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Dissertations / Theses on the topic 'Mitochondrial pathology'

Author: Grafiati

Published: 4 June 2021

Last updated: 31 January 2023

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1

Blaikie, Frances H., and n/a. "Synthesis and characterisation of probes that influence mitochondrial function." University of Otago. Department of Chemistry, 2008. http://adt.otago.ac.nz./public/adt-NZDU20080212.091116.

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The production of reactive oxygen species by mitochondria is implicated in mitochondrial dysfunction associated with a range of diseases and ageing. In addition, reactive oxygen species produced by mitochondria are involved in redox signalling pathways that modulate a number of cell processes. Mitochondria targeted antioxidants comprised of an antioxidant moiety linked to a lipophilic triphenylphosphonium cation have recently been used to decrease oxidative damage to mitochondria and to investigate the involvement of mitochondrial reactive oxygen species in redox signalling. These lipophilic c

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2

Renken, Christian Wolfgang. "The structure of mitochondria /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2004. http://wwwlib.umi.com/cr/ucsd/fullcit?p3141929.

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3

Jiang, Sirui. "Mitochondrial Dynamic Abnormalities in Alzheimer's Diease." Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1536608714970424.

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4

Shum, Laura C. "Mitochondrial Metabolism in Bone Physiology and Pathology." Thesis, University of Rochester, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10792056.

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<p> Worldwide, 1 in 3 women and 1 in 5 men over age 50 will experience fractures due to a decline in bone quality. Elucidating the mechanisms for declining bone quality can lead to better therapeutics. A vital, yet overlooked aspect of bone health is the role of mitochondrial metabolism in both bone physiology and pathology. We have found that the ability of stem cells to differentiate into bone forming osteoblasts is sensitive to mitochondrial dysfunction, and therefore preserving mitochondrial function is essential to maintaining bone quality. In human patient samples, we found that osteogen

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5

Hanson, Bonnie Jean. "Protein based methods for the identification and classification of mitochondrial disorders /." view abstract or download file of text, 2001. http://wwwlib.umi.com/cr/uoregon/fullcit?p3018367.

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Thesis (Ph. D.)--University of Oregon, 2001.<br>Typescript. Includes vita and abstract. Includes bibliographical references (leaves 96-103). Also available for download via the World Wide Web; free to University of Oregon users.

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6

Oglesbee, Devin. "Improving the diagnosis of mitochondrial diseases : application of monoclonal antibody technologies to NADH:ubiquinone oxidoreductase and cytochrome c oxidase defects /." view abstract or download file of text, 2004. http://wwwlib.umi.com/cr/uoregon/fullcit?p3136436.

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Thesis (Ph. D.)--University of Oregon, 2004.<br>Typescript. Includes vita and abstract. Includes bibliographical references (leaves 113-119). Also available for download via the World Wide Web; free to University of Oregon users.

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7

Slipetz, Deborah M. "Characterization of mutations in pediatric mitochondrial myopathies." Thesis, McGill University, 1990. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=60101.

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Mitochondrial myopathies are a group of diverse neuromuscular disorders. Defects in electron transport chain (ETC) subunits have been implicated in pediatric and adult onset cases. Skin fibroblasts from four patients were studied to elucidate the biochemical defects.<br>Cells from two patients with ETC complex I deficiency, showed reduced oxidation of alanine with normal oxidation of succinate. Analysis of complex I subunits indicated deficient synthesis of the 20 kDa subunit in the severely affected patient. In the milder patient, subunit abnormalities were not detected.<br>Fibroblasts from a

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8

Malik, Safarina Golfiani 1963. "Human disorder of energy transduction : molecular pathology." Monash University, Dept. of Biochemistry and Molecular Biology, 2001. http://arrow.monash.edu.au/hdl/1959.1/8335.

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9

Taylor, Robert William. "Mitochondrial respiratory chain dysfunction in human pathology : investigation, pathogenicity and treatment." Thesis, University of Newcastle Upon Tyne, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.577189.

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The work presented in this thesis comprises 100 peer-reviewed publications, mostly original research papers but some key review articles are included, which highlight my ongoing research in understanding the role of mitochondrial respiratory chain dysfunction and mitochondrial DNA (mtDNA) mutation in human pathologies over a twenty year period, and in no small part have contributed to the development of my laboratory as a national referral centre in the UK for diagnostic biochemical and molecular genetic testing, funded by the NHS Specialist Commissioners. A significant proportion (at least 50

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10

van, der Watt George Frederick. "Whole Blood Mitochondrial DNA Depletion in Human Immunodeficiency Virus-Infected Children." Master's thesis, University of Cape Town, 2010. http://hdl.handle.net/11427/2705.

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Background: Nucleoside reverse transcriptase inhibitors (NRTIs) interfere with mitochondrial DNA polymerase gamma causing significant toxic effects, including fatal lactic acidosis. Little is known about mitochondrial DNA (mtDNA) in human immunodeficiency virus (HIV) infected children who face a lifetime exposure to these agents. We performed a cross sectional observation of mtDNA levels in whole blood in a pediatric population to ascertain the relationship between mtDNA, NRTI regimens and parameters of HIV-infection severity. Methods: Whole blood mt:nDNA ratios were determined by real-time PC

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11

Holowiecki, Andrew. "Catalysis of mitochondrial NADH:NAD+ transhydrogenation in adult Ascaris suum (nematoda)." Bowling Green, Ohio : Bowling Green State University, 2009. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=bgsu1256953439.

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12

Phillips, Jonathan. "The investigation of axonal pathology in the cerebellum of patients with mitochondrial disease." Thesis, University of Newcastle upon Tyne, 2016. http://hdl.handle.net/10443/3557.

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Cerebellar ataxia affects 68% of adult patients with mitochondrial disease and is associated with progressive loss of co-ordination, impaired balance, and speech difficulties. In these patients, the cerebellum shows numerous neuropathological changes, and a prominent feature is the appearance of axonal torpedoes which represent swollen axons from Purkinje cells. Axonal torpedoes occur in the proximal portion of the Purkinje cell axon projecting into the granular cell layer and are mainly comprised of hyper phosphorylated neurofilament H. Although they have been reported in mitochondrial diseas

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13

Chrysostomou, Alexia. "Investigating the contribution of synaptic and vascular pathology to neurodegeneration in mitochondrial disease." Thesis, University of Newcastle upon Tyne, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.701152.

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Mutations in mitochondrial DNA (mtDNA) lead to a genetically and phenotypically heterogeneous group of human diseases, mitochondrial disorders. Though patients with mtDNA disease present with multisystemic abnormalities, the central nervous system is usually severely affected. Of the neurological deficits, cerebellar ataxia is the most frequently presenting symptom of patients recruited to the UK MRC Mitochondrial Disease Patient cohort, with a prevalence of 70%. Furthermore, stroke-like episodes are prominent, but not restricted, to patients with the Mitochondrial Encephalomyopathy, Lactic Ac

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14

Gonzalez, Serrano Ligia Elena. "Caractérisation de l'ArgRS mitochondriale humaine et contribution à la compréhension des pathologies liées aux mutations des aminoacyl-ARNt synthétases mitochondriales." Thesis, Strasbourg, 2018. http://www.theses.fr/2018STRAJ074/document.

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Les aminoacyl-ARNt synthétases mitochondriales humaines (aaRS mt) sont des enzymes clés de la traduction mitochondriale. Elles catalysent l'aminoacylation des ARNt par les acides aminés correspondent. Des mutations dans leurs gènes sont corrélées à des pathologies avec un large spectre de phénotypes cliniques, mais aux mécanismes moléculaires sous-jacents encore incompris. L'objectif de ce travail de thèse s'intègre dans les axes scientifiques du laboratoire, mais élargit l'intérêt et les connaissance à un système encore peu exploré: l'arginyl-ARNt synthétase mitochondriale (ArgRS mt). Des mut

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15

Thomas, Kelly Jean. "Pten-induced kinase 1 (PINK1) and its role in mitochondrial function and dynamics." Connect to Electronic Thesis (ProQuest) Connect to Electronic Thesis (CONTENTdm), 2008. http://worldcat.org/oclc/457179676/viewonline.

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16

Ling, Jiqiang. "Role of phenylalanyl-tRNA synthetase in translation quality control." Columbus, Ohio : Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1212111223.

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17

Ohland, Derek Paul. "Systematics of cetaceans using restriction site mapping of mitochondrial DNA." Master's thesis, University of Cape Town, 1992. http://hdl.handle.net/11427/27119.

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A phylogenetic study of eleven cetaceans was undertaken using Restriction Endonuclease Maps (RSM) of mitochondrial DNA (mtDNA). One species from the suborder mysticeti (baleen whales) was sampled, and of the ten odontocetes (toothed whales) sampled two were from the family Ziphiidae (beaked whales) and eight were from the family Delphinidae (dolphins) (each representing a different genus). The primarily opportunistically obtained (i.e. from strandings or accidental death in commercial trawl nets) heart tissue generally yielded high quantities of mtDNA which is needed for double digest fragment

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18

Pang, Wei Wei. "The role of mitochondria in regulating MAPK signalling pathways during oxidative stress." University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2006. http://theses.library.uwa.edu.au/adt-WU2007.0026.

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[Truncated abstract] Reactive oxygen species (ROS) have been implicated to play a major role in many pathological conditions including heart attack and stroke. Their ability to modulate the extracellular signal-regulated protein kinase (ERK) and c-Jun Nterminal kinase (JNK) signalling pathways, thereby influencing cellular response has been well-documented. Recent studies implicate a central role for mitochondria in ERK and JNK activation by ROS although the mechanisms remained unresolved. Using Jurkat T-lymphocyte as a cell model, this study demonstrated increased mitochondrial ROS production

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19

Snell, Cameron Edward. "Mitochondrial modulators of hypoxia-related pathways in tumours." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:33742557-6da8-452d-8374-60ccb9a2dd17.

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The Lon protease is a mitochondrial matrix quality-control protease belonging to the family of AAA+ proteins (ATPases associated with many cellular activities). We had previously found Lon to be upregulated in lung tumours with a non-angiogenic phenotype in a microarray study comparing these to conventional angiogenic tumours. In this project I set out to investigate whether Lon had any role in modulating the hypoxic response of tumour cells. Using a novel monoclonal antibody against Lon, I found that upregulation of Lon was present in breast and lung tumours and that higher levels of Lon are

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20

Price, Nathan Loftus. "The Role of SIRT1 in Preventing Mitochondrial Dysfunction with Obesity and Aging." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10363.

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Mitochondrial function declines with aging and obesity, and has been implicated in the development of many age-related diseases. Caloric restriction (CR) prevents aging and has been shown to induce mitochondrial biogenesis and improve mitochondrial function. These effects may involve increased activity of the \(NAD^+\)-dependent deacetylase SIRT1. Indeed, overexpression of SIRT1 reproduces many of the health benefits of CR including induction of mitochondrial biogenesis by deacetylation and activation of the transcriptional co-activator \(PGC-1\alpha\). Because mitochondria regulate cell

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21

Ho, Lois H. M. "Functional analysis of the promoter regions of alternative oxidase genes from Arabidopsis thaliana." University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2009. http://theses.library.uwa.edu.au/adt-WU2010.0047.

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[Truncated abstract] Mitochondria are semi-autonomous organelles found in almost all eukaryotic cells to contain more than 1000 different proteins. The majority of these proteins are encoded in the nucleus, translated in the cytosol and imported into mitochondria. The overall aim of this study was to characterise the regulation of nuclear-encoded mitochondrial proteins (NEMP). This was carried out in the plant, Arabidopsis thaliana, using the alternative oxidase (AOX) as a model. Specifically, the aims were to i) determine how regulation of NEMP interact with known regulatory pathways/mechani

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22

Bowen, Lance Daniel. "Mitochondrial response to hypoxia and assessment of sub-cellular directed DNA repair on mitigating the effects of ROS induced DNA damage /." abstract and full text PDF (free order & download UNR users only), 2006. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3250680.

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Thesis (Ph. D.)--University of Nevada, Reno, 2006.<br>"December 2006." Includes bibliographical references. Online version available on the World Wide Web. Library also has microfilm. Ann Arbor, Mich. : ProQuest Information and Learning Company, [2006]. 1 microfilm reel ; 35 mm.

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23

Taivassalo, Tanja. "Exercise training as therapy for mitochondrial myopathies : physiological, biochemical and genetic effects." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=37845.

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Patients with mitochondrial myopathies characteristically exhibit pronounced exercise intolerance, often associated with lactic acidosis, tachycardia and muscle weakness. These clinical features are attributable to impaired electron transport chain function in skeletal muscle. The usual etiology is a primary defect in mitochondrial DNA (mtDNA), where the severity of impairment is presumably linked to the ratio of mutant to wild-type mtDNA. This dissertation presents novel therapeutic approaches to these genetic defects, aimed at attenuating mitochondrial dysfunction and ameliorating the clinic

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24

Tai, Yi-Heng [Verfasser], Martin [Akademischer Betreuer] Kerschensteiner, Thomas [Gutachter] Misgeld, and Mikael [Gutachter] Simons. "Mitochondrial pathology in acute and chronic neuroinflammation / Yi-Heng Tai ; Gutachter: Thomas Misgeld, Mikael Simons ; Betreuer: Martin Kerschensteiner." München : Universitätsbibliothek der TU München, 2020. http://d-nb.info/1241740224/34.

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25

Wang, Xinglong. "Impaired Balance of Mitochondria Fission and Fusion in Alzheimer Disease." Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1228318762.

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26

Le, Gris Masha. "Mitochondrial protein expression in the developing brain and in pathological conditions." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670248.

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27

Pandit, Ashish V. "REGULATION OF MITOCHONDRIAL GENE EXPRESSION IN MULTIPLE SCLEROSIS CORTEX." Kent State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=kent1334214461.

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28

Sacks, Jessica Erin. "Targeting Mitochondrial Pathways in Obesity and Type 2 Diabetes." Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1522935947635474.

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29

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." UKnowledge, 2011. http://uknowledge.uky.edu/gradschool_diss/133.

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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 can produce pathology in humans has proved difficult. Exposure to trichloroethylene (TCE) or traumatic brain injury (TBI) has been shown to be linked to PD and it has also been proposed that multiple insults may be needed for disease development. The present studies show that exposure to TCE prior to a TBI can result in pathology similar to early PD and that the interaction of both insults is required for impairment in behaviora

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30

Worgan, Lisa Catherine Women &amp Children's Health UNSW. "The role of nuclear-encoded subunit genes in mitochondrial complex 1 deficiency." Awarded by:University of New South Wales. Women and Children's Health, 2005. http://handle.unsw.edu.au/1959.4/22307.

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BACKGROUND: Mitochondrial complex I deficiency often leads to a devastating neurodegenerative disorder of childhood. In most cases, the underlying genetic defect is unknown. Recessive nuclear gene mutations, rather than mitochondrial DNA mutations, account for the majority of cases. AIM: Our aim was to identify the genetic basis of complex I deficiency in 34 patients with isolated complex I deficiency, by studying six of the 39 nuclear encoded complex I subunit genes (NDUFV1, NDUFS1, NDUFS2, NDUFS4, NDUFS7 and NDUFS8). These genes have been conserved throughout evolution and carry out essentia

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31

Schwitlick, Christina [Verfasser]. "The influence of specific mitochondrial polymorphisms on the α-synuclein-induced pathology in a mouse model of Parkinson's disease / Christina Schwitlick". Magdeburg : Universitätsbibliothek, 2015. http://d-nb.info/1078666679/34.

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32

Szunyogová, Eva. "Understanding the pathogenesis of spinal muscular atrophy by determining the role of survival motor neuron protein in early development." Thesis, University of Aberdeen, 2017. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=237002.

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Spinal Muscular Atrophy (SMA) is caused by mutation or deletion of the Survival Motor Neuron 1 (SMN1), which encodes cell-ubiquitous SMN protein. Although classified as a neuromuscular disease, a range of systemic pathologies is reported in SMA patients. Despite a clear understanding of the genetics, the role of SMN protein in SMA pathogenesis is somewhat unclear, especially in tissues outside the CNS. Here, we describe failed liver development in response to reduced SMN levels, in a Taiwanese mouse model of severe SMA. Molecular analysis revealed significant changes in proteins involved in ce

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33

Breckwoldt, Michael [Verfasser], Thomas [Akademischer Betreuer] Misgeld, Martin [Akademischer Betreuer] Kerschensteiner, Thomas [Akademischer Betreuer] Korn, and Edgar [Akademischer Betreuer] Meinl. "Imaging of mitochondrial redox signals in neuronal physiology and pathology / Michael Breckwoldt. Gutachter: Martin Kerschensteiner ; Thomas Korn ; Edgar Meinl. Betreuer: Thomas Misgeld." München : Universitätsbibliothek der TU München, 2014. http://d-nb.info/1068315911/34.

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34

Breckwoldt, Michael O. [Verfasser], Thomas [Akademischer Betreuer] Misgeld, Martin [Akademischer Betreuer] Kerschensteiner, Thomas [Akademischer Betreuer] Korn, and Edgar [Akademischer Betreuer] Meinl. "Imaging of mitochondrial redox signals in neuronal physiology and pathology / Michael Breckwoldt. Gutachter: Martin Kerschensteiner ; Thomas Korn ; Edgar Meinl. Betreuer: Thomas Misgeld." München : Universitätsbibliothek der TU München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:91-diss-20140225-1171922-0-6.

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35

Schwenzer, Hagen. "Aminoacyl-ARNt synthétases mitochondriales humaines : aspects fondamentaux et contribution à la compréhension de pathologies reliées." Thesis, Strasbourg, 2013. http://www.theses.fr/2013STRAJ045/document.

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Les aminoacyl-ARNt synthetases (aaRS) sont impliquées dans le mécanismes de la traduction. Dans les cellules humaines, il existe deux jeux de gènes nucléaires codant pour les aaRS : un pour les aaRS cytosolique (cyt), le second pour les aaRS mitochondriales (mt). Les aaRS mt sont traduites dans le cytosole, adressées et importées dans la mitochondrie.Mutations dans 9 gènes d’aaRS mt ont été démontrées comme responsables de pathologies mitochondriales. Certaines des mutations n’affectent pas la propriété originelle d’aminoacylation. Il a été proposé que certaines de ces mutations puissent affec

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36

Harland, Micah Thomas. "Neuronal Mitofusin 2 Modulates Neuroinflammation in Acute Systemic Inflammation and Alleviates Pathologies in a Mouse Model for Neurodegenerative Diseases." Case Western Reserve University School of Graduate Studies / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=case1586468876190716.

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37

Wagner, Gregory Randall. "Identification and characterization of altered mitochondrial protein acetylation in Friedreich's ataxia cardiomyopathy." Thesis, Hindawi Publishing Corporation and Oxford Journals and SAGE Journals, 2011. http://hdl.handle.net/1805/4209.

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Indiana University-Purdue University Indianapolis (IUPUI)<br>Friedreich’s Ataxia (FRDA) is a rare and poorly understood autosomal recessive disease caused by a pathological deficiency of the mitochondrial protein frataxin. Patients suffer neurodegeneration, ataxia, diabetes, and heart failure. In an effort to understand the mechanisms of heart failure in FRDA, we investigated the role of the protein modification acetylation, which is highly abundant on mitochondrial proteins and has been implicated in regulating intermediary metabolism. Using mouse models of FRDA, we found that cardiac frataxi

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38

Van, der Merwe Celia. "An investigation into the role of mitochondrial dysfunction in South African Parkinson’s disease patients." Thesis, Stellenbosch : Stellenbosch University, 2012. http://hdl.handle.net/10019.1/71647.

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Thesis (MScMedSC)--Stellenbosch University, 2012.<br>Bibliography<br>ENGLISH ABSTRACT: Parkinson’s disease (PD) is a neurodegenerative movement disorder characterized by the loss of dopaminergic neurons in the substantia nigra of the midbrain. Although the aetiology of PD is still not fully understood, it is thought to involve a combination of environmental (such as exposure to pesticides and neurotoxins) and genetic factors. A number of PD-causing genes have been found including SNCA, LRRK2, EIF4G1 and VPS35 (for autosomal dominant forms of PD) and parkin, PINK1, DJ-1 and ATP13A2 (for autosom

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Bashir-Tanoli, Sumayia. "Impact of mitochondrial genetic variation and immunity costs on life-history traits in Drosophila melanogaster." Thesis, University of Stirling, 2014. http://hdl.handle.net/1893/21855.

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Immune activation is generally acknowledged to be costly. These costs are frequently assumed to result from trade-offs arising due to the reallocation of resources from other life-history traits to be invested in immunity. Here, I investigated the energetic basis of the costs associated with immune activation in Drosophila melanogaster. I found that immune activation significantly reduced fly fecundity (45%) and also caused a decline in metabolic rate (6%) but had no effect on body weight. To understand the factors behind reduced fecundity and metabolic rate I measured feeding and found that f

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Weerakoon, Tasmeen Shiny. "Investigation of a putative mitochondrial Twin Arginine Translocation pathway in Arabidopsis thaliana." Miami University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=miami1501256746410956.

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Assaly, Rana. "Protection du myocarde ischémique et pore géant mitochondrial : applications pharmacologiques." Phd thesis, Université Paris Sud - Paris XI, 2011. http://tel.archives-ouvertes.fr/tel-00734466.

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La maladie coronaire d'origine ischémique reste l'une des principales causes de mortalité dans le monde industrialisé. Le traitement de l'ischémie aiguë du myocarde est cependant entré dans une nouvelle ère où la mortalité peut être diminuée de moitié en utilisant des procédures qui permettent un retour rapide du débit sanguin dans la zone ischémique du myocarde, c'est-à-dire la revascularisation. Toutefois, cette reperfusion entraîne par elle-même des complications appelées lésions de la reperfusion qui ont été décrites pour la première fois par Jennings et al., en 1960. Par conséquent, le dé

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Bris, Céline. "Influence de la génétique mitochondriale en pathologie : apport des techniques de séquençage haut débit Deep sequencing shows that oocytes are not prone to accumulate mtDNA heteroplasmic mutations during ovarian ageing Novel NDUFS4 gene mutation in an atypical late-onset mitochondrial form of multifocal dystonia." Thesis, Angers, 2017. http://www.theses.fr/2017ANGE0093.

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Les maladies mitochondriales sont des pathologies fréquentes du métabolisme caractérisées par une forte hétérogénéité clinique et génétique, notamment par la dépendance à 2 génomes, nucléaire (ADNn) et mitochondrial (ADNmt), et le concept d’hétéroplasmie (HT). L’objectif de ce travail de thèse a été de développer une stratégie d’analyse de l’ADNmt par séquençage haut-débit (NGS), puis de l’appliquer à l’étude des maladies mitochondriales et des pathologies liées au vieillissement : glaucome à angle ouvert (GPAO) et vieillissement ovarien précoce. Après validation des performances de notre stra

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Carneiro, Lionel. "Détection hypothalamique de l'hyperglycémie : rôle de la dynamique mitochondriale dans la signalisation par les espèces actives de l'oxygène." Phd thesis, Université de Bourgogne, 2011. http://tel.archives-ouvertes.fr/tel-00689166.

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L'homéostasie énergétique se définit comme le maintien de l'équilibre entre les apports et les dépenses d'énergie. La régulation nerveuse de cet équilibre est principalement assurée par l'hypothalamus. Il existe dans cette structure des neurones spécialisés dont l'activité électrique est modifiée par des signaux nerveux, métaboliques et hormonaux.Nous avons travaillé sur la détection du glucose dans cette structure, qui permet l'élaboration d'une réponse adaptée en termes de prise alimentaire et de contrôle du métabolisme. Lors de cette détection, l'utilisation du glucose conduit à la formatio

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Taylor, Matthew A. "The effect of varying times of ischemia on the levels of glutathione in the cytosol and mitochondria of the rat kidney." Virtual Press, 2002. http://liblink.bsu.edu/uhtbin/catkey/1236375.

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Ischemia caused by the disruption of blood flow results in kidney damage and dysfunction. This study investigated the effects of 30, 60 or 120 minutes of renal ischemia on the levels of glutathione (GSH), the major antioxidant inside cells. Kidneys from anesthetized female Lewis rats (9 months old) were clamped to induce ischemia and then homogenized and separated into cytosolic and mitochondria fractions by differential centrifugation. The levels of GSH and oxidized glutathione (GSSG) in the fractions were measured spectrophotometrically or by capillary electrophoresis. A significant reductio

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Bedoya, Felipe. "Identification and Characterization of Mitochondrial Genome Concatemers in AIDS-Associated Lymphomas and Lymphoma Cell Lines." [Tampa, Fla] : University of South Florida, 2009. http://purl.fcla.edu/usf/dc/et/SFE0003030.

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Montaigne, David. "Pathologie du métabolisme énergétique cardiaque induite par la doxorubicine." Lille 2, 2010. http://www.theses.fr/2010LIL2S018.

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La doxorubicine est une anthracycline utilisée largement dans le traitement des cancers du sein et des hémopathies malignes, mais présente une cardiotoxicité qui en limite l’utilisation. Cette toxicité est attribuée en grande partie aux conséquences des anthracyclines sur le métabolisme énergétique cardiaque : les anthracyclines produisent au niveau cellulaire des espèces radicalaires de l’oxygène à l’origine d’une inhibition de la chaîne respiratoire mitochondriale, d’une dissipation du potentiel de membrane mitochondriale, d’une surcharge calcique mitochondriale. L’hypothèse de notre travail

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Beauvais, Geneviève. "Molecular and cellular bases for the protective effects of dopamine D1 receptor antagonist, SCH23390, against methamphetamine-induced neurotoxicity in the rat brain." Phd thesis, Université René Descartes - Paris V, 2012. http://tel.archives-ouvertes.fr/tel-00691924.

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Methamphetamine (METH) is a potent psychostimulant known to cause cognitive abnormalities and neurodegenerative changes in the brains of METH abusers. One approach for developing therapies for METH abuse is to understand the molecular mechanisms of toxicity of the drug. Investigations in our laboratory and elsewhere have shown that single intraperitoneal injections of METH (30-40 mg/kg of body weight) can cause damage to striatal and cortical monoaminergic systems and induce neuronal apoptosis in the striatum of rodents via activation of endoplasmic reticulum (ER) and mitochondrial death pathw

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Mary, Arnaud. "Implications de la signalisation de la protéine kinase activée par l’AMP (AMPK) dans les dysfonctions mitochondriales, la pathologie amyloïde et Tau, et la neuroinflammation dans la maladie d’Alzheimer." Electronic Thesis or Diss., Université Côte d'Azur, 2022. http://theses.univ-cotedazur.fr/2022COAZ6001.

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La maladie d’Alzheimer (MA) est la pathologie neurodégénérative la plus répandue dans le monde. L’échec des traitements ciblant l’amyloïde beta (Aβ), un catabolite de la protéine précurseur de l’amyloïde (APP), souligne le caractère multifactoriel de cette pathologie. Ainsi, les défauts précoces de la structure et de la fonction des mitochondries et la neuroinflammation sont impliqués dans le développement de la MA. Différentes études décrivent l’AMPK (AMP-activated protein kinase) comme étant un acteur majeur de l'homéostasie mitochondriale notamment via l’élimination des mitochondries altéré

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Marmolino, Daniele. "Alterations of mitochondrial biogenesis and alterations of mitochondrial antioxidant defense in Friedreich's ataxia." Doctoral thesis, Universite Libre de Bruxelles, 2011. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209972.

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Friedreich’s ataxia (FRDA) is an autosomal recessive inherited disorder affecting approximately 1 every 40,000 individuals in Western Europe, is characterized by progressive gait and limb ataxia, dysarthria, areflexia, loss of vibratory and position sense, and a progressive weakness of central origin. Additional features particularly include an hypertrophic cardiomyopathy that can cause premature death. A large GAA repeat expansion in the first intron of the FXN gene is the most common mutation underlying FRDA. Patients show severely reduced levels of the FXN-encoded mitochondrial protein frat

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Haut, Sandrine. "Place de la biologie moléculaire dans le diagnostic des cytopathies mitochondriales." Paris 5, 1998. http://www.theses.fr/1998PA05P151.

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