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Dissertations / Theses on the topic 'Myasthenic'

Author: Grafiati

Published: 4 June 2021

Last updated: 17 February 2022

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1

Carr, A. S. "An epidemiological study of myasthenia gravis and congenital myasthenic syndromes in Northern Ireland." Thesis, Queen's University Belfast, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.546021.

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2

Abdelgany, Amr. "Gene therapy for congenital myasthenic syndromes." Thesis, University of Oxford, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441062.

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3

Finlayson, Sarah E. "Congenital myasthenic syndromes : current diagnostic and therapeutic aspects." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:5e08ab86-8a20-48b3-86b9-683eb8b2c6e4.

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4

Zoltowska, Katarzyna Marta. "Novel pathogenic mechanisms of myasthenic disorders and potential therapeutic approaches." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:e817f50a-0318-4944-bf67-773af523c4c3.

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Congenital myasthenic syndrome (CMS) and myasthenia gravis (MG) are, respectively, inherited or autoimmunological disorders caused by aberrant neuromuscular transmission, which manifests as fatiguable muscle weakness. A novel subtype of CMS, resulting from mutations in GFPT1 and characterised by a limb girdle pattern of muscle weakness, has been described. The gene encodes L glutamine:D fructose-6-phosphate amidotransferase 1 (GFAT1) – a key rate limiting enzyme in the hexosamine biosynthetic pathway, providing building blocks for glycosylation of proteins and lipids. The research focused on t

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5

Cheung, Jonathan Yu. "Pathogenic mechanisms of RAPSN mutations in congenital myasthenic syndromes." Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:c343ca03-563e-4b4a-9e35-aac09bfc5ea7.

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Rapsyn is essential for clustering acetylcholine receptors (AChR) at the neuromuscular junction (NMJ). Congenital myasthenic syndrome (CMS) due to RAPSN mutations compromises neuromuscular transmission through a deficiency of AChR at the NMJ. RAPSN-CMS is autosomal recessive, and most patients harbour a common mutation p.Asn88Lys. A definitive genetic diagnosis for patients who do not carry the p.Asn88Lys allele can be challenging. In this thesis 10 novel variants in RAPSN are shown to impair AChR clustering in vitro, and are thus defined as pathogenic. The properties of RAPSN mutations p.Val4

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6

Issop, Yasmin. "A GFPT1 deficient mouse model of congenital myasthenic syndrome." Thesis, University of Newcastle upon Tyne, 2017. http://hdl.handle.net/10443/3902.

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Congenital myasthenic syndromes (CMS) are inherited disorders characterised by fatigable muscle weakness resulting from impaired transmission at the neuromuscular junction (NMJ). CMS occur due to mutations in genes encoding proteins responsible for maintaining the structure and function of the NMJ. Glutamine-fructose-6-phosphate transaminase 1 (GFPT1) is the rate-limiting enzyme in the hexosamine biosynthetic pathway which yields precursors required for protein and lipid glycosylation. Mutations in GFPT1 and genes downstream of this pathway are pathogenic for CMS. One hypothesis is that hypogl

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7

Chaouch, Amina. "The clinical and genetic characteristics of congenital myasthenic syndromes." Thesis, University of Newcastle upon Tyne, 2014. http://hdl.handle.net/10443/2748.

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Congenital myasthenic syndromes (CMS) are inherited disorders in which the safety margin of the neuromuscular transmission is compromised. The clinical hallmark of CMS is fatigable weakness. To date, nineteen genes have been implicated in causing this disorder, with most mutations located in postsynaptic proteins. Nevertheless, a great proportion of patients remains with no molecular diagnosis and cannot therefore access optimum therapy. In this thesis, each topic is summarized in one chapter that corresponds to one or part of a selected journal publication, or a book chapter. Chapter 1 is ded

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8

Childs, Lisbeth Ann. "The effects of myasthenic serum on skeletal muscle cells in culture." Thesis, University of Bath, 1985. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.484407.

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Rat muscle cells were grown in culture for use as an experimental model in which to study the myolytic effects of myasthenic serum in vitro. Use was made of a procedure which depends upon the selective uptake of tritium-labelled carnitine by cultured myotubes, loss of which can be monitored following cytolytic damage. The studies demonstrated that heat-inactivated myasthenic serum samples caused myotube-specific lysis in a manner that was dependent on the addition of complement. The concentration and activity of the complement source was shown to be a major factor in detecting myotoxicity. Usi

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9

Nichols, Philip Paul. "Transcriptional regulation of the human nicotinic acetylcholine receptor." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326016.

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10

Pinto, Ashwin. "Specificity of autoantibodies in Lambert-Eaton myasthenic syndrome for neuronal calcium channels." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.342539.

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11

Clausen, Lisa K. J. "Effects of beta-2 adrenergic receptor agonists in DOK7 congenital myasthenic syndromes." Thesis, University of Oxford, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.712079.

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12

Clausen, Lisa. "Effects of beta-2 adrenergic receptor agonists in DOK7 congenital myasthenic syndrome." Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:9360c51b-8497-47ca-bd16-e917a3614a25.

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Congenital myasthenic syndromes (CMS) are a rare group of heterogeneous disorders, characterised by compromised neuromuscular transmission and symptoms of fatiguable muscle weakness. CMS is caused by mutations in genes that affect the structure and function of the neuromuscular junction (NMJ). In about 20% of CMS cases, patients have mutations in the gene DOK7; the protein product, DOK7, is crucial for maintaining the dense aggregation of acetylcholine receptor (AChR) clusters at the NMJ. DOK7-CMS patients do not respond to treatment with acetylcholinesterase inhibitors which are the first lin

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13

Ealing, John. "The use of catalytic nucleic acids in the treatment of congenital myasthenic syndromes." Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393481.

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14

Domville, Jaimee Allison. "Mapping the Allosteric Pathway Leading from a Mutation in the Nicotinic Acetylcholine Receptor to a Congenital Myasthenic Syndrome." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/37037.

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The peripheral and highly lipid-exposed M4 α-helix, although distant from the agonist binding site, channel gate, and other important gating structures, is involved in modulating function of the nicotinic acetylcholine receptor. M4 "senses" changes in the surrounding lipid environment and may consequently affect receptor function by altering specific interactions between the M4 C-terminus and the Cys-loop. An example of this lipid sensing ability is demonstrated by a lipid-facing Cys418 to Trp substitution on αM4 (αM4 C418W) of the muscle-type receptor, which subtly alters protein-lipid inte

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15

Maddison, Paul. "A quantitative study of the immune-mediated neuromuscular disorders of acquired neuromyotonia and Lambert-Eaton myasthenic syndrome." Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285378.

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16

Cruz, Pedro M. Rodríguez. "Undefined myasthenias : clinical and molecular characterisation and optimised therapy." Thesis, University of Oxford, 2017. http://ora.ox.ac.uk/objects/uuid:90f1b53c-a5ec-4fe3-8589-8ea076fc4cbf.

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Congenital myasthenic syndromes (CMS) are a group of heterogeneous disorders caused by mutations in genes encoding for proteins that are essential for neuromuscular transmission. All CMS share the clinical feature of fatigable muscle weakness. The differential diagnosis of CMS is wide, with a range of diseases going from autoimmune myasthenia gravis to muscle disorders. In this thesis, it was shown that measuring antibodies to clustered acetylcholine receptors (AChRs) by cell-based assay is helpful in the differential diagnosis of CMS. The findings of the current investigations showed that mut

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17

Duffield, Michael. "Comparison of the expression pattern of voltage-gated calcium channel subunits and Lambert-Eaton myasthenic syndrome autoantibodies in the mouse colon /." Adelaide, 1999. http://web4.library.adelaide.edu.au/theses/09SB/09sbd857.pdf.

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18

von, Rosch Anthony Stanislav Wierzbicki. "The isolation and characterisation of the genes coding for the calcium channel affected by Lambert-Eaton myasthenic syndrome antibodies in NG108-15 cells." Thesis, University of Oxford, 1992. https://ora.ox.ac.uk/objects/uuid:096b02c9-8c80-4f82-8d4c-8ed2ca59aa2e.

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Lambert-Eaton myasthenic syndrome is a rare paraneoplastic and autoimmune disorder affecting the presynaptic voltage gated calcium channels at the neuromuscular junction. The aim of this project was to isolate the genes coding for the Î±1 and Î±2 subunits of the voltage-gated calcium channel from hybrid neuronal cell lines including NG108-15 whose potassium stimulated <sup>45</sup>Ca<sup>2+</sup> flux is reduced by IgG from patients with Lambert-Eaton myasthenic syndrome. The cDNA libraries were constructed in Î»gt10 from NG108-15 mRNA and screened with PCR products derived from the rabbit ske

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19

Trecenti, Anelize de Souza. "Investigação das mutações responsáveis pela doença de acúmulo de glicogênio tipo II e pela miastenia hereditária em bovinos da raça Brahman no Brasil." Universidade Estadual Paulista (UNESP), 2017. http://hdl.handle.net/11449/152155.

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20

da, Silva Leite Maria Isabel. "Myasthenia Gravis: Investigations into Seronegative Myasthenia." Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.490100.

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Myasdienia gravis (MG) is an antibody-mediated autoimmune disease causing muscle weakness and fatigue. Over 80% of patients with generalised MG have IgG autoantibodies (mostly IgUlj to the native muscle acetylcholine receptor (AChR) at the neuromuscular junction (NM]). AChR-antibody-positive MG (AChR-MG) patients often benefit from thymectomy. Their thymus usually has epithelial hyperplasia and the thymus is thought to be the site of autoimmunisation against AChR. Of the remaining 15-20% of patients with generalised MG, a variable proportion (0-50%) have autoantibodies to muscle-specific kinas

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21

Simpson, John Alexander. "Myasthenia gravis." Thesis, University of Edinburgh, 1991. http://hdl.handle.net/1842/27395.

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The thesis is 72 publications describing the author's hypothesis of an autoimmune basis for myasthenia gravis (MG) and its validation. At the time of the first 24 papers many considered that MG was a syndrome rather than a disease entity, due to a biochemical disorder of the neuromuscular junction. Favoured models were a circulating 'curare-like' substance released from the thymus gland, or a pre-junctional abnormality, possibly causing release of small quanta of acetylcholine at the motor nerve terminals. Endplate receptor substance was speculative. The immunological role of the thymus was un

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22

Armbruster, Lena. "Lambert-Eaton Myasthenie Syndrom." Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-112592.

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23

Verschuuren, Johannes Justus Gerard Maria. "Experimental autoimmune myasthenia gravis." Maastricht : Maastricht : Datawyse ; University Library, Maastricht University [Host], 1989. http://arno.unimaas.nl/show.cgi?fid=5471.

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24

Robb, S. A. "T cells in myasthenia." Thesis, University of Newcastle Upon Tyne, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376234.

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25

Schaffert, Hanne. "Immunpathogenese der Myasthenia gravis." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2015. http://dx.doi.org/10.18452/17213.

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Die Myasthenia Gravis (MG) ist ein Prototyp einer Antikörper-vermittelte Autoimmunerkrankung. Die Autoantikörper richten sich hauptsächlich gegen den Acetylcholinrezeptor (AChR). Welche Bedeutung TH17-Zellen für die Pathogenese der MG haben, konnte bisher noch nie direkt gezeigt werden. Mithilfe des Tiermodells Experimentelle Autoimmune Myasthenia Gravis (EAMG) sollte die Rolle der TH17-Zellen im Rahmen dieser Arbeit analysiert werden. Eine signifikante Anzahl tAChR-spezifischer CD4+ T-Zellen, die IL17 exprimieren, konnte nach der Immunisierung mit torpedo AChR in CFA in Wildtyp-Mäusen (WT) be

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26

Kaufman, Robin L. "Immunoregulation in myasthenia gravis." Thesis, University of British Columbia, 1989. http://hdl.handle.net/2429/30683.

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Myasthenia Gravis (MG) is an autoimmune disorder of neuromuscular transmission. Clinically, the disease is manifested by abnormal muscle fatigue with recovery on resting. Circulating nicotinic acetylcholine receptor antibodies (nAchR Ab) are highly characteristic of myasthenia gravis. These antibodies have been shown to be directly pathogenic at the muscle endplate and are responsible for impaired neuromuscular transmission through several mechanisms. While it is clear that the immune system does not function normally in MG, the mechanisms by which the response to nAchR is initiated and perpe

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27

McConville, John Paul. "Autoantibodies in seronegative myasthenia gravis." Thesis, University of Oxford, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.400295.

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28

EL, KHAILI HASSAN. "Myasthenie, myasthenie grave experimentale auto-immune et syndromes myastheniques induits par l'alphabungarotoxine : effets des glucocorticoides." Strasbourg 1, 1991. http://www.theses.fr/1991STR15068.

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29

Härönen, H. (Heli). "Collagen XIII as a neuromuscular synapse organizer:roles of collagen XIII and its transmembrane form, and effects of shedding and overexpression in the neuromuscular system in mouse models." Doctoral thesis, Oulun yliopisto, 2018. http://urn.fi/urn:isbn:9789526218014.

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Abstract Collagen XIII is a transmembrane protein consisting of intracellular, transmembrane and extracellular domains. The latter can be cleaved by proteases of the furin family at the plasma membrane and in the trans-Golgi network. Both the transmembrane and shed collagen XIII are expressed at the neuromuscular junctions of mice and humans. Such motor synapse passes the contraction signal from the central nervous system to the muscles and brings about all voluntary movements. Loss of both forms of collagen XIII in mice and loss-of-function mutations in the COL13A1 gene in humans leads to con

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30

Labouret, Pascale. "Etude rétrospective de 67 patients myasthéniques." Université Louis Pasteur (Strasbourg) (1971-2008), 1991. http://www.theses.fr/1991STR1M116.

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31

Wang, Hua-Bing. "Immunoregulation in experimental autoimmune myasthenia gravis /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4437-7/.

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32

Buckley, Camilla. "Autoimmunity in thymoma-associated Myasthenia gravis." Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394014.

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33

Burke, Georgina. "Genotype - phenotype correlations in congenital myasthenia." Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.437178.

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34

Betty, Maria. "Molecular genetic studies in hereditary myasthenia." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240536.

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35

RAVEL, CHRISTOPHE. "Myasthenie et pathologies auto-immunes associees." Clermont-Ferrand 1, 1992. http://www.theses.fr/1992CLF13029.

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36

Pereira, Antonio. "Myasthenia gravis : l'histoire de madame h." Lille 2, 1988. http://www.theses.fr/1988LIL2M375.

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37

Koneczny, Inga. "Potential mechanisms in MuSK-myasthenia gravis." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:7b81b941-92c0-47ae-a747-62277394638e.

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Autoimmunity is a failure to tolerate circulating or cell surface expressed self antigens,leading to activation of the immune system and attack of self tissues. Muscle-specific kinase (MuSK) myasthenia gravis (MG) is a disease caused by antibodies to MuSK and hallmarked by fatigable muscle weakness. MuSK is a tyrosine kinase that interacts with low-density lipoprotein receptor-related protein 4 (LRP4), resulting in maintenance of the high density of acetylcholine receptors (AChRs) at the neuromuscular junction; this high density is essential for efficient transmission of signals from nerve to

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38

Gärtner, Sabine Luise. "Kongenitale myasthene Syndrome." Diss., lmu, 2008. http://nbn-resolving.de/urn:nbn:de:bvb:19-87075.

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39

Shi, Fu-Dong. "Immunopathogenesis and nasal tolerance in experimental autoimmune myasthenia gravis /." Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19980525shi.

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40

Glasner, Stefan. "Wirbelsäulendegeneration und Muskelschwäche eine Studie zur Spondylolisthesis und zu myopathologischen Befunden des Musculus erector spinae." Berlin dissertation.de, 2005. http://d-nb.info/98988385X/04.

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41

MARTINENT, LOUIS. "Place de la radiotherapie dans le traitement de la myasthenie : a propos de 30 observations." Lyon 1, 1990. http://www.theses.fr/1990LYO1M439.

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42

PLUCHON, YVES-MARIE. "Evolution des conceptions therapeutiques dans la myasthenie generalisee : a propos de 29 observations recueillies sur 20 ans dans le service de neurologie du c.h.r.u. de nantes." Nantes, 1988. http://www.theses.fr/1988NANT144M.

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43

WADOUX, SYLVIE. "Myasthenie grave : a propos d'un cas clinique ; etude du mecanisme physiopathologique." Amiens, 1994. http://www.theses.fr/1994AMIEM120.

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44

Mayer, Anne. "Antibiotiques contre-indiques dans le traitement de la myasthenie." Strasbourg 1, 1991. http://www.theses.fr/1991STR15076.

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45

VILQUIN, JEAN-THOMAS. "Contribution a la comprehension, au traitement et au diagnostic de la myasthenia gravis." Strasbourg 1, 1992. http://www.theses.fr/1992STR15067.

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46

Messéant, Julien. "Rôle des protéines Wnt et de leurs voies de signalisation associées dans la formation de la jonction neuromusculaire." Thesis, Paris 5, 2014. http://www.theses.fr/2014PA05T068.

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La formation de la jonction neuromusculaire des vertébrés (JNM), une synapse cholinergique périphérique entre les motoneurones et les fibres musculaires squelettiques repose sur la reconnaissance et l’apposition précise des motoneurones présynaptiques sur leurs cibles musculaires postsynaptiques. Les données de la littérature montrent que les morphogènes Wnt agissent comme des régulateurs clés de la formation de la JNM. Cependant, l'identité précise des Wnts, leur collaboration et les mécanismes moléculaires de la signalisation Wnt régissant la formation de la JNM restent encore incompris. A l

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47

Xu, Biying. "Studies of immune mechanisms in myasthenia gravis /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-3265-4/.

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48

Plested, Charles Paul. "Mechanism of action of seronegative myasthenia gravis." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301392.

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49

Moody, Anne Marie. "T-cell receptor studies in myasthenia gravis." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337448.

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50

Croxen, Rebecca. "Molecular genetic studies in hereditary/congenital myasthenia." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267938.

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