Accedi

Bibliografie tematiche / Muscular dystrophy / Tesi

Segui questo link per vedere altri tipi di pubblicazioni sul tema: Muscular dystrophy.

Tesi sul tema "Muscular dystrophy"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 25 luglio 2025

Cita una fonte nei formati APA, MLA, Chicago, Harvard e in molti altri stili

Scegli il tipo di fonte:

Vedi i top-50 saggi (tesi di laurea o di dottorato) per l'attività di ricerca sul tema "Muscular dystrophy".

Accanto a ogni fonte nell'elenco di riferimenti c'è un pulsante "Aggiungi alla bibliografia". Premilo e genereremo automaticamente la citazione bibliografica dell'opera scelta nello stile citazionale di cui hai bisogno: APA, MLA, Harvard, Chicago, Vancouver ecc.

Puoi anche scaricare il testo completo della pubblicazione scientifica nel formato .pdf e leggere online l'abstract (il sommario) dell'opera se è presente nei metadati.

Vedi le tesi di molte aree scientifiche e compila una bibliografia corretta.

1

Gaschen, Lorrie. "Cardiomyopathy in dystrophin-deficient hypertrophic feline muscular dystrophy /." [S.l.] : [s.n.], 1998. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

2

Howard, Judith. "Electrodiagnostic evaluation of dystrophin-deficient hypertrophic feline muscular dystrophy /." [S.l.] : [s.n.], 2000. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

3

Coovert, Daniel David. "Analysis of dystrophin in duchenne muscular dystrophy and SMN in spinal muscular atrophy /." The Ohio State University, 1998. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487951595500021.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

4

Holst, Holst. "The history of muscular dystrophy." Thesis, University of British Columbia, 1989. http://hdl.handle.net/2429/27477.

Testo completo

Abstract (sommario):

The muscular dystrophies, Duchenne muscular dystrophy being the most common type, are a group for which there is no apparent pathology to the spinal motor neurons concomitant to progressive muscular degeneration. After this fact was established during the nineteenth century through postmortem examination, Charcot divided muscular disease into the "Great Classes" of myopathy and neuropathy. Erb's study of the histopathology brought a further division between the two before death and therefore the muscle biopsy became a tool for differential diagnosis. He also discovered that the response of mus

Gli stili APA, Harvard, Vancouver, ISO e altri

5

Clement, E. "Congenital muscular dystrophy in 2010." Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1318071/.

Testo completo

Abstract (sommario):

Congenital Muscular Dystrophies (CMDs) are a heterogeneous group of conditions that usually present in the first months of life with weakness and hypotonia. Extramuscular manifestations are common and may include brain, skin and eye abnormalities. CMDs are relatively rare disorders and despite the major progress made over the last 2 decades in identifying, mapping and investigating these conditions, there remains a lot to be learned. Little is known about the relative frequency of the various forms of CMD in the UK population. Experience had shown that founder mutations are common in different

Gli stili APA, Harvard, Vancouver, ISO e altri

6

Montanaro, Federica. "The role of dystroglycan in muscular dystrophy and synaptogenesis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0020/NQ55361.pdf.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

7

Rabinowitz, Adam Howard. "Antisense therapies for Duchenne muscular dystrophy." Thesis, Imperial College London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.444590.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

8

Smith, T. J. "Molecular analysis of Duchenne muscular dystrophy." Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233559.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

9

Hodgson, Shirley V. "Genetic studies in Duchenne muscular dystrophy." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235878.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

10

Wakefield, Philip M. "Gene therapy for duchenne muscular dystrophy." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365743.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

11

Bakir, Hadil. "Studies on muscular dystrophy associated genes." Thesis, Durham University, 2007. http://etheses.dur.ac.uk/2143/.

Testo completo

Abstract (sommario):

Muscular dystrophy is a collective group of genetic disorder that results in progressive wasting of skeletal muscle. Dysferlin, the gene responsible for Limb Girdle Muscular Dystrophy type 2B (LGMD2B) and Miyoshi Myopathy (MM) was found to be a member of a newly identified protein family named the ferlins. Recent work has suggested that dysferlin is necessary for efficient calcium sensitive membrane resealing therefore is involved in membrane repair, a mechanism which if defective results in progressive muscle wasting. In this project, the involvement of other genes that could possibly be asso

Gli stili APA, Harvard, Vancouver, ISO e altri

12

Koppaka, Sisir. "Imaging biomarkers for Duchenne muscular dystrophy." Thesis, Massachusetts Institute of Technology, 2015. http://hdl.handle.net/1721.1/106959.

Testo completo

Abstract (sommario):

Thesis: S.M., Massachusetts Institute of Technology, School of Engineering, Center for Computational Engineering, Computation for Design and Optimization Program, 2015.<br>Cataloged from PDF version of thesis.<br>Includes bibliographical references (pages 75-78).<br>Duchenne muscular dystrophy (DMD) is the most common muscular dystrophy of childhood and affects 1 in 3600 male births. The disease is caused by mutations in the dystrophin gene leading to progressive muscle weakness which ultimately results in death due to respiratory and cardiac failure. Accurate, practical, and painless tests to

Gli stili APA, Harvard, Vancouver, ISO e altri

13

Tay, Shaun Li Jian. "Duchenne Muscular Dystrophy—Insight and Treatment." Thesis, The University of Arizona, 2015. http://hdl.handle.net/10150/595055.

Testo completo

Abstract (sommario):

Duchenne Muscular Dystrophy (DMD) is a genetic disorder characterized by progressive degeneration of muscle fibers and dystrophic changes on muscle biopsy¹. DMD accounts for approximately 50% of all dystrophinopathies, with around 21,000 male babies born with the disease each year², ³, ⁴, ⁵. It is also the most lethal X-linked recessive disorder as phenotypic traits are not immediately present at birth¹¹, ³. Patients usually do not live past their 20's without medical intervention to treat associated respiratory and cardiac dysfunctions¹¹, ³. For these reasons DMD remains one of the greatest t

Gli stili APA, Harvard, Vancouver, ISO e altri

14

Wallace, Lindsay M. "Gene Therapy for Facioscapulohumeral Muscular Dystrophy." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1338315498.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

15

Beers, Leanne. "Living With Muscular Dystrophy: Sexual Education." ScholarWorks, 2018. https://scholarworks.waldenu.edu/dissertations/4908.

Testo completo

Abstract (sommario):

Sexual pleasure and intimacy are fundamental and innate human needs. Individuals with physical disabilities often find it difficult to meet these needs because of such factors as impaired mobility and lack of knowledge about sexual health. People with physical disabilities are often seen as asexual and not capable of having sex, and sexuality is often not considered a concern among this population. These misconceptions can result in individuals with physical disabilities not receiving basic sex education or advice and guidance when issues arise. Not receiving this attention may impede disabled

Gli stili APA, Harvard, Vancouver, ISO e altri

16

vianello, sara. "Molecular modifiers in Duchenne muscular dystrophy." Doctoral thesis, Università degli studi di Padova, 2018. http://hdl.handle.net/11577/3426720.

Testo completo

Abstract (sommario):

Duchenne muscular dystrophy (DMD) is an X-linked progressive neuromuscular disease affecting 1:3500 –1/5000 boys at birth. It is caused by the absence of dystrophin, a subsarcolemmal protein that confers membrane stability linking cytoskeletal actin to the extracellular matrix. Dystrophin is part of a multi-protein complex called dystrophin associated protein complex (DAPC), which contains, among the other components, β-dystroglycan and nitric oxide synthase (NOS). The consequences of the absence of dystrophin are: deregulation of calcium homeostasis, tissue necrosis, and progressive accumulat

Gli stili APA, Harvard, Vancouver, ISO e altri

17

Laws, Nicola. "Characterisation and strategic treatment of dystrophic muscle." University of Southern Queensland, Faculty of Sciences, 2005. http://eprints.usq.edu.au/archive/00001457/.

Testo completo

Abstract (sommario):

The mdx mouse is widely used as a model for Duchenne Muscular Dystrophy, a fatal X-linked disease caused by a deficiency of the sub-sarcolemmal protein, dystrophin. This dissertation reports characterisation of the features of dystrophy in the mdx mouse, including parameters such as electrophysiological and contractile properties of dystrophic cardiac tissue, quantitative evaluation of kyphosis throughout the mdx lifespan, and contractile properties of respiratory and paraspinal muscles. Following these characterisation studies, the efficacy of antisense oligonucleotides (AOs) to induce altern

Gli stili APA, Harvard, Vancouver, ISO e altri

18

Anderson, Jennifer Louise Medical Sciences Faculty of Medicine UNSW. "Cerebellar synaptic plasticity in two animal models of muscular dystrophy." Publisher:University of New South Wales. Medical Sciences, 2008. http://handle.unsw.edu.au/1959.4/43524.

Testo completo

Abstract (sommario):

Duchenne muscular dystrophy (DMD) and congenital muscular dystrophy 1A (MDC1A) are the two most common forms of muscular dystrophy in humans, caused by mutations in dystrophin and laminin α2 genes respectively. Both are severe forms of the disease that lead to premature death due and are both now known to have a significant effect on the central nervous system. This project investigated the role of both proteins involved in each of these diseases in cerebellar Purkinje cells of two murine models of disease: the mdx mouse a dystrophin-deficient model of DMD and the dy2J a laminin α2-deficient m

Gli stili APA, Harvard, Vancouver, ISO e altri

19

Abmayr, Simone. "Gene therapy for muscular dystrophy using secondary modifiers of the dystrophic phenotype." [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=973452595.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

20

Judge, Luke Milburn. "Dissecting the signaling and mechanical functions of the dystrophin-glycoprotein complex in skeletal muscle /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/4989.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

21

Kim, Jihee. "Evaluating pathogenesis in FKRP related muscular dystrophy." Thesis, Royal Veterinary College (University of London), 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.731277.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

22

Brais, Bernard. "Oculopharyngeal muscular dystrophy : from phenotype to genotype." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0002/NQ44369.pdf.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

23

Smith, Philip E. M. "Breathing during sleep in Duchenne muscular dystrophy." Thesis, University of Liverpool, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235539.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

24

Babaria, Arati. "Molecular Mechanisms that Underlie Duchenne Muscular Dystrophy." Thesis, The University of Arizona, 2016. http://hdl.handle.net/10150/612573.

Testo completo

Abstract (sommario):

Duchenne muscular dystrophy is an inherited, X-linked recessive skeletal muscle disorder that is characterized by mutations in the dystrophin gene [1]. Therefore, the disease affects primarily males and women are typically carriers. 1 in 3500 males in the United States are affected [1]. Dystrophin is a critical, large scaffolding protein in the dystrophin-glycoprotein complex found at the sarcolemma of skeletal muscle [1]. The complex helps maintain sarcolemma integrity and stability during muscle contractions by coupling the extracellular matrix proteins to the intracellular cytoskeleton in s

Gli stili APA, Harvard, Vancouver, ISO e altri

25

Skyrme, Sarah Louise. "Research decisions : living with Duchenne muscular dystrophy." Thesis, University of Newcastle upon Tyne, 2014. http://hdl.handle.net/10443/2678.

Testo completo

Abstract (sommario):

Duchenne muscular dystrophy (DMD) is a severe form of muscular dystrophy that affects males. Muscle deterioration leads to increasing levels of disability during childhood and adolescence, with death commonly occurring in the late teens or early twenties, although changes in care and treatment are leading to increasing numbers of boys with DMD living into adulthood. Parents and parent-led charities are raising funds to find effective treatments and a cure, and much of the medical research they promote requires the participation of those with DMD. This raises questions about children and young

Gli stili APA, Harvard, Vancouver, ISO e altri

26

Pearce, Marcela. "Genomic structure of the human utrophin gene." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318897.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

27

Reza, Mojgan. "Engineering and optimisation of mini-dystrophin constructs for Duchenne muscular dystrophy gene therapy." Thesis, University of Newcastle upon Tyne, 2015. http://hdl.handle.net/10443/2827.

Testo completo

Abstract (sommario):

Muscular dystrophies (MDs) are inherited disorders characterised by muscle weakness and atrophy. One of the most severe forms is Duchenne muscular dystrophy (DMD) which together with the milder allelic form Becker muscular dystrophy (BMD) are known as the dystrophinopathies and result from defects in the X-linked gene encoding dystrophin. Dystrophin is a structural protein of the muscle that connects the internal cytoskeleton of muscle fibres to the extracellular matrix. DMD is also amongst the most common forms of muscular dystrophy, affecting ~1 in 4000 live male birth and manifests as rapid

Gli stili APA, Harvard, Vancouver, ISO e altri

28

Woolf, Peter James. "Cardiac calcium handling in the mouse model of Duchenne Muscular Dystrophy." University of Southern Queensland, Faculty of Sciences, 2003. http://eprints.usq.edu.au/archive/00001525/.

Testo completo

Abstract (sommario):

The dystrophinopathies are a group of disorders characterised by cellular absence of the membrane stabilising protein, dystrophin. Duchenne muscular dystrophy is the most severe disorder clinically. The deficiency of dystrophin, in the muscular dystrophy X-linked (mdx) mouse causes an elevation in intracellular calcium in cardiac myocytes. Potential mechanisms contributing to increased calcium include enhanced influx, sarcoplasmic reticular calcium release and\or reduced sequestration or sarcolemmal efflux. This dissertation examined the potential mechanisms that may contribute to an intracell

Gli stili APA, Harvard, Vancouver, ISO e altri

29

Cockburn, David James. "Analysis of DMD translocations." Thesis, University of Oxford, 1991. http://ora.ox.ac.uk/objects/uuid:ab53825b-b18e-4f60-954a-4ea9e0435126.

Testo completo

Abstract (sommario):

Duchenne and Becker muscular dystrophies (DMD, BMD) are allelic X-linked diseases which affect approximately one in 3500 male newborns. They are caused by mutations in a gene positioned on the short arm of the X chromosome at Xp21. The first indication of the location of this gene was the description of rare females expressing DMD and who were found to have constitutional X;autosome translocations with an X chromosome breakpoint at this site. There are now 24 such females known worldwide. They express DMD as a consequence of preferential inactivation of the normal X chromosome. In order to con

Gli stili APA, Harvard, Vancouver, ISO e altri

30

Dunant, Patrick. "Strategies for Molecular Therapy of Duchenne Muscular Dystrophy." Diss., lmu, 2003. http://nbn-resolving.de/urn:nbn:de:bvb:19-12429.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

31

Longman, Cheryl Amanda. "Clinical and molecular studies of congenital muscular dystrophy." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.423211.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

32

Weiler, Tracey. "Limb girdle muscular dystrophy in unique Manitoba populations." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ62676.pdf.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

33

Bia, Britta Lydia. "Cardiomyopathy in mouse models of Duchenne muscular dystrophy." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301799.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

34

Clapp, Jannine. "Investigating the molecular genetics of FSH muscular dystrophy." Thesis, University of Nottingham, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.435765.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

35

Bolland, Daniel J. "Comparative mapping of the FSH muscular dystrophy region." Thesis, University of Nottingham, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394920.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

36

Chang, C. F. "Studies of muscle regeneration in avian muscular dystrophy." Thesis, Imperial College London, 1987. http://hdl.handle.net/10044/1/38258.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

37

Crisp, Edmund Alastair D. "Heart function in mouse models of muscular dystrophy." Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:b0dedd86-00d8-4f89-a197-3b78ab989524.

Testo completo

Abstract (sommario):

Duchenne muscular dystrophy (DMD) is an X-linked recessive disease caused, in most cases, by the complete absence of the 427 kD cytoskeletal protein, dystrophin. Without dystrophin, the dystrophin-associated protein complex (DAPC) does not form and the plasma membrane is destabilised. There is no effective treatment and affected individuals die from respiratory failure and cardiomyopathy by age 30. This thesis describes experiments in which in vivo cardiac function was measured using non-invasive magnetic resonance imaging in a number of mouse models relevant to muscular dystrophy. As syncoili

Gli stili APA, Harvard, Vancouver, ISO e altri

38

Winnard, Alissa Vira. "Exception patients in Duchenne and Becker muscular dystrophy /." The Ohio State University, 1993. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487847309050842.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

39

Meredith, Christopher. "Molecular genetic investigation of autosomal dominant muscular dystrophy." Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2001. https://ro.ecu.edu.au/theses/1509.

Testo completo

Abstract (sommario):

This thesis contributes to the Human Genome Project by adding detail to the physical and genetic maps of the human genome, and by identifying a strong candidate gene for a form of distal myopathy. Genomic clones for the human skeletal muscle genes slow troponin (TNN/1), alpha actin (ACTA1), and (3-tropomyosin (TPM2) were isolated for use in the fluorescent in situ hybridisation localisation of these genes on the cytogenetic map of the human genome. The localisation of these genes made them potential candidates for inherited skeletal muscle diseases, including the muscular dystrophies investiga

Gli stili APA, Harvard, Vancouver, ISO e altri

40

Fusto, Aurora. "Genetic and clinical modifiers in Duchenne muscular dystrophy." Doctoral thesis, Università degli studi di Padova, 2019. http://hdl.handle.net/11577/3423193.

Testo completo

Abstract (sommario):

La distrofia muscolare di Duchenne (DMD) è una malattia neuromuscolare causata da mutazioni del gene codificante per la distrofina (DMD) che ne impediscono la produzione. Sebbene tutti i pazienti affetti da DMD condividano lo stesso difetto biochimico di distofina, a livello fenotipico è osservabile una grande varietà in termini di progressione della malattia, ad esempio nell'età di perdita della deambulazione o nell'età di insorgenza di complicanze cardiache e respiratorie. Questa variabilità è dovuta a diversi fattori, alcuni di origine ambientale (ad esempio la qualità delle cure a cui hann

Gli stili APA, Harvard, Vancouver, ISO e altri

41

Dutton, Anna Louise. "An investigation into the effects of dystrophin on the lateral mobility of muscle membrane components." Thesis, Durham University, 1999. http://etheses.dur.ac.uk/4576/.

Testo completo

Abstract (sommario):

Dystrophin is the product of the Duchenne Muscular Dystrophy gene locus, whose absence results in progressive skeletal muscle breakdown. Despite considerable work on the localisation of dystrophin and its associated complex, its role in muscle function remains unclear. In the light of the structural and mechanical instability of the dystrophic membrane, the idea was tested that dystrophin might impart membrane integrity and strength by anchoring membrane proteins and/or delineating the surface into specialised subcellular functional domains. Specifically, because dystrophin shows high sequence

Gli stili APA, Harvard, Vancouver, ISO e altri

42

Lekan, Jaimy Marie. "Exercise-induced mechanisms of muscle adaptation in mdx mice." The Ohio State University, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=osu1095372379.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

43

Johnson, Eric K. "A new model for the dystrophin associated protein complex in striated muscles." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1354554580.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

44

Kaspar, Rita Wen. "Genotype-Phenotype Association Analysis of Dilated Cardiomyopathy in Becker Muscular Dystrophy." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1243469474.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

45

Messaed, Christiane. "Investigation of molecular mechanisms underlying Oculopharyngeal Muscular Dystrophy (OPMD)." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111879.

Testo completo

Abstract (sommario):

Oculopharyngeal Muscular Dystrophy (OPMD) is a late-onset dominant/recessive myopathy caused by the expansion of a polyalanine repeat in exon 1 of the PABPN1 gene. The expression of expanded PABPN1 (expPABPN1) triggers the formation of insoluble nuclear aggregates within muscle fiber nuclei of OPMD patients. These aggregates are enriched in poly(A)RNA and sequester molecular chaperones, ubiquitin and proteasome subunits. In addition to these cellular components, we first identified two novel PABPN1 interacting partners, hnRNPA1 and hnRNPA/B that also localized to the insoluble expPABPN1 aggreg

Gli stili APA, Harvard, Vancouver, ISO e altri

46

Winchester, Catherine Louisa. "Expression of myotonic dystrophy candidate proteins." Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265141.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

47

Fair, Jeanette L. "Effects of compensatory hypertrophy on dystrophic (Bio 14.6) hamster muscle : changes in collagen and myofibrillar protein content." Virtual Press, 1987. http://liblink.bsu.edu/uhtbin/catkey/494971.

Testo completo

Abstract (sommario):

Compensatory hypertrophy was induced on the plantaris (PL) and soleus (SOL) muscles of five week old normal and dystrophic (strain 14.6) hamsters. This was done to indicate whether submaximal exercise would be beneficial in reducing the progression of the muscular dystrophy (i.e., by causing muscle hypertrophy, reducing the total collagen content, and increasing the total protein content of the diseased muscle to approximate that of normal tissue).The hamsters were divided into four groups: 1) dystrophic overload (DO), 2) dystrophic control (DC), 3) normal overload (NO), and 4) normal control

Gli stili APA, Harvard, Vancouver, ISO e altri

48

Newman, Emma E. "An investigation into molecular basis of myotonic dystrophy." Thesis, University of Nottingham, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310951.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

49

Harris, Sarah Elizabeth. "Expression and functional analysis of the transcription factor DMAHP." Thesis, University of Glasgow, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284736.

Testo completo

Gli stili APA, Harvard, Vancouver, ISO e altri

50

Betts, Corinne A. "Exon skipping peptide-pmos for correction of dystrophin in mouse models of duchenne muscular dystrophy." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:545d586a-ad7b-4089-8537-b2677957b874.

Testo completo

Abstract (sommario):

Duchenne muscular dystrophy (DMD) is a fatal, muscle-wasting disorder due to mutations/deletions in the dystrophin gene. Whilst improvements in palliative care have increased the life expectancy of patients, cardiomyopathy and respiratory complications are still the leading causes of death. A potential therapy for the treatment of DMD is antisense oligonucleotides (AOs), which modulate dystrophin pre-mRNA splicing to restore the dystrophin reading frame and generate a truncated functional protein. Conjugation of AOs to cell penetrating peptides (CPP), such as Pip5e-, significantly improves del

Gli stili APA, Harvard, Vancouver, ISO e altri

Offriamo sconti su tutti i piani premium per gli autori le cui opere sono incluse in raccolte letterarie tematiche. Contattaci per ottenere un codice promozionale unico!