessed November 27, 2020. http://hdl.handle.net/2144/38668.

MLA Handbook (7th Edition):

Mukerji, Shivali. “Mitochondrial dysfunction in C. elegans model of Parkinson's disease.” 2019. Web. 27 Nov 2020.

Vancouver:

Mukerji S. Mitochondrial dysfunction in C. elegans model of Parkinson's disease. [Internet] [Masters thesis]. Boston University; 2019. [cited 2020 Nov 27]. Available from: http://hdl.handle.net/2144/38668.

Council of Science Editors:

Mukerji S. Mitochondrial dysfunction in C. elegans model of Parkinson's disease. [Masters Thesis]. Boston University; 2019. Available from: http://hdl.handle.net/2144/38668


Washington State University

22. [No author]. Identifying Disease Characteristics, Parent Experience, and Coping Strategies When Predicting Pediatric Illness-Related Stress in Parents of Children with Mitochondrial Disease .

Degree: 2013, Washington State University

Mitochondrial disease (mito) is a group of rare, inherited, chronic, life-limiting, incurable neurodegenerative disorders known to affect children early in life that result from failure… (more)

Subjects/Keywords: Nursing; Childhood Illness; Coping; Mitochondrial Disease; Parent Experience; Parents; Stress

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APA (6th Edition):

author], [. (2013). Identifying Disease Characteristics, Parent Experience, and Coping Strategies When Predicting Pediatric Illness-Related Stress in Parents of Children with Mitochondrial Disease . (Thesis). Washington State University. Retrieved from http://hdl.handle.net/2376/5035

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

author], [No. “Identifying Disease Characteristics, Parent Experience, and Coping Strategies When Predicting Pediatric Illness-Related Stress in Parents of Children with Mitochondrial Disease .” 2013. Thesis, Washington State University. Accessed November 27, 2020. http://hdl.handle.net/2376/5035.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

author], [No. “Identifying Disease Characteristics, Parent Experience, and Coping Strategies When Predicting Pediatric Illness-Related Stress in Parents of Children with Mitochondrial Disease .” 2013. Web. 27 Nov 2020.

Vancouver:

author] [. Identifying Disease Characteristics, Parent Experience, and Coping Strategies When Predicting Pediatric Illness-Related Stress in Parents of Children with Mitochondrial Disease . [Internet] [Thesis]. Washington State University; 2013. [cited 2020 Nov 27]. Available from: http://hdl.handle.net/2376/5035.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

author] [. Identifying Disease Characteristics, Parent Experience, and Coping Strategies When Predicting Pediatric Illness-Related Stress in Parents of Children with Mitochondrial Disease . [Thesis]. Washington State University; 2013. Available from: http://hdl.handle.net/2376/5035

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


University of Hong Kong

23. 文兆晴. Can drugs modulating mitochondrial dynamics be translated into neuroprotection in Parkinson's disease?.

Degree: 2016, University of Hong Kong

 Mitochondria are dynamic and mobile organelles undergoing continuous membrane remodeling. The separating and merging processes of mitochondrial membranes are named fission and fusion respectively. Proper… (more)

Subjects/Keywords: Mitochondrial pathology; Parkinson's disease

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APA (6th Edition):

文兆晴. (2016). Can drugs modulating mitochondrial dynamics be translated into neuroprotection in Parkinson's disease?. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/236253

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

文兆晴. “Can drugs modulating mitochondrial dynamics be translated into neuroprotection in Parkinson's disease?.” 2016. Thesis, University of Hong Kong. Accessed November 27, 2020. http://hdl.handle.net/10722/236253.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

文兆晴. “Can drugs modulating mitochondrial dynamics be translated into neuroprotection in Parkinson's disease?.” 2016. Web. 27 Nov 2020.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

文兆晴. Can drugs modulating mitochondrial dynamics be translated into neuroprotection in Parkinson's disease?. [Internet] [Thesis]. University of Hong Kong; 2016. [cited 2020 Nov 27]. Available from: http://hdl.handle.net/10722/236253.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

文兆晴. Can drugs modulating mitochondrial dynamics be translated into neuroprotection in Parkinson's disease?. [Thesis]. University of Hong Kong; 2016. Available from: http://hdl.handle.net/10722/236253

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation


University of Kentucky

24. Sauerbeck, Andrew David. TRICHLOROETHYLENE EXPOSURE AND TRAUMATIC BRAIN INJURY INTERACT AND PRODUCE DUAL INJURY BASED PATHOLOGY AND PIOGLITAZONE CAN ATTENUATE DEFICITS FOLLOWING TRAUMATIC BRAIN INJURY.

Degree: 2011, University of Kentucky

 The development of Parkinson's disease (PD) in humans has been linked to genetic and environmental factors for many years. However, finding common single insults which… (more)

Subjects/Keywords: Trichloroethylene; Traumatic brain injury; Parkinson's disease; Mitochondrial dysfunction; Pioglitazone; Medical Neurobiology

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APA (6th Edition):

Sauerbeck, A. D. (2011). TRICHLOROETHYLENE EXPOSURE AND TRAUMATIC BRAIN INJURY INTERACT AND PRODUCE DUAL INJURY BASED PATHOLOGY AND PIOGLITAZONE CAN ATTENUATE DEFICITS FOLLOWING TRAUMATIC BRAIN INJURY. (Doctoral Dissertation). University of Kentucky. Retrieved from https://uknowledge.uky.edu/gradschool_diss/133

Chicago Manual of Style (16th Edition):

Sauerbeck, Andrew David. “TRICHLOROETHYLENE EXPOSURE AND TRAUMATIC BRAIN INJURY INTERACT AND PRODUCE DUAL INJURY BASED PATHOLOGY AND PIOGLITAZONE CAN ATTENUATE DEFICITS FOLLOWING TRAUMATIC BRAIN INJURY.” 2011. Doctoral Dissertation, University of Kentucky. Accessed November 27, 2020. https://uknowledge.uky.edu/gradschool_diss/133.

MLA Handbook (7th Edition):

Sauerbeck, Andrew David. “TRICHLOROETHYLENE EXPOSURE AND TRAUMATIC BRAIN INJURY INTERACT AND PRODUCE DUAL INJURY BASED PATHOLOGY AND PIOGLITAZONE CAN ATTENUATE DEFICITS FOLLOWING TRAUMATIC BRAIN INJURY.” 2011. Web. 27 Nov 2020.

Vancouver:

Sauerbeck AD. TRICHLOROETHYLENE EXPOSURE AND TRAUMATIC BRAIN INJURY INTERACT AND PRODUCE DUAL INJURY BASED PATHOLOGY AND PIOGLITAZONE CAN ATTENUATE DEFICITS FOLLOWING TRAUMATIC BRAIN INJURY. [Internet] [Doctoral dissertation]. University of Kentucky; 2011. [cited 2020 Nov 27]. Available from: https://uknowledge.uky.edu/gradschool_diss/133.

Council of Science Editors:

Sauerbeck AD. TRICHLOROETHYLENE EXPOSURE AND TRAUMATIC BRAIN INJURY INTERACT AND PRODUCE DUAL INJURY BASED PATHOLOGY AND PIOGLITAZONE CAN ATTENUATE DEFICITS FOLLOWING TRAUMATIC BRAIN INJURY. [Doctoral Dissertation]. University of Kentucky; 2011. Available from: https://uknowledge.uky.edu/gradschool_diss/133


Georgia State University

25. Chang, Jihye S. Relationships among Processing Speed, Attention, and Biochemical Features in Children Identified with Mitochondrial Disease.

Degree: MA, Psychology, 2011, Georgia State University

Mitochondrial Diseases (MD) are disorders of function in cellular oxidative phosphorylation caused by diverse nuclear DNA and mtDNA mutations and seen in 1/5,000 births.… (more)

Subjects/Keywords: Mitochondrial disease; Oxidative phosphorylation; Neuropsychological outcome; Attention; Processing Speed; Children; Psychology

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APA (6th Edition):

Chang, J. S. (2011). Relationships among Processing Speed, Attention, and Biochemical Features in Children Identified with Mitochondrial Disease. (Thesis). Georgia State University. Retrieved from https://scholarworks.gsu.edu/psych_theses/80

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Chang, Jihye S. “Relationships among Processing Speed, Attention, and Biochemical Features in Children Identified with Mitochondrial Disease.” 2011. Thesis, Georgia State University. Accessed November 27, 2020. https://scholarworks.gsu.edu/psych_theses/80.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Chang, Jihye S. “Relationships among Processing Speed, Attention, and Biochemical Features in Children Identified with Mitochondrial Disease.” 2011. Web. 27 Nov 2020.

Vancouver:

Chang JS. Relationships among Processing Speed, Attention, and Biochemical Features in Children Identified with Mitochondrial Disease. [Internet] [Thesis]. Georgia State University; 2011. [cited 2020 Nov 27]. Available from: https://scholarworks.gsu.edu/psych_theses/80.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Chang JS. Relationships among Processing Speed, Attention, and Biochemical Features in Children Identified with Mitochondrial Disease. [Thesis]. Georgia State University; 2011. Available from: https://scholarworks.gsu.edu/psych_theses/80

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


Universiteit Utrecht

26. Lim, J.L. The relationship between the 'use it or lose it' theory and the mechanisms underpinning Alzheimer's disease.

Degree: 2010, Universiteit Utrecht

 In light of recent research, which has demonstrated a significant energy deficiency in the brains of individuals with Alzheimer’s disease (AD), it has been proposed… (more)

Subjects/Keywords: Geneeskunde; Alzheimer's disease; 'use it or lose it'; neuronal activation; amyloid-beta; soluble amyloid-beta; mitochondrial impairment; mitochondrial theory of aging

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APA (6th Edition):

Lim, J. L. (2010). The relationship between the 'use it or lose it' theory and the mechanisms underpinning Alzheimer's disease. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/179298

Chicago Manual of Style (16th Edition):

Lim, J L. “The relationship between the 'use it or lose it' theory and the mechanisms underpinning Alzheimer's disease.” 2010. Masters Thesis, Universiteit Utrecht. Accessed November 27, 2020. http://dspace.library.uu.nl:8080/handle/1874/179298.

MLA Handbook (7th Edition):

Lim, J L. “The relationship between the 'use it or lose it' theory and the mechanisms underpinning Alzheimer's disease.” 2010. Web. 27 Nov 2020.

Vancouver:

Lim JL. The relationship between the 'use it or lose it' theory and the mechanisms underpinning Alzheimer's disease. [Internet] [Masters thesis]. Universiteit Utrecht; 2010. [cited 2020 Nov 27]. Available from: http://dspace.library.uu.nl:8080/handle/1874/179298.

Council of Science Editors:

Lim JL. The relationship between the 'use it or lose it' theory and the mechanisms underpinning Alzheimer's disease. [Masters Thesis]. Universiteit Utrecht; 2010. Available from: http://dspace.library.uu.nl:8080/handle/1874/179298


Texas Medical Center

27. Moats, Allison. Hypoglycemia in Mitochondrial Disorders.

Degree: MS, 2019, Texas Medical Center

  INTRODUCTION: The electron transport chain (ETC) in mitochondria functions to produce energy in the form of adenosine triphosphate (ATP). Defects in the mitochondrial or… (more)

Subjects/Keywords: hypoglycemia; mitochondria; mitochondrial disorder; mitochondrial disease; glucose; Genetics; Medicine and Health Sciences; Other Genetics and Genomics

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APA (6th Edition):

Moats, A. (2019). Hypoglycemia in Mitochondrial Disorders. (Thesis). Texas Medical Center. Retrieved from https://digitalcommons.library.tmc.edu/utgsbs_dissertations/934

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Moats, Allison. “Hypoglycemia in Mitochondrial Disorders.” 2019. Thesis, Texas Medical Center. Accessed November 27, 2020. https://digitalcommons.library.tmc.edu/utgsbs_dissertations/934.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Moats, Allison. “Hypoglycemia in Mitochondrial Disorders.” 2019. Web. 27 Nov 2020.

Vancouver:

Moats A. Hypoglycemia in Mitochondrial Disorders. [Internet] [Thesis]. Texas Medical Center; 2019. [cited 2020 Nov 27]. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/934.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Moats A. Hypoglycemia in Mitochondrial Disorders. [Thesis]. Texas Medical Center; 2019. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/934

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


North-West University

28. Pretorius, Marianne. Evaluation of metallothionein involvement in the modulation of mitochondrial respiration in mice / Marianne Pretorius.

Degree: 2011, North-West University

 Metallothioneins (MTs) are small, non-enzymatic proteins that are involved in cellular detoxification and metal homeostasis because of their high cysteine content. MTs have also been… (more)

Subjects/Keywords: mitochondrion; metallothionein; oxidative phosphorylation; respiratory chain; mitochondrial disease; MTKO mouse model; complex I deficiency; rotenone; enzyme activity analyses; mitochondrial respiration analyses

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APA (6th Edition):

Pretorius, M. (2011). Evaluation of metallothionein involvement in the modulation of mitochondrial respiration in mice / Marianne Pretorius. (Thesis). North-West University. Retrieved from http://hdl.handle.net/10394/9195

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Pretorius, Marianne. “Evaluation of metallothionein involvement in the modulation of mitochondrial respiration in mice / Marianne Pretorius. ” 2011. Thesis, North-West University. Accessed November 27, 2020. http://hdl.handle.net/10394/9195.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Pretorius, Marianne. “Evaluation of metallothionein involvement in the modulation of mitochondrial respiration in mice / Marianne Pretorius. ” 2011. Web. 27 Nov 2020.

Vancouver:

Pretorius M. Evaluation of metallothionein involvement in the modulation of mitochondrial respiration in mice / Marianne Pretorius. [Internet] [Thesis]. North-West University; 2011. [cited 2020 Nov 27]. Available from: http://hdl.handle.net/10394/9195.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Pretorius M. Evaluation of metallothionein involvement in the modulation of mitochondrial respiration in mice / Marianne Pretorius. [Thesis]. North-West University; 2011. Available from: http://hdl.handle.net/10394/9195

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

29. Jacoupy, Maxime. Perte de fonction de la voie de signalisation <<PINK1/Parkine>> dans la physiopathologie de la maladie de Parkinson - Mécanismes et conséquences : Loss of function of the « PINK1/Parkin » signaling pathway in the pathophysiology of Parkinson’s disease – Mechanisms and consequences.

Degree: Docteur es, Neurobiologie, 2016, Université Pierre et Marie Curie – Paris VI

La maladie de Parkinson (MP) est caractérisée par une dégénérescence des neurones dopaminergiques de la substance noire. Elle est le plus souvent sporadique mais des… (more)

Subjects/Keywords: Parkine; PINK1; Maladie de Parkinson; Machinerie TOM; Import mitochondrial; Biogenèse mitochondriale; Parkine; Parkinson's disease; Mitochondrial biogenesis; 616.8

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

APA (6th Edition):

Jacoupy, M. (2016). Perte de fonction de la voie de signalisation <<PINK1/Parkine>> dans la physiopathologie de la maladie de Parkinson - Mécanismes et conséquences : Loss of function of the « PINK1/Parkin » signaling pathway in the pathophysiology of Parkinson’s disease – Mechanisms and consequences. (Doctoral Dissertation). Université Pierre et Marie Curie – Paris VI. Retrieved from http://www.theses.fr/2016PA066387

Chicago Manual of Style (16th Edition):

Jacoupy, Maxime. “Perte de fonction de la voie de signalisation <<PINK1/Parkine>> dans la physiopathologie de la maladie de Parkinson - Mécanismes et conséquences : Loss of function of the « PINK1/Parkin » signaling pathway in the pathophysiology of Parkinson’s disease – Mechanisms and consequences.” 2016. Doctoral Dissertation, Université Pierre et Marie Curie – Paris VI. Accessed November 27, 2020. http://www.theses.fr/2016PA066387.

MLA Handbook (7th Edition):

Jacoupy, Maxime. “Perte de fonction de la voie de signalisation <<PINK1/Parkine>> dans la physiopathologie de la maladie de Parkinson - Mécanismes et conséquences : Loss of function of the « PINK1/Parkin » signaling pathway in the pathophysiology of Parkinson’s disease – Mechanisms and consequences.” 2016. Web. 27 Nov 2020.

Vancouver:

Jacoupy M. Perte de fonction de la voie de signalisation <<PINK1/Parkine>> dans la physiopathologie de la maladie de Parkinson - Mécanismes et conséquences : Loss of function of the « PINK1/Parkin » signaling pathway in the pathophysiology of Parkinson’s disease – Mechanisms and consequences. [Internet] [Doctoral dissertation]. Université Pierre et Marie Curie – Paris VI; 2016. [cited 2020 Nov 27]. Available from: http://www.theses.fr/2016PA066387.

Council of Science Editors:

Jacoupy M. Perte de fonction de la voie de signalisation <<PINK1/Parkine>> dans la physiopathologie de la maladie de Parkinson - Mécanismes et conséquences : Loss of function of the « PINK1/Parkin » signaling pathway in the pathophysiology of Parkinson’s disease – Mechanisms and consequences. [Doctoral Dissertation]. Université Pierre et Marie Curie – Paris VI; 2016. Available from: http://www.theses.fr/2016PA066387


University of Lund

30. Piel, Sarah. Mitochondrial medicine. New strategies to evaluate drug toxicity and develop pharmacological protection of the cell’s powerhouse.

Degree: 2018, University of Lund

 Mitochondria produce the majority of the cell’s energy. Any dysfunction in, or interference with mitochondrial function can have severe consequences. And yet, it was only… (more)

Subjects/Keywords: Medical and Health Sciences; mitochondria; drug-induced mitochondrial toxicity; mitochondrial disease; mitochondrial medicine; drug development; succinate; methylene blue; metformin; acetaminophen; paracetamol; Kolliphor® EL

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

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

APA (6th Edition):

Piel, S. (2018). Mitochondrial medicine. New strategies to evaluate drug toxicity and develop pharmacological protection of the cell’s powerhouse. (Doctoral Dissertation). University of Lund. Retrieved from https://lup.lub.lu.se/record/86ddb2bd-297e-4c00-a88a-9a0b540c885d ; https://portal.research.lu.se/ws/files/39904541/e_nailing_Sarah.pdf

Chicago Manual of Style (16th Edition):

Piel, Sarah. “Mitochondrial medicine. New strategies to evaluate drug toxicity and develop pharmacological protection of the cell’s powerhouse.” 2018. Doctoral Dissertation, University of Lund. Accessed November 27, 2020. https://lup.lub.lu.se/record/86ddb2bd-297e-4c00-a88a-9a0b540c885d ; https://portal.research.lu.se/ws/files/39904541/e_nailing_Sarah.pdf.

MLA Handbook (7th Edition):

Piel, Sarah. “Mitochondrial medicine. New strategies to evaluate drug toxicity and develop pharmacological protection of the cell’s powerhouse.” 2018. Web. 27 Nov 2020.

Vancouver:

Piel S. Mitochondrial medicine. New strategies to evaluate drug toxicity and develop pharmacological protection of the cell’s powerhouse. [Internet] [Doctoral dissertation]. University of Lund; 2018. [cited 2020 Nov 27]. Available from: https://lup.lub.lu.se/record/86ddb2bd-297e-4c00-a88a-9a0b540c885d ; https://portal.research.lu.se/ws/files/39904541/e_nailing_Sarah.pdf.

Council of Science Editors:

Piel S. Mitochondrial medicine. New strategies to evaluate drug toxicity and develop pharmacological protection of the cell’s powerhouse. [Doctoral Dissertation]. University of Lund; 2018. Available from: https://lup.lub.lu.se/record/86ddb2bd-297e-4c00-a88a-9a0b540c885d ; https://portal.research.lu.se/ws/files/39904541/e_nailing_Sarah.pdf

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