Rozprawy doktorskie na temat „Skeletal muscle”
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Foxton, Ruth. "Dysferlin in skeletal muscle and skeletal muscle disease". Thesis, University of Newcastle Upon Tyne, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268429.
Pełny tekst źródłaPathare, Neeti C. "Metabolic adaptations following disuse and their impact on skeletal muscle function". [Gainesville, Fla.] : University of Florida, 2005. http://purl.fcla.edu/fcla/etd/UFE0010024.
Pełny tekst źródłaTypescript. Title from title page of source document. Document formatted into pages; contains 171 pages. Includes Vita. Includes bibliographical references.
Peoples, Gregory Edward. "Skeletal muscle fatigue can omega-3 fatty acids optimise skeletal muscle function? /". Access electronically, 2004. http://www.library.uow.edu.au/adt-NWU/public/adt-NWU20041217.123607.
Pełny tekst źródłaTypescript. This thesis is subject to a 12 month embargo (06/09/05 - 14/09/05) and may only be viewed and copied with the permission of the author. For further information please contact the Archivist. Includes bibliographical references: leaf 195-216.
Salman, Mahmoud M. "Preconditioning in skeletal muscle". Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1446109/.
Pełny tekst źródłaBlackwell, Danielle. "The role of Talpid3 in skeletal muscle satellite cells and skeletal muscle regeneration". Thesis, University of East Anglia, 2017. https://ueaeprints.uea.ac.uk/66948/.
Pełny tekst źródłaBaker, Brent A. "Characterization of skeletal muscle performance and morphology following acute and chronic mechanical loading paradigms". Morgantown, W. Va. : [West Virginia University Libraries], 2007. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=5325.
Pełny tekst źródłaTitle from document title page. Document formatted into pages; contains xii, 270 p. : ill. (some col.). Includes abstract. Includes bibliographical references.
Zhang, Yan. "Cytokines and skeletal muscle wasting". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ47124.pdf.
Pełny tekst źródłaOude, Vrielink Hubertus Hermanus Egbert. "Vasomotion and skeletal muscle perfusion". Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1988. http://arno.unimaas.nl/show.cgi?fid=5409.
Pełny tekst źródłaWalsh, Garrett Lyndon. "Skeletal muscle powered cardiac assist". Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=63879.
Pełny tekst źródłaKochamba, Gary. "Skeletal muscle powered cardiac assist". Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=61746.
Pełny tekst źródłaMofarrahi, Mahroo. "Angiopoietins and skeletal muscle function". Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=106387.
Pełny tekst źródłaLes Angiopoétines sont des ligands pour les cellules endothéliales spécifiques aux récepteurs Tie-2. L'angiopoétine-1 (Ang-1) active les récepteurs Tie-2 dans la vasculature et favorise la survie, la prolifération, la migration et la différentiation. L'Angiopoétine-2 (Ang-2) est synthétisé principalement par les cellules endothéliales et antagonise l'activation des récepteurs Tie-2 induits par Ang-1. Dans des circonstances spéciales, Ang-2 active les récepteurs Tie-2 et favorise l'angiogénèse. Dans cette thèse, j'adresse la régulation et la signification fonctionnelle des Angiopoétines et des récepteurs Tie-2 dans des muscles squelettiques normaux et en régénération. Je décris en premier que les cellules souches musculaires squelettiques produisent Ang-1 et Ang-2 et expriment les récepteurs Tie-2. La production d'Ang-1 et Ang-2 du muscle squelettique augmente de façon significative pendant la différenciation des cellules souches en myotubes. Les conditions d'inflammation systémique telle que la septicémie sévère entraîne une baisse significative des niveaux d'Ang-1 et Tie-2 dans le muscle squelettique et induit simultanément une production d'Ang-2 à travers la voie de signalisation NFκB dépendante. La production d'Ang-2 des muscles squelettiques est aussi sur-régulée par le stress oxydatif. Les expériences in-vitro qui utilisent les ascendants isolés de muscles squelettiques révèlent que ensemble Ang-1 et Ang-2 favorisent la survie, la différentiation de ces cellules mais que seulement Ang-1 induit la prolifération et la migration des muscles ascendants. Ces effets sont négociés partiellement à travers la phosphorylation des récepteurs Tie-2 dérivés de muscles et l'activation des voies de signalisation PI-3 Kinase/AKT et ERK1/2. Dans le modèle cardiotoxique nécrotique induit de muscle blessé chez la souris, l'administration d'adénovirus exprimant Ang-1 quatre jours après l'initiation du muscle blessé montre une amélioration significative de la capacité régénérative du muscle, augmentant l'angiogenèse et la récupération complète de la contractilité du muscle. Ces résultats dévoilent un nouveau et important rôle d'Ang-1 dans la promotion de la régénération du muscle squelettique à travers l'augmentation de l'angiogenèse et de la myogenèse.
Sanderson, Alison Louise. "Regulation of skeletal muscle metabolism". Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318615.
Pełny tekst źródłaWang, Zai, i 王在. "Kinesin-1 in skeletal muscle". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B41757877.
Pełny tekst źródłaSlee, Adrian. "Regulation of skeletal muscle proteolysis". Thesis, University of Nottingham, 2005. http://eprints.nottingham.ac.uk/13105/.
Pełny tekst źródłaSpencer, C. I. "Chemomechanical coupling in skeletal muscle". Thesis, Open University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383710.
Pełny tekst źródłaJones, Garrett Collier. "Skeletal Muscle Recovery and Vibration". BYU ScholarsArchive, 2019. https://scholarsarchive.byu.edu/etd/8285.
Pełny tekst źródłaShue, Guay-Haur. "System models of skeletal muscle". Case Western Reserve University School of Graduate Studies / OhioLINK, 1995. http://rave.ohiolink.edu/etdc/view?acc_num=case1058448071.
Pełny tekst źródłaWang, Zai. "Kinesin-1 in skeletal muscle". Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B41757877.
Pełny tekst źródłaStone, Michael H. "Mechanisms of Skeletal Muscle Hypertrophy". Digital Commons @ East Tennessee State University, 2010. https://dc.etsu.edu/etsu-works/4532.
Pełny tekst źródłaStone, Michael H. "Mechanisms of Skeletal Muscle Hypertrophy". Digital Commons @ East Tennessee State University, 2011. https://dc.etsu.edu/etsu-works/4544.
Pełny tekst źródłaStone, Michael H. "Development of Skeletal Muscle Hypertrophy". Digital Commons @ East Tennessee State University, 2010. https://dc.etsu.edu/etsu-works/4579.
Pełny tekst źródłaDunaway, Dwayne Lee. "Nano-mechanics of skeletal muscle structures /". Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/8022.
Pełny tekst źródłaScionti, Isabella. "Epigenetic Regulation of Skeletal Muscle Differentiation". Thesis, Lyon, 2017. http://www.theses.fr/2017LYSEN084/document.
Pełny tekst źródłaLSD1 and PHF2 are lysine de-methylases that can de-methylate both histone proteins, influencing gene expression and non-histone proteins, affecting their activity or stability. Functional approaches using Lsd1 or Phf2 inactivation in mouse have demonstrated the involvement of these enzymes in the engagement of progenitor cells into differentiation. One of the best-characterized examples of how progenitor cells multiply and differentiate to form functional organ is myogenesis. It is initiated by the specific timing expression of the specific regulatory genes; among these factors, MYOD is a key regulator of the engagement into differentiation of muscle progenitor cells. Although the action of MYOD during muscle differentiation has been extensively studied, still little is known about the chromatin remodeling events associated with the activation of MyoD expression. Among the regulatory regions of MyoD expression, the Core Enhancer region (CE), which transcribes for a non-coding enhancer RNA (CEeRNA), has been demonstrated to control the initiation of MyoD expression during myoblast commitment. We identified LSD1 and PHF2 as key activators of the MyoD CE. In vitro and in vivo ablation of LSD1 or inhibition of LSD1 enzymatic activity impaired the recruitment of RNA PolII on the CE, resulting in a failed expression of the CEeRNA. According to our results, forced expression of the CEeRNA efficiently rescue MyoD expression and myoblast fusion in the absence of LSD1. Moreover PHF2 interacts with LSD1 regulating its protein stability. Indeed in vitro ablation of PHF2 results in a massive LSD1 degradation and thus absence of CEeRNA expression. However, all the histone modifications occurring on the CE region upon activation cannot be directly attributed to LSD1 or PHF2 enzymatic activity. These results raise the question of the identity of LSD1 and PHF2 partners, which co-participate to CEeRNA expression and thus to the engagement of myoblast cells into differentiation
Yeung, Wai Ella, i 楊慧. "Eccentric contraction-induced injury in mammalian skeletal muscle". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29750313.
Pełny tekst źródłaPillitteri, Paul J. "Regeneration of Rat Skeletal Muscle Following a Muscle Biopsy". Ohio University / OhioLINK, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1118087917.
Pełny tekst źródłaArc-Chagnaud, Coralie. "Regulation of antioxidant defenses in the prevention of skeletal muscle deconditioning". Thesis, Montpellier, 2019. http://www.theses.fr/2019MONT4005.
Pełny tekst źródłaMusculoskeletal system plays a key role in organism’s well-functioning and is responsible for a large variety of functions such as posture, locomotion, balance, and activities of daily life. The quality of the skeletal muscle is therefore capital to maintain quality of life and, in the long term, survival. Hypoactivity and aging are two situations that cause skeletal muscle deconditioning, therefore sharing common characteristics: loss of muscle strength, muscular atrophy and MyHC redistribution, as well as IMAT accumulation. To date, there is plenty of evidence supporting a causative link between oxidative stress phenomenon and muscle deconditioning.The general aim of this PhD thesis was to evaluate the impact of the modulation of the antioxidant defenses on the prevention of muscle deconditioning. It has been studied from two perspectives, the first one in the context of aging and the second in the context of hypoactivity.The first study aimed to evaluate frailty in old female animals, using WT and G6PD-overexpressing mice. We evaluated muscle quality parameters and oxidative stress markers. Finally, we performed a transcriptomic analysis of muscle samples and highlighted differentially expressed genes in both groups of mice.The second study was conducted to evaluate the effects of a cocktail enriched in antioxidant/anti-inflammatory molecules in a 2-month hypoactivity experiment (Bedrest model). Our results clearly demonstrate the ineffectiveness of this type of supplementation in the prevention of muscle mass and strength loss. Moreover, data regarding muscle molecular mechanisms highlight an alteration of recovery processes in the supplemented subjects.Finally, the conclusions of our two studies gave clues on the suitable antioxidant modulation strategy for the prevention of skeletal muscle deconditioning. It seems preferable to focus on the stimulation of endogenous defense system whether than towards exogenous supply of nutritional antioxidants. Nevertheless, the complexity of redox signaling requires better understanding to optimize countermeasures in muscle wasting situations
Wood, Stephanie Ann Cardinal Trevor R. "A morphological and hemodynamic analysis of skeletal muscle vasculature : a thesis /". [San Luis Obispo, Calif. : California Polytechnic State University], 2008. http://digitalcommons.calpoly.edu/theses/16/.
Pełny tekst źródła"July 2008." "In partial fulfillment of the requirements for the degree [of] Master of Science in Engineering with a specialization in Biomedical Engineering." "Presented to the faculty of California Polytechnic State University, San Luis Obispo." Major professor: Trevor Cardinal, Ph.D. Includes bibliographical references (leaves 96-101). Also available on microfiche and online.
Aydin, Jan. "Skeletal muscle calcium homeostasis during fatigue : modulation by kinases and mitochondria /". Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-247-7/.
Pełny tekst źródłaVlahovich, Nicole. "The role of cytoskeletal tropomyosins in skeletal muscle and muscle disease". Thesis, View thesis, 2007. http://handle.uws.edu.au:8081/1959.7/32176.
Pełny tekst źródłaMaenhout, Mascha. "Strain fields within contracting skeletal muscle". Eindhoven : Maastricht : Technische Universiteit Eindhoven ; University Library, Maastricht University [Host], 2002. http://arno.unimaas.nl/show.cgi?fid=7018.
Pełny tekst źródłaGeukes, Foppen Remco Jan. "Electrical bistability of skeletal muscle membrane". [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2005. http://dare.uva.nl/document/78574.
Pełny tekst źródłaRaue, Ulrika. "Skeletal muscle gene expression with age". Virtual Press, 2007. http://liblink.bsu.edu/uhtbin/catkey/1370882.
Pełny tekst źródłaSchool of Physical Education, Sport, and Exercise Science
Tallon, Mark J. "Carnosine metabolism in human skeletal muscle". Thesis, University of Chichester, 2005. http://eprints.chi.ac.uk/843/.
Pełny tekst źródłaKwende, Martin M. N. "The biomechanics of skeletal muscle ventricles". Thesis, University of Liverpool, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283451.
Pełny tekst źródłaLevy, Louis Bernard. "Nutrition, infection and skeletal muscle function". Thesis, University of Southampton, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316459.
Pełny tekst źródłaCampbell, Robert N. "Glucose-regulated transcription in skeletal muscle". Thesis, University of Newcastle Upon Tyne, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.427295.
Pełny tekst źródłaAlam, Nasreen. "Malonyl-coa metabolism in skeletal muscle". Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300485.
Pełny tekst źródłaSmith, N. "Thiol signalling in skeletal muscle ageing". Thesis, University of Liverpool, 2018. http://livrepository.liverpool.ac.uk/3026986/.
Pełny tekst źródłaStickland, Neil Charles. "Development and growth of skeletal muscle". Thesis, University of Edinburgh, 1998. http://hdl.handle.net/1842/30012.
Pełny tekst źródłaNikoi, Naa-Dei. "Cellulose nanowhiskers for skeletal muscle engineering". Thesis, University of Manchester, 2017. https://www.research.manchester.ac.uk/portal/en/theses/cellulose-nanowhiskers-for-skeletal-muscle-engineering(30db0446-d55b-40aa-b759-c8e2c71a4cf6).html.
Pełny tekst źródłaWilson, Emma. "Force response of locust skeletal muscle". Thesis, University of Southampton, 2010. https://eprints.soton.ac.uk/190857/.
Pełny tekst źródłaMetzger, Sabrina Kinzie. "Modeling of excitation in skeletal muscle". Wright State University / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=wright1620983611677044.
Pełny tekst źródłaEngland, Eric M. "Postmortem metabolism in porcine skeletal muscle". Diss., Virginia Tech, 2015. http://hdl.handle.net/10919/54580.
Pełny tekst źródłaPh. D.
Myhal, Mark. "Skeletal muscle, age, overload, and oxandrolone/". The Ohio State University, 1999. http://rave.ohiolink.edu/etdc/view?acc_num=osu1488190109868676.
Pełny tekst źródłaJohnston, Nicholas Ian Falkinder. "Arginine vasopressin in foetal skeletal muscle". Thesis, University of Edinburgh, 2000. http://hdl.handle.net/1842/22358.
Pełny tekst źródłaFry, William Mark. "K+ channels in Xenopus skeletal muscle /". St. John's NF : [s.n.], 2001.
Znajdź pełny tekst źródłaNeedham, Elise. "Personalised phosphoproteomics of skeletal muscle metabolism". Thesis, The University of Sydney, 2022. https://hdl.handle.net/2123/28191.
Pełny tekst źródłaEbert, Scott Matthew. "Molecular mechanisms of skeletal muscle atrophy". Diss., University of Iowa, 2012. https://ir.uiowa.edu/etd/4967.
Pełny tekst źródłaSimmers, Jessica L. "nNos localization, muscle function and atrophy in skeletal muscle disorders". Thesis, The Johns Hopkins University, 2013. http://pqdtopen.proquest.com/#viewpdf?dispub=3573097.
Pełny tekst źródłaIn skeletal muscle, loss of neuronal nitric oxide synthase (nNOS) from the sarcolemma has been observed in a few muscular dystrophies and myopathies. However, the extent of this phenomenon, its mechanism, and its physiological impact are not well understood. Using immunofluorescent staining for nNOS, a survey of 161 patient biopsies found absent or reduced sarcolemmal nNOS in 43% of patients. Patient mobility and muscle functional status correlated with nNOS mislocalization from the sarcolemma. Mouse models of inherited and acquired myopathies showed similar loss of sarcolemmal nNOS and impaired mobility and muscle function. A proteomic approach, using mass spectrometry and differentially labeled control and steroid-induced myopathy (SIM) mouse samples, found novel nNOS binding proteins including alpha-actinin-3 (ACTN3), which exhibited decreased interaction with nNOS after steroid treatment. It revealed a potential explanation for impaired muscle function in SIM as nNOS interactions were lost at the sarcomere and gained at the sarcoplasmic reticulum impairing contractility. Treating nNOS-deficient mice with steroids demonstrated that loss of sarcolemmal nNOS reduces muscle contractility and strength in SIM through increased nitric oxide (NO) signaling. In SIM mice treated with a nitric oxide donor and steroids, nitric oxide partially protects the muscle from atrophy and improves muscle fatigability and recovery suggesting nNOS mislocalization also decreases NO availability. These findings show that loss of sarcolemmal nNOS is a common phenomenon that negatively impacts muscle function. Therapeutic strategies targeting nNOS or NO signaling need to allow for the complexity of local nitric oxide content and cellular context.
Tarabees, Reda Zakaria Ibrahim. "Endotoxin induced muscle wasting in avian and murine skeletal muscle". Thesis, University of Nottingham, 2011. http://eprints.nottingham.ac.uk/13001/.
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